Perelman School of Medicine at the University of Pennsylvania

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Gastroenterology Pearls

Esophagus/Stomach: Achalasia

What are the findings for achalasia on barium swallow and manometry?

  • Barium swallow: bird’s beak appearance with narrowing of the lower esophagus and esophageal dilatation with stasis of barium in the lower esophagus
  • Esophageal manometry: incomplete relaxation of the lower esophageal sphincter (LES), high resting LES pressure, absent esophageal peristalsis
  • 2016 article on the use of manometry in diagnosing esophageal motility disorders: http://www.ncbi.nlm.nih.gov/pubmed/26631942

How do we treat achalasia?

  • Medical: calcium channel blockers, nitrates, endoscopic injection of botulinum toxin at the lower esophageal sphincter
  • Surgical: Heller myotomy or partial fundoplication
  • 2016 update on endoscopic treatment of achalasia: http://www.ncbi.nlm.nih.gov/pubmed/26839644

 

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Esophagus/Stomach: Autoimmune Atrophic Gastritis

What are the systemic manifestations of autoimmune atrophic gastritis?

  • Most of the manifestations of atrophic gastritis are related to the inability to absorb B12 (cobalamin)
    • Megaloblastic anemia
    • Glossitis and soreness of tongue
    • Diarrhea from malabsoprtion related to megaloblastic changes of the small intestine
    • Peripheral neuropathy
  • A pathologist’s view on autoimmune atrophic gastritis: http://www.ncbi.nlm.nih.gov/pubmed/26576102

 

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Esophagus/Stomach: Barrett Esophagus

How do you manage dysplasia in a patient with Barrett esophagus?

  • Once high-grade dysplasia has been detected there are three options:
    • Surveillance endoscopy with biopsies every three months until cancer is detected
    • Endoscopic ablation
    • Surgical resection/esophagectomy
  • American College of Gastroenterology 2015 guidelines on managing Barrett esophagus: http://www.ncbi.nlm.nih.gov/pubmed?term=26526079

Describe the progression from GERD to Barrett esophagus to adenocarcinoma.

  • GERD to
  • Barrett esophagus (with intestinal metaplasia of the esophagus) to
  • Barrett esophagus with high grade dysplasia to
  • Adenocarcinoma
  • American College of Gastroenterology 2015 guidelines on managing Barrett esophagus: http://www.ncbi.nlm.nih.gov/pubmed?term=26526079

What is the risk of esophageal cancer in a patient with Barrett esophagus?

  • For patients without dysplasia on EGD biopsy, the risk of progression to esophageal cancer is about 0.5% per year

 

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Esophagus/Stomach: Esophagitis (Candida)

 

How do we treat Candida esophagitis?

  • Fluconazole
  • Nystatin
  • Caspofungin (for refractory cases)
  • Amphotericin (for refractory cases)
  • 2016 article on treatment of Candida esophagitis in immunocompetent and immunocompromised patients: http://www.ncbi.nlm.nih.gov/pubmed/26847359

What are the four major triggers of pill esophagitis?

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Esophagus/Stomach: Gastric Bypass

What are the indications for gastric bypass surgery?

  • BMI > 40
  • BMI 35-40 plus an obesity-related illness:
    • Severe diabetes
    • Pickwickian syndrome (obesity hypoventilation syndrome)
    • Obesity-related cardiomyopathy
    • Severe sleep apnea
    • Severe osteoarthritis

 

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Esophagus/Stomach: GERD

 

Which lifestyle modifications can reduce GERD?

  • Avoid alcohol, chocolate, citrus products, tomato products, coffee, peppermint, onion
  • Avoid large meals
  • Wait at least 3 hours after a meal before laying down
  • Lose weight
  • Elevate the head of the bed by 8 inches
  • JAMA Surgery article about efficacy of GERD treatments: http://www.ncbi.nlm.nih.gov/pubmed/26629969

What are the adverse effects of PPIs?

How is a hiatal hernia diagnosed?

  • On a barium swallow, the following three findings suggest a hiatal hernia diagnosis:
    • An outpouching of barium in the lower esophagus
    • Gastric folds forming a wide hiatus that is in continuum with the stomach
    • Free reflux of barium

What are the red flag signs in peptic ulcer disease?

