pathology of the exocrine pancreas/Bernardino
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| the exocrine portion of the pancreas is what percent of it? | about 85%
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| this is used to describe the part of the pancreas composed of acinal cellst hat produce enzymes necessary for digestion and the series of ducts and ductules that convey secretions into the duodenum | exocrine pancreas
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| list some mechanisms to prevent self digestion of the pancreatic tissue | enzymes made as inactive proenzymes, enzymes sequestered in membrane bound zymogen granules, actiation of proenzymes requires activation of tripsinogen by enterokinase, trypsin inhiibtors are npresent within acinar and ductal secretions,
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| are acinar cells remarkably resistant to the action of trypsin, chymotrypsin, and phospholipase A2? | yes
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| list some congenital anomalies of the pancreas | agenesis, annular pancreas, ectopic pancreas, pancreas divisum
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| in this congenital anomaly of the pancreas, the pancreas fails to form | agenesis
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| in this congenital anomaly of the pancreas, there is a band like ring of normal pancreatic tissue that encircles the duodenum and can result in duodenal obstruction | annular pancreas
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| in this congenital anomaly of the pancreas, there is embryologic rests located in the submucosa of the gallbladder, and may cause pain from localized infection | ectopic pancreas
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| this type of congenital anomaly is the most common with the pancreas, and results from a failure of the dorsal and ventral pancreatic ducts to fuse. | pancreas divisum
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| what is a consequence of pancreas divisum? | pancreatitis, because the ducts don't fuse, so they can become blocked.
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| this symptom describnes inflammation in the pancreas associated with injury to the exocrine pancreas parenchyma | pancreatitis
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| what are some clinical symptoms of pancreatitis? | they can range in severity from mild disease to a life threatening situation: acute or chronic pancreatitis
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| this is reversible pancreateic parenchymal injury associated with inflammation. | acute pancreatitis
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| list some major causes of acute pancreatitis | chronic alcohol abuse, gallstones
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| what is the pathophysiology of alcoholand gallstones causing acute pancreatitis? | alcohol causes secretion of protein rich fluid, causing ductal obstruction. there is increased pressure from ductal edema, leading to fat digestion.
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| list some mechanisms for the pathogenesis of acute pancreatitis... | duct obstruction, acute cell injury, defective intracellular transport.
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| the changes in morphology of acute pancreatitis are due to what? | autodigestion of the pancreatic substances by inappropriately activated pancreatic enzymes.
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| list symptoms of interstitial pancreatitis (mild) | mild inflammation, interstitial edema, focal areas of fat necrosis.
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| list some symptoms of necrotizing pancreatitis | parenchymal necrosis
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| list symptoms of hemorrhagic pancreatitits (most severe) | vascular injury accompanied by parenchymal necrosis leading to hemorrhage within the glands.
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| list some general clinical features of acute pancreatitis | intense, constant abdominal pain, referred pain to the upper back and left shoulder, anorexia, nausea, vomitting, fever.
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| can acute pancreatitis be a medical emergency? why? | yes. due to severe systemic inflammatory activation of leukocytes, hemolysis, DIC, fluid sequestration, ARDS, diffuse fat necrosis, shock
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| list some lab findings in acute pancreatitis | elevated serum amylase within first twenty four hours, rising serum lipase level: 72-96 hours, glycosuria, hypocalcemia-precipitates of calcium soap in necrotic fat
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| list some ways to manage acute pancreatitis | NPO, IV fluids, analgesia.
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| what are some complications of acute pancreatitis | death from shock, ARDS and acute renal failure, sterile pancreatic abscess, infection by gram negative bacteria
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| this is a physical sign of acute pancreatitis where you have echymosis around the umbullical area following hematoma in acute pancreatitis | cullen sign
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| this is a physical sign of acute pancreatitis where you have echymosis in teh skin overlying the flanks | grey-turner
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| this is a symptom of irreversible destruciton of the pancreas, fibrosis, in late stages, you can even have destruction of the endocrine parenchyma. | chronic pancreatitis
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| what is the pathogenesisi of chronic pancreatitis? | repeated episodes of acute pancreatitis that over time leads to loss of pancreatic parenchyma and fibrosis
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| what are some clinical features of acute pancreatitis? | repeated attacks of moerately severe abdominal pain or mild pain, persistent abdominal and back pain, may be silent until pancreatic insufficiency and diabetes develop. attacks may be precipitated by alcohol abuse, overeating, or drugs
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| what disease develops over time from chronic pancreatitis? | diabetes
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| list some histologic findings of acute pancreatitis | parenchymal fibrosis, reduced number and size of acinar cells, chronic inflammatory infiltrate, dilated ducts with inspissated eosinophilic ductal secretions
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| this is a disease of autoimmune pancreatitis, distinct from chronic pancreatitis where you have duct centric mixed inflammatory cell infiltrate, venulitis, and increased numeber of IgG4-producing plasma cells. | lymphoplasmocytic sclerosing pancreatitis
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| what is the clinical significance of lymphoplasmocytic sclerosing pancreatitis? | it can clinically mimic pancreatic cancer, and responds to steroid therapy
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| what is a complication from chronic pancreatitis? | pancreatic calcifications may obstruct the pancreatic duct, fat malabsorption, pancreatic pseudocyst, diabetes, pain from peripheral fibrosis, stones in pancreatic duct.
