A Case Presentation on NSAID – induced PUD: Gastric Antral Ulcer

Saint Padre Pio of Pietrelcina 2019 – RLE Group C

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I. INTRODUCTION

PEPTIC ULCER DISEASE (PUD)

I. DEFINITION:

Peptic ulcer disease (PUD), also known as a peptic 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.1

II. CAUSES:

1. Helicobacter pylori
A major causative factor (60% of gastric and up to 50–75%of duodenal ulcers) is
chronic inflammation due to Helicobacter pylori that colonizes the antral mucosa. The immune
system is unable to clear the infection, despite the appearance of antibodies. Thus, the bacterium
can cause a chronic active gastritis (type B gastritis). Gastrin stimulates the production of gastric
acid by parietal cells. In H. pylori colonization, responses to increased gastrin, the increase in acid
can contribute to the erosion of the mucosa and therefore ulcer formation. 2

2. Non-Steroidal Anti-Inflammatory Drugs (NSAIDS)

Another major cause is the use of NSAIDs, such as ibuprofen and aspirin. The gastric
mucosa protects itself from gastric acid with a layer of mucus, the secretion of which is
stimulated by certain prostaglandins. NSAIDs block the function of cyclooxygenase 1 (COX-1),
which is essential for the production of these prostaglandins. COX-2 selective anti-
inflammatories (such as celecoxib or the since withdrawn rofecoxib) preferentially inhibit COX-
2, which is less essential in the gastric mucosa, and roughly halve the risk of NSAID-related
gastric ulceration.3

3. Stress
Stress due to serious health problems such as those requiring treatment in an intensive
care unit is well described as a cause of peptic ulcers, which are termed stress ulcers.
While chronic life stress was once believed to be the main cause of ulcers, this is no
longer the case. It is, however, still occasionally believed to play a role. This may be by
increasing the risk in those with other causes such as H. pylori or NSAID use.3

4. Diet
Dietary factors such as spice consumption were hypothesized to cause ulcers until late in
the 20th century, but have been shown to be of relatively minor importance. Caffeine and coffee,
also commonly thought to cause or exacerbate ulcers, appear to have little effect. Similarly, while
studies have found that alcohol consumption increases risk when associated with H.
pylori infection, it does not seem to independently increase risk. Even when coupled with H.
pylori infection, the increase is modest in comparison to the primary risk factor. 4

1. 1 "Definition and Facts for Peptic Ulcer Disease". National Institute of Diabetes and Digestive and Kidney Diseases.
2. http://www.niddk.nih.gov/health-information/digestive-diseases/peptic. Retrieved 11 April 2017.
3. 2 "Antral mucosa - Humpath.com - Human pathology". Archived from the original on 2011-11-09.

4. https://web.archive.org/web/20111109174244/http:/humpath.com. Retrieved 11 April 2017.

5. 3 "Stomach ulcer - Causes - NHS Choices." http://www.nhs.uk/Conditions/peptic-ulcer/Pages/causes.aspx

6. 4. "Ulcer Disease Facts and Myths". http://www.ulcerdisease.net. Retrieved 11 April 2017

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 A Case Presentation on NSAID – induced PUD: Gastric Antral Ulcer
Saint Padre Pio of Pietrelcina 2019 – RLE Group C
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5. Other cause
A rare condition known as Zollinger-Ellison syndrome can cause gastric and
duodenal ulcers. This condition causes cancerous and noncancerous tumors to develop in
the stomach and duodenum. 5

III. RISK FACTORS:

The following are the factors that may cause peptic ulcer disease: 6
 While doctors often recommend NSAIDs for health conditions such as arthritis or
joint inflammation, NSAIDs can increase your risk for developing peptic ulcers.
Additional medications that may increase your risk for gastric and duodenal ulcers
include:
 alendronate (Fosamax)
 Anticoagulants
 risedronate (Actonel)
 selective serotonin reuptake inhibitors (SSRIs)
 Spicy foods don’t increase your risk for ulcers but they can irritate your stomach
further.
 Other risk factors known to increase your risk for developing gastric and duodenal
ulcers include:
 being 70 years old or older
 drinking alcohol
 history of peptic ulcers
 smoking

