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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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 Global Developmental Delay Causes Perinatal TORCH infections: Toxoplasmosis, CMV, Rubella, HSV Hypoxic-ischaemic injury: Placental abruption, uterine rupture, prolonged labour Birth trauma: Macrosomia, improper forceps/vacuum use, intracranial haemorrhage Congenital/Genetic Fetal Alcohol Syndrome: Microcephaly, smooth philtrum, small palpebral fissures, developmental delays Inborn Errors of Metabolism: Congenital hypothyroidism (delayed milestones, hypotonia, lethargy) Neuromuscular Disorders: Duchenne Muscular Dystrophy, Spinal Muscular Atrophy Cerebral Palsy: Prenatal (75%): Intrauterine insults, congenital infections, genetic causes Perinatal (15%): Birth asphyxia, stroke Postnatal (10%): Meningitis, trauma, kernicterus Genetic Syndromes: Fragile X (intellectual disability, speech delay, hyperactivity), Down Syndrome, Prader-Willi Syndrome Postnatal Environmental factors: Neglect, malnutrition (iron, iodine deficiencies) CNS infections: Meningitis, encephalitis, severe sepsis Examination Growth Plot weight, height, head circumference (OFC), BMI on growth charts Dysmorphic Features Microcephaly, flat nasal bridge, single palmar crease, hypotonia Vision/Hearing Assess tracking, visual fixation, response to sounds Developmental Assessment Gross motor: Head control, rolling, sitting, walking Fine motor: Pincer grasp, hand use, object transfer Speech/language: Babbling, first words, sentence formation Social interaction: Smiling, eye contact, joint attention Neurological Examination Tone abnormalities: Hypotonia (floppy infant), hypertonia (spasticity) Deep tendon reflexes: Increased in spasticity (e.g., cerebral palsy), reduced in hypotonia (e.g., neuromuscular disorders) Posture and movement patterns Management Referrals Developmental paediatrician for assessment Genetic testing (chromosomal microarray, Fragile X screening) if syndromic features present Neurologist if seizures, regression, or abnormal tone Investigations Brain MRI if structural abnormalities, perinatal insults, or neurological signs Vision and hearing assessment to rule out sensory causes Thyroid function tests (TFTs) for congenital hypothyroidism Metabolic screening if metabolic disorders suspected Early Intervention NDIS funding for therapy and support services Occupational therapy (OT), physiotherapy, speech therapy Specialist educational programs for developmental support Follow-Up Multidisciplinary team reviews with paediatrics, allied health, and education specialists Regular monitoring of developmental progress and intervention effectiveness Additional Notes Hypotonia is a common feature across most causes ("floppy infant") Prognosis depends on the underlying cause and timing of intervention Early diagnosis and therapy significantly improve long-term outcomes Global Developmental Delay Causes Perinatal TORCH infections such as toxoplasmosis, cytomegalovirus, rubella, and herpes simplex Hypoxic-ischaemic encephalopathy from events like placental abruption, uterine rupture, or prolonged labour Birth trauma associated with macrosomia or improper use of forceps/vacuum extraction Congenital/Genetic Fetal alcohol syndrome characterised by microcephaly, smooth philtrum, and small palpebral fissures Inborn errors of metabolism including congenital hypothyroidism leading to delayed milestones and hypotonia Genetic syndromes such as Down syndrome, Fragile X syndrome, and Prader-Willi syndrome Neuromuscular Disorders Conditions like Duchenne muscular dystrophy or spinal muscular atrophy causing motor deficits Cerebral Palsy Often prenatal in origin, though perinatal or postnatal insults may contribute Postnatal Environmental factors including neglect, nutritional deficiencies, and central nervous system infections (e.g. meningitis) Other Contributory Factors Exposure to toxins such as lead and socioeconomic deprivation affecting early development Examination Anthropometric Measurements Record weight, height, and BMI using Down syndrome-specific or standard growth charts as appropriate Dysmorphic Features Identify features such as microcephaly, flat nasal bridge, epicanthal folds, or single palmar crease Sensory Screening Assess vision with cover-uncover tests and hearing by evaluating responses to auditory stimuli Developmental Assessment Evaluate gross and fine motor skills, language abilities, social interactions, and adaptive behaviours using age-appropriate tools Neurological Examination Check muscle tone (noting hypotonia or “floppy infant” presentation), reflexes, posture, and coordination Spine Examination Inspect for structural anomalies such as spina bifida or scoliosis Investigations Genetic Testing Perform chromosomal microarray as first-line when a genetic aetiology is suspected Neuroimaging MRI brain for structural abnormalities if indicated by neurological findings Metabolic Screening Assess thyroid function and perform relevant metabolic panels Sensory Assessments Conduct formal vision and hearing tests to rule out contributory sensory deficits Developmental Screening Use standardised developmental assessments to quantify delays Management Multidisciplinary Approach Refer to a developmental paediatrician for comprehensive evaluation and management Include geneticists, neurologists, and allied health professionals as indicated Early Intervention Initiate speech, occupational, and physical therapies as early as possible Develop individualised educational and behavioural support plans Support Services Facilitate access to funding and community resources (e.g. disability support schemes) Provide caregiver education and psychological support Regular Follow-Up Schedule multidisciplinary reviews to monitor progress and adjust interventions accordingly Complications and Prognosis Prognosis depends on the underlying cause and the timeliness of intervention Early, targeted therapy can significantly improve outcomes Some children may catch up to peers, while others may require lifelong support Potential long-term complications include persistent learning difficulties and social or adaptive challenges Notes Hypotonia is a frequent finding contributing to motor delays Global developmental delay may coexist with other neurodevelopmental disorders necessitating comprehensive evaluation Ongoing monitoring is essential to adjust interventions and support developmental progress 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 Grover’s Disease (Transient Acantholytic Dermatosis) Definition Pruritic, red, crusted or eroded papules/vesicles Sites: Central back, mid-chest, upper arms Common in: Caucasian men >50 with sun-damaged skin Duration: Days to decades, often seasonal Risk Factors Sweating, sun exposure, fever Malignancy, hospitalisation, prolonged bed rest Clinical Features Small, red, crusted/eroded papules Intense itch, worsened by sweating Primarily affects back, chest, upper arms Management Self-limiting, but