Cell Death Flashcards

1
Q

necrosis

A

*cell death by injury
*characterized by loss of membrane integrity, enzymatic digestion of cells, host reaction/response
*ALWAYS PATHOLOGIC
*affects LARGE fields of cells

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2
Q

nuclei changes associated with cell death

A

*pyknosis
*karyorrhexis
*karyolysis

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3
Q

pyknosis

A

nuclear shrinkage, condensed chromatin
*indicates cell death

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4
Q

karyorrhexis

A

nuclear fragmentation
*indicates cell death

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5
Q

karyolysis

A

faded chromatin
*indicates cell death

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6
Q

coagulative necrosis - overview

A

*hypoxic cell death in tissue (all except brain)
*most common type of necrosis
*caused by ischemic necrosis (cutoff of blood supply)

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7
Q

coagulative necrosis - pathologic features

A

*“GHOST ARCHITECTURE” - preserved structural outline of tissues (can still identify the tissue)
*acids denature proteins
*ex. = myocardial infarction

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8
Q

liquefactive necrosis - overview

A

*enzymatic liquefaction of dead cells/tissue
*caused by ischemic necrosis in brain, pancreatitis (enzymatic digestion), or suppurative infection

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9
Q

liquefactive necrosis - pathologic features

A

*cavitations with liquid centers
*NO ghost architected
*contains cell debris and inflammatory cells

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10
Q

caseous necrosis - disease that causes

A

TUBERCULOSIS

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11
Q

caseous necrosis - pathologic features

A

*caseous - “cheese-like” consistency
*granulomatous inflammation
*obliterates structure, resulting in cavitation

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12
Q

gangrenous necrosis - overview

A

*sudden vascular occlusion / blood supply interruption of lower extremities or bowel

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13
Q

dry gangrene

A

*presents as coagulative ischemic necrosis

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14
Q

wet gangrene

A

*secondary complication with bacterial/infective heterolysis

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15
Q

gas gangrene

A

*Clostridium perfringens myconecrosis produces GAS in tissues to cause gangrene
*bubbles up

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16
Q

fibrinoid necrosis - overview

A

*vascular necrosis with “fibrin-like” deposition
*associated with autoimmune vasculitis

17
Q

fat necrosis - overview

A

*enzymatic proteolytic/lipolytic digestion
*caused by trauma to adipose tissues or pancreatitis

18
Q

fat necrosis - pathologic features

A

*foamy appearing macrophages
*fat saponification (chalky fats)

19
Q

apoptosis

A

*cell death by suicide
*tightly controlled programmed cell death program
*affects SINGLE cells
*LACK of inflammation
*could be physiologic or pathologic

20
Q

series of changes in apoptosis

A
  1. cytoplasmic shrinkage
  2. nuclear changes (pyknosis, etc)
  3. apoptotic bodies
  4. phagocytosis of the apoptotic bodies
21
Q

biochemical features of apoptosis

A
  1. caspase cascade
  2. activation of transglutaminases
  3. activation of endonucleases
  4. rapid phagocytosis
22
Q

mitochondrial pathway for initiation of apoptosis

A

*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

23
Q

death receptor pathway for initiation of apoptosis

A

*plasma membrane “death receptor” mediated
1. T cell expression of FasL binds to FAS, forming a trimer (death domain)
2. activation of caspase cascade

24
Q

cytotoxic pathway for initiation of apoptosis

A
  1. CD8+ cytotoxic T cells secrete perforin
  2. granzyme B goes through the pore and into target cell
  3. activation of caspase cascade
25
Q

examples of physiologic apoptosis

A

*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)

26
Q

apoptosis and cancer

A

*some viruses (HPV and EBV) produce oncogenes that inhibit or evade apoptosis