  • Age > 50
  • Weight loss
  • Bleeding/anemia
  • Early satiety
  • Recurrent vomiting
  • Progressive dysphagia or odynophagia
  • Family history of GI cancer

How do you manage dysplasia in a patient with Barrett esophagus?

  • Once high-grade dysplasia has been detected there are three options:
    • Surveillance endoscopy with biopsies every three months until cancer is detected
    • Endoscopic ablation
    • Surgical resection/esophagectomy
  • American College of Gastroenterology 2015 guidelines on managing Barrett esophagus: http://www.ncbi.nlm.nih.gov/pubmed?term=26526079

Describe the progression from GERD to Barrett esophagus to adenocarcinoma.

  • GERD to
  • Barrett esophagus (with intestinal metaplasia of the esophagus) to
  • Barrett esophagus with high grade dysplasia to
  • Adenocarcinoma
  • American College of Gastroenterology 2015 guidelines on managing Barrett esophagus: http://www.ncbi.nlm.nih.gov/pubmed?term=26526079

What is the risk of esophageal cancer in a patient with Barrett esophagus?

  • For patients without dysplasia on EGD biopsy, the risk of progression to esophageal cancer is about 0.5% per year

 

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Esophagus/Stomach: H.pylori

How do we test for H.pylori?

  • H.pylori stool antigen (sensitivity and specificity > 90%, can be used to confirm eradication after therapy)
  • Urea breath test (sensitivity and specificity > 90%, can be used to confirm eradication after therapy)
  • H.pylori serum antibody (can be positive even 3 years after prior infection, CANNOT be used to confirm eradication of bacteria)
  • Endoscopic rapid urease test, bacterial culture, or histologic detection via biopsy.

How do we treat H.pylori?

 

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Esophagus/Stomach: Upper GI Bleed

How does heart rate correlate with upper GI blood loss?

  • Class 1: <750cc blood loss, HR <100
  • Class 2: 750-1500cc blood loss, HR >100
  • Class 3: 1500-2000cc blood loss, HR >120
  • Class 4: >2000cc blood loss, HR > 140
  • Correlation of heart rate and hypovolemic shock in peptic ulcer bleeding: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1416867/

How do we define upper or lower GI bleeding?

  • Upper/lower GI bleeding is defined as being proximal or distal to the ligament of Treitz

What are the esophageal, gastric, and duodenal causes of upper GI bleed?

  • Esophageal causes
    • Esophageal varices, esophagitis, esophageal ulcers, Mallory-Weiss tear, esophageal cancer
  • Gastric causes
    • Gastric varices, gastritis, gastric ulcers, GAVE (gastric antral vascular ectasia), Dieulafoy’s lesions, gastric cancer
  • Duodenal causes
    • Duodenal ulcer, vascular malformations (aorto-enteric fistula), bleeding from biliary tree or pancreatic duct
  • JAMA Rational Clinical Examination Series on Does this Patient Have a Severe Upper GI Bleed? http://jama.jamanetwork.com/article.aspx?articleid=1105075&resultClick=3

 

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Gallbladder/Biliary System: Cholelithiasis/Acute Cholecystitis/Cholangitis

What are the risk factors for acalculous cholecystitis?

What are the two main theories of how acalculous cholecystitis occurs?

  • The pathophysiology is still unclear though these are two major theories:
    • When a patient has been fasting (no enteral nutrition), CCK (cholecystokinin) is not released so there is no stimulus for the gallbladder to empty.  Thus the bile remains stagnant.  Retained concentrated bile is extremely noxious.
    • An endotoxin causes areas of necrosis and mucosal loss as part of an acute ischemic process and also prevents the contractile response of CCK leading to further gallbladder stasis.

How does biliary colic usually present?

  • Generally pain in the right upper quadrant or epigastrium and can radiate to the right scapula
  • Pain is usually post-prandial within an hour after a fatty meal
  • Pain increases for about 10-20 minutes then subsides when the gallbladder stops contracting and the stone falls back into the gallbladder

What are the Charcot’s Triad and Reynold’s Pentad of cholecystitis?

  • Charcot’s Triad
    • Abdominal pain, jaundice, fever
  • Reynold’s Pentad
    • The above, plus hypotension and altered mental status

What are the most common imaging studies for cholecystitis?

