Stomach Flashcards

1
Q

What is the incidence of peptic ulcer disease in the US?

A

0.1-0.3% or 300,000 new cases per year

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2
Q

What are the main indications for surgical intervention for gastric ulcers?

A
  1. hemorrhage
  2. perforation
  3. obstruction
  4. refractory disease
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3
Q

2 most common etiologies of gastric ulcers?

A
  1. H pylori

2. NSAIDs

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4
Q

What is the definition of failure of medical therapy for gastric ulcers?

A

12 weeks of treatment with persistence of symptoms

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5
Q

Where are type I gastric ulcers located?

A

near the incisura on the lesser curvature

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6
Q

What is the most common type/location for gastric ulcers? What percent of all gastric ulcers do they account for?

A
  • Type I (near the incisura on the lesser curvature

- 60%

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7
Q

What is the first line treatment of all gastric ulcers?

A
  • acid suppression

- H pylori eradication

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8
Q

What is the treatment for H pylori

A
Triple therapy
1. clarithromycin 500 mg BID
2. amoxicillin  1000 mg BID
3. PPI BID
all x 14 days.
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9
Q

What is the preferred surgical treatment for type I gastric ulcers?

A

Antrectomy and vagotomy with Billroth I reconstruction

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10
Q

Where are type II gastric ulcers located? What is the cause?

A
  • concominant gastric ulcer near the incisura and a duodenal ulcer
  • acid hypersecretion
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11
Q

What is the preferred surgical treatment for type II gastric ulcers?

A

distal gastrectomy with vagotomy and Billroth I reconstruction

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12
Q

Where are type II gastric ulcers? What is the cause?

A
  • prepyloric

- acid hypersecretion

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13
Q

What is the preferred surgical treatment of type III gastric ulcers?

A

distal gastrectomy with vagotomy and Billroth I reconstruction (occasionally amenable to full-thickness excision with highly selective vagotomy)

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14
Q

Where are type IV gastric ulcers located?

A
  • along the lesser curvature near the GE junction
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15
Q

What are the surgical options for type IV gastric ulcers?

A
  • Pauchet procedure: antrectomy with extension along the lesser curvature to include the ulcer
  • Csendes procedure: distal gastrectomy with extension along the lesser curvature to include the ulcer
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16
Q

Where are type V gastric ulcers located? What is the cause?

A
  • Diffuse ulceration of the stomach

- NSAIDs

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17
Q

What is a Cushing’s ulcer?

A

gastric ulcer after head injury

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18
Q

What is a Curling’s ulcer?

A

gastric ulcer after a burn. typically need >30% TBSA burn

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19
Q

What is the definition of a giant ulcer? What is a special consideration in regards to giant ulcers?

A
  • ulcer > 3 cm

- 30% will harbour malignancy

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20
Q

What is the most common complication of gastric ulcers?

A

perforation

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21
Q

What is the difference between a truncal vagotomy, selective vagotomy, and highly selective vagotomy?

A
  • truncal vagotomy is division of the anterior and posterior vagus nerves 4 cm proximal to the GE junction
  • selective vagotomy is division of the vagus nerves after the posterior branches that innervate the pancreas and small intestine and the anterior branches that innervate the liver and gallbladder branch off
  • a highly selective vagotomy involves division of the terminal branches of the vagus nerve sparring the nerve of Latarjet
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22
Q

What is the criminal nerve of grassi? Why is it important?

A
  • It is the first branch of the posterior vagus nerve, that can separate from the vagus nerve proximally to the celiac division
  • It is important because 2/3 of failure of vagotomies are due to failure to transect the criminal nerve of grass resulting in recurrent ulcers
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23
Q

What are the advantages of a selective vagotomy over a truncal vagotomy?

A

selective vagotomy is not associated with diarrhea and dumping syndrome like truncal vagotomy is due to the preservation of the posterior branches to the pancreas and duodenum and the anterior branches to the liver and gallbladder

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24
Q

What is the advantage of a highly selective vagotomy over a selective vagotomy?

