Atherosclerosis MCQ — NEET PG Practice Question | NEETPGAI
Atherosclerosis
medium
microscope Pathology
Regarding the pathogenesis of atherosclerosis, all of the following are recognized mechanisms EXCEPT:
A. High-density lipoprotein (HDL) directly inhibits the formation of foam cells by blocking LDL oxidation
B. Oxidation of low-density lipoprotein (LDL) in the subendothelial space promotes uptake by macrophages via scavenger receptors
C. Smooth muscle cell migration from the media to the intima is mediated by platelet-derived growth factor (PDGF) released from activated platelets and macrophages
D. Endothelial dysfunction leads to increased expression of adhesion molecules (ICAM-1, VCAM-1) and recruitment of monocytes
Explanation
Pathogenesis of Atherosclerosis: Mechanisms and Misconceptions
Overview
Atherosclerosis is a multistep inflammatory process involving endothelial dysfunction, lipid accumulation, and smooth muscle proliferation. The question tests understanding of which mechanisms are actually operative versus which are misconceptions.
Correct Mechanisms (Options 0, 1, 3)
Option 0: LDL Oxidation and Foam Cell Formation
Oxidized LDL (oxLDL) accumulates in the subendothelial space
Macrophages recognize oxLDL via scavenger receptors (SR-A, LOX-1), not the classical LDL receptor
This leads to unregulated lipid uptake and foam cell formation
Robbins 10e Ch 11
Option 1: Endothelial Dysfunction
Loss of endothelial barrier function and increased permeability
Upregulation of adhesion molecules (ICAM-1, VCAM-1, E-selectin)
Recruitment and transmigration of monocytes into the intima
This is a critical early step in atherogenesis
Option 3: Smooth Muscle Proliferation
PDGF is released from activated platelets and macrophages
Acts as a potent chemoattractant and mitogen for smooth muscle cells
Drives migration from media to intima and subsequent proliferation
Forms the fibrous cap of advanced plaques
The Incorrect Mechanism (Option 2)
Option 2: HDL and Foam Cell Prevention
This is FALSE. HDL does NOT directly inhibit foam cell formation by blocking LDL oxidation
HDL's protective role is through reverse cholesterol transport — it removes cholesterol from peripheral tissues and foam cells, facilitating hepatic clearance
HDL also has antioxidant and anti-inflammatory properties, but it does NOT prevent oxLDL formation
Once LDL is oxidized, HDL cannot "undo" that oxidation
The question stem asks for the mechanism that is NOT true — this is the answer
Key Point
HDL protects against atherosclerosis by:
Reverse cholesterol transport (ABCA1-mediated efflux)
NOT by preventing LDL oxidation in the first place
High-Yield Distinction
Warning
Students often confuse HDL's protective mechanisms. HDL is reactive (removes lipids after damage) not preventive (stops oxidation before it happens). Prevention of LDL oxidation is the role of antioxidant vitamins (vitamin E, C) and endogenous antioxidant enzymes, not HDL.
