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PHP 327: Lecture 3 Introduction To CV Disease: Clinical Pathophysiology - Vascular Dysfunction Questions And Answers

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PHP 327: Lecture 3 Introduction To CV Disease: Clinical Pathophysiology - Vascular Dysfunction Questions And Answers Different risk factors (cholesterol, hypertension, diabetes, & tobacco) can each injure the lining endothelial cells Injury will elicit a series of cellular interactions (inflammatory response) forming the lesions in atheroscerosis Explain the "Response to Injury" hypothesis Oxidized LDL --> endothelial injury --> endothelial receptors --> attracting & adhering to circulating monocytes --> monocyte migration into subendothelial space --> macrophage --> ingestion of oxidized LDL --> formation of foam cell

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PHP 327: Lecture 3 Introduction To CV
Disease: Clinical Pathophysiology - Vascular
Dysfunction Questions And Answers

Different risk factors (cholesterol, hypertension, diabetes, & tobacco) can each injure the lining
endothelial cells

Injury will elicit a series of cellular interactions (inflammatory response) forming the lesions in
atheroscerosis Explain the "Response to Injury" hypothesis



Oxidized LDL --> endothelial injury --> endothelial receptors --> attracting & adhering to
circulating monocytes --> monocyte migration into subendothelial space --> macrophage -->
ingestion of oxidized LDL --> formation of foam cells



Foam cells become fatty streak

Fibrous collagen connective tissue become fibroproliferative plaque How are fatty streaks
formed?



Soft lipid-rich core

Hard collagen-rich sclerotic tissue What are the 2 components of plaque?




sclerotic component of plaque More voluminous

70% average plaque

Innocuous

,Stabilizes plaque

Prevents disruption



Lipid core of plaque Less voluminous

Dangerous component

Destabilizes plaque

More vulnerable to rupture



gruel exposed to flowing blood What causes thrombus formation?



Injury to the lining of the blood vessel provoking inflammatory response

Early fatty streak formation

Late fibrous plaque formation

Encroachment of the lumen of the vessel impairing the blood flow - chronic stable angina

Plaque rupture - unstable angina and MI Review the process of atherosclerosis formation



Oxygen-carrying capacity

Perfusion pressure

Vascular resistance Whatever are the myocardial determinants of oxygen supply?




hemoglobin content and systemic oxygenation What is Oxygen-carrying capacity
dependent on?

, aortic diastolic pressure Maximal flow is during diastole (relaxation) and perfusion
pressure is approximated by the _________________



atherosclerosis in the epicardial arteries (usually > 70% obstruction)

coronary tone of the epicardial arteries (vasoconstriction)

intrinsic coronary tone of small resistance arteries What is resistance to flow caused by?



wall tension

heart rate

contractility What are the myocardial determinants of oxygen demand?




increase; rise As our heart rate accelerates, the number of contractions and the amount of
ATP consumed per minute ____________ and oxygen requirements ______



decrease As heart rate slows, the amount of ATP consumed and the oxygen demand
________



Positive _______ inotropes directly increase the force of contraction and increases oxygen
demand



Negative _________ inotropic drugs decrease myocardial oxygen demand

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