Disturbances of

GastroIntestinal Tract (GIT)

(peptic ulcer disease; gerd; erosive esophagitis; dyspepsia)

Erwin Budi Cahyono

Department of Internal Medicine
School of Medicine UNISSULA
Islamic Teaching Hospital SULTAN AGUNG
 THE GASTROINTESTINAL TRACT - function

 Ingestion of food
 Digestion
- mechanical digestion of food particles
- breaks up food particles
 Motility
- movements of organs and food
- mechanical digestion of food particles
 Secretion
- secretion of digestive juices
- chemical digestion of food particles
 Absorption
- absorption of digestion products to
blood or lymphatic vessels
 Storage and Elimination
- non-digested food particles
 Protective function – mechanical, chemical, immunological
- not only GIT organs but also the body as a whole, against the potential harmful food
components
THE GASTROINTESTINAL TRACT - function
CARBOHYDRATE DIGESTION AND ABSORPTION
PROTEIN DIGESTION AND ABSORPTION
FAT DIGESTION AND ABSORPTION
THE GASTROINTESTINAL TRACT - absorption
THE GASTROINTESTINAL TRACT - structure
 DISORDERS OF THE DIGESTIVE SYSTEM

• Disorders of the digestive system have serious consequences for the activity of
the organism as a whole
 congenital malformations  traumatic processes
 inflammatory processes  neoplastic processes
 infectious processes

• Digestive system communicates with the external environment through the

intake of fluids and food

 Toxic substances in food and fluids

 GIT itself contains toxic substances - secretion components - enzymes, HCl
- waste products of digestion of food, bacterial
flora
THE MOST COMMON DISORDERS of the digestive system

 Motor dysfunction of smooth muscle of the individual parts of the digestive

system

 Indigestion of food and absorption of nutrients - malabsorption syndrome

 Bleeding into the individual parts of the digestive tract

 Perforation of the wall of the digestive system with subsequent leakage of the
contents to the peritoneal cavity

 Obstruction in moving of the contents of one part of the digestive system to the
next section

 Circulation disorders in the wall of the individual parts of the digestive system
 CLINICAL MANIFESTATIONS of GI dysfunction

 Vomiting
 Dyspepsia
 Constipation
 Diarrhea
 Abdominal Pain
 Gastrointestinal Bleeding
 Disorders of the GastroIntestinal Tract

Esophagus Intestinal system

 Dysphagia  inflammatory bowel disease
 Achalasia  Crohn disease
 Gastroesophageal reflux  Ulcerative colitis
 Colon Cancer

Stomach  Ileus

 Gastritis
 Peptic Ulcer
 Gastric Cancer
 Disorders of the GIT - GASTROESOPHAGEAL
REFLUX DISEASE (GERD)

 Gastroesophageal reflux disease (GERD)

is the reflux of acid and pepsin from the
stomach to the esophagus that causes
esophagitis.

• HCl, pepsin and bile - induce mucosal

inflammation, erosion and ulceration

• It is a consequence of weaken function of the lower esophageal sphincter, delayed

gastric emptying with an increase in the pressure of its content and weaken
clearing function of the esophagus (lack of saliva, poor esophageal peristalsis, and
decreased production of the esophageal mucosal glands).
 GASTROESOPHAGEAL REFLUX DISEASE (GERD)

Clinical manifestation:
− heartburn, chronic cough, asthma attacks
− abdominal pain (within 1 hour after meals, repeating)
− symptoms may worsen if the individual lies down, or in
the case of increasing intra-abdominal pressure (as a
result of coughing, vomiting, or of hard stool)
− symptoms may be present even if the acid is not present
in the esophagus

− heartburn can be seen as chest pain, which requires the exclusion of cardiac
ischemia
 Disorders of the GIT – PEPTIC ULCER

- is a result of imbalance between the

mucosal defense mechanisms in the
esophagus, stomach and duodenum,
and gastric mucosa-damaging
mechanisms

- relates to digestion of mucous

membrane and lower parts of the
stomach, duodenum, and lower
esophagus by HCl and pepsin
 PEPTIC ULCER

Risk factors for peptic ulcer disease:

• genetic predisposition
• H.pylori infection of the gastric
mucosa
• age greater than 65 years
• psychologic stress (mechanism
unknown)
• excessive use of alcohol
• smoking
• acute pancreatitis
• chronic obstructive pulmonary
disease
• obesity
• cirrhosis
PEPTIC ULCER
 EPITHELIAL GASTRODUODENAL BARRIER

