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 Tremor History (RACGP) Onset, duration, progression (acute vs chronic) Location (unilateral, bilateral, head) Pattern (resting, postural, intention) Triggers (caffeine, stress, alcohol – ET improves with alcohol) Family history (AD inheritance in ET) Medications (including OTCs) Functional impact Types of Tremor Resting Tremor (Parkinson’s) Worst at rest, improves with movement Pill-rolling tremor, more obvious with distraction Associated with rigidity, bradykinesia Action/Postural Tremors Essential Tremor (ET) >40 years, autosomal dominant inheritance Bilateral postural tremor, persists during movement May involve head (titubation), affects speech/writing, normal gait Improves with alcohol, worsens with caffeine Other Causes of Action/Postural Tremor Hyperthyroidism Anxiety Phaeochromocytoma Drug withdrawal (e.g. benzodiazepines) Intention Tremor Cerebellar dysfunction (stroke, alcohol, MS, mass lesion) Worsens at movement’s end (fails finger-to-nose test) Look for cerebellar signs: Gait ataxia Slurred speech Nystagmus Dysmetria, dysdiadochokinesia Tremor: Key Points History (RACGP Approach) Onset, Duration, Progression: Acute vs. chronic development Location: Unilateral, bilateral, head involvement Pattern: Resting (at rest), postural (holding posture), intention (worsens with movement towards a target) Triggers: Caffeine, stress, alcohol (notably improves essential tremor) Family History: Autosomal dominant inheritance in essential tremor (ET) Medications: Including over-the-counter, possible drug-induced tremors Functional Impact: Effect on daily activities (writing, eating, social) Types of Tremor 1. Resting Tremor (e.g., Parkinson’s Disease) Worst at rest, improves with voluntary movement. Often described as a “pill-rolling” tremor of the hands. More obvious with distraction (e.g. counting backward). Associated Parkinsonian features: Rigidity, bradykinesia, postural instability. 2. Action / Postural Tremors Essential Tremor (ET) Onset typically >40 years. Often autosomal dominant pattern. Bilateral postural tremor, can persist during movement (slight amplitude increase). May involve the head (titubation) and affect speech/writing. Improves with alcohol, worsens with stimulants (caffeine). Normal gait (distinguishes it from cerebellar causes). Other Causes of Action/Postural Tremor Hyperthyroidism Anxiety (adrenergic surge) Phaeochromocytoma Drug withdrawal: e.g., benzodiazepines, alcohol (in chronic use) 3. Intention Tremor Associated with cerebellar dysfunction (stroke, MS, mass lesion, chronic alcohol effects). Worsens as the limb approaches the target (finger-nose test). Cerebellar Signs: Gait ataxia Slurred speech (dysarthria) Nystagmus Dysmetria, dysdiadochokinesia 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 Cushing Syndrome Causes Primary Causes: Pituitary Adenoma (Cushing Disease) - Most common endogenous cause Adrenal Adenoma/Carcinoma - Autonomous cortisol secretion Ectopic ACTH Production - Commonly from small cell lung cancer or other neuroendocrine tumours Secondary Causes: Iatrogenic Cushing Syndrome - Most common cause overall, due to chronic corticosteroid use History and Examination Features Psych: Mood changes, depression, psychosis Neuro: Headaches, fatigue Derma/Haema: Thin skin, easy bruising, purple striae Skin atrophy (subcutaneous fat loss), poor wound healing Immunosuppression (e.g., recurrent infections) Ophtha: Blurred vision, glaucoma (via increased intraocular pressure) Endo: Hypertension, peripheral oedema Hypokalaemia (mineralocorticoid effects), hyperglycaemia GI: Central obesity, "moon face," "buffalo hump" Gastritis or peptic ulcers MSK: Proximal myopathy, osteoporosis, fractures Pertinent Long-term Steroid Side Effects Osteoporosis, fractures Hyperglycaemia, insulin resistance Hypertension Immunosuppression Cataracts Muscle weakness Notes: Testing for Cushing Syndrome: Initial: 1 mg overnight dexamethasone suppression test, 24-hour urinary cortisol, or late-night salivary cortisol Beware of false positives (e.g., estrogen-containing drugs, rifampicin) Treatment: Surgical resection of the pituitary or adrenal tumour Pharmacological cortisol blockade preoperatively or if surgery fails Technically, corticosteroid = glucocorticoid + mineralocorticoid but is often used as synonym for glucocorticoid Cortisol is most important type of glucocorticoid Investigations: If low suspicion of Cushing’s, select any 1 test; if high suspicion, use 2 tests Late-night salivary cortisol 24h urinary free cortisol excretion (requires ≥2x normal levels for diagnosis) Overnight 1 mg dexamethasone suppression test (first choice if performing a single test) Overnight 1 mg Dexamethasone Suppression Test: Measures morning cortisol following dexamethasone administration the night before Spare blood tube for ACTH levels if elevated cortisol is detected Normal or low cortisol: Excludes Cushing’s High cortisol: Inappropriate suppression → Indicates Cushing’s syndrome 8 mg Dexamethasone Suppression Test (to find cause): Differentiates pituitary, adrenal, or ectopic sources: Pituitary (Cushing’s disease): Low ACTH and cortisol suppressed with 8 mg (but not 1 mg) Adrenal: Low ACTH but high cortisol (autonomous adrenal cortisol secretion) Ectopic ACTH production: High ACTH and high cortisol (failure to suppress) Additional Notes: If ACTH-independent Cushing’s syndrome is suspected (e.g., adrenal adenoma), perform an adrenal CT or MRI Use a high-dose dexamethasone suppression test to distinguish between pituitary and ectopic ACTH sources Key Considerations: Pseudo-Cushing’s syndrome (e.g., obesity, alcoholism, depression) may mimic biochemical findings; repeat tests in equivocal cases Consider measuring midnight plasma cortisol if salivary cortisol is unavailable Cushing's syndrome Aetiology: Primary Causes: Pituitary Adenoma (Cushing's Disease): ACTH-secreting pituitary adenoma, the most common endogenous cause, is approximately five times more frequent than adrenal causes. Adrenal Adenoma: Produces cortisol independently. Ectopic ACTH Production: Tumours, such as small cell lung cancer, secrete ACTH, leading to cortisol overproduction. Bilateral Adrenal Hyperplasia (BAH): Rare, can also contribute to cortisol overproduction. Secondary Cause: Iatrogenic Cushing's Syndrome: Due to long-term oral corticosteroid use, which is the most common cause overall. Symptoms: General Appearance: Moon Face, Buffalo Hump, Central Obesity: Classic appearance includes a rounded face (moon face), fat pad between shoulders (buffalo hump), and truncal obesity with thin extremities (resembling "lemon with matchsticks" sign). Skin Changes: Purple abdominal striae, hirsutism (androgen excess in females), acne, spontaneous bruising, and delayed wound healing due to skin thinning. Musculoskeletal: Proximal myopathy, osteoporosis, and pathological fractures. Psychiatric: Mood disturbances, depression, and insomnia. Metabolic and Endocrine: Hypertension, hyperglycaemia (diabetes mellitus), polyuria, and polydipsia. Long-term Side Effects of Steroid Use: Osteoporosis, hyperglycaemia, hypertension, immunosuppression, cataracts, and muscle weakness. Differential Diagnosis: Metabolic syndrome (due to overlapping obesity and hypertension). Polycystic ovary syndrome (PCOS) with similar features of obesity and androgen excess in females. Investigations: Screening Tests: Late-night Salivary Cortisol: Detects abnormal diurnal cortisol rhythm. 