How do macrophages contribute to the initiation of an atherosclerotic plaque ?

Macrophages ingest oxidized LDL particles trapped in the tunica intima . This consumption process converts them into foam cells , which accumulate to form the initial fatty streak.

What is the physiological role of growth factors in the progression from a fatty streak to a fibrous plaque ?

Growth factors, such as platelet-derived growth factor , stimulate the proliferation of smooth muscle cells and matrix production to encapsulate the lipid core, thereby stabilizing the lesion.

Why is plaque rupture considered the critical event in the transition to an acute myocardial infarction ?

Rupture exposes the underlying thrombogenic material to the bloodstream, triggering rapid platelet aggregation and thrombus formation, which can cause sudden, complete occlusion of the coronary artery.

How does hypertension increase the risk of atherosclerosis at the cellular level?

Hypertension creates persistent mechanical stress on the arterial walls, which injures the endothelial lining and increases vascular permeability, allowing LDL cholesterol to enter the sub-endothelial space.

Which specific lipid profile component is considered cardiovascular protective and why?

HDL (High-Density Lipoprotein) is considered protective because it facilitates reverse cholesterol transport , removing excess cholesterol from arterial walls and returning it to the liver for excretion.

Why is family history of cardiovascular disease categorized as a non-modifiable risk factor ?

It represents an inherent genetic predisposition to vascular pathology that cannot be altered by lifestyle changes, necessitating earlier or more aggressive clinical cardiovascular surveillance .

What key clinical feature distinguishes stable angina from unstable angina regarding resolution?

Stable angina occurs predictably with exertion and resolves with rest or GTN . Unstable angina occurs at rest, is unpredictable, and does not resolve with standard rest or nitrate therapy .

Why might a patient experiencing an NSTEMI present with a normal or non-diagnostic ECG ?

An NSTEMI often involves only partial vessel occlusion or subendocardial ischemia , which may not produce the transmural electrical changes required to show ST-segment elevation on a standard 12-lead ECG.

What is the gold standard diagnostic test used in hospital settings to differentiate NSTEMI from unstable angina ?

Troponin testing is the gold standard. Elevated troponin levels indicate myocardial cell death (infarction), confirming NSTEMI , whereas unstable angina typically does not show elevated cardiac biomarkers.

How does GTN reduce myocardial oxygen demand in a patient with angina ?

GTN acts as a vasodilator. By promoting venous dilation, it reduces venous return (preload), which decreases the volume of blood the heart must pump, thereby reducing its metabolic workload and oxygen consumption.

At higher doses, what additional cardiovascular effect does GTN exert beyond venous dilation?

At higher doses, GTN causes significant arterial dilation , which reduces systemic vascular resistance or afterload , further decreasing the pressure the heart must work against.

What is the pharmacological mechanism by which Aspirin prevents thrombus growth?

Aspirin acts as an antiplatelet agent that irreversibly inhibits the COX-1 enzyme . This prevents the conversion of arachidonic acid into Thromboxane A2 , a potent molecule required for platelet aggregation.

Why is the 70% occlusion threshold clinically significant in the context of coronary artery disease?

It is the threshold where the arterial lumen is sufficiently narrowed that blood flow can no longer meet the increased metabolic demand of the myocardium during exercise, resulting in exertional chest pain .

What is the difference between transmural and subendocardial damage in the context of myocardial infarction?

Transmural damage involves the full thickness of the myocardial wall, typically associated with STEMI . Subendocardial damage is limited to the inner, oxygen-sensitive layers and is typically associated with NSTEMI .

Why is smoking considered a major modifiable risk factor in the pathogenesis of atherosclerosis?

Smoking contributes to endothelial damage through the release of catecholamines (which increase heart rate and BP) and the disruption of the lipid profile , favoring the oxidation of LDL and the formation of plaques.

Pathophysiology And Clinical Management Of Acute Coronary Syndrome Flashcards

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Flashcard Sets

Pathophysiology and Clinical Management of Acute Coronary Syndrome

This deck covers the biological progression of atherosclerosis, cardiovascular risk assessment, clinical presentations of ACS, and the pharmacological management of cardiac events.

15 cards

intermediate

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by @eli_shanna

Q: How do macrophages contribute to the initiation of an atherosclerotic plaqu...

Q: What is the physiological role of growth factors in the progression from a ...

Q: Why is plaque rupture considered the critical event in the transition to an <strong...

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