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64 Cards in this Set

  • Front
  • Back
Most common congenital anomaly of the pancreas
Pancreas Divisum
Anomaly caused by a failure of the fetal duct systems of the ventral and dorsal pancreatic primordia to fuse? Where does the bulk of the pancreas drain
Pancreas Divisum:
It drains through a dorsal duct and the small calliber papilla
In pancreas divisum, what happens to the main pancreatic duct
It becomes short and drains only a small portion of the pancreas
Most common location of ectopic pancreas
Submucosa of the stomach and duodenum
Band-like ring ring of normal pancreatic tissue that completely encircles what portion of the duodenum? What may this cause?
Annular pancreas:
Around the 2nd part of the duodenum
Duodenal obstruction
Trypsin inhibitors are what type of protease inhibitors
Several mechanisms of protection against self-digestion in the pancreas
Synthesized as Inactive proenzymes
Enzymes are within membrane bound zymogen-granules within the acinar cells.
Proenzymes must be activated by trypsin
Trypsin inhibitors are present within acinar and ductal secretions
Acinar cells are resistant to enzyme action
Activates trypsinogen into trypsin
Duodenal enteropeptidase(enterokinase)
The pancreas arises from the fusion of dorsal and ventral outpouchings of? The majority of the pancreas is derived from?
the foregut
the dorsal primordium of the foregut
Gives rise to the posterior/inferior part of the head of the pancreas
Ventral primordium of the foregut
Type of exocrine cell of the pancreas
Account for approximately 80% of cases in acute pancreatitis
Alcohol and biliary disease
Reversible pancreatic parenchymal injury associated with inflammation
Acute pancreatitis
Most cases of idiopathic pancreatitis are caused by germline mutations of
Cationic trypsinogen gene:
This mutation abrogates a critical fail-safe mechanism by altering a site on the cationic trypsinogen molecule that is essential for the cleavage of trypsin by trypsin itself. When this site is mutated, trypsin becomes resistant to cleavage by another trypsin molecule.
Viral infection that may cause acute pancreatitis? Parasite?
Ascaris lumbricoides
The serine protease inhibitor Kasal type 1 gene encodes for?
A trypsin inhibitor
Fat necrosis in pancreatitis is due to What appearance do the released fatty acids give on microscopic examination
activation of lipase
They combine with Ca2+ to form insoluble salts that impart a blue appearance
Pancreatitis with mild inflammation, interstitial edema, and focal areas of fat necrosis
Acute interstitial pancreatitis
In acute necrotizing pancreatitis, where may foci of fat be found
within the pancreas, but also on the omentum and mesentery of bowel, and even outside the abd cavity, such as in subcutaneous fat
Extensive parenchymal necrosis with dramatic hemorrhage within the gland
Hemorrhagic pancreatitis
Pancreatitis with microvascular edema, interstitial inflammation, necrosis of fat, proteolytic destruction of pancreatic parenchyma, and destruction of blood vessels w/ hemorrhage
Acute necrotizing pancreatitis
What pancreatic cells are destroyed in acute necrotizing pancreatitis
acinar, ductal, and islets of Langerhans
the inappropriate activation of what, is an important triggering event in acute pancreatitis
Besides the digestive enzymes, what else does trypsin activate?
Converts prekalikrein to kalikrein, thus activating kinin: inflammation and vasodilation/increased vascular permeability
Activates Hageman factor (XII):
Clotting factor
Mechanism of injury in acute pancreatitis caused by certain viruses, drugs, trauma, or ischemia.
Primary acinar cell injury.
Initiates local inflammation and promotes the development of interstitial edema via leaky microvasculature
Injured tissues periacinar fibroblasts, and leukocytes release proinflammatory factors such as IL-1, IL-6, TNF, PAF, and substance P.
At what time is pancreatic amylase elevated during pancreatitis? Lipase?
24 hrs
72-96 hrs
How does hypocalcemia occur in pancreatitis?
Due to the amount of fatty acids of necrotic fat cells combining with Ca2+ to form insoluble salts.
This is a poor prognostic sign
In half of pts with acute necrotizing pancreatitis, the necrotic debris become infected with?
gram- organisms
How defective transport of digestive enzymes lead to acute pancreatitis?
Pancreatic proenzymes are delivered to the intracellular compartmentcontaing lysosomal hydrolases, which activate the proenzymes, leading to injury.
What primarily causes activated enzymes?
acinar cell injury from:
Duct obstruction
Primary injury (virus, drugs,trauma)
Defective intracellular transport
How does duct obstruction lead to acute pancreatitis?
Cholelithiasis causes ampulla obstruction which increases intrapancreatic ductal pressure and lead to accumulation of enzyme rich fluid which cannot be entirely inactivated by anti-trypsin. This leads to injury, edema, impaired blood flow, and ischemia, which cause acinar injury, and activate enzymes.
