PLENARY DISCUSSION

PEPTIC ULCER DISEASE

CREATED BY:

2
 5th TUTORIAL GROUP

PHARMACY DEPARTMENT

FACULTY OF MEDICAL AND HEALTH SCIENCE

MUHAMMADIYAH UNIVERSITY OF YOGYAKARTA

2018

Member’s Name:
20160350082 Facetha Intan Pramana

20160350100 Annisa Zulfarrahmah

20160350070 Rifka Syaida Fitria

20160350023 Dwi Asih Ramadhani

20160350067 Puji Septiana

20160350096 Suci Apriliyanti

20160350074 Firly Amila Nazar

20160350077 Isna Aura Dewayanti

20160350058 Hanan Nisa Prabaswari

20160350104 Avisena

20160350028 Linta Sabila Hanik

20160350050 Elma Safitri

3
 PREFACE
Praise and Gratitude we thank God Almighty, because it has been
bestowed Thanks, Grace and His gift so that we can arrange this paper properly
and on time. In this paper we will discuss about " Diarrhea Diseases And The
Treatment".

This paper has been prepared by a variety of observations and some

support from other parties to help resolve the challenges and obstacles during
work on this paper. Therefore, we would like to thank the coach and also all those
who have helped in the preparation of this paper.

We realize that there are still many fundamental flaws in this paper.
Therefore, criticism and suggestions from readers so we expect to enhance the
next paper.

Final words I hope this paper can provide benefits for us all.

Yogyakarta, January 5th 2016

4
 Writer

Table of content
Member’s Name:......................................................................................................2

PREFACE.................................................................................................................3

CHAPTER I.............................................................................................................7

INTRODUCTION....................................................................................................7

A. Purpose.........................................................................................................7

B. Formulation of the problem..........................................................................7

C. Background...................................................................................................7

CHAPTER II............................................................................................................9

LITERATURE REVIEW........................................................................................9

A. Digestive system (gaster).............................................................................9

Structure.....................................................................................................9

Regions of the stomach............................................................................10

Layers of the stomach wall.......................................................................11

Function....................................................................................................11

5
 Regulation of Acid Secretion...................................................................12

B. Peptic Ulcer................................................................................................13

B.1 Definition...........................................................................................13

B.2 Epidemiology ...................................................................................14

B.3 Pathophysiology................................................................................14

B.4 Ethiology...........................................................................................16

B.5 Symtom..............................................................................................17

B.6 Diagnosis...........................................................................................17

B.8 Therapy of Peptic Ulcer.....................................................................19

B.7 Algorithm...........................................................................................24

CHAPTER III.........................................................................................................26

DISCUSSION........................................................................................................26

A. What are the functions and mechanisms of each drug...............................26

B. Comparison, which drug is better ppi or h2 blocker (along with EBM)....27

C. are there interactions between trexenamic acid and cetriaxone? how the
solution............................................................................................................27

D.Role of the Pharmacist................................................................................27

CHAPTER IV........................................................................................................29

CONCLUSION......................................................................................................29

BIBLIOGRAPHY..................................................................................................30

6
 CHAPTER I

INTRODUCTION
A. Purpose

1. Students understand about peptic ulcer

2. Students are able to know the medicine for peptic ulcer
3. Students are able to know the role of pharmacists in patients
with peptic ulcer

B. Formulation of the problem

A. What are the functions and mechanisms of each drug

B. comparison, which drug is better ppi or h2 blocker (along with EBM)

C. are there interactions between trexenamic acid and cetriaxone? how the
solution

D. Role of Pharmacist for peptic ulcer patient.

C. Background

In the United States about four million people have active peptic ulcers and about
350,000 new cases are diagnosed each year. Four times as many duodenal ulcers
as gastric ulcers are diagnosed. Approximately 3000 deaths per year in the United
States are due to duodenal ulcer and 3000 to gastric ulcer. There has been a
marked decrease in reported hospitalization and mortality rates for peptic ulcer in
the United States. Changes in criteria for selecting the underlying cause of death
might account for some of the apparent decrease in ulcer mortality rates.