24-hour Urinary Free Cortisol (UFC): Assesses overall cortisol production. Overnight 1 mg Dexamethasone Suppression Test (DST): Preferred for initial screening; lack of suppression indicates Cushing’s syndrome. Dexamethasone Suppression Test (DST) Interpretation: Low-dose DST: Measures cortisol level the morning after 1 mg dexamethasone at night. Non-suppressed cortisol levels suggest Cushing’s. High-dose DST: Differentiates causes: Pituitary (Cushing's Disease): Suppressed cortisol and low ACTH. Adrenal: Low ACTH, high cortisol (non-suppressible). Ectopic ACTH Production: Both ACTH and cortisol remain elevated and non-suppressible. Imaging Studies: Pituitary MRI: For suspected pituitary adenoma. Abdominal CT/MRI: For adrenal adenomas or carcinomas. Chest CT: If ectopic ACTH production is suspected. Management: Pituitary Tumour: Transsphenoidal surgery for pituitary adenoma, followed by radiotherapy if needed. Adrenal Tumour: Surgical resection for adrenal adenomas. Ectopic ACTH-producing Tumour: Tumour resection if possible; otherwise, medical therapy to control cortisol. Iatrogenic Cushing's (from Steroid Use): Gradual tapering of corticosteroid dosage under medical supervision to prevent adrenal crisis. Complications: Cardiovascular issues i.e., hypertension and increased risk of myocardial infarction. Metabolic issues such as diabetes and hypokalaemia. Osteoporosis with increased fracture risk due to prolonged cortisol exposure. Prognosis: Prognosis depends on cause and treatment success. Surgical intervention for pituitary or adrenal causes can lead to remission. Chronic corticosteroid use requires careful management and monitoring to mitigate complications. Notes: Terminology Note: Corticosteroid refers to glucocorticoid plus mineralocorticoid, but it is often used synonymously with glucocorticoid. Feedback Mechanism: Cortisol exerts a negative feedback loop on the hypothalamic-pituitary axis, reducing ACTH secretion under normal conditions. Depression Link: Cortisol levels in Cushing’s resemble stress-induced profiles, often resulting in psychiatric symptoms like depression and mood disturbances 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 Angular Cheilitis Definition Inflammatory condition affecting the corners of the mouth Can be acute or chronic, depending on the underlying cause Affects children and adults, particularly those with poor general health or immunosuppression Risk Factors Moisture retention at mouth corners (saliva pooling) Oral thrush (Candida albicans) Poorly fitting dentures Systemic conditions (e.g., Crohn’s disease, Sjögren’s syndrome) Aetiology & Causes Excess saliva and local irritation → maceration and secondary infection Common pathogens: Fungal: Candida albicans (most common) Bacterial: Staphylococcus aureus Viral: Herpes simplex virus (HSV) (less common) Nutritional deficiencies: Iron, zinc, B vitamins (B2, B6, B12) Clinical Features Painful cracks and fissures at the mouth corners Redness, blistering, bleeding, crusting Burning or stinging sensation, worsened by mouth movement Complications Chronic cases → scarring, persistent infection, spread to adjacent skin Diagnosis Clinical diagnosis based on appearance Swabs (if needed) to identify Candida, S. aureus, or HSV Management General Measures Keep lips hydrated (lip balm, emollients) Avoid lip-licking Improve oral hygiene Ensure dentures fit properly Targeted Treatment Fungal (Candida suspected): Topical antifungals (miconazole, clotrimazole) Bacterial (S. aureus suspected): Topical antibiotics (mupirocin, fusidic acid) Inflammatory (without infection): Mild topical steroids (e.g., hydrocortisone 1%) Nutritional deficiencies: Iron, zinc, B vitamin supplementation Prevention Prevent saliva pooling (use barrier creams, lip balm) Correct underlying causes (e.g., treat oral thrush, improve denture fit) Maintain good oral hygiene Angular Cheilitis Definition Angular Cheilitis (also called angular stomatitis or perlèche) is an inflammatory condition primarily affecting the corners (angles) of the mouth. May present as acute or chronic, often recurrent if underlying factors persist. Common in both children and adults, especially those with poor general health or immunocompromise. Risk Factors Saliva pooling at the mouth corners (excess drooling, mouth breathing, poorly fitting dentures). Candida overgrowth (oral thrush). Poor denture fit (especially in older adults). Systemic diseases: Crohn’s disease, coeliac disease, Sjögren’s syndrome, diabetes mellitus (due to dryness or immunosuppression). Nutritional deficiencies (iron, zinc, B vitamins). Immunosuppression (e.g. HIV, chronic steroid use). Aetiology & Pathophysiology Excess saliva and local irritation lead to maceration of the skin at the angles of the mouth. Secondary infection can develop, most commonly: Fungal: Candida albicans (most frequent overall) Bacterial: Staphylococcus aureus Viral: Herpes simplex virus (less common) Nutritional factors (e.g., low iron, zinc, vitamins B2, B6, B12) can predispose or exacerbate. Clinical Features Skin Lesions Painful cracks (fissures) and sores at the corners of the mouth. Redness, erythema, possible blistering or bleeding. Crusting or scaling may develop in chronic cases. Symptoms Burning, stinging, or pain aggravated by mouth movements (talking, chewing). May have associated dryness or chapping of the lips. Complications Chronic angular cheilitis can lead to scarring, persistent infection, or extension to adjacent skin. Diagnosis Usually a clinical diagnosis based on characteristic lesions at the mouth corners. Swab for microbiological culture (fungal, bacterial) if the lesion is resistant to standard therapies or if the diagnosis is uncertain. Consider patch testing for allergic contact dermatitis in atypical presentations. Evaluate for nutritional deficiencies (iron, folate, B12) and dental/oral factors (denture fit, oral candidiasis). Management General Measures Lip care: Use emollients or lip balms to keep lips hydrated and prevent further cracking. Avoid lip-licking: Saliva evaporation worsens dryness and maceration. Oral hygiene: Regular dental checks; ensure dentures are well-fitting. Saliva pooling reduction: Barrier creams (e.g. petroleum jelly) at the mouth corners. Targeted Treatment Antifungal Treatment (suspected or confirmed Candida): Topical miconazole gel or clotrimazole cream applied to the angles of the mouth 2–3 times daily. Continue for at least 2 weeks or until complete resolution. If intra-oral candidiasis is present, treat accordingly (e.g. nystatin oral suspension, miconazole oral gel). Antibacterial Treatment (suspected or confirmed Staphylococcus aureus): Topical antibiotics such as mupirocin or fusidic acid 2–3 times daily. Consider oral antibiotics if severe or refractory infection. Mild Topical Steroids Low potency (e.g. hydrocortisone 1%) if inflammation is prominent and infection is ruled out or concurrently addressed. Short-term use to reduce inflammation; avoid prolonged steroid monotherapy if infection is a concern. Nutritional Supplementation Iron, zinc, or B vitamins if deficiency is suspected or confirmed. Encourage a balanced diet or refer to a dietitian if indicated. Prevention Maintain good oral hygiene and denture care (clean dentures daily; adjust for proper fit). Use of barrier agents (lip balm, petroleum jelly) if there is a tendency for saliva pooling. Correct underlying causes: Manage oral thrush promptly. Identify and treat nutritional deficiencies. Monitor for dermatological or systemic conditions (e.g. Crohn’s, Sjögren’s). Key Points Multifactorial Aetiology: Usually a combination of moisture, friction, and infectious agents (often Candida). Common in Older Adults: Denture-related issues and xerostomia (dry mouth) are often implicated. Simple Measures: Lip hydration, barrier creams, improved oral hygiene frequently help mild cases. Topical Therapy: Select based on most likely pathogen—antifungal (for Candida), antibiotic (for Staph.), mild steroid if primarily inflammatory. Investigate Persistence: Chronic or recurrent angular cheilitis warrants further evaluation (nutritional, immunological, mechanical factors). 