Log In Get started Bookmarks Help Progress 0% Cardiovascular AAA + Rupture AC dislocation ATSI Abdominal pain in kids Abnormal/Dysfunctional Uterine Bleeding (AUB/DUB) Acanthosis Nigricans Acne Acromegaly Actinic Cheilitis Acute Kidney Injury (AKI) Acute Swollen Joint with Fever Acute Vision Loss Acute and Progressive Vision Loss Addisons Adjustment Disorder and Anxiety Adjustment Disorder with Depressed Mood Age related macular degeneration Alcohol Cessation Allergic rhinitis Alopecia Amenorrhoea Anaphylaxis Angina Angular Cheilitis Ankylosing Spondylitis (AS) Anorexia Nervosa Anticholinergics and TCAs Antidepressants Antimetabolite drugs Antiphospholipid syndrome Antipsychotics Anxiety Disorders Aortic Dissection Arrhythmia Asthma Asthma Atrial Fibrillation Back pain Behavioural / learning disorders Behavioural disturbances Bell’s palsy and Ramsey Hunt syndrome Beta-Human Chorionic Gonadotropin (β-hCG) Biologic agents Bipolar Disorder Bleeding disorders Blepharitis Breast Cancer Breast Lump Bronchiectasis (Updated) CA-125 (Cancer Antigen 125) CRPS CVD Risk Assessment Calluses and Corns Candida (Candidiasis as an STI) Carpal tunnel syndrome and de quervains tenosynovitis Cellulite Cervical spondylosis Chest pain Chickenpox (Varicella) Chilblains Cholesteatoma Chronic Cough in Children Chronic Fatigue Syndrome (CFS) Chronic Kidney Disease (CKD) Chronic Rhinosinusitis Chronic Stridor Clavicular fracture Clozapine Coeliacs Colorectal Cancer Screening Recommendations Congestive Cardiac Failure Connective Tissue Diseases Constipation Contact Dermatitis Cracked Heel Croup Cushings Cutaneous Drug Eruptions DKA vs HHS Dacrocystitis, dacyrostenosis, dacyrocystocoele Deep Vein Thrombosis (DVT) Delerium Dementia Depression and Delirium Dermal melanocystosis (mongolian spot) Developmental Dysplasia of the Hip (DDH) Diabetes Diabetes Insipidus (DI) vs Primary Polydipsia Diabetic Neuropathy Diarrhoea Diplopia Dizziness / syncope Down syndrome Duchenne muscular dystrophy Dupuytrens / trigger finger Dyspepsia Dyspnoea (Shortness of Breath) ECG ECG Findings ECG Patterns CONCISE COMPREHENSIVE Eating Disorders Risk Factors Female Family history Body dissatisfaction Negative self-evaluation Idealisation of thinness Dieting Perfectionism or high personal standards History of trauma or abuse Peer pressure or societal influences promoting thinness Sports or activities emphasizing leanness (e.g., ballet, gymnastics) Comorbid psychiatric conditions (depression, anxiety, OCD) Diagnostic Questions SCOFF Questionnaire Sick: Do you make yourself sick because you feel uncomfortably full? Control: Do you worry you have lost control over how much you eat? One stone: Have you lost >6 kg in 3 months? Fat: Do you believe you are fat despite others saying you are thin? Food: Does food dominate your life?Interpretation: Score ≥2 → likely eating disorder, needs further evaluation Additional Questions Does your weight affect how you feel about yourself? Do you feel guilty after eating? Do you compare your body to others? Any mood or anxiety changes related to eating? Any eating rituals (e.g., cutting food into small pieces)? Physical symptoms (dizziness, fatigue)? Do you avoid certain foods/food groups? Why? Notes: Screen for comorbid mental health issues (depression, anxiety, substance abuse) Assess the impact of eating behaviours on daily life (e.g., school, work) Consider cultural and societal influences on body image and eating patterns Evaluate for physical complications: malnutrition, electrolyte imbalances, cardiac issues Use a multidisciplinary approach (mental health, dietitians, medical team) Early intervention: Improves prognosis, reduces long-term complications Approach: Non-judgmental, supportive conversations about body image and eating Follow-up: Regular reviews to monitor progress and adjust treatment Eating Disorders Risk Factors Female sex: Eating disorders are more prevalent in females, although males are increasingly affected. Family history: Genetic predisposition or shared environmental factors. Body dissatisfaction: Negative body image; idealisation of thinness. Negative self-evaluation: Low self-esteem, perfectionism, or high personal standards. Dieting behaviour: Restrictive eating patterns can precede an eating disorder. History of trauma or abuse: Physical, sexual, or emotional trauma can be a contributing factor. Peer or societal pressure: Emphasis on thinness in social groups, media, or certain cultures. Sports or activities emphasising leanness: Ballet, gymnastics, distance running, etc. Comorbid psychiatric conditions: Depression, anxiety, OCD, substance use disorders. Diagnostic Questions SCOFF Questionnaire (quick screening tool): Sick: Do you make yourself sick because you feel uncomfortably full? Control: Do you worry you have lost control over how much you eat? One stone: Have you lost more than 6 kg in a 3-month period? Fat: Do you believe you are fat when others say you are too thin? Food: Does food dominate your life? Interpretation: A score ≥2 suggests a likely eating disorder; further assessment is warranted. Additional Questions Does your weight influence your self-esteem or how you feel about yourself? Do you feel guilty after eating? Do you frequently compare your body shape or weight to others? Do you experience mood or anxiety changes related to eating? Are there any eating rituals (e.g. cutting food into small pieces, food avoidance)? Do you experience physical symptoms like dizziness or fatigue? Do you avoid specific foods or entire food groups? Why? Bookmark Failed! Bookmark Saved! Add Bookmark Refresh Refresh

Log In Get started Bookmarks Help Progress 0% Cardiovascular AAA + Rupture AC dislocation ATSI Abdominal pain in kids Abnormal/Dysfunctional Uterine Bleeding (AUB/DUB) Acanthosis Nigricans Acne Acromegaly Actinic Cheilitis Acute Kidney Injury (AKI) Acute Swollen Joint with Fever Acute Vision Loss Acute and Progressive Vision Loss Addisons Adjustment Disorder and Anxiety Adjustment Disorder with Depressed Mood Age related macular degeneration Alcohol Cessation Allergic rhinitis Alopecia Amenorrhoea Anaphylaxis Angina Angular Cheilitis Ankylosing Spondylitis (AS) Anorexia Nervosa Anticholinergics and TCAs Antidepressants Antimetabolite drugs Antiphospholipid syndrome Antipsychotics Anxiety Disorders Aortic Dissection Arrhythmia Asthma Asthma Atrial Fibrillation Back pain Behavioural / learning disorders Behavioural disturbances Bell’s palsy and Ramsey Hunt syndrome Beta-Human Chorionic Gonadotropin (β-hCG) Biologic agents Bipolar Disorder Bleeding disorders Blepharitis Breast Cancer Breast Lump Bronchiectasis (Updated) CA-125 (Cancer Antigen 125) CRPS CVD Risk Assessment Calluses and Corns Candida (Candidiasis as an STI) Carpal tunnel syndrome and de quervains tenosynovitis Cellulite Cervical spondylosis Chest pain Chickenpox (Varicella) Chilblains Cholesteatoma Chronic Cough in Children Chronic Fatigue Syndrome (CFS) Chronic Kidney Disease (CKD) Chronic Rhinosinusitis Chronic Stridor Clavicular fracture Clozapine Coeliacs Colorectal Cancer Screening Recommendations Congestive Cardiac Failure Connective Tissue Diseases Constipation Contact Dermatitis Cracked Heel Croup Cushings Cutaneous Drug Eruptions DKA vs HHS Dacrocystitis, dacyrostenosis, dacyrocystocoele Deep Vein Thrombosis (DVT) Delerium Dementia Depression and Delirium Dermal melanocystosis (mongolian spot) Developmental Dysplasia of the Hip (DDH) Diabetes Diabetes Insipidus (DI) vs Primary Polydipsia Diabetic Neuropathy Diarrhoea Diplopia Dizziness / syncope Down syndrome Duchenne muscular dystrophy Dupuytrens / trigger finger Dyspepsia Dyspnoea (Shortness of Breath) ECG ECG Findings ECG Patterns CONCISE COMPREHENSIVE Short Stature Definition Height below the 3rd centile for age and sex Growth Drivers Neonatal: Nutrition Childhood: Growth hormone (GH), insulin-like growth factor 1 (IGF-1) Adolescence: Sex steroids Differentials Physiological Constitutional