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DDSEP® 9 Quick Quiz
Q2. Correct answer: D
Rationale
Episodic hepatic encephalopathy is usually precipitant-induced in over 80% of cases and includes dehydration, infections, over diuresis, gastrointestinal bleeding, constipation, and the use of narcotics and sedatives. Key is to identify and treat the precipitant. A diagnostic workup to rule out other disorders that can alter brain function and mimic hepatic encephalopathy should also be performed.
Reference
1. Viltstrup H et al. Hepatic encephalopathy in chronic liver disease: 2014 Practice Guideline by the American Association for the Study of Liver Diseases and the European Association for the Study of the Liver. Hepatology. 2014;60(2):715-35.
ginews@gastro.org
Q2. Correct answer: D
Rationale
Episodic hepatic encephalopathy is usually precipitant-induced in over 80% of cases and includes dehydration, infections, over diuresis, gastrointestinal bleeding, constipation, and the use of narcotics and sedatives. Key is to identify and treat the precipitant. A diagnostic workup to rule out other disorders that can alter brain function and mimic hepatic encephalopathy should also be performed.
Reference
1. Viltstrup H et al. Hepatic encephalopathy in chronic liver disease: 2014 Practice Guideline by the American Association for the Study of Liver Diseases and the European Association for the Study of the Liver. Hepatology. 2014;60(2):715-35.
ginews@gastro.org
Q2. Correct answer: D
Rationale
Episodic hepatic encephalopathy is usually precipitant-induced in over 80% of cases and includes dehydration, infections, over diuresis, gastrointestinal bleeding, constipation, and the use of narcotics and sedatives. Key is to identify and treat the precipitant. A diagnostic workup to rule out other disorders that can alter brain function and mimic hepatic encephalopathy should also be performed.
Reference
1. Viltstrup H et al. Hepatic encephalopathy in chronic liver disease: 2014 Practice Guideline by the American Association for the Study of Liver Diseases and the European Association for the Study of the Liver. Hepatology. 2014;60(2):715-35.
ginews@gastro.org
A 62-year-old man with hepatitis C cirrhosis is admitted with altered mental status. He had a recent dental procedure and was given pain medication and a short course of antibiotics. He is only taking spironolactone 50 mg for small ascites. Patient is alert but not oriented to place and time. He has evidence of asterixis. His mucous membranes are dry and he has no evidence of ascites on exam. His labs include WBC, 4.7 × 103 mm3; AST, 45 U/L; ALT, 40 U/L; total bilirubin of 2.5 mg/dL; albumin of 3.7 g/dL; sodium 142 mEq/L; and a creatinine of 0.5 mg/dL.
DDSEP® 9 Quick Quiz
Q1. Correct answer: A
Rationale
In the United States, pigmented stones (black and brown) are less common than cholesterol gallstones. Both types of pigmented stones contain an excess of unconjugated bilirubin and are composed of calcium hydrogen bilirubinate, which is oxidized and polymerized in the hard black stones but unpolymerized in softer brown stones. Black pigmented gallstones are frequently radiopaque and form in sterile bile. Risk factors for black pigmented stones include hemolysis (example, sickle cell disease), cirrhosis, cystic fibrosis, and diseases affecting the ileum (example, Crohn's disease). In contrast, brown stones are more likely to occur in the bile ducts, are radiolucent, and form secondary to biliary stasis (example, biliary stricture) and infection (example, Clonorchis sinensis).
Obesity, female sex, and hyperlipidemia are risk factors for cholesterol gallstone formation. Octreotide decreases gallbladder motility and long-term use can increase the risk of cholelithiasis.
References
1. Stinton LM, Myers RP, Shaffer EA. Epidemiology of gallstones. Gastroenterol Clin N Am. 2010;39:157-69.
2. Vitek L, Carey MC. New pathophysiological concepts underlying pathogenesis of pigment gallstones. Clin Res Hepatol Gastroenterol. 2012;36:122-9.
ginews@gastro.org
Q1. Correct answer: A
Rationale
In the United States, pigmented stones (black and brown) are less common than cholesterol gallstones. Both types of pigmented stones contain an excess of unconjugated bilirubin and are composed of calcium hydrogen bilirubinate, which is oxidized and polymerized in the hard black stones but unpolymerized in softer brown stones. Black pigmented gallstones are frequently radiopaque and form in sterile bile. Risk factors for black pigmented stones include hemolysis (example, sickle cell disease), cirrhosis, cystic fibrosis, and diseases affecting the ileum (example, Crohn's disease). In contrast, brown stones are more likely to occur in the bile ducts, are radiolucent, and form secondary to biliary stasis (example, biliary stricture) and infection (example, Clonorchis sinensis).
