Cell Death Flashcards
necrosis
*cell death by injury
*characterized by loss of membrane integrity, enzymatic digestion of cells, host reaction/response
*ALWAYS PATHOLOGIC
*affects LARGE fields of cells
nuclei changes associated with cell death
*pyknosis
*karyorrhexis
*karyolysis
pyknosis
nuclear shrinkage, condensed chromatin
*indicates cell death
karyorrhexis
nuclear fragmentation
*indicates cell death
karyolysis
faded chromatin
*indicates cell death
coagulative necrosis - overview
*hypoxic cell death in tissue (all except brain)
*most common type of necrosis
*caused by ischemic necrosis (cutoff of blood supply)
coagulative necrosis - pathologic features
*“GHOST ARCHITECTURE” - preserved structural outline of tissues (can still identify the tissue)
*acids denature proteins
*ex. = myocardial infarction
liquefactive necrosis - overview
*enzymatic liquefaction of dead cells/tissue
*caused by ischemic necrosis in brain, pancreatitis (enzymatic digestion), or suppurative infection
liquefactive necrosis - pathologic features
*cavitations with liquid centers
*NO ghost architected
*contains cell debris and inflammatory cells
caseous necrosis - disease that causes
TUBERCULOSIS
caseous necrosis - pathologic features
*caseous - “cheese-like” consistency
*granulomatous inflammation
*obliterates structure, resulting in cavitation
gangrenous necrosis - overview
*sudden vascular occlusion / blood supply interruption of lower extremities or bowel
dry gangrene
*presents as coagulative ischemic necrosis
wet gangrene
*secondary complication with bacterial/infective heterolysis
gas gangrene
*Clostridium perfringens myconecrosis produces GAS in tissues to cause gangrene
*bubbles up
fibrinoid necrosis - overview
*vascular necrosis with “fibrin-like” deposition
*associated with autoimmune vasculitis
fat necrosis - overview
*enzymatic proteolytic/lipolytic digestion
*caused by trauma to adipose tissues or pancreatitis
fat necrosis - pathologic features
*foamy appearing macrophages
*fat saponification (chalky fats)
apoptosis
*cell death by suicide
*tightly controlled programmed cell death program
*affects SINGLE cells
*LACK of inflammation
*could be physiologic or pathologic
series of changes in apoptosis
- cytoplasmic shrinkage
- nuclear changes (pyknosis, etc)
- apoptotic bodies
- phagocytosis of the apoptotic bodies
biochemical features of apoptosis
- caspase cascade
- activation of transglutaminases
- activation of endonucleases
- rapid phagocytosis
mitochondrial pathway for initiation of apoptosis
*non-receptor mediated
*injury to the mitochondria stimulates apoptosis through:
1. INACTIVATION of BCL-2 (an anti-apoptotic signal)
2. stimulation of BAX/BAK
3. release of cytochrome C
4. activation of caspase cascade
death receptor pathway for initiation of apoptosis
*plasma membrane “death receptor” mediated
1. T cell expression of FasL binds to FAS, forming a trimer (death domain)
2. activation of caspase cascade
cytotoxic pathway for initiation of apoptosis
- CD8+ cytotoxic T cells secrete perforin
- granzyme B goes through the pore and into target cell
- activation of caspase cascade
examples of physiologic apoptosis
*involution (ex. get rid of yolk sac after embryogenesis; lactating breast returning to normal)
*replace cells for maintenance (ex. GI tract)
*destroy cells that represent a threat (ex. virally infected cells, cells with DNA damage)
apoptosis and cancer
*some viruses (HPV and EBV) produce oncogenes that inhibit or evade apoptosis