delay of growth and puberty (CDGP): Delayed puberty, family history, normal predicted adult height Familial short stature: Genetically short but following mid-parental height trajectory Pathological Perinatal: Prematurity, intrauterine growth restriction (IUGR), low birth weight Nutritional: Malnutrition, poor feeding, anorexia nervosa Chronic illness: Coeliac disease, inflammatory bowel disease, renal or cardiac disease Endocrine: Growth hormone deficiency (↓ velocity, delayed bone age), hypothyroidism, Turner syndrome Psychosocial: Chronic stress, neglect Investigations Bloods: FBC, ESR, UEC, LFTs, TFTs, coeliac serology, IGF-1 Bone age X-ray: Wrist X-ray to assess skeletal maturation Specialist tests: Karyotype for Turner syndrome, GH stimulation test for suspected deficiency Management Physiological Causes CDGP: Reassurance, monitoring, short-course sex steroids if significant distress Pathological Causes Treat underlying condition (e.g., gluten-free diet for coeliac disease, thyroxine for hypothyroidism) GH therapy for growth hormone deficiency (specialist-led) Referral Height below the 1st centile Crossing ≥2 centile lines downward Significant deviation from mid-parental height Delayed puberty: Girls: No breast development by 13 Boys: Testes <4 mL by 14 Notes Monitor growth velocity over time CDGP: Delayed bone age but normal growth velocity Short Stature Definition Height below the 3rd centile for age and sex on standard growth charts Often defined by significant deviation from mid-parental height Growth Drivers Neonatal: Primarily influenced by nutrition Childhood: Governed by growth hormone (GH) and insulin-like growth factor 1 (IGF-1) levels Adolescence: Driven by sex steroids contributing to the pubertal growth spurt Differential Diagnosis Physiological Constitutional delay of growth and puberty (CDGP) with normal adult height and family history Familial short stature based on genetic potential from mid-parental height Pathological Perinatal factors such as prematurity, intrauterine growth restriction (IUGR) and low birth weight Nutritional deficiencies from malnutrition, poor feeding or anorexia Chronic illnesses including coeliac disease, inflammatory bowel disease, renal or cardiac disorders Endocrine disorders such as growth hormone deficiency (evidenced by low growth velocity and delayed bone age), hypothyroidism, Turner syndrome, Prader-Willi syndrome and SHOX gene disorders Psychosocial factors including stress, neglect and chronic emotional deprivation Investigations Blood tests Full blood count, urea and electrolytes, comprehensive metabolic panel and liver function tests Thyroid function tests and coeliac serology to exclude nutritional or endocrine causes Insulin-like growth factor 1 (IGF-1) levels to assess GH status Bone age assessment Wrist X-ray to compare bone age with chronological age and assess growth potential Growth velocity Serial height measurements over at least 12 months (minimum three readings, spaced 3 months apart) Specialist evaluations GH stimulation test if growth hormone deficiency is suspected Chromosomal analysis (karyotyping) for conditions such as Turner syndrome Management Physiological causes (CDGP, familial short stature) Reassure families and monitor growth and pubertal progression with regular follow-up Consider short-course sex steroids if the delay causes significant distress Pathological causes Address underlying nutritional deficiencies and chronic illnesses with appropriate dietary or medical therapy Treat endocrine disorders with thyroxine replacement for hypothyroidism or initiate GH therapy for confirmed growth hormone deficiency under specialist guidance Referral criteria Height below the 1st centile or crossing two or more centile lines downward Significant deviation from mid-parental height Delayed puberty with no breast development by 13 in girls or testicular volume <4 mL by 14 in boys Notes Most cases of short stature are due to constitutional delay; pathological causes account for only 10–15% of cases Interpretation of a child’s growth should always be contextualised with parental heights and family history Regular monitoring of growth velocity and bone age is essential to guide management Growth hormone therapy is available through specialist referral and is indicated for children with confirmed GH deficiency or other endocrine causes Early identification and treatment of underlying conditions optimise adult height and long-term health outcomes A multidisciplinary approach involving paediatric endocrinologists, gynaecologists and dietitians improves management of complex cases 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Log In Get started Bookmarks Help Progress 0% Cardiovascular AAA + Rupture AC dislocation ATSI Abdominal pain in kids Abnormal/Dysfunctional Uterine Bleeding (AUB/DUB) Acanthosis Nigricans Acne Acromegaly Actinic Cheilitis Acute Kidney Injury (AKI) Acute Swollen Joint with Fever Acute Vision Loss Acute and Progressive Vision Loss Addisons Adjustment Disorder and Anxiety Adjustment Disorder with Depressed Mood Age related macular degeneration Alcohol Cessation Allergic rhinitis Alopecia Amenorrhoea Anaphylaxis Angina Angular Cheilitis Ankylosing Spondylitis (AS) Anorexia Nervosa Anticholinergics and TCAs Antidepressants Antimetabolite drugs Antiphospholipid syndrome Antipsychotics Anxiety Disorders Aortic Dissection Arrhythmia Asthma Asthma Atrial Fibrillation Back pain Behavioural / learning disorders Behavioural disturbances Bell’s palsy and Ramsey Hunt syndrome Beta-Human Chorionic Gonadotropin (β-hCG) Biologic agents Bipolar Disorder Bleeding disorders Blepharitis Breast Cancer Breast Lump Bronchiectasis (Updated) CA-125 (Cancer Antigen 125) CRPS CVD Risk Assessment Calluses and Corns Candida (Candidiasis as an STI) Carpal tunnel syndrome and de quervains tenosynovitis Cellulite Cervical spondylosis Chest pain Chickenpox (Varicella) Chilblains Cholesteatoma Chronic Cough in Children Chronic Fatigue Syndrome (CFS) Chronic Kidney Disease (CKD) Chronic Rhinosinusitis Chronic Stridor Clavicular fracture Clozapine Coeliacs Colorectal Cancer Screening Recommendations Congestive Cardiac Failure Connective Tissue Diseases Constipation Contact Dermatitis Cracked Heel Croup Cushings Cutaneous Drug Eruptions DKA vs HHS Dacrocystitis, dacyrostenosis, dacyrocystocoele Deep Vein Thrombosis (DVT) Delerium Dementia Depression and Delirium Dermal melanocystosis (mongolian spot) Developmental Dysplasia of the Hip (DDH) Diabetes Diabetes Insipidus (DI) vs Primary Polydipsia Diabetic Neuropathy Diarrhoea Diplopia Dizziness / syncope Down syndrome Duchenne muscular dystrophy Dupuytrens / trigger finger Dyspepsia Dyspnoea (Shortness of Breath) ECG ECG Findings ECG Patterns CONCISE COMPREHENSIVE Stroke Acute Management (Ischaemic) Aspirin 300mg stat if CT excludes bleed; continue 100mg daily thereafter BP target pre-thrombolysis: <185/110mmHg; post-thrombolysis: <140/90mmHg (use GTN or labetalol) Thrombolysis: Within 4.5 hours of symptom onset (e.g., alteplase) Endovascular thrombectomy: Perform within 6 hours (up to 24hrs if salvageable tissue seen on imaging) Thrombectomy: Indications and Timing Large vessel occlusion (MCA, basilar artery), salvageable penumbra on CT/MR perfusion imaging Standard within 6 hours, extended up to 24 hours with salvageable tissue Haemorrhagic Stroke Stop anticoagulants/antiplatelets; reverse anticoagulation if needed (e.g., vitamin K, FFP) BP target: <140mmHg systolic Avoid chemical DVT prophylaxis for 48hrs; use mechanical prophylaxis instead Refer to neurosurgery urgently Contraindications to Thrombolysis/Thrombectomy Intracranial haemorrhage, active bleeding/coagulopathy Ischaemic stroke or major trauma in the past 3 months BP >185/110mmHg Rehabilitation (Multidisciplinary) Early stroke unit involvement: Physiotherapy: Mobility, balance, strength training Occupational therapy: ADLs, adaptive techniques Speech therapy: Swallowing, speech recovery Dietitian: Nutrition support, dysphagia management Social worker: Support services, discharge planning Goals: Maximise independence, prevent complications (DVT, contractures, aspiration) Secondary Prevention BP control: Target <140/90mmHg (ACEI/ARB, CCB preferred) Diabetes management: Optimise HbA1c target ≤7%, lifestyle measures + metformin 1st line if T2DM Smoking cessation: Strong recommendation with NRT, behavioural support, or pharmacotherapy Other measures: Statins: High-potency (e.g., atorvastatin 40–80mg) Antiplatelets: Aspirin + dipyridamole or clopidogrel SNAP risk factors: Smoking, Nutrition, Alcohol, Physical activity Post-hospital Discharge Assess suitability of care plan for post-stroke impairment/disability Ensure carer support (e.g., discuss respite care if necessary) Facilitate ongoing rehabilitation (OT, physiotherapy) Prescribe secondary prevention medications as appropriate Advise on SNAP goals (support for smoking cessation) Inform about driving restrictions: 2 weeks for TIA, 4 weeks for stroke Ensure diet is suitable for swallow function to prevent aspiration Refer to Stroke Foundation Australia for additional support Longer-term Goals Review for residual disability/impairment and optimise lifestyle Monitor for fatigue or depression, offering psychological interventions if necessary Screen for aspiration risks (e.g., cough, chest infections) Optimise comorbidities such as diabetes, hypertension Stroke Acute Management (Ischaemic) Aspirin 300mg stat if non-haemorrhagic stroke confirmed on imaging, continue 100mg daily thereafter Blood pressure control Pre-thrombolysis: <185/110mmHg Post-thrombolysis: <140/90mmHg (use IV antihypertensives such as GTN or labetalol) Thrombolysis Give IV alteplase within 4.5 hours of symptom onset Ensure CT/MRI excludes haemorrhage and no contraindications Aim for door-to-needle time <60 minutes Endovascular Thrombectomy Recommended for large vessel occlusion (MCA, basilar) Ideally within 6 hours of onset Extended window (up to 24 hours) for selected patients with salvageable tissue on advanced imaging Thrombectomy: Indications and Timing Large vessel occlusion in anterior circulation, confirmed on CTA/MRA Perfusion imaging (CTP/MR perfusion) demonstrates salvageable penumbra Key time frames Standard up to 6 hours Extended up to 24 hours if perfusion imaging shows ongoing viability Haemorrhagic Stroke Reverse anticoagulation if present (vitamin K, prothrombin complex concentrate or FFP) Target systolic BP <140mmHg Avoid chemical DVT prophylaxis for first 48 hours, use mechanical prophylaxis (intermittent pneumatic compression) Urgent neurosurgical referral for possible surgical intervention if large haematoma or elevated intracranial pressure Contraindications to Thrombolysis/Thrombectomy Intracranial haemorrhage, active bleeding, coagulopathy Recent ischaemic stroke or significant trauma in the past 3 months Persistent severe hypertension >185/110mmHg Uncertain time of onset beyond approved windows Rehabilitation (Multidisciplinary) Early stroke unit involvement improves outcomes Physiotherapy: Mobility, balance, and strength training Occupational therapy: Activities of daily living, adaptive techniques Speech therapy: Swallowing, speech and language recovery Dietitian: Nutrition optimisation, dysphagia management Social work: Support services, carer planning, discharge coordination Aim to maximise functional recovery and prevent complications such as aspiration pneumonia, contractures, and DVT Secondary Prevention Blood pressure control Target <140/90mmHg in most patients ACEI/ARB or CCB often first-line, especially if accompanied by diabetes or LVH Diabetes management Aim for HbA1c ≤7% in type 2 diabetes Emphasise dietary measures, exercise, and optimal medication adjustments Smoking cessation Strongly recommended (NRT, varenicline, or bupropion plus behavioural support) Lipid management High-potency statins (e.g. atorvastatin 40–80mg) Consider ezetimibe if statin intolerance Antiplatelet therapy Aspirin 100mg daily plus dipyridamole SR 200mg twice daily Alternatively, clopidogrel monotherapy 75mg daily Some guidelines recommend short-term dual antiplatelet therapy (e.g. aspirin + clopidogrel for 21–90 days) in minor stroke/TIA SNAP risk factor optimisation (Smoking, Nutrition, Alcohol, Physical activity) Post-Hospital Discharge Assess ongoing rehabilitation needs and develop tailored care plan Ensure adequate carer support and consider respite care if required Ongoing therapy (physiotherapy, occupational therapy) for at least 6–12 weeks Long-term secondary prevention medications (antiplatelet/antihypertensive/statin) Driving restrictions TIA: No driving for 2 weeks Stroke: Minimum 4 weeks, then conditional on medical clearance Ensure safe swallow (monitor for aspiration risk) Advise on lifestyle measures and regular follow-up with GP or stroke clinic Longer-Term Goals Review for residual impairments and address complications such as spasticity or neuropathic pain Monitor mood and cognition, as post-stroke depression and fatigue are common Encourage ongoing exercise or community programs for fitness and social support Optimise comorbidities such as hypertension, hyperlipidaemia, and diabetes to reduce recurrent stroke risk Assess for persistent dysphagia and malnutrition if patient has recurrent chest infections or weight loss Notes: Early recognition of stroke is crucial (FAST: Face, Arms, Speech, Time), and immediate ED referral can reduce morbidity Telestroke services can expedite thrombolysis decisions for rural areas Uncomplicated haemorrhagic strokes with stable imaging may require conservative management, but close observation for expansion is essential Stroke Foundation resources can support patients and families with education and self-management strategies Bookmark Failed! 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Log In Get started Bookmarks Help Progress 0% Cardiovascular AAA + Rupture AC dislocation ATSI Abdominal pain in kids Abnormal/Dysfunctional Uterine Bleeding (AUB/DUB) Acanthosis Nigricans Acne Acromegaly Actinic Cheilitis Acute Kidney Injury (AKI) Acute Swollen Joint with Fever Acute Vision Loss Acute and Progressive Vision Loss Addisons Adjustment Disorder and Anxiety Adjustment Disorder with Depressed Mood Age related macular degeneration Alcohol Cessation Allergic rhinitis Alopecia Amenorrhoea Anaphylaxis Angina Angular Cheilitis Ankylosing Spondylitis (AS) Anorexia Nervosa Anticholinergics and TCAs Antidepressants Antimetabolite drugs Antiphospholipid syndrome Antipsychotics Anxiety Disorders Aortic Dissection Arrhythmia Asthma Asthma Atrial Fibrillation Back pain Behavioural / learning disorders Behavioural disturbances Bell’s palsy and Ramsey Hunt syndrome Beta-Human Chorionic Gonadotropin (β-hCG) Biologic agents Bipolar Disorder Bleeding disorders Blepharitis Breast Cancer Breast Lump Bronchiectasis (Updated) CA-125 (Cancer Antigen 125) CRPS CVD Risk Assessment Calluses and Corns Candida (Candidiasis as an STI) Carpal tunnel syndrome and de quervains tenosynovitis Cellulite Cervical spondylosis Chest pain Chickenpox (Varicella) Chilblains Cholesteatoma Chronic Cough in Children Chronic Fatigue Syndrome (CFS) Chronic Kidney Disease (CKD) Chronic Rhinosinusitis Chronic Stridor Clavicular fracture Clozapine Coeliacs Colorectal Cancer Screening Recommendations Congestive Cardiac Failure Connective Tissue Diseases Constipation Contact Dermatitis Cracked Heel Croup Cushings Cutaneous Drug Eruptions DKA vs HHS Dacrocystitis, dacyrostenosis, dacyrocystocoele Deep Vein Thrombosis (DVT) Delerium Dementia Depression and Delirium Dermal melanocystosis (mongolian spot) Developmental Dysplasia of the Hip (DDH) Diabetes Diabetes Insipidus (DI) vs Primary Polydipsia Diabetic Neuropathy Diarrhoea Diplopia Dizziness / syncope Down syndrome Duchenne muscular dystrophy Dupuytrens / trigger finger Dyspepsia Dyspnoea (Shortness of