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 Metabolic Syndrome Diagnostic Criteria Increases risk of CVD, diabetes, CKD by 2–3x and complications by 1.6x when diagnosed Confirmed by ≥3/5 of the following criteria: Weight Circumference: Men: >102 cm (white), >94 cm (non-white) Women: >88 cm (white), >80 cm (non-white) TG >1.7 mmol/L HDL cholesterol: <1 mmol/L in men <1.3 mmol/L in women BP: ≥130/85 mmHg or treated HTN Fasting Glucose: ≥5.5 mmol/L or diagnosed T2DM Management Intensive Lifestyle Modifications: Weight loss, exercise, diet adjustment crucial Pharmacological Review: Address potential culprits (e.g., antipsychotics, antidepressants) Pharmacological Treatment: No first-line indication for metformin unless T2DM Lifestyle Changes Dietary Recommendations: Mediterranean-style diet: High in vegetables, whole grains, lean protein, healthy fats (e.g., olive oil, nuts) Limit refined carbs, sugar-sweetened beverages, saturated fats, processed foods Increase omega-3 fatty acid intake (e.g., fish) Exercise Regimens: Aim for 150 mins/week of moderate-intensity aerobic activity (e.g., brisk walking, swimming) Resistance training 2–3x per week improves insulin sensitivity Weight Loss Targets: Aim for 5–10% body weight reduction over 6 months Encourage sustainable strategies (e.g., portion control, meal planning) Notes: HDL Cutoff Variations: Women <1.3 mmol/L vs men <1 mmol/L Waist Circumference Variance: Non-white populations have lower cutoff values Metabolic Syndrome Aetiology / Pathophysiology Insulin resistance is central, leading to compensatory hyperinsulinaemia and disrupted glucose–lipid metabolism. Excess visceral fat contributes to pro-inflammatory cytokine release and exacerbates insulin resistance. Common contributory factors include obesity, poor diet (high refined sugars/fats), sedentary lifestyle, certain medications (e.g. antipsychotics), and familial/genetic influences. Diagnostic Criteria Most guidelines require ≥3 of the following 5 criteria. Cut-offs may vary by ethnicity: Waist Circumference (WC) European/North American men: ≥102 cm European/North American women: ≥88 cm Non-white or Asian men: >90–94 cm (varies by guideline) Non-white or Asian women: >80–88 cm (varies by guideline) Elevated Triglycerides (TG): ≥1.7 mmol/L Reduced HDL-C Men: <1.0 mmol/L Women: <1.3 mmol/L Elevated Blood Pressure: ≥130/85 mmHg or on treatment for hypertension Elevated Fasting Glucose: ≥5.5 mmol/L or previously diagnosed T2DM Having metabolic syndrome increases the risk of CVD, T2DM, and CKD by approximately 2–3 times. Clinical Features Often asymptomatic, discovered incidentally on routine health checks. Abdominal obesity (central adiposity). Hypertension (may manifest as headache or found on screening). Dyslipidaemia (can be asymptomatic unless severe). Possible mild hyperglycaemic symptoms if borderline T2DM (e.g. fatigue, increased thirst). Differential Diagnosis T2DM alone: Overlaps with metabolic syndrome but focuses primarily on hyperglycaemia. Hypothyroidism: Can cause weight gain and dyslipidaemia, important to exclude. Cushing’s syndrome: Features include central obesity, hypertension, skin changes. PCOS: Women may exhibit insulin resistance, obesity, and dyslipidaemia. Investigations Fasting Lipid Profile (total cholesterol, HDL, LDL, TG). Fasting Glucose / HbA1c. Waist Circumference (annual measurement if high risk or overweight/obese). Blood Pressure (regular measurement). Consider OGTT if borderline glucose or additional risk factors for T2DM. Screen for microalbuminuria in patients with elevated BP and/or hyperglycaemia. Management 1. Lifestyle Modifications (First-Line Intervention) Weight Loss Aim for 5–10% reduction in body weight over 3–6 months. Bariatric surgery can be considered in severe obesity or if lifestyle measures are insufficient and comorbidities are significant. Diet Emphasise Mediterranean-style or similarly balanced diets rich in vegetables, whole grains, lean protein, and healthy fats (e.g. olive oil, nuts). Limit refined carbohydrates, sugar-sweetened beverages, and processed foods. Increase intake of omega-3 fatty acids (e.g. fish twice weekly). Physical Activity At least 150 minutes per week of moderate-intensity aerobic exercise (e.g. brisk walking, cycling, swimming). Incorporate resistance training 2–3 times per week to improve insulin sensitivity and maintain lean body mass. Behavioural Interventions Support for smoking cessation, stress reduction, and adequate sleep. 2. Pharmacological Review Identify and adjust any medications that exacerbate metabolic risks (e.g. certain antipsychotics, corticosteroids). Consider antihypertensives, lipid-lowering agents, or antidiabetic drugs if indicated by comorbidities or severity of each metabolic abnormality. Metformin not routinely indicated for metabolic syndrome alone but recommended if T2DM is present or in prediabetes with high risk of progression. 3. Monitoring and Ongoing Care Regular reassessment of waist circumference, blood pressure, lipids, and glycaemic parameters (fasting glucose/HbA1c) every 3–6 months, or as clinically indicated. Use absolute cardiovascular risk calculators to guide intensity of interventions. Encourage long-term adherence to lifestyle modifications and follow-up to prevent progression to T2DM and CVD. Complications 2–3 times higher CVD risk compared with those without metabolic syndrome. Significantly increased risk of developing T2DM. Increased CKD likelihood due to hypertension, hyperglycaemia, and other related factors. Prognosis Early and effective lifestyle interventions can substantially reduce the risk of progression to T2DM and major cardiovascular events. Pharmacotherapy for specific components (e.g. statins, antihypertensives, antidiabetics) further reduces morbidity and mortality if instituted early. Notes: Metabolic syndrome is a useful clinical concept to identify patients at high risk who benefit most from preventive measures. Lifestyle modifications remain the cornerstone of treatment. Ethnic-specific waist circumference cut-offs are crucial for accurate diagnosis. Regular follow-up and a team-based approach (GP, dietitian, exercise physiologist) improve outcomes and patient adherence. 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 Vulvovaginitis Differential Diagnoses Infectious Causes: Candidiasis: Thick, white discharge, itching Bacterial vaginosis: Thin, grey discharge, fishy odour Trichomoniasis: Frothy, yellow-green discharge, vaginal irritation Dermatological Conditions: Lichen sclerosus: White, atrophic patches, intense itching Eczema/dermatitis: Erythema, scaling, itching Psoriasis: Well-demarcated erythematous plaques, silvery scales Other Causes: Atrophic vaginitis: Oestrogen deficiency (postmenopause) → Dryness, itching, dyspareunia Allergic/irritant reactions: Soaps, detergents, sanitary products, spermicides Foreign bodies: Retained tampon → Discharge, irritation History Onset, duration, severity Discharge: Colour, consistency, odour Associated symptoms: Itching, burning, dyspareunia, dysuria Recent antibiotics, new hygiene products Menstrual & sexual history Past episodes or dermatological conditions Management General Measures: Avoid irritants: No douches, perfumed products, tight clothing Use soap-free cleansers Loose cotton underwear to reduce moisture Gentle drying after bathing, avoid excessive washing Specific Treatments: Candidiasis: Topical or oral antifungals Bacterial vaginosis: Oral/topical metronidazole or clindamycin Trichomoniasis: Oral metronidazole Dermatological conditions: Topical corticosteroids or immunomodulators Atrophic vaginitis: Topical oestrogen Key Notes Confirm diagnosis with microscopy, culture, or NAAT before treatment Persistent/recurrent symptoms → Further evaluation to rule out other causes Refer to RACGP guidelines for detailed management Vulvovaginitis Definition Vulvovaginitis is inflammation of the vulva and vagina, presenting with a range of symptoms including irritation and discharge Differential Diagnoses Infectious causes Candidiasis: Thick, white discharge; intense itching; may be associated with dysuria and dyspareunia Bacterial vaginosis: Thin, grey discharge; fishy odour (often more pronounced after intercourse) Trichomoniasis: Frothy, yellow-green discharge; vaginal irritation; possible cervical motion tenderness Dermatological conditions Lichen sclerosus: White, atrophic patches; severe itching; potential risk for squamous cell carcinoma if untreated Eczema/dermatitis: Erythema and scaling; pruritus; may be related to irritants Psoriasis: Well-demarcated erythematous plaques; silvery scales; typically chronic with variable severity Other causes Atrophic vaginitis: Due to oestrogen deficiency in postmenopausal women; dryness, itching, dyspareunia Allergic or irritant reactions: Triggered by soaps, detergents, sanitary products or spermicides Foreign bodies: Retained tampon or other objects causing persistent discharge and irritation History Document onset, duration and severity of symptoms Characterise discharge by colour, consistency and odour Ask about associated symptoms such as itching, burning, dyspareunia, and dysuria Review recent antibiotic use, new hygiene or cosmetic products, and changes in sexual activity Inquire about menstrual history and previous episodes