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 Arrhythmia Assessment for HD Compromise Key Indicators: Hypotension, hypoperfusion Syncope Altered LOC Chest pain Heart failure Tachyarrhythmias Management: Assess narrow vs broad complex tachy If unstable tachy: synchronised DC cardioversion If unstable brady: transcutaneous pacing General management: Maintain airway Assist breathing as required Administer oxygen to maintain sats >94% Cardiac monitoring / BP monitoring Establish IV access Bradyarrhythmias SA Node: Sick sinus syndrome (tachy-brady often w/ paroxysmal AF), sinus brady AV Node: Heart blocks Atropine 0.5mg IV bolus q3-5 min up to 3mg max Transcutaneous pacing if atropine ineffective IV adrenaline/isoprenaline while awaiting pacing: Care: chronotropes like isoprenaline/adrenaline may provoke arrhythmias Adrenaline better in BP <80 as isoprenaline can decrease BP Long-term: Permanent Pacemaker (PPM) Tachyarrhythmias: Specifics Narrow Complex: SVT (incl WPW), AF, A flutter Broad Complex: VT, VF, torsades Valsalva, carotid massage: Effective in SVT including WPW Avoid in elderly or those w/ vagal disease Adenosine: 6 mg IV bolus → 12mg, 18mg (1st line in SVT incl WPW) Prep resus equipment due to risk of accelerated ventricular response Differential Diagnosis for Arrhythmias Non-cardiac causes: Anxiety/panic attack, hyperventilation Thyrotoxicosis Electrolyte disturbances (e.g., hyperkalaemia, hypomagnesaemia) Drugs: beta-agonists, digoxin toxicity, QT-prolonging medications Structural: Cardiomyopathies, ischaemic heart disease, valvular pathology Electrical: Long QT syndrome, Brugada syndrome, WPW Prophylaxis BBs prevent tachyarrhythmias in AF, SVT, VT Antiarrhythmics (e.g., amiodarone, sotalol): Recurrent symptomatic arrhythmias Electrolyte optimisation: Maintain K+ 4–5 mmol/L and Mg2+ >1 mmol/L Lifestyle modification: Avoid stimulants (e.g., caffeine, alcohol), stress management Complications Heart failure (due to persistent tachy/brady) Thromboembolism (e.g., AF → stroke, systemic embolism) Sudden cardiac death (e.g., VF, torsades, VT progression) Syncope and falls (especially in elderly with bradyarrhythmias) Risk Stratification: Identifying Patients at Risk for Life-Threatening Arrhythmias Structural Heart Disease: Hx of MI, cardiomyopathy (EF <35%) Genetic Syndromes: Long QT syndrome, Brugada syndrome, WPW ECG Findings: Prolonged QT interval, ventricular ectopics, nonsustained VT Symptoms: Syncope, presyncope, exertional dizziness Family History: Sudden cardiac death Device Therapy: Indications for Pacemakers and Defibrillators Pacemaker (PPM): Symptomatic bradycardia, heart block, sick sinus syndrome ICD (Implantable Cardioverter Defibrillator): Survivors of VF/VT arrest Severe LV dysfunction (EF <35%) for primary prevention Arrhythmia Aetiology/Causes Cardiac Causes Ischaemic heart disease, cardiomyopathies, valvular disease, congenital heart abnormalities Structural heart disease (e.g., left ventricular dysfunction, previous MI) Non-Cardiac Causes Electrolyte disturbances: Hyperkalaemia, hypokalaemia, hypomagnesaemia, hypocalcaemia Medications: Beta-blockers, digoxin, antiarrhythmics, QT-prolonging drugs Systemic: Thyrotoxicosis, infections, metabolic disorders Lifestyle: Excess caffeine, alcohol, smoking, stimulant use Pathophysiology Impulse formation disorders: Altered automaticity (e.g., increased pacemaker activity), afterdepolarisations Impulse conduction disorders: Re-entry circuits (e.g., AV nodal re-entrant tachycardia), conduction blocks (e.g., AV block) Clinical Assessment Haemodynamic Compromise Indicators Hypotension, hypoperfusion Syncope, altered level of consciousness Chest pain, heart failure symptoms Tachyarrhythmia Assessment Narrow vs Broad Complex: Narrow: SVT, AF, Atrial Flutter Broad: VT, VF, Torsades de Pointes If unstable: synchronised DC cardioversion Bradyarrhythmia Assessment SA Node Dysfunction: Sick sinus syndrome, sinus bradycardia AV Node Dysfunction: Heart blocks (1st, 2nd, 3rd-degree) If unstable: transcutaneous pacing Symptoms Palpitations, dizziness, syncope Chest pain, dyspnoea Fatigue, reduced exercise tolerance Investigations Initial Assessment ECG: Essential for diagnosis; identifies rhythm type and conduction abnormalities Blood tests: U&E, cardiac enzymes (if ACS suspected), TFTs Imaging: CXR (if structural disease suspected) Further Testing Holter monitor: Intermittent arrhythmias Echocardiography: Structural heart disease assessment Electrophysiology Studies (EPS): For diagnosing complex arrhythmias ____________________________________ Management General Management Principles Maintain airway, assist breathing as needed Administer oxygen to maintain SpO2 >94% Continuous cardiac and BP monitoring Establish IV access Bradyarrhythmias Atropine: 0.5mg IV every 3-5 min (max 3mg) Transcutaneous pacing if atropine ineffective IV adrenaline/isoprenaline while awaiting pacing Adrenaline preferred if BP <80 mmHg (isoprenaline may reduce BP) Long-term: Permanent Pacemaker (PPM) for symptomatic bradycardia Tachyarrhythmias Narrow Complex (SVT, AF, Atrial Flutter) Vagal Manoeuvres: Valsalva, carotid massage (avoid in elderly) Adenosine: 6mg IV → 12mg → 18mg (caution in WPW) Beta-blockers or CCBs: If adenosine contraindicated Electric Cardioversion: If resistant to pharmacotherapy Broad Complex (VT, VF, Torsades de Pointes) Antiarrhythmics: Amiodarone or Lidocaine Immediate defibrillation: VF or pulseless VT Magnesium sulphate: If Torsades suspected Differential Diagnosis Non-Cardiac Causes Anxiety/panic attacks, hyperventilation Thyrotoxicosis Electrolyte disturbances (hyperkalaemia, hypomagnesaemia) Drugs: Beta-agonists, digoxin toxicity, QT-prolonging medications Structural Causes Cardiomyopathies, ischaemic heart disease, valvular pathology Electrical Causes Long QT Syndrome, Brugada Syndrome, WPW Prophylaxis & Long-Term Management Beta-blockers: Atenolol 25mg daily, Metoprolol 25mg BD Antiarrhythmics: Amiodarone, Sotalol for recurrent symptomatic arrhythmias Electrolyte optimisation: Maintain K+ 4–5 mmol/L, Mg2+ >1 mmol/L Lifestyle modification: Avoid stimulants (caffeine, alcohol), stress management Complications Heart Failure: Due to persistent tachyarrhythmia or bradyarrhythmia Thromboembolism: AF → Stroke, systemic embolism Sudden Cardiac Death: VF, Torsades, VT progression Syncope & Falls: Especially in elderly with bradyarrhythmias Risk Stratification: Identifying High-Risk Patients Structural heart disease: Previous MI, EF <35% Genetic syndromes: Long QT syndrome, Brugada, WPW ECG abnormalities: Prolonged QT, ventricular ectopics, non-sustained VT Symptoms: Syncope, exertional dizziness Family history: Sudden cardiac death Device Therapy: Pacemakers & ICDs Pacemaker (PPM) Indications Symptomatic bradycardia, heart block, sick sinus syndrome Implantable Cardioverter Defibrillator (ICD) Indications Survivors of VF/VT arrest Severe LV dysfunction (EF <35%) for primary prevention Notes: Unstable patients require urgent intervention (cardioversion/pacing/defibrillation) Adenosine first-line for SVT, but contraindicated in WPW with AF VF and pulseless VT require immediate defibrillation Long-term management includes rate/rhythm control, lifestyle modifications, and risk stratification Bookmark Failed! 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Log In Get started Bookmarks Help Progress 0% Cardiovascular AAA + Rupture AC dislocation ATSI Abdominal pain in kids Abnormal/Dysfunctional Uterine Bleeding (AUB/DUB) Acanthosis Nigricans Acne Acromegaly Actinic Cheilitis Acute Kidney Injury (AKI) Acute Swollen Joint with Fever Acute Vision Loss Acute and Progressive Vision Loss Addisons Adjustment Disorder and Anxiety Adjustment Disorder with Depressed Mood Age related macular degeneration Alcohol Cessation Allergic rhinitis Alopecia Amenorrhoea Anaphylaxis Angina Angular Cheilitis Ankylosing Spondylitis (AS) Anorexia Nervosa Anticholinergics and TCAs Antidepressants Antimetabolite drugs Antiphospholipid syndrome Antipsychotics Anxiety Disorders Aortic Dissection Arrhythmia Asthma Asthma Atrial Fibrillation Back pain Behavioural / learning disorders Behavioural disturbances Bell’s palsy and Ramsey Hunt syndrome Beta-Human Chorionic Gonadotropin (β-hCG) Biologic agents Bipolar Disorder Bleeding disorders Blepharitis Breast Cancer Breast Lump Bronchiectasis (Updated) CA-125 (Cancer Antigen 125) CRPS CVD Risk Assessment Calluses and Corns Candida (Candidiasis as an STI) Carpal tunnel syndrome and de quervains tenosynovitis Cellulite Cervical spondylosis Chest pain Chickenpox (Varicella) Chilblains Cholesteatoma Chronic Cough in Children Chronic Fatigue Syndrome (CFS) Chronic Kidney Disease (CKD) Chronic Rhinosinusitis Chronic Stridor Clavicular fracture Clozapine Coeliacs Colorectal Cancer Screening Recommendations Congestive Cardiac Failure Connective Tissue Diseases Constipation Contact Dermatitis Cracked Heel Croup Cushings Cutaneous Drug Eruptions DKA vs HHS Dacrocystitis, dacyrostenosis, dacyrocystocoele Deep Vein Thrombosis (DVT) Delerium Dementia Depression and Delirium Dermal melanocystosis (mongolian spot) Developmental Dysplasia of the Hip (DDH) Diabetes Diabetes