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 Endometriosis Pathophysiology Exact cause unknown Theories: Retrograde menstruation, haematogenous spread, genetic predisposition (7× risk with family history) History Common symptoms: Dysmenorrhoea, dyspareunia, dyschezia, dysuria, infertility, lower back pain GI symptoms: Nausea, vomiting, diarrhoea, constipation, bloating Consider if: Severe dysmenorrhoea resistant to NSAIDs/OCPs or impacting daily life Examination Possible findings: Cervical fixation, tender adnexal/ovarian mass Investigations TVUS: May detect endometriomas CA125: Can be elevated, but non-specific Definitive diagnosis: Laparoscopy + histology Management Medical Therapy (First-Line) Goal: Hypoestrogenic state → Atrophy of ectopic endometrium First-line: COCPs or Mirena IUD GnRH agonists (goserelin, leuprorelin): Second-line due to side effects Surgical Management Laparoscopy (gold standard for diagnosis & treatment) Excision/ablation of lesions, adhesion lysis, endometrioma removal Severe cases: Bilateral salpingo-oophorectomy ± hysterectomy (if fertility not a concern) Multidisciplinary Approach Physiotherapy, psychological support, pain management Endometriosis Pathophysiology Endometriosis is a chronic inflammatory gynaecological condition characterised by hormone-dependent growth of endometrial-like tissue outside the uterus Theories include retrograde menstruation, haematogenous spread and genetic predisposition with a significantly increased risk in individuals with a positive family history Lesions may be superficial or deep infiltrating, and invasion into the myometrium is referred to as adenomyosis History Common symptoms include dysmenorrhoea, dyspareunia, dyschezia, dysuria and chronic pelvic pain lasting six months or more Gastrointestinal symptoms such as nausea, vomiting, diarrhoea, constipation and bloating may occur alongside premenstrual spotting and heavy menstrual bleeding Infertility is a frequent presenting complaint, and severe symptoms unresponsive to NSAIDs or oral contraceptives should prompt further evaluation Early symptom onset in adolescence and a first-degree relative with endometriosis markedly increase clinical suspicion Examination Pelvic examination may reveal cervical fixation, tender adnexal or ovarian masses and fixed pelvic organs Abdominal examination can demonstrate lower quadrant tenderness or palpable masses A detailed assessment should include evaluation for nodularity in the posterior vaginal fornix suggestive of deep infiltrating disease Investigations Transvaginal ultrasound can detect endometriomas, although deep infiltrating endometriosis may be missed and normal findings do not exclude the diagnosis CA125 levels may be elevated but are non-specific Laparoscopy with histological confirmation remains the gold standard, although treatment may begin on a presumed clinical diagnosis Management Medical Therapy (First-Line) Aim to create a hypoestrogenic state to induce atrophy of ectopic endometrium First-line options include combined oral contraceptive pills (with extended or continuous regimens) or a levonorgestrel-releasing intrauterine device Oral progestogens may be utilised when oestrogen is contraindicated, despite potential adverse effects such as irregular bleeding and breast tenderness GnRH agonists are reserved as second-line due to their side-effect profile and require add-back therapy to mitigate hypoestrogenic effects Surgical Management Laparoscopy is the gold standard for both diagnosis and treatment, allowing for excision or ablation of lesions, adhesion lysis and endometrioma removal In severe cases where fertility is not a concern, bilateral salpingo-oophorectomy with or without hysterectomy may be considered Multidisciplinary Approach Integrate physiotherapy, pelvic floor therapy, psychological support and specialised pain management into the treatment plan Encourage patients to maintain a symptom diary to monitor cyclical patterns and impact on quality of life Referral and Special Considerations Refer to a specialist gynaecology service if symptoms persist or worsen after three months of first-line treatment or if deep infiltrating disease is suspected Early referral for fertility assessment is advised for individuals over 35 years or those unable to conceive after six months of trying Consider additional multidisciplinary input for complex cases, including pain specialists and mental health professionals Ongoing Management Regular follow-up is essential to monitor treatment response and adjust therapy as needed Develop a tailored management plan addressing both physical symptoms and quality of life Long-term management may involve combining medical and surgical interventions based on evolving reproductive goals 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 β-hCG in Pregnancy Use & Actions Placental hormone that stimulates progesterone release from the corpus luteum Useful in the first 6 weeks before confirming an intrauterine pregnancy (not useful after) Fetal cardiac activity should be visible by 6 weeks on transvaginal ultrasound (TVUS) Trajectory Doubles every 2–3 days, peaks at 10 weeks Red flag: <50% rise in 48 hours suggests abnormal pregnancy (e.g., ectopic, early pregnancy failure) TVUS Findings Based on β-hCG Gestational sac visible when β-hCG >1500–2000 IU/L If non-viable pregnancy suspected: Serial β-hCG q2–3 days + repeat TVUS in 1 week Monitoring in Failed Pregnancy Monitor β-hCG weekly until it returns to negative (<5 mIU/mL) Notes Early pregnancy bleeding + no visible gestational sac → Examine adnexa for ectopic Adnexal mass (seen in >88% of ectopics) is the most common ultrasound finding Discriminatory