QCM : Understanding Atherosclerosis Formation and Risks — 16 questions

Explication

The initiation of atherosclerosis involves endothelial dysfunction that allows LDL cholesterol to cross the endothelium and become oxidized beneath it. Oxidized LDL plays a key role in attracting immune cells and promoting lesion formation.

Explication

Fatty streaks, the earliest lesions in atherosclerosis, typically start forming in individuals aged 10-20 years, establishing the beginning stage of the disease.

Explication

Foam cells are macrophages that have ingested oxidized low-density lipoprotein (LDL). They appear as lipid-laden macrophages within the arterial intima and are the hallmark feature of early fatty streaks in atherosclerosis. These foam cells contribute to the formation of fatty streaks, which are the earliest visible lesions in atherogenesis.

Explication

VSMCs migrate into the intima and produce collagen, forming the fibrous cap that stabilizes the plaque.

Explication

VSMC migration is a crucial step in atherogenesis where smooth muscle cells move from the media to the intima, where they produce collagen and other extracellular matrix components. This collagen forms a fibrous cap that stabilizes the plaque, preventing rupture. Therefore, the correct process involves VSMC migration reaching the intima and producing collagen, which contributes to plaque stability.

Explication

High LDL cholesterol is a major risk factor because it leads to fatty deposits beneath the endothelium, promoting plaque formation.

Explication

A stable atherosclerotic plaque is characterized by a thick fibrous cap that is rich in collagen, which provides mechanical strength and reduces the likelihood of rupture. In contrast, unstable plaques tend to have a thin fibrous cap with a large lipid core and are more prone to rupture leading to thrombosis.

Explication

Unstable plaques are characterized by a large lipid/necrotic core, making them more prone to rupture compared to collagen-rich stable plaques.

Explication

Unstable plaques are typically lipid-rich and soft, making them vulnerable to fissuring or rupture. These plaques have a thin fibrous cap and a large necrotic core, which predisposes them to rupture, leading to thrombosis. In contrast, stable plaques usually have a collagen-rich fibrous cap that provides stability and reduces the likelihood of rupture.

Explication

Critical stenosis causing symptoms is generally defined as greater than 70-75% narrowing of the artery, impairing blood flow.

Explication

A stable atherosclerotic plaque is characterized by a fibrous cap rich in collagen that covers a core of lipids and necrotic material, making it less prone to rupture. The thick collagen cap provides structural integrity, reducing the risk of fissuring or rupture, unlike unstable plaques that are lipid-rich and have a thin fibrous cap.

Explication

Plaque rupture exposes the necrotic core to blood, activating clotting and leading to thrombosis, which can cause vessel occlusion.

Explication

Ischemic symptoms usually manifest when arterial lumen narrowing exceeds 70-75%, as this level of stenosis significantly impairs blood flow. When the stenosis is less severe, collateral circulation or residual flow often prevents symptoms. Therefore, the critical threshold for symptom development is generally in the >70-75% range of vessel narrowing, making option one correct.

Explication

Angina in coronary artery disease often results from the rupture of an unstable atheromatous plaque, leading to thrombus formation and subsequent obstruction of blood flow. The process typically involves plaque disruption rather than mere gradual narrowing or vasospasm alone. The rupture exposes thrombogenic material, activating clot formation that can suddenly occlude the vessel, causing ischemic chest pain.

Explication

The middle cerebral artery is the most commonly affected cerebral artery in large vessel strokes, accounting for a significant proportion of ischemic strokes. It supplies large portions of the lateral cerebral cortex, including areas responsible for motor and sensory functions of the face and limbs. Occlusion often leads to contralateral hemiparesis and sensory loss, aphasia if in dominant hemisphere.

Explication

Claudication results from gradual narrowing of peripheral arteries caused by atherosclerotic plaques, which reduces blood flow during increased demand such as exercise. This ischemia manifests as pain or cramping in the affected limbs. The process is primarily due to atherosclerosis, not rupture, spasm, or infection.