Stomach & Duodenum

• 
• Celiac trunk → left gastric artery → lesser curve
• Celiac trunk → common hepatic artery → right gastric artery OR GDA → right gastric artery → lesser curve
• Celiac trunk → common hepatic → GDA → right gastroepiploic artery → greater curve
• Celiac trunk → splenic artery → left gastroepiploic artery → greater curve
• Celiac trunk → splenic artery → short gastric arteries → fundus
• Inferior phrenic arteries → fundus

Originates from the left gastric artery 15-24%

Runs in the gastrohepatic ligament

Can represent the only arterial blood supply to the left hepatic lobe

Right gastroepiploic artery

At or just above/below the diaphragmatic esophageal hiatus before giving off celiac & hepatic branches

Distal to the branching which spares the celiac and hepatic branches

• Division of the terminal branches of the nerve of Latarjet in the fundus and corpus of the stomach.  
• Spares the vagal branches to the antrum and pylorus, which control gastric motility and emptying - thus obviating need for a drainage procedure.

Located in the gastric fundus & corpus

Secrete hydrochloric acid, intrinsic factor

Located in the gastric fundus & corpus

Secrete pepsinogen

Located in the antrum

Secrete gastrin

Located in duodenum & jejunum

• Secrete motilin
• (stimulated by erythromycin)

Motilin → stimulates upper GI motility

Located in the gastric corpus & antrum

Secrete somatostatin

Somatostatin → Inhibits release of all GI hormones, inhibits enteric water & electrolyte secretion, inhibits motility

Located in duodenum & jejunum

Secrete secretin 

secretin → induces release of water & bicarb from pancreatic ductal cells, also inhibits release of gastrin, gastric acid secretion, & gastric motility

Located in the gastric body

Secrete ghrelin

Acetylcholine, histamine, and gastrin receptors on parietal cells

Activation of the H⁺, K⁺-ATPase pump which results in the secretion of a hydrogen ion for potassium

Depends on specific membrane phospholipases

Increases intracellular calcium levels → phosphorylase kinase-induced phosphorylation → activates H⁺, K⁺-ATPase pump

       

Depends on specific membrane phospholipases

Increases intracellular calcium levels → phosphorylase kinase-induced phosphorylation → activates H⁺, K⁺-ATPase pump

       

Histamine → activates adenylate cyclase → protein phosphorylation via protein kinase → activates H⁺, K⁺-ATPase pump

       

• Somatostatin
• Cholecystokinin
• Secretin

Cephalic phase - mediated by vagus nerve → Ach → parietal cells release HCl & G cells release gastrin

Gastric phase - initiated by gastric distention, intraluminal peptides, & amino acids → G cells release gastrin

Intestinal phase - thought to be mediated by duodenal gastrin & enterooxyntin (accounts for 10% of acid secretion)

Luminal acidity releases secretin & somatostatin which inhibit acid secretion

• Induces release of water & bicarb from pancreatic ductal cells
• Inhibits release of gastrin, gastric acid secretion, & gastric motility

• Universal "on" switch
• Stimulates all GI hormones except secretin, stimulates GI secretions & motility

• Universal "off" switch
• Inhibits release of all GI hormones, inhibits enteric water & electrolyte secretion, inhibits motility

Stimulates upper GI motility

Potent stimulator of intestinal secretion

Stimulate gallbladder contraction

Used to help diagnose biliary dyskinesia or acalculous cholecystitis

Measure maximal gastric acid secretion

Inhibit the release of GI hormones in the following conditions:

• - Zollinger-Ellison syndrome
• - VIPoma
• - Insulinoma
• - carcinoid tumors
• - pancreatic fustulas
• - pancreatic ascites
• - enterocutaneous fistulas
• - GI bleed

Relax the sphincter of Oddi to facilitate ERCP

Identify gastrinoma (causes paradoxical increase in serum gastrin levels)

Evaluate intact vagal nerve function

Food stimulates release of pancreatic peptide via efferent vagal activity.  This increase is not seen if there has been a vagotomy

Neural and hormonal factors triggered by gastric volume & composition.

• Faster emptying:
• - larger volume
• - liquids

• Slower emptying:
• - high lipid intake

fundal tone

• mechanical obstruction
• metabolic derangements (myxedema, hyperglycemia)
• electrolyte abnormalities (hypokalemia, hypocalcemia)
• drugs (narcotics, anticholinergics)
• systemic diseases (DM, scleroderma)
• iatrogenic - postvagotomy (40%)

• previous gastric resection
• impaired fat absorption (pancreatic insufficiency, short bowel syndrome)
• hypergastrinemia (Zollinger-Ellison syndrome)

• 90-95% of duodenal ulcers
• 75-80% of gastric ulcers

• duodenal/gastric ulcers
• chronic atrophic gastritis (which can lead to gastric cancer)
• mucosa-associated lymphoid tissue lymphoma (MALT)

[Negative association with GERD]

Endoscopic mucosal biopsy (gold standard) with histologic exam (s&s 90%), rapid urease test, & culture (only if suspicious of abx resistance)

Noninvasive tests: urea breath test (s&s 95%), serology

Urea breath test

(Serologic tests cannot distinguish between active infection and previous exposure)

1-8mmol/hr

6-40mmol/hr

• Zollinger-Ellison syndrome (>1000pg/mL)
• antral G-cell hyperplasia
• retained antrum
• gastric outlet obstruction
• short bowel syndrome
• renal failure

• pernicious anemia
• postvagotomy states
• chronic gastritis
• gastric cancer
• pharmacologic acid suppression
• duodenal ulcer (although may be elevated postprandially)

serum gastrin response to provocative testing

Administer secretin → pronounced increase in serum gastrin  = ZE

NSAIDS

also associated with older age, multiple medical problems, and sepsis

Truncal vagotomy and antrectomy

• diarrhea
• bile reflux
• post-prandial dumping syndrome

Denervates parietal cell-bearing portion but preserves innervation of pyeloroantral region

Advantage - more normal gastric emptying, lowest mortality, lowest incidence of side effects

Disadvantage - highest recurrence rate (5-15%)

Omental patch (Graham patch) of the perforation without primary closure of defect.

Non-operative treatment is reserved for old contained perforations or terminally ill patients who are too unstable for surgery

20%

Excision of ulcer to rule out malignancy.

1/3 have no further problems, 1/3 have recurrence amenable to medical management, 1/3 require reoperation

[Can also do omental patch with biopsy of ulcer edges. (Source)]

Cancer

• Adenocarcinomas of the pancreas, stomach, and duodenum (decreasing order of frequency) are the leading cause.
• Other causes: Gastrointestinal stromal tumors (GIST), primary lymphomas, extrinsic compression from metastatic disease to the porta hepatis

hypochloremic, hypokalemic metabolic alkalosis

• barf → loss of HCl → decreased Cl & mild alkalosis → compensated by renal excretion of bicarb
• continued barfing → severe extracellular fluid deficit → kidneys conserve Na+ & H2O by excreting hydrogen (?), potassium, & bicarb
• Alkaline serum pH → ionized calcium (mildly alkaline) shifts to non-ionized form

• Active arterial bleeding (~100%)
• Non-bleeding "visible vessel" (~50%)
• Non-bleeding ulcer with an overlying clot (~30-35%)
• Oozing ulcer (~10%-27%)
• Clean based ulcer (<3%)

Proximal and distal gastroduodenal and transverse pancreatic arteries