Pathology & Morphology — Quick Bullets

1. Myocardial Infarction (MI)

• Vast majority caused by acute coronary thrombosis on a disrupted/eroded atherosclerotic plaque
• Plaque rupture → platelet aggregation → thromboxane A2/ADP/serotonin release → occlusion
• ~10% occur without occlusive atherosclerosis (vasospasm, mural thrombi, embolism)

• Transmural - full-thickness necrosis; epicardial vessel occlusion + thrombus
• Subendocardial - limited to inner 1/3 of myocardium; thrombus lysed before transmural spread; most vulnerable zone due to distance from epicardial vessels

• LAD occlusion (40-50%): anterior LV, anterior 2/3 of septum, apex
• RCA occlusion (30-40%): posterior/inferior LV, posterior 1/3 of septum
• LCX occlusion (15-20%): lateral LV

• Contractile dysfunction, arrhythmias, papillary muscle rupture (MR), free wall rupture → haemopericardium, ventricular aneurysm, mural thrombus, Dressler syndrome

2. Rheumatic Heart Disease (RHD)

• Group A streptococcal pharyngitis → 2-3 wk delay → immune response
• Anti-streptococcal antibodies (against M protein) cross-react with cardiac antigens (molecular mimicry)
• CD4+ T cells + complement activation → pancarditis
• Streptococci are absent from lesions

• Focal inflammatory nodules in myocardium, pericardium, endocardium
• Composed of: T lymphocytes, plasma cells, plump macrophages called Anitschkow cells (abundant cytoplasm, central chromatin condensed into a wavy ribbon = "caterpillar cells")
• Pancarditis = all three layers involved
• Endocarditis: fibrinoid necrosis → small 1-2 mm verrucae along valve closure lines
• MacCallum plaques: subendocardial thickenings in left atrium (from regurgitant jets)

• Mitral valve always involved (isolated in 2/3; mitral + aortic in 25%)
• Leaflet thickening, commissural fusion, chordal thickening and shortening
• "Fish mouth" / "button-hole" stenosis - fusion creates this appearance
• Neovascularization of valve leaflets in chronic disease
• Pulmonary valve - rarely affected

3. Lung Carcinoma

• Peripheral location; associated with pleural scars
• Lepidic growth pattern (along alveolar walls without architectural destruction) in adenocarcinoma in situ (AIS, ≤3 cm)
• Invasive: glandular, papillary, micropapillary, solid, or acinar patterns; desmoplasia present

• Central location; arises in major bronchi
• Preceded by squamous metaplasia → dysplasia → carcinoma in situ (over years)
• Keratin pearls + intercellular bridges (well-differentiated)
• Large lesions may undergo central necrosis → cavitation

• Central, pale gray mass extending into parenchyma
• Cells: small, round to fusiform, scant cytoplasm, finely granular "salt-and-pepper" chromatin
• Numerous mitoses; extensive necrosis
• Azzopardi effect: DNA staining blue along vessel walls (crush artifact in biopsies)
• Neuroendocrine markers: synaptophysin, chromogranin, CD56
• Metastasizes early (hilar + mediastinal nodes); associated with paraneoplastic syndromes
• Grouped with large cell neuroendocrine carcinoma in 2021 WHO Classification

• Diagnosis of exclusion (~10%)
• Large nuclei, prominent nucleoli, moderate cytoplasm; no squamous or glandular features

4. Inflammatory Bowel Disease (IBD)

Crohn Disease

• Any site from mouth to anus; most common = terminal ileum + cecum
• Skip lesions (multiple, separated areas of disease interspersed with normal mucosa)
• Earliest lesion: aphthous ulcers → progress to serpentine ulcers along long axis
• Cobblestone appearance: edematous mucosa elevated around depressed ulcers
• Transmural inflammation → intestinal wall thickening, fibrosis, strictures
• Creeping fat: mesenteric fat adherent to serosa
• Fissures → fistulas (to bladder, vagina, skin) or perforation
• Microscopy: crypt abscesses, distorted crypts, noncaseating granulomas (~35% of cases) - hallmark but not required for diagnosis; may be in any layer; pseudopyloric metaplasia

Ulcerative Colitis (UC)

• Always starts in rectum, extends proximally, continuously - no skip lesions
• Limited to colon; pancolitis = entire colon
• Gross: broad-based ulcers; pseudopolyps (islands of regenerating mucosa)
• No mural thickening, no strictures (unlike Crohn); serosal surface normal
• Microscopy: inflammation limited to mucosa and superficial submucosa; crypt abscesses; crypt distortion; no granulomas
• Toxic megacolon: inflammation damages muscularis propria → colonic dilation → perforation risk

