Gastroduodenal ulcer disease

A disease characterized by the presence of one or more ulcers in the wall of the stomach or duodenum.


 * ulcer (ulcus) – a mucosal defect, reaching deeper into the submucosa,
 * erosion – mucosal defect limited to the mucosa (does not penetrate through the muscularis interna into the submucosa).

Location of ulcers



 * Type I – small curvature mediogastrically,
 * Type II – combined chronic duodenal and gastric ulcer,
 * Type III – prepyloric ulcer up to a distance of 2 cm from the pylori,
 * Type IV – ulcer high on a small curvature near the GE junction.


 * duodenal ulcer – 95 % in the bulb of the duodenum on the anterior and/or posterior wall (kissing ulcer),
 * multiple duodenal ulcers – especially in Zollinger-Ellison syndrome,
 * ulcers on a large curvature – suspected malignancy.

Note: Duodenal ulcers are four times more common (80 %) than gastric ulcers, they also bleed more often.

Etiology



 * 1) the main etiological agent is Helicobater pylori,
 * 2) abusus NSAID,
 * 3) imbalance between protective and aggressive factors acting on the mucosa:

Protective factors

 * Mucus and bicarbonates (from saliva, food - the best neutralizer),
 * prostaglandins,
 * mucosal regenerative capacity,
 * good mucosal perfusion.

Aggressive factors

 * HCl,
 * pepsin,
 * Helicobater pylori (colonizes only the gastric mucosa, gastric metaplastic mucosa in the duodenum),
 * ischemia of the wall,
 * bile acids (duodenogastric reflux),
 * drugs (NSAID – ASA, Glucocorticoids, Cytostatics),
 * hyperparathyroidism hypercalcaemia stimulates gastrin secretion),
 * smoking alcohol coffee spice,
 * psychosomatic diseases.

Note: HP infection is the main cause of the gastric ulcer and HCl in duodenal hypersecretion.

Special types of ulcers

 * Cushing's ulcer – for trauma or CNS surgery (vagus irritation - HCl hypersecretion),
 * Curling's ulcer – for burns (hyperhistamina - hypersecretion HCl),
 * Zollinger-Ellison syndrome - ↑ gastrin production (stimulates HCl secretion) in pancreatic gastrinoma,
 * Stress ulcer – a disorder of mucosal perfusion.

Dividing ulcers

 * acute – funnel-shaped defect with sharp edges, often multiple, with a black base (digested blood),
 * chronic – round defect with bulging edges, light base (cleaned with enzymes and HCl, red-pink - granulation tissue, white - connective tissue), it is solitary, algae of the surrounding mucosa converge radially to it..

Clinical manifestations

 * 1) Gastric ulcer,
 * 2) *pain (visceral) in the epigastrium after a meal (Antacids do not usually bring relief),
 * 3) *anorexia, feeling full, heartburn, occasional vomiting with bile - the sick prefer to starve for fear,
 * 4) *affects older individuals,
 * 5) Duodenal ulcer,
 * 6) *epigastric pain on an empty stomach (often wakes the patient at night - nocturnal hunger pains),
 * 7) *food and antacids bring relief,
 * 8) *typical seasonal occurrence with exacerbation in spring and autumn (duration 1-2 weeks),
 * 9) *affects younger individuals.



Diagnostics

 * 1) anamnesis (pain, Nausea, vomiting, heartburn , loss of appetite, weight loss, foetor ex ore + physical examination (palpable pain in the epigastrium),
 * 2) imaging methods,
 * 3) *endoscopy – endoscopy - in uncomplicated ulcer (incl. biopsy, pH of the gastric mucosa and evidence of HP), bleeding,
 * 4) *'Native X-ray - evidence of pneumoperitoneum during perforation,
 * 5) *'Contrasting X-ray - in case of stenosis, event. during perforation (KL flow into the peritoneal cavity),
 * 6) biochemical examinations,
 * 7) *''Helicobacter pylori' identification:
 * 8) **invasive - rapid urease test, biopsy (microscopy, culture, PCR),
 * 9) **non-invasive - breath test with labeled urea, antibodies against HP in serum and urine, eventually saliva PCR, fecal HP antigens.

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