Acute Appendicitis MCQ — NEET PG Practice Question | NEETPGAI
Acute Appendicitis
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A 22-year-old male presents with a 36-hour history of periumbilical pain that has migrated to the right lower quadrant, with anorexia and low-grade fever. On examination, he has focal tenderness over McBurney point with a positive Rovsing sign. Graded-compression ultrasound of the right lower quadrant reveals the structure marked **A** — a non-compressible, blind-ending tubular structure measuring 8 mm in outer diameter. Which of the following pathophysiological mechanisms BEST explains the initial development of this acute condition?
A. Luminal obstruction (typically by fecalith in adults or lymphoid hyperplasia in children) leading to mucus accumulation, distension, venous congestion, and bacterial overgrowth
B. Spontaneous perforation of the appendix due to increased intraluminal pressure alone
C. Primary bacterial invasion of the appendiceal wall without preceding luminal obstruction
D. Acute mesenteric ischemia from appendiceal artery thrombosis
Explanation
Why option 1 is correct
The structure marked A — a non-compressible, blind-ending tubular structure >6 mm — is the acutely inflamed appendix on ultrasound. The clinical anchor from Sabiston and WSES guidelines is that acute appendicitis pathophysiology BEGINS with luminal obstruction (fecalith in adults, lymphoid hyperplasia in children), which triggers mucus accumulation, distension, venous and lymphatic congestion, bacterial overgrowth (E. coli, Bacteroides fragilis, Peptostreptococcus), and mucosal ulceration. This is the initiating mechanism in the vast majority of cases and is the foundation of understanding why appendicitis develops. The patient's clinical presentation (periumbilical pain migrating to RLQ, McBurney tenderness, Rovsing sign) and the sonographic finding of a dilated non-compressible appendix are consistent with acute appendicitis secondary to luminal obstruction.
Why each distractor is wrong
Option 2 (Primary bacterial invasion without obstruction): While bacterial overgrowth is part of the pathophysiology, it is a CONSEQUENCE of luminal obstruction and stasis, not the primary initiating event. Bacteria do not spontaneously invade a healthy appendiceal mucosa without preceding obstruction.
Option 3 (Mesenteric ischemia from artery thrombosis): Ischemia is a LATE complication of untreated appendicitis (within 48–72 hours if perforation occurs), not the initial mechanism. It results from progressive venous congestion and bacterial invasion, not primary vascular thrombosis.
Option 4 (Spontaneous perforation from pressure alone): Perforation is a complication that occurs if obstruction and infection are left untreated; it is not the initiating mechanism. Increased pressure alone does not cause perforation without preceding inflammation and mucosal ulceration.
