GROUP

C2
Physiology Laboratory
Small Group Discussion
Output

March 9, 2016

[PEPTIC ULCER DISEASE]

By: ASUBARIO, Olufunmilola Omonike; BALADAD, Alvin Byron; DE JESUS, Chrislou; GURUNG, Man
Bahadur; KALANYEG, Kristie; MAHALEE, Naphitcharak; MONTHATHONG, Thanapol; PANLASIGUI,
Rikkimae Maria; SAMSON, Chino Paolo; SOLONIO, Natalie Keith; VALDEZ, Gregorio
 PEPTIC ULCER DISEASE

Peptic ulcer disease (PUD), also known

Deep gastric ulcer
as a peptic ulcer or stomach ulcer, is a break in
the lining of the stomach, first part of the small
intestine, or occasionally the lower esophagus. An
ulcer in the stomach is known as a gastric
ulcer while that in the first part of the intestines is
known as a duodenal ulcer. The most common
symptoms are waking at night with upper
abdominal pain or upper abdominal pain that
improves with eating. The pain is often described
as a burning or dull ache. Other symptoms include
belching, vomiting, weight loss, or poor appetite.
About a third of older people have no symptoms.
Complications may include bleeding, perforation,
and blockage of the stomach. Bleeding occurs in
as many as 15% of people.

EPIDEMIOLOGY

In the United States, PUD affects approximately 4.5 million people annually.
Approximately 10% of the US population has evidence of a duodenal ulcer at some
time. Of those infected with H pylori, the lifetime prevalence is approximately 20%. Only
about 10% of young persons have H pylori infection; the proportion of people with the
infection increases steadily with age.

Overall, the incidence of duodenal ulcers has been decreasing over the past 3-4
decades. Although the rate of simple gastric ulcer is in decline, the incidence of
complicated gastric ulcer and hospitalization has remained stable, partly due to the
concomitant use of aspirin in an aging population. The hospitalization rate for PUD is
approximately 30 patients per 100,000 cases.

The prevalence of PUD has shifted from predominance in males to similar

occurrences in males and females. Lifetime prevalence is approximately 11-14% in men
and 8-11% in women. Age trends for ulcer occurrence reveal declining rates in younger
men, particularly for duodenal ulcer, and increasing rates in older women. Trends reflect
complex changes in risk factors for PUD, including age-cohort phenomena with the
prevalence of H pylori infection and the use of NSAIDs in older populations.

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International statistics

The frequency of PUD in other countries is variable and is determined primarily

by association with the major causes of PUD: H pylori and NSAIDs

SIGNS & SYMPTOMS

An ulcer may or may not have symptoms. When symptoms occur, they may include:
 A gnawing or burning pain in the middle or upper stomach between meals or at
night
 Bloating
 Heartburn
 Nausea or vomiting
In severe cases, symptoms can include:
 Dark or black stool (due to bleeding)
 Vomiting blood (that can look like "coffee-grounds")
 Weight loss
 Severe pain in the mid to upper abdomen
CAUSES

Different factors can cause the lining of the stomach, the esophagus, and the small
intestine to break down. These include:

 Helicobacter pylori (H. pylori): a bacteria that can cause a stomach infection and
inflammation
 frequent use of aspirin, ibuprofen, and other anti-inflammatory drugs (risk associated
with this behavior increases in women and people over the age of 60)
 smoking
 drinking too much alcohol
 radiation therapy
 stomach cancer

PATHOPHYSIOLOGY

Peptic ulcers result from an imbalance between factors that can damage the
gastroduodenal mucosal lining and defense mechanisms that normally limit the injury.
Aggressive factors include gastric juice (including hydrochloric acid, pepsin, and bile
salts refluxed from the duodenum), H pylori, and NSAIDs.

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 Mucosal defenses comprise a mucus bicarbonate layer secreted by surface
mucus cells forming a viscous gel over the gastric mucosa; the integrity of tight
junctions between adjacent epithelial cells; and the process of restitution, whereby any
break in the epithelial lining is rapidly filled by adjacent epithelial and mucosal stromal
cells migrating and flattening to fill the gap. Mucosal defenses depend on an adequate
blood supply and on formation within the gastric mucosa.

In general, duodenal ulcers are the result of hypersecretion of gastric acid related
to H pylori infection (the majority of cases), whereas secretion is normal or low in
patients with gastric ulcers.

In duodenal ulcers, chronic H pylori infection confined mainly to the gastric

antrum leads to impaired secretion of somatostatin and consequently increased gastrin
release, resulting in gastric acid hypersecretion. In Zollinger-Ellison syndrome, a
gastrin-secreting neuro-endocrine tumour is the stimulus for high rates of gastric acid
secretion.

