Stomach

1 . The consistently largest artery to the stomach is the Answer: B

A. Right gastric The consistently largest artery to the stomach is the left gas­
B. Left gastric tric artery, which usually arises directly from the celiac trunk
C. Right gastroepiploic and divides into an ascending and descending branch along
D. Left gastroepiploic the lesser gastric curvature. Approximately 20% of the time,
the left gastric artery supplies an aberrant vessel that travels
in the gastrohepatic ligament (lesser omentum) to the left side
of the liver. Rarely, this is the only arterial blood supply to this
part of the liver, and inadvertent ligation may lead to clinically
significant hepatic ischemia in this unusual circumstance. (See
Schwartz l Oth ed., p. 1037.)

2. Which of the following inhibits gastrin secretion? Answer: D

A. Histamine Luminal peptides and amino acids are the most potent
B. Acetylcholine stimulants of gastrin release, and luminal acid is the most
C. Amino acids potent inhibitor of gastrin secretion. The latter effect is pre­
D. Acid dominantly mediated in a paracrine fashion by somatostatin
released from antral D cells. Gastrin-stimulated acid secretion
is significantly blocked by H2 antagonists, suggesting that the
principal mediator of gastrin-stimulated acid production is
histamine from mucosal enterochromaffin-like (ECL) cells.
Acetylcholine released by the vagus nerve leads to stimulation
of ECL cells, which in turn produce histamine. (See Schwartz
l Oth ed., p. 1045.)

3. Helicobacter pylori infection primarily mediates duodenal Answer: A

ulcer pathogenesis via Helicobacter pylori possess the enzyme urease, which converts
A. Antral alkalinization leading to inhibition of soma- urea into ammonia and bicarbonate, thus creating an environ­
tostatin release ment around the bacteria that buffers the acid secreted by the
B. Direct stimulation of gastrin release stomach. H. pylori infection is associated with decreased lev­
C. Local inflammation with autoimmune response els of somatostatin, decreased somatostatin messenger RNA
D. Upregulation of parietal cell acid production production, and fewer somatostatin-producing D cells. These
effects are probably mediated by H. pylori-induced local
alkalinization of the antrum (antral acidification is the most
potent antagonist to antral gastrin secretion), and H. pylori­
mediated increases in other local mediators and cytokines.
The result is hypergastrinemia and acid hypersecretion, pre­
sumably leading to the parietal cell hyperplasia seen in many
patients with duodenal ulcer. Other mechanisms whereby
H. pylori can induce gastroduodenal mucosal injury include
the production of toxins (vacA and cagA), local elaboration
of cytokines (particularly interleukin-8) by infected mucosa,

203
204
recruitment of inflammatory cells and release of inflamma­
tory mediators, recruitment and activation of local immune
factors, and increased apoptosis. (See Schwartz l Oth ed.,
pp. 1 054- 1 055.)

4. The effect of erythromycin on gastric emptying is through Answer: C

its function as a Erythromycin is a common prokinetic agent used to treat
A. Dopamine antagonist delayed gastric empting, and works as a motilin agonist. Dom­
B. Cholinergic agonist peridone and metoclopramide, two other commonly used
C. Motilin agonist medications, function as dopamine antagonists (Table 26- 1 ) .
D. Cholinergic antagonist (See Schwartz l Oth ed., Table 26-4, p . 1 050.)

TA B L E 2 6 - 1 Drugs that accelerate gastric emptyi ng

Agent Typical Adult Dose Mechanism of Action

Metoclopramide l O mg PO q i d Dopa m i n e a ntag o n i st

t.n Eryt h romyc i n 250 mg PO q i d Moti l i n agon ist

r+
0
Domperidone l O mg PO q i d Dopa m i n e a ntag o n i st
3
Cl.J
(")
-::::;
5. Which of the following is secreted by gastric parietal cells? Answer: B
A. Pepsinogen Activated parietal cells secrete intrinsic factor in addition to
B. Intrinsic factor hydrochloric acid. Presumably the stimulants are similar, but
C. Gastrin-releasing peptide acid secretion and intrinsic factor secretion may not be linked.
D. Ghrelin Intrinsic factor binds to luminal vitamin B 12 , and the com­
E. Histamine plex is absorbed in the terminal ileum via mucosal receptors.
Vitamin B 12 deficiency can be life-threatening, and patients
with total gastrectomy or pernicious anemia require B 2
1
supplementation by a nonenteric route. (See Schwartz 1 Oth ed.,
p. 1044.)

6. The most accurate diagnostic test for Zollinger-Ellison Answer: D

syndrome (ZES) is All patients with gastrinoma have an elevated gastrin level,
A. Fasting serum gastrin and hypergastrinemia in the presence of elevated basal acid
B. Computed tomography ( CT) scan output (BAO) strongly suggests gastrinoma. Patients with gas­
C. Endoscopy trinoma usually have a BAO > 1 5 mEq/h or >5 mEq/h if they
D. Secretin stimulation test have had a previous procedure for peptic ulcer. Acid secretory
medications should be held for several days before gastrin
measurement, because acid suppression may falsely elevate
gastrin levels. Causes of hypergastrinemia can be divided
into those associated with hyperacidity and those associated
with hypoacidity (Fig. 26- 1 ) . The diagnosis of Zollinger­
Ellison syndrome (ZES) is confirmed by the secretin stimu­
lation test. An intravenous (IV) bolus of secretin (2 U/kg) is
given and gastrin levels are checked before and after inj ection.
An increase in serum gastrin of 200 pg/mL or greater sug­
gests the presence of gastrinoma. Patients with gastrinoma
should have serum calcium and parathyroid hormone levels
determined to rule out multiple endocrine neoplasia type 1
(MENl ) and, if present, parathyroidectomy should be consid­
ered before resection of gastrinoma. (See Schwartz l Oth ed.,
Figure 26-46, p. 1 072.)
 205

Measure BAO and gastric pH

BAO low pH >2

P revious G l surgery
• Vagotomy?
• Massive S B resection

V1
..-+
Sign ificant elevation i n serum Confirm with EG D/Bx 0
gastrin m response to I V secret1n ? test/treat H. pylori 3
Cl.J
give B 1 2 ()
:::1

Zol l i n ger-E I I ison

syndrome

Octreotide scan
R/0 MEN 1

Consider resection Resect retained antru m

Or
Convert 82 to 81

F I G . 2 6- 1 . A l g o rith m for d ia g n o s i s and m a nagement of hyperg a stri n e m i a . B = B i l l roth I ; B = B i l l roth II; BAO = basa l acid output; Bx = bio psy;
1 2
ECL = enteroc h romaffi n-l i ke; EGO = esophagogastrod uodenoscopy; GJ = g a strojej u nosto my; H 2 RA = h i sta m i ne 2 receptor a ntag o n i st; i n suff =
i n s uffi c i e n cy; M E N 1 = m u lt i p l e e n d ocri n e n e o p l a s i a type 1 ; P P I = proto n p u m p i n h i b itor; R/0 = r u l e out; SB = s m a l l bowe l ; S/P = stat u s post;
TV = tru n c a l va gotomy; TV a n d A = tru n c a l va gotomy a n d a ntrectomy.

7. Which of the following is the preoperative imaging study Answer: £

of choice for gastrinoma? CT will detect most lesions > l cm in size and magnetic reso­
A. CT scan nance imaging (MRI) is comparable. Endoscopic ultrasound
B. Magnetic resonance imaging (MRI) (EUS) is more sensitive than these other noninvasive imaging
C. Endoscopic ultrasound (EUS) tests, but it still misses many of the smaller lesions, and may
D. Angiographic localization confuse normal lymph nodes for gastrinomas. Currently,
E. Somatostatin receptor scintigraphy the preoperative imaging study of choice for gastrinoma is
somatostatin-receptor scintigraphy (the octreotide scan) .
When the pretest probability of gastrinoma is high, the sen­
sitivity and specificity of this modality approach 1 00%. Gas­
trinoma cells contain type II somatostatin receptors that bind
the indium-labeled somatostatin analogue (octreotide) with
high affinity, making imaging with a gamma camera pos­
sible. Currently, angiographic localization studies are infre­
quently performed for gastrinoma. (See Schwartz l Oth ed.,
pp. l 072- 1 073.)
206
8. Patients taking nonsteroidal anti-inflammatory drugs Answer: C
(NSAIDs) or aspirin need concomitant acid suppressing The overall risk of significant serious adverse gastrointestinal
medication if which of the following is present? ( GI) events in patients taking nonsteroidal anti-inflammatory
A. Age over 50 drugs (NSAIDs) is more than three times that of controls
B. Heavy smoking history (Table 26-2). This risk increases to five times in patients older
C. Concurrent steroid intake than 60 years. Factors that clearly put patients at increased
D. Heavy alcohol consumption risk for NSAID-induced GI complications include age >60,
prior GI event, high NSAID dose, concurrent steroid intake,
and concurrent anticoagulant intake. Alcohol is commonly
mentioned as a risk factor for peptic ulcer disease (PUD),
but confirmatory data are lacking. High doses of H 2 blockers
have been shown to be less effective than proton pump inhibi­
tors (PPis) in preventing GI complications in these high risk
patients on antiplatelet therapy, but clearly they are better than
no acid suppression. (See Schwartz lOth ed., Table 26-6, p. 1 058.)
t.n
r+
0 TA B L E 26-2 Hospita l ization rates for Gl events with and without NSAID use in selected large popu lations
3
Cl.J Annualized l ncidenceb
(J
-::::; Thera pies Used C linical Upper G l Events' Com plicated Upper Gl Events•

Study• NSAID Control Study Drugs Control Study Drug Control Study Drug

M U COSA NSAIDs (n = 443 9) M isoprostol 200 �g 3.1 % 1 .6% 1 5% 0.7%

qid + NSAI D (n = 4404)

CLASS I bu p rofen 800 mg tid, Celecox i b 400 mg bid 35% 2.1 % 1 5% 0.8%
d i c l ofe nac 75 mg bid (n = 3995)
(n = 3987)

(No a s p i r i n': 2.9%) 1 .4% 1 .3% 0.4%

VIGOR N a p roxen 500 mg bid Rofecox i b 50 mg qd 45% 2.1 % 1 .4% 0.6%

(n = 4047) (n = 4029)
"MUCOSA and VIGOR tria l s i n c l uded only rheumatoi d a rthritis patients; C LASS trial i n c l uded osteoa rthritis (73%) a n d rheu matoid a rthritis (27%).
b l n c idence for M U COSA trial represents d o u b l i n g of resu lts provided at 6 months (a lthough m e d i a n fol l ow-up was <6 months). I nc i dences for VIGOR and CLASS trials re present rates
per 1 00 patient-yea rs, a lt h o u g h VIGOR med i a n fo l low- u p was 9 months and C LASS data i n c l u d e only the fi rst 6 months of the study.
'Incl udes perforatio n s, obstructions, bleed i ng, and u ncompl icated u lcers d i s covered on c l i n ica l l y i n d icated work-up.
'Incl udes perforation, obstruction, bleed i n g (doc u m e nted due to u l c e r or erosions i n M U COSA and CLASS; major bleed i n g in VIGOR).
'2 1 o/o of patients i n CLASS study were ta king low-dose a s p i r i n .
Note: A l l d i ffere nces between contro l s a n d s t u d y d ru g s were s i g n ificant except c l i n ical u pper G l events i n overa l l C LASS s t u d y (P = .09).
Source: Reproduced with perm ission from La i n e L. Approaches to nonstero i d a l a nti-i n A a m m atory d rug use i n the h i g h-risk patient Gastroen terology 1 20:594, 200 1 . Copyright Elsevier.

9. The optimal initial management of a patient hospitalized Answer: D

for a bleeding peptic ulcer is The management of bleeding peptic ulcer is summarized in
A. Ulcer oversew the algorithm in Fig. 26-2. All patients admitted to hospital
B. Vagotomy and pyloroplasty with bleeding peptic ulcer should be adequately resuscitated
C. Distal gastrectomy and started on continuous IV PPI. Seventy-five percent of
D. Intravenous PPis patients will stop bleeding with these measures alone, but 25%
will continue to bleed or will rebleed in hospital. Among the
high risk group, endoscopic hemostatic therapy is indicated
and usually successful. Only then should surgical interven­
tion be considered, with indications including massive hem­
orrhage unresponsive to endoscopic control and transfusion
requirement of more than four to six units of blood, despite
attempts at endoscopic control. Long-term maintenance
PPI therapy should be considered in all patients admitted
to hospital with ulcer complications. (See Schwartz l Oth ed.,
Figure 26-42, pp. 1 06 1 , 1 064- 1065, and 1 069.)
 207

Hospital admission Bleeding peptic ulcer

Resuscitate
Conti nuous IV P P I drip
EGO

20% high risk 80% Low risk

Yes : Shock? : No
-----�----------------------�-----

: :
V1
Yes Transfusion? No .---+
0
-----�----------------------�-----

: 3
Yes Active bleeding o n EGO? : No Cl.J
-----+----------------------+----- ()
: :
:::1
Yes Visible vessel o n EGO? No
-----+----------------------+-----
1 I
Yes 1 Abnormal PT, PTT, or platelets? 1 No
I I

Lifelong P P I
Test + R x H . pylori
Avoid N SAI Os/ASA if possible

FIG. 26-2. A l g o rith m for the treatment of b l eed i n g peptic u l cer. ASA = acetyl sal icyl i c acid; EGO = esophagogastrod uodenoscopy; IV =
i ntrave n o u s; OR = operati n g roo m; P P I = proton p u m p i n h i bitor; PRBC = u n it of packed red b l ood ce l l s; PT = prot h ro m b i n ti me; PTI = p a rt i a l
t h ro m bo p l a sti n time; R x = treatme nt.

10. Which of the following options is the least preferable Answer: C

reconstruction for patients undergoing antrectomy for Following antrectomy, GI continuity may be reestablished
PUD? with a Billroth I gastroduodenostomy or a Billroth II loop
A. Billroth I. gastrojejunostomy. Since antrectomy routinely leaves a 60 to
B. Billroth II. 70% gastric remnant, routine reconstruction as a Roux-en-Y
C. Roux-en-Y gastrojejunostomy. gastrojejunostomy should be avoided. Although the Roux-en-Y
D. All are equally preferable. operation is an excellent procedure for keeping duodenal
contents out of the stomach and esophagus, in the presence of
a large gastric remnant, this reconstruction will predispose to
marginal ulceration and/or gastric stasis. (See Schwartz lOth ed.,
p. 1 063.)
208
1 1 . A 55-year-old executive who is seen because of severe Answer: A
epigastric pain is found on esophagogastroduodenos­ The indications for surgery in PUD are bleeding, perforation,
copy to have a large ulcer in the duodenal bulb and tests obstruction, and intractability or nonhealing. Intractability
positive for H. pylori. He is treated for H. pylori and should be an unusual indication for peptic ulcer operation
instructed to quit smoking, but his symptoms persist and nowadays. The patient referred for surgical evaluation because
he is referred to you for further management. At this of intractable PUD should raise red flags for the surgeon:
time, it would be most appropriate to recommend maybe the patient has a missed cancer, is noncompliant, or
A. NSAID cessation and urea breath test has Helicobacter despite the presence of a negative test or pre­
B. Highly selective vagotomy vious treatment (differential for intractability, Table 26-3).
C. Truncal vagotomy and antrectomy In this setting, the patient with persistent symptoms despite
D. Truncal vagotomy and pyloroplasty appropriate treatment requires further evaluation before any
consideration of operative treatment. If surgery is necessary,
a lesser operation may be preferable. (See Schwartz l Oth ed.,
Table 26- 1 3 , pp. 1 059 and 1069- 1071.)

(J)
r+
TA B L E 26-3 Differential diagnosis of intracta bil ity or
0 non hea l i ng peptic ulcer disease
3
Cl.J Cancer
(")
-::::; Gastric
Pa ncreatic
Duode n a l
Persistent H. pylori i nfection
Tests may be fa l se-negative
Co nsider e m p i ric treatment
N o n c o m p l i a nt patient
Fa i l u re to take prescri bed med icatio n
S u r re ptiti o u s u se o f NSAIDs
Mot i l ity d isorder
Zo l l i nger-E I I ison syndrome

12. Which blood group is associated with an increased risk of Answer: A

gastric cancer? Gastric cancer is more common in patients with pernicious
A. A anemia, blood group A, or a family history of gastric cancer.
B. B When patients migrate from a high-incidence region to a
C. AB low-incidence region, the risk of gastric cancer decreases
D. 0 in the subsequent generations born in the new region. This
strongly suggests an environmental influence on the devel­
opment of gastric cancer. Environmental factors appear to
be more related etiologically to the intestinal form of gastric
cancer than the more aggressive diffuse form. The commonly
accepted risk factors for gastric cancer are listed in Table 26-4.
(See Schwartz l Oth ed., Table 26- 1 5, pp. 1 074- 1075.)

