Episode five closes the chapter with two tumors that share the same pancreas and almost nothing else. Adenocarcinoma is desmoplastic, poorly enhancing, presents late with painless jaundice, and is staged by its relationship to four vessels into the resectability categories that drive surgery-versus-systemic-therapy. The neuroendocrine tumors are islet-derived, hypervascular, and often announce themselves with a hormone syndrome while still small, sorted by functional pattern and grade. The same core biopsy and multiphase CT serve both, but everything downstream diverges, so the work is holding the two algorithms apart. Biology sets the staging language, and the staging language sets the treatment, from neoadjuvant FOLFIRINOX to somatostatin analogs and radionuclide therapy. Topics covered Adenocarcinoma biology and late presentation Risk factors: modifiable, hereditary, conditioning Diagnostic sequence and core biopsy The autoimmune pancreatitis mimic trap Four-vessel resectability staging Neoadjuvant, adjuvant, and metastatic chemotherapy Neuroendocrine tumor biology and imaging Functional syndromes: insulinoma and gastrinoma VIPoma, glucagonoma, somatostatinoma Treatment stratified by size and receptor status Key decisions A patient over sixty with a painless head mass and obstructive jaundice has adenocarcinoma until proven otherwise, so a mildly elevated IgG4 does not justify empiric prednisone that would cost the curative window. Resectability is defined by the tumor relationship to the celiac axis, common hepatic artery, superior mesenteric artery, and superior mesenteric and portal veins, with borderline disease showing arterial contact under one hundred eighty degrees or reconstructable venous involvement. Borderline resectable and many resectable patients receive neoadjuvant modified FOLFIRINOX for four to six months before re-staging, and upfront-surgery patients receive adjuvant modified FOLFIRINOX when fit. Metastatic disease is treated with modified FOLFIRINOX or gemcitabine plus nab-paclitaxel by performance status, with olaparib maintenance for germline BRCA or PALB2 mutations whose tumors respond to platinum. In suspected insulinoma, a suppressed C-peptide with high insulin during hypoglycemia indicates factitious insulin use rather than tumor, and endoscopic ultrasound is the dominant localization tool because most insulinomas are somatostatin-receptor negative. Gastrinoma diagnosis requires a fasting serum gastrin measured off proton pump inhibitor for seven days, with a gastrin above one thousand picograms per milliliter and gastric pH under two diagnostic, and intermediate values prompting a secretin stimulation test. Non-functional neuroendocrine tumors under one centimeter may be observed while those over two centimeters warrant resection, and unresectable disease is managed with somatostatin analogs, everolimus or sunitinib, and lutetium-DOTATATE radionuclide therapy. For the full chapter with MCQs, tables, and primary-guideline references, visit www.boardpearls.com. Questions or feedback: [email protected].

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“What did the council decide on item 42?” — answered with the speaker and the moment.

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