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Flashcards in hepatobil: 3/6 Deck (108)
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1

Histological features of cirrhosis

-Portal bridging fibrosis and nodular hepatocyte
regeneration.

2

Fetor hepaticus
-what is it?
-what disease is it found in?

-breath smells musty.
-cirrhosis. Due to hepatocyte failure.

3

Inc or dec estrogen in cirrhosis?

increased estrogen
-liver plays role in removing estrogen.

4

Name some sxs of inc. estrogen in cirrhosis

-spider nevi
-gynecomstia
-testicular atophy
-palmar erythema

5

How does cirrhosis cause anemia?

-Cytopenias along with the splenomegaly suggest hypersplenism as a cause for this patient’s anemia, leukopenia, and thrombocytopenia.
-The circulating blood cells are sequestered within the large spleen.
-One of the most common causes is congestive splenomegaly from portal hypertension resulting from cirrhosis.

6

Cirrhosis
-is PTT, PTT, or bleeding time changed?

-PT time is increased.
-factor 7 = shortest half life of pro-coag factors, its made in the liver.

7

Is ALT or AST specific for liver?

ALT
-L for Liver.

8

GGT
-where is it found?
-what causes increase?

-SER of hepatocytes
-P450 induction b/c leads to SER hyperplasia.
*ie. chronic alcoholism.

9

Reye syndrome
-Sxs
-mechanism
-associated w/which bugs most commonly?

-hepatoencephalopathy. mitochondrial abnormalities, fatty
liver (microvesicular fatty change), hypoglycemia, vomiting, hepatomegaly, coma.

-aspirin metabolites dec. β-oxidation by reversible inhibition of mitochondrial enzyme.

-VZV and influenza B.
*okay to give kawasaki disease kids aspirin!

10

alcoholic hepatitis
-mechanism of damage to hepatocytes?
-is there any WBC infiltration?
-intracytoplasmic findings?

-ethanol does direct chemical damage to hepatocytes.
*mediator = acetaldehyde.
-neutrophil infiltration
-mallory bodies (damaged IFs).

11

Mallory bodies found in which diseases?

-alcoholic hepatitis.

12

Micronodular, irregularly shrunken liver with “hobnail”
appearance.

-alcoholic cirrhosis

13

alcoholic cirrhosis
-sclerosis seen predominantly where?

-Sclerosis around central vein (zone III).

14

2 contributing factors to hyperammonemia in cirrhosis.

1-urea cycle happens in the liver.

2- w/portal HTN, you get more portosystemic shunts so things bypass your liver. This leads to less ammonia being brought to the liver for urea cycle in the first place.

15

hepatic encephalopathy
-hyper or hyporeflexia?

-hyperreflexia

16

gaurding and rebound tenderness in HCC pt?
-why?

-tumor can rupture and leak stuff & cause bloody ascites & peritonitis.

17

Tumor marker for HCC?

-AFP
-levels do not correlate w/size, stage, or prognosis. Just let you know its there.

18

Cavernous hemangioma
-do you biopsy these?

-no, risk of hemorrhage.

19

Hepatic adenoma
-associated w/use of what?

Oral contraceptives & anabolic steroids.

20

Budd chiari
-JVD present?

-no.
-associated w/absence of JVD.

21

α 1-antitrypsin deficiency
-where does it accumulate?
-how do you stain for it?

-ER of hepatocytes
-PAS (+)
*remember, its a co-dominant trait.

22

Crigler Najjar
-what is it?
-leads to what?
-whats the milder version called?

-Absent UDP-glucuronosyltransferase
-indirect hyperbili
-Gilbert = Mild dec. of UDP-glucuronosyltransferase

23

Dubin-Johnson syndrome
-what is it?
-leads to what?
-whats liver look like?
-whats the milder version called?

-Defective liver excretion of bile. Defect in canalicular transport. So instead the conjugated bili spills into blood.
-direct hyperbili
-grossly black liver.
-Rotor syndrome

24

Too much cholesterol in bile can lead to gallstones.
-too much of what else can lead to gallstones?

-billirubin.
-pigmented gallstones.

25

Mnemonic for Rotor syndrome

Rotor rooter = getting stuff out (of toilet). Like getting
stuff out of liver. Defect in canalicular transport of bile, spills into blood stream instead.
-conjugated hyperbili.

26

What gives urine a dark color?

conjugated bilirubin or excess urobilin.

27

Physiologic neonatal jaundice
-causes?
-what type of hyperbili?

1-immature UDP-glucuronosyltransferase
2-lots of RBC destruction at birth b/c newborns have Hb-F - so these cells destroyed and replaced w/Hb-A (Hb-F not resposive to 2,3-DPG, Hb-A is).

-unconjugated hyperbilirubinemia

28

Tx for physiologic neonatal jaundice

-we use BLUE light.
-bilirubin absorbs light and fragments into water soluble fragments, and baby can pee it out.
-it does NOT conjugate the bilirubin! it just makes it more water soluble!

29

Mild icterus w/stress or fasting.

Gilbert syndrome
-Mildly dec. UDP-glucuronosyltransferase conjugation activity.

30

Type 2 Crigler Najjar
-Tx:

-Phenobarbital, which inc. liver enzyme synthesis.
-type 2 = less severe.