zone: β-hCG level where a gestational sac should be seen (typically 1500–2000 IU/L) Below zone: Diagnosis based on inadequate β-hCG rise Above zone: Diagnosis based on absent intrauterine pregnancy on TVUS β-hCG in Pregnancy Definition and Physiology β-hCG is a placental hormone produced by syncytiotrophoblast cells that supports the corpus luteum by stimulating progesterone release It plays a critical role in maintaining early pregnancy until the placenta takes over hormone production Use and Actions Essential for confirming early pregnancy status in the first 6 weeks before intrauterine pregnancy can be reliably visualised Fetal cardiac activity is expected to be visible by approximately 6 weeks of gestation on ultrasound Trajectory β-hCG levels typically double every 2–3 days during early pregnancy Levels peak around 10 weeks of gestation A rise of less than 50% over 48 hours is a red flag for a non-viable or ectopic pregnancy TVUS Findings Based on β-hCG A gestational sac is usually visible on transvaginal ultrasound when β-hCG exceeds the discriminatory zone of 1500–2000 IU/L In cases of suspected non-viable pregnancy, serial β-hCG measurements every 2–3 days are indicated along with a repeat TVUS in 1 week Monitoring in Failed Pregnancy β-hCG should be monitored weekly until levels become undetectable to ensure complete resolution of a failed pregnancy Notes In early pregnancy bleeding with no visible gestational sac on TVUS, careful examination of the adnexa is critical to rule out ectopic pregnancy An adnexal mass is the most common ultrasound finding in ectopic pregnancies, observed in over 88% of cases The discriminatory zone is key; below this threshold, diagnosis relies on inadequate β-hCG rise, while above this level, absence of an intrauterine pregnancy on TVUS indicates pathology Serial β-hCG trends help differentiate between viable intrauterine pregnancies, failing pregnancies and ectopic pregnancies Plateaued or suboptimal β-hCG rises warrant further investigation even if a gestational sac is not visualised Combining biochemical monitoring with TVUS findings enhances diagnostic accuracy in early pregnancy complications 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 Antiphospholipid Syndrome (APS) Presentation Acquired thrombophilia → increased risk of arterial and venous thrombi Recurrent miscarriages, pre-eclampsia, fetal growth restriction, MI, CVA Associated with SLE and autoimmune disorders May present with livedo reticularis or thrombocytopenia Pathophysiology Antiphospholipid antibodies attack phospholipids in vessel linings → clot formation Triple positivity (lupus anticoagulant, anticardiolipin, beta-2 glycoprotein 1) confers higher risk of recurrent thrombosis Investigations Antibody tests: Lupus anticoagulant Anticardiolipin antibody Beta-2 glycoprotein 1 antibody Other tests: FBC (for thrombocytopenia), coagulation studies Repeat aPL testing at least 12 weeks apart to confirm persistent positivity Assess modifiable risk factors (smoking, hypertension, dyslipidaemia) to reduce vascular risk Diagnosis Requires 1 clinical manifestation (thrombotic or obstetric) + positive aPL antibodies on 2 occasions, 12 weeks apart Higher-risk profiles include triple positivity and history of severe thrombotic or obstetric complications Treatment Lifelong warfarin for thrombotic APS (target INR 2.5–3.5) Avoid NOACs (less effective in APS) Aspirin/clopidogrel for certain cases Specialist anticoagulation management during pregnancy Bridge warfarin with LMWH if anticoagulation must be paused Regular INR monitoring is crucial, especially in high-risk (triple-positive) patients (RACGP) Obstetric vs Thrombotic APS Clinical Manifestations Obstetric APS ≥3 early miscarriages (<10 weeks) ≥1 fetal death (>10 weeks) Preterm birth (<34 weeks) due to pre-eclampsia / placental insufficiency Thrombotic APS DVT/PE (most common initial presentation) Stroke/TIA in young patients Other: Myocardial infarction, retinal occlusion, microvascular thrombosis Management Obstetric APS Low-dose aspirin + LMWH during pregnancy and 6–12 weeks postpartum High-risk cases: Add hydroxychloroquine or IVIG (specialist decision) Postpartum period remains high risk for thrombosis; prophylaxis continuation advised Thrombotic APS Lifelong anticoagulation with warfarin Recurrent events: Combine warfarin with antiplatelet therapy (aspirin/dipyridamole) Antiphospholipid Syndrome (APS) Presentation Acquired thrombophilia → increased risk of arterial and venous thrombi Recurrent miscarriages, pre-eclampsia, fetal growth restriction, MI, CVA Associated with SLE and autoimmune disorders, also seen in Sjögren’s syndrome, RA, systemic sclerosis May present with livedo reticularis, thrombocytopenia, or cardiac valve disease (valve thickening and regurgitation) Catastrophic APS (CAPS) is a rare, life-threatening variant causing multi-organ failure due to microvascular thrombosis Pathophysiology Antiphospholipid antibodies (aPL) interact with inflammatory endothelial factors → disrupt coagulation → clot formation Triple positivity (lupus anticoagulant, anticardiolipin, beta-2 glycoprotein 1) confers highest risk of recurrent thrombosis aPL antibodies may be additive to traditional risk factors (smoking, hypertension, hyperlipidaemia) Investigations Antibody tests: Lupus anticoagulant Anticardiolipin antibody Beta-2 glycoprotein 1 antibody Other tests: FBC (thrombocytopenia, anaemia) Coagulation studies (aPTT prolongation, INR monitoring) Repeat aPL testing at least 12 weeks apart to confirm persistent positivity Assess modifiable risk factors (smoking, hypertension, dyslipidaemia) to reduce vascular risk Diagnosis Requires one clinical