PEPTIC

ULCER DISEASE
ABDALLAH AL JAZZAZI
STOMACH

• The stomach occupies a small area immediately distal to the oesophagus (the cardia), the upper
region (the fundus, under the left diaphragm), the mid-region or body and the antrum, which
extends to the pylorus.
• It serves as a reservoir where food can be retained and broken up before being actively expelled
in to the proximal small intestine.
• Acid secretion is central to the functionality of the stomach
• It is under neural and hormonal control and both stimulate acid secretion through the direct
action of histamine on the parietal cell.
• Somatostatin inhibits both histamine and gastrin release and therefore acid secretion.
Histamine stimulates Gs via the H2 receptors and acts via
cyclic AMP;
acetylcholine (ACh) acts via the vagus M3 receptors; ACh
also acts via the ECL cell;
gastrin acts via the gastrin receptor, increasing the
intracellular free calcium, and also via the ECL cell
stimulating histamine.
prostaglandin E2 activates the Gi protein and inhibits acid
secretion;
MUCOSAL LAYER

• The ‘mucosal barrier’, made up of the plasma membranes of mucosal cells and the mucus layer,
protects the gastric epithelium from damage by acid and, for example, alcohol, aspirin, NSAIDs
and bile salts. Prostaglandins stimulate secretion of mucus, and their synthesis is inhibited by
aspirin and NSAIDs, which inhibit cyclo-oxygenase.
Notes: Alcohol is not ulcerogenic!
Corticosteroids alone are not ulcerogenic, but
they double the risk of serious NSAID-
associated gastrointestinal complication-risk
of bleeding may be 10-fold!
EPIDEMIOLOGY

• Either NSAIDs or H. pylori infection alone increased the risk of ulcer approximately 20-fold.
• NSAID users with H. pylori infection were about 60 times more likely to have a peptic ulcer than
uninfected non- NSAID patients.
• NSAIDs and H. pylori infection alone increased the risk of ulcer bleeding by 4.8-fold and 1.8-fold,
respectively.
• NSAID users with H. pylori infection had a 6-fold increase in risk of bleeding compared to uninfected
NSAID users.
PUD SYMPTOMS

• Recurrent, burning epigastric pain.

• patient points with a single finger to the epigastrium as the site of the pain this is strongly suggestive
of peptic ulcer disease.
• The relationship of the pain to food is variable and on the whole not helpful in diagnosis.
• The pain of a DU classically occurs at night (as well as during the day) and is worse when the patient
is hungry, but this is not reliable.
• The pain of both gastric and duodenal ulcers may be relieved by antacids.
• Nausea may accompany the pain; vomiting is infrequent but can relieve the pain. Anorexia and weight
loss may occur, particularly with GUs.
• Persistent and severe pain suggests complications such as penetration into other organs
• No relation between symptoms, endoscopic and histological findings (Sørreisa study)
H PYLORI

• Spiral, gram negative, micro-aerophilic rod.

• H. pylori infection can cause gastritis, PUD, gastric adenocarcinoma, and
gastric B-cell (MALT) lymphoma.
EPIDEMIOLOGY OF H PYLORI INFECTION

• The prevalence of H. pylori is high in developing countries (80–90% of

the population), and much lower (20–50%) in developed countries.
• Infection rates are highest in lower income groups.
• Infection is usually acquired in childhood
• The incidence increases with age, probably due to acquisition in
childhood when hygiene was poorer (cohort effect) rather than infection
in adult life
• Infection rates in adults are probably far less than 1% per year in
developed countries.
WHEN TO TEST

• Test for H. pylori when:

• there is any prior history of PUD, complicated or uncomplicated, and especially duodenal ulcer;
• current findings on EGO show ulcer disease, erosive gastritis, or duodenitis;
• MALT lymphoma is present; and/or there is a family history of gastric cancer.
• The strategy is "test and treat" in dyspeptic patients < 55 years of age even with no alarm
symptoms/features.
TESTS FOR H PYLORI

• Invasive tests:
• The gold standard for H. pylori testing is histologic examination of biopsied antral mucosa-obtained
during EGO.
• Urease tests are based on the finding that H. pylori breaks down urea into ammonia and C02. Urease
tests are good for checking for active disease and for response to therapy. These tests are sensitive
(95%) and specific (95%). Urease tests are less sensitive if the patient is on a drug that may blunt the
effect of H. pylori infection, such as PPis and antibiotics. In such patients, it is appropriate to obtain
biopsies for histologic evaluation with or without RUT or to plan testing with a urea breath test or fecal
antigen test later (after withholding the offending agents for 2--4 weeks).
NON INVASIVE TESTS

• Noninvasive tests include a urea breath test, a fecal antigen test, and a serologic test:
• A urea breath test (UBT), which uses labeled urea, is the 1st choice for checking effectiveness of
treatment.
• A fecal antigen test (FAT) is a good method for primary diagnosis, and if the patient is on PPI, it is the
best test for checking effectiveness of treatment (S&S = 94% & 98%).
• Serologic tests are no longer recommended due to their low PPV (positive predictive value;< 50%). Also,
serum tests are poor for checking effectiveness of treatment as they can stay positive for years after
eradication.
ENDOSCOPIC FINDINGS

• Gastritis: erythematous and edematous mucosa

• Histopathologic diagnosis
• Biopsies from antrum and gastric body
• Malignant potential if intestinal metaplasia and atrophic gastritis.
WHEN TO TREAT

