{
  "version": "2026-11-06-completion",
  "reviewed_at": "2026-11-06",
  "domains": [
    {
      "id": "GP",
      "name": "General practice"
    },
    {
      "id": "CAH",
      "name": "Child and adolescent health"
    },
    {
      "id": "OGN",
      "name": "Obstetrics, gynaecology and the newborn"
    },
    {
      "id": "MH",
      "name": "Mental health"
    },
    {
      "id": "RAPP",
      "name": "Rehabilitation, aged care and palliative care"
    },
    {
      "id": "Bridge",
      "name": "Acute presentations"
    }
  ],
  "gp_groups": [
    "Prevention and lifestyle",
    "Cardiovascular, metabolic and renal",
    "Respiratory and sleep",
    "General symptoms and blood",
    "Gastrointestinal and liver",
    "Urinary and men’s health",
    "Sexual health and relationships",
    "Breast and skin",
    "Eye, ear, nose and throat",
    "Neurology and musculoskeletal",
    "Surgery"
  ],
  "presentations": {
    "P001": "Abdominal distension",
    "P002": "Abdominal pain (including but not limited to: generalised, centralised, upper, lower, flank)",
    "P003": "Abnormal antenatal presentations (including: reduced fetal movement)",
    "P004": "Abnormal bleeding and bruising",
    "P005": "Abnormal development",
    "P006": "Abnormal growth (including abnormal feeding)",
    "P007": "Abnormal speech and communication (including unclear communication and speech)",
    "P008": "Abnormal uterine bleeding (including: metrorrhagia, menorrhagia, amenorrhea)",
    "P009": "Agitation (including aggression)",
    "P010": "Alcohol-related presentations",
    "P011": "Altered body image",
    "P012": "Altered bowel habit",
    "P013": "Altered conscious state (including but not limited to: intoxication, shock, trauma)",
    "P014": "Altered eating pattern",
    "P015": "Altered sleep",
    "P016": "Altered urinary volume (including but not limited to: anuria, oliguria, polyuria)",
    "P017": "Antenatal care",
    "P018": "Anxiety (with or without worrying)",
    "P019": "Breast lump",
    "P020": "Breast pain (mastalgia)",
    "P021": "Cognitive impairment",
    "P022": "Chest pain",
    "P023": "Chronic disease assessment (including but not limited to: diabetes mellitus, asthma, chronic obstructive pulmonary disease, chronic kidney disease, degenerative joint disease, rheumatoid arthritis, chronic pain)",
    "P024": "Confusion",
    "P025": "Constipation",
    "P026": "Cough",
    "P027": "Depressed mood",
    "P028": "Diarrhoea",
    "P029": "Difficulty walking",
    "P030": "Dizziness",
    "P031": "Drug misuse",
    "P032": "Dying/terminal care",
    "P033": "Dysphagia",
    "P034": "Dyspnoea",
    "P035": "Ear pain",
    "P036": "Elevated mood",
    "P037": "Erectile dysfunction",
    "P038": "Eye pain",
    "P039": "Facial pain (including jaw pain)",
    "P040": "Falls",
    "P041": "Fertility visit (including subfertility and unwanted fertility)",
    "P042": "Fever (including post-operative fever)",
    "P043": "Frailty",
    "P044": "Functional impairment (including but not limited to: poor self-care, social withdrawal)",
    "P045": "Geriatric assessment visit",
    "P046": "Haematemesis",
    "P047": "Haematuria",
    "P048": "Haemoptysis",
    "P049": "Headache",
    "P050": "Hearing loss",
    "P051": "Heart murmur",
    "P052": "High blood pressure",
    "P053": "Inguinoscrotal lumps",
    "P054": "Inguinoscrotal pain",
    "P055": "Jaundice",
    "P056": "Joint pain (including but not limited to: back, hip, knee, neck, shoulder, pelvic instability, sacroiliac joint, lower back)",
    "P057": "Joint swelling",
    "P058": "Labour and birth",
    "P059": "Lack of energy (including but not limited to: lethargy, fatigue, tiredness, malaise, non-specific presentations)",
    "P060": "Loss of consciousness (including but not limited to: anaesthetised patient, transient, trauma)",
    "P061": "Low blood pressure",
    "P062": "Lump",
    "P063": "Melaena",
    "P064": "Muscle weakness – generalised and regional",
    "P065": "Musculoskeletal pain – generalised and regional (including but not limited to: bone, muscle ache, lower limb, loin pain, pelvic floor/perineum)",
    "P066": "Neck lump",
    "P067": "Nipple discharge (including: lactation)",
    "P068": "Paediatric behavioural problems",
    "P069": "Paediatric mental health issues",
    "P070": "Pain (chronic, acute, neuropathic, nociceptive, radicular)",
    "P071": "Pallor",
    "P072": "Palpitations",
    "P073": "Perianal lump",
    "P074": "Perianal pain",
    "P075": "Polydipsia",
    "P076": "Pre-operative assessment",
    "P077": "Preventative health assessment",
    "P078": "Pruritus",
    "P079": "Psychological trauma",
    "P080": "Rash",
    "P081": "Rectal bleeding",
    "P082": "Red eye",
    "P083": "Rehabilitation assessment visit (including SMART goal setting)",
    "P084": "Rhinorrhoea",
    "P085": "Seizure",
    "P086": "Self-harm (including: suicidality)",
    "P087": "Sensory disturbance",
    "P088": "Sexual dysfunction",
    "P089": "Skin lumps",
    "P090": "Skin ulcers",
    "P091": "Somatic complaints",
    "P092": "Sore throat",
    "P093": "Sweating",
    "P094": "Swelling – generalised and regional (including but not limited to: generalised, lower limb, peripheral oedema)",
    "P095": "Tinnitus",
    "P096": "The seriously unwell child",
    "P097": "The unsettled infant",
    "P098": "Trauma (including but not limited to: lacerations, head injuries, soft tissue injuries, joint injuries, fracture, dislocations, non-accidental injury)",
    "P099": "Tremor",
    "P100": "Unusual thoughts or behaviours",
    "P101": "Urinary symptoms (including but not limited to: frequency, dysuria, nocturia, lower urinary tract symptoms, incontinence)",
    "P102": "Vision loss",
    "P103": "Vomiting (including nausea)",
    "P104": "Weight gain",
    "P105": "Weight loss",
    "P106": "Well child visit",
    "P107": "Wheeze/stridor (including: respiratory distress, noisy breathing)",
    "P108": "Wounds"
  },
  "units": [
    {
      "id": "G01",
      "domain": "GP",
      "group": "Prevention and lifestyle",
      "title": "Prevention, screening and vaccination",
      "focus": "Age/risk-appropriate screening, shared decisions, follow-up of abnormal results, care after a cancer diagnosis and immunisations.",
      "first_pass": true,
      "priority": "Core",
      "saq_cases": [
        {
          "id": "deck-gp-cervical-breast-screening",
          "title": "Cervical and breast cancer screening",
          "set": "MD3 SAQ Revision Deck"
        },
        {
          "id": "deck-gp-bowel-cancer-screening",
          "title": "Bowel cancer screening",
          "set": "MD3 SAQ Revision Deck"
        },
        {
          "id": "deck-gp-herpes-zoster-older-adult",
          "title": "Herpes zoster and immunisation in older adults",
          "set": "MD3 SAQ Revision Deck"
        }
      ],
      "core_ids": [
        "P077",
        "P106"
      ],
      "gp_tasks": [
        "Counsel on age/risk-based cancer screening and vaccination",
        "Use SNAP/5As and follow up positive screening results"
      ],
      "notes": "### Principles\n\nScreening is for asymptomatic people. **Symptoms require diagnostic assessment**, not a screening test.\n\nDiscuss harms alongside benefit: false-positive results, unnecessary procedures, overdiagnosis and false reassurance. Agree who will convey each result and act on an abnormal test.\n\nTailor prevention to the person's risks: smoking, alcohol, nutrition, activity, blood pressure, mental health, sexual health, family history and previous screening.\n\nAsk Aboriginal and Torres Strait Islander patients whether they wish to identify, and offer culturally safe care, an Aboriginal health worker or a community-controlled service where preferred. Use a qualified interpreter and teach-back to confirm understanding. Missed care often reflects transport, cost, disability or competing priorities; address those barriers.\n\n### Cervical screening\n\n- **Eligibility:** people with a cervix aged `25–74` who have ever had sexual contact, including those vaccinated against HPV, since vaccines do not cover every oncogenic type.\n- **Test:** HPV testing every `five years`, on a self-collected vaginal or clinician-collected cervical sample. Self-collection tests for HPV only and cannot provide cytology.\n- **HPV 16/18:** refer for colposcopy. These types carry the highest risk of high-grade disease.\n- **Other oncogenic HPV:** reflex cytology on the same sample; a self-collected sample needs a clinician-collected sample for cytology. High-grade or glandular cytology means colposcopy.\n\nWith other oncogenic HPV and negative or low-grade cytology (pLSIL or LSIL), most infections clear and the risk of high-grade disease is low, so the HPV test is repeated in `12 months` rather than referring at once. If HPV is no longer detected, five-yearly screening resumes; HPV 16/18 at any repeat means colposcopy. Persisting other oncogenic HPV with negative or low-grade cytology leads to a second repeat at `24 months`, and any HPV then means colposcopy. People who identify as Aboriginal or Torres Strait Islander, those aged 50 or over and those at least two years overdue at the first test are referred for colposcopy if any HPV is found at the 12-month repeat. Follow-up after treatment for high-grade disease, and screening in immune deficiency, have separate pathways.\n\n> [!counsel]\n> HPV is very common and the immune system usually clears it within one to two years. A positive result is not a diagnosis of cancer; the repeat test checks whether the infection has cleared, and colposcopy is arranged if it persists.\n\n> [!pitfall]\n> Persistent postcoital or unexplained bleeding needs examination and diagnostic investigation, even after a negative screen.\n\n### Clinician-collected cervical sample\n\nOffer self-collection to eligible asymptomatic patients once HPV screening has been explained. For clinician collection:\n\n1. Explain the speculum, the brief brushing sensation, possible spotting and the right to stop.\n2. Obtain consent, offer a chaperone, and position and drape comfortably.\n3. Insert a suitable speculum gently, visualise the cervix and collect into the medium specified by the kit.\n4. Arrange result follow-up.\n\nSymptomatic bleeding may need a clinician-collected co-test and diagnostic examination; self-collection alone is insufficient.\n\n### Breast screening\n\nBreastScreen invites women aged `50–74` every `two years`. Women aged 40–49 or 75 and over can attend after weighing individual benefits and harms.\n\nA lump or nipple change needs diagnostic imaging and triple assessment, not a screening booking; see G23 (Triple assessment).\n\n### Bowel screening\n\niFOBT every `two years` at ages `45–74` for people at average risk; those aged 45–49 request their first kit. Collect small samples from two separate bowel motions, uncontaminated by urine or toilet water, and return the kit promptly.\n\n**A positive result requires colonoscopy.** Do not repeat the stool test: bleeding from a lesion is intermittent, so a negative repeat does not exclude it. Family history may place the person on a different pathway.\n\n### Lung screening\n\nLow-dose CT for asymptomatic people aged `50–70` with `≥30 pack-years` who currently smoke or quit within the past `ten years`. Repeat screening is generally two-yearly; nodules may need earlier review. Discuss radiation exposure, incidental findings and smoking cessation.\n\n### After a cancer diagnosis\n\nA suspected or confirmed cancer creates follow-up responsibilities that are easily lost between services, so be clear who will act on each result and referral, and when the patient will next be seen.\n\nGive the diagnosis in person where possible, in private, with time and a support person if the patient wishes. The SPIKES sequence is a useful guide: set up the conversation, find out what the patient already understands, ask how much they want to know, give the information in plain language and in small amounts, respond to their emotion, and summarise with an agreed plan and next step. Little is retained after bad news, so check understanding and offer a follow-up appointment soon afterwards.\n\nReferral follows the Optimal Care Pathway for the cancer type, which sets out the expected investigations and timeframes. Distance and travel costs, work and caring commitments, language and cultural safety can delay or prevent treatment, so ask about them and use the supports available, such as patient travel schemes, Aboriginal liaison services and the Cancer Council.\n\nAfter treatment, *survivorship care* covers surveillance for recurrence and new cancers, the late effects of treatment, prevention and the person's psychosocial needs, coordinated between the specialist team and general practice. In shared care, the GP undertakes some scheduled follow-up with rapid access back to the specialist; for selected cancers, such as low- to moderate-risk prostate cancer, it has proved as safe as hospital follow-up and is preferred by many patients. A written survivorship care plan states the surveillance schedule, who orders and acts on each test, and which symptoms need earlier review. At follow-up, consider:\n\n- Physical effects: fatigue, pain, continence, sexual function and fertility, lymphoedema, and cardiovascular and bone health after hormonal or cardiotoxic treatment.\n- Mood, fear of recurrence and distress in the patient and family.\n- Work, finances, insurance and carer strain.\n- Smoking, alcohol, activity and weight, and screening for other cancers.\n- Family history and genetic testing where relevant.\n\nNew or persistent symptoms are assessed as a possible recurrence rather than left for the next scheduled visit.\n\n### Vaccination counselling\n\nCheck the Australian Immunisation Register for previous doses. Ask about pregnancy, immunosuppression, allergies and previous serious reactions, which determine what is safe.\n\nExplain what the vaccine prevents, the common local pain, redness and swelling, transient systemic symptoms, and the rare risk of severe allergy.\n\nA mild afebrile illness or current antibiotics is generally not a reason to defer. Severe allergy to a previous dose or component, and live vaccines in pregnancy or significant immunosuppression, need specific assessment.\n\n1. Obtain consent; confirm the product, site and dose.\n2. Observe for at least `15 minutes`, the period in which most anaphylaxis occurs.\n3. Record the product, batch and next dose; report significant adverse events.\n4. Advise return for breathing difficulty, collapse or persistent concerning symptoms.\n\nSee C02 (Immunisation and follow-up) for childhood vaccination and O01 (Vaccination in pregnancy) for pregnancy.\n\n### Adult schedule (checked November 2026)\n\n- **Influenza:** annual. Funded for older adults, pregnancy, First Nations people and specified risk groups.\n- **Pneumococcal:** from July 2026, one 21vPCV (Capvaxive) dose for adults `≥65`, First Nations adults `≥25` and eligible medical-risk groups `≥18`. Allow at least `12 months` after any previous pneumococcal vaccine. This replaces the older age-70/13vPCV advice.\n- **Shingles (Shingrix):** two non-live doses `2–6 months` apart. NIP-funded at `≥65`, for First Nations adults `≥50` and for specified immunocompromised adults. Previous shingles does not remove the benefit.\n- **COVID-19:** twice yearly at `≥75` and annually at 65–74, with further age- and risk-specific recommendations.\n- **RSV:** a single dose for adults `≥75`, First Nations adults `≥60` and adults `≥60` with specified risk factors. NIP-funded (Arexvy, from May 2026) for those `≥75` and First Nations adults `≥60`; adults 60–74 and younger people with risk conditions may purchase it privately. Protection lasts at least two years, and it is not an annual vaccine.\n\nFunding and catch-up rules differ from recommendations. Check individual scheduling, especially after previous vaccines or with immunocompromise, against the current [Australian Immunisation Handbook](https://immunisationhandbook.health.gov.au/).",
      "formerly": [
        "G07",
        "G18"
      ]
    },
    {
      "id": "G02",
      "domain": "GP",
      "group": "Prevention and lifestyle",
      "title": "Smoking, alcohol and behaviour change",
      "focus": "Brief intervention, readiness to change, dependence treatment, motivational interviewing and harm reduction.",
      "first_pass": false,
      "priority": "Core",
      "saq_cases": [
        {
          "id": "2016-mhagp-q5",
          "title": "Lower urinary tract symptoms, bowel screening and smoking/alcohol",
          "set": "2016 MH/GP"
        },
        {
          "id": "deck-mh-alcohol-use-disorder",
          "title": "Alcohol use disorder and withdrawal",
          "set": "MD3 SAQ Revision Deck"
        }
      ],
      "core_ids": [
        "P010",
        "P031",
        "P077"
      ],
      "gp_tasks": [
        "Brief intervention and motivational interviewing for smoking/alcohol",
        "Offer practical cessation support and relapse follow-up"
      ],
      "notes": "### Assessment of use and dependence\n\nAsk permission to discuss smoking, vaping or alcohol, and link the discussion to the person's own priorities.\n\n- **Tobacco:** quantity and time to first cigarette indicate nicotine dependence. Previous quit attempts and triggers inform the plan.\n- **Alcohol:** quantity, frequency, binges, morning drinking, loss of control, consequences, last drink and previous withdrawal distinguish risky use from dependence and identify withdrawal risk.\n\nOne Australian **standard drink** contains `10 g` of alcohol; a large glass of wine or a strong beer may contain several.\n\n> [!pitfall]\n> AUDIT-C is a screening aid, not a diagnosis of dependence.\n\nLower-risk guidance for healthy adults is no more than `ten standard drinks a week` and `four on any day`; less carries less risk. No alcohol is safest in pregnancy and when planning pregnancy, and children and adolescents should not drink. Relevant harms include driving, medication interactions, falls, liver disease, mental health and effects on family.\n\n### Brief intervention\n\nThe **5As** are ask, assess, advise, assist and arrange. For example: establish smoking and dependence, assess readiness, explain its relevance to the patient's breathlessness, agree a quit strategy and book review.\n\n**Motivational interviewing** uses open questions, reflections and the patient's own reasons for change: \"What would be better if you smoked less?\" After a readiness scale, ask \"Why that number and not a lower one?\" to draw out existing motivation.\n\nEnd with a specific, achievable step, such as a quit date, alcohol-free days, recording drinks or avoiding a trigger. Discuss barriers and plan for slips without blame. Arrange support, medication where indicated and follow-up; advice alone achieves less.\n\n### Smoking cessation treatment\n\nCombine behavioural support, including Quitline (13 7848), with medication; together they outperform either alone.\n\n- **Combination NRT:** a daily patch covers background need; gum, lozenge, inhalator or spray handles breakthrough cravings. Match the dose to dependence and review cravings and adverse effects.\n- **Nicotine gum:** chew until it tingles, then park it between cheek and gum, since nicotine is absorbed through the oral mucosa. Avoid acidic drinks around use, which reduce absorption. Rapid repeated chewing releases nicotine to be swallowed, causing nausea and hiccups.\n- **Varenicline:** reduces nicotine reward and withdrawal. The dose is titrated over the first week to `1 mg twice daily`, starting `one to two weeks` before the quit date and continuing for `12 weeks`. Counsel about nausea and vivid dreams, adjust for renal impairment, and review mood or unusual behaviour.\n- **Bupropion:** lowers the seizure threshold, so avoid it with seizure disorders or eating disorders. Check interactions.\n- **Pregnancy:** behavioural support first; supervised NRT if needed, which delivers nicotine without the carbon monoxide and other toxins in smoke.\n\nReview soon after the quit date and again over the following weeks, when withdrawal and relapse are most likely.\n\n> [!pitfall]\n> Stopping smoking can raise clozapine and olanzapine levels, because tobacco smoke, not nicotine, induces their metabolism (CYP1A2). Coordinate monitoring with the prescriber.\n\n### Alcohol dependence\n\n> [!pitfall]\n> **Abrupt cessation is unsafe** for an alcohol-dependent person at high withdrawal risk. Assess before advising them to stop.\n\nSupervised withdrawal is indicated by previous withdrawal seizures or delirium, severe dependence, major medical illness, pregnancy or inadequate support. Assess nutrition, electrolytes and liver disease, and give thiamine where indicated.\n\nSee M06 (Alcohol and sedative withdrawal) for withdrawal management and M06 (Treating the disorder beyond withdrawal) for relapse prevention.",
      "formerly": [
        "G08"
      ]
    },
    {
      "id": "G03",
      "domain": "GP",
      "group": "Prevention and lifestyle",
      "title": "Travel health and returned traveller",
      "focus": "Vaccine counselling, travel risk assessment, malaria prevention and fever after travel.",
      "first_pass": false,
      "priority": "Selective",
      "saq_cases": [],
      "core_ids": [
        "P042",
        "P077",
        "P093"
      ],
      "gp_tasks": [
        "Assess itinerary and explain relevant travel vaccination and prevention",
        "Identify red flags when evaluating a febrile returned traveller"
      ],
      "notes": "### Pre-travel assessment\n\n- **Itinerary:** exact countries and regions, season, rural exposure, accommodation, activities, duration, visiting friends and relatives, and access to care.\n- **Traveller:** pregnancy, age, immunosuppression, chronic illness, medicines and vaccination history. These alter both the risk and which vaccines and drugs are safe.\n\nAttending several weeks before travel allows vaccine courses to be completed, but late attendance still allows useful protection and advice.\n\nReview routine vaccination first, then destination-specific vaccines: hepatitis A and B, typhoid, rabies, Japanese encephalitis and yellow fever. Yellow fever vaccine is live; it is given by an accredited provider after careful contraindication assessment. Entry requirements and disease risk are separate questions.\n\nAlso cover travel insurance, medicine supply, a medication list, a plan for exacerbations of chronic illness, and access to safe care.\n\n### Malaria prevention\n\nChoose prophylaxis according to destination resistance, pregnancy, age, renal function and interactions. No agent suits every traveller.\n\n- **Atovaquone–proguanil:** daily, from `1–2 days` before exposure until `7 days` after leaving.\n- **Doxycycline:** `100 mg daily`, from `1–2 days` before until `4 weeks` after. Causes photosensitivity and oesophagitis; unsuitable in pregnancy.\n- **Mefloquine:** weekly, from `2–3 weeks` before until `4 weeks` after. Unsuitable with relevant psychiatric or seizure history.\n\nContinuing after departure covers parasites acquired late in the trip. Confirm the schedule against current travel guidance for the destination.\n\nAdvise repellent, covering clothing, screened or air-conditioned rooms and insecticide-treated bed nets. Protect against daytime bites as well: the mosquitoes that transmit dengue and other arboviruses bite during the day.\n\n> [!pitfall]\n> **Prophylaxis does not exclude malaria** in a returned febrile traveller.\n\n### Other travel advice\n\n- **Food and water:** safe water and food preparation, hand hygiene, and oral rehydration for diarrhoea. Routine antibiotics are unnecessary for mild traveller's diarrhoea.\n- **Invasive diarrhoea:** bloody diarrhoea, high fever, severe abdominal pain or dehydration needs medical assessment. Avoid antimotility agents in invasive infection, because slowing transit delays clearance of the pathogen.\n- **Injury:** road trauma is a major travel risk. Advise seatbelts, helmets and no impaired driving.\n- **Other exposures** as relevant: sun and heat, altitude or diving, sexual health, and avoiding contact with animals.\n\n> [!escalate]\n> After a bite or scratch with rabies risk, wash the wound with soap and running water for about `15 minutes` and seek same-day post-exposure assessment, even after pre-exposure vaccination. Prior vaccination changes the regimen but does not remove the need for post-exposure care.\n\n### Fever after travel\n\n- **History:** destinations and dates, onset, mosquito or tick exposure, freshwater swimming, animal contact, food, sexual exposure and sick contacts. Incubation periods define which infections are plausible.\n- **Differential:** malaria, dengue, enteric fever, rickettsial illness, hepatitis and common local infections.\n- **Examination:** hydration, perfusion, rash, jaundice, respiratory signs and neurological state.\n\n> [!escalate]\n> Plausible malaria exposure requires same-day blood films and a rapid antigen test. Falciparum malaria can deteriorate within hours. If suspicion persists after a negative result, repeat the films, commonly three sets over `12–24 hours`.\n\nAdd FBE and platelets, renal and liver function, and cultures according to the syndrome. Avoid NSAIDs where dengue is possible until bleeding risk is assessed, because dengue causes thrombocytopenia and haemorrhage.\n\n> [!escalate]\n> Hypotension, confusion, respiratory distress, significant bleeding or jaundice needs emergency department care, with infectious diseases input.\n\nGive receiving staff the travel history early and use appropriate infection precautions. Check current destination risks and entry requirements for any real itinerary.",
      "formerly": [
        "G25"
      ]
    },
    {
      "id": "G04",
      "domain": "GP",
      "group": "Cardiovascular, metabolic and renal",
      "title": "Type 2 diabetes in primary care",
      "focus": "Screen, diagnose, stage complications, set goals, optimise treatment and follow-up.",
      "first_pass": true,
      "priority": "Core",
      "saq_cases": [
        {
          "id": "deck-gp-type2-diabetes",
          "title": "Type 2 diabetes: screening and management",
          "set": "MD3 SAQ Revision Deck"
        }
      ],
      "core_ids": [
        "P016",
        "P023",
        "P075",
        "P087",
        "P104",
        "P105"
      ],
      "gp_tasks": [
        "AUSDRISK, diagnostic criteria and complication screening",
        "Explain a follow-up plan: targets, monitoring, referrals and recall"
      ],
      "notes": "### Recognition\n\n**Type 2 diabetes** develops when insulin resistance outstrips pancreatic insulin secretion. Onset is gradual and many people are asymptomatic at diagnosis; others notice thirst, polyuria, blurred vision, fatigue, recurrent infection or weight loss. Previous gestational diabetes, family history, weight gain and cardiovascular disease raise the likelihood.\n\nScreen with AUSDRISK every `three years` from age `40`, and test HbA1c or fasting glucose when the score is `≥12`.\n\nMarked weight loss, ketosis or rapid onset suggests absolute insulin deficiency. Type 1 diabetes also occurs in adults and needs insulin, not a stepwise oral approach.\n\n### Diagnosis\n\nAny one of the following establishes diabetes:\n\n- HbA1c `≥6.5%` (`48 mmol/mol`).\n- Fasting venous glucose `≥7.0 mmol/L`.\n- Two-hour glucose `≥11.1 mmol/L` on a 75 g oral glucose tolerance test (OGTT).\n- Random venous glucose `≥11.1 mmol/L` with typical symptoms.\n\nWithout symptoms, **confirm a single abnormal result on a second sample** before making a lifelong diagnosis.\n\nHbA1c reflects haemoglobin glycation over about three months. Anaemia, haemoglobin variants and recent transfusion alter red-cell survival or haemoglobin structure and can make it misleading; use glucose-based tests instead. A capillary meter shows hyperglycaemia immediately but is not a diagnostic test.\n\n> [!escalate]\n> Vomiting, dehydration, abdominal pain, deep breathing or altered consciousness suggests metabolic decompensation. Check glucose and ketones and arrange emergency hospital care.\n\n### Complications assessment\n\nHyperglycaemia damages small vessels in the eyes, kidneys and nerves, while BP, lipids and smoking drive heart and stroke risk. Either may be present at diagnosis. Assess:\n\n- BP, weight, smoking and lipids.\n- eGFR and urine albumin:creatinine ratio (ACR).\n- Retinal examination.\n- Feet: skin breaks, deformity, pulses, and protective sensation with a `10 g` monofilament.\n\nAsk directly about neuropathic pain, erectile dysfunction, dental health, mood, diet, activity, finances and ability to manage medicines. These determine what treatment is realistic.\n\n### Management\n\nPractical nutrition and activity changes, with dietitian and diabetes educator support, underpin every later step.\n\nAn HbA1c target of about `7%` (`53 mmol/mol`) is common. Frailty, recurrent hypoglycaemia, comorbidity or preference may justify a less intensive target: the harms of hypoglycaemia arrive sooner than the microvascular benefits of tight control.\n\nChoose medicines for the clinical problem (heart failure, kidney disease, weight, hypoglycaemia risk), together with renal function, adverse effects, cost and eligibility.\n\n#### Metformin\n\nThe usual first-line drug. Start low, for example `500 mg` with the evening meal, and increase gradually to limit gastrointestinal upset; a modified-release preparation may help.\n\n- Metformin is renally cleared and accumulates as kidney function falls, increasing lactic acidosis risk. It is **contraindicated at eGFR `<30`**; reduce the dose and review more often with lesser impairment.\n- Long-term use can lower B12.\n\n#### SGLT2 inhibitors\n\nTheir benefit in heart failure, kidney disease and cardiovascular disease extends beyond glucose lowering. They increase urinary glucose loss, which explains genital fungal infection, polyuria and dehydration. Ketoacidosis can occur without very high glucose.\n\n#### GLP-1 receptor agonists\n\nThey lower glucose and weight, and selected agents reduce cardiovascular events. Nausea reflects slowed gastric emptying, so titrate gradually. Teach injection technique and assess persistent severe abdominal pain. Avoid in pregnancy.\n\n#### Insulin and sulfonylureas\n\nBoth cause hypoglycaemia, which shapes counselling and monitoring. Insulin is often needed for severe symptomatic hyperglycaemia or catabolism, when endogenous insulin is clearly inadequate.\n\n### Weight gain\n\nTiming and the measured change are the first clues.\n\n- **Rapid gain with oedema, orthopnoea or ascites:** fluid retention, not fat. Consider cardiac, renal and hepatic disease.\n- **Gradual gain:** consider pregnancy, diet, activity, sleep, alcohol, mood and medicines such as corticosteroids, antipsychotics and insulin.\n\nTest thyroid function when there is cold intolerance, constipation or another endocrine feature; weight gain alone does not establish hypothyroidism.\n\nWith permission, measure BMI, waist circumference and BP, assess metabolic risk, and ask about sleep apnoea, joint symptoms and functional impact. Discuss weight without blame.\n\nAgree a few achievable changes to nutrition, activity and sleep, supported by dietetic and behavioural input, progressive strength and aerobic activity, and planned follow-up. Selected patients may benefit from weight-management medication or bariatric assessment. Ask about body-image distress and disordered eating before recommending a restrictive diet; see M05 (The eating disorders, at any body weight).\n\n### Glucose self-monitoring\n\nHome testing is useful when the result informs a decision: insulin use, hypoglycaemia risk, illness or treatment adjustment. Routine frequent finger-pricks add little for most people taking metformin alone.\n\n1. Wash and dry hands; sugar on the skin falsely raises the reading.\n2. Insert an in-date strip and prick the side of a fingertip, which hurts less than the pad.\n3. Record the result and its timing.\n\n### Hypoglycaemia\n\nFor a conscious adult with glucose `<4 mmol/L`, give about `15 g` of fast-acting carbohydrate, recheck after `15 minutes` and repeat if still low. Then give longer-acting carbohydrate if the next meal is not soon.\n\n> [!escalate]\n> An unconscious person needs emergency help and parenteral treatment (glucagon or IV glucose), never oral food or drink.\n\n### Sick-day plan\n\nProvide a written plan:\n\n- Maintain fluids and check glucose more often.\n- **Temporarily withhold metformin and SGLT2 inhibitors** during significant dehydrating illness. They increase the risks of lactic acidosis and ketoacidosis respectively.\n- Seek advice for vomiting, ketones or persistent hyperglycaemia.\n- Adjust insulin with advice; do not simply stop it, because insulin deficiency during illness can precipitate ketoacidosis.\n\n### Follow-up\n\n- **HbA1c:** about three months after a treatment change.\n- **Feet, urine ACR and renal function:** at least annually.\n- **Retinal examination:** every one to two years, or sooner according to findings.\n\nRecord who recalls the patient and who follows up results.",
      "formerly": [
        "G01"
      ]
    },
    {
      "id": "G05",
      "domain": "GP",
      "group": "Cardiovascular, metabolic and renal",
      "title": "Cardiovascular risk and hypertension",
      "focus": "Absolute CVD risk, lipids, non-pregnant adult BP confirmation/treatment, lifestyle and follow-up.",
      "first_pass": true,
      "priority": "Core",
      "saq_cases": [
        {
          "id": "deck-gp-dyslipidaemia-cvd",
          "title": "Dyslipidaemia and cardiovascular risk",
          "set": "MD3 SAQ Revision Deck"
        }
      ],
      "core_ids": [
        "P023",
        "P052",
        "P072",
        "P077"
      ],
      "gp_tasks": [
        "Estimate and explain absolute CVD risk",
        "Confirm BP, interpret lipids, counsel about treatment and follow-up"
      ],
      "notes": "### Absolute cardiovascular risk\n\nBase treatment on absolute risk, the combined effect of age, smoking, BP, lipids, diabetes, kidney disease and other factors, not on any single measurement.\n\nUse the Australian CVD risk calculator for people without established cardiovascular disease aged `45–79`, from `35` with diabetes, and from `30` for Aboriginal and Torres Strait Islander people. Assess individual risk factors earlier when indicated.\n\nFive-year risk is classified as:\n\n- **Low:** `<5%`.\n- **Intermediate:** `5–<10%`.\n- **High:** `≥10%`.\n\nA 10% risk means that about 10 in 100 similar people will have a cardiovascular event over five years.\n\nTreat without calculating in established vascular disease (secondary prevention), familial hypercholesterolaemia and specified moderate-to-severe CKD; the calculator underestimates risk in these groups.\n\nAbsolute benefit rises with baseline risk. At high risk, generally offer both lipid- and BP-lowering treatment. At intermediate risk, discuss expected benefit, adverse effects and preferences.\n\n### Measuring blood pressure\n\n1. Seat the patient quietly for `five minutes`, back supported, feet flat and uncrossed, arm supported at heart level, with a correctly sized cuff.\n2. Avoid talking, take repeated readings and check both arms initially.\n\nAnxiety and poor technique often raise a single clinic reading. Confirm hypertension over repeated visits or with home or ambulatory monitoring, unless urgent treatment is needed. Diagnostic thresholds:\n\n- Clinic BP `≥140/90 mmHg`.\n- Average home or daytime ambulatory BP `≥135/85 mmHg`.\n\nFor home monitoring, take two readings morning and evening for `seven days`. Discard the first day, when readings run higher, and average the rest.\n\n### Assessment of hypertension\n\n- **Contributors:** NSAIDs, decongestants, stimulants, alcohol, sleep apnoea and poor adherence. These are often correctable.\n- **Secondary causes:** suggested by young onset, abrupt worsening, hypokalaemia or resistant hypertension.\n- **Target organs:** electrolytes and creatinine, urine ACR and ECG.\n- **Overall risk:** glucose or HbA1c and lipids.\n\n### Management\n\nAdvise smoking cessation, regular aerobic and resistance activity, a better diet, salt reduction, moderate alcohol and sustainable weight change. Hypertension rarely causes symptoms, so explain that treatment prevents future stroke, heart and kidney damage; adherence depends on that understanding.\n\nChoose drugs and combinations by comorbidity and tolerability.\n\n#### ACE inhibitor or ARB\n\nPreferred with albuminuric kidney disease or heart failure.\n\n- They reduce efferent arteriolar tone and aldosterone secretion, so check potassium and creatinine before and about `1–2 weeks` after starting or increasing.\n- ACE inhibitors cause cough and, rarely, angioedema. Neither class is used in pregnancy.\n- **Do not combine them**: dual blockade increases hyperkalaemia and kidney injury without added benefit.\n\n#### Dihydropyridine calcium-channel blocker (e.g. amlodipine)\n\nCauses ankle oedema, flushing and headache. The oedema comes from arteriolar dilatation raising capillary pressure; it is not fluid overload and does not need a diuretic.\n\n#### Thiazide-like diuretic (e.g. indapamide)\n\nCauses sodium and potassium loss and reduces urate excretion. Monitor electrolytes, renal function and gout.\n\n#### Statin\n\nLowers LDL cholesterol and atherosclerotic events. Discuss muscle symptoms, interactions and the small diabetes risk against the cardiovascular benefit. Check baseline liver tests, then review response and adherence. Investigate significant muscle pain or weakness; routine creatine kinase testing in everyone is unnecessary.\n\n#### Targets and review\n\nA common initial target is `<140/90`, lower for some high-risk people if tolerated. In frailty, check standing BP and falls before intensifying treatment: postural hypotension can turn a modest cardiovascular benefit into fall-related harm.\n\nReview BP and adverse effects within weeks of a change, and lipids once treatment has had time to work.\n\n### Severe hypertension\n\n> [!escalate]\n> Severe BP with chest pain, dyspnoea, confusion, focal neurological signs, visual disturbance or acute kidney injury suggests a hypertensive emergency and needs emergency department assessment.\n\nSevere asymptomatic hypertension (commonly `≥180/110`) needs prompt reassessment and a treatment plan. Avoid rapid, uncontrolled outpatient reduction: chronically hypertensive circulations autoregulate at higher pressures, so an abrupt fall risks cerebral, coronary or renal ischaemia.",
      "formerly": [
        "G02"
      ]
    },
    {
      "id": "G06",
      "domain": "GP",
      "group": "Cardiovascular, metabolic and renal",
      "title": "Heart failure, atrial fibrillation and leg swelling",
      "focus": "Heart failure and AF in the community: assessment, optimisation, anticoagulation, escalation, the differential of leg swelling and suspected PE.",
      "first_pass": false,
      "priority": "Core",
      "saq_cases": [
        {
          "id": "deck-geri-heart-failure",
          "title": "Heart failure and acute pulmonary oedema",
          "set": "MD3 SAQ Revision Deck"
        },
        {
          "id": "deck-geri-atrial-fibrillation",
          "title": "Atrial fibrillation and post-stroke care",
          "set": "MD3 SAQ Revision Deck"
        }
      ],
      "core_ids": [
        "P023",
        "P034",
        "P051",
        "P072",
        "P094"
      ],
      "gp_tasks": [
        "Review worsening heart-failure symptoms and medication harms",
        "Assess AF stroke risk, anticoagulation and secondary stroke prevention"
      ],
      "notes": "### Heart failure: definitions and assessment\n\n**Heart failure** is a clinical syndrome in which cardiac dysfunction produces congestion and/or inadequate cardiac output. **Ejection fraction** is the proportion of end-diastolic left ventricular volume ejected with each beat; it can remain preserved despite impaired filling and raised filling pressures. Heart failure with reduced ejection fraction (**HFrEF**) has an EF of `≤40%`; heart failure with preserved ejection fraction (**HFpEF**) has an EF of `≥50%`.\n\nThe typical symptoms are exertional dyspnoea, orthopnoea, paroxysmal nocturnal dyspnoea, oedema and fatigue. On examination, the weight trend, JVP and lung bases show how congested the patient is, while pulse, BP and peripheral perfusion show whether cardiac output is adequate. Function and adherence determine what care plan is practical.\n\nInvestigations establish the cause and severity, which determine treatment:\n\n- **ECG.**\n- **Echocardiography:** separates reduced from preserved ejection fraction and identifies valve disease.\n- **Bloods:** renal function and electrolytes, FBE and iron studies, and natriuretic peptide when the diagnosis is uncertain.\n\n### Long-term management of heart failure\n\nIn stable HFrEF, introduce and titrate four disease-modifying classes as tolerated:\n\n- An angiotensin receptor–neprilysin inhibitor (ARNI, sacubitril–valsartan) or an ACE inhibitor/ARB.\n- An evidence-based beta blocker: bisoprolol, carvedilol, metoprolol succinate or nebivolol.\n- A mineralocorticoid receptor antagonist: spironolactone or eplerenone.\n- An SGLT2 inhibitor: dapagliflozin or empagliflozin.\n\nLoop diuretics relieve congestion but have not been shown to improve survival, so they **supplement these treatments rather than replacing them**.\n\nBP, pulse, renal function and potassium usually limit titration, so check them as doses rise. ACE inhibitors, ARBs, ARNI and spironolactone can cause hyperkalaemia; diuretics can cause dehydration, renal impairment and electrolyte loss. An ACE inhibitor needs a `36-hour` washout before sacubitril–valsartan to reduce the risk of angioedema. Start a beta blocker only once the patient is stable, because its initial negative inotropic effect can worsen shock or severe congestion.\n\nIn HFpEF, treat congestion and the contributing conditions: BP, AF and obesity. An SGLT2 inhibitor benefits suitable patients. In either type, avoid NSAIDs and review medicines that cause fluid retention.\n\nFluid accumulates before breathlessness becomes obvious, so daily weights allow treatment to be adjusted before admission is needed. Agree in advance what the patient should do when oedema or breathlessness worsens; a rise of about `2 kg over two days` should prompt contact under the individual plan. Exercise or cardiac rehabilitation, vaccination and a reliable medication supply complete the plan. Fluid restriction is individualised and not needed for everyone with stable heart failure.\n\n### Atrial fibrillation: diagnosis\n\n**Atrial fibrillation** (AF) is disorganised atrial electrical activity with loss of coordinated atrial contraction; the resulting blood stasis explains its thromboembolic risk. The ECG shows an irregularly irregular ventricular rhythm without consistent P waves.\n\nLook for precipitants: infection, thyroid disease, alcohol, ischaemia, electrolyte disturbance and valve disease. Treating them can make rate or rhythm easier to control. Record onset, symptoms, haemodynamic stability and any previous stroke or bleeding.\n\n### Stroke prevention\n\nThe Australian **CHA2DS2-VA** score assigns:\n\n- **One point each:** heart failure, hypertension, diabetes, vascular disease, age 65–74.\n- **Two points each:** age ≥75, previous stroke or TIA.\n\nAnticoagulation is **recommended at `≥2` and considered at `1`**.\n\nBleeding-risk assessment identifies correctable risks such as uncontrolled BP, NSAIDs, alcohol and renal impairment. It is not a reason to withhold anticoagulation automatically.\n\nDirect oral anticoagulants (DOACs) are preferred for eligible patients; the dose depends on the drug, renal function, age and sometimes weight. Mechanical valves and moderate-to-severe rheumatic mitral stenosis require warfarin, which targets an INR of `2–3` in AF and needs extra checks when interacting drugs change. Patients on warfarin should keep vitamin K intake consistent rather than avoiding it, because fluctuations shift the INR.\n\nCounselling for either drug covers adherence, the missed-dose rule for the specific agent, bleeding signs, interactions and planned procedures.\n\n> [!pitfall]\n> **Aspirin is not a substitute** for anticoagulation in AF. It offers little stroke protection and still causes bleeding.\n\n> [!pitfall]\n> Sinus rhythm on the day, or intermittent AF, does not remove the indication for anticoagulation. Stroke risk follows the patient's risk profile, not the rhythm at review.\n\n### Rate and rhythm control\n\nRate control commonly uses a beta blocker. Verapamil or diltiazem suits patients without HFrEF; both depress contractility, so avoid them in HFrEF.\n\nRhythm control, cardioversion and ablation depend on symptoms, duration and cardiac context. When AF has lasted `≥48 hours` or for an unknown time, cardioversion requires at least `three weeks` of anticoagulation or transoesophageal echocardiography first, because restoring atrial contraction can dislodge thrombus that has already formed.\n\n### Murmurs\n\n- **Aortic stenosis:** exertional dyspnoea, angina or syncope, with an ejection systolic murmur radiating to the carotids.\n- **Mitral regurgitation:** a pansystolic apical murmur radiating to the axilla.\n\nRefer a new symptomatic murmur for echocardiography and cardiology review. Acute breathlessness, syncope or instability makes it urgent or an emergency.\n\n### Leg swelling\n\nWhether the swelling is unilateral or bilateral, how quickly it developed and whether it pits narrow the differential:\n\n- **Unilateral, acute:** DVT, cellulitis, injury or a ruptured Baker cyst.\n- **Bilateral, pitting:** chronic venous insufficiency, heart failure, renal disease including nephrotic syndrome, liver disease or hypoalbuminaemia, pregnancy, and medicines such as dihydropyridine calcium-channel blockers, NSAIDs, corticosteroids and pregabalin.\n- **Non-pitting:** lymphoedema, or myxoedema in thyroid disease.\n\nFor suspected DVT, a clinical probability score such as Wells guides testing. When DVT is unlikely, a normal D-dimer excludes it; when DVT is likely, or the D-dimer is raised, arrange compression ultrasound. Breathlessness, pleuritic chest pain or haemoptysis alongside leg swelling suggests pulmonary embolism and needs emergency assessment, as described in the next section.\n\nBilateral swelling calls for a medication review, urinalysis for protein, renal and liver function, albumin and assessment for heart failure. Compression helps venous oedema once significant arterial disease has been excluded; see R08 (Assessing arterial supply before compression).\n\n### Suspected pulmonary embolism\n\nPulmonary embolism presents with sudden breathlessness, pleuritic pain, haemoptysis, syncope, tachycardia or unexplained hypoxaemia, sometimes with signs of DVT. These features overlap with pneumonia, ACS, pneumothorax and heart failure, so the ECG and chest X-ray mainly look for alternatives; neither can exclude PE.\n\nAs with DVT, estimate clinical probability first, because it determines what a D-dimer can do:\n\n- **PE unlikely** (Wells `≤4`): a normal D-dimer excludes PE. In a patient with low clinical suspicion who meets all eight PERC criteria (age under 50, heart rate `<100`, SpO₂ `≥95%`, and no haemoptysis, oestrogen use, previous VTE, unilateral leg swelling or recent surgery or trauma), PE is excluded without a D-dimer. An age-adjusted cut-off (age × `10 µg/L` over 50) reduces false positives in older people.\n- **PE likely**, or a raised D-dimer: arrange CT pulmonary angiography (CTPA). A ventilation–perfusion (V/Q) scan is used when contrast is unsuitable, as in significant renal impairment or contrast allergy.\n\nIn general practice, suspected PE that cannot be excluded clinically needs same-day hospital assessment. Where imaging will be delayed and the probability is high, anticoagulation is usually started before the result, unless bleeding risk prevents it.\n\n**Hypotension or shock suggests massive PE**, which needs emergency resuscitation and consideration of thrombolysis. Right-ventricular strain on echocardiography or a raised troponin in a normotensive patient indicates higher risk and admission.\n\nPregnancy raises the risk of VTE while making the D-dimer unreliable, because it rises physiologically. When there are leg symptoms, compression ultrasound comes first, since a DVT establishes the need for anticoagulation without lung imaging; otherwise CTPA or V/Q is chosen with the obstetric and radiology teams. Treatment is with LMWH; see O05 (Other medical conditions in pregnancy).\n\nConfirmed PE in a stable patient is treated with a DOAC for most people, for at least `three months`. Whether to continue depends on whether the clot was provoked by a transient risk factor, the bleeding risk and the patient's preference.\n\n### Escalation and follow-up\n\n> [!escalate]\n> Pulmonary oedema, chest pain, syncope, shock, or rapid AF with haemodynamic compromise needs emergency care.\n\nAfter each treatment change, review symptoms, observations and relevant blood tests. Agree which responsibilities sit with the GP and which with cardiology.",
      "formerly": [
        "B02",
        "G04"
      ]
    },
    {
      "id": "G07",
      "domain": "GP",
      "group": "Cardiovascular, metabolic and renal",
      "title": "Chest pain and palpitations in the community",
      "focus": "Recognising time-critical chest pain and arrhythmia, safe referral, ECG recording and reading, and follow-up of stable symptoms.",
      "first_pass": false,
      "priority": "Selective",
      "saq_cases": [
        {
          "id": "deck-geri-atrial-fibrillation",
          "title": "Atrial fibrillation and post-stroke care",
          "set": "MD3 SAQ Revision Deck"
        },
        {
          "id": "deck-gp-dyslipidaemia-cvd",
          "title": "Dyslipidaemia and cardiovascular risk",
          "set": "MD3 SAQ Revision Deck"
        }
      ],
      "core_ids": [
        "P022",
        "P048",
        "P061",
        "P072"
      ],
      "gp_tasks": [
        "Recognise emergency red flags and organise safe referral",
        "Assess palpitations and use ECG in community assessment"
      ],
      "notes": "### Time-critical causes\n\n- **Acute coronary syndrome (ACS):** pressure or heaviness, radiation, dyspnoea, sweating or nausea. Older people and people with diabetes may have less typical pain.\n- **Others:** pulmonary embolism, aortic dissection, pneumothorax, pericarditis and oesophageal rupture.\n\nReproducible chest-wall tenderness or a normal initial ECG does not exclude ACS.\n\n### Assessment\n\n- **Chest pain:** onset, duration, exertion, radiation, pleuritic or positional features, syncope, haemoptysis and vascular risk factors.\n- **Palpitations:** abrupt onset and offset suggests a re-entrant arrhythmia rather than sinus tachycardia. Ask about regularity, duration, triggers, stimulants and associated chest pain or presyncope.\n- **Examination:** observations, pulse, perfusion and cardiorespiratory examination determine how urgently the patient must be transferred.\n\n> [!escalate]\n> Call an ambulance for current or recent suspected ischaemic pain, significant dyspnoea or an unstable tachyarrhythmia.\n\nIn suspected ACS, give chewable aspirin `300 mg` unless there is serious allergy, active major bleeding, or concern for a contraindicating diagnosis such as dissection.\n\n> [!pitfall]\n> Do not delay transfer for outpatient troponin testing. An early single result cannot exclude ACS and delays definitive care.\n\nGive oxygen only for hypoxaemia. Before nitrates, check BP and contraindications, including recent PDE5 inhibitor use, which combines with nitrates to cause profound hypotension.\n\n### Recording an ECG\n\nExplain the test, preserve privacy, clean and dry the skin and position the patient comfortably. Place the chest leads:\n\n- **V1, V2:** fourth intercostal space either side of the sternum.\n- **V4:** fifth intercostal space, midclavicular line.\n- **V3:** midway between V2 and V4.\n- **V5, V6:** level with V4, at the anterior and midaxillary lines.\n\nMisplaced chest leads can create misleading changes.\n\n### Reading an ECG\n\nCheck identity, date, calibration and artefact. Then assess rate, rhythm, axis, PR, QRS and QT intervals, P waves, QRS morphology and ST/T changes. Compare with a previous ECG if available, since many abnormalities matter only if new.\n\n- **AF:** irregular rhythm without consistent P waves.\n- **SVT:** regular narrow-complex tachycardia.\n- **Broad-complex tachycardia:** treat as ventricular until proven otherwise.\n\nSignificant ST elevation or depression, high-grade block or dangerous QT prolongation requires immediate action.\n\n### Stable intermittent symptoms\n\n> [!pitfall]\n> A normal resting ECG between episodes does not exclude an intermittent arrhythmia.\n\nOnce urgent causes are reasonably excluded, choose monitoring by episode frequency: Holter for frequent symptoms, a longer event or patch monitor for infrequent ones. Ask the patient to record the timing and symptoms of episodes so they can be matched to the trace. Check FBE, thyroid function and electrolytes, and arrange echocardiography if structural disease is suspected.\n\nFor stable exertional chest discomfort, assess cardiovascular risk and arrange timely diagnostic testing or cardiology review. Address smoking, BP and lipids while the diagnosis is clarified. Do not attribute symptoms to anxiety until the pattern and risk factors have been evaluated.\n\n### Handover and follow-up\n\nUse ISBAR: identity, suspected problem, onset and time of last symptoms, relevant background, observations and ECG findings, treatment given and the urgency required. Send copies of the ECGs and the medicine and allergy list with the patient.\n\nFor outpatient care, tell the patient which symptoms require an ambulance and who will review the monitoring and test results.",
      "formerly": [
        "G17"
      ]
    },
    {
      "id": "G08",
      "domain": "GP",
      "group": "Cardiovascular, metabolic and renal",
      "title": "Chronic kidney disease follow-up",
      "focus": "Screen, stage CKD and plan community monitoring, risk reduction, medicine review and recall.",
      "first_pass": true,
      "priority": "Core",
      "saq_cases": [],
      "core_ids": [
        "P016",
        "P023",
        "P094"
      ],
      "gp_tasks": [
        "Identify CKD risk and interpret eGFR/albuminuria over time",
        "Plan monitoring, medication precautions and chronic-condition follow-up"
      ],
      "notes": "### Definition and staging\n\n**Chronic kidney disease** (CKD) is reduced kidney function or a marker of kidney damage persisting for at least `three months`. The time criterion separates it from acute kidney injury, such as a single low eGFR during dehydration.\n\neGFR describes filtration capacity; urinary albumin reveals glomerular damage even when filtration is normal. Confirm both eGFR and urine albumin:creatinine ratio (ACR) on repeat testing. Use an early-morning urine specimen, which reduces variation from posture and activity, and exclude transient rises from infection, strenuous exercise or menstruation.\n\nStage by both kidney function and albuminuria:\n\n- **eGFR (mL/min/1.73 m²):** G1 `≥90`; G2 `60–89`; G3a `45–59`; G3b `30–44`; G4 `15–29`; G5 `<15`. **G1 and G2 count as CKD only with another marker of damage.**\n- **Urine ACR (mg/mmol):** A1 `<3`; A2 `3–30`; A3 `>30`. Some Australian pathways use sex-specific thresholds; follow the laboratory or pathway in use.\n\nCause, eGFR and albuminuria together predict progression and cardiovascular risk better than creatinine alone.\n\n### Assessment\n\n- **Causes:** diabetes and hypertension are the commonest. Also consider vascular disease, family history, stones or obstruction, systemic inflammatory symptoms, and medicines including NSAIDs, contrast and herbal products.\n- **Examination:** BP, volume status and weight.\n- **Urine:** persistent haematuria with proteinuria suggests glomerular disease.\n- **Imaging:** renal ultrasound for suspected obstruction.\n\nA normal creatinine can conceal impairment in someone with low muscle mass.\n\n### Investigations for complications\n\nCheck electrolytes, bicarbonate and FBE, and add calcium and phosphate as disease advances. Anaemia may reflect low erythropoietin but still needs evaluation for iron deficiency and blood loss. The rate of eGFR change is more informative than any single result.\n\n### Management\n\nCardiovascular events are more likely than kidney failure for most people with CKD. Control of BP and diabetes and smoking cessation reduce both.\n\n#### ACE inhibitor or ARB\n\nIndicated in albuminuric disease. Check creatinine and potassium before and about `1–2 weeks` after starting or increasing.\n\nA small creatinine rise reflects the intended fall in glomerular pressure. A rise of `>30%` or significant hyperkalaemia needs reassessment for dehydration, interactions, renal artery disease or another cause. Do not combine an ACE inhibitor with an ARB.\n\n#### SGLT2 inhibitor\n\nAn SGLT2 inhibitor slows progression in suitable patients with CKD, including some without diabetes; eligibility depends on eGFR, albuminuria and indication. Give sick-day and perioperative advice.\n\n#### Safe prescribing\n\nAvoid NSAIDs and adjust renally cleared drugs. Use the renal estimate appropriate to each medicine: DOAC dosing often uses calculated creatinine clearance, the measure used in their dosing trials, not laboratory eGFR.\n\n#### Care plan\n\nExplain that monitoring aims to prevent complications, since kidney disease is often silent. Record review intervals for BP, ACR and eGFR, the medicines, dietitian input when needed, and who follows results.\n\nSodium moderation and individualised nutrition help; indiscriminate fluid restriction and highly restrictive diets do not help early CKD.\n\n### Referral\n\nRefer to nephrology for:\n\n- eGFR `<30`.\n- Rapid sustained decline.\n- Significant persistent albuminuria: urine ACR `>30 mg/mmol` (Kidney Health Australia).\n- Haematuria with renal impairment.\n- Resistant hypertension.\n- Uncertain cause or systemic disease.\n\nDiscuss kidney replacement options and conservative kidney management early enough to allow an informed choice in advanced disease.\n\n### Acute deterioration\n\n> [!escalate]\n> Acute oliguria or anuria, pulmonary oedema, severe hyperkalaemia, uraemic complications or an infected obstructed kidney needs emergency care.\n\nUse intake and output, recent weight, BP, oedema and medicines to judge whether fluid is needed. Give fluid only when assessment supports volume depletion, and reassess after each volume; do not start automatic maintenance fluid.",
      "formerly": [
        "G20"
      ]
    },
    {
      "id": "G09",
      "domain": "GP",
      "group": "Cardiovascular, metabolic and renal",
      "title": "Thyroid disease in general practice",
      "focus": "Hypo/hyperthyroidism, interpretation of thyroid tests, medication counselling and neck lump triage.",
      "first_pass": true,
      "priority": "Core",
      "saq_cases": [],
      "core_ids": [
        "P059",
        "P066",
        "P072",
        "P093",
        "P099",
        "P104",
        "P105"
      ],
      "gp_tasks": [
        "Interpret TSH/FT4 patterns in context",
        "Counsel on levothyroxine or antithyroid treatment and follow-up"
      ],
      "notes": "### Definitions\n\n**Thyrotoxicosis** is excess thyroid-hormone action from any cause. **Hyperthyroidism** is increased hormone synthesis and secretion by the thyroid gland. The distinction matters for treatment: Graves disease and toxic nodules synthesise new hormone, whereas thyroiditis releases stored hormone.\n\n### Interpreting TSH and free T4\n\nTSH is regulated by negative feedback from thyroid hormone, so reading it with free T4 locates the problem.\n\n- **High TSH, low free T4:** primary hypothyroidism.\n- **High TSH, normal free T4:** subclinical hypothyroidism.\n- **Suppressed TSH, raised free T4 and/or T3:** primary thyrotoxicosis.\n- **Low free T4 with normal or low TSH:** the pituitary is not responding. Consider central hypothyroidism or severe non-thyroidal illness.\n\nBiotin supplements distort some assays; ask about them when results and presentation disagree.\n\n### Clinical features\n\n- **Hypothyroidism:** fatigue, cold intolerance, constipation, dry skin, weight gain, bradycardia and menstrual change.\n- **Hyperthyroidism:** heat intolerance, sweating, weight loss, tremor, palpitations, diarrhoea and anxiety.\n\nExamine pulse and rhythm, BP, reflexes, proximal strength, the thyroid and the eyes. Graves disease may cause a diffuse goitre and ophthalmopathy.\n\n### Investigations for cause\n\n- **Thyroid peroxidase antibodies:** support autoimmune hypothyroidism.\n- **TSH-receptor antibodies:** support Graves disease.\n- **Ultrasound:** for a structural abnormality, not for every abnormal TSH. A nodule needs ultrasound risk assessment and possible FNA. If TSH is suppressed, functional imaging may be relevant after specialist assessment.\n\nPainful thyroiditis may follow a viral illness and often passes through hyperthyroid then hypothyroid phases.\n\nRepeat a mild isolated abnormality before committing to lifelong treatment; transient changes during non-thyroidal illness or thyroiditis are common. Persistently marked TSH elevation, symptoms, pregnancy plans and antibodies favour treating subclinical disease. Pregnancy has its own targets and monitoring.\n\n### Levothyroxine\n\nReplaces deficient hormone.\n\n- Take it consistently, usually on an empty stomach, several hours apart from iron and calcium.\n- Start cautiously in older people and in coronary disease: a rapid rise in metabolic demand can provoke angina or arrhythmia.\n- Titrate by TSH after about `6–8 weeks`. Levothyroxine's long half-life means TSH takes weeks to reach a new steady state.\n- Warn about overtreatment (palpitations, tremor), which increases AF and bone-loss risk.\n\nReview stable patients annually, and test earlier in pregnancy, after major weight change or when interacting medicines change.\n\n### Carbimazole\n\nReduces hormone synthesis in Graves disease and toxic nodular disease. It does not help most destructive thyroiditis, in which preformed hormone leaks from damaged follicles. A beta blocker can relieve tremor and palpitations while definitive treatment takes effect.\n\nCheck baseline FBE and liver tests. Use free T4 and T3 to guide early treatment, because TSH can stay suppressed after they improve.\n\n> [!counsel]\n> Fever, sore throat or mouth ulcers mean **stop carbimazole and have an urgent FBE** to exclude agranulocytosis. Jaundice or significant abdominal symptoms need urgent review for liver injury.\n\nPregnancy or planned pregnancy needs specialist medication advice; do not stop treatment abruptly.\n\n### Radioiodine and surgery\n\nRadioiodine and thyroidectomy are definitive alternatives to antithyroid drugs for selected patients, and both commonly lead to later hypothyroidism. Radioiodine is contraindicated in pregnancy and breastfeeding and can worsen active Graves eye disease. The choice depends on the diagnosis, goitre size, relapse and preference.\n\n### Escalation\n\n> [!escalate]\n> Fever, tachyarrhythmia, agitation and systemic illness may indicate thyroid storm. Hypothermia, bradycardia and reduced consciousness may indicate myxoedema coma. Both are emergencies.\n\n> [!escalate]\n> Stridor from a thyroid mass is an emergency because the airway is threatened.\n\nProgressive compressive symptoms, rapid nodule growth, a hard fixed mass or concerning nodes need prompt specialist referral for possible malignancy.",
      "formerly": [
        "G21"
      ]
    },
    {
      "id": "G10",
      "domain": "GP",
      "group": "Respiratory and sleep",
      "title": "Asthma and COPD in adults",
      "focus": "Diagnose and stage obstructive disease, inhaler technique, acute adult asthma, exacerbation prevention, community-acquired pneumonia, vaccination, smoking cessation.",
      "first_pass": true,
      "priority": "Core",
      "saq_cases": [
        {
          "id": "deck-geri-copd",
          "title": "COPD",
          "set": "MD3 SAQ Revision Deck"
        },
        {
          "id": "deck-paeds-acute-asthma",
          "title": "Acute asthma",
          "set": "MD3 SAQ Revision Deck"
        }
      ],
      "core_ids": [
        "P023",
        "P026",
        "P034",
        "P107"
      ],
      "gp_tasks": [
        "Interpret spirometry/PEFR and demonstrate inhaler/spacer technique",
        "Explain action plans, prevent exacerbations and support smoking cessation"
      ],