manifestation (thrombotic or obstetric) plus persistent aPL antibodies (two positive tests, 12 weeks apart) Higher-risk profiles: Triple positivity and history of severe thrombotic or obstetric complications Catastrophic APS diagnosed when thrombosis affects ≥3 organs in <1 week Treatment Thrombotic APS: Lifelong warfarin (target INR 2.5–3.5) Avoid NOACs (less effective in APS, increased risk of recurrent thrombosis) Recurrent events: Warfarin + antiplatelet therapy (aspirin/dipyridamole) Consider hydroxychloroquine for added protection in high-risk patients Statins may be considered in high-risk patients with atherosclerotic risk factors Specialist input for refractory cases, catastrophic APS Obstetric APS: Low-dose aspirin + LMWH during pregnancy and for 6–12 weeks postpartum High-risk cases: Add hydroxychloroquine or IVIG (specialist decision) Warfarin contraindicated in pregnancy → switch to therapeutic LMWH Postpartum remains high risk for thrombosis; extended prophylaxis advised Obstetric vs Thrombotic APS Clinical Manifestations Obstetric APS ≥3 early miscarriages (<10 weeks) ≥1 fetal death (>10 weeks) Preterm birth (<34 weeks) due to pre-eclampsia/placental insufficiency Thrombotic APS DVT/PE (most common initial presentation) Stroke/TIA in young patients Other: Myocardial infarction, retinal occlusion, microvascular thrombosis Management Obstetric APS Low-dose aspirin + LMWH during pregnancy and 6–12 weeks postpartum High-risk cases: Add hydroxychloroquine or IVIG (specialist decision) Postpartum period remains high risk for thrombosis; prophylaxis continuation advised Thrombotic APS Lifelong anticoagulation with warfarin Recurrent events: Combine warfarin with antiplatelet therapy (aspirin/dipyridamole) Catastrophic APS (CAPS) Acute multi-organ failure due to widespread microvascular thrombosis Precipitated by infection, surgery, malignancy, anticoagulation withdrawal Requires urgent hospitalisation, anticoagulation, high-dose steroids, IVIG, and plasma exchange Key Considerations Screening for aPL antibodies only in specific clinical contexts (young stroke, unprovoked VTE, recurrent pregnancy loss) Asymptomatic aPL positivity does not warrant routine anticoagulation, but may justify aspirin in high-risk individuals Hydroxychloroquine recommended for SLE patients with aPL antibodies Regular INR monitoring crucial, especially in high-risk (triple-positive) patients Avoid oestrogen-containing contraceptives and HRT in APS due to increased thrombotic 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 Mastalgia Differential Diagnoses Cyclical mastalgia (typically bilateral, worse premenstrually) Non-cyclical mastalgia (unilateral or bilateral) Pregnancy Breast cancer Contraceptive use Mastitis/breast abscess Costochondritis/thoracic back pain Management Reassurance & breast awareness Appropriate breast screening Supportive bra (sports bra may help) Analgesia: Paracetamol 1g QID PRN Topical NSAIDs for localised pain Evening primrose oil (EPO): 1000 mg 2–3× daily for 2–3 months may help Cease smoking Aim for ideal body weight Severe cases affecting lifestyle: Danazol, tamoxifen may be considered → Limited by side effects, specialist review required Mastalgia Definition Mastalgia is breast pain that affects up to 77% of women at some point in their lives It may be accompanied by tenderness, lumpiness, fullness, heaviness or an increase in breast size It is typically benign and not indicative of breast cancer, although it can cause significant discomfort and anxiety Differential Diagnoses Cyclical mastalgia, usually bilateral, worsening premenstrually and most common in premenopausal women in their 30s Non-cyclical mastalgia, which may be unilateral or bilateral, with burning, stabbing or throbbing pain, more common in women in their 40s Pregnancy-related breast changes Breast cancer Effects of hormonal contraceptive use Mastitis or breast abscess Chest wall pain from costochondritis or thoracic back pain Investigation Obtain a thorough history and encourage completion of a pain chart to characterise the pattern of pain Conduct a detailed physical examination of the breasts, including palpation for masses or asymmetry Arrange breast imaging with ultrasound and/or mammography based on clinical findings and patient age Consider triple assessment (clinical examination, imaging and non-surgical biopsy) for any significant findings such as asymmetrical thickening or a discrete palpable mass Management Reassure the patient that mastalgia is typically benign and not caused by breast cancer Promote breast awareness and ensure appropriate breast screening is in place Advise the use of a well-fitting supportive bra, for example a sports bra Recommend analgesia with paracetamol 1 g QID as needed Use topical NSAIDs for localised pain relief Suggest evening primrose oil at a dose of 1000 mg 2–3 times daily for 2–3 months Encourage lifestyle modifications such as smoking cessation and achieving an ideal body weight For severe cases affecting quality of life, consider hormonal treatments such as danazol or tamoxifen with referral for specialist review Notes Cyclical mastalgia typically improves with the onset of menstruation, whereas non-cyclical mastalgia does not vary with the menstrual cycle and may warrant further evaluation Chest wall pain should be considered when breast imaging is normal and the pain may originate from muscles, ribs or ligaments A combination of reassurance, conservative measures and tailored pharmacological therapy often yields the best outcomes Ongoing patient education and follow-up are crucial, as most cases of mastalgia tend to improve over time regardless of treatment 