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 Erythrasma Definition Superficial bacterial skin infection, often in skin folds (axillae, groin, between toes) Hyperpigmented, thin patches Wood’s lamp: Coral-pink fluorescence Aetiology & Causes Corynebacterium minutissimum (Gram-positive, non-spore-forming) Often mistaken for fungal infections (tinea, Candida) Risk Factors Warm climates Excessive sweating Skin of colour Diabetes, obesity, poor hygiene Advanced age Clinical Features Well-defined pink/brown patches with fine scaling ± superficial fissures Sites: Axillae, groin, between toes Mild itching possible Diagnosis Wood’s lamp: Coral-pink fluorescence (porphyrin production) Microscopy (Gram/methylene blue stain): Identifies C. minutissimum Management Topical Treatment (First-Line) Fusidic acid 2% ointment BD x 2 weeks Whitfield’s ointment Oral Treatment (If Extensive) Clarithromycin 1g stat Erythromycin or tetracycline Other Options Photodynamic therapy (red light) Prevention Antibacterial soap to prevent recurrence Repeat treatment as needed Erythrasma Definition Erythrasma is a superficial bacterial skin infection typically found in skin folds (e.g. axillae, groin, interdigital spaces). It presents as hyperpigmented, thin patches that may be mistaken for fungal infections. Under a Wood’s lamp, erythrasma demonstrates a characteristic coral-pink fluorescence. Aetiology & Causes Caused by Corynebacterium minutissimum (Gram-positive, non-spore-forming bacillus). Commonly misdiagnosed as tinea or candidal infection due to similar rash patterns. Risk Factors Warm, humid climates Excessive sweating (hyperhidrosis) Skin of colour (hyperpigmentation more evident) Diabetes, obesity, poor hygiene Advanced age (compromised skin barrier) Clinical Features Well-demarcated pinkish-brown patches with fine scaling; can sometimes have superficial fissures. Usually mildly pruritic or asymptomatic, though some patients report mild itch or discomfort. Common sites: Axillae Groin (inguinal folds) Interdigital spaces (especially between the 4th and 5th toes) Submammary folds in women May co-exist with fungal infections (e.g. tinea). Diagnosis Wood’s Lamp Examination: Coral-pink fluorescence due to porphyrin production by C. minutissimum. Microscopy: Gram stain or methylene blue stain can identify C. minutissimum. Differential: Tinea cruris, intertrigo (candida), inverse psoriasis. Further Assessments: Check for underlying risk factors like diabetes if recurrent or extensive. Management Topical Treatment (First-Line) Fusidic Acid 2% Ointment BD for 2 weeks Whitfield’s Ointment (benzoic acid and salicylic acid) can also be used Alternatives: Topical clindamycin or erythromycin if fusidic acid is unavailable Oral Treatment (If Extensive or Recurrent) Clarithromycin 1 g stat (single dose) Erythromycin or Tetracycline (doxycycline) for 7–14 days if needed Oral therapy is particularly beneficial in widespread disease or if topical therapy fails Other Options Photodynamic Therapy (red light): Reported in some cases, though not routinely used in Australian practice Ensure adequate dryness of skin folds; consider antifungal if co-existing tinea Prevention Antibacterial soaps or washes to reduce skin colonisation Keep skin folds dry (use absorptive powders, wear loose clothing) Repeat treatment or maintenance topical therapy if recurring Address underlying factors: Weight reduction (if obesity) Optimise glycaemic control in diabetes Improve hygiene Notes Erythrasma can recur, especially if risk factors (e.g. sweating, obesity, diabetes) are not addressed. Consider checking for co-infection with dermatophytes (tinea) as it may coexist in similar sites. Some guidelines suggest combining topical antibacterial with antifungal if diagnosis is uncertain. 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 Medications Most Likely to Cause Depression and Delirium Medications Causing Depression Antihypertensives Beta blockers (e.g., metoprolol) Calcium channel blockers Anticonvulsants Carbamazepine, topiramate Sedatives Benzodiazepines, anticholinergics Antihistamines Ranitidine Corticosteroids High doses or chronic use Medications Causing Delirium Anticholinergics Oxybutynin, promethazine (common in elderly due to heightened sensitivity) Benzodiazepines Especially in high doses or chronic use Opioids Morphine (higher risk in elderly or renal impairment) Corticosteroids High-dose or long-term use Dopaminergic Drugs Levodopa (Parkinson’s medications) Alcohol/Illicit Drugs Intoxication or withdrawal Additional Notes Polypharmacy: Increases risk of both depression and delirium, particularly in elderly patients or those with multiple comorbidities Steroids: Can cause depression, euphoria, anxiety, or psychosis Prevention: Conduct regular medication reviews in elderly or psychiatric history patients Adjust doses or discontinue causative agents when possible Medications Most Likely to Cause Depression and Delirium Medications Causing Depression Antihypertensives: Beta blockers (e.g. metoprolol) Calcium channel blockers Anticonvulsants: Carbamazepine, topiramate Sedatives: Benzodiazepines, anticholinergics Antihistamines: Ranitidine (H2 receptor antagonist, historically) Corticosteroids: High-dose or chronic use Medications Causing Delirium Anticholinergics: Oxybutynin, promethazine Common in older adults due to heightened sensitivity Benzodiazepines: Especially in high doses or prolonged use Opioids: Morphine, particularly in older adults or renal impairment Corticosteroids: High-dose or long-term therapy Dopaminergic Drugs: Levodopa, used in Parkinson’s disease Alcohol/Illicit Drugs: Intoxication or withdrawal can precipitate delirium Additional Notes Polypharmacy raises the risk for both depression and delirium, especially in the elderly or those with multiple comorbidities. Steroids can cause mood changes ranging from depression to euphoria, anxiety, or even psychosis. Prevention: Conduct regular medication reviews in older adults or those with a psychiatric history. Adjust doses or discontinue offending agents when feasible. 