General Pathology Revision: Cell Injury, OmpathStudy

For Tuesday, the most voluminous and easiest-to-forget material is General Pathology (Systemic Pathology Paper 1) : it has 28 essay questions covering cell injury, inflammation, wound healing, and neoplasia — dense, enumeration-heavy content that's hard to recall under exam pressure. I'll start there, then Female Genital System (Paper 2's biggest, cervical Ca is the most-repeated essay in the whole document), then work down. --- TUESDAY — PART 1: GENERAL PATHOLOGY (MBPA 3500 Paper 1) --- 1. CELL INJURY & ADAPTATION Cell regeneration hierarchy (know this cold — classic trap below): Labile cells — continuously dividing (skin epithelium, GI mucosa, bone marrow) Stable cells — normally quiescent, can regenerate if stimulated (liver, kidney tubules, smooth muscle ) Permanent cells — cannot regenerate (neurons, skeletal muscle, cardiac muscle ) ⚠️ Trap: Smooth muscle is STABLE, not permanent. Cardiac muscle is the LEAST regenerative of all (permanent). Cell cycle phases: G0 (resting) → G1 (growth) → S (DNA synthesis) → G2 (growth/preparation) → M (mitosis) Mechanisms of cell injury: Mitochondrial damage — ↓ATP production Membrane damage — loss of ion gradients, cell swelling Calcium derangement — influx activates destructive enzymes (proteases, phospholipases) Lysosomal enzyme leakage — self-digestion ⚠️ "Normal/increased protein synthesis" is always the FALSE option in MCQs — injury impairs protein synthesis Reversible vs irreversible injury: Reversible — cellular swelling, fatty change Irreversible — pyknosis (nuclear shrinkage), karyorrhexis (nuclear fragmentation), karyolysis (nuclear dissolution) — these three are the classic nuclear changes of necrosis, occurring in that sequence Cardiac injury marker: Creatine kinase-MB (CK-MB) — see also cardiac markers table from Monday's Chemical Pathology Cellular adaptations (essay-favourite, asked twice): Hypertrophy — increase in cell SIZE (e.g. cardiac muscle in hypertension) Hyperplasia — increase in cell NUMBER (e.g. endometrium in oestrogen excess) Atrophy — decrease in cell size/number from disuse, denervation, ischaemia, or ageing Metaplasia — reversible change of one differentiated cell type to another, e.g. bronchial columnar → squamous epithelium in smokers ; always reversible, but persistent stimulus can progress to dysplasia and cancer Historical fact: Elie Metchnikoff discovered phagocytosis. Chediak-Higashi syndrome: impairs phagolysosome formation → recurrent infections, partial albinism, giant granules in leukocytes. --- 2. ACUTE INFLAMMATION (asked 3× as an essay — master this fully) Vascular events (in order): 1. Transient vasoconstriction (seconds) 2. Vasodilation — increased blood flow (causes redness/heat) 3. Increased vascular permeability — fluid leaks into tissue (causes swelling) 4. Stasis — slowed blood flow allows leukocyte margination Cellular events (in chronological order — this exact sequence is asked separately too): 1. Margination — leukocytes move to vessel periphery 2. Rolling — leukocytes roll along endothelium (selectins) 3. Adhesion — firm attachment (integrins, ICAM/VCAM) 4. Diapedesis — migration through endothelial junctions into tissue 5. Chemotaxis — directed migration toward the injury site (via chemokines, complement C5a, leukotriene B4) 6. Phagocytosis — recognition, engulfment, and killing of the pathogen/debris Key inflammatory mediators and actions: Histamine/serotonin (from mast cells) — vasodilation, increased permeability Bradykinin — pain, vasodilation, smooth muscle contraction (⚠️ NOT involved in opsonization — common false-option trap) Prostaglandins — vasodilation, pain, fever Leukotrienes — chemotaxis, bronchoconstriction Complement (C3a, C5a) — anaphylatoxins, chemotaxis, opsonization (C3b) Cell types: Acute inflammation — neutrophil is the main cell Chronic inflammation — macrophage is the main cell Exudate vs Transudate (commonly asked to differentiate): Feature Exudate Transudate --- --- --- Protein content High Low Cause Inflammation (increased permeability) ↓Oncotic pressure or ↑hydrostatic pressure Cellularity High (inflammatory cells) Low Specific gravity 1.020 <1.012 Example Pneumonia, abscess Heart failure, cirrhosis, nephrotic syndrome Oedema: Commonest cause overall: ↓plasma oncotic pressure (e.g. liver cirrhosis, nephrotic syndrome, malnutrition) ⚠️ Potassium retention is NOT a cause of oedema — sodium retention is --- 3. CHRONIC INFLAMMATION Histological hallmarks: Mononuclear cell infiltrate (macrophages, lymphocytes, plasma cells) Tissue destruction Attempts at healing — angiogenesis and fibrosis occurring simultaneously Mediators and actions: Macrophage-derived cytokines (TNF-α, IL-1) — sustain inflammation, cause systemic effects (fever) Growth factors — stimulate fibroblast proliferation and angiogenesis Interferon-gamma (from T-lymphocytes) — activates macrophages Granuloma formation (essay-favourite): Definition: organised collection of activated macrophages (epithelioid cells), often with