Hospitalization rates for duodenal ulcers decreased nearly 50 per cent from 1970
to 1978, but hospitalization rates for gastric ulcers did not decrease. Although this
decrease in hospitalization rates may reflect a decrease in duodenal ulcer disease
incidence, it appears that changes in coding practices, hospitalization criteria, and

7
diagnostic procedures have contributed to the reported declines in peptic ulcer
hospitalization and mortality rates. There is no good evidence to support the
popular belief that peptic ulcer is most common in the spring and autumn. The
most consistent pattern appears to be low ulcer rates in the summer. There is
strong evidence that cigarette smoking, regular use of aspirin, and prolonged use
of steroids are associated with the development of peptic ulcer. There is some
evidence that coffee and aspirin substitutes may affect ulcers, but most studies do
not implicate alcohol, food, or psychological stress as causes of ulcer disease.
Genetic factors play a role in both duodenal and gastric ulcer.

The first-degree relatives of patients with duodenal ulcer have a two- to threefold
increase in risk of getting duodenal ulcer and relatives of gastric ulcer patients
have a similarly increased risk of getting a gastric ulcer. About half of the patients
with duodenal ulcer have elevated plasma pepsinogen I. A small increase in risk of
duodenal ulcer is found in persons with blood group O and in subjects who fail to
secrete blood group antigens into the saliva. In most Western countries, morbidity
from duodenal ulcer is more common than from gastric ulcer, even though deaths
from gastric ulcer exceed or equal those from duodenal ulcer. In Japan, both
morbidity and mortality are higher for gastric ulcer than for duodenal ulcer.

8
 CHAPTER II

LITERATURE REVIEW
A. Digestive system (gaster)

The stomach is a muscular, J-shaped organ in the upper part of the abdomen. It is
part of the digestive system, which extends from the mouth to the anus. The size
of the stomach varies from person to person, and from meal to meal.

Structure
The stomach is part of the digestive system and is connected to the:

 esophagus – a tube-like organ that connects the mouth and throat to the
stomach. The area where the esophagus joins the stomach is called the
gastroesophageal (GE) junction.
 small intestine (small bowel) – a long tube-like organ that extends from
the stomach to the colon (large intestine or large bowel). The first part of

9
 the small intestine is called the duodenum, and it is this part that is
connected to the stomach.
The stomach is surrounded by a large number of lymph nodes.

Regions of the stomach

The stomach is divided into 5 regions:

 The cardia is the first part of the stomach below the esophagus. It contains
the cardiac sphincter, which is a thin ring of muscle that helps to prevent
stomach contents from going back up into the esophagus.
 The fundus is the rounded area that lies to the left of the cardia and below
the diaphragm.
 The body is the largest and main part of the stomach. This is where food is
mixed and starts to break down.
 The antrum is the lower part of the stomach. The antrum holds the broken-
down food until it is ready to be released into the small intestine. It is
sometimes called the pyloric antrum.
 The pylorus is the part of the stomach that connects to the small intestine.
This region includes the pyloric sphincter, which is a thick ring of muscle
that acts as a valve to control the emptying of stomach contents (chyme)
into the duodenum (first part of the small intestine). The pyloric sphincter
also prevents the contents of the duodenum from going back into the
stomach.

10
Layers of the stomach wall
The stomach is made up of several layers of tissue:

 The mucosa (mucous membrane) is the inner lining of the stomach. When
the stomach is empty the mucosa has a ridged appearance. These ridges
(rugae) flatten out as the stomach fills with food.
 The next layer that covers the mucosa is the submucosa. It is made up of
connective tissue that contains larger blood and lymph vessels, nerve cells
and fibres.
 The muscularis propria (or muscularis externa) is the next layer that covers
the submucosa. It is the main muscle of the stomach and is made up of 3
layers of muscle.
 The serosa is the fibrous membrane that covers the outside of the stomach.
The serosa of the stomach is also called the visceral peritoneum.

Function
The stomach has 3 main functions:

 temporary storage for food, which passes from the esophagus to the
stomach where it is held for 2 hours or longer
 mixing and breakdown of food by contraction and relaxation of the muscle
layers in the stomach
 digestion of food
The mucosa contains specialized cells and glands that produce hydrochloric acid
and digestive enzymes to help digest food. The mucosa in the cardiac and pyloric
regions of the stomach release mucus that helps protect the lining of the stomach
from the acid produced for digestion. Other specialized cells in the mucosa of the
pylorus release the hormone gastrin into the blood. Gastrin helps to stimulate the
release of acid and enzymes from the mucosa. Gastrin also helps the muscles of
the stomach to start contracting.

