Dyspepsia and Dysphagia
Dyspepsia
•  Common symptom
•  Extensive differential diagnosis
•  25% of the population each year (majority don’t
seek treatment)
•  Original definition: disordered digestion of food
•  Symptoms of “indigestion,” bloating, early satiety,
nausea, vomiting
Dyspepsia
International committee definition (Rome III criteria):
•  Postprandial fullness
•  Early satiation
•  Epigastric pain or burning
Dyspepsia—Differential Dx
•  Most common: functional dyspepsia (60%)
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NSAID induced dyspepsia
Peptic ulcers
GERD
Neoplasm (<2%)
Dyspepsia
Dyspepsia
Dyspepsia: Alarm Symptoms •
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Unintended weight loss
Persistent vomiting
Progressive dysphagia
Odynophagia
Anemia
Hematemesis
Palpable mass
Family hx GI cancer
Previous gastric surgery
Jaundice
GERD •  Symptoms or mucosal damage produced by
abnormal reflux of gastric contents into the
esophagus
•  Some degree of reflux physiologic
•  Excessive reflux of gastric juice
•  Impaired esophageal clearance of the
refluxate
•  Symptoms: retrosternal burning (postprandial),
regurgitation, dysphagia, chest pain, water
brash, globus, odynophagia, nausea, cough
GERD: Mild-Mod Sx
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Mild sx: lifestyle/diet modification, OTC H2
Head of bed elevation: 6-8 inches
Avoid chocolate/mint/EtOH/fatty food
Avoid food triggers
Avoid lying supine after meals
Obesity—increased risk—weight loss
Promotion of salivation: gum, lozenges
Smoking cessation
GERD: Severe
•  Step up or Step down approach
In ascending order of potency
•  OTC antacids and/or H2 blockers
•  Prescription H2 blockers (bid)
•  Intermittent (2 weeks) use of PPI
•  Omeprazole 20 mg daily or equivalent
•  Omeprazole 20 mg bid or equivalent
GERD therapeutic regimens
•  H2 blockers (six week is adequate trial)
•  PPI more effective than H2
•  No studies showing one PPI more effective than
others
•  Prokinetic agents: high side effect profile
•  H.pylori and GERD: complex
Proton Pump Inhibitors
•  Stomach parietal cells secrete HCl in
response to histamine, acetylcholine, gastrin
•  H-K-ATPase (proton pump) final pathway by
which acid secreted
•  Most potent inhibition of gastric acid
available
•  Administer before first meal of the day
(highest H-K-ATPase)
•  Should not be given concomitantly (at the
same time of day) with H2 blocker
Proton Pump Inhibitors
•  Inhibits only activated enzyme
•  Once daily dosing inhibits maximum acid
output by 66% after five days
•  Occasional use does not reliably provide
adequate acid inhibition (in contrast to H2
blocker)
•  Max acid secretion may not restored for 24-48
hours after discontinuing
•  BID dosing of PPI for first 2-3 days may be helpful
in achieving more rapid acid inhibition
•  Rebound gastric secretion with discontinuation,
consider taper if on high dose or on for > 6 mos
•  Chronic atrophic gastritis
PPI and clopidogrel
•  FDA 2009 Concomitant should be avoided due to
decreased clopidogrel activity
•  Only large scale randomized trial (2010) of
omeprazole vs placebo in clopidogrel users showed
no significant difference in CV events along with a
significant reduction in GI events
•  Postulated mechanism is competitive inhibition of
clopidogrel metabolism
•  Take home: if patient truly requires PPI then
continue, but if patient has been on PPI with
questionable indication consider d/c
GERD: Maintenance Rx
•  Treat acute GERD for at least 8 weeks
•  Consider maintenance therapy if recurrent
symptoms in < 3 months
GERD: Maintenance Rx
Potential risks
•  Increased CAP
•  Increased enteric infections (c.diff)
•  Decreased Vit B12 absorption
•  Increased bone fracture risk due to
decreased calcium absorption and
osteoclast inhibition (dose dependent and
therapy dependent)
•  Hypomagnesemia (check if on PPI for > one
year or on dig/diuretics)
Peptic Ulcer Disease
Pain in epigastrium (2/3)
Burning, gnawing, hungerlike
Vague, cramping
Pattern: symptomatic periods x several weeks
followed by symptoms period of weeks/months
