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Approach To Dyspepsia

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FUNCTIONAL DYSPEPSIA

DEFINITION
The term dyspepsia derives from the
Greek “dys,” meaning bad, and
“pepsis,” meaning digestion.
Dyspepsia refers to pain or discomfort
centered in the upper abdomen
 Dyspepsia is a common symptom having either an
organic
or a functional cause; distinguishing between the two
can
be a challenge.
 Clinical features of functional dyspepsia,
gastroesophageal
reflux disease, and gastrointestinal motility disorders
overlap, making diagnosis difficult.
 Most patients with functional dyspepsia have normal
esophagogastroduodenoscopy (EGD) findings.
 Endoscopy is indicated for patients with new-onset
symptoms who are > 55 years of age or have alarm
features.
 Functional dyspepsia remains a diagnosis of exclusion
Centered implies that the
pain or discomfort is mainly
in or around the midline.

Pain in the right or left


hypochondrium is not
considered to be
representative of dyspepsia
Dyspepsia

Discomfort may be characterized by or


associated with upper abdominal fullness,
early satiety, bloating , or nausea

These symptoms typically are


accompanied by a component of upper
abdominal distress
Dyspepsia

The painful or uncomfortable symptoms


may be intermittent or continuous , and
may or may not be related to meals
Differential
Diagnosis

Organic Functional
40% =“Non-
Ulcer
Dyspepsia”
60%
Organic Causes

 Peptic Ulcer Disease


 GERD Most common organic causes,
 Gastric cancer according to AGA
 Medications (ASA/NSAIDS, Abx)
 Gastroparesis
 Cholelithiasis, Choledocholithiasis
 Pancreatitis (acute or chronic)
 Carbohydrate malabsorption
 Ischemic bowel
 Other GI malignancy (ep. Pancreatic cancer)
 Systemic disease (DM, Thyroid, Parathyroid, CTD)
 Intestinal parasite
FUNCTIONAL
DYSPEPSIA
FD is a clinical syndrome which is
defined by chronic or recurrent upper
abdominal symptoms without a cause
that is identifiable by conventional
diagnostic means such as endoscopy,
radiology or histology.
Risk Factors and Past Hx
 Risk Factors
 Smoker, NSAID use, Heavy EtOH, FHx
ulcer
 Personal Hx
 Previous ulcer, GI bleed
 DM, hypo/hyperthyroidism, parathyroid
dis.
 Colitis, diverticulosis, liver disease
 Anxiety, stress, depression
 Previous Upper GI series, OGD, Abdo U/S
Diagnostic approach
 Symptom alone are unable to discriminate organic
dyspepsia from non organic dyspepsia
 Patients need to have further examination to rule
out relevant organic disease
 Functional dyspepsia is a diagnosis of exclusion
Definition of
Functional Dyspepsia
FUNCTIONAL DYSPEPSIA

Dyspepsia is a very common


complaint.
In western country:
The prevalence rate of FD :10-40%.
The remission rate :10-20% annually
The recurrence rate :20-55%
PATHOPHYSIOLOGY OF
FUNCTIONAL DYSPEPSIA
Pathophysiology of FD is poorly understood
The symptoms can be associated with

Motility abnormality of the stomach

Visceral hyperalgesia/hypersensitivity

Hp gastritis

Psychosocial factor
PATHOPHYSIOLOGY OF FUNCTIONAL
DYSPEPSIA

In such a group of patient the symptoms


are associated with abnormal motor function
of the stomach:
 Impairment of gastric accommodation
 Delayed gastric emptying
 Antral hypomotility
 Bradygastria / Tachygastria
 Intragastric maldistribution of solid and liquid food
 small bowel dysmotility
(Malagelada etal.1985;Camilleri etal.1986;Waldron etal.1991;Hveem etal.1996;Stanghellini
etal.1996)
Disorders of gastric neuromuscular
function:
myoelectrical and contractile
abnormalities Impaired fundic relaxation
Abnormal fundic emptying

