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 Gambling Disorder Gambling disorder: Persistent gambling causing actual harm, characterised by: Impaired control (escalating time/money spent) Prioritising gambling over other life areas Continued gambling despite negative consequences Risk Factors Early onset (adolescence) Family history Comorbidities: Mood/anxiety disorders, substance use disorders, personality disorders Aboriginal and Torres Strait Islander background Parkinson’s disease (dopamine agonists, e.g. pramipexole) Clinical Features & Harms Escalation: Increased frequency, bets, multiple venues, neglect of responsibilities Financial distress: Debt, unpaid bills, illegal activities (fraud/theft) Psychological distress: Depression, anxiety, suicidal thoughts, substance misuse Social consequences: Relationship breakdown, family violence, job loss Screening & Assessment Routine Enquiry Ask routinely in new patients, or opportunistically if risk factors present 2-Item Screening “In the past 12 months, have you been preoccupied with gambling or had a strong urge to gamble?” “Have you often gambled longer, with more money, or more frequently than intended?” → A "yes" to either suggests potential gambling disorder Lie/Bet Questionnaire (Adolescents 12–25 years) “Have you ever had to lie about how much you gambled?” “Have you ever felt the need to bet more and more money?” → A "yes" to either warrants further assessment Further Evaluation Detailed history (time/money spent, impulsivity) Psychosocial assessment (financial stress, relationships, mental health) Screen for comorbidities (substance use, mood disorders) Validated tools: Problem Gambling Severity Index (PGSI) Management Therapeutic Approach Non-judgemental, collaborative style Instil hope (relapses may occur but recovery is possible) Early Referral Gambling support services (phone, online, face-to-face) Specialist advice for complex cases (state-based gambling hotlines) Long-Term Follow-Up Monitor relapse risk, mental health, finances Ongoing motivation and behaviour change support Specific Management Strategies Brief Interventions Motivational interviewing: Explore patient’s concerns about gambling Address ambivalence, strengthen motivation for change Small reductions in gambling can be an important first step Gambling Support Services Helplines & websites (e.g. Gambling Help Online) offer: Behavioural assessment Money management strategies & self-exclusion Referrals to financial counselling, peer support (e.g. Gamblers Anonymous), therapy Money Management Cancel credit cards or limit gambling-related financial access Some banks offer transaction blocking for gambling-related spending Self-Exclusion ("Self-Barring") Voluntary exclusion from venues or online platforms Venues keep photo register to enforce exclusion Psychological Therapies Cognitive Behavioural Therapy (CBT) (strongest evidence) Corrects distorted beliefs (illusion of control, gambler’s fallacy) Behavioural strategies: Avoidance of triggers vs. controlled exposure Urge-control techniques Delivered via group or individual therapy through specialist gambling services Motivational Enhancement Therapy may also help Pharmacological Therapy No TGA-approved medication for gambling disorder in Australia Naltrexone (opioid antagonist) may be used off-label as adjunct therapy in severe cases Limited evidence for pharmacotherapy Managing Comorbidities Substance use disorder: Treat concurrently Mood/anxiety disorders: Consider CBT or medication if indicated Parkinson’s disease: Review dopamine agonists if compulsive gambling emerges Special Populations Aboriginal & Torres Strait Islander communities: Higher prevalence; require culturally sensitive approaches Young people: May not see gambling as problematic; address gaming/gambling overlap (e.g. loot boxes) Older adults: Risks include social isolation, cognitive decline, medication effects (dopamine agonists) Gambling Disorder According to the ICD-11, pathological gambling is conceptualised as: Hazardous gambling: Escalating behaviour that increases the risk of harm to the individual or others (but harm may not yet have occurred) Gambling disorder: Gambling leads to actual harm for the person or those close to them, and is characterised by: Impaired control (escalation of time, money, or venues). Increased priority given to gambling over other life areas. Persistence despite negative consequences. Risk Factors Early age of onset (adolescence). Family history of gambling disorder. Mental health conditions: Mood disorders, anxiety, personality disorders, and substance use disorders often co-occur. Aboriginal or Torres Strait Islander origin. Parkinson disease (possibly due to dopamine agonist use, eg pramipexole). Clinical Features and Harms Markers of escalation: Increasing frequency, higher bets, multiple venues, neglect of other life areas. Financial impacts: Mounting debts, inability to pay bills, or engaging in illegal activities (fraud/theft). Psychological distress: Comorbid depression, anxiety, substance misuse, and suicidal thoughts. Social consequences: Relationship conflict or breakdown, family violence, job loss. Screening and Assessment Routine Enquiry Given the high prevalence and significant stigma, it is recommended to: Ask routinely about gambling in new patients. Enquire opportunistically in ongoing patients, particularly if risk factors or suspicious presentations (eg financial stress, mood changes). Simple 2-Item Screening If a patient admits to gambling, consider: “In the past 12 months, have you been preoccupied with gambling or had a strong urge to gamble?” “In the past 12 months, have you often gambled longer, with more money, or more frequently than intended?” A “yes” to either suggests potential hazardous or disordered gambling. Adolescents (12–25 years) – Lie/Bet Questionnaire “Have you ever had to lie to people important to you about how much you gambled?” “Have you ever felt the need to bet more and more money?” A “yes” to either warrants further assessment. Further Evaluation Detailed history of gambling patterns (time, money, impulsivity). Psychosocial assessment (financial stress, relationship strain, mental health). Explore coexisting substance use or mental disorders. Use validated tools like the 9-item Problem Gambling Severity Index (PGSI) to grade severity. Management