The dividing line is mitochondrial permeability and membrane integrity — not swelling or blebbing.
Why this is true
Injury begins with ATP depletion: the Na⁺/K⁺-ATPase fails, sodium and water enter, and the cell swells. All of that is recoverable. The point of no return is opening of the mitochondrial permeability transition pore, which collapses the proton gradient so that even restored oxygen cannot regenerate ATP, and releases cytochrome c. Combined with plasma membrane defects and massive calcium influx activating phospholipases and proteases, the cell can no longer be rescued. This is also why restoring blood flow can *worsen* infarction — oxygen returning to damaged mitochondria generates free radicals rather than ATP.
Key points
Necrosis patterns
| Pattern | Typical site | Mechanism |
|---|---|---|
| Coagulative | Heart, kidney, spleen | Ischaemia with protein denaturation |
| Liquefactive | Brain, abscess | Enzymatic digestion |
| Caseous | Tuberculosis, fungi | Granulomatous inflammation |
| Fat | Pancreas, breast | Lipase-mediated saponification |
| Fibrinoid | Vessel walls | Immune complex deposition |
Common traps
- Cellular swelling is reversible; mitochondrial vacuolisation is not. Both look like 'swelling' in a stem.
- Apoptotic bodies are cleared without inflammation — a stem mentioning a neutrophil infiltrate is describing necrosis.
Clinical case
Three days after successful thrombolysis a myocardial infarct is larger than the initial perfusion defect predicted.
High-yield
Reperfusion injury is oxygen-radical and calcium mediated, worsening the initial infarct.