Signs and symptoms
Signs and symptoms of a peptic ulcer can include one or more of the following:
· abdominal pain, classically epigastric strongly correlated to mealtimes. In case of duodenal ulcers the pain appears about three hours after taking a meal;
· bloating and abdominal fullness;
· water brash (rush of saliva after an episode of regurgitation to dilute the acid in esophagus - although this is more associated with gastroesophageal reflux disease);
· nausea, and copious vomiting;
· loss of appetite and weight loss;
· hematemesis (vomiting of blood); this can occur due to bleeding directly from a gastric ulcer, or from damage to the esophagus from severe/continuing vomiting.
· melena (tarry, foul-smelling feces due to presence of oxidized iron from hemoglobin);
· rarely, an ulcer can lead to a gastric or duodenal perforation, which leads to acute peritonitis, extreme, stabbing pain, and requires immediate surgery.
Complications
· Gastrointestinal bleeding is the most common complication. Sudden large bleeding can be life-threatening. It occurs when the ulcer erodes one of the blood vessels, such as the gastroduodenal artery.
· Perforation (a hole in the wall of the gastrointestinal tract) often leads to catastrophic consequences if left untreated. Erosion of the gastro-intestinal wall by the ulcer leads to spillage of stomach or intestinal content into the abdominal cavity. Perforation at the anterior surface of the stomach leads to acute peritonitis, initially chemical and later bacterial peritonitis. The first sign is often sudden intense abdominal pain; an example is Valentino's syndrome, named after the silent-film actor who experienced this pain before his death. Posterior wall perforation leads to bleeding due to the involvement of gastroduodenal artery that lies posterior to the first part of the duodenum.
· Penetration is a form of perforation in which the hole leads to and the ulcer continues into adjacent organs such as the liver and pancreas.
· Gastric outlet obstruction is a narrowing of the pyloric canal by scarring and swelling of the gastric antrum and duodenum due to peptic ulcers. The person often presents with severe vomiting without bile.
· Cancer is included in the differential diagnosis (elucidated by biopsy), Helicobacter pylori as the etiological factor making it 3 to 6 times more likely to develop stomach cancer from the ulcer.
Cause
H. pylori
A major causative factor (60% of gastric and up to 50–75% of duodenal ulcers) is chronic inflammation due to Helicobacter pylori that colonizes the antral mucosa. The immune system is unable to clear the infection, despite the appearance of antibodies. Thus, the bacterium can cause a chronic active gastritis (type B gastritis). Gastrin stimulates the production of
· Gastrointestinal bleeding is the most common complication. Sudden large bleeding can be life-threatening. It occurs when the ulcer erodes one of the blood vessels, such as the gastroduodenal artery.
· Perforation (a hole in the wall of the gastrointestinal tract) often leads to catastrophic consequences if left untreated. Erosion of the gastro-intestinal wall by the ulcer leads to spillage of stomach or intestinal content into the abdominal cavity. Perforation at the anterior surface of the stomach leads to acute peritonitis, initially chemical and later bacterial peritonitis. The first sign is often sudden intense abdominal pain; an example is Valentino's syndrome, named after the silent-film actor who experienced this pain before his death. Posterior wall perforation leads to bleeding due to the involvement of gastroduodenal artery that lies posterior to the first part of the duodenum.
· Penetration is a form of perforation in which the hole leads to and the ulcer continues into adjacent organs such as the liver and pancreas.
· Gastric outlet obstruction is a narrowing of the pyloric canal by scarring and swelling of the gastric antrum and duodenum due to peptic ulcers. The person often presents with severe vomiting without bile.
· Cancer is included in the differential diagnosis (elucidated by biopsy), Helicobacter pylori as the etiological factor making it 3 to 6 times more likely to develop stomach cancer from the ulcer.
Cause
H. pylori
A major causative factor (60% of gastric and up to 50–75% of duodenal ulcers) is chronic inflammation due to Helicobacter pylori that colonizes the antral mucosa. The immune system is unable to clear the infection, despite the appearance of antibodies. Thus, the bacterium can cause a chronic active gastritis (type B gastritis). Gastrin stimulates the production of
gastric acid by parietal cells. In H. pylori colonization responses to increased gastrin, the increase in acid can contribute to the erosion of the mucosa and therefore ulcer formation.