Principles Therapeutic Relationship Non-judgemental, collaborative approach. Provide hope by explaining that recovery is possible, although relapses can occur. Early Referral Encourage patients to use gambling support services (phone, online, or face-to-face). Seek specialist advice (via state-based gambling hotlines or referral systems) in complex cases. Long-Term Care Ongoing follow-up is crucial to address relapse, comorbid mental health, and lifestyle factors. Specific Management Strategies Brief Interventions Motivational interviewing: Elicit patient’s own concerns about gambling. Explore ambivalence and strengthen motivation for change. Small but significant short-term reduction in gambling behaviour is documented. Brief interventions can act as a gateway to more intensive therapy. Gambling Support Services Gambling hotlines and websites (e.g. Gambling Help Online, state-based helplines). They offer: Assessment of gambling behaviour. Practical support for money management and self-exclusion (“self-barring”) from venues or online gambling platforms. Referrals to financial counselling, peer support groups (e.g. Gambler’s Anonymous), and specialist therapy. Money Management Cancel credit cards or arrange finances to limit access to gambling funds. Banks may offer blocking of gambling transactions. Self-Barring Individuals can voluntarily exclude themselves from specific gambling venues or online sites. Venues keep a photo register to help enforce exclusion. Specialist Psychological Therapies Cognitive Behavioural Therapy (CBT) has the strongest evidence for reducing gambling frequency and improving outcomes. Addresses distorted beliefs (illusion of control, gambler’s fallacy). Teaches behavioural strategies: Avoidance of triggers vs. graded exposure (recognising triggers, controlling urges). Motivational Enhancement Therapy and extended motivational interviewing approaches are also beneficial. Group CBT or individual sessions can be used, often through specialist gambling services. Pharmacological Therapy No medication is TGA-approved for gambling disorder in Australia. Naltrexone (an opioid antagonist) may be used off-label by specialist services as an adjunct to therapy where other interventions have not succeeded. Evidence for pharmacotherapy remains limited. Comorbidities Substance use disorders (particularly alcohol) commonly co-occur; treat concurrently. Mood and anxiety disorders (assess and manage, potentially with psychological therapy and/or medication if indicated). Parkinson disease: consider careful review of dopaminergic medications if gambling behaviours arise. Self-Help Resources Online Self-Assessments: Gambling Help Online offers screening tools and immediate advice. Mobile Applications: The “Reset” app, “100 Day Challenge,” and “Gamble Less” help with motivational tracking and coping strategies. Peer Support Groups: Gambler’s Anonymous (in-person or online). These can be first-step interventions for patients reluctant to engage in formal treatment or those preferring anonymity. Special Populations Aboriginal and Torres Strait Islander Peoples Higher prevalence of gambling disorder. Tailored, culturally sensitive strategies recommended. Young People May not identify gambling as a problem. Lie/Bet questionnaire is useful for screening. Address gaming vs. gambling overlap (loot boxes, micro-transactions). Older Adults Risks include social isolation, cognitive decline, and certain medications (eg dopamine agonists). Follow-Up and Relapse Prevention Reinforce the therapeutic alliance; schedule regular reviews to monitor gambling behaviour, finances, and mental health. Address early warning signs of relapse: strong urges, changes in mood, or access to funds. Offer re-referral to support services or specialist therapy if the patient disengages or relapses. 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 Low Breast Milk Supply Symptoms Weight Gain: Birth weight not regained by 10–14 days Weekly gain: 150–200 g (0–3 mths), 100–150 g (3–6 mths), 70–90 g (6–12 mths) Wet Nappies: <5/day, dark urine, or uric acid crystals Dehydration: Fewer stools, dry mucosa Other Signs: Post-feed irritability, soft breasts Treatment Feeding: 2–3 hourly, wake infant if needed Feed both breasts; use compressions Support: Refer lactation consultant for latch/positioning Skin-to-skin contact for oxytocin release Maternal Care: Hydration, nutrition, rest Galactagogues: Domperidone 10 mg TDS if non-pharmacological measures fail Notes Monitor: 6–8 wet nappies/day, yellow stools by day 5 Avoid formula unless medically necessary Reassess: Weight gain, feeding progress Low Breast Milk Supply Definition Insufficient production of breast milk to meet an infant’s nutritional requirements, leading to inadequate weight gain and hydration issues Often a perception issue when breasts are less full as milk supply adjusts to demand Clinically assessed by monitoring infant weight gain and effective feeding Symptoms Poor weight gain: Failure to regain birth weight by 2 weeks postpartum Decreased wet nappies: Fewer than five per day, concentrated urine or presence of uric acid crystals Infant irritability after feeds and signs of dehydration such as dry mucous membranes Maternal reports of soft or less full breasts between feeds Treatment Increase breastfeeding frequency: Encourage feeding at least 12 times in 24 hours and wake the infant if necessary Optimise feeding technique: Ensure effective latch by feeding from both breasts at each session and using proper positioning and attachment Promote skin-to-skin contact: Enhances bonding and stimulates oxytocin release to increase milk production Adjust feeds according to demand: Feed on demand rather than strict schedules to maintain a proper supply-demand cycle Use of galactagogues: Consider domperidone 10 mg TDS if non-pharmacological measures fail, with caution in patients with cardiac history Consider supplemental feeding cautiously: Use expressed breast milk rather than formula unless medically indicated; paced bottle feeding may help if top-up feeds are required Address contributing factors: Manage maternal conditions such as hypothyroidism or anaemia, ensure proper maternal nutrition and hydration, and counsel on lifestyle modifications including avoiding smoking and excessive alcohol Additional Considerations Assess infant factors: Evaluate for