Obesity, female sex, and hyperlipidemia are risk factors for cholesterol gallstone formation. Octreotide decreases gallbladder motility and long-term use can increase the risk of cholelithiasis.
References
1. Stinton LM, Myers RP, Shaffer EA. Epidemiology of gallstones. Gastroenterol Clin N Am. 2010;39:157-69.
2. Vitek L, Carey MC. New pathophysiological concepts underlying pathogenesis of pigment gallstones. Clin Res Hepatol Gastroenterol. 2012;36:122-9.
ginews@gastro.org
Q1. Correct answer: A
Rationale
In the United States, pigmented stones (black and brown) are less common than cholesterol gallstones. Both types of pigmented stones contain an excess of unconjugated bilirubin and are composed of calcium hydrogen bilirubinate, which is oxidized and polymerized in the hard black stones but unpolymerized in softer brown stones. Black pigmented gallstones are frequently radiopaque and form in sterile bile. Risk factors for black pigmented stones include hemolysis (example, sickle cell disease), cirrhosis, cystic fibrosis, and diseases affecting the ileum (example, Crohn's disease). In contrast, brown stones are more likely to occur in the bile ducts, are radiolucent, and form secondary to biliary stasis (example, biliary stricture) and infection (example, Clonorchis sinensis).
Obesity, female sex, and hyperlipidemia are risk factors for cholesterol gallstone formation. Octreotide decreases gallbladder motility and long-term use can increase the risk of cholelithiasis.
References
1. Stinton LM, Myers RP, Shaffer EA. Epidemiology of gallstones. Gastroenterol Clin N Am. 2010;39:157-69.
2. Vitek L, Carey MC. New pathophysiological concepts underlying pathogenesis of pigment gallstones. Clin Res Hepatol Gastroenterol. 2012;36:122-9.
ginews@gastro.org
A 56-year-old woman presents for evaluation of right upper-quadrant pain. Her medical history is remarkable for obesity with a BMI of 31 kg/m2, hyperlipidemia, diabetes mellitus, NASH cirrhosis, and a recent admission for melena. During her prior admission, she was treated with a proton pump inhibitor and octreotide. Esophagogastroduodenoscopy revealed a gastric ulcer with signs of recent bleeding and small esophageal varices without red wale signs.
Her lab evaluation is as follows: AST, 69 U/L; ALT, 35 U/L; total bilirubin, 1.6 mg/dL; alkaline phosphatase, 121 U/L, leukocytes 7,500/microL. An abdominal ultrasound is notable for a positive sonographic Murphy's sign, cholelithiasis, an 8-mm gallbladder wall, normal appearing bile ducts, and a cirrhotic appearing liver with splenomegaly. She undergoes cholecystectomy. Examination of the gallbladder reveals numerous hard gallstones, which are predominately composed of calcium bilirubinate.
DDSEP® 9 Quick Quiz Question 2
Q2. Correct answer: D
Rationale
This patient has tropical sprue based on her travel to an endemic country, negative celiac serologies, labs revealing a macrocytic anemia and low albumin and characteristic histology (villous blunting, increased intraepithelial lymphocytes). Treatment is with tetracycline and folate. Diagnosis of tropical sprue is ultimately confirmed by a response to treatment. A gluten-free diet is not appropriate, as the patient does not have celiac disease, confirmed by normal celiac serologies. Ceftriaxone IV followed by Bactrim PO is the correct treatment for Whipple's disease. A diet low in fermentable oligo-, di-, and monosaccharides and polyols (FODMAPs) is beneficial treatment in some patients with IBS with abdominal bloating or pain. Rifaximin is the correct treatment for small intestine bacterial overgrowth or IBS-D.
References
1. Brown IS, Bettington A, Bettington M, Rosty C. Tropical sprue: revisiting an underrecognized disease. Am J Surg Pathol. 2014;38:666.
