Dyspepsia

Agung F. Sumantri, dr, SpPD

Departemen Penyakit Dalam
FK UNISBA

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 Dyspepsia is a term usually only used
by medical practitioners.

Definision : Dyspepsia is persistent or

recurrent pain or discomfort
centred in the upper abdomen

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 Definitions & Etiology

Dyspepsia : syndrome or symptom

complex consisting of episodic epigastric
pain (often associated with bloating,
distention, and eructation with or without
cramping), which is precipitated by the
ingestion of food.

4 weeks
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 dyspepsia
 structural abnormality (40%) :
- peptic ulcer (25%)
- reflux esophagitis
- gastric cancer
- biliary and pancreatic disorders

 Functional (60%)
- POSTPRANDIAL DISTRESS SYNDROME
- EPIGASTRIC PAIN SYNDROME

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 Rome III
They consist of one or more of the following symptoms :
a. Bothersome postprandial fullness
b. Early satiation
c. Epigastric pain
d. Epigastric burning
AND
No evidence of structural disease (including at upper
endoscopy) that is likely to explain the symptoms.

Criteria fulfilled for the last 3 months

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Ulcer and Nonulcer Dyspepsia
Distinguishing ulcer dyspepsia from nonulcer
dyspepsia is clinically important
Because:
• Patients with ulcer are easily treated & their
dyspepsia typically resolves
• Nonulcer dyspepsia have a variety of
potential causes for their pain none of
which is easily treated.

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Causes of nonulcear dyspepsia
- Erosive esophagitis
- Gastric cancer
- Hepatobiliary disease
- Pancreatitis
or
Nongastrointestinal disease (eg, pyelonephritis) and
functional dyspepsia such as
Nonerosive esophageal disease
Motility disorders
Nongastrointestinal disorders (eg, psychiatric Illness)

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 Functional Dyspepsia

Is a disorder of GI function resulting in a

dyspeptic syndrome

May result from :

 motility disturbance
 phychiatric disorder
 unknown

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 Dyspepsia Subtypes
Dominant
Subtype Symptomps Comments
Ulcer-like Abdominal pain Cannot distinguish ulcer
dyspepsia pain clinically

Motility-like Bloating and gas May overlap with irritable

dyspepsia production bowel syndrome

Reflux-like Heartburn May be similar to

dyspepsia nonerosive reflux disease

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 Symptom-based dyspepsia subgroups

SUBGROUP CLINICAL FEATURES

Ulcer-like Localised epigastric pain
Pain relieved by food
Pain relieved by antacids
Hunger pain
Night pain (waking the patients from sleep )
Episodic pain
Dysmotility-like Early satiety
Postprandial fullness
Nausea
Retching and/or vomiting
Upper abdominal bloating
Discomfort aggrarated by food
Unspecified Symptoms not compatible with ulcer-like or
dysmotility-like subgroups

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 Pathophysiology

Although the pathogenesis dyspepsia

remains unknows, a number of
physiological factors appear to be
associated with the disorder. Most
attention has been directed towards
assessment of upper gut sensorimotor
function.

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PATHOPHYSIOLOGY

1. Acid Hypersecretion
2. Motor disorders
3. Abnormal visceral perception
4. Psychologic factors
5. Gastritis
6. Environmental agents

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 Factors Supporting and Opposing Pathophysiologic Mechanisms of
Dyspepsia

Mechanism Supporting Opposing Studies

Relative acid Helicobacter pylori-positive patients have Patients with nonulcer dyspepsia Nyren
Hypersecretion a graded increase in acid output produce normal amounts of acid Talley
Acid hypersensitivity reported in some Antisecretory agents fail to El-Oemar
studies prevent pain after acid Collen
stimulation in some studies George
Bates

Motor disorders Various specific manometric abnormalities Correction of motor abnormalities Nyren
have been identified does not correlate with Talley
symptomatic responses Tucci
Duodenogastric reflux is not Waldron
more common in patients with Malagelada
Dyspepsia Jian
Bost

Abnormal Gastric ballon distension causes Studies involving therapeutic Nyren

visceral symptoms blocking agents are lacking Talley
Perception Mearin
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Psychologic Psychologic distress and sexual abuse No characteristic personality Nyren
factors are more common in patients with profile exists Talley
dyspepsia Life-event stresses are not Talley
increased

Gastritis Mucosal inflammation is pathologic Resolution fails to alter Nyren

Patients commonly report associations symptoms convincingly or Talley
between foods and symptoms reverse motility abnormalities El-Omar
Malferteiner
Pieramico
Talley

Environmental NSAIDs commonly cause distress, often Studies do not reliabily Nyren
agents without endoscopic changes demonstrate an association Talley
between specific foods and Talley
Dyspepsia

