DDSEP® 8 Quick Quiz

Q2. CORRECT ANSWER: C

RATIONALE
In a population study of U.S. veterans infected with hepatitis C (n = 110,484), a cox proportional hazards model was used to determine risk of developing cirrhosis and hepatocellular carcinoma for genotypes 1-4, after adjusting for age, period of service, race, sex, human immunodeficiency virus (HIV) infection, alcohol use, diabetes, body mass index, and antiviral treatment. Despite genotype 3 patients being younger, their risk of developing cirrhosis was highest with hazard ratio = 1.30 (1.22, 1.39), compared to genotype 1 (reference, HR 1.0), genotype 2 with HR = 0.68 (0.64, 0.73), and genotype 4 with HR = 0.94 (0.78, 1.14). Likewise, the risk of development of HCC was highest for genotype 3 HCV with HR = 1.80 (1.60, 2.03), compared to a genotype 2 (HR = 0.55; 0.47, 0.63), and genotype 4 (0.99; 0.68, 1.45).
It is speculated that the hepatic steatosis that is a direct result of genotype 3 HCV may contribute to the accelerated progression to cirrhosis and HCC, but this has not been proven and was not evaluated in this Veteran Affairs study.

REFERENCE
1. Kanwal F., Kramer J.R., Ilyas J., et al. HCV genotype 3 is associated with an increased risk of cirrhosis and hepatocellular cancer in a national sample of U.S. Veterans with HCV. Hepatology. 2014;60(1):98-105.

Q2. CORRECT ANSWER: C

RATIONALE
In a population study of U.S. veterans infected with hepatitis C (n = 110,484), a cox proportional hazards model was used to determine risk of developing cirrhosis and hepatocellular carcinoma for genotypes 1-4, after adjusting for age, period of service, race, sex, human immunodeficiency virus (HIV) infection, alcohol use, diabetes, body mass index, and antiviral treatment. Despite genotype 3 patients being younger, their risk of developing cirrhosis was highest with hazard ratio = 1.30 (1.22, 1.39), compared to genotype 1 (reference, HR 1.0), genotype 2 with HR = 0.68 (0.64, 0.73), and genotype 4 with HR = 0.94 (0.78, 1.14). Likewise, the risk of development of HCC was highest for genotype 3 HCV with HR = 1.80 (1.60, 2.03), compared to a genotype 2 (HR = 0.55; 0.47, 0.63), and genotype 4 (0.99; 0.68, 1.45).
It is speculated that the hepatic steatosis that is a direct result of genotype 3 HCV may contribute to the accelerated progression to cirrhosis and HCC, but this has not been proven and was not evaluated in this Veteran Affairs study.

REFERENCE
1. Kanwal F., Kramer J.R., Ilyas J., et al. HCV genotype 3 is associated with an increased risk of cirrhosis and hepatocellular cancer in a national sample of U.S. Veterans with HCV. Hepatology. 2014;60(1):98-105.

Q2. CORRECT ANSWER: C

RATIONALE
In a population study of U.S. veterans infected with hepatitis C (n = 110,484), a cox proportional hazards model was used to determine risk of developing cirrhosis and hepatocellular carcinoma for genotypes 1-4, after adjusting for age, period of service, race, sex, human immunodeficiency virus (HIV) infection, alcohol use, diabetes, body mass index, and antiviral treatment. Despite genotype 3 patients being younger, their risk of developing cirrhosis was highest with hazard ratio = 1.30 (1.22, 1.39), compared to genotype 1 (reference, HR 1.0), genotype 2 with HR = 0.68 (0.64, 0.73), and genotype 4 with HR = 0.94 (0.78, 1.14). Likewise, the risk of development of HCC was highest for genotype 3 HCV with HR = 1.80 (1.60, 2.03), compared to a genotype 2 (HR = 0.55; 0.47, 0.63), and genotype 4 (0.99; 0.68, 1.45).
It is speculated that the hepatic steatosis that is a direct result of genotype 3 HCV may contribute to the accelerated progression to cirrhosis and HCC, but this has not been proven and was not evaluated in this Veteran Affairs study.

REFERENCE
1. Kanwal F., Kramer J.R., Ilyas J., et al. HCV genotype 3 is associated with an increased risk of cirrhosis and hepatocellular cancer in a national sample of U.S. Veterans with HCV. Hepatology. 2014;60(1):98-105.