Insipidus (DI) vs Primary Polydipsia Diabetic Neuropathy Diarrhoea Diplopia Dizziness / syncope Down syndrome Duchenne muscular dystrophy Dupuytrens / trigger finger Dyspepsia Dyspnoea (Shortness of Breath) ECG ECG Findings ECG Patterns CONCISE COMPREHENSIVE Atrial Fibrillation (AF) Aetiology Structural/Electrical: CAD, HF, HTN, valvular heart disease Metabolic: Hyperthyroidism, obesity Reactive: Infection/sepsis, PE Risk Factors Cardiovascular risk factors (obesity, diabetes, smoking, OSA) Increasing age Male sex Triggers Psychological stress Infection Caffeine, dehydration Alcohol Screening Screen patients aged ≥65 years annually; if irregular pulse, perform ECG Classifications Paroxysmal: Self-terminating, duration <7 days (usually <48 hours) Persistent: >7 days, requires intervention to restore sinus rhythm Chronic: Persistent AF where restoration to sinus rhythm is not attempted Valvular: Associated with moderate-severe mitral stenosis or mechanical heart valves Investigations Baseline bloods: FBC, UEC, TFT Urine MCS and CXR: To identify infection or contributing pathology ECG: Confirms diagnosis; evaluate for ischaemia, LVH, or valvular disease Echocardiogram: Assess for mural thrombus, atrial/ventricular size, and valvular function LFTs: Consider for alcohol-related AF or medication monitoring Catheter Ablation: Indications and Considerations for Referral Indications: Symptomatic AF refractory to medical therapy Paroxysmal AF uncontrolled with antiarrhythmic drugs Younger patients with minimal comorbidities Considerations: Requires specialist cardiology referral Success higher in paroxysmal AF than persistent or chronic AF Risks include cardiac tamponade, pulmonary vein stenosis, thromboembolism Additional Notes HAS-BLED Score: Assess bleeding risk prior to initiating anticoagulation Criteria for Rhythm Control Most cases of AF focus on rate control, except in the following situations: Symptomatic AF (e.g., palpitations, dizziness, dyspnoea) Patient is physically active Ventricular dysfunction (e.g., LVEF <40%) First presentation within <48 hours Difficulty attaining rate control with medications Haemodynamic instability: Requires electrical cardioversion (100J biphasic, 200J monophasic) Note: Pharmacological cardioversion with IV flecainide or amiodarone can be attempted if the patient is haemodynamically stable CHA2DS2-VASc Scoring Criteria Used to assess stroke risk and guide anticoagulation: C: CHF ≤40% = 1 H: HTN = 1 A: ≥75 years = 2 D: Diabetes = 1 S2: Stroke/TIA/thromboembolism = 2 V: Vascular disease (e.g., MI, PAD) = 1 A: 65–74 years = 1 Sex: Female = 1(if other risk factors present) Scoring: If score ≥2 (men) or ≥3 (women), initiate anticoagulation. For males with a score of 1 and females with a score of 2, anticoagulation is considered. Anticoagulation Pharm Management First-Line Direct Oral Anticoagulants (DOACs): Apixaban: 5mg BD (reduce to 2.5mg BD if ≥80 years, weight ≤60kg, or Cr ≥133µmol/L) For VTE, initial dose is 10mg BD for 1/52, then 5mg BD Rivaroxaban: 20mg OD(15mg OD if CrCl 30–49mL/min) For VTE, initial dose is 15mg BD for 3/52, then 20mg OD Dabigatran 150mg BD (reduce to 110mg BD if ≥75 years, CrCl 30–49mL/min, or high bleeding risk) Warfarin use: Recommended for patients with rheumatic mitral stenosis, mechanical heart valves, or severe kidney impairment; Target INR 2–3 Special Considerations: If AF detected asymptomatically and onset is unclear: Pre-Cardioversion: ≥3 weeks anticoagulation unless TOE excludes thrombus Post-Cardioversion: Continue for ≥4 weeks. Criteria for Hospitalisation Hypotension RVR (HR >110) Significant symptoms: Chest pain, presyncope, syncope Pharmacological Management Rate Control: BBs: Metoprolol 25–100mg BD, atenolol 25–100mg OD Calcium channel blockers (if BBs not tolerated): Verapamil, diltiazem (180–360mg OD) Digoxin: Add-on in sedentary patients or if rate control is insufficient Amiodarone: Reserved for refractory cases Rhythm Control: Flecainide: For structurally normal hearts Amiodarone/Sotalol: If structural or significant heart disease present Note: Rate control is not required if HR <100 and asymptomatic Non-Pharmacological Management Avoid triggers (e.g., caffeine, stress) Optimise risk factors (e.g., manage HTN, OSA) Smoking and alcohol cessation Regular aerobic exercise (e.g., 150min/week) Maintain healthy BMI <25 Notes: Use dihydropyridine CCBs + flecainide cautiously in patients with LV dysfunction or HF Atrial flutter follows similar management, but cardioversion is more effective compared to AF Atrial Fibrillation (AF) Aetiology: Structural/electrical abnormalities, such as coronary artery disease (CAD), heart failure (HF), hypertension (HTN), and valvular heart disease. Metabolic causes: Hyperthyroidism, alcohol (ethanol) use. Reactive causes: Infections, sepsis, pulmonary embolism (PE). Risk Factors: Cardiovascular risk factors: obesity, diabetes, smoking, OSA. Older age, male sex. Triggers: psychological stress, caffeine, dehydration Rheumatic mitral stenosis or mechanical heart valve elevates risk. Triggers: Stress, infections, caffeine, dehydration, alcohol. Classifications: Paroxysmal AF: Self-terminating episodes lasting less than 7 days, often within 48 hours. Persistent AF: Lasts longer than 7 days and may require intervention. Long-Standing Persistent AF: Continuous AF lasting for more than 1 year, with rhythm control attempts. Permanent AF: Rhythm control is not pursued or is unsuccessful. All types of AF present a similar risk of thromboembolism and stroke. Conditions That Increase the Risk of AF: HTN Diabetes Obesity OSA HF Thyrotoxicosis VHD (esp. rheumatic mitral stenosis) Alcohol use Acute events (i.e., sepsis, pneumonia, surgery) Screening: Annual ECG for those >65; check if pulse is irregular. Diagnostic workup: FBE, UEC, TFTs, CMP, TTE. Use the PIRATES mnemonic for new-onset AF causes: Pulmonary (i.e., pHTN, PE, COPD, OSA) Ischemic (MI) Rheumatic heart disease Alcohol, arrhythmias (i.e., WPW) Thyrotoxicosis, toxins (i.e., adenosine) Electrolytes (i.e., hypokalaemia) Sepsis, surgery Investigations: Labs: FBE, UEC, TFTs, LFTs if alcohol-related. MCS and CXR. ECG, Echo for thrombus, valvular issues, atrial/ventricular assessment. Others: HbA1c, TTE (for VHD, ejection fraction). Scoring and Anticoagulation: CHADSVa Score: Determines stroke risk in AF: CHF – 1 HTN – 1 Age 65-74 – 1, ≥75 – 2 Diabetes – 1 Stroke/TIA – 2 Vascular disease – 1 Female – 1 (if other risks present) HAS-BLED Score: Evaluates bleeding risk to balance with anticoagulation therapy. Anticoagulate at least 3 weeks pre-cardioversion if AF onset unclear. Management: Treat the Underlying Cause: Address conditions that increase AF risk, including hypertension, diabetes, obesity, and alcohol consumption. Anticoagulation Therapy: Required for stroke prevention in AF patients, especially those with risk factors as per CHADSVa and CHA₂DS₂VASc scoring. Non-Valvular AF: Preferably managed with a NOAC (e.g., Apixaban or Rivaroxaban). Valvular AF (moderate to severe mitral stenosis or mechanical heart valves): Requires warfarin regardless of other risk factors. Address Underlying Causes: Manage factors raising AF risk (i.e., HTN, diabetes, obesity, alcohol). Anticoagulation: Prevents stroke in AF, following CHADSVa score. Non-Valvular AF: Use NOAC (i.e., Apixaban, Rivaroxaban). Valvular AF (rheumatic mitral stenosis, mechanical valves): Warfarin preferred. Dosing for NOACs based on renal function and bleeding risk: NOAC Dosing Criteria Apixaban 5 mg BID Standard dose Apixaban 2.5 mg BID ≥2 risk factors (i.e., age ≥80, weight ≤60 kg) Rivaroxaban 20 mg daily CrCl ≥50 Rivaroxaban 15 mg daily CrCl 30–49 Rate Control: Aim for a resting heart rate of less than 110 bpm. First-Line: Beta-blockers (e.g., Atenolol 25–100 mg or Metoprolol 25–100 mg). Second-Line: Calcium channel blockers like Diltiazem or Verapamil for patients who cannot tolerate beta-blockers. Alternative Options: Digoxin or Amiodarone if beta-blockers or CCBs are ineffective or contraindicated. Rhythm Control (if indicated): Acute Rhythm Control: Direct current (DC) cardioversion or pharmacological agents (e.g., Flecainide, Amiodarone) for haemodynamically unstable patients. Long-Term Rhythm Control: Consider for symptomatic patients or those who prefer it; options include Flecainide, Sotalol, or Amiodarone. Note: Pill-in-the-pocket approach may be used for infrequent symptomatic episodes. Non-Pharmacological Management: Lifestyle modifications, including smoking cessation, limiting alcohol intake, maintaining a BMI <27, and regular aerobic exercise (at least 150 minutes per week). Optimising control of underlying cardiovascular risk factors. Criteria for Hospitalisation: Indicator Description Hypotension Low blood pressure RVR >110 bpm Rapid ventricular rate Severe symptoms i.e., chest pain, syncope Complications: Increased risk of thromboembolism, stroke, heart failure, and quality of life impairment. Notes: Rate Control vs Rhythm Control: Rate control is generally preferred, except in symptomatic or physically active patients, or those with LV dysfunction. Acute Management Considerations: Haemodynamic stability and duration