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 CLINICAL FEATURES

Typical presentation : epigastric pain – usually

occurring in relation to meals
Associated symptoms – GIT
postprandial bloating
heartburn
nausea
vomiting

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Differential Diagnosis

Peptic ulcer disease

Biliary tract disease
Pancreatic disease

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 Differential diagnosis of upper abdominal pain or
discomfort
“ORGANIC”
 Cronic peptic ulcer (gastric ulcer,
duodenal ulcer)
 Gastro-oesophageal reflux disease
(with or without oesophagitis)
 Drugs/medications
 Symptomatic cholelithiasis
 Cronic pancreatitis
 Malignancy (gastric, pancreatic,
colonic)
 Mesenteric vascular insufficiency
 Metabolic causes (eg uraemia, hyper-
calcaemia, diabetes mellitus with
gastroparesis)
 Abdominal wall pain
“FUNCTIONAL DYSPEPSIA”
 Sensorimotor dysfunction of
gastroduodenum :
- idiopathic gastroparesis/gastric
antral hypomotility
- gastric dysrhythmias
- gastric/duodenal hypersensitivity
 Psychosocial factors :
- chronic life stress
 ? H, pylori gastritis
 Idiophatic
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 Possible pathogenesis of of chronic
duodenal ulcer
Duodenal acid load
increased

Gastric metaplasia H. Pylori gastritis

H. Pylori colonisation Increased gastrin

Of duodenum ?? role

Active duodenitis Other factors

Duodenal ulcer
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A rapid urease test

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 Diagnostic tests for H. pylori

METHODS ADVANTAGES DISADVANTAGES USEFULNESS

Noninvalsive
Serology Noninvalsive, Requires validation Initial diagnosis,
relatively cheap in local patient epidemiology
population
14C urea breath test Rapid, allows Involves ingestion of Initial diagnosis,
distinction between radioactivity follow-up of
acute & past treatment
infection regimens
13C urea breath test No radioactivity, as Complex equipment, Initial diagnosis,
for 14C expensive follow-up of
treatment
regiment

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Invasive
Rapid urease test Rapid, inexpensive Invasive Initial diagnosis

Histology Allows assessment Invasive, costly Assess gastritis,

Of mucosa metaplasia &
atrophy etc. initial
diagnosis

Culture Specificity: 100% Invasive, costly, Initial diagnosis,

Slow, less sensitive antimicrobial
sensitivities, strain
typing

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Schematic representation of the 14C and 13C
breath test.

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 Treatment of H. pylori: current regimens
REGIMEN DOSE DURATION ERADICATION
RATE

Proton pump inhibitor combination:

Omeprazole 20 mg bid 2 weeks 80-90 %
or lansoprazole 30 mg bid
- plus amoxycillin 1000 mg bid
- plus clarithromycin 500 mg bid
2 week 80-90 %
Omeprazole 20 mg bid
- plus clarithromycin 500 mg bid
- plus metronidazole 500 mg bid

2 weeks 80-90 %
Bismuth combinations:
Bismuth subsalicylates 525 mg qid
- plus tetracycline 500 mg qid
- plus metronidazole 250 mg qid
- plus PPI

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 Investigations

Early endoscopy

Helicobacter pylori-guided endoscopy

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 Therapy for Dyspepsia
Antisecretory agents
H2-receptors antagonists (eg, cimetidine, ranitidine)
Proton pump inhibitors (eg, omeprazole, lansoprazole)
Prokinetics
Metoclopramide
Domperidone
Cisapride
Anti-Helicobacter pylori theraphy
Bismuth salts
Antibiotics
Anticholinergics (with or without benzodiazepines)
Tricyclic antidepressants (eg, amitriptyline)
Other
Serotonergic agent (eg, fedotozine)
Fiber
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 PRIMARY MANAGEMENT OF NEW ONSET
UNINVESTIGATED DYSPEPSIA IN INDONESIA
EXCLUDE BY HISTORY ; IF < 2 – 4 WKS.
BILIARY PAIN, IRRITABLE DYSPEPSIA DIETARY ADVICE, OBSERVE
BOWEL, REFLUX REVIEW CURRENT MEDS

AGE > 55 YRS AGE > 55 YRS

WITHOUT ALARM FEATURES WITH ALARM FEATURES :
SEVERE VOMITING
FEVER
TREATMENT TRIAL : 2 WKS HEMATEMESIS / MELENA
SUCCESS
'ANTACIDS ICTERUS
'ANTISECRETORY  BW
'PROKINETICS FOLLOW UP NSAIDs
STRONG FEAR OF SERIOUS DIS.
FAILURE OR FAMILY HISTORY : GASTRIC CA
EARLY RELAPSE RELAPSE