Q1. CORRECT ANSWER: A

RATIONALE
In patients with a good response to anti-reflux surgery who develop new dysphagia, an upper endoscopy is the test of choice. This will evaluate the structural integrity of the fundoplication, and evaluate for disruption and paraesophageal herniation. The esophagus can be inspected for esophagitis, and dilation of the fundoplication site can be performed. In the absence of heartburn or the original reflux symptoms, empiric acid suppression is not expected to improve the dysphagia. If the endoscopy is negative, esophageal manometry and barium swallow are the next studies of value. A pH study off PPI therapy is performed if recurrent reflux is suspected that does not respond to anti-reflux medications.

REFERENCE
1. Johnson D.A., Younes Z., Hogan W.J. Endoscopic assessment of hiatal hernia repair. Gastrointest Endosc. 2000;52(5):650-9.

Q1. CORRECT ANSWER: A

RATIONALE
In patients with a good response to anti-reflux surgery who develop new dysphagia, an upper endoscopy is the test of choice. This will evaluate the structural integrity of the fundoplication, and evaluate for disruption and paraesophageal herniation. The esophagus can be inspected for esophagitis, and dilation of the fundoplication site can be performed. In the absence of heartburn or the original reflux symptoms, empiric acid suppression is not expected to improve the dysphagia. If the endoscopy is negative, esophageal manometry and barium swallow are the next studies of value. A pH study off PPI therapy is performed if recurrent reflux is suspected that does not respond to anti-reflux medications.

REFERENCE
1. Johnson D.A., Younes Z., Hogan W.J. Endoscopic assessment of hiatal hernia repair. Gastrointest Endosc. 2000;52(5):650-9.

Q1. CORRECT ANSWER: A

RATIONALE
In patients with a good response to anti-reflux surgery who develop new dysphagia, an upper endoscopy is the test of choice. This will evaluate the structural integrity of the fundoplication, and evaluate for disruption and paraesophageal herniation. The esophagus can be inspected for esophagitis, and dilation of the fundoplication site can be performed. In the absence of heartburn or the original reflux symptoms, empiric acid suppression is not expected to improve the dysphagia. If the endoscopy is negative, esophageal manometry and barium swallow are the next studies of value. A pH study off PPI therapy is performed if recurrent reflux is suspected that does not respond to anti-reflux medications.

REFERENCE
1. Johnson D.A., Younes Z., Hogan W.J. Endoscopic assessment of hiatal hernia repair. Gastrointest Endosc. 2000;52(5):650-9.

Correct Answer: E

Rationale

On serial imaging, two worrisome features have developed in the pancreas cyst, i.e., an enhancing mural nodule and dilation of the main pancreatic duct. These features are high-risk stigmata, and therefore surgical resection is recommended. EUS FNA can be considered but is unlikely to change management if cytology is negative. Radiologic surveillance is not appropriate unless the patient refuses surgery.

Reference

1. Tanaka M., Fernández-del Castillo C., Adsay V., et al. International consensus guidelines 2012 for the management of IPMN and MCN of the pancreas. Pancreatology. 2012;12(3):183-97.

Correct Answer: E

Rationale

On serial imaging, two worrisome features have developed in the pancreas cyst, i.e., an enhancing mural nodule and dilation of the main pancreatic duct. These features are high-risk stigmata, and therefore surgical resection is recommended. EUS FNA can be considered but is unlikely to change management if cytology is negative. Radiologic surveillance is not appropriate unless the patient refuses surgery.

Reference

1. Tanaka M., Fernández-del Castillo C., Adsay V., et al. International consensus guidelines 2012 for the management of IPMN and MCN of the pancreas. Pancreatology. 2012;12(3):183-97.

Correct Answer: E

Rationale

On serial imaging, two worrisome features have developed in the pancreas cyst, i.e., an enhancing mural nodule and dilation of the main pancreatic duct. These features are high-risk stigmata, and therefore surgical resection is recommended. EUS FNA can be considered but is unlikely to change management if cytology is negative. Radiologic surveillance is not appropriate unless the patient refuses surgery.

Reference

1. Tanaka M., Fernández-del Castillo C., Adsay V., et al. International consensus guidelines 2012 for the management of IPMN and MCN of the pancreas. Pancreatology. 2012;12(3):183-97.

Correct Answer: C

Rationale

Mixed connective tissue disease can be associated with atrophy of the smooth muscle of the gut, like scleroderma. In the esophagus, this can manifest as a hypotensive lower esophageal sphincter and impaired esophageal smooth muscle peristalsis; in extreme cases, there is absent contractility in the esophagus. This contributes to impaired esophageal clearance of refluxed material, leading to prolonged acid residence times in the esophagus and severe reflux esophagitis. Many patients with mixed connective tissue disease have overlap Sjogren’s syndrome, reducing salivary neutralization of esophageal mucosal acidification and further contributing to esophagitis. While esophageal body motor function can be suboptimal in diabetes mellitus and Barrett’s esophagus, the mechanism of hypomotility is not smooth muscle atrophy and fibrosis. Polymyositis can affect skeletal muscle of the proximal esophagus, but not the smooth muscle. Lichen planus affects mucosa but not muscle.

