MBBS Curriculum
The MBBS library.
349 evidence-graded topics across 27 subjects and 23 systems — written for NEET-PG, INICET, and MBBS final-professional exams. Filter by year or sub-specialty.
Topics349
Subjects27
High yield299
349 topics
General Medicine
138 topicsCardiology
2
★ High yieldCardiology
Infective Endocarditis
Infective endocarditis (IE) is a microbial infection of the endocardial surface, usually a heart valve, forming friable vegetations of platelets and fibrin that entrap organisms. It classically presents with fever, a new or changing murmur, and embolic, immunologic or septic phenomena. Diagnosis rests on blood cultures and echocardiography integrated through the Duke criteria. Management combines prolonged bactericidal antibiotics (benzylpenicillin/ceftriaxone ± gentamicin for streptococci; flucloxacillin for MSSA; vancomycin for MRSA) with early surgery for heart failure, uncontrolled infection or the prevention of embolism.
NEET-PGINICET
★ High yieldCardiology
Peripheral Arterial Disease
Peripheral arterial disease (PAD) is atherosclerotic narrowing of the lower-limb arteries — a clinical expression of systemic atherosclerosis and a powerful marker of coronary and cerebrovascular risk. The hallmark symptom is intermittent claudication, reproducible calf (or buttock/thigh) pain on walking that is relieved within minutes by rest, progressing in advanced disease to rest pain and chronic limb-threatening ischaemia with ulceration or gangrene. The bedside test is the ankle–brachial index (ABI): a value below 0.9 confirms PAD, below 0.4 indicates critical ischaemia, and over 1.3 signals non-compressible calcified vessels. Management has two aims — reduce cardiovascular risk (smoking cessation, high-intensity statin, antiplatelet, tight blood-pressure and glycaemic control, supervised exercise) and improve the leg (cilostazol or naftidrofuryl for claudication; endovascular or surgical bypass revascularisation for disabling symptoms or limb threat). Acute limb ischaemia, the sudden 6-P occlusion from embolism or thrombosis, is a vascular emergency requiring immediate heparin and revascularisation. Smoking and diabetes dominate the risk profile.
NEET-PGINICET
Dermatology
10
★ High yieldDermatology
Alopecia & Hair Disorders
Hair loss (alopecia) is the single most psychologically charged dermatological presentation. The pivotal skill is the scarring vs non-scarring distinction: non-scarring (reversible — androgenetic, alopecia areata, telogen effluvium, anagen effluvium, traction, trichotillomania, tinea capitis) preserves the follicle and is potentially recoverable, whereas scarring (cicatricial) (lichen planopilaris, frontal fibrosing alopecia, central centrifugal cicatricial alopecia, discoid lupus, folliculitis decalvans, pseudopelade) destroys follicular stem cells and is permanent and irreversible. Androgenetic alopecia (miniaturisation by dihydrotestosterone via 5-alpha-reductase type II) is graded by the Hamilton-Norwood scale in men and the Ludwig scale in women and treated with topical minoxidil 5% and oral finasteride 1 mg daily (men only). Alopecia areata (autoimmune T-cell attack on anagen follicles) presents as a smooth patch with exclamation-mark hairs and is now treated with JAK inhibitors (baricitinib, ritlecitinib) for severe disease — FDA-approved 2022-2023. Telogen effluvium is diffuse shedding two to three months after a trigger and is self-limiting.
NEET-PGINICET
Dermatology
Benign Skin Lesions
Benign skin lesions are the most common tumours in medicine. The high-yield catalogue: seborrhoeic keratosis ('stuck-on' waxy brown plaques, older adults, most common benign tumour of all — comedo-like horn cysts on dermoscopy), melanocytic naevi (moles — junctional, compound, intradermal; plus Spitz, halo, blue, dysplastic variants), pyogenic granuloma (lobular capillary haemangioma — friable bleeding papule after trauma), dermatofibroma (firm brown leg papule, dimple sign), sebaceous hyperplasia (yellow umbilicated facial papule), epidermoid and pilar cysts (firm subcutaneous nodule with punctum — keratin not sebum), lipoma (soft doughy mobile mass), milia, syringoma, cherry angioma, neurofibroma (buttonhole sign, NF1) and xanthelasma (yellow eyelid plaque — check lipids). The cardinal skill: distinguish benign from malignant with dermoscopy and the ABCDE/ugly-duckling screen, and biopsy any changing or atypical lesion before destructive treatment.
NEET-PGINICET
★ High yieldDermatology
Burns & Thermal Injury
Burns are skin and deeper-tissue injuries caused by thermal, chemical, electrical or radiation energy, classified by depth (first-degree / epidermal — erythema, pain, no blisters; superficial second-degree / superficial partial-thickness — blisters, moist, painful, blanches; deep second-degree / deep dermal — dry, pale, slow capillary refill; third-degree / full-thickness — dry, leathery, insensate, no blanching; fourth-degree — muscle, tendon, bone) and by total body surface area (TBSA) using the Rule of Nines (adults), the Lund-Browder chart (children) or the palm method (patient palm equals 1 percent TBSA). Major burn criteria: over 10 percent TBSA in adults, over 5 percent in children or elderly, any full-thickness burn over 5 percent, burns to face, hands, feet, genitals, perineum or major joints, inhalation injury, electrical or chemical burns, or burns with comorbidity. Management is ABCDE with early airway control, cooling with running water for 20 minutes within 3 hours, Parkland formula resuscitation (4 mL Ringer lactate x kg x percent TBSA, half in first 8 hours), wound care (silver sulfadiazine, hydrocolloids, biological membranes), escharotomy for circumferential full-thickness burns, tetanus prophylaxis, early enteral nutrition and referral to a burns unit.
NEET-PGINICET
Dermatology
Keloids & Hypertrophic Scars
Keloids and hypertrophic scars are fibroproliferative disorders of wound healing characterised by excessive collagen deposition in response to skin injury. The pivotal distinction: hypertrophic scars stay within the original wound boundaries and often regress spontaneously, whereas keloids extend beyond the wound margins into surrounding normal skin, do not regress, and recur after excision. Risk factors include darker skin (Fitzpatrick IV-VI, up to 15-fold higher risk), age 10 to 30, genetic predisposition, wound tension (chest, shoulders, upper back, jawline, earlobes), infection, burns, foreign body, and piercings. Diagnosis is clinical. First-line treatment is intralesional corticosteroid (triamcinolone acetonide 10-40 mg/mL every 4-6 weeks), with silicone gel sheeting for prevention and early lesions. Surgical excision of keloids must be combined with adjuvant therapy (intralesional steroid or radiation within 24-48 hours), because excision alone has a 50-100 percent recurrence rate.
NEET-PGINICET
★ High yieldDermatology
Melanoma & Skin Cancer
Skin cancer is the commonest malignancy worldwide and splits into melanoma (aggressive melanocytic cancer with high metastatic potential) and the non-melanoma skin cancers (NMSC) — basal cell carcinoma (BCC, commonest and locally invasive, rarely metastasises) and squamous cell carcinoma (SCC, keratinising, can metastasise to nodes) — plus the rarer, aggressive Merkel cell carcinoma (neuroendocrine, polyomavirus-related). Risk factors centre on ultraviolet radiation (sun exposure, sunburn, tanning beds), fair skin, freckles, red hair (MC1R), immunosuppression, older age, family/genetic predisposition (FAMM/CDKN2A, xeroderma pigmentosum, Gorlin), and previous skin cancer. Melanoma is recognised by the ABCDE criteria and the ugly-duckling sign; subtypes are superficial spreading (commonest), nodular (worst), lentigo maligna, acral lentiginous and amelanotic. Staging rests on Breslow thickness, ulceration, and sentinel lymph node biopsy, with AJCC TNM 8th edition defining the T categories. Treatment is surgical (wide local excision with margins dictated by Breslow thickness; Mohs for facial/high-risk BCC/SCC) and, for advanced melanoma, transformed by anti-PD-1 immunotherapy (pembrolizumab, nivolumab) +/- anti-CTLA-4 (ipilimumab) and BRAF/MEK targeted therapy (dabrafenib + trametinib). Sun protection and early detection remain the preventive cornerstones.
NEET-PGINICET
★ High yieldDermatology
Pemphigus Vulgaris & Bullous Pemphigoid
Pemphigus vulgaris (PV) and bullous pemphigoid (BP) are the two archetype autoimmune blistering diseases of the skin and mucosa, distinguished by the level of the split and the target antigen. PV: pathogenic IgG against desmoglein 3 (Dsg3, mucosal) ± desmoglein 1 (Dsg1, cutaneous) → suprabasal intraepidermal acantholysis → flaccid blisters, raw erosions, oral ulceration, positive Nikolsky sign; affects middle-aged adults (40 to 60), Mediterranean/Jewish/Indian predilection; potentially fatal without immunosuppression. BP (commonest autoimmune blistering disease overall, and especially in the elderly): IgG against BP180 (BPAG2) and BP230 (BPAG1) of the hemidesmosome → subepidermal split → tense bullae on flexural skin, pruritic, oral mucosa spared, Nikolsky negative. Diagnosis rests on a triad: skin biopsy H&E + peri-lesional direct immunofluorescence + serum ELISA. DIF: PV = intercellular fishnet IgG/C3; BP = linear BMZ IgG/C3. Salt-split skin: BP binds roof, EBA binds floor. Treatment revolutionised by rituximab — now first-line for moderate-severe PV (PEMPHIX) and refractory BP — and by doxycycline + potent topical steroid as the safer first-line BP strategy (BLISTER).
NEET-PGINICET
★ High yieldDermatology
Stevens-Johnson Syndrome & Toxic Epidermal Necrolysis
Stevens-Johnson syndrome (SJS) and toxic epidermal necrolysis (TEN) are severe, immune-mediated mucocutaneous reactions, usually drug-induced (rarely infection), characterised by full-thickness epidermal necrosis, sheet-like epidermal detachment, mucosal ulceration of at least two sites, and systemic toxicity. By the Bastuji-Garin consensus spectrum SJS is under 10 percent body surface area (BSA) detachment, SJS-TEN overlap is 10 to 30 percent, and TEN is over 30 percent. Commonest causative drugs are allopurinol, anticonvulsants (carbamazepine, lamotrigine, phenytoin), sulphonamide antibiotics, oxicam NSAIDs and nevirapine, with onset one to eight weeks after the drug is started. Clinical features are a prodromal flu-like illness, painful burn…
NEET-PGINICET
★ High yieldDermatology
Tinea & Dermatophytosis (Ringworm)
Tinea (dermatophytosis, ringworm) is a superficial fungal infection of keratinised tissue by dermatophyte moulds of three genera — Trichophyton (skin, hair, nails), Microsporum (hair, skin; many fluoresce green under Wood's lamp), and Epidermophyton floccosum (skin and nails, never hair). Dermatophytes secrete keratinases that digest keratin in the stratum corneum, hair shafts, and nails; they cannot invade living tissue. The clinical lesion is the annular, erythematous, scaly plaque with a raised, advancing, scaly border (active edge) and central clearing — the ringworm pattern — and is named by site: corporis, cruris, pedis (interdigital/moccasin/vesicular), capitis (black-dot/kerion/favus), unguium (onychomycosis), manuum, faciei, barbae, and incognito (steroid-modified). The diagnosis rests on clinical morphology + KOH mount of the active border showing branching septate hyphae, supported by fungal culture on Sabouraud dextrose agar, Wood's lamp (Microsporum green hair fluorescence), dermatoscopy (comma/corkscrew hairs; Morse-code nails), and PAS/GMS stain on biopsy. Topical antifungals (clotrimazole 1% BD 4 weeks, terbinafine 1% OD one to two weeks) cure most localised skin disease; ORAL therapy is mandatory for tinea capitis, onychomycosis, extensive/recurrent/steroid-modified tinea, Majocchi granuloma, and immunosuppression. Terbinafine 250 mg OD is first-line systemic (allylamine, fungicidal, inhibits squalene epoxidase); griseofulvin remains the gold standard for Microsporum tinea capitis in children; itraconazole (pulse for nails) and fluconazole 150 mg weekly are alternatives. Kerion — boggy inflammatory tinea capitis — needs oral antifungal plus oral corticosteroid, NOT incision. Tinea incognito from misuse of fixed-dose corticosteroid-antifungal-antibacterial creams is a major Indian epidemic (AAA syndrome: Abuse, Application, Addiction), requires oral antifungal and steroid withdrawal. Recurrence is reduced by treating coexisting tinea pedis (the reservoir), washing clothing/bedding, addressing diabetes/HIV, and treating household and animal contacts.
NEET-PGINICET
Dermatology
Viral Warts (Verrucae)
Viral warts (verrucae) are benign epidermal proliferations caused by human papillomavirus (HPV) infection of basal keratinocytes. Clinical subtypes: common (verruca vulgaris) — rough, hyperkeratotic papules on hands, fingers and knees (HPV 1, 2, 4, 27); plantar (verruca plantaris/myrmecia) — tender, inward-growing on soles with pathognomonic black dots that are thrombosed capillary loops (HPV 1); flat (verruca plana) — smooth, flat-topped papules on face and hands (HPV 3, 10, 28); filiform — finger-like projections on face and neck; genital (condyloma acuminata) — sexually transmitted cauliflower-like lesions (HPV 6, 11; oncogenic 16, 18, 31, 33). Most cutaneous warts resolve spontaneously in immunocompetent children (approximately 50 percent in 1 year, two-thirds in 2 years). First-line treatment is salicylic acid 12 to 40 percent for up to 12 weeks; cryotherapy with liquid nitrogen every 1 to 3 weeks is the main clinic alternative; imiquimod 5 percent or podophyllotoxin 0.5 percent for genital warts; intralesional bleomycin and immunotherapy for recalcitrant plantar warts. The 9-valent HPV vaccine (types 6, 11, 16, 18, 31, 33, 45, 52, 58) prevents genital warts and HPV-related cancer. Biopsy atypical, persistent or rapidly growing lesions to exclude squamous cell carcinoma or verrucous carcinoma.
NEET-PGINICET
★ High yieldDermatology
Vitiligo & Pigmentation Disorders
Vitiligo is an acquired autoimmune destruction of epidermal melanocytes producing well-demarcated, chalk-white (depigmented) macules and patches on the periorificial face, hands, extensor surfaces, genitalia and body folds; classified as segmental (unilateral, dermatomal, early onset, stabilises within 1 to 2 years) or non-segmental (bilateral, symmetrical, progressive). It is associated with autoimmune thyroid disease, type 1 diabetes, pernicious anaemia, Addison disease and alopecia areata, and carries a major psychological burden, especially in darker skin. Melasma (chloasma) is acquired symmetrical facial hyperpigmentation (forehead, malar cheeks, upper lip) triggered by sun, pregnancy, oral contraceptives and genetics. Post-inflammatory pigment change, oculocutaneous albinism, and drug-induced pigmentation (minocycline, amiodarone, chloroquine) complete the pigmentary differential. Diagnosis is clinical, confirmed with the Wood lamp; management combines topical corticosteroids, calcineurin inhibitors, JAK inhibitors, narrowband UVB phototherapy, excimer laser, surgery, camouflage and depigmentation for vitiligo, and strict sun protection with hydroquinone-based regimens for melasma.
NEET-PGINICET
Emergency & Toxicology
11
★ High yieldEmergency & Toxicology
Heat Stroke
Heat stroke is a life-threatening hyperthermic emergency defined by a core body temperature above 40 degrees C (104 F) with central nervous system dysfunction (confusion, agitation, seizures, ataxia, coma) and, in many cases, multi-organ failure. It is the severe end of the heat-illness spectrum (heat cramps, heat exhaustion, heat stroke). Two forms: (1) Classic (non-exertional, epidemic) — elderly and chronically ill patients during heatwaves, with impaired thermoregulation, polypharmacy and hot dry skin; (2) Exertional — young, fit individuals (athletes, military, firefighters, labourers) during strenuous exercise in heat, in whom sweating is often still present. The mechanism is thermoregulatory failure: environmental heat gain plus endogenous heat production exceed sweating and radiation capacity, producing direct heat injury to proteins and a gut-ischaemia / endotoxaemia-driven cytokine storm that mimics sepsis, driving disseminated intravascular coagulation, rhabdomyolysis, acute kidney injury, hepatic necrosis and ARDS. Heat stroke is a hyperthermia, not a pyrexia — the hypothalamic set-point is normal, so antipyretics are useless. Treatment is RAPID COOLING started within the first 30 minutes: cold-water immersion (gold standard for exertional), evaporative cooling (spray plus fans, preferred for classic), ice packs, and cooled IV fluids; cool to below 39 C then stop to avoid overshoot hypothermia.
NEET-PGINICET
★ High yieldEmergency & Toxicology
High-Altitude Illness
High-altitude illness is the spectrum of syndromes caused by ascent to altitude (usually above 2500 m) under hypobaric hypoxia: (1) Acute Mountain Sickness (AMS) — common and self-limiting, defined as headache plus one or more of nausea/anorexia, fatigue/weakness, dizziness/vertigo and sleep disturbance (2018 Lake Louise score); (2) High-Altitude Cerebral Oedema (HACE) — severe, with ataxia and altered consciousness from vasogenic cerebral oedema, fatal if untreated; (3) High-Altitude Pulmonary Oedema (HAPE) — severe, with exertional dyspnoea, dry then pink-frothy cough, cyanosis and reduced exercise performance from uneven hypoxic pulmonary vasoconstriction and non-cardiogenic pulmonary oedema — the commonest cause of altitude-related death. Onset is hours to days after ascent; risk rises with rate of ascent, altitude reached and individual susceptibility. Prevention is gradual ascent plus acetazolamide 125 to 250 mg twice daily. AMS — stop ascent, rest, acetazolamide; HACE and HAPE — immediate descent plus oxygen plus dexamethasone (HACE) or nifedipine (HAPE), with a portable hyperbaric chamber if descent is impossible.
NEET-PGINICET
★ High yieldEmergency & Toxicology
Hypothermia
Hypothermia is defined as a core (rectal, bladder or oesophageal) body temperature below 35 degrees C (95 F), caused by excessive heat loss, impaired thermogenesis, or both. Severity by core temperature: mild 35 to 32 C — conscious, shivering; moderate 32 to 28 C — impaired consciousness, shivering ceases; severe 28 to 24 C — unconscious with vital signs possibly present, arrhythmia risk; profound below 24 C — apparent death (coma, fixed dilated pupils, asystole possible). The Swiss (Durrer) HT staging (HT I to HT V) maps clinical state to temperature and drives the rewarming strategy. Presentation: cold pale skin, shivering (which stops below 32 C), bradycardia, bradypnoea, confusion then coma, and the classic Osborn (J) wave on ECG. Management: handle GENTLY (rough handling triggers ventricular fibrillation), remove from cold, and rewarm by stage — passive external (mild) then active external (forced warm air) then active internal (warmed fluids and gases, lavage, and ECMO/CPB for severe/arrest). The cardinal rule of arrest is 'no one is dead until warm and dead' — continue CPR and rewarm to at least 32 C before ceasing. Always search for a secondary cause (myxoedema coma, sepsis, hypoglycaemia, drugs).
NEET-PGINICET
★ High yieldEmergency & Toxicology
Lead Poisoning (Plumbism)
Lead poisoning (plumbism/saturnism) is toxic accumulation of lead (Pb), a heavy metal with NO biological role and NO safe blood level, causing multisystem harm — neurotoxic (especially irreversible IQ loss in children), microcytic sideroblastic anaemia with basophilic stippling, lead colic, motor peripheral neuropathy (wrist drop), nephropathy, saturnine gout, hypertension, and reproductive damage. Sources: lead-based paint (pre-1970s housing, children ingest flakes/dust), contaminated water (lead pipes/solder), industrial exposure (smelting, battery recycling, ammunition, soldering, foundry, demolition), traditional cosmetics (surma/kohl, sindoor), Ayurvedic/herbal medicines, ceramic glazes, leaded petrol (legacy environmental), moonshine, toys/jewellery, retained bullets. Lead mimics calcium (deposits in bone/teeth — metaphyseal 'lead lines'; crosses placenta and blood-brain barrier) and inhibits ALA dehydratase and ferrochelatase → sideroblastic anaemia with basophilic stippling. Diagnosis: whole blood lead level + FBC (basophilic stippling). Treat: remove source + chelation — succimer (DMSA, oral) for moderate; calcium disodium EDTA (IV) for moderate-severe; dimercaprol (BAL, IM) FIRST then EDTA for encephalopathy. Prevention (public health) is paramount — neurodevelopmental damage is irreversible.
NEET-PGINICET
★ High yieldEmergency & Toxicology
Methaemoglobinaemia
Methaemoglobinaemia is the presence of methaemoglobin (MetHb) — haemoglobin in which the haem iron is in the ferric (Fe3+) state (normal haemoglobin is ferrous, Fe2+) — which cannot bind or transport oxygen and, worse, shifts the oxygen-haemoglobin dissociation curve to the LEFT, so that oxygen bound to neighbouring normal haemoglobin subunits is held more tightly and released less readily to tissues. Normal MetHb is under 1 percent of total haemoglobin; levels over 1.5 percent are abnormal. Two mechanisms: ACQUIRED (oxidant drugs/chemicals — over 99 percent of cases) — nitrates/nitrites (contaminated well water in infants, sodium nitrite food preservative, amyl/sodium/butyl nitrite 'poppers'), local anaesthetics (benzocaine, prilocaine, lidocaine), dapsone (hydroxylamine metabolite), aniline dyes, chlorates, phenazopyridine, nitroprusside, nitroglycerin, sulphonamides, primaquine, smoke; and CONGENITAL (rare) — cytochrome b5 reductase deficiency (autosomal recessive) and haemoglobin M disease (autosomal dominant). The cardinal clinical clue is cyanosis REFRACTORY to oxygen with chocolate-brown blood and a saturation gap (SpO2 stuck around 85 percent with a normal PaO2). Diagnose with CO-OXIMETRY (the only test that measures MetHb directly). Treat by stopping the oxidant, high-flow oxygen, and the elegant cofactor antidote METHYLENE BLUE 1-2 mg/kg IV — which acts via the NADPH-methaemoglobin reductase pathway and is therefore CONTRAINDICATED in G6PD deficiency (it fails and causes haemolysis). Alternatives in G6PD deficiency or methylene-blue failure are ascorbic acid, N-acetylcysteine, exchange transfusion and hyperbaric oxygen.
NEET-PGINICET
★ High yieldEmergency & Toxicology
Organophosphate Poisoning
Organophosphate (OP) poisoning (agricultural pesticides such as malathion, parathion, chlorpyrifos, dimethoate, monocrotophos, profenofos; military nerve agents such as sarin, soman, tabun, VX) is one of the commonest causes of deliberate self-harm death in agricultural regions of South and South-East Asia. OPs irreversibly phosphorylate and inhibit acetylcholinesterase (AChE), causing accumulation of acetylcholine at muscarinic, nicotinic and central receptors — a cholinergic crisis. The classic muscarinic toxidrome is the DUMBELSS / SLUDGE mnemonic (Diarrhoea, Urination, Miosis, Bronchorrhoea/bronchospasm, Emesis, Lacrimation, Salivation, Sweating); nicotinic effects include muscle fasciculations, weakness, paralysis; central effects include seizures, coma, central respiratory depression. Death is from respiratory failure. Treatment is the two-antidote doctrine — atropine (muscarinic antagonist; titrate to a dry patient) PLUS pralidoxime (reactivates AChE; nicotinic effects; give EARLY before enzyme ageing), plus benzodiazepines (seizures), decontamination with staff PPE and ventilation. Three phases follow: acute cholinergic crisis (minutes to hours), intermediate syndrome (24 to 96 hours) and organophosphate-induced delayed polyneuropathy, OPIDP (1 to 3 weeks).
NEET-PGINICET
★ High yieldEmergency & Toxicology
Poisoning Overview & Toxidromes
A structured, examiner-grade overview of the approach to the acutely poisoned patient — resuscitation (ABCDE), toxidrome recognition, gastrointestinal decontamination, enhanced elimination, and the antidote armamentarium. Designed as a self-contained chapter covering all 15 examiner dimensions for NEET-PG, INICET, USMLE and PLAB.
NEET-PGINICET
★ High yieldEmergency & Toxicology
Rhabdomyolysis
Rhabdomyolysis is the breakdown of skeletal muscle with release of intracellular contents (myoglobin, creatine kinase, potassium, phosphate, urate, lactate dehydrogenase) into the circulation, causing acute kidney injury, electrolyte disturbance, compartment syndrome and disseminated intravascular coagulation. Causes span trauma/crush (earthquakes, prolonged immobilisation), exertion (strenuous exercise, seizures, delirium), muscle ischaemia (arterial occlusion, compartment syndrome), drugs and toxins (statins, fibrates, alcohol, cocaine, amphetamines, MDMA, succinylcholine, neuroleptic malignant syndrome, serotonin syndrome, snake venom), infection (influenza, coxsackie, malaria, legionella, sepsis), electrolyte disorders (hypokalaemia, hypophosphataemia), temperature extremes (heat stroke, hypothermia) and inherited metabolic myopathies (McArdle, carnitine palmitoyltransferase II deficiency). Presents with the classic triad of muscle pain, weakness and dark tea-coloured urine (often incomplete). Diagnosis rests on a raised creatine kinase (over 5 times the upper limit of normal, frequently over 1000 U/L; over 5000 U/L marks high acute-kidney-injury risk), urine dipstick positive for blood but with no red cells on microscopy (myoglobin), hyperkalaemia, and a creatinine that rises disproportionate to urea. The cornerstone of treatment is aggressive IV crystalloid to maintain urine output 1 to 3 mL/kg/h (around 300 mL/h, often 6 to 12 L in the first 24 h), started before extrication in crush injury, with treatment of hyperkalaemia, treatment of the cause, fasciotomy for compartment syndrome, and renal replacement therapy for established AKI. Sodium bicarbonate and mannitol are controversial adjuncts, not first-line; early hypocalcaemia is not treated.
NEET-PGINICET
★ High yieldEmergency & Toxicology
Snake Envenomation
Snake envenomation is a WHO category-A neglected tropical disease and a leading cause of accidental rural death in the tropics — India alone bears the largest global burden (~45,000 deaths/year). Medically important snakes divide into two clinical families. Elapids (cobra, krait, mamba, coral, Australian taipan/brown) deliver neurotoxic venom — alpha-neurotoxins block the postsynaptic nicotinic acetylcholine receptor and phospholipase A2 destroys the presynaptic nerve terminal, producing descending flaccid paralysis (ptosis, ophthalmoplegia, bulbar palsy, respiratory failure) with little local swelling. Vipers (Russell's, saw-scaled, puff adder, rattlesnake) deliver haemato/cytotoxic venom — procoagulant enzymes activate prothrombin/factor X causing venom-induced consumption coagulopathy (VICC) with incoagulable blood, spontaneous bleeding, and AKI, shock and local necrosis. Sea snakes / Australian elapids add rhabdomyolysis (myoglobinuric AKI). First aid: reassure, immobilise the limb, pressure-immobilisation bandage for elapids, rapid transport; avoid cut/suck/tourniquet/ice. Diagnosis is clinical + 20-minute whole blood clotting test (20WBCT). Treatment is resuscitation + specific antivenom (ASV) IV for significant envenomation (neurotoxicity, VICC, bleeding, shock, AKI, rhabdomyolysis, severe local), early ventilation for respiratory failure, dialysis for AKI, blood products after antivenom, and fasciotomy only after coagulopathy is corrected.
NEET-PGINICET
★ High yieldEmergency & Toxicology
Toxic Alcohols: Methanol & Ethylene Glycol Poisoning
Methanol (wood alcohol; antifreeze, windscreen washer, illicit spirits, paint thinner, denatured alcohol, hand sanitiser) and ethylene glycol (antifreeze) are toxic alcohols that are themselves relatively harmless but are metabolised by hepatic alcohol dehydrogenase to highly toxic organic acids — methanol to formic acid (causes blindness, optic nerve injury, basal ganglia necrosis, severe metabolic acidosis) and ethylene glycol to glycolic and oxalic acid (causes acute kidney injury, severe metabolic acidosis, hypocalcaemia, calcium oxalate crystalluria). The defining laboratory signature is a high anion-gap metabolic acidosis AND an elevated osmolal gap early in the course; as the parent alcohol is metabolised the osmolal gap falls while the anion gap rises. Clinical discriminator: methanol causes visual disturbance, 'snowstorm' vision, optic disc oedema, blindness; ethylene glycol causes renal failure, hypocalcaemia and calcium oxalate crystals in the urine. Treatment is mechanism-directed: block alcohol dehydrogenase with fomepizole (preferred) or ethanol, give sodium bicarbonate for acidosis, haemodialyse severe cases, and give folinic acid (methanol) and thiamine + pyridoxine (ethylene glycol) as cofactors.
NEET-PGINICET
★ High yieldEmergency & Toxicology
Toxic Shock Syndrome
Toxic shock syndrome (TSS) is an acute, life-threatening, toxin-mediated multisystem illness caused by bacterial superantigen exotoxins that bypass normal MHC-restricted antigen presentation, activating up to 20 to 30 percent of all T-cells simultaneously (versus ~0.01 percent normally) and producing a massive cytokine storm (IL-1, IL-2, TNF-alpha, IFN-gamma) that drives capillary leak, systemic vasodilation, hypotension and multi-organ failure. Two forms: staphylococcal TSS (Staphylococcus aureus producing TSST-1, staphylococcal enterotoxins B and C — classically associated with tampons/menstruation but now more often non-menstrual — surgical wounds, postpartum, burns, skin infection, nasal packing — and typically NOT bacteraemic; mortality 3 to 5 percent) versus streptococcal toxic shock syndrome (STSS) (Group A beta-haemolytic strep, Streptococcus pyogenes, producing streptococcal pyrogenic exotoxins SpeA, SpeC — associated with invasive soft-tissue infection / necrotising fasciitis, myonecrosis, bacteraemia in ~60 percent, mortality 30 to 60 percent). Clinical: acute high fever (over 38.9 deg C), hypotension, diffuse macular 'sunburn-like' rash that desquamates 1 to 2 weeks later (especially palms and soles), mucous membrane hyperaemia and multi-organ failure. Diagnosis is CLINICAL (CDC criteria) — blood culture isolation is NOT required for staphylococcal TSS. Treat: aggressive fluid resuscitation + immediate SOURCE CONTROL (remove tampon / foreign body, surgical debridement of necrotising fasciitis) + empirical IV antibiotics including an ANTI-TOXIN agent (clindamycin 600 to 900 mg IV q8h) + beta-lactam + IVIG (1 to 2 g/kg) in severe disease + vasopressors + ICU.
NEET-PGINICET
Endocrinology
14
★ High yieldEndocrinology
Acromegaly
Acromegaly is chronic growth hormone (GH) excess, nearly always from a pituitary somatotroph adenoma, driving hepatic IGF-1 overproduction and progressive somatic overgrowth. Features include enlarging hands and feet, coarse facial features (prognathism, frontal bossing), dental malocclusion, macroglossia, headache, hyperhidrosis, carpal tunnel and bitemporal visual field loss (optic chiasm compression), with hypertension, diabetes, obstructive sleep apnoea and acromegalic cardiomyopathy. Screening is by elevated age/sex-matched IGF-1, confirmed by a 75 g oral glucose tolerance test in which GH fails to suppress under 1 ng/mL, and a pituitary MRI localises the adenoma. Transsphenoidal surgery is first-line and curative when complete; somatostatin receptor ligands (octreotide LAR, lanreotide, pasireotide), the GH receptor antagonist pegvisomant, the dopamine agonist cabergoline and stereotactic radiotherapy treat residual disease. Cardiovascular disease is the leading cause of death.
NEET-PGINICET
★ High yieldEndocrinology
Hypercalcaemia and Hyperparathyroidism
Hypercalcaemia is a corrected serum calcium over 2.6 mmol/L (10.4 mg/dL); it is dangerous above 3.5 mmol/L (14 mg/dL) — hypercalcaemic crisis with confusion, dehydration, AKI and shortened QT. Causes split by PTH: PTH-dependent (primary and tertiary hyperparathyroidism, lithium, familial hypocalciuric hypercalcaemia) versus PTH-independent (malignancy via PTHrP, osteolytic metastases (breast, myeloma), granulomatous disease (sarcoid, TB), vitamin D intoxication, thiazides, immobilisation, thyrotoxicosis). Primary hyperparathyroidism is the commonest outpatient cause (single parathyroid adenoma 80 percent, hyperplasia 15 percent, double adenoma 4 percent, carcinoma under 1 percent); malignancy is the commonest inpatient cause and the commonest cause overall in a sick patient. Acute severe hypercalcaemia is treated with isotonic saline rehydration then an IV bisphosphonate (zoledronic acid 4 mg or pamidronate 90 mg) — denosumab for refractory disease — plus calcitonin for the fastest onset. Primary hyperparathyroidism is cured by parathyroidectomy; cinacalcet is for those who decline or fail surgery.
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Hypocalcaemia
Hypocalcaemia (corrected calcium under 2.20 mmol/L or under 8.5 mg/dL) presents with neuromuscular irritability — perioral numbness and paraesthesia, tetany, carpopedal spasm, Chvostek and Trousseau signs, and in severe cases generalised seizures, laryngeal stridor and a prolonged QT interval. Causes are split by PTH: low or inappropriately normal PTH (post-surgical hypoparathyroidism — the commonest hospital cause, autoimmune / APS-1, DiGeorge 22q11.2 deletion, infiltrative, hypomagnesaemia, activating CaSR mutations, pseudohypoparathyroidism with end-organ resistance) versus high PTH with appropriate secondary hyperparathyroidism (vitamin D deficiency, CKD-MBD, malabsorption, hungry bone syndrome, bisphosphonates / denosumab / foscarnet, citrated massive transfusion). Always correct for albumin and check magnesium — hypomagnesaemia causes reversible PTH resistance and refractory hypocalcaemia. Acute severe symptomatic hypocalcaemia (tetany, seizures, prolonged QT) is treated with IV calcium gluconate 10 percent, 10 to 20 mL (1 to 2 g) over 10 to 20 minutes with cardiac monitoring; chronic management is oral calcium plus active vitamin D (calcitriol 0.25 to 1 mcg daily) and correction of the underlying cause.
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Hypopituitarism
Hypopituitarism is the partial or complete deficiency of one or more anterior pituitary hormones (GH, PRL, ACTH, TSH, LH/FSH); loss of all anterior hormones is panhypopuitarism. It is caused most commonly by a pituitary adenoma, surgery or radiation, Sheehan syndrome (postpartum ischaemic necrosis), pituitary apoplexy, infiltrative disease (sarcoidosis, haemochromatosis, Langerhans cell histiocytosis), autoimmune hypophysitis (including immune-checkpoint inhibitors), genetic mutations (PROP1, POU1F1), or traumatic brain injury. Each hormone deficiency produces distinct features: ACTH deficiency causes secondary adrenal insufficiency (fatigue, postural hypotension, hypoglycaemia, hyponatraemia — but no hyperpigmentation and no hyperkalaemia, distinguishing it from primary Addison disease); TSH causes secondary hypothyroidism; LH/FSH causes hypogonadism (loss of libido, amenorrhoea, erectile dysfunction, infertility); GH causes reduced muscle mass, central adiposity and, in children, growth failure; prolactin causes failure of lactation. Large lesions cause bitemporal hemianopia and headache. Diagnosis shows low target hormones with low or inappropriately normal trophic hormones, confirmed by pituitary MRI. Management is hormone replacement — hydrocortisone FIRST (always before levothyroxine, to avoid precipitating adrenal crisis), then levothyroxine, sex steroids, growth hormone, and desmopressin for diabetes insipidus.
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Endocrinology
Multiple Endocrine Neoplasia (MEN) Syndromes
Multiple endocrine neoplasia (MEN) syndromes are autosomal dominant disorders in which a single germline mutation predisposes to tumours of two or more endocrine glands throughout life. MEN 1 (Wermer syndrome) is caused by the MEN1 gene (menin) tumour suppressor on chromosome 11q13 and follows the 3 P's rule: Primary hyperparathyroidism (commonest, multi-gland hyperplasia), Pituitary adenoma (prolactinoma commonest) and Pancreatic neuroendocrine tumour (gastrinoma with Zollinger-Ellison commonest; insulinoma second). MEN 2A (Sipple syndrome) and MEN 2B are caused by the RET proto-oncogene on chromosome 10q11.2: MEN 2A features medullary thyroid carcinoma (near 100 percent), phaeochromocytoma (around 50 percent, often bilateral) and parathyroid hyperplasia (around 20 percent), while MEN 2B features aggressive medullary thyroid cancer, phaeochromocytoma, mucosal neuromas and marfanoid habitus with no parathyroid disease. MEN 4 is caused by a CDKN1B (p27) mutation and mimics MEN 1. Diagnosis is by genetic testing (RET for MEN 2, MEN1 gene for MEN 1) combined with biochemical surveillance. Management includes prophylactic thyroidectomy in MEN 2 RET carriers (timing by ATA mutation risk), treating each tumour, alpha-blockade before any surgery in MEN 2, and lifelong cascade screening of first-degree relatives (MEN 2 from birth, MEN 1 from age 5).
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Osteoporosis
Osteoporosis is a systemic skeletal disease of low bone mass and microarchitectural deterioration, increasing the risk of fragility fractures (hip, spine, wrist). Diagnosis is by DEXA T-score of minus 2.5 or less (osteopenia minus 1 to minus 2.5; a fragility fracture establishes the diagnosis regardless of score), and the FRAX score estimates 10-year fracture risk to guide treatment. Risk factors include age, female sex, postmenopausal status, family history, low BMI, glucocorticoids, smoking, hypogonadism and hyperthyroidism. It is often silent until a fracture. Management is lifestyle (weight-bearing exercise, no smoking, calcium and vitamin D) plus first-line bisphosphonates (alendronate, zoledronate), with denosumab and anabolic teriparatide for high-risk or refractory disease. After 3 to 5 years of a bisphosphonate, a drug holiday is considered. The goal is preventing the first fragility fracture, especially hip and vertebral, which carry high morbidity and mortality.
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Endocrinology
Paget Disease of Bone
Paget disease of bone (osteitis deformans) is a chronic, focal disorder of adult bone remodeling in which excessive, disorganised osteoclast activity is followed by chaotic osteoblast repair, producing bone that is thick and hypervascular but mechanically weak (a disordered woven/mosaic pattern). It is usually asymptomatic and found on incidental raised alkaline phosphatase with normal calcium and phosphate; symptoms include bone pain (often nocturnal), bony deformity (sabre tibia, enlarging skull, kyphosis), sensorineural deafness and, rarely, neurological or cardiac complications. Common sites are the pelvis, spine, femur, skull and tibia. Diagnosis rests on raised ALP with normal Ca/PO4, characteristic X-rays (cortical thickening, mixed lytic-sclerotic lesions, cotton-wool skull, blade-of-grass, picture-frame vertebrae) and an isotope bone scan showing focal hot spots. The cornerstone treatment is a single 5 mg IV infusion of zoledronic acid (plus calcium and vitamin D) for symptomatic or complication-risk disease, with ALP monitoring. The feared complication is osteosarcoma transformation (under 1 percent), heralded by new or rapidly worsening pain.
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Phaeochromocytoma
Phaeochromocytoma is a catecholamine-secreting tumour arising from chromaffin cells of the adrenal medulla; an identical tumour outside the adrenal (organ of Zuckerkandl, sympathetic chain, bladder) is a paraganglioma. About 80 to 85 percent are intra-adrenal and 15 to 20 percent extra-adrenal. It presents with the classic triad of episodic headache, sweating and palpitations with paroxysmal or sustained hypertension and striking pallor. The historical rule of 10 (about 10 percent each bilateral, malignant, extra-adrenal, familial and paediatric) is outdated for heritability: modern genotyping shows 30 to 40 percent carry a germline mutation (RET/MEN 2, VHL, NF1, SDHx, MAX, TMEM127). Diagnosis rests on plasma free metanephrines or 24-hour urine fractionated metanephrines, with CT/MRI for localisation and MIBG or 68Ga-DOTATATE PET for extra-adrenal and metastatic disease. The cardinal management rule is ALPHA-block before beta-block — phenoxybenzamine for 10 to 14 days, then a beta-blocker for tachycardia, then laparoscopic adrenalectomy. A beta-blocker given first leaves alpha-1 vasoconstriction unopposed and triggers a fatal hypertensive crisis; intra-operative crisis is treated with IV phentolamine or sodium nitroprusside.
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Polycystic Ovary Syndrome (PCOS)
Polycystic ovary syndrome (PCOS) is the commonest endocrine disorder of reproductive-age women (around 8 to 13 percent), diagnosed by the Rotterdam criteria — TWO of THREE: oligo/anovulation, clinical or biochemical hyperandrogenism (hirsutism, acne, elevated free testosterone), and polycystic ovaries on ultrasound — after excluding mimics (thyroid, prolactin, Cushing, non-classic CAH, androgen-secreting tumour). Insulin resistance and the metabolic syndrome are central, driving obesity, type 2 diabetes and cardiovascular risk. Presentation includes irregular periods, hirsutism, acne, infertility and weight gain. Management is lifestyle first (5 to 10 percent weight loss), then combined oral contraceptive pill (cycle control, endometrial protection, hirsutism), metformin (insulin resistance), letrozole (first-line for fertility — PPCOS II, NEJM 2014) and spironolactone (hirsutism, with reliable contraception). Long-term care includes endometrial protection, type 2 diabetes screening and cardiovascular risk reduction.
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Endocrinology
Primary Aldosteronism (Conn Syndrome)
Primary aldosteronism is autonomous aldosterone secretion that is independent of renin (high aldosterone, suppressed renin), causing sodium retention with hypertension, and potassium and hydrogen loss with hypokalaemic metabolic alkalosis. It is the commonest cause of secondary hypertension, affecting 5 to 10 percent of all hypertensives and over 20 percent of those with resistant hypertension, yet is frequently missed because most patients are normokalaemic. Causes are bilateral idiopathic adrenal hyperplasia (commonest), a unilateral aldosterone-producing adenoma (Conn syndrome), unilateral adrenal hyperplasia, and familial hyperaldosteronism types I to IV. Screen at-risk patients with the aldosterone-to-renin ratio (ARR), confirm autonomy with a suppression test, then localise with CT and adrenal venous sampling (AVS). Treat unilateral disease with laparoscopic adrenalectomy (curative) and bilateral disease with a mineralocorticoid receptor antagonist (spironolactone or eplerenone).
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Prolactinoma
Prolactinoma is a benign pituitary lactotroph adenoma that autonomously secretes prolactin — the most common hormonally active pituitary tumour, accounting for around 40 to 45 percent of functioning pituitary adenomas. Hyperprolactinaemia inhibits hypothalamic GnRH, lowering FSH and LH and producing hypogonadotropic hypogonadism: in women oligomenorrhoea or amenorrhoea, galactorrhoea, infertility and low libido; in men reduced libido, erectile dysfunction and infertility. A macroprolactinoma (10 mm or more) adds mass effect — bitemporal hemianopia (optic chiasm compression), hypopituitarism and cranial nerve palsies. Diagnosis rests on a fasting serum prolactin (over 4000 mU/L or 200 ng/mL essentially diagnostic), exclusion of pregnancy, drugs, hypothyroidism and renal failure, a macroprolactin screen, and a pituitary MRI. First-line treatment is medical — a dopamine agonist, cabergoline (preferred over bromocriptine) — which normalises prolactin, shrinks the tumour and restores fertility. Surgery is reserved for resistance, intolerance, apoplexy, CSF leak or chiasmal compression unresponsive to drugs.
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Endocrinology
Thyroid Nodules & Thyroid Cancer
Thyroid nodules are very common but mostly benign — palpable in around 5 percent of adults and seen on ultrasound in 30 to 50 percent — yet only 5 to 10 percent are malignant. The clinical task is to identify that minority through ultrasound risk-stratification (ACR TI-RADS) and fine-needle aspiration cytology (Bethesda System), guided by clinical risk (neck radiation, family history, rapid growth, hoarseness, fixed nodule, lymphadenopathy). The four main thyroid cancers are papillary (commonest, around 80 percent; excellent prognosis; BRAF V600E, RET-PTC, psammoma bodies, orphan Annie-eye nuclei), follicular (10 percent; vascular and capsular invasion; haematogenous spread to bone and lung; RAS mutation), medullary (5 percent; parafollicular C cells; calcitonin; MEN-2; RET proto-oncogene) and anaplastic (1 to 2 percent; undifferentiated; elderly; survival measured in months). Differentiated cancer is treated with thyroidectomy plus or minus radioactive iodine-131 ablation and TSH suppression; medullary needs surgery plus RET genetic testing (no RAI benefit); anaplastic is largely palliative. Always check serum TSH first in any thyroid nodule.
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Endocrinology
Thyroiditis & Goitre
Thyroiditis is inflammation of the thyroid gland, producing a spectrum from transient thyrotoxicosis (leak of preformed hormone) through hypothyroidism (gland destruction). Hashimoto thyroiditis (autoimmune, anti-TPO) is the commonest cause of hypothyroidism and goitre in iodine-sufficient areas. Subacute (De Quervain) thyroiditis presents with a painful tender goitre, fever and transient thyrotoxicosis after a viral illness, a raised ESR and a low radioactive iodine uptake. Postpartum and silent (painless) thyroiditis cause a transient thyrotoxicosis then hypothyroidism. Amiodarone causes both hypothyroidism (Wolff-Chaikoff effect) and thyrotoxicosis (Jod-Basedow, type 1 synthetic vs type 2 destructive). Riedel thyroiditis is a rare IgG4-related fibrosing disease with a stony-hard goitre. A goitre may be diffuse (Graves, Hashimoto, iodine deficiency, puberty) or multinodular (nodular hyperplasia, toxic or compressive). Thyroid storm is the endocrine emergency, treated with beta-blocker, thionamide, iodine and glucocorticoid.
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Vitamin D Deficiency (Rickets & Osteomalacia)
Vitamin D deficiency is the commonest nutritional deficiency worldwide, caused by inadequate UVB skin synthesis, dark skin, malabsorption, CKD, liver disease, obesity and enzyme-inducing drugs. In the growing skeleton it causes nutritional rickets — craniotabes, rachitic rosary, Harrison sulcus, widened wrists, genu varum, delayed fontanelle closure and dental defects. In the mature skeleton it causes osteomalacia — diffuse bone pain, proximal muscle weakness, a waddling gait and Looser zones (pseudofractures). The diagnostic test is 25-hydroxyvitamin D (calcidiol): under 50 nmol/L (20 ng/mL) deficient, severe deficiency under 30 nmol/L (12 ng/mL), over 50 nmol/L the treatment goal, with the classical biochemical tetrad of low or normal calcium, low phosphate, high PTH (secondary hyperparathyroidism) and raised alkaline phosphatase. Treatment is high-dose cholecalciferol or ergocalciferol daily for at least 12 weeks (e.g. 50,000 IU weekly for 8 weeks) followed by maintenance supplementation — with adequate calcium; CKD and malabsorption require higher doses or active vitamin D.