•  2-5 hours after meals or btwn 2300-0200
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H.pylori testing
ACG recommendations
•  Only if clinician plans to offer treatment
•  Active peptic ulcer disease or past history of
documented peptic ulcer (untreated)
•  “Test and treat” strategy: patients under 55 with
uninvestigated dyspepsia with no alarm features
H.pylori stool Ag assay
•  Sens 94%, Spec 86-92%
•  Can be used to determine eradication after four
weeks
•  False negatives: PPI, bismuth
Urea breath testing
•  Based on hydrolysis of urea by H.pylori to produce
CO2 and ammonia
•  Labeled carbon isotope given by mouth, presence
of h.pylori liberates CO2 that can be detected
•  Sensitivity 88-95%, Spec 95-100%
•  False negatives: anti-secretory therapy, bismuth,
antibiotics (off abx 4 wks, PPI 2 wks)
H.pylori serology
•  ELISA to detect IgG antibodies
•  Highly sensitive 90-100%, Variable specificity 76-96%
•  At 18 months 60% of patients cured of infection had
undetectable antibody titers
Confirmation of
Eradication
•  Recommended by ACG
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An patient with h.pylori associated ulcer
Persistent dyspepsia despite treatment
H.pylori MALT lymphoma
Resection of early gastric cancer
UBT or stool Ag testing
Antibiotics/bismuth d/c for at least 4 wks
PPI discontinued at least one week
UTD authors recommend consideration of testing for
confirmation of eradication in all patients treated
for h.pylori
H.pylori treatment
•  Multiple treatment regimens evaluated in
RCT, no optimal therapy identified
•  Consider efficacy, cost, side effects, ease of
administration
•  Most common is triple therapy with PPI,
amoxicillin 1 g bid, and clarithromycin 500
bid for 7-14 days
•  A meta-analysis suggested that longer
duration of treatment (14 vs 7 days) was
associated with 5% increase in eradication
rates
H.pylori treatment
•  Prevpac: lansoprazole, amoxicillin,
clarithromycin
•  Quadruple therapy consists of PPI, bismuth,
two abx (metronidazole, tetracycline)
•  Pylera/Helidac: bismuth, metronidazole,
tetracycline (Helidac )
•  LOAD therapy: levofloxacin, omeprazole,
nitazoxanide, doxycycline
Dyspepsia:Functional
Dysphagia: Classification
Oropharyngeal dysphagia
Esophageal dysphagia
Dysphagia: Classification
Oropharyngeal dysphagia (transfer
dysphagia)
•  Disease of the upper esophagus and
pharynx
•  Upper esophageal sphincter dysfunction
•  Patient will complain of food getting stuck
immediately upon swallowing.
•  They will point to cervical region as location
of symptoms.
Dysphagia: Classification
Esophageal dysphagia
•  Disease in body of the esophagus, lower
esophageal sphincter, or cardia
•  Symptoms occur several seconds after swallowing
•  Symptoms usually located retrosternal or at the
suprasternal notch
Dysphagia: What to ask?
•  Differentiate odynophagia (pain with swallowing)
from globus sensation (feeling of a lump in the
throat)
•  Type of food that causes symptoms: solid, liquid or
both?
•  Progressive symptoms or intermittent?
•  Timeline of symptoms
•  Other medical problems: DM, scleroderma, AIDS,
NM d/o, hx radiation
Dysphagia: What to ask? Mechanical
•  Dysphagia to solids
which progress to
liquids
•  Progressive: think
cancer or stricture
•  Intermittent: think lower
esophageal ring
Motility
•  Dysphagia to solids
AND liquids
•  May be progressive or
intermittent
Dysphagia: Testing •  Barium swallow: if proximal lesion suspected
by history
•  EGD: for mid and lower esophagus lesions
•  Esophageal manometry: Diagnosis of
motility disorders
•  Videofluoroscopy: visualization and analysis
of swallow.
•  Nasopharyngeal laryngoscopy: visualization
of oropharynx, hypopharynx, larynx, vocal
cords
Dysphagia: Treatments
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Reflux esophagitis: H2, PPI
Lower esophageal ring: pneumatic dilation
Achalasia: myotomy, pneumatic dilation, botox
Peptic stricture: dilation, antireflux Rx
Carcinoma: surgery, radiation
Spastic motility: Ca Channel blockers, nitrates
Functional dysphagia: Ca channel blockers,
nitrates, SSRI, anxiolytics, smooth muscle
relaxants