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My own copies of absite stuff > stomach final absite > Flashcards

stomach final absite Flashcards

1
Q

Inferiorly, the stomach is attached to ___ via___

A

Transverse colon via gastrocolic omentum

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2
Q

The lesser curvature is thethered to the liver by

A

Hepatogastric ligament (lesser omentum)

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3
Q

What’s posterior to the stomach

A

Lesser omental bursa and pancreas

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4
Q

Right gastroepiploic artery rises from

A

Gastroduodenal artery (GDA) behind the first portion of the duodenum

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5
Q

Left gastroepiploic artery arises from

A

Splenic artery, meets the right one on the greater curvature

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6
Q

The right gastric artery arises from

A

The hepatic artery (proper hepatic) near the pylorus and hepatoduodenal ligament

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7
Q

The right and left gastric veins drain into

A

Portal vein

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8
Q

Right gastroepiploic vein drains into

A

SMV near the inferior border of pancreatic neck

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9
Q

Components of the celiac trunk

A

Left gastricCommon hepatic arterySplenic artery

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10
Q

Branches of the splenic artery that supply the stomach

A

Left gastroepiploic and short gastric

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11
Q

Blood supply to the greater curvature

A

Right and left gastroepiploics, short gastrics

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12
Q

What is the right gastroepiploic a branch of?

A

Gastroduodenal artery

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13
Q

Blood supply of lesser curvature

A

Right and left gastrics

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14
Q

What is the right gastric a branch off?

A

The common hepatic artery

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15
Q

Blood supply of the pylorus

A

Gastroduodenal artery

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16
Q

Left gastroepiploic vein drains into the

A

Splenic vein

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17
Q

What supplies the gastric remnant following a radical subtotal gastrectomy

A

Short gastric as long as spelling artery is ok

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18
Q

Common hepatic branches into

A

Proper hepatic and GDA

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19
Q

Type of cells making up the stomach

A

Simple columnar cells, and mucus secreting cells mostly in cardiac

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20
Q

Fundus and body cells and stimulation

A

Parietal cells (release acid and intrinsic factor), chief cells secrete pepsinogen (chief role so chief cells).

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21
Q

Stimulation of parietal cells

A

Stimulated by Vagus via Ach, gastrin from g cell, and histamine

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22
Q

Stomach antrum secretes

A

G cells and D cells (somatostatin)

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23
Q

Produces pepsinogen (1st enzyme in proteolysis)

A

Chief cells

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24
Q

Release hydrogen and intrinsic factor

A

Parietal cells

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25
Q

If retained antrum syndrome, basal stomach acid, gastrin level in response to secretin

A

Basal high bc still masking gastrin, gastrin high, gastric acid secretion in response to secretion stimulations test would drop in comparison to gastronoma.
Secretin normally would decrease gastric acid, high in gastronoma.
Antrum syndrome, hyperstimualtion of gastrin from lack of acid hitting g cells and downregulating them 


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26
Q

Role of somatostatin

A

Inhibits secretin of gastric acid, pepsinogen , pancreatic secretions, decreased GB contraction, decreased insulin and glucagon release

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27
Q

organioaxial vulvus - stomach

A

Triggered by reduceding volvues, need Nissan. GE junction to pylorus.

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28
Q

Forceful vomiting and hematemesis following

A

Mallory weiss tear, mucosal tear, EGD and clip along lesser curve MC

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29
Q

Truncal vagotomy

A

Go 5 cm up one esphagus and get left and right, trying to get criminal nerve of grassi, increase emptying of liquid. Lose innervation fo pylorus so solids also affected. Unless you perform a pyloroplasty. Decrease gastric acid production by 90%, increase gastrin overall from gastrin cell hyperplasia, decrease exocrine pancreatic function, decrease bile flow, increase GB volume, decreased in vagaly mediated hormones

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30
Q

Selected vagotomy

A

Trying to Maintain vagus innervation below the liver, so below hepatic branches to get stomach fibers. Normal solid emptying

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31
Q

Hepatic branches

A

LARP- left become anterior continues over to the liver, posterior becomes the celiac

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32
Q

Emptying of stomach following vagotomy

A

Increased because lose the receptor reflex, increased emptying liquid of stomach.