A

highly selective vagotomy spares the nerve of latarjet which allows the pylorus to function properly and thus no drainage procedure is required

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25
Q

What is a Heineken-Mikulicz pyloroplasty?

A

a longitudinal incision through the pylorus with a transverse closure

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26
Q

What is a Finney pyloroplasty?

A

a longitudinal incision through the pylorus extending from the duodenum onto the antrum of the stomach with a side to side anastomosis from the duodenum to the antrum

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27
Q

What is the anatomical landmark the distinguishes the antrum from the body of the stomach?

A
  • a line drawn 2/5 the distance from the pylorus to the cardia on the lesser curvature and 1/8 the distance on the greater curvature
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28
Q

Where are most duodenal ulcers located?

A

first portion of the duodenum; 90%

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29
Q

Ulceration of more distal portions of the duodenum should raise concern for what?

A

gastrinoma

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30
Q

What is the first line treatment for duodenal ulcers?

A
Triple therapy
1. clarithromycin 500 mg BID
2. amoxicillin 1000 mg BID
3. PPI
all x 14 days
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31
Q

What are the indications for surgical management of duodenal ulcers?

A
  • hemorrhage
  • obstruction
  • perforation
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32
Q

What is the most common fatal complication of duodenal ulcers?

A

perforation, with the majority being on the anterior surface of the first part of the duodenum

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33
Q

How would you repair a perforated duodenal ulcer?

A
  • anterior surface 5mm: omental patch with peritoneal irrigation
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34
Q

What is the re-bleed rate for duodenal ulcers?

A

30-40%

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35
Q

What is the first step in treatment of a bleeding duodenal ulcer?

A

PPI drip

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36
Q

Where are bleeding duodenal ulcers most commonly located?

A

posterior proximal duodenum

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37
Q

What is the surgical treatment for bleeding duodenal ulcer?

A

anterior duodenotomy, heavy permanent sutures with a u stitch to incorporate any bleeding vessels, and a two layer closure of the duodenotomy

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38
Q

What structure must one be sure to not incorporate when placing u stitches to stop a bleeding duodenal ulcer?

A

common bile duct

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39
Q

How do you manage acute gastric outlet obstruction due to a duodenal ulcer?

A

ng tube decompression, fluid resuscitation, and IV PPI. These are due to acute inflammation and medically management typically resolves the inflammation and relieves the obstruction

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40
Q

How do you manage chronic gastric outlet obstruction due to a duodenal ulcer?

A

after ruling out malignancy, balloon dilation can be attempted. however this often fails and surgical intervention with a highly selective vagotomy and gastrojejunostomy or vagotomy and antrectomy can be performed.

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41
Q

If a gastric ulcer is not resected, what must be done prior to finishing any operation?

A

biopsy of the ulcer

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42
Q

What is the definition of a giant duodenal ulcer?

A

> 2 cm

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43
Q

What is Zollinger-Ellision Syndrome?

A

gastrinoma

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44
Q

What are the 3 characteristics of ZES?

A
  • ulceration of the upper jejunum
  • hyper secretion of gastric acid
  • non-beta islet cell tumor
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45
Q

What familial disorder is ZES associated with?

A

Multiple Endocrine Neoplasia I (MEN I) - 20%

80% are sporadic

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46
Q

What are the typical symptoms of ZES?

A
  • diarrhea
  • peptic ulcers
  • abdominal pain
  • heartburn
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47
Q

What percent of patients with ZES present with mets? Where are the mets usually located?

A
  • 1/3

- liver or bone

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48
Q

How is ZES diagnosed?

A
  1. Fasting serum gastrin: patient should be off any PPI for >72 hours and fasting for 12 hours. A level > 1000 pg/mL is considered diagnostic. Normal levels are 110 pg/mL
  2. Secretin stimulation test: 0.4 microg/kg of secretin is infused. Gastrin levels are measured at 2,5,10,15, and 30 minutes. An increase of > 110 pg/mL is considered a positive test
  3. MEN I must be ruled out with serum calcium, parathyroid hormone, prolactin, and fasting insulin levels
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49
Q

What imaging test is best to localize a gastrinoma? Why?