TA B L E 26-4 Factors increasing or decreasing the risk of

gastric ca ncer
I nc rease risk
Fa m i ly h i story
Diet (high i n n itrates, sa lt, fat)
Fa m i l ia l polyposis
Gastric adenomas
Hered ita ry n o n polyposis colorecta l cancer
H. pylori infection
Atro p h ic g a stritis, i ntest i n a l meta p l a s ia, dysplasia
Previo u s ga strectomy or ga strojej u nostomy (> 1 0 yea rs ago)
To bacco u se
M e n etrier's d i sease
Decrease r i s k
Aspirin
D iet (high fresh fru it a n d vegeta b l e i nta ke)
Vita m i n C
 209
1 3 . A subtotal gastrectomy with D2 dissection performed for Answer: B
Stage 3 gastric adenocarcinoma in the antrum includes Surgical resection is the only curative treatment for gastric
A. Grossly negative margins of 2 em cancer and most patients with clinically resectable locore­
B. More than 1 5 lymph nodes removed gional disease should have gastric resection. The standard
C. Billroth II reconstruction operation for gastric cancer is radical subtotal gastrectomy,
D. Splenectomy which entails ligation of the left and right gastric and gastro­
epiploic arteries at the origin, as well as the en bloc removal of
the distal 75% of the stomach, including the pylorus and 2 em
of duodenum, the greater and lesser omentum, and all asso­
ciated lymphatic tissue. Generally, the surgeon strives for a
grossly negative margin of at least 5 em. More than 1 5 resected
lymph nodes are required for adequate staging, even in the
low-risk patient. The operation is deemed an adequate cancer
operation provided that tumor-free margins are obtained,
> 1 5 lymph nodes are removed, and all gross tumor is resected.
In the absence of involvement by direct extension, the spleen V1
..-+
and pancreatic tail are not removed. Reconstruction is usually 0
by Billroth I gastrojejunostomy or Roux-en-Y reconstruction. 3
Cl.J
(See Schwartz l Oth ed., p. 108 1 . ) ()
:::1

14. The standard treatment for an isolated 3 em gastrointesti­ Answer: C

nal stromal tumor (GIST) in the body of the stomach is Gastrointestinal stromal tumors (GISTs) are submucosal
A. Imatinib tumors that are slow growing, and arise from interstitial cells
B. Endoscopic ablation of Cajal (ICC) . Prognosis in patients with GISTs depends
C. Wedge resection mostly on tumor size and mitotic count, and metastasis, when
D. Subtotal gastrectomy it occurs, is typically by the hematogenous route. Any lesion
> l cm can behave in a malignant fashion and may recur. Thus,
all GISTs are best resected along with a margin of normal
tissue-wedge resection with clear margins is adequate sur­
gical treatment. True invasion of adjacent structures by the
primary tumor is evidence of malignancy. If safe, en bloc
resection of involved surrounding organs is appropriate to
remove all tumor when the primary is large and invasive.
Five-year survival following resection for GIST is about 50%.
Most patients with low-grade lesions are cured (80% 5-year
survival) , but most patients with high-grade lesions are not
(30% 5-year survival) . Imatinib, a chemotherapeutic agent
that blocks the activity of the tyrosine kinase product of c-kit,
yields excellent results in many patients with metastatic or
unresectable GIST, and is also recommended in high risk
groups as an adjuvant therapy. Fig. 26-3 shows an algorithm
for treatment of patients with GIST (See Schwartz l Oth ed.,
Figure 26-59, pp. 1 085- 1 086.)
21 0

U nresectable or resection Consider resection of primary

requ i ring extensive surgery with min imal metastatic disease
or risk of organ dysfu nction especially when symptomatic

l/)
r+
0
3
Cl.J
(")
-::::;
Sunitinib
Postop i matin i b
Other new agents

R FA = radiofrequency ablation *If all g ross disease or all

i mati nib-resistant disease
is treatable

F I G . 26-3. A l g o rith m for the treatment of g a stroi ntest i n a l stro m a l t u m o r. (Reprod uced with perm ission fro m Gold JS, DeMatteo RP,
Co m b i ned s u rg i c a l a n d m o l ec u l a r thera py: The gastroin testinal stromal tumor model. A n n S u rg 244: 1 76, 2006.)

1 5 . Which of the following options is the best management of Answer: A

a low-grade gastric lymphoma of the gastric antrum? Low-grade mucosa-associated lymphoid tissue (MALT)
A. H. pylori eradication lymphoma, essentially a monoclonal proliferation of B cells,
B. Chemotherapy ± radiation therapy presumably arises from a background of chronic gastritis
C. Wedge resection associated with H. pylori. These relatively innocuous tumors
D. Antrectomy then undergo degeneration to high-grade lymphoma, which
is the usual variety seen by the surgeon. Remarkably, when the
H. pylori are eradicated and the gastritis improves, the low­
grade MALT lymphoma often disappears. Thus, low-grade
MALT lymphoma is not a surgical lesion. An algorithm for
gastric lymphoma treatment is found in Fig. 26-4. (See
Schwartz l Oth ed., Figure 26-58, pp. 1084- 1085.)
 21 1

H. pylori eradication therapy

and chemo** +1- XRT*

V1
.-+
Stage I I 0
Close follow-up
Chemo** + X RT* 3
Cl.J
()
:::1
*X RT: external beam radiation therapy, approxi mately 30 Gy with 1 0 Gy boost
**Chemo: chemotherapy regimens include ch lorambucil , fludarabinel,
and cyclosphospham ide, vincristine, prednisone ( COP ) +1- rituximab

Further chemotherapy

*Chemo: chemotherapy regimen usually cyclophosphamide,

doxorobicin , vincristine, predn isone ( CHOP ) +1- rituximab
**XRT: external beam radiatio n , approximately 30 Gy with 1 0 Gy boost

F I G . 26-4. A l g o rith m for the treatment of g a stric l y m p h o m a . MALT = m u cosa-associated l y m p h o i d tissue. (Reprod uced with perm ission from
Yoo n SS, Co it DG, Portl ock CS, et a l , The diminishing role of surgery in the treatmen t of gastric lymphoma. A n n S u rg 240:28, 2004.)

16. Type III gastric carcinoid tumors Answer: C

A. Often do not require resection Type III gastric carcinoids are sporadic tumors, most often soli­
B. Are associated with hypergastrinemia tary (usually > 2 em), occur more commonly in men, and behave
C. Are sporadic lesions more aggressively than types I and II. Unlike types 1 and II,
D. Have better outcomes than type I and II tumors they are not associated with hypergastrinemia. Type I gastric
carcinoids are the most common type of gastric carcinoid, and
occur in patients with chronic hypergastrinemia secondary
to pernicious anemia or chronic atrophic gastritis. Type II is
rare, and is associated with MEN1 and ZES. Gastric carcinoids
should all be resected, and small lesions ( <2 em) confined to the
mucosa may be treated endoscopically with endoscopic muco­
sal resection (EMR) if there are only a few lesions ( <5) and if
margins are histologically negative. Locally invasive lesions, or
those >2 em, should be removed by radical gastric resection
and lymphadenectomy. Survival is excellent for node-negative
patients (>90% 5-year survival); node-positive patients have
21 2
a 50% 5-year survival. The 5-year survival for patients
with type I gastric carcinoid is close to 1 00%; for patients
with type III lesions, the 5-year survival is less than 50%.
Most type III patients have nodal or distant metastases at
the time of diagnosis, and some present with symptoms of
carcinoid syndrome. (See Schwartz l Oth ed., p. 1 086.)

1 7. Watermelon stomach is best treated by Answer: C

A. Acid-reducing agents The parallel red stripes atop the mucosal folds of the distal
B. Beta blockers stomach give this rare entity its name. Histologically, gastric
C. Antrectomy antral vascular ectasia (GAVE) is characterized by dilated
D. Total gastrectomy mucosal blood vessels that often contain thrombi, in the
lamina propria. Mucosal fibromuscular hyperplasia and hya­
linization often are present (Fig. 26-5) . The histologic appear­
ance can resemble portal hypertensive gastropathy, but the
l/)
latter usually affects the proximal stomach, whereas water­
r+
0 melon stomach predominantly affects the distal stomach.
3 Beta blockers and nitrates, useful in the treatment of por­
Cl.J
(") tal hypertensive gastropathy, are ineffective in patients with
-::::;
gastric antral vascular ectasia. Patients with GAVE are usually
elderly women with chronic GI blood loss requiring transfu­
sion. Most have an associated autoimmune connective tissue
disorder, and at least 25% have chronic liver disease. Nonsur­
gical treatment options include estrogen and progesterone,
and endoscopic treatment with the neodymium yttrium­
aluminum garnet (Nd:YAG) laser or argon plasma coagulator.
Antrectomy may be required to control blood loss, and this
operation is quite effective but carries increased morbidity in
this elderly patient group. Patients with portal hypertension
and antral vascular ectasia should be considered for transjug­
ular intrahepatic portosystemic shunt (TIPSS). (See Schwartz
l Oth ed., Figure 26-6 1 , pp. 1088- 1 089.)

FIG. 26-5. Gastric a ntra l vascu l a r ecta s i a (wate r m e l o n stomach).

(Reproduced with perm ission fro m Gold m a n H . M ucosa l
hypertrophy a n d hyperp l a s i a of the stomach, i n M i n g S-C, G o l d m a n
H, e d s . Pathology of the Gastroin testinal Tract, 2 n d ed. B a l t i m o re:
Wi l l ia m s & Wi l ki n s; 1 998, p. 548.)
 21 3
18. Treatment for severe early dumping after gastrectomy Answer: C
that is persistent despite an antidumping diet and fiber is Dumping is a phenomenon consisting of a constellation of
A. Expectant management postprandial symptoms thought to be the result of the abrupt
B. Oral glucose for symptoms delivery of a hyperosmolar load into the small bowel due to
C. Octreotide ablation of the pylorus or decreased gastric compliance. Early
D. Surgical conversion to a Roux-en-Y drainage dumping occurs 1 5 to 30 minutes after a meal, with patients
becoming diaphoretic, weak, light-headed, and tachycardic.
Late dumping occurs hours later, and is due to a reactive
hypoglycemia. Late dumping is relieved by the administra­
tion of sugar. The medical therapy for the dumping syndrome
consists of dietary management and somatostatin analogue
(octreotide) . Often, symptoms improve if the patient avoids
liquids during meals. Hyperosmolar liquids (eg, milk shakes)
may be particularly troublesome. There is some evidence that
adding dietary fiber compounds at mealtime may improve
the syndrome. If dietary manipulation fails, the patient is V1
..-+
started on octreotide, 1 00 f.lg subcutaneously twice daily. This 0
can be increased up to 500 f.lg twice daily if necessary. The 3
Cl.J
long -acting depot octreotide preparation is useful. Octreotide ()
:::1
not only ameliorates the abnormal hormonal pattern seen in
patients with dumping symptoms, but also promotes resto­
ration of a fasting motility pattern in the small intestine (ie,
restoration of the migrating motor complex [MMC] ) . Only
a very small percentage of patients with dumping symptoms
ultimately require surgery. Therefore, the surgeon should not
rush to re-operate on the patient with dumping syndromes.
(See Schwartz l Oth ed., p. 109 1 . )

19. Menetrier disease is characterized by Answer: A

A. Hypertrophic gastric folds and hypoproteinemia There are two clinical syndromes characterized by epithelial
B. A tortuous submucosal congenital arteriovenous hyperplasia and giant gastric folds: ZES and Menetrier dis­
malformation ease. The latter is characteristically associated with protein­
C. Gastric antral vascular ectasia losing gastropathy and hypochlorhydria. A few patients with
D. Epithelial hyperplasia and hypergastrinemia these unusual diseases have been successfully treated with the
epidermal growth factor receptor blocking monoclonal anti­
body cetuximab. There may be an increased risk of gastric
cancer with this disease, and gastric resection may be indi­
cated for bleeding, severe hypoproteinemia, or cancer. The
other options describe Dieulafoy lesions, watermelon stom­
ach, and ZES, respectively. (See Schwartz l Oth ed., p. 1088.)
 C H A P T E R 2 1

STOMACHANDDUODENUM
Lia Jordano, M.D., and Minh B. Luu, M.D.

1. One month after an antrectomy with Billroth II reconstruction, a eitherirondeficiencyormegaloblasticsecondarytoB12deficiency.

patient presents with colicky abdominal pain, distention, bilious Lossofasignificantportionofthestomachreducestheamountof
emesis, and failure to pass gas. This most likely represents: intrinsic factor that is required to absorb vitamin B12. Calcium
A. Blind loop syndrome e ciencies are also observed, leading to osteoporosis and osteo-
malacia, as calcium is primarily absorbed in the duodenum. All of
B. Afferent loop syndrome
these conditions are treated with supplementation. Afferent loop
 C. Refluxgastritis syndrome occurs as a result of a partial or complete obstruction in
D. Efferent loop syndrome the afferent limb. It can be acute or chronic and progress to blind
 E. Vitamindeficiency loop syndrome in which bacterial overgrowth occurs. In the case
of blind loop syndrome, megaloblastic anemia can develop due to
ANSWER: D bacterial consumption of vitamin B12. The presentation of afferent
loop syndrome includes postprandial pain and fullness with even-
COMMENTS: See Question 3. tual purely bilious emesis, which relieves the pain. Diagnosis is
Ref.: 1 made with a CT scan. Treatment consists of antibiotics for bacterial
overgrowth and conversion to a Roux-en-Y with a short afferent
2. As opposed to the above condition, the patient presents with limb. Efferent loop obstruction presents the same as a small
chronic vague abdominal discomfort and cramping with bowel obstruction. Diagnosis can be established by demonstrating
postprandialexplosivebiliousemesis,whichrelievesthe alackoffillingoftheefferentlimbonbariumswalloworbyCT
pain. He continues to be able to pass gas. What is the best scan. Operative management consists of correction of the cause for
management for this patient? the obstruction be it adhesions, internal herniation, etc. Finally,
 A. Dietarymodificationtoreducethemealsize al aline reflux gastritis most commonly plagues patients who
B. Emergent surgery to reduce the internal hernia have undergone a Billroth II reconstruction and consists of bile
refluxing into the stomach remnant. Patients present with bilious
C. Iron and calcium supplementation
emesis that does not tend to relieve their pain. Diagnosis can be
 D. ConversiontoaRoux-en-Ywithalongerafferentlimb made with a HIDA scan, demonstrating biliary secretion into the
 E. ConversiontoaRoux-en-Ywithashorterafferentlimb! stomach. The surgical management of this condition involves con-
version to a Roux-en-Y with a Roux limb that is greater than 40
ANSWER: E cm in length.
COMMENTS: See Question 3. Ref.: 1
Ref.: 1 4. Which of the following pairs of diagnostic measures and
3. Following a Billroth II reconstruction, a patient presents with their role in the management of a patient with gastric cancer
epigastric abdominal pain, bilious emesis that does not is correct?
relieve the pain, and weight loss. Which of the following  A. Physicalexamination/identifyoccultmetastaticdisease
tests would reveal the diagnosis?  B. Esophagogastroduodenoscopy(EGD)withendoscopic
 A. Hydroxyiminodiaceticacid(HIDA)scan ultrasound(EUS)/examineforlocoregionalstaging
 B. Computedtomography(CT)scan  C. CTscan/monitorforresponsetoneoadjuvanttherapy
C. Barium swallow  D. Positronemissiontomography(PET)scan/detect
 D. Kidney,ureter,andbladder(KUB)test intraabdominal metastatic disease
E. Gastric emptying study!  E. Diagnosticlaparoscopy/resectintraabdominalmetastases!

ANSWER: A ANSWER: B
COMMENTS: Postgastrectomy complications range from nutri- COMMENTS: The workup of a patient with gastric cancer
tional deficiencies to mechanical malfunctions requiring surgical begins with a thorough p ysical exa ination in which care is
intervention. The most common metabolic disturbance is anemia, taken to identify signs of advanced disease. Prominent
 CHAPTER 21 / Stomach and Duodenum 301

supraclavicular or periumbilical nodes, hepatomegaly, ascites,

ANSWER: A
palpableovariesonpelvicexamination,orafirmBlumer’sshelf
onrectalexaminationallrepresentpossiblemetastasis.Afteran COMMENTS: Both H2 blockers and PPIs work to decrease acid
initialexamination,patientsshouldundergoanEGD with EUS secretion by parietal cells. H2 blockers function as histamine receptor
for locoregional staging purposes and a CT scan for the detection antagonists at the level of the parietal cell but do not influence the
of intraabdominal metastatic spread. PET scans do not have a releaseofhistaminefromtheECLcells.PPIsmorecompletelyinhibit
reliable role in the staging workup of a patient; however, they acidsecretionbyirreversiblyinhibitingthefinalcommonpathway,the
havebeenusedtotrackresponsetoneoadjuvanttherapy.Because proton pump. For the recovery of acid secretion to occur, new proton
CT scan has an overall detection rate of 85% for intraabdominal pumpsneedtobesynthesized,givingthemalongerdurationofaction
spreadandonly50%forperitonealmetastasis, diagnostic lapa- than H2 blockers. All antisecretory agents result in the elevation of
roscopycanbeutilizedtoidentifytheoccultmetastaticdisease. serum gastrin levels and hyperplasia of the G cells and ECL cells.
In a 2007 study that included 106 patients with gastric cancer, Ref.: 1
33% of patients previously thought to be resection candidates
based on preoperative imaging were found to have CT occult 7. A patient presents after several episodes of violent emesis,
disease on laparoscopy. There is no role for the laparoscopic which eventually turned bloody. Which of the following is
resection of intraabdominal metastases. the best diagnostic tactic?
Ref.: 1  A. Uprightchestx-ray
 B. Placementofanasogastric(NG)tube
5. Which of the following is true regarding dumping syndrome?
C. Barium swallow
 A. Latedumpingsyndromeistheresultofamassiveinflux
of high osmolarity contents into the intestines. D. CT of the chest and abdomen
B. It is more common after Billroth I reconstructions versus E. Endoscopy!
Billroth II.
ANSWER: E
C. It can include cardiovascular effects such as palpitations,
diaphoresis,fainting,andflushing. COMMENTS: Mallory-Weiss tears are the result of violent
 D. Earlydumpingsyndromeismadeworsebyhigh-carbo- retching, vomiting, or coughing. They generally occur high on the
hydrate foods. lesser curvature and involve only the mucosa, not a full perfora-
tion. They comprise around 15% of upper gastrointestinal (GI)
 E. Mostpatientsrequirelong-actingoctreotideagoniststo hemorrhages.Themajorityofpatientscanbeeffectivelydiagnosed
control their symptoms.! and managed with endoscopy alone. In the rare case that endo-
scopic control is unsuccessful, operative intervention can be carried
ANSWER: C out via an anterior gastrotomyandoversewingoftheinjurywith
COMMENTS: Dumping syndrome can be divided into early and ucosal reapproxi ation. None of the other answers would accu-
latephases,withtheearlyoccurring20to30minaftereatingand rately diagnose this condition.
the late 2 to 3 h after eating. Early dumping occurs when high Ref.: 1
osmolarity contents enter the intestines at a rapid rate, inducing
a large shift of extracellular fluid into the lumen. Symptoms 8. Concerning duodenal diverticula, which of the following
include cramping, nausea and vomiting, epigastric fullness, and statements is false?
diarrhea. Late dumping occurs when contents high in carbohy- A. They are twice as common in women as in men.
drates enter the intestines, stimulating an overcompensatory B. Duodenal diverticula are the second most common
insulin release that, in turn, results in profound hypoglycemia. congenitaldiverticulaoftheintestineafterMeckel’s
Cardiovascular effects occur with both types; however, they are diverticulum.
more common with late dumping. Most patients find effective
 C. Themajorityofduodenaldiverticulaarefoundinthe
reliefwithdietarymodificationaloneincludingsmallerportions,
periampullary region.
slower eating, avoiding foods high in sugars, and separating
liquidsfromsolids.Octreotideagonistsarereservedforthefew D. Most of them are asymptomatic and found incidentally.
who do not respond to these measures. Overall, dumping is more E. They can result in cholangitis and pancreatitis from the
common after Billroth II reconstructions. obstruction of the biliary or pancreatic ducts, respectively.!
Ref.: 1
ANSWER: B
6. Which of the following is true concerning the pharmacologic
COMMENTS: Duodenal diverticula are false diverticula contain-
regulation of acid secretion?
ing only mucosa and submucosa, as opposed to a true diverticulum,
 A. Protonpumpinhibitors(PPIs)exerttheireffectatafinal whichcontainsalllayersoftheintestinalwall(e.g.,Meckel’sdiver-
common pathway of acid secretion. ticulum).Duodenaldiverticulaarethesecondmostcommoncause
B. H2 blockers inhibit the release of histamine from the ofacquireddiverticulaafterthoseinthecolon.Theyaremorecom-
enterochromaffin-like(ECL)cells. monlyseeninwomenthaninmen(2:1)andusuallyoccurlaterin
 C. PPIsfunctionasreversiblereceptorantagonists. life,similartocolonicdiverticula.Themajorityofthesediverticula
(∼75%) arefound within a2-cmradiusfrom theampulla ofVater
D. H2 blockers have a more prolonged inhibition of gastric
and generally protrude through the medial wall of the duodenum.
acidsecretionthandoPPIs.
Theseduodenaldiverticulaarerarelysymptomaticanddonotrequire
E. Antisecretory agents do not affect serum gastrin intervention. Surgery is reserved for those that are symptomatic and
levels.! in which complications develop. Symptoms are usually the result of
302 SECTION V / Alimentary Tract