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33
Q

What are patients complain off after a vagotomy, treatment?

A

Diarrhea, give cholestyramine for treatment

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34
Q

What causes bile secretion?

A

Cholinergic stimulationcausescontraction of the gallbladder and relaxation of the sphincter of Oddi, which means thatbileissecretedinto the intestine.

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35
Q

Upper GI bleed?

A

Above ligament of treitz

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36
Q

Upper GI bleed first line?

A

ABC, 2 large bores, resuscitation, early endoscopy

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37
Q

Bleeding ulcers, types?

A

Active bleeding - 60% of re-bleed
Base of ulcer - 40%
Diffuse oozing - 30%

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38
Q

Upper endoscopy and can’t control bleeding?

A

OR, empiric treatment for h pylori

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39
Q

Already on h pylori tx, but are going to OR for uncontrolled bleeding?

A

Think about vagotomy

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40
Q

Duodenal ulcers location

A

Duodenal bulb, first portion

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41
Q

Anterior ulceration of duodenum, presentation?

A

Free perf in peritoneum, pneumoperitoneum

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42
Q

Posterior ulceration of duodenum, presentation?

A

Into GDA (bleed), more common.

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43
Q

Posterior ulceration of duodenum with significant bleed that can’t be controlled by endoscopy. Needle and suture? Careful with what

A

Duodenotomy, GDA ligation, 3 suture ligation. Proximal , distal and transverse pancreatic branch . Use O vycryl suture, UR6 needle. Careful with CBD.

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44
Q

Anterior perforation tx?

A

Graham patch using omentum

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45
Q

Graham patch?

A

2 suture into anterior portion of duodenum and bring omentum , if on PPI and + h.pylori treatment = vagal

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46
Q

Quadruple therapy?

A

Amox, clarithromycin, PPI +bismuth

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47
Q

Best test for h pylori?

A

EGD with biopsy and histology

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48
Q

Most sensitive test for h pylori?

A

Antibody test

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49
Q

Best test for documenting resolution?

A

Breath test - urease

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50
Q

Young patient, multiple ulcers, some in distal portions?

A

Zollinger

Gastronome - secretin test if not super diagnostic, gastrin level (>200, def > 1000),

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51
Q

Gastric ulcers - type I?

A

Low along body lesser curve, 50-60%

Poor mucosa protection

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52
Q

Gastric ulcers - type IV?

A

high lesser curve < 10%, poor mucosa protection

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53
Q

Type 2 gastric ulcer

A

2 ulcers (lesser curve and duodenal); similar to duodenal ulcer with high acid secretion

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54
Q

Type 3 gastric ulcer

A

pre-pyloric ulcer; similar to duodenal ulcer with high acid secretion

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55
Q

Types related to high acid secretion?

A

Type II, lesser curve and duodenum from high acid

Type III, prepylorus also high acid

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56
Q

Which gastric ulcer is secondary to meds?

A

Type 5, 5% NSAID use

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57
Q

Main-stem treatment?

A

Trugnal vagotomy, antrectomy, consider separate ulcer excision and exclude cancer

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58
Q

Antrectomy, reconstructions

A

Vagotomy first

  • Bilroth I - hooking stomach directly to duodenum, complications
  • Bilroth II - hooking stomach into jejunum, symptoms of dumping and alkaline, common complications: afferent loop obstruction
  • RNY - preferred in younger patients.

Anatomy of modern Roux-en-Y gastric bypass. Modern gastric bypass consists of a divided pouch gastroplasty with Rouxen-Y jejunojejunal reconstruction. The Roux limb is most commonly placed in the antecolic position. Intestinal limbs are termed with either standard Roux (Roux, afferent, efferent) or bariatric (alimentary, biliopancreatic, common channel) nomenclature as shown.

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59
Q

Afferent loop syndrome, tx?

A

Overgrowth of bacteria can present with megaloblastic anemia, b12 deficiency, bile reflux gastritis (tx to convert to RNY, need at least 6 cm from pancreatic/biliary limb to avoid this)

Conversion of Billroth II gastrojejunostomy to Roux-en-Y gastrojejunostomy. The afferent limb is divided (A) and intestinal continuity is reestablished by anastomosis 50 to 60 cm downstream from the original gastrojejunostomy (B).

