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Flashcards in Alimentary Tract - Stomach Deck (49):

gastric arterial supply

  • right and left gastrics - lesser curvature
  • right and left gastroepiploics - greater curvature 
  • short gastrics - fundus



gastric venous system

  • right and left gastric veins - portal
  • right gastroepiploic - SMV
  • left gastroepiploic - splenic 


duodenal blood supply

  • first and second portions - celiac axis, GDA, superior pancreaticoduodenal artery 
  • third and fourth portions - SMA, inferior pancreaticoduodenal artery 
  • venous drainage parallels arterial supply 


The vagus nerve is the predominant branch of the parasympathetic nervous system within the foregut. Describe its 

  • There are left anterior and right posterior branches at the esophageal hiatus.
  • The left anterior branch innervates the liver via the hepatic branch and the anterior lesser curvature as the nerve of Latarjet.
  • The right posterior branch supplies the celiac plexus and the posterior lesser curvature. The criminal nerve of Grassi is a branch of the posterior vagus supplying the fundus.


What is the sympathetic innervation to the stomach?

T5 to T10 travel to the celiac ganglion and onward to the stomach


List the different types of gastric glands and what they secrete

  • Mucous cells: mucous and bicarb
  • Parietal cells: secrete acid and intrinsic factor
  • Chief cells: secrete pepsinogen
  • G cells: secrete gastrin
  • Enterochromaffin-like (ECL) cells: secrete histamine
  • D cells: secrete somatostatin


What are the histological layers of the stomach?

  • mucosa: secretory cells - columnar glandular epithelial
  • submucosa: NV and lymph structures, Meissner's plexus, collagen
  • musculris propria: inner circular muscle, outer longitudinal, Auerbach's plexus
  • serosa: visceral peritoneum


most bleeding duodenal ulcers represent posterior erosions into...



surgical options for bleeding vessel associated with PUD

suture ligation +/- definitive ulcer operation (eg HSV)

may require distal gastrctomy or vagotomy and drainage


normal stimulatory mechanisms for acid secreting cells in the stomach

parietal cells secrete acid 2/2 stimulation from

  1. acetylcholine from vagus
  2. gastrin from G cells
  3. histamine from ECL cells


what is the normal negative feedback for stomach acid secretion

somatostatin release from D cells → inhibits ECL (histamine) and G cells (gastrin) → inhibits parietal cell acid secretion


physiologic protective mechanisms the stomach utilizes to remain intact

mucus cells - secrete bicarb and mucus


a patient has a bleeding peptic ulcer, what are risk factors that must be identified

  • H pylori
  • aspirin
  • ZES
  • trauma
  • burn
  • cigarette smoking
  • psychosocial stress
  • cocaine


what is the HPI of a patient with a peptic ulcer

abd pain, nausea, vomiting, dyspepsia, reflux, weight loss

history of H. pylori infection or NSAID/aspirin use

gastric ulcer: pain when eating

duodenal ulcer: post-prandial pain

exam: epigastric tenderness, heme-positive stool


Diagnostic testing in a patient with suspected peptic ulcer

  • labs: CBC, BMP, gastric, ELISA H. pylori (90% sens/spec)
  • imaging: upper GI XRs (can show ulcer craters), consider CT depending on psx
  • EGD w/ biopsies
  • urea breath test can be used to document eradication


treat uncomplicated peptic ulcer disease w/ neg H pylori

can use PPI, H2 blocker, antacid, sucralfate

smoking cessation

avoid NSAID/aspirin


treat uncomplicated peptic ulcer disease w/ H pylori

multiple versions of triple therapy available, including the following

  • PPI + clarithromycin + amoxicillin
  • PPI + clarithromycin + metronidazole


Describe the medical and endoscopic treatment for acute hemorrhage or gastric outlet obstruction secondary to peptic ulcer disease

  • Hemorrhage: upper endoscopy for diagnosis and hemostasis via epinephrine injection, electrocautery, or clip application.
  • Obstruction: endoscopic balloon dilation


Describe the indications for operative intervention of peptic ulcer disease

bleeding uncontrolled by endoscopic therapy, bleeding in a hemodynamically unstable patient, transfusion requirement of >4–6 units of blood, perforation, obstruction, or ulcer disease refractory to maximal medical therapy


Describe historic acid-reducing surgical procedures:

Truncal vagotomy

Involves dividing the left and right vagus nerves just proximal to the GE junction, thus sacrificing the hepatic and celiac branches.  A drainage procedure is usually performed as well, either the Heineke-Mikulicz or Finney pyloroplasty or a Jaboulay gastroduodenostomy.


Describe historic acid-reducing surgical procedures:

selective vagotomy

more distal division of the vagus nerves beyond the takeoff of the hepatic and celiac branches


Describe historic acid-reducing surgical procedures: HSV

Denervation of the parietal cells of the body and fundus. Since the antrum is not denervated drainage procedures are not required. The nerves of Latarjet are identified and the branches providing innervation to the body and fundus are divided, leaving the antral innervation (“crow’s feet”) intact. This line of division proceeds from 5 cm proximal to the esophagus to about 7 cm proximal to the pylorus. The criminal nerve of Grassi should be identified and divided.