2. Shah VH, Rotterdam H, Kotler DP, et al. All that scallops is not celiac disease. Gastrointest Endosc. 2000;51:717.
ginews@gastro.org
Q2. Correct answer: D
Rationale
This patient has tropical sprue based on her travel to an endemic country, negative celiac serologies, labs revealing a macrocytic anemia and low albumin and characteristic histology (villous blunting, increased intraepithelial lymphocytes). Treatment is with tetracycline and folate. Diagnosis of tropical sprue is ultimately confirmed by a response to treatment. A gluten-free diet is not appropriate, as the patient does not have celiac disease, confirmed by normal celiac serologies. Ceftriaxone IV followed by Bactrim PO is the correct treatment for Whipple's disease. A diet low in fermentable oligo-, di-, and monosaccharides and polyols (FODMAPs) is beneficial treatment in some patients with IBS with abdominal bloating or pain. Rifaximin is the correct treatment for small intestine bacterial overgrowth or IBS-D.
References
1. Brown IS, Bettington A, Bettington M, Rosty C. Tropical sprue: revisiting an underrecognized disease. Am J Surg Pathol. 2014;38:666.
2. Shah VH, Rotterdam H, Kotler DP, et al. All that scallops is not celiac disease. Gastrointest Endosc. 2000;51:717.
ginews@gastro.org
Q2. Correct answer: D
Rationale
This patient has tropical sprue based on her travel to an endemic country, negative celiac serologies, labs revealing a macrocytic anemia and low albumin and characteristic histology (villous blunting, increased intraepithelial lymphocytes). Treatment is with tetracycline and folate. Diagnosis of tropical sprue is ultimately confirmed by a response to treatment. A gluten-free diet is not appropriate, as the patient does not have celiac disease, confirmed by normal celiac serologies. Ceftriaxone IV followed by Bactrim PO is the correct treatment for Whipple's disease. A diet low in fermentable oligo-, di-, and monosaccharides and polyols (FODMAPs) is beneficial treatment in some patients with IBS with abdominal bloating or pain. Rifaximin is the correct treatment for small intestine bacterial overgrowth or IBS-D.
References
1. Brown IS, Bettington A, Bettington M, Rosty C. Tropical sprue: revisiting an underrecognized disease. Am J Surg Pathol. 2014;38:666.
2. Shah VH, Rotterdam H, Kotler DP, et al. All that scallops is not celiac disease. Gastrointest Endosc. 2000;51:717.
ginews@gastro.org
An 18-year-old woman presents for evaluation of chronic diarrhea, fatigue, and abdominal cramping. She was recently in Puerto Rico for 6 months visiting family and returned a few weeks ago. Her labs are significant for a hemoglobin of 11 g/L with an MCV of 109 fL. Her albumin is 3.6 g/dL. She had stool studies which ruled out infection, including parasites. TtG IgA and total IgA were within normal limits. EGD with multiple duodenal biopsies showed villous blunting with increased intraepithelial lymphocytes.
March 2020 - Question 1
Correct answer: C
Rationale
This patient has been exposed to HBV in the past and has cleared the virus. The HBVcore total Ab is indicative of prior exposure while the HBV surface Ab is detectable and gives immunity against reinfection under most routine clinical scenarios. Patients who have been exposed to HBV still have HBV ccc DNA within their hepatocytes that is dormant, but under extreme combined B and T cell immunosuppression, the patients are at risk for reverse seroconversion where they can lose HBV surface Ab and manifest HBV surface antigen and present as an acute HBV infection. Prophylaxis is required during therapy and for at least 12-18 months after therapy due to the long-lasting effects of anti-B cell monoclonal antibodies like rituximab. Reactivation of HCV in HCV Ab–positive, RNA-negative patients has not been reported.
Reference
1. Pauly MP, Tucker LY, Szpakowski JL, et al. Incidence of hepatitis B virus reactivation and hepatotoxicity in patients receiving long-term treatment with tumor necrosis factor antagonists. Clin Gastroenterol Hepatol. 2018 Apr 24. doi: 10.1016/j. cgh.2018.04.033.
ginews@gastro.org
Correct answer: C
Rationale
This patient has been exposed to HBV in the past and has cleared the virus. The HBVcore total Ab is indicative of prior exposure while the HBV surface Ab is detectable and gives immunity against reinfection under most routine clinical scenarios. Patients who have been exposed to HBV still have HBV ccc DNA within their hepatocytes that is dormant, but under extreme combined B and T cell immunosuppression, the patients are at risk for reverse seroconversion where they can lose HBV surface Ab and manifest HBV surface antigen and present as an acute HBV infection. Prophylaxis is required during therapy and for at least 12-18 months after therapy due to the long-lasting effects of anti-B cell monoclonal antibodies like rituximab. Reactivation of HCV in HCV Ab–positive, RNA-negative patients has not been reported.
