Stomach & Duodenum

Card Set Information

Author:
anders
ID:
250046
Filename:
Stomach & Duodenum
Updated:
2013-12-06 01:41:50
Tags:
Absite
Folders:
Absite
Description:
Stomach & Duodenum
Show Answers:

Home > Flashcards > Print Preview

The flashcards below were created by user anders on FreezingBlue Flashcards. What would you like to do?


  1. Describe the stomach's blood supply:
    • 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
  2. Incidence of aberrant/replaced left hepatic artery =
    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
  3. After esophagectomy, the arterial blood supply of a gastric conduit is primarily based on what vessel?
    Right gastroepiploic artery
  4. Truncal vagotomy is conventionally performed where?
    At or just above/below the diaphragmatic esophageal hiatus before giving off celiac & hepatic branches

  5. Selective vagotomy is performed where?
    Distal to the branching which spares the celiac and hepatic branches

  6. Describe divisions made during a Highly Selective Vagotomy.
    (aka Proximal Gastric or Parietal Cell Vagotomy)
    • 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.

  7. Location & product of Parietal Cells:
    Located in the gastric fundus & corpus

    Secrete hydrochloric acid, intrinsic factor
  8. Location & product of Chief Cells:
    Located in the gastric fundus & corpus

    Secrete pepsinogen
  9. Location & product of G Cells:
    Located in the antrum

    Secrete gastrin
  10. Location & product of M cells:
    Located in duodenum & jejunum

    • Secrete motilin
    • (stimulated by erythromycin)

    Motilin → stimulates upper GI motility
  11. Location & product of Delta Cells:
    Located in the gastric corpus & antrum

    Secrete somatostatin

    Somatostatin → Inhibits release of all GI hormones, inhibits enteric water & electrolyte secretion, inhibits motility
  12. Location and product of S cells:
    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
  13. Location & product of endocrine cells:
    Located in the gastric body

    Secrete ghrelin
  14. Acid secretion is stimulated by....
    Acetylcholine, histamine, and gastrin receptors on parietal cells
  15. Activation of the acetylcholine, histamine, or gastric receptors on parietal cells causes...
    Activation of the H+, K+-ATPase pump which results in the secretion of a hydrogen ion for potassium
  16. Describe the acetylcholine receptor pathway of acid secretion in parietal cells:
    Depends on specific membrane phospholipases

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

           
  17. Describe the gastrin receptor pathway of acid secretion in parietal cells:
    Depends on specific membrane phospholipases

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

           
  18. Describe the histamine receptor pathway of acid secretion in parietal cells:
    Histamine → activates adenylate cyclase → protein phosphorylation via protein kinase → activates H+, K+-ATPase pump

           
  19. Acid secretion is inhibited by...
    • Somatostatin
    • Cholecystokinin
    • Secretin
  20. Describe the 3 phases of gastric acid secretion:
    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
  21. What is the function of Secretin?
    • Induces release of water & bicarb from pancreatic ductal cells
    • Inhibits release of gastrin, gastric acid secretion, & gastric motility
  22. What is the function of Gastrin-releasing Peptide (aka Bombesin)?
    • Universal "on" switch
    • Stimulates all GI hormones except secretin, stimulates GI secretions & motility
  23. What is the function of Somatostatin?
    • Universal "off" switch
    • Inhibits release of all GI hormones, inhibits enteric water & electrolyte secretion, inhibits motility
  24. What is the function of Motilin?
    Stimulates upper GI motility
  25. What is the function of Vasoactive Intestinal Peptide (VIP)?
    Potent stimulator of intestinal secretion
  26. Administration of cholecystokinin (CCK) is used to...
    Stimulate gallbladder contraction

    Used to help diagnose biliary dyskinesia or acalculous cholecystitis
  27. Administration of pentagastrin (gastrin analogue) is used to...
    Measure maximal gastric acid secretion
  28. Administration of somatostatin (or analogue) is used to...
    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
  29. Administration of glucagon is used to...
    Relax the sphincter of Oddi to facilitate ERCP
  30. Administration of secretin is used to...
    Identify gastrinoma (causes paradoxical increase in serum gastrin levels)
  31. Measurement of pancreatic peptide (PP) in response to sham feedings is used to...
    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
  32. What factors influence gastric emptying?
    Neural and hormonal factors triggered by gastric volume & composition.