ineffective suck due to congenital conditions (e.g., cleft palate) that may reduce milk transfer Recognise normal lactogenesis: Decreased breast fullness after the initial weeks is common and not necessarily a sign of low supply Encourage proper breast emptying: Express milk after feeds if necessary to stimulate further production Monitor weight gain: Infants should return to birth weight by 10–14 days and gain 150–200 g/week (0–3 months), 100–150 g/week (3–6 months), and 70–90 g/week (6–12 months) Educate on avoiding disruptive practices: Strict feeding schedules and unnecessary bottle top-ups can interfere with the supply-demand cycle Notes Maternal anxiety about low milk supply is common and often unwarranted if the infant is gaining weight appropriately Regular follow-up is essential to monitor weight gain, wet nappies, and overall feeding progress Multidisciplinary support from lactation consultants and breastfeeding counsellors can optimise outcomes Emphasis on maternal self-care and family support is vital, as stress can adversely affect milk production 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 Pompholyx (Dyshidrotic Eczema) Definition Vesicular hand & foot dermatitis, presenting with deep-seated vesicles or bullae Also called: Vesicular endogenous eczema Key Features: More common in young adults & females Linked to hyperhidrosis (excessive sweating of palms/soles) 50% have atopic eczema history Triggered by stress, humidity, sweating Aetiology & Risk Factors Genetics Irritants (water, detergents, friction) Nickel/allergen exposure Tinea (dermatophyte infections) Drug reactions (esp. immunoglobulin therapy) Clinical Features Recurrent crops of deep-seated blisters on palms/soles → intense itching/burning Blisters rupture → red, dry, cracked skin May involve: Paronychia (nail fold swelling) Nail dystrophy (pitting, ridges) Duration: Weeks, with frequent recurrences Differential Diagnosis Condition Key Features Palmoplantar Pustular Psoriasis Sterile pustules, scaling Contact Dermatitis History of irritant/allergen exposure Tinea Manuum/Pedis Asymmetric involvement, KOH positive Scabies Burrows, intense night itch Bullous Pemphigoid Elderly, widespread tense bullae Management General Measures Avoid triggers: Irritants, sweating, allergens Protective gloves during wet/dirty work Regular emollients to prevent dryness Potent antiperspirants (e.g., aluminium chloride) at night for palms/soles Pharmacological Treatment Drying agents: Potassium permanganate soaks Saltwater soaks Topical corticosteroids: Betamethasone dipropionate 0.05% cream (occlusive dressing for severe cases) Systemic steroids (for severe cases): Oral prednisolone 25 mg OD x 3–4 days, taper over 2–3 weeks Notes: Recurrent vesicular rash on hands/feet? Think dyshidrotic eczema! Strong link with hyperhidrosis, stress, and humidity Avoid irritants, use emollients & protective gloves Topical steroids first-line, oral steroids for severe cases Pompholyx (Dyshidrotic Eczema) Definition A vesicular hand and foot dermatitis presenting with deep-seated vesicles or bullae on the palms and soles. Also called vesicular endogenous eczema. Key Features More common in young adults and females Often linked to hyperhidrosis (excessive sweating) ~50% have a history of atopic eczema Triggered by stress, humidity, sweating Aetiology & Risk Factors Genetics Irritants: Prolonged contact with water, detergents, friction Nickel/Allergen Exposure: Common allergic trigger for hand dermatitis Tinea (dermatophyte infections): May incite an id reaction Drug Reactions (e.g., immunoglobulin therapy in rare cases) Clinical Features Recurrent crops of deep-seated blisters on palms/soles → intense itching/burning Blisters rupture → red, dry, cracked skin prone to secondary infection May involve: Paronychia (nail fold swelling) Nail dystrophy (pitting, ridges) Duration: Weeks, often with frequent recurrences Differential Diagnosis Condition Key Features Palmoplantar Pustular Psoriasis Sterile pustules, possible scaling, psoriasis hx Contact Dermatitis Irritant/allergen exposure history Tinea Manuum/Pedis Asymmetric involvement, KOH positive Scabies Burrows, intense nocturnal pruritus Bullous Pemphigoid Tense bullae, often elderly, widespread Management General Measures Avoid Triggers: Limit exposure to water, detergents, allergens, friction Protective Gloves for wet/dirty tasks Regular Emollients to prevent dryness, cracking Potent Antiperspirants (e.g. aluminium chloride) applied at night for hyperhidrosis Pharmacological Treatment Drying Agents: Potassium permanganate soaks, saltwater soaks for acute vesicular eruptions Topical Corticosteroids: e.g. Betamethasone dipropionate 0.05% cream Use under occlusive dressing for severe or recalcitrant lesions Systemic Steroids (severe cases): Oral prednisolone 25 mg daily for 3–4 days, then taper over 2–3 weeks Notes Recurrent vesicular rash on hands/feet → suspect dyshidrotic eczema. Strong link with hyperhidrosis, stress, and high humidity. Avoid irritants, maintain emollients, use protective gloves. Topical steroids are first-line, oral steroids for severe flares. 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 Mallet Finger Types Tendinous: Extensor tendon disruption, no fracture on XR Bony: Avulsion fracture of the dorsal distal phalanx Management Conservative: Splinting: DIP in full extension, PIP free, 6 weeks continuous wear (even at night) Restart splinting if DIP flexes during the period Indications for Splint Alone: No volar subluxation Bony involvement <30% of articular surface Preserved passive extension Surgical Referral: 30% articular surface involvement Inability to maintain passive extension Volar subluxation or high functional demand Timing of Referral Refer within 7 days for assessment Low threshold for diagnostic/management uncertainty Key Notes Continuous splinting is critical for success Hand therapy post-splinting for functional recovery Mallet Finger Types Tendinous: Extensor tendon disruption, no fracture on XR Bony: Avulsion fracture of the dorsal distal phalanx Clinical Features Pain and swelling at the DIP joint Inability to actively extend the DIP joint while passive extension is preserved Often occurs after forced flexion of an extended finger (e.g., catching a ball) Management Conservative Splinting: DIP in full extension, PIP free, 6–8 weeks continuous wear (including at night) If DIP flexes at any point, restart the splinting period After the initial phase, night-time splinting may be continued for an additional 2–4 weeks to prevent recurrence Indications for Splint Alone: No volar subluxation Bony involvement <30% of the articular surface Preserved passive extension No significant gap between bone fragments on imaging Surgical Referral 30% articular surface involvement Inability to maintain passive extension Volar subluxation of the distal phalanx High functional demand (e.g., athletes, manual workers) Large displaced bony fragment or joint malalignment Timing of Referral Refer within 7 days for assessment Low threshold for referral in cases of diagnostic uncertainty, joint instability, or failure of conservative management Key Notes Continuous splinting is critical for success Hand therapy post-splinting for functional recovery, focusing on DIP joint mobility and strengthening Late presentation can still be treated conservatively, but prolonged splinting may be required Monitor for complications such as extensor lag or stiffness 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 Hypercholesterolaemia Secondary Causes Most Common: Excessive alcohol intake (↑ TGs); Diabetes Other Causes Hypothyroidism Nephrotic syndrome Cholestatic or chronic liver disease Obesity Pharm Management 1st Line High-intensity statins: Atorvastatin 40–80mg OD Rosuvastatin 20–40mg OD Statins remain the cornerstone for LDL-C reduction and cardiovascular risk reduction 2nd Line Ezetimibe 10mg OD: Reduces cholesterol absorption; used as monotherapy if statins are not tolerated Fibrates: Stimulate PPAR-alpha to reduce TGs and mildly reduce LDL while increasing HDL Fenofibrate 145mg OD: Preferred fibrate Consider in combination with statins if TG >4mmol/L, especially if HDL <1mmol/L Dose reduction required for eGFR 20–60 (96mg OD) and eGFR 10–20 (48mg OD) Also used in diabetic retinopathy treatment Bile Acid Binding Resins (e.g., cholestyramine 4–8g OD): Effective for cholesterol reduction but avoid in elevated TGs as they increase TG levels Note: TGs >10mmol/L significantly increase the risk of pancreatitis; fibrates or fish oils are preferred for initial management of severe hypertriglyceridaemia Non-Pharm Management Increase intake of plant sterol-enriched foods (milk, margarine, cheese): Can reduce LDL-C by ~15% Increase soluble fibre intake (e.g., oats, legumes) Reduce saturated fats (and avoid trans fats) Replace saturated fats with monounsaturated and polyunsaturated fats (e.g., nuts, olive oil, fish) Notes TG-lowering focus: Severe hypertriglyceridaemia (>10mmol/L) warrants urgent management to prevent pancreatitis Combination therapy: Statins can be safely combined with ezetimibe or fibrates (except gemfibrozil, due to rhabdomyolysis risk) Hypercholesterolaemia Secondary Causes Common: Excess alcohol (↑ triglycerides) Diabetes mellitus (dyslipidaemia) Other: Hypothyroidism, nephrotic syndrome, chronic liver disease, obesity Pharmacological Management First-Line High-intensity statins (first choice for LDL-C reduction & CVD risk reduction) Atorvastatin 40–80 mg once daily Rosuvastatin 20–40 mg once daily Second-Line (if LDL-C targets unmet or statin intolerance) Ezetimibe 10 mg once daily (↓ cholesterol absorption; monotherapy or add-on) Fibrates (↓ triglycerides, modest LDL-C reduction, ↑ HDL-C) Fenofibrate 145 mg once daily (adjust for renal impairment) Bile Acid Binding Resins (e.g., Cholestyramine 4–8 g once daily) Avoid in hypertriglyceridaemia (may ↑ TG levels) Non-Pharmacological Management Dietary Modifications Plant sterols (fortified milk, margarine, cheese) → ~15% LDL-C reduction Soluble fibre (oats, legumes) Reduce saturated & trans fats; replace with monounsaturated & polyunsaturated fats (nuts, olive oil, fish) Lifestyle Modifications Exercise: ≥150 min moderate-intensity/week Weight management Limit alcohol, avoid smoking Notes: Triglyceride Management (if TG >10 mmol/L to prevent pancreatitis) Fibrates or omega-3 fatty acids (first-line) Combination Therapy Statins + ezetimibe or fibrates may be used Avoid gemfibrozil + statins (↑ rhabdomyolysis risk) 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 Seizure Acute Pharmacological Treatment When to treat: Start treatment if seizure lasts >5 min or if seizures recur without full recovery. First-line (Midazolam): Adults: 10 mg IM (if >40 kg) or 5 mg IM (if <40 kg) Alternatives: IV (10 mg over 2 min), intranasal, or buccal Paediatrics: 0.2 mg/kg IV, IM, buccal, intranasal If seizure persists: Repeat midazolam once after 5 min OR Second-line: IV phenytoin/fosphenytoin, valproate, or levetiracetam Key considerations: Check blood glucose early; correct hypoglycaemia promptly Non-Pharmacological Management No driving: 6 months (private), 5 years (commercial) Max alcohol: 2 drinks/day Notify employer Optimise sleep hygiene No unsupervised swimming Avoid illicit substances & antihistamines Relaxation therapies Plan pregnancy (consider depot or Mirena) Refer for EEG Risk: 50% recurrence after first unprovoked seizure Household education on seizure first aid Shower instead of bath if alone Seizure – First Episode Differentials Seizure-related: First presentation epilepsy, psychogenic non-epileptic seizure (PNES) Syncopal causes: Cardiac (arrhythmia), vasovagal, postural Neurological: Bleed, infection, tumour, stroke, basilar migraine, narcolepsy Metabolic: Hypoglycaemia, hypo/hypernatremia, hypo/hyperkalaemia, hypomagnesaemia Other: Drug/alcohol intoxication or withdrawal, hyperventilation attack, conversion disorder Always exclude correctable metabolic causes – check serum electrolytes, including magnesium. History Prior similar attacks Urinary incontinence/tongue biting Emotional triggers Palpitations before event Substance use Headaches Anxiety/recent stressors Head injury Family history of seizures Examination Track marks Alcohol smell Pupil abnormalities Meningism Tongue laceration Fever Arrhythmia Notes: HLA-B*1502 screening (Han Chinese & SE Asians) before carbamazepine (SJS risk) Brain tumour suspicion: Dull, constant bifrontal headache, unilateral predominance, nocturnal, wakes patient, worsened by Valsalva PNES clues: Anxiety, PTSD, psychosis, substance abuse Seizure features suggesting immediate treatment: History of absence, myoclonic, focal seizures, or aura Urgent neuroimaging