      "notes": "### Asthma versus COPD\n\nBoth obstruct airflow; they differ in how the obstruction behaves.\n\n- **Asthma:** variable wheeze, cough, chest tightness and breathlessness, often with night symptoms or exercise and allergen triggers.\n- **COPD:** persistent airflow obstruction, usually after tobacco smoke or other inhalational exposure.\n\nAn atypical pattern raises heart failure, bronchiectasis, upper-airway disease and lung cancer.\n\n### Spirometry\n\nSpirometry measures FEV1, FVC and their ratio after maximal inspiration and a sustained forceful expiration. It is effort dependent, so require acceptable, repeatable blows. A low FEV1/FVC indicates obstruction; bronchodilator testing shows whether it reverses.\n\n- **Asthma:** a rise in FEV1 of `≥12%` and `≥200 mL` after bronchodilator supports variable airflow limitation in an adult. A negative test does not exclude asthma, which may be quiescent on the day; repeat when symptomatic or use other variability testing.\n- **COPD:** persistent post-bronchodilator FEV1/FVC `<0.70` in the right clinical setting. Measuring after bronchodilator stops reversible narrowing being mistaken for fixed obstruction.\n\nFEV1 grades airflow limitation; symptoms and exacerbations guide treatment.\n\n### Asthma review\n\nAssess current control (daytime symptoms, night waking, activity limitation, reliever use) and future risk (oral steroid courses, admissions, previous ICU care).\n\nBefore increasing treatment, watch the patient use their inhaler and ask about adherence; poor technique and non-adherence commonly explain apparent failure. Address smoking, rhinitis, obesity, occupational exposure and triggers.\n\n### Asthma treatment\n\nAsthma is inflammatory, so adults and adolescents need **inhaled corticosteroid (ICS)-containing treatment**.\n\n> [!pitfall]\n> SABA-only treatment is no longer recommended. It relieves symptoms without treating inflammation and is associated with severe exacerbations.\n\nMatch the regimen to symptom burden:\n\n- **Mild asthma:** as-needed low-dose budesonide–formoterol, so each reliever dose also delivers ICS.\n- **More persistent disease:** maintenance-and-reliever therapy (MART) with a suitable ICS–formoterol product.\n- **Alternative:** regular ICS-containing maintenance with salbutamol as reliever.\n\nFormoterol acts rapidly, so ICS–formoterol products can serve as relievers; ICS/LABA products containing salmeterol cannot. State the product and the action-plan maximum explicitly.\n\nExplain that ICS treats airway inflammation while bronchodilators relieve narrowing. Rinse and spit after maintenance ICS to reduce thrush and dysphonia.\n\nProvide a written action plan stating usual treatment, what to do when symptoms or reliever use rise, and when to seek urgent help. Name the medicines, doses and device; do not rely on inhaler colour.\n\n### Inhaler, spacer and peak-flow technique\n\n**Pressurised metered-dose inhaler with spacer:**\n\n1. Remove the cap, check the mouthpiece, shake, insert into the spacer and make a firm lip seal.\n2. Fire **one puff at a time**; several puffs fired into the spacer together reduce the dose inhaled.\n3. Inhale slowly and deeply and hold the breath if able, or take several normal breaths through the spacer.\n4. Shake again before each puff.\n\nA young child needs a well-fitting mask over nose and mouth. Ask the patient or carer to demonstrate the technique back.\n\n**Dry-powder inhalers** rely on the patient's own inspiration to disperse the powder. They need a forceful deep inhalation and are not used with a spacer.\n\n**Peak flow:** reset the marker, stand or sit upright, inhale fully, seal the lips and blow out hard and fast. Record the best of three. Compare with the person's best and their action plan. Peak flow is effort dependent and does not replace diagnostic spirometry.\n\n### Acute asthma\n\nJudge severity from how the person speaks, breathes and responds, not from the wheeze, which needs airflow and can fade as an attack worsens. Arrange transfer to hospital when they cannot speak in whole sentences, SpO₂ is `≤94%`, or breathing has not improved within minutes of bronchodilator. Drowsiness, exhaustion, cyanosis, a silent chest or falling respiratory effort is life-threatening: call an ambulance and treat while waiting.\n\n1. Give salbutamol `100 micrograms` per puff by pMDI and spacer, one puff at a time with tidal breathing: `4–12 puffs` for a mild to moderate attack, `12 puffs` for a severe one. Repeat every `20 minutes` in the first hour if breathing has not settled. Use a nebuliser (`5 mg`, or two `5 mg` nebules if life-threatening) only when a spacer cannot be used.\n2. Give oxygen when SpO₂ is `<92%`, titrated to `93–95%`, or `88–92%` with a risk of hypercapnia. Over-oxygenation causes harm without benefit.\n3. Start oral prednisolone early, because it takes hours to act: `37.5–50 mg` daily for a total of `5–10 days`. A short course needs no taper.\n4. In a severe attack, ipratropium is added to salbutamol, and IV magnesium is a hospital treatment for a poor response.\n\nA patient who recovers in the clinic is observed for at least `four hours` before going home, with an interim written plan, enough reliever, a preventer containing at least a medium dose of ICS, and the prednisolone course. Review within `3–5 days` and again a couple of weeks later, asking why the attack happened: adherence, technique, triggers and an inadequate preventer are the usual answers.\n\nTreatment in children differs in doses and in the place of corticosteroids; see C06 (Treatment by severity (RCH)).\n\n### COPD management\n\n**COPD-X** organises long-term care:\n\n- **C**onfirm the diagnosis.\n- **O**ptimise function with bronchodilators and pulmonary rehabilitation.\n- **P**revent deterioration through smoking cessation and vaccination.\n- **D**evelop self-management.\n- **X**: manage exacerbations.\n\nLAMA and/or LABA improve symptoms. Add ICS selectively, for frequent exacerbations, eosinophilic inflammation or coexisting asthma, because its benefit must be balanced against pneumonia risk.\n\nAssess nutrition, exercise, ability to use the inhaler, mood and oxygen eligibility. Long-term oxygen requires documented hypoxaemia on formal assessment.\n\n### COPD exacerbation\n\nRecord observations and oxygen saturation and assess severity. Consider pneumonia, PE and heart failure as alternatives or precipitants.\n\n- Increase short-acting bronchodilator.\n- Give a short course of oral corticosteroid for significant exacerbations: prednisolone `30–50 mg daily` for `5 days`.\n- Give an antibiotic when bacterial features such as purulent sputum are present: amoxicillin or doxycycline for `5 days`.\n- With hypercapnia risk, titrate oxygen to `88–92%` pending blood gases; uncontrolled oxygen can worsen CO2 retention.\n\n> [!escalate]\n> In an exacerbation of either asthma or COPD, a silent chest, inability to speak, cyanosis, exhaustion or confusion needs emergency treatment.\n\nReview after every exacerbation of asthma or COPD to adjust treatment and to check that the written plan worked.\n\n### Community-acquired pneumonia\n\n*Community-acquired pneumonia* (CAP) is acute infection of the lung parenchyma acquired outside hospital. The usual picture is cough, fever, breathlessness, sputum and pleuritic pain, with tachypnoea and focal signs such as crackles, bronchial breathing or dullness. Older people often present instead with confusion, falls or reduced intake, sometimes without fever. Atypical organisms (Mycoplasma, Chlamydia and Legionella species) more often cause a dry cough, headache and systemic symptoms out of proportion to the chest signs.\n\nAcute bronchitis causes cough with normal observations and no focal signs, and does not need antibiotics. Consider heart failure, PE, an exacerbation of asthma or COPD, and an obstructing lung cancer presenting as infection.\n\nSeverity decides where treatment happens. Measure respiratory rate, SpO₂, BP and conscious state. *CRB-65* gives one point each for new confusion, respiratory rate `≥30`, systolic BP `<90` or diastolic `≤60 mmHg`, and age `≥65`. A score of `0` usually allows treatment at home; `≥2` calls for hospital assessment, as does hypoxaemia, multilobar disease, inability to take oral treatment, significant comorbidity or lack of support at home. SMART-COP is used in Australian hospitals to predict the need for intensive respiratory or vasopressor support.\n\nA chest X-ray is not needed for a well adult with a clear clinical picture. Arrange one when the diagnosis is uncertain, a complication such as effusion is suspected, the patient is not improving, or lung cancer is a risk; then repeat it at about `six weeks` to confirm resolution. Test for influenza and COVID-19 when they are circulating, since antivirals may be indicated. Sputum culture is not routine in the community.\n\nFor low-severity CAP:\n\n- **First-line:** amoxicillin `1 g orally three times daily`, for `5 days` if the patient is improving.\n- **Atypical infection likely, or penicillin allergy:** doxycycline `100 mg twice daily`, or clarithromycin.\n- **Not improving at `48 hours`:** add doxycycline or clarithromycin and reassess; combination treatment from the start is reasonable when review at 48 hours is not possible.\n\n> [!counsel]\n> Cough and tiredness can last several weeks, but fever should settle within a few days. Seek review within two days if you are not improving, and urgently for worsening breathlessness, confusion, chest pain or inability to keep fluids down.\n\nChildren are managed differently; see C06 (Pneumonia).",
      "formerly": [
        "G03"
      ]
    },
    {
      "id": "G11",
      "domain": "GP",
      "group": "Respiratory and sleep",
      "title": "Sleep concerns and obstructive sleep apnoea",
      "focus": "Insomnia history, behavioural management and adult OSA assessment; medication and safety review.",
      "first_pass": false,
      "priority": "Selective",
      "saq_cases": [],
      "core_ids": [
        "P015",
        "P034",
        "P059"
      ],
      "gp_tasks": [
        "Take a sleep/medication history and provide sleep advice",
        "Recognise OSA features and when to refer for testing"
      ],
      "notes": "### Sleep history\n\nAsk about bedtime, sleep onset, awakenings, waking time, naps, shift work, caffeine and alcohol, screens, pain, mood and medicines. Recall of sleep is often inaccurate; a two-week sleep diary can reveal circadian delay, excessive time in bed or an irregular routine.\n\n- **Chronic insomnia:** persistent difficulty starting or maintaining sleep, with daytime impairment, despite adequate opportunity.\n- **Sleepiness** differs from fatigue and points to a sleep disorder.\n- **Restless legs:** an evening or rest-related urge to move the legs, relieved by movement.\n\n### Obstructive sleep apnoea\n\nIn **obstructive sleep apnoea** (OSA), the upper airway repeatedly narrows or closes during sleep despite ongoing respiratory effort, fragmenting sleep and often causing intermittent hypoxaemia. Loud snoring, witnessed apnoeas, choking, morning headache and daytime sleepiness suggest it.\n\nExamine BMI and neck habitus, airway features and BP, and assess cardiometabolic disease. STOP-Bang estimates OSA risk and the Epworth scale quantifies subjective sleepiness; neither confirms nor excludes the diagnosis.\n\nIn children, snoring with witnessed pauses, restless sleep, daytime behaviour change or growth problems suggests OSA. Tonsil and adenoid assessment and referral depend on severity.\n\n### Investigations\n\nA home sleep study suits selected uncomplicated patients; polysomnography is preferred for complex disease or a possible alternative sleep disorder.\n\nThe **apnoea–hypopnoea index** (AHI) counts respiratory events per hour. Adult categories:\n\n- **Mild:** `5–14`.\n- **Moderate:** `15–29`.\n- **Severe:** `≥30`.\n\nSymptoms, oxygenation, cardiovascular risk and occupation also determine management; the AHI does not capture impact.\n\nCheck ferritin and iron studies in restless legs, since iron deficiency aggravates it and is treatable. Otherwise, test only for a suspected medical cause of insomnia.\n\n### Insomnia management\n\nCBT for insomnia (CBT-I) is first-line for persistent insomnia. It combines:\n\n- **A regular rising time.**\n- **Stimulus control:** use the bed mainly for sleep. If persistently awake, get up for a quiet activity and return when sleepy, so the bed is reassociated with sleep.\n- **Sleep restriction or compression:** a supervised, tailored sleep window that reduces awake time in bed and builds sleep pressure, expanded as sleep consolidates. It causes initial sleepiness, so adapt it for severe sleepiness, bipolar disorder, seizures or safety-critical work.\n- **Cognitive work** on sleep-related worry, and relaxation.\n\nSleep hygiene supports treatment but is not the whole intervention. Reduce late caffeine, avoid alcohol as a sleep aid (it fragments later sleep), and align light and activity with the desired schedule. Treat pain, depression or anxiety at the same time.\n\nBenzodiazepines and Z-drugs carry dependence, falls and next-day impairment risks. If used, agree a limited indication and duration and review; do not issue indefinite repeats.\n\n### OSA management\n\n- **Lifestyle and positional measures:** weight management where relevant, exercise, avoiding evening alcohol and sedatives, and positional therapy for positional disease.\n- **CPAP:** splints the upper airway open and works only when used. Review mask fit, nasal dryness, pressure comfort and nightly use.\n- **Mandibular advancement device:** for selected patients after dental assessment.\n- **Surgery:** for selected anatomical problems or treatment failure.\n\nAsk specifically about drowsy driving and near misses. Advise a person with significant sleepiness not to drive or do hazardous work until assessed and controlled, considering licensing and occupational requirements.\n\nAt follow-up, review daytime function and treatment use. Unexplained severe somnolence, hypoventilation or major psychiatric risk needs prompt referral.",
      "formerly": [
        "G24"
      ]
    },
    {
      "id": "G12",
      "domain": "GP",
      "group": "General symptoms and blood",
      "title": "Fatigue, night sweats and unintentional weight loss",
      "focus": "Clarifying tiredness and weight loss, focused examination, first-line tests, and dated review when tests are unrevealing.",
      "first_pass": true,
      "priority": "Core",
      "saq_cases": [
        {
          "id": "deck-geri-unintentional-weight-loss",
          "title": "Unintentional weight loss",
          "set": "MD3 SAQ Revision Deck"
        },
        {
          "id": "2021-ummss-q8",
          "title": "Low mood and fatigue in a young adult",
          "set": "2021 UMMSS"
        }
      ],
      "core_ids": [
        "P059",
        "P093",
        "P105"
      ],
      "gp_tasks": [
        "Prioritise red flags, initial investigations and safety-netting",
        "Interpret FBC, iron studies and B12 where relevant"
      ],
      "notes": "### Clarifying the symptom\n\n\"Tired\" may mean sleepiness, weakness, breathlessness or lack of motivation, and each points in a different direction, so establish which the patient means before going further. The history then looks for an explanation and for features of serious disease:\n\n- Duration and effect on function.\n- Sleep, mood and alcohol.\n- Diet and weight change.\n- Bleeding and bowel symptoms.\n- Fever and night sweats.\n- Medicines.\n- Possible pregnancy.\n\n**Unintentional weight loss** of `>5%` of body weight over `6–12 months` is significant, particularly with focal symptoms or appetite change. The main causes to consider are:\n\n- Malignancy.\n- Chronic infection.\n- Inflammatory disease.\n- Hyperthyroidism and diabetes.\n- Malabsorption.\n- Depression.\n- Difficulty obtaining or swallowing food.\n\n**Night sweats** occur with menopause, medicines, anxiety, infection and malignancy. Drenching, persistent sweats with fever, weight loss, lymphadenopathy or a relevant exposure need targeted investigation, but an isolated symptom does not imply lymphoma.\n\n### Examination\n\nRecord observations and weight, and compare the weight with previous measurements; a documented trajectory is more informative than the patient's estimate. Then examine for:\n\n- Pallor and lymphadenopathy.\n- Thyroid enlargement.\n- Cardiorespiratory and abdominal signs, including organomegaly.\n- Relevant neurological findings.\n\nBruising, petechiae, bone pain, recurrent infection or organomegaly suggests marrow or haematological disease rather than uncomplicated iron deficiency.\n\n### Investigations\n\nInitial tests are:\n\n- FBE and ferritin.\n- Renal function and liver tests.\n- TSH.\n- Glucose.\n\nAdd CRP, B12 and folate, coeliac serology, a pregnancy test or infection testing according to the presentation.\n\n### Follow-up\n\nWhen initial tests are unrevealing, book a dated review with serial weights and targeted investigation. An evolving cause often declares itself only over time, so an open-ended \"return if needed\" is unsafe. A likely benign cause can be treated, but unexplained or persistent symptoms, outstanding results and referrals still need tracking.\n\n> [!escalate]\n> New systemic signs, bleeding, a neurological deficit or rapid progression needs same-day reassessment.",
      "formerly": [
        "B02",
        "G09"
      ]
    },
    {
      "id": "G13",
      "domain": "GP",
      "group": "General symptoms and blood",
      "also_in": [
        "CAH"
      ],
      "title": "Anaemia, bruising and bleeding",
      "focus": "Interpreting anaemia and iron studies, finding the cause, replacement, bleeding patterns, and pallor or bruising in children.",
      "first_pass": true,
      "priority": "Core",
      "saq_cases": [
        {
          "id": "deck-paeds-iron-deficiency",
          "title": "Anaemia in infancy",
          "set": "MD3 SAQ Revision Deck"
        },
        {
          "id": "deck-paeds-leukaemia",
          "title": "Childhood leukaemia",
          "set": "MD3 SAQ Revision Deck"
        }
      ],
      "core_ids": [
        "P004",
        "P071"
      ],
      "notes": "### Definitions\n\n**Anaemia** is haemoglobin below the appropriate reference range. **Iron deficiency** is depleted iron stores; it can occur before anaemia develops. The FBE and iron studies therefore answer different questions.\n\n### Classifying anaemia\n\nCell size is the first branch. The reticulocyte count then separates reduced production from an appropriate marrow response to bleeding or haemolysis. Request a blood film with abnormal counts, haemolysis or suspected marrow disease.\n\n- **Microcytic:** iron deficiency, thalassaemia or chronic inflammation. Low ferritin confirms iron deficiency, but **ferritin is an acute-phase reactant and can be normal or high during inflammation**; interpret it with transferrin saturation and CRP. Thalassaemia trait often shows marked microcytosis with a relatively preserved red-cell count.\n- **Normocytic:** early iron deficiency, chronic disease, CKD, acute bleeding or haemolysis. Reticulocytosis, raised unconjugated bilirubin and LDH, and low haptoglobin support haemolysis.\n- **Macrocytic:** B12 or folate deficiency, alcohol, liver disease, hypothyroidism, medicines or marrow disorders. Neuropathy, impaired vibration or proprioception, or cognitive change raises B12 deficiency.\n\n### Iron deficiency\n\nIron deficiency needs a cause. In a man or postmenopausal woman, investigate for gastrointestinal loss or malabsorption, chiefly occult bleeding from colorectal or gastric cancer: arrange gastroscopy and colonoscopy, with coeliac serology. Menstrual loss may explain deficiency in a premenopausal woman but should not obscure other red flags.\n\n> [!pitfall]\n> A negative screening iFOBT does not remove the diagnostic need for endoscopy.\n\n### Treatment\n\n**Oral iron** suits many stable patients. Choose the preparation by its **elemental iron** content; a typical adult dose is about `100 mg` elemental iron daily, or on alternate days if poorly tolerated.\n\n- Warn about dark stools, nausea and constipation. Taking iron with food improves tolerance but reduces absorption.\n- Separate from interacting medicines such as thyroxine.\n- Recheck FBE after `2–4 weeks` for a response. Continue for about `three months` after haemoglobin normalises to replenish stores.\n\nPoor response suggests non-adherence, ongoing loss, malabsorption or the wrong diagnosis. IV iron suits selected patients.\n\n**B12 deficiency:** replace parenterally when there is neurological disease or significant malabsorption.\n\n> [!pitfall]\n> **Do not give folate alone without excluding B12 deficiency.** The anaemia can improve while neurological injury progresses.\n\nBase transfusion on symptoms, haemodynamics and context, not a haemoglobin number alone.\n\n### Bruising and bleeding\n\nThe bleeding pattern points to the mechanism:\n\n- **Mucocutaneous bleeding** (bruising, epistaxis, menorrhagia, gum bleeding): platelet disorder or von Willebrand disease.\n- **Deep muscle or joint bleeding:** coagulation-factor deficiency.\n\nLifelong versus new symptoms, family history, anticoagulants and liver disease narrow the cause further. Investigate with FBE and platelets, blood film, PT/INR and APTT.\n\n> [!escalate]\n> Major bleeding, pancytopenia, severe symptomatic anaemia or suspected acute leukaemia needs emergency care or same-day haematology review, according to stability.\n\n### Pallor and bruising in children\n\nPallor, persistent fever, bruising or petechiae, bone pain, limp, lymphadenopathy or hepatosplenomegaly may indicate leukaemia from marrow infiltration. Ordinary infection symptoms do not exclude it.\n\n> [!escalate]\n> Suspected leukaemia needs an FBE and blood film and same-day paediatric assessment.\n\n> [!pitfall]\n> Do not give steroids before specialist assessment of suspected leukaemia; they can obscure the diagnosis.",
      "formerly": [
        "C12",
        "G09"
      ]
    },
    {
      "id": "G14",
      "domain": "GP",
      "group": "Gastrointestinal and liver",
      "title": "Reflux, dyspepsia, dysphagia and H. pylori",
      "focus": "Upper GI symptoms in general practice: alarm features, PPI use and step-down, dysphagia patterns and H. pylori testing.",
      "first_pass": true,
      "priority": "Core",
      "saq_cases": [],
      "core_ids": [
        "P002",
        "P033",
        "P046",
        "P063"
      ],
      "gp_tasks": [
        "Explain initial GORD/IBS care, coeliac test pitfalls and gastroscopy red flags",
        "Interpret LFT patterns, counsel on fatty liver and consider hepatitis testing"
      ],
      "notes": "### Definitions\n\n**Gastro-oesophageal reflux disease** (GORD) causes heartburn and regurgitation. **Dyspepsia** is upper abdominal discomfort, fullness or early satiety.\n\n### Assessment and alarm features\n\nAsk about NSAIDs, alcohol, weight, meal timing and alarm features. Acute severe epigastric pain is a different problem from dyspepsia and is assessed as in B01 (Acute abdominal pain), because pancreatitis, biliary disease, perforation and myocardial infarction can present this way.\n\n> [!pitfall]\n> Dysphagia, bleeding, persistent vomiting, iron-deficiency anaemia or weight loss raises malignancy, stricture or ulcer disease. Refer for gastroscopy; do not continue empirical acid suppression indefinitely.\n\nThe dysphagia pattern suggests its mechanism:\n\n- **Solids, progressing to liquids:** mechanical obstruction.\n- **Solids and liquids from the outset:** dysmotility.\n- **Choking or coughing on swallowing:** oropharyngeal dysphagia; arrange swallowing assessment.\n\n### Management of reflux\n\nAdvise smaller and earlier meals, not lying down after eating, weight loss when appropriate and avoidance of individual triggers.\n\nOffer a time-limited proton-pump inhibitor (PPI) trial, commonly `4–8 weeks`, then review and step down to the lowest effective regimen. Take it before a meal, because PPIs inhibit only actively secreting proton pumps.\n\n### H. pylori\n\nTest for H. pylori in dyspepsia without an immediate indication for endoscopy.\n\n- **Test:** urea breath test or stool antigen, both of which detect active infection.\n- **Preparation:** stop PPIs for `two weeks` and antibiotics or bismuth for `four weeks` beforehand when safe; these suppress bacterial load and cause false negatives.\n- **Treatment:** first-line triple therapy is a PPI plus amoxicillin `1 g` plus clarithromycin `500 mg`, all twice daily for `14 days`. Adjust for penicillin allergy and previous antibiotic exposure.\n- **Confirm eradication** with a breath or stool test at least `four weeks` after treatment. Do not use serology, which stays positive after cure.",
      "formerly": [
        "G22"
      ]
    },
    {
      "id": "G15",
      "domain": "GP",
      "group": "Gastrointestinal and liver",
      "title": "Bowel symptoms, coeliac disease, IBD and rectal bleeding",
      "focus": "Change in bowel habit, investigation by risk, IBS, coeliac disease, IBD, perianal problems and referral.",
      "first_pass": true,
      "priority": "Core",
      "saq_cases": [
        {
          "id": "deck-gp-bowel-cancer-screening",
          "title": "Bowel cancer screening",
          "set": "MD3 SAQ Revision Deck"
        },
        {
          "id": "deck-geri-unintentional-weight-loss",
          "title": "Unintentional weight loss",
          "set": "MD3 SAQ Revision Deck"
        }
      ],
      "core_ids": [
        "P002",
        "P012",
        "P025",
        "P028",
        "P073",
        "P074",
        "P081"
      ],
      "gp_tasks": [
        "Assess change in bowel habit and colorectal cancer risks",
        "Explain screening, red flags and community referral"
      ],
      "notes": "### History\n\nAsk about stool frequency and consistency, duration, pain, blood or mucus, urgency, nocturnal symptoms, weight loss, fever, recent antibiotics or travel, and family history. Review medicines such as metformin, laxatives, opioids and iron.\n\n- **Overflow:** constipation with watery leakage may be overflow around impaction.\n- **Organic disease:** diarrhoea with blood, nocturnal waking, anaemia or weight loss **suggests organic disease**, not irritable bowel syndrome; functional symptoms rarely wake people, cause bleeding or cause weight loss.\n\n### Examination\n\nAssess hydration, weight and the abdomen. When it will answer a clinical question, perform consented perianal inspection and digital rectal examination for tenderness, masses, blood and impacted stool. Explain the examination, offer a chaperone and use lubrication; do not force it through severe pain.\n\n### Investigations\n\nFor chronic diarrhoea or concerning change in bowel habit:\n\n- **Bloods:** FBE and ferritin, inflammatory markers, renal function, and coeliac serology **while the patient is eating gluten**.\n- **Faecal calprotectin:** separates intestinal inflammation from functional symptoms; infection and NSAIDs also raise it.\n- **Stool pathogen testing:** for severe or bloody illness, prolonged symptoms, outbreak or travel risk, or immunocompromise. Test for C. difficile after antibiotics or healthcare exposure.\n\nRefer for colonoscopy with persistent rectal bleeding, iron-deficiency anaemia, a mass or a concerning change in bowel habit. Haemorrhoids can coexist with colorectal cancer.\n\n> [!pitfall]\n> Population bowel screening does not replace diagnostic referral. Do not repeat a positive screening iFOBT to avoid colonoscopy.\n\n### Irritable bowel syndrome\n\n**IBS** is a disorder of gut–brain interaction: altered bowel sensitivity and motility cause real pain without destructive inflammation.\n\n> [!current]\n> **Rome V (2026)** criteria: recurrent, non-continuous abdominal pain or discomfort on average at least `three days per month` over the last three months, with onset at least six months earlier, associated with **at least two** of:\n>\n> - Defaecation.\n> - A change in stool frequency.\n> - A change in stool form.\n\nThe older **Rome IV** criteria require abdominal pain on average at least `one day a week`, with the same duration and associations. After red-flag assessment, the criteria support a positive diagnosis without endless normal tests.\n\nReference: [Australian Prescriber: IBS diagnosis and management (2026)](https://australianprescriber.tg.org.au/articles/diagnosis-and-management-of-irritable-bowel-syndrome.html).\n\n- **General measures:** regular meals, soluble fibre, physical activity and attention to triggers.\n- **Low-FODMAP diet:** a dietitian-supervised trial for selected patients, followed by structured reintroduction. Lifelong broad exclusion risks unnecessary restriction.\n- **Drug treatment:** directed at the dominant symptom, constipation or diarrhoea.\n- **Gut-directed psychological therapy:** where distress and symptom amplification are prominent.\n\nFor constipation without IBS features, including faecal impaction, see R07 (Building a bowel regimen).\n\n### Coeliac disease\n\nGluten triggers immune-mediated small-bowel injury, not an immediate food allergy, so trace exposure matters and symptoms can be delayed.\n\nConsider it with chronic diarrhoea, bloating, iron deficiency, weight loss, osteoporosis or a family history.\n\n- **Serology:** tissue transglutaminase IgA plus total IgA, **taken while eating gluten**. Total IgA identifies IgA deficiency, in which the IgA test is falsely negative; use IgG-based tests instead.\n- **Confirmation:** refer a positive result to gastroenterology for duodenal biopsy before starting a lifelong gluten-free diet.\n\n> [!pitfall]\n> Normal serology after gluten avoidance does not exclude coeliac disease.\n\nAfter diagnosis, arrange dietitian-led avoidance of wheat, barley and rye, check for deficiencies and bone health, and repeat serology to confirm response. Offer testing to first-degree relatives.\n\n### Inflammatory bowel disease\n\n- **Ulcerative colitis:** continuous mucosal inflammation, usually starting at the rectum.\n- **Crohn disease:** discontinuous, transmural inflammation anywhere in the GI tract, causing strictures, fistulas or perianal disease.\n\nDiagnosis requires endoscopy with biopsy and appropriate imaging.\n\nIn shared care with gastroenterology, manage nutrition and anaemia, complete vaccination (ideally before immunosuppression), and monitor medication.\n\n- **Mesalazine:** used in many ulcerative colitis regimens.\n- **Corticosteroids:** induce remission in selected flares; unsuitable for maintenance.\n- **Immunomodulators and biologics:** require specialist monitoring and infection-risk assessment.\n\n> [!escalate]\n> Frequent bloody stools with systemic illness, severe pain or distension needs same-day hospital review for acute severe colitis.\n\n### Perianal problems\n\n- **Haemorrhoids:** bright-red bleeding or prolapse. Soften stools and avoid straining. Persistent symptoms may need procedural treatment after diagnostic assessment.\n- **Fissure:** sharp pain during and after defaecation with a little fresh blood. Soften stools and use local treatment. A chronic fissure may need topical glyceryl trinitrate or diltiazem ointment to relieve the sphincter spasm that impairs healing. An off-midline or multiple fissures suggest another cause, including Crohn disease.\n- **Abscess:** constant focal pain, swelling and sometimes fever. Needs urgent surgical drainage; antibiotics alone are inadequate.\n\n> [!pitfall]\n> Do not attribute bleeding to haemorrhoids without considering age, anaemia, change in bowel habit and cancer risk.\n\n### Escalation and follow-up\n\n> [!escalate]\n> Large-volume bleeding, melaena with instability, severe dehydration, peritonism or obstruction needs emergency care.\n\nBook explicit review of persistent symptoms and outstanding results, even after a plausible benign diagnosis.\n\nAcute abdominal pain, including suspected diverticulitis, is assessed as in B01 (Acute abdominal pain).",
      "formerly": [
        "B02",
        "G10",
        "G22"
      ]
    },
    {
      "id": "G16",
      "domain": "GP",
      "group": "Gastrointestinal and liver",
      "title": "Liver tests, hepatitis and jaundice",
      "focus": "Liver enzyme patterns, hepatitis serology, gallstone disease, jaundice, fatty liver, abdominal distension and escalation.",
      "first_pass": true,
      "priority": "Core",
      "saq_cases": [],
      "core_ids": [
        "P001",
        "P055"
      ],
      "gp_tasks": [
        "Explain initial GORD/IBS care, coeliac test pitfalls and gastroscopy red flags",
        "Interpret LFT patterns, counsel on fatty liver and consider hepatitis testing"
      ],
      "notes": "### Liver test patterns\n\n- **ALT/AST predominant:** hepatocellular injury.\n- **ALP/GGT predominant:** cholestasis, meaning impaired bile formation or flow.\n- **Isolated raised bilirubin:** haemolysis or Gilbert syndrome.\n\nAlbumin and INR reflect synthetic function but have non-hepatic influences too. Alcohol, metabolic risk, medicines and supplements, viral exposure and symptoms often identify the cause. Ultrasound assesses biliary obstruction and liver structure.\n\n### Hepatitis B serology\n\n- **HBsAg:** current infection.\n- **Anti-HBs:** immunity.\n- **Anti-HBc:** previous or current natural infection, not vaccination alone, because the vaccine contains only surface antigen.\n\nFurther markers, HBV DNA, ALT and fibrosis assessment determine phase and treatment need. Normal ALT does not exclude chronic hepatitis or fibrosis.\n\n### Hepatitis C serology\n\nAntibody indicates exposure; HCV RNA confirms current infection. Direct-acting antivirals cure most infections but do not prevent reinfection. Before treatment, assess fibrosis, interactions and hepatitis B status.\n\n### Counselling in viral hepatitis\n\nAdvise avoiding blood exposure and sharing injecting equipment, safer sex when indicated, and alcohol reduction. Offer hepatitis B vaccination to household and sexual contacts.\n\n### Fatty liver disease\n\n**Metabolic dysfunction-associated steatotic liver disease** (MASLD) is associated with diabetes and metabolic risk. **Steatosis** is fat accumulation in hepatocytes; **fibrosis** is scar deposition that can distort liver architecture and progress to cirrhosis.\n\nFibrosis, not fat, determines liver prognosis. Estimate fibrosis risk with FIB-4, followed by elastography when indicated; ultrasound shows fat but cannot stage fibrosis.\n\nSupport activity, nutrition and weight loss where appropriate, and reduce cardiovascular risk, since cardiovascular disease is a major cause of death in this group.\n\n### Gallstone disease\n\nGallstones are common and usually asymptomatic; incidental stones need no treatment. Symptoms arise when a stone obstructs the cystic or common bile duct:\n\n- **Biliary colic:** a stone transiently obstructing the cystic duct. Steady, severe right upper-quadrant or epigastric pain, often after a fatty meal, sometimes radiating to the right scapula, lasting from about half an hour to several hours and then resolving. The patient is afebrile and well between attacks, and liver tests are usually normal.\n- **Acute cholecystitis:** persistent obstruction with inflammation of the gallbladder wall. Pain lasting more than about `six hours`, fever, right upper-quadrant tenderness with Murphy's sign, and raised WCC and CRP.\n- **Common bile duct stone:** jaundice, dark urine and a cholestatic enzyme pattern; with infection it causes cholangitis (below). A stone can also cause pancreatitis, with epigastric pain radiating to the back and a raised lipase.\n\nUltrasound shows stones, gallbladder wall thickening, pericholecystic fluid and duct dilatation. Check liver function, lipase, FBE and CRP, and record an ECG for epigastric pain, since an inferior myocardial infarction can mimic biliary pain. Peptic ulcer, pancreatitis, hepatitis, right lower-lobe pneumonia and renal colic are the other alternatives.\n\nBiliary colic is treated with analgesia, an NSAID with an opioid if needed, and referral for elective laparoscopic cholecystectomy, because further attacks and complications are common. Suspected cholecystitis, or any jaundice, fever or raised lipase, needs same-day hospital assessment; cholecystitis is treated with antibiotics and early cholecystectomy.\n\n### Jaundice\n\nAsk about pain, fever, pale stools and dark urine, itch, alcohol and medicines, travel and weight loss. Bilirubin and the enzyme pattern separate hepatocellular, cholestatic and haemolytic processes; arrange ultrasound for suspected obstruction.\n\n> [!escalate]\n> **Fever, right upper-quadrant pain and jaundice suggest cholangitis**, which needs emergency hospital care.\n\nPainless progressive jaundice raises pancreatic or biliary malignancy and needs prompt referral, as does unexplained weight loss.\n\n### Abdominal distension\n\nCauses include gas, constipation, obesity, pregnancy, a mass and ascites. Investigate new ascites for liver, cardiac and malignant causes, often with diagnostic paracentesis.\n\n### Escalation\n\n> [!escalate]\n> Encephalopathy, rising INR, haematemesis or melaena, or features of acute liver failure need emergency care.",
      "formerly": [
        "B02",
        "G22"
      ]
    },
    {
      "id": "G17",
      "domain": "GP",
      "group": "Urinary and men’s health",
      "title": "Urinary symptoms, UTI, retention and haematuria",
      "focus": "Characterising LUTS, urine specimens, UTI treatment, renal colic, acute retention and investigation of visible haematuria.",
      "first_pass": true,
      "priority": "Core",
      "saq_cases": [
        {
          "id": "2016-mhagp-q5",
          "title": "Lower urinary tract symptoms, bowel screening and smoking/alcohol",
          "set": "2016 MH/GP"
        }
      ],
      "core_ids": [
        "P016",
        "P047",
        "P101"
      ],
      "gp_tasks": [
        "Take a targeted LUTS history and consider IPSS",
        "Assess infection, obstruction or haematuria and decide referral"
      ],
      "notes": "### Lower urinary tract symptoms\n\n- **Storage symptoms:** urgency, frequency and nocturia.\n- **Voiding symptoms:** hesitancy, weak or intermittent stream, straining and incomplete emptying.\n\nAsk about dysuria, fever, flank pain, blood, sexual exposure, pregnancy, constipation, neurological symptoms, medicines, and fluid and caffeine intake.\n\nFrequent small voids differ from **true polyuria**, which suggests excess intake, diabetes or impaired concentrating ability. Chronic symptoms often improve once fluid timing, constipation and contributing medicines are addressed. For longer-term management see G19 (Treating LUTS) and G18 (Conservative and medical treatment).\n\n### Urine specimens\n\nA midstream sample collects bladder urine after the urethra has been flushed.\n\n1. Wash hands; separate the labia or retract the foreskin.\n2. Pass the first urine into the toilet, then collect the middle portion without touching the inside of the container; finish in the toilet.\n3. Label and send promptly, refrigerating if delayed.\n\nFor chlamydia and gonorrhoea NAAT, use **first-catch urine, not midstream**, because the first portion carries urethral organisms. A self-collected vaginal swab is often preferable in women.\n\n### Interpreting urine tests\n\nNitrites and leucocyte esterase support UTI but do not replace symptoms or culture. Send culture in pregnancy, men, children, recurrent or complicated infection, pyelonephritis and treatment failure.\n\nA positive culture without urinary or systemic symptoms is usually **asymptomatic bacteriuria**: do not treat, except in pregnancy or before selected invasive urological procedures. It is especially common in older people and catheter users, so test urine only when symptoms or systemic findings suggest infection.\n\n> [!pitfall]\n> **Cloudy or smelly urine alone does not establish a UTI.**\n\n### Lower UTI\n\nUncomplicated cystitis causes dysuria and frequency without fever or flank pain. For a non-pregnant adult woman:\n\n- **Trimethoprim:** `300 mg orally at night for three days`, or\n- **Nitrofurantoin:** `100 mg orally every six hours for five days`.\n\nChoose by renal function (nitrofurantoin is less effective and more toxic in renal impairment), previous culture, allergy and local resistance. Pregnancy, men and other complicated infections need different regimens; for pregnancy, see O05 (Urinary tract infection in pregnancy).\n\n### Upper or complicated UTI\n\nFever, rigors, flank pain or systemic illness suggests pyelonephritis or complicated infection. Send culture and assess further. Nitrofurantoin is unsuitable, because renal tissue concentrations are inadequate.\n\n> [!escalate]\n> Sepsis or an infected obstructed kidney is an emergency.\n\nReference for antibiotic examples: [SA Health adult UTI guideline](https://www.sahealth.sa.gov.au/wps/wcm/connect/c7a3f980432af25ca680f68cd21c605e/UTI%2Bguideline%2Bv2.1_FINAL.pdf?MOD=AJPERES).\n\n### Renal colic\n\nA stone obstructing the ureter causes sudden, severe loin pain radiating to the groin, testis or labium, coming in waves. The patient is restless and cannot find a comfortable position, unlike someone with peritonitis, who lies still. Nausea and vomiting are common, and most have haematuria on dipstick.\n\n**In a person over 60 with a first episode of apparent renal colic, consider a leaking abdominal aortic aneurysm.** Pyelonephritis, ectopic pregnancy, appendicitis, biliary disease and testicular torsion are the other important alternatives.\n\nSend urine for microscopy and culture, and check FBE, renal function, calcium and urate, with a pregnancy test where relevant. Non-contrast low-dose CT of the kidneys, ureters and bladder is the diagnostic test; ultrasound shows hydronephrosis and avoids radiation in pregnancy and younger patients.\n\nAn NSAID is first-line analgesia, as effective as an opioid, if renal function allows; add an opioid and an antiemetic as needed. Stones under `5 mm` usually pass. Tamsulosin can help distal stones of about `5–10 mm` to pass. Ask the patient to strain the urine so a stone can be analysed.\n\nA patient whose pain is controlled, who is afebrile and has normal renal function and two functioning kidneys can usually be managed at home, with imaging to confirm passage and urology follow-up if it has not occurred within a few weeks. **Infection behind an obstructing stone needs emergency decompression**, by stent or nephrostomy, as well as antibiotics. AKI, a solitary kidney, bilateral obstruction, uncontrolled pain or vomiting, and a large stone also need urgent urology. To prevent recurrence, advise enough fluid for about `2.5 L` of urine a day, and investigate recurrent stones metabolically.\n\n### Acute urinary retention\n\n> [!escalate]\n> Acute painful retention needs same-day bladder drainage by a trained clinician.\n\nInvestigate obstruction, constipation, medicines and neurological disease. Record residual volume, renal function and urine output; large-volume retention can be followed by post-obstructive diuresis needing monitoring.\n\n> [!pitfall]\n> Blood at the meatus after pelvic trauma suggests urethral injury. Obtain specialist assessment before catheterising.\n\n### Visible haematuria\n\nCauses include malignancy, infection, stones, renal disease and trauma.\n\n> [!pitfall]\n> Anticoagulation does not explain visible haematuria. It commonly unmasks bleeding from an underlying lesion, so investigate as usual.\n\nArrange urine microscopy and culture, renal function and imaging. Refer promptly to urology; assessment usually includes cystoscopy because imaging can miss small bladder tumours. Recheck haematuria attributed to a genuine UTI after treatment; refer if it persists or is otherwise unexplained.\n\n> [!escalate]\n> Clot retention, heavy bleeding, renal impairment or systemic illness needs emergency care.",
      "formerly": [
        "G11",
        "R07"
      ]
    },
    {
      "id": "G18",
      "domain": "GP",
      "group": "Urinary and men’s health",
      "also_in": [
        "OGN",
        "RAPP"
      ],
      "title": "Urinary incontinence and pelvic organ prolapse",
      "focus": "Incontinence types and contributors, assessment, pelvic floor and bladder training, medicines, catheters and prolapse.",
      "first_pass": true,
      "priority": "Core",
      "saq_cases": [
        {
          "id": "2021-ummss-q2",
          "title": "Urinary incontinence in an older woman",
          "set": "2021 UMMSS"
        },
        {
          "id": "2016-wcah-q2",
          "title": "Urinary incontinence",
          "set": "2016 WH/CAH"
        }
      ],
      "core_ids": [
        "P101"
      ],
      "notes": "### Types of incontinence\n\n- **Stress:** leakage with coughing, exertion or raised abdominal pressure.\n- **Urgency:** leakage after a sudden compelling urge to void. Mixed stress and urgency symptoms are common.\n- **Overflow:** leakage from incomplete emptying.\n- **Functional:** difficulty reaching or using the toilet.\n\nThe type determines treatment.\n\n**Pelvic organ prolapse** may cause a vaginal bulge, heaviness, difficulty emptying bladder or bowel, or needing to support the prolapse digitally.\n\n### Contributors\n\nCommon contributors are childbirth, previous surgery, menopause, chronic cough, constipation and medicines. Older people often have several causes; diuretics, sedatives and anticholinergics are frequent reversible ones.\n\n### History\n\nAsk about onset, dysuria, haematuria, stream, incomplete emptying, nocturia, fluid and caffeine intake, bowel function, mobility and cognition. Effects on activity and sexual life indicate how much treatment the person wants.\n\n### Assessment\n\n- **Examination:** with consent, examine the abdomen for a full bladder, the vulva and vaginal tissues or the prostate, and the nervous system as the history suggests. Assess prolapse on straining and pelvic floor contraction; perform a cough stress test when appropriate.\n- **Bladder diary:** three days of voiding times and volumes, fluid intake, urgency and leakage.\n- **Urinalysis:** for infection and haematuria.\n- **Post-void bladder scan:** for retention when emptying is impaired.\n\nUrodynamics is not a routine first test for straightforward symptoms.\n\n### Conservative and medical treatment\n\nSupervised pelvic floor training for at least `three months` is **first-line** for stress and mixed incontinence. A correct contraction lifts and squeezes around the vagina and anus without straining or breath-holding. Many people contract the wrong muscles, so a pelvic health physiotherapist confirms technique and tailors sustained and rapid contractions.\n\n> [!pitfall]\n> Repeatedly stopping urine midstream is not a training programme and can disrupt normal bladder emptying.\n\n**Bladder training** for urgency gradually lengthens planned voiding intervals with urge-suppression strategies. Reduce excessive caffeine and fluid without causing dehydration, and address constipation, cough and weight, each of which loads the pelvic floor.\n\n- **Vaginal oestrogen:** helps postmenopausal tissue and urinary symptoms.\n- **Antimuscarinics:** cause dry mouth, constipation, retention and cognitive effects, which matter particularly in frail older people.\n- **Beta-3 agonists (e.g. mirabegron):** avoid anticholinergic effects but need BP and contraindication review.\n\nFunctional incontinence often responds to practical change: toilet access, clothing, lighting, mobility, and scheduled or prompted toileting. Maintain hydration and treat constipation, which presses on the bladder and impairs emptying.\n\n### Catheters\n\n> [!pitfall]\n> Do not insert an indwelling catheter for staff convenience or uncomplicated incontinence. Catheters cause infection, trauma and loss of mobility.\n\nWhen a catheter is necessary, record the indication, insert it aseptically, keep a closed freely draining system and review daily whether it can come out. Intermittent catheterisation may be better for selected persistent emptying problems. Investigate haematuria, recurrent infection, obstruction or renal impairment.\n\nCall experienced help for difficult catheterisation or suspected urethral injury; do not make repeated traumatic attempts.\n\n### Pelvic organ prolapse\n\n- **Pessary:** supports symptomatic prolapse. Requires fitting, vaginal tissue care and scheduled review and removal to prevent ulceration.\n- **Surgery:** for persistent bothersome symptoms, after discussing benefits, recurrence and procedure-specific harms.\n\nUrinary retention, recurrent infection, haematuria, obstructive renal injury or an ulcerated or bleeding prolapse needs further assessment, not just continence medication.",
      "formerly": [
        "G11",
        "O13",
        "R07"
      ]
    },
    {
      "id": "G19",
      "domain": "GP",
      "group": "Urinary and men’s health",
      "title": "Men’s health: prostate, erectile dysfunction and scrotal lumps",
      "focus": "BPH/IPSS, sexual dysfunction and cardiovascular risk, PSA discussions, what follows a raised PSA, and selective androgen assessment.",
      "first_pass": false,
      "priority": "Selective",
      "saq_cases": [
        {
          "id": "2016-mhagp-q5",
          "title": "Lower urinary tract symptoms, bowel screening and smoking/alcohol",
          "set": "2016 MH/GP"
        }
      ],
      "core_ids": [
        "P037",
        "P053",
        "P054",
        "P077",
        "P088",
        "P101"
      ],
      "gp_tasks": [
        "Use IPSS and assess bothersome LUTS",
        "Discuss PSA testing and ED medication safely and without overtesting"
      ],
      "notes": "### Benign prostatic hyperplasia\n\n**Benign prostatic hyperplasia** (BPH) is proliferation of glandular and stromal tissue around the prostatic urethra, which can obstruct outflow. Gland size, obstruction and symptom severity do not necessarily correlate.\n\nThe **International Prostate Symptom Score** (IPSS) rates seven symptoms (incomplete emptying, frequency, intermittency, urgency, weak stream, straining and nocturia) plus a separate quality-of-life question. Bother, more than symptom count, determines treatment.\n\nThe same symptoms occur with diabetes, infection, medicines, neurological disease and bladder dysfunction.\n\n### Assessment\n\n- **Examination:** abdomen for retention, external genitalia and, when relevant and consented, the prostate. A smooth enlarged prostate supports BPH; a hard nodule is concerning, but a normal examination does not exclude cancer.\n- **Investigations:** urinalysis and culture, renal function and post-void residual, selected by symptoms.\n\nEvaluate haematuria and recurrent infection in their own right.\n\n### Treating LUTS\n\nFor mild symptoms, adjust evening fluids, caffeine and alcohol, treat constipation and review contributing medicines.\n\n- **Alpha blocker (e.g. tamsulosin):** relaxes prostatic smooth muscle and improves flow within days to weeks. Warn about postural dizziness, falls and ejaculatory change, and tell the patient to inform an ophthalmologist before cataract surgery.\n- **5-alpha-reductase inhibitor (e.g. finasteride):** shrinks a substantially enlarged prostate over months. Discuss sexual adverse effects. It roughly halves measured PSA, which affects interpretation.\n\nCombination treatment or surgery may suit persistent symptoms or complications. Acute retention needs same-day drainage.\n\nRefer to urology for recurrent retention, recurrent infection, bladder stones, obstructive renal impairment or refractory symptoms.\n\n> [!pitfall]\n> LUTS do not imply prostate cancer, and prostate cancer is often asymptomatic.\n\n### Erectile dysfunction\n\n- **History:** in private, ask about onset, consistency, spontaneous and morning erections, libido, ejaculation, pain, relationship context, distress and medicines. Preserved morning erections suggest intact vascular and neural function.\n- **Contributors:** diabetes, vascular disease, smoking, depression, antihypertensives and pelvic surgery.\n- **Cardiovascular risk:** ED shares risk factors with coronary disease and can precede it. Check BP, metabolic risk and exercise tolerance.\n- **Testosterone:** measure a morning level when there is low libido or other hypogonadal features. Confirm a low result on a separate morning and investigate the cause.\n\nTreat underlying disease and medication contributors, with psychosexual support when useful.\n\n**PDE5 inhibitors (e.g. sildenafil)** enhance the response to sexual stimulation; they do not produce an erection without it. Explain timing, headache, flushing and dyspepsia, and when to seek help for a prolonged erection or sudden visual symptoms.\n\n> [!pitfall]\n> **Nitrates are contraindicated** with PDE5 inhibitors because the combination causes profound hypotension. Check cardiovascular stability, interaction with alpha blockers, and the product-specific interval before a nitrate can be given.\n\n> [!pitfall]\n> Do not prescribe testosterone for an isolated low result or normal ageing without a confirmed diagnosis of hypogonadism.\n\n### Scrotal lumps\n\nExamine both testes and the groins with consent and a chaperone. Decide whether the lump lies within the testis, beside it or above it, because **intratesticular masses carry the malignancy risk**.\n\n- **Painless firm intratesticular lump:** prompt ultrasound and urology referral for possible cancer.\n- **Epididymal cyst:** separate from the testis.\n- **Varicocele:** dilated veins, more apparent on standing.\n- **Hydrocele:** surrounds the testis and often transilluminates.\n\nThese findings guide imaging but do not reliably exclude cancer.\n\n### Scrotal and groin pain\n\n> [!escalate]\n> Sudden severe unilateral testicular pain with vomiting or an abnormal lie is **torsion until proven otherwise** and needs emergency surgical review; do not delay for imaging.\n\n> [!escalate]\n> A tender irreducible groin lump with vomiting suggests an incarcerated hernia, which is an emergency.\n\nGradual epididymal pain with urinary symptoms or sexual exposure suggests epididymo-orchitis, but consider torsion first. Send urine and STI tests and treat according to the likely source.\n\nChildhood genital presentations are covered in C12 (Acute scrotum).\n\n### PSA testing\n\nPSA is **prostate-specific, not cancer-specific**: BPH, inflammation and infection also raise it.\n\nTesting may detect treatable cancer earlier, but it also causes false positives, biopsy complications, overdiagnosis, and treatment-related incontinence and sexual dysfunction. The balance depends on age, family history, life expectancy and preference. Under the 2026 Australian guideline, men aged 50–69 are offered a PSA test every `two years` after an informed discussion. Men at about twice the usual risk, because of a brother with prostate cancer, a father diagnosed before 65, a BRCA2 variant or Black African ancestry, are offered it from `45`. From 70, testing depends on health and a life expectancy of more than about seven years.\n\nAvoid testing during UTI or prostatitis and soon after urological instrumentation, which transiently raise PSA. An abnormal result may need repeating before referral, depending on its level.\n\nA raised PSA is not a diagnosis of cancer. At 50–69, a result of `≥3.0 µg/L` (`≥2.0 µg/L` at higher risk; `≥5.5 µg/L` from 70) is repeated within `1–3 months`. A confirmed result or an abnormal examination leads to urology referral, where MRI comes before any biopsy and spares some men a biopsy. A confirmed cancer is graded and staged, and these findings, with life expectancy and preference, determine management:\n\n- **Active surveillance:** for low-risk cancer. Regular PSA, MRI and repeat biopsy, with curative treatment offered if the cancer progresses.\n- **Radical prostatectomy or radiotherapy:** for clinically significant localised cancer. Both can cause urinary incontinence and erectile dysfunction, and radiotherapy can also affect the bowel.\n- **Watchful waiting:** for men with limited life expectancy. Symptoms are treated as they arise, without curative intent.\n\nShared follow-up and survivorship are in G01 (After a cancer diagnosis).\n\nSymptoms or a suspicious examination need assessment regardless of screening preference. Record the agreed testing and follow-up plan.",
      "formerly": [
        "G23"
      ]
    },
    {
      "id": "G20",
      "domain": "GP",
      "group": "Sexual health and relationships",
      "title": "Sexual health and sexually transmitted infections",
      "focus": "Confidential sexual history, STI testing, treatment of common infections, syphilis serology, PEP, partner management, vaginal discharge and trichomoniasis.",
      "first_pass": false,
      "priority": "Core",
      "saq_cases": [
        {
          "id": "deck-og-pid",
          "title": "Pelvic inflammatory disease",
          "set": "MD3 SAQ Revision Deck"
        },
        {
          "id": "2016-mhagp-q6",
          "title": "Late period, sexual health screening and contraception",
          "set": "2016 MH/GP"
        }
      ],
      "core_ids": [
        "P088"
      ],
      "gp_tasks": [
        "Take a confidential sexual history and offer STI tests/contraception",
        "Provide patient-centred counselling and follow-up"
      ],
      "notes": "### Sexual history\n\nBegin by explaining confidentiality and its safety and legal limits; patients disclose more when they know what will happen to the information. Use inclusive language, without assuming gender, anatomy or relationship structure, and offer time alone, a qualified interpreter and a chaperone for examination. The patient can decline or stop an examination at any point.\n\nThe history covers:\n\n- Partners: number, gender and recent change.\n- Practices and sites of exposure (genital, anal, oral).\n- Condom and other protection use.\n- Previous STIs and testing.\n- Contraception and pregnancy intentions.\n- Symptoms: pain, bleeding, discharge, sexual dysfunction.\n- Coercion or violence.\n\n### Testing\n\n- **NAAT for chlamydia and gonorrhoea:** vaginal swab or first-catch urine, plus rectal and pharyngeal swabs when those sites were exposed.\n- **Blood tests:** HIV, syphilis and hepatitis according to risk, vaccination and pregnancy.\n\nBefore testing, discuss window periods, how results will be given, and partner notification.\n\n> [!escalate]\n> HIV post-exposure prophylaxis is time-critical: start immediately, and within `72 hours` of a qualifying exposure. Offer PrEP for ongoing risk.\n\n### Chlamydia\n\n- **Uncomplicated genital infection:** doxycycline `100 mg orally twice daily for seven days`.\n- **Pregnancy:** azithromycin `1 g orally once`.\n\nRetest at `three months`, because reinfection, often from an untreated partner, is common. A test of cure is not routine, but is indicated in pregnancy and selected circumstances, no earlier than `four weeks` after treatment; NAAT can detect non-viable organisms before then.\n\n### Gonorrhoea\n\nUncomplicated genital or anorectal infection: ceftriaxone `500 mg IM once` plus azithromycin `1 g orally once`.\n\nTake gonococcal cultures before antibiotics, but do not wait for results: culture provides antimicrobial susceptibility, which NAAT cannot. Pharyngeal infection, co-infection and complicated disease have specific regimens.\n\nPerform a site-specific test of cure, usually at `two weeks`, and retest for reinfection at `three months`.\n\n### Syphilis\n\nSyphilis is increasing in Australia, including congenital syphilis, so test whenever there is risk and in every pregnancy.\n\n- **Primary:** a painless chancre at the site of inoculation, with regional lymphadenopathy.\n- **Secondary:** a widespread rash that often involves the palms and soles, mucosal lesions, lymphadenopathy and systemic symptoms.\n- **Latent:** no symptoms, detected only by serology.\n\nDiagnosis is serological, with a PCR swab of any lesion. Early syphilis is treated with benzathine benzylpenicillin `2.4 million units IM once`; late latent syphilis needs three weekly doses. Two kinds of serological test answer different questions:\n\n- **Treponemal tests (an EIA or CMIA screen, confirmed by TPPA):** detect antibody to the organism itself. They become positive early and usually stay positive for life, so they show that infection has occurred, not whether it is active.\n- **Non-treponemal test (RPR):** detects antibody to lipid released by tissue damage. Its titre rises with active disease and falls after treatment, so it measures activity and response.\n\nA positive treponemal test with a reactive RPR and no documented treatment needs treatment. A positive treponemal test with a non-reactive RPR usually means past treated infection or a false positive, but can be very early infection; repeat it after a recent exposure. A primary chancre can precede seroconversion, which is why the lesion is swabbed for PCR.\n\nAfter treatment, repeat the RPR at `3, 6 and 12 months`. A `fourfold` fall in titre (two dilutions, for example from 1:32 to 1:8) indicates an adequate response; a fourfold rise suggests reinfection or treatment failure, and a titre that has not fallen fourfold by 12 months needs specialist advice. In pregnancy, involve a sexual health or infectious diseases specialist and the obstetric team, since penicillin is the only treatment that reliably prevents congenital syphilis.\n\nSyphilis is notifiable, and partner notification and follow-up serology confirm the response.\n\n### Advice after treatment\n\n> [!counsel]\n> Avoid sex for at least `seven days` after starting treatment, and until the course is complete, symptoms have resolved and partners have been treated.\n\nSupport contact tracing and complete any required notification.\n\n### Vaginal discharge\n\n- **Candidiasis:** itch with thick discharge. Treat with topical clotrimazole or oral fluconazole `150 mg once` (avoid fluconazole in pregnancy).\n- **Bacterial vaginosis:** thin, malodorous discharge. Treat with metronidazole `400 mg orally twice daily for seven days`.\n- **Cervicitis:** discharge or postcoital bleeding.\n\nExamination and appropriate swabs distinguish these from trichomoniasis and non-infective irritation. Pelvic pain or tenderness raises PID; see O11 (Pelvic inflammatory disease).\n\n> [!pitfall]\n> Reassess persistent symptoms; do not keep repeating empirical thrush treatment.\n\n### Trichomoniasis\n\nTrichomonas vaginalis is a sexually transmitted protozoan. In women it can cause a frothy, yellow-green, malodorous discharge, vulvovaginal irritation and dysuria, but many infections are asymptomatic; men are usually asymptomatic or have urethritis. Diagnose by NAAT on a vaginal swab or first-catch urine, since microscopy misses many infections, and offer testing for other STIs.\n\n- **Women:** metronidazole `400 mg twice daily for seven days`.\n- **Men:** metronidazole `2 g orally once`.\n\nMetronidazole can be used in pregnancy. Treat current partners at the same time and advise avoiding sex until both have completed treatment, because untreated partners cause reinfection. A test of cure is needed only if symptoms persist, about `three weeks` after treatment.\n\nReference: [Australian STI Management Guidelines](https://sti.guidelines.org.au/).",
      "formerly": [
        "G18"
      ]
    },
    {
      "id": "G21",
      "domain": "GP",
      "group": "Sexual health and relationships",
      "also_in": [
        "OGN"
      ],
      "title": "Contraception and emergency contraception",
      "focus": "Comparing methods by typical-use effectiveness, contraindications, missed pills and emergency contraception.",
      "first_pass": true,
      "priority": "Core",
      "saq_cases": [
        {
          "id": "2016-mhagp-q6",
          "title": "Late period, sexual health screening and contraception",
          "set": "2016 MH/GP"
        },
        {
          "id": "deck-og-postpartum-contraception",
          "title": "Postpartum contraception",
          "set": "MD3 SAQ Revision Deck"
        }
      ],
      "core_ids": [
        "P041"
      ],
      "gp_tasks": [
        "Take a confidential sexual history and offer STI tests/contraception",
        "Provide patient-centred counselling and follow-up"
      ],
