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2012-01-07 18:00:39

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  1. What is transit time through the stomach?
    3-4 hours
  2. Where does peristalsis occur in the stomach?
    occurs only in the distal stomach
  3. How is gastroduodenal pain sensed?
    Gastroduodenal pain sensed through afferent sympathetic fibers T5-T10
  4. Whats the blood supply to the stomach?
    Celiac Trunk- left gastric, common hepatic artery, splenic artery

    Left gastroepiploic and short gastric are branches of splenic artery

    Greater curvature- right and left gastroepiploics, short gastrics

    Lesser curvature- right and left gastrics

    Right gastric is a branch of the common hepatic artery

    Pylorus- gastroduodenal artery
  5. Describe the histology of the mucosa of the stomach
    Mucosa- lined with simple columnar epithelium
  6. Cardia glands
    mucus secreting
  7. What are the glands of the fundus and body of the stomach, what do they secrete?
    Fundus and body (oxyntic) glands

    Chief cells- pepsinogen
    (1st enzyme in proteolysis)

    Parietal cells- release H+ and intrinsic factor

    - Acetylcholine, gastrin and histamine cause HCl release

    - Acetylcholine (vagus) and gastrin act on phospholipase--> PIP--> DAG+IP3 to increase Ca; activates phosphorylase kinase--> increase HCl production

    - Histamine acts on adenylate cyclase--> cAMP--> protein kinase A to increase HCl

    Phosphorylase kinase and protein kinase C phosphorylate H/K ATPase to increase acid production

    Omeprazole blocks H/K ATPase in parietal cell membrane (final pathway for H+ release)

    Inhibitors of parietal cells- somatostatin, secretin, PGE1, and CCK

    Intrinsic factor- binds B12 and the complex is reabsorbed in the terminal ileum

  8. What are the atrum and pylorus glands?
    • * Mucus and HCO3 secreting glands- protect stomach
    • G-cells release Gastrin- why antrectomy is helpful
    • - inhibited by H+ in duodenum
    • - stimulated by aminoacids, acetylcholine

    secrete somatostatin; inhibit gastrin and acid release

    Brunner's glands- in duodenum; secrete pepsinogen and alkaline mucus

    Somatostatin, CCK, and secretin- released with antral and duodenal acidification

  9. What increases acid and gastrin?
    • 1. ZES
    • 2. antral cell hyperplasia
    • 3. retained antrum
    • 4. renal failure
    • 5. gastric outlet obstruction
    • 6. short bowel syndrome
  10. What causes increased gastrin and normal/decreased acid?
    • 1. pernicious anemia
    • 2. chronic gastritis
    • 3. gastric Ca
    • 4. postvagotomy
    • 5. medical acid suppression
  11. What causes rapid gastric emptying?
    • 1. previous surgery (#1)
    • 2. ZES
    • 3. ulcers
  12. What causes delayed gastric emptying?
    • 1. opiates
    • 2. anticholinergics
    • 3. myxedema (hypothyroidism)
    • 4. hyperglycemia
    • 5. diabetes
  13. Billroth I-
    Billroth II-
    • Billroth I- antrectomy with gastroduodenal anastomosis
    • Billroth II- antrectomy with gastrojejunal anastomosis
  14. What are trichobezoars?
    • hair- hard to pull out
    • Tx: EGD generally inadequate; likely need gastrostomy and removal
  15. What are phytobezoars?
    • fiber- often in diabetics with poor gastric emptying
    • Tx: enzymes, EGD, diet changes
  16. What will be more likely to give you marginal ulceration and diarrhea?
    Billroth I and II versus Roux-en-Y gastrojejunostomy
  17. Whats a dieulafoy's ulcer?
    vascular malformation (large tortuous arteriole in the stomach wall that erodes and bleeds)
  18. Whats menetrier's disease?
    mucous cell hyperplasia, increased rugal folds
  19. Gastric Voluvulus
    • 1) Associated with type II (paraesophageal) hernia
    • 2) Nausea without vomiting; severe pain, usually organoaxial volvulus
    • Tx: reduction and Nissen
  20. Mallory Weiss Tear
    • 1) secondary to forceful vomiting
    • 2) presents as hematemesis following severe retching
    • 3) bleeding often stops spontaneously
    • 4) Dx/Tx: EGD; tear is usually near lesser curvature of the stomach (near GE junction), PPI, transfusion
    • 5) If continuous bleeding, may need gastrostomy and oversewing of the vessel
  21. Vagotomies
    • Vagal denervation- all forms increase liquid emptying--> vagally mediated receptive relaxation is removed
    • * results in increased gastric pressure that accelerates liquid emptying

    • Truncal vagotomy- divides vagal truncks at level of esophagus
    • Selective Vagotomy- divides nerves of Latarjet
    • Highly selective (proximal) vagotomy- divides individual fibers, preserves "crow's foot"

    • Complete vagotomy (truncal or selective)- decreased emptying of solids
    • Highly selective vagotomy- normal emptying of solids
    • Addition of pyloroplasty to either of the above results in increased solid emptying

    • Other physiologic alterations caused by truncal vagotomy:
    • -Gastric effects- decreased acid output by 90%, increased gastrin, gastrin cell hyperplasia
    • -Nongastric effects-
    • 1- decreased exocrine pancreas function
    • 2- decreased postprandial bile flow
    • 3- increased gallbladder volumes
    • 4- decreased release of vagally mediated hormones

    • Diarrhea (30-50%)- most common problem following vagotomy
    • - caused by sustained MMCs forcing bile acids into colon
  22. Upper gastrointestinal bleeding:
    • Risk Factors:
    • 1. previous UGI bleed
    • 2. peptic ulcer disease
    • 3. NSAID use
    • 4. smoking
    • 5. liver disease
    • 6. esophageal varices
    • 7. splenic vein thrombosis
    • 8. sepsis
    • 9. burn injuries
    • 10. trauma
    • 11. severe vomiting

    • 1st NGT and EGD to confirm bleeding is from ulcer, can potentially treat the ulcer with EGD
    • - EGD for bleeding duodenal ulcer- does not change mortality or operative rates; most important predictor of continued or recurrent bleeding is bleeding at time of EGD.

    If patient hypotensive despite resuscitation and thought to be bleeding from ulcer--> go to OR

    Having trouble localizing bleeding source--> tagged RBC scan

    • Biggest risk factor for rebleeding at time of EGD:
    • #1- spurting blood vessel (60% chance of rebleed)
    • #2- visible blood vessel (40% chance of rebleed)
    • #3- diffuse oozing (30% chance of rebleed)

    • Patient with liver failure is likely bleeding from esophageal varices, not an ulcer
    • Tx: EGD with sclerotherapy or TIPS, no OR
  23. Duodenal Ulcers
    increased acid production and decreased defense
  24. Pathogenesis of peptic ulcer:
    What are the endocrine consequences of H. Pylori infection:
    • 1. Increased basal serum gastrin
    • 2. Increased gastrin response to a meal
    • 3. Increased responsiveness to gastrin-releasing peptid
    • 4. Production of N-alpha methylhistamine
    • 5. Decreased density of somatostatin cells
    • 6. Decreased mucosal somatostatin content
  25. Pathogenesis of peptic ulcer
    Gastric Acid sectretion:
    • 1. Increased acid secretory capacity
    • 2. Increased basal secretion
    • 3. Increased pentagastrin-stimulated output
    • 4. Increased meal response
    • 5. Abnormal gastric emptying
  26. Pathogenesis of peptic ulcer
    Mucosal defense:
    • 1. Decreased duodenal bicarbonate production
    • 2. Decreased gastric mucosal prostaglandin production

    • Environment:
    • Cigarrette Smoking
    • NSAIDs
  27. Duodenal Ulcers:
    1. Most frequent peptic ulcer; more common in men

    • 2. Usually 1st part of the duodenum; usually anterior
    • - anterior ulcers perforate
    • - posterior ulcers bleed from gastroduodenal artery
    • 3. Symptoms: epigastric pain radiating to the back; abates with eating but recurs 30 min after

