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Appendix > Stomach > Flashcards

Stomach Flashcards

1
Q

Most of blood supply of stomach supplied by?

A

celiac artery

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2
Q

4 main arteries that supply the stomach?

A

right and left gastric arteries along lesser curve

left and right gastro-epiploics along greater curve

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3
Q

What are some collateral arteries that supply the stomach?

A

inferior phrenic arteries

short gastrics from spleen

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4
Q

Largest artery to stomach?

A

left gastric

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5
Q

15-20% of the time, left gastric artery gives off aberrant what?

A

left hepatic artery

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6
Q

Sometimes ligating the proximal left gastric artery can result in left lobe hepatic ischemia, why?

A

15-20% of time, left gastric can give off left hepatic artery

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7
Q

Origins of left gastro-epiploics and right gastro-epiploic?

A

L–> from splenic

R–> from gastroduodenal

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8
Q

Venous drainage of the stomach?

A

L-gastro epiploic–> splenic vein
R- gastro epiploic–> SMV
L+R gastric veins–> portal vein

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9
Q

Innervation fo stomach occurs via?

A

PSNS: vagus
SNS: celiac plexus

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10
Q

Position of left and right vagus nerves at GE junction?

A

LARP

left vagus–anterior

right vagus–posterior

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11
Q

Branches off of the left vagus include:

A

hepatic branch

anterior nerve of Latarjet

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12
Q

Hepatic branches and anterior nerve of Latarjet are branches off what?

A

left vagus

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13
Q

First branch off of the right vagus?

A

criminal nerve of Grassi

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14
Q

Criminal nerve of Grassi comes off of what nerve?

A

right vagus

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15
Q

Criminal nerve of Grassi, off of the right vagus, can cause problems why?

A

when left undivided, cause of recurrent ulcers

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16
Q

This vagus gives off a celiac branch:

A

right vagus

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17
Q

Anatomically where do we perform a truncal vagotomy?

A

above the celiac and hepatic branches of the vagi

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18
Q

Anatomically where do we perform a selective vagotomy?

A

below the celiac and hepatic branches of the vagi

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19
Q

What;s a highly selective vagotomy?

A

divide the crow’s feet to proximal stomach

preserve innervation to antum and pyloric parts of stomach

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20
Q

What are the layers of the stomach wall?

A

mucosa
submucosa
muscularis layer (3 layers of muscle; incomplete inner oblique layer, middle circular, outer longtidunal)
serosa

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21
Q

Where do we find Aurbach’s plexus in stomach wall?

A

within muscle layer

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22
Q

Strongest layer of gastric wall?

A

submucosa –> collagen rich

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23
Q

Where do we find Meissner’s plexus?

A

submucosa

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24
Q

Where do we find Auerbach’s and Meissner’s plexi?

A

Auerbachs–muscle layer

Meissner’s–submucosa

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25
Q

Gastric mucosa is made up of what type of epithelium?

A

glandular columnar

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26
Q

These cells secrete HCl acid and IF:

A

parietal cells

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27
Q

What do parietal cells make?

A

HCl acid + IF

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28
Q

Where do we find parietal cells:

A

body of stomach

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29
Q

What do chief cells make?

A

pepsin

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30
Q

Pepsin made by ?

A

chief cells

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31
Q

Chief cells and parietal cells reside where?

A

body

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32
Q

Enterochromaffin like cells of stomach make what?

A

histamine

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33
Q

G cells of antrum make what?

A

gastrin

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34
Q

Gastrin made by?

A

G cells

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35
Q

Somatostatin made by?

A

D cells

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36
Q

What do D cells of body and antrum make?

A

somatostatin

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37
Q

Stomach begins digestion of a meal, primary by braking down starches thru activity of what enzyme?

A

salivary amylase

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38
Q

Gastrin produced by?

A

G cells in antrum

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39
Q

Release of gastrin stimulated by?

A

food components of a meal, especially protein digestion products

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40
Q

Gastrin levels become inappropriately elevated in pts with?

A

Zollinger-Ellison syndrome

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41
Q

What are the specialized pacemaker cells of stomach?

A

interstitial cells of Cajal

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42
Q

Where do we find the interstitial cells of Cajal in stomach?

A

muscularis layer

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43
Q

Outer layer of stomach is the serosa, AKA?

