Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Copy ABSITE Review: Fiser, Decker, SCORE, UpToDate, TrueLearn > Chapter 30 - Stomach+ > Flashcards

Chapter 30 - Stomach+ Flashcards

1
Q

What is the transit time of the stomach?

A

3-4h

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What level of afferent sympathetic fibers sense gastroduodenal pain?

A

T5-10

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What type of mucosa does the stomach have?

A

Simple columnar epithelium

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What do the cardia glands secrete?

A

Mucus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What do Chief cells secrete? Location?

A

Pepsinogen; fundus and body

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What do Parietal cells secrete? Location?

A

H+ and intrisic factor; fundus and body

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What stimulates HCl release?

A

Gastrin, ACh, histamine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What mediator does ACh and gastrin work on to inc. HCl?

A

Phospholipase → PIP → DAG + IP3 → inc. Ca, activates phosphorylase kinase

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Histamine acts on what mediator to inc. HCl?

A

Adenylate cyclase → cAMP → protein kinase A

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What are inhibitors of parietal cells?

A

Somatostatin, PGE1, secretin, CCK

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What does intrinsic factor do?

A

Binds B12 and the complex is reabsorbed in the terminal ileum

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

G cells release what? Location?

A

Gastrin; Antrum and pylorus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

G cells inhibited by? Stimulated by?

A

Inhibited by H+ in duodenum; stimulated by amino acids, ACh

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

D cell secrete what? Location?

A

Somatostatin; antrum and pylorus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Response to somatostatin in the stomach?

A

Inhibit gastrin and acid release

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Brunner’s glands secrete what? Location?

A

Pepsinogen and alkaline mucus; duodenum

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

DDx for elevated acid and gastrin?

A

ZES, antral cell hyperplasia, retained antrum, renal failure, gastric outlet obstruction, short bowel syndrome

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

DDx for elevated gastrin and normal/decreased acid?

A

Pernicious anemia, chronic gastritis, gastric ca, postvagotomy, medical acid suppression

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

DDx for rapid gastric emptying?

A

1 previous surgery, ZES, ulcers

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

DDx for delayed gastric emptying?

A

Opiates, anticholinergics, myxedema, hyperglycemia, diabetes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Components of Billroth I?

A

Antrectomy with gastroduodenal anastamosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Components of Billroth II?

A

Antrectomy with gastrojejunal anastamosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

What is a trichobezoar? Treatment?

A

Hair, hard to pull out; EGD inadequate, likely need gastrostomy and removal

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

What is a phytobezoar? Treatment?

A

Fiber, often in diabetics with poor gastric emptying; enzymes, EGD, diet changes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

What is Dieulafoy’s ulcer?

A

Vascular malformation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

What is Menetrier’s disease?

A

Mucous cell hyperplasia, increased rugal folds

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

Gastric volvulus is associated with what condition?

A

Type II hiatal hernia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

Symptoms of gastric volvulus? Treatment?

A

Nausea without vomiting, severe pain; usually organoaxial volvulus; reduction and Nissen

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

What is a Mallory-Weiss tear? Presentation?

A

Secondary to forceful vomiting; hematemesis following severe retching

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

Diagnosis of Mallory-Weiss? Treatment?

A

EGD; tear usually near lesser curve of stomach, PPE, transfusion; if continued bleeding, may need gastrostomy and oversewing of the vessel

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

Effects of all forms of vagal denervation?

A

Increased liquid emptying; vagally mediated receptive relaxation is removed; results in increased gastric pressure that accelerates liquid emptying

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

Where is the denervation in truncal vagotomy? Effect on solid emptying?

A

Divides vagal trunks at level of esophagus; decreased emptying of solids

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

Where is the level of denervation in selective vagotomy? Effect on solid emptying?

A

Divides nerves of Latarjet; decreased emptying of solids

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

Where is the level of denervation in highly-selective vagotomy? Effect on solid emptying?

A

Divides individual fibers, preserves “crow’s foot”; normal emptying of solids

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

What are the gastric effects of truncal vagotomy?

A

Dec. acid output by 90%, increased gastrin, gastrin cell hyperplasia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

What are the nongastric effects of truncal vagotomy?

A

Decreased exocrine pancreas function, decreased postprandial bile flow, increased gallbladder volumes, decreased release of vagally mediated hormones

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

What is the most common problem following vagotomy?

A

Diarrhea (30-50%), caused by sustained MMCs forcing bile acids into colon

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

Risk factors for upper GI bleed?