Reference

1. Savarino E., Mei F., Parodi A., et al. Gastrointestinal motility disorder assessment in systemic sclerosis. Rheumatology (Oxford). 2013 Jun;52(6):1095-100.

2. Langdon P.C., Mulcahy K., Shepherd K.L., et al. Pharyngeal dysphagia in inflammatory muscle diseases resulting from impaired suprahyoid musculature. Dysphagia. 2012 Sep;27(3):408-17.

Correct Answer: C

Rationale

Mixed connective tissue disease can be associated with atrophy of the smooth muscle of the gut, like scleroderma. In the esophagus, this can manifest as a hypotensive lower esophageal sphincter and impaired esophageal smooth muscle peristalsis; in extreme cases, there is absent contractility in the esophagus. This contributes to impaired esophageal clearance of refluxed material, leading to prolonged acid residence times in the esophagus and severe reflux esophagitis. Many patients with mixed connective tissue disease have overlap Sjogren’s syndrome, reducing salivary neutralization of esophageal mucosal acidification and further contributing to esophagitis. While esophageal body motor function can be suboptimal in diabetes mellitus and Barrett’s esophagus, the mechanism of hypomotility is not smooth muscle atrophy and fibrosis. Polymyositis can affect skeletal muscle of the proximal esophagus, but not the smooth muscle. Lichen planus affects mucosa but not muscle.

Reference

1. Savarino E., Mei F., Parodi A., et al. Gastrointestinal motility disorder assessment in systemic sclerosis. Rheumatology (Oxford). 2013 Jun;52(6):1095-100.

2. Langdon P.C., Mulcahy K., Shepherd K.L., et al. Pharyngeal dysphagia in inflammatory muscle diseases resulting from impaired suprahyoid musculature. Dysphagia. 2012 Sep;27(3):408-17.

Correct Answer: C

Rationale

Mixed connective tissue disease can be associated with atrophy of the smooth muscle of the gut, like scleroderma. In the esophagus, this can manifest as a hypotensive lower esophageal sphincter and impaired esophageal smooth muscle peristalsis; in extreme cases, there is absent contractility in the esophagus. This contributes to impaired esophageal clearance of refluxed material, leading to prolonged acid residence times in the esophagus and severe reflux esophagitis. Many patients with mixed connective tissue disease have overlap Sjogren’s syndrome, reducing salivary neutralization of esophageal mucosal acidification and further contributing to esophagitis. While esophageal body motor function can be suboptimal in diabetes mellitus and Barrett’s esophagus, the mechanism of hypomotility is not smooth muscle atrophy and fibrosis. Polymyositis can affect skeletal muscle of the proximal esophagus, but not the smooth muscle. Lichen planus affects mucosa but not muscle.

Reference

1. Savarino E., Mei F., Parodi A., et al. Gastrointestinal motility disorder assessment in systemic sclerosis. Rheumatology (Oxford). 2013 Jun;52(6):1095-100.

2. Langdon P.C., Mulcahy K., Shepherd K.L., et al. Pharyngeal dysphagia in inflammatory muscle diseases resulting from impaired suprahyoid musculature. Dysphagia. 2012 Sep;27(3):408-17.

Answer: C

Rationale: Binge-eating disorder (BED) is a distinct clinical entity, which gastroenterologists are likely to encounter. A substantial fraction of patients evaluated for weight loss therapy will have BED, yet it can be difficult to recognize. Similar to bulimia, BED is characterized by binge-eating episodes, which must occur an average of once a week for at least 3 months. However, there are no recurrent inappropriate behaviors such as purging with laxatives, diuretics, or emetics (e.g., syrup of ipecac) or excessive exercise. BED patients most often do not have any specific symptoms or physical exam findings other than being overweight or obese. Very subtle characteristics include very rapid eating, eating despite satiety, eating alone due to feelings of shame, and a negative emotional context after binge eating. BED will negatively impact any interventions for obesity, unless recognized and addressed.

Nocturnal eating syndrome is similar, yet distinct, in that it is also characterized by binge eating without inappropriate compensatory purging behaviors, but prominent features include morning anorexia, nocturnal hyperphagia, and sleep disturbances. The sleep disturbances are characterized by an average of 3-4 awakenings per night, during which an average of roughly 1,100 calories might be consumed during half the episodes.