symptom relief may be needed Key Treatments Cooling measures (avoid heat, reduce sweating) Moisturisers (prevent dryness) Topical steroids (e.g. betamethasone, triamcinolone) for itch/inflammation Oral retinoids, phototherapy (for severe cases) Grover’s Disease (Transient Acantholytic Dermatosis) Definition Grover’s disease is an itchy dermatosis characterised by small, red, crusted or eroded papules/vesicles, primarily affecting the central back, mid-chest, and upper arms. Most common in Caucasian men over 50 years with sun-damaged Can be short-lived or persist for days to decades, often exhibiting a seasonal fluctuation (e.g. worse in winter) Risk Factors Sweating, sun exposure, fever: Heat and perspiration can exacerbate or precipitate lesions Malignancy or Prolonged Bed Rest: Hospitalised, bed-bound, or debilitated patients sometimes develop Grover’s disease Other: Chronic sun-damaged skin, older age, and fair complexion Clinical Features Lesions: Small, red, sometimes crusted or eroded papules, occasionally vesicular Pruritus: Often intense itch, worsened by sweating or heat Distribution: Typically the central back, chest, upper arms, though it can appear on the trunk generally Course: May last days to weeks, spontaneously resolving, but can persist for months or even years in recurrent or chronic forms Management Self-Limiting Many cases resolve spontaneously without specific treatment; focus on symptomatic relief. General Measures Cooling Measures: Keep ambient temperatures comfortable; avoid excessive heat or sweaty environments Moisturisers: Prevent dryness and reduce itching; apply after bathing Avoid Triggers: Minimising sweating (light clothing, air-conditioned environment), gentle sun exposure if triggers are known Topical Treatments Topical Corticosteroids (e.g. betamethasone dipropionate, triamcinolone) to reduce inflammation and pruritus Apply once or twice daily, for short courses (1–2 weeks), with caution around skin thinning Calamine or menthol-based lotions for mild cooling effect More Severe Cases Oral Retinoids (e.g. acitretin) under specialist guidance if refractory Phototherapy (NB-UVB or PUVA) can be beneficial for extensive or resistant disease Oral Antihistamines for significant itch, though efficacy varies Notes Patients often benefit from reducing friction or sweating on affected areas; wearing loose, breathable clothing. Differential diagnoses include eczema, psoriasis, pityriasis rosea, Darier’s disease, or pemphigus foliaceus (in acantholytic conditions). If lesions do not respond to standard topical therapies or have unusual features, consider referral to a dermatologist for biopsy and advanced management. Bookmark Failed! Bookmark Saved! Add Bookmark Refresh Refresh

Log In Get started Bookmarks Help Progress 0% Cardiovascular AAA + Rupture AC dislocation ATSI Abdominal pain in kids Abnormal/Dysfunctional Uterine Bleeding (AUB/DUB) Acanthosis Nigricans Acne Acromegaly Actinic Cheilitis Acute Kidney Injury (AKI) Acute Swollen Joint with Fever Acute Vision Loss Acute and Progressive Vision Loss Addisons Adjustment Disorder and Anxiety Adjustment Disorder with Depressed Mood Age related macular degeneration Alcohol Cessation Allergic rhinitis Alopecia Amenorrhoea Anaphylaxis Angina Angular Cheilitis Ankylosing Spondylitis (AS) Anorexia Nervosa Anticholinergics and TCAs Antidepressants Antimetabolite drugs Antiphospholipid syndrome Antipsychotics Anxiety Disorders Aortic Dissection Arrhythmia Asthma Asthma Atrial Fibrillation Back pain Behavioural / learning disorders Behavioural disturbances Bell’s palsy and Ramsey Hunt syndrome Beta-Human Chorionic Gonadotropin (β-hCG) Biologic agents Bipolar Disorder Bleeding disorders Blepharitis Breast Cancer Breast Lump Bronchiectasis (Updated) CA-125 (Cancer Antigen 125) CRPS CVD Risk Assessment Calluses and Corns Candida (Candidiasis as an STI) Carpal tunnel syndrome and de quervains tenosynovitis Cellulite Cervical spondylosis Chest pain Chickenpox (Varicella) Chilblains Cholesteatoma Chronic Cough in Children Chronic Fatigue Syndrome (CFS) Chronic Kidney Disease (CKD) Chronic Rhinosinusitis Chronic Stridor Clavicular fracture Clozapine Coeliacs Colorectal Cancer Screening Recommendations Congestive Cardiac Failure Connective Tissue Diseases Constipation Contact Dermatitis Cracked Heel Croup Cushings Cutaneous Drug Eruptions DKA vs HHS Dacrocystitis, dacyrostenosis, dacyrocystocoele Deep Vein Thrombosis (DVT) Delerium Dementia Depression and Delirium Dermal melanocystosis (mongolian spot) Developmental Dysplasia of the Hip (DDH) Diabetes Diabetes Insipidus (DI) vs Primary Polydipsia Diabetic Neuropathy Diarrhoea Diplopia Dizziness / syncope Down syndrome Duchenne muscular dystrophy Dupuytrens / trigger finger Dyspepsia Dyspnoea (Shortness of Breath) ECG ECG Findings ECG Patterns CONCISE COMPREHENSIVE Chronic Fatigue Syndrome (CFS) Diagnostic Criteria Fatigue: Persistent, unexplained fatigue >6 months, not relieved by rest, with significant functional impairment. Associated Symptoms (≥4, lasting >6 months): Impaired memory/concentration Post-exertional malaise Unrefreshing sleep Muscle or multi-joint pain (no swelling/redness) New/severe headaches Sore throat or tender cervical/axillary lymph nodes Symptoms and Key Features Hallmark Symptoms: Post-exertional malaise, unrefreshing sleep, cognitive impairment Common Features: Orthostatic intolerance, acute onset (often post-viral), crimson crescents in the oropharynx Triggers Post-viral fatigue (e.g., Epstein-Barr virus) Psychological or physical stress Immune Dysregulation: Possible role in pathogenesis Vitamin D deficiency Differentials Obstructive sleep apnoea Hypothyroidism, hyperthyroidism Anaemia, iron deficiency Fibromyalgia Depression, generalised anxiety disorder Multiple sclerosis HIV, hepatitis Investigations Initial Screening FBC ESR/CRP UEC, LFT, TFT Vitamin D: Exclude deficiency Further Testing (if indicated): Coeliac serology: Malabsorption Cortisol: Adrenal insufficiency Infectious workup: EBV serology Management Non-Pharmacological Graded Exercise Therapy: Low-level activity with rest periods CBT: For coexisting depression/anxiety Pacing: Avoid over-exertion to manage post-exertional malaise Sleep Hygiene: Address unrefreshing sleep Pharmacological Pain: NSAIDs or paracetamol Sleep Issues: Sedatives or low-dose antidepressants (e.g., amitriptyline) Avoid polypharmacy—limited evidence for specific medications Chronic Fatigue Syndrome (CFS) Diagnostic Criteria Fatigue: Persistent, unexplained fatigue >6 months, not relieved by rest, causing significant functional impairment. Associated Symptoms (≥4, lasting >6 months): Impaired memory or concentration Post-exertional malaise Unrefreshing sleep Muscle or multi-joint pain (without swelling/redness) New or severe headaches Sore throat or tender cervical/axillary lymph nodes Symptoms and Key Features Hallmark Symptoms: Post-exertional malaise, unrefreshing sleep, cognitive impairment Common Features: Orthostatic intolerance, often acute onset (post-viral), crimson