Pathology 3 Flashcards
What causes physiological neonatal jaundice?
unconjugated hyperbilirubinemia from increased bilirubin - hemolysis going from low oxygen environment to high
What disorders can cause prolonged jaundice or jaundice after the first week of life?
sepsis neonatal hepatitis biliary atresia choledochal cysts syndromes or diseases that result in paucity of intrahepatic bile ducts
What are extra hepatic biliary tract tumors?
adenocarcinoma of gallbladder
extrahepatic cholangiocarcinoma
What are extrahepatic biliary tract tumors associated with?
cholelithiasis fibrocystic diseases of bile ducts biliary tract inf IBD PSC thorotrast exposure
Where do cholangiocarcinomas develop?
20-25% intrahepatic
50-60% perihilar - fork of hepatic ducts
20-25% distal, extrahepatic
What is periampullary carcinoma?
carcinoma of distal common bile duct, proximal pancreatic carcinoma, and carcinoma of small intestine in ampulla of Vater
obstruction and jaundice at early stage
What are risk factors for the development of pigment stones?
non-western countries
chronic hemolytic anemias and GI dz, CF
What is a possible complication of cholelithiasis?
gallstone ileus - stones at ileocecal valve
What causes cholecystitis?
phospholipases from damaged mucosa hydrolyze other molecules which become toxic to mucosa - detergent action of bile salts further damages wall - released prostaglandins inflame
distension of gallbladder increases pressure and compromises flow since cystic A. is end artery
What can cause acalculous cholecystitis?
ischemic injury of GB - PAN, bile sludge, post-op, postpartum, trauma/burns, sepsis
What histologic findings are present in acute vs. chronic cholecystitis?
acute - neutrophils, ulcers, possible empyema
chronic - lymphocytes, plasma cells, Rokitansky-Aschoff sinuses
Other than secretion of enzmes in inactive form, what other protective mechanisms are in place to protect pancreas from damage?
proenzymes in zymogen granules in acinar cells - enzymes in lysosomes can degrade if normal acinar secretion blocked
acinar cells resistant to many activated enzymes
most enzymes inactive in bicarb rich pancreatic fluid
trypsinogen and trypsin inhibitors (SPINK1) present in ductal secretions
trypsin has self recognition cleavage site in situations of high local concentrations
What three processes cause acute pancreatitis?
ductal obstruction
direct acinar cell injury
defective intracellular transport of enzymes
What is the histology of acute pancreatitis?
fat necrosis w/i and outside pancreas
acute inflammation
parenchymal destruction
fibrinoid necrosis of blood vessel walls - hemorrhage if severe
What are causes of/risk factors for acute pancreatitis?
Alcoholism and biliary tract disease (stones) Infection/inflammatory Ischemia Drugs Metabolic Congenital anomalies - pancreas divisum Trauma Hereditary - PRSS1 (trypsinogen) and SPINK1 (trypsin inhibitor) gene mutations
What are complications that can result from acute pancreatitis?
hypocalcemia and electrolyte imbalance
shock and multiorgan failure
DIC
pancreatic abscess
pancreatic pseudocyst formation - no epithelium, lined by fibrotic tissue
chronic pancreatitis and pancreatic insufficiency
What are complications that can result from chronic pancreatitis?
exocrine pancreatic insufficiency (steatorrhea, malabsorption)
diabetes
pancreatic pseudocyst
pancreatic carcinoma if hereditary causes
What are the different types of pancreatic neoplasias?
pancreatic ductal adenocarcinoma - most common
pancreatic serous neoplasms - benign or malignant
mucinous cystic neoplasms - benign or malignant
intraductal papillary mucinous neoplasms - adenomas or carcinomas growing into lumen
acinar cell carcinoma
neuroendocrine (or endocrine) tumors - low grade functional or non-functional, small and large cell carcinomas
solid psuedopapillary tumor - benign in young women
pancreaticoblastoma - malignant, infants/children
What are risk factors for pancreatic ductal adenocarcinoma development?
smoking - doubles risk
chronic pancreatitis and diabetes
hereditary disorders - Tumor syndromes (Peutz Jegher syndrome, BRCA2 mutation, HNPCC and FAP syndromes), hereditary pancreatitis mutations (PRSS1), CFTR mutation
Where are most pancreatic ductal adenocarcinomas located?
head of pancreas - can lead to biliary obstruction and jaundice
What genetic alterations lead to the dev of pancreatic ductal adenocarcinoma?
telomere shortening K-ras mutations and activation inactivation of p16 SMAD4 tumor suppressor activation p53 tumor suppressor gene activation
What are the features of IPMN?
more common in men
arise in main ducts
lack cell stroma of mucinous neoplasms
can have dysplasia and invasion
