Page 980 - Clinical Immunology_ Principles and Practice ( PDFDrive )
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CHaPter 69 Inflammation and Atherothrombosis 946.e1
MUL t IPL e -CHOIC e QU est IO ns
1. Indicate which of the following represents the correct timeline 2. Which of the following represents a recognized mechanism
in the natural history of atherosclerosis: involved in plaque instability?
A. Subendothelial retention of lipoproteins and flow-mediated A. Increase in regulatory T cells (Tregs) around the plaque
inflammatory changes → endothelial dysfunction → B. Widespread coronary inflammation
self-maintaining inflammatory state → fatty streak → C. Smooth muscle cells hyperreactivity
atheroma→ fibroatheroma D. Metabolic disturbances
B. Fatty streak → endothelial dysfunction → self-maintaining 3. The mechanisms involved in plaque erosion are still poorly
inflammatory state → subendothelial retention of lipo- understood; according to recent experimental evidence, which
proteins and flow-mediated inflammatory changes → of the following seems to be the most probable trigger involved
atheroma→ fibroatheroma in endothelial erosion?
C. Fibroatheroma → endothelial dysfunction → fatty streak A. Inflammasome activation through cholesterol crystals inside
→ self-maintaining inflammatory state → subendothelial the plaque
retention of lipoproteins and flow-mediated inflammatory B. Coronary artery dissection
changes → atheroma C. Fibrous cap rupture
D. Self-maintaining inflammatory state → atheroma → D. Toll-like receptor (TLR) activation, extracellular matrix
fibroatheroma → endothelial dysfunction → fatty streak and hyaluronan exposure, neutrophil recruitment
→ subendothelial retention of lipoproteins and flow-
mediated inflammatory changes

