Path IV Flashcards

1
Q

What are some cytoplasmic features of necrosis?

A

increased cytoplasmic eosinophilia, calcification

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2
Q

What are some nuclear features of necrosis?

A

karyolysis leading to fading of basophilia of DNA

pyknosis: nculear shrinkage into a ball with increased basophilia
karyorrhexis: fragemntation of of pyknotic or karyolyitic nuclei

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3
Q

What is the morphology of an apoptotic cell?

A

shrunken, dark cell with pyknotic nucleus and fragmentation of the the cell into apoptotic bodies. followed by phagocytosis.

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4
Q

How do we regulate the size of a cell population?

A

altering the rate of cell death or changing the rate of cell proliferation and differentiation.

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5
Q

What are the three kinds of cells in the body, grouped by how often they divide?

A
  1. continuously dividing cells: epithelium, hematopoetic cells
  2. quiescent cells: low levels of activity and division but can be greatly upregulated in times of need: kidney, liver, pancreas, endothelial cells
  3. non-dividing cells: cells that don’t divide post-natally: neurons, cardiac myocytes, most skeletal muscle
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6
Q

What signaling goes on in the extrinsic pathway for apoptosis?

A

cell surface molecules like TNFR1 or Fas bind TNF-family molecules.
this leads to the aggregation of intracellulatr death domains (FADD)
we then se a proteolytic cascade where the final result is the activation of caspases.

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7
Q

What roles does TNF play in the cell?

A

may promote apoptosis by leading to the aggregation of intracellular death domains or may oppose apoptosis by degrading inhibitors of anit-apoptotic proteins (like NF-kB).

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8
Q

How do cytotoxic T cells promote apoptosis using the extrinsic death pathway?

A

via interacting with Fas receptors of the (soon-to-be) apoptotic cells. T cells have Fas ligand on their surfaces.

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9
Q

How does the intrinsic apopotic pathway work?

A

Normally, Bcl-2 is found on the surface of the mitochondria and is bound by growth factors and hormones. If this stimulus disappears, Bcl-2 decreases. Or, sensors of damage and stress like Bim, Bad, and Bid are activated leading tho the insertion of Bax and Bak into the mitochondrial membrane. Mitochondria leaks cytochrome c, cytochrome c binds cytoplasmic Apaf-1, and caspases are activated.

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10
Q

How does severe DNA damage promote apoptosis?

A

severe DNA damage leads to the accumulation of p53, which interacts with Bcl-2 and promotes apopotosis.

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11
Q

What happens during the execution phase of apoptosis?

A

activation of executioner caspases 3 and 6 by initiator caspases 8 and 9. they cleave each other, the cytoskeleton, and nuclear matrix proteins. DNases are activated and macrophage stimulatory factors are released.

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12
Q

How do cytotoxic T cells promote apoptosis directly?

A

they perforate the cell membrane with perforin and inject granzyme protease, which activates executioner caspases.

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13
Q

What happens during autophagy- what is its function and what occurs?

A

this is the lysosomal degradation of a cell’s own components.
it removes organelles that were damaged during injury or aren’t needed due to cellular remodeling. it also digests unneeded proteins. stuff is organelles are sequestered in an autophagic vaculue, which fuses w/ lysosome to make an autolysosome. digested materials may be recycled.

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14
Q

What is the difference between exogenous and endogenous intracellular accumulation?

A

endogenous: describes materials that are naturally occuring in the body
exogenous: describes materials that are ingested or absorbed from the environment.

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15
Q

Why do normal endogenous/exogenous things accumulate?

A

synthesis/absorption is up or degradation/metabolism/export is down.

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16
Q

Why do abnormal things accumulate?

A

usually due to metabolism or export defects, or when environmental exposures happen with materials for which there is no effective metabolism/excretion mechanism.

17
Q

What are some markers for phagocytic recognition?

A

PS is flipped and expressed on the outer cell membrane- can bind to annexin V.

18
Q

What is fatty change?

A

abnormal accumulation of triglycerides withing cells, esp. hepatocytes and cardiac myocytes.

19
Q

What are causes of fatty change/steatosis?

A

alcohol abuse, diabetes, obesity, toxins, protein malnutrition, anoxia,

20
Q

What are examples of pathologic processes characterized by the accumulation of cholesterol and cholesterol esters?

A

atherosclerosis: smooth muscle cells and macrophages fill with cholesterol and cholesterol esters and become foam cells.
xanthomas- foam cells in skin
cholesterolosis- foam cells in gall bladder mucosa

21
Q

What are three diseases characterized by cytoskeletal protein accumulation?

A

alpha-1 antitrypsin deficiency, mallory bodies of alcohol intoxication, neurfibrillary tangles of alzheimer’s disease

22
Q

What is alpha-1 antitrypsin dificiency?

A

accumulation of poorly folded cytoskeletal proteins in the liver

23
Q

What are mallory bodies?

A

due to alcohol intoxication, they are eosinophilic keratin filaments in hepatocytes (cytoskeletal protein accumulation)

24
Q

What proteins make up the tangles of alzheimer’s disease?

A

neurofilaments and microtubule-asociated proteins

25
Q

What are two examples of intracellular accumulations of pigments?

A

carbon from cigarettes and industrial smoke in lungs (anthracosis) and lymph nodes
tattoos: pigments in intradermal macrophages

26
Q

What is lipofuscin?

A

It is a polymer of lipids and phospholipids bound to protein
it increases with aging
it has yellowish brown cytoplasmic granules

27
Q

What is hemosiderin?

A

storage form of iron incells exposed to high iron concentrations. Often seen in bruises and at sites of hemorrhage or during hemolytic anemia course golden brown granular pigment. Very easy to see if you stain for iron.

28
Q

What is dystrophic calcification?

A

occurs in sites of necrosis and in atherosclerosis, some papillary cancers
white granules or larger aggregates; basophilic in H and E stains.

29
Q

What is the pathogenesis of dystrophic calcification?

A

formation of crystalline calcium phosphate mineral. initiation: begins in mitochondria of dead or dying cells, which seed crystals.