Stomach Flashcards
Most of blood supply of stomach supplied by?
celiac artery
4 main arteries that supply the stomach?
right and left gastric arteries along lesser curve
left and right gastro-epiploics along greater curve
What are some collateral arteries that supply the stomach?
inferior phrenic arteries
short gastrics from spleen
Largest artery to stomach?
left gastric
15-20% of the time, left gastric artery gives off aberrant what?
left hepatic artery
Sometimes ligating the proximal left gastric artery can result in left lobe hepatic ischemia, why?
15-20% of time, left gastric can give off left hepatic artery
Origins of left gastro-epiploics and right gastro-epiploic?
L–> from splenic
R–> from gastroduodenal
Venous drainage of the stomach?
L-gastro epiploic–> splenic vein
R- gastro epiploic–> SMV
L+R gastric veins–> portal vein
Innervation fo stomach occurs via?
PSNS: vagus
SNS: celiac plexus
Position of left and right vagus nerves at GE junction?
LARP
left vagus–anterior
right vagus–posterior
Branches off of the left vagus include:
hepatic branch
anterior nerve of Latarjet
Hepatic branches and anterior nerve of Latarjet are branches off what?
left vagus
First branch off of the right vagus?
criminal nerve of Grassi
Criminal nerve of Grassi comes off of what nerve?
right vagus
Criminal nerve of Grassi, off of the right vagus, can cause problems why?
when left undivided, cause of recurrent ulcers
This vagus gives off a celiac branch:
right vagus
Anatomically where do we perform a truncal vagotomy?
above the celiac and hepatic branches of the vagi
Anatomically where do we perform a selective vagotomy?
below the celiac and hepatic branches of the vagi
What;s a highly selective vagotomy?
divide the crow’s feet to proximal stomach
preserve innervation to antum and pyloric parts of stomach
What are the layers of the stomach wall?
mucosa
submucosa
muscularis layer (3 layers of muscle; incomplete inner oblique layer, middle circular, outer longtidunal)
serosa
Where do we find Aurbach’s plexus in stomach wall?
within muscle layer
Strongest layer of gastric wall?
submucosa –> collagen rich
Where do we find Meissner’s plexus?
submucosa
Where do we find Auerbach’s and Meissner’s plexi?
Auerbachs–muscle layer
Meissner’s–submucosa
Gastric mucosa is made up of what type of epithelium?
glandular columnar
These cells secrete HCl acid and IF:
parietal cells
What do parietal cells make?
HCl acid + IF
Where do we find parietal cells:
body of stomach
What do chief cells make?
pepsin
Pepsin made by ?
chief cells
Chief cells and parietal cells reside where?
body
Enterochromaffin like cells of stomach make what?
histamine
G cells of antrum make what?
gastrin
Gastrin made by?
G cells
Somatostatin made by?
D cells
What do D cells of body and antrum make?
somatostatin
Stomach begins digestion of a meal, primary by braking down starches thru activity of what enzyme?
salivary amylase
Gastrin produced by?
G cells in antrum
Release of gastrin stimulated by?
food components of a meal, especially protein digestion products
Gastrin levels become inappropriately elevated in pts with?
Zollinger-Ellison syndrome
What are the specialized pacemaker cells of stomach?
interstitial cells of Cajal
Where do we find the interstitial cells of Cajal in stomach?
muscularis layer
Outer layer of stomach is the serosa, AKA?
visceral peritoneum
What do parietal cells make?
HCL
IF
HCO3
What stimulates parietal cells to make HCL?
gastrin
ACh
histamine
Somatostatin made by D cells does what?
inhibits parietal cell HCL
somatostatin inhibited by Ach
How does somatostatin inhibit cell regulation?
inhibits adenylate cyclase
reduces cAMP
This stomach hormone enhances appetite and increases food intake:
ghrelin
Principal neurotransmitter modulating parietal cell HCL secretion?
Ach
Eating a meal causes vagal fibers to release ACh, which does what?
stimulates parietal cells–> HCL
stimulates ECL cells–> histamine
stimulates G cells–> gastrin
binds D cells–> inhibits somatostatin
Main stimulus for D cells to release somatostatin is?
acidification of antral lumen
Three phases of gastric secretions following a meal?
cephalic
gastric
luminal
Cephalic phase produces how much acid following a meal?
