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Pathology Exam 2-5

Terms in this set (71)

hepatocytes
the liver is composed of _____ arranged in flat plates supported by a reticulin framework
hepatic artery and portal vein
blood is supplied to the liver by the ______ and _______
hepatic vein
blood drains from the liver via the _____
zone 3 (near central vein)
hepatocytes in this area are supplied by blood that is relatively depleted of oxygen;
most vulnerable to damage by hypoxia or poor perfusion
vulnerable to certain toxins (e.g. acetaminophen)
zone 1 (near portal tracts)
well supplied with blood, resist damage by poor perfusion
not damaged by certain agents, b/c lack enzymes needed for conversion to toxic intermediates
cholestasis and obstructive jaundice
damage or blockage to either intrahepatic or extrahepatic bile ducts
acute hepatitis
disease causing necrosis of liver cells with inflammation
viral or toxic mediated
chronic hepatitis
continued inflammation for over 6 months
viral or immune mediated
cirrhosis
end-point of long-standing damage and resulting fibrosis
bilirubin
derived from breakdown of hemoglobin
unconjugated bilirubin
bound to albumin --> cannot be excreted in urine --> circulates to the liver --> conjugated to glucouronic acid
lipid soluble
kernicterus
in neonates, unconjugated bilirubin can enter the brain and cause damage
conjugated bilirubin
water soluble
excreted in bile--> enters gut where bacteria split it into urobilinogen --> most is excreted in feces, 20% is reabsorbed in the blood and is re-excreted by the liver (enterohepatic circulation)
small amounts into urine
jaundice
yellow discoloration of the sclera and skin
caused by abnormalities in bilirubin metabolism and excretion
unconjugated hyperbilirubinemia
excess unconjugated bilirubin in the blood - exceeds the livers capacity to conjugate and secrete
gilbert syndrome
inherited defect in hepatic conjugation of bilirubin
autosomal dominant
liver is normal
decreased activity of glucuronyl transferase activity
neonatal jaundice
low activity of glucuronyl transferase in the 1st 2 weeks of life
crigler-najjar syndrome
hereditary lack of glucuronyl transferase activity (Type 1)
hereditary decreased in function of glucuronyl transferase activity (Type 2)
autosomal recessive
80-90%
_____% of hepatic function must be lost before acute liver failure ensues
non-alcoholic fatty liver disease (NAFLD)
a complication of metabolic syndrome, and is increasingly recognized cause of chronic liver disease
cholestasis
characterized by:
conjugated hyperbilirubinemia
increased serum alkaline phosphatase (enzyme normally located on the cell membrane of bile canaliculi)
intrahepatic cholestasis
disease affecting bile secretion in the liver:
abnormalities of liver cells and bile canaliculi
disease of intrahepatic bile ducts
extrahepatic cholestasis
blockage of the main bile ducts outside the liver
right sided heart failure
causes passive congestion of the liver
back-pressure in systemic venous system
nutmeg liver or chronic passive congestion
centrilobular hemorrhagic necrosis
portal hypertension
continued elevation in portal venous pressure
splenomegaly and ascites
back-flow in portal vascular bed leads to ____ and _____
budd-chiari syndrome
occlusion of the main hepatic vein
pts develop severe acute disease, with massive vascular congestion causing acute portal hypertension and jaundice
liver enlargement is painful with rapid development of ascites
hepatitis
inflammatory disease of the liver
hepatitis A
RNA enterovirus
transmitted by feco-oral route
small epidemics occur in institutions, water contamination, raw fish
incubation period 1-4 weeks
infection gives immunity
hepatitis E
similar to HAV(but more severe)
RNA calcivirus
transmitted by feco-oral route
incubation period of 1 month
can result in acute fulminant hepatitis in pregnant women
immunity not lifelong
hepatitis B
DNA virus of hepadna group
transmitted in blood, semen, and saliva
vertical transmission
acute self-limited hepatitis
fulminant acute hepatitis
chronic hepatitis
asymptomatic chronic infection
4 clinical patterns of hepatitis B infection
hepatocellular carcinoma
patients with chronic hepatitis B are at risk for _____
HBsAg
hepatitis B surface protein
peaks before clinical disease
HBeAg
hepatitis B core component, associated with replication
HBV DNA
detected by PCR to measure viral replication (hepatitis B)
transaminase
______ levels rise just before symptoms in hepatitis B infection
3-6 months
incubation time for acute hepatits B
hepatitis D
can only cause infection in the presence of HBV
same transmission as HBV
60% of pts develop cirrhosis
hepatitis C
RNA flavivirus
same transmission as HBV
incubation period of 2 months
most have asymptomatic acute infection
some will recover with complete elimination of virue