Anorexia nervosa is characterized by a restriction in food intake relative to needs which results in an inappropriately low body weight (below BMI of 17.5 kg/m2), a fear of gaining weight or being fat despite being underweight, and inappropriate perception/experience of body image. Roughly half of patient with anorexia nervosa may also engage in binge-eating behaviors or purging behaviors.

Purging disorder is a distinct variant recognized as purging behaviors in the absence of the binge-eating behavior.

Answer: C

Rationale: Binge-eating disorder (BED) is a distinct clinical entity, which gastroenterologists are likely to encounter. A substantial fraction of patients evaluated for weight loss therapy will have BED, yet it can be difficult to recognize. Similar to bulimia, BED is characterized by binge-eating episodes, which must occur an average of once a week for at least 3 months. However, there are no recurrent inappropriate behaviors such as purging with laxatives, diuretics, or emetics (e.g., syrup of ipecac) or excessive exercise. BED patients most often do not have any specific symptoms or physical exam findings other than being overweight or obese. Very subtle characteristics include very rapid eating, eating despite satiety, eating alone due to feelings of shame, and a negative emotional context after binge eating. BED will negatively impact any interventions for obesity, unless recognized and addressed.

Nocturnal eating syndrome is similar, yet distinct, in that it is also characterized by binge eating without inappropriate compensatory purging behaviors, but prominent features include morning anorexia, nocturnal hyperphagia, and sleep disturbances. The sleep disturbances are characterized by an average of 3-4 awakenings per night, during which an average of roughly 1,100 calories might be consumed during half the episodes.

Anorexia nervosa is characterized by a restriction in food intake relative to needs which results in an inappropriately low body weight (below BMI of 17.5 kg/m2), a fear of gaining weight or being fat despite being underweight, and inappropriate perception/experience of body image. Roughly half of patient with anorexia nervosa may also engage in binge-eating behaviors or purging behaviors.

Purging disorder is a distinct variant recognized as purging behaviors in the absence of the binge-eating behavior.

Answer: C

Rationale: Binge-eating disorder (BED) is a distinct clinical entity, which gastroenterologists are likely to encounter. A substantial fraction of patients evaluated for weight loss therapy will have BED, yet it can be difficult to recognize. Similar to bulimia, BED is characterized by binge-eating episodes, which must occur an average of once a week for at least 3 months. However, there are no recurrent inappropriate behaviors such as purging with laxatives, diuretics, or emetics (e.g., syrup of ipecac) or excessive exercise. BED patients most often do not have any specific symptoms or physical exam findings other than being overweight or obese. Very subtle characteristics include very rapid eating, eating despite satiety, eating alone due to feelings of shame, and a negative emotional context after binge eating. BED will negatively impact any interventions for obesity, unless recognized and addressed.

Nocturnal eating syndrome is similar, yet distinct, in that it is also characterized by binge eating without inappropriate compensatory purging behaviors, but prominent features include morning anorexia, nocturnal hyperphagia, and sleep disturbances. The sleep disturbances are characterized by an average of 3-4 awakenings per night, during which an average of roughly 1,100 calories might be consumed during half the episodes.

Anorexia nervosa is characterized by a restriction in food intake relative to needs which results in an inappropriately low body weight (below BMI of 17.5 kg/m2), a fear of gaining weight or being fat despite being underweight, and inappropriate perception/experience of body image. Roughly half of patient with anorexia nervosa may also engage in binge-eating behaviors or purging behaviors.

Purging disorder is a distinct variant recognized as purging behaviors in the absence of the binge-eating behavior.

Answer: C

Rationale: The patient presents with acute gallstone pancreatitis. In patients with gallstone pancreatitis and evidence of cholangitis, ERCP with sphincterotomy and stone extraction should be performed. The patient’s fever, jaundice, and right upper-quadrant pain are sufficient to make the diagnosis of cholangitis. It is too early in the course of the disease to evaluate for pancreatic necrosis. Typically, triglyceride levels above 1,000 mg/dL are required to induce pancreatitis. Finally, while the patient has cholelithiasis, there is no evidence of cholecystitis. Therefore, a HIDA scan is not warranted.

Reference

1. Behrns K.E., Ashley S.W., Hunter J.G., Carr-Locke D. Early ERCP for gallstone pancreatitis: for whom and when? J Gastrointest Surg. 2008;12(4):629-33.

Answer: C

Rationale: The patient presents with acute gallstone pancreatitis. In patients with gallstone pancreatitis and evidence of cholangitis, ERCP with sphincterotomy and stone extraction should be performed. The patient’s fever, jaundice, and right upper-quadrant pain are sufficient to make the diagnosis of cholangitis. It is too early in the course of the disease to evaluate for pancreatic necrosis. Typically, triglyceride levels above 1,000 mg/dL are required to induce pancreatitis. Finally, while the patient has cholelithiasis, there is no evidence of cholecystitis. Therefore, a HIDA scan is not warranted.