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Gastroenterology
11
★ High yieldGastroenterology
Acute & Chronic Diarrhoea
Diarrhoea is three or more loose or watery stools in 24 hours (or more frequent than is normal for the individual). Acute diarrhoea (under 14 days) is usually infective and self-limiting — viral (norovirus, rotavirus), bacterial (enterotoxigenic E. coli, Campylobacter, Salmonella, Shigella), Clostridioides difficile (after antibiotics) or parasitic (Giardia, Cryptosporidium, Entamoeba) — and the central clinical task is to separate the self-limiting viral illness (reassure, rehydrate) from disease that needs testing or specific treatment: invasive bacterial infection, C. difficile, or an underlying chronic cause. Chronic diarrhoea (over 4 weeks) has a wide differential including irritable bo…
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Acute Liver Failure
Acute liver failure (ALF) is severe acute liver injury with coagulopathy (INR at least 1.5) and any degree of hepatic encephalopathy, developing within 26 weeks in a patient without pre-existing cirrhosis (Wilson's disease and reactivation of chronic hepatitis B are the accepted exceptions). The commonest cause in the developed world is paracetamol (acetaminophen) toxicity; in the developing world viral hepatitis (HAV, HBV, HEV) predominates. Other causes are idiosyncratic drug-induced liver injury (anti-TB, antiepileptics), autoimmune hepatitis, ischaemic/shock liver, Budd-Chiari, Wilson's disease, mushroom (Amanita phalloides) poisoning and pregnancy-related syndromes (HELLP, acute fatty liver of pregnancy). AL…
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Acute Pancreatitis
Acute pancreatitis is an acute inflammatory process of the pancreas caused by premature intracellular activation of trypsinogen to trypsin within pancreatic acinar cells, with autodigestion of the gland and a systemic inflammatory response. Diagnosed when 2 of 3 criteria are met: characteristic epigastric pain radiating to the back, serum lipase or amylase over 3 times the upper limit of normal, or characteristic imaging (CT/MRI). The two commonest causes are gallstones (40 to 50%) and alcohol (25 to 35%); remember I GET SMASHED for the full list. Severity is graded by the Revised Atlanta classification into mild (no organ failure, no complications — 80% of cases), moderately severe (transient organ failure under 48 h, or local complications), and severe (persistent organ failure over 48 h). Manage with goal-directed moderate lactated Ringer's (WATERFALL — aggressive fluids harm), adequate IV opioid analgesia, early enteral feeding within 24 to 48 h (no prolonged nil by mouth), no routine prophylactic antibiotics, ERCP within 24 h only for cholangitis or persistent obstruction, and a step-up drainage approach at ~4 weeks for infected necrosis.
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Alcoholic & MASLD Liver Disease
Alcohol-related liver disease and metabolic dysfunction-associated steatotic liver disease (MASLD, formerly NAFLD) are the two leading causes of chronic liver disease worldwide. Both follow the same histological spectrum — steatosis to steatohepatitis to fibrosis to cirrhosis (and hepatocellular carcinoma) — driven by different insults (alcohol versus obesity, type 2 diabetes and metabolic syndrome). Alcoholic hepatitis is the severe inflammatory form: AST greater than ALT (ratio over 2), both under 300, with jaundice and a high MCV, graded by the Maddrey Discriminant Function (32 or more is severe) and MELD. Management centres on abstinence and addiction care for alcohol-related disease (with corticosteroids for severe alcoholic hepatitis, response assessed by the Lille score at day 7), and weight loss of 7 to 10 percent, metabolic control and emerging pharmacotherapy (pioglitazone, GLP-1 agonists, resmetirom) for MASLD. Both warrant 6-monthly hepatocellular carcinoma surveillance once cirrhotic.
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Gastroenterology
Autoimmune Liver Disease (PBC, PSC & AIH)
Autoimmune liver disease comprises three distinct immune-mediated conditions. Primary biliary cholangitis (PBC) affects predominantly middle-aged women, destroys small intrahepatic bile ducts, is marked by antimitochondrial antibody (AMA) and a raised ALP, and is treated with ursodeoxycholic acid 13 to 15 mg/kg/day. Primary sclerosing cholangitis (PSC) causes multifocal biliary strictures (best shown by MRCP), is strongly associated with inflammatory bowel disease (especially ulcerative colitis, 60 to 80% of cases), carries a cholangiocarcinoma risk, has no proven medical therapy and often needs ERCP or transplant. Autoimmune hepatitis (AIH) causes a hepatitic picture (raised transaminases, high IgG, characteristic autoantibodies and histology), and is steroid-responsive.
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Colorectal Cancer
Colorectal cancer (CRC) is an adenocarcinoma of the colonic or rectal mucosa that evolves from a benign adenomatous polyp through the stepwise accumulation of genetic hits — the adenoma-carcinoma sequence (APC, then KRAS, then TP53) over 10 to 15 years. It is the third most commonly diagnosed cancer worldwide and the second leading cause of cancer death. About 85 percent are sporadic; the remainder arise in hereditary syndromes (Lynch syndrome, familial adenomatous polyposis) or long-standing inflammatory bowel disease. Presentation differs by site — left-sided causes obstruction, a change in bowel habit and bright-red bleeding; right-sided presents with iron-deficiency anaemia and occult blood loss. Diagnosis is by colonoscopy and biopsy; staging with CT chest/abdomen/pelvis and MRI rectum; monitoring with CEA. Treatment is surgical (segmental colectomy with lymphadenectomy; total mesorectal excision for rectal cancer) for localised disease, adjuvant FOLFOX or CAPOX for 6 months for stage III, neoadjuvant radiotherapy (short course 25 Gy in 5 fractions, or long course 45 to 50.4 Gy with 5-FU or capecitabine) for T3 or N-plus rectal cancer, and FOLFOX or FOLFIRI plus bevacizumab or anti-EGFR therapy (cetuximab or panitumumab, RAS wild-type only) for metastatic disease. Screening with FIT or colonoscopy from age 45 to 50 exploits the long pre-malignant polyp phase to prevent cancer outright.
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★ High yieldGastroenterology
Diverticular Disease
Diverticular disease is the clinical spectrum arising from acquired pseudodiverticula — outpouchings of mucosa and submucosa through the colonic muscle wall, most numerous in the sigmoid colon where raised segmental intraluminal pressure (driven by a low-fibre, low-residue diet) forces mucosa through the points where vasa recta arteries penetrate the circular muscle. The spectrum runs from asymptomatic diverticulosis (over half of people aged over 60), to symptomatic uncomplicated diverticular disease (SUDD), to acute diverticulitis — the classic triad of left-lower-quadrant pain, fever and a raised CRP diagnosed by CT abdomen/pelvis (NOT colonoscopy) — and on to complicated disease (abscess, perforation, fistula, stricture, bleeding). The Modified Hinchey classification grades perforated diverticulitis; the Ambrosetti CT grade and the DICA score grade severity. Uncomplicated diverticulitis is managed with selective antibiotics (co-amoxiclav + metronidazole) and bowel rest — modern RCTs (AVOD, DIABOLO, van Dijk) allow selected mild cases to be managed without antibiotics; a pericolic/pelvic abscess over 3-4 cm needs CT-guided drainage; generalised peritonitis needs emergency surgery — Hartmann's procedure for faecal peritonitis (Hinchey IV) or primary anastomosis with defunctioning ileostomy. Diverticular bleeding is the commonest cause of acute lower GI bleeding — painless, arterial, brisk, and self-limiting in 75-80%, managed by CT angiography with embolisation then colonoscopy with surgery reserved for failure. After recovery, elective sigmoid colectomy is offered for recurrent disease or immunosuppression rather than by a rigid episode count. The old advice to avoid seeds, nuts and popcorn has been debunked (Strate 2008, JAMA).
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Malabsorption
Malabsorption is impaired absorption of nutrients across the gut, divided into three mechanistic classes: luminal (defective digestion — pancreatic exocrine insufficiency, bile-salt deficiency, small-intestinal bacterial overgrowth, lactase deficiency), mucosal (defective uptake — coeliac disease, tropical sprue, Crohn's disease, radiation enteritis, Whipple disease) and transport/post-mucosal (short bowel syndrome, post-gastrectomy, intestinal lymphangiectasia). The hallmark is steatorrhoea (pale, bulky, greasy, foul-smelling, difficult-to-flush stool) with weight loss, bloating and deficiency signs (iron, B12, folate, calcium, and the fat-soluble vitamins A, D, E, K). Diagnosis combines blood deficiency screens, coeliac serology (anti-tTG IgA + total IgA), faecal elastase, breath tests and endoscopy with duodenal biopsy (Marsh classification). Management is to treat the underlying cause (e.g. lifelong gluten-free diet for coeliac, pancreatic enzyme replacement for insufficiency, rotating antibiotics for SIBO, teduglutide for short bowel) and replace deficiencies and support nutrition.
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Peptic Ulcer Disease
Peptic ulcer disease (PUD) is a break in the gastric or duodenal mucosa extending through the muscularis mucosae, caused by an imbalance between aggressive acid-peptic factors and mucosal defence. The two dominant causes are Helicobacter pylori (about 90 percent of duodenal ulcers) and NSAIDs/aspirin; less common are Zollinger-Ellison syndrome (gastrinoma), stress ulcers (ICU; Curling/Cushing), and malignant ulcers. It presents with epigastric burning or gnawing pain (duodenal eased by food and waking at night; gastric worsened by food) with dyspepsia; complications are bleeding (haematemesis/melaena), perforation (peritonitis, free gas), penetration, and gastric outlet obstruction. Oesophagogastroduodenosc…
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Variceal Haemorrhage
Variceal haemorrhage is massive upper gastrointestinal bleeding from ruptured oesophageal or gastric varices — dilated submucosal portosystemic collaterals that form when portal venous pressure rises. It is defined by a hepatic venous pressure gradient (HVPG) over 12 mmHg, and almost always occurs in cirrhosis. Each bleed carries 15 to 25 percent 6-week mortality. Acute management follows a four-step bundle: resuscitation with a restrictive transfusion strategy (Hb target 70 to 80), vasoactive drug (terlipressin or octreotide) plus prophylactic ceftriaxone (both proven to reduce mortality), urgent endoscopy within 12 hours for band ligation (or cyanoacrylate for gastric varices), and rescue or pre-emptive TIPS for failure or high-risk. Prevention: primary (NSBB or band ligation), secondary (NSBB plus serial band ligation) — all aimed at lowering the HVPG.
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Viral Hepatitis (Hepatitis A, B, C, D, E)
Viral hepatitis is inflammation of the liver caused by the five hepatotropic viruses — A (RNA, faecal-oral, never chronic), B (DNA, parenteral/vertical/sexual, chronic in 90 percent neonates), C (RNA, blood-borne, chronic in 75 percent, curable with DAAs), D (defective RNA requiring HBsAg), E (RNA, faecal-oral, fulminant in pregnancy). Acute infection presents with prodrome (anorexia, nausea, fatigue, arthralgia) then jaundice, dark urine, tender hepatomegaly; chronic infection is often asymptomatic until cirrhosis or HCC. Diagnosis by serology: HBsAg/anti-HBc (HBV), anti-HCV/HCV RNA (HCV), IgM anti-HAV/anti-HEV. Management: supportive for HAV/HEV; long-term nucleos(t)ide analogues (tenofovir, entecavir) for HBV; direct-acting antivirals (DAAs) 8-12 weeks with over 95 percent SVR for HCV. Prevention: HAV and HBV vaccines, universal HBV birth-dose, post-exposure prophylaxis, screening before immunosuppression to prevent fatal HBV reactivation.
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Haematology
11
Haematology
Anaemia of Chronic Disease (Anaemia of Inflammation)
Anaemia of chronic disease (anaemia of inflammation) is the commonest anaemia in hospitalised and chronically ill patients. It arises from chronic immune activation (infection, autoimmune disease, malignancy, chronic kidney disease) driving hepcidin-mediated iron sequestration (iron trapped in macrophages, reduced gut absorption), suppressed erythropoiesis, and a moderately shortened red-cell lifespan. Classically a normocytic, normochromic anaemia, occasionally mild microcytic; iron profile shows low serum iron, LOW TIBC/transferrin (vs HIGH in iron deficiency), normal or raised ferritin (an acute-phase reactant) and low transferrin saturation. Treat the underlying cause; IV iron when oral iron is ineffective (hepcidin blocks absorption); ESA in CKD and cancer.
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Antiphospholipid Syndrome (APS)
Antiphospholipid syndrome (APS, Hughes syndrome) is an acquired autoimmune thrombophilia defined by persistent antiphospholipid antibodies (lupus anticoagulant, anticardiolipin, anti-beta-2-glycoprotein-I) causing venous and arterial thrombosis and pregnancy morbidity (recurrent early miscarriage, late fetal death, severe pre-eclampsia/HELLP, placental insufficiency). It is primary (no autoimmune disease) or secondary (most often to SLE). Diagnosis needs one clinical criterion (thrombosis or pregnancy morbidity) plus one laboratory criterion, the antibody persistent on two occasions at least 12 weeks apart (revised Sapporo 2006). The lupus anticoagulant paradox — it prolongs the APTT in vitro yet thromboses in vivo — is the signature concept. Treat thrombosis with lifelong anticoagulation (warfarin preferred; avoid DOACs in high-risk APS); pregnancy uses aspirin plus LMWH; catastrophic APS needs combined anticoagulation plus corticosteroids plus plasma exchange plus IVIG.
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Coagulation Disorders (Haemophilia & von Willebrand)
Haemophilia A (factor VIII deficiency, X-linked recessive, F8 gene, 1 in 5000 males) and haemophilia B (factor IX deficiency / Christmas disease, F9 gene, 1 in 30 000 males) are the classic inherited coagulopathies, presenting with deep-tissue bleeds — haemarthrosis of knees/elbows/ankles, intramuscular bleeds, and (in severe disease) spontaneous intracranial haemorrhage. Von Willebrand disease (VWD) is the commonest inherited bleeding disorder (up to 1 in 100, autosomal dominant), causing mucocutaneous bleeding (menorrhagia, epistaxis, gum, dental). Diagnosis rests on a prolonged APTT with normal PT and platelets that corrects on mixing, confirmed by factor VIII/IX assays (haemophilia) and vWF antigen plus…
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Haematology
Inherited Thrombophilia (Factor V Leiden & Protein C/S Deficiency)
Inherited thrombophilias are genetic disorders increasing the risk of venous thromboembolism (VTE). The commonest are factor V Leiden (activated protein C resistance; the single commonest inherited thrombophilia in Europeans, autosomal dominant, carrier rate 3 to 8 percent) and the prothrombin G20210A mutation (raised prothrombin; 2 percent of Europeans). Less common but higher-risk are deficiencies of the natural anticoagulants — antithrombin, protein C, protein S — which cause more severe, younger-onset, unusual-site thrombosis and warfarin-induced skin necrosis (protein C/S). Hyperhomocysteinaemia (MTHFR mutations) raises both venous and arterial thrombosis risk. Indications to test: VTE under 50, unusual site (cerebral, mesenteric, portal, hepatic), recurrent unprovoked VTE, family history, VTE in pregnancy/OCP, warfarin-induced skin necrosis. Testing is selective, not universal; the result does NOT change anticoagulation duration for low-risk defects alone. Treat with anticoagulation; high-risk defects (AT deficiency, homozygous FVL) warrant extended/lifelong therapy. Pregnancy uses LMWH (warfarin teratogenic).
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Lymphoma (Hodgkin & Non-Hodgkin)
Lymphoma is a clonal malignancy of lymphocytes arising in lymphoid tissue, divided by the Reed-Sternberg cell into Hodgkin lymphoma (HL) and non-Hodgkin lymphoma (NHL). HL spreads contiguously, is driven by the CD15+/CD30+ Reed-Sternberg cell, presents with cervical/supraclavicular nodes and a mediastinal mass, and is treated with ABVD (doxorubicin, bleomycin, vinblastine, dacarbazine). NHL is heterogeneous — follicular (indolent, t(14;18) BCL2), DLBCL (commonest aggressive, R-CHOP), mantle cell (t(11;14) cyclin D1, CD5+), Burkitt (t(8;14) MYC, fastest human tumour, Ki67 ~100 percent), MALT (H. pylori, gastric). Diagnosis = EXCISIONAL biopsy (not FNA — need architecture). Ann Arbor staging (Cotswolds) with B symptoms (fever over 38C, drenching night sweats, weight loss over 10 percent in 6 months). PET-CT for staging and Deauville 5-point scale for response. IPS (HL) and IPI (NHL) for prognosis. Emergencies: SVC syndrome, mediastinal-mass airway, tumour lysis, cord compression.
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★ High yieldHaematology
Multiple Myeloma
Multiple myeloma is a malignant clonal neoplasm of terminally differentiated B-cells (plasma cells) that accumulates in the bone marrow and secretes a monoclonal protein (paraprotein / M-band) and/or free light chains. End-organ damage is summarised by CRAB — hyperCalcaemia, Renal impairment (cast nephropathy), Anaemia, Bone lesions (lytic). Diagnosis (IMWG 2014) requires clonal marrow plasma cells at least 10 percent (or biopsy-proven plasmacytoma) plus a myeloma-defining event: CRAB features or a biomarker of malignancy (serum involved-to-uninvolved free light chain ratio at least 100, more than one focal lesion on MRI, or 60 percent or more clonal marrow plasma cells). Workup: SPEP + immunofixation, serum free light chains, urine Bence Jones, marrow biopsy with FISH, whole-body low-dose CT, beta-2 microglobulin, LDH, albumin (R-ISS). Treatment: VRd (bortezomib + lenalidomide + dexamethasone) induction then autologous stem-cell transplant for fit patients then lenalidomide maintenance; relapsed disease — daratumumab (anti-CD38), carfilzomib, pomalidomide, bispecific antibodies, anti-BCMA CAR-T. Supportive: zoledronic acid or denosumab for bone. Median survival now 7 to 10 years.
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★ High yieldHaematology
Myelodysplastic Syndromes
Myelodysplastic syndromes (MDS) are a heterogeneous group of clonal haematopoietic stem-cell neoplasms defined by dysplastic, ineffective haematopoiesis, peripheral cytopenia(s) and a variable risk of transformation to acute myeloid leukaemia. Diagnosis requires dysplasia of at least 10 percent in one or more myeloid lineages (or an MDS-defining cytogenetic lesion) plus a persistent unexplained cytopenia after excluding secondary causes (B12, folate, copper deficiency, alcohol, infection). The 20 percent blast threshold separates MDS from AML. Risk is stratified by the IPSS-R and, increasingly, the molecular IPSS-M (blast percentage, cytogenetics, haemoglobin, platelets, plus TP53, SF3B1, FLT3 mutations). Lower-risk disease is managed with supportive care, erythropoiesis-stimulating agents, lenalidomide for del(5q) and luspatercept for ringed sideroblasts; higher-risk disease gets a hypomethylating agent (azacitidine or decitabine), often with venetoclax and the only curative modality — allogeneic stem-cell transplant. Median survival spans from over eight years in very-low-risk disease to under a year in very-high-risk or multi-hit TP53 disease.
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★ High yieldHaematology
Myeloproliferative Disorders (PV, ET, MF & CML)
Myeloproliferative neoplasms (MPN) are clonal disorders of haematopoietic stem cells causing overproduction of mature myeloid lineages. Polycythaemia vera (PV) = raised haematocrit (over 0.52 M / over 0.48 F) plus JAK2 V617F (~95%) and low serum erythropoietin; presents with hyperviscosity (headache, visual disturbance, thrombosis, aquagenic pruritus), splenomegaly, gout; treat with venesection to haematocrit under 0.45 plus low-dose aspirin plus cytoreduction (hydroxycarbamide 15 to 35 mg/kg/day). Essential thrombocythemia (ET) = sustained platelet count over 450 with megakaryocytic hyperplasia (JAK2 50 to 60 percent, CALR 25 percent, MPL 5 percent); risk of thrombosis and bleeding; treat with aspirin 75 mg and cytoreduction if high-risk. Primary myelofibrosis (PMF) = marrow fibrosis, massive splenomegaly, tear-drop cells, leukoerythroblastic film; treat with ruxolitinib (JAK1/2 inhibitor); allogeneic stem cell transplant is the only cure. Chronic myeloid leukaemia (CML) is driven by the BCR-ABL1 fusion (Philadelphia chromosome, t(9;22)) and treated with tyrosine-kinase inhibitors (imatinib 400 mg, dasatinib 100 mg, nilotinib 300 mg twice daily) with RT-PCR BCR-ABL1 transcript monitoring; allogeneic stem cell transplant is reserved for blast phase or T315I mutation. Splanchnic vein thrombosis (Budd-Chiari) warrants JAK2 testing even with normal counts. Thrombosis is the leading cause of death in PV and ET.
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★ High yieldHaematology
Thalassaemia (Alpha & Beta)
Thalassaemia is an inherited disorder of haemoglobin synthesis causing reduced (plus) or absent (zero) globin chain production, leading to microcytic hypochromic anaemia. Beta-thalassaemia (autosomal recessive, HBB on chromosome 11): major (Cooley anaemia; transfusion-dependent from 6 to 12 months with severe microcytic anaemia, failure to thrive, frontal bossing, hepatosplenomegaly, raised HbF and HbA2), intermedia (milder, transfusion-independent), minor/trait (asymptomatic, microcytosis out of proportion to anaemia, high RBC count, normal iron, raised HbA2). Alpha-thalassaemia (HBA on chromosome 16, four genes): one gene silent carrier, two trait (mild microcytosis, NORMAL electrophoresis), three HbH disease (moderate haemolytic anaemia, beta-4 tetramers), four Hb Bart hydrops fetalis (gamma-4 tetramers, lethal). Diagnosis: Hb electrophoresis/HPLC (raised HbF/HbA2 in beta), DNA testing for alpha trait (electrophoresis normal). Management: lifelong regular red-cell transfusion, mandatory iron chelation (deferasirox 20 to 40 or deferiprone 75 to 100 mg/kg/day oral, or deferoxamine infusion), splenectomy for hypersplenism, curative HSCT (matched sibling) and gene therapy (betibeglogene autotemcel, approved 2023/24). Iron-overload cardiomyopathy is the leading cause of death — chelation is non-negotiable.
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★ High yieldHaematology
Transfusion Medicine & Transfusion Reactions
Blood transfusion is a liquid transplant: each unit places donor cells, plasma proteins and donor leucocyte-fragments into a recipient, with benefits (oxygen carriage, haemostasis, volume) balanced against immune, infectious, and circulatory risks. The two universal safety principles are correct ABO/Rh matching (the commonest fatal error is clerical mislabelling of a sample or unit) and a restrictive transfusion strategy — red-cell threshold haemoglobin under 70 g/L (under 80 g/L in cardiac surgery, symptomatic anaemia, or active bleeding), one unit then reassess. Components: PRBCs (anaemia/haemorrhage), platelets (thrombocytopenia, prophylaxis under 10 x 10^9/L), fresh frozen plasma (INR over 1.5 with bleeding), cryoprecipitate (fibrinogen under 1.5 g/L), prothrombin complex concentrate (urgent warfarin reversal), albumin, IVIG, CMV-negative and irradiated products for the immunocompromised. Acute transfusion reactions (under 24 h): acute haemolytic (ABO mismatch — fever, flank pain, hypotension, haemoglobinuria, DIC; STOP), febrile non-haemolytic (cytokines from donor WBCs; commonest), allergic/urticarial (mild) to anaphylactic (anti-IgA in IgA-deficient patients), TRALI (donor anti-WBC antibodies, bilateral non-cardiogenic infiltrates within 6 h), TACO (circulatory overload), bacterial contamination (room-temperature platelets), and transfusion-associated graft-versus-host disease (immunocompromised — use irradiated). Delayed reactions (over 24 h): delayed haemolytic (anamnestic IgG, 3 to 14 days), post-transfusion purpura, transfusion-transmitted infection (HIV, HepB/C — now extremely rare with nucleic-acid testing), and iron overload (chronic transfusion; desferrioxamine/deferasirox). The universal reaction rule for ANY reaction: STOP, maintain IV access with normal saline, assess ABCDE, keep the unit and giving set, send fresh patient samples, return unit to blood bank, and report.
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Haematology
Waldenström Macroglobulinaemia, MGUS & Hyperviscosity Syndrome
Monoclonal gammopathy of undetermined significance (MGUS) is an asymptomatic clonal plasma-cell or B-cell disorder defined by a serum monoclonal protein (M-protein) under 30 g/L, bone-marrow plasma cells under 10 percent, and absence of end-organ damage (CRAB); it is common in older adults (over 3 percent of those over 50) and carries a roughly 1 percent per year lifelong progression risk, so requires lifelong monitoring. Waldenstrom macroglobulinaemia is an indolent B-cell lymphoma (lymphoplasmacytic lymphoma) of post-germinal-centre B cells driven in over 90 percent of cases by the MYD88 L265P mutation, secreting a monoclonal IgM paraprotein. Its signature emergency is hyperviscosity syndrome — the triad of mucosal bleeding, visual change and neurological symptoms with sausage-string retinal veins on fundoscopy — because the 970-kDa pentameric IgM is largely confined to the intravascular space. Hyperviscosity is an emergency: confirm with serum viscosity and fundoscopy, treat with urgent plasmapheresis (which physically removes intravascular IgM and reverses symptoms within hours), then rituximab-based chemoimmunotherapy (BR, DRC) or a BTK inhibitor (zanubrutinib, ibrutinib) for definitive disease control.
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Infectious Diseases
18
★ High yieldInfectious Diseases
Bacterial Meningitis & Acute Meningoencephalitis
Bacterial meningitis is a life-threatening medical emergency — acute inflammation of the meninges and subarachnoid space, most often from haematogenous spread of Streptococcus pneumoniae or Neisseria meningitidis. Classic triad: fever, headache, neck stiffness plus photophobia, vomiting, altered mental status and seizures; meningococcal disease adds a rapidly evolving petechial/purpuric rash and septicaemia. Organisms by age: neonate — Group B strep, E. coli, Listeria; child — meningococcus, pneumococcus, Hib; adult — pneumococcus, meningococcus; over 50 / immunocompromised / pregnant — add Listeria. Diagnosis rests on lumbar puncture CSF (cloudy, neutrophil-predominant pleocytosis, protein high, glucose low, positive Gram stain/culture; CSF lactate is the best bacterial-versus-viral discriminator) — but CT head first when red flags are present, and empirical IV antibiotics must never be delayed for the LP or CT. Treatment: a third-generation cephalosporin (± vancomycin) + ampicillin (Listeria) + aciclovir (HSV) plus adjunctive dexamethasone with the first antibiotic dose. Mortality around 19-23% in contemporary adult series; sensorineural hearing loss is the commonest sequel and is reduced by corticosteroids.
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Candidiasis & Invasive Fungal Infection
Candidiasis is infection by Candida yeasts (commonly C. albicans and increasingly non-albicans species), spanning mucocutaneous forms — oral thrush, vulvovaginal candidiasis, oesophageal (AIDS-defining), cutaneous (intertrigo, balanitis) — and invasive candidiasis (candidaemia and deep-seated infection) in the critically ill, immunocompromised, post-surgical, central-line, broad-spectrum-antibiotic, parenteral-nutrition patient. Risk factors: neutropenia, ICU/critically ill, central venous catheter, TPN, broad-spectrum antibiotics, diabetes, steroids, abdominal surgery, malignancy. Invasive candidiasis presents with fever unresponsive to antibiotics, sepsis, and may seed the eye (endophthalmitis), heart (endocarditis), liver/spleen, bone, CNS, skin. Diagnosis: blood cultures, beta-D-glucan, T2Candida/PCR, sterile-site culture/histology. Treat mucocutaneous with topical or oral azoles/nystatin; invasive with echinocandin first-line (caspofungin, micafungin, anidulafungin, rezafungin), step-down to fluconazole when stable and susceptible, remove central lines, ophthalmology exam for endophthalmitis, 2 weeks after first negative culture.
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Cellulitis & Skin / Soft-Tissue Infection
Cellulitis is an acute, spreading, non-suppurative infection of the dermis and subcutaneous tissue, usually caused by Streptococcus pyogenes or Staphylococcus aureus (including community-acquired MRSA), presenting with erythema, warmth, swelling and tenderness with poorly demarcated margins, usually on a leg and often through a portal of entry (tinea pedis, ulcer, trauma, IV site). Erysipelas is the superficial variant with raised, sharply demarcated margins. Necrotising fasciitis is the life-threatening deep-fascial variant — severe pain out of proportion, systemic toxicity, skin necrosis or bruising, bullae, crepitus, rapid spread — needing urgent surgical debridement. Management is driven by the purulent vs non-purulent and mild vs moderate vs severe axes: non-purulent cellulitis gets oral flucloxacillin (or cefalexin); purulent disease gets incision and drainage plus or minus antibiotics; MRSA cover (clindamycin, co-trimoxazole, doxycycline, vancomycin, linezolid) is added for purulent, severe, or at-risk patients. Mark the border, elevate the limb, and treat the portal of entry (tinea, lymphoedema, ulcer) to prevent recurrence.
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Dengue & Dengue Haemorrhagic Fever
Dengue is an acute mosquito-borne flaviviral illness caused by four antigenically distinct serotypes (DENV-1 to DENV-4), transmitted mainly by the day-biting Aedes aegypti mosquito (also A. albopictus). It is the most important arboviral disease of humans, endemic across the tropics with ~100 million symptomatic cases a year. The clinical spectrum runs from undifferentiated fever through classic dengue fever (DF) to dengue haemorrhagic fever (DHF) and dengue shock syndrome (DSS) — the latter driven by plasma leakage, thrombocytopenia and bleeding. A secondary infection with a different serotype is markedly more severe through antibody-dependent enhancement (ADE). The illness has three phases — febrile (2-7 days), critical (24-48 h around defervescence) when leakage peaks and shock supervenes, and recovery. Diagnosis rests on NS1 antigen (days 1-5) and IgM ELISA (after day 5). There is no specific antiviral: management is fluid titration — oral fluids and paracetamol in mild disease (AVOID NSAIDs and aspirin); isotonic crystalloid for the leaking patient; bolus resuscitation for shock. Treated DSS mortality is under 1%; untreated, 10-20%. Dengvaxia (CYD-TDV) and Qdenga (TAK-003) vaccines now exist.
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Gonorrhoea & Chlamydia (Urogenital STIs)
Gonorrhoea (Neisseria gonorrhoeae) and chlamydia (Chlamydia trachomatis serovars D-K) are the commonest bacterial sexually transmitted infections, causing urethritis, cervicitis, proctitis and pharyngitis, and — in women — ascending infection causing pelvic inflammatory disease (PID), ectopic pregnancy and tubal-factor infertility, plus neonatal conjunctivitis/pneumonia. Most infections are asymptomatic, so the clinical skill is screening high-risk, asymptomatic people and treating empirically + tracing partners. Disseminated gonococcal infection produces migratory polyarthralgia, tenosynovitis and a pustular rash. Diagnosis is NAAT on urine and genital, rectal and pharyngeal swabs. Gonorrhoea: ceftriaxone IM (single dose); chlamydia: doxycycline 7 days (azithromycin in pregnancy); PID adds metronidazole for 14 days. Antimicrobial resistance drives the gonococcal regimen; newer oral agents (zoliflodacin) are emerging.
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Infectious Mononucleosis (Epstein-Barr Virus)
Infectious mononucleosis is the acute, self-limiting clinical syndrome of primary Epstein-Barr virus (EBV, human herpesvirus 4) infection, transmitted mainly by saliva ('kissing disease') and classically affecting adolescents and young adults. The classic triad is fever, exudative tonsillar pharyngitis and (especially posterior cervical) lymphadenopathy, with prolonged fatigue, palatal petechiae, splenomegaly, hepatitis and atypical lymphocytes on the blood film. EBV enters B lymphocytes via the CD21 (CR2) receptor; the atypical lymphocytes are reactive CD8+ cytotoxic T cells (Downey cells). Diagnosis is by heterophile antibody (Monospot) plus EBV-specific serology (VCA IgM = acute). Management is supportive (rest, analgesia); AVOID ampicillin/amoxicillin (diffuse rash), alcohol (hepatitis), and contact sport for at least 3 to 4 weeks (splenic rupture). Corticosteroids are reserved for impending airway obstruction, severe cytopenia/haemolysis or neurology. Key complications: splenic rupture, airway obstruction, autoimmune haemolytic anaemia/thrombocytopenia, neurological disease, and EBV-driven malignancy (Burkitt, Hodgkin, nasopharyngeal carcinoma, PTLD).
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Intestinal & Tissue Helminth Infections (STH, Tapeworms, Schistosomiasis, Strongyloides, Filariasis)
Helminth infections are parasitic worm infestations caused by nematodes (roundworms), cestodes (tapeworms), and trematodes (flukes), infecting approximately 1.5 billion people worldwide and dominating the tropical infectious-disease burden alongside malaria and tuberculosis. The soil-transmitted helminths (STH) - Ascaris lumbricoides, hookworm (Necator americanus / Ancylostoma duodenale), and Trichuris trichiura - are acquired by egg ingestion or larval skin penetration from contaminated soil; tapeworms (Taenia solium/saginata) by undercooked meat; schistosomes by freshwater cercariae; filarial worms by insect vectors. Many infections are asymptomatic or pauci-symptomatic, but heavy burdens cause iron-deficiency anaemia (hookworm), growth and cognitive impairment in children (all STH), intestinal obstruction and biliary migration (Ascaris), Loeffler eosinophilic pneumonitis (larval migration), neurocysticercosis (Taenia solium eggs), portal hypertension and bladder cancer (schistosomiasis), elephantiasis (lymphatic filariasis), and fatal hyperinfection (Strongyloides in the immunosuppressed). The unifying laboratory signature is peripheral eosinophilia, and the unifying diagnostic test is stool microscopy for ova, cysts, and parasites (OCP) with species-specific serology or antigen tests for tissue stages. Treatment is with benzimidazoles (albendazole/mebendazole) for STH, praziquantel for cestodes and trematodes, ivermectin for Strongyloides and onchocerciasis, and diethylcarbamazine for lymphatic filariasis. Prevention rests on sanitation, safe water, footwear, thorough cooking of meat and fish, and mass drug administration (MDA) to at-risk children in endemic regions.
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Intra-Abdominal Infection & Peritonitis
Intra-abdominal infection (IAI) and peritonitis are time-critical emergencies that span two very different diseases. Primary peritonitis — spontaneous bacterial peritonitis (SBP) — is infection of cirrhotic ascites without an intra-abdominal source, presenting subtly (fever, abdominal pain, hepatic encephalopathy, renal failure) and treated medically with cefotaxime/ceftriaxone plus IV albumin (the ascitic neutrophil count over 250 cells per mm³ is diagnostic). Secondary peritonitis is polymicrobial contamination of the peritoneum from a perforated or translocating hollow viscus (perforated peptic ulcer, appendicitis, diverticulitis, ischaemic bowel, post-operative leak, trauma) and is a surgical emergency: resuscitation, broad-spectrum antibiotics covering enteric Gram-negatives and anaerobes, and urgent source control. Tertiary peritonitis is persistent or recurrent infection in the critically ill, often with multi-drug-resistant organisms (Pseudomonas, Enterococcus, Candida). Presents with abdominal pain, peritonism (rigidity, guarding, rebound tenderness), fever, sepsis and ileus. Diagnose with diagnostic ascitic tap (PMN over 250), CT abdomen with contrast and blood cultures. Treat with antibiotics plus source control (surgery or radiological drainage); SBP additionally receives albumin to prevent hepatorenal syndrome.
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Leprosy (Hansen Disease)
Leprosy (Hansen disease) is a chronic granulomatous mycobacterial infection caused by Mycobacterium leprae (and the related M. lepromatosis), an obligate intracellular, acid-fast bacillus with tropism for Schwann cells of peripheral nerves and dermal macrophages in cooler tissues (skin, peripheral nerves, nasal mucosa, eyes, testes). Transmission is via prolonged close contact through nasal droplets from untreated multibacillary cases, with a long incubation (2 to 12 years). The clinical spectrum is determined by host cell-mediated immunity — strong Th1 immunity gives the paucibacillary/tuberculoid pole (single anaesthetic hypopigmented patches with thickened nerves), whereas absent CMI gives the multibacillary/lepromatous pole (numerous symmetric lesions, nodules, leonine facies, madarosis, glove-and-stocking neuropathy, saddle nose). Lepra reactions — type 1 (reversal) and type 2 (erythema nodosum leprosum, ENL) — cause acute, irreversible nerve damage and disability. Diagnosis is clinical (anaesthetic patch + thickened nerve) plus slit-skin smear, skin biopsy (Fite-Faraco acid-fast bacilli) and PCR. Treatment is WHO multidrug therapy (MDT) — paucibacillary: rifampicin + dapsone for 6 months; multibacillary: rifampicin + dapsone + clofazimine for 12 months. Reactions are treated with corticosteroids (type 1) and thalidomide/clofazimine/steroids (type 2).
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Measles (Rubeola)
Measles (rubeola) is a highly contagious, vaccine-preventable acute viral exanthem caused by the measles morbillivirus (Paramyxoviridae), transmitted by respiratory droplets and airborne aerosols. After a 10 to 14 day incubation, a prodrome of high fever with the '3 Cs' (cough, coryza, conjunctivitis) and the pathognomonic Koplik spots (blue-white grains on the buccal mucosa) precedes a maculopapular rash that spreads head to toe. With a basic reproduction number (R0) of 12 to 18 it is one of the most infectious human pathogens; herd immunity needs about 95 percent coverage. Complications are common and severe — otitis media, pneumonia (the commonest cause of death), diarrhoea, keratitis/blindness, acute encephalitis, and the late, fatal subacute sclerosing panencephalitis (SSPE) — and measles induces a transient 'immune amnesia' that erases pre-existing immunity to other pathogens. Diagnosis is clinical plus IgM serology or RT-PCR (throat/urine). There is no specific antiviral; treatment is supportive plus vitamin A (two doses, reduces mortality and blindness). Prevention is the MMR vaccine (two doses, over 97 percent effective). Suspected measles is notifiable and isolated with airborne precautions.
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Mumps (Epidemic Parotitis)
Mumps (epidemic parotitis) is an acute, vaccine-preventable, self-limiting viral infection caused by the mumps virus — a Rubulavirus within the Paramyxoviridae (enveloped, non-segmented, negative-sense single-stranded RNA) — transmitted by respiratory droplets and saliva. The cardinal feature is nonsuppurative, painful parotid swelling (parotitis) that lifts the ear lobe and obliterates the jaw angle (bilateral in 70 percent), accompanied by fever and malaise. After a 16 to 18 day incubation, illness lasts 7 to 10 days. The clinical importance of mumps lies less in the parotitis than in its complications — orchitis/oophoritis (post-pubertal), aseptic meningitis/meningoencephalitis, pancreatitis, sensorineural deafness and myocarditis — which can occur without parotitis. Diagnosis is clinical, confirmed by buccal-swab RT-PCR or mumps IgM (PCR preferred in the vaccinated, who may be IgM-negative). Treatment is supportive (hydration, analgesia, compresses); no antiviral is of proven benefit. Isolate (droplet) for 5 days after parotitis onset; mumps is notifiable. Prevention: MMR vaccine — two doses, ~88 percent effective; live vaccine, CONTRAINDICATED in pregnancy and immunocompromise.
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Osteomyelitis
Osteomyelitis is an infection of bone and bone marrow (myelo = marrow) by microbes (usually bacteria), producing inflammation, bone destruction (osteolysis), necrosis and reactive new bone formation. By pathogenesis (Lew-Waldvogel): haematogenous (bloodstream seeding — children: long-bone metaphysis; adults: vertebrae), contiguous-focus (adjacent wound, ulcer, diabetic foot, surgery) and chronic (sequestrum, involucrum, sinus tract, biofilm). Staphylococcus aureus is the commonest organism across all ages and types. Acute disease presents with localised bone pain, tenderness, swelling and fever; chronic disease with a draining sinus tract and relapsing pain. X-ray may be normal for the first 1 to 2 weeks — MRI is the modality of choice (sensitivity about 90%). The microbiological gold standard is bone biopsy culture (sinus tract culture is contaminated). Management is orthopaedic + infectious diseases co-management: dead bone cannot be cured by antibiotics, so surgical debridement of necrotic/sequestered bone is the cornerstone of chronic disease, combined with prolonged culture-directed antibiotics (4 to 6 weeks acute, 6 weeks plus chronic; add rifampin for staphylococcal biofilm).
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Pneumonia (Community-Acquired)
Community-acquired pneumonia (CAP) is an acute infection of the lung parenchyma acquired outside hospital (or within 48 h of admission). Commonest organism Streptococcus pneumoniae; atypicals (Mycoplasma, Chlamydophila, Legionella); viruses (influenza, COVID-19, RSV); Staphylococcus aureus and Gram-negatives in severe/chronic disease; Klebsiella in alcoholics. Presents with productive cough, fever, dyspnoea, pleuritic chest pain and signs of consolidation; atypical pneumonias have a dry cough, prominent systemic features and a normal/mildly abnormal CXR. Diagnosis is clinical plus chest X-ray; severity by CURB-65 (Confusion, Urea over 7, RR over 30, BP under 90/60, age over 65). Treat with antibiotics within 4 hours: low severity amoxicillin/doxycycline; moderate/severe beta-lactam plus macrolide; give oxygen, fluids, cover atypicals. Admit if CURB-65 at least 2; ICU if 3 to 5. Vaccinate (pneumococcal, influenza, COVID-19).
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Sepsis & Septic Shock
Sepsis is a life-threatening organ dysfunction caused by a dysregulated host response to infection (Sepsis-3 definition, Singer 2016). Operationally it is identified at the bedside as an acute change in total SOFA score of 2 or more points consequent to infection. Septic shock is a subset of sepsis with circulatory and cellular/metabolic abnormalities substantial enough to substantially increase mortality — clinically hypotension requiring vasopressors to maintain a mean arterial pressure of at least 65 mmHg AND a serum lactate over 2 mmol/L despite adequate volume resuscitation, carrying a hospital mortality over 40 percent. Common sources are respiratory, abdominal, urinary, skin/soft tissue and device-related. Recognition is clinical (suspected infection with qSOFA at least 2: RR 22 or more, altered mentation, SBP 100 or less), and management is the Surviving Sepsis Campaign Hour-1 bundle — measure lactate, obtain blood cultures, give broad-spectrum antibiotics immediately (within 1 hour in shock), give at least 30 mL/kg crystalloid within the first 3 hours for sepsis-induced hypoperfusion, and start vasopressors for hypotension — plus source control and organ support.
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Syphilis (Treponema pallidum)
Syphilis is a chronic systemic infection by the spirochete Treponema pallidum subsp. pallidum, acquired sexually or vertically, that progresses through four clinical stages if untreated: primary (painless indurated chancre at the inoculation site with rubbery regional lymphadenopathy), secondary (systemic illness with a diffuse non-itchy maculopapular rash involving the palms and soles, mucous patches, condylomata lata, generalised lymphadenopathy and moth-eaten alopecia), latent (asymptomatic but seropositive), and tertiary (years later: gummas, cardiovascular syphilis with ascending aortic aneurysm and aortic regurgitation, and neurosyphilis — tabes dorsalis, general paresis, Argyll Robertson pupil, meningovascular stroke, ocular and otic syphilis). Neurosyphilis can occur at any stage. Congenital syphilis causes stillbirth, hydrops and the late stigmata (Hutchinson triad, saddle nose, saber shin, snuffles). Diagnosis rests on two-tier serology: non-treponemal (RPR/VDRL — activity, titre and treatment response) plus treponemal (TPPA/FTA — confirm, lifelong positive); dark-field microscopy shows the motile spirochete from moist lesions. Penicillin is first-line for every stage — benzathine penicillin G IM (single dose for primary/secondary/early latent; weekly x 3 for late latent/tertiary) and IV aqueous crystalline penicillin for neurosyphilis for 10 to 14 days. The Jarisch-Herxheimer reaction is common after the first dose. All patients must be tested for HIV, partners notified and treated, and every pregnancy screened and treated urgently to prevent congenital syphilis.
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Tetanus
Tetanus is an acute, toxin-mediated neurological disease caused by Clostridium tetani tetanospasmin released from spores germinating in anaerobic, necrotic wounds. The toxin travels retrogradely in motor nerves to the spinal cord and brainstem, cleaves synaptobrevin (VAMP), and blocks release of the inhibitory neurotransmitters glycine and GABA, producing unopposed sustained muscle contraction and reflex spasms with a preserved sensorium. The classic phenotype is trismus (lockjaw), risus sardonicus, opisthotonos and stimulus-triggered spasms, progressing to autonomic instability and respiratory failure. Diagnosis is clinical — there is no useful laboratory test. Management rests on three pillars: neutralise unbound toxin (human tetanus immunoglobulin, HTIG), eradicate the organism (wound debridement plus metronidazole), and control spasms and support vital functions in ICU (benzodiazepines, magnesium sulphate, mechanical ventilation, autonomic control) — followed by active vaccination, because the disease does not confer immunity. Tetanus is entirely preventable by DTaP/Tdap vaccination every 10 years, wound prophylaxis, and maternal immunisation.
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Typhoid & Enteric Fever (Salmonella Typhi)
Enteric (typhoid) fever is a prolonged systemic bacteraemic illness caused by Salmonella enterica serovars Typhi and Paratyphi A, B, C, transmitted faecal-orally through contaminated food and water. It is endemic in South Asia (India, Pakistan, Bangladesh), sub-Saharan Africa and parts of SE Asia, with an incubation of 7 to 14 days. The clinical signature is a step-ladder (stepwise-rising) fever with relative bradycardia (Faget sign), dull headache, constipation then 'pea-soup' diarrhoea, rose spots, splenomegaly and a coated tongue. Untreated it progresses over weeks to intestinal perforation and haemorrhage (Peyer's patch necrosis, week 3 to 4), severe typhoid with encephalopathy, myocarditis and hepatitis. Blood culture is the gold standard (first week); bone marrow culture is the most sensitive, remaining positive even after antibiotics; the Widal test is unreliable alone. Treatment is culture-guided: ciprofloxacin (where susceptible), ceftriaxone/cefixime for quinolone-resistant strains, azithromycin for XDR, and dexamethasone (Hoffman regimen) for severe typhoid. Prevention: Vi conjugate (Typbar-TCV), Ty21a and Vi polysaccharide vaccines, safe water and food hygiene.
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★ High yieldInfectious Diseases
Varicella & Herpes Zoster (Chickenpox and Shingles)
Varicella-zoster virus (VZV, human herpesvirus 3 / HHV-3) is a neurotropic double-stranded DNA alpha-herpesvirus that produces two distinct clinical syndromes. Primary infection — varicella (chickenpox) is a generalised, pruritic, vesicular rash appearing in crops at different stages simultaneously (papules, vesicles, pustules, crusts together), with fever and malaise, mainly in children. The virus then becomes latent in the dorsal root and cranial-nerve ganglia and reactivates decades later as herpes zoster (shingles) — a painful, unilateral, dermatomal vesicular rash that does not cross the midline, typically in older or immunosuppressed adults. Zoster complications: postherpetic neuralgia (the commonest, persistent pain beyond 90/120 days, especially in the elderly), ophthalmic zoster (Hutchinson sign — ophthalmology emergency, corneal involvement), Ramsay Hunt syndrome (geniculate ganglion — ear vesicles, facial palsy, deafness), dissemination in the immunocompromised, meningitis/encephalitis/myelitis, and VZV vasculopathy/stroke. Varicella complications: pneumonia (adults, smokers, pregnant, immunocompromised — IV aciclovir), secondary bacterial skin infection (commonest, Strep/Staph, necrotising fasciitis), cerebellar ataxia (children), encephalitis, congenital varicella syndrome (limb hypoplasia, scarring) and neonatal varicella. Treatment: uncomplicated varicella/zoster is supportive ± antivirals; oral aciclovir, valaciclovir or famciclovir started within 72 hours of the zoster rash reduces severity, duration and postherpetic neuralgia; IV aciclovir for severe, ophthalmic, disseminated, immunocompromised, pregnant-with-pneumonia and neonatal disease. Vaccines: live-attenuated varicella (children) and recombinant zoster vaccine / Shingrix (adults over 50, over 90% efficacy). VZIG for post-exposure prophylaxis in high-risk contacts.
