General Pathology: Mechanisms, Patterns, and Pitfalls
General Pathology tests whether you can connect a clinical insult to a cellular and tissue pattern, then distinguish reversible from irreversible disease. Expect cell injury, inflammation, repair, neoplasia and hemodynamics to be examined as mechanisms rather than lists.
Core rules
- Reversible injury shows swelling, blebs and ribosome detachment; irreversible injury shows membrane rupture, mitochondrial permeability transition and nuclear changes such as pyknosis, karyolysis and karyorrhexis.
- Necrosis is usually accompanied by inflammation; apoptosis is energy-dependent, caspase-mediated and usually not.
- Acute inflammation has vasodilation, increased permeability and neutrophil recruitment; chronic inflammation has mononuclear cells, fibrosis and sometimes granulomas.
- Healing by primary intention gives a fine scar; secondary intention has more granulation tissue and contraction.
- Neoplasia is assessed by differentiation, grade, stage, invasion and metastasis; carcinoma in situ has full-thickness atypia without basement-membrane breach.
- Thrombus forms in flowing blood; embolism travels; infarction depends on vascular supply and oxygen demand.
Worked example
A 58-year-old man dies 36 hours after myocardial infarction. Histology of the left ventricular wall shows loss of nuclei, eosinophilic cytoplasm and neutrophil infiltration. This is coagulative necrosis, typical of ischemic injury except in brain. The neutrophils date the lesion to roughly 1 to 3 days; granulation tissue would appear later. The mechanism is ATP failure, calcium influx and membrane damage, not apoptosis.
Traps
Do not label liquefactive necrosis in brain as coagulative. Fibrinoid necrosis occurs in immune vasculitis and malignant hypertension. Dystrophic calcification occurs in damaged tissue with normal serum calcium; metastatic calcification occurs with hypercalcemia. Dysplasia is not invasion. Hyperplasia increases cell number; hypertrophy increases cell size.