      "notes": "### Comparing methods\n\nCompare methods by typical-use effectiveness, bleeding, reversibility, administration, contraindications and STI protection. Typical use is the figure that matters, because methods that depend on daily action fail more often in real life than in ideal use. Only condoms reduce STI transmission.\n\n- **Etonogestrel implant:** highly effective for `three years`; irregular bleeding is common. Explain insertion and removal under local anaesthetic. Check for enzyme-inducing drugs, which lower progestogen levels enough to cause failure.\n- **Hormonal IUD:** highly effective and usually reduces bleeding and cramps. Mirena lasts `eight years` for contraception and Kyleena `five`; Mirena used for endometrial protection with systemic oestrogen is replaced at `five years`. Discuss insertion discomfort, early irregular bleeding, expulsion and rare perforation. Exclude pregnancy and assess infection risk.\n- **Copper IUD:** hormone-free, highly effective, and the most effective emergency contraceptive. May increase bleeding and cramps. Duration is product-specific.\n- **Combined pill or vaginal ring:** reliable cycle control when used correctly, with a small increase in VTE risk. Check BP, smoking, migraine with aura, VTE history or thrombophilia, vascular disease, liver disease and postpartum status.\n- **Progestogen-only pill or depot medroxyprogesterone:** options when oestrogen is unsuitable. Discuss bleeding changes and adherence. Depot can cause weight gain, reversible loss of bone density and delayed return of fertility.\n\n> [!pitfall]\n> Migraine with aura and significant thrombotic risk generally contraindicate oestrogen-containing contraception, which further increases ischaemic stroke and VTE risk.\n\n### Starting a method\n\nExclude pregnancy reasonably before starting.\n\n> [!pitfall]\n> A negative test immediately after unprotected sex cannot exclude conception; hCG may not be detectable until about `three weeks` afterwards. Quick-start may be possible with backup contraception and a repeat test.\n\n### Missed combined pill\n\n- Take a late active pill as soon as remembered.\n- If more than `24 hours` late: take the most recent missed pill, continue the pack and use condoms for `seven days`.\n- If fewer than `seven active pills` remain: skip the hormone-free interval, which would otherwise extend the time without ovarian suppression.\n- Consider emergency contraception if the missed pills follow the hormone-free interval and there was recent unprotected sex.\n\nUnusual formulations have product-specific instructions.\n\n### Missed progestogen-only pill\n\n- **Norethisterone or levonorgestrel:** `three-hour` window; `three days` of backup.\n- **Drospirenone:** `24-hour` window; `seven days` of backup.\n\nTake the missed pill promptly and continue. Backup periods follow current Sexual Health Victoria advice. Vomiting, severe diarrhoea and enzyme-inducing medicines also reduce protection.\n\n### Emergency contraception\n\n- **Copper IUD:** within `five days`.\n- **Ulipristal `30 mg`:** within `120 hours`.\n- **Levonorgestrel `1.5 mg`:** as early as possible, preferably within `72 hours`; Australian guidance allows use up to `96 hours`.\n\nChoose by timing, weight, medicines, breastfeeding and suitability.\n\n- **After ulipristal:** **wait five days before starting hormonal contraception**, because progestogens reduce its effect; then use backup until the method is effective.\n- **After levonorgestrel:** hormonal contraception can start immediately.\n\n> [!counsel]\n> Oral emergency contraception does not cover later intercourse. Take a pregnancy test `three weeks` after the exposure, or sooner if symptoms develop.\n\nReference for formulation-specific advice: [Sexual Health Victoria](https://www.shvic.org.au/).",
      "formerly": [
        "G18"
      ]
    },
    {
      "id": "G22",
      "domain": "GP",
      "group": "Sexual health and relationships",
      "also_in": [
        "OGN",
        "MH"
      ],
      "title": "Family violence and reproductive coercion",
      "focus": "Asking safely, assessing immediate danger, collaborative safety planning, referral and documentation.",
      "first_pass": false,
      "priority": "Core",
      "saq_cases": [],
      "core_ids": [],
      "gp_tasks": [
        "Take a confidential sexual history and offer STI tests/contraception",
        "Provide patient-centred counselling and follow-up"
      ],
      "notes": "### Asking\n\nAsk privately whether anyone makes the patient afraid, controls their activities, money or contraception, or threatens or hurts them. **Reproductive coercion** includes interfering with contraception or pressuring decisions about pregnancy.\n\nAcknowledge and validate the disclosure.\n\n### Risk assessment\n\nAssess immediate safety, children, escalating violence, strangulation, weapons and threats to kill. In Victoria, the MARAM framework provides the structured approach to risk assessment used across services.\n\n> [!escalate]\n> Strangulation can cause serious occult injury and strongly predicts future lethal violence, so it needs same-day medical assessment.\n\n### Safety planning and referral\n\nPlan collaboratively, since the person knows the risks of their situation best: a safe destination, a trusted contact, access to documents and money, and a safe way for services to make contact.\n\nChildren exposed to family violence are at risk of harm, and a reasonable belief that a child is at risk of significant harm requires a report to Child Protection. Victorian information-sharing schemes allow relevant information to be shared with other services to assess or manage family violence risk.\n\nWith consent, and within applicable reporting duties, make a warm referral to social work, The Orange Door or a specialist family violence service. Give 24-hour contacts: Safe Steps (1800 015 188) in Victoria and 1800RESPECT (1800 737 732) nationally; 000 for immediate danger.\n\n> [!pitfall]\n> Do not pressure the person to leave, and do not contact the alleged perpetrator. Separation is a period of heightened danger.\n\n### Documentation\n\nDocument objectively: record disclosures in the patient's own words, describe injuries with their size and site (a body map helps), and note who was present. Consider whether shared records, electronic messages, appointment reminders or printed material could be seen by the perpetrator and increase danger.",
      "formerly": [
        "G18"
      ]
    },
    {
      "id": "G23",
      "domain": "GP",
      "group": "Breast and skin",
      "title": "Breast lump, nipple change and breast symptoms",
      "focus": "Triple assessment concept, risk assessment, urgent referral, lactational vs non-lactational symptoms.",
      "first_pass": true,
      "priority": "Core",
      "saq_cases": [
        {
          "id": "2016-wcah-q1",
          "title": "Breastfeeding problems and postpartum contraception",
          "set": "2016 WH/CAH"
        },
        {
          "id": "deck-og-breastfeeding-mastitis",
          "title": "Breastfeeding and lactation problems",
          "set": "MD3 SAQ Revision Deck"
        }
      ],
      "core_ids": [
        "P019",
        "P020",
        "P062",
        "P067"
      ],
      "gp_tasks": [
        "Characterise a breast lump and arrange appropriate assessment",
        "Distinguish symptom assessment from screening"
      ],
      "notes": "### History\n\nAsk when the lump appeared, whether it changes with the cycle, and about pain, pregnancy or lactation, trauma, previous breast disease, hormones and family history. Cyclical change favours a benign hormonally responsive process; family history lowers the threshold for investigation.\n\nCharacterise nipple discharge as spontaneous or expressed, unilateral or bilateral, single-duct or multiduct, and bloody, serous or milky. **Persistent unilateral spontaneous bloody or serous discharge** points to a single-duct lesion such as papilloma or carcinoma and is more concerning than bilateral expressed milky discharge.\n\n### Examination\n\nExplain the examination, obtain consent, offer a chaperone and preserve privacy.\n\n1. **Inspect** both breasts with arms relaxed and then raised, for asymmetry, dimpling, erythema, nipple retraction or peau d'orange; tethering and lymphatic involvement produce these signs.\n2. **Palpate systematically**, recording the lump's location, size, consistency, mobility and attachment to skin or chest wall.\n3. Examine axillary and supraclavicular nodes.\n\nA hard, irregular, fixed lump is suspicious, but **palpation alone cannot establish that a lump is benign**.\n\n### Triple assessment\n\nTriple assessment combines three sources of evidence, because no single test is reliable alone:\n\n- **Clinical:** history and examination.\n- **Imaging:** ultrasound first in younger, pregnant or lactating patients, whose denser breast tissue limits mammography; diagnostic mammography with targeted ultrasound in older patients.\n- **Tissue:** core biopsy of suspicious solid lesions, which provides tissue architecture.\n\n**The three components must be concordant.** A clinically suspicious mass needs specialist evaluation even if one imaging test is reassuring.\n\nExplain what each test is for and how results will be given.\n\n> [!pitfall]\n> Do not send a symptomatic patient to routine BreastScreen in place of diagnostic assessment.\n\nRefer promptly to a breast clinic for a suspicious mass, skin or nipple distortion, pathological discharge or concerning nodes.\n\n### Common benign conditions\n\n- **Fibroadenoma:** a smooth, mobile solid mass in a younger patient. Confirm with concordant clinical and imaging assessment, and biopsy when indicated.\n- **Cyst:** may be tender and fluctuate; ultrasound distinguishes fluid from solid. Aspirate a symptomatic cyst. Investigate bloody fluid, recurrence or a residual mass.\n- **Cyclical mastalgia:** usually bilateral and related to the menstrual cycle. After assessment, reassure and suggest a supportive bra and simple or topical analgesia. Evaluate persistent focal non-cyclical pain.\n- **Galactorrhoea:** causes include pregnancy, breastfeeding, prolactin-raising medicines, hypothyroidism (raised TRH stimulates prolactin) and pituitary disease. Check a pregnancy test, prolactin and TSH. Headache or visual-field symptoms raise a pituitary lesion.\n- **Persistent nipple eczema:** unilateral disease, ulceration or failure to respond to skin treatment raises Paget disease; refer to a specialist.\n\n### Lactational and inflammatory symptoms\n\n**Mastitis** causes local inflammation and may cause systemic symptoms. An **abscess** is a focal collection requiring ultrasound and drainage.\n\nSupport normal breastfeeding or expression; avoid aggressive deep massage and over-pumping. Add analgesia, and antibiotics when bacterial mastitis is likely. See O09 (Mastitis) for feeding assessment and treatment.\n\n> [!pitfall]\n> Diffuse redness and peau d'orange outside a typical, resolving lactational episode may be inflammatory breast cancer, which mimics infection.\n\nIf presumed infection does not improve, re-examine and reassess; do not issue repeated antibiotics without review.\n\n### Follow-up\n\nSet a review point for every pathway and confirm that imaging and biopsy results have been received. Communication, shared care and survivorship after a cancer diagnosis are in G01 (After a cancer diagnosis).",
      "formerly": [
        "G12"
      ]
    },
    {
      "id": "G24",
      "domain": "GP",
      "group": "Breast and skin",
      "title": "Skin lesions, lumps, rashes and itch",
      "focus": "Describing lesions, suspicious pigmented lesions, biopsy, eczema, psoriasis, acne, cellulitis and abscess, other infections, lumps and itch.",
      "first_pass": true,
      "priority": "Core",
      "saq_cases": [
        {
          "id": "deck-gp-hand-dermatitis",
          "title": "Occupational hand dermatitis",
          "set": "MD3 SAQ Revision Deck"
        },
        {
          "id": "deck-gp-shingles-phn",
          "title": "Shingles and post-herpetic neuralgia",
          "set": "MD3 SAQ Revision Deck"
        }
      ],
      "core_ids": [
        "P062",
        "P078",
        "P080",
        "P089"
      ],
      "gp_tasks": [
        "Describe a skin lesion or rash and decide if biopsy/referral is needed",
        "Understand dermoscopy, common treatments and wound follow-up"
      ],
      "notes": "### Describing a lesion\n\nPrecise morphology narrows the differential and makes change detectable.\n\n- **Macule:** flat colour change.\n- **Papule or plaque:** superficial solid elevation.\n- **Nodule:** deeper solid lesion.\n- **Vesicle:** clear fluid.\n- **Pustule:** pus.\n- **Ulcer:** loss of epidermis extending into the dermis.\n\nRecord site, distribution, size, colour, shape, border, surface and evolution, with any scale, crust, excoriation or mucosal involvement. Ask about itch or pain, medicines, contacts, occupation, sun exposure and previous treatment. Photograph with consent to document change.\n\n### Suspicious pigmented lesions\n\nLook for asymmetry, an irregular border, varied colour and above all **evolution**, or an \"ugly duckling\" unlike the person's other lesions. Change and difference from the person's own pattern are more telling than any single static feature.\n\nDermoscopy examines pigment structures, symmetry and vascular patterns. It improves assessment in trained hands but does not replace biopsy of a concerning lesion.\n\n- **BCC:** pearly lesion with telangiectasia.\n- **SCC:** keratotic, tender or ulcerated growing lesion.\n\n> [!pitfall]\n> Amelanotic melanoma is pink, not dark.\n\n### Biopsy\n\nSuspected melanoma needs complete excisional biopsy with a narrow (`2 mm`) clinical margin where feasible, or specialist planning for difficult sites and large lesions. Narrow excision gives the pathologist the whole lesion without compromising later wide excision or lymphatic mapping.\n\n> [!pitfall]\n> **Do not destroy a suspicious lesion before histology.** Breslow thickness determines staging and excision margins.\n\nBiopsy or refer any non-healing or bleeding lesion. A punch biopsy samples only part of a lesion and must suit the diagnostic question.\n\nFor biopsy consent, explain the purpose, local anaesthetic, scar, bleeding and infection, wound care, and how pathology results will be followed up. Review treatment response and results: failure to heal can indicate malignancy, ischaemia or the wrong diagnosis.\n\nCryotherapy treats selected warts and actinic keratoses after diagnosis. Warn about pain, blistering, pigment change and possible repeat treatment.\n\n### Eczema and contact dermatitis\n\nThe skin barrier is defective. Use regular fragrance-free emollient and reduce irritant exposure, with a topical corticosteroid of suitable potency for the site during flares.\n\n- A **fingertip unit** is about `0.5 g` and covers about two adult palms.\n- An adequate short course is safer than prolonged undertreatment. Use weaker products on the face and folds and stronger ones on thick hand skin.\n- For occupational dermatitis, plan glove use and consider patch testing for suspected allergic contact dermatitis.\n\n### Psoriasis\n\n*Psoriasis* is a chronic immune-mediated disease in which epidermal turnover accelerates, producing well-demarcated red plaques with thick silvery scale. Typical sites are the extensor elbows and knees, scalp, natal cleft and umbilicus, and nail pitting and onycholysis are common. *Guttate psoriasis*, a shower of small drop-shaped plaques, can follow streptococcal throat infection. A sharp border, heavy scale and extensor distribution separate psoriasis from eczema, which is ill-defined, itchy and flexural in adults; an annular lesion with an active edge suggests tinea, so scrape it if in doubt.\n\nAsk about joint pain, morning stiffness, swollen digits and heel pain, because psoriatic arthritis affects a substantial minority and early rheumatology referral limits joint damage. Psoriasis is also associated with cardiovascular and metabolic disease and with depression.\n\nTreatment starts with emollients and topical therapy. A potent corticosteroid combined with calcipotriol, a vitamin D analogue, is first-line for plaques; scalp disease responds to corticosteroid and keratolytic preparations, and the face and flexures need weaker corticosteroids. Avoid oral corticosteroids, because withdrawal can provoke a severe pustular or erythrodermic flare. Refer extensive, refractory or nail-dominant disease for phototherapy or systemic treatment, and treat erythroderma or widespread pustules as an emergency.\n\n### Acne\n\nComedones indicate follicular obstruction; papules and pustules indicate inflammation.\n\n- **Foundation:** a topical retinoid plus benzoyl peroxide. The retinoid reduces follicular plugging; benzoyl peroxide is antibacterial without inducing resistance. Warn about initial irritation and that benefit takes weeks.\n- **Moderate inflammatory acne:** add an oral tetracycline, such as doxycycline, with topical non-antibiotic treatment. Avoid antibiotic monotherapy and prolonged unreviewed courses, which promote resistance.\n- **Scarring, nodules or refractory disease:** refer for isotretinoin assessment, including pregnancy-prevention requirements.\n\nRetinoids and tetracyclines require pregnancy precautions.\n\n### Shingles\n\nUnilateral dermatomal pain and vesicles reflect reactivation of varicella-zoster virus.\n\n- Oral antivirals work best started early, within `72 hours`, and may still be indicated later with new lesions or complications. Valaciclovir `1 g three times daily for seven days` is the standard choice.\n- Ophthalmic involvement, immunocompromise or disseminated disease needs urgent assessment.\n- Vesicle fluid can transmit varicella. Cover lesions and avoid contact with susceptible pregnant or immunocompromised people until the lesions have crusted.\n\n### Scabies\n\nNocturnal itch and affected contacts. Treat the patient and close contacts at the same time, since an untreated contact reinfests the patient, and launder clothing and bedding. Permethrin `5%` cream, applied from the neck down, left on overnight and repeated after `one week`, is standard.\n\nItch can persist for weeks while the hypersensitivity reaction settles; it does not necessarily mean treatment failure.\n\n### Cellulitis and skin abscess\n\n*Cellulitis* is bacterial infection of the dermis and subcutaneous tissue, usually streptococcal or staphylococcal; *erysipelas* is a more superficial form with a raised, sharply demarcated edge. The typical picture is spreading, warm, tender erythema, usually on one lower leg, with a portal of entry such as a fissured toe web, wound or ulcer. Fever and malaise can precede the rash.\n\n**Bilateral red legs are rarely cellulitis.** Venous stasis dermatitis, lipodermatosclerosis, contact dermatitis and gout are common mimics, and a swollen calf with little erythema raises DVT; see G06 (Leg swelling). A fluctuant, tender swelling, often pointing, with surrounding erythema is an abscess, usually caused by S. aureus.\n\n- **Uncomplicated cellulitis in a well patient:** oral flucloxacillin or cefalexin `500 mg four times daily` for `5 days`, extended only if improvement is incomplete. Mark the edge of the erythema to judge progress, elevate the limb, and treat the portal of entry, such as tinea between the toes. Redness can spread a little in the first day even when treatment is working.\n- **Abscess:** incision and drainage is the main treatment, since antibiotics penetrate a collection poorly. Add an antibiotic when there is surrounding cellulitis, systemic illness, immunosuppression or a difficult site, and send pus for culture, as community-acquired MRSA is common in some populations.\n\nRefer to hospital for systemic illness, rapid spread, failure to improve on oral treatment within `48 hours`, or facial involvement; see G27 (Periorbital and orbital cellulitis). Pain out of proportion to the signs, tense swelling, bullae, crepitus or skin necrosis suggests necrotising infection, which needs the emergency response below.\n\n### Urgent skin presentations\n\n> [!escalate]\n> Rapidly spreading pain and redness, systemic illness, necrosis, or mucosal blistering after a new drug needs same-day review, or emergency care if necrotising infection or a severe drug reaction is suspected.\n\n### Lumps\n\nAssess location, duration, growth, tenderness, mobility, overlying skin and regional nodes. Lipomas and cysts are common. Refer a rapidly growing, deep, fixed or persistent unexplained mass for imaging.\n\n> [!pitfall]\n> Do not incise an assumed abscess when the diagnosis is uncertain; a vascular lesion or tumour can mimic one.\n\n### Generalised itch\n\n- **With a primary rash:** eczema, urticaria, scabies or another skin disorder.\n- **Without a clear rash:** medicines, cholestasis, renal disease, thyroid disease or a haematological disorder.\n\nFor persistent unexplained itch, check FBE, renal and liver function and TSH, with further tests according to findings.",
      "formerly": [
        "B02",
        "G13"
      ]
    },
    {
      "id": "G25",
      "domain": "GP",
      "group": "Eye, ear, nose and throat",
      "title": "Red eye and acute visual symptoms",
      "focus": "Excluding sight-threatening causes of a red or painful eye, sudden vision loss, eyelid lumps and blepharitis, fluorescein and injuries.",
      "first_pass": true,
      "priority": "Core",
      "saq_cases": [
        {
          "id": "deck-geri-multiple-sclerosis",
          "title": "Multiple sclerosis",
          "set": "MD3 SAQ Revision Deck"
        }
      ],
      "core_ids": [
        "P038",
        "P082",
        "P102"
      ],
      "gp_tasks": [
        "Perform focused eye/ear examination and recognise urgent referral",
        "Interpret otoscopy/audiogram; recognise sight-threatening presentations"
      ],
      "notes": "### Assessment\n\nAsk about onset, pain, photophobia, change in vision, discharge, contact lens use, injury and chemical exposure. Check visual acuity in each eye separately with usual correction, then examine pupils, eye movements, visual fields and the cornea.\n\nConjunctivitis affects only the surface. Pain, reduced vision, marked photophobia, a cloudy cornea or an abnormal pupil is **inconsistent with simple conjunctivitis** and needs same-day ophthalmic assessment.\n\n### Causes of a red or painful eye\n\n- **Conjunctivitis:** gritty discomfort and discharge with preserved vision. Viral disease often starts in one eye and spreads to the other; allergic disease is itchy and bilateral. Advise hygiene and symptom care. Most cases are viral or allergic, so antibiotics are selective; chloramphenicol drops are the usual choice for bacterial conjunctivitis.\n- **Keratitis or corneal ulcer:** corneal inflammation, with epithelial loss and stromal damage in ulceration. Painful red eye with photophobia, reduced vision or corneal opacity, especially in a contact lens wearer. Remove lenses and refer the same day.\n- **Anterior uveitis:** inflammation of the iris and ciliary body. Photophobia, ciliary injection and a small or irregular pupil. Refer the same day.\n- **Acute angle closure:** blocked aqueous drainage causes a rapid rise in intraocular pressure. Severe eye or head pain, haloes, nausea, a hazy cornea and a fixed mid-dilated pupil. This is an emergency.\n\n### Sudden visual loss\n\n> [!escalate]\n> Flashes, floaters, a curtain-like field defect or sudden painless monocular loss suggests retinal detachment or vascular occlusion and needs emergency ophthalmology or stroke assessment.\n\n> [!escalate]\n> In an older person, jaw claudication, new temporal headache or scalp tenderness suggests giant cell arteritis. Check ESR and CRP the same day and assess for immediate corticosteroid treatment to protect vision.\n\n### Eyelid lumps and blepharitis\n\n- **Hordeolum (stye):** an acute, painful staphylococcal infection of a lash follicle or eyelid gland, pointing as a tender red swelling at the lid margin. Warm compresses several times a day help it drain, usually within a week. Do not squeeze it; antibiotics are not routinely needed.\n- **Chalazion:** a firm, painless lump within the lid, developing over weeks as a blocked meibomian gland leads to granulomatous inflammation. Warm compresses and lid massage help most to resolve within a few months. A persistent or troublesome chalazion can be incised and curetted by an ophthalmologist.\n- **Blepharitis:** chronic inflammation of the lid margins, with crusting at the lash bases, gritty or burning eyes and recurrent styes and chalazia, often alongside rosacea or seborrhoeic dermatitis. Daily lid hygiene, with warm compresses and gentle cleaning of the lid margins, controls rather than cures it. Selected patients need a short course of topical antibiotic or oral doxycycline.\n\nLid swelling that spreads, with fever, suggests preseptal cellulitis, and pain on eye movement or reduced vision suggests orbital cellulitis; see G27 (Periorbital and orbital cellulitis). A recurrent chalazion at the same site, loss of lashes, ulceration or distortion of the lid margin needs biopsy to exclude a malignancy such as BCC or sebaceous carcinoma.\n\n### Fluorescein examination\n\nFluorescein highlights epithelial defects under blue light. Explain the temporary staining, avoid contaminating the strip, and look for an abrasion, an ulcer or a dendritic pattern (herpes simplex).\n\n> [!pitfall]\n> Do not prescribe topical steroid or take-home anaesthetic drops without specialist direction. Steroid worsens herpetic and fungal keratitis; repeated anaesthetic delays epithelial healing and masks deterioration.\n\n### Eye injuries\n\n> [!escalate]\n> For a suspected penetrating injury, apply a protective shield, avoid any pressure or manipulation, and transfer as an emergency.\n\n> [!escalate]\n> After chemical exposure, irrigate immediately and copiously; do not delay irrigation to take a detailed history.",
      "formerly": [
        "G14"
      ]
    },
    {
      "id": "G26",
      "domain": "GP",
      "group": "Eye, ear, nose and throat",
      "title": "Ear pain, hearing loss and tinnitus",
      "focus": "Otoscopy, tuning-fork tests and audiograms, otitis externa, cerumen, sudden hearing loss and tinnitus.",
      "first_pass": true,
      "priority": "Core",
      "saq_cases": [
        {
          "id": "deck-paeds-otitis-media",
          "title": "Acute otitis media",
          "set": "MD3 SAQ Revision Deck"
        }
      ],
      "core_ids": [
        "P035",
        "P050",
        "P095"
      ],
      "gp_tasks": [
        "Perform focused eye/ear examination and recognise urgent referral",
        "Interpret otoscopy/audiogram; recognise sight-threatening presentations"
      ],
      "notes": "### History\n\nAsk whether loss is sudden or gradual, and about pain or discharge, tinnitus, vertigo, noise and ototoxic exposure, and the effect on communication.\n\n### Otoscopy\n\nInspect the pinna and mastoid. Brace the hand holding the otoscope against the patient's head, so that a sudden movement carries the otoscope with the head instead of into the canal. Use a comfortable speculum and inspect the canal and tympanic membrane without force.\n\n- **Acute otitis media:** bulging, opaque drum.\n- **Middle-ear effusion:** dull or retracted drum, or a fluid level.\n- **Otitis externa:** tragal tenderness and an inflamed canal.\n\n### Tuning-fork tests\n\n**Conductive loss** impairs sound transmission through the outer or middle ear. **Sensorineural loss** reflects dysfunction of the cochlea or auditory nerve. Use a 512 Hz fork:\n\n- **Rinne:** air conduction normally exceeds bone conduction. Bone ≥ air suggests conductive loss in that ear.\n- **Weber:** lateralises towards the ear with conductive loss and away from the ear with sensorineural loss.\n\nInterpret the two tests together and confirm with audiometry.\n\n### Audiogram\n\nAn audiogram plots hearing threshold against frequency. An air–bone gap indicates conductive loss. In sensorineural loss, air and bone thresholds are raised together.\n\n### Treatment\n\n- **Otitis externa:** topical treatment and keeping the ear dry, for example dexamethasone–framycetin–gramicidin drops. Choose drops according to whether the tympanic membrane is intact: aminoglycoside-containing preparations such as this are ototoxic in the middle ear, so use ciprofloxacin–hydrocortisone drops if the drum may be perforated.\n- **Cerumen:** softening or removal may relieve conductive loss. Do not irrigate with a perforation, grommets, relevant ear surgery or active infection. Stop if pain or vertigo occurs.\n\n> [!escalate]\n> Button batteries and sharp foreign bodies need same-day specialist removal. Do not irrigate a battery.\n\n> [!escalate]\n> Sudden sensorineural hearing loss is **time-critical**: treatment works best when started early, so arrange same-day ENT assessment.\n\n### Referral\n\nRefer pulsatile tinnitus, persistent unilateral tinnitus or asymmetric hearing loss, mastoid swelling, facial palsy or neurological signs to ENT.\n\nIn children, persistent effusion or hearing loss can affect language and learning. Arrange audiology and ENT or developmental review instead of repeated antibiotics. For paediatric infection see C07 (Acute otitis media).\n\n### Tinnitus\n\nFor persistent non-pulsatile tinnitus without red flags, explain its association with hearing loss, advise reducing harmful noise exposure and arrange hearing assessment. Hearing aids, background sound and psychological strategies reduce distress. Avoid promising a cure.",
      "formerly": [
        "G14"
      ]
    },
    {
      "id": "G27",
      "domain": "GP",
      "group": "Eye, ear, nose and throat",
      "title": "Sore throat, nasal symptoms, neck lumps and facial pain",
      "focus": "Sore throat and deep-space infection, rhinitis and sinusitis, epistaxis, orbital cellulitis, neck lumps, facial pain and red flags.",
      "first_pass": false,
      "priority": "Selective",
      "saq_cases": [
        {
          "id": "deck-paeds-tonsillitis",
          "title": "Sore throat and tonsillitis",
          "set": "MD3 SAQ Revision Deck"
        }
      ],
      "core_ids": [
        "P039",
        "P066",
        "P084",
        "P092"
      ],
      "gp_tasks": [
        "Use antibiotic stewardship in URTI and sinusitis",
        "Assess sore throat, nasal symptoms and persistent neck lump"
      ],
      "notes": "### Sore throat\n\nMost acute sore throats are viral. Cough, rhinorrhoea and conjunctivitis support a viral cause. Fever, tonsillar exudate and tender anterior cervical nodes may suggest streptococcal infection but do not confirm it. A clinical score alone should not override age, epidemiology or signs of complications.\n\nMarked fatigue, posterior cervical nodes or splenomegaly suggests glandular fever. Advise avoiding contact sport while splenic enlargement is possible, because of the risk of rupture.\n\n### Sore throat: management\n\nFluids and analgesia are the mainstay. For viral illness, antibiotics give little benefit and cause diarrhoea, allergy and resistance.\n\nGive antibiotics when bacterial infection is likely and the patient is at increased risk of acute rheumatic fever (for example, Aboriginal and Torres Strait Islander people in high-risk settings, or previous rheumatic fever):\n\n- **Phenoxymethylpenicillin** `15 mg/kg up to 500 mg orally twice daily for 10 days`. The full course is needed to eradicate the organism and prevent rheumatic fever.\n- **Alternative:** a single IM dose of benzathine benzylpenicillin, particularly where adherence is uncertain.\n\nFor recurrent tonsillitis or persistent hoarseness, record frequency and impact and review before considering surgery.\n\n### Peritonsillar abscess and airway obstruction\n\nUnilateral severe pain, a muffled voice, trismus and uvular displacement suggest peritonsillar abscess (quinsy).\n\n> [!escalate]\n> Drooling, stridor, inability to swallow secretions, a toxic appearance or rapidly progressive neck swelling suggests airway obstruction or deep-space infection and needs emergency care. In a child with suspected critical upper-airway obstruction, avoid distressing throat examination.\n\n### Allergic rhinitis\n\nItching, sneezing and clear rhinorrhoea, often with eye symptoms. An intranasal corticosteroid is effective for persistent symptoms; an oral antihistamine helps itch and sneezing.\n\nNasal spray technique:\n\n1. Gently clear the nose and tilt the head slightly forward.\n2. Aim the nozzle away from the septum, towards the outer eye or ear on the same side.\n3. Sniff gently; do not draw the spray into the throat.\n\nCorrect direction and regular use reduce irritation and epistaxis.\n\n### Acute rhinosinusitis\n\nUsually viral. Bacterial infection is suggested by symptoms persisting beyond `10 days` without improvement, marked unilateral pain with fever, or worsening after initial improvement. Saline irrigation and symptom relief help most patients. When an antibiotic is indicated, amoxicillin `500 mg orally three times daily for five days` is the usual choice.\n\n### Epistaxis\n\nMost nosebleeds come from Little's area on the anterior septum and stop with first aid. Posterior bleeds are less common, heavier and more frequent in older people and those taking anticoagulants, and blood may run from both nostrils and down the throat.\n\n1. Sit the person up and lean them forward, so blood drains out rather than being swallowed or aspirated.\n2. Pinch the soft lower part of the nose firmly and continuously for `10–15 minutes` without releasing to check; pressure on the bony bridge does not compress the bleeding vessels.\n3. Ask them to spit out blood rather than swallow it.\n\nMeanwhile assess duration and volume, pulse and BP, anticoagulant or antiplatelet use, a bleeding disorder, trauma and recurrence. If bleeding continues, clear clots, apply a topical vasoconstrictor with local anaesthetic, and inspect with a headlight. A visible anterior vessel can be cauterised with silver nitrate, one side of the septum only, because bilateral cautery risks perforation; otherwise insert an anterior nasal pack and refer. Do not routinely stop an anticoagulant for a controlled bleed, but check the INR in a patient on warfarin.\n\n> [!escalate]\n> Bleeding that continues despite pressure and packing, a suspected posterior bleed, haemodynamic compromise or any patient with a pack in place needs emergency department or ENT care.\n\nAfterwards, advise avoiding nose-blowing, straining and heavy lifting for a few days. Recurrent anterior bleeds, common in children, often settle with an antiseptic nasal cream; recurrent unilateral bleeding in an adult needs ENT examination, as noted under neck lumps.\n\n### Periorbital and orbital cellulitis\n\n**Preseptal cellulitis** affects the eyelid tissues anterior to the orbital septum. **Orbital cellulitis** involves the tissues behind the septum, within the orbit.\n\n> [!escalate]\n> Periorbital swelling with painful or restricted eye movements, proptosis or impaired vision suggests **orbital cellulitis**, which needs emergency imaging and specialist treatment.\n\nPreseptal cellulitis lacks these orbital signs but still needs assessment and antibiotic treatment.\n\n### Nasal problems in children\n\nUnilateral foul discharge in a child suggests a nasal foreign body.\n\n> [!escalate]\n> A nasal button battery requires immediate removal, because tissue injury progresses within hours.\n\nInfants breathe preferentially through the nose, so nasal obstruction impairs both breathing and feeding. Review the same day if there is respiratory distress or poor intake.\n\n### Neck lumps\n\nA neck node may drain a primary elsewhere, so examine the oral cavity, scalp and skin, salivary glands and thyroid as well as the nodes.\n\nRefer a persistent adult neck mass promptly for imaging and ENT assessment, particularly with smoking or alcohol exposure, weight loss, dysphagia, unilateral otalgia or hoarseness. FNA is preferred to open biopsy, which can seed tumour and compromise definitive surgery.\n\nA thyroid mass moves with swallowing; investigate with ultrasound and TSH.\n\nPersistent unilateral nasal obstruction, recurrent unilateral epistaxis, hoarseness or an oral ulcer needs examination and ENT or dental referral, because persistent unilateral symptoms can indicate a tumour.\n\n### Facial pain\n\nCommon causes are dental disease, temporomandibular dysfunction, sinusitis and neuropathic pain.\n\n- **Trigeminal neuralgia:** brief electric-shock pain triggered by touch or chewing. Carbamazepine is first-line.\n- **Structural lesion:** persistent sensory loss or other neurological signs; arrange imaging and specialist assessment.\n\n> [!escalate]\n> Facial swelling with trismus, drooling, floor-of-mouth swelling or airway symptoms suggests spreading dental or deep-space infection and needs emergency care.\n\nIn an older person, new temporal pain, jaw claudication or visual symptoms suggests giant cell arteritis; same-day assessment and treatment protect vision.\n\nFor the fuller eye and headache approaches, see G25 (Sudden visual loss) and G28 (Headache: assessment and red flags).",
      "formerly": [
        "B02",
        "G15"
      ]
    },
    {
      "id": "G28",
      "domain": "GP",
      "group": "Neurology and musculoskeletal",
      "title": "Headache, dizziness and syncope",
      "focus": "Symptom-first community assessment: red flags, orthostasis, vertigo vs presyncope, selective referral.",
      "first_pass": false,
      "priority": "Core",
      "saq_cases": [
        {
          "id": "deck-geri-balance-falls-meds",
          "title": "Disequilibrium, falls and medication review",
          "set": "MD3 SAQ Revision Deck"
        },
        {
          "id": "deck-paeds-migraine",
          "title": "Migraine in childhood",
          "set": "MD3 SAQ Revision Deck"
        }
      ],
      "core_ids": [
        "P030",
        "P049",
        "P060",
        "P061",
        "P087",
        "P099"
      ],
      "gp_tasks": [
        "Assess headache red flags and use a focused neurological exam",
        "Separate vertigo, presyncope and persistent dizziness"
      ],
      "notes": "### Primary headache patterns\n\nMost headaches are primary, and the diagnosis is made clinically from the history of the attacks.\n\n- **Migraine:** recurrent moderate to severe headache with nausea and light or sound sensitivity, worsened by activity. **Aura** consists of reversible neurological symptoms that usually evolve gradually.\n- **Tension-type headache:** usually bilateral and pressing, without prominent nausea.\n- **Cluster headache:** very severe unilateral orbital or temporal attacks with ipsilateral tearing or nasal symptoms. The patient is typically agitated rather than lying still.\n\n### Headache: assessment and red flags\n\nTo separate primary from secondary headache, ask about onset, frequency and duration, triggers, and the number of days each month that analgesics or triptans are taken. A new or changing pattern raises concern, as does headache in pregnancy or postpartum, or in someone with cancer or immunosuppression. Examine BP, temperature and neurology, and the fundi when appropriate.\n\n> [!escalate]\n> Arrange emergency assessment for thunderclap onset, fever or meningism, papilloedema, a new focal deficit, significant head injury, or a new headache in an older person.\n\nIn pregnancy or postpartum, consider pre-eclampsia, cerebral venous thrombosis and other secondary causes.\n\nA stable, typical primary headache with a normal examination does not need imaging.\n\n### Managing migraine\n\n- **General measures:** regular sleep and meals and adequate hydration. A headache diary identifies triggers and records medication use.\n- **Acute treatment:** an NSAID or paracetamol, adding a triptan when appropriate and an antiemetic if needed. Triptans are vasoconstrictors, so check for vascular contraindications first.\n- **Prevention:** offer preventive treatment for frequent disabling attacks, choosing the agent according to comorbidity and pregnancy potential.\n- **Medication overuse:** frequent analgesic or triptan use can itself cause headache. Ask about actual monthly use.\n\n### Dizziness: clarify the symptom\n\n\"Dizzy\" may mean vertigo (a sense of spinning), presyncope (an impending faint), imbalance or nonspecific light-headedness. Each has a different differential, so establish which the patient means before going further.\n\n### Vertigo: timing and triggers\n\n- **Seconds, provoked by head movement such as turning in bed:** BPPV.\n- **Continuous for hours to days:** vestibular neuritis or posterior circulation stroke.\n- **With hearing loss or tinnitus:** another peripheral syndrome, including Ménière disease. Hearing symptoms do not guarantee a benign cause.\n\nExamine gait, eye movements and nystagmus, cranial nerves and limb coordination to separate peripheral vestibular disease from a central cause.\n\n> [!escalate]\n> Arrange emergency assessment for severe inability to walk, focal neurological signs, new headache or neck pain, or high clinical concern for stroke.\n\nHINTS is for trained clinicians assessing a **continuous acute vestibular syndrome**. It is not a general test for every dizzy patient.\n\n### BPPV\n\n**Benign paroxysmal positional vertigo** occurs when displaced otoconia stimulate a semicircular canal during head movement.\n\n- **Diagnosis:** for suspected posterior-canal BPPV, a trained examiner performs the Dix–Hallpike test. With the head turned, the patient moves from sitting to a supported head-hanging position; characteristic transient positional nystagmus supports the diagnosis.\n- **Treatment:** the Epley manoeuvre repositions the displaced canaliths. Check neck and mobility limitations first.\n\nAvoid long-term vestibular suppressants. They blunt the signals the brain needs for central compensation.\n\n### Syncope: history\n\n**Syncope** is transient loss of consciousness from reduced global cerebral perfusion, with rapid onset and spontaneous recovery.\n\nA witness account is often the most useful part of the assessment. Ask about posture, prodrome, exertion, palpitations, duration, movements and recovery.\n\n> [!pitfall]\n> Brief jerking movements can occur during syncope and do not by themselves indicate a seizure. Prolonged confusion afterwards or a lateral tongue bite favours seizure.\n\n### Syncope: examination and investigations\n\nCardiac causes carry the greatest risk, so record an ECG and examine the cardiovascular system in every patient. Review medicines, and examine neurology and check glucose when relevant.\n\n> [!escalate]\n> Arrange urgent cardiac assessment for syncope on exertion or when supine, associated chest pain, an abnormal ECG, known structural heart disease, or a family history of sudden death. These suggest an arrhythmic or structural cause.\n\n### Orthostatic hypotension\n\n1. Measure BP and pulse after at least `five minutes` supine.\n2. Stand the patient and repeat at `one and three minutes`, recording symptoms.\n\nA fall of `≥20 mmHg systolic` or `≥10 mmHg diastolic` within `three minutes` supports orthostatic hypotension. Common causes are dehydration, blood loss, antihypertensives and autonomic disease.\n\n### Vasovagal syncope\n\nTypical vasovagal episodes may improve with trigger recognition, adequate fluids, lying down at the first prodromal symptoms and counter-pressure manoeuvres.\n\n### Driving and follow-up\n\nDriving and occupational advice depends on the cause and the current Austroads standards. Arrange planned follow-up for unexplained episodes.",
      "formerly": [
        "G16"
      ]
    },
    {
      "id": "G29",
      "domain": "GP",
      "group": "Neurology and musculoskeletal",
      "title": "Musculoskeletal pain and low back pain",
      "focus": "Back pain patterns and red flags, osteoarthritis, rheumatoid arthritis, polymyalgia rheumatica, the hot swollen joint and gout, imaging, conservative care and safe analgesia.",
      "first_pass": false,
      "priority": "Core",
      "saq_cases": [
        {
          "id": "2016-mhagp-q4",
          "title": "Chronic non-specific low back pain",
          "set": "2016 MH/GP"
        },
        {
          "id": "deck-gp-low-back-pain",
          "title": "Low back pain",
          "set": "MD3 SAQ Revision Deck"
        }
      ],
      "core_ids": [
        "P023",
        "P056",
        "P057",
        "P065",
        "P070"
      ],
      "gp_tasks": [
        "Back-pain red flags, imaging decisions and function-based goals",
        "OA/inflammatory arthritis assessment and allied-health care plan"
      ],
      "notes": "### Patterns of back pain\n\nBack pain is usually benign, and its pattern indicates the likely source.\n\n- **Mechanical:** varies with movement or loading.\n- **Radicular:** radiates in a nerve-root distribution, sometimes with sensory change, weakness or altered reflexes.\n- **Inflammatory:** improves with movement, causes prolonged morning stiffness, and may accompany psoriasis, uveitis or inflammatory bowel disease.\n\nFracture, infection, malignancy and renal, vascular or pelvic causes are less common but important.\n\n### Assessment and red flags\n\nAsk about red flags for serious pathology: previous cancer, trauma, osteoporosis or steroid use, infection risk, fever, weight loss, progressive weakness, saddle sensory change and bladder or bowel disturbance.\n\nExamine gait, the spine and relevant joints, lower-limb power, sensation and reflexes, with straight-leg raise when radiculopathy is suspected.\n\n> [!escalate]\n> New urinary retention, saddle anaesthesia or a progressive motor deficit needs emergency assessment for **cauda equina or cord compression**.\n\n### Osteoarthritis\n\n**Osteoarthritis** involves cartilage loss with changes throughout the joint, including bone and surrounding tissues. It causes activity-related pain, brief stiffness, reduced range and bony enlargement. Hand disease typically affects the DIP and PIP joints and thumb base. Symptoms and function matter more than radiographic severity.\n\n### Rheumatoid arthritis\n\n**Rheumatoid arthritis** is an autoimmune disease in which persistent synovial inflammation damages cartilage and bone and can cause systemic disease. It causes persistent inflammatory swelling and prolonged morning stiffness, often in a symmetrical MCP and PIP distribution.\n\nAssess extra-articular features. FBE, inflammatory markers, rheumatoid factor and anti-CCP support the diagnosis; negative serology does not exclude it. Refer early to rheumatology: disease-modifying treatment started promptly limits joint damage, which NSAIDs alone do not.\n\n### Polymyalgia rheumatica\n\n*Polymyalgia rheumatica* (PMR) is an inflammatory disorder of people over 50 that causes bilateral aching and morning stiffness of the shoulder and hip girdles and neck, developing over days to weeks and lasting more than `45 minutes` each morning, often with fatigue, low-grade fever or weight loss. Strength is preserved; pain limits movement, but true weakness points to another diagnosis. ESR and CRP are usually raised, and CK is normal.\n\nThe main alternatives are late-onset rheumatoid arthritis, inflammatory myopathy (weakness and a raised CK), hypothyroidism, malignancy, infection such as endocarditis, and bilateral shoulder disease. Baseline tests cover FBE, ESR and CRP, renal and liver function, calcium, TSH, CK, rheumatoid factor and anti-CCP, protein electrophoresis and glucose.\n\n**Ask every patient about symptoms of giant cell arteritis**: new headache, scalp tenderness, jaw claudication or visual disturbance. GCA accompanies PMR in a substantial minority and needs same-day assessment and higher-dose corticosteroid to protect vision; see G25 (Sudden visual loss).\n\nTreat PMR with prednisolone, commonly `15 mg daily`. The response is usually dramatic within days, and a poor response should prompt reconsideration of the diagnosis. Reduce slowly over one to two years, as relapse is common during tapering. Protect bone (see G30), monitor glucose and BP, and refer atypical presentations: onset before 60, normal inflammatory markers, peripheral synovitis, a poor response or repeated relapse.\n\n### Acute hot swollen joint\n\nConsider septic arthritis, crystal arthritis and haemarthrosis. Fever may be absent. Gout typically affects the first metatarsophalangeal joint, ankle or knee, while a prosthetic joint, immunosuppression, diabetes or injecting drug use increases the risk of infection.\n\n> [!escalate]\n> When infection is possible, arrange same-day joint aspiration for cell count, microscopy for crystals, and culture. Crystals do not exclude coexisting infection.\n\n### Gout\n\n*Gout* is inflammation provoked by monosodium urate crystals, which form in and around joints when urate has been chronically supersaturated. A flare builds over hours to a peak within a day, with intense pain, redness and tenderness, classically at the first metatarsophalangeal joint. Alcohol, large meals, dehydration, intercurrent illness, surgery, diuretics and starting urate-lowering treatment are common triggers. Gout clusters with CKD, obesity, hypertension and diabetes, so assess cardiovascular risk as well.\n\nAspiration showing negatively birefringent, needle-shaped crystals is definitive, and is needed whenever infection is possible. A typical recurrence in a person with established gout can be diagnosed clinically. Serum urate can fall to normal during a flare, so measure it again once the flare has settled.\n\nTreat a flare as early as possible with whichever suits the patient's comorbidities:\n\n- **NSAID:** at full dose for a few days, if renal, gastrointestinal and cardiovascular risks allow.\n- **Colchicine:** low dose, `1 mg` then `0.5 mg` an hour later. Higher doses add toxicity without benefit. Reduce the dose in renal impairment and check for interactions, including clarithromycin and some statins.\n- **Corticosteroid:** oral prednisolone, or an intra-articular injection once infection is excluded; useful when NSAIDs and colchicine are unsafe, as in CKD.\n\nContinue established urate-lowering treatment through a flare.\n\nOffer urate-lowering treatment for recurrent flares (more than one a year), tophi, erosions, CKD or urate stones. Start allopurinol at `100 mg daily` (`50 mg` in CKD) and increase monthly until serum urate is `<0.36 mmol/L`, or `<0.30 mmol/L` with tophi; it can be started during a flare. Falling urate mobilises crystals, so give prophylactic colchicine, commonly `0.5 mg daily`, for at least the first `six months`. Test for HLA-B5801 before starting in people of Han Chinese, Korean or Thai ancestry, who carry a higher risk of severe allopurinol hypersensitivity.\n\n> [!counsel]\n> Allopurinol prevents attacks rather than treating them, and is usually lifelong. Attacks may become more frequent for the first few months, which is why a second medicine is given to prevent them; keep taking both.\n\n### Imaging\n\nDo not image uncomplicated acute nonspecific back pain. Imaging commonly shows degenerative findings that also occur in people without pain; explain that such findings do not necessarily identify the cause.\n\nReserve imaging for red flags, persistent or progressive neurological findings, or when the result will change specialist management.\n\n### Explaining chronic pain\n\nChronic pain can persist through sensitisation of pain pathways after tissue healing. Acknowledge that the pain is real, and link treatment to restoring activity, sleep and confidence. Mood, work, fear of movement, previous treatment and the person's goals influence recovery; this does not make the problem psychological.\n\n### Management\n\nRestoring activity matters more than finding an ideal analgesic. Continued activity, graded exercise and physiotherapy aid recovery; bed rest delays it.\n\n- **Knee or hip OA:** strengthening, aerobic activity, weight loss when relevant and appropriate aids are first-line.\n- **Occupational therapy:** adapts tasks.\n- **Psychology:** CBT or acceptance-based strategies for pain, avoidance and distress.\n\nMedicines play a supporting role, and their harms often outweigh their benefit here.\n\n- **Topical NSAIDs:** useful for OA of accessible joints such as the knee and hand, with little systemic exposure.\n- **Oral NSAIDs:** lowest effective dose for the shortest time, after assessing renal, gastrointestinal and cardiovascular risk.\n- **Paracetamol:** limited benefit for nonspecific back pain.\n- **Opioids, benzodiazepines and gabapentinoids:** inappropriate for routine nonspecific back pain; they add dependence and sedation risk for little benefit. Use neuropathic medicines only with a clear indication, and review benefit against sedation and falls.\n\n> [!pitfall]\n> Avoid the \"triple whammy\" of ACE inhibitor or ARB, diuretic and NSAID. Each undermines a different part of renal perfusion, and together they can precipitate acute kidney injury.\n\n### Follow-up\n\nReview progress in terms of function. Set an observable goal, such as walking for ten minutes daily or returning to modified work, and review it in a few weeks with adverse effects and any change in the diagnosis.\n\nRefer persistent major disability despite appropriate care for multidisciplinary or specialist review. Reassess earlier for new neurological or systemic red flags.",
      "formerly": [
        "G05"
      ]
    },
    {
      "id": "G30",
      "domain": "GP",
      "group": "Neurology and musculoskeletal",
      "title": "Osteoporosis and fragility fracture prevention",
      "focus": "Fracture risk, DXA interpretation, secondary causes, bone-protective treatment and follow-up.",
      "first_pass": false,
      "priority": "Core",
      "saq_cases": [
        {
          "id": "deck-gp-osteoporosis",
          "title": "Osteoporosis",
          "set": "MD3 SAQ Revision Deck"
        },
        {
          "id": "deck-geri-balance-falls-meds",
          "title": "Disequilibrium, falls and medication review",
          "set": "MD3 SAQ Revision Deck"
        }
      ],
      "core_ids": [
        "P029",
        "P040",
        "P098"
      ],
      "gp_tasks": [
        "Estimate fragility risk and interpret DXA",
        "Plan falls prevention, rehabilitation and osteoporosis treatment review"
      ],
      "notes": "### Definitions\n\n**Osteoporosis** reduces bone strength through loss of bone mass and deterioration of microarchitecture. A **fragility fracture** follows trauma that would not normally break healthy bone, typically a fall from standing height or less.\n\nFracture risk has two components: bone strength, which osteoporosis reduces, and exposure to injury, which falls determine.\n\nA low-trauma hip or vertebral fracture is usually an indication for treatment **regardless of the DXA result**: the fracture itself demonstrates fragility and predicts further fractures.\n\nOther risk factors include previous fracture, height loss, falls, parental hip fracture, glucocorticoids, smoking, alcohol, early menopause, hypogonadism and malabsorption.\n\n### DXA interpretation\n\n- **T-score:** comparison with a young-adult reference. In postmenopausal women and men aged `≥50`, **T-score `≤−2.5` defines osteoporosis**; between −1 and −2.5 is low bone mass.\n- **Z-score:** comparison with age-matched peers. Use it in younger patients, in whom low density is more often secondary, and evaluate secondary causes.\n\nFRAX or the Garvan calculator estimates absolute fracture risk but does not replace clinical judgement after a significant fragility fracture.\n\n### Assessment\n\n- **Examination:** height and kyphosis (for unrecognised vertebral fracture); gait, balance, vision, footwear and standing BP (for falls).\n- **Bloods for secondary causes:** calcium, phosphate, renal function, vitamin D and FBE; thyroid, coeliac or myeloma tests according to the history.\n- **Vertebral imaging:** for unexplained height loss or compatible back pain.\n\n### Prevention of further injury\n\nAdvise weight-bearing and progressive resistance exercise, which load bone and build muscle, and balance training, which reduces falls. Ensure adequate protein and dietary calcium, smoking cessation and moderate alcohol.\n\nSupplement calcium when dietary intake is insufficient and replace vitamin D deficiency. Supplements are not a substitute for osteoporosis medication in a high-risk patient.\n\nReview sedatives, vision, home hazards and walking aids with physiotherapy and OT; see R02 (Preventing recurrence and planning safe activity).\n\n### Oral bisphosphonate\n\nFor example, alendronate `70 mg weekly`. Reduces bone resorption and fracture risk.\n\n- Absorption is poor and the tablet can injure the oesophagus. Take it fasting with plain water, stay upright for at least `30 minutes`, and delay food and other medicines for the product's required interval.\n- Avoid with major oesophageal disease, inability to stay upright, or substantial renal impairment.\n- Discuss upper-GI irritation and the rare risks of jaw osteonecrosis and atypical femoral fracture. Investigate persistent thigh or groin pain.\n\n### IV bisphosphonate\n\nZoledronic acid `5 mg IV yearly`, when oral treatment is unsuitable.\n\nCheck renal function, calcium and vitamin D first: the drug is renally cleared and can precipitate hypocalcaemia when vitamin D is deficient. Transient flu-like symptoms may follow the infusion.\n\n### Denosumab\n\n`60 mg` subcutaneously every `six months`. Correct hypocalcaemia first and assess hypocalcaemia risk in renal impairment.\n\n> [!pitfall]\n> Doses must be on time, and **stopping denosumab requires a planned transition to another antiresorptive**. Rapid bone loss and vertebral fractures can follow cessation. There is no drug holiday as with bisphosphonates.\n\n### Anabolic treatment\n\nTeriparatide or romosozumab, which build bone rather than only slowing its loss, is a specialist option for very high fracture risk or selected treatment failure. It is followed by antiresorptive therapy, because the gain is otherwise lost.\n\n### Before and during treatment\n\nReview oral health and any planned invasive dental work before antiresorptive treatment, but do not let routine dental care delay fracture prevention indefinitely.\n\nDiscuss expected benefit, administration, cost, and planned duration and review. Bisphosphonates persist in bone, so reassess the need after several years (commonly `5 years` oral or `3 years` IV) according to fracture risk.\n\n### Follow-up\n\nSecondary prevention is often missed after a fragility fracture. Link fracture liaison, GP, rehabilitation and osteoporosis care. Review adherence, new falls or fractures, and calcium and renal issues as relevant. Repeat DXA when the result can change management.\n\n> [!escalate]\n> Acute hip pain with inability to bear weight, or suspected vertebral fracture with neurological symptoms needs emergency assessment.",
      "formerly": [
        "G06"
      ]
    },
    {
      "id": "G31",
      "domain": "GP",
      "group": "Surgery",
      "title": "Pre-operative and perioperative review",
      "focus": "Perioperative risk, medication reconciliation, consent, preparation for surgery and postoperative review.",
      "first_pass": false,
      "priority": "Selective",
      "saq_cases": [],
      "core_ids": [
        "P042",
        "P076"
      ],
      "gp_tasks": [
        "Review comorbidities, relevant medications and perioperative risk",
        "Communicate with treating team; do not drill hospital anaesthesia"
      ],
      "notes": "### Perioperative risk\n\nPerioperative risk depends on the operation, its urgency and the physiological stress it imposes, as well as on the patient. The review therefore asks how well this person is likely to tolerate this procedure, which problems can be improved beforehand, and what the surgical and anaesthetic teams need to know about the rest.\n\nRelevant history includes:\n\n- Exercise tolerance, chest pain, dyspnoea and syncope.\n- Heart, lung, kidney and liver disease; diabetes; obstructive sleep apnoea.\n- Frailty, nutrition, anaemia and current infection.\n- Previous anaesthetic problems and family anaesthetic complications.\n- Smoking, alcohol and withdrawal risk.\n- Allergies, dental problems and supports at home.\n\n### Examination and investigations\n\nExamination focuses on the observations, cardiorespiratory findings, features that may make the airway difficult, and functional status. Order FBE, renal function, ECG or other tests when the operation and the patient's comorbidities justify them. Routine panels in healthy patients generate follow-up without improving safety.\n\n> [!escalate]\n> New angina, decompensated heart failure, a major arrhythmia or acute illness needs medical and anaesthetic review before elective surgery proceeds.\n\n### Medication reconciliation\n\nBuild a complete list that includes over-the-counter drugs and supplements as well as prescribed medicines. For each, record the indication, dose and relevant renal function, and who is responsible for any perioperative change. The medicines that most often need a specific plan are:\n\n- **Anticoagulants:** interruption balances bleeding risk against thromboembolic risk, with timing set by the drug's half-life and renal function. **Bridging is not routine.** It means temporary use of a short-acting anticoagulant while longer-acting anticoagulation, usually warfarin, is interrupted. Coronary stents and mechanical valves need coordinated specialist advice.\n- **SGLT2 inhibitors:** increase the risk of euglycaemic ketoacidosis. Under ADS–ANZCA advice, withhold them for the `two days` before surgery and on the day of surgery; for minor day procedures with brief fasting, such as gastroscopy, omit only on the day. Check ketones on the day of surgery and whenever illness suggests DKA despite modest glucose.\n- **Insulin:** needs an explicit fasting-day plan. In type 1 diabetes, basal insulin must not be omitted, because insulin deficiency can cause ketoacidosis within hours.\n- **GLP-1 medicines:** slow gastric emptying, which raises aspiration risk. Under current ANZCA advice they are usually continued, with a clear-fluid diet for the whole day before an elective procedure followed by standard fasting. Tell the anaesthetic team, who may still manage the patient as having a full stomach.\n- **Corticosteroids:** long-term use may suppress the adrenal axis, which then cannot mount the cortisol response that surgery demands. Assess suppression and plan perioperative supplementation.\n- **Parkinson medicines and long-term benzodiazepines:** stopping these abruptly can cause dangerous withdrawal syndromes, so continue them or plan an alternative.\n\nThe written plan states when each withheld drug restarts and who will check renal function, bleeding and oral intake. Share it with the patient, surgeon, anaesthetist and GP.\n\n### Consent\n\nValid consent requires capacity, voluntariness and relevant information. The discussion covers the procedure and why it is recommended, its expected benefits, the material risks that matter to this patient, alternatives including no intervention, and the likely recovery.\n\nConsent is a shared understanding rather than a signature. Check that the patient has understood, use an interpreter when needed, and allow time for questions. A student needs supervision and should not consent a patient for a procedure beyond their own knowledge.\n\n### Preparation\n\nSeveral factors can be improved before elective surgery: anaemia, nutrition, smoking, alcohol use and fitness (prehabilitation).\n\nPractical preparation covers fasting instructions, transport, the expected pain plan, early mobilisation and help at home. When frailty or major illness changes the balance of benefit and burden, goals of care belong in the discussion.\n\n### Postoperative review and handover\n\nReview the wound, pain, medication changes, bowel and bladder function, nutrition, mobility and VTE prevention.\n\n> [!pitfall]\n> Serious postoperative complications in an older person can occur without fever.\n\n> [!escalate]\n> New chest pain, dyspnoea, tachycardia, hypoxaemia, bleeding, severe pain or confusion needs same-day assessment for a complication; do not attribute it to normal recovery.\n\nThe discharge handover records the diagnosis, complications, medication changes, pending results and who is responsible for each follow-up task.",
      "formerly": [
        "G19"
      ]
    },
    {
      "id": "C01",
      "domain": "CAH",
      "also_in": [
        "OGN"
      ],
      "title": "The newborn: transition, jaundice and heart murmurs",
      "focus": "Newborn transition and respiratory distress, neonatal jaundice by age in hours, innocent versus structural murmurs.",
      "first_pass": true,
      "priority": "Core",
      "saq_cases": [
        {
          "id": "deck-paeds-murmurs-chd",
          "title": "Murmurs and congenital heart disease",
          "set": "MD3 SAQ Revision Deck"
        },
        {
          "id": "deck-og-newborn-rds",
          "title": "Newborn respiratory distress",
          "set": "MD3 SAQ Revision Deck"
        }
      ],
      "core_ids": [
        "P051",
        "P055",
        "P107"
      ],
      "notes": "### Newborn transition\n\nBreathing, temperature, feeding, urine and stools, and weight show how well a newborn is adapting after birth. Babies of mothers with diabetes, and preterm, small or large babies, need scheduled glucose checks; see O05 (The baby of a mother with diabetes).\n\nGrunting, recession, cyanosis or apnoea suggests infection, respiratory distress syndrome, transient tachypnoea or cardiac disease. Prematurity raises the risk of surfactant deficiency, and elective caesarean birth raises the risk of retained lung fluid and transient tachypnoea, but neither label should delay assessment of a sick infant.\n\n### Neonatal jaundice\n\nNewborns produce more bilirubin and conjugate it less efficiently than older infants, so unconjugated hyperbilirubinaemia is common. **Physiological jaundice** appears after the first day in an otherwise well baby.\n\nJaundice needs investigation when it:\n\n- Appears within the first `24 hours`.\n- Rises rapidly.\n- Occurs with poor feeding or illness.\n- Is prolonged, beyond `14 days` in a term infant.\n- Occurs with dark urine or pale stools.\n\nThese features suggest haemolysis, infection or biliary disease.\n\nMeasure bilirubin and plot it against **age in hours**, gestation and the risk-specific treatment chart; visual inspection and a single universal threshold are inadequate. Phototherapy lowers unconjugated bilirubin, and very high levels may need exchange transfusion. Support feeding and check hydration while investigation proceeds.\n\n> [!escalate]\n> Pale stools or conjugated hyperbilirubinaemia suggests biliary obstruction and needs urgent specialist assessment. The outcome of surgery for biliary atresia depends on operating early.\n\n### Heart murmurs in infants and children\n\nAn **innocent murmur** is usually soft, systolic and position-dependent, in a thriving, asymptomatic child with normal pulses and heart sounds.\n\nFeatures that suggest structural heart disease are:\n\n- A diastolic, loud, harsh or continuous murmur.\n- An abnormal second heart sound.\n- Cyanosis or poor growth.\n- Weak femoral pulses.\n- Breathlessness or sweating with feeds, exercise intolerance, chest pain or syncope.\n- A family history of sudden death.\n\nThe common lesions produce recognisable patterns. VSD, ASD and PDA cause left-to-right shunting after birth, increasing pulmonary blood flow, while coarctation obstructs systemic flow:\n\n- **VSD:** pansystolic murmur at the lower left sternal edge.\n- **ASD:** fixed split second sound with a pulmonary flow murmur.\n- **PDA:** continuous murmur.\n- **Coarctation:** weak or delayed femoral pulses and a higher BP in the arms than the legs.\n\nThese findings guide assessment but do not replace echocardiography. Saturation, pulses, perfusion, growth, liver size and respiratory signs show the haemodynamic effect. Keep a low threshold for echocardiography and cardiology review for any murmur in a newborn and for a symptomatic child.\n\n> [!escalate]\n> In **duct-dependent disease**, pulmonary or systemic blood flow relies on the ductus arteriosus, so the baby deteriorates as the duct closes in the first days. Cyanosis, shock or poor feeding in a newborn needs emergency neonatal care, not outpatient investigation.",
      "formerly": [
        "C12"
      ]
    },
    {
      "id": "C02",
      "domain": "CAH",
      "title": "Well child visit, feeding and growth",
      "focus": "Developmental surveillance, growth chart reasoning, feeding review, health promotion and parent concerns.",
      "first_pass": true,
      "priority": "Core",
      "saq_cases": [
        {
          "id": "2016-wcah-q4",
          "title": "Growth, development, immunisation and nocturnal enuresis",
          "set": "2016 WH/CAH"
        },
        {
          "id": "deck-paeds-six-week-check",
          "title": "Six-week check",
          "set": "MD3 SAQ Revision Deck"
        }
      ],
      "core_ids": [
        "P005",
        "P006",
        "P102",
        "P106"
      ],
      "notes": "### The well-child visit\n\nStart with the parents' concerns, then review pregnancy and birth, feeding, urine and stools, sleep, growth, development, immunisation, and hearing and vision. Parental mood, support, housing and safety affect the child directly, so ask about them too, without assuming any particular family structure.\n\nObserve the child before touching them. Alertness, colour, interaction, posture and spontaneous movement are informative, and handling quickly changes them.\n\n### Measuring and plotting growth\n\n- **Weight:** infants unclothed, without a nappy where practical.\n- **Length or height:** recumbent length under two years; standing height thereafter.\n- **Head circumference:** the maximum occipitofrontal circumference, around the forehead and the most prominent part of the occiput, with a non-stretch tape.\n\nPlot on age- and sex-appropriate charts. For a premature baby, use **corrected age** (chronological age minus the weeks born before 40 weeks' gestation) through early childhood.\n\nInterpret the trajectory across serial measurements, not a single centile. Weight loss or downward crossing of centiles may reflect inadequate intake, whereas **poor linear growth with preserved or increased weight suggests an endocrine cause**. Disproportionate head growth needs assessment.\n\n### Six-week examination\n\nThe six-week check looks for conditions in which early detection changes the outcome:\n\n- Growth, fontanelle and head shape.\n- Eyes and red reflex; palate.\n- Heart, lungs and femoral pulses.\n- Abdomen, spine and genitalia, including testicular position.\n- Hips.\n- Tone and symmetry of movement.\n\n> [!escalate]\n> An absent or asymmetric red reflex, or a white pupil, needs urgent ophthalmology review for cataract or retinoblastoma.\n\nWeak femoral pulses, cyanosis, or sweating and tachypnoea with feeds suggest congenital heart disease.\n\nFor the hips, assess abduction and leg length, and perform Barlow and Ortolani manoeuvres gently and only with appropriate training. Refer an unstable or dislocated hip promptly. Breech presentation or a strong family history is an indication for hip ultrasound even when the examination is normal.\n\n> [!pitfall]\n> Repeated forceful hip testing can itself destabilise the joint.\n\nInfantile haemangiomas appear in the first weeks of life, grow fastest in the first few months and then slowly involute, so most need only observation. Refer early, while propranolol can still limit growth, for lesions near the eye, nose, lip or airway, large facial or segmental lesions, ulceration, or five or more skin lesions, which can accompany liver haemangiomas.\n\n### Developmental milestones\n\nMilestones are ranges, not deadlines. Useful anchors are:\n\n- **About six weeks:** social smile.\n- **Three to four months:** good head control.\n- **Six to nine months:** sitting.\n- **About 12 months:** pincer grasp and first words.\n- **12–18 months:** walking independently.\n- **By two years:** two-word phrases.\n\nAssess gross motor, fine motor, language and social development together, because a delay confined to one domain has different implications from a global delay. Assess further when there is parental concern, regression, persistent asymmetry, no response to sound, or no independent walking by `18 months`; one normal skill does not provide reassurance.\n\n### Feeding and safety advice\n\nBreastmilk or correctly prepared formula is the foundation. Observe a feed if intake, pain or weight is a concern.\n\n- **Solids:** introduce iron-rich foods at around `six months`, when the infant is developmentally ready and prenatal iron stores are falling, and not before `four months`. Breastmilk or formula continues alongside.\n- **Allergens:** offer common allergens, including peanut and egg, in safe forms during the first year, one new food at a time. Keep tolerated foods in the diet, since regular exposure helps maintain tolerance.\n- **Food safety:** whole nuts are a choking risk. Avoid honey before `12 months` because of infant botulism, and do not give cow's milk as the main drink before `12 months`, partly because it is low in iron.\n- **Formula:** make it up at exactly the stated concentration. Dilution or extra scoops cause poor growth or electrolyte disturbance.\n\n**Safe sleep** means placing the baby on their back on a firm, flat, clear surface, with the face and head uncovered, in a smoke-free environment, in their own cot in the caregiver's room. Tummy time is for supervised play while awake.\n\nOther anticipatory guidance covers car restraints, water safety, choking and burn prevention, dental care, and limiting screen time that displaces sleep and interaction.\n\n### Immunisation and follow-up\n\nCheck the Australian Immunisation Register for what is due. Catch up missed vaccines without restarting each series. The routine schedule is:\n\n- **Birth:** hepatitis B.\n- **2, 4 and 6 months:** DTPa–IPV–Hib–hepatitis B combination.\n- **2 and 4 months:** rotavirus, within strict age limits, because intussusception risk is higher with later doses.\n- **2, 4 and 12 months:** pneumococcal conjugate vaccine (currently 20vPCV). First Nations children and risk groups may need extra doses.\n- **12 months:** MMR and meningococcal ACWY.\n- **18 months:** MMRV, Hib and DTPa.\n- **Four years:** DTPa–IPV.\n\nInfluenza vaccine is recommended every year from `six months`, and is funded for young children and risk groups. School programs give HPV and adolescent boosters.\n\nExplain the common reactions (pain, redness and swelling, mild fever and irritability), the rare risk of severe allergy, and vaccine-specific effects. Fever and rash about a week after a measles-containing vaccine reflect replication of the attenuated virus; rotavirus vaccine carries a small risk of intussusception.\n\nObserve after vaccination, record the doses and give the next appointment. End every well-child visit with an agreed follow-up for any growth, developmental or family concern.",
      "formerly": [
        "C01"
      ]
    },
    {
      "id": "C03",
      "domain": "CAH",
      "title": "Development, autism, ADHD and behaviour",
      "focus": "Developmental history, red flags, differential, family support, referral and school context; mental health assessment in intellectual disability.",
      "first_pass": true,
      "priority": "Core",
      "saq_cases": [
        {
          "id": "deck-paeds-autism",
          "title": "Language delay and autism",
          "set": "MD3 SAQ Revision Deck"
        },
        {
          "id": "deck-paeds-adhd",
          "title": "ADHD",
          "set": "MD3 SAQ Revision Deck"
        },
        {
          "id": "deck-paeds-down-fragile-x",
          "title": "Down syndrome and fragile X syndrome",
          "set": "MD3 SAQ Revision Deck"
        }
      ],
      "core_ids": [
        "P005",
        "P007",
        "P050",
        "P068",
        "P069"
      ],
      "notes": "### Developmental assessment\n\nThe history establishes when the concern began, which skills are delayed and whether any acquired skills have been lost. Pregnancy, prematurity, growth and head circumference, seizures, hearing and vision, sleep, family history and the social environment complete it.\n\n**Global developmental delay** affects at least two developmental domains in a young child.\n\n> [!pitfall]\n> Isolated speech delay still needs hearing and broader developmental assessment. Hearing loss and wider developmental difference commonly present first as delayed speech.\n\nPlay is the most natural way to assess function. Observe reaching, transferring objects and pincer grip; sitting and walking; comprehension and expressive language; and joint attention, pretend play and interaction. Caregivers and teachers can describe skills the child will not show in an unfamiliar room, so a single reluctant performance does not prove a skill is absent. Examine tone, strength, reflexes, symmetry, dysmorphic features and skin when relevant.\n\nHearing and vision problems, poor sleep, learning difficulty, trauma and medical illness can all present as behavioural difficulty, so consider them before accepting behaviour as the explanation.\n\n> [!escalate]\n> Regression, early marked hand preference (which may reflect weakness on the other side), abnormal head growth, progressive weakness or new seizures needs urgent paediatric or neurological assessment.\n\n### Autism\n\n**Autism** involves persistent differences in social communication and interaction, together with restricted or repetitive behaviours, interests or sensory patterns. These arise in early development and affect function.\n\nExplore reciprocal interaction, gestures, shared attention, play, routines, sensory distress and how the child adapts across environments. Screening tools identify children who need assessment; the diagnosis rests on detailed clinical assessment, with multidisciplinary input as needed.\n\n### Intellectual disability\n\n**Intellectual disability** requires deficits in both intellectual and adaptive functioning, beginning in the developmental period. An IQ score alone is insufficient, because support needs depend on how the person manages conceptual, social and practical tasks.\n\nConsider genetic evaluation for unexplained global delay or intellectual disability, with consent and counselling; examples include chromosomal causes, Down syndrome and fragile X. Tailor testing to the phenotype and specialist advice.\n\n### Support while assessment continues\n\nExplain the child's strengths and support needs in accessible language, without blame. Start hearing assessment, speech therapy, occupational therapy, educational adjustments and family support according to need; they do not have to wait for a final diagnosis. Set functional goals, such as expressing needs, taking part in class or managing a daily routine, and check eligibility for developmental and disability services, including the NDIS.\n\n### ADHD\n\n**ADHD** is persistent, developmentally inappropriate inattention and/or hyperactivity–impulsivity that impairs function. The diagnostic criteria require:\n\n- Symptoms for at least `six months`.\n- At least `six symptoms` in the relevant domain below age 17, or `five` from age 17.\n- Several symptoms present before age `12`.\n- Impairment in more than one setting.\n\nBecause impairment must be present across settings, observations from both home and school help separate a persistent pattern from difficulty confined to one environment.\n\nSleep deprivation or obstructive sleep apnoea, anxiety, depression, learning disorder, sensory impairment and trauma can mimic ADHD, and comorbidity is common.\n\n#### Management of ADHD\n\nCombine psychoeducation, predictable routines, clear brief instructions, positive reinforcement, school adjustments and parent support.\n\nStimulants such as methylphenidate may be appropriate after specialist assessment; non-stimulants are alternatives for selected children. Stimulants can suppress appetite and growth and raise pulse and BP, so before starting record:\n\n- Growth, appetite and sleep.\n- Pulse and BP.\n- Personal and family cardiac history.\n\nECG is reserved for a concerning history or examination. Monitor benefit in actual daily functioning, as well as appetite, weight and growth, sleep, mood, pulse and BP, and the risk of misuse or diversion.\n\n### Common behavioural problems\n\nTantrums in a toddler are often developmentally normal, reflecting frustration that outruns language. Triggers, communication, tiredness and caregiver responses usually explain the pattern. Agree a consistent, achievable approach with the family and, where relevant, the school, and review it.\n\nSevere aggression, persistent distress, loss of function or a safeguarding concern needs broader assessment.\n\n### Mental health in intellectual disability\n\nMental illness is more common in people with intellectual disability than in the general population, psychosis especially, yet it is often missed. *Diagnostic overshadowing* is the attribution of new symptoms to the disability, or to \"behaviour\", rather than to a physical or mental illness. Presentations may also be atypical: a person with limited language may show depression as withdrawal, loss of skills, sleep or appetite change, or new aggression or self-injury, and acute stress can produce confusion that resembles psychosis.\n\nThe assessment turns on change from the person's own baseline:\n\n- **Collateral history:** with consent where possible, ask familiar carers, family and support staff about usual communication, function, behaviour and supports, and when and how things changed; review previous assessments.\n- **Physical causes:** pain, including dental pain and constipation, infection, delirium, epilepsy, thyroid disease, sensory loss and medication effects commonly present as behavioural change.\n- **Circumstances:** changes in carers, accommodation or routine, conflict, bullying and abuse.\n- **The interview:** use simple language, allow extra time or several short sessions, and use the person's communication aids. Avoid leading and yes/no questions, because many people acquiesce to an authority figure; observation carries more weight in the mental state examination.\n\nCapacity is assessed for each decision, as for anyone else; an intellectual disability does not by itself establish incapacity (R11 (Capacity)). Behavioural and environmental approaches come first for challenging behaviour. Psychotropic medication is for a diagnosed or suspected psychiatric disorder, with a defined target and planned review, and restrictive practices are a last resort under disability law. Care works best when mental health and disability services, the GP and the NDIS plan are coordinated.",
      "formerly": [
        "C02"
      ],
      "also_in": [
        "MH"
      ]
    },
    {
      "id": "C04",
      "domain": "CAH",
      "title": "Unsettled infant, vomiting and feeding difficulty",
      "focus": "Colic versus reflux versus allergy/obstruction, hydration, safeguarding and reassurance.",
      "first_pass": true,
      "priority": "Core",
      "saq_cases": [
        {
          "id": "deck-paeds-infant-colic",
          "title": "Persistent crying and infant colic",
          "set": "MD3 SAQ Revision Deck"
        },
        {
          "id": "deck-paeds-gord",
          "title": "Infant vomiting and gastro-oesophageal reflux",
          "set": "MD3 SAQ Revision Deck"
        },
        {
          "id": "2016-wcah-q6",
          "title": "Vomiting infant: pyloric stenosis",
          "set": "2016 WH/CAH"
        }
      ],
      "core_ids": [
        "P002",
        "P006",
        "P014",
        "P097",
        "P103"
      ],
      "notes": "### Assessment\n\nThe history covers age, onset, whether the infant can be consoled, feeding volume and technique, wet nappies, stools, fever, weight change and the character of any vomit. Watching a whole feed often reveals problems with technique, volume or distress that the history misses.\n\nExamine the general appearance, hydration, abdomen, fontanelle, skin, groins and genitalia. For unexplained acute crying, look specifically for a hair tourniquet on a digit or the penis, a corneal abrasion and occult injury.\n\n### Obstruction and other serious causes\n\n#### Bilious vomiting\n\nGreen vomit means obstruction beyond the ampulla of Vater. Malrotation with **volvulus**, in which the bowel twists on its mesentery and cuts off its own blood supply, can infarct the gut within hours.\n\n> [!escalate]\n> Bilious vomiting needs emergency surgical assessment, even if the infant looks well.\n\n#### Pyloric stenosis\n\nProjectile non-bilious vomiting at about `2–8 weeks` suggests pyloric stenosis. The hypertrophied pyloric muscle narrows the gastric outlet above the point where bile enters, so the vomit is not bile-stained. Loss of gastric acid causes dehydration and **hypochloraemic, hypokalaemic metabolic alkalosis**.\n\nUltrasound confirms the diagnosis. **Correct fluids and electrolytes before surgery**: uncorrected alkalosis increases anaesthetic and postoperative apnoea risk.\n\n#### Intussusception\n\nEpisodic inconsolable distress with pallor, drawing up of the legs, vomiting or lethargy suggests intussusception, in which one segment of bowel telescopes into the next. Bloody \"redcurrant jelly\" stool is a late sign and is often absent.\n\n> [!escalate]\n> Suspected intussusception needs emergency assessment and ultrasound.\n\nSepsis, UTI, intracranial illness and metabolic disease are important alternatives in an unsettled, vomiting infant.\n\n### Normal crying and physiological reflux\n\nCrying normally increases over the first weeks of life and settles over the following months. A well infant who feeds, grows and examines normally may simply be showing developmental crying. Acknowledge caregiver exhaustion and review feeding, sleep and supports; promising a single cure is unhelpful.\n\nEffortless regurgitation is common because infant feeds are liquid and the antireflux barrier is immature. If the infant is thriving and comfortable, explain the natural history, avoid overfeeding and support feeding technique. Sleep remains on the back on a flat, safe surface; wedges and prone sleeping are not reflux treatments.\n\n> [!pitfall]\n> Acid suppression does not treat uncomplicated regurgitation or unexplained crying, and it can cause harm.\n\nConsider reflux disease when there is poor growth, haematemesis, feeding refusal or another complication, once alternative causes have been assessed.\n\n### Feeding adequacy\n\nFor breastfeeding, positioning, deep attachment, audible swallowing, nipple pain, wet nappies and the weight trajectory together show whether milk is being transferred. For formula, check the exact preparation and feed volumes.\n\nPoor transfer, over-dilution or frequent small ineffective feeds can explain faltering growth. Arrange lactation or child-health nurse support, and treat dehydration or illness promptly.\n\n### Cow's milk protein allergy\n\nCow's milk protein allergy can cause blood or mucus in the stools, eczema, vomiting or poor growth. Immediate hives, wheeze or collapse suggests an **IgE-mediated** reaction; delayed gut symptoms reflect a **non-IgE** mechanism.\n\n> [!pitfall]\n> Isolated crying or a nonspecific change in stools is not enough to diagnose allergy.\n\nConfirm suspected non-IgE allergy with a supervised elimination trial followed by planned reintroduction, since improvement during elimination may be coincidental. Involve a dietitian to prevent nutritional deficiency.\n\nUse extensively hydrolysed formula when a formula is needed, reserving amino-acid formula for selected severe cases. Do not casually stop breastfeeding or impose multiple maternal food exclusions.\n\n### Supporting the caregiver\n\nSoothing strategies, a predictable but flexible routine and practical respite all help.\n\n> [!counsel]\n> If you feel overwhelmed, put the baby safely in the cot, step away briefly and call for help. **Never shake a baby.**\n\nAsk sensitively about parental mental health and whether anyone feels unable to keep the baby safe.\n\n### Escalation and follow-up\n\nFever in a young infant, bilious or bloody vomit, abdominal distension, lethargy, apnoea, dehydration, poor perfusion, or failure to regain or gain weight needs same-day assessment.\n\nFor a well infant, arrange a specific review of growth and feeding, and explain what change would need earlier assessment.",
      "formerly": [
        "C03"
      ]
    },
    {
      "id": "C05",
      "domain": "CAH",
      "title": "The seriously unwell or febrile child",
      "focus": "Recognise sepsis, meningitis, dehydration and red flags by age; maintenance and replacement fluids; paediatric assessment and escalation.",
      "first_pass": true,
      "priority": "Core",
      "saq_cases": [
        {
          "id": "deck-paeds-neonatal-sepsis",
          "title": "Neonatal sepsis",
          "set": "MD3 SAQ Revision Deck"
        },
        {
          "id": "deck-paeds-meningitis",
          "title": "Infant meningitis",
          "set": "MD3 SAQ Revision Deck"
        },
        {
          "id": "2020-ummss-q9",
          "title": "Paediatric dehydration and fluid management",
          "set": "2020 UMMSS"
        }
      ],
      "core_ids": [
        "P042",
        "P096"
      ],
      "notes": "### Definitions\n\n**Sepsis** is life-threatening organ dysfunction caused by a dysregulated response to infection; fever or a positive culture alone is not sepsis. **Shock** is inadequate tissue perfusion, and it can be present before hypotension develops.\n\nChildren compensate for circulatory failure with tachycardia and vasoconstriction and may maintain their BP until shock is advanced. The early signs of deterioration therefore lie in behaviour, breathing and perfusion.\n\n### Recognising the seriously unwell child\n\nObserve interaction, alertness, colour, breathing and circulation before a detailed examination. Caregivers can say how the child differs from normal; ask also about intake, wet nappies, vomiting, rash, pain, breathing and vaccination status. Young age, prematurity, immunocompromise and significant chronic disease lower the threshold for escalation.\n\nAssess systematically:\n\n- **Airway:** patency.\n- **Breathing:** rate and work of breathing, air entry and oxygen saturation. Count an infant's respiratory rate for a full minute, because infant breathing is irregular.\n- **Circulation:** heart rate, capillary refill, limb temperature and BP.\n- **Disability:** conscious state, pupils and glucose.\n- **Exposure:** look for rash or injury while keeping the child warm.\n\nInterpret vital signs against age-specific ranges. Grunting, apnoea, exhaustion, mottling, poor perfusion, altered responsiveness, or a non-blanching rash in an unwell child is concerning.\n\n> [!pitfall]\n> A normal BP, or improvement after an antipyretic, **does not exclude sepsis**.\n\n### Fever by age\n\nFever is a temperature of `≥38°C`. Sources to consider include UTI, pneumonia, meningitis, bone and joint infection and bacteraemia, not only viral illness. A positive viral test does not exclude bacterial co-infection.\n\nIn young infants, meningitis may cause only poor feeding, lethargy, irritability or a bulging fontanelle, without neck stiffness. Their immature immunity and lack of localising signs mean that age largely determines management.\n\n> [!escalate]\n> Fever in a neonate needs urgent paediatric assessment and admission. Infants under `three months` need a low threshold for investigation and treatment; an unwell infant of any age needs emergency care.\n\n> [!current]\n> The RCH febrile child guideline (October 2026) requires a full septic work-up and empiric IV antibiotics for infants `≤21 days` corrected age. Well infants aged `22–28 days` still need admission, with lumbar puncture and antibiotic decisions made by a senior clinician using inflammatory markers.\n\nThese hospital distinctions do not justify delaying the referral of an unwell nine-week-old from general practice.\n\n### Investigations and initial treatment\n\nFor suspected serious infection, take:\n\n- Blood culture, FBE and inflammatory markers.\n- Electrolytes, renal function and glucose.\n- A properly collected urine specimen.\n- Other samples according to the likely source.\n\nPerform a lumbar puncture when meningitis is possible and it is safe to do so, but **do not delay antibiotics** or perform an LP in an unstable child. Order a chest X-ray for respiratory findings, not routinely.\n\nCall senior help or an ambulance early. Give oxygen for hypoxaemia, obtain IV or IO access when indicated, and give empiric antibiotics promptly according to the age-specific guideline; for example, ceftriaxone for suspected sepsis beyond the neonatal period.\n\nFor shock, give a `10–20 mL/kg` bolus of 0.9% sodium chloride and reassess perfusion and signs of fluid overload after each bolus, involving senior staff early. Children with leaky capillaries or poor cardiac function can be tipped into fluid overload, so take particular care in cardiac disease. Correct hypoglycaemia promptly.\n\nHand over the age and weight, observations, time of onset, suspected source, fluids and drugs given, and allergies.\n\n### Hydration\n\nJudge hydration from intake and output, mucous membranes, tears, sunken eyes, heart rate and perfusion, alertness and weight change. Mild to moderate dehydration can usually be treated enterally; severe dehydration or shock needs hospital care.\n\nA fluid plan has three separate components: maintenance needs, the deficit and ongoing losses. Record the response and urine output.\n\nEnteral fluid, by mouth or nasogastric tube, is preferred whenever the child can take it; see C08 (Gastroenteritis). When IV fluid is needed beyond the neonatal period, the hourly maintenance rate follows the *4–2–1 rule*:\n\n- `4 mL/kg/h` for the first 10 kg.\n- `2 mL/kg/h` for the next 10 kg.\n- `1 mL/kg/h` for each kilogram above 20 kg, to a usual maximum of `100 mL/h`.\n\nA 15 kg child therefore needs 40 + 10 = `50 mL/h`. Use 0.9% sodium chloride with 5% glucose, adding potassium once electrolytes and renal function are known; hypotonic fluids are no longer used routinely, because they cause hyponatraemia.\n\nUnwell children often secrete excess ADH, which retains water and lowers sodium, so RCH gives most unwell children who are not dehydrated `two-thirds` of the calculated maintenance, with further restriction after some neurological, respiratory or postoperative conditions on senior advice. A deficit is added to maintenance and replaced at no more than about `5%` of body weight (50 mL/kg) in each `24 hours`, since clinical estimates of dehydration are imprecise; measured ongoing losses are replaced over the following hours. Resuscitation boluses are separate and are not counted in these calculations.\n\nWeigh the child at the start and at least daily, keep a strict fluid balance, and check electrolytes and glucose before starting and at least daily, or after `4–6 hours` in an unwell child. A sodium below `135 mmol/L`, or a rapid change, needs senior review. Neonates have different requirements, and DKA is managed as in C09 (New type 1 diabetes).\n\n### Safe discharge\n\nA child can be managed at home when they are alert enough to interact, are maintaining adequate intake, have a reassuring assessment and can be reliably followed up. Give weight-appropriate analgesia or antipyretic for comfort; there is no need to chase a normal temperature, because fever itself is not harmful.\n\n> [!counsel]\n> Return urgently for difficult breathing, unusual sleepiness, a non-blanching rash, poor intake or reduced urine output, persistent vomiting or worsening pain.\n\nTime the review according to age and uncertainty. Reassess prolonged fever for Kawasaki disease or another source.\n\nReference: [RCH Febrile child](https://www.rch.org.au/clinicalguide/guideline_index/Febrile_child/) (October 2026 update).",
      "formerly": [
        "C04"
      ]
    },
    {
      "id": "C06",
      "domain": "CAH",
      "title": "Childhood wheeze, asthma and respiratory infection",
      "focus": "Bronchiolitis, croup, pneumonia and asthma: differentiate, treat and communicate with parents.",
      "first_pass": true,
      "priority": "Core",
      "saq_cases": [
        {
          "id": "deck-paeds-bronchiolitis",
          "title": "Bronchiolitis",
          "set": "MD3 SAQ Revision Deck"
        },
        {
          "id": "deck-paeds-acute-asthma",
          "title": "Acute asthma",
          "set": "MD3 SAQ Revision Deck"
        },
        {
          "id": "deck-paeds-croup",
          "title": "Croup",
          "set": "MD3 SAQ Revision Deck"
        }
      ],
      "core_ids": [
        "P026",
        "P034",
        "P107"
      ],
      "notes": "### Wheeze and stridor\n\n**Wheeze** usually reflects narrowing of the intrathoracic airways and is loudest on expiration. **Stridor** is a harsh sound from upper-airway narrowing, usually most obvious on inspiration.\n\nAge, onset and the noise the child makes usually identify the illness:\n\n- **Bronchiolitis:** an infant with coryza followed by cough, feeding difficulty and widespread crackles and wheeze.\n- **Croup:** barking cough, hoarse voice and inspiratory stridor from subglottic narrowing, typically from six months to three years.\n- **Asthma:** recurrent, variable expiratory wheeze and cough, often with exercise or night symptoms, or atopy.\n- **Pneumonia:** fever, tachypnoea and sometimes focal chest signs.\n- **Inhaled foreign body:** sudden onset during eating or play, unilateral wheeze or persistent focal signs, even with a normal chest X-ray.\n\nSeverity shows in alertness, the ability to feed or speak, recession, grunting, respiratory rate, air entry and oxygen saturation.\n\n> [!escalate]\n> Apnoea, cyanosis, exhaustion, a silent chest or altered consciousness needs emergency care.\n\nKeep a distressed child with their caregiver and avoid unnecessary upsetting examination in upper-airway obstruction, because distress can precipitate complete obstruction.\n\n### Bronchiolitis\n\nTypical bronchiolitis is a **clinical diagnosis**. Obstruction comes from viral inflammation, oedema and mucus in the small airways, not bronchospasm, so routine chest X-ray, blood tests, salbutamol, corticosteroids and antibiotics do not help.\n\nManagement is supportive:\n\n- **Feeding and hydration:** maintain intake, using nasogastric feeds or fluids if needed.\n- **Oxygen:** RCH recommends oxygen for persistent saturation `<90%`; brief dips do not determine treatment. Reserve high-flow oxygen for failure of standard support.\n\nThe need for admission depends on age, apnoea, work of breathing, intake and underlying disease.\n\n### Croup\n\nA corticosteroid reduces subglottic oedema over hours and helps croup with stridor or clinically significant symptoms. A barking cough alone without stridor may not need it.\n\n- **Mild to moderate:** oral dexamethasone `0.15 mg/kg`, or prednisolone `1 mg/kg`.\n- **Severe:** dexamethasone `0.6 mg/kg` (`maximum 12 mg`).\n\nNebulised adrenaline relieves significant stridor or distress within minutes, but the effect wears off. Observe for at least `three hours` afterwards, and discharge only when there is no stridor at rest.\n\nDrooling, a toxic appearance, a poor response to treatment or an atypical age suggests another diagnosis, such as bacterial tracheitis or epiglottitis.\n\n### Acute asthma\n\nJudge severity clinically, from work of breathing, respiratory rate, alertness, activity and air entry. Oxygen saturation, heart rate and the ability to talk add to the picture, but tachycardia can reflect salbutamol as much as severity.\n\n- **Mild:** mildly increased work of breathing, a normal respiratory rate, alert and active.\n- **Moderate:** moderately increased work of breathing and respiratory rate, still alert and active.\n- **Severe:** markedly increased work of breathing and respiratory rate, with agitation or pallor.\n- **Life-threatening:** maximal work of breathing, drowsiness or confusion, reduced movement or cyanosis.\n\n> [!pitfall]\n> The loudness of the wheeze is unreliable, because wheeze needs airflow. A silent chest in an unwell child may signal impending respiratory collapse.\n\nWheeze under `12 months` is more likely to be bronchiolitis, which does not respond to bronchodilators. Sudden symptoms after a food, medicine or sting raise anaphylaxis; when the two are hard to distinguish, treat as anaphylaxis (see B02 (Recognition and adrenaline)). Routine chest X-ray and blood gases are not needed, and sampling blood can distress a child into deterioration.\n\n#### Treatment by severity (RCH)\n\nSalbutamol by metered-dose inhaler and spacer, with a mask for young children, works as well as a nebuliser with fewer adverse effects. Doses differ at 1–5 years and from 6 years:\n\n- **Mild:** salbutamol once, `2–6 puffs` (1–5 years) or `12 puffs` (6 years and over), then reassess after `20 minutes`. Persisting work of breathing or an oxygen need moves the child to moderate treatment.\n- **Moderate:** salbutamol every `20 minutes` for `three doses`, `6 puffs` or `12 puffs` by age, with oxygen to keep SpO₂ `≥90%`. Children of 6 and over also receive oral prednisolone `1 mg/kg` (`maximum 50 mg`), or dexamethasone. **In children aged 1–5, steroids are initially withheld** and considered only if the response is poor. Reassess `30 minutes` after the third dose; if improvement is inadequate, add ipratropium every `20 minutes` for three doses alongside further salbutamol.\n- **Severe:** early senior involvement, salbutamol plus ipratropium every `20 minutes` for three doses, a systemic corticosteroid given early by mouth or IV, and IV access. Persisting severe symptoms need admission and consideration of IV magnesium sulfate or aminophylline with critical-care input.\n- **Life-threatening:** resuscitation area, paediatric critical-care involvement and respiratory support. Give continuous nebulised salbutamol with ipratropium, IV corticosteroid and IV magnesium sulfate, and consider IM adrenaline for poor respiratory effort.\n\nA poor response to salbutamol is a reason to reconsider the diagnosis, including foreign body or pneumothorax when air entry is persistently asymmetric. Frequent salbutamol itself causes tachycardia, tremor, tachypnoea, hypokalaemia and lactic acidosis, which can be mistaken for respiratory deterioration. Adolescents who use budesonide–formoterol as their reliever are given salbutamol for an attack that needs hospital treatment.\n\nFor community first aid, give salbutamol `4 separate puffs` through a spacer, with four breaths after each puff. Wait `4 minutes` and repeat if needed, calling an ambulance for severe symptoms. An individual action plan may specify a different regimen.\n\n#### Discharge\n\nMost children are ready for discharge once they have gone `3 hours` without salbutamol, are drinking and are clinically well. An SpO₂ of `90–94%` alone does not prevent discharge in a child who has responded well. A few children with fully resolved signs may go after `1 hour`, following senior review, if their carers are competent and emergency care is accessible.\n\nBefore the child goes home:\n\n- Demonstrate one-puff-at-a-time spacer technique and have the caregiver show it back; see G10 (Inhaler, spacer and peak-flow technique).\n- Provide a written action plan covering daily treatment, what to do when symptoms increase, emergency signs and whom to contact.\n- Address smoke exposure, access to medicines at school or childcare, and follow-up.\n\n### Ongoing asthma control\n\n> [!pitfall]\n> A single episode of preschool viral wheeze does not establish persistent asthma.\n\nInterval symptoms, night waking, exercise limitation, atopy, reliever use and previous severe attacks distinguish ongoing asthma from episodic viral wheeze. Recurrent or persistent symptoms may need low-dose inhaled corticosteroid through an age-appropriate spacer, with monitoring of technique, adherence, symptom response and growth. Do not simply copy adult ICS–formoterol regimens into preschool care.\n\n### Pneumonia\n\nBacterial community-acquired pneumonia in a child who is stable and drinking can be managed at home with symptomatic treatment and review. RCH advises considering oral amoxicillin `30 mg/kg` (`maximum 1 g`) three times daily for `3–5 days`. This high-dose regimen is chosen to overcome the reduced penicillin susceptibility of some pneumococci.\n\nHypoxaemia, dehydration, very young age or significant work of breathing needs hospital assessment. In hospital, oral amoxicillin remains appropriate if it is tolerated, with IV benzylpenicillin for a child who is vomiting or cannot take oral treatment. Severe pneumonia, marked by severe respiratory distress, SpO₂ `<80%` or a need for respiratory support, marked tachycardia, altered mental state or a complicated pneumonia, is treated with IV ceftriaxone, and most of these children need intensive care.\n\nRe-evaluate at `24–48 hours`. A child who is not improving needs the diagnosis and treatment reconsidered, and a chest X-ray to look for effusion or empyema if they are deteriorating; otherwise reserve chest X-ray for severe or uncertain disease. Complicated pneumonia may need a longer course.\n\nA chronic wet cough, recurrent focal infection, clubbing or poor growth needs assessment for bronchiectasis, cystic fibrosis or another underlying disorder.",
      "formerly": [
        "C05"
      ]
    },
    {
      "id": "C07",
      "domain": "CAH",
      "title": "Childhood infections, fever and rash",
      "focus": "Viral exanthems, otitis media, sore throat, impetigo and nappy dermatitis, eczema herpeticum, Kawasaki disease and IgA vasculitis.",
      "first_pass": false,
      "priority": "Core",
      "saq_cases": [
        {
          "id": "deck-paeds-otitis-media",
          "title": "Acute otitis media",
          "set": "MD3 SAQ Revision Deck"
        },
        {
          "id": "deck-paeds-tonsillitis",
          "title": "Sore throat and tonsillitis",
          "set": "MD3 SAQ Revision Deck"
        },
        {
          "id": "2020-ummss-q1",
          "title": "Atopic dermatitis and eczema herpeticum",
          "set": "2020 UMMSS"
        }
      ],
      "core_ids": [
        "P035",
        "P042",
        "P050",
        "P080",
        "P092"
      ],
      "notes": "### Fever and rash: assessment\n\nMost childhood rashes are viral and self-limiting. The task is to recognise the common patterns while actively looking for the few serious causes.\n\nAsk about the duration of fever, exposures and travel, vaccination, medicines, itch or pain, mucosal symptoms and intake. Describe the distribution of the rash and whether it blanches, and examine the ears and throat, lymph nodes, joints and hydration.\n\n> [!escalate]\n> A non-blanching rash in an unwell child, mucosal sloughing, or rapidly progressive painful skin disease needs emergency care.\n\n### Common viral exanthems\n\n- **Roseola:** high fever for several days, then a rash as the fever settles, in a young child who is generally improving.\n- **Parvovirus B19:** \"slapped cheek\" followed by a lacy rash on the limbs. The virus infects red-cell precursors, so consider pregnant contacts and children with haemolytic disease.\n- **Hand, foot and mouth disease:** oral ulcers with lesions on the hands and feet. Hydration and pain relief matter most.\n- **Varicella:** itchy vesicles in successive crops. Keep the child away from susceptible pregnant or immunocompromised people, and exclude from childcare and school until all lesions have crusted.\n- **Measles:** fever, cough, coryza and conjunctivitis, followed by a rash spreading from the face downwards.\n\n> [!escalate]\n> Measles is airborne and highly contagious. Isolate a suspected case immediately, arrange testing without exposing a waiting room, and notify public health the same day. Vaccination history changes the probability, not the need to act on a convincing presentation.\n\n### Acute otitis media\n\nDiagnosis requires compatible symptoms and a bulging or inflamed drum; redness alone is not enough, because crying reddens the drum. Most uncomplicated cases resolve spontaneously, so analgesia and review are often sufficient.\n\nGive antibiotics to infants under six months, to children who are systemically unwell or have complications, and in high-risk groups such as Aboriginal and Torres Strait Islander children. Amoxicillin is first-line.\n\n> [!escalate]\n> Redness or swelling over the mastoid, a protruding pinna or systemic deterioration suggests mastoiditis and needs same-day assessment.\n\n**Otitis media with effusion** causes hearing difficulty without acute infection; adenoidal or nasal disease can contribute through Eustachian-tube dysfunction. Antibiotics do not reliably clear a persistent effusion. Refer to audiology and ENT for persistent hearing concerns, language delay or recurrent disease.\n\n### Sore throat\n\nMost sore throats are viral. Assess the risk of acute rheumatic fever and look for signs of deep-space infection; see G27 (Sore throat: management).\n\n### Skin infections and eczema\n\n- **Impetigo:** superficial infection with S. aureus or S. pyogenes, causing honey-coloured crusted lesions, often around the nose and mouth, or flaccid blisters in bullous impetigo. Hygiene and covering the lesions reduce spread: soften and remove crusts with soap and water, pat dry and cover with a waterproof dressing. A topical antibiotic suits a few localised lesions; extensive, bullous or recurrent impetigo, or systemic features, needs an oral antibiotic such as cefalexin, guided by local resistance and culture. In Victoria, the child is excluded from school or childcare until appropriate antibiotic treatment has started, with lesions on exposed skin covered.\n- **Nappy dermatitis:** usually an irritant dermatitis from urine and faeces held against the skin, affecting the convex surfaces of the buttocks and genitals and sparing the skin folds. Candidal infection is suggested by involvement of the folds, a beefy red colour and satellite papules or pustules, especially after antibiotics. Change nappies frequently, allow nappy-free time, clean with water rather than fragranced wipes, and apply a thick zinc oxide or petrolatum barrier at each change. Add a topical imidazole such as clotrimazole for candidal features, and a mild corticosteroid briefly for marked inflammation. Review a rash that fails to improve within about a week, blisters or erosions (secondary infection), extension beyond the nappy area (seborrhoeic or atopic dermatitis, psoriasis), or an infant who is unwell or not thriving.\n- **Scabies:** treat the child and all close contacts at the same time.\n- **Eczema:** regular emollient plus adequate topical anti-inflammatory treatment.\n\n> [!escalate]\n> Fever with rapidly spreading painful vesicles or punched-out erosions in a child with eczema suggests eczema herpeticum and needs same-day assessment for antiviral treatment.\n\nExclusion periods follow the current Victorian rules for each infection; there is no generic \"24 hours of antibiotics\" rule.\n\n### Kawasaki disease and IgA vasculitis\n\nBoth are forms of **vasculitis**, inflammation of blood-vessel walls. Kawasaki disease mainly affects medium-sized arteries, especially the coronary arteries. IgA vasculitis results from immune-complex deposition in small vessels, typically of the skin, joints, bowel and kidneys.\n\n#### Kawasaki disease\n\nPersistent fever with:\n\n- Bilateral non-purulent conjunctivitis.\n- Oral changes: red cracked lips, strawberry tongue.\n- Polymorphous rash.\n- Changes in the hands and feet: redness, swelling, later peeling.\n- Cervical lymphadenopathy.\n\nIncomplete presentations are common, especially in infants. Consider the diagnosis when fever lasts `four or more days` with suggestive features, and **do not wait for every sign**: coronary injury can develop before the full picture appears, and timely treatment reduces it.\n\n> [!escalate]\n> Suspected Kawasaki disease needs same-day paediatric review, inflammatory markers and echocardiography. IV immunoglobulin and aspirin are specialist treatments.\n\n#### IgA vasculitis\n\nPalpable purpura on the legs and buttocks, arthralgia and abdominal pain, sometimes with renal involvement.\n\n> [!pitfall]\n> Nephritis can appear weeks after the rash. Check BP and urinalysis at diagnosis and during follow-up, even if the child feels well.\n\nSevere abdominal pain, gastrointestinal bleeding, intussusception or significant nephritis needs emergency care.",
      "formerly": [
        "C06"
      ]
    },
    {
      "id": "C08",
      "domain": "CAH",
      "title": "Paediatric bowel symptoms, nutrition and growth failure",
      "focus": "Constipation, gastroenteritis, coeliac disease and IBD: assessment, red flags, family guidance.",
      "first_pass": false,
      "priority": "Core",
      "saq_cases": [
        {
          "id": "deck-paeds-constipation",
          "title": "Functional constipation",
          "set": "MD3 SAQ Revision Deck"
        },
        {
          "id": "deck-paeds-gastroenteritis",
          "title": "Gastroenteritis",
          "set": "MD3 SAQ Revision Deck"
        },
        {
          "id": "deck-paeds-coeliac",
          "title": "Faltering growth and coeliac disease",
          "set": "MD3 SAQ Revision Deck"
        }
      ],
      "core_ids": [
        "P002",
        "P006",
        "P012",
        "P025",
        "P028",
        "P081",
        "P103",
        "P105"
      ],
      "notes": "### Functional constipation\n\nFunctional constipation is usually a self-reinforcing cycle. A painful stool leads to withholding; retained stool becomes harder and the rectum distends, so the next stool is also painful. **Overflow soiling** is involuntary leakage of liquid stool around the retained mass, not deliberate behaviour.\n\nAsk about stool consistency and frequency, painful defaecation, withholding postures, toilet training, diet, medicines and urinary symptoms. Examine growth and the abdomen, inspect the perianal area, and examine the lumbosacral spine and lower-limb neurology when indicated.\n\nFeatures that suggest an organic cause:\n\n- Delayed passage of meconium (beyond `48 hours`) or symptoms from early infancy.\n- Bilious vomiting or severe distension.\n- An abnormal anus or spine.\n- Faltering growth.\n\nIn **Hirschsprung disease**, absent enteric ganglion cells stop the affected distal bowel relaxing, producing functional obstruction.\n\nOtherwise the diagnosis is clinical. A typical, uncomplicated functional presentation does not need abdominal X-ray, rectal examination or blood tests.\n\n### Management of constipation\n\nTreatment breaks the cycle in two phases:\n\n1. **Disimpaction**, if the child is impacted, with an age- and weight-appropriate oral macrogol regimen. Soiling may increase temporarily during clearance.\n2. **Maintenance** with a lower dose that produces soft, painless stools. This often continues for months, because rectal sensation takes time to recover.\n\nCombine medication with unhurried toilet sitting after meals, feet supported, praise for trying and a stool diary. Fibre and fluids support treatment but rarely clear established impaction alone. Taper gradually after sustained recovery; stopping early commonly leads to relapse.\n\n### Gastroenteritis\n\nMost acute diarrhoea in children is viral. The duration, blood in the stool, fever, exposures, urine output and hydration determine severity. Focal severe pain, bilious vomiting or marked lethargy suggests another diagnosis. Weight change is useful when a reliable pre-illness weight is known.\n\nFor mild to moderate dehydration, give oral rehydration solution in frequent small amounts, starting at about `10 mL/kg/hour` (RCH) and reassessing. ORS works because glucose-coupled sodium absorption in the gut remains intact in most gastroenteritis.\n\n- Continue breastfeeding and normal age-appropriate feeding as tolerated.\n- Avoid juice and soft drinks; their high sugar content can worsen diarrhoea.\n- Oral ondansetron can help a child over `six months` with persistent vomiting tolerate ORS.\n\nIf oral rehydration fails, nasogastric rehydration is often preferable to IV fluid in a stable child. Shock or severe dehydration needs hospital care. Antibiotics and antidiarrhoeal medicines are not routine.\n\n> [!counsel]\n> Return urgently for reduced urine output, drowsiness, persistent vomiting or blood in the stool.\n\n### Faltering growth\n\nConfirm the measurements, then plot weight, length or height and head circumference over time. Inadequate intake is the commonest cause; a description of a typical day, milk volumes, food availability, feeding behaviour and oral-motor skills often reveals it.\n\nThe order in which growth parameters fall helps separate causes. Weight usually falls first in undernutrition, whereas endocrine disorders more often slow height velocity while weight is preserved or increased. Parental heights, pubertal stage and bone age help distinguish familial short stature and constitutional delay from disease.\n\n### Chronic gut disease\n\nPersistent diarrhoea, greasy stools, abdominal pain, recurrent infection or poor growth suggests malabsorption or chronic disease. Initial tests include FBE and ferritin, renal and liver function, inflammatory markers, coeliac serology and targeted stool tests.\n\n- **Coeliac disease:** test tTG-IgA with total IgA while the child is eating gluten. Refer to paediatric gastroenterology before starting a gluten-free diet. Specialist pathways permit diagnosis without biopsy in selected children; this is not a general rule for every positive test.\n- **Inflammatory bowel disease:** bloody or nocturnal diarrhoea, perianal disease, oral ulcers, delayed growth or puberty, and a raised faecal calprotectin increase concern. Endoscopy and specialist care establish the diagnosis and treatment, and growth and nutrition are major treatment outcomes.\n- **Cystic fibrosis:** an inherited disorder of the CFTR ion channel that dehydrates secretions and often causes pancreatic insufficiency, linking airway disease with poor fat absorption. Consider it with recurrent chest infections, greasy stools and poor growth; newborn screening lowers but does not remove the possibility. Arrange sweat testing and specialist evaluation when it is suspected.\n\n### Management and follow-up\n\nTreat the specific cause and support nutrition with a dietitian and a family-centred feeding plan, with documented goals for weight trajectory, intake, symptoms and function. Avoid indiscriminate restrictive diets, which deepen the energy deficit.\n\n> [!escalate]\n> Severe abdominal pain, obstruction, significant gastrointestinal bleeding, marked dehydration or rapid nutritional decline needs same-day assessment.\n\nPlan reassessment for any persisting growth concern, even after reassuring initial tests.",
      "formerly": [
        "C07"
      ]
    },
    {
      "id": "C09",
      "domain": "CAH",
      "title": "Childhood diabetes, renal and urinary presentations",
      "focus": "DKA/hypoglycaemia, UTI, nephritic presentation, fluid balance and relevant referral.",
      "first_pass": false,
      "priority": "Core",
      "saq_cases": [
        {
          "id": "deck-paeds-dka",
          "title": "Diabetic ketoacidosis",
          "set": "MD3 SAQ Revision Deck"
        },
        {
          "id": "deck-paeds-uti",
          "title": "Urinary tract infection in a child",
          "set": "MD3 SAQ Revision Deck"
        },
        {
          "id": "deck-paeds-psgn",
          "title": "Post-streptococcal glomerulonephritis",
          "set": "MD3 SAQ Revision Deck"
        }
      ],
      "core_ids": [
        "P016",
        "P047",
        "P075",
        "P094",
        "P101"
      ],
      "notes": "### New type 1 diabetes\n\n**Type 1 diabetes** results from autoimmune destruction of pancreatic beta cells. Without insulin, the body burns fat for fuel and produces ketones. Polyuria, polydipsia, weight loss, fatigue or new bedwetting should prompt an immediate capillary glucose and ketone check. Do not defer testing to a fasting appointment, because ketoacidosis can develop within hours.\n\n> [!escalate]\n> A child with newly suspected diabetes needs same-day paediatric assessment, even before ketoacidosis develops.\n\n### Diabetic ketoacidosis\n\n**Diabetic ketoacidosis** (DKA) is metabolic acidosis caused by ketone accumulation during marked insulin deficiency. It adds vomiting, abdominal pain, dehydration, deep (Kussmaul) breathing and altered consciousness to the picture of new diabetes. Hospital diagnostic criteria are:\n\n- Glucose usually `>11 mmol/L`.\n- Blood ketones usually `≥3 mmol/L`.\n- Venous pH `<7.3` or bicarbonate `<18 mmol/L`.\n\nAssess glucose, blood ketones, a venous gas, electrolytes and neurological state. Treatment corrects the deficit slowly and replaces insulin steadily (RCH):\n\n- **Fluids:** a `10 mL/kg` bolus of 0.9% sodium chloride only for poor perfusion, then maintenance plus the deficit over `48 hours`, starting with 0.9% sodium chloride.\n- **Insulin:** an infusion at `0.05–0.1 units/kg/h`, started at least `one hour` after IV fluids and without a bolus.\n- **Potassium:** total body potassium is depleted and insulin drives it into cells, so add potassium to the fluids once the level is known and the child is passing urine.\n- **Glucose:** add 5% glucose once blood glucose falls to `15 mmol/L`, so that insulin can continue until the ketosis clears.\n- **Monitoring:** glucose, ketones, fluid balance and neurological observations hourly, with a venous gas and electrolytes every `2–4 hours`. An insulin bolus or rapid, unplanned correction is harmful, raising the risks of hypokalaemia and cerebral oedema.\n\n> [!escalate]\n> **Headache, falling conscious state or bradycardia during treatment** suggests cerebral oedema and needs emergency action.\n\n### Living with type 1 diabetes\n\nFamily education covers insulin administration and storage, carbohydrate awareness, glucose monitoring, hypoglycaemia, sick-day ketone checks and a school plan.\n\n> [!counsel]\n> Never simply stop insulin during illness. Stress hormones increase insulin requirements, and stopping it precipitates ketoacidosis.\n\nFor a conscious child with hypoglycaemia, give weight-appropriate fast-acting carbohydrate and recheck after about `15 minutes`, following the diabetes plan.\n\n> [!escalate]\n> An unconscious child with hypoglycaemia needs emergency glucagon or IV glucose and nothing by mouth.\n\n### Urinary tract infection\n\nInfants with UTI may have only fever, poor feeding or vomiting. Older children may report dysuria, frequency, abdominal or flank pain, or new incontinence. Collect urine before antibiotics where feasible, but do not delay treatment in a seriously ill child.\n\nThe diagnosis is only as reliable as the specimen. Use a clean-catch sample when it can be obtained; young infants may need a catheter or suprapubic sample.\n\n> [!pitfall]\n> Bag specimens are highly prone to contamination and **cannot reliably confirm a positive culture**.\n\nRecord the collection method, and interpret pyuria, colony count and organism in that light. Constipation and voiding dysfunction predispose to recurrence, so check for them as well as for anatomical risk.\n\n#### Treatment\n\n- **Unwell child, or infant under `three months`:** hospital assessment and usually initial IV antibiotics.\n- **Stable older child with cystitis:** oral cefalexin `20 mg/kg per dose three times daily` (`maximum 750 mg per dose`) for `3–5 days` (RCH), adjusted for culture, allergy and local guidance.\n- **Pyelonephritis:** a different dose and duration, with severity assessment.\n\nReview the culture promptly. Reserve imaging for atypical or recurrent infection and specific age and risk features; it is not needed after every uncomplicated episode.\n\n### Nephritic and nephrotic syndromes\n\nThe two syndromes reflect different kinds of glomerular injury.\n\n#### Nephritic syndrome\n\nGlomerular inflammation causes haematuria, hypertension, oedema and reduced renal function. Post-streptococcal glomerulonephritis follows throat or skin infection by one to several weeks.\n\nAssess with urine microscopy and protein, creatinine and electrolytes, complement (low C3) and evidence of preceding streptococcal infection. Monitor BP, urine output and fluid overload. Antibiotics treat any active infection but do not reverse established glomerular inflammation.\n\n#### Nephrotic syndrome\n\nA leaky filtration barrier causes heavy proteinuria, hypoalbuminaemia and oedema, often first noticed around the eyes. Assess urine protein, albumin and renal function, and look for its complications:\n\n- Infection.\n- Thrombosis.\n- Intravascular depletion despite visible oedema, because fluid has shifted from the circulation into the tissues.\n\nSteroid treatment and monitoring need paediatric supervision. Do not assume that every oedematous child needs unrestricted diuresis.\n\nIn either syndrome, severe hypertension, oliguria, pulmonary oedema or sepsis needs emergency care.\n\n### Nocturnal enuresis\n\nPrimary nocturnal enuresis differs from new wetting after a dry period, and from daytime symptoms, both of which more often have an underlying cause. Screen for constipation, diabetes, UTI, sleep apnoea and psychosocial change.\n\nExplain that bedwetting is not deliberate. Regular daytime voiding, sensible fluid timing and, once the child and family are ready, an enuresis alarm form the core of treatment. Desmopressin may help in selected short-term situations but requires evening fluid restriction to avoid hyponatraemia.",
      "formerly": [
        "C08"
      ]
    },
    {
      "id": "C10",
      "domain": "CAH",
      "title": "Seizures, headache and developmental neurology",
      "focus": "Seizure assessment and emergency treatment, febrile and afebrile seizures, childhood headache and developmental neurology.",
      "first_pass": false,
      "priority": "Core",
      "saq_cases": [
        {
          "id": "2020-ummss-q10",
          "title": "Seizure in a child: febrile convulsion",
          "set": "2020 UMMSS"
        },
        {
          "id": "deck-paeds-migraine",
          "title": "Migraine in childhood",
          "set": "MD3 SAQ Revision Deck"
        }
      ],
      "core_ids": [
        "P013",
        "P049",
        "P064",
        "P085"
      ],
      "notes": "### Definitions\n\nA **seizure** is a transient disturbance of neurological function caused by abnormal, excessive or synchronous neuronal activity. **Epilepsy** is an enduring predisposition to unprovoked seizures; a single seizure is not epilepsy.\n\nSeizure type matters for diagnosis and treatment. **Focal seizures** begin in one hemisphere. **Generalised seizures** involve bilateral networks from the outset; absence seizures cause brief lapses of awareness. Staring episodes need careful description to distinguish focal seizures, absences and simple inattention.\n\n### Assessing the event\n\nThe diagnosis rests largely on the description, so obtain a witness account or a safely recorded video covering onset, duration, focal features, eye or head deviation, movements, colour, awareness and recovery. Fever, illness, trauma, ingestion, sleep deprivation, development and family history help identify a cause. Mimics include syncope, rigors, breath-holding spells and behavioural events.\n\nDuring a seizure, assess and support airway, breathing and circulation, and protect the child from injury. Time the seizure, because its duration determines when rescue medication is needed, and check glucose to exclude a treatable cause.\n\n> [!escalate]\n> A convulsive seizure lasting `five minutes or longer` needs emergency treatment with a benzodiazepine, such as buccal or intranasal midazolam `0.3 mg/kg` (maximum `10 mg`), repeated once after a further `five minutes` if needed. A seizure continuing after two doses needs a second-line IV drug, such as levetiracetam, and senior help. Seizures that have lasted this long are less likely to stop on their own.\n\nCount any doses already given before repeating, because respiratory depression risk rises with each dose. After recovery, examine neurological function and look for infection, injury and raised intracranial pressure.\n\n### Febrile seizures\n\nA **simple febrile seizure** is generalised, lasts `<15 minutes` and does not recur within the same illness, with full recovery within an hour, in a developmentally and neurologically normal child, usually aged `six months to six years`.\n\nFocality, a prolonged or repeated seizure, persistent altered consciousness or an atypical age needs broader assessment. Investigate the fever for its cause. EEG, neuroimaging and long-term antiseizure medication are not needed after a typical simple febrile seizure.\n\nExplain that brief simple febrile seizures are frightening but usually benign. They can recur, and they do not cause brain damage. Antipyretics improve comfort but **do not reliably prevent another seizure**.\n\n> [!counsel]\n> During a seizure, place the child on their side when safe, move nearby hazards away, do not restrain them and put nothing in their mouth. Call an ambulance if the seizure lasts `five minutes`, if there is difficulty breathing or injury, or if the child does not recover; follow any individual rescue plan.\n\n### Afebrile seizures\n\nAn afebrile seizure needs paediatric assessment, with EEG and imaging according to the history and examination. Treatment is not usually started after a single unprovoked seizure, because many children do not have another.\n\nSome seizure types are easily missed. Absence seizures are brief staring spells with abrupt onset and offset, often many times a day and provoked by hyperventilation. Infantile spasms are clusters of sudden flexion or extension, often on waking, sometimes with developmental regression; they need urgent same-day paediatric referral, because delay worsens the developmental outcome. Advise on safety around water, heights and roads, supervision, sleep, and medication adherence if treatment is started.\n\n### Headache in children\n\nMigraine in children can be bilateral and shorter than in adults, with nausea, sensitivity to light and sound, and activity limitation. Ask about school, sleep, meals, hydration, stress, medication use and family history, and examine BP, gait, cranial nerves, coordination and, when appropriate, the fundi.\n\nManage a typical migraine pattern with early age- and weight-appropriate analgesia, a quiet environment and a headache diary. Some children need migraine-specific or preventive treatment through paediatric care. Support school attendance and avoid frequent analgesic use.\n\n> [!escalate]\n> Progressive morning headache with vomiting, a focal deficit, papilloedema, changed behaviour, headache that wakes the child, or systemic illness suggests raised intracranial pressure or another secondary cause and needs urgent investigation.\n\n### Weakness and developmental neurology\n\nLoss of skills, an abnormal gait, frequent falls or difficulty rising from the floor needs assessment. Localisation guides investigation:\n\n- **Upper motor neurone signs:** spasticity and brisk reflexes.\n- **Lower motor neurone pattern:** weakness, wasting and reduced reflexes.\n- **Gowers manoeuvre** (climbing up the legs to stand): suggests proximal weakness, but is not diagnostic alone.\n\n**Cerebral palsy** reflects a non-progressive disturbance of the developing brain, although functional needs change with growth. Regression points to another explanation.\n\n> [!escalate]\n> Progressive weakness, bulbar symptoms or respiratory compromise needs urgent referral.\n\nLong-term disability needs coordinated therapy, communication support and family support.",