NEET-PGINICET
Nephrology
14
★ High yieldNephrology
Acid-Base Disorders
Acid-base disorders arise from disturbance of the bicarbonate-carbon-dioxide buffer system. There are four primary disorders: metabolic acidosis (low pH, low bicarbonate) — raised anion gap from ketoacidosis, lactic acidosis, renal failure or toxins (MUDPILES) or normal gap from diarrhoea and renal tubular acidosis (HARDUP); metabolic alkalosis (high pH, high bicarbonate — vomiting, diuretics); respiratory acidosis (low pH, high CO2 — COPD, opiates); respiratory alkalosis (high pH, low CO2 — anxiety, pain, sepsis, altitude). The stepwise approach is check the pH, identify the primary disorder, assess compensation (Winter's and the respiratory rules), calculate the anion gap, then treat the cause. Bicarbonate is reserved for severe acidosis (pH under 7.1 to 7.15 with instability), hyperkalaemia with ECG change, and tricyclic overdose. Always correct potassium and chloride.
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★ High yieldNephrology
Acute Kidney Injury
Acute kidney injury (AKI) is a rapid (hours to days) decline in kidney function defined by KDIGO as a serum creatinine rise of 0.3 mg/dL (26.5 micromol/L) or more within 48 hours, a creatinine 1.5 times baseline or more within 7 days, or urine output under 0.5 mL/kg/h for 6 hours or more. It is classified into pre-renal (hypoperfusion, around 60 per cent), intrinsic/renal (acute tubular necrosis, glomerular, interstitial, vascular) and post-renal (obstruction, around 5 per cent). Commonest intrinsic cause is acute tubular necrosis (ATN) from ischaemia or nephrotoxins. Presents with oliguria, fluid overload, uraemia, hyperkalaemia; diagnose with creatining trend, FENa, urine sediment, renal ultrasound. Management: treat the cause, restore perfusion with balanced crystalloid, stop nephrotoxins (NSAIDs, ACE inhibitors, aminoglycosides, contrast), manage hyperkalaemia and acidosis, and dialyse for AEIOU (Acidosis, Electrolytes, Ingestion, Overload, Uraemia). Mortality 10 per cent uncomplicated to over 50 per cent in ICU; survivors carry increased risk of future CKD.
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★ High yieldNephrology
Contrast-Associated AKI (Contrast Nephropathy) & Acute Tubular Necrosis vs Pre-Renal AKI
Contrast-associated AKI (CA-AKI, contrast nephropathy) is an intrinsic AKI developing within 48 to 72 hours of iodinated contrast, driven by renal medullary vasoconstriction and direct tubular cytotoxicity, highest-risk in CKD and diabetes. It is one cause of acute tubular necrosis (ATN), which must be distinguished from pre-renal AKI at the bedside: pre-renal (hypovolaemia, hypoperfusion with intact tubules) shows a FENa under 1 percent, urine sodium under 20, urine osmolality over 500, BUN/Cr over 20 and responds to fluids; ATN (ischaemia, nephrotoxins, contrast) shows a FENa over 2 percent, urine sodium over 40, urine osmolality under 350, muddy brown granular casts and a slower recovery over days to weeks. There is no specific treatment for established contrast AKI, so prevention dominates: risk-stratify, isotonic saline hydration, lowest contrast dose, hold nephrotoxins (metformin held if AKI develops, not because of a direct contrast-metformin interaction).
NEET-PGINICET
★ High yieldNephrology
Diabetic Kidney Disease
Diabetic kidney disease (DKD, diabetic nephropathy) is the commonest single cause of end-stage kidney disease (ESKD) worldwide, developing over years through a predictable pathway of glomerular hyperfiltration, microalbuminuria, macroproteinuria and declining GFR. Its histological hallmark is nodular glomerulosclerosis (Kimmelstiel-Wilson nodules) with thickening of the glomerular basement membrane and mesangial expansion, driven by chronic hyperglycaemia and intraglomerular hypertension. The earliest clinical marker is albuminuria measured as the urine albumin-to-creatinine ratio (UACR): screen annually from diagnosis in type 2 diabetes and from 5 years after diagnosis in type 1 diabetes. Renal biopsy is reserved for atypical features (short diabetes duration, absence of retinopathy, rapid decline, haematuria, more than 30 percent creatinine rise on RAAS blockade). Management is multifactorial and combination-based: RAAS blockade (ACE inhibitor or ARB), an SGLT2 inhibitor (dapagliflozin, empagliflozin or canagliflozin) as a glucose-independent disease-modifying agent, the non-steroidal mineralocorticoid receptor antagonist finerenone, plus glycaemic and blood pressure control, statin and lifestyle. Combined, these slow progression and reduce cardiovascular events, the leading cause of death in this population.
NEET-PGINICET
★ High yieldNephrology
Drug Dosing in Kidney Disease
Safe prescribing in kidney disease is a repeated clinical decision, not a universal renal-dose table: define the indication, assess current kidney-function trajectory, use the estimator and units specified by the current product label or local monograph, account for body size and dialysis, design loading and maintenance doses from pharmacokinetics, monitor effect and toxicity, and reassess whenever physiology or renal replacement therapy changes.
NEET-PGINICET
★ High yieldNephrology
Haematuria (Evaluation)
Haematuria (red blood cells in the urine) is a sign, not a diagnosis. It is divided into visible (macroscopic/gross) and non-visible (microscopic, defined as more than 3 RBCs per high-power field on microscopy). The pivotal diagnostic distinction is glomerular vs urological source: glomerular bleeding shows dysmorphic red cells, red-cell casts and proteinuria and is managed by nephrology; urological bleeding shows isomorphic (intact) red cells and needs cystoscopy and CT urogram. Painless visible haematuria is cancer until proven otherwise and warrants an urgent suspected-cancer referral. Evaluation first excludes infection and transient causes, then uses urine microscopy to direct either a urological or nephrological work-up.
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★ High yieldNephrology
Hypertensive Nephrosclerosis
Hypertensive nephrosclerosis is chronic kidney injury caused by long-standing systemic hypertension — after diabetic kidney disease, the commonest cause of CKD and ESKD worldwide. Benign (chronic) nephrosclerosis produces hyaline arteriolosclerosis of the afferent arteriole, small granular kidneys and slowly progressive CKD with sub-nephrotic proteinuria. Malignant-phase (accelerated) hypertension — severe BP (typically over 180 over 120 mmHg) with acute target-organ damage (retinopathy grade III-IV, encephalopathy, AKI, microangiopathic haemolysis) — is a medical emergency whose histology is fibrinoid necrosis of arterioles and onion-skinning of interlobular arteries. Chronic management is strict BP control with an ACE inhibitor or ARB (BP target under 130 over 80, or SBP under 120 if tolerated — KDIGO 2021), an SGLT2 inhibitor added to CKD (DAPA-CKD, EMPA-KIDNEY), and aggressive cardiovascular risk reduction. Malignant hypertension requires CONTROLLED IV BP lowering (labetalol, nicardipine) — about a 25 percent reduction in mean arterial pressure in the first hour — because a rapid or excessive fall precipitates ischaemic stroke, MI or AKI. Resistant or early-onset hypertension mandates screening for a secondary cause (renal artery stenosis, primary aldosteronism).
NEET-PGINICET
★ High yieldNephrology
Membranous Nephropathy & FSGS
Membranous nephropathy and focal segmental glomerulosclerosis (FSGS) are the two commonest primary glomerular causes of nephrotic syndrome in adults. Membranous nephropathy is an antibody-mediated subepithelial immune-complex disease: about 80% is primary, driven by IgG4 autoantibodies against the podocyte M-type phospholipase A2 receptor (PLA2R) (and rarely THSD7A); secondary forms arise from solid-organ malignancy, hepatitis viruses, lupus class V, drugs and other exposures. It carries the highest thrombotic risk of any nephrotic cause (renal vein thrombosis), and about a third remit spontaneously (the rule of thirds). FSGS is a podocytopathy defined by focal, segmental glomerular scarring from podocyte injury — primary (permeability factor), genetic (APOL1, NPHS1, NPHS2, TRPC6, INF2), virus-associated (HIV), drug-induced (heroin, pamidronate, interferon) and adaptive (hyperfiltration from obesity, reduced renal mass, reflux). It is often steroid-resistant, progresses frequently to ESKD, and recurs in about a third of renal transplants. Both present as nephrotic syndrome and require renal biopsy. Management combines shared nephrotic care (RAAS blockade, anticoagulation decisions when albumin is very low, vaccination, lipid and oedema control) with disease-specific immunosuppression risk-stratified by proteinuria and renal function: modified Ponticelli (steroid plus cyclophosphamide) or rituximab for high-risk membranous (MENTOR, NEJM 2019); a prolonged high-dose steroid trial, then calcineurin inhibitor for primary FSGS.
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★ High yieldNephrology
Nephritic Syndrome & Acute Glomerulonephritis
Nephritic syndrome is the glomerular inflammatory counterpart of nephrotic syndrome: haematuria (dysmorphic red cells and red-cell casts), subnephrotic proteinuria (typically under 3.5 g/day), hypertension, oedema and an acute rise in creatinine (AKI), caused by glomerular inflammation and cellular proliferation. Causes are split by serum complement: low C3/C4 (post-streptococcal GN, membranoproliferative GN, lupus nephritis, endocarditis-associated GN, cryoglobulinaemia, shunt nephritis) versus normal complement (IgA nephropathy — the commonest primary GN worldwide, IgA vasculitis/Henoch-Schonlein purpura, anti-GBM disease/Goodpasture, ANCA-associated vasculitis). The pivotal clinical decision is distinguishing a self-limiting post-streptococcal GN (supportive care, excellent prognosis in children) from a renal emergency such as rapidly progressive (crescentic) GN, which destroys glomeruli within days and needs urgent steroids, cyclophosphamide or rituximab, and plasma exchange for anti-GBM and severe ANCA disease. Work-up: urine microscopy (dysmorphic RBCs and RBC casts), C3/C4, ANA/anti-dsDNA, ANCA (MPO/PR3), anti-GBM antibody, ASO/anti-DNase B, hepatitis B/C and HIV, and renal biopsy in adults and atypical cases.
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★ High yieldNephrology
Nephrolithiasis (Kidney & Ureteric Stones)
Nephrolithiasis (renal and ureteric stones) is the formation of crystalline calculi within the urinary tract, driven by urinary supersaturation of stone-forming salts, and presenting classically as acute, severe colicky flank pain radiating from loin to groin with nausea, restlessness and haematuria. Calcium oxalate is the commonest stone type (~75%, radio-opaque); the other three pillars are uric acid (radio-lucent, acidic urine, gout, dissolvable with alkalinisation), struvite (urease-producing Proteus infection, alkaline urine, staghorn calculi) and cystine (autosomal-recessive cystinuria, hexagonal crystals). Risk factors cluster around low fluid intake, high sodium/animal-protein/fructose intake, obesity, gout, primary hyperparathyroidism, inflammatory bowel disease and renal tubular acidosis. Non-contrast CT KUB is the diagnostic standard (95 to 98 percent sensitive). Most stones under 5 mm pass spontaneously with NSAIDs, fluids and an alpha-blocker; larger or obstructing stones need ESWL, ureteroscopy with laser, or PCNL, chosen by size and site. Prevention rests on fluids over 2.5 to 3 L/day, low salt, low animal protein, normal dietary calcium, and targeted metabolic therapy (thiazide, potassium citrate, allopurinol, tiopronin). The single most dangerous scenario is an obstructing stone with infection, which destroys a kidney within hours and demands urgent decompression before definitive stone treatment.
NEET-PGINICET
★ High yieldNephrology
Nephrotic Syndrome
Nephrotic syndrome is the clinical expression of severe glomerular filtration-barrier (podocyte) injury, defined by the tetrad of heavy proteinuria (over 3.5 g/day, or over 50 mg/kg/day in children, or urine protein-to-creatinine ratio over 300 mg/mmol), hypoalbuminaemia (under 30 g/L, often under 25 g/L), oedema and hyperlipidaemia with lipiduria. It is distinguished from the nephritic syndrome by proteinuria-dominant features (few cells in the sediment) versus haematuria, hypertension, renal failure and low complement. In children (peak age 2-6 years, male predominance) the commonest cause is minimal change disease; in adults (equal sex ratio) membranous nephropathy and FSGS lead, with secondary causes — diabetic nephropathy, lupus nephritis, amyloidosis, malignancy, pre-eclampsia, and drugs (NSAIDs, pamidronate, lithium) — important. Malignancy associations are high-yield: membranous = solid-organ carcinoma (lung, colon, stomach); MCD = Hodgkin lymphoma. Complications arise from urinary losses — infection (encapsulated organisms from IgG and complement factor B/D loss), thromboembolism (renal vein, DVT, PE from antithrombin-III loss), hyperlipidaemia, AKI and malnutrition. Diagnosis combines protein quantification, urine microscopy, complement, autoimmune/viral/anti-PLA2R serology and renal biopsy (all adults). Management is to treat the cause (e.g. prednisolone 60 mg/m²/day for MCD), reduce proteinuria (ACE inhibitor/ARB; SGLT2 inhibitor for diabetic kidney disease), control fluid and lipids, and prevent complications (anticoagulation, vaccination).
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★ High yieldNephrology
Polycystic Kidney Disease
Autosomal dominant polycystic kidney disease (ADPKD) is the commonest inherited kidney disease (prevalence 1 in 400 to 1 in 1000), caused in 95 percent of families by mutations in PKD1 (85 percent, chromosome 16, severe) or PKD2 (15 percent, chromosome 4, milder). It produces bilateral, progressively enlarging renal cysts arising from any nephron segment, leading to hypertension, grossly enlarged kidneys, and progression to end-stage kidney disease by the fifth or sixth decade (about 50 percent by age 60). Important extrarenal features include liver cysts (commonest, ~80 percent by age 60), intracranial berry aneurysms (~10 percent, with subarachnoid haemorrhage risk), mitral valve prolapse (~25 percent), pancreatic cysts and diverticular disease. Diagnosis is by ultrasound using age-adjusted cyst count (Pei criteria), cross-sectional imaging for height-adjusted total kidney volume (Mayo classification), or genetic testing. Management centres on strict blood-pressure control (ACE inhibitor or ARB, target under 110 over 80), tolvaptan (a vasopressin V2 antagonist) in rapidly progressive disease, treatment of cyst complications (infection, bleeding, pain), and dialysis or transplantation for ESKD — with selective aneurysm screening when there is a family history of haemorrhage.
NEET-PGINICET
★ High yieldNephrology
Rapidly Progressive Glomerulonephritis
Rapidly progressive glomerulonephritis (RPGN) is the most aggressive form of glomerulonephritis and a true renal emergency: a syndrome of rapid loss of renal function (loss of over 50 per cent of GFR within under 3 months), unified by the histological hallmark of crescents — fibrin and proliferating parietal epithelial cells — in Bowman's space. Untreated it progresses to end-stage kidney disease within weeks. It is classified by immunofluorescence into three types: Type I anti-GBM (linear IgG; Goodpasture syndrome with pulmonary haemorrhage), Type II immune-complex (granular; lupus, post-infectious, IgA) and Type III pauci-immune (ANCA-associated vasculitis — GPA, microscopic polyangiitis; the commonest form in adults). Presentation is a rapidly rising creatinine with haematuria and dysmorphic red cells / red-cell casts, often with systemic vasculitic features or haemoptysis (the pulmonary-renal syndrome). Work-up is ANCA (anti-PR3, anti-MPO), anti-GBM antibody, complement, and urgent renal biopsy. The overriding principle is treat first, refine later — start high-dose IV methylprednisolone on suspicion before biopsy results, then add cyclophosphamide or rituximab, with plasma exchange for anti-GBM disease and selected severe ANCA (dialysis-dependent or life-threatening alveolar haemorrhage), followed by maintenance rituximab or azathioprine to prevent ANCA relapse. Speed of treatment determines whether the kidney survives — once crescents become fibrous the damage is irreversible.
NEET-PGINICET
★ High yieldNephrology
Urinary Tract Infection & Pyelonephritis
A source-first framework for urinary infection: distinguish localized cystitis from systemic UTI or pyelonephritis, identify risk factors and mimics, collect and interpret urine correctly, select empirical therapy from current syndrome-specific regional guidance, add prior susceptibility and a recent relevant antibiogram for septic complicated UTI, narrow to susceptibility, adjust for renal function, and obtain urgent source control for an infected obstruction.
NEET-PGINICET
Neurology
12
★ High yieldNeurology
CNS Infections — Meningitis, Encephalitis, Brain Abscess, TB, Cryptococcal, Neurocysticercosis
CNS infections span the meninges (meningitis), brain parenchyma (encephalitis, abscess), or both (meningoencephalitis). Acute bacterial meningitis is a time-critical emergency: the classic triad of fever, neck stiffness and altered mental status is complete in only 44 percent of adults, yet 95 percent have at least two of headache, fever, neck stiffness and altered mental status — and empiric IV antibiotics must start within one hour (per the ESCMID guideline), with dexamethasone 10 mg every six hours for four days given before or with the first antibiotic dose. CSF analysis distinguishes bacterial (neutrophil-predominant pleocytosis, low glucose, high protein) from viral (lymphocytic, negative Gram stain) patterns. HSV encephalitis needs early IV aciclovir 10 mg/kg every eight hours; brain abscess needs imaging, stereotactic aspiration and prolonged antibiotics; TB meningitis needs antituberculosis drugs plus dexamethasone; cryptococcal meningitis needs short-course amphotericin-based induction with flucytosine; neurocysticercosis needs antiparasitic therapy with corticosteroids for viable cysts.
NEET-PGINICET
★ High yieldNeurology
Concussion & Traumatic Brain Injury
Traumatic brain injury (TBI) is a disruption of brain function from external mechanical force, graded by the Glasgow Coma Scale (GCS) into mild (GCS 13 to 15, about 80 percent — concussion), moderate (GCS 9 to 12, about 10 percent) and severe (GCS 3 to 8, about 10 percent). Injury is divided into primary (mechanical, instantaneous, largely irreversible — skull fracture, contusion, diffuse axonal injury) and secondary (delayed, PREVENTABLE — hypoxia, hypotension, raised intracranial pressure, ischaemia, infection); preventing secondary injury is the main target of treatment. Concussion produces transient headache, dizziness, confusion, nausea and amnesia without structural injury on imaging, and is managed with 24 to 48 hours of physical and cognitive rest followed by a graduated return. Moderate to severe TBI requires ABCDE resuscitation, urgent CT, ICP monitoring (target under 22 mmHg, CPP 60 to 70 mmHg), surgical evacuation of mass lesions and anticonvulsant prophylaxis. The extradural haematoma (lucid interval, biconvex/lens-shaped, middle meningeal artery, temporal) and subdural haematoma (crescent-shaped, cortical bridging veins, elderly/alcoholic) are the two neurosurgical emergencies every student must distinguish.
NEET-PGINICET
★ High yieldNeurology
Guillain-Barré Syndrome
Guillain-Barré syndrome (GBS) is an acute, monophasic, immune-mediated polyradiculoneuropathy producing symmetric, ascending flaccid paralysis with areflexia, progressing to a nadir within four weeks and often preceded by an infection one to six weeks earlier. The commonest subtype is acute inflammatory demyelinating polyradiculoneuropathy (AIDP, 85 to 90 percent in Western countries), with axonal motor (AMAN) forms commoner in Asia. The antecedent trigger is classically Campylobacter jejuni gastroenteritis, but cytomegalovirus, Epstein-Barr virus, Mycoplasma pneumoniae, influenza and Zika are also recognised. Diagnosis is clinical, supported by CSF albuminocytological dissociation (high protein, normal cell count) and nerve conduction studies showing demyelination or axonal loss. Twenty to thirty percent of patients need mechanical ventilation, and autonomic instability is the leading cause of death. The two equally effective first-line treatments are intravenous immunoglobulin (IVIg, 2 g/kg over five days) and plasma exchange (5 sessions over one to two weeks); corticosteroids are NOT effective. Mortality is 3 to 7 percent and about one in five patients has residual disability.
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★ High yieldNeurology
Motor Neuron Disease (ALS)
Motor neuron disease is an umbrella term; amyotrophic lateral sclerosis is its commonest adult phenotype and usually combines progressive upper- and lower-motor-neuron dysfunction. Diagnosis is clinical using the Gold Coast framework, with EMG/NCS and imaging used to support localization and exclude mimics. Care integrates riluzole, jurisdiction-specific edaravone or SOD1-directed tofersen, respiratory and nutritional support, communication, symptom control, genetic counselling, advance care planning and palliative care.
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★ High yieldNeurology
Myasthenia Gravis
Myasthenia gravis is an autoimmune postsynaptic neuromuscular-junction disorder that causes fluctuating, fatigable ocular, bulbar, limb, axial or respiratory weakness. Diagnosis is clinical and supported by antibody and electrophysiological testing; crisis requires trajectory-led airway and ventilatory assessment rather than a rigid spirometric threshold.
NEET-PGINICET
★ High yieldNeurology
Peripheral Neuropathy
Peripheral neuropathy is any disorder of the peripheral nerves; clinically the term usually denotes polyneuropathy — a diffuse, usually symmetric process. The commonest pattern worldwide is a distal symmetric (length-dependent), sensorimotor, axonal polyneuropathy producing numbness, tingling and burning pain in a glove-and-stocking distribution, with loss of ankle reflexes. The commonest cause is diabetes mellitus (diabetic peripheral neuropathy, DPN); other leading causes are alcohol, vitamin B12 deficiency, drugs (chemotherapy, vincristine, isoniazid, metronidazole, amiodarone, phenytoin), uraemia, hereditary (Charcot-Marie-Tooth), vasculitic and CIDP. Diagnosis combines the clinical pattern, blood tests (HbA1c, B12, TSH, U&E, SPEP) and nerve conduction studies distinguishing axonal from demyelinating injury. Management is treat the underlying cause plus neuropathic pain relief (gabapentinoids, duloxetine, TCAs — not opioids) and meticulous foot care to prevent ulceration and amputation.
NEET-PGINICET
★ High yieldNeurology
Raised Intracranial Pressure
Raised intracranial pressure (ICP) occurs when the volume of brain, blood or CSF exceeds the rigid skull's capacity (Monro-Kellie doctrine). Normal ICP is 5 to 15 mmHg in a supine adult; in traumatic brain injury, ICP over 22 mmHg defines raised ICP and warrants treatment. Causes include space-occupying lesions (tumour, haematoma, abscess), hydrocephalus (obstructive and communicating), cerebral oedema (vasogenic, cytotoxic, osmotic), traumatic brain injury, cerebral venous sinus thrombosis and idiopathic intracranial hypertension (IIH). Presentation: headache (worse on waking, coughing, bending), nausea and vomiting, papilloedema, altered consciousness, and the Cushing triad (bradycardia, hypertension, irregular respiration — a pre-terminal sign). The four herniation syndromes — uncal, central, tonsillar (coning), and subfalcine — are the feared complications. Cerebral perfusion pressure (CPP) = MAP minus ICP; target CPP 60 to 70 mmHg. Management: head up 30 degrees, normocapnia (PaCO2 4.0 to 5.0 kPa), mannitol 0.5 to 1 g/kg or 3 percent hypertonic saline, dexamethasone for vasogenic oedema, treat the cause; refractory: induced coma, decompressive craniectomy. IIH (young obese women; headache, papilloedema, visual loss; normal MRI/MRV; LP opening pressure over 25 cmH2O) is treated with weight loss, acetazolamide 1 to 2 g/day, and CSF shunting or optic nerve sheath fenestration if vision is threatened.
NEET-PGINICET
Neurology
Restless Legs Syndrome & Sleep Disorders
Restless legs syndrome (RLS) is an irresistible urge to move the legs, worse at rest and in the evening, relieved by movement, and tightly linked to brain-iron deficiency — so check ferritin and replace it if under 75 ug/L before anything else. First-line drug therapy is an alpha-2-delta ligand (gabapentin, pregabalin) or, alternatively, a non-ergot dopamine agonist (pramipexole 0.125 to 0.5 mg, ropinirole 0.25 to 4 mg, rotigotine patch) — but beware augmentation with long-term dopamine agonists. Obstructive sleep apnoea (OSA) is recurrent upper-airway obstruction during sleep producing snoring, witnessed apnoeas and daytime somnolence; screen with STOP-BANG, confirm with polysomnography (Apnoea-Hypopnoea Index over 5) and treat with CPAP plus weight loss — untreated OSA drives resistant hypertension, atrial fibrillation, stroke and heart failure. Insomnia is managed first-line with CBT-I (more effective than hypnotics), reserving short-term z-drugs (zopiclone 3.75 to 7.5 mg, zolpidem 5 to 10 mg). Narcolepsy (daytime sleepiness with cataplexy and REM-sleep intrusion, from autoimmune loss of hypothalamic hypocretin neurons) is treated with modafinil 200 mg once daily and sodium oxybate.
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★ High yieldNeurology
Spinal Cord Compression
Spinal cord compression is a neurological emergency in which the spinal cord, conus medullaris or cauda equina is compressed by metastatic cancer (commonest: breast, prostate, lung, myeloma, kidney), intervertebral disc herniation, epidural abscess, epidural haematoma or vertebral collapse. Presentation: progressive, often nocturnal back pain, a sensory level, weakness, and — late and ominous — bladder and bowel dysfunction. Cauda equina syndrome adds saddle anaesthesia, bilateral sciatica, urinary retention and erectile dysfunction. Diagnosis is urgent whole-spine MRI. Malignant spinal cord compression: dexamethasone 16 mg immediately, then radiotherapy or surgical decompression within 24 to 48 hours. Cauda equina from disc: emergency surgical decompression within 24 to 48 hours. Time is cord — delay causes permanent paralysis.
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★ High yieldNeurology
Subarachnoid Haemorrhage
Subarachnoid haemorrhage (SAH) is bleeding into the subarachnoid space, usually from a ruptured intracranial aneurysm (85 percent), presenting with a sudden, severe 'thunderclap' headache (maximum intensity within 1 minute) — often described as 'the worst headache of my life' — with neck stiffness, photophobia, nausea, vomiting, altered consciousness and sometimes seizures. Non-contrast CT brain (sensitivity about 100 percent within 6 hours on a modern scanner) is the first investigation; if the CT is negative or performed later than 6 hours, lumbar puncture for xanthochromia (yellow CSF supernatant from bilirubin) confirms the diagnosis. Management includes securing the aneurysm (endovascular coiling preferred over surgical clipping per ISAT), nimodipine 60 mg orally every 4 hours for 21 days (prevents delayed cerebral ischaemia from vasospasm), blood pressure control, and management of complications (rebleeding, vasospasm, hydrocephalus, hyponatraemia). SAH carries a 30-day mortality of around 30 percent; vasospasm is the leading cause of preventable death and disability.
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★ High yieldNeurology
Transient Ischaemic Attack (TIA)
Transient ischaemic attack (TIA) is a transient episode of neurological dysfunction caused by focal brain, spinal cord or retinal ischaemia without acute infarction (tissue-based definition). It is a medical emergency, not a benign event — the risk of completed stroke is 5 to 10 percent within 48 hours and 10 to 20 percent within 90 days without treatment. The ABCD2 score (Age, Blood pressure, Clinical features, Duration, Diabetes) stratifies early stroke risk and drives triage urgency. Presentation is a sudden focal neurological deficit that resolves within 24 hours (usually under 1 hour) — unilateral weakness, aphasia, or monocular visual loss (amaurosis fugax). Urgent workup includes CT then MRI-DWI brain, carotid Doppler or CT angiography, ECG (atrial fibrillation) and echocardiography. Management is aggressive secondary prevention: dual antiplatelet therapy (aspirin plus clopidogrel for 21 days, then monotherapy), high-intensity statin, blood-pressure control, anticoagulation for atrial fibrillation, and carotid endarterectomy for symptomatic stenosis over 50 percent (especially over 70 percent) within 2 weeks — together preventing up to 80 percent of predicted strokes.
NEET-PGINICET
Neurology
Trigeminal Neuralgia & Bell Palsy
Trigeminal neuralgia (TN, tic douloureux) is severe, paroxysmal, electric-shock-like facial pain in the distribution of the trigeminal nerve (usually V2/V3), lasting seconds and provoked by light touch (washing, eating, cold air). It is usually caused by neurovascular compression of the trigeminal root at the root-entry zone, producing focal demyelination and ephaptic transmission. Carbamazepine is first-line; refractory cases need microvascular decompression (Jannetta), gamma knife or percutaneous procedures. Bell palsy is an acute, unilateral lower motor neurone (LMN) facial nerve (CN VII) palsy of idiopathic (likely viral) cause producing facial asymmetry with forehead involvement, inability to close the eye, drooping mouth and altered taste. Treatment is oral prednisolone 60 mg daily for 5 days then taper, started within 72 hours, plus mandatory eye protection; antivirals add limited benefit. Most recover within 3 to 6 months. The single highest-yield discriminating fact: forehead spared = upper motor neurone (stroke); forehead involved = LMN (Bell palsy).
NEET-PGINICET
Psychiatry
4
★ High yieldPsychiatry
Autism Spectrum Disorder
Autism spectrum disorder (ASD) is a neurodevelopmental disorder defined in DSM-5 and ICD-11 by persistent deficits in social communication and social interaction across multiple contexts (the three sub-domains of social-emotional reciprocity, nonverbal communicative behaviour, and relationships) PLUS restricted, repetitive patterns of behaviour, interests or activities (at least 2 of 4: stereotyped/repetitive movements, speech or object use; insistence on sameness/rituals; restricted interests of abnormal intensity; and hyper- or hypo-reactive sensory behaviour). Onset is in the early developmental period, the symptoms are present across contexts, and they cause clinically significant functional impairment. Global prevalence is about 1 in 100 children and the most recent US CDC ADDM surveillance reports 1 in 36 (2.8 percent) among 8-year-olds; the male-to-female ratio is about 3 to 4:1; heritability is approximately 80 percent. There is no medication that treats the core ASD — management is early intensive behavioural and developmental intervention, multidisciplinary support, and symptom-targeted pharmacotherapy for comorbidities (risperidone and aripiprazole are the two FDA-approved drugs for irritability associated with paediatric ASD).
NEET-PGINICET
★ High yieldPsychiatry
Perinatal Psychiatry (Postnatal Depression & Postpartum Psychosis)
Perinatal mental health covers psychiatric disorders arising in pregnancy and the first 12 months postpartum. Three conditions dominate and must be distinguished: baby blues (50 to 80 percent of mothers; days 2 to 14; tearfulness, mood lability; self-limiting — reassure); postnatal depression (PND) (10 to 15 percent; weeks to months postpartum; depressed mood, anhedonia, poor bonding, intrusive thoughts; screen with the Edinburgh Postnatal Depression Scale (EPDS) at 6 to 8 weeks; treat with CBT/IPT and an SSRI, sertraline preferred in breastfeeding); and postpartum (puerperal) psychosis (0.1 to 0.2 percent; onset within 2 to 4 weeks, usually the first 2 weeks; acute delusions, hallucinations, mood disturbance, insomnia; risk 25 to 50 percent in bipolar disorder; a PSYCHIATRIC EMERGENCY — admit to a mother-and-baby unit; risk of infanticide and suicide). Suicide is a leading indirect cause of maternal death — risk assessment is mandatory in every perinatal presentation.
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Psychopharmacology Overview
Psychopharmacology is the framework every doctor uses when prescribing psychiatric drugs, organised around four pillars — antidepressants, antipsychotics, mood stabilisers, and anxiolytics (plus ADHD stimulants and the antidotes). For each class the exam wants four facts: receptor target, first-line agent, signature side-effect profile, and the named emergency (toxidrome). Antidepressants — SSRIs first-line (sertraline preferred; nausea, sexual dysfunction, hyponatraemia in the elderly, GI bleed, QT with citalopram; serotonin syndrome with serotonergic combinations — hyperreflexia, clonus, autonomic instability — stop, cyproheptadine, benzodiazepine, cooling). Antipsychotics — 2nd-generation first-line (olanzapine, risperidone, quetiapine, aripiprazole); D2 blockade is the mechanism (efficacy in mesolimbic, EPS in nigrostriatal, hyperprolactinaemia in tuberoinfundibular); the EPS quartet is acute dystonia, akathisia, parkinsonism, tardive dyskinesia; clozapine is the only drug proven superior in treatment-resistant schizophrenia (mandatory regular FBC monitoring throughout treatment); NMS (fever, lead-pipe rigidity, high CK, altered consciousness) is the emergency — stop, dantrolene, bromocriptine, ICU. Mood stabilisers — lithium gold standard (level 0.6 to 0.8 mmol/L (guideline-consensus maintenance), monitor renal/thyroid/calcium 6-monthly, toxicity over 1.5 = dialysis if severe); valproate is teratogenic (avoid pregnancy); lamotrigine risks Stevens-Johnson (titrate slowly); carbamazepine needs HLA-B*1502 testing in Asian populations. Benzodiazepines enhance GABA-A — short-term only (dependence, withdrawal seizures; flumazenil reverses cautiously). Antidote mnemonic: NMS dantrolene, serotonin syndrome cyproheptadine, lithium toxicity saline/dialysis, TCA overdose NaHCO3, benzodiazepine overdose flumazenil, acute dystonia anticholinergic. Universal prescribing rule: start low, go slow, monitor, never stop abruptly.
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Substance Use Disorders (Alcohol & Opioids)
Substance use disorders (SUD) are chronic relapsing brain diseases defined by pathological substance use despite harm, with tolerance, withdrawal, craving, loss of control, and continued use despite consequences (DSM-5: 2+ of 11 criteria over 12 months — mild 2 to 3, moderate 4 to 5, severe 6+). The two highest-yield subtypes are alcohol use disorder (AUD) and opioid use disorder (OUD). Alcohol withdrawal ranges from tremor to generalised seizures (24 to 48 h) to delirium tremens (48 to 72 h, mortality 5 percent untreated); treated with benzodiazepines via CIWA-Ar scoring (chlordiazepoxide preferred; lorazepam if liver disease) plus IV thiamine BEFORE any glucose (Wernicke encephalopathy). Opioid overdose is the triad of coma + pinpoint pupils + respiratory depression — naloxone 0.4 to 0.8 mg IV/IM/IN immediately, repeat and observe for long-acting agents. Opioid withdrawal (lacrimation, rhinorrhoea, myalgia, piloerection, diarrhoea, yawning, mydriasis) is miserable but rarely fatal. Maintenance therapy (methadone, buprenorphine-naloxone, naltrexone) is the single most effective intervention for OUD, reducing mortality by over 50 percent. AUD relapse prevention: naltrexone, acamprosate, disulfiram alongside CBT, motivational interviewing and AA/NA.
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Respiratory
17
Respiratory
Acute Bronchitis
Acute bronchitis is acute inflammation of the trachea and large bronchi producing a self-limiting cough of up to three weeks, nearly always viral (rhinovirus, influenza, RSV, coronavirus, parainfluenza, adenovirus) and without the radiographic consolidation of pneumonia. The cough often lasts one to three weeks (sometimes up to eight from post-viral airway hyper-reactivity). The pivotal clinical tasks are to exclude pneumonia (normal vital signs, no focal chest signs, normal oxygenation) and to avoid unnecessary antibiotics — they offer minimal benefit and real harm, because the cause is viral. Management is symptomatic (rest, fluids, analgesia, honey or an antitussive). Consider pertussis (cough beyond three weeks, whoop, post-tussive vomiting, exposure) — treat with a macrolide and notify public health.
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Allergic Bronchopulmonary Aspergillosis & Aspergillus Lung Disease
Current 2024 revised ISHAM approach to ABPA and ABPM: diagnosis, radiological and clinical classification, treatment response, prednisolone and azole regimens, interactions, biologics, special populations, and boundaries with sensitisation, aspergilloma, chronic pulmonary aspergillosis and invasive disease.
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Aspiration Pneumonia & Pneumonitis
Aspiration pneumonitis is acute chemical lung injury after macroaspiration; aspiration pneumonia is infection in a host who aspirates. Distinguish the syndromes clinically, stabilise first, treat pneumonia according to CAP or HAP/VAP guidance, and reserve extra anaerobic therapy for abscess, empyema, or necrotising infection.
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Respiratory
Chronic Cough
Chronic cough is a cough lasting more than 8 weeks in an adult. After a chest X-ray to exclude serious disease (lung cancer, TB, ILD, heart failure, bronchiectasis) and review of smoking and the drug list (especially ACE inhibitors, which must be stopped), a non-smoker with a normal X-ray off ACE inhibitors has one of the 'big three' common, treatable causes in most cases: upper-airway cough syndrome (UACS, post-nasal drip), asthma / eosinophilic bronchitis, and gastro-oesophageal reflux disease (GORD, often silent). Work-up is the 'anatomical diagnostic protocol' — empirical, sequential therapy of each cause, re-assessing response. Cough that persists despite this is refractory and reflects cough-reflex hypersensitivity (sensitisation of vagal afferents TRPV1, TRPA1, P2X3); it is treated with speech-language therapy and neuromodulators (gabapentin, pregabalin, low-dose morphine), or P2X3 antagonists (gefapixant), at a specialist cough clinic.
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Chronic Obstructive Pulmonary Disease (COPD)
COPD is a common, preventable and treatable disease characterised by persistent, progressive, not-fully-reversible airflow limitation driven by chronic inflammation from inhaled noxious particles (chiefly cigarette smoke). It comprises two overlapping phenotypes — chronic bronchitis (productive cough for at least 3 months in 2 successive years) and emphysema (destruction of alveolar parenchyma). Diagnosis is spirometric: a post-bronchodilator FEV1/FVC below 0.70. Severity is graded by FEV1 percent predicted (GOLD grades 1 to 4), while therapy is escalated by symptoms (mMRC/CAT) and exacerbation history (GOLD ABE). Smoking cessation and long-term oxygen therapy are the only interventions that change survival. An acute exacerbation is treated with controlled oxygen (SpO2 88 to 92 percent), nebulised bronchodilators, prednisolone 40 mg for 5 days, antibiotics when Anthonisen criteria are met, and non-invasive ventilation (BiPAP) for acute hypercapnic respiratory failure.
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Respiratory
Cor Pulmonale
Cor pulmonale is right ventricular hypertrophy, dilatation and failure caused by lung disease (NOT by a primary cardiac problem), via pulmonary hypertension driven by chronic hypoxia and loss of the pulmonary vascular bed. The commonest cause is COPD; others include interstitial lung disease, obstructive sleep apnoea/obesity hypoventilation, chronic thromboembolic disease and restrictive chest-wall disease. Patients show the features of the underlying lung disease plus right-heart failure — raised JVP, peripheral oedema, hepatomegaly, a loud pulmonary second sound (P2), a parasternal right-ventricular heave and tricuspid regurgitation. Echocardiography demonstrates RV hypertrophy/dilatation and raised estimated pulmonary pressures (right heart catheterisation is the gold standard). Management is to treat the underlying lung disease, give long-term oxygen therapy (which improves survival, per the MRC and NOTT trials), optimise ventilation (NIV/CPAP), and diurese cautiously; pulmonary vasodilators are NOT routinely used in COPD/ILD, and chronic thromboembolic PH is the one cause that can be cured by pulmonary endarterectomy.
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Influenza (Seasonal & Pandemic)
Influenza is an acute, highly contagious respiratory infection caused by orthomyxoviruses of types A, B and (rarely) C. Type A is subtyped by two surface glycoproteins — haemagglutinin (H, 18 subtypes) and neuraminidase (N, 11 subtypes); current human strains are A/H1N1pdm09 and A/H3N2; type B is divided into Victoria and Yamagata lineages. Antigenic drift (point mutations in H and N) drives annual seasonal epidemics; antigenic shift (reassortment of genome segments when two viruses co-infect a host, e.g. swine as a 'mixing vessel') produces a novel subtype → pandemic (1918 H1N1 'Spanish flu', 1957 H2N2 'Asian flu', 1968 H3N2 'Hong Kong flu', 2009 H1N1pdm09 'swine flu'). Transmission is by respiratory droplets and aerosols with an incubation period of 1–4 days. Clinically: abrupt high fever, rigors, headache, myalgia, dry cough, sore throat, extreme prostration — distinguished from the common cold by sudden onset and severity of systemic symptoms. Diagnosis is clinical in season; RT-PCR (nasopharyngeal swab) is the gold standard; RIDTs give a result in 15 min but have moderate sensitivity (50–70%) and high specificity (90–95%), so a negative RIDT does NOT exclude influenza. Treat with oral oseltamivir 75 mg twice daily for 5 days, started within 48 hours of onset (reduces duration by ~1 day and prevents complications); always treat hospitalised, pregnant, immunocompromised, and high-risk patients regardless of delay. Annual quadrivalent vaccine (2 A + 2 B strains) is the cornerstone of prevention — recommended for all over 6 months, with priority for elderly, pregnant, children under 5, chronic disease, immunocompromise, healthcare workers. Complications: primary viral pneumonia, secondary bacterial pneumonia (Strep pneumoniae, Staph aureus — classically post-influenza), bronchiolitis, otitis media (children), myocarditis, encephalitis, Guillain–Barre syndrome, Reye syndrome (children given aspirin), rhabdomyolysis, ARDS. Global mortality: 290,000–650,000 respiratory deaths and up to 1 million deaths annually.
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Interstitial Lung Disease
Interstitial lung disease (ILD), also called diffuse parenchymal lung disease (DPLD), is a heterogeneous group of over 200 disorders that share inflammation and/or fibrosis of the lung interstitium (alveolar walls, septa, peribronchovascular and perilymphatic spaces), producing a restrictive ventilatory defect (low total lung capacity, low FVC, low DLCO with preserved or raised FEV1/FVC) and a diffuse abnormality on imaging. The clinical archetype is idiopathic pulmonary fibrosis (IPF) — chronic, progressive fibrosis of older adults with a usual interstitial pneumonia (UIP) pattern on HRCT (basal, subpleural reticulation, honeycombing, traction bronchiectasis, with little ground-glass) and a median survival of three to five years, worse than many common cancers. Diagnosis is multidisciplinary (MDT) and excludes known causes (CTD, drugs, occupation, hypersensitivity). Treatment is pirfenidone or nintedanib (slow decline), long-term oxygen, pulmonary rehabilitation, and lung transplantation (the only cure).
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Lung Abscess
A lung abscess is a localised collection of pus within a cavitating area of lung parenchyma, classically produced by aspiration of oropharyngeal contents (a mixed anaerobic inoculum) in a host with impaired consciousness or swallowing — alcoholism, seizures, poor dentition, dysphagia, stroke. Other mechanisms are necrotising pneumonia (Staphylococcus aureus, Klebsiella, Pseudomonas), septic emboli (right-sided endocarditis in intravenous drug use, Lemierre syndrome), and abscess distal to an obstructing tumour or foreign body. The presentation is insidious over weeks with fever, foul-smelling (fetid) sputum, cough, weight loss and night sweats, and imaging shows a thick-walled cavity with an air-fluid level in a dependent segment. Treatment is prolonged antibiotics covering anaerobes — clindamycin or amoxicillin-clavulanate for 4 to 6 weeks, percutaneous or surgical drainage for large or failing abscesses, treatment of the predisposing cause, and bronchoscopy to exclude an obstructing tumour in any non-resolving case.
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Lung Cancer
Lung cancer is a malignant tumour arising from the bronchial or alveolar epithelium, the leading cause of cancer death worldwide. The fundamental divide is non-small cell lung cancer (NSCLC, ~85%) — adenocarcinoma (commonest, peripheral, never-smokers, EGFR/ALK-driven), squamous cell carcinoma (central, cavitates, PTHrP hypercalcaemia), large cell — versus small cell lung cancer (SCLC, ~15%) (central, smoker, neuroendocrine, paraneoplastic SIADH and Lambert-Eaton, early metastasis, chemo- and radio-sensitive). Risk is dominated by tobacco smoking (80 to 90%); also asbestos, radon, second-hand smoke. Presentation: persistent cough, haemoptysis, dyspnoea, weight loss, chest pain, plus paraneoplastic syndromes and metastatic manifestations (bone, brain, liver, adrenal). Diagnosis by CT chest ± PET-CT, confirmed on histology/cytology (bronchoscopy, EBUS-TBNA, CT-guided biopsy); molecular testing (EGFR, ALK, ROS1, BRAF, PD-L1) drives targeted therapy. Stage by TNM 8th edition (NSCLC) or limited vs extensive (SCLC). Management: NSCLC early stage (I to II) — surgical resection (lobectomy) ± adjuvant chemo; locally advanced (III) — chemoradiotherapy ± durvalumab; advanced (IV) — platinum doublet plus pembrolizumab/atezolizumab, with EGFR/ALK-targeted TKIs for driver-mutant disease. SCLC — etoposide plus platinum ± radiotherapy; prophylactic cranial irradiation. Prognosis overall 5-year survival ~20%; stage I ~60%, stage IV under 10%. Low-dose CT screening reduces mortality in high-risk smokers.
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Obstructive Sleep Apnoea
Obstructive sleep apnoea (OSA) is recurrent collapse of the upper airway during sleep, causing apnoeas and hypopnoeas with oxygen desaturation and arousal. It presents with loud snoring, witnessed apnoeas (reported by a partner), excessive daytime sleepiness and unrefreshing sleep. Risk factors are obesity (large neck), male sex, middle age, alcohol/sedatives and craniofacial narrowing. Untreated, it drives systemic hypertension, atrial fibrillation, myocardial infarction, stroke, type 2 diabetes and a high risk of road-traffic accidents. Polysomnography is diagnostic, quantifying the apnoea-hypopnoea index (AHI) — mild 5-15, moderate 15-30, severe over 30 — and STOP-BANG screens for risk. Management is weight loss and lifestyle change, CPAP (the gold standard for moderate-severe disease), a mandibular advancement device for mild/CPAP-intolerant cases, and surgery only in selected patients.
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Pleural Effusion
Pleural effusion is an accumulation of fluid in the normally near-dry pleural space. It is classified by Light's criteria (1972) as a transudate (systemic cause: heart failure, cirrhosis, nephrotic syndrome, peritoneal dialysis, myxoedema, pulmonary embolism) or an exudate (local pleural disease: parapneumonic, malignancy, tuberculosis, pulmonary embolism, autoimmune, pancreatitis, chylothorax, haemothorax). Diagnosis rests on chest X-ray (blunted costophrenic angle over 200 mL, meniscus sign, mediastinal shift), thoracic ultrasound (loculation, septation, guidance) and diagnostic thoracentesis with pleural fluid analysis (protein, LDH, glucose, pH, cell count, Gram stain and culture, cytology, ADA, amylase, triglycerides, NT-proBNP). Treatment is cause-specific plus therapeutic thoracentesis, chest drain, talc pleurodesis or indwelling pleural catheter for recurrent malignant effusion.