crescents in the oropharynx Triggers Post-viral fatigue (e.g. Epstein-Barr virus) Psychological or physical stress Immune dysregulation (potential role) Vitamin D deficiency Differentials Obstructive sleep apnoea Thyroid dysfunction (hypothyroidism/hyperthyroidism) Anaemia or iron deficiency Fibromyalgia Depression or generalised anxiety disorder Multiple sclerosis HIV, hepatitis Investigations Initial Screening: FBC ESR/CRP UEC, LFT, TFT Vitamin D (exclude deficiency) Further Testing (if indicated): Coeliac serology (malabsorption) Cortisol (adrenal insufficiency) Infectious workup (e.g. EBV serology) Management Non-Pharmacological: Graded Exercise Therapy (low-level activity with planned rest periods) CBT for coexisting depression/anxiety Pacing to avoid over-exertion and manage post-exertional malaise Sleep hygiene to address unrefreshing sleep Pharmacological: Pain relief (NSAIDs or paracetamol) Sedatives or low-dose antidepressants (e.g. amitriptyline) for sleep issues Avoid polypharmacy; limited evidence for specific medications 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 Interstitial Lung Disease (ILD) Types Idiopathic Pulmonary Fibrosis (IPF): >50 yrs, linked to smoking, GORD; antifibrotics (pirfenidone, nintedanib) slow progression CTD-ILD: RA, SLE, systemic sclerosis; may respond to immunosuppressants Pneumoconioses: Asbestos, silica, coal dust exposure Hypersensitivity Pneumonitis: Inhaled organic allergens (e.g. bird proteins, mould) Drug-Induced: Amiodarone, methotrexate, nitrofurantoin Smoking-Related: Respiratory bronchiolitis-ILD, Langerhans cell histiocytosis Presentation Dry cough, dyspnoea, velcro crackles, clubbing (IPF), rash/Raynaud’s (CTD-ILD) Specialist referral for HRCT to confirm; DLCO helps distinguish parenchymal from extraparenchymal causes Vaccinate (influenza, pneumococcal) due to infection risk Investigations Initial: Pulse oximetry, spirometry (restrictive: ↓FVC, ↑FEV₁/FVC), CXR Specialist: HRCT (diagnosis, pattern differentiation), ANA, RF, DLCO, lung biopsy if unclear Monitor: ≥10% ↓FVC or ≥15% ↓DLCO = significant decline Management IPF: Antifibrotics (pirfenidone, nintedanib), pulmonary rehab, long-term O₂ if hypoxaemic CTD-ILD: Immunosuppressants (e.g., mycophenolate, cyclophosphamide) Smoking-Related ILD: Smoking cessation; corticosteroids if progressive; consider lung transplant Hypersensitivity Pneumonitis: Allergen avoidance, corticosteroids if severe Pneumoconioses: Manage symptoms, monitor occupational exposures Special Notes HRCT Patterns: UIP: Honeycombing, basal/subpleural (IPF, RA-ILD) NSIP: Bilateral ground-glass opacities (CTD-ILD) Childhood ILD: Rare; refer to paediatric specialist, genetic testing for familial cases Monitoring Regular lung function tests to track progression and comorbidities Pulmonary rehab improves QoL; O₂ for hypoxaemia Interstitial Lung Disease (ILD) Types Idiopathic Pulmonary Fibrosis (IPF) Typically age >50, associated with smoking, gastro-oesophageal reflux disease (GORD) Antifibrotic agents (pirfenidone, nintedanib) may slow disease progression Connective Tissue Disease–Related ILD (CTD-ILD) Common in RA, SLE, systemic sclerosis May respond to immunosuppressive therapy (e.g. mycophenolate mofetil, cyclophosphamide) Pneumoconioses From occupational exposures: Asbestos, silica, coal dust Hypersensitivity Pneumonitis Inhaled organic allergens (e.g. bird proteins, mould) → alveolar inflammation Drug-Induced Amiodarone, methotrexate, nitrofurantoin can all cause ILD Smoking-Related Includes respiratory bronchiolitis–ILD and Langerhans cell histiocytosis (often younger smokers) Presentation Dry cough, progressive dyspnoea Velcro crackles on auscultation, clubbing (particularly in IPF) Signs of underlying CTD if relevant (rash, Raynaud’s, arthralgias) Specialist referral for HRCT (high-resolution CT) to confirm pattern; DLCO helps differentiate parenchymal from extraparenchymal causes Vaccinations (influenza, pneumococcal) recommended due to increased infection risk Investigations Initial Pulse oximetry → check resting SpO₂ and possible desaturation on exertion Spirometry → restrictive pattern: ↓FVC with preserved or increased FEV₁/FVC ratio CXR → reticular or reticulonodular opacities, possible honeycombing Specialist HRCT → critical for diagnosis and pattern differentiation (e.g. UIP, NSIP) Autoimmune markers (ANA, RF) if CTD suspected DLCO (diffusing capacity) → often reduced in ILD Lung biopsy (rarely needed) for unclear cases Monitoring: ≥10% ↓FVC or ≥15% ↓DLCO signals significant decline in disease status Management IPF Antifibrotics: Pirfenidone or nintedanib to slow fibrotic progression Pulmonary rehabilitation: Improves functional capacity and QoL Long-term oxygen if hypoxaemic; consider lung transplant evaluation in advanced disease CTD-ILD Immunosuppressants: Mycophenolate mofetil, cyclophosphamide (especially in scleroderma-related ILD) Treat underlying rheumatologic disease concurrently (e.g. DMARDs for RA, lupus therapy) Smoking-Related ILD Smoking cessation is fundamental Corticosteroids if progressive or inflammatory Consider lung transplant if advanced Hypersensitivity Pneumonitis Allergen avoidance is critical Corticosteroids if severe or progressive disease Pneumoconioses Manage symptoms, avoid ongoing occupational exposures, monitor for progressive fibrotic changes Special Notes HRCT Patterns UIP (usual interstitial pneumonia): Honeycombing, basal/subpleural predominance (classic in IPF, can also appear in RA-ILD) NSIP (nonspecific interstitial pneumonia): More bilateral ground-glass opacities, often linked to CTDs Childhood ILD is rare and may require paediatric respiratory referral, genetic testing for familial ILD Monitoring Regular lung function tests (FVC, DLCO) track progression and comorbidities Pulmonary rehabilitation improves quality of life and exercise tolerance Long-term oxygen therapy if hypoxaemic (PaO₂ <55 mmHg or SpO₂ <88%) Refer to specialist (respiratory physician) if uncertain diagnosis, significant disease progression, or complicated comorbidities 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 Paracetamol Hepatotoxicity Overdose Dose Single Dose: ≥10 g or 200 mg/kg in 24 hours Chronic Use: ≥6 g or 150 mg/kg/day over 48 hours Clinical Features Nausea, vomiting Right upper quadrant pain Elevated liver enzymes (AST/ALT >1000 IU/L) Jaundice Coagulopathy Hypoglycaemia Management Initial Steps Assess ingestion history and time Activated charcoal if within 1 hour of ingestion N-Acetylcysteine (NAC) Start immediately per dosing protocol (based on time post-ingestion) Continue NAC even if delayed presentation Monitoring Liver function tests (AST/ALT, bilirubin) Coagulation profile (INR/PT) Glucose levels Supportive Care Manage liver dysfunction Avoid hepatotoxic drugs Referral Criteria AST/ALT >1000 IU/L Acute liver failure (encephalopathy, coagulopathy) Uncertain ingestion time or beyond treatment window Massive overdose requiring ICU care Failure to respond to initial therapy Paracetamol Hepatotoxicity Overdose Dose Single