Peptic Ulcer Disease (PUD) is characterized by the development of ulcers in the stomach or duodenal mucosa. Its pathophysiology is complex, involving a balance between damaging and protective elements.
Damaging agents such as Helicobacter pylori, gastric acid, pepsin, and nonsteroidal anti-inflammatory drugs (NSAIDs) can weaken the mucosal defense, allowing hydrogen ions to infiltrate back and harm epithelial cells.
On the protective side:
The interplay of these factors either heightens acid-pepsin levels or weakens the mucosal barrier's resistance. Damaged mucosa struggles to produce sufficient mucus as a defense, leading to inflammation, harm, and mucosal erosion.
A peptic ulcer implies a sore in the stomach or duodenal mucosa associated with the following pathophysiology:
The gastric and duodenal mucosa have a superficial gel layer that functions as a barrier, preventing the penetration of gastric juices like hydrochloric acid and pepsin.
Typically, a balance exists between gastric juice secretion and mucosal defenses.
An imbalance between aggressive factors and mucosal defenses can lead to mucosal injury and ulcers.
Aggressive factors such as NSAIDs, alcohol, H pylori, and gastric juices can compromise the mucosal defense, allow the back diffusion of hydrogen ions, and injure epithelial cells.
Mucosal defensive mechanisms include tight intercellular junctions, the generation of mucus, bicarbonate, prostaglandins, mucosal blood flow, cellular restitution, and epithelial renewal.
Disruptions in these mechanisms may increase the concentration or activity of acid-pepsin or decrease the resistance of the protective mucosal barrier.
A compromised mucosa secretes less mucus, lowering resistance to aggressive factors. This leads to inflammation, injury, and erosion of the mucosa.
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