Fiser Chapter 30. STOMACH Flashcards

1
Q

Stomach transit time

A

3-4 hours

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2
Q

Where in stomach does peristalsis occur?

A

Just antrum (distal stomach)

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3
Q

What sympathetic fibers does gastroduodenal pain get sensed?

A

T5-10

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4
Q

Blood supply of stomach

A

Celiac: left gastric, CHA, splenic (L gastroepiploic and short gastrics are branches of splenic)

Greater curvature: R and L gastroepiploics, short gastrics. (R gastroepiploic is a branch of GDA)

Lesser curvature: R and L gastrics, R is branch off CHA

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5
Q

Stomach mucosa hitso

A

Simple columnar epithelium

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6
Q

Cardia glands versus fundus and body glands

A

Cardia: mucus secreting

Fundus and body glands:
Chief cells pepsinogen
Parietal cells H+ and IF

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7
Q

Chief cells

A

Pepsinogen (1st enzyme in proteolysis)

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8
Q

Parietal cells

A

H+ and IF

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9
Q

What causes H+ release from parietal cells?

A

Ach (vagus)

Gastrin (G cells in antrum)

Histamine (from mast cells)

Phosphorylase kinase and protein kinase A

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10
Q

Achetylcholine and gastrin MoA to increase H+ release

A

Activates phospholipase (PIP) –> DAG + IP3 to increase calcium -> calcium-calmodulin activated phosphorylase kinase -> increased H+ relaease

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11
Q

Histamine MoA to increase H+ release

A

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

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12
Q

Phosphorylase kinase and proteine kinase A MoA to increase H+ release

A

They phosphorylate H+/K+ ATPase to increase H+ secretion and K+ absorption

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13
Q

How does omeprazole work?

A

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

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14
Q

What are inhibitors of parietal cells (which release H+)?

A

Somatotatin

Prostaglandins (PGE1)

Secretin

CCK

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15
Q

What does intrinsic factor do?

A

Binds B12, and then the complex is reabsorbed in the TI

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16
Q

Fundus and body glands versus antrum and pylorus glands

A

Fundus and body: chief cells and parietal cells with pepsinogen and H+ and IF release

Antrum and pylorus: G cells (release gastrin in antrum) and mucus and HCO3- secreting glands; and D cells (secrete somatostatin)

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17
Q

Why is an antrectomy helpful for ulcer disease?

A

G cells release gastrin (taken out)

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18
Q

What inhibits and stimulates G cells

A

G cells release gastrin

Inhibited by H+ in duodenum

Stimulated by amino acids and acetylcholine

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19
Q

What do D cells do?

A

Secrete somatostatin, which inhibits gastrin and H+ release

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20
Q

What do Brunner’s glands do?

A

Secrete alkaline mucus

in duodenum

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21
Q

Antral and duodenal acidification causes what?

A

Somatostatin, CCK, and secretin release

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22
Q

MCC rapid and delayed gastric emptying

A

Rapid: previous surgery, ulcers

Delayed: DM, opiates, anticholinergics, hypothyroid

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23
Q

Trichobezoars and phytobezoars

A

Trychobezoars: Hair, hard to pull out, EGD generally inadequate and likely need gastrostomy and removal

Phytobezoars: Fiber, often in diabetics with poor gastric emptying, tx with enzymes, EGD and diet changes

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24
Q

Dieulafoy’s ulcer

A

vascular malformation that can bleed

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25
Q

Menetrier’s disease

A

Mucous cell hyperplasia, increased rugal folds

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26
Q

Nausea without vomiting, severe pains

A

Gastric volvulus, usually organoaxial

Associated with type 2 (paraesophageal) hernia

Tx: Reduction and Nissen

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27
Q

Hematemesis following severe retching

A

Mallory-Weiss tear

EGD with hemo-clips; Tear is usually on lesser curvature near GEJ

Bleeding often stops spontaneously, if continued bleeding may need gastrostomy and vessel oversewing

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28
Q

Truncal and proximal vagotomies

A

Both increase liquid emptying by removing vagally mediated receptive relaxation, causing increased gastric pressure that accelerates fluid emptying

Truncal (at level of esophagus): decreases solid emptying; add pyloroplasty to increase solid emptying

Proximal (high selective, divides individual fibers, preserves “crow’s foot”): Normal emptying of solids

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29
Q

Truncal vagotomy effects

A

decreased solid emptying (and increased liquid emptying like all vagotomies); decreases acid output by 90%, increases gastrin and gastrin cell hyperplasia; decreases exocrine pancreas function and postprandial bile flow; increases gallbladder volumes, and decreases release of vagally mediated hormons; diarrhea in 40% (most common problem after vagotomy) due to sustained MMCs forcing bile acids into colon

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30
Q

MCC problem after vagotomy

A

Diarrhea

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31
Q

Risk factors for UGIB

A

Prior UGIB, PUD, NSAIDs, smoking, liver dz, esophageal varices, splenic vein thrombosis, sepsis, burns, trauma, severe vomiting

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32
Q

Dx/Tx of UGIB

A

EGD, can potentially treat with hemo-clips, epi injection, cautery

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33
Q

Slow bleeding and having trouble localizing source?