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60
Q

Most common benign gastric neoplasm, although can be malignant
Symptoms: usually asymptomatic, but obstruction and bleeding can occur

A

GIST

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61
Q

What will be positive in biopsy of GIST?

A

C-KIT

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62
Q

GIST receptor

A

Receptor CK

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63
Q

What are poor options for surgical repair of gastric ulcers?

A

Omental patch and ligation of bleeding vessels are poor options for gastric ulcers due to high recurrence of symptoms and risk of gastric CA in the ulcer.

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64
Q

What’s CK

A

Tyrosine kinase receptor

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65
Q

Dx and tx of GIST

A

Dx: biopsy - are C-KIT positiveTx: resection with 1 cm margins; Chemotherapy with imatinib (Gleevac, tyrosine kinase inhibitor) if malignant

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66
Q

When are GIST considered malignant?

A

> 5 cm or > 5 mitoses / 50 HPF (high-powered field)

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67
Q

TK inhibitor that can be treatment for malignant GIST?

A

Imatinib (Gleevax; tyrosine kinase inhibitor)look at pathology report and seize, if > 5 cm: tx with adjuvantGleevax, look at mitosis per hpf, If >5, use this.

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68
Q

Resection margins for GIST

A

1 cm margins

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69
Q

How do GISTs look on ultrasound?

A

Hypoechoic on ultrasound; smooth edges

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70
Q

Macroscopic margins

A

Don’t need macroscopic margins

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71
Q

Lymphomas - maltoma tx

A

Triple therapy ABX given relationship with h pylori or radiation if non-responsive

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72
Q

Extraenodal lymphoma, MC site

A

stomach, non-hodgkin B cell type, tx with chemo and radiation, expect if stage 1 and confined to

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73
Q

cushings ulcer

A

Head injury patient

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74
Q

Curlings culer

A

Burn patient

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75
Q

Camerons ulcer

A

Pressure point next to hiatal hernia

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76
Q

Gastric cancer with mets to ovaries

A

Kruckenberg tumor

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77
Q

Enlarged supraclavicular node associated with metastatic gastric cancer

A

Virchows node

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78
Q

Supra umbilical

A

Sister Mary Joseph node

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79
Q

Hiatal hernia - type 1

A

Sliding

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80
Q

Hiatal hernia - type 2

A

Para-esophageal hernia

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81
Q

Hiatal hernia - type 3

A

Combining sliding and paraesophageal

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82
Q

Hiatal hernia - type 4

A

Entire stomach into chest + another organ***

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83
Q

Hiatal hernia treatments

A

2,3,4 all need surgical intervention - 2,3 risk stratified if too frail may need to avoid surgery
Ultimately: nissen fundoplication 


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84
Q

Bouchards triad

A

Chest pain retching without vomiting and inability to pass NGT

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85
Q

Tenets to nissen

A

Reduce hernia and sac, excise sac out of chest, mediastinal mobilization of esophagus (2-3 cm intraadbominally) reaproxiamte crura, perform wrap over a large 50-54 French bougie to recreate natural valve to prevent reflux

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86
Q

Complication after Nissen

A

MC: dysphagia, some is expected so put them on CLD, if worried barium swallow. Ar they tolerating their own secretions? If not, then OR too tight wrap and swelling.

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87
Q

What if you cant get esophagus down the stomach?

A

Coulis gastroplasty - elongate esophagus by coming down to tubliainzg stomach in greater curve

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88
Q

What stimulates parietal cells?

A

Acetylcholine (vagus nerve), gastrin (from G cells in antrum), and histamine (from mast cells) cause H+ release

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89
Q

What is the pathway of acetylcholine (vagus nerve) and gastrin?

A

Activates phospholipase (PIP -> DAG + IP3 + Increase Ca); Ca-calmodulin activates phosphorylase kinase -> H+ release

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90
Q

What is the pathway of histamine?

A

Activates adenylate cyclase -> cAMP -> activates protein kinase A -> increased H+ release

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91
Q

How do phosphorylase and protein kinase A work?

