Aortic Dissection Stanford Type A - False Lumen & Intimal Flap MCQ — NEET PG Practice Question | NEETPGAI
Aortic Dissection Stanford Type A - False Lumen & Intimal Flap
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microscope Pathology
A 60-year-old hypertensive man presents with sudden, tearing chest pain radiating to the back, blood pressure 200/110 mmHg in the right arm and 140/80 mmHg in the left arm, and an early diastolic murmur. CT angiography confirms an ascending aortic dissection. The autopsy specimen shows the ascending aorta opened longitudinally. The structure marked **A** in the diagram—the thin intimal flap separating the true lumen from the false lumen—is the pathological hallmark of this dissection. Which of the following BEST explains the pathogenesis of the intimal tear that initiates this dissection?
A. Chronic hypertension and age causing cystic medial degeneration with fragmentation of elastic lamellae and loss of smooth muscle
B. Genetic mutation in COL3A1 causing acute collagen type III deficiency in the media
C. Atherosclerotic plaque rupture in the ascending aorta with secondary intimal ulceration
D. Acute bacterial infection of the aortic wall leading to inflammatory weakening of the intima
Explanation
Why option 1 is right
Chronic hypertension and age produce cystic medial degeneration—fragmentation of elastic lamellae, loss of smooth muscle, and accumulation of myxoid (proteoglycan) material—which weakens the media. This weakened media allows pulsatile blood to drive longitudinally between the inner two-thirds and outer one-third of the media, creating the false lumen and the characteristic intimal flap (structure A) that separates the true from the false lumen. This is the gross hallmark and pathogenesis of Stanford Type A aortic dissection as described in Robbins and Braunwald Cardiology.
Why each distractor is wrong
Option 2 (Acute bacterial infection): While syphilitic aortitis can affect the ascending aorta, it typically causes aneurysm formation with a tree-bark intima, not acute intimal dissection with a false lumen and intimal flap. Bacterial infection is not the primary mechanism in this hypertensive patient.
Option 3 (COL3A1 mutation): COL3A1 mutations cause Ehlers-Danlos type IV (vascular), which is a predisposing condition for dissection but not the mechanism in this 60-year-old with chronic hypertension. The acute pathogenesis here is medial degeneration from hypertension, not genetic collagen deficiency.
Option 4 (Atherosclerotic plaque rupture): Atherosclerotic ulceration causes intimal damage but does not produce the characteristic false lumen with laminated thrombus and intimal flap separation seen in aortic dissection. This describes acute coronary syndrome, not dissection pathogenesis.
High-YieldNEET PG
Stanford Type A dissection = ANY ascending aorta involvement; pathogenesis = hypertension → cystic medial degeneration → intimal tear → pulsatile blood cleaves media → false lumen + intimal flap; surgical emergency.
Robbins Pathology; Braunwald Cardiology
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