A

Previous UGI bleed, PUD, NSAIDs, smoking, liver disease, esophageal varices, splenic v thrombosis, sepsis, burn injuries, trauma, severe vomiting

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

Risk factors for rebleeding at time of EGD for UGIB?

A

1 spurting blood vessel (60%), #2 visible blood vessel (40%), #3 diffuse oozing (30%)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

Likely source of UGI bleed in liver failure patient? Treatment?

A

Bleeding from esophageal varices. Do EGD with sclerotherapy, TIPS, not OR

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

What is the cause of duodenal ulcers?

A

Increased acid production, decreased host defense

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

Most common location of duodenal ulcers?

A

1st part of duodenum, usually anterior

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

Most common presentation of anterior duodenal ulcers? Posterior?

A

Anterior: perforation, posterior: bleed

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

Treatment of duodenal ulcers?

A

H2 blockers, PPI, triple therapy for pts with H. pylori

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

Surgical indications for duodenal ulcer?

A

Perforation, protracted bleeding despite EGD therapy, obstruction, intractability despite medical therapy, inability to r/o cancer

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

Surgical options for duodenal ulcers?

A

Truncal vagotomy and pyloroplasty, truncal vagotomy and antrectomy with BI or BII. Highly selective vagotomy.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

Ulcer surgery with lowest rate of recurrence?

A

Truncal vagotomy and antrectomy with BI/BII

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

Ulcer surgery with lowest rate of complications?

A

Proximal or highly selective vagotomy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

What is the most frequent complication of duodenal ulcers?

A

Bleeding

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
50
Q

What is the initial treatment of choice for obstruction secondary to duodenal ulcers?

A

Serial dilation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
51
Q

Surgical options for duodenal ulcer causing obstruction?

A

Near ampulla: gastroj (BII, bypasses obstruction), antrectomy, truncal vagotomy; proximal to ampulla: antrectomy with ulcer excision, BII, truncal vagotomy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
52
Q

% of patients with perforation that will have free air?

A

80%

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
53
Q

Treatment of perforation in elderly, high risk patients?

A

Possibility that high risk patients can be safely observed with UGI to make sure perforation has sealed

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
54
Q

Surgical option for perforated duodenal ulcer?

A

Graham patch and highly selective vagotomy (for pts on PPI); truncal vagotomy and pyloroplsty (include ulcer in pyloroplasty); truncal vagotomy and antrectomy with BI or BII (need to include ulcer)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
55
Q

What defines intractability with duodenal ulcers?

A

> 3mo without relief on PPI or recurrence <1y after medical therapy; based on EGD findings, not symptoms

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
56
Q

Risk factors for gastric ulcers?

A

Male, tobacco, ETOH, NSAIDs, H. pylori, uremia, stress, steroids, chemo

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
57
Q

Most common cause of gastric ulcers?

A

H. Pylori.

Most (type I/IV) have normal acid secretion, due to abnormal mucosal defense.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
58
Q

% of gastric ulcers on lesser curve of stomach?

A

70-80%

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
59
Q

Where do biopsies for H. pylori need to be taken from?

A

Antrum

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
60
Q

What type of blood is associated with type I ulcers?

A

Type A

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
61
Q

What type of blood is associated with type II-IV ulcers?

A

Type O

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
62
Q

Indications for surgery with gastric ulcers?

A

Perforation, bleeding, obstruction, cannot exclude malignancy, intractability

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
63
Q

Location of type I gastric ulcer? Cause?

A

Lesser curvature; due to decreased mucosal protection

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
64
Q

Treatment of type I gastric ulcer?

A

Distal gastrectomy including ulcer with BI/BII

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
65
Q

Location of type II gastric ulcer? Cause?

A

Lesser curve and duodenal; high acid secretion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
66
Q

Treatment of type II gastric ulcer?

A

Distal gastrectomy with BI/BII and truncal vagotomy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
67
Q

Location of type III gastric ulcer? Cause?

A

Prepyloric; similar to duodenal, high acid secretion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
68
Q

Treatment for type III gastric ulcer?

A

Distal gastrectomy with BI/BII and truncal vagotomy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
69
Q

Location of type IV? Cause?

A

Lesser curve high along cardia of stomach; decreased mucosal protection

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
70
Q

Treatment for type IV gastric ulcer?

A

Ulcer excision +/- vagotomy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
71
Q

Location of type V gastric ulcer? Cause?

A

Anywhere; NSAID-related

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
72
Q

How many days after the event does stress gastritis occur?

