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FA - Pathology > Path - Inflammation (Apoptosis, Necrosis, & Cell injury) > Flashcards

Path - Inflammation (Apoptosis, Necrosis, & Cell injury) Flashcards

Pg. 220-221 in First Aid 2014 Sections include: -Apoptosis -Necrosis -Cell injury

1
Q

In brief, what is apoptosis? Does it require ATP?

A

Programmed cell death; ATP requires

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2
Q

What are the 2 pathways for apoptosis? What is the common goal of both pathways?

A

Intrinsic or extrinsic pathway; both pathways –> activation of cytosolic caspases that mediate cellular breakdown

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3
Q

What is important to remember about inflammation in the context of apoptosis, especially as it compares/contrasts to necrosis?

A

No significant inflammation (unlike necrosis)

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4
Q

What are 6 histological findings that characterize apoptotic cells?

A

Characterized by (1) deeply eosinophlic cytoplasm (2) cell shrinkage (3) nuclear shrinkage (pyknosis) and basophilia (4) membrane blebbing (5) nuclear fragmentation (karyorrhexis) (6) Formation of apoptotic bodies, which are then phagocytosed

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5
Q

What is the fate of apoptotic bodies?

A

Formation of apoptotic bodies, which are then phagocytosed

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6
Q

What is a sensitive indicator of apoptosis, and why?

A

DNA laddering is a sensitive indicator of apoptosis; during karyorrhexis, endonucleases cleave at internucleosomal regions, yielding 180-bp fragments

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7
Q

How does radiation therapy cause apoptosis? What kind of cells are very susceptible to this? Give 2 examples of this kind of cell.

A

Radiation therapy causes apoptosis of tumors and surrounding tissue via free radical formation and dsDNA breakage; Rapidly dividing cells (e.g., skin, GI mucosa) are very susceptible to radiation therapy-induced apoptosis

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8
Q

What is an important correlation between apoptosis and embryology?

A

Intrinsic pathway (of apoptosis) - Involved in tissue remodeling in embryogenesis

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9
Q

What are 2 contexts in which apoptosis via the intrinsic pathway occurs? Give at least one example of each context/trigger.

A

(1) Occurs when a regulating factor is withdrawn from a proliferating cell population (e.g., decreased IL-2 after a complete immunological reaction –> apoptosis of proliferating effector cells.) (2) Also occurs after exposure to injurious stimuli (e.g., radiation, toxins, hypoxia).

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10
Q

What is the mechanism of the intrinsic pathway?

A

Changes in proportions of anti- and pro-apoptotic factors lead to increased mitochondrial permeability and cytochrome c release

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11
Q

What are 2 examples of pro-apoptotic proteins?

A

BAX and BAK are pro-apoptotic proteins

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12
Q

What is an example of an anti-apoptotic protein?

A

Bcl-2 is anti-apoptotic

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13
Q

What function does Bcl-2 normally serve, and via what mechanism?

A

Bcl-2 prevents cytochrome c release by binding to and inhibiting Apaf-1. Apaf-1 normally induces the activation of caspases.

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14
Q

What is the normal function of Apaf-1? What important protein inhibits its action?

A

Bcl-2 prevents cytochrome c release by binding to and inhibiting Apaf-1. Apaf-1 normally induces the activation of caspases.

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15
Q

What occurs due to overexpression of Bcl-2?

A

If Bcl-2 is overexpressed (e.g., follicular lymphoma), then Apaf-1 is overly inhibited, leading to decreased caspase activation and tumorigenesis.

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16
Q

What 2 pathways within the extrinsic pathway of apoptosis? Give the mechanism associated with each of these pathways.

A

2 pathways: (1) Ligand receptor interactions (FasL binding to Fas [CD95]) (2) Immune cell (cytotoxic T-cell release of perforin and granzyme B)

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17
Q

What is an important process that requires Fas-FasL interaction? What pathway(s) of apoptosis does this exemplify? Be specific.

A

Fas-FasL interaction is necessary in thymic medullary negative selection; Extrinsic pathway -Ligand receptor interactions

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18
Q

What results from mutations in Fas, and why?

A

Mutations in Fas increase numbers of circulating self-reacting lymphocytes due to failure of clonal deletion (via ligand receptor interactions of Fas L binding to Fas [CD95])

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19
Q

What ensues after Fas crosslinks with FasL? Briefly summarize downstream events.

A

After Fas crosslinks with FasL, forming a binding site for a death domain-containing adapter protein, FADD. FADD binds inactive caspases, activating them.

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20
Q

What is FADD? What is its action? What is needed for it to take this action?

A

After Fas crosslinks with FasL, forming a binding site for a death domain-containing adapter protein, FADD. FADD binds inactive caspases, activating them.

21
Q

What is the pathophysiological basis for autoimmune disorders?

A

Defective Fas-FasL interaction is the basis for autoimmune disorders

22
Q

Draw the intrinsic versus extrinsic pathways occurring within one cell, highlighting the key steps of each and their shared mechanism(s).

A

See p. 220 in First Aid 2014 for visual

23
Q

From what does necrosis result, and what are its major consequences?

A

Enzymatic degradation and protein denaturation of a cell resulting from exogenous injury. Intracellular components leak; inflammatory process (unlike apoptosis)

24
Q

In what setting does coagulative necrosis occur? Give 3 examples of organs in which it occurs?

A

Heart, liver, kidney; Occurs in tissues supplied by end-arteries

25
Q

What histological finding may be apparent in coagulative necrosis?

A

Increased cytoplasmic binding of acidophilic dye

26
Q

What processes occur in coagulative necrosis, and in what order?

A

Proteins denature first, followed by enzyme degradation

27
Q

Give 2 examples of locations/types of liquefactive necrosis. In what setting does liquefactive necrosis occur, and why?

A

Brain, bacterial abscess; occurs in CNS due to high fat content

28
Q

What process occurs first in coagulative necrosis? Compare/contrast this to liquefactive necrosis.

A

In contrast to coagulative necrosis, enzymatic degradation due to release of lysosomal enzymes occurs first.

29
Q

What are 3 examples of organisms that cause caseous necrosis?

A

(1) TB (2) Systemic fungi (3) Nocardia

30
Q

What are 2 ways in which fatty necrosis can occur? Give an example of each.

A

Enzymatic (pancreatitis [saponification]) and nonenzymatic (e.g., breast trauma)

31
Q

What is a histological finding of fatty necrosis?

A

Calcium deposits appear dark blue on staining

32
Q

What are 2 general causes of fibrinoid necrosis?

A

(1) Vasculitidies (e.g., Henoch-Schonlein purpura, Churg-Strauss syndrome) (2) Malignant hypertension

33
Q

What are 2 ways that fibrinoid necrosis appears on histology?

A

Amorphous and pink on H & E

34
Q

Give 2 examples of vasculitidies that may cause fibrinoid necrosis.

A

Vasculitidies (e.g., Henoch-Schonlein purpura, Churg-Strauss syndrome)

35
Q

What are the 2 kinds of gangrenous necrosis? Define each.

A

Dry (ischemic coagulative) and wet (infection)

36
Q

In what parts of the body is gangrenous necrosis common?

A

Common in limbs and GI tract

37
Q

With what substance/factor is reversible injury reversible?

A

Reversible with O2

38
Q

Reversible or Irreversible cell injury: ATP depletion?

A

Reversible with O2

39
Q

Reversible or Irreversible cell injury: Plasma membrane damage (degradation of membrane phospholipid)?

A

Irreversible

40
Q

Reversible or Irreversible cell injury: Mitochondrial permeability/vacuolization? Explain more about the reversible versus irreversible aspects of this.

A

Irreversible; Mitochondrial permeability/vacuolization; phospholipid-containing amorphous densities within mitochondria (swelling alone is reversible)

41
Q

Reversible or Irreversible cell injury: Cellular/mitochondrial swelling? What is the mechanism behind this?

A

Reversible with O2; Cellular/mitochondrial swelling (decreased ATP –> decreased activity of Na+/ pumps

42
Q

Reversible or Irreversible cell injury: Nuclear chromatin clumping?

A

Reversible with O2

43
Q

Reversible or Irreversible cell injury: Decreased glycogen?

A

Reversible with O2

44
Q

Reversible or Irreversible cell injury: Lysosomal rupture?

A

Irreversible

45
Q

Reversible or Irreversible cell injury: fatty change?

A

Reversible with O2

46
Q

Reversible or Irreversible cell injury: ribosomal/polysomal detachment? What effect does this have?

A

Reversible with O2; Ribosomal/polysomal detachment (decreased protein synthesis)

47
Q

Reversible or Irreversible cell injury: Membrane blebbing?

A

Reversible with O2

48
Q

What are the 3 hallmark changes associated with irreversible cell injury?

A

Nuclear pyknosis, karyorrhexis, karyolysis (i.e., hallmarks of cell death)

FA - Pathology (12 decks)

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