Cell Death and Perfusion Disorders III Flashcards

1
Q

autolysis

A

cell destruction that occurs after death (by a cells own enzymes)

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2
Q

putrefaction

A

decomposition of dead tissues by microorganisms

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3
Q

ischemia

A

decrease in blood supply to a tissue with resultant hypoxia, decreased glucose and other nutrients and decreased removal of metabolic waste

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4
Q

infarct

A

local area of peracute ischemia that causes coagulative necrosis

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5
Q

what is the time progression of necrosis types

A

coagulative -> caseous -> liquifactive

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6
Q

common causes of coagulative necrosis

A

hypoxia, ischemia, toxins

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7
Q

common cause of caseous necrosis

A

infectious agents

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8
Q

common area of liquefactive necrosis

A

nervous tissue

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9
Q

gangrenous necrosis occurs at

A

extremities or dependent portions of organs

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10
Q

dry gangrenous necrosis resembles

A

coagulative necrosis

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11
Q

wet gangrenous necrosis resembles

A

liquefactive necrosis

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12
Q

gross appearance of coagulative necrosis

A

pale tan to gray, sharply demarcated, solid

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13
Q

histologic appearance of coagulative necrosis

A

retained architecture, cytoplasmic eosinophilia

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14
Q

gross appearance of caseous necrosis

A

dry or moist, crumbly, granular or laminated, may have central exudate

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15
Q

histologic appearance of caseous necrosis

A

architecture lost, lysed cells, granular to amorphous debris, nuclear debris

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16
Q

gross appearance of liquefactive necrosis

A

pale to translucent, soft to liquid, cavitated

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17
Q

histologic appearance of liquefactive necrosis

A

architecture lost, parenchymal cells lost, space filled with inflammatory cells

18
Q

gross appearance of dry gangrene

A

dry, leathery

19
Q

histologic appearance of dry gangrene

A

(coagulative necrosis): cytoplasmic eosinophilia, architecture retained

20
Q

gross appearance of wet gangrene

A

red-black, wet

21
Q

histologic appearance of wet gangrene

A

(liquefactive necrosis): architecture lost, parenchyma lost, inflammatory cells

22
Q

describe what hematogenous agents would cause a zonal pattern and what would cause a random multifocal pattern

A

toxins would cause zonal patterns; bacteria would cause a random multifocal pattern

23
Q

what pattern would inhaled pathogens cause on the lung

A

cranioventral distribution

24
Q

what would the presence of fibrin in a lesion tell you

A

the lesion was an ulcer (reached the blood vessels) as opposed to an erosion

25
Q

what layers does erosion go through vs an ulcer

A

erosion: just mucosa; ulcer: mucosa, submucosa, muscularis

26
Q

what part of the kidney is most susceptible to NSAID overdose

A

medulla; specifically the medullary capillary plexus

27
Q

what is a clinical sign of growth plate necrosis

A

affected limb is shorter than non-affected limb

28
Q

anemic hypoxia would impact what part of the liver first

A

zone III (last to receive oxygen)

29
Q

causes of oxygen deprivation (4)

A
  1. inadequate blood oxygenation
  2. inadequate oxygen-carrying capacity of blood
  3. inadequate delivery of oxygenated blood to tissue
  4. inhibition of cellular respiration enzymes
30
Q

what is reperfusion syndrome

A

reperfusion of tissues -> ROS/free-radical generation -> further damage to tissue

31
Q

how does ischemia of watershed zones appear

A

segmental

32
Q

example of end-artery ischemia

A

coagulative necrosis of a renal pyramid

33
Q

difference between arterial and venous occlusion

A

arterial causes an immediate infarction, whereas venous first causes congestion and edema, which promotes the infarction

34
Q

what would cause a pale and non-swollen infarct

A

ACUTE arterial infarct

35
Q

what would cause a dark red/swollen infarct

A

venous infarct; slightly later arterial infarct with damage of blood vessels in the infarcted tissue and backflow of blood from other tissues

36
Q

what would cause a pale, swollen, red-rimmed infarct

A

cell swelling and necrosis that pushes blood out of the infarct, macrophage cleaning
red rim = hyperemia/hemorrhage/acute inflammation

37
Q

what would cause a multicoloured infarct

A

RBC breakdown, inflammation, neovascularization

38
Q

what would cause a white and contracted infarct

A

chronic infarction with subsequent scarring

39
Q

what is the endpoint of infarction

A

scarring with contraction

40
Q

what is DIC

A

loss of localization of the coagulation process and generation of excess thrombin, with widespread microvascular thrombi

41
Q

name 3 causes of DIC

A

sepsis, shock, extensive trauma

42
Q

DIC sequela

A

bleeding due to consumption of all coagulation factors; ischemic tissue damage