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 HSV (Herpes Simplex Virus) Oral HSV vs Herpetic Whitlow Oral HSV (Herpetic Gingivostomatitis) Cause: HSV1 (oral mucocutaneous herpes) Primarily affects the oral mucosa, including the gums, lips, and inside of the mouth Herpetic Whitlow (Finger Infection) Cause: HSV1 or HSV2 (usually from contact with infected oral lesions) Affects the fingertip (digital infection) Risk Factors: children who suck fingers, immunocompromised patients, health worker exposure is described in practice literature Diagnosis Primary infection: usually a clinical diagnosis. If confirmation is required, take a PCR swab or use rapid immunofluorescence. Recurrent flares: Typically diagnosed clinically, as lesions recur in the same spot Note Rapid immunofluorescence testing is an alternative confirmatory test in unclear cases Tzanck smear is outdated Treatment 1ry Infection (Primary HSV) If minor: Symptomatic relief with topical anaesthetic gel q2h PRN (e.g., anaesthetic mouthwash in hospital) Analgesia, ensure adequate hydration If severe: Oral antiviral, for ex: valaciclovir 1 g BD for 7 days, or famciclovir 500 mg BD for 7 days, or aciclovir 200 mg 5x daily for 7 days 2ry Infection (Recurrent HSV) If minor: Topical antiviral, aciclovir 5% cream q4h while awake for 5 days on lesions on skin around the mouth, OR oral famciclovir 1.5 g stat If severe: Oral famciclovir 1.5 g stat, OR valaciclovir 2 g q12h for 1 day, OR aciclovir 200 mg 5x daily for 5 days Suppressive therapy: For frequent disabling recurrences or complications (e.g., erythema multiforme), use valaciclovir 500 mg daily for 6 months, then review. Early treatment initiation during the prodromal stage, tingling or burning, can reduce symptom duration and severity Herpetic whitlow caused by HSV1 or HSV2: treat with an oral antiviral as for a severe initial oral episode, for ex: valaciclovir 1 g BD for 7 days, start early Non-Pharm Management Advise patients to avoid direct contact with the lesion to reduce transmission. Children who do not have control of oral secretions should be excluded from childcare and school. Barrier cream can prevent lip adhesions Educate on the recurring nature of the condition Highlight triggers that provoke flare ups, trauma, sun or wind exposure, viral infections, stress Tingling or burning is an early sign of a flare Advise avoidance of sharing utensils, lip products, or towels during active outbreaks Emphasise hand hygiene to minimise autoinoculation or spread HSV (Herpes Simplex Virus) Common viral infection caused by HSV-1 (oral-labial lesions, herpetic whitlow) or HSV-2 (often genital, but can infect other sites) Primary infection typically more symptomatic than recurrences Transmitted via direct contact with lesion fluid or mucosal secretions Oral HSV (Herpetic Gingivostomatitis) Often due to HSV-1 Affects oral mucosa, gums, lips, inside of the mouth Presentation: painful vesicles or ulcers, gingivitis, possible fever, malaise Risk of dehydration in children if oral intake is reduced due to pain Herpetic Whitlow (Finger Infection) Caused by HSV-1 or HSV-2 through direct contact with infected oral or genital lesions Infection of the fingertip or nail bed Risk factors: healthcare workers (dentists), children with thumb-sucking habit, immunocompromised patients Presents with painful vesicles or ulcers on the finger, local swelling and erythema Diagnosis Primary Infection PCR swab from lesion is the gold standard for confirmation Direct fluorescent antibody (DFA) testing can be used if PCR unavailable Tzanck smear is outdated (reveals multinucleated giant cells but lacks specificity) Recurrent Lesions Usually diagnosed clinically, lesions recur in the same site Serological tests (HSV IgG/IgM) may help distinguish HSV-1 vs HSV-2, though not routinely required Management Primary HSV Infection If mild: supportive care with topical anaesthetic gel or mouthwash, regular analgesia, adequate hydration If severe or extensive lesions: oral antivirals (e.g. valaciclovir 1 g BD for 7 days) Consider IV antivirals in severe immunocompromise or disseminated infection Recurrent HSV Infection If mild or limited: topical aciclovir 5% cream q4h for 5 days or one-off oral therapy (famciclovir 1.5 g stat) If severe or frequent: oral famciclovir 1.5 g stat can shorten the episode Suppressive therapy with valaciclovir 500 mg daily for ≥6 months if recurrent episodes are frequent or complicated (e.g. erythema multiforme) Early initiation during the prodromal phase (tingling or burning) significantly reduces lesion severity and duration Herpetic Whitlow Oral antiviral (valaciclovir or famciclovir) if pain or extensive involvement Keep lesion covered, practise meticulous hand hygiene In immunocompromised individuals, consider longer antiviral courses Non-Pharmacological Measures Avoid direct contact with active lesions (no sharing utensils, lip balms) Identify triggers for recurrent flares (trauma, UV exposure, stress, immunosuppression) Emphasise hand washing to prevent autoinoculation (e.g. from lip to finger or eye) Advise patients to watch for ocular involvement (urgent ophthalmology referral if suspected) Complications Local Secondary bacterial infection of lesions Severe pain or dehydration if lesions in oropharynx Neurological Encephalitis (HSV is the most common sporadic encephalitis cause) Aseptic meningitis Bell’s palsy (rare) Haematological or Mucocutaneous Erythema multiforme triggered by HSV Other Disseminated infection in immunocompromised hosts Notes: Early recognition of primary infection can prompt timely antiviral therapy and reduce complications Recurrent cold sores are very common, and patient education on prodromal symptoms plus early antiviral use is crucial Herpetic whitlow in healthcare workers emphasises need for gloves and protection Children with gingivostomatitis may require careful hydration management Investigate severe or atypical presentations for immunodeficiency or other underlying pathologies 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 Red Eye: Optic Neuritis, Uveitis, Herpes Ophthalmicus Optic Neuritis Pathology: Optic nerve inflammation, often linked to MS or autoimmune/infectious causes (e.g., sarcoidosis, neuromyelitis optica) Features: Monocular vision loss (central scotoma, colour desaturation, esp. red) Pain (90%), worsens with extraocular movements Afferent pupillary defect Management: Urgent neurologist/ophthalmologist referral High-dose IV corticosteroids (e.g., methylprednisolone) MRI to evaluate for MS Uveitis Pathology: Inflammation of the uveal tract (iris, ciliary body, choroid) linked to autoimmune (IBD, ankylosing spondylitis) or infectious (TB, syphilis, HSV) causes Features: Anterior: Painful red eye, perilimbal injection, photophobia, blurred vision Posterior: Painless, floaters, vision loss Severe cases: Hypopyon Management: Urgent ophthalmology referral Anterior: Topical steroids (e.g., prednisolone acetate), cycloplegics (e.g., atropine) Posterior/recurrent: Systemic steroids or immunosuppressants Herpes Ophthalmicus Pathology: VZV reactivation in CN V1; can cause corneal ulceration, scarring, vision loss Features: Painful red eye, vesicular rash in V1 distribution (forehead, scalp, nose) Hutchinson’s sign (nose vesicles → high ocular involvement risk) Photophobia, decreased vision, corneal dendrites Management: Oral antivirals (within 72 hrs): Valaciclovir 1g TDS or aciclovir 800mg 5x/day (7–10 days) Lubricants for comfort Urgent ophthalmology referral for ocular involvement Avoid topical antivirals; steroids only after ophthalmology review Notes Posterior uveitis: Systemic workup for infectious/autoimmune causes (imaging, fundus photography) Herpes ophthalmicus: Steroids only post-antivirals (to prevent replication). Red Eye - Conjunctivitis (Viral/Allergic/Bacterial/Neonatal) Management General Measures Hygiene: Avoid eye rubbing, sharing towels, contact lenses Saline bathing for soothing (esp. bacterial) Swab for PCR/culture: Herpes simplex, chlamydia, gonorrhoea suspicion Bacterial conjunctivitis if treatment fails Urgent referral: Severe pain, photophobia, reduced vision Viral Conjunctivitis Features: Gritty burning, watery discharge, preauricular lymphadenopathy (adenovirus, highly contagious) Management: Cool compresses, lubricating eye drops Sunglasses for photophobia Allergic Conjunctivitis Features: Itchy, burning eyes, sneezing, watery rhinorrhoea; linked to asthma, eczema Management: Avoid allergens, eye rubbing, contact lenses Cool compresses, lubricating drops Topical antihistamine drops (e.g., azelastine) Oral antihistamines, nasal steroids for systemic symptoms Bacterial Conjunctivitis Features: Purulent discharge, redness, often bilateral; severe cases → consider chlamydia/gonorrhoea Management: Chloramphenicol 0.5% drops, 1 drop QID x 7 days (or framycetin drops) Swab/culture if persistent Gonococcal: Ceftriaxone 1g IM Neonatal Conjunctivitis Features: Chlamydia: Purulent discharge, onset 1–2 weeks post-delivery Gonococcal: Severe discharge, early onset (ophthalmic emergency) Management: Chlamydia: Azithromycin 20 mg/kg orally x 3 days Gonococcal: Ceftriaxone 1g IM Treat household contacts Regular face washing for hygiene NB Preauricular lymphadenopathy → viral, absent in bacterial Neonatal gonococcal conjunctivitis → risk of perforation/corneal scarring (urgent care needed) Red Eye: Summaries of Key Conditions Below is an overview of optic neuritis, uveitis, herpes ophthalmicus, and various types of conjunctivitis, including their clinical features, investigations, and management strategies. 