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RUSVM Pathology 1 > Exam II: ALL > Flashcards

Exam II: ALL Flashcards

1
Q

What does an influx of Ca into cells cause?

A

Activation of : phospholipases,

proteases,

endonucleases

and ATPases

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2
Q

This histology slide is characteristic for what kind of cell change?

A

Hydrophic change

  • enlarged cells,
  • clear cytoplasm,
  • normal nucleus location
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3
Q

The organ on the left is exhibiting what type of change?

A

hydropic degeneration from cell injury (reversible)

-accumulation of water in the cell, caused by multiple injuries agents

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4
Q

True or false: fatty changes can be seen in all cell types?

A

false; occurs only in cells that participate in fat metabolism (hepatocytes), cardiomyocytes and renal tubular epithelium

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5
Q

Name the histological change shown here

A

Lipidosis (fatty degeneration)

  • accumulation of fat in cells,
  • nucleus pushed to periphery,
  • fat accumulation DOES NOT STAIN
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6
Q

true or false: when necrosis is present there is always inflammation?

A

TRUE

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7
Q

This nuclear change is called:

A

Karyolysis (nuclear fading)

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8
Q

This nuclear change is called:

A

Pyknosis (nuclear shrinking)

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9
Q

This nuclear change is called:

A

karyorrhexis (fragmentation)

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10
Q

Name the necrosis pattern associated with hypoxic injury

A

coagulative

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11
Q

pattern of necrosis where cell architecture is preserved

A

coagulative

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12
Q

Name the injury

A

infarct

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13
Q

What type of necrosis is associated with ischemia?

A

coagulative

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14
Q

Most common cause of caseous necrosis in cattle

A

mycobacterium

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15
Q

most common cause of caseous necrosis in sheep

A

cornyebacterium

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16
Q

prolonged lack of adequate blood supply is called

A

ischemia

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17
Q

What type of necrosis is shown here?

A

Liquefactive

  • abscess
  • tissue unrecognizable
  • not fibrous capsule
  • center has eosinophilic or basophilic material and bacterial colonies
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18
Q

What type of necrosis is shown here?

A

caseous

  • abscess,
  • chronic (usually)
  • ring of macrophages and MNGC,
  • obliterated tissue,
  • dystrophic calcification
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19
Q

main cause of dry gangrene

A

ischemia

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20
Q

main difference between dry and wet gangrene

A

wet gangrene = bacteria

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21
Q

what are the ONLY 3 types of fat necrosis?

A

enzymatic (saponification in the pancreas–looks cooked),

traumatic (dystocia),

necrosis of abdominal fat (Jersey/Guernsey, unknown cause)

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22
Q

What is shown here?

A

saponification of fat in pancreas (fat necrosis)

23
Q

What is shown here?

A

Necrosis of abdominal fat:

-fatty acids are acting with calcium and therefore can become pigmented (normal fat does not stain)

24
Q

what is happening in this vascular wall?

A

fibrinoid necrosis – typical of immune rxns involving BV

25
Q

What is happening in this image?

A

cell undering apoptosis – hypereosinophilia and condensation of chromatin

26
Q

What are the initiator caspases of apoptosis

A

9 & 8

27
Q

what are the executioner caspases of apoptosis?

A

3 & 6

28
Q

what triggers the intrinsic pathway of apoptosis?

A

mitochondrial pathway – release of cytochrome C

29
Q

what triggers the extrinsic pathway of apoptosis?

A

death receptor initiated pathway

30
Q

What 4 things initiate apoptosis?

A

injury, withdrawal of growth factors/hormones, receptor-ligand interactions and cytotoxic T lymphocytes

31
Q

what are the four markers used to ID apoptotic cells?

A

annexin V, thrombospodin, caspases, C1q

32
Q

the receptor-ligand interactions that trigger apoptosis involve what?

A

Fas and TNF receptor

33
Q

disorders of defective apoptosis with INCREASED cell survival

A

cell with mutated p53,

lymphocytes that react to self antigen,

failure to eliminate dead cells

*may be the basis of autoimmune disorders

34
Q

disorders with increased apoptosis and excessive cell death

A

neurodegenerative diseases,

ischemic injury (myocardial infarction and stroke),

death of virus-infected cell

35
Q

normal vascular endothelium is ___thrombotic and ___fibrinolytic

A

antithrombotic,

pro-fibrinolytic

(we do not want clots forming normally)

36
Q

action of nitrous oxide on blood vessel

A

vasodilator

37
Q

action of endothelin on blood vessel

A

vasoconstrictor

38
Q

4 causes of edema

A

increased blood hydrostatic pressure,

decreased plasma colloid oncotic pressure,

lymphatic obstruction,

increased vascular permeability

39
Q

right sided congestive heart failure and a tightly bandaged limb are both examples of what cause of edema?

A

increased blood hydrostatic pressure

40
Q

Starvation, GI malabsorption, Liver disease and increased protein loss are examples of what cause of edema?

A

decreased plasma colloid oncotic pressure (decreased proteins being absorbed or made in vasculature)

41
Q

inflammatory edema is called?

A

exudate; protein rich, caused by increased vascular permeability

42
Q

non-inflammatory edema is called?

A

transudate; pale, protein-poor

43
Q

anasarca

A

generalized edema (puppy pic)

44
Q

frothy, moist enlarged lungs are associated with

A

pulmonary edema – left sided congestive heart failure

45
Q

heart failure cells are characteristic of ___sided cardiac failure

A

left -sideded.

46
Q

Hepatic congestion is seen in ___ sided heart failure

A

right sided

47
Q

nutmeg liver is caused by

A

right sided congestive heart failure

48
Q

This is tissue from a cow. Could this be coagulative necrosis caused by mycobacterium?

A

No; coagulative necrosis starts with hypoxia; this is caseous necrosis

49
Q

use of improperly buffered formalin may lead to what type of artifact on a histological exam?

A

acid hematin

50
Q

what pigment is contained in heart failure cells and what do you stain it with?

A

hemosiderin; iron’s pearl

51
Q

What’s the most likely etiology:

A

vit E/selenium deficiency

52
Q

true or false: fibrosis on lungs of ruminants is normal

A

true

53
Q
A

RUSVM Pathology 1 (14 decks)

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