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May 2019 - Question 2
Q2. Correct Answer: B
Rationale:
The PRSS1 mutation has been shown to be the causative genetic factor in hereditary pancreatitis. Hereditary pancreatitis is an autosomal dominant gene mutation with 80% penetrance. Symptoms start in childhood with acute recurrent pancreatitis and progress to chronic pancreatitis, diabetes, and exocrine insufficiency. The incidence of pancreatic cancer is increased to 40% by age 70. BRCA1 mutations have been associated with familial pancreas cancer families. SPINK mutations have been associated with chronic tropical pancreatitis. Delta F508 is the most common mutation in cystic fibrosis that leads to pancreas insufficiency in childhood. The clinical scenario is classic for hereditary pancreatitis.
Reference
1. Shelton CA, Umapathy C, Stello K, Yadav D, Whitcomb DC. Hereditary pancreatitis in the United States: Survival and rates of pancreatic cancer. Am J Gastroenterol. 2018 Sep;113(9):1376-84.
Q2. Correct Answer: B
Rationale:
The PRSS1 mutation has been shown to be the causative genetic factor in hereditary pancreatitis. Hereditary pancreatitis is an autosomal dominant gene mutation with 80% penetrance. Symptoms start in childhood with acute recurrent pancreatitis and progress to chronic pancreatitis, diabetes, and exocrine insufficiency. The incidence of pancreatic cancer is increased to 40% by age 70. BRCA1 mutations have been associated with familial pancreas cancer families. SPINK mutations have been associated with chronic tropical pancreatitis. Delta F508 is the most common mutation in cystic fibrosis that leads to pancreas insufficiency in childhood. The clinical scenario is classic for hereditary pancreatitis.
Reference
1. Shelton CA, Umapathy C, Stello K, Yadav D, Whitcomb DC. Hereditary pancreatitis in the United States: Survival and rates of pancreatic cancer. Am J Gastroenterol. 2018 Sep;113(9):1376-84.
Q2. Correct Answer: B
Rationale:
The PRSS1 mutation has been shown to be the causative genetic factor in hereditary pancreatitis. Hereditary pancreatitis is an autosomal dominant gene mutation with 80% penetrance. Symptoms start in childhood with acute recurrent pancreatitis and progress to chronic pancreatitis, diabetes, and exocrine insufficiency. The incidence of pancreatic cancer is increased to 40% by age 70. BRCA1 mutations have been associated with familial pancreas cancer families. SPINK mutations have been associated with chronic tropical pancreatitis. Delta F508 is the most common mutation in cystic fibrosis that leads to pancreas insufficiency in childhood. The clinical scenario is classic for hereditary pancreatitis.
Reference
1. Shelton CA, Umapathy C, Stello K, Yadav D, Whitcomb DC. Hereditary pancreatitis in the United States: Survival and rates of pancreatic cancer. Am J Gastroenterol. 2018 Sep;113(9):1376-84.
Q2. A 25-year-old male presents to the emergency department with severe epigastric pain and mild elevations in lipase (3 x ULN) diagnostic of acute pancreatitis. The patient describes multiple episodes of pain and associated pancreas enzyme elevations since early childhood that generally respond to brief hospitalizations and conservative treatment including intravenous fluids and IV analgesics. CT imaging reveals parenchymal calcifications seen throughout the pancreas. Further history discloses two relatives with similar pain attacks.
May 2019 - Question 1
Q1. Correct Answer: A
Rationale:
This is an example of Yersinia infection. Transmission of yersiniosis is largely foodborne.
Risk factors associated with yersiniosis include consumption of undercooked or raw pork products and exposure to untreated water. Y. enterocolitica infection has also been associated with iron-overload states (such as hemochromatosis) and blood transfusions, because iron likely promotes virulence of this organism. The incubation period for yersiniosis is typically 4-6 days. Clinical manifestations of acute yersiniosis include diarrhea, abdominal pain, and fever; nausea and vomiting may also occur. Localization of abdominal pain to the right lower quadrant is also a diagnostic clue for yersiniosis. However, both Yersinia and Campylobacter can present with right lower quadrant pain that may be confused as appendicitis (pseudo appendicitis). Another diagnostic clue is pharyngitis, which may be an accompanying symptom. Yersinia causes diarrhea through penetration of the mucosa and proliferation in the submucosa. Pathogenic Y. enterocolitica pass through the stomach, adhere to gut epithelial cells, invade the gut wall, localize in lymphoid tissue within the gut wall and in regional mesenteric lymph nodes, and evade the host’s cell-mediated immune response. Vibrio cholerae and enterotoxigenic E. coli (ETEC) secrete enterotoxins that stimulate secretion and/or impair absorption.