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 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 Gender Dysphoria Terminology & Definitions Sex: Assigned at birth based on external anatomy (e.g. male/female) Gender: Social construct encompassing roles, behaviours, and identities beyond a binary model Gender Identity: Internal sense of being male, female, both, neither, or another identity (may/may not align with assigned sex) Gender Dysphoria (DSM-5): Distress due to incongruence between experienced gender and assigned sex Aetiology Multifactorial: Biological, psychological, and sociocultural influences Possible contributors: Genetic, hormonal, and neurodevelopmental factors, though no single causative mechanism identified Clinical Presentation & Diagnosis Key features: Incongruence between experienced gender and assigned sex Discomfort with primary/secondary sex characteristics Desire to be of another gender and/or treated as another gender Distress/impairment in social, occupational, or personal functioning Adolescents & Children Gender exploration may be a normal developmental process Persistent, consistent, and insistent cross-gender identification → consider specialist referral Screening & Assessment Non-judgemental approach (use open-ended questions) Psychosocial assessment: HEADSS tool (adolescents) Comprehensive biopsychosocial evaluation: Mental health: Screen for depression, anxiety, self-harm Physical health: Sexual health, fertility considerations Family/social support Role of the GP Safe & inclusive environment: Use chosen names/pronouns, ensure clinic staff are respectful Screen for comorbidities: Depression, anxiety, eating disorders, self-harm, suicidal ideation Coordinate care: Liaise with mental health, endocrinology, speech pathology, and other specialists Documentation support: Letters for name changes, identity documents, workplace accommodations Management Approaches Psychosocial Support Counselling (with transgender-competent clinicians) Family therapy, especially for adolescents Hormone Therapy (typically managed with endocrinologist or trained GP) Transfeminine: Oestrogen ± anti-androgens Transmasculine: Testosterone therapy Monitoring: Hormone levels, lipids, liver function, risk-benefit discussions Puberty Suppression (Adolescents) GnRH analogues (puberty blockers) to pause secondary sexual development, allowing time for identity exploration Requires specialist paediatric endocrinology and mental health support Surgical Interventions (older adolescents/adults with persistent dysphoria) Top surgery: Chest reconstruction (transmasculine), breast augmentation (transfeminine) Bottom surgery: Vaginoplasty, phalloplasty, metoidioplasty Requires robust assessment, psychological support, and informed consent Gender Dysphoria Terminology and Definitions Sex: Typically assigned at birth based on external anatomy (e.g. male/female). Gender: A social and cultural construct, referring to the roles, behaviours, and identities deemed appropriate for men and women (or beyond a binary understanding). Gender Identity: A person’s internal, deeply felt sense of being male, female, both, neither, or another identity. This may or may not align with the sex assigned at birth. Gender Dysphoria (DSM-5): Refers to the distress or discomfort that may arise when one’s experienced or expressed gender is incongruent with one’s assigned sex. It replaces the older term “gender identity disorder.” Aetiology and Contributing Factors The aetiology of gender dysphoria is considered multifactorial, involving biological, psychological, and sociocultural components. Genetic, hormonal, and neurodevelopmental studies suggest a possible biological underpinning; however, conclusive causal mechanisms remain under investigation. Clinical Presentation and Diagnosis GPs may be the first health professionals approached by patients experiencing gender incongruence. Key features: Marked incongruence between one’s experienced/expressed gender and assigned sex. Discomfort with one’s primary and/or secondary sex characteristics. Desire to be of another gender and/or to be treated as another gender. This incongruence often leads to significant distress or impairment in social, occupational, or other important areas of functioning. Adolescents and Children Presentation can start in childhood or adolescence but must be interpreted with caution, recognising that gender exploration can be a normal developmental process for some. Persistent, consistent, and insistent expression of cross-gender identification in a child or adolescent warrants further evaluation and possibly referral to specialist services. Screening and Assessment A non-judgemental approach is essential. Begin with open-ended questions about gender identity and explore the patient’s experiences, expectations, and goals. Consider using psychosocial assessment tools (e.g. HEADSS for adolescents). In cases of suspected gender dysphoria, a comprehensive biopsychosocial evaluation is important: Mental health history (screen for depression, anxiety, self-harm). Physical health (including sexual health, fertility considerations). Family and social context, support systems. Role of the GP GPs play a crucial role in early recognition, support, referral, and ongoing primary care for patients with gender dysphoria. Key responsibilities: Provide a safe, inclusive environment: Use chosen names/pronouns and ensure clinic staff are similarly respectful. Screen for comorbidities: Higher rates of depression, anxiety, eating disorders, self-harm, and suicidal ideation have been noted among trans and gender diverse people. Coordinate care: Liaise with mental health professionals, endocrinologists, speech