• Mucus-bicarbonate barrier
− smooth adhesive mucus layer
− pH gradient (lumen – epithelial surfice)
− bicarbonate secretion by epithelial cells

• H+ disposal in gastric wall

− mucoid barrier damage
− back diffusion of H+ into the wall
− mucosal blood flow

• Proliferation and epithelial repair

− mitosis and cell migration along the basal membrane
− mucoid cap after epithelial damage
Disorders of the GIT – PEPTIC ULCER
 Outline
• Terminologi GERD
• Faktor-faktor presipitasi GERD
• Diagnosis GERD
• Alur penegakkan diagnosis GERD
• Terapi non medikamentosa
• Terapi medikamentosa
 The American College of Gastroenterology (ACG)
guidelines define gastroesophageal reflux disease
(GERD) as “symptoms or complications resulting
from the reflux of gastric contents into the
esophagus or beyond, into the oral cavity
(including larynx) or lung.”
 What is GERD

 A condition that occurs when

the lower esophageal
sphincter (LES) does not close
properly and stomach
contents leak back, or reflux,
into the esophagus.

 The LES is a ring of muscle at

the bottom of the esophagus
that acts like a valve between
the esophagus and stomach.
 Prevalence of GERD

 Gastroesophageal reflux disease (GERD) characterized

by heartburn and/or regurgitation symptoms is one of
the most common gastrointestinal disorders managed
by gastroenterologists and primary care physicians.
There has been an increase in GERD prevalence,
particularly in North America and East Asia.
How many people are affected?
 GERD is one of the most prevalent gastrointestinal disorders

 Heartburn is a significant problem in Western societies

 Annual prevalence of GERD is between 10 % and 23%1 and is

increasing

– about 25% of individuals have heartburn and/or regurgitation

at least once a month

– about 15% have symptoms at least once a week

– about 7% have symptoms daily

 Reflux symptoms are less common in East Asian populations

1Eslick GD et al., J Clin Gastroenterol. 2009;43(2):111-7

ID/PAN/2017-00035
 Causes of GERD
• Abnormalities with the
Lower Esophageal
Sphincter, or LES
• Stomach Abnormalities
–Hiatal hernia
Figure 1 A simple overview of the pathogenesis of gastroesophageal reflux disease.

GI Motility online (May 2006) | doi:10.1038/gimo21

 Reflux of acid is the dominant irritant to the esophagus in the
development and progression of GERD, although the presence of
bile and other compounds in gastric juice may contribute to the
"reflux burden" when combined with the acid or on their own.
The reflux burden of acid requires the presence of acid
secretion, and is further determined by dysfunction of the
gastroesophageal competence mechanism that allows increased
reflux, and by decreased esophageal clearance that increases
contact time of acid with the mucosa. However, there are a
number of relevant issues that arise in regard to gastric acid
secretion and the development of GERD.
Release of Gastric Acid
 Release of Gastric Acid
• Histamine stimulates
acid release by
interacting with the
histamine receptor, H2
• Acetylcholine activates
the cholinergic
receptors
• Gastrin is released
when food is present in
the stomach
 Figure 2 Gastroesophageal reflux disease initiates a vicious cycle of increasing
esophageal acid exposure.

GI Motility online (May 2006) | doi:10.1038/gimo21

Other factors that may contribute to GERD

• Alcohol use
• Overweight
• Pregnancy
• Smoking
 Certain foods can be associated with reflux events

• Citrus fruits
• Chocolate
• Drinks with caffeine
• Fatty and fried foods
• Garlic and onions
• Mint flavorings
• Spicy foods
• Tomato-based foods, like spaghetti sauce, chili, and pizza
 What are the symptoms of GERD

The cardinal symptoms of GERD are heartburn and regurgitation.