if: Focal onset, abnormal exam, or first seizure in patient >25 years Seizures Acute management of prolonged seizure According to Therapeutic Guidelines, immediate treatment is indicated if A seizure lasts longer than 5 minutes, or Seizures recur without full recovery of consciousness between events First-line pharmacological treatment Midazolam is recommended as first-line benzodiazepine treatment Adults ≥40 kg: 10 mg IM <40 kg: 5 mg IM Alternative routes: IV (10 mg over 2 minutes), intranasal, or buccal Paediatric dose 0.2 mg/kg IV, IM, buccal, or intranasal If the seizure continues beyond 5 minutes after the first dose of midazolam Repeat midazolam (one additional dose), or Proceed to second-line agents IV phenytoin/fosphenytoin IV valproate IV levetiracetam Key considerations during acute seizure Check blood glucose early: Hypoglycaemia must be corrected promptly Ensure a safe environment: Position the patient to avoid injury, loosen tight clothing, protect the airway, and do not place objects in their mouth Non-pharmacological and long-term management Driving restrictions In Australia, driving regulations for patients with seizure are enforced through the Austroads guidelines, also reflected in RACGP recommendations. Generally Private vehicle licence: No driving for 6 months if a patient has had a seizure Commercial licence: No driving for 5 years Always advise patients to inform the local driving authority if they experience any seizure activity Lifestyle modifications Alcohol: Limit to a maximum of 2 standard drinks per day (though individual advice may vary based on overall risk) Substances: Avoid illicit drugs and caution with sedating medications (e.g. antihistamines) Sleep hygiene: Encourage regular sleep patterns and adequate rest Swimming/bathing: Recommend supervised swimming; advise showering rather than bathing if alone, to reduce the risk of drowning in case of a seizure Stress reduction: Relaxation therapies, mindfulness, and other stress-management techniques Family/household education: Train family members or housemates in seizure first aid Occupational considerations: Advise to notify their employer if safety at work could be compromised Contraception and pregnancy planning Contraceptive choices: Depot medroxyprogesterone injection or levonorgestrel intrauterine device (Mirena) may be preferable when avoiding interactions with enzyme-inducing antiepileptics Pre-pregnancy planning: Women with epilepsy should seek preconception counselling, as certain antiepileptic drugs carry teratogenic risks Referral and further investigations EEG (electroencephalogram): Often indicated in new-onset suspected epilepsy or if the clinical picture is unclear Neuroimaging: Urgent imaging (CT or MRI) if Seizure has a focal onset Abnormal neurological examination First seizure occurs in a patient over 25 years of age (to exclude intracranial pathology) Neurologist referral: If recurrent seizures, diagnostic uncertainty, or concern for complex comorbidities Seizure – first episode When encountering a first seizure in general practice, consider the broad range of differentials and always exclude correctable metabolic or structural causes Differential diagnosis Seizure-related First presentation of epilepsy Psychogenic non-epileptic seizure (PNES) Syncope Cardiac: Arrhythmias, structural heart disease Vasovagal (common faint) Postural (orthostatic) hypotension Neurological Intracranial bleed (subarachnoid, intracerebral) CNS infection (meningitis, encephalitis) Tumour Stroke or transient ischaemic attack Basilar migraine Narcolepsy (rare mimic) Metabolic Hypoglycaemia Hypo/hypernatraemia Hypo/hyperkalaemia Hypomagnesaemia Other Drug/alcohol intoxication or withdrawal Hyperventilation attack Conversion disorder Investigations for first seizure Serum electrolytes, including magnesium Blood glucose (capillary and serum) Full blood count, renal function, liver function tests Possibly toxicology screen if clinical suspicion History and examination Key historical features Prior similar events or childhood seizures Event description: Witness accounts, urinary incontinence, tongue biting Triggers: Emotional stress, sleep deprivation, flashing lights Precipitating factors: Palpitations (cardiac cause), substance use, recent head trauma Associated symptoms: Headaches, confusion, focal neurological signs Family history: Seizures or epilepsy Psychosocial: Anxiety, recent stressors, history of psychological trauma (may point to PNES) Examination findings General: Look for track marks (IV drug use), smell of alcohol Vital signs: Fever (possible infection), arrhythmias Neurological: Pupil abnormalities, meningism, focal deficits Tongue laceration: Suggestive of a generalised convulsive event Integument: Injuries consistent with a fall or convulsion 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 Herpetic Whitlow Definition Painful HSV infection of fingers or thumbs Often due to autoinoculation from oral or genital herpes Vesicular or pustular presentation Aetiology Autoinoculation from oral/genital HSV Direct inoculation from external sources HSV-1 (60%), HSV-2 (40%) Clinical Features Local swelling, itching, burning Clear/turbid vesicles, crusting over time Prodromal fever or malaise may occur Differential Diagnosis Paronychia Hand-foot-and-mouth disease Management Same antivirals as severe oral herpes Children >3 months: Aciclovir 10 mg/kg PO 5× daily x 5–7 days Pain relief: Topical/oral analgesics Severe cases: Aciclovir or valaciclovir Herpetic Whitlow Definition Herpetic whitlow is a painful HSV infection affecting the fingers or thumbs, often arising from autoinoculation of the virus (commonly HSV-1 or HSV-2) from an existing oral or genital herpes lesion. It typically presents with vesicular or pustular lesions on the distal phalanx. Aetiology Autoinoculation from existing oral/genital herpes (e.g. lip cold sores, genital sores) Direct inoculation from external sources (e.g. contact with someone else’s active HSV lesion) HSV-1 accounts for about 60% of cases, HSV-2 about 40% Clinical Features Local Swelling, Itching, Burning: Prodromal sensation before vesicles appear Clear/Turbid Vesicles over the affected fingertip area, possibly crusting with time Prodromal Fever or Malaise may occur in more significant infections Lesions can be quite painful, leading to difficulty in using the