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 Neutropenia and Normocytic Anaemia Neutropenia Differentials Common: Acute infections (EBV, CMV, hepatitis, influenza) Others: Autoimmune (SLE), bone marrow suppression (malignancies, chemo), drug reactions When to Refer WCC <1 × 10⁹/L Persistent/recurrent infections Systemic illness Key Points Febrile Neutropenia: Emergency → IV antibiotics Severe/Prolonged: Consider G-CSF Normocytic Anaemia Differentials Anaemia of chronic disease (RA, T2DM, HF, IHD, IBD) Acute blood loss Early iron deficiency Haemolytic anaemia (e.g., sickle cell) Key Points Reticulocyte Count: Distinguish underproduction vs haemolysis Haemolysis Workup: LDH, bilirubin, haptoglobin Chronic Disease: Check CRP, ESR Note: Neutropenia: Acute infections are most common and often self-limiting Normocytic Anaemia: Chronic inflammation suppresses erythropoiesis despite adequate iron Neutropenia and Normocytic Anaemia NEUTROPENIA Differential Diagnoses Acute Infections (viral: EBV, CMV, influenza, hepatitis) Often self-limiting, mild neutropenia resolving once infection clears Autoimmune Conditions (SLE, RA) Immune-mediated peripheral destruction or bone marrow suppression Bone Marrow Suppression Malignancies (leukaemia, myelodysplastic syndromes), infiltration, aplastic anaemia Chemotherapy or radiation-induced (common iatrogenic cause) Drug-Induced Certain antibiotics (trimethoprim-sulfamethoxazole), antipsychotics, anticonvulsants can cause neutropenia Monitor FBC if on long-term or high-risk medications When to Refer WCC <1 × 10^9/L or severe neutropenia (ANC <0.5 × 10^9/L) High risk of severe infections (bacterial/fungal) Persistent / Recurrent Infections suggesting inadequate immune defence Systemic Illness with unexplained cytopenias or suspicion of bone marrow failure Key Points Febrile Neutropenia: Medical emergency → urgent hospital referral for broad-spectrum IV antibiotics Sepsis risk is high, especially with ANC <0.5 × 10^9/L Severe / Prolonged Neutropenia Consider G-CSF (granulocyte colony-stimulating factor) to stimulate neutrophil production if recurrent infections or post-chemotherapy Evaluate marrow function (bone marrow biopsy if indicated) Common, Mild Neutropenia Often benign, especially with mild viral infections in children or transient autoimmune neutropenia Monitor FBC trend over weeks to ensure recovery NORMOCYTIC ANAEMIA Differential Diagnoses Anaemia of Chronic Disease (ACD) / Anaemia of Chronic Inflammation Associated with RA, CKD, T2DM, HF, IBD, malignancies Inflammatory cytokines reduce erythropoietin responsiveness and iron mobilisation Ferritin often normal or elevated, low TIBC, normal/low serum iron Acute Blood Loss Initially normocytic before iron deficiency develops if bleeding continues Early Iron Deficiency MCV may remain normal initially, eventually becomes microcytic Haemolytic Anaemia RBC destruction (hereditary spherocytosis, sickle cell disease, autoimmune haemolysis) Reticulocytosis with elevated unconjugated bilirubin, LDH, low haptoglobin Key Investigations Reticulocyte Count Differentiates underproduction (low retic) vs increased RBC destruction or blood loss (high retic) Haemolysis Workup LDH, bilirubin, haptoglobin, peripheral smear (schistocytes, spherocytes, sickle cells) Markers of Inflammation CRP, ESR often elevated in chronic disease Renal and Endocrine Status CKD or hypothyroidism may present with normocytic anaemia Bone Marrow Assessment If unexplained cytopenias or suspicion of marrow pathology Management Anaemia of Chronic Disease Address underlying inflammatory condition (RA control, infection treatment, better CKD management) IV iron supplementation may help if functional iron deficiency present (low transferrin saturation, normal/high ferritin) Erythropoiesis-stimulating agents in selected CKD patients with severe anaemia Acute Blood Loss Identify and treat source of bleeding (GI bleed, trauma) RBC transfusion if haemodynamically unstable or Hb <70 g/L in most stable adults (target higher threshold in cardiac disease) Early Iron Deficiency Oral iron therapy (100–200 mg elemental iron daily) or IV iron if malabsorption or intolerance Reassess MCV and iron studies over 2–3 months Haemolytic Anaemia Tailor therapy based on aetiology (e.g. steroids for autoimmune, hydroxycarbamide for sickle cell, splenectomy in certain conditions) Supportive Care Regular follow-up, monitor CBC trends to ensure response to therapy Treat comorbidities (CKD, hypothyroidism) contributing to anaemia Check for B12/folate deficiency if RBC indices shift or if clinical suspicion Notes: Neutropenia and normocytic anaemia may co-exist in marrow disorders (myelodysplasia) or systemic diseases (SLE, chronic infections) Febrile Neutropenia requires urgent IV antibiotics and possible G-CSF if severe/prolonged For normocytic anaemia, always check reticulocyte count to distinguish underproduction vs blood loss/haemolysis Anaemia of Chronic Disease is common in older adults with multiple comorbidities (HF, T2DM, CKD) – treat underlying cause, consider IV iron if functional deficiency Consider referral to haematology if complex aetiologies, persistent cytopenias, or uncertain diagnosis 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 STEMI / NSTEMI Chest Pain Management (Pre-Hospital or Initial) Transfer to ED via ambulance urgently Aspirin 300mg orally stat GTN spray 400mcg sublingually every 5 minutes (max 3 doses) IV morphine 5mg stat every 5 minutes (if needed) Oxygen to maintain saturations >94% Large bore IV access and cardiac monitoring (ECG and vitals) Discuss with nearest tertiary hospital regarding clopidogrel or advanced care Note: STEMI - Possibly if rural - in consultation w. Cardiologist; above + clopidogrel 300mg stat Reperfusion Strategies STEMI: Primary PCI: Within 90 minutes of presentation if available Fibrinolysis: If PCI unavailable, give within 30 minutes of presentation Reperfusion must occur within 12 hours of symptom onset NSTEMI: PCI within 24–72 hours, depending on risk stratification Fibrinolysis not recommended Antiplatelet Therapy (DAPT Protocols) Aspirin: 300mg stat → then 100mg daily lifelong Clopidogrel: 300mg stat → then 75mg daily For PCI: Consider ticagrelor or prasugrel instead of clopidogrel Continue DAPT for 12 months post-MI Post-MI Medications Beta Blockers: Within 24hrs unless contraindicated (reduces mortality, arrhythmias) ACE Inhibitors: Especially in HF, LV dysfunction, or diabetes Statins: High-potency (e.g., atorvastatin 40–80mg) Aldosterone Antagonists: Add if LV dysfunction and symptomatic HF (e.g., eplerenone) Cardiac Rehabilitation Structured multidisciplinary programs focusing on: Gradual supervised return to activity Manage BP, lipids, diabetes, smoking cessation Lifestyle modifications, adherence to medications Anxiety and depression management post-MI Long-Term Management Cardiac Rehabilitation Refer for structured multidisciplinary cardiac rehab, similar to stroke long-term management All should be on ACEI, statin (highest tolerated dose), antiplatelet Dual Antiplatelet Therapy (DAPT): Continue for 12 months post-ACS, regardless of stent: Aspirin 100mg daily Clopidogrel 75mg daily (or ticagrelor/prasugrel if PCI performed) Include exercise training, SNAP risk factor optimisation, and psychological support Beta Blockers: Atenolol 25mg OD or metoprolol 25mg BD (as per eTG) LVEF <40%: Use bisoprolol 1.25mg OD, titrate up to 10mg daily Notes: Anticoagulation (e.g., warfarin/DOACs) may be required if mural thrombus or AF present post-MI ACEI primarily indicated for specific conditions (e.g., HF, LV dysfunction, diabetes, anterior MI) STEMI / NSTEMI Chest Pain Management (Pre-Hospital or Initial) Transfer to ED via ambulance urgently. Aspirin 300mg orally stat. GTN spray 400mcg sublingually every 5 minutes (max 3 doses). IV morphine 5mg stat every 5 minutes if needed. Oxygen to maintain saturations >94%. Large-bore IV access and cardiac monitoring (ECG and vitals). Consult nearest tertiary hospital for possible additional antiplatelet (clopidogrel or ticagrelor) and advanced care. In a rural setting (after consulting a cardiologist), administer clopidogrel 300mg stat for a confirmed STEMI if primary PCI is not immediately available. Reperfusion Strategies STEMI Primary PCI Aim to perform within 90 minutes of first medical contact. Radial approach preferred if expertise available (reduces bleeding risk). Fibrinolysis If PCI is unavailable or delayed, fibrinolysis should be given within 30 minutes of presentation. Most beneficial if within 12 hours of symptom onset. Contraindications include active bleeding, recent stroke, uncontrolled hypertension. NSTEMI Fibrinolysis not recommended. Early invasive strategy (PCI) within 24–72 hours, guided by risk stratification. High-risk features (recurrent chest pain, dynamic ECG changes, haemodynamic instability) may warrant expedited angiography (<24 hours). Antiplatelet Therapy (DAPT Protocols) Aspirin: 300mg stat then 100mg daily lifelong. Clopidogrel: 300mg stat then 75mg daily. Ticagrelor or Prasugrel: Consider in patients undergoing PCI. Often preferred over clopidogrel due to greater efficacy in reducing ischaemic events (check contraindications such as prior intracranial haemorrhage for prasugrel). Duration: Continue dual antiplatelet therapy (DAPT) for 12 months post-ACS or as recommended by a cardiologist. Post-MI Medications Beta Blockers Start within 24 hours unless contraindicated. Reduce mortality and arrhythmic risk. ACE Inhibitors (or ARBs) Especially indicated in HF, LV dysfunction, anterior MI, or diabetes. Start low and titrate (monitor renal function and potassium levels). Statins (High-Potency) E.g. atorvastatin 40–80mg daily. Reduces recurrent events and improves survival. Aldosterone Antagonists Indicated if LV dysfunction and symptomatic HF (e.g. eplerenone). Monitor potassium and renal function. Cardiac Rehabilitation Structured multidisciplinary programs focusing on gradual supervised return to activity. Manage BP, lipids, diabetes, smoking cessation. Emphasise lifestyle modifications and medication adherence. Include psychological support for anxiety or depression. Long-Term Management All patients should be on an ACEI (or ARB), statin (highest tolerated dose), beta blocker, and aspirin. DAPT for 12 months post-ACS (aspirin 100mg plus clopidogrel 75mg daily, or ticagrelor/prasugrel if indicated). Ongoing exercise training, SNAP risk factor optimisation (Smoking, Nutrition, Alcohol, Physical activity). Cardiologist follow-up to evaluate the need for further investigations (e.g. stress echo or imaging). Beta Blockers Common options include atenolol 25mg once daily or metoprolol 25mg twice daily. If LVEF <40%, consider heart failure-specific beta blockers (e.g. bisoprolol 1.25mg once daily, titrate to 10mg). Monitor BP, heart rate, and for signs of decompensated HF. Notes Anticoagulation (LMWH or unfractionated heparin) may be used short-term in hospital if high risk of thrombus or if awaiting PCI. Consider warfarin or DOAC in select patients (e.g. mural thrombus, concurrent AF). ACEI indicated for anterior STEMI, LV dysfunction, diabetes, or clinical HF. SGLT2 Inhibitors may be considered in patients with T2DM and HF to improve outcomes. Emphasise lifestyle changes (diet modification, weight management, ongoing smoking cessation, stress management) in primary care follow-up Overview of management of ST elevation myocardial infarction (STEMI) 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 Iron Deficiency Anaemia (IDA) Causes Chronic blood loss (menorrhagia, GI) Dietary deficiency Malabsorption (e.g., coeliac disease) Increased demand (e.g., pregnancy) Management Diet: Increase iron-rich foods (red meat, leafy greens) Oral Iron: Elemental iron 100–200 mg daily or second daily Check reticulocytes after 1–2 weeks for response Continue 3 months after Hb normalises to replenish stores IV Iron: Ferric carboxymaltose for poor oral tolerance, severe deficiency, or ongoing blood loss Counselling Oral Iron: Take on an empty stomach ± vitamin C (improves absorption) Avoid calcium, milk, tea, PPIs Side effects: Nausea, constipation, black stools (consider second-daily dosing) IV Iron: Side effects: Nausea, flushing, rare anaphylaxis or skin staining Rapid correction, generally well-tolerated Special Considerations (IBD) IDA → Most common systemic complication of IBD Active Disease: Parenteral iron preferred (oral iron can worsen symptoms) Mild/Inactive Disease: Oral iron acceptable Monitor ferritin/Hb every 3 months (1st year), then 6–12 months Notes Avoid oral iron in active IBD Supplementation must continue 3 months after Hb normalises Iron Deficiency Anaemia (IDA) Causes Chronic Blood Loss Menorrhagia, GI losses (peptic ulcer, malignancy, diverticular disease), haemorrhoids In men or postmenopausal women, investigate GI causes (colonoscopy, endoscopy) Dietary Deficiency Limited intake of iron-rich foods (e.g. vegetarian/vegan diets) Malabsorption Coeliac disease (screen via anti-tTG), H. pylori infection Increased Demand Pregnancy, rapid growth (adolescents), lactation Clinical Features Fatigue, pallor, dyspnoea on exertion, reduced exercise tolerance Pica (pagophagia → craving ice), restless legs syndrome Brittle nails, koilonychia, angular cheilitis Chronic IDA can be well-tolerated until Hb drops significantly Investigations FBC: Microcytosis (low MCV), hypochromia (low MCH), possibly elevated RDW Iron Studies: Low ferritin (<30 µg/L diagnostic), high TIBC, low serum iron, low transferrin saturation Other Tests: Coeliac screen (anti-tTG), colonoscopy/gastroscopy if suspicion of GI loss or unexplained IDA in adults, especially men or postmenopausal women Peripheral Smear: Pencil cells, target cells, anisopoikilocytosis Management Dietary Measures Increase iron-rich foods: red meat, organ meats, seafood, leafy greens, iron-fortified cereals Address contributors such as heavy menstrual bleeding, GI pathology Oral Iron Supplementation Elemental iron 100–200 mg daily or alternate days improves tolerability Take on an empty stomach with vitamin C (e.g. orange juice) to enhance absorption Avoid concurrent intake of calcium, tea, coffee, PPIs (reduce iron absorption) Common side effects: nausea, constipation, black stools Check reticulocyte count in 1–2 weeks as an early indicator of response Continue iron therapy for at least 3 months after normalisation of Hb to replenish stores IV Iron Ferric carboxymaltose or iron polymaltose if severe deficiency, poor oral tolerance, ongoing blood loss, or active inflammatory bowel disease Side effects: transient nausea, flushing, rare anaphylaxis or extravasation with skin staining Rapid repletion of iron stores Transfusion Usually reserved for severe or symptomatic anaemia (e.g. Hb <70 g/L or <80 g/L if cardiovascular compromise) Post-transfusion, still require oral/IV iron to correct stores Counselling Points Oral Iron Take with vitamin C, separate from calcium or antacids by 2 hours Alternate day dosing can reduce GI side effects and maintain efficacy IV Iron Short infusion time but risk of hypersensitivity or infusion reactions Inform about possible local skin staining if extravasation occurs Special Considerations IBD (Crohn’s / Ulcerative Colitis) IDA is the most common systemic complication In active disease, parenteral (IV) iron is preferred to avoid worsening GI inflammation In mild or inactive disease, oral iron can be used, but monitor for flare-ups Recheck ferritin/Hb every 3 months in the first year, then 6–12 months thereafter Pregnancy Increased iron requirement, routine supplementation if deficiency confirmed or risk factors present Check for compliance and tolerance Notes Diagnosis: Confirm low ferritin (gold standard). If microcytosis is unexplained, rule out coeliac disease and chronic GI blood loss Duration of Therapy: Continue 3 months beyond normal Hb to replete iron stores Monitoring Response: Reticulocyte rise ~1–2 weeks, normal Hb by ~6–8 weeks if well-tolerated and no ongoing losses Long-Term Follow-Up: Identify and address the cause of IDA, especially GI pathology in older patients. Recurrent or refractory IDA warrants specialist referral (e.g. gastroenterology) 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 PSA Screening and Prostate Cancer PSA Screening Benefits Negative test can reassure Early detection may enable curative treatment Negatives False negatives lead to missed cancers False positives from benign causes (e.g., BPH, prostatitis) Most prostate cancers grow slowly and may not harm Diagnostic procedures (e.g., biopsy) have risks like bleeding, infection, or urinary symptoms General Australia: PSA screening not routine In asymptomatic people there is no evidence to show that screening decreases mortality (applies for ovarian + prostate) Testing (if chosen): Every 2 years until age 69 Prostate Cancer Risk Factors First-degree relative with prostate cancer <65 years BRCA1/2 mutations Key Notes Discuss risks/benefits of PSA testing for higher-risk men but do not mandate it LUTS (e.g., BPH): Not linked to increased prostate cancer risk Early prostate cancer is usually asymptomatic Causes of Elevated PSA Prostatitis BPH Recent ejaculation or strenuous exercise (<48 hours) Recent DRE (<1 week) Prostate biopsy (<6 weeks) UTI Management of Elevated PSA Thresholds for Action Total PSA >3 ng/mL (if ≥50 years) Repeat total PSA + free-to-total ratio in 1–3 months Biopsy if Total PSA >5.5 ng/mL, OR Total PSA 3–5.5 ng/mL + free-to-total ratio <25% Age <50 years Use age-specific PSA percentiles <75th percentile: Reassess at age 50 75–95th percentile: Test every 2 years (3x increased risk) 95th percentile: Further investigation Free-to-total PSA ratio less reliable in this group Special Considerations Prostatitis/UTI: Defer testing until resolved Biopsy: Consider only after thorough discussion of risks/benefits Age >70: Rarely recommended unless strong family history Testing Recommendations Test only in well-informed men after shared decision-making Focus on men >45 years with risk factors Avoid frequent testing in men with normal age-specific PSA levels PSA Screening and Prostate Cancer PSA Screening Benefits Negative test can reassure men who are concerned about prostate cancer. Early detection of an aggressive cancer may enable curative treatment (e.g. radical prostatectomy, radiotherapy). Negatives False Negatives: May miss some cancers if PSA is “normal.” False Positives: PSA can be elevated by benign causes (BPH, prostatitis) → leads to unnecessary investigations or biopsy. Overdiagnosis: Many prostate cancers grow slowly and pose minimal harm; detection might lead to overtreatment. Diagnostic Risks: Biopsy complications like bleeding, infection, or urinary issues. Australian Context Routine population-wide PSA screening is not universally recommended. No conclusive evidence that PSA screening reduces mortality at the population level. (Applies similarly to ovarian cancer screening, which is also not recommended in asymptomatic women.) If men opt for screening (after informed discussion), testing is typically every 2 years up to age 69. Prostate Cancer Risk Factors Family History: First-degree relative with prostate cancer <65 