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Peptic Ulcer – Definition, Incidence, Related anatomy physiology, Etiology

DEFINITION

A peptic ulcer is a sore on the lining of the stomach or duodenum, the beginning of the small intestine. Less commonly, a peptic ulcer may develop just above the stomach in the esophagus, the tube that connects the mouth to the stomach.

A peptic ulcer in the stomach is called a gastric ulcer. One that occurs in the duodenum is called a duodenal ulcer. People can have both gastric and duodenal ulcers at the same time. They also can develop peptic ulcers more than once in their lifetime.

Peptic Ulcer

INCIDENCE

Occurrence of peptic ulcer-  4 million individuals (newcases and recurrences) affected per year. Lifetime prevalence of PUD is 12% in men and 10% in women. Moreover, an estimated 15,000 deaths per year occur as a consequence of complicated PUD.

RELATED ANATOMY

The gastric epithelial lining consists of rugae that contain microscopic gastric pits, each branching into four or five gastric glands made up of highly specialized epithelial cells. Glands within the gastric cardia comprise 5% of the gastric gland area and contain mucous and endocrine cells. The majority of gastric glands (75%) are found within the oxyntic mucosa.

Gastroduodenal Mucosal Defense

The gastric epithelium is under a constant assault by a series of endogenous noxious factors including HCl, pepsinogen/pepsin, and bile salts. In addition, a steady flow of exogenous substances such as medications, alcohol, and bacteria encounter the gastric mucosa. The mucosal defense system can be envisioned as a three-level barrier, composed of preepithelial, epithelial and subepithelial elements.

Preepithelial

  • Mucus
  • Bicarbonate
  • Surface active phospholipids

Epithelial

  • Cellular resistance
  • Restitution
  • Growth factors, Prostaglandins
  • Cell proliferation

Subepithelial

  • Blood flow
  • Leukocyte

PHYSIOLOGY OF GASTRIC SECRETION

  • Hydrochloric acid and pepsinogen are the two principal gastric secretory products capable of inducing mucosal injury.
  • Basal acid production occurs in a circadian pattern, with highest levels occurring during the night and lowest levels during the morning hours.
  • Stimulated gastric acid secretion occurs primarily in three phases based on the site where the signal originates (cephalic, gastric, and intestinal).
  • Sight, smell, and taste of food are the components of the cephalic phase, which stimulates gastric secretion via the vagus nerve.
  • The gastric phase is activated once food enters the stomach. This component of secretion is driven by nutrients (amino acids and amines) that directly stimulate the G cell to release gastrin, which in turn activates the parietal cell via direct and indirect mechanisms.
  • Distention of the stomach wall also leads to gastrin release and acid production. The last phase of gastric acid secretion is initiated as food enters the intestine and is mediated by luminal distention and nutrient assimilation.
  • Additional neural (central and peripheral) and hormonal (secretin, cholecystokinin) factors play a role in counterbalancing acid secretion. Under physiologic circumstances, these phases are occurring simultaneously.

ETIOLOGY

  • Family tendency
  • Age (between 40 to 60 years)
  • Gender (more in men and menopausal women)
  • Stress
  • Anxiety
  • Infection with gram negative bacteria H.pylori
  • Use of NSAIDs
  • Eating spicy food
  • Smoking and drinking alcohol
  • Blood group O+ve
  • Patients with COPD or CRF
  • Excessive production of hormone gastrin

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