A
  • somatostatin receptor scintigraphy

- because 80% of gastrinomas express type 2 somatostatin receipts

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50
Q

Who should be offered surgery for gastrinoma?

A

any patient with acceptable surgical risk factors and no evidence of mets

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51
Q

How does surgical management of ZES differ in patients with MEN I?

A

hyperparathyroidism should be treated first with parathyroidectomy and autotransplantation or partial parathyroidectomy because this in itself can decrease serum gastrin levels and basal acid secretion by decreasing serum calcium levels

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52
Q

What is the endoscopic finding (besides distal small bowel ulcers or recurrent, non healing ulcers) that should raise suspicion for ZES?

A

prominent gastric folds. This is caused by the trophic gastrin effect

53
Q

Hypersecretory causes of hypergastrinemia?

A
  • gastrinoma (ZES)
  • Gastric outlet obstruction
  • Retained gastric antrum
  • Antral hyperplasia
  • H pylori infection
  • Pheochromocytoma
  • Short gut syndrome
54
Q

Hyposecretory causes of hypergastrinemia?

A
  • pernicious anemia
  • atrophic gastritis
  • previous vagotomy
  • DM
  • renal failure
  • acid-reducing medications
55
Q

What test is used to differentiate between ZES and other causes of hypergastrinemia?

A

secretin secretion test. Dramatic increases in gastrin levels after administration of secretin, >110 pg/mL over baseline is considered a positive test and diagnostic of ZES

56
Q

Where do most gastrinomas occur?

A
  • 70% in the duodenum
  • 20% in the pancreas
  • 10% in adjacent lymph nodes
57
Q

What is the gastrinoma triangle?

A

where 80% of gastrinomas are located. This is the area between:

1) the confluence of the cystic and common bile duct
2) the junction 2nd the 3rd portion of the duodenum
3) the junction of the neck and the body of the pancreas

58
Q

What is the treatment for ZES?

A

control of the symptoms with acid blocking medications, typically high dose PPI followed by surgery in patients who are good surgical candidates. (The idea behind surgery is that a large number of these will be malignant)

59
Q

How does surgical management of ZES differ in cases of MEN1 compared to sporadic cases?

A

MEN1 ZES typically results in multiple tumors with a high recurrence rate; more than 95% have biochemical recurrence in 3-5 years. Current recommendations suggest surgery only for those with tumors >2-2.5 cm in size

60
Q

What percentage of patients with sporadic ZES are cured by surgery? MEN1 ZES?

A
  • 60%

- rarely

61
Q

T/F: the higher the gastrin level at diagnosis of ZES, the worse the 10 year prognosis.

A

True.

62
Q

What is Mallory-Weiss Syndrome?

A

linear mucosal lacerations of the gastroesophageal junction that leads to upper GI bleeding

63
Q

What is the classic presentation of Mallory-Weiss Syndrome?

A

retching and vomiting followed by hematemesis. Of note, majority of these tears are painless.

64
Q

What is the standard for evaluation of upper GI bleeding?

A

upper endoscopy

65
Q

Where is the most common location for Mallory-Weiss tears?

A

1) below the GE junction along the lesser curve of the stomach (50-80%)
2) below the GE junction along the greater curve of the stomach (10-20%)

66
Q

What is the initial management of Mallory-Weiss Syndrome?

A
  • placement of large bore IVs
  • Fluid resuscitation
  • type and cross blood products for potential use
  • correct any coagulation abnormalities
  • once the patient is stabilized upper endoscopy is the test of choice to evaluate upper GI bleeding
67
Q

What percentage of cases of Mallory-Weiss syndrome are self-limiting?

