Peptic Ulcer Disease

Buyucan, Cueto, Cunanan, Dadgardoust

Peptic Ulcer DiseaseUlcer

- break in the mucosal surface > 5 mm in size with a depth to the submucosa

Doudenal UlcerPUD

Gastric Ulcer

Peptic Ulcer Disease

Aggressive

Agents

Mucosal Defense

and Repair

Preepithelial

EpithelialSubepithel

ial

Hydrochloric Acid

Pepsinogen


Aggressive

Agents

Mucosal Defense

and Repair


Aggressive

Agents

Mucosal Defense

and Repair


Aggressive

Agents

Mucosal Defense

and Repair


Major Causes

H. Pylori InfectionNSAID Induced

Peptic Ulcer DiseaseComplications

GI BleedingPerforationGastric Outlet obstruction

Peptic Ulcer DiseaseIncreased Acid secretion and/ o rDecreased

Mucosal Defenses

Mucosal Injury/ Ulceration

GI Bleeding

Incidence and Epidemiology• Peptic ulcers are the most common source of

upper GI bleeding accounting up to ~50% of cases

• 2 most common causes of PUD: Helicobacter pylori infection and NSAID use.

• As the prevalence of H. pylori infection decreases and NSAID use increases, the relative contribution of each factor to the incidence of PUD will change.

References: Harrison’s Principles of Internal Medicine 17th editionWong, et al. Changing trends in peptic ulcer prevalence in a tertiary care setting in the Philippines: A seven-year study. Journal of Gastroenterology and Hepatology, Vol 20, Number 4, April 2005: 628-632(5)

Incidence and EpidemiologyDUODENAL ULCERS

6-15% of the Western populationIncidence declined steadily from 1960 to 1980

and has remained stable since then >50% over visits have decreased over the past 30 years

The declining global prevalence is due to declining prevalence of Helicobacter pylori infections

Eradication of H. pylori has greatly reduced the recurrence rates after initial therapy

GASTRIC ULCERSTend to occur later in life than duodenal

lesions, with peak incidence reported in the 6th decade

More than half of GUs occur in malesLess common than duodenal ulcers, perhaps

due to higher likelihood of Gus being silent and presenting only after a complication develops

Clinical Manisfestation

Abdominal pain Burning or gnawing

discomfort at epigatriumIll-defined, aching

sensation, hunger painOccurs 90mins – 3 hrs

after meal, empty stomach, early morning

Relieved by foods or antacids

Nausea, vomiting, weight lossEpigastric tenderness

Right of midline (20%)

Other posible manifestation GI bleeding

Bloody or dark tarry stoolsCoffee ground emesisChest painFatigue

PerforationSudden, severe, generalized abdominal painTender, boardlike abdomen

Barium StudiesStill commonly used as a first test for

documenting an ulcer80% sensitivity : single contrast barium study90% sensitivity: double contrast barium studySensitivity is low for small ulcers (<0.5 cm)Duodenal ulcers appear as a well demarcated

crater most often seen at the bulbGastric ulcers may either be benign or

malignant

Barium StudiesBenign gastric ulcer appears as a discrete

crater with radiating mucosal folds originating from the mucosal margin

Ulcers >3 cm are more often malignant

Radiographic studies that show a gastric ulcer must be followed by endoscopy and biopsy.

Fauci, et. al. Harrison’s Principles of Internal Medicine, 17 th ed.

EndoscopyMost sensitive and specific Direct visualization of the mucosaPhotographic documentation of the defectTissue biopsy to rule out malignancy or H.

pylori.Helpful in identifying lesions too small to

detect by radiographic examination, evaluation of atypical radiographic abnormalities, or to determine if an ulcer is a source of blood loss


Detection of H. pyloriNON-INVASIVE

Serology Detection of antibodies in the serum

Urea Breath Test Simple, rapid, early follow up

Stool antigen Sensitive, specific, and inexpensive


Detection of H. pyloriINVASIVE (Endoscopy/Biopsy required)

Rapid urease Simple, false negative with recent use of PPIs,

antibiotics, or bismuth compounds

Histology Provides histologic information

Culture Time-consuming, expensive


ObjectivesPain reliefHealingPrevention of complicationsPrevention of recurrences

AntacidsRarely used as a primary therapeutic agents

but are instead used for symptomatic reliefMixture of aluminum hydroxide and

magnesium hydroxideEg. Maalox, Mylanta


H2 Receptor AntagonistsInhibit basal and stimulated acid secretionOften used for treatment of active ulcers (4-6

weeks) in combination with an antibiotic directed at eradicating H. pylori.

Eg. Cimetidine, Ranitidine, Famotidine, Nizatidine


Proton Pump InhibitorsSubstituted benzimidazole derivatives that

covalently bind and irreversibly inhibit H+K+-ATPase

Eg. Omeprazole, Esomeprazole, Lansoprazole, Rabeprazole, Pantoprazole


Cytoprotective AgentsSucralfate

Insoluble in waterViscous paste within the stomach and duodenum,

binding primarily to sites of active ulceration

Bismuth-containing compoundsUlcer coating; prevention of further pepsin/HCl-

induced damage; binding of pepsin; and stimulation of PGs, bicarbonate, and mucous secretion

Prostaglandin AnaloguesEnhancement of mucosal defense and repairEg. Misoprostol


THERAPY FOR H. pyloriEradication of H. pylori is the primary goal

DRUG DOSETRIPLE THERAPY1. Bismuth subsalicylate plus

Metronidazole plus Tetracycline

2. Ranitidine bismuth citrate plus Tetracycline plus

Clarithromycin or Metronidazole

3. Omeprazole (lansoprazole) plus Clarithromycin plus

Metronidazole or Amoxicillin

2 tabs qid250 mg qid500 mg qid

400 mg bid500 mg bid500 mg bid

20 mg bid (30 mg bid)250 or 500 mg bid500 mg bid1 g bid

DRUG DOSEQUADRUPLE THERAPYOmeprazoleBismuth subsalicylateMetronidazoleTetracycline

20 mg (30 mg) daily2 tablets qid250 mg qid500 mg qid


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Peptic Ulcer Disease