      "formerly": [
        "C09"
      ]
    },
    {
      "id": "C11",
      "domain": "CAH",
      "title": "Limp, joints, trauma and safeguarding",
      "focus": "Assess limp/injury, septic joint red flags, non-accidental injury, documentation and escalation.",
      "first_pass": true,
      "priority": "Core",
      "saq_cases": [
        {
          "id": "deck-paeds-limp-septic-arthritis",
          "title": "Limping child and septic arthritis",
          "set": "MD3 SAQ Revision Deck"
        },
        {
          "id": "2016-wcah-q5",
          "title": "Developmental dysplasia of the hip, development and non-accidental injury",
          "set": "2016 WH/CAH"
        },
        {
          "id": "deck-paeds-nai-toddler-fracture",
          "title": "Possible non-accidental injury and toddler's fracture",
          "set": "MD3 SAQ Revision Deck"
        }
      ],
      "core_ids": [
        "P029",
        "P056",
        "P057",
        "P065",
        "P098",
        "P108"
      ],
      "notes": "### Causes of a limp by age\n\nTrauma, septic arthritis, osteomyelitis, malignancy and inflammatory arthritis occur at any age. Other causes cluster by age:\n\n- **Toddlers:** occult spiral tibial fracture (toddler's fracture).\n- **Younger school-age children:** transient synovitis and Perthes disease.\n- **Adolescents, particularly with obesity:** slipped upper femoral epiphysis (SUFE).\n\n**Transient synovitis** is self-limiting inflammation of the hip synovium, often after a viral illness. **Perthes disease** is avascular necrosis of the developing femoral head. **SUFE** is displacement of the femoral head epiphysis on the femoral neck through the growth plate.\n\nHip disease can present as **referred knee pain**, so examine the hip in any limping child with a normal knee.\n\n### Assessment\n\nAsk about onset, fever, preceding illness, night pain, injury, ability to bear weight and systemic symptoms. Observe the gait if safe, and examine the spine, hips and the joints above and below the complaint, with neurovascular assessment.\n\nSevere pain on passive joint movement with refusal to bear weight is concerning even without fever.\n\n> [!escalate]\n> A febrile child who will not bear weight needs same-day assessment for septic arthritis. Joint destruction can follow within days.\n\n### Investigations and initial management\n\n- **X-ray:** targeted films for suspected fracture or structural disease. A normal early X-ray does not exclude infection or an occult fracture.\n- **Ultrasound:** shows a hip effusion but cannot reliably separate septic arthritis from transient synovitis.\n- **Suspected bone or joint infection:** FBE and CRP, blood cultures and sometimes MRI; urgent orthopaedic assessment for aspiration or drainage and IV antibiotics.\n\nSUFE needs **immediate non-weight-bearing** and orthopaedic review, because further slippage risks avascular necrosis. Do not repeatedly manipulate a painful hip.\n\nManage transient synovitis with rest from provoking activity, analgesia and early review, but only once serious alternatives have been reasonably excluded. Reassess persisting symptoms.\n\n### Juvenile idiopathic arthritis\n\n**Juvenile idiopathic arthritis** (JIA) is arthritis lasting `>6 weeks` with onset before age `16`, after other causes have been excluded. Morning stiffness and swelling may be more prominent than pain. Refer to rheumatology and arrange slit-lamp uveitis screening even when the eyes are asymptomatic, because JIA-associated uveitis is often silent until vision is damaged.\n\n### Fractures\n\nGive analgesia early. Assess skin, deformity, pulses, capillary refill, sensation and movement before and after splinting, since a splint can itself compromise circulation.\n\nA true uncomplicated distal radius buckle fracture is stable and can be managed in a removable wrist splint for about `three weeks`. Confirm that the X-ray shows a genuine buckle injury with the opposite cortex intact. Displaced, physeal, open, neurovascularly compromised or uncertain fractures need specialist care.\n\n> [!pitfall]\n> Increasing pain despite analgesia, pain on passive stretch or tense swelling suggests compartment syndrome. Normal pulses do not exclude it: tissue pressure stops capillary perfusion well before it occludes arterial flow.\n\n> [!counsel]\n> Keep the limb raised for the first two days and move the fingers or toes often. Keep the cast or splint dry and put nothing inside it. Come back at once if pain is increasing, the fingers or toes become numb, tingling, pale, blue or cold or cannot be moved, or the cast feels too tight.\n\n### Burns and wounds\n\nCool a burn under running water for `20 minutes` as soon as possible, ideally within `three hours`, while keeping the rest of the child warm. Remove constricting items before swelling develops and avoid ice, which causes further vasoconstrictive injury. Assess depth, extent, special sites (face, hands, feet, perineum, joints) and inhalation injury. Refer significant burns to a paediatric burns service.\n\nFor a wound, irrigate it, look for foreign bodies and tendon or nerve injury, check tetanus status, and choose closure and dressing according to contamination and tissue damage.\n\n- **Closure:** a clean, recent laceration can be closed primarily with adhesive strips, tissue glue or sutures. Heavily contaminated, older or bite wounds are often left open or closed later, since closure traps bacteria; bites usually need prophylactic amoxicillin–clavulanate.\n- **Tetanus:** give a tetanus-containing vaccine if the person is not fully vaccinated, or if the last dose was more than `five years` ago for a tetanus-prone wound (`ten years` for a clean minor one). Add tetanus immunoglobulin for a tetanus-prone wound in someone with fewer than three previous doses or an unknown history.\n- **Aftercare:** keep the wound clean and dry for the first day or two and watch for spreading redness, pain, discharge or fever. Sutures are commonly removed at about `3–5 days` on the face, `7 days` on the scalp and trunk, and `10–14 days` over joints.\n\nThese principles apply equally to adults.\n\n### Safeguarding\n\nConcern arises from:\n\n- Injuries inconsistent with the child's developmental ability or the history given.\n- Any unexplained bruising in a non-mobile infant; accidental mechanisms are very limited before a baby can move independently.\n- Patterned injuries.\n- Repeated presentations or delayed presentation.\n\nAsk open, neutral questions and record the caregiver's and child's words verbatim. Document objective findings and seek senior child-protection advice.\n\n> [!pitfall]\n> Do not conduct a leading interrogation, and do not promise absolute secrecy.\n\nIn Victoria, doctors are mandatory reporters when they form a reasonable belief that a child needs protection from significant harm due to physical or sexual abuse and the parents have not protected, or are unlikely to protect, the child. Other concerns also need appropriate safeguarding action. Act on reasonable grounds; do not wait for proof.\n\nImmediate danger needs urgent protection, and discharge must be safe. Where possible, explain to the family what information will be shared, provided this does not increase the risk to the child.",
      "formerly": [
        "C10"
      ]
    },
    {
      "id": "C12",
      "domain": "CAH",
      "title": "Scrotal, groin and genital problems in children",
      "focus": "Acute scrotum and torsion, hernia, hydrocele, undescended testis, foreskin problems and prepubertal vulvovaginitis.",
      "first_pass": false,
      "priority": "Selective",
      "saq_cases": [
        {
          "id": "deck-paeds-testicular-torsion",
          "title": "Testicular torsion",
          "set": "MD3 SAQ Revision Deck"
        }
      ],
      "core_ids": [
        "P053",
        "P054"
      ],
      "notes": "Adapt the examination to the child's development, obtain assent as well as consent, explain the findings to caregivers, and give a specific plan for review.\n\n### Acute scrotum\n\n> [!escalate]\n> Sudden unilateral testicular pain, a high-riding or horizontal testis, vomiting or an absent cremasteric reflex suggests **testicular torsion**. Arrange emergency surgical assessment; do not let ultrasound delay surgery when suspicion is high, because testicular viability falls within hours.\n\nOther causes of an acute scrotum include torsion of a testicular appendage, epididymitis and an incarcerated inguinal hernia.\n\n> [!escalate]\n> A painful irreducible groin lump with vomiting is an emergency.\n\n### Hydrocele and undescended testis\n\nA hydrocele is usually painless and transilluminates. Refer for surgical review if it persists beyond infancy or the diagnosis is uncertain.\n\nSpontaneous descent is unlikely after the first few months, so **refer a persistently undescended testis by about `six months`**. Orchidopexy is planned during infancy, commonly from about `nine months`, to protect fertility and allow the testis to be examined. Distinguish a retractile testis, which can be brought into the scrotum.\n\n### Foreskin problems\n\nThe foreskin is normally non-retractable in young children and should not be forcibly retracted, which can tear it and cause scarring.\n\n**Balanitis** usually responds to gentle hygiene and treatment of the cause.\n\n> [!escalate]\n> **Paraphimosis**, a retracted foreskin trapped behind the glans, needs same-day reduction, because the constricting ring obstructs venous return from the glans.\n\n### Prepubertal vulvovaginitis\n\nPrepubertal vulvovaginitis usually relates to irritation, moisture or hygiene, since the thin, unoestrogenised tissue is easily irritated. Ask about soaps, tight clothing, urinary and bowel symptoms, and nocturnal itch, which suggests threadworm.\n\nExamine externally and gently, with assent, consent and a chaperone; routine internal vaginal examination is inappropriate. Refer for specialist assessment if there is persistent foul discharge, bleeding, a suspected foreign body, a specific infection or a safeguarding concern.\n\n> [!pitfall]\n> Thrush is not the usual cause of vulvovaginitis in a prepubertal child.",
      "formerly": [
        "C12"
      ]
    },
    {
      "id": "C13",
      "domain": "CAH",
      "title": "Adolescent health: confidentiality, mood and eating",
      "focus": "Eating disorders, self-harm risk, consent, adolescent confidentiality and support.",
      "first_pass": true,
      "priority": "Core",
      "saq_cases": [
        {
          "id": "deck-paeds-anorexia-nervosa",
          "title": "Eating disorders in adolescence",
          "set": "MD3 SAQ Revision Deck"
        },
        {
          "id": "deck-gp-youth-depression",
          "title": "Adolescent depression and confidentiality",
          "set": "MD3 SAQ Revision Deck"
        }
      ],
      "core_ids": [
        "P011",
        "P014",
        "P027",
        "P069",
        "P086"
      ],
      "notes": "### Setting up the consultation\n\nAddress the young person directly, ask about their own concerns, and arrange to see them alone for part of the visit; sensitive disclosures are unlikely with a parent present.\n\nExplain confidentiality honestly. Information is normally private, but a serious risk to safety or a legal reporting duty may require sharing relevant information. Avoid promising absolute confidentiality, and avoid implying that every disclosure of distress triggers a report. Where possible, discuss who would be told and why.\n\nCapacity to consent depends on understanding the particular decision, its consequences and the alternatives, not on age alone. A sufficiently mature adolescent (a \"mature minor\") may consent to some care. Assess and document understanding, voluntariness and any coercion. Encourage the involvement of a supportive adult where safe, while respecting legitimate privacy.\n\nConfidentiality can be undone by practical details, so consider billing, patient portals, text messages and appointment reminders.\n\n### HEEADSSS assessment\n\nHEEADSSS is a structured psychosocial history:\n\n- **Home:** living situation and safety.\n- **Education and employment:** participation and attendance.\n- **Eating and exercise.**\n- **Activities:** friendships and online life.\n- **Drugs:** alcohol, smoking and vaping, and other drugs.\n- **Sexuality:** relationships, consent and contraception.\n- **Suicide and depression:** mood and self-harm.\n- **Safety:** risks, strengths and supports.\n\nStart with the less threatening areas to build rapport before more personal questions, and use the young person's own language. Ask about bullying, discrimination, family violence and identity-related distress, without assuming these explain everything.\n\n### Depression and self-harm\n\nAdolescent depression may present as irritability, withdrawal, school refusal, loss of interest, changes in sleep and appetite, and declining function. Ask directly about suicidal thoughts, intent, preparations, access to means, previous attempts and the person's current ability to stay safe.\n\n> [!pitfall]\n> Denial of current intent does not cancel the significance of a suicide note, a recent attempt or severe deterioration.\n\nThe response is a collaborative safety plan, involvement of a safe support person, reduced access to means and timely follow-up; see M01 (Formulating suicide and self-harm risk). A promise not to self-harm is not a safety intervention.\n\n> [!escalate]\n> Active intent, serious recent self-harm, psychosis, intoxication or inability to establish safety needs emergency specialist or emergency department assessment.\n\nTreatment combines psychological therapy, family and school support, restoration of sleep and activity, and action on bullying or adversity. Among antidepressants, **fluoxetine** has the strongest evidence in adolescent depression and may be used within a careful clinical plan. Warn about early activation, agitation or increased suicidal thinking, arrange close early review, and screen for bipolar symptoms first. Medication does not replace safety assessment or psychosocial care.\n\n### Eating and body image\n\nA concrete account of what the young person ate and drank yesterday is more revealing than general questions. Follow it with food rules, body checking, bingeing, vomiting or laxative use, exercise, and the weight trajectory.\n\n> [!pitfall]\n> **Serious malnutrition can occur at a normal or high BMI.**\n\nWhen an eating disorder is suspected, check the indicators of medical risk: lying and standing pulse and BP, temperature, hydration, glucose, an ECG, and electrolytes including phosphate and magnesium. Bradycardia, postural instability and electrolyte disturbance indicate medical instability.\n\n> [!escalate]\n> Rapid weight loss, bradycardia, syncope, electrolyte disturbance or refusal of food or fluid needs urgent medical assessment. M05 (Setting of care) gives the admission criteria.\n\nExplain that nutritional rehabilitation improves thinking, emotions and physical health, and that the family is a source of support, not the cause of the illness. Coordinate paediatric or adolescent, mental health and dietetic care, with a named clinician responsible for physical monitoring.\n\nNot all restrictive eating is driven by weight concerns: sensory aversion (ARFID) and neurodevelopmental differences are important alternatives.\n\n### Follow-through\n\nAgree a small number of priorities with the young person, provide confidential sexual health and contraception care when appropriate, and book the next visit. Young people often disengage between appointments, so help arrange contact with youth services or school supports and confirm that referrals have been received. Document the safety plan, confidentiality decisions, and who is following up results and referrals.",
      "formerly": [
        "C11"
      ]
    },
    {
      "id": "O01",
      "domain": "OGN",
      "title": "Preconception and routine antenatal care",
      "focus": "Antenatal visit structure, screening, risk counselling, supplements and prevention.",
      "first_pass": true,
      "priority": "Core",
      "saq_cases": [
        {
          "id": "deck-og-prenatal-counselling",
          "title": "Preconception counselling",
          "set": "MD3 SAQ Revision Deck"
        },
        {
          "id": "deck-og-antenatal-screening",
          "title": "First antenatal visit and screening",
          "set": "MD3 SAQ Revision Deck"
        }
      ],
      "core_ids": [
        "P017",
        "P041",
        "P077"
      ],
      "notes": "### Preconception care\n\nOrgans form in the first weeks after conception, often before the pregnancy is recognised, so the best opportunity to reduce many risks comes before conception.\n\nA preconception review covers pregnancy intentions, previous pregnancies and complications, medical and mental health, medicines, family and genetic history, infections and vaccination, smoking and alcohol, and social safety. Review potentially harmful medicines with the relevant specialist; abruptly stopping antiseizure or psychiatric treatment can also cause harm. Optimise diabetes, epilepsy, thyroid disease and hypertension before conception where possible.\n\nSupplements and preventive advice:\n\n- **Folic acid:** `400–500 micrograms daily` from at least `one month` before conception until the end of the first trimester. Use `5 mg` daily in higher-risk situations, such as a previous neural tube defect pregnancy, pre-existing diabetes or relevant antiseizure therapy.\n- **Iodine:** `150 micrograms daily` when planning pregnancy, during pregnancy and while breastfeeding, with individual advice in thyroid disease.\n- **Lifestyle:** nutrition, activity, a healthy weight, food safety, smoking cessation and no alcohol. Avoid high-dose vitamin A supplements, which are teratogenic.\n- **Immunity:** check rubella and varicella immunity and give indicated live vaccines before pregnancy, avoiding conception for `28 days` afterwards.\n\n### First antenatal visit\n\nConfirm the pregnancy and estimate gestation from the last menstrual period and cycle history, with a dating ultrasound. Accurate dating underpins screening and later decisions about timing.\n\nThe obstetric history records gravidity and parity, and previous caesarean birth, postpartum haemorrhage, preterm birth or ectopic pregnancy. Record medical and surgical history, allergies and medicines. Ask privately, with an interpreter if needed, about coercion and violence, housing, support and mental health, and discuss the preferred model of maternity care.\n\nMeasure BP and weight or BMI, and examine as indicated. An early BP provides the baseline against which later hypertension is judged.\n\nInitial tests are:\n\n- FBE, blood group and RhD status, and red-cell antibodies.\n- Rubella immunity.\n- Hepatitis B, hepatitis C, HIV and syphilis serology.\n- Urine culture; asymptomatic bacteriuria is treated in pregnancy because of the risk of pyelonephritis; see O05 (Urinary tract infection in pregnancy).\n- Varicella immunity, STI tests and others according to history.\n\nOffer reproductive carrier screening (cystic fibrosis, spinal muscular atrophy and fragile X), explaining residual risk and the implications for the reproductive partner.\n\n### Screening versus diagnosis\n\n**A screening test estimates chance; it does not diagnose a fetal condition.**\n\nCell-free DNA testing can be offered from about `10 weeks`; combined first-trimester screening uses ultrasound and serum markers. Explain that false positives and inconclusive results can occur, that there may be a cost, and that the patient may decline.\n\nA high-chance result needs counselling and a diagnostic test before any irreversible decision: chorionic villus sampling or amniocentesis, depending on gestation. Discuss the procedure-related risk and what the test can and cannot detect.\n\n### Routine tests later in pregnancy\n\n- **Morphology ultrasound:** `18–22 weeks`, after a first-trimester scan.\n- **Gestational diabetes:** OGTT at `24–28 weeks`, when insulin resistance has risen enough to reveal it, with earlier testing for higher-risk patients; see O05 (Testing and current Australian thresholds).\n- **Syphilis:** at the first visit, at `26–28 weeks`, and at `36 weeks` or birth, whichever comes first; more often with ongoing risk or symptoms.\n- **Other tests:** FBE at `28 weeks`, repeated at `36 weeks` if low; a red-cell antibody screen at `28 weeks` in RhD-negative patients; and GBS screening at `35–37 weeks` where the service screens all patients (O06 (Group B streptococcus)).\n\n### Ongoing antenatal care\n\nEach visit reviews wellbeing, symptoms, BP, fetal growth and movements, mental health and any new risks. From mid-pregnancy, symphysis–fundal height tracks growth; an unexpected measurement needs review and ultrasound, since a tape measure alone does not diagnose a growth problem. Later in pregnancy, abdominal examination assesses lie, presentation and engagement; confirm a suspected malpresentation with ultrasound.\n\n### Vaccination in pregnancy\n\nMaternal antibody crosses the placenta and protects the infant in the first months of life.\n\n- **Influenza:** at any stage.\n- **dTpa (pertussis):** ideally at `20–32 weeks`, in every pregnancy.\n- **RSV (Abrysvo):** from `28 weeks`, preferably `28–36 weeks`, in each pregnancy.\n- **COVID-19:** follow current Handbook advice, which depends on age, risk and pregnancy.\n\nLive vaccines such as MMR and varicella are not given in pregnancy because of the theoretical risk to the fetus.\n\n### Anti-D prophylaxis\n\nIn an unsensitised RhD-negative patient, anti-D prevents the formation of antibodies against fetal red cells, which would otherwise threaten this and future RhD-positive pregnancies. Routine prophylaxis is commonly given at `28 and 34 weeks` and after the birth of an RhD-positive baby, `625 IU` each time, with the antibody screen repeated at 28 weeks before the first dose. A sensitising event, such as bleeding, abdominal trauma, external cephalic version or amniocentesis, needs anti-D as soon as practical and ideally within `72 hours`: `250 IU` in the first 12 weeks and `625 IU` after. After 20 weeks, the size of the fetomaternal haemorrhage is measured in case more is needed.\n\n> [!pitfall]\n> Anti-D does not treat established sensitisation.\n\n### Safety-netting and planning for birth\n\n> [!counsel]\n> Contact maternity services for bleeding, severe pain, loss of fluid, severe headache or visual change, fever, or reduced fetal movements.\n\nMake sure the patient has the service's contact number, the next appointment and a named owner for every screening result.\n\nNear term, discuss birth plans, feeding, newborn care and postpartum support, explaining that a birth plan states preferences rather than guaranteeing how labour will go.",
      "formerly": [
        "O01"
      ]
    },
    {
      "id": "O02",
      "domain": "OGN",
      "title": "Fetal wellbeing and reduced movements",
      "focus": "Growth restriction, abnormal fetal surveillance and reduced fetal movement assessment/escalation.",
      "first_pass": true,
      "priority": "Core",
      "saq_cases": [
        {
          "id": "deck-og-sga-fgr",
          "title": "Small for gestational age and fetal growth restriction",
          "set": "MD3 SAQ Revision Deck"
        }
      ],
      "core_ids": [
        "P003"
      ],
      "notes": "### Reduced fetal movements\n\nReduced fetal movement can be an early sign of fetal compromise, so the patient's own report of change is the trigger for assessment. Ask about gestation, the usual pattern of movements, when it changed, the last clearly felt movement, previous episodes, pain, bleeding, fluid loss and maternal illness.\n\nMovements may feel different near term, but they should not become progressively less frequent because \"there is less room\". A fixed kick count is not a substitute for the patient's concern.\n\n> [!escalate]\n> Reduced or absent movements in the third trimester need same-day maternity assessment. Absent movements, or reduced movements with bleeding or pain, are an emergency.\n\n> [!pitfall]\n> Do not advise waiting until the next day, relying on a home Doppler (which may pick up the maternal pulse and falsely reassure), or delaying for a cold drink.\n\nAt earlier gestations, assessment depends on the gestation and on whether movements had been established.\n\n### Assessment\n\nMaternal observations, BP, abdominal tenderness and pre-eclampsia symptoms point to maternal or placental causes. Uterine size, growth and the fetal heart assess the fetus. Risk factors for placental dysfunction lower the threshold for further testing.\n\n- **CTG:** commonly used from about `28 weeks`, once it is interpretable.\n- **Ultrasound:** growth, amniotic fluid and Doppler studies when indicated, especially with persistent or recurrent symptoms or risk factors.\n\n> [!pitfall]\n> Hearing a fetal heartbeat confirms current cardiac activity, not wellbeing.\n\nInterpret the results together. A reassuring CTG may allow discharge after appropriate assessment, but recurrent reduced movements need reassessment and an explicit plan. Persistent concern, abnormal testing or maternal illness needs obstetric review and consideration of delivery according to gestation and risk.\n\n### Small for gestational age and fetal growth restriction\n\nA fetus is **small for gestational age** (SGA) when the estimated fetal weight or abdominal circumference is below the `10th centile`. **Fetal growth restriction** (FGR) is failure to reach growth potential, and it can occur above that centile when growth slows. Size and growth are different: some fetuses are constitutionally small and healthy.\n\nCauses include placental insufficiency, maternal vascular disease and smoking, fetal anomalies and infection.\n\nUltrasound assesses size, interval growth, liquor volume and Doppler studies:\n\n- **Umbilical artery:** increased resistance suggests placental dysfunction; absent or reversed end-diastolic flow is particularly concerning.\n- **Middle cerebral artery:** reduced resistance reflects redistribution of blood flow to the brain (\"brain sparing\").\n\nA single estimated fetal weight is imprecise, so serial trends and clinical context matter. If pre-eclampsia is suspected, check maternal BP, urine protein and blood tests; the two conditions share a placental origin.\n\n### Management of FGR\n\nSurveillance balances the risks of continuing a compromised pregnancy against the risks of prematurity. It may include serial ultrasound and Doppler, CTG, specialist review and a defined threshold for delivery.\n\nIf early delivery is planned, give corticosteroids for fetal lung maturation and magnesium sulfate for neuroprotection at the appropriate gestations. The route of birth depends on fetal reserve, presentation and the obstetric situation; FGR does not automatically mean caesarean birth.\n\nAddress modifiable factors such as smoking, and practical barriers to attending surveillance. Give clear advice to return if movements reduce again, even after a reassuring visit.\n\n### Suspected fetal death\n\nConfirm with ultrasound and senior review. Communicate privately and compassionately, offer support, explain the options for investigation, and arrange follow-up. Avoid premature statements about cause or blame.",
      "formerly": [
        "O02"
      ]
    },
    {
      "id": "O03",
      "domain": "OGN",
      "title": "Early pregnancy pain and bleeding",
      "focus": "Ectopic pregnancy/miscarriage differential, tests, ultrasound and safe escalation.",
      "first_pass": true,
      "priority": "Core",
      "saq_cases": [
        {
          "id": "deck-og-miscarriage",
          "title": "Early pregnancy loss",
          "set": "MD3 SAQ Revision Deck"
        },
        {
          "id": "2021-ummss-q11",
          "title": "Acute pelvic pain in a young woman",
          "set": "2021 UMMSS"
        }
      ],
      "core_ids": [
        "P002",
        "P008",
        "P041",
        "P103"
      ],
      "notes": "### Initial assessment\n\nAssess haemodynamic status first: observations, perfusion, pain, bleeding volume, syncope, and shoulder-tip pain, which suggests diaphragmatic irritation from intraperitoneal blood.\n\nDo a pregnancy test in anyone of reproductive potential with pelvic or abdominal pain, even if they report using contraception. Methods fail, and a pregnancy that occurs with an IUD or after sterilisation is more likely to be ectopic.\n\nThe differential is:\n\n- Ectopic pregnancy.\n- Viable intrauterine pregnancy with bleeding (threatened miscarriage).\n- Miscarriage.\n- Molar pregnancy, an abnormal proliferation of trophoblast with swollen chorionic villi.\n- Non-obstetric causes.\n\n> [!pitfall]\n> **An ectopic pregnancy can rupture with a low or falling hCG**, and without a known risk factor.\n\n> [!escalate]\n> Hypotension, peritonism, severe pain or heavy bleeding is an emergency. Resuscitate, insert large-bore IV access, send FBE and group and crossmatch, and call gynaecology urgently.\n\nIn a stable patient, quantitative hCG and transvaginal ultrasound establish the location and viability of the pregnancy. With consent, a speculum examination can identify the source of bleeding and cervical findings.\n\n### Pregnancy of unknown location\n\nA positive pregnancy test with no intrauterine or ectopic pregnancy seen on ultrasound is a **pregnancy of unknown location**. It is not proof of either miscarriage or ectopic pregnancy.\n\nRepeat hCG, commonly after about `48 hours`. A rise of more than about `63%` suggests a viable intrauterine pregnancy, to be confirmed on a later scan; a fall of more than about `50%` suggests a failing pregnancy; and a plateau or smaller rise raises concern for ectopic pregnancy and needs repeat ultrasound and specialist review. A healthy pregnancy does not always double its hCG in 48 hours, and **hCG trends alone cannot establish the location** or safely exclude an ectopic pregnancy.\n\nOn a technically adequate transvaginal scan, either finding supports pregnancy loss, confirmed by an experienced sonographer:\n\n- Crown–rump length `≥7 mm` without cardiac activity.\n- Mean sac diameter `≥25 mm` without an embryo.\n\nThese thresholds are deliberately conservative so that a viable pregnancy is not misdiagnosed. When an earlier scan is equivocal, repeat it after the appropriate interval, commonly `7–14 days`, before making the diagnosis.\n\nUntil the location or outcome is known, the patient carries an unquantified ectopic risk.\n\n> [!counsel]\n> Explain why follow-up matters, and return immediately for worsening pain, shoulder-tip pain, dizziness, collapse or heavy bleeding. Surveillance continues until the outcome is clear.\n\n### Management of early pregnancy loss\n\nFor a stable patient with confirmed early pregnancy loss, the options differ mainly in speed, predictability and procedural risk:\n\n- **Expectant management.**\n- **Medical management:** mifepristone followed by misoprostol.\n- **Surgical evacuation:** prompt completion, but with anaesthetic and procedural risks.\n\nExplain the likely bleeding and cramping, the time to completion, analgesia, the possibility of incomplete evacuation, and how completion will be confirmed. Infection, haemodynamic instability or heavy ongoing bleeding changes the choice.\n\nAcknowledge the loss, and explain that ordinary activity did not cause it. Offer support, follow-up and, if wanted, discussion of future pregnancy and contraception.\n\n### Unintended pregnancy\n\nDiscuss the options of continuing the pregnancy, parenting or adoption, and termination in a non-directive way, with timely referral. In Victoria, abortion is available on request up to `24 weeks`; after that, a second doctor must agree that it is appropriate in all the circumstances. A practitioner with a conscientious objection must still refer the patient to one without, and 1800 My Options lists local services.\n\nGestation, ectopic risk, preference and clinical eligibility determine whether medical or surgical termination is suitable. Medical termination with mifepristone and misoprostol is used in the community up to `63 days` of gestation. Before either, confirm gestation and intrauterine location, check blood group, offer STI testing and plan contraception.\n\n### Ectopic pregnancy\n\nA stable ectopic pregnancy may be managed with methotrexate, surgery or, in selected cases, observation under specialist criteria.\n\nBefore methotrexate, exclude a viable intrauterine pregnancy, check renal and liver function and the blood count, and confirm that the patient can attend serial hCG follow-up. Rupture remains possible during follow-up, so explain that risk together with the medication and pregnancy-avoidance instructions. An unstable or ruptured ectopic pregnancy needs surgery.\n\n### Anti-D in early pregnancy\n\n> [!current]\n> RANZCOG's March 2025 guideline no longer recommends routine RhD testing or prophylaxis for threatened miscarriage or miscarriage before `10 weeks`. Surgically managed ectopic pregnancy remains an indication for anti-D in an unsensitised RhD-negative patient. The 2024 national Rh D immunoglobulin guideline is broader, recommending `250 IU` after miscarriage, ectopic or molar pregnancy within the first `12 weeks`. Both therefore support `250 IU` for an unsensitised RhD-negative patient after a surgically managed ectopic pregnancy, and after miscarriage or bleeding from `10 weeks`; they differ only before 10 weeks, where services choose between them.\n\n### Hyperemesis gravidarum\n\nNausea and vomiting are common in pregnancy. Inability to maintain intake, dehydration, electrolyte disturbance or functional impairment suggests **hyperemesis gravidarum**. Assess weight, hydration, renal function and electrolytes, and consider alternative causes. Ultrasound may show a multiple or molar pregnancy, both of which raise hCG.\n\n- Give antiemetics, fluids and nutritional support according to severity.\n- **Give thiamine before dextrose** after prolonged poor intake, to reduce the risk of Wernicke encephalopathy; acute hypoglycaemia still needs prompt treatment.\n- Consider thromboprophylaxis on admission.\n- Judge response clinically; ketonuria is not the sole marker of severity.\n\nReference: [RANZCOG miscarriage and ectopic pregnancy guideline](https://ranzcog.edu.au/wp-content/uploads/Miscarriage-Ectopic-Pregnancy.pdf).",
      "formerly": [
        "O03"
      ]
    },
    {
      "id": "O04",
      "domain": "OGN",
      "title": "Hypertension and pre-eclampsia",
      "focus": "Recognition, maternal/fetal assessment, tests, treatment principles and timing of delivery.",
      "first_pass": true,
      "priority": "Core",
      "saq_cases": [
        {
          "id": "deck-og-preeclampsia",
          "title": "Hypertension in pregnancy and pre-eclampsia",
          "set": "MD3 SAQ Revision Deck"
        }
      ],
      "core_ids": [
        "P003",
        "P049",
        "P052",
        "P085",
        "P093"
      ],
      "notes": "### Definitions\n\n**Hypertension in pregnancy** is BP `≥140 mmHg systolic` and/or `≥90 mmHg diastolic` on appropriate repeat measurement. Its timing indicates the likely type:\n\n- **Before `20 weeks`:** usually chronic (pre-existing) hypertension.\n- **New after `20 weeks`:** gestational hypertension or pre-eclampsia.\n\n**Pre-eclampsia** is a placental disorder with systemic endothelial effects. It is new hypertension after 20 weeks with maternal organ dysfunction and/or uteroplacental dysfunction. Proteinuria is common but **not required** when other features are present.\n\n**Severe hypertension** is BP `≥160 systolic` or `≥110 diastolic`. It needs urgent confirmation and treatment because of the risk of maternal stroke.\n\nDisease can first appear, or worsen, after birth.\n\n### Symptoms\n\nHeadache, visual disturbance, epigastric or right upper-quadrant pain, nausea and vomiting, breathlessness and reduced fetal movements suggest maternal end-organ or placental involvement.\n\n> [!pitfall]\n> Oedema is neither specific nor sufficient for the diagnosis.\n\n### Assessment\n\nMeasure BP with the correct cuff size and position. Examination looks for the organ involvement that defines severity: respiratory status (pulmonary oedema), neurological symptoms and reflexes, abdominal tenderness (hepatic involvement), urine output and fetal growth.\n\nInvestigations:\n\n- FBE and platelets.\n- Creatinine and electrolytes.\n- Liver function tests.\n- Urine protein:creatinine ratio; `≥30 mg/mmol` indicates significant proteinuria.\n- Haemolysis screen (LDH, blood film) if HELLP syndrome is suspected.\n\nThrombocytopenia, renal or liver injury, pulmonary oedema or neurological features indicate significant disease even when proteinuria is modest.\n\nAssess the fetus with CTG, ultrasound for growth, amniotic fluid and Doppler studies as appropriate.\n\n**HELLP syndrome** is haemolysis, elevated liver enzymes and low platelets. A seizure in this setting suggests **eclampsia**, although other neurological causes remain possible.\n\n### Management\n\nSuspected pre-eclampsia needs maternity assessment and a documented plan for maternal and fetal surveillance.\n\n> [!escalate]\n> Severe BP, neurological symptoms, pulmonary oedema, deteriorating organ function or fetal compromise needs emergency senior care.\n\n- **Antihypertensives:** labetalol, nifedipine or methyldopa, according to severity and setting. Acute severe hypertension may need IV labetalol or hydralazine, or oral immediate-release nifedipine, with close monitoring. Avoid ACE inhibitors and ARBs, which are fetotoxic.\n- **Magnesium sulfate:** treats eclamptic seizures and prevents them in severe disease. It is renally excreted, so renal impairment increases toxicity. Monitor respiratory rate, tendon reflexes and urine output; calcium gluconate is the antidote.\n- **Fluids:** give cautiously, because capillary leak increases the risk of pulmonary oedema. Monitor intake and output, renal function and clinical state.\n\n### Timing of birth\n\nBirth removes the placental driver of the disease, but its timing balances maternal and fetal danger against prematurity. Stabilise before delivery where possible. Pre-eclampsia does not by itself require caesarean birth. When preterm birth is anticipated, give antenatal corticosteroids, without delaying necessary delivery in an emergency.\n\n### Prevention\n\nIdentify high-risk patients early: previous pre-eclampsia, chronic hypertension, renal disease, diabetes or autoimmune disease.\n\n- **Aspirin:** low-dose aspirin, commonly `100–150 mg at night`, started ideally before `16 weeks`, while placentation is still developing.\n- **Calcium:** supplement where dietary intake is low.\n\n> [!counsel]\n> Know the warning symptoms (severe headache, visual change, upper abdominal pain, breathlessness, reduced fetal movements) and how to contact the maternity service.\n\n### Postpartum follow-up\n\nContinue BP and symptom monitoring after birth, since recovery is not immediate. Review the need for antihypertensives and the renal and urine protein findings. A postpartum medical review addresses the increased risk of future cardiovascular disease and of recurrence in a later pregnancy, with ongoing BP and metabolic prevention in general practice.",
      "formerly": [
        "O04"
      ]
    },
    {
      "id": "O05",
      "domain": "OGN",
      "title": "Gestational diabetes and medical pregnancy",
      "focus": "Gestational diabetes, newborn glucose screening after maternal diabetes, other medical conditions in pregnancy, cholestasis of pregnancy and urinary tract infection in pregnancy.",
      "first_pass": false,
      "priority": "Core",
      "saq_cases": [
        {
          "id": "deck-og-gestational-diabetes",
          "title": "Gestational diabetes",
          "set": "MD3 SAQ Revision Deck"
        }
      ],
      "core_ids": [
        "P016",
        "P023"
      ],
      "notes": "### Mechanism\n\nPlacental hormones increase insulin resistance as pregnancy advances. Gestational diabetes (GDM) develops when maternal insulin secretion cannot compensate. Glucose crosses the placenta but insulin does not, so the fetus responds with its own hyperinsulinaemia, which drives excess growth.\n\nThe consequences are:\n\n- Macrosomia and shoulder dystocia.\n- Polyhydramnios.\n- Hypertensive disease.\n- Neonatal hypoglycaemia, because fetal hyperinsulinaemia persists briefly after the maternal glucose supply ends at birth.\n\nPre-existing diabetes also raises the risk of congenital anomalies when glucose is high during organ formation, so it needs specialist preconception care.\n\n### Testing and current Australian thresholds\n\n- **All patients:** a 75 g two-hour OGTT at `24–28 weeks`, unless diabetes has already been diagnosed.\n- **Higher-risk patients, including previous GDM:** first-trimester HbA1c to detect early hyperglycaemia. HbA1c `≥6.5%` indicates overt diabetes; `6.0–6.4%` is managed as GDM, with referral for diabetes education.\n- **Higher-risk patients without a first-trimester HbA1c:** an early OGTT before `20 weeks`, ideally at `10–14 weeks`, using the same diagnostic thresholds.\n\nFasting glucose alone is not used in the first trimester.\n\n> [!pitfall]\n> Insulin resistance keeps rising later in pregnancy, so a normal early test does not remove the need for the 24–28-week OGTT.\n\n> [!current]\n> Under ADIPS 2025, GDM is diagnosed when **one or more** OGTT values meets these thresholds:\n>\n> - Fasting plasma glucose `5.3–6.9 mmol/L`.\n> - One-hour plasma glucose `≥10.6 mmol/L`.\n> - Two-hour plasma glucose `9.0–11.0 mmol/L`.\n>\n> Fasting `≥7.0`, two-hour `≥11.1` or HbA1c `≥6.5%` indicates overt diabetes in pregnancy. Victoria adopted these criteria in August 2025, replacing the older 5.1/10.0/8.5 cut-offs.\n\nHbA1c cannot replace the OGTT later in pregnancy, because pregnancy alters red-cell turnover and HbA1c misses post-load hyperglycaemia.\n\n### The OGTT\n\n1. Eat normally in the days before, then fast overnight as the laboratory instructs.\n2. Have the fasting sample taken, then drink the glucose solution.\n3. Stay seated, without food or smoking, for the timed samples; water is usually allowed.\n\nVomiting may invalidate the test. If the OGTT cannot be tolerated, arrange an alternative clinical plan; do not treat an incomplete test as negative.\n\n### Management\n\nStart with diabetes and maternity education and a dietitian. Regular meals, sensible carbohydrate distribution and safe activity form the basis of treatment; it is not a starvation diet.\n\nTeach fasting and post-meal glucose monitoring, with written targets and timing. Common service targets are fasting `<5.3` and two-hour post-meal `<6.7 mmol/L`, although services vary. These are **treatment targets, not diagnostic thresholds**.\n\nIf targets are not met with lifestyle measures, insulin is well established. Metformin may be offered after discussing its benefits, placental transfer and local practice. Teach injection technique and hypoglycaemia prevention, and how to contact the team about repeated out-of-range results.\n\nFetal growth surveillance and planning for birth depend on glucose control, medication use and fetal and maternal findings, not simply on the diagnosis.\n\n### After birth\n\nInsulin resistance falls rapidly once the placenta is delivered. GDM treatment is usually stopped after birth with glucose review; pre-existing diabetes needs an adjusted ongoing regimen.\n\n- **Baby:** early feeding and glucose monitoring (below).\n- **Mother:** a 75 g OGTT at about `6–12 weeks` postpartum.\n- **Long term:** diabetes screening every `1–3 years`, because GDM indicates a substantially raised lifetime risk of type 2 diabetes.\n\nDiscuss testing in a future pregnancy, breastfeeding, contraception and sustainable prevention at the same time.\n\n### The baby of a mother with diabetes\n\nAny maternal diabetes, pre-existing or gestational and whether or not insulin was needed, puts the baby at risk of hypoglycaemia in the first day or two while fetal hyperinsulinaemia persists; macrosomia or growth restriction adds to the risk. Many hypoglycaemic babies have no symptoms, so the risk is managed by screening rather than by waiting for signs.\n\nKeep mother and baby together, with skin-to-skin contact, a first feed within the first hour and feeds at least every `three hours`. Under the Safer Care Victoria guideline (2024), the first glucose is measured no later than `2 hours` after birth, then before feeds every `3–4 hours` until three consecutive values are `≥2.6 mmol/L` with adequate feeding.\n\n- **Well baby with a low value:** for glucose `1.5–2.5 mmol/L`, give buccal 40% glucose gel `0.5 mL/kg`, a breastfeed and a top-up of expressed milk or formula, and recheck within the hour.\n- **Urgent neonatal review:** glucose `<1.5 mmol/L`, jitteriness, lethargy, poor feeding, hypotonia, apnoea or seizures, inability to feed, or hypoglycaemia that persists despite gel and feeds. These babies need IV glucose, typically a `2 mL/kg` bolus of 10% glucose followed by an infusion.\n\nExplain to parents before birth why the heel-prick tests are done and why early, frequent feeding matters, and ask them to report a baby who is sleepy, floppy or not feeding. Jitteriness can also reflect hypocalcaemia, which is more common in these babies.\n\n### Other medical conditions in pregnancy\n\n- **Iron-deficiency anaemia:** confirm, replace and reassess; do not assume it is physiological.\n- **Epilepsy:** specialist review of medication and levels, and high-dose folic acid. Do not stop treatment abruptly.\n- **Hypothyroidism:** levothyroxine requirements often rise, as binding proteins and placental demand increase.\n- **Suspected VTE:** urgent objective testing. Pregnancy is no reason to avoid indicated imaging; the radiation dose is small compared with the danger of untreated thromboembolism. LMWH is used for pregnancy-associated VTE, with a coordinated plan for birth and neuraxial anaesthesia.\n- **DKA:** can occur at lower glucose levels in pregnancy and is an emergency.\n\n### Intrahepatic cholestasis of pregnancy\n\n*Intrahepatic cholestasis of pregnancy* (ICP) is a pregnancy-specific liver disorder in which bile acids accumulate, usually from late in the second or in the third trimester. The typical complaint is **itch without a primary rash**, often starting on the palms and soles and worst at night; excoriations may be the only skin finding. Dark urine or mild jaundice occasionally follows. ICP resolves within days of birth and often recurs in later pregnancies.\n\nItch with a rash points instead to eczema, scabies or a dermatosis of pregnancy such as polymorphic eruption. Itch alone is common in pregnancy, so testing decides.\n\nCheck non-fasting serum bile acids and liver function. Bile acids of `≥19 µmol/L` support the diagnosis, and raised transaminases are common. If the results are normal and itch persists, repeat them in `two weeks`. Exclude other liver disease with viral hepatitis serology and ultrasound for gallstones, and check BP and urine: pre-eclampsia and acute fatty liver of pregnancy can coexist and are more dangerous.\n\nMaternal effects are mostly itch and disturbed sleep. The fetal risks are spontaneous preterm birth, meconium-stained liquor and, at very high bile acid levels (`≥100 µmol/L`), stillbirth, which tends to occur near term with little warning.\n\n> [!pitfall]\n> Do not treat late-pregnancy itch with emollients and antihistamines alone without checking bile acids.\n\nRefer to the obstetric team promptly, urgently if bile acids are `≥40 µmol/L`. Ursodeoxycholic acid relieves itch but has not been shown to prevent stillbirth. Bile acids and liver function are monitored, and the timing of birth is planned from the peak bile acid level because stillbirth risk rises with it: commonly by `40 weeks` below 40 µmol/L, at `38–39 weeks` for `40–99 µmol/L`, and at `35–36 weeks` for `≥100 µmol/L` (RCOG 2022). The patient should report reduced fetal movements at once. Check liver function at about `six weeks` postpartum; persisting abnormality suggests underlying liver disease.\n\n### Urinary tract infection in pregnancy\n\nIn pregnancy, progesterone relaxes ureteric smooth muscle and the enlarging uterus compresses the ureters, so bacteria ascend from the bladder more readily. Untreated asymptomatic bacteriuria progresses to pyelonephritis in a substantial minority, and pyelonephritis is associated with sepsis and preterm birth. This is why urine is cultured at the first antenatal visit, and why **asymptomatic bacteriuria is treated in pregnancy** although not otherwise; see O01 (First antenatal visit) and G17 (Interpreting urine tests).\n\nSend a culture for bacteriuria and for symptomatic cystitis, and choose the antibiotic by susceptibility:\n\n- **Cefalexin:** `500 mg` twice daily for `5 days`, a common choice in any trimester.\n- **Nitrofurantoin:** `100 mg` every six hours for `5 days`; avoid near term, when it can cause haemolysis in the newborn.\n- **Trimethoprim:** avoid in the first trimester, because it is a folate antagonist.\n\nFluoroquinolones and tetracyclines are avoided. Repeat the culture `one to two weeks` after treatment as a test of cure, and periodically for the rest of the pregnancy after a recurrence.\n\n> [!escalate]\n> Fever, rigors, loin pain or vomiting in pregnancy suggests pyelonephritis and needs same-day hospital assessment for IV antibiotics and fetal monitoring.\n\nReference: [Safer Care Victoria: ADIPS implementation](https://www.safercare.vic.gov.au/news/new-gestational-diabetes-guideline-from-the-australian-diabetes-in-pregnancy-society-adips).",
      "formerly": [
        "O05"
      ]
    },
    {
      "id": "O06",
      "domain": "OGN",
      "title": "Antepartum bleeding, membrane rupture and infection",
      "focus": "Placental causes, PPROM, chorioamnionitis, sepsis in pregnancy and after birth, GBS and obstetric escalation.",
      "first_pass": true,
      "priority": "Core",
      "saq_cases": [
        {
          "id": "deck-og-aph-placenta-praevia",
          "title": "Antepartum haemorrhage and placenta praevia",
          "set": "MD3 SAQ Revision Deck"
        },
        {
          "id": "deck-og-pprom-gbs",
          "title": "Prelabour rupture of membranes and group B streptococcus",
          "set": "MD3 SAQ Revision Deck"
        },
        {
          "id": "deck-og-chorioamnionitis",
          "title": "Fever in late pregnancy and chorioamnionitis",
          "set": "MD3 SAQ Revision Deck"
        }
      ],
      "core_ids": [
        "P003",
        "P004",
        "P042"
      ],
      "notes": "### Antepartum haemorrhage\n\n**Antepartum haemorrhage** is bleeding from the genital tract after `20 weeks` and before birth. Two patients are at risk. Assess maternal airway, breathing and circulation, observations and perfusion, gestation, the amount of bleeding, pain and contractions, uterine tenderness, fetal movements and the known placental position.\n\n> [!pitfall]\n> Visible loss may underestimate the haemorrhage, especially in abruption, when blood can be concealed behind the placenta.\n\nObtain IV access, FBE, group and crossmatch, and coagulation studies with fibrinogen according to severity, with early obstetric involvement and fetal assessment.\n\n### Causes\n\n- **Placenta praevia:** the placenta covers the internal cervical os; a placental edge within `20 mm` of the os without covering it is called low-lying. Bleeding is typically painless. Ultrasound, including transvaginal imaging, defines the placental position.\n- **Placental abruption:** separation of the placenta causes pain, uterine tenderness or a hard uterus, and fetal compromise, sometimes with little visible bleeding. A normal ultrasound does not exclude it, and severe abruption can cause coagulopathy.\n- **Vasa praevia:** unprotected fetal vessels cross near the cervix. Bleeding after membrane rupture with fetal compromise may be fetal blood, and the fetal blood volume is small, so it needs immediate assessment for delivery.\n- **Uterine rupture:** consider it with previous uterine surgery, sudden pain, an abnormal fetal heart rate and maternal deterioration.\n\n> [!pitfall]\n> Do not perform a digital vaginal examination until placenta praevia has been excluded; it can provoke major haemorrhage.\n\n> [!escalate]\n> Suspected abruption, vasa praevia or uterine rupture, or any heavy bleeding, is an obstetric emergency.\n\nAssess an unsensitised RhD-negative patient for anti-D. Stabilisation, admission, surveillance and timing of birth depend on the cause, recurrence, gestation and maternal and fetal condition. Both praevia and abruption can recur, so observation continues even when bleeding stops; explain why.\n\n### Suspected rupture of membranes\n\nAsk about a gush or ongoing leakage, the colour and odour of the fluid, contractions, bleeding, fever and fetal movements. Urine and vaginal discharge are the main mimics.\n\nPerform a sterile speculum examination to look for pooling of fluid, with a fluid test if needed. Ultrasound liquor volume supports the assessment but neither confirms nor excludes rupture.\n\n> [!pitfall]\n> Avoid unnecessary digital examinations, which increase the risk of infection, particularly before labour.\n\n### PPROM\n\nPrelabour rupture of membranes before `37 weeks` is **PPROM**. With the membranes open, the risks are ascending infection, labour, cord prolapse and prematurity. Management weighs these against gestation and fetal wellbeing, and may include:\n\n- Admission.\n- Latency antibiotics, which prolong the pregnancy and reduce infection: commonly oral erythromycin `250 mg` four times daily for `10 days`, given in Victoria with IV benzylpenicillin for the first `48 hours`.\n- Antenatal corticosteroids, and magnesium sulfate for neuroprotection at the appropriate gestations.\n- Delivery if infection, fetal compromise or another indication develops.\n\nTocolysis is not routine in PPROM.\n\nAt term, most women labour within a day. Induction with oxytocin is offered, and expectant management for up to about `24 hours` is an alternative when there are no signs of infection; GBS colonisation, meconium or any sign of infection favours prompt induction, with intrapartum antibiotics for GBS.\n\n### Intra-amniotic infection\n\nMaternal fever, uterine tenderness, foul or purulent fluid and maternal or fetal tachycardia suggest intra-amniotic infection (chorioamnionitis), although no single sign is diagnostic. Take cultures where appropriate, give prompt broad-spectrum IV antibiotics, assess for sepsis and plan the birth with obstetrics. Infection alone does not require caesarean birth; the route depends on the obstetric circumstances.\n\n### Sepsis in pregnancy and after birth\n\nSepsis is a leading direct cause of maternal death, and group A streptococcus is the commonest cause of these deaths. It is harder to recognise in pregnancy, because the normal rise in heart rate and fall in blood pressure, and the rise in white cell count during labour and soon after birth, overlap with early sepsis; deterioration can then be rapid. Use the maternity observation chart, and treat a pregnant or recently pregnant woman with signs of infection and tachypnoea, hypotension or altered mentation as possibly septic.\n\nBesides the genital tract (intra-amniotic infection, endometritis, retained products and wound infection), common sources are pyelonephritis, pneumonia and mastitis. Pulmonary embolism, concealed haemorrhage and acute fatty liver of pregnancy can mimic sepsis. Management follows the adult sepsis response (B01 (Sepsis and meningitis)), with these changes:\n\n1. Call the obstetric team early, and anaesthetics and intensive care for organ dysfunction.\n2. Resuscitate the mother first, with left lateral tilt or manual uterine displacement after about `20 weeks` to relieve aortocaval compression.\n3. Take blood cultures and cultures from the likely source, and measure lactate, without delaying antibiotics; interpret results against pregnancy reference ranges.\n4. Give broad-spectrum IV antibiotics within `one hour`. Without an obvious source, SOMANZ suggests amoxicillin or ampicillin with gentamicin and metronidazole, adding clindamycin when group A streptococcal infection is suspected.\n5. Assess the fetus once the mother is stabilising; an abnormal CTG often reflects maternal hypoperfusion and may improve with resuscitation.\n6. Control the source, which may mean birth for intrauterine infection or removing retained products.\n\n### Group B streptococcus\n\nGBS is common colonisation, not an STI or a sign of poor hygiene. It matters because it can be transmitted to the newborn during labour. Screening is commonly by a lower vaginal and rectal swab at `35–37 weeks`, or by a risk-based strategy, according to the local service.\n\nGive **intrapartum antibiotic prophylaxis**, usually IV benzylpenicillin, for:\n\n- A positive screening swab.\n- GBS bacteriuria in this pregnancy.\n- A previous infant with invasive GBS disease.\n- Specified risk factors when screening is risk-based.\n\nChoose alternatives according to allergy and susceptibility.\n\n> [!pitfall]\n> Treating colonisation weeks before labour does not replace intrapartum prophylaxis, because recolonisation is common.\n\nA planned caesarean before labour with intact membranes does not need GBS prophylaxis.\n\n### Emergencies\n\n> [!escalate]\n> **Cord prolapse** after membrane rupture needs immediate help, relief of pressure on the cord by a trained clinician, and expedited birth. Maternal shock, severe bleeding, sepsis or fetal bradycardia is an emergency.\n\nThe handover should give the gestation, placental position, GBS and RhD status, observations, fetal assessment and treatment already given.",
      "formerly": [
        "O06"
      ]
    },
    {
      "id": "O07",
      "domain": "OGN",
      "title": "Labour, CTG and birth",
      "focus": "Stages of labour, abnormal CTG, intervention/escalation and birth complications.",
      "first_pass": false,
      "priority": "Core",
      "saq_cases": [
        {
          "id": "2020-ummss-q2",
          "title": "Intrapartum CTG and postpartum haemorrhage after caesarean",
          "set": "2020 UMMSS"
        }
      ],
      "core_ids": [
        "P058"
      ],
      "notes": "### Stages of labour\n\n- **First stage:** from the onset of labour to full cervical dilatation. Established active labour involves regular painful contractions with progressive cervical change, commonly from about `5 cm` under current guidance.\n- **Second stage:** from full dilatation to the birth of the baby.\n- **Third stage:** from the birth of the baby to delivery of the placenta.\n\n### Assessing progress\n\nAssess maternal observations, pain and coping, contractions, membrane status, fetal presentation and wellbeing, and progress together. Normal labour varies widely in pace, so progress is a trend across examinations; neither one examination nor a universal centimetres-per-hour rule is a reliable guide.\n\nVaginal examinations are uncomfortable and add infection risk after membrane rupture, so perform them when the findings will inform a decision. Explain, obtain consent, preserve privacy and offer support. The examination assesses:\n\n- Cervical dilatation and **effacement** (shortening and thinning of the cervix).\n- Position of the presenting part.\n- **Station**: the level of the presenting part relative to the maternal ischial spines.\n- Membrane status.\n\n### Support and analgesia\n\nContinuous support, comfortable positions, hydration and appropriate analgesia help the patient cope. Nitrous oxide, systemic opioids and epidural differ in effectiveness and side effects. Epidural is the most effective, but needs anaesthetic assessment and monitoring for hypotension, motor block, urinary retention and rare complications.\n\n### CTG interpretation\n\nFirst confirm that the trace is the fetal heart and not the maternal pulse, then check trace quality, gestation and clinical risk. Describe the baseline, variability, accelerations, decelerations and contraction frequency, and finish with an overall interpretation and an action.\n\nNormal features under current RANZCOG guidance:\n\n- **Baseline:** `110–160 bpm`.\n- **Variability:** `6–25 bpm`.\n- Accelerations present.\n- No concerning decelerations, and uterine activity not excessive.\n\nDecelerations are classified by their timing relative to contractions, which reflects their cause:\n\n- **Early:** mirror the contraction; usually head compression.\n- **Variable:** vary in shape and timing; suggest cord compression. Depth, duration, recovery, baseline and variability determine concern.\n- **Late:** begin after the peak of the contraction; suggest impaired placental oxygen transfer.\n\n> [!pitfall]\n> Absent accelerations alone, on an otherwise reassuring trace, do not indicate hypoxia.\n\nA rising baseline, reduced or absent variability, a prolonged deceleration or bradycardia needs prompt assessment. Combinations of features and their evolution matter more than any single feature.\n\n### Responding to an abnormal CTG\n\nAddress the reversible causes of reduced fetal oxygenation:\n\n1. Call for help and assess the mother.\n2. Turn her to the left lateral position to relieve aortocaval compression, stop any oxytocin infusion, and correct hypotension.\n3. Look for excessive uterine activity, cord prolapse and rapid progress. Tocolysis may be needed for uterine hyperstimulation.\n\nGive oxygen for maternal hypoxaemia, not routinely.\n\n> [!escalate]\n> A persistently abnormal CTG needs senior review and may require urgent birth; do not continue observation without a defined escalation plan.\n\n### Induction of labour\n\nOffer induction when the expected benefit of birth outweighs the risk of continuing the pregnancy, for example post-dates or a maternal or fetal complication. Counselling covers the indication and alternatives; cervical ripening with a balloon catheter or prostaglandin; amniotomy and oxytocin; monitoring; the risk of hyperstimulation; and the possibility of failed induction and caesarean birth. Previous uterine surgery changes which methods are safe.\n\n### Assisted vaginal birth\n\nAssisted birth may be appropriate for fetal concern or a prolonged second stage when its prerequisites are met:\n\n- Full dilatation and ruptured membranes.\n- Known fetal head position and adequate descent.\n- An adequate pelvis.\n- Analgesia and an empty bladder.\n- A safe back-up plan.\n\nCounselling covers perineal injury and the instrument-specific neonatal risks.\n\n### Caesarean birth and breech\n\nCounselling for caesarean birth covers the reason it is recommended and its risks: bleeding, infection, VTE, injury to bladder or bowel, recovery, and placental and uterine risks in future pregnancies.\n\nFor persistent breech presentation, offer external cephalic version at about `37 weeks`, alongside a discussion of the options for birth.\n\nFor **vaginal birth after caesarean**, weigh the likelihood and benefits of vaginal birth against the risk of uterine rupture and emergency surgery, considering the previous incision, the current pregnancy and the service's capability.\n\n### Obstetric emergencies\n\n**Shoulder dystocia** needs immediate help. Stop excessive traction, use McRoberts positioning (which rotates the pelvis to free the impacted anterior shoulder) and apply suprapubic pressure, followed by trained internal manoeuvres if needed.\n\n> [!pitfall]\n> **Do not use fundal pressure** in shoulder dystocia; it worsens impaction of the shoulder.\n\n**Cord prolapse** needs urgent relief of pressure on the cord and expedited birth. Document timings and actions in both emergencies, and offer a debrief afterwards.\n\n### Third stage and the newborn\n\nActive management of the third stage uses a prophylactic uterotonic, usually oxytocin `10 units IM`, and controlled cord traction by a trained clinician, with the timing of cord clamping adapted to the circumstances of mother and baby. Check that the placenta is complete, the uterus is contracted, bleeding is controlled and maternal observations are stable.\n\nDry and warm the newborn, assess breathing and heart rate, and begin neonatal resuscitation promptly when needed.\n\nReference: [RANZCOG intrapartum fetal surveillance, fifth edition](https://fsep.ranzcog.edu.au/what-we-offer/clinical-guideline/).",
