Acute peptic ulcer
Acute ulcers are often multiple and may be due to;
Shock especially burns - local ischaemia, increased histamine release increases gastric juice secretion
Drugs eg. aspirin, NSAIDS
Uraemia Acute ulcers usually heal rapidly
Chronic peptic ulcer
HP (helicobacter pylori), stimulates gastrin secretion and damages mucosa.
Psychological stress raises acid levels
Gastric - Men : women 2 : 1
DU, - Men : women 4 : 1
More in blood group O, (for DU)
More common in elderly
Alteration in mucus production
Intake of methylxanthines, eg tea coffee, cola, chocolate
DU are 10 times more common than gastric
Gastric juices contain hydrochloric acid and digestive enzymes.
Acidity of stomach (HCl) may be as low as pH 1
Peptic ulcers occur at sites where there are peptic juices
Up to 15% of individuals may have DU at some time in their life.
Ulceration extends through the lining mucosa into the muscle layer of the gut.
Craters up to 5 cm in diameter occur.
A sharply "punched out" edge with a smooth clean floor.
Often local thickening occurs due to fibrous tissue.
Fibrous tissue often contract causing folding of the gut wall.
Most gastric ulcers are singular and occur on the lesser curve of the stomach
Duodenogastric reflux, (bile damage to gastric mucosa)
Prostaglandins increase mucus production and vasodilate so are cytoprotective
Duodenum (most common) Meckel`s diverticulum, (ectopic gastric mucosa)
Jejunum (after anastomosis)
Signs and Symptoms
Exacerbations of several days or weeks
Remissions may last for months or years
Pain or tenderness in the epigastrium probably with Pointing sign
Pain is burning or gnawing
Usually worse at night
Occasional vomiting occurs in 40% of cases
Pain is relieved by vomiting and antacids
Anorexia and nausea
Dyspepsia (pain or upper abdominal discomfort)
Some ulcers are `silent` and present with complications
Haemorrhage - coffee grounds, melaena, haematemesis
Perforation - peritonitis
Stenosis, pyloric or gastric
Perforation of the pancreas
Deficiencies, haemorrhage and poor diet.
Gastroscopy (always exclude malignancy) Biopsy
Barium meal Blood profiling
Decreasing the amount of acid present
Giving alkali tablets
PPIs e.g. omperazole, lansoprazole
H2 receptor antagonists, e.g. ranitidine
No bed rest
No special diets
Indications for surgery are haemorrhage, perforation, gastric outflow obstruction, recurrence of ulcer following gastric surgery
H2-receptor antagonists Cimetidine, ranitidine
Inhibit action of histamine at H2 receptor sites on parietal cells
Reduce volume and acidity of gastric juice
Accelerates ulcer healing, reduces relapse rate
Proton pump inhibitors Esomeprazole, omeprazole
Inhibit gastric parietal cell H+/K+-ATPase
Work faster and heal ulcers faster than H2 blockers
Also improve symptoms and heal GORD
Cytoprotectants Sucralfate, bismuth
Helicobacter pylori infection
Confirm diagnosis with culture, 13C-urea breath test or antibodies.
Eradication can achieve rapid and long term healing of peptic ulcers.
Acid inhibition combined with antibiotics.
One week triple therapy, PPI, amoxicillin and either clarithromycin or metronidazole gives 90% eradication rates
Locality of pain
How pain is relieved, eating antacids, vomiting etc
Time of day of pain
Foods which increase symptoms
Type A personality
Intake of drugs or other gastric irritants
Vomit/ stool specimen
Level of patient anxiety about the condition
Patients understanding of the condition
Potential for the development of complications
Situation of significant others
Adequate balanced diet
Drug education to improve compliance
Alert to possible gastric irritants, eg aspirin
Observation for haemorrhage, anaemia
Chew food thoroughly, eat in a leisurely manner
Ovoid over large meals