A

3-5d

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
73
Q

Where is type A chronic gastritis located? Associated with what conditions?

A

Fundus; pernicious anemia, autoimmune disease

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
74
Q

Location of type B chronic gastritis? Associated conditions?

A

Antrum; H. pylori

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
75
Q

Symptoms associated with gastric cancer?

A

Pain unrelieved by eating, weight loss

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
76
Q

Where are the majority of gastric cancers located?

A

Antrum (40%)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
77
Q

Risk factors for gastric cancer?

A

Adenomatous polyps, tobacco, previous gastric operations, intestinal metaplasia, atrophic gastritis, pernicious anemia, type A blood, nitrosamines

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
78
Q

Adenomatous polyps carry what % cancer risk? Treatment?

A

10-20% risk of cancer; endoscopic resection

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
79
Q

What is Krukenberg tumor?

A

Metastases to ovaries

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
80
Q

What is Virchow’s node?

A

Mets to supraclavicular node

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
81
Q

What is intestinal gastric cancer associated with?

A

High risk populations, older men (rare in US); associated with chronic atrophy, dysplasia, blood invasion, glands on histology

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
82
Q

Characteristics of diffuse gastric cancer (linitis plastica)?

A

Low risk populations, women, lymphatic invasion, NO glands

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
83
Q

Surgical treatment of linitis plastica?

A

Total gastrectomy plus chemo

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
84
Q

Options for palliation for gastric cancer causing obstruction? Bleeding or pain?

A

Obstruction: stenting; bleeding/pain: XRT or palliative gastrectomy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
85
Q

What is the most common benign gastric neoplasm?

A

Gastric leiomyomas (GIST)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
86
Q

US findings of GIST?

A

Hypoechoic, smooth edges

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
87
Q

Treatment of GIST?

A

Resection - offer to all. Potentially curable. Consider chemo if >5cm or 5-10 mitoses/HPF; need 1cm margins (as opposed to 5 cm for adenocarcinoma). GIST involves muscularis propria, so endoscopic resection is not recommended.

88
Q

Gene mutation associated with GIST?

A

c-KIT

89
Q

Chemo used with GIST?

A

Gleevec (tyrosine kinase inhibitor)

90
Q

Treatment for gastric leiomyosarcoma?

A

En bloc resection

91
Q

What is the diagnosis of cancer with gastric leiomyosarcomas based on?

A

Mitoses/HPF (>5-10)

92
Q

Spread of leiomyosarcoma via what?

A

Hematogenous

93
Q

Symptoms of gastric lymphomas?

A

Ulcer symptoms

94
Q

Most common type of lymphoma of the stomach?

A

Non-Hodgkins

95
Q

Treatment for gastric lymphomas?

A

Chemo and XRT; surgery for complications

96
Q

Overall 5y survival rate of gastric lymphoma?

A

> 50%

97
Q

Mucosa-associated lymphoid tissue lymphoma (MALT) associated with what condition?

A

H. pylori infection

98
Q

Where are MALTs located?

A

Usually in GI, can also be in lung and Waldeyer’s ring

99
Q

Treatment for MALT?

A

Triple therapy abx for H. pylori and surveillance; if does not regress, need chemo (CHOP). Factors that predict MALT lymphoma treatment failure after H. pylori eradication alone include the presence of transmural tumor extension, nodal involvement, transformation into a large cell phenotype, and t(11;18) or nuclear BCL-10 expression.

100
Q

Procedure that should be performed with gastric bypass?

A

Cholecystectomy

101
Q

Failure rate of roux-en-y?

A

10-15% due to high carb snacking

102
Q

What is the most common cause of leak with roux-en-y? Signs? Tx?

A

Ischemia; tachycardia, tachypnea, pain, fever, elevated WBCs. Abx, nutritional support, IR drain (stent can’t be used for Roux-en-Y, but can for sleeve). If IR cannot control the drainage, may require OR washout with an omental patch and potentially jejunostomy.

103
Q

% of roux-en-y that develop marginal ulcers? Treatment?

A

10%; omeprazole

104
Q

Tx for stenosis following roux-en-y?

A

Dilation

105
Q

What are signs of obstruction following roux-en-y surgery?

A

Hiccups, large stomach bubble

106
Q

Why are jejunoileal bypass operations no longer done?

A

Associated with increased liver cirrhosis and kidney stones, osteoporosis

107
Q

What is the treatment for jejunoileal bypass when encountered?

A

Correction with roux-en-y

108
Q

What causes dumping syndrome post-gastrectomy?

