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DISPEPSIA

Primary regions of gastric


acid-related disease
Acid reflux
Oesophagitis
Strictures
Barretts
oesophagus
Oesophageal
adenocarcinoma

Gastritis
Peptic ulcer
disease
(Includes NSAIDinduced ulcers)

Duodenitis
Duodenal ulcer

Functional
dyspepsia

Defines :
Abdominal

symptoms : discomfort, pain,


aching, bloating, fullness, burning, or
indigestion

Definition of dyspepsia (Rome II)

Pain or discomfort occurring


in the upper abdomen
Dyspepsia subgroups

Ulcer-like (predominantly pain)

Dysmotility-like (predominantly discomfort)

Unspecified (non-specific, no predominant


symptom)
Talley et al., Gut 1999; 45(Suppl II): II3742.
Malfertheiner, Eur J Gastroenterol Hepatol 1999; 11(Suppl 1): S259.

Dyspepsia covers a range of symptoms

GORD

DYSPEPSIA
PAIN OR DISCOMFORT

IBS

centred in upper abdomen

UNINVESTIGATED

INVESTIGATED
ORGANIC

FUNCTIONAL
(or idiopathic)
(use of the term non-ulcer
is discouraged)

Talley et al., Gut 1999; 45(Suppl II): II3742.

Dyspepsia:
the size of the problem
1525% of the general population experience dyspepsia within
a 12-month period
Much more common than peptic ulcer
Up to 5% of primary care visits are due to dyspepsia
Most patients have no detectable abnormality on radiological
upper GI series or endoscopy
Endoscopy findings and symptoms do not correlate

Talley, J Clin Gastroenterol 2001; 32: 28693.


Locke, Ballieres Clin Gastroenterol 1998; 12: 43542.
Par, Can J Gastroenterol 1999; 13: 64754.
van Bommel et al., Postgrad Med J 2001; 77: 51418.
Talley et al., BMJ 2001; 323: 12947.

Dyspepsia:
pathogenic mechanisms
Dysmotility
H. pylori infection/
inflammation

Altered gastric
acid secretion
Mechanisms of
dyspepsia

Psychosocial
factors

Gut hypersensitivity
Witteman & Tytgat, Netherlands J Med 1995; 46: 20511.
Talley et al., BMJ 2001; 323:12947.
Tack et al., Curr Gastroenterol Rep 2001; 3: 5038.

Dyspepsia:
symptom assessment
Nature of symptoms
Character
Radiation
Timing, duration
and frequency
Modifying factors

Patients degree
of distress

Severity of
symptoms

Assessment
of symptoms

Alarm features

Par, Can J Gastroenterol 1999; 13: 64754.

Table. Causes of chronic dyspepsia


Disease

Clues on clinical evaluation

Functional (non-ulcer) dyspepsia


Chronic peptic ulceration

Young patient; no alarm features


NSAID use; Helicobacter pylori-positive serologically;
smoker; history of bleeding or anemia
Heartburn or acid regurgitation dominant complaint
Advanced age at onset; alarm features such as
weight loss; H.pylori positive serologically

Gastro-oesophageal reflux
Gastric cancer
Miscellaneous:
Biliary tract disease
Chronic pancreatitis
Intestinal angina
Diabetes mellitus
Drugs

Biliary type pain


Constant pain; radiates to back; alcohol abuse;
diabetes mellitus
Only postprandrial pain; afraid to eat; weight loss;
smoker
History of diabetes; other diabetic complications
Theophylline; iron; potassium; digoxin; antibiotics

Important to distinguish the terms:

Dyspepsia encompasses all relevant upper


abdominal symptoms regardless of their underlying
cause
Uninvestigated D : refers to new onset or recurrent
D for which no diagnostic investigation yet have
been performed and therefore a specific diagnosis
has not been determined
Functional D: refers to persistent or recurrent D for
which diagnostic investigation (including endoscopy)
has not determined an obvious organic cause of
symptoms

Uninvestigated dyspepsia
vs functional dyspepsia
Uninvestigated dyspepsia

All symptomatic patients, regardless of whether a


cause
has been sought

Functional dyspepsia

Symptomatic patients in whom


an organic cause has been
sought and excluded

Talley et al., Gut 1999; 45(Suppl II): II3742.