of vulvovaginitis or dermatological conditions Examination Perform a thorough vulval examination to inspect for erythema, swelling, fissuring or lichenification Check for signs of atrophy in postmenopausal women Evaluate for signs of foreign bodies or trauma Consider a pelvic examination if deeper pathology is suspected Investigations Obtain a high vaginal swab for microscopy, culture, and nucleic acid amplification testing (NAAT) to confirm the diagnosis Use Gram stain for detection of clue cells in bacterial vaginosis or budding yeast and hyphae in candidiasis Consider pH testing of vaginal secretions (vaginal pH >4.5 supports bacterial vaginosis) In cases of persistent or recurrent symptoms, further evaluation including biopsy may be warranted Management General measures Advise avoidance of irritants such as douches, perfumed products and tight clothing Recommend the use of soap-free cleansers and loose, cotton underwear to reduce moisture Instruct on gentle drying after bathing and to avoid excessive washing Specific treatments Candidiasis: Treat with topical antifungals (e.g. clotrimazole 1% cream or pessaries for six nights) or, if severe, consider oral antifungals (fluconazole 150 mg single dose, noting contraindications in pregnancy) Bacterial vaginosis: Treat with oral or topical metronidazole (400 mg twice daily for five to seven days) or clindamycin (oral or 2% cream at night for seven days) Trichomoniasis: Treat with oral metronidazole (2 g single dose or 400 mg twice daily for 5–7 days); ensure partner treatment Dermatological conditions: Manage with appropriate topical corticosteroids or immunomodulators as indicated Atrophic vaginitis: Use topical oestrogen therapy to alleviate symptoms and improve vaginal health Patient education Emphasise proper genital hygiene and avoidance of known irritants Provide advice on lifestyle modifications to reduce recurrence In cases of recurrent or persistent symptoms, consider referral for specialist evaluation Notes Confirm diagnosis with appropriate laboratory investigations including microscopy, culture, and NAAT before initiating treatment Persistent or recurrent symptoms warrant further evaluation to rule out alternative or coexisting pathology Treatment choices may be influenced by patient preference, cost considerations, and pregnancy status Individualised treatment plans are essential for optimal patient outcomes and long-term symptom control 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 Morphoea (Localised Scleroderma) Definition Inflammation & fibrosis due to excess collagen deposition Affects skin only, no systemic involvement Starts as purplish erythema → ivory-white plaques (smooth, shiny, hairless) May resolve spontaneously, but specialist assessment advised Rare, mainly in children (1–3 per 100,000) Differences from Systemic Sclerosis No skin thickening of fingers/toes No specific autoantibodies No small vessel disease (Raynaud’s, digital ulcers) No internal organ damage Pathophysiology Collagen overproduction → inflammation & fibrosis Diagnosis Biopsy, blood tests if needed Possible findings: ↑ Eosinophils ↑ ESR, CRP ANA may be positive (but ENA negative) Management No cure, treatment aims to halt progression Topical Steroids, tacrolimus, calcipotriol, imiquimod Phototherapy UVA1 for deeper lesions Systemic Therapy (Severe cases) Methotrexate, systemic steroids, mycophenolate mofetil Complications if Untreated Joint contractures, growth defects, severe cosmetic deformity Morphoea (Localised Scleroderma) Definition Morphoea (also called localised scleroderma) is an inflammatory and fibrotic process affecting only the skin, characterised by excess collagen deposition. It typically presents with purple erythematous patches that evolve into ivory-white, shiny plaques, often lacking hair (alopecia in the lesion). Unlike systemic sclerosis, morphoea does notinvolve internal organs. Differences from Systemic Sclerosis No skin thickening of the fingers or toes No specific autoantibodies commonly linked to systemic disease (e.g., anti-Scl-70, anti-centromere) No small vessel disease: Absent Raynaud’s phenomenon, digital ulcers No internal organ (lung, GI, renal) involvement Pathophysiology Collagen overproduction leads to inflammation and fibrosis in the skin’s dermal and sometimes subcutaneous layers. Incidence is rare, mainly in children (~1–3 per 100,000). Diagnosis Often clinical but can require biopsy for confirmation. Blood Tests: May show eosinophilia, raised ESR/CRP. ANA can be positive, but ENA is usually negative or unremarkable. Management No definitive cure; aim to halt progression and limit complications. Topical Therapy Potent topical steroids (reduce local inflammation) Tacrolimus ointment, calcipotriol, or imiquimod in some cases Phototherapy UVA1 can help deeper lesions by reducing collagen deposition Systemic Therapy (Severe Cases) Methotrexate plus short-course systemic steroids Mycophenolate mofetil as an alternative immunosuppressant Supportive Measures Monitor for joint contractures in lesions crossing joints Physiotherapy may be needed if limb range of motion is threatened Complications if Untreated Joint contractures, especially in children Growth defects (when affecting growth plates) Severe cosmetic deformity (atrophy, disfigurement) 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 Thyroid Radionucleotide scan Indications When the clinical presentation and laboratory tests cannot differentiate causes of thyrotoxicosis (e.g., when TSH receptor antibodies are negative, ~10% of cases) Evaluate thyroid nodules to assess "cold" or "hot" nodules Suspected hyperthyroidism with goitre Pathologies Detected Toxic Adenoma: Focal increased uptake Toxic Multinodular Goitre: Multiple focal increased uptake areas Graves' Disease: Diffuse increased uptake Subacute Thyroiditis: Decreased or absent uptake Drug-Induced Thyroiditis: Decreased or absent uptake Contraindications Pregnancy Breastfeeding (should discontinue breastfeeding for 48 hours post-scan) Thyroid Radionuclide Scan Indications When clinical presentation and laboratory tests cannot differentiate causes of thyrotoxicosis (e.g., when TSH receptor antibodies are negative, ~10% of cases) Evaluate thyroid nodules to assess "cold" or "hot" nodules Suspected hyperthyroidism with goitre Assessing the functional status of thyroid nodules in patients with a subnormal TSH Pathologies Detected Toxic Adenoma: Focal increased uptake Toxic Multinodular Goitre: Multiple focal increased uptake areas Graves' Disease: Diffuse increased uptake Subacute Thyroiditis: Decreased or absent uptake Drug-Induced Thyroiditis: Decreased or absent uptake Autonomous Nodule: Intense focal uptake with suppression of surrounding thyroid tissue. Contraindications Pregnancy. Breastfeeding (should discontinue breastfeeding for 24–48 hours post-scan) Recent exposure to iodine-containing contrast agents or medications (e.g., amiodarone) may affect scan results Patient Preparation Inform patients about the procedure, including the need for an intravenous injection and the duration of the scan (45–60 minutes) Advise patients to remove neck jewellery and wear clothing that allows easy access to the arm for injection Discuss potential radiation exposure and ensure women of childbearing age are assessed for pregnancy or breastfeeding status Medications and Substances Affecting Scan Results Water-soluble intravenous contrast agents (used in CT scans) Amiodarone Thyroxine or liothyronine (Tertroxin) Some mineral/vitamin supplements containing iodine Patients should discontinue these substances for an appropriate period before the scan to minimise the risk of a nondiagnostic result Interpretation of Results The pattern of radionuclide uptake helps differentiate causes of hyperthyroidism, guiding treatment decisions Functioning ("hot") nodules in hyperthyroid patients typically lead to treatment of hyperthyroidism Non-functioning ("cold") nodules may require further investigation, such as ultrasound and/or fine-needle biopsy, due to a higher risk of malignancy 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 Hypoglycaemia Management Mild Hypoglycaemia (BSL <4 mmol/L, Patient Conscious) 15g fast-acting carbohydrate (e.g., 125mL fruit juice, 6–7 jelly beans, 1 tube of glucose gel). Recheck BSL in 15 minutes; repeat if still <4 mmol/L. Follow with a longer-acting carbohydrate (e.g., sandwich, yoghurt) to prevent recurrence. Severe Hypoglycaemia (Unconscious or Unable to Swallow) IM Glucagon: Adults: 1 mg. Children <25 kg: 0.5 mg; ≥25 kg: 1 mg. IV Glucose: Adults: Glucose 10% 150–200mL over 15 mins. Glucose 20% 75–100mL over 15 mins. Children: Glucose 10% 1–2 mL/kg over 20 mins until BSL >4 mmol/L. Recheck BSL every 15 mins until stabilised. Risk Factors Insulin or sulfonylurea use Missed meals, fasting, or prolonged exercise Alcohol consumption Long-standing diabetes with hypoglycaemia unawareness Cognitive impairment, kidney/liver disease Hypoglycaemia Pathophysiology During hypoglycaemia, the body activates glycogenolysis and gluconeogenesis via counter-regulatory hormones (glucagon, adrenaline, cortisol, growth hormone). Common precipitants: Reduced dietary carbohydrate intake Increased physical activity Inappropriate timing/use of diabetes medication Renal impairment (reduced