Breath) ECG ECG Findings ECG Patterns CONCISE COMPREHENSIVE Type 1 Diabetes Mellitus (T1DM) History Questions Weight loss in a person with normal BMI (<25) Polyuria, polydipsia, and nocturia Sudden onset of sx Ketosis or ketonuria Age <50 years Personal or family history of autoimmune diseases (e.g., coeliac disease, autoimmune thyroiditis) Investigations Blood glucose levels (random ≥11.1 mmol/L or fasting ≥7.0 mmol/L) Ketones: Blood ketones >0.5 mmol/L indicate ketosis; >1.5 mmol/L is an emergency Urine ketones (used if blood ketone testing is unavailable) Autoimmune markers: Glutamic acid decarboxylase (GAD) antibodies Insulinoma antigen-2 (IA-2) antibodies Zinc transporter-8 (ZnT8) antibodies (if avail) C-peptide (low in T1DM, helps differentiate from T2DM and latent autoimmune diabetes in adults) Notes: Islet-cell antibodies are no longer routinely used; IA-2 antibodies are preferred A blood ketone level >1.5 mmol/L suggests DKA, requiring urgent specialist input. T1DM in Adults vs Children/Adolescents Honeymoon Phase Adults: Often over 12 months. Children: Typically lasts 6–12 months. Glycaemic Targets Adults: HbA1c ≤ 7% (53 mmol/mol), fasting glucose 4–7 mmol/L, postprandial glucose 6–10 mmol/L. Children/Adolescents: HbA1c ≤ 7% (same target), but higher caution required in young children to avoid severe hypoglycaemia during rapid brain growth. Complication Screening Adults: Annual screening for microvascular (e.g., retinopathy, nephropathy) and macrovascular complications (e.g., cardiovascular disease). Children/Adolescents: Chronic complications (e.g., retinopathy, kidney disease) are rare in childhood; routine screening begins after 5 years of disease onset or age 11. Dietary Management Adults: Focus on glycaemic control and weight management. Children: Nutritional intake tailored to growth, energy needs, and puberty; education for family members is critical. T1DM Classic Symptoms: Polyuria and Polydipsia: Frequent urination and excessive thirst due to osmotic diuresis from hyperglycemia. Polyphagia: Increased hunger resulting from energy depletion in tissues. Weight Loss: Typically occurs despite normal or increased food intake, especially in individuals with a normal BMI (<25). Ketosis/Ketonuria: Presence of ketone bodies in urine or blood due to lipolysis when insulin is deficient. Onset of Symptoms: Sudden Onset: Rapid development of symptoms is common, unlike in Type 2 diabetes. Often presents in individuals aged <50 years, though it can develop at any age. Family and Personal History: Autoimmune Diseases: Ask about a personal or family history of autoimmune conditions, as T1DM is associated with other autoimmune disorders (e.g., thyroid disease, coeliac disease). Pathophysiology Mechanism: Autoimmune destruction of beta cells leads to absolute insulin deficiency, causing hyperglycaemia and associated metabolic disturbances. Stages in Development: Genetic predisposition, followed by autoimmune activation and eventual beta-cell destruction. Investigations Blood Glucose Testing: Random Blood Glucose: Elevated levels (>11.1 mmol/L) with classic symptoms can confirm the diagnosis. Fasting Blood Glucose: Elevated levels (>7 mmol/L) support the diagnosis. Blood Glucose with Ketones: Blood Ketones: Suspect T1DM if blood glucose is elevated with blood ketones >0.5 mmol/L (levels >1.5 mmol/L indicate a high risk for DKA and are an emergency). Autoantibodies: Glutamic Acid Decarboxylase (GAD) Antibodies: Commonly present in T1DM and used to differentiate from Type 2 diabetes. Insulinoma Antigen-2 (IA-2) Antibodies: Another marker for T1DM. Other Autoantibodies: Occasionally, zinc transporter 8 (ZnT8) antibodies may also be tested. C-Peptide: Low C-Peptide: Indicates low endogenous insulin production, which is characteristic of T1DM. Helps differentiate from Type 2 diabetes, where C-peptide levels are usually normal or elevated. <0.2 nmol/L in fasting or non-fasting state suggests T1DM. Note: Islet-Cell Antibodies: Previously used but now IA-2 antibodies are preferred for diagnosis. Management Insulin Therapy: Basal-Bolus Regimen: Combination of long-acting basal insulin (e.g., glargine or detemir) and short-acting bolus insulin (e.g., aspart or lispro) before meals. Continuous Subcutaneous Insulin Infusion (CSII): Insulin pumps may be considered in patients with difficulty achieving control on injections. Monitoring: Self-Monitoring of Blood Glucose (SMBG): Regular checks to adjust insulin doses and prevent hypoglycemia. Continuous Glucose Monitoring (CGM): Can provide real-time glucose levels and trends to aid in glycemic control. Education: Carbohydrate Counting: Essential for adjusting insulin doses based on meal content. Hypoglycemia Management: Education on recognising and treating low blood glucose episodes, including using glucagon in emergencies. Preventive Care: Screening for Complications: Regular checks for retinopathy, nephropathy, and neuropathy. Vaccinations: Recommend vaccinations (e.g., influenza, pneumococcal) due to increased risk of infections. Complications Diabetic Ketoacidosis (DKA): A life-threatening emergency due to insulin deficiency, resulting in hyperglycemia, acidosis, and dehydration. Management includes IV fluids, insulin infusion, electrolyte replacement, and monitoring. Long-Term Complications: Microvascular: Retinopathy, nephropathy, and neuropathy. Macrovascular: Increased risk of cardiovascular disease. Special Considerations: Adolescents and young adults may experience challenges with adherence and glycemic variability. Screen for other autoimmune disorders, such as autoimmune thyroid disease and coeliac disease, at diagnosis and periodically thereafter Bookmark Failed! Bookmark Saved! Refresh Refresh Refresh

Log In Get started Bookmarks Help Progress 0% Cardiovascular AAA + Rupture AC dislocation ATSI Abdominal pain in kids Abnormal/Dysfunctional Uterine Bleeding (AUB/DUB) Acanthosis Nigricans Acne Acromegaly Actinic Cheilitis Acute Kidney Injury (AKI) Acute Swollen Joint with Fever Acute Vision Loss Acute and Progressive Vision Loss Addisons Adjustment Disorder and Anxiety Adjustment Disorder with Depressed Mood Age related macular degeneration Alcohol Cessation Allergic rhinitis Alopecia Amenorrhoea Anaphylaxis Angina Angular Cheilitis Ankylosing Spondylitis (AS) Anorexia Nervosa Anticholinergics and TCAs Antidepressants Antimetabolite drugs Antiphospholipid syndrome Antipsychotics Anxiety Disorders Aortic Dissection Arrhythmia Asthma Asthma Atrial Fibrillation Back pain Behavioural / learning disorders Behavioural disturbances Bell’s palsy and Ramsey Hunt syndrome Beta-Human Chorionic Gonadotropin (β-hCG) Biologic agents Bipolar Disorder Bleeding disorders Blepharitis Breast Cancer Breast Lump Bronchiectasis (Updated) CA-125 (Cancer Antigen 125) CRPS CVD Risk Assessment Calluses and Corns Candida (Candidiasis as an STI) Carpal tunnel syndrome and de quervains tenosynovitis Cellulite Cervical spondylosis Chest pain Chickenpox (Varicella) Chilblains Cholesteatoma Chronic Cough in Children Chronic Fatigue Syndrome (CFS) Chronic Kidney Disease (CKD) Chronic Rhinosinusitis Chronic Stridor Clavicular fracture Clozapine Coeliacs Colorectal Cancer Screening Recommendations Congestive Cardiac Failure Connective Tissue Diseases Constipation Contact Dermatitis Cracked Heel Croup Cushings Cutaneous Drug Eruptions DKA vs HHS Dacrocystitis, dacyrostenosis, dacyrocystocoele Deep Vein Thrombosis (DVT) Delerium Dementia Depression and Delirium Dermal melanocystosis (mongolian spot) Developmental Dysplasia of the Hip (DDH) Diabetes Diabetes Insipidus (DI) vs Primary Polydipsia Diabetic Neuropathy Diarrhoea Diplopia Dizziness / syncope Down syndrome Duchenne muscular dystrophy Dupuytrens / trigger finger Dyspepsia Dyspnoea (Shortness of Breath) ECG ECG Findings ECG Patterns CONCISE COMPREHENSIVE Pneumothorax Definition & Classification Air in the pleural space causing lung collapse. Spontaneous Primary: No