21.2 : 소화성 궤양 질환의 병태생리: 점막 방어 요인

Peptic ulcer disease, or PUD, involves discontinuous gastrointestinal tract lining due to gastric acid or pepsin secretion.

The mucus-bicarbonate barrier is crucial in defending against gastric acid's corrosive effects in the stomach. The mucus layer prevents direct acid contact, while bicarbonate secretion neutralizes stomach acid, maintaining a protective pH.

Various factors can weaken this barrier and increase gastric acidity, injuring the stomach lining and contributing to PUD.

Helicobacter pylori infection impairs somatostatin production, increasing acid secretion, and reducing bicarbonate levels, further weakening the defense barrier.

Prostaglandins stimulate bicarbonate secretion, reduce gastric acid production, and protect the gastric mucosa.

Nonsteroidal anti-inflammatory drugs or NSAIDs inhibit prostaglandins, reducing gastric mucus and mucosal blood flow, raising PUD risk.

Disturbances like duodenogastric reflux and atrophic gastritis can also lead to chronic PUD.

In summary, PUD's pathophysiology involves an imbalance between mucosal defense and aggressive factors.