  • According to the 2010 American College of Radiology Appropriateness Criteria:
    • Ultrasound is the preferred initial test to diagnose acute cholecystitis.
    • Hepatobiliary scintigraphy (HIDA) is the alternative initial test.
    • CT without contrast or MRI with gadolinium are second line imaging tests.  CT is especially useful if you suspect gangrene, perforation, or gas.
    • MRCP and ERCP can be used for high risk patients.
    • Ultrasound sensitivity/specificity in cholecystitis: http://www.ncbi.nlm.nih.gov/pubmed?term=7979854

What are the three main types of gallstones?

  • There are three main types of gallstones
    • Cholesterol gallstones: comprises 80% of gallstones in the US, related to cholesterol secreted by liver cells relative to bile salts
    • Bilirubin gallstones: comprises 10-20% of gallstones in the US, related to hemolysis or cirrhosis (from portal hypertension leading to splenomegaly and then red cell sequestration) with high heme turnover
    • Mixed gallstones: cholesterol gallstones become colonized with bacteria and end up accumulating bilirubin

Describe Murphy’s sign in relation to gallbladder pathology.

  • Murphy’s sign
    • While the patient takes a deep breath in, you press on the right upper quadrant they stop breathing.
    • Concern for acute cholecystitis.
    • Sensitivity for cholecystitis 97%, specificity 48%
    • More on sensitivity/specificity of Murphy’s sign: http://www.ncbi.nlm.nih.gov/pubmed?term=8780468

Describe the Sonographic Murphy’s sign in relation to gallbladder pathology.

  • Sonographic Murphy’s sign
    • The patient takes a deep breath in and holds (unlike the physician Murphy sign where they are inhaling). When an ultrasound probe is used to press down on the gallbladder (visible on the ultrasound) the patient has pain.
    • Concern for acute cholecystitis.

Describe the Courvoisier’s sign in relation to gallbladder pathology.

What is the pathophysiology of post-cholecystectomy syndrome?

  • When there are changes in biliary flow (no gallbladder reservoir) two issues arise related to post-cholecystectomy syndrome
    • There is a continuous flow of bile into the GI tract which can cause esophagitis and gastritis.
    • In the lower GI tract diarrhea and lower abdominal pain can result.     
  • Review of post-cholecystectomy syndrome: http://www.ncbi.nlm.nih.gov/pubmed/26622110

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Gallbladder/Biliary System: Hepatitis

 

What labs should you send to detect Hepatitis B immunity or acute infection?

  • To indicate Hepatitis B immunity: surface antibody and surface antigen
  • To indicate Hepatitis B acute infection: surface antibody, surface antigen, core IgM (usually paired with core IgG), e antigen and e antibody (if antigen positive is associated with higher rates of replication and infectivity), Hepatitis B DNA (viral load)

What diseases are associated with Hepatitis C?

  • Cryoglobulinemia
  • Lichen planus
  • Idiopathic thrombocytopenic purpura (ITP)
  • Prophyria cutanea tarda
  • Sjogren’s syndrome
  • Positive rheumatoid factor (up to 38% of patients with hepatitis C)
  • Extrahepatic manifestations of Hepatitis C: http://www.ncbi.nlm.nih.gov/pubmed/26862398

 

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Gallbladder/Biliary System: Jaundice

At what levels of bilirubin do you see scleral icterus and skin jaundice?

  • Scleral icterus is generally visible when the serum total bilirubin is above 2.5mg/dl.
  • Jaundice of the skin is generally visible when the serum total bilirubin is above 3.0mg/dl.

 

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Gallbladder/Biliary System: Primary Sclerosing Cholangitis

What is the association between primary sclerosing cholangitis and inflammatory bowel disease?

  • Approximately 5% of IBD patients (predominantly ulcerative colitis) have PSC.
  • Approximately 70% of PSC patients have IBD.
  • Patients with both IBD and PSC are at 30 fold greater risk for colon cancer.
  • Patients with PSC are at 160 fold greater risk for cholangiocarcinoma.
  • 2016 article with an update on the association between PSC and IBD: http://www.ncbi.nlm.nih.gov/pubmed/26636407

What is the pathophysiology of primary sclerosing cholangitis?