A

90% will heal without intervention in 48-72 hours

68
Q

What is the first line treatment modality for Mallory-Weiss syndrome?

A

upper endoscopy. This allows for diagnosis and treatment. Most cases require no treatment (90%). When active bleeding is present on upper endoscopy, endoscopy treatments are usually capable of stopping it. Surgery is only indicated in

69
Q

When is surgery indicated for Mallory-Weiss Syndrome? How would you surgically treat it?

A
  • when bleeding continues after endoscopic treatment has failed.
  • oversewing of the tears with absorbable suture
70
Q

What is a Sengstaken-Blakemore tube?

A

it is a NG or OG tube with a two balloons on the end, on of which sits in the stomach, the other is longer and sits along the GE junction. The lower balloon can be insufflated to place pressure on the lower esophagus/GE junction in the event of bleeding from varices or Mallory-Weiss tears

71
Q

What are the risk factors for gastric adenocarcinoma?

A
  • H pylori infection
  • diets high in smoked or salty foods
  • pernicious anemia
  • prior gastric surgery
  • chronic atrophic gastritis
  • intestinal metaplasia
72
Q

What genetic cancer syndromes are associated with an increased risk of gastric cancer?

A
  • Hereditary Nonpolyposis colon cancer (HNPCC)
  • Li-Fraumeni syndrome
  • Peutz-Jeghers syndrome
  • Hereditary Diffuse Gastric Cancer (HDGC syndrome)
73
Q

What is the common presentation for gastric adenocarcinoma?

A
  • weight loss
  • epigastric or abdominal pain
  • anorexia
74
Q

What is the work up of gastric adenocarcinoma?

A
  • Upper endoscopy with biopsy
  • EUS can give additional information about T stage (specifically better describe tumor depth)
  • CT abdomen/pelvis
  • PET can be useful if neoadjuvant treatment is given to evaluate response, but is not indicated if no neoadjuvant treatment is given
  • Diagnostic laparoscopy with peritoneal washings can be performed in patients with suspected carcinomatosis that is not overtly seen on CT
75
Q

What is the surgery for distal or middle stomach gastric adenocarcinoma?

A

distal or subtotal gastrectomy. (multiple studies have shown no difference in 5 year survival when comparing distal or subtotal gastrectomy to total gastrectomy for these tumors)

76
Q

What is the treatment for proximal gastric adenocarcinomas?

A

surgeons choice between proximal gastrectomy and total gastrectomy. However, some studies have shown higher complication rates with proximal gastrectomies, but no difference in survival has been shown between the 2.

77
Q

What is the preferred reconstruction technique after distal gastrectomy or subtotal gastrectomy for gastric adenocarcinoma?

A

surgeon preference between Billroth I, Billroth II, or Roux-en-Y

78
Q

What is the preferred reconstruction technique after total gastrectomy for gastric adenocarcinoma?

A

Roux-en-Y esophagojejunostomy with or without jejunal pouch (some studies have shown improved quality of life in patients with pouch)

79
Q

When should a D1 lymphadenectomy be performed in the setting of gastric adenocarcinoma? When should a D2 lymphadenectomy be performed?

A
  • D1 for all tumors
  • D2 for any tumors T2 or larger or with clinically positive nodes
    All according to the Japanese Gastric Cancer Association
80
Q

How many lymph nodes must be obtained for proper N staging of gastric cancer?

A

minimum of 16

81
Q

Which tumor markers are associated with gastric cancer?

A
  • CA19-9

- HER2/neu

82
Q

What is the most common sarcoma, especially of the GI tract?

A

Gastrointestinal Stromal Tumors (GIST)

83
Q

What is the cell is believed to be the cell of origin for GISTs?

A

Interstitial cells of Cajal

84
Q

What is the mutation that causes nearly all GISTs?

A

gain of function mutation in the c-KIT proto-oncogene which results in expression and activation of the transmembrane tyrosine kinase receptor KIT

85
Q

What is the estimated yearly incidence of GIST in the US?

