DDSEP® 8 Quick Quiz

Q2: Answer: B

This patient, with no imaging or laboratory findings to suggest cirrhosis, most likely has noncirrhotic portal hypertension (NCPH). There is now a well-described association between HIV and NCPH with the prevalence of NCPH in HIV estimated to be –0.5% to 1%. Patients typically are unaware of any underlying liver disease until presentation with variceal bleeding. Variceal bleeding is a much more common manifestation of NCPH than ascites. Clinical presentation with normal hepatic enzymes and normal hepatic synthetic function is a very typical feature in these patients.  Although the exact etiology is not fully understood, NCPH in HIV is likely related to HAART, particularly didanosine use, hypercoagulability, microbial translocation from the gut, and direct effects of HIV. NCPH is a presinusoidal lesion, and liver biopsy may reveal paucity of portal vasculature and focal obliteration of small portal veins. Portal vein thrombosis in patients with HIV and NCPH is common and has been observed in 25%-75% of patients.  
 

Reference

1. Vispo E., Morello J., Rodriguez-Novoa S., Soriano V. Noncirrhotic portal hypertension in HIV infection. Curr Opin Infect Dis. 2011;24:12-8.
2. Khanna R., Sarin S.K. Noncirrhotic portal hypertension – Diagnosis and management. J Hepatol. 2014;60:421-41. 
 

Q2: Answer: B

This patient, with no imaging or laboratory findings to suggest cirrhosis, most likely has noncirrhotic portal hypertension (NCPH). There is now a well-described association between HIV and NCPH with the prevalence of NCPH in HIV estimated to be –0.5% to 1%. Patients typically are unaware of any underlying liver disease until presentation with variceal bleeding. Variceal bleeding is a much more common manifestation of NCPH than ascites. Clinical presentation with normal hepatic enzymes and normal hepatic synthetic function is a very typical feature in these patients.  Although the exact etiology is not fully understood, NCPH in HIV is likely related to HAART, particularly didanosine use, hypercoagulability, microbial translocation from the gut, and direct effects of HIV. NCPH is a presinusoidal lesion, and liver biopsy may reveal paucity of portal vasculature and focal obliteration of small portal veins. Portal vein thrombosis in patients with HIV and NCPH is common and has been observed in 25%-75% of patients.  
 

Reference

1. Vispo E., Morello J., Rodriguez-Novoa S., Soriano V. Noncirrhotic portal hypertension in HIV infection. Curr Opin Infect Dis. 2011;24:12-8.
2. Khanna R., Sarin S.K. Noncirrhotic portal hypertension – Diagnosis and management. J Hepatol. 2014;60:421-41. 
 

Q2: Answer: B

This patient, with no imaging or laboratory findings to suggest cirrhosis, most likely has noncirrhotic portal hypertension (NCPH). There is now a well-described association between HIV and NCPH with the prevalence of NCPH in HIV estimated to be –0.5% to 1%. Patients typically are unaware of any underlying liver disease until presentation with variceal bleeding. Variceal bleeding is a much more common manifestation of NCPH than ascites. Clinical presentation with normal hepatic enzymes and normal hepatic synthetic function is a very typical feature in these patients.  Although the exact etiology is not fully understood, NCPH in HIV is likely related to HAART, particularly didanosine use, hypercoagulability, microbial translocation from the gut, and direct effects of HIV. NCPH is a presinusoidal lesion, and liver biopsy may reveal paucity of portal vasculature and focal obliteration of small portal veins. Portal vein thrombosis in patients with HIV and NCPH is common and has been observed in 25%-75% of patients.  
 

Reference

1. Vispo E., Morello J., Rodriguez-Novoa S., Soriano V. Noncirrhotic portal hypertension in HIV infection. Curr Opin Infect Dis. 2011;24:12-8.
2. Khanna R., Sarin S.K. Noncirrhotic portal hypertension – Diagnosis and management. J Hepatol. 2014;60:421-41. 
 

Q1: Answer: A

Critique: This is a classic presentation of eosinophilic esophagitis (EoE). As many as half of older children with food impactions suffer from EoE. EoE is characterized by a severe, eosinophilic infiltration of the esophagus that may respond to acid inhibition, systemic or topical steroid therapy, or removal of dietary allergens. Epidemiologic studies suggest a rising incidence in the United States in both children and adults, with at least one case occurring in every 10,000 children each year. Treatment is aimed at alleviating symptoms and healing esophageal inflammation. Allergy testing should be performed at the time of diagnosis; however, radioallergosorbent  tests and skin-prick tests are often negative, and only half of affected children have a antecedent history of other allergic symptoms. 