  • In the bile ducts there is inflammation (likely immune mediated) that leads to sclerosis (hardening and narrowing) of bile ducts which then blocks bile flow (cholestasis).
  • Cholestasis and back pressure lead to focal epithelial cell proliferation and destruction of liver parenchyma forming bile lakes.

 

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Intestines: C.difficile Infection

Which antibiotics are most associated with C.diff?

  • Most frequently associated: fluoroquinolones, clindamycin, cephalosporins
  • Less associated: macrolides, trimethoprim-sulfamethoxazole, penicillins

How often does C.diff recur?

How do we grade the severity of C.diff?

  • Qualifies as severe C.diff infection if:
    • WBC > 15
    • Cr > 1.5x original
    • Albumin < 3
    • Hemodynamically unstable or ICU admission

How do we treat C.diff?

 

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Intestines: Celiac Disease

 

What blood tests would you order to diagnose Celiac disease?

How do we stage endoscopic biopsy results for Celiac disease?

  • Stage 0: normal
  • Stage 1: increased percentage of intra-epithelial lymphocytes
  • Stage 2: increased inflammatory cells and crypt cell proliferation but villous architecture is preserved
  • Stage 3: mild, moderate, or subtotal villous atrophy
  • Stage 4: total mucosal hypoplasia

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Intestines: Constipation

What are the options for bowel regimens in constipation?

  • Initial oral choices: psyllium (Metamucil), senna, docusate (Colace), polyethylene glycol (MiraLax), bisacodyl (Dulcolax), lactulose
  • Rectal administration: bisacodyl (Dulcolax) suppository, tap water enema, soap suds enema, sodium-phosphate (Fleet) enema
  • Advanced oral options: polyethylene glycol as Golytely (four liter administration), lubiprostone, linaclotide
  • Opiate constipation: naloxegol

What are the major causes of ileus?

  • Post-operative/trauma
    • Sepsis/infection
    • Drugs (opiates, anesthesia, anticholinergics)
    • Metabolic (electrolytes)
    • Myocardial infarction
    • Intra-abdominal inflammation/infection/hematoma
    • Biliary and renal colic

 

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Intestines: Colon Cancer Screening

When should you repeat a colonoscopy based on prior biopsies?

  • Age 50+ or 10yrs before family members colon cancer diagnosis
  • Hyperplastic polyp: in 10 years
  • 1-2 small (<1cm) tubular adenomas without high grade dysplasia: in 5 years
  • 3+ adenomas, villous, high grade dysplasia, or adenoma>1cm: in 3 years
  • 10+ adenomas or >2cm polyp: <3 years
  • The only people who need it less than one year is large polyp > 2cm taken out in pieces
  • 2015 NCCN Clinical Practice Guidelines in Oncology for Colorectal Cancer Screening http://www.ncbi.nlm.nih.gov/pubmed/26285241

 

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Intestines: Inflammatory Bowel Disease (Crohn's/Ulcerative Colitis)

Why do we test TPMT in Crohn’s disease patients?

  • Some patients may need 6-mercaptopurine (6-MP) for Crohn’s therapy
  • Keep in mind that if you use 6-MP you should check a TPMT enzyme activity test.
  • 0.3% of the population has TPMT coding mutations and thus will have excess levels of 6-mercaptopurine which can increase the risk of bone marrow suppression.

Crohn’s Disease vs Ulcerative Colitis: Areas of Involvement

  • Terminal ileum involvement: commonly in Crohn’s, rare in UC
  • Colon involvement: commonly in Crohn’s, always in UC
  • Rectum involvement: rarely in Crohn’s, usually in UC
  • Anal involvement: common in Crohn’s, rare in UC
  • Distribution of disease: patchy/skip lesions in Crohn’s, continuous area in UC
  • Depth of inflammation: transmural in Crohn’s, shallow and mucosal in UC

Crohn’s Disease vs Ulcerative Colitis: Serological Testing

  • Two tests that can be used to help differentiate Crohn’s disease from ulcerative colitis include:
    • Anti-Saccharomyces cerevisiae antibodies (ASCA) are more commonly found in Crohn’s disease
    • Perinuclear anti-neutrophil cytoplasmic antibody (p-ANCA) is more commonly found in UC
  • Comparison of p-ANCA and anti-Saccharomyces cerevisiae antibodies in IBD: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2659117/

What is the association between primary sclerosing cholangitis and inflammatory bowel disease?

