Cardiovascular, Respiratory & OmpathStudy

TUESDAY — PART 3: CARDIOVASCULAR, RESPIRATORY & GI/HEPATOBILIARY PATHOLOGY (MBPA 3500 Paper 2) --- SECTION A: CARDIOVASCULAR PATHOLOGY--- A1. ATHEROSCLEROSIS (recap + expansion from Part 1)- Stages: fatty streak → fibrous plaque → complicated plaque (calcification, ulceration, haemorrhage, thrombosis) Complicated plaque is what causes clinical events — MI, stroke, peripheral vascular disease Risk factors: hyperlipidaemia, hypertension, smoking, diabetes, age, male sex, family history --- A2. MYOCARDIAL INFARCTION Timeline of morphological changes (classic exam table): Time after MI Gross/microscopic change --- --- <24 hours Coagulative necrosis (earliest change) — grossly may look normal 1–3 days Neutrophil infiltration, yellow pallor 3–7 days Macrophages clear debris, yellow-tan, soft 1–3 weeks Granulation tissue formation, red-grey border Weeks–months Collagen scar formation (fibrosis), grey-white, firm Earliest identifiable change (<24h) — coagulative necrosis Cardiac marker timeline (troponin, CK-MB) — see Monday's Chemical Pathology notes --- A3. DILATED CARDIOMYOPATHY (essay-favourite) Morphologic changes in the heart: Cardiomegaly — all four chambers dilated Ventricular walls may be thinned or normal thickness (dilation predominates over hypertrophy) Mural thrombi commonly form in the dilated chambers (risk of embolism) Microscopically — non-specific myocyte hypertrophy and interstitial fibrosis Functional consequence — systolic dysfunction (poor contractility), leads to congestive heart failure Causes: idiopathic (most common), viral myocarditis, alcohol, peripartum, genetic, doxorubicin toxicity --- A4. VASCULITIS — classified by vessel size Vessel size Examples --- --- Large vessel Takayasu arteritis (young Asian women, aortic arch), Giant cell (temporal) arteritis (elderly, headache, jaw claudication) Medium vessel Polyarteritis nodosa (PAN — necrotising, associated with Hep B), Kawasaki disease (children, coronary artery aneurysms) Small vessel Granulomatosis with polyangiitis/Wegener's (c-ANCA, upper/lower respiratory + renal), Microscopic polyangiitis (p-ANCA) --- A5. RHEUMATIC HEART DISEASE Pathogenesis: Follows group A streptococcal pharyngitis (untreated) Molecular mimicry — antibodies against streptococcal M protein cross-react with cardiac tissue Causes acute rheumatic fever → chronic rheumatic heart disease with repeated episodes Morphology: Aschoff bodies — pathognomonic granulomatous lesions containing Anitschkow cells (activated macrophages), found in the myocardium Mitral valve is most commonly affected — leads to mitral stenosis over time (fish-mouth/buttonhole deformity) Valve changes: leaflet thickening, fusion of commissures, chordae tendineae shortening --- A6. INFECTIVE ENDOCARDITIS — Acute vs Sub-acute (commonly compared) Feature Acute IE Sub-acute IE --- --- --- Organism Staphylococcus aureus (virulent) Streptococcus viridans (less virulent) Valve affected Often previously normal valve Usually previously damaged/abnormal valve Onset Rapid, days Slow, weeks–months Vegetations Large, destructive Smaller Course Severe, rapidly fatal if untreated Indolent --- A7. PULMONARY THROMBOEMBOLISM Pathogenesis: Most emboli arise from deep vein thrombosis (DVT) of the lower limbs (femoral, iliac veins) Virchow's triad predisposes: venous stasis, hypercoagulability, endothelial injury Thrombus dislodges → travels through venous system → right heart → pulmonary arteries Morphology/consequences: Small emboli — often asymptomatic or clinically silent Large emboli — can cause sudden death via saddle embolus occluding the pulmonary artery bifurcation Medium emboli — pulmonary infarction (wedge-shaped, haemorrhagic) if collateral circulation is inadequate Chronic recurrent emboli — pulmonary hypertension, cor pulmonale --- SECTION B: RESPIRATORY PATHOLOGY--- B1. EMPHYSEMA vs CHRONIC BRONCHITIS (always compared — the classic COPD pair) Feature Emphysema ("Pink puffer") Chronic bronchitis ("Blue bloater") --- --- --- Definition Permanent airspace enlargement distal to terminal bronchiole, with wall destruction Chronic productive cough for ≥3 months in 2 consecutive years Main mechanism Protease-antiprotease imbalance (↓alpha-1 antitrypsin), destroys elastin Chronic irritation (smoking) → mucous gland hyperplasia Appearance Thin, breathless, pink complexion Overweight, cyanotic, oedematous Hypoxia/CO2 retention Mild, compensates by hyperventilating Marked hypoxia and CO2 retention Cor pulmonale Late Early and more severe Pathogenesis of emphysema: Cigarette smoke → recruits neutrophils/macrophages → release proteases (elastase) Normally alpha-1 antitrypsin inhibits elastase — smoking also inactivates alpha-1 antitrypsin Net effect — unopposed elastase activity destroys alveolar walls → permanent airspace enlargement Alpha-1 antitrypsin deficiency (genetic) — causes early-onset panacinar emphysema, especially in lower lobes --- B2. ASTHMA — microscopic bronchiole changes (5 features)- Bronchial smoot