Pathophysiology of ASCVD

Question 1

What is ASCVD ins layman’s terms

Answer 1

Clogged arteries

Question 2

What are the modifiable ASCVD risk factors

Answer 2

Hypertension, Dyslipidemia, Diabetes, Smoking

Question 3

What are the non-modifiable ASCVD risk factors

Answer 3

Male gender, Age, genetics (family history)

Question 4

How does atherosclerosis start

Answer 4

LDL particles enter intima layer due to endothelial breakdown

Question 5

What happens once the LDL particles enter the intima layer

Answer 5

LDL particles become oxidized, this oxidation leads to activation of plasminogen activator inhibitor promoting coagulation inside the blood vessel

Question 6

Why is there increased vasoconstriction when LDL particles enter the intima

Answer 6

Oxidized LDL particles increase endothelin ( a potent vasoconstrictor) while leading to less nitric oxide

Question 7

T/F: When oxidized LDL enter the intima they can cause inflammation that attracts monocyte

Answer 7

True

Question 8

What do monocytes become when they engulf oxidized LDL in the intima of a blood vessel

Answer 8

Foam cells

Question 9

How does the plaque become more developed and form inward

Answer 9

Accumulation of Foam cells, T cells, and inflammation mediators/ smooth muscles cells move to intima adding bulk

Question 10

What are the two ways that a growing plaque loses its fibourous cap

Answer 10

Decrease in collagen production and increasing collagen degradation

Question 11

How do foam cells lead to hypercoagulation

Answer 11

Increase the production of tissue factor

Question 12

What causes a necrotic core in a plaque

Answer 12

Foam cells degrade and die and they are not able be cleared from the area due to diminished blood vessels functions

Question 13

What can occur if there is plaque rupture that cause a break in the blood vessel, what can occur if this is out of control

Answer 13

thrombosis, thrombous formation becomes greater than endogenous fibrinolysis leading to arterial occlusion

Question 14

What can occur if there is a plaque rupture and thrombosis occurs but endogenous fibrinolysis keeps up with the thrombosis

Answer 14

More fibrous eccentric occlusive plaque that will also lead to a narrow lumen

Question 15

What endothelial dysfunction of ASCVD can occur from the first decade of life

Answer 15

Fatty streak formation

Question 16

What endothelial dysfunction of ASCVD can occur from the third decade of life

Answer 16

Intermediate lesion and athreoma

Question 17

What endothelial dysfunction of ASCVD can occur from the fourth decade of life

Answer 17

Fibroatheroma and Complicated lesion

Question 18

What ASCVD diseases can occur due to these lipid complications

Answer 18

Intracranial atherosclerosis, flow reducing carotid stenosis, cardiogenic emboli, carotid plaque with atriogenic emboli, artery spasm

Question 19

What are the two most vital organs that can be affect by ASCVD, what diseases are associated with these organs

Answer 19

Brain (cerebrovascular disease), Heart (coronary heart disease and coronary artery disease)

Question 20

T/F: If there is a decrease in luminal area there is a decrease in peripheral resistance

Answer 20

False: A small decrease in luminal area leads to a large change in peripheral resistance and pressure gradient across stenosis

Question 21

What determines oxygen supply

Answer 21

Arterial pO2 (oxygenation and hemoglobin stores), Diastolic filling time (heart rate), coronary blood flow

Question 22

What determines oxygen demand

Answer 22

heart rate, Myocardial contractility, ventricular wall tension

Question 23

T/F: Large blood vessels are more likely to cause coronary resistance

Answer 23

False: Small blood vessels are the major determinant of coronary resistance

Question 24

How can coronary resistance of small vessels lead to ischemia

Answer 24

Maximal dilation at rest lead to less perfusion pressure when it is need most, such as exercising

Question 25

What happens to the brain when it is no longer able to regulate the increase in blood flow

Answer 25

Forced dilation leads to an increase in pressure and increased risk for vasogenic edema

Question 26

What are the cascade of consequences that can happen due to decreasing cerebral perfusion pressure after extended periods of increased pressure

Answer 26

increased vasodilation --> increase cerebral blood volume--> increased intracranial pressure

Question 27

What is collateral circulation

Answer 27

Maturation of smaller, capillary like vessels from preexisting arteries providing flow to areas of ischemia

Question 28

What growth factors lead to the collateral circulation vessels

Answer 28

VEGF and BFGF

Question 29

What is infarction

Answer 29

Death of tissue due to little blood supply

Question 30

What is ischemic penumbra

Answer 30

Tissue that surrounds an infarction but is metabolically active and vulnerable to an infarction

Question 31

What is a consequence caused by the tissue in a ischemic penumbra

Answer 31

Metabolic toxins and oxygen free radicals accumulate causing an ionic shift

Question 32

What major events are more likely to occur in the brain and heart due to depolarization due to the ionic shift (pneumbra growth)

Answer 32

Seizures and/or arrhythymias

Question 33

What is the equation that determines Cerebral Perfusion Pressure, what is the main determinant from the equation

Answer 33

CPP= MAP-ICP, mean arterial pressure

Question 34

T/F: Too little CPP can lead to ischemia while too much CPP can lead to edema

Answer 34

True

Question 35

What is the percent of coronary stenosis (occlusion) where there are generally no symptoms, when would symptoms start to occur and why

Answer 35

less than 40%, 40%-50% due NO depletion

Question 36

At what percentage of coronary stenosis does non obstructive coronary artery disease become obstructive

Answer 36

70%, symptoms are more likely to become present

Question 37

T/F: At 80% to 85% plaques are most likely to rupture

Answer 37

False: At 40% to 70% plaques are most prone to rupturing, at 80% to 85% symptoms occur at rest