clearance of insulin/oral hypoglycaemic agents) Symptoms Adrenergic Symptoms (mediated by sympathetic nervous system): Dizziness Lightheadedness Shakiness Sweating Palpitations Anxiety Neuroglycopenic Symptoms (due to altered brain function): Hunger Confusion Behavioral changes Coma Seizures Threshold for Symptoms: Initial symptoms arise at ~3.0 mmol/L. Hypoglycaemic unawareness can occur with repeated episodes (no symptoms until severe hypoglycaemia). Aetiology Iatrogenic: Insulin or sulfonylurea overdose (most common cause). Advanced diabetic nephropathy (reduced drug clearance). Medications: Beta-blockers (masks hypoglycaemia symptoms). Lifestyle Factors: Missed meals, alcohol intake, weight loss, increased physical activity. Risk Factors Common or important patient risk factors for hypoglycaemia: Previous severe hypoglycaemia Hypoglycaemia unawareness Long duration of diabetes Insulin therapy Increased age Cognitive impairment Kidney or liver impairment Primary GI disease with malabsorption (e.g., coeliac disease) Primary failure of hormones that raise blood glucose (e.g., adrenal cortical failure) Acute Precipitants (especially in insulin users): Irregular carbohydrate intake Suppressed gluconeogenesis by alcohol Incorrect insulin administration Vigorous exercise Diagnostics Patient History: Physical activity, diet, medication, alcohol use. Laboratory Tests: Blood glucose (FBG <4 mmol/L). C-peptide (helps differentiate causes): High insulin + high C-peptide: likely insulinoma. High insulin + low C-peptide: exogenous insulin. Management Mild Hypoglycaemia Treatment: 15, 15 rule: 15g of fast-acting carbohydrate (i.e., 6-7 jelly beans or half a cup of apple juice) Recheck blood glucose level after 15 minutes Repeat treatment if blood glucose remains below 4 mmol/L Severe Hypoglycaemia Glucagon: 1 mg IM or SC (may be given by another person) IV Glucose: 20 mL of 50% glucose (adults) or 2 mL/kg of 10% glucose (children) Recheck blood glucose level after 15 minutes Transfer to hospital if patient remains unconscious or requires more than two doses Note: Avoid 50% glucose IV in children or adolescents, as it increases risks of hyperosmolarity and necrosis. Monitoring After Hypoglycaemic Episode Monitor blood glucose every 1-2 hours for first 4 hours, then resume usual testing. Investigate and address underlying causes. Review medications and diet to prevent recurrence. Hypoglycaemia Unawareness Often occurs in patients with diabetes for over 10 years. Repeated mild hypoglycaemic episodes impair adrenergic response, increasing the risk of severe hypoglycaemia. Management: Patients should avoid driving until awareness improves, which may take several weeks. Special Considerations Alcohol-Associated Hypoglycaemia Alcohol impairs liver glucose production, increasing hypoglycaemia risk. Guidelines for patients with type 1 diabetes: Use a medical alert device Avoid skipping meals or drinking on an empty stomach Monitor blood glucose closely, especially at night Sulfonylurea-Induced Hypoglycaemia Prolonged hypoglycaemia may occur, particularly in patients with kidney impairment. Management: Hospital admission and frequent glucose monitoring are often necessary. Notes: Hypoglycaemia Awareness: Establish by maintaining stable glucose levels. Consider dietary adjustments or insulin modifications if recurrent episodes occur. Driving Advisory: Individuals should avoid driving if they are at risk of hypoglycaemia or until hypoglycaemia awareness is restored. Avoidance: Educate patients on the "Rule of 15" for mild hypoglycaemia management 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 Chronic Kidney Disease Classification – Green, Yellow, Orange, Red Criteria Remember: Each column (normal urine ACR, microalbuminuria, macroalbuminuria) has six rows corresponding to different eGFR ranges (first row = eGFR >90). Below each number corresponds to number of rows it occupies: Left (normal urine ACR) column - 2, 1, 1, 2 (green, yellow, orange, red) Middle (microalbuminuria) column - 2, 2, 2 (yellow, orange, red) Right (macroalbuminuria) column - 1 (red) CKD Yellow & Orange Categories Yellow (Moderate Risk CKD) Criteria: eGFR 45-59 (normal ACR) eGFR 60-90 (microalbuminuria) Review & Investigations (Every 12 Months): Kidney health check: Urine ACR, eGFR, BP Add-on tests: Weight, lipid profile HbA1c (if diabetic) Assess cardiovascular risk Optimise BP, lipid profile, glycaemic control Avoid nephrotoxic medications Orange (High-Risk CKD) Criteria: eGFR 30-44 (normal ACR) eGFR 30-59 (microalbuminuria) Review & Investigations (Every 3-6 Months): Yellow category tests + Calcium & phosphate FBC (for EPO deficiency, anaemia) PTH (if eGFR <45) Check medication doses appropriate for eGFR Monitor for CKD complications Note: Red Category CKD requires 1-3 monthly review Risk Factors & Screening Risk Factors: Age >60 Hypertension Diabetes Smoking Obesity Previous cardiovascular disease ATSI >30 (or >18 if CKD risk factors present) Family history of kidney disease How Often to Screen: Annual screening (eGFR, BP, urine ACR) if diabetes or hypertension 1-2 yearly kidney check for other high-risk individuals Medications Medications to Withhold When Unwell (SADMANS) Sulfonylureas ACE inhibitors Diuretics (safe if eGFR <30, but adjust doses) Metformin (CI if eGFR <30) ARBs NSAIDs (except low-dose aspirin) SGLT2 inhibitors (CI if eGFR <45) Initiating ACE/ARB Therapy Acceptable eGFR drop <25% within 2 months If >25% decline → Nephrology referral Caution if K >5.5 before starting (as it will increase ~0.5, risk hyperkalaemia) If K >6.5 → Requires urgent ED referral Best Diabetic Medications for CKD SGLT2 Inhibitors (Preferred if eGFR >45 for renal & CV protection) DPP-4 Inhibitors (Preferred if eGFR <30, as they require minimal dose adjustment) Symptoms, Diagnosis, and Investigations Symptoms: Anaemia (Fatigue, dyspnoea from EPO deficiency) Uraemia (Pruritus, encephalopathy, nausea, restless legs, anorexia) Hypoalbuminaemia (Peripheral oedema) Diagnosis: eGFR <60 on at least 3 readings over >3 months Urine ACR >2.5 (men) or >3.5 (women) on at least 2 out of 3 tests over 3 months Persistent haematuria (after excluding urological causes) Structural kidney abnormalities (e.g., single kidney, PCKD, hydronephrosis) Pathological abnormalities (nephritic or nephrotic features) Investigations: FBC, UEC ESR/CRP (if considering inflammatory cause) Lipid profile, glucose (diabetes assessment) Urine microscopy (Look for dysmorphic RBCs or casts) Renal ultrasound Consider Further Testing If: Rash, arthralgia, pulmonary symptoms (SLE, vasculitis): Anti-GBM, ANCA, ANA, ENA, complement Risk factors for infection: HIV, Hep B/C serology >40 years old with possible myeloma: Serum and urine protein electrophoresis Management Lifestyle Modifications: Smoking cessation Alcohol <2 standard drinks/day (max 4 per occasion) Avoid nephrotoxic medications (even if not on NSAIDs) Monitor BP (target <140/90, or <130/80 if diabetes/microalbuminuria/high CVD risk) Reduce salt intake <6g/day 150 min of moderate-intensity exercise per week Maintain BMI <25 Drink fluids to satisfy thirst (no need to increase fluid intake) Pharmacological Management: ACE/ARB: BP targets: <140/90 (standard CKD) <130/80 (diabetes, microalbuminuria, high CVD risk) Essential for all except eGFR 45-60 and normotensive patients Statins: All CKD patients >50 years If <50 years, only if high CVD risk or diabetic Use atorvastatin or pravastatin (no dose adjustment needed) Diabetes control: Metformin 500 mg (if eGFR >30, dose-adjust below 60) Additional Notes: Request "RBC morphology" on pathology form when assessing haematuria No need for routine urine MCS in CKD unless infection suspected Causes of False eGFR & Urine ACR Readings eGFR False Readings (Creatinine-Based Formula) Extremes of body mass (underweight = overestimation, very muscular = underestimation) Strict vegetarian or high-protein diet (affects creatinine production) AKI, dialysis, immobilisation, pregnancy Urine ACR False Readings UTI, febrile illness Heavy exercise (if done within 24 hours before testing) High protein intake Congestive heart failure (CCF) Notes: eGFR drop >25% after starting ACEI/ARB → Nephrology referral Urine ACR >2.5-3.5 is abnormal, even if eGFR >60 Screen annually in diabetes, hypertension, or ATSI >30 years old CKD is an independent risk factor for cardiovascular disease SGLT2 inhibitors are first-line in CKD with diabetes, provided eGFR >45 NSAIDs are a major cause of AKI in CKD – avoid chronic use Severe hyperkalaemia (>6.5) requires urgent ED review Chronic Kidney Disease Classification – Green, Yellow, Orange, Red Criteria Below is a simplified version of the CKD risk matrix, showing eGFR stages on the left (rows) and urine ACR categories in the top row (columns). Each cell indicates a colour-coded level of risk: eGFR (mL/min/1.73m²) Normal ACR (<3 mg/mmol) Microalbuminuria (3–30 mg/mmol) Macroalbuminuria (>30 mg/mmol) >90 (G1) Green (Low risk) Yellow (Moderate risk) Red (Very high risk) 60–89 (G2) Green (Low risk) Yellow (Moderate risk) Red (Very high risk) 45–59 (G3a) Yellow (Moderate risk) Orange (High risk) Red (Very high risk) 30–44 (G3b) Orange (High risk) Orange (High risk) Red (Very high risk) 15–29 (G4) Red (Very high risk) Red (Very high risk) Red (Very high risk) <15 (G5) Red (Very high risk) Red (Very high risk) Red (Very high risk) CKD Yellow & Orange Categories Yellow (Moderate Risk) Criteria: eGFR 45–59 with normal ACR eGFR 60–90 with microalbuminuria Review & Investigations (every 12 months): Kidney health check (urine ACR, eGFR, BP) Weight, lipid profile HbA1c (if diabetic) Cardiovascular risk assessment Optimise BP, lipids, glycaemic control Avoid nephrotoxic drugs Orange (High Risk) Criteria: eGFR 30–44 with normal ACR eGFR 30–59 with microalbuminuria Review & Investigations (every 3–6 months): All yellow category tests plus: Calcium & phosphate FBC (EPO deficiency, anaemia) PTH (if eGFR <45) Check medication doses appropriate for eGFR Monitor for CKD complications Note: Red category CKD requires 1–3 monthly review Risk Factors & Screening Risk Factors: Age >60 Hypertension Diabetes Smoking Obesity Previous cardiovascular disease ATSI people (>30 years, or >18 if other risk factors) Family history of kidney disease How Often to Screen: Annual eGFR, BP, and urine ACR if diabetes or hypertension 1–2 yearly kidney check for other high-risk groups Medications Medications to Withhold When Unwell (SADMANS): Sulfonylureas ACE inhibitors Diuretics (safe if eGFR <30, but dose adjustments required) Metformin (contraindicated if eGFR <30) ARBs NSAIDs (except low-dose aspirin) SGLT2 inhibitors (contraindicated if eGFR <45) Initiating ACE/ARB Therapy: Acceptable eGFR drop <25% within 2 months If >25% decline → Refer nephrology Caution if K >5.5 (risk hyperkalaemia on commencement) If K >6.5 → Urgent ED referral Best Diabetic Medications for CKD: SGLT2 inhibitors if eGFR >45 (for renal & cardiovascular protection) DPP-4 inhibitors if eGFR <30 (minimal dose adjustments) Symptoms, Diagnosis, and Investigations Symptoms: Anaemia (fatigue, dyspnoea due to EPO deficiency) Uraemia (pruritus, nausea, restless legs, encephalopathy) Hypoalbuminaemia (oedema) Diagnosis: eGFR <60 on ≥3 readings over >3 months Urine ACR >2.5 (men) or >3.5 (women) on ≥2 of 3 tests over 3 months Persistent haematuria (after excluding urological causes) Structural abnormalities (e.g. polycystic kidneys, hydronephrosis) Pathological abnormalities (e.g. nephrotic or nephritic syndrome) Investigations: FBC, UEC ESR/CRP if inflammatory causes suspected Lipid profile, glucose/HbA1c Urine microscopy for RBC casts or dysmorphic cells Renal ultrasound Further tests if indicated (e.g. ANCA, HIV, myeloma screen) Management Lifestyle Modifications: Smoking cessation Alcohol <2 standard drinks/day Avoid nephrotoxic medications Optimal BP control (<140/90 generally, <130/80 if diabetes/high CVD risk) Salt restriction <6 g/day 150 min moderate-intensity exercise/week Maintain BMI <25 Adequate (but not excessive) fluid intake Pharmacological Management: ACE/ARB Indicated unless eGFR 45–60 and normotensive BP targets: <140/90 or <130/80 if high-risk (e.g. diabetes, microalbuminuria) Statins For all CKD patients >50 years In <50 years, consider if high CVD risk or diabetic Diabetes Control Metformin 500 mg if eGFR >30 (dose adjust under 60) Causes of False eGFR & Urine ACR Readings eGFR False Readings: Extremes of body mass (underweight → overestimation, very muscular → underestimation) Strict vegetarian or high-protein diets Acute kidney injury, dialysis, immobilisation, pregnancy Urine ACR False Readings: UTI, febrile illness Heavy exercise within 24 hours prior High protein intake Congestive heart failure Notes eGFR drop >25% after starting ACEI/ARB → Refer nephrology Urine ACR >2.5–3.5 is abnormal even if eGFR >60 Screen annually for diabetes, hypertension, ATSI >30 CKD is an independent CVD risk factor SGLT2 inhibitors first-line in CKD + diabetes if eGFR >45 NSAIDs can precipitate AKI in CKD; avoid long-term use Severe hyperkalaemia (>6.5) → Urgent ED review 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 Head Injury History Mechanism: Height, speed, force, helmet use Symptoms: LOC (duration), seizures, vomiting (frequency), headache, confusion, amnesia Injuries: Suspected/visible injuries PMH: Bleeding disorders, anticoagulants, prior head injuries Examination General: Visible injuries, shock Neurological: GCS, pupils (size/reactivity), motor strength, reflexes Skull Fracture Signs: Base: Haemotympanum, raccoon eyes, Battle’s sign, CSF leak Depressed: Step-off deformity Management Mild (GCS 13–15) Monitor: Neurological checks every 30 mins for 6 hours Discharge: Baseline behaviour, tolerating fluids, no concerning symptoms Advice: Rest, gradual activity return, educate on red flags (e.g., persistent vomiting, drowsiness) Moderate/Severe CT Brain: GCS <13, skull fracture signs, focal deficit, seizures, NAI suspicion Stabilisation: Intubate if GCS <8, urgent ED transfer Red Flags Deteriorating GCS, persistent vomiting, raised ICP signs (e.g., unequal pupils) Non-blanching rash, suspicious injury history (NAI) Special Populations <2 Years: Higher fracture risk; assess scalp swelling, irritability, feeding issues Anticoagulated: Lower imaging threshold Head Injury History Mechanism: Detailed account of injury including height, speed, force, and use of protective equipment (e.g., helmet) Loss of consciousness: Duration and associated seizure activity are critical Amnesia: Document both anterograde and retrograde memory loss Associated symptoms: Multiple episodes of vomiting, persistent headache, confusion, drowsiness, or focal neurological deficits Other injuries: Presence of external injuries or signs of non-accidental injury Past medical history: Bleeding disorders, anticoagulant use, prior head injuries, neurodevelopmental conditions, VP shunt status Examination General: Observe for visible injuries, signs of shock, and overall appearance Glasgow Coma Scale: Assess eye, verbal, and motor responses to gauge level of consciousness Neurological: Check for focal deficits, abnormal posturing, and signs of raised intracranial pressure (e.g., unequal pupils, posturing) Skull assessment: Palpate for step-off deformities, swelling, or tenderness Basal skull fracture signs: Look for haemotympanum, Battle’s sign, raccoon eyes, and any CSF rhinorrhoea or otorrhoea Vital signs: Monitor blood pressure, heart rate, and respiratory rate as indicators of systemic stability Investigations CT Brain (+/- C-spine): Gold standard for moderate to severe injuries or when red flags are present (GCS ≤13, focal deficits, suspected NAI, signs of basal skull fracture) Indications for CT: Persistent altered mental status, history of loss of consciousness, post-traumatic seizure, severe mechanism, scalp haematoma MRI: Consider if specific lesions are suspected and CT is inconclusive Other tests: Urgent imaging for suspected non-accidental injury; plain skull X-ray rarely used in acute head trauma Management Mild Head Injury (GCS 15 without risk factors): Discharge with head injury advice if stable with no red flags Advise rest, gradual return to normal activities, and monitoring for symptom change Mild Head Injury (with risk factors, GCS 14–15): Observe for up to 4 hours with neurological checks every 30 minutes Discharge if returning to baseline and tolerating oral intake Moderate Head Injury (GCS 9–13): Require urgent CT brain (+/- C-spine) and neurosurgical consultation Continuous monitoring and early involvement of a senior clinician Severe Head Injury (GCS ≤8): Activate trauma protocol with airway protection, possible intubation Urgent neuroimaging and neurosurgical involvement Initiate measures to reduce raised intracranial pressure (e.g., elevate head, hyperosmolar therapy with mannitol or hypertonic saline) Discharge Advice Provide caregivers with clear instructions on red flag symptoms (worsening headache, confusion, persistent vomiting, new neurological deficits) Advise on gradual return to cognitive and physical activities, especially following concussion Arrange follow-up to reassess neurological status and recovery progress Red Flags Deteriorating or persistently low GCS (<13) Signs of basal skull fracture (haemotympanum, Battle’s sign, raccoon eyes, CSF leak) Focal neurological deficits or post-traumatic seizures Evidence of raised intracranial pressure (unequal pupils, abnormal posturing) Suspected non-accidental injury or severe mechanism of injury (high-impact MVC, significant fall) Additional Notes Children under 6 months, those with neurodevelopmental disorders, or special conditions (e.g., VP shunt, bleeding disorders) require lower thresholds for neuroimaging and careful evaluation In remote or rural settings, stabilise airway, breathing, and circulation while arranging prompt transfer Continuous monitoring post-injury is critical to detect delayed complications such as intracranial bleeding or raised ICP 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 LFT Derangement History Recent antibiotics, herbal medications (e.g., mistletoe), hepatotoxic chemicals (e.g., mushroom toxins, vinyl chloride) Alcohol intake Hepatitis B risk factors: IV drug use, travel, vaccination status Obesity Stool/urine colour change Family history: autoimmune liver disease Haemochromatosis: arthralgia, skin pigment changes Associated Conditions Inflammatory bowel disease (PSC) Right heart failure (congestive hepatopathy) Dilated cardiomyopathy, diabetes (hemochromatosis) Emphysema (esp <40, α1-antitrypsin