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Pneumothorax
Pneumothorax is air in the pleural space. Loss of the normal negative intrapleural pressure uncouples the lung from the chest wall, and elastic recoil collapses the lung. It is classified as primary spontaneous (PSP — no underlying lung disease; tall, thin, young male smoker, ruptured apical subpleural bleb), secondary spontaneous (SSP — underlying disease: COPD, asthma, cystic fibrosis, Pneumocystis, TB, LAM), traumatic/iatrogenic, and the life-threatening tension pneumothorax (a one-way valve raising intrathoracic pressure until venous return and cardiac output collapse — hypotension, tracheal deviation away, distended neck veins). Diagnosis is clinical plus an erect chest X-ray (pleural line, absent lung markings), except tension which is a clinical diagnosis — decompress before imaging. Management is size- and type-driven per the BTS 2023 guideline: small/asymptomatic PSP — observe plus high-flow oxygen; large or symptomatic PSP — aspiration or small-bore drain; SSP — intercostal drain; recurrent/persistent air leak — surgical pleurodesis (VATS). Tension — immediate needle/finger decompression then a definitive chest drain.
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Respiratory Failure
Respiratory failure is the failure of the respiratory system to maintain adequate gas exchange, defined by the arterial blood gas: PaO2 below 8 kPa (60 mmHg) at room air, with or without a raised PaCO2. Type 1 (hypoxaemic) is low oxygen with normal or low CO2, caused by ventilation-perfusion mismatch or shunt — pneumonia, pulmonary embolism, pulmonary oedema, ARDS, asthma. Type 2 (hypercapnic) is low oxygen AND high CO2 (PaCO2 above 6 kPa / 45 mmHg), caused by alveolar hypoventilation — COPD, neuromuscular disease, opiates, obesity hypoventilation, brainstem depression. The ABG diagnoses it and the type drives treatment. Management is oxygen (target SpO2 94–98% for type 1; 88–92% for COPD/type 2 to avoid CO2 narcosis), non-invasive ventilation (BiPAP) for type 2 with acidosis, CPAP/HFNC for refractory type 1 hypoxia, intubation if NIV fails or the airway is threatened, lung-protective ventilation in ARDS, and treatment of the underlying cause.
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Respiratory
Sarcoidosis
Sarcoidosis is a multisystem granulomatous disease of unknown cause characterised by non-caseating (hard) granulomas in one or more organs. It most often affects the lungs and intrathoracic lymph nodes of young and middle-aged adults (peak age 20 to 40 years), with a striking predilection for African ancestry (about three times the incidence of white Americans) and Scandinavians. Presentation ranges from an incidental finding of bilateral hilar lymphadenopathy through acute Löfgren syndrome (erythema nodosum plus bilateral hilar lymphadenopathy plus ankle arthritis, with fever) to chronic multisystem disease involving the skin (lupus pernio), eyes (uveitis), heart (arrhythmia, sudden death), nervous system (cranial nerve VII palsy) and calcium metabolism (hypercalcaemia, nephrocalcinosis). Diagnosis rests on a compatible clinical-radiological picture plus histological non-caseating granulomas, after excluding tuberculosis and fungal infection; Scadding chest X-ray stages 0 to IV grade pulmonary involvement. Treatment is observe asymptomatic disease; corticosteroids (prednisolone 20 to 40 mg) for symptomatic or organ-threatening disease; methotrexate as first steroid-sparing agent; infliximab for refractory disease.
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Respiratory
Solitary Pulmonary Nodule
A solitary pulmonary nodule (SPN) is a single, well-defined, roughly spherical opacity 3 cm or less in diameter, surrounded by aerated lung, with no associated atelectasis, adenopathy or pleural effusion — most often found incidentally on CT or on low-dose CT lung cancer screening. The clinical task is to distinguish benign from malignant using size, density (solid, part-solid, ground-glass), border (smooth vs spiculated), growth rate, calcification, and patient risk (age, smoking, prior cancer). Benign features favour a smooth border, dense central/popcorn calcification, and no growth over two years; malignant features are a spiculated or part-solid nodule that grows in an older smoker. A validated risk model (Brock, then Herder; Mayo/Swensen classically) quantifies the probability of cancer. Low risk means CT surveillance (Fleischner or BTS intervals); intermediate means PET-CT and biopsy; high risk means tissue diagnosis, surgical resection if malignant. A nodule over 3 cm is a mass (presumed malignant).
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Tuberculosis
Tuberculosis (TB) is infection by Mycobacterium tuberculosis complex, transmitted by the airborne route via droplet nuclei. It is usually pulmonary but can affect any organ. Distinguish latent TB infection (LTBI) — contained, non-infectious bacilli — from active TB disease — multiplying, transmissible infection causing chronic cough (often with haemoptysis), weight loss, night sweats and fever, with apical cavitation on chest X-ray. Diagnosis is by sputum smear and culture, with Xpert MTB/RIF Ultra providing rapid molecular detection and rifampicin-resistance testing. Standard drug-susceptible TB is treated with a 6-month, four-drug regimen — 2 months of HRZE (rifampicin, isoniazid, pyrazinamide, ethambutol) plus 4 months of HR (rifampicin, isoniazid) — given as directly observed therapy (DOTS). MDR-TB is treated with a prolonged all-oral regimen; the BPaLM regimen (bedaquiline, pretomanid, linezolid, moxifloxacin) is used for eligible cases. BCG protects against childhood disseminated TB and TB meningitis.
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Rheumatology
14
Rheumatology
Adult-Onset Still's Disease
Adult-onset Still's disease (AOSD) is a rare systemic autoinflammatory disorder (the adult counterpart of systemic juvenile idiopathic arthritis) presenting with quotidian spiking fevers (evening peak), an evanescent salmon-pink rash, arthritis, sore throat, and markedly raised inflammatory markers (ferritin often very high) with negative autoantibodies (ANA, RF negative). It affects young adults (16 to 35). Three patterns: self-limited monocyclic, polycyclic (relapsing-remitting), or chronic articular. The feared complication is macrophage activation syndrome (MAS) / secondary HLH — a life-threatening hyperinflammatory emergency. Diagnosis is clinical (Yamaguchi or Fautrel criteria), after excluding infection, malignancy and other rheumatic disease. Treatment: NSAIDs and glucocorticoids first-line; methotrexate; IL-1 inhibitors (anakinra, canakinumab) for refractory systemic disease and IL-6 inhibitor (tocilizumab) for the chronic articular pattern.
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ANCA-Associated Vasculitis (GPA, MPA & EGPA)
ANCA-associated vasculitis (AAV) comprises three necrotising small-vessel vasculitides associated with anti-neutrophil cytoplasmic antibodies (ANCA): granulomatosis with polyangiitis (GPA, formerly Wegener) — PR3-ANCA (c-ANCA), ENT (epistaxis, saddle nose, deafness) plus respiratory (sinusitis, lung nodules/cavitation) plus renal (pauci-immune glomerulonephritis); microscopic polyangiitis (MPA) — MPO-ANCA (p-ANCA), renal plus pulmonary without granulomatous ENT; eosinophilic granulomatosis with polyangiitis (EGPA, Churg-Strauss) — asthma, eosinophilia, sinus/nasal polyposis then vasculitic phase (neuropathy, cardiomyopathy, renal). The feared pulmonary-renal syndrome (alveolar haemorrhage plus rapidly progressive glomerulonephritis) is a medical emergency. Diagnosis combines ANCA (immunofluorescence plus PR3/MPO ELISA), urinalysis, renal biopsy (pauci-immune necrotising crescentic GN), and CT chest. Induction is high-dose glucocorticoids plus rituximab or cyclophosphamide, with plasma exchange for severe renal/pulmonary disease; maintenance is rituximab or azathioprine; mepolizumab (anti-IL-5) for EGPA.
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Rheumatology
Behçet's Syndrome
Behçet's syndrome is a relapsing-remitting multisystem vasculitis (affects both arteries and veins of all sizes) classically defined by recurrent oral aphthous ulcers plus any two of: genital ulcers, eye lesions (uveitis/retinal vasculitis), skin lesions (erythema nodosum, papulopustular, pathergy), and positive pathergy test. Commonest along the Silk Road (Turkey, Mediterranean, Middle East, East Asia); rare in Northern Europeans. HLA-B51 association. Can involve vessels (venous thrombosis, arterial aneurysm, pulmonary artery aneurysm — major cause of death), eyes (panuveitis, retinal vasculitis — blindness), gastrointestinal (ileocaecal ulcers), joints (arthritis), neurological, and skin. Oral ulcers are universal and the gateway to diagnosis; genital ulcers scar. Diagnosis is clinical (ICBD criteria) with no specific test. Treat mucocutaneous disease conservatively (colchicine, apremilast); ocular, vascular, neuro and GI involvement need aggressive immunosuppression (azathioprine, ciclosporin, interferon-alpha, anti-TNF, cyclophosphamide). Thrombosis is inflammatory — immunosuppression matters more than anticoagulation.
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Dermatomyositis & Polymyositis (Idiopathic Inflammatory Myopathies)
Idiopathic inflammatory myopathies (IIM) are acquired autoimmune muscle diseases causing symmetric, proximal muscle weakness (difficulty combing hair, rising from a chair, climbing stairs) with raised creatine kinase. Dermatomyositis (DM) features characteristic skin manifestations (heliotrope rash — violaceous periorbital; Gottron papules/sign — over knuckles; shawl/V-sign, nailfold changes); polymyositis (PM) is muscle-only. Other IIM: inclusion body myositis (IBM) (older, distal + quadriceps/finger flexor weakness, poor steroid response), immune-mediated necrotising myopathy (IMNM) (anti-SRP/HMGCR), antisynthetase syndrome (anti-Jo-1, ILD, fever, mechanic's hands, arthritis), juvenile DM. Strong association of adult DM with occult malignancy and of antisynthetase/anti-MDA5 disease with interstitial lung disease (ILD). Diagnosis combines proximal weakness + high CK + myopathic EMG + muscle biopsy (DM perifascicular; PM endomysial) plus myositis-specific antibodies and MRI. Treat with high-dose steroids then MTX/azathioprine/MMF/IVIG/rituximab; IBM is largely refractory.
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Rheumatology
IgG4-Related Disease
IgG4-related disease (IgG4-RD) is a fibro-inflammatory immune-mediated disorder characterised by tumefactive (mass-like) lesions, a dense lymphoplasmacytic infiltrate rich in IgG4-positive plasma cells, storiform fibrosis and obliterative phlebitis, and often elevated serum IgG4. It can affect nearly any organ — type 1 autoimmune pancreatitis, IgG4-related sclerosing cholangitis, sialadenitis (Mikulicz syndrome), dacryoadenitis, retroperitoneal fibrosis, tubulointerstitial nephritis, aortitis, Riedel thyroiditis and hypertrophic pachymeningitis. It predominantly affects older men and often presents as painless organ enlargement or a mass that mimics malignancy. Diagnosis rests on histology (the gold standard) plus serum IgG4 and imaging. Treatment gives a dramatic response to glucocorticoids; rituximab is the key steroid-sparing and refractory agent. The cardinal rule: biopsy mass-like lesions before assuming cancer or proceeding to surgery.
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Low Back Pain (Approach & Red Flags)
Low back pain is the leading cause of disability worldwide; the vast majority is non-specific (mechanical) and self-limiting (over 90 percent recover within 6 weeks). The central clinical skill is identifying red flags (serious pathology — fracture, infection, malignancy, cauda equina, inflammatory) that mandate imaging and referral, while reassuring and mobilising the remainder. Red flags: significant trauma; age over 50 with new pain; history of cancer; fever/weight loss/night sweats; immunosuppression, IV drug use; night pain or pain unrelieved by rest; recent bacterial infection; corticosteroid use; cauda equina (saddle anaesthesia, urinary retention/incontinence, bilateral neurology, progressive weakness) = surgical emergency. Manage non-specific pain: reassure, stay active, simple analgesia (avoid opioids), exercise + CBT; surgery only for severe persistent radiculopathy or cauda equina.
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Osteoarthritis
Osteoarthritis (OA) is the commonest joint disorder — a degenerative, mechanically driven arthritis of articular (hyaline) cartilage with bony remodelling (osteophytes, subchondral sclerosis and cysts), meniscal damage and low-grade synovial inflammation. It predominantly affects the knees, hips, hands (DIP — Heberden nodes, PIP — Bouchard nodes, first CMC) and spine. Risk factors are age, obesity, female sex, prior joint injury, repetitive occupational stress and genetics. It presents with use-related joint pain (worse with activity, better with rest, brief morning stiffness under 30 minutes), functional limitation, crepitus and bony swelling, with late deformity. Diagnosis is clinical, supported by X-ray (LOSS — joint-space narrowing, osteophytes, subchondral sclerosis and cysts), though imaging severity correlates poorly with symptoms. Management is built on education, exercise and weight loss (core, disease-modifying), plus topical NSAIDs, short-course oral NSAIDs, intra-articular steroid for flares and joint replacement for end-stage disease.
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Osteoporosis
Osteoporosis is a progressive systemic skeletal disease of low bone mass and microarchitectural deterioration of bone tissue, leading to increased bone fragility and a consequent increase in fracture risk. Operationally (WHO) it is defined by a DEXA T-score of minus 2.5 or less at the femoral neck, total hip or lumbar spine; a low-trauma (fragility) fracture establishes the diagnosis regardless of the T-score. It is the commonest metabolic bone disease of older adults and the underlying cause of most fragility fractures (low-trauma — fall from standing height or less) of the vertebra, hip, distal forearm (Colles) and proximal humerus. Commonest in postmenopausal women and older adults; secondary causes include glucocorticoids, hypogonadism, hyperthyroidism, hyperparathyroidism, CKD, malabsorption, chronic liver disease, smoking, alcohol, low BMI and immobility. Often silent until a fragility fracture. Diagnosis: DEXA T-score plus FRAX 10-year fracture probability. Treat: lifestyle (weight-bearing exercise, calcium 1000 to 1200 mg, vitamin D 800 to 1000 IU, smoking cessation, fall prevention) + bisphosphonates first-line (alendronate weekly, zoledronate IV annually), denosumab SC 6-monthly; anabolic agents (teriparatide, romosozumab) for very-high-risk disease; drug holiday after 3 to 5 years.
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Rheumatology
Polyarteritis Nodosa (PAN)
Polyarteritis nodosa (PAN) is a necrotising vasculitis of medium-sized muscular arteries characterised by transmural inflammation, fibrinoid necrosis, disruption of the internal elastic lamina and microaneurysm formation. It is defined by what it is NOT: it does not involve glomeruli or capillaries, does not involve the lungs (no pulmonary capillaritis), and is not ANCA-associated — the three findings that distinguish it from the ANCA-associated vasculitides (especially microscopic polyangiitis). Presentation: constitutional symptoms, mononeuritis multiplex (wrist/foot drop from nerve infarction), mesenteric ischaemia (abdominal angina), renovascular hypertension with bland urinalysis, livedo reticularis, tender subcutaneous nodules, ulcers, testicular pain. Diagnosis: mesenteric/renal angiography (microaneurysms and beading — the 'rosary sign'), tissue biopsy (medium-vessel transmural fibrinoid necrosis), ANCA negative, bland urinalysis, HBV serology mandatory. Forms: idiopathic and hepatitis B-associated. Treatment: idiopathic — high-dose corticosteroids (+ cyclophosphamide for severe); HBV-associated — antivirals (entecavir/tenofovir) + plasma exchange + short steroids (goal is HBV clearance, not long-term immunosuppression). Five-year survival is around 80 percent treated (versus 13 percent untreated).
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★ High yieldRheumatology
Psoriatic Arthritis
Psoriatic arthritis (PsA) is an inflammatory arthritis associated with psoriasis, usually rheumatoid-factor negative, classified within the seronegative spondyloarthropathies. Diagnosis is clinical using the CASPAR criteria (established inflammatory articular disease plus at least 3 points from current psoriasis, personal or family history of psoriasis, current or historical dactylitis, juxta-articular new bone formation, rheumatoid-factor negativity, and nail dystrophy). The five Moll and Wright patterns are asymmetric oligoarthritis (commonest), symmetric polyarthritis, DIP-predominant, arthritis mutilans, and predominant spondylitis or sacroiliitis. Hallmarks: dactylitis (sausage digit), enthesitis (Achilles, plantar fascia), nail disease (pitting, onycholysis, hyperkeratosis), and DIP involvement. Pathophysiology is genetic (HLA-Cw6 for skin, HLA-B27 for axial) plus environmental triggers (Koebner phenomenon, infection, obesity, drugs) driving the IL-23 / Th17 / IL-17 axis and TNF, producing the unique paradoxical bone remodelling in which erosions and pathological new bone formation coexist. Treat-to-target aims for minimal disease activity or remission: NSAIDs first-line, conventional DMARDs (methotrexate) for moderate peripheral disease, TNF inhibitors first-line biologic, then IL-17 and IL-23 inhibitors for refractory or skin-predominant disease, with JAK inhibitors as oral alternatives.
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Rheumatology
Raynaud Phenomenon
Raynaud phenomenon is episodic reversible vasospasm of the digital arteries and cutaneous arterioles, classically producing the triphasic colour change: white (pallor / ischaemia), blue (cyanosis) and red (reperfusion hyperaemia) of the fingers and toes on cold exposure or emotional stress. Two forms: primary (benign, idiopathic, young women, symmetric, no tissue loss, normal nailfold capillaries, negative autoantibodies) and secondary (associated with connective tissue disease — systemic sclerosis above all, plus SLE, MCTD; occupational vibration; drugs such as beta-blockers, bleomycin, cisplatin, ergotamine; thromboembolic and hyperviscosity states; older onset, asymmetric, abnormal nailfold capillaroscopy with dilated tortuous loops and avascular dropout, positive ANA, risk of digital ulcers and critical ischaemia). Diagnosis is clinical, supported by nailfold capillaroscopy and an autoantibody screen. Management: cold avoidance, smoking cessation, hand and whole-body warming + calcium-channel blockers (nifedipine 10 to 40 mg OD, amlodipine 5 to 10 mg OD) first-line; in secondary Raynaud add PDE-5 inhibitors (sildenafil, tadalafil), IV prostacyclin (iloprost) for severe disease, and bosentan to prevent new digital ulcers; critical digital ischaemia is a rheumatological emergency.
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Reactive Arthritis (Reiter Syndrome)
Reactive arthritis (ReA, formerly Reiter syndrome) is a sterile inflammatory arthritis arising 1 to 4 weeks after an extra-articular infection (classically genitourinary — Chlamydia trachomatis; or gastrointestinal — Campylobacter, Salmonella, Shigella, Yersinia, Clostridioides difficile), belonging to the HLA-B27-associated seronegative spondyloarthropathies. The classic triad (Reiter): arthritis (asymmetric, lower-limb oligoarthritis), urethritis/cervicitis, and conjunctivitis/uveitis ('can't see, can't pee, can't climb a tree'). Characteristic features include enthesitis, dactylitis (sausage digit), sacroiliitis, keratoderma blennorrhagicum, circinate balanitis, painless oral ulcers, and nail changes. Usually self-limiting (3 to 12 months); 15 to 30 percent develop chronic or recurrent spondyloarthritis. Diagnosis is clinical, supported by a culture-negative, crystal-negative inflammatory synovial fluid. Management: treat the trigger and sexual contacts, NSAIDs first-line, intra-articular corticosteroids, DMARDs (sulfasalazine) for persistent disease, and TNF inhibitors for refractory cases.
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Septic Arthritis
Septic arthritis is a medical and surgical emergency — direct microbial invasion of a joint space (usually bacterial and haematogenous) causing purulent synovial inflammation, rapid articular cartilage destruction, sepsis and death if untreated. Incidence is 4 to 10 per 100,000 in the West and rises steeply with prosthetic joints, rheumatoid arthritis, diabetes, immunosuppression, IV drug use and age over 80. The knee is the commonest joint (about half of cases). Staphylococcus aureus is the commonest organism in all ages; Neisseria gonorrhoeae in young sexually active adults (migratory polyarthralgia, tenosynovitis, pustular rash); Group B streptococcus in neonates; Haemophilus influenzae and Streptococcus pneumoniae in unvaccinated children; Salmonella in sickle-cell disease; Pseudomonas and Gram-negatives in IV drug users; coagulase-negative staphylococci in prosthetic joints. Presentation is a single hot, swollen, very tender joint with severe pain on movement ± fever (fever may be absent). Diagnosis rests on urgent joint aspiration: synovial WBC typically over 50,000 per cubic millimetre (50,000 to 200,000), neutrophil-predominant, positive Gram stain and culture (positive in about 75% of Gram-positive, 50% overall), low glucose, raised lactate; blood cultures are positive in about half. The Kocher criteria stratify the irritable paediatric hip. Crystals do NOT exclude infection — sepsis coexists with gout/CPPD in up to a fifth of cases. Treatment is urgent surgical washout/drainage plus empirical IV antibiotics started immediately after aspiration — flucloxacillin 2 g IV QID (clindamycin if allergic, vancomycin 1 g IV BD if MRSA suspected) plus Gram-negative cover (ceftriaxone 2 g IV OD), narrowed to culture, total 4 to 6 weeks (about 2 IV then oral). Gonococcal arthritis: ceftriaxone 1 g IV/IM OD plus azithromycin 1 g PO. Prosthetic joint infection follows a specialist staged surgical pathway with biofilm-aware antibiotics. Mortality is 7 to 15%; up to half retain joint damage.
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★ High yieldRheumatology
Systemic Sclerosis (Scleroderma)
Systemic sclerosis (scleroderma) is a chronic multisystem autoimmune connective tissue disease defined by a pathophysiological triad of microvascular vasculopathy, immune dysregulation and generalised fibrosis (excess collagen deposition) of the skin and internal organs, with disease-specific autoantibodies (anti-centromere, anti-Scl-70/topoisomerase I, anti-RNA polymerase III). The two principal subtypes are limited cutaneous (CREST — Calcinosis, Raynaud, oEsophageal dysmotility, Sclerodactyly, Telangiectasia; anti-centromere; late pulmonary arterial hypertension) and diffuse cutaneous (anti-Scl-70 or anti-RNA polymerase III; early interstitial lung disease, renal crisis, rapidly progressive skin). Raynaud phenomenon is the first manifestation in over 90 percent. It is the rheumatic disease with the highest case fatality — interstitial lung disease and pulmonary arterial hypertension are the leading causes of death, and scleroderma renal crisis is the classical emergency demanding an urgent ACE inhibitor.
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General Surgery
40 topicsGastroenterology
2
★ High yieldGastroenterology
Gallstone Disease & Cholecystitis
Gallstone disease (cholelithiasis) is the formation of solid crystalline concretions in the gallbladder or biliary tree from precipitated bile components — most commonly cholesterol (the classic risk profile of the 5 Fs — female, forty, fat, fertile, fair, plus rapid weight loss, family history and OCP use) and less often pigment stones from chronic haemolysis (black) or bacterial biliary infection (brown). Sixty to eighty per cent are silent; symptomatic disease spans biliary colic (postprandial RUQ pain, self-limiting), acute cholecystitis (persistent RUQ pain, fever, positive Murphy sign), choledocholithiasis (obstructive jaundice) and the septic emergency of ascending cholangitis (Charcot triad of fever, jaundice and RUQ pain; Reynolds pentad adds hypotension and confusion). Severity is graded by the Tokyo Guidelines 2018 for both cholecystitis and cholangitis. Ultrasound is first-line; MRCP images the ducts non-invasively; ERCP removes common-duct stones and drains an obstructed system. Management is conservative for asymptomatic stones, laparoscopic cholecystectomy (using the critical view of safety) for symptomatic disease, early cholecystectomy within 72 hours for acute cholecystitis, ERCP with sphincterotomy for CBD stones, and antibiotics plus urgent ERCP biliary decompression for cholangitis.
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★ High yieldGastroenterology
Pancreatic Cancer
Pancreatic ductal adenocarcinoma (PDAC) is a highly lethal malignancy of the pancreatic exocrine cells, driven by an obligate KRAS mutation in over 90 percent of tumours followed by CDKN2A, TP53 and SMAD4 loss, and by a dense desmoplastic stroma that shields it from drugs and the immune system. It is the third to fourth leading cause of cancer death in developed countries, with an overall five-year survival of about 10 to 12 percent because over 80 percent are unresectable at presentation. Risk factors are smoking (the biggest modifiable risk), chronic pancreatitis, obesity, new-onset diabetes, advancing age, and hereditary syndromes (BRCA2/PALB2, Peutz-Jeghers, Lynch, hereditary pancreatitis, FAMMM). Site defines the picture: a head tumour (60 to 70 percent) causes painless obstructive jaundice with pale stools, dark urine and pruritus, and Courvoisier sign (a palpable non-tender gallbladder), while a body or tail tumour presents late with epigastric pain radiating to the back, weight loss and new-onset diabetes. Trousseau migratory thrombophlebitis is a paraneoplastic clue. Diagnosis rests on CT pancreas protocol, endoscopic ultrasound with FNA biopsy for tissue, and CA 19-9 for monitoring. Only a minority are resectable: pancreaticoduodenectomy (Whipple) for the head, distal pancreatectomy with splenectomy for body or tail, followed by adjuvant modified FOLFIRINOX (PRODIGE 24). Borderline resectable and locally advanced disease receive neoadjuvant FOLFIRINOX or gemcitabine plus nab-paclitaxel then reassessment; metastatic disease is treated with FOLFIRINOX (fit patients) or gemcitabine plus nab-paclitaxel, with olaparib maintenance for germline BRCA-mutated tumours (POLO), plus palliative biliary and duodenal stenting, coeliac plexus neurolysis and early palliative care.
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General Surgery
38
★ High yieldGeneral Surgery
Abdominal Aortic Aneurysm
Abdominal aortic aneurysm (AAA) is a permanent, localised dilation of the abdominal aorta to 3 cm or more (or 1.5 times the expected normal diameter), with over 90% infrarenal. Most are asymptomatic until rupture. Risk: male sex, age over 65, smoking (the dominant modifiable factor), family history, hypertension. Screening: one-off ultrasound for men at 65 (NHS AAA Screening Programme); USPSTF for men 65 to 75 who ever smoked. Surveillance thresholds: under 3 cm normal; 3.0 to 4.4 cm yearly; 4.5 to 5.4 cm every 3 months; over 5.5 cm refer for elective repair (open or EVAR). Rupture triad: severe abdominal/back/flank pain plus hypotension plus a pulsatile abdominal mass (complete in only half). Ruptured AAA mortality 80 to 90% overall; 40 to 50% perioperative. Elective mortality 2 to 5% open, 1.5 to 2% EVAR. Laplace law: Wall Tension = Pressure x Radius / Wall Thickness explains the vicious cycle of growth. EVAR is less invasive but needs lifelong surveillance for endoleak.
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Abdominal Wall Hernias
Hernia = abnormal protrusion of a viscus (or part of a viscus) through a defect in the wall of its containing cavity. Inguinal hernias are commonest (75%, above and medial to the pubic tubercle): indirect (through the deep ring, lateral to the inferior epigastric, congenital) versus direct (through Hesselbach's triangle, medial, acquired). Femoral hernias lie below and lateral to the pubic tubercle and carry the highest strangulation risk. Lichtenstein tension-free mesh repair is the open gold standard for inguinal hernia; strangulation (irreducible plus tender plus obstructive signs) is a surgical emergency. Always check the hernial orifices in any unexplained small-bowel obstruction.
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★ High yieldGeneral Surgery
Acute Appendicitis
Acute appendicitis is the most common acute surgical abdomen. Classic presentation: periumbilical pain migrating to the right iliac fossa over 12 to 24 hours, with anorexia, nausea, and low-grade fever. Pathophysiology: luminal obstruction (fecalith, lymphoid hyperplasia) → bacterial overgrowth → increased intraluminal pressure → venous obstruction → ischemia → gangrene → perforation (appendicular artery is an end artery). Alvarado score (MANTRELS) guides bedside diagnosis. CT is gold standard in adults; ultrasound first-line in children/pregnancy. Laparoscopic appendectomy is definitive treatment. Appendicular mass: conservative management → interval appendectomy 6 to 8 weeks. Perforated peritonitis: emergency laparotomy.
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Acute Cholecystitis
Acute cholecystitis is acute inflammation of the gallbladder, 90% caused by a gallstone impacting the cystic duct. Classic: right upper quadrant pain + Murphy sign (inspiratory arrest on RUQ palpation) + fever. Ultrasound is first-line: gallbladder wall thickening, pericholecystic fluid, stones, sonographic Murphy sign. Management: early laparoscopic cholecystectomy within 72 hours (Tokyo Guidelines 2018). If unfit: percutaneous cholecystostomy. Complications: gangrene, perforation, empyema, emphysematous cholecystitis. Acalculous cholecystitis (10%): ICU patients, high mortality.
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Anorectal Disorders
Anorectal disorders span haemorrhoids (Grade I–IV; rubber band ligation first-line for II–III), anal fissure (posterior midline 90%; topical GTN 0.4% or diltiazem 2%; chronic = lateral internal sphincterotomy), anorectal abscess/fistula (cryptoglandular origin; Goodsall rule: anterior = straight, posterior = curved to midline; fistulotomy for low, seton/LIFT/advancement flap for high), pilonidal sinus (natal cleft, hirsute young males; excision ± Limberg flap), anal cancer (HPV 16/18; Nigro protocol 5-FU + mitomycin C chemoradiation), rectal prolapse (elderly women; rectopexy/Delorme/Altemeier) and pruritus ani.
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Benign Prostatic Hyperplasia
Benign prostatic hyperplasia (BPH) is age-related nodular hyperplasia of the periurethral transition zone causing bladder outlet obstruction. Affects 50% of men over 50, up to 90% over 80. Presents with LUTS: voiding (hesitancy, weak stream, straining, incomplete emptying) and storage (frequency, urgency, nocturia) symptoms. DRE: smooth, symmetrically enlarged, rubbery prostate (vs hard, irregular in cancer). PSA over 4 ng/mL warrants cancer investigation. IPSS scores severity: mild 0 to 7, moderate 8 to 19, severe 20 to 35. Treat: alpha-1-blocker (tamsulosin 0.4 mg OD — rapid relief) plus 5-alpha-reductase inhibitor (finasteride 5 mg OD — shrinks gland over 6 months) for moderate symptoms. TURP (transurethral resection) is the surgical gold standard. TURP syndrome = dilutional hyponatraemia from glycine irrigation. Acute urinary retention = catheterise immediately.
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Breast Cancer
Breast cancer is the most common cancer in women worldwide (about 24% of all female cancers, lifetime risk roughly 1 in 8). Classic presentation: painless, hard, irregular, fixed breast lump. Diagnosis via triple assessment (clinical + imaging + biopsy, about 98% accurate). Molecular subtypes drive treatment: ER/PR+ (endocrine therapy), HER2+ (trastuzumab), triple-negative (chemotherapy). Surgery: wide local excision + radiotherapy (breast-conserving) or mastectomy. Sentinel lymph node biopsy for axillary staging. Commonest metastasis: bone (about 70%). BRCA1/2 mutations in about 5 to 10%.
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Burns
Burns are tissue injuries caused by thermal, chemical, electrical, or radiation energy. Severity is determined by depth (superficial / superficial-partial / deep-partial / full-thickness / 4th degree), total body surface area (TBSA), and site (face, hands, feet, perineum, airway). Inhalational injury and burns over 25% TBSA (adults) or 10% (children) are life-threatening. Fluid resuscitation with the Parkland formula (4 mL Ringer-lactate x kg x %TBSA, first half in 8 h, second half over next 16 h) is critical for burns over 15% TBSA. Escharotomy for circumferential full-thickness burns compromising circulation or ventilation. Refer to a burns centre for over 10% TBSA, full-thickness burns, special sites, electrical or chemical injury, or inhalational injury. Complications: hypovolaemic (burn) shock, infection or sepsis, Curling's stress ulcer, compartment syndrome, contractures, hypertrophic scarring.
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Carotid Artery Disease
Carotid artery disease is atherosclerotic narrowing of the extracranial carotid artery (commonest: bifurcation/internal carotid). Presents as TIA (focal deficit under 24 h), amaurosis fugax (transient monocular blindness from retinal embolus), or completed stroke. Or asymptomatic (incidental bruit). NASCET method measures stenosis: (normal ICA diameter − minimal lumen) / normal ICA diameter × 100. Symptomatic stenosis 70–99%: CEA within 2 weeks (NASCET, ARR 17%, NNT 6). Symptomatic 50–69%: CEA for selected (modest benefit). Asymptomatic over 60–70%: CEA if perioperative risk under 3% (ACAS/ACST). All patients receive best medical therapy (antiplatelet + high-intensity statin + BP control + smoking cessation + diabetes control). CEA: open plaque removal + patch closure. CAS: endovascular stent for high-risk surgical patients (CREST).
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★ High yieldGeneral Surgery
Colorectal Carcinoma
Colorectal carcinoma (CRC) arises from the colonic or rectal epithelium (adenocarcinoma in 95%). Third most common cancer worldwide; risk factors include age over 50, family history, Lynch syndrome (HNPCC), FAP, IBD (ulcerative colitis), red/processed meat, smoking, obesity. Presents with altered bowel habit, rectal bleeding, weight loss, abdominal pain; right-sided tumours cause anaemia/weight loss (insidious), left-sided/rectal cause obstruction, tenesmus, fresh bleeding. Diagnosis by colonoscopy + biopsy; staging by CT chest/abdomen/pelvis + MRI rectum (for rectal) and CEA. TNM staging drives treatment: surgery is curative for stages I to III (TME for rectal); adjuvant chemotherapy (FOLFOX/CAPOX) for stage III; neoadjuvant chemoradiotherapy for locally advanced rectal cancer. Screening from age 45 to 50 (colonoscopy, FIT) saves lives.
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★ High yieldGeneral Surgery
Common Fractures
Common fractures covers the most frequently encountered fractures in clinical practice: Colles, Smith, scaphoid, neck of femur, intertrochanteric, tibial plateau, ankle, clavicular, humeral neck, and supracondylar fractures. Each has characteristic mechanisms, deformities, and management principles following AO/OTA classification and Garden classification for femoral neck fractures. Management follows the AO principles: anatomical reduction, stable fixation, preservation of blood supply, early mobilisation. Open fractures require emergency debridement (within 24h), IV antibiotics, tetanus prophylaxis, and stabilisation per Gustilo-Anderson classification.
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Diverticular Disease
Diverticular disease encompasses a spectrum from asymptomatic diverticulosis (70 to 80% of cases) through symptomatic uncomplicated diverticular disease (SUDD) to acute diverticulitis and its life-threatening complications. False (pseudodiverticula) = mucosa and submucosa herniate through the muscularis propria at sites of vasa recta penetration. The sigmoid colon is affected in 90% of Western populations (right-sided in 15 to 75% of Asians). Over 50% of people older than 60 are affected. Hinchey classification (stages I to IV) and the WSES 2015 severity grade guide surgical management of perforated diverticulitis. Management ranges from dietary modification to emergency Hartmann's procedure for faecal peritonitis.
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Ductal Carcinoma In Situ
Ductal carcinoma in situ (DCIS) is a non-invasive breast neoplasm in which malignant epithelial cells proliferate within the ductal-lobular system but do not breach the basement membrane. It is a non-obligate precursor of invasive ductal carcinoma — untreated, about 30 to 50% progress over 10 to 20 years, but many lesions never become invasive. With screening mammography, DCIS now makes up about 20 to 25% of all new breast cancer diagnoses and is nearly always detected as microcalcifications. Treatment: breast-conserving surgery (wide local excision with at least 2 mm clear margins) plus whole-breast radiotherapy, or mastectomy for large or multicentric disease. Tamoxifen for ER-positive DCIS reduces ipsilateral and contralateral recurrence (NSABP B-24). The Van Nuys Prognostic Index (VNPI) guides treatment intensity. Pure DCIS cannot metastasise, so the axilla is not routinely staged.
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General Surgery
Enhanced Recovery After Surgery (ERAS)
ERAS (Enhanced Recovery After Surgery) is a multimodal, evidence-based, protocolised perioperative care pathway that attenuates the surgical stress response, preserves organ function, and accelerates functional recovery. Pioneered by Henrik Kehlet in 1990s colorectal surgery, it reduces length of stay by 2-3 days and complications by approximately 50% without increasing readmission or mortality. The four pillars are: attenuation of the stress response (no fasting, carb loading, regional anaesthesia), maintenance of organ function (goal-directed fluids, normothermia, no tubes), early return of gut function (early feeding, opioid-sparing), and early mobilisation (day 0).
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★ High yieldGeneral Surgery
Gallstone Disease
Gallstone disease encompasses the spectrum from asymptomatic stones (80%) through biliary colic (RUQ pain after fatty meal, 2 to 6 hours, resolves spontaneously) to acute cholecystitis (fever + Murphy sign + RUQ pain lasting over 6 hours) and its complications (choledocholithiasis, cholangitis, pancreatitis, gallstone ileus). Risk: the 5 Fs (Female, Fat, Forty, Fertile, Family). Ultrasound is first-line (95% sensitive for stones over 2 mm). Asymptomatic: observe. Biliary colic: elective laparoscopic cholecystectomy. Acute cholecystitis: early laparoscopic cholecystectomy within 72 hours. CBD stone: ERCP with sphincterotomy. Cholangitis: IV antibiotics + urgent ERCP. Courvoisier's law: palpable gallbladder + jaundice = NOT stones (malignant obstruction).
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Gastric Carcinoma
Gastric carcinoma is an adenocarcinoma arising from the gastric epithelium. It is the fifth most commonly diagnosed cancer worldwide and the fourth leading cause of cancer death, with the highest incidence in East Asia (Japan, Korea, China), Eastern Europe, and parts of South America. The dominant risk factor is Helicobacter pylori (a WHO Class I carcinogen), followed by diet (salted/smoked/pickled foods, N-nitroso compounds, low fruit and vegetables), smoking, chronic atrophic gastritis, pernicious anaemia, and the hereditary diffuse gastric cancer syndrome (CDH1/E-cadherin mutation). Most tumours arise through the Correa cascade (chronic gastritis to atrophic gastritis to intestinal metaplasia to dysplasia to adenocarcinoma) over decades. Presentation is characteristically late and insidious — epigastric pain, weight loss, early satiety, dysphagia (proximal), vomiting (distal), and anaemia — with eponymous metastatic signs (Virchow's node, Sister Mary Joseph nodule, Krukenberg tumour, Blumer's shelf). Diagnosis is by OGD with biopsy; staging combines CT, EUS, and staging laparoscopy (for occult peritoneal disease). Surgery — gastrectomy with D2 lymphadenectomy — is the only cure; perioperative FLOT chemotherapy (built on the MAGIC trial) is standard for resectable locally advanced disease; trastuzumab is added for HER2-positive and nivolumab/pembrolizumab for PD-L1-positive or MSI-H metastatic disease. Prognosis is poor overall (20 to 30 per cent five-year survival) because of late presentation, though Japan and Korea achieve far better outcomes through national endoscopic screening.
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Haemorrhoids
Haemorrhoids (piles) are engorged, displaced anal vascular cushions at the anorectal junction. Internal (above dentate line, painless bleeding) vs external (below dentate line, painful thrombosis). Goligher grading: Grade I (bleed, no prolapse), II (prolapse, reduce spontaneously), III (prolapse, need manual reduction), IV (prolapsed, irreducible). Risk: constipation, straining, pregnancy, prolonged sitting. Present with painless bright red bleeding per rectum (on toilet paper, dripping), prolapse, pruritus ani. Thrombosed external haemorrhoid = acutely painful perianal lump. Always exclude colorectal cancer in patients over 40 with rectal bleeding. Manage: Grade I to II (dietary, topical, rubber band ligation); Grade III to IV (surgical — open/closed haemorrhoidectomy, stapled haemorrhoidopexy, THD/HALO).
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Hepatocellular Carcinoma
Hepatocellular carcinoma (HCC) is the 6th most common cancer and 3rd leading cause of cancer death worldwide. Most cases arise in the setting of cirrhosis (HBV, HCV, alcohol, NASH). Surveillance: 6-monthly USS +/- AFP in at-risk patients. Diagnosis: non-invasive (LI-RADS) by typical arterial enhancement + portal venous washout on CT/MRI. BCLC staging guides treatment: resection (early), transplant (Milan criteria), TACE (intermediate), sorafenib/atezolizumab+bevacizumab (advanced).
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Hydrocele
Hydrocele is an abnormal collection of serous fluid within the tunica vaginalis of the testis (vaginal type) or along a patent processus vaginalis (congenital type). It presents as painless, gradually enlarging scrotal swelling that is positive on transillumination and that the examiner can get above (confirming it is scrotal, not inguinal). Congenital hydrocele (patent processus vaginalis) is common in infants and resolves by age 2 in over 90 percent of cases. Adult hydrocele is idiopathic or secondary to infection, trauma, tumour, or filariasis. The clinical skill is excluding the dangerous mimics — inguinal hernia (cough impulse positive, reducible, cannot get above), testicular tumour (heavy, opaque to transillumination), and testicular torsion (painful). Diagnosis is clinical, confirmed by ultrasound scrotum (excludes underlying testicular pathology). Treatment: Lord plication, Jaboulay eversion, or sac excision for adults; observe until age 2 then herniotomy for congenital. Aspiration is not recommended (recurs and risks infection); sclerotherapy is an alternative for unfit patients.
★ High yieldGeneral Surgery
Inflammatory Bowel Disease — Surgical Management
Surgical management of IBD differs between Crohn's disease (surgery is not curative — recurrence is expected) and ulcerative colitis (proctocolectomy is curative). UC: indications include acute severe colitis (failure of IV steroids), toxic megacolon, perforation, dysplasia/cancer. Definitive: proctocolectomy with ileal pouch-anal anastomosis (IPAA/J-pouch). Crohn's: strictureplasty (Heineke-Mikulicz, Finney, Michelassi), resection with anastomosis, abscess drainage, fistula management.
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Intestinal Obstruction
Intestinal obstruction is the partial or complete blockage of the bowel that prevents normal transit of intestinal contents. Small bowel obstruction (SBO) is caused by adhesions (60 to 75%), hernias (15 to 20%) and malignancy (10 to 15%); large bowel obstruction (LBO) by colorectal cancer (60%), volvulus (10 to 15%) and diverticulitis (10%). The classic tetrad is colicky abdominal pain, vomiting, distension and absolute constipation (obstipation). CT is the gold standard. The single decision that saves life is recognising strangulation (constant severe pain, tachycardia, fever, peritonism, raised lactate) which mandates emergency laparotomy. Adhesive SBO without strangulation resolves with conservative drip-and-suck management (NBM + NG tube + IV fluids) in 70 to 80% within 48 to 72 hours. Bologna guidelines (2018) and WSES volvulus guidelines (2023) standardise management.
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Neck Swellings
Neck swellings are classified by location: midline (thyroid goitre moves on swallowing; thyroglossal duct cyst moves on swallowing AND tongue protrusion; dermoid does not move) versus lateral (cervical lymphadenopathy is the commonest cause; also branchial cyst in young adults, salivary gland tumour, cystic hygroma). In an adult over 40, a new neck lump is malignancy until proven otherwise. Ultrasound plus FNA is the standard workup. Sistrunk procedure (excise cyst + tract + central hyoid) for thyroglossal cyst; surgical excision for branchial cyst; superficial parotidectomy with facial nerve preservation for pleomorphic adenoma; do NOT biopsy a carotid body tumour. Metastatic SCC node mandates panendoscopy to find the head and neck primary.
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Obstructive Jaundice
Obstructive jaundice is mechanical blockage of bile flow anywhere from the intrahepatic ducts to the ampulla of Vater, producing conjugated hyperbilirubinaemia with a cholestatic enzyme pattern (ALP and GGT raised, AST and ALT near-normal). Painless progressive jaundice with weight loss and a palpable gallbladder (Courvoisier's law) = pancreatic head cancer until proven otherwise. Fever, jaundice and right-upper-quadrant pain (Charcot's triad) = ascending cholangitis — an emergency needing IV antibiotics and urgent ERCP for biliary drainage. Ultrasound is first-line imaging; MRCP is the non-invasive gold standard for the biliary tree; ERCP is both diagnostic and therapeutic (stone extraction, stent, brush cytology). Vitamin K 10 mg IV corrects the coagulopathy of cholestasis before any procedure.
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Oesophageal Cancer
Oesophageal cancer is the 8th most common cancer worldwide. Squamous cell carcinoma predominates globally (Asia, Africa); adenocarcinoma predominates in Western countries (Barrett's oesophagus from GORD). Presentation: progressive dysphagia (solids then liquids), weight loss. Staging: endoscopy + biopsy, EUS (T/N staging), CT/PET-CT (M staging), laparoscopy for GOJ tumours. Multimodal treatment: neoadjuvant ChemoRT (CROSS: carboplatin + paclitaxel + 41.4 Gy) then surgery (Ivor Lewis oesophagectomy).
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Pancreatic Carcinoma
Pancreatic carcinoma (ductal adenocarcinoma) is an aggressive malignancy with a 5-year survival under 10% — the worst of any solid organ cancer. Risk factors: smoking, chronic pancreatitis, diabetes, obesity, family history, BRCA2. Head of pancreas (70%): presents with painless obstructive jaundice, weight loss, Courvoisier's sign (palpable non-tender gallbladder). Body/tail: presents late with pain radiating to the back. Diagnosis: CT pancreas protocol + CA 19-9 + EUS-FNA biopsy. Only 15 to 20% are resectable at presentation (Whipple / pancreatoduodenectomy for head tumours). FOLFIRINOX or gemcitabine/nab-paclitaxel for metastatic. Jaundice relief by ERCP stenting. Almost uniformly fatal.
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Peptic Ulcer Disease
Peptic ulcer disease (PUD) is a break in the gastric or duodenal mucosa caused by an imbalance between acid-peptic injury and mucosal defence. Two major causes: Helicobacter pylori (60 to 80%) and NSAIDs (20 to 30%). Duodenal ulcer: epigastric pain relieved by food/antacids, wakes at night. Gastric ulcer: pain worsened by food, weight loss. Diagnosis: OGD + biopsy (gastric ulcers are always biopsied to exclude malignancy); H. pylori testing (CLO test, urea breath, stool antigen). Treatment: H. pylori eradication triple therapy (PPI + clarithromycin + amoxicillin) 14 days; PPI for 4 to 8 weeks; stop NSAIDs. Surgical complications: perforation (Graham omental patch), haemorrhage (under-run bleeding vessel), gastric outlet obstruction (scarring from chronic DU).
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★ High yieldGeneral Surgery
Perianal Abscess and Anal Fistula
Perianal abscess and anal fistula (fistula-in-ano) are two stages of a single cryptoglandular disease process. Obstruction of an anal gland duct at the dentate line produces an acute pus collection (abscess) which, on drainage, may leave a permanent epithelialised tract (fistula) in 30 to 50 percent of patients. Abscess presents with severe throbbing perianal pain, fever, and a tender fluctuant mass; fistula presents with recurrent discharge and recurrent abscesses. Goodsall's rule predicts the internal opening. Park's classification grades fistulas by sphincter involvement. Abscess is treated by incision and drainage; low fistula by fistulotomy; high or complex fistula by a loose seton, LIFT, or advancement flap to preserve the sphincter. Crohn's perianal fistula demands anti-TNF and sphincter-conserving surgery.