Dose: ≥10 g or 200 mg/kg in 24 hours (whichever is less) Chronic Use: ≥6 g or 150 mg/kg/day over 48 hours (especially in low-weight or malnourished patients) Clinical Features Nausea, vomiting Right upper quadrant (RUQ) abdominal pain Elevated liver enzymes (AST/ALT often >1000 IU/L in severe cases) Jaundice if significant liver damage Coagulopathy (↑ INR, prolonged PT) Hypoglycaemia (due to impaired gluconeogenesis in severe cases) Management Initial Steps Assess Ingestion History & Timing Confirm dose, time of ingestion, and any co-ingestants Activated Charcoal If presentation <1 hour post-ingestion (reduces paracetamol absorption) N-Acetylcysteine (NAC) Begin as soon as possible according to an approved dosing protocol Continue NAC even if patient presents late (beyond the typical 8-hour window) NAC prevents hepatocellular damage by replenishing glutathione Monitoring Liver Function Tests: AST, ALT, bilirubin Coagulation Profile: INR/PT (detects hepatic synthetic failure) Glucose Levels: Hypoglycaemia risk in severe liver injury Supportive Care Manage potential hypoglycaemia with IV dextrose if needed Monitor fluid balance, renal function Avoid hepatotoxic drugs (e.g. further paracetamol, certain antibiotics) Consider ICU admission if severe toxicity or acute liver failure Referral Criteria AST/ALT >1000 IU/L (suggests severe hepatic injury) Acute Liver Failure: Encephalopathy, coagulopathy (INR >1.5), significant jaundice Uncertain ingestion time or beyond typical treatment window (≥8 hours) Massive Overdose requiring closer monitoring or ICU Failure to respond to initial NAC therapy (persistent or rising transaminases, coagulopathy) 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 Haematuria Differentials Most common Bladder calculi (or renal) Urethritis (men, STI) UTI Prostatitis Bladder (70%) causes Others: Exercise induced haematuria (kidney/bladder microtrauma) Menstrual contamination PCKD Pelvic or renal trauma Prostate cancer Bladder cancer (transitional cell) Renal cell carcinoma (renal cell) Glomerulonephritis - IgA nephropathy, interstitial nephritis, PSGN Anticoags Trauma Risk Factors Age History of gross haematuria Irritative lower urinary tract symptoms Smoking (current or past history) Occupational exposure (dyes, benzenes, aromatic amines) Cyclophosphamide exposure History of chronic urinary tract infection History of pelvic irradiation History Flank pain: Suggests renal pathology (stones, PCKD) Haematuria timing: Start of stream = Urethral source Throughout = Bladder/kidney End of stream = Prostatic or bladder neck cause Recent trauma (loin, pelvis, genitals) Dysuria, LUTS, weight loss, abdominal/lower back pain (consider bladder cancer) Travel history (schistosomiasis risk) Strenuous exercise (possible exercise-induced haematuria) Bleeding elsewhere (easy bruising, epistaxis – consider coagulopathy or vasculitis) Urethral discharge (possible STI-related cause) Investigations Microscopic Haematuria First step: Urine MCS to exclude infection Confirm persistence: Repeat dipstick testing 1 week apart (≥1+ on 2 out of 3 tests, NOT trace) Risk stratification: High risk (e.g., male, >40, smoker, macrohaematuria history, dye exposure) → Urine cytology x3, US KUB Refer to urology (consider cystoscopy) Glomerular signs (albuminuria, red eGFR, red cell casts, dysmorphic RBCs) → Refer to nephrology Low risk (no risk factors, normal renal function) → Annual monitoring with kidney health check (BP, ACR, eGFR) Macroscopic Haematuria Always requires investigation Urine MCS first to exclude infection Urine cytology x3, CT IVP Refer to Urology (consider PSA in men >50) Diagnosis (Prior to Referral) Urine MCS (infection, sterile pyuria) Urine microscopy (red cell morphology, casts) Dysmorphic RBCs, red cell casts → Glomerular disease Normal RBCs → Non-glomerular cause UEC (renal function, possible CKD) US KUB or CT IVP (depending on micro vs macrohaematuria) Cytology x3 (for urothelial malignancy) FBC (only for referral preparation) When to Refer Refer to Nephrology: Persistent microscopic haematuria with proteinuria or renal impairment (eGFR decline, albuminuria) Dysmorphic RBCs or red cell casts (suggests glomerular pathology) Strong suspicion of IgA nephropathy, vasculitis, or lupus nephritis Refer to Urology: Any episode of macroscopic haematuria Persistent microscopic haematuria with risk factors (male >40, smoker, occupational dye exposure, recurrent UTIs) Unexplained haematuria with normal renal function Abnormal imaging findings (renal mass, bladder lesion, obstructive uropathy) Recurrent haematuria with LUTS despite normal PSA Management Microscopic Haematuria Low-risk cases: Annual urine dipstick, BP, ACR, eGFR monitoring High-risk cases: Immediate workup and referral (Urology or Nephrology) Macroscopic Haematuria Requires full investigation If symptomatic with significant pain, clot retention, or haemodynamic instability → Refer to ED Notes Red cell casts are virtually diagnostic of glomerulonephritis or vasculitis Dysmorphic RBCs = Glomerular disease, normal RBCs = Non-glomerular cause Bladder cancer is the most common malignancy-related cause of haematuria (70%) Exercise-induced haematuria is a diagnosis of exclusion Haematuria Differentials Common Causes Bladder calculi, renal calculi Urethritis (especially in men with STI risk) UTI, prostatitis Bladder pathologies (~70% of haematuria causes; e.g. transitional cell carcinoma) Other Causes Exercise-induced microtrauma to kidney/bladder Menstrual contamination (in women) PCKD (polycystic kidney disease) Prostate cancer Renal cell carcinoma Glomerulonephritis (e.g. IgA nephropathy, interstitial nephritis, post-streptococcal GN) Anticoagulants use Trauma to the renal tract Risk Factors Age (≥40–50 years) Gross (macroscopic) haematuria history Irritative LUTS (frequency, urgency) Smoking (current or past) Occupational exposure to dyes, benzenes, aromatic amines Cyclophosphamide exposure Chronic/recurrent UTIs Pelvic irradiation history History Flank pain: Suggestive of renal pathology (stones, PCKD) Timing of haematuria: Start of stream → Urethral source Throughout → Bladder or kidney origin End of stream → Prostatic or bladder neck cause Recent trauma (loin, pelvis, genitals) Associated symptoms: Dysuria, LUTS, weight loss, or abdominal/back pain (possible malignancy) Travel history: Schistosomiasis if relevant exposures Exercise: Strenuous exercise might cause exercise-induced haematuria Bleeding elsewhere (e.g. nose, gums) → Coagulopathy or vasculitis? Urethral discharge → STI cause (gonococcal or chlamydial infection) Investigations Microscopic Haematuria Urine MCS: Exclude infection Confirm persistence: Repeat dipstick 1 week apart (≥1+ on 2 of 3 tests, ignoring “trace” results) Risk Stratification: High Risk (male >40, smoker, occupational exposure, previous macrohaematuria) Urine cytology ×3 samples (suspected urothelial malignancy) Ultrasound KUB or CT IVP Refer to urology (cystoscopy) Glomerular Signs: Albuminuria, RBC casts, dysmorphic RBCs, eGFR decline → Nephrology