A five-food elimination diet can be helpful for many affected children and adults, although adherence to the diet can be difficult. There is a group of affected children who respond to high doses of proton pump inhibitors, and most patients respond to either systemic or topical steroid therapy. Even with therapy, some patients go on to develop esophageal strictures and may need serial or repeated dilatations.  

While eosinophilic infiltration and inflammation may be present with gastroesophageal reflux disease and associated esophagitis, the number of eosinophils seen in this boy’s biopsies is much more consistent with EoE. Moreover, stricture formation as a result of peptic esophagitis in a child this age would be extremely rare. While inflammatory bowel disease may be associated with eosinophilic infiltration of the intestinal tract, isolated esophageal Crohn’s disease would be extraordinarily rare.Our patient has no history of any immune deficiency or steroid use that would predispose to fungal esophagitis. Achalasia typically presents with gradually worsening symptoms, and the obstruction would be at the lower esophageal sphincter, not in the mid-esophagus.  
 

Reference

<sup>1. Liacouras C., Furuta G., Hirano I., et al. Eosinophilic esophagitis: updated consensus recommendations for children and adults. J Allergy Clin Immunol. 2011;128:3-20. 
2. Furuta G., Liacouras C., Collins M., et al. Eosinophilic esophagitis in children and adults: A systematic review and consensus recommendations for diagnosis and treatment. Gastroenterology. 2007;133:1342-63.</sup>

Q1: Answer: A

Critique: This is a classic presentation of eosinophilic esophagitis (EoE). As many as half of older children with food impactions suffer from EoE. EoE is characterized by a severe, eosinophilic infiltration of the esophagus that may respond to acid inhibition, systemic or topical steroid therapy, or removal of dietary allergens. Epidemiologic studies suggest a rising incidence in the United States in both children and adults, with at least one case occurring in every 10,000 children each year. Treatment is aimed at alleviating symptoms and healing esophageal inflammation. Allergy testing should be performed at the time of diagnosis; however, radioallergosorbent  tests and skin-prick tests are often negative, and only half of affected children have a antecedent history of other allergic symptoms. 

A five-food elimination diet can be helpful for many affected children and adults, although adherence to the diet can be difficult. There is a group of affected children who respond to high doses of proton pump inhibitors, and most patients respond to either systemic or topical steroid therapy. Even with therapy, some patients go on to develop esophageal strictures and may need serial or repeated dilatations.  

While eosinophilic infiltration and inflammation may be present with gastroesophageal reflux disease and associated esophagitis, the number of eosinophils seen in this boy’s biopsies is much more consistent with EoE. Moreover, stricture formation as a result of peptic esophagitis in a child this age would be extremely rare. While inflammatory bowel disease may be associated with eosinophilic infiltration of the intestinal tract, isolated esophageal Crohn’s disease would be extraordinarily rare.Our patient has no history of any immune deficiency or steroid use that would predispose to fungal esophagitis. Achalasia typically presents with gradually worsening symptoms, and the obstruction would be at the lower esophageal sphincter, not in the mid-esophagus.  
 

Reference

<sup>1. Liacouras C., Furuta G., Hirano I., et al. Eosinophilic esophagitis: updated consensus recommendations for children and adults. J Allergy Clin Immunol. 2011;128:3-20. 
2. Furuta G., Liacouras C., Collins M., et al. Eosinophilic esophagitis in children and adults: A systematic review and consensus recommendations for diagnosis and treatment. Gastroenterology. 2007;133:1342-63.</sup>

Q1: Answer: A

Critique: This is a classic presentation of eosinophilic esophagitis (EoE). As many as half of older children with food impactions suffer from EoE. EoE is characterized by a severe, eosinophilic infiltration of the esophagus that may respond to acid inhibition, systemic or topical steroid therapy, or removal of dietary allergens. Epidemiologic studies suggest a rising incidence in the United States in both children and adults, with at least one case occurring in every 10,000 children each year. Treatment is aimed at alleviating symptoms and healing esophageal inflammation. Allergy testing should be performed at the time of diagnosis; however, radioallergosorbent  tests and skin-prick tests are often negative, and only half of affected children have a antecedent history of other allergic symptoms. 

A five-food elimination diet can be helpful for many affected children and adults, although adherence to the diet can be difficult. There is a group of affected children who respond to high doses of proton pump inhibitors, and most patients respond to either systemic or topical steroid therapy. Even with therapy, some patients go on to develop esophageal strictures and may need serial or repeated dilatations.  

