Disorders of the Stomach
and Duodenum
J.B. Handler, M.D.
Physician Assistant Program
University of New England
1
Abbreviations
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R/O- rule out
ETOH- alcohol
UGI- upper GI
bid- twice daily
qid- 4x daily
Dx- diagnosis
Rx- treatment
Sx- symptoms
DDx- differential diagnosis
Abd- abdomen
ZE- Zollinger-Ellison
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PUD- peptic ulcer disease
PPI- proton pump inhibitor
H2- histamine 2 receptor
EGD- esophago-gastroduodenoscopy
COX- cyclooxygenase
ARF- acute renal failure
DU- duodenal ulcer
GU- gastric ulcer
CNS- central nervous
system
ETOH- alcohol
2
Case 1
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A 44 y/o man presents with several wk hx of
mid-epigastric burning pain that improves with
eating or antacids. No other medical problems.
Meds: Ibuprofen 3-4x wk for HA’s. Smokes 1
ppd. ETOH: 1-2 glasses of wine daily.
PE- VS normal; Resp and CV examsunremarkable; Abd- Nl BS; no tenderness,
masses or guarding. Rectal- no masses; stoolhemmocult neg.
DDx?
3
Peptic Ulcer Disease
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Definition: A break in the gastric or
duodenal mucosa as a result of:
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Impaired normal mucosal defense factors
(e.g. NSAIDS)
Defensive factors overwhelmed by
aggressive luminal factors (acid, pepsin,
infection)
>5 mm in diameter- extend through
muscularis mucosa
Location: duodenal bulb, pyloris, stomach
4
Peptic Ulcer
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Epidemiology
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500,000 new cases/year/USA.
10-20% lifetime incidence in adults.
Decreasing incidence since ’70’s: death
rates, provider visits; need for
surgery has decreased by 50%.
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Decrease correlates with H pylori
infection/successful treatment and
development of anti-secretory drugs.
Duodenal ulcers 5x more common than
gastric: gastric antrum (60%), lesser
curvature (25%); Benign vs malignant.
6
Case 1 DDx
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Peptic ulcer disease associated with:
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Gastritis from:
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H pylori
NSAIDS
Idiopathic
NSAIDS
Alcohol
Stress (unlikely in absence of major medical problems)
H pylori
GERD
7
Ulcer Pathology
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NSAIDS: ulcers and/or gastritis-usually
associated with long term use.
Helicobacter pylori infection
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Duodenal and gastric ulcers
Idiopathic- H pylori negative and not
taking NSAIDs (5-10% of all ulcers)
Hypersecretory States (Z-E syndromesee below)
Smoking is a risk factor for all ulcers.
8
Ulcer Pathology Hypotheses
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DU: H pylori infection (gastric antrum)
acid gastric metaplasia in duodenal
bulb further H pylori infection
duodenitis mucosal breakdown 
duodenal ulcer.
GU: H pylori infection of stomach (body)
 gastritis with chronic inflammation
overwhelms defenses mucosal
breakdowngastric ulcer.
NSAIDS impaired defensesmucosal
breakdown gastric ulcer.
9
Helicobacter pylori
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Necessary cofactor for majority (7590%) of duodenal/gastric ulcers; not
associated with NSAID ulcers.
A “hearty” bacteria: spiral, gram (–) rod
Urease production
Transmission: Unknown; likely oral-oral,
fecal-oral, gastro-oral (via vomitus,
NG/endo tube).
Incidence correlates with socioeconomic
status; 25-30% adults in US, varies with
age.
10
Helicobacter pylori
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May be associated with acute infectious
syndrome: “gastroenteritis”, nausea, abd
pain.
Chronic local infection: diffuse superficial
mucosal inflammation with polys,
lymphocytes; majority of patients
asymptomatic (see H pylori gastritis
below).
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15% of infected individuals develop PUD.
Eradication crucial to prevent ulcer
recurrence (85% recurrence if not).
11
Signs and Symptoms: PUD
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Epigastric pain common (80-90% pts with
PUD); burning, gnawing, aching,
“hunger-like”. Not sensitive/specific
enough to serve alone as a reliable
diagnostic marker of PUD.
Pain relief with eating (50%), antacids,
with subsequent return in 2-4 hrs.
Nocturnal awakening with pain common.