IV. SIGNS AND SYMPTOMS:

Signs and symptoms of a peptic ulcer can include one or more of the following: 7
 Abdominal pain, classically epigastric strongly correlated to mealtimes. In case of
duodenal ulcers the pain appears about three hours after taking a meal;
 Bloating and abdominal fullness;
 Waterbrash (rush of saliva after an episode of regurgitation to dilute the acid in
esophagus - although this is more associated with gastroesophageal reflux disease);
 Nausea, and copious vomiting;
 Loss of appetite and weight loss;
 Hematemesis (vomiting of blood); this can occur due to bleeding directly from a
gastric ulcer, or from damage to the esophagus from severe/continuing vomiting.
 Melena (tarry, foul-smelling feces due to presence of oxidized iron
from hemoglobin);
 Rarely, an ulcer can lead to a gastric or duodenal perforation, which leads to acute
peritonitis, extreme, stabbing pain, and requires immediate surgery. 8

5 “Allabout Peptic Ulcer Disease”. http://www.merckmanuals.com/professional/gastrointestinal-

disorders/gastritis-and-peptic-ulcer-disease. Retrieved 11 April 2017
6 "Peptic Ulcer". Home Health Handbook for Patients & Caregivers. Merck Manuals. October 2006.

1. 7 "Stomach ulcer – Signs and Symptoms”. http://www.nhs.uk/Conditions/peptic-ulcer/Pages/causes.aspx

2. 8 "Ulcer: Facts and Myths". http://www.diseaseulceration.net. Retrieved 12 April 2017

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 A Case Presentation on NSAID – induced PUD: Gastric Antral Ulcer
Saint Padre Pio of Pietrelcina 2019 – RLE Group C
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A history of heartburn, gastroesophageal reflux disease (GERD) and use of

certain forms of medication can raise the suspicion for peptic ulcer. Medicines associated
with peptic ulcer include NSAIDs (non-steroid anti-inflammatory drugs) that
inhibit cyclooxygenase, and most glucocorticoids (eg. prednisolone). 9
In patients over 45 with more than two weeks of the above symptoms, the odds
for peptic ulceration are high enough to warrant rapid investigation by esophagogastro
duodenoscopy (EGD).
The timing of the symptoms in relation to the meal may differentiate between
gastric and duodenal ulcers: A gastric ulcer would give epigastric pain during the meal,
as gastric acid production is increased as food enters the stomach. Symptoms of duodenal
ulcers would initially be relieved by a meal, as the pyloric sphincter closes to concentrate
the stomach contents; therefore acid is not reaching the duodenum. Duodenal ulcer pain
would manifest mostly 2–3 hours after the meal, when the stomach begins to release
digested food and acid into the duodenum. 9
Also, the symptoms of peptic ulcers may vary with the location of the ulcer and
the patient's age. Furthermore, typical ulcers tend to heal and recur and as a result the
pain may occur for few days and weeks and then wane or disappear. Usually, children
and the elderly do not develop any symptoms unless complications have arisen. 9
Burning or gnawing feeling in the stomach area lasting between 30 minutes and
3 hours commonly accompanies ulcers. This pain can be misinterpreted
as hunger, indigestion or heartburn. Pain is usually caused by the ulcer but it may be
aggravated by the stomach acid when it comes into contact with the ulcerated area. The
pain caused by peptic ulcers can be felt anywhere from the navel up to the sternum, it
may last from few minutes to several hours and it may be worse when the stomach is
empty. Also, sometimes the pain may flare at night and it can commonly be temporarily
relieved by eating foods that buffer stomach acid or by taking anti-acid medication.
However, peptic ulcer disease symptoms may be different for every sufferer. 9

V. TESTS AND DIAGNOSTIC EXAMINATIONS:

The diagnosis of peptic ulcer disease is mainly established based on the
characteristic symptoms. Stomach pain is usually the first signal of a peptic ulcer. In
some cases, doctors may treat ulcers without diagnosing them with specific tests and
observe whether the symptoms resolve, thus indicating that their primary diagnosis was
accurate.10
More specifically, peptic ulcers erode the muscularis mucosae, at least to the level
of the submucosa.11
Confirmation of the diagnosis is made with the help of tests such as endoscopies
or barium contrast x-rays. The tests are typically ordered if the symptoms do not resolve
after a few weeks of treatment, or when they first appear in a person who is over age 45
or who has other symptoms such as weight loss, because stomach cancer can cause
similar symptoms. Also, when severe ulcers resist treatment, particularly if a person has
several ulcers or the ulcers are in unusual places, a doctor may suspect an underlying
condition that causes the stomach to overproduce acid.10

9 “Hole:Peptic Ulcer Disease”. http://www.thepepticproject.com/peptic-ulcer-disease. Retrieved 11 April 2017