Some bacteria produce toxins in contaminated food; when ingested, the toxins cause acute symptoms, usually nausea and vomiting. Examples of these are Staphylococcus aureus and Bacillus cereus. Enteropathogenic E. coli (EPEC) and enterohemorrhagic E. coli (EHEC) adhere to the intestinal mucosa, where they attach and cause effacement of the microvilli. Shigella, enteroinvasive E. coli, and Campylobacter jejuni penetrate the mucosa, spread, and cause mucosal damage with erosions and ulcers.
Reference
1. Cover TL, Aber RC. Yersinia enterocolitica. N Engl J Med. Jul 6 1989;321(1):16-24.
Q1. Correct Answer: A
Rationale:
This is an example of Yersinia infection. Transmission of yersiniosis is largely foodborne.
Risk factors associated with yersiniosis include consumption of undercooked or raw pork products and exposure to untreated water. Y. enterocolitica infection has also been associated with iron-overload states (such as hemochromatosis) and blood transfusions, because iron likely promotes virulence of this organism. The incubation period for yersiniosis is typically 4-6 days. Clinical manifestations of acute yersiniosis include diarrhea, abdominal pain, and fever; nausea and vomiting may also occur. Localization of abdominal pain to the right lower quadrant is also a diagnostic clue for yersiniosis. However, both Yersinia and Campylobacter can present with right lower quadrant pain that may be confused as appendicitis (pseudo appendicitis). Another diagnostic clue is pharyngitis, which may be an accompanying symptom. Yersinia causes diarrhea through penetration of the mucosa and proliferation in the submucosa. Pathogenic Y. enterocolitica pass through the stomach, adhere to gut epithelial cells, invade the gut wall, localize in lymphoid tissue within the gut wall and in regional mesenteric lymph nodes, and evade the host’s cell-mediated immune response. Vibrio cholerae and enterotoxigenic E. coli (ETEC) secrete enterotoxins that stimulate secretion and/or impair absorption.
Some bacteria produce toxins in contaminated food; when ingested, the toxins cause acute symptoms, usually nausea and vomiting. Examples of these are Staphylococcus aureus and Bacillus cereus. Enteropathogenic E. coli (EPEC) and enterohemorrhagic E. coli (EHEC) adhere to the intestinal mucosa, where they attach and cause effacement of the microvilli. Shigella, enteroinvasive E. coli, and Campylobacter jejuni penetrate the mucosa, spread, and cause mucosal damage with erosions and ulcers.
Reference
1. Cover TL, Aber RC. Yersinia enterocolitica. N Engl J Med. Jul 6 1989;321(1):16-24.
Q1. Correct Answer: A
Rationale:
This is an example of Yersinia infection. Transmission of yersiniosis is largely foodborne.
Risk factors associated with yersiniosis include consumption of undercooked or raw pork products and exposure to untreated water. Y. enterocolitica infection has also been associated with iron-overload states (such as hemochromatosis) and blood transfusions, because iron likely promotes virulence of this organism. The incubation period for yersiniosis is typically 4-6 days. Clinical manifestations of acute yersiniosis include diarrhea, abdominal pain, and fever; nausea and vomiting may also occur. Localization of abdominal pain to the right lower quadrant is also a diagnostic clue for yersiniosis. However, both Yersinia and Campylobacter can present with right lower quadrant pain that may be confused as appendicitis (pseudo appendicitis). Another diagnostic clue is pharyngitis, which may be an accompanying symptom. Yersinia causes diarrhea through penetration of the mucosa and proliferation in the submucosa. Pathogenic Y. enterocolitica pass through the stomach, adhere to gut epithelial cells, invade the gut wall, localize in lymphoid tissue within the gut wall and in regional mesenteric lymph nodes, and evade the host’s cell-mediated immune response. Vibrio cholerae and enterotoxigenic E. coli (ETEC) secrete enterotoxins that stimulate secretion and/or impair absorption.