12
Signs and Symptoms
Caution: change in pain patternpenetration or perforation.
 Gastric ulcers: nausea/anorexia may
be associated symptoms.
 Physical Exam more often
unremarkable; rectal for occult
blood is important.
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13
Case 1
Based on the history and PE, you
decide that his presentation is most
consistent with PUD although
gastritis remains a possibility.
 Which diagnostic tests are indicated
to further sort this out?
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Investigative Findings:PUD
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Hgb/Hct for anemia; +/-amylase.
Endoscopy- EGD- best diagnostic
tool: visualize ulcer, biopsy (GU); can
test for H pylori via histology and/or
rapid urease biopsy testing if not yet
done noninvasively (below).
Imaging: Barium UGI: screening tool for
dyspepsia; helpful but limited- cannot
identify malignant vs benign gastric
ulcers; may be unable to identify some
ulcers.
15
Endoscopy
What language??
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Non-Invasive H pylori Testing
*Fecal antigen test- indicates
active infection, >90% S/S.
 *13C-urea breath test- indicates
active infection, >90% S/S.
 Serologic blood tests no longer
recommended- lack S/S.
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*Tests of choice for active PUD, recurrent PUD, proof of eradication
Must D/C PPI 7-14 days before test or can have false (-)
17
Gastric vs Duodenal Ulcer
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Major difference is gastric ulcers may be
malignant (3-5% incidence). Essential
to biopsy at time of endoscopy.
Gastric ulcers often take longer to heal
than duodenal ulcers, require length of
Rx. Non-healing (ongoing or recurrent
Sx) GU warrants repeat endoscopy and
biopsy for malignancy.
18
Case 1
His EGD reveals an oval shaped (2.5
x 3 cm) duodenal ulcer without
evidence of bleeding.
 H pylori breath test is positive.
 How should this man be managed?
 Is there any indication to repeat the
above tests following treatment?
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PUD Treatment
Acid-antisecretory agents
 H pylori eradication
 Enhanced mucosal defense agents
 What happens if H pylori not
eradicated?
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Acid-Antisecretory Agents
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Proton Pump Inhibitors (PPI):
inactivate the H+ K+ ATPase or “proton
pump” in stomach. Short T1/2 but 24 hr
pump inactivation allows 1-2x daily Rx
(see below); mostly oral agents; inhibit
>90% acid secretion.
>90% of duodenal ulcers heal in 4 wks
>90 of gastric ulcers heal in 8 weeks
21
Acid-Antisecretory Agents
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Safe, low side effect profile; minor GI,
CNS side effects.
Omeprazole (Prilosec), lansoprazole
(Protonix), others.
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Esomeprazole & pantoprazole available IV
2x daily dosing while eradicating H pylori,
then once daily (e.g. Omeprazole 20 mg).
Ulcers likely to recur unless H pylori
eradicated.
22
Acid-Antisecretory Agents
H2 receptor antagonists: inhibit
histamine mediated gastric acid
secretion.
 Suppress nocturnal> waking/post
meal acid secretion.
 Less effective than PPI, but most
ulcers heal (85-90% efficacy) over
6-8 weeks.
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Acid-Antisecretory Agents
Ranitidine (Zantac), famotidine
(Pepcid), others, all over-the
counter.
 Safe, usually taken as single large
oral dose in the PM (e.g. ranitidine
300 mg)
 Available in IV forms (see belowstress gastritis).
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Mucosal Defense Agents
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These are 2nd line or adjunct therapy
for Rx of PUD. Antisecretory agents
are drugs of choice.
Antacids- buffer acid; rapid symptom
relief; useful for supplemental Rx.
Sucralfate- (Carafate)- adheres to ulcer
craters and protects cells from acid and
pepsin; allows healing- 2nd line to PPI or
H2-blockers.
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Mucosal Defense Agents
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Bismuth- anti-bacterial vs H pylori;
enhances mucosal defenses.
Misoprostol (Cytotec)- for prophylaxis
vs. NSAID induced ulcer or gastritis;
prostaglandin analog, stimulates
gastroduodenal mucus and HCO3
secretion; side effect is diarrhea.
Infrequently used.
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Preferred Rx for prophylaxis is a PPI (see
below).
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H pylori Eradication
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Difficult to eradicate; requires “triple”
therapy- 2 antibiotics plus PPI bismuth.
