Acid Related Disease_Acid Related Disease

Acid Related Disease.ppt

1. ACID RELATED DISEASES

2. Acid Related Disease
Acid Related Disease
Upper
GI Bleeding
Functional
Dyspepsia
Gastroduodenal
ulcus
GERD
Stress Ulcer
Wolfe MM. Gastroenterology 2000;118:S9-S31

3. DYSPEPSIA
Talley et al. Am J Gastroenterol 2005;100:2324–2337)
Dyspepsiaisdefinedaschronicor
recurrentpainordiscomfortcenteredinthe
upperabdomen
Discomfortisdefinedasasubjective
negativefeelingthatisnonpainful,andcan
incorporateavarietyofsymptoms
includingearlysatietyorupperabdominal
fullness
Patientspresentingwithpredominantor
frequent(morethanonceaweek)heartburn
oracidregurgitationshouldbeconsidered
tohavegastroesophagealrefluxdisease
(GERD)untilprovenotherwise.

4. DIAGNOSTIC TESTING
patients more than 55 yr old, or those with alarm features should
undergo prompt endoscopy to rule out peptic ulcer disease,
esophagogastric malignancy, and other rare upper gastrointestinal
tract disease.
In patients aged 55 yr or younger with no alarm features
test and treat for H. pylori using a validated noninvasive test and
a trial of acid suppression if eradication is successful but
symptoms do not resolve
an empiric trial of acid suppression with a proton pump
inhibitor (PPI) for 4–8 wk.
The test-and-treat option is preferable in populations with
a moderate to high prevalence of H. pylori infection (≥10%), whereas
the empirical PPI strategy is preferable in low prevalence situations.
Talley et al. Am J Gastroenterol 2005;100:2324–2337

5. Management of Dyspepsia Uninvestigated
Dyspepsia (uninvestigated)
Age > 55 or alarm
features
Age < 55
No alarm features
EGD
HP prevalence
< 10%
HP prevalence
> 10%
PPI trial
Test and treat
for H pylori
Consider EGD
Test and treat
For H pylori
PPI Trial
Consider EGD
Fails
Fails
Fails
Fails
Talley et al. Am J Gastroenterol 2005;100:2324–2337)
EGD: Esophagogastroduodenoscopy

6. EMPIRIC ANTISECRETORY THERAPY IN
UNINVESTIGATED DYSPEPSIA
In H. pylori-negative cases with uninvestigated dyspepsia
and no alarm features, an empiric trial of acid suppression
for 4–8 wk is recommended first-line therapy
1985 H2 receptor antagonist for 6–8 wk
PPIs replace H2RANow
There are limited data that prokinetic therapy employed as an
empiric strategy may be efficacious in uninvestigated dyspepsia
Talley et al. Am J Gastroenterol 2005;100:2324–2337)

7. MANAGEMENT OF DOCUMENTED
FUNCTIONAL DYSPEPSIA
Onceadiagnosisoffunctionaldyspepsiaisconfirmedbyanegative
endoscopy,anempirictrialoftherapyiscommonlyprescribed
Manypatientsdonotrequiremedicationfordyspepsiaaftertheyhave
hadreassuranceandeducationsuchasHigh-fatmealsshouldbeavoided;
eatingfrequentandsmallermealsthroughouttheday
Antacidsandsucralfatewerenotsuperiortoplaceboinfunctional
dyspepsiabasedonaCochranereview
ACochranereviewof8trialsofH2receptorantagonistswith1,125
patientsshowedarelativeriskreductionof30%butthequalityofthe
trialswasgenerallypoor
PPIsinthisreviewalsoproducedarelativeriskreductionof
approximately30%andthequalityofthetrialswasbetter
Talley et al. Am J Gastroenterol 2005;100:2324–2337)

8. SKEMAPENATALAKSANAAN PASIEN
DI PELAYANAN KESEHATAN LINI PERTAMA
DISPEPSIA
ENDOSKOPI
Terapi dihentikan
Tidak ada sarana
Umur < 45 tahun tanpa tanda-
tanda bahaya
Usia > 45 atau < usia 45 tahun
dengan tanda-tanda bahaya
DISPEPSIA(-)
Terapi Eradiksi
SEROLOGI (Tervalidasi secara lokal)
DISPEPSIA (+)
Terapi empiris selama 2 minggu
-Antasid
-H2 antagonis
Penghambat Pompa Proton (PPI)
-Obat-obat prokinetik
Hasil (+)
Hasil (-)
RUJUK
Internis, internis plus,
Gastroenterologist atau dokter
anak dengan fasilitas endoskopi
UBT/HpSA
Hasil (-) Hasil (+)
Gagal