While eosinophilic infiltration and inflammation may be present with gastroesophageal reflux disease and associated esophagitis, the number of eosinophils seen in this boy’s biopsies is much more consistent with EoE. Moreover, stricture formation as a result of peptic esophagitis in a child this age would be extremely rare. While inflammatory bowel disease may be associated with eosinophilic infiltration of the intestinal tract, isolated esophageal Crohn’s disease would be extraordinarily rare.Our patient has no history of any immune deficiency or steroid use that would predispose to fungal esophagitis. Achalasia typically presents with gradually worsening symptoms, and the obstruction would be at the lower esophageal sphincter, not in the mid-esophagus.  
 

Reference

<sup>1. Liacouras C., Furuta G., Hirano I., et al. Eosinophilic esophagitis: updated consensus recommendations for children and adults. J Allergy Clin Immunol. 2011;128:3-20. 
2. Furuta G., Liacouras C., Collins M., et al. Eosinophilic esophagitis in children and adults: A systematic review and consensus recommendations for diagnosis and treatment. Gastroenterology. 2007;133:1342-63.</sup>

Q2: Answer: B

Objective: Recognize the features of CVID-associated noninfectious gastrointestinal manifestations.

Explanation: This patient has gastrointestinal manifestations of common variable immune deficiency (CVID), which can present similarly to celiac disease or inflammatory bowel disease. Histologically, intestinal biopsies will reveal villous atrophy, crypt hyperplasia, and intraepithelial lymphocytosis similar to celiac disease. However, while plasma cells are increased in celiac disease, they are absent in CVID.

The initial treatment strategy for CVID typically includes oral corticosteroids, either prednisone or budesonide, with other immunosuppressants such as the thiopurines or anti–tumor necrosis factor agents reserved for steroid-dependent or refractory disease.

Gluten-free diet is ineffective for the treatment of CVID-associated enteropathy. Intravenous immunoglobulin therapy reduces the frequency of infections associated with CVID, but does not affect the noninfectious GI symptoms. While bacterial overgrowth can occur in CVID, it is typically the consequence of the luminal changes, not the cause.

Reference

1. Agarwal S., Mayer L. Gastrointestinal manifestations in primary immune disorders. Inflamm Bowel Dis. 2010;16:703-11.

Q2: Answer: B

Objective: Recognize the features of CVID-associated noninfectious gastrointestinal manifestations.

Explanation: This patient has gastrointestinal manifestations of common variable immune deficiency (CVID), which can present similarly to celiac disease or inflammatory bowel disease. Histologically, intestinal biopsies will reveal villous atrophy, crypt hyperplasia, and intraepithelial lymphocytosis similar to celiac disease. However, while plasma cells are increased in celiac disease, they are absent in CVID.

The initial treatment strategy for CVID typically includes oral corticosteroids, either prednisone or budesonide, with other immunosuppressants such as the thiopurines or anti–tumor necrosis factor agents reserved for steroid-dependent or refractory disease.

Gluten-free diet is ineffective for the treatment of CVID-associated enteropathy. Intravenous immunoglobulin therapy reduces the frequency of infections associated with CVID, but does not affect the noninfectious GI symptoms. While bacterial overgrowth can occur in CVID, it is typically the consequence of the luminal changes, not the cause.

Reference

1. Agarwal S., Mayer L. Gastrointestinal manifestations in primary immune disorders. Inflamm Bowel Dis. 2010;16:703-11.

Q2: Answer: B

Objective: Recognize the features of CVID-associated noninfectious gastrointestinal manifestations.

Explanation: This patient has gastrointestinal manifestations of common variable immune deficiency (CVID), which can present similarly to celiac disease or inflammatory bowel disease. Histologically, intestinal biopsies will reveal villous atrophy, crypt hyperplasia, and intraepithelial lymphocytosis similar to celiac disease. However, while plasma cells are increased in celiac disease, they are absent in CVID.

The initial treatment strategy for CVID typically includes oral corticosteroids, either prednisone or budesonide, with other immunosuppressants such as the thiopurines or anti–tumor necrosis factor agents reserved for steroid-dependent or refractory disease.

Gluten-free diet is ineffective for the treatment of CVID-associated enteropathy. Intravenous immunoglobulin therapy reduces the frequency of infections associated with CVID, but does not affect the noninfectious GI symptoms. While bacterial overgrowth can occur in CVID, it is typically the consequence of the luminal changes, not the cause.

Reference

1. Agarwal S., Mayer L. Gastrointestinal manifestations in primary immune disorders. Inflamm Bowel Dis. 2010;16:703-11.

Q1: Answer: D

Current recommendations suggest H. pylori testing for patients with active or a documented history of peptic ulcer disease, gastric MALT lymphoma, or gastric carcinoma. The H. pylori test-and-treat strategy is also recommended for patients less than 55 years of age who present with dyspepsia symptoms without “alarm features.”