      "formerly": [
        "O07"
      ]
    },
    {
      "id": "O08",
      "domain": "OGN",
      "title": "Postpartum haemorrhage, recovery and contraception",
      "focus": "Primary/secondary PPH, complications, contraception and postnatal follow-up.",
      "first_pass": true,
      "priority": "Core",
      "saq_cases": [
        {
          "id": "deck-og-pph-ida",
          "title": "Primary postpartum haemorrhage",
          "set": "MD3 SAQ Revision Deck"
        },
        {
          "id": "deck-og-pph-secondary",
          "title": "Primary and secondary postpartum haemorrhage",
          "set": "MD3 SAQ Revision Deck"
        },
        {
          "id": "deck-og-postpartum-contraception",
          "title": "Postpartum contraception",
          "set": "MD3 SAQ Revision Deck"
        }
      ],
      "core_ids": [
        "P004",
        "P041",
        "P058"
      ],
      "notes": "### Primary postpartum haemorrhage\n\n**Primary postpartum haemorrhage** (PPH) occurs within `24 hours` of birth. Blood loss of `≥500 mL`, or any loss causing haemodynamic compromise, needs assessment; do not wait for a number in a deteriorating patient. Healthy pregnant women compensate well and may not become hypotensive until the loss is large, and visible loss is often underestimated, so quantify blood loss where possible and watch observations and perfusion closely.\n\nThe **4 Ts** organise the causes:\n\n- **Tone:** uterine atony, the commonest cause.\n- **Trauma:** genital tract injury or uterine rupture.\n- **Tissue:** retained placenta or products of conception.\n- **Thrombin:** coagulopathy.\n\nAfter the placenta separates, contraction of the myometrium compresses the vessels supplying the placental bed. **Uterine atony** is failure of this contraction. A soft, enlarged uterus suggests atony; continued bleeding with a firm uterus suggests trauma or another cause. More than one cause can coexist.\n\n### Management of PPH\n\nResuscitation and control of the source proceed together. Call the obstetric haemorrhage team, assess airway, breathing and circulation, insert large-bore IV access and send FBE, coagulation studies with fibrinogen, and crossmatch. Use warmed fluids and blood, activating the massive transfusion protocol when indicated, and monitor urine output, temperature and response.\n\n> [!pitfall]\n> Repeated crystalloid dilutes clotting factors. Do not let it delay blood components or definitive control of bleeding.\n\n- **Atony:** rub up the fundus, empty the bladder (a full bladder impedes uterine contraction), and give oxytocin `10 IU` IM or slowly IV, followed by an infusion (commonly `40 IU` over `4 hours`).\n- **Additional uterotonics:** ergometrine, carboprost or misoprostol. Avoid ergometrine in significant hypertension or pre-eclampsia, because its vasoconstriction can provoke severe hypertension. Carboprost can cause bronchospasm and is avoided in asthma unless specialist judgement supports it.\n- **Tranexamic acid:** `1 g IV over about 10 minutes`, as early as possible and within `3 hours` of birth for clinically diagnosed PPH. A second `1 g` may be given if bleeding continues after `30 minutes` or restarts.\n- **Other sources:** examine and repair trauma, remove retained tissue appropriately and correct coagulopathy.\n\nIf bleeding persists, the options are bimanual compression, balloon tamponade, return to theatre, embolisation and surgery up to hysterectomy. Escalate while the initial treatments are being given, not after they have failed.\n\n> [!counsel]\n> Afterwards, explain to the patient and their support person what happened and what was done, and offer a debrief.\n\nAssess and treat anaemia, and support feeding and recovery.\n\n### Secondary postpartum haemorrhage\n\nAbnormal heavy bleeding between 24 hours and `12 weeks` after birth may reflect retained products, endometritis or **subinvolution** (delayed return of the uterus towards its non-pregnant size). Bleeding, pain, fever, uterine tenderness and observations help separate these; use FBE, cultures and ultrasound as indicated. Sepsis or heavy bleeding needs hospital care. Treatment may include antibiotics and removal of retained tissue.\n\n### Postnatal review\n\nThe routine postnatal review covers bleeding, healing of the wound or perineum, pain, bowel and bladder function, VTE symptoms, feeding, sleep, mood, bonding and safety. Condition-specific follow-up includes:\n\n- **Hypertensive disease:** BP review.\n- **PPH:** anaemia.\n- **GDM:** the postnatal OGTT; see O05 (After birth).\n\nAlso ask about pelvic-floor symptoms, and advise a gradual return to activity and sex according to comfort and healing.\n\n> [!escalate]\n> Severe headache, chest pain, breathlessness, unilateral leg swelling, fever or heavy bleeding after discharge needs urgent assessment. Pre-eclampsia, VTE and sepsis can all present postpartum.\n\n### Postpartum contraception\n\nOvulation can return before the first period, so fertility may resume without warning. **Lactational amenorrhoea** is reliable only when **all three criteria** are met:\n\n- Under `six months` postpartum.\n- No periods.\n- Fully or nearly fully breastfeeding, frequently, day and night.\n\nIf any criterion changes, another method is needed.\n\n- **Progestogen-only pill and implant:** usually suitable early postpartum and during breastfeeding.\n- **IUD:** can be placed immediately after delivery of the placenta in an appropriate service, or at a later postpartum visit; the timing affects expulsion and perforation risk.\n- **Combined (oestrogen-containing) methods:** restricted early postpartum because of VTE risk and effects on breastfeeding. They are avoided in the first `21 days` after birth, and later when there are VTE risk factors; during breastfeeding they are generally avoided until `six weeks`.\n\nChoose according to effectiveness, bleeding, reversibility and preference (see G21 (Comparing methods)), aiming to have a method in place before fertility returns if contraception is wanted.",
      "formerly": [
        "O08"
      ]
    },
    {
      "id": "O09",
      "domain": "OGN",
      "title": "Breastfeeding and lactational symptoms",
      "focus": "Attachment, lactation counselling, mastitis, abscess and medication compatibility.",
      "first_pass": false,
      "priority": "Core",
      "saq_cases": [
        {
          "id": "2016-wcah-q1",
          "title": "Breastfeeding problems and postpartum contraception",
          "set": "2016 WH/CAH"
        },
        {
          "id": "deck-og-breastfeeding-mastitis",
          "title": "Breastfeeding and lactation problems",
          "set": "MD3 SAQ Revision Deck"
        }
      ],
      "core_ids": [
        "P020",
        "P067"
      ],
      "notes": "### Assessing milk transfer\n\n> [!pitfall]\n> Frequent feeding does not prove adequate intake. What matters is whether milk is being transferred.\n\nStart with the parent's feeding goals, pain, breast and nipple changes, feeding pattern, expressing, formula use and medicines. Then assess the infant's alertness, weight trajectory, wet nappies and stools.\n\nWith consent, observe a feed. In good attachment the baby is held close with head and body aligned, opens the mouth wide and takes a deep mouthful of breast, with rhythmic sucking and audible swallowing. Persistent pain, clicking, shallow attachment, or a nipple that looks compressed after the feed suggests a problem with attachment.\n\nInterpret early newborn weight loss against age, intake and clinical state. Excessive loss, failure to regain birth weight, jaundice or reduced urine output needs assessment. A skilled lactation review then informs a feeding plan based on milk transfer and the infant's clinical state. Address infant oral anatomy or maternal factors when indicated, without attributing every problem to tongue-tie.\n\n### Milk supply\n\nMilk production responds to effective, regular removal of milk: prolactin drives production and oxytocin the let-down reflex. Responsive feeding follows from this.\n\nIf the infant cannot feed effectively, an individual plan for expressing and supplementation protects both maternal comfort and infant nutrition. Formula can be part of an informed feeding plan; avoid pressure or language that implies failure.\n\n### Engorgement\n\n**Engorgement** is diffuse fullness of the breasts, which can make attachment difficult. Cool packs, analgesia, and gentle expression only as needed for comfort or attachment can help.\n\n> [!pitfall]\n> Removal of milk drives production, so repeatedly pumping to \"empty\" the breast, or deep aggressive massage, can worsen swelling and oversupply.\n\nWhen weaning, reduce stimulation gradually to limit engorgement.\n\n### Mastitis\n\nMastitis causes local pain and redness and may cause systemic symptoms. Not every episode is bacterial.\n\n**Continue breastfeeding or expressing in the usual pattern if possible**; the milk is safe for the baby. Add rest, fluids, cold packs and paracetamol or ibuprofen if suitable, and correct attachment problems and oversupply, which often underlie mastitis.\n\nGive antibiotics for likely bacterial mastitis, persistent or worsening symptoms, or significant illness:\n\n- **Flucloxacillin** `500 mg orally four times daily`, covering the staphylococci usually responsible. The duration follows response, often `5–10 days`.\n- Allergy, a resistant organism or severe illness changes the regimen.\n\nReview within `24–48 hours`. Culture milk in recurrent, severe or non-responding disease.\n\n### Breast abscess\n\nA persistent focal mass or fluctuant area suggests an abscess, which needs ultrasound and drainage, with culture and antibiotics. Severe systemic illness needs hospital assessment. Breastfeeding can often continue, with advice tailored to the drainage site.\n\nRecurrent presumed mastitis, or persistent redness or a mass outside lactation, needs breast assessment to exclude another diagnosis; see G23 (Lactational and inflammatory symptoms).\n\n### Nipple pain\n\nMechanical trauma, dermatitis, vasospasm and infection can all cause nipple pain. Examination is more reliable than diagnosing Candida from burning pain alone.\n\n- **Vasospasm:** blanching or colour change, often with cold. Warmth and correcting trauma help; consider medication (such as nifedipine) for persistent symptoms.\n- **Dermatitis:** treat the skin and avoid irritants.\n\n### Medicines during breastfeeding\n\nCheck medicine safety in a reliable lactation reference, such as the Royal Women's Hospital Pregnancy and Breastfeeding Medicines Guide or LactMed. Many medicines are compatible, and unnecessarily stopping breastfeeding or essential treatment causes harm. Infant prematurity and age, and the drug and dose, determine exposure more than any single rule.\n\n### Follow-up\n\nFollow-up covers both feeding and the baby's weight, as well as maternal sleep, mood and the help available.",
      "formerly": [
        "O09"
      ]
    },
    {
      "id": "O10",
      "domain": "OGN",
      "title": "Abnormal uterine bleeding and amenorrhoea",
      "focus": "Heavy, intermenstrual and postmenopausal bleeding; pregnancy exclusion, investigations and referral.",
      "first_pass": true,
      "priority": "Core",
      "saq_cases": [
        {
          "id": "2016-wcah-q3",
          "title": "Heavy menstrual bleeding",
          "set": "2016 WH/CAH"
        },
        {
          "id": "deck-og-imb-prolapse",
          "title": "Intermenstrual bleeding and pelvic organ prolapse",
          "set": "MD3 SAQ Revision Deck"
        },
        {
          "id": "deck-og-postmenopausal-bleeding",
          "title": "Postmenopausal bleeding and cervical screening",
          "set": "MD3 SAQ Revision Deck"
        }
      ],
      "core_ids": [
        "P008"
      ],
      "notes": "### Characterising abnormal bleeding\n\nEstablish the frequency, duration and heaviness of bleeding, any intermenstrual or postcoital bleeding, pain, contraception, the possibility of pregnancy and the effect on daily life. **Heavy menstrual bleeding** is defined partly by its effect on quality of life, not only by measured volume.\n\nAssess haemodynamic status and anaemia first. Do a pregnancy test where relevant before treating the bleeding as non-pregnant, since pregnancy complications are the commonest serious mimic.\n\n### Causes: PALM–COEIN\n\n**PALM** covers the structural causes:\n\n- **Polyp:** a localised overgrowth of the endometrium.\n- **Adenomyosis:** endometrial-type tissue within the myometrium.\n- **Leiomyoma (fibroid):** a benign smooth-muscle tumour.\n- **Malignancy and hyperplasia.**\n\n**COEIN** covers the non-structural causes: coagulopathy, ovulatory dysfunction, endometrial disorders, iatrogenic causes and those not otherwise classified.\n\nAnovulation causes irregular, unpredictable bleeding: the endometrium builds under oestrogen without the organised shedding that follows progesterone withdrawal. It is common in adolescence, PCOS and the perimenopause. Anticoagulants and hormonal contraception also change bleeding patterns. Heavy periods since menarche, with bruising or other bleeding, suggest an inherited bleeding disorder such as von Willebrand disease.\n\n### Examination and investigations\n\nRecord observations, look for pallor and examine the abdomen. With consent, perform a pelvic and speculum examination when indicated, to identify cervical or vaginal pathology and assess uterine size and tenderness.\n\n- **FBE and ferritin:** anaemia and iron deficiency.\n- **TSH, coagulation studies and STI tests:** according to the history.\n- **Pelvic ultrasound:** fibroids, polyps, adenomyosis and adnexal pathology.\n\nConsider endometrial sampling for persistent abnormal bleeding from about age `45`, or earlier with risk factors such as obesity, prolonged anovulation, tamoxifen or hereditary cancer risk, which increase the chance of hyperplasia or cancer.\n\n> [!pitfall]\n> Before menopause, endometrial thickness alone cannot exclude pathology, because it changes across the cycle.\n\nHysteroscopy helps with focal lesions or when sampling and imaging are insufficient.\n\n### Management of heavy menstrual bleeding\n\nTreat iron deficiency, then choose among the options according to fertility goals, contraindications and preference:\n\n- **Levonorgestrel IUD:** the most effective medical treatment; thins the endometrium locally and provides contraception.\n- **Combined hormonal contraception:** regulates or suppresses cycles when oestrogen is suitable.\n- **Oral progestogens:** protect the endometrium in anovulation.\n- **Tranexamic acid:** reduces bleeding on heavy days; it is not a contraceptive.\n- **NSAIDs:** reduce prostaglandin-mediated bleeding and pain; assess renal, gastrointestinal and bleeding risk.\n\nStructural disease may need polypectomy, fibroid treatment or other surgery. Endometrial ablation is unsuitable when future pregnancy is wanted and is not contraception. Hysterectomy is definitive but carries greater operative and recovery burden.\n\n> [!escalate]\n> Acute heavy bleeding with haemodynamic instability needs emergency resuscitation and gynaecological treatment.\n\n### Amenorrhoea\n\n- **Primary amenorrhoea:** assess if menarche has not occurred by about age `15`, or earlier if pubertal development is absent or abnormal.\n- **Secondary amenorrhoea:** absence of periods for `three months` in previously regular cycles, or `six months` in previously irregular cycles.\n\nExclude pregnancy first. Then ask about nutrition, exercise, stress, weight change, medicines, galactorrhoea, androgen excess and menopausal symptoms.\n\nTSH, prolactin, FSH and oestradiol locate the problem along the hypothalamic–pituitary–ovarian axis:\n\n- **High FSH with low oestradiol:** the ovary is not responding to pituitary drive; primary ovarian insufficiency.\n- **Low or normal gonadotrophins with low oestradiol:** hypothalamic or pituitary suppression, for example from low energy availability.\n- **Raised prolactin:** medicines, hypothyroidism or pituitary disease; confirm before further investigation.\n- **Ovulatory dysfunction with hyperandrogenism:** PCOS; see O12 (PCOS diagnosis).\n\nPrimary amenorrhoea with cyclical pain suggests outflow obstruction, such as an imperforate hymen.\n\n### Postmenopausal bleeding\n\n**Any new bleeding after menopause needs prompt assessment**, because endometrial cancer must be excluded. Transvaginal ultrasound and endometrial sampling or gynaecology referral follow the findings:\n\n- Examine the vulva, vagina and cervix for atrophy, a polyp or a tumour, and check that cervical screening is up to date. Confirm that the blood is vaginal rather than urinary or rectal.\n- On transvaginal ultrasound in a patient not using hormone therapy, an evenly thin endometrium of `≤4 mm` makes cancer unlikely, so a single episode can be observed. A thicker endometrium, a focal lesion or an endometrium that cannot be seen clearly needs endometrial sampling, usually with hysteroscopy, through gynaecology. Some units use `3 mm`.\n- Tamoxifen thickens the endometrium, so thickness is unreliable and referral is needed. On hormone therapy, an expected withdrawal bleed on a cyclical regimen is not postmenopausal bleeding, but unscheduled bleeding, or bleeding after the first `six months` of a continuous combined regimen, needs assessment.\n\nPersistent or recurrent bleeding needs evaluation even when the endometrium is thin, usually hysteroscopy and biopsy, because ultrasound can miss focal disease.\n\n> [!pitfall]\n> Do not attribute postmenopausal bleeding to atrophy or hormone therapy without assessment.",
      "formerly": [
        "O10"
      ]
    },
    {
      "id": "O11",
      "domain": "OGN",
      "title": "Pelvic pain, endometriosis and pelvic infection",
      "focus": "History, differential, STI considerations, imaging, treatment principles and safety-netting.",
      "first_pass": false,
      "priority": "Core",
      "saq_cases": [
        {
          "id": "deck-og-endometriosis",
          "title": "Chronic pelvic pain and endometriosis",
          "set": "MD3 SAQ Revision Deck"
        },
        {
          "id": "deck-og-pid",
          "title": "Pelvic inflammatory disease",
          "set": "MD3 SAQ Revision Deck"
        }
      ],
      "core_ids": [
        "P002",
        "P056",
        "P065",
        "P070",
        "P088"
      ],
      "notes": "### Assessment of pelvic pain\n\nPelvic pain can arise from reproductive, urinary, gastrointestinal or musculoskeletal disease, and a few causes threaten life or fertility within hours. Do a pregnancy test early in anyone who could be pregnant, including those using contraception.\n\n- **Ectopic pregnancy:** pain or bleeding with a positive pregnancy test; see O03 (Initial assessment).\n- **Ovarian torsion:** sudden unilateral pain with vomiting, often with an ovarian cyst or mass. Ultrasound supports the diagnosis, but it is confirmed and treated at laparoscopy, which should not wait when suspicion is high, because ovarian viability falls within hours; detorsion usually saves the ovary even when it looks dusky.\n- **Tubo-ovarian abscess:** fever, systemic illness and a tender adnexal mass.\n\n> [!escalate]\n> Haemodynamic instability, peritonism, fever with systemic illness, suspected torsion or a suspected tubo-ovarian abscess needs emergency hospital assessment.\n\n> [!pitfall]\n> **Doppler flow on ultrasound does not reliably exclude torsion** when the clinical picture is convincing.\n\nAsk about onset and timing in the menstrual cycle, bleeding, discharge, dyspareunia, pain on defaecation, urinary symptoms, fever, STI exposure, previous surgery and fertility goals. The effect on work, relationships and daily activity indicates how much treatment the patient wants.\n\nWith consent, examine the abdomen, and examine the pelvis when the findings will change management; offer a chaperone and stop if asked. Urinalysis, a pregnancy test, STI swabs and pelvic ultrasound each answer a different question, so choose them for the presentation.\n\n### Dysmenorrhoea\n\n**Primary dysmenorrhoea** is prostaglandin-mediated cramping around menstruation without underlying pelvic pathology. NSAIDs inhibit prostaglandin synthesis and work best when started at the onset of pain, or just before a predictable period. Hormonal contraception is also effective.\n\nNew or progressively worsening pain, deep dyspareunia, intermenstrual bleeding, heavy bleeding, infertility or an abnormal examination suggests **secondary dysmenorrhoea**.\n\n### Endometriosis and adenomyosis\n\n**Endometriosis** is endometrial-like tissue outside the uterus that causes inflammation, pain and sometimes adhesions or infertility. Typical symptoms are cyclical pelvic pain, painful defaecation or urination, and deep dyspareunia. The severity of pain does not reliably indicate the extent of disease.\n\n**Adenomyosis** is endometrial tissue within the myometrium. It more often causes heavy, painful periods with a tender, enlarged uterus.\n\nUltrasound identifies ovarian endometriomas, adenomyosis and other structural disease, but a normal scan does not exclude superficial endometriosis. A clinical diagnosis is enough to start treatment; laparoscopy is not required before symptom relief.\n\nInitial management:\n\n- NSAIDs if suitable, heat, and activity adapted to symptoms.\n- When pregnancy is not wanted now: continuous combined hormonal contraception, a progestogen (such as dienogest) or a levonorgestrel IUD. These suppress the cyclical stimulation that drives the lesions; explain the expected changes in bleeding and review the response.\n- Pelvic floor physiotherapy, and management of bowel, bladder and persistent pain contributors when relevant.\n\nRefer to gynaecology for persistent disabling symptoms, a mass, suspected deep disease or fertility concerns. Surgery and specialist hormonal treatments depend on goals, risks and previous response.\n\n### Pelvic inflammatory disease\n\n**Pelvic inflammatory disease** (PID) is infection of the upper genital tract, often polymicrobial. Lower abdominal pain, cervical motion tenderness, uterine or adnexal tenderness, abnormal discharge, intermenstrual or postcoital bleeding and dyspareunia support the diagnosis. Fever may be absent.\n\n> [!pitfall]\n> **A negative chlamydia or gonorrhoea test does not exclude PID.** Untreated infection risks tubal infertility, ectopic pregnancy and chronic pain.\n\nTake vaginal or endocervical NAAT for chlamydia and gonorrhoea, a pregnancy test and relevant STI serology, with gonococcal culture where indicated. Ultrasound helps when an abscess, mass or alternative diagnosis is possible; a normal scan does not exclude uncomplicated PID.\n\nStart empirical treatment when the clinical diagnosis is likely, without waiting for swab results, because delay increases the risk of tubal damage. For mild to moderate PID, the standard Australian outpatient regimen covers gonorrhoea, chlamydia and anaerobes:\n\n- **Ceftriaxone** `500 mg IM once`, plus\n- **Doxycycline** `100 mg orally twice daily for 14 days`, plus\n- **Metronidazole** `400 mg orally twice daily for 14 days`.\n\nPregnancy, severe illness, inability to take oral treatment or a suspected abscess needs hospital or specialist management. Review within `48–72 hours`; if there is no improvement, reassess the diagnosis, adherence and complications.\n\n> [!counsel]\n> Complete the full course. Avoid sex until treatment is finished, symptoms have resolved and partners have been treated, since an untreated partner causes reinfection.\n\nArrange partner notification and testing, organism-specific retesting, and ongoing contraception and STI prevention. An existing IUD does not routinely need removal if the patient wishes to keep it; reassess promptly if there is no improvement.\n\nReference: [Australian STI Management Guidelines: PID](https://sti.guidelines.org.au/syndromes/pelvic-inflammatory-diseases-pid/).",
      "formerly": [
        "O11"
      ]
    },
    {
      "id": "O12",
      "domain": "OGN",
      "title": "Subfertility and PCOS",
      "focus": "Assessing both partners, timing of referral, PCOS diagnosis by age, metabolic risk and goal-based management.",
      "first_pass": false,
      "priority": "Core",
      "saq_cases": [
        {
          "id": "deck-og-infertility",
          "title": "Infertility",
          "set": "MD3 SAQ Revision Deck"
        },
        {
          "id": "deck-og-pcos",
          "title": "Polycystic ovary syndrome",
          "set": "MD3 SAQ Revision Deck"
        }
      ],
      "core_ids": [
        "P041",
        "P104"
      ],
      "notes": "### Subfertility: when to investigate\n\nInvestigate after `12 months` of regular unprotected intercourse, or after `six months` when the female partner is `35 or older`, since declining ovarian reserve makes delay more costly. Investigate earlier with amenorrhoea, suspected tubal disease, a significant male risk factor or older reproductive age.\n\nAsk about the duration and timing of attempts, previous pregnancies, the menstrual pattern, pelvic infection or surgery, endometriosis, medicines, sexual function and lifestyle in both partners. Use non-judgemental language and acknowledge the emotional and financial burden.\n\n### Investigations\n\nConception requires ovulation, adequate sperm and a patent reproductive tract, so investigate all three in both partners rather than assuming the problem lies with one.\n\n- **Semen analysis:** an early test. An abnormal result usually needs repeating and specialist interpretation.\n- **Ovulation:** a mid-luteal progesterone, taken about `seven days` before the expected period. A fixed \"day 21\" sample is correct only for a 28-day cycle.\n- **Anatomy and tubal patency:** pelvic ultrasound for uterine and ovarian anatomy; specialist tubal patency testing according to the history.\n- **AMH:** estimates ovarian reserve and the likely response to stimulation. It is not a test of natural fertility or egg quality.\n\nBegin preconception care from the outset: folic acid, vaccination and medication review, smoking cessation and help with alcohol or other drugs. Intercourse every `two to three days` covers the fertile window without intensive tracking. Refer for ovulation induction, management of tubal or male-factor infertility, or assisted reproduction according to the findings; age and cause determine the likely benefit.\n\n### PCOS diagnosis\n\n> [!current]\n> PCOS was renamed **polyendocrine metabolic ovarian syndrome (PMOS)** by international consensus in May 2026. The clinical recommendations remain those of the 2023 international guideline; the familiar curriculum term is used here.\n\nIn adults, the diagnosis requires **two of the following, after excluding other causes**:\n\n- Ovulatory dysfunction (irregular cycles).\n- Clinical or biochemical hyperandrogenism.\n- Polycystic ovarian morphology on ultrasound, or an elevated AMH.\n\nIf irregular cycles and hyperandrogenism are both present, ultrasound and AMH are unnecessary.\n\nIn **adolescents**, both persistent ovulatory dysfunction and hyperandrogenism are required. Ultrasound and AMH are not used, because multifollicular ovaries are common in normal adolescence.\n\n> [!pitfall]\n> Ovarian \"cysts\" on ultrasound do not by themselves establish PCOS.\n\nExclude pregnancy, thyroid dysfunction, hyperprolactinaemia and non-classic congenital adrenal hyperplasia as appropriate. Rapid virilisation or very high androgen levels suggest an androgen-secreting tumour.\n\n### PCOS: metabolic and psychological assessment\n\nPCOS is a metabolic as well as a reproductive condition. Assess BP, glucose tolerance, lipids, symptoms of sleep apnoea, depression and eating concerns, and fertility intentions. A 75 g OGTT is the most accurate test of glycaemic status. Reassess metabolic risk over time.\n\n### PCOS management\n\nManagement follows the patient's main goal:\n\n- **Lifestyle:** sustainable nutrition, activity and weight support, offered without stigma. Health benefits occur even without weight loss.\n- **Endometrial protection:** combined hormonal contraception or cyclical progestogen during prolonged anovulation, when unopposed oestrogen would otherwise stimulate the endometrium. A levonorgestrel IUD protects the endometrium and provides contraception.\n- **Acne and hirsutism:** combined hormonal contraception. Antiandrogens need reliable contraception and monitoring because of fetal risk.\n- **Metabolic risk:** metformin for metabolic indications in selected patients. It does not replace endometrial protection or fertility treatment.\n- **Anovulatory infertility:** letrozole is the preferred first-line drug for ovulation induction when there is no other infertility factor, under specialist fertility care.\n\nReference: [Monash international PCOS guideline](https://www.monash.edu/medicine/mchri/pcos/guideline).",
      "formerly": [
        "O12"
      ]
    },
    {
      "id": "O13",
      "domain": "OGN",
      "title": "Menopause and menopausal hormone therapy",
      "focus": "Diagnosis, early menopause, MHT benefits, risks and endometrial protection, non-hormonal options and contraception.",
      "first_pass": false,
      "priority": "Core",
      "saq_cases": [
        {
          "id": "deck-og-menopause-mht",
          "title": "Menopause and menopausal hormone therapy",
          "set": "MD3 SAQ Revision Deck"
        }
      ],
      "core_ids": [
        "P088",
        "P093"
      ],
      "notes": "### Diagnosis of menopause\n\n**Menopause** is diagnosed retrospectively after `12 months` without a period at the expected age. After age `45`, typical symptoms and menstrual change are usually enough; FSH fluctuates during the perimenopause, so routine testing does not help.\n\nMenopause before `45`, and especially **premature ovarian insufficiency** before `40`, needs investigation and specialist input, because the longer period of oestrogen deficiency has bone and cardiovascular consequences.\n\nExplore hot flushes, sleep, mood, vaginal dryness, dyspareunia and urinary symptoms, as well as bleeding and contraception.\n\n### Menopausal hormone therapy\n\nMenopausal hormone therapy (MHT) is the most effective treatment for vasomotor symptoms and prevents bone loss while it is taken. The balance of benefit and risk is generally most favourable when it is started before age `60` or within `10 years` of menopause.\n\n- **Endometrial protection:** with a uterus present, systemic oestrogen must be combined with a progestogen, because unopposed oestrogen causes endometrial hyperplasia and cancer. A Mirena used for this purpose is replaced at `five years`, despite its longer contraceptive life.\n- **Route:** transdermal oestrogen carries a lower thrombotic risk than oral oestrogen, because it avoids first-pass hepatic effects on clotting factors.\n\nBefore prescribing, assess unexplained bleeding, hormone-dependent cancer, cardiovascular disease, liver disease and VTE history; significant histories need specialist advice. Discuss breast tenderness, bleeding, and breast cancer and thrombotic risks in relation to the formulation and duration, and review benefit and tolerability.\n\n### Other treatments\n\n- **Genitourinary symptoms alone:** vaginal moisturisers and lubricants, and low-dose vaginal oestrogen. Systemic therapy is unnecessary.\n- **When MHT is unsuitable:** selected SSRIs or SNRIs, or gabapentin, can reduce vasomotor symptoms.\n\n### Contraception around menopause\n\n> [!pitfall]\n> MHT is not a contraceptive. After the last natural period, contraception is needed for `two years` if under `50` and `one year` if `50 or older`.\n\nHormonal contraception can mask the menstrual pattern and make this harder to judge.\n\nReference: [Australasian Menopause Society information sheets](https://www.menopause.org.au/hp/information-sheets).",
      "formerly": [
        "O12"
      ]
    },
    {
      "id": "O14",
      "domain": "OGN",
      "title": "Gynaecological cancer: warning features and referral",
      "focus": "Endometrial, ovarian, cervical and vulval warning features, investigation, referral and hereditary risk.",
      "first_pass": false,
      "priority": "Core",
      "saq_cases": [
        {
          "id": "deck-og-ovarian-cancer",
          "title": "Ovarian cancer",
          "set": "MD3 SAQ Revision Deck"
        },
        {
          "id": "deck-og-postmenopausal-bleeding",
          "title": "Postmenopausal bleeding and cervical screening",
          "set": "MD3 SAQ Revision Deck"
        }
      ],
      "core_ids": [
        "P001",
        "P062"
      ],
      "notes": "Population screening does not replace investigation of symptoms. Each gynaecological cancer has its own warning features, and the referral pathway follows from them.\n\n### Endometrial cancer\n\nPostmenopausal bleeding is the key presentation. Prolonged unopposed oestrogen exposure, obesity and chronic anovulation increase the risk.\n\nTransvaginal ultrasound and endometrial sampling are arranged through the gynaecology pathway. Persistent or recurrent bleeding needs evaluation even after an initially reassuring scan.\n\n### Ovarian cancer\n\nSymptoms are often vague and attributed to the gut. Examine and arrange pelvic ultrasound for persistent, new:\n\n- Bloating or abdominal distension.\n- Early satiety.\n- Pelvic or abdominal pain.\n- Urinary frequency.\n- Weight loss or a palpable mass.\n\nCA-125 contributes to the assessment of a suspicious mass but is neither specific nor a population screening test: benign disease can raise it, and cancer can occur with a normal value. Refer suspicious findings promptly; do not observe indefinitely.\n\n### Cervical cancer\n\nPostcoital or intermenstrual bleeding, persistent unusual discharge or a visible lesion needs speculum examination and diagnostic assessment. In a symptomatic patient, do a clinician-collected co-test (HPV and cytology); routine self-collected screening does not evaluate symptoms.\n\nRefer a suspicious-looking cervix regardless of screening results. Persistent or recurrent postcoital bleeding also needs gynaecological assessment.\n\n### Vulval cancer\n\nPersistent itch, pain, ulceration, a lump or altered pigmentation needs examination. Repeated treatment for presumed thrush can delay the diagnosis, so biopsy or refer persistent or suspicious lesions.\n\nLichen sclerosus needs potent topical corticosteroid treatment and long-term surveillance, because of its association with vulval cancer.\n\n### Referral and hereditary risk\n\nExplain the reason for referral without presenting cancer as certain. Check for anaemia and symptom burden, and make a review plan that tracks the referral and results.\n\nA family history suggesting hereditary breast and ovarian cancer (BRCA) or Lynch syndrome needs referral to a familial cancer service, since confirmed carriers may be offered risk-reducing surgery or surveillance.",
      "formerly": [
        "O13"
      ]
    },
    {
      "id": "M01",
      "domain": "MH",
      "title": "Depression and suicide risk assessment",
      "focus": "Diagnose, identify differential, perform risk formulation, select treatment including ECT and rTMS, and plan follow-up.",
      "first_pass": true,
      "priority": "Core",
      "saq_cases": [
        {
          "id": "2021-ummss-q8",
          "title": "Low mood and fatigue in a young adult",
          "set": "2021 UMMSS"
        },
        {
          "id": "deck-mh-depression-young-adult",
          "title": "Major depressive disorder",
          "set": "MD3 SAQ Revision Deck"
        }
      ],
      "core_ids": [
        "P027",
        "P059",
        "P086"
      ],
      "notes": "### Diagnosis of a depressive episode\n\nA **major depressive episode** requires at least `five symptoms` during the same `two-week` period, including low mood or loss of interest or pleasure, with clinically significant distress or impairment. The other symptoms are:\n\n- Change in appetite or weight.\n- Sleep disturbance.\n- Psychomotor slowing or agitation.\n- Fatigue.\n- Guilt or worthlessness.\n- Poor concentration or indecision.\n- Recurrent thoughts of death or suicide.\n\nPersistence, functional impact and the person's usual baseline matter as much as the symptom count, so the diagnosis rests on clinical assessment rather than a questionnaire. PHQ-9 helps quantify symptoms and monitor response, but clinical assessment determines the diagnosis and safety.\n\n### Assessment\n\n- **Background:** previous episodes and treatment, anxiety, trauma, grief, substance use, medicines and medical symptoms.\n- **Bipolar history:** ask about previous mania or hypomania before prescribing an antidepressant, which can precipitate a switch in bipolar disorder.\n- **Medical contributors:** examine and test for possible contributors such as thyroid disease, anaemia, sleep apnoea or neurological illness.\n\nBereavement does not exclude a depressive episode. Grief usually comes in waves linked to the loss, with some positive emotion preserved; pervasive worthlessness, sustained anhedonia and suicidality suggest depression.\n\nThe **mental state examination** describes appearance and behaviour, speech, subjective mood and observed affect, thought form and content, perception, cognition, insight and judgement.\n\nSevere guilt or nihilistic delusions, hallucinations, catatonia or profound self-neglect indicate psychotic or severe depression, which changes both urgency and treatment.\n\n### Formulating suicide and self-harm risk\n\nAsk directly and calmly about suicide; asking does not increase risk. Explore, in turn:\n\n- Passive wishes to be dead, and active thoughts of suicide.\n- Intent, a specific plan, preparations and access to means.\n- Previous attempts, their lethality and the circumstances of rescue.\n- Recent losses, hopelessness, agitation, insomnia, intoxication and psychosis.\n- The ability to seek help.\n\nSelf-harm can regulate distress without an intention to die, but the two can coexist, and intent can change.\n\nProtective factors are as important to explore as risk factors: relationships, responsibilities, reasons for living, coping strategies and willingness to accept support. Obtain collateral where appropriate, explaining confidentiality and its safety limits. The aim is a formulation that summarises the person's current drivers, available means, supports and foreseeable changes.\n\n> [!pitfall]\n> A risk score or a \"low-risk\" label **does not predict an individual's safety**. Risk fluctuates, and most people who die by suicide were not classified as high risk.\n\n> [!escalate]\n> Immediate intent with a feasible plan, inability to stay safe, severe psychosis, intoxication or major self-neglect needs emergency assessment and supported transfer. **Do not leave an acutely unsafe person alone** while arranging care.\n\nWhen outpatient care is appropriate, agree a written **safety plan**:\n\n- Personal warning signs and coping steps.\n- People and places that help, and clinical and crisis contacts (such as Lifeline, 13 11 14).\n- Safer storage or removal of lethal means.\n- A definite follow-up appointment.\n\nRestricting means matters because suicidal crises are often brief, and the method available at that moment influences the outcome. A promise not to self-harm is no substitute for a plan.\n\n### The four Ps\n\nThe **four Ps** organise a broader formulation:\n\n- **Predisposing:** vulnerabilities.\n- **Precipitating:** the events leading to the current episode.\n- **Perpetuating:** problems maintaining it.\n- **Protective:** factors supporting safety and recovery.\n\nLink each modifiable factor to treatment. For example, insomnia and alcohol may be perpetuating the low mood, while a supportive partner may help put the safety and recovery plan into practice.\n\n### Treatment\n\nMilder depression often responds to behavioural activation, structured psychological therapy, support for sleep and activity, and practical help with stressors.\n\n- **Behavioural activation** schedules small, achievable activities that restore routine, connection and reward. It does not wait for motivation, which usually returns after activity rather than before it.\n- **CBT** addresses unhelpful interpretations and behaviours.\n- **Interpersonal therapy** focuses on relationships and role transitions.\n\nPersistent, moderate or severe depression is often treated with an antidepressant, psychotherapy or both. An SSRI such as sertraline (commonly starting at `50 mg daily`) is a common first choice after considering previous response, interactions, pregnancy plans and adverse effects.\n\nBenefit develops over weeks, while adverse effects appear early, so explain both. Early nausea or jitteriness can occur; sexual dysfunction, sleep change, hyponatraemia and bleeding interactions may also matter. Review within `one to two weeks` of starting, sooner with suicidal thoughts or deterioration. If the response is inadequate after an adequate trial, reassess the dose, adherence and diagnosis.\n\nArrange a GP Mental Health Treatment Plan and referral for psychological therapy where appropriate, explaining access, likely costs and follow-up.\n\nContinue effective treatment for at least `six months` after remission, and longer for recurrent or severe illness, because stopping early carries a high risk of relapse. Then plan a gradual reduction when appropriate.\n\nIn *psychotic depression*, delusions or hallucinations accompany a depressive episode and are usually mood-congruent: guilt, poverty, illness or nihilism, or voices that accuse or condemn. It carries a high risk of suicide and responds poorly to an antidepressant alone, so it needs urgent specialist care and treatment with an antidepressant combined with an antipsychotic, or ECT. Catatonia, life-threatening refusal of food or fluid, or treatment-resistant illness also needs specialist care. ECT may be indicated and can work faster than medication, which matters most when the patient's life is at risk.\n\n*Electroconvulsive therapy* (ECT) induces a brief generalised seizure under general anaesthesia and muscle relaxation, usually two or three times a week over several weeks. It is the most effective treatment for severe depression and is also used for catatonia and selected mania and psychosis. Headache, muscle aches and confusion after each treatment are common. Memory loss for events around the course, and difficulty forming new memories during it, usually improve over weeks to months, although some gaps may remain. In Victoria an adult with capacity gives written consent personally; ECT for an adult without capacity, and for anyone under 18, needs Mental Health Tribunal approval.\n\n*Repetitive transcranial magnetic stimulation* (rTMS) stimulates the prefrontal cortex with a magnetic coil held over the scalp, in daily outpatient sessions over several weeks, without anaesthesia. It is less effective than ECT and is used for depression that has not responded to adequate trials of at least two antidepressants.\n\nThe plan also covers restoring function, the warning signs of relapse and the patient's support network. See M08 (Antidepressants) for prescribing detail.",
      "formerly": [
        "M01"
      ]
    },
    {
      "id": "M02",
      "domain": "MH",
      "title": "Anxiety and panic in primary care",
      "focus": "GAD, panic, social anxiety, medical mimics, psychological/medication treatment and follow-up.",
      "first_pass": true,
      "priority": "Core",
      "saq_cases": [
        {
          "id": "deck-mh-gad",
          "title": "Generalised anxiety disorder",
          "set": "MD3 SAQ Revision Deck"
        },
        {
          "id": "deck-mh-panic-disorder",
          "title": "Panic disorder",
          "set": "MD3 SAQ Revision Deck"
        }
      ],
      "core_ids": [
        "P015",
        "P018",
        "P030"
      ],
      "notes": "### The anxiety disorders\n\nThe anxiety disorders are distinguished mainly by what the fear is about:\n\n- **Generalised anxiety disorder (GAD):** excessive, hard-to-control worry about several areas of life on most days for at least `six months`, with symptoms such as restlessness, fatigue, poor concentration, irritability, muscle tension and disturbed sleep.\n- **Social anxiety disorder:** fear of scrutiny or embarrassment.\n- **Specific phobia:** fear of a circumscribed trigger.\n- **Agoraphobia:** fear and avoidance of situations where escape or help may be difficult, such as public transport, crowds or being out alone. It can occur with or without panic disorder.\n\nWhat the person avoids, and how that affects study, work, relationships and daily tasks, indicates severity.\n\n### Panic attacks and panic disorder\n\nA **panic attack** is a sudden surge of intense fear or discomfort, peaking within minutes, with symptoms such as palpitations, sweating, tremor, breathlessness, chest discomfort, nausea, dizziness, paraesthesia, or fear of dying or losing control.\n\n**Panic disorder** requires recurrent unexpected attacks followed by at least `one month` of persistent worry about further attacks or maladaptive avoidance. Panic attacks also occur in other psychiatric and medical conditions.\n\n### Assessment and medical mimics\n\nAnxiety produces genuine physical symptoms, so medical causes need active consideration. Ask about onset, triggers and duration; caffeine, stimulants and alcohol withdrawal; medicines; sleep; trauma; and depression and suicidal thoughts. Target examination and tests to plausible causes such as arrhythmia, hyperthyroidism, hypoglycaemia or asthma. GAD-7 supports assessment and follow-up but does not replace the history.\n\n> [!pitfall]\n> New exertional chest pain, syncope, persistent hypoxaemia or focal neurological findings needs medical assessment. A previous anxiety diagnosis does not explain every new episode.\n\n### The maintaining cycle\n\nAnxiety activates a normal threat response, which produces real bodily symptoms. Interpreting those symptoms as dangerous amplifies the arousal. Avoidance and repeated reassurance relieve distress briefly but strengthen the belief that the situation is unsafe. Explaining this cycle validates the patient's experience and gives a rationale for treatment.\n\nDuring a likely panic attack, once medical concerns have been checked, provide a calm environment, a clear explanation and slow, comfortable breathing.\n\n> [!pitfall]\n> Do not use paper-bag rebreathing. It can cause hypoxaemia and is dangerous when the cause is cardiac or respiratory.\n\nWhen the episode settles, discuss ongoing treatment and when to return; a sedative alone is not an adequate response.\n\n### Psychological treatment\n\nCBT targets the maintaining cycle directly, combining cognitive work with **graded exposure** to feared situations or bodily sensations. Exposure is planned collaboratively, repeated and progressed, so that the person learns the feared outcome does not happen. Simply telling someone to confront their worst fear is unlikely to help.\n\nAddress excessive caffeine, poor sleep, substance use and practical stressors, and frame goals in functional terms, such as travelling independently or attending classes.\n\n### Medication\n\nAn SSRI or SNRI is appropriate for persistent, impairing anxiety when the patient prefers it or psychological treatment is insufficient or unavailable. Start at a low dose and titrate, because early activation can worsen symptoms. Explain that improvement takes several weeks, describe the common adverse effects, and plan a gradual taper after sustained recovery.\n\nReview early for tolerability, mood and safety, and later for symptoms and avoidance, not only a questionnaire score.\n\nBenzodiazepines cause sedation, impaired driving, falls, dependence and withdrawal. They are **not routine long-term treatment** for anxiety or panic, and relieving anxiety on demand can reinforce avoidance. If one is used for a short-term crisis, specify the duration and review, and assess for alcohol and opioid interactions.\n\n> [!escalate]\n> Significant suicidality, psychosis, severe self-neglect or dangerous withdrawal needs urgent assessment.",
      "formerly": [
        "M02"
      ]
    },
    {
      "id": "M03",
      "domain": "MH",
      "title": "Mania, bipolar disorder and psychosis",
      "focus": "MSE, differentials, risk and capacity, treatment/monitoring, urgent referral.",
      "first_pass": true,
      "priority": "Core",
      "saq_cases": [
        {
          "id": "2020-ummss-q3",
          "title": "Mania and bipolar I disorder",
          "set": "2020 UMMSS"
        },
        {
          "id": "deck-mh-schizophrenia",
          "title": "Schizophrenia and related psychotic disorders",
          "set": "MD3 SAQ Revision Deck"
        }
      ],
      "core_ids": [
        "P009",
        "P036",
        "P100"
      ],
      "notes": "### Mania and hypomania\n\n**Mania** is elevated, expansive or irritable mood with increased energy or activity lasting at least `one week`, or any duration if hospitalisation is needed. At least **three** of the following are present, or **four** if the mood is only irritable:\n\n- Grandiosity.\n- Reduced need for sleep.\n- Pressured speech.\n- Racing thoughts or flight of ideas.\n- Distractibility.\n- Increased goal-directed activity or agitation.\n- Risky behaviour, such as spending, sexual or business risks.\n\n**Hypomania** has the same features for at least `four days`, as an observable change, but without psychosis or marked functional impairment. Marked impairment, psychosis or the need for admission makes an episode manic.\n\n- **Bipolar I disorder:** at least one manic episode.\n- **Bipolar II disorder:** hypomania and a major depressive episode, with no previous mania.\n\nPast hypomania is easily missed. Ask about periods of needing little sleep while still energetic, overspending, increased sexuality, unusual confidence, and activation on antidepressants or stimulants. Ordinary mood fluctuation does not qualify.\n\n### Psychosis\n\n**Psychosis** is impaired reality testing, shown by delusions, hallucinations and disorganised thought or behaviour. It is a syndrome with several causes: schizophrenia-spectrum disorders, mood disorders, substances and medical illness.\n\n- **Hallucination:** a sensory experience without a corresponding external stimulus.\n- **Delusion:** a fixed belief held despite contrary evidence and not explained by the person's cultural or religious context.\n\n**Schizophrenia** requires characteristic active symptoms for about `one month`, within at least `six months` of disturbance, with functional decline and exclusion of other causes. A first presentation can be treated before the eventual diagnosis is clear.\n\nAcute, fluctuating inattention, abnormal observations or neurological signs suggest delirium or medical illness.\n\n### Assessment and engagement\n\nA calm setting, simple language and respectful curiosity make assessment possible. Acknowledge distress without endorsing a delusion or arguing about it, since confrontation tends to entrench the belief.\n\n- **Symptoms:** ask about voices, including commands and whether the person feels able to resist them, which bears directly on risk; persecutory beliefs; sleep; self-care; and substance use.\n- **Collateral:** family or carers can describe the onset, behaviour, function and previous episodes.\n- **Risk:** suicide, violence, vulnerability to exploitation, reckless spending or sexual risk, dependants, and decision-specific capacity.\n\nA first or atypical presentation needs physical and neurological assessment:\n\n- **Common tests:** glucose, FBE, electrolytes and renal function, liver function, TSH and ECG. The ECG also provides a baseline before antipsychotic treatment.\n- **Targeted tests:** urine drug screen, pregnancy test, infection tests or brain imaging, according to findings and with consent.\n\n> [!escalate]\n> Rapid onset with seizures, dyskinesia, autonomic instability or altered consciousness needs emergency investigation for causes such as autoimmune encephalitis; do not assume a primary psychiatric disorder.\n\n### Acute treatment\n\nSevere mania or psychosis usually needs urgent psychiatric involvement and often admission. Reduce stimulation, support hydration, nutrition and sleep, and use verbal de-escalation first.\n\n- **Antipsychotics** treat acute psychosis and mania.\n- **Lithium or another mood stabiliser** may be added in bipolar disorder.\n- **Antidepressants and stimulants:** stop or review with the treating team. **Avoid antidepressant monotherapy in bipolar I disorder**, because it can destabilise mood.\n\nWhen de-escalation fails and the risk is high, offer oral medication first, such as olanzapine or diazepam. If parenteral sedation is needed, give a single agent, commonly IM droperidol, olanzapine or midazolam, to a defined maximum dose rather than an improvised combination. Monitor the airway, observations and level of sedation afterwards, and do not give IM olanzapine with a parenteral benzodiazepine, because together they can cause cardiorespiratory depression.\n\n### Preventing relapse\n\nRecovery depends on preventing relapse as much as on treating the episode. Combine maintenance medication with psychological intervention, family education, reduced substance use and support for study or work. Identify early warning signs in advance, especially reduced sleep, and agree how the person will obtain help.\n\nMonitor for metabolic, cardiovascular, movement and reproductive adverse effects; see M08 (Antipsychotics). Clozapine is considered for treatment-resistant schizophrenia after adequate trials of other antipsychotics, with its specific monitoring.\n\n### Compulsory assessment in Victoria\n\nUse voluntary, supported care whenever possible. Under the **Mental Health and Wellbeing Act 2022**, an assessment order requires that:\n\n- The person appears to have mental illness.\n- They appear to need immediate treatment to prevent serious deterioration or serious harm.\n- An assessment can be carried out under the order.\n- No less restrictive means is reasonably available.\n\nA registered doctor or authorised mental health practitioner must have examined the person within the previous `24 hours`.\n\nAn assessment order **authorises assessment**; it is not general authority for treatment. Compulsory treatment has separate criteria and authorisation. Explain the person's rights, advocacy and review, document the criteria, and seek senior help.\n\n> [!pitfall]\n> A psychiatric diagnosis or order does not remove capacity for unrelated medical decisions.\n\nReference: [Victorian Department of Health: Mental Health and Wellbeing Act](https://www.health.vic.gov.au/mental-health-and-wellbeing-act).",
      "formerly": [
        "M03"
      ]
    },
    {
      "id": "M04",
      "domain": "MH",
      "title": "OCD, trauma and adjustment disorders",
      "focus": "Obsessions/compulsions, PTSD/acute stress, non-pharmacological management and risk.",
      "first_pass": false,
      "priority": "Core",
      "saq_cases": [
        {
          "id": "deck-mh-ocd",
          "title": "Obsessive-compulsive disorder",
          "set": "MD3 SAQ Revision Deck"
        },
        {
          "id": "deck-mh-ptsd",
          "title": "PTSD, acute stress disorder and adjustment disorder",
          "set": "MD3 SAQ Revision Deck"
        }
      ],
      "core_ids": [
        "P018",
        "P079"
      ],
      "notes": "### Obsessive–compulsive disorder\n\n**Obsessions** are intrusive, unwanted thoughts, images or urges that cause distress. **Compulsions** are repeated actions or mental rituals performed to reduce that distress or prevent a feared outcome, often without a realistic connection to it or to an excessive degree. Each ritual brings brief relief, which keeps the cycle going.\n\nOCD is clinically significant when obsessions and compulsions are time-consuming, commonly more than `one hour` a day, or cause substantial distress or impairment. Common themes are contamination, checking, symmetry, and taboo thoughts about harm, sex or religion.\n\nShame often stops people volunteering hidden mental rituals, avoidance, reassurance seeking, time lost and family accommodation, so ask directly.\n\n> [!pitfall]\n> An unwanted intrusive thought about harm is different from a wish or plan to act. Assess intent and risk directly; do not assume either safety or danger.\n\nInsight varies. Distinguish OCD from a fixed delusion, generalised worry and a personality preference for order, and screen for depression and suicidality, which the same shame can conceal.\n\n### Treatment of OCD\n\nThe main psychological treatment is CBT with **exposure and response prevention**: the person gradually faces feared cues while resisting rituals. Repeated exposure teaches that the distress can be tolerated and subsides without the compulsion.\n\nAn SSRI is useful for moderate to severe OCD or by preference. It often needs a longer trial and higher doses than in depression, and the response may take around `12 weeks`.\n\nFamily accommodation sustains the cycle in the same way as the person's own rituals. Help relatives reduce their participation gradually and support functional goals; demanding abrupt cessation does not work.\n\n### PTSD and acute stress disorder\n\n**PTSD** follows exposure to actual or threatened death, serious injury or sexual violence, with symptoms lasting more than `one month` and causing impairment. The symptom groups are:\n\n- Intrusions: memories, nightmares and flashbacks.\n- Avoidance.\n- Negative changes in mood and beliefs.\n- Heightened arousal and reactivity.\n\n**Acute stress disorder** describes similar symptoms from `three days to one month` after the trauma.\n\nNightmares and flashbacks, dissociation, hypervigilance, sleep, guilt, substance use, and effects on relationships and work indicate severity and impact.\n\n### Trauma-informed assessment\n\nTrauma often takes away privacy, choice and control, so give them back during assessment. Explain why questions or examinations are needed, ask permission, allow pauses, and do not press for a detailed account at a first consultation.\n\nDetermine whether the threat is ongoing, including family violence, and address immediate safety first; processing trauma is difficult while danger continues. Assess suicide risk, self-neglect and supports.\n\n### Treatment of PTSD\n\n- **Psychological therapy:** trauma-focused CBT and EMDR are the established first-line treatments.\n- **Medication:** an SSRI or SNRI may help selected patients, particularly with comorbid depression or by preference.\n- **Benzodiazepines** are not routine treatment for PTSD.\n\nPractical support, sleep care, social connection and planned follow-up complement treatment.\n\n> [!pitfall]\n> Do not impose a compulsory single-session emotional debriefing after trauma. It does not prevent PTSD and may worsen outcomes.\n\n### Adjustment disorder and grief\n\n**Adjustment disorder** is distress or functional impairment linked to an identifiable stressor, beginning within `three months` of it and not better explained by another disorder. Symptoms usually resolve within `six months` after the stressor or its consequences end. The diagnosis still requires assessment of safety and function; an understandable cause does not make distress trivial.\n\nManagement supports problem solving, manageable routines, psychological care and social and practical help.\n\nGrief varies with culture and circumstance and has no fixed timetable. Persistent disabling grief, depression, substance use or suicidal thinking needs further assessment. Revisit the working diagnosis if symptoms persist, worsen or develop the features of a more specific disorder.",
      "formerly": [
        "M04"
      ]
    },
    {
      "id": "M05",
      "domain": "MH",
      "title": "Eating disorders and body image",
      "focus": "Medical risk, physical complications, psychological management and multidisciplinary care.",
      "first_pass": true,
      "priority": "Core",
      "saq_cases": [
        {
          "id": "2016-mhagp-q2",
          "title": "Eating disorders",
          "set": "2016 MH/GP"
        },
        {
          "id": "deck-mh-anorexia-adult",
          "title": "Anorexia nervosa in an adult",
          "set": "MD3 SAQ Revision Deck"
        }
      ],
      "core_ids": [
        "P011",
        "P014",
        "P104",
        "P105"
      ],
      "notes": "### The eating disorders, at any body weight\n\nThe eating disorders are distinguished by the behaviours involved and the beliefs that drive them. A **binge** is an unusually large amount of food eaten in a discrete period with a sense of loss of control. **Compensatory behaviours** aim to offset eating and include vomiting, laxatives, fasting and excessive exercise.\n\n- **Anorexia nervosa:** restriction leading to significantly low weight; fear of weight gain or behaviour that prevents it; and disturbed experience of weight or shape, or limited recognition of the seriousness of the illness.\n- **Atypical anorexia nervosa:** the same psychopathology and significant weight loss, without a currently low weight.\n- **Bulimia nervosa:** recurrent binges with compensatory behaviours, usually at least weekly for three months, with self-evaluation unduly influenced by weight and shape.\n- **Binge-eating disorder:** distressing binges at least weekly for three months, without regular compensatory behaviour.\n- **Avoidant/restrictive food intake disorder (ARFID):** restriction because of sensory aversion, low interest in food or fear of consequences such as choking, without weight or shape concerns.\n\n> [!pitfall]\n> **Dangerous starvation can occur at any body size.**\n\nThe rate and percentage of weight loss, intake, purging and physiological state matter more than appearance. Assumptions based on sex, ethnicity or BMI mislead, and families should not be blamed.\n\n### History\n\nA concrete account of a typical day's food, fluid and caffeine intake is more revealing than general questions. Follow it with skipped meals, food rules, bingeing, vomiting, laxative or diuretic use, exercise and body checking.\n\nEstablish the recent and longer-term weight trajectory, and ask about dizziness or syncope, palpitations, cold intolerance, constipation, menstrual change and concentration. Explore mood, suicide and self-harm, trauma, neurodiversity, school or work, social eating and readiness for help.\n\nOffer weighing with consent, including the option of not being told the number.\n\n### Examination and investigations\n\nExamine temperature, lying and standing pulse and BP, hydration and muscle wasting. Bradycardia and hypothermia in this setting reflect adaptation to starvation, not fitness. Lanugo, dental erosion, parotid swelling and calluses on the knuckles (Russell sign) support the history but need not be present.\n\nBaseline investigations:\n\n- ECG.\n- Glucose.\n- FBE.\n- Electrolytes and renal function.\n- Calcium, magnesium and phosphate.\n- Liver function tests.\n\n> [!pitfall]\n> Normal albumin or electrolytes **do not exclude serious malnutrition**; serum levels are maintained while total-body stores are depleted.\n\nVomiting causes a hypokalaemic, hypochloraemic metabolic alkalosis; water loading causes hyponatraemia.\n\n### Setting of care\n\n> [!escalate]\n> Medical instability, severe dehydration, inability or refusal to maintain intake, uncontrolled purging, rapid weight loss or significant suicidality needs urgent specialist assessment.\n\nRCH red flags for admission in **adolescents** are:\n\n- **Heart rate:** awake heart rate below `50`, or a postural rise of more than `50`.\n- **BP:** systolic below `80`, or a postural systolic fall of more than `20 mmHg`.\n- **Temperature:** below `35.5°C`.\n- **ECG:** QTc over `450 ms`.\n- **Bloods:** glucose below `3.0`, potassium below `3.0`, sodium below `130` or phosphate below `0.9 mmol/L`.\n\nThese guide escalation; do not wait for a threshold to be crossed, since several milder abnormalities together can also justify admission. Adult services use their own criteria.\n\n### Nutritional rehabilitation and refeeding\n\nStarvation impairs cardiac function, endocrine activity, gut motility, thinking and emotion. Restoring nutrition is therefore part of medical and psychological treatment, not merely a step before it.\n\nAfter prolonged undernutrition, carbohydrate stimulates insulin release. Phosphate, potassium and magnesium shift into cells and the body retains salt and water, which can cause arrhythmia, oedema, and cardiac or respiratory failure: the **refeeding syndrome**.\n\nStart nutritional rehabilitation under an agreed medical and dietetic plan:\n\n- Assess refeeding risk.\n- Give thiamine when indicated.\n- Correct deficits.\n- Monitor electrolytes, glucose, fluid balance and clinical state.\n\n> [!pitfall]\n> The shifts occur after feeding begins, so a normal baseline phosphate does not remove the risk.\n\nRefeeding precautions must never delay emergency treatment of hypoglycaemia or shock.\n\n### Ongoing treatment\n\nOngoing care coordinates medical monitoring, dietetic support and evidence-based psychological treatment. **Family-based treatment** is central for many adolescents with anorexia; **CBT-E** (enhanced CBT) is used for bulimia and other eating disorders. Practical goals are regular, adequate and varied eating and a gradual return to social eating.\n\nMedication is an adjunct for selected disorders and comorbidities, not a replacement for nutrition and psychological care. Do not prescribe for weight loss as a routine response to binge eating, because restriction often drives the binge cycle.\n\nThe team, patient and family need an agreed way of communicating, a clear owner for monitoring physical risk, and a defined level of deterioration that triggers hospital assessment. Judge recovery by physical stability, eating behaviour, cognition, participation and wellbeing, as well as weight.\n\nReference: [RCH: eating disorders in the emergency department](https://www.rch.org.au/clinicalguide/guideline_index/Management_of_Eating_Disorders_in_the_Emergency_Department/).",
