Pathophysiology
- Excessive Acid Production: PUD involves an overproduction of gastric acid, which is normally secreted for digestion but can lead to mucosal damage if in excess.
- Disruption of Mucosal Barrier: Factors like Helicobacter pylori infection, NSAID use, and certain stress-related conditions compromise the protective mechanisms of the gastric and duodenal mucosa.
- Helicobacter pylori Infection: H. pylori is a bacterium that colonizes the stomach lining, leading to inflammation and weakening of the mucosal barrier. It also stimulates increased acid production.
- NSAID-Induced Injury: Nonsteroidal anti-inflammatory drugs (NSAIDs) inhibit prostaglandin synthesis, reducing the protective effects on the gastric mucosa. This makes it more susceptible to damage from gastric acid and pepsin.
- Impaired Blood Flow: Conditions that reduce blood flow to the gastric mucosa, such as severe illness or systemic conditions, can lead to ischemic ulcers due to inadequate oxygen and nutrient delivery.
- Genetic Predisposition: Some individuals may be genetically predisposed to PUD, potentially due to variations in mucosal defense mechanisms or response to acid exposure.
- Psychological Stress: While not a direct cause, stress and certain behaviors like smoking or excessive alcohol consumption can exacerbate existing ulcers and hinder the healing process.
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