yrs old → higher risk. BRCA1/2 Mutations: Increase risk of early or aggressive disease. Age: Risk rises from ~50 yrs onward (earlier in high-risk groups). Other: Possibly diets high in saturated fats, but evidence is mixed. Key Notes Shared Decision-Making: Always discuss potential benefits and harms of PSA testing. LUTS (from BPH) is not a proven risk factor for prostate cancer. Early prostate cancer is commonly asymptomatic. Causes of Elevated PSA Prostatitis or recent UTI Benign Prostatic Hyperplasia (BPH) Recent Ejaculation or strenuous physical activity involving the perineum (<48 hours) Recent DRE (within 1 week) Prostate Biopsy (up to 6 weeks post-procedure) Management of Elevated PSA Thresholds for Action If Total PSA >3 ng/mL (≥50 years), repeat total PSA ± free-to-total ratio in 1–3 months. Biopsy if: Total PSA >5.5 ng/mL OR Total PSA 3–5.5 ng/mL + free-to-total ratio <25% For men <50 years, use age-specific PSA percentiles: <75th percentile: Reassess at age 50 75–95th percentile: Test every 2 years (3× increased risk) 95th percentile: Further investigation (Free-to-total ratio less reliable in younger men) Special Considerations Prostatitis/UTI: Defer PSA testing until infection/inflammation has resolved (usually ~6 weeks). Biopsy: Consider only after thorough discussion of benefits vs. risks (bleeding, infection, anxiety). Age >70: Rarely recommended unless strong family history or high-risk factors. Testing Recommendations Test only in well-informed men after shared decision-making, focusing on men >45 years with risk factors (family history, known genetic predisposition). Avoid frequent testing if normal for age. If deciding to screen, typically every 2 years until age 69 (or older if clinically indicated and in robust health). 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 Hypertension Exam Irreg HR Waist circum / BMI Fundoscopy: Retinal haemorrhages, cotton wool spots, AV nipping, papilloedema Goitre: Hyperthyroidism as a secondary HTN cause HF signs: Displaced apex, elevated JVP, bibasal crackles, ± peripheral oedema Renal bruits: Suggest renovascular HTN Radiofemoral delay: Seen in coarctation of the aorta Palp for enlarged kidneys: Suggests ADPKD Investigations FBC, UECs, FBG (no LFTs) Urinalysis (blood), urine ACR Fasting lipids ECG ABPM Consider echo and carotid US (if smoker, diabetic, old) Ambulatory BP Borderline HTN: Confirms or excludes sustained BP elevation, particularly in white coat or masked HTN Blood Pressure Targets General population: <140/90 mmHg Diabetes: <130/80 mmHg CKD: <130/80 mmHg Elderly (≥75 years): <150/90 mmHg, individualised based on frailty and sx Monitoring and Follow-Up Initial diagnosis: Review within 4 weeks Stable HTN: Review every 3–6 months Monitor: Home BP readings if available Electrolytes and renal function (6–12 monthly with ACEi/ARBs) Adherence and SEs of medications Annual fundoscopy and CV risk reassessment Management of Hypertensive Emergencies BP >180/120 mmHg with acute end-organ damage: Immediate intervention required Common presentations: Encephalopathy: Confusion, headache, seizures Papilloedema ± retinal haemorrhages Acute pulmonary oedema AKI Immediate management: Admit to hospital IV antihypertensives (e.g., labetalol, GTN, sodium nitroprusside) Gradual BP reduction over 24–48 hours (to avoid ischaemia) Notes: 24-hr ABPM: Diagnostic threshold = SBP ≥130/80 mmHg Electrolyte imbalances: Hyperaldosteronism causes fatigue, weakness, and cramps Diabetes insipidus-related hypokalaemia can cause polydipsia and polyuria Stepwise Progression Start with first-line agents (ACE-I, ARB, CCB, thiazides) based on patient-specific factors Combination therapy is often required to achieve BP targets, starting with a low dose and titrating upwards Monitoring Baseline UEC and repeat testing 1–2 weeks after starting ACE-I or ARB to monitor renal function and potassium Accept a 25% drop in eGFR or 30% rise in creatinine, provided it stabilises within 1–2 months Pharmacological Management 1st Line Agents ACE-I / ARB Indications: Preferred in patients with HFrEF, CKD (including diabetic nephropathy), or younger patients Examples: Perindopril: 5mg daily (max 10mg) Telmisartan: 40mg daily (max 80mg) Key SEs: Hyperkalaemia, angioedema, and renal impairment Avoid in bilateral renal artery stenosis CCB Use: Effective for older patients and in those with stable angina Example: Amlodipine 5mg daily (max 10mg) Key SEs: Peripheral oedema (dose-dependent) Thiazides Indication: Particularly effective in patients >65 years and those with isolated systolic hypertension Example: Hydrochlorothiazide or indapamide 1.25–2.5mg daily Caution: Worsens gout and increases diabetes risk Monitoring: Repeat UEC at 4 weeks for hypokalaemia or hyponatraemia 2nd Line Agents Beta Blockers Indications: HFrEF, post-MI, or stable angina Example: Metoprolol XR 25mg daily (max 100mg BD) Caution: Avoid in asthma and bradycardia Non-Dihydropyridine CCBs Use: Stable angina when BBs are contraindicated Example: Diltiazem XR 180mg daily (max 360mg) Key SEs: Avoid in HFrEF due to negative inotropic and chronotropic effects Other Agents Potassium-Sparing Diuretics: Used adjunctively in resistant HTN; monitor for hyperkalaemia Alpha Blockers: Considered in resistant HTN or those with concurrent benign prostatic hyperplasia (BPH) Notes: Resistant HTN: If BP remains uncontrolled on maximum tolerated doses of 2–3 agents, consider secondary HTN investigations Combination Therapy: ACE-I or ARB + CCB is recommended as initial dual therapy in most patients CKD Guidelines: A 25% drop in eGFR within 2 months is acceptable but warrants close monitoring if decline continues Severe HTN with No Symptoms Diagnosis: BP >180/110, asymptomatic Can be managed in GP unless high-risk features: coagulopathy/anticoags, severe HF (e.g., APO), kidney impairment, recent surgery needing tight BP control, aortic dissection, pregnancy Treatment: Observe with repeated BP measurements to confirm persistence Start/continue regular antihypertensive (e.g., ramipril 5mg daily) Follow up within days to monitor response Hypertensive Urgency Diagnosis: BP >180/110 with symptoms and mild end-organ dysfunction Symptoms: mild headache, epistaxis, agitation, dizziness, blurry vision, proteinuria Treatment: Start or adjust BP meds (e.g., ACEi, CCB) if not already initiated ED referral only if symptoms worsen; otherwise monitor in GP Advise low salt diet and avoid acute stressors Hypertensive Emergency Diagnosis: BP >200–220/140 with severe symptoms and end-organ damage Symptoms: APO, chest pain (MI), confusion (HTN encephalopathy), seizures, intracranial haemorrhage Investigations: ECG, UEC, LFT, urinalysis Treatment: Immediate ED referral for ICU care IV hydralazine 1mg/min or labetalol GTN infusion (reduce BP <25% over 2 hrs) Special considerations: Aortic dissection/pregnancy: Use BB Adrenergic crisis (meth OD): Avoid BB APO: Use GTN Additional notes: Reassess long-term BP control once acute phase resolves Ensure lifestyle advice includes sodium reduction (<6g/day), weight management, and increased physical activity Causes of Resistant HTN Measurement-related: (only if question asks for “causes of high BP reading” not “causes of patient’s HTN”) Measurement error from incorrect cuff size Anxiety during measurement (White coat HTN—common in up to 20% of patients) Poor technique, e.g., patient talking or unsupported arm during measurement Patient-related: Non-adherence to medications (common and under-reported) High dietary salt intake or hidden sources (e.g., processed foods) Sedentary lifestyle and low physical activity Recent weight gain Excessive alcohol consumption (>2 standard drinks/day in men, >1 in women) Illicit substance use (e.g., cocaine, amphetamines) Effects of other medications: NSAIDs Corticosteroids (e.g., prednisone) Decongestants (e.g., pseudoephedrine) Oral contraceptives Calcineurin inhibitors (e.g., cyclosporine, tacrolimus) Secondary hypertension causes: Renal failure (e.g., CKD, renovascular disease) Primary aldosteronism Obstructive sleep apnoea (OSA) Phaeochromocytoma Additional Notes: Evaluate adherence and lifestyle factors before considering further investigations or adding medications. 