Reference

1. Behrns K.E., Ashley S.W., Hunter J.G., Carr-Locke D. Early ERCP for gallstone pancreatitis: for whom and when? J Gastrointest Surg. 2008;12(4):629-33.

Answer: C

Rationale: The patient presents with acute gallstone pancreatitis. In patients with gallstone pancreatitis and evidence of cholangitis, ERCP with sphincterotomy and stone extraction should be performed. The patient’s fever, jaundice, and right upper-quadrant pain are sufficient to make the diagnosis of cholangitis. It is too early in the course of the disease to evaluate for pancreatic necrosis. Typically, triglyceride levels above 1,000 mg/dL are required to induce pancreatitis. Finally, while the patient has cholelithiasis, there is no evidence of cholecystitis. Therefore, a HIDA scan is not warranted.

Reference

1. Behrns K.E., Ashley S.W., Hunter J.G., Carr-Locke D. Early ERCP for gallstone pancreatitis: for whom and when? J Gastrointest Surg. 2008;12(4):629-33.

Q2: Answer: E 

This patient has elevated transaminases with normal alkaline phosphatase and total bilirubin levels. His AST is greater than his ALT. He does not meet criteria for having nonalcolholic steatohepatitis because of his history of drinking at least five drinks per day. Additionally, his AST:ALT ratio would be atypical for classic NASH presentation. This patient does not have chronic hepatitis B as his serologies reveal that he is hepatitis B immune. This patient’s labs are not suggestive of iron overload with a normal serum ferritin and normal iron saturation. Although this patient has emphysema diagnosed at a young age and an undetectable alpha-1-antitrypsin level, this patient’s liver enzyme elevations are not due to alpha-1-antitrypsin deficiency. Alpha-1-antitrypsin is a glycoprotein that functions as a serine protease inhibitor and is produced predominantly in hepatocytes and then secreted from the cell.

In alpha-1-antitrypsin mutations that affect the liver (most commonly the ZZ phenotype), there is an amino acid substitution that results in the production of an abnormal alpha-1-antitrypsin molecule that polymerizes within the hepatocyte preventing secretion from the cell and resulting in abnormal accumulation of the alpha-1-antitrypsin in hepatocytes with resulting hepatic damage over time. This patient, however, has the alpha-1-antitrypsin phenotype null/null, which results in the absence of alpha-1-antitrypsin production. As such, null/null individuals are at very high risk for emphysema due to the complete absence of the alpha-1-antitrypsin enzyme. However, since null/null individuals produce no alpha-1-antitrypsin at all, there is no abnormally polymerized alpha-1-antitrypsin protein build-up. Based upon the clinical history and laboratory data, this patient’s liver enzyme elevations are most likely due to alcohol abuse.  

References

1. Fairbanks K.D., Tavill A.S. Liver disease in alpha-1-antitrypsin deficiency: A review. Am J Gastro. 2008;103:2136-41.

2. Silverman E.A., Sandhaus R.A. Alpha-1 antitrypsin deficiency. N Engl J Med. 2009;360;2749-5.

Q2: Answer: E 

This patient has elevated transaminases with normal alkaline phosphatase and total bilirubin levels. His AST is greater than his ALT. He does not meet criteria for having nonalcolholic steatohepatitis because of his history of drinking at least five drinks per day. Additionally, his AST:ALT ratio would be atypical for classic NASH presentation. This patient does not have chronic hepatitis B as his serologies reveal that he is hepatitis B immune. This patient’s labs are not suggestive of iron overload with a normal serum ferritin and normal iron saturation. Although this patient has emphysema diagnosed at a young age and an undetectable alpha-1-antitrypsin level, this patient’s liver enzyme elevations are not due to alpha-1-antitrypsin deficiency. Alpha-1-antitrypsin is a glycoprotein that functions as a serine protease inhibitor and is produced predominantly in hepatocytes and then secreted from the cell.

In alpha-1-antitrypsin mutations that affect the liver (most commonly the ZZ phenotype), there is an amino acid substitution that results in the production of an abnormal alpha-1-antitrypsin molecule that polymerizes within the hepatocyte preventing secretion from the cell and resulting in abnormal accumulation of the alpha-1-antitrypsin in hepatocytes with resulting hepatic damage over time. This patient, however, has the alpha-1-antitrypsin phenotype null/null, which results in the absence of alpha-1-antitrypsin production. As such, null/null individuals are at very high risk for emphysema due to the complete absence of the alpha-1-antitrypsin enzyme. However, since null/null individuals produce no alpha-1-antitrypsin at all, there is no abnormally polymerized alpha-1-antitrypsin protein build-up. Based upon the clinical history and laboratory data, this patient’s liver enzyme elevations are most likely due to alcohol abuse.  