underlying lung disease Secondary: Associated with COPD, asthma, ILD, cystic fibrosis Traumatic Blunt/penetrating trauma Iatrogenic (e.g. pleural aspiration, lung biopsy) Decompensated (Tension) Pneumothorax Large, rapidly expanding pneumothorax → severe breathlessness, hypotension, hypoxaemia Requires immediate decompression Clinical Presentation Sudden pleuritic chest pain, dyspnoea If large: ↓ Breath sounds Tachypnoea ↓ Chest wall movement Hyperresonance Tracheal deviation (if decompensated) Investigations CXR (upright inspiratory): First-line for diagnosis CT Chest: If equivocal CXR or complex lung disease Decompensated Pneumothorax: Clinical diagnosis → do not delay needle decompression Decompensated (Tension) Pneumothorax – Emergency Management Immediate needle decompression Insert cannula in 2nd intercostal space, midclavicular line Remove needle to allow air escape Definitive management: Insert intercostal catheter (chest drain) Primary Spontaneous Pneumothorax Assess Stability Unstable? → Immediate aspiration or chest drain Stable? → Conservative management Management Options Observe with analgesia (if small, no distress) Aspiration (midaxillary line) → repeat CXR at 4h Intercostal catheter (10–14G) if aspiration fails or large pneumothorax Recurrence Prevention 30–50% recurrence risk Smoking cessation strongly advised Second ipsilateral recurrence → consider pleurodesis Secondary Spontaneous Pneumothorax Higher risk of respiratory compromise More likely to require early intercostal catheter drainage Aspiration may be attempted if small & stable Do NOT use CPAP/BPAP unless pneumothorax is drained Traumatic & Iatrogenic Pneumothorax Traumatic: Chest drain if large or unstable Iatrogenic: Often resolves; aspirate if symptomatic/large Pneumothorax Definition & Classification Pneumothorax: Air in the pleural space. Primary Spontaneous: No underlying lung disease. Secondary Spontaneous: Involves underlying lung disease (eg COPD, asthma, ILD, cystic fibrosis). Traumatic: Blunt/penetrating chest injury or iatrogenic (procedural). Decompensated (Tension): Rapid onset, unstable patient (hypotension, severe dyspnoea); requires urgent needle decompression. Clinical Clues Presentation: Sudden pleuritic chest pain + breathlessness. Signs (large pneumothorax): Absent breath sounds, hyperresonance on percussion, possible tracheal deviation away from the affected side. Diagnosed: Primarily via upright inspiratory chest X‐ray (CT if needed). Decompensated (Tension) Pneumothorax Emergency: Immediate needle decompression (above 3rd rib, midclavicular line), then chest tube. Rare in primary spontaneous pneumothorax but more common in secondary disease or trauma. Suspect in any unstable patient, especially on positive‐pressure ventilation. Primary Spontaneous Pneumothorax Many are not dangerous and can resolve spontaneously in stable patients. Conservative management often sufficient if patient is stable (analgesia ± oxygen if hypoxaemic). Catheter aspiration or intercostal drain if large or patient unstable. Recurrence ~30–50%. Smoking cessation reduces recurrence. Second ipsilateral episode → consider pleurodesis. Secondary Spontaneous Pneumothorax Underlying lung disease → more severe, even if small. More likely to require early intervention (eg intercostal drain). Do not use non‐invasive ventilation (CPAP/BPAP) unless the pneumothorax is definitively drained. Traumatic & Iatrogenic Pneumothorax Traumatic: Usually chest tube if large/unstable; consider larger‐bore tube if blood is present. Iatrogenic: Often small; manage conservatively if stable, or aspirate if needed. Persistent Air Leak Common with intercostal drains; many resolve within ~14 days without surgery. Small‐bore catheter with a one‐way valve (Heimlich) can facilitate outpatient management if stable. Bookmark Failed! Bookmark Saved! Add Bookmark Refresh Refresh

Log In Get started Bookmarks Help Progress 0% Cardiovascular AAA + Rupture AC dislocation ATSI Abdominal pain in kids Abnormal/Dysfunctional Uterine Bleeding (AUB/DUB) Acanthosis Nigricans Acne Acromegaly Actinic Cheilitis Acute Kidney Injury (AKI) Acute Swollen Joint with Fever Acute Vision Loss Acute and Progressive Vision Loss Addisons Adjustment Disorder and Anxiety Adjustment Disorder with Depressed Mood Age related macular degeneration Alcohol Cessation Allergic rhinitis Alopecia Amenorrhoea Anaphylaxis Angina Angular Cheilitis Ankylosing Spondylitis (AS) Anorexia Nervosa Anticholinergics and TCAs Antidepressants Antimetabolite drugs Antiphospholipid syndrome Antipsychotics Anxiety Disorders Aortic Dissection Arrhythmia Asthma Asthma Atrial Fibrillation Back pain Behavioural / learning disorders Behavioural disturbances Bell’s palsy and Ramsey Hunt syndrome Beta-Human Chorionic Gonadotropin (β-hCG) Biologic agents Bipolar Disorder Bleeding disorders Blepharitis Breast Cancer Breast Lump Bronchiectasis (Updated) CA-125 (Cancer Antigen 125) CRPS CVD Risk Assessment Calluses and Corns Candida (Candidiasis as an STI) Carpal tunnel syndrome and de quervains tenosynovitis Cellulite Cervical spondylosis Chest pain Chickenpox (Varicella) Chilblains Cholesteatoma Chronic Cough in Children Chronic Fatigue Syndrome (CFS) Chronic Kidney Disease (CKD) Chronic Rhinosinusitis Chronic Stridor Clavicular fracture Clozapine Coeliacs Colorectal Cancer Screening Recommendations Congestive Cardiac Failure Connective Tissue Diseases Constipation Contact Dermatitis Cracked Heel Croup Cushings Cutaneous Drug Eruptions DKA vs HHS Dacrocystitis, dacyrostenosis, dacyrocystocoele Deep Vein Thrombosis (DVT) Delerium Dementia Depression and Delirium Dermal melanocystosis (mongolian spot) Developmental Dysplasia of the Hip (DDH) Diabetes Diabetes Insipidus (DI) vs Primary Polydipsia Diabetic Neuropathy Diarrhoea Diplopia Dizziness / syncope Down syndrome Duchenne muscular dystrophy Dupuytrens / trigger finger Dyspepsia Dyspnoea (Shortness of Breath) ECG ECG Findings ECG Patterns CONCISE COMPREHENSIVE Heel Pain Key Note Consider posterior tibial tendinopathy even if tenderness localised to heel, especially with symptoms around malleoli Differentials Achilles: Rupture, tendinopathy, retrocalcaneal/ostcalcaneal bursitis Calcaneus: Sever’s disease (children), fracture, fat pad atrophy, FB Medial malleolus: Tibialis posterior/FHL tendinopathy, tarsal tunnel syndrome Plantar: Plantar fasciitis (most common in adults) Systemic: Spondyloarthritides (e.g., reactive arthritis), OA/RA, gout, septic arthritis History Activity-related: Ballet, jumping sports, running on hard surfaces Systemic symptoms: Diarrhoea, urethritis, iritis (reactive arthritis), morning stiffness Burning pain: Suggests tarsal tunnel syndrome Arch collapse: Posterior tibial tendon dysfunction Footwear: Recent changes or worn-out shoes Examination Medial malleolus: Reduced inversion → posterior tibial tendinopathy Calcaneus: Tender fat pad; swelling/erythema → bursitis/fracture Functional tests: Heel raise difficulty: Tibialis posterior dysfunction, Achilles issues Flatfoot: Posterior tibial tendon dysfunction Great toe flexion: Flexor hallucis longus tendinopathy Thompson test: No plantar flexion → Achilles rupture Management General: Heel pads/orthotics → pressure reduction Rest, NSAIDs, weight loss Ice after activity Specific: Physiotherapy: Stretch/strengthen plantar fascia, Achilles Steroid injections: Caution with Achilles (rupture risk) Podiatry referral: Footwear/orthotics advice Imaging: X-ray/MRI if no improvement Notes Sever’s disease: Supportive care (rest, ice, heel cups) in active children Tarsal tunnel: Nerve compression; treat with orthotics/activity changes Posterior tibial tendinopathy: Early treatment prevents adult flatfoot Heel Pain Key Note Consider posterior tibial tendinopathy even if tenderness is localised to the heel, especially with medial malleolus pain or progressive arch lowering Differentials Achilles: Rupture, mid-portion or insertional