SEROLOGIC Hp TESTING SPECIALIST REFERAL :

GASTROENTEROLOGIST
INTERNAL MED./PED.WITH
NEG POS ENDOSCOPIC FACILITIES
FINAL EVALUATION AFTER 8 WKS
> 3 X RELAPSE Page 26
 MANAGEMENT OF DYSPEPSIA IN REFFERAL CENTER
DYSPEPSIA

FROM ALGORHYTM 1 UGI ENDOSCOPY CLO TEST, PA

CLO (+), PA (+) CLO (-), PA (+) CLO (+), PA (-) CLO (-), PA (-)

CASE SELECTION
NO ERADICATION
EMPIRIC TREATMENT
ERADICATION THERAPY
FIND OTHER CAUSES

SUCCESS EVALUATION 4 EKS FAILURE

AFTER ERADICATION

REEVALUATE : ENDOSC., PA, CLO FAILURE

QUADRUPLE TREATMENT
REEVALUATE : ENDOSC., PA, Hp CULTURE

Hp ERADICATION ACCORDING
TO THE RESISTANCY TEST Page 27
Page 28
Alarm symptoms :

Age > 50 yrs

Family history of digestive malignancy
Involuntary weight loss
Gastrointestinal bleeding of feriprive anemia
Progressive dysphagia
Odinophagia
Recurrent vomiting
Palpable tumor or adenopathy
Icterus

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 GERD

(Gastro-Esophageal Reflux Disease)

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Definition :
Symptoms or mucosal damage produced
by the abnormal reflux of gastric contents
into the esophagus

Cardinal symptoms :
Heartburn & regurgitation& dysphagia
 AS : chest pain, water brash
(Hypersalivation), globus sensation,
odynophagia (Esophageal ulcer), nausea

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Diferential diagnosis
Another esophagitis (Inf, eosinophilic)
Peptic ulcer
CAD
Esophageal motor disorder

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 Who gets reflux disease?
*Inherited and acquired factors both contribute to
the development of GERD.
*The prevalence of reflux symptoms is high in the
parents of affected people, and in identical twin
pairs than it is in non-identical twin pairs.
*Genetic factors contribute 18-31% to the cause
of GERD.
*Lifestyle factors. Smokers are more likely to have
reflux symptoms.
*Obesity is also associated with GERD; Moreover
obese people tend to eat larger meals and choose
rich, energy dense foods , dietary factors that
increase the risk of reflux.
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 In contrast, although patients often
think that coffee, chocolate, and
alcohol can trigger symptoms

*Advice on lifestyle, such as stopping smoking,

losing weight, and avoiding large, late meals can
reduce the frequency and severity of reflux
symptoms, although it is rare for these
measures to remove the need for acid
suppression.

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 Why does reflux occur?
*Everybody experiences gastro-oesophageal reflux
at some time.
*In health, reflux of air (belching) occurs during
transient relaxations of the lower oesophageal
sphincter triggered by gastric distension (bloating).
Small volumes of ingested food and gastric acid may
pass into the oesophagus during such episodes.
*But GERD is present only when the reflux of
gastric contents causes frequent, severe symptoms
or mucosal damage

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Why does reflux occur?

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Dignostic tools
Esophagoscopy
Ambulatory esophageal PH monitoring
Esophageal manometry
Bernstein test
Hystology
Radiography vs endoscopy

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 Endoscopic findings in GERD

NERD.
65%
Barrett's Esoph.
10%
ERD
25%

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Classification
Savary-Miller classification
• Grade I exhibits one or more supravestibular,
non-confluent reddish spots, with or without
exudate
• Grade II demonstrates erosive and exudative
lesions in the distal esophagus that may be
confluent, but not circumferential
• Grade III is characterized by circumferential
erosions in the distal esophagus, covered by
hemorrhagic and pseudomembranous exudate
• Grade IV is defined by the presence of chronic
complications such as deep ulcers, stenosis, or
scarring with Barrett's metaplasia

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Los Angeles classification
• Grade A — one or more mucosal breaks each ≤
5 mm in length
• Grade B — at least one mucosal break >5 mm
long, but not continuous between the tops of
adjacent mucosal folds
• Grade C — at least one mucosal break that is
continuous between the tops of adjacent
mucosal folds, but which is not circumferential
• Grade D — mucosal break that involves at least
three-fourths of the luminal circumference

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 Extraesophageal disorders in GERD

