Definition_x0000_ A break in the lining of the lower part of the esophagus, the stomach, or the upper part of the small intestine. Peptic ulcers form when cells on the surface of the lining become inflamed and die.
The term peptic ulcer disease (PUD) refers to
both duodenal ulcer and gastric ulcer disease. ﻋﺒﺎرت از ﺿﺎﯾﻌﻪ ﻏﺸﺎی ﻣﺨﺎﻃﯽ اﺳﺖ اﮐﺜﺮا از اﺛﺮ اﻟﺘﻬﺎب ﺣﺎد ﺑﻪ وﺟﻮد ً در ﻣﻌﺪه وﯾﺎ اﺛﻨﺎ ﻋﺸﺮه _. ﻣﯿﮕﺮددFocal defect آﻣﺪه وﻣﻨﺠﺮ ﺑﻪ اﯾﺠﺎد Causes
1.Most common causes
a. Helicobacter pylori infection b. NSAIDs—inhibit prostaglandin production, which leads to impaired mucosal defenses c. Acid hypersecretory states, such as Zollinger– Ellison syndrome Other Causes.
a. Smoking—ulcers twice as likely in cigarette
smokers as in nonsmokers
b. Alcohol and coffee—may exacerbate
symptoms,but causal relationship as yet unproven
c. Other potential but unproven causes include
emotional stress, personality type (“type A”), and dietary factors. Clinical featurs. 1 Epigastric pain
a. Aching or gnawing in nature
b. Nocturnal symptoms and the effect of food on symptoms are variable
2. May be complicated by upper GI bleeding
3. Other symptoms: nausea/vomiting, early
satiety, and weight loss. Diagnosis 1.... Endoscopy A. Most accurate test in diagnosing ulcers.
B. Essential in diagnosis of gastric ulcers
because biopsy is necessary to rule out malignancy—duodenal ulcers do not require biopsy.
C. Preferred when severe or acute bleeding
is present (can perform electrocautery of bleeding ulcers).
D. Can obtain endoscopic biopsy for
diagnosis of H. pylori. Dx. contin..... • 2. Barium swallow
a. Sometimes used initially but is less reliable
than endoscopy.
b. Double-contrast techniques preferred due
to improved accuracy. Dx. contin....
3. Laboratory test—for diagnosis of H. pylori
infection
a. Biopsy: Histologic evaluation of endoscopic
biopsy is the gold standard.
b. Urease detection via urea breath test is the
most convenient test (sensitivity and specificity > 95%). It documents active infection and helps to assess the results of antibiotic therapy._ • c. Serology (lower specificity)—The presence of antibodies to H. pylori does not necessarily indicate current infection—Antibodies to H. pylori can remain ele vated for months or even years after eradication of infection (90% sensitive).
• The following may lead to false-negative test
results: proton pump inhibitors (PPIs), bismuth, many antibiotics and upper GI bleeding.
4. Serum gastrin measurement—if
considering Zollinger–Ellison syndrome as a diagnosis_ Note.
If a peptic ulcer is uncomplicated, a barium
study or endoscopy is not needed initially.
Initiate empiric therapy. However,
if you suspect any of the complications of PUD, order confirmatory studies._ Treatment 1. Medical—Majority of patients with PUD can be successfully treated by curing H. pylori infection, avoidance of NSAIDs, and appropriate use of antisecretory drugs.
A. Supportive (patient directive)
٠ Discontinue aspirin/NSAIDs. • Restrict alcohol use but do not restrict any foods. • Stop smoking, decrease emotional stress. • Avoid eating before bedtime (eating stimulates nocturnal gastric acid levels); decrease coffee intake (although no strong link has been established with ulcer disease). B. Acid suppression therapy • H2 receptor blockers—Cimetidine (Tagamet) and Ranitidine (Zantac). Block histamine–based parietal cell acid secretion. Accelerate healing of ulcers. • PPIs—omeprazole (Prilosec), lansoprazole (Prevacid), Block H+/K+ ATPase pump directly in parietal cell membrane. Most effective antisecretory agents (although expensive). • Antacids—somewhat outdated for primary therapy and more appropriately used for adjunctive therapy/symptomatic relief. Examples include alumi num hydroxide (Mylanta), calcium carbonate (Tums), Bismuth subsalicylate (Pepto-Bismol). C. Eradicate H. pylori with triple or quadruple therapy Once infec tion is cleared, the rate of recurrence is very low. • For initial therapy, triple therapy (PPI, amoxicillin and clarithromycin) for 10 days to 2 weeks. • For retreatment, quadruple therapy (PPI, bismuth, metronidazole, and tetra cycline). D. Cytoprotection • Sucralfate—facilitates ulcer healing, must be taken frequently, is costly, and can cause GI upset. • Misoprostol—reduces risk for ulcer formation associated with NSAID therapy, is costly, and can cause GI upset (common side effect). E.. Treatment regimens • If H. pylori test is positive, begin eradication therapy with either triple or qua druple therapy . Also begin acid suppression with antacids, an H2 blocker, or a PPI. • If the patient has an active NSAID-induced ulcer, stop NSAID use (may switch to acetaminophen). Also begin with either a PPI or misoprostol. Continue for 4 to 8 weeks, depending on severity. Treat the H. pylori infection as above if present. E........
• Antisecretory drugs can be discontinued after 4
to 6 weeks in patients with uncomplicated ulcers who are asymptomatic. Patients at increased risk of recurrence (especially if underlying cause of ulcer is not reversed) may ben efit from maintenance therapy.
• H. pylori-negative ulcers that are NOT caused
by NSAIDs can be treated with antisecretory drugs (either H2 blockers or PPI). 2. Surgical