Spencer C. Knox, MD

Internal Medicine Resident Physician, PGY-3

Category: Gastroenterology & Hepatology (Page 1 of 2)

Endoscopy Simulator

Thought I’d share a photo of my residency program’s GI endoscopy simulator!  Earlier today, I had fun testing out some of the EGD and Colonoscopy scenarios on this machine.  Once a month, our program allows for “Simulation (sim) Lab.”  Essentially, it’s an hour-long block wherein residents practice code blue 90’s, rapid responses, central line insertions, and even practice with the simulator.

Interestingly, not only does this simulator attempt to recreate life-like images while you manipulate the endoscope, but it also includes a fully-functional biopsy/intervention channel.  This allows the user to position biopsy forceps, epinephrine injection needles, and more.  Really cool technology!

GI endoscopy simulator

Simulator is ready-to-go for the next clinical scenario!

Acute and Chronic Pancreatitis

In this section, I’ll outline important facts about Acute Pancreatitis and Chronic Pancreatitis that most residents and hospitalists should be aware of.



Acute Pancreatitis

  • Hospitalists, listen up!  This is the #1 GI cause of hospitalization in the States.
  • Clinically:
    • c/c severe epigastric pain
    • 80% are classified as “Mild Pancreatitis”
      • Recovery within few days
    • 20% are classified as either Moderate or Severe
      • Moderate:  pancreatic necrosis, fluid collections, and temporary organ dysfunction outside of pancreas.
      • Severe:  3+ days of organ failure, predictor of death.
        • BUN > 20 mg/dL, Hct > 44%, and elevated Creatinine are POOR PROGNOSTIC criteria.
  • Pathophysiology:
    • Capillary leak syndrome is caused by SIRS; led by premature activation of pancreatic enzymes leading to autodigestion.
    • 80% of acute pancreatitis is caused by gallstones and alcohol.
    • Remaining 20%:
      • Meds – lasix, asparaginase, didanosine, mesalamine, HCTZ, 6-MP/AZA, simvastatin.
      • Triglyceridemia (1,000 and up) and/or Hypercalcemia
      • Choledochocele
      • Post-ERCP
      • Very rarely:  viral/parasitic infection, trauma, ischemia, Celiac disease, autoimmune.
  • Diagnosis of Acute Pancreatitis:
    • Need 2/3 of the following:
      • acute epigastric pain (may radiate to back), better when leaning forward
      • serum lipase > 3x upper limit of normal
      • CT or MRI findings consistent with inflammatory process.
    • Symptomatic pleural effusion may result, due to SIRS process.
    • LFT elevation – think common bile duct obstruction.
    • A common etiology is gallstones, therefore all patients need transabdominal US.
    • CT Abdomen with contrast is NOT required for the diagnosis; it may miss some gallstones.
  • Treatment of Acute Pancreatitis:
    • IV Fluid hydration, NPO, pain control PRN, and Zofran/Phenergan PRN nausea.
      • IVF @ 250-500 mL/hr is critical in the immediate setting (12-24 hours)
    • When to begin ORAL feeding:
      • Severe pancreatitis = in 72 hours
        • This protocol actually reduces mortality, infections, and organ failure!
      • Mild-moderate = when nausea/vomiting abates.
    • AVOID TPN.
  • Acute Pancreatitis Complications:
    • Pseudocysts = persistent interstitial fluid collections (peripancreatic) with encapsulation after 4 weeks.
    • Walled-off necrosis = after 4 weeks, once necrotic tissue becomes encapsulated.
    • Most will resolves on their own.
    • Diabetes mellitus, gastric outlet obstruction, splenic vein thrombosis, colonic necrosis, gastric variceal bleeding.

Chronic Pancreatitis

  • Clinically:
    • c/c Epigastric pain with radiation to the back, waxes and wanes.
    • Consider pseudocyst or biliary/pancreatic duct stricture if constant pain.
    • Bulky/greasy stool owing to pancreatic lipase insufficiency.
    • Diabetes mellitus due to malfunction of endocrine portion of pancreas.
  • Pathophysiology:
    • Chronic inflammatory condition, usually caused by alcohol use exceeding 50-80 g/day (single drink = 14 g of alcohol)
    • Other important causes:
      • Tobacco is independent risk factor.
      • Genetic mutations of certain genes
      • Obstructive, secondary to pancreatic head tumor, intraductal mucinous neoplasm, trauma with ductal stricture.
      • Recurrent severe acute pancreatitis
      • Irradiation-induced
      • Celiac disease or autoimmune pancreatitis
      • Idiopathic
  • Diagnosis of Chronic Pancreatitis:
    • Amylase and lipase levels are typically normal
    • Typical clinical features and calcifications on abdominal imaging.
    • Supporting criteria:  bulky/greasy stools, diabetes
    • If CT abdomen cannot find calcifications of pancreas, consult GI for endoscopic US (EUS).
    • Quantitative 72-hour fecal fat testing, direct CCK or secretin stim. tests also available.
  • Treatment of Chronic Pancreatitis:
    • Educate patient:  STOP smoking.
    • Pain control with acetaminophen, ibuprofen, and tramadol.
    • Low-dose TCAs and gabapentinoids if none of above work.
    • Pancreatic enzymes, including 90,000 USP lipase with meals, half dose with snacks.
    • Endoscopic stenting of culprit ductal lesions.


