The document outlines the approach to diagnosing and managing acid peptic disease, emphasizing the mechanisms behind excessive acid secretion and reduced mucosal defense. Key symptoms include epigastric pain and alarm features necessitating gastroenterology referral. Diagnostic methods range from H. pylori testing to upper GI endoscopy, with treatment strategies addressing both acute bleeding and infection management.

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.