hemorrhage, perforation, blind loop syndrome, cholangitis, or pan- Zollinger-Ellison syndrome, VIPoma, insulinoma, and carcinoid
creatitisfromtheobstructionofthebiliaryorpancreaticducts.Jux- tumors. They are also useful in patients with pancreatic stulas,
tapyloric diverticula have been noted to be associated with pancreatic ascites, and enterocutaneous stulas by decreasing GI
choledocholithiasis. Their presence increases the difficulty of suc- secretions. Additionally, they have been used as a treatment to decrease
cessful completion of endoscopic retrograde cholangiopancreato- bleeding from the GI tract. Glucagon is used by endoscopists to relax
graphy (ERCP). When treatment is required, surgical excision the sphincter of OdditofacilitateERCP.Secretin, which inhibits acid
(diverticulectomy)isrecommended. secretion, causes a paradoxical increase in serum gastrin levels in
Ref.: 1 patients with gastrinoma. Pancreatic polypeptide (PP) is predomi-
nantlysecretedinthepancreatichead.PPserumlevelsdropfollowing
9. A
 23-year-oldthin(92lb)womanwithahistoryofsurgical the Whipple procedure and may be related to the delayed gastric
correction of her scoliosis is evaluated for symptoms of emptying observed after pyloric-preserving pancreatoduodenectomy.
postprandial epigastric pain, fullness, nausea, and vomiting. Inaddition,PPsecretionnecessitatesintactvagalnervefunction;thus
Herphysicalexaminationisunremarkableexceptforherthin a blunt response to stimulation by sham feedings has been used to
physique/stature.BariumupperGIseriesshowedadilated evaluate intact vagal nerve function, particularly in patients suspected
duodenumandstomachwithminimalflowofbariumintothe ofhavingiatrogenicvagusnerveinjury.
jejunum.Whichofthefollowingistheoperativemanage- Ref.: 1, 2
mentofchoiceforthispatient’scondition?
A. Segmental duodenectomy 11. A patient with gastric outlet obstruction and prolonged
vomiting has which of the following metabolic
 B. Pancreaticoduodenectomy
abnormalities?
 C. Gastrojejunostomy
A. Hypochloremic, hyperkalemic metabolic alkalosis
 D. Duodenojejunostomy
B. Hyperchloremic, hypokalemic metabolic acidosis
 E. Roux-en-Yhepaticojejunostomy!
C. Hyponatremic, hypokalemic metabolic acidosis
ANSWER: D D. Hypochloremic, hypokalemic metabolic alkalosis
COMMENTS: The patient in this scenario has compression of the E. Hyperchloremic, hyperkalemic metabolic acidosis!
third portion of the duodenum by the superior mesenteric artery
(SMA) as it passes over it. This rare condition is known as SMA
ANSWER: D
syndrome or Wilkie syndrome. This syndrome is usually seen in COMMENTS: The most common cause of gastric outlet obstruc-
young asthenic females with predisposing conditions of weight loss, tion is malignancy. The classic metabolic abnormality resulting from
scoliosisorcorrectivesurgeryforit,supinemobilization,andplace- gastric outlet obstruction and prolonged vomiting is hypochloremic,
ment of a body cast. The diagnosis is usually made with either a hypokalemic metabolic alkalosis. Initial loss of hydrochloric acid
barium upper GI series or a CT, with oral and intravenous (IV) causes hypochloremia and mild alkalosis compensated for by renal
contrast enhancement demonstrating a dilated duodenum and excretionofbicarbonate.Thereforeintheearlystages,theurineis
stomach with an abrupt or nearly complete cutoff of contrast agent alkaline. Continued vomiting produces a severe extracellular fluid
at the third portion of the duodenum and minimal flow into the deficit and sodium deficit from both renal and gastric losses. The
jejunum.Conservativemanagementconsistingofnutritionalsupple- kidneysbegintoconservesodiumand,inexchange,excretehydro-
mentation can be tried initially. In patients who fail medical manage- gen and potassium cations to accompany bicarbonate. The kidneys
ment, the operative treatment of choice is duodenojejunostomy. arethepredominantsiteofpotassiumloss,andtheurineisparadoxi-
Ref.: 1 cally acidic. Urine chloride content is reduced throughout and is
eventually absent. Serum ionized calcium levels are decreased
10. W
 hichhormoneismatchedwiththecorrectdiagnostic/ becausecalciumismildlyalkalineandshiftstoitsnonionizedform
therapeutic function? to reduce alkalosis. Treatment of this metabolic situation is accom-
 A. Cholecystokinin(CCK)/treatmentofesophagealvariceal plished primarily by the administration of isotonic saline solution,
bleeding which replenishes the deficits in volume, sodium, and chloride.
 B. Somatostatin/reliefofspasmofthesphincterofOddi Potassiumisreplacedoncetherenalfunctionisoptimized.
 C. Gastrin/measurementofmaximalgastricacidsecretion Ref.: 1, 2
 D. Glucagon/provocativetestforgastrinoma 12. Which of the following statements is true with regard to the
 E. Secretin/stimulationofgallbladdercontraction! arterial blood supply of the stomach?
A. The left gastroepiploic artery is the main blood supply to
ANSWER: C the gastric conduit used in esophagectomies.
COMMENTS: GI hormones or their analogues have been used clini- B. Ligation of the left gastric artery can result in acute
cally as diagnostic or therapeutic agents. CCK is used to stimulate left-sidedhepaticischemia.
gallbladder contraction. This is useful in identifying patients with C. The stomach is susceptible to ischemia because of poor
biliary dyskinesia or acalculous cholecystitis with the help of CCK collateral circulation.
cholescintigraphy. Pentagastrin, a gastrin analogue, is used to
D. The inferior phrenic and short gastric arteries provide
measure gastric acid secretion. Somatostatin or its analogues are used
significantbloodsupplytothebodyofthestomach.
in various conditions as a result of their universal inhibitory function.
Because they inhibit the release of GI hormones, somatostatin ana- E. A replaced right hepatic artery may originate from the
logues are used for various endocrine neoplasms such as left gastric artery.!
 CHAPTER 21 / Stomach and Duodenum 303

 C. Duodenaltumorsusuallyrequirepancreaticoduodenectomy.
ANSWER: B
 D. Antrectomyisindicatedifthetumorcannotbelocalized.
COMMENTS: The arterial blood supply of the stomach is
E. Resection of liver metastases is not indicated.!
derived primarily from the celiac artery. The left gastric artery
comes off of the celiac artery and supplies the stomach along the
ANSWER: A
lessercurvature.Anaberrant/replacedleft hepatic artery origi-
nates from the left gastric artery (15%–24%) and can represent COMMENTS: Treatment of Zollinger-Ellison syndrome is
the only arterial blood supply to the left hepatic lobe. This aber- two pronged and aimed at both resecting the tumor when pos-
rant/replaced left hepatic artery runs in the gastrohepatic liga- sible and protecting the gastric end organ. Therapy must be
ment. The right gastric artery typically arises from the common individualized. Patients with known endocrine tumors should
hepatic artery distal to the gastroduodenal artery. The right and undergo careful evaluation for other potential endocrine tumors.
left gastroepiploic arteries usually originate from the gastroduo- In patients with gastrinoma and hyperparathyroidism, para-
denal artery and splenic artery, respectively. It is the right estro- thyroidectomyshouldbeperformedfirsttoeliminatehypercal-
epiploic artery that functions as the main blood supply to the cemia. Abdominal surgery is not urgent with the current
gastric conduit used in esophagectomies. The short gastric arteries antisecretory medications. Although gastrinomas are often mul-
arising from the splenic artery and inferior phrenic arteries also tipleandareusuallymetastatic,long-termsurvivalispossible.
contribute significant blood volume to the proximal part of the Aggressiveattemptstolocalizeandresecttumorscanprovidea
stomach. The stomach is well protected from ischemia and can curein5%–20%ofpatientsandcandiminishgastrinsecretion
easily survive with ligation of three of four arteries because of its in others. Digital palpation through a duodenotomy and intraop-
rich collateral circulation. erativeultrasoundareusefuloperativeadjuncts.Bothpancreatic
Ref.: 1, 2 and duodenal gastrinomas can be resected by enucleation when
appropriately located. Blind pancreatic resections are not gener-
13. Choose the correct type of vagotomy with the appropriate ally indicated. When complete tumor removal is not possible, a
level of vagal transection from the pairs listed below: gastric operation may be appropriate. Proximal gastric vagot-
 A. Truncalvagotomy/criminalnerveofGrassi omy may be useful, but total gastrectomy still provides the best
 B. Highlyselectivevagotomy/anteriorandposteriorvagal long-termqualityoflifeforsomepatients.Life-longpharmaco-
trunks below the celiac and hepatic branches logic treatment with antisecretory agents may control the ulcer
diathesis in some patients, but problems with high doses, com-
 C. Selectivevagotomy/anteriorandposteriorvagaltrunks pliance, and side effects may occur. Resection or ablation of
above the celiac and hepatic branches metastatic disease, although not curative, can provide important
 D. Parietalcellvagotomy/terminalbranchesofthenerveof palliation and decrease the need for drug therapy.
Latarjet Ref.: 1–3
 E. Highlyselectivevagotomy/hepaticbranches!
15. Which of the following clinical conditions is not associated
ANSWER: D with delayed gastric emptying?
A. Hypocalcemia
COMMENTS: In the chest, the vagal trunks are situated to the right
and left of the esophagus. At the level of the cardia, the left vagal B. Scleroderma
trunk is found anterior and the right vagal trunk is found posterior C. Hyperglycemia
secondary to the embryonic gastric rotation. The anterior vagal trunk  D. Myxedema
dividesintohepaticandanteriorgastric(anteriornerveofLatarjet)
 E. Zollinger-Ellisonsyndrome!
branches. The posterior vagus divides into the posterior nerve of
Latarjetandceliacbranches.Oneoftheproximalposteriorbranches
ANSWER: E
of the posterior vagal trunk is known as the criminal nerve of Grassi
andisidentifiedasapossiblecauseofrecurrentulcersifleftundi- COMMENTS: Disorders of gastric emptying can be divided
vided during selective vagotomy. Truncal vagotomy is convention- into rapid or delayed emptying, both of which can be signifi-
allyperformedatorjustaboveorbelowthediaphragmaticesophageal cantly disabling conditions. Delayed gastric emptying is the
hiatus before it gives off celiac and hepatic branches. In contrast, morefrequentlyencounteredproblemofgastricmotility.Exclud-
a selective vagotomy is performed distal to this location and spares ing mechanical obstruction, important causes of delayed gastric
the celiac and hepatic branches. Highly selective vagotomy (also emptying include metabolic derangements (e.g., yxe e a
known as proxi al gastric or parietal cell vagoto y)dividesindi- and hyperglycemia),electrolyte abnormalities(e.g.,hypoka-
vidual terminal branches of the nerve of Latarjet in the fundus lemia and hypocalcemia),drugs(e.g.,narcotics and anticho-
and corpus of the stomach but spares the vagal branches to the linergics), and systemic diseases (e.g., diabetes mellitus and
antrum and pylorus, which control gastric motility and emptying— scleroderma).Upto40%ofpostvagotomypatientsexperience
thus obviating the need for a drainage procedure. delayed gastric emptying. Rapid gastric emptying is less com-
Ref.: 1, 2 monly observed. Causes of rapid gastric emptying include previ-
ous gastric resection, conditions with impaired fat absorption
14. C
 oncerningthetreatmentofpatientswithZollinger-Ellison resultinginthelossoftheinhibitionofgastricemptying(e.g.,
syndrome, which of the following statements is true? pancreatic insu ciency and short bowel syndrome),andcon-
A. Operative treatment of associated hyperparathyroidism ditions with hypergastrinemia such as Zollinger-Ellison
takes precedence over abdominal surgery. syndrome.
 B. Pancreatictumorsshouldnotberemovedbyenucleation. Ref.: 1–3
304 SECTION V / Alimentary Tract

16. Which of the following conditions is not associated with the operative intervention besides closure of the
Helicobacter pylori infection? perforation?
A. Duodenal ulcer  A. Feedingjejunostomy
B. Gastric cancer  B. Gastrojejunostomy
 C. Mucosa-associatedlymphoidtissue(MALT)lymphoma C. Gastrostomy tube placement
 D. Gastroesophagealrefluxdisease  D. Excisionorbiopsyoftheulcer
E. Chronic gastritis!  E. Pyloroplasty!

ANSWER: D ANSWER: D
COMMENTS: H. pyloriisacurvedorS-shaped,gram-negative COMMENTS: The preferred treatment of a perforated duodenal
microaerophilic motile bacterium whose natural habitat is the ulcer is resuscitation and prompt surgery. Nonoperative manage-
human stomach. H. pylori infection has been demonstrated to be ment is reserved for old contained perforations or for terminally ill
associated with 90% of duodenal ulcers and 75% of gastric patients who otherwise cannot undergo surgery. The diagnosis is a
ulcers. After eradication of the organism as a part of ulcer treat- presumptive one based on clinical grounds and should not be
ment,recurrenceofulcerisextremelyrare.Inaddition,H. pylori excluded if pneumoperitoneum cannot be demonstrated, because
has been associated with chronic atrophic gastritis, which in turn about 20% of patients with perforations do not have this typical
leads to gastric atrophy and intestinal metaplasia, a suspected radiographic feature. Operative management requires the closure
precursor of gastric cancer. H. pylori infection also increases the of the perforation, which is generally best accomplished with an
risk for low-grade MALT lymphoma; eradication of H. pylori omental (Graham) patch. Closure of the perforation is usually
results in the resolution of MALT lymphomas in most cases. There sufficientinpatientswithduodenalulcers;however,excisionofthe
appears to be a negative association between H. pylori infection ulcer is necessary to rule out malignancy in patients with gastric
and G reflux isease. ulcers before closure. Following simple repair alone, the traditional
Ref.: 1,2,4 natural history has been that about one-third of patients have no
further ulcer problems, one-third have ulcer recurrence amenable
17. With regard to H. pylori–negativeduodenalulcerdisease, tomedicalmanagement,andone-thirdrequireasubsequentopera-
which of the following statements is true? tion for ulcer disease. It is not clear how precisely this applies to
 A. Nonsteroidalantiinflammatorydrugs(NSAIDs)arenota patients with H. pylori infection or those with NSAID-induced
cause of duodenal ulcers in patients who are H. pylori ulcers. Definitive operations should be performed only in stable
negative. patients and in those with documented failure after appropriate H.
B. Because of the high prevalence of H. pylori–positive pylori eradication. Truncal vagotomy can be performed expedi-
duodenal ulcers, patients should be treated for H. pylori tiously but has a greater incidence of side effects. Highly selective
withoutconfirmatorytesting. vagotomyisanexcellentchoicebutistimeconsumingandrequires
asurgeonwiththeexpertisetoperformit.Resectiveproceduresare
C. In contrast to H. pylori–positiveduodenalulcers, generally avoided in the setting of perforation because of higher
NSAID-inducedulcersarefrequentlyassociatedwith morbidity. Following surgery, ulcerogenic drugs should be with-
chronic active gastritis. held, and any concomitant H. pylori infection should be treated.
D. H. pylori–negativeduodenalulcersareusuallylarge Ref.: 1,6
ulcers that are not often associated with bleeding.
E. Older age, multiple comorbid conditions, and sepsis are 19. A
 45-year-oldmanrequiressurgeryforanintractable
independently associated with H. pylori–negative duodenal ulcer. Which operation best prevents ulcer
duodenal ulcers.! recurrence?
A. Subtotal gastrectomy
ANSWER: E B. Truncal vagotomy and pyloroplasty
COMMENTS: Initial studies have demonstrated that H. pylori C. Truncal vagotomy and antrectomy
infection is present in more than 90% of patients with duodenal D. Selective vagotomy
ulcers. However, more recently, it has been shown that the preva-
E. Highly selective vagotomy!
lence of H. pylori–associatedduodenalulcersisonly75%andis
foundtobedecreasing.Thusitisimportanttofirstmakethediag-
ANSWER: C
nosis of an active H. pylori infection rather than initiating empiri-
cal therapy. H. pylori–negative duodenal ulcers are independently COMMENTS:SeeQuestion20.
associated with NSAID use, older age, multiple medical prob- Ref.: 1,2,6
lems, and sepsis.UseofNSAIDsisthemajorcauseofduodenal
ulcers in patients who are H. pylori negative. Bleeding is the initial 20. Which operation for duodenal ulcer is least likely to produce
manifestation in these patients, and they have large and multiple undesirable postoperative symptoms?
ulcers. A. Subtotal gastrectomy
Ref.: 1, 6 B. Truncal vagotomy and pyloroplasty
18. If the patient in Question 21 was found to have a perfo- C. Truncal vagotomy and antrectomy
rated gastric ulcer instead of a duodenal ulcer, which D. Selective vagotomy
additional procedure would need to be conducted during E. Highly selective vagotomy!
 CHAPTER 21 / Stomach and Duodenum 305

is entered and a longitudinal pyloroduodenotomy is performed.