  • Approximately 5% of IBD patients (predominantly ulcerative colitis) have PSC.
  • Approximately 70% of PSC patients have IBD.
  • Patients with both IBD and PSC are at 30 fold greater risk for colon cancer.
  • Patients with PSC are at 160 fold greater risk for cholangiocarcinoma.
  • 2016 article with an update on the association between PSC and IBD: http://www.ncbi.nlm.nih.gov/pubmed/26636407

Crohn’s Disease vs Ulcerative Colitis: Symptom Comparison

  • Fevers: ore common in Crohn’s, if occurs in UC generally indicates more severe disease
  • Fistulae: common in Crohn’s, rare in UC
  • Weight loss: common in Crohn’s, rare in UC
  • Diarrhea: more porridge-like in Crohn’s, more mucus-like and bloody in UC
  • Tenesmus: less in Crohn’s, more in UC

 

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Intestines: Irritable Bowel Syndrome (IBS)

What are the Rome III criteria for irritable bowel syndrome?

  • Diagnosis requires recurrent abdominal discomfort/pain for at least three days per month over the last three months, with at least two of the following:
    • Pain relieved by defecation
    • Onset associated with a change in stool frequency
    • Onset associated with a change in stool form
  • Comparison of Rome II and III criteria for IBS: http://www.ncbi.nlm.nih.gov/pubmed/17489052

What are the subtypes of irritable bowel syndrome?

  • IBS-D (diarrhea predominant)
  • IBS-C (constipation predominant
  • IBS-M (mixed diarrhea and constipation)
  • IBS-A (alternating diarrhea and constipation)
  • Up to 75% of patients can switch between subtypes within a year.
  • Review of IBS: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4161800/

 

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Intestines: Lower GI Bleed

How does heart rate correlate with lower GI bleed?

  • Class 1: <750cc blood loss, HR <100
  • Class 2: 750-1500cc blood loss, HR >100
  • Class 3: 1500-2000cc blood loss, HR >120
  • Class 4: >2000cc blood loss, HR > 140

How do we define upper or lower GI bleeding?

  • Upper/lower GI bleeding is defined as being proximal or distal to the ligament of Treitz

What is the differential diagnosis of lower GI bleeding?

  • Inflammatory
    • Ulcerative colitis, Crohn’s disease
  • Infectious
    • Gastroenteritis (bacterial or viral)
  • Anatomic
    • Hemorrhoids, anal fissure, diverticulosis
  • Vascular
    • Arteriovenous malformations (AVMs), angiodysplasia, ischemic colitis, radiation colitis
  • Coagulopathy
    • Bleeding disorder
  • Cancer
    • Intestinal cancer

What are symptoms of chronic mesenteric ischemia?

 

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Liver: Alcoholic Hepatitis

What is the modified Maddrey’s Discriminant Function in alcoholic hepatitis?

  • Use the modified Maddrey’s discriminant function to determine prognosis in alcoholic hepatitis
  • Formula: 4.6 x (prothrombin time – control) + serum bilirubin
  • If the value is >32 consider treatment with methylprednisolone because a value > 32 implies one month mortality of 35-45%
  • 2015 article challenging that the MELD is more useful than the Discriminant Function in alcoholic hepatitis: http://www.ncbi.nlm.nih.gov/pubmed/15826720

Do patients recover from alcoholic hepatitis after alcohol cessation?

  • If a patient stops drinking, alcoholic hepatitis can either resolve or greatly improve after about 6-12 months.
  • In milder cases complete resolution is possible.
  • In severe cases, alcoholic hepatitis can lead to residual cirrhosis.

How long does a patient have be abstinent from alcohol to be transplanted?

  • To be considered for liver transplantation a patient must abstain from alcohol for at least 6 months.
  • In milder cases, alcoholic hepatitis that does not lead to cirrhosis can improve significantly after about 6-12 months of abstinence.
  • Commentary challenging mandatory abstinence period: http://www.ncbi.nlm.nih.gov/pubmed/25892898

 

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Liver: Autoimmune Hepatitis

Which antibody assays are used to detect each type of autoimmune hepatitis?