A

From rapid entering of carbs into small bowel; can occur after gastrectomy, vagotomy, pyloroplasty

109
Q

What are the 2 phases of dumping syndrome?

A

Hyperosmotic load causes fluid shift into bowel (diarrhea, dizziness, hypotension); reactive increase in insulin and decrease in glucose (rarely occurs)

110
Q

Treatment for dumping syndrome?

A

Small, low-fat, low-carb, increased-protein meals; no liquids with meals, no lying down after meals

111
Q

Surgical options for dumping syndrome?

A

Rarely necessary; Conversion of BI or BII to Roux-en-y, operations to increase gastric reservoir (jejunal pouch), or increase emptying time (reversed jejunal loop)

112
Q

What are symptoms of alkaline reflux gastritis?

A

Postprandial epigastric pain associated with n/v; pain not relieved with vomiting

113
Q

Diagnosis of alkaline reflux gastritis?

A

Evidence of bile reflux into stomach, histologic evidence of gastritis

114
Q

Medical treatment for alkaline reflux gastritis?

A

H2 blockers, cholestyramine, metoclopramide

115
Q

Surgical options for alkaline reflux gastritis?

A

Conversion of BI/BII to roux-en-y with afferent limb 60cm distal to original gastroj

116
Q

What is roux stasis? Diagnosis?

A

Stasis of chyme in roux limb due to loss of jejunal motility; EGD, emptying studies

117
Q

Treatment for roux stasis? Surgical options?

A

Metoclopramide, prokinetics; shorten roux limb to 40cm

118
Q

What is chronic gastric atony? Symptoms? Diagnosis?

A

Delayed gastric emptying after vagotomy; n/v, pain, early satiety; gastric emptying study

119
Q

Treatment for chronic gastric atony? Surgical options?

A

Metoclopramide, prokinetics; near-total gastrectomy with roux-en-y

120
Q

Treatment for duodenal stump blow-out?

A

place duodenostomy and drains

121
Q

What is blind-loop syndrome?

A

With BII or roux-en-y; pain, diarrhea, malabsorption, b12 deficiency, steatorrhea; caused by bacterial overgrowth and stasis in afferent limb

122
Q

Treatment for blind-loop syndrome?

A

Tetracycline, flagyl, reglan; reanastomosis with shorter (40cm) afferent limb

123
Q

What is afferent-loop obstruction?

A

With B-II or roux-en-y; nonbilious vomiting, pain relieved with bilious emesis; ruq pain, steatorrhea; caused by obstruction of afferent limb

124
Q

Treatment of afferent-loop obstruction?

A

Balloon dilation may be possible; reanastomosis with shorter (40cm) afferent limb. Can also convert to Roux-en-y if B-II.

125
Q

What is efferent-loop obstruction?

A

Symptoms of obstruction

126
Q

Treatment for efferent loop obstruction?

A

Dilation; find site of obstruction and relieve it

127
Q

What is postvagotomy diarrhea secondary to?

A

Nonconjugated bile salts in colon and sustained postprandial organized MMCs

128
Q

Define upper GI bleed.

A

Proximal to the ligament of Treitz

129
Q

Causes of upper GI bleed.

A

PUD, varices, Mallory-Weiss tears, vascular lesions, malignancy

130
Q

Presentation of upper GI bleed.

A

Hematemesis, but hematochezia and melena are more common. Hypotension, AMS, dyspnea, chest pain.

131
Q

What is the initial management of upper GI bleed?

A

Start w/ ABCs - airway, access, MTP/resuscitate, Foley to monitor. Then workup - CBC, chem 10, LFTs, type and cross, ROTEM. Begin treating with IV PPI. This sets up a successful EGD. IV erythromycin used to improve visualization (or NGT lavage if already in place)

132
Q

What is the role for NGT in a suspected upper GI bleed?

A

During initial workup, if there is a question about the source (melena, hematochezia), NGT can be used to approximate the site - blood is upper GI, bile is lower GI, nonbloody/nonbilious rules out stomach but doesn’t exclude duodenum. No need for NGT if location of bleed is clear.

133
Q

What can be done during initial management of upper GI bleed to improve EGD visualization?

A

If NGT is in place, can do lavage. If not, give IV erythromycin.

134
Q

If hematemesis is the presentation of upper GI bleed, how quickly should an EGD be done?

A

Within 1 hour. If melena is the presentation, EGD should be done within 12 hours.

135
Q

What is the role for tagged RBC scan in upper GI bleed?