ANSWER: E
Digital pressure is applied over the ulcer base to temporize the
COMMENTS: The goal of surgical therapy for duodenal ulcers bleeding and allow resuscitation before suture control is obtained.
is to reduce acid production in a manner that is safe and has the Propercontrolofbleedingrequiresthree-pointsutureligationof
fewest possible side effects. Acid can be reduced by eliminating the duodenal ulcer. These “U” stitches are placed superior and
vagal stimulation, removing the antral source of gastrin, and remov- inferiortothesiteofpenetrationtoligatetheproximalanddistal
ingtheparietalcellmass.Traditionally,subtotaltwo-thirdsgastrec- gastroduodenal artery. A third suture is placed on the medial
tomy has carried the highest mortality rate. Truncal vagotomy aspect of the ulcer to control the transverse pancreatic branch
with antrectomy has the lowest recurrence rate. Procedures coming off the gastroduodenal artery. After the bleeding is con-
involving antrectomy, pyloroplasty, or truncal vagotomy may be trolled, biopsy of gastric mucosa should be performed for histo-
complicated by diarrhea, postprandial dumping, or bile reflux. logic analysis of H. pylori. The longitudinal pyloroduodenotomy
Selective vagotomy, which preserves the hepatic and celiac vagal is then closed transversely (Heineke-Mikulicz or Weinberg
branches, has been associated with a lower rate of diarrhea than pyloroplasty).
truncal vagotomy. Highly selective vagotomy, also known as pari- Ref.: 1,2,4,6
etal cell vagotomy, aims to denervate the parietal cell–bearing
portion of the stomach but preserves innervations to the pyloroan- 23. Which gastric ulcer corresponds with the correct recom-
tral region and thus maintains more normal gastric emptying. This mended surgical management?
operation carries the lowest mortality rate and the lowest incidence  A. TypeI/BillrothIorIIreconstruction
of side effects, but the highest recurrence rate, which ranges from
 B. TypeII/truncalvagotomyandpyloroplasty
5% to 15%.
 C. TypeIII/CsendesgastrectomywithRoux-en-Ygastrojeju-
Ref.: 1,2,6
nostomyorPauchetgastrectomyandBillrothI
21. A
 75-year-oldmantakingNSAIDsforarthritishasanacute reconstruction
abdomenandpneumoperitoneum.Hissymptomsare6hold,  D. TypeIV/BillrothIorIIreconstructionwithtruncal
and his vital signs are stable after the infusion of 1 L of vagotomy
normalsalinesolution.Whatshouldbethenextstepinthe  E. TypeIV/totalgastrectomy!
management of this patient?
A. CT of the abdomen ANSWER: A
B. EGD
COMMENTS: Benign gastric ulcers have been classified in
 C. Antisecretorydrugs,broad-spectrumantibiotics,and terms of their anatomic location. Type I ulcers are the most
surgeryifhefailstoimprovein6h common(50%)andoccurinthebodyofthestomachalongthe
D. Antisecretory drugs, antibiotics for H. pylori, and surgery lesser curvature. These ulcers are associated with low to normal
ifhefailstoimprovein6h acid secretion. Type IIgastriculcers(25%)alsooccurinthebody
E. Surgery! of the stomach but have associated duodenal ulcers. Type III
gastric ulcers (20%) are located in the prepyloric region. Both
ANSWER: E type II and type III ulcers are associated with excessive acid
secretion. Type IVulcersaretheleastcommon(<10%)andoccur
COMMENTS: See Question 18. near the GE junction along the lesser curve. Like type I ulcers,
Ref.: 1,2,6 they are associated with low or normal acid secretion. Surgical
intervention is indicated for patients who have failed maximal
22. D
 uringanoperationforableedingduodenalulcer,three-
medical therapy (12 weeks), for those in whom complications
point“U”stitchesareplacedtoligatewhichofthefollowing
develop, or for those in whom malignancy cannot be ruled out.
arteries after longitudinal pyloroduodenotomy?
Surgical therapy for benign gastric ulcers depends on the type of
A. Common hepatic, right gastric, and gastroduodenal ulcer and its associated acid secretion. Type I ulcers are usually
arteries well treated with antrectomy or hemigastrectomy (including
 B. Proximalanddistalgastroduodenalandtransverse removal of the ulcer) without vagotomy. Type IV ulcers do not
pancreatic arteries requirevagotomyeither.TypeIVulcersneartheGEjunctioncan
C. Right gastric, gastroduodenal, and right gastroepiploic be treated by modifications of distal gastrectomy that include
arteries ulcerexcision.Distalgastrectomywithextensionalongthelesser
curvaturetoincludetheulcer(Pauchet procedure)andBillroth
D. Right gastric and anterior and posterior inferior pancreati- I reconstruction can be performed for ulcers that are 2 to 5 cm
coduodenal arteries from the GE junction. For type IV ulcers at the GE junction,
E. Common hepatic, gastroduodenal, and superior mesen- subtotal gastrectomy with Roux-en-Y jejunal reconstruction
teric arteries! (Csendes procedure), a rotational Tanner gastrectomy, or a
Kahler-Muhlenberg procedure should be performed. Because
ANSWER: B type II and type III ulcers are associated with acid hypersecretion,
COMMENTS: Massive bleeding is usually the result of posterior they are treated as duodenal ulcers. Truncal vagotomy with Bill-
erosion of a duodenal ulcer into the gastroduodenal artery. Emer- roth I or II reconstruction is the preferred surgical therapy because
gency surgical intervention is indicated when bleeding is refrac- it accomplishes both goals of a decrease in acid secretion and
tory to endoscopic therapy or in the presence of hemorrhagic excisionoftheulcer.
shock.Afterexpeditiouspreoperativeresuscitation,theabdomen Ref.: 1,4,6
306 SECTION V / Alimentary Tract

24. Which of the following tests is best to document eradication of potential similar to colonic adenomatous polyps. The risk increases
H. pyloriinfectioninpatientswithpepticulcerdisease(PUD)? withincreasingsizeofthepolyp.Fundic gland polyps are benign
 A. Ureabreathtest and have no malignant potential.
 B. Histologicexaminationofmucosa Ref.: 1,6,7
C. Rapid urease test 26. With regard to the surgical treatment of gastric adenocarci-
D. Culture and sensitivity testing noma, which of the following statements is true?
E. H. pylori serology! A. Total gastrectomy for antral lesions results in longer
survival than does partial gastrectomy.
ANSWER: A B. Routine splenectomy does not improve survival rates.
COMMENTS: It is important to document the presence or absence  C. Extendedlymphnodedissectionimprovessurvivalrates
of H. pyloritoadequatelytreatpatientswithPUD.Bothinvasive in patients with stages I and II lesions.
and noninvasive tests are available for the diagnosis of H. pylori D. Total gastrectomy for palliation is contraindicated.
infection. Invasive tests require endoscopic mucosal biopsy and E. Linitis plastica should be resected to histologically
include istologic exa ination, rapid urease test, and culture. negative margins.!
Noninvasive tests include the urea breath test and serology. His-
tologic examination can accurately diagnose H. pylori with two ANSWER: B
biopsyspecimenswithhighsensitivityandspecificity(90%).The
rapid urease test on a mucosal biopsy specimen uses a change in COMMENTS: Gastric adenocarcinoma is preferably treated by
pHresultingfromthebreakdownofureabyaureaseenzymepro- resection, although resection usually proves to be palliative. The
duced by H. pylori. This test is considered the initial test of choice general strategy for curative resection is to remove as much of the
because of its simplicity, accuracy, and rapid results. Culture of H. stomach as necessary to obtain free margins and to perform limited
pylori has the most specificity (100%) but is difficult to perform node dissection. Although data from Japan support the benefit of
and is currently not widely available. Cultures should usually be extendednodaldissection(celiac,mesenteric,hepatic,andparaaortic),
reserved for research purposes or for patients with suspected anti- studiesintheUnitedStateshavenotgenerallyconfirmedthisbenefit.
biotic resistance. The urea breath test is a noninvasive test that Furthermore,theseextendeddissectionscanbeassociatedwithsub-
analyzes breath for labeled carbon dioxide produced by bacterial stantial morbidity. Most resections entail distal subtotal gastrectomy.
urease from the conversion of ingested labeled urea. Because of its Totalgastrectomyisappropriateforlocallyextensivetumors,proximal
noninvasiveness plus high sensitivity and specificity (95%), the tumors (to avoid esophageal anastomosis to the distal stomach
urea breath test is considered the test of choice for documentation remnant),andevenpalliationifnecessary.Extendingclearmarginson
of H. pylorieradication.Serologictestsarequickandinexpensive adistaltumorbytotalratherthansubtotalgastrectomyisofnobenefit.
but cannot differentiate between active infection and previous Resections for linitis plastica are palliative, usually necessitate total
exposure. Serologyis useful for theinitialdiagnosisofH. pylori gastrectomy, and are carried out to grossly negative margins only.
infection in patients in whom endoscopy is not indicated. Splenectomy is performed according to the location of gastric resec-
Ref.: 1,5,6 tion, but its routine performance does not improve the survival rate.
The number of lymph nodes resected, the number of positive nodes,
25. Which of the following conditions is not associated with and the ratio of positive to the total number of lymph nodes have
gastric cancer? important staging implications. Furthermore, a minimum number of
A. Chronic atrophic gastritis 15lymphnodesshouldroutinelybeexamined.
B. H. pylori infection Ref.: 1,6,7
C. Hereditary nonpolyposis colorectal cancer 27. W
 ithregardtogastrointestinalstromaltumors(GISTs),
D. Adenomatous gastric polyps which of the following statements is incorrect?
E. Fundic gland polyps!  A. Acombinationofcellularmorphologyonhematoxylin–
eosin staining and KIT immunohistochemistry are
ANSWER: E requiredforthediagnosisofGIST.

COMMENTS:Certaingastriclesionshaveasignificantassocia- B. After the small intestine, the stomach is the second most
tion with gastric adenocarcinoma and can be considered precursors common location for GISTs, followed by the colon and
to malignancy. Chronic atrophic gastritis, of which several forms rectum.
are recognized, underlies most gastric cancers. The epithelial  C. ThemajorityofGISTshaveanactivatingmutationinthe
changes of intestinal metaplasia and dysplasia are premalignant. KIT oncogene.
Autoimmune chronic gastritis involves the body and fundus of the D. GISTs are usually resistant to conventional chemotherapy
stomach. It is associated with pernicious anemia, achlorhydria, very and radiation therapy.
high gastrin levels, and a high risk for cancer. Hypersecretory E. Complete surgical resection is the standard of treatment.!
chronic gastritis involves the gastric antrum and is associated with
PUD but not malignancy. H. pylori infection may be the most ANSWER: B
important risk factor for gastric adenocarcinoma worldwide. The
immunoglobulin (Ig)G antibody positivity in various populations COMMENTS: GI stromal tumors are the most common mes-
correlates with the local incidence of gastric cancer. Hereditary enchymal neoplasms of the GI tract. The majority of these
nonpolyposis colorectal cancer is an inheritable risk factor for GISTsoccurinthestomach(60%),followedbythesmallbowel
gastric cancer. Adenomatous gastric polyps have malignant (30%), esophagus (1%–5%), and colon and rectum (5%). The
 CHAPTER 21 / Stomach and Duodenum 307

diagnosis of GIST is based on the presence of characteristic

ANSWER: A
pathologic findings on hematoxylin–eosin staining and expres-
sion of the KIT receptor on immunohistochemistry. Rarely, COMMENTS: Gastric volvulus is a serious complication of para-
KIT might not be overexpressed, and in such cases molecular esophageal hernia. Two types of gastric volvulus may occur, depend-
evaluation may be necessary. These tumors do not usually ingontheaxisofrotation. rganoaxial volvulus, the more common
metastasizetolymphnodes.Completesurgicalresectionisthe type,involvesrotationaroundtheaxisofalineconnectingthecardia
standardoftreatmentofprimary,localizedGISTs.Themajority and pylorus. esenteroaxial volvulus is not associated with a dia-
of GISTs have an activating mutation in the KIT protooncogene phragmatic defect and involves rotation around the line that bisects the
that can be effectively inhibited by tyrosine kinase inhibitors greater and lesser curvatures. Combined types have also been described.
such as imatinib mesylate (Gleevec). GISTs are resistant to Patients classically present with Borchardt’s triad, which includes
conventional chemoradiation therapy. Laparoscopic resection is acute epigastric pain, violent retching without vomiting, and the inabil-
increasingly being used, provided that a negative margin can be ity to pass an NG tube. Acute gastric volvulus is a surgical emergency
obtained. Both the size and number of mitoses per 50 high- andrequirespromptreductionviaatransabdominalapproach.Repair
powerfieldhavebeenusedtocategorizetumoraggressiveness. of the diaphragmatic defect should follow with possible fundoplica-
Tumorlocationmayhaveprognosticimplicationsinthatextra- tion. In the setting of volvulus without an associated diaphragmatic
gastric tumors may carry a worse prognosis. Large or unresect- defect,detorsionofthestomachandeithergastropexyortubegastros-
able tumors that show KIT overexpression may initially be tomy is performed to reduce the risk for recurrence.
treated with Gleevec. Ref.: 1, 11
Ref.: 1, 8
30. In a patient who presents with intractable ulcer disease,
28. W
 hichofthefollowingstatementsregardingCrohn’sdisease which of the following statements is true?
of the duodenum is false?  A. Afastingserumgastrinlevelof>200pg/mLisdiagnostic
 A. DuodenalCrohn’sdiseaseaccountsonlyfor2%–4%of of a gastrinoma.
allpatientswithCrohn’sdisease. B. A CT scan may demonstrate a mass within the tail of the
B. Because of its location, operative intervention is fre- pancreas.
quentlyneededforduodenalCrohn’sdisease.  C. InthesettingofZollinger-Ellisonsyndrome,endoscopy
 C. Whenanoperationisrequired,abypasssuchasgastroje- would demonstrate atrophic gastric mucosa.
junostomyisperformedratherthanduodenalresection.  D. Themostsensitiveandspecificdiagnostictestfor
 D. Inwell-selectedpatients,strictureplastycanbecarriedout Zollinger-Ellisonsyndromeisthesecretinstimulationtest.
with good results. E. Testing for associated multiple endocrine neoplasia II
 E. Adenocarcinomaistheleadingcauseofdisease-specific (MENII)endocrinetumorsshouldbeconsidered.!
deathinpatientswithCrohn’sdisease.!
ANSWER: D
ANSWER: B COMMENTS: Intractable ulcer diseaseisdefinedasthatoccurring
COMMENTS: Crohn’s disease of the duodenum is not common afteranadequatedurationofantacidtherapy,documentationoferadi-
and is seen in only 2%–4% of patients with Crohn’s disease. cation of H. pylori infection, and elimination of NSAID use. In these
Medical therapy remains the mainstay of treatment of duodenal patients, malignancy must be ruled out and a serum gastrin level should
Crohn’s disease, with surgical intervention being reserved for be drawn to evaluate for a gastrinoma. Zollinger-Ellison syndrome is
patients who do not respond to medical therapy or in whom a thetriadofgastricacidhypersecretion,severePUD,andnon–betaislet
complication such as obstruction or perforation develops. In cell tumors of the pancreas. Gastrinomas occur most commonly within
patients who do need a surgical procedure, bypass is preferred over the gastrinoma triangleasdefinedbytheconfluenceofthecysticand
duodenal resection. In a few select patients, their anatomy might commonbileduct,thejunctionofthesecondandthirdportionsofthe
be amenable to strictureplasty. duodenum,andthejunctionoftheneckandbodyofthepancreas.They
Irrespective of the location of Crohn’s disease, GI cancer arefoundalmostequallywithinthewalloftheduodenumasthehead
remainstheleadingcauseofdeathinpatientswithCrohn’sdisease. of the pancreas but not in the tail of the pancreas. Endoscopy often
reveals prominent rugal folds, which result from the trophic effect of
Ref.: 1,9,10
the hypergastrinemia. Fasting serum gastrin levels are usually elevated
29. With regard to gastric volvulus, which of the following above200pg/mL,butavaluegreaterthan1000pg/mLisdiagnostic.
statements is true? Inthesettingofequivocalgastrinlevels,themostsensitivetestisthe
 A. TheBorchardt’striadincludesacuteepigastricpain, secretinstimulationtest.Ariseingastrinlevelsofgreaterthan200pg/
retching without vomiting, and inability to pass an NG mLabovebaselineisspecificforgastrinoma.Gastrinomasareassoci-
tube. ated with MEN I syndrome, not MEN II syndrome. Testing for associ-
ated endocrine tumors should be performed.
B. Its symptoms consist of severe nausea with bilious
emesis. Ref.: 1, 11

 C. Itmorefrequentlyinvolvesrotationaroundtheaxisthat 31. Which of the following is true with regard to gastric
bisects the greater and lesser curvatures. carcinoid neoplasms?
D. Its surgical management is via a transthoracic approach. A. The incidence is decreasing.
E. Surgical management of volvulus without a diaphrag- B. They commonly present with abdominal pain, bleeding,
matic defect involves only detorsion of the stomach.! and carcinoid syndrome.
308 SECTION V / Alimentary Tract

