Parsa- Cell injury 3 and 4 Flashcards

1
Q

how does ATP become depleted?

A

stop oxygen supply or nutrient supply in an artery, toxins (cyanides). without oxygen than the mitochondria wont be able to do oxidative phosphorylation.

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2
Q

if a patient is experiencing anaerobic ATP production due to lack of oxygen, what would you notice in the cell?

A

clumping of nuclear chromatin due to a decrease in pH

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3
Q

if there is an influx of calcium, water, sodium and an efflux of potassium; what is not working correctly? and how will it effect the cell?

A

sodium pump is faulty.

leads to ER swelling, cellular swelling, blebs and loss of microvilli

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4
Q

if cytochrome c is released from the mitochondria what will happen?

A

apoptosis

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5
Q

how does loss of membrane potential lead to necrosis?

A

decrease oxidative phosphorylation-> inability to make ATP

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6
Q

what can independently activate caspases to undergo apoptosis?

A

calcium

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7
Q

how does oxidative stress occur in a cell?

A

when the production of ROS increases or the scavenging systems are ineffective.

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8
Q

what mechanisms in the cell help to reduce the amount of ROS in the cell?

A

antioxidant mechanisms (Superoxide dismutase, glutathione peroxidase, catalase)

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9
Q

what generally accompanies ischemic injury?

A

inflammation because neutrophils and other leukocytes are usually present

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10
Q

how does inflammation further antagonize ischemic injuries?

A

Reperfusion. (inflammation also leads to ROS byproducts. so ROS increases due to inflammation and ischemia)

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11
Q

what is considered to be a sign of cell death?

A

leakage of enzymes

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12
Q

ischemic attacks like sickle cell disease tend to disrupt blood supplies. if an organ like a liver exhibit a firm texture in which the architecture of dead tissues is preserved for a span of a few days, what type of necrosis is it?

A

coagulative necrosis

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13
Q

what type of tissues tend to experience hemorrhagic necrosis?

A

in tissues when venous supply is obstructed and leads to rupture. (common in the lungs and reproductive system)

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14
Q

what is the difference between coagulative necrosis and liquefactive necrosis?

A

in contrast to coagulative necrosis, it is characterized by digestion of dead cells, resulting in transformation of the tissue into a liquid viscous mass (ischemic attack in the brain).

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15
Q

what kind of necrosis is exemplified by blockage of arteries in the lower extremities in diabetic patients?

A

gangrenous necrosis

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16
Q

what kind of necrosis to patients with TB experience?

A

caseous necrosis (collection of fragmented or lysed cells and amorphous granular debris enclosed within a distinctive inflammatory border).

17
Q

what is similar to caseous necrosis, but also contains a lot of plasma cells?

A

gumma (common in syphilis)

18
Q

what happens to a fat cell during fat necrosis?

A

irregular large bubble cell with no nucleus

19
Q

what necrosis is usually deposited in the vascular walls due to the deposition of antigens and antibodies?

A

fibrinoid necrosis

20
Q

what type of cells most commonly experience direct chemical injury (mercury binding to cell membrane sulfhydryl groups)?

A

absorption/ excretion cells (G.I and kidney)

21
Q

when a person takes tylenol (acetaminophen) how much of it is converted to cytochrome P-450? and how is it detoxified?

A

5%

the free radical interacts with reduced glutathione (GSH) to become detoxified

22
Q

are Bax and Bak considered anti-apoptotic?

A

nope. Bcl-2 and Bcl-x are anti-apoptotic

23
Q

FADD is known to be the death signal domain in the extrinsic pathway. what activates the FADD?

A

when FasL bind to Fas

24
Q

what can inhibit the pro-caspases-8 in the extrinsic pathway and ultimately inhibit apoptosis after FADD domain is active?

A

FLIP

25
Q

what are the responses to misfolded proteins?

A

repair (chaperones), decreased translation of proteins, activation of ubiquitin pathway (degradation) and activation of caspases (apoptosis)