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GI > Liver > Flashcards

Liver Flashcards

1
Q

Top 4 causes of chronic liver disease

A

Hep C, Alcoholic liver disease, non alcoholic fatty liver, hepatitis B

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2
Q

Liver tests-Hepatocyte integrity

A

Aminotransferases(AST, ALT), LDH

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3
Q

Is LDH specific to liver?

A

No

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4
Q

Tests to measure hepatocyte function

A

serum albumin, prothrombin time, serum ammonia

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5
Q

Liver tests-Bile canaliculus enzymes. Present during times of bile obstruction

A

Alkaline phosphatase, 5’-Nucleotidase, Gamma glutamyl transpeptidase

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6
Q

Equation for total bilirubin

A

Unconjugated+conjugated

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7
Q

normal levels of total bilirubin

A

0.1-1.2 mg/dL

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8
Q

Level of bilirubin leading to jaundice

A

> 2 mg/dL

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9
Q

where does conjugation take place

A

in hepatocytes

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10
Q

Clinical manifestations of hyperbilirubinemia

A

jaundice and cholestasis

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11
Q

3 mechanisms of jaundice and cholestasis

A

Isolated disorders of bilirubin metabolism, liver disease, bile duct obstruction

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12
Q

Prehepatic

A

too much red cell breakdown, leads to increased levels of unconjugated bilirubin. Heme gets into splenic macrophages, enzymes convert heme to biliverdon which is converted to bilirubin in unconguated form.

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13
Q

Hepatic

A

Bilirubin conjugated, but can’t leave liver. Could also be unconjugated

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14
Q

Posthepatic

A

Conjugated bilirubin

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15
Q

Where in hepatocyte does conjugation take place

A

ER. UGT1A1 adds sugar moities to bilirubin.

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16
Q

Function of MRP2,3

A

Excretion of conjugated bilirubin

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17
Q

Mechanisms of unconjugated bilirubin

A

overproduction, reduced uptake, defective conjugation

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18
Q

Mechanisms of conjugated hyperbilirubinemia

A

Defective excretion, Defective secretion

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19
Q

Age group with difficulties with impaired uptake of bilirubin and reduced glucuronyl transferase activity

A

Newborn

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20
Q

Diseases causing conjugated hyperbilirubinemia

A

Crigler-Najjar syndrome Types I and II, Gilbert syndrome. Born with all these

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21
Q

Diseases causing conjugated hyperbilirubinemia

A

Dubin Johnson syndrome, Rotor syndrome

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22
Q

Describe Gilbert syndrome

A

Autosomal recessive, UGTIAI promoter mutation leads to decreased activity, jaundice during times of stress, normal liver/healthy life. No treatment

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23
Q

Describe Crigler Najjar syndrome Type I

A

UGTIAI ABSENT. Get super high levels of unconjugated bilirubin. At birth, BB barrier not fully developed, bilirubin can get into brain and cause kernicterus. Very severe. Mental retardation if not death. Treat with phototherapy, transplant

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24
Q

Crigler Najjar Syndrome Type II

A

Decreased activity of UGT1A1, but more severe than Gilbert. Do respond to phenobarbital unlike CNS Type I.

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25
Q

Describe Dubin Johnson Syndrome

A

Defect in multidrug resistance protein 2, so bilirubin can’t get into canicular system, can’t be secreted from hepatocyte. Pt gets black liver due to metabolic products of epinephrine? No inflammation/fibrosis

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26
Q

Rotor syndrome

A

asymptomatic jaundice. Normal liver labs, increased total coproporphyrin, normal isomer I.

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27
Q

Describe progressive familial intrahepatic cholestasis

A

Defect in biliary epithelial transporters. Presents usually in childhood with progressive cholestasis. Leads to fibrosis/cirrhosis. Leads to failure to thrive, hepatic failure and need for liver transplant

28
Q

Contents of normal bile

A

cholic, chenodeoxycholic acid taurine/glycine salts, cholesterol, lecithin, bilirubin, bicarbonate.

29
Q

PFIC-2

A

problem with transport of bile salts

30
Q

PFIC-3

A

problem with transport of phosphatidylcholine

31
Q

PFIC-1

A

problem with ATPase in canicular area, trouble shunting stuff into canicular system

32
Q

complications of progressive familial intrahepatic cholestasis

A

cholestasis, fat malabsorption, fat soluble vitamin deficiency, osteopenia, liver failure

33
Q

Diseases that can occur that effect hepatocellular function with bilirubin. These effect the cells themselves

A

Viruses, alcoholic liver disease, drugs including chlorpromazine, erythromycin, hepatotoxins, metabolic disorders, pregnancy-toxemia, preclampsyia, immune-PBC and PSC

34
Q

2 most common causes of posthepatic dysfunction (obstruction of bile duct)

A

gallstones and carcinoma of ampulla of vater

35
Q

clinical presentation of pt with cholestasis

A

Pruritis, jaundice, clay colored stools, dark urine, bleeding diathesis (prothrombin time elevated), xanthomas, osteoporosis.