24-hour ambulatory BP monitoring (ABPM) may help differentiate between true resistant HTN and white coat HTN. Secondary Causes of Hypertension Most Common Causes OSA Kidney pathology Simplified classification: Parenchyma Primary kidney diseases: PCKD, nephritis (e.g., IgA nephropathy), and CKD Vessels Renal artery stenosis (via atherosclerosis or fibromuscular dysplasia): Investigate with renal artery duplex ultrasound or CT angiogram Hormones Primary aldosteronism: Most common cause is bilateral adrenal hyperplasia (60%) Investigations: Plasma renin/aldosterone ratio (requires specialist interpretation, especially if on antihypertensives) CT adrenal scan (with contrast) Adrenal-secreting adenoma (Conn’s syndrome): Accounts for 40% of primary aldosteronism Less Common Causes Cushings Hypothyroid Hyperparathyroid Coarctation of aorta Pheochromocytoma Presents with episodic headaches, palpitations, and flushing Investigations: 24-hour urinary catecholamines or metanephrines (screening) Plasma free metanephrines for confirmation Notes: Always assess for these conditions in patients with resistant hypertension, especially if aged <40 or with sudden-onset or severe hypertension. Secondary hypertension accounts for ~10% of cases, so ensure thorough workup in refractory cases. eTG recommends specific testing based on clinical presentation to avoid unnecessary investigations. Hypertension Diagnostic thresholds (in clinic): ≥140/90 mmHg for most patients Alternative out-of-clinic threshold via ambulatory/home monitoring: ≥135/85 mmHg Types of hypertension Primary (essential) hypertension Accounts for the majority of cases (≈90%). No single identifiable cause; associated with genetics, aging, and lifestyle factors (diet, obesity, inactivity). Secondary hypertension Due to an underlying condition such as renal disease, endocrine disorders (e.g., primary aldosteronism), medication use (e.g., NSAIDs, steroids), or other specific pathologies (e.g., coarctation of aorta). Accounts for ~10% of cases; should be suspected in younger patients (<40 years), resistant HTN, or abrupt onset. Clinical features Often asymptomatic (“silent killer”); most individuals present with high BP on routine checks. Possible symptoms (usually in severe or rapidly rising BP): headaches, dizziness, blurred vision, palpitations, epistaxis (nosebleeds). Examination clues General: BMI/waist circumference (obesity), irregular heart rate (e.g., atrial fibrillation). Fundoscopy: Cotton wool spots, retinal hemorrhages, papilledema. Cardiac: Displaced apex beat (left ventricular hypertrophy), elevated JVP, signs of heart failure. Renal: Abdominal or flank bruits (renovascular disease), palpable enlarged kidneys (e.g., polycystic kidney). Vascular: Radiofemoral delay (coarctation of the aorta). Endocrine: Goiter (hyperthyroidism) or other features suggesting endocrine abnormalities. Investigations Initial tests Blood tests: UEC (urea, electrolytes, creatinine) – assess renal function and electrolyte balance. FBC (full blood count). Blood glucose or HbA1c – screen for diabetes. Lipid profile – cardiovascular risk assessment. LFTs may be done if indicated, although not always essential. Urinalysis: Check for proteinuria, hematuria, or microalbuminuria (urine ACR). ECG: Look for signs of left ventricular hypertrophy (LVH) or ischemic changes. Out-of-clinic BP monitoring Ambulatory blood pressure monitoring (ABPM) (24-hour) Gold standard for diagnosing white-coat or masked hypertension. Diagnostic threshold: SBP ≥130 mmHg or DBP ≥80 mmHg over 24 hours. Home blood pressure monitoring (HBPM) Useful alternative if ABPM not available. Confirm sustained BP elevation or diagnose white-coat effect. Additional/optional tests Echocardiogram: If LVH or cardiac dysfunction is suspected. Carotid ultrasound: In older patients or those with significant atherosclerotic risk factors. Further testing for suspected secondary causes (e.g., renal artery duplex, endocrine workup) if resistant or atypical presentation. Blood pressure targets General population: <140/90 mmHg Diabetes or CKD: <130/80 mmHg Elderly (≥75 years): Often <150/90 mmHg, but individualized based on frailty and symptoms. Current guidelines vary; many still aim for <140/90 unless there is a good reason to be more lenient. Management Lifestyle modifications (cornerstone for all patients) Diet Reduce salt intake (<6 g/day). Increase fruit/vegetables; DASH or Mediterranean diet patterns recommended. Weight loss Aim for 5–10% reduction in overweight/obese patients. Exercise Moderate aerobic activity ≥150 minutes/week (e.g., brisk walking). Alcohol Limit intake (≤2 standard drinks/day for men, ≤1 for women). Smoking cessation Essential to reduce overall cardiovascular risk. Pharmacological therapy Initiation criteria Based on absolute cardiovascular (CV) risk and BP level. Generally start medication in: Persistent BP ≥140/90 mmHg with moderate-to-high CV risk. Any patient with BP ≥160/100 mmHg. Those with established CV disease or ≥10% 5-year absolute risk. First-line options ACE inhibitors (ACEi) or ARBs Preferred in younger patients, diabetes, CKD, heart failure. Examples: Perindopril 5–10 mg daily, Telmisartan 40–80 mg daily. Calcium channel blockers (CCBs) Effective in older patients, people of African descent, and those with angina. Example: Amlodipine 5–10 mg daily. Thiazide or thiazide-like diuretics Useful in older adults or isolated systolic hypertension. Examples: Hydrochlorothiazide, Indapamide. Second-line or add-on options Beta-blockers Non-dihydropyridine CCBs (e.g., Diltiazem) Potassium-sparing diuretics (e.g., Spironolactone) Alpha blockers (e.g., Prazosin) Titration and monitoring Combination therapy often required to reach target. Start at low dose; titrate as needed. Repeat UEC ~1–2 weeks after initiating ACEi/ARB to monitor renal function. Hypertensive crises Hypertensive urgency: BP often >180/110 mmHg but no severe end-organ damage. Usually managed with oral medications in outpatient or GP setting. Hypertensive emergency: BP typically >200–220/140 mmHg with acute end-organ damage (e.g., encephalopathy, pulmonary edema, acute kidney injury). Requires IV antihypertensives. Resistant hypertension Defined as BP remaining above target despite an appropriate regimen of at least 3 antihypertensives (ideally including a diuretic) at maximally tolerated doses Common contributing factors: measurement error, non-adherence, lifestyle factors, drug interactions, secondary HTN Secondary causes of hypertension Renal: CKD, glomerulonephritis, polycystic kidney disease, renal artery stenosis Endocrine: Primary hyperaldosteronism, Cushing’s syndrome, pheochromocytoma, thyroid disorders Vascular: Coarctation of the aorta Monitoring & follow-up Initial diagnosis: Reassess within 4 weeks Stable HTN: Routine follow-up every 3–6 months Annual: Fundoscopy, CV risk reassessment Notes: Confirm the diagnosis with proper BP measurements. Lifestyle modification is essential. Tailor pharmacotherapy to comorbidities. Most patients require ≥2 agents for optimal control. Address adherence and secondary causes in resistant cases. Heart Foundation recommendations for consideration of ambulatory blood pressure monitoring (AFP) 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 Pancreatitis Causes GETSMASH'D: Gallstones Ethanol Trauma (blunt abdo usually) Steroids Mumps Autoimmune Scorpion bites Hyperlipidaemia Drugs (ACEi, GLP1/DPP4, sulfa) Initial Ix: LFTs, TGs, calcium, abdo U/S Note: Elevated lipase (>3x normal) is more specific for acute pancreatitis than amylase Management General Principles: Hospital admission required for all cases IV fluids: Goal-directed with Hartmann’s solution (monitor BP, HR, urine output >0.5 mL/kg/hr) Analgesia: IV morphine or fentanyl Antiemetics as needed Feeding: Early oral feeding as tolerated (reduces hospital stay) If NBM >72hrs → enteral feeding via NGT Avoid TPN unless enteral nutrition fails Gallstone Pancreatitis: Early cholecystectomy (during initial admission) recommended Alcohol-Induced: Cease alcohol, refer to alcohol cessation programmes Note: Prophylactic antibiotics are not recommended unless infection is confirmed (e.g., infected necrosis) Complications Early: Hypovolaemia Acute respiratory distress syndrome (ARDS) Renal failure Late: Pancreatic pseudocyst (can resolve spontaneously; symptomatic ones → endoscopic/percutaneous drainage) Pancreatic necrosis → drainage and antibiotics if infected Fistulas, pseudoaneurysm formation Walled-off necrosis typically forms after 4 weeks and may require surgical intervention if symptomatic Chronic Causes: Chronic alcohol use (most common in AUS) Hereditary pancreatitis Recurrent acute pancreatitis Autoimmune disease Management: Pain Management: Cease alcohol Pancreatic enzyme supplements (if pain due to malabsorption) Refractory pain: ERCP ± pancreatic duct stenting, lithotripsy, surgery Malabsorption: Pancreatic enzyme replacement (steatorrhoea, fat-soluble vitamin deficiencies) Vit D supplementation until nutrition normalises Refer to dietitian for tailored nutritional advice Complications: Osteoporosis: Screen and manage Diabetes: Regular monitoring and treatment Note: Annual HbA1c and fasting BGL are recommended in chronic pancreatitis for early diabetes detection Pancreatitis CausesGET SMASH’D Gallstones Ethanol (alcohol) Trauma (blunt abdominal trauma) Steroids Mumps (and other infections, e.g. Coxsackie, EBV) Autoimmune pancreatitis Scorpion bites (rare, e.g. Tityus species) Hyperlipidaemia (TGs usually >11 mmol/L) Drugs (ACE inhibitors, GLP-1/DPP-4 inhibitors, sulfonamides, etc.) Acute Pancreatitis Initial Investigations Lipase (>3× normal) is more specific than amylase for acute pancreatitis. LFTs to detect possible gallstone aetiology (↑ ALP, GGT) Serum TGs if hypertriglyceridaemia is suspected Calcium (hypocalcaemia can be seen in pancreatitis) Abdominal Ultrasound to check for gallstones or biliary dilation Management General Principles Hospital Admission: All cases of moderate to severe acute pancreatitis require admission for supportive care. IV Fluids: Goal-directed fluid resuscitation (e.g. Hartmann’s solution), aiming for urine output >0.5 mL/kg/hr Analgesia: IV morphine or fentanyl (avoid pethidine due to toxic metabolites) Antiemetics if needed Feeding: Encourage early oral feeding as tolerated (reduces hospital stay) If NBM >72 hours, use enteral feeding via nasogastric tube (avoids TPN) Reserve TPN only if enteral routes are not feasible Specific Scenarios Gallstone Pancreatitis: Early cholecystectomy (ideally during the same hospital admission) to prevent recurrence Alcohol-Induced: Cease alcohol; referral to alcohol cessation programs Prophylactic Antibiotics Not recommended unless there is proven or strongly suspected infected necrosis or sepsis Complications Early (within 1–2 weeks) Hypovolaemia / shock from massive fluid shifts ARDS (acute respiratory distress syndrome) Renal failure (acute kidney injury due to hypoperfusion, severe sepsis) Late (after 2–4 weeks) Pancreatic