General Pathology: Cell Injury, Inflammation, Repair, Neoplasia, and Hemodynamics
Core framework
Cell injury begins with ATP depletion, mitochondrial permeability transition, calcium influx, and reactive oxygen species. Reversible injury shows swelling and blebs; irreversible injury shows membrane rupture, mitochondrial cristae loss, and nuclear changes (pyknosis, karyorrhexis, karyolysis). Apoptosis is energy-dependent, caspase-mediated, and produces no inflammation; necrosis is passive and inflames. Learn the necrosis patterns: coagulative (ischemia except brain), liquefactive (brain, abscess), caseous (TB, fungi), and fibrinoid (vasculitis). Fat necrosis follows pancreatitis; dystrophic calcification occurs in damaged tissue with normal serum calcium, metastatic calcification with hypercalcemia.
Inflammation: acute inflammation uses neutrophils, vasodilation, increased permeability, and mediators (histamine, bradykinin, leukotrienes, IL-1, TNF, complement). Chronic inflammation uses lymphocytes, plasma cells, macrophages, and granulomas. Repair: primary intention for clean wounds, secondary for gaping wounds; type III collagen early, type I later; wound strength is low early and rises over months.
Neoplasia: distinguish dysplasia (reversible, basement membrane intact) from carcinoma in situ (full thickness, intact membrane) from invasive carcinoma. Hallmarks include self-sufficiency, insensitivity to growth inhibition, evading apoptosis, immortalization, angiogenesis, invasion, and metastasis. Grading describes differentiation; staging describes spread and predicts prognosis better.
Hemodynamics: Virchow triad (stasis, endothelial injury, hypercoagulability). Infarcts are pale in solid organs with end-arterial supply and red in loose tissues or dual supply.
Traps and a worked rule
Questions often swap coagulative and liquefactive necrosis, or ask which change is earliest. They also confuse grade with stage, and granuloma with neoplasm.
Rule of thumb: if tissue architecture is preserved, think coagulative necrosis; if it is destroyed, think liquefactive.
Worked example: a myocardial infarct at 24 hours shows coagulative necrosis with neutrophils; at 2 months, a collagenous scar. The earliest visible light-microscopic change is at 12–24 hours.