Ana de Luca
Complications of peptic ulcers include perforation and bleeding.
Gastric and Duodenal Malignancies also tend to ulcerate, so one should biopsy ulcers
Pathology during endoscopy to rule out cancer.
Perforation: acute onset of abdominal pain and peritonitis. An
Gastritis upright radiograph may reveal free air under the diaphragm
(pneumoperitoneum).
Gastric in ammation and associated mucosal injury found on
Bleeding ulcer: if the ulcer overlies a vein or artery
biopsy. Causes of gastritis include Helicobacter pylori infection,
alcohol, NSAIDs, and autoimmune conditions. (gastroduodenal or gastric artery) → melena, or even high volume
bleeding.
PEPTIC ULCER DISEASE
Peptic ulcers are open sores that develop on the inside lining of
erosions of gastric mucosa associated with gnawing, aching, your stomach and the upper portion of your small intestine.
burning epigastric abdominal pain.
- Ulcers are most commonly caused by H. pylori infection or 2 types:
heavy NSAID use. 1. Gastric ulcers → on the inside of the stomach. Worsened by
- Physiologic stress can also contribute to ulcer formation. eating → weight loss. Relieved by antiacids.
- H. Pylori: patients with active H.pylori infection will 2. Duodenal ulcers → inside of the upper portion of the small
have positive stool antigen and urease breath test. intestine (duodenum). Before meals and at night, relieved by
eating.
The urease breath test involves a patient consuming radiolabeled
urea. In the presence of urease from H. pylori, the urea will be
broken down into CO2 and ammonia. The radiolabeled CO2 can
then be detected on exhalation. Endoscopy, however, remains
the gold standard.
- NSAIDs: cause ulcers by inhibiting the production of
protective prostaglandins. In general, NSAIDs inhibit
cyclooxygenase-1 (COX-1) and COX-2. Because
COX-1 is more responsible for the production of
protective prostaglandin E2 (PGE2) in the stomach,
selective COX-2 inhibitors such as celecoxib are
somewhat less likely to contribute to gastritis or ulcer
formation.
- Physiologic stress: ill (trauma, infection, surgery) may
develop gastric ulcers caused by inadequate tissue
If perforation occurs, it results in acute sudden onset abdominal
perfusion due to splanchnic vasoconstriction and/or
pain, peritonism and board like rigidity.
systemic hypotension.
May see free air under diaphragm (pneumoperitoneum) A with
referred pain to the shoulder.
Curling ulcers: stress associated with severe trauma/burns
caused by systemic hypovolemia, hypotension and
Today, elective surgery is uncommon due to the development of
hypoperfusion.
antisecretory drugs (proton pump inhibitors and histamine
Cushing ulcers: stress ulcers associated with brain lesions.
blockers0 and helicobacter pylori treatment.
Elevated intracranial pressure, from tumors or traumatic bleeding,
increases vagal stimulation of gastric parietal cells and H+
A ulcer is the mucosal break greater than 5mm in diameter that
secretion.
extends beyond the muscularis mucosa.
fl
Complications of peptic ulcers include perforation and bleeding.
Gastric and Duodenal Malignancies also tend to ulcerate, so one should biopsy ulcers
Pathology during endoscopy to rule out cancer.
Perforation: acute onset of abdominal pain and peritonitis. An
Gastritis upright radiograph may reveal free air under the diaphragm
(pneumoperitoneum).
Gastric in ammation and associated mucosal injury found on
Bleeding ulcer: if the ulcer overlies a vein or artery
biopsy. Causes of gastritis include Helicobacter pylori infection,
alcohol, NSAIDs, and autoimmune conditions. (gastroduodenal or gastric artery) → melena, or even high volume
bleeding.
PEPTIC ULCER DISEASE
Peptic ulcers are open sores that develop on the inside lining of
erosions of gastric mucosa associated with gnawing, aching, your stomach and the upper portion of your small intestine.
burning epigastric abdominal pain.
- Ulcers are most commonly caused by H. pylori infection or 2 types:
heavy NSAID use. 1. Gastric ulcers → on the inside of the stomach. Worsened by
- Physiologic stress can also contribute to ulcer formation. eating → weight loss. Relieved by antiacids.
- H. Pylori: patients with active H.pylori infection will 2. Duodenal ulcers → inside of the upper portion of the small
have positive stool antigen and urease breath test. intestine (duodenum). Before meals and at night, relieved by
eating.
The urease breath test involves a patient consuming radiolabeled
urea. In the presence of urease from H. pylori, the urea will be
broken down into CO2 and ammonia. The radiolabeled CO2 can
then be detected on exhalation. Endoscopy, however, remains
the gold standard.
- NSAIDs: cause ulcers by inhibiting the production of
protective prostaglandins. In general, NSAIDs inhibit
cyclooxygenase-1 (COX-1) and COX-2. Because
COX-1 is more responsible for the production of
protective prostaglandin E2 (PGE2) in the stomach,
selective COX-2 inhibitors such as celecoxib are
somewhat less likely to contribute to gastritis or ulcer
formation.
- Physiologic stress: ill (trauma, infection, surgery) may
develop gastric ulcers caused by inadequate tissue
If perforation occurs, it results in acute sudden onset abdominal
perfusion due to splanchnic vasoconstriction and/or
pain, peritonism and board like rigidity.
systemic hypotension.
May see free air under diaphragm (pneumoperitoneum) A with
referred pain to the shoulder.
Curling ulcers: stress associated with severe trauma/burns
caused by systemic hypovolemia, hypotension and
Today, elective surgery is uncommon due to the development of
hypoperfusion.
antisecretory drugs (proton pump inhibitors and histamine
Cushing ulcers: stress ulcers associated with brain lesions.
blockers0 and helicobacter pylori treatment.
Elevated intracranial pressure, from tumors or traumatic bleeding,
increases vagal stimulation of gastric parietal cells and H+
A ulcer is the mucosal break greater than 5mm in diameter that
secretion.
extends beyond the muscularis mucosa.
fl