Food is broken down into a thick, acidic, soupy mixture called chyme. The pyloric
sphincter relaxes once chyme formation is complete. Chyme then passes into the
duodenum. The duodenum plays a big role in absorption of the food we eat. The

11
stomach does not play a big role in absorption of food. It only absorbs water,
alcohol and some drugs.

Regulation of Acid Secretion

Parietal cells in the stomach secrete roughly two liters of acid a day in the form
of hydrochloric acid. Acid in the stomach functions to kill bacteria, and to aid
digestion by solubilizing food. The acid is also important to establish the optimal
pH (between 1.8-3.5) for the function of the digestive enzyme pepsin.

A key protein for acid secretion is the H+/K+-ATPase (or proton pump). This
protein, which is expressed on the apical membrane of parietal cells, uses the
energy derived from ATP hydrolysis to pump hydrogen ions into the lumen in
exchange for potassium ions.

Stimulation of acid secretion involves the translocation of H+/K+-ATPases to the

apical membrane of the parietal cell. When the cell is resting (not stimulated),
H+/K+-ATPases are located in vesicles inside the cell. When the cell is stimulated,
these vesicles fuse with the plasma membrane, thereby increasing the surface area

12
of the plasma membrane and the number of proton pumps in the membrane.

There are three regulatory molecules that stimulate acid secretion

(acetylcholine, histamine, gastrin) and one regulatory molecule that inhibits acid
secretion (somatostatin). Acetylcholine is a neurotransmitter that is released
by enteric neurons. Histamine is a paracrine that is released
from ECL (enterochromaffin-like) cells. Gastrin is a hormone that is released
by G cells, endocrine cells that are located in the gastric
epithelium. Somatostatin is also secreted by endocrine cells of the gastric
epithelium; it can act as either a paracrine or a hormone.

The figure (same as on the handout) shows how the positive and negative
regulators interact to stimulate acid secretion. Acetylcholine and histamine
directly stimulate parietal cells to increase acid secretion. Gastrin stimulates acid
secretion by stimulating histamine release from ECL cells. (Gastrin also has a
direct effect on parietal cells, which is to stimulate their proliferation). When the
pH of the stomach gets too low, somatostatin secretion is stimulated. Somatostatin
inhibits acid secretion by direct effects on parietal cells, and also by inhibiting
release of the positive regulators histamine and gastrin. The balance of activity of

13
the different regulators changes as food is consumed and passes through different
segments of the upper GI track.

B. Peptic Ulcer

B.1 Definition
Peptic ulcer (peptic ulcer disease) is a lesion in the stomach or duodenum caused
by an imbalance between aggressive factors (gastric acid secretion, pepsin, and
bacterial infection Helicobacter pylori) with defensive factors / protective factors
mucosa (prostagladin production, gastric mucus, bicarbonate, and mucosal blood
flow) (Berardy and Lynda, 2005).

Peptic ulcer is a state of continuity of discontinuous gastric mucosa and extends

below the epithelium. Mucous damage that does not extend to the bottom
epithelium is called erosion. Although often considered as ulcers (for example
ulcers because of stress) (Wilson and Lindseth, 2005).

The epidemiology of peptic ulcer disease largely reflects the epidemiology of the
2 major aetiologic factors, Helicobacter pylori infection and use of nonsteroidal
anti-inflammatory drugs (NSAIDs).  In the developed world, H pylori incidence
has been slowly declining over the past 50 years and NSAID use has increased.
This has resulted in a decline in duodenal ulcers and an increase in gastric ulcers.
Peptic ulcers remain common worldwide, especially in the developing world
where H pylori infection is highly prevalent.

The epidemiology of peptic ulcer has been changing over the past decades.
Indonesia was reported have a low prevalence of peptic ulcer compared to other
countries in Asia. Some studies in Indonesia have evaluated that poor sanitation,
age, religion, ethnicity are the risk factors for peptic ulcer.

