Spencer C. Knox, MD

Internal Medicine Resident Physician, PGY-3

Tag: GI (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!

I Matched into GI Fellowship!

Matching into a three-year clinical Gastroenterology fellowship program is a dream come true.  Match Day was December 6th, 2017.  I remember anxiously driving home to meet my wife Claudia and puppy Chloe so that everyone was there to hear the news as soon as I pulled up the NRMP 2017 Medical Specialties results online.

Sitting down at my desk, I opened Chrome and started to type the NRMP’s website address.  My web browser filled in the rest.  I scrolled down to the results area, and was stunned to see I matched!! 🙂

NRMP Fellowship Results

We shared a celebratory toast, thanking God, our family, and my new GI program for… the opportunity.

Hugging Claudia, we both instantly knew our lives would change.  “I’m going to be a GI doctor!” I exclaimed to my wife.  We shared a celebratory toast, thanking God, our family, and my new GI program for allowing me the opportunity to train in the art and science-based medicine of Gastroenterology.

Suddenly, the text messages and Facebook posts came in.  I recall thinking, I feel so blessed to have family and friends in my life who are so supportive and genuinely happy for me.

In the hours and days after the shock gradually wore off and reality set in, my mind began running through all of the things that need to happen before starting day one.  Licensure in Massachusetts, finding a suitable home for the next three years, the unknown of who our new Massachusetts friends might be, and so much more.  It’s such an exciting time!


Fellowship Candidacy

Life in residency is always busy.  Time flies by.  I am nearly three months into my third and final year of residency (PGY-3).  I was scrolling through social media earlier today, and noticed a familiar big announcement:

The start of a brand new cycle of residency applications is a momentous event.  For MS4’s, it marks the official beginning of what will be a life-altering season.  Interviews will be sent out to deserving applicants, and both the programs and applicants work towards a match.  I can’t help but remember the feeling of pure joy at the sight of each invitation email.  It’s been over two full years since I went through the process.

Right now, as I enter the fourth month of my last year of residency, I can say that I am so very honored and happy at my current residency program.   I like my co-residents, and call many of them friends.  Attendings have been extremely supportive.

Now, I am a candidate for a fellowship in Gastroenterology (GI).  I recently went on my first interview for a 2018 position, and felt very, very honored to be in the presence of so many professionals who are making GI their life’s work.  Meeting current GI fellows and attendings is extraordinarily invigorating.  I can see myself diagnosing and treating patients with disorders of the small intestinal including Celiac Disease and malabsorption.  I want to make it my career to protect and prevent complications of Barrett Esophagus, IBD, colon cancer, and various other downstream problems of the gastrointestinal system.  A Gastroenterology fellowship would mean the world to me!

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.

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.

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