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Cell death — types of necrosis, apoptosis and regulated pathways
Necrosis is uncontrolled cell death with membrane rupture and surrounding inflammation, and apoptosis is programmed death in which the cell shrinks and breaks into bodies without inflammation — and between the two lie further regulated pathways: necroptosis, pyroptosis and ferroptosis.
Why it matters in the exam
The bank asks about necrosis types by organ and the molecules of apoptosis. Coagulative necrosis — tissue architecture preserved and "ghost" cells — characterises infarcts in all organs except the brain. Liquefactive necrosis characterises the brain and abscesses. Caseous necrosis — cheesy material without structure — characterises tuberculosis. Fat necrosis forms in pancreatitis from lipases (with calcium soaps) and in the breast after trauma. Fibrinoid necrosis in vessel walls appears in vasculitis and malignant hypertension. "Gangrene" is a clinical term for necrosis of a limb. Nuclear changes: shrinkage (pyknosis), fragmentation (karyorrhexis) and dissolution (karyolysis).
Apoptosis occurs through two pathways. The intrinsic (mitochondrial) pathway is triggered by DNA damage, growth-factor withdrawal and reticulum stress; the proteins BAX and BAK open the mitochondrial membrane, cytochrome c escapes and activates caspase 9, while BCL-2 and BCL-XL inhibit the process. The extrinsic pathway is triggered through death receptors — Fas with FasL and the TNF receptor — and activates caspase 8. Both pathways converge on executioner caspases, mainly caspase 3. Many tumour cells evade apoptosis by excess BCL-2 (for example follicular lymphoma with t(14;18)) or by loss of p53.
Necroptosis is regulated necrosis mediated by RIPK1, RIPK3 and MLKL, when caspases are inhibited. Pyroptosis is mediated by the inflammasome and caspase 1, releases IL-1 and provokes inflammation. Ferroptosis is iron-dependent death from membrane lipid peroxidation. Reperfusion injury increases damage through free radicals, calcium overload and inflammation. In morphology questions, apoptosis appears as a single shrunken eosinophilic cell with condensed chromatin and no surrounding inflammation.
Key points
- Coagulative in infarcts; liquefactive in brain and abscess; caseous in tuberculosis.
- Fat necrosis: pancreas and breast; fibrinoid necrosis: vasculitis.
- Intrinsic pathway: BAX and BAK, cytochrome c, caspase 9; BCL-2 inhibits.
- Extrinsic pathway: Fas and TNF, caspase 8; convergence on caspase 3.
- Necroptosis, pyroptosis and ferroptosis are further regulated pathways.
Summary table
| Type | Feature | Example | Mechanism |
|---|---|---|---|
| Coagulative necrosis | Architecture preserved, ghost cells | Infarct of heart and kidney | Protein denaturation |
| Liquefactive necrosis | Tissue dissolved | Brain infarct, abscess | Hydrolytic enzymes |
| Caseous necrosis | Cheesy material without structure | Tuberculosis | Granulomatous reaction |
| Fat necrosis | Calcium soaps | Pancreatitis, breast trauma | Lipases |
| Apoptosis | Shrunken cell without inflammation | Developmental regulation, DNA damage | Caspases 8, 9 and 3 |
Free exam questions
באבחנה של Infiltrating astrocytoma אנחנו משתמשים בקריטריונים היסטולוגים שונים. איזה מבין הממצאים ההיסטולוגיי ם הבאים לא מהווה קריטריון לאבחון דרגת הממאירות לפי ה WHO ? (the question as examined, in Hebrew)
- א. ( דרגת ההסננה של הנגע degree of infiltration )
- ב. נמק
- ג. מיטוזות
- ד. Microvascular cell proliferation בחינת של ב א' אנטומיה פתולוגית 21.06.22
איזה מבין הממצאים המורפולוגיים הבאים אינו אופייני ל apoptosis? (the question as examined, in Hebrew)
- א. Shrinkage of cell size
- ב. Disruption of plasma membrane
- ג. Absence of accompanying inflammation
- ד. Chromatin condensation and nuclear fragmentation
) בתהליך האפופטוזיס apoptosis ( משתחרר החלבון cytochrome c מהמיטוכונדריה אל הציטופלזמה. כיצד פועל חלבון זה בתוך הציטופלזמה? (the question as examined, in Hebrew)
- א. דרך קישור אל APAF-1
- ב. דרך קישור אל TNF
- ג. דרך קישור אל BCL2
- ד. דרך קישור אל FADD
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Sources
- Robbins and Cotran Pathologic Basis of Disease, 10th edition (2021) — Cell death: necrosis, apoptosis and other pathways
- Galluzzi L et al. Molecular mechanisms of cell death: recommendations of the Nomenclature Committee on Cell Death, Cell Death and Differentiation, 2018 — Definitions of regulated cell death
- Rubin's Pathology: Mechanisms of Human Disease, 8th edition (2020) — Cell death
Sources are given for further reading; the text is written afresh and not copied from them.
Reviewed by the Examqo AI Professor · 2026-11-06. The text may contain errors; when in doubt, check the source.