A

visceral peritoneum

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44
Q

What do parietal cells make?

A

HCL
IF
HCO3

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45
Q

What stimulates parietal cells to make HCL?

A

gastrin
ACh
histamine

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46
Q

Somatostatin made by D cells does what?

A

inhibits parietal cell HCL

somatostatin inhibited by Ach

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47
Q

How does somatostatin inhibit cell regulation?

A

inhibits adenylate cyclase

reduces cAMP

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48
Q

This stomach hormone enhances appetite and increases food intake:

A

ghrelin

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49
Q

Principal neurotransmitter modulating parietal cell HCL secretion?

A

Ach

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50
Q

Eating a meal causes vagal fibers to release ACh, which does what?

A

stimulates parietal cells–> HCL
stimulates ECL cells–> histamine
stimulates G cells–> gastrin

binds D cells–> inhibits somatostatin

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51
Q

Main stimulus for D cells to release somatostatin is?

A

acidification of antral lumen

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52
Q

Three phases of gastric secretions following a meal?

A

cephalic
gastric
luminal

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53
Q

Cephalic phase produces how much acid following a meal?

A

20-30%

*** gastric phase produces 60-70% of acid

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54
Q

What two secondary messengers involved in acid secretion from parietal cells>

A

Ca

cAMP

55
Q

MOA of famotidine?

A

H2 receptor blocker

t 1/2; 3 hrs

56
Q

MOA of PPIs?

A

irreversible inhibition of proton pump

57
Q

Side effect of PPIs?

A

hyperplasia of G cells and ECL cells

increase in gastrin

58
Q

Eating a meal relaxes proximal stomach, termed gastric accomodation and receptive relaxation, mediated by vagus nerve, what happens in a truncal vagotomy?

A

these reflexes are eliminated

see early satiety
rapid clearance of fluids

59
Q

What are some protective factors in PUD?

A 
HCO3
mucus production
blood flow
growth factors
cell renewal
prostaglandins
60
Q

What are some damaging factors in PUD?

A 
HCl
pepsins
ethanol
smoking 
ischemia
NSAIDs
H. pylori
61
Q

What % of duodenal ulcers assc. with h pylori?

A

90%

62
Q

What % of gastric ulcers assc. with h. pylori?

A

75%

63
Q

This bug is a spiral/helical gram negative rod with 4-6 flagella that resides in gastric epithelium:

A

h. pylori

64
Q

H. pylori contains what enzyme?

A

urease

65
Q

H. pylori contains urease enzyme, which does what?

A

splits urea into ammonia and bicarb–> creates an alkaline environment

66
Q

How does h pylori cause GI injury?

A

production of toxic products that causes local tissue injury

induce a local inflammatory immune response

increase gastrin levels which leads to increased acid secretion

67
Q

NSAID induced ulcers are more commonly found where ?

A

stomach

68
Q

H pylori induced ulcers are more commonly found where?

A

duodenum

69
Q

Clinical presentation of someone with a suspected duodenal ulcer?

A

mid-epigastric localized pain

pain relieved by food

70
Q

How do we document h pylori eradication after tx?

A

perform a urea breath test 4 weeks after treatment

h pylori has urease enzyme which splits urea into ammonia and bicarb

71
Q

Most reliable method of diagnosing a duodenal ulcer?

A

endoscopy

can also sample tissue and provide treatment

72
Q

Medical management of duodenal ulcers split into three categories:

A

tx against h pylori

ant-acid protection

mucosal barrier protection

73
Q

Most potent and weakest H2 receptor antagonists?

A

famotidine most potent

cimetidine is weakest

74
Q

Why dont we combine H2 antagonists and PPI?

A

PPI need an acidic environment to work

H2 antagonists promote an alkaline environment

75
Q

Triple therapy for h pylori?

A

PPI
amoxicillin
clarithromycin (or metronidazole)

for 2 weeks

76
Q

For pt’s not responsive to triple therapy eradication what do we do?

A

quadruple therapy with bismuth

77
Q

For pt withs an upper GI bleed, endoscopy often used to visualize source and gain control, control usually gained via injection of:

A

epinephrine + second method (sclerosing agent and thermal coagulation)

dual therapy shown to be superior to epinephrine injection alone in controlling bleeding

78
Q

In PUD, the vessel most likely to be bleeding is?