20-30%
*** gastric phase produces 60-70% of acid
What two secondary messengers involved in acid secretion from parietal cells>
Ca
cAMP
MOA of famotidine?
H2 receptor blocker
t 1/2; 3 hrs
MOA of PPIs?
irreversible inhibition of proton pump
Side effect of PPIs?
hyperplasia of G cells and ECL cells
increase in gastrin
Eating a meal relaxes proximal stomach, termed gastric accomodation and receptive relaxation, mediated by vagus nerve, what happens in a truncal vagotomy?
these reflexes are eliminated
see early satiety
rapid clearance of fluids
What are some protective factors in PUD?
HCO3 mucus production blood flow growth factors cell renewal prostaglandins
What are some damaging factors in PUD?
HCl pepsins ethanol smoking ischemia NSAIDs H. pylori
What % of duodenal ulcers assc. with h pylori?
90%
What % of gastric ulcers assc. with h. pylori?
75%
This bug is a spiral/helical gram negative rod with 4-6 flagella that resides in gastric epithelium:
h. pylori
H. pylori contains what enzyme?
urease
H. pylori contains urease enzyme, which does what?
splits urea into ammonia and bicarb–> creates an alkaline environment
How does h pylori cause GI injury?
production of toxic products that causes local tissue injury
induce a local inflammatory immune response
increase gastrin levels which leads to increased acid secretion
NSAID induced ulcers are more commonly found where ?
stomach
H pylori induced ulcers are more commonly found where?
duodenum
Clinical presentation of someone with a suspected duodenal ulcer?
mid-epigastric localized pain
pain relieved by food
How do we document h pylori eradication after tx?
perform a urea breath test 4 weeks after treatment
h pylori has urease enzyme which splits urea into ammonia and bicarb
Most reliable method of diagnosing a duodenal ulcer?
endoscopy
can also sample tissue and provide treatment
Medical management of duodenal ulcers split into three categories:
tx against h pylori
ant-acid protection
mucosal barrier protection
Most potent and weakest H2 receptor antagonists?
famotidine most potent
cimetidine is weakest
Why dont we combine H2 antagonists and PPI?
PPI need an acidic environment to work
H2 antagonists promote an alkaline environment
Triple therapy for h pylori?
PPI
amoxicillin
clarithromycin (or metronidazole)
for 2 weeks
For pt’s not responsive to triple therapy eradication what do we do?
quadruple therapy with bismuth
For pt withs an upper GI bleed, endoscopy often used to visualize source and gain control, control usually gained via injection of:
epinephrine + second method (sclerosing agent and thermal coagulation)
dual therapy shown to be superior to epinephrine injection alone in controlling bleeding
In PUD, the vessel most likely to be bleeding is?
gastroduodenal artery from a posterior ulcer
What artery most likely source of bleeding in PUD?
gastroduodenal artery
How do we control a bleeding gastroduodenal artery from PUD?
open the duodenum longitudinally
extend incision thru pylorus
vessel is oversewn with a 3-point U-stitch
duodenotomy is closed transversely (Heineke-Mikulicz pyloroplasty)
Duodenal ulcer perforations usually occur in what part of duodenum?
1st part
How do we close perforations < 1 cm in duodenal ulcer dx?
repair primarily
How do we close duodenal ulcer perforations >1 cm but < 3 cm?
Graham patch
How do we close duodenal perforations >3 cm?
can apply jejunal serosa or Graham patch
place a duodenostomy tube for wide drainage
Surgical therapy for PUD seeks to do what?
reduce acid secretion by;
removing vagal stimuli
antrectomy to remove gastrin
Anatomically where do we perform a truncal vagotomy?
divide the right and left vagus above the hepatic and celiac branches
**just above the GE junction
What is a highly selective vagotomy?
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)
Describe a highly selective vagotomy;
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
Antrectomy and vagotomy usually performed for what type of ulcers?
gastric
An antrectomy usually requires GI continuity via what?
Billroth I (gastro duodenostomy)
Billroth II (gastro jejunostomy )
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?
decreases chance of twisting/kinking of jejunum
decreases chance of duodenal stump leak
Gastric ulcers can occur anywhere along stomach, but most commonly in what location?
along lesser curve at incisura (60%)
Most gastric ulcers found in this location and are classified as this type;
lesser cuve at incisura (60%)
type I
What are the 5 different types of gastric ulcers?
