Grace Guzman, M.D.
Assistant Professor of Pathology, UIC Phone: 312-996-9288 e-mail: email@example.com
UIC College of Medicine
M2 Pathology Course Lecture #69 Friday, February 13, 2004 11:30-12:20
Reading Assignment: My lecture notes; Robbins Pathologic Basis of Disease (Cotran, Kumar, Robbins) 6th Ed., Chapter 20, pp 902-929. EDUCATIONAL GOALS AND OBJECTIVES: 1. DEFINE THE FOLLOWING TERMS: -Pancreatitis -Pseudocyst Obstructive Jaundice -Migratory Thrombophlebitis 2. 3. 4. 5. 6. 7. 8. VIPoma Somatostatinoma Gastrinoma Ectopic Pancreas
Review the normal anatomy, histology, and physiology of the pancreas. Describe the pathophysiology of acute pancreatitis. Describe the etiologic causes of acute and chronic pancreatitis. Describe the morphologic findings in acute and chronic pancreatitis Describe the clinical events leading to pseudocyst formation. Describe the events leading to obstructive jaundice Describe the pathology and clinical manifestations of pancreatic adenocarcinoma.
Describe the pathology and clinical manifestations of Zollinger-Ellison Syndrome.
Describe the pathology and clinical manifestations of insulinoma. Describe the pathology and clinical manifestations of glucagonoma. Page 1 of 12
Pathology of the Pancreas
I. Introduction A. Anatomy The pancreas is a comma shaped organ that lies in the upper retroperitoneal space. The head of the pancreas is nestled within the curvature of the duodenum. It surrounds or is in close contact with the common bile duct. The body of the pancreas lies posterior to the stomach. The tail of the pancreas inserts into the hilus of the spleen. The entire pancreas is in close association with many nerves. In 60-70% of individuals, the main pancreatic duct joins the CBD to drain through a common channel. In the remaining, the two ducts run parallel without joining. B. Normal pancreas •Exocrine component secretes 20 different digestive enzymes •Endocrine component is a group of cells (six types) which form the islet of Langerhans Humoral factors involved in pancreatic digestive enzyme secretion • Secretin – stimulates water and bicarbonate secretion by pancreatic duct cells • Cholecystokinin – also produced in the duodenum promotes discharge of digestive enzyme by acinar cells in response to fatty acids and protein digestive products (peptides and amino acids) Digestive enzymes: •Trypsin •Chymotrypsin •Aminopeptidases •Elastases •Amylases •Lipases •Phospholipases •Nucleases Autodigestion is prevented by the following: Page 2 of 12
Pathology of the Pancreas
•Enzymes are synthesized as an inactive proenzyme with the exception of amylase and lipase •Proenzymes are sequestered in membrane bound zymogen granules in the acinar cells •Activation of proenzyme requires conversion of inactive trypsinogen to trypsin by duodenal enteropeptidase: enterokinase •Trypsin inhibitors in acinar and ductal cells •Intrapancreatic release of trypsin activates enzyme/s that degrade/s other digestive enzymes to inert products •Lysosomal hydrolases are capable of degrading zymogen granules when normal acinar secretion is impaired or blocked •Acinar cells are remarkably resistant to the action of trypsin, chymotrypsin and phospholipase A -primary stimulus for duodenal secretin production are increased acid load and fatty acids C. Physiology The pancreas is a mixed exocrineendocrine gland. The exocrine component secretes 20 different digestive enzymes. The endocrine component is a group of cells (six types) that form the islets of Langerhans. II. Inflammation A. 1. a. Acute pancreatitis Pathology The anatomic changes of acute pancreatitis strongly suggests autodigestion of the pancreatic substance
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Pathology of the Pancreas by inappropriately activated pancreatic enzymes: i. Microvascular leakage causing edema Necrosis of fat by lipolytic enzymes (may occur in pancreas as well as in omentum, mesentery, and bowel) Acute