A

Used to determine if further intervention is necessary in a patient with occult bleed.

136
Q

What is the role for arteriography in upper GI bleed?

A

Used in patient with high surgical risk that continue to bleed after EGD attempts. Can be diagnostic and therapeutic.

137
Q

What is the role of surgery in upper GI bleed? What maneuvers are performed?

A

If EGD and arteriogram fail, and the patient is dying (hemodynamic instability continues, requires 6 units of blood), operative exploration can be done. Do upper midline incision, perform duodenotomy, extend this proximally or distally depending on findings/susupicion.

138
Q

What should be tested for if a patient with upper GI bleed is found to have an ulcer?

A

Gastric biopsies of healthy mucosa for H pylori. Treat if found.

139
Q

In a patient presenting with upper GI bleed, EGD is performed and an ulcer is found. What are high-risk features for re-bleeding?

A

Active pulsatile bleeding, active oozing, visible vessel, adherent clot, pigmented spot.

140
Q

What will you do if a patient’s bleeding duodenal ulcer cannot be controlled with EGD/arteriogram/medical management? What are the steps?

A

OR: upper midline incision, mobilize the duodenum with Kocher, anterior longitudinal duodenotomy at the duodenal bulb. 3 nonabsorbable stitches are placed in the superior, inferior, and medial locations to ligate the GDA and transverse pancreatic artery. Avoid the CBD - consider cannulating the ampulla.

141
Q

How are gastric ulcers classified?

A

Location and contribution of gastric acid to development: I - lesser curve, not associated with high acid. II - simultaneous on lesser curve and duodenal bulb, asssociated with high acid output. III - prepylorus and associated with high acid output. IV - cardia near GEJ, not associated with acid. V - diffuse, associated with medication (NSAIDs, aspirin).

142
Q

How does management with bleeding gastric ulcers differ from duodenal ulcers?

A

Initial management is the same. During EGD, do NOT do biopsy or you risk bleeding. Repeat EGD with biopsy can happen later. If operative management is required, resect the affected stomach.

143
Q

What are the operative options for bleeding gastric ulcers?

A

Type I requires wedge resection. Type II and III require antrectomy with BI and BII. Type IV gets Csendes - distal gastrectomy w/ Roux-en-y.

144
Q

A patient presents with upper GI bleed and is found to have varices, what other medication can be given in conjunction with management with EGD?

A

Somatostatin or octreotide. Ceftriaxone if cirrhotic.

145
Q

If a patient with upper GI bleed is found to have varices that cannot be controlled with EGD banding and sclerotherapy, what should be done next?

A

Balloon tamponade

146
Q

What is the role for surgical management in a cirrhotic patient presenting with upper GI bleed?

A

Determine whether the patient is a transplant candidate. If so, avoid surgery by doing TIPS. If not a transplant candidate, the urgency of the procedure is considered - if no active bleed, do splenorenal shunt; if actively bleeding, do central portacaval shunt.

147
Q

In a patient with upper GI bleed d/t variceal bleeding, what other medication can be added post-recovery?

A

Propranolol. Not to be used in an acute setting.

148
Q

In a patient with left-sided portal hypertension causing gastric varices, what is a likely cause and what can be done?

A

Pancreatic disease causing splenic vein thrombosis causing selective left-sided portal HTN. Do splenectomy.

149
Q

In a patient with upper GI bleed d/t Mallory Weiss tear who is requiring surgical intervention, what is the approach?

A

Anterior gastrotomy and direct suture ligation

150
Q

In a patient with upper GI bleed d/t acute hemorrhagic gastritis who is requiring surgical intervention, what is the approach?

A

Near-total/total gastrectomy

151
Q

What is the procedure of choice for a benign mass found to be the cause of an upper GI bleed?

A

GIST, hamartoma, hemangioma - wedge resection

152
Q

What is the management for a malignant mass found to be the cause of an upper GI bleed?

A

Stabilize, stage, and resect as appropriate when stable. If the disease is advanced, avoid surgery.

153
Q

If an upper GI bleed is caused by a Cameron ulcer, what must be included in the operative plan if feasible?

A

These are ulcers in a hiatal hernia near GE. Must repair the hiatal hernia and do a Nissen.

154
Q

What is the presentation of hemobilia as an upper GI bleed? How do you manage?

A

Hx of biliary pathology or recent instrumentation with upper GI bleed, RUQ pain, obstructive jaundice. EGD to rule out other UGIB causes, then mesenteric angiography with angioembolization will cure. Hepatic artery ligation and/or liver resection are last resorts.