Some bacteria produce toxins in contaminated food; when ingested, the toxins cause acute symptoms, usually nausea and vomiting. Examples of these are Staphylococcus aureus and Bacillus cereus. Enteropathogenic E. coli (EPEC) and enterohemorrhagic E. coli (EHEC) adhere to the intestinal mucosa, where they attach and cause effacement of the microvilli. Shigella, enteroinvasive E. coli, and Campylobacter jejuni penetrate the mucosa, spread, and cause mucosal damage with erosions and ulcers.
Reference
1. Cover TL, Aber RC. Yersinia enterocolitica. N Engl J Med. Jul 6 1989;321(1):16-24.
Q1. A 45-year-old man presents to the clinic with worsening right lower quadrant pain and diarrhea for the last 2 days. His past medical history is significant for hemochromatosis and he undergoes regular therapeutic phlebotomies. He admits to dining out in a newly-opened restaurant in his town 4 days ago. He describes having 5 nonbloody watery stools and also has been experiencing sore throat for the last 2 days. His physical examination is unremarkable except some mild abdominal tenderness at the right lower quadrant.
There was no rebound tenderness. Laboratory data shows mild leukocytosis.
April 2019 - Question 2
Critique:
Factors raising suspicion for Zollinger-Ellison syndrome include recurrent peptic ulcer disease, multiple ulcers, post-bulbar ulcer, non-H. pylori/non-NSAID-related duodenal ulcer, diarrhea, erosive esophagitis, and family or personal history of multiple endocrine neoplasia type 1. The patient in this question presents with duodenal ulcer without H. pylori or NSAID use, erosive esophagitis, and diarrhea, which raises suspicion for hypergastrinemia.
His laboratory evaluation also showed hypercalcemia, which may be due to hyperparathyroidism, a condition related to MEN I. The initial test to obtain when gastrinoma is suspected includes a fasting serum gastrin level. In follow-up of gastrin elevations, a gastric pH assessment should be performed and, depending on these results, a secretin stimulation test may be useful. Routine repeat upper endoscopy is not indicated after hemostasis of duodenal ulcer bleeding.
A restrictive transfusion strategy with a hemoglobin threshold of 7 g/dL has been shown to result in improved clinical outcome compared to a liberal transfusion strategy. While sucralfate may help the healing of duodenal ulcers, it is not the first-line therapy for long-term secondary prevention.
References
1. Roy PK, Venzon DJ, Shojamanesh H, et al. Zollinger-Ellison syndrome. Clinical presentation in 261 patients. Medicine (Baltimore) 2000;79:379.
2. Murugesan SV, Varro A, Pritchard DM. Review article: Strategies to determine whether hypergastrinaemia is due to Zollinger-Ellison syndrome rather than a more common benign cause. Aliment Pharmacol Ther 2009;29:1055-68.
3. Villaneuva C, Colomo A, Bosch A, et al. Transfusion strategies for acute upper gastrointestinal bleeding. N Engl J Med. 2013 Jan 3;368(1):11-21.
Critique:
Factors raising suspicion for Zollinger-Ellison syndrome include recurrent peptic ulcer disease, multiple ulcers, post-bulbar ulcer, non-H. pylori/non-NSAID-related duodenal ulcer, diarrhea, erosive esophagitis, and family or personal history of multiple endocrine neoplasia type 1. The patient in this question presents with duodenal ulcer without H. pylori or NSAID use, erosive esophagitis, and diarrhea, which raises suspicion for hypergastrinemia.
His laboratory evaluation also showed hypercalcemia, which may be due to hyperparathyroidism, a condition related to MEN I. The initial test to obtain when gastrinoma is suspected includes a fasting serum gastrin level. In follow-up of gastrin elevations, a gastric pH assessment should be performed and, depending on these results, a secretin stimulation test may be useful. Routine repeat upper endoscopy is not indicated after hemostasis of duodenal ulcer bleeding.