Weak 3 cpm rhythm

Gastric dysrhythmias

Dilated gastric antrum


Small bowel Antral hypomotility
dysmotility Gastroparesis
DIAGNOSTIC APPROACH
 Careful history taking and Physical
examination
 Alcohol,smoking, drugs (NSAID), weight loss,
abdml surgery , intractable pain,dysphagia,
recurrent vomiting GI bleeding, pallor, jaundice
abdominal mass, abdominal scar.
 Laboratory examination
 CBC, Liver function test, Renal function test, ECG,
Test for Hp
 X ray examination and USG upper abdomen
 Endoscopy examination and biopsy
 EGG, Gastric emptying study, Manometry, 24
h
pH monitoring
History & Physical

 PUD
 Past history of ulcers, NSAIDs, Smoking
 GERD
 Heartburn or regurg symptoms, aggravated
when supine, chronic cough
 Gastric Cancer
 Older (>50), wt. loss, dysphagia, smoker, long-
standing GERD
History & Physical

 Biliary Tract disease


 Episodic RUQ pain > 1 hr,
associated with meals, post-
prandial
 Meds
 iron,NSAIDs, bisphosphonates,
antibiotics, etc.
 Metabolic disorder/Gastroparesis
 DM, Hyper or Hypo -
Thyroidism,
Hyperparathyroidism
History & Physical

 IBS
 Pain relieved with defectation
 more freq stools at onset of pain
 abdominal distention
 passage of mucus
 sense of incomplete evacuation
Examination

 Fever, weight loss,  Signs anemia


hypotension,  Brittle nails
tachycardia
 Cheilosis
 Abdo
 Pallor palpebral
 Epigastric
mucosa or nail beds
tenderness  Other
 Palpable mass
 Teeth (loss enamel)
 Distention  Lymphadenopathy -
 Colon tenderness Virchow’s node
 Jaundice  Acanthosis nigrans

 Murphy’s sign  Hypo/Hyperthyroid.

 Stool for OB
Alarm symtoms
 Weight loss
 Anaemia
 Dysphagia
 Recurrent vomiting
 Haematemesis and or maelena
 Abdominal mass
From AGA Guidelines

Dyspepsia

Clinical evaluation

Exclude by History: + Manage


GERD; biliary; IBS; Meds;
appropriately
aerophagia

 45 years and >45 or red flags


no red flags

Endoscopy
From AGA Guidelines

 45 years and
no red flags

H. pylori Testing
+ -

Treat H.p. Empiric H2, PPI, or


prokinetic x 1 month
From AGA Guidelines

 45 years and
no red flags

H. pylori Testing
+ -

Treat H.p. Empiric H2, PPI, or


prokinetic x 1 month
fails
success
fails success

Endoscopy Follow-up
Follow-up
From AGA Guidelines

Endoscopy

Organic Disease H. pylori detected Functional

Rx & Follow-up H2/PPI or prokinetic

success 4 weeks

fails
Switch to other agent

success Re-evaluate

fails
? Behavioral/ Psychotherapy/
Antidepressant
Treatment

Empirical treatment could be started to the


patient with uninvestigated dyspepsia
without alarm symptoms. The treatment
should be individualize
First line treatment is prokinetic agent or anti
secretory drug. However the placebo
response is high (20-60%)
Some patients should be avoid precipitating
food or drink
Other patients may be need anti anxiety or
anti depressant drugs
Pharmacologic Treatment for
FD
 Prokinetic agent
 Dopaminergic ( Metoclopramid , Domperidone)
 Serotonergic ( Cisapride, Ondansetron, Granisetron)
 Anti secretion
 H2
blockers(Cimetidin,Ranitidin,Nizatidin,Famotidin,Roxatidin)
 PPI
( Omeprazole,Mesomeprazole,Lansoprazole,Rabeprazole,
Pantopprazole)
 Antacid
 Cytoprotector agent
 Sucralfate
 Rebamipide
 Trepenon
 Anti anxiety or Anti depression
ANTACIDS
Drug Side effect
Magnesium severe osmotic
•MOA: Weak bases that diarrhoea
react with gastric acid to (therefore
form H20+salt. ↓pepsin combined with
activity as pepsin inactive AlOH)
at pH>4 ↓ drug
absorption

