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
Q

In DNA damage what activates proapoptic forms of Bcl-2

A

p53

26
Q

stimulation of proapoptic forms of Bcl-2 stimulates

A

Bax and Bak

27
Q

apoptosis extrinsic pathway

A

Fas, TNF activate adaptor proteins which bind caspases

28
Q

Apoptosis instrinsice pathway

A

Bax and Bak dimerize and form channels in the mitochondrial membrane leading to permeability of cytochromc C leakage and activation of caspases

29
Q

cell size of necrosis

A

enlarges

30
Q

cell size of apoptosis

A

reduces

31
Q

nuclues of necrosis

A

pyknosis, karyorrhexis, karyolysis

32
Q

nucleus of apoptosis

A

fragmentation

33
Q

plasma membrane of necrosis

A

disrupted

34
Q

plasma membrane of apoptosis

A

intact

35
Q

cellular contents of necrosis

A

enzymatic digestion, may leak out of cell

36
Q

cellular contents of apoptosis

A

intact

37
Q

acetaminophen

A

it’s metabolite is a highly reactive quinone that reacts with protein, DNA< causes oxygen stress - massive liver necrosis

38
Q

CCl4

A

reacts with membrane and ER

39
Q

heavy metals and cyanide

A

act on mitochondria

reduce ATP

40
Q

phalloidin, paclitaxel

A

act on cytoskeletal

prevent cell from replicating

41
Q

chemotherapeutic alkylating agents

A

damage DNA directly