5. Liver Cirrhosis

• Diffuse transformation of entire liver into regenerative parenchymal nodules surrounded by fibrous bands

• Gross: nodular liver surface; broad fibrous scars between bulging nodules
• Micronodular (<3 mm, uniform) vs. macronodular (>3 mm, irregular) - alcohol typically micronodular early
• Microscopy: regenerative nodules; portal-portal or portal-central fibrous bridging; ductular reactions (stem cell-derived duct-like structures, prominent in cirrhosis)
• Fibrosis can regress if disease is cured (scars thin → fragment → nodules coalesce)

• Chronic HBV, HCV, NAFLD/NASH, alcohol-related liver disease

• Portal hypertension → esophageal varices, ascites, splenomegaly
• Hepatic encephalopathy (ammonia, GABA)
• Hepatocellular carcinoma (especially in HBV, HCV, alcohol cirrhosis)
• Coagulopathy, jaundice, pruritus, hypoalbuminemia

6. Cholelithiasis (Gallstones)

• Supersaturation of bile with cholesterol → nucleation → crystal growth
• Three factors: (1) supersaturation, (2) accelerated nucleation, (3) biliary stasis
• Cholesterol stones contain calcium salts, proteins, and bile pigments admixed

• Cholesterol stones: pale yellow, round to faceted, hard, may be multiple; cross-section shows radial crystalline pattern
• Pigment stones: black - small, irregular, multiple, crumble easily; brown - soft, greasy
• Gallbladder wall: may show chronic cholecystitis (fibrosis, Rokitansky-Aschoff sinuses), or acute cholecystitis (edema, neutrophils, mucosal necrosis)

• Biliary colic, cholecystitis (acute/chronic), choledocholithiasis, cholangitis, gallstone ileus, Mirizzi syndrome; risk factor for gallbladder carcinoma

7. Breast Carcinoma

• Malignant cells confined within ductal-lobular system, no basement membrane invasion
• Comedo type (high-grade): large cells with pleomorphic nuclei, central necrosis, calcifications → linear/branching calcifications on mammography
• Non-comedo types: cribriform, micropapillary, solid, papillary patterns
• Paget disease of nipple = DCIS extending into nipple epidermis; associated with invasive carcinoma

• Monomorphic, small, discohesive cells filling the lobule; loss of E-cadherin
• Rarely forms calcifications; usually incidental
• Risk marker for invasive carcinoma in either breast

• Hard, gritty mass on cut section; dense fibrotic stroma (desmoplasia)
• Forms irregular nests, cords, or glands infiltrating stroma
• Graded by Nottingham system: tubule formation, nuclear pleomorphism, mitotic count

• Single file ("Indian file") invasion through stroma; targetoid pattern around ducts
• Loss of E-cadherin (CDH1 mutations)
• Discohesive cells with intracytoplasmic mucin vacuoles (signet ring-like)
• Bilateral in ~20%; may metastasize to serosal surfaces, GI tract, meninges

Cardamom - Pods / "Strands"

What It Is

Culinary Uses

• Added whole to rice dishes, biryanis, curries, stews, and braised meats - impart flavour while cooking, then removed before eating (like a bay leaf or whole clove)
• Indian biryani typically uses 4 whole pods
• Crushed and steeped in chai tea and Arabic coffee (gahwa)

• Toasted and ground with a mortar and pestle for maximum fresh flavour
• Used in desserts, pastries, Scandinavian breads, Indian sweets (mithai), garam masala spice blend

• Convenient but loses flavour faster; used in baking, coffee, spice rubs

Flavour Profile

• α-terpinyl acetate and α-terpineol - sweet, warm, floral notes
• 1,8-cineole (eucalyptol) - the sharp, mentholated, woody impression

Health Benefits (Evidence-Based)

• Antioxidant - rich in phenols, flavonoids, terpenoids, tannins
• Anti-inflammatory - bioactive compounds reduce inflammatory markers
• Digestive aid - soothes stomach, reduces bloating, relieves nausea/morning sickness
• Blood pressure - some evidence of lipid-modifying and BP-lowering effects
• Antimicrobial - essential oils active against certain bacteria

How to Use the Whole Pod (Strands)

1. Crush lightly with the flat of a knife or mortar to crack the husk - this releases the seeds and their aroma into the dish
2. Infuse in hot liquid (tea, coffee, simmering sauces, rice water)
3. Remove before serving - the pod itself is fibrous and unpleasant to bite into
4. For grinding: split pod, extract seeds, discard husk, grind seeds fresh

Storage

• Store whole pods in an airtight container, cool and dark
• Whole pods last up to 1 year with good flavour retention
• Ground cardamom loses potency within a few months - buy whole pods and grind as needed for best results