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 Amenorrhoea & Infertility Primary & Secondary Amenorrhoea Primary: No menarche by 15 years (if normal secondary sexual characteristics) or 13 years (if absent) Secondary: No menstruation for 3 cycles or 6 months in previously regular cycles Differential Diagnoses Hypothalamic Causes Functional hypothalamic amenorrhoea (stress, excessive exercise, weight loss) Pituitary Causes Hyperprolactinaemia (prolactinoma, medications) Thyroid dysfunction (hypothyroidism, hyperthyroidism) Ovarian Causes Premature ovarian insufficiency (POI): ↑FSH, ↓oestradiol Polycystic ovary syndrome (PCOS): Hyperandrogenism, oligo-/amenorrhoea Uterine/Vaginal Causes Asherman’s syndrome (intrauterine adhesions) Müllerian agenesis (congenital absence of uterus/vagina) Investigations Initial Tests β-hCG: Exclude pregnancy TSH, free T4: Thyroid dysfunction Serum prolactin: Hyperprolactinaemia FSH, LH: Differentiate hypogonadotropic vs hypergonadotropic states Oestradiol: Assess ovarian function Additional Tests if Indicated Total testosterone, DHEAS: Hyperandrogenism (e.g., PCOS) 17-hydroxyprogesterone: Congenital adrenal hyperplasia Imaging Pelvic ultrasound: Assess uterine and ovarian anatomy Brain MRI: Evaluate for pituitary lesions if hyperprolactinaemia or central cause suspected Infertility Differentials Ovulatory Disorders PCOS: Chronic anovulation, hyperandrogenism POI: ↑FSH, ↓oestradiol Tubal Factors Pelvic inflammatory disease (PID) → Tubal occlusion Endometriosis → Peritubal adhesions Uterine Factors Fibroids (submucosal) → Implantation failure Congenital anomalies → Structural abnormalities Male Factors Semen abnormalities (oligospermia, asthenozoospermia) Investigations Ovulation Assessment Mid-luteal progesterone: Confirms ovulation Ovarian Reserve Testing AMH levels: Estimates oocyte quantity Antral follicle count (ultrasound): Assesses ovarian reserve Tubal Patency Testing Hysterosalpingogram (HSG): Detects tubal occlusion Male Partner Assessment Semen analysis: Performed after 2–3 days of abstinence Key Considerations Evaluate both partners to identify contributing factors Early assessment optimises management and treatment planning Amenorrhoea & Infertility Primary Amenorrhoea Consider evaluation if no menses by age 15 with normal secondary sexual development or by age 13 without secondary sexual characteristics Differential diagnoses include constitutional delay, Müllerian agenesis, androgen insensitivity syndrome, imperforate hymen and hypogonadotrophic hypogonadism A detailed history should include family pubertal timing and any history of endocrine disorders Secondary Amenorrhoea Common causes include polycystic ovary syndrome (PCOS), functional hypothalamic amenorrhoea due to stress, weight loss or excessive exercise, and hyperprolactinaemia Other aetiologies encompass thyroid dysfunction, premature ovarian insufficiency and iatrogenic causes such as medications History should assess changes in menstrual pattern and associated systemic or psychosocial symptoms Investigations for Amenorrhoea Exclude pregnancy with a Beta-hCG test Hormonal evaluation: Measure FSH, LH, estradiol, prolactin and TSH to distinguish between hypogonadotrophic and hypergonadotrophic states Bone age assessment via wrist X-ray to assess skeletal maturation Pelvic ultrasound to evaluate uterine and ovarian anatomy; transvaginal ultrasound provides superior detail if acceptable Consider GnRH stimulation testing to differentiate central from peripheral causes Chromosome analysis is indicated for suspected genetic causes such as Turner syndrome or androgen insensitivity syndrome Infertility Differential Diagnoses Ovulatory disorders: PCOS characterised by hyperandrogenism and chronic anovulation Premature ovarian insufficiency indicated by elevated FSH and low oestradiol Tubal factors: History of pelvic inflammatory disease leading to tubal occlusion Endometriosis causing peritubal adhesions Uterine factors: Structural abnormalities such as fibroids (especially submucosal) or congenital anomalies impairing implantation Male factors: Semen abnormalities including oligospermia and asthenozoospermia should be evaluated via semen analysis Investigations for Infertility Ovulation assessment: Mid-luteal progesterone measurement to confirm ovulation Ovarian reserve testing: Anti-Müllerian hormone (AMH) levels and antral follicle count by ultrasound Tubal patency: Hysterosalpingography (HSG) to detect tubal occlusion Evaluation of the male partner: Semen analysis following 2–3 days of abstinence Management Address underlying causes of amenorrhoea: Central amenorrhoea managed with GnRH analogues to delay premature pubertal progression For secondary amenorrhoea, treat conditions such as thyroid dysfunction, hyperprolactinaemia or PCOS with appropriate medical therapy and lifestyle modifications Infertility management: Ovulatory disorders may be treated with ovulation induction agents and, in PCOS, with combined oral contraceptives or insulin sensitisers Anatomical causes (eg, tubal or uterine factors) may require surgical intervention Evaluate both partners comprehensively to guide treatment planning and optimise fertility outcomes Notes: Early evaluation and intervention are essential to prevent long-term complications such as premature epiphyseal closure in amenorrhoea and to optimise fertility outcomes A detailed history, including parental heights, family pubertal timing and psychosocial factors, is critical for distinguishing between normal variants and pathological conditions Regular monitoring of growth, bone age, and pubertal progression, as well as ongoing assessment of menstrual patterns, informs clinical management A multidisciplinary approach involving endocrinologists, gynaecologists, fertility specialists and mental health professionals is recommended for complex cases In cases of infertility, timely investigation of both partners facilitates targeted therapy and improves chances of conception Lifestyle modifications, including nutritional support and stress management, play a crucial role in managing functional hypothalamic amenorrhoea and improving fertility outcomes 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 Enuresis Definitions Monosymptomatic: Nocturnal only, no daytime LUTS Non-monosymptomatic: With LUTS (daytime incontinence, urgency) Differentials Constipation: Rectal distension impairs bladder emptying UTI: Dysuria, frequency, fever OSA: Snoring, somnolence Overactive bladder: Urgency, small voids Diabetes: Polyuria, polydipsia, weight loss Psychological stressors/NAI: Family dysfunction, trauma ADHD: Impulsivity, inattentiveness Spinal dysraphism: Neurological bladder, abnormal gait History Onset: Acute or gradual? >6 months dry? Daytime symptoms: Incontinence, urgency Family hx: Bedwetting common Constipation: Straining, infrequent stools Systemic: Polyuria (diabetes), snoring (OSA), dysuria (UTI) Psychosocial: Stress, trauma, NAI risk Dietary: Evening fluids, caffeine ADHD symptoms: Hyperactivity, inattentiveness Previous interventions: Alarms, meds Examination Growth: Poor → consider diabetes, OSA Tonsils: Hypertrophy → OSA Abdomen: Mass → constipation/bladder distension Genitalia: Anatomical abnormalities Spine: Dysraphism (dimples, hair patches) Lower limbs: Reflexes, tone, gait (neurogenic bladder) Management Non-Pharmacological: Regular toileting, avoid evening fluids/caffeine Prevent constipation Educate parents: Avoid punishment, use rewards Bedwetting alarms: Effective ≥6 years, 6–8 weeks consistent use Pharmacological: Desmopressin: For ≥7 years, especially for sleepovers/camps Start 200 mcg PO at bedtime; ↑ to 400 mcg if needed Address daytime LUTS before nocturnal enuresis Notes Red flags: Poor growth, neuro signs, trauma → refer Combine behavioural and medication for refractory cases Parental involvement is key for success Enuresis Definitions Monosymptomatic: Nocturnal bedwetting only, without daytime lower urinary tract symptoms Non-monosymptomatic: Enuresis accompanied by daytime incontinence, urgency, or other bladder symptoms Differentials Constipation: Rectal distension impacting bladder emptying Urinary tract infection: Dysuria, frequency, fever Obstructive sleep apnoea: Snoring, daytime somnolence, poor growth Overactive bladder: Urgency, frequent small-volume voids Diabetes mellitus: Polyuria, polydipsia, weight loss Psychological stressors or abuse: Family dysfunction, trauma history Attention deficit hyperactivity disorder: Impulsivity, inattentiveness Spinal dysraphism: Neurological bladder, abnormal gait, possible cutaneous spine markers History Onset of bedwetting: Whether acute, gradual, or occurring after a dry period of more than 6 months Daytime symptoms: Urgency, frequency, incontinence Family history: High prevalence of enuresis in families Constipation: Signs such as straining, infrequent stools Systemic issues: Polyuria (diabetes), snoring (OSA), dysuria or fever (UTI) Psychosocial factors: Stress, NAI risk, recent changes in family dynamics Dietary factors: High evening fluid intake, caffeine consumption ADHD symptoms: Hyperactivity, inattention impacting toileting routines Previous interventions: Use of alarms, medications, or behavioural strategies Examination Growth parameters: Poor growth may suggest OSA or chronic illness Tonsillar hypertrophy: Potential indication of OSA Abdominal exam: Identify faecal mass or palpable bladder distension Genital exam: Rule out anatomical abnormalities or signs of abuse Spine inspection: Look for dimples or hair patches indicating spinal dysraphism Neurological screening: Assess lower limb reflexes, tone, and gait for neurogenic bladder clues Management Non-Pharmacological Regular toileting and timed voids throughout the day Limit evening fluids and caffeine Address constipation early with adequate dietary fibre and hydration Encourage positive reinforcement rather than punishment Bedwetting alarms for children over 6 years, used consistently for at least 6–8 weeks Consider urotherapy techniques such as bladder training and scheduled voiding Pharmacological Desmopressin (for children 7 years and older), starting at 200 micrograms at bedtime and increasing to 400 micrograms if needed Ensure daytime bladder dysfunction is managed before focusing on nocturnal enuresis Combine medication with behavioural strategies in refractory cases Notes Red flags: Poor growth, abnormal neurological signs, or signs of abuse requiring prompt referral Obtain urine dipstick if diagnosis is uncertain to rule out glycosuria or proteinuria Parental involvement and consistent follow-up improve long-term success rates Many children outgrow enuresis spontaneously, but support and appropriate interventions can expedite dryness and reduce psychosocial impact 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 Parkinson’s Disease History Tremor (resting, hands) Difficulty rising from chair Stiffness (arms, legs) Constipation Loss of smell Falls Non-motor symptoms (fatigue, depression, REM sleep behaviour disorder) may precede motor signs Examination Resting "pill-rolling" tremor Shuffling gait, loss of arm swing Stooped posture Masked facies Cogwheel rigidity Bradykinesia Power, reflexes, sensation usually normal Postural instability develops later Investigations Clinical diagnosis (based on response to levodopa) DaTScan (dopamine transporter scan) for atypical cases Management Neurology referral for confirmation Patient education (chronic nature of disease) Levodopa + carbidopa (first-line) Dopamine agonists (pramipexole, ropinirole) or anticholinergics (consider in younger or tremor-dominant cases) Physiotherapy (mobility) Psychology (CBT), Parkinson’s support group Speech therapy Manage comorbidities (dementia, depression, anxiety) Falls prevention, regular exercise Avoid metoclopramide & prochlorperazine, use domperidone 10 mg TDS (max 7 days) for nausea Note: Parkinsonism (Parkinson-plus syndromes) does not improve with levodopa/carbidopa. Parkinson’s Disease History Tremor: Resting, often “pill-rolling” in the hands Mobility Issues: Difficulty rising from a chair, stiffness in arms/legs, slower movements Constipation: Common non-motor feature Loss of Smell (anosmia) Falls (postural instability in later disease) Non-Motor Symptoms: Fatigue, depression, REM sleep behaviour disorder (may precede motor signs) Examination Resting Tremor: Pill-rolling type, reduces with intentional movement Shuffling Gait: Reduced arm swing, stooped posture Rigidity: “Cogwheel” or “lead-pipe” in arms/legs Bradykinesia: Slowness of movements, reduced facial expression (masked facies) Power, Reflexes, Sensation: Typically normal Postural Instability: Tends to occur in later disease stages Investigations Primarily a clinical diagnosis. Response to Levodopa can support diagnosis. DaTScan (dopamine transporter scan) sometimes used in atypical or uncertain presentations. Management Neurology Referral For confirmation of diagnosis and tailoring therapy. Patient Education Chronic, progressive nature of