pathologists, and other allied health services involved in transgender care. Assist with documentation: Offer letters of support for name changes, official identity documents, and workplace accommodations if needed. Management Approaches Psychosocial Support Counselling or psychotherapy (with a clinician experienced in transgender health) to support exploration of gender identity, address dysphoria, and foster resilience. Family therapy or parental support, especially for adolescents, to facilitate a positive family environment. Hormone Therapy Typically managed in collaboration with an endocrinologist experienced in transgender care, or a GP with appropriate additional training/experience. Gender-affirming hormones can greatly alleviate dysphoria but require comprehensive assessment and informed consent. Oestrogen-based therapy for transfeminine patients; testosterone-based therapy for transmasculine patients. Monitoring includes regular blood tests (e.g. hormone levels, lipids, liver function) and ongoing risk-benefit discussions. Puberty Suppression (Adolescents) In early puberty, gonadotrophin-releasing hormone (GnRH) analogues (puberty blockers) may be offered, typically in consultation with specialist paediatric endocrinology and mental health support. Puberty suppression aims to pause irreversible secondary sexual characteristic development, giving the young person time to explore their gender identity. Surgical Interventions Gender-affirming surgeries (e.g. chest reconstruction, vaginoplasty, phalloplasty) can be considered in older adolescents or adults with persistent gender dysphoria. Surgical decisions require robust assessment, psychological support, and ensuring realistic expectations about outcomes, risks, and benefits. Ethical, Legal, and Cultural Considerations Informed Consent and Capacity Assess capacity to consent, especially in minors. For individuals under 18, decision-making often involves a multidisciplinary team plus parental/guardian involvement. In some complex cases, legal processes may be required. Confidentiality Strict adherence to privacy and confidentiality laws is critical due to high rates of discrimination and stigma. Cultural Competence Aboriginal and Torres Strait Islander, CALD (Culturally and Linguistically Diverse) communities, and faith-based backgrounds may have unique needs. Ensure culturally sensitive approaches and, where appropriate, engage multicultural or Indigenous liaison workers. Mental Health Risks and Co-Management High rates of suicidal ideation and self-harm in transgender populations highlight the need for vigilant mental health support. GPs should screen for depression, anxiety, eating disorders, and substance misuse. Early referral to mental health professionals is recommended if risk factors are present. 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 Lichen Planus Definition Chronic inflammatory disorder affecting skin and mucosa Affects ~1 in 100 people, usually >40 years Autoimmune, possibly triggered by stress, trauma, medications Targets keratinocytes Clinical Features 5 Ps: Polygonal, Pruritic, Purple, Papular, Plaques Lesions: Scaly plaques with Wickham’s striae (white lacy lines) Common sites: Wrists, ankles, lower back, oral mucosa (cheeks, tongue, lips) Types Cutaneous Lichen Planus Shiny, flat-topped polygonal plaques (wrists, ankles, mucosa) Wickham’s striae Severe cases: Persistent ulcers, erosions Oral Lichen Planus Cheeks, gums, lips Painful erosions, redness, Wickham’s striae Increased risk of oral SCC Management General Measures Avoid irritating soaps Regular emollients Specific Treatments Potent topical corticosteroids Topical calcineurin inhibitors Retinoids (topical/systemic) Intralesional steroids (severe cases) Prognosis Resolves within 6–9 months, but chronic/severe cases may persist Biopsy if uncertain diagnosis (rule out SCC) Lichen Planus Definition Lichen planus is a chronic inflammatory disorder affecting the skin and mucosa, typically seen in adults over 40. It is considered autoimmune in nature, possibly triggered by stress, trauma, or certain medications. The immune response primarily targets keratinocytes, leading to characteristic lesions. Clinical Features Known by the “5 Ps”: Polygonal Pruritic Purple Papular Plaques Lesions often show Wickham’s striae (fine white, lacy lines) on the surface. Common sites: Wrists, ankles, lower back, and oral mucosa (cheeks, tongue, lips). Approximately 1 in 100 people affected, slightly more in middle-aged or older adults. Types Cutaneous Lichen Planus Shiny, flat-topped polygonal plaques on the skin (wrists, ankles). Wickham’s striae on the surface. Severe cases can have persistent ulcers or erosions. Oral Lichen Planus Involves cheeks, gums, or lips. Painful erosions, redness, Wickham’s striae are common. Increased risk of oral squamous cell carcinoma if persistent erosive lesions. Management General Measures Avoid irritating soaps, minimise friction/trauma to lesions. Regular emollients to reduce dryness and itching. Specific Treatments Potent Topical Corticosteroids (e.g. clobetasol propionate) → first-line for localised cutaneous lesions. Topical Calcineurin Inhibitors (e.g. tacrolimus ointment) → especially for oral or genital lesions. Retinoids (topical or systemic) → help reduce thickness of plaques, can be considered in severe or recalcitrant cases. Intralesional Steroids (e.g. triamcinolone) → for persistent plaques or hypertrophic lesions. Prognosis Many cases resolve spontaneously within 6–9 months, but some can become chronic or severe. Oral lichen planus may persist longer; regular follow-up is essential to rule out malignant transformation. Biopsy if diagnosis is uncertain or if lesions show suspicious changes (to exclude SCC). 