NSAIDs
Another major cause is the use of NSAIDs, such as ibuprofen and aspirin. The gastric mucosa protects itself from gastric acid with a layer of mucus, the secretion of which is stimulated by certain prostaglandins. NSAIDs block the function of cyclooxygenase 1 (cox-1), which is essential for the production of these prostaglandins. COX-2 selective anti-inflammatories (such as celecoxib or the since withdrawn rofecoxib) preferentially inhibit cox-2, which is less essential in the gastric mucosa, and roughly halve the risk of NSAID-related gastric ulceration.
Stress
Stress due to serious health problems such as those requiring treatment in an intensive care unit is well described as a cause of peptic ulcers, which are termed stress ulcers.
While chronic life stress was once believed to be the main cause of ulcers, this is no longer the case. It is, however, still occasionally believed to play a role. This may be by increasing the risk in those with other causes such as H. pylori or NSAID use.
Diet
Dietary factors such as spice consumption, were hypothesized to cause ulcers until late in the 20th century, but have been shown to be of relatively minor importance. Caffeine and coffee, also commonly thought to cause or exacerbate ulcers, appear to have little effect. Similarly, while studies have found that alcohol consumption increases risk when associated with H. pylori infection, it does not seem to independently increase risk. Even when coupled with H. pylori infection, the increase is modest in comparison to the primary risk factor.
Diagnosis
The diagnosis of Helicobacter pylori can be made by:
· Urea breath test (noninvasive and does not require EGD);
· Direct culture from an EGD biopsy specimen; this is difficult to do, and can be expensive. Most labs are not set up to perform H. pylori cultures;
· Direct detection of urease activity in a biopsy specimen by rapid urease test;
· Measurement of antibody levels in the blood (does not require EGD). It is still somewhat controversial whether a positive antibody without EGD is enough to warrant eradication therapy;
· Stool antigen test;
· Histological examination and staining of an EGD biopsy.
Classification
1. Esophagus 5.Mucosa
2. Stomach 6.Submucosa
3. Ulcers 7.Muscle
4. Duodenum
Another major cause is the use of NSAIDs, such as ibuprofen and aspirin. The gastric mucosa protects itself from gastric acid with a layer of mucus, the secretion of which is stimulated by certain prostaglandins. NSAIDs block the function of cyclooxygenase 1 (cox-1), which is essential for the production of these prostaglandins. COX-2 selective anti-inflammatories (such as celecoxib or the since withdrawn rofecoxib) preferentially inhibit cox-2, which is less essential in the gastric mucosa, and roughly halve the risk of NSAID-related gastric ulceration.
Stress
Stress due to serious health problems such as those requiring treatment in an intensive care unit is well described as a cause of peptic ulcers, which are termed stress ulcers.
While chronic life stress was once believed to be the main cause of ulcers, this is no longer the case. It is, however, still occasionally believed to play a role. This may be by increasing the risk in those with other causes such as H. pylori or NSAID use.
Diet
Dietary factors such as spice consumption, were hypothesized to cause ulcers until late in the 20th century, but have been shown to be of relatively minor importance. Caffeine and coffee, also commonly thought to cause or exacerbate ulcers, appear to have little effect. Similarly, while studies have found that alcohol consumption increases risk when associated with H. pylori infection, it does not seem to independently increase risk. Even when coupled with H. pylori infection, the increase is modest in comparison to the primary risk factor.
Diagnosis
The diagnosis of Helicobacter pylori can be made by:
· Urea breath test (noninvasive and does not require EGD);
· Direct culture from an EGD biopsy specimen; this is difficult to do, and can be expensive. Most labs are not set up to perform H. pylori cultures;
· Direct detection of urease activity in a biopsy specimen by rapid urease test;
· Measurement of antibody levels in the blood (does not require EGD). It is still somewhat controversial whether a positive antibody without EGD is enough to warrant eradication therapy;
· Stool antigen test;
· Histological examination and staining of an EGD biopsy.