of AF episode (< or >48 hour) guide the decision for immediate cardioversion. Cardioversion should be deferred if left atrial thrombus presence is suspected unless the patient has been on therapeutic anticoagulation for at least 3 weeks. Anticoagulant Choice in Special Populations: Use warfarin over NOACs in patients with valvular AF (rheumatic mitral stenosis, mechanical heart valves) or severe kidney disease. Antiplatelet therapy is generally not recommended for stroke prevention in AF. Additional Recommendations (Heart Foundation 2018): Intensive risk factor management for weight, exercise, and sleep apnoea is recommended to reduce AF burden. Regular screening for sleep apnoea and adherence to Continuous Positive Airway Pressure (CPAP) if diagnosed 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 Intellectual Disability (ID) Definition IQ <70 plus deficits in adaptive functioning (communication, social skills, daily living) Often diagnosed in early childhood, linked with global developmental delay (delay in ≥2 domains: motor, cognitive, social, language) Causes Prenatal Prematurity, intrauterine growth restriction (IUGR) Maternal infections (TORCH: Toxoplasmosis, Other [syphilis], Rubella, CMV, Herpes) Fetal alcohol syndrome, maternal substance use Perinatal Birth hypoxia, perinatal brain injury Severe neonatal jaundice (kernicterus) Postnatal Lead poisoning, severe malnutrition Head trauma, non-accidental injury Genetic Chromosomal disorders: Down syndrome, Turner syndrome Single-gene disorders: Fragile X syndrome, Rett syndrome Metabolic disorders: Phenylketonuria (PKU), mitochondrial diseases Investigations First-Line Chromosomal microarray (CMA): Identifies copy number variations (e.g., microdeletions, duplications) Other Investigations (As Indicated) Metabolic screening: Inborn errors of metabolism (PKU, mitochondrial disorders) Thyroid function tests: Congenital or acquired hypothyroidism Lead levels: If environmental exposure suspected Management Referral Paediatrician or developmental specialist for comprehensive assessment and diagnosis GP Role Early identification of developmental concerns Initiate chromosomal microarray (CMA) and consider other relevant tests Support families: Provide education, coordinate with allied health services, assist with disability funding applications Allied Health Support Speech therapy: If communication delays Occupational therapy: Support adaptive skills and sensory integration Physiotherapy: For motor delays if present Psychology: Behavioural management and emotional support Long-Term Considerations Education and special needs planning: Individualised learning plans (ILP) Disability support services: NDIS funding, Centrelink assistance Transition planning for adulthood: Vocational training, supported employment, independent living skills Intellectual Disability (ID) Definition Significantly reduced intellectual functioning with an IQ below 70 Deficits in adaptive behaviour across areas such as communication, social participation, and self-care Onset usually during the developmental period and often accompanied by global developmental delay in two or more domains (motor, cognitive, social, language) Causes Prenatal Prematurity, maternal infections, fetal alcohol spectrum disorders Exposure to teratogens affecting brain development Perinatal Hypoxic-ischaemic injury, intracranial haemorrhage Complications during delivery Postnatal Lead toxicity, traumatic head injury, severe malnutrition Central nervous system infections (e.g. meningitis, encephalitis) Genetic Down syndrome, Fragile X syndrome, other chromosomal abnormalities Inherited metabolic disorders (e.g. phenylketonuria) Psychosocial Extreme neglect or prolonged institutional care in early childhood Investigations Chromosomal Microarray First-line genetic test to identify microdeletions or duplications Additional Testing (as indicated) Metabolic screening if an inborn error of metabolism is suspected Thyroid function to exclude hypothyroidism Serum lead levels if environmental exposure is possible MRI brain for structural anomalies if clinically relevant Management Referral Involve a paediatrician or developmental specialist for comprehensive assessment Multidisciplinary input from geneticists, allied health, and educational services GP Role Early recognition of developmental delays and initiation of investigations (including chromosomal microarray) Coordinate ongoing care and support for families Early Intervention Access to speech therapy, occupational therapy, and physiotherapy for skill development Special education programmes tailored to cognitive level Support and Planning Guidance on behaviour management and social skills training Assistance with community resources, respite care, and educational entitlements Monitoring Regular follow-up to reassess developmental progress, comorbidities (e.g. epilepsy, visual/hearing impairment) Transition planning into adolescence and adulthood, ensuring appropriate vocational and social support Bookmark Failed! 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Log In Get started Bookmarks Help Progress 0% Cardiovascular AAA + Rupture AC dislocation ATSI Abdominal pain in kids Abnormal/Dysfunctional Uterine Bleeding (AUB/DUB) Acanthosis Nigricans Acne Acromegaly Actinic Cheilitis Acute Kidney Injury (AKI) Acute Swollen Joint with Fever Acute Vision Loss Acute and Progressive Vision Loss Addisons Adjustment Disorder and Anxiety Adjustment Disorder with Depressed Mood Age related macular degeneration Alcohol Cessation Allergic rhinitis Alopecia Amenorrhoea Anaphylaxis Angina Angular Cheilitis Ankylosing Spondylitis (AS) Anorexia Nervosa Anticholinergics and TCAs Antidepressants Antimetabolite drugs Antiphospholipid syndrome Antipsychotics Anxiety Disorders Aortic Dissection Arrhythmia Asthma Asthma Atrial Fibrillation Back pain Behavioural / learning disorders Behavioural disturbances Bell’s palsy and Ramsey Hunt syndrome Beta-Human Chorionic Gonadotropin (β-hCG) Biologic agents Bipolar Disorder Bleeding disorders Blepharitis Breast Cancer Breast Lump Bronchiectasis (Updated) CA-125 (Cancer Antigen 125) CRPS CVD Risk Assessment Calluses and Corns Candida (Candidiasis as an STI) Carpal tunnel syndrome and de quervains tenosynovitis Cellulite Cervical spondylosis Chest pain Chickenpox (Varicella) Chilblains Cholesteatoma Chronic Cough in Children Chronic Fatigue Syndrome (CFS) Chronic Kidney Disease (CKD) Chronic Rhinosinusitis Chronic Stridor Clavicular fracture Clozapine Coeliacs Colorectal Cancer Screening Recommendations Congestive Cardiac Failure Connective Tissue Diseases Constipation Contact Dermatitis Cracked Heel Croup Cushings Cutaneous Drug Eruptions DKA vs HHS Dacrocystitis, dacyrostenosis, dacyrocystocoele Deep Vein Thrombosis (DVT) Delerium Dementia Depression and Delirium Dermal melanocystosis (mongolian spot) Developmental Dysplasia of the Hip (DDH) Diabetes Diabetes Insipidus (DI) vs Primary Polydipsia Diabetic Neuropathy Diarrhoea Diplopia Dizziness / syncope Down syndrome Duchenne muscular dystrophy Dupuytrens / trigger finger Dyspepsia Dyspnoea (Shortness of Breath) ECG ECG Findings ECG Patterns CONCISE COMPREHENSIVE Clavicular Fracture Management Conservative: Immobilisation: Sling for ~2 weeks Analgesia: Paracetamol ± ibuprofen (2–3 weeks) Restrictions: No contact sports for 6 weeks post-sling Follow-Up: Reassess if pain, deformity, or neurovascular changes Education: Normal: Lump at fracture site (may persist ~1 year) Complications: W atch for skin irritation, malunion, nonunion Orthopaedic Referral Displaced middle/lateral-third fracture Shortened middle-third >2 cm (>12 years) Open fracture or skin tenting Neurovascular injury Follow-Up Guidelines <11 years: No follow-up unless symptomatic ≥11 years: GP/fracture clinic in 1 week with repeat XR (if displaced) Clavicular Fracture Classification Fractures are often categorised by their location along the clavicle: Middle (mid-shaft) third: Most common site Lateral (distal) third Medial (proximal) third Mechanism Typically results from a direct blow to the lateral shoulder, a fall on an outstretched hand, or a high-impact collision in sports. The proximal fragment may be pulled superiorly by the sternocleidomastoid, while the distal fragment can be displaced downward by the weight of the arm. Management (when no severe neurovascular compromise) Immobilisation: A broad arm sling for approximately 2 weeks to minimise movement and allow early callus formation Analgesia: Paracetamol (regular dosing) and/or NSAIDs (e.g. ibuprofen) for pain control over 2–3 weeks, unless contraindicated Activity restrictions: Avoid contact or high-risk sports for at least 6 weeks after sling removal to reduce re-injury risk Follow-up: Patients should return for re-assessment if pain worsens, deformity increases, or neurovascular symptoms develop Education: A palpable lump at the fracture site is common and may persist for about a year. Skin irritation can occur from the sling. Malunion and nonunion are possible but relatively uncommon with mid-shaft fractures managed conservatively Indications for orthopaedic referral Displaced middle or