Sabiston Stomach Flashcards
The embryonic stomach
-two mesenteries:
dorsal (which becomes the gastrosplenic, gastrocolic, and gastrophrenic ligaments)
ventral (which becomes the hepatoduodenal and gastrohepatic ligaments of the lesser omentum and the falciform ligament).
Blood Supply
-The celiac artery
-four main arteries :
the left and right gastric arteries along the lesser curvature
the left and right gastroepiploic arteries along the greater curvature
the left gastric artery being the largest.
proximal stomach > inferior phrenic arteries and short gastric arteries from the spleen.
15% to 20% of patients > aberrant left hepatic artery originating from the left gastric artery.
-proximal ligation of the left gastric artery can result in acute left-sided hepatic ischemia.
-The right gastric artery from the hepatic artery or the gastroduodenal artery
-The left gastroepiploic artery from the splenic artery
-the right gastroepiploic artery from the gastroduodenal artery.
Venous Supply
the veins of the stomach parallel the arteries.
-The left gastric (coronary) and right gastric veins usually drain into the portal vein.
-The right gastroepiploic vein drains into the superior mesenteric vein
-the left gastroepiploic vein drains into the splenic vein
Gastric LN
-The superior gastric group : drains lymph from the upper lesser curvature into the left gastric and paracardial nodes.
-The suprapyloric group of nodes drains the antral segment on the lesser curvature of the stomach into the right suprapancreatic nodes.
-The pancreaticolienal group of nodes drains lymph high on the greater curvature into the left gastroepiploic and splenic nodes.
-The inferior gastric and subpyloric group of nodes drains lymph along the right gastroepiploic vascular pedicle.
All four zones of lymph nodes drain into the celiac nodes and eventually into the thoracic duct.
Vagus Nerve
LARP
Left : Anterior
Right : Posterior
Vagus Nerve Again
-The left vagus > hepatic branch to the liver and continues along the lesser curvature as the nerve of Latarjet.
-criminal nerve of Grassi > first branch of the right posterior vagus nerve;
it is recognized as a potential cause of recurrent ulcers when left undivided.
The right vagus nerve > branch off to the celiac plexus and continues posteriorly along the lesser curvature.
Vagotomies
A truncal vagotomy > above the celiac and hepatic branches of the vagi
selective vagotomy > below.
A highly selective vagotomy > dividing the crow’s feet to the proximal stomach while preserving the innervation of the antral and pyloric parts of the stomach.
Morphology
-muscularis propria or externa > three layers of smooth muscles.
-The middle layer > circular and is the only complete muscle layer of the stomach wall.
The outer muscle layer > Longitudinal and predominates in the distal two thirds of the stomach.
Within the muscularis externa > Auerbach myenteric plexus.
The submucosa > strongest layer of the gastric wall contains network of blood vessels and lymphatics + Meissner plexus of autonomic nerves.
Gastric acid secretion by the parietal cell is regulated mainly by three stimuli
acetylcholine, gastrin, and histamine
Helicobacter pylori
secretes various proteases and lipases that break down mucin and impair the protective function of the mucous layer.
Vagotomy and gastric emptying
results in loss of receptive relaxation and gastric accommodation in response to meal ingestion
with resultant early satiety, postprandial bloating, accelerated emptying of liquids, and delay in emptying of solids.
hyperglycemia on gastric motility
decrease in contractility of the gastric antrum
increase in pyloric contractility
relax the proximal stomach
suppress the migrating myoelectric complexes
How to assess gastric emptying
The most common is a radionucleotide scan
meal of radiolabeled food.
Scans are obtained immediately after ingestion of the meal and at 1, 2, and 4 hours after the meal.
Measurement of residual gastric contents at 4 hours
> At 4 hours, retention of 10% to 15% signifies mild gastroparesis, 15% to 35% is moderate, and greater than 35% is severe.
Other Diagnostic Studies
-upper abdominal x-ray series after barium swallow > mechanical causes
-electrogastrogram or antroduodenal motility study assesses for nerve and muscle abnormalities
-Wireless motility capsules > alternative to scintigraphy
Tx of Gastroparesis
first-line for mild gastroparesis
> dietary modification > multiple, small meals with little fat or insoluble fiber, Acidic and spicy foods avoided.
opioids, calcium channel blockers, tricyclic antidepressants, and dopamine agonists, should be stopped
Glycemic control
Pharmacologic therapy for persistent symptoms despite nonpharmacologic modifications.
First-line therapy > metoclopramide a dopamine 2 receptor antagonist stimulates antral contractions and decreases postprandial relaxation of the fundus.
domperidone, dopamine 2 antagonist, patients who do not respond to metoclopramide
Macrolide antibiotics (erythromycin and azithromycin) are motilin agonists that act by stimulating fundal contraction (second-line therapy)
H. pylori
-spiral-shaped, flagellate, gram-negative bacteria
-potent producer of urease, which is capable of splitting urea into ammonia and bicarbonate
H. pylori can also be found in heterotopic gastric mucosa
-proximal esophagus
-in Barrett esophagus
-in gastric metaplasia in the duodenum
-within a Meckel diverticulum
-in heterotopic gastric mucosa in the rectum
Mechanism of H. pylori–induced GI injury
1- Production of toxic products > breakdown products from urease activity (e.g., ammonia), cytotoxins, mucinase
2-Induction of a local mucosal immune response > proinflammatory cytokines and reactive oxygen metabolites
3- Increased gastrin levels and changes in acid secretion
4- Gastric metaplasia occurring in the duodenum.
Invasive Tests for H.Pylori
Endoscopic biopsy > gastric body and the antrum > tested for urease.
Endoscopy > biopsy gastric mucosa, > histologic visualization of H. pylori
Culturing of gastric mucosa obtained at endoscopy
Noninvasive Tests
Urea breath test :
ability of H. pylori to hydrolyze urea
discontinue antibiotics for 4 weeks and PPIs for 2 weeks
Stool Antigen :
monoclonal antibodies to H. pylori antigens to test fecal specimens
the most cost-effective method for assessing treatment efficacy.
Serology :
presence of IgG antibodies to H. pylori.
Antibody titers can remain high for 1 year or longer after eradication > not used to check Tx Efficacy
Gastric Perforation Site
Most perforations occur along the anterior aspect of the lesser curvature.
gastric outlet obstruction can also occur in which type of ulcer
in patients with type II or III gastric ulcers
Gastric Ulcer Pain Description
pain > becomes constant > deeper penetration of the ulcer.
Referral of pain to the back > penetration into the pancreas
diffuse peritoneal irritation > free perforation.
PPIs have a healing rate of
85% at 4 weeks
96% at 8 weeks