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 Limping Child Differentials Developmental/Mechanical: Perthes: Gradual painless limp, knee pain, short limb SCFE: Knee/hip pain, externally rotated, shortened leg Transient synovitis: Post-URTI, self-limiting Overuse injury: Stress fractures, growth plate irritation Minor injuries: Common in active children Infective/Inflammatory: Septic arthritis: Fever, NWB, effusion Osteomyelitis: Local tenderness, erythema, systemic signs Post-viral myositis: Resolves in days JIA: Chronic joint pain, stiffness Other: Malignancy: Night pain, systemic signs Trauma/NAI: Fractures, unexplained injuries HSP: Petechiae, joint swelling, abdominal pain Red Flags Systemic signs: Fever, weight loss, fatigue Pain: Night pain, worsening, localised tenderness Persistent limp >7 days NWB: Suspect septic arthritis or SCFE Petechiae/bruising: HSP, malignancy, NAI Examination Gait: Antalgic, Trendelenburg, stiff ROM: Restricted internal rotation → early pathology Joint/knee: Pain, effusion Systemic signs: Fever, pallor, bruising Position: External rotation/short limb → SCFE Investigations No tests: Mild limp <7 days, no red flags Bloods: FBC, CRP, ESR; cultures if infection suspected Imaging: X-ray: Structural issues US: Effusion (septic arthritis/synovitis) MRI: Suspected malignancy/osteomyelitis Management Transient synovitis: Rest, weight-bearing as tolerated, paracetamol/ibuprofen Perthes: Urgent: >8 yrs (surgery likely) Semi-urgent: <8 yrs (activity restriction, physio) SCFE: NWB, urgent ortho referral Risk: Osteonecrosis, early OA Hallmarks Perthes: Boys 4–8 yrs, gradual limp, ↓ internal rotation SCFE: Adolescents (obese), knee/hip pain, external rotation Transient synovitis: Boys 3–10 yrs, post-URTI, resolves <7 days Limping Child Differentials Developmental/Mechanical Perthes disease: Gradual, painless limp; knee pain; limb shortening; decreased internal rotation Slipped upper femoral epiphysis (SCFE): Presents in adolescents; knee or hip pain; externally rotated, shortened leg; often linked to obesity Transient synovitis: Occurs post-URTI or fever; self-limiting; typical in children aged 3–10 Overuse injury/stress fracture: Associated with increased physical activity and growth plate irritation Minor musculoskeletal injury: Common in active children with trivial trauma Infective/Inflammatory Septic arthritis: Presents with fever, inability to bear weight, and joint effusion; requires urgent treatment Osteomyelitis: Localised bone pain with tenderness, erythema, and systemic signs Juvenile idiopathic arthritis: Chronic joint pain and morning stiffness with persistent swelling Postviral myositis: Generally self-limiting and resolves within days Other Malignancy: Leukaemia, lymphoma, or bone tumour; characterised by night pain, systemic symptoms, and localized tenderness Non-accidental injury: Unexplained trauma with inconsistent history and possible bruising Henoch-Schönlein purpura: May present with petechiae, joint swelling, and abdominal pain Red Flags Systemic symptoms including fever, weight loss, night sweats and fatigue indicating severe infection or malignancy Persistent limp lasting over 7 days or non-weight bearing status suggestive of septic arthritis or SCFE Localised, worsening or nocturnal pain raising suspicion of bone tumour Skin findings such as petechiae or bruising which may point to HSP, malignancy or non-accidental injury Examination Gait analysis: Look for antalgic, Trendelenburg or stiff gait patterns Hip range of motion: Assess for limitation, especially reduced internal rotation which may indicate Perthes disease or SCFE Knee examination: Evaluate for pain, effusion and tenderness Limb alignment: Note external rotation or shortening suggestive of SCFE Systemic assessment: Check for fever, pallor or bruising and inspect skin for petechiae Investigations No immediate tests if limp is mild and lasts <7 days without red flags Blood tests: Full blood count, CRP and ESR to assess for infection or inflammation Imaging: X-ray of the hip and knee to evaluate for structural abnormalities such as Perthes disease or SCFE; Ultrasound of the hip to detect joint effusion in cases of suspected septic arthritis or transient synovitis MRI: Consider if there is a suspicion of osteomyelitis, malignancy or if initial imaging is inconclusive Management Observation: Review in 3 days if the child is otherwise well and symptoms are mild Activity modification: Encourage rest from aggravating activities and allow weight bearing as tolerated in transient synovitis Pain management: Use paracetamol 15 mg/kg QID as required Perthes disease: Semi-urgent orthopaedic referral for children <8 years with activity restriction and physiotherapy; urgent referral for children >8 years as surgery may be indicated SCFE: Non-weight bearing measures and urgent orthopaedic referral to prevent complications such as osteonecrosis and early osteoarthritis Provide safety netting advice and arrange close follow-up if symptoms persist or worsen Notes Perthes disease commonly affects boys aged 4–8 years and is typically painless with decreased internal rotation SCFE is seen in adolescents, frequently associated with obesity, and may present with knee pain rather than hip pain Transient synovitis usually follows an URTI and resolves within 7 days Persistent or worsening symptoms require further investigation to exclude serious pathology such as septic arthritis, malignancy or non-accidental injury Multidisciplinary management including orthopaedics and physiotherapy improves long-term 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 