Classification
1. Esophagus 5.Mucosa
2. Stomach 6.Submucosa
3. Ulcers 7.Muscle
4. Duodenum
By area
· Duodenum (called duodenal ulcer)
· Esophagus (called esophageal ulcer)
· Stomach (called gastric ulcer)
· Meckel's diverticulum (called Meckel's diverticulum ulcer; is very tender with palpation)
Modified Johnson
· Type I: Ulcer along the body of the stomach, most often along the lesser curve at incisura angularis along the locus minoris resistantiae. Not associated with acid hypersecretion.
· Type II: Ulcer in the body in combination with duodenal ulcers. Associated with acid oversecretion.
· Type III: In the pyloric channel within 3 cm of pylorus. Associated with acid oversecretion.
· Type IV: Proximal gastroesophageal ulcer
· Type V: Can occur throughout the stomach. Associated with the chronic use of NSAIDs (such as ibuprofen).
· Esophagus (called esophageal ulcer)
· Stomach (called gastric ulcer)
· Meckel's diverticulum (called Meckel's diverticulum ulcer; is very tender with palpation)
Modified Johnson
· Type I: Ulcer along the body of the stomach, most often along the lesser curve at incisura angularis along the locus minoris resistantiae. Not associated with acid hypersecretion.
· Type II: Ulcer in the body in combination with duodenal ulcers. Associated with acid oversecretion.
· Type III: In the pyloric channel within 3 cm of pylorus. Associated with acid oversecretion.
· Type IV: Proximal gastroesophageal ulcer
· Type V: Can occur throughout the stomach. Associated with the chronic use of NSAIDs (such as ibuprofen).
Macroscopic appearance
Gastric ulcers are most often localized on the lesser curvature of the stomach. The ulcer is a round to oval parietal defect ("hole"), 2 to 4 cm diameter, with a smooth base and perpendicular borders. These borders are not elevated or irregular in the acute form of peptic ulcer, regular but with elevated borders and inflammatory surrounding in the chronic form. In the ulcerative form of gastric cancer the borders are irregular. Surrounding mucosa may present radial folds, as a consequence of the parietal scarring.
Microscopic appearance
Micrograph showing erosive gastric ulcer. (H&E stain)
A gastric peptic ulcer is a mucosal defect which penetrates the muscularis mucosae and lamina propria, produced by acid-pepsin aggression. Ulcer margins are perpendicular and present chronic gastritis. During the active phase, the base of the ulcer shows 4 zones: inflammatory exudate, fibrinoid necrosis, granulation tissue and fibrous tissue. The fibrous base of the ulcer may contain vessels with thickened wall or with thrombosis.
Differential diagnosis
· Gastritis
· Stomach cancer
· Gastroesophageal reflux disease
· Pancreatitis
· Hepatic congestion
· Cholecystitis
· Biliary colic
· Inferior myocardial infarction
· Referred pain (pleurisy, pericarditis)
· Superior mesenteric artery syndrome
Treatment
Younger patients with ulcer-like symptoms are often treated with antacids or H2 antagonists before endoscopy is undertaken.
People who are taking nonsteroidal anti-inflammatories (NSAIDs) may also be prescribed a prostaglandin analogue (misoprostol) in order to help prevent peptic ulcers.
Acid reducing medication
H2 antagonists or proton-pump inhibitors decrease the amount of acid in the stomach, helping with healing of ulcers.
H. pylori
When H. pylori infection is present, the most effective treatments are combinations of 2 antibiotics (e.g. clarithromycin, amoxicillin, tetracycline, metronidazole) and a proton-pump inhibitor (PPI), sometimes together with a bismuth compound. In complicated, treatment-resistant cases, 3 antibiotics (e.g. amoxicillin + clarithromycin + metronidazole) may be used together with a PPI and sometimes with bismuth compound. An effective first-line therapy for uncomplicated cases would be amoxicillin + metronidazole + pantoprazole (a PPI).
Surgery
Perforated peptic ulcer is a surgical emergency and requires surgical repair of the perforation. Most bleeding ulcers require endoscopy urgently to stop bleeding with cautery, injection, or clipping.
No comments:
Post a Comment