Cell Injury Flashcards

1
Q

what is steatosis? how does it occur?

A

fatty change in the liver; alcohol changes fat metabolism by decreasing fatty acid oxidation, decreasing lipoprotein synthesis and increasing triglyceride synthesis.

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2
Q

What is Mallory’s hyaline?

A

an example of permanent damage to a hepatocyte. abstinence from alcohol will still leave a damaged hepatocyte. dense pink rope like body in the cytoplasm of hepatocytes and is an accumulation of Cytokeratin filaments.

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3
Q

what is hemochromatosis?

A

a genetic disease that results in abnormal accumulation of iron in tissues. seen as rusty tan color in stain.

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4
Q

Burkitt lymphoma is an example of:

what histological pattern is associated with this:

A

macrophage phagocytosis of apoptotic B cells
“starry sky” – lightly stained macrophages with apoptotic bodies surrounded by the dense infiltrate of malignant lymphocytes

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5
Q

what is ischemia?

A

the effect of oxygen deprivation on cell morphology

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6
Q

what are some of the early, reversible effects of hypoxia on a cell?
a histologic example of early hypoxia would be:

A

increased cell volume as Na enters w/water, increased Ca influx causes damage to cell membrane
myocardial edema

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7
Q

what is necrosis?

A

cell death at tissue level.&raquo_space; morphological changes of tissue due to enzymatic degradation of dead cells by lysosomal enzymes, and denaturation of proteins

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8
Q

The two types of necrosis are _____ and _____

A

coagulative and liquifactive

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9
Q

Coagulative necrosis results from:

A

denaturation of proteins (dominate picture). ex: mycoardial/renal/pulmonary infarction

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10
Q

Liquifactive necrosis results from:

A

extensive inflammation due to bacteria or fungus&raquo_space; complete digestion of tissue. ex: abcess & cerebral infarction

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11
Q

what is caseous necrosis?

A

usually associated w/TB. combo of liquifactive and coagulative necrosis&raquo_space; cheese like morphology

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12
Q

1) Distinguish reversible from irreversible cell injury.

A

reversible ex: steatosis. Liver hepatocyte–> steatosis (fatty change)&raquo_space; abstinence&raquo_space;healthy hepatocyte
permanent: ex: hepatocyte –> mallory’s hyaline (cytokeratin) –> abstinence –> damaged hepatocyte
reversible ex2: excess iron absorption&raquo_space; hemosiderosis&raquo_space; treatment&raquo_space; normal hepatocyte
permant ex 2: hemosiderosis&raquo_space; no treatment&raquo_space; cirrhosis

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13
Q

2) Identify the cytological changes that are associated with irreversible injury.

A

Mitochondrial swelling, loss of nuclear envelope/cell membrane, invasion by keratin filaments

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14
Q

3) Explain how steatosis occurs due to alcohol ingestion.

A

Mobilizization of fatty acids from stores
Decreased fatty acid oxidation
Increased triglyceride synthesis
Increased lipoprotein synthesis
Decreased glycosylation & transport of VLDL = accumulation of tryglycerides in liver

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15
Q

4) Name and distinguish 4 types of pathological necrosis.

A

Liquifactive: necrosis w/significant inflammation often due to bacterial or fungal infection. ex: abcess or cerebral infarction
Coagulative: most common. denaturation of cellular proteins. ex: ischemic origin, “white necrosis”
Caseous: combo of L & C necrosis
Gangrenous: overlay of liquifactive on already necrosed tissue

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16
Q

5) Explain the relationship between hemochromatosis and cirrhosis.

A

Hemochromatosis (genetic increase in iron absorption) results in liver cirrhosis if untreated. Overaccumulation of iron&raquo_space; scarring (cirrhosis)

17
Q

6) Diagram the mechanisms active in cellular apoptosis.

A

1

18
Q

7) Name four features of cellular injury that are reversible.

A
cellular swelling
loss of microvilli
Bleb
myelin figures
ER swelling
19
Q

8) Describe the electrolyte shifts that occur in ischemic cell injury leading to cell death.

A

Cells lose ability to maintain Na/K gradient via ATPase (no O2 = no oxidative phosphorylation). Na and Ca enter the cell and result in additional injury to cytoskeletal and membrane integrity

20
Q

9) Explain the role of Ca++ ions in irreversible cell injury.

A

Enters cell freely and causes release of phospholipases, proteases, endonucleases, and decreased ATPase activity. Mitochondria swell and Ca deposits are seen on EM.