Gastritis
Peptic ulcer
disease
(Includes NSAIDinduced ulcers)
Duodenitis
Duodenal ulcer
Functional
dyspepsia
Defines :
Abdominal
GORD
DYSPEPSIA
PAIN OR DISCOMFORT
IBS
UNINVESTIGATED
INVESTIGATED
ORGANIC
FUNCTIONAL
(or idiopathic)
(use of the term non-ulcer
is discouraged)
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
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
Gastro-oesophageal reflux
Gastric cancer
Miscellaneous:
Biliary tract disease
Chronic pancreatitis
Intestinal angina
Diabetes mellitus
Drugs
Uninvestigated dyspepsia
vs functional dyspepsia
Uninvestigated dyspepsia
Functional dyspepsia
Management of
uninvestigated
dyspepsia
GP management of
uninvestigated dyspepsia
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.
If H. pyloripositive,
treat the infection
When to refer
Presence of alarm symptoms
Failure to respond to appropriate therapy
Patients 45 years of age with new-onset
symptoms
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.
Anak-anak >10%
Dewasa : 2% terutama wanita sebagain besar
keluhan GI kronis (NUD & gangguan usus)
CAP
Dyspepsia fungsional
IBS
Kelainan kandung empedu fungsional
Patofisiologi
2006)
Terapi FGID
IBS tipe C
DF
GERD
IBS tipe D
Dispepsia
Bifidobacterium
Kesimpulan
Nyeri
Pathofisiology
PUD
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
Burning
Discomfort
2.
Diffential Diagnosis
Non
ulcer dyspepsia
GI tumors
GERD
Vascular disease
Pancreatobiliary disease
Gastro duodenal Cohn's disease
Diagnosis
Diagnosis
Endoscopy
Gambar H. pylori
Sensitivity/specifity, %
Comments
80 - 95/95 100
Histology
80 90/>95
Culture
--/--
NON-INVASIVE
Serology
>80/>90
>90/>90
Stool antigen
>90/>90
Examples
Dose
Sucralfate
Misoprostol
Bismuth sub-salicylate (BSS)
1 g qid
200 g qid
See anti H.pylori regimens
Dose
TRIPLE THERAPY
1.
2.
3.
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
GASTRITIS
Gastritis
Time course
Histology features
Anatomical distribution
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
Acute gastritis
Chronic gastritis
Histologic
Superficial atrophic
Gastric atrophy
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