A

Tagged RBCscan

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34
Q

Biggest risk factor for rebleeding at time of EGD

A
  1. Spurting blood vessel (60% chance)
  2. Visible vessel (40%)
  3. Diffuse oozing (30%)
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35
Q

HIghest risk factor for mortality with non-varicealm UGIB

A

Continued or rebleeding

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36
Q

Patient with liver failure MCC UGIB

A

Esophageal varices (NOT an ulcer)

Tx EGD with bands or sclerotherapy; TIPS if that fails

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37
Q

Duodenal ulcers cause

A

Increased acid production and less defese

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38
Q

Most common peptic ulcer

A

Duodenal

More common in men

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39
Q

Most common place for duodenal ulcer

A

Anterior, first part of duodenum

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40
Q

Anterior versus posterior duodenal ulcers

A

Anterior: Perforate

Posterior: Bleed from GDA

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41
Q

Epigastric pain radiating to the back, abates with eating but recurs 30 min after

A

Duodenal ulcer

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42
Q

Dx and Tx of duodenal ulcer

A

EGD; PPI, triple therapy for H pylori

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43
Q

Tripe therapy

A

Amoxicillin, Metronidazole/tetracyclene, PPI (PAM or PAT)

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44
Q

Surgery for ulcer?

A

Rarely indicated since PPIs

  • Perforated
  • Protracted bleeding despite EGD therapy
  • Obstruction
  • Intractability despite medical therapy
  • Inability to rule out cancer (ulcer remains despite treatment) requires resection
  • If a patient has been on a a PPI, an acid-reducing surgical procedure is required in addition to surgery for any complications
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45
Q

PUD mgt

A

Rule out gastrinoma in patients with complicated ulcer disease (ZES - gastric acid hypersecretion, peptic ulcers, and gastrinoma)

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46
Q

Surgical options for PUD (acid-reducing surgery)

A

Proximal vagotomy: lowest rate of complications, no need for antral or pylorus procedure; 10-15% ulcer recurrence and 0.1% mortality

Truncal vagotomy and pyloroplasty: 5-10% ulcer recurrence, 1% mortality

Truncal vagotomy and antrectomy: 1-2% ulcer recurrence (lowest rate of recurrence) and 2% mortality

Reconstruction after antrectomy: Roux-en-Y gastrojejunostomy is best: less dumping syndrome and reflux gastritis compared to Billroth I (gastroduodenal anastomosis) and Billroth II (gastrojejunal anastomosis)

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47
Q

Acid-reducing surgery with lowest rate of PUD recurrence?

A

Truncal vagotomy and antrectomy

48
Q

Reconstruction after antrectomy with lowest rate of dumping syndrome and reflux gastritis

A

Roux-en-Y gastrojejunostomy

49
Q

Most frequent complication of duodenal ulcers

A

Bleeding

Usually minor but can be life threatening

If > 6 units of blood in 24hr or hypotensive despite transfusion = major bleeding

50
Q

Tx of duodenal ulcer bleeding

A

EGD 1st: hemoclips, cauterize, epi injection

  1. Surgery: duodenotomy and GDA ligation. Avoid hitting CBD (posterior). If patient has been on a PPI, need acid-reducing surgery too
51
Q

Risk of duodenotomy and GDA ligation for duodenal ulcer bleed?

A

Hitting CBd (posterior)

52
Q

PUD obstruction tx

A

PPI and serial dilation initially

Surgical options: antrectomy and truncal vagotomy (best); include ulcer in resection if located proximal to ampulla of Vater; need to bx area of resection to rule out Ca

53
Q

Sudden sharp epigastric pain, generalized peritonitis, free air

A

PUD perforation: 80% will have free air

Pain can radiate to pericolic gutters with dependent drainage of gastric content

54
Q

Tx of perforated PUD

A

Graham patch (place omentum over perforation)

Also need acite-reducing surgery if patient has been on a PPI

55
Q

PUD intractability (no relief after >3 months of escalating PPI dose) tx

A

Based in EGD findings, not symptoms

Tx: Acid-reducing surgery

56
Q

Gastric ulcers characteristics and risk factors

A

Older men, slow healing, 80% on lesser curvature

RF: male, tobacco, EtOH, NSAIDs, H pylori, uremia, stress (burns, sepsis, trauma), steroids, chemotx

57
Q

GIB from stomach versus duodenal ulcer

A

Stomach hemorrhage associated with higher mortality

58
Q

Epigastric pain radiating to back, relieved with eating but recurs 30 min later, melena or guaiac-positive stools

A

Stomach ulcer bleed?

59
Q

Best test of H pylori

A

Histiologic examination of biopsies from antrum

Other: CLO test (rapid urease test): detects urease released from H pylori

60
Q

Stomach ulcer types

A

I: lesser curve LOW along body of stomach, due to decreased mucosal protection

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

III: Pre-pyloric; similar to duodenal with high acid secretion

IV: lesser curve HIGH along cardia; decreased mucosal protection

V: ulcer associated with NSAIDs

61
Q

Surgical indications for stomach ulcer

A

Perforation

Bleeding not controlled with EGD

Obstruction

Cannot exclude malignance

Intractability (> 3 months without relief; based on mucosal findings)

62
Q

Surgical options for stomach ulcer disease

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); 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 ulcer

63
Q

Fundus ulcer 3-10 days after an event

A

Stress gastritis; tx PPI; EGD with cautery of specific bleeding point may be effective

64
Q

Chronic gastritis types A and B

A

A: Fundus, associated with pernicious anemia; autoimnune disease; tx PPI

B: Antral, associated with H pylori; tx PPI

65
Q

Pain UNRELIEVED by eating; weight loss

A

Gastric cancer

40% in antrum

Accounts for 50% of cancer-related deaths in Japan

66
Q

Dx of gastric ca

A

EGD

67
Q

Risk factors for gastric ca

A

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

68
Q

Gastric adenomatous polyps and cancer risk?

A

15% cancer risk, tx with endoscopic resection

69
Q

Krukenberg tumor

A

Gastric mets to ovaries

70
Q

Virchow’s nodes

A

gastric mets to supraclavicular node

71
Q

Intestinal type gastric Ca risk factors and tx

A

Increased in high risk populations, older men; Japan, rare in US

Tx: Try to perform subtotal gastrectomy (need 10 cm margins)

72
Q

Diffuse gastric ca (linitis plastica)

A

In low-risk populations, woman; most common type in US

Diffuse lymphatic invascion; NO glands

Less favorable prognosis than intestinal type gastric ca (overall 5 YS of 25%)

Total gastrectomy because of diffuse nature of linitis plastica

73
Q

Gastric ca chemotx

A

5-FU, doxorubicin, mitomycin C

Poor response

74
Q

Contraindication to resection in gastric ca

A

Metastatic disease outside area of resection (unless it’s for palliation)

75
Q

Palliation of obstructed gastric Ca

A

Stent proximal lesions

Gastrojejunostomy for distal lesions

76
Q

Palliative of bleeding or painful gastric Ca

A

XRT

77
Q

Palliative gastrectomy?

A

If other options for obstruction or bleeding fail

78
Q

Most common benign gastric neoplasm

A

GISTS (though can be malignant)

79
Q

GIST symptoms

A

usually asymptomatic, but obstruction and bleeding can occur

80
Q

GISTS on US

A

Hypoechoid with smooth edges

81
Q

GIST dx

A

Biopsy: C-KIT positive

82
Q

GIST malignant characteristics

A

> 5 cm or > 5 mitoses/50 HPF

If malignant, chemo with imatinib (gleevec; tyrosine kinase inhibitor)

83
Q

Treatment of GIST

A

Resect with 1cm margins

84
Q

MALT lymphoma

A

Related to H pylori

Usually regresses after H pylori tx

Stomach most common location

Tx: triple therapy abx and surveillance; if MALT does not regress, need XRT

85
Q

What if MALT lymphoma doesn’t regress after H pylori tx?

A

XRT

86
Q

Most common location for extranodal lymphoma

A

Stomach; usually NHL (B cell); have ulcer symptoms

87
Q

Dx of gastric lymphoma

A

EGD with biopsy

88
Q

Tx of gastric lymphoma

A

Chemotx and XRT

Surgery for complications; possibly indicated only for stage I disease (tumor confined to stomach mucosa) and then only partial resection indicated

89
Q

Gastric lymphoma prognosis

A

5YS of >50%

90
Q

Bariatric surgery indications

A
  1. BMI>40 or BMI>35 with coexisting comorbidities

Failure of nonsurgical methods

Psychological stability

Absence of drug and alcohol abuse

91
Q

Obesity worse prognoses

A

Central obesity

92
Q

Bariatric operative mortality

A

~1%

93
Q

What conditions get better after bariatric surgery?