• Treat only symptomatic patients

• those with history of gastric/duodenal ulcer
• personal/family history of gastric cancer
• personal history of MALT lymphoma.
NOTES

• H. pylori develops resistance to metronidazole and clarithromycin

• Previous macrolide antibiotic use precludes the use of clarithromycin
• Metronidazole resistance can be overcome with increased dose (500 mg bid)
• If the first course of therapy (PPI and 2 antibiotics) fails to eradicate H. pylori,
then some recommend PPI + amoxicillin + levofloxacin or quadruple therapy
using bismuth+ 2 antibiotics + PPL
ERADICATION FOLLOW UP

• Universal post-treatment testing is not recommended. The accepted indications

include the following:
• History of H. pylori-associated ulcer
• Persistent dyspepsia despite the test-and-treat strategy
• H. pylori-associated MALT lymphoma
• Resection of early gastric carcinoma
• When confirmation is necessary, testing should be performed no sooner than 4
weeks after the completion of therapy. In general, noninvasive tests (not serology)
should be done for post-treatment testing unless there is a need for repeat EGD.
NSAIDS

• NSAIDs cause the majority of peptic ulcers not caused by H. pylori. The prevalence of ulcers in patients
on NSAIDs is 25%. NSAIDs cause both gastric and duodenal ulcers-but typically gastric.
• If NSAIDs are required, and the patient is having or has had trouble, use any of the following:
• Nonacetylated NSAIDs (e.g., salsalate).
• NSAIDs that are non-acidic prodrugs (e.g., nabumetone; Relafen®).
• NSAIDs with a PPI or prostaglandin E analog (e.g., misoprostol). PPis are superior to H2 blockers and
sucralfate in the prevention of NSAID-induced ulcers.
• COX-2 NSAIDs
RISK FACTORS FOR CONVENTIONAL NSAID-INDUCED
PUD
• First 3 months of use
• high doses
• elderly patient
• history of ulcer disease or prior UGI bleed
• cardiac disease
• concurrent steroid use
• serious illness
• concurrent ASA use.
RECOMMENDATIONS

• H pylori eradication is beneficial before starting NSAID treatment.

• It is mandatory in patients with a peptic ulcer history.
• H pylori eradication alone does not reduce the incidence of gastroduodenal ulcers in patients already
receiving long- term NSAID treatment. They require continued PPI treatment as well as eradication
treatment.
• The long-term incidence of peptic ulcer bleeding is low in these patients after receiving eradication
even in the absence of gastroprotective treatment.
• Enteric-coated NSAIDs have been recommended in the past; but the 2008 ACC/ ACG guidelines on
NSAIDs in patients with coronary artery disease highlights data that demonstrates no increased benefit
of enteric-coated formulations in reduction of GI adverse events.
PUD TREATMENT

• H. pylori treatment
• Decrease acid secretion (H2 receptor antagonists, PPis)
• Stop exacerbating processes (smoking, taking NSAIDs)
INDICATIONS FOR SURGERY

• UGI bleed(most common) active bleed unable to stop via endoscopic therapy.
Surgery is required in 5% of UGI bleeds.
• Gastric outlet obstruction-initial treatment is balloon dilation. Surgery
required in 25%.
• Perforation-laparoscopic repair may be possible.
• Recurrent/refractory ulcers (rare).
• Zollinger-Ellison syndrome (ZES)-surgery is for underlying gastrinoma.
COMPLICATIONS

• Bleeding : Most common (15-20%). Melena, hematemesis, coffee ground and

hematochezia, Iron deficiency anemia and occult blood in stool (chronic
ulcer). Rebleeding risk: active bleeding at gastoscopy, size >1-2 cm, posterior
wall DU, location at minor curvature, Visible vessels on a non-bleeding ulcer,
Visible clot
• Perforation
• Penetration: pancreas, liver, biliary ducts, colon. • Treatment: NG catheter, PPI
• Obstruction.
BLEEDING ULCER TREATMENT

• EGD is the diagnostic and treatment procedure of choice for UGI bleeding
• It should be done emergently if the patient is unstable or has recurrent
hematochezia or hematemesis.
• Increasing the gastric pH to > 6.0 reduces the risk of rebleeding-PPis given
either IV or orally bid achieve this.
• Initial treatment of actively bleeding ulcers (or adherent clot/visible vessel)
shows best results with combination therapy consisting of injection
(epinephrine or sclerosant) followed by either thermal/laser coagulation or a
hemoclip.
PERFORATION

• Acute severe pain

• Circulatory shock
• Peritonitis
• Abdominal Exam.: tenderness, rigidity, no liver dullness, bowel sounds are first hyperactive then
disappear upon clinical worsening.
• Plain abd. X-ray: free air under diaphragm
• Gastroscopy is contraindicated >> Gastrosurgery.
OBSTRUCTION

• N/V (30-60 min after meals)

• Early satiety and bloating
• Weight loss
• Gastroscopy and CT abdomen.
• N-G tube if gastric retention.
• PPI tx. (ulcer heals and edema disappears)
OTHER CAUSES OF GASTRITIS

• Autoimmune gastritis (Antibodies: Anti- intrinsic factor, Anti-parietal cell

antigen
• Eosinophillic gastritis
• Hypertrophic gastritis
• Chemical gastritis
• Hypertensive gastropathy/gastroduodenopathy (liver cirrhosis)
Thank you for listening