disease. Discuss realistic goals, importance of exercise, and support services. Pharmacotherapy Levodopa + Carbidopa (first-line) Dopamine Agonists (pramipexole, ropinirole) or Anticholinergics (e.g. benztropine) in younger patients or tremor-dominant disease to delay levodopa side effects. Manage side effects (dyskinesias, motor fluctuations) as disease progresses. Allied Health and Support Physiotherapy: Improves mobility, gait training, reduces falls. Psychology or counselling: CBT for depression or anxiety, connect with Parkinson’s support groups. Speech Therapy: If dysarthria, swallowing issues. Occupational Therapy: Home safety, assistive devices, falls prevention. Comorbidities & Lifestyle Screen for dementia, depression, anxiety (common in Parkinson’s). Falls prevention strategies, regular exercise. Avoid dopamine-blocking medications (e.g. typical antipsychotics, metoclopramide, prochlorperazine) that worsen symptoms. If antiemetic needed → use domperidone (10 mg TDS, max 7 days) as it doesn’t cross BBB significantly. Note Parkinson-plus syndromes (e.g. progressive supranuclear palsy) do not improve well with levodopa/carbidopa, often have additional features atypical for PD (vertical gaze palsy, early falls, etc.) 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 Blepharitis Types: Anterior: Affects eyelid margins/eyelashes (crusting/scales) Posterior: Affects meibomian glands (blocked glands, foamy tears) Associations: Staphylococcal infection, seborrhoea, rosacea, allergy Treatment: General: Warm compress 2–4x daily Eyelid hygiene (proprietary cleansers; avoid baby shampoo) Lubricating eye drops Anterior: Chloramphenicol 1% ointment OD (if bacterial) Posterior: Doxycycline 100 mg OD (4–8 weeks, reduce to 50 mg) Topical azithromycin if severe (doxycycline contraindicated) Firm eyelid massage (express blocked oils) NB: Address underlying rosacea/seborrhoea to prevent recurrence Complications: Keratitis, chalazion, dry eye syndrome Blepharitis Types Anterior Blepharitis: Inflammation at the eyelid margins and eyelashes (outer edge) Can be staphylococcal (crusting, scales at lash base) or seborrhoeic (greasy scales) Often presents with redness, irritation, and possible lash debris Posterior Blepharitis: Involves the meibomian glands (inner lid margin) Gland dysfunction leads to blocked orifices and foamy tears Commonly associated with rosacea or seborrhoeic dermatitis Associations Staphylococcal infection (commonly S. aureus) Seborrhoea (e.g. scalp dandruff) Rosacea (facial redness, telangiectasia, papulopustular lesions) Allergy (chronic inflammatory response) Treatment General Measures Warm Compresses: 2–4 times daily, 5–10 minutes each, helps soften crusts and improve meibomian gland flow Eyelid Hygiene: Use proprietary eyelid cleansers specifically formulated for blepharitis (e.g. lid scrubs) Avoid baby shampoo (can irritate eyes and disrupt tear film) Lubricating Eye Drops: Alleviate dryness and irritation Anterior Blepharitis Topical Antibiotic Ointment: e.g. Chloramphenicol 1% ointment once daily (HS) or BD if staphylococcal involvement is suspected Apply to the lid margin, not just the conjunctival sac Ensure concurrent lid hygiene to remove crusting Posterior Blepharitis Oral Doxycycline: 100 mg once daily for 4–8 weeks, then consider reducing to 50 mg daily Monitor for GI side effects, consider sun protection due to photosensitivity Topical Azithromycin (off-label or specialist recommended) if severe or doxycycline contraindicated Firm Eyelid Massage: Gently express meibomian glands to improve lipid flow Address underlying rosacea or seborrhoea (e.g. with topical metronidazole for facial rosacea, anti-seborrhoeic shampoos) Complications Keratitis: Corneal involvement can cause vision changes Chalazion: Blocked meibomian gland cyst Dry Eye Syndrome: Reduced tear film quality Recurrent Infections: If poor lid hygiene persists Notes Blepharitis tends to be chronic and recurrent. Consistent lid hygiene is key to preventing flare-ups. In rosacea-related blepharitis, controlling facial rosacea (topical or systemic therapies) helps reduce eyelid inflammation. If severe pain, visual disturbance, or atypical presentation occurs, consider ophthalmology referral. Bookmark Failed! Bookmark Saved! Refresh Refresh Refresh

Log In Get started Bookmarks Help Progress 0% Cardiovascular AAA + Rupture AC dislocation ATSI Abdominal pain in kids Abnormal/Dysfunctional Uterine Bleeding (AUB/DUB) Acanthosis Nigricans Acne Acromegaly Actinic Cheilitis Acute Kidney Injury (AKI) Acute Swollen Joint with Fever Acute Vision Loss Acute and Progressive Vision Loss Addisons Adjustment Disorder and Anxiety Adjustment Disorder with Depressed Mood Age related macular degeneration Alcohol Cessation Allergic rhinitis Alopecia Amenorrhoea Anaphylaxis Angina Angular Cheilitis Ankylosing Spondylitis (AS) Anorexia Nervosa Anticholinergics and TCAs Antidepressants Antimetabolite drugs Antiphospholipid syndrome Antipsychotics Anxiety Disorders Aortic Dissection Arrhythmia Asthma Asthma Atrial Fibrillation Back pain Behavioural / learning disorders Behavioural disturbances Bell’s palsy and Ramsey Hunt syndrome Beta-Human Chorionic Gonadotropin (β-hCG) Biologic agents Bipolar Disorder Bleeding disorders Blepharitis Breast Cancer Breast Lump Bronchiectasis (Updated) CA-125 (Cancer Antigen 125) CRPS CVD Risk Assessment Calluses and Corns Candida (Candidiasis as an STI) Carpal tunnel syndrome and de quervains tenosynovitis Cellulite Cervical spondylosis Chest pain Chickenpox (Varicella) Chilblains Cholesteatoma Chronic Cough in Children Chronic Fatigue Syndrome (CFS) Chronic Kidney Disease (CKD) Chronic Rhinosinusitis Chronic Stridor Clavicular fracture Clozapine Coeliacs Colorectal Cancer Screening Recommendations Congestive Cardiac Failure Connective Tissue Diseases Constipation Contact Dermatitis Cracked Heel Croup Cushings Cutaneous Drug Eruptions DKA vs HHS Dacrocystitis, dacyrostenosis, dacyrocystocoele Deep Vein Thrombosis (DVT) Delerium Dementia Depression and Delirium Dermal melanocystosis (mongolian spot) Developmental Dysplasia of the Hip (DDH) Diabetes Diabetes Insipidus (DI) vs Primary Polydipsia Diabetic Neuropathy Diarrhoea Diplopia Dizziness / syncope Down syndrome Duchenne muscular dystrophy Dupuytrens / trigger finger Dyspepsia Dyspnoea (Shortness of Breath) ECG ECG Findings ECG Patterns CONCISE COMPREHENSIVE 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 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 Acute Vision Loss Differentials Neurological: Cerebellar: Stroke (posterior circulation), retinal migraine, migraine aura Optic Nerve: Tumours (glioma, meningioma), optic neuritis, papilloedema Vascular: Arterial: Amaurosis fugax, GCA, CRAO Venous: CRVO Ocular: Retina: Detachment, macular hole Vitreous: Haemorrhage, posterior vitreous detachment (PVD) Cornea: Keratitis, abrasions Key History Flashing lights: Retinal or PVD Floaters: PVD, retinal detachment, vitreous haemorrhage Precipitating factors: Coughing, exertion (embolism, detachment) Headache/scalp pain: GCA Painful loss: Optic neuritis, glaucoma, uveitis Painless loss: CRAO, CRVO, detachment, amaurosis fugax Investigations Bloods: ESR, CRP (rule out GCA) Imaging: Carotid US/Echo: Embolic source (CRAO) MRI/MRV: Optic neuritis, compressive lesions CTA/MRA: Stroke assessment (posterior circulation) CT Orbit: Trauma, tumour, abscess LP: For raised ICP (papilloedema) Ophthalmology: Fundoscopy: Retinal detachment, CRAO, CRVO, optic disc changes Ocular US: Vitreous haemorrhage, retinal detachment Key Notes PVD: Common (age 40–70), benign but monitor for detachment Retinal Detachment: Emergency if vision loss + floaters/flashes Vitreous Haemorrhage: Red-tinted vision, reduced acuity Acute Vision Loss Differential Diagnoses It can be helpful to categorise causes based on anatomical location or pathophysiology (neurological, vascular, ocular). Neurological Causes Cerebellar stroke (posterior circulation): Typically associated with other neurological deficits (e.g. ataxia, dysarthria). May present with visual field defects if the occipital lobe is involved. Retinal migraine: Transient monocular or binocular visual disturbance, often followed by typical migraine headache. Migraine aura: Visual aura can cause flashing lights, scotomas, or transient visual loss. Optic nerve lesions: Optic neuritis: Painful vision loss, common in multiple sclerosis or post-viral. Compressive tumours (e.g. glioma, meningioma): Gradual vision changes, may see optic disc swelling on fundus exam. Papilloedema: Usually bilateral; raised intracranial pressure signs (headache, vomiting). Vascular Causes Arterial: Amaurosis fugax: Transient monocular vision loss (“curtain coming down”), often due to an embolus from the carotid or cardiac source. Giant cell arteritis (GCA): Usually in patients >50 years; often presents with headache, jaw claudication, scalp tenderness, elevated inflammatory markers. Emergency—risk of permanent blindness. Central retinal artery occlusion (CRAO): Sudden, painless, severe monocular vision loss; fundoscopy shows a pale retina with a cherry-red spot at the fovea. Venous: Central retinal vein occlusion (CRVO): Painless vision loss; fundoscopy shows “blood and thunder” appearance (widespread retinal haemorrhages). Ocular Causes Retinal: Retinal detachment: Flashes of light, floaters, and a “curtain” or shadow over vision. This is an ophthalmic emergency. Macular hole: Central vision loss, metamorphopsia (distorted vision). Vitreous: Vitreous haemorrhage: Presents with sudden visual loss, possibly “red haze” or floaters; common in diabetic retinopathy or trauma. Posterior vitreous detachment (PVD): Often causes flashes and floaters; usually benign but can precede retinal detachment. Corneal: Keratitis (e.g. microbial, herpetic), corneal abrasions: Painful, red eye, photophobia, blurred vision. Other: Acute glaucoma (angle-closure crisis): Painful red eye, halos around lights, mid-dilated pupil, elevated intraocular pressure. Uveitis/Iridocyclitis: Pain, photophobia, possible floaters. Key History Features Flashing lights Suggestive of retinal involvement or posterior vitreous detachment. Floaters Seen in PVD, retinal detachment, or vitreous haemorrhage. Precipitating factors (e.g. coughing, exertion) Can point to embolism or acute mechanical strain that leads to retinal detachment or haemorrhage. Headache/scalp pain Alert for Giant Cell Arteritis. Painful vs. Painless Loss Painful: Optic neuritis, acute glaucoma, uveitis. Painless: CRAO, CRVO, retinal detachment, amaurosis fugax, vitreous haemorrhage. Temporal profile Sudden onset: Vascular occlusion (CRAO, CRVO), retinal detachment, haemorrhage. Progressive: Tumours, papilloedema, corneal opacities. Associated symptoms Jaw claudication (GCA). Neurological deficits (stroke). Floaters/flashes (retinal detachment/PVD). Investigations Depending on clinical suspicion, investigations may include: Blood tests ESR, CRP: Rule out GCA if patient >50 years or suspicious symptoms. Imaging Carotid ultrasound / Echocardiogram: Searching for an embolic source in CRAO or amaurosis fugax. MRI/MRV (brain and orbit): For optic neuritis, compressive lesions, venous sinus thrombosis. CTA/MRA: Assessment of the posterior circulation in suspected stroke or vascular anomalies. CT Orbit: Trauma, suspected tumour or abscess. Lumbar puncture (LP): If raised intracranial pressure or suspected papilloedema (only after imaging to exclude mass lesion). Ophthalmology-specific Fundoscopy: Look for retinal detachment (elevated retina), CRAO (pale retina, cherry-red spot), CRVO (blood and thunder), optic disc swelling, or papilloedema. Ocular ultrasound: Helps confirm retinal detachment or vitreous haemorrhage if fundoscopy is difficult. Management Approaches Retinal Detachment Ophthalmic emergency. Urgent referral to ophthalmology for possible surgical intervention (e.g. pneumatic retinopexy, vitrectomy). Giant Cell Arteritis If strongly suspected, start high-dose corticosteroids immediately (e.g. oral prednisone 1 mg/kg/day) to prevent further vision loss. Arrange urgent temporal artery biopsy (ideally within 1–2 weeks of starting steroids). CRAO (Central Retinal Artery Occlusion) Emergency; immediate ophthalmology referral. Possible acute treatments include ocular massage, lowering intraocular pressure (e.g. IV acetazolamide), hyperbaric oxygen (in some centres). Investigate embolic sources (carotid, cardiac). CRVO (Central Retinal Vein Occlusion) Ophthalmology referral; may benefit from intravitreal anti-VEGF injections. Control risk factors (hypertension, diabetes, hyperlipidaemia). Optic Neuritis Often associated with multiple sclerosis. High-dose IV methylprednisolone can hasten recovery (but does not change final visual outcome). Vitreous Haemorrhage Identify and treat underlying cause (e.g. diabetic retinopathy, trauma, retinal tear). If unresolved, might require surgical intervention (vitrectomy). Acute Glaucoma Immediate referral for reducing intraocular pressure (e.g. IV acetazolamide, topical beta-blockers, pilocarpine). Migraine Aura / Retinal Migraine Usually transient; manage as per migraine protocols if no other cause found. Supportive Measures Pain management if required. Ensure the other eye is protected; address modifiable risk factors (e.g. controlling BP, diabetes, cessation of smoking). Key Notes Posterior Vitreous Detachment (PVD): Common between ages 40–70. Usually benign but must be evaluated to rule out or monitor for retinal detachment. Retinal Detachment: Sudden vision loss with floaters and flashes is urgent. “Curtain coming down” or shadow. Prompt surgical intervention is crucial. Vitreous Haemorrhage: Often presents with “red-tinted” vision or dark floating spots; treat underlying cause (e.g. diabetic retinopathy). GCA: Requires immediate high-dose steroids if suspected, even before confirmation, to prevent bilateral blindness. Painful vs. Painless: Distinguish quickly in history for direction of investigations. Imaging: Must be performed if neurological or vascular cause is suspected, or if papilloedema is a possibility. 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 Epistaxis Causes Idiopathic: 85% of cases Local: Digital trauma (nose picking) URTI, cocaine use, dry air (dries out nasal passage making it more fragile, especially in winter) Septal deviation, incorrect use of intranasal steroids, NSAIDs Systemic: HTN Coagulopathy (e.g., bleeding disorders due to EtOH abuse, malignancy, liver disease) Medications (anticoagulants, SSRIs, NSAIDs) Leukemia History Thrombocytopaenia: Ask about bleeding gums, easy bruising OTC NSAID use Family hx of bleeding disorder Bilateral or unilateral bleeding Night sweats/weight loss/bone pain (malignancy or systemic causes) EtOH use (liver disease or thrombocytopaenia) Repetitive trauma to nose Postnasal drip of blood Haematemesis/melaena (swallowed blood) Symptoms of anaemia or previously diagnosed anaemia Current URTI Illicit substance use (e.g., cocaine) ____________________________________ Examination Postural hypotension Signs of anaemia (tachycardia, conjunctival pallor) Stigmata of coagulopathy (e.g., petechiae, bruising) Stigmata of chronic liver disease (e.g., jaundice, spider naevi) Excoriated Little's area (common site of anterior bleeds) Bilateral nose bleeding (more likely posterior) Postnasal drip of blood (posterior source) Investigations Anterior rhinoscopy to locate bleeding source FBC, coagulation profile if recurrent or severe bleeding CT scan if tumour or structural lesion is suspected Consider LFTs if chronic liver disease is suspected Management Long-term Avoid nose picking, strenuous activity, and nose blowing Use Kenacomb ointment for crusting or minor irritation Address systemic contributors (e.g., HTN control or managing coagulopathy) Acute Sit upright and exclude shock Insert IVC and perform blood tests, including coagulation studies Lean forward, applying digital pressure to the nose for 10 minutes Apply ice packs to the neck or mouth to reduce bleeding Use phenylephrine spray with lignocaine for vasoconstriction and analgesia Cauterise visible vessels with silver nitrate Apply anterior/posterior nasal packing as required If uncontrolled, refer to ED for surgical intervention (ligation or embolisation) ____________________________________ Complications Hypovolaemia or anaemia due to blood loss Infection Septal haematoma (may lead to septal perforation if untreated) Aspiration of blood (especially in posterior bleeds) ____________________________________ Notes: Patients on anticoagulants may require temporary reversal if bleeding is severe or recurrent Recurrent idiopathic epistaxis may benefit from referral to ENT for further evaluation and potential endoscopic cautery Epistaxis Causes Idiopathic (approximately 85% of cases) Local Digital trauma (nose picking) Dry air (especially during winter) Structural issues (septal deviation), nasal irritants (cocaine, intranasal steroids) Chronic nasal inflammation (recurrent URTI) Tumours (rare) Systemic Hypertension Coagulopathies (e.g. liver disease, alcohol misuse, hereditary bleeding disorders) Medications (anticoagulants, NSAIDs, SSRIs) Haematological conditions (leukaemia, thrombocytopenia) History Frequency and duration of nosebleeds Medications (NSAIDs, anticoagulants) and over-the-counter remedies Signs of bleeding disorder (gum bleeding, easy bruising, menorrhagia) Possible triggers (nose picking, illicit substances, heavy alcohol use) Unilateral or bilateral bleeding Any postnasal drip, haematemesis, or melaena from swallowed blood Red flag symptoms (night sweats, weight loss, bone pain) Symptoms of anaemia (fatigue, dizziness, pallor) Examination Check vital signs (postural hypotension, tachycardia) Look for signs of anaemia (pallor, tachycardia) or chronic liver disease (jaundice, spider naevi) Inspect for stigmata of coagulopathy (bruising, petechiae) Anterior rhinoscopy Evaluate Little’s area (common site of anterior bleeds) Note excoriations, granulations, or visible vessels Bilateral bleeding or prominent postnasal drip suggests posterior source Consider nasal endoscopy if bleeding source is unclear Investigations Usually clinical diagnosis for mild, recurrent anterior bleeds FBC and coagulation profile if epistaxis is recurrent, severe, or suspected coagulopathy LFTs if chronic liver disease is suspected CT scan of the sinuses or nasopharynx if structural lesion or tumour is suspected Management Acute Sit patient upright, leaning forward, to prevent blood swallowing Pinch soft part of the nostrils firmly for at least 10 minutes Apply cold packs to the nose or neck to induce vasoconstriction Consider topical vasoconstrictors (phenylephrine) with local anaesthesia (lignocaine) if available If visible bleeding site, cauterise with silver nitrate under good visualisation Anterior nasal packing if bleeding persists or source not clearly identified Posterior packing or balloon catheter if posterior bleed is suspected (often bilateral or heavy bleed) Insert IV cannula if risk of significant blood loss and check bloods including coags Refer