Cardiovascular & Respiratory Pathology: OmpathStudy

. CARDIOVASCULAR PATHOLOGY Atherosclerosis Pathogenesis (response-to-injury): Chronic endothelial injury (HTN, smoking, hyperlipidaemia, hyperglycaemia, turbulent flow at branch points) Injured endothelium → permeable to LDL → LDL enters intima, oxidizes Oxidized LDL attracts monocytes → become macrophages → engulf lipid → foam cells Foam cell accumulation = fatty streak (earliest lesion) Growth factors → smooth muscle migrates from media to intima, proliferates, lays collagen → fibrous cap over lipid core = fibrous plaque Plaque calcifies, ulcerates, haemorrhages, or ruptures = complicated plaque → thrombus → acute occlusion Morphology by stage: fatty streak (flat, yellow, macrophages only) → fibrous plaque (raised, fibrous cap + necrotic core) → complicated plaque (calcification, haemorrhage, ulceration, superimposed thrombus) Risk factors: hyperlipidaemia, hypertension, smoking, diabetes, age, male sex, genetics --- Rheumatic Heart Disease Follows group A β-haemolytic strep pharyngitis (not skin infection) Mechanism: molecular mimicry — antibodies to strep M protein cross-react with cardiac tissue (Type II hypersensitivity) Acute RHD: pancarditis — fibrinous pericarditis, myocarditis with Aschoff bodies (pathognomonic — fibrinoid necrosis + lymphocytes + Anitschkow/"caterpillar" cells), verrucous endocarditis along valve closure lines Chronic RHD: valve leaflet fibrosis/fusion, chordae shortening, "fish-mouth"/"buttonhole" mitral stenosis Mitral valve most affected aortic Clinical (Jones criteria): fever, migratory polyarthritis, carditis, subcutaneous nodules, erythema marginatum, Sydenham chorea --- Infective Endocarditis Acute Subacute --- --- --- Organism S. aureus (virulent) Strep viridans (low virulence) Valve Previously normal Previously damaged Course Rapid, fulminant Indolent, weeks-months Destruction Extensive Minimal Shared features: vegetations (fibrin+platelets+organisms+inflammatory cells), septic emboli, Janeway lesions, Osler nodes, Roth spots, immune-complex glomerulonephritis --- Dilated Cardiomyopathy Morphology: all 4 chambers dilated, walls thin/normal, mural thrombi common, nonspecific fibrosis on microscopy Mechanism: loss of contractility → systolic dysfunction → dilation → increased wall stress → worsening (vicious cycle) Causes: idiopathic/genetic, viral myocarditis (Coxsackie B), alcohol, peripartum, doxorubicin Other cardiomyopathies (likely add-on) Hypertrophic: asymmetric septal hypertrophy, diastolic dysfunction, myocyte disarray, cause of sudden death in young athletes, genetic (sarcomere protein mutations) Restrictive: normal chamber size, stiff walls, diastolic dysfunction — amyloidosis, sarcoidosis, endomyocardial fibrosis --- Vasculitis by vessel size Large: Takayasu (young Asian women, aortic arch), Giant Cell/Temporal Arteritis (elderly, headache, jaw claudication, blindness risk) Medium: PAN (Hep B association, spares lungs), Kawasaki (children, coronary aneurysms) Small: GPA/Wegener's (c-ANCA, resp tract + kidney), Microscopic Polyangiitis (p-ANCA, no granulomas), Henoch-Schönlein purpura (IgA-mediated) --- Pulmonary Thromboembolism Source: 95% from DVT (femoral/iliac/popliteal) — Virchow's triad Saddle embolus → sudden death (acute cor pulmonale) Medium embolus → haemorrhagic wedge infarct Small/recurrent → chronic pulmonary hypertension Ischaemic Heart Disease / MI (add-on — high-yield, not in your list but commonly examined) Coagulative necrosis at 4-24h (earliest microscopic change ~12-24h) Neutrophil infiltrate 1-3 days Macrophages/granulation tissue 3-7 days Scar formation by 6 weeks Complications: arrhythmia (early, commonest cause of death), cardiogenic shock, free wall rupture (day 3-7, weakest point), papillary muscle rupture, mural thrombus, Dressler syndrome (autoimmune pericarditis weeks later) Cor Pulmonale (add-on) Right heart failure secondary to pulmonary hypertension from lung disease Commonest cause: COPD Right ventricular hypertrophy ± dilation --- RESPIRATORY PATHOLOGY Chronic Obstructive Pulmonary Disease — Emphysema vs Chronic Bronchitis Emphysema pathogenesis: Protease-antiprotease imbalance Smoking recruits neutrophils/macrophages → release elastase Smoking also oxidizes/inactivates α1-antitrypsin; genetic deficiency worsens this Unchecked elastase destroys alveolar septae → permanent airspace enlargement distal to terminal bronchiole Loss of elastic recoil → air trapping "Pink puffer": thin, dyspnoeic, compensatory hyperventilation Chronic bronchitis: Clinical definition: productive cough 3 months/year, 2 consecutive years Mucus gland hyperplasia — measured by Reid index (increased) "Blue bloater": cyanotic, obese, hypoxic/hypercapnic, less compensation Emphysema Chronic Bronchitis --- --- --- Site Alveoli/acinus Bronchi Mechanism Protease-antiprotease imbalance Gland hyperplasia Marker ↓Elastic recoil ↑Reid index Cor pulmonale Late Early Bronchiectasis (add-on — often paired with COPD topics) Permanent dilation of bronchi due to destructi