  • Autoimmune Hepatitis Type 1: anti-smooth muscle antibodies, ANA
  • Autoimmune Hepatitis Type 2: anti-liver-kidney microsomal type 1 (anti-LKM-1) antibody
  • Autoimmune Hepatitis Type 3: anti-soluble liver antigen antibody (anti-SLA)

How do we treat autoimmune hepatitis?

  • Generally treat autoimmune hepatitis with prednisone and azathioprine.
  • Keep in mind that if you use azathioprine you should check a TPMT enzyme activity test.
  • 0.3% of the population has TPMT coding mutations and thus will have excess levels of 6-mercaptopurine (the azathioprine metabolite) which can cause increase the risk of bone marrow suppression.

 

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Liver: Cirrhosis

 

What are the most common causes of ascites in the U.S.?

  • Cirrhosis
  • Neoplasm
  • Congestive heart failure
  • Tuberculous peritonitis

What SAAG and total protein values are suggestive of cirrhosis?

What is a MELD score?

  • MELD stands for Model for End-Stage Liver Disease.
  • Originally designed to assess three-month mortality of surgery in patients who had undergone a TIPS (transjugular intrahepatic shunt).
  • Now used to determine prognosis and prioritization for liver transplant.
  • Involves the total bilirubin, INR, and creatinine
  • Can be modified if the patient is also on hemodialysis or based on the patient’s sodium
  • Comparison of MELD and CTP score in extrahepatic surgery mortality: http://www.ncbi.nlm.nih.gov/pubmed/23647879

How do NSAIDs affect cirrhotic patients?

  • Can cause bleeding in the setting of varices
  • NSAIDs also inhibit prostaglandin synthesis which leads to worsening of the renal vasoconstriction that already is present in decompensated cirrhosis leading to a drop in GFR

What is the Child-Turcotte-Pugh (CTP) score?

  • Used to grade the severity of liver disease
  • One, two, or three points are assigned to each of five categories:
    • Encephalopathy
    • Ascites
    • Albumin
    • Bilirubin
    • INR
  • Child Class A: 0-6 points
  • Child Class B: 7-9 points
  • Child Class C: 10+ points
  • Comparison of MELD and CTP score in extrahepatic surgery mortality: http://www.ncbi.nlm.nih.gov/pubmed/23647879

What are the most common physical exam signs of cirrhosis/liver disease?

  • Systemic: fatigue, anorexia, weight loss, muscle wasting
  • Skin: jaundice, spider angioma, skin telangiectasis (“paper money skin”), palmar erythema
  • Ascites: abdominal distention, bulging flanks, shifting dullness, “puddle sign” when patients kneel onto their elbows and knees
  • Encephalopathy: asterixis, Milkmaid’s grip
  • JAMA Rational Clinical Examination Series: Does this Patient with Liver Disease Have Cirrhosis? http://jama.jamanetwork.com/article.aspx?articleid=1355997&resultClick=3

What are the most common causes of cirrhosis in the U.S.?

  • Hepatitis C (26%)
  • Alcoholic liver disease (21%)
  • Cryptogenic causes including NAFLD (18%)
  • Hepatitis C plus alcoholic liver disease (15%)
  • Hepatitis B (15%)

How does cirrhosis alter blood flow?

  • Patients with cirrhosis and portal hypertension alter blood flow in two main ways:
    • Increased nitric oxide leads to peripheral vascular dilation and increased cardiac output which lead to increased splanchnic arterial flow which results in more splanchnic venous flow into the liver which can get backed up into other organs.
    • Splanchnic vasodilation occurs through multiple vasodilating substances which also includes nitric oxide.

 

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Liver: Hemochromatosis

 

What lab tests can be used to diagnose hemochromatosis?

  • Transferrin saturation > 45% is the preferred initial test
  • Next step would be to check for a C282Y or H63D mutation to confirm the diagnosis
  • Often see serum iron concentration greater than 150mcg/dL
  • TIBC may range 200-300mcg/dL (technically in the normal lab range)
  • Ferritin is considered less sensitive
  • Diagnostic testing in hemochromatosis: http://www.ncbi.nlm.nih.gov/pubmed/25976957

What are the most common signs of hemochromatosis?