A

5000-6000 cases per year

86
Q

Where do GISTs arise? What is the most common location?

A
  • Gastric = 50=70%
  • small intestine = 25=35%
  • colon and rectum = 5-10%
  • mesentery, omentum, and esophagus
87
Q

What is the most common presentation of a GIST?

A

GI bleeding. This is because they are highly vascular, soft, and friable

88
Q

Is a tissue diagnosis needed for a GIST?

A
  • No. EUS with FNA is not consistently diagnostic and upper endoscopy with biopsy may rupture a GIST causing dissemination.
  • A biopsy should only be performed if another diagnosis such as lymphoma is suspected or if there is metastatic disease
89
Q

What is the surgery of choice for GISTs?

A
  • wedge resection or segmental resection without wide margins necessary for adenocarcinoma
  • care must be taken to not rupture the tumor or violate it as these are associated with an increased risk of recurrance
  • lymphadenectomy is not required as GISTs rarely involve the lymph nodes
90
Q

What are the 2 medical treatment options for GISTs? How do they work?

A
  • Imatinib and Sunitinib

- Both work by inhibiting the tyrosine kinase receptors

91
Q

When should neoadjuvant therapy with imatinib or sunitinib be administered for GISTs?

A
  • to downstage tumors in order to perform a less extensive operation
92
Q

What is the current recommendation for adjuvant chemotherapy for GISTs?

A

36 months of imatinib or sunitinib for high risk lesions

93
Q

What are the indications for bariatric surgery?

A
  • BMI >/= 40 or BMI >/= 35 with a significant obesity-related comorbidity
  • Patients also must have documented, unsuccessful attempts at weight loss typically for a 6 month period
94
Q

How long should a biliopancreatic limb be in a Roux-en-Y?

A

at least 40 cm

95
Q

How long is a Roux limb in a typical Roux-en-Y?

A

approximately 100 cm

96
Q

Where is the typical origin of the left hepatic artery? Where is the origin of the replaced/accessory left hepatic artery?

A
  • Common hepatic artery which is a continuation of the proper hepatic artery from the celiac trunk
  • Left gastric artery
97
Q

Where is the typical origin of the right hepatic artery? Where is the origin of the replaced/accessory right hepatic artery?

A
  • Common hepatic artery which is a continuation the proper hepatic artery from the celiac trunk
  • SMA
98
Q

Where is the origin of the left gastric artery?

A
  • Celiac trunk or aorta
99
Q

Where is the origin of the right gastric artery?

A
  • Proper hepatic artery, but can also originate from the common hepatic artery or gastroduodenal artery
100
Q

Where is the origin of the right gastroepiploic artery?

A
  • GDA
101
Q

Where is the origin of the left gastroepiploic artery?

A
  • splenic artery
102
Q

How many short gastric arteries does a person typically have?

A
  • 5 to 7 (one more than you think)
103
Q

What is a Siewert type I tumor?

A

an adenocarcinoma with the center of the tumor located 1-5 cm above the GE junction

104
Q

What is a Siewert type II tumor?

A

a true adenocarcinoma of the cardia located within 1 cm above the GE junction to 2 cm below

105
Q

What is a Siewert type III tumor?

A

a subcardial adenocarcinoma with the tumor center located 2-5 cm below the GE junction which infiltrates the GE junction and esophagus from below

106
Q

In regards to Siewert tumors, which are treated as gastric cancers and which are treated as esophageal cancers?

A
  • Type III is treated as a gastric cancer

- Type I and II are treated as esophageal cancers

107
Q

When is laparoscopy with peritoneal washings indicated for gastric adenocarcinoma?

A
  • According to the NCCN, laparoscopy with peritoneal washing and cytology is indicated for any tumor clinically T1b or larger
  • The NCCN also recommends it in patients receiving pre-operative therapy
108
Q

What is the accepted margin for a gastric adenocarcinoma?