Based on riset in Indonesia (2013), Annual Mortality Rate 4.6 / 100.000 people.
Annual Years of Healthy Life Lost 124.4 / 100.000 people − Change in Annual
Years of Healthy Life Lost - 32.6% in the past 20 years

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B.3 Pathophysiology
Historically, our understanding of the pathophysiology of peptic ulcer disease
focused on abnormalities in the secretion of gastric acid and pepsin, and on the
suppression of acid as a treatment strategy. Today, gastric hyper secretion—
associated with gastrinoma in Zollinger–Ellison syndrome, antral G-cell
hyperplasia, an increase in parietal-cell mass, and a physiological imbalance
between the antagonistic gastric hormones gastrin and somatostatin—is still an
important issue in peptic ulcer disease. Moreover, it is known that cholinergic
hypersensitivity and parasympathetic dominance are related to the stimulation not
only of hydrochloric acid but also pepsin, which is often neglected as a cofactor in
the development of erosive injury to the gastric mucosa. Psychologic stress,
cigarette smoking, alcohol consumption, use of nonsteroidal anti- inflammatory
drugs (NSAIDs) including aspirin, oral bisphosphonates, potassium chloride,
immuno suppressive medications, and an agerelated decline in prostaglandin
levels have all been shown to contribute to peptic ulcer disease.6 It was, however,
the isolation of H. pylori and its identification as the most important cause of
peptic ulcer disease that led to exploration of the role of inflammation and its
associated cytokine cascade in gastric acid secretion.

H. pylori evades attack by the host immune system and causes chronic, indolent
inflammation by several mechanisms. H. pylori can damage the mucosal defense
system by reducing the thickness of the mucus gel layer, diminishing mucosal
blood flow, and interacting with the gastric epithelium throughout all stages of the
infection. H. pylori infection can also increase gastric acid secretion; by producing
various antigens, virulence factors, and soluble mediators, H. pylori induces
inflammation, which increases parietal-cell mass and, therefore, the capacity to
secrete acid. The H. pylori cytotoxinassociated gene CagA also has an important
role: it interferes with gastric epithelial cell-signaling pathways, thereby
regulating cellular responses and possibly contributing to apical junction barrier
disruption, interleukin-8 secretion and phenotypic changes to gastric epithelial
cells.7 Understanding the pathophysiology of peptic ulcer disease is at something
of a crossroads: mechanisms of injury differ distinctly between duodenal and
gastric ulcers. Duodenal ulcer is essentially an H. pylori-related disease and is

15
caused mainly by an increase in acid and pepsin load, and gastric metaplasia in the
duodenal cap.8 Gastric ulcer, at least in Western countries, is most commonly
associated with NSAID ingestion, although H. pylori infection might also be
present.9 Chronic, superficial and atrophic gastritis predominate in patients with
gastric ulcers, when even normal acid levels can be associated with mucosal
ulceration.10 In both conditions, ulcer is associated with an imbalance between
protective and aggressive factors, with inflammation being a leading cause of this
imbalance. The isolation of H. pylori in the early 1980s was one of the most
exciting advances in the history of peptic ulcer disease,11 and it has dramatically
changed the management of peptic ulcer. Eradication of H. pylori infection is now
the mainstay of treatment for peptic ulcer disease, and has resulted in very high
ulcer healing rates and recurrence rates that have dropped dramatically, especially
for individuals with a duodenal ulcer. The greater recognition of the role of
NSAIDs and aspirin in gastrointestinaltract injury has led to the development of
therapeutic and preventive strategies that rely on the use of antisecretory drugs,
the prostaglandin analog misoprostol, or selective cyclo-oxygenase (COX)-2
inhibitors (coxibs).

B.4 Ethiology
Peptic ulcus risk factors:

• Helicobacter pylori,

16
• use of NSAIDs

• smoking

• food habits

B.5 Symtom
 Burning stomach pain

 Feeling of fullness, bloating or belching

 Fatty food intolerance

 Heartburn

 Nausea

The most common peptic ulcer symptom is burning stomach pain. Stomach acid
makes the pain worse, as does having an empty stomach. The pain can often be
relieved by eating certain foods that buffer stomach acid or by taking an acid-
reducing medication, but then it may come back. The pain may be worse between
meals and at night.

B.6 Diagnosis
The history and physical examination are important to identify patients at risk of
ulcer, perforation, bleeding, or malignancy. However, a systematic review of
models using risk factors, history, and symptoms found that they did not reliably
distinguish between functional dyspepsia and organic disease.