others will have persistent abnormal liver function tests for over a year
chronic hepatitis
inflammation of the liver persisting for more than 6 months
intrinsic hepatotoxins
dose dependent, predictable, high incidence of toxic damage to liver
idiosyncratic hepatotoxins
cause liver disease in a small percentage of exposed individuals, b/c hypersensitivity or abnormal drug metabolism
alcohol
the most common cause of chronic liver disease in western countries
fatty liver (reversible)
acute hepatitis (reversible)
cirrhosis (irreversible)
alcohol causes these 3 liver diseases
cirrhosis of the liver
normal architecture is replaced by nodules of regenerated liver cells separated by bands of collagenous fibrosis
irreversible form of chronic liver disease
end stage of many processes
long-standing destruction of liver cells
chronic inflammation that stimulates fibrosis
regeneration of hepatocytes to cause nodules
three key characteristics of cirrhosis
hepatic adenoma
neoplasm
well-circumscribed nodule up to 20cm
women in the reproductive period
predisposed by estrogen-containing oral contraceptives
histologically resemble normal liver but WITHOUT PORTAL AREAS
can rupture and cause intra-abdominal bleeding
focal nodular hyperplasia
hyperplasia of hepatocytes
often has a central scar
detected incidentally
HAS PORTAL AREAS
bile duct adenoma
very common
thought to be hamartomas
small white nodules
subcapsular
composed of abnormal bile ducts in a collagenous stroma
may be mistaken for metastatic tumor deposits
hemangioma
common
subcapsular
dark, almost black
histologically composed of abnormal vascular channels
hepatocellular carcinoma
common in asia and africa
incidence is increasing in US
main etiologic agents are hepatitis B and C, alcoholic cirrhosis
may be unifocal or multifocal
tend to invade blood vessels
cholangiocarcinoma
adenocarcinoma arising from the intrahepatic bile duct epithelium
predisposed to by chronic inflammatory diseases of the intrahepatic biliary tree
very poor prognosis with survival rates of 15% at 2 years
cholelithiasis (gallstones)
over 95% of biliary tract disease is attributable to _____
calcium bilirubinate
pigment stones are mostly composed of _____
acute cholecystitis
can be caused by gallstones
gallbladder is enlarged, red and edematou
histologically, acute inflammation with epithelial erosion and/or ulceration
gallbladder carcinoma
usually associated with stones and chronic chloecystitis
mostly seen in women >70 years
most tumors arise in the fundus and are adenocarcinomas
prognosis is poor
acute (exocrine) pancreatitis
results autodigestion of the pancreatic substance by inappropriately activated enzymes
severe acute inflammation and necrosis leads to liberation of digestive enzymes --> enzyme-mediated local tissue necrosis, particularly fat necrosis
a complication is the development of a pseudocyst
amylase and lipase
laboratory findings of a patient with acute pancreatitis would show an increase in serum _____ and ______
chronic pancreatitis
inflammation of the pancreas with irreversible destruction of exocrine parenchyma, fibrosis, and, in the late stages, the destruction of endocrine parenchyma
irreversible damage
the distinction between chronic and acute pancreatitis is the ______
chronic alcohol abuse
chronic pancreatitis is mainly caused by ______
pancreatic pseudocyst
localized collections of necrotic-hemorrhagic material rich in pancreatic enzymes
arise after an episode of acute pancreatitis, often in the setting of chronic alcoholic pancreatitis
serous cystadenoma
women>men
oresent in 70's with non-specific pain
usually benign
surgery is curative
mucinous cystic neoplasm
~95% arise in women
arise in the body or tail of the pancreas and present as painless, slow-growing masses
the cysts are larger than in serous cystadenomas
cysts are filled with thick, tenacious mucin and lined with a columnar mucin-producing epithelium with an associated dense stroma similar to ovarian stroma
1/3rd harbor an invasive adenocarcinoma
intraductal papillary mucinous neoplasms (IPMNs)
men>women
involve the head of the pancreas more than the tail
10-20% are multifocal
lack the dense "ovarian" stroma seen in mucinous cystic neoplasms
involve a larger pancreatic duct
cigarette smoking
strongest environmental influence on pancreatic carcinoma
courvoisier's sign
obstructive jaundice with painless palpable dilation of the gallbladder (associated with pancreatic carcinoma)
trousseau's syndrome
migratory thrombophlebitis, in which there is development of multiple thrombi in superficial and deep leg veins (associated with pancreatic carcinoma)
chronic cholecystitis
thickened gallbladder wall
chronic inflammation
choledocholithiasis
stone in bile ducts
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