A

DM

HLD

OSA

HTN

Urinary incontinence

GERD
VSU

Pseudotumor cerebri

Joint pain

Migraines

Depression

PCOS

NASH

94
Q

Gastric bypass

A

Better weight loss than just banding

Risk of marginal ulcers, leak, necrosis, B12 deficiency (intrinsic factor needs acidic environment to bind B12), IDA (bypasses duodenum where Fe absorbed), gallstones from rapid weight loss

Perform chole during operation if stones present

UGI on POD2

10% failure rate due to high carb snacking

95
Q

Gastric bypass leaks

A

MCC is ischemia

96
Q

Increased RR, tachy, abd pain, fever, elevated WBCs after bypass

A

Leak; MCC is ischemia; dx with UGI; tx with re-op if early not-contained leak; percutaneous drain and abx if weeks out from surgery and likely contained

97
Q

Marginal ulcer risk after RYGB

A

10%; tx with PP

98
Q

Stenosis after RYGB

A

Usually responds to serial dilation

99
Q

Hiccoughs and large stomach bubble after RYGB

A

Dilation of excluded stomach; Dx with AXR; Tx with G-tube

100
Q

SBO after RYGB

A

Surgical emergency due to high risk of small bowel herniation, strangulation, infarction, and necrosis

Surgical exploration

101
Q

Jejunoileal bypass

A

No longer done; associated with liver cirrhosis, kdieny stones, osteoporosis

Need to correct these patients and perform RYGB if ileojejunal bypasses are encountered

102
Q

Postgastrectomy complications

A

Dumping syndrome

Alkaline reflux gastritis

Chronic gastric atony

Small gastric remnant

Blind-loop syndrome

Afferent-loop syndrome

Efferent-loop syndrome

Post-vagotomy diarrhea

Duodenal stump blow-out

PEG complications

103
Q

Hypotension, diarrhea, and dizziness after gastrectomy

A

Dumping syndrome, hyperosomotic load causing fluid shift into bowel

Occurs from rapid entering of carbs into small bowel

Can occur after gastrectomy or after vagotomy and pyloroplasty

90% resolve with medical therapy

104
Q

Hypglycemia after gastrectomy

A

Dumping syndrome, 2nd phase (rare); reactive increase in insulin and decrease in glucose

105
Q

Tx of dumping syndrome

A

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

106
Q

Dumping syndrome surgery (rarely needed)

A

Conversion of billroth I or II to RYGJ

Jejunal pouch or reversed jejunal loop to increase gastric reservoir or increase emptying time

107
Q

Postprandial epigastric pain associated with N/V; pain not relieved with vomiting; after gastrectomy

A

Alkaline reflux gastritis

Ex: e/o bile reflux into stomach and histologic evidence of gastritis

Tx: PPI, cholestyramine, metoclopramide

Surgery: conversion of billroth I or II to RYGJ with afferent limb 60cm distal to gastroJ

108
Q

SDelayedNausea, vomiting, pain, eraly satiety ater gastrectomy

A

Chronic gastric atony from delayed gastric emptying

Dx: Gastric emptying study

Tx: Metoclopramide, prokinetics

Surgery: Near-total gastrectomy with Roux-en-Y

109
Q

Early satiety after gastrectomy

A

Small gastric remnant, actually want this for gastric bypass patients

Dx: EGD

Tx: Small meals

Surgery: jejunal pouch construction

110
Q

Pain, steatorrhea, B12 deficiency, and malabsorption after gastrectomy

A

Blind-loop syndrome after Billroth II or Roux-en-Y

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

Dx: EGD of afferent limb with aspirate and culture for organisms

Tx: Tetracycline and flagyl, metoclopramide to improve motility

Surgery: Re-anastomosis with shorter (40cm) afferent limb

111
Q

RUQ pain, steatorrhea, nonbilious vomiting, pain relieved with bilious emesis after gastrectomy

A

Afferent-loop obstruction after billroth II or Roux-en-Y

Caused by mechanical obstruction of afferent limb (long afferent limb is a risk factor)

Dx: CT scan

Tx: Balloon dilation may be possible

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

112
Q

Nausea, vomiting, abdominal pain after gastrectomy

A

Efferent-loop obstruction

Dx: UGI, EGD

Tx: Balloon dilation

Surgery: find site of obstruction and relieve it

113
Q

Diarrhea after vagotomy

A

Secondary to non-conjugated bile salts in the colon (osmotic diarrhea), with sustained postprandial organized MMCs

Tx: cholestyramine, octreotide

Surgery: Reversed interposition jejunal graft

114
Q

Duodenal stump blow out tx

A

Lateral duodenostomy tube and drains

115
Q

PEG complications

A

Insertion into liver or colon