Pathology Liver/biliary

Front 1

C. sinensis

Back 1

liver fluke, risk factor for biliary tract cancer

Front 2

Cryptosporidiosis

Back 2

imunocompromised pts, can occasionally occur in biliary tract and elsewhere

Front 3

Cytomegalovirus

Back 3

immunocompromised pts, hepatitis like picture w/o biliary tract disease

Front 4

Entameoba Histolytica

Back 4

present w/ diarrhea + blood +mucus, and then now cysts

Front 5

cholithiasis, risk factor for what microbe?

Back 5

E. Coli. reaches liver by ascending in biliary tree.
+/- cysts in liver

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so will present like patient w/ gallstones, and then see cystic lesions. what microbe caused cysts? E.coli

Front 6

cholesterol gallstones

Back 6

- yellow, but can get varied color appearance b/c of bile pigment trapping. but still dont' look like hemolytic anemia stones which are uniformly dark.
- risk factors:
- native american
- female
-fat
- older age

Front 7

Pigmented gallstones

Back 7

- hemolytic anemia
- Crohn's disease (ileal dysfunction)
-

Front 8

jaundice pruritis, ulcerative colitis. associated with?

Back 8

primary sclerosing cholangitis

Front 9

Wilson's disease.

Back 9

- AR
- accumulation of toxic levels of copper, mostly in liver, brain, eye
- normally ~50% ingested Cu absorbed in stomach/duodenum,
- transported to liver complexed to albumin
- taken up by hepatocytes and made into ceruloplasmin, Cu containing protein, which is secreted into plasma.
- so ~90-95% bound as ceruloplasmin in plasma
- ATP&B gene on chromosome 13
- codes Cu transporter ATPase on hepatocyte canalicular membrane
- mutations --> defective biliary excretion of Cu and Cu accumulation in liver
- exceeds binding capacity and then toxic liver injury via Cu catalyzed formation of reactive O2 species
- eventualy decreased Ceruloplasmin levels w/ liver injury b/c made in liver, and increased free Cu (serum Cu levels) but decreased TOTAL Cu levels (b/c most existed as bound to Ceruloplasmin remember?)
- usual liver injuries, fatty change, hepatitis, nerosis
- Kayser-Fleischer rings (eye, limbus of cornea)
- Hepatolenticular degeneration (basal ganglia) --> parkinson's type: corea, rigidity, dimentia?
- usually manifests b/f 6 yrs old
- also increased urinary excretion of Cu

Front 10

if former alcoholic, stopped drinking 10 years ago, will you see fatty change in liver?

Back 10

no. reversible thing. would have gone away if not drinking currently

Front 11

pathogenesis of yellow gallstones?

Back 11

-cholesterol
- usually only soluble w/ bile's help
- when too much cholesterol, solubilizing capacity of bile exceeded so cholesterol makes monohydrate crystals and entrapped in gallbladder, aggregate into stones
- pure cholesterol stones are radiolucent, but usually have calcium carbonate so radio-opaque
- increased risk for carcinoma of gallbladder

Front 12

pathogenesis of pigmented gallstones?

Back 12

-mix of insoluble calcium salts of unconjugated bilirubin and inorganic calcium salts
- infection of gallbladder causes release of microbial Beta-glucuronidases which hydrolyze bilirubin glucuronides (conjugated), so more unconjugated.
- infections from E. coli, Ascaris lumbricoides, Opisthorchis sinensis (liver fluke)
- hemlytic anemia too increases unconjugated bilirubin.
- increased risk for carcinoma of gallbladder

Front 13

primary sclerosing cholangitis?

