1.3 Cell Death Flashcards

1
Q

What is the morphological hallmark of cell death?

A

Loss of the nucleus

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2
Q

What is pyknosis?

A

Shrinkage of the nucleus

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3
Q

What is Karyorrhexis?

A

Breakdown of the nucleus into pieces

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4
Q

What is karyolysis?

A

The complete dissolution of the chromatin of a dying cell due to the enzymatic degradation by endonucleases

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5
Q

What are the three major stages of cell death?

A
  1. Pyknosis
  2. Karyorrhexis
  3. Karyolysis
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6
Q

True or false: necrosis is alway pathologic

A

True

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7
Q

What is the major difference between necrosis and apoptosis?

A

Necrosis is followed by inflammation

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8
Q

What, generally, is coagulative necrosis?

A

Necrotic tissue that retains its shape and firmness d/t preservation of the organ structure and coagulation of cellular proteins

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9
Q

What happens to the nucleus with coagulative necrosis?

A

Disappears

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10
Q

Coagulative necrosis can be characteristic of necrosis in any organ, except for which?

A

Brain

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11
Q

What process produces coagulative necrosis?

A

Ischemic infarction

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12
Q

What is the general shape of areas of infarcts?

A

Wedge shaped

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13
Q

What causes a red infarction?

A

If blood reenters an area of loosely organized tissue that underwent necrosis

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14
Q

Why is it essential that CT is loose if a red infarct is to occur?

A

Needs to be able to hold the blood

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15
Q

What occurs with liquefactive necrosis?

A

Enzymatic lysis of cells and proteins resulting in liquefaction

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16
Q

What are the three classic circumstances in which liquefactive necrosis occurs?

A
  • Brain infarction
  • Abscesses
  • Pancreatitis
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17
Q

Why is it that the brain in particular undergoes liquefactive necrosis?

A

Microglial cells release oxygen radicals and crush the brain tissue like Stalin

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18
Q

Why is different about the cells that mediate liquefactive necrosis in abscesses as compared to the brain?

A

PMNs do it in abscesses

Microglial cells do it in the brain

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19
Q

What causes the liquefactive necrosis of the pancreas?

A

Enzymes of the pancreas digest pancreas

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20
Q

What is gangrenous necrosis?

A

Coagulative necrosis that resembles mummified tissue

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21
Q

Where in the body does gangrenous necrosis classically occur (but not the only place)?

A

Lower limb and GI tract

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22
Q

What makes gangrene “wet”?

A

Superimposed infection on the gangrenous necrosis

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23
Q

What is caseous necrosis? What classically causes this type of necrosis?

A

Combination of coagulative and liquefactive necrosis

Granulomatous inflammation d/t TB or fungal infx

24
Q

What is the gross appearance of caseous necrosis?

A

Cottage cheese

25
Q

What is the classic gross appearance of fat necrosis? What causes this?

A

Chalky white appearance d/t Ca deposition

26
Q

What is saponification?

A

the alkaline hydrolysis of the fatty acid ester–FAs released by trauma or lipase join with Ca

27
Q

What type of necrosis does the pancreas undergo?

A

Pancreas itself = liquefactive

Fat necrosis of the peripancreatic fat

28
Q

What are the two classic regions of the body that undergo fat necrosis?

A

Peripancreatic fat

Breast trauma

29
Q

What type of cell might be seen with fat necrosis?

A

Giant cells

30
Q

What are the two general processes of Ca deposition in the body?

A
  • Necrotic tissue become a nidus for Ca deposition

- psammoma bodies

31
Q

What happens to serum Ca levels with dystrophic calcification? Serum phosphate?

A

Both normal

32
Q

What is metastatic calcification? What are the relative serum Ca and phosphate levels with this?

A

Increased concentration of Ca and phosphate in the serum pathologically deposit Ca into tissues

33
Q

True or false: metastatic calcification always occurs d/t a cancer somewhere?

A

False–just means that Ca levels are high. Cancers can however, cause this, but it is not required.

34
Q

What is fibrinoid necrosis?

A

Necrotic damage to the blood vessel wall from the leakage of proteins from serum

35
Q

What causes the bright pink staining characteristics of fibrinoid necrosis?

A

Leakage of proteins into vessel wall

36
Q

What are the two major (general) causes of fibrinoid necrosis?

A

Malignant HTN or vasculitis

37
Q

What causes fibrinoid necrosis of the placenta?

A

Preeclampsia

38
Q

True or false: apoptosis requires energy

A

True

39
Q

Does apoptosis involve a single cell, or groups of cells

A

Either

40
Q

What is the process that causes separation of the fingers during embryogenesis?

A

Apoptosis

41
Q

What causes the endometrial lining to be shed during menses?

A

Apoptosis of the endometrial lining

42
Q

Does CD8+ T cell killing cause necrosis or apoptosis?

A

Apoptosis

43
Q

What are the general morphological changes that occur with apoptosis?

A

Shrinkage of the cell with intense eosinophilia, and budding off of cell contents

44
Q

What happens to the nucleus with apoptosis?

A

Nucleus condenses and fragments

45
Q

What happens to the apoptotic bodies that fall off of the cell?

A

Macrophages eat ‘em up

46
Q

What enzymes are the key mediators of apoptosis?

A

Caspases

47
Q

What is the role of the proteases that caspases activate?

A

Break down the cell cytoskeleton

48
Q

What is the function of the endonucleases that caspases activate?

A

Break down DNA

49
Q

What is the key sign of irreversible damage?

A

membrane damage

50
Q

What is the intrinsic mitochondrial pathway that leads to apoptosis?

A

Damage of some sort deactivates Bcl2

51
Q

What is the role of Bcl2?

A

Stabilizes the mitochondrial membrane, to prevent cytochrome C from leaking out and killing the cell

52
Q

What is the receptor that activates the extrinsic receptor-ligand pathway of apoptosis?

A

Fas ligand binds to Fas death receptor (CD95)

53
Q

How are maturing T cells killed in the thymus if they do not pass positive or negative selection?

A

Fas-L and receptor

54
Q

What are the three major pathways of apoptosis activation?

A
  1. Intrinsic mito pathway
  2. Fas-Fas-L interaction
  3. Cytotoxic CD8 T cell
55
Q

How do CD8+ T cells cause apoptosis? (2 enzymes)

A

Perforins create pores in membrane or target cell, and granzyme enters pore and activates caspases