155
Q

How do you treat upper GI bleed caused by duodenal diverticula?

A

Last resort for symptomatic pts - segmental resection. Watch for pancreatic and bile ducts. If intraluminal, do duodenotomy and excision.

156
Q

Define obesity.

A

BMI >30

157
Q

What is the only intervention for morbid obesity that consistently induces sustained weight loss with proven long-term outcomes?

A

bariatric surgery - results are better than those of a combination of diet, exercise, and behavioral modification, even with the addition of weight loss drugs

158
Q

What are the indications for bariatric surgery?

A

BMI >40 or BMI > 30 in patients with high-risk conditions - DM, cardiomyopathy, OSA. Documented failure of non-surgical attempts at weight loss is included as well.

159
Q

What types of preoperative assessments must one undergo before bariatric surgery?

A

Nutrition, psychological, compliance, social

160
Q

What are the comorbid goals in preoperative management of bariatric surgery patients?

A

HbA1c <6.5 to 7 (>8 is assd w/ worst outcomes). Screen (H&P) for OSA and treat w/ CPAP. If >30 yrs, need EKG. For DVT, chemical ppx should be given 30 min preop, ambulation starts POD0, and ppx IVC can be considered for pts w/ PAH.

161
Q

What surgery should be considered if the bariatric surgery patient has GERD?

A

Roux-en-y

162
Q

In patients with epigastric pain, ulcers, or gastritis, what should be screened for pre-operatively?

A

H. pylori.

163
Q

How are patients with Crohns and UC managed if they are being considered for bariatric surgery?

A

Contraindication for active disease. Vertical sleeve gastrectomy is the only potential option.

164
Q

How should gallstones be managed in a patient undergoing bariatric surgery?

A

Do concurrent lap chole if symptomatic gallstones.

165
Q

What complications plague lap adjusted gastric band?

A

It’s easy to do, but risk band slip and pouch dilation.

166
Q

What are the major steps for a lap roux-en-y gastric bypass for bariatric surgery?

A

1) Gastric pouch formation. 2) Gastrojejunostomy. 3) Jejunojejunostomy. 4) Closure of mesenteric defects.

167
Q

What is the most concerning early complication for LRYGB?

A

anastomotic leak - can present with subtle signs of intra-abdominal sepsis and tachycardia

168
Q

How do you manage the long-term complication of marginal ulcers s/p LRYGB?

A

Often occur at the GJ site. Manage medically - stop smoking, stop NSAIDs. Revision for ulcer causing stenosis and as last resort for nonhealing ulcer. Graham patch perforations.

169
Q

How do you manage a LRYGB complicated by stenosis at GJ?

A

EGD and dilation works well. Revision if associated with ulcer.

170
Q

How do you decide between sleeve gastrectomy or roux-en-y for bariatric surgery?

A

lean towards roux-en-y for T2DM

171
Q

In sleeve gastrectomy for bariatric surgery, what is the significance of removing the stomach fundus?

A

Other than shrinking the size of the stomach, it decreases ghrelin, which is secreted from the fundus.

172
Q

Why is LSG often preferred for bariatric surgery?

A

Low complication rate - staple line leak, stricture, GERD.

173
Q

How are strictures managed in a postop sleeve gastrectomy done for bariatric surgery?

A

Observation can be attempted. EGD dilation is next step. Seromyotomy if dilation fails. Conversion to a roux-en-y is the last resort.

174
Q

Where are postop sleeve gastrectomy strictures most likely to occur? How do you prevent them?

A

At the incisura angularis (distal “break” at distal lesser curve). Prevent by using a bougie, staying away from the incisura, and maintaining symmetricla lateral traction.

175
Q

How do you manage a staple line leak after sleeve gastrectomy for bariatric surgery?

A

EGD stent placement with IR perc drainage or lap exploration with washout and drain placement.

176
Q

A postop sleeve gastrectomy presents with fever and tachycardia. UGI is normal.

A

Immediate exploration. Washout. Place a feeding j-tube.

177
Q

What are the pros/cons for biliopancreatic diversion/duodenal switch?

A

Excellent long-term weight loss, highest level of comorbid condition improvement; comparable

178
Q

How is GERD initially diagnosed?

A

History and physical

179
Q

What is the first line treatment in a patient presenting with typical GERD symptoms?

A

Daily PPI trial 3-6 months. Head of bed elevation. Weight loss.

