Regarding the cardinal signs and mediators of acute inflammation, all of the following are correct EXCEPT:

Question

Accepted Answer

B. Prostaglandin E2 (PGE2) causes vasoconstriction and decreases vascular permeability, thereby limiting inflammation. ## Mediators of Acute Inflammation — Mechanism and Effects

**Key Point:** PGE2 is a pro-inflammatory mediator that causes vasodilation and increases vascular permeability — it does NOT cause vasoconstriction or limit inflammation. This is the incorrect statement.

### Correct Mediators and Their Actions

| Mediator | Source | Primary Action | Effect |
|----------|--------|-----------------|--------|
| Histamine | Mast cells, basophils | H1/H2 receptor activation | Vasodilation, ↑ permeability, pain |
| Bradykinin | Kinin cascade (HMWK) | B2 receptor activation | Vasodilation, pain, smooth muscle contraction |
| C5a | Complement activation | G-protein coupled receptor | Chemotaxis, degranulation, vasodilation |
| PGE2 | COX pathway (arachidonic acid) | EP receptors | **Vasodilation, ↑ permeability, potentiates pain** |
| Leukotrienes (LTC4, LTD4) | 5-lipoxygenase pathway | CysLT receptors | Potent vasodilation, ↑ permeability, chemotaxis |

**High-Yield:** PGE2 and other prostaglandins (PGD2, PGI2) are pro-inflammatory — they amplify the inflammatory response, not suppress it. NSAIDs work by inhibiting COX enzymes, thereby reducing PG synthesis and inflammation.

**Clinical Pearl:** The distinction between vasodilators (histamine, bradykinin, PGE2, leukotrienes) and vasoconstrictors (norepinephrine, angiotensin II) is clinically important. Acute inflammation is characterized by net vasodilation and increased permeability.

### Why Option 3 Is Wrong

PGE2 causes:
- Vasodilation (not vasoconstriction)
- Increased vascular permeability (not decreased)
- Potentiation of pain (synergizes with bradykinin)
- Pro-inflammatory effects (not anti-inflammatory)

**Warning:** Do not confuse PGE2 with catecholamines or vasopressin, which cause vasoconstriction. PGE2 is fundamentally a vasodilator and permeability-increasing agent.

Answer

A. Histamine causes vasodilation and increased vascular permeability primarily through H1 and H2 receptors

Answer

C. Bradykinin is a nonapeptide generated from high-molecular-weight kininogen and causes pain and vasodilation

Answer

D. Complement component C5a is a potent chemotactic agent that recruits neutrophils to the site of injury

Regarding the cardinal signs and mediators of acute inflammation, all of the following are correct EXCEPT:

Explanation

Mediators of Acute Inflammation — Mechanism and Effects

Correct Mediators and Their Actions

Why Option 3 Is Wrong

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Mediator	Source	Primary Action	Effect
Histamine	Mast cells, basophils	H1/H2 receptor activation	Vasodilation, ↑ permeability, pain
Bradykinin	Kinin cascade (HMWK)	B2 receptor activation	Vasodilation, pain, smooth muscle contraction
C5a	Complement activation	G-protein coupled receptor	Chemotaxis, degranulation, vasodilation
PGE2	COX pathway (arachidonic acid)	EP receptors	Vasodilation, ↑ permeability, potentiates pain
Leukotrienes (LTC4, LTD4)	5-lipoxygenase pathway	CysLT receptors	Potent vasodilation, ↑ permeability, chemotaxis