Pathology Cheat Sheet
Necrosis or Quiet Deletion
Necrosis and apoptosis for NEET-PG: coagulative vs liquefactive vs caseous vs fibrinoid necrosis, gas gangrene, caspase pathways, and apoptosis vs necrosis.
MedNext Academy | 3 min read
Necrosis or Quiet Deletion
Necrosis and apoptosis for NEET-PG: coagulative vs liquefactive vs caseous vs fibrinoid necrosis, gas gangrene, caspase pathways, and apoptosis vs necrosis.
The patterns of necrosis and the mechanisms of apoptosis, with the key features that separate the two forms of cell death.
High-yield lines
- Coagulative necrosis preserves cell outlines and follows ischaemic infarction in heart, kidney, and spleen.
- Brain infarction produces liquefactive rather than coagulative necrosis, the most tested exception.
- Caseous necrosis shows amorphous granular debris surrounded by granulomas and is classic for tuberculosis.
- Fat necrosis in acute pancreatitis forms chalky calcium soaps through saponification of released fatty acids.
- Fibrinoid necrosis is a vessel-wall lesion seen in immune vasculitis and malignant hypertension.
- Gas gangrene is caused by Clostridium perfringens, whose alpha-toxin is a lecithinase producing muscle necrosis and crepitus.
- The first nuclear change in necrosis is pyknosis, followed by karyorrhexis and then karyolysis.
- The first cytoplasmic change in necrosis is increased eosinophilia from RNA loss and protein denaturation.
- Apoptosis is energy-dependent, causes cell shrinkage, and does not incite inflammation because the membrane stays intact.
- The intrinsic apoptotic pathway releases cytochrome c, forms the apoptosome, and activates caspase-9.
- The extrinsic pathway acts through death receptors such as Fas, assembles the DISC, and activates caspase-8.
- Caspase-3 is the final executioner caspase common to both apoptotic pathways, and BCL-2 overexpression from t(14;18) drives follicular lymphoma.
Mapped competency codes
- PA2.4
- PA2.8
Continue into the full chapter
This summary maps to PA2-cell-injury-and-adaptation.
Frequently Asked Questions
Which type of necrosis occurs in the brain after infarction?
Liquefactive necrosis, because the brain is rich in lipids and lysosomal enzymes, unlike the coagulative necrosis of most other organs.
What is the first nuclear change seen in a necrotic cell?
Pyknosis (nuclear shrinkage and chromatin condensation), followed by karyorrhexis (fragmentation) and karyolysis (dissolution).
How does apoptosis differ from necrosis?
Apoptosis is energy-dependent and causes cell shrinkage without inflammation because the membrane remains intact, whereas necrosis causes swelling, membrane rupture, and inflammation.
Which caspase is activated by the apoptosome?
Caspase-9, the initiator caspase of the intrinsic mitochondrial pathway, which then activates the executioner caspase-3.
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