180
Q

What is there is no response to the initial PPI trial for GERD?

A

BID PPI

181
Q

What if there is no response to the BID PPI trial for GERD?

A

Workup: esophagogram, upper endoscopy, pH study, esophageal manometry.

182
Q

What should be done endoscopically to confirm the presence of Barrett and assess for dysplasia?

A

four quadrant biopsies at 2 cm intervals

183
Q

What is the gold standard to determine esophageal acid exposure?

A

24 hr ambulatory pH monitoring. This can be omitted for severe erosive esophagitis or biopsy proven long-segment Barrett. Stop PPIs before testing.

184
Q

During endoluminal pH testing, what is the DeMeester score that indicates abnormal acid exposure?

A

> 14.7 - most important predictor of Nissen success. Also typical GERD symptoms.

185
Q

What test best identifies esophageal motility in GERD workup?

A

manometry

186
Q

What GERD patients are eligible for surgery?

A

failed medical management, Barrett, peptic stricture, severe esophagitis

187
Q

In GERD patients what surgery should be done for patients with reflux and morbid obesity?

A

roux-en-y gastric bypass, otherwise do Nissen

188
Q

What are the principles of laparoscopic paraesophageal hernia repair?

A

1) reduction of the stomach and excision of the hernia sac. 2) adequate mediastinal esophageal mobilization. 3) repair of the diaphragmatic hiatus. 4) fundoplication.

189
Q

How does erythromycin work as a promotility agent?

A

binds motilin receptors on smooth muscle cells in GI tract

190
Q

What are the steps for sleeve gastrectomy?

A

Devascularic the greater curvature of the stomach. Use a 34-40 Fr bougie to size the sleeve. Transect the stomach starting 2-6 cm proximal to the pylorus. Extract the stomach.

191
Q

What can be added as an adjunct to pH monitoring to determine if the cause is bile reflux (pt w/ hx of Bilroth)?

A

esophageal impedance testing - tests for nonacid reflux

192
Q

Discuss gastroparesis.

A

Delayed gastric emptying w/o obstruction. Usually idiopathic, diabetic, or post-surgical.
Psx: nausea, vomiting, satiety, abd pain, bloating, weight loss.
Dx: endoscopy first to rule out mechanical obstruction. A dx is confirmed by scintigraphy w/ retention >10% at 4 hrs or 60% at 2 hrs.
Mgmt: find cause - TSH, Hgb, glucose, protein, albumin, ANA; manometry. Change diet, prokinetic, antiemetics; venting gastrostomy if still symptomatic

193
Q

What is an advantage of the Belsey Mark IV

A

partial fundoplication performed by transthoracic approach, which allows full esophageal mobilization; used for an obese pt w/ previous abdominal surgery and esophagus shortened by inflammation

194
Q

Most common pattern of inflammation with H pylori?

A

The most common pattern is associated with mild to moderate inflammation of all regions of the stomach. Antral gastritis is associated with high acid output and development of ulcers in the duodenum and prepyloric areas. The third pattern of inflammation is predominantly affecting the body of the stomach. It is associated with gastric atrophy, hypergastrinemia, achlorhydria, and it is considered a precursor for gastric cancer.

195
Q

Compare the expected weight loss of the three major bariatric surgery procedures.

A

Laparoscopic adjustable gastric bands (LAGB) have an expected excess weight loss of approximately 50%, while Roux-en-Y gastric bypass and sleeve gastrectomy have an expected excess weight loss of 75% and 60% respectively.

196
Q

Describe the final position of a lap adjusted gastric band.

A

Laparoscopic adjustable gastric band placement involves placing a band with an adjustable reservoir around the proximal stomach. The band should be oriented in a medial to lateral direction with an inferior-to-superior slant.

197
Q

After treatment, the best test for eradication of the H pylori is with?

A

Urea breath test. Testing should be delayed for 4 weeks to ensure reliable results.

198
Q

What do gastrin, motilin, and secretin do to LES pressure?

A

The hormones gastrin and motilin have been shown to increase lower esophageal sphincter pressure. Secretin decrease LES pressure.

199
Q

What do you do for a slipped gastric band?

A

remove saline from the band, take to OR for removal of the gastric band

200
Q

Does highly selective vagotomy require a drainage procedure?

A

Highly selective vagotomy removes only the innervation to the lesser curvature of the stomach and preserves the innervation to the pylorus. Consequently, a highly selective vagotomy does not require a concomitant drainage procedure.

201
Q

Does highly selective vagotomy have an increased or decreased risk of dumping compared to standard vagotomy?

