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Gastrointestinal > Liver path I > Flashcards

Liver path I Flashcards

1
Q

What is the most common cause of chronic liver disease? Second most common?

A
  1. Hep C

2. EtOH

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2
Q

What are the two enzymes that are used in LFTs?

A

AST

ALT

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3
Q

Which is more specific for the liver: AST or ALT

A

ALT

AST is in muscles

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4
Q

What does LDH measure?

A

RBC destruction

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5
Q

What causes increase LFTs?

A

Breakage of hepatocytes

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6
Q

What are the three tests that measure the liver synthesis function?

A

Serum albumin
INR
Serum ammonia

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7
Q

What is the test that you want to order to differentiate if there is an isolated elevated alk phos to determine if it comes from the liver vs from the bone?

A

Gamma-glutamyl-transpeptidase

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8
Q

Isolated elevation in alk phos is suspicious for what disease?

A

Bile duct problems

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9
Q

Primary sclerosing cholangitis vs primary biliary cholangitis***

A
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10
Q

What form of bilirubin is conjugated: direct or indirect?

A

Direct

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11
Q

What is the normal range of direct bilirubin?

A

0.1-1.2 mg/dL

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12
Q

Greater than what level of direct bili causes jaundice?

A

> 2 mg/dL

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13
Q

Why is direct bilirubin named as such?

A

Can be directly measured in the lab since it’s water soluble?

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14
Q

How do they calculate indirect bili?

A

Subtract direct from the total bili

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15
Q

Where does bili concentrate?

A

Hepatocytes

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16
Q

Why is it that there is an increase in direct bili with alcoholic cirrhosis?

A

Edema of the hepatocytes causing obstruction of bile flow

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17
Q

Where are the best places to tell if an AA pt hwat jaundice?

A

Sclera

Mucous membranes

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18
Q

What are the prehepatic causes of increased bili

A

Hemolysis

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19
Q

What are the hepatic causes of increased bili?

A

Cirrhosis

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20
Q

What are the post hepatic causes of jaundice?

A

Obstruction of the bile duct

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21
Q

Heme is converted to what? What are the enzymes at each of these steps?

A

Biliverdin to bilirubin

heme oxygenase and biliverdin reductase respectively

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22
Q

Where does bilirubin formation occur?

A

Hepatocytes

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23
Q

Prehepatic causes of bilirubin cause an increase in what type of bilirubin?

A

Unconjugated

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24
Q

Hepatic causes of hyperbilirubinemia usually has what type of bilirubin?

A

Conjugated or unconjugated

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25
Q

Obstructive causes of hyperbilirubinemia usually has what type of bilirubin?

A

Conjugated

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26
Q

What is stercobilinogen?

A

Color of bili in the stool

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27
Q

What is the bili found in urine?

A

Urobilinogen

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28
Q

How is urobilinogen formed?

A

made by bacteria

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29
Q

What is the enzymes that conjugated heme?

A

UGT1A1–uridine diphosphate-glucuronyltransferase 1 A1

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30
Q

What is the transporter for bilirubin into hepatocyte ER?

A

Bilirubin-glutathione S tranferas

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31
Q

What is the chemical change that occurs with bilirubin metabolism?

A

add sugar moieties

32
Q

What are the two causes of elevation of unconjugated bili?

A

Overproduction

Reduce uptake

33
Q

What are the causes of elevated levels of conjugated bili?

A

Defective conjugation
Defective excretion
Defective secretion

34
Q

What are the causes of impaired uptake of bili? (3)

A

Hepatocellular injury
Drugs
Newborn

35
Q

What is the cause of Gilbert syndrome? How is this inherited?

A

Impaired UDP glucuronyl transferase activity, causing jaundice with stress

AR

36
Q

What is the cause of Crigler-Najjar syndrome type I? How is this inherited? Is this fatal?

A

Absent UDP glucuronyl transferase activity

AD

Causes death in infants

37
Q

What is the cause of dubin-Johnson syndrome? How is this inherited?

A

Impaired secretion of bili

AR

38
Q

What is the cause of Rotor syndrome?

A

AR decreased hepatic uptake and storage

39
Q

What is the liver pathology with Dubin-Johnson syndrome?

A

Pigmented cytoplasmic globules

40
Q

What is the cause of Crigler-Najjar syndrome type II? How is this inherited? Is this fatal?

A

Decreased Glucuronyl transferase activity

AD with variable penetrance

Generally mild

41
Q

What is the underlying genetic cause of Gilbert syndrome?

A

promoter mutation for UGT1A1

42
Q

What is the treatment for Gilbert syndrome?

43
Q

What is the treatment for Crigler-Najjar syndrome type I?

A

Liver transplant and phototherapy

No response to phenobarbital

44
Q

What causes death with Crigler-Najjar syndrome type I?

A

Kernicterus

45
Q

Which type of Crigler-Najjar syndrome responds to phenobarbital?

46
Q

What is the underlying defect with Dubin-Johnson syndrome?

A

MDR protein 2 defect, causing inability to transport

47
Q

What happens to the liver with Dubin-Johnson syndrome? What causes this?

A

Blackened

Build up of epi in lysosomes

48
Q

What is the diagnostic test for Dubin-Johnson syndrome?

A

Total urinary porphyrins are normal, but increased isomer I (usually III is higher)

49
Q

What happens with total coproporphyrin in Rotor syndrome?

A

Increased total, but normal isomer I

50
Q

What is the treatment for Rotor syndrome?

A

None required

51
Q

What is progressive familial intrahepatic cholestasis? What causes it?

A

A group of familial cholestatic conditions caused by defects in biliary epithelial transporters, that progresses to hepatic failure.

52
Q

What are the normal contents of bile? (4)

A

Cholic
Cholesterol
Lecithin
Bicarb

53
Q

What is (PFIC-1) Byler’s syndrome?

A

Problems with ATPase (ATP8B1) in liver, so not enough energy for transfer into the canalicular system

54
Q

What is PFIC-2?

A

ABCb11; bile salt export pump

55
Q

What is PFIC-3?

A

ABCB4; MDR3 phosphatidylcholine transfer

56
Q

What is the end result of PFIC 1, 2, and 3?

A

Cirrhosis/liver failure
Fat soluble vit deficiency
Cholestasis

57
Q

What are the histological characteristics of Progressive familial intrahepatic cholestasis?

A

Liver cell rosettes

Feathery degeneration

58
Q

What are the drugs that cause hepatocellular dysfunