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petic ulcer/ulcer, etiology, risk factor, ulcer symptoms, pthophysiology, diagnosis, treatment

Peptic ulcer/stomach ulcer/ulcer
Etiology of ulcer, risk factor for ulcer
Can you get ulcer from stress
How to know if you have stomach ulcer/ulcer symptoms
Pathophysiology of ulcer
How to diagnose an ulcer
Treatment for ulcer


peptic ulcer

Peptic ulcer disease (PUD) refers to a group of ulcerative disorders of the upper gastrointestinal(GI) tract that require acid and pepsin for their formation.


peptic ulcer



Etiology of ulcer


common cause 

Helicobacter pylori infectionNSAIDs, Critical illness (stress-related mucosal damage).

uncommon cause 

Idiopathic (non–H. pylori, non-NSAID peptic ulcer)
Hypersecretion of gastric acid (eg, Zollinger-Ellison syndrome)
Viral infections (eg, cytomegalovirus)
Vascular insufficiency (eg, crack cocaine associated)
Radiation therapy
Chemotherapy (eg, hepatic artery infusions)
Infiltrating disease (eg, Crohn disease)
Diseases and medical conditions associated with chronic peptic ulcer:
Cirrhosis
Chronic renal failure
Chronic obstructive pulmonary disease
Cardiovascular disease
Organ transplantation
NSAIDs(nonsteroidal anti-inflammatory drugs)

Can you get ulcer from stress

The importance of psychological factors in the pathogenesis of PUD remains controversial.1 Clinical observation suggests that ulcer patients are adversely affected by stressful life events. However, results from controlled trials are conflicting and have failed to document a cause-and-effect relationship. Emotional stress may induce behavioral risks such as smoking and the use of NSAIDs or alter the inflammatory response or resistance to H. pylori infection. The role of stress and how it affects PUD(peptic ulcer disease) is complex and probably multifactorial.

How to know if you have stomach ulcer/ulcer symptoms

Abdominal pain is the most frequent PUD symptom. Pain is often epigastric and described as burning but can present as vague discomfort, abdominal fullness, or cramping. Nocturnal pain may awaken patients from sleep, especially between 12 am and 3 am.

Pain from duodenal ulcers often occurs 1 to 3 hours after meals and is usually relieved by food, whereas food may precipitate or accentuate ulcer pain in gastric ulcers. Antacids provide rapid pain relief in most ulcer patients.

Heartburn, belching, and bloating often accompany pain. Nausea, vomiting, and anorexia are more common in gastric than duodenal ulcers.

Severity of symptoms varies among patients and may be seasonal, occurring more frequently in spring or fall.

Presence or absence of epigastric pain does not define an ulcer. Ulcer healing does not necessarily render the patient asymptomatic. Conversely, absence of pain does not preclude an ulcer diagnosis, especially in the elderly who may present with a “silent” ulcer complication.

Ulcer complications include upper GI bleeding, perforation into the peritoneal cavity, penetration into an adjacent structure (eg, pancreas, biliary tract, or liver), and gastric.

Pathophysiology

Pathogenesis of duodenal and gastric ulcers involves pathophysiologic abnormalities and environmental and genetic factors:

Most peptic ulcers occur in presence of acid and pepsin when Helicobacter pylori(HP), nonsteroidal anti-inflammatory drugs (NSAIDs), or other factors disrupt normal mucosal defense and healing mechanisms. Increased gastric acid secretion may occur with duodenal ulcers, but patients with gastric ulcers usually have normal or reduced rates of acid secretion.
damaged gastric mucosa
Damaged gastric mucosa by H.pylori
Normal mucosal defense and repair mechanisms include mucus and bicarbonate secretion, intrinsic epithelial cell defense, and mucosal blood flow. Maintenance of mucosal integrity and repair is mediated by endogenous prostaglandin production.

HP(helicobacter pylori) infection causes gastric mucosal inflammation in all infected individuals, but only a minority develop an ulcer or gastric cancer. Mucosal injury is produced by elaborating bacterial enzymes (urease, lipases, and proteases), adherence, and HP virulence factors. HP induces gastric inflammation by altering the host inflammatory response and damaging epithelial cells.

Nonselective NSAIDs (including aspirin) cause gastric mucosal damage by two mechanisms:
 (1) a direct or topical irritation of the gastric epithelium, and (2) systemic inhibition of endogenous mucosal prostaglandin synthesis.

Use of corticosteroids alone does not increase risk of ulcer or complications, but ulcer risk is doubled in corticosteroid users taking NSAIDs concurrently.

Epidemiologic evidence links cigarette smoking to PUD, impaired ulcer healing, and ulcer-related GI complications. Risk is proportional to amount smoked per day.

Although clinical observation suggests that ulcer patients are adversely affected by stressful life events, controlled studies have not documented a cause-and-effect relationship.

Coffee, tea, cola beverages, beer, milk, and spices may cause dyspepsia but do not increase PUD risk. Ethanol ingestion in high concentrations is associated with acute gastric mucosal damage and upper GI bleeding but is not clearly the cause of ulcers.

How to diagnose an ulcer

Physical examination may reveal epigastric tenderness between the umbilicus and the xiphoid process that less commonly radiates to the back.

Routine laboratory tests are not helpful in establishing a diagnosis of PUD. Hematocrit, hemoglobin, and stool guaiac tests are used to detect bleeding.

Diagnosis of HP infection can be made using endoscopic or nonendoscopic (urea breath test [UBT], serologic antibody detection, and stool antigen) tests. Testing for HP is recommended only if eradication therapy is planned. If endoscopy is not planned, serologic antibody testing is reasonable to determine HP status. The UBT is the preferred nonendoscopic method to verify HP eradication but must be delayed at least 4 weeks after completion of treatment to avoid confusing bacterial suppression with eradication.

Diagnosis of PUD depends on visualizing the ulcer crater either by upper GI radiography or endoscopy. Endoscopy has largely replaced radiography because it provides a more accurate diagnosis and permits direct visualization of the ulcer.

Treatment for ulcer

Non pharmaclogical treatment

Patients with peptic ulcer disease should eliminate or reduce psychological stress, cigarette smoking, and use of NSAIDs (including aspirin). If possible, alternative agents such as acetaminophen or a nonacetylated salicylate (eg, salsalate) should be used for pain relief.

Although there is no need for a special diet, patients should avoid foods and beverages that cause dyspepsia or exacerbate ulcer symptoms (eg, spicy foods, caffeine, and alcohol).

Elective surgery is rarely performed because of highly effective medical management. Emergency surgery may be required for bleeding, perforation, or obstruction.

Pharmacological treatment

First-line therapy to eradicate HP infection is usually initiated with a proton pump inhibitor (PPI)–based, three-drug regimen for 10 to 14 days. If a second treatment course is required, the regimen should contain different antibiotics, or a four-drug regimen with a bismuth salt, metronidazole, tetracycline, and a PPI should be used. Bismuth-based quadruple therapy is recommended as an alternative for patients allergic to penicillin. All medications except the PPI should be taken with meals and at bedtime.
Treatment guidelines for peptic ulcer
Treatment guidelines for peptic ulcer
In sequential therapy, the antibiotics are administered in a sequence rather than all together. The rationale is to treat initially with antibiotics that rarely promote resistance (eg, amoxicillin) to reduce bacterial load and preexisting resistant organisms and then to follow with different antibiotics (eg, clarithromycin and metronidazole) to kill the remaining organisms. The potential advantage of superior eradication rates requires confirmation in the United States before this regimen can be recommended as first-line therapy 

If initial treatment fails to eradicate H.pylori, second-line (salvage) treatment should:(1) use antibiotics that were not included in the initial regimen, (2) use antibiotics that are not associated with resistance, (3) use a drug that has a topical effect (eg, bismuth), and (4) extend the treatment duration to 14 days. A 14-day course of the PPI-based quadruple regimen is the most commonly used second-line therapy after failure of a PPI–amoxicillin–clarithromycin regimen.

Patients with NSAID-induced ulcers should be tested to determine H.pylori status. If H.pylori positive, start treatment with a PPI-based three-drug regimen. If HP negative, discontinue the NSAID and treat with either a PPI, H2RA, or sucralfate.

If the NSAID must be continued despite ulceration, initiate treatment with a PPI (if HP negative) or a PPI-based three-drug regimen (if HP positive). Cotherapy with a PPI or misoprostol or switching to a selective cyclooxygenase-2 (COX-2) inhibitor is recommended for patients at risk of developing an ulcer-related complication

Limit maintenance therapy with a PPI or H2 receptor antagonist to high-risk patients with ulcer complications, patients who fail HP eradication, and those with HP-negative ulcers.

Patients with ulcers refractory to treatment should undergo upper endoscopy to confirm a nonhealing ulcer, exclude malignancy, and assess HP status. HP-positive patients should receive eradication therapy. In HP-negative patients, higher PPI doses (eg, omeprazole 40 mg/day) heal the majority of ulcers. Continuous PPI treatment is often necessary to maintain healing. Patients with refractory gastric ulcer may require surgery because of the possibility of malignancy.
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