A

4 cm; whichever surgery achieves this is acceptable

109
Q

What determines low risk gastric GIST?

A
110
Q

What determines moderate risk gastric GIST?

A

2-5 cm and

111
Q

What determines high risk gastric GIST?

A

> 5 cm and > 5 mitoses/50 HPF

112
Q

What is the definition of gastroparesis?

A

delayed gastric emptying in the absence of mechanical obstruction

113
Q

Are males or females more commonly affected by gastroparesis?

A

females, some sources say as high as 7:1

114
Q

What surgical procedures are associated with gastroparesis?

A
  • fundoplication (most common)
  • Billroth II gastrectomy
  • botox injection for achalasia
  • vatical sclerotherapy
  • heart or lung transplant
115
Q

What test can be performed to help establish a vagal nerve injury in the setting of gastroparesis?

A
  • plasma pancreatic polypeptide level; this normally increases by 25 pg/mL in the first 20 minutes after a sham feeding. In vagal nerve injury this can be blunted or absent
116
Q

What medications are implicated in gastroparesis?

A
  • narcotics
  • clonidine (alpha agonists)
  • TCAs
  • calcium channel blockers
  • dopamine agonists
  • anticholingerics
  • octreotide
117
Q

What medical conditions are associated with gastroparesis?

A
  • connective tissue disorders (scleroderma)
  • infection (Norwalk virus, rotavirus)
  • amyloidosis
  • thyroid dysfunction
  • metabolic derangements
118
Q

What tests should be obtained if gastroparesis is suspected?

A
  • metabolic panel looking for derangements
  • upper endoscopy looking for mucosal disease or obstruction
  • upper GI series looking for obstruction
  • gastric emptying scintigraphy
119
Q

What is the gold standard for test for diagnosing gastroparesis?

A

gastric emptying scintigraphy; a technetium 99m labeled meal is consumed and scintigraphy is performed at 1, 2, and 4 hours.
If >10% is retained at 4 hours or >60% at 2 hours the test is positive and gastroparesis is diagnosed

120
Q

Why should you always wait the entire 4 hours when performing a gastric emptying scintigraphy study for gastroparesis?

A

because 20% of patients will have a normal 2 hour test but an abnormal 4 hour test

121
Q

What is first line therapy for gastroparesis?

A
  • tight glycemic control
  • low fat, low fiber diet (fat and fiber slow gastric transit)
  • frequent meals
122
Q

How does a gastric electric stimulator help gastroparesis?

A
  • improves symptoms specifically less vomiting (it does not cause contraction of the stomach and increased motility)
123
Q

What are the most common surgeries associated with the development of dumping syndrome?

A
  • gastrectomy
  • Roux-en-Y gastric bypass
  • gastroenterostomy
  • vagotomy
124
Q

What are the symptoms of early dumping syndrome?

A

nausea, abdominal pain, diaphoresis, and palpitations 15-30 minutes after eating followed by diarrhea 30-60 minutes later

125
Q

What are the symptoms of late dumping syndrome?

A

lightheadedness, palpitations, diaphoresis, and tremulousness 1-3 hours after eating due to release of GLP-1 which causes an exaggerated release of insulin leading to hypoglycemia

126
Q

How is dumping syndrome diagnosed?

A
  • patient is given a 50g oral glucose challenge and HCT, glucose and HR are measured every 30 minutes for 3 hours.
  • a positive test shows an increase in HCT of 3%, glucose level
127
Q

What is the first line management of dumping syndrome?

A

dietary modifications. Symptoms generally improve overtime with dietary modifications.

128
Q

What medications are available to treat dumping syndrome?

A
  • Acarbose (poorly tolerated due to gas and diarrhea side effects)
  • Octreotide
129
Q

When should patients with dumping syndrome be considered for surgical treatment? What are the options?

A
  • intractable disease which is not improved by dietary modifications or medical treatment
  • conversion to a Roux-en-Y gastrojejunostomy or jejunal interposition graft