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Perioperative VTE Prophylaxis
Venous thromboembolism (VTE) = deep vein thrombosis (DVT) + pulmonary embolism (PE). It is the leading preventable cause of hospital death. Surgical patients carry a ten- to twenty-fold increased risk. Prevention rests on Virchow's triad (stasis, hypercoagulability, endothelial injury), risk stratification (Caprini for surgical, Padua for medical patients) and a stepwise ladder: early mobilisation, mechanical methods (TEDS, IPC) and pharmacological prophylaxis (enoxaparin 40 mg SC OD, fondaparinux 2.5 mg SC OD, rivaroxaban 10 mg PO OD). High-risk patients get both. Extended prophylaxis for twenty-eight days after major orthopaedic or cancer surgery. Massive PE is an emergency: oxygen, haemodynamic support, systemic thrombolysis (alteplase).
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Peripheral Arterial Disease
Peripheral arterial disease (PAD) is atherosclerotic narrowing of the lower limb arteries. Presents on a spectrum: asymptomatic PAD (ABPI under 0.9, no symptoms), intermittent claudication (calf pain on walking, relieved by rest), chronic limb-threatening ischaemia (CLTI) with rest pain (severe nocturnal foot pain relieved by dependency) and tissue loss (ulceration, gangrene), and acute limb ischaemia (ALI) with the 6 Ps. Smoking is the dominant modifiable risk factor; diabetes multiplies risk 2-4 fold. ABPI under 0.9 confirms PAD; toe-brachial index replaces ABPI when medial Mönckeberg calcinosis makes ankle vessels non-compressible (diabetes, CKD). Fontaine classification: I (asymptomatic), II (claudication), III (rest pain), IV (gangrene). TASC II grades aortoiliac and femoropopliteal lesions A-D, guiding endovascular vs surgical revascularisation. WIfI (Wound-Ischaemia-foot Infection) risk-stratifies CLTI amputation risk. Management ladder: stop smoking + supervised exercise + antiplatelet + statin (best medical therapy, BMT, for all), cilostazol for symptomatic claudication, low-dose rivaroxaban + aspirin (COMPASS regimen) for symptomatic PAD, angioplasty ± stent for focal TASC A-B disease, bypass with autologous vein for extensive TASC C-D disease, fasciotomy after revascularisation for reperfusion compartment syndrome, and amputation for unsalvageable limb. Acute limb ischaemia: emergency IV unfractionated heparin, Fogarty catheter embolectomy for embolic, catheter-directed thrombolysis for thrombotic. Time window 4-6 hours before irreversible muscle necrosis.
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Portal Hypertension
Portal hypertension is sustained elevation of the portal venous pressure gradient (HVPG over 5 mmHg). Commonest cause worldwide is cirrhosis (sinusoidal); the commonest pre-sinusoidal cause globally is schistosomiasis. Four consequences: varices (oesophageal and gastric), ascites, splenomegaly with hypersplenism, and hepatic encephalopathy. Acute variceal bleed: resuscitate with restrictive transfusion (Hb target 70 to 80), terlipressin 2 mg IV every 4 h, ceftriaxone 1 g IV daily (mandatory antibiotic prophylaxis), and endoscopic band ligation within 12 h. Refractory bleeding: balloon tamponade (Sengstaken-Blakemore) as a bridge, then TIPSS. Primary prophylaxis: non-selective beta-blocker (propranolol, nadolol, carvedilol) or EVL. Secondary prophylaxis: beta-blocker plus serial EVL. HVPG over 10 = clinically significant; over 12 = bleeding risk; over 16 = high mortality.
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Splenic Injury and Splenectomy
Splenic injury is the most common intra-abdominal organ injury in blunt trauma (25% of cases). The AAST grading system (Grade I–V, revised 2018) guides management. Non-operative management (NOM) is successful in over 90% of haemodynamically stable patients. Splenectomy is reserved for haemodynamic instability, peritonitis, or failed NOM. The critical post-operative concern is overwhelming post-splenectomy infection (OPSI) — a 1–5% lifetime risk of fulminant sepsis from encapsulated organisms (S. pneumoniae, H. influenzae, N. meningitidis) with up to 50–70% mortality. Prevention requires vaccination (pneumococcal, meningococcal, Hib), lifelong antibiotic prophylaxis, and patient education.
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Surgical Site Infection
SSI = infection at the surgical site within 30 days (or 90 days if implant placed), classified by CDC into superficial incisional (skin/subcut), deep incisional (fascia/muscle) and organ/space. Affects 2 to 5% of procedures, doubles mortality, and adds 7 to 10 days to length of stay. Most common organism in clean surgery: Staphylococcus aureus. Prevention bundle: prophylactic antibiotics within 60 min of incision (re-dose at 4 h or after 1500 mL blood loss), normothermia, glycaemic control, clipping (not shaving), supplemental oxygen, chlorhexidine skin prep, WHO Surgical Safety Checklist.
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Testicular Torsion
Testicular torsion is a urological surgical emergency — twisting of the spermatic cord on its longitudinal axis compromises the testicular blood supply, producing ischaemia and, within hours, irreversible infarction. The salvage window is the 6-hour rule: 90 to 100 percent salvage if detorsed within 6 hours, about 50 percent at 6 to 12 hours, and less than 10 percent after 24 hours. Classic presentation: sudden severe unilateral testicular pain, an absent cremasteric reflex, and a high-riding testis lying horizontally. Diagnosis is clinical — never delay surgery for imaging when suspicion is high. Definitive management is immediate scrotal exploration with detorsion, assessment of viability, ipsilateral orchidopexy or orchidectomy, and routine contralateral orchidopexy (the bell-clapper deformity is bilateral in roughly 12 percent anatomically and fixation protects the only remaining testis).
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Thyroid Carcinoma
Thyroid carcinoma arises from thyroid follicular cells (papillary 80%, follicular 10%) or parafollicular C cells (medullary 5%); anaplastic (1 to 2%) is undifferentiated and near-uniformly fatal. Presents as a thyroid nodule (palpable or incidental on ultrasound); risk factors: radiation exposure in childhood, female sex, family history, iodine deficiency (follicular), RET germline mutation / MEN-2 (medullary). Workup: TSH, ultrasound with TI-RADS risk stratification, FNA cytology using the Bethesda system, plus serum calcitonin when medullary is suspected. Papillary: best prognosis, BRAF V600E, lymphatic spread, psammoma bodies; treated with total thyroidectomy with or without prophylactic central neck dissection, then radioiodine 131I ablation and TSH suppression. Follicular: RAS mutation, haematogenous spread to bone and lung, diagnosed on vascular or capsular invasion. Medullary: calcitonin from C cells, RET proto-oncogene, 25% familial (MEN-2), amyloid stroma; total thyroidectomy plus central and lateral neck dissection, no role for radioiodine. Anaplastic: undifferentiated, TP53/TERT, all stage IV, median survival months; surgery rarely possible, external beam radiotherapy and chemotherapy are palliative. Most thyroid nodules are benign (over 90%); cancer is confirmed on FNA or histology.
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Trauma Management (ATLS)
Trauma management follows the ATLS primary survey (cABCDE): catastrophic haemorrhage control first, then Airway with cervical spine protection, Breathing, Circulation, Disability (GCS), Exposure. Life-threatening injuries are identified and treated in order — not all at once. Tension pneumothorax = immediate needle decompression (2nd ICS mid-clavicular or 5th ICS anterior axillary). Massive haemothorax (over 1500 mL initial or over 200 mL/h) = thoracotomy. Cardiac tamponade = Beck's triad. Pelvic fracture = pelvic binder. GCS under 8 = intubate. FAST scan for intraperitoneal blood. Damage control surgery: control bleeding/contamination, temporary closure, ICU, re-operation. Lethal triad: hypothermia + acidosis + coagulopathy. CRASH-2: tranexamic acid 1 g IV within 3 hours.
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Umbilical and Epigastric Hernia
Umbilical hernias occur through the umbilical ring and are common in infants (95% close spontaneously by 5 years) and adults (associated with obesity, pregnancy, ascites). Epigastric hernias occur through the linea alba between the umbilicus and xiphisternum and always contain preperitoneal fat (often no peritoneal sac). Management: infantile — observe until age 4-5; adult — surgical repair (open or laparoscopic mesh). Richter's hernia (only anti-mesenteric border of bowel in sac) is a particular risk in small umbilical/epigastric hernias.
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Urinary Tract Stones
Urinary tract stones (urolithiasis) are crystalline formations arising anywhere from the renal collecting system to the urethra when urine becomes supersaturated with stone-forming solutes. They present with renal colic — sudden, severe pain radiating from loin to groin that makes the patient writhe and roll (unlike the stillness of peritonitis). CT KUB is the gold standard (97% sensitive, sees all stone types). Calcium oxalate is the commonest (75%); uric acid stones are radiolucent and dissolvable; struvite stones form staghorn calculi with urease-producing infection. Stones under 5 mm pass spontaneously in 80%; over 10 mm need intervention (ESWL, ureteroscopy + laser, or PCNL). NSAIDs are first-line analgesia. Obstruction with infection is a urological emergency requiring urgent decompression (JJ stent or nephrostomy). Prevention rests on fluids over 3 L/day, low salt, normal dietary calcium, and targeted metabolic therapy.
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General Surgery
Varicose Veins
Varicose veins are permanently dilated, tortuous, elongated superficial leg veins (greater than or equal to 3 mm) caused by incompetent venous valves. Most arise in the great saphenous vein (medial leg, around 80 percent) from saphenofemoral junction incompetence. The disease is graded by the CEAP classification (C0 to C6). Duplex ultrasound is the gold-standard investigation. Endovenous thermal ablation (EVLA or RFA) is the first-line definitive treatment. Venous ulcers (medial gaiter area) are managed with four-layer compression bandaging after confirming an ABPI above 0.8. Never strip if the deep veins are obstructed; biopsy any change in a chronic ulcer to exclude Marjolin ulcer.
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Paediatrics
19 topicsPaediatrics
19
★ High yieldPaediatrics
Acute Gastroenteritis in Children
Acute gastroenteritis (AGE) = inflammation of stomach and intestines causing 3 or more loose/watery stools in 24 hours and/or vomiting, of infectious origin, lasting under 14 days. The 2nd leading cause of under-5 mortality worldwide. Most common pathogen globally is rotavirus (pre-vaccine); post-vaccine, norovirus is rising. WHO classifies dehydration as no / some / severe and treats with Plan A (home ORS), Plan B (ORS 75 mL/kg over 4 h), Plan C (IV bolus 20 mL/kg normal saline). Zinc 20 mg/day for 10 to 14 days shortens the episode. Continue feeding throughout. EHEC (E coli O157:H7) → HUS (microangiopathic haemolytic anaemia + thrombocytopenia + AKI). Antibiotics are reserved for Shigella, cholera, severe Salmonella in infants under 3 months, and amoebic dysentery.
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Bronchiolitis
Bronchiolitis is an acute viral lower respiratory tract infection of the small airways (bronchioles) in infants, typically under 2 years (peak 2 to 6 months), caused mainly by respiratory syncytial virus (RSV, 70 to 80 percent). Presentation: coryzal prodrome for 1 to 3 days, then worsening cough, wheeze, tachypnoea, and respiratory distress (nasal flaring, recession, grunting, head bobbing), with bilateral crackles and wheeze on auscultation. Most cases are mild and self-limiting. Treatment is supportive: oxygen if SpO2 persistently under 92 percent, nasal suctioning, and hydration (oral, NG, or IV). Bronchodilators, corticosteroids, antibiotics, chest physiotherapy, and routine imaging are NOT recommended. Severe disease may need high-flow nasal cannula, CPAP, or mechanical ventilation. Prevention: palivizumab 15 mg/kg monthly IM for high-risk infants during RSV season; nirsevimab (single long-acting dose) for all infants in regions where it is funded.
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Childhood Immunisation
Childhood immunisation prevents an estimated 2 to 3 million deaths per year worldwide. Active immunity (vaccine drives own antibody and memory-cell production) is contrasted with passive (pre-formed antibody: IVIG, tetanus immunoglobulin, transplacental). Live attenuated vaccines (BCG, OPV, MMR, rotavirus, varicella, yellow fever, LAIV) are contraindicated in severe immunocompromise and in pregnancy; inactivated, toxoid, conjugate, and recombinant vaccines are safe. UK routine schedule (verbatim): birth BCG/HepB for at-risk; 8wk 6-in-1 + MenB + rotavirus; 12wk 6-in-1 + PCV + rotavirus; 16wk 6-in-1 + MenB; 1yr Hib/MenC + MMR + PCV + MenB; 2 to 4yr influenza nasal; 3yr4mo MMR-2 + DTaP/IPV pre-school booster; 12 to 13yr HPV 2 doses; 14yr Td/IPV + MenACWY; pregnancy pertussis 16 to 32wk + influenza. BCG: intradermal, prevents TB meningitis and miliary TB (not pulmonary). OPV (Sabin) carries VAPP risk — global switch to IPV (Salk). Cold chain: 2 to 8 degrees C with VVM monitoring. Premature: vaccinate by chronological age. MMR does NOT cause autism (Wakefield retracted; Madsen, Hviid, Cochrane).
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Childhood Leukaemia
Childhood leukaemia is the most common childhood malignancy (30% of all childhood cancers). Acute lymphoblastic leukaemia (ALL) accounts for 75-80%; acute myeloid leukaemia (AML) 15-20%. Peak age: 2-5 years. Presentation: bone marrow failure (anaemia, infection, bleeding), organ infiltration (hepatosplenomegaly, lymphadenopathy, CNS). Diagnosis: FBC + blood film + bone marrow aspirate (morphology, flow cytometry, cytogenetics). Treatment: risk-stratified chemotherapy. 5-year survival ALL: 90%, AML: 65-70%.
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Congenital Heart Disease
Congenital heart disease (CHD) = structural heart defect present at birth. Incidence: 8-9 per 1000 live births. Classification: acyanotic (left-to-right shunt: VSD, ASD, PDA, AVSD; obstructive: coarctation, AS, PS) vs cyanotic (right-to-left shunt: TOF, TGA, tricuspid atresia, TAPVD, HLHS). Duct-dependent lesions (TGA, HLHS, critical PS/AS, severe coarctation) present with collapse at duct closure — maintain PGE1. Hyperoxia test distinguishes cardiac from pulmonary cyanosis.
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Congenital Hypothyroidism
Congenital hypothyroidism (CH) is thyroid hormone deficiency present at birth, resulting from abnormal thyroid gland development (dysgenesis, about 80%) or inborn errors of hormone biosynthesis (dyshormonogenesis, about 15 to 20%), with a minority due to transient maternal or environmental causes. Affected neonates are usually asymptomatic at birth because maternal thyroxine crosses the placenta; untreated, the disease produces irreversible intellectual disability, short stature and developmental delay, making CH the most common preventable cause of intellectual disability worldwide. Universal newborn screening (TSH on a heel-prick dried blood spot) detects CH before symptoms, and immediate levothyroxine 10 to 15 mcg/kg/day started within the first 2 weeks restores normal cognitive outcome. The cardinal rule is treat first, investigate later — never delay therapy for imaging or genetic tests.
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Croup
Croup (acute laryngotracheobronchitis) is the most common cause of acute upper airway obstruction in young children, peaking at 6 months to 3 years, caused mainly by parainfluenza virus type 1 and 2. Presentation: barking seal-like cough, harsh inspiratory stridor, hoarse voice, low-grade fever, worse at night. Most are mild and self-limiting over 3 to 7 days. Severe croup: stridor at rest, marked retractions, cyanosis, altered mental state. Treatment: oral dexamethasone 0.15 to 0.6 mg/kg single dose for all children; nebulised adrenaline 1:1000, 0.5 mL/kg max 5 mL, for moderate to severe with stridor at rest; observe at least 2 to 4 hours after adrenaline for rebound.
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Developmental Dysplasia of the Hip
Developmental dysplasia of the hip (DDH) is a spectrum of hip joint abnormalities in the infant and child ranging from a lax, dislocatable hip to a frankly dislocated hip with a shallow (dysplastic) acetabulum. Formerly called congenital dislocation of the hip (CDH); renamed because the disorder can develop after birth. Risk factors: breech presentation, female sex, firstborn, oligohydramnios, family history, foot deformity. Newborn: Barlow test (dislocatable) and Ortolani test (reducible clunk). Older infant: limited abduction, asymmetric skin folds, Galeazzi sign. Walker: Trendelenburg gait, leg-length discrepancy. Image with ultrasound under 4 to 6 months, plain X-ray over 4 to 6 months. Treat by age: Pavlik harness 0 to 6 months; closed reduction and spica cast 6 to 18 months; open reduction over 18 months; osteotomy for residual dysplasia. Feared complication: avascular necrosis of the femoral head.
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Developmental Milestones
Developmental milestones are age-specific functional skills achieved by children across four domains: gross motor, fine motor, language, and social/adaptive. Principles: cephalocaudal (head to toe), proximodistal (centre to periphery). Screening tools: ASQ-3, Denver II, Bayley scales. Red flags: loss of any skill (regression), no smile by 8 weeks, no words by 16 months, no 2-word phrases by 24 months, asymmetric movements. Global developmental delay = delay in 2+ domains; specific delay = 1 domain.
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Down Syndrome
Down syndrome is the commonest autosomal chromosomal abnormality in liveborn infants, caused by a full or partial extra copy of chromosome 21 (trisomy 21). It produces a characteristic facial phenotype, intellectual disability, and a cluster of associated conditions — congenital heart disease (AVSD), duodenal atresia, hypothyroidism, leukaemia, and atlantoaxial instability. Three cytogenetic forms: non-disjunction (95%), Robertsonian translocation (4%), and mosaicism (1%). Maternal age is the dominant risk factor. Diagnose with karyotype; screen antenatally with combined first-trimester screen and cell-free DNA (NIPT). Management is lifelong, multidisciplinary, anticipatory (AAP 2022 schedule) — early intervention, cardiac surveillance, thyroid and FBC monitoring, atlantoaxial precautions. Life expectancy now 50 to 60 years.
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Failure to Thrive
Failure to thrive (FTT) = weight consistently below the 3rd centile or crossing 2 major centile lines downward. Preferred term: faltering growth. Affects 5-10% of children. Classification: organic (identifiable pathology) vs non-organic/psychosocial (most common, 70-80%). Causes: inadequate intake, malabsorption (coeliac, CF), increased requirements (CHD), increased losses (GERD). Management: MDT approach (dietitian, health visitor, paediatrician), nutritional rehabilitation.
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Febrile Seizures
Febrile seizure = a seizure accompanied by fever (over 38 C / 100.4 F) in a child aged 6 months to 60 months (5 years), without evidence of central nervous system infection or a prior afebrile seizure, and without a defined acute neurological cause. Simple febrile seizure (SFS, about 70%): primary generalized, lasts under 15 minutes, does not recur within 24 hours. Complex febrile seizure (CFS, about 30%): any of focal onset, duration over 15 minutes, or recurs within 24 hours. Febrile status epilepticus: a febrile seizure lasting over 30 minutes. Affects 2 to 5% of children; peak age 12 to 18 months. Affects boys slightly more. Does NOT cause brain damage, cognitive impairment or epilepsy in the vast majority. Recurrence risk after a first febrile seizure is about 30% (50% if under 12 months). Subsequent epilepsy risk is 2 to 5% (simple) and 4 to 15% (complex). Active seizure lasting over 5 minutes: terminate with a benzodiazepine — IV lorazepam 0.1 mg/kg, buccal midazolam 0.5 mg/kg, or rectal diazepam 0.5 mg/kg. Always exclude meningitis (lumbar puncture in any child under 12 months with fever and seizure). No routine EEG, neuroimaging, or prophylactic antiepileptic drugs for simple febrile seizures.
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Henoch-Schonlein Purpura (IgA Vasculitis)
Henoch-Schonlein purpura (HSP), now officially renamed IgA vasculitis (IgAV) by the Chapel Hill Consensus Conference, is an immune-complex-mediated small-vessel (leukocytoclastic) vasculitis characterised by dominant IgA1 immune-complex deposition in the skin, gastrointestinal tract, joints and glomeruli. It is the most common vasculitis of childhood. Classically presents after a recent upper respiratory infection with the tetrad of palpable purpura (lower limbs/buttocks, mandatory), arthritis/arthralgia (knees, ankles), colicky abdominal pain, and renal involvement (haematuria/proteinuria). Platelets are NORMAL (key distinction from ITP). Diagnosis is clinical using EULAR/PRINTO/PRES 2010 or 1990 ACR criteria. Management is supportive in most cases (rest, hydration, analgesia, NSAIDs for arthritis); corticosteroids for severe gastrointestinal or renal involvement. Crucially, steroids do NOT prevent nephritis (Jauhola, 2011). Long-term outcome is excellent in children but renal involvement must be monitored for 6 to 12 months as nephritis can develop late, after the rash has resolved; ~1 to 2% progress to end-stage renal disease.
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Kawasaki Disease
Kawasaki disease is an acute, self-limited, medium-vessel vasculitis of childhood of unknown cause that preferentially involves the coronary arteries. It is the leading cause of acquired heart disease in children in developed nations. Diagnosis is clinical: fever for at least five days PLUS four of five principal features (bilateral non-purulent conjunctivitis, oral changes, polymorphous rash, extremity changes, cervical lymphadenopathy); an incomplete form (two to three features) is common in young infants and carries a higher coronary aneurysm risk. Cornerstone treatment is intravenous immunoglobulin 2 g/kg as a single infusion over 10 to 12 hours PLUS aspirin (high-dose anti-inflammatory then low-dose anti-platelet) within the first 10 days of illness, which reduces coronary artery aneurysm risk from roughly 25 per cent to 3 to 5 per cent. Echocardiography is mandatory at baseline, one to two weeks, and four to six weeks. Intravenous immunoglobulin resistance occurs in 10 to 20 per cent; repeat immunoglobulin, infliximab, corticosteroids, anakinra or cyclosporine are used in refractory disease.
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Neonatal Jaundice
Neonatal jaundice = yellow skin and sclera from elevated bilirubin in the first 28 days of life, visible when total serum bilirubin (TSB) exceeds 5 to 7 mg per dL (85 to 120 micromol per L). Jaundice within the FIRST 24 HOURS is always PATHOLOGICAL and demands urgent investigation for haemolysis and sepsis. Unconjugated (indirect) hyperbilirubinaemia (about 85%) is fat-soluble, crosses the immature blood-brain barrier, and causes kernicterus (acute bilirubin encephalopathy with lethargy, high-pitched cry, opisthotonus; chronic choreoathetoid cerebral palsy, sensorineural hearing loss). Conjugated (direct) hyperbilirubinaemia (about 15%) is water-soluble, does not cause kernicterus, but signals hepatobiliary disease — most importantly biliary atresia (pale stool, dark urine, conjugated jaundice) needing Kasai portoenterostomy before 60 days. Treatment is phototherapy (blue light converts unconjugated bilirubin to water-soluble photoisomers) and exchange transfusion for dangerous levels. Thresholds are age-, gestation- and risk-factor-specific on the Bhutani nomogram.
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Neonatal Sepsis
Neonatal sepsis is a systemic inflammatory response to a documented or suspected infection in the first 28 days of life. It is the great mimic of neonatology: presentation is non-specific (temperature instability, poor feeding, lethargy, respiratory distress, apnoea). Divided into early-onset sepsis (EOS, within 72 hours or 7 days) — vertically acquired from the maternal genital tract, organisms Group B Streptococcus (GBS), E coli (K1 capsule), Listeria monocytogenes — and late-onset sepsis (LOS, after 72 hours or 7 days) — horizontally/nosocomially acquired, organisms coagulase-negative staphylococci (CoNS, S epidermidis), S aureus (incl MRSA), Klebsiella, E coli, Pseudomonas, Candida. Mortality 10 to 30% overall, higher in premature and LBW infants. Take a blood culture before antibiotics and start empirical IV antibiotics within 1 hour: UK benzylpenicillin + gentamicin (EOS) or flucloxacillin + gentamicin (LOS); US ampicillin + gentamicin (EOS). Lumbar puncture for suspected meningitis. Maternal intrapartum GBS prophylaxis with IV benzylpenicillin reduces early-onset GBS disease by approximately 80%.
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Pneumonia in Children
Pneumonia in children = inflammation of the lung parenchyma, the single leading infectious cause of under-5 mortality globally, responsible for ~700,000 deaths/year (≈14% of all under-5 deaths). The WHO operational definition is cough or difficulty breathing with fast breathing defined by age (over 50/min at 2-12 months, over 40/min at 12 months-5 years, over 20/min at over 5 years). WHO classifies severity into pneumonia (fast breathing only, treat at home with oral amoxicillin), severe pneumonia (lower chest wall indrawing, hospitalise), and very severe pneumonia (danger signs: inability to drink, convulsions, vomiting everything, severe malnutrition, grunting — IV/IM antibiotics urgently). Leading viral cause under 1 year = RSV. Leading bacterial cause = Streptococcus pneumoniae; Hib pneumonia has fallen dramatically with conjugate vaccination. Empirical treatment: oral amoxicillin 80-90 mg/kg/day divided twice daily for 5-7 days for non-severe pneumonia, IV ampicillin + gentamicin (or ceftriaxone) for severe/very severe disease. Complicated empyema requires chest drain ± fibrinolysis with tPA + DNase (MIST2) or VATS. Prevention: PCV13/PCV10, Hib conjugate, measles, influenza annual, exclusive breastfeeding 6 months, hand hygiene, indoor air-pollution reduction, complementary feeding with zinc and vitamin A per WHO.
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Seizures in Children
Seizures affect 5% of children (at least one seizure); epilepsy affects 1%. Febrile seizures are most common (2-5% of children aged 6 months to 5 years). ILAE classification 2017: focal, generalised, unknown onset. Key syndromes: childhood absence (3Hz spike-wave, ethosuximide), juvenile myoclonic (valproate), infantile spasms (ACTH/vigabatrin). Status epilepticus: over 5 min — lorazepam → levetiracetam → phenytoin.
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Urinary Tract Infection in Children
Urinary tract infection (UTI) in children is common (8 percent of girls, 2 percent of boys by age 7), and in young infants the presentation is often non-specific (fever without source, poor feeding, vomiting, irritability, jaundice) — so a urine sample must be obtained in any unwell or febrile child under 3 months (and considered under 3 years). Causes: E. coli (75 to 85 percent), Klebsiella, Proteus, Enterococcus, Pseudomonas. Risk factors: female sex, uncircumcised boys, constipation, voiding dysfunction, vesicoureteric reflux (VUR), posterior urethral valves (boys), neurogenic bladder. Diagnosis rests on urine culture (SPA gold standard in infants; catheter 10^4 to 10^5; clean-catch over 10^5 CFU/mL). Treat: lower UTI 3 days oral; upper UTI/pyelonephritis 7 to 10 days oral or IV. Investigate recurrent, atypical, or any UTI under 6 months: renal ultrasound, DMSA scintigraphy (scarring at 4 to 6 months), MCUG (VUR selective). Untreated or recurrent pyelonephritis, especially with high-grade VUR, causes permanent renal scarring - hypertension and CKD.
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Obstetrics & Gynaecology
15 topicsObstetrics & Gynaecology
15
★ High yieldObstetrics & Gynaecology
Antepartum Haemorrhage
Antepartum haemorrhage (APH) is vaginal bleeding from the genital tract from 24 weeks of gestation until the birth of the baby. The three placental causes are placenta praevia (low placenta over/near the internal os — classically painless, bright-red, recurrent bleeding, soft relaxed non-tender uterus, often abnormal lie — diagnosed by transvaginal ultrasound, never digital vaginal examination until praevia excluded, caesarean if the placenta covers the os or lies within 2 cm), placental abruption (premature separation of a normally-sited placenta — painful, tense tender woody-hard uterus, dark or concealed bleeding, fetal distress, shock disproportionate to visible loss; risks hypertension/pre-eclampsia, previous abruption, smoking, cocaine; resuscitate and deliver), and vasa praevia (fetal vessels running over the membranes across the internal os — painless bleeding at rupture of membranes with sudden fetal compromise (sinusoidal CTG) in a haemodynamically normal mother; prenatal diagnosis carries 98.6% perinatal survival versus 72.1% when missed — planned caesarean before membrane rupture). Always resuscitate, cross-match as indicated, FBC/coagulation/fibrinogen, continuous CTG, anti-D to Rh-negative women, tranexamic acid if major bleeding, and deliver when there is maternal or fetal compromise.
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Cervical Cancer
Cervical cancer arises at the cervical transformation zone from persistent infection with high-risk HPV (16/18), whose E6 and E7 oncoproteins disable the p53 and Rb tumour suppressors. Over 10 to 15 years a minority of persistent infections progress through CIN 1 to 3 to invasive carcinoma. Presentation: postcoital or intermenstrual bleeding. Diagnosis: cervical cytology and HPV testing, colposcopy, directed biopsy. FIGO 2018 staging is clinical and radiological. Early disease: radical hysterectomy (Wertheim) or fertility-sparing trachelectomy. Locally advanced: concurrent chemoradiotherapy (cisplatin + EBRT + brachytherapy). Metastatic: cisplatin, paclitaxel, bevacizumab (GOG-240). Largely preventable through HPV vaccination and organised screening.
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Ectopic Pregnancy
Ectopic pregnancy = implantation of a fertilized ovum outside the uterine cavity. About 95% are tubal (ampulla 75%, isthmus 12%, fimbria 5%, interstitial 2%). Incidence 1 to 2% of pregnancies and 2 to 3% with IVF. Classic triad: missed period + unilateral abdominal pain + dark vaginal bleeding. Diagnosis: quantitative serum beta-hCG + transvaginal ultrasound. Discriminatory zone: at beta-hCG over 1500 to 2000 IU/L an intrauterine gestational sac should be visible on TVS. Shoulder tip pain + collapse = ruptured ectopic (haemoperitoneum). Stable unruptured: methotrexate 50mg per metre squared IM (under 3.5cm, beta-hCG under 5000, no cardiac activity) or laparoscopic salpingostomy or salpingectomy. Ruptured: emergency laparoscopy or laparotomy + salpingectomy. Always give Anti-D to Rh-negative women.
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★ High yieldObstetrics & Gynaecology
Gestational Diabetes Mellitus
A source-verified, region-aware guide to gestational diabetes: distinguish GDM from overt diabetes, keep WHO/IADPSG, ACOG and NICE pathways separate, individualise lifestyle and pharmacotherapy, plan fetal surveillance and birth, protect the newborn, and complete postpartum prevention and future-pregnancy care.
NEET-PGINICET
★ High yieldObstetrics & Gynaecology
Menopause & Hormone Replacement Therapy
Menopause is the permanent cessation of menstruation, defined retrospectively as 12 months of amenorrhoea without any other cause (average age 50 to 52; premature ovarian insufficiency before 40). It results from depletion of ovarian follicles producing loss of oestradiol and inhibin, so FSH and LH rise. Symptoms cluster into vasomotor (hot flushes, night sweats — over 75 percent), the genitourinary syndrome of menopause (vaginal dryness, dyspareunia, urinary symptoms) and psychological / sleep disturbance. Long-term oestrogen deficiency drives osteoporosis, cardiovascular disease and urogenital atrophy. Diagnosis is clinical in women over 45; measure FSH only if under 45, after hysterectomy, suspected POI, or atypical. Treatment is individualised HRT — oestrogen (most effective for vasomotor, bone and GSM) plus a progestogen if the uterus is intact (unopposed oestrogen causes endometrial cancer). Transdermal oestrogen carries lower VTE risk; vaginal oestrogen treats isolated GSM. Start HRT under 60 or within 10 years of menopause ('timing hypothesis'). Postmenopausal bleeding = endometrial cancer until proven.
NEET-PGINICET
★ High yieldObstetrics & Gynaecology
Menstrual Disorders
Menstrual disorders encompass abnormalities in menstrual cycle frequency, duration, volume, or associated symptoms. FIGO PALM-COEIN classification (2011/2018) categorises abnormal uterine bleeding: Polyps, Adenomyosis, Leiomyoma, Malignancy/hyperplasia (structural); Coagulopathy, Ovulatory dysfunction, Endometrial, Iatrogenic, Not classified (non-structural). Management follows NICE NG88: LNG-IUS first-line for HMB; tranexamic acid/mefenamic acid/COCP alternatives.
NEET-PGINICET
★ High yieldObstetrics & Gynaecology
Miscarriage & Recurrent Pregnancy Loss
Miscarriage (spontaneous abortion) is the loss of a pregnancy before 24 weeks of gestation (the threshold of viability). It is the commonest complication of pregnancy, affecting about 1 in 5 clinically recognised pregnancies (and far more when biochemical losses are counted). The clinical types are distinguished by the cervical os and ultrasound viability: threatened (bleeding, closed os, viable fetus), inevitable (bleeding, open os), incomplete (partial passage, open os, ongoing bleeding), complete (all passed, closed os), missed (fetal demise, retained), and septic (infection — an emergency). Recurrent pregnancy loss (RPL) is 3 or more consecutive first-trimester losses. The commonest cause overall is chromosomal abnormality of the embryo (over 50 percent); the most important treatable cause of RPL is antiphospholipid syndrome. Diagnosis rests on transvaginal ultrasound (TVS) using the NICE non-viability criteria plus serial beta-hCG; management offers expectant, medical (mifepristone plus misoprostol) or surgical (suction evacuation) options, with anti-D for all Rh-negative women.
NEET-PGINICET
★ High yieldObstetrics & Gynaecology
Normal Labour and Delivery
Normal labour = physiological expulsion of fetus, placenta, and membranes after 24 weeks gestation, via regular painful uterine contractions causing progressive cervical effacement, dilatation, descent, and expulsion. Four stages: 1st (latent 0 to 4cm + active 4 to 10cm), 2nd (full dilatation to baby), 3rd (placenta, active vs expectant management), 4th (golden hour). Eight cardinal movements: engagement, descent, flexion, internal rotation, extension, restitution, external rotation, expulsion. Three Ps: Powers, Passenger, Passage. Molecular switch: myometrial connexin-43 gap junctions plus oxytocin receptor upregulation. Active management of 3rd stage (oxytocin 10 IU IM + CCT + uterine massage) reduces PPH by 60%. APGAR at 1, 5, and 10 min.
NEET-PGINICET
★ High yieldObstetrics & Gynaecology
Ovarian Cancer
Ovarian cancer is the leading cause of gynaecological cancer death in the UK and the sixth most common cancer in women (lifetime risk about 2 per cent, 1 in 50). The dominant subtype, high-grade serous carcinoma, arises from the fimbrial end of the fallopian tube (serous tubal intraepithelial carcinoma, STIC), not the ovarian surface — a paradigm shift that drives risk-reducing salpingo-oophorectomy in BRCA1/2 carriers. The classical presentation is late and non-specific — bloating, distension, early satiety — so most women are Stage III/IV at diagnosis. CA-125 plus transvaginal ultrasound triage via IOTA simple rules and the Risk of Malignancy Index (RMI), with RMI over 250 mandating specialist referral. FIGO 2014 staging is surgical. Standard care is surgical staging and maximal cytoreduction (TAH + BSO + omentectomy + peritoneal biopsies + lymphadenectomy) plus carboplatin and paclitaxel for six 3-weekly cycles. Maintenance PARP inhibitors (olaparib, niraparib) and bevacizumab have transformed first-line therapy. Stage I survival is 90 per cent; Stage IV under 15 per cent. Population screening does not work (UKCTOCS, PLCO).
NEET-PGINICET
★ High yieldObstetrics & Gynaecology
Pelvic Inflammatory Disease
Pelvic inflammatory disease (PID) is an ascending, polymicrobial infection of the upper female genital tract — endometrium (endometritis), fallopian tubes (salpingitis), ovaries (oophoritis) and pelvic peritoneum. The classical organisms are Chlamydia trachomatis and Neisseria gonorrhoeae, with Mycoplasma genitalium, anaerobes and bacterial-vaginosis-associated organisms also important. Presents with bilateral lower abdominal pain, deep dyspareunia, abnormal vaginal discharge and cervical motion tenderness, but is often subtle or silent — the missed case is the one that causes tubal infertility. Diagnosis is clinical (minimum criterion: cervical motion, uterine or adnexal tenderness in a sexually active young woman with no other cause). Outpatient therapy: ceftriaxone 500 mg IM once + doxycycline 100 mg BD 14 days + metronidazole 500 mg BD 14 days; treat partners (60-day window); admit if pregnant, severe, TOA, failed oral therapy or diagnostic uncertainty. Complications: tubal infertility (12 percent after one episode), ectopic pregnancy (6 to 10-fold risk), chronic pelvic pain, tubo-ovarian abscess and Fitz-Hugh-Curtis perihepatitis.
NEET-PGINICET
★ High yieldObstetrics & Gynaecology
Placenta Praevia
Placenta praevia = placenta implanted wholly or partly in the lower uterine segment, over or near the internal cervical os. Incidence about 0.3 to 0.5 percent of pregnancies at term (higher earlier because most low placentas migrate). Classic: painless, causeless, recurrent bright-red vaginal bleeding after 20 to 24 weeks; uterus soft and non-tender (unlike abruption). Transvaginal ultrasound is the gold standard; NEVER do a digital vaginal examination until praevia is excluded. Caesarean for praevia where the placenta overlaps the os, at 36 to 37 weeks. Previous caesarean + praevia = high placenta accreta spectrum risk.
NEET-PGINICET
★ High yieldObstetrics & Gynaecology
Placental Abruption
Placental abruption (abruptio placentae) = premature separation of a normally-situated placenta from the uterine wall before delivery of the fetus. Incidence about 1 in 100 pregnancies; severe (fetal death) about 1 in 1000. Classic triad: painful vaginal bleeding + hard, woody, tender hypertonic uterus + fetal distress. Two patterns: revealed (about 80%, blood tracks via cervix, visible, less dangerous) and concealed (about 20%, blood trapped behind placenta, shock disproportionate to visible loss, more dangerous). Pathology: decidual vasculopathy (pre-eclampsia) leads to spiral artery rupture, retroplacental clot, extension of separation, and in severe cases Couvelaire uterus (blood infiltrates myometrium to serosa, uteroplacental apoplexy) and DIC (thromboplastin release, fibrinogen under 2 g/L). Top risk factor: pre-eclampsia/hypertension; recurrence 6 to 25 percent. Management: resuscitate in parallel with delivery planning; correct coagulopathy before any surgery; fetus alive + distress leads to emergency caesarean; fetus dead leads to vaginal delivery unless maternal indication. Watch for refractory atonic PPH, AKI and Sheehan syndrome.
NEET-PGINICET
★ High yieldObstetrics & Gynaecology
Postpartum Haemorrhage
Postpartum haemorrhage (PPH) = blood loss over 500 mL after birth within 24 h; over 1000 mL is severe PPH. Secondary PPH = 24 h to 12 weeks postpartum. 4 Ts: Tone (atony — the dominant cause), Trauma, Tissue, Thrombin. Resuscitate and treat the cause in parallel. Uterotonics: oxytocin first-line, misoprostol 800 µg sublingual as best-evidenced alternative; add tranexamic acid 1 g IV as soon as possible after onset (WOMAN trial). Refractory atony: uterine balloon tamponade (pooled success about 86%), compression sutures, hysterectomy (last resort).
NEET-PGINICET
★ High yieldObstetrics & Gynaecology
Pre-eclampsia & Eclampsia
Pre-eclampsia is new hypertension at or after 20 weeks with proteinuria or specified maternal or uteroplacental dysfunction, interpreted using a named regional guideline. Severe hypertension and eclampsia are obstetric emergencies: stabilize, prevent or terminate seizures with protocolised magnesium sulphate, treat blood pressure urgently, assess mother and fetus, and plan birth after stabilization.
NEET-PGINICET
★ High yieldObstetrics & Gynaecology
Preterm Labour & Preterm Birth
Preterm labour (PTL) is the onset of regular painful uterine contractions with cervical change before 37 completed weeks of gestation; preterm birth (PTB) is delivery before 37 weeks — the commonest cause of neonatal mortality and a leading cause of childhood disability. Risk factors: infection (intra-amniotic, BV, UTI, STI — the biggest reversible driver), previous preterm birth (recurrence 20 to 30 percent), multiple pregnancy, short cervix, PPROM, uterine anomaly, prior cervical surgery, smoking, low BMI, short interpregnancy interval, IVF. Diagnosis: contractions with cervical change; prediction by TVUS cervical length under 25 mm and fetal fibronectin (negative is a powerful rule-out). Management goal: delay birth 48 h for antenatal corticosteroids (24 to 34w) + magnesium sulfate neuroprotection (under 32w) + in-utero transfer — tocolysis with nifedipine (first-line); PPROM → erythromycin + surveillance, deliver at 34w; never tocolyse chorioamnionitis or fetal compromise. Prevention: vaginal progesterone (short cervix), cervical cerclage (history/ultrasound-indicated), smoking cessation, treat infection, interval planning.
NEET-PGINICET
Medicine
20 topicsDermatology
20
Dermatology
Antihistamines and itch
H1 antihistamines are first-line pharmacotherapy for histamine-mediated pruritus (urticaria, angioedema, insect bites, allergic rhinitis). They act as inverse agonists at the H1 receptor, not simple competitive antagonists. First-generation agents (chlorpheniramine, diphenhydramine, hydroxyzine, promethazine) cross the blood-brain barrier, are sedating and anticholinergic, and are avoided in the elderly per the Beers Criteria. Second-generation agents (cetirizine, levocetirizine, loratadine, desloratadine, fexofenadine, bilastine) are non-sedating and preferred for chronic use. Terfenadine and astemizole were withdrawn because of hERG K+ channel blockade causing QT prolongation and Torsades de Pointes. In chronic spontaneous urticaria the EAACI/GA²LEN algorithm up-titrates second-generation H1 antihistamines up to 4 times the standard dose before adding omalizumab, the only licensed next-line therapy. Antihistamines have limited efficacy in non-histaminergic itch (atopic dermatitis, cholestasis, uraemia, neuropathic pruritus), where cause-specific treatment is required.
NEET-PGINICET
Dermatology
Atypical / Dysplastic Naevus
An atypical (dysplastic) naevus is a benign melanocytic naevus with clinical features of irregularity (asymmetry, border irregularity, colour variegation, diameter 5 mm) and/or histological features of architectural disorder and cytological atypia. It is primarily a melanoma risk marker rather than a direct precursor, and management is risk-stratified: observation and surveillance for most, with excision of changing or suspicious lesions.
NEET-PGINICET
★ High yieldDermatology
Candidiasis
Candidiasis is a yeast infection caused predominantly by Candida albicans and increasingly by non-albicans species (C. glabrata, C. tropicalis, C. parapsilosis) and the multidrug-resistant C. auris. For MBBS final-proficiency, candidates must master the cutaneous forms (intertrigo, napkin/diaper dermatitis, candidal paronychia), the mucosal forms (oral thrush, angular cheilitis, vulvovaginal candidiasis, balanitis), the risk factors (moisture, occlusion, antibiotics, diabetes, immunosuppression, pregnancy), the bedside diagnosis by KOH showing budding yeasts and pseudohyphae, and the stepwise antifungal ladder (topical nystatin/azoles, oral fluconazole/itraconazole, echinocandins for invasive disease). They must also recognise chronic mucocutaneous candidiasis as a signal of immune dysregulation, and Candida auris as a healthcare-associated infection-control emergency.
NEET-PGINICET
Dermatology
Cicatricial alopecia
Cicatricial (scarring) alopecia is a group of disorders in which hair follicles are destroyed and replaced by fibrous tissue, producing permanent, irreversible hair loss. The hallmark clinical sign is loss of follicular ostia. The North American Hair Research Society (NAHRS) classifies primary cases by inflammatory infiltrate into lymphocytic (lichen planopilaris, frontal fibrosing alopecia, discoid lupus, CCCA, pseudopelade of Brocq), neutrophilic (folliculitis decalvans, dissecting cellulitis) and mixed (acne keloidalis nuchae) forms. Early diagnosis by trichoscopy and biopsy of the active margin is essential because destroyed follicles cannot regrow. Management targets the inflammatory mechanism: lymphocytic disease uses corticosteroids, hydroxychloroquine, mycophenolate and JAK inhibitors; neutrophilic disease uses antibiotics, isotretinoin and TNF inhibitors. Hair transplantation is reserved for burnt-out, quiescent disease.
NEET-PGINICET
Dermatology
Cryoglobulinaemia
Cryoglobulinaemia is the presence of immunoglobulins that precipitate below 37°C and redissolve on warming. Type I is predominantly a monoclonal occlusive disorder; mixed Types II and III usually cause immune-complex vasculitis. Diagnosis depends on exact warm sample handling, and treatment is directed by cause and severity.
NEET-PGINICET
Dermatology
Dermatitis herpetiformis
Exam-focused dermatitis herpetiformis: presentation, correctly sited biopsy, TG3 pathogenesis, coeliac assessment, gluten-free diet, and safe dapsone use.
NEET-PGINICET
Dermatology
Dermatology in pregnancy
Exam-exhaustive MBBS guide to physiologic skin changes in pregnancy, atopic eruption of pregnancy, polymorphic eruption of pregnancy/PUPPP, pemphigoid gestationis, intrahepatic cholestasis of pregnancy, pustular psoriasis of pregnancy/impetigo herpetiformis, fetal-risk triage, investigations, drug safety in pregnancy and lactation, and red flags.
NEET-PGINICET
Dermatology
Epidermal naevus and naevus sebaceous
Epidermal naevi are congenital hamartomas of keratinocytes or epidermal appendages that follow Blaschko lines, reflecting postzygotic somatic mosaicism. Verrucous epidermal naevus presents as linear warty papules; naevus sebaceous is a yellow-orange hairless scalp or facial plaque that thickens at puberty; ILVEN is a pruritic psoriasiform linear plaque. Epidermal naevus syndrome (Schimmelpenning) associates cutaneous lesions with neurological, skeletal, and ocular anomalies. Modern management of naevus sebaceous is conservative with biopsy of suspicious nodules, because the risk of basal cell carcinoma is low.
NEET-PGINICET
★ High yieldDermatology
Epidermolysis Bullosa
Epidermolysis bullosa (EB) is a group of inherited mechanobullous disorders caused by mutations in structural proteins of the skin and mucosa. Blistering follows minor mechanical trauma. Classification is by the level of cleavage: EB simplex (intraepidermal; KRT5/14), junctional EB (lamina lucida; laminin-332/COL17A1), dystrophic EB (sublamina densa; COL7A1/type VII collagen), and Kindler syndrome (mixed plane; FERMT1). Severe recessive dystrophic EB carries a cumulative cutaneous squamous cell carcinoma risk of around 90% by age 55 and remains the leading cause of early death. Diagnosis rests on immunofluorescence mapping and genetic testing; management is multidisciplinary supportive care, with topical gene therapy (beremagene geperpavec / Vyjuvek) now FDA-approved for dystrophic EB.
FRCDermABD
Dermatology
Erythema multiforme
Erythema multiforme is an acute immune-mediated eruption recognised by raised acral target lesions. It is clinically distinct from SJS/TEN; RIME and MIRM are infection-triggered mucositis syndromes whose relationship to EM remains debated.