Reference
1. Pauly MP, Tucker LY, Szpakowski JL, et al. Incidence of hepatitis B virus reactivation and hepatotoxicity in patients receiving long-term treatment with tumor necrosis factor antagonists. Clin Gastroenterol Hepatol. 2018 Apr 24. doi: 10.1016/j. cgh.2018.04.033.
ginews@gastro.org
Correct answer: C
Rationale
This patient has been exposed to HBV in the past and has cleared the virus. The HBVcore total Ab is indicative of prior exposure while the HBV surface Ab is detectable and gives immunity against reinfection under most routine clinical scenarios. Patients who have been exposed to HBV still have HBV ccc DNA within their hepatocytes that is dormant, but under extreme combined B and T cell immunosuppression, the patients are at risk for reverse seroconversion where they can lose HBV surface Ab and manifest HBV surface antigen and present as an acute HBV infection. Prophylaxis is required during therapy and for at least 12-18 months after therapy due to the long-lasting effects of anti-B cell monoclonal antibodies like rituximab. Reactivation of HCV in HCV Ab–positive, RNA-negative patients has not been reported.
Reference
1. Pauly MP, Tucker LY, Szpakowski JL, et al. Incidence of hepatitis B virus reactivation and hepatotoxicity in patients receiving long-term treatment with tumor necrosis factor antagonists. Clin Gastroenterol Hepatol. 2018 Apr 24. doi: 10.1016/j. cgh.2018.04.033.
ginews@gastro.org
Q1. A 45-year-old man has recently been diagnosed with leukemia. The chemotherapeutic regimen will include rituximab and high-dose steroids. He is a former IV drug user but has been sober for 20 years. His lab work is as follows: ALT 25 U/L, HAV total antibody positive, HBs antibody positive, HBs antigen negative, HBc total positive, HCV antibody positive, HCV RNA undetected.
February 2020: Question 2
Q2. Correct Answer: C
Rationale
Carvedilol is a nonselective beta-blocker with vasodilating properties that is used to decrease portal pressure and prevent first variceal hemorrhage. It has more robust effect on the reduction of portal pressure than nadolol or propranolol. A safe and effective dose is 12.5 mg/day. Doses higher than 12.5 mg a day are associated with increased side effects and hypotension in patients with impaired liver function caused alpha1 antagonist action and excessive first pass metabolism.
References
1. Tripathi D, Ferguson JW, Kochar N, et al. Randomized controlled trial of carvedilol versus variceal band ligation for the prevention of the first variceal bleed. Hepatology. 2009 Sep;50(3):825-33.
2. Carvedilol (coreg) package insert Philadelphia. SmithKline Beecham Pharmaceuticals. May 1997.
ginews@gastro.org
Q2. Correct Answer: C
Rationale
Carvedilol is a nonselective beta-blocker with vasodilating properties that is used to decrease portal pressure and prevent first variceal hemorrhage. It has more robust effect on the reduction of portal pressure than nadolol or propranolol. A safe and effective dose is 12.5 mg/day. Doses higher than 12.5 mg a day are associated with increased side effects and hypotension in patients with impaired liver function caused alpha1 antagonist action and excessive first pass metabolism.
References
1. Tripathi D, Ferguson JW, Kochar N, et al. Randomized controlled trial of carvedilol versus variceal band ligation for the prevention of the first variceal bleed. Hepatology. 2009 Sep;50(3):825-33.
2. Carvedilol (coreg) package insert Philadelphia. SmithKline Beecham Pharmaceuticals. May 1997.
ginews@gastro.org
Q2. Correct Answer: C
Rationale
Carvedilol is a nonselective beta-blocker with vasodilating properties that is used to decrease portal pressure and prevent first variceal hemorrhage. It has more robust effect on the reduction of portal pressure than nadolol or propranolol. A safe and effective dose is 12.5 mg/day. Doses higher than 12.5 mg a day are associated with increased side effects and hypotension in patients with impaired liver function caused alpha1 antagonist action and excessive first pass metabolism.
References
1. Tripathi D, Ferguson JW, Kochar N, et al. Randomized controlled trial of carvedilol versus variceal band ligation for the prevention of the first variceal bleed. Hepatology. 2009 Sep;50(3):825-33.