A restrictive transfusion strategy with a hemoglobin threshold of 7 g/dL has been shown to result in improved clinical outcome compared to a liberal transfusion strategy. While sucralfate may help the healing of duodenal ulcers, it is not the first-line therapy for long-term secondary prevention.
References
1. Roy PK, Venzon DJ, Shojamanesh H, et al. Zollinger-Ellison syndrome. Clinical presentation in 261 patients. Medicine (Baltimore) 2000;79:379.
2. Murugesan SV, Varro A, Pritchard DM. Review article: Strategies to determine whether hypergastrinaemia is due to Zollinger-Ellison syndrome rather than a more common benign cause. Aliment Pharmacol Ther 2009;29:1055-68.
3. Villaneuva C, Colomo A, Bosch A, et al. Transfusion strategies for acute upper gastrointestinal bleeding. N Engl J Med. 2013 Jan 3;368(1):11-21.
Critique:
Factors raising suspicion for Zollinger-Ellison syndrome include recurrent peptic ulcer disease, multiple ulcers, post-bulbar ulcer, non-H. pylori/non-NSAID-related duodenal ulcer, diarrhea, erosive esophagitis, and family or personal history of multiple endocrine neoplasia type 1. The patient in this question presents with duodenal ulcer without H. pylori or NSAID use, erosive esophagitis, and diarrhea, which raises suspicion for hypergastrinemia.
His laboratory evaluation also showed hypercalcemia, which may be due to hyperparathyroidism, a condition related to MEN I. The initial test to obtain when gastrinoma is suspected includes a fasting serum gastrin level. In follow-up of gastrin elevations, a gastric pH assessment should be performed and, depending on these results, a secretin stimulation test may be useful. Routine repeat upper endoscopy is not indicated after hemostasis of duodenal ulcer bleeding.
A restrictive transfusion strategy with a hemoglobin threshold of 7 g/dL has been shown to result in improved clinical outcome compared to a liberal transfusion strategy. While sucralfate may help the healing of duodenal ulcers, it is not the first-line therapy for long-term secondary prevention.
References
1. Roy PK, Venzon DJ, Shojamanesh H, et al. Zollinger-Ellison syndrome. Clinical presentation in 261 patients. Medicine (Baltimore) 2000;79:379.
2. Murugesan SV, Varro A, Pritchard DM. Review article: Strategies to determine whether hypergastrinaemia is due to Zollinger-Ellison syndrome rather than a more common benign cause. Aliment Pharmacol Ther 2009;29:1055-68.
3. Villaneuva C, Colomo A, Bosch A, et al. Transfusion strategies for acute upper gastrointestinal bleeding. N Engl J Med. 2013 Jan 3;368(1):11-21.
A 47-year-old man with a history of chronic diarrhea presents with black, tarry stools for 2 days. Laboratory evaluation shows hemoglobin 8.9 g/dL (normal: 14-17 g/dL), platelet 201 x 103/mcL (normal: 150-350 mcL), blood urea nitrogen 40 mg/dL (normal: 8-20 mg/dL), creatinine 0.8 mg/dL (normal: 0.7-1.3 mg/dL), and calcium 12.5 mg/dL (normal: 9-10.5 mg/dL). An upper endoscopy reveals LA grade C esophagitis and a 1-cm clean-based ulcer in the duodenal bulb. Gastric biopsies show no H. pylori on H&E stain. He denies any history of NSAID or aspirin use.
April 2019 - Question 1
Rationale:
ICP has a 60%-70% recurrence rate, and therefore, this patient is at high risk of recurrence. Ursodeoxycholic acid (UDCA) has been shown to reduce pruritus and improve bile acid levels and liver-associated enzymes. There is also evidence that UDCA is safe late in pregnancy and likely improves fetal outcomes. Cholestyramine is not as effective as UCDA at reducing pruritus, reducing bile acid levels, or normalizing aminotransferase. In addition, babies are delivered closer to term with UDCA as opposed to cholestyramine. Hydroxyzine improves pruritus but can aggravate respiratory issues in preterm babies and is not recommended in ICP. Given these findings, UDCA is considered first-line therapy in treatment of ICP. A recent study showed that the perinatal mortality is decreased with delivery of the baby at 36 weeks gestation, or if ICP develops past 36 weeks, delivery with onset of symptoms. Thus, optimal management if her current pregnancy mimics the previous pregnancy if UDCA is given with development of symptoms with planned delivery at approximately 36-37 weeks gestation.
References
1. Bacq Y, Sentilhes L, Reyes HB, et al. Efficacy of ursodeoxycholic acid in treating intrahepatic cholestasis of pregnancy: a meta-analysis. Gastroenterology. 2012;143(6):1492-501.
2. Kondrackiene J, Beurers U, Kupcinskas L. Efficacy and safety of ursodeoxycholic acid versus cholestyramine in intrahepatic cholestasis of pregnancy. Gastroenterology. 2005;129(3):894-901.
3. Puljic A, Kim E, Page J, et al. The risk of fetal death by each additional week of expectant management in intrahepatic cholestasis of pregnancy by gestational age. Am J Obstet Gynecol. 2015;212(5):667e1-5.
Rationale:
ICP has a 60%-70% recurrence rate, and therefore, this patient is at high risk of recurrence. Ursodeoxycholic acid (UDCA) has been shown to reduce pruritus and improve bile acid levels and liver-associated enzymes. There is also evidence that UDCA is safe late in pregnancy and likely improves fetal outcomes. Cholestyramine is not as effective as UCDA at reducing pruritus, reducing bile acid levels, or normalizing aminotransferase. In addition, babies are delivered closer to term with UDCA as opposed to cholestyramine. Hydroxyzine improves pruritus but can aggravate respiratory issues in preterm babies and is not recommended in ICP. Given these findings, UDCA is considered first-line therapy in treatment of ICP. A recent study showed that the perinatal mortality is decreased with delivery of the baby at 36 weeks gestation, or if ICP develops past 36 weeks, delivery with onset of symptoms. Thus, optimal management if her current pregnancy mimics the previous pregnancy if UDCA is given with development of symptoms with planned delivery at approximately 36-37 weeks gestation.
References
1. Bacq Y, Sentilhes L, Reyes HB, et al. Efficacy of ursodeoxycholic acid in treating intrahepatic cholestasis of pregnancy: a meta-analysis. Gastroenterology. 2012;143(6):1492-501.
2. Kondrackiene J, Beurers U, Kupcinskas L. Efficacy and safety of ursodeoxycholic acid versus cholestyramine in intrahepatic cholestasis of pregnancy. Gastroenterology. 2005;129(3):894-901.
3. Puljic A, Kim E, Page J, et al. The risk of fetal death by each additional week of expectant management in intrahepatic cholestasis of pregnancy by gestational age. Am J Obstet Gynecol. 2015;212(5):667e1-5.
Rationale:
ICP has a 60%-70% recurrence rate, and therefore, this patient is at high risk of recurrence. Ursodeoxycholic acid (UDCA) has been shown to reduce pruritus and improve bile acid levels and liver-associated enzymes. There is also evidence that UDCA is safe late in pregnancy and likely improves fetal outcomes. Cholestyramine is not as effective as UCDA at reducing pruritus, reducing bile acid levels, or normalizing aminotransferase. In addition, babies are delivered closer to term with UDCA as opposed to cholestyramine. Hydroxyzine improves pruritus but can aggravate respiratory issues in preterm babies and is not recommended in ICP. Given these findings, UDCA is considered first-line therapy in treatment of ICP. A recent study showed that the perinatal mortality is decreased with delivery of the baby at 36 weeks gestation, or if ICP develops past 36 weeks, delivery with onset of symptoms. Thus, optimal management if her current pregnancy mimics the previous pregnancy if UDCA is given with development of symptoms with planned delivery at approximately 36-37 weeks gestation.
References
1. Bacq Y, Sentilhes L, Reyes HB, et al. Efficacy of ursodeoxycholic acid in treating intrahepatic cholestasis of pregnancy: a meta-analysis. Gastroenterology. 2012;143(6):1492-501.
2. Kondrackiene J, Beurers U, Kupcinskas L. Efficacy and safety of ursodeoxycholic acid versus cholestyramine in intrahepatic cholestasis of pregnancy. Gastroenterology. 2005;129(3):894-901.
3. Puljic A, Kim E, Page J, et al. The risk of fetal death by each additional week of expectant management in intrahepatic cholestasis of pregnancy by gestational age. Am J Obstet Gynecol. 2015;212(5):667e1-5.
A 31-year-old G2P1 woman presents to your clinic for pregnancy counseling. She is currently 12 weeks pregnant, and states that her first pregnancy was complicated by intrahepatic cholestasis of pregnancy (ICP) development at 29 weeks. She developed severe pruritus, and the baby was delivered prematurely. She is concerned about complications with her current pregnancy and is wondering about therapy if ICP recurred at the same point in her pregnancy.
March 2019 - Question 2
Correct Answer: E
Rationale
This patient has slow-transit constipation without concomitant defecatory disorder, which is unresponsive to newer pharmacologic agents. According to the recently published AGA medical position paper on constipation, the next step in this patient's evaluation should be to repeat colon transit testing on medications. If abnormal, the next step would be evaluation for possible upper GI motility disorder including a gastric-emptying scan. There is no role for repeat anorectal manometry, balloon expulsion testing, or a trial of biofeedback therapy in this patient.
References
1. Wald A, Bharucha AE, Cosman BC, Whitehead WE. ACG clinical guideline: management of benign anorectal disorders. Am J Gastroenterol. 2014;109(8):1141-57.
2. Bharucha AE, Pemberton JH, Locke GR 3rd. American Gastroenterological Association technical review on constipation. Gastroenterology. 2013;144:218.
[email protected]
Correct Answer: E
Rationale
This patient has slow-transit constipation without concomitant defecatory disorder, which is unresponsive to newer pharmacologic agents. According to the recently published AGA medical position paper on constipation, the next step in this patient's evaluation should be to repeat colon transit testing on medications. If abnormal, the next step would be evaluation for possible upper GI motility disorder including a gastric-emptying scan. There is no role for repeat anorectal manometry, balloon expulsion testing, or a trial of biofeedback therapy in this patient.
References
1. Wald A, Bharucha AE, Cosman BC, Whitehead WE. ACG clinical guideline: management of benign anorectal disorders. Am J Gastroenterol. 2014;109(8):1141-57.
2. Bharucha AE, Pemberton JH, Locke GR 3rd. American Gastroenterological Association technical review on constipation. Gastroenterology. 2013;144:218.
[email protected]
Correct Answer: E
Rationale
This patient has slow-transit constipation without concomitant defecatory disorder, which is unresponsive to newer pharmacologic agents. According to the recently published AGA medical position paper on constipation, the next step in this patient's evaluation should be to repeat colon transit testing on medications. If abnormal, the next step would be evaluation for possible upper GI motility disorder including a gastric-emptying scan. There is no role for repeat anorectal manometry, balloon expulsion testing, or a trial of biofeedback therapy in this patient.
References
1. Wald A, Bharucha AE, Cosman BC, Whitehead WE. ACG clinical guideline: management of benign anorectal disorders. Am J Gastroenterol. 2014;109(8):1141-57.
2. Bharucha AE, Pemberton JH, Locke GR 3rd. American Gastroenterological Association technical review on constipation. Gastroenterology. 2013;144:218.
[email protected]
A 66-year-old woman presents for an evaluation of a 3-year history of constipation. She reports some mild abdominal pain, which is related to constipation. She denies GI bleeding and any relevant family history of colorectal neoplasia or IBD. A previous trial of fiber and polyethylene glycol was unsuccessful. Physical examination is normal, including the rectal examination. Evaluation including routine blood work and thyroid evaluation is normal. Her last colonoscopy was 1 year ago and was normal. She undergoes anorectal manometry, balloon expulsion testing and defecography, which do not reveal any significant abnormalities. Sitz marker test reveals 14 markers remaining in the colon on day 5. She is started on intestinal secretagogue therapy with no significant improvement in symptoms.
What is the next best step in the evaluation of this patient?
March 2019 - Question 1
Correct Answer: B
Rationale
The ultrasound finding of a hyperechoic protrusion is suggestive of a gallbladder polyp. These polyps can have malignant potential and should be monitored or referred for surgical management depending on their size. There is consensus that polyps larger than 10 mm should be referred for cholecystectomy. There is some debate about whether polyps greater than 6 mm should also be referred for surgery or whether they can be surveyed. For gallbladder polyps less than 6 mm, surveillance with ultrasound in 6-12 months is the recommended surveillance strategy.
Reference
1. Gallahan WC, Conway JD. Diagnosis and management of gallbladder polyps. Gastroenterol Clin North Am. 2010;39(2):359-67.
Correct Answer: B
Rationale
The ultrasound finding of a hyperechoic protrusion is suggestive of a gallbladder polyp. These polyps can have malignant potential and should be monitored or referred for surgical management depending on their size. There is consensus that polyps larger than 10 mm should be referred for cholecystectomy. There is some debate about whether polyps greater than 6 mm should also be referred for surgery or whether they can be surveyed. For gallbladder polyps less than 6 mm, surveillance with ultrasound in 6-12 months is the recommended surveillance strategy.
Reference
1. Gallahan WC, Conway JD. Diagnosis and management of gallbladder polyps. Gastroenterol Clin North Am. 2010;39(2):359-67.
Correct Answer: B
Rationale
The ultrasound finding of a hyperechoic protrusion is suggestive of a gallbladder polyp. These polyps can have malignant potential and should be monitored or referred for surgical management depending on their size. There is consensus that polyps larger than 10 mm should be referred for cholecystectomy. There is some debate about whether polyps greater than 6 mm should also be referred for surgery or whether they can be surveyed. For gallbladder polyps less than 6 mm, surveillance with ultrasound in 6-12 months is the recommended surveillance strategy.
Reference
1. Gallahan WC, Conway JD. Diagnosis and management of gallbladder polyps. Gastroenterol Clin North Am. 2010;39(2):359-67.
A 63-year-old woman undergoes a right upper quadrant ultrasound for intermittent epigastric pain. A 5-mm fixed hyperechoic protrusion in the gallbladder is identified, but there are no gallstones or wall thickening. Upper endoscopy shows moderate gastritis. Biopsies reveal active H. pylori gastritis. She is treated with triple therapy and reports complete resolution of her symptoms.
What is the best next step in management?
January 2019 Question 2
A 54-year-old woman presents for management of moderately severe ileocolonic Crohn’s disease. She has a strong family history of multiple sclerosis and recently noted some tingling in her toes for which she is undergoing neurologic evaluation. She has had two small basal cell carcinomas removed from her cheek in the last year. She received the BCG vaccine as a child and had a positive PPD skin test within the last year. Laboratory evaluation reveals HBsAg negative, anti-HBs positive, and anti-HBc positive; JC virus antibody is positive.
January 2019 Question 1
A 31-year-old man is seen for a 1-week history of epigastric pain and scleral icterus. One month earlier, he developed diarrhea and fatigue, which has continued to persist. He denies any prior medical problems, though he admits he has not seen a doctor in years. He is currently visiting family in the United States, but he resides in South Africa. His laboratory tests are as follows: total bilirubin, 3.5 mg/dL; direct bilirubin, 2.9 mg/dL; alkaline phosphatase, 720 U/L; ALT, 105 U/L; AST, 117 U/L; albumin, 2.1 g/dL; INR, 1.2; HIV viral load 450,000 copies/mL, CD4 count, 25 cells/mm3. An abdominal ultrasound shows intra- and extrahepatic ductal dilation and an ERCP shows strictured intrahepatic ducts with papillary stenosis.
December 2018 Question 2
A 26-year-old woman presents for an evaluation of an 8-month history of intermittent abdominal pain, which is associated with diarrhea. Her pain improves with bowel movements. She denies weight loss, GI bleeding, or nocturnal symptoms. There is no family history of IBD or celiac disease. Physical examination is normal. Thyroid function testing, C-reactive protein, celiac serology, stool studies for infectious pathogens, stool calprotectin, and colonoscopy with biopsies are all negative.
December 2018 Question 1
A 45-year-old woman presents with a 3-year history of a sense of incomplete evacuation, excessive straining to defecate, and rectal bleeding. Colonoscopy demonstrates an irregular, polypoid lesion on the anterior wall of the rectum. Biopsies reveal fibromuscular obliteration of the lamina propria and hypertrophied muscularis mucosa with extension of muscle fibers upward between the crypts.