  • Liver disease and cirrhosis
  • Skin hyperpigmentation and bronzing
  • Diabetes
  • Arthritis
  • Cardiomyopathy
  • Hormonal disturbances: impotence, hypogonadism, amenorrhea

 

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Liver: Hepatic Encephalopathy

What EEG changes are seen in hepatic encephalopathy?

  • High amplitude, low frequency waves
  • Triphasic waves
  • These are nonspecific but classic signs of hepatic encephalopathy
  • 2016 article on using EEG to assess for hepatic encephalopathy: http://www.ncbi.nlm.nih.gov/pubmed/26833704

How is hepatic encephalopathy severity graded?

  • Grade 0: subclinical with normal mental status
  • Grade 1: mild confusion, slowing, mood changes or irritability, inverted sleep cycle
  • Grade 2: drowsiness, obvious personality changes, inappropriate behavior, gross deficits during mental tasks
  • Grade 3: somnolent but arousable, unable to perform mental tasks, marked confusion and disorientation, speech is incomprehensible, can have fits of rage
  • Grade 4: coma with or without response to painful stimuli
  • Correlation between ammonia levels and severity of hepatic encephalopathy: http://www.ncbi.nlm.nih.gov/pubmed/12637132

What are common precipitants of hepatic encephalopathy?

  • Infection
  • Diuretic therapy/Hypovolemia
  • GI bleeding
  • Renal failure
  • Constipation

How do we treat hepatic encephalopathy?

  • First treat the underlying cause.
  • Lactulose: stimulates movement of ammonia from tissues to the gut lumen and inhibits intestinal ammonia production
  • Neomycin or Rifaximin: decrease colonic concentration of ammoniagenic bacteria
  • Zinc: zinc is a cofactor for the pathway that allows ammonia to be converted to urea
  • Less commonly: L-ornithine, L-aspartate, sodium benzoate
  • Protein restriction
  • Review of hepatic encephalopathy treatment: http://www.ncbi.nlm.nih.gov/pubmed/26692331

 

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Liver: Hepatorenal Syndrome

 

How do we diagnose hepatorenal syndrome?

  • Major criteria:
    • Serum creatinine greater than 1.5mg/dl or creatinine clearance less than 40mL/min
    • When no other cause of renal dysfunction can be found (shock, infection, fluid losses, nephrotoxic medications)
    • Absence of proteinuria (less than 500mg/day)
    • No improvement of renal function after at least 1.5L of plasma expander has been infused
  • Minor criteria:
    • Less than 500mL/day of urine
    • Urine sodium less than 10 mEq/L present
    • Urine osmolality greater than blood
    • Absence of hematuria
    • Serum sodium less than 130
  • Serum creatinine greater than 1.5mg/dl or creatinine clearance less than 40mL/min
  • Review of management of AKI in cirrhotic patients: http://www.ncbi.nlm.nih.gov/pubmed/26724589

What is the standard treatment cocktail for hepatorenal syndrome?

What are the two types of hepatorenal syndrome?

  • Pathophysiology: vasoconstriction of small and large renal arteries causing hypoperfusion
  • Type I HRS: rapid onset liver failure requiring liver transplantation
  • Type II HRS: slower progression and may develop ascites resistant to diuretics

 

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Liver: Spontaneous Bacterial Peritonitis (SBP)

 

How do you diagnose spontaneous bacterial peritonitis

  • Paracentesis with peritoneal fluid showing greater than 250 polymorphonuclear cells (PMNs) per mm3 of ascites with a positive ascites culture.
  • For every 250 red blood cells in the ascites subtract one PMN
  • More commonly the ascites cultures are negative making it culture-negative neutrocytic ascites.
  • Both culture positive and culture negative ascites carry a 20-30% mortality rate.
  • 2016 review of SBP treatment: http://www.ncbi.nlm.nih.gov/pubmed/26671516

 

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Liver: Wilson's Disease

How do you diagnose Wilson’s disease?