A

gastroduodenal artery from a posterior ulcer

79
Q

What artery most likely source of bleeding in PUD?

A

gastroduodenal artery

80
Q

How do we control a bleeding gastroduodenal artery from PUD?

A

open the duodenum longitudinally

extend incision thru pylorus

vessel is oversewn with a 3-point U-stitch

duodenotomy is closed transversely (Heineke-Mikulicz pyloroplasty)

81
Q

Duodenal ulcer perforations usually occur in what part of duodenum?

A

1st part

82
Q

How do we close perforations < 1 cm in duodenal ulcer dx?

A

repair primarily

83
Q

How do we close duodenal ulcer perforations >1 cm but < 3 cm?

A

Graham patch

84
Q

How do we close duodenal perforations >3 cm?

A

can apply jejunal serosa or Graham patch

place a duodenostomy tube for wide drainage

85
Q

Surgical therapy for PUD seeks to do what?

A

reduce acid secretion by;

removing vagal stimuli
antrectomy to remove gastrin

86
Q

Anatomically where do we perform a truncal vagotomy?

A

divide the right and left vagus above the hepatic and celiac branches

**just above the GE junction

87
Q

What is a highly selective vagotomy?

A

divides only the vagus nerves supplying the acid producing portions of the stomach body and fundus

the innervation of the antrum is preserved (so there is no need for a drainage procedure)

88
Q

Describe a highly selective vagotomy;

A

nerves of Latarjet are identified anteriorly/posteriorly and crows feet innervating body of stomach are divided

7 cm proximal to pylorus extending up to 5 cm proximal to GE junction

89
Q

Antrectomy and vagotomy usually performed for what type of ulcers?

A

gastric

90
Q

An antrectomy usually requires GI continuity via what?

A

Billroth I (gastro duodenostomy)

Billroth II (gastro jejunostomy )

91
Q

When performing a Billroth II after a distal antrectomy, why do we bring the loop of jejunum up in a retrocolic fashion to anastomose to the stomach?

A

decreases chance of twisting/kinking of jejunum

decreases chance of duodenal stump leak

92
Q

Gastric ulcers can occur anywhere along stomach, but most commonly in what location?

A

along lesser curve at incisura (60%)

93
Q

Most gastric ulcers found in this location and are classified as this type;

A

lesser cuve at incisura (60%)

type I

94
Q

What are the 5 different types of gastric ulcers?

A

I–> lesser curve at incisura (normal acid)

II–> gastric body + duodenal ulcer (ACID)

III–> prepyloric (ACID)

IV—> high on lesser curve (normal acid)

V—> anywhere (normal acid, NSAID induced)

95
Q

Peak incidence of gastric ulcers?

A

55-65

96
Q

What type of gastric ulcers are prone to see bleeding with?

A

type II &; III

97
Q

MOst gastric ulcer perforations occur where?

A

lesser curve

98
Q

Key difference between gastric and duodenal ulcers?

A

in gastric ulcers we need to rule out cancer

99
Q

What is a giant gastric ulcer?

A

ulcer diameter >2 cm

100
Q

Where do we normally find giant gastric ulcers?

A

lesser curve

have 10% incidence of malignancy

101
Q

What Zollinger Ellison syndrome?

A

triad of;

gastric acid hypersecretion
severe PUD
non-B islet cell pancreatic tumors

102
Q

What do we see with gastrinomas in ZES?

A

elevated gastrin levels

fasting and stimulated plasma gastrin levels elevated

> 1000 are diagnostic

103
Q

In pts with ZES (gastrinomas), where their gastrinomas levels are equival, how can we find out if they have a gastrinoma or not?

A

secretin stimulation test

give IV secretin every 5 minutes for 30 minutes

a number > 200 above basal level is diagnostic

104
Q

This occurs after physical trauma, shock, sepsis, hemorrhage, or resp failure and may lead to life threatening gastric bleeding:

A

stress gastritis

105
Q

Ulcers in the setting of CNS disease?

A

cushing ulcers

106
Q

Ulcers in setting of thermal burns?

A

Curling ulcers

107
Q

When do we see frank bleeding with stress ulcers?

A

when they erode into submucosa (which contains the blood supply)

108
Q

What causes stress ulcers?

