Cell Injury and Death II Flashcards

1
Q

Necrosis

A

cell death that is not controlled by the cell, does not require the signals or activation of genes

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2
Q

cytoplasmic changes in necrosis

A

eosinophilia, glassy appearance, vacuolation

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3
Q

nuclear changes in necrosis

A

pyknosis, karyorrhexis, karolysis

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4
Q

6 types of necrosis

A
coagulative
liqufactive
caseous
enzymatic fat
fibrinoid
gangrenous
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5
Q

coagulative necrosis

A

seen in death due to ischemia, hypoxia, reperfusion injury

basic outline of cell preserved but with no nuclei (ghost like)

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6
Q

liquefactive necrosis

A

death of brain tissue
abscesses where the center is made of pus.
amoorphous, granular under microscope

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7
Q

caseous necrosis

A

accumulation of mononuclear cells that mediate the chronic inflammatory reaction and granuloma formation. looks cheesy.

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8
Q

caseous necrosis is characteristic of what

A

TB

certain fungi

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9
Q

enzymatic fat necrosis

A

due to action of lipases

fatty acids that are released reach with calcium to form a soap-like substance

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10
Q

what does enzymatic fat necrosis look like under a microscope

A

material in fat cells

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11
Q

what does enzymatic fat necrosis look like in gross

A

white, chalky

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12
Q

If there is enough calcium the deposits in enzymatic fat necrosis will be _____-

A

basophilic

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13
Q

what is enzymatic fat necrosis seen in

A

pancreatitis

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14
Q

fibrinoid necrosis

A

injury in blood vessels with accumulation of plasma proteins causing wall to stain eosiohpilic

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15
Q

gangrenous necrosis

A

affects multiple types of tissue, happens when there is no blood going to that tissue. not a specific pattern of cell death

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16
Q

what is gangrenous necrosis often applied to

A

a limb lost from diabetes

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17
Q

wet gangrene

A

gangrene + bacterial infection

18
Q

ischemia

A

caused by reduction of available oxygen, leads to tissue death

19
Q

reperfusion

A

blood flow/oxygenation of tissue is restored, leads to large amount of ROS damage

20
Q

what does ROS react with

A

lipid peroxide radicals
oxidation of proteins
oxidation of DNA

21
Q

other findings in ischemia/reperfusion injury

A

accumulation of neutrophils

activation of complement pathway

22
Q

roles of apoptosis (non-pathological)

A

em bryogenesis
hormone dependent involution
cell deletion in proliferating cell population
immune defense
removal of self-reactive lymphocytes
removal of cells that have served their purpose

23
Q

apoptosis (pathologic)

A
cell death in tumors
DNA damages
transplant rejection
atrophy after duct obstruction
some viral diseases
24
Q

stages of apoptosis

A

signaling pathways
intracellular signals
execution phase
removal of dead cells

25
In DNA damage what activates proapoptic forms of Bcl-2
p53
26
stimulation of proapoptic forms of Bcl-2 stimulates
Bax and Bak
27
apoptosis extrinsic pathway
Fas, TNF activate adaptor proteins which bind caspases
28
Apoptosis instrinsice pathway
Bax and Bak dimerize and form channels in the mitochondrial membrane leading to permeability of cytochromc C leakage and activation of caspases
29
cell size of necrosis
enlarges
30
cell size of apoptosis
reduces
31
nuclues of necrosis
pyknosis, karyorrhexis, karyolysis
32
nucleus of apoptosis
fragmentation
33
plasma membrane of necrosis
disrupted
34
plasma membrane of apoptosis
intact
35
cellular contents of necrosis
enzymatic digestion, may leak out of cell
36
cellular contents of apoptosis
intact
37
acetaminophen
it's metabolite is a highly reactive quinone that reacts with protein, DNA< causes oxygen stress - massive liver necrosis
38
CCl4
reacts with membrane and ER
39
heavy metals and cyanide
act on mitochondria | reduce ATP
40
phalloidin, paclitaxel
act on cytoskeletal | prevent cell from replicating
41
chemotherapeutic alkylating agents
damage DNA directly