There is currently no recommendation for asymptomatic family members of patients diagnosed with H. pylori infection to be tested, unless there are known factors that may increase the patient’s risk for gastric malignancy (e.g., family history of gastric carcinoma, and ethnic background from areas with high prevalence of H. pylori and gastric cancer such as East Asia, Latin America, and Eastern Europe).

References

1. Chey W.D., Wong B.C. Practice Parameters Committee of the American College of Gastroenterology. American College of Gastroenterology guideline on the management of Helicobacter pylori infection. Am J Gastroenterol. 2007;102:1808-25.

2. Talley N.J., Vakil N.B., Moayyedi P. American Gastroenterological Association technical review on the evaluation of dyspepsia. Gastroenterology 2005;129:1756-80.

3. Suerbaum S., Michetti P. Helicobacter pylori infection. N Engl J Med. 2002;347:1175-86.

4. Everhart J.E., Kruszon-Moran D., Perez-Perez G.I., et al. Seroprevalence and ethnic differences in Helicobacter pylori infection among adults in the United States. J Infect Dis. 2000;181:1359-63.

Q1: Answer: D

Current recommendations suggest H. pylori testing for patients with active or a documented history of peptic ulcer disease, gastric MALT lymphoma, or gastric carcinoma. The H. pylori test-and-treat strategy is also recommended for patients less than 55 years of age who present with dyspepsia symptoms without “alarm features.”

There is currently no recommendation for asymptomatic family members of patients diagnosed with H. pylori infection to be tested, unless there are known factors that may increase the patient’s risk for gastric malignancy (e.g., family history of gastric carcinoma, and ethnic background from areas with high prevalence of H. pylori and gastric cancer such as East Asia, Latin America, and Eastern Europe).

References

1. Chey W.D., Wong B.C. Practice Parameters Committee of the American College of Gastroenterology. American College of Gastroenterology guideline on the management of Helicobacter pylori infection. Am J Gastroenterol. 2007;102:1808-25.

2. Talley N.J., Vakil N.B., Moayyedi P. American Gastroenterological Association technical review on the evaluation of dyspepsia. Gastroenterology 2005;129:1756-80.

3. Suerbaum S., Michetti P. Helicobacter pylori infection. N Engl J Med. 2002;347:1175-86.

4. Everhart J.E., Kruszon-Moran D., Perez-Perez G.I., et al. Seroprevalence and ethnic differences in Helicobacter pylori infection among adults in the United States. J Infect Dis. 2000;181:1359-63.

Q1: Answer: D

Current recommendations suggest H. pylori testing for patients with active or a documented history of peptic ulcer disease, gastric MALT lymphoma, or gastric carcinoma. The H. pylori test-and-treat strategy is also recommended for patients less than 55 years of age who present with dyspepsia symptoms without “alarm features.”

There is currently no recommendation for asymptomatic family members of patients diagnosed with H. pylori infection to be tested, unless there are known factors that may increase the patient’s risk for gastric malignancy (e.g., family history of gastric carcinoma, and ethnic background from areas with high prevalence of H. pylori and gastric cancer such as East Asia, Latin America, and Eastern Europe).

References

1. Chey W.D., Wong B.C. Practice Parameters Committee of the American College of Gastroenterology. American College of Gastroenterology guideline on the management of Helicobacter pylori infection. Am J Gastroenterol. 2007;102:1808-25.

2. Talley N.J., Vakil N.B., Moayyedi P. American Gastroenterological Association technical review on the evaluation of dyspepsia. Gastroenterology 2005;129:1756-80.

3. Suerbaum S., Michetti P. Helicobacter pylori infection. N Engl J Med. 2002;347:1175-86.

4. Everhart J.E., Kruszon-Moran D., Perez-Perez G.I., et al. Seroprevalence and ethnic differences in Helicobacter pylori infection among adults in the United States. J Infect Dis. 2000;181:1359-63.

Q2: Answer: E

Objective: Recall that the major risk to pregnant patients with inflammatory bowel disease (IBD) is a flare of IBD.

Rationale: The most important factor in a successful pregnancy is the maintenance of IBD in a quiescent state. Most of the medications typically used to treat IBD are considered relatively safe in pregnancy. In fact, the risk of a flare of disease during pregnancy usually outweighs the risk of these medications.