referral Low Risk (no risk factors, normal renal function) → Annual monitoring: dipstick, BP, ACR, eGFR Macroscopic Haematuria Requires urgent investigation Urine MCS first to rule out infection Urine cytology ×3, CT IVP (or US KUB if CT contraindicated) Refer urology for cystoscopy Consider PSA in men >50 with other risk factors Diagnosis (Prior to Referral) Urine MCS to identify infection or sterile pyuria Urine Microscopy: RBC morphology → Dysmorphic RBCs or RBC casts indicate glomerular disease UEC for renal function, possible CKD Imaging: US KUB or CT IVP (depending on micro vs macrohaematuria) Identify masses, stones, hydronephrosis Cytology ×3 for urothelial malignancy screening if indicated FBC: Part of referral preparation (haemoglobin, WCC, platelets) When to Refer Nephrology Persistent microscopic haematuria with proteinuria or renal impairment (eGFR decline, albuminuria) Dysmorphic RBCs or red cell casts (glomerular origin) Suspected IgA nephropathy, vasculitis, or lupus nephritis Urology Any macroscopic haematuria (painful or painless) Persistent microscopic haematuria with risk factors (male >40, smoker, occupational exposures, recurrent UTIs) Unexplained haematuria with normal renal function Abnormal imaging findings (renal mass, bladder lesion, obstructive uropathy) Recurrent haematuria with LUTS despite normal PSA Management Microscopic Haematuria Low-Risk Cases: Annual check of urine dipstick, BP, ACR, eGFR High-Risk Cases: Immediate full workup and urological or nephrological referral Macroscopic Haematuria Requires full investigation If symptomatic with severe pain, clot retention, or haemodynamic instability, consider urgent ED referral Evaluate for possible bleeding disorder if repeated or unexplained Notes Red cell casts indicate glomerulonephritis or vasculitis. Dysmorphic RBCs suggest a glomerular source; normal RBCs indicate non-glomerular cause. Bladder cancer is the most common malignancy linked to haematuria (70% of malignant haematuria). Exercise-induced haematuria is a diagnosis of exclusion (rule out other pathology first). 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 Primary Adrenal Insufficiency (Addison's Disease) Causes Primary Causes: Autoimmune adrenalitis (most common in developed countries) TB, fungal infections, CMV Metastatic cancer, adrenal haemorrhage Congenital adrenal hyperplasia (e.g., 21-hydroxylase deficiency), adrenoleukodystrophy Secondary Causes: Chronic steroid use (suppressing ACTH production) Pituitary or hypothalamic dysfunction Presentation Cortisol deficiency - weakness (99%), weight loss (98%), N/V/D, hypoglycaemia Aldosterone Deficiency - Postural hypotension, tachycardia, hyponatraemia, hyperkalaemia ACTH Excess - Hyperpigmentation (sun-exposed, palmar creases), vitiligo. Diagnosis Initial Tests: Morning cortisol, ACTH, renin, aldosterone. Short Synacthen Test: Administer synthetic ACTH (tetracosactide) Cortisol fails to rise significantly in Addison’s Autoimmune Workup: Check anti-adrenal antibodies if autoimmune cause suspected Management Acute Management (Adrenal Crisis): Hydrocortisone: 100 mg IV initially, then 50 mg IV q6h until stable Can also give IM however eTG states give 40 mg oral pred if IV access impossible Rehydration: IV 0.9% saline +/- dextrose for hypoglycaemia Correct hyperkalaemia (usually resolves with fluids and steroids) Chronic Replacement Therapy: In Addison’s, the adrenal cortex is damaged, leading to deficiencies in both cortisol and aldosterone. Replace both with: Hydrocortisone 15–25 mg daily (split doses, e.g., 2/3 in the morning, 1/3 in the afternoon) AND Fludrocortisone 100 mcg daily (adjust based on renin, potassium, and blood pressure) Patient education: Wear a medical alert bracelet and have a "sick day" glucocorticoid plan If sx persist despite optimised therapy, consider DHEA Stress Dose Adjustments: Double or triple hydrocortisone dose during intercurrent illness or surgery Note 21-Hydroxylase deficiency: Common cause of CAH, causing cortisol and aldosterone deficiency with androgen excess due to shunting of 17-hydroxyprogesterone. Long-term Management Managed by endocrinologist; adjust glucocorticoids during illness/surgery. Replacement Therapy: Glucocorticoids: Oral hydrocortisone split into 2–3 daily doses (e.g., 2/3 AM, 1/3 PM) Mineralocorticoids: Fludrocortisone 50–300 mcg/day (adjust by BP, renin, K). Annual check: Na, K, renin. BMD every 2 years. Education on Associated Risks: Co-existing autoimmune conditions: Hashimoto’s thyroiditis, coeliac disease, T1DM Sx and signs of excess or insufficient glucocorticoid or mineralocorticoid replacement Self-Care Counselling Sick Day Rules: Increase glucocorticoid dose during acute illness (typically 2–3x usual dose for 2–3 days) Adrenal Crisis Preparedness: Recognise early signs: N/V, hypotension, dehydration Carry injectable hydrocortisone for emergencies Wear medical alert bracelet or necklace Lifestyle Adjustments: Regular follow-ups to reinforce self-care education Carry wallet card with treatment details (template available from Hormones Australia) Notes: Excess Glucocorticoid Replacement: Monitor for signs of Cushing’s syndrome (e.g., weight gain, elevated blood pressure) Plasma ACTH levels are unreliable for assessing glucocorticoid dosing adequacy Primary Adrenal Insufficiency (Addison's Disease) Aetiology: Primary Causes: Autoimmune adrenalitis is the most common cause, leading to gradual adrenal cortex destruction. Globally, infectious causes like tuberculosis, fungal infections, and cytomegalovirus (CMV) can also lead to adrenal insufficiency. Paediatric Cases: Congenital adrenal hyperplasia (e.g., 21-hydroxylase deficiency) is a frequent cause in children, where enzyme deficiencies affect cortisol synthesis. Secondary Causes: Long-term corticosteroid use suppresses adrenal function. Pituitary adenomas can also decrease adrenocorticotropic hormone (ACTH) production, leading to adrenal atrophy. Symptoms (Clinical Features): Cortisol Deficiency: Weakness (common in 99% of cases), weight loss (98%), nausea, vomiting, diarrhoea, and hypoglycaemia. Aldosterone Deficiency: Postural hypotension, tachycardia, hyponatraemia, and hyperkalaemia. Excess ACTH: Hyperpigmentation (characteristic of Addison's disease), particularly in sun-exposed areas and skin creases, and potentially vitiligo. Differential Diagnosis: Other causes of chronic fatigue and weight loss i.e., hypothyroidism, chronic infections. Conditions associated with skin pigmentation changes i.e., haemochromatosis. Investigations: Cortisol Levels: Measured in serum and 24-hour urine samples; low cortisol confirms adrenal insufficiency. Plasma ACTH: Elevated ACTH supports primary adrenal insufficiency (Addison’s), while low ACTH suggests secondary causes. Short Synacthen Test: Assesses adrenal function by administering synthetic ACTH; minimal cortisol response indicates Addison's disease. Plasma Renin Activity: Increased renin due to aldosterone deficiency. Autoantibodies: Positive anti-adrenal antibodies suggest autoimmune