B1 git med1 peptic ulcer disease

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PEPTIC ULCER DISEASE Dr. HUSSEIN SAAD Assistant Professor and Consultant, MRCP(UK) FAMILY and COMMUNITY MEDICINE College of Medicine King Saud University 26/09/2016

Transcript of B1 git med1 peptic ulcer disease

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PEPTIC ULCER DISEASE

Dr. HUSSEIN SAAD Assistant Professor and Consultant, MRCP(UK)

FAMILY and COMMUNITY MEDICINE College of Medicine

King Saud University26/09/2016

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• Aetiology• Presentation• Approash: Diagnosis H pylori Management

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Case• A 36-year-old man, smoker, presents with 2 months H/O epigastric pain mainly post meals. He sometimes awake by night because of burning pain to which he used to drink milk to relieve the pain.

• No vomiting• He has no H/o any chronic illnesses• No H/o of drugs

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Peptic ulcer Refers to erosion of the mucosa lining any portion of the G.I. tract.

It is defined as: A circumscribed ulceration of the gastrointestinal

mucosa occurring in areas exposed to acid and pepsin and most often

caused by Helicobacter pylori infection. (Uphold & Graham, 2003)

Gastric ulcer : the ulcer that occurs in the stomach lining ,some of them

may be malignant

Duodenal ulcer : most often seen in first portion of duodenum (>95%)

Peptic Ulcer Disease (PUD)Definition

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Peptic ulcer disease

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Peptic Ulcer DiseasePathogenesis :

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Aetiology

•H pylori infection•Drugs like NSAIDs, Aspirin or Corticosteroids

•Smoking•Stress like trauma, surgery•Excess gastrin secretion

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ETIOLOGIC FACTORS OF PUD

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Presentation• Gastric and duodenal ulcers usually cannot be

differentiated based on history alone.

• Epigastric pain is the most common symptom.

• It is characterized by a burning sensation and occurs after meals—classically, shortly after meals with gastric ulcer and 2-3 hours afterward with duodenal ulcer.

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Presentation• Food or antacids relieve the pain of duodenal ulcers

but provide minimal relief of gastric ulcer pain.

• Duodenal ulcer pain often awakens the patient at night.

• About 50-80% of patients with duodenal ulcers experience nightly pain, as opposed to only 30-40% of patients with gastric ulcers and 20-40% of patients with nonulcer dyspepsia (NUD).

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Case• A 36-year-old man, smoker, presents with 2 months H/O epigastric pain mainly post meals. He sometimes awake by night because of burning pain to which he used to drink milk to relieve the pain.

• No vomiting• He has no H/o any chronic illnesses• No H/o of drugs

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Presentation• Pain with radiation to the back is suggestive of a

posterior penetrating gastric ulcer complicated by pancreatitis.

• Patients who develop gastric outlet obstruction as a result of a chronic, untreated duodenal ulcer usually report a history of fullness and bloating associated with nausea and emesis that occurs several hours after food intake.

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PresentationOther possible manifestations include the following:Dyspepsia, including belching, bloating, distention, and

fatty food intoleranceHeartburnChest discomfortHematemesis or melena resulting from gastrointestinal

bleeding. Melena may be intermittent over several days or multiple episodes in a single day.

Symptoms consistent with IDA (eg, fatigue, dyspnea). NSAID-induced gastritis or ulcers may be silent, especially in elderly patients.

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Alarm FeaturesWarrant prompt gastroenterology referral: 

• Bleeding or anemia• Early satiety• Unexplained weight loss• Progressive dysphagia or odynophagia• Recurrent vomiting• Family history of GI cancer

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Serum Gastrin Level

• A fasting serum gastrin level should be obtained in certain cases to screen for Zollinger-Ellison syndrome.

• Patients with multiple ulcers• Strong family history of PUD• Peptic ulcer associated with diarrhea, steatorrhea, or weight

loss• Peptic ulcer not associated with H pylori infection or NSAID

use• Peptic ulcer associated with hypercalcemia or renal stones• Ulcer refractory to medical therapy• Ulcer recurring after surgery

•  

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Differential Diagnoses

• Acute Cholangitis• Acute Coronary Syndrome• Acute Gastritis• Cholecystitis and Biliary Colic • Chronic Gastritis• Diverticulitis• Esophagitis• Gallstones (Cholelithiasis)• Gastroesophageal Reflux Disease• Inflammatory Bowel Disease• Viral Hepatitis

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Types of Ulcer• Benign ulcers tend to have a smooth, regular, rounded

edge with a flat smooth base and surrounding mucosa that shows radiating folds.

• Malignant ulcers usually have irregular heaped-up or overhanging margins. The ulcerated mass often protrudes into the lumen, and the folds surrounding the ulcer crater are often nodular and irregular.

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Benign Ulcers

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Malignant Ulcer

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Helicobacter pylori Gram negative, Spiral bacilli Spirochetes Do not invade cells – only mucous Breakdown urea - ammonia Break down mucosal defense Chronic Superficial inflammation

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H pylori Testing

• Testing for H pylori infection is essential in all patients with peptic ulcers.