2. Carvedilol (coreg) package insert Philadelphia. SmithKline Beecham Pharmaceuticals. May 1997.
ginews@gastro.org
Q2.
February 2020: Question 1
Q1. Correct Answer: B
Rationale
The leading cause of death in patients with NASH is cardiovascular disease. Death from liver-related causes is much more common in NASH than in the general population, but is not the leading cause of death. Cancer-related death is among the top three causes of death in patients with NASH, but is not the most common.
References
1. Adams LA, Lymp JF, St Sauver J, et al. The natural history of nonalcoholic fatty liver disease: a population-based cohort study. Gastroenterology 2005;129:113-21.
2. Chalasani N, Younossi Z, Lavine JE, et al. The Diagnosis and Management of Nonalcoholic Fatty Liver Disease: Practice Guidance from the American Association for the Study of Liver Disease. Hepatology 2018;67:328-57.
Q1. Correct Answer: B
Rationale
The leading cause of death in patients with NASH is cardiovascular disease. Death from liver-related causes is much more common in NASH than in the general population, but is not the leading cause of death. Cancer-related death is among the top three causes of death in patients with NASH, but is not the most common.
References
1. Adams LA, Lymp JF, St Sauver J, et al. The natural history of nonalcoholic fatty liver disease: a population-based cohort study. Gastroenterology 2005;129:113-21.
2. Chalasani N, Younossi Z, Lavine JE, et al. The Diagnosis and Management of Nonalcoholic Fatty Liver Disease: Practice Guidance from the American Association for the Study of Liver Disease. Hepatology 2018;67:328-57.
Q1. Correct Answer: B
Rationale
The leading cause of death in patients with NASH is cardiovascular disease. Death from liver-related causes is much more common in NASH than in the general population, but is not the leading cause of death. Cancer-related death is among the top three causes of death in patients with NASH, but is not the most common.
References
1. Adams LA, Lymp JF, St Sauver J, et al. The natural history of nonalcoholic fatty liver disease: a population-based cohort study. Gastroenterology 2005;129:113-21.
2. Chalasani N, Younossi Z, Lavine JE, et al. The Diagnosis and Management of Nonalcoholic Fatty Liver Disease: Practice Guidance from the American Association for the Study of Liver Disease. Hepatology 2018;67:328-57.
You recently diagnosed a 66-year-old man with cirrhosis due to nonalcoholic steatohepatitis. The patient presents to your clinic now inquiring about his long-term prognosis.
Question 2
Q2. Correct Answer: D
Rationale
Elbasvir and grazoprevir are hepaticaly metabo¬lized and undergo minimal renal elimination making them safe for use in patients with end stage renal disease. The C-Surfer trial evaluated elbasvir and grazoprevir in genotype 1 patients with advanced renal disease inclusive of patients on hemodialysis. Cure rates in this trial were 94- 99 percent. Sofosbuvir containing regimen are not approved for patient with CKD stage 4-5 or those on hemodialysis, even when given in a dose reduced or post-dialysis fashion.
References
https://www.hcvguidelines.org/unique-popula¬tions/renal-impairment
Roth D, Nelson DR, Bruchfeld A, et al. Grazoprevir plus elbasvir in treatment-naive and treat¬ment experienced patients with hepatitis C virus genotype 1 infection and stage 4-5 chronic kidney disease (the C-SURFER study): a combination phase 3 study. Lancet. 2015;386(10003):1537-45.
Q2. Correct Answer: D
Rationale
Elbasvir and grazoprevir are hepaticaly metabo¬lized and undergo minimal renal elimination making them safe for use in patients with end stage renal disease. The C-Surfer trial evaluated elbasvir and grazoprevir in genotype 1 patients with advanced renal disease inclusive of patients on hemodialysis. Cure rates in this trial were 94- 99 percent. Sofosbuvir containing regimen are not approved for patient with CKD stage 4-5 or those on hemodialysis, even when given in a dose reduced or post-dialysis fashion.
References
https://www.hcvguidelines.org/unique-popula¬tions/renal-impairment
Roth D, Nelson DR, Bruchfeld A, et al. Grazoprevir plus elbasvir in treatment-naive and treat¬ment experienced patients with hepatitis C virus genotype 1 infection and stage 4-5 chronic kidney disease (the C-SURFER study): a combination phase 3 study. Lancet. 2015;386(10003):1537-45.