to ENT or ED if uncontrolled bleeding, shock, or suspicion of posterior source Long-Term and Preventive Avoid nasal trauma (picking, forceful blowing) and reduce aggravating factors (dry air, irritants) Use topical emollients or antibiotic-steroid ointments (e.g. Kenacomb) to keep nasal mucosa moist and prevent crusting Optimise management of systemic factors (control hypertension, review anticoagulants if recurrent bleeds) ENT follow-up for recurrent idiopathic bleeds or suspected anatomical abnormality Consider antibiotic prophylaxis in certain cases of nasal packing to prevent toxic shock syndrome (depending on pack type and clinical risk) Complications Significant blood loss, leading to hypovolaemia or anaemia Nasal septal haematoma, which can cause cartilage necrosis if untreated Infection, including rare toxic shock syndrome Aspiration of blood, particularly with posterior bleeds Need for surgical intervention (arterial ligation or embolisation) if conservative measures fail Key Points Most epistaxis arises from Kiesselbach’s plexus in Little’s area (anterior bleeds) and is easily managed with pressure and local cautery Posterior bleeds tend to be more severe, often requiring specialist involvement Patients on anticoagulants may need dose adjustment or temporary reversal if bleeding is severe or uncontrolled Early referral to ENT is indicated for refractory cases, high suspicion of posterior source, or structural lesions 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 Duchenne Muscular Dystrophy (DMD) Pathophysiology X-linked recessive DMD gene mutation → dystrophin deficiency Progressive skeletal & cardiac muscle atrophy Most common muscular dystrophy, onset in early childhood Markedly elevated CK (muscle fibre degeneration) Patient Profile Boys aged 2–3 years (rare in girls) Family history may warrant genetic counselling Presentation Delayed motor milestones (shuffling/crawling instead of walking) Waddling gait, calf pseudohypertrophy (fat/fibrosis replacement) Hypotonia, hyporeflexia Mild-moderate intellectual impairment Positive Gower’s sign (child “climbs” legs to stand) Progressive difficulty running, jumping, climbing stairs Diagnosis Genetic testing (DMD gene mutation, ↑ CK) Muscle biopsy (dystrophin staining if genetic test inconclusive) Cardiac evaluation (ECG, echocardiogram) for cardiomyopathy Treatment Neurology referral (specialist in neuromuscular disorders) Corticosteroids (prednisone/deflazacort) (slow progression, prolong ambulation) Physio/OT (maintain mobility, prevent contractures) Cardiac meds, respiratory support (as complications develop) Genetic counselling (family planning, risk assessment) Complications Respiratory failure (diaphragmatic weakness → lung complications) Cardiomyopathy & arrhythmias (life-threatening) Scoliosis (requires intervention) Duchenne Muscular Dystrophy (DMD) Pathophysiology X-linked recessive mutation in the DMD gene Deficiency of dystrophin → progressive skeletal and cardiac muscle atrophy Most common muscular dystrophy, presenting in early childhood Markedly elevated CK due to muscle fibre degeneration Patient Profile Typically affects boys aged 2–3 years (very rare in girls) Family history might indicate the need for genetic counselling Presentation Delayed motor milestones (e.g. crawling instead of walking) Waddling gait, calf pseudohypertrophy (calf muscle replaced by fat/fibrosis) Hypotonia, hyporeflexia Mild-to-moderate intellectual impairment Positive Gower’s sign (child uses arms to “climb” up legs when standing) Progressive difficulty with running, jumping, climbing stairs Diagnosis Genetic testing (mutation in DMD gene, elevated CK) Muscle biopsy (assessing dystrophin staining if genetic test inconclusive) Cardiac evaluation (ECG, echocardiogram) to monitor for cardiomyopathy Treatment Neurology referral (specialist in neuromuscular disorders) Corticosteroids (prednisone or deflazacort) to slow progression and prolong ambulation Physiotherapy and occupational therapy for mobility maintenance and contracture prevention Cardiac medications and respiratory support as needed Genetic counselling for family planning and risk assessment Complications Respiratory failure (due to diaphragmatic and intercostal muscle weakness) Cardiomyopathy and arrhythmias (potentially life-threatening) Scoliosis (may require surgical intervention) 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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 Anorexia Nervosa Diagnosis Intense fear of weight gain → restrictive eating & low body weight Poor recognition of seriousness of low weight Subtypes: Restrictive type: Limits food intake ± compulsive exercise Binge-eating/purging type: Episodes of binge eating or purging DSM-5 Criteria Restriction of energy intake → significantly low weight Intense fear of weight gain or persistent behaviours preventing weight gain Disturbance in self-perceived weight/shape or undue influence of body weight on self-evaluation Investigations Routine labs: FBC, eLFTs, CMP, FBG Specific tests: Iron studies, B12/folate, TSH Hormonal tests: FSH, LH, prolactin, oestradiol Bone health: Bone densitometry Cardiac: ECG (arrhythmias, QT prolongation) Management First-line: Family-based therapy (children/adolescents) Nutritional restoration with dietitian Psychiatric support for comorbidities Monitor for refeeding syndrome (electrolytes, phosphate, magnesium) Multidisciplinary care essential Hospital Admission Criteria BP <90 mmHg (<80 mmHg in children) HR <40 bpm (<50 bpm) Postural tachycardia/hypotension (>20 mmHg drop) Temp <36°C or >38°C BGL <3 mmol/L BMI <14 kg/m² Screening: SCOFF Questionnaire Sick: Induce vomiting when uncomfortably full? Control: Fear losing control of eating? One stone: Lost >6.35 kg in 3 months? Fat: Feel fat despite being told otherwise? Food: Does food dominate life? Interpretation: Score ≥2 → likely eating disorder, warrants further evaluation Common Presentations Severe weight loss, dieting obsession, excessive exercise Amenorrhoea/delayed menarche GI symptoms: early satiety, constipation Fainting, dizziness, palpitations Cold intolerance, brittle hair, lanugo Special Populations Adolescents: Early intervention to avoid long-term complications Childbearing age: Delay pregnancy until stable; risk of low birth weight, hyperemesis Postpartum: Relapse risk ↑ due to stress, sleep deprivation, body