    • 4. Dx. endoscopy
    • 5. Tx:
    • H2 blockers (cimetidine, ranitidine)
    • H-pump inhibitor (omeprazole)
    • triple therapy for patients with H. pylori on biopsy--> bismuth salts, amoxicillin, metronidazole/tetracyclin (BAM/BAT)

    6. Surgery for ulcer rarely indicated since introduction of proton pump inhibitors

    • Surgical Indications
    • 1) perforation
    • 2) protracted bleeding despite EGD therapy
    • 3) obstruction
    • 4) intractability despite medical therapy
    • 5) inability to rule out cancer (ulcer remains despite treatment)--> requires resection of ulcer

    7. If patient has been on proton pump inhibitor therapy, acid-reducing surgical procedure is required in addition to surgery for the complication.

    8. need to rule out gastrinoma in patients with complicated ulcer disease

    • 9. Surgical options
    • 1. Truncal vagotomy and pyloroplasty
    • 2. Truncal vagotomy and antrectomy with Billroth I or Billroth II- best surgery for prevention of recurrence
    • 3. Proximal or highly selective vagotomy- lowest rate of postoperative complications, 10% recurrence, no need for antral or pylorus procedure.
  28. Name complications of duodenal ulcers:
    • Bleeding
    • 1. most frequent complication of duodenal ulcers
    • 2. usually minor but can be life-threatening
    • 3. Major bleeding- >6units of blood in 24hrs or patient remains hypotensive despite transfusion
    • 4. Tx: EGD 1st- sclerose, cauterize; vasopressin, omeprazole

    • Surgical options
    • 1. duodenostomy and gastroduodenal artery ligation
    • 2.avoid hitting common bile duct with GDA ligation
    • 3. if patient has been on H-pump inhibitor therapy, need surgical ulcer procedure as well --> truncal vagotomy and pyloroplasty probably best option (does not get rid of ulcer).
    • 4. can consider highly selective vagotomy as an alternative.

    • Obstruction
    • 1. serial dilation is the initial treatment of choice
    • Surgical options
    • - if near the ampulla of vater or if removing ulcer would be very difficult--> gastrojejunostomy (billroth II, bypasses obstruction), antrectomy, and truncal vagotomy--> probably best option for most patients
    • - if proximal to ampulla of Vater--> antrectomy (with ulcer excision) with Billroth II and truncal vagotomy

    • Perforation
    • 1. 80% will have free air
    • 2. Patients usually have sudden sharp epigastric pain; can have generalized peritonitis
    • 3. Pain can radiate to the pericolic gutters with dependent drainage of gastric content
    • 4. Elderly- some believe that elderly, high-risk patients can be safely observed
    • -Need to get UGI to make sure that the perforation has sealed

    • Surgical options
    • -Graham patch and highly selective vagotomy- probably best option for most if patient has been on H-pump inhibitor; otherwise just do a Graham patch and place on omeprazole.
    • - truncal vagotomy and pyloroplasty- need to include ulcer in pyloroplasty
    • - truncal vagotomy and antrectomy with billroth I or II- need to include ulcer

    • Intractability
    • 1. > 3months without relief while on H-pump inhibitor therapy or recurrence <1 year after medical therapy
    • 2. Based on EGD mucosal findings, not symptoms
    • Surgical options:
    • * Highly selective vagotomy (does not get rid of ulcer)- probably best option for most patients
    • * Truncal vagotomy and pyloroplasty (does not get rid of ulcer)
    • * Truncal vagotomy and antrectomy with Billroth I or Billroth II
  29. Zollinger-Ellison Syndrome:
    • 1. Pancreatic tumors <2cm can be enucleated
    • 2. Secretin test results in high gastrin level
    • 3. Can often be multiple and metastatic
    • 4. Blind pancreatic resections are generally not indicated
    • 5. When the tumor is not resectable, total gastrectomy best for long-term quality of life
    • 6. Resection and ablation of metasases are important for palliation and decreased need for drug treatment
  30. Gastric Ulcers
    • 1. Older men, slow healing
    • 2. Risk factors:

    • 1. male
    • 2. tobacco
    • 3. EtOH
    • 4. NSAIDs
    • 5. H. Pylori
    • 6. Uremia
    • 7. Stress (burns/sepsis/trauma)
    • 8. Steroids
    • 9. Chemotherapy

    3. Most (type I and type IV) have normal acid secretion, due to abnormal mucosal defense

    4. 70-80% on lesser curvature of the stomach

    5. Hemorrhage is associated with higher mortality than duodenal ulcers

    6. Symptoms: epigastric pain radiating to the back; relieved with eating but recurs 30min later; melena or guiac-positive stools

    7. CLO test- test for H. pylori --> detects urease released from H. pylori

    8. Biopsy for H. pylori needs to be from the antrum

    • 9.
    • Type A blood- assocaited with type I ulcers
    • Type O blood- associated with type II-IV ulcers

    • 10. Surgical Indications
    • 1. perforation
    • 2. bleeding
    • 3. obstruction
    • 4. cannot exclude malignancy
    • 5. intractability; >3 months without relief or 2nd recurrence (based on mucosal findings)

    • Type I- lesser curvature along the body of the stomach; due to decreased mucosal protection
    • Type II- 2 ulcers (lesser curve and duodenal); similar to duodenal ulcer with high acid secretion
    • -Tx: distal gastrectomy with Billroth I or Billroth II and truncal vagotomy probably best option
    • - alternative--> truncal vagotomy and pyloroplasty (does not get rid of ulcers)
    • Type III- prepyloric ulcer; similar to duodenal ulcer with high acid secretion; increased bleeding
    • Tx: distal gastrectomy with Billroth I or Billroth II and truncal vagotomy probably best option
    • - Alternative --> truncal vagotomy and pyloroplasty (does not get rid of ulcer)
    • Type IV-lesser curve high along cardia of stomach; increased risk of bleeding due to decreased mucosal protection
    • Tx: ulcer excision +/- highly selective vagotomy or truncal vagotomy and pyloroplasty
    • Type V- ulcer associated with NSAIDS
  31. Stress Gastritis
    • 1. Occurs 3-10 days after event
    • 2. Lesions appear in fundus first
    • 3. Tx: proton pump inhibitor
    • 4. Seletive angiography with vassopressin injection may help with bleeding
    • 5. EGD with cautery of specific bleeding point may be effective
  32. Chronic Gastritis:
    • Type A (fundus)- associated with pernicious anemia, autoimmune disease
    • Type B (antral)- associated w/H. Pylori
  33. Gastric Cancer:
    • 1. pain unrelieved by eating, weight loss
    • 2. Antrum has 40% of gastric cancers
    • 3. 50% of cancer-related deaths in Japan
    • 4. Dx: EGD
    • 5. Risk Factors:
    • 1. adenomatous polyps
    • 2. tobacco
    • 3. previous gastric operations
    • 4. intestinal metaplasia
    • 5. atrophic gastritis
    • 6. pernicious anemia
    • 7. Type A blood
    • 8 nitrosamines
  34. Adenomatous polyps
    • 1. 10-20% risk of cancer
    • 2. Tx: endoscopic resection
  35. Krukenberg tumor:
    metastases to ovaries
  36. Virchow's nodes
    metastases to supraclavicular node
  37. Intestinal gastric cancer:
    • 1. high in high-risk populations
    • 2. older men in the US
    • 3. Associated with chronic atrophy, dysplasia, has blood invasions; glands on histology
    • 4. stage I disease- 85% cure rate; overall 5 year survival rate 10%
    • 5. Surgical Tx: try to perform subtotal gastrectomy (need 5cm margins)
  38. Diffuse gastric cancer (linitis plastica)
    • 1. in low risk populations, women
    • 2. Lymphatic invasion; no glands
    • 3. Less favorable prognosis than intestinal gastric cancer
    • 4. Stage II disease- <50% 5yr survival rate
    • 5. Surgical Tx: patients require total gastrectomy because of diffuse nature of linitis plastica