This procedure has the highest recurrence but lowest morbidity.


Describe historic acid-reducing surgical procedures: Vagotomy and drainage

Truncal vagotomy and pyloroplasty or gastroduodenostomy.  Denervation of the antrum and pylorus followed by bypassing the denervated area via gastroduodenostomy or pyloroplasty. Side effects include dumping syndrome, diarrhea, marginal ulceration


Describe historic acid-reducing surgical procedures: Vagotomy and antrectomy

More commonly indicated for gastric ulcer disease than peptic ulcer disease. Antrectomy must be followed by gastroduodenostomy (Billroth I) or gastrojejunostomy (Billroth II). Billroth I procedures are preferred when possible due to lower complication rates. This procedure has the highest rate of post-procedure complications such as dumping syndrome and alkaline reflux gastritis but the lowest recurrence rates.


Describe complications of PUD operaiton: dumping syndrome

Rapid passage of hypertonic food bolus from stomach into the small intestine causes extracellular to intraluminal fluid shifts, causing intestinal distension, nausea, vomiting, crampy abdominal pain, palpitations, tachycardia, diaphoresis, flushing, dizziness as a result of autonomic stimulation and hormone release. Early symptoms usually occur 20–30 minutes after eating. Late dumping is due to the rapid delivery of carbohydrates to the intestines triggering hyperglycemia and resultant hyperinsulinemia which can then precipitate severe hypoglycemia. The catecholamine response causes lightheadedness, tachycardia, diaphoresis, and sometimes altered mental status. To prevent this, patients should avoid large carbohydrate heavy meals and avoid having liquids with meals. Some patients require octreotide. In some cases Roux-en-Y reconstruction is necessary.


Describe complications of PUD operaiton: Afferent loop syndrome

Due to obstruction of the afferent loop, causing distension, abdominal pain and cramps, reflux of intestinal contents into the stomach, and bilious emesis. Blind loop syndrome can result from bacterial overgrowth causing vitamin B12 deficiency. Acute complete occlusion is a surgical emergency putting the bowel at risk of ischemia and perforation. Diagnosis can be obtained via upper endoscopy with inability to visualize the afferent loop. Correction involves Roux-en-Y reconstruction with shorter afferent loop.


Describe complications of PUD operaiton: Efferent loop obstruction

Less common. Presents with abdominal pain, bilious emesis, distension. Diagnosed via upper GI contrast study with lack of contrast transit. Requires surgical correction as it is usually due to internal herniation of the efferent loop or adhesive disease (form of SBO).


Describe complications of PUD operaiton: Alkaline reflux gastritis

Due to reflux of bile into the stomach. Can be diagnosed clinically or via endoscopy or HIDA scan. More common in V + A with Billroth II reconstruction. Bile acid sequestrants such as cholestyramine may help but Roux-en-Y conversion may be required.


Describe complications of PUD operaiton: Delayed gastric emptying

Due to gastric atony, but most rule out metabolic, neurogenic, and anatomic causes. Seen more commonly in truncal or selective vagotomies. Usually affects emptying of food only, not liquids. Can be treated with metoclopramide, erythromycin, or resection in severe cases.


Describe complications of PUD operaiton: Marginal ulceration

Due to exposure of gastric G-cells to alkaline duodenal secretions, causing acid hypersecretion and recurrent ulceration at the anastomosis. Can be treated with PPIs or surgical resection of gastric remnant with hyperplastic G-cells or vagotomy.


Describe complications of PUD operaiton: Diarrhea

Can be due to bile acid or fat malabsorption, bacterial overgrowth, or dumping syndrome. Usually treated medically.


Describe the potential operative procedures for perforated gastric ulcers

Small perforations can be closed primarily with an omental patch. Perforations >1 cm should be repaired with a Graham patch in which a piece of omentum is sutured in place over the perforation. Some surgeons perform acid-reducing procedures in stable patients.


Describe the potential operative procedures for GI ulcers with acute hemorrhage

The most common bleeding vessel is the gastroduodenal artery from a posterior ulcer. The vessel should be oversewn and a Heineke-Mikulicz pyloroplasty performed. The duodenum is opened longitudinally across the pylorus, the vessel is oversewn with a three-point stitch, and the duodenotomy is closed transversely.


Describe the potential operative procedures for GI ulcers w/ GOO

Usually requires vagotomy and antrectomy with gastrojejunostomy. Cancer must be ruled out as the underlying cause.


Identify the areas of nodal drainage for gastric tumors and describe what nodal basins contribute to a D1, D2, D3 and D4 surgical resection.

  • D1: perigastric nodes along lesser/greater curvature (stations 1-6, N1)
  • D2: D1 plus nodes along left gastric artery, common hepatic artery, celiac trunk, splenic hilum, and splenic artery (stations 7-11, N2)
  • D3: D2 plus nodes along the hepatoduodenal ligament near porta hepatis, retropancreatic space, and along the root of the SMA/SMV extending to vessels of the transverse mesocolon (stations 12-15, N3).
  • D3 - often described as including peri-aortic nodes AND LNs along porta hepatis/root of the mesentery.
  • D4: D3 plus peri-aortic LNs (station 16)


Identify patient populations at risk for gastric cancer.