C. The subtypes associated with low acid states have a 33. Which of the following statements is true regarding the gross
better prognosis. or microscopic anatomy of the stomach?
 D. Long-termuseofPPIshasnotbeenshowntoincrease A. The angularis incisura marks the transition from the body
the risk for developing a gastric carcinoid neoplasm. of the stomach to the antrum along the greater curvature.
E. The treatment is based largely on nonsurgical manage-  B. TheangleofHisisformedbythejunctionofthefundus
ment with somatostatin analogues.! with the left diaphragmatic crus.
 C. Thecardiaisdominatedbymucus-secretingcells.
ANSWER: C
 D. Themajorityoftheparietalcellsexistinthefundusand
COMMENTS: Long thought to be a rare location for carcinoid theproximalbody.
malignancies, gastric carcinoid neoplasms (or neuroendocrine  E. TheGEjunctionisnormallyfoundatthediaphragmatic
tumors, NET) are increasing in incidence. Many patients are hiatus.!
asymptomatic and diagnosed incidentally during endoscopy,
though rarely they can present with abdominal pain, bleeding, and ANSWER: C
symptoms of carcinoid syndrome. The rise in the use of endos-
copy has been postulated to account for some of the increase in COMMENTS: The most proximal region of the stomach is the
incidence; however, the increase in the long-term use of PPIs cardia. This is dominated by mucus-secreting cells, which provide
may also play a part as it has been shown to be an independent amechanicalbarriertoinjury.Gastriculcersinthisareaaredeemed
risk factor for the development of gastric carcinoid tumors. There type IV ulcers and are associated with a breakdown of this mucus
are three types of gastric carcinoids. The majority of these are barrier. The uppermost part of the stomach is the fundus.Thejunc-
type 1 and are associated with a low acid state (normally from tion of the fundus and the left margin of the esophagus forms the
atrophicgastritis),resultinginhypergastrinemia, which in turn angle of His. The GE junction is normally found about 2 to 3 cm
is thought to cause ECL cell hyperplasia and eventual dysplasia. below the diaphragmatic esophageal hiatus.The extension of the
This type carries a better prognosis than sporadic types, type 3, esophagus into the abdominal cavity creates an anatomically
notassociatedwithlowacidstates.Thefinaltypeistype2,which important pressure differential between the distal esophagus within
is associated with Zollinger-Ellison syndrome and high gastrin the positive pressure abdomen and the midesophagus within the
levels. Treatment is based on complete resection whether accom- negativepressurethoraciccavitythathelpstopreventreflux.This
plished via endoscopic removal, wedge resection, or total gastrec- relationship is disturbed in patients with type I hiatal hernias. The
tomy, depending on the extent of the disease. Somatostatin body is bound by the lesser curvature on the right and greater
analogues can serve to decrease tumor burden and address symp- curvature on the left. Parietal cellsexistprimarilywithinthebody,
toms of carcinoid syndrome in patients with recurrent or meta- with few in the fundus and antrum and none in the cardia or pre-
static disease. pyloric antrum. As the lesser curvature meets the pylorus, it angles
Ref.: 1, 11 abruptly to the right, identifying the angularis incisura.
Ref.: 1, 11
32. On the cellular level, which of the following is true regarding
acid secretion? 34. Which of the following statements is true regarding the
A. Acid secretion is stimulated only by gastrin. management of upper GI bleeding?
B. Acid secretion is stimulated by gastrin and secretin.  A. ThereturnofclearfluidfromanNGlavagerulesout
upper GI bleeding.
 C. Thefinalcommonpathwayofacidsecretionisthe
hydrogen-potassiumadenosinetriphosphatase(H+,  B. Primaryhemostasisisonlyachievedin60%ofpatients
K+-ATPase). by endoscopy alone.
D. Histamine activates acid secretion via increases in  C. ThemajorityofupperGIbleedingwillrequire
intracellular calcium. intervention.
E. Acid secretion is stimulated by CCK.!  D. PatientswithanupperGIbleedshouldundergoendos-
copywithin24hofpresentation.
ANSWER: C  E. AllpatientsshouldbeplacedonPPIandoctreotide
infusions.!
COMMENTS: It is important to have the knowledge of the
cellular basis for parietal cell acid secretion to understand the
ANSWER: D
pharmacologic control of acid. The parietal cell has three spe-
cific plasma membrane receptors that stimulate acid secretion: COMMENTS:ThemajorityofupperGIbleedingrequiresnointer-
acetylcholine, histamine, and gastrin receptors. All three vention and ceases spontaneously. However, if it persists, it is associ-
receptors eventually activate the H+, K+-ATPase pump via dif- ated with a mortality rate of 6%–8%. Initial management should
ferent mechanisms, which results in the secretion of a hydrogen include IV access, fluid resuscitation, and blood products as indi-
ionforpotassium.Acetylcholine-andgastrin-stimulatedsecre- cated.PlacementofanNGtubecanconfirmupperGIbleedingwith
tion depends on increases in intracellular calcium levels, with return of bloody or coffee ground lavage; however, only return of
subsequent phosphorylase kinase–induced phosphorylation bilious lavage can effectively rule out an upper GI source of a bleed.
and H+, K+-ATPaseactivity.Histamineactivatestheadenylate Regardless of the degree of severity, patients who present with upper
cyclase pathway. Somatostatin, CCK, and secretin inhibit acid GIbleedingshouldundergoendoscopywithin24hofpresentation
secretion. for both diagnostic and therapeutic purposes. Endoscopic control
Ref.: 1, 11 results in primary hemostasis in approximately 90% of patients.
Patientsshouldbecloselymonitoredinanintensivecareunit(ICU)
 CHAPTER 21 / Stomach and Duodenum 309

settingincaseofpersistentbleeding,andallhigh-riskpatientsshould
ANSWER: C
be placed on PPI infusion. Octreotide infusions are reserved for
upper GI bleeding as a result of esophageal varices. COMMENTS: Gastric MALT lymphoma is associated with
Ref.: 1, 11 chronic H. pylori infection in more than 90% of cases. Chronic
infection with H. pyloriresultsinmonoclonalB-cellproliferation
35. Which cell type is matched with the appropriate secretory anddevelopmentoflymphoidtissueresemblingPeyer’spatchesin
product? the stomach. Treatment directed toward H. pylori eradication
 A. Chiefcell/gastrin results in the resolution of MALT lymphomas in 75% of cases.
Upper endoscopy with biopsy is the diagnostic test of choice.
 B. Deltacell/somatostatin
Gastric biopsies are used to evaluate the presence of H. pylori and
 C. Parietalcell/pepsin the histologic type of lymphoma. The depth of gastric wall invasion
 D. Gcell/histamine and the presence of nodal involvement can be determined with the
 E. ECLcell/intrinsicfactor! help of endoscopic ultrasonography. Histologically, H. pylori–
negative MALT lymphomas should be confirmed as such with
ANSWER: B serologic testing. Staging is completed with a chest radiograph,
bone marrow biopsy, and CT of the abdomen. Surveillance is
COMMENTS:SeeQuestion36. achieved with repeat endoscopy in 2 months with biopsy to docu-
Ref.: 1, 2, 11 ment clearance of infection and subsequent endoscopy every 6
months for 3 years. Certain genetic translocations, large cell phe-
36. Which cell type is matched with the correct primary
notype, nodal involvement, or transmural tumor extension all
anatomic location?
predict failure of H. pylori eradication alone.
 A. Chiefcell/gastricantrum
Ref.: 1,6,11
 B. Gcell/gastriccardia
38. W
 hichofthefollowingstatementsabouthigh-gradegastric
 C. Dcell/gastricfundus
lymphoma is true?
 D. Parietalcell/gastricfundus
 A. DiffuselargeB-celllymphomaisthesecondmost
 E. Endocrinecell/gastricbody! common gastric lymphoma after MALT lymphoma.
B. The addition of surgery to chemotherapy alone has been
ANSWER: E
shown to improve outcomes.
COMMENTS: The gastric mucosa consists of surface columnar  C. Hemorrhageisafrequentcomplicationofchemotherapy.
epithelial cells and glands containing various cell types. The mucosal
D. Surgical treatment is usually reserved for patients with
cells vary in their anatomic location and secretory function. Within
limitedgastricdisease,localizedpersistentlymphoma,or
thecardia,theglandscontainprimarilymucus-secretingcellsandthe
complications associated with nonsurgical treatment.
pits are short. In the body of the stomach, the glands retain their
mucus-secretingcellsattheirluminalendbutthepitsextenddeeper  E. Perforationisafrequentcomplicationafterchemotherapy.!
andbegintoincludeothersecretorycells.Parietalandchiefcellsare
ANSWER: D
located predominately in the body. Parietal cells produce hydro-
chloric acid and intrinsic factor, whereas chief cells secrete pep- COMMENTS: Diffuse large B-cell lymphoma is the most
sinogen. The G cells of the antrum are the primary source of gastrin. common type of gastric lymphoma, with MALT lymphoma being
Somatostatinissynthesizedandstoredindelta cells located in the thesecondmostcommon.High-gradegastriclymphomaisgener-
gastric corpus and antrum. Ghrelin, produced by endocrine cells of ally treated with chemotherapy or chemoradiation. Compared with
the gastric body, probably plays a role in the neuroendocrine response surgicaltreatment,patientsurvivalhasbeenshowntobeequivalent
to changes in nutritional status and has been shown to enhance or better with nonsurgical treatment in several prospective clinical
appetiteandincreasefoodintake.Removalofasignificantportion trials(randomizedandnonrandomized).Itwaspreviouslybelieved
of the gastric body resulting in decreased ghrelin levels is thought to that surgery was superior to chemotherapy due to the risk for com-
be the mechanism of appetite control after a sleeve gastrectomy. plications such as perforation and hemorrhage with chemother-
Ref.: 1, 2, 11 apy.However,theseriskshavebeenfoundtobeonlyapproximately
5%. It is postulated that these risks may be increased with full-
37. Which of the following statements is true regarding gastric thickness involvement of the gastric wall. EUS can be used to
MALT lymphoma? determine the depth of invasion, and this information can be offered
A. Negative histologic H. pyloritestingconfirmsanH. to the patient when discussing risks and benefits of treatment
pylori–negativeMALTlymphoma. options. Operative intervention is therefore largely reserved for
limitedgastricdiseaseinwhichR0resectionisareasonablegoal,
 B. Lessthan10%ofgastriclymphomashaveassociatedH.
patients undergoing chemoradiation with treatment failure, or for
pylori infection.
the management of rare complications of nonsurgical treatment
 C. UpperGIendoscopywithgastricbiopsyforthedetermi- including perforation, hemorrhage, and obstruction.
nation of the presence of H. pylori and the histologic type
Ref.: 1,6,11
of lymphoma is the diagnostic test of choice.
 D. Surveillanceincludesrepeatendoscopyin6monthsto 39. Regarding gastric varices, which of the following is false?
document clearance of the infection.  A. Gastricvaricesdevelopviaincreasedflowandpressure
E. CT of the abdomen, chest radiography, bone marrow transmitted through the short and posterior gastric veins.
biopsy,anddiagnosticlaparoscopyarerequiredfor B. Isolated gastric varices are the result of splenic vein
complete staging.! thrombosis.
310 SECTION V / Alimentary Tract

 C. Gastricvaricesaremoreoftenassociatedwithgeneralized
ANSWER: A
portal hypertension than with splenic vein thrombosis.
D. Isolated gastric varices should be managed with endo- COMMENTS: Small bowel adenocarcinoma accounts for the
scopic banding and sclerotherapy. majority(35%–50%)ofsmallbowelmalignantneoplasms,followed
by carcinoid tumors, lymphomas, and sarcomas. Adenocarcinoma of
E. Gastric varices associated with portal hypertension should
the small bowel is more common in the duodenum, whereas carci-
be managed with endoscopic banding and sclerotherapy.!
noid tumors and lymphomaaremorefrequentlyseenintheileum.
Small bowel adenocarcinoma is found in decreasing order of fre-
ANSWER: D
quency in the duodenum, jejunum, and ileum. Most patients have
COMMENTS: There are two types of gastric varices: those that nonspecific symptoms initially; however, adenocarcinoma of the
occur in the setting of portal hypertension and those that are sec- duodenum is manifested earlier with signs and symptoms of obstruc-
ondary to splenic vein thrombosis (isolated gastric varices). To tivejaundice,gastricoutletobstruction,andabdominalpain.Opera-
establish the diagnosis of isolated gastric varices, there must be no tive resection (pancreaticoduodenectomy and local excision) is the
evidence of portal hypertension, cirrhosis, or esophageal varices on treatmentofchoice,dependingonthesizeandlocationoftheadeno-
endoscopy.Ineithertype,anincreasedflowandpressureistrans- carcinoma,thepatient’shealth,andthesurgeon’sexpertise.Although
mitted via the short and posterior gastric veins. For isolated rare in the small bowel, villous adenomasarefrequentlyfoundin
gastric varices, splenectomy is curative. Splenectomy is neither the duodenum and are associated with FAP syndrome(31%–92%).
curative nor indicated when the varices are associated with portal These villous adenomas have high malignant potential, especially if
hypertension. Rather, this type is best managed similarly to esopha- they are larger than 5 cm or are accompanied by bleeding or obstruc-
geal varices with endoscopy, banding, and sclerotherapy. tion. The Spigelman criteria are used to grade duodenal polyposis
Ref.: 1, 12 seeninFAP.Theyconsistoffiveincrementalstagesofseverity(0to
IV). Points are earned for the number of polyps, size of polyps,
40. Regarding the gross anatomy of the duodenum, which of the histology,andgradeofdysplasia.Thisclassificationalsocorrelates
following is true? with the risk for malignancy as follows: stage II, 2.3% risk; stage III,
 A. Thelengthoftheduodenumisapproximately20cm. 2.4%risk;andstageIV,36%risk.Pancreaticoduodenectomyisrec-
ommended for stage IV.
B. The second, third, and fourth portions of the duodenum
are retroperitoneal. Ref.: 1,2,6,14
C. The SMA marks the transition point between the second
and third portions. R E F E R E N C E S
D. Lack of collateral blood supply puts the duodenum at a 1. Mercer DW, Robinson EK. Stomach. In: Townsend CM, Beauchamp
RD, Evers BM, et al., eds. Sabiston Textbook of Surgery: The Biologi-
high risk for ischemia. cal Basis of Modern Surgical Practice. 18th ed. Philadelphia: WB
 E. Theminorpapillaislocatedinthefirstportionofthe Saunders;2008.
duodenumandthemajorinthesecond.! 2. Dempsey DT. Stomach. In: Brunicardi FC, Andersen DK, Billiar TR,
et al., eds. Schwartz’s Principles of Surgery. 9th ed. New York:
McGraw-Hill;2010.
ANSWER: A  3. Rice-Townsend SE, Norton JA. Zollinger-Ellison syndrome. In:
Cameron JL, ed. Current Surgical Therapy.9thed.Philadelphia:CV
COMMENTS:Theduodenumisthefirstportionofthesmallintestine Mosby;2008.
andthemostdistalforegut-derivedstructure.Itisapproximately20cm  4. Winkleman BJ, UsatiiA, Ellison EC. Duodenal ulcer. In: Cameron
in length and is divided into four portions, of which the second and JL, ed. Current Surgical Therapy.9thed.Philadelphia:CVMosby;
third are found retroperitoneally. Although the minor papilla is found 2008.
5. Fisher WE, Brunicardi FC. Benign gastric ulcer. In: Cameron JL, ed.
superiorlytothemajor,theyarebothlocatedwithinthesecondportion. Current Surgical Therapy.9thed.Philadelphia:CVMosby;2008.
The acute angle between the aorta and the SMA marks the transition  6. Bland KI, Büchler MW, Csendes A, Garden OJ, Wong J. General
point between the third and fourth portions. The blood supply to the Surgery: Principles and International Practice. 2nd ed. New York:
duodenum is via the superior and inferior pancreaticoduodenal arteries, Springer-Verlag;2008.
both of which have posterior and anterior divisions and constitute a rich  7. Cho CS, Brennan MF. Gastric adenocarcinoma. In: Cameron JL, ed.
Current Surgical Therapy.9thed.Philadelphia:CVMosby;2008.
bed of vascular collaterals. The anastomosis of these two vessels also 8. Efron DT. Gastrointestinal stromal tumors. In: Cameron JL, ed. Current
represents the only connection between celiac and SMA blood supply. Surgical Therapy.9thed.Philadelphia:CVMosby;2008.
Ref.: 1, 13  9. Mintz Y, Talamini MA. Crohn’s disease of the small bowel. In:
Cameron JL, ed. Current Surgical Therapy.9thed.Philadelphia:CV
41. With regard to adenocarcinoma of the small bowel, which of Mosby;2008.
10. TavakkolizadehA, Whang EE, Ashley SW, Zinner MJ. Small intestine.
the following statements is false? In: Brunicardi FC, Andersen DK, Billiar TR, et al., eds. Schwartz’s
A. Small bowel adenocarcinoma is found in decreasing order Principles of Surgery.9thed.NewYork:McGraw-Hill;2010.
offrequencyintheileum,jejunum,andduodenum. 11. Mulholland M. Stomach and duodenum. In: Mulholland M, Lillemoe
K, Doherty GM, et al., eds. Greenfield’s Surgery: Scientific Principles
B. Villous adenomas of the small bowel are commonly and Practice. 5th ed. Ann Arbor: Lippincott Williams & Wilkins;
found in the duodenum around the ampulla of Vater. 2010.
12. Fraker D. The spleen. In: Mulholland M, Lillemoe K, Doherty GM,
C. Adenocarcinoma of the duodenum usually occurs earlier et al., eds. Greenfield’s Surgery: Scientific Principles and Practice. 5th
than small bowel adenocarcinoma elsewhere in the ed.AnnArbor:LippincottWilliams Wilkins;2010.
jejunumandileum. 13. Drake R, Vogl A, Mitchell A. Gray’s Anatomy. 2nd ed. Philadelphia:
ChurchillLivingstoneElsevier;2010.
 D. Villousadenomasoftheduodenumarefrequently 14. Groves CJ, Saunders BP, Spigelman AD, Phillips RKS. Duodenal
associatedwithfamilialadenomatouspolyposis(FAP). cancer in patient with familial adenomatous polyposis (FAP): results
E. Operative resection is the treatment modality of choice ofa10-yearprospectivestudy.Gut.2002;50:636–641.
and has curative potential.!
 C H A P T E R 2 0

Stomach and Duodenum

Kamran Idrees, M.D., and John D. Christein, M.D.

