Pathophysiology of ASCVD Flashcards
What is ASCVD ins layman’s terms
Clogged arteries
What are the modifiable ASCVD risk factors
Hypertension, Dyslipidemia, Diabetes, Smoking
What are the non-modifiable ASCVD risk factors
Male gender, Age, genetics (family history)
How does atherosclerosis start
LDL particles enter intima layer due to endothelial breakdown
What happens once the LDL particles enter the intima layer
LDL particles become oxidized, this oxidation leads to activation of plasminogen activator inhibitor promoting coagulation inside the blood vessel
Why is there increased vasoconstriction when LDL particles enter the intima
Oxidized LDL particles increase endothelin ( a potent vasoconstrictor) while leading to less nitric oxide
T/F: When oxidized LDL enter the intima they can cause inflammation that attracts monocyte
True
What do monocytes become when they engulf oxidized LDL in the intima of a blood vessel
Foam cells
How does the plaque become more developed and form inward
Accumulation of Foam cells, T cells, and inflammation mediators/ smooth muscles cells move to intima adding bulk
What are the two ways that a growing plaque loses its fibourous cap
Decrease in collagen production and increasing collagen degradation
How do foam cells lead to hypercoagulation
Increase the production of tissue factor
What causes a necrotic core in a plaque
Foam cells degrade and die and they are not able be cleared from the area due to diminished blood vessels functions
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
thrombosis, thrombous formation becomes greater than endogenous fibrinolysis leading to arterial occlusion
What can occur if there is a plaque rupture and thrombosis occurs but endogenous fibrinolysis keeps up with the thrombosis
More fibrous eccentric occlusive plaque that will also lead to a narrow lumen
What endothelial dysfunction of ASCVD can occur from the first decade of life
Fatty streak formation
What endothelial dysfunction of ASCVD can occur from the third decade of life
Intermediate lesion and athreoma
What endothelial dysfunction of ASCVD can occur from the fourth decade of life
Fibroatheroma and Complicated lesion
What ASCVD diseases can occur due to these lipid complications
Intracranial atherosclerosis, flow reducing carotid stenosis, cardiogenic emboli, carotid plaque with atriogenic emboli, artery spasm
What are the two most vital organs that can be affect by ASCVD, what diseases are associated with these organs
Brain (cerebrovascular disease), Heart (coronary heart disease and coronary artery disease)
T/F: If there is a decrease in luminal area there is a decrease in peripheral resistance
False: A small decrease in luminal area leads to a large change in peripheral resistance and pressure gradient across stenosis
What determines oxygen supply
Arterial pO2 (oxygenation and hemoglobin stores), Diastolic filling time (heart rate), coronary blood flow
What determines oxygen demand
heart rate, Myocardial contractility, ventricular wall tension
T/F: Large blood vessels are more likely to cause coronary resistance
False: Small blood vessels are the major determinant of coronary resistance
How can coronary resistance of small vessels lead to ischemia
Maximal dilation at rest lead to less perfusion pressure when it is need most, such as exercising
What happens to the brain when it is no longer able to regulate the increase in blood flow
Forced dilation leads to an increase in pressure and increased risk for vasogenic edema
What are the cascade of consequences that can happen due to decreasing cerebral perfusion pressure after extended periods of increased pressure
increased vasodilation –> increase cerebral blood volume–> increased intracranial pressure
What is collateral circulation
Maturation of smaller, capillary like vessels from preexisting arteries providing flow to areas of ischemia
What growth factors lead to the collateral circulation vessels
VEGF and BFGF
What is infarction
Death of tissue due to little blood supply
What is ischemic penumbra
Tissue that surrounds an infarction but is metabolically active and vulnerable to an infarction
What is a consequence caused by the tissue in a ischemic penumbra
Metabolic toxins and oxygen free radicals accumulate causing an ionic shift
What major events are more likely to occur in the brain and heart due to depolarization due to the ionic shift (pneumbra growth)
Seizures and/or arrhythymias
What is the equation that determines Cerebral Perfusion Pressure, what is the main determinant from the equation
CPP= MAP-ICP, mean arterial pressure
T/F: Too little CPP can lead to ischemia while too much CPP can lead to edema
True
What is the percent of coronary stenosis (occlusion) where there are generally no symptoms, when would symptoms start to occur and why
less than 40%, 40%-50% due NO depletion
At what percentage of coronary stenosis does non obstructive coronary artery disease become obstructive
70%, symptoms are more likely to become present
T/F: At 80% to 85% plaques are most likely to rupture
False: At 40% to 70% plaques are most prone to rupturing, at 80% to 85% symptoms occur at rest