A

Phosphorylate H+/K+ ATPase to increase H+ secretion and K+ absorption

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92
Q

Blocks H+/K+ ATPase in parietal cell membrane (final pathway for H+ release)

A

Omeprazole

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93
Q

Inhibitors of parietal cells

A

Somatostatin, prostaglandins (PGE1), secretin, CCK

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94
Q

Binds B12 and the complex is reabsorbed in the terminal ileum

A

Intrinsic factor

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95
Q

Antrum and pylorus glands

A

Mucus and HCO3- secreting glands.G cells (gastrin).D cells (somatostatin)

96
Q

Secreting glands - protect stomach

A

Mucus and HCO3- (Antrum and pylorus glands)

97
Q

Release gastrin - reason why antrectomy is helpful for ulcer disease

A

G cells

98
Q

What inhibits G cells?

A

H+ in duodenum

99
Q

What stimulates G cells?

A

Amino acids, acetylcholine

100
Q

Secrete somatostatin, inhibit gastrin and acid release

A

D cells

101
Q

In duodenum; secrete alkaline mucus

A

Brunner’s glands

102
Q

Released with antral and duodenal acidification

A

Somatostain, CCK, and secretin

103
Q

Stomach transit time

A

3-4 hours

104
Q

Where does stomach peristalsis occur?

A

Distal stomach (antrum)

105
Q

How is gastroduodenal pain sensed

A

Through afferent sympathetic fibers T5-T10

106
Q

What do cardia glands secrete?

A

Mucus

107
Q

What are the causes of rapid gastric emptying?

A

Previous surgery (#1), ulcers

108
Q

What are the causes of delayed gastric emptying?

A

Diabetes, opiates, anticholingerics, hypothyroidism

109
Q

(Hair) - hard to pull outTx?

A

Trichobezoars- Tx: EGD generally inadequate; likely need gastrostomy and removal

110
Q

(fiber) - often in diabetics with poor gastric emptyingTx?

A

Phytobezoars (fiber)Tx: enzymes, EGD, diet changes

111
Q

Vascular malformation; can bleed

A

Dieulafoy’s ulcer

112
Q

Mucous cell hyperplasia, increased rugal folds

A

Menetrier’s disease

113
Q
  • Associated with type II (paraesophageal) hernia- Nausea without vomiting; severe pain; usually organoaxial volvulusTreatment?
A

Gastric volvulusTx: reduction and Nissen

114
Q
  • Secondary to forceful vomiting- Presents as hematemesis following severe retching- Bleeding often stops spontaneously
A

Mallory-Weiss tear

115
Q

What type of volvulus is a gastric volvulus?

A

Organoaxial volvulus

116
Q

Dx/Tx: Mallory Weiss Tear

A

EGD with hemo-clips; tear is usually on the lesser curvature (near GE junction)

117
Q

Where is the Mallory Weiss Tear located?

A

Usually on the lesser curvature (near GE junction)

118
Q

What if you have continued bleeding after EGD with hemo-clips for Mallory Weiss tear?

A

If continued bleeding, may need gastrostomy and oversewing of the vessel.

119
Q

What is the physiologic effect of vagotomy?

A

Both truncal and proximal forms increase liquid emptying -> vaguely mediated receptive relaxation if removed (results in increased gastric pressure that accelerates liquid emptying)

120
Q

Vagotomy:Divides vagal trunks at the level of the esophagus; decreases emptying of solids

A

Truncal vagotomy

121
Q

Vagotomy:- highly selective- divides individual fibers, preserves “crow’s foot”, normal emptying of solids

A

Proximal vagotomy

122
Q

Emptying of solids: truncal vs proximal vagotomy

A

Truncal: decreased emptying of solidsProximal: normal emptying of solids

123
Q

How can you increase solid emptying with truncal vagotomy?

A

Addition of pyloroplasty to truncal vagotomy results in increased solid emptying.

124
Q

Physiologic effects of truncal vagotomy- Gastric effects- Nongastric effects- Diarrhea

A
  • Gastric: decreased acid output by 90%, increased gastrin cell hyperplasia- Nongastric: decreased exocrine pancreas function, decreased postprandial bile flow, increased gallbladder volumes, decreased release of vaguely mediated hormones - Diarrhea: MC problem following vagotomy
125
Q

MC common problem following vagotomy

A

Diarrhea (40%)

126
Q

What causes diarrhea following vagotomy?

