This topic helps you , how to approach a patient having peptic ulcer disease and how to diagnose finally how to end up with treatment. Peptic ulcer disease a chronic disease of stomach and duodenum where the protective layer of stomach and duodenum weakens by many factors most common is H Pylori infection. Infection of H Pylori cause ulcer over time.

1. APPROACH TO A
PATIENT WITH ACID
PEPTIC DISEASE
25/6/2020

2. • Acid peptic disorders are the result of distinctive, but overlapping pathogenic
mechanisms leading to either excessive acid secretion or diminished mucosal
defense.

3. PHYSIOLOGY OF ACID SECRETION
• The stomach consists of an epithelium made up of pits and glands. The two
primary functional zones are the oxyntic gland area, representing approximately
80% of the organ, and the pyloric gland area representing the remaining 20%

4. REGULATION OF ACID SECRETION
• Parietal cell acid secretion is initiated by a variety of factors related to food
ingestion.
• Regulation is via central, peripheral and cellular mechanisms.
• Acid is generated by the carbonic anhydrase-mediated catalysis of CO2 and H2O
to form H+ and HCO3

5. How does patient approaches to you

6. HISTORY
• Epigastric pain is the most common symptom of both gastric and duodenal
ulcers.
• It is characterized by a gnawing or burning sensation and occurs after meals—
classically, shortly after meals with gastric ulcer and 2-3 hours afterward with
duodenal ulcer.
• 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.

7. • Pain typically follows a daily pattern specific to the patient.
• Pain with radiation to the back is suggestive of a posterior penetrating gastric
ulcer complicated by pancreatitis.

8. • Dyspepsia, including belching, bloating, distention, and fatty food intolerance
• Heartburn
• Chest discomfort
• Hematemesis or melena resulting from gastrointestinal bleeding. Melena may be intermittent over several days or multiple
episodes in a single day.
• Rarely, a briskly bleeding ulcer can present as hematochezia.
• Symptoms consistent with anemia (eg, fatigue, dyspnea) may be present
• Sudden onset of symptoms may indicate perforation.
• NSAID-induced gastritis or ulcers may be silent, especially in elderly patients.
• Only 20-25% of patients with symptoms suggestive of peptic ulceration are found on investigation to have a peptic ulcer.

9. ALARM FEATURES
Alarm features that warrant prompt gastroenterology referral include the following:
• Bleeding or anemia
• Early satiety
• Unexplained weight loss
• Progressive dysphagia or odynophagia
• Recurrent vomiting
• Family history of gastrointestinal cancer

10. DIFFERENTIAL DIAGNOSES
• Acute Cholangitis
• Acute Cholecystitis/Cholelithiasis
• Acute Coronary Syndrome
• Acute/ chronic Gastritis Cholecystitis
• Diverticulitis
• Esophagitis
• Gastroesophageal Reflux Disease
• Inflammatory Bowel Disease

11. H PYLORI TESTING
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.

12. ENDOSCOPY
• Upper gastrointestinal (GI) endoscopy is the preferred diagnostic test in the evaluation
of patients with suspected peptic ulcer disease.
• It is highly sensitive for the diagnosis of gastric and duodenal ulcers,
• It allows for biopsies.

13. RADIOGRAPHY
• In patients presenting acutely, a chest radiograph may be useful to detect free
abdominal air when perforation is suspected.
• On upper gastrointestinal (GI) contrast study with water-soluble contrast, the
extravasation of contrast indicates gastric perforation.

14. ANGIOGRAPHY
• Angiography may be necessary in patients with a massive gastrointestinal bleed
in whom endoscopy cannot be performed.
• An ongoing bleeding rate of 0.5 mL/min or more is needed for the angiography
to be able to accurately identify the bleeding source.

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

16. SECRETIN STIMULATION TEST
• A secretin stimulation test may be required if the diagnosis of Zollinger-Ellison
syndrome cannot be made on the basis of the serum gastrin level alone.
• This test can distinguish Zollinger-Ellison syndrome from other conditions with a
high serum gastrin level, such as use of antisecretory therapy with a proton pump
inhibitor, renal failure, or gastric outlet obstruction.