A

stress in the form of hypoxia, sepsis or organ failure usually inciting event

this leads to mucosal ischemia–> leads to breakdown in natural defenses

109
Q

When do most pts develop stress gastritis?

A

50% will develop it within 1-2 days after a traumatic event

110
Q

Usually bleeding from stress gastritis stops with conservative measures, when it doesn’t stop, what’s an indication to operate?

A

> 6 U of blood

111
Q

There are two clinical manifestations of dumping syndrome, they are?

A

early (more common)

late

112
Q

When does early dumping syndrome occur?

A

20-30 mins after eating

113
Q

When does late dumping syndrome occur?

A

2-3 hrs after a meal

114
Q

What procedures do we usually see dumping syndrome with?

A

gastrectomy w/Billroth II

115
Q

Sxs of dumping syndrome?

A

GI: N/V, fullness, cramps, diarrhea

Cardiac: tachy, palpatations, flushing, faintness

116
Q

Pathophys of early dumping syndrome?

A

due to rapid passage of high osmolarity food from stomach to small intestine

b/c you’re missing parts of stomach, which prevents stomach from fully mobilizing the food and preparing it into small particles in an isotonic solution

stomach thus delivers a hypertonic food bolus to small intestine

this causes rapid shift of extracellular fluid in small intestinal lumen to make solution isotonic

after all this fluid enters small intestine, you get distention and symptoms

117
Q

Pathophys of late dumping syndrome?

A

rapid delivery of carbs from stomach to the intestines

carbs quickly absorbed by small intestine causing hyperglycemia

large amt of insulin released to control rising blood sugar

this causes a profound hypoglycemia in return

adrenal gland activated then and releases catecholamines–> diaphoresis, tremulousness, tachy, confusion

118
Q

Treatment for dumping syndrome?

A

dietary measures sufficient to treat most patients

avoid sugary foods
frequent feeding w/small meals rich in protein/fat
separate liquids from solids during a meal

119
Q

Medical therapy for dumping syndrome?

A

ocreotide antagonists==> slow gastric/intestinal motility

120
Q

After gastrectomy, what’s the most common metabolic affect?

A

anima (seen in 30% of pts going gastrectomy)

121
Q

Megaloblastic anemia after gastrectomy?

A

rare **due to how much stomach removed and if B12 affected

122
Q

What’s afferent loop syndrome?

A

due to partial obstruction of afferent limb, can;’t empty its contents

pancreatic and hepatibiliary secretions build up –> causes distention and cramping

pressures build up and eventually you get spillage of contents into stomach–> bilious vomiting and relief

123
Q

Blind loop syndrome?

A

if an obstruction has been present in afferent limb for a long time;

you get bacterial overgrowth

bind B12 and deconjugated bile acids–> anemia

124
Q

How do we treat afferent loop syndrome?

A

usually a long afferent limb is the problem

convert Billroth II into a Roux-en-Y

125
Q

What is efferent loop obstruction?

A

50% seen within 1st month

do a GI contrast study of stomach, see failure of contrast to enter efferent limb

surgery needed to close retroanastomotic hernia and close potential hernia space

126
Q

What’s alkaline reflux gastritis?

A

after gastrectomy, reflux of bile is common

in some pts this bile reflux assc. w/severe epigastric pain, bilious vomiting, weight loss

127
Q

How do we diagnose alkaline reflux gastritis?

A

HIDA scan, bile seen in stomach

128
Q

Alkaline reflux gastritis commonly seen in pts who underwent a Billroth II, how do we correct this surgically?

A

convert to a Roux-en-y

129
Q

Gastric emptying usually delayed after gastrectomy and truncal and selective vagotomies, what two meds do we use?

A

metoclopramide (reglan)–> prokinetic effects via DA antagonism, also stimulates Ach release from enteric cholinergic neurons

erythormycin–> binds to motilin receptos in smooth muscle cells

130
Q

Men vs women most commonly affected by gastric cancer?

A

MEN 60%

131
Q

How does H pylori cause gastric cancer?

A

having H pylori causes chronic inflammation

this chronic gastritis leads to metaplasia, dysplasia, adenocarcinoma

132
Q

What h pylori gene associated with increased virulence and risk of gastric cancer?

A

CagA

133
Q

What is Borchards triad?

A

assc with gastric volvulus

severe epigastric pain
inability to vomit
inability to pass an NG tube

Appendix (39 decks)

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