lateral-third fracture, especially if significantly angulated Shortened middle-third fracture >2 cm in individuals over 12 years of age Open fractures or those with skin tenting, given the risk of compromised soft tissues Neurovascular injury, including evidence of brachial plexus compromise or compromised subclavian vessels Follow-up guidelines Children under 11 years: Usually no routine follow-up needed if the fracture is not severely displaced and the child is pain-free. Significant remodelling potential means these fractures often heal well Children 11 years and older: GP or fracture clinic review in 1 week, ideally with repeat X-ray if there is displacement, to ensure ongoing acceptable alignment Adults: Reassess clinically within 1–2 weeks. If persistent or severe pain, repeat imaging may be considered to evaluate for nonunion or excessive displacement Additional considerations Healing times vary: Children typically heal more quickly (4–6 weeks) than adults (8–12 weeks). Compliance with immobilisation and gradual return to activity is crucial for optimal recovery Physiotherapy can be introduced after the initial immobilisation phase to maintain shoulder range of motion and prevent stiffness. Early gentle pendulum exercises may be advised depending on pain levels Complications include malunion, nonunion (especially in smokers or older patients), and rare neurovascular compromise. Medial third fractures carry a higher risk of complications due to proximity to great vessels and brachial plexus Athletes and manual labourers may require extended rehabilitation or, in some cases, surgical fixation if the fracture is severely displaced or if early functional return is critical Bookmark Failed! Bookmark Saved! 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Log In Get started Bookmarks Help Progress 0% Cardiovascular AAA + Rupture AC dislocation ATSI Abdominal pain in kids Abnormal/Dysfunctional Uterine Bleeding (AUB/DUB) Acanthosis Nigricans Acne Acromegaly Actinic Cheilitis Acute Kidney Injury (AKI) Acute Swollen Joint with Fever Acute Vision Loss Acute and Progressive Vision Loss Addisons Adjustment Disorder and Anxiety Adjustment Disorder with Depressed Mood Age related macular degeneration Alcohol Cessation Allergic rhinitis Alopecia Amenorrhoea Anaphylaxis Angina Angular Cheilitis Ankylosing Spondylitis (AS) Anorexia Nervosa Anticholinergics and TCAs Antidepressants Antimetabolite drugs Antiphospholipid syndrome Antipsychotics Anxiety Disorders Aortic Dissection Arrhythmia Asthma Asthma Atrial Fibrillation Back pain Behavioural / learning disorders Behavioural disturbances Bell’s palsy and Ramsey Hunt syndrome Beta-Human Chorionic Gonadotropin (β-hCG) Biologic agents Bipolar Disorder Bleeding disorders Blepharitis Breast Cancer Breast Lump Bronchiectasis (Updated) CA-125 (Cancer Antigen 125) CRPS CVD Risk Assessment Calluses and Corns Candida (Candidiasis as an STI) Carpal tunnel syndrome and de quervains tenosynovitis Cellulite Cervical spondylosis Chest pain Chickenpox (Varicella) Chilblains Cholesteatoma Chronic Cough in Children Chronic Fatigue Syndrome (CFS) Chronic Kidney Disease (CKD) Chronic Rhinosinusitis Chronic Stridor Clavicular fracture Clozapine Coeliacs Colorectal Cancer Screening Recommendations Congestive Cardiac Failure Connective Tissue Diseases Constipation Contact Dermatitis Cracked Heel Croup Cushings Cutaneous Drug Eruptions DKA vs HHS Dacrocystitis, dacyrostenosis, dacyrocystocoele Deep Vein Thrombosis (DVT) Delerium Dementia Depression and Delirium Dermal melanocystosis (mongolian spot) Developmental Dysplasia of the Hip (DDH) Diabetes Diabetes Insipidus (DI) vs Primary Polydipsia Diabetic Neuropathy Diarrhoea Diplopia Dizziness / syncope Down syndrome Duchenne muscular dystrophy Dupuytrens / trigger finger Dyspepsia Dyspnoea (Shortness of Breath) ECG ECG Findings ECG Patterns CONCISE COMPREHENSIVE Antipsychotics 1st vs 2nd Generation Antipsychotics 1st Gen (Typical) Chlorpromazine (Largactil): Low potency → more sedation and anticholinergic effects, fewer EPSE Haloperidol: High potency → less sedation, more EPSE 2nd Gen (Atypical) Aripiprazole: Fewer metabolic side effects, minimal weight gain/diabetes risk Olanzapine: Highest metabolic risk (weight gain, diabetes, hyperlipidaemia); minimal hyperprolactinaemia Risperidone/Paliperidone: Most likely to cause hyperprolactinaemia (galactorrhoea, menstrual irregularities) Clozapine: Superior in treatment-resistant schizophrenia; agranulocytosis risk → regular blood monitoring Quetiapine: Low EPSE risk; often used for sedation Monitoring of Side Effects 1. Metabolic At Every Visit: Weight, BMI, waist circumference Annually: Blood pressure, fasting glucose, lipids, LFTs 2. Cardiovascular ECG annually (monitor QTc, especially for haloperidol/ziprasidone) 3. Other Side Effects Anticholinergic: Dry mouth, constipation (review every visit) EPSE: Tremor, rigidity, akathisia (check every 6 months) Hyperprolactinaemia: Annual history of galactorrhoea, menstrual irregularities, sexual dysfunction Management of Side Effects 1. Metabolic Lifestyle: SNAP (Smoking, Nutrition, Alcohol, Physical activity) Pharmacological: Metformin for impaired glucose tolerance or rapid weight gain Statins or ACE inhibitors for dyslipidaemia or hypertension 2. EPSE Lower dose or switch to lower-risk agents (e.g., quetiapine, clozapine) Acute dystonia/parkinsonism: Benztropine Akathisia: Propranolol or lorazepam 3. Hyperprolactinaemia Switch to a low-prolactin agent (e.g., aripiprazole) if symptomatic Key History Questions Recent weight gain, dietary/exercise changes Sedation, fatigue, or functional difficulties Menstrual irregularities, galactorrhoea, sexual dysfunction Stiffness, restlessness, tremor (EPSE symptoms) History of fainting or palpitations (QTc prolongation) Smoking, alcohol use, and medication compliance Additional Notes Regular monitoring reduces cardiovascular risks from long-term antipsychotic use Clozapine: Blood monitoring mandatory (weekly for 18 weeks, then less frequent) Antipsychotics 1st vs 2nd Generation Antipsychotics Drug/Generation Key Features 1st Gen (Typical) Chlorpromazine (Largactil) – Low potency More sedation, anticholinergic effects; fewer extrapyramidal side effects (EPSE) Haloperidol – High potency Less sedation, more prone to EPSE (parkinsonism, akathisia, dystonia) 2nd Gen (Atypical) Aripiprazole Minimal metabolic side effects, low risk of weight gain/diabetes, lower hyperprolactinaemia Olanzapine Highest metabolic risk (weight gain, diabetes, hyperlipidaemia), minimal hyperprolactinaemia Risperidone/Paliperidone Most likely among atypicals to cause hyperprolactinaemia (galactorrhoea, menstrual irregularities) Clozapine Superior efficacy in treatment-resistant schizophrenia; risk of agranulocytosis requires mandatory blood monitoring (weekly for 18 weeks, then less frequently) Quetiapine Low risk of EPSE, frequently used for sedation purposes Monitoring of Side Effects Parameter Frequency Notes Metabolic At every visit: weight/BMI/waist Annually: Blood pressure, fasting glucose, lipids, LFTs Cardiovascular (ECG) Annually Monitor QTc, especially if on haloperidol or ziprasidone Anticholinergic Effects Review every visit Dry mouth, constipation, blurred vision, urinary retention EPSE Every 6 months Check for tremor, rigidity, akathisia, tardive dyskinesia Hyperprolactinaemia Annually (or if symptomatic) Ask about galactorrhoea, menstrual irregularities, reduced libido Management of Side Effects Metabolic Lifestyle interventions (SNAP: Smoking, Nutrition, Alcohol, Physical activity) Metformin if glucose intolerance or rapid weight gain Statins or ACE inhibitors for dyslipidaemia/hypertension Extrapyramidal Side Effects (EPSE) Lower the dose or switch to a lower-risk agent (quetiapine, clozapine) Acute dystonia/parkinsonism → benztropine Akathisia → propranolol or lorazepam Hyperprolactinaemia Switch to a lower-prolactin agent (aripiprazole) if symptomatic Key History Questions Recent weight gain, dietary/exercise changes Sedation, fatigue, or difficulties in daily functioning Menstrual irregularities, galactorrhoea, or sexual dysfunction (hyperprolactinaemia) Stiffness, restlessness, tremor (possible EPSE) History of fainting or palpitations (QTc concerns) Smoking, alcohol use, medication compliance Additional Notes Regular monitoring can prevent long-term cardiovascular complications from antipsychotic-induced metabolic changes. Clozapine requires mandatory blood monitoring due to agranulocytosis risk (weekly for 18 weeks, then at longer intervals). 