Management of
uninvestigated
dyspepsia

GP management of
uninvestigated dyspepsia

No alarm features (and/or <45 years?)

Alarm features (and/or >45 years?)

Symptom-based diagnosis
4 weeks therapy based on predominant symptom

Refer/investigate

Treat accordingly
Responders

Non-responders/early relapses
1st-line investigation (13CUBT/stool test)

H. pylori +ve
Eradication therapy

Responders

H. pylori -ve

Non-responders
2nd-line investigation Increase doses/combination therapies

Stanghellini, 2001.

The Maastricht European Consensus Guidelines on the


management of dyspeptic patients in primary care
Dyspeptic patient
First primary care visit
Age <45 years* without
alarm symptoms
Review patients history
Test for H. pylori
13C-UBT or
Laboratory serology

Age 45 years or with alarm


symptoms (irrespective of age)
Refer to
gastroenterologist

* The cut-off age may be below 45 years,

If H. pyloripositive,
treat the infection

depending on regional differences in the


incidence of gastric malignancy

The European Helicobacter Pylori Study Group 1997

When to refer
Presence of alarm symptoms
Failure to respond to appropriate therapy
Patients 45 years of age with new-onset
symptoms

Talley et al., Gut 1999; 45(Suppl II): II3742.


Talley et al., BMJ 2001; 323: 12947.
Bytzer & Talley, Ann Intern Med 2001; 134: 81522.

Treatment options in functional dyspepsia

Acid inhibition

Muco-protective
agents

Functional
Functional
dyspepsia
Dyspepsia
Prokinetic
motility agents

H. pylori eradication
Phytotherapeutics
Carminatives
Anti-depressants
Anti-serotoninergics
Opioids
Talley et al., Aliment Pharmacol Ther 1999; 13: 113548.
Talley et al., Gut 1999; 45(Suppl II): II3742.

Nyeri Perut Berulang


(Recurrent Abdominal Pain/RAP)
Chronic

abdominal Pain (CAP) : nyeri perut


lebih dari 3 bulan terus menerus atau
kambuh-kambuhan)
RAP : nyeri perut lebih dari 3 bulan tidak
berlangsung terus menerus namun intermiten.
Prevalensi :

Anak-anak >10%
Dewasa : 2% terutama wanita sebagain besar
keluhan GI kronis (NUD & gangguan usus)

CAP

: biasanya fungsional : adanya gejalagejala nyeri perut berhubungan GI pada


pemeriksaan fisik, struktur maupun
biokimiawi tidak ditemukan kelainan
CAP :

FAPS / FGID 90%


CAP 10%
(Collins & Thomas Pediatric in Review, 2007)

Kriteria diagnostik FGID :


Kriteria

Roma III : gejala sudah terjadi seja 6


bulan dan harus aktif saat ini (harus
memenuhi kriteria selama 3 bulan)
FGID :

Dyspepsia fungsional
IBS
Kelainan kandung empedu fungsional

(Chang, 2006; Mustafa, 2008)

Kriteria Diagnostik Roma III


Dyspepsia Fungsional (Chang, 2006)
Paling

sedikit dalam waktu 3 bulan pada 6


bulan terakhir terdapat 1 atau lebih gejala
dibawah ini :

Rasa penuh setelah makan


Cepat kenyang
Nyeri epigastrik
Rasa terbakar di ulu hati
Tidak ada penyakit yang mendasari (endoskopi
atas)

IBS (Kriteria Diagnostik Roma III)


Paling

sedikit dalam waktu 3 bulan pada 6


bulan terakhir,nyeri abdomen berulang atau
tasa tida enak di perut, yang terdiri dari 2
atau lebih gejala dibawah ini :

Perubahan pola BAB dan / atau


Perubahan fulmen BAB, dan / atau
Perubahan bentuk feses

Patofisiologi

2006)

FGID gambar 1 (Crowell,

Terapi FGID

Tegaserol efek pada serotonin

Acute depresan : trisiklik efek langsung pada usus


mengurangi somatisasi
Kolesistokinin (CCK) : IBS tipe C
Probiotik : perubahan mikroflora usus

IBS tipe C
DF
GERD

IBS tipe D
Dispepsia

Bifidobacterium

Kesimpulan
Nyeri

perut berulang sebagian besar


fungsional, pemeriksaan endoskopi
atas/bawah tidak ditemukan kelainan.
Peranan endoskopi untuk diagnosis sangat
penting dilakukan lebih-lebih bila ada tandatanda bahaya.
Terapi sesuai gejala-gejalanya.

