Anatomy, embryology, pathophysiology
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Adenocarcinoma: inactivation of multiple antioncogenes, as well as issues with deoxyribonucleic acid mismatch repair ( BRCA2 ). Smoking, diet high in meat and solvent exposure are risk factors.
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Neuroendocrine tumors: multiple chromosomal losses. Associated with Von-Hippel Lindau syndrome and multiple endocrine neoplasia.
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Pancreatic lymphoma: usually non-Hodgkin lymphoma.
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Acinar cell carcinoma: mutations in adenomatous polyposis coli beta-catenin gene and loss of chromosome 11.
Techniques
Computed tomography
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Detects and characterizes the lesion based on the enhancement pattern on dynamic imaging.
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Pancreatic adenocarcinomas are hypodense on pancreatic phase whereas neuroendocrine tumors are hyperdense.
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Venous phase imaging allows for evaluation of vascular invasion and metastases, including regional lymph nodes, hepatic and omental metastases.
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Used as primary imaging tool for staging of pancreatic cancer at most institutions.
Magnetic resonance imaging
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Problem solving tool.
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Good for detection of small tumors and metastases.
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Used as primary imaging tool for local staging at some institutions.
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Magnetic resonance (MR) angiography can be used to assess vascular involvement.
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MR cholangiopancreatography (MRCP) can be used to visualize the effect of the tumor on the biliary tree.
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Secretin enhanced MRCP can improve assessment of ductal stenosis and help differentiate benign from malignant strictures.
Ultrasonography
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Operator dependent with limitations based on bowel gas and patient body habitus.
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Endoscopic ultrasound usually performed by gastroenterologists. Provides high resolution images of pancreas and allows biopsy (fine needle aspiration) of lesions.
Nuclear medicine
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Positron emission tomography (PET)/computed tomography (CT).
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Normal pancreas should not have significant fluorodeoxyglucose (FDG) uptake.
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Focal uptake is abnormal and could represent a primary malignancy.
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Specific disease processes
Pancreatic adenocarcinoma
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90% of malignant pancreatic tumors.
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Fifth leading cause of death in Western countries.
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Five-year survival of 4%.
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Males more than females between seventh and eighth decade.
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Presentation: painless jaundice (75% of patients), new onset diabetes (10%), vague abdominal pain, weight loss.
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Tumors at head are more common (two-thirds) ( Figs. 13.1–13.3 ) and have better prognosis. Smaller at presentation with average size of 3 cm.
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Tumors in body (5%–15%) or tail (10%–15%) may present with back pain. Worse prognosis. Larger at prognosis with average size of 5 cm ( Fig. 13.4 ).
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May be focal masses or may be infiltrative.
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Cystic changes may happen because of necrosis or ductal obstruction.
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Incites extensive desmoplastic reaction leading to main pancreatic ductal (MPD) obstruction ( Fig. 13.5 ), pancreatitis, and/or parenchymal atrophy.
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Mode of spread: local ( Fig. 13.6 ), retroperitoneum, peritoneal lymph nodes ( Fig. 13.7 ), and liver.
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Mass conspicuity higher in pancreatic phase. Appears as low density mass compared with surrounding parenchyma but may be isoattenuating in 10% of cases.
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Indirect evidence: ductal dilation ( Fig. 13.8 ), parenchymal atrophy, double duct sign (common bile duct and MPD dilation) ( Fig. 13.9 ).
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Portal venous phase important for evaluation of metastases, visualization of tumor in respect to vasculature.
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Vessel encasement evaluation on CT is important prognostic factor in resection.
Less than 90 degrees, less than 3% infiltration; 90 to 180 degrees, 29% to 57% infiltration; more than 180 degrees, more than 80% infiltration.
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T1 hypointense, variable T2 signal (usually hypointense), enhances less than parenchyma but demonstrates progressive enhancement.
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MRCP can demonstrate ductal abnormalities, including stenosis, double duct sign, etc. Secretin MRCP better at characterization than MRCP.
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On ultrasound, pancreatic mass appears hypoechoic.
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Endoscopic ultrasound is most accurate for detection of duodenal infiltration and lymph node staging ( Fig. 13.10 ).
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