However, GERD may present with a variety of other symptoms,
including water brash (sudden excess of saliva), chest pain or
discomfort, difficulty or pain when swallowing, belching,
epigastric pain, nausea, and bloating.
In addition, patients may experience extraesophageal symptoms
like dry cough, hoarseness, throat clearing, choking or throat
tightness, throat pain or burning, wheezing, and sleep
disturbances.
 Range of Presentation GERD

Typical Symptoms
(Heartburn/ Atypical Symptoms Complications
Regurgitation)

With Chest pain Oesophageal

Oesophagitis (visceral errosions
hyperalgesia) & or ulcers
without Hoarseness strictures
Oesophagitis (“reflux
laryngitis) Barrett’s
Asthma, Oesophagus
Chronic cough,
wheezing Oesophageal
dental adenocarcinoma
Natheo, Int J Clin Pract errosions
2001 ; 55 :465-9
 The Montreal New Definition of GERD 2006

The Global Definition of GERD :

•GERD is a condition which develops when the reflux of stomach
contents causes troublesome symptoms and/ or complications
•Symptoms related to gastro-esophageal reflux become
troublesome when they adversly affect an individual’s well-being
•Reflux symptoms that are not troublesome should not be
diagnosed as GERD
•In Clinical Practice, the patients should determine if their reflux
symptoms are troublesome

Schoeider HR. GERD. The Montreal definition and classification. SA Fam Pract 2007;49(1):19-26
 The Montreal Definition of GERD 2006
GERD is a condition which develops when the reflux
of stomach content causes trouble some symptoms
and/or complications

Extra-Esophageal
Esophageal
Syndromes
Syndromes

Syndromes with Established Proposed

Symptomatic
Esophageal Association Association
Syndromes
injury

Pharingitis
Typical Reflux Refluks Esophagitis Reflux Cough
Sinusitis
Reflux Stricture Reflux Laryngitis
Syndromes Barrett’s Esophageus Reflux asthma Idiopathic
Reflux Chest Adenocarcinoma Reflux dental Erotion Pulmonary Fibrosis
Pain Syndromes Recurrent Otitis
Media

Vakil N et al. Am J Gastroenterol 2006;101:1900-1920

HOW IS GERD DIAGNOSED ?
GERD diagnosis
Initial management of patients with symptoms suggestive of GERD

Symptom-based
diagnosis enGERD
Alarm
features
Risk Endoscopy ERD
assessment

CRD
Empirical
therapy

enGERD : non-erosive GERD

ERD = erosive reflux disease Labenz J and Malfertheiner P. World J Gastroenterol 2005; 11: 4291–9
CRD = complicated reflux disease
ID/PAN/2017-00035
 Alarm features
• Dysphagia
• Odynophagia (painful swallowing)
• Recurrent bronchial symptoms, aspiration pneumonia
• Dysphonia
• Recurrent or persistent cough
• Gastrointestinal tract bleeding
• Frequent nausea and/or vomiting
• Persistent pain
• Iron-deficiency anemia
• Progressive unintentional weight loss
• Lymphadenopathy
• Epigastric mass
• New-onset atypical symptoms at age 45–55 years. A lower age threshold
may be appropriate, depending on local recommendations.
• Family history of either esophageal or gastric adenocarcinoma.
Tools in diagnosing and managing GERD

National consensus on the management of GERD in Indonesia, 2013

ID/PAN/2017-00035
 GERD management algorithm
Symptoms suggestive of GERD
(burning retrosternal pain responding to antacids)
PPI therapy for 1 year, age <40 years
Alarm symptoms?
and/or lifestyle reasons**

Long-term medical therapy

Increase dose
(with episodic attempts to reduce the dose)

NO Yes
Persistant/recur Symptoms Asymptomatic

Maintain for 3 months Discontinue medication

Antacids and simple antireflux measures No/mild PPI low

(eg, raising bed, weight loss, avoidance of esophagitis Maintain for 3 months Symptoms Remit Reduce to half dose
dose
precipitating foods and drugs)
Symptoms persistent Symptoms
and/or nocturnal remit

Mod/severe
esophagitis or PPI full dose PPI full dose and Maintain for 3 months
Symptoms Nocturnal Laparoscopic fundoplication
troublesome prokinetic
persist predominance Surgery**
symptoms
Diagnostic EGD Maintain for 3 months Resection

No dysplasia Surveillance programme

Barrett’s
PPI Symptoms persist or recur esophagus
Dysplasia* Low grade Surveillance at 1 year

Maintain on treatment
Symptoms controlled 4 weeks, then stop High grade
High-dose PPI for 3 months,
then repeat biopsy Low grade
No symptoms
Other
diagnoses Manage as appropriate
High grade
No further measures

EGD = esophagogastroduodenoscopy Modlin IM and Sachs G (eds). Acid-related diseases:

* By 2 expert independent pathologists Biology and treatment. Philadelphia, USA: Lippincott
** Decided by patient after joint consultation with physician Williams and Wilkins, 2004: 1–522
and/or surgeon ID/PAN/2017-00035
enGERD algorithm

