peptic_ulcer
peptic ulcer disease (PUD)
introduction
Peptic ulcers are defects in the gastric or duodenal mucosa that extend through the muscularis mucosa.
Western society has a 10% lifetime prevalence of developing PUD.
Under normal conditions, a physiologic balance exists between peptic acid secretion and gastroduodenal mucosal defense. Mucosal injury and, thus, peptic ulcer occur when the balance between the aggressive factors and the defensive mechanisms is disrupted.
Aggressive factors allowing back diffusion of hydrogen ions and subsequent epithelial cell injury and include NSAIDs, H pylori, alcohol, bile salts, acid, and pepsin.
The defensive mechanisms include tight intercellular junctions, mucus, mucosal blood flow, cellular restitution, and epithelial renewal.
aetiology:
types of ulcers
idiopathic ulcers:
90% of DU's & 2/3rds of GU's are due to interplay between mucosal damage by Helicobacter pylori and luminal acid
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Other less common causes are hypersecretory states, such as:
stress ulcers:
complications of peptic ulcer
bleeding
penetration
Ulcer penetration refers to penetration of the ulcer through the bowel wall without free perforation and leakage of luminal contents into the peritoneal cavity.
Surgical series suggest that penetration occurs in 20 percent of ulcers, but only a small proportion of penetrating ulcers become clinically evident.
Penetration occurs in descending order of frequency into the pancreas, gastrohepatic omentum, biliary tract, liver, greater omentum, mesocolon, colon, and vascular structures.
The change in symptom pattern may be gradual or sudden; it usually involves a loss of cyclicity of the pain with meals, and loss of food and antacid relief. The pain typically becomes more intense, of longer duration, and is frequently referred to the lower thoracic or upper lumbar region.
serum amylase may be raised mildy but clinical
pancreatitis is uncommon
may cause uncommon complications such as:
erosion into vascular structures leading to exsanguinating hemorrhage (aortoenteric fistula)
perivisceral abscess
erosion into the cystic artery
Rare biliary tract complications include erosion into the biliary tree with choledochoduodenal fistula, extra hepatic obstruction, or hematobilia.
perforation
Duodenal, antral, and gastric body ulcers account for 60, 20 and 20 percent of perforations due to peptic ulcer, respectively.
One-third to one-half of perforated ulcers are associated with NSAID use; these usually occur in elderly patients
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gastric outlet obstruction
management of peptic ulceration:
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For all complicated ulcers, large gastric ulcers, ulcers occurring in high-risk patients or ulcers associated with NSAID use, ongoing antisecretory therapy with a proton pump inhibitor (PPI) for about 8 weeks is appropriate. This maximises the likelihood of ulcer healing, particularly in patients destined to remain infected after eradication therapy.
duodenal ulcer:
gastric ulcer:
idiopathic ulcers:
as for DU but:
PPI bd dosing not once daily
acute therapy should be 2-4weeks longer than for DU, depending on ulcer size
exclude NSAID aetiology as cause before embarking on Helicobacter eradication therapy
NSAID-induced ulcers:
stress ulcers:
prophylaxis:=
ranitidine 50mg slow IV or 2hr infusion 6-8h, or,
famotidine 20mg IV over 30min 12h, or,
sucralfate 1g (crushed tablets, or suspension) via NGT every 6h
bleeding ulcers:
perforated ulcer
penetrating ulcer
Other references
peptic_ulcer.txt · Last modified: 2013/06/05 15:31 (external edit)