affected finger Differential Diagnosis Paronychia (infection of the nail fold, often bacterial) Hand-Foot-and-Mouth Disease (Coxsackie virus) – typically also with oral lesions and foot involvement Management Antiviral Therapy (similar approach as for severe or complicated HSV infections): Children ≥3 months: Aciclovir 10 mg/kg orally, five times daily for 5–7 days Adults with moderate–severe herpetic whitlow: Aciclovir (e.g. 200 mg five times daily) or Valaciclovir (e.g. 1 g BD) for 5–7 days Pain Relief: Topical anaesthetics (e.g. lignocaine gel) or systemic analgesics (NSAIDs, paracetamol) General Care: Keep the area clean, cover with a light dressing if needed, avoid picking or squeezing vesicles to prevent secondary bacterial infection Notes Prevent autoinoculation: Educate patients with cold sores/genital HSV to avoid touching lesions or to wear gloves if contact is unavoidable (e.g. healthcare workers). Consider that herpetic whitlow may recur if patients have recurrent HSV episodes. If infection is severe or complicated, or if immunocompromised, consult specialist advice or consider IV aciclovir. 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 Mesenteric Adenitis Presentation Cause: Often follows viral URTI or tonsillitis (Yersinia enterocolitica possible) Symptoms: RLQ pain, less localised than appendicitis, no rebound tenderness Mild fever, nausea, anorexia (less severe than appendicitis) May include cervical lymphadenopathy or pharyngitis Progression Resolves in 3–5 days without residual effects Red Flags: Persistent pain, fever, or generalised tenderness → exclude appendicitis Management Symptomatic: Hydration (oral/IV), paracetamol or ibuprofen for pain Avoid antibiotics unless bacterial cause confirmed Monitor: Ensure improvement; follow up if worsening Differentiating from Appendicitis Mesenteric Adenitis: Less localised pain, higher fever, milder rigidity Associated with recent URTI/pharyngitis Appendicitis: Generalised tenderness or peritonitis → urgent surgical review Notes US: Consider to exclude appendicitis if uncertain Common in children/adolescents but possible at any age Educate parents to seek care for worsening pain, fever, or vomiting Mesenteric Adenitis Definition Inflammation or infection of mesenteric lymph nodes in the abdomen Often follows a viral URTI or tonsillitis; bacterial causes such as Yersinia enterocolitica may be involved Common in children and adolescents, though it can occur at any age Presentation Right lower quadrant pain that is less localised than in appendicitis and may shift in location Mild fever, nausea, and anorexia that are generally less severe than with appendicitis May be associated with cervical lymphadenopathy or pharyngitis following a recent infection Typically self-limiting with resolution in 3–5 days without residual effects Differential Diagnosis Appendicitis More localized RLQ pain with rebound tenderness and peritonitis Typically lacks a preceding URTI Gastroenteritis Diffuse abdominal pain accompanied by diarrhoea and vomiting Intussusception Colicky pain with red currant jelly stools and a palpable abdominal mass Pelvic inflammatory disease (in females) Lower abdominal pain with associated vaginal discharge Urinary tract infection Fever, dysuria, and malodorous urine Other causes such as inflammatory bowel disease or mesenteric adenitis secondary to Yersinia infection Investigations Abdominal ultrasound Visualises enlarged mesenteric lymph nodes and helps exclude appendicitis Blood tests Full blood count may reveal mild leucocytosis; CRP can be mildly elevated Additional imaging (CT scan) is rarely required unless the diagnosis remains uncertain Urinalysis To exclude urinary tract infection as a cause of abdominal pain Management Symptomatic treatment with rest and adequate hydration Provide analgesia and antipyretics such as paracetamol or ibuprofen Avoid antibiotics unless there is clear evidence of a bacterial infection Observation and follow-up to ensure improvement; re-evaluate if symptoms persist or worsen beyond 3–5 days Differentiating from Appendicitis Mesenteric adenitis presents with more diffuse, less localized RLQ pain and milder abdominal rigidity Often preceded by an upper respiratory tract infection or pharyngitis Appendicitis typically shows localized tenderness, rebound, and signs of peritonitis requiring urgent surgical review Notes Diagnosis is primarily clinical and made by exclusion once appendicitis and other serious causes are ruled out Educate caregivers to monitor for worsening symptoms such as persistent fever, increasing pain, or vomiting Follow-up is essential to confirm resolution and to manage any complications promptly Mesenteric adenitis is self-limiting and usually resolves without long-term sequelae 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 Nephrotic Syndrome Pathophysiology Glomerular damage → massive proteinuria (>3.5 g/day) Hypoalbuminaemia → oedema Hyperlipidaemia → compensatory hepatic lipid synthesis Hypercoagulability → urinary loss of antithrombin III, protein C/S Causes DM, SLE, amyloidosis cause 1/3 cases Other inc IgA nephropathy, minimal change disease (most common kids), membranous nephropathy (most common adults), focal segmental glomerulosclerosis, HIV Clinical Presentation Severe oedema: Periorbital, lower limb, anasarca Foamy urine: Proteinuria Dyspnoea: Pulmonary oedema, pleural effusion Underlying disease features: Rash, arthralgia (SLE) Peripheral neuropathy (amyloidosis, diabetes) Hepatosplenomegaly (amyloidosis, chronic infection) Key Lab Features Proteinuria >3.5 g/day (ACR >300 mg/mmol) Hypoalbuminaemia <25 g/L Hyperlipidaemia Hypercoagulability: ↑ risk of DVT/PE ↑ Infection risk: Loss of IgG, impaired immune response Investigations Initial Workup: UEC: Renal function, creatinine clearance Urine MCS: Exclude infection, check casts Urine PCR/ACR or 24-hour protein: Quantify proteinuria LFTs: Hypoalbuminaemia, rule out liver disease Lipid profile: Assess hyperlipidaemia Coagulation studies: Hypercoagulability risk Identify Underlying Cause: ANA, C3/C4: SLE HbA1c, fasting glucose: Diabetes Urine Bence-Jones proteins, protein electrophoresis: Amyloidosis, myeloma Hepatitis B/C serology, HIV test: Viral nephropathies Imaging: Renal US: Chronic changes, renal vein thrombosis Definitive Diagnosis: Renal biopsy (gold standard, except in clear diabetic