Q2. Correct Answer: D
Rationale
Elbasvir and grazoprevir are hepaticaly metabo¬lized and undergo minimal renal elimination making them safe for use in patients with end stage renal disease. The C-Surfer trial evaluated elbasvir and grazoprevir in genotype 1 patients with advanced renal disease inclusive of patients on hemodialysis. Cure rates in this trial were 94- 99 percent. Sofosbuvir containing regimen are not approved for patient with CKD stage 4-5 or those on hemodialysis, even when given in a dose reduced or post-dialysis fashion.
References
https://www.hcvguidelines.org/unique-popula¬tions/renal-impairment
Roth D, Nelson DR, Bruchfeld A, et al. Grazoprevir plus elbasvir in treatment-naive and treat¬ment experienced patients with hepatitis C virus genotype 1 infection and stage 4-5 chronic kidney disease (the C-SURFER study): a combination phase 3 study. Lancet. 2015;386(10003):1537-45.
A 47-year-old man with stage 5 chronic kidney disease on hemodialysis is referred to your clinic. He has genotype 1a HCV and F2 fibrosis. He wants to discuss treatment options.
Question 1
Q1. Correct answer: C
Rationale
There are many potential reasons for PPI failure in patients with symptoms of gastroesophageal reflux. However, the single most important reason is inappropriate drug administration. Patients should be counseled to take their medication 30-60 minutes prior to meals for optimal physiologic gastric acid inhibition, with the morning meal favored over the evening meal due to relative more gastric acid production at this time.
Reference
Fass R, Shapiro M, Dekel R. Systematic review: proton-pump inhibitor failure in gastro-oesophageal reflux disease – where next? Aliment Pharmacol Ther. 2005;22:79-94.
Q1. Correct answer: C
Rationale
There are many potential reasons for PPI failure in patients with symptoms of gastroesophageal reflux. However, the single most important reason is inappropriate drug administration. Patients should be counseled to take their medication 30-60 minutes prior to meals for optimal physiologic gastric acid inhibition, with the morning meal favored over the evening meal due to relative more gastric acid production at this time.
Reference
Fass R, Shapiro M, Dekel R. Systematic review: proton-pump inhibitor failure in gastro-oesophageal reflux disease – where next? Aliment Pharmacol Ther. 2005;22:79-94.
Q1. Correct answer: C
Rationale
There are many potential reasons for PPI failure in patients with symptoms of gastroesophageal reflux. However, the single most important reason is inappropriate drug administration. Patients should be counseled to take their medication 30-60 minutes prior to meals for optimal physiologic gastric acid inhibition, with the morning meal favored over the evening meal due to relative more gastric acid production at this time.
Reference
Fass R, Shapiro M, Dekel R. Systematic review: proton-pump inhibitor failure in gastro-oesophageal reflux disease – where next? Aliment Pharmacol Ther. 2005;22:79-94.
.
November 2019
Q2. Correct answer: D
Rationale
HELLP syndrome is a multisystemic disorder that is characterized by the development of hemolytic anemia, elevated liver enzymes, and low platelets. Most cases occur between 28 and 36 weeks of gestation, but it can also develop up to 1 week postpartum in 30% of cases.
Reference
Fitzpatrick KE, et al. Risk factors, management, and outcomes of hemolysis, elevated liver enzymes, and low platelets syndrome and elevated liver enzymes, low platelets syndrome. Obstet Gynecol. 2014 Mar;123(3):618-27.
Q2. Correct answer: D
Rationale
HELLP syndrome is a multisystemic disorder that is characterized by the development of hemolytic anemia, elevated liver enzymes, and low platelets. Most cases occur between 28 and 36 weeks of gestation, but it can also develop up to 1 week postpartum in 30% of cases.
Reference
Fitzpatrick KE, et al. Risk factors, management, and outcomes of hemolysis, elevated liver enzymes, and low platelets syndrome and elevated liver enzymes, low platelets syndrome. Obstet Gynecol. 2014 Mar;123(3):618-27.
Q2. Correct answer: D
Rationale
HELLP syndrome is a multisystemic disorder that is characterized by the development of hemolytic anemia, elevated liver enzymes, and low platelets. Most cases occur between 28 and 36 weeks of gestation, but it can also develop up to 1 week postpartum in 30% of cases.