Endoscopic procedures are generally well tolerated when proper precautions are taken, but should be deferred until the second trimester if possible, and performed only when there is a strong indication. The decision to proceed with endoscopy should be made in consultation with an obstetrician, regardless of gestational age.

References

1. Schulze H., Esters P., Dignass A. Review article: The management of Crohn’s disease and ulcerative colitis during pregnancy and lactation. Aliment Pharmacol Ther. 2014;40:991-1008.

2. ASGE Standard of Practice Committee. Shergill A.K., Ben-Menachem T., Chandrasekhara V., et al. Guidelines for endoscopy in pregnant and lactating women. Gastrointest Endosc. 2012:76:18-24.

Q2: Answer: E

Objective: Recall that the major risk to pregnant patients with inflammatory bowel disease (IBD) is a flare of IBD.

Rationale: The most important factor in a successful pregnancy is the maintenance of IBD in a quiescent state. Most of the medications typically used to treat IBD are considered relatively safe in pregnancy. In fact, the risk of a flare of disease during pregnancy usually outweighs the risk of these medications.

Endoscopic procedures are generally well tolerated when proper precautions are taken, but should be deferred until the second trimester if possible, and performed only when there is a strong indication. The decision to proceed with endoscopy should be made in consultation with an obstetrician, regardless of gestational age.

References

1. Schulze H., Esters P., Dignass A. Review article: The management of Crohn’s disease and ulcerative colitis during pregnancy and lactation. Aliment Pharmacol Ther. 2014;40:991-1008.

2. ASGE Standard of Practice Committee. Shergill A.K., Ben-Menachem T., Chandrasekhara V., et al. Guidelines for endoscopy in pregnant and lactating women. Gastrointest Endosc. 2012:76:18-24.

Q2: Answer: E

Objective: Recall that the major risk to pregnant patients with inflammatory bowel disease (IBD) is a flare of IBD.

Rationale: The most important factor in a successful pregnancy is the maintenance of IBD in a quiescent state. Most of the medications typically used to treat IBD are considered relatively safe in pregnancy. In fact, the risk of a flare of disease during pregnancy usually outweighs the risk of these medications.

Endoscopic procedures are generally well tolerated when proper precautions are taken, but should be deferred until the second trimester if possible, and performed only when there is a strong indication. The decision to proceed with endoscopy should be made in consultation with an obstetrician, regardless of gestational age.

References

1. Schulze H., Esters P., Dignass A. Review article: The management of Crohn’s disease and ulcerative colitis during pregnancy and lactation. Aliment Pharmacol Ther. 2014;40:991-1008.

2. ASGE Standard of Practice Committee. Shergill A.K., Ben-Menachem T., Chandrasekhara V., et al. Guidelines for endoscopy in pregnant and lactating women. Gastrointest Endosc. 2012:76:18-24.

Q1: Answer: B

Rationale: Although copper deficiency could be a complication of extensive enteropathy from conditions such as Crohn’s disease, celiac disease, short gut syndrome, or HIV enteropathy, it is more commonly recognized as a complication of gastric bypass surgeries. Copper absorption is thought to be primarily in the stomach and proximal small intestine. Copper is partially excreted in the bile, and patients with chronic external biliary drains may also develop copper deficiency. Deficiency in copper has also been recognized as a complication of zinc toxicity from deliberate chronic ingestion of zinc or unintentional industrial overexposure to zinc, and can also be a complication of chronic total parenteral nutrition in the absence of routine micronutrient supplementation. Complaints of muscle weakness and gait disturbance with copper deficiency are secondary to a myeloneuropathy similar to vitamin B12 deficiency. Copper deficiency may present as a microcytic anemia and neutropenia and, in advanced cases, may mimic a myelodysplastic syndrome. The microcytic anemia of copper deficiency is worsened by iron supplementation, which can reduce copper absorption.

Riboflavin deficiency may manifest with photophobia, burning mouth sensation, and glossitis. Zinc deficiency may manifest as diarrhea, altered taste sensation (dysgeusia), night blindness, and a characteristic acrodermatitis. Iron deficiency principally manifests as a microcytic anemia. Vitamin B12 deficiency is associated with gastric bypass surgery, as well as resection of the ileum, and may result in myeloneuropathy, but characteristically is associated with a megaloblastic, macrocytic anemia.

