The stomach and duodenum comprise two well elucidated, critical organs in the digestive process.  I will review Peptic Ulcer Disease, Dyspepsia, H. pylori, gastroparesis, and other similar pathology in this post.

 

 

Peptic Ulcer Disease (PUD)

  • Clinically:
    • Typical symptoms = epigastric pain; eating may either hurt/help the pain, early satiety, nausea, bloating, nocturnal pain (suggesting duodenal ulcer).
  • Diagnosis:
    • Upper endoscopy (EGD) is gold standard
    • Mucosal breakdown 5mm or bigger
    • “Complicated PUD:”
      • Usually alarm symptoms:  GI bleeding (hematemesis/melena), penetration (think pancreatitis), perforation (severe, sudden abdominal pain and peritoneal signs), obstruction (anorexia, weight loss, vomiting)
      • On labs:  iron deficiency anemia (low ferritin)
  • Treatment:
    • Generally speaking, indefinite use of PPI (unless young, uncomplicated, and associated with NSAID use – then co-therapy with PPI while using NSAID).
    • Appropriate therapy if H. pylori identified.

Dyspepsia

  • Definition via clinical symptoms:  bloating, belching, +/- weight loss, epigastric pain/burning, belly fullness, nausea/vomiting.
  • Functional Dyspepsia is a diagnosis of exclusion; therefore, must rule out:
    • GERD, malignancy, PUD, gastroparesis, Celiac sprue, H. pylori infection, lactose intolerance, biliary tract disease, pancreatitis, ischemic bowel disease, abdominal muscle pathology, EtOH, pregnancy, etc.
  • Diagnosis of Functional Dyspepsia:
    • Rome III consensus group:  post-prandial fullness, early satiety, epigastric pain, epigastric burning for 3+ months, with initial onset 6 months prior to diagnosis.
    • No structural defect (see above)
  • Treatment:
    • Patients < 55 years of age without alarm symptoms (e.g. BRBPR, melena, weight loss, loss of appetite, odynophagia, family history of GI malignancy, prior abdominal surgery, anemia), first step is test and treat for H. pylori infection or trial of PPI.
    • Patients > 55years with alarm symptoms and/or persistence of symptoms, first step is upper endoscopy (EGD).
    • Diet/lifestyle modification (low fat, small portions)
    • H2 blocker or PPI similar efficacy.
    • Severe/refractory FD, try TCAs or SSRIs

Implications of H. pylori Infection

  • The WHO designates H. pylori as a human carcinogen (cancer-causing organism), therefore proper diagnosis and treatment is imperative.
  • Specific indications for H. pylori testing:
    • Active PUD
    • History of PUD
    • MALT lymphoma
    • Bothersome dyspepsia with unknown etiology
    • s/p resection of gastric cancer
    • Less evidence:  iron deficiency anemia of unknown etiology and primary ITP.
  • Diagnosis:
    • Ways to identify active infection:
      • Fecal antigen test or urea breath test
      • HOLD antibiotics and bismuth for 28 days before testing
      • HOLD PPIs for 7-14 days before testing
      • HOLD H2-antagonists 1-2 days before testing.
    • If active bleeding from PUD, incidence of false-negative testing rises.  Get serologic antibody testing as well in these cases.
      • Serum IgG Ab has good negative predictive value
    • Most accurate way to identify H. pylori = Urea breath test
  • Treatment:
    • Triple therapy (two antibiotics and one PPI) for 10-14 days.
      • Protonix 40mg BID, clarithromycin 500mg BID, and amoxicillin 1000mg BID (check clarithro. resistance rates in your area)
        • Substitute amoxicillin with metronidazole 500mg BID when penicillin allergic.
    • Quadruple therapy also exists as first-line option.
      • Protonix 40mg BID, bismuth subsalicylate 525mg four times daily, metronidazole 250mg four times daily, tetracycline 500mg four times daily
  • How to confirm eradication:
    • Note:  wait at least 4 weeks after triple therapy, must be off PPI for 2+ weeks.
    • Recommended in all cases due to common treatment failure (rate of 25%)
    • Urea breath test, or
    • Fecal antigen test

Atrophic Gastritis

  • Two types:  H. pylori-associated and autoimmune
    • Autoimmune type is untreatable
  • Be on the lookout for the following sequelae:
    • Pernicious anemia
    • Iron deficiency anemia
    • Hypergastrinemia (due to parietal cell loss and loss of HCl, breaking feedback cycle)
  • No endoscopy surveillance is advised.

Intestinal Metaplasia

  • PRECANCEROUS lesion of stomach mucosa (for adenocarcinoma)
  • H. pylori stool Ag test or urea breath test should be performed, given its association.

Eosinophilic Gastritis

  • Very rare inflammatory entity.
  • Can cause gastric outlet obstruction; rarely causes ascites
  • Treatment:
    • Diet and/or steroid therapy.