•Symptom relief, Aluminium ↓phosphate,


liquids>tablets ↓absorption of
tetracycline,
thyroxine &
•E.g. Maalox = Mg(OH)2 + chlorpromazine
Al(OH)3 , constipation
Calcium ↑Ca in blood &
urine (high
doses)
MUCOSAL PROTECTIVE AGENTS

1) Sulcralfate
MOA: Binds to positively charged proteins present on damaged mucosa forming a
protective coat

Useful in “stress ulceration”

As effective as H2-R antagonists/high dose antacids

SE: Constipation

↓absorption of cimetidine, digoxin, phenytoin & tetracycline

2) Bismuth
MOA: Antimicrobial action. Also inhibit pepsin activity, ↑mucus secretion &
interact with proteins in necrotic mucosal tissue to coat & protect the ulcer crater
H2-RECEPTOR ANTAGONISTS

Drug Side effects


Cimetidine -reversible impotence, gynaecomastia & ↓
sperm count (high doses) (nonsteroidal
antiandrogen)
-mental status abnormalities-confusion,
hallucinations (elderly/renal impairment)
-leukopenia & thrombocytopenia (rare)
-cytochrome P450 inhibitor (e.g. impairs
metabolism of warfarin, theophylline &
phenytoin)
Ranitidine,famotidi -Impotence, gynaecomastia & confusion less
ne frequently than cimetidine.
-Little interference with cytochrome P450
-Reversible drug-induced hepatitis with all H2-
antagonists
PROTON-PUMP INHIBITORS (PPI)

• MOA: block parietal cell H+/K+ ATPase enzyme


system (proton pump) ↓ secretion of H+ ions into
gastric lumen

• More effective than H2-antagonists or antacids

• Used in antimicrobial regimens to eradicate H. pylori

• SE: n&v, diarrhoea, dizziness, headaches,


gynaecomastia & impotence (rare),
thrombocytopenia, rashes
H. PYLORI ERADICATION

1st line eradication tx 2nd line tx


for H. pylori
Preferred tx= PPI PO + PPI + Bismuth 120mg QDS PO
Clarithromycin 500mg BD PO + + Metronidazole 500mg TDS
Amoxicillin 1 gm BD PO for 7 PO + Tetracycline 500mg QDS
days PO for 7 days

If Penicillin allergic= PPI +


Clarithromycin 500mg BD PO +
Metronidazole 400mg BD PO for Subsequent failures handled
7 days on individual basis with advice
from gastro/micro
E.g. of PPI: Lansoprazole 30mg
BD PO
H. PYLORI ERADICATION

1 week triple-therapy regimens eradicate H. Pylori


in >90% cases. Usually no need for continued
antisecretory tx unless ulcer complicated by
bleeding/perforation

2 week triple-therapy offer higher eradication


rates cf 1 week but SE common & poor compliance

2-week dual-therapy with PPI & antibacterial


produce low rates of H. pylori eradication & not
recommended
H. PYLORI ERADICATION
Treatment failure may be due to
- Resistance to antibacterial drugs
- Poor compliance

Drug Side effects


Bismuth n&v, unpleasant taste, darkening of tongue &
stools, caution in renal disease
Metronidazol n&v, unpleasant taste, ↓effectiveness OCP, care
e with lithium/warfarin
Amoxicillin GI side effects, ↓ effectiveness OCP,
& tetracycline pseudomenbranous colitis
Lansoprazole ↓ effectiveness OCP

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