How does chronic alcohol ingestion cause pancreatitis?
1. secretion of protein-rich fluid that obstructs small pancreatic ducts.
2. Transiently increases pancreatic exocrine secretion and contraction of the sphincter of oddi
3. Direct toxic affect on acinar cells.
many of the systemic features of severe acute pancreatitis can be attributed to?
Release of toxic enzymes, cytokines, and other mediators that activate systemic inflammatory response, resulting in leukocytosis, hemolysis, DIC, acute respiratory sydrome, and shock.
Inflammation of the pancreas with irreversible destruction of the exocrine parenchyma, fibrosis, and in late stages, the endocrine parenchyma
chronic pancreatitis
Most common cause of chronic pancreatitis
Mutations in the CFTR gene often lead to?
Chronic pancreatitis:
Due to decreased bicarb secretion, which promotes protein plugging.
Events that cause the development of chronic pancreatitis
1. Ductal obstruction by concretions:
Increase in protein concentrations of the pancreatic juice. Prominent in chronic alcoholics.
2. Toxic effects on acinar cells
3. Oxidative stress
Promote the activation of periacinar myofibroblasts, resulting in deposition of collagen and fibrosis

This predominates in chronic pancreatitis
Characterized by parenchymal fibrosis, reduced size and number of acinar cells, variable dilation of the pancreatic ducts, and relative sparing of the islets of langerhans
chronic pancreatitis
Loss of what cells is a constant feature of chronic pancreatitis
acinar cells
Presentation of ductal epithelium in chronic pancreatitis
may be hyperplastic, atrophied, or may show squamous metaplasia
Chronic pancreatitis characterized by a duct-centric mixed inflammatory cell infiltrate, venulitis, and increased numbers of IgG4-producing plasma cells. Txmt?
Lymphoplasmocytic sclerosing pancreatitis
In chronic pancreatitis, development of what disease may be associated with destruction of the islets of langerhans
Syndrome of vascular neoplasms are found in the retina and cerebellum or brain stem in association with congenital cysts in the pancreas, liver, and kidneys
von Hippel-Lindau disease
Believed to result from anamolous development of the pancreatic ducts
Congenital cysts
Congenital cysts are usually lined by?
uniform cuboidal epithelium
Localized collections of necrotic-hemorrhagic material rich in pancreatic enzymes. When do they usually occur?
Psuedocyts, because they have no epithelial lining
Occur during an episode of acute pancreatitis in the setting of chronic pancreatitis.
Most common type of cyst in the pancreas
Pseudocysts are formed by the walling off of?
areas of peripancreatic hemorrhagic fat necrosis with fibrous tissue
Manysurgically resected mucinous cystic neoplasms harbor an associated ?
invasive adenocarcinoma
Benign cystic neoplasms composed of glycogen rich cuboidal cells surrounding small cysts containing clear, thin, fluid
serous cystadenomas
Mucinous cystic neoplasms usually arise in what area of the pancreas? Lined by what type of epithelium?
Body or tail
Columnar mucin producing epi with associated dense stroma similar to ovarian stroma.
Mucin producing intraductal neoplasms? How do they differ from mucinous cystic neoplasms?
Intraductal papillary mucinous neoplasms (IPMNs):
Occur in the head of the pancreas, rather than the body or tail.
Lack the dense "ovarian" stroma
Individuals present with metastatic fat necrosis caused by release of lipase into the systemic circulation.
Acinar cell carcinomas:
Prominent acinar cell differentiation, formation of zymogen granules, and production of exocrine enzymes.
Precursor lesions to pancreatic carcinoma. Show dramatic shortening of?
pancreatic intraepithelial neoplasias
Most frequently altered oncogene in pancreatic CA
Impair GTP activity of the K-ras protein, causing it to be constitutively active.
Most frequently inactivated tumor suppressor gene in pancreatic CA
Strongest environmental influence in pancreatic cancer
cigarette smoking
Most pancreatic CA arise in what part of the pancreas? What may this cause?
Causes obstruction of the common bile duct leading to marked dilation of the biliary tree and jaundice.
Ampulla of vater
Joining of the common bile duct and pancreatic duct just prior to emptying in the papilla of vater
Carcinomas in this part of the pancreas are often silent and therefore very disseminated by the time they are discovered
Body and tail
Two features characteristic of pancreatic ca
highly invasive
elicits an intense non-neiplastic host rxn composed of fibroblasts, lymphocytes, and extracellular matrix (desmplastic response).
The vast majority of pancreatic carcinomas are?
ductal adenocarcinomas that form ductal glands and secrete mucin