A

It also preserves pyloric function and therefore has a lower risk of dumping syndrome.

202
Q

On postoperative day 5 following a Billroth II procedure, you note that your patient has a change in the character of his right upper quadrant drain from serosanguinous to bilious. The most likely cause is…

A

Duodenal stump leak from technical error.

203
Q

Describe gastric polyps and their management.

A

Most commonly discovered incidentally during endoscopic evaluation. Polyps are more common in patients who have a history of H. pylori infection and atrophic gastritis. Polyps found in the fundus have no malignant potential. Similar to colonic polyps, gastric polyps are either hyperplastic (low malignant potential) or adenomatous. Adenomatous polyps can be tubular, tubulovillous, or villous and increase in their malignant potential, respectively. Gastric polyps should be excised endoscopically and sent to pathology to determine if any invasive cancer is involved.

204
Q

Definitive treatment for gastric cancer?

A

surgical resection with at least 5 cm margins; splenectomy not needed; 15 nodes in D1 resection

205
Q

What is the role for neoadjuvant chemo in gastric cancer?

A

Neoadjuvant chemotherapy is indicated for lesions ≥T2 or any N. (like esophageal or rectal cancer)

206
Q

How do you manage proximal vs distal gastric cancer?

A

Proximal gastric cancer require total gastrectomy in order to obtain adequate 5 cm margins. Distal tumors can usually achieve an adequate margin and a subtotal gastrectomy.

207
Q

A 44-year-old female who is 4 years status post laparoscopic adjustable gastric banding presents with erythema and tenderness on her abdomen around her port. What is the suspected diagnosis?

A

Band erosion. Do upper endoscopy. Go to OR for removal of the band and closure of the defect.

208
Q

During an esophagogastrectomy, what can be done to help the gastric conduit meet the proximal esophagus for a tension-free anastomosis?

A

Kocher

209
Q

What are the main steps of an esophagogastrectomy?

A

proper oncologic resection of the tumor, creation of an esophageal conduit (either from the stomach or intestine), and the creation of a tension-free anastomosis

210
Q

What are the two factors that put patients at greatest risk for stress ulcers?

A

ventilation >48 hrs, coagulopathy

211
Q

What do you tell pts about a diagnostic laparoscopy given gastric adenocarcinoma diagnosis and advanced stage?

A

Advanced tumor stage may warrant diagnostic laparoscopy because position emission tomography is about 50% sensitive for detection of peritoneal carcinomatosis.

212
Q

What are important prognostic indicators of gastrointestinal stromal tumor, with the first listed being the most important?

A

Mitotic index, tumor size, and site of tumor origin (small bowel worse than gastric)

213
Q

Gastric carcinoids have been described as three types. What are they?

A

Type I is most common and associated with pernicious anemia and chronic atrophic gastritis. These tumors have less malignant potential and are slow growing. Type II tumors occur in patients with MEN 1 and Zollinger-Ellison syndrome, and have intermediate malignant potential. Type III gastric carcinoid tumors are aggressive, usually solitary lesions that are associated with normal gastrin levels. Five-year survival is 85% for type I and II tumors whereas the overall 5-year survival for type III is 33% or less.

214
Q

How do you treat gastric carcinoid tumors?

A

The treatment of patients with gastric carcinoid tumors depends on the size of the tumor and the cause. Sporadic tumors are assumed to be malignant until proven otherwise. Tumors associated with hypergastrinemia (Zollinger-Ellison syndrome or atrophic gastritis) are less aggressive, and treatment of these 2 populations is directed toward eradication of hypergastrinemia. In fact, complete regression of all tumors after antrectomy alone has been documented in patients with atrophic gastritis and multiple small carcinoids.

215
Q

If a plasma gastrin determination of 400 pg/ml is obtained, the single best test to establish the diagnosis of Zollinger-Ellison syndrome (gastrinoma) is?

A

A secretin stimulation test. A baseline gastrin level is drawn, then 2 units per kilogram of secretin are administered intravenously as a bolus, and gastrin levels are drawn at 5 minute intervals for 30 minutes. An increase in gastrin of more than 200pg/ml above the basal level supports the diagnosis of a gastrinoma.

Initially, fasting serum gastrin levels are measured, and if greater than 1,000pg/ml in the setting of hyperacidity and ulcer disease, it is pathognomic for gastrinoma.

Copy ABSITE Review: Fiser, Decker, SCORE, UpToDate, TrueLearn (50 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions