Pathology

Acute inflammation is the body's emergency service, and its steps map onto the cardinal signs taught since Celsus. Vascular phase: momentary arteriolar constriction, then sustained vasodilatation driven by histamine (mast cells), prostaglandins and nitric oxide — hyperaemia producing redness (rubor) and heat (calor); simultaneously venular endothelial cells contract, opening intercellular gaps: protein-rich fluid (exudate — protein above ~30 g/L with cells, distinguishing it from the low-protein transudate of pure pressure/oncotic imbalance, the distinction used in effusion and ascites analysis) pours into tissue, causing swelling (tumor), diluting toxins and delivering fibrin, complement and antibodies. Pain (dolor) is mediated — bradykinin and PGE2 sensitise nociceptors (the pharmacological address of NSAIDs) — plus tension from swelling; together with reflex guarding these produce loss of function (functio laesa), which is real and protective. Cellular phase: slowed flow lets neutrophils marginate; selectins roll them, chemokine-activated integrins bind them firmly (ICAM/VCAM), they transmigrate (diapedesis) and follow chemotactic gradients — C5a, leukotriene B4, IL-8, bacterial peptides — to the focus, where opsonisation (IgG, C3b) enables phagocytosis and killing by the NADPH-oxidase respiratory burst and lysosomal enzymes (the mechanism whose failure — diabetes, hypothermia, steroids — explains this bank's wound infection risk factors). Outcomes: complete resolution; organisation and fibrosis; suppuration — the walled abscess whose antibiotic-impenetrability underlies the source-control doctrine; or transition to chronic inflammation.

Why the others are wrong: A, B, C and E — inflammation is protective (its absence, as in neutropenia, is deadly, and its signs are then muted); neutrophils arrive first (lymphocytes belong to chronicity); exudate is protein-rich and permeability-driven; functio laesa has mechanistic grounding.

Key point: Vasodilatation (rubor, calor), permeable venules leaking protein-rich exudate (tumor), mediator-sensitised pain (dolor) and neutrophils delivered by the selectin-integrin-chemotaxis relay — acute inflammation's machinery explains the cardinal signs, the exudate/transudate divide, and why pus needs a drain, not just a drug.

Chronic inflammation is not prolonged acute inflammation but a different programme, and its histology changes surgical diagnoses. Cellular cast: macrophages — recruited monocytes activated classically by T-cell interferon-gamma — dominate, flanked by lymphocytes and plasma cells; the tissue shows the signature paradox of destruction (macrophage enzymes, reactive oxygen species) proceeding alongside attempted repair — angiogenesis, fibroblast proliferation, collagen: the fibrosis that is chronic inflammation's monument (the strictures of Crohn's disease, the contracted gallbladder of chronic cholecystitis, the frozen fields of chronic pancreatitis met throughout this bank). Causes: persistent low-virulence infection (TB, H. pylori — whose gastritis-to-cancer sequence appears elsewhere), indigestible material (suture, mesh, urate, silica), and autoimmunity. The granuloma is the specialised solution to the indigestible: a organised focus of epithelioid macrophages (secretory, adherent transformation), often fused into Langhans-type giant cells, ringed by lymphocytes — immunological quarantine, T-cell-dependent (which is why anti-TNF therapy dissolves granuloma integrity and reactivates TB, the screening rationale before biologics in the Crohn's questions). Reading granulomas surgically: central caseous necrosis points to mycobacteria (the terminal-ileal or nodal TB masquerading as Crohn's or malignancy — send tissue for culture and PCR, not just formalin); non-caseating granulomas suggest Crohn's disease (a diagnostic criterion in the resected specimen), sarcoidosis, foreign-body reaction or vasculitides. The practical rule embedded here: unexpected granulomas in a surgical specimen mandate fresh-tissue microbiology and a TB question before immunosuppression.

Why the others are wrong: B, C, D and E — the cellular programme differs; granulomas are macrophage, not neutrophil, structures; caseation flags TB, its absence the others; fibrosis is chronicity's hallmark companion.

Key point: Chronic inflammation = mononuclear cells destroying and repairing at once, ending in fibrosis; the granuloma is T-cell-orchestrated macrophage quarantine — caseating: think TB (culture the tissue), non-caseating: think Crohn's, sarcoid or foreign body — and anti-TNF therapy unlocks the quarantine.

Guidelines: NICE tuberculosis guidance (NG33): granulomatous inflammation on histology should prompt fresh (unfixed) tissue for mycobacterial culture and molecular testing, since caseating granulomas suggest TB and culture confirms sensitivity — fixation destroys the organism's viability.