1. Optic Neuritis Pathology Inflammation of the optic nerve often associated with multiple sclerosis or autoimmune/infectious aetiologies (sarcoidosis, neuromyelitis optica). Features Monocular vision loss: Central scotoma, colour desaturation (especially red). Pain: Worsening with extraocular movements (90% cases). Afferent pupillary defect (Marcus Gunn pupil). Management Urgent referral to neurologist/ophthalmologist. High-dose IV corticosteroids (e.g. methylprednisolone). MRI to evaluate for MS or demyelinating lesions. 2. Uveitis Pathology Inflammation of the uveal tract (iris, ciliary body, choroid). Linked to autoimmune (IBD, ankylosing spondylitis) or infectious (TB, syphilis, HSV) causes. Features Anterior Uveitis (Iritis): Painful red eye, ciliary/perilimbal injection, photophobia, blurred vision. Severe cases: Hypopyon (layer of WBCs in anterior chamber). Posterior Uveitis: Often painless, presents with floaters, visual field defects, blurred vision. Management Urgent ophthalmology referral. Anterior: Topical steroids (e.g. prednisolone acetate), cycloplegics (e.g. atropine). Posterior/recurrent: Systemic steroids or immunosuppressants. 3. Herpes Ophthalmicus Pathology Varicella Zoster Virus reactivation in the ophthalmic branch (V1) of CN V. Can cause corneal ulceration, scarring, vision loss if untreated. Features Painful red eye, vesicular rash in V1 distribution (forehead, scalp, nose). Hutchinson’s sign: Vesicle on tip/side of nose → high risk of ocular involvement. Photophobia, decreased vision, possible corneal dendritic ulcers. Management Oral antivirals (within 72 hrs): Valaciclovir 1 g TDS or aciclovir 800 mg 5×/day for 7–10 days. Lubricants for comfort. Urgent ophthalmology referral if ocular involvement. Avoid topical antivirals unless directed; topical steroids only after ophthalmology review. Conjunctivitis (Red Eye) General Management Emphasise hygiene: Avoid eye rubbing, sharing towels, contact lenses. Saline bathing can soothe symptoms. Swab for suspected herpes simplex, chlamydia, gonorrhoea, or if treatment failure. Urgent referral if severe pain, photophobia, or reduced vision. Viral Conjunctivitis Features: Gritty/burning sensation, watery discharge, preauricular lymphadenopathy (common with adenovirus). Management: Cool compresses, lubricating drops, symptomatic relief; highly contagious. Allergic Conjunctivitis Features: Itchy, burning eyes, sneezing, watery rhinorrhoea (often associated with asthma/eczema). Management: Avoid allergens, compresses. Topical antihistamine drops (e.g. azelastine). Oral antihistamines, nasal steroids for systemic symptoms. Bacterial Conjunctivitis Features: Purulent discharge, redness, often bilateral. Management: Chloramphenicol 0.5% drops 1 drop QID × 7 days (or framycetin). Swab if persistent or atypical. Gonococcal: Ceftriaxone 1 g IM. Neonatal Conjunctivitis Causes: Chlamydia: Onset ~1–2 weeks post-delivery, purulent discharge. Gonococcal: Severe discharge, early onset (ophthalmic emergency). Management: Chlamydia: Azithromycin 20 mg/kg PO × 3 days. Gonococcal: Ceftriaxone 1 g IM. Treat household contacts; ensure regular hygiene. Notes and Takeaways Posterior Uveitis: Systemic workup for infectious/autoimmune causes. Herpes Ophthalmicus: Steroids only after starting antivirals. Preauricular Lymphadenopathy: Suggestive of viral conjunctivitis. Neonatal gonococcal conjunctivitis → risk of corneal perforation, urgent referral. Bookmark Failed! Bookmark Saved! Refresh Refresh Refresh

Log In Get started Bookmarks Help Progress 0% Cardiovascular AAA + Rupture AC dislocation ATSI Abdominal pain in kids Abnormal/Dysfunctional Uterine Bleeding (AUB/DUB) Acanthosis Nigricans Acne Acromegaly Actinic Cheilitis Acute Kidney Injury (AKI) Acute Swollen Joint with Fever Acute Vision Loss Acute and Progressive Vision Loss Addisons Adjustment Disorder and Anxiety Adjustment Disorder with Depressed Mood Age related macular degeneration Alcohol Cessation Allergic rhinitis Alopecia Amenorrhoea Anaphylaxis Angina Angular Cheilitis Ankylosing Spondylitis (AS) Anorexia Nervosa Anticholinergics and TCAs Antidepressants Antimetabolite drugs Antiphospholipid syndrome Antipsychotics Anxiety Disorders Aortic Dissection Arrhythmia Asthma Asthma Atrial Fibrillation Back pain Behavioural / learning disorders Behavioural disturbances Bell’s palsy and Ramsey Hunt syndrome Beta-Human Chorionic Gonadotropin (β-hCG) Biologic agents Bipolar Disorder Bleeding disorders Blepharitis Breast Cancer Breast Lump Bronchiectasis (Updated) CA-125 (Cancer Antigen 125) CRPS CVD Risk Assessment Calluses and Corns Candida (Candidiasis as an STI) Carpal tunnel syndrome and de quervains tenosynovitis Cellulite Cervical spondylosis Chest pain Chickenpox (Varicella) Chilblains Cholesteatoma Chronic Cough in Children Chronic Fatigue Syndrome (CFS) Chronic Kidney Disease (CKD) Chronic Rhinosinusitis Chronic Stridor Clavicular fracture Clozapine Coeliacs Colorectal Cancer Screening Recommendations Congestive Cardiac Failure Connective Tissue Diseases Constipation Contact Dermatitis Cracked Heel Croup Cushings Cutaneous Drug Eruptions DKA vs HHS Dacrocystitis, dacyrostenosis, dacyrocystocoele Deep Vein Thrombosis (DVT) Delerium Dementia Depression and Delirium Dermal melanocystosis (mongolian spot) Developmental Dysplasia of the Hip (DDH) Diabetes Diabetes Insipidus (DI) vs Primary Polydipsia Diabetic Neuropathy Diarrhoea Diplopia Dizziness / syncope Down syndrome Duchenne muscular dystrophy Dupuytrens / trigger finger Dyspepsia Dyspnoea (Shortness of Breath) ECG ECG Findings ECG Patterns CONCISE COMPREHENSIVE Chest pain Differentiation of Cardiac vs. Non-Cardiac Causes: Thorough Evaluation Frameworks Cardiac causes: Ischaemic: ACS, stable angina, coronary vasospasm Non-ischaemic: Pericarditis, myocarditis, aortic dissection, cardiomyopathy Non-cardiac causes: Gastrointestinal: GORD, oesophageal spasm, peptic ulcer disease Musculoskeletal: Costochondritis, rib fracture Respiratory: PE, pneumothorax, pneumonia Psychogenic: Panic attack, anxiety Evaluation: History: Pain type, duration, triggers, associated symptoms (e.g., SOB, diaphoresis) Examination: Vital signs, chest tenderness, heart/lung auscultation Investigations: ECG, troponins, CXR, bloods (FBC, UECs) With Chest Pain Low-risk chest pain: Perform stress ECG to assess for inducible ischaemia High-risk chest pain: Conduct stress echocardiography to evaluate for wall motion abnormalities Without Chest Pain Low risk: No immediate investigation necessary Intermediate risk (10–20%): Consider CTCA High family history risk: Consider CTCA if no prior CAD diagnosis ACS Pathways: Management Based on RACGP/eTG Guidelines Initial assessment: ECG within 10 minutes Troponins: 0-hour and repeat at 3 hours, if required Risk stratification: High risk: Immediate cardiology referral ± coronary angiography Intermediate risk: Admit for serial troponins, monitoring, and stress testing Low risk: Outpatient stress testing or CTCA if no concerning features Management: Antiplatelets: Aspirin 300 mg ± clopidogrel/ticagrelor if ACS confirmed Symptomatic relief: GTN Long-term therapy: Beta-blockers ± statin Imaging Modalities: Stress Tests, Coronary CT Angiography, and Echocardiography Indications Stress ECG: For low-risk patients with suspected stable angina Stress Echo: For intermediate to high-risk chest pain; assess for regional wall motion abnormalities CTCA: For intermediate-risk chest pain (10–20%) No prior CAD but equivocal symptoms Strong family history of premature CVD Echocardiography: Assess LV function, valve disease, or pericardial effusion Evaluate suspected structural heart disease (e.g., cardiomyopathy) Chest Pain Differentiation of Cardiac vs Non-Cardiac Causes: Thorough Evaluation Frameworks Cardiac causes Ischaemic: ACS (unstable angina, NSTEMI, STEMI), stable angina, coronary vasospasm (Prinzmetal angina) Non-ischaemic: Pericarditis, myocarditis, aortic dissection, cardiomyopathy, significant arrhythmias (e.g. tachyarrhythmias) Non-cardiac causes Gastrointestinal: GORD, oesophageal spasm, peptic ulcer disease, pancreatitis Musculoskeletal: Costochondritis, rib fracture, Tietze’s syndrome