A

Caused by sustained MMCs (migrating motor complex) forcing bile acids into the colon

127
Q

Name that vagotomy: both nerve trunks are divided at the level of the diaphragmatic hiatus

A

Truncal vagotomy

128
Q

Name that vagotomy: division of the vagal fibers that supply the gastric funds. Branches to the antropyloric region of the stomach are not transected, and the hepatic and celiac divisions of the vagus nerves remain intact.

A

Proximal gastric vagotomy

129
Q

Risk factors: upper gastroinestinal bleeding

A

Previous UGIB, PUD, NSAIDs, smoking, liver disease, esophageal varices, splenic vein thrombosis, sepsis, burn injuries, trauma, severe vomiting.

130
Q

Dx/Tx: UGIB

A

EGD (confirm bleeding is from ulcer); can potentially treat with hemo-clips, Epi injection, cautery

131
Q

Mgmt: UGIB with slow bleeding and having trouble localizing source

A

Tagged RBC scan

132
Q

UGIB: biggest risk factor for rebleeding at the time of EGD

A

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

133
Q

Highest risk factor for mortality with non-variceal UGIB

A

Continued or re-bleeding

134
Q

Treatment: patient with liver failure is likely bleeding from esophageal varices, not an ulcer

A

EGD with variceal bands or sclerotherapy; TIPS if that fails

135
Q
  • From increased acid production and decreased defense- Most common peptic ulcer; more common in men
A

Duodenal ulcers

136
Q

Location of duodenal ulcers

A

Usually in 1st part of the duodenum; usually anterior.

137
Q

Complications of duodenal ulcers:- Anterior- Posterior

A
  • Anterior ulcers perforate- Posterior ulcers bleed from gastroduodenal artery
138
Q

Symptoms: epigastric pain radiating to the back; abates with eating but recurs 30 minutes after- Dx/Tx?

A

Duodenal ulcer- Dx: endoscopy- Tx: PPI, triple therapy for H. pylori -> bismuth salts, amoxicillin, and metronidazole/tetracycline (BAM or BAT)

139
Q

What has decreased incidence of surgery for ulcer?

A

Surgery for ulcer rarely indicated since PPIs

140
Q

What do you need to rule out in patients with complicated ulcer disease?

A

Need to rule out gastrinoma

141
Q

Gastric acid hyper secretion.Peptic ulcers.Gastrinoma.

A

Zollinger-Ellison Syndrome

142
Q

Surgical indications for duodenal ulcer

A

Perforation. Protracted bleeding despite EGD therapy. Obstruction. Intractability despite medical therapy. Inability to rule out cancer. PPI with duodenal ulcer complication.

143
Q

Duodenal ulcer: if patient has been on a PPI and has complications

A

If a patient has been on a PPI, an acid-reducing surgical procedure is required in addition to surgery for any complications

144
Q

Surgical options (acid-reducing surgery) for duodenal ulcers

A
  • Proximal vagotomy- Truncal vagotomy and pyloroplasty- Truncal vagotomy and antrectomy- Reconstruction after antrectomy - Roux-en-Y gastro-jejunostomy (best)
145
Q

Surgery duodenal ulcer: lowest rate of complications, no need for astral or pylorus procedure; 10-15% ulcer recurrence, 0.1% mortality

A

Proximal vagotomy

146
Q

Ulcer recurrence / mortality after proximal vagotomy

A
  • 10-15% ulcer recurrence- 0.1% mortality
147
Q

Ulcer recurrence / mortality after truncal vagotomy and pyloroplasty

A
  • 5-10% ulcer recurrence- 1% mortality
148
Q

Ulcer recurrence / mortality after truncal vagotomy and antrectomy

A
  • 1-2% ulcer recurrence (lowest rate of recurrence)- 2% mortality
149
Q

Why is roux-en-y gastro-jejunostomy the best procedure for reconstruction after antrectomy?