NEET-PGINICET
★ High yieldDermatology
Erythrasma
Erythrasma is a chronic, superficial bacterial infection of intertriginous skin caused by Corynebacterium minutissimum (reclassified by some taxonomic schemes as Kocuria or retained within Corynebacterium), presenting as well-demarcated, reddish-brown, finely scaly macules and patches in the groin, axillae, toe webs, submammary folds and gluteal cleft. The pathognomonic diagnostic sign is coral-red fluorescence under Wood's lamp (UV-A 365 nm) produced by coproporphyrin III. NEET-PG/INICET high-yield topics include differentiation from tinea cruris, candidal intertrigo and inverse psoriasis; the fact that imidazole antifungals are effective against this bacterial infection; and oral erythromycin or clarithromycin for extensive disease.
NEET-PGINICET
Dermatology
Granuloma annulare
Granuloma annulare (GA) is a benign, usually self-limiting granulomatous dermatosis. Histology: palisading granulomas with central necrobiotic collagen + mucin surrounded by histiocytes. Localized (commonest): annular skin-coloured papules on dorsa of hands/feet; self-limiting. Generalized: disseminated; may associate with diabetes, dyslipidaemia, thyroid disease and HIV; refractory. Subcutaneous (deep): firm nodules in children; mimics rheumatoid nodules (but RF negative). Perforating: crusted papules (trans-epidermal elimination). DDx: tinea corporis, annular psoriasis, necrobiosis lipoidica, rheumatoid nodules, sarcoidosis, interstitial granulomatous dermatitis, erythema annulare centrifugum, actinic granuloma. Management: localized — observe or potent topical corticosteroids / intralesional triamcinolone, cryotherapy, tacrolimus; generalized — topical dapsone, hydroxychloroquine, nbUVB, methotrexate, isotretinoin, adalimumab; observation for mild localised. Prognosis is generally excellent.
NEET-PGINICET
Dermatology
Hyperhidrosis
Hyperhidrosis is sweating beyond the physiological requirement for thermoregulation. It is divided into primary focal (idiopathic, bilateral, symmetric, focal onset before age 25, ceases during sleep, often familial) and secondary generalised (endocrine, neurological, malignant, infectious, drug-related or autonomic cause). Primary focal hyperhidrosis affects roughly 1-3% of people and causes substantial psychosocial and occupational disability. Eccrine sweat glands are innervated by sympathetic cholinergic post-ganglionic fibres that release acetylcholine onto muscarinic-3 (M3) receptors; this explains why anticholinergics and botulinum toxin are effective. Site drives therapy: aluminium chloride 20% for axillary disease, tap-water iontophoresis for palmar/plantar disease, botulinum toxin A for refractory axillary or palmar disease, oral anticholinergics for generalised disease, and endoscopic thoracic sympathectomy (ETS) only as a last resort for severe palmar disease because of compensatory hyperhidrosis.
NEET-PGINICET
★ High yieldDermatology
IgA vasculitis (Henoch-Schönlein purpura)
IgA vasculitis is an IgA1 immune-complex small-vessel leukocytoclastic vasculitis, classically presenting with lower-limb palpable purpura, arthralgia or arthritis, colicky abdominal pain or GI bleeding, and renal involvement with haematuria or proteinuria. Diagnosis is clinical when purpura is typical and platelets are normal; early skin biopsy shows leukocytoclastic vasculitis with IgA-dominant direct immunofluorescence. Management is supportive for most children, with urinalysis, blood pressure, proteinuria, and renal function surveillance; corticosteroids are reserved for severe abdominal or renal disease, and persistent proteinuria or renal impairment needs nephrology-led care.
NEET-PGINICET
★ High yieldDermatology
Incontinentia Pigmenti
Incontinentia pigmenti (IP; Bloch-Sulzberger syndrome) is an X-linked dominant genodermatosis caused by mutation in the IKBKG/NEMO gene (Xq28). It is lethal in most hemizygous males and almost exclusively affects females. The hallmark is a 4-stage Blaschkoid cutaneous eruption (vesicular, verrucous, hyperpigmented, atrophic/hypopigmented) with extracutaneous involvement of teeth, eyes, CNS, hair and nails.
NEET-PGINICET
Dermatology
Melasma
Melasma is an acquired, bilateral, symmetrical hyperpigmentation of sun-exposed facial skin, classically affecting women with Fitzpatrick III-IV skin. It is driven by UV and visible light, hormonal triggers, genetic predisposition and local skin microenvironmental changes. Wood's lamp examination separates epidermal (accentuated, responds to topicals), dermal (not accentuated, resistant) and mixed types. Management is built on strict photoprotection, then topical depigmenting agents such as hydroquinone, tretinoin and azelaic acid, with oral tranexamic acid and carefully selected procedures for refractory disease. It is chronic and relapsing.
NEET-PGINICET
Dermatology
Necrobiosis lipoidica
Necrobiosis lipoidica is a chronic granulomatous dermatosis of collagen degeneration, classically producing yellow-brown atrophic telangiectatic plaques with a violaceous rim on the anterior shins. It is strongly associated with diabetes mellitus but does not reliably improve with glycaemic control. Diagnosis is clinical when typical and biopsy shows palisading or layered granulomas around necrobiotic collagen with plasma cells and vascular change. Management centres on smoking cessation, trauma avoidance, topical or intralesional corticosteroid to the active rim, tacrolimus or phototherapy for steroid-sparing control, antiplatelet or pentoxifylline in selected cases, biologics for refractory disease, and meticulous ulcer care.
NEET-PGINICET
Dermatology
Telogen effluvium
Telogen effluvium (TE) is a non-scarring, diffuse hair loss caused by a premature shift of anagen follicles into the telogen (resting) phase, producing synchronous shedding 2-3 months after a triggering event. Headington classified five functional types (immediate anagen release, delayed anagen release, short anagen, immediate telogen release, delayed telogen release) and the Whiting entity of chronic telogen effluvium (CTE) is a distinct middle-aged female phenotype that fluctuates for years. Common triggers include childbirth, severe illness or fever (including COVID-19), iron deficiency, thyroid dysfunction, crash dieting or bariatric surgery, retinoids, anticoagulants, beta-blockers, lithium, valproate, interferon and severe emotional stress. The hallmark bedside signs are diffuse thinning (not patterned, not patchy), a positive hair pull test (5-6 of 50-60 hairs), trichoscopic empty follicles and upright regrowing hairs, and ABSENT follicular diameter diversity. Investigation is targeted: ferritin (target 70 microg/L), TSH, vitamin D, zinc and CBC. Management is identify-and-treat-the-trigger plus reassurance; acute TE is self-limiting within 6-12 months. Topical or oral minoxidil is reserved for chronic TE or TE overlapping with female pattern hair loss (FPHL).
NEET-PGINICET
★ High yieldDermatology
Tinea pedis, tinea cruris and tinea unguium (onychomycosis)
Tinea pedis (athlete's foot), tinea cruris (jock itch) and tinea unguium/onychomycosis (nail infection) are the commonest dermatophyte infections, sharing Trichophyton rubrum and the warm, occluded foot-and-shoe ecological niche. The topic covers the interdigital, moccasin, vesicobullous and acute ulcerative patterns of tinea pedis, the scrotal-sparing groin rash of tinea cruris, the four patterns of onychomycosis, the 'two feet, one hand' sign, KOH/culture/PAS diagnosis, topical allylamine and azole therapy for skin disease, systemic terbinafine and itraconazole for nails, the emerging terbinafine-resistant Trichophyton indotineae, and the public-health importance of treating the foot and nail reservoir to prevent recurrent cellulitis and groin disease.
NEET-PGINICET
★ High yieldDermatology
Topical Corticosteroids
Topical corticosteroids (TCS) are the most widely prescribed dermatological therapy. Safe use requires matching potency (mild to very potent), vehicle (ointment cream lotion), and body site (face/flexures = low potency; palms/soles = high potency). The fingertip unit (FTU; ~0.5 g) standardizes dosing. Adverse effects include local atrophy, striae, telangiectasia, periorificial dermatitis, tinea incognito, and systemic HPA axis suppression. Steroid-sparing agents (tacrolimus, pimecrolimus, calcipotriene) and patient counselling about corticophobia improve outcomes.
NEET-PGINICET
Cardiology
19 topicsCardiology
19
★ High yieldCardiology
Acute Aortic Syndrome
Acute aortic syndrome (AAS) is a spectrum of life-threatening aortic emergencies — classic aortic dissection (intimal tear with a false lumen), intramural haematoma (IMH), and penetrating aortic ulcer (PAU) — that share a common pathophysiology (medial degeneration and wall shear) and an identical initial resuscitation strategy. Stanford type A (ascending aorta involvement) is a surgical emergency — mortality rises roughly 1 to 2 percent per untreated hour, and emergency open repair (supracoronary tube graft or valve-sparing root replacement, plus aortic arch replacement if required) carries an operative mortality of 15 to 25 percent in IRAD and saves the patient's life in most cases. Stanford type B (descending aorta only, distal to the left subclavian artery) is initially managed medically — impulse-control with IV beta-blockade (esmolol or labetalol) targeting a heart rate under 60 bpm and a systolic blood pressure 100 to 120 mmHg, plus analgesia (morphine 5 to 10 mg IV) — with thoracic endovascular aortic repair (TEVAR) reserved for complicated type B (malperfusion, rupture, refractory pain, expansion, uncontrolled hypertension). The classic presentation is sudden severe tearing or ripping chest or back pain, often with a blood-pressure differential of more than 20 mmHg between arms or between arm and leg, a widened mediastinum on chest X-ray, and a pulse or neurological deficit. Independent risk factors include uncontrolled hypertension (the dominant factor), connective-tissue disease (Marfan, Loeys-Dietz, Ehlers-Danlos type IV), bicuspid aortic valve, aortic coarctation, cocaine use, pregnancy (especially the third trimester and peripartum), smoking and family history of aortic disease. Diagnosis is by CT aortography (first-line in stable patients — sensitivity and specificity both above 95 percent), transoesophageal echocardiography (TEE) (the bedside test of choice in haemodynamically unstable patients in the resuscitation room or operating theatre), or MRI (second-line, e.g. young/ pregnant/renal failure patients who cannot have iodinated contrast). D-dimer can be a useful rule-out in low-probability patients presenting under 24 hours (sensitivity about 95 to 99 percent when below 500 ng/mL but specificity poor). Complications include cardiac tamponade, acute aortic regurgitation, myocardial infarction (if a coronary ostium is involved), stroke (carotid or intercostal malperfusion), paraplegia (spinal cord ischaemia from intercostal artery loss), mesenteric ischaemia, renal failure and limb ischaemia. Key drugs: esmolol 500 mcg/kg IV bolus then 50 to 200 mcg/kg/min infusion, labetalol 20 to 80 mg IV bolus every 10 minutes (max 300 mg), nicardipine 5 to 15 mg/hour IV infusion, nitroprusside 0.25 to 10 mcg/kg/min (added after rate control), and morphine 5 to 10 mg IV for pain. Anchored to the 2022 ACC/AHA (Isselbacher) and 2014 ESC (Erbel) aortic disease guidelines.
NEET-PGINICET
★ High yieldCardiology
Acute Coronary Syndrome
Acute coronary syndrome (ACS) spans STEMI (ST elevation, complete coronary occlusion, emergency reperfusion), NSTEMI (troponin-positive, no ST elevation), and unstable angina (troponin-negative). Diagnosis rests on the 12-lead ECG within 10 minutes and high-sensitivity troponin. Immediate treatment: aspirin 300 mg + a P2Y12 inhibitor + parenteral anticoagulant; STEMI needs primary PCI within 120 minutes (or fibrinolysis if unavailable); NSTE-ACS is risk-stratified with the GRACE score to choose invasive-strategy timing.
NEET-PGINICET
★ High yieldCardiology
Adult Congenital Heart Disease
Adult congenital heart disease (ACHD) is the lifetime management of patients with structural heart disease present since birth who survive into adulthood. The commonest lesions encountered in adults are secundum atrial septal defect (ASD), repaired Tetralogy of Fallot (TOF), coarctation of the aorta, bicuspid aortic valve, Ebstein anomaly and the late consequences of atrial-switch (Mustard/Senning) or Fontan surgery. The central diagnostic skill is recognising an unrepaired shunt, the central decision is shunt closure before irreversible pulmonary vascular disease, and the irreversible end-stage of an uncorrected L-to-R shunt is Eisenmenger syndrome — pulmonary arterial hypertension (PAH) at or above systemic level with shunt reversal (R-to-L), central cyanosis, clubbing and secondary erythrocytosis. Pregnancy is contraindicated in Eisenmenger physiology (maternal mortality 30–50%).
NEET-PGINICET
★ High yieldCardiology
Aortic Regurgitation
Aortic regurgitation (AR) is diastolic incompetence of the aortic-valve complex permitting backflow from the aorta into the left ventricle. In chronic AR the LV remodels by eccentric hypertrophy, giving the classic signs — early-diastolic decrescendo murmur at Erb point, wide pulse pressure, water-hammer (Corrigan) pulse and a constellation of peripheral signs (de Musset, Quincke, Traube, Duroziez, Hill). Causes are leaflet disease (rheumatic, bicuspid, endocarditis) or aortic-root dilation (Marfan, hypertension, ankylosing spondylitis, syphilis). Acute severe AR (endocarditis, type A dissection, trauma) presents as sudden pulmonary oedema without the classic signs. Diagnosis is by echocardiography, which grades severity (regurgitant volume, fraction, EROA, vena contracta). Definitive treatment is aortic valve surgery (AVR) when symptomatic, when EF is 50 percent or below, or when LV end-systolic diameter exceeds 50 mm. Never use an intra-aortic balloon pump in significant AR.
NEET-PGINICET
★ High yieldCardiology
Aortic Stenosis
Aortic stenosis (AS) is obstruction of left ventricular outflow at the valve level, caused most often by calcific degeneration (elderly) or a bicuspid valve (younger); rheumatic disease predominates in young Indian patients. Severe AS produces the classic symptom triad of angina, syncope and heart failure, a slow-rising small-volume pulse (pulsus parvus et tardus) and a crescendo-decrescendo ejection systolic murmur radiating to the carotids. Diagnosis rests on echocardiography with the continuity equation. Aortic valve replacement (AVR) is the only survival-modifying therapy; choice of surgical AVR (SAVR) versus transcatheter AVR (TAVI/TAVR) is driven by age, surgical risk and anatomy.
NEET-PGINICET
★ High yieldCardiology
Bradycardia and AV Block
Bradyarrhythmia in adults means a resting heart rate below 60 bpm (the clinical threshold drops to below 50 bpm when truly symptomatic, and athletic resting bradycardia of 30 to 40 bpm is physiological). The two master categories are sinus node dysfunction (sinus bradycardia, sinus arrest, sinoatrial block, sick sinus syndrome) and atrioventricular (AV) block — 1st degree (PR over 200 ms, benign), 2nd degree Mobitz I (Wenckebach, usually benign, AV nodal, atropine-responsive), 2nd degree Mobitz II (infranodal, high risk of progression to complete block, Class I indication for pacing even when asymptomatic), and 3rd degree (complete heart block, AV dissociation, Class I pacing). Common aetiologies include age-related idiopathic fibrosis and calcification (Lev disease and Lenegre disease), inferior MI with right coronary artery occlusion supplying the AV node, iatrogenic drug toxicity (beta-blocker, calcium-channel blocker, digoxin), electrolyte disturbance (hyperkalaemia, hypermagnesaemia), post-cardiac surgery (aortic valve replacement, septal myectomy, TAVI, congenital repair), Lyme carditis, Chagas disease, sarcoidosis, amyloidosis, myocarditis, and high vagal tone (athletes, sleep apnoea, cough, micturition). Pathophysiology centres on failure of impulse formation (SA node) or conduction (AV node, His–Purkinje), often with ischaemia (the SA and AV nodes are supplied by the RCA in 80–90 percent of patients, making inferior MI the classic cause). Clinical presentation ranges from asymptomatic through fatigue, exercise intolerance, dizziness, breathlessness, to Stokes-Adams syncope, falls and sudden cardiac death when long pauses occur. Diagnosis rests on the 12-lead ECG (PR interval, Mobitz pattern, dissociation) extended by ambulatory ECG/Holter (24 h), patch/event monitors (7–14 days), implantable loop recorder (up to 3 years), exercise testing and electrophysiology study with AV Wenckebach cycle length. Management is the Resuscitation Council UK / ACC/AHA/HRS 2018 bradycardia algorithm: atropine 500 mcg IV bolus (max 3 mg), second-line isoprenaline 5 mcg/min IV infusion titrated, adrenaline 1 mg IV for arrest, transcutaneous or transvenous pacing, and the definitive single-chamber (VVI) or dual-chamber (DDD) permanent pacemaker for irreversible block. Mobitz II, high-grade AV block, complete heart block and symptomatic sinus node dysfunction are Class I indications for pacing per 2018 ACC/AHA/HRS and 2013 ESC pacing guidelines. Temporary pacing is required when the cause may reverse (drug toxicity, inferior MI, post-cardiac surgery, Lyme, myocarditis) — a bridge to recovery or to definitive permanent device implantation.
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★ High yieldCardiology
Cardiogenic Shock
Cardiogenic shock (CS) is a state of end-organ hypoperfusion due to cardiac pump failure, defined for acute MI as systolic blood pressure below 90 mmHg for at least 30 minutes (or needing inotropes/vasopressors to keep it above this), cardiac index below 2.2 L/min/m2, and signs of hypoperfusion (cool peripheries, oliguria under 0.5 mL/kg/hour, altered mentation, raised lactate), with pulmonary capillary wedge pressure over 18 mmHg (confirming a cardiac cause). The commonest cause is acute MI with left ventricular failure (about 80 percent) — typically large anterior STEMI, but also right ventricular infarction and mechanical complications (papillary muscle rupture, ventricular septal rupture, free-wall rupture) at a mean of 3 to 6 days post-MI. Other causes: acute decompensated heart failure, fulminant myocarditis, end-stage cardiomyopathy, arrhythmia, valvular catastrophe (acute severe MR/AR), massive pulmonary embolism, tamponade, drug toxicity (beta-blocker, CCB, digoxin). Pathophysiology is a vicious downward spiral: myocardial injury reduces stroke volume, falling cardiac output drops systemic and coronary perfusion pressure, which worsens ischaemia, which further reduces contractility — the spiral is broken only by early reperfusion and circulatory support. The SCAI SHOCK stages (A to E) stratify severity from 'at risk' through 'extremis' and predict mortality (A roughly 4 percent, E over 80 percent). Diagnosis is clinical (hypoperfusion) plus echo (cardiac cause) plus invasive haemodynamics (PA catheter); raised lactate and low cardiac power output (CPO below 0.6 W) confirm severity. Management is the SHOCK-funnel / National Cardiogenic Shock Initiative protocol: ABCDE and oxygen; early escalation to a shock centre; bed-side echo; arterial line and PA catheter; pharmacological haemodynamic support (inotrope — dobutamine or milrinone; vasopressor — noradrenaline); prompt revascularisation (PCI within 90 minutes; culprit-lesion-only PCI per CULPRIT-SHOCK); mechanical circulatory support (IABP, Impella, VA-ECMO) as bridge to recovery, decision, transplant or LVAD. Early revascularisation reduced 6-month and 1-year mortality in the SHOCK trial (benefit confined to under-75s). Routine IABP did NOT reduce mortality in IABP-SHOCK II (demoted from Class I). Despite modern care, in-hospital mortality remains 40 to 50 percent.
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★ High yieldCardiology
Chronic Coronary Syndrome
Chronic coronary syndrome (CCS) is the modern umbrella term replacing "stable angina" for the long-term presentations of coronary artery disease. Defined by the 2019 ESC Guidelines as the spectrum of clinical presentations driven by chronic, often predictable, myocardial ischaemia typically precipitated by exertion or emotional stress and relieved by rest or sublingual nitrates. Anatomically it is the consequence of fixed or dynamic epicardial coronary stenosis (atherosclerotic plaque with intact fibrous cap), microvascular dysfunction, or vasospasm. The classic presentation is substernal chest discomfort provoked by exertion, lasting under 10 minutes, and relieved by rest or nitroglycerin (CCS grade I-IV / Canadian Cardiovascular Society grading). Diagnosis is clinical plus exclusion of ACS (serial hs-troponin negative, no dynamic ST-T changes); risk stratification uses pre-test probability, coronary CT angiography or functional stress imaging, with invasive angiography reserved for high event risk or refractory symptoms. Management rests on four pillars: (1) disease-modifying secondary prevention (aspirin, high-intensity statin with LDL target below 1.4 mmol/L in very high risk, ACE inhibitor where indicated), (2) symptom control (beta-blocker or calcium-channel blocker first-line, nitrates for acute relief, ranolazine/ivabradine second-line), (3) lifestyle and risk-factor modification, and (4) revascularisation for prognostic left-main/multivessel disease or refractory angina despite optimal medical therapy.
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★ High yieldCardiology
Dilated Cardiomyopathy
Dilated cardiomyopathy (DCM) is a disease of the heart muscle defined by dilatation and systolic impairment of one or both ventricles (LV end-diastolic dimension corrected for body surface area and sex, more than 117% of predicted; or Z-score over 2; with ejection fraction under 45%) unexplained by abnormal loading (hypertension, valve disease) or coronary artery disease sufficient to cause the impairment. It is the commonest cardiomyopathy and a leading cause of heart failure with reduced ejection fraction (HFrEF), sudden cardiac death (SCD) and heart transplantation in the young. Aetiology is genetic in 30 to 50% (titin-truncating variants TTnTV in roughly 15 to 25%), but also myocarditis (viral: coxsackie, parvovirus B19, SARS-CoV-2), alcohol, anthracycline chemotherapy (doxorubicin), peripartum, tachycardia-induced, haemochromatosis, sarcoidosis, hypothyroidism and Chagas disease (Latin America). Presentation is heart failure (dyspnoea, oedema, fatigue, S3 gallop, displaced apex), arrhythmia, thromboembolism, or incidentally (asymptomatic LV dysfunction on imaging). Diagnosis is echocardiography (dilated thin-walled LV, EF under 45%); cardiac MRI adds late-gadolinium-enhancement pattern (mid-wall, subepicardial, or diffuse) for aetiology and prognosis; family screening and genetic testing are mandatory. Management is the four pillars of HFrEF (ARNI/ACE-inhibitor, beta-blocker, MRA, SGLT2 inhibitor) + cause-specific therapy (alcohol abstinence, viral/immune myocarditis therapy, iron repletion, treat endocrine disease) + device therapy. ICD for primary prevention if EF under 35% after at least 3 months of optimal medical therapy (with the DANISH-trial caveat in non-ischaemic DCM); CRT if QRS over 150 ms with LBBB; anticoagulation if atrial fibrillation, prior thromboembolism, or LV thrombus. Cardiac transplantation for end-stage DCM.
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★ High yieldCardiology
Dyslipidaemia
Dyslipidaemia is an abnormality of circulating lipids or lipoproteins (high LDL-C/apoB, high triglycerides, low HDL-C, or elevated lipoprotein(a)). LDL-C is the primary atherogenic particle and the main target of therapy. Treatment is risk-stratified: high-intensity statin (atorvastatin 40–80 mg or rosuvastatin 20–40 mg) for established/very-high cardiovascular risk, with LDL-C under 1.4 mmol/L (ESC 2019 very-high risk). Add ezetimibe then a PCSK9 inhibitor (alirocumab/evolocumab) if target is unmet. Fibrates/icosapent ethyl treat hypertriglyceridaemia; triglycerides over 10 mmol/L risk pancreatitis.
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★ High yieldCardiology
Hypertrophic Cardiomyopathy
Hypertrophic cardiomyopathy (HCM) is an autosomal dominant sarcomere-protein mutation disease producing unexplained left ventricular hypertrophy, classically asymmetric septal. Histology shows myocyte disarray, interstitial fibrosis and intramural small-vessel disease. Dynamic left ventricular outflow tract (LVOT) obstruction with systolic anterior motion (SAM) of the mitral valve and secondary mitral regurgitation occurs in about two-thirds. The cardinal clinical threats are sudden cardiac death (SCD) in the young, diastolic heart failure, atrial fibrillation and angina from microvascular ischaemia. The bedside signature is an ejection systolic murmur at the left sternal edge that increases with Valsalva and standing and decreases with squatting — the opposite of fixed aortic stenosis. Diagnosis is by echocardiography (LV wall thickness 15 mm or more in adults, or a lower threshold in relatives), with cardiac MRI and genetic testing as core adjuncts. Beta-blockers are first-line; disopyramide or non-dihydropyridine calcium-channel blockers are second-line; septal reduction therapy (Morrow surgical myectomy or alcohol septal ablation) is reserved for drug-refractory obstructive disease; and an implantable cardioverter-defibrillator (ICD) is given to patients at high risk of SCD. The cardiac myosin inhibitor mavacamten is a new disease-modifying option for symptomatic obstructive HCM.
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★ High yieldCardiology
Long QT and Channelopathies
Long QT syndrome and the related cardiac channelopathies (Brugada, CPVT, short QT, early repolarisation) are inherited arrhythmia syndromes caused by mutations in cardiac ion-channel genes that predispose young, structurally normal hearts to syncope, torsades de pointes, ventricular fibrillation and sudden cardiac death. The dominant therapy is beta-blockade (nadolol or propranolol for LQTS and CPVT), avoidance of QT-prolonging drugs, lifestyle modification, and ICD implantation for secondary prevention or high-risk primary prevention. Acute torsades de pointes is treated with IV magnesium 2 g, defibrillation if sustained, and overdrive pacing or isoprenaline for pause-dependent forms.
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★ High yieldCardiology
Mitral Regurgitation
Mitral regurgitation (MR) is systolic backflow of blood from the left ventricle (LV) into the left atrium (LA) through an incompetent mitral valve. Chronic MR runs an asymptomatic compensated phase (LA and LV dilate, eccentric hypertrophy) before decompensation with dyspnoea, fatigue and atrial fibrillation. Acute MR (papillary-muscle or chordal rupture post-MI) presents as fulminant pulmonary oedema and cardiogenic shock. Cardinal sign: pansystolic murmur at the apex radiating to the axilla, soft S1, and a third heart sound. Diagnosis and grading are by echocardiography (EROA, regurgitant volume/fraction, vena contracta). Definitive treatment is mitral valve repair (preferred) or replacement; surgery timing rests on symptoms or LV dysfunction (EF under 60% or LV end-systolic diameter at least 40 mm). Transcatheter edge-to-edge repair (MitraClip) is an option for inoperable functional MR (COAPT).
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★ High yieldCardiology
Mitral Stenosis
Mitral stenosis (MS) is a narrowing of the mitral valve orifice that obstructs flow from the left atrium to the left ventricle during diastole. The normal mitral valve area (MVA) is 4 to 6 cm squared; symptoms emerge as the area falls (severe under 1.5, very severe under 1.0). The leading cause worldwide is rheumatic heart disease (RHD) — commissural fusion, leaflet thickening, subvalvular chordal shortening producing the fish-mouth valve. The classic triad of auscultation is a loud (tapping) S1, an opening snap after S2, and a low-pitched mid-diastolic rumble at the apex with presystolic accentuation in sinus rhythm. Pathophysiology is a rising transmitral gradient cascade: raised LA pressure transmits back through the pulmonary veins, causing pulmonary venous hypertension, reactive pulmonary arterial hypertension, right ventricular pressure overload, and right-heart failure. Atrial fibrillation develops in 40 to 60 percent and is dangerous because loss of atrial contraction and irregular ventricular rate both reduce diastolic filling and precipitate acute pulmonary oedema. Severity is graded by valve area, mean transmitral gradient, and pulmonary artery systolic pressure (PASP), not by murmur loudness. Management rests on three arms: medical (rate control with beta-blockers or digoxin, diuretic, anticoagulation), secondary rheumatic prophylaxis with benzathine penicillin G, and definitive mechanical relief by percutaneous mitral commissurotomy (PMC) or mitral valve replacement (MVR). Favourable anatomy (pliable non-calcified leaflets, no LA thrombus, no or mild MR, Wilkins score at or below 8) → PMC; unfavourable → MVR. The PMC-versus-surgery equivalence is established by the Ben Farhat (Circulation 1998) and Reyes (NEJM 1994) trials. MS with atrial fibrillation is valvular AF — warfarin INR 2 to 3; DOACs are not recommended in moderate-to-severe MS.
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★ High yieldCardiology
Non-ST-Elevation Acute Coronary Syndrome (NSTE-ACS)
Non-ST-elevation acute coronary syndrome (NSTE-ACS) is myocardial ischaemia at rest or on minimal exertion caused by a partially or intermittently occlusive intra-coronary thrombus over a disrupted atherosclerotic plaque, but without the ST elevation that mandates immediate reperfusion. It comprises NSTEMI (myocardial necrosis demonstrated by a rise and/or fall of high-sensitivity cardiac troponin with at least one value above the 99th centile) and unstable angina (ischaemia without troponin release). Diagnosis rests on the 12-lead ECG within 10 minutes plus serial high-sensitivity troponin (0-hour/1-hour or 0-hour/3-hour algorithms). Risk-stratify with the GRACE (death) and TIMI (composite endpoint) scores to triage the timing of invasive coronary angiography: immediate (within 2 hours) for very high-risk (haemodynamic instability, life-threatening arrhythmia, mechanical complication, acute heart failure, recurrent dynamic ST-T change), early (within 24 hours) for high risk (GRACE above 140, dynamic ST-T change, troponin rise-fall), and within 72 hours for intermediate risk. Every patient receives immediate dual antiplatelet therapy (aspirin 300 mg load then 75 mg daily plus ticagrelor 180 mg load then 90 mg twice daily, or prasugrel/clopidogrel) and a parenteral anticoagulant (fondaparinux 2.5 mg subcutaneous daily, enoxaparin, unfractionated heparin, or bivalirudin), a high-intensity statin (atorvastatin 80 mg) within 24 hours, and beta-blockade and an ACE inhibitor where not contraindicated. NSTE-ACS is more common than STEMI in contemporary registries and carries a long-term mortality that equals or exceeds STEMI because of the larger burden of multivessel disease and recurrent events.
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★ High yieldCardiology
Prosthetic Valves and Anticoagulation
Prosthetic heart valves are either mechanical (pyrolytic carbon bileaflet, tilting disc, or caged ball; durable for life but thrombogenic, mandating lifelong warfarin — INR 2.5 to 3.5 mitral, 2.0 to 3.0 aortic) or bioprosthetic / tissue (bovine pericardial Carpentier-Edwards, porcine Hancock; no lifelong anticoagulation but structural deterioration over 10 to 15 years). Transcatheter (TAVI/TAVR) Edwards SAPIEN and Medtronic CoreValve/Evolut serve elderly high-risk severe aortic stenosis. DOACs are contraindicated in mechanical valves (RE-ALIGN trial). Bioprosthetic valves need warfarin for 3 months then aspirin. Acute valve thrombosis is an emergency: surgery if obstructive, thrombolysis if surgery unavailable.
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★ High yieldCardiology
Pulmonary Hypertension
Pulmonary hypertension (PH) is a haemodynamic and pathophysiological syndrome defined as a mean pulmonary arterial pressure (mPAP) above 20 mmHg at rest measured by right heart catheterisation (RHC), confirmed by a pulmonary arterial wedge pressure (PAWP) of 15 mmHg or less in pre-capillary disease and pulmonary vascular resistance (PVR) above 2 Wood units (WU) in pulmonary arterial hypertension (PAH). The 2022 ESC/ERS Guidelines classify PH into five groups by aetiology: Group 1 — pulmonary arterial hypertension (PAH) (idiopathic, heritable, drug- and toxin-induced, and associated with connective tissue disease, HIV, portal hypertension, congenital heart disease); Group 2 — PH due to left heart disease (heart failure with preserved or reduced ejection fraction, valvular disease); Group 3 — PH due to lung disease or hypoxia (COPD, interstitial lung disease, sleep-disordered breathing); Group 4 — PH due to pulmonary artery obstruction (chronic thromboembolic pulmonary hypertension, CTEPH); Group 5 — PH with unclear or multifactorial mechanisms (haematological, systemic, metabolic disorders, sarcoidosis). Clinical presentation is dominated by progressive exertional dyspnoea, fatigue, pre-syncope or syncope on exertion, signs of right ventricular (RV) failure (raised JVP, peripheral oedema, hepatomegaly, ascites), and on examination a loud pulmonary component of the second heart sound (P2), a left parasternal (RV) heave, a pansystolic murmur of tricuspid regurgitation, and a right ventricular S4. The diagnostic algorithm is stepwise: transthoracic echocardiography with Doppler estimation of peak tricuspid regurgitant velocity (TR Vmax) — used to derive right ventricular systolic pressure (RVSP) — is the screening test of choice, followed by confirmation with RHC (the only definitive test, providing mPAP, PAWP, PVR, cardiac output, and vasoreactivity testing). Ventilation–perfusion (V/Q) scan is mandatory to exclude CTEPH (Group 4). The mainstay of management is risk-stratified PAH-specific therapy in Group 1 (endothelin receptor antagonists [ERAs — bosentan 62.5 mg BD for 4 weeks then 125 mg BD, ambrisentan 5 to 10 mg daily, macitentan 10 mg daily], phosphodiesterase-5 inhibitors [PDE5i — sildenafil 20 mg three times daily, tadalafil 40 mg daily], the soluble guanylate-cyclase stimulator riociguat 1 mg three times daily titrated to 2.5 mg three times daily, prostacyclin analogues [epoprostenol 1 to 2 ng/kg/min IV titrated to 10 to 20 ng/kg/min, iloprost 5 mcg inhaled 6 to 9 times daily, treprostinil subcutaneous or inhaled], and the selective IP-receptor agonist selexipag 200 mcg twice daily titrated up by 200 mcg twice daily every 2 weeks to a maximum of 1600 mcg twice daily), combined with supportive measures (oxygen, furosemide 40 mg IV or PO daily with metolazone if needed, supervised rehabilitation, iron replacement when deficient, cautious anticoagulation in selected idiopathic PAH). CTEPH (Group 4) is potentially curable by pulmonary endarterectomy, with riociguat as the only licensed medical therapy in inoperable or residual disease. Acute RV failure in PH is resuscitated with parenteral prostacyclin (epoprostenol or iloprost), cautious diuresis with furosemide 40 mg IV, inotropic support (dobutamine or milrinone) to maintain systemic blood pressure and RV perfusion, and — for refractory cases — intubation with avoidance of positive-pressure ventilation, mechanical RV support (VA-ECMO), and urgent transfer to a PH centre. Pulmonary hypertension remains a progressive disease with mortality dominated by RV failure, with five-year survival in untreated idiopathic PAH historically around 30 to 40 percent but improving to more than 60 percent at five years on modern combination therapy.
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★ High yieldCardiology
Sudden Cardiac Death
Sudden cardiac death (SCD) is the sudden, unexpected death from a cardiac cause occurring within one hour of symptom onset (witnessed), or within 24 hours of last being seen alive and well (unwitnessed). It is the leading natural cause of death in the industrialised world, accounting for roughly 300,000 to 400,000 events per year in the United States and 4 to 5 million globally. The final common pathway in 80 to 90 percent of cases is a ventricular tachyarrhythmia (rapid polymorphic VT degenerating to ventricular fibrillation), with bradyasystole and pulseless electrical activity accounting for the rest. Coronary artery disease underlies 75 to 80 percent of adult SCD; the remainder arise from cardiomyopathies (hypertrophic, dilated, arrhythmogenic right ventricular), inherited channelopathies (long QT, Brugada, CPVT), severe valvular disease, myocarditis, drug toxicity, electrolyte disturbance, anomalous coronary arteries, commotio cordis, and massive pulmonary embolism. Management is the chain of survival (early CPR, early defibrillation, early advanced life support), targeted temperature management at 32 to 36 degrees C for 24 hours, urgent coronary angiography when a cardiac cause is suspected, and ICD implantation for survivors (secondary prevention) and for high-risk primary-prevention subgroups defined by the landmark trials (MADIT, MADIT-II, MUSTT, SCD-HeFT, DINAMIT, DANISH). First-degree relatives of young SCD victims require cascade clinical and genetic screening.
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★ High yieldCardiology
Syncope
Syncope is a transient loss of consciousness (TLoC) due to transient global cerebral hypoperfusion, characterised by rapid onset, short duration, and spontaneous complete recovery without electrical brain injury. It must be separated from seizures and psychogenic collapse. The three mechanism-based categories are reflex (neurally-mediated, commonest in the young), orthostatic hypotension (drugs, volume depletion, autonomic failure), and cardiac (arrhythmic or structural — highest mortality). The initial evaluation — a focused history, eyewitness account, examination and a 12-lead ECG in every patient — yields a diagnosis in the majority. Reproduce the San Francisco Syncope Rule (CHEAT) and the Canadian Syncope Risk Score to risk-stratify; admit the high-risk group, manage vasovagal with lifestyle measures and countermanoeuvres, treat OH with volume/salt expansion and midodrine/fludrocortisone, and treat cardiac syncope by correcting the underlying arrhythmia or obstruction. Red flags: exertional, supine or unprovoked syncope, palpitations, abnormal ECG, structural heart disease, family history of sudden cardiac death (SCD) under 40.
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Psychiatry
18 topicsPsychiatry
18
★ High yieldPsychiatry
Adjustment Disorders & Grief
Adjustment disorders are emotional or behavioural symptoms arising within 3 months of an identifiable stressor, disproportionate to the stressor and causing impairment, that do not meet criteria for another mental disorder and resolve within 6 months of the stressor (or its consequences) ending. Normal grief (bereavement) is the universal human response to loss: sadness that comes in waves, longing for the deceased, preserved self-esteem and capacity for positive memories, with gradual re-engagement in life over weeks to months. Prolonged grief disorder (PGD) — added to the DSM-5-TR in 2022 and to the ICD-11 (6B42) — is intense yearning/longing for, or preoccupation with, the deceased, plus at least 3 of identity disruption, disbelief, avoidance, emotional pain, difficulty reintegrating, numbness, meaninglessness and loneliness, present most days for at least 12 months in adults (6 months in children), causing impairment beyond cultural norms. PGD affects 7 to 10 percent of bereaved people and is treated with complicated grief therapy (CGT), a 16-session dual-process treatment that outperforms interpersonal therapy and standard CBT.
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★ High yieldPsychiatry
Anxiety and Panic Disorder
Anxiety disorders are the most prevalent of all mental disorders. A panic attack is an abrupt surge of intense fear peaking within minutes with at least 4 of 13 autonomic/cognitive symptoms; it is a specifier, not a diagnosis. Panic disorder requires recurrent unexpected panic attacks followed by at least 1 month of persistent concern about further attacks, anticipatory anxiety, or maladaptive behaviour change. Generalised anxiety disorder (GAD) is excessive, difficult-to-control worry occurring more days than not for at least 6 months plus at least 3 of 6 somatic/cognitive symptoms (restlessness, fatigue, concentration, irritability, muscle tension, sleep). Lifetime prevalence: panic disorder about 2 to 5%, GAD about 5 to 6%; female 2:1; onset late teens to early 30s. First-line treatment is an SSRI (sertraline, escitalopram) — onset 4 to 6 weeks, full effect 8 to 12 weeks — combined with cognitive-behavioural therapy. Benzodiazepines are for short-term (2 to 4 weeks) rescue only because of dependence. Always exclude cardiac, thyroid and substance causes before diagnosing primary panic.
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★ High yieldPsychiatry
Attention Deficit Hyperactivity Disorder (ADHD)
ADHD is a neurodevelopmental disorder characterised by persistent, pervasive, impairing inattention, hyperactivity, and impulsivity with onset before age 12 and symptoms present in two or more settings (home, school, work). Prevalence about 5 percent of children, 2.5 percent of adults; clinic male-to-female ratio 3:1 (community 2:1); heritability 74 to 88 percent — among the highest in psychiatry. DSM-5-TR: 6+ inattention and/or 6+ hyperactivity-impulsivity symptoms in children (5+ in adults 17+), for at least 6 months, several before age 12, in 2+ settings, causing impairment, not better explained. Three presentations: predominantly inattentive, predominantly hyperactive-impulsive, combined. Treat: behavioural parent-training first for children under 6; stimulants first-line for 6+ (methylphenidate blocks dopamine/noradrenaline transporters; lisdexamfetamine promotes release — 70 to 80 percent response); atomoxetine (non-stimulant SNRI, for substance use, tics, anxiety); alpha-2 agonists (guanfacine, clonidine — hyperactivity, tics, sleep). Combined stimulant + behavioural therapy best for moderate-severe. Adult ADHD: lisdexamfetamine first-line (NICE). Monitor on stimulants: growth (height/weight 6-monthly), BP/HR, appetite, sleep, mood, tics. ADHD persists into adulthood in ~60 percent.
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★ High yieldPsychiatry
Bipolar Affective Disorder
Bipolar affective disorder is a chronic, relapsing episodic mood disorder defined by one or more manic or hypomanic episodes, usually alternating with major depressive episodes. Lifetime prevalence about 1% for Bipolar I (Bipolar spectrum up to 2 to 4%); equal sex ratio; onset 15 to 30; the most heritable major psychiatric disorder (heritability 60 to 85%). A manic episode is distinctly elevated, expansive or irritable mood with abnormally increased energy for at least 1 week; hypomania is 4 days plus, observable, no marked impairment and no psychosis. Acute mania is treated by stopping any antidepressant and giving an antipsychotic plus a mood stabiliser; lithium is the gold-standard mood stabiliser (therapeutic 0.4 to 1.0 mmol/L, narrow index), reduces relapse by about a third and suicide by up to 60%. Valproate is teratogenic (neural tube defects) and is contraindicated in women of childbearing potential; lithium carries a small Ebstein-anomaly risk. Lifetime suicide mortality is the highest of any mental disorder (about 6 to 15% die by suicide).
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★ High yieldPsychiatry
Child & Adolescent Psychiatry
Child and adolescent psychiatry covers mental disorders from birth to age 18, with every symptom assessed in developmental context against age-appropriate norms. The high-yield disorders are: Conduct disorder (CD) — a repetitive, persistent pattern of behaviour that violates the rights of others or age-appropriate norms (aggression to people/animals, destruction of property, deceit/theft, serious rule violation; at least 3 of 15 criteria in 12 months); Oppositional defiant disorder (ODD) — angry/irritable mood, argumentative/defiant behaviour, vindictiveness without aggression or rights violation; Separation anxiety disorder — excessive, developmentally inappropriate fear of separation lasting at least 4 weeks; Selective mutism — consistent failure to speak in social situations despite speaking elsewhere; Enuresis — repeated involuntary urination, age at least 5; Encopresis — repeated faecal soiling, age at least 4; and the attachment disorders (reactive attachment disorder, disinhibited social engagement disorder) that follow grossly pathogenic care. Management is built on one principle: behavioural and psychological interventions are first-line — parent training programmes (Triple P, Incredible Years, PCIT) for ODD/CD, CBT for anxiety/depression, the enuresis alarm (not drugs) for bedwetting, treating constipation first for encopresis, and safeguarding every child. Medication is a last resort in children.
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★ High yieldPsychiatry
Depression
Major depressive disorder is a common, relapsing-remitting mood disorder defined by 5 or more SIGECAPS symptoms present most of the day, nearly every day, for at least 2 weeks, including depressed mood or anhedonia. First-line treatment is an SSRI (sertraline) combined with CBT; ECT is reserved for severe, psychotic, or catatonic depression. Suicide risk must be assessed at every contact.
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★ High yieldPsychiatry
Eating Disorders
Eating disorders are persistent disturbances in eating or eating-related behaviour that impair physical health or psychosocial function and are not better explained by another disorder or a cultural practice. DSM-5-TR groups them under 'Feeding and Eating Disorders' and removed the amenorrhoea criterion for anorexia nervosa. The four examinable entities are anorexia nervosa (AN) — restriction leading to significantly low body weight with intense fear of weight gain and body-image distortion; bulimia nervosa (BN) — recurrent binge eating plus inappropriate compensatory behaviour (vomiting, laxatives, exercise, fasting) at normal weight; binge eating disorder (BED) — recurrent binges without regular compensatory behaviour; and avoidant/restrictive food intake disorder (ARFID) — food restriction driven by sensory aversion, fear of aversive consequences, or lack of interest — not by body image. Lifetime prevalence is about 1 to 4 percent in women, female-to-male roughly 10 to 1 for AN/BN (closer to 2 to 1 for BED); peak onset 15 to 19 years. Anorexia nervosa has the highest mortality of any psychiatric disorder (standardised mortality ratio about 5.9; Arcelus 2011) — deaths from cardiac arrhythmia, refeeding syndrome, medical complications, and suicide. Pathophysiology is bio-psycho-social: genetic (heritability 28 to 74 percent; GWAS shows a metabolic-psychiatric origin, Watson 2019), serotonergic and dopaminergic dysregulation, altered hypothalamic-pituitary axes, starvation-induced neuroplastic change (the 'Minnesota semi-starvation' experiment), and sociocultural thin-ideal pressure. Bedside exam: lanugo, hypothermia, bradycardia, hypotension, acrocyanosis, parotid enlargement, Russell sign (knuckle calluses from induced vomiting), dental erosion, proximal myopathy. SCOFF screens (≥2 positive = likely). Investigations: FBC, U&E (hypokalaemia from vomiting), LFTs, glucose, phosphate, magnesium, calcium, TFTs, cortisol, ECG (QTc prolongation), DEXA (osteoporosis). Management: refeeding syndrome is the time-critical medical risk — give thiamine before feeding, start calories low (about 5 to 20 kcal/kg/day, NICE/MARSIPAN/MEED), supplement phosphate, potassium, magnesium, and escalate slowly. Anorexia: weight restoration first; family-based treatment (Maudsley model) for adolescents is first-line; CBT-ED for adults; no drug is effective for the core symptoms; olanzapine may aid weight gain. Bulimia: fluoxetine 60 mg once daily is the evidence-based drug (Fluoxetine Bulimia Nervosa Collaborative Study Group 1992); CBT-ED first-line. Binge eating disorder: CBT, IPT, and lisdexamfetamine (FDA-approved). Avoid bupropion in any purging patient (seizure threshold). Compulsory admission under the Mental Health Act is used when the patient lacks capacity and the disorder is life-threatening.
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★ High yieldPsychiatry
ECT and Brain Stimulation Therapies
A source-verified, jurisdiction-aware guide to selecting, consenting, delivering and following electroconvulsive therapy, with evidence and regulatory boundaries for TMS, tES, VNS, DBS, MST and esketamine.