1. Which of the following statements is true with regard to the gastric (vasa brevia) arteries are routinely divided. The major arte-
arterial blood supply of the stomach? rial source for the neoesophagus (gastric conduit) is derived from
the right gastroepiploic artery.
A. The left gastroepiploic artery commonly arises from the
left gastric artery. ANSWER: C
B. Ligation of the left gastric artery can result in acute left-
sided hepatic ischemia. 3. Choose the correct type of vagotomy with the appropriate level
of vagal transection from the pairs listed below:
C. The stomach is extremely susceptible to ischemia because
of poor collateral circulation. A. Truncal vagotomy/criminal nerve of Grassi
D. The inferior phrenic and short gastric arteries provide sig- B. Highly selective vagotomy/anterior and posterior vagal
nificant blood supply to the body of the stomach. trunks below the celiac and hepatic branches
E. A replaced right hepatic artery may originate from the left C. Selective vagotomy/anterior and posterior vagal trunks
gastric artery. above the celiac and hepatic branches
Ref.: 1, 2 D. Parietal cell vagotomy/terminal branches of the nerve of
Latarjet
COMMENTS: The arterial blood supply of the stomach is
E. Highly selective vagotomy/hepatic branches
derived primarily from the celiac artery. The left gastric artery
comes off of the celiac artery and supplies the stomach along the Ref.: 1, 2
lesser curvature. An aberrant/replaced left hepatic artery origi-
nates from the left gastric artery (15% to 24%) and can represent COMMENTS: In the chest, the vagal trunks are situated to the
the only arterial blood supply to the left hepatic lobe. This aberrant/ right and left of the esophagus. At the level of the cardia, the left
replaced left hepatic artery runs in the gastrohepatic ligament. The vagal trunk is found anterior and the right vagal trunk is found
right gastric artery typically arises from the common hepatic posterior secondary to embryonic gastric rotation. The anterior
artery distal to the gastroduodenal artery. The right and left gas- vagal trunk divides into hepatic and anterior gastric (anterior nerve
troepiploic arteries usually originate from the gastroduodenal of Latarjet) branches. The posterior vagus divides into the posterior
artery and splenic artery, respectively. The short gastric arteries nerve of Latarjet and celiac branches. One of the proximal posterior
arising from the splenic artery and inferior phrenic arteries also branches of the posterior vagal trunk is known as the criminal
contribute significant blood volume to the proximal part of the nerve of Grassi and is identified as a possible cause of recurrent
stomach. The stomach is well protected from ischemia and can ulcers if left undivided during selective vagotomy. Truncal vagot-
easily survive with ligation of three of four arteries because of its omy is conventionally performed at or just above or below the
rich collateral circulation. diaphragmatic esophageal hiatus before it gives off celiac and
hepatic branches. In contrast, selective vagotomy is performed
ANSWER: B distal to this location and spares the celiac and hepatic branches.
Highly selective vagotomy (also known as proximal gastric or
parietal cell vagotomy) divides individual terminal branches of
2. After esophagectomy, the arterial blood supply of a gastric the nerve of Latarjet in the fundus and corpus of the stomach but
conduit is primarily based on which of the following vessels? spares the vagal branches to the antrum and pylorus, which control
gastric motility and emptying—thus obviating the need for a drain-
A. Left gastroepiploic artery
age procedure.
B. Left gastric artery
ANSWER: D
C. Right gastroepiploic artery
D. Right gastric artery 4. Which cell type is matched with the appropriate secretory
product?
E. Inferior phrenic arteries
A. Parietal cell/ghrelin
Ref.: 1, 2
B. Chief cell/pepsinogen
COMMENTS: During gastric mobilization for esophageal
replacement after esophagectomy, the left gastric artery and short C. G cell/intrinsic factor

259
260 SECTION V / Alimentary Tract

D. Delta cell/gastrin COMMENTS: It is important to have knowledge of the cellular

basis for parietal cell acid secretion to understand the pharmaco-
E. Endocrine cell/somatostatin
logic control of acid. The parietal cell has three specific plasma
Ref.: 1, 2 membrane receptors that stimulate acid secretion: acetylcholine,
histamine, and gastrin receptors. All three receptors activate the
COMMENTS: See Question 5. H+,K+-ATPase pump, which results in secretion of hydrogen ion
for potassium. Acetylcholine- and gastrin-stimulated secretion
ANSWER: B depends on specific membrane phospholipases and increases
intracellular calcium levels, with subsequent phosphorylase
5. Which cell type is matched with the correct primary anatomic kinase–induced phosphorylation and H+,K+-ATPase activity.
location? Histamine activates adenylate cyclase, which in turn leads to
protein phosphorylation via protein kinase and H+,K+-ATPase
A. Parietal cell/gastric cardia
activation. Somatostatin, cholecystokinin, and secretin inhibit
B. Chief cell/gastric cardia acid secretion.
C. G cell/gastric antrum ANSWER: C
D. Delta cell/duodenum
8. All of the following stimulate gastric acid secretion except:
E. Endocrine cell/gastric corpus and fundus
A. Gastric distention
Ref.: 1, 2
B. Duodenal gastrin
C. Acetylcholine
COMMENTS: The gastric mucosa consists of surface columnar
epithelial cells and glands containing various cell types. The D. Intraluminal protein
mucosal cells vary in their anatomic location and secretory func-
E. Somatostatin
tion. Parietal and chief cells are located predominantly in the
gastric fundus and corpus. Parietal cells produce hydrochloric Ref.: 1, 2
acid and intrinsic factors, whereas chief cells secrete pepsinogen.
The G cells of the antrum are the primary source of gastrin. COMMENTS: Gastric acid secretion is regulated in three phases:
Somatostatin is synthesized and stored in delta cells located in cephalic, gastric, and intestinal. The cephalic phase is primarily
the gastric corpus and antrum. Mucus is secreted by gastric surface mediated by the vagus nerve. Vagal stimulation (acetylcholine)
epithelial cells, neck cells, and the Brunner gland. Ghrelin, pro- directly releases acid from the parietal cells, in addition to releasing
duced by endocrine cells of the gastric body, probably plays a role gastrin from the antrum. The gastric phase is initiated by gastric
in the neuroendocrine response to changes in nutritional status and distention, intraluminal peptides, and amino acids and results
may be used to help in the treatment or prevention of obesity, or in the release of gastrin. The majority of gastrin is released in the
both, in the future. antrum with a small amount being secreted from the duodenal
mucosa. The intestinal phase of gastric secretion accounts for only
ANSWER: C 10% of the total acid volume. Duodenal gastrin and the hypotheti-
cal peptide hormone enterooxyntin have been postulated to mediate
the intestinal phase of acid secretion. Luminal acidity releases
6. Acid secretion is stimulated by the following parietal cell secretin and somatostatin, which inhibit acid secretion.
receptors except:
ANSWER: E
A. Acetylcholine
B. Secretin 9. Which intestinal hormone is matched with the correct
function?
C. Histamine
A. Secretin/acts as a universal “on” switch
D. Gastrin
B. Gastrin-releasing peptide/acts as a universal “off” switch
E. All of the above
C. Somatostatin/stimulates intestinal secretion and motility
Ref.: 1, 2
D. Motilin/acts as a universal “on” switch
COMMENTS: See Question 7.
E. Vasoactive intestinal peptide (VIP)/stimulates intestinal
ANSWER: B secretion and motility

Ref.: 1, 2
7. The final common pathway of acid secretion by parietal cells
involves which of the following?
COMMENTS: Gastrointestinal (GI) hormones are secreted by
A. Protein kinase
endocrine cells that are widely distributed and localized to specific
B. Increased intracellular Ca2+ GI mucosa. These hormones regulate GI secretion, motility, and
C. Hydrogen-potassium adenosine triphosphatase (H+,K+- absorption in a complex fashion. Secretin is released by S cells
ATPase) located in the duodenum and jejunum. The primary function of
secretin is to induce the release of water and bicarbonate from
D. Phosphorylase kinase pancreatic ductal cells. Secretin also inhibits the release of gastrin,
E. Adenylate cyclase gastric acid secretion, and gastric motility. Gastrin-releasing
peptide (also known as bombesin) is found throughout the GI
Ref.: 1, 2 tract. It acts as the universal “on” switch by stimulating all GI
 CHAPTER 20 / Stomach and Duodenum 261

hormones (except secretin), as well as GI secretions and motility. D. Emptying of liquids is dependent on antral propulsion.
Somatostatin is produced by delta cells located primarily in the
E. The lower esophageal sphincter regulates gastric volume.
pancreas and gastric antrum. Because of its wide inhibitory action,
somatostatin is known as the universal “off” switch of the intestinal
Ref.: 1, 2
tract. It inhibits the release of all GI hormones along with the
inhibition of enteric water, electrolyte secretion, and motility.
Motilin, secreted by M cells in the duodenum and jejunum, stimu- COMMENTS: Gastric emptying is regulated largely by neural
lates upper GI motility. Erythromycin is thought to increase GI and hormonal factors triggered by gastric volume and composition.
motility through the activation of motilin receptors. Vasoactive Generally, the greater the volume, the faster the contents empty.
intestinal peptide is present throughout the length of the intestinal Liquids empty faster than solids. The pattern of liquid emptying is
tract and the central nervous system. It is a potent stimulator of exponential and is largely determined by fundal tone. Solids are
intestinal secretion. VIP is the chief culprit in the watery diarrhea, reduced in size to particles 1 to 2 mm in diameter by propulsive
hypokalemia, and achlorhydria syndrome (WDHA) associated and retropulsive activity. Gastric emptying is linear after an
with pancreatic endocrine tumors (also known as Verner-Morrison initial lag and depends on mechanical action of the pyloroantral
syndrome or VIPoma). region. Higher caloric intake, in the form of lipids, slows gastric
emptying. The lower esophageal sphincter does not control
ANSWER: E gastric volume.

10. Which hormone is matched with the correct diagnostic/thera- ANSWER: B

peutic function?
12. Which of the following clinical conditions is not associated
A. Cholecystokinin/treatment of esophageal variceal bleeding
with delayed gastric emptying?
B. Somatostatin/relief of spasm of the sphincter of Oddi
A. Hypocalcaemia
C. Gastrin/measurement of maximal gastric acid secretion
B. Scleroderma
D. Glucagon/provocative test for gastrinoma
C. Hyperglycemia
E. Secretin/stimulation of gallbladder contraction
D. Myxedema
Ref.: 1, 2 E. Zollinger-Ellison syndrome

Ref.: 1-3
COMMENTS: GI hormones or their analogues have been used
clinically as diagnostic or therapeutic agents. Cholecystokinin
(CCK) is used to stimulate gallbladder contraction. This is useful COMMENTS: Disorders of gastric emptying can be divided into
in identifying patients with biliary dyskinesia or acalculous cho- rapid or delayed emptying, both of which can be significantly
lecystitis with the help of CCK cholescintigraphy. Pentagastrin, a disabling conditions. Delayed gastric emptying is the more fre-
gastrin analogue, is used to measure gastric acid secretion. Soma- quently encountered problem of gastric motility. Excluding
tostatin or its analogues are used in various conditions as a result mechanical obstruction, important causes of delayed gastric empty-
of their universal inhibitory function. Because they inhibit the ing include metabolic derangements (e.g., myxedema and
release of GI hormones, somatostatin analogues are used for hyperglycemia), electrolyte abnormalities (e.g., hypokalemia
various endocrine neoplasms such as Zollinger-Ellison syndrome, and hypocalcaemia), drugs (e.g., narcotics and anticholiner-
VIPoma, insulinoma, and carcinoid tumors. They are also useful gics), and systemic diseases (e.g., diabetes mellitus and sclero-
in patients with pancreatic fistulas, pancreatic ascites, and derma). Up to 40% of postvagotomy patients experience delayed
enterocutaneous fistulas by decreasing GI secretions. Addition- gastric emptying. Rapid gastric emptying is less commonly
ally, they have been used as a treatment to decrease bleeding from observed. Causes of rapid gastric emptying include previous
the GI tract. Glucagon is used by endoscopists to relax the gastric resection, conditions with impaired fat absorption result-
Sphincter of Oddi to facilitate endoscopic retrograde cholangio- ing in loss of the inhibition of gastric emptying (e.g., pancreatic
pancreatography (ERCP). Secretin, which inhibits acid secretion, insufficiency and short bowel syndrome), and conditions with
causes a paradoxical increase in serum gastrin levels in patients hypergastrinemia such as Zollinger-Ellison syndrome.
with gastrinoma. Pancreatic polypeptide (PP) is predominantly
secreted in the pancreatic head. PP serum levels drop following the ANSWER: E
Whipple procedure and may be related to the delayed gastric emp-
tying observed after pyloric-preserving pancreatoduodenectomy. 13. Infection with Helicobacter pylori has been associated with all
In addition, PP secretion necessitates intact vagal nerve function; but which of the following conditions?
thus, a blunt response to stimulation by sham feedings has been
A. Duodenal ulcer
used to evaluate intact vagal nerve function, particularly in patients
suspected of having iatrogenic vagus nerve injury. B. Gastric cancer
ANSWER: C C. Mucosa-associated lymphoid tissue (MALT) lymphoma
D. Gastroesophageal reflux disease (GERD)
11. With regard to regulation of gastric emptying, which of the
E. Chronic gastritis
following statements is true?
Ref.: 1, 2, 4
A. The greater the volume present in the stomach, the slower
the gastric emptying. COMMENTS: H. pylori is a curved or S-shaped, gram-negative
B. Higher intake of lipids slows gastric emptying. microaerophilic motile bacterium whose natural habitat is the
human stomach. H. pylori infection has been demonstrated to be
C. Emptying of solids is dependent on fundal tone. associated with 90% of duodenal ulcers and 75% of gastric
262 SECTION V / Alimentary Tract

ulcers. After eradication of the organism as part of ulcer treatment, diagnosis of H. pylori infection in patients in whom endoscopy is
recurrence of ulcer is extremely rare. In addition, H. pylori has not indicated.
been associated with chronic atrophic gastritis, which in turn
leads to gastric atrophy and intestinal metaplasia, a suspected ANSWER: A
precursor of gastric cancer. H. pylori infection also increases the
risk for low-grade mucosa-associated lymphoid tissue lym-
phoma; eradication of H. pylori results in resolution of MALT 16. Which condition corresponds to the appropriate basal and
lymphomas in most cases. There appears to be a negative associa- pentagastrin-stimulated acid output?
tion between H. pylori infection and gastrointestinal reflux
A. Duodenal ulcer/basal and pentagastrin-stimulated acid
disease.
output is decreased
ANSWER: D B. Pernicious anemia/basal and pentagastrin-stimulated acid
output is decreased
C. Gastric cancer/basal and pentagastrin-stimulated acid
14. Which of the following tests is not appropriate for the initial
output is decreased
detection of H. pylori infection in patients with peptic ulcer
disease? D. Zollinger-Ellison syndrome/basal and pentagastrin-stimu-
lated acid output is increased
A. Urea breath test
E. Gastric atrophy/basal and pentagastrin-stimulated acid
B. Histologic examination of mucosa
output is decreased
C. Rapid urease test
Ref.: 1, 2
D. Culture and sensitivity testing
E. H. pylori serology
COMMENTS: The normal mean basal acid output is in the range
Ref.: 1, 5, 6 of 1 to 8 mmol/h, and the response to pentagastrin-stimulated
output ranges from 6 to 40 mmol/h. In patients with duodenal
COMMENTS: See Question 15. ulcer and Zollinger-Ellison syndrome, both basal acid output
and pentagastrin-stimulated acid output are decreased. In con-
ANSWER: D trast, adults with pernicious anemia, gastric atrophy, and gastric
cancer are achlorhydric or have subnormal acid output. In these
patients, maximal acid output remains decreased despite pentagas-
15. Which of the following tests is best to document eradication trin evaluation.
of H. pylori infection in patients with peptic ulcer disease?
ANSWER: A
A. Urea breath test
B. Histologic examination of mucosa
17. Elevated serum gastrin levels during fasting are typical in all
C. Rapid urease test
but which of the following conditions?
D. Culture and sensitivity testing
A. Short bowel syndrome
E. H. pylori serology
B. Pernicious anemia
Ref.: 1, 5, 6 C. Chronic gastritis
COMMENTS: It is important to document the presence or D. Duodenal ulcer
absence of Helicobacter pylori to adequately treat patients with
E. Gastric outlet obstruction
peptic ulcer disease. Both invasive and noninvasive tests are avail-
able for the diagnosis of H. pylori infection. Invasive tests require Ref.: 1, 2, 6
endoscopic mucosal biopsy and include histologic examination,
the rapid urease test, and culture. Noninvasive tests include the COMMENTS: Conditions associated with hypergastrinemia
urea breath test and serology. Histologic examination can accu- and increased acid secretion include Zollinger-Ellison syndrome,
rately diagnose H. pylori with two biopsy specimens with high antral G-cell hyperplasia, retained antrum, renal failure,
sensitivity and specificity (90%). The rapid urease test on a mucosal gastric outlet obstruction, and short bowel syndrome. In contra-
biopsy specimen uses a change in pH resulting from the breakdown distinction, an elevated serum gastrin level with normal or
of urea by a urease enzyme produced by H. pylori. This test is diminished acid output is seen in patients with pernicious
considered the initial test of choice because of its simplicity, accu- anemia, postvagotomy states, chronic gastritis, and gastric
racy, and rapid results. Culture of H. pylori has the most specificity cancer and in patients with pharmacologic acid suppression.
(100%) but is difficult to perform and is currently not widely avail- Serum gastrin levels during fasting are normal in patients with
able. Cultures should usually be reserved for research purposes or duodenal ulcer but may be excessively elevated postprandially.
patients with suspected antibiotic resistance. The urea breath test The absolute level of an abnormally elevated serum gastrin level
is a noninvasive test that analyzes breath for labeled carbon dioxide is not necessarily indicative of the cause. However, marked eleva-
produced by bacterial urease from the conversion of ingested tions (>1000 pg/mL) are often associated with Zollinger-Ellison
labeled urea. Because of its noninvasiveness plus high sensitivity syndrome. Ulcerogenic causes of hypergastrinemia resulting
and specificity (95%), the urea breath test is considered the test of from elevated gastric acid secretion include Zollinger-Ellison syn-
choice for documentation of H. pylori eradication. Serologic tests drome, antral G-cell hyperplasia, retained antrum, short bowel
are quick and inexpensive but cannot differentiate between active syndrome, and gastric outlet obstruction. Zollinger-Ellison syn-
infection and previous exposure. Serology is useful for the initial drome and antral G-cell hyperplasia are uncommon, but they must
 CHAPTER 20 / Stomach and Duodenum 263

be differentiated to determine proper therapy. Both are associated 20. Which operation for duodenal ulcer is least likely to produce
with elevated gastrin and gastric acid levels. They can be differenti- undesirable postoperative symptoms?
ated on the basis of the serum gastrin response to several provoca-
A. Subtotal gastrectomy
tive tests. A pronounced increase in serum gastrin levels after the
intravenous infusion of secretin is typically seen with Zollinger- B. Truncal vagotomy and pyloroplasty
Ellison syndrome. Elevations can occur with other conditions, but
C. Truncal vagotomy and antrectomy
they are not as dramatic. In contradistinction, more marked
increases in gastrin levels occur after stimulation by a protein in D. Selective vagotomy
Zollinger-Ellison syndrome.
E. Highly selective vagotomy
ANSWER: D
Ref.: 1, 2, 6