adrenalitis. Management: Immediate Management (Crisis): IV hydrocortisone 100 mg initially, followed by 50 mg every 6 hours. Intramuscular (IM) hydrocortisone if IV access is not available; alternatively, oral prednisolone 40 mg if IM access is also challenging. IV 0.9% saline bolus (10–20 mL/kg) for dehydration, alongside 5–10% dextrose to prevent hypoglycaemia. Hyperkalaemia usually resolves with fluid therapy. Long-term Management: Referral to an endocrinologist for specialist management. Lifelong glucocorticoid (e.g., hydrocortisone) and mineralocorticoid (e.g., fludrocortisone) replacement. Bone mineral density (BMD) assessment at diagnosis and every two years to monitor for osteoporosis. Annual biochemical and clinical evaluations (including Na, K, renin levels) to monitor response and adjust hormone replacement. Patient education on recognising signs of insufficient or excessive hormone replacement. Self-Care Counselling: Sick Day Management: Increase glucocorticoid dose (usually 3x normal dose for 2–3 days) during illness or stress. Emergency Preparedness: Carry an emergency injectable form of hydrocortisone for acute adrenal crisis. Symptom Awareness: Educate on signs of deterioration i.e., nausea, vomiting, dehydration. Medical Identification: Advise wearing a medical alert bracelet indicating adrenal insufficiency. Notes: Congenital adrenal hyperplasia (CAH): In cases of 21-hydroxylase deficiency, there is a buildup of 17-hydroxyprogesterone, leading to shunting of steroid synthesis toward androgen production due to impaired cortisol/aldosterone synthesis. Excess glucocorticoid replacement can lead to Cushingoid symptoms. Plasma ACTH may not be a reliable marker for assessing the adequacy of glucocorticoid replacement in such cases. 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 Hyperhidrosis Definition Excessive sweating, usually localised (palms, soles, axillae, face) Affects 2–3%, worsened by stress, often independent of temperature Aetiology & Causes Rule out thyroid dysfunction (TSH disorders) Secondary causes: Diabetes mellitus, phaeochromocytoma, lymphoma Post-surgery, spinal cord injury SSRIs Management First-Line Topical aluminium chloride 20% solution, applied daily (morning or night) Specialist Treatments (Severe Cases) Palmar/plantar hyperhidrosis: Iontophoresis (tap water + electrical stimulation) Anticholinergic drugs Axillary hyperhidrosis: Botulinum toxin A injections (effective up to 6 months) Generalised hyperhidrosis: Systemic anticholinergics (e.g. oxybutynin 2.5–5 mg PO) Botulinum toxin, iontophoresis (temporary sweat gland blockade) Hyperhidrosis Definition Hyperhidrosis is excessive sweating, usually in localised areas (palms, soles, axillae, face) but can also be generalised. It affects approximately 2–3% of the population and can be exacerbated by stress. It often occurs independently of ambient temperature or exertion. Aetiology & Causes Primary Hyperhidrosis: Often idiopathic, with no underlying pathology. Rule out secondary causes: Thyroid dysfunction (check TSH) Diabetes mellitus (poor glycaemic control) Phaeochromocytoma (adrenal tumour → episodic sweating) Lymphoma (night sweats) Post-Surgical changes, spinal cord injury Certain medications (e.g. SSRIs) Management First-Line Topical Aluminium Chloride 20% Solution: Apply daily (morning or night) to dry skin in affected area. Gradual reduction in sweating over days to weeks. Possible skin irritation → consider lower concentrations or less frequent application. Specialist Treatments (Severe Cases) Palmar/Plantar Hyperhidrosis: Iontophoresis: Immersion of hands/feet in tap water with a mild electric current (repeated sessions). Anticholinergic Drugs (e.g. glycopyrrolate, oxybutynin) if severe or resistant; watch for side effects (dry mouth, blurred vision). Axillary Hyperhidrosis: Botulinum Toxin A Injections: Effective for ~6 months, repeated as needed. Consider surgical options (e.g. local excision of sweat glands, endoscopic thoracic sympathectomy) only in refractory cases. Generalised Hyperhidrosis: Systemic Anticholinergics (e.g. oxybutynin 2.5–5 mg PO) if multiple areas affected. Botulinum toxin or iontophoresis can help localised severe sweating. Address underlying triggers or conditions where possible. Notes Emphasise lifestyle measures: Loose clothing, breathable fabrics, daily hygiene, use of absorbent foot/shoe products. Psychosocial impact can be significant → Offer support or referral to mental health counselling if needed. If suspicion of secondary hyperhidrosis (e.g. night sweats, weight loss, palpitations, etc.), conduct appropriate investigations (TSH, FBC, glucose, consider imaging if indicated). 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 Thrombophlebitis Shouldn’t be able to see the actual veins in DVT Same risk factors as DVT Tender on palpation Still do US doppler as can prog to DVT/PE Treatment Ibuprofen 400mg tds (not paracetamol) Elevate leg Compression stockings Warm compresses Continue to mobilise Enoxaparin 40mg SC od for 4/52 (consider esp if high risk prog deeper) Thrombophlebitis Risk Factors Prolonged immobilisation (e.g. long-haul flights, bed rest) Recent surgery (especially orthopaedic procedures of the lower limb) Active cancer or malignancy Pregnancy or postpartum period Use of oral contraceptives or hormone replacement therapy Obesity Varicose veins Inherited thrombophilias (e.g. Factor V Leiden mutation) Many of these risk factors overlap with those for DVT, often summarised by Virchow’s Triad (stasis, endothelial injury, hypercoagulability). Clinical Presentation Superficial thrombophlebitis Localised tenderness, pain, redness, and a palpable cord-like vein The affected vein is often visible or palpable just below the skin surface Swelling is usually localised along the inflamed vein rather than the entire limb Patients might notice local warmth over the area Deep vein thrombosis Typically presents with diffuse swelling of the entire calf or leg Pain, possibly worse on dorsiflexion (Homan’s sign), though this sign is neither sensitive nor specific The overlying veins are often not visible as dilated, cord-like structures More pronounced risk of pulmonary embolism if untreated Because superficial thrombophlebitis can progress to DVT in certain scenarios, careful assessment is required. Investigations A thorough history (including risk factors) and physical examination are essentialLook for signs suggestive of DVT (e.g. diffuse swelling) or superficial thrombophlebitis (a palpable cord, local redness, tenderness) Clinical Assessment Assess for extension beyond superficial veins or suspicion of concomitant DVTCheck for risk factors such as recent immobilisation, active malignancy, or previous venous thromboembolic events Ultrasound (Doppler) Examination Duplex ultrasound is the main investigation to confirm superficial thrombophlebitis and assess for extension into the deep venous systemEven if the clinical suspicion is high for superficial thrombophlebitis, a Doppler ultrasound is recommended to