3. 10 "Stomach ulcer – Tests and Diagnostics”. http://www.nhs.uk/peptic-ulcer/Pages/tests. Retrieved 11 April 2017
4. 11 "PUD: How do you know you have it?". http://www.pepticulcerdisease.net. Retrieved 12 April 2017

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 A Case Presentation on NSAID – induced PUD: Gastric Antral Ulcer
Saint Padre Pio of Pietrelcina 2019 – RLE Group C
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An esophagogastroduodenoscopy (EGD), a form of endoscopy, also known as

a gastroscopy, is carried out on patients in whom a peptic ulcer is suspected. By direct
visual identification, the location and severity of an ulcer can be described. Moreover, if
no ulcer is present, EGD can often provide an alternative diagnosis.10
One of the reasons that blood tests are not reliable for accurate peptic ulcer
diagnosis on their own is their inability to differentiate between past exposure to the
bacteria and current infection. Additionally, a false negative result is possible with a
blood test if the patient has recently been taking certain drugs, such
as antibiotics or proton-pump inhibitors.
The diagnosis of Helicobacter pylori can be made by: 11
 Urea breath test (noninvasive and does not require EGD);
 Direct culture from an EGD biopsy specimen; this is difficult to do, and can be
expensive. Most labs are not set up to perform H. pylori cultures;
 Direct detection of urease activity in a biopsy specimen by rapid urease test;
 Measurement of antibody levels in the blood (does not require EGD). It is still
somewhat controversial whether a positive antibody without EGD is enough to
warrant eradication therapy;
 Stool antigen test;
 Histological examination and staining of an EGD biopsy.
The breath test uses radioactive carbon to detect H. pylori. To perform this exam
the patient will be asked to drink a tasteless liquid which contains the carbon as part of
the substance that the bacteria breaks down. After an hour, the patient will be asked to
blow into a bag that is sealed. If the patient is infected with H. pylori, the breath sample
will contain radioactive carbon dioxide. This test provides the advantage of being able to
monitor the response to treatment used to kill the bacteria.11
The possibility of other causes of ulcers, notably malignancy (gastric cancer)
needs to be kept in mind. This is especially true in ulcers of the greater (large)
curvature of the stomach; most are also a consequence of chronic H. pylori infection.
If a peptic ulcer perforates, air will leak from the inside of the gastrointestinal
tract (which always contains some air) to the peritoneal cavity (which normally never
contains air). This leads to "free gas" within the peritoneal cavity. If the patient stands
erect, as when having a chest X-ray, the gas will float to a position underneath the
diaphragm. Therefore, gas in the peritoneal cavity, shown on an erect chest X-ray or
supine lateral abdominal X-ray, is an omen of perforated peptic ulcer disease.11

VI. TREATMENTS:
The following are treatments given to patients with PUD: 12
 Younger patients with ulcer-like symptoms are often treated with antacids or H2
antagonists before endoscopy is undertaken.
 People who are taking nonsteroidal anti-inflammatories (NSAIDs) may also be
prescribed a prostaglandin analogue (misoprostol) in order to help prevent peptic
ulcers.
 Some are prescribed with H2 antagonists or proton-pump inhibitors which
decrease the amount of acid in the stomach, helping with the healing of ulcers.

10 "Stomach ulcer – Tests and Diagnostics”. http://www.nhs.uk/peptic-ulcer/Pages/tests. Retrieved 11 April 2017

5. 11 "PUD: How do you know you have it?". http://www.pepticulcerdisease.net. Retrieved 12 April 2017
6. 12 "Stomach ulcer – Treatments”. http://www.nhs.uk/peptic-ulcer/Pages/treatments. Retrieved 11 April 2017

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 A Case Presentation on NSAID – induced PUD: Gastric Antral Ulcer
Saint Padre Pio of Pietrelcina 2019 – RLE Group C
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 When H. pylori infection is present, the most effective treatments are