tendinopathy, retrocalcaneal/subcutaneous calcaneal bursitis Calcaneus: Sever’s disease (children), stress/traumatic fracture, fat pad atrophy, foreign body Medial Malleolus: Tibialis posterior or flexor hallucis longus tendinopathy, tarsal tunnel syndrome Plantar: Plantar fasciitis (worse with first steps in the morning) Systemic: Spondyloarthritides (reactive arthritis, RA, OA), gout, septic arthritis History Activity-related pain (dancers, jumping sports, running on hard surfaces) Systemic signs: Diarrhoea, urethritis, ocular inflammation (reactive arthritis), morning stiffness (inflammatory cause) Burning/tingling pain → Neural involvement (tarsal tunnel syndrome) Progressive arch collapse → Posterior tibial tendon dysfunction Footwear changes (pronation control, worn-out shoes) affecting biomechanics Examination Medial malleolus: Tenderness, reduced inversion strength (posterior tibial tendinopathy) Calcaneus: Fat pad tenderness, swelling (bursitis/stress fracture) Functional tests: Single heel raise → Tibialis posterior/Achilles dysfunction Flatfoot posture → Posterior tibial tendon collapse Great toe flexion → Flexor hallucis longus tendinopathy Thompson test → Achilles rupture Windlass test → Plantar fasciitis Nerve entrapment signs → Burning pain radiating to medial ankle/foot Management General Heel pads, orthotics, offloading devices Activity modification, NSAIDs, weight reduction Ice post-activity (plantar fasciitis, Achilles tendinopathy) Specific Physiotherapy: Stretching/strengthening (plantar fascia, Achilles, tibialis posterior), eccentric loading for chronic Achilles tendinopathy/plantar fasciitis Steroid injections (resistant cases, caution near Achilles due to rupture risk) Podiatry referral for recurrent/bilateral cases or footwear assessment Imaging (X-ray, US, MRI) if no improvement in 6–8 weeks, suspected fracture/tendon tear, or inflammatory/infectious concerns Shockwave therapy for chronic plantar fasciitis Additional Notes Sever’s disease: Calcaneal apophysitis in children → Rest, ice, heel cups, activity reduction Tarsal tunnel syndrome: Posterior tibial nerve compression → Orthotic support, activity modification Posterior tibial tendinopathy: Risk of adult-acquired flatfoot if untreated → Strengthening, posture correction, immobilisation if severe Consider spondyloarthropathy/inflammatory arthritis if bilateral heel pain, prolonged morning stiffness, or systemic features (uveitis, GI symptoms) Bookmark Failed! 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Experience RACGP CCE coaching with free sample cases and videos. Master exam prep with Fellow Academy’s All-in-One CCE System. Home AKT/KFP CCE Cases CCE Coaching Clinical Team Topics Summary Testimonial Blogs Exam notes Menu Close Experience Fellow Academy’s CCE Coaching with Free Sample Sessions Watch how our expert GP examiners guide you through real CCE-style patient simulations and case discussions Coaching Sessions #1. Elderly man with hip pain, cognitive decline, VAD request Case discussion #2: Aboriginal GP registrar with Anxiety/PTSD #3. Infant with Vomiting, Weight Loss, and Eczema Patient Simulation #1. Heavy Painful Periods (Menorrhagia) #2. Sudden Vision Loss in a Diabetic Patient #3. Hypertension and Metabolic Syndrome Summary Key points Timestamps Viva Case 1: James Andrews Elderly man with hip pain, cognitive decline, and VAD request James, 85M, living in residential aged care presents with a four-week history of persistent right hip pain. The pain has led to a decline in mobility and overall functioning. He has mild cognitive impairment, hearing impairment, and has experienced unintentional weight loss. Nursing staff report that James appears more withdrawn, raising concern about low mood. His daughter is involved in his care, and during the consultation James raises the issue of voluntary assisted dying, seeking to discuss his options. 5:02 – Key features and likely ddx 85M in aged care, 4 weeks hip pain, cognitive impairment, weight loss, functional decline Concerns: malignancy, occult fracture, OA, trochanteric bursitis, Paget’s disease 6:45 – Initial Investigations/Assessments X-ray, bloods (FBC, CRP/ESR) Mobility/falls risk assessments Cognitive screening (MMSE), hearing checks 8:20 – Management strategies Non-pharma: activity modification, physio, footwear, heat packs, massage Pharma: analgesia (cautious with NSAIDs, opioids very low-dose PRN) Allied health involvement 10:32– Voluntary Assisted Dying Discussion Respectful language, ensure no coercion, confirm capacity Outline eligibility (age, residency, prognosis ≤12 months, voluntary decision) Involve specialists 12:29 – Capacity Assessment Must understand, retain, weigh risks/benefits, communicate clearly. 13:03 – Prognosis, End-of-Life Care Discuss advance care planning, CPR/ICU, comfort measures Involve daughter in palliative planning 16:24 – Death in Aged Care Facility Expected vs unexpected death (coroner if unexpected) Provide death certificate, inform family compassionately 17:23 – Communication Before/After Death Use simple language, active listening, address concerns Offer bereavement support, community groups, social work 18:50 – If Imaging Suggests Malignancy, next steps? Urgent referral (oncology, geriatrics, palliative care) Clarify findings with patient/family 20:20 – Debrief and Shaun’s feedback Clarify questions if confused Structure answers slowly, pause between sentences In geriatrics: mention falls risk, ACP, EPOA, referrals Be precise with meds (frail → low opioid doses, cautious NSAIDs) Always mention bereavement support/community groups Ethics → 4 pillars (autonomy, beneficence, non-maleficence, justice) Viva Case 3: Christopher Ryan Infant with Vomiting, Weight Loss, and Eczema Christopher is an infant with persistent vomiting and faltering growth, dropping from the 60th to the 30th percentile on growth charts. His mother reports increasing distress as the vomiting continues despite feeding. Alongside this, Christopher’s eczema has worsened. The combination of vomiting, weight loss, and skin changes raises concern for underlying medical conditions requiring further assessment. 4:53 – Key clinical concerns Aamer summarises: vomiting, growth faltering (dropped percentiles), eczema worsening. Key concerns: failure to thrive, distress to mother. 6:23 – Differentials Pyloric stenosis Cow’s milk protein allergy Reflux UTI Gastroenteritis Lactose intolerance (less likely at this age) Malrotation/volvulus Coeliac (less likely at infancy) 8:17 – Day-to-Day Factors influencing current symptoms Feeding frequency and technique Positioning after feeds Cow’s milk formula Environmental eczema triggers (heat, allergens) 9:18 – Management Plan Reduce feed volume, upright positioning post-feed Trial extensively hydrolysed formula → escalate to amino acid formula if no response Growth monitoring, child health nurse reviews Safety-net: blood in vomit/stool, worsening vomiting, distress, dehydration Review in 1–2 weeks, consider paediatric referral, ultrasound for pyloric stenosis, urine tests 11:33 – Eczema Management Soap-free moisturisers, trigger avoidance Topical steroids if needed Monitor for infection 12:35 – Addressing Parental Concerns Explore concerns, provide information, use motivational interviewing, shared decision-making, leaflets Soy formula not recommended due to cross-reactivity risk 14:46 – Escalation If symptoms persist after 4-week trial → switch to amino acid formula, refer to paediatrics Specialist investigations may include allergy testing, ultrasound, bloods, urine tests 16:29 – Social Red Flags Screen for domestic violence, neglect, financial hardship, parental mental health, substance abuse, overcrowding 17:43 – Reviews/Red Flags for Parents Monitor feeds, urination, dehydration, worsening vomiting, fevers, further percentile drops Urgent if forceful vomiting, bilious vomit, blood in vomit/stool, lethargy, severe irritability 20:00 – Debrief and Shaun’s feedback Strong differential coverage, but slow down and summarise confidently. Use structured 5-minute notes (problem list, differentials, investigations, management) Use mnemonics like RECAP and SNAP Always mention safety-netting (worst-case scenario, e.g., anaphylaxis for cow’s milk allergy) Geriatric/paediatric red flags are vital Viva Case 2: Marlee West Aboriginal GP registrar with Anxiety/PTS Mali is an Aboriginal GP registrar presenting with anxiety, sleep disturbance, and nightmares. Since relocating to a rural town, she has become socially isolated and is worried about making mistakes at work and being judged. She also describes distress linked to her mother’s passing and her grandmother’s experiences of the Stolen Generations, raising issues of cultural trauma and discrimination. 