exclude concurrent DVT or extension toward the deep system Management Management aims to reduce inflammation, relieve pain, and prevent extension into deep veins Conservative Measures Leg elevation Warm compresses Compression stockings (graduated compression helps reduce pain and swelling) Mobilisation rather than strict bed rest Analgesia and Anti-Inflammatory Treatment NSAIDs (e.g. ibuprofen 400 mg three times daily) for pain and inflammation Consider contraindications (e.g. peptic ulcer disease, renal impairment, cardiovascular disease) Paracetamol alone is less effective for the inflammatory component Anticoagulation Consider anticoagulation if the thrombus is extensive, close to the deep venous system, or the patient is high risk (e.g. previous VTE, active cancer, thrombophilia) Low molecular weight heparin (e.g. enoxaparin 40 mg subcut once daily) for up to 4 weeks is often used Alternative agents (such as DOACs or fondaparinux) may be considered in specific circumstances Follow current Therapeutic Guidelines for dosing and duration Monitoring and Follow-Up Ensure symptomatic improvement (decreasing pain, erythema, swelling) Consider repeat ultrasound if symptoms worsen or do not improve Advise patients to seek urgent review if signs of DVT or PE develop Complications Propagation of the clot into deeper veins (leading to secondary DVT) Pulmonary embolism if extension reaches the deep system Recurrent superficial thrombophlebitis, especially in patients with varicose veins or thrombophilias Chronic venous insufficiency if repeated episodes damage venous valves Prevention Address modifiable risk factors (weight reduction, smoking cessation, regular mobilisation) Optimise management of varicose veins (consider surgical intervention if recurrent issues) Provide prophylaxis in high-risk situations (e.g. prophylactic LMWH during high-risk periods for patients with previous VTE or known thrombophilias) 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 Calluses & Corns Definition Calluses (Tyloma): Diffuse thickening of the stratum corneum due to repeated friction/pressure; usually painless Corns (Clavus, Heloma): Localized hyperkeratosis with a painful central core, often due to pressure over bony prominences (e.g. ill-fitting shoes, abnormal gait) Aetiology & Causes Chronic friction or pressure due to: Ill-fitting shoes Bony prominences Abnormal gait Pathophysiology Calluses: Thickened skin develops as a protective response Corns: Pressure over bony areas → central core formation, causing pain Symptoms Calluses: Thick, rough skin; usually painless unless irritated Corns: Hard, painful areas over pressure points (feet, toes) Differential Diagnosis Plantar warts (HPV infection): Punctate capillary thromboses (dark spots after paring) Disrupted skin lines (unlike calluses/corns) Management Pharmacological Treatment Salicylic Acid 40% Plasters Debulking: Pare the lesion with a #15 scalpel blade Application: Cut plaster to lesion size, apply for 48–72 hours Keep area dry Follow-up: Remove softened skin, repeat if necessary Non-Pharmacological Treatment Prevention: Avoid ill-fitting shoes Consider orthotic consultation for recurrent issues Follow-up: If no resolution in 2 weeks, re-evaluate Avoid salicylic acid in peripheral neuropathy (risk of misplacement & injury) Calluses & Corns Definition Calluses (Tyloma): A diffuse thickening of the stratum corneum caused by repeated friction or pressure on the skin. Typically painless but can become tender if there is ongoing irritation. Corns (Clavus, Heloma): A more localised form of hyperkeratosis that presents with a hardened, central core. They commonly occur over bony prominences (e.g. the dorsal aspect of toes) and are often painful. Aetiology & Causes Chronic friction or pressure due to: Ill-fitting shoes (narrow toe box, high heels, shoes too small or too large) Bony prominences (hammer toes, bunions, foot deformities) Abnormal gait or biomechanics (uneven weight distribution) Pathophysiology Calluses: The skin thickens in response to repeated pressure or friction as a protective mechanism. The thickening tends to be more diffuse. Corns: Persistent or focused pressure over a bony prominence leads to a concentrated hyperkeratotic plug, or “core,” which can impinge on deeper structures and cause pain. Symptoms Calluses: Thick, rough, yellowish skin patches. Usually painless, although they can become sore if further irritated. Common sites: plantar aspect of the foot (especially under metatarsal heads), palms (if related to occupational friction). Corns: Hard, cone-shaped lesions that press into the deeper dermis, causing sharp or burning pain. Often appear on the dorsal surface of toes or between toes if moisture is retained (soft corns). May limit mobility and footwear choices due to discomfort. Differential Diagnosis Plantar warts (verrucae caused by HPV): May show punctate capillary thromboses (“black dots”) upon debridement. Disruption of normal skin lines (whereas calluses/corns tend to preserve skin lines). Often painful when pinched side-to-side rather than direct pressure. Other causes of foot pain: Metatarsalgia (pain in the forefoot region). Morton’s neuroma. Fungal infections (tinea pedis) if there is scaling and itching. Management Pharmacological Treatment: Salicylic Acid 40% Plasters: Debulking: Pare the lesion gently with a #15 scalpel blade (or an emery board/pumice stone at home) to reduce thickness. Application: Cut the plaster to the size of the lesion. Apply for 48–72 hours, keeping the area dry. Check the site regularly for irritation. Follow-up: Carefully remove softened skin. Repeat if necessary until improvement. Non-Pharmacological Treatment: Prevention: Avoid ill-fitting or high-heeled shoes that concentrate pressure on a small area. Consider orthotics or customised insoles for biomechanical issues, especially if recurrent lesions occur at the same spot. Footwear advice: Wide toe box, adequate cushioning, and correct sizing help reduce pressure points. Foot care: Regularly soak feet in warm water and use a pumice stone or foot file to keep calluses from building up excessively. Moisturise feet to prevent drying and fissuring of calluses. Follow-up: If no resolution or improvement in 2 weeks, re-evaluate diagnosis and consider referral to a podiatrist. Use caution with salicylic acid in patients with peripheral neuropathy or peripheral vascular disease (risk of unnoticed injury or ulceration). Notes Comorbidities: In diabetic or immunocompromised patients, careful foot inspection and podiatry referral might be warranted to avoid complications such as foot ulcers. Painful or persistent corns: May need ongoing paring or removal by a trained professional (e.g. podiatrist). Surgery: Rarely indicated unless there is an underlying severe foot deformity (e.g. bunions, claw toes) that repeatedly causes corns/calluses. 