Q1: Answer: B

Rationale: Although copper deficiency could be a complication of extensive enteropathy from conditions such as Crohn’s disease, celiac disease, short gut syndrome, or HIV enteropathy, it is more commonly recognized as a complication of gastric bypass surgeries. Copper absorption is thought to be primarily in the stomach and proximal small intestine. Copper is partially excreted in the bile, and patients with chronic external biliary drains may also develop copper deficiency. Deficiency in copper has also been recognized as a complication of zinc toxicity from deliberate chronic ingestion of zinc or unintentional industrial overexposure to zinc, and can also be a complication of chronic total parenteral nutrition in the absence of routine micronutrient supplementation. Complaints of muscle weakness and gait disturbance with copper deficiency are secondary to a myeloneuropathy similar to vitamin B12 deficiency. Copper deficiency may present as a microcytic anemia and neutropenia and, in advanced cases, may mimic a myelodysplastic syndrome. The microcytic anemia of copper deficiency is worsened by iron supplementation, which can reduce copper absorption.

Riboflavin deficiency may manifest with photophobia, burning mouth sensation, and glossitis. Zinc deficiency may manifest as diarrhea, altered taste sensation (dysgeusia), night blindness, and a characteristic acrodermatitis. Iron deficiency principally manifests as a microcytic anemia. Vitamin B12 deficiency is associated with gastric bypass surgery, as well as resection of the ileum, and may result in myeloneuropathy, but characteristically is associated with a megaloblastic, macrocytic anemia.

Q1: Answer: B

Rationale: Although copper deficiency could be a complication of extensive enteropathy from conditions such as Crohn’s disease, celiac disease, short gut syndrome, or HIV enteropathy, it is more commonly recognized as a complication of gastric bypass surgeries. Copper absorption is thought to be primarily in the stomach and proximal small intestine. Copper is partially excreted in the bile, and patients with chronic external biliary drains may also develop copper deficiency. Deficiency in copper has also been recognized as a complication of zinc toxicity from deliberate chronic ingestion of zinc or unintentional industrial overexposure to zinc, and can also be a complication of chronic total parenteral nutrition in the absence of routine micronutrient supplementation. Complaints of muscle weakness and gait disturbance with copper deficiency are secondary to a myeloneuropathy similar to vitamin B12 deficiency. Copper deficiency may present as a microcytic anemia and neutropenia and, in advanced cases, may mimic a myelodysplastic syndrome. The microcytic anemia of copper deficiency is worsened by iron supplementation, which can reduce copper absorption.

Riboflavin deficiency may manifest with photophobia, burning mouth sensation, and glossitis. Zinc deficiency may manifest as diarrhea, altered taste sensation (dysgeusia), night blindness, and a characteristic acrodermatitis. Iron deficiency principally manifests as a microcytic anemia. Vitamin B12 deficiency is associated with gastric bypass surgery, as well as resection of the ileum, and may result in myeloneuropathy, but characteristically is associated with a megaloblastic, macrocytic anemia.

Q2: Answer: B

Rationale: This patient has a sessile serrated polyp without dysplasia located in the right colon as well as hyperplastic polyps in the rectosigmoid. Serrated polyps are thought to be precursor lesions to colon cancers arising from gene hypermethylation. Serrated polyps may be difficult to detect as they are flat or sessile, have indiscrete borders, and adherent mucus. Recent guidelines from the Multi-Society Task Force recommend that these lesions be treated in a way similar to that of adenomas for surveillance. Serrated polyps less than 10 mm without dysplasia should be surveyed in 5 years. Serrated polyps greater than 10 mm with or without dysplasia should be managed in a way similar to that of high-risk adenomas, with surveillance in 3 years. Hyperplastic polyps in the rectum do not require intensified surveillance.

Reference

1. Lieberman, D.A., Rex, D.K., Winawer, S.J., et al. Guidelines for colonoscopy surveillance after screening and polypectomy: A consensus update by the US Multi-Society Task Force on Colorectal Cancer. Gastroenterology 2012;143:844.

Q2: Answer: B

Rationale: This patient has a sessile serrated polyp without dysplasia located in the right colon as well as hyperplastic polyps in the rectosigmoid. Serrated polyps are thought to be precursor lesions to colon cancers arising from gene hypermethylation. Serrated polyps may be difficult to detect as they are flat or sessile, have indiscrete borders, and adherent mucus. Recent guidelines from the Multi-Society Task Force recommend that these lesions be treated in a way similar to that of adenomas for surveillance. Serrated polyps less than 10 mm without dysplasia should be surveyed in 5 years. Serrated polyps greater than 10 mm with or without dysplasia should be managed in a way similar to that of high-risk adenomas, with surveillance in 3 years. Hyperplastic polyps in the rectum do not require intensified surveillance.

Reference

1. Lieberman, D.A., Rex, D.K., Winawer, S.J., et al. Guidelines for colonoscopy surveillance after screening and polypectomy: A consensus update by the US Multi-Society Task Force on Colorectal Cancer. Gastroenterology 2012;143:844.

