LEC 4: Cell Death Flashcards
(16 cards)
Apoptosis
Programmed cell death
- Pathways that enzymatically degrades DNA and proteins
- Fragmentation into bodies (blebbing -> apoptotic bodies)
- Intact plasma membrane
- No inflammatory response
Necrosis
Premature Cell Death
- Caused by external factors (infection, toxins, trauma)
- Cell initially swells, then loses membrane integrity, causing cell lysis
- Inflammation response
Nuclear Changes during Cell Death
Karyolysis: nuclear fading
Pyknosis: nuclear shrinkage
Karyorrhexis: nuclear fragmentation
Physiological Apoptosis
Eliminates redundant cells
- maintains constant number of cells in tissue
- elimination of autoreactive cells, infected/tumour cells
Pathological Apoptosis
Eliminates cells that are genetically altered or injured beyond repair
- occurs without severe host reaction
Clearing the Dead
- Prevents further tissue damage by stimulating production of anti-inflam cytokines and chemokines
- Recruitment of macrophages for phagocytosis
Caspade-Cascade Apoptotic Cell Death
Caspases = Cysteine Aspertate Proteases
Mitochondrial (Intrinsic) Pathway
Mitochondrial Damage and Leakage of Cytochrome-C
- activation of Caspase 9
- results in cell death
Death Receptor (Extrinsic) Pathway
Activation of death receptors (cell mediated)
- activation of Caspase 8
Morphological Subgroups of Necrosis
- Liquefactive Necrosis
- Coagulative Necrosis
- Fibrinoid Necrosis
- Enzymatic Fat Necrosis
- Caseous Necrosis
- Ischemic (non-specific)
- Gangrenous Necrosis
Coagulative Necrosis
Cell is dead but basic tissue architecture is initially preserved.
- characteristic of hypoxic cell deaths in all solid organs (except the brain)
Liquefactive Necrosis
Loss of organ/cellular architecture with enzymatic breakdown of tissue (complete cell digestion)
- initial inflammation -> pus
Caseous Necrosis
Loss of cellular architecture with rim of inflammatory cells (granuloma)
- no visible outlines
- encountered most often in foci of tuberculosis infection
Enzymatic Fat Necrosis
Focal areas of fat destruction
- fatty acids released via hydrolysis reaction with Ca and forms chalky white areas (fat saponification)
Gangrenous Necrosis
Most commonly due to lack of blood flow, ‘ischemic’ necrosis or physical injury/trauma
- Dry Grangrene: no bacterial superinfection, tissue appears dry (black and dead)
- Wet Grangrene: bacterial superinfection
- tissue looks wet and liquefactive
Fibrinoid Necrosis
Caused by immune reactions where complexes of Ag’s and Ab’s deposited in arterial walls
- Fibrin leaks out of vessels
- Complexes react with Fibrin to form Eosinophilic areas (Fibrinoid)