References

1. Fairbanks K.D., Tavill A.S. Liver disease in alpha-1-antitrypsin deficiency: A review. Am J Gastro. 2008;103:2136-41.

2. Silverman E.A., Sandhaus R.A. Alpha-1 antitrypsin deficiency. N Engl J Med. 2009;360;2749-5.

Q2: Answer: E 

This patient has elevated transaminases with normal alkaline phosphatase and total bilirubin levels. His AST is greater than his ALT. He does not meet criteria for having nonalcolholic steatohepatitis because of his history of drinking at least five drinks per day. Additionally, his AST:ALT ratio would be atypical for classic NASH presentation. This patient does not have chronic hepatitis B as his serologies reveal that he is hepatitis B immune. This patient’s labs are not suggestive of iron overload with a normal serum ferritin and normal iron saturation. Although this patient has emphysema diagnosed at a young age and an undetectable alpha-1-antitrypsin level, this patient’s liver enzyme elevations are not due to alpha-1-antitrypsin deficiency. Alpha-1-antitrypsin is a glycoprotein that functions as a serine protease inhibitor and is produced predominantly in hepatocytes and then secreted from the cell.

In alpha-1-antitrypsin mutations that affect the liver (most commonly the ZZ phenotype), there is an amino acid substitution that results in the production of an abnormal alpha-1-antitrypsin molecule that polymerizes within the hepatocyte preventing secretion from the cell and resulting in abnormal accumulation of the alpha-1-antitrypsin in hepatocytes with resulting hepatic damage over time. This patient, however, has the alpha-1-antitrypsin phenotype null/null, which results in the absence of alpha-1-antitrypsin production. As such, null/null individuals are at very high risk for emphysema due to the complete absence of the alpha-1-antitrypsin enzyme. However, since null/null individuals produce no alpha-1-antitrypsin at all, there is no abnormally polymerized alpha-1-antitrypsin protein build-up. Based upon the clinical history and laboratory data, this patient’s liver enzyme elevations are most likely due to alcohol abuse.  

References

1. Fairbanks K.D., Tavill A.S. Liver disease in alpha-1-antitrypsin deficiency: A review. Am J Gastro. 2008;103:2136-41.

2. Silverman E.A., Sandhaus R.A. Alpha-1 antitrypsin deficiency. N Engl J Med. 2009;360;2749-5.

Q1: Answer: A

Campylobacter species are a major cause of diarrheal illness in the world. The organism inhabits the intestinal tracts of a wide range of animal hosts, notably poultry; contamination from these sources can lead to foodborne disease. Given the self-limited nature of most Campylobacter infections and the limited efficacy of routine antimicrobial therapy, treatment is warranted only for patients with features of severe disease or risk for severe disease.

Patients with severe disease include individuals with bloody stools, high fever, extra-intestinal infection, worsening or relapsing symptoms, or symptoms lasting longer than 1 week. Those at risk for severe disease include patients who are elderly, pregnant, or immunocompromised. First-line agents for treatment of Campylobacter infection include fluoroquinolones (if sensitive) or azithromycin. Campylobacter is inherently resistant to trimethoprim and beta-lactam antibiotics, including penicillin and most cephalosporins.

In the United States, the rate of resistance to fluoroquinolones is also increasing. The rate of ciprofloxacin resistance among Campylobacter isolated in the United States increased from 0% to 19% between 1989 and 2001. Inappropriate and overprescription of fluoroquinolones in humans combined with increased fluoroquinolone use in the poultry industry in particular have contributed to the increased prevalence of fluoroquinolone resistance.

The rate of macrolide-resistance among Campylobacter has remained stable at less than 5% in most parts of the world.

References

1. Dasti J.I., Tareen A.M., Lugert R., et al. Campylobacter jejuni: A brief overview on pathogenicity-associated factors and disease-mediating mechanisms. Int J Med Microbiol. 2010;300:205–11.

2. Gupta A., Nelson J.M., Barrett T.J., et al. Antimicrobial resistance among Campylobacter strains, United States, 1997-2001. Emerging infectious diseases. Jun 2004;10(6):1102-9.

Q1: Answer: A

Campylobacter species are a major cause of diarrheal illness in the world. The organism inhabits the intestinal tracts of a wide range of animal hosts, notably poultry; contamination from these sources can lead to foodborne disease. Given the self-limited nature of most Campylobacter infections and the limited efficacy of routine antimicrobial therapy, treatment is warranted only for patients with features of severe disease or risk for severe disease.