nephropathy) Management General Measures: ACEi/ARBs: Reduce proteinuria, target BP <130/80 Fluid restriction, low salt diet, daily weights Pharmacological: Diuretics: Loop ± spironolactone for oedema Statins: If persistent dyslipidaemia Aspirin: If high atherosclerotic risk (e.g., diabetes, previous MI/stroke) Immunosuppression: Prednisolone: First-line for MCD, FSGS, lupus nephritis Cyclophosphamide/calcineurin inhibitors (tacrolimus, cyclosporine): Steroid-resistant cases Infection & Thrombosis Prevention: Vaccination: Influenza, pneumococcal, hepatitis B Prophylactic antibiotics: If recurrent infections Anticoagulation: If albumin <20 g/L or history of DVT/PE Key Notes MCD: Most common in children, steroid-responsive Membranous nephropathy: Most common in adults, linked to malignancy/infection ACEi/ARBs: Essential for reducing proteinuria, slowing progression High risk of infections & thrombosis → Monitor closely Renal biopsy needed unless clear secondary cause (e.g., diabetes) Nephrotic Syndrome Pathophysiology Glomerular injury leading to massive proteinuria (>3.5 g/day) Hypoalbuminaemia due to urinary loss of protein → oedema Hyperlipidaemia due to compensatory hepatic lipid synthesis Hypercoagulability from loss of antithrombin III, protein C, and protein S in urine Causes Diabetes, SLE, Amyloidosis: Account for ~⅓ of cases (secondary causes) Primary Glomerular Diseases: Minimal Change Disease (MCD): Most common in children; typically steroid-responsive Membranous Nephropathy: Most common in adults; can be linked to malignancy, infections, autoimmune Focal Segmental Glomerulosclerosis (FSGS): May be idiopathic or secondary (obesity, HIV) IgA Nephropathy: More commonly nephritic, but can have nephrotic-range proteinuria HIV-Associated nephropathy Clinical Presentation Severe Oedema: Periorbital (in mornings), lower limb, anasarca Foamy Urine: Due to proteinuria Dyspnoea: Secondary to fluid overload (pulmonary oedema, pleural effusions) Features of underlying disease: e.g. rash/arthralgia (SLE), neuropathy (amyloidosis/diabetes), hepatosplenomegaly (amyloidosis) Key Lab Features Proteinuria >3.5 g/day (ACR >300 mg/mmol) Hypoalbuminaemia <25 g/L Hyperlipidaemia (high LDL, triglycerides) Hypercoagulability → ↑ risk of DVT/PE ↑ Infection Risk: Loss of immunoglobulins (IgG) in urine Investigations Initial Workup UEC: Assess renal function Urine MCS: Exclude infection; check for casts Urine PCR/ACR or 24-hour protein: Quantify proteinuria LFTs: Assess hypoalbuminaemia, exclude liver disease Lipid Profile: Evaluate hyperlipidaemia Coagulation Studies: Risk of thrombosis Identify Underlying Cause Autoimmune: ANA, C3/C4 (SLE) Diabetes: HbA1c, fasting glucose Paraproteins: Serum/urine electrophoresis for amyloidosis or multiple myeloma Hepatitis B/C, HIV serologies Renal Ultrasound: Rule out structural issues, detect possible renal vein thrombosis Renal Biopsy: Definitive diagnosis unless a clear secondary cause (e.g. longstanding diabetes with typical changes) Management General Measures ACE Inhibitors / ARBs: Reduce proteinuria, target BP <130/80 mmHg Salt & Fluid Restriction if oedema is significant Daily Weights: Track fluid overload Diuretics (loop ± spironolactone) for volume management Statins if persistent dyslipidaemia or high cardiovascular risk Aspirin for atherosclerotic risk if indicated (e.g., diabetes, prior MI/stroke) Immunosuppression (if primary GN or immune-mediated): Corticosteroids: First-line in minimal change, can be used in FSGS, SLE nephritis Cyclophosphamide / Calcineurin Inhibitors (cyclosporine, tacrolimus) for steroid-resistant or relapsing cases Mycophenolate Mofetil: Alternative in some glomerulopathies Infection & Thrombosis Prevention Vaccinations: Influenza, pneumococcal, hepatitis B Prophylactic Antibiotics if recurrent infections or significant immunosuppression Anticoagulation: Consider if albumin <20 g/L or history of DVT/PE Notes Minimal Change Disease: Common in children, highly steroid-responsive Membranous Nephropathy: Most frequent adult cause, often associated with malignancies/infections/autoimmune ACE/ARB therapy is essential to slow progression and reduce proteinuria Patients have high risk of infections & thrombosis → monitor carefully Renal Biopsy needed for definitive diagnosis unless the cause is clearly secondary (longstanding T2DM with typical features) 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 Perianal Streptococcal Dermatitis Presentation Common in children, rare in adults Bright red, well-defined perianal rash Itching, tenderness, burning, bleeding, mucoid discharge, painful defecation Often linked to recent streptococcal throat or skin infection Diagnosis Perianal swab: MCS confirms Group A Streptococcus (GAS) Rule out: Pinworms: Tape test Candidiasis: More common in infants Irritant dermatitis: Soaps, poor hygiene Management Antibiotics Cefalexin: 25 mg/kg (max 1 g) BD for 10 days Penicillin allergy: Clindamycin or azithromycin (seek specialist advice) Supportive Care Gentle cleansing with warm water Barrier cream (e.g., zinc oxide) Reassess if no improvement Prevention Handwashing to prevent recurrence Treat symptomatic household streptococcal infections Notes Follow-up: Confirm resolution, especially in persistent cases Mimics other conditions: Consider alternative diagnoses if unclear Perianal Streptococcal Dermatitis Definition Bacterial infection of the perianal skin caused by Streptococcus pyogenes (Group A Streptococcus) Primarily affects young children, with rare occurrence in adults Presents as a sharply demarcated erythematous rash around the anus Presentation Bright red, well-defined rash around the perianal region Symptoms include itching, tenderness, burning, and pain during defaecation May be associated with mucoid or purulent discharge and minor bleeding Often follows a recent episode of streptococcal pharyngitis or skin infection Can be accompanied by perineal discomfort and, in some cases, mild systemic symptoms Differential Diagnosis Pinworms: Rule out with a tape test if perianal itching is prominent Candidiasis: Common in infants, characterised by satellite lesions and a red rash Irritant dermatitis: Due to soaps, wipes or poor hygiene Contact dermatitis: Reaction to topical agents or detergents Other bacterial infections: Consider if atypical features are present Diagnosis Perianal swab for