9. SKEMA PENATALAKSANAAN PASIEN DISPEPSIA OLEH
GASTROENTEROLOGIS/INTERNIS DENGAN FASILITAS ENDOSKOPI
DISPEPSIA
Umur > 45 tahun Tanda
bahaya/alarm
Gagal terapi
Riwayat ulkus peptikum +
komplikasi
Permintaan pasien
Pengguna aspirin / NSAID
Gastroeshopageal Reflux Disease
(GERD)
Tidak YA
UBT/HpSA
Hasi
l (-)
Hasi
l (+)
ENDOSKOPI
PemeriksaanRapid Urease Test
(CLO, MIO, Prontodry*)
Histopatology
Hasil (-)Hasil (+)
Terapi Eradikasi Terapi Simtomatik
Reevaluasi diagnostik
GagalTerapi Simtomatik

10. Peptic Ulcer
Apepticulcerisadeepandsharplydemarcatedbreakinthe
liningofthestomachorduodenum–wheninthestomachit
isdescribedasagastriculcerandwhenintheduodenuma
duodenalulcer.
Themostcommoncausalfactorinthisdamageisinfectionof
thestomachwiththebacteriumHelicobacterpylori.
Theothermajorcauseofpepticulcerdisease,particularly
gastriculcerdisease,istheuseofnonsteroidalanti-
inflammatorydrugs

11. Treatment of H.pylori Infection
First choice treatment ~ Triple Therapy
•PPI (standard dose bid), clarithromycin (500 mg bid), amoxicillin (1000 mg bid) or
metronidazole (400 or 500 mg bid), 14 day treatment is more effective than 7days (by
12% (95% confidence interval 7% to 17%).
•A seven day treatment may be acceptable where local studies show that it is effective
•Combination options
•PPI-clarithromycin-amoxicillin or metronidazole treatment if less than 15–20%
population resistance to clarithromycin
•PPI-clarithromycin-metronidazole is preferable, if less than 40% population
metronidazole resistance
Malfertheiner P et al. Gut 2007;56:772-781

12. Second choice treatments ~ Quadruple treatments
•Bismuth-containing quadruple treatments remain the best second
choice treatment
•PPI-amoxicillin or tetracycline and metronidazole are
•recommended if bismuth is not available
Treatment of H.pylori Infection
Malfertheiner P et al. Gut 2007;56:772-781
Maastricht 3–2006

13. Test H.pylori
•Non Invasive
•
13
C urea breath test (UBT)
•The diagnostic accuracy ~ 95%
•Accurate, practical and readily available test
•Result on 1 hour
•False negative occur in patients taking antisecretory drug
•Stool antigen tests
•Appropriate when multiple specimen are tested as a batch
•Need to store stool sample –20o C before testing
•Sensitivity decrease to 69% after 2-3 days at room temperature
Malfertheiner P et al. Gut 2007;56:772-781
Maastricht 3–2006

14. •Immunological test / serology test
Widely used, inexpensive non-invasive test
Diagnostic accuracy is low (80-84%)
Recommend to assess H.pylori in patients with a bleeding ulcer
and conditions associated with a low bacterial density
Invansive
•endoscopy with gastric biopsy for rapid urease test
Test H.pylori
Malfertheiner P et al. Gut 2007;56:772-781
Maastricht 3–2006

15. Baskin et al 1976
NSAIDs can cause
gastroduodenalinjury
NSAID damage to the gastric mucosa
Scanning electron micrographs of normal gastric mucosa (left) and
mucosal surface (right) 16 minutes after administration of aspirin

16. Arachidonic acid
COX-1
(constitutive)
COX-2
(induced by inflammatory stimuli)
Non-selective NSAIDs
•Gastrointestinal cytoprotection
•Platelet activity
•Inflammation
•Pain
•Fever
Prostaglandins Prostaglandins