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 Polycythaemia Vera (PV) Symptoms Headache, dizziness, tinnitus, angina, vision changes Splenomegaly (70%), hepatomegaly (30%) Pruritus (especially post-hot shower), erythromelalgia (burning pain in extremities with redness) ↑ Thrombosis risk (arterial/venous) Causes Primary (True PV): ↑Hb, ↓EPO, Positive JAK2 mutation (diagnostic) Secondary: Chronic hypoxia (COPD, OSA), EPO-secreting tumours (RCC, HCC) Smoking (↑carboxyhaemoglobin) Investigations Baseline: FBC, EPO, JAK2 mutation Secondary Workup (if JAK2-negative):: LFT, UEC, urinalysis, imaging (CXR, CT, US) for tumours or hypoxia Bone marrow biopsy for suspected myeloproliferative disorders Monitoring: Regular HCT (<45%), iron studies (risk of deficiency with venesection) Management First-Line: Phlebotomy (venesection) to maintain HCT <45% Medications: Hydroxyurea (for high-risk patients, age >60 or thrombotic hx) Low-dose aspirin (to reduce thrombosis risk) Ruxolitinib (if hydroxyurea intolerant) Lifestyle: Smoking cessation, manage OSA Notes: PV = Myeloproliferative disorder with high risk of thrombotic events Exclude secondary causes before diagnosing PV JAK2 mutation is present in over 95% of true PV cases Venesection → iron deficiency → ↓HCT rises, ↓phlebotomy need Polycythaemia Vera A myeloproliferative neoplasm characterised by autonomous red blood cell overproduction Associated with elevated haematocrit (HCT), often >0.45 in men and women Involves risk of thrombotic events (arterial or venous) and progression to myelofibrosis or acute leukaemia Symptoms & Clinical Features Increased RBC Mass Headache, dizziness, tinnitus Visual disturbances (blurred vision or scotomas) Erythromelalgia (burning pain in extremities with redness) Splenomegaly (~70%), possible hepatomegaly (~30%) Pruritus (often severe after a hot shower or bath due to histamine release from basophils) Thrombosis High risk of both arterial (stroke, MI) and venous events (DVT, PE, hepatic/portal vein thrombosis) Thrombotic complications are a major cause of morbidity and mortality Causes Primary (True PV) JAK2 mutation in >95% of cases (JAK2 V617F or exon 12) Elevated RBC mass, suppressed EPO level Often elevated WBC and platelets, reflecting panmyelosis Secondary Chronic hypoxia (COPD, obstructive sleep apnoea, high altitude) Smoking (↑carboxyhaemoglobin) EPO-secreting tumours (renal cell carcinoma, hepatocellular carcinoma, haemangioblastoma) Inappropriate exogenous EPO use (athletes, doping) Investigations Initial Labs FBC: Elevated Hb/HCT, often elevated platelets/WBC EPO level: Low in primary PV, elevated or normal in secondary causes Serum ferritin/iron studies: Identify coexisting iron deficiency or confirm functional iron deficiency (due to repeated venesections) JAK2 mutation testing: Confirmatory for PV if positive Imaging and Further Workup CXR, abdominal ultrasound, or CT if suspicion of an underlying tumour or chronic hypoxia Sleep study if clinically suspect OSA Bone marrow biopsy in uncertain cases or if additional cytopenias suggest other myeloproliferative disorders Monitoring Regular haematocrit checks (target <0.45 to reduce thrombosis risk) Periodic iron studies to monitor for depletion from phlebotomy Assess for new symptoms (e.g. splenomegaly, thrombosis) Management Phlebotomy (Venesection) First-line to maintain HCT <0.45 Decreases blood viscosity, reducing thrombotic complications Long-term venesection may induce functional iron deficiency, which can reduce RBC production Cytoreductive Therapy (in high-risk patients) Hydroxyurea Considered if age >60, history of thrombosis, or significant cardiovascular risk factors Monitor FBC regularly for cytopenias Interferon-α Used in pregnancy or younger patients desiring to avoid potential mutagenicity Ruxolitinib JAK1/JAK2 inhibitor for hydroxyurea-intolerant or resistant PV Improves splenomegaly, controls haematocrit, reduces symptoms Low-Dose Aspirin Indicated for most PV patients (unless contraindicated) to reduce thrombotic risk Monitor for GI bleeding risk, especially if combined with venesection-induced iron deficiency Lifestyle & Supportive Measures Smoking cessation (reduces secondary elevation of carboxyhaemoglobin) Manage OSA if present Encourage hydration to reduce blood viscosity Advise against high-altitude travel if feasible Other Considerations Avoid iron supplementation unless clear evidence of symptomatic iron deficiency VTE prophylaxis in high-risk scenarios (long-haul flights, perioperative) Monitor for transformation to myelofibrosis or acute leukaemia Notes: PV is a chronic condition requiring lifelong monitoring of haematocrit and risk factors for thrombosis Exclude secondary causes (chronic hypoxia, EPO-secreting tumours) before diagnosing true PV JAK2 positivity >95% in primary PV, typically with suppressed EPO Mainstay therapy: phlebotomy + aspirin, cytoreductive therapy for high-risk patients Control modifiable cardiovascular risk factors (smoking, hypertension) to mitigate clot risk Regular follow-up is crucial: watch for pruritus, splenomegaly changes, or new thrombotic events Bookmark Failed! 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Log In Get started Bookmarks Help Progress 0% Cardiovascular AAA + Rupture AC dislocation ATSI Abdominal pain in kids Abnormal/Dysfunctional Uterine Bleeding (AUB/DUB) Acanthosis Nigricans Acne Acromegaly Actinic Cheilitis Acute Kidney Injury (AKI) Acute Swollen Joint with Fever Acute Vision Loss Acute and Progressive Vision Loss Addisons Adjustment Disorder and Anxiety Adjustment Disorder with Depressed Mood Age related macular degeneration Alcohol Cessation Allergic rhinitis Alopecia Amenorrhoea Anaphylaxis Angina Angular Cheilitis Ankylosing Spondylitis (AS) Anorexia Nervosa Anticholinergics and TCAs Antidepressants Antimetabolite drugs Antiphospholipid syndrome Antipsychotics Anxiety Disorders Aortic Dissection Arrhythmia Asthma Asthma Atrial Fibrillation Back pain Behavioural / learning disorders Behavioural disturbances Bell’s palsy and Ramsey Hunt syndrome Beta-Human Chorionic Gonadotropin (β-hCG) Biologic agents Bipolar Disorder Bleeding disorders Blepharitis Breast Cancer Breast Lump Bronchiectasis (Updated) CA-125 (Cancer Antigen 125) CRPS CVD Risk Assessment Calluses and Corns Candida (Candidiasis as an STI) Carpal tunnel syndrome and de quervains tenosynovitis Cellulite Cervical spondylosis Chest pain Chickenpox (Varicella) Chilblains Cholesteatoma Chronic Cough in Children Chronic Fatigue Syndrome (CFS) Chronic Kidney Disease (CKD) Chronic Rhinosinusitis Chronic Stridor Clavicular fracture Clozapine Coeliacs Colorectal Cancer Screening Recommendations Congestive Cardiac Failure Connective Tissue Diseases Constipation Contact Dermatitis Cracked Heel Croup Cushings Cutaneous Drug Eruptions DKA vs HHS Dacrocystitis, dacyrostenosis, dacyrocystocoele Deep Vein Thrombosis (DVT) Delerium Dementia Depression and Delirium Dermal melanocystosis (mongolian spot) Developmental Dysplasia of the Hip (DDH) Diabetes Diabetes Insipidus (DI) vs Primary Polydipsia Diabetic Neuropathy Diarrhoea Diplopia Dizziness / syncope Down syndrome Duchenne muscular dystrophy Dupuytrens / trigger finger Dyspepsia Dyspnoea (Shortness of Breath) ECG ECG Findings ECG Patterns CONCISE COMPREHENSIVE PTSD & Acute Stress Disorder Definitions & Core Concepts Acute Stress Disorder (ASD) Duration: Symptoms last ≥3 days to ≤1 month post-trauma Key Features: Dissociation (numbness, detachment) Intrusions, avoidance, hyperarousal, anxiety Post-Traumatic Stress Disorder (PTSD) Core Symptom Clusters (DSM-5): Intrusions: Flashbacks, distressing memories, nightmares Avoidance: Avoiding trauma-related thoughts, places, conversations Negative Cognition & Mood: Guilt, shame, persistent negative beliefs Arousal & Reactivity: Hypervigilance, exaggerated startle, irritability Risk Factors Type of trauma: Interpersonal trauma (e.g. assault, sexual violence, combat) → higher PTSD risk than natural disasters Previous trauma: Childhood abuse, multiple traumatic exposures Pre-existing mental health conditions: Anxiety, depression, substance use Poor social support Family history of mental illness, socioeconomic disadvantage Clinical Features Intrusive symptoms: Flashbacks, nightmares, distressing memories Avoidance: Of trauma reminders (places, conversations) Negative mood: Emotional numbness, guilt, detachment Hyperarousal: Irritability, insomnia, hypervigilance, startle response Somatic symptoms: Palpitations, GI distress, headaches When to Suspect ASD/PTSD Recent trauma history New-onset anxiety, panic attacks, depression Social withdrawal, substance use changes Unexplained physical symptoms Diagnosis Diagnostic Criteria Highlights ASD: Symptoms last 3 days to 1 month post-trauma, ≥9 symptoms from intrusion, mood, dissociation, avoidance, arousal clusters PTSD: Symptoms persist >1 month, must include symptoms from all 4 DSM-5 clusters Screening Tools PC-PTSD-5 (Primary Care PTSD Screen) – 5-item tool PCL-5 (PTSD Checklist) – Assesses PTSD severity K10 (Kessler Psychological Distress Scale) – Screens for comorbid mental distress Differential Diagnoses Adjustment Disorder: Emotional distress post-stressor, but less severe, no flashbacks/avoidance Major Depression: Overlaps but lacks trauma-specific intrusions/avoidance Anxiety Disorders (GAD, Panic Disorder): No trauma-related re-experiencing Personality Disorders: Long-standing maladaptive patterns Traumatic Brain Injury: Can mimic PTSD, common in combat/accidents Management Approach Guiding Principles Trauma-informed care: Validate experiences, avoid re-traumatisation Stepped care model: Tailor interventions to symptom severity Early identification: ASD treatment may prevent chronic PTSD Non-Pharmacological (First-Line) Therapy Psychoeducation & Support Normalise post-trauma reactions, discuss treatment options Encourage social support Trauma-Focused Therapies (First-line for PTSD) Trauma-focused Cognitive Behavioural Therapy (tf-CBT): Identifies negative beliefs, exposure therapy Eye Movement Desensitisation & Reprocessing (EMDR): Guided eye movements during trauma recall Prolonged Exposure Therapy: Gradual confrontation with trauma-related cues Stress Management Techniques Relaxation training, mindfulness, grounding exercises Sleep hygiene strategies Avoid single-session debriefing (e.g. Critical Incident Stress Debriefing) – May worsen distress Pharmacological Therapy (Second-Line or Adjunctive Treatment) First-Line Medications SSRIs: Sertraline, paroxetine, fluoxetine SNRIs: Venlafaxine Second-Line or Adjunctive Options Mirtazapine (if SSRIs/SNRIs ineffective or not tolerated) Prazosin (for nightmares; mixed evidence) Avoid Benzodiazepines – Risk of dependence, worsens recovery Monitoring & Duration Continue ≥12 months post-symptom resolution to prevent relapse Regular review for side effects & adherence Prognosis ASD: Many recover without progressing to PTSD PTSD: Chronic if untreated → early intervention improves outcomes Trauma-focused therapies +/− medication → significant symptom reduction, better quality of life PTSD and Acute Stress Disorder Definitions and Core Concepts Acute Stress Disorder (ASD) Definition: A trauma- and stressor-related disorder that occurs within one month of exposure to a traumatic event (actual/threatened death, serious injury, or sexual violation). Onset and Duration: Symptoms begin immediately (or soon after) the trauma and last at least three days up to one month. Key Features: Prominent dissociative symptoms (e.g. numbness, detachment) may be present, alongside intrusive re-experiencing, avoidance, anxiety, and hyperarousal. Post-Traumatic Stress Disorder (PTSD) Definition: A trauma-related condition that persists beyond one month of exposure to a traumatic event. Core Symptom Clusters (DSM-5): Intrusions (e.g. flashbacks, distressing memories, nightmares). Avoidance of trauma-related stimuli. Negative alterations in cognition and mood (e.g. guilt, shame, persistent negative beliefs). Alterations in arousal and reactivity (e.g. hypervigilance, startle response, irritability). Epidemiology PTSD has a lifetime prevalence of approximately 5–10% in Australia (varies depending on the study). Rates are higher in specific populations (e.g. veterans, first responders, refugees). Women are more likely to develop PTSD than men after exposure to a traumatic event. Risk Factors and Vulnerabilities Type of Trauma: Interpersonal traumas (e.g. assault, sexual violence, combat) tend to be more likely to result in PTSD compared to natural disasters. Previous Trauma: History of childhood abuse or multiple traumatic exposures increases susceptibility. Pre-existing Psychiatric History: Anxiety, depression, or substance misuse. Lack of Social Support: Poor support networks contribute to worse outcomes. Other Factors: Family history of mental health disorders, socioeconomic disadvantage. Clinical Presentation Both ASD and PTSD can present with: Distressing memories or flashbacks of the traumatic event(s). Persistent avoidance of reminders (people, places, conversations). Emotional numbness, detachment, or negative mood states. Hypervigilance and exaggerated startle reflex. Sleep disturbance (e.g. insomnia, nightmares). Irritability or angry outbursts. Poor concentration. Somatic symptoms (including autonomic hyperarousal, palpitations, headaches, gastrointestinal upset). When to Suspect A GP should consider ASD or PTSD in any patient presenting with: Recent traumatic life events. New-onset anxiety, panic attacks, or depressive features post-trauma. Changes in behaviour (social withdrawal, substance use) post-trauma. Unexplained somatic complaints. Diagnosis Diagnostic Criteria Highlights ASD: Symptoms last 3 days to 1 month post-trauma. Presence of at least 9 symptoms from any of these categories: intrusion, negative mood, dissociation, avoidance, arousal. PTSD: Symptoms present >1 month post-trauma. Must have symptoms from each of the four clusters (intrusion, avoidance, negative thoughts/mood, arousal) and clinically significant distress or impairment. Screening Tools Primary Care PTSD Screen (PC-PTSD) or PC-PTSD-5: Simple 4–5 item questionnaire. PTSD Checklist (PCL-5): More comprehensive scale to gauge severity of PTSD symptoms. Kessler Psychological Distress Scale (K10): A measure for general psychological distress; can indicate comorbid issues. Differential Diagnoses Adjustment Disorder: Emotional/behavioural symptoms in response to stressor(s), but typically milder and less enduring than PTSD, and not meeting full criteria. Major Depressive Disorder: Can overlap but lacks the hallmark re-experiencing and avoidance symptoms tied to a specific trauma. Anxiety Disorders (including Generalised Anxiety Disorder, Panic Disorder): May present with overlapping features but lack trauma-specific re-experiencing. Personality Disorders: Long-standing patterns of interpersonal difficulty and maladaptive coping can confound or coexist with PTSD. Traumatic Brain Injury: Particularly relevant in accidents or combat; can mimic or coexist with PTSD. Management Approach Guiding Principles Trauma-informed Care: Recognise the trauma experience; minimise re-traumatisation by adopting a patient-centred and empathetic approach. Stepped Care Model: Tailor interventions to symptom severity and functional impairment. Early Identification: Prompt detection of ASD might allow early intervention, which can reduce the risk of developing chronic PTSD. Non-Pharmacological (Psychological) Interventions Psychoeducation and Support Provide the patient with information about common responses to trauma, expected course, and available treatments. Encourage social support and involvement of family/friends if appropriate. Trauma-Focused Psychological Therapies (First-line treatments for PTSD) Trauma-focused Cognitive Behavioural Therapy (tf-CBT): Helps patients reframe negative cognitions and progressively desensitise to trauma memories. Eye Movement Desensitisation and Reprocessing (EMDR): Uses directed eye movements to facilitate processing of traumatic memories. Prolonged Exposure Therapy: Systematic confrontation with trauma memories and cues to reduce avoidance. Stress Management and Coping Skills Relaxation training, mindfulness, grounding techniques. Self-care strategies (e.g. regular exercise, structured routine). Avoidance of Single-Session “Psychological Debriefing” Formal single-session debriefing soon after trauma (critical incident stress debriefing) is not recommended, as it may exacerbate distress. Pharmacological Interventions Per current Australian Therapeutic Guidelines (eTG) and the RACGP: First-Line Pharmacotherapy: Selective Serotonin Reuptake Inhibitors (SSRIs) Serotonin-Noradrenaline Reuptake Inhibitors (SNRIs) Examples include sertraline, paroxetine, fluoxetine, venlafaxine. Second-Line or Adjunctive Options: Mirtazapine or other antidepressants if SSRIs/SNRIs not tolerated or ineffective. Prazosin for trauma-related nightmares and sleep disturbances (though evidence is mixed, some practitioners find it helpful). Avoiding Benzodiazepines Generally contraindicated for long-term management due to dependence risk and potential to worsen recovery. Monitoring and Duration Continue medication for at least 12 months after symptom resolution to reduce relapse risk. Regular reviews to monitor side effects, efficacy, and patient adherence. Comorbidities Depression and Anxiety Disorders: Very common with PTSD/ASD. Substance Use Disorders: Patients may attempt self-medication to cope with distress. Chronic Pain: Especially if the trauma was associated with a physical injury (e.g. motor vehicle accidents). Personality Disorders: May complicate the clinical picture and require more intensive therapy. Ensuring a comprehensive assessment for comorbid conditions is essential for an effective management plan. Prognosis Many individuals with ASD will recover without developing PTSD, especially with early intervention and adequate support. PTSD can become chronic if unrecognised or poorly managed, leading to significant functional impairment. With evidence-based trauma-focused therapies and/or pharmacotherapy, a substantial proportion of patients experience symptom reduction and improved quality of life. 