No acid

No ulcerOLD TESTAMENT

No HP No ulcer

NEW TESTAMENT

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Rapid Urease TestsAre considered the endoscopic diagnostic test of choice.

The presence of H pylori in gastric mucosal biopsy specimens is detected by testing for the bacterial product urease.

The kit contains a combination of a urea substrate and a pH sensitive indicator. One or more gastric biopsy specimens are placed in the rapid urease test kit. If H pylori is present, bacterial urease converts urea to ammonia, which changes the pH, resulting in a color change.

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Urease Test

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Histopathology

• Often considered the criterion standard to establish a diagnosis of H pylori infection , if the rapid urease test result is negative and a high suspicion for H pylori persists (presence of a duodenal ulcer).

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Urea Breath Tests (13C and14C)• Detect active H pylori infection by testing for the

enzymatic activity of bacterial urease.• In the presence of urease produced by H pylori, labeled

carbon dioxide (heavy isotope, carbon-13, or radioactive isotope, carbon-14) is produced in the stomach, absorbed into the bloodstream, diffused into the lungs, and exhaled.

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Fecal Antigen Testing• Identifies active H pylori infection by detecting the

presence of H pylori antigens in stools.

• This test is more accurate than antibody testing and is less expensive than urea breath tests.

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Antibodies

• (Immunoglobulin G [IgG]) to H pylori can be measured in serum, plasma, or whole blood.

• Not effective in follow up after eradication.

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Approach Considerations

Treatment of peptic ulcers varies depending on:• The etiology and clinical presentation. • Stable patient with dyspepsia • An unstable patient with Alarm Features

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Treatment Options• Empiric anti-secretory therapy, • Empiric triple therapy for H pylori infection, • Endoscopy followed by appropriate therapy based on

findings, • H pylori serology followed by triple therapy for patients

who are infected. • Breath testing for active H pylori infection may be used.• Endoscopy is required to document healing of gastric

ulcers and to rule out gastric cancer. • This usually is performed 6-8 weeks after the initial

diagnosis of PUD.

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EndoscopyPerform endoscopy early in:

• Patients older than 45-50 years • Patients with alarm symptoms, such as dysphagia,

recurrent vomiting, weight loss, or bleeding.

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Case• A 42-year-old man came to follow the result of endoscopy

done few days ago.Endoscopy Result:• Antral erosions• Duodenal erosions• Urease test is positive for H pylori

• How are you going to manage him?

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Acid Suppression

Two classes of acid-suppressing medications currently in use are:• Histamine-2 receptor antagonists (H2RAs) • Proton pump inhibitors (PPIs).

• Both classes are available in intravenous and oral preparations.

• Examples of H2RAs include ranitidine, cimetidine, .... Examples of PPIs include omeprazole, pantoprazole, lansoprazole, …..

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Proton Pump Inhibitors (PPIs)

• Good safety profile • Adverse effects, especially with long-term and/or high-

dose therapy, such as:• Clostridium difficile infection, • community-acquired pneumonia, • hip fracture, • and vitamin B12 deficiency.  

• PPIs impair gastric secretion of acid; thus, absorption of any medication that depends on gastric acidity, such as iron, is impaired with long-term PPI therapy.

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Triple-therapy regimens for H pylori

A 14-day regimen as shown below:• Omeprazole: 20 mg PO bid• or• Esomeprazole (Nexium): 40 mg PO qd• Plus• Clarithromycin: 500 mg PO bid• and• Amoxicillin: 1 g PO bid

Alternative triple-therapy regimens•The alternative triple therapies, also administered for 14 days, are as follows:

• Omeprazole : 20 mg PO bid• Or • Esomeprazole (Nexium): 40 mg PO qd• Plus• Clarithromycin: 500 mg PO bid• and• Metronidazole (Flagyl): 500 mg PO bid

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A 62-year-old lady, known case of IHD presents with one week H/O black stools which is documented to be melena on PR. She was pale and abdomen is soft.

Investigations revealed:HGB ....................... 96 120 – 160 g/LPLT .................. .......260 140 – 450 x10.e9/L

What is the most common cause could be responsible for this condition?

Aspirin The most appropriate next step to do is:A- Start her on ferrous sulphateB- Start her on H2 blockerC- Start her on proton pump inhibitorD- Refer her for gastroscopy Answer D

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Medical Management of NSAID Ulcers

• According to the ACG guideline, all patients who are beginning long-term NSAID therapy should first be tested for H pylori.

• NSAIDs should be immediately discontinued in patients with positive H pylori test results if clinically feasible and given eradication therapy.

• For patients who must continue with their NSAIDs, PPI maintenance is recommended to prevent recurrences even after eradication of H pylori.

• If NSAIDs must be continued, changing to a COX-2 selective inhibitor is an option. 

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Prophylactic or Preventive Therapy• Patients with NSAID-induced ulcers who require chronic,

daily NSAID therapy

• Patients older than 60 years

• Patients with a history of PUD or a complication such as gastrointestinal bleeding

• Patients taking concomitant steroids or anticoagulants or patients with significant comorbid medical illnesses

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Reference

• American College of Gastroenterology 2012

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