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 IBS Causes Unsure aetiology Involves hypersensitive nerves of the bowel which easily upset Women in young 20s Sx come and go Triggers Infection, stress, meds (abs), food FODMAPs (lactose, fructose) Post-infectious IBS more likely after severe gastroenteritis or foodborne illnesses History Bloating / abdo pain Chronic diarrhoea / constipation or alternating Rectal urgency Mucous in stools Excess flatus Nausea Examination Usually normal but can have mild abdo pain on palp May detect tenderness in the sigmoid region; exclude masses or other pathology Alarm Features (usually req endo/colonoscopy) Nocturnal diarrhoea Weight loss Progressive abdo pain Iron def Rectal bleeding Onset over 50 yrs Family history IBD, colon ca Diagnosis Abdo pain 1d/week for 3 months: Related to defaecation (relieved by passing wind/faeces) o Assoc with change in stool freq/form Consider ROME IV criteria for functional GI disorders Investigations FBC, CRP, coeliac serology, faecal calprotectin (if diarrhoea) Consider faeces cultures / FOBT if relevant Exclude IBD, coeliac, colorectal cancer in older pop, gastro esp parasites Thyroid function tests (exclude hyperthyroidism or hypothyroidism contributing to GI sx) Management Non-Pharm Food diary for identification of common food triggers (dietary therapy) Refer to dietitian for trial of a low FODMAP diet (usually post diary) Increase dietary fibre intake from vegetables (esp constipation) Adequate fluid intake of at least 2L/day Refer to psychologist for CBT Pharm Loperamide Movicol Symptom-Specific Management Constipation Avoid fermentable fibres (e.g., wheat bran) Osmotic laxatives (e.g., lactulose) may cause bloating and pain Stimulant laxatives may cause cramping Diarrhoea Loperamide for intermittent or pre-emptive use (e.g., at night if morning diarrhoea or before meals out) Non-fermentable insoluble fibre (e.g., sterculia) may be used as bulking agent Consider rifaximin for general sx improvement Specialist consideration: 5-HT3 antagonists (e.g., ondansetron) Abdominal Pain Antispasmodics: Peppermint oil 0.2mL/capsule, 1-2 capsules TDS before meals o Hyoscine butylbromide 20mg up to QID Mebeverine 135mg TDS Refractory pain: Consider low-dose TCAs/SSRIs to address visceral hypersensitivity Bloating Managed as for functional bloating Psychological Therapy IBS often associated with anxiety or depression – treating these may improve GI sx Cognitive Behavioural Therapy (CBT): Useful for sx exacerbations in predictable situations (e.g., exams, public transport) Modified CBT for IBS provided by counsellors familiar with the condition Gut-directed hypnotherapy: Effective in refractory cases, with benefits sustained over time Neuromodulation Using Antidepressants TCAs, SSRIs can be used for brain-gut neuromodulation in IBS: Effective for reducing visceral hypersensitivity, esp abdominal pain and global sx relief 1st Line: Low-dose TCAs (e.g., amitriptyline or nortriptyline): Start 5-10mg nocte and increase weekly as tolerated to a max of 50 mg nocte Trial should continue for at least 4 weeks with full benefit taking up to 3 months If sx persists despite optimal dose → stop TCA 2nd Line: SSRIs at standard doses if TCAs are contraindicated or ineffective, particularly for concurrent anxiety or depression If sx still persists → refer to gastroenterologist Additional Notes: Long-term management often requires a multi-disciplinary approach, including dietitians and gastroenterologists. Consider probiotics in those with recurrent GI infections or those trialling FODMAP diets as adjunctive therapy. Irritable Bowel Syndrome (IBS) Causes Irritable Bowel Syndrome (IBS) is a functional gastrointestinal disorder characterised by hypersensitive nerves in the bowel, leading to abdominal pain and altered bowel habits. Although the exact aetiology is unclear, triggers often include infection, stress, certain medications (e.g. antibiotics), and FODMAP-rich foods. Post-infectious IBS frequently follows severe gastroenteritis or foodborne illnesses. History Bloating, abdominal pain (commonly relieved by defaecation or passing wind) Chronic diarrhoea/constipation or an alternating pattern Rectal urgency; sometimes with mucus in stools Excess flatulence and occasional nausea Usually no systemic signs (weight loss, fever) Alarm Features (require further investigations, often endoscopy): Nocturnal diarrhoea Weight loss Progressive abdominal pain Iron deficiency Rectal bleeding Onset over 50 years Family history of IBD, colorectal cancer Examination Often normal but may detect mild abdominal tenderness (e.g. in the sigmoid region). Exclude masses or organomegaly. Assess for anxiety/depression if relevant. Diagnosis Rome IV Criteria: Abdominal pain ≥1 day/week for 3 months plus ≥2 features: Related to defaecation Associated with change in stool frequency Associated with change in stool form/appearance Investigations (to exclude organic disease): FBC (anaemia?), CRP, coeliac serology, and faecal calprotectin if diarrhoea predominant. Consider stool culture if travel or infection suspicion. Thyroid function tests to rule out hyper-/hypothyroidism. No alarm features → IBS likely if investigations normal. Management Non-Pharmacological Dietary Measures Food diary to identify specific triggers. Low FODMAP diet trial with dietitian support. Fibre: Increase from vegetables/fruit for constipation-predominant IBS; avoid excessive fermentable fibres (like bran) if bloating worsens. Adequate fluids (≥2L/day). Lifestyle Regular exercise, stress reduction. Smoking cessation. Psychological Cognitive Behavioural Therapy (CBT) for stress-related exacerbations. Gut-directed hypnotherapy if refractory. Address comorbid anxiety or depression (therapeutic or pharmacological). Pharmacological Bowel Habit Management Constipation: Osmotic laxatives (e.g. Movicol); caution with lactulose (can cause bloating). Stimulant laxatives short-term if needed. Diarrhoea: Loperamide PRN or prophylactically if lifestyle requires (avoid with alarm features). Non-fermentable bulking agents (e.g. sterculia). Antibiotic rifaximin can be considered in some IBS-D for global symptom improvement (specialist advice). Antispasmodics (for Abdominal Pain/Bloating) Peppermint oil 0.2 mL capsules 1–2 TDS before meals. Hyoscine butylbromide 20 mg up to QID. Mebeverine 135 mg TDS. Neuromodulation (if persistent pain, recalcitrant IBS) Low-dose TCAs (e.g. amitriptyline 5–10 mg nocte) → can titrate up to 50 mg. SSRI if TCA contraindicated or coexisting depression/anxiety. Maintain therapy for at least 4 weeks; benefits may take 3 months to fully establish. Probiotics: May help in some patients, but evidence is variable. Notes IBS is a chronic condition requiring long-term management with a multidisciplinary approach (dietitian, GP, possible gastroenterologist). Emphasise reassurance that IBS is benign but can greatly impact quality of life. Symptom diaries help track patterns/triggers. Follow-up: Monitor symptom response and adjust diet/pharmacotherapy. FODMAP diet compliance for 6–8 weeks, then systematic reintroduction to identify specific triggers. Bookmark Failed! Bookmark Saved! Refresh Refresh Refresh