  • Serum ceruloplasmin less than 20mg/dL
  • Urine copper excretion greater than 100mcg/day
  • If the patient has Kayser-Fleischer rings, then having a ceruloplasmin of 0 and urine copper excretion > 40mcg/day is diagnostic
  • Liver biopsy specimen with > 250 mcg/g hepatic copper concentration
  • Wilson’s disease review article: http://www.ncbi.nlm.nih.gov/pubmed/26692151

What is the role of Kayser-Fleischer rings in Wilson’s disease?

  • Represent copper deposition in the Descemet membrane of the limbus of the cornea.
  • Rings can be visible to the naked eye, visible using an ophthalmoscope, or may require slit-lamp exam.
  • Not pathognomonic for Wilson’s disease unless there are neurologic manifestations.
  • 90% of patients with symptomatic Wilson’s disease will have Kayser-Fleischer rings.
  • JAMA Ophthalmology article on Kayser-Fleischer rings in Wilson’s disease: http://www.ncbi.nlm.nih.gov/pubmed/24809467

What are the stages of Wilson’s disease?

  • Stage I: accumulation of copper in liver
  • Stage II: redistribution of copper in the liver and release into circulation
  • Stage III: accumulation of copper in brain and other extrahepatic tissue with progressive and fatal disease
  • Stage IV: chelation therapy leads to copper balance
  • Wilson’s disease review article: http://www.ncbi.nlm.nih.gov/pubmed/26692151

 

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Pancreas: Acute Pancreatitis

How do we use the APACHE II score in acute pancreatitis?

  • APACHE II score is used only within the first 24 hours of admission to assess severity of pancreatitis and morbidity/mortality
  • There are 12 physiologic variables (use the worst value of each) and 2 disease-related variables to form a score from 0 to 71
  • A score of 0-4 indicates a 4% non-operative mortality and a 1% post-operative mortality
  • A score greater than 35 indicates an 85% non-operative mortality and an 88% post-operative mortality
  • Comparison of APACHE II, Ranson, and Glasgow scoring systems in pancreatitis: http://www.ncbi.nlm.nih.gov/pubmed/15720995

What are the most common causes of acute pancreatitis?

  • Gallstones
  • Alcohol
  • ERCP-induced
  • Drug-induced
  • Developmental abnormalities of the pancreas (pancreas divisum, annular pancreas, and Sphicter of Oddi dysfunction)
  • Hypertriglyceridemia

What are the physical exam findings in acute pancreatitis?

  • These three physical exam findings are classically seen in severe necrotizing pancreatitis
    • Cullen sign: blue discoloration around the umbilicus caused by hemoperitoneum
    • Grey-Turner sign: red/brown discoloration at the flanks from retroperitoneal bleed or extravasated pancreatic exudates
    • Erythematous skin nodules: from fat necrosis usually less than 1cm

How do we treat acute pancreatitis?

  • Supportive therapy unless you have necrotizing pancreatitis in which case a carbapenem should be started
  • Bowel rest, fluids, pain control
  • Treat the underlying cause of pancreatitis if possible
  • Italian Association for the Study of the Pancreas Guidelines on acute pancreatitis treatment: Wilson’s disease review article: http://www.ncbi.nlm.nih.gov/pubmed/26692151

 

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Pancreas: Pancreatic Cancer

What are the physical exam eponym findings in pancreatic cancer?

  • Most common: painless obstructive jaundice (especially when the tumor is at the head of the pancreas)
  • Trousseau sign: migratory thrombophlebitis
  • Courvoisier sign: palpable gallbladder
  • Sister Mary Joseph nodule: paraumbilical nodules
  • Blumer’s shelf: palpable mass in the rectal pouch (Blumer’s shelf)
  • Virchow’s node: palpable lymph node behind the left clavicle

What risk factors predispose a patient to pancreatic cancer?

  • Smoking
  • Age, gender, ethnicity
  • Family history
  • Chronic pancreatitis
  • Obesity/diabetes

What tumor markers are often sent in pancreatic cancer?

  • As with many other cancers, tumor markers are helpful but often nonspecific
  • CA 19-9: about 80% of patients with pancreatic cancer will have elevated CA 19-9 levels, but notably early stage tumors may not have detectable CA 19-9 and 5-10% of patients lack the enzyme to make CA 19-9
  • CEA: only 40-45% of patients with pancreatic cancer have elevated CEA levels, and notably both benign and malignant pancreatic conditions can lead to elevated CEA levels

 

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