In gastric ulcers, longstanding H pylori infection throughout the stomach

accompanied by severe inflammation results in gastric mucin degradation, disruption of
tight junctions between gastric epithelial cells, and the induction of gastric epithelial cell
death. NSAIDs cause injury directly (involving trapping hydrogen ions) and indirectly (a
systemic effect involving the inhibition of cyclo-oxygenases, especially COX-1) and
increase bleeding risk through anti-platelet actions. Chronic gastric ischaemia underlies
the stress ulcers of patients in intensive care.

DIAGNOSIS:

 Tests for H. pylori- Your doctor may recommend tests to determine whether the
bacterium H. pylori is present in your body. Tests can test for H. pylori using:

> Blood
> Breath
> Stool

 Endoscopy- using a scope to examine your upper digestive system.During

endoscopy, your doctor passes a hollow tube equipped with a lens (endoscope)
down your throat and into your esophagus, stomach and small intestine. Using
the endoscope, your doctor looks for ulcers. If your doctor detects an ulcer, small
tissue samples (biopsy) may be removed for examination in a lab. A biopsy can
also identify the presence of H. pylori in your stomach lining. Your doctor is more
likely to recommend endoscopy if you are older, have signs of bleeding, or have
experienced recent weight loss or difficulty eating and swallowing
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  X-ray of your upper digestive system- sometimes called a barium swallow or
upper gastrointestinal series, this series of X-rays creates images of your
esophagus, stomach and small intestine. During the X-ray, you swallow a white
liquid (containing barium) that coats your digestive tract and makes an ulcer
more visible.

TREATMENT & MANAGEMENT:

Treatment for peptic ulcers depends on the cause. Treatments can include:

 Antibiotic medications to kill H. pylori. If H. pylori is found in your digestive tract, your
doctor may recommend a combination of antibiotics to kill the bacterium.
 Proton pump inhibitors reduce stomach acid by blocking the action of the parts of
cells that produce acid. These drugs include the prescription and over-the-counter
medications omeprazole (Prilosec), lansoprazole (Prevacid), rabeprazole (Aciphex),
esomeprazole (Nexium) and pantoprazole (Protonix).

 Acid blockers — also called histamine (H-2) blockers — reduce the amount of
stomach acid released into your digestive tract, which relieves ulcer pain and
encourages healing.

 Antacids that neutralize stomach acid. Antacids neutralize existing stomach acid and
can provide rapid pain relief. Side effects can include constipation or diarrhea,
depending on the main ingredients.

 In some cases, your doctor may prescribe medications called cytoprotective agents
that help protect the tissues that line your stomach and small intestine. Options
include the prescription medications sucralfate (Carafate) and misoprostol (Cytotec).
Another nonprescription cytoprotective agent is bismuth subsalicylate (Pepto-
Bismol).

PROGNOSIS

When the underlying cause is addressed, the prognosis is excellent. Most

patients are treated successfully with eradication of H pylori infection, avoidance of
NSAIDs, and the appropriate use of antisecretory therapy. Eradication of H
pyloriinfection changes the natural history of the disease, with a decrease in the ulcer
recurrence rate from 60-90% to approximately 10-20%. However, this is a higher
recurrence rate than previously reported, suggesting an increased number of ulcers not
caused by H pylori infection.

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 With regard to NSAID-related ulcers, the incidence of perforation is
approximately 0.3% per patient year, and the incidence of obstruction is approximately
0.1% per patient year. Combining both duodenal ulcers and gastric ulcers, the rate of
any complication in all age groups combined is approximately 1-2% per ulcer per year.

The mortality rate for PUD, which has decreased modestly in the last few
decades, is approximately 1 death per 100,000 cases. If one considers all patients with
duodenal ulcers, the mortality rate due to ulcer hemorrhage is approximately 5%. Over
the last 20 years, the mortality rate in the setting of ulcer hemorrhage has not changed
appreciably despite the advent of histamine-2 receptor antagonists (H2RAs) and proton
pump inhibitors (PPIs). However, evidence from meta-analyses and other studies has
shown a decreased mortality rate from bleeding peptic ulcers when intravenous PPIs
are used after successful endoscopic therapy.[19, 20, 21, 22]

Emergency operations for peptic ulcer perforation carry a mortality risk of 6-30%.

Factors associated with higher mortality in this setting include the following:

 Shock at the time of admission

 Renal insufficiency
 Delaying the initiation of surgery for more than 12 hours after presentation
 Concurrent medical illness (eg, cardiovascular disease, diabetes mellitus
 Age older than 70 years
 Cirrhosis
 Immunocompromised state

Location of ulcer (mortality associated with perforated gastric ulcer is twice that
associated with perforated

References:

1. Guyton, AC; Hall, JE: Textbook of Medical Physiology, 11th edition. Elsevier Inc.
2006.

2. Koeppen, BM; Stanton, BA: Berne and Levy Physiology, 6 th edition. Elsevier Inc.
2010.

3. en.wikipedia.org

4. http://www.webmd.com/digestive-disorders/digestive-diseases-peptic-ulcer-disease

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