GASTROENTEROLOGY LITERATURE REVIEW SESSION

May 17, 2001

 Etemad B, Whitcomb DC. Chronic pancreatitis:  diagnosis, classification, and new genetic developments.  Gastroenterology 2001;120:682-707.

 1. The first test in the evaluation of possible chronic pancreatitis should be

            a.  pancreatic biopsy

            b.  pancreatic EUS

            c.  Computed tomography

            d.  ERP

 2.  CT techniques used to evaluate for possible chronic pancreatitis include

            a.  an initial non-contrasted scan to detect pancreatic calcification

            b.  using water as an oral contrast agent to maximize pancreatic visualization

            c.  using a helical CT scan

            d.  obtaining thin cuts through the pancreas

 3.  A person who tests positive for one of the cationic trypsinogen gene mutations should be advised that

            a.  smoking increases risk of pancreatitis and pancreatic cancer

            b.  alcohol, emotional stress and fatty foods may precipitate pancreatitis attacks

            c.  the risk of developing pancreatitis depends on the type of mutation

            d.  the risk of the first attack of pancreatitis increases with age

            e.  no specific treatment exists for the prevention or treatment of chronic

pancreatitis

f.  prophylactic pancreatectomy after age 50 is recommended because of the

high risk of pancreatic cancer

 4.  Features of autoimmune pancreatitis include

            a.  a positive high-titer AMA (anti-mitochondrial antibody)

            b.  hypergammaglobulinemia

            c.  histologic findings of duct destruction, atrophy of acinar tissue with no

calcification, lymphocytic infiltration, plasma cells and fibrosis.

            d.  a normal pancreas on CT scan is required for diagnosis

            e.  prompt response to corticosteroids

 True or False

 5.  Over 50% of heavy alcohol users develop pancreatitis.

 6.  Tissue diagnosis of chronic pancreatitis is the gold standard to establish the diagnosis.

 7.  Findings on CT that suggest chronic pancreatitis include calcifications within the pancreatic ducts or parenchyma, and/or dilated main pancreatic ducts combined with parenchymal atrophy.

 8.  Testing for CFTR mutations to explain chronic pancreatitis is difficult because many different types and combinations of CFTR mutations must be considered and tested for, and the presence of some of these mutations may not be associated with pancreatitis.

 9.  The “gold standard” for measuring pancreatic function is the “tubed” secretin test

 10.  Individuals with mutations in the cationic trypsinogen gene have a 80% likelihood of developing pancreatitis and a 40% likelihood of developing chronic pancreatitis.

 11.  Endosonographic features suggestive of chronic pancreatitis found during EUS examination of the pancreas have been correlated with histologic findings and are accurate predictors of chronic pancreatitis.

 12.  Tobacco smoking is considered an independent risk factor for the development of chronic pancreatitis.

 13.  A normal carefully done helical CT with pancreatic protocol excludes the diagnosis of chronic pancreatitis.

 14.  Chronic renal failure is associated with increased rates of both acute and chronic pancreatitis, etiology may be multifactorial. 

15.  Most individuals with genetic mutations in the pancreatic secretory trypsin inhibitor (SPINK1) and the cystic fibrosis transmembrane conductance regulator (CFTR) develop clinical pancreatitis.

 16.  ERP findings of chronic pancreatitis include

            a.  early changes consist of dilation and irregularity of the smaller ducts and

branches of the pancreas

            b.  changes in the main pancreatic duct reflects more advanced disease

            c.  tortuosity stricture and calcifications suggest malignancy

            d.  findings in severe cases are pathognomonic, changes seen in minimal

disease are difficult to distinguish from a normal pancreatogram

 17.  Mutations in the cationic trypsinogen gene (PRSS1):

            a.  is associated with an autosomal dominant form of hereditary pancreatitis

            b.  allows premature activation of trypsinogen within the pancreas leading to

pancreatic autodigestion and repeated episodes of acute pancreatitis.

            c.  the prevalence of this mutation varies from 0% to 19% among patients

presumed to have idiopathic chronic pancreatitis 

            d.  any mutation in this gene is associated with a high probability of pancreatitis.

 18.  SPINK1 Mutations

            a.  are mutations of the pancreatic secretory trypsin inhibitor

            b.  SPINK1 acts as the first line defense against prematurely activated

trypsinogen

            c. SPINK1 mutations causes autosomal dominant hereditary pancreatitis

            d.  SPINK1 mutations are associated with idiopathic chronic pancreatitis

            e.  People with SPINK1 mutations have a low probability of developing

pancreatitis.

            f.  SPINK1 mutations appear to increase the likelihood that other toxic or

environmental agents may trigger pancreatitis.

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