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34 Cards in this Set

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why gets cholelethiasis?
Fat, 40, fertile, frantically fasting, Fe, Family, Faulty fecal flow, inFlammatory bowel, cloFibrate

especially Native americans, African Americans, and those with diabetes, cirrhosis, and crhonic extravascular hemolysis

NOT RELATED TO HYPERCHOLESTEROLEMIA
What are the the types of cholelethiasis stones?

What are more common?
Cholesterol 80%
Black (hemolytic, TPN, high protein diet)
Brown (infection, flukes)
What are the tests to dx cholelethiasis?
U/S >95% (>2mm), CT 74-79%, X-ray, HIDA (ductal), and MRI (incidental)
Other than surgery, what is the treatment option for cholelethiasis?
UCDA (urodiol/ursodeoxycholic acid) - decreases absorption, synthesis, and storage of cholesterol after 6-18 months
How does UCDA (urodiol/ursodeoxycholic acid) work?
decreases absorption, synthesis, and storage of cholesterol after 6-18 months
What is the most common symptomatic disorder of the gallbladder?
chronic cholecystitis (often 90% associated with stones, most NOT associated with bacteria)
What is acaoculous cholecystitis?
in the seriously ill (burns, major trauma, surgery) --> large tense, thickened gallbladder with fluid
What is the cancer of the gallbladder?
porcelain gallbladder resulting from chronically inflamed gallbladder with dystrophic calcification.
What part of the liver does primary biliary cirrhosis effect?
small-medium bile duct destruction associated with disease of altered immunity
Who is affected by primary biliary cirrhosis
75-90% are women
Where is AST from?
mitochondrial enzyme of liver/hepatic cells

elevated more in alcoholism than in viral infection because EtOh is a mitochondrial poison.
Where is ALT from?
cytosol of hepatic cells

It is especially elevated in viral infections
This indicates what condition?
ALT>AST
viral hep
This indicates what condition?
AST>ALT, increased GGT
alcoholic liver
Why is GGT elevated in alcoholic hep?
synthesis induced by alcohol
What cells have GGT and AP?
GGT in liver duct cells

AP in liver bone placenta, and WBC's
What effect will granulomas (focal, benign liver dz) have on LFT's?
increase AP adn GGT slightly

Bilirubin, LDH, and transaminases (AST, ALT) are normal
What effect will focal metastatic liver dz have on LFTs?
LDH, AP, GGT will be slightly increased

AST, ALT, and bili will be normal
<20% CB fraction = >80% unconjugated bilirubin (UCB) means???
extravascular hemolysis (problem with uptake for conjugation)

bilirubin won't go out urine because it is unconjugated but there is a lot of urobilinogen in the urine
mixed (20-50%) CB and UCB means what?
hepatitis

Moderate amount of bilirubin and urobilinogen in the urine
CB >50% means what?
obstructive jaundice so the bilirubin will go out the urine
What LFTs show necrosis numbers/results?
AST and ALT
With what disease are antimitochondrial antibodies present?
primary biliary cirrhosis
With what disease are anti-smooth muscle, anti-liver/kidney microsome, and antinuclear Ab's present?
autoimmune hepatitis (mostly young women)

Special sx: itching, rashes, amenorrhea, and joint pain
With what disease is AFP (alpha-Fetoprotein) and AAT (alpha-antitrypsin) elevated?
hepatocellular Ca (adults) or hepatoblastoma (kids)
What are the histological findings of acute hepatitis?
hypertrophy/hyperplasia of Kupffer's cells, partal tract inflammation --> lymphocytic infiltrate, Councilman bodies (apoptosis) in focal ballooning
What are the histologic and serologic findings of chronic hepatitis B?
only 10% progress to chronic in adults. Most cases 90% are children HBsAg and ground glass hepatocytes with mild portal triaditis
Which types of hepatitis have carriers?
B and C

NOT A
What are the Ig findings in symptomatic and previous infection Hep A?
Symptomatic = + IgM
Previous infection = - IgM, + IgG
What is the pathologic progression of Hep B?
replication is not cytotoxic --> CD8+ release IFN gamma and TNF (host immunity causes damage) --> cirrhosis & fibrosis --> hepatocellular Ca
hepatocellular Ca is associated with what viral infection?
Hepatitis B

replication doesn't cause damage --> CD8+, release TNF and IFN gamma --> fibrosis, cirrhosis --> hepatocellular Ca
HBeAg indicates what?
highly infective state early in the disease. Usually the begining of presentating symptoms. There are only anti-HBc IgM at this point
What does HBsAg presence indicate?
first to appear and last to disappear
What benefit does anti-HBc-IgM provide? When is it present?
nonprotective
arrives shortly after HBsAg and persists when all antigens are gone, but Ab levels are not detectable.

changes to anti-HBc-IgG after 3-6 months