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| in 10-20% of the population, individuals have no known associated process and episodes of pancreatitis begin in childhood. | hereditary pancreatitis
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| hereditary pancreatitis develops from mutation in which genes? | cationic trypsinogen gene PRSS1: trypsin is continually produced. can also have inactivatin gmutation of serine protease inhibitar (SPINK I), which keeps trypsin active
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| what is the mediator in acute pancreatitis? | you have activation of proteolytic enzymes leading to inflammatory and vascular injury event. i
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| what are the mediators in chronic pancreatitis? | aside from activation of proteolytic enzymes, you have things that produce growth factors beta and collagen, which stimulate pancreatic fibrosis and eventually you lose your acinar cells.
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| this is cancer of the ductal system of the pancreas and is an infiltrating ductal adenocarcinoma | pancreatic carcinoma
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| pancreatic carcinoma is most common in which race? | African Americans
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| what is the survival rate of pancreatic cancer? | five year survival rate is only five percent. very low.
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| what are some risk factors for pancreatic carcinoma? | cigarette smoking, fat rich diet, chronic pancreatitis, diabetes mellitis.
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| this is a precursor lesion to pancreatic cancer | pancreatic intraepithelial neoplasia (PanIn)
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| where are PanINs found? | pancreatic parenchyma adjacent to infiltrating carcinomas.
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| what changes in terms of mutations can help in the development of pancreatic cancer? | telomere shortening, mutation in KRAS, inactivation of p16, inactivation of p63, SMAD4, BRCA2
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| what is the morphology of pancreatic carcinoma? | majority are a ductal carcinoma. there are two characteristic features: highly invasive, desmoplastic response
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| most of the pancreatic carcinomas occur in which part of the pancreas? | the head
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| can pancreatic carcinoma be diagnosed right after onset? | no. carcinoma of the pancreas remain silent until they invade into adjacent structures.
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| give some signs and symptoms of pancreatic carcinoma | pain, obstructive jaundice (head of pancreas), weight loss, anorexia, generalized malaise and wekness.
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| this is a sign of pancreatic carcinoma where you have migratory thrombophlebnitis manifesting as tender erythematous rash, due to elaboration of platelet aggregating factors and procoagulants from the carcinoma or its necrotic products. | Trosseau sign
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| this is the most common cystic lesion of the pancreas. there is no epithelial lining, formed by walling off areas of peripancreatic hemorrhage fat necrosis with fibrous tissue. made of central necrotic hemorrhagic material rich in amylase and lipase. | pseudycyst. they usually arise after an episode of acute pancreatitis, often in the setting of chronic alcoholic pancreatitis.
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| this is a benign neoplasm composed of numerous small cysts lined by uniform glycogen rich cuboidal epithelium that produce a watery fluid similar to serum. associated with VHL disease. good prognosis, minimal risk of malignant transformation. | serous cystadenoma
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| this is a cystic neoplasm lined by columnar mucin producing epithelium supported by ovarian type stroma. no communication with the pancreatic duct system. mostly in body and tail of pancreas. painless slow growing masses. good prognosis if no invasion | mucinous cystic neoplasm
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| this arise sin the main pancreatic duct or its major branches; no spindle cell type stroma. arise more frequently in men. involve pancreatic head than tail. invasive neoplasms are staged as ductal adenocarcinoma. | intraductal papillary mucinous neoplasm
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| this is an indolent neoplasm with large, well circumscribed with solid and cystic components. there is a hemorrhagic cystic mass, neoplastic cells can grow in solid sheets or as papillary projections. mainly in young women, no preferred location on pancre | solid pseudopapillary neoplasm
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| solid pseudopapillary neoplasm is due to mutations in what? | Beta-cantenin
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| these are cysts associated with solid neoplasms such as: cystic endocrine neoplasm, ductal adenocarcinoma with cystic degeneration, acinar cell cystadenocarcinoma | degenerative cysts.
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