bacterial culture and sensitivity (MCS) to confirm Group A Streptococcus Clinical examination focusing on the distribution and character of the rash Rule out alternative causes such as fungal infection or irritant dermatitis through history and appropriate tests Management Antibiotic Therapy Oral cephalexin at 25 mg/kg up to a maximum of 1 g, administered twice daily for 5–10 days depending on severity In cases of penicillin allergy, consider clindamycin or azithromycin with specialist advice Supportive Measures Gentle cleansing of the perianal area with warm water and soap-free cleansers Application of a barrier cream, such as zinc oxide, to protect the skin Follow-Up Monitor for symptom resolution and ensure adherence to the prescribed antibiotic regimen Re-evaluate if there is no improvement or if symptoms persist beyond the treatment period Prevention Educate caregivers on the importance of regular handwashing and proper perianal hygiene Advise on thorough cleaning after defaecation to minimise residual bacterial contamination Treat symptomatic household members with strep infections to prevent recurrence Encourage prompt medical review for any new or worsening perianal symptoms Additional Notes Early recognition and treatment are essential to prevent complications such as secondary bacterial infection The condition may mimic other perianal dermatoses, so a high index of suspicion is required Reinforce that perianal streptococcal dermatitis is usually self-limiting with appropriate antibiotic therapy Routine follow-up helps confirm resolution and identify any recurrent or resistant cases promptly 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 Hyperlipidaemia Causes Primary: Genetic factors (e.g., familial hypercholesterolaemia) Secondary: Diabetes Excessive alcohol consumption Hypothyroidism Liver or renal disease Obesity Certain medications (e.g., thiazide diuretics) Symptoms Generally asymptomatic Severe hypertriglyceridaemia (>10 mmol/L) may cause pancreatitis Differential Diagnosis Hypothyroidism Uncontrolled diabetes Alcohol-related liver disease Investigations Lipid Profile: Total cholesterol LDL-C HDL-C Triglycerides Additional Tests: Thyroid function tests Liver function tests Renal function tests HbA1c for diabetes screening Management Exclude Secondary Causes: Manage underlying contributors (e.g., diabetes) Pharmacological: Statins: First-line for CVD risk reduction (e.g., atorvastatin 40–80 mg) Ezetimibe: Add if LDL-C targets are unmet Fibrates: For triglycerides >4 mmol/L; caution with renal impairment Fish Oils: For severe hypertriglyceridaemia Non-Pharmacological: Increase fibre intake Reduce saturated fats Regular exercise Weight loss Limit alcohol consumption Complications Cardiovascular events (MI, stroke) Pancreatitis with high triglycerides Hyperlipidaemia Aetiology/Causes Primary Causes: Genetic predispositions (e.g., familial hypercholesterolaemia) Secondary Causes: Excessive alcohol intake: Raises TG levels Diabetes: Poorly controlled diabetes often results in elevated TG Hypothyroidism Nephrotic syndrome Cholestatic or chronic liver disease Obesity Certain medications (e.g., thiazide diuretics, beta-blockers, oral oestrogens, atypical antipsychotics) Pathophysiology Elevated LDL-C and triglycerides contribute to the formation of atherosclerotic plaques, increasing the risk of coronary artery disease, stroke, and peripheral vascular disease. Low HDL-C further exacerbates CVD risk due to its role in reverse cholesterol transport. Symptoms and Examination Findings Symptoms: Generally asymptomatic Severe hypertriglyceridaemia (>10 mmol/L) may cause pancreatitis Examination Findings: Xanthelasma: Yellowish deposits on the eyelids Arcus cornealis: Greyish-white ring around the cornea Tendon xanthomas: Nodules on tendons (Achilles, hands) indicating familial hypercholesterolaemia Differential Diagnosis Primary lipid disorders Hypothyroidism Uncontrolled diabetes Alcohol-related liver disease Investigations Lipid Profile Testing: Measures total cholesterol, HDL-C, LDL-C, and TG Use fasting sample to accurately assess TG if elevated Other Tests: Thyroid function tests (TFTs) to rule out hypothyroidism Liver function tests (LFTs) for underlying liver disease Renal function tests to evaluate nephrotic syndrome HbA1c for diabetes screening Management Algorithm Exclude Secondary Causes: Identify and manage conditions contributing to elevated lipids Assess Absolute CVD Risk: Estimate the 5-year CVD risk to guide treatment intensity Pharmacological Management: Statins: First-line therapy for CVD risk reduction High-Intensity Doses: Atorvastatin (40–80 mg) or Rosuvastatin (20–40 mg) Indications: All patients with established CVD or high CVD risk Ezetimibe (10 mg daily): Add-on if LDL-C targets are unmet with statin monotherapy PCSK9 Inhibitors (e.g., Evolocumab): For familial hypercholesterolaemia or uncontrolled lipid levels on other therapies Fibrates: Effective for lowering TG, particularly when >4 mmol/L Dosage Adjustment: Based on renal function (eGFR) Combination Therapy: Use with statins when TG remains elevated Fish Oils: 2–4 g/day for TG reduction in severe cases Bile Acid Binding Resins: Avoid in high TG due to risk of further elevation Non-Pharmacological Management: Dietary Changes: Increase intake of plant sterols Reduce saturated fats; replace with monounsaturated or polyunsaturated fats Soluble fibre (e.g., oats, psyllium) Exercise: At least 30 minutes, five times weekly Weight Loss: Particularly if overweight or obese Limit Alcohol Consumption: Reduces TG levels Smoking Cessation Treatment Targets LDL-C: <2.0 mmol/L (primary prevention); <1.8 mmol/L (secondary prevention) Non-HDL-C: <2.5 mmol/L TG: <2.0 mmol/L HDL-C: >1.0 mmol/L Complications Cardiovascular events (e.g., myocardial infarction, stroke) Pancreatitis with high triglycerides Atherosclerosis Prognosis Long-term outcomes are significantly improved with adequate lipid management and lifestyle changes, reducing the risk of cardiovascular events. Notes Diabetes and Hypertriglyceridaemia: Control of diabetes can rapidly reduce TG levels Statin Use in High TG: Statins can be used in combination with fibrates to lower CVD risk, even if TG reduction is modest Monitoring: No routine CK 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 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