COX-2 selective NSAIDs
Vane & Botting 1995
NSAIDs inhibit the COX enzyme, which exists in two
forms

17. Gastric acid plays a central role in
NSAID-associated gastroduodenaldamage
Aspirin
and other
NSAIDs
PROTECTIVE
FACTORS
Mucus layer
Ionic gradient
Bicarbonate layer
Prostaglandins
Surface epithelial
cells
Mucosal blood
supply
H. pylori
PepsinGastric
acid
AGGRESSIVE FACTORS
Aspirin and
other NSAIDs
Prostaglandin
production
Bicarbonate
production
Mucus
production
Acidic
environment
Neutral environment

18. 0
1
2
3
4
5
2.0 4.0 5.5 7.0
Gastric luminal pH
Total haemorrhagic mucosal area
%
Intraduodenal saline
Intraduodenal indomethacin
40 mg/kg
Elliott et al 1996
NSAID-associated gastroduodenal
damage is pH-dependent

19. Cheatum et al 1999
0
10
20
30
40
50
Fenoprofen
Diclofenac
Naproxen
Sulindac
Ibuprofen
Indomethacin
Piroxicam
Flurbiprofen
Etodolac
Ketoprofen
Aspirin
>1 NSAID
Other NSAIDs
High prevalence ofpeptic ulceration during NSAID
treatment
Patients with peptic ulcers
%

20. “GERD is a condition which develops when the reflux
of stomach content causes troublesome symptoms
and / or complications”
Esophageal
Syndromes
Extra-esophageal
Syndromes
Symptomatic
Syndromes
Typical Reflux
Syndrome
Reflux Chest
Pain Syndrome
Syndromes
with Esophageal
Injury
Reflux Esophagitis
Reflux Stricture
Barrett’s Esophagus
Adenocarcinoma
Established
Associations
Reflux Cough
Reflux Laryngitis
Reflux Asthma
Reflux Dental Eros.
Proposed
Associations
Pharyngitis
Sinusitis
Idiopathic
Pulmonary Fibrosis
Recurrent Otitis
Media
The Montréal definition of GERD
Vakil N et al. Am J Gastroenterol 2006; in press

21. Katzka DA, DiMarino AJ. In: The esophagus, second edition, Castell DO (editor).
Little, Brown & Company, Boston, USA. 1995:443–53.
Defective esophageal
clearance
LES ‘dysfunction’
Hiatal hernia
Delayed gastric emptying
Increased intra-abdominal pressure
Causes of increased exposure of
the esophagusto gastric refluxate

22. GERD can be diagnosed based
on symptoms alone
Troublesome symptoms
Heartburn
Regurgitation
Epigastric pain
Extra-esophageal
symptoms
(chronic cough,
hoarseness etc)
Dysphagia –
mayindicate GERD
*When cardiac causes have been excluded
Retrosternal pain*
(chest pain)

23. Symptom-based
diagnosis
Risk
assessment
Non-erosive
reflux disease
Reflux
esophagitis
~35%
Complicated
reflux disease
~5%
~60%
Endoscopy
Alarm
symptoms
Empirical
therapy
1
DeVault KR, Castell DO. Am J Gastroenterol 2005;100:190–200;
Rao G. J Fam Pract 2005;54 (12 Suppl):3–8.
Adapted from Labenz J et al. World J
Gastroenterol 2005;11:4291-99.
Following a symptom-based diagnosis, almost all
patients can be managed in primary care
Treatment
failure
~95% of
patients in
primary
care
1

24. Guidelines NSAID therapy 2006
No/low NSAID GI risk NSAID GI risk
No CV risk
(no aspirin)
Traditional NSAID
COX-2 selective inhibitors
or
Traditional NSAID + PPI
or
Consider non-NSAID therapy
CV risk (aspirin)
Traditional NSAID* + PPI
if GI risk warrants gastroprotection
or
Consider non-NSAID therapy
A “gastroprotective”agent
mustbe added if any
NSAID* is prescribed
or
Consider non-NSAID therapy
Scheiman, JM, Fendrick AM. Arthritis ResTher 2005, 7(suppl 4):S23-S29
*Ibuprofen should be used cautiously in individuals taking aspirin.