Respiratory: PE, pneumothorax, pneumonia, pleuritis Psychogenic: Panic attack, anxiety disorders, hyperventilation Evaluation History: Nature of pain (sharp, crushing, burning), duration, triggers (exertion, stress), associated features (SOB, diaphoresis, palpitations), risk factors (age, smoking, diabetes) Examination: Vital signs (BP in both arms if dissection suspected), chest wall tenderness, heart/lung auscultation, signs of heart failure or shock Investigations: ECG, troponins, chest X-ray, bloods (FBC, UECs, possibly D-dimer if PE suspected), consideration of risk scores (e.g. HEART, GRACE, TIMI in acute presentations) With Chest Pain Low-risk chest pain Perform stress ECG if no high-risk features, normal baseline ECG, and stable symptoms Useful for detecting inducible ischaemia in suspected stable angina High-risk chest pain Consider stress echocardiography to visualise regional wall motion abnormalities under stress Pharmacological stress (dobutamine) if patient cannot exercise If suspicion of ACS, proceed with immediate hospital assessment Without Chest Pain Low risk No immediate investigation required if completely asymptomatic and no significant risk factors Intermediate risk (10–20%) Consider coronary CT angiography (CTCA) for anatomical assessment of coronary arteries High family history risk CTCA can be helpful if no prior CAD diagnosis and the patient has a strong family history of premature coronary artery disease ACS Pathways: Management Based on Guidelines Initial assessment ECG within 10 minutes of arrival or symptom presentation Troponins at 0 hours and repeat at 3 hours if needed (hs-troponin can facilitate earlier diagnosis) Risk stratification High risk: Immediate cardiology referral ± urgent angiography Intermediate risk: Admit for serial troponins, continuous monitoring, possible inpatient stress testing Low risk: Outpatient stress testing or CTCA if no ongoing chest pain, normal ECG, and stable vitals Management Antiplatelets: Aspirin 300 mg loading, add clopidogrel or ticagrelor if ACS confirmed Symptom relief: GTN sublingual or IV for persistent pain, IV morphine if severe Long-term therapy: Beta-blockers (if no contraindications) and statins for secondary prevention, consider ACE inhibitors in LV dysfunction, hypertension, or diabetes Imaging Modalities: Stress Tests, Coronary CT Angiography, and Echocardiography Indications Stress ECG Low-risk patients with a normal baseline ECG and suspected stable angina Limited utility if baseline ST/T changes, LBBB, or paced rhythm Stress Echocardiography Intermediate to high-risk chest pain to detect wall motion abnormalities Useful when baseline ECG abnormalities limit interpretation of a standard stress ECG CTCA Intermediate-risk chest pain (~10–20% estimated pre-test probability) No prior diagnosis of CAD but equivocal or atypical symptoms Strong family history of early coronary artery disease Helps rule out significant stenoses, can reduce need for invasive angiography Echocardiography Assess LV function, valve pathology, or pericardial effusion Evaluate suspected structural heart disease such as dilated or hypertrophic cardiomyopathies Additional Considerations Rapid identification of red flags (ongoing chest pain at rest, hypotension, arrhythmias, syncope, signs of heart failure) dictates urgent ED referral GORD or oesophageal spasm can mimic cardiac chest pain; a trial of proton pump inhibitors may help clarify diagnosis Panic attacks may present with chest tightness, palpitations, hyperventilation; differentiate from cardiac aetiologies through thorough assessment and risk stratification Chronic stable chest pain in the setting of known CAD warrants optimisation of anti-anginal therapy (beta-blockers, nitrates, possibly calcium channel blockers) and risk factor management (lipids, BP, diabetes control, smoking cessation) Thorough GP follow-up for borderline or recurrent symptoms ensures timely escalation if patients deteriorate or new features emerge ____________________________________ Features of typical and atypical acute cardiac chest pain (AJGP) 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 Age-Related Macular Degeneration (AMD) Wet vs Dry AMD Dry AMD (Non-Exudative): Pathophysiology: Retinal pigment degeneration → drusen, geographic atrophy Progression: Gradual central vision loss Signs: Drusen deposits, macular atrophy Wet AMD (Exudative): Pathophysiology: Subretinal neovascularisation → bleeding, fluid leakage, scarring Progression: Rapid/severe central vision loss Signs: Metamorphopsia (Amsler grid), subretinal fluid/haemorrhage Prevalence Dry AMD: ~90% of cases; 2%/year progress to wet AMD Risk Factors Non-Modifiable: Age >60 (strongest) Modifiable: Smoking (strongest), obesity (BMI >30), hypertension, low omega-3, CVD Presentation Central Vision Loss: Gradual (dry), rapid (wet) Metamorphopsia: Early sign of wet AMD (Amsler grid) Functional Impact: Difficulty reading, recognising faces Management For Both Dry/Wet AMD: Lifestyle: Quit smoking, BMI <25, omega-3-rich diet (fatty fish, leafy greens) Supplements: AREDS2 vitamins (Vit C/E, zinc, lutein, zeaxanthin) Monitoring: Self-check with Amsler grid; routine eye reviews (1–2 years for dry AMD) For Wet AMD: VEGF Inhibitors: Intravitreal injections (e.g., ranibizumab, bevacizumab) Urgent Referral: Signs of wet AMD → urgent ophthalmology Age-Related Macular Degeneration (AMD) Pathophysiology & Types Dry AMD (Non-Exudative) Pathophysiology: Characterised by retinal pigment epithelial (RPE) degeneration and the accumulation of drusen (yellowish deposits) beneath the retina. Progression can lead to geographic atrophy, where areas of the RPE and overlying photoreceptors become atrophic. Clinical Course: Typically gradual decline in central vision over months to years. Signs: Drusen deposits on fundoscopy Macular atrophy in later stages Generally slower progression than wet AMD Wet AMD (Exudative) Pathophysiology: Choroidal neovascularisation develops beneath the retina; new vessels leak fluid and blood, leading to subretinal haemorrhage, exudation, and eventual scar formation. Clinical Course: Often rapid and more severe loss of central vision. Signs: Metamorphopsia (distortion of straight lines) detectable with an Amsler grid Subretinal fluid or haemorrhages on ophthalmoscopic or OCT (Optical Coherence Tomography) exam Prevalence Dry AMD: Accounts for ~90% of cases, though 2% per year can progress to wet AMD. Wet AMD: Although less common, it causes the majority of severe vision loss in AMD. Risk Factors Non-Modifiable Age >60 (most significant factor) Genetic predisposition (family history) Caucasian ethnicity Modifiable Smoking (strongest modifiable risk factor) Obesity (BMI >30) Hypertension Diet low in omega-3 fatty acids and leafy greens Cardiovascular disease (CVD) Presentation Central Vision Loss Gradual onset in dry AMD Sudden or rapid worsening in wet AMD Metamorphopsia Early sign of wet AMD Detected via Amsler grid self-checks Functional Impact Difficulty with reading, recognising faces, and fine detail tasks (e.g. driving, crafts) Management Shared Measures for Both Dry & Wet AMD Lifestyle Modifications Smoking cessation: Greatest potential to reduce disease progression in smokers Healthy diet: Increase intake of omega-3 (fatty fish) and leafy green vegetables; maintain a BMI <25 Blood pressure control and management of cardiovascular risk factors Nutritional Supplements AREDS2 formulation (Age-Related Eye Disease Study 2): Typically contains vitamin C, vitamin E, zinc, copper, lutein, and zeaxanthin Can reduce progression in intermediate and advanced AMD, although not a cure Monitoring Self-check with Amsler grid (ideally daily or weekly) to detect early changes in vision Routine eye reviews: At least every 1–2 years for patients with dry AMD or those at risk More frequent if there is evidence of progression Additional Management for Wet AMD Intravitreal Anti-VEGF Injections Medications such as ranibizumab, aflibercept, or bevacizumab (off-label) Aim to reduce neovascularisation and stabilise or improve vision Typically administered every 4–8 weeks depending on clinical response Urgent Referral Sudden vision loss or signs of active wet AMD (new metamorphopsia, subretinal fluid/bleeding) warrant urgent ophthalmology assessment Early treatment significantly improves outcomes Notes: Early Identification: Patients with dry AMD should be vigilant for signs of progression (metamorphopsia, acute vision change) and know how to use an Amsler grid. Smoking Cessation: Strong recommendation to quit smoking to slow disease progression. Anti-VEGF Therapy: A mainstay for wet AMD; can stabilise or improve vision if started promptly. Comprehensive Management: Control blood pressure, maintain healthy weight, and optimise diet and exercise to reduce progression risk. 