Q2: Answer: B

Rationale: This patient has a sessile serrated polyp without dysplasia located in the right colon as well as hyperplastic polyps in the rectosigmoid. Serrated polyps are thought to be precursor lesions to colon cancers arising from gene hypermethylation. Serrated polyps may be difficult to detect as they are flat or sessile, have indiscrete borders, and adherent mucus. Recent guidelines from the Multi-Society Task Force recommend that these lesions be treated in a way similar to that of adenomas for surveillance. Serrated polyps less than 10 mm without dysplasia should be surveyed in 5 years. Serrated polyps greater than 10 mm with or without dysplasia should be managed in a way similar to that of high-risk adenomas, with surveillance in 3 years. Hyperplastic polyps in the rectum do not require intensified surveillance.

Reference

1. Lieberman, D.A., Rex, D.K., Winawer, S.J., et al. Guidelines for colonoscopy surveillance after screening and polypectomy: A consensus update by the US Multi-Society Task Force on Colorectal Cancer. Gastroenterology 2012;143:844.

Q1: Answer: C

Cystoisospora belli (formerly known as Isospora belli) is a gastrointestinal protozoan. In patients with AIDS and other immunodeficiencies, it is an opportunistic pathogen that can cause watery diarrhea and weight loss. Infections are acquired by the ingestion of sporulated oocysts from food or water contaminated with human feces. In general, protozoal infections do not cause peripheral or tissue eosinophilia; however, Cystoisospora infection is an exception to this rule.

Diarrhea and peripheral eosinophilia in an immunocompromised individual should raise concern for Cystoisospora infection. The other protozoal infections listed can cause diarrhea, but do not cause eosinophilia.

Reference

1. Goodgame, R.W. Understanding intestinal spore-forming protozoa: Cryptosporidia, microsporidia, isospora, and cyclospora. Ann Intern Med. 1996;124:429-41.

Q1: Answer: C

Cystoisospora belli (formerly known as Isospora belli) is a gastrointestinal protozoan. In patients with AIDS and other immunodeficiencies, it is an opportunistic pathogen that can cause watery diarrhea and weight loss. Infections are acquired by the ingestion of sporulated oocysts from food or water contaminated with human feces. In general, protozoal infections do not cause peripheral or tissue eosinophilia; however, Cystoisospora infection is an exception to this rule.

Diarrhea and peripheral eosinophilia in an immunocompromised individual should raise concern for Cystoisospora infection. The other protozoal infections listed can cause diarrhea, but do not cause eosinophilia.

Reference

1. Goodgame, R.W. Understanding intestinal spore-forming protozoa: Cryptosporidia, microsporidia, isospora, and cyclospora. Ann Intern Med. 1996;124:429-41.

Q1: Answer: C

Cystoisospora belli (formerly known as Isospora belli) is a gastrointestinal protozoan. In patients with AIDS and other immunodeficiencies, it is an opportunistic pathogen that can cause watery diarrhea and weight loss. Infections are acquired by the ingestion of sporulated oocysts from food or water contaminated with human feces. In general, protozoal infections do not cause peripheral or tissue eosinophilia; however, Cystoisospora infection is an exception to this rule.

Diarrhea and peripheral eosinophilia in an immunocompromised individual should raise concern for Cystoisospora infection. The other protozoal infections listed can cause diarrhea, but do not cause eosinophilia.

Reference

1. Goodgame, R.W. Understanding intestinal spore-forming protozoa: Cryptosporidia, microsporidia, isospora, and cyclospora. Ann Intern Med. 1996;124:429-41.

Q2: Answer: B

This is likely a tapeworm infection with Diphyllobothrium latum, and most tapeworm infections are treated with praziquantel. D. latum infection can be acquired by ingesting certain forms of freshwater fish, and those who consume raw fish, including sushi, are at increased risk. Patients infected with D. latum may develop a megaloblastic anemia secondary to vitamin B12 deficiency given that D. latum competitively interferes with normal host absorption. All the other agents listed would not be used for treatment of tapeworm infection. 

Reference

1. Scholz T., et al. Update on the human broad tapeworm (genus Diphyllobothrium), including clinical relevance. Clin Microbiol Rev. 2009;22:146-60.

Q2: Answer: B

This is likely a tapeworm infection with Diphyllobothrium latum, and most tapeworm infections are treated with praziquantel. D. latum infection can be acquired by ingesting certain forms of freshwater fish, and those who consume raw fish, including sushi, are at increased risk. Patients infected with D. latum may develop a megaloblastic anemia secondary to vitamin B12 deficiency given that D. latum competitively interferes with normal host absorption. All the other agents listed would not be used for treatment of tapeworm infection. 