      "formerly": [
        "M05"
      ]
    },
    {
      "id": "M06",
      "domain": "MH",
      "title": "Alcohol, cannabis and other substance use",
      "focus": "Assessing use and dependence, alcohol and benzodiazepine withdrawal, Wernicke encephalopathy, opioid, cannabis and stimulant use, and harm reduction.",
      "first_pass": false,
      "priority": "Core",
      "saq_cases": [
        {
          "id": "deck-mh-alcohol-use-disorder",
          "title": "Alcohol use disorder and withdrawal",
          "set": "MD3 SAQ Revision Deck"
        },
        {
          "id": "2021-ummss-q6",
          "title": "Cannabis use disorder",
          "set": "2021 UMMSS"
        }
      ],
      "core_ids": [
        "P010",
        "P013",
        "P031",
        "P099"
      ],
      "notes": "### Use, dependence and harm\n\nTake a substance history covering what is used, the amount and potency, route, frequency, last use, combinations, and prescribed and over-the-counter medicines. Quantify alcohol in Australian standard drinks of `10 g` each. A non-judgemental approach improves disclosure.\n\nDependence is suggested by:\n\n- Craving and impaired control.\n- Tolerance and withdrawal.\n- Unsuccessful attempts to cut down.\n- Continued use despite harm.\n\n**Physical dependence** is physiological adaptation that causes withdrawal when a substance is reduced or stopped. It can develop during appropriate prescribed treatment and does not by itself establish a substance use disorder.\n\nExplore harms: overdose, withdrawal seizures, driving, finances, injecting, sexual risk, mood and psychosis, violence, and dependent children.\n\nAddress immediate safety before a longer motivational discussion: intoxication, respiratory depression, altered consciousness, agitation and medical complications. Capillary glucose, observations and targeted ECG and blood tests help when the person is acutely unwell. A urine drug screen can support selected assessments, but it does not establish impairment or replace the history.\n\n### Alcohol and sedative withdrawal\n\nAlcohol is a central nervous system depressant. With chronic use the brain adapts to its presence, so a fall in intake produces rebound excitation.\n\n- **Early withdrawal:** begins within hours, with tremor, sweating, nausea, anxiety and tachycardia.\n- **Withdrawal seizures:** most often within the first `48 hours`.\n- **Delirium tremens:** usually later, often at `48–72 hours`, with delirium and autonomic instability.\n\n> [!pitfall]\n> **A detectable blood alcohol level does not exclude withdrawal** in a dependent person.\n\nSupervised inpatient withdrawal is indicated by previous seizures or delirium tremens, heavy dependence, pregnancy, frailty, major medical or psychiatric illness, or inadequate support at home.\n\nTreat with a monitored benzodiazepine regimen, usually diazepam, which acts on the same GABA system and has a long half-life, guided by a withdrawal scale. Add hydration, correction of electrolytes and thiamine. Other causes of delirium or seizures still need investigation.\n\n> [!pitfall]\n> Phenytoin does not prevent or treat alcohol-withdrawal seizures.\n\n### Wernicke encephalopathy\n\nConfusion, ataxia or eye-movement abnormalities in a nutritionally depleted drinker suggest **Wernicke encephalopathy**, although the full triad is often absent.\n\n> [!escalate]\n> Give high-dose parenteral thiamine promptly when Wernicke encephalopathy is suspected or absorption is unreliable, commonly `300–500 mg IV three times daily` for `3–5 days`; protocols vary.\n\nGive thiamine before or with carbohydrate where feasible, because glucose metabolism consumes thiamine, but never delay urgent glucose for hypoglycaemia.\n\n### Benzodiazepine withdrawal\n\nWithdrawal causes anxiety, insomnia, tremor, perceptual disturbance and, after abrupt cessation of regular high doses, seizures or delirium. Its onset depends on the half-life of the drug. Dependence needs a planned gradual taper, usually after conversion to a long-acting benzodiazepine such as diazepam, over weeks to months, agreed with the patient and prescribed by a single clinician. Combining benzodiazepines with opioids or alcohol increases the risk of fatal respiratory depression.\n\n### Treating the disorder beyond withdrawal\n\nWithdrawal alone does not prevent relapse. **Motivational interviewing** asks permission, explores the person's goals and ambivalence, reflects their reasons for change and agrees an achievable next step. Psychological care, peer and community support, and treatment of coexisting illness form the foundation.\n\nMedicines for alcohol dependence:\n\n- **Naltrexone:** reduces craving and the rewarding effect of alcohol. It blocks opioid receptors, so it is unsuitable with current opioid use; check liver function.\n- **Acamprosate:** supports abstinence; check renal function. Three-times-daily dosing can affect adherence.\n- **Disulfiram:** for carefully selected, supervised patients after discussing the alcohol reaction and contraindications.\n\n### Opioid use disorder\n\nOpioid use disorder responds to buprenorphine or methadone with appropriate prescribing and psychosocial care. Standard buprenorphine induction begins once withdrawal has developed, because buprenorphine is a high-affinity partial agonist that displaces other opioids and can precipitate withdrawal if started too early. Specialist low-dose induction methods differ.\n\n> [!counsel]\n> Take-home naloxone can reverse an overdose, but call 000 and support breathing as well. Naloxone is short-acting and toxicity can return.\n\nTolerance falls after a period of abstinence, so the overdose risk rises sharply on relapse, especially with alcohol or benzodiazepines.\n\n### Cannabis and stimulants\n\nCannabis use disorder follows the same pattern of impaired control, craving and continued use despite harm. Heavy use impairs attention, memory, motivation and driving. Early, frequent and high-potency use increases the risk of psychosis and worsens established psychotic illness.\n\n- **Cannabis withdrawal:** irritability, anxiety, insomnia, vivid dreams, reduced appetite and craving, starting within one or two days and lasting up to two weeks or more. It is uncomfortable rather than dangerous, but often drives relapse.\n- **Cannabinoid hyperemesis syndrome:** recurrent bouts of vomiting in long-term heavy users, often relieved by hot showers, which resolve only with stopping cannabis.\n- **Stimulants:** can cause chest pain, hypertension, hyperthermia, agitation, aggression and psychosis, followed by low mood and exhaustion on withdrawal.\n\nPsychosocial interventions are central: motivational interviewing, CBT and contingency management, with treatment of coexisting anxiety, depression or psychosis. No medicine is established for cannabis or stimulant dependence. Severe toxicity or a safety concern needs urgent medical or psychiatric treatment.\n\n### Harm reduction and follow-up\n\nOffer sterile injecting equipment, hepatitis B vaccination, HIV and hepatitis testing, and treatment pathways where relevant. Advise against using alone, warn that potency is unpredictable and that sedative combinations are dangerous, and advise safe storage away from children.\n\nAgree a follow-up appointment and a relapse plan that encourages a return to care without blame. GP, addiction, mental health and social services work best in coordination, and making access conditional on complete abstinence tends to exclude the people at greatest risk.\n\nReference: [NSW Health: withdrawal clinical guidance](https://www.health.nsw.gov.au/aod/professionals/Pages/clinical-guidance.aspx).",
      "formerly": [
        "M06"
      ]
    },
    {
      "id": "M07",
      "domain": "MH",
      "title": "Personality disorders, distress and self-harm",
      "focus": "Personality disorders, self-harm, crisis response, discharge planning after self-harm and longer-term care.",
      "first_pass": true,
      "priority": "Core",
      "saq_cases": [
        {
          "id": "2021-ummss-q5",
          "title": "Discharge planning after an overdose (borderline personality disorder)",
          "set": "2021 UMMSS"
        },
        {
          "id": "deck-mh-borderline-pd",
          "title": "Borderline personality disorder",
          "set": "MD3 SAQ Revision Deck"
        }
      ],
      "core_ids": [
        "P044",
        "P079",
        "P086",
        "P091",
        "P100"
      ],
      "notes": "### Personality disorder\n\nA *personality disorder* is an enduring pattern of inner experience and behaviour that differs markedly from cultural expectations, is pervasive and inflexible across situations, begins by adolescence or early adulthood, and causes distress or impairment. The diagnosis describes a long-standing pattern, not a single difficult encounter or a reaction to acute stress.\n\nDSM-5 groups the personality disorders into three clusters, which are more useful as a memory aid than as a clinical distinction:\n\n- **Cluster A (odd or eccentric):** paranoid, schizoid and schizotypal.\n- **Cluster B (dramatic, emotional or erratic):** antisocial, borderline, histrionic and narcissistic.\n- **Cluster C (anxious or fearful):** avoidant, dependent and obsessive–compulsive.\n\nICD-11 instead rates personality disorder by severity (mild, moderate or severe) and describes the prominent traits, with an optional borderline pattern specifier.\n\nTemperament and early experience combine in the development of these patterns. In the biosocial account of borderline personality disorder, which underpins dialectical behaviour therapy, an emotionally sensitive child grows up in an environment that repeatedly dismisses or punishes emotional experience, and so does not learn to recognise, tolerate or regulate strong emotion. Childhood abuse, neglect and disrupted attachment are common in the history, but they are neither necessary nor sufficient for the diagnosis.\n\n#### Borderline personality disorder\n\nThe core features are instability of emotion, relationships and self-image, together with impulsivity. DSM-5 requires five of the following nine:\n\n- Frantic efforts to avoid real or imagined abandonment.\n- Unstable, intense relationships that swing between idealisation and devaluation.\n- An unstable sense of self.\n- Impulsivity in at least two potentially self-damaging areas, such as spending, sex, substances, driving or binge eating.\n- Recurrent suicidal behaviour, threats or self-harm.\n- Marked emotional reactivity, with intense dysphoria, irritability or anxiety lasting hours to a few days.\n- Chronic emptiness.\n- Intense, poorly controlled anger.\n- Transient stress-related paranoia or dissociation.\n\nOnset is usually in adolescence or early adulthood. Many people no longer meet the criteria some years later, although difficulties with relationships and work can persist. Australian guidance supports making the diagnosis in adolescents when the features are clear, because early treatment helps.\n\nDepression, bipolar disorder, PTSD and complex PTSD, substance use, autism, ADHD and medical illness are alternatives or comorbidities. Rapid mood changes in response to interpersonal events differ from sustained manic episodes with reduced need for sleep and increased energy. Complex PTSD shares emotional dysregulation, a negative self-concept and relationship difficulty, but follows prolonged or repeated trauma and includes core PTSD symptoms.\n\n> [!pitfall]\n> A personality disorder diagnosis does not make new physical symptoms less credible.\n\n#### Other personality disorders\n\n- **Antisocial:** persistent disregard for and violation of the rights of others, with deceitfulness, impulsivity, aggression and lack of remorse. The diagnosis requires an age of at least 18 and evidence of conduct disorder before 15.\n- **Narcissistic:** grandiosity, a need for admiration and limited empathy, often with fragile self-esteem.\n- **Schizotypal:** odd beliefs, perceptual distortions, eccentricity and social anxiety without sustained psychosis; it is genetically related to schizophrenia.\n- **Avoidant:** pervasive social inhibition and fear of rejection, overlapping heavily with social anxiety disorder.\n- **Obsessive–compulsive personality disorder:** perfectionism, rigidity and preoccupation with order and control. Unlike OCD, the traits are usually experienced as reasonable rather than as unwanted intrusions; see M04 (Obsessive–compulsive disorder).\n\nThe same principles apply across these types. Make the diagnosis only after enough contact to see an enduring pattern, and look for comorbid depression, anxiety and substance use, which are common, treatable and often the reason the person presents. Explain the pattern in terms of its effects on the person's life rather than as a label. Consistent, predictable care with clear and explained boundaries suits most people. Psychological therapy has the best evidence: CBT-based approaches for avoidant personality, as for social anxiety, and schema or other structured therapies through specialist services. In antisocial personality disorder, the priorities are managing violence risk, substance use and comorbidity; no medication treats the disorder itself.\n\n### Self-harm\n\n*Self-harm* is intentional self-poisoning or self-injury, whatever the motive or the degree of suicidal intent. Cutting and overdose of prescribed or over-the-counter medicines, particularly paracetamol, are the methods most often seen in hospital.\n\nSelf-harm often relieves unbearable emotion, ends dissociation, punishes the self or communicates distress, and understanding what it does for the person guides the response. It is not confined to personality disorder: it occurs with depression, substance use, psychosis and acute crises, and acute distress after a loss or interpersonal crisis is not in itself a disorder; see M04 (Adjustment disorder and grief).\n\n> [!pitfall]\n> Recurrent self-harm can regulate distress and still coexist with substantial suicide risk.\n\n**Previous self-harm is the strongest single predictor of suicide**, and the risk is highest in the weeks after discharge from hospital. Ask about suicide and formulate risk as described in M01 (Formulating suicide and self-harm risk).\n\n### Responding to a crisis\n\nAssess injury, poisoning, intoxication and medical stability first. After an overdose, establish what was taken, how much and when, including whether doses were staggered over hours, and assume other substances until shown otherwise. Measure a paracetamol level in every deliberate overdose, at `four hours` or later after a single ingestion, because early toxicity is silent and treatment is time-critical. An ECG helps when a drug may affect cardiac conduction, and the Poisons Information Centre (13 11 26) advises on specific agents.\n\nPsychiatric assessment proceeds once the person is medically fit and no longer intoxicated. Explore the episode: the sequence of events, what the person was feeling, what the self-harm did for them, any intent to die, planning, access to means, and what has changed since. Current capacity, supports, dependants and the ability to use a safety plan complete the assessment.\n\nUse calm, validating language: acknowledge the distress and explore what would help over the next few hours. **Validation** means recognising the experience, not agreeing that self-harm is the only solution.\n\nExplain limits and decisions consistently, avoid threats and punitive responses, and include the person in practical choices; inconsistency and punishment tend to escalate distress. Obtain collateral and involve supports with consent where possible, explaining the safety exceptions.\n\n> [!escalate]\n> Urgent admission or specialist assessment is needed when safety cannot be maintained or there is severe comorbid illness. If the person refuses and the criteria are met, compulsory assessment may be needed; see M03 (Compulsory assessment in Victoria).\n\nWhen admission is needed, clarify its purpose and the review plan. Automatic, open-ended admission for every crisis can disrupt effective longer-term care and undermine the person's confidence in their own coping.\n\n### Discharge after self-harm\n\nDischarge is a period of high risk, so the plan needs to be concrete, shared with the people who will carry it out, and followed up actively rather than left to the person to return if things get worse. It covers:\n\n- **Medical clearance:** toxicity treated or excluded, and injuries managed.\n- **Assessment and formulation:** a documented psychosocial assessment and risk formulation, with the precipitants, such as relationship breakdown, housing, debt or substance use, addressed where possible.\n- **Safety plan:** agreed collaboratively, identifying triggers, warning signs, coping and distraction strategies, supportive people and crisis contacts such as Lifeline (13 11 14) and the Suicide Call Back Service (1300 659 467).\n- **Means safety:** removal of stockpiled medicines, limited supply (for example, staged or weekly dispensing by a pharmacy) and questions about access to firearms.\n- **Supports:** family or other supports involved with consent, and the welfare of any dependent children checked.\n- **Follow-up:** a specific appointment within days and contact within the first week. In Victoria, the Hospital Outreach Post-suicidal Engagement (HOPE) program provides assertive aftercare; young people can be linked with headspace.\n- **Communication:** a prompt discharge summary to the GP and community team, stating the plan, medication changes and who is responsible for each part of the follow-up.\n\n### Longer-term care\n\n**Structured psychotherapy is the main treatment for borderline personality disorder.** Dialectical behaviour therapy (DBT) teaches mindfulness, distress tolerance, emotion regulation and interpersonal skills. Mentalisation-based treatment and good psychiatric management are other effective approaches.\n\nA consistent team, a shared formulation and predictable contact reduce the fragmentation of care that tends to escalate crises. In general practice, regular scheduled appointments, rather than appointments only in crisis, reduce reactive presentations, and a GP Mental Health Treatment Plan supports access to psychological therapy. Goals should include relationships, study or work and meaningful activity, not only fewer crises.\n\nNo medication treats a personality disorder as a whole. Prescribe only for a defined comorbid disorder or a specific, time-limited target, and review benefit and harm. Avoid accumulating sedatives or multiple drugs without a clear purpose, particularly where overdose or dependence is a concern.\n\nDocument observations and reasoning neutrally, avoiding labels such as \"manipulative\" or \"attention seeking\". Recovery is possible, and an understandable explanation of the diagnosis can support engagement.",
      "formerly": [
        "M07"
      ]
    },
    {
      "id": "M08",
      "domain": "MH",
      "title": "Psychiatric prescribing and monitoring",
      "focus": "SSRI counselling, antipsychotics, clozapine/lithium monitoring, interactions, side effects and consent.",
      "first_pass": true,
      "priority": "Core",
      "saq_cases": [
        {
          "id": "2021-ummss-q3",
          "title": "Counselling on starting an SSRI",
          "set": "2021 UMMSS"
        },
        {
          "id": "2021-ummss-q4",
          "title": "Clozapine monitoring",
          "set": "2021 UMMSS"
        },
        {
          "id": "2016-mhagp-q1",
          "title": "Altered sleep and behaviour in a young adult",
          "set": "2016 MH/GP"
        }
      ],
      "core_ids": [
        "P023",
        "P100"
      ],
      "notes": "### Principles of psychiatric prescribing\n\nBase prescribing on the working diagnosis, previous responses, current medicines and substances, pregnancy potential, medical comorbidities and the patient's priorities. Counselling covers the expected benefit and when it starts, common adverse effects, serious warning symptoms, interactions, what to do after a missed dose, and how treatment will be reviewed. Use teach-back to check understanding.\n\nA measurable target, such as better sleep and function or fewer hallucinations, makes review meaningful.\n\n### Antidepressants\n\nSSRIs are the common first-line medicines for depression and anxiety. For a typical adult, sertraline starts at `50 mg daily`; `25 mg` may be better tolerated initially in anxiety or frailty. Titrate according to response and adverse effects, without frequent changes before benefit has had time to emerge. Check for bipolar history first, and review early after starting or increasing the dose.\n\nThe adverse effects differ by class:\n\n- **SSRIs:** nausea, headache, sleep change, sexual dysfunction and initial activation. Hyponatraemia is more likely in older people and with diuretics. SSRIs increase bleeding risk, especially with NSAIDs, antiplatelets or anticoagulants, because platelets depend on serotonin uptake for aggregation.\n- **SNRIs:** as for SSRIs, and can raise BP.\n- **Mirtazapine:** sedation and increased appetite and weight.\n- **Tricyclics:** anticholinergic, orthostatic and cardiac effects; dangerous in overdose.\n\n> [!escalate]\n> **Serotonin toxicity** presents with agitation, sweating, diarrhoea, tremor, hyperreflexia and clonus, sometimes with hyperthermia, after serotonergic combinations or dose changes. Stop the causative medicines and arrange emergency care.\n\nStopping an antidepressant abruptly can cause dizziness, flu-like symptoms, sensory disturbance and anxiety. Plan a gradual, individualised taper, particularly after long treatment or with drugs prone to discontinuation symptoms.\n\n### Antipsychotics\n\nRecord weight or BMI, waist circumference, BP, glucose or HbA1c and lipids at baseline. Repeat them early after starting, commonly at about `three months`, because weight and metabolic changes are often greatest in the first months, then periodically. Also review movement symptoms, sedation, orthostatic hypotension, prolactin-related effects and sexual function, with an ECG when QT or cardiac risk, or the chosen drug, requires it. Discuss adherence openly; long-acting injections are a collaborative option.\n\nMost movement effects reflect dopamine blockade in the basal ganglia:\n\n- **Acute dystonia:** painful sustained muscle contractions, often within days of starting.\n- **Akathisia:** distressing inner restlessness, which can be mistaken for worsening agitation.\n- **Parkinsonism:** slowed movement with rigidity and/or tremor.\n- **Tardive dyskinesia:** delayed-onset involuntary movements, often of the mouth and tongue.\n\nParkinsonism and tardive dyskinesia need medication review.\n\n> [!escalate]\n> Fever, marked rigidity, altered mental state and autonomic instability suggest **neuroleptic malignant syndrome**. Stop the antipsychotic and arrange emergency care.\n\nNeuroleptic malignant syndrome is distinguished from serotonin toxicity by \"lead-pipe\" rigidity and slower onset, whereas clonus and hyperreflexia dominate serotonin toxicity; both can be fatal.\n\n### Lithium\n\nLithium has a narrow therapeutic range.\n\n- **Before starting:** renal function and electrolytes, TSH, calcium, cardiac risk and pregnancy status. Lithium can cause renal impairment, hypothyroidism and hyperparathyroidism.\n- **After starting or changing the dose:** measure a level `12 hours` after the last dose, once steady state is reached at about `five to seven days`. A maintenance range of `0.6–0.8 mmol/L` is common; the specialist sets the individual target, often lower in older people.\n- **Ongoing:** recheck the level and renal, thyroid and calcium status regularly, and sooner with illness, dehydration or interacting medicines.\n\nThe kidney handles lithium much like sodium. NSAIDs, ACE inhibitors, ARBs and thiazides reduce its clearance and raise levels.\n\n> [!counsel]\n> Keep fluid and salt intake steady, because sodium depletion increases lithium reabsorption. Seek advice during vomiting, diarrhoea or fever.\n\n> [!escalate]\n> A new coarse tremor, vomiting, ataxia, confusion or marked drowsiness suggests lithium toxicity. Withhold lithium and arrange an urgent level, renal assessment and treatment; do not wait for a trough time when toxicity is suspected.\n\n### Other mood stabilisers\n\n- **Valproate:** high risk of major fetal malformation and neurodevelopmental harm. Avoid it for psychiatric indications in anyone who could become pregnant unless exceptional specialist circumstances apply. Monitor liver and haematological effects.\n- **Lamotrigine:** titrate slowly because of the risk of serious rash. A significant new rash needs prompt assessment.\n\nPregnancy planning on any mood stabiliser needs specialist advice balancing fetal exposure against the risk of relapse; patients should not stop treatment abruptly on their own.\n\n### Clozapine\n\nClozapine requires registered prescribing and dispensing and mandatory neutrophil monitoring, because it can cause agranulocytosis.\n\n> [!escalate]\n> Fever or sore throat on clozapine needs urgent assessment for infection and a same-day FBE.\n\n- **Myocarditis:** persistent tachycardia, chest pain, breathlessness or fever in the first weeks; check troponin and CRP.\n- **Constipation:** anticholinergic slowing of the gut can progress to fatal ileus. Ask about bowel function at every review, prevent constipation actively, and assess pain, distension or vomiting urgently.\n- **Levels:** stopping smoking (smoke induces CYP1A2) and acute infection can raise clozapine levels; notify the treating service.\n- **Interruption:** after missed doses, tolerance to its cardiovascular and sedative effects is lost, so re-titration may be needed. Check before restarting the previous dose.\n\nReferences: [Australian Prescriber: lithium](https://australianprescriber.tg.org.au/articles/lithium-therapy-and-its-interactions.html); [Australian clozapine product information](https://www.safetyandquality.gov.au/medicine-finder/clozaril).",
      "formerly": [
        "M08"
      ]
    },
    {
      "id": "M09",
      "domain": "MH",
      "also_in": [
        "GP"
      ],
      "title": "Somatic symptom and related disorders",
      "focus": "Somatic symptom disorder, illness anxiety and functional neurological symptoms; investigation and structured care.",
      "first_pass": false,
      "priority": "Selective",
      "saq_cases": [
        {
          "id": "deck-mh-somatic-symptom",
          "title": "Somatic symptom and related disorders",
          "set": "MD3 SAQ Revision Deck"
        }
      ],
      "core_ids": [
        "P091"
      ],
      "notes": "### Persistent physical symptoms\n\nPhysical symptoms may reflect organic disease, functional mechanisms, psychological distress or a combination.\n\n- **Somatic symptom disorder:** distressing physical symptoms with persistent, disproportionate thoughts, feelings or behaviours about them. It does not require proof that no physical disease exists.\n- **Illness anxiety disorder:** fear of having a serious illness despite few or no symptoms.\n- **Functional neurological disorder:** diagnosed from positive clinical features showing inconsistency with recognised neurological disease, such as Hoover sign, not simply from normal imaging.\n\nIn these disorders the symptoms are not consciously produced. In *factitious disorder* symptoms are deliberately feigned or induced to occupy the sick role, and in malingering they are feigned for external gain. Depression, anxiety and past trauma commonly coexist and need treatment in their own right.\n\n### Assessment\n\nThe symptoms are real, and acknowledging that is the basis of a working relationship. The chronology, red flags, previous investigations, functional effects, and the patient's beliefs and worries determine how much further testing is justified.\n\nAppropriate examination, review of records and investigation of plausible disease are still needed. Repeated low-yield tests without a new indication tend to reinforce worry rather than relieve it, so agree in advance which new features would prompt further investigation. Ask what the patient believes is causing the symptoms and what they fear, and screen for depression, anxiety and medicine or substance use.\n\n> [!pitfall]\n> A functional diagnosis does not protect against organic disease, which develops at the usual rate. Reassess any new objective change on its merits.\n\n### Management\n\nExplain a coherent mechanism, such as altered threat processing and heightened sensitivity to bodily signals, without implying that the symptoms are imagined. Name what the diagnosis is, rather than ending with what the tests have excluded; \"nothing is wrong\" is heard as disbelief.\n\nGive care a predictable structure: regular scheduled reviews, one coordinating clinician, and goals for sleep, activity and participation. CBT helps across these disorders, physiotherapy-led rehabilitation helps functional neurological disorder, and an antidepressant may help comorbid depression or anxiety.",
      "formerly": [
        "M09"
      ]
    },
    {
      "id": "M10",
      "domain": "MH",
      "also_in": [
        "OGN"
      ],
      "title": "Perinatal mental health",
      "focus": "Perinatal depression and anxiety, EPDS, baby blues, intrusive thoughts and postpartum psychosis.",
      "first_pass": true,
      "priority": "Core",
      "saq_cases": [
        {
          "id": "deck-mh-postpartum-depression",
          "title": "Postpartum depression",
          "set": "MD3 SAQ Revision Deck"
        }
      ],
      "core_ids": [
        "P027"
      ],
      "notes": "### Perinatal depression and anxiety\n\nDuring pregnancy and after birth, ask about mood, anxiety, sleep, bonding, support, family violence, previous psychiatric illness and substance use. Risk is higher with previous depression or anxiety, bipolar disorder, earlier perinatal illness, limited support, relationship conflict, adverse life events, and a traumatic birth or a baby needing intensive care.\n\nThe **Edinburgh Postnatal Depression Scale** (EPDS) is a screening tool, used in pregnancy and again after birth. A score of `≥13` suggests probable depression, and any positive response to the self-harm question needs immediate assessment of safety. Follow concerning responses with clinical assessment rather than treating the score as a diagnosis. Practical infant care and feeding, maternal physical illness, and whether the person can rest with the support available complete the assessment.\n\n**Baby blues** cause tearfulness and emotional lability in the first days after birth and settle within `two weeks`.\n\nPersistent low mood or anhedonia, functional impairment, severe anxiety or suicidality suggests a perinatal mood or anxiety disorder that needs treatment; depression may begin during pregnancy. Treatment includes psychological therapy, practical and partner or family support, and medication when indicated after weighing the risks of illness against those of exposure. SSRIs, commonly sertraline, are the usual first-line medicines in pregnancy and breastfeeding. Valproate should be avoided in anyone who may become pregnant; see M08 (Other mood stabilisers). The maternal and child health nurse and PANDA (1300 726 306) provide support, and partners can also develop perinatal depression.\n\n> [!pitfall]\n> Untreated maternal illness carries risks for both mother and baby. Do not stop effective psychiatric treatment abruptly because of pregnancy or breastfeeding; coordinate perinatal specialist advice.\n\n### Intrusive thoughts of harm\n\nUnwanted intrusive thoughts of accidental or deliberate harm to the baby are common in perinatal anxiety and OCD and can be intensely distressing. Ask whether the thoughts are unwanted, whether there is any intent, and whether the person holds delusional explanations or hears commands. These distinguish common intrusive thoughts from immediate danger; do not assume either.\n\n### Postpartum psychosis\n\n> [!escalate]\n> Rapid onset of insomnia, agitation, elevated or depressed mood, confusion, bizarre beliefs or hallucinations after birth suggests **postpartum psychosis**, often related to bipolar disorder. It is **an emergency** even if the person denies suicidal thoughts: the illness can escalate within hours and judgement about self and baby is impaired.\n\nBipolar disorder or a previous episode of postpartum psychosis greatly increases the risk, so these patients need a perinatal mental health plan before birth and close review in the first weeks afterwards.\n\n- Arrange emergency specialist assessment and admission; a mother–baby unit may be suitable where available.\n- Make sure the mother is supported and the baby is safely cared for, and assess both suicide risk and risk to the infant.\n- Do not leave the mother solely responsible for the baby while acute psychosis is being assessed.",
      "formerly": [
        "M09"
      ]
    },
    {
      "id": "R01",
      "domain": "RAPP",
      "title": "Comprehensive geriatric assessment and frailty",
      "focus": "Domains: illness, function, cognition, mood, nutrition, medication, falls, social supports; priorities and care plan.",
      "first_pass": true,
      "priority": "Core",
      "saq_cases": [
        {
          "id": "deck-geri-balance-falls-meds",
          "title": "Disequilibrium, falls and medication review",
          "set": "MD3 SAQ Revision Deck"
        },
        {
          "id": "2020-ummss-q7",
          "title": "Rehabilitation after hip arthroplasty",
          "set": "2020 UMMSS"
        }
      ],
      "core_ids": [
        "P043",
        "P044",
        "P045",
        "P059"
      ],
      "notes": "### Definitions\n\n**Comprehensive geriatric assessment** (CGA) is a coordinated, multidisciplinary assessment of medical problems, function, cognition, mood and social circumstances that leads to an agreed care plan.\n\n**Frailty** is reduced physiological reserve with increased vulnerability to stressors. It overlaps with multimorbidity and disability but is not the same as either, or as chronological age.\n\n> [!pitfall]\n> Do not label a person with stable lifelong disability as frail solely because they need assistance.\n\n### The baseline\n\nCGA starts with the person's priorities and their usual function before the current illness. Together these define the goal and the baseline against which recovery is judged. Collateral from family, carers, the GP or services is often essential, obtained with consent and alongside the patient's own account.\n\nScore frailty on pre-illness function; scoring temporary dependence during an acute illness underestimates what recovery can achieve.\n\nUse a professional interpreter when needed and make sure glasses and hearing aids are working, because language and sensory barriers can mimic cognitive impairment. Speak to the patient directly, allow time to respond and confirm understanding. For Aboriginal and Torres Strait Islander patients, ask about preferred family involvement, community connections and Aboriginal health services; do not assume a uniform cultural preference.\n\n### The assessment domains\n\n- **Medical:** active diagnoses, pain, recent falls and admissions, cardiorespiratory symptoms, continence and constipation, nutrition, sleep, vision and hearing, oral health and medication harms. Older people often present with falls, delirium or loss of function instead of a typical focal symptom.\n- **Basic activities of daily living (ADLs):** bathing, dressing, toileting, transfers, continence and eating. Record whether each needs prompting, supervision or physical help; Barthel or Katz scales structure this.\n- **Instrumental ADLs:** shopping, cooking, housework, transport, phone and technology, medicines and finances. These often decline before basic self-care, because they demand more of cognition and mobility.\n- **Mobility:** walking distance and aid, transfers, stairs, balance, gait speed, chair rises and fear of falling. A corridor walk does not establish safety at home.\n- **Cognition and mood:** acute change and inattention, longer-term memory or executive problems, depression, anxiety, alcohol use, and decision-specific capacity. Screening tools support history and collateral; they do not replace them.\n- **Social and environmental:** who lives at home, whether carers are available and willing, housing and access, finances, isolation, cultural needs, concerns about abuse or neglect, and existing services.\n\n### From findings to a care plan\n\nDeal with reversible contributors first: dehydration, infection, undertreated pain, depression, medication effects and undernutrition. Group interacting problems: a sedating drug may worsen balance, continence, cognition and participation at once, so stopping it can improve all four.\n\nWeigh preventive treatments against their time to benefit and treatment burden. A frailty score informs risk and planning but **does not by itself determine eligibility for treatment or a ceiling of care**.\n\nChoose a small number of useful goals, such as walking to the toilet with one aid, eating enough, or returning home with reliable support for medicines. Allocate each action to a team member with a review date:\n\n- **Physiotherapy:** strength and balance.\n- **Occupational therapy:** daily activities, equipment and the home.\n- **Dietetics:** nutrition.\n- **Pharmacy:** medicines.\n- **Social work:** supports and services.\n\nMeasure progress in function as well as laboratory results.\n\n### Community care\n\nMy Aged Care is the entry point for aged-care assessment.\n\n> [!current]\n> **Support at Home** replaced Home Care Packages and Short-Term Restorative Care in November 2025. The Commonwealth Home Support Programme (CHSP) remains a separate entry-level programme.\n\nPeople may also need community rehabilitation, nursing, respite, residential care or disability services. Check eligibility and actual availability. Family carers need their own assessment and support, since carer breakdown is a common reason that a home plan fails.\n\n### Elder abuse and safeguarding\n\nAsk privately whether the person feels safe, who controls their money and medicines, and whether they feel neglected or pressured. Assess immediate danger and capacity, document objective findings, and seek senior and social work advice. Respect an informed adult's choices while addressing coercion and practical barriers.\n\nA plan is complete only when the patient and the receiving team know who will carry it out.\n\nReference: [Australian Government: Support at Home](https://www.health.gov.au/our-work/support-at-home).",
      "formerly": [
        "R01"
      ]
    },
    {
      "id": "R02",
      "domain": "RAPP",
      "title": "Falls, fracture and mobility impairment",
      "focus": "Multifactorial falls assessment, gait aids, osteoporosis, delirium prevention and discharge.",
      "first_pass": true,
      "priority": "Core",
      "saq_cases": [
        {
          "id": "2020-ummss-q4",
          "title": "Falls and hip fracture",
          "set": "2020 UMMSS"
        },
        {
          "id": "2021-ummss-q1",
          "title": "Fall in an anticoagulated older woman",
          "set": "2021 UMMSS"
        }
      ],
      "core_ids": [
        "P029",
        "P040",
        "P098"
      ],
      "notes": "### Why the fall happened\n\nFalls in older people usually result from several interacting factors, so even a \"trip\" needs assessment. The circumstances, activity, environment, warning symptoms, loss of consciousness, witness account and recovery suggest the mechanism. Previous falls, medicines, alcohol, vision, footwear, urinary urgency, dizziness and usual mobility identify the contributing risks.\n\nA **long lie** on the floor adds the risks of dehydration, hypothermia, pressure injury and rhabdomyolysis.\n\n### Injuries\n\nLook for head injury, bleeding, spinal injury and fracture, particularly in people taking anticoagulants. Hip pain, a shortened and externally rotated leg, or inability to bear weight suggests hip fracture.\n\n> [!pitfall]\n> Persistent inability to bear weight despite a normal initial X-ray **needs further imaging**, because an occult hip fracture may not be visible on the first films.\n\n> [!escalate]\n> Syncope, a new neurological deficit, acute confusion or abnormal observations needs same-day investigation of the underlying illness.\n\n### Examination and investigations\n\nExamine for intrinsic contributors: cardiovascular and neurological disease, vision, the feet, lower-limb strength and joint movement.\n\nMeasure lying BP after rest, then standing BP at about `one and three minutes` if safe. A fall of at least `20 mmHg systolic` or `10 mmHg diastolic` supports orthostatic hypotension, but symptoms and the timing of medicines also matter.\n\nRecord an ECG for unexplained falls or suspected syncope, and target blood tests to plausible causes such as anaemia, electrolyte disturbance or infection.\n\nWatching the person move is often more informative than a formal examination. Observe rising from a chair, starting to walk, turning and use of aids. The **Timed Up and Go** test involves standing up, walking `three metres`, turning, returning and sitting down; note the quality and safety of movement as well as the time.\n\nCommon intrinsic contributors are poor balance, proximal weakness, peripheral neuropathy, parkinsonism and vestibular disease. An occupational therapy home assessment identifies loose rugs, poor lighting, unsafe bathroom access and barriers to using an aid.\n\n### Hip fracture\n\nGive analgesia promptly, including a regional nerve block where available, which reduces opioid requirements, within coordinated orthopaedic and geriatric care. Review hydration, anaemia, anticoagulation, delirium risk, pressure care and thromboprophylaxis.\n\nProlonged immobility causes its own complications, so early surgery (ideally within `48 hours`) and early mobilisation are usual goals, rather than prolonged bed rest to perfect the control of chronic disease.\n\n### Rehabilitation after hip surgery\n\nPhysiotherapy works on transfers, strength, range of movement, gait and endurance, progressing from bed and chair to toilet, stairs and community tasks. Weight-bearing status and hip precautions depend on the procedure and the surgeon's instructions. If posterior precautions are prescribed, the usual restrictions are avoiding deep flexion, crossing the legs (adduction) and internal rotation, the movements that risk posterior dislocation; they do not apply after every hip operation.\n\nA new refusal or inability to mobilise needs reassessment. Tachycardia and low oxygen saturation after surgery suggest pulmonary embolism, pneumonia, anaemia or cardiopulmonary decompensation, as well as pain, dislocation and delirium.\n\n> [!pitfall]\n> Fear of falling may contribute to reluctance to mobilise, but do not assume it until abnormal observations have been explained.\n\n### Preventing recurrence and planning safe activity\n\nFalls usually have several causes, so prevention combines several measures:\n\n- Progressive strength and balance exercise, and a suitable walking aid.\n- Medication review and treatment of orthostatic hypotension.\n- Vision and footwear care, and home modifications.\n- Osteoporosis treatment after a fragility fracture; see G30 (Oral bisphosphonate). Nutrition, and treatment of vitamin D deficiency when relevant.\n\nAgree how the person will summon help after another fall, and how carers can assist safely.\n\nReturn to driving requires adequate strength, movement and reaction time, safe cognition and vision, and freedom from impairing analgesia. Postoperative restrictions and the Austroads standards apply, with an occupational therapy driving assessment when there is doubt. A fixed number of weeks, or the ability to walk independently, does not by itself establish fitness to drive.\n\nFollow-up covers healing, function, falls prevention and bone protection.",
      "formerly": [
        "R02"
      ]
    },
    {
      "id": "R03",
      "domain": "RAPP",
      "title": "Delirium, dementia and cognitive assessment",
      "focus": "Distinguish acute from chronic changes, causes, cognitive tools and appropriate management.",
      "first_pass": true,
      "priority": "Core",
      "saq_cases": [
        {
          "id": "2020-ummss-q6",
          "title": "Delirium versus dementia",
          "set": "2020 UMMSS"
        },
        {
          "id": "deck-geri-cognitive-assessment",
          "title": "Cognitive assessment in older people",
          "set": "MD3 SAQ Revision Deck"
        },
        {
          "id": "deck-geri-delirium",
          "title": "Delirium",
          "set": "MD3 SAQ Revision Deck"
        }
      ],
      "core_ids": [
        "P009",
        "P021",
        "P024",
        "P100"
      ],
      "notes": "### Delirium, dementia and mild cognitive impairment\n\n- **Delirium:** acute, fluctuating impairment of attention and awareness, with other cognitive changes. It may be hyperactive, hypoactive or mixed. Hypoactive delirium is the form most often missed; a quiet, drowsy patient may be seriously unwell.\n- **Dementia:** acquired, persistent cognitive decline that interferes with independent function.\n- **Mild cognitive impairment:** measurable deficits with preserved independence.\n\nDelirium often occurs on top of dementia, so a reliable account of the baseline and the time course is essential.\n\n### Finding the cause of delirium\n\nDelirium signals an underlying physiological disturbance, which must be found.\n\n- Check observations, oxygen saturation, glucose, hydration and pain.\n- Review recent medication changes, and look for urinary retention, constipation and focal neurological signs.\n- Look for infection or metabolic illness by examination and targeted tests: FBE, electrolytes and renal function, calcium, inflammatory markers and others as indicated.\n\n> [!pitfall]\n> **Bacteriuria alone does not establish UTI** in a confused older person; asymptomatic bacteriuria is common at this age. Look for supporting clinical features.\n\nOrder a CT brain for head injury, focal signs, reduced consciousness or another specific concern, not routinely for every delirium.\n\n### Delirium screening tools\n\nThe **4AT** assesses alertness, brief orientation (AMT4), attention (months of the year backwards) and acute change or fluctuation:\n\n- Score of `4 or more`: possible delirium, with or without cognitive impairment.\n- Score of `1–3`: possible cognitive impairment.\n\n> [!pitfall]\n> A score of zero does not exclude fluctuating illness.\n\nThe **Confusion Assessment Method** (CAM) identifies delirium as an acute or fluctuating change with inattention, plus either disorganised thinking or altered consciousness. Neither tool identifies the cause.\n\n### Cognitive screening tools\n\nFor a chronic complaint, ask for concrete examples of difficulty with memory, language, visuospatial skills and executive function, and relate them to medicines, finances, cooking, navigation and safety. Choose a tool that suits the person's language, education and sensory ability, as well as the question being asked:\n\n- **MMSE or SMMSE:** 30-point test of orientation, registration and recall, attention, language and construction. Insensitive to executive deficits and mild impairment.\n- **MoCA:** 30-point test that adds executive, visuospatial and attention tasks; often more useful in mild impairment. Interpret against education and local norms; a cut-off is not a diagnosis.\n- **RUDAS:** 30-point tool designed to reduce cultural and language bias, covering memory, body orientation, praxis, drawing, judgement and language. Use a professional interpreter where needed; it is not free of every contextual influence.\n- **GPCOG:** brief patient test, with an informant component when indicated; suited to general practice.\n- **KICA:** culturally adapted assessment developed for older Aboriginal people, with versions for different settings; choose the version with local expertise.\n- **NUCOG:** broader assessment of attention, memory, executive, language and visuoconstructional function when more detail is needed.\n\nClock drawing adds visuospatial and executive information but is not culturally or educationally neutral.\n\nFollow standard administration instructions and record the test, version and circumstances. A result obtained during delirium does not represent the person's stable ability. A normal score does not exclude meaningful decline in a previously high-functioning person.\n\n### Dementia subtypes\n\nThe early pattern of deficits points to the underlying disease:\n\n- **Alzheimer disease:** usually begins with episodic memory decline.\n- **Vascular dementia:** executive and gait problems with a vascular history, often with stepwise decline.\n- **Dementia with Lewy bodies:** fluctuating cognition, visual hallucinations, parkinsonism and REM sleep behaviour disorder.\n- **Frontotemporal dementia:** often begins with change in behaviour or language.\n\nMixed pathology is common.\n\n### Evaluation and management of dementia\n\nReview depression, hearing, sleep, alcohol, and anticholinergic or sedating medicines, all of which can worsen cognition. Routine tests include FBE, electrolytes, renal and liver function, calcium, TSH and B12, with structural brain imaging and other tests according to the presentation. Refer rapid progression, young onset, focal findings or an atypical syndrome for specialist assessment.\n\nExplain the diagnosis sensitively, with the person's preferred supports present. Address driving, safety with medicines and finances, carer support, exercise, social activity and future planning while capacity remains.\n\nCholinesterase inhibitors (donepezil, rivastigmine, galantamine) can give symptomatic benefit in selected dementias. They increase vagal tone, so they can cause gastrointestinal upset, weight loss, bradycardia and syncope. Memantine is another option for selected patients. Neither class reverses the underlying disease.\n\n### Managing delirium\n\nTreat the precipitant and the factors that perpetuate confusion: restore hydration and nutrition, manage pain, and support mobility, toileting, sleep and sensory aids. Familiar people and repeated gentle reorientation help. Avoid restraints and unnecessary catheters, which increase agitation, falls and other complications.\n\n> [!pitfall]\n> Antipsychotics do not cure delirium. Reserve them for severe distress or immediate risk of harm after non-drug measures, at a low dose with short-term review.\n\nBenzodiazepines generally worsen delirium, except in specific situations such as alcohol withdrawal.\n\nAfter recovery, reassess cognition and record the episode in the discharge summary, since delirium often signals vulnerability to later decline.\n\nReferences: [4AT guidance](https://www.the4at.com/userguide); [Dementia Australia: RUDAS](https://www.dementia.org.au/professionals/assessment-and-diagnosis-dementia/rowland-universal-dementia-assessment-scale-rudas).",
      "formerly": [
        "R03"
      ]
    },
    {
      "id": "R04",
      "domain": "RAPP",
      "also_in": [
        "MH"
      ],
      "title": "Psychiatry of old age: BPSD, depression and late-life psychosis",
      "focus": "Describing behaviour and its causes, non-drug plans, antipsychotic caution, late-life depression and new psychosis.",
      "first_pass": false,
      "priority": "Core",
      "saq_cases": [
        {
          "id": "2020-ummss-q8",
          "title": "Agitation and paranoia in an older person",
          "set": "2020 UMMSS"
        },
        {
          "id": "deck-geri-late-life-depression",
          "title": "Depression and suicide risk in later life",
          "set": "MD3 SAQ Revision Deck"
        },
        {
          "id": "2021-ummss-q12",
          "title": "Delirium, dementia and BPSD in Parkinson disease",
          "set": "2021 UMMSS"
        }
      ],
      "core_ids": [
        "P009",
        "P015",
        "P018",
        "P021",
        "P027",
        "P100"
      ],
      "notes": "### Behavioural and psychological symptoms of dementia\n\n**Behavioural and psychological symptoms of dementia** (BPSD) include agitation, aggression, wandering, apathy, sleep disturbance, hallucinations and distress. Behaviour in dementia is often the person's way of communicating a need they can no longer express.\n\nDescribe the behaviour precisely: what it is, how often it occurs, its triggers and its consequences. \"Agitated\" is not a description. A sudden change should prompt assessment for delirium, pain, infection, urinary retention, constipation, medication effects and other illness.\n\nWhat happens before, during and after an episode often explains it. A person resisting a shower may be cold, frightened, unable to understand the task, or in pain; a person who keeps walking may need the toilet or be following a familiar routine. Hunger, thirst, overstimulation, boredom, poor hearing or vision, unfamiliar carers and communication difficulties are common contributors. Collateral and the effect on the patient, staff and family, including any immediate risk of harm, complete the assessment.\n\n### Non-drug management\n\nTreat pain and other unmet physical needs, keep regular sleep, daylight and activity, and use familiar routines and meaningful occupation. Practical approaches:\n\n- Approach from the front so the person is not startled, introduce yourself, give one simple instruction at a time and allow time to respond.\n- Reassure rather than repeatedly correcting memory errors, which the person cannot correct and which increases distress.\n- Modify environmental triggers, provide safe space to walk and use sensory aids.\n\nDocument approaches that work so that different carers respond consistently. Carers need education, respite and referral to dementia support services (such as Dementia Support Australia), and it is worth asking whether the current setting can meet the person's needs. Measure improvement by the target behaviour and the person's distress, not by sedation.\n\n### Antipsychotics in dementia\n\nAntipsychotics may be justified for severe, persistent psychosis or aggression causing distress or risk, once reversible causes have been addressed. Their benefit is modest and their harms substantial. Discuss the increased risk of stroke and death, sedation, falls and movement effects with the person or their substitute decision-maker.\n\nSpecify the target symptom, the lowest effective dose, a short review interval, and a plan to reduce and stop if the drug is ineffective or no longer needed.\n\n> [!pitfall]\n> Do not use antipsychotics as routine chemical restraint for staff convenience.\n\n> [!pitfall]\n> Dementia with Lewy bodies and Parkinson disease can cause **severe sensitivity to dopamine-blocking drugs**. Seek specialist advice before using them.\n\nBenzodiazepines can worsen confusion, increase falls and cause paradoxical disinhibition. Medicines should not substitute for an environmental or staffing solution. If acute risk requires emergency medication, use a single drug at a low dose, orally where possible (for example, risperidone `0.25–0.5 mg`), avoid combining sedatives, monitor observations and falls risk afterwards, and document the rationale and response.\n\n### Late-life depression and anxiety\n\nDepression in older adults may present as withdrawal, pain, poor intake, sleep change or memory complaints, rather than reported low mood. Seek collateral and consider bereavement and isolation, medicines, sensory impairment, physical illness and suicide risk. Depression and dementia can coexist; do not dismiss cognitive difficulty as either without assessment.\n\nNew fluctuating inattention or altered alertness suggests delirium and needs medical work-up; see R03 (Finding the cause of delirium).\n\nPersistent low mood or anhedonia, guilt, hopelessness, changes in appetite and sleep, and suicidal thinking suggest depression rather than apathy alone, which lacks the distress. Ask directly about suicide, including access to medicines and social isolation; older men have particularly high suicide rates.\n\nThe **15-item Geriatric Depression Scale** (GDS-15) supports assessment. In significant cognitive impairment, combine the patient's account with observation and collateral rather than relying on a self-report score.\n\nPain, sensory loss, loneliness and loss of role are often treatable contributors. Accessible psychological therapy, behavioural activation and social support help. An antidepressant may be appropriate, with monitoring for hyponatraemia, falls, interactions, and gastrointestinal and sexual effects.\n\n> [!escalate]\n> Severe psychotic depression, refusal of food or fluid, or suicidality needs urgent psychiatric assessment and may need ECT.\n\n### Late-life psychosis\n\nNew psychosis in later life needs review of cognition, medicines, sensory impairment, neurological disease and other medical causes before schizophrenia is considered. Visual hallucinations with visual impairment and preserved insight (Charles Bonnet syndrome) still need assessment.\n\nPlan follow-up with the GP, the older persons' mental health team and carers, preserving autonomy and decision-specific capacity wherever possible.",
      "formerly": [
        "M09",
        "R04"
      ]
    },
    {
      "id": "R05",
      "domain": "RAPP",
      "title": "Polypharmacy, deprescribing and medication harms",
      "focus": "Medication reconciliation, high-risk drugs, renal/functional considerations, monitoring and withdrawal.",
      "first_pass": true,
      "priority": "Core",
      "saq_cases": [
        {
          "id": "deck-geri-balance-falls-meds",
          "title": "Disequilibrium, falls and medication review",
          "set": "MD3 SAQ Revision Deck"
        },
        {
          "id": "2021-ummss-q1",
          "title": "Fall in an anticoagulated older woman",
          "set": "2021 UMMSS"
        }
      ],
      "core_ids": [
        "P023",
        "P030",
        "P059",
        "P061"
      ],
      "notes": "### Medication reconciliation\n\nA printed list often differs from what the person actually takes. Build the list from the patient or carer, the pharmacy record, the discharge summary and the actual packs and devices. Include prescribed, over-the-counter and complementary medicines, as-needed doses, patches, inhalers, eye drops and recently stopped drugs, and clarify the indication, dose, timing, adherence and who gives each medicine.\n\n### Why older people are vulnerable\n\nAgeing changes both how drugs are handled and how the body responds to them. Older people are more vulnerable to renal accumulation, anticholinergic effects, orthostatic hypotension, hypoglycaemia and sedation.\n\n**Polypharmacy** becomes a problem when harm, burden or unnecessary treatment outweighs benefit; the number of medicines alone is not the diagnosis. Undertreatment also matters, including of pain, osteoporosis and indicated stroke prevention.\n\n### Reviewing each medicine\n\nFor each medicine, ask whether:\n\n- It still has a valid indication and evident benefit.\n- Its time to benefit fits the person's goals and prognosis.\n- The dose and route remain suitable, given renal function, interactions, swallowing and dexterity.\n- Its cost and complexity are justified.\n\nA frail person with low muscle mass may have a deceptively normal creatinine, so use the appropriate renal estimate and drug-specific dosing guidance.\n\n### High-risk medicines\n\n- **Anticholinergics:** dry mouth, constipation, urinary retention, blurred vision and confusion. The effects add up across several medicines.\n- **Benzodiazepines, sedating antihistamines and opioids:** impair balance and alertness, especially in combination.\n- **NSAIDs:** gastrointestinal bleeding, fluid retention and kidney injury. An NSAID with an ACE inhibitor or ARB and a diuretic markedly increases AKI risk.\n- **Insulin and sulfonylureas:** hypoglycaemia when intake falls or renal function worsens.\n- **Antihypertensives, diuretics and alpha blockers:** orthostatic hypotension, dehydration and falls.\n- **Anticoagulants:** bleeding when the dose, renal function or interactions are overlooked.\n\n> [!pitfall]\n> **Falls risk alone is not a reason to stop an indicated anticoagulant.** The strokes it prevents usually outweigh the extra bleeding risk from falls.\n\n### Prescribing cascades\n\nA **prescribing cascade** occurs when an adverse effect is mistaken for a new condition and treated with another drug. For example, amlodipine-related ankle oedema leads to a diuretic, which leads to dehydration and falls. Revisiting the original cause is often better than adding a treatment for each adverse effect.\n\n### Deprescribing\n\nFrame deprescribing around the patient's goals: \"This tablet may now be making you dizzy; we can reduce it and check your blood pressure and symptoms.\" Agree priorities, usually starting with the medicine of highest harm and lowest benefit, and change one or a few at a time so the response can be interpreted.\n\nSome medicines can stop directly; others need tapering to avoid withdrawal or rebound, including benzodiazepines, antidepressants, opioids, beta blockers and long-term corticosteroids. The taper is drug-specific and often slower after prolonged use. The plan states what to monitor, who reviews and when, and what would justify restarting.\n\nRecord changes on every relevant list and notify the pharmacy or care facility. STOPP/START and the Beers criteria prompt review but do not replace individual judgement.\n\n### Making the regimen usable\n\nSimpler dosing and clear written instructions linked to daily routines make a regimen easier to follow. Dose administration aids help selected patients, but they can obscure which drug is which, complicate changes, and leave out as-needed and inhaled medicines; check whether the patient can actually use one.\n\nPharmacist-led review (such as a Home Medicines Review) and teach-back help. Where needed, give a specific sick-day plan that names which medicines to withhold during dehydrating illness and when to restart them; a vague instruction to stop everything can cause harm.\n\nAfter changes, review falls, alertness, standing BP, renal function, glucose and symptom control. Report and record significant adverse reactions, distinguishing allergy from intolerance; mislabelling an intolerance as an allergy can exclude useful treatment later. A successful review may simplify the regimen, add an omitted useful treatment, or leave an appropriate medicine unchanged.",
      "formerly": [
        "R05"
      ]
    },
    {
      "id": "R06",
      "domain": "RAPP",
      "title": "Undernutrition, sarcopenia and dysphagia in older people",
      "focus": "Sarcopenia, undernutrition, swallowing, low reserves, reversible causes, achievable care plans.",
      "first_pass": false,
      "priority": "Selective",
      "saq_cases": [
        {
          "id": "deck-geri-unintentional-weight-loss",
          "title": "Unintentional weight loss",
          "set": "MD3 SAQ Revision Deck"
        }
      ],
      "core_ids": [
        "P014",
        "P033",
        "P043",
        "P059",
        "P071",
        "P105"
      ],
