Presentation on theme: "Al-Qassim University Faculty of Medicine Phase II – Year III GIT Block (CMD332) EXOCRINE PANCREASE Lecture Dr. Gamal Hamra Wednesday 01/12/1430 (18/11/2009)"— Presentation transcript:
Al-Qassim University Faculty of Medicine Phase II – Year III GIT Block (CMD332) EXOCRINE PANCREASE Lecture Dr. Gamal Hamra Wednesday 01/12/1430 (18/11/2009)
Describe etio-pathogenesis and morphology of: Acute and chronic pancreatitis Carcinomas of the exocrine pancreas
Acute Pancreatitis Activation of pancreatic enzymes → autodigestion of the gland. Abdominal pain + raised levels of pancreatic enzymes (amylase and lipase) Mild (acute interstitial pancreatitis), edema & inflamation Severe ( acute hemorrhagic pancreatitis), extensive hemorrhage 80% associated with cholelithiasis & alcoholism.
Pathogenesis of acute pancreatitis
Morphology of Acute Pancreatitis –Leakage of the vasculature to cause edema –Necrosis of regional fat by lipolytic enzymes –Acute inflammatory reaction –Proteolytic destruction of the pancreatic substance –Destruction of the blood vessels with subsequent interstitial hemorrhage
Chronic Pancreatitis Repeated bouts of mild to moderate pancreatic inflammation → loss of pancreatic parenchyma & replacement by fibrous tissue. → loss of pancreatic function CT scan ( pancreas hard with foci of calcifications) Fibrosis number & size of acini Sparing of the islets of Langerhans Obstruction of pancreatic ducts
Chronic pancreatitis : pancreas (P) atrophic and replaced by rubbery, fibrous tissue, dilated ducts (D), duodenum (A)
Clinical features Chronic pancreatitis Silent or recurrent attacks of pain Precipitated by alcohol abuse, overeating & drugs Mild serum amylase and lipase, Late complications include: –Diarrhea (malabsorbtion) –Steatorrhea –Diabetes –Pseudocyst
Carcinoma of the Pancreas Arising from ductal epithelial cells (adenocarcinoma). Common cause of death in the US Poor prognosis Alcohol consumption increased risk Y More in men and blacks
Development of pancreatic cancer : 1- K-RAS oncogene mutations (early stages) 2- p16 tumor suppressor gene inactivation (intermediate stages) 3- p53& BRCA2 tumor suppressor genes inactivation ( late stages) ( Multiple mutations is more important )
Morphology of pancreatic cancer Distribution is as follows: –Head 60% –Body 15% –Tail 5% –Diffuse or widely spread 20% Tumors may be small and ill defined or large (8-10 cm), with extensive local invasion and regional metastases. Microscopically, more or less differentiated glandular patterns (adenocarcinoma) arise from ductal epithelium, mucous or non-mucous secreting.
Carcinoma of the head of the pancreas T umours appear as gritty, grey, hard nodules (T), irregularly invading the adjacent gland and local structures
Carcinoma of the pancreas. Poorly formed glands in densely fibrotic stroma, inflammatory cells
Diagnosis of Carcinoma of pancreas Tumor markers : CEA, CA 19-9 & CA 125 CT, MRI, US & ERCP Cytologic and histologic specimen