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 Temporomandibular Dysfunction (TMD) Causes Muscular (most common): Bruxism (grinding/clenching), stress/anxiety Joint-related: Disc displacement, TMJ OA, trauma, RA History Pain with jaw movement (chewing, yawning) Crepitus, locking, or trismus Associated: Tension headache, otalgia, tinnitus, vertigo, hearing loss Psychosocial stressors: Anxiety, poor sleep Examination Inspection/Palpation: TMJ/muscle tenderness, clicking/popping on jaw opening Functional: Restricted jaw ROM, locking, or deviation Other: Otoscopy to rule out ear pathology Investigations First-line: Clinical diagnosis If severe/atypical: MRI: Gold standard (disc displacement) CT/X-ray: Degenerative changes/fracture Ultrasound: Intra-articular disc (operator-dependent) Management Non-Pharm: Education: Role of stress, bruxism, posture Lifestyle: Avoid hard foods, stress management, sleep hygiene Warm compresses, jaw stretching exercises Dental referral: Occlusal splint (if persistent) Pharm: 1st-line: NSAIDs 2nd-line: Muscle relaxants (short-term, e.g., benzodiazepines) TCAs (chronic pain/tension headaches) Botox (refractory myofascial pain) Red Flags Persistent swelling/erythema/fever → Septic arthritis/malignancy Weight loss or unresponsive trismus → Malignancy/systemic inflammatory condition Unilateral jaw deviation + neuro deficits Other Interventions Physio: Jaw/postural exercises Referral: Dentist/maxillofacial surgeon → Persistent joint dysfunction Psychologist → CBT for stress-related bruxism Temporomandibular Dysfunction (TMD) Causes Muscular (most common): Bruxism (grinding or clenching), stress or anxiety, tension Joint-related: Disc displacement, osteoarthritis, trauma, rheumatoid arthritis History Pain exacerbated by jaw movements such as chewing or yawning Clicking, popping, or locking of the jaw, sometimes leading to trismus Associated symptoms including tension headache, ear pain, tinnitus, vertigo, or hearing loss Psychosocial factors like anxiety, poor sleep, or high stress Examination Palpation of the TMJ and masticatory muscles, assessing for tenderness or clicking Observation of jaw opening for restriction, deviation, or locking Otoscopy to rule out primary ear pathology Investigations Primarily clinical diagnosis MRI for detailed assessment of disc displacement CT or X-ray if degenerative changes or trauma are suspected Ultrasound for intra-articular disc visualisation, noting operator dependency Management Non-Pharm Education on the role of bruxism, stress, posture, and avoidance of hard foods Jaw relaxation exercises, warm compresses, and good sleep hygiene Occlusal splint via dental referral if bruxism persists Pharm NSAIDs as first-line pain relief Muscle relaxants (e.g. short-term benzodiazepines) or TCAs for chronic pain and tension headaches Botulinum toxin for refractory myofascial pain Red Flags Persistent swelling or fever suggestive of septic arthritis or malignancy Weight loss or unresponsive trismus pointing to malignancy or systemic inflammatory conditions Unilateral jaw deviation with neurological deficits requiring urgent evaluation Other Interventions Physiotherapy for specific jaw and postural exercises Referral to dentist or maxillofacial surgeon for joint dysfunction resistant to conservative measures Psychological support or CBT for stress-related bruxism 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 Leukaemia Classification Acute Leukaemias: AML: Age 67; M3 (Auer rods) → ATRA, non-M3 → chemo ALL: Age 7; CNS involvement (↑ICP) → intrathecal chemo, TLS prophylaxis (allopurinol/rasburicase) Chronic Leukaemias: CML: Age 47; Philadelphia chromosome (t9;22); risk of blast crisis CLL: Age 87; asymptomatic or chemo (progression); IVIG for hypogammaglobulinemia Presentation Acute: RBC: Fatigue, lethargy (anaemia) Platelets: Bleeding (thrombocytopenia) WBC: Infections (leukopenia), bone pain, rapid onset Chronic: Often asymptomatic; hepatosplenomegaly, lymphadenopathy, insidious onset Diagnosis Blood Film: Acute: >20% blasts Chronic: ↑lymphocytes (>60%) Bone Marrow Biopsy: Hypercellular, blasts in acute cases Cytogenetics: Philadelphia chromosome (CML) Labs: LDH, uric acid (tumor lysis risk) Management Acute (AML/ALL): Induction chemo ± transplant RBC/platelet transfusions, infection prophylaxis Chronic (CML/CLL): CML: Tyrosine kinase inhibitors (imatinib) CLL: Monitor asymptomatic; chemo/IVIG if progression Complications Tumor Lysis Syndrome: Prophylaxis with allopurinol/rasburicase Infections: Neutropenia → bacterial/viral/fungal risks Bleeding: Thrombocytopenia, coagulopathy (acute cases) Organ Infiltration: Hepatosplenomegaly, lymphadenopathy, CNS (ALL) Blast Crisis (CML): Mimics acute leukaemia, poor prognosis Leukaemia Classification Acute Leukaemias Acute Myeloid Leukaemia (AML) Median age ~67 Subtype M3 (acute promyelocytic leukaemia) associated with Auer rods, responds well to ATRA (all-trans retinoic acid) Other AML subtypes treated with standard induction chemotherapy (e.g. cytarabine + anthracycline) ± haematopoietic stem cell transplant Acute Lymphoblastic Leukaemia (ALL) Median age ~7 (most common paediatric leukaemia) CNS involvement common → prophylactic intrathecal chemotherapy High risk of tumour lysis syndrome (TLS) with intensive chemo → prophylaxis with allopurinol or rasburicase Chronic Leukaemias Chronic Myeloid Leukaemia (CML) Median age ~47 Philadelphia chromosome (t[9;22], BCR-ABL fusion) → dysregulated tyrosine kinase → proliferation of myeloid line Risk of blast crisis (transforming to acute leukaemia) if untreated Chronic Lymphocytic Leukaemia (CLL) Median age ~87 (often older adults) Often asymptomatic; may find on routine FBC with elevated lymphocyte count Hypogammaglobulinaemia can occur → recurrent infections Treatment deferred unless symptomatic or evidence of progression Presentation Acute Leukaemias (AML, ALL) Rapid onset over weeks to months RBC: Fatigue, pallor, anaemia Platelets: Bleeding tendency (bruising, petechiae, haemorrhage) WBC: Infections due to neutropenia or dysfunctional blasts Bone pain (marrow expansion), fever, night sweats CNS involvement more common in ALL (headache, cranial nerve palsies, ↑ICP) Chronic Leukaemias (CML, CLL) Insidious onset over months to years Often asymptomatic or mild symptoms (fatigue, weight loss, low-grade fevers) Hepatosplenomegaly, lymphadenopathy, incidental finding of ↑WBC on routine labs CLL can present with recurrent infections (hypogammaglobulinaemia) Diagnosis Peripheral Blood Film AML/ALL: >20% blasts (myeloblasts or lymphoblasts) CLL: Marked lymphocytosis, often >60% mature lymphocytes CML: Elevated WBC (often >100 × 10^9/L), basophilia, myelocytes in peripheral smear Bone Marrow Biopsy Hypercellular marrow, ≥20% blasts for acute leukaemias Assessment of lineage markers (flow cytometry) to distinguish AML vs ALL Cytogenetics/Molecular Testing Philadelphia chromosome t(9;22) in CML PML-RARA t(15;17) in APL (M3 AML) Other rearrangements guide prognosis and treatment (e.g. FLT3, NPM1 in AML) Additional Labs LDH, uric acid (risk of tumour lysis), LFTs, renal function, coagulation profile Infectious screening (HBV, HCV, HIV) prior to immunosuppressive therapy Management Acute Leukaemias (AML, ALL) Induction Chemotherapy (e.g. cytarabine + anthracycline for AML, hyper-CVAD for ALL) to achieve remission Consolidation ± stem cell transplant depending on risk stratification (cytogenetics, minimal residual disease) Supportive Care RBC and platelet transfusions for cytopenias Infection prophylaxis (antibacterial, antifungal, antiviral) if severe neutropenia Allopurinol/rasburicase for TLS prophylaxis in high tumour burden CNS prophylaxis in ALL (intrathecal methotrexate) APL (Acute Promyelocytic Leukaemia, M3 AML) High risk of DIC, treat with ATRA ± arsenic trioxide, can be highly curable if managed early Chronic Myeloid Leukaemia (CML) Tyrosine Kinase Inhibitors (TKIs) (e.g. imatinib, dasatinib, nilotinib) mainstay therapy Monitor BCR-ABL transcript levels for response Allogeneic stem cell transplant considered if TKI resistance or advanced disease (blast crisis) Chronic Lymphocytic Leukaemia (CLL) Watchful Waiting if asymptomatic with stable blood counts Active Therapy for progressive disease (lymphadenopathy, B symptoms, cytopenias) Options: chemoimmunotherapy (e.g. FCR - fludarabine, cyclophosphamide, rituximab), novel agents (BTK inhibitors like ibrutinib), anti-CD20 (obinutuzumab) Supportive IVIG replacement in recurrent infections due to hypogammaglobulinaemia Palliative radiotherapy for bulky nodes or splenomegaly Complications Tumour Lysis Syndrome (TLS) Spontaneous or post-therapy (especially ALL, high WBC AML) Hyperuricaemia, hyperkalaemia, hyperphosphataemia, hypocalcaemia Prophylaxis: aggressive hydration, allopurinol or rasburicase Infections Severe neutropenia → bacterial/fungal/viral infections Prophylactic antimicrobials for high-risk patients (fluoroquinolones, fluconazole, aciclovir) Bleeding Thrombocytopenia, coagulopathy (particularly in APL) Platelet transfusions, cryoprecipitate, FFP as needed Organ Infiltration Hepatosplenomegaly, lymphadenopathy, CNS infiltration (ALL) Leukaemic infiltration of gums (monocytic AML) Blast Crisis (CML) Transformation to acute leukaemia with poor prognosis Notes: Suspicion: Unexplained fatigue, bruising, infections, high WBC or blasts on FBC → urgent referral to haematology Diagnosis: Peripheral smear + bone marrow biopsy ± cytogenetics essential for accurate classification Acute: Rapid intervention needed for AML/ALL to prevent life-threatening complications Chronic: Monitor stable CLL or manage progressive disease with modern agents (imatinib for CML, BTK inhibitors for CLL) Supportive Care: Vigilance for febrile neutropenia (urgent broad-spectrum antibiotics), tumour lysis prophylaxis, transfusion support Follow-Up: Long-term monitoring for treatment side effects, secondary malignancies, relapse, and psychosocial support. 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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 Precocious Puberty Definition Onset before 8 years in girls or 9 years in boys Normal puberty onset: ~10.5 years in girls, ~11.5 years in boys Tanner Stages Stage 1: Prepubertal Stage 2: Girls: Breast buds, sparse pubic hair Boys: Testes >4 mL, sparse pubic hair Stages 3–5: Progressive pubertal changes, menstruation in girls Differentials Central (Gonadotropin-Dependent) Idiopathic: Most common cause Hypothalamic hamartoma CNS tumours: Gliomas, astrocytomas, hydrocephalus Peripheral (Gonadotropin-Independent) Adrenal causes: Congenital adrenal hyperplasia (CAH), adrenal tumours Gonadal causes: Ovarian cysts/tumours, testicular tumours Exogenous hormone exposure: Oestrogen/testosterone creams, medications Investigations Hormonal Testing Central: High LH/FSH Peripheral: Low LH/FSH, high oestradiol/testosterone Imaging Bone age X-ray: Advanced age suggests hormonal activation MRI brain: Rule out CNS lesions Pelvic/testicular ultrasound: Assess gonadal pathology Adrenal imaging: Evaluate for adrenal tumours GnRH stimulation test: High LH confirms central cause Management Central: GnRH agonists (e.g., leuprolide) to delay further progression Peripheral: Treat the underlying cause (e.g., tumour resection, CAH management) Key Points Refer to paediatric endocrinology if precocious puberty is suspected Untreated cases risk short stature due to early epiphyseal plate closure Precocious Puberty Definition Onset of secondary sexual characteristics before age 8 in girls and before age 9 in boys Classified as central (gonadotropin-dependent) or peripheral (gonadotropin-independent) based on underlying pathophysiology Early pubertal changes include breast development in girls and testicular enlargement (volume >4 mL) in boys Normal Age of Puberty Girls typically begin at approximately 10.5 years Boys typically begin at approximately 11.5 years Tanner Stages Stage 1: Prepubertal Stage 2: Girls: Breast budding and sparse pubic hair Boys: Testicular enlargement and sparse pubic hair Stages 3–5: Progressive development of secondary sexual characteristics, with menarche occurring in girls Differential Diagnosis Central Precocious Puberty (Gonadotropin-Dependent) Idiopathic (most common) Hypothalamic hamartoma or other CNS tumours Peripheral Precocious Puberty (Gonadotropin-Independent) Adrenal causes such as congenital adrenal hyperplasia or adrenal tumours Gonadal causes including ovarian cysts or testicular tumours Exogenous hormone exposure from topical creams or medications Investigations Hormonal Evaluation Measure LH, FSH, and sex steroids (estradiol in girls, testosterone in boys) GnRH stimulation test: A rise in LH confirms central cause Bone Age Assessment Wrist X-ray to assess for advanced bone age indicative of increased hormonal activity Imaging MRI brain to exclude CNS lesions in central precocious puberty Pelvic ultrasound in girls or testicular ultrasound in boys to evaluate gonadal pathology Adrenal imaging if adrenal pathology is suspected Management Central Precocious Puberty GnRH analogues (eg, leuprolide) to suppress premature gonadotropin release Peripheral Precocious Puberty Target underlying cause (eg, tumour resection or cessation of exogenous hormone exposure) Supportive Care Provide psychological counselling to address social and emotional impacts Regular monitoring of growth, bone age, and pubertal progression to prevent early epiphyseal closure Notes: Early intervention prevents premature growth plate closure and short stature Rapid progression or neurological symptoms necessitate urgent evaluation Family history of early puberty may contribute and should be documented Monitoring should include regular assessment of growth velocity and pubertal staging Long-term follow-up is important to adjust treatment and optimise adult height Psychosocial support is crucial to help children manage the challenges of early puberty Emerging evidence on maternal factors may influence pubertal timing and warrants further research Differentiation between central and peripheral causes is key to appropriate management A multidisciplinary approach involving endocrinologists, paediatricians and psychologists is recommended for optimal care Comprehensive history, physical examination and targeted investigations are essential to guide treatment decisions 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 Extrapyramidal Side Effects (EPSE) Symptoms & Timeframes 1. Acute Dystonia (4 Hours) Symptoms: Muscle spasms (face, neck, back) Onset: Within hours (90% within 5 days, 50% within 2 days) Management: Benztropine 1 mg IM, then oral as needed 2. Akinesia (4 Days) Symptoms: Parkinsonism (bradykinesia, rigidity, tremor) Management: Oral benztropine 3. Akathisia (4 Weeks) Symptoms: Inner restlessness, inability to stay still Management: Propranolol or diazepam 4. Tardive Dyskinesia (4 Months) Symptoms: Involuntary repetitive movements (face, mouth) Management: Switch to lower-risk antipsychotic (e.g., clozapine, quetiapine) Consider dose reduction Emerging treatments: VMAT2 inhibitors (valbenazine, tetrabenazine) Extrapyramidal Side Effects (EPSE) Overview Extrapyramidal side effects are drug-induced movement disorders most often associated with typical (first-generation) antipsychotics, though they can also occur with some atypical antipsychotics (particularly at higher doses). These side effects arise from dopamine D2 receptor blockade in the nigrostriatal pathway. The mnemonic “4 hours, 4 days, 4 weeks, 4 months” helps recall typical onset timelines of various EPSE. 1. Acute Dystonia (4 Hours) Symptoms: Sudden muscle spasms (often affecting face, neck, back) Oculogyric crisis (eyes deviated upward) Laryngospasm (rare but potentially severe) Onset: Typically within hours of initiating or escalating dose (about 90% within 5 days, 50% within 2 days) Management: IM benztropine (1 mg) or IV/IM anticholinergics Transition to oral benztropine or other anticholinergic for short-term prophylaxis If recurrent, consider dose reduction or switching antipsychotic 2. Akinesia (4 Days) Symptoms: Parkinsonism features: Bradykinesia, rigidity, tremor, postural instability May also present with masked facies or a