PEPTIC ULCER DISEASE


(PUD)
Siti Nurdjanah

Peptic Ulcer Disease (PUD)


Peptic

Ulcer (gastric and duodenal)


Defect in the gastrointestinal mucosa that
extend through the muscularis mucosa

Pathofisiology
PUD

: the end result of an imbalance


between aggressive and defensive factors in
the gastro duodenal mucosa

AGGRESSIVE FACTORS
Acidic
environment

Mucus layer
Ionic gradient
Bicarbonate layer
Prostaglandins

Gastric
NSAIDs Bile acid

H. pylori
Pepsin

Neutral environment

Surface epithelial
cells
Mucosal blood
supply

PROTECTIVE FACTORS
Imbalanced between aggressive factors and protective factors

Clinical Features of PU

Abdominal pain common


Epigastric pain :

Burning
Discomfort

Typical pain pattern DU :

Occurs 90 mn to 3 hr after meal frequently relieved by


antacids or food
Awakes the patients from sleep (midnight 3 A.M)
Discomfort precipitated by food
Nausea weight loss

The mechanism of pain


unknown
1.

2.

Acid induced activation of clinical receptors in


duodenum enhanced duodenal sensitivity to
bile acids and pepsin
Altered gastro duodenal motility :
Variation in the intensity or distribution of the abdominal
pain indicative of an ulcer complication

Dyspepsia constant no longer relieved by food


or antacids or radiation to the back penetrating
ulcer (pancreas)
Sudden onset of severe perforation
Pain worsening with meal, nausea, vomiting of
undigested food suggesting gastric outlet
obstruction

Diffential Diagnosis
Non

ulcer dyspepsia
GI tumors
GERD
Vascular disease
Pancreatobiliary disease
Gastro duodenal Cohn's disease

Diagnosis

Predictive value of abdominal pain poor for the


presence of a gastro duodenal ulcer
A radiographic ( barium study)

Single-contrast barium meals sensitivity defecting DU :


80%
Double contras sensitivity 90%

DU : appears as a well demarcated scarring


GU : as a discrete crater with radiating mucosal folds
originating from the ulcer margin

Diagnosis
Endoscopy

most sensitive and specific

Gambar H. pylori

Table 1. Test for detection of H.pylori


Test

Sensitivity/specifity, %

Comments

INVASIVE (ENDOSCOPY/BIOPSY REQUIRED)


Rapid urease

80 - 95/95 100

Histology

80 90/>95

Culture

--/--

Simple, false negative with recent use of PPIs,


antibiotics, or bismuth compounds
Requires pathology processing and information
Time-consuming, expensive, dependent on
experience; allows determination of antibiotic
susceptibility

NON-INVASIVE
Serology

>80/>90

Urea breath test

>90/>90

Stool antigen

>90/>90

Inexpensive, convenient; not useful for early follow-up


Simple, rapid; useful for early follow-up; false
negatives with recent therapy (see rapid urease test);
exposure to low-dose radiation with 14C test
Inexpensive, convenient; not established for
eradication but promising

Table2. Drugs used in the treatment of Peptic Ulcer Disease


Drug type/Mechanism
Acid-suppressing drugs
Antacids
H2 receptor antagonists

Proton pump inhibitors

Mucosal protective agents


Sucralfate
Prostaglandin analogue
Bismuth-containing
compounds

Examples

Dose

Mylanta, Maalox, Tums,


Gaviscon
Cimetidine,
Ranitidine,
Famotidine,
Nizatidine
Omeprazole,
Lansoprazole,
Rabeprazole,
Pantoprazole,
Esomeprazole

100-140 meq/L 1 and


3 h after meals and hs
400 mg bid
300 mg hs
40 mg hs
300 mg hs
20 mg/d
30 mg/d
20 mg/d
40 mg/d
20 mg/d

Sucralfate
Misoprostol
Bismuth sub-salicylate (BSS)

1 g qid
200 g qid
See anti H.pylori regimens

Table3. Regimens Recommended for Eradication


of H.pylori Infection
Drug

Dose

TRIPLE THERAPY
1.