Pseudocyst: Fluid collection; may resolve spontaneously, endoscopic/percutaneous drainage if symptomatic Pancreatic Necrosis: Drain if infected or symptomatic; antibiotics if infection proven Fistulas, pseudoaneurysm formation (risk of haemorrhage) Walled-Off Necrosis: Typically after 4 weeks, may need surgical or endoscopic intervention if symptomatic Chronic Pancreatitis Causes Chronic Alcohol Use (most common in Australia) Hereditary Pancreatitis Recurrent Severe Acute Pancreatitis Autoimmune Disease (IgG4-related disease) Management Pain Management Cease Alcohol (absolute requirement for slowing progression) Pancreatic Enzyme Supplements if malabsorption or if enzyme replacement helps pain Refractory Pain: Consider ERCP with pancreatic duct stenting or lithotripsy if ductal stones; surgery if needed Malabsorption Pancreatic Enzyme Replacement for steatorrhoea, vitamin malabsorption (especially fat-soluble vitamins A, D, E, K) Vitamin D supplementation until nutritional status normalises Dietitian Referral for tailored nutrition advice Complications Osteoporosis: Chronic malabsorption, vitamin D deficiency → screen and manage Diabetes: Exocrine insufficiency can extend to endocrine insufficiency → check HbA1c, fasting BGL annually for early detection Key Points Always consider gallstones and alcohol as leading causes for acute pancreatitis in adults. Lipase is the preferred enzyme test for diagnosis over amylase. Early cholecystectomy advised in gallstone pancreatitis to prevent recurrence. Chronic pancreatitis leads to chronic pain, malabsorption, and risk of insulin-dependent diabetes. Smoking cessation recommended, as smoking exacerbates pancreatic damage. 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 Ankylosing Spondylitis (AS) Characteristics: Inflammatory vs Mechanical Back Pain Inflammatory Back Pain: Onset <40 years, insidious, >3 months duration Improves with exercise, worsens with rest Morning stiffness >45 minutes Alternating buttock pain, night pain (2nd half of night) Mechanical Back Pain: Any age, often acute Worsens with activity, improves with rest Short-lived stiffness Presentation Chronic back pain <45 years, >3 months Morning stiffness relieved by exercise/NSAIDs Extra-axial features: Asymmetric oligoarthritis (lower limbs) Enthesitis: Achilles, plantar fascia, chest wall Dactylitis (sausage digit) Extra-Articular Features Eye: Anterior uveitis (~40%) Lung: Apical pulmonary fibrosis (late-stage, ~15%) Heart: Aortic regurgitation (~10%) Bone: Osteopenia/osteoporosis → vertebral fractures Bowel: IBD (~10%) Pathogenesis Chronic inflammation of sacroiliac joints/spine → erosion → bony fusion (syndesmophytes) HLA-B27 positive in ~85–90%, but only ~5% of carriers develop AS Risk Factors Family history of spondyloarthritis Male sex HLA-B27 positive status Smoking (worsens prognosis) Diagnosis Clinical suspicion: Inflammatory back pain + extra-articular features Imaging: X-ray: Bilateral sacroiliitis (grade ≥2) or unilateral sacroiliitis (grade ≥3) MRI: Early marrow oedema or sacroiliitis Bamboo spine: Advanced spinal fusion Labs: ESR/CRP elevated in 50–70% HLA-B27: Supportive but not diagnostic Investigations X-ray: Pelvis AP view for sacroiliitis MRI: For early disease or inconclusive X-ray Labs: ESR, CRP, HLA-B27 Treatment Non-Pharmacological: Exercise program: Stretching, hydrotherapy, physiotherapy Smoking cessation Patient education and support groups Pharmacological: First-line: NSAIDs (symptom relief and disease modification) Biologics: TNF inhibitors (e.g., etanercept, adalimumab) if NSAIDs fail DMARDs: For peripheral arthritis (e.g., sulfasalazine, methotrexate) Complications Spinal: Ankylosis, severe stiffness, deformity Fractures: Vertebral fractures from osteopenia Neurological: Cauda equina syndrome Cardiovascular: Aortic regurgitation, increased CV risk Notes NSAIDs are both symptom-relieving and disease-modifying Early diagnosis requires high suspicion as symptoms may be subtle Regularly assess spinal mobility to monitor progression When to Refer Diagnostic uncertainty or poor response to NSAIDs Extra-articular complications (e.g., uveitis, cardiac issues) Initiation of biologics for refractory disease Ankylosing Spondylitis (AS) Characteristics of Back Pain Distinguishing inflammatory from mechanical back pain is critical: Inflammatory Back Pain Onset: Age <40, insidious onset >3 months Improves with exercise, worsens with rest Morning stiffness >45 minutes Night pain (often in second half of night) Alternating buttock pain may occur Good symptomatic response to NSAIDs Mechanical Back Pain Any age, often acute onset Worsens with activity, improves with rest Stiffness short-lived, typically <30 minutes in the morning Usually no major improvement with NSAIDs Clinical Presentation Chronic back pain in individuals <45 years of age, lasting >3 months Morning stiffness that significantly improves with exercise or NSAIDs Extra-axial features: Asymmetric oligoarthritis (predominantly lower limbs) Enthesitis: Inflammation where tendons insert into bone (e.g. Achilles tendon, plantar fascia, chest wall) Dactylitis (“sausage digit”) Extra-Articular Features Eye: Acute anterior uveitis (~40%); presents with unilateral eye pain, redness, photophobia Lung: Apical pulmonary fibrosis, typically late stage (~15%) Heart: Aortic regurgitation (~10%); conduction abnormalities Bone: Osteopenia/osteoporosis → risk of vertebral fractures Bowel: Inflammatory bowel disease (~10%) Pathogenesis Chronic inflammation of sacroiliac joints and the spine leads to erosion followed by bony fusion(syndesmophytes). HLA-B27 positivity: ~85–90% of AS patients carry the gene, but only ~5% of HLA-B27 carriers develop AS. Risk factors: Family history, male sex, HLA-B27 positivity, smoking (which worsens prognosis). Diagnosis Clinical Suspicion: Age <45, insidious onset of chronic back pain lasting >3 months. Inflammatory features (morning stiffness, improvement with exercise, etc.). Extra-articular manifestations (e.g. uveitis, enthesitis). Imaging: X-ray of the pelvis (AP view) to assess for sacroiliitis. Bilateral sacroiliitis (grade ≥2) or unilateral sacroiliitis (grade ≥3) is diagnostic. Bamboo spine in advanced disease, where vertebral bodies show marginal syndesmophytes. MRI of the sacroiliac joints: Can detect early inflammatory changes (bone marrow oedema) before X-ray changes appear. Laboratory Tests: ESR/CRP: Elevated in ~50–70% of cases (indicates ongoing inflammation). HLA-B27: Supportive but not definitive; a negative test does not exclude AS. Investigations X-ray: Pelvis (AP view) for sacroiliitis; spine X-ray if indicated. MRI: Sacroiliac joints if suspicion is high but X-ray is inconclusive (early disease). Bloods: ESR, CRP, HLA-B27. Additional tests if required (e.g. ECG or echocardiogram for cardiac involvement). Treatment Non-Pharmacological Measures Exercise & Physiotherapy Stretching and range-of-motion exercises reduce stiffness. Hydrotherapy can be particularly beneficial. Consider supervised physiotherapy programmes. Smoking Cessation Smoking exacerbates the disease and is associated with worse outcomes. Patient Education Understanding the chronic nature of AS, importance of adherence to exercise and medication. Pharmacological Therapies NSAIDs First-line for symptom relief and possible disease-modifying effects. Monitor for gastrointestinal, renal, and cardiovascular side effects. Biologics TNF inhibitors (e.g. etanercept, adalimumab) or IL-17 inhibitors (e.g. secukinumab) if insufficient response to NSAIDs. Require rheumatology input; indications typically include high disease activity or progressive structural damage. DMARDs Generally limited role for axial disease, but can be used for peripheral arthritis. Sulfasalazine, methotrexate for peripheral joint involvement. Complications Spinal Ankylosis: Advanced bony fusion can cause severe stiffness and reduced chest expansion. Fractures: Osteopenia or osteoporosis can lead to vertebral fractures with minimal trauma. Neurological: Risk of cauda equina syndrome due to dural ectasia or spinal lesions. Cardiovascular: Aortic regurgitation, increased cardiovascular risk due to chronic inflammation. Notes NSAIDs: Symptom-relieving and may slow radiographic progression in early disease. Early Diagnosis: Requires a high index of suspicion, especially in younger patients with unexplained back pain. Monitoring: Regular assessment of spinal mobility (e.g. Schober’s test), chest expansion, and posture. Referral: To rheumatology if diagnosis is uncertain, poor response to initial therapy, or consideration of biologic treatment. When to Refer Diagnostic uncertainty or suspicion of other spondyloarthropathies. Poor response to NSAIDs or significant side effects limiting treatment. Extra-articular complications: Uveitis, cardiac involvement (valvular disease), or severe peripheral arthritis needing advanced therapies. Biologics: Require specialist initiation and monitoring. 