shuffling gait Onset: Within days to weeks of antipsychotic use (often around 4 days in acute presentations) Management: Oral benztropine (1–2 mg up to TDS) or trihexyphenidyl Amantadine may be used if anticholinergics are contraindicated Consider lowering dose of antipsychotic or switching to a lower-risk agent (e.g. second-generation antipsychotic) 3. Akathisia (4 Weeks) Symptoms: Subjective restlessness, inner tension, inability to stay still Patient may pace around, fidget, or shift weight frequently Can significantly impact compliance with antipsychotics Onset: Usually within weeks of starting or increasing dose Management: Propranolol (10–40 mg BD) often first-line Benzodiazepines (e.g. diazepam) if severe anxiety Dose reduction or switching to a lower-risk antipsychotic may help Short-term use of anticholinergics is less effective for akathisia 4. Tardive Dyskinesia (4 Months) Symptoms: Involuntary, repetitive movements, often orofacial (lip smacking, tongue protrusion) or choreoathetoid limb movements Can be socially stigmatizing and sometimes irreversible Onset: Usually after months to years of antipsychotic therapy (the mnemonic “4 months” is a memory aid, but real onset can be much longer) Management: Switch to a lower-risk agent (e.g. clozapine, quetiapine) Consider reducing or discontinuing the offending drug if feasible VMAT2 inhibitors (e.g. valbenazine, tetrabenazine) have emerging evidence to reduce tardive dyskinesia Early recognition is key; permanent changes can occur if not addressed promptly Additional Notes Risk Factors: Older age, higher doses, longer duration of antipsychotic use, presence of organic brain syndromes (e.g. dementia). Preventive Strategies: Use the lowest effective dose of antipsychotic; prefer second-generation agents (some still carry EPSE risk, albeit lower). Monitoring: Regular assessment of extrapyramidal function using tools like the Simpson-Angus Scale or the Abnormal Involuntary Movement Scale (AIMS) for tardive dyskinesia. Clinical Pearls: If early onset EPSE occur, addressing them quickly (dose adjustment, medication switch, or short-term anticholinergics) can prevent non-adherence and more severe complications. 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 Obesity Medications for Weight Management Phentermine (sympathomimetic) - Avoid in cardiovascular disease, anxiety, or substance misuse Orlistat - Decreases fat absorption; can cause steatorrhoea Liraglutide/Semaglutide (GLP-1 analogues) - Improves glycaemic control; preferred in patients with diabetes Naltrexone/Bupropion - Avoid in epilepsy or uncontrolled hypertension Note: VLEDs can also be appropriate with similar BMI criteria (caution in patients on SGLT2 inhibitors, insulin, sulfonylureas). Indications for Starting Medications BMI ≥ 30 kg/m², or ≥ 27 kg/m² with obesity-related complications (e.g., Type 2 diabetes, hypertension) Must be combined with lifestyle interventions Consider surgery (sleeve gastrectomy) In diabetics w BMI >40 (or >35 w 1 or more obesity related complication) Referral Criteria for Bariatric Surgery BMI >35 BMI >30 w comorbidities Comorbidities requiring specialist management ie OSA Non-Pharmacological Management Dietary Approaches: Tailored to patient preferences (e.g., Mediterranean, low-carb) Emphasis on energy intake reduction and long-term adherence Physical Activity: Moderate/vigorous activity ≥ 150 minutes per week to maintain weight loss Reduces ASCVD risk independent of weight loss Behavioural Support: Goal setting, cognitive behavioural interventions, self-monitoring Prevent relapse with structured maintenance programs Notes: Obesity related complications: Diabetes, HTN, IHD, OSA, NAFLD Consider bariatric surgery if >30 BMI w obesity related comp esp diabetes w difficult to attain BSL control Avoid all medications in pregnancy except liraglutide (seek specialist input) Topiramate - Assoc with weight loss, but not TGA-approved for weight loss; avoid in glaucoma Obesity Medications for Weight Management Phentermine (sympathomimetic) Mechanism: Appetite suppression Avoid in patients with cardiovascular disease, uncontrolled hypertension, anxiety, or substance misuse TGA-approved for short-term use (≤12 weeks) Orlistat Mechanism: Inhibits pancreatic lipase, reducing fat absorption Side effects: Steatorrhoea, flatulence, potential deficiency of fat-soluble vitamins (A, D, E, K) Liraglutide / Semaglutide (GLP-1 Receptor Agonists) Mechanism: Slows gastric emptying, promotes satiety Preferred in patients with T2DM or high cardiovascular risk Monitor for gastrointestinal side effects (nausea, vomiting) Naltrexone / Bupropion Mechanism: Central appetite suppression and reward pathway modulation Avoid in epilepsy, severe uncontrolled hypertension, or patients at high risk of seizures Caution: May raise blood pressure and heart rate Notes VLED (Very Low Energy Diet) can be used with similar BMI thresholds (≥30, or ≥27 with obesity-related comorbidities), but take care in those using insulin, sulfonylureas, or SGLT2 inhibitors (increased risk of hypoglycaemia or euglycaemic DKA) Avoid all anti-obesity medications in pregnancy (liraglutide not specifically TGA-indicated in pregnancy) Topiramate has off-label weight loss effects but is not TGA-approved for obesity management and has ocular side effects (risk of acute angle-closure glaucoma) Indications for Starting Medications BMI ≥30 kg/m², or ≥27 kg/m² with obesity-related complications (e.g. T2DM, hypertension, NAFLD, OSA) Must be combined with lifestyle interventions (diet, physical activity, behavioural support) Continue only if clinically meaningful weight loss (≥5% from baseline) is achieved within 12 weeks Regularly review safety profile and ongoing adherence Consider Surgery (Sleeve Gastrectomy or Other Bariatric Procedures) In diabetic patients with BMI >40 or BMI >35 plus ≥1 obesity-related complication, especially if glycaemic control is difficult to achieve Surgical approach can result in significant and sustained weight reduction, remission or improvement in T2DM, and reduced cardiovascular risk Referral Criteria for Bariatric Surgery BMI >35 kg/m² regardless of comorbidities BMI >30 kg/m² with obesity-related comorbidities (e.g. T2DM, OSA, uncontrolled hypertension) Conditions requiring specialist management (severe OSA, complex T2DM) Psychological readiness and commitment to long-term follow-up Non-Pharmacological Management Dietary Approaches Tailor to patient preferences (Mediterranean, low-carb, meal replacements) Energy deficit of ~500–750 kcal/day for gradual, sustainable weight loss Monitor calcium and protein intake if using VLED or meal replacements Physical Activity At least 150–300 minutes per week of moderate-to-vigorous activity Include resistance training 2–3 times per week for muscle preservation Even without major weight loss, exercise reduces ASCVD risk and improves metabolic health Behavioural Support SMART goal-setting, self-monitoring of weight and dietary intake Cognitive behavioural strategies to prevent relapse (stress management, problem-solving) Regular follow-up and accountability (group programs, online tools) Lifestyle Targets Aim for ≥5–10% weight reduction over 6–12 months Address psychosocial factors (sleep hygiene, mental health, readiness for change) Notes: Obesity-related complications include T2DM, hypertension, IHD, OSA, NAFLD, PCOS, and arthritis Bariatric surgery considered at lower BMI thresholds (≥30) if severe comorbidities exist (e.g. difficult-to-control diabetes) In pregnancy planning, discontinue weight loss medications except under specialist guidance (risks vs benefits) Regular reviews are important to reassess treatment efficacy, potential adverse effects, and patient adherence Implement a comprehensive approach: diet, exercise, behavioural therapy, plus medication or surgery if indicated Use motivational interviewing and shared decision-making to support lifestyle changes Monitor for medication side effects (e.g. orlistat’s GI effects, phentermine’s cardiovascular effects) Refer patients with significant comorbidities or inadequate response to lifestyle interventions for specialist evaluation, including bariatric surgery assessment Long-term follow-up is vital for maintaining weight loss and optimising metabolic health Bookmark Failed! 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