Reference
Fitzpatrick KE, et al. Risk factors, management, and outcomes of hemolysis, elevated liver enzymes, and low platelets syndrome and elevated liver enzymes, low platelets syndrome. Obstet Gynecol. 2014 Mar;123(3):618-27.
Q2. A 29-year-old woman at 37 weeks gestation presents to the emergency room with right upper quadrant pain, nausea, vomiting. She is diagnosed with preeclampsia. She is treated with intravenous magnesium, antihypertensive therapy, and labor is induced. Prior to delivery, laboratory values were as follows: aspartate aminotransferase, 240 U/L; alanine aminotransferase, 220 U/L; total bilirubin, 1.8 mg/dL; hemoglobin, 10.1 g/dL; platelets, 110,000 microL. Forty-eight hours following delivery, she complained of worsening right upper quadrant pain and headache. Repeat laboratory values 48 hours postpartum were as follows: AST, 410 U/L; ALT, 390 U/L; total bilirubin, 5.1 mg/dL; hemoglobin, 7.9 g/dL; and platelets 75,000 microL.
November 2019
Q1. Correct answer: F
Rationale
There are a number of known risk factors for cholangiocarcinoma including PSC, choledochal cysts, obesity, chronic liver disease, toxins such as Thorotrast as well as liver flukes including those in the Opisthorchis and Clonorchis genus. While Fasciola does infect the liver, an association has not been reported with cholangiocarcinoma.
References
1. Fevery J, et al. Malignancies and mortality in 200 patients with primary sclerosering cholan¬gitis: a long-term single-centre study. Liver Int. 2012;32(2):214-22.
2. Razumilava N, Gores GJ, Lindor KD. Cancer surveillance in patients with primary sclerosing cholangitis. Hepatology. 2011;54(5): 1842-52.
3. Williamson KD, Chapman RW. Primary sclerosing cholangitis: a clinical update. Br Med Bull. 2015;114(1):53-64.
Q1. Correct answer: F
Rationale
There are a number of known risk factors for cholangiocarcinoma including PSC, choledochal cysts, obesity, chronic liver disease, toxins such as Thorotrast as well as liver flukes including those in the Opisthorchis and Clonorchis genus. While Fasciola does infect the liver, an association has not been reported with cholangiocarcinoma.
References
1. Fevery J, et al. Malignancies and mortality in 200 patients with primary sclerosering cholan¬gitis: a long-term single-centre study. Liver Int. 2012;32(2):214-22.
2. Razumilava N, Gores GJ, Lindor KD. Cancer surveillance in patients with primary sclerosing cholangitis. Hepatology. 2011;54(5): 1842-52.
3. Williamson KD, Chapman RW. Primary sclerosing cholangitis: a clinical update. Br Med Bull. 2015;114(1):53-64.
Q1. Correct answer: F
Rationale
There are a number of known risk factors for cholangiocarcinoma including PSC, choledochal cysts, obesity, chronic liver disease, toxins such as Thorotrast as well as liver flukes including those in the Opisthorchis and Clonorchis genus. While Fasciola does infect the liver, an association has not been reported with cholangiocarcinoma.
References
1. Fevery J, et al. Malignancies and mortality in 200 patients with primary sclerosering cholan¬gitis: a long-term single-centre study. Liver Int. 2012;32(2):214-22.
2. Razumilava N, Gores GJ, Lindor KD. Cancer surveillance in patients with primary sclerosing cholangitis. Hepatology. 2011;54(5): 1842-52.
3. Williamson KD, Chapman RW. Primary sclerosing cholangitis: a clinical update. Br Med Bull. 2015;114(1):53-64.
Q1. You are evaluating a 77-year-old man for obstructive jaundice and weight loss. The patient reports an approximate 25-pound weight loss over the last month. He denies abdominal pain. Labs reveal a total bilirubin of 17.5 mg/dL, alkaline phosphatase of 441 IU/L, aspartate aminotransferase of 60 IU/L, alanine aminotransferase of 70 IU/L, lipase of 41 U (ULN 50 U) and WBC of 8 × 109/L. A right upper quadrant ultrasound is obtained and shows intra- and extrahepatic biliary dilation up to 2 cm. A subsequent pancreas protocol CT is notable for narrowing of the mid bile duct with a normal downstream common bile duct. A mass is not visualized within the pancreas. CA 19-9 is elevated to 1900 U/mL and CEA is 8 ng/ mL. You are concerned for a possible extrahepatic cholangiocarcinoma.