4:38 – Key issues in presentation Anxiety, nightmares, poor sleep Social isolation after relocation Fear of mistakes and judgement at work Distress linked to family trauma and discrimination 5:33 – Structured problem list Clinical: anxiety, nightmares, assess for self-harm Cultural: bereavement, intergenerational trauma, Stolen Generations Psychosocial: isolation, anxiety, sleep disturbance Professional: fear of mistakes at work, judgement by colleagues 7:01 – Exploring psychosocial & cultural background Use safe, respectful language Offer Aboriginal health worker involvement (with consent) Explore family supports and cultural background Apply trauma-informed care: avoid retraumatisation, ensure safety, confidentiality 8:29 – Communication strategies Empathetic listening and collaboration Ask one issue at a time, check understanding Maintain safety in consultation Use affirmations and open-ended questions 9:28 – Avoiding stereotypes Treat as individual, not defined by race Avoid assumptions about Aboriginal identity or experiences Ask open-ended questions, listen actively Respectful language, no presumption 10:49 – Differential diagnoses PTSD (nightmares, trauma, flashbacks) Adjustment disorder (relocation, work stress) Anxiety disorder Depression Bipolar disorder (less likely) 11:31 – Differentiating & red flags PTSD: trauma history, nightmares, poor sleep Adjustment disorder: triggered by move/workplace Depression/anxiety: low mood, anxiety, poor concentration Red flags: suicidality, risk to self/others 12:37 – Culturally safe management plan Offer Aboriginal health worker support Link with Aboriginal medical services Ask about gender-concordant doctor preference Involve family/support person if desired 13:53 – Non-pharmacological supports Psychologist with Indigenous health experience GP registrar/college wellbeing services (RACGP, Doctors for Doctors, supervisor support) Counsellor, support groups 15:01 – Trauma-informed care principles Acknowledge trauma, avoid retraumatisation Empower patient to set pace and boundaries Confidentiality unless risk present Collaboration, active listening, open-ended questions Use silence appropriately to support sharing 16:40 – If symptoms worsen or she cannot work Assess patient and workplace safety Sick leave if necessary Liaise with supervisor/college Psychologist referral, CBT, counselling Ensure improvement before return to work; consider modified duties Monitor closely, weekly reviews if needed Reassess for suicidality 18:31 – Debrief and Shaun’s Feedback Recognised key principles well: anxiety/PTSD, cultural trauma, professional stressors. Always structure your problem list across clinical, cultural, psychosocial, and professional domains to show breadth. Avoid over-sensitising. Let the patient define what cultural safety means to them. Don’t assume negative experiences; ask what matters to them. You listed differentials well, but the question also asked about red flags. Strategy: jot “Differentials | Red flags” on paper so you don’t forget. Management was strong: good mention of registrar support. Always include SNAP to capture lifestyle, stress management, and sleep hygiene. Don’t forget crisis supports (helplines, acute referral if deteriorating). Cultural safety management should include pharma and non-pharma. You could add SSRIs as an option, with a discussion about cultural acceptability. Use strength-based framing: highlight resilience, achievements, and community ties to build empowerment. Include return-to-work planning: discuss fit for work, safe duties, or modifications, not just binary “fit/unfit”. Patient Simulation Case: Michelle Dunbar Heavy Painful Periods (Menorrhagia) A woman presents with a 12–18 month history of progressively heavier and more painful periods. Her menstrual bleeding has increased in duration from 5–6 days to 7–8 days, now requiring overnight pads and frequent changes. She reports passing clots up to the size of a 50 cent coin and worsening cramping pain. The symptoms are affecting her sleep, leading to daytime fatigue, irritability, and low mood. She has experienced unintentional weight loss of 2–3 kg and reduced appetite. There is no history of intermenstrual or postcoital bleeding. She is worried that her symptoms may be due to fibroids or cancer. 05:18 Case start Patient describes progressively heavier, longer, and more painful periods. 16:19 – Menstrual history Periods now last 7–8 days (previously 5–6); requires overnight pads; clots present 08:53 – Functional impact & associated symptoms Disturbed sleep, missed social/work events, 2–3 kg weight loss, poor appetite, irritability, low mood. 13:01 – Patient concern States fear of fibroids or cancer; family history of endometriosis. 16:00 – Investigations proposed Full blood count Iron studies Thyroid function tests Coagulation screen Pelvic ultrasound (abdominal + transvaginal) Pelvic examination with chaperone 19:00 – Management plan Analgesia: paracetamol, NSAIDs Antifibrinolytic: tranexamic acid Hormonal options: Mirena IUD, combined oral contraceptive pill 20:30 – Shaun’s feedback: History : good structure but too much back-and-forth. Aim to finish by 6–8 minutes. Break history into sections : menstrual, functional impact, pain (Socrates), psychological, sexual, red flags. Use the 5-minute prep to jot headings and key red flags. Summarise midway if blank. Empathy : better to say fewer but more genuine statements (rehearse lines, avoid over-apologising). Differential list: include fibroids, adenomyosis, endometriosis, thyroid disease, clotting disorder, malignancy. Investigations : add β-hCG, always specify timeframe for review. Management : good mention of NSAIDs & tranexamic acid, but also mention Mirena or OCP. Mental health : add SNAP advice, psychologist if needed. Patient Simulation Case: Denise Ellison Sudden Vision Loss in a Diabetic Patient Patient with a history of diabetes presents with sudden loss of vision in her left eye, first noticed while reading the newspaper two days earlier. She describes it as a dark patch or curtain in the lower visual field of the affected eye. There is no pain, discharge, headache, or neurological symptoms. He checks his blood glucose regularly, usually 7–8 mmol/L, and his BP averages 130/80 mmHg. He recalls being told he had mild diabetic retinopathy by an optometrist one year ago. He is anxious about going blind, especially after witnessing a friend lose vision due to diabetes. 5:08 – Case start Patient reports sudden patch of darkness in the left eye, ongoing for 2 days 5:55 – Symptom description Dark smudge/curtain in the lower visual field; no pain, discharge, photophobia, or eye movement restriction. 7:23 – Associated symptoms excluded No headache, no weakness, no numbness, no prior similar episodes. 8:25 – Impact and concerns Patient expresses anxiety about blindness; recalls a friend who went blind from diabetes. 