Lymphocytic Gastritis

  • Rare, benign chronic inflammation of stomach mucosa.
  • Clinically:
    • Dyspepsia, Fe-deficiency anemia, diarrhea
  • Associated with:
    • Celiac disease and H. pylori gastritis
    • Less commonly –
      • Varioliform gastritis = endoscopy findings of nodules, erosions, beefed-up rugae.
      • Crohn disease, HIV, lymphocytic gastroenterocolitis, lymphomas.
  • No endoscopic surveillance required.

Impact of NSAIDs, ASA, Anticoagulation

  • Aspirin 81mg daily = 2-4x increase in upper GI pathology.
  • 25% of chronic NSAID people will get PUD.
    • Risk factors:  age 65+, H. pylori infection, hx of PUD, same-time ASA use, anticoagulants, steroids, comorbid disease.
  • Prevention:
    • Proton Pump Inhibitors (PPIs) are first line!

Gastroparesis

  • Very difficult to manage patient population, often with underlying poorly controlled diabetes mellitus, thyroid dysfunction, and/or previous abdominal surgery.
  • Patients frequently complain of intractable nausea/vomiting +/- labile blood glucose levels.
  • Diagnosis:
    • First step is to exclude mechanical/anatomic defects via upper endoscopy (EGD).
      • May substitute with upper GI series if unavailable.
    • Next step is NM gastric emptying study of solid foods, 4-hour test is best.
      • AVOID medications with effect on gastric emptying (HOLD for 48 hours+ before test):
        • opioids, anticholinergic, TCAs, CCBs, PPIs, octreotide, H2-blockers, and many others.
      • Hyperglycemia (275 mg/dL) can cause slowed gastric transit.  Treat first.
  • Treatment:
    • IVF, electrolyte replacement PRN
    • Diet modification:  small, low-fat, low-soluble-fiber meals (4-5x/day)
    • Zofran or Phenergan PRN nausea
    • Reglan 5mg tid starting dose; warn about neuroligic effect.
    • Erythromycin for acute exacerbations.

Gastric Polyps

  • 90% of the gastric polyps found on EGD are hyperplastic or fundic gland polyps.
    • 1-5mm in size, <10 total.
  • If >30 gastric polyps, consider more serious path., including FAP or MYH-associated polyposis.
    • 10mm or larger in size
    • First test is Colonoscopy to rule out these oft-dysplastic disease entities.

Gastrointestinal Stromal Tumors (GISTs)

  • Less than 1% of GI tumors; stomach is most common location.
  • Arise from interstitial cells of Cajal.
  • Etiology:
    • KIT oncogene mutation (95% of GISTs); CD117+

Gastric Carcinoid Tumors

  • Also known as Neuroendocrine tumors (NETs), comprise 1% of gastric cancers.
  • Arise from enterochromaffin cells of stomach mucosa.
  • Type I (80% of this type) = assoc. w/autoimmune atrophic gastritis and hypergastrinemia.
  • Pathophysiology:
    • Secrete 5-hydroxytryptophan, therefore rarely classic carcinoid syndrome.
      • More likely to see lacrimation, swelling, heart/valve dz., and wheezing.
  • Treatment:
    • EGD with polypectomy can be curative for Type I and II.

Gastric Adenocarcinoma

  • #4 most common cancer in the world; think Asia (China), S. American, Eastern Europe.
  • 5-year survival rate 28%
  • Gastric adenocarcinoma comprises 90%+ of all gastric-origin cancers.
  • Hereditary diffuse gastric cancer:
    • Mutation of E-cadherin gene — translates into 80% lifetime risk.  If found, recommend prophylactic gastrectomy in 20+ yo patients.
  • Screening:
    • General screening with EGD not recommended, unless there is presence of adenomatous polyps (1 year f/u).
  • Clinically:
    • “Warning signs” as described above.
  • Diagnosis:
    • TOC is EGD with biopsy

Post-op Gastric Surgery Issues

  • Post-operative mortality rates are best for laparoscopic restrictive procedures (sleeve gastrectomy and banding).
  • Increased mortality is due to:
    • DVT, PE, OSA, old age, surgical technique, and functional status.
  • Gastric banding complications:
    • Malpositioning (slippage) of band, leading to pouch dilation; band erosion.
  • Sleeve gastrectomy complications:
    • Leaks are the worst!
    • Stenosis (narrowing) is the most common #1 complication.
  • Roux-en-Y gastric bypass issues:
    • Cholelithiasis and/or nephrolithiasis (increased urine oxalate excretion)
    • Dumping syndrome
  • Follow up:
    • For malabsorptive surgeries (Roux-en-Y), test for albumin/prealbumin, iron studies, other vitamins and bone mineral density test.

Bibliography

  • ACP MKSAP 17:  Gastroenterology and Hepatology, pgs. 12-23
  • Image source:  https://en.wikipedia.org/wiki/Helicobacter_pylori
    • H. pylori immunohistochemical stain, gastric tissue

TOC = treatment of choice.

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