2.

3.

Bismuth subsalicylate plus


Metronidazole plus
Tetracycline
Ranitidine bismuth citrate plus,
Tetracycline plus,
Clarithromycin or metronidazole
Omeprazole (lansoprazole) plus,
Clarithromycin plus
Metronidazole or Amoxicillin

2 tablets qid
250 mg qid
500 mg qid
400 mg bid
500 mg bid
500 mg bid
20 mg bid (30 mg bid)
500 mg bid
1 gr bid

QUADRUPLE THERAPY
Omeprazole (lansoprazole)
Bismuth subsalicylate
Metronidazole
Tetracycline

20 mg (30 mg) daily


2 tablets qid
250 mg qid
500 mg qid

GASTRITIS

Gastritis

Inflammation of the gastric mucosa should be


reserve for histologically documented
Gastritis :

is not the mucosal erythema seen during endoscopy


Is not interchangeable with dyspepsia

Classification of gastritis based on:

Time course
Histology features
Anatomical distribution

Table. Classification of gastritis


I.
A.
B.

Acute Gastritis
Acute H.pylori infection
Other acute infectious gastritides
1. Bacterial (other than H.pylori)
2. Helicobacter helmanni
3. Phlegmonous
4. Mycobacterial
5. Syphilitic
6. Viral
7. Parasitic
8. Fungal

II. Chronic atrophic gastritis


A.
Type A: Autoimmune bodypredominant
B.
B. Type B: H.pylori-related, antralpredominant
C.
Indeterminant
III. Uncommon Forms of Gastritis
A.
Lymphocytic
B.
Eosinophilic
C.
Cohn's disease
D.
Sarcoidosis
E.
Isolated granulomatous gastritis

Acute gastritis

The most common causes: infectious H.pylori


histologic mucosal:

Marked infiltrate of neutrophils


Edema
Hyperemia

Bacterial infection phlegmonous gastritis: diffuse


acute inflammatory infiltrates of the entire gastric
wall.
Causes: Streptococci, Staphylococci, E-coli,
Proteus, Haemophilus sp.

Chronic gastritis
Histologic

mucosal : inflammatory cell


infiltrate: lymphocytes, plasma cell, with very
scant neutrophil involvement.
Distribution of inflammation: patchy,
superficial and glandular portions of the
gastric mucosa progress glandular
destruction, atrophy and metaplasia.
Classification of chronic G accoding to
histologic characteritis

Superficial atrophic
Gastric atrophy

Early phase of chronic gastritis & superficial gastritis


inflammatory changes : limited to the lamina propria
of the surface mucosa, edema and cellular infiltrates
separating intact gastric glands decrease mucus
and mitotic figures in the gland cells.
Atropy gastritis: inflammatory infiltrate extends
deeper into the mucosa progressive distortion and
destruction of the glands.
Gastric atrophy: glandular structures are lost
endoscopically the mucosa: substantially their,
permitting clear visualization of the underlying blood
vessels.

Type A gastritis

Less common
The predominant site: fundus and body, with antral
sparing
This form associate with permicious anemia
Antibody to parietal cell detected in > 90% of
patients with permicious anemia and in up to 50% of
patients with type A gastritis
Is also called autoimmune gastritis
Gastric and plays role in feedback inhibition of
gastrin release from G cells. Achlorhydric, conpled
with relative sparing of the antral mucosa (site G
cells) hypergastrinemia.

Type B gastritis
Antral-predominant
More

common
H.pylori infection is the cause of this entity

Histologically
The

quantity of H.pylori is highest and a


dense chronic inflammatory infiltrate of the
laminapropria.
Epithelial cell infiltration with pmn lenkocytes
Multifocal atrophic gastritis, gastric atrophy
with subsequent metaplasia development
of gastric adenoca.