COMMENTS: The goal of surgical therapy for duodenal ulcers

18. With regard to H. pylori–negative duodenal ulcer disease, all is to reduce acid production in a manner that is safe and has the
of the following statements are correct except: fewest possible side effects. Acid can be reduced by eliminating
vagal stimulation, removing the antral source of gastrin, and remov-
A. Nonsteroidal anti-inflammatory drugs (NSAIDs) are a
ing the parietal cell mass. Traditionally, subtotal two-thirds gastrec-
major cause of duodenal ulcers in patients who are H.
tomy has carried the highest mortality rate. Truncal vagotomy
pylori negative.
with antrectomy has the lowest recurrence rate. Procedures involv-
B. Because of the high prevalence of H. pylori–positive duo- ing antrectomy, pyloroplasty, or truncal vagotomy may be compli-
denal ulcers, patients should be treated for H. pylori cated by diarrhea, postprandial dumping, or bile reflux. Selective
without confirmatory testing. vagotomy, which preserves the hepatic and celiac vagal branches,
has been associated with a lower rate of diarrhea than truncal
C. In contrast to H. pylori–positive duodenal ulcers, NSAID-
vagotomy has. Highly selective vagotomy, also known as parietal
induced ulcers are not frequently associated with chronic
cell vagotomy, aims to denervate the parietal cell–bearing portion
active gastritis.
of the stomach but preserve innervations to the pyloroantral region
D. H. pylori–negative duodenal ulcers are usually large ulcers and thus maintain more normal gastric emptying. This operation
and multiple and are often associated with bleeding. carries the lowest mortality rate, the lowest incidence of side effects,
but the highest recurrence rate, which ranges from 5% to 15%.
E. Older age, multiple comorbid conditions, and sepsis are
independently associated with H. pylori–negative duodenal ANSWER: E
ulcers.

Ref.: 1, 6
21. A 75-year-old man taking NSAIDs for arthritis has an acute
abdomen and pneumoperitoneum. His symptoms are 6 hours
COMMENTS: Initial studies have demonstrated that Helico- old and his vital signs are stable after the infusion of 1 L of
bacter pylori infection is present in more than 90% of patients with normal saline solution. What should be the next step in the
duodenal ulcers. However, more recently it has been shown that management of this patient?
the prevalence of H. pylori–associated duodenal ulcers is only 75%
A. Computed tomography of the abdomen
and is found to be decreasing. Thus, it is important to first make
the diagnosis of an active H. pylori infection rather than initiating B. Esophagogastroduodenoscopy (EGD)
empirical therapy. Helicobacter pylori–negative duodenal
C. Antisecretory drugs, broad-spectrum antibiotics, and
ulcers are independently associated with nonsteroidal anti-
surgery if he fails to improve in 6 hours
inflammatory drug use, older age, multiple medical problems,
and sepsis. Use of NSAIDs is the major cause of duodenal ulcers D. Antisecretory drugs, antibiotics for H. pylori, and surgery
in patients who are H. pylori–negative. Bleeding is the initial if he fails to improve in 6 hours
manifestation in these patients and they have large and multiple
E. Surgery
ulcers.
ANSWER: B Ref.: 1, 2, 6

COMMENTS: See Question 23.

19. A 45-year old man requires surgery for an intractable duodenal ANSWER: E
ulcer. Which operation best prevents ulcer recurrence?
A. Subtotal gastrectomy
22. The patient in Question 21 is found to have a perforated duo-
B. Truncal vagotomy and pyloroplasty denal ulcer. Which of the following best describes the required
operation?
C. Truncal vagotomy and antrectomy
A. Suture closure of the perforation
D. Selective vagotomy
B. Omental patch of the perforation
E. Highly selective vagotomy
C. Repair of the perforation and highly selective vagotomy
Ref.: 1, 2, 6
D. Repair of the perforation and truncal vagotomy
COMMENTS: See Question 20. E. Repair of the perforation and gastric resection
ANSWER: C Ref.: 1, 2, 6
264 SECTION V / Alimentary Tract

COMMENTS: See Question 23. instead of peptic ulcer disease. Among malignancies, primary
adenocarcinomas of the pancreas, stomach, and duodenum (in
ANSWER: B decreasing order of frequency) are the leading cause of gastric
outlet obstruction. Gastrointestinal stromal tumors (GISTs) of the
stomach and duodenum and primary lymphomas of the stomach,
23. If the patient in Question 21 were found to have a perforated duodenum, and pancreas are other causes of gastric outlet obstruc-
gastric ulcer instead of a duodenal ulcer, what additional steps, tion. Extrinsic compression from metastatic disease to the porta
if any, need to be performed at the time of operative interven- hepatis can also lead to obstruction. It is therefore important to
tion beside closure of the perforation? have a high index of suspicion for a malignancy when a patient
has gastric outlet obstruction rather than mistaking it for a benign
A. Feeding jejunostomy
obstruction from peptic ulcer disease.
B. Gastrojejunostomy
ANSWER: C
C. Gastrostomy tube placement
D. Excision or biopsy of the ulcer
25. A patient with gastric outlet obstruction and prolonged vomit-
E. Pyloroplasty
ing has which of the following metabolic abnormalities?
Ref.: 1, 6 A. Hypochloremic, hyperkalemic metabolic alkalosis
COMMENTS: The preferred treatment of a perforated duode- B. Hyperchloremic, hypokalemic metabolic acidosis
nal ulcer is resuscitation and prompt surgery. Nonoperative man-
C. Hyponatremic, hypokalemic metabolic acidosis
agement is reserved for old contained perforations or for terminally
ill patients who otherwise cannot undergo surgery. The diagnosis D. Hypochloremic, hypokalemic metabolic alkalosis
is a presumptive one based on clinical grounds and should not be
E. Hyperchloremic, hyperkalemic metabolic acidosis
excluded if pneumoperitoneum cannot be demonstrated, because
about 20% of patients with perforations do not have this typical
Ref.: 1, 2
radiographic feature. Operative management requires closure of
the perforation, which is generally best accomplished with an
omental (Graham) patch. Closure of the perforation is usually COMMENTS: The classic metabolic abnormality resulting from
sufficient in patients with duodenal ulcers; however, excision of gastric outlet obstruction and prolonged vomiting is hypochlore-
the ulcer is necessary to rule out malignancy in patients with gastric mic, hypokalemic metabolic alkalosis. Initial loss of hydrochloric
ulcers before closure. Following simple repair alone, the traditional acid causes hypochloremia and mild alkalosis compensated for by
natural history has been that about one third of patients have no renal excretion of bicarbonate. Therefore, in the early stages the
further ulcer problems, one third have ulcer recurrence amenable urine is alkaline. Continued vomiting produces a severe extracel-
to medical management, and one third require a subsequent opera- lular fluid deficit and sodium deficit from both renal and gastric
tion for ulcer disease. It is not clear how precisely this applies to losses. The kidneys begin to conserve sodium and, in exchange,
patients with H. pylori infection or those with NSAID-induced excrete hydrogen and potassium cations to accompany bicarbonate.
ulcers. Definitive operations should be performed only in stable The kidneys are the predominant site of potassium loss, and the urine
patients and those with documented failure after appropriate H. is paradoxically acidic. Urine chloride content is reduced throughout
pylori eradication. Truncal vagotomy can be performed expedi- and eventually absent. Serum ionized calcium levels are decreased
tiously but has a greater incidence of side effects. Highly selective because calcium is mildly alkaline and shifts to its nonionized form
vagotomy is an excellent choice but is time-consuming and requires to reduce alkalosis. Treatment of this metabolic situation is accom-
a surgeon with the expertise to perform it. Resective procedures plished primarily by the administration of isotonic saline solution,
are generally avoided in the setting of perforation because of higher which replenishes the deficits in volume, sodium, and chloride.
morbidity. Following surgery, ulcerogenic drugs should be with- Potassium is replaced once renal function is optimized.
held, and any concomitant H. pylori infection should be treated.
ANSWER: D
ANSWER: D

26. Which of the following endoscopic ulcer characteristics has

24. The most common cause of gastric outlet obstruction in the highest risk for recurrent bleeding?
adults is:
A. Oozing ulcer
A. Peptic ulcer disease
B. Clean based ulcer
B. Extrinsic neoplastic compression
C. Nonbleeding “visible vessel”
C. Cancer
D. Nonbleeding ulcer with an overlying clot
D. Primary lymphoma of the stomach
E. Dieulafoy ulcer
E. Duodenal Crohn’s disease
Ref.: 6
Ref.: 1, 5, 6
COMMENTS: Esophagogastroduodenoscopy is not only the
diagnostic test of choice but can also be therapeutic in patients with
COMMENTS: With increased use of histamine receptor blockers upper gastrointestinal bleeding. EGD can localize the bleeding
and proton pump inhibitors in the medical management of peptic site and determine the risk for rebleeding based on the appearance
ulcer disease and effective treatment of H. pylori infection, malig- of the ulcer bed. The endoscopic features of ulcers with a risk for
nancy is the most common cause of gastric outlet obstruction rebleeding in decreasing order of frequency are active arterial
 CHAPTER 20 / Stomach and Duodenum 265

bleeding (approaches 100%), nonbleeding “visible vessel” (≈50%), 29. Which type of gastric ulcer corresponds with the associated
nonbleeding ulcer with an overlying clot (≈30% to 35%), oozing acid secretion?
ulcer (≈10% to 27%), and a clean based ulcer (<3%). Dieulafoy
A. Type I/high acid secretion
ulcers are vascular malformations that bleed when superficial
erosion into the vessel occurs. Unless actively bleeding, they are B. Type II/high acid secretion
difficult to diagnose endoscopically.
C. Type III/normal or low acid secretion
ANSWER: C D. Type IV/high acid secretion
E. All of the above
27. During an operation for a bleeding duodenal ulcer, three-point
Ref.: 1, 4, 6
“U” stitches are placed to ligate which of the following arteries
after longitudinal pyloroduodenotomy?
COMMENTS: See Question 30.
A. Common hepatic, right gastric, and gastroduodenal
arteries ANSWER: B
B. Proximal and distal gastroduodenal and transverse pancre-
atic arteries
30. Which gastric ulcer corresponds with the correct recommended
C. Right gastric, gastroduodenal, and right gastroepiploic
surgical management?
arteries
A. Type I/Billroth I or II reconstruction
D. Right gastric and anterior and posterior inferior pancreati-
coduodenal arteries B. Type II/truncal vagotomy and pyloroplasty
E. Common hepatic, gastroduodenal, and superior mesenteric C. Type III/Csendes gastrectomy with Roux-en-Y gastrojeju-
arteries nostomy or Pauchet gastrectomy and Billroth I
reconstruction
Ref.: 1, 2, 4, 6
D. Type IV/Billroth I or II reconstruction with truncal
vagotomy
COMMENTS: Massive bleeding is usually the result of posterior
E. Type IV/total gastrectomy
erosion of a duodenal ulcer into the gastroduodenal artery. Emer-
gency surgical intervention is indicated when bleeding is refractory
Ref.: 1, 4, 6
to endoscopic therapy or in the presence of hemorrhagic shock.
After expeditious preoperative resuscitation, the abdomen is entered
and a longitudinal pyloroduodenotomy is performed. Digital COMMENTS: Benign gastric ulcers have been classified in
pressure is applied over the ulcer base to temporize the bleeding terms of their anatomic location. Type I ulcers are the most
and allow resuscitation before suture control is obtained. Proper common (50%) and occur in the body of the stomach along the
control of bleeding requires three-point suture ligation of the duo- lesser curvature. These ulcers are associated with low to normal
denal ulcer. These “U” stitches are placed superior and inferior to acid secretion. Type II gastric ulcers (25%) also occur in the body
the site of penetration to ligate the proximal and distal gastroduo- of the stomach but have associated duodenal ulcers. Type III
denal artery. A third suture is placed on medial aspect of the ulcer gastric ulcers (20%) are located in the prepyloric region. Both type
to control the transverse pancreatic branch coming off the gas- II and type III ulcers are associated with excessive acid secretion.
troduodenal artery. After the bleeding is controlled, biopsy of Type IV ulcers are the least common (<10%) and occur near the
gastric mucosa should be performed for histologic analysis for GE junction along the lesser curve. Like type I ulcers, they are
H. pylori. The longitudinal pyloroduodenotomy is then closed associated with low or normal acid secretion. Surgical intervention
transversely (Heineke-Mikulicz or Weinberg pyloroplasty). is indicated for patients who have failed maximal medical therapy
(12 weeks), for those in whom complications develop, or for those
ANSWER: B in whom malignancy cannot be ruled out. Surgical therapy for
benign gastric ulcers depends on the type of ulcer and its associated
acid secretion. Type I ulcers are usually well treated with antrec-
28. Which type of gastric ulcer corresponds with the correct ana- tomy or hemigastrectomy (including removal of the ulcer) without
tomic location? vagotomy. Type IV ulcers do not require vagotomy either. Type IV
ulcers near the GE junction can be treated by modifications of distal
A. Type I/prepyloric region
gastrectomy that include ulcer excision. Distal gastrectomy with
B. Type II/lesser curvature of the stomach near the GE extension along the lesser curvature to include the ulcer (Pauchet
junction procedure) and Billroth I reconstruction can be performed for
ulcers that are 2 to 5 cm from the GE junction. For type IV ulcers
C. Type III/body of the stomach along the lesser curvature
at the GE junction, subtotal gastrectomy with Roux-en-Y jejunal
D. Type IV/lesser curvature of the stomach near the GE reconstruction (Csendes procedure), a rotational Tanner gastrec-
junction tomy, or a Kahler-Muhlenberg procedure should be performed.
Because type II and type III ulcers are associated with acid hyper-
E. Type IV/prepyloric region
secretion, they are treated as duodenal ulcers. Truncal vagotomy
Ref.: 1, 4, 6 with Billroth I or II reconstruction is the preferred surgical therapy
because it accomplishes both goals of a decrease in acid secretion
COMMENTS: See Question 30. and excision of the ulcer.
ANSWER: D ANSWER: A
266 SECTION V / Alimentary Tract

31. Concerning the treatment of patients with Zollinger-Ellison in males all over the world, and the incidence is higher in African-
syndrome, which of the following statements is true? American men than in white men in the United States. The inci-
dence of adenocarcinoma of the gastric cardia and GE junction has
A. Operative treatment of associated hyperparathyroidism
gradually increased, whereas that of the distal part of the stomach
takes precedence over abdominal surgery.
has decreased over the past few decades. Although most risk
B. Pancreatic tumors should not be removed by enucleation. factors for gastric cancer are probably exogenous, genetic factors
may also be involved, as exemplified by patients with pernicious
C. Duodenal tumors usually require pancreaticoduodenec-
anemia and by slightly increased risk in patients with blood group
tomy.
A. There is also an increased risk 10 to 15 years after gastric
D. Total gastrectomy is indicated if the tumor cannot be resection for benign disease, perhaps indicative of the role of bile
localized. reflux.
E. Resection of liver metastases is not indicated. ANSWER: C

Ref.: 1-3
33. All of the following conditions are associated with gastric
COMMENTS: Treatment of Zollinger-Ellison syndrome is two cancer except:
pronged and aimed at both resecting the tumor when possible and
A. Chronic atrophic gastritis
protecting the gastric end-organ. Therapy must be individualized.
Patients with known endocrine tumors should undergo careful B. H. pylori infection
evaluation for other potential endocrine tumors. In patients with
C. Hereditary nonpolyposis colorectal cancer
gastrinoma and hyperparathyroidism, parathyroidectomy
should be performed first to eliminate hypercalcemia. Abdominal D. Adenomatous gastric polyps
surgery is not urgent with the current antisecretory medications.
E. Fundic gland polyps
Although gastrinomas are often multiple and are usually meta-
static, long-term survival is possible. Aggressive attempts to Ref.: 1, 6, 7
localize and resect tumors can provide cure in 5% to 20% of
patients and can diminish gastrin secretion in others. Most gastri- COMMENTS: Certain gastric lesions have a significant associa-
nomas can be found in the triangle of Passaro. Digital palpation tion with gastric adenocarcinoma and can be considered precursors
through a duodenotomy and intraoperative ultrasound are useful to malignancy. Chronic atrophic gastritis, of which several forms
operative adjuncts. Both pancreatic and duodenal gastrinomas are recognized, underlies most gastric cancers. The epithelial
can be resected by enucleation when appropriately located. Blind changes of intestinal metaplasia and dysplasia are premalignant.
pancreatic resections are not generally indicated. When complete Autoimmune chronic gastritis involves the body and fundus of the
tumor removal is not possible, a gastric operation may be appropri- stomach. It is associated with pernicious anemia, achlorhydria,
ate. Proximal gastric vagotomy may be useful, but total gastrec- very high gastrin levels, and a high risk for cancer. Hypersecretory
tomy still provides the best long-term quality of life for some chronic gastritis involves the gastric antrum and is associated with
patients. Life-long pharmacologic treatment with antisecretory peptic ulcer disease but not malignancy. Helicobacter pylori infec-
agents may control the ulcer diathesis in some patients, but prob- tion may be the most important risk factor for gastric adenocarci-
lems with high doses, compliance, and side effects may occur. noma worldwide. The IgG antibody positivity in various populations
Resection or ablation of metastatic disease, although not curative, correlates with the local incidence of gastric cancer. Hereditary
can provide important palliation and decrease the need for drug nonpolyposis colorectal cancer is an inheritable risk factor for
therapy. gastric cancer. Adenomatous gastric polyps have malignant
potential similar to colonic adenomatous polyps. The risk increases
ANSWER: A with increasing size of the polyp. Fundic gland polyps are benign
and have no malignant potential.