A

Less dumping syndrome and reflux gastritis compared to Bilroth I (gastro-duodenal anastomosis) and Billroth II (gastro-jejunal anastomosis)

150
Q

Most frequent complication of duodenal ulcers

A

Bleeding (usually minor but can be life threatening)

151
Q

Definition of major bleeding in duodenal ulcer

A

> 6 units of blood in 24 hours or patient remains hypotensive despite transfusion

152
Q

Tx: bleeding from duodenal ulcer

A

EGD 1st - hemoclips , cauterize, Epi injection

153
Q

Surgery: bleeding duodenal ulcers

A

Duodenotomy and gastroduodenal artery (GDA) ligation.- Avoid hitting common bile duct (posterior) with GDA ligation- If patient has been on a PPI, need acid-reducing surgery as well

154
Q

Initial treatment of choice for obstruction from duodenal ulcer

A

PPI and serial dilation

155
Q

Surgical options: duodenal ulcer obstruction

A

Antrectomy and truncal vagotomy (best); include ulcer in resection if it’s located proximal to ampulla of Vater

156
Q

What do you need to rule out in duodenal ulcer obstruction?

A

Need to biopsy area of resection to rule out CA

157
Q

Duodenal ulcer perforation: % will have free air

A

80% will have free air

158
Q
  • patient usually have sudden epigastric pain; can have generalized peritonitis- pain can radiate to the prevocalic gutters with dependent drainage of gastric content
A

Duodenal ulcer perforation

159
Q

Tx: duodenal ulcer perforation

A

Graham patch (place momentum over the perforation)- Also need acid-reducing surgery if the patient has been on a PPI

160
Q

Definition of intractable duodenal ulcers

A

> 3 months without relief while on escalating doses of PPI

161
Q

What is diagnosis of intractable duodenal ulcers based on?

A

Based in EGD mucosal findings, not symptoms

162
Q

Tx: intractability of duodenal ulcers

A

Acid-reducing surgery

163
Q
  • Older men, slow healing- 80% on lesser curvature of the stomach- Symptoms: epigastric pain radiating to the back; relieved with eating but recurs 30 minutes later; melena or guaiac-positive stools
A

Gastric ulcers

164
Q

Risk factors for gastric ulcer

A

Male, tobacco, ETOH, NSAIDs, H. pylori, uremia, stress (burns, sepsis, and trauma), steroids, chemotherapy

165
Q

Where are most gastric ulcers located?

A

80% on lesser curvature of the stomach

166
Q

What is difference in mortality between gastric and duodenal ulcer hemorrhage?

A

Hemorrhage is associated with higher mortality than duodenal ulcers.

167
Q

Gastric ulcers: best test for H. pylori

A

Histiologic examination of biopsies from antrum

168
Q

Test for H.pylori, detects urease released from H. pylori

A

CLO test (rapid urease test)

169
Q

Surgical indications for gastric ulcers

A

Perforation, bleeding not controlled with EGD, obstruction, cannot exclude malignancy, intractability (> 3 months without relief - based on mucosal findings)

170
Q

Tx: gastric ulcer

A

Truncal vagotomy and antrectomy best for complications; try to include the ulcer with resection (extended antrectomy) - need separate ulcer excision if that is not possible (gastric ulcers are resected at time of surgery due to high risk of gastric CA)

171
Q
  • Occurs 3-10 days after event; lesions appear in fundus first- Tx: PPI- EGD with cautery of specific bleeding point may be effective
A

Stress gastritis

172
Q

Where do lesions in stress gastritis appear?

A

Lesions appear in fundus first

173
Q

Chronic gastritis type: associated with pernicious anemia, autoimmune disease

A

Type A (fundus)

174
Q

Chronic gastritis type: associated with H. pylori

A

Type B (antral)

175
Q

Treatment Chronic Gastritis

A

PPI

176
Q

Pain unrelieved by eating, weight loss

A

Gastric cancer

177
Q

Where are 40% of gastric cancers located?

A

Antrum

178
Q

Gastric cancer-related deaths in Japan

A

Accounts for 50% of cancer-related deaths in Japan

179
Q

Dx: gastric cancer

A

EGD

180
Q

Risk factors: gastric cancer

A

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

181
Q

15% risk of gastric cancer.- Tx: endoscopic resection

A

Adenomatous polpys

182
Q

Gastric metastasis to supraclavicular node

A

Virchow’s node

183
Q

Increased in high-risk populations. Older men. Japan. Rare in United StatesSurgical treatment: try to perform subtotal gastrectomy (need 10-cm margins)