  • men, 70s, Asian
  • diets w/ salt and smoked meats, nitrates
  • smokers
  • H pylori
  • hereditary diffuse gastric ca, FAP, Li-Fraumeni, HNPCC
  • pernicious anemia
  • large polyps


Signs and symptoms of gastric cancer

  • constant epigastric pain unaffected by food
  • fatigue, weight loss, early satiety
  • dysphagia if proximal
  • obstruction if distal
  • iron deficiency anemia, unlikely frank hematemesis 
  • non-healing gastric ulcers


For gastric cancer is the number or location of lymph nodes more prognostic? What is N-stage based on?

Number. N-stage is based on number.


How many lymph nodes are required for accurate staging in gastric cancer? How many are recommended?

15 is accurate, 30 is recommended


What extent of lymph node resection should be done (D1-4)?

D1 vs D2.

Western studies show higher mortality w/ D2 w/o benefit.

Japanese studies show increased recurrence-free survival w/o increased morbidity.

Prefer D2 at high-volume centers.


What is the role of chemo and radiation?

Adjuvant chemo/XRT shows increased survival


DDx in a patient w/ epigastric pain, weight loss, iron deficiency anemia.

PUD, GERD, DGE, biliary dysfunction (e.g., cholecystitis, cholangitis, biliary dyskinesia), pancreatitis, pancreatic neoplasm, MI or dysrhythmia, hepatitis, gastric outlet obstruction, perforation, mesenteric ischemia, IBD, viral or bacterial gastritis/enteritis, SBP, AAA, constipation, diverticulosis/diverticulitis.


What is the definitive diagnostic test for patients with suspected gastric cancer?

Endoscopy w/ EUS and biopsy


In a patient with biopsy-proven gastric carcinoma, describe the proper workup for lymph node metastasis needed for adequate staging.

  • CT  abd/pelvis required for mets and can help with T/N staging.
  • EUS is superior for T staging and possible nodal involvement (N), and is recommended if no M1 disease is present on CT (NCCN guidelines)
  • Perform FNA of suspicious nodes as it increases staging accuracy.
  • PET/CT is clinically indicated or recommended by multidisciplinary board.


Given a patient with localized biopsy-proven gastric carcinoma, select the extent of gastrectomy and lymphadenectomy that appropriately treats and accurately stages the disease.

  • Resection is based on location: distal gastrectomy is appropriate for distal tumors including body and antrum; proximal transection at incisura w/ 6-cm margins, distal transection point is proximal duodenum w/ 2-cm margins; reconstruction w/ Billroth II vs. Roux-en-Y
  • Tumors of gastric body require total gastrectomy w/ Roux-en-Y.
  • For proximal tumors of cardia or fundus - prefer total gastrectomy, some advocate for proximal gastrectomy.
  • D2 nodal dissection should be attempted if technically capable.


Given a patient with distant metastases from gastric carcinoma, implement an appropriate overall therapeutic strategy for disease management, in cooperation with oncology consultants.

  • Prognosis is poor; some studies quote 3- to 5-month median survival.
  • Asymptomatic unresectable patients may opt for chemotherapy; triple therapy with 5FU, cisplatin, and anthracycline-based compound (epirubicin) is recommended; for those with increased age or comorbidities, dual or single agent therapy is appropriate.
  • Symptomatic unresectable patients may be resected for palliation of symptoms; endoscopic stent placement is also an option.


Implement an appropriate surveillance follow-up plan for a patient who has completed primary and adjuvant therapy for a locally confined gastric carcinoma.

  • Per NCCN guidelines: all stages require H&P q3–6 months for 1-2 years, q6–12 months for 3–5 years, annually thereafter w/ CBC and CMP prn.
  • For endoscopic resection: endoscopy q6 months for 1 year, annually for 3 years thereafter; for partial gastrectomy, EGD as clinically indicated
  • For pathologic stage II or greater: CT chest/abd/pelvis q6–12 months for 2 years, annually for up to 5 years; consider PET/CT on individual patient basis or provider preference; CT C/A/P as needed if lower than stage II.


Given a patient with a defined stage of gastric carcinoma who has undergone successful resectional therapy, explain the likelihood and potential modes of recurrent disease, ensuring accurate patient understanding.

  • Recurrence rates range from 40–80% and most occur within the first 3 years.
  • Peritoneal dissemination occurs ~54% vs. locoregional recurrence at 38–45%.
  • Locoregional recurrence is typically at anastomotic site, gastric bed or regional LNs; hematogenous spread can occur, commonly to liver, lung or bone.


What is the neoadjuvant therapy for stage III gastric cancer?

Perioperative chemotherapy is given in the neoadjuvant setting in contrast to adjuvant therapy that consists of chemotherapy plus radiation.

Common chemotherapy regimen consists of: Epirubicin, Cisplatin and 5-Fluorouracil.