deficiency) Coeliac disease, hypothyroidism Exam Findings (RACGP Exam Grid) Spider naevi Ascites Peripheral oedema Palmar erythema Asterixis Hepatomegaly/splenomegaly Jaundice Finger clubbing Caput medusae Enlarged left supraclavicular node (Virchow’s) Gynaecomastia, testicular atrophy (male hypogonadism) Bruising, leukonychia, IV drug use stigmata Investigations Bloods: Hepatitis B/C, iron studies Autoimmune screen: ASMA, AMA, ANA TFTs, coeliac serology α1-antitrypsin level Serum caeruloplasmin (Wilson's disease) Imaging: Ultrasound abdomen: biliary duct dilatation suggests extrahepatic; normal bile ducts suggest intrahepatic pathology MRCP/ERCP if bile ducts dilated or ALP >50% normal; inconclusive ultrasound Other Tests: Albumin: low in chronic liver disease, normal in acute liver disease Prothrombin time When to Refer Unexplained, persistent: AST/ALT > 2x normal ALP > 1.5x normal If no improvement after 6 months of monitoring New: Refer if ferritin >1,000 µg/L with liver enzyme elevation (hemochromatosis workup) LFT Derangement History Recent Antibiotics, Herbal Medications (e.g. mistletoe), hepatotoxic substances (mushroom toxins, vinyl chloride) Alcohol Intake: Quantify standard drinks per week Hepatitis B Risk Factors: IV drug use, overseas travel, vaccination status Obesity: Non-alcoholic fatty liver disease (NAFLD/NASH) Stool/Urine Colour Changes (pale stools, dark urine → cholestatic picture) Family History: Autoimmune liver disease, haemochromatosis (arthralgia, skin pigmentation) Associated Conditions Inflammatory Bowel Disease: PSC (primary sclerosing cholangitis) Right Heart Failure: Congestive hepatopathy (raised JVP, oedema) Haemochromatosis: Arthropathy, diabetes, cardiomyopathy, skin pigmentation Alpha-1 Antitrypsin Deficiency: Emphysema < age 40, liver dysfunction Coeliac Disease, Hypothyroidism: Can contribute to mild LFT elevation Exam Findings (RACGP Exam Grid) Spider Naevi, Palmar Erythema, Jaundice → Chronic liver disease Ascites, Peripheral Oedema → Decompensated cirrhosis Asterixis (flapping tremor) → Hepatic encephalopathy Hepatosplenomegaly → Chronic liver disease, haemolysis Finger Clubbing → Chronic hypoxia or GI/liver disease Caput Medusae → Portal hypertension Virchow’s Node (left supraclavicular) → Malignancy Gynaecomastia, Testicular Atrophy → Chronic liver disease (male hypogonadism) Bruising, Leukonychia, stigmata of IV drug use if suspect viral hepatitis Investigations Bloods Hepatitis B/C Serologies, Iron Studies (haemochromatosis) Autoimmune Markers: ASMA (autoimmune hepatitis), AMA (PBC), ANA (SLE overlap) TFTs, Coeliac Serology if indicated α1-Antitrypsin level → deficiency? Serum Caeruloplasmin for Wilson’s disease (especially in younger patients with neurological/liver issues) Imaging Ultrasound Abdomen: Assess for biliary duct dilatation → possible obstructive or cholestatic pattern MRCP/ERCP: If bile ducts are dilated or ALP significantly elevated, and initial ultrasound is inconclusive Other Tests Albumin: Often low in chronic liver disease, can be normal in acute disease Prothrombin Time: Prolonged in significant hepatic synthetic dysfunction When to Refer Unexplained, persistent LFT abnormalities, e.g. AST/ALT > 2× normal ALP > 1.5× normal No improvement after 6 months of monitoring High Ferritin > 1000 µg/L with elevated liver enzymes → assess for haemochromatosis Suspicion of advanced or complex liver disease (signs of portal hypertension, coagulopathy, significant cholestasis) Progressive jaundice, potential malignancy or complicated biliary obstruction → urgent referral 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 Acute Kidney Injury (AKI) Common Causes Prerenal: Dehydration Intrarenal: Sepsis, nephrotoxins (drugs, contrast, rhabdomyolysis, myeloma) Classification of AKI Causes Prerenal (↓ Renal Perfusion) Causes: Volume depletion: Vomiting, diarrhoea, dehydration, haemorrhage Cardiac failure (low output) Hypoalbuminaemia (cirrhosis, nephrotic syndrome) Plan: BUN/Cr ratio >20 → Suggests prerenal AKI IV fluids (if volume depleted) Diuretics (if overloaded, e.g., CHF) Postrenal (Obstruction) Causes: Ureteric stones Malignancy (bladder, prostate, pelvic) BPH (bladder outlet obstruction) Plan: US or CT KUB → Assess for hydronephrosis, stones, mass Catheterisation if bladder obstruction Intrarenal (Direct Kidney Damage) Causes: Glomerular: Nephritic syndrome (IgA nephropathy, lupus nephritis) Interstitial: Drug-induced (beta-lactams, NSAIDs, PPIs) Acute Tubular Necrosis (ATN): Hypoperfusion, toxins (contrast, myoglobin in rhabdomyolysis) Sepsis-related injury Plan: Urine microscopy: RBC casts → Glomerulonephritis WBC casts → Infection, interstitial nephritis Muddy brown casts → ATN Urinalysis: Proteinuria, haematuria, leukocyturia Medications That Cause AKI SADMANS (Hold in Dehydration/AKI Risk Situations) Sulfonylureas ACE inhibitors (ACEi) Diuretics Metformin (Adjust if eGFR <60, stop if eGFR <30) ARBs NSAIDs (except low-dose aspirin) SGLT2 inhibitors Triple Whammy (Avoid in Dehydration/CKD) NSAIDs (except low-dose aspirin) Diuretics ACEi/ARB Management After AKI Recovery BP Control: Avoid ACEi/ARB for 2–4 weeks post-AKI (reintroduce cautiously if stable) Use CCBs or beta-blockers if hypertension persists Medication Review: Reassess nephrotoxic drugs Restart SADMANS meds only if renal function recovers Renal Function Monitoring: Check eGFR & electrolytes: 1–2 weeks post-discharge Monthly if ongoing CKD risk Monitor for proteinuria/haematuria Assess for CKD Progression: eGFR decline or albuminuria >3 months → Nephrology referral CKD risk: Diabetes, hypertension, recurrent AKI Lifestyle: Ensure hydration (unless fluid-restricted, e.g., CHF) Reduce sodium/protein intake in at-risk patients Follow-Up Imaging (If Required): Renal US: Structural abnormalities, recurrent UTIs, persistent proteinuria Notes Most AKI cases are reversible with prompt treatment Monitor for CKD progression, especially after multiple AKI episodes Avoid contrast in high-risk patients (consider IV fluids if necessary) Early nephrology referral if persistent eGFR decline post-AKI Acute Kidney Injury (AKI) Overview & Definition Acute Kidney Injury (AKI) is a rapid decrease in renal function leading to a failure of the kidneys to excrete nitrogenous waste products and maintain fluid–electrolyte balance. According to KDIGO criteria, AKI is defined by any of the following: Rise in serum creatinine by ≥26.5 µmol/L within 48 hours, or Increase in serum creatinine to ≥1.5 times baseline within the previous 7 days, or Urine output <0.5 mL/kg/h for 6 hours. Common Causes Prerenal (↓ Renal Perfusion) Dehydration (e.g. vomiting, diarrhoea, poor oral intake) Haemorrhage Cardiac failure (low cardiac output) Hypoalbuminaemia (e.g. cirrhosis, nephrotic syndrome) Intrarenal (Direct Kidney Damage) Sepsis (systemic inflammatory response → acute tubular necrosis) Nephrotoxins: Drugs (e.g. NSAIDs, aminoglycosides, IV contrast, some chemotherapy agents) Rhabdomyolysis (myoglobin) Multiple myeloma (light chains) Postrenal (Obstruction) Ureteric stones Malignancy (bladder, prostate, pelvic) Benign prostatic hyperplasia (BPH; bladder outlet obstruction) Classification of AKI Causes 1. Prerenal AKI (Decreased Renal Perfusion) Causes Volume depletion: Vomiting, diarrhoea, dehydration, haemorrhage Cardiac failure (reduced renal blood flow) Hypoalbuminaemia (e.g. cirrhosis, nephrotic syndrome) Typical Laboratory Findings High BUN/Cr ratio (often > 20:1) Low fractional excretion of sodium (FENa) <1% (if the patient is not on diuretics) Initial Management Plan IV fluids if volume depletion is suspected (e.g. normal saline or balanced crystalloids) Diuretics if signs of volume overload (e.g. in heart failure) Optimise cardiac output if relevant (e.g. treat arrhythmias, consider inotropes if severe) 2. Postrenal AKI (Obstruction) Causes Ureteric stones Pelvic or retroperitoneal malignancy BPH (common in older men) Investigations Renal ultrasound (US) or CT KUB (kidneys, ureters, bladder) to assess for hydronephrosis, stones, or masses Bladder scan or urethral catheter to check for urinary retention Management Plan Relieve obstruction: Catheterisation if bladder outlet obstruction Urological intervention if stones are large or obstructing Specialist referral if malignancy or complex obstruction suspected 3. Intrarenal AKI (Direct Kidney Parenchyma Damage) Causes Glomerular: Nephritic syndromes (e.g. IgA nephropathy, lupus nephritis) Interstitial: Drug-induced interstitial nephritis (e.g. beta-lactams, NSAIDs, PPIs), autoimmune conditions Acute Tubular Necrosis (ATN): Hypoperfusion, contrast nephropathy, myoglobin (rhabdomyolysis), toxins Sepsis-related: Prolonged hypotension, inflammatory damage to renal tubules Urine Microscopy Clues RBC casts → Glomerulonephritis WBC casts → Pyelonephritis or interstitial nephritis Muddy brown casts → ATN (common in prolonged hypotension or nephrotoxic injury) Management Plan Identify and remove offending agent (e.g. nephrotoxic drugs) Manage sepsis aggressively (appropriate antibiotics, fluid resuscitation, haemodynamic support) Correct electrolyte disturbances (hyperkalaemia, acidosis) Medications That Can Cause or Worsen AKI SADMANS (Hold in Dehydration/AKI Risk Situations) Sulfonylureas (risk of hypoglycaemia if renal function drops) ACE Inhibitors (ACEi) Diuretics Metformin (risk of lactic acidosis; adjust if eGFR <60 mL/min/1.73m^2, stop if eGFR <30) ARBs (Angiotensin II Receptor Blockers) NSAIDs (except low-dose aspirin) SGLT2 inhibitors Triple Whammy (Avoid in Dehydration/CKD) NSAIDs (except low-dose aspirin) Diuretics ACEi/ARB Combining these three increases the risk of AKI significantly due to reduced renal perfusion and altered autoregulation. Management After AKI Recovery Blood Pressure Control Avoid restarting ACEi/ARB immediately post-AKI; typically wait 2–4 weeks until stable renal function is demonstrated. If hypertension persists, consider alternative antihypertensives such as calcium channel blockers or beta-blockers. Reintroduce ACEi/ARB cautiously if needed for cardiovascular or diabetic indications. Medication Review Reassess all nephrotoxic drugs. Restart SADMANS medications only if renal function has clearly recovered and there are compelling indications (e.g. heart failure, diabetic nephropathy). Renal Function Monitoring Check eGFR & electrolytes: 1–2 weeks post-discharge or post-AKI episode. Monthly if ongoing chronic kidney disease (CKD) risk. Monitor for proteinuria or haematuria (urinalysis, ACR) as signs of progressive CKD. Assess for CKD Progression If eGFR decline or persistent albuminuria (>3 months), consider referral to nephrology. Patients with diabetes, hypertension, or recurrent AKI are at higher risk of CKD progression. Lifestyle Advice Ensure adequate hydration (unless fluid-restriction indicated for heart failure). Reduce sodium intake if hypertensive or fluid-overloaded. Consider protein intake moderation in established CKD, though individualised advice is needed. Maintain a healthy weight and manage comorbidities (diabetes, hypertension, dyslipidaemia). Follow-Up Imaging (If Required) Renal ultrasound to assess for structural abnormalities if persistent deranged renal function or recurrent UTIs. Repeat imaging in cases of high suspicion of obstruction or complex renal pathology. Notes Many AKI cases are reversible with prompt identification and management of the underlying cause (e.g. volume replacement, stopping nephrotoxic agents). Monitor for progression to chronic kidney disease (CKD), especially after multiple AKI episodes. Avoid or minimise IV contrast in high-risk patients (eGFR <30 mL/min/1.73m^2, diabetic nephropathy) or consider prophylactic IV fluids if contrast is essential. Early nephrology referral is indicated if there is persistent eGFR decline, resistant electrolyte issues (e.g. hyperkalaemia), or diagnostic uncertainty. 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 Dyspnoea (Shortness of Breath) Pathophysiology & Aetiology Dyspnoea results from complex interactions between respiratory, cardiovascular, and psychological mechanisms. Respiratory Causes Obstructive: Asthma, COPD (exacerbation) Infective: Pneumonia (bacterial, viral, atypical) Vascular: Pulmonary embolism (PE) Structural: Pneumothorax, interstitial lung disease, upper airway obstruction (e.g. anaphylaxis, foreign body) Cardiac Causes Heart failure (acute or chronic) Ischaemic heart disease (unstable angina, MI) Arrhythmias (AF, SVT) Valvular disease (e.g. aortic stenosis) Pericardial disease (tamponade, constrictive pericarditis) Other Causes Anaemia (exertional dyspnoea) Metabolic acidosis (e.g. DKA) Anxiety (hyperventilation syndrome) Thyroid disorders (e.g. hyperthyroidism → AF, increased metabolic demand) History Onset & duration: Acute (mins–hrs), subacute (days–weeks), chronic (weeks–months) Nature: Exertional vs. rest, nocturnal (PND in heart failure), positional (orthopnoea) Associated symptoms: Chest pain: PE, ACS, pleurisy Wheeze, cough, sputum: Asthma, COPD, infection Fever, chills: Infection Leg swelling, calf pain: DVT/PE Palpitations, dizziness: Arrhythmia PMHx: Cardiac or respiratory disease, recent surgery/immobilisation (PE risk), medications (beta-blockers, ACE inhibitors) Social history: Smoking, occupational exposures, recent travel (PE risk) Examination Vitals: RR, SpO₂, HR, BP, temp Tachypnoea >20 breaths/min → Cardiorespiratory compromise Hypoxia (SpO₂ <94% or <88–92% in COPD) → Urgent assessment General: Speech, accessory muscle use, cyanosis Cardiorespiratory: Auscultation: Wheeze (asthma), crackles (pulmonary oedema, pneumonia), reduced breath sounds (effusion, pneumothorax) Percussion: Hyperresonance (pneumothorax), dullness (consolidation, effusion) Heart sounds: Murmurs (valvular disease), gallops (heart failure) Peripheral: Oedema, raised JVP (heart failure), calf tenderness (DVT) Immediate Assessment & Red Flags PE: Sudden onset dyspnoea, pleuritic chest pain, risk factors Tension pneumothorax: Tracheal deviation, hypotension Severe asthma: Silent chest, exhaustion, unable to speak Anaphylaxis: Urticaria, angio-oedema, hypotension Acute pulmonary oedema: Frothy sputum, high respiratory distress ACS/arrhythmias with shock ⚡ Urgent interventions: Oxygen therapy (except COPD target SpO₂ 88–92%), CXR, ECG, ABG, consider thrombolysis or emergency procedures if needed. Investigations CXR: Pneumonia, pulmonary oedema, pleural effusion, pneumothorax, interstitial lung disease ECG: Arrhythmias, ischaemia, right heart strain (PE) Pulse oximetry / ABG: Hypoxia, acidosis (e.g. DKA, COPD exacerbation) FBC: Anaemia, leucocytosis (infection) Biochemistry: Electrolytes, renal function, BNP (if suspecting heart failure) D-dimer: Low probability PE (use Wells score), confirm with CTPA if high suspicion Spirometry: Asthma, COPD, restrictive lung disease CTPA: Gold standard for PE HRCT: Interstitial lung disease Echocardiogram: Suspected heart failure or valvular disease Management Respiratory Causes Asthma/COPD: Acute: Bronchodilators, steroids, oxygen (88–92% in COPD), consider antibiotics in COPD Chronic: Optimise inhalers, pulmonary rehab, smoking cessation Pneumonia: Antibiotics as per Therapeutic Guidelines, supportive therapy, hospital admission if severe PE: Anticoagulation (DOACs or LMWH), risk stratification for inpatient vs. outpatient treatment Pneumothorax: Needle decompression if tension pneumothorax, chest drain if large/symptomatic Cardiac Causes Heart Failure: Acute: IV diuretics (furosemide), oxygen if hypoxic Chronic: ACE inhibitors/ARBs, beta-blockers, diuretics, address triggers (arrhythmias, ischaemia) ACS: MONA-B (Morphine, Oxygen [if hypoxic], Nitrates, Aspirin, Beta-blocker), urgent cardiology input if STEMI Arrhythmias: Rate/rhythm control (e.g. beta-blockers, digoxin for AF), anticoagulation (if indicated by CHA₂DS₂-VASc score) Other Causes Anaemia: Treat underlying cause (iron/B12/folate deficiency, chronic disease) Anxiety: Exclude organic pathology first; consider CBT, relaxation techniques, SSRIs if needed Metabolic: Correct underlying disorder (e.g. insulin + fluids in DKA) Dyspnoea (Shortness of Breath) Pathophysiology and Aetiology Dyspnoea results from complex interactions between physiological (respiratory and cardiovascular) and psychological (anxiety) mechanisms. Common underlying causes can be classified by system: Respiratory Causes Asthma (acute exacerbation, poorly controlled chronic asthma) Chronic Obstructive Pulmonary Disease (COPD) (exacerbation) Pneumonia (bacterial, viral, atypical) Pulmonary Embolism (PE) Pneumothorax Interstitial lung disease Upper airway obstruction (e.g. anaphylaxis, epiglottitis, foreign body) Cardiac Causes Heart failure (acute decompensation or chronic) Ischaemic heart disease (unstable angina, myocardial infarction) Arrhythmias (e.g. atrial fibrillation, supraventricular tachycardias) Valvular heart disease (e.g. aortic stenosis) Pericardial disease (tamponade, constrictive pericarditis) Others Anaemia (may present with exertional dyspnoea) Metabolic acidosis (e.g. diabetic ketoacidosis) Anxiety and panic disorders (hyperventilation syndrome) Thyroid disorders (e.g. hyperthyroidism, which can precipitate atrial fibrillation or cause generalised hypermetabolic state) History and Examination History Onset and duration: acute (minutes to hours), subacute (days to weeks), or chronic (weeks to months). Nature of dyspnoea: exertional vs. rest, nocturnal episodes (e.g. paroxysmal nocturnal dyspnoea in heart failure), positional changes (orthopnoea). Associated symptoms: Chest pain (could indicate PE, ACS, or pleurisy). Wheeze, cough, sputum (suggestive of asthma, COPD, infection). Fever, chills (infection). Leg swelling or calf pain (DVT leading to PE). Palpitations or light-headedness (arrhythmia). Past medical history: Cardiac or respiratory disease (e.g. COPD, asthma, heart failure). Recent surgery or immobilisation (risk for thromboembolism). Medications (e.g. beta-blockers, ACE inhibitors). Social history: Smoking status, occupational exposures, or inhaled irritants. Recent travel (risk for DVT/PE if long-haul flights). Physical Examination Vital signs: respiratory rate, oxygen saturation (SpO₂), heart rate, blood pressure, temperature. Tachypnoea (>20 breaths/min) often indicates significant cardiorespiratory compromise. Hypoxia (SpO₂ <94% in healthy adults; <88–92% for COPD target range) warrants urgent assessment. General appearance: can the patient speak in full sentences? Are they using accessory muscles? Are there signs of cyanosis? Cardiorespiratory exam: Auscultation for wheezes, crackles, decreased breath