Initial therapy and long-term care of patients with enGERD

Symptom
resolution
On-demand
enGERD PPI for 2–4 weeks therapy

Troublesome symptoms
Failure: after 4-week PPI
Symptom Symptoms
resolution persistent
Double-dose Prolongation of
Step down
PPI (bid) for 4 weeks therapy

Symptoms persistent Symptom resolution

pH-metry during therapy

Step down
 individual care
enGERD : non-erosive GERD
Labenz J and Malfertheiner P. World J Gastroenterol 2005; 11: 4291–9
ID/PAN/2017-00035
 Mild-to-moderate EE algorithm

Management of patients with mild-to-moderate erosive esophagitis/EE

LA grade A/B
esophagitis

Symptoms Full-dose PPI Symptoms

controlled (4 weeks) persistent
Symptoms
controlled
Trial withdrawal Double-dose PPI (bid)

Symptoms persistent
Symptomatic relapse
Clinical course Patient preference Reassess symptoms
pH monitoring

Intermittent Continuous Antireflux

PPI therapy PPI therapy surgery

*Includes stepdown Labenz J and Malfertheiner P. World J Gastroenterol 2005; 11: 4291–9
 Moderate-to-severe EE algorithm

Management of patients moderate to severe esophagitis

LA grade C/D
esophagitis

Symptoms Full-dose PPI Symptoms

controlled (8 weeks) persistent
Symptoms
Continue full- or controlled Double-dose PPI (bid)
double-dose PPI (8 weeks)

Symptoms persistent

Patient preference Reassess symptoms

pH monitoring
Surgeon skill

Continuous Antireflux Higher dose

PPI therapy* surgery PPI
*Individual dose titration Labenz J and Malfertheiner P. World J Gastroenterol 2005; 11: 4291–9
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 Endoscopy

ID/PAN/2017-00035
Esofagogastroduodenoskopi
The Los Angeles Classification System for the endoscopic
assessment of reflux oesophagitis

GRADE A:
One or more mucosal breaks no
longer than 5 mm, non of which
extends between the tops of the
mucosal folds
The Los Angeles Classification System for the endoscopic
assessment of reflux oesophagitis

GRADE B:
One or more mucosal breaks
more than 5 mm long, none
of which extends between
the tops of two mucosal folds
The Los Angeles Classification System for the endoscopic
assessment of reflux oesophagitis

GRADE C:
Mucosal breaks that extend
between the tops of two or more
mucosal folds, but which involve
less than 75% of the oesophageal
circumference
The Los Angeles Classification System for the endoscopic
assessment of reflux oesophagitis

GRADE D:
Mucosal breaks which involve
at least 75% of the
oesophageal circumference
Endoscopic view of GERD complications
 How is GERD treated?

• Lifestyle Changes
• Medications
New treatments
• Surgery
 Treatment guidelines: American College of
Gastroenterologists
Recommendation Level of
evidence
Although lifestyle modifications may benefit some GERD patients, alone they are 4
unlikely to control symptoms in most patients
Patient-orientated therapy for symptoms: antacids and OTC acid suppressants 4

Acid suppression is the mainstay of therapy for GERD. PPIs are superior to H2RAs, 1
although the latter may be effective in some patients with less severe GERD
Promotility agents may be used in some patients adjunctive to acid suppression 2

Continuous therapy to control symptoms and prevent complications is appropriate 1

Antireflux surgery is a maintenance option for those with well-documented GERD 2

Endoscopic therapy controls symptoms in some patients with well-documented 3

GERD
GERD refractory to medical therapy is rare. Diagnosis should be carefully 4
confirmed (ambulatory pH testing) before antireflux surgery

1. Strong evidence from systematic review of RCTs; 2. Strong evidence from an RCT; 3. Evidence from
non-randomized trials; 4. Evidence from well designed nonexperimental studies
DeVault KR and Castell DO. Am J Gastroenterol 2005; 100: 190–200
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 Lifestyle Changes
• If you smoke, stop.
• Do not drink alcohol.
• Lose weight if needed.
• Eat small meals.
• Wear loose-fitting clothes.
• Avoid lying down for 3 hours after a meal.
• Raise the head of your bed 6 to 8 inches by putting
blocks of wood under the bedposts--just using extra
pillows will not help.
 Lifestyle modifications