FRANZCPMRCPsych
★ High yieldPsychiatry
Intellectual Disability (Developmental Delay)
Intellectual disability (ID) is a neurodevelopmental disorder defined by deficits in intellectual functioning (IQ under 70) AND in adaptive functioning (conceptual, social and practical domains), with onset during the developmental period (before age 18). Severity by DSM-5 / ICD-11: mild (IQ 50 to 69, approximately 85 percent), moderate (IQ 35 to 49, 10 percent), severe (IQ 20 to 34, 3 to 4 percent), profound (IQ under 20, 1 to 2 percent). Causes are genetic (Down syndrome is the commonest chromosomal cause; Fragile X the commonest inherited single-gene cause; Rett, PKU, Prader-Willi, Angelman), prenatal (TORCH, fetal alcohol syndrome), perinatal (hypoxic-ischaemic encephalopathy, prematurity) and postnatal (meningitis, traumatic brain injury, lead, severe neglect); in about 30 percent no cause is found. Common comorbidities: epilepsy (20 to 30 percent), autism (30 to 40 percent of severe ID), ADHD, sensory impairment, mental illness (30 to 40 percent), challenging behaviour. Management: identify cause (chromosomal microarray first-line, then fragile X, metabolic, MRI/EEG), early intensive multidisciplinary intervention (speech, OT, physio, special education, positive behaviour support), symptom-targeted pharmacotherapy, family support, annual health checks, transition to adult services. There is no medication for the core cognitive deficit of ID — all drug therapy targets comorbid symptoms.
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Obsessive-Compulsive Disorder (OCD)
Obsessive-compulsive disorder (OCD) is a chronic, disabling mental disorder characterised by obsessions (intrusive, unwanted, recurrent thoughts, images or urges that cause marked anxiety or distress) and/or compulsions (repetitive behaviours or mental acts the person feels driven to perform to neutralise the obsession or prevent a dreaded outcome), that are time-consuming (over 1 hour per day) or cause clinically significant distress and impairment. Patients have insight (recognise the obsessions as irrational) but cannot resist them — this distinguishes OCD from psychosis (no insight), delusional disorder and OCPD (ego-syntonic). Common themes: contamination/washing, doubt/checking, symmetry/ordering/counting, forbidden/taboo thoughts (sexual, religious, aggressive, somatic), hoarding. Lifetime prevalence about 2 to 3 percent; onset typically adolescence to early adulthood; average 11 to 17 years delay to diagnosis because patients hide symptoms. DSM-5-TR moved OCD out of the Anxiety Disorders into its own 'Obsessive-Compulsive and Related Disorders' category (siblings: body dysmorphic disorder, hoarding disorder, trichotillomania, excoriation disorder). Treatment: ERP (exposure and response prevention) is the gold-standard psychological therapy; SSRIs at HIGH doses (higher than depression — fluoxetine up to 60 mg, sertraline 200 mg, paroxetine 60 mg, fluvoxamine 300 mg); clomipramine when SSRI fails; antipsychotic augmentation (risperidone, aripiprazole) for refractory. Sudden-onset OCD in a child: consider PANDAS (post-strep autoimmune); check ASO titre.
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★ High yieldPsychiatry
Personality Disorders
Personality disorders (PD) are enduring, inflexible, and pervasive patterns of inner experience and behaviour that deviate markedly from the expectations of the individual's culture, are stable over time, begin by adolescence or early adulthood, lead to distress or impairment, and are not better explained by another mental disorder, substance use, or a medical condition. DSM-5 groups them into three clusters: Cluster A (odd, eccentric) — paranoid, schizoid, schizotypal; Cluster B (dramatic, emotional, erratic) — antisocial, borderline, histrionic, narcissistic; Cluster C (anxious, fearful) — avoidant, dependent, obsessive-compulsive (OCPD). Borderline personality disorder (BPD) is the most clinically important and most examined: frantic efforts to avoid abandonment, unstable intense relationships, identity disturbance, impulsivity, recurrent self-harm/suicidal behaviour, affective instability, chronic emptiness, inappropriate anger, and transient stress-related paranoia or dissociation. Dialectical behaviour therapy (DBT) is first-line, with mentalization-based therapy (MBT) and schema therapy as alternatives; pharmacotherapy is symptom-targeted only, and benzodiazepines are avoided.
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Post-Traumatic Stress Disorder (PTSD)
Post-traumatic stress disorder (PTSD) is a trauma- and stressor-related disorder that develops after exposure to actual or threatened death, serious injury, or sexual violence (directly experienced, witnessed, learned about when a violent/accidental event occurred to a close other, or through repeated extreme exposure to aversive details such as in first responders). Symptoms last more than 1 month and cluster in four domains: (1) intrusion (flashbacks, nightmares, intrusive memories, distress at reminders); (2) avoidance (of internal and external reminders); (3) negative alterations in cognition and mood (negative beliefs, blame, detachment, inability to recall key aspects); and (4) alterations in arousal and reactivity (hypervigilance, exaggerated startle, irritability, sleep disturbance, recklessness). Lifetime prevalence is 6 to 9 percent of the general adult population; women are 2 to 3 times more likely than men to develop it. The neurobiology is a hyperreactive amygdala, hypoactive ventromedial prefrontal cortex, smaller hippocampus, paradoxically low cortisol with high corticotropin-releasing hormone, and noradrenergic excess. First-line treatment is trauma-focused cognitive behavioural therapy or Eye Movement Desensitisation and Reprocessing (EMDR) — at least as effective as medication; SSRIs (sertraline, paroxetine are the only two FDA-approved) are first-line pharmacotherapy; prazosin reduces trauma-related nightmares. Benzodiazepines and single-session debriefing are harmful and should not be used. ICD-11 Complex PTSD adds affect dysregulation, negative self-concept and relationship disturbance to the core picture, typically after prolonged repeated interpersonal trauma.
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Psychiatric Emergencies & Acute Agitation
Psychiatric emergencies are acute situations requiring immediate intervention to prevent harm to the patient or others. The core scenarios are: acute agitation/aggression (de-escalation first, then oral, then rapid tranquillisation — IM lorazepam, olanzapine or aripiprazole, with IM haloperidol 5–10 mg plus promethazine up to 50 mg second-line per TREC), acute psychosis (risk assessment, antipsychotic, admission if risk), suicide attempt / self-harm (medical stabilisation, psychosocial assessment before discharge), delirium (identify and treat cause; antipsychotics increase mortality in dementia), neuroleptic malignant syndrome (stop antipsychotic — this reduces mortality; dantrolene best-evidenced; 2-week washout), serotonin syndrome (stop serotonergic agents, supportive care, cyproheptadine 4–8 mg orally), lithium poisoning (saline; haemodialysis preferred when renal impairment with level over 4.0 mEq/L or dangerous features at any level), acute dystonia (anticholinergic), akathisia (mirtazapine, biperiden or vitamin B6), catatonia (parenteral lorazepam, ECT for failures), excited delirium (chemical sedation over restraint), and postpartum psychosis (emergency admission; antipsychotic plus lithium).
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Schizophrenia
Schizophrenia is a chronic major mental disorder characterised by positive symptoms (delusions, hallucinations, thought disorder), negative symptoms (flat affect, alogia, avolition, anhedonia, asociality), and cognitive impairment, causing functional decline, present for over 6 months with at least 1 month of active-phase symptoms. Lifetime prevalence about 1%; onset males 15 to 25, females 25 to 35. Dopamine hypothesis: mesolimbic hyperdopaminergia (positive), mesocortical hypodopaminergia (negative/cognitive). Atypical antipsychotics first-line (olanzapine, risperidone); clozapine for treatment-resistant schizophrenia after 2 failed adequate trials, with mandatory FBC monitoring for agranulocytosis. Watch for EPSE, NMS, metabolic syndrome, hyperprolactinaemia, QT prolongation. Lifetime suicide risk about 5%; life expectancy reduced 15 to 20 years.
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Somatic Symptom Disorder & Related Disorders
The somatic symptom and related disorders (SSRD) are a DSM-5-TR cluster defined by EXCESSIVE thoughts, feelings, and behaviours related to somatic symptoms or health concerns, NOT by absence of disease. Somatic Symptom Disorder (SSD): one or more distressing somatic symptoms plus disproportionate concern, persistent health anxiety, or excessive time/energy devoted to symptoms for at least 6 months. Illness Anxiety Disorder (IAD, hypochondriasis): preoccupation with having or acquiring a serious illness with minimal/no somatic symptoms. Conversion/FND: motor or sensory symptoms incompatible with recognised neurological disease, NOT consciously produced. Factitious = falsification/induction for the sick role; malingering = feigning for external gain. Pathophysiology: catastrophic misinterpretation of bodily sensation in a hyperactivated interoceptive network (anterior insula + ACC), reinforced by checking/reassurance/avoidance. Diagnosis is clinical (use PHQ-15 and Whiteley-7), with targeted (not shotgun) investigations. Management: CBT first-line, antidepressants (SSRIs even without depression), regular scheduled GP visits, single medical home, AVOID repeated unnecessary tests and opioids. ALWAYS reassess an acute change in a known SSD patient for genuine new disease.
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Psychiatry
Specific Phobias & Agoraphobia
Specific phobias are marked, persistent, excessive fear of a circumscribed object or situation, provoking immediate anxiety, recognised as out of proportion, leading to avoidance, lasting 6 months or more, with impairment. DSM-5 subtypes: animal, natural environment, blood-injection-injury (BII — UNIQUE: vasovagal bradycardia/syncope, not tachycardia), situational, other. Agoraphobia is marked fear of 2 or more of 5 situations where escape might be difficult or help unavailable. Treatment of choice and often curative: CBT with exposure therapy (graded / systematic desensitisation); applied tension for BII phobia; SSRIs reserved for severe/agoraphobic or comorbid cases.
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Suicide Risk Assessment & Prevention
Suicide is a leading cause of death worldwide. Risk assessment is a core clinical skill: ask directly about ideation, plan, intent, means, and preparatory acts. Risk factors (male sex, older/young adult age, psychiatric disorder — depression in 60 percent, previous attempt = strongest predictor, hopelessness, substance use, access to lethal means) are weighed against protective factors (social support, reasons for living). Risk stratification drives disposition: high risk = urgent admission; moderate = crisis team, remove means, safety plan; low = outpatient plus safety plan. ALWAYS document.
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Psychiatry
Tourette Syndrome & Tic Disorders
Tourette syndrome (TS) is a neurodevelopmental disorder defined by multiple motor tics and one or more vocal (phonic) tics, present for at least 1 year, with onset before age 18. Tics are sudden, rapid, recurrent, non-rhythmic movements or vocalisations that are temporarily suppressible and usually preceded by a premonitory urge (a building internal sensation that the tic transiently relieves). Motor tics classically begin in the head and neck (eye blinking, facial grimacing, head jerking, shoulder shrugging) and march caudally over years; vocal tics follow (throat clearing, sniffing, grunting; coprolalia in only 8 to 15 percent). Tics wax and wane, peak in severity around 10 to 12 years, and improve substantially in adolescence and adulthood in about two-thirds. Comorbidity is the rule: ADHD in about 60 percent (the commonest and most impairing comorbidity) and OCD in 30 to 50 percent. The popular stereotype of involuntary swearing affects only a minority and is the single biggest misconception. Management is stepwise: education and reassurance for mild tics; Comprehensive Behavioural Intervention for Tics (CBIT) / Habit Reversal Training (HRT) first-line for impairing tics; alpha-2 agonists (clonidine, guanfacine) first-line drug (also treat ADHD); antipsychotics (risperidone, aripiprazole) for severe tics; botulinum toxin for focal disabling tics; deep brain stimulation only for severe refractory adult disease.
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Haematology
3 topicsHaematology
3
★ High yieldHaematology
Anaemia
Anaemia (low Hb for age, sex and physiological state) is not a diagnosis but a sign of disease. The examinable skill is the MCV-based framework — microcytic (iron deficiency, thalassaemia, anaemia of chronic disease, sideroblastic, lead), normocytic (acute blood loss, anaemia of chronic disease, haemolysis, aplastic, mixed deficiency) and macrocytic (megaloblastic B12/folate, alcohol, liver disease, hypothyroid, MDS, drugs) — plus the reticulocyte count splitting causes into underproduction versus destruction/loss. Iron deficiency (most common worldwide): ferritin is the most powerful single test; oral iron is given both to correct anaemia and replenish stores (alternate-day dosing improves fractional absorption), parenteral iron when oral is not tolerated, and always find the cause (GI blood loss until proven otherwise in men and post-menopausal women). Megaloblastic anaemia (B12/folate): hypersegmented neutrophils, macro-ovalocytes, pancytopenia — treat B12 deficiency without delay to avoid neurological impairment; parenteral B12 is standard and oral 2000 micrograms daily is effective. Transfuse at restrictive thresholds (Hb under 7 g per dL in stable critical illness; symptoms-guided in older cardiovascular-risk patients) — restrictive is at least as safe as liberal.
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Asplenia and Post-Splenectomy Care
Asplenia (surgical, congenital, or functional from sickle cell) predisposes to overwhelming post-splenectomy infection (OPSI) from encapsulated organisms (Strep pneumoniae, Neisseria meningitidis, Haemophilus influenzae). Management: vaccination (PCV13, PPSV23, MenACWY, MenB, Hib) at least 2 weeks before elective splenectomy or 2 weeks after emergency; lifelong daily antibiotic prophylaxis (phenoxymethylpenicillin 250 to 500 mg BD, or amoxicillin); patient education and alert card; prompt empirical antibiotics for fever (ceftriaxone 2 g IV/IM).
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Haemolytic Anaemia
Haemolytic anaemia is anaemia caused by premature destruction of red blood cells (lifespan shortened from the normal 120 days) at a rate that exceeds marrow compensation. Classify by site (intravascular vs extravascular) and by origin (inherited vs acquired). Biochemical signature: raised reticulocytes, raised LDH, raised unconjugated bilirubin, low/absent haptoglobin, with haemoglobinaemia/haemoglobinuria in intravascular forms. The direct antiglobulin (DAT/Coombs) test is the single most important discriminator: positive = immune (warm IgG AIHA, cold IgM agglutinin, paroxysmal cold haemoglobinuria), negative = non-immune (hereditary spherocytosis, G6PD deficiency, PNH, microangiopathic, sickle cell, thalassaemia). Management is cause-specific: warm AIHA — prednisolone 1–1.5 mg/kg; cold agglutinin — avoid cold + rituximab; hereditary spherocytosis — folate +/- splenectomy (vaccinate before); G6PD — avoid triggers; PNH — eculizumab/ravulizumab; MAHA — treat underlying (TTP = plasma exchange + caplacizumab).
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emergency-toxicology
2 topicsemergency-toxicology
2
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Anaphylaxis
Anaphylaxis is a severe, life-threatening systemic hypersensitivity reaction that is rapid in onset (minutes to hours) and may cause death. It is a CLINICAL diagnosis — treat on suspicion. FIRST-LINE treatment is INTRAMUSCULAR ADRENALINE 0.5 mg (adult) into the anterolateral thigh, repeat after 5 minutes. Position the patient SUPINE with legs elevated (never sit/stand). Adjuncts (antihistamine, corticosteroid, oxygen, IV fluid) come AFTER adrenaline. Observe for 6 to 12 hours because a BIPHASIC reaction recurs in up to 15 percent of cases. Discharge with TWO adrenaline autoinjectors, an action plan, and an allergy referral.
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Opioid Overdose
Opioid overdose produces the opioid (narcotic) triad: depressed consciousness/coma, respiratory depression (bradypnoea), and pinpoint pupils (miosis). Diagnosis is clinical plus response to naloxone. Resuscitate with bag-valve-mask ventilation and oxygen FIRST, then give naloxone (a competitive mu-opioid receptor antagonist) titrated to respiratory rate, not full alertness. Because naloxone's half-life (1 to 2 h) is shorter than most opioids, monitor for re-narcotisation for at least 2 to 4 h (24 to 48 h for methadone, sustained-release formulations, and fentanyl).
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Rheumatology
8 topicsRheumatology
8
★ High yieldRheumatology
Ankylosing Spondylitis
Ankylosing spondylitis (AS) is a chronic, progressive inflammatory disease of the axial skeleton and entheses — the prototype of the seronegative spondyloarthropathies. Strongly associated with HLA-B27 (about 90 percent). Presents as inflammatory back pain (insidious onset under 40 years, worse with rest, better with exercise, morning stiffness over 30 minutes, alternating buttock pain) with sacroiliitis (often bilateral and symmetric) and, late, a bamboo spine. Extra-articular: acute anterior uveitis (unilateral painful red eye), aortic regurgitation, apical lung fibrosis, secondary amyloidosis. Diagnosis by the modified New York criteria (1984) for established AS, or the ASAS 2009 criteria for the wider axial spondyloarthritis spectrum (which includes non-radiographic disease detectable on MRI). Management: continuous full-dose NSAIDs plus physiotherapy first-line; TNF inhibitors (adalimumab, etanercept, infliximab, golimumab, certolizumab) or IL-17 inhibitors (secukinumab, ixekizumab) for active disease; total hip replacement for hip arthritis. Treat to target: ASDAS under 1.3 or low disease activity.
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Rheumatology
Calcium Pyrophosphate Deposition Disease (CPPD / Pseudogout)
Calcium pyrophosphate deposition (CPPD) disease is a crystal-deposition arthritis caused by calcium pyrophosphate dihydrate (CPP) crystals forming in articular cartilage and fibrocartilage (chondrocalcinosis) and shedding into joints. It is the commonest crystal arthritis of the elderly and the second commonest overall after gout. Prevalence rises sharply with age, reaching 30 to 60 per cent in those over 85. Presentation is a spectrum: acute CPP arthritis ('pseudogout') mimicking gout (classically the knee, wrist); chronic CPP crystal inflammatory arthritis (RA-like); osteoarthritis with CPPD (pseudo-OA); or asymptomatic chondrocalcinosis. Associations are ageing, osteoarthritis and metabolic triggers (hyperparathyroidism, haemochromatosis, hypothyroidism, hypomagnesaemia) — screen for these in younger (under 55) patients. Diagnosis: rhomboid, weakly positively birefringent crystals plus chondrocalcinosis on X-ray. Treatment mirrors gout (NSAIDs, colchicine, intra-articular or oral corticosteroid); treat the metabolic cause; always aspirate acute monoarthritis to exclude sepsis. Unlike gout, no drug dissolves CPP crystals.
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Fibromyalgia
Fibromyalgia is a chronic disorder of central pain processing (nociplastic pain) causing widespread musculoskeletal pain, fatigue, unrefreshing sleep, cognitive dysfunction ('fibro-fog') and multiple somatic symptoms (irritable bowel, headache, dysmenorrhoea), with no tissue inflammation or damage. Predominantly women, onset 30 to 60 years; often triggered by physical or emotional stress, infection, trauma. Strongly associated with depression, anxiety and other functional syndromes. Examination is normal apart from tenderness; investigations are normal (rule out mimics). Diagnosis is clinical — Widespread Pain Index (WPI) plus Symptom Severity Scale (SSS), lasting over 3 months, with no alternative explanation. Management is non-pharmacological first (education, graded aerobic exercise, CBT, sleep hygiene) and pharmacological adjunct (duloxetine, pregabalin, amitriptyline). Avoid opioids. Treat comorbid depression and anxiety.
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Giant Cell Arteritis
Giant cell arteritis (GCA, temporal arteritis) is the most common primary vasculitis in adults over 50, affecting large and medium arteries (especially the extracranial branches of the carotid, particularly the temporal arteries, and the aorta and its branches). Symptoms: new-onset headache, scalp tenderness, jaw claudication, visual disturbance (ischaemic optic neuropathy, amaurosis fugax, diplopia), constitutional symptoms, polymyalgia rheumatica. Diagnosis: ESR/CRP markedly elevated; temporal artery biopsy confirms. Treatment: high-dose corticosteroids started immediately on clinical suspicion (do not wait for biopsy); tocilizumab for relapse or steroid-sparing.
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Gout
Gout is a crystal-deposition disease caused by monosodium urate (MSU) crystal accumulation in joints and soft tissues, the end result of chronic hyperuricaemia. It is the commonest inflammatory arthritis in adults. The clinical spectrum runs from asymptomatic hyperuricaemia to explosive acute monoarthritis (classically the first MTP — podagra), through intercritical periods, to chronic tophaceous gout with erosive joint destruction, urate nephropathy and uric acid urolithiasis. Risks: male sex, obesity, metabolic syndrome, CKD, alcohol (especially beer), high-purine diet, fructose, diuretics, cyclosporin, lead. The diagnostic hallmark is the negatively birefringent, needle-shaped monosodium urate crystal on polarised-light microscopy of synovial fluid. Acute attacks are treated with an anti-inflammatory-dose NSAID, low-dose colchicine or corticosteroid (all equally first-line, chosen by comorbidity). Long-term urate-lowering therapy (allopurinol first-line) is titrated to a target serum urate below 6 mg/dL (360 micromol/L), with low-dose colchicine prophylaxis against mobilisation flares.
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Rheumatoid Arthritis
Rheumatoid arthritis (RA) is a chronic, symmetric, erosive, autoimmune polyarthritis of unknown cause that preferentially targets the synovial small joints (MCP, PIP, wrists, MTP), spares the DIP, and produces morning stiffness lasting more than 1 hour. Diagnosis is clinical plus anti-CCP antibody (highly specific) and characteristic X-ray erosions; disease activity is graded with the DAS28. Management is treat-to-target to remission or low disease activity, beginning with methotrexate (weekly + folic acid) and escalating through csDMARDs, bDMARDs (anti-TNF, anti-IL-6, anti-CD20, abatacept) and tsDMARDs/JAK inhibitors. Untreated disease causes deformity, disability, atlantoaxial subluxation and premature cardiovascular death.
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Sjogren's Syndrome
Sjogren's syndrome is a chronic systemic autoimmune epithelitis characterised by focal lymphocytic infiltration of exocrine glands leading to sicca syndrome (dry eyes plus dry mouth), with variable extraglandular involvement. It is the second most common autoimmune rheumatic disease after rheumatoid arthritis, with a 9 to 1 female preponderance and peak onset at age 40 to 60. Anti-Ro/SSA is the key serological marker. Primary Sjogren's is classified by the ACR/EULAR 2016 weighted score of at least 4. Management is symptomatic first (artificial tears, saliva substitutes, secretagogues such as pilocarpine 5 mg four times daily), with immunosuppression reserved for organ-threatening disease. Lifelong surveillance for B-cell (MALT) lymphoma is essential.
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Systemic Lupus Erythematosus
Systemic lupus erythematosus (SLE) is a multisystem autoimmune disease driven by loss of self-tolerance, autoantibody formation (ANA, anti-dsDNA, anti-Sm), immune complex deposition, and type I interferon activation. 9:1 female predominance, peak 15-45 years, worse in African, Hispanic, Asian populations. Classification: EULAR/ACR 2019 (ANA entry + additive weighted criteria, score 10+). Manifestations span skin (malar rash sparing nasolabial folds, discoid, photosensitivity), joints (non-erosive, Jaccoud), kidneys (lupus nephritis ISN/RPS class I-VI), serosae (pericarditis, pleuritis), CNS (neuropsychiatric lupus), blood (cytopenias, antiphospholipid), and heart (Libman-Sacks endocarditis). Management: hydroxychloroquine for ALL patients; NSAIDs and short-course steroids for flares; mycophenolate, cyclophosphamide, azathioprine for organ disease; belimumab, anifrolumab, rituximab for refractory. Treat-to-target: remission or low disease activity.
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haematology
4 topicshaematology
3
★ High yieldhaematology
Aplastic Anaemia
Aplastic anaemia is a life-threatening bone marrow failure syndrome defined by pancytopenia (anaemia + neutropenia + thrombocytopenia) with a markedly hypocellular marrow and no abnormal infiltrate. Most cases are acquired and idiopathic (immune-mediated); recognised triggers include drugs (chloramphenicol, carbamazepine, NSAIDs), toxins (benzene, radiation), and viruses (seronegative hepatitis, EBV, parvovirus B19, HIV); inherited forms include Fanconi anaemia and dyskeratosis congenita. Presents with fatigue, bleeding and infection in a well-looking patient without organomegaly. Diagnose with full blood count, film, reticulocyte count and a trephine biopsy (cellularity under 25 percent). Severe AA (Camitta criteria): cellularity under 25 percent plus at least two of neutrophils under 0.5, platelets under 20, reticulocytes under 20 (all x 10^9/L). Treat young patients (under 40) with an HLA-matched sibling donor by allogeneic haematopoietic stem cell transplant; everyone else with horse anti-thymocyte globulin plus ciclosporin, plus eltrombopag in selected cases. Supportive care: transfusions, neutropenic-sepsis antibiotics, infection prophylaxis.
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Chronic Leukaemia (CLL & CML)
Chronic leukaemia encompasses two distinct indolent clonal marrow stem-cell disorders. Chronic lymphocytic leukaemia (CLL) is a CD5-positive B-cell neoplasm of mature-appearing lymphocytes (lymphocytosis over 5×10⁹/L, smudge cells, lymphadenopathy, splenomegaly), staged by Rai or Binet, treated only when symptomatic (watch-and-wait early), with FCR chemoimmunotherapy or targeted agents (ibrutinib BTK inhibitor, venetoclax BCL2 inhibitor). Chronic myeloid leukaemia (CML) is a BCR-ABL1 myeloproliferative neoplasm driven by the Philadelphia chromosome t(9;22), characterised by leucocytosis with left shift, basophilia, splenomegaly and low LAP score, divided into chronic, accelerated and blast-crisi…
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haematology
Hereditary Haemochromatosis
Hereditary haemochromatosis (HH) is an autosomal recessive disorder of iron homeostasis causing inappropriate, unregulated intestinal iron absorption that progressively deposits in parenchymal organs — liver (cirrhosis, hepatocellular carcinoma), pancreas (diabetes), heart (cardiomyopathy, arrhythmia), skin (bronzing), joints (arthropathy), pituitary and gonads (hypogonadism). The commonest cause is homozygous C282Y mutation in the HFE gene on chromosome 6p (Type 1). Screen with transferrin saturation over 45 percent and serum ferritin; confirm with HFE genetic testing. Cornerstone treatment is therapeutic venesection (phlebotomy) to target ferritin 50 to 100 micrograms per litre, with iron chelation reserved for those who cannot be venesected. Treated before cirrhosis, life expectancy is normal.
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Haematology
1
cardiology
8 topicscardiology
8
cardiology
Arrhythmogenic Cardiomyopathy
Arrhythmogenic cardiomyopathy (ACM) is an inherited heart-muscle disease in which progressive fibro-fatty replacement of ventricular myocardium (classically the right ventricle) produces ventricular arrhythmias, heart failure and sudden cardiac death (SCD) in apparently healthy young people — most notably competitive athletes. Inheritance is usually autosomal dominant and the genes are predominantly desmosomal (PKP2 plakophilin-2, DSP desmoplakin, DSG2 desmoglein-2, DSC2 desmocollin-2, JUP plakoglobin); non-desmosomal genes include TMEM43, LMNA, PLN, DES, CDH2, SCN5A, CTNNA3. The ECG hallmark is the epsilon wave (a low-amplitude deflection at the end of the QRS in V1-V3) with T-wave inversion V1-V3 (without RBBB); cardiac MRI shows RV dilatation, regional wall-motion abnormalities and late gadolinium enhancement. Diagnosis uses the 2010 Modified Task Force Criteria (six categories — imaging, biopsy, repolarisation, depolarisation, arrhythmia, family history) refined by the 2020 Padua criteria for CMR quantification. Management combines lifestyle restriction (no competitive or endurance sport), beta-blockade (sotalol, metoprolol, bisoprolol), ICD for the high-risk (sustained VT, aborted SCD, severe RV/LV dysfunction, unexplained syncope), catheter ablation of drug-refractory VT, and heart failure therapy / transplantation for the burnt-out phase.
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★ High yieldcardiology
Mitral Valve Prolapse
Mitral valve prolapse (MVP) is the systolic billowing of one or both mitral leaflets above the mitral annulus into the left atrium, defined echocardiographically as leaflet displacement of at least 2 mm beyond the mitral annular plane in the parasternal long-axis view during systole. The underlying pathology is myxomatous degeneration of the leaflet (proteoglycan-rich matrix, fragmented collagen) with chordal elongation and often annular dilatation or mitral annular disjunction (MAD). MVP is the commonest primary valve abnormality in developed countries, with a population prevalence of 2 to 3 percent and a 2:1 female predominance in classic (younger) forms. Clinically, two morphological phenotypes are recognised: fibroelastic deficiency (younger patients, thinner leaflets, focal prolapse, often P2 scallop, sudden chordal rupture, acute MR) and diffuse myxomatous Barlow's disease (multisegmental billowing, bileaflet, redundant tissue, marked annular dilatation, chronic severe MR). Most patients are asymptomatic; the classic clinical triad is the mid-systolic click and late systolic murmur that responds to dynamic manoeuvres: the click moves earlier with Valsalva and standing (reduced preload — leaflet prolapses sooner) and later with squatting (raised preload — leaflet prolapses later). Symptoms — when present — include palpitations (often PVCs, NSVT), atypical chest pain, dyspnoea on exertion, fatigue, syncope and panic-like attacks; a small but important subset has arrhythmic MVP with MAD and ventricular tachycardia/fibrillation and sudden cardiac death. The 2020 ACC/AHA valvular heart disease guideline and the 2014 AHA/ACC VHD guideline (Nishimura, Otto) anchor management, and the EHRA expert consensus (2022) addresses arrhythmic MVP. Diagnosis is transthoracic echo (TTE) with leaflet displacement, MR severity (EROA, regurgitant volume), LV size and function, MAD and pulmonary pressures; transoesophageal echo (TOE) refines repair planning. Treatment is risk-stratified — reassurance for asymptomatic patients, beta-blocker for symptoms, endocarditis prophylaxis only for the highest-risk, and mitral valve surgery (repair preferred over replacement) for severe MR, LV dysfunction, new AF or endocarditis.
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Myocarditis
Myocarditis is an inflammatory disease of the myocardium confirmed by histological, immunological and immunohistochemical criteria, most commonly caused by viruses (coxsackievirus B3, adenovirus, parvovirus B19, enteroviruses, SARS-CoV-2). It presents with a clinical triad of chest pain, heart-failure symptoms and arrhythmia, frequently after a viral prodrome 1 to 2 weeks earlier. Diagnosis is suspected on chest pain plus raised high-sensitivity troponin with normal coronary angiography, and confirmed by cardiac MRI using the Lake Louise Criteria; endomyocardial biopsy remains the gold standard. Management is predominantly supportive (heart-failure therapy, arrhythmia control, activity restriction) — NSAIDs are avoided; giant cell, eosinophilic and sarcoid myocarditis respond to immunosuppression. Most patients recover fully; a minority progress to dilated cardiomyopathy or suffer sudden cardiac death, especially athletes.
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Pericardial Disease
Pericardial disease spans three overlapping syndromes: acute pericarditis (inflammation of the pericardium with pleuritic chest pain, pericardial rub and diffuse ST elevation with PR depression), pericardial effusion with cardiac tamponade (fluid under pressure impairing diastolic filling; Beck triad, pulsus paradoxus), and constrictive pericarditis (chronic thickening producing Kussmaul sign and a pericardial knock). Commonest cause is idiopathic/viral; in India TB pericarditis is a major differential. Diagnose clinically plus ECG; echocardiography is the key imaging. Treat acute pericarditis with high-dose NSAIDs plus colchicine 0.5 mg once or twice daily (weight-based) for 3 months; corticosteroids are NOT first-line (raise recurrence). Tamponade is drained by echo-guided pericardiocentesis; constriction needs pericardiectomy.
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cardiology
Restrictive Cardiomyopathy
Restrictive cardiomyopathy (RCM) is the rarest of the three WHO cardiomyopathies, defined by non-compliant, stiff ventricles that resist filling in diastole, with reduced diastolic volume and preserved (or near-normal) systolic function, producing biventricular diastolic heart failure with bi-atrial enlargement. Leading cause in the developed world is cardiac amyloidosis (AL light-chain, and ATTR — wild-type/senile and hereditary variant); other causes are sarcoidosis, haemochromatosis, endomyocardial fibrosis (EMF) / Loffler endocarditis, radiation, carcinoid heart disease, glycogen storage diseases (Fabry, Pompe, Danon) and scleroderma. Presents with right-heart-failure signs (raised JVP, Kussmaul's sign, hepatomegaly, ascites, oedema), dyspnoea, fatigue and atrial fibrillation, in a patient with preserved EF. Differentiate from constrictive pericarditis by BNP (high in RCM, low in constriction), pericardial calcification (constriction only), septal bounce (constriction) and the square-root sign in both. Investigate with ECG (low voltages with thick walls = amyloid), echo (bi-atrial enlargement, granular myocardium, restrictive mitral inflow, low tissue e'), cardiac MRI (diffuse subendocardial LGE, T1/ECV mapping), serum free light chains for AL, bone-tracer scintigraphy for ATTR, and endomyocardial biopsy (gold standard). Treat the underlying cause; tafamidis 61 mg daily for ATTR-CM (ATTR-ACT trial); CyBorD/daratumumab for AL; steroids for sarcoid; phlebotomy/chelation for haemochromatosis. Cautious diuretics; avoid digoxin and calcium-channel blockers in amyloid. Heart transplant for end-stage.
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★ High yieldcardiology
Supraventricular Tachycardia
Supraventricular tachycardia (SVT) is a rapid, usually regular tachyarrhythmia originating at or above the atrioventricular (AV) node with a narrow QRS (under 120 ms) and a rate usually 150 to 250 bpm. The two re-entrant mechanisms dominate: AV nodal re-entrant tachycardia (AVNRT) — a circuit within the AV node using dual slow-fast pathways (commonest, ~60%) — and AV re-entrant tachycardia (AVRT) — a circuit using an accessory pathway bypassing the AV node, classically Wolff-Parkinson-White (WPW). Presents with paroxysmal palpitations of abrupt onset/offset, dyspnoea, lightheadedness and, characteristically, polyuria after termination. Management: if haemodynamically unstable — synchronised DC cardioversion; if stable — modified Valsalva manoeuvre, then IV adenosine 6 mg rapid bolus escalating to 12 mg then 12 mg. IV verapamil or a beta-blocker if adenosine is contraindicated. Catheter ablation is curative and first-line for recurrent disease. WPW with pre-excited atrial fibrillation is an emergency: avoid all AV-nodal-blocking agents (adenosine, verapamil, diltiazem, beta-blockers, digoxin) — they preferentially conduct down the accessory pathway and can precipitate ventricular fibrillation; use flecainide/amiodarone or DC cardioversion.
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★ High yieldcardiology
Venous Thromboembolism
Venous thromboembolism (VTE) is the combined disease of deep vein thrombosis (DVT) and pulmonary embolism (PE) — a single pathophysiological continuum in which a thrombus, most often originating in the deep veins of the lower limb, propagates or embolises through the right heart into the pulmonary arterial tree. It is the third commonest cardiovascular disease after acute MI and stroke, with an annual incidence of 1 to 2 per 1000 adults, rising sharply after the age of 70. The pathophysiological substrate is Virchow's triad — venous stasis, endothelial injury and hypercoagulability — and a single episode may be provoked (recent surgery, immobility, cancer, pregnancy, oestrogen, hospitalisation) or unprovoked (idiopathic, often the first signal of an occult cancer or thrombophilia). DVT presents with unilateral leg swelling, pain, pitting oedema, warmth and erythema along the deep venous distribution; proximal (iliofemoral) DVT carries a 50 percent risk of embolisation if untreated, whereas distal (calf) DVT carries a much lower embolic risk. PE presents with pleuritic chest pain, dyspnoea, tachycardia and tachypnoea; massive PE (about 5 percent — hypotension, syncope, cardiac arrest) has a mortality of over 30 percent untreated, falling to 6 to 8 percent with thrombolysis; submassive (intermediate-risk) PE (about 25 percent — RV strain on echo or CT, raised troponin/BNP) has a 30-day mortality of 3 to 15 percent; low-risk PE is normotensive without RV dysfunction. Diagnosis uses the Wells score for clinical probability, D-dimer (rule-out in low/moderate probability), compression ultrasound for DVT, and CT pulmonary angiography as the gold standard for PE. Treatment is prompt anticoagulation — DOACs (apixaban, rivaroxaban, dabigatran, edoxaban) first-line for the majority (Konstantinides 2019 ESC, Witt 2018 ASH), LMWH for cancer-associated VTE and pregnancy (still preferred in some cancer settings per Agnelli 2020 ADAM VTE), with systemic thrombolysis (alteplase 100 mg over 2 hours, or 0.6 mg/kg over 15 minutes in arrest) for massive / high-risk PE and rescue/catheter-directed thrombolysis for selected intermediate-risk PE (PEITHO). The complications are chronic thromboembolic pulmonary hypertension (CTEPH, incidence about 2 to 4 percent after PE — Pengo), post-thrombotic syndrome (up to 50 percent after proximal DVT), recurrent VTE (about 10 percent at 1 year, 25 percent at 5 years after unprovoked VTE), and anticoagulant-associated bleeding (major bleed rate 1 to 2 percent per year on DOACs).
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★ High yieldcardiology
Ventricular Tachyarrhythmias
Ventricular tachyarrhythmias are rapid rhythms originating below the bundle of His that produce a broad QRS complex and span a continuum from monomorphic ventricular tachycardia (VT) through polymorphic VT (including torsades de pointes) to ventricular fibrillation (VF). Sustained VT with pulse is treated with IV procainamide 10 mg/kg or amiodarone 5 mg/kg over 20 minutes (PROCAMIO) if stable, or synchronised DC cardioversion if unstable; pulseless VT and VF are shockable rhythms managed by the ALS algorithm (immediate unsynchronised defibrillation, high-quality CPR, epinephrine, and amiodarone 300 mg IV after three or more failed shocks). Long-term prevention is the implantable cardioverter-defibrillator (ICD): primary prevention at LVEF 35% or less in NYHA II–III heart failure (SCD-HeFT) or EF 30% or less post-MI (MADIT-II), deferred within 40 days of MI (DINAMIT). Torsades is treated by stopping the offending drug and giving IV magnesium sulfate, the treatment of choice. The single highest-yield exam rule: any broad-complex tachycardia in a patient with structural heart disease is VT until proven otherwise; the Vereckei aVR criteria (initial R wave, AV dissociation, vi/vt of 1 or less) confirm VT.
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Gastroenterology
7 topicsGastroenterology
7
★ High yieldGastroenterology
Ascites and Spontaneous Bacterial Peritonitis
Ascites is the pathological accumulation of fluid in the peritoneal cavity and the most common presentation of decompensated cirrhosis. The serum-ascites albumin gradient (SAAG) of 1.1 g/dL or more separates portal-hypertensive from non-portal causes. Spontaneous bacterial peritonitis (SBP) is a monomicrobial infection of ascitic fluid without an obvious intra-abdominal source, defined by an ascitic polymorphonuclear neutrophil count of 250 cells/mm3 or more, treated with a third-generation cephalosporin (cefotaxime 2 g IV every 8 hours) plus intravenous albumin (1.5 g/kg on day 1 and 1 g/kg on day 3). Ascites management is built on sodium restriction, combined spironolactone with furosemide, large-volume paracentesis with albumin, TIPS for refractory ascites, and liver transplantation.
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★ High yieldGastroenterology
Chronic Pancreatitis
Chronic pancreatitis (CP) is a progressive, inflammatory, fibrotic disease of the pancreas producing irreversible morphological damage with permanent loss of exocrine (acinar) and endocrine (islet) function. Commonest cause worldwide is alcohol (60 to 70 percent); tobacco is an independent co-factor; tropical calcific pancreatitis dominates in southern India; hereditary (PRSS1), autoimmune (IgG4) and obstructive subtypes complete the spectrum (TIGAR-O classification). Presents with the classic triad of recurrent epigastric pain radiating to the back, steatorrhoea, and diabetes with weight loss; atypical painless CP presents with new diabetes and cachexia. Diagnosis rests on a combination of structural imaging (calcification, ductal change, atrophy) and functional testing (faecal elastase under 200); there is no single gold standard. Management is multidisciplinary: alcohol and smoking cessation, stepwise analgesia, pancreatic enzyme replacement (PERT: pancreatin 25,000 to 40,000 units lipase per meal with a PPI), insulin for type 3c diabetes, then endoscopic (ESWL, stenting) and surgical (Puestow drainage for duct over 7 mm, resection for head mass) options for refractory pain; corticosteroids for autoimmune pancreatitis. Complications include pseudocyst, biliary stricture, splenic vein thrombosis with isolated gastric varices (splenectomy curative), pseudoaneurysm with catastrophic bleed, and pancreatic cancer (cumulative risk around 4 percent at 20 years). Prognosis: progressive, life expectancy shortened by 10 to 20 years.
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★ High yieldGastroenterology
Cirrhosis
Cirrhosis is the diffuse, irreversible distortion of hepatic architecture by fibrosis and regenerative nodules that follows chronic hepatocellular injury. It is the final common pathway of virtually every chronic liver disease (alcohol, viral hepatitis B/C, MASLD, autoimmune, cholestatic, metabolic, vascular). Clinically it is divided into a long compensated phase (asymptomatic with stigmata) and a decompensated phase defined by ascites, variceal haemorrhage, hepatic encephalopathy and jaundice. The pathophysiology centres on portal hypertension (mechanical distortion plus dynamic vasoconstriction) and loss of hepatocellular mass (synthetic and detoxification failure). Diagnosis is clinical, biochemical (low albumin, raised INR, thrombocytopenia), radiological (nodular liver, splenomegaly) and by elastography (liver stiffness over 12 to 15 kPa). Severity is graded by Child-Pugh and MELD-Na. Management is treat the cause, prevent decompensation (NSBB, HCC surveillance), and manage each complication — with liver transplantation as the definitive therapy.
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★ High yieldGastroenterology
Coeliac Disease
Coeliac disease is a chronic, immune-mediated small-intestinal enteropathy triggered by gluten (prolamins — gliadin in wheat, hordein in barley, secalin in rye) in genetically predisposed (HLA-DQ2/DQ8) individuals. Presents across a spectrum from classical malabsorption (diarrhoea, weight loss, bloating, steatorrhoea) to atypical/extraintestinal disease (iron-deficiency anaemia, osteoporosis, aphthous ulcers, short stature, dermatitis herpetiformis, transaminitis) and silent/latent forms found on screening. Diagnosis requires serology while on a gluten-containing diet — anti-tissue transglutaminase IgA (anti-tTG IgA, most sensitive ~90–95%) and anti-endomysial IgA (EMA, most specific ~99%) — PLUS a total IgA to exclude selective IgA deficiency (5–10x more common in coeliac); in IgA deficiency use anti-deamidated gliadin peptide (DGP) IgG. Diagnosis is confirmed by duodenal biopsies (greater than or equal to 6 biopsies from bulb and distal duodenum) showing villous atrophy, crypt hyperplasia and intraepithelial lymphocytosis — graded by the Marsh classification (0 to 3c). Definitive treatment is a strict lifelong gluten-free diet (GFD) (avoid wheat, barley, rye; oats if uncontaminated, Codex threshold under 20 ppm). Correct deficiencies (iron, B12, folate, calcium, vitamin D), vaccinate against encapsulated organisms (functional hyposplenism), and monitor annually. Refractory coeliac disease and enteropathy-associated T-cell lymphoma (EATL) are the feared complications. Never start a gluten-free diet before serology and biopsy — it sero-negatives the work-up.
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Gastroenterology
Gastro-Oesophageal Reflux Disease (GORD)
Gastro-oesophageal reflux disease (GORD) is the condition in which stomach content refluxes into the oesophagus causing troublesome symptoms and/or complications. The cardinal symptoms are retrosternal burning (heartburn) and acid regurgitation; atypical features include chest pain, chronic cough, laryngitis, dental erosion and worsening asthma. Two endoscopic phenotypes: erosive reflux disease (ERD) with visible mucosal breaks graded by the Los Angeles classification (A to D), and non-erosive reflux disease (NERD) (normal mucosa). Pathophysiology centres on transient lower-oesophageal sphincter relaxations (TLESRs), a weak/hypotensive LES, hiatus hernia, impaired oesophageal clearance and delayed gastric emptying. Diagnosis is clinical, confirmed by empirical PPI trial; endoscopy for alarm features or persistent symptoms; ambulatory pH / pH-impedance monitoring (acid exposure time over 6 percent is conclusive — Lyon Consensus 2.0). Management is stepwise: lifestyle, antacids / alginates, H2-receptor antagonists, then proton-pump inhibitors (PPIs) as first-line — omeprazole 20 mg once daily for 4 to 8 weeks. Refractory disease: double-dose PPI, then anti-reflux surgery (Nissen fundoplication) or endoscopic therapy. Barrett oesophagus (intestinal metaplasia of the distal oesophagus) is the key premalignant complication driving adenocarcinoma surveillance.
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★ High yieldGastroenterology
Gastrointestinal Bleeding
Gastrointestinal (GI) bleeding is any haemorrhage from the lumen of the gastrointestinal tract, divided anatomically at the ligament of Treitz into upper GI bleeding (UGIB) — haematemesis (fresh red blood), coffee-ground vomiting, and melaena (black tarry stool) — and lower GI bleeding (LGIB) — haematochezia (fresh red or maroon blood per rectum). The commonest UGIB cause is peptic ulcer disease (about a third to half of all cases), followed by erosive gastritis, oesophago-gastric varices, Mallory-Weiss tear, oesophagitis and malignancy; the commonest LGIB cause in older adults is diverticular bleeding, with colonic angiodysplasia, ischaemic colitis, colitis (inflammatory/infective), neoplasia and haemorrhoids following. Management is ABCDE resuscitation (two large-bore cannulae, crossmatch, restrictive transfusion to Hb at least 7 g/dL), risk-stratify with the Glasgow-Blatchford Score pre-endoscopy and Rockall with endoscopy, OGD within 24 hours (within 12 hours if variceal). Bleeding ulcer = adrenaline injection plus a clip/thermal method plus IV PPI (omeprazole 80 mg then 8 mg/hour for 72 hours). Variceal bundle = terlipressin 2 mg IV every 4 hours plus ceftriaxone 1 g IV daily plus endoscopic band ligation within 12 hours plus restrictive transfusion; TIPS if refractory. Antibiotics to all cirrhotics with GI bleed.
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★ High yieldGastroenterology
Inflammatory Bowel Disease
Inflammatory bowel disease (IBD) is a group of chronic relapsing immune-mediated disorders of the gastrointestinal tract comprising Crohn disease (CD) — transmural inflammation in a skip-lesion distribution anywhere from mouth to anus, frequently involving terminal ileum, with fistula, stricture, abscess and perianal disease — and ulcerative colitis (UC) — diffuse mucosal inflammation continuous from the rectum proximally, presenting with bloody diarrhoea, urgency and tenesmus. A third working group, IBD-unclassified (IBDU) or colonic IBD type-unclassified, is used when differentiation is not possible on initial work-up. Incidence is highest in the second and third decades (a smaller second peak in the seventh decade) in…
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Respiratory
5 topicsRespiratory
5
★ High yieldRespiratory
Asthma
Asthma is a chronic inflammatory airway disease with variable and reversible airflow obstruction, bronchial hyperresponsiveness, and airway inflammation. GINA: ICS-containing therapy for every patient (SABA-only is unsafe), as-needed low-dose ICS-formoterol as the preferred reliever (MART), add-on LAMA, azithromycin or biologics for severe asthma. Acute severe attacks: oxygen, nebulised short-acting beta-2 agonist and early systemic corticosteroid, with IV magnesium sulphate 1.2 to 2 g over 15 to 30 minutes when response is insufficient.