    • 6. Chemotherapy (poor respose to chemo) 5 FU, doxorubicin, mitomycin C
    • 7. Metastatic disease outside the area of resection- contraindication to resection unless performing surgery for palliation
  39. Palliation of gastric cancer
    • 1. Obstruction- proximal lesion can be stented; distal lesion bypasses with gastrojejunostomy
    • 2. Low to moderate bleeding or pain- XRT
    • 3. if these fail, consider palliative gastrectomy for obstruction or bleeding
  40. Gastric Leiomyomas (also called GIST tumors)
    • 1. Most common benign gastric neoplasm
    • 2. Symptoms: usually asymptomatic but obstruction and bleeding can occur
    • 3. Hypoechoic on ultrasound; smooth edges
    • 4. Dx. biopsy
    • 5. Tx: resection
    • 6. Consider chemotherapy is >5cm or >5-10 mitoses/HPF
    • 7. Need 1cm margins
    • 8. Most are C-KIT positive
    • 9. Chemotherapy- Gleevec (tyrosine kinase inhibitor)
  41. Gastric Leiomyosarcomas
    • 1. need en bloc resection
    • 2. Cancer diagnosis based on mitoses/HPF (>5-10 associated with increased risk of metastases)
    • 3. Hematogenous spread
  42. Gastric Lymphomas
    • 1. have ulcer symptoms; organ most commonly involved in extranodal lymphoma
    • 2. Usually non-hodgkin's lymphoma
    • 3. Dx: EGD
    • 4. Chemotherapy and XRT are primary treatment modalities; surgery for complications
    • 5. Surgery possibly indicated only for stage I disease (tumor confined to stomach mucosa) and then only partial resection is indicated
    • 6. Overall 5 year survival rate >50%
  43. Mucosa-associated Lymphoproliferative Tissue
    • 1. Related to H. Pylori infection; considered a precursor for gastric lymphoma
    • 2. should regress after treatment for H. pylori
    • 3. Usually in GI tract; can also occur in lung and Waldeyer's ring
    • 4. Tx: triple therapy antibiotics for H. pylori and surveillance; if MALT does not regress, need chemotherapy (CHOP)
  44. Morbid obesity
    • 1) Central obesity- worse prognosis
    • 2) Surgical eligibility: BMI >40 or BMI >35 w/comorbidities
    • 3) NIDDM, HTN, and sleep apnea often resolve after surgery
  45. Criteria for patient selection for bariatric surgery
    • 1) BMI >40
    • 2) BMI >35 w/coexisting comorbidities
    • 3) failure of nonsurgical methods of weight reduction
    • 4) psychological stability
    • 5) abscence of drug and alcohol use
  46. Whats the operation mortality of gastric bypass
    about 1%
  47. Roux-en-y gastric bypass
    1) better weight loss than just stapling

    • 2) Risks:
    • 1- marginal ulcers
    • 2- leak
    • 3- necrosis
    • 4- B12 deficiency (intrinsic factor needs acidic environment to bind B12)
    • 5- iron-deficiency anemia (bypasses duodenum, where Fe absorbed)
    • 6- gallstones (from rapid weight loss)

    3) perform cholecystectomy during operation if stones present

    4) UGI on postop day 2

    5) 10%-15% failure rate due to high carbohydrate snacking

    • 6) Ischemia- most common cause of leak
    • -signs of leak: increased RR, HR, pain, fever, elevated WBCs

    7) marginal ulcers- develop in 10%. Tx-omeprazole

    8) stenosis- usually responds to serial dilation

    9) signs of obstruction following surgery- hiccups, large stomach bubble
  48. Jejunoileal bypass
    • 1) these operations are no longer done
    • 2) associated with increased liver cirrhosis and kidney (stones) problems, osteoporosis (decreased Ca)
    • 3) need to correct these patients and perform roux-en-y gastric bypass if ileojejunal bypasses are encountered
  49. Postgastrectomy complications:

    Dumping syndrome:
    • 1- can occur after gastrectomy or after vagotomy and pyloroplasty
    • 2- occurs from rapid entering of carbohydrates into the small bowel
    • 3- 90% resolve with medical therapy

    • 4- There are 2 phases:
    • -hyperosmotic load causes fluid shift into bowel (diarrhea, dizziness, hypotension)
    • -reactive increase in insulin and decrease in glucose (2nd phase rarely occurs)

    5- can almost always be treated with medical and conservative (dietary changes) therapy

    6- treatment: small, low fat, low carbohydrate, increased protein meals; no liquids with meals, no lying down after meals

    7- octreotide may be effective

    • 8- surgical options (rarely needed)
    • 1- conversion of billroth I or billroth II to roux-en-y gastrojejunostomy
    • 2- operations to increase gastric reservoir (jejunal pouch) or increase emptying time (reversed jejunal loop)
  50. Postgastrectomy complications:
    Alkaline reflux gastritis
    1) postprandial epigastric pain associated with N/V; pain not relieved with vomiting

    2) Diagnosis: evidence of bile reflux into stomach, histologic evidence of gastritis

    3) Treatment: H2 blockers, cholestyramine, metochlopramide

    4) surgical option: conversion of billroth I or billroth II to roux-en-y gastrojejunostomy with afferent limb 60cm distal to original gastrojejunostomy
  51. Postgastrectomy complications:
    Roux stasis:
    • 1) stasis of chyme in roux limb due to loss of jejunal mobility
    • 2) Diagnosis: EGD, emptying studies
    • 3) Treatment: metochlopramide, prokinetics
    • 4) Surgical option: shorten to roux limb to 40cm
  52. Postgastrectomy complications:
    Chronic gastric atony:
    • 1) delayed gastric emptying after vagotomy
    • 2) symptoms: nausea, vomiting, pain, early satiety
    • 3) diagnosis: gastric emptying study
    • 4) metoclopramide, prokinetics
    • 5) Surgical option: near total gastrectomy with Roux-en-y
  53. Postgastrectomy complications:
    Small gastric remnant:
    • 1) actually want this for gastric bypass patients
    • 2) Dx: EGD
    • 3) Treatment: small meals
    • 4) surgical option: jejunal pouch reconstruction
  54. Postgastrectomy complications:
    Duodenal stump blow-out-
    place duodenostomy and drains
  55. Postgastrectomy complications:
    Blind-Loop syndrome:
    • 1) with billroth II or Roux-en y
    • 2) symptoms: pain, diarrhea, malabsorption, B12 deficiency (bacteria use it up), steatorrhea (bacterial deconjugation of bile)
    • 3) caused by bacterial (E.coli, GNRs) overgrowth and stasis in afferent limb
    • 4)Treatment: tetracycline, flagyl, metoclopramide
    • 5)Surgical option: reanastomosis with shorter (40cm) afferent limb
  56. Postgastrectomy complications:
    afferent loop obstruction
    • 1) with billroth II or roux en y
    • 2) nonbillious vomiting, pain relieved with bilious emesis
    • 3) symptoms: RUQ pain, steatorrhea
    • 4)caused by obstruction of afferent limb
    • 5) risk factors: long afferent limb with billroth II or roux-en-y
    • 6) diagnosis: CT scan
    • 7)balloon dilation may be possible
    • 8)surgical option: reanastomosis with shorter 40cm afferent limb
  57. Postgastrectomy complications:
    efferent loop obstruction:
    • 1) symptoms of obstruction
    • 2) Diagnosis: UGI, EGD
    • 3) treatment: balloon dilation
    • 4) surgical option: find the site of obstruction an relieve it
  58. Postgastrectomy complications:
    Postvagotomy diarrhea:
    • 1) secondary to nonconjugated bile salts in the colon
    • 2) caused by sustained postprandial organized MMCs
    • 3) treatment: cholestyramine, octreotide
    • 4)surgical option: reversed interpostion jejunal graft
  59. PEG complications:
    insertion into liver or colon