10-14 day course:
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PPI 2x daily
Clarithromycin* 500 mg 2x daily
Amoxicillin 1 gram 2x daily
Alternative antibiotics include
metronidazole*, tetracycline.
*Resistant strains common.
See CMDT for other regimens
27
Ulcer Treatment
H pylori assoc ulcers: goal is
symptoms, promote healing,
eradicate H pylori.
 Antibiotic regimen + PPI (2x/d) for
10-14 days.
 PPI continued 1x/d:
Duodenal ulcer- additional 2-4 wks
Gastric ulcer– additional 4-6 wks
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Ulcer Treatment
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H2 blockers as alternative if cost a
concern; may require longer treatment.
Most will heal; key to preventing
recurrence is eradication of H pylori
(>85% success rate).
Proof of H pylori eradication not needed
unless: ulcer complication, recurrent or
refractory ulcers.
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Ulcer Recurrence
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For recurrent ulcers: essential to R/O
ongoing H pylori infection and/or
NSAID use.
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NSAID use can promote recurrence.
<20% incidence if H pylori eradicated.
Once gone, H pylori reinfection rates are
very low (<.5%/year).
Multiple recurrences suggest alternative
pathology, i.e hypersecretory states.
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NSAID Ulcers
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Selective Cox-2 vs. non-selective (N-S)
NSAIDs.
Long term use of N-S NSAIDS can cause both
gastritis and ulcers; inhibit gastric COX-1,
prostaglandin synthesis impair gastric
mucus/HCO3 secretion and other protective
mechanisms.
NSAID anti-inflammatory effects via inhibition of
COX-2. Selective COX-2 agents (Celecoxib)
risk of ulcers/gastritis, but associated with
risk of coronary events in susceptible patients
(see below).
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NSAID Ulcers
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Complications: bleeding & perforation
occur in 1-2% patients with NSAID
ulcers.
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Risk factors for complications: hx PUD or
complications; corticosteroids; anticoagulants;
age> 60; also on ASA; underlying medical
illness.
Treatment once present: PPI or H2 blocker
4-8 wks, plus D/C NSAID; rapid vs
delayed healing if NSAID continued.
H pylori not a cofactor but often presentmust eradicate if present.
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Prevention/Prophylaxis
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Reserved for high risk patientsprevent
ulcer complications (see above).
PPI prophylaxis (omeprazole 20 mgs
daily) while taking NSAID.
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Alternative is Misoprostol (see above).
COX-2 NSAIDS as alternative to nonselective NSAIDcardiac events/MI in
patients with underlying CHD.
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If dose of celecoxib is low ( 200mg/d) and
duration short (<3 mos.), there is very low
risk.
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Refractory Ulcers
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Uncommon; non-compliance is major
cause.
Cigarettes retard healing.
NSAIDS (including low dose ASA).
Failure to eradicate H pylori.
Malignancy (non-healing gastric ulcer).
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Ulcer Complications
Bleeding
 Penetration/Perforation
 Gastric outlet obstruction
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Bleeding Ulcers
Common; seen in 10-20% patients
with active PUD; 6-10% mortality;
50% of UGI bleeding is from
ulcers.
 May be first sign/symptom vs
antecedant ulcer symptoms.
 Hematemesis and/or melena vs
hematochezia dependent on amount.
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Bleeding Ulcer
Endoscopic appearance of ulcer predicts likelihood or re-bleeding
Images.google.com
Bleeding Ulcers
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Gastric lavage/emesis: BRB vs “coffee
grounds”.
PE: vital signs, postural changes, palor
etc. dependent on amount of blood loss.
Lab: decrease Hgb, Hct (will drop further
with volume expansion); check PTT, INR
and platelets; BUN may be increased
from digested blood.
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Treatment: Bleeding Ulcer
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Volume expansion (isotonic fluids);
transfuse when needed.
Bleeding stops spontaneously in 80%.
Endoscopy identifies site, stability of
bleeding site; also used to stop bleeding
when necessary (theromocoag,
vasoconstricters, clips/staples, etc.).
IV PPI or high dose oral PPI- decrease rebleeding, need for transfusion or repeat
interventions, including surgery.
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Treatment: Bleeding Ulcer
H pylori eradication if present
(most)essential in preventing rebleeding.