32. With regard to the epidemiologic characteristics of gastric ANSWER: E

cancer, which of the following statements is false?
A. The highest incidence is found in Japan.
34. With regard to the surgical treatment of gastric adenocarci-
B. Gastric cancer is twice as common in males as in females. noma, which of the following statements is true?
C. The incidence of gastric adenocarcinoma of the distal A. Total gastrectomy for antral lesions results in longer sur-
portion of the stomach has increased in the past several vival than does partial gastrectomy.
decades.
B. Routine splenectomy does not improve survival rates.
D. There is a higher incidence in patients with blood group A.
C. Extended lymph node dissection improves survival rates in
E. There is a higher incidence in patients who have undergone patients with stages I and II lesions.
gastric resection for duodenal ulcer.
D. Total gastrectomy for palliation is contraindicated.
Ref.: 1, 6, 7 E. Linitis plastica should be resected to histologically nega-
tive margins.
COMMENTS: The significant geographic variations in the inci-
dence of gastric cancer are probably related to environmental and Ref.: 1, 6, 7
dietary differences that result in exposure to N-nitroso compounds,
polycyclic hydrocarbons, and other potential carcinogens. The COMMENTS: Gastric adenocarcinoma is preferably treated by
highest incidence is found in Japan, with lower rates in the United resection, although resection usually proves to be palliative. The
States and Western Europe. Gastric cancer occurs more frequently general strategy for curative resection is to remove as much of the
 CHAPTER 20 / Stomach and Duodenum 267

stomach as necessary to obtain free margins and to perform limited C. The majority of GISTs have an activating mutation in the
node dissection. Although data from Japan support the benefit of KIT oncogene.
extended nodal dissection (celiac, mesenteric, hepatic, and para-
D. GISTs are usually resistant to conventional chemotherapy
aortic), studies in the United States have not generally confirmed
and radiation therapy.
this benefit. Furthermore, these extended dissections can be associ-
ated with substantial morbidity. Most resections entail distal sub- E. Complete surgical resection is the standard of treatment.
total gastrectomy. Total gastrectomy is appropriate for locally
extensive tumors, proximal tumors (to avoid esophageal anastomo- Ref.: 1, 8
sis to the distal stomach remnant), and even palliation if necessary.
Extending clear margins on a distal tumor by total rather than COMMENTS: Gastrointestinal stromal tumors are the most
subtotal gastrectomy is of no benefit. Resections for linitis plastica common mesenchymal neoplasms of the GI tract. The majority of
are palliative, usually necessitate total gastrectomy, and are carried these GISTs occur in the stomach (60%), followed by the small
out to grossly negative margins only. Splenectomy is performed bowel (30%), esophagus (1% to 5%), and colon and rectum (5%).
according to the location of gastric resection, but its routine per- The diagnosis of GIST is based on the presence of characteristic
formance does not improve the survival rate. The number of lymph pathologic findings on hematoxylin-eosin staining and expression
nodes resected, the number of positive nodes, and the ratio of posi- of the KIT receptor on immunohistochemistry. Rarely, KIT might
tive to the total number of lymph nodes have important staging not be overexpressed, and in such cases molecular evaluation may
implications. Furthermore, a minimum number of 15 lymph nodes be necessary. These tumors do not usually metastasize to lymph
should routinely be examined. nodes. Complete surgical resection is the standard of treatment of
primary, localized GISTs. The majority of GISTs have an activating
ANSWER: B mutation in the KIT protooncogene that can be effectively inhibited
by tyrosine kinase inhibitors such as imatinib mesylate (Gleevec).
GISTs are resistant to conventional chemoradiation therapy. Lapa-
35. With regard to gastric volvulus, which of the following state- roscopic resection is increasingly being used, provided that clean
ments is true? margins can be obtained. Both the size and number of mitoses per
50 high-power field have been used to categorize tumor aggres-
A. Symptoms consist of severe nausea with an inability to
siveness. Tumor location may have prognostic implications in that
vomit.
extragastric tumors may carry a worse prognosis. Large or unre-
B. The Borchardt triad includes acute epigastric pain, nausea, sectable tumors that show KIT overexpression may initially be
and bilious vomiting. treated with Gleevec.
C. It is frequently relieved simply by passage of a nasogastric ANSWER: B
tube.
D. Gastric volvulus should always be managed
conservatively. 37. Which of the following statements is not true regarding gastric
MALT lymphoma?
E. It is associated with an increased incidence of sigmoid
volvulus. A. Gastric MALT lymphomas result from the monoclonal pro-
liferation of B cells as a result of stimulation of a specific
Ref.: 1, 2 infecting strain of H. pylori.
COMMENTS: Gastric volvulus is a serious complication of B. Unresponsive gastric MALT lymphoma can usually be sal-
paraesophageal hernia. Two types of gastric volvulus may occur, vaged by gastric resection.
depending on the axis of rotation. Organoaxial volvulus, the
C. Chromosomal translocations and genetic mutations can
more common type, involves rotation around the axis of a line
predict failure of H. pylori treatment.
connecting the cardia and pylorus. With mesenteroaxial volvulus,
the axis is approximately at a right angle to the cardiopyloric D. Less than 10% of gastric lymphomas have no associated
line. Combined types have also been described. Patients generally H. pylori infection.
have severe pain and nausea but are unable to vomit. Gastric
E. External beam radiation is used to treat refractory MALT
volvulus should be suspected in patients with the Borchardt
lymphoma.
triad, which includes acute epigastric pain, violent retching, and
inability to pass a nasogastric tube. Strangulation can follow.
Ref.: 1, 6
Hence, acute gastric volvulus requires prompt surgical interven-
tion. It is not associated with an increased incidence of sigmoid
volvulus. COMMENTS: Gastric MALT lymphoma is associated with
chronic Helicobacter pylori infection in more than 90% of
ANSWER: A cases. This chronic infection with H. pylori results in monoclonal
B-cell proliferation controlled by T lymphocytes. Treatment
directed toward H. pylori eradication results in the resolution
36. With regard to GISTs, which of the following statements is of MALT lymphomas in most cases. Certain chromosomal trans-
incorrect? locations and genetic mutations can predict resistance to H.
pylori therapy and progression to a high-grade gastric lymphoma.
A. A combination of cellular morphology on hematoxylin-
Resistant gastric MALT lymphomas are usually salvaged with
eosin staining and KIT immunohistochemistry are required
radiation therapy, cyclophosphamide-based chemotherapy regi-
for the diagnosis of GIST.
mens, monoclonal anti-CD20 antibody, or combinations of these
B. After the small intestine, the stomach is the second most treatments.
common location for GISTs, followed by the colon and
rectum. ANSWER: B
268 SECTION V / Alimentary Tract

38. With regard to the diagnosis and treatment of MALT lym- 40. A 23-year-old thin (92 lb) woman with a history of surgical
phoma, which of the following statements is correct? correction of her scoliosis is evaluated for symptoms of post-
prandial epigastric pain, fullness, nausea, and vomiting. Her
A. Upper GI endoscopy with gastric biopsy for determination
physical examination is unremarkable except for her thin phy-
of the presence of H. pylori and the histologic type of
sique/stature. Barium upper GI series showed a dilated duode-
lymphoma is the diagnostic test of choice.
num and stomach with minimal flow of barium into the
B. Computed tomography of the abdomen, lymphangiogra- jejunum. Which of the following is the operative management
phy, chest radiography, and bone marrow biopsy are of choice for this patient’s condition?
required for complete staging.
A. Segmental duodenectomy
C. H. pylori serology is sufficient to document remission.
B. Pancreaticoduodenectomy
D. H. pylori–negative gastric MALT lymphoma should ini-
C. Gastrojejunostomy
tially be treated with clarithromycin, amoxicillin, and a
proton pump inhibitor. D. Duodenojejunostomy
E. H. pylori Gram stain is sufficient to make the diagnosis E. Roux-en-Y hepaticojejunostomy
alone.
Ref.: 1
Ref.: 1, 6
COMMENTS: The patient in this scenario has compression of
COMMENTS: Upper endoscopy with biopsy is the diagnostic the third portion of the duodenum by the superior mesenteric artery
test of choice. Gastric biopsies are used to evaluate for the presence as it passes over it. This rare condition is known as superior mes-
of H. pylori and the histologic type of lymphoma. The depth of enteric artery syndrome or Wilkie syndrome. This syndrome is
gastric wall invasion and the presence of nodal involvement can usually seen in young asthenic females with predisposing condi-
be determined with the help of endoscopic ultrasonography. tions of weight loss, scoliosis or corrective surgery for it, supine
Staging is completed with a chest radiograph, bone marrow biopsy, mobilization, and placement of a body cast. The diagnosis is
and computed tomography of the abdomen. Lymphangiography is usually made with either a barium upper GI series or computed
not required for staging. Surveillance is achieved with upper endos- tomography, with oral and intravenous contrast enhancement dem-
copy, biopsy, and endoscopic ultrasound every 3 months until his- onstrating a dilated duodenum and stomach with abrupt or nearly
tologic and radiographic resolution. Complete resolution is usually complete cutoff of contrast agent at the third portion of the duode-
achieved in 3 to 6 months on average. H. pylori–negative gastric num and minimal flow into the jejunum. Conservative management
MALT lymphoma, which accounts for less than 10% of all gastric consisting of nutritional supplementation can be tried initially. In
lymphomas, does not respond to bacterial eradication therapy. patients who fail medical management, the operative treatment of
choice is duodenojejunostomy.
ANSWER: A
ANSWER: D
39. All of the following statements are correct about high-grade
gastric lymphoma except: 41. All of the following statements regarding Crohn’s disease of
the duodenum are correct except:
A. Treatment usually requires combination chemotherapy and
radiation therapy. A. Duodenal Crohn’s disease accounts only for 2% to 4% of
all patients with Crohn’s disease.
B. Randomized clinical trials for early stages IE and IIE
disease demonstrate nonsurgical therapy to be equivalent B. Because of its location, operative intervention is frequently
or superior to surgical treatment in regard to patient needed for duodenal Crohn’s disease.
survival.
C. When an operation is required, a bypass such as gastroje-
C. Hemorrhage is a frequent complication of chemotherapy. junostomy is performed rather than duodenal resection.
D. Surgical treatment is usually reserved for patients with D. In well-selected patients, strictureplasty can be carried out
localized persistent lymphoma or complications associated with good results.
with nonsurgical treatment.
E. Adenocarcinoma is the leading cause of disease-specific
E. Perforation is very rare after chemotherapy. death in patients with Crohn’s disease.
Ref.: 1, 6 Ref.: 1, 9, 10
COMMENTS: High-grade gastric lymphomas require treat-
ment with combination chemotherapy and the addition of radiation COMMENTS: Crohn’s disease of the duodenum is not common
therapy for bulky or residual disease. Patient survival has been and is seen in only 2% to 4% of patients with Crohn’s disease.
shown to be equivalent or better with nonsurgical treatment than Medical therapy remains the mainstay of treatment of duodenal
with surgical treatment in several prospective clinical trials (ran- Crohn’s disease, with surgical intervention being reserved for
domized and nonrandomized). Complications were more frequent patients who do not respond to medical therapy or in whom a
in the surgical groups than in the nonsurgical groups. Complica- complication develops such as obstruction or perforation. In
tions such as perforation and hemorrhage are very infrequent in patients who do need a surgical procedure, bypass is preferred over
patients undergoing chemotherapy or radiation therapy. Complica- duodenal resection. In a few select patients, their anatomy might
tions from chemoradiation therapy or persistent localized lym- be amenable to strictureplasty.
phoma are current indications for operative intervention in patients Irrespective of the location of Crohn’s disease, GI cancer
with gastric lymphoma. remains the leading cause of death in patients with Crohn’s disease.
ANSWER: C ANSWER: B
 CHAPTER 20 / Stomach and Duodenum 269

42. With regard to adenocarcinoma of the small bowel, all of the majority of these diverticula (≈75%) are found within a 2-cm radius
following statements are correct except: from the ampulla of Vater and generally protrude through the
medial wall of the duodenum. These duodenal diverticula are rarely
A. Small bowel adenocarcinoma is found in decreasing order
symptomatic, and symptoms are usually the results of hemorrhage,
of frequency in the ileum, jejunum, and duodenum.
perforation, blind loop syndrome, cholangitis, or pancreatitis from
B. Villous adenomas of the small bowel are commonly found obstruction of the biliary or pancreatic ducts. Juxtapyloric diver-
in the duodenum around the ampulla of Vater. ticula have been noted to be associated with choledocholithiasis.
Their presence increases the difficulty of successful completion of
C. Adenocarcinoma of the duodenum usually occurs earlier
ERCP.
than small bowel adenocarcinoma elsewhere in the jejunum
and ileum. ANSWER: B
D. Villous adenomas of the duodenum are frequently associ-
ated with familial adenomatous polyposis.
44. Which of the following is the preferred treatment of a symp-
E. Operative resection is the treatment modality of choice and
tomatic duodenal diverticulum?
has curative potential.
A. Observation
Ref.: 1, 2, 6
B. Broad-spectrum antibiotics
COMMENTS: Small bowel adenocarcinoma accounts for the
C. Duodenal diverticulectomy
majority (35% to 50%) of small bowel malignant neoplasms, fol-
lowed by carcinoid tumors, lymphomas, and sarcomas. Adenocar- D. Pancreas-sparing duodenectomy
cinoma of the small bowel is more common in the duodenum,
E. Pancreaticoduodenectomy
whereas carcinoid tumors and lymphoma are more frequently
seen in the ileum. Small bowel adenocarcinoma is found in decreas- Ref.: 1
ing order of frequency in the duodenum, jejunum, and ileum.
Although rare in the small bowel, villous adenomas are frequently COMMENTS: As discussed earlier, most of the duodenal diver-
found in the duodenum and are associated with familial adenoma- ticula are asymptomatic and do not warrant any intervention.
tous polyposis syndrome (31% to 92%). These villous adenomas Surgery is reserved for patients in whom complications develop.
have high malignant potential, especially if they are larger than They can cause abdominal pain, obstruction, perforation, bleeding,
5 cm or are accompanied by bleeding or obstruction. Most patients bacterial overgrowth, and pancreaticobiliary complications. When
have nonspecific symptoms initially; however, adenocarcinoma of treatment is required, surgical excision (diverticulectomy) is
the duodenum is manifested earlier with signs and symptoms of recommended.
obstructive jaundice, gastric outlet obstruction, and abdominal
pain. Operative resection (pancreaticoduodenectomy and local ANSWER: C
excision) is the treatment of choice, depending on the size and
location of the adenocarcinoma, the patient’s health, and the sur- R E F E R E N C E S
geon’s expertise.
1. Mercer DW, Robinson EK: Stomach. In Townsend CM, Beauchamp
ANSWER: A RD, Evers BM, et al, editors: Sabiston textbook of surgery: the biologi-
cal basis of modern surgical practice, ed 18, Philadelphia, 2008, WB
Saunders.
2. Dempsey DT: Stomach. In Brunicardi FC, Andersen DK, Billiar TR,
43. Concerning duodenal diverticula, all of the following state- et al, editors: Schwartz’s principles of surgery, ed 9, New York, 2010,
ments are correct except: McGraw-Hill.
3. Rice-Townsend SE, Norton JA: Zollinger-Ellison syndrome. In
A. They are twice as common in women as in men.
Cameron JL, editor: Current surgical therapy, ed 9, Philadelphia, 2008,
B. Duodenal diverticula are the second most common CV Mosby.
congenital diverticula of the intestine after Meckel 4. Winkleman BJ, Usatii A, Ellison EC: Duodenal ulcer. In Cameron JL,
diverticulum. editor: Current surgical therapy, ed 9, Philadelphia, 2008, CV Mosby.
5. Fisher WE, Brunicardi FC: Benign gastric ulcer. In Cameron JL, editor:
C. The majority of duodenal diverticula are found in the peri- Current surgical therapy, ed 9, Philadelphia, 2008, CV Mosby.
ampullary region. 6. Bland KI, Büchler MW, Csendes A, et al: General surgery: principles
and international practice, ed 2, New York, 2008, Springer-Verlag.
D. Most of them are asymptomatic and found incidentally. 7. Cho CS, Brennan MF: Gastric adenocarcinoma. In Cameron JL, editor:
Current surgical therapy, ed 9, Philadelphia, 2008, CV Mosby.
E. They can result in cholangitis and pancreatitis from obstruc-
8. Efron DT: Gastrointestinal stromal tumors. In Cameron JL, editor:
tion of the biliary or pancreatic ducts, respectively. Current surgical therapy, ed 9, Philadelphia, 2008, CV Mosby.
9. Mintz Y, Talamini MA: Crohn’s disease of the small bowel. In Cameron
Ref.: 1
JL, editor: Current surgical therapy, ed 9, Philadelphia, 2008, CV
Mosby.
COMMENTS: Duodenal diverticula are false diverticula con-
10. Tavakkolizadeh A, Whang EE, Ashley SW, et al: Small intestine. In
taining only mucosa and submucosa, as opposed to a true diver- Brunicardi FC, Andersen DK, Billiar TR, et al, editors: Schwartz’s
ticulum, which contains all layers of the intestinal wall (e.g., principles of surgery, ed 9, New York, 2010, McGraw-Hill.
Meckel diverticulum). Duodenal diverticula are the second most
common cause of acquired diverticula after those in the colon.
They are more commonly seen in women than in men (2 : 1) and
usually occur later in life, similar to colonic diverticula. The