Patients with severe disease include individuals with bloody stools, high fever, extra-intestinal infection, worsening or relapsing symptoms, or symptoms lasting longer than 1 week. Those at risk for severe disease include patients who are elderly, pregnant, or immunocompromised. First-line agents for treatment of Campylobacter infection include fluoroquinolones (if sensitive) or azithromycin. Campylobacter is inherently resistant to trimethoprim and beta-lactam antibiotics, including penicillin and most cephalosporins.

In the United States, the rate of resistance to fluoroquinolones is also increasing. The rate of ciprofloxacin resistance among Campylobacter isolated in the United States increased from 0% to 19% between 1989 and 2001. Inappropriate and overprescription of fluoroquinolones in humans combined with increased fluoroquinolone use in the poultry industry in particular have contributed to the increased prevalence of fluoroquinolone resistance.

The rate of macrolide-resistance among Campylobacter has remained stable at less than 5% in most parts of the world.

References

1. Dasti J.I., Tareen A.M., Lugert R., et al. Campylobacter jejuni: A brief overview on pathogenicity-associated factors and disease-mediating mechanisms. Int J Med Microbiol. 2010;300:205–11.

2. Gupta A., Nelson J.M., Barrett T.J., et al. Antimicrobial resistance among Campylobacter strains, United States, 1997-2001. Emerging infectious diseases. Jun 2004;10(6):1102-9.

Q1: Answer: A

Campylobacter species are a major cause of diarrheal illness in the world. The organism inhabits the intestinal tracts of a wide range of animal hosts, notably poultry; contamination from these sources can lead to foodborne disease. Given the self-limited nature of most Campylobacter infections and the limited efficacy of routine antimicrobial therapy, treatment is warranted only for patients with features of severe disease or risk for severe disease.

Patients with severe disease include individuals with bloody stools, high fever, extra-intestinal infection, worsening or relapsing symptoms, or symptoms lasting longer than 1 week. Those at risk for severe disease include patients who are elderly, pregnant, or immunocompromised. First-line agents for treatment of Campylobacter infection include fluoroquinolones (if sensitive) or azithromycin. Campylobacter is inherently resistant to trimethoprim and beta-lactam antibiotics, including penicillin and most cephalosporins.

In the United States, the rate of resistance to fluoroquinolones is also increasing. The rate of ciprofloxacin resistance among Campylobacter isolated in the United States increased from 0% to 19% between 1989 and 2001. Inappropriate and overprescription of fluoroquinolones in humans combined with increased fluoroquinolone use in the poultry industry in particular have contributed to the increased prevalence of fluoroquinolone resistance.

The rate of macrolide-resistance among Campylobacter has remained stable at less than 5% in most parts of the world.

References

1. Dasti J.I., Tareen A.M., Lugert R., et al. Campylobacter jejuni: A brief overview on pathogenicity-associated factors and disease-mediating mechanisms. Int J Med Microbiol. 2010;300:205–11.

2. Gupta A., Nelson J.M., Barrett T.J., et al. Antimicrobial resistance among Campylobacter strains, United States, 1997-2001. Emerging infectious diseases. Jun 2004;10(6):1102-9.

Answer B

Objective: Recognize the clinical presentation and imaging features of main duct intraductal papillary mucinous neoplasm (IPMN)

Critique: The patient’s imaging is consistent with main duct IPMN and the mild pancreatitis is likely a consequence of mucin plugging and obstruction. Main duct IPMN is associated with a higher incidence of malignancy, compared with branch duct IPMN and surgical resection is recommended if the patient is a surgical candidate.

While further sampling with endoscopic ultrasound or endoscopic retrograde cholangiopancreatography may be helpful, these tests have a low sensitivity for identifying dysplasia and are unlikely to change management. Surveillance with MRI would be appropriate if the patient does not wish to undergo surgery at this time.

Answer B

Objective: Recognize the clinical presentation and imaging features of main duct intraductal papillary mucinous neoplasm (IPMN)

Critique: The patient’s imaging is consistent with main duct IPMN and the mild pancreatitis is likely a consequence of mucin plugging and obstruction. Main duct IPMN is associated with a higher incidence of malignancy, compared with branch duct IPMN and surgical resection is recommended if the patient is a surgical candidate.

While further sampling with endoscopic ultrasound or endoscopic retrograde cholangiopancreatography may be helpful, these tests have a low sensitivity for identifying dysplasia and are unlikely to change management. Surveillance with MRI would be appropriate if the patient does not wish to undergo surgery at this time.