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)
Peak incidence of gastric ulcers?
55-65
What type of gastric ulcers are prone to see bleeding with?
type II &; III
MOst gastric ulcer perforations occur where?
lesser curve
Key difference between gastric and duodenal ulcers?
in gastric ulcers we need to rule out cancer
What is a giant gastric ulcer?
ulcer diameter >2 cm
Where do we normally find giant gastric ulcers?
lesser curve
have 10% incidence of malignancy
What Zollinger Ellison syndrome?
triad of;
gastric acid hypersecretion
severe PUD
non-B islet cell pancreatic tumors
What do we see with gastrinomas in ZES?
elevated gastrin levels
fasting and stimulated plasma gastrin levels elevated
> 1000 are diagnostic
In pts with ZES (gastrinomas), where their gastrinomas levels are equival, how can we find out if they have a gastrinoma or not?
secretin stimulation test
give IV secretin every 5 minutes for 30 minutes
a number > 200 above basal level is diagnostic
This occurs after physical trauma, shock, sepsis, hemorrhage, or resp failure and may lead to life threatening gastric bleeding:
stress gastritis
Ulcers in the setting of CNS disease?
cushing ulcers
Ulcers in setting of thermal burns?
Curling ulcers
When do we see frank bleeding with stress ulcers?
when they erode into submucosa (which contains the blood supply)
What causes stress ulcers?
stress in the form of hypoxia, sepsis or organ failure usually inciting event
this leads to mucosal ischemia–> leads to breakdown in natural defenses
When do most pts develop stress gastritis?
50% will develop it within 1-2 days after a traumatic event
Usually bleeding from stress gastritis stops with conservative measures, when it doesn’t stop, what’s an indication to operate?
> 6 U of blood
There are two clinical manifestations of dumping syndrome, they are?
early (more common)
late
When does early dumping syndrome occur?
20-30 mins after eating
When does late dumping syndrome occur?
2-3 hrs after a meal
What procedures do we usually see dumping syndrome with?
gastrectomy w/Billroth II
Sxs of dumping syndrome?
GI: N/V, fullness, cramps, diarrhea
Cardiac: tachy, palpatations, flushing, faintness
Pathophys of early dumping syndrome?
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
Pathophys of late dumping syndrome?
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
Treatment for dumping syndrome?
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
Medical therapy for dumping syndrome?
ocreotide antagonists==> slow gastric/intestinal motility
After gastrectomy, what’s the most common metabolic affect?
anima (seen in 30% of pts going gastrectomy)
Megaloblastic anemia after gastrectomy?
rare **due to how much stomach removed and if B12 affected
What’s afferent loop syndrome?
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
Blind loop syndrome?
if an obstruction has been present in afferent limb for a long time;
you get bacterial overgrowth
bind B12 and deconjugated bile acids–> anemia
How do we treat afferent loop syndrome?
usually a long afferent limb is the problem
convert Billroth II into a Roux-en-Y
What is efferent loop obstruction?
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
What’s alkaline reflux gastritis?
after gastrectomy, reflux of bile is common
in some pts this bile reflux assc. w/severe epigastric pain, bilious vomiting, weight loss
How do we diagnose alkaline reflux gastritis?
HIDA scan, bile seen in stomach
Alkaline reflux gastritis commonly seen in pts who underwent a Billroth II, how do we correct this surgically?
convert to a Roux-en-y
Gastric emptying usually delayed after gastrectomy and truncal and selective vagotomies, what two meds do we use?
metoclopramide (reglan)–> prokinetic effects via DA antagonism, also stimulates Ach release from enteric cholinergic neurons
erythormycin–> binds to motilin receptos in smooth muscle cells
Men vs women most commonly affected by gastric cancer?
MEN 60%
How does H pylori cause gastric cancer?
having H pylori causes chronic inflammation
this chronic gastritis leads to metaplasia, dysplasia, adenocarcinoma
What h pylori gene associated with increased virulence and risk of gastric cancer?
CagA
What is Borchards triad?
assc with gastric volvulus
severe epigastric pain
inability to vomit
inability to pass an NG tube