17
UREA BREATH TESTS Urea breath tests require the ingestion of urea labeled
with the nonradioactive isotope carbon 13 or carbon 14. Specificity and sensitivity
approach 100%. Urea breath testing is one option for test of cure and should be
performed four to six weeks after completion of eradication therapy. Proton pump
inhibitors (PPIs) must be stopped for at least two weeks before the test, and
accuracy is lower in patients who have had distal gastrectomy. Cost and
inconvenience are disadvantages of this test.8

TOOL MONOCLONAL ANTIGEN TESTS Stool antigen tests using

monoclonal antibodies are as accurate as urea breath tests if a validated
laboratorybased monoclonal test is used.1,11 They are cheaper and require less
equipment than urea breath tests. Like urea breath tests, stool antigen tests detect
only active infection and can be used as a test of cure. PPIs should be stopped for
two weeks before testing, but stool antigen tests are not as affected by PPI use as
are urea breath tests.

18
SEROLOGIC TESTS Serologic antibody testing detects immunoglobulin G
specific to H. pylori in serum and cannot distinguish between an active infection
and a past infection. Serologic tests may be most useful in mass population
surveys and in patients who cannot stop taking PPIs (e.g., those with
gastrointestinal bleeding or continuous NSAID use) because the tests are not
affected by PPI or antibiotic use.1,2

ENDOSCOPY WITH BIOPSY Endoscopy with biopsy is recommended to rule

out cancer and other serious causes in patients 55 years or older, or with one or
more alarm symptoms. In patients who have not been taking a PPI within one to
two weeks of endoscopy, or bismuth or an antibiotic within four weeks, the rapid
urease test performed on the biopsy specimen provides an accurate, inexpensive
means ofdiagnosing H. pylori infection.2 Patients who have been on these
medications will require histology, with or without rapid urease testing. Culture
and polymerase chain reaction allow for susceptibility testing but are not readily
available for clinical use in the United States.

B.8 Therapy of Peptic Ulcer

Non-Pharmacology

 Choose a healthy diet. Choose a healthy diet full of fruits, especially with
vitamins A and C, vegetables, and whole grains. Not eating vitamin-rich
foods may make it difficult for your body to heal your ulcer.

 Consider foods containing probiotics. These include yogurt, aged cheeses,

miso, and sauerkraut.

 Consider eliminating milk. Sometimes drinking milk will make your ulcer
pain better, but then later cause excess acid, which increases pain. Talk to
your doctor about drinking milk.

 Consider switching pain relievers. If you use pain relievers regularly, ask
your doctor whether acetaminophen (Tylenol, others) may be an option for
you.

19
  Control stress. Stress may worsen the signs and symptoms of a peptic ulcer.
Consider the sources of your stress and do what you can to address the
causes. Some stress is unavoidable, but you can learn to cope with stress
with exercise, spending time with friends or writing in a journal.

 Don't smoke. Smoking may interfere with the protective lining of the
stomach, making your stomach more susceptible to the development of an
ulcer. Smoking also increases stomach acid.

 Limit or avoid alcohol. Excessive use of alcohol can irritate and erode the
mucous lining in your stomach and intestines, causing inflammation and
bleeding.

 Try to get enough sleep. Sleep can help your immune system, and therefore
counter stress. Also, avoid eating shortly before bedtime.

Pharmacology

Treatment of PUD varies depending on the etiology and clinical presentation. The
goals of pharmacotherapy are to eradicate HPI infection, to reduce morbidity, and
to prevent complications in patients with PUD.1-4 Acid suppression is the general
pharmacologic principle of medical management of acute bleeding from a peptic
ulcer, using histamine-2 receptor antagonists and proton pump inhibitors (PPIs)
(table 2).2

20
Medications can include:

Medications that block acid production and promote healing. Proton

pump inhibitors — also called PPIs — 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).

Long-term use of proton pump inhibitors, particularly at high doses, may

increase your risk of hip, wrist and spine fracture. Ask your doctor whether a
calcium supplement may reduce this risk.

Medications to reduce acid production. 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.

Available by prescription or over-the-counter, acid blockers include the

medications ranitidine (Zantac), famotidine (Pepcid), cimetidine (Tagamet
HB) and nizatidine (Axid AR).

Antacids that neutralize stomach acid. Your doctor may include an

antacid in your drug regimen. Antacids neutralize existing stomach acid and
can provide rapid pain relief. Side effects can include constipation or
diarrhea, depending on the main ingredients

Antacids can provide symptom relief, but generally aren't used to heal your
ulcer.

Medications that protect the lining of your stomach and small

intestine. In some cases, your doctor may prescribe medications called
cytoprotective agents that help protect the tissues that line your stomach and
small intestine.