Extraesophageal manifestations of gastroesophageal reflux disorder

(GERD) are frequent, and consist broadly of

• Noncardiac chest pain

• pulmonary diseases
– Asthma
– chronic cough
– recurrent bronchitis
– sleep apnea
– pulmonary fibrosis
• laryngeal diseases
– Laryngitis
– subglottic stenosis
– laryngeal cancer
• other ENT (ear, nose, throat) disorders
– Sinusitis
– Otitis media
– Pharyngitis
– dental erosion

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 Noncardiac chest pain is associated with GERD

• Among patients with angina-like chest pain

– 30% will have normal coronary arteries; of these, 40% to 50% have
objective evidence of GERD by endoscopy or ambulatory pH monitoring

• Prevalence of GERD symptoms is 23% to 100%

• Esophagitis is seen in 0% to 47%

• Abnormal ambulatory pH recordings noted in 20% to 63%

• Empiric trial of PPI

– 78% sensitivity and 86% specificity , for diagnosing GERD association with
noncardiac chest pain.

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 Diagnosis

• The majority of patients with extraesophageal

manifestations of GERD do not have the classic
symptoms of heartburn or regurgitation

• less than 30% have endoscopic evidence of reflux

esophagitis

• Twenty-four-hour pH monitoring has been commonly

used to look for evidence of acid reflux into the lower
esophagus, upper esophagus, and pharynx. However,
this test is not comfortable for most patients

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Mempertahankan pH >4 adalah penting untuk
penatalaksanaan GERD

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 pH > 4 memegang peranan penting dalam
aktivitas pepsin
Aktivitas maksimum pepsin (%)
100

80

60

40

20

0
1 2 3 4 pH asam lambung
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Berstad A. Scand J Gastroenterol 1970;5:343-8
 Lama mempertahankan pH >4 berbanding lurus
dengan angka kesembuhan pasien GERD
Pasien sembuh
setelah 8 minggu (%)
100

80

60

40

20

0
2 4 6 8 10 12 14 16 18 20 22
Lama pH lambung >4 ( jam)
Joelson & Johnson. GUT 1989; 30:1523-1525
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Bell et al. Digestion 1992;51 Suppl1:59-67
 Efikasi pengontrolan asam lambung pada pH > 4
antar PPI berbeda

Data hari ke-5, penelitian five-way crossover pada pasien GERD

esomeprazole 40 mg 15,3 **
sekali sehari *

rabeprazole 20 mg 13,3
sekali sehari
n=34
omeprazole 20 mg 12,9
sekali sehari
*** p=0,0004 vs rabeprazole;
p<0,0001 vs lansoprazole,
lansoprazole 30 mg 12,7
omeprazole dan pantoprazole
sekali sehari

pantoprazole 40 mg 11,2
sekali sehari
0 5 10 15 20
Lama pH lambung >4 (jam)
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Miner P et al. Am J Gastroenterol 2006;101:404–406
 Esomeprazole mengatasi gejala lebih cepat
dibandingkan PPI oral lainnya

Kahrilas
5 hari p < 0,05 Esomeprazole 40 mg
et al.1 sekali sehari
n=1304 9 hari
omeprazole 20 mg sekali
sehari
Castell
7 hari p  0,01 lansoprazole 30 mg sekali
et al.2
n=5241 8 hari sehari

pantoprazole 40 mg
sekali sehari
Labenz 6 hari p < 0,001
et al.3
n=3151 8 hari
*Sustained symptom resolution:
Pasien bebas heartburn selama
0 7 hari berturut-turut
1 2 3 4 5 6 7 8 9 hari
Lama pasien mengalami sustained symptom resolution*

1Kahrilas PJ, et al. Aliment Pharmacol Ther 2000;14:1249–1258, 2 Castell, et al. Am J Gastroenterol 2002;97(2):575–
583, 3 Labenz, et al. Aliment Pharmacol Ther 2005;21:739–746

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 Coclusions

 Gastroesophageal reflux is extremely common and may

manifest with typical and atypical symptoms.

 At present it is extremely difficult to establish a definite

diagnosis of extraesophageal GERD.

 Typical esophageal symptoms (heartburn, regurgitation)

may be absent in a large number of patients.

 Neither the type of ENT symptoms nor the ENT findings

are of predictive value in determining underlying GERD.

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 Conclusions

 Although interesting new modalities for reflux testing are available

(capsule pH monitoring, impedance testing) it remains to be seen
whether these modalities improve diagnostic accuracy

 Currently, the most cost-effective approach for most patients with

suspected reflux-related symptoms is a trial of a high-dose proton-
pump inhibitor for 3 months.

 pH testing reserved to confirm adequate acid suppression in those

with refractory symptoms.

 Although improvement in cough symptoms may be evident within 2

weeks of treatment, improvement in other ENT disorders may
require 3 or more months of therapy.

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