2. Objectives
• By the end of this seminar you will:
– have a working definition of dyspepsia
– know the main causes of dyspepsia
– have a rational, cost-effective, evidencebased approach to dyspepsia
4. Differential Diagnosis and Pathophysiology
Diagnosis
Typical Features
Epigastric pain or burning, postprandial
fullness, early satiety
60%
Peptic ulcer
Postprandial epigastric burning pain
15%–25%
disease
Reflux esophagitis
Heartburn, sour taste in the mouth
5%–15%
Gastric or
Abdominal pain or heartburn, dysphagia
,weight loss
2%
Functional
dyspepsia
esophageal cancer
Frequency %
Rare causes*
*Rare causes include carbohydrate malabsorption, small intestinal mucosal disorders (e.g., sprue,
intestinal parasites, chronicpancreatitis), infiltrative diseases of the stomach (e.g., Crohndisease),
ischemic bowel disease, metabolic disorders (hypothyroidism, hyperkalemia), medications (e.g.,
erythromycin), cardiac conditions (e.g., inferior myocardial ischemia), and pulmonaryconditions
(e.g., lower lobe pneumonia).
Frequency of diagnosis on endoscopy. The diagnosis of functional dyspepsia is made if there are no
findings on endoscopy.
5. Functional dyspepsia :
• It refers to the dyspepsia that occurs without
identifiable abnormality in the digestive
system (most common).
Usually affecting young adults .
Women affected twice as men .
Morning symptoms (pain and nausea are
characterstics).
But No diagnostic signs .= diagnosis
of exclusion .
6. Rome III Diagnostic Criteria For
Functional Dyspepsia:
Presence of at least one of the following symptoms with no evidence
of structural disease (including at upper endoscopy) that is likely to
explain the symptoms:
•Bothersome postprandial fullness
•Early satiation
•Epigastric pain
•Epigastric burning
•Note: criteria must be fulfilled for the past three months, with
symptom onset at least six months before the diagnosis.
7. • Three major potential pathophysiologic
mechanisms of functional dyspepsia have
been identified
• 1.delayed gastric emptying
• about 30% of patient
• associated with postprandial fullness,
nausea and vomiting
8. • 2.impaired gastric accommodation
• about 40% of patients
• associated with early satiety
• 3.hypersensitivity to gastric distention
• 37% of patients
• associated with postprandial pain, belching
and weight loss
9. Peptic Ulcer Disease (PUD)
•
•
•
The primary causes of PUD are Helicobacter pylori infection
and nonsteroidal anti-inflammatory drug (NSAID) use.
Cigarette smoking is an additional risk factor that may impair
the healing of an ulcer and increase the likelihood of recurrence
after successful treatment .
Zollinger-Ellison syndrome is an uncommon cause of PUD that
results from tumors of the small intestine or pancreas that
secrete excessive amounts of gastrin hormone which leads to an
overproduction of stomach acid.
10. Gastroesophageal Reflux Disease
• is a condition in which the reflux of gastric contents into the It may
also cause evidence of inflammation (esophagitis) and erosions in the
esophageal mucosa.
•
One important causative factor is esophago-gastric junction (EGJ)
incompetence.
• After the reflux occurs, another key factor is ineffective esophageal
clearance of acid and reflux material that may result from impaired
esophageal emptying, esophageal peristalsis dysfunction.
13. History
1- patiant profile.
2-present complaint :
-what do you mean by dyspepsia?
-then try to analyze the pain (SOCRATES)
-what other symptoms ?
ALSO DON’T FORGET TO ASK ABOUT
RISK FACTORS ????
14. Risk Factors and Past Hx
• Risk Factors
– Smoker, NSAID use, FHx ulcer
• Personal Hx
– Previous ulcer, GI bleed
– DM, hypo/hyperthyroidism, parathyroid dis.
– Colitis, diverticulosis, liver disease
– Anxiety, stress, depression
– Previous Upper GI series, Abdo U/S
15. History
• 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
16. History
• 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
17. History
• IBS
– Rome criteria
• Pain relieved with defectation
• more freq stools at onset of pain
• abdominal distention
• passage of mucus
• sense of incomplete evacuation
18. Examination
• Fever, weight loss,
hypotension, tachycardia
• Abdo
– Epigastric tenderness
– Palpable mass
– Distention
– Colon tenderness
– Jaundice
– Murphy’s sign
– Stool for OB
• Signs anemia
– Brittle nails
– Cheilosis
– Pallor palpebral
mucosa or nail beds
• Other
– Teeth (loss enamel)
– Lymphadenopathy Virchow’s node
– Acanthosis nigrans
– Hypo/Hyperthyroid.