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 Premenstrual Syndrome (PMS) & Premenstrual Dysphoric Disorder (PMDD) Presentation Psychological Symptoms: Mood swings, irritability, depression, anxiety Inability to cope Physical Symptoms: Bloating, headaches, breast tenderness, fatigue Management Lifestyle Modifications: Regular exercise Cognitive behavioural therapy (CBT) Relaxation techniques Pharmacological Treatments: SSRIs (first-line for PMDD) → Continuous or luteal-phase dosing (14 days pre-menses) COCP (drospirenone + low-dose oestrogen) → Modest efficacy in PMDD Severe Cases (Refractory to Treatment): Bilateral salpingo-oophorectomy → Last-line, induces surgical menopause, requiring HRT Notes Lifestyle changes help but severe cases need medical treatment PMDD often worsens with age/stress but ceases at menopause SSRIs (continuous dosing) offer better symptom control COCP’s effect is modest; placebo response cannot be ruled out Premenstrual Syndrome (PMS) & Premenstrual Dysphoric Disorder (PMDD) Definition Premenstrual syndrome (PMS) comprises a range of psychological and physical symptoms occurring cyclically in the luteal phase of the menstrual cycle Premenstrual dysphoric disorder (PMDD) represents a severe form of PMS with marked mood disturbances that significantly impair daily functioning Presentation Psychological Symptoms Mood swings, irritability, depression and anxiety Emotional lability and inability to cope with daily stressors Increased interpersonal conflicts and decreased social functioning Physical Symptoms Bloating and breast tenderness Headaches and fatigue Other somatic complaints such as joint or muscle pain Management Lifestyle Modifications Regular exercise, particularly aerobic activities, to improve mood and reduce stress Cognitive behavioural therapy (CBT) to address negative thought patterns and coping strategies Use of relaxation techniques such as yoga, meditation or progressive muscle relaxation Dietary modifications including balanced nutrition and reduced caffeine intake Pharmacological Treatments First-line treatment with SSRIs for PMDD using either continuous or luteal-phase dosing (approximately 14 days pre-menses) for optimal symptom control Combined oral contraceptive pills containing drospirenone and low-dose oestrogen, which may offer modest symptom relief Adjunctive use of analgesics and NSAIDs for alleviating physical symptoms Consider calcium supplementation as an additional option in some cases Severe or Refractory Cases Referral to specialist care for further evaluation in cases refractory to first-line treatments Last-line option includes bilateral salpingo-oophorectomy, which induces surgical menopause and necessitates subsequent hormone replacement therapy Short-term use of anxiolytics may be considered during acute episodes of severe distress Notes Lifestyle modifications are essential; however, severe cases of PMDD often require pharmacological intervention PMDD symptoms tend to worsen with age and stress but typically resolve at menopause Continuous dosing of SSRIs generally provides superior symptom control compared with intermittent dosing The efficacy of COCPs in PMDD is modest and may be influenced by placebo effects Patient education, psychological support and regular follow-up are critical components of management 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 Antidepressants: SSRIs, SNRIs, Atypical Antidepressants, MAOIs Drug Names & Dosing 1. SSRIs Sertraline: 50 mg PO OD, ↑ to 100 mg after 7 days (max 200 mg) Escitalopram: 10 mg PO OD (max 20 mg) Fluoxetine: 20 mg PO OD (max 60 mg) Fluvoxamine: 50–100 mg PO OD (max 300 mg in divided doses) Citalopram: 20 mg PO OD (max 40 mg; max 20 mg if >65 years due to QTc risk) Paroxetine: 20 mg PO OD (max 50 mg) 2. SNRIs Duloxetine: 60 mg PO OD (max 120 mg) Venlafaxine XR: 75 mg PO OD (max 375 mg; monitor BP at higher doses) Desvenlafaxine XR: 50 mg PO OD (max 200 mg) Reboxetine: 4 mg PO BD (max 12 mg; second-line) 3. Atypical Antidepressants Mirtazapine: 15–30 mg PO nocte (max 60 mg; lower doses more sedating) Agomelatine: 25 mg PO nocte (max 50 mg; requires LFT monitoring) 4. MAOIs Selegiline: 5 mg PO BD (also for Parkinson’s disease) Phenelzine: 15 mg PO TDS (max 90 mg; irreversible, non-selective) Moclobemide: 150 mg PO BD (max 600 mg; reversible MAOI-A, second-line) Pharmacological Considerations First-Line Options: SSRIs, SNRIs, mirtazapine Second-Line: MAOIs, reboxetine (due to safety/tolerability concerns) MAOIs: Risk of hypertensive crisis with dietary tyramine (e.g., aged cheese, cured meats) Special Populations: Elderly: SSRIs preferred; avoid citalopram (>65 years) due to QTc prolongation risk SNRIs: Venlafaxine may ↑ BP at higher doses → monitor BP Mirtazapine: Useful for insomnia or poor appetite Monitoring & Interactions 1. SSRIs/SNRIs Monitor for serotonin syndrome with other serotonergic drugs (e.g., tramadol, linezolid) Regular BP checks for venlafaxine (high doses) 2. MAOIs Dietary Restrictions: Avoid tyramine-rich foods to prevent hypertensive crisis Washout Periods: Strict when switching to/from other antidepressants to avoid serotonin syndrome or hypertensive crisis 3. Additional Monitoring Monitor for weight changes LFTs: Periodic monitoring for agomelatine BP: Regular checks, especially with venlafaxine or SNRIs at high Notes Antidepressants are typically dosed once daily (OD) unless specified Educate patients on potential interactions and the need for adherence to monitoring schedules Antidepressants: Considerations When Prescribing Key Considerations Before Prescribing Symptom Assessment Evaluate severity, duration, and impact on functioning Comorbidities Tailor choice based on coexisting conditions (e.g., anxiety, chronic pain, insomnia) Drug Interactions Review concurrent medications: SSRIs + warfarin: Increased bleeding risk Serotonergic agents (e.g., tramadol): Serotonin syndrome risk Previous Treatments Assess response and tolerability of past antidepressants Patient Profile Consider: Age, pregnancy status, renal/hepatic function, QT prolongation risk Patient Education Points Starting Treatment Explain dose titration and review plan Onset of Action Improvement typically takes 2–6 weeks Duration of Treatment Minimum 12 months; longer for recurrent depression Side Effects Short-Term (1–2 weeks): Nausea, increased anxiety, possible worsening suicidality (temporary) Long-Term: Weight gain, sexual dysfunction, sedation Alcohol Exacerbates depression and counteracts medication effects → avoid Stopping Antidepressants Warn against abrupt cessation → taper gradually to avoid withdrawal symptoms (e.g., agitation, dizziness, flu-like symptoms) Safety in Pregnancy Avoid paroxetine (congenital malformations); sertraline is preferred Additional Notes Address myths about dependency (antidepressants are not addictive) Incorporate CBT or non-pharmacological therapies in the plan Monitor for worsening symptoms, especially in: First month of treatment Patients <25 years old Antidepressant Classes & Common Dosing 1. SSRIs (Selective Serotonin Reuptake Inhibitors) Drug Typical Starting Dose Usual Maximum Dose Key Notes Sertraline 50 mg PO OD 200 mg/day May increase to 100 mg after 7 days. Commonly first-line for depression/anxiety. Escitalopram 10 mg PO OD 20 mg/day Elderly/sensitive: start at 5 mg. Fluoxetine 20 mg PO OD 60 mg/day Long half-life; useful for non-adherent patients; caution in hepatic impairment. Fluvoxamine 50–100 mg PO OD 300 mg/day (divided) Often used for OCD at higher doses. Citalopram 20 mg PO OD 40 mg/day If >65 years or risk of QTc prolongation: max 20 mg/day. Paroxetine 20 mg PO OD 50 mg/day Higher risk of weight gain, sedation, and withdrawal effects; avoid in pregnancy. General Notes: First-line for major depression, anxiety disorders, OCD. Adverse effects: GI upset, headaches, sexual dysfunction, potential initial increase in anxiety. 2. SNRIs (Serotonin-Noradrenaline Reuptake Inhibitors) Drug Starting Dose Usual Max Dose Key Notes Duloxetine 60 mg PO OD 120 mg/day Also indicated for diabetic neuropathy, fibromyalgia. Monitor BP. Venlafaxine XR 75 mg PO OD 375 mg/day Monitor BP, particularly at doses ≥225 mg/day. Can cause withdrawal symptoms if stopped abruptly. Desvenlafaxine XR 50 mg PO OD 200 mg/day Active metabolite of venlafaxine; similar side effect profile. Reboxetine 4 mg PO BD 12 mg/day Selective noradrenaline reuptake inhibitor; second-line due to tolerability issues (e.g., insomnia, dry mouth). General Notes: Commonly used if SSRIs are ineffective or poorly tolerated. Can elevate BP at higher doses (especially venlafaxine). Common side effects include headache, insomnia, GI upset, sexual dysfunction. 3. Atypical Antidepressants Drug Starting Dose Maximum Dose Key Notes Mirtazapine 15–30 mg PO nocte 60 mg/day Lower doses can be more sedating; useful if insomnia or poor appetite. May cause weight gain, sedation. Agomelatine 25 mg PO nocte 50 mg/day Melatonin receptor agonist & 5-HT2C antagonist. LFT monitoring required (baseline, then 3, 6, 12, 24 weeks). General Notes: Mirtazapine is helpful in patients with insomnia or reduced appetite. Agomelatine is generally well-tolerated but must monitor liver function. 