B2.004 Acute MI Deep Dive Flashcards

1
Q

What is the universal definition of MI?

A

evidence of myocardial necrosis in a clinical setting consistent with acute myocardial ischemia

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2
Q

What is necrosis?

A

a type of cell death

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3
Q

What is hypertrophy?

A

increase in size of cells resulting in increase in size of organ; due to synthesis of more cellular components and more structural/functional proteins

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4
Q

What is hyperplasia?

A

increase in number of cells in response to stimulus

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5
Q

Why can hyperplasia be dangerous?

A

more proliferation can lead to more chance of DNA mutations during mutations; this can potentially lead to cancer

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6
Q

Is hyperplasia always pathologic?

A

NO, can be a part of a physiologic process

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7
Q

What is atrophy?

A

decrease in size and number of cells resulting in a decrease in organ size

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8
Q

Why does atrophy occur?

A

autophagocytosis causes cell to cannibalize its own internal proteins for fuel

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9
Q

What is metaplasia?

A

replacement of one differentiated cell type by another differentiated cell time; usually accompanied by increased cell division

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10
Q

What are the main features of necrosis?

A

accidental death due to ATP depletion, loss of membrane integrity and leakage of cytoplasmic contents, always pathogenic

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11
Q

What are the main features of apoptosis?

A

programmed death that is energy dependent, membrane integrity preserved to avoid inflammation, can be physiologic or pathologic

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12
Q

What are 5 causes for necrosis?

A

hypoxia, physical agents, chemical agents, infectious agents, immunologic reactions, genetic derangements, nutritional imbalances

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13
Q

What are 5 causes of physiologic apoptosis?

A

embryogenesis, hormonal involution, cell loss in proliferating cell pops, elimination of potentially harmful self reactive lymphocytes, immunologically mediated cell death

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14
Q

What are 4 causes of pathogenic apoptosis?

A

DNA damage, accumulation of misfolded proteins, infections/ immunologic reactions, cell loss in organs after duct obstruction

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15
Q

What are some mechanisms that facilitate necrosis?

A

depletion of ATP, mitochondrial damage, loss of Ca homeostasis, accumulation of ROS, defects in membrane permeability, damage to DNA/proteins

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16
Q

How does an influx of Ca damage a cell?

A

activates cellular enzymes that cause damage and increase mitochondrial permeability which decreases ATP production

17
Q

How do ROS’s damage a cell?

A

can damage DNA, modify proteins, or cause lipid peroxidation

18
Q

How are ROS’s typically removed in a healthy cell?

A

O2 radical converted to H2O2 which is decomposed along with OH radicals to H2O by enzymes

19
Q

What are the two pathways for apoptosis?

A

intrinsic (mitochondrial)

extrinsic (death receptor initiated)

20
Q

Which protein family mediates the intrinsic apoptosis pathway?

A

BCL2 sensors and effectors cause mitochondria to release cytochrome c

21
Q

Which receptors mediate the extrinsic apoptosis pathway?

A

Fas and TNF

22
Q

Which proteins initiate and execute final apoptosis pathways?

A

capases

23
Q

What are 3 types of necrosis and how do they differ?

A

coagulative: seen in MI, substructure still exists
liquefactive: underlying substructure collapses leaving a cavity of dead cells and neutrophils (pus)
caseous: due to infectious agents, long acting response which results in granulous (hard) imflammation

24
Q

What is the biochemical effect of hypoxia?

A

no aerobic metabolism

25
Q

What is the biochemical effect of ischemia?

A

no aerobic metabolism or anaerobic glycolysis once substrates are exhaused

26
Q

What are some causes of arterial compromise?

A

thrombosis, embolism, vasospasm, hemorrhange into plaque, extrinsic compression, torsion, rupture, entrapment

27
Q

What are some causes of venous compromise?

A

thrombosis, common in tissue/organs w single drainage

28
Q

Where does liquefactive necrosis mostly occur?

A

CNS due to lack of collagen based infrastructure

29
Q

What is the source of reperfusion injury?

A

oxidative stress after prolonged oxygen depletion, intracellular calcium overload, imflammation