Essential Cardiovascular Pathology: OmpathStudy

Year 3 Pathology — Cardiovascular, Respiratory & GI/Hepatobiliary SECTION A: CARDIOVASCULAR PATHOLOGY A1. Atherosclerosis Stages: fatty streak → fibrous plaque → complicated plaque (calcification, ulceration, haemorrhage, thrombosis) Complicated plaque causes clinical events: MI, stroke, peripheral vascular disease, aneurysm Risk factors: hyperlipidaemia, hypertension, smoking, diabetes, age, male sex, family history Pathogenesis (response-to-injury hypothesis): endothelial injury → lipid insudation → macrophage foam cell formation → smooth muscle proliferation → fibrous cap formation A2. Myocardial Infarction Time after MI Gross/microscopic change --- --- <24 hours Coagulative necrosis (earliest change) — may look normal grossly 1–3 days Neutrophil infiltration, yellow pallor 3–7 days Macrophages clear debris, yellow-tan, soft (weakest point, highest rupture risk) 1–3 weeks Granulation tissue formation, red-grey border Weeks–months Collagen scar formation, grey-white, firm Complications by timing: arrhythmia (first hours, #1 cause of death) → cardiogenic shock → papillary muscle rupture (day 3–5) → free wall rupture (day 4–7, coincides with softest phase above) → ventricular aneurysm (weeks–months, in the scarred phase) A3. Dilated Cardiomyopathy Cardiomegaly, all four chambers dilated; dilation predominates over hypertrophy Mural thrombi common in dilated chambers (embolism risk) Microscopic: non-specific myocyte hypertrophy, interstitial fibrosis Functional consequence: systolic (contractile) dysfunction → congestive heart failure Causes: idiopathic (most common), viral myocarditis (esp. Coxsackie B), alcohol, peripartum, genetic, doxorubicin toxicity Compare with: Hypertrophic cardiomyopathy — diastolic dysfunction, asymmetric septal hypertrophy, myocyte disarray, cause of sudden death in young athletes Restrictive cardiomyopathy — diastolic dysfunction from myocardial infiltration (amyloid, sarcoidosis) A4. Vasculitis — Classified by Vessel Size Vessel size Examples --- --- Large Takayasu arteritis (young Asian women, aortic arch); Giant cell/temporal arteritis (elderly, headache, jaw claudication, blindness risk) Medium Polyarteritis nodosa (necrotising, Hep B-associated); Kawasaki disease (children, coronary artery aneurysms) Small Granulomatosis with polyangiitis/Wegener's (c-ANCA, upper/lower respiratory + renal); Microscopic polyangiitis (p-ANC A) A5. Rheumatic Heart Disease Pathogenesis: follows untreated Group A streptococcal pharyngitis; molecular mimicry — antibodies against streptococcal M protein cross-react with cardiac tissue; acute rheumatic fever → chronic RHD with repeated episodes Morphology: Aschoff bodies — pathognomonic granulomatous lesions containing Anitschkow cells, found in myocardium Mitral valve most commonly affected → mitral stenosis (fish-mouth/buttonhole deformity) Valve changes: leaflet thickening, commissural fusion, chordae tendineae shortening Diagnosis (Jones criteria): Major — carditis, polyarthritis, chorea, erythema marginatum, subcutaneous nodules. Minor — fever, arthralgia, raised ESR/CRP A6. Infective Endocarditis — Acute vs Sub-acute Feature Acute IE Sub-acute IE --- --- --- Organism Staphylococcus aureus (virulent) Streptococcus viridans (less virulent) Valve affected Often previously normal Usually previously damaged Onset Rapid, days Slow, weeks–months Vegetations Large, destructive Smaller Course Severe, rapidly fatal if untreated Indolent Related non-infective forms: Non-bacterial thrombotic (marantic) endocarditis — sterile vegetations, associated with malignancy/hypercoagulable states. Libman-Sacks endocarditis — associated with SL E. A7. Pulmonary Thromboembolism Pathogenesis: most emboli arise from DVT of the lower limbs (femoral, iliac veins); Virchow's triad predisposes — venous stasis, hypercoagulability, endothelial injury; thrombus dislodges → right heart → pulmonary arteries Consequences by size: Small — often asymptomatic/silent Large — sudden death via saddle embolus occluding the pulmonary artery bifurcation Medium — pulmonary infarction (wedge-shaped, haemorrhagic) if collateral circulation inadequate Chronic recurrent — pulmonary hypertension, cor pulmonale --- SECTION B: RESPIRATORY PATHOLOGY B1. Emphysema vs Chronic Bronchitis Feature Emphysema (pink puffer) Chronic bronchitis (blue bloater) --- --- --- Definition Permanent airspace enlargement distal to terminal bronchiole, wall destruction Chronic productive cough ≥3 months, 2 consecutive years Main mechanism Protease-antiprotease imbalance (↓alpha-1 antitrypsin), elastin destruction Chronic irritation (smoking) → mucous gland hyperplasia (↑Reid index) 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 ant