Al-Qassim University Faculty of Medicine

Phase II – Year IIIGIT Block (CMD332)

EXOCRINE PANCREASELecture

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

Etiologic FactorsMetabolic

• Alcoholism

• Drugs (e.g., thiazide diuretics)

Mechanical

• Trauma

• Gallstones• Iatrogenic injury( Perioperative injury , Endoscopic procedures with dye injection)  

Vascular

• Shock

• Atheroembolism

Infectious

• Mumps

• Coxsackievirus

 

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

Acute pancreatitis: hemorrhage & fat necrosis

Acute pancreatitis : fat necrosis , adipose tissue & hemorrhage

Chronic Pancreatitis

Etiologic Factors

• Long-term alcohol abuse

• Long-standing pancreatic duct obstruction

(pseudocysts, calculi, neoplasms)

• Tropical pancreatitis (malnutrition)

• Hereditary pancreatitis (gene mutation)

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)

Chronic pancreatitis : fibrous tissue, dilated ducts & residual acinar tissue

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

• 65 - 80 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 pancreasT 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