4. MAOIs (Monoamine Oxidase Inhibitors) Drug Starting Dose Maximum Dose Key Notes Selegiline 5 mg PO BD Variable Primarily used in Parkinson’s disease; selective for MAO-B at low doses. Phenelzine 15 mg PO TDS 90 mg/day Irreversible, non-selective MAOI. Dietary tyramine restriction crucial. Risk of hypertensive crisis. Moclobemide 150 mg PO BD 600 mg/day Reversible inhibitor of MAO-A (RIMA). Fewer dietary restrictions vs. irreversible MAOIs, but caution still advised. Typically second-line. General Notes: Generally reserved for treatment-resistant depression due to side effects and dietary restrictions. Washout periods required when switching from/to SSRIs or other serotonergic drugs to prevent serotonin syndrome. Pharmacological Considerations First-line agents are often SSRIs, SNRIs, or mirtazapine. MAOIs (phenelzine, moclobemide) and reboxetine are usually second-line due to safety/tolerability issues. MAOIs carry a risk of hypertensive crisis with tyramine-rich foods. Venlafaxine can raise blood pressure at higher doses; monitor BP. Avoid citalopram in older patients (>65 years) due to QTc prolongation. Mirtazapine helps if insomnia or poor appetite are major symptoms. Monitoring & Interactions SSRIs/SNRIs: Monitor for serotonin syndrome if combined with other serotonergic drugs (e.g., tramadol). Venlafaxine or high-dose SNRIs: Regular BP checks. MAOIs: Dietary restrictions to avoid tyramine. Ensure adequate washout when switching antidepressants. LFTs: Required for agomelatine monitoring. Key Considerations Before Prescribing Assess symptom severity, duration, and functional impact. Check for comorbidities (e.g., anxiety, chronic pain) to guide agent selection. Review potential drug interactions (e.g. SSRIs + warfarin → bleeding risk). Consider previous treatments (efficacy/tolerability). Factor in patient’s age, pregnancy status, possible QT prolongation risk. Patient Education Points Explain the 2–6 week onset of antidepressant effects; adherence is crucial. Advise at least 12 months of treatment for first-episode depression. Common early side effects: nausea, increased anxiety, possible mood dip. Long-term issues: potential weight gain, sexual dysfunction, sedation. Warn not to stop abruptly; taper to avoid withdrawal (especially venlafaxine, paroxetine). Avoid excess alcohol, as it may worsen depression. In pregnancy, avoid paroxetine if possible; sertraline is often preferred. Notes Combine medication with psychological therapies (e.g., CBT) and lifestyle changes for optimal results. Monitor closely in the first month and in patients <25 years for any worsening of mood or suicidal ideation. 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 Rectal Bleeding Differentials Most Common: Diverticulosis Haemorrhoids Other Causes: Anal fissure Colorectal cancer/polyp Infectious colitis (Campylobacter, Shigella, Salmonella, EHEC) Ischaemic colitis Angiodysplasia IBD (ulcerative colitis, Crohn’s disease) Anal cancer/polyp Bleeding peptic ulcer/gastritis Coagulopathy Oesophagitis/oesophageal varices History Questions Medication use (e.g., anticoagulants, antiplatelets, NSAIDs) Bowel habit changes Blood mixed in with stools/colour of the blood Fever Palpitations, hypotension (suggestive of ischaemia or hypovolaemia) Unintentional weight loss/family history of bowel cancer Perianal pruritus, lump (haemorrhoids) Painful defecation, constipation (anal fissures) Abdominal pain, nocturnal diarrhoea, diarrhoea with urgency (IBD) Travel history, recent antibiotics, undercooked foods, vomiting (gastroenteritis) Enquire about previous colonoscopy or FOBT results Investigations FBC, ELFTs CRP Coags, iron studies CT with contrast (suspicion for malignancy or diverticular disease) Nil indication for FOBT if symptomatic Consider flexible sigmoidoscopy for suspected left-sided pathology or full colonoscopy if red flags are present Red Flags Age >50 years Age <50 years and: Abdominal pain Bowel habit change Weight loss Iron deficiency Family history of bowel cancer Persistent symptoms >6 weeks Note: UpToDate + SA Health Recommendation: No need for scope if age <40 years and bright red rectal bleeding, with source identified on physical examination (e.g., haemorrhoids) If >40 years, a scope is required even without red flags Ensure patients with iron deficiency anaemia undergo investigation for GI bleeding, particularly in men and postmenopausal women Rectal Bleeding Differentials Most Common Diverticulosis Haemorrhoids Other Causes Anal Fissure Colorectal Cancer or Polyp Infectious Colitis (Campylobacter, Shigella, Salmonella, EHEC) Ischaemic Colitis Angiodysplasia Inflammatory Bowel Disease (Ulcerative Colitis, Crohn’s Disease) Anal Cancer or Polyp Peptic Ulcer/Gastritis (rarely presents with bright red bleeding, more typically melena) Coagulopathy (e.g. warfarin, DOAC use) Oesophagitis/Oesophageal Varices (more commonly melena or haematemesis) History Questions Medication Use: Anticoagulants (warfarin, DOACs), antiplatelets, NSAIDs Bowel Habit Changes: Diarrhoea, constipation, changes in calibre/frequency Character/Colour of Blood: Bright red vs. mixed with stool vs. melena Fever: Suggestive of infection or IBD flare Cardiovascular: Palpitations, hypotension if significant blood loss Weight Loss, family history of bowel cancer (red flag) Perianal Symptoms: Pruritus, lumps (haemorrhoids), painful defecation (anal fissures) Abdominal Pain: Nocturnal diarrhoea, urgency → IBD, or postprandial pain → ischaemic colitis Travel History, recent antibiotics, undercooked foods → Infectious colitis/gastroenteritis Previous Investigations: Recent colonoscopy or FOBT results Investigations Blood Tests FBC: Anaemia? ELFTs: Electrolytes, renal/liver function CRP: Inflammatory markers (IBD, infection) Coagulation Profile, Iron Studies if suspect chronic blood loss Imaging CT Abdomen/Pelvis with contrast if malignancy or diverticular disease suspected Endoscopic Evaluation Flexible Sigmoidoscopy for suspected left-sided pathology (e.g. haemorrhoids, rectal disease, distal colitis) Colonoscopy if red flags are present or suspicion of proximal lesions No indication for FOBT if actively symptomatic Red Flags Age >50 years, new-onset bleeding Age <50 with additional risk factors: Unexplained abdominal pain Change in bowel habit Weight loss Iron deficiency Family History of bowel cancer Persistent symptoms >6 weeks Management Guidelines Identify Source: Thorough physical exam (digital rectal exam, proctoscopy) and ensure no suspicious lesions. No Need for Scope if: Age <40, bright red rectal bleeding, and clear benign cause on exam (e.g. haemorrhoids, fissure), no other risk factors. Scope Required if: Age >40, or Presence of red flags (weight loss, anaemia, persistent changes), or Uncertain diagnosis. Iron Deficiency Anaemia requires investigation of GI tract bleeding, especially in men or postmenopausal women. Notes Assess severity of bleeding (haemodynamic stability, repeated episodes). Treat underlying cause: e.g. haemorrhoids (topical agents, banding), diverticular disease (diet/fibre, possible surgical consult if recurrent bleeds), IBD management. Refer for colonoscopy if suspicion of polyp, cancer, or persistent unexplained rectal bleeding. 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 Non-Accidental Injury (NAI) Red Flags General Indicators Poor attachment, neglect, prior child protection involvement Delayed medical attention, DNA (Did Not Attend), inconsistent explanations Suspicious Bruising Any bruising in non-mobile infants Bruises away from bony prominences (e.g., face, abdomen, ears, back, buttocks) Clustered, patterned bruises (e.g., belt marks, cords), differing healing stages Red Flag Fractures Highly Suspicious Metaphyseal (“bucket handle”) fractures, posterior rib fractures Scapula, sternum, or vertebral fractures Bilateral fractures, multiple stages of healing Additional Considerations Digital fractures in infants, complex skull fractures Inconsistent injury patterns with mechanism or developmental age History Questions Injury Details Mechanism, timeline, and who was present Consistency Conflicting caregiver accounts, implausible explanations Caregiver Capacity Mental health issues, substance use, family violence Previous History Unexplained injuries, neglect, sibling abuse Management Immediate Actions Treat injuries and assess immediate safety (admit if needed) Reporting Mandatory report to child protection Forensic consultation if uncertainty or confirmation is needed Documentation Use body diagrams for injuries, include direct quotes from caregivers Investigations Skeletal survey for occult fractures Rule out coagulopathies for unexplained bruising Family Support Multidisciplinary involvement (social workers, psychologists) Parenting support referrals as needed Key Notes High suspicion if injuries are inconsistent with history Collaboration with child protection agencies is essential to prioritise safety Non-Accidental Injury Definition Physical harm inflicted deliberately on a child or resulting from neglect Involves injuries inconsistent with accidental mechanisms Requires comprehensive evaluation of medical, social, and family history Red Flags Bruising in non-mobile children or infants under 9 months Bruises on protected areas such as ears, face, abdomen, back, buttocks, arms, and hands Patterned bruising suggestive of object use (e.g. belt marks, rope injuries) Fractures highly suspicious for abuse such as metaphyseal ("bucket handle") fractures, posterior rib fractures, scapular, sternal, vertebral, digital, and complex skull fractures Multiple fractures at different stages of healing Inconsistent or evolving explanations for injury not matching developmental capabilities Delayed presentation for medical care and history of repeated injuries or neglect History Detailed account of injury mechanism, timeline, and circumstances from caregivers Inconsistencies or conflicting reports between different caregivers Assess caregiver capacity, including mental health issues, substance misuse, and domestic violence Previous history of unexplained injuries or sibling abuse Social factors such as missed appointments and inadequate supervision Examination Comprehensive physical examination documenting all bruises, lacerations, and fractures using body diagrams Evaluate for signs of neglect, including poor hygiene, malnutrition, and developmental delay Assess for retinal haemorrhages with ophthalmologic examination in suspected abusive head trauma Check for other signs of abuse such as burns, patterned injuries, and injuries in atypical locations Investigations Skeletal survey to identify occult fractures and determine stages of healing CT