Cervical Spondylosis Presentation Pain: Dull, aching suboccipital pain ± tension-like headaches Unilateral, worsens with activity or prolonged neck positions ROM: Restricted neck rotation or lateral flexion Neurological: Upper limb paraesthesia (dermatomal) Possible cervical radiculopathy or myelopathy Spurling’s Test: Neck extension, lateral flexion, rotation + downward pressure Positive: Limb pain/paraesthesia (not neck pain alone) Investigations MRI Spine: Preferred for: Motor symptoms, red flags (e.g., malignancy, infection), progressive symptoms Failure to respond to conservative management Other: XR Cervical Spine: Degenerative changes (osteophytes, narrowing) Nerve Conduction Studies: If MRI unavailable Management (No Severe Neuro Deficits) Lifestyle: Avoid aggravating activities (e.g., prolonged flexion) Postural correction Pain Relief: NSAIDs ± short steroids for acute radicular pain Physiotherapy: Strengthening/stretching exercises, mobilisation Adjuncts: Soft cervical collar (short-term only) Steroid injections (epidural/facet joint) for persistent radicular pain Follow-Up 6–8 weeks: Assess symptom resolution/improvement Refer for advanced imaging or specialist review if worsening Cervical spondylosis Definition A degenerative disorder of the cervical spine characterised by age-related wear of the intervertebral discs, facet joints, and other surrounding structures. It commonly leads to osteophyte formation, disc narrowing, and ligamentous thickening, which can impinge on nerve roots or the spinal cord. Presentation Pain: Often presents as a dull, aching discomfort in the suboccipital region and may radiate unilaterally to the neck and shoulders. Some patients experience tension-type headaches Range of motion: Restricted neck rotation or lateral flexion due to pain or stiffness. Pain may worsen after prolonged neck positions (e.g. computer or desk work) Neurological involvement: Upper limb paraesthesia following a dermatomal pattern. Cervical radiculopathy (root compression) can lead to arm pain, while cervical myelopathy (spinal cord compression) can cause gait disturbance, hand clumsiness, or bowel/bladder issues in advanced cases Spurling’s test: Performed by extending the neck, laterally flexing and rotating it towards the symptomatic side, then applying gentle downward pressure. A positive test reproduces limb pain or paraesthesia, suggesting nerve root irritation Investigations MRI of the cervical spine: The imaging of choice when red flags (e.g. motor weakness, malignancy, infection) are present, or if conservative measures fail. It is sensitive for detecting neural element compression, disc herniation, and soft-tissue changes Plain X-ray: Demonstrates degenerative changes such as osteophytes, disc space narrowing, and spondylolisthesis. Often an initial screening tool but less sensitive for nerve root or cord pathology Nerve conduction studies or electromyography: Consider if MRI is unavailable, or to further clarify nerve root involvement, especially in complicated or atypical presentations Management (when no severe neurological deficits) Lifestyle and postural advice: Avoid prolonged neck flexion or extension (e.g. extended computer use without breaks) Encourage ergonomic assessment in the workplace Pain relief: NSAIDs can be used first-line for musculoskeletal neck pain, and short courses of oral corticosteroids may help in acute radicular episodes. Paracetamol can be added or substituted if NSAIDs are contraindicated Physiotherapy: Tailored exercises focusing on neck-strengthening, mobilisation, and postural training. Techniques may include gentle manual therapy and advice on maintaining flexibility and core neck stability Soft cervical collar: Can be used briefly for acute exacerbations, though prolonged use is generally discouraged to avoid neck muscle deconditioning Steroid injections: Epidural or facet joint injections can be considered for persistent radicular pain or localised facet joint inflammation. Ultrasound or fluoroscopic guidance may improve accuracy and efficacy Follow-up: Review at 6–8 weeks to assess improvement in pain and function. Escalation to advanced imaging or specialist referral is recommended if there is clinical deterioration, persistent severe pain, or developing neurological deficits Additional considerations Red flags prompting urgent imaging or specialist review include progressive neurological deficits, suspected cervical myelopathy (e.g. unsteady gait, hyperreflexia, bowel/bladder dysfunction), history of malignancy, weight loss, or severe unremitting night pain Physiotherapists and exercise physiologists can provide home-based exercise programmes to improve neck strength and mobility, with an emphasis on posture correction and activity modification Adjunct measures, such as topical analgesics or neuropathic pain agents (in radicular pain), may be utilised according to clinical judgement Prognosis varies depending on the degree of degenerative change and nerve involvement, but most mild-to-moderate cases respond well to conservative measures over weeks to months Bookmark Failed! Bookmark Saved! 