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Pathology > Cell injury and death II > Flashcards

Cell injury and death II Flashcards

1
Q

What is coagulative necrosis? How does it appear histologically?

A

the outline of the dead cells are maintained and the tissue is somewhat firm. Nucleus disappears, and there is a wedge shaped and pale area where clot was

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2
Q

What is liquefactive necrosis?

A

the dead cells undergo disintegration and affected tissue is liquified via enzymatic lysis

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3
Q

What is caseous necrosis?

A

Accumulation of mononuclear cells that mediate the chronic inflammatory reaction and granuloma formation to an offending organism. The lipid in the wall of the organism can’t be fully broken down. The dead cells persist indefinitely as amorphous, coarsely granular eosinophilic debris

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4
Q

What is fat necrosis?

A

enzymatic digestion of fat via lipases. The FAs that are released react with Ca to form a soap-like substance

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5
Q

What is gangrenous necrosis?

A

Not a specific pattern of cell death, but usually describes limb loss due to lack of circulation

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6
Q

What type of cell injury results in coagulative necrosis?

A

Ischemia

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7
Q

What causes the maintenance of the outline of coagulative cells?

A

The CT framework

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8
Q

Why doesn’t the brain undergo coagulative necrosis? What type of necrosis does it undergo?

A

There is no CT framework, thus undergoes liquefaction necrosis

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9
Q

What type of necrosis occurs in abscesses? Why?

A

Liquefactive, b/c center made up of PMNs (thus no CT)

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10
Q

How does Liquefactive necrosis appear under the microscope?

A

Amorphus, granular

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11
Q

What is an abscess filled with? Does it have vascular supply?

A

Area filled with PMNs.

No vascular supply

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12
Q

How does caseous necrosis appear grossly?

A

Grayish, whitish or yellowish

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13
Q

What are the two organisms that cause caseous necrosis?

A

TB

Fungi (especially histoplasmosis)

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14
Q

What does caseous necrosis appear like beneath the microscope?

A

Granulated material with surrounding giant cells

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15
Q

What does enzymatic fat necrosis look like grossly?

A

White, chalky

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16
Q

What does enzymatic fat necrosis look like microscopically?

A

Stuff in fat cells rather than their normal, clear appearance

Potentially basophilic if there is enough Ca

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17
Q

In what disease does enzymatic fat necrosis usually take place? Why?

A

In pancreatitis

Because lipases produced solely in the pancreas

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18
Q

Why is fat necrosis seen more often in pts with hyperthyroidism?

A

Increased Ca in the blood activates enzymes

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19
Q

What is fibroid necrosis?

A

Injury in blood vessels with accumulation of plasma proteins causing the wall to stain intensely eosinophilic

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20
Q

What causes fibroid necrosis?

A

Antigen-ab complexes activated clotting cascade

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21
Q

What is wet gangrene?

A

Combination of gangrene with superimposed bacterial infection

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22
Q

Green discoloration around a wound indicates what?

A

Pseudomonas

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23
Q

What causes reperfusion injury?

A

lack of enzymes that reduce ROS, leading to a sudden burst of ROS

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24
Q

What are the three things that ROS damage?

A

Membranes (via lipd radicals)

Protein (abnormal folding)

DNA (mutations)

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25
Q

What are the two findings of reperfusion injury besides increased ROS?

A
  1. Expression of cytokines and cell adhesion molecules

2. Activation of complement pathway

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26
Q

What are the proteins that activate apoptosis?

A

Caspases

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27
Q

What happens to the plasma membrane in apoptosis?

A

Remain intact, but it is altered such that the cell and its fragments become targets for phagocytes

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28
Q

What are the stages of apoptosis?

A
  1. Signal to initiate
  2. Intracellular signals
  3. Execution phase via caspases
  4. Removal of dead cells
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29
Q

What is function of caspases in apoptosis?

A

Catabolize the cytoskeletons and activate endonucleases

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30
Q

What are the two pro-apoptotic proteins in a cell that form holes in the mitochondria? What does this cause?

A

Bax
Bak

Causes cyt C to leak out and activate initiator caspases

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31
Q

What is the function of Bcl-2 and Bcl-X?

A

Block Bax and Bak, thereby inhibiting the apoptosis pathway

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32
Q

What is the ligand used for the extrinsic apoptotic pathway? What happens when this is bound to a signalling protein?

A

Fas ligand.TNF receptor

Causes adaptor proteins to activate the initiator caspases

33
Q

Where do the intrinsic and extrinsic pathways of apoptosis converge? What happens after this?

A

Activation of initiator caspases

Leads to executioner caspases

34
Q

What is the role of p53 in apoptosis?

A

Activates Bax and Bak to start the intrinsic pathway

35
Q

What are the morphological changes in apoptosis? (4)

A
  1. Shrinkage of cells
  2. Condensation of chromatin
  3. Formation of apoptotic bodies
  4. Phagocytosis of apoptotic bodies
36
Q

Swelling is seen in what, and shrinkage is seen in what (necrosis/apoptosis)?