 Weight reduction

 Sleeping with the head of the bed elevated

 Elimination of factors that increase abdominal pressure

 Patients should not smoke

 Patients should avoid

X
X Coffee
X Alcohol
Fatty
foods ID/PAN/2017-00035
 Medications

• Antacids:
– Maalox,
– Mylanta Magnesium salt can lead to diarrhea, and
aluminum salts can cause constipation
– Pepto-Bismol
– Rolaids

• H2 blockers
– Cimetidine
– Famotidine
– Ranitidine
 Medications

• Proton pump inhibitors

– omeprazole
– lansoprazole
– pantoprazole
– rabeprazole
– esomeprazole

• Prokinetics

– Metoclopramide
– Domperidone
GERD : Clinical Management

Initial Long-Term
Management Management
 Mainstream Options for Therapy of GERD
Highest Efficacy
2x daily PPI + H2RA

2x daily PPI
Recommended
1x daily PPI

1x daily ½ PPI
Current

guidelines Prokinetic + H2RA

Prokinetic Or H2RA
Should be Antacide + lifestyle
abandoned
Antacide
Lowest Efficacy
Lifestyle

*no clear dose-response established After Dent et al. Gut 1999 (Suppl 2)
 GERD : Long Term Management

Continuous daily
Step down to therapy
Empirical
The Lowest dose
therapy Intermittent Courses
That Controls of therapy
Successful
symptoms On-demand
therapy

Dent & Talley, Aliment Pharmacol Ther 2003 (Suppl 1)

Dent et al. Gut 2004 (Suppl 4)
Effects of GERD drugs
 New Treatments
• Cholecystokinin2 receptor
antagonists (CCK2)
• Potassium competitive acid
blockers (P-CABs)
 Surgery

most commonly Nissen fundoplication

 stomach is wrapped around

the esophagus to create an
antireflux barrier

Poorer-than-anticipated outcomes1, 2

1Vakil N et al., Am J Med 2003;114:1-5

2Rantanen TK et al., Am J Gastroenterol 1999;94:1777-81
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PEPTIC ULCER DISEASE
 Objectives
• Definition of peptic ulcer
• Comparison of duodenal & gastric ulcers
• Aetiology
• Clinical presentation
• Medications
• Helicobacter pylori infection
What is a peptic ulcer?
 PEPTIC ULCER
A break in superficial epithelial cells penetrating down to muscularis mucosa
 Differences between duodenal &
gastric ulcers?

DUODENAL GASTRIC
INCIDENCE

ANATOMY

DURATION (acute/chronic)

MALIGNANCY
 Duodenal vs Gastric

DUODENAL GASTRIC
INCIDENCE More common Less common

ANATOMY First part of duodenum – Lesser curvature of stomach

anterior wall
DURATION Acute or chronic Chronic

MALIGNANCY Rare Benign or malignant

Risk factors of peptic ulcer disease
• HELICOBACTER PYLORI
• Non Steroidal Anti-inflammatory Drugs
• Steroid therapy
• Smoking
• Excess alcohol intake
• Genetic factors
• Zollinger Ellison syndrome – rare syndrome caused by
gastrin-secreting tumour
• Blood group O
• Hyperparathyroidism
 Helicobacter pylori infection
• Urease producing, gram negative bacillus
• Developing countries
• Infection increases with age
• Infects mucosa of stomach > inflammatory
response > gastritis > increased gastrin
secretion > gastric metaplasia > damage to
mucosa > ulceration
• Increased risk of developing gastric
adenocarcinoma
 Symptoms of PUD
• Asymptomatic
• Epigastric pain
• Nausea
• Oral flatulence, bloating, distension and
intolerance of fatty food
• Heartburn
• Pain radiating to the back
 ALARM signs for epigastric pain
• Chronic GI bleeding
• Iron-deficiency anaemia
• Progressive unintentional weight loss
• Progressive dysphagia
• Persistent vomiting
• Epigastric mass
• Patients aged 55 years and older with
unexplained and persistent recent- onset
dyspepsia alone
Mechanism urea breath test
UREA IS A NITROGEN-CONTAINING COMPOUND THAT IS
PRODUCED DURING DECARBOXYLATION OF THE AMINO
ACID ARGININE IN THE UREA CYCLE. UREA IS A MAJOR
ORGANIC WASTE PRODUCT OF PROTEIN DIGESTION IN
MOST VERTEBRATE AND IS EXCRETED IN URINE. SOME
BACTERIA HAVE THE ABILITY TO PRODUCE AN ENZYME
UREASE AS PART OF ITS METABOLISM TO BREAK DOWN
UREA. THE UREASE IS A HYDROLYTIC ENZYME WHICH
ATTACKS THE CARBON AND NITROGEN BOND WITH THE
LIBERATION OF AMMONIA AND CARBON DIOXIDE. IT IS A
USEFUL DIAGNOSTIC TEST FOR IDENTIFYING BACTERIA,
SUCH AS HELICOBACTER PYLORI
 H pylori investigations
• C urea breath tests