21
 Options include the prescription medications sucralfate (Carafate) and
misoprostol (Cytotec).

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. These may include amoxicillin (Amoxil), clarithromycin
(Biaxin), metronidazole (Flagyl), tinidazole (Tindamax), tetracycline
(Tetracycline HCL) and levofloxacin (Levaquin).

The antibiotics used will be determined by where you live and current
antibiotic resistance rates. You'll likely need to take antibiotics for two
weeks, as well as additional medications to reduce stomach acid, including a
proton pump inhibitor and possibly bismuth subsalicylate (Pepto-Bismol).

The 2017 ACG guidelines for the treatment of H pylori infection have
reaffirmed testing for HPI before starting NSAID therapy. 3 The suggested
primary therapy for HPI is PPI–based triple therapy. Antacids or a GI
cocktail, classically an antacid with an anesthetic, such as viscous lidocaine
and/or an antispasmodic, may be used as symptomatic therapy in the
emergency department.2,3 Maintenance treatment with H2 blockers and/or
PPIs for 1 year is indicated in high-risk patients.2,3

The ACG guidelines indicate that selection of an HPI management regimen

should take into account previous antibiotic exposure(s). The ACG also
includes the following therapeutic strategies for first- line treatment3:

 Ten to 14 days of bismuth quadruple therapy (bismuth, a PPI, tetracycline,

and a nitroimidazole), especially in those with previous macrolide
exposure or who are penicillin allergic (strong recommendation)
 Ten to 14 days of a concomitant PPI, clarithromycin, amoxicil- lin, and a
nitroimidazole (strong recommendation)

 Fourteen days of clarithromycin triple therapy (clarithromycin, a PPI, and

amoxicillin or metronidazole) should be reserved for patients with no

22
 previous history of macrolide exposure who live in regions where
clarithromycin resistance among H pyloriisolates is known to be low
(<15%)(conditional recommendation)

 Five to 7 days of sequential therapy with a PPI and amoxicillin, followed

by 5 to 7 days with clarithromycin, a PPI, and a nitroimidazole
(conditional recommendation)

 Seven days of a hybrid therapy with a PPI and amoxicillin, followed by 7

days with a PPI, amoxicillin, clarithromycin, and a nitroimidazole
(conditional recommendation)

 Ten to 14 days of levofloxacin triple therapy (levofloxacin, a PPI, and

amoxicillin)(conditional recommendation)

 Five to 7 days of fluoroquinolone sequential therapy (a PPI and

amoxicillin), followed by 5 to 7 days of a PPI, fluoroquinolone, and
nitroimidazol (conditional recommendation)

23
B.7 Algorithm

A. Noncompliance increases with duration and with number of drugs employed.

24
B. Cost = Average wholesale price based -10% for brand products and Maximum
Allowable Cost (MAC) + $3 for generics on 30-day supply or less, Amerisource
AWP 01/05 & Blue Cross Blue Shield of Michigan Mac List, 01/31/05.
C. PPIs for PPI triple therapy: Omeprazole 20 mg bid ($3/day generic; $8/day
brand) or Lansoprazole 15 or 30 mg bid (both $9/day brand).
D. H2 blockers with conventional triple therapy: Cimetidine 400 mg bid ($1/day
generic; $3/day brand), Famotidine 20 mg bid ($1/day generic; $4/day brand),
Nizatidine 150 mg bid ($1/day generic; $6/day brand), or Ranitidine 150 mg bid
($1/day generic; $4/day brand)
E. PPIs with conventional triple therapy: Lansoprazole 15 or 30 mg daily ($9/day
generic & brand) or Omeprazole 20 mg daily ($3/day generic; $8/day brand)

CHAPTER III

DISCUSSION
A. What are the functions and mechanisms of each drug

1. Ringer lactate is an infusion fluid commonly used in adult and children patients
as a source of electrolytes and water for hydration.

2. Paracetamol is used to relieve pain. This drug has activity as an analgesic, but
its anti-inflammatory activity is very weak. Paracetamol is more tolerable for
patients who have a history of digestive disorders, such as excessive gastric acid
secretion and gastric bleeding, compared to aspirin.

3. Omeprazole is a drug to treat stomach and esophageal problems caused by

stomach acid. The way it works is by lowering the acid levels produced by the
stomach.
25
4. -Domperidone is a drug used to relieve nausea, vomiting or stomach problems.

