Exam 2: Cell injury Flashcards

1
Q

What are the two types of reversible cell injury

A
  1. Cellular swelling

2. Fatty changes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What are the 3 types of irreversible cell injury and cell death

A
  1. Necrosis
  2. Apoptosis
  3. Cellular death
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Early, sub-lethal manifestation of cell damage, characterized by inc. cell size and volume due to water overload

A

Acute cell swelling

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What is the most common and fundamental expression of cell injury

A

Acute cell swelling

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What is the Gross appearance of acute cell swelling

A
  1. Slightly swollen organ with rounded edges
  2. pallor
  3. tissue bulges when cut
  4. heavy/wet
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Histologic appearance of cellular swelling

A
  1. Enlarged
  2. pals cytoplasm
  3. Inc. cytoplasmic eosinophila
  4. no morphologic change to nucleus
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What are the 4 ultrastructural changes of cellular swelling

A
  1. PM alterations
  2. Mitochondrial changes
  3. Dilation of ER
  4. Nuclear alterations
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

An inc. in cell size can be due to what two things

A
  1. cell swelling

2. hypertrophy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What is the diff. b/t cell swelling and hypertrophy

A

Cell swelling: due to water

Hypertrophy: cell enlargement is caused by inc. of normal organelles

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

T/F. the prognosis of cellular swelling depends on the number of cells affected and importance of cells

A

T

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Sub-lethal cell damage characterized by intracytoplasmic fatty vacuolation

A

Fatty change

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Accumulation of triglycerides and other lipid metabolites within parenchymal cells

A

Lipidosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

what are the 3 main causes of fatty changes in tissues

A
  1. hypoxia
  2. Toxicity
  3. Metabolic disorders
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What are the 3 steps of the pathogenesis of fatty change

A
  1. Impaired metabolism of fatty acids
  2. Accumulation of triglycerides
  3. Formation of intracytoplasmic fat vacuoles
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Common liver change in obese cats, secondary to anorexia

A

Hepatic lipidosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Irreversible injury is usually associated morphalogically with what 3 things?

A
  1. Severe swelling of mitochondria
  2. Extensive damage to PM
  3. Swelling of lysosomes
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Necrotic change that occurs less than 6 hrs

A

Ultrastructurally

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Necrotic change that occurs from 6-12 hrs

A

Histologically

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Necrotic change that occurs 24-58 hrs

A

Grossly

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Cell death after irreversible cell injury by hopoxia, ischemia, and direct cell memb. injury

A

Necrosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

The morphologic aspect of Necrosis is due to what 2 concurrent processes

A
  1. Denaturation of proteins

2. enzymatic digestion of the cell

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

What is the common outcome of necrosis

A

Inflammation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

What are the 6 types of necrosis?

A
  1. Coagulative necrosis
  2. Liquefactive necrosis
  3. Gangrenous necrosis
  4. Caseous necrosis
  5. Fat necrosis
  6. Fibrinoid necrosis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

when architecture of dead tissues is preserved, ultimately the necrotic cells was removed

A

Coagulative necrosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

What are the 2 ways necrotic cells are removed in coagulative necrosis

A
  1. phagocytosis by WBCs

2. Digestion by lysosomal enzymes from WBCs

26
Q

What is the common cause of coagulative necrosis in solid organs minus the brain?

A

ischemia

27
Q

What type of necrosis is caused by vit. E/selenium deficiency?

A

Coagulative necrosis

28
Q

Type of necrosis typically seen in the CNS

A

Liquefactive necrosis

29
Q

Necrosis where architecture is liquefied, dead cells are digested

A

Liquefactive necrosis

30
Q

what are the 2 types of tissue that can undergo liquefactive necrosis

A
  1. tissue with high neutrophil recruitment and enzymatic release with digestion of tissue
  2. tissue with high lipid content
31
Q

happens when F. moniliforme containing B1 toxin-producing moldy corn is ingested

A

Leukoencephalomalacia

32
Q

Which spp. are infected with leukoencephalomalacia

A

Horse, chicken, pig

33
Q

Characterized by necrosis of white matter of cerebral hemishperes, brain stem, and cerebellum

A

Leukoncephalomalacia

34
Q

A localized collection of pus in a cavity formed by disintegration of tissues surrounded by fibrous CT

A

Absces

35
Q

What are the 2 types of abscess?

A
  1. Septic: infection, release of enzymes from WBCs and infectious agent
  2. Sterile: process caused by nonliving irritants such as drugs
36
Q

Type of necrosis without a specific pattern of cell death but begins mostly as coagulative necrosis

A

Gangrenous necrosis

37
Q

Gangrenous necrosis is likely due to ____

A

ischemia

38
Q

What is dry gangrene?

A

no bacterial superinfection,

39
Q

what is wet gangrene?

A

bacterial superinfection has occured

40
Q

Necrosis that white, friable, and represents dead WBCs

A

Caseous necrosis

41
Q

What are 3 possible causes of caseous necrosis?

A
  1. Mycobacterium
  2. Corynebacterium
  3. fusobacterium
  4. fungal infections
42
Q

Compared with Coagulation necrosis, caseous necrosis is acute/chronic

A

Chronic

43
Q

Type of necrosis that is often associated with poorly degradable lipids of bacterial origin

A

Caseous necrosis

44
Q

Necrosis associated with obliterated tissue architecture

A

Caseous

45
Q

Commonly seen in the center of caseous necrosis

A

Dystrophilic calcification

46
Q

What are the 3 types of fat necrosis?

A
  1. enzymatic necrosis
  2. Traumatic necrosis of fat
  3. Necrosis of abdominal fat
47
Q

what is another name for fat necrosis

A

Pancreatic necrosis of fat

48
Q

Type of necrosis caused by activated pancreatic lipases in escaped pancreatic fluid

A

Enzymatic necrosis

49
Q

Type of necrosis that is associated with dystocia, it is subcutaneously in the intermuscular fat

A

Traumatic necrosis of fat

50
Q

What is the cause of necrosis of abdominal fat?

A

unknown

51
Q

A special form of necrosis usually seen in immune reactions involving blood vessels

A

Fibrinoid necrosis

52
Q

Fibrinoid necrosis occurs when _______ are depositied in the walls of arteries

A

Ag-Ab complexes

53
Q

A pathway of cell death induced by tightly regulated suicide program

A

Apoptosis

54
Q

Apoptic cells break up into fragments called ____, which contain portions of the cytoplasm and nucleus

A

Apoptoic bodies

55
Q

T/F. during apoptosis the PM stays intact

A

T

56
Q

T/F. apoptosis cause inflammation

A

F. no inflam

57
Q

What are the 2 pathways of apoptosis

A
  1. intrinsic/ mitochondrial

2. Extrinsic pathwat/ death receptor initiated

58
Q

What are the 2 initator caspases of apoptosis

A

8 and 9

59
Q

What are the 2 executioner caspases of apoptosis

A

3 and 6

60
Q

what is the major mech. of apoptosis in all mammals

A

Intrinsic pathway

61
Q

released into the cytoplasm and initiates suicide program of apoptosis

A

Cytochrome C

62
Q

what initiates the extrinsic pathway

A

Death receptors