21. Red Flag Symptoms
There are certain red flags to look for which may
indicate the possibility for serious disease :
Age > 55 y
anorexia,
unexplained recent weight loss,
dysphagia,
odynophagia,
persistent vomiting,
hematemesis,
longstanding gastroesophageal reflux
symptoms,
22. blood
in the stool,
anemia,
previous gastric surgery,
a palpable abdominal mass,
gastrointestinal perforation,
jaundice
melena
23. From AGA Guidelines
Dyspepsia
Clinical evaluation
Exclude by History:
GERD; biliary; IBS;
Meds; aerophagia
≤ 45 years
and no red
flags
+
Manage
appropriately
>45 or red flags
Endoscopy
25. The Role of H. pylori in NonUlcer Dyspepsia
• Association between H. pylori & Non-Ulcer
dyspepsia not clear
• Role in pathogenesis disputed
26. Non-invasive tests for H. pylori
SENS
14
C Urea Breath Test
Serology*
SPEC
90-95
90-95
85-95
85-90
*cannot discriminate between active & previous infection
(therefore, do not use to diagnose recurrence)
27. Treatment of H. pylori
• Multiple Regimens
• UHN/MSH Guidelines...
1st line: Most cost-effective (for the hosp.)
Lansoprazole 30mg BID
Clarithromycin 500 BID
HP Pack
7 days
Amoxicillin 1000mg BID
Alternate regimens substitute metronidazole for amoxil
(but some H.pylori are resistant)
28. NICE guidance – Indigestion
‘eradication therapy’ for H.pylori
• a PPI to take for 7 days, and
• two types of antibiotics, which are either:
metronidazole and clarithromycin, or
amoxicillin and clarithromycin.
29.
30.
31. American College of
Gastroenterology Position
• "There is no conclusive evidence that
eradication of H. pylori infection will
reverse the symptoms of nonulcer
dyspepsia. Patients may be tested for H.
pylori on a case-by-case basis, and
treatment offered to those with a positive
result."
32. What if H. pylori is negative?
• Minimal evidence supports:
– H2 blockers
– Antiacid
– Proton Pump Inhibitors
– Prokinetic agents
• metoclopramide, domperidone
• cisapride no longer available
33. Antacids:
Usually the first drugs recommended to
relieve symptoms of indigestion.
Side effects: Magnesium salt → diarrhea
aluminum salt → constipation.
Calcium carbonate antacids, can also be a
supplemental source of calcium, though they
may → constipation.
34. H2 receptor antagonists
(H2RAs)
include ranitidine, cimetidine, famotidine,
and nizatidine
reduce stomach acid.
Side effects: headache, nausea, vomiting,
constipation, diarrhea, and unusual bleeding
or bruising.
35. Proton pump inhibitors
(PPIs)
Include omeprazole, lansoprazole,
pantoprazole and esomeprazole
Most effective in people who also have
GERD
Side effects: back pain, aching, cough,
headache, dizziness, vomiting, constipation,
and diarrhea.
36. Prokinetics
As metoclopramide, may be helpful for people
who have a problem with the stomach
emptying
Improves muscle action in the digestive tract
Side effects: limit their use, as sleepiness,
depression and involuntary muscle spasms or
movements.
37. From AGA Guidelines
≤ 45 years
and no red
flags
H. pylori Testing
+
Treat H.p.
success
Follow-up
Empiric H2, PPI, or
prokinetic x 1 month
fails
fails
Endoscopy
success
Follow-up
39. Upper GI series
The upper GI
inexpensive.
series
is
noninvasive
and
relatively
It is sensitive in detecting gastric and duodenal ulcers
(80%–90%). Its accuracy improves with disease severity.
The double-contrast technique including spot views during
vigorous compression with the barium-filled bulb improves
detection of duodenal ulcers.
In patients with GERD, only severe esophagitis may be
detected, although reflux and motility disorders of the
esophagus can be seen.
The presence of a hiatal hernia does not correlate with GERD.
40. Upper GI Endoscopy
Upper GI endoscopy is the gold standard for
identifying esophagogastroduodenal
pathology and is the investigation of choice
for patients older than 55 with uninvestigated
dyspepsia or in the presence of alarm features.
Upper endoscopy is preferred to upper GI
barium study, because lesions can be directly
visualized and biopsy can be performed. In
addition, testing for H pylori can be
performed.
41. Intraesophageal pH monitoring
Most physicians consider this procedure to be
the
single best test for diagnosis for GERD.
Coupled with a symptom diary, 24-hour
monitoring has a sensitivity between 87% 93% and a specificity of 92% - 97% for GERD.
42. Scintigraphy
Scintigraphy is best used to detect delayed
gastric emptying. GERD and delayed
gastric emptying can be detected using
[99mTc]
sulfur
colloid,
although
intraesophageal pH monitoring is a better
test for reflux.