B2.004 Acute MI Deep Dive Flashcards Preview

MCM Test 1 > B2.004 Acute MI Deep Dive > Flashcards

Flashcards in B2.004 Acute MI Deep Dive Deck (29):
1

What is the universal definition of MI?

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

2

What is necrosis?

a type of cell death

3

What is hypertrophy?

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

4

What is hyperplasia?

increase in number of cells in response to stimulus

5

Why can hyperplasia be dangerous?

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

6

Is hyperplasia always pathologic?

NO, can be a part of a physiologic process

7

What is atrophy?

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

8

Why does atrophy occur?

autophagocytosis causes cell to cannibalize its own internal proteins for fuel

9

What is metaplasia?

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

10

What are the main features of necrosis?

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

11

What are the main features of apoptosis?

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

12

What are 5 causes for necrosis?

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

13

What are 5 causes of physiologic apoptosis?

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

14

What are 4 causes of pathogenic apoptosis?

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

15

What are some mechanisms that facilitate necrosis?

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

16

How does an influx of Ca damage a cell?

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

17

How do ROS's damage a cell?

can damage DNA, modify proteins, or cause lipid peroxidation

18

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

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

19

What are the two pathways for apoptosis?

intrinsic (mitochondrial)
extrinsic (death receptor initiated)

20

Which protein family mediates the intrinsic apoptosis pathway?

BCL2 sensors and effectors cause mitochondria to release cytochrome c

21

Which receptors mediate the extrinsic apoptosis pathway?

Fas and TNF

22

Which proteins initiate and execute final apoptosis pathways?

capases

23

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

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

What is the biochemical effect of hypoxia?

no aerobic metabolism

25

What is the biochemical effect of ischemia?

no aerobic metabolism or anaerobic glycolysis once substrates are exhaused

26

What are some causes of arterial compromise?

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

27

What are some causes of venous compromise?

thrombosis, common in tissue/organs w single drainage

28

Where does liquefactive necrosis mostly occur?

CNS due to lack of collagen based infrastructure

29

What is the source of reperfusion injury?

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