      "notes": "### Definitions\n\n- **Malnutrition:** inadequate intake or absorption relative to requirements.\n- **Sarcopenia:** reduced muscle strength with reduced muscle quantity or quality. Poor physical performance indicates more severe sarcopenia.\n- **Frailty:** a broader vulnerability to stressors.\n- **Cachexia:** disease-associated muscle loss driven partly by inflammation and metabolic change, which nutrition alone may not reverse.\n\nThese can coexist, including in a person with obesity.\n\n### Assessment\n\nThe measured weight trajectory matters more than the current BMI, which can look normal despite substantial recent loss. Unintentional loss of about `5%` of body weight over `six months` is clinically important, especially with poor intake or functional decline.\n\nGrip strength, chair-rise ability, gait and the effect on daily tasks show whether muscle function is affected. A screening tool such as the Mini Nutritional Assessment short form (MNA-SF) or the Malnutrition Universal Screening Tool (MUST) identifies who needs fuller assessment; it does not explain the cause.\n\n> [!pitfall]\n> Albumin is affected by inflammation and fluid status and is **not a test of nutrition**.\n\n### Contributing causes\n\nWeight loss in older people usually has several contributors, many of them treatable:\n\n- **Physical symptoms:** poor appetite, early satiety, nausea, diarrhoea or constipation, pain, altered taste or smell, chewing problems or ill-fitting dentures, and difficulty swallowing.\n- **Practical barriers:** inability to shop, prepare food, open packaging or feed oneself; loneliness; finances; cultural preferences; dietary restrictions.\n- **Other causes:** medicines, alcohol, depression, cognitive impairment, infection, malignancy, and endocrine or chronic disease.\n\nExamine oral health, hydration, muscle and fat stores, the abdomen, lymph nodes and other relevant systems. Target tests to the presentation: FBE, renal and liver function, calcium, TSH, inflammatory markers, iron studies and B12, and specific investigations for concerning symptoms.\n\n> [!pitfall]\n> Rapid weight loss, severe anaemia, a mass, bleeding or focal symptoms needs investigation; do not attribute it to ageing.\n\nNew fatigue may reflect anaemia, a sleep disorder, depression, medicines or acute illness as well as frailty.\n\n### Management\n\nTreat pain, nausea, constipation, oral disease and other reversible causes first. Small frequent meals, food fortification and protein-rich foods that suit the person's preferences then help, with oral nutritional supplements to fill gaps when ordinary food is not enough.\n\nDietary advice should account for renal disease, diabetes, swallowing and goals. In frail older people, undernutrition usually poses the greater risk, so burdensome restrictions that make adequate intake impossible need a clear benefit to justify them.\n\nCombine nutrition with progressive resistance and balance exercise where feasible. Calories alone do not restore strength, because muscle is rebuilt in response to load.\n\nMeal delivery, help with shopping, assisted feeding, adapted utensils and social eating are useful when they address the actual barrier. Review intake, weight trend, strength and function, and whether the patient finds the plan tolerable.\n\n### Dysphagia\n\nCoughing or choking with eating, a wet voice, prolonged meals, recurrent chest infections or unexplained weight loss suggests dysphagia. Aspiration can also be silent.\n\nSpeech pathology assesses swallowing, with instrumental testing when indicated, and recommends posture, pacing and food and fluid textures. Reassess hydration and nutrition, because texture-modified diets can reduce intake. Oral hygiene matters whether the person eats or is tube-fed, because aspiration of oral bacteria causes pneumonia.\n\n### Feeding decisions\n\n> [!pitfall]\n> Tube feeding has disease-specific benefits and burdens, and it does not remove the risk of aspiration.\n\nIn advanced dementia or the last phase of life, supported oral or comfort feeding may fit the person's goals better than a tube. Discuss the likely outcomes, the person's preferences, and capacity and substitute decision-making; tube placement is not an automatic response to weight loss.\n\nAfter substantial recent starvation or prolonged minimal intake, there is a risk of refeeding syndrome. Assess thiamine and electrolytes and feed under monitoring with dietetic and medical input; see M05 (Nutritional rehabilitation and refeeding).\n\nIn advanced cachexia, declining appetite can reflect the biology of the illness. Relieving distressing symptoms and supporting comfortable eating, without blaming the patient or family, helps more than pressing for intake.",
      "formerly": [
        "R13"
      ]
    },
    {
      "id": "R07",
      "domain": "RAPP",
      "also_in": [
        "GP"
      ],
      "title": "Constipation, faecal impaction and faecal incontinence",
      "focus": "Bowel history, red flags, laxatives by mechanism, opioid constipation, disimpaction and faecal incontinence.",
      "first_pass": false,
      "priority": "Core",
      "saq_cases": [
        {
          "id": "deck-geri-faecal-incontinence",
          "title": "Faecal incontinence",
          "set": "MD3 SAQ Revision Deck"
        }
      ],
      "core_ids": [
        "P012",
        "P025"
      ],
      "notes": "### Assessment and red flags\n\nAsk about the usual bowel pattern, stool consistency, straining, incomplete emptying, painful defaecation, medicines, diet and fluid intake, and mobility. Examine the abdomen. Perform a consented rectal examination when impaction, an outlet problem or neurological dysfunction is suspected.\n\n> [!pitfall]\n> **Overflow of liquid stool around an impaction can be mistaken for diarrhoea.** Check before giving an antidiarrhoeal, which would worsen the impaction.\n\nRectal bleeding, iron deficiency, a progressive unexplained change in bowel habit, weight loss, severe pain or distension, or vomiting needs investigation.\n\n> [!escalate]\n> Suspected bowel obstruction needs emergency assessment; do not simply escalate oral laxatives. New saddle sensory loss, leg weakness, or urinary retention or incontinence suggests cauda equina compression and is an emergency.\n\n### Building a bowel regimen\n\nThe foundations are regular toileting with privacy, a good posture (feet supported, knees above hips), mobility and adequate fluid. Fibre helps uncomplicated constipation when intake and hydration are adequate, but can worsen severe impaction, obstruction or constipation in a poorly hydrated patient, because it adds bulk without the water to move it.\n\nChoose laxatives by mechanism:\n\n- **Osmotic (e.g. macrogol):** retains water in the stool.\n- **Stimulant (e.g. senna, bisacodyl):** increases motility.\n\nOpioid-induced constipation reflects both reduced motility and drier stool, so it usually needs both an osmotic and a stimulant laxative, prescribed proactively when the opioid is started. Titrate to comfortable regular stools; a daily motion is not required. Docusate alone is often inadequate.\n\n### Faecal impaction\n\nImpaction needs a specific disimpaction plan, using oral macrogol and/or rectal treatment according to the location, severity and tolerance, followed by maintenance therapy to prevent recurrence. Manual disimpaction, when necessary, needs consent, analgesia and an experienced clinician.\n\n### Faecal incontinence\n\nFaecal incontinence is common in older people and under-reported, so ask directly. The pattern points to the mechanism:\n\n- **Urge incontinence:** external sphincter injury (often obstetric), reduced rectal capacity or diarrhoea.\n- **Passive soiling:** internal sphincter weakness, neurological disease, or overflow around an impaction.\n- **Functional incontinence:** reduced mobility or cognition that prevents reaching the toilet in time.\n\nAsk about obstetric injury, anorectal surgery, neurological disease, stool consistency (a stool chart using the Bristol scale helps) and the effect on daily life. Examine the perineum and perform a rectal examination to assess resting tone, squeeze and impaction.\n\nTreat the underlying cause. Disimpaction comes first when there is overflow. Once impaction and infective diarrhoea have been excluded, firming the stool with fibre and, where needed, loperamide often helps. Scheduled toileting after meals uses the gastrocolic reflex, and access to the toilet, clothing and mobility aids matter as much as medicines. Pelvic floor training and biofeedback help sphincter weakness; refer to a colorectal service for sphincter injury or when conservative treatment fails.\n\nProtect the skin, involve continence nursing, and review stool charts, symptoms and adverse effects after each change. Pads manage the consequences but do not replace assessment of a treatable cause.",
      "formerly": [
        "R07"
      ]
    },
    {
      "id": "R08",
      "domain": "RAPP",
      "also_in": [
        "GP"
      ],
      "title": "Pressure injuries, leg ulcers and immobility",
      "focus": "Pressure injury staging, venous, arterial and neuropathic ulcers, ABPI before compression, wound care and immobility.",
      "first_pass": false,
      "priority": "Core",
      "saq_cases": [],
      "core_ids": [
        "P044",
        "P090",
        "P108"
      ],
      "notes": "### Pressure injury\n\nPressure and shear reduce blood flow to tissue, typically over the heels, sacrum and other bony prominences, or beneath medical devices. Immobility, sensory loss, poor nutrition, moisture and impaired circulation increase risk, both by increasing load on the tissue and by reducing its tolerance.\n\nInspect the whole skin and every device contact point, not just a known wound. In darker skin, warmth, tenderness, firmness and colour change may be more informative than visible redness.\n\n### Pressure injury staging\n\nStaging describes the deepest tissue involved:\n\n- **Stage 1:** intact skin with persistent non-blanching erythema or colour change.\n- **Stage 2:** partial-thickness skin loss with exposed dermis, or an intact or ruptured serum-filled blister. Moisture damage and skin tears are not stage 2 injuries.\n- **Stage 3:** full-thickness skin loss, often with visible fat, but without exposed fascia, muscle, tendon or bone.\n- **Stage 4:** full-thickness tissue loss with exposed or directly palpable fascia, muscle, tendon or bone.\n- **Unstageable:** slough or eschar obscures the depth.\n- **Deep tissue pressure injury:** persistent deep red, maroon or purple discolouration, or a blood-filled blister. It can deteriorate rapidly.\n\nDocument the site, dimensions, depth, undermining, tissue type, exudate, surrounding skin, pain and signs of infection.\n\n> [!pitfall]\n> Do not \"reverse-stage\" a healing wound; lost tissue is replaced by scar, not regenerated. Record the original stage and the healing progress.\n\n### Leg ulcers\n\nThe location and character of an ulcer reflect its cause:\n\n- **Venous:** usually in the gaiter area, with oedema, haemosiderin pigmentation and other venous skin changes.\n- **Arterial:** often distal and painful, with cool skin and reduced pulses.\n- **Neuropathic:** at pressure points on an insensate foot; may be relatively painless.\n\nMixed causes are common. In every case assess pulses, sensation, footwear, diabetes and vascular risk; a healthy-looking wound does not establish adequate perfusion.\n\n### Assessing arterial supply before compression\n\nAssess arterial supply before applying compression, because compressing an ischaemic limb can cause tissue necrosis.\n\nAn **ankle–brachial pressure index** (ABPI) of about `0.8–1.3` generally supports standard compression when the clinical assessment agrees. Lower values need modified compression or specialist decisions. A high or non-compressible reading, especially in diabetes or CKD, can be falsely reassuring because calcified arteries resist the cuff; toe pressures or vascular assessment may be needed.\n\n> [!escalate]\n> Rest pain, gangrene, or an acutely cold, pulseless limb needs emergency vascular care.\n\n### Wound management\n\nHealing depends on perfusion, sensation, pressure, oedema, nutrition and infection, so assess these before choosing a dressing. Dressings cannot overcome continuing pressure or ischaemia.\n\n- **Pressure:** relieve it with individualised repositioning, heel offloading, appropriate mattresses and cushions, and early supported mobilisation. A support surface does not replace repositioning.\n- **Moisture and incontinence:** gentle cleansing and barrier products.\n- **Venous ulcers:** appropriately selected compression, with movement and elevation.\n- **Neuropathic ulcers:** offloading and foot care.\n- **Arterial ulcers:** vascular assessment.\n\nAdd analgesia, and attend to nutrition and perfusion.\n\nChoose cleansing and dressings by tissue type and exudate, maintaining a moist healing environment without maceration. Debridement depends on perfusion, tissue and goals. Leave stable, dry heel eschar or an ischaemic wound alone unless perfusion has been assessed, because the eschar acts as a protective cover when the blood supply is too poor to heal an open wound.\n\n> [!pitfall]\n> Antibiotics treat spreading clinical infection or deeper infection, not colonisation.\n\nSuspected osteomyelitis, rapidly progressive necrosis, systemic illness or an atypical or non-healing edge needs further investigation, biopsy or referral. Review objective healing, and whether the patient can manage the plan at home.\n\n### Complications of immobility\n\nBed rest causes muscle loss, contractures, atelectasis, thrombosis, constipation, urinary retention, delirium and dependence. Prevent them with mobilisation, range-of-motion exercises, breathing support where needed, bowel and continence care, and VTE prophylaxis according to risk. Keep the call bell within reach, provide sensory aids and meaningful interaction, and ensure adequate food and fluid.\n\nRestore activity where possible. Confining a person to bed to avoid falls trades one harm for several others.",
      "formerly": [
        "G13",
        "R12"
      ]
    },
    {
      "id": "R09",
      "domain": "RAPP",
      "title": "Parkinsonism, weakness and neurological disability",
      "focus": "Functional impacts of PD/MS/MND, falls, dysphagia, spasticity, supportive care.",
      "first_pass": false,
      "priority": "Selective",
      "saq_cases": [
        {
          "id": "deck-geri-parkinson",
          "title": "Parkinson disease",
          "set": "MD3 SAQ Revision Deck"
        },
        {
          "id": "deck-geri-mnd",
          "title": "Motor neurone disease",
          "set": "MD3 SAQ Revision Deck"
        }
      ],
      "core_ids": [
        "P007",
        "P029",
        "P033",
        "P064",
        "P087",
        "P099"
      ],
      "notes": "### Localising weakness\n\nLocalise weakness within the nervous system first; the site of the lesion narrows the differential far more than the symptom does. Onset, progression, distribution, fatigability, pain, sensory change, and swallowing, breathing, bladder and bowel symptoms help localise it. Sudden focal weakness suggests stroke; a sensory level with sphincter dysfunction suggests spinal cord disease.\n\n> [!escalate]\n> Rapidly progressive symmetrical weakness, bulbar symptoms or breathing difficulty needs emergency assessment, not routine rehabilitation referral.\n\nExamine the cranial nerves, muscle bulk, tone, power, reflexes, plantar responses, sensation, coordination and gait. The findings fall into recognisable patterns:\n\n- **Upper motor neurone:** spasticity, brisk reflexes and an extensor plantar response.\n- **Lower motor neurone:** weakness with wasting, reduced reflexes and sometimes fasciculations.\n- **Peripheral neuropathy:** usually distal sensory loss and reduced ankle reflexes.\n- **Myopathy:** usually proximal weakness with normal sensation.\n- **Neuromuscular junction:** fatigable weakness, often ocular or bulbar, without sensory loss.\n\nChoose investigations by the localisation: electrolytes, glucose, CK, thyroid function and B12, neuroimaging or nerve conduction studies as indicated.\n\n- **Guillain–Barré syndrome:** new ascending weakness with reduced reflexes. Assess respiratory and autonomic function urgently.\n- **Myasthenia gravis:** fatigable ptosis or diplopia; dysphagia or breathlessness suggests possible crisis.\n\n> [!pitfall]\n> Normal oxygen saturation does not exclude early ventilatory failure; saturation falls late. Serial forced vital capacity is more informative.\n\n### Parkinson disease\n\n**Parkinsonism** is a motor syndrome with several causes. **Parkinson disease** is a neurodegenerative cause involving loss of dopaminergic neurones in the substantia nigra.\n\nParkinsonism requires bradykinesia with rigidity and/or rest tremor. Shuffling gait and freezing, reduced arm swing, small handwriting, falls, constipation, orthostatic symptoms, REM sleep behaviour disorder, mood change, cognitive change and hallucinations together describe the motor and non-motor burden.\n\n- **Atypical parkinsonism:** suggested by early severe falls, marked autonomic failure or a poor response to levodopa.\n- **Drug-induced parkinsonism:** caused by dopamine-blocking medicines.\n- **Tremor:** a bilateral postural or action tremor with otherwise normal movement and tone suggests essential or enhanced physiological tremor; review caffeine, anxiety, thyroid disease and medicines. Rest tremor alone does not establish Parkinson disease.\n\n### Treatment of Parkinson disease\n\nLevodopa combined with a peripheral decarboxylase inhibitor (carbidopa or benserazide) is the main symptomatic treatment. The inhibitor prevents peripheral conversion of levodopa, reducing nausea and allowing more to reach the brain.\n\n> [!pitfall]\n> **Give levodopa at the person's usual times, including in hospital.** Its short half-life means delayed or missed doses can cause severe immobility, swallowing problems and a dangerous withdrawal syndrome. If oral intake stops, arrange an alternative route promptly.\n\nReview wearing-off, dyskinesia, hallucinations and postural hypotension. Dopamine agonists can cause sudden sleep attacks and impulse-control disorders, such as gambling or hypersexuality, which patients rarely volunteer; ask directly.\n\n> [!pitfall]\n> Avoid dopamine-blocking antiemetics such as metoclopramide and prochlorperazine, which oppose treatment and can cause marked deterioration. Domperidone is the safer choice. Seek advice before using any antipsychotic.\n\nCombine medication with physiotherapy (cueing, strength and balance), occupational therapy adaptations, speech and swallowing care, management of constipation, and support for carers. Swallowing problems, falls and cognitive change should prompt reassessment of home safety and treatment.\n\n### Multiple sclerosis\n\n**Multiple sclerosis** is an immune-mediated disease of the CNS involving demyelination and neuroaxonal injury. It causes relapses or progression of visual, sensory, motor, balance and sphincter dysfunction. Diagnosis and disease-modifying treatment need neurology and appropriate MRI and other evidence.\n\nInfection or heat can worsen old symptoms without a true relapse (a pseudo-relapse), because demyelinated nerves conduct less reliably under these stresses. Rehabilitation addresses fatigue, spasticity, mood, bladder function and participation alongside disease treatment.\n\n### Motor neurone disease\n\n**Motor neurone disease** causes progressive weakness with upper and/or lower motor neurone signs, usually without prominent sensory loss. Bulbar dysfunction, a weak cough and respiratory symptoms need multidisciplinary assessment. Support may include non-invasive ventilation, assisted cough, nutrition and gastrostomy discussions, communication aids and symptom treatment. Cognitive and behavioural involvement can occur and affects planning.\n\n### Communication and independence\n\nFunction with aids or extra time, not only unaided performance, shows what the person can do. Support includes accessible communication, swallowing assessment, suitable seating and mobility equipment and help with personal care, together with attention to pain, contractures, pressure injury, bowel and bladder function, sexuality and emotional adjustment.\n\nDiscuss future decisions about breathing support and nutrition, and preferred supports, while communication and capacity allow, without assuming that disability means a poor quality of life.",
      "formerly": [
        "R09"
      ]
    },
    {
      "id": "R10",
      "domain": "RAPP",
      "title": "Rehabilitation goals and discharge planning",
      "focus": "Impairments/activities/participation, SMART goals, allied health, stroke secondary prevention, spinal cord injury, safe destination and supports.",
      "first_pass": true,
      "priority": "Core",
      "saq_cases": [
        {
          "id": "2020-ummss-q7",
          "title": "Rehabilitation after hip arthroplasty",
          "set": "2020 UMMSS"
        }
      ],
      "core_ids": [
        "P007",
        "P044",
        "P083"
      ],
      "notes": "### The ICF framework\n\nThe WHO **International Classification of Functioning, Disability and Health** (ICF) separates impairment, activity, participation, and environmental and personal factors. After a stroke, for example:\n\n- **Body impairment:** arm weakness.\n- **Activity limitation:** difficulty dressing.\n- **Participation restriction:** unable to return to work.\n- **Environmental barrier:** an inaccessible bathroom.\n\nThe framework explains why rehabilitation can improve function by adapting tasks and the environment even when an impairment cannot be reversed.\n\n### Setting goals\n\nPre-event function, current abilities, the person's priorities, likely recovery, and barriers such as pain, fatigue, cognition, mood, communication and social support shape the goals.\n\nMake goals specific, measurable, achievable, relevant and time-bound (SMART). \"Within two weeks, transfer from bed to chair using a frame with supervision only\" is more useful than \"improve mobility\", because it tells every team member what to work towards and when to review. Agree goals with the patient, review them with the team and adjust them as recovery unfolds.\n\n### The multidisciplinary team\n\n- **Physiotherapy:** strength, balance, gait, endurance, transfers, respiratory function and walking aids.\n- **Occupational therapy:** dressing, toileting, meal preparation, cognition in daily tasks, equipment, home modifications and driving assessment.\n- **Speech pathology:** swallowing safety and communication, including supported communication for aphasia.\n- **Dietetics:** energy and protein needs, malnutrition and nutrition plans.\n- **Nursing:** daily practice of skills, skin and continence care, education and monitoring between therapy sessions.\n- **Social work, psychology and neuropsychology:** adjustment, family and carer needs, cognition and behaviour, funding and community participation.\n- **Medical team and pharmacy:** treat complications and optimise medicines, pain, spasticity and comorbid disease without compromising alertness or mobility.\n\n### Stroke rehabilitation\n\n**Screen swallowing before any oral food, fluid or medication after an acute stroke**, whether or not dysphagia is suspected. An abnormal screen needs formal swallowing assessment.\n\nRehabilitation also addresses aspiration, communication, neglect, visual field loss, mood, continence, shoulder pain and secondary prevention.\n\n- **Aphasia:** impaired language.\n- **Dysarthria:** impaired motor production of speech.\n- **Neglect:** reduced attention to one side of space or of the body; distinct from a visual field defect.\n\n> [!pitfall]\n> Aphasia does not mean incapacity. Support communication before judging capacity.\n\nHandle a weak arm carefully and avoid traction on the shoulder, which can subluxate because the supporting muscles are paralysed.\n\n### Secondary prevention after stroke or TIA\n\nRecurrence risk is highest in the first days and weeks, so prevention begins in hospital and continues in general practice. The cause of an ischaemic event determines the antithrombotic treatment, which is why brain imaging, ECG and rhythm monitoring for AF, echocardiography and carotid imaging are part of the work-up.\n\n- **Non-cardioembolic ischaemic stroke or TIA:** antiplatelet treatment. After a minor stroke or high-risk TIA, aspirin plus clopidogrel is started early and continued for about `21 days`, then a single antiplatelet agent long term; longer dual therapy adds bleeding without further benefit. Symptomatic carotid stenosis of `70–99%` is referred for endarterectomy, ideally within `two weeks`, and `50–69%` is considered.\n- **AF or another cardioembolic source:** anticoagulation, usually with a DOAC, rather than antiplatelet treatment; adding aspirin increases bleeding without a separate indication. The stroke team times the start according to infarct size and bleeding risk. See G06 (Stroke prevention).\n- **Intracerebral haemorrhage:** BP control matters most; antithrombotic treatment is a specialist decision.\n\nFor all patients:\n\n- **Lipids:** a high-intensity statin after ischaemic stroke or TIA, aiming for LDL cholesterol `<1.8 mmol/L`.\n- **BP:** start or intensify treatment once the patient is stable, aiming for `<130/80` in most people.\n- **Other risks:** smoking cessation, diabetes management, alcohol reduction, physical activity, diet and weight, and assessment for obstructive sleep apnoea.\n\nDriving is restricted after stroke or TIA, for a minimum period and then according to residual deficits; follow the current Assessing Fitness to Drive standards. Review adherence, adverse effects, mood and function at each visit; post-stroke depression is common and slows recovery.\n\n### Traumatic brain injury\n\nAfter **traumatic brain injury**, executive dysfunction, memory problems, fatigue, impulsivity and sensory overload may be disabling even when walking is preserved.\n\n**Post-traumatic amnesia** (PTA) is a period of disorientation and impaired continuous new learning. Track it with serial standardised testing, such as the Westmead PTA scale. Because new learning is impaired, provide a predictable, low-stimulation environment, consistent staff, short instructions and supervision, followed by graded cognitive and physical rehabilitation and support to return to study or work.\n\n> [!pitfall]\n> Challenging behaviour after brain injury may reflect the injury itself, not unwillingness.\n\n### Spinal cord injury\n\nRehabilitation after **spinal cord injury** covers skin protection, bowel and bladder management, respiratory support, spasticity, sexual function and equipment.\n\nThe *neurological level* is the lowest segment with normal sensation and strength on both sides. An injury is *complete* when no sensory or motor function is preserved in the lowest sacral segments (ASIA Impairment Scale A); incomplete injuries carry a better prognosis for recovery.\n\n- **Neurogenic bladder:** an injury above the sacral cord usually leaves an overactive detrusor contracting against an uncoordinated sphincter, which raises bladder pressure and causes incomplete emptying, reflux and renal damage; a sacral or cauda equina injury leaves a flaccid bladder that retains and overflows. Clean intermittent catheterisation, about four to six times a day, is preferred when hand function or a carer allows, with an indwelling or suprapubic catheter as the alternative, and the renal tract is monitored for life. Bacteriuria is almost universal, so treat UTI on symptoms such as fever, new incontinence, increased spasticity or dysreflexia, not on culture alone.\n- **Neurogenic bowel:** a planned routine at a consistent time, daily or on alternate days, using stool softeners, suppositories and digital stimulation (or manual evacuation after a sacral injury), prevents both incontinence and impaction.\n- **Skin:** pressure injuries develop quickly over insensate skin, so repositioning, pressure-relieving surfaces and daily skin checks are part of the routine; see R08 (Pressure injury).\n\n**Autonomic dysreflexia** occurs with lesions at or above `T6`: a stimulus below the lesion triggers unopposed sympathetic activity, causing a sudden rise in BP, headache, flushing and sweating above the lesion, and sometimes bradycardia.\n\n> [!escalate]\n> Autonomic dysreflexia is an emergency.\n>\n> 1. Sit the person upright to lower BP, and loosen tight clothing.\n> 2. Monitor BP and call for help.\n> 3. Look for the trigger, most often a blocked catheter or full bladder, then the bowel.\n>\n> If systolic BP remains `≥150 mmHg`, give a short-acting antihypertensive, commonly sublingual glyceryl trinitrate `300 micrograms`, repeated every `5–10 minutes` if needed, or sublingual captopril if a PDE5 inhibitor has been taken recently. Watch for hypotension once the trigger is removed. Bowel manipulation can worsen the episode, so use appropriate precautions such as local anaesthetic gel.\n\n### Discharge planning\n\nDischarge is safe when the person can manage in the intended environment, not just on the ward. Assess:\n\n- Transfers, walking and stairs, and toileting, as performed in practice.\n- Eating, swallowing and managing medicines.\n- Cognition, judgement and the ability to call for help in an emergency.\n- Whether carers are willing and able, and what training they need; family cannot provide unlimited care.\n\nArrange equipment before discharge, confirm services and appointments, and give a named contact and a plan for deterioration.\n\nThe handover states the diagnoses, restrictions, functional change, goals, medication changes, outstanding results and who will follow them up. Community rehabilitation may continue once inpatient progress slows.\n\nMy Aged Care, the NDIS, injury compensation schemes (such as the TAC and WorkSafe in Victoria) and community health services have different eligibility and purposes. A disability pension provides income support, not rehabilitation.\n\nReturn to driving or work needs a task-specific assessment and any relevant medical restrictions; hospital discharge is not clearance.\n\nReferences: [Australian Stroke Clinical Care Standard](https://www.safetyandquality.gov.au/clinical-care-standards/stroke); [ACI: autonomic dysreflexia](https://aci.health.nsw.gov.au/networks/spinal-cord-injury/resources/autonomic-dysreflexia).",
      "formerly": [
        "R06"
      ]
    },
    {
      "id": "R11",
      "domain": "RAPP",
      "title": "Consent, capacity and goals of care",
      "focus": "Informed consent, decision-specific capacity, the Victorian framework and substitute decision-makers, goals-of-care discussions.",
      "first_pass": true,
      "priority": "Core",
      "saq_cases": [
        {
          "id": "deck-geri-capacity",
          "title": "Capacity, enduring powers of attorney and wills",
          "set": "MD3 SAQ Revision Deck"
        }
      ],
      "core_ids": [
        "P021",
        "P044"
      ],
      "notes": "### Informed consent\n\nValid consent requires **capacity, adequate information and a voluntary decision**. The information is what a reasonable person in this patient's position would want to know:\n\n- The proposed treatment and its expected benefit.\n- The material risks relevant to this person.\n- The alternatives.\n- The likely consequences of declining.\n\nCheck understanding with teach-back, allow questions and use an interpreter or communication aid when needed. Consent to one procedure does not cover unrelated interventions, and an adult with capacity may refuse treatment even when clinicians disagree.\n\n### Capacity\n\nCapacity is presumed, and the person is supported to make the decision before their capacity is questioned. Assess whether the person can:\n\n- **Understand** the relevant information.\n- **Retain** it long enough to decide.\n- **Use or weigh** it.\n- **Communicate** a choice, by any means.\n\nUseful questions include \"What is the treatment for?\", \"What might happen with or without it?\" and \"How did you weigh those options?\" Record the explanation given and the person's answers.\n\nCapacity can fluctuate, so treat reversible barriers such as delirium, pain, intoxication, hearing loss or language difficulty, and reassess at a better time when possible.\n\n> [!pitfall]\n> A diagnosis of dementia, an abnormal cognitive score, detention under mental health law, or an unwise decision **does not by itself establish incapacity**.\n\nCapacity is decision-specific: a person may be able to decide about a simple treatment but not a complex financial matter.\n\n### Victorian medical treatment decisions\n\nUnder the **Medical Treatment Planning and Decisions Act 2016**, an **advance care directive** may contain:\n\n- An **instructional directive:** consent to or refusal of specified future treatment, which is legally binding if valid and applicable.\n- A **values directive:** the person's values and preferences, to guide decisions.\n\nConfirm that a directive is valid and applies to the situation, and that the person currently lacks capacity, before relying on it.\n\nWhen a substitute decision is needed, the **medical treatment decision maker** is the first of the following who is reasonably available and willing and able to act:\n\n1. A medical treatment decision maker appointed by the person.\n2. A guardian appointed by VCAT with power to make medical treatment decisions.\n3. The spouse or domestic partner, if in a close and continuing relationship.\n4. The primary unpaid carer.\n5. An adult child, then a parent, then an adult sibling, each in a close and continuing relationship. Where relatives rank equally, the eldest has precedence.\n\nThe decision maker must decide as the person would have, based on their known preferences and values, following the statutory process when these are unknown.\n\n> [!pitfall]\n> \"Next of kin\" has no automatic legal authority, and a financial power of attorney does not confer medical decision-making power.\n\nA support person helps the patient communicate and decide but does not thereby become the decision maker.\n\nWhen no authorised person is available, or there is conflict, seek senior and Office of the Public Advocate advice; do not construct consent from a family vote. The Act has specific provisions for emergency treatment, but a known valid and applicable refusal must still be considered.\n\n### Goals-of-care discussions\n\nStart from the person's own understanding: what they know about their illness, what matters most to them, what worries them, and what outcomes they would find unacceptable. Then explain the likely outcomes of treatment in concrete terms, including function and burden, and make the relevant decisions: CPR, hospital transfer, ventilation, antibiotics, nutrition and preferred place of care.\n\nA decision not to attempt CPR is separate from stopping other useful treatment. Document the agreed plan, who took part and what would prompt review, and share it across settings.\n\nWhen there is conflict, clarify whether the disagreement is about facts, values, authority or communication, because each is resolved differently. Seek senior, ethics or legal support, while continuing symptom relief and respectful discussion.\n\n### Testamentary capacity\n\n**Testamentary capacity** to make a will is a separate legal test: understanding the nature of a will, the extent of one's property and the people with a claim on it. A brief cognitive score or a medical treatment assessment cannot establish it.\n\nReference: [Victorian Department of Health: when a person does not have decision-making capacity](https://www.health.vic.gov.au/advance-care-planning/when-a-person-does-not-have-decision-making-capacity).",
      "formerly": [
        "R11"
      ]
    },
    {
      "id": "R12",
      "domain": "RAPP",
      "title": "Advanced chronic illness and multimorbidity",
      "focus": "COPD/HF, goals of care, symptom management, prognostic uncertainty, hospital avoidance and review.",
      "first_pass": false,
      "priority": "Core",
      "saq_cases": [
        {
          "id": "deck-geri-copd",
          "title": "COPD",
          "set": "MD3 SAQ Revision Deck"
        },
        {
          "id": "deck-geri-heart-failure",
          "title": "Heart failure and acute pulmonary oedema",
          "set": "MD3 SAQ Revision Deck"
        }
      ],
      "core_ids": [
        "P023",
        "P034",
        "P061",
        "P094"
      ],
      "notes": "### Trajectory and priorities\n\nIn advanced heart, lung, renal or neurological disease, the trajectory of admissions, exacerbations, weight and functional loss, dependence and symptom burden shows where the person is in their illness. What the person most wants to preserve, and which burdens they would find unacceptable, determines how that information is used. Prognosis is often uncertain, but useful planning does not need an exact survival estimate.\n\nReview each treatment for its benefit, burden and fit with the person's goals. Disease-modifying and palliative care can run together: a diuretic may improve both heart failure physiology and comfort, whereas a long-term preventive medicine may offer little near-term benefit to someone dying of another illness.\n\n> [!pitfall]\n> Involving palliative care is not in itself a reason to stop chronic treatment.\n\n### Progression or a reversible exacerbation\n\nNot every decline is progression of the disease; some is a treatable exacerbation. Observations, hydration or fluid overload, infection, adherence, medication changes and new cardiorespiratory symptoms help make the distinction.\n\n- **Heart failure:** increasing orthopnoea, oedema and weight suggest congestion. Over-diuresis can cause dizziness, kidney injury and falls.\n- **COPD:** distinguish an infective or bronchospastic exacerbation from pneumonia, heart failure, pulmonary embolism and anxiety.\n\n> [!escalate]\n> New confusion, chest pain, severe hypoxaemia or focal neurology needs same-day assessment, in line with the agreed treatment plan.\n\n### Fluid assessment in frail older people\n\nJudge fluid need from intake and losses, weight, mucous membranes, perfusion, postural symptoms, urine output and signs of congestion.\n\n> [!pitfall]\n> Neither a dry mouth nor a raised urea alone proves dehydration.\n\nIf IV fluid is needed, prescribe a defined volume and rate cautiously, check electrolytes and reassess early, especially in heart or kidney failure, where the margin between too little and too much is narrow. Repeated unreviewed bags of fluid can cause pulmonary oedema.\n\n### Symptom and exacerbation plan\n\nOptimise the main condition first: inhaler technique and an action plan in obstructive lung disease, diuretics and weight monitoring in heart failure, and renal medication and diet advice where relevant.\n\nSupportive measures for breathlessness include pacing, positioning, a handheld fan, rehabilitation or activity as tolerated, anxiety support and carer education. Prescribe oxygen for a physiological or demonstrated individual indication, not for every sensation of breathlessness; breathlessness without hypoxaemia rarely improves with oxygen. Refractory symptoms need specialist palliative advice; see R13 (Other common symptoms).\n\nA written plan lets the person and carers respond early to change. It states which changes can be managed at home, whom to contact, which medicines may be adjusted and who reviews the result, with clear thresholds for calling the team, for example for worsening breathlessness, reduced intake or rapid weight change. Avoid unsupervised dose increases without attention to renal function, BP and adverse effects.\n\n### Anticipating decisions\n\nBegin with the person's understanding, hopes and concerns, then discuss likely future decisions such as hospital transfer, ventilation, dialysis or nutritional support. Explain the expected benefits and burdens in terms of the person's function and priorities.\n\nDocument resuscitation decisions and other treatment limitations separately. A decision not to attempt CPR **does not mean withholding other useful treatment**.\n\nIdentify the medical treatment decision maker and any advance care directive **while the patient can still take part**. Arrange community nursing, palliative or rehabilitation input, equipment, medication access and after-hours support according to need.\n\nCarer exhaustion can cause a crisis even when the disease is stable. Revisit the plan after significant deterioration, after discharge, or when the person's preferences change.",
      "formerly": [
        "R08"
      ]
    },
    {
      "id": "R13",
      "domain": "RAPP",
      "title": "Palliative care: symptoms, the last days and death certification",
      "focus": "Pain mechanisms and opioid prescribing, other symptoms including terminal agitation, care in the last days, verification, certification and reporting of death.",
      "first_pass": true,
      "priority": "Core",
      "saq_cases": [
        {
          "id": "deck-geri-palliative-bowel-cancer",
          "title": "Palliative care in advanced bowel cancer",
          "set": "MD3 SAQ Revision Deck"
        },
        {
          "id": "deck-geri-end-of-life-care",
          "title": "End-of-life care and death certification",
          "set": "MD3 SAQ Revision Deck"
        }
      ],
      "core_ids": [
        "P032",
        "P065",
        "P070",
        "P103"
      ],
      "notes": "### Pain assessment\n\nThe mechanism of pain influences which treatments help:\n\n- **Somatic pain:** from skin, muscle or bone; usually well localised.\n- **Visceral pain:** from internal organs; usually diffuse or referred.\n- **Neuropathic pain:** from a lesion or disease of the somatosensory nervous system; often burning, shooting or associated with altered sensation.\n\nPain is often mixed. Assess the site, quality, severity, timing, triggers, breakthrough episodes and effect on sleep and function, together with previous treatment, opioid exposure, renal and hepatic function, constipation, cognition and sedation.\n\nPsychological, social and spiritual distress can amplify suffering and need attention alongside analgesia. Investigate reversible causes when the likely benefit fits the person's goals.\n\n> [!escalate]\n> New severe back pain with weakness or sphincter symptoms suggests spinal cord compression. Focal bone pain may indicate a fracture. Colic, distension and vomiting suggest bowel obstruction. Each needs prompt assessment, not simply a higher opioid dose.\n\n### Starting opioids\n\nNon-drug measures, paracetamol and selected anti-inflammatory or adjuvant drugs form the foundation where appropriate.\n\nFor an opioid-naive adult with significant pain who can swallow, a common starting regimen is immediate-release oral morphine `2.5–5 mg every four hours` as needed, reduced or spaced further in frailty, with close review. Significant renal impairment needs a different dose or drug, because morphine metabolites accumulate; involve palliative care.\n\n> [!pitfall]\n> A fentanyl patch is unsuitable for starting opioids or for rapid titration; it takes many hours to reach steady state.\n\n### Regular and breakthrough doses\n\nOnce the requirement is stable, a modified-release preparation can provide background control, with immediate-release doses for breakthrough pain. A breakthrough dose is usually **one-twelfth to one-sixth of the total 24-hour dose of the same opioid by the same route**. For example, 60 mg oral morphine a day corresponds to a `5–10 mg` immediate-release oral breakthrough dose.\n\nSpecify the minimum interval and a review threshold for every as-needed dose. Breakthrough doses also give information: repeated effective doses suggest the background dose needs increasing, while ineffective doses call for reassessment of the mechanism and cause.\n\nChanging route or opioid requires an equianalgesic calculation from a current conversion chart, usually followed by a dose reduction for incomplete cross-tolerance, and close monitoring. Oral, subcutaneous and transdermal doses are not interchangeable milligram for milligram. Seek specialist help with methadone, fentanyl conversions, severe renal failure or rapidly escalating pain.\n\n### Opioid counselling and adverse effects\n\nPrescribe a laxative, usually an osmotic and/or stimulant, from the start, and an antiemetic if needed. Explain regular versus breakthrough doses, safe storage, sedation and driving, and when to seek help. Early nausea and drowsiness often improve; constipation usually persists, because tolerance does not develop to it.\n\n> [!escalate]\n> Marked sedation, slow breathing, new myoclonus or confusion suggests opioid toxicity and needs urgent review.\n\nTolerance and physical dependence are expected pharmacological effects and differ from addiction. Titrating opioids for comfort does not hasten death.\n\n### Other common symptoms\n\n#### Breathlessness\n\nAssess reversible causes, then use upright positioning, a fan or airflow, pacing and reassurance. Oxygen helps mainly with hypoxaemia or demonstrated individual benefit. A monitored low-dose opioid trial may help selected patients with refractory breathlessness by reducing the sensation of air hunger; attend to anxiety and sedation risks.\n\n#### Nausea and vomiting\n\nMatch treatment to the cause, since different causes act through different receptors:\n\n- **Gastric stasis:** metoclopramide. Avoid it in complete mechanical obstruction and in Parkinson disease.\n- **Drug-induced or metabolic nausea:** a dopamine antagonist such as low-dose haloperidol; consider QT and movement effects.\n- **Vestibular nausea:** an antihistamine such as cyclizine.\n\nBowel obstruction, raised intracranial pressure (dexamethasone may help) or persistent symptoms need a specific plan, often specialist-led.\n\n#### Constipation and urinary retention\n\nAsk actively, examine when needed and treat; do not assume abdominal distress is disease progression. Overflow diarrhoea may indicate impaction. Urinary retention, often from opioids or anticholinergic drugs, can present as restlessness or lower abdominal pain; a bladder scan confirms it.\n\n#### Dry mouth\n\nFrequent mouth care, sips or ice chips if safe, and saliva substitutes often help more than IV fluid. Review anticholinergic medicines and look for oral candidiasis.\n\n#### Agitation and terminal restlessness\n\nRestlessness in a dying person is often *delirium*, a fluctuating disturbance of attention and awareness, but it can also be anxiety, existential distress or unrelieved physical discomfort, each of which needs a different response. Look first for causes that can be relieved simply: pain, a full bladder, constipation, nausea, breathlessness, an uncomfortable position, fever, and medicines, including opioid toxicity, anticholinergics, corticosteroids and withdrawal from alcohol, nicotine or benzodiazepines. In the last days, investigate only what could change comfort.\n\nA calm, familiar environment, the presence of people the patient knows, gentle reassurance and reduced noise help, and family can often provide them. Medicines are added when distress persists or the patient is at risk of harm:\n\n- **Haloperidol:** `0.5–1 mg` subcutaneously as needed for delirium with agitation or hallucinations. Avoid it in Parkinson disease and dementia with Lewy bodies.\n- **Midazolam:** `2.5–5 mg` subcutaneously as needed, at most hourly, for anxiety or severe agitation. Benzodiazepines can worsen delirium earlier in illness (see R03 (Managing delirium)), but in the last days, when the aim is comfort, midazolam is used alone or with an antipsychotic.\n\nSeek palliative care advice when symptoms are not controlled within one to two hours or repeated doses are needed; a subcutaneous infusion may follow.\n\nExplain to the family that restlessness can be part of dying, that medicines are given to relieve distress rather than to hasten death, and that any sedation is proportionate to the distress.\n\n### Care in the last days\n\n> [!counsel]\n> Families cope better when they know what to expect: increasing sleep, reduced intake, changes in breathing and noisy secretions.\n\nContinue comfort care, repositioning, mouth care and family support. Offer food and drink as wanted and safe, without forcing intake. Review burdensome monitoring and preventive medicines. Clinically assisted hydration is an individual trial when a benefit is plausible, with review for oedema or increased secretions.\n\n- **Anticipatory medicines:** prescribe subcutaneous medicines for pain or breathlessness, nausea, agitation and secretions, with clear indications and nursing access, so that symptoms can be treated promptly once oral intake stops.\n- **Secretions:** an antimuscarinic may reduce new secretions but does not clear existing fluid. Explain that noisy breathing does not necessarily mean the person is distressed.\n- **Refractory distress:** palliative sedation needs specialist assessment, explicit goals and proportionate treatment.\n\nAfter-hours help, equipment and bereavement support matter as much as the prescriptions.\n\n### Verification, certification and reporting of death\n\n**Verification** confirms that death has occurred, by the required clinical examination and local procedure: absent responsiveness, circulation and breathing. Document the findings, time and identity. **Certification** states the medical cause of death.\n\nFor a natural death that can be certified, the medical certificate of cause of death lists the causal sequence from the immediate cause to the underlying disease, with other contributing conditions listed separately. \"Cardiac arrest\" alone describes a mechanism, not a cause.\n\nReport to, or seek advice from, the Coroner when a death is unexpected, violent, unnatural or injury-related; when the cause or identity is unknown; when it may be related to a procedure; or when it falls into a statutory category of care or custody. An old injury can still have contributed.\n\nNot every death of a person with a psychiatric history is reportable, but specified circumstances under mental health legislation carry additional obligations. Do not issue an ordinary certificate when a coronial process is required.\n\n### Voluntary assisted dying\n\nLawful voluntary assisted dying (VAD) is distinct from symptom relief and from withholding unwanted treatment. In Victoria, a death following lawful VAD is excluded from the definition of a reportable death, but the certifying doctor must notify the Coroner if aware that the person had a VAD permit. Follow the current VAD and certification pathway; amendments commencing in April 2027 are not yet in force in November 2026.\n\nReferences: [WA Health: palliative care prescribing](https://www.kemh.health.wa.gov.au/~/media/HSPs/NMHS/Hospitals/WNHS/Documents/Clinical-guidelines/Obs-Gyn-Guidelines/Palliative-Care.pdf); [Victorian community palliative care guidance](https://www.health.vic.gov.au/ready-for-community-palliative-care/referring-to-community-services); [Coroners Court: reportable deaths](https://www.coronerscourt.vic.gov.au/report-death-or-fire/reportable-deaths); [BDM: legal requirements for doctors](https://www.bdm.vic.gov.au/legal-requirements-doctors).",
      "formerly": [
        "R10",
        "R11"
      ]
    },
    {
      "id": "B01",
      "domain": "Bridge",
      "title": "Acute adult presentations: recognition and first response",
      "focus": "Instability and time-critical patterns, first treatments, acute abdominal pain, smaller-volume haemoptysis and handover.",
      "first_pass": false,
      "priority": "Safety",
      "saq_cases": [
        {
          "id": "deck-geri-acute-stroke",
          "title": "Acute ischaemic stroke",
          "set": "MD3 SAQ Revision Deck"
        },
        {
          "id": "deck-geri-heart-failure",
          "title": "Heart failure and acute pulmonary oedema",
          "set": "MD3 SAQ Revision Deck"
        }
      ],
      "core_ids": [
        "P013",
        "P022",
        "P046",
        "P048",
        "P060",
        "P061",
        "P063",
        "P072",
        "P085",
        "P098"
      ],
      "notes": "### First response\n\nAssess airway, breathing, circulation, disability and exposure, including observations, oxygen saturation, capillary glucose and conscious state. In the community, the priority is to recognise instability and get the patient to definitive care quickly. Call an ambulance early, start basic life support when needed, and give treatment within the skills and resources available.\n\n> [!pitfall]\n> Do not delay transfer to complete an outpatient set of investigations.\n\n### Time-critical patterns\n\n#### Acute coronary syndrome and aortic dissection\n\nPersistent pressure-like chest pain with sweating or breathlessness suggests ACS. Sudden severe chest or back pain with collapse, or a difference in pulses or new neurological signs, suggests aortic dissection.\n\nRecord an ECG if immediately available; a normal tracing does not exclude ACS. Give aspirin for suspected ACS when appropriate, but not when major bleeding or dissection is a concern. Arrange ambulance transfer. See G07 (Assessment) for the community approach.\n\n#### Stroke and TIA\n\nSudden face or arm weakness, speech or visual disturbance, ataxia or another focal deficit suggests stroke or TIA. Record the **time last known well**, which determines eligibility for reperfusion, check glucose, and transfer as an emergency even if the symptoms have resolved, since the early stroke risk after TIA is high.\n\nGive nothing by mouth, including medicines, until swallowing has been screened, because dysphagia after stroke causes aspiration.\n\nSecondary prevention, which differs for cardioembolic and other ischaemic events, is in R10 (Secondary prevention after stroke or TIA).\n\n#### Sepsis and meningitis\n\nInfection with poor perfusion, altered consciousness, respiratory compromise or organ dysfunction suggests sepsis; fever may be absent. Meningism, a non-blanching rash or a rapidly worsening headache raises concern for meningitis. Transfer urgently. The hospital sepsis response takes blood cultures and a lactate, gives IV antibiotics chosen by the likely source within the first hour, and gives crystalloid boluses for hypotension or poor perfusion (commonly `500 mL` in an adult, reassessing after each), without delaying for a lumbar puncture or non-essential tests. Where meningococcal disease is suspected and transfer will be delayed, give benzylpenicillin or ceftriaxone before transfer.\n\n#### Pulmonary embolism and severe respiratory illness\n\nAcute unexplained breathlessness, pleuritic pain, haemoptysis, syncope or hypoxaemia raises pulmonary embolism; consider VTE risk factors, as well as pneumonia, severe asthma or COPD, and pulmonary oedema. Severe work of breathing, exhaustion, a silent chest or altered consciousness needs immediate support. Titrate oxygen to an appropriate target, using a controlled target (`88–92%`) when there is a risk of hypercapnic respiratory failure.\n\nThe probability-based work-up for PE is in G06 (Suspected pulmonary embolism). The first treatment of acute asthma in adults, and pneumonia severity assessment, are in G10 (Acute asthma; Community-acquired pneumonia).\n\n#### Major bleeding and the acute abdomen\n\nHaematemesis, melaena with compromise, heavy haemoptysis, peritonism, obstruction or sudden severe abdominal pain needs emergency assessment and resuscitation. Anticoagulants and possible pregnancy change the differential and must be included in the handover.\n\nThe assessment of acute abdominal pain, including appendicitis and the colics, is in Acute abdominal pain below.\n\n### First treatments\n\n#### Anaphylaxis\n\nGive IM adrenaline promptly. The dose, positioning, devices and observation period are in B02 (Recognition and adrenaline).\n\n#### Seizures and altered consciousness\n\nProtect the person from injury, time the seizure, maintain the airway and check glucose. Do not restrain the person or put anything in their mouth. A seizure lasting `five minutes`, or recurrent seizures without recovery, needs a benzodiazepine, commonly midazolam `10 mg` buccal, intranasal or IM in an adult (less in a frail or small adult), repeated once after `five minutes` if the seizure continues, and ambulance transfer. The main causes to consider are hypoglycaemia, stroke, infection, intoxication and withdrawal.\n\n#### Opioid toxicity\n\nOpioid toxicity with respiratory depression needs breathing support and naloxone (for example `400 micrograms IM`, repeated as needed), followed by continued observation and transfer. Naloxone is shorter-acting than many opioids, so sedation can return.\n\n#### Diabetic emergencies\n\nSweating and confusion may be hypoglycaemia. Give fast-acting carbohydrate only if the person can swallow safely; otherwise give emergency parenteral treatment (glucagon `1 mg IM`).\n\nHyperglycaemia with dehydration, vomiting, abdominal pain or deep breathing suggests DKA or the hyperosmolar hyperglycaemic state. Check ketones where available and transfer. DKA associated with SGLT2 inhibitors can occur without marked hyperglycaemia.\n\n### Acute abdominal pain\n\nThe first decision is whether the patient needs emergency care, and it does not depend on reaching a diagnosis. Shock or tachycardia, peritonism (guarding, rigidity, or pain on moving or coughing), features of obstruction, significant gastrointestinal bleeding, pain out of proportion to the examination, and pain or bleeding with a positive pregnancy test each need same-day emergency, surgical or gynaecological assessment rather than outpatient tests.\n\n> [!pitfall]\n> Older people, and those who are immunosuppressed or taking corticosteroids, can have perforation, ischaemia or appendicitis with few signs, a normal temperature and a normal white cell count. Lower the threshold for referral.\n\nThe history covers the site and onset of the pain, its progression and radiation, vomiting, bowel and urinary symptoms, fever, previous episodes and operations, NSAIDs, alcohol and anticoagulants, and the menstrual, sexual and pregnancy history. Examine the hernial orifices, and the testes in males, since torsion can present as lower abdominal pain; perform a pelvic examination, with consent, when gynaecological disease is suspected.\n\nAppendicitis typically begins as vague periumbilical pain, because the inflamed appendix first stimulates visceral afferents, then localises to the right iliac fossa once the parietal peritoneum is irritated. Anorexia, nausea and low-grade fever are usual, followed by localised tenderness and guarding. Presentations are less typical in older people, in pregnancy and with a retrocaecal appendix. Suspected appendicitis needs same-day surgical assessment: test for pregnancy, give analgesia, which does not obscure the diagnosis, and keep the patient fasted.\n\nOther common and dangerous causes have recognisable patterns:\n\n- **Biliary disease:** right upper-quadrant or epigastric pain, often after meals; fever and persisting tenderness suggest cholecystitis, and jaundice suggests a duct stone or cholangitis. See G16 (Gallstone disease).\n- **Acute pancreatitis:** severe, constant epigastric pain radiating to the back, with vomiting, most often caused by gallstones or alcohol. A lipase above `three times` the upper limit of normal supports the diagnosis, and every suspected case needs hospital care.\n- **Perforated peptic ulcer:** sudden severe epigastric pain that becomes generalised, with a rigid abdomen, often after NSAID use.\n- **Bowel obstruction:** colicky central pain, vomiting, distension and absent flatus and stool. Adhesions from previous surgery, a hernia and colorectal cancer are the usual causes.\n- **Diverticulitis:** left iliac fossa pain and tenderness, fever and altered bowel habit, usually in an older adult.\n- **Renal colic:** waves of loin-to-groin pain in a restless patient, with haematuria. See G17 (Renal colic).\n- **Vascular emergencies:** mesenteric ischaemia causes pain out of proportion to the signs, typically with AF or vascular disease; a leaking aortic aneurysm causes abdominal, back or loin pain and collapse in an older person. Both are easily mistaken for colic.\n- **Gynaecological and pregnancy-related causes:** ectopic pregnancy, ovarian torsion, pelvic inflammatory disease and a ruptured or haemorrhagic cyst. See O03 (Initial assessment) and O11 (Assessment of pelvic pain).\n- **Medical causes:** inferior myocardial infarction, DKA, lower-lobe pneumonia and pyelonephritis.\n\nTest for pregnancy in anyone who could be pregnant, and test the urine. Choose blood tests by the likely cause: FBE and CRP for inflammation, electrolytes and renal function when the patient is vomiting or unwell, and liver function and lipase for upper abdominal pain, with an ECG for epigastric pain. Ultrasound is the first imaging for biliary and pelvic disease and in pregnancy. CT is the usual test for suspected diverticulitis, obstruction, perforation or ischaemia, and for uncertain appendicitis in adults.\n\nGive analgesia and an antiemetic, and keep the patient fasted if surgery is possible. A stable patient with localised pain and no warning features can be investigated as an outpatient, provided there is a definite review within `24 hours` and clear advice about what should prompt earlier return. Uncomplicated diverticulitis in a well, afebrile patient who can drink is usually managed at home with analgesia and fluids; antibiotics are no longer routine and are reserved for systemic features, significant comorbidity or immunosuppression. Colonoscopy follows complicated diverticulitis, and uncomplicated disease when CT is suspicious or bowel screening is due.\n\nA referral to the emergency department gives the onset and course of the pain, the observations and examination findings, the tests and treatment already given, pregnancy status, anticoagulants and the question being asked; see Handover and safety-netting below.\n\n### Smaller-volume haemoptysis\n\nConfirm that the blood has been coughed up, not vomited or coming from the nose or mouth; each source has a different differential. The amount, recurrence, fever, sputum, weight loss, smoking, tuberculosis exposure and VTE risk point to the likely cause. Check observations, oxygen saturation and the chest. The main causes to consider are infection, bronchiectasis, malignancy and pulmonary embolism.\n\nA stable patient needs a chest X-ray and investigation guided by the pattern. Persistent or recurrent unexplained haemoptysis needs CT and respiratory assessment even if the chest X-ray is normal, because a plain film can miss a central tumour.\n\n> [!escalate]\n> Increasing bleeding, respiratory compromise or haemodynamic instability needs emergency transfer.\n\n### Handover and safety-netting\n\nUse **ISBAR**: identify yourself and the patient, state the immediate concern, give relevant background, the observations, onset and treatment given, and make a clear request. Include allergies, anticoagulants, the time last known well, possible pregnancy and any treatment limitations.\n\nFor a patient judged suitable for outpatient care, state which symptoms mean deterioration, when the review will be, and who will follow up outstanding results.\n\n> [!pitfall]\n> \"Return if worse\" without saying what to look for is not a safety net.",
      "formerly": [
        "B01"
      ]
    },
    {
      "id": "B02",
      "domain": "Bridge",
      "also_in": [
        "CAH"
      ],
      "title": "Anaphylaxis",
      "focus": "Recognition, IM adrenaline dose and technique, positioning, observation, and follow-up after recovery, for all ages.",
      "first_pass": true,
      "priority": "Safety",
      "saq_cases": [
        {
          "id": "deck-paeds-anaphylaxis",
          "title": "Anaphylaxis",
          "set": "MD3 SAQ Revision Deck"
        }
      ],
      "core_ids": [
        "P061"
      ],
      "notes": "### Recognition and adrenaline\n\n**Anaphylaxis** is a rapid-onset systemic allergic reaction with airway, breathing or circulatory involvement after a likely exposure. Skin signs are often present but can be absent.\n\n> [!escalate]\n> Give **IM adrenaline into the outer mid-thigh** and call an ambulance:\n>\n> - **Dose:** `0.01 mg/kg` of 1 mg/mL (1:1000) adrenaline.\n> - **Maximum:** `0.5 mg` per dose.\n> - **Repeat:** every `five minutes` if needed.\n\nLay the person flat, or let them sit with legs extended if breathing is difficult. In pregnancy, use a left-lateral position that supports breathing and circulation. Do not let the person stand or walk, because a sudden change of posture can precipitate cardiovascular collapse. Hold infants horizontally.\n\n> [!pitfall]\n> Antihistamines and corticosteroids do not replace adrenaline. Only adrenaline reverses airway oedema and vasodilatory shock.\n\nSudden swelling of the tongue or lips with airway symptoms is an emergency.\n\n### Adrenaline autoinjector\n\nFor an **EpiPen**:\n\n1. Remove the blue safety release.\n2. Place the orange end against the outer mid-thigh and push down firmly; hold for `three seconds`, stabilising a young child's leg.\n3. Call an ambulance, and give another dose after `five minutes` if symptoms persist.\n\nOther devices have different instructions.\n\n### Observation and follow-up\n\nObserve for at least `four hours` after the last dose of adrenaline, in a setting able to manage deterioration, because symptoms can return after apparent recovery (biphasic reaction).\n\nAfter recovery, prescribe adrenaline autoinjectors, provide an ASCIA action plan, refer to an allergist, and train caregivers and the school or childcare service.",
      "formerly": [
        "B01",
        "B02",
        "C06"
      ]
    }
  ]
}