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Respiratory
Bronchiectasis (non-CF)
Bronchiectasis is the permanent, abnormal dilation of one or more bronchi caused by destruction of the muscular and elastic wall components. It is not a single disease but the end-result of a vicious cycle of impaired mucociliary clearance, chronic infection and neutrophilic inflammation (Cole's hypothesis). The classic presentation is a chronic productive cough with daily mucopurulent sputum, recurrent exacerbations, coarse crackles, finger clubbing and, in advanced disease, haemoptysis and cor pulmonale. Diagnosis is clinical plus high-resolution CT (the signet-ring sign — bronchus wider than its accompanying artery — is the radiological hallmark). Commonest organisms are Haemophilus influenzae (early) and Pseudomonas aeruginosa (severe, accelerating decline). Management rests on four pillars: treat the underlying cause, airway-clearance physiotherapy, infection control (acute 14-day antibiotics plus long-term macrolides and/or inhaled antibiotics for frequent exacerbators), and prevention (vaccination, smoking cessation). Dornase alfa helps in CF but not in non-CF bronchiectasis (the O'Donnell trial).
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★ High yieldRespiratory
Community-Acquired Pneumonia
Community-acquired pneumonia (CAP) is an acute infection of the lung parenchyma acquired outside hospital (or within the first 48 hours of admission). The commonest pathogen is Streptococcus pneumoniae; atypicals (Mycoplasma pneumoniae, Chlamydophila pneumoniae/psittaci, Legionella pneumophila), respiratory viruses (influenza, SARS-CoV-2, RSV), Haemophilus influenzae, Moraxella catarrhalis, and in selected hosts Staphylococcus aureus, Klebsiella pneumoniae and anaerobes. Typical CAP presents abruptly with fever, productive or rust-coloured sputum, dyspnoea, pleuritic chest pain and signs of consolidation; atypical CAP is insidious with a dry cough and prominent systemic features. Diagnosis is clinical plus chest X-ray; severity is graded with CURB-65 (Confusion, Urea over 7, RR 30 or more, systolic BP under 90 or diastolic 60 or less, age 65 or more). Treat with empirical antibiotics within 4 hours: low severity amoxicillin or doxycycline; moderate or severe a beta-lactam plus a macrolide; oxygen, fluids and sepsis care as needed. Admit if CURB-65 score is 2 or more; consider ICU if 3 or more. Prevention is vaccination (pneumococcal, influenza, COVID-19).
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★ High yieldRespiratory
Cystic Fibrosis
Cystic fibrosis (CF) is an autosomal recessive multi-system disorder caused by loss-of-function mutations in the CFTR gene on chromosome 7 (Phe508del is the most common mutation; nearly 90 percent of patients carry at least one copy). CFTR is an epithelial anion channel; its dysfunction produces dehydrated, viscous secretions across lungs, pancreas, gut, liver, sweat glands and reproductive tract. Pulmonary disease — chronic endobronchial infection (Staphylococcus aureus, Pseudomonas aeruginosa) with bronchiectasis and respiratory failure — dominates morbidity and mortality. Diagnosis rests on newborn screening (immunoreactive trypsinogen with confirmatory testing), a sweat chloride over 60 mmol/L and CFTR genotyping interpreted through CFTR2. Treatment layers airway clearance and mucolytics (dornase alfa, hypertonic saline), inhaled antibiotics and azithromycin, pancreatic enzyme and nutritional support, insulin for CF-related diabetes, and mutation-directed CFTR modulators — most powerfully elexacaftor-tezacaftor-ivacaftor.
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★ High yieldRespiratory
Haemoptysis
Haemoptysis is the coughing up of blood that originates from the lower respiratory tract (below the vocal cords). It ranges from blood-streaked sputum to massive, life-threatening haemoptysis. Worldwide the commonest cause is tuberculosis; in developed countries bronchial carcinoma, bronchiectasis and pneumonia predominate. Massive haemoptysis (any volume threatening the airway or gas exchange, classically over 100 to 240 mL/24h) kills by asphyxia, not exsanguination — because over 90 percent of such bleeds arise from the high-pressure bronchial arteries. Management is stepwise: protect the airway, oxygenate, put the BLEEDING LUNG DOWN, reverse anticoagulation, then rigid bronchoscopy with tamponade and bronchial artery embolisation (BAE) first-line; surgery is last resort. Always exclude PE, TB, carcinoma and diffuse alveolar haemorrhage (ANCA / anti-GBM).
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Emergency & Toxicology
9 topicsEmergency & Toxicology
8
★ High yieldEmergency & Toxicology
Beta-Blocker & Calcium-Channel Blocker Overdose
Beta-blocker (BB) and calcium-channel blocker (CCB) overdoses are two of the most lethal prescription drug poisonings and are taught together because they produce an overlapping toxidrome — bradycardia, hypotension, AV conduction block and cardiogenic shock refractory to standard ACLS — and share an overlapping antidote ladder (IV calcium, high-dose insulin euglycaemia therapy, glucagon, vasopressors, lipid emulsion, pacing, ECMO). Beta-blockers antagonise beta-adrenergic G-protein-coupled receptors - reduced cAMP/PKA - reduced L-type calcium-channel opening - negative inotropy, chronotropy and dromotropy; lipophilic agents (propranolol, metoprolol, carvedilol) cross the blood-brain barrier causing CNS depression, seizures and coma (membrane-stabilising Na-channel effect), and sotalol uniquely prolongs the QT (torsades risk). Calcium-channel blockers directly block the L-type voltage-gated calcium channel: the non-dihydropyridines (verapamil, diltiazem) are predominantly cardiac (negative inotropy/chronotropy/dromotropy and AV block) and are the most lethal in overdose, while the dihydropyridines (amlodipine, nifedipine) are predominantly vasodilatory. The single most exam-relevant discriminator is that CCBs block calcium entry into pancreatic beta cells - impaired insulin release - HYPERGLYCAEMIA + metabolic acidosis, a clue that distinguishes CCB from BB overdose (BBs do not cause hyperglycaemia and may instead cause hypoglycaemia). The most effective single inotropic therapy is high-dose insulin euglycaemia therapy (HIET). Sustained-release verapamil/diltiazem is the lethal subtype with delayed and prolonged toxicity.
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★ High yieldEmergency & Toxicology
Digoxin Toxicity
Digoxin toxicity results from excess of the cardiac glycoside digoxin (used for rate control in atrial fibrillation and as an adjunct in heart failure with reduced ejection fraction). Digoxin inhibits the Na+/K+ ATPase - raised intracellular Na+ - reduced Na+/Ca2+ exchange - raised intracellular Ca2+ (positive inotropy) and increased vagal tone (AV nodal blockade). Toxicity produces gastrointestinal (anorexia, nausea, vomiting), neurological/visual (confusion, weakness, yellow-green halos = xanthopsia) and cardiac effects — the hallmark being arrhythmia from automaticity AND conduction block together (atrial tachycardia WITH AV block classic; bidirectional VT pathognomonic). Chronic toxicity is potentiated by hypokalaemia, renal failure, hypomagnesaemia and drug interactions (amiodarone, verapamil, macrolides). Treatment: stop digoxin, correct K+/Mg2+, atropine/pacing for bradycardia, lidocaine/phenytoin/magnesium for ventricular tachyarrhythmia, and digoxin-specific Fab fragments (DigiFab) for life-threatening features (VT/VF, severe brady/AV block, K+ over 5.5, shock, massive overdose). Avoid IV calcium (classic 'stone heart' teaching), class Ia/Ic agents, and dialysis.
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★ High yieldEmergency & Toxicology
Drowning
Drowning is defined by the WHO as the process of experiencing respiratory impairment from submersion or immersion in liquid; outcomes are fatal drowning, non-fatal drowning with morbidity, or non-fatal drowning without morbidity (a rescue). The old terms 'near-drowning', 'dry drowning', 'wet drowning', 'active drowning' and 'secondary drowning' are obsolete. The primary injury is hypoxia produced by laryngospasm and/or aspiration of liquid into the alveoli, which washes out surfactant, collapses alveoli, causes non-cardiogenic pulmonary oedema and ventilation-perfusion mismatch, and may evolve over hours into acute respiratory distress syndrome (ARDS). The downstream killer is hypoxic cardiac arrest, which in drowning is asystolic or PEA — NOT ventricular fibrillation. The defining management principle is therefore oxygenation first: in cardiac arrest give 5 initial rescue breaths before chest compressions, then continue 30:2; for the hypoxic but breathing victim give high-flow oxygen, escalate to CPAP/NIV or intubation, and observe for at least 6 to 24 hours because ARDS can develop after rescue. Never use the Heimlich manoeuvre, do not routinely immobilise the cervical spine (only if a concerning mechanism), give no routine prophylactic antibiotics or corticosteroids, and do not terminate resuscitation prematurely in the hypothermic victim ('not dead until warm and dead'). Risk factors: alcohol, inability to swim, unsupervised children, seizures, trauma (diving), hypothermia, and hyperventilation before a breath-hold dive (shallow-water blackout); swimming is also a recognised trigger of arrhythmia in long-QT syndrome, Brugada syndrome and CPVT, so an unexplained drowning demands an ECG and family screening.
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★ High yieldEmergency & Toxicology
Iron Overdose
Iron overdose is one of the leading causes of accidental poisoning death in children (adult prenatal/iron tablets look like sweets) and an occasional means of deliberate self-harm in adults. Iron is corrosive to the gastrointestinal mucosa (haemorrhagic gastritis, vomiting, diarrhoea) and, once absorbed iron exceeds transferrin binding capacity, becomes a systemic free-radical toxin via the Fenton reaction — it uncouples oxidative phosphorylation, blocks the Krebs cycle and produces lactic (high-anion-gap) acidosis, centrilobular hepatic necrosis, coagulopathy (direct thrombin inhibition), shock and multi-organ failure. Toxic dose (elemental iron): under 20 mg/kg usually asymptomatic; over 20 mg/kg mild; over 40 mg/kg significant; over 60 mg/kg severe, potentially lethal. Four clinical stages: Stage 1 (0 to 6 h) GI corrosive injury + hypovolaemic shock; Stage 2 (6 to 24 h) deceptive latent phase; Stage 3 (12 to 48 h) shock + acidosis + hepatic/renal failure + coma (the killer); Stage 4 (4 to 6 weeks) gastric/pyloric outlet stricture. Diagnosis: serum iron at 4 to 6 h (over 500 microgram/dL significant), abdominal X-ray (radiopaque tablets), anion-gap metabolic acidosis with hyperglycaemia and leucocytosis. Management: ABCDE + aggressive crystalloid; activated charcoal is USELESS — whole bowel irrigation is the decontamination of choice; IV desferrioxamine 15 mg/kg/h (urine turns 'vin rose') for iron over 500, acidosis, or shock; supportive care for organ failure.
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★ High yieldEmergency & Toxicology
Lithium Toxicity
Lithium toxicity results from excess of lithium carbonate (the mood-stabiliser used for bipolar affective disorder prophylaxis), a drug with a narrow therapeutic index (therapeutic 0.6-1.2 mmol/L). Lithium is a small monovalent cation handled by the kidney like sodium — freely filtered, reabsorbed proximally, almost entirely renally excreted — so reduced GFR or sodium/water loss (dehydration, vomiting, diarrhoea, fever, low-salt diet) and interacting drugs (thiazides, NSAIDs, ACE-inhibitors/ARBs) are the classic precipitants of accumulation. Three patterns exist: acute overdose, acute-on-chronic, and chronic accumulation (the commonest and most dangerous). Toxicity is predominantly NEUROLOGICAL — fine tremor (earliest) progressing to coarse tremor, fasciculations, hyperreflexia, ataxia, dysarthria, seizures and coma — with nephrogenic diabetes insipidus (polyuria/polydipsia), GI (nausea/vomiting/diarrhoea, more in acute), cardiac (T-wave flattening, QT prolongation) and endocrine (hypothyroidism, hypercalcaemia) features. The key exam trap: acute overdose looks mild initially (distribution into the CNS lags serum by hours) whereas chronic toxicity is dangerous at lower levels (tissue already saturated) — so clinical correlation trumps the level. Diagnosis: serum lithium (over 1.5 mild, over 2.5 moderate, over 3.5-4.0 severe) plus renal function, electrolytes (Na, K, Ca), ECG, TFTs. Management: stop lithium, aggressive isotonic saline (the cornerstone — enhances renal excretion), haemodialysis for severe (EXTRIP criteria: impaired renal function with level over 4.0 mmol/L, or decreased consciousness/seizures/life-threatening dysrhythmia at any level), whole-bowel irrigation for sustained-release ingestion, and avoid activated charcoal (does not adsorb lithium), loop/thiazide diuretics, NSAIDs and ACE-inhibitors. Recheck levels after dialysis because of rebound.
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★ High yieldEmergency & Toxicology
Paracetamol (Acetaminophen) Overdose
Paracetamol (acetaminophen) overdose is the commonest cause of acute liver failure (ALF) in the developed world. At therapeutic doses paracetamol is safely metabolised by glucuronidation and sulfation; in overdose these saturate and the CYP2E1 pathway generates the toxic intermediate NAPQI (N-acetyl-p-benzoquinone imine), which depletes glutathione and produces centrilobular (zone 3) hepatic necrosis. The diagnostic pivot is a serum paracetamol level at 4 hours post-ingestion plotted on the treatment nomogram (Rumack-Matthew 150 mg/L line or UK 100 mg/L line); above the line = treat with IV N-acetylcysteine (NAC), which replenishes glutathione and gives virtually complete protection when given within 8 hours. Staggered, unknown-time, modified-release, or repeated supratherapeutic ingestion INVALIDATES the nomogram — treat empirically with NAC. King's College Criteria (arterial pH under 7.3 OR prothrombin time over 100 s plus creatinine over 300 micromol/L plus severe encephalopathy) trigger urgent liver transplant referral.
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★ High yieldEmergency & Toxicology
Salicylate (Aspirin) Overdose
Salicylate (aspirin) overdose produces a characteristically mixed acid-base disorder: direct stimulation of the medullary respiratory centre (respiratory alkalosis) plus uncoupling of oxidative phosphorylation, inhibition of citric-acid-cycle dehydrogenases and increased keto-acid production (high anion-gap metabolic acidosis). Early features include tinnitus, nausea, vomiting and hyperventilation; severe poisoning causes agitation, altered mental status, seizures, non-cardiogenic pulmonary oedema and coma. Treatment is gastrointestinal decontamination, fluid resuscitation, urinary alkalinisation with IV sodium bicarbonate to a urine pH of at least 7.5 (first line for moderately severe poisoning not needing dialysis), and intermittent haemodialysis for altered mental status, ARDS on oxygen, failing standard therapy, severe acidaemia or high concentrations. If the patient is intubated, maintain a high minute ventilation and arrange timely haemodialysis.
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★ High yieldEmergency & Toxicology
Tricyclic Antidepressant (TCA) Overdose
Tricyclic antidepressant (TCA) overdose (amitriptyline, imipramine, dothiepin, nortriptyline, clomipramine) is one of the most lethal common poisonings — even a handful of tablets can kill. TCAs exert three toxic effects that define the syndrome: (1) fast voltage-gated SODIUM-CHANNEL BLOCKADE in cardiac myocytes and cortical neurons (slows phase 0 depolarisation - QRS widening, AV block, re-entrant ventricular arrhythmia, hypotension, seizures, coma); (2) ANTICHOLINERGIC (antimuscarinic) blockade (the classic toxidrome — mydriasis, dry mucosae, flushed dry skin, hyperthermia, ileus, urinary retention, sinus tachycardia, agitated delirium); and (3) ALPHA-1 ADRENERGIC blockade plus norepinephrine/serotonin reuptake inhibition (vasodilation, hypotension, initial sympathomimetic features). The hallmark of severe poisoning is QRS widening over 120 ms on ECG (predicts seizures and ventricular arrhythmias); other ECG markers are the terminal R wave over 3 mm in aVR (right-axis deviation of the terminal 40 ms) and QT prolongation. The specific antidote is IV SODIUM BICARBONATE (1-2 mmol/kg bolus, alkalinise serum to pH 7.45-7.55) for QRS over 120 ms, ventricular arrhythmia or hypotension. AVOID class Ia/Ic antiarrhythmics (procainamide, flecainide), phenytoin, and flumazenil — all worsen the cardiotoxicity or precipitate seizures. Seizures are treated with benzodiazepines; refractory cardiovascular collapse is treated with intravenous lipid emulsion and ECMO. An asymptomatic patient with a normal ECG for 6 hours after an immediate-release ingestion can be safely discharged (GEMNet 6-hour rule).
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Emergency Medicine
1
Neurology
5 topicsNeurology
5
★ High yieldNeurology
Brain Tumours
Brain tumours are intracranial neoplasms — primary (arising from glia, meninges, cranial nerves, pituitary or germ cells) or secondary (metastatic, roughly five to ten times commoner than primary). The WHO 2021 classification defines them by integrated histology and molecular markers (IDH mutation, 1p/19q codeletion, MGMT methylation, BRAF, H3 K27). Presentation: raised ICP (morning headache, vomiting, papilloedema), seizures, progressive focal deficit. MRI with gadolinium is the imaging gold standard. Management: maximal safe resection, radiotherapy, chemotherapy (Stupp protocol for glioblastoma — radiotherapy 60 Gy plus concomitant and adjuvant temozolomide), dexamethasone for vasogenic oedema, anticonvulsants for seizures. Glioblastoma median survival is about 15 months with Stupp protocol.
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★ High yieldNeurology
Headache
Headache (cephalalgia) is pain arising from the pain-sensitive structures of the head (dura, vessels, sinuses, scalp, cervical roots, cranial nerves V, VII, IX, X) but NOT the brain parenchyma itself (it is insensate). The single most important clinical step is to separate primary from secondary headache using the SNNOOP10 red-flag screen: a secondary headache has an underlying cause (haemorrhage, infection, mass, giant-cell arteritis, raised pressure) and may be life-threatening. The three primary headaches are migraine (unilateral throbbing, 4 to 72 h, photophobia, phonophobia, nausea, aura in one-third), tension-type (bilateral pressing band, no nausea, not aggravated by routine), and cluster (unilateral periorbital excruciating 15 to 180 min attacks in bouts, ipsilateral autonomic features and Horner syndrome). A thunderclap headache (peak intensity within 1 minute) is subarachnoid haemorrhage until proven otherwise — emergency CT then LP if CT negative (xanthochromia, between 12 hours and 2 weeks). Acute migraine: oral sumatriptan 100 mg or NSAID + antiemetic; migraine prophylaxis if 4 or more days/month: propranolol, topiramate, amitriptyline, candesartan, flunarizine, or a CGRP-pathway monoclonal antibody (erenumab, fremanezumab, galcanezumab). Cluster acute: 100 percent oxygen at 12 L/min for 15 minutes OR subcutaneous sumatriptan 6 mg; cluster prophylaxis verapamil at a daily dose of at least 240 mg. Medication-overuse headache: triptans/opioids/combination analgesics on 10 or more days/month for over 3 months — education, withdraw the offending drug, add prevention.
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★ High yieldNeurology
Meningitis and Encephalitis
Meningitis is inflammation of the meninges, most often infective; encephalitis is inflammation of the brain parenchyma, and meningoencephalitis is both together. Bacterial meningitis is a time-critical emergency — fever plus headache plus neck stiffness plus altered mental status is bacterial meningitis until proven otherwise, and empirical therapy (ceftriaxone plus vancomycin where ceftriaxone-resistant pneumococcus is prevalent, ampicillin added for neonates, older and immunocompromised patients, and dexamethasone 10 mg before or with the first antibiotic) must start without delay, before lumbar puncture or imaging. Herpes simplex encephalitis is the treatable encephalitis not to miss — fever plus altered mental status plus seizures needs empirical IV aciclovir 10 mg/kg every 8 hours for 10 to 21 days, without waiting for PCR. CSF analysis (cell count, glucose, protein, Gram stain, culture, PCR) distinguishes bacterial, viral, tuberculous and fungal causes.
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★ High yieldNeurology
Multiple Sclerosis
Multiple sclerosis (MS) is a chronic, immune-mediated, inflammatory demyelinating disease of the central nervous system (CNS) defined by episodes of neurological dysfunction (disseminated in time and space) that, untreated, progress to irreversible disability. It is the commonest non-traumatic cause of neurological disability in young adults. Onset is typically between 20 and 40 years, female predominance about 3:1. About 85% present with relapsing-remitting MS (RRMS); 10 to 15% have primary progressive MS (PPMS) from onset. Diagnosis is clinical and anchored on the McDonald 2017 criteria — MRI showing periventricular, juxtacortical, infratentorial and spinal-cord plaques (Dawson fingers), with CSF oligoclonal bands (intrathecal IgG) substituting for dissemination in time. Acute relapse = IV methylprednisolone 1000 mg daily for 3 to 5 days; plasma exchange if steroid-refractory. Disease-modifying therapy (DMT) ranges from interferon-beta / glatiramer, oral agents (fingolimod, dimethyl fumarate, teriflunomide) to monoclonal antibodies (natalizumab, ocrelizumab) — ocrelizumab is the only approved DMT for PPMS (ORATORIO). Always exclude NMOSD (AQP4) and MOGAD first — interferon worsens NMOSD.
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★ High yieldNeurology
Stroke
Stroke is sudden focal neurological deficit from vascular injury to the brain: ischaemic (85%) from arterial occlusion, or haemorrhagic (15%) from vessel rupture. FAST (Face, Arm, Speech, Time) triggers recognition; a non-contrast CT brain is the first, most urgent investigation to distinguish the two — since the acute treatments are opposite. Ischaemic stroke: IV alteplase within 4.5 hours, thrombectomy up to 24 hours for large-vessel occlusion with favourable imaging. Haemorrhagic stroke: blood-pressure control, reversal of anticoagulation, and neurosurgical evacuation where indicated.
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Nephrology
6 topicsNephrology
6
★ High yieldNephrology
Chronic Kidney Disease
Chronic kidney disease (CKD) is defined by KDIGO as abnormalities of kidney structure or function present for more than 3 months, with implications for health. The operational definition is kidney damage markers (albuminuria, urine sediment abnormalities, imaging or histology) OR eGFR below 60 mL/min/1.73 m squared for over 3 months. CKD is classified by cause, GFR category (G1 to G5) and albuminuria category (A1 to A3) — the CGA staging that predicts risk of progression, cardiovascular events and mortality. CKD affects 10 to 13 percent of adults worldwide; diabetic kidney disease is the single largest cause (30 to 50 percent), followed by hypertensive nephrosclerosis (around 25 percent), glomerulonephritis, ADPKD, and obstructive or reflux nephropathy. CKD is usually silent until G3b to G4: uraemic symptoms, fluid overload, hyperkalaemia, acidosis, anaemia and renal bone disease emerge late. Management rests on four pillars: RAAS blockade (ACE inhibitor or ARB) for proteinuria, SGLT2 inhibition (dapagliflozin or empagliflozin) for cardiorenal protection, finerenone in diabetic CKD, and multifactorial cardiovascular risk reduction (statin, BP, glycaemia, smoking cessation, salt restriction, weight loss, avoidance of nephrotoxins) — plus treatment of anaemia (iron then ESA), CKD-MBD (phosphate binders, active vitamin D, calcimimetics), acidosis (sodium bicarbonate) and hyperkalaemia (diet, potassium binders). Renal replacement therapy planning (AV fistula 6 months ahead, transplant referral) starts at eGFR below 30. Dialysis is indicated for the AEIOU emergencies. Cardiovascular disease is the leading cause of death.
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★ High yieldNephrology
Hepatorenal Syndrome
Hepatorenal syndrome (HRS) is a functional, potentially reversible acute kidney injury (AKI) that occurs in patients with ascites and advanced cirrhosis (or acute liver failure / acute-on-chronic liver failure), in the absence of any other identifiable renal injury. The kidneys are structurally normal and recover after liver transplantation. The dominant mechanism is splanchnic and peripheral arterial vasodilation (driven by portal hypertension, nitric oxide and other vasodilators) producing a reduced effective arterial blood volume, with compensatory activation of the renin-angiotensin-aldosterone system, sympathetic nervous system and non-osmotic vasopressin causing intense renal vasoconstriction. HRS is a diagnosis of exclusion — cirrhosis with ascites plus AKI plus no response to albumin and diuretic withdrawal, and no shock, nephrotoxin or structural renal disease. Treat with terlipressin plus albumin (or noradrenaline plus albumin); liver transplantation is the only definitive cure. Untreated HRS type 1 carries a median survival of under 2 weeks.
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★ High yieldNephrology
Hyperkalaemia
Hyperkalaemia is a serum potassium concentration above 5.5 mmol/L and is one of the few electrolyte emergencies because it can precipitate fatal cardiac arrhythmia. Severe hyperkalaemia is a potassium at or above 6.5 mmol/L or any hyperkalaemia with ECG change (peaked T waves, PR prolongation, QRS widening, sine-wave morphology, ventricular fibrillation or asystole). The clinical priority is to exclude pseudohyperkalaemia (in vitro haemolysis, thrombocytosis or leucocytosis), identify the cause (CKD, ACEi or ARB, potassium-sparing diuretics, NSAIDs, acidosis, Addison disease, hypoaldosteronism, tumour lysis, massive transfusion) and deliver the three-step ladder: stabilise the membrane with calcium, shift potassium into cells with insulin-dextrose and nebulised salbutamol, and remove total-body potassium with binders or haemodialysis.
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★ High yieldNephrology
IgA Nephropathy
IgA nephropathy (Berger disease) is the commonest primary glomerulonephritis worldwide, defined by mesangial deposition of galactose-deficient IgA1 immune complexes. Classically presents with synpharyngitic gross haematuria 1 to 2 days after a mucosal infection. Diagnosis is renal biopsy showing dominant mesangial IgA on immunofluorescence. Foundation of management is RAAS blockade plus an SGLT2 inhibitor; steroids, targeted-release budesonide and complement-directed therapy are reserved for high-risk progressive disease.
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★ High yieldNephrology
Minimal Change Disease
Minimal change disease (MCD) is the leading cause of nephrotic syndrome in children and the prototype of steroid-responsive podocytopathy. It accounts for roughly 70-90 percent of nephrotic syndrome in children over one year and about 10-15 percent of adult primary nephrotic syndrome, with selective albuminuria, normal light microscopy, no immune deposits on immunofluorescence, and diffuse foot process effacement on electron microscopy. Most children achieve complete remission within 4-6 weeks of glucocorticoids, with calcineurin inhibitors, mycophenolate, cyclophosphamide and rituximab reserved for frequently relapsing and steroid-dependent disease.
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★ High yieldNephrology
Renal Replacement Therapy
Renal replacement therapy (RRT) is the substitution of the kidney's excretory, fluid-balance and electrolyte/acid-base functions when they fail — applied either as planned maintenance therapy in end-stage kidney disease (ESKD) or as emergency support in severe acute kidney injury (AKI). There are three modalities — haemodialysis (HD) (extracorporeal clearance across a semipermeable membrane by diffusion; AV fistula is the best access, 3 times weekly, target Kt/V over 1.2; risks access infection, intradialytic hypotension, amyloidosis), peritoneal dialysis (PD) (the peritoneal membrane as the filter, glucose osmotic gradient, home-based, gentler; main risk peritonitis, usually Staph epidermidis), and kidney transplantation (the best survival and quality of life, living-donor and pre-emptive preferred, requiring lifelong immunosuppression — calcineurin inhibitor + mycophenolate + steroid; twin threats rejection and opportunistic infection CMV/BK/PJP). A fourth, legitimate option is conservative (non-dialytic) care for the frail elderly. Start dialysis for symptoms (eGFR around 5-10) or for AEIOU emergencies (Acidosis, Electrolytes, Ingestion, Overload, Uraemia) — never for a number alone.
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Obstetrics and Gynaecology
2 topicsObstetrics and Gynaecology
2
★ High yieldObstetrics and Gynaecology
Contraception
Contraception methods span hormonal (combined oral contraceptive pill, progestogen-only pill, implant, injectable, hormonal intrauterine system), intrauterine (copper IUD), barrier (condom, diaphragm), natural (fertility awareness, lactational amenorrhoea), emergency contraception, and permanent sterilisation. Choice depends on efficacy, safety, side effects, reversibility, coital independence, age, comorbidities, and patient preference. Long-acting reversible contraception (LARC) — copper IUD, LNG-IUS, implant — is most effective and offered first-line. UK Medical Eligibility Criteria (UKMEC) categorise every method from 1 (no restriction) to 4 (unacceptable risk) across medical conditions.
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★ High yieldObstetrics and Gynaecology
Endometrial Cancer
Endometrial cancer is the most common gynaecological malignancy in developed countries and the sixth most common cancer in women. Around 90 per cent present with postmenopausal bleeding, which is cancer until proven otherwise. Two pathogenetic types exist: Type I (endometrioid, 80 per cent) is oestrogen-driven, arising through unopposed oestrogen stimulation, endometrial hyperplasia with atypia and well-differentiated carcinoma, with PTEN, PIK3CA, KRAS and ARID1A mutations and a favourable prognosis; Type II (serous, clear cell, carcinosarcoma, 20 per cent) is not oestrogen-driven, arises in atrophic endometrium, carries TP53 mutations, and is aggressive. Diagnosis is by transvaginal ultrasound (endometrial thickness over 4 to 5 mm in a postmenopausal woman prompts biopsy), pipelle or hysteroscopy and dilation and curettage, and pelvic MRI for myometrial invasion and staging. Treatment is total hysterectomy, bilateral salpingo-oophorectomy, plus sentinel or full lymph node assessment, with adjuvant vault brachytherapy for intermediate risk (PORTEC), external beam radiotherapy and chemotherapy (carboplatin and paclitaxel) for high-risk and advanced disease, and high-dose progestin for fertility-sparing management of grade 1 disease.
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Infectious Diseases
4 topicsInfectious Diseases
4
★ High yieldInfectious Diseases
COVID-19 (SARS-CoV-2)
COVID-19 is the disease caused by the betacoronavirus SARS-CoV-2, declared a pandemic by the WHO in March 2020. The S1 subunit of the spike protein binds the ACE2 receptor (high density in type-II pneumocytes, nasal goblet cells, enterocytes, renal tubules, myocardium) and S2 is primed by TMPRSS2 and furin before membrane fusion. Spectrum runs from asymptomatic through mild upper-respiratory illness, pneumonia with hypoxaemia, ARDS and multi-organ failure. Hallmarks: anosmia/ageusia, silent hypoxaemia, bilateral peripheral ground-glass opacities on CT, and a lymphopenia/raised CRP/ferritin/D-dimer/IL-6 profile. Severe disease is driven by a cytokine storm with endothelialitis and microthrombi. Dexamethasone 6 mg OD reduces mortality in patients on oxygen (RECOVERY); remdesivir shortens recovery; nirmatrelvir-ritonavir (Paxlovid) prevents hospitalisation in high-risk outpatients; tocilizumab/baricitinib in rapidly progressing severe disease; mandatory VTE prophylaxis with LMWH. Vaccines (mRNA: Pfizer BNT162b2, Moderna mRNA-1273; viral-vector: ChAdOx1 Covishield/AstraZeneca, Ad26.COV2.S Janssen; inactivated: Covaxin BBV152, CoronaVac; protein subunit: Novavax) are the single most effective prevention and reduce severe disease by more than 90%.
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★ High yieldInfectious Diseases
HIV / AIDS
HIV is a retrovirus (lentivirus) that infects and depletes CD4+ T-helper lymphocytes, producing progressive cell-mediated immunodeficiency. AIDS is the advanced stage, defined by CD4 under 200 cells/uL, a CD4 percentage below 14%, or any AIDS-defining illness (PJP, toxoplasmosis, CMV, MAC, Kaposi sarcoma, CNS lymphoma, etc.). Transmitted by sexual contact, blood/blood products, needle-sharing, and mother-to-child. Acute infection is a mononucleosis-like illness 2 to 4 weeks after exposure, followed by years of clinical latency, then opportunistic infections and tumours as CD4 falls. Diagnosis: 4th-generation Ag/Ab combo assay (p24 + antibody) confirmed by HIV-1/2 differentiation; staging by CD4 count and HIV RNA viral load. Treatment is combination antiretroviral therapy (cART) for every person with HIV regardless of CD4 (START trial): a backbone of 2 NRTIs plus an integrase strand-transfer inhibitor (INSTI) — e.g. tenofovir + emtricitabine + dolutegravir or bictegravir. Suppression to undetectable viral load prevents sexual transmission (U=U, HPTN 052). PCP prophylaxis with co-trimoxazole at CD4 under 200; toxo at under 100; MAC and CMV at under 50. PrEP (tenofovir-emtricitabine or long-acting cabotegravir) for high-risk negatives; PEP is a 28-day 3-drug regimen started within 72 hours. With modern ART, near-normal life expectancy is achievable.
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★ High yieldInfectious Diseases
Malaria
Malaria is a mosquito-borne protozoan illness caused by the apicomplexan parasite Plasmodium and transmitted by the bite of an infected female Anopheles mosquito. Five species infect humans — P. falciparum (most lethal), P. vivax (commonest relapsing form), P. ovale, P. malariae and the zoonotic P. knowlesi. Classical presentation is a fever paroxysm (cold, hot and sweating stages) with chills, rigors, headache and splenomegaly, but in many endemic areas the periodicity is irregular and the illness is indistinguishable from other febrile syndromes. P. falciparum causes severe malaria — cerebral malaria, severe malarial anaemia, ARDS, acute kidney injury, hypoglycaemia and acidosis — through cytoadherence, sequestration and rosetting of parasitised erythrocytes in the microvasculature. Diagnosis is by thick blood film (detection sensitivity) and thin film (species identification and parasitaemia quantification) plus rapid diagnostic tests (HRP-2 / pLDH). Treatment is species- and severity-driven: artemisinin-based combination therapy (ACT) — artemether-lumefantrine, artesunate-amodiaquine, dihydroartemisinin-piperaquine — for uncomplicated falciparum; intravenous artesunate (2.4 mg/kg at 0, 12 and 24 h) for severe disease; primaquine (after G6PD screening) for radical cure of vivax/ovale; chemoprophylaxis (atovaquone-proguanil, doxycycline, mefloquine) for travellers. With prompt, correct treatment uncomplicated malaria is cured in three days; cerebral malaria still carries 15 to 20 per cent mortality.
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★ High yieldInfectious Diseases
Tuberculosis
Tuberculosis (TB) is a chronic granulomatous infection caused by Mycobacterium tuberculosis (Mtb), an acid-fast aerobic bacillus that classically attacks the lungs (pulmonary TB, 70-80 percent) but can affect any organ (extrapulmonary TB). It exists in two states: latent TB infection (LTBI) — the bacilli are contained by host immunity in a granuloma, the patient is asymptomatic and non-infectious; and active TB disease — replication resumes, symptoms develop, and the patient becomes infectious. Globally TB causes about 10 million new cases and 1.4 million deaths per year and is the leading cause of death from a single infectious agent. Diagnosis rests on microbiology — sputum AFB smear (Ziehl-Neelsen or auramine), mycobacterial culture (the gold standard), and rapid molecular NAAT (Xpert MTB/RIF or Xpert Ultra, which simultaneously detects rifampicin resistance); the interferon-gamma release assay (IGRA) or tuberculin skin test (TST/PPD) detects latent infection. Treatment of drug-susceptible active pulmonary TB is the six-month RIPE regimen — rifampicin (RIF) 10 mg/kg daily max 600 mg, isoniazid (INH) 5 mg/kg daily max 300 mg, pyrazinamide (PZA) 25 mg/kg daily max 2 g, and ethambutol (EMB) 15-20 mg/kg daily for 2 months (intensive), then rifampicin + isoniazid for 4 months (continuation), with pyridoxine (vitamin B6) 25 mg daily to prevent INH-induced peripheral neuropathy. Drug-resistant TB — MDR (resistant to at least INH + RIF), XDR (MDR plus resistance to any fluoroquinolone and at least one of bedaquiline/linezolid), and pre-XDR (MDR plus fluoroquinolone resistance) — requires all-oral bedaquiline-based regimens — the 24-26-week BPaLM/BPaL regimens (bedaquiline, pretomanid, linezolid, plus moxifloxacin in BPaLM) for fluoroquinolone-resistant disease, or longer individualised regimens. LTBI is treated with shorter rifapentine-based regimens — 3HP (INH + rifapentine weekly for 12 weeks) or 1HP (INH + rifapentine daily for 4 weeks) — to prevent progression to active disease. BCG vaccination at birth protects children against severe forms (miliary TB, TB meningitis) but has variable efficacy against adult pulmonary TB.
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Endocrinology
5 topicsEndocrinology
5
★ High yieldEndocrinology
Cushing Syndrome
Cushing syndrome is the clinical and biochemical syndrome resulting from chronic exposure to excess glucocorticoid (endogenous cortisol or exogenous steroid). Exogenous (iatrogenic) steroid therapy is the commonest cause overall; of endogenous causes, ACTH-dependent forms (Cushing disease from a pituitary corticotroph adenoma ~70%, ectopic ACTH/CRH ~10%) outnumber ACTH-independent adrenal causes (adrenal adenoma, carcinoma, bilateral macronodular hyperplasia ~20%). The phenotype combines central obesity, moon face, dorsocervical and supraclavicular fat pads, purple striae, proximal myopathy, easy bruising, thin skin, hypertension, hyperglycaemia and osteoporosis. Diagnosis requires two abnormal first-line screening tests of the three endorsed by the Endocrine Society (24-hour urine free cortisol, late-night salivary cortisol, 1-mg overnight dexamethasone suppression test), then plasma ACTH to localise (ACTH-dependent vs ACTH-independent), then imaging ± bilateral inferior petrosal sinus sampling for ACTH-dependent disease. Transsphenoidal resection is first-line for Cushing disease; adrenalectomy for adrenal tumours; tumour resection for ectopic ACTH. Steroidogenesis inhibitors (metapyrapone, ketoconazole, osilodrostat, mitotane) and the pituitary-directed pasireotide bridge control and treat unresectable disease.
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★ High yieldEndocrinology
Diabetes Mellitus
Diabetes mellitus is a group of chronic metabolic disorders unified by sustained hyperglycaemia arising from absolute insulin deficiency (T1DM), insulin resistance plus progressive beta-cell failure (T2DM), gestation (GDM), specific monogenic and secondary forms (MODY, LADA, drug-induced, pancreatic). Diagnostic thresholds (ADA 2019): HbA1c over 6.5 percent (48 mmol/mol), fasting plasma glucose over 7.0 mmol/L (126 mg/dL), or 2-hour 75 g OGTT plasma glucose over 11.1 mmol/L (200 mg/dL), or a random plasma glucose over 11.1 mmol/L in a symptomatic patient. Management is cause-specific: lifestyle and metformin remain the T2DM foundation (UKPDS-34 metformin), with SGLT2 inhibitors and GLP-1 receptor agonists added for cardiovascular and renal protection (EMPA-REG, 2019 ESC/EASD), and multiple daily injections of insulin for T1DM (DCCT/EDIC). Targets HbA1c generally under 7 percent (53 mmol/mol), individualised. Complications are microvascular (retinopathy, nephropathy, neuropathy) and macrovascular (coronary artery disease, stroke, peripheral arterial disease), plus the acute emergencies of DKA, HHS and hypoglycaemia.
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★ High yieldEndocrinology
Diabetic Ketoacidosis and Hyperosmolar Hyperglycaemic State (DKA / HHS)
Diabetic ketoacidosis (DKA) is the triad of hyperglycaemia, ketosis and metabolic acidosis arising from absolute insulin deficiency (most often new or known type 1 diabetes). Hyperosmolar hyperglycaemic state (HHS) is severe hyperglycaemia with high osmolality and dehydration but minimal ketosis, classically in older type 2 patients. Both are medical emergencies triggered by infection, missed insulin, infarction or new diabetes. Treatment pillars are IV fluids first, fixed-rate IV insulin 0.1 units/kg/hr, careful potassium replacement, and treat the precipitant. The killing complications are hypokalaemia (a leading preventable death during treatment) and cerebral oedema (chiefly in children).
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★ High yieldEndocrinology
Hyperthyroidism
Hyperthyroidism is the syndrome of excess thyroid-hormone synthesis and secretion by the thyroid gland; thyrotoxicosis is the broader clinical state of excess circulating hormone from any source. The commonest cause is Graves disease (TSH-receptor stimulating antibody), followed by toxic multinodular goitre and toxic adenoma; destructive thyroiditis and exogenous hormone produce low-uptake thyrotoxicosis. The biochemical hallmark is a suppressed TSH with raised free T4 and/or free T3. Treatment options are antithyroid drugs (carbimazole/methimazole; propylthiouracil in pregnancy first trimester and thyroid storm), radioactive iodine (I-131) and surgery. Thyroid storm is the decompensated, life-threatening extreme — thionamide then iodine one hour later, beta-blocker, hydrocortisone, cooling, and treatment of the precipitant.
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★ High yieldEndocrinology
Hypoglycaemia
Hypoglycaemia is plasma glucose low enough to cause symptoms (typically under 3.0 mmol/L / 54 mg/dL). It produces a biphasic clinical syndrome: first autonomic / sympathetic activation (sweating, tremor, palpitations, hunger, anxiety) at glucose about 3.2 mmol/L (58 mg/dL), then neuroglycopenia (confusion, drowsiness, seizures, coma, and at its extreme, death) as glucose falls below 3.0 mmol/L. In adults in the community the dominant cause is glucose-lowering therapy in diabetes (insulin, sulfonylureas, glinides); in non-diabetics, insulinoma, non-islet cell tumour hypoglycaemia (IGF-II), adrenal insufficiency, alcohol, sepsis/critical illness, and autoimmune insulin syndrome must each be excluded. The diagnostic cornerstone is Whipple's triad (symptoms + low documented glucose + relief with glucose). Treatment is layered: mild — 15 g fast-acting oral carbohydrate, recheck at 15 minutes; severe (unconscious or unable to swallow) — IV 10% dextrose or IM glucagon 1 mg, but glucagon is ineffective in sulfonylurea overdose and depleted glycogen states and octreotide is added for sulfonylurea poisoning. Recurrent hypoglycaemia causes hypoglycaemia-associated autonomic failure (HAAF) and hypoglycaemia unawareness, resetting the glycaemic threshold at which symptoms occur — the most dangerous complication of long-term insulin therapy. Avoidance through structured glucose targets, patient education, CGM, and the 15-15 rule prevents the morbidity that the ACCORD, ADVANCE and VADT trials linked to intensive glucose lowering.
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obstetrics-gynaecology
3 topicsobstetrics-gynaecology
3
★ High yieldobstetrics-gynaecology
Endometriosis
Endometriosis is the presence of functional endometrial glands and stroma outside the uterine cavity, producing a chronic, oestrogen-dependent, inflammatory condition. It classically presents with the triad of secondary dysmenorrhoea, deep dyspareunia and chronic pelvic pain, with infertility a frequent sole presentation. The ovary is the commonest site; the three phenotypes are superficial peritoneal, ovarian endometrioma ('chocolate cyst') and deep infiltrating endometriosis (DIE). Diagnosis is clinical plus transvaginal ultrasound; MRI maps DIE; laparoscopy with histology is the gold standard. Management is NSAIDs plus hormonal suppression (combined OCP, progestogens, GnRH analogues/antagonists) and surgery (excision/ablation, cystectomy) for refractory disease, DIE and selected infertility.
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★ High yieldobstetrics-gynaecology
Polycystic Ovary Syndrome
Polycystic ovary syndrome (PCOS) is a heterogeneous, lifelong reproductive and metabolic disorder of reproductive-age women characterised by ovulatory dysfunction, hyperandrogenism (clinical or biochemical), and polycystic ovarian morphology (PCOM), defined by the Rotterdam 2003 consensus as any two of those three features, after exclusion of other causes. Insulin resistance with compensatory hyperinsulinaemia is the central driver in 70 to 80% of patients, augmented by gonadotropin dysregulation (elevated LH:FSH ratio) and low-grade chronic inflammation. Presentation clusters around oligomenorrhoea or amenorrhoea, hirsutism (modified Ferriman-Gallwey score over 4 to 6), acne, central obesity, acanthosis nigricans, and anovulatory infertility. Management is stratified by the patient's presenting complaint: lifestyle (5 to 10% weight loss) for all; combined oral contraceptive pill (COCP) for cycle control, endometrial protection and acne; anti-androgens (spironolactone, cyproterone acetate) for hirsutism; letrozole as first-line ovulation induction (superior to clomiphene, PPCOS II); metformin for insulin resistance or metabolic features. Lifelong surveillance is mandatory: type 2 diabetes mellitus (3 to 7x risk), metabolic syndrome in 40%, endometrial cancer (around 3x), and cardiovascular disease. The 2023 International Evidence-based Guideline reaffirms letrozole as first-line fertility therapy and introduces the use of anti-Mullerian hormone as a substitute marker for PCOM in adults.
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★ High yieldobstetrics-gynaecology
Uterine Fibroids (Leiomyomas)
Uterine fibroids (leiomyomas) are benign, monoclonal, oestrogen- and progesterone-responsive smooth-muscle tumours of the myometrium — the commonest benign tumour of women (up to 70 to 80 per cent by age 50). Most are asymptomatic; when symptomatic the leading complaint is abnormal uterine bleeding (heavy/prolonged menses), followed by bulk/pressure symptoms (pelvic heaviness, urinary frequency, constipation) and infertility (predominantly submucosal). Classified by location (FIGO 0 to 8): submucosal cause bleeding and subfertility, intramural are commonest, subserosal cause pressure. Diagnosis is clinical plus transvaginal ultrasound; MRI maps submucosal extent and excludes sarcoma. Management is goal- and fertility-directed: observe if asymptomatic; medical (tranexamic acid, NSAIDs, LNG-IUS, GnRH agonist with add-back, GnRH antagonist); surgery (myomectomy for uterus/fertility preservation, hysterectomy definitive cure for completed family); and uterus-sparing radiological options (uterine artery embolisation, MRgFUS, radiofrequency ablation).
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gastroenterology
3 topicsgastroenterology
1
Gastroenterology
2
Gastroenterology
Functional Dyspepsia
Functional dyspepsia is chronic (at least 3 months) epigastric pain or burning, bothersome postprandial fullness or early satiety, with no structural cause on endoscopy (including normal OGD). It is a disorder of gut-brain interaction driven by gastroduodenal dysmotility, visceral hypersensitivity, duodenal eosinophilic inflammation and low-grade mucosal immune activation, and is divided into two subtypes — postprandial distress syndrome (fullness, early satiety) and epigastric pain syndrome (pain, burning). Diagnosis requires excluding alarm features (age 55 or over, weight loss, bleeding, dysphagia, anaemia, family history) with OGD in selected patients and testing for H. pylori. Management is stepwise — reassurance and lifestyle measures, then test-and-treat H. pylori, a PPI trial, prokinetics, and for refractory disease low-dose tricyclic antidepressants or CBT.
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Gastroenterology
Irritable Bowel Syndrome
Irritable Bowel Syndrome (IBS) is a Disorder of Gut-Brain Interaction (DGBI) defined by the Rome IV criteria as recurrent abdominal pain at least one day per week in the last three months, associated with two or more of: (1) relation to defaecation, (2) associated change in stool frequency, (3) associated change in stool form (appearance) — in the absence of alarm features or structural disease. Prevalence is 10 to 15 percent of adults worldwide, with a female-to-male ratio of about 2:1 and peak onset before age 50. The four Rome IV subtypes are IBS-C (constipation), IBS-D (diarrhoea), IBS-M (mixed) and IBS-U (unclassified); severity is graded mild, moderate or severe by impact on daily activities…
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