sounds. Percussion note changes (hyper-resonance in pneumothorax, dullness in consolidation or effusion). Heart sounds (murmurs, gallops suggesting heart failure). Peripheral signs: oedema, raised JVP (heart failure), calf tenderness (possible DVT). Immediate Assessment and Red Flags Identify life-threatening causes of acute dyspnoea: Pulmonary Embolism: sudden onset breathlessness, pleuritic chest pain, risk factors (recent surgery, immobility). Pneumothorax: especially tension pneumothorax (tracheal deviation, hypotension). Acute Severe Asthma: inability to speak, silent chest, exhaustion. Anaphylaxis: urticaria, angio-oedema, hypotension. Acute Pulmonary Oedema: frothy sputum, acute onset, high respiratory distress. Acute Coronary Syndrome or arrhythmias causing cardiogenic shock. Immediate oxygen therapy (except in certain COPD patients where target SpO₂ is typically 88–92%), urgent imaging (chest X-ray) and further investigations (ECG, blood gas analysis) may be needed. Investigations The choice of investigations depends on the clinical scenario, guided by the most likely differential diagnoses: Chest X-ray (CXR) Essential initial investigation for most causes of acute or chronic dyspnoea. Identifies pneumonia, pulmonary oedema, pleural effusion, pneumothorax, interstitial patterns, or mass lesions. Electrocardiogram (ECG) Helps detect arrhythmias, signs of ischaemia, or right heart strain (in acute PE). Pulse Oximetry and Arterial Blood Gas (ABG) Pulse oximetry is a quick, non-invasive method to assess oxygen saturation. ABG may be necessary if the oximetry is unreliable or if acid-base status requires evaluation (e.g. suspected DKA, severe asthma). Full Blood Count (FBC) Anaemia can contribute to exertional dyspnoea. Leucocytosis may indicate infection. Biochemistry Electrolytes, renal function, and liver function can be relevant, especially in chronic conditions or when starting diuretic therapy. BNP or NT-proBNP if heart failure is suspected. D-dimer Used with validated risk scores (e.g. Wells score) to rule out pulmonary embolism in a low-probability setting. A positive D-dimer is non-specific; proceed to imaging (CT pulmonary angiogram) if PE is still suspected. Spirometry In subacute or chronic dyspnoea, spirometry can diagnose or monitor COPD, asthma, restrictive lung disease. Imaging CT Pulmonary Angiogram (CTPA) is the gold standard for diagnosing PE. High-resolution CT (HRCT) can be used to investigate interstitial lung disease. Echocardiogram for suspected heart failure or valvular disease. Management Principles Tailor management based on the underlying cause, patient comorbidities, and severity of presentation: Respiratory Causes Asthma/COPD Ensure optimal inhaler technique and adherence to prevent exacerbations. Oral corticosteroids for acute exacerbations. Bronchodilators (short-acting and long-acting). Consider antibiotics if a bacterial infection is suspected in a COPD exacerbation. Oxygen therapy: aim for target SpO₂ of 88–92% in COPD to avoid CO₂ retention. Pneumonia Empirical antibiotics guided by guidelines (e.g. Therapeutic Guidelines). Supportive measures: fluids, antipyretics, oxygen if hypoxic. Hospital admission if moderate-severe pneumonia or significant comorbidity. Pulmonary Embolism Anticoagulation (low molecular weight heparin or direct oral anticoagulants). Risk stratification (e.g. simplified PESI or Hestia criteria) to determine outpatient vs. inpatient treatment. Pneumothorax Immediate needle decompression if tension pneumothorax. Otherwise, chest tube insertion or observation depending on size, symptoms, and underlying lung disease. Cardiac Causes Heart Failure Address acute decompensation with diuretics (e.g. IV furosemide) for pulmonary oedema. Chronic management with ACE inhibitors/ARBs, beta-blockers, and diuretics. Control exacerbating factors (arrhythmias, ischaemia, infection). Coronary Artery Disease / ACS MONA-B (Morphine, Oxygen [if hypoxic], Nitrates, Aspirin, Beta-blocker) as indicated. Urgent cardiology input if ST-elevation MI or ongoing ischaemia. Arrhythmias Rate control or rhythm control for tachyarrhythmias such as AF. Consider anticoagulation if indicated (CHA₂DS₂-VASc score). Other Causes Anaemia Investigate for iron deficiency, B12/folate deficiency, chronic disease. Correct underlying cause. Anxiety / Panic Disorder Evaluate for organic pathology first. Cognitive Behavioural Therapy, relaxation techniques, sometimes pharmacotherapy (SSRIs). Metabolic Causes Manage underlying cause (e.g. insulin and fluids in DKA). Chronic Dyspnoea: Ongoing Management and Follow-up Multidisciplinary care is often required (e.g. physiotherapy, chronic disease management nurses, respiratory or cardiac specialists). Optimise comorbidities: blood pressure control, glycaemic management, smoking cessation. Pulmonary rehabilitation for COPD or chronic respiratory disease. Home oxygen assessment if chronic hypoxaemia in advanced cardiorespiratory disease. Advance care planning in end-stage diseases (e.g. palliative approach where appropriate). 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 Acute and Progressive Vision Loss Acute Vision Loss Vascular: CRAO: Sudden painless monocular loss, "cherry red spot" on fundoscopy CRVO: Painless monocular loss, "blood and thunder" fundus Amaurosis Fugax: Transient monocular loss; embolic source GCA: Vision loss, headache, scalp tenderness, jaw claudication, ↑ESR/CRP Retinal: Detachment: "Curtain" over vision, flashes, floaters; urgent referral PVD: Floaters/flashes, mild unless retinal detachment occurs Vitreous Haemorrhage: Red-tinted vision, floaters, severe blurring Neurological: Optic Neuritis: Pain with eye movement, scotoma, colour vision loss Posterior Stroke: Binocular field defects, ataxia, dizziness Ocular: Acute Glaucoma: Severe pain, nausea, halos, red eye, mid-dilated pupil Corneal Ulcer/Oedema: Pain, photophobia, reduced vision Endophthalmitis: Pain, red eye, vision loss; post-surgical/trauma Progressive Vision Loss Refractive Errors: Gradual blurring, correctable with lenses Cataracts: Glare, halos, poor night vision, central blurring ARMD: Dry: Gradual central scotoma, preserved periphery Wet: Sudden distortion or rapid loss due to neovascularisation Glaucoma: Gradual peripheral loss → tunnel vision Diabetic Retinopathy: Blurring (early), floaters or sudden loss (advanced) Other: Myopic Maculopathy: Central loss in high myopia Retinitis Pigmentosa: Night blindness → tunnel vision Optic Neuropathies: Gradual loss; field defects (e.g., bitemporal hemianopia) Key Features Acute: CRAO: Painless, monocular, "cherry red spot" CRVO: "Blood and thunder" Retinal Detachment: "Curtain," flashes, floaters Optic Neuritis: Pain with movement, scotoma, dyschromatopsia Acute Glaucoma: Severe pain, halos, red eye Progressive: Cataracts: Gradual blurring, glare ARMD: Dry (scotoma), wet (distortion/rapid loss) Diabetic Retinopathy: Blurring, floaters, haemorrhage Glaucoma: Gradual tunnel vision Acute Vision Loss Acute vision loss is defined as a sudden decrease in vision (minutes to days). Important causes include vascular events (occlusions), retinal pathology (detachment, vitreous haemorrhage), optic nerve lesions (neuritis, ischaemia), and acute ocular conditions (acute glaucoma, corneal pathology). Vascular Causes Central Retinal Artery Occlusion (CRAO) Presentation: Sudden, painless monocular vision loss (“like a curtain descending”) Fundoscopy: Pale retina with a cherry red spot at the fovea Urgency: Ophthalmic emergency; immediate referral (possible ocular massage, lowering IOP, search for embolic source) Associated Factors: GCA in older patients, carotid atheroma, cardiac emboli Central Retinal Vein Occlusion (CRVO) Presentation: Sudden, painless monocular loss of vision Fundoscopy: “Blood and thunder” appearance (widespread retinal haemorrhages, dilated veins, cotton wool spots) Risk Factors: Hypertension, diabetes, hyperlipidaemia, glaucoma Management: Urgent ophthalmology referral (possible intravitreal anti-VEGF injections), address cardiovascular risk factors Amaurosis Fugax Presentation: Transient monocular “blackout” of vision, often described as a curtain coming down then lifting Cause: Embolic phenomenon from carotid or cardiac source Workup: Carotid Doppler, echocardiogram, vascular risk assessment (lipids, BP, glucose) Giant Cell Arteritis (GCA) Presentation: Vision loss (often sudden), headache, scalp tenderness, jaw claudication, age >50 Lab findings: Elevated ESR and CRP Management: Immediate high-dose corticosteroids to prevent further or bilateral vision loss, urgent temporal artery biopsy Retinal Causes Retinal Detachment Symptoms: “Curtain” or veil spreading across vision, flashes, floaters Risk Factors: Myopia, trauma, previous ocular surgery Management: Urgent ophthalmology referral (laser, surgical repair) Posterior Vitreous Detachment (PVD) Symptoms: Flashes, floaters; usually mild vision disturbance unless retinal tear/detachment ensues Management: Ophthalmology assessment to exclude retinal detachment Vitreous Haemorrhage Presentation: “Red-tinted” vision, sudden floaters, severe blurring Causes: Diabetic retinopathy, retinal tear, trauma Management: Treat underlying cause (urgent referral if vision severely compromised) Neurological Causes Optic Neuritis Presentation: Subacute vision loss, often painful with eye movement; reduced colour vision (red desaturation) Association: Multiple sclerosis, autoimmune conditions Management: Neuro-imaging (MRI) if indicated, high-dose IV steroids can hasten recovery Posterior Circulation Stroke Presentation: Visual field defects (often bilateral or homonymous), ataxia, possible brainstem signs (dizziness, dysarthria) Management: Urgent neuroimaging (CT/MRI), stroke protocol Ocular Causes Acute Angle-Closure Glaucoma Presentation: Severe eye pain, nausea/vomiting, halos around lights, red eye, mid-dilated pupil non-reactive Management: Emergency; reduce intraocular pressure (e.g. IV acetazolamide), urgent ophthalmology review Corneal Ulcer/Oedema Presentation: Pain, photophobia, reduced visual acuity, corneal haze/opacification Causes: Infectious (bacterial, viral, fungal), contact lens misuse Management: Urgent ophthalmic assessment (corneal scraping, topical antimicrobials) Endophthalmitis Presentation: Severe pain, red eye, marked vision loss, often post-surgery or trauma Management: Emergency ophthalmology referral for intraocular antibiotics Progressive Vision Loss Progressive vision loss typically occurs over weeks to years, often due to chronic degenerative changes or systemic diseases impacting the eyes. Refractive Errors (Myopia, Hyperopia, Astigmatism) Presentation: Gradual blurring of vision, improved by prescription lenses Management: Refraction test, corrective glasses or contact lenses Cataracts Symptoms: Gradual blurring, glare, difficulty with night driving, halos around lights Risk Factors: Ageing, diabetes, steroid use, UV exposure Management: Surgical lens extraction if functionally limiting Age-Related Macular Degeneration (ARMD) Dry (atrophic): Gradual central vision loss, drusen on fundoscopy Wet (exudative): Sudden distortion or rapid deterioration of central vision due to choroidal neovascularisation Management: Dry: Antioxidant supplements, lifestyle modifications (smoking cessation), monitoring Wet: Urgent referral for intravitreal anti-VEGF therapy Chronic (Open-Angle) Glaucoma Symptoms: Gradual peripheral vision loss → “tunnel vision”; often asymptomatic until advanced Risk Factors: Raised intraocular pressure, family history, age >50, African or Asian heritage Management: Intraocular pressure-lowering medications (topical prostaglandin analogues, beta-blockers), laser trabeculoplasty, or surgery Diabetic Retinopathy Presentation: Blurring in early stages; floaters or sudden vision loss if vitreous haemorrhage or retinal detachment Management: Optimal glycaemic, BP, lipid control; regular ophthalmic review; laser or intravitreal therapy if proliferative changes Other Myopic Maculopathy: High myopia leads to macular thinning and degeneration → central vision loss Retinitis Pigmentosa: Night blindness, progressive peripheral vision loss → tunnel vision Optic Neuropathies (e.g. pituitary adenoma → bitemporal hemianopia): Gradual field defects; requires imaging Key Features & Distinguishing Points Acute CRAO: Sudden painless monocular loss, “cherry red spot” CRVO: “Blood and thunder” fundus appearance Retinal Detachment: “Curtain” over vision, flashes, floaters Optic Neuritis: Pain on eye movement, colour desaturation Acute Glaucoma: Severe pain, red eye, halos, mid-dilated pupil Progressive Cataracts: Gradual blurring, glare, halos around lights ARMD: Dry → slow central loss Wet → sudden distortion or rapid deterioration Diabetic Retinopathy: May be asymptomatic early; risk of sudden loss if haemorrhage Glaucoma: Gradual peripheral loss → tunnel vision Practical Tips & Management Pathways History & Exam Onset: Sudden vs. gradual Pain: Painful conditions (acute glaucoma, optic neuritis, corneal ulcer) vs. painless (CRAO, CRVO, detachment) Associated symptoms: Headache/jaw claudication (GCA), flashes/floaters (retinal detachment), metamorphopsia (wet ARMD) Visual Acuity Test: With and without pinhole (to exclude refractive error) Fundoscopy: Essential for vascular occlusions, retinopathies, disc swelling Immediate Actions Suspected Retinal Detachment, CRAO, CRVO, GCA, or Acute Glaucoma → Urgent ophthalmology referral High-dose corticosteroids if GCA is strongly suspected Reduce IOP if acute angle-closure glaucoma Stroke protocol if posterior circulation stroke suspected Ongoing Management Optimise systemic risk factors: BP, glucose, lipids Lifestyle: Smoking cessation, UV eye protection, healthy diet (particularly for ARMD) Follow-up: Regular eye checks for chronic conditions (e.g. diabetic retinopathy screening) 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 Transient Ischaemic Attack (TIA) Presentation Face: Drooping, slurred speech, vision loss Limbs: Weakness, paraesthesia, imbalance Investigations ABCD2 score: Stroke risk stratification tool (add 1 point B for HTN history) Bloods: FBC, UEC, LFT, lipid profile Imaging: Carotid US, ECG, Echo (for AF or embolic source) Management Urgent imaging (CT/MRI): If ABCD2 score >3, AF, carotid symptoms, or crescendo TIA (≥2 events within 1 week) → Refer immediately or within 24hrs If score ≤3 or symptom onset >1 week → Manage in GP setting with imaging within 48hrs Carotid management: Symptomatic stenosis >70% → Refer for endarterectomy within 2 weeks Asymptomatic stenosis → Refer for specialist review within 1 week Pharmacological Management Antiplatelets: First-line: Aspirin 100mg OD Alternatives: Clopidogrel or aspirin + dipyridamole if aspirin contraindicated Anticoagulation: Use if CHA2DS2-VASc score ≥2 and no contraindications Warfarin: For valvular AF, mural thrombus, or mechanical valves DOACs: For non-valvular AF Delay if large stroke due to risk of haemorrhagic transformation Statins: High-potency statin (e.g., atorvastatin 40mg OD), regardless of cholesterol levels Lifestyle (SNAP) and BP Management Lifestyle: No smoking, regular exercise, healthy BMI, <2 standard drinks/day BP: ACE inhibitors or diuretics (even if normotensive, unless symptomatic hypotension) Notes: Urgent referrals may include TIA clinics, ED, or vascular specialists Migraine aura can mimic TIA—consider in differential Transient Ischaemic Attack (TIA) Presentation Sudden onset neurological deficit resolving within 24 hours (often <1 hour) Common symptoms include facial droop, slurred speech, vision loss (amaurosis fugax), limb weakness, paraesthesia, imbalance, speech disturbance Investigations ABCD2 score for stroke risk stratification (Age ≥60, BP ≥140/90, Clinical features of TIA, Duration of symptoms, Diabetes) Add 1 point for history of hypertension Higher scores indicate increased stroke risk Blood tests: FBC, UEC, LFT, lipid profile, fasting glucose/HbA1c Cardiac evaluation: ECG to exclude arrhythmias (e.g. AF), transthoracic echo (or TOE if suspicion of cardiac embolic source) Imaging: Urgent CT/MRI brain to exclude haemorrhage or established infarction Carotid duplex ultrasound for anterior circulation TIAs (especially if carotid territory) Management Urgent imaging (CT/MRI) If ABCD2 score >3, atrial fibrillation, carotid symptoms, or crescendo TIA (≥2 events in 1 week) → refer immediately or within 24 hours If score ≤3 or symptom onset >1 week → manage in GP setting with imaging within 48 hours Carotid management Symptomatic stenosis >70% → refer for endarterectomy within 2 weeks of the event Asymptomatic stenosis → specialist review within 1 week Early antiplatelet therapy Aspirin 300mg stat, then 100mg daily Alternatively, clopidogrel monotherapy (75mg daily) or aspirin plus dipyridamole if aspirin contraindicated Consider short-term dual antiplatelet therapy (DAPT) with aspirin and clopidogrel for up to 21 days if TIA or minor stroke and no high bleeding risk Anticoagulation Indicated if CHA2DS2-VASc ≥2 in atrial fibrillation Warfarin for valvular AF, mural thrombus, or mechanical valves DOACs for non-valvular AF Delay anticoagulation if large infarct present (to reduce risk of haemorrhagic transformation) Statins High-potency statin (e.g. atorvastatin 40mg or 80mg daily) regardless of baseline cholesterol levels Blood pressure control Target <140/90 in most patients ACE inhibitors or thiazide diuretics commonly used, even if BP not significantly elevated, unless symptomatic hypotension occurs Lifestyle (SNAP) Smoking cessation, nutrition (healthy diet), reduce alcohol intake (<2 standard drinks/day), increase physical activity Aim for healthy BMI and regular exercise Post-TIA Care Rapid referral to TIA clinic or stroke prevention service if moderate-high risk features Ongoing risk-factor modification (hypertension, hyperlipidaemia, diabetes, smoking) Consider screening for carotid stenosis if not done earlier Arrange timely follow-up and reinforcement of compliance with secondary prevention measures Differential Diagnosis Migraine aura (can mimic TIA) Hypoglycaemia Focal seizure with Todd’s paresis Notes TIA is a warning sign: up to 10–15% risk of stroke within 90 days, with half occurring in the first 48 hours Urgent carotid intervention and antiplatelet therapy can significantly reduce stroke risk Monitor for recurrent episodes or crescendo TIAs (increased stroke risk) Educate patients about recognising stroke-like symptoms (FAST) and seeking immediate care if they recur Bookmark Failed! Bookmark Saved! Add Bookmark Refresh Refresh