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Log In Get started Bookmarks Help Progress 0% Cardiovascular AAA + Rupture AC dislocation ATSI Abdominal pain in kids Abnormal/Dysfunctional Uterine Bleeding (AUB/DUB) Acanthosis Nigricans Acne Acromegaly Actinic Cheilitis Acute Kidney Injury (AKI) Acute Swollen Joint with Fever Acute Vision Loss Acute and Progressive Vision Loss Addisons Adjustment Disorder and Anxiety Adjustment Disorder with Depressed Mood Age related macular degeneration Alcohol Cessation Allergic rhinitis Alopecia Amenorrhoea Anaphylaxis Angina Angular Cheilitis Ankylosing Spondylitis (AS) Anorexia Nervosa Anticholinergics and TCAs Antidepressants Antimetabolite drugs Antiphospholipid syndrome Antipsychotics Anxiety Disorders Aortic Dissection Arrhythmia Asthma Asthma Atrial Fibrillation Back pain Behavioural / learning disorders Behavioural disturbances Bell’s palsy and Ramsey Hunt syndrome Beta-Human Chorionic Gonadotropin (β-hCG) Biologic agents Bipolar Disorder Bleeding disorders Blepharitis Breast Cancer Breast Lump Bronchiectasis (Updated) CA-125 (Cancer Antigen 125) CRPS CVD Risk Assessment Calluses and Corns Candida (Candidiasis as an STI) Carpal tunnel syndrome and de quervains tenosynovitis Cellulite Cervical spondylosis Chest pain Chickenpox (Varicella) Chilblains Cholesteatoma Chronic Cough in Children Chronic Fatigue Syndrome (CFS) Chronic Kidney Disease (CKD) Chronic Rhinosinusitis Chronic Stridor Clavicular fracture Clozapine Coeliacs Colorectal Cancer Screening Recommendations Congestive Cardiac Failure Connective Tissue Diseases Constipation Contact Dermatitis Cracked Heel Croup Cushings Cutaneous Drug Eruptions DKA vs HHS Dacrocystitis, dacyrostenosis, dacyrocystocoele Deep Vein Thrombosis (DVT) Delerium Dementia Depression and Delirium Dermal melanocystosis (mongolian spot) Developmental Dysplasia of the Hip (DDH) Diabetes Diabetes Insipidus (DI) vs Primary Polydipsia Diabetic Neuropathy Diarrhoea Diplopia Dizziness / syncope Down syndrome Duchenne muscular dystrophy Dupuytrens / trigger finger Dyspepsia Dyspnoea (Shortness of Breath) ECG ECG Findings ECG Patterns CONCISE COMPREHENSIVE External Auditory Exostosis Aetiology / Pathology Chronic cold water/air exposure → periosteal bone growth in the external auditory canal (EAC) Common in surfers, divers, and swimmers ("surfer’s ear") Typically multiple, broad-based bony outgrowths near the tympanic ring Symptoms / Presentation Recurrent otitis externa (narrowed canal traps debris/moisture) Ear blockage or discomfort Progressive conductive hearing loss (advanced cases) Frequent cerumen impaction due to restricted canal diameter Examination Otoscopic findings: Bony mounds narrowing the EAC May limit TM visualisation, especially if inflamed or debris present Diagnosis Clinical: History of cold water exposure + otoscopic findings Audiometry: If hearing loss suspected CT temporal bone: If severe or for surgical planning Management Prevention Earplugs/neoprene hood in cold water Thorough drying after water exposure Avoid repeated cold exposure if possible Medical Treat infections/otitis externa with topical agents Manage wax impaction with drops or gentle suction Surgical (if severe stenosis, recurrent infections, or hearing loss) Exostoses removal under microscope with specialised drills Risks: SNHL, facial nerve injury, infection Long-term follow-up for regrowth monitoring ENT Referral Persistent symptoms, progressive hearing loss, frequent infections Obstructive exostoses affecting quality of life Notes Early prevention minimises complications Regular ear hygiene reduces cerumen impaction and infection risk Significant bony overgrowth increases risk of recurrent infections, warranting ENT assessment if persistent/worsening symptoms External Auditory Exostosis Aetiology / Pathology Chronic exposure to cold water and air stimulates periosteal bone growth in the canal Common in surfers, divers, swimmers, and others frequently in cold aquatic environments Typically presents as multiple, broad-based bony outgrowths near the tympanic ring Symptoms / Presentation Recurrent ear infections or otitis externa (due to narrowed canal trapping debris and moisture) Sensation of ear blockage or discomfort Progressive conductive hearing loss in advanced cases (from canal narrowing or impacted cerumen) May notice frequent ear wax impaction due to restricted canal diameter Examination Otoscopic inspection reveals bony mounds protruding into the EAC Canal may appear narrowed, limiting visualisation of the tympanic membrane Inflammation or debris can complicate the view if infection is present Diagnosis Primarily clinical based on history (repeated cold water exposure) and otoscopic findings Audiometry if hearing impairment is suspected Imaging (e.g. CT temporal bones) may be considered for severe cases or surgical planning Management Preventive Measures Wear earplugs or neoprene hood when surfing or swimming in cold conditions Thoroughly dry the ears after water exposure Encourage avoidance of repeated exposure to cold wind or water if possible Medical Management Treat infections or otitis externa promptly with topical agents to reduce inflammation and debris Ear drops or gentle suctioning to manage impacted wax Surgical Removal Indicated if canal stenosis is severe, recurrent infections, or significant hearing loss Performed under microscope, removing exostoses with specialised drills Risks include sensorineural hearing loss, facial nerve injury, and infection Long-term follow-up may be required to monitor for regrowth Referral to ENT Persistent or symptomatic cases Progressive hearing loss, frequent infections, or difficulty in removing obstructive exostoses Consideration of operative intervention if quality of life is affected Notes: Early intervention and consistent preventive strategies can minimise complications Regular ear hygiene and protection help prevent recurrent exostosis formation and reduce infection risk Patients with significant bony overgrowth are at higher risk of cerumen impaction and external ear canal infections, emphasising the importance of ENT assessment if symptoms persist or worsen Bookmark Failed! 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