A

Intestinal-type gastric CA

184
Q

Low risk populations. Women. Most common type in the United States.Diffuse lymphatic invasion, no glands.Surgery: total gastrectomy bc of diffuse nature of linitis plastica

A

Diffuse gastric cancer

185
Q

Prognosis: intestinal-type gastric CA vs diffuse gastric cancer

A

Less favorable prognosis than intestinal-type gastric CA (overall 5-YS - 25%)

186
Q

Margins for intestinal-type gastric CA

A

need 10 cm margins

187
Q

Chemotherapy for gastric cancer

A

Poor prognosis:- 5 FU, doxorubicin, mitomycin C

188
Q

Gastric cancer: management of metastatic disease outside area of resection

A

Contraindication to resection unless performing surgery for palliation.

189
Q

When to consider palliation of gastric cancer?

A
  • Obstruction - proximal lesions can be scented; distal lesions can be bypassed with gastrojejunostomy- Low to moderate bleeding or pain - Tx: XRT
190
Q

What if surgical management fails for palliation of gastric cancer (stents, gastrojejunostomy, XRT)?

A

If these fail, consider palliative gastrectomy for obstruction or bleeding.

191
Q
  • Related to H. pylori infection- Usually regresses after treatment for H. pylori
A

Mucosa-associated lymphoid tissue lymphoma (MALT lymphoma)

192
Q

MC location of MALT lymphoma

A

Stomach

193
Q

Treatment: MALT lymphoma

A

Triple-therapy antibiotics for H. pylori and surveillance.If MALT does not regress, need XRT.

194
Q

What if MALT lymphoma does not resolve with triple therapy antibiotics for H.pylori?

A

If MALT does not regress, need XRT

195
Q
  • Have ulcer symptoms- Usually non-Hodgkin’s lymphoma (B cell)- Overall 5-year survival rate > 50%
A

Gastric lymphomas

196
Q

MC location for extra-nodal gastric lympoma

A

Stomach

197
Q

Dx: Gastric lymphoma

A

EGD with biopsy

198
Q

Primary treatment modalities of gastric lymphoma

A

Chemotherapy and XRT are primary treatment modalities; surgery for complications

199
Q

When is surgery indicated for gastric lymphoma?

A

Surgery possibly indicated only for stage 1 disease (tumor confined to stomach mucosa) and then only partial resection is indicated

200
Q

Overall 5-year survival rate for gastric lymphoma

A

> 50%

201
Q

Criteria for patient selection for bariatric surgery (need all 4)

A
  • BMI > 40 kg/m^2 or BMI > 35 kg/m^2 with coexisting comorbidities- Failure of nonsurgical methods of weight reduction- Psychological stability- Absence of drug or alcohol abuse
202
Q

What type of obesity is worse prognosis in general population?

A

Central obesity

203
Q

What gets better are surgery for morbid obesity?

A

DM, cholesterol, sleep apnea, HTN, urinary incontinence, GERD, venous stasis ulcers, pseudotumor cerebri, joint pain, migraines, depressions, PCOS, NASH

204
Q
  • Better weight loss than just banding.- Risk of marginal ulcers, leak, necrosis, B12 deficiency, IDA, gallstones- Perform cholecystectomy during operation if stones present- UGI on POD 2
A

Roux-en-Y gastric bypass

205
Q

Failure rate of roux-en-y gastric bypass

A

10% failure rate due to high-carbohydrate snacking

206
Q

What are the signs of a leak after roux-en-y gastric bypass?

A
  • Ischemia: MCC leak- Signs of leak: increased RR, increased HR, abdominal pain, fever, elevated WBCs
207
Q

Dx / Tx: leak after roux-en-y gastric bypass

A

Dx: UGITx: early leak (not contained) -> re-op; late leak (Weeks out from surgery, likely contained) -> percutaneous drain, antibiotics

208
Q

Incidence of marginal ulcers after roux-en-y gastric bypass

A

Develop in 10%Tx: PPI

209
Q

Management of stenosis after roux-en-y gastric bypass

A

Usually responds to serial dilation

210
Q

Complications of roux-en-y gastric bypass

A
  • Leak- Marginal ulcers- Stenosis
211
Q

MCC leak after roux-en-y gastric bypass

A

Ischemia

212
Q

After roux-en-y gastric bypass:- Hiccoughs, large stomach bubble- Dx: AXR- Tx: G-tube (gastrostomy tube)

A

Dilation of excluded stomach postop

213
Q

s/p roux-en-y gastric bypass:- nausea and vomiting, intermittent abodminal pain- AXR shows dilated SB

A

Small bowel obstruction- Surgical emergency

214
Q

Why is SBO s/p roux-en-y gastric bypass a surgical emergency?