8:55 – Past medical history Known diabetes, checks BGL daily (7–8 mmol/L) BP ~130/80 Prior optometrist visit showed mild retinopathy 9:38 – Differential explanations Retinal detachment (most likely – “curtain” of vision loss) Vitreous haemorrhage (small vessel bleed) Glaucoma (less likely – no pain) Vitreous changes (detachment) 12:10 – Next steps, safety-netting & urgency Urgent ophthalmology referral required; cannot be left untreated. Interim advice: avoid straining or heavy lifting; minimise sudden head movements. 13:28 – Patient query: “Can I wait and see?” Aamer strongly advises against waiting; emphasises risk to vision and need for urgent specialist review. 16:25 – Preventive health Checks immunisations (flu, pneumonia, shingles) and cancer screening (bowel, cervical, breast) as part of overall care. 17:20 – Shaun’s feedback Shaun confirms strong performance and safe management. Adds high-yield refinements: Clarify sudden onset (minutes/hours) Ask about scalp tenderness (exclude giant cell arteritis) Confirm right eye is unaffected Emphasise home/social supports (elderly patient + vision loss) Differential phrasing: retinal detachment, vitreous haemorrhage, ischaemic optic neuropathy Patient Simulation Case: Alice Derrington Hypertension and Metabolic Syndrome Alice is a woman presenting with concerns about elevated blood pressure readings. At home, her BP has averaged 142/88 mmHg, with occasional higher clinic readings (148/92 mmHg). She reports morning headaches, daytime tiredness, and stress related to work. She also notes poor sleep and irritability. She is overweight, and investigations show raised cholesterol, elevated fasting glucose, and increased BMI. Alice is worried about starting medication and prefers to try “natural” options first. 4:42 - Case start Patient reports home BP readings elevated, occasional morning headaches, tiredness, stress. Aamer explores headache features, fatigue, stressors, menstrual status, sleep, mood. Also screens for systemic symptoms (polyuria, weight change, hot flushes, night sweats, snoring). Patient reluctant to start medications, preferring “natural” management. 13:24 – Review of Investigations Clinic BP: 148/92, Home: 142/88. High cholesterol, high fasting glucose, raised BMI. Aamer explains these findings, introduces concept of metabolic syndrome 17:10 – Management discussion Lifestyle modifications: diet, exercise, weight reduction, stress reduction, caffeine moderation. Referral to dietitian, exercise physiologist, psychologist if needed. Plans 6-week review, repeat tests, possible initiation of medications if no improvement. 20:30– Shaun’s Feedback Core case focus = investigations & management (hypertension + cholesterol). Aamer lost too much time on headaches/fatigue; should rule out red flags briefly (15–20s), then focus on “bread and butter” management. Strengths: asked about caffeine, OTC meds, lifestyle, used correct terms like “metabolic syndrome.” Improvements: Be more specific about lifestyle advice (exercise type, diet detail). Explain why high BP/cholesterol matter → translate into cardiovascular risk (heart attack/stroke) terms patients understand. Mention both non-pharma + pharma, plus investigations for end-organ damage (urine ACR, ECG, renal tests). Use jargon for examiner, then explain simply for patient. Explore why patient is medication-averse to tailor reassurance. Summary Keypoints Timestamps Summary Keypoints Timestamps Summary Keypoints Timestamps Video Sections Case Discussion Patient Simulation Video #1 Subject Title 13:03 Video #2 Subject Title 21:20 Video #3 Subject Title 08:19 Video #1 Subject Title 13:03 Video #2 Subject Title 21:20 Video #3 Subject Title 08:19 Summary Keypoints Timestamps Overview In this case discussion, Dr Shaun reviews a [patient age + gender] presenting with [main complaint/clinical context]. The session highlights how to structure responses under exam conditions, demonstrate clear clinical reasoning, and align answers with RACGP examiner expectations. Why Our CCE Coaching Works One Integrated System. One Clear Goal: To Help You Pass Every component is designed to strengthen the others. You’ll practise under exam-style conditions, get structured feedback, and learn exactly how to meet examiner expectations. It’s a smarter, more effective way to prepare — so you walk into the CCE with confidence. Buy Complete CCE Mock Exam Experience The All-in-One CCE Preparation System: Everything You Need to Pass with Confidence BUY CCE PREP BUNDLE 100+ CCE Cases Viva and Patient Sim cases that mirror the official RACGP format 300+ Topics Exam Notes Clear summaries that help you structure your CCE answers 1500+ Flashcards Practise “speaking your answers” out loud Every resource is designed to complement the others. You’ll build exam-ready skills by working through realistic cases, reinforcing knowledge with concise notes, and locking it in with high-yield flashcards. It’s a complete, integrated approach to preparation + + Concise & Comprehensive Exam Notes 1500+ High Yield-Aligned Flashcards 100+ Exam-Standard CCE Cases The All-in-One CCE Preparation System: Everything You Need to Pass BUY CCE PREP BUNDLE Every resource is designed to complement the others. You’ll build exam-ready skills by working through realistic cases, reinforcing knowledge with concise notes, and locking it in with high-yield flashcards. It’s a complete, integrated approach to preparation BUY CCE PREP BUNDLE + + Concise & Comprehensive Exam Notes 1500+ High Yield-Aligned Flashcards 100+ Exam-Standard CCE Cases The All-in-One CCE Preparation System: Everything You Need to Pass BUY CCE PREP BUNDLE Ready to try our CCE Cases for FREE ? Get instant access to a selection of Fellow Academy’s exam-standard CCE cases at no cost. These free cases are designed to mirror the exact RACGP CCE format so you can experience the quality and structure of our resources for yourself. Each case contains: Candidate Instructions – replicating the exact prompts you’ll receive in the exam Case Scenario – realistic, detail-rich, and based on common GP presentations Patient Record Summary – aligned with RACGP formatting for clinical accuracy Examiner Questions (for viva cases) – targeted to test your clinical reasoning, depth of knowledge, and safe management planning Role-Player Script (for patient simulation cases) – opening lines, general information, specific details, and typical patient questions Competent Candidate Criteria (CCC) – benchmarks to self-assess against examiner expectations Which RACGP pathway are you preparing under?* Australian GP Trainee (AGPT) Fellowship Support Program (FSP – IMG) Specialist Pathway Program (SPP) RVTS (Remote Vocational Training Scheme) Other Next Which RACGP pathway are you preparing under?* Australian GP Trainee (AGPT) Fellowship Support Program (FSP – IMG) Specialist Pathway Program (SPP) RVTS (Remote Vocational Training Scheme) Other Next Ready to try our CCE Cases for FREE ? Get instant access to a selection of Fellow Academy’s exam-standard CCE cases at no cost. These free cases are designed to mirror the exact RACGP CCE format so you can experience the quality and structure of our resources for yourself. Each case contains: Candidate Instructions – replicating the exact prompts you’ll receive in the exam Case Scenario – realistic, detail-rich, and based on common GP presentations Patient Record Summary – aligned with RACGP formatting for clinical accuracy Examiner Questions (for viva cases) – targeted to test your clinical reasoning, depth of knowledge, and safe management planning Role-Player Script (for patient simulation cases) – opening lines, general information, specific details, and typical patient questions Competent Candidate Criteria (CCC) – benchmarks to self-assess against examiner expectations Premium Coaching All-In-One CCE System: Complete CCE Mock Exam Experience $2500 CCE Pack + Exam Notes $800 $599 CCE Pack $499 $399 Best Value CCE Prep Bundle CCE Pack + Flashcards + Exam Notes $1200 $699 CCE Pack + Exam Notes $599.00 $800.00 Best Value CCE Prep Bundle $699.00 $1200.00 Complete CCE Mock Exam Experience $2500.00 ELEVATE YOUR CCE PREP TODAY CCE Pack $399.00 $499.00 Premium Coaching