    • Faster emptying:
    • - larger volume
    • - liquids

    • Slower emptying:
    • - high lipid intake
  33. Pattern of liquid emptying is largely determined by...
    fundal tone
  34. Disorders of gastric emptying can be divided into rapid or delayed emptying.
    Causes of delayed emptying (more common):
    • mechanical obstruction
    • metabolic derangements (myxedema, hyperglycemia)
    • electrolyte abnormalities (hypokalemia, hypocalcemia)
    • drugs (narcotics, anticholinergics)
    • systemic diseases (DM, scleroderma)
    • iatrogenic - postvagotomy (40%)
  35. Disorders of gastric emptying can be divided into rapid or delayed emptying.
    Causes of rapid emptying:
    • previous gastric resection
    • impaired fat absorption (pancreatic insufficiency, short bowel syndrome)
    • hypergastrinemia (Zollinger-Ellison syndrome)
  36. Helicobacter pylori infection is associated with what percentage of duodenal and gastric ulcers?
    • 90-95% of duodenal ulcers
    • 75-80% of gastric ulcers
  37. Helicobacter pylori infection is associated with what conditions?
    • duodenal/gastric ulcers
    • chronic atrophic gastritis (which can lead to gastric cancer)
    • mucosa-associated lymphoid tissue lymphoma (MALT)

    [Negative association with GERD]
  38. Helicobacter pylori infection diagnosis:
    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
  39. Test of choice to demonstrate eradication of H. pylori =
    Urea breath test

    (Serologic tests cannot distinguish between active infection and previous exposure)
  40. What is the normal mean basal acid output?

    What is the expected acid response to pentagastrin administration?
    1-8mmol/hr

    6-40mmol/hr
  41. Conditions associated with hypergastrinemia & increased acid secretion:
    • Zollinger-Ellison syndrome (>1000pg/mL)
    • antral G-cell hyperplasia
    • retained antrum
    • gastric outlet obstruction
    • short bowel syndrome
    • renal failure
  42. Conditions associated with hypergastrinemia & normal/low acid secretion:
    • pernicious anemia
    • postvagotomy states
    • chronic gastritis
    • gastric cancer
    • pharmacologic acid suppression
    • duodenal ulcer (although may be elevated postprandially)
  43. How to differentiate Zollinger-Ellison syndrome from G-cell hyperplasia:
    serum gastrin response to provocative testing

    Administer secretin → pronounced increase in serum gastrin  = ZE
  44. Major cause of duodenal ulcers in H pylori negative patients =
    NSAIDS

    also associated with older age, multiple medical problems, and sepsis
  45. Surgical procedure for duodenal ulcer with the lowest recurrence rate =
    Truncal vagotomy and antrectomy

  46. Post operative symptoms associated with antrectomy, pyloroplasty, or truncal vagotomy:
    • diarrhea
    • bile reflux
    • post-prandial dumping syndrome
  47. Advantage & disadvantages of highly selective vagotomy for duodenal ulcers:
    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%)
  48. Treatment of perforated duodenal ulcer =
    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
  49. What percentage of perforated duodenal ulcers do NOT demonstrate pneumoperitoneum on abdominal CT?
    20%
  50. Treatment of perforated gastric ulcer =
    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)]
  51. Most common  cause of gastric outlet obstruction in adults =
    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
  52. What is the classic metabolic abnormality resulting from gastric outlet obstruction and prolonged vomiting?
    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

  53. What endoscopic ulcer characteristic has the highest risk for recurrent bleeding?
    • 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%)
  54. During an operation for a bleeding duodenal ulcer, three-point "U" stitches are placed to ligate which arteries after a longitudinal pyloroduodenenotomy?
    Proximal and distal gastroduodenal and transverse pancreatic arteries

What would you like to do?

Home > Flashcards > Print Preview