-Domperidone is a dopamine antagonist which peroferal works selectively at D2

receptors.

5. Ceftriaxone is an antibiotic drug with a function to treat various types of

bacterial infections. Ceftriaxone belongs to an antibiotic class called
cephalosporin which works by stopping bacterial growth.

6. -Tanexamic acid is a drug that affects blood. Fibrinolytic drugs that inhibit the
termination of the fibrin thread. Tranexamic acid is used for prophylaxis and
treatment of bleeding caused by excessive fibrinolysis and angioedema of
heredity.

- Tranexamic acid works by blocking plasminogen and plasmin bonds against

fibrin; This inhibition of plasmin is very limited to a certain level

{Department of health}

B. Comparison, which drug is better ppi or h2 blocker (along with EBM)

Proton Pump Inhibitor (PPIs,) when compared to Histamine-2-Receptor

Antagonists (H2RAs), lower the risk of clinically important and overt GI bleeding
among critically ill patients. Based on journal below:

26
PPIs, more potent at increasing gastric pH than H2RAs and maintaining gastric
pH between 3.5 and 5.0, may minimize the risk of gastric mucosal injury [10]. Of
four meta-analyses comparing PPIs to H2RAs, three suggested that PPIs are
superior to H2RAs] and one did not.

C. Whether the use of trexenamic acid and cetriaxone drugs is correct ? how
the solution

Cetriaxone antibiotics; iv prophylactic therapy is recommended, it is used if it is

resistant to quinolone goals and liver cirrhosis.

As traxenamic: there is no evidence of upper saline bleeding, ppi can for bleeding
Pud can maintain pH above 6 can reduce gastroinestinal bleeding.

Same as PPI, there are benefits but still need to be studied.

Comparison of Ppi and H2Ra, the result is that Ppi is more effective in treating
gastrointestinal both major and minor bleeding.

27
D.Role of the Pharmacist

Pharmacists should be prepared to answer patients’ concerns and be familiar with

the basics of PUD. They can screen for possible drug/ drug interactions and
contraindications as well as counsel patients on the proper use of pharmacological
agents used for the treatment of PUD, including adverse effects. Patients
experiencing worsening symptoms should be directed to immediately seek
medical care to prevent further complications.
Yvette C. Terrie, BSPharm, RPh is a consultant pharmacist and medical writer
based in Haymarket, Virginia.

And also the pharmacist should give information about

Patients should be warned of known or potentially injurious drugs and agents.
Some examples are as follows:

 nonsteroidal anti-inflammatory drugs (NSAIDs)

 Aspirin
 Tobacco
 Caffeine (eg, coffee, tea, colas)
Obesity has been shown to have an association with peptic ulcer disease (PUD),
and patients should be counseled regarding benefits of weight loss. Stress
reduction counseling might be helpful in individual cases but is not needed
routinely.
For patient education resources, see Digestive Disorders Center as well as Peptic
Ulcer, Heartburn, and GERD and Heartburn Medications.

28
 CHAPTER IV

CONCLUSION
Peptic ulcer is a disease caused by disorders of the gastrointestinal tract above
caused by excessive secretion of acid and pepsin by the gastric mucosa (Avunduk,
2008).

Helicobacter pylori is known to be the main cause of stomach ulcers, besides

NSAIDs and a rare cause is Zollinger Ellison Syndrome and disease Chron
disease (Sanusi, 2011). These bacteria are present in the gastric mucosa and also
found on the surface of the epithelium in the gastric antrum (Hadi, 2013). Study at
Indonesia shows a relationship between the level of environmental sanitation to
prevalence of H. pylory infection and an estimated 36-46.1% of the population
has been infected with H. pylory (Rani & Fauzi, 2006).

Peptic ulcer treatment is intended to improve the quality of life of patients,

eliminate complaints, cure ulcers, prevent recurrence and complications (Sanusi,
2011). The most appropriate treatment choice for peptic ulcer disease depending
on the cause. Drug combination therapy is needed for ulcer disease peptic. A
combination of two types of antibiotics with PPI (Proton Pump Inhibitor) or
bismuth used for H. pylory eradication therapy, while the combination of H2
receptor antagonists, PPI or sucralfate can be used for therapy caused by NSAIDs.

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 BIBLIOGRAPHY
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