36
Q

labs results for cholestasis

A

increased AP, GGT, 5-Nucleotidase. Hyperbilirubinemia greater than 1.2, hyperlipidemia

37
Q

what causes bile lake

A

extrahepatic cholestasis due to obstruction

38
Q

Cirrhosis

A

inflammation, fibrosis, bridging bw microscopic structures of liver. Once nodules form have full blown cirrhosis

39
Q

4 common causes of cirrhosis

A

Mainly alcholic liver disease, viral hepatitis, obesity. Cryptogenic to a lesser extent

40
Q

Problems associated with decompensated cirrhosis.

A

Portal hypertension>12 mmHg, hepatorenal syndrome, liver failure, hepatic encephalopathy

41
Q

complications of portal hypertension

A

Gastroesophageal varices, rectal varices, caput medusae, ascites, hypersplenism

42
Q

Ascities- SAAG level in portal hypertension, non portal HTN

A

greater than 1.1 g/dL, less than 1.1 g/dL

43
Q

Hepatic failure

A

Loss of >80% of liver function
Fulminant is entire wipe out of architecture of liver
Subfulminant-Central veins and around outside of lobules will be destroyed

44
Q

clinical manifestation of hepatic failure

A

Encephalopathy, coagulopathy, jaundice, multi organ failure

45
Q

Hepatorenal failure

A

renal failure occurs bc cirrhosis or fulminant liver failure. Altered blood flow to kidney causes failure.

46
Q

Hepatorenal syndrome

A

Liver failure plus renal failure, normal kidney, oliguria/anuria, increased BUN, creatinine, low urinary Na, normal urinary sediment, poor prognosis

47
Q

Type 1 vs Type 2 hepatorenal syndrome

A

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48
Q

Hepatopulmonary syndrome

A

jkjk;j

49
Q

Hepatic encephalopathy

A

potentially reversible neuropsychiatric abnormality in setting of acute or chronic liver failure. Increased NH3 brain diffusion with edema is the cause

50
Q

Clinical features of hepatic encephalopathy

A

spatial perception distortion, sleep disturbances, personatlity changes, asterixis, abnormal EEG, lethargy, coma, decerebrate posture.

51
Q

Acute asymptomatic hepatitis infection with recover: serologic evidence only

A

Hep A, B most, C, D coninfection, E

52
Q

Acute symptomatic hepatitis with recovery: anicteric or icteric

A

Hep A, B, C, D coinfection, E

53
Q

Chronic hepatitis: without or with progression to cirrhosis

A

Hep B few, C 85%, D superinfection most

54
Q

Fulminant hepatitis: with massive to submassive hepatic necrosis

A

Hep A rare, B rare, C rare, D co and super, E pregnant

55
Q

Picorna virus-RNA, transmission is fecal oral, no carrier state or chronic hepatitis, rarely causes fulminant hepatitis. Clinical disease mild/asymptomatic and rare after childhood.

A

Hep A

56
Q

Only dsDNA, hepadnavirus, most common cause of cirrhosis and hepatocellular carcinoma (background of cirrhosis needed), transmission via parenteral, sexual, vertical

A

Hep B

57
Q

Chronic Hep B extrahepatic manifestations

A

Glomerulonephritis in children, polyarteritis nodosa in adults.

58
Q

Hep D needs what other Hep to replicate

A

Hep D needs Hep B

59
Q

Chronic Hep C extrahepatic manifestations

A

Cryoglobulinemia, thyroiditis, glomerulonephritis, thrombocytopenia

60
Q

When is Hep E not benign

A

When you’re preggers

61
Q

Primary biliary cirrhosis

A

Antimitochondrial antibody. Genetic predisposition. Get cirrhosis, gallstones, hepatocellular carcinoma. Liver failure over long period of time.

62
Q

Diagnosis of primary biliary cirrhosis

A

Increased AMA, anti M2, anti PDH E2. Increased IgM, increased AP/5-NT/GGT, increased cholesterol

63
Q

Primary sclerosing cholangitis diagnosis

A

Increased AP, GGT, 5-NT.
p ANCA positive in 80% of cases
Also do ERCP

64
Q

PSC complications

A

Chronic cholestasis, cholangitis, secondary biliary ciffhosis, liver failure, cholangiocarcinoma.

65
Q

Type I autoimmune hepatitis

A

SMA, ANA, most common

66
Q

Type II autoimmune hep

A

Anti LKM1

67
Q

Type III autoimmune hep

A

Anti SLA/LP

GI (13 decks)

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