Apoptosis and necrosis

Initiation

Phase where caspases become active.

Execution

Phase where caspases cause cell death.

Caspases

Lipid enzymes inducing apoptosis by activating cell death.

Cytochrome c release

Leading to protein activation and cell death.

Altered mitochondrial membrane

Cytochrome c release.

P53 protein

Accumulates within the nucleus if DNA is damaged.

Mitochondrial permeability

Results in apoptosis.

Mitochondrial permeability regulators

BCl-2 and p53.

Apoptosis types

Extrinsic and intrinsic.

Intrinsic

Mitochondrial.

Extrinsic

TNF and Fas receptor-mediated.

Efferocytosis

The process of apoptotic cell phagocytosis.

Coagulative necrosis

Type of necrosis in which protein denaturation is more prominent than enzymatic breakdown.

Infarct

A localized area of coagulative necrosis.

**Ischemia caused by obstruction in a vessel may lead to coagulative necrosis of the supplied tissue in all organs except

the brain.

Liquefactive necrosis

Occurs in situations in which enzymatic breakdown is more prominent than protein denaturation.

Hypoxic death of cells within the central nervous system

Often manifests as liquefactive necrosis.

Caseous necrosis

A "cheesy-looking" necrosis associated with tuberculosis infections.

Fat Necrosis

Breakdown of lipid and a release of fatty acids, which combine with calcium to form chalky deposits. Saponification happens with calcium.

Gangrenous necrosis types

Wet, dry, and gas.

Wet gangrene

Coagulative necrosis followed by liquefactive necrosis because of bacteria. No clear demarcation and related to diabetes.

Dry Gangrene

Usually seen on distal limbs of elderly; Blood supply is little = ischemia.

Gas gangrene

When palpated, it produces a sound called "cryptus" and is caused by clostridium perfringens.

Fibrinoid Necrosis

It typically occurs when complexes of antigens and antibodies are deposited in the walls of arteries.