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 Failure to Thrive (FTT) Definition "Poor growth" defined as weight <3rd centile or crossing two centile lines downward Adjust growth charts for prematurity (<37 weeks) until 2 years of age Use condition-specific growth charts for syndromic conditions (e.g., Down syndrome) Red Flags Child-Related Dehydration, malnutrition, lethargy, recurrent infections, fever Caregiver-Related Signs of abuse or neglect, poor attachment, mental health concerns Non-English speaking background (NESB) with potential communication barriers Social Factors Domestic violence, parental substance abuse, social isolation, missed appointments Causes Inadequate Intake Breastfeeding or latch difficulties, incorrect formula preparation Restricted diet, delayed introduction of solids Malabsorption Coeliac disease, cystic fibrosis, chronic liver disease, cow’s milk protein allergy Excessive Caloric Use Congenital heart disease, diabetes, hyperthyroidism, chronic infections Other Causes Genetic syndromes (e.g., Prader-Willi, Turner syndrome) Inborn errors of metabolism (e.g., phenylketonuria) ____________________________________ History Feeding history: Vomiting, food refusal, introduction of solids, formula preparation errors Family history: Parental height, social factors (e.g., refugee status, food insecurity) Medical history: Diarrhoea, fatty stools, chronic illness signs, developmental milestones Investigations Bloods FBC, UEC, CMP, LFT, ESR, iron studies, TFTs, glucose Urine and Stool Tests Urine MCS for infection Stool MCS, fat globules for malabsorption Special Tests Coeliac serology (anti-TTG, total IgA) Management Weight Monitoring Weekly weight checks at most to track progress Parental Support Feeding guidance, correcting formula preparation errors Encouragement of appropriate complementary feeding Referrals Paediatrician for complex cases or persistent growth failure Dietitian or lactation consultant for feeding difficulties Multidisciplinary team involvement if concerns for neglect or significant psychosocial issues Child Protection Mandatory reporting if neglect or abuse is suspected Notes Early intervention improves outcomes and prevents long-term developmental impacts Treating the underlying cause restores the child’s growth trajectory Failure to Thrive (FTT) Definition Poor growth defined as weight below the 3rd centile or crossing two centile lines downward Adjust growth charts for prematurity (infants <37 weeks) until 2 years of age Use condition-specific growth charts for syndromic conditions such as Down syndrome Red Flags Child-related signs: Dehydration, malnutrition, lethargy, recurrent infections, persistent fever Caregiver-related concerns: Indicators of neglect or abuse, poor attachment behaviours, mental health issues Social factors: Domestic violence, parental substance misuse, social isolation, frequent missed appointments Causes Inadequate intake: Breastfeeding difficulties (poor latch), incorrect formula preparation, restricted diet, delayed introduction of solids Malabsorption: Coeliac disease, cystic fibrosis, chronic liver disease, cow’s milk protein allergy Excessive caloric use: Congenital heart disease, diabetes, hyperthyroidism, chronic infections Other causes: Genetic syndromes (e.g., Prader-Willi, Turner syndrome), inborn errors of metabolism (e.g., phenylketonuria) History Feeding history: Evaluate frequency of feeds, vomiting, food refusal, introduction of solids, and formula preparation errors Family history: Document parental height, socioeconomic status, refugee status, and food insecurity Medical history: Look for diarrhoea, fatty stools, chronic illness signs, and developmental milestones Social history: Assess for factors that may impact nutritional intake and healthcare access Investigations Blood tests: Full blood count, urea, electrolytes and creatinine, comprehensive metabolic panel, liver function tests, ESR, iron studies, thyroid function tests, and blood glucose Urine and stool tests: Urine MCS for infection; stool microscopy and fat globules evaluation for malabsorption Special tests: Coeliac serology (anti-TTG and total IgA); consider vitamin D levels if indicated Management Weight monitoring: Weekly weight checks to track progress Parental support: Provide detailed feeding guidance, correct formula preparation, and encourage appropriate complementary feeding Nutritional rehabilitation: Refer to a dietitian or paediatric nutrition service if growth remains suboptimal Referrals: Refer to a paediatrician for complex or persistent growth failure; involve a lactation consultant for breastfeeding difficulties Multidisciplinary approach: Involve social services and child protection if neglect or significant psychosocial issues are identified Notes Early intervention improves outcomes and prevents long-term developmental impacts Treating the underlying cause usually restores normal growth trajectory Regular follow-up is essential to monitor progress and adjust management as needed Bookmark Failed! 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Log In Get started Bookmarks Help Progress 0% Cardiovascular AAA + Rupture AC dislocation ATSI Abdominal pain in kids Abnormal/Dysfunctional Uterine Bleeding (AUB/DUB) Acanthosis Nigricans Acne Acromegaly Actinic Cheilitis Acute Kidney Injury (AKI) Acute Swollen Joint with Fever Acute Vision Loss Acute and Progressive Vision Loss Addisons Adjustment Disorder and Anxiety Adjustment Disorder with Depressed Mood Age related macular degeneration Alcohol Cessation Allergic rhinitis Alopecia Amenorrhoea Anaphylaxis Angina Angular Cheilitis Ankylosing Spondylitis (AS) Anorexia Nervosa Anticholinergics and TCAs Antidepressants Antimetabolite drugs Antiphospholipid syndrome Antipsychotics Anxiety Disorders Aortic Dissection Arrhythmia Asthma Asthma Atrial Fibrillation Back pain Behavioural / learning disorders Behavioural disturbances Bell’s palsy and Ramsey Hunt syndrome Beta-Human Chorionic Gonadotropin (β-hCG) Biologic agents Bipolar Disorder Bleeding disorders Blepharitis Breast Cancer Breast Lump Bronchiectasis (Updated) CA-125 (Cancer Antigen 125) CRPS CVD Risk Assessment Calluses and Corns Candida (Candidiasis as an STI) Carpal tunnel syndrome and de quervains tenosynovitis Cellulite Cervical spondylosis Chest pain Chickenpox (Varicella) Chilblains Cholesteatoma Chronic Cough in Children Chronic Fatigue Syndrome (CFS) Chronic Kidney Disease (CKD) Chronic Rhinosinusitis Chronic Stridor Clavicular fracture Clozapine Coeliacs Colorectal Cancer Screening Recommendations Congestive Cardiac Failure Connective Tissue Diseases Constipation Contact Dermatitis Cracked Heel Croup Cushings Cutaneous Drug Eruptions DKA vs HHS Dacrocystitis, dacyrostenosis, dacyrocystocoele Deep Vein Thrombosis (DVT) Delerium Dementia Depression and Delirium Dermal melanocystosis (mongolian spot) Developmental Dysplasia of the Hip (DDH) Diabetes Diabetes Insipidus (DI) vs Primary Polydipsia Diabetic Neuropathy Diarrhoea Diplopia Dizziness / syncope Down syndrome Duchenne muscular dystrophy Dupuytrens / trigger finger Dyspepsia Dyspnoea (Shortness of Breath) ECG ECG Findings ECG Patterns CONCISE COMPREHENSIVE Pinguecula vs Pterygium Causes Chronic irritation from UV exposure, dust, wind, or dryness Common in outdoor workers or high UV exposure Pinguecula Features: Localised yellow, elevated conjunctival lesion Does not cross the cornea Found nasally or temporally on the conjunctiva Complications: Pingueculitis → redness, irritation Management: Lubricants for symptoms Topical steroids/NSAIDs for inflammation Pterygium Features: Wing-shaped fibrovascular tissue crossing the cornea Arises nasally; may distort vision if affecting the visual axis or causing astigmatism Complications: Persistent redness, irritation, visual impairment Management: Conservative: Lubricants for dryness Surgical: If affecting vision, inducing astigmatism, or causing irritation Post-surgical recurrence → reduced by adjunctive mitomycin C Prevention (Both) Sunglasses with UV protection Protective eyewear in dusty/windy environments Lubricants for dry eye prevention Note: Pinguecula: Benign, asymptomatic Pterygium: Progressive, may impair vision More common in tropical climates (high UV exposure) Pinguecula vs Pterygium Causes (Shared) Chronic irritation from UV exposure, dust, wind, or dryness Common in outdoor workers or regions with high UV (tropical climates) Pinguecula Features Localised, yellowish, elevated lesion on the conjunctiva Does not cross the cornea Often located nasally or temporally Can become inflamed (pingueculitis) → redness, irritation Management Lubricating Eye Drops for dryness/irritation Topical Steroids/NSAIDs for occasional inflammation Typically benign and asymptomatic, no surgical intervention required unless persistent irritation Pterygium Features Wing-shaped, fibrovascular tissue that crosses the cornea Usually arises nasally, can distort vision if it grows into the visual axis or induces astigmatism Can cause persistent redness, irritation, foreign body sensation Management Conservative: Lubricants for dryness, mild irritation Surgical: Indicated if vision affected, significant astigmatism, or chronic irritation Adjunct: Mitomycin C used intraoperatively can reduce recurrence risk More progressive than pinguecula; can impair vision Prevention (Both) Sunglasses with UV protection (wrap-around style ideal) Protective Eyewear in dusty or windy conditions Lubricants for dry eyes if indicated Key Differences Pinguecula: Confined to the conjunctiva, does not invade cornea, generally benign Pterygium: Extends onto the cornea, more likely to affect vision, may require surgical removal 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 Croup Pathogen Parainfluenza virus type 1 (most common) Others: RSV, influenza A/B, adenovirus Severity Mild: Barking cough, no stridor at rest No/minimal WOB Moderate: Frequent barking cough, inspiratory stridor at rest Mild-moderate WOB (nasal flaring, intercostal retractions) No agitation or drowsiness Severe: Marked WOB (accessory muscle use, retractions) Persistent stridor (inspiratory/expiratory) Agitation/drowsiness, tachypnoea/bradypnoea Life-threatening: Cyanosis, lethargy, exhaustion Treatment General: Minimal handling, comfortable position Mild/Moderate: Prednisolone 1 mg/kg PO or dexamethasone 0.15 mg/kg PO (max 10 mg) Review if stridor recurs → transfer to ED Severe: Nebulised adrenaline: 0.5 mL/kg (1:1000, max 5 mL) Dexamethasone 0.6 mg/kg (max 12 mg, any route) Monitor for 4 hrs post-adrenaline for rebound symptoms Notes Hypoxia: Late sign, indicates life-threatening croup Oxygen: Rare, for severe hypoxaemia only IV access: Defer unless essential (may agitate the child) Croup Definition Viral inflammation of the larynx, trachea, and bronchi, typically affecting children aged 6 months to 3 years Characterised by a barking cough, inspiratory stridor, and varying degrees of respiratory distress Common Pathogens Parainfluenza virus type 1 is most common Other causes include RSV, influenza A/B, and adenovirus Severity Mild Barking cough without stridor at rest Minimal work of breathing Moderate Frequent barking cough Stridor at rest with mild to moderate work of breathing No significant agitation or drowsiness Severe Marked work of breathing, accessory muscle use, possible inspiratory and expiratory stridor Agitation or altered level of consciousness Tachypnoea or occasional bradypnoea Life-Threatening Cyanosis, significant lethargy, exhaustion Treatment General Measures Minimise distress and handling Allow the child to sit upright or choose a comfortable position Mild to Moderate Croup Oral prednisolone 1 mg/kg or dexamethasone 0.15 mg/kg (maximum 10 mg) Observe for recurrence of stridor at rest, which may warrant further intervention Severe Croup Nebulised adrenaline 0.5 mL/kg of 1:1000 (maximum 5 mL) Dexamethasone 0.6 mg/kg by any route (maximum 12 mg) Monitor for at least 4 hours to watch for rebound symptoms Additional Points Nebulised budesonide can be an alternative if oral or IV steroids are not tolerated Oxygen is rarely needed unless severe hypoxaemia is present Notes Hypoxia is a late and ominous sign IV access should be avoided unless absolutely necessary Most children improve within 48 hours, though residual cough can persist Consider hospital admission if there is persistent stridor at rest, severe work of breathing, or poor oral intake Advise parents to seek urgent care if breathing worsens or stridor returns at rest at home 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 Glaucoma Risk Factors: Age >60, family history, ↑IOP Diabetes, hypertension, myopia, trauma, African/Asian ancestry Acute Angle-Closure Management: Position: Lay flat (improves optic nerve perfusion) Symptom Control: Morphine (pain), ondansetron (nausea) IOP Reduction: Beta-Blocker: Timolol 0.5% (↓aqueous humour; avoid in asthma, heart block) Alpha-Agonist: Apraclonidine 1% (↓production, ↑outflow) Cholinergic: Pilocarpine 2% (↑outflow via miosis) Carbonic Anhydrase Inhibitor: Acetazolamide IV/oral 500 mg (↓production) Referral: Urgent for laser iridotomy or surgery Glaucoma Risk Factors Age >60: Prevalence increases significantly with advancing age. Family History: Genetic predisposition, especially in primary open-angle glaucoma (POAG). Elevated IOP (intraocular pressure): Central risk factor across glaucoma subtypes. Diabetes, Hypertension: Possibly linked to vascular factors and microvascular damage. Myopia: High myopia can predispose to angle changes and optic nerve vulnerability. Trauma: Direct injury can damage drainage structures. Ethnicity: African and Asian ancestries have higher rates of certain glaucoma forms. Acute Angle-Closure Glaucoma Management Patient Position Lay flat or slightly elevated: Helps improve optic nerve perfusion by facilitating venous return. Provide analgesia (morphine if severe pain) and antiemetics (e.g. ondansetron) for symptom control. IOP Reduction Measures Beta-Blocker (topical): Timolol 0.5% eye drops reduce aqueous humour production. Avoid in asthma, COPD, heart block due to systemic β2 and β1 blockade. Alpha-Agonist (topical): Apraclonidine 1% or brimonidine: Decrease aqueous humour production and enhance outflow. Cholinergic (topical): Pilocarpine 2% constricts the pupil (miosis), pulling the iris away from the trabecular meshwork and increasing aqueous outflow. More effective once IOP is partially lowered. Carbonic Anhydrase Inhibitor: Acetazolamide 500 mg IV or oral reduces aqueous production. Monitor for metabolic acidosis, electrolyte disturbances, sulfonamide allergy. Osmotic Agents (e.g. IV mannitol) can be used if extremely high IOP and unresponsive to first-line measures. Definitive Treatment Urgent Referral to ophthalmology for laser peripheral iridotomy or surgical intervention to create an alternative pathway for aqueous humour. Ongoing prophylaxis for the fellow eye, as it is at high risk of similar angle-closure episodes. Notes Acute Angle-Closure Glaucoma: Presents with severe eye pain, blurred vision, halos around lights, red eye, mid-dilated pupil, headache, nausea, vomiting. Open-Angle Glaucoma: More common overall, often asymptomatic until late; managed with topical IOP-lowering drops (prostaglandin analogues, β-blockers, alpha-agonists, etc.) Long-Term Monitoring: Once stabilized, patients require regular optic nerve assessments, visual field testing, and IOP checks. 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 Golfer’s Vasculitis / Exercise-Induced Vasculitis Definition Harmless small vessel vasculitis, triggered by prolonged physical activity Pathophysiology Neutrophilic inflammation of small to medium vessels in skin/subcutaneous tissue Occurs after strenuous exercise Clinical Features Sites: Lower legs, thighs (unilateral or bilateral) Rash: Red patches, urticarial weals, purpura Oedema, sparing areas covered by socks/stockings Itching, stinging, pain, burning No systemic symptoms (no fever, malaise) Resolves in 3–4 weeks, may leave purple-brown discolouration Common Triggers: Running, jogging, hiking, climbing Step aerobics, golf, swimming Diagnosis Clinical history + examination Investigations only if systemic vasculitis suspected Management General Measures Rest, limb elevation Compression stockings for symptom relief/prevention NSAIDs, antihistamines for itching/discomfort Recurrent Cases Avoid vigorous exercise in hot weather Consider colchicine, dapsone, hydroxychloroquine Steroids only for severe ulceration/blistering Golfer’s Vasculitis / Exercise-Induced Vasculitis Definition Golfer’s vasculitis (also known as exercise-induced vasculitis) is a benign small vessel vasculitis that typically arises after prolonged physical activity. It primarily involves a neutrophilic inflammation of the skin’s small to medium-sized vessels and presents with superficial rash on the lower extremities. Pathophysiology Neutrophilic infiltration in vessel walls occurs in response to the mechanical and thermal stress of exercise. Commonly triggered by prolonged or strenuous physical activities, often in hot weather. Clinical Features Sites: Lower legs, possibly thighs, either unilateral or bilateral. Rash Characteristics: Red patches, urticarial weals, purpura Oedema, sometimes sparing areas covered by socks or stockings Itching, stinging, pain, or burning sensations Typically no systemic symptoms (e.g., no fever or malaise) Rash resolves spontaneously in ~3–4 weeks; may leave purple-brown pigmentation. Common Triggers: Running, jogging, hiking, climbing, step aerobics, golf, swimming. Diagnosis Mostly clinical, based on history of onset during or after exercise, characteristic distribution, and lack of systemic involvement. Investigations are generally unnecessary unless systemic or atypical signs raise suspicion of other vasculitides (e.g. ANA, ESR, CRP if needed). Management General Measures Rest and limb elevation to reduce swelling and discomfort. Compression stockings may help prevent or alleviate symptoms by improving venous return. NSAIDs (e.g. ibuprofen) or antihistamines (e.g. cetirizine) can relieve itching or mild pain. Recurrent or More Severe Cases Avoid vigorous exercise in hot weather if this pattern is recurrent. Consider colchicine, dapsone, or hydroxychloroquine under specialist guidance for recurrent or persistent cases. Topical or oral corticosteroids are typically reserved for severe ulceration or blistering (rare). Notes Also called “golfer’s vasculitis” because it often appears after golfing or similar prolonged outdoor activity, especially in warm climates. Education and reassurance are important; the condition is benign and usually resolves without scarring. If you encounter unusual or persistent features (systemic illness, extensive purpura, blistering, necrosis), consider referring to a dermatologist or rheumatologist to exclude systemic vasculitis. Bookmark Failed! Bookmark Saved! Add Bookmark Refresh Refresh