combinations of 2 antibiotics (e.g. clarithromycin, amoxicillin, tetracycline, and
metronidazole) and a proton-pump inhibitor (PPI), sometimes together with a
bismuth compound. In complicated, treatment-resistant cases, 3 antibiotics (e.g.
amoxicillin + clarithromycin + metronidazole) may be used together with a PPI
and sometimes with bismuth compound. An effective first-line therapy for
uncomplicated cases would be amoxicillin + metronidazole + pantoprazole (a
PPI).
 Perforated peptic ulcer is a surgical emergency and requires surgical repair of the
perforation. Most bleeding ulcers require endoscopy urgently to stop bleeding
with cautery, injection, or clipping.
 Various elective procedures for peptic ulceration have been assessed. The
operations that have been used traditionally are: 13
 Billroth I gastrectomy - is an operation in which the pylorus is removed and the
proximal stomach is anastomosed directly to the duodenum.
 Billroth II or Pólya gastrectomy - is an operation in which the greater curvature of
the stomach is connected to the first part of the jejunum in end-to-side
anastomosis.
 Truncal vagotomy and pyloroplasty - includes division of the main trunk of the
vagus (including its celiac/hepatic branch) and denervation of the pylorus;
therefore, a pyloric drainage procedure, such as pyloric dilatation or disruption
(pyloromyotomy or pyloroplasty) or gastrojejunostomy, is needed.
 Highly selective vagotomy - refers to denervation of only those branches
supplying the lower esophagus and stomach

VII. COMPLICATIONS: 14
 Gastrointestinal bleeding is the most common complication. Sudden large
bleeding can be life-threatening. It occurs when the ulcer erodes one of the blood
vessels, such as the gastroduodenal artery.
 Perforation (a hole in the wall of the gastrointestinal tract) often leads to
catastrophic consequences if left untreated. Erosion of the gastro-intestinal wall
by the ulcer leads to spillage of stomach or intestinal content into the abdominal
cavity. Perforation at the anterior surface of the stomach leads to acute peritonitis,
initially chemical and later bacterial peritonitis. The first sign is often sudden
intense abdominal pain; an example is Valentino's syndrome, named after the
silent-film actor who experienced this pain before his death. Posterior wall
perforation leads to bleeding due to the involvement of gastroduodenal artery that
lies posterior to the first part of the duodenum.
 Penetration is a form of perforation in which the hole leads to and the ulcer
continues into adjacent organs such as the liver and pancreas.
 Gastric outlet obstruction is a narrowing of the pyloric canal by scarring and
swelling of the gastric antrum and duodenum due to peptic ulcers. The person
often presents with severe vomiting without bile.

13 Millat B, Fingerhut A; Surgical treatment of complicated duodenal ulcers: controlled trials. World J Surg. 2000 Mar 24.
7. 14 "Stomach ulcer – Complications”. http://www.nhs.uk/peptic-ulcer/Pages/complications. Retrieved 11 April 2017

8.

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 A Case Presentation on NSAID – induced PUD: Gastric Antral Ulcer
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 Cancer is included in the differential diagnosis (elucidated

by biopsy), Helicobacter pylori as the etiological factor making it 3 to 6 times
more likely to develop stomach cancer from the ulcer.

VIII. PREVENTIONS:
You can reduce your risk for ulcers by lowering your intake of NSAIDs or
switching to another medication, if you’re taking NSAIDs.
Other methods for prevention include:
 Take NSAIDs with meals or medications that protect your stomach lining, if you
need NSAIDs.
 Avoid or limit caffeinated drinks and alcohol. They may worsen your symptoms.
 Refrain from smoking, as it can slow healing.
 Take all of your antibiotics, if prescribed, for H. pylori infections. Not taking the
entire amount can bring the infection back.
 Take steps to reduce the stress in your life. From sleeping more to taking time to
do something you enjoy (reading, exercising, or writing in a journal), reducing
stress can keep gastric and duodenal ulcer symptoms from getting worse.

IX. EPIDEMIOLOGY:
The three most deadly digestive diseases in Philippines during 2013 were peptic
ulcer disease, pancreatitis, and paralytic ileus and intestinal obstruction respectively. 15
The annual mortality rate per 100,000 people from peptic ulcer disease in
Philippines has decreased by 12.9% since 1990, and this has been shown to decrease in
an average of 0.6% a year. 15
For men, the deadliness of peptic ulcer disease in Philippines peaks at age 80+. It
kills men at the lowest rate at age 5-9. At 341.5 deaths per 100,000 men in 2013, the peak
mortality rate for men was higher than that of women, which was 202 per 100,000
women. Women are killed at the highest rate from peptic ulcer disease in Philippines at
age 80+. It was least deadly to women at age 5-9. 15
According to the latest WHO data published in may 2014, Peptic Ulcer Disease
deaths in Philippines reached 6,234 or 1.20% of total deaths in the said year. The age
adjusted death rate is 10.98 per 100,000 of population. 16

9. 15 “Health Grove”. http://global-disease-burden. com/Peptic-Ulcer-Disease-in-Philippines. Retrieved 10 May 2017

10. 16 "World Health Rankings”. http://www.worldlifeexpectancy.com/philippines-peptic-ulcer-disease. Retrieved 10 May 2017
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