image concerns Complications Medical: Osteopenia, fractures Electrolyte imbalances (e.g., hypokalaemia, hypophosphataemia) Cardiac: arrhythmias, bradycardia GI: constipation, gastric atony Amenorrhoea, infertility Psychiatric: Anxiety, depression, OCD traits Suicide risk in severe cases Anorexia Nervosa Diagnostic Criteria According to DSM-5, the key features of anorexia nervosa are: Restriction of energy intake leading to a significantly low body weight (in context of age, sex, developmental trajectory, and physical health). Intense fear of gaining weight or persistent behaviour that interferes with weight gain. Disturbance in the way one’s body weight or shape is experienced, undue influence of body weight or shape on self-evaluation, or lack of recognition of the seriousness of current low body weight. Subtypes: Restrictive Type: Weight loss primarily through dieting, fasting, or excessive exercise. Binge-Eating/Purging Type: Regular episodes of binge eating or purging (e.g. self-induced vomiting, misuse of laxatives/diuretics). Clinical Features Psychological/Behavioural Intense preoccupation with food, weight, calories Fear of weight gain; body-image distortion Restrictive eating patterns, obsessive calorie counting In adolescents: Possible amenorrhoea or delayed menarche Physical Low BMI (often <17.5 kg/m² in adults) Lanugo hair (fine downy hair on body) Cold intolerance, hypothermia Cardiovascular changes: Bradycardia, hypotension, arrhythmias Amenorrhoea or oligomenorrhoea in females; low libido in males Bone density loss (osteopenia/osteoporosis) GI issues: Early satiety, constipation Common Presentations in General Practice Persistent, significant weight loss or failure to gain weight (in adolescents) Excessive exercise routines despite low weight Fatigue, dizziness, fainting episodes (due to hypoglycaemia or low blood pressure) Psychological distress about body shape, weight, and food Investigations A thorough medical assessment is essential to evaluate nutritional status, complications, and potential aetiological factors: Routine Blood Tests FBC (Full Blood Count) eLFTs (Electrolytes, Liver Function Tests) CMP (Calcium, Magnesium, Phosphate) FBG (Fasting Blood Glucose) Endocrine & Nutritional Tests Iron studies, B12/folate for anaemia TSH (thyroid disorders) FSH, LH, oestradiol, prolactin (menstrual irregularities, hypogonadism) Cardiac ECG to detect arrhythmias, QT prolongation Bone Health DXA (Bone Densitometry) if prolonged low weight or amenorrhoea >6 months Additional Assessments as indicated (e.g. coeliac serology if malabsorption is suspected) Management Principles A multidisciplinary approach is key, involving GP, dietitian, mental health professionals, and sometimes specialist eating disorder services. Nutritional Rehabilitation Goal: Gradual weight restoration, typically 0.5–1.0 kg/week inpatient or 0.25–0.5 kg/week outpatient. Dietitian: Structured meal plans, addressing energy requirements, portion sizes. Psychological Therapies Family-Based Therapy (FBT): First-line in children and adolescents. Focuses on empowering parents to manage the child’s eating and weight restoration. Individual Therapy: Cognitive Behavioural Therapy (CBT-E), Interpersonal Therapy (IPT), or psychodynamic approaches depending on individual needs. Motivational interviewing for engagement if low insight or ambivalence. Monitoring & Medical Support Regular physical exams: Check vital signs, BMI/weight, electrolytes. Refeeding Syndrome: Monitor phosphate, magnesium, potassium closely when reintroducing calories; consider prophylactic supplementation if high risk. Psychiatric comorbidities: Depression, anxiety, OCD traits may require additional treatment (e.g. SSRIs). When to Consider Pharmacotherapy Pharmacological treatment is not a primary intervention for anorexia nervosa, but SSRIs or other medications may help with comorbid depression or anxiety once partial weight restoration is achieved. Hospital Admission Criteria Admission is warranted for acute medical risk or severe psychiatric instability. Common thresholds include: Severe Hypotension: BP <90 mmHg in adults; <80 mmHg in children Bradycardia: HR <40 bpm (adults); <50 bpm (children/adolescents) Postural Tachycardia/Hypotension: >20 mmHg drop on standing Hypothermia: <36°C, or fever >38°C indicating possible infection Hypoglycaemia: BGL <3 mmol/L Critically low BMI: <14 kg/m² in adults or rapid weight loss in adolescents Electrolyte abnormalities: e.g. severe hypokalaemia, hypophosphataemia Screening Tool: SCOFF Questionnaire Sick: Do you make yourself sick when you feel uncomfortably full? Control: Do you worry you have lost control over how much you eat? One stone: Have you recently lost more than 6.35 kg (one stone) in a 3-month period? Fat: Do you believe yourself to be fat when others say you are too thin? Food: Would you say that food dominates your life? Interpretation: Scoring ≥2 suggests a likely eating disorder and warrants further assessment. Special Populations Adolescents Early intervention can prevent long-term complications (growth and pubertal delay). Family involvement is crucial, especially with FBT. Childbearing Age Infertility and obstetric risks (low birth weight, miscarriages). Advisable to delay pregnancy until stable nutritional status. Postpartum Increased risk of relapse due to stress, sleep deprivation, body image changes. Complications Medical Osteopenia/osteoporosis: Increased fracture risk. Electrolyte imbalances (e.g. hypokalaemia, hypophosphataemia → arrhythmias, refeeding syndrome). Cardiac: Bradycardia, arrhythmias, risk of sudden death. Amenorrhoea, infertility. GI: Gastroparesis, constipation. Psychiatric Comorbidity: Depression, anxiety disorders, OCD traits. Suicide Risk: Highest among eating disorders; requires vigilant monitoring. Notes: Early detection is critical; consider screening with SCOFF in high-risk individuals (adolescents, underweight patients, females with menstrual irregularities). Family-based therapy is first-line in younger patients. Monitor refeeding syndrome when increasing caloric intake. Multidisciplinary approach: GP, dietitian, psychologist/psychiatrist, and others as needed (endocrinology, cardiology). Hospital admission thresholds are based on physiological instability, severe malnutrition, or psychiatric crisis. Bookmark Failed! Bookmark Saved! Refresh Refresh Refresh