Acute Inflammation MCQ — NEET PG Practice Question | NEETPGAI
Acute Inflammation
medium
microscope Pathology
A 32-year-old male presents to the emergency department with acute onset of severe right lower abdominal pain, fever (38.5°C), and vomiting for 6 hours. On examination, he has localized tenderness at McBurney's point with guarding and rebound tenderness. Blood investigations show WBC 14,500/μL with left shift (80% neutrophils). Ultrasound confirms acute appendicitis. During emergency appendectomy, the surgeon notes the appendiceal wall is hyperemic, edematous, and infiltrated with purulent exudate. Histopathology shows neutrophilic infiltration with fibrin deposition and tissue destruction. Which of the following mediators is MOST responsible for the vascular permeability increase and neutrophil recruitment observed in this acute inflammatory response?
A. Tumor necrosis factor-alpha and interleukin-1
B. Histamine and bradykinin
C. Prostaglandin E2 and leukotriene B4
D. Complement C3a and C5a
Explanation
Pathophysiology of Acute Inflammation in Appendicitis
Vascular and Cellular Events
Acute appendicitis triggers the classic acute inflammatory response characterized by:
1.
Increased vascular permeability (exudation)
2.
Neutrophil recruitment and infiltration
3.
Tissue damage and fibrin deposition
Role of Complement Fragments C3a and C5a
Key Point
C3a and C5a are the most potent anaphylatoxins and are the PRIMARY mediators of both vascular permeability increase and neutrophil chemotaxis in acute inflammation.
High-YieldNEET PG
C5a is the most powerful neutrophil chemoattractant (100× more potent than C3a)
Both C3a and C5a increase vascular permeability by acting on endothelial cells and mast cells
They promote neutrophil adhesion to endothelium via upregulation of adhesion molecules (integrins, selectins)
C5a also triggers the respiratory burst in neutrophils, enhancing their bactericidal capacity
Comparative Role of Other Mediators
Table
Mediator
Primary Role
Potency
Timeline
Histamine & Bradykinin
Vascular permeability (early)
Moderate
Immediate (minutes)
PGE₂ & LTB₄
Pain, vasodilation, weak chemotaxis
Moderate
Early (minutes–hours)
TNF-α & IL-1
Systemic effects, endothelial activation
Moderate–High
Delayed (hours)
C3a & C5a
Permeability + potent chemotaxis
Highest
Rapid (minutes)
Clinical Pearl
In bacterial peritonitis (as in perforated appendicitis), the complement cascade is activated via both classical and alternative pathways, making C3a/C5a generation the dominant mechanism driving the acute inflammatory infiltrate.
Why This Matters in Appendicitis
The histological finding of neutrophilic infiltration with fibrin deposition is the hallmark of acute suppurative inflammation, and this is orchestrated primarily by complement-mediated neutrophil recruitment and vascular leak.
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