• Stool antigen tests

• Serology
• Endoscopy with biopsy
 DYSPEPSIA
• DEFINITION :

Symptoms like pain or nausea in epigastrium

accompanied by disgust, vomit, bloat, easy to
full, fullness or nitre, which is suspected come
from the abnormality of upper gastro-
intestinal tractus.
 Dyspepsia:
pathogenic mechanisms

Dysmotility
H. pylori infection/ Altered gastric acid
inflammation secretion

Mechanisms of
dyspepsia

Psychosocial Gut hypersensitivity

factors
Witteman & Tytgat, Netherlands J Med 1995; 46: 205–11.
Talley et al., BMJ 2001; 323:1294–7.
Tack et al., Curr Gastroenterol Rep 2001; 3: 503–8.
 Dyspepsia:
symptom assessment

Nature of symptoms Severity of

Character symptoms
Radiation
Timing, duration
and frequency
Modifying factors
Assessment
of symptoms

Patient’s degree Alarm features

of distress

Paré, Can J Gastroenterol 1999; 13: 647–54.

 Classification
• acute dyspepsia (new onset dyspepsia)
– Suddenly Sigh with the quality of sigh which is
usually more tremendous with a longer response
to the medication.
• chronic dyspepsia
– Sigh which is sometimes disappear, sometimes
appear, more than two weeks. The sigh is not as
tremendous as acute dyspepsia with a quick
response to the medication.
 Ethiology

• Organic Dyspepsia :
– There is an organ abnormality as ulcer gastro-
duodenal, gastro esofageal reflux and gastric
carcinoma (Talley, 1998)
 Functional Dyspepsia
 A common term which is given to the patient as : abdominal
pain or nausea on the upper of stomach which is repeatedly
happen more than three months, and at least a long of that
time 25% symptoms of dyspepsia appear and no evidence
organic disease which is responsible to that symptoms
clinically, biochemistrically, endoscopy and ultrasonografy
(Talley et al, 1991). But, patient with gastritis and duodenitis
non erosif is included in this term (Hu & Kren, 1998)
 Rome III Diagnostic Criteria for Functional
Dyspepsia
Functional Dyspepsia
At least 3 months, with onset at least 6 months previously,
of 1 or more of the following:
• Bothersome postprandial fullness
• Early satiation
• Epigastric pain
• Epigastric burning
And
•No evidence of structural disease (including at upper
endoscopy) that is likely to explain the symptoms
 Rome III Diagnostic Criteria for Epigastric
Pain Syndrome
Epigastric Pain Syndrome
At least 3 months, with onset at least 6 months previously, with ALL of
the following:
Pain and burning that is:
• intermittent
• localized to the epigastrium of at least moderate severity, at least once
per week,
• and NOT:
generalized or localized to other abdominal or chest regions
2. relieved by defecation or flatulence
3. fulfilling criteria for gallbladder or sphincter of Oddi disorders
 Rome III Diagnostic Criteria for
Postprandial Distress Syndrome
Postprandial Distress Syndrome
At least 3 months, with onset at least 6 months
previously, of 1 or more of the following:
• Bothersome postprandial fullness
1. occurring after ordinary-sized meals
2. at least several times a week
• Early satiation
1. that prevents finishing a regular meal
2. and occurs at least several times a week
 Management of dyspepsia
• NICE guidance for dyspepsia
 Medications

• Antacids:
– Maalox,
– Mylanta Magnesium salt can lead to diarrhea, and
aluminum salts can cause constipation
– Pepto-Bismol
– Rolaids

• H2 blockers
– Cimetidine
– Famotidine
– Ranitidine
 Medications

• Proton pump inhibitors

– omeprazole
– lansoprazole
– pantoprazole
– rabeprazole
– esomeprazole

• Prokinetics

– Metoclopramide
– Domperidone