Normal histology	Histopathology	Pathological basis of disease	Clinical findings	
Tissue architecture:
•	The pancreas is a highly lobulated gland invested by a thin loose collagenous capsule which extends as delicate septa between the lobule.
•	The exocrine component of the pancreas consists of closely packed secretory acini which drain into a highly branched duct system.
•	Most of the secretion drains into the main pancreatic duct which joins the common bile duct to drain into the duodenum via the ampulla of Vater.

Cellular characteristics:
•	The acinar cells are typical protein-secreting cells.
•	The nuclei are basally located & surrounded by basophilic cytoplasm crammed with rough endoplasmic reticulum.
•	The apices of the cells are packed with eosinophilic zymogen secretory granules.
•	The cells lining the intercalated ducts are responsible for elaborating the water & bicarbonate component of pancreatic secretion. 	Abnormal histology:
•	Gray-white necrosis of the parenchyma & chalky white fat necrosis.
•	Adipocytes: instead of a thin cell membrane & peripherally placed nuclei, the cells now have no nuclei & there are cloudy markings in the central regions of cells.
•	Large areas of coagulative necrosis & complete destruction & replacement of pancreatic acinic by extensive infiltration of inflammatory cells.
•	Purplish appearance of fat cells due to saponification of fat.
•	Variegated pattern of blue-black hemorrhages & gray-white necrotic softening alternating with foci of yellow-white, chalky fat necrosis.
•	Resolution leaves diffuse or focal parenchymal fibrosis, calcification & irregular ductal dilation.

Pancreatic alterations:
•	Leakage of vasculature to cause edema.
•	Necrosis of regional fat by lipolytic enzymes.
•	An acute inflammatory reaction.
•	Proteolytic destruction of the pancreatic substances.
•	Destruction of blood vessels with subsequent interstitial hemorrhage.	Etiologic factors:
•	80% associated with alcoholism & cholelithiasis.
•	Vascular: shock, atheroembolism, polyarteritis nodosa.
•	Infectious: mumps, coxsackievirus, mycoplasma pneumoniae.

Pathogenesis:
•	Tissue proteolysis, lipolysis & hemorrhage resulting from release of pancreatic enzymes from acinar cells.
•	Local activated trypsin converts other proenzymes to active enzymes & prekallikrien to kallikrein, activating the kinin system & clotting, leading to local inflammation & thrombosis.
•	Pancreatic duct obstruction leads to accumulation of enzyme-rich interstitial fluid & resident tissue leukocytes release cytokines promoting local inflammation & edema.
•	Primary acinar cell injury: caused by alcohol which promotes deposition of protein plugs within pancreatic ducts leading to local obstruction & inflammation.
•	Defective intracellular transport of proenzymes.	Clinical signs:
•	Acute abdomen
•	Constant & intense abdominal pain with upper back radiation
•	Peripheral vascular collapse
•	Shock 
•	Disseminated intravascular coagulation

Causes of death:
•	Shock
•	Acute respiratory distress syndrome
•	Acute renal failure

Laboratory findings:
•	Marked elevation of serum amylase during first 24 hours.
•	Followed within 72-96 hours by a rising serum lipase.
•	Glycosuria in 10% of cases.
•	Hypocalcemia may result from precipitation of calcium soaps in the fat necrosis.

Sequelae:
•	A sterile pancreatic abscess from liquefaction of tissue.
•	Pancreatic pseudocyst from aberrant drainage of pancreatic secretions.
•	Chronic pancreatitis.