Back 13

inflammation and obliterative fibrosis of intrahepatic and extrahepatic bile ducts w/ dilation of preserved segments = BEADING
- 70% coexist w/ inflamm bowel disease esp Chronic Ulcerative Colitis
- 30-50 yrs old
- lymphocytic infiltrate hence cholangITIS
-concentric PERIDUCTAL FIBROSIS = ONION SKIN
-liver becomes cholestatic
- DON'T REALLY SEE ASSOCIATED AUTOANTIBODIES
-cholangiocarcinoma risk
-treat w/ liver transplantation

Front 14

Primary Biliary Cirrhosis

Back 14

progressive often fatal cholestatic liver disease
- destruction of medium sized INTRAHEPATIC bile ducts, portal inflamm, scarring
- SEE expanded portal tract b/c of lymphocytic and plasma cell infiltrate
GRANULOMATOUS REACTION
-middle aged women, onset anywhere from 20-80 yrs
- xanthomas b/c cholesterol retention
- insidious onset
- eventual chronic liver disease (portal HTN etc)
- hyperbilirubinemia late development (b/c still have many functioning ducts)
- ANTIMITOCHONDRIAL ANTIBODIES
-can be associated w/ other AI things (Sjogren, Raynaud's)
- steathorrea, malabsorption of course
-usually die b/c liver failure via cirrhosis

Front 15

piecemeal hepatocellular necrosis at interface of portal tracts (limiting plate?)

Back 15

chronic hepatitis, like hep C

Front 16

risk factors for?
1. ulcerative cholitis
2. C. Sinensis
3. gallstones

Back 16

1. primary sclerosing cholangitis (cholangiocarcinoma)
2. Biliary tract cancer
3. gall bladder adenocarcinoma

Front 17

oral contraceptives and anabolic steroids effect on liver?

Back 17

cause intrahepatic cholestatsis and predispose to hepatic adenoma, which has a bad tendency to rupture, causing rapid dangerous fall in blood pressure; can be fatal. may not have signs of the liver cell adenoma. can just rupture.

Front 18

1. aflatoxin.
2. oysters.
3. aspirin

Back 18

1. from aspergillus flavus, which grows on moldy peanuts. carcinogenic = hepatic carcinoma
2. oysters w/ HAV from sea water that's contaminated w/ sewage (fecal-oral)
3. Reye syndrome in kids w/ microvesicular steatosis

Front 19

transient jaundice under stress/fasting w/ normal enzyme levels. cause?

Back 19

Gilbert's syndrome. don't treat. goes away in like a day or two.

Front 20

alcoholic hepatitis vs. cirrhosis?

Back 20

cirrhosis has fibrosis and lobular disruption w/ portal HTN tendency, etc.
alcoholic hepatitis is like any hepatitis: has necrosis and inflamm infiltrate (PMN usually) around necrosis.

Front 21

Reye syndrome

Back 21

aspirin in kids. caused by mitochondrial dysfunction affecting liver, brain, other orgs.
- death from hepatic failure can happen
- microvesicular steatosis in hepatocytes
- so can die of cerebral edema too.

Front 22

male w/ dyspnea due to idiopathic pulmonary fibrosis. increased liver enzymes AST ALT. what's going on?

Back 22

idiopathic pulmonary fibrosis led to pulmonary HTN which caused cor pulmonale. this leads to passive backward congestion due to failure and passive liver congestion thus. if this happens in liver, necrosis seen, first in centrilobular areas around central vein (zone 3, least oxygenated, most susceptible)

Front 23

bronze diabetes. associated with?

Back 23

hereditary hemachromatosis.

Front 24

mallory bodies

Back 24

seen in hepatitis. like alcoholic hepatitis. not specific for this though.

Front 25

asterexis in liver problems. why?

Back 25

b/c ammonia metabolism interrupted (urea cycle interrupted in hepatocytes) so build up of ammonia, encephalopathy.
-flapping tremor of hand

Front 26

what lesion are these environmental factors associated with in liver:
1. oral contraceptives
2. aflatoxin from aspergillus flavus
3. vinyl chloride exposure
4. chronic hep B infection

Back 26

1. hepatic adenoma (also anabolic steroids, have tendency to rupture even though benign so dangerous)
2. hepatocellular adenoma
3. angiosarcoma
4. hepatocellular carcinoma

Front 27

most common form of liver cancer?
hepatocellular carcinoma in Western world most often associated with?

Back 27

- metastasis
- cirrhosis (remember all those charts where chronic ends in either cirrhosis or hepatocellular carcinoma?)

Front 28

the most common cause of cryptogenic cirrhosis is?

Back 28

nonalcoholic fatty liver disease and steatohepatitis