17. ACID SUPPRESSION
• Acid suppression is the general pharmacologic principle of medical management
of acute bleeding from a peptic ulcer. Reducing gastric acidity is believed to
improve hemostasis primarily through the decreased activity of pepsin in the
presence of a more alkaline environment.
• Pepsin is believed to antagonize the hemostatic process by degrading fibrin
clots. By suppressing acid production and maintaining a pH above 6, pepsin
becomes markedly less active. Concomitant H pylori infection in the setting of
bleeding peptic ulcers should be eradicated, as this lowers the rate of rebleeding.

18. • Parenteral PPI administration is used after successful endoscopic therapy for
ulcers with high-risk signs, such as active bleeding, visible vessels, and adherent
clots.

19. H PYLORI INFECTION
Triple-therapy regimens
• PPI-based triple therapy regimens for H pylori consist of a PPI, amoxicillin, and
clarithromycin for 7-14 days. A longer duration of treatment (14 d vs 7 d) appears to
be more effective and is currently the recommended treatment.
• Amoxicillin should be replaced with metronidazole in penicillin-allergic patients only,
because of the high rate of metronidazole resistance.
• In patients with complicated ulcers caused by H pylori, treatment with a PPI beyond
the 14-day course of antibiotics and until the confirmation of the eradication of H
pylori is recommended.

20. 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.
• For patients who must continue with their NSAIDs, PPI maintenance is
recommended to prevent recurrences even after eradication of H pylori.

21. MEDICAL MANAGEMENT OF NSAID ULCERS
Consider prophylactic or preventive therapy for the following patients:
• Patients with NSAID-induced ulcers who require chronic, daily NSAID therapy
• Patients older than 60 years
• Patients with a history of peptic ulcer disease or a complication such as
gastrointestinal bleeding
• Patients taking concomitant steroids or anticoagulants or patients with significant
comorbid medical illnesses

22. COMPLICATIONS OF PEPTIC ULCER DISEASE
• Refractory, symptomatic peptic ulcers, though rare after eradication of H pylori infection and
the appropriate use of antisecretory therapy, are a potential complication of peptic ulcer
disease.
• Obstruction is particularly likely to complicate peptic ulcer disease in cases refractory to
aggressive antisecretory therapy. Obstruction may persist or recur despite endoscopic balloon
dilation.
• Perforation is also a possibility. Penetration, particularly if not walled off or if a gastrocolic
fistula develops, is a potential complication.
• ulcer bleeding, particularly in patients with a history of massive hemorrhage and
hemodynamic instability, recurrent bleeding on medical therapy, and failure of therapeutic
endoscopy to control bleeding is a serious complication.

23. COMPLICATIONS
• Patients with gastric ulcers are also at risk of developing gastric malignancy. The risk is
approximately 2% in the initial 3 years.
• One of the important risk factors is related to H pylori infection. H pylori is associated with
atrophic gastritis, which, in turn, predisposes to gastric cancer. H pylori infection is associated
with gastric lymphoma or mucosa-associated lymphoid tissue (MALT) lymphoma.
• Normal gastric mucosa is devoid of organized lymphoid tissue. H pylori infection promotes
acquisition of lymphocytic infiltration and often the formation of lymphocytic aggregates and
follicles from which MALT lymphoma develops.
• Eradication of H pylori is very important in this group of patients because it has shown to cause
a remission of MALT lymphoma.
• Malignancy should be strongly considered in the case of a persistent nonhealing gastric ulcer.

24. LONG-TERM MONITORING
• Maintenance therapy with antisecretory medications (eg, H2 blockers, PPIs) for 1
year is indicated in high-risk patients. High-risk patients include those with recurrent
ulcers and those with complicated or giant ulcers.
• Consider maintenance therapy with half of the standard doses of H2-receptor
antagonists at bedtime in patients with recurrent, refractory, or complicated ulcers,
particularly if cure of H pylori has not been documented or if an H pylori –negative
ulcer is present.
• Patients with refractory ulcers may continue receiving once-daily PPI therapy
indefinitely. If H pylori is absent, consider a secondary cause of duodenal ulcer, such
as Zollinger-Ellison syndrome.