Answer B

Objective: Recognize the clinical presentation and imaging features of main duct intraductal papillary mucinous neoplasm (IPMN)

Critique: The patient’s imaging is consistent with main duct IPMN and the mild pancreatitis is likely a consequence of mucin plugging and obstruction. Main duct IPMN is associated with a higher incidence of malignancy, compared with branch duct IPMN and surgical resection is recommended if the patient is a surgical candidate.

While further sampling with endoscopic ultrasound or endoscopic retrograde cholangiopancreatography may be helpful, these tests have a low sensitivity for identifying dysplasia and are unlikely to change management. Surveillance with MRI would be appropriate if the patient does not wish to undergo surgery at this time.

Answer D

Objective: Identify the clinical presentation and risk factors for small intestinal bacterial overgrowth.

Rationale: This patient likely has small intestinal bacterial overgrowth (SIBO) based on her symptoms, the steatorrhea with the positive Sudan stain for fat, and a slight anemia with an elevated MCV suggestive of vitamin B12 deficiency secondary to the bacterial overgrowth. She also has scleroderma, a condition commonly associated with SIBO, because it impairs gastrointestinal motility. 

While hydrogen breath testing may help establish the diagnosis of SIBO, there is variable sensitivity and specificity of the testing with false-positive and false-negative test results frequently occurring. An alternative strategy is to treat empirically with an accepted antibiotic regimen and assess response after the course is completed. 

References

1. Bures J., Cyrany J., Kohoutova D., et al. Small intestinal bacterial overgrowth syndrome. World J Gastroenterol. 2010 Jun 28;16(24):2978-90.

2. Abu-Shanab A., Quigley E.M.. Diagnosis of small intestinal bacterial overgrowth: The challenges persist! Expert Rev Gastroenterol Hepatol. 2009 Feb;3(1):77-87.

3. Khoshini R., Dai S.C., Lezcano S., Pimentel M. A systematic review of diagnostic tests for small intestinal bacterial overgrowth. Dig Dis Sci. 2008 Jun;53(6):1443-54.

Answer D

Objective: Identify the clinical presentation and risk factors for small intestinal bacterial overgrowth.

Rationale: This patient likely has small intestinal bacterial overgrowth (SIBO) based on her symptoms, the steatorrhea with the positive Sudan stain for fat, and a slight anemia with an elevated MCV suggestive of vitamin B12 deficiency secondary to the bacterial overgrowth. She also has scleroderma, a condition commonly associated with SIBO, because it impairs gastrointestinal motility. 

While hydrogen breath testing may help establish the diagnosis of SIBO, there is variable sensitivity and specificity of the testing with false-positive and false-negative test results frequently occurring. An alternative strategy is to treat empirically with an accepted antibiotic regimen and assess response after the course is completed. 

References

1. Bures J., Cyrany J., Kohoutova D., et al. Small intestinal bacterial overgrowth syndrome. World J Gastroenterol. 2010 Jun 28;16(24):2978-90.

2. Abu-Shanab A., Quigley E.M.. Diagnosis of small intestinal bacterial overgrowth: The challenges persist! Expert Rev Gastroenterol Hepatol. 2009 Feb;3(1):77-87.

3. Khoshini R., Dai S.C., Lezcano S., Pimentel M. A systematic review of diagnostic tests for small intestinal bacterial overgrowth. Dig Dis Sci. 2008 Jun;53(6):1443-54.

Answer D

Objective: Identify the clinical presentation and risk factors for small intestinal bacterial overgrowth.

Rationale: This patient likely has small intestinal bacterial overgrowth (SIBO) based on her symptoms, the steatorrhea with the positive Sudan stain for fat, and a slight anemia with an elevated MCV suggestive of vitamin B12 deficiency secondary to the bacterial overgrowth. She also has scleroderma, a condition commonly associated with SIBO, because it impairs gastrointestinal motility. 

While hydrogen breath testing may help establish the diagnosis of SIBO, there is variable sensitivity and specificity of the testing with false-positive and false-negative test results frequently occurring. An alternative strategy is to treat empirically with an accepted antibiotic regimen and assess response after the course is completed. 

References

1. Bures J., Cyrany J., Kohoutova D., et al. Small intestinal bacterial overgrowth syndrome. World J Gastroenterol. 2010 Jun 28;16(24):2978-90.

2. Abu-Shanab A., Quigley E.M.. Diagnosis of small intestinal bacterial overgrowth: The challenges persist! Expert Rev Gastroenterol Hepatol. 2009 Feb;3(1):77-87.

3. Khoshini R., Dai S.C., Lezcano S., Pimentel M. A systematic review of diagnostic tests for small intestinal bacterial overgrowth. Dig Dis Sci. 2008 Jun;53(6):1443-54.