A 
Apoptosis = shrinkage
necrosis = swelling
37
Q

What are the changes in the nucleus for necrosis?

A

Pyknosis to karyorrhexis to karyolysis

38
Q

What are the changes in the nucleus for apoptosis?

A

Fragmentation

39
Q

What happens to the plasma membrane in necrosis? Apoptosis?

A 
Necrosis = Disrupted
Apoptosis = intact
40
Q

What happens to the cellular contents in necrosis?

A

Enzymatic digestion; may leak out of cell

41
Q

What happens to the cellular contents in apoptosis?

A

Intact; may be released in apoptotic bodies

42
Q

Which has inflammation: necrosis or apoptosis?

A

Necrosis

43
Q

How can a virus-infected cell undergo apoptosis via the intrinsic pathway?

A

Activation of p53

44
Q

What are the cells that destroy virus-infected cells?

A

Granzymes (cytotoxic T cells)

45
Q

How can meds indirectly kill cells?

A

metabolites

46
Q

What is the MOA of acetominphen causing cell death?

A

Produces a highly reactive quinone that reacts with proteins/DNA and causes oxidative stress

47
Q

What is the MOA of CCl4?

A

CCl4 goes through p450. Metabolite CCl3 radical reacts with apoproteins in the liver, causing FAs to build up

48
Q

Where do heavy metals affect cells?

A

ETC in mito

49
Q

What is the MOA of phalloidin and paclitaxel?

A

Binds and inhibits cytoskeleton

50
Q

Which zone of hepatocytes are most affected by drugs? Why?

A

Zone 3–farthest from initial site of contact with metabolizing hepatocytes

51
Q

Name the type of necrosis: the outline of the dead cells are maintained and the tissue is somewhat firm.

A

Coagulative necrosis

52
Q

Name the type of necrosis:the dead cells undergo disintegration and affected tissue is liquified.

A

Liquifactive necrosis

53
Q

Name the type of necrosis: a form of coagulative necrosis (cheese-like). Example: tuberculosis lesions.

A

Caseous necrosis

54
Q

Name the type of necrosis: enzymatic digestion of fat. Example: necrosis of fat by pancreatic enzymes.

A

Fat necrosis

55
Q

Name the type of necrosis: Necrosis (usually secondary to ischemia) affecting multiple tissue types (skin, nerve, muscle, etc). It can be dry where the tissue is mummified or wet (usually with superimposed infection). Example: necrosis of distal limbs, usually foot and toes in diabetes.

A

Gangrenous necrosis

56
Q

What is the effect of caspases?

A

Cleavage of proteins

57
Q

What is the crucial event in apoptosis?

A

abnormal mitochondrial membrane permeability which allows escape of cytochrome-c into the cystosol which, in turn, activates proteolytic enzymes (caspases)

58
Q

What does coagulative necrosis look like histologically?

A

Increased acidophilic uptake

59
Q

What is the order of protein degradation and enzymatic degradation in coagulative vs liquefactive necrosis?

A 
Coag = Proteins denature first, then enzymatic destruction
Liq = Enzymes first, then protein denaturation
60
Q

What is the histological appearance of fatty necrosis?

A

Blue staining d/t Ca deposits

61
Q

How does fibrinoid necrosis appear histologically?

A

Amorphous and pink

62
Q

Reversible or irreversible: ATP depletion cell injury

A

Reversible

63
Q

Reversible or irreversible: mito swelling

A

Reversible

64
Q

Reversible or irreversible:membrane blebing

A

Reversible

65
Q

Reversible or irreversible: Nuclear pyknosis/karyorrhexis/karyolysis

A

Irreversible

66
Q

Reversible or irreversible: lysosomal rupture

A

Irreversible

67
Q

Reversible or irreversible: increased mitochondrial permeability

A

Irreversible

68
Q

What are red infarcts seen in? White?

A 
Red = multiple blood supply (red = reperfusion)
White = Solid tissues with single blood supply
69
Q

What is the most damaging ROS?

A

OH* radical

70
Q

What are the three causes of decreased oxygen in a tissue?

A
  1. Ischemia (lowered blood flow)
  2. Hypoxemia (pO2)
  3. Anemia/CO binding
71
Q

What are the three membranes that are damages in Irreversible injury?

A

Plasmalemma
Mitochondrial inner membrane
Lysosomal

72
Q

What are the two signs of CO poisoning?

A

HA

Cherry red face

73
Q

What does the blood look like in methemoglobinemia?

A

Chocolate-colored

74
Q

Is apocrine metaplasia a risk for CA?

A

No

75
Q

What is keratomalacia?

A

Loss of Vit A, leading to loss of conjunctiva

76
Q

What is myositis ossificans?

A

Mesenchymal tissues undergone metaplasia to bone.

77
Q

Streak injury in an ovary = ?

A

Turner’s syndrome

78
Q

Is metaplasia reversible?

A

yes

Pathology (32 decks)

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