Reference

1. Scholz T., et al. Update on the human broad tapeworm (genus Diphyllobothrium), including clinical relevance. Clin Microbiol Rev. 2009;22:146-60.

Q2: Answer: B

This is likely a tapeworm infection with Diphyllobothrium latum, and most tapeworm infections are treated with praziquantel. D. latum infection can be acquired by ingesting certain forms of freshwater fish, and those who consume raw fish, including sushi, are at increased risk. Patients infected with D. latum may develop a megaloblastic anemia secondary to vitamin B12 deficiency given that D. latum competitively interferes with normal host absorption. All the other agents listed would not be used for treatment of tapeworm infection. 

Reference

1. Scholz T., et al. Update on the human broad tapeworm (genus Diphyllobothrium), including clinical relevance. Clin Microbiol Rev. 2009;22:146-60.

Q1: Answer: B

Rationale: Bile acid diarrhea (BAD) is becoming more widely recognized as a cause of chronic diarrhea. There are four associated types of BAD: Type 1 BAD is associated with ileal dysfunction with impaired reabsorption; type 2 BAD is considered primary or idiopathic BAD and occurs in the absence of ileal or obvious gastrointestinal disease; type 3 BAD is associated with gastrointestinal disorders, such as small intestinal bacterial overgrowth, celiac disease, or chronic pancreatitis; a fourth category of BAD may result from excessive hepatic bile acid synthesis caused by medications. This patient appears to have type 2 BAD; therefore, Answer B is correct. BAD has been shown to account for about one-third of patients with chronic diarrhea or irritable bowel syndrome with diarrhea.

References

1. Camilleri M. Bile acid diarrhea: prevalence, pathogenesis, and therapy.  Gut Liver. 2015 May 23;9[3]:332-9.

2. Wedlake L., et al. Systematic review: The prevalence of idiopathic bile acid malabsorption as diagnosed by SeHCAT scanning in patients with diarrhoea-predominant irritable bowel syndrome. Aliment Pharmacol Ther. 2009;30:707-17.

Q1: Answer: B

Rationale: Bile acid diarrhea (BAD) is becoming more widely recognized as a cause of chronic diarrhea. There are four associated types of BAD: Type 1 BAD is associated with ileal dysfunction with impaired reabsorption; type 2 BAD is considered primary or idiopathic BAD and occurs in the absence of ileal or obvious gastrointestinal disease; type 3 BAD is associated with gastrointestinal disorders, such as small intestinal bacterial overgrowth, celiac disease, or chronic pancreatitis; a fourth category of BAD may result from excessive hepatic bile acid synthesis caused by medications. This patient appears to have type 2 BAD; therefore, Answer B is correct. BAD has been shown to account for about one-third of patients with chronic diarrhea or irritable bowel syndrome with diarrhea.

References

1. Camilleri M. Bile acid diarrhea: prevalence, pathogenesis, and therapy.  Gut Liver. 2015 May 23;9[3]:332-9.

2. Wedlake L., et al. Systematic review: The prevalence of idiopathic bile acid malabsorption as diagnosed by SeHCAT scanning in patients with diarrhoea-predominant irritable bowel syndrome. Aliment Pharmacol Ther. 2009;30:707-17.

Q1: Answer: B

Rationale: Bile acid diarrhea (BAD) is becoming more widely recognized as a cause of chronic diarrhea. There are four associated types of BAD: Type 1 BAD is associated with ileal dysfunction with impaired reabsorption; type 2 BAD is considered primary or idiopathic BAD and occurs in the absence of ileal or obvious gastrointestinal disease; type 3 BAD is associated with gastrointestinal disorders, such as small intestinal bacterial overgrowth, celiac disease, or chronic pancreatitis; a fourth category of BAD may result from excessive hepatic bile acid synthesis caused by medications. This patient appears to have type 2 BAD; therefore, Answer B is correct. BAD has been shown to account for about one-third of patients with chronic diarrhea or irritable bowel syndrome with diarrhea.

References

1. Camilleri M. Bile acid diarrhea: prevalence, pathogenesis, and therapy.  Gut Liver. 2015 May 23;9[3]:332-9.

2. Wedlake L., et al. Systematic review: The prevalence of idiopathic bile acid malabsorption as diagnosed by SeHCAT scanning in patients with diarrhoea-predominant irritable bowel syndrome. Aliment Pharmacol Ther. 2009;30:707-17.