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Pathology I — Cellular Injury, Adaptation & Death — USMLE Step 2 CK Notes
Free, high-yield revision notes for USMLE Step 2 CK. Read here, or drill the same material as questions and flashcards in the app.
Shared for free public use by a practising clinician who has sat the exam, with their permission. These notes are a revision aid and are not editorially reviewed, so verify against a primary source before relying on anything clinically.
Why this chapter is worth the most
Cell injury, inflammation and neoplasia are the general principles the rest of pathology is built on. Test-takers report several questions drawn straight from them, and their logic recurs in every organ system.
Cellular adaptations (reversible, purposeful)
| Adaptation | Meaning | Example |
|---|---|---|
| Hypertrophy | Bigger cells | Cardiac muscle in hypertension |
| Hyperplasia | More cells | Endometrium, prostate (BPH) |
| Atrophy | Smaller / fewer cells | Disuse, denervation, ischaemia |
| Metaplasia | One mature type → another | Barrett oesophagus |
| Dysplasia | Disordered, pre-malignant | Cervical CIN |
Reversible vs irreversible injury
- Reversible: cellular swelling (failed Na/K ATPase), ribosomal detachment, fatty change
- Irreversible marker: membrane damage with calcium influx; mitochondrial vacuolisation; the point of no return
- Ischaemia depletes ATP → the earliest lesion is cellular swelling
Necrosis — six patterns to recognise
- Coagulative — ischaemia in solid organs; preserved outlines, lost nuclei
- Liquefactive — brain infarct, and abscesses (neutrophil enzymes)
- Caseous — TB and fungi; granuloma with central 'cheese'
- Fat — pancreatitis (saponification) and breast trauma
- Fibrinoid — vessel walls in vasculitis and malignant hypertension
- Gangrenous — dry (coagulative) or wet (superimposed infection)
Apoptosis vs necrosis
| Apoptosis | Necrosis | |
|---|---|---|
| Trigger | Programmed signal | Injury |
| Cell | Shrinks | Swells |
| Membrane | Intact | Ruptures |
| Inflammation | None | Yes |
| Enzymes | Caspases | — |
Intrinsic pathway: BCL-2 family, mitochondrial cytochrome c. Extrinsic: Fas/FasL and TNF death receptors.
Free radicals and pigments
- Reactive oxygen species cause reperfusion injury, CCl4 toxicity, ageing; scavenged by SOD, catalase, glutathione
- Lipofuscin ('wear and tear'), haemosiderin (iron overload), and amyloid (Congo red, apple-green birefringence)
AI-authored Step 1 pathology · not editorially reviewed · study aid only.
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