or MRI of the head if neurological signs or suspected abusive head trauma are present Ophthalmologic examination to assess for retinal haemorrhages Laboratory tests including coagulation studies to exclude bleeding disorders Multidisciplinary assessment if injury patterns remain unexplained Management Provide immediate care to address acute injuries and ensure the child's safety Meticulously document clinical findings and caregiver statements, using photographs and body diagrams where possible Mandatory reporting to child protection services as per local legislation Consult with forensic specialists or child abuse paediatricians in cases of uncertainty Arrange multidisciplinary follow-up involving social workers, psychologists, and allied health professionals for ongoing support Additional Notes Non-accidental injury is often a diagnosis of exclusion and must be considered in the context of overlapping features with neglect or failure to thrive Legal obligations for reporting vary by jurisdiction; ensure compliance with local guidelines Parental and caregiver education on injury prevention and supervision is vital to safeguarding child welfare Regular team training and clear documentation practices are essential for early recognition and appropriate response to suspected abuse 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 Diabetic Neuropathy Non-Pharmacological Management Foot Care: Wear well-fitting footwear Perform daily self-examination of feet for wounds, blisters, or skin changes Regular podiatry reviews Refer to high-risk foot clinic if necessary Refer to vascular surgeon for advanced complications Optimise Systemic Health: Achieve good glycaemic control Manage cardiovascular risk factors (e.g., smoking cessation, blood pressure, lipids) Pharmacological Management 1st-line Meds for Painful Neuropathy may either be: Amitriptyline: 25 mg at night (titrated up to 150 mg nocte if tolerated) Duloxetine: 60 mg daily (max 120 mg/day) Pregabalin: 75 mg twice daily (titrate up to 300 mg bd) Gabapentin: Start at 300 mg daily (max 1200 mg tid) Adjuncts: Topical capsaicin cream (if oral medications are not tolerated) Note: Titrate medications gradually to minimise SEs. Lower starting doses for elderly patients. Topical nitrate spray (not on eTG but on racgp T2DM handbook) Important Considerations Screen for other causes of neuropathy (e.g., vitamin B12 deficiency, hypothyroidism) Patients with loss of protective sensation (e.g., insensate neuropathy) are at high risk for foot ulcers and Charcot arthropathy Regular foot assessments can prevent complications Differentials for general and unilateral neuropathy Differentials for general neuropathy Diabetic neuropathy Prolonged excessive alcohol use Peripheral arterial disease B12 deficiency Hypothyroidism Chronic kidney disease (peripheral oedema, change in urinary frequency) Multiple myeloma Idiopathic (25%) Restless legs syndrome (strong urge to move legs) Raynauds phenomenon Differentials for unilateral neuropathy L5/S1 nerve root compression (shooting pain from the back) Chronic regional pain syndrome (recent trauma to the limb) Mortons neuroma (worse with tight shoes) Tarsal tunnel syndrome (PT nerve (medial)) Hallmark and Atypical Symptoms Classic symptoms: Numbness, tingling, or burning pain starting in the toes and progressing proximally (stocking-glove distribution) Symmetrical and slow progression Sensory loss that can coexist with pain (e.g., "painful insensate foot") Atypical features: Sudden or asymmetrical onset (e.g., diabetic amyotrophy or mononeuropathies) Involvement of proximal muscles, such as pelvic or thigh girdle weakness (diabetic radiculoplexus neuropathy) History Typical symptoms: Burning, aching pain and paraesthesia Numbness or reduced sensation Difficulty with balance, especially in the dark Assess risk factors: Poor glycaemic control History of smoking, hypertension, or dyslipidaemia (risk factors for peripheral arterial disease) Past foot ulcers or Charcot foot Features of Examination for Peripheral Neuropathy Neurological assessment: Loss of protective sensation (e.g., absent 10 g monofilament response) Reduced vibration perception (e.g., using a 128 Hz tuning fork) Reduced ankle reflexes Loss of pinprick or temperature sensation MSK assessment: Deformities such as claw toes, prominent metatarsal heads, or collapsed arches (Charcot foot features) Other findings: Signs of neuropathic ulceration or infection Reduced peripheral pulses (if concomitant peripheral arterial disease is present) Notes Screening: Routine annual screening is essential, even in asymptomatic patients, as neuropathy increases the risk of foot ulcers and amputations. Prevention and Management: Optimise glycaemic control to slow progression but note that established neuropathy is irreversible. Address risk factors (e.g., smoking cessation, blood pressure, and lipid management). Pain management options include amitriptyline, duloxetine, gabapentin, or pregabalin, titrated to response Diabetic Neuropathy Hallmark and Atypical Symptoms Classic Symptoms: Numbness, tingling, and pain, primarily in the toes and feet. Sensory changes begin at toes, progressing to calves, then hands (nerve length-dependent, with proximal spread). Symptoms present at rest but improve with mobility. Symmetrical and slow progression over time. Atypical Symptoms: Calf pain greater than foot pain, worsens with movement (often linked with Peripheral Vascular Disease - PVD). Acute onset, asymmetry, motor symptoms predominant over sensory, with symptoms in proximal extremities more than distal (non-length dependent). Neuropathic Arthropathy / Charcot Foot Lack of proprioception leading to ligament laxity, instability, and increased risk of minor trauma Progressive degenerative changes in joint architecture Presents as swelling, redness, warmth, with a history of trauma or overuse Relatively painless despite significant deformity and abnormal weight-bearing Can result in fractures, deformity, and ulceration History Longstanding diabetes with poor glycemic control. Presence of other cardiovascular risk factors (e.g., smoking, hyperlipidemia, hypertension). Duration and severity of diabetes directly correlate with neuropathy risk. Clinical Features of Peripheral Neuropathy Peripheral Neuropathy Symptom Score: 1 point for each symptom occurring a few times a week for the past 2 weeks. Symptoms: Unsteadiness, burning/aching/tenderness, prickling, numbness. Scoring system for neuropathy symptoms (assign 1 point for symptoms that occur a few times per week over the past 2 weeks): 1 - Unsteadiness 2 - Burning, aching, tenderness 3 - Prickling 4 – Numbness Score ≥ 1 indicates polyneuropathy Peripheral Neuropathy Examination: Reduced ankle tendon reflexes Loss of 10g monofilament pressure sensation. Loss of vibration perception. Loss of pinprick pain sensation. Charcot Neuropathy Acute: swollen, warm, red foot with minimal pain despite significant structural damage Chronic: deformity such as “rocker bottom” foot due to bone collapse and progressive joint destruction Diagnosis Imaging for Charcot Neuropathy X-rays may show osteolysis, fractures, and deformity, especially in later stages MRI or nuclear imaging can confirm stress fractures and soft tissue involvement, as plain radiographs may miss early changes Management Non-Pharmacological: Well-fitting footwear. Daily self-examination of feet. Control of diabetes and cardiovascular risk factors. Regular podiatry reviews. Referral to high-risk foot clinics if necessary. Surgical referral for vascular assessment if warranted. Pharmacological: Amitriptyline 25 mg at night, up to 150 mg as needed. Duloxetine 60 mg daily, may increase to 60 mg twice daily. Pregabalin 75 mg twice daily, up to 300 mg daily if needed. Topical nitrate spray for localized pain (not in ETG, but referenced in RACGP guidelines). Note: Treatment options align closely with management strategies for fibromyalgia. Charcot Foot - A Medical Emergency Requires a multidisciplinary high-risk foot team Management options: Offloading with a total contact cast or Charcot restraint orthotic walker to prevent further weight-bearing injury Antibiotics if cellulitis is present Optimal diabetic control to prevent progression Differential Diagnosis for Neuropathy General Neuropathy: Diabetic neuropathy. Prolonged alcohol use. Peripheral arterial disease (PAD). B12 deficiency. Hypothyroidism. Chronic kidney disease (with peripheral oedema). Multiple myeloma. Idiopathic (25% cases). Restless legs syndrome. Raynaud's phenomenon. Unilateral Neuropathy: L5/S1 nerve root compression (back pain with radiation). Chronic regional pain syndrome (often post-trauma). Morton's neuroma (aggravated by tight shoes). Tarsal tunnel syndrome (compression of posterior tibial nerve). Notes Diabetic neuropathy is progressive and managing blood glucose levels can slow its progression. Regular monitoring and lifestyle modifications are crucial. Early recognition and management can prevent complications, especially in foot care to avoid ulcers and infections. Pathophysiology of Charcot Foot: Charcot neuropathy is attributed to repeated minor trauma and loss of protective sensation, which leads to joint destruction and bone resorption. The affected foot is often warm, red, and swollen, but relatively painless. Patient Education: Emphasize the importance of regular foot checks and immediate reporting of new symptoms (e.g., redness, warmth, or swelling in feet). Discuss the role of glycaemic control in preventing neuropathy progression Bookmark Failed! Bookmark Saved! Add Bookmark Refresh Refresh