**Core Concept**
The question describes a patient with joint pain on NSAID use presenting with punctate hemorrhagic lesions and mucosal erosions without ulcers, which is characteristic of acute inflammation of the gastric mucosa due to direct irritation from ibuprofen.

**Why the Correct Answer is Right**
Ibuprofen, as a nonsteroidal anti-inflammatory drug (NSAID), inhibits cyclooxygenase (COX) enzymes, reducing protective prostaglandins in the gastric mucosa. This leads to decreased mucus and bicarbonate secretion and increased acid exposure, causing acute mucosal injury. The findings of scattered punctate hemorrhagic areas with edema and erosions, but no ulcers, are classic for **acute gastritis**—a reversible, inflammation-driven condition with transient mucosal damage. The absence of ulceration and the presence of focal, hemorrhagic erosions distinguish it from chronic or autoimmune forms.

**Why Each Wrong Option is Incorrect**
Option A: Active chronic gastritis involves long-standing inflammation, often with atrophy, intestinal metaplasia, and H. pylori infection—absent here.
Option C: Autoimmune gastritis is characterized by lymphocytic infiltration, parietal cell destruction, and pernicious anemia—no such features are present.
Option D: Chronic gastritis typically presents with gradual, persistent symptoms and histological signs of atrophy or metaplasia, not acute erosions.

**Clinical Pearl / High-Yield Fact**
NSAID-induced gastritis is a common cause of acute gastric mucosal injury; patients on long-term NSAID therapy should be monitored for GI bleeding. Early recognition and discontinuation of the offending agent can prevent progression to ulcers.

✓ Correct Answer: B. Acute gastritis