 Surgery for re-bleeding/refractory
bleeding in selected patients.
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Ulcer Perforation
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5% incidence in ulcer patients.
Anterior wall of stomach or duodenum.
Results in chemical peritonitis- severe,
generalized abdominal pain, rigid abd,
rebound, WBC, free air on KUB/upright.
Laparoscopic perforation closure carries
morbidity compared to laparotomy with
vagotomy, antrectomy.
Intensive medical Rx also required.
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Other Complications (IO)
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Ulcer Penetration of posterior wall of
stomach/duodenum into pancreas, liver
or biliary tract.
Symptoms: increase in pain, radiates to
back, unresponsive to antacids and other
meds; amylase may be elevated. Rx is
intensive PPI regimen or IV H2 blocker.
IO- interest only
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Erosive & Hemorrhagic Gastritis
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Etiologies: ETOH, NSAIDS; stress from
underlying severe medical/surgical
disease (common in ICU patients).
Symptoms: Often asymptomatic;
anorexia, N&V, “dyspepsia”; initial
presentation may be GI bleeding.
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UGI bleeding: hematemesis, “coffee ground”
emesis, melena as above; usually self-limited.
Dx often requires endoscopy: DDx:
bleeding peptic ulcer, esophageal
varices, mallory-weiss tear.
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Gastritis
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Stress Gastritis/Ulcers
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Superficial erosions common and
develop quickly in critically ill/ICU
patients; bleeding in up to 6% with 
associated mortality.
Pathophys: gastric mucosal blood flow.
Risk factors for bleeding: trauma, burns,
sepsis, shock, hypotension, respiratory
failure/mechanical ventilation,
coagulation problem, ARF, CNS injury.
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Prophylaxis: High Risk Patient
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IV H2 blockers bleeding incidence by
50% or more in high risk patients.
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PPI- Oral/NG* (omeprazole suspension) or IV
(expensive) may be better than H2 blocker,
but controlled comparison trials are lacking.
Goal: gastric pH>4
Sucralfate not as effective: alternative if
patient intolerant to antisecretory agents.
Improve hemodynamics where possible.
Enteral feedings when indicated; risk of
bleeding.
*NG- nasogastric or nasoenteric tube
46
NSAID Gastritis
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Very common in patients on chronic
NSAIDs; most unrecognized because
no Sx.
Dyspepsia in 25% of patients with NSAID
gastritis.
If on NSAIDS with Sx, empiric Rx is
reasonable: D/C NSAID; PPI for 2 wks.
Persistent or worsening symptoms
endoscopy (EGD) PPI 2-4 wks.
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Alcohol Gastritis
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Excessive ETOH intakenausea,
dyspepsia, emesis, hematemesis (usually
minor UGI bleeding.)
Responds to H2 receptor blocker, PPI or
sucralfate therapy- 4 week course.
DDX of UGI bleeding in alcoholics includes
PUD and esophageal varices from portal
hypertensionmore significant bleeding.
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H pylori Gastritis
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Non-erosive, non-specific picture.
Usually asymptomatic; unlikely cause
of dyspepsia.
Co-factor for PUD
Associations:
1. Gastric adenocarcinoma
2. B-cell gastric lymphoma (mucosa
associated lymphoid tissue lymphoma or
MALToma).
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Zollinger-Ellison Syndrome
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Hypersecretory state from a gastrin
secreting tumor (gastrinoma).
Tumor found in pancreas, duodenum,
lymph nodes; 2/3 malignant, metastasize
to liver; slow growth.
Excess acid secretion leads to recurrent
or refractory duodenal ulcers.
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Associated Sx: GERD, diarrhea.
Can lead to malabsorbtion, weight loss.
50
Zollinger-Ellison Syndrome
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Testing: Increased serum gastrin (often
>500 pg/ml) levels (nl< 100pg/ml), +
document gastric pH <3 (to r/o
hypochlorhydria which can also raise
gastrin levels)
Special imaging required to find primary
tumor and/or metastasis:
somatostatin receptor scintigraphy
endoscopic ultrasonography
51
Treatment of Z-E
If isolated primary tumor: PPI +
resection.
 If metastasis: PPI in high dose to
decrease basal acid output.
 Prognosis: good for isolated tumor.
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52