  • ACP MKSAP 17:  Gastroenterology and Hepatology, pgs. 23-27
  • Image source:  https://en.wikipedia.org/wiki/Chronic_pancreatitis
    • CT image showing numerous calcifications within parenchyma of pancreas.

Stomach and Duodenal Disease

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.


  • 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!


  • 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.


  • 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.

Esophageal Metaplasia and Neoplasia

Esophageal cancer accounts for a jaw-dropping amount of cancer-related deaths, and is now classified as the 6th-highest cause of death in this group.  In this installment of the study guide series, I will discuss Barrett Esophagus (I learned this entity as Barrett Metaplasia) and esophageal cancer (neoplasia).


Barrett Metaplasia

  • Metaplasia:  columnar epithelium replaces the physiologic squamous epithelium in the distal portion of the food pipe.
    • Cancer risk of 0.5% per year in those who have Barrett Esophagus.
    • Usual pathway (if progresses to ca):  intestinal metaplasia –> low-grade dysplasia –> high-grade dysplasia.
  • NO evidence that routine screening for BE based on GERD symptoms is helpful.
  • Clinically:
    • Think of this in an older obese white male with chronic reflux and a history of chain-smoking.
    • Protective = average wine consumption, fruits/veggies.
    • Barrett Esophagus occurs in the presence or absence of reflux!
  • Diagnosis:
    • Upper endoscopy showing typical intestinal metaplasia of distal esophagus.
      • Salmon-colored mucosa
      • Further classifications:  Short segment (< 3cm) or long segment (> 3cm)
  • Treatment:
    • PPI are useful for reflux symptom improvement, not preventing progression to dysplasia.
    • HIGH-grade dysplasia = destroy bad tissue with radiofrequency ablation or other resection.
  • Surveillance
    • EGD is primary modality.
    • Based on dysplasia grade:
      • none = repeat EGD 3-5 years.
      • low-grade = repeat EGD 6-12 months
      • high-grade = look for focal lesions, which may harbor more progressive disease; repeat EGD q3 months with resection/surgery.

Esophageal Carcinoma

  • Adenocarcinoma is most common type (#1) in US; SCC is also very common.
  • Typically presents in males, aged 50-60’s.
  • 5-year survival rate 15-25%, depending on stage at presentation.
  • Risk factors:
    • Adenocarcinoma = GERD, Barrett metaplasia, tobacco, radiation, male, old age, poor diet.
    • SCC = tobacco and alcohol, direct toxic injury, Zn and selenium deficiency, prior radiation to region, poor population, poor oral hygiene, HPV, nitrosamine exposure (occupational hazards), nonepidermolytic palmoplantar keratoderma.
  • Diagnosis:
    • #1 symptom = SOLID-food dysphagia
    • Weight loss, low appetite, low hemoglobin/hematocrit.
    • EGD is best way to diagnose.
    • Squamous Cell Carcinoma is proximal
    • Adenocarcinoma is distal
    • CT scan is useful to evaluate for metastatic disease; PET used for questionable lesions.
  • Treatment
    • Refer to Oncology, resection versus chemotherapy is stage dependent at time of diagnosis.


  • ACP MKSAP 17:  Gastroenterology and Hepatology, pgs. 9-12
  • Image source:  https://en.wikipedia.org/wiki/Barrett’s_esophagus
    • Intestinal metaplasia consistent with Barrett esophagus (left side of main image) and normal stratified squamous epithelium (right side), Alcian blue stain.

Gastroesophageal Reflux Disease (GERD)

GERD is incredibly common, with an estimated prevalence of 10-20% in the Western hemisphere.  It’s important to note that GERD has many overlap symptoms with cardiac chest pain, thus cardiovascular causes should be ruled out first before the diagnosis of GERD.



  • Clinically
    • Insomnia/poor sleep quality, diminished work output
    • Typical heartburn, liquid regurgitation with resultant metallic or acidic quality
    • Alarm symptoms:  dysphagia (r/o malignancy, ring, web), weight loss, bloody vomitus, and black tarry stools).
      • Upper endoscopy is generally a preferred modality in these cases
    • Pregnancy-induced GERD is common
    • Risk factors:  obesity, “trigger” foods (caffeine, spices, oranges/grape fruit, alcohol, foods high in fat)
    • GERD can lead to:
      • erosive esophagitis, Barrett metaplasia, cancer, and stricture.
  • Diagnosis of GERD
    • Clinical history, response to PPI, and pH testing.
    • If NO alarm symptoms, then response to empiric PPI will confirm dx.
    • If no response to empiric PPI, perform EGD.
    • If + alarm symptoms, first step is to perform EGD.
    • Ambulatory pH testing; Impedance pH exam can see acid and non-acid reflux.
  • Treatment
    • Lifestyle changes including diet/exercise.
    • Raise head of bed (pillows, incline) and stop nocturnal eating.
    • If a food leads to heartburn, eliminate it.
    • Best regimen:  PPI qdaily for 8 weeks
      • 30-60 minutes prior to first meal
      • OK for use in pregnancy
    • Alternative:  H2 blocker
    • Laparoscopic fundoplication or bariatric surgery only indicated when:
      • patient preference, side effects to meds, refractory GERD, and large hiatal hernia.
      • Will need pH-impedance testing, manometry to objectively identify GERD
      • May still need PPI 5-10 years down the road, despite therapeutic surgery.


  • ACP MKSAP 17:  Gastroenterology and Hepatology, pgs. 7-9
  • Image source:  https://en.wikipedia.org/wiki/Gastroesophageal_reflux_disease

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