A

Due to the high risk of small bowel herniation, strangulation, infarction and subsequent necrosis.- Tx: surgical exploration

215
Q
  • these operations are no longer done- a/w liver cirrhosis, kidney stones, and osteoporosis (decreased calcium)- need to correct these patients and perform roux-en-y gastric bypass if encountered
A

jejunoileal bypass

216
Q
  • can occur after gastrectomy or after vagotomy and pyloroplasty- occurs form rapid entering of carbohydrates into the small bowel.- can almost always be treated medically (and dietary changes)
A

Dumping syndrome

217
Q

2 phases of dumping syndrome

A
  • Hyperosmotic load causes fluid shift into bowel (hypotension, diarrhea, dizziness)- hypoglycemia from reactive increase in insulin and decrease in glucose (2nd phase rarely occurs)
218
Q

Tx: dumping syndrome

A

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

219
Q

Surgical options for dumping syndrome (Rarely needed)

A
  • Conversion of Billroth 1 or Billroth 2 to Roux-en-y gastrojejunostomy- Operations to increase gastric reservoir (jejunal pouch) or increased emptying time (Reversed jejunal loop)
220
Q

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

A

Alkaline reflux gastritis

221
Q

Dx / Tx: alkaline reflux gastritis

A

Dx: evidence of bile reflux into the stomach; histologic evidence of gastritisTx: PPI, cholestyramine, metoclopramide

222
Q

Surgical options for alkaline reflux gastritis

A

Conversion of Billroth 1 or Billroth 2 to Roux-en-Y gastrojejunostomy with afferent limb 60 cm distal to gastro jejunostomy

223
Q
  • Delayed gastric emptying- Symptoms: n/v, pain, early satiety
A

Chronic gastric atony

224
Q

Chronic gastric atony:Dx / Tx / Surgical options

A

Dx: gastric emptying studyTx: metoclopramide, prokineticsSurgical option: near total gastrectomy with roux-en y

225
Q
  • Early satiety- Actually want this for gastric bypass patients
A

Small gastric remnant

226
Q

Small gastric remnant:Dx / Tx / Surgical option

A
  • Dx: EGD- Tx: small meals- Surgical option: jejunal pouch reconstruction
227
Q
  • With billroth 2 or roux-en-y; caused by poor motility- Symptoms: pain, steatorrhea (bacterial beconjugation of bile), B12 deficiency (bacteria use it up), malabsorption
A

Blind-loop syndrome

228
Q

What causes blind-loop syndrome with billroth 2 or roux-en-y?

A

Caused by bacterial overgrowth (E coli, GNRs) from stasis in afferent limb

229
Q

Dx: blind-loop syndrome

A

EGD of afferent limb with aspirate and culture for organisms

230
Q

Tx: blind loop syndrome

A

Tetracycline and flagyl, metoclopramide to improve motility

231
Q

Surgical option: blind-loop syndrome

A

Re-anastomosis with shorter (40-cm) afferent limb to relieve obstruction

232
Q
  • Symptoms of obstruction - n/v, abdominal pain- Dx: UGI, EGD- Tx: balloon dilation- Surgical option: find site of obstruction and relieve it
A

Efferent-loop obstruction

233
Q
  • Secondary to non-conjugated bile salts in the colon (osmotic diarrhea)- Causes by sustained postprandial organized MMCs
A

Post-vagotomy diarrhea

234
Q

Tx / Surgical option: post-vagotomy diarrhea

A

Tx: cholestyramine, octreotideSurgical option: reversed interposition jejunal graft

235
Q

What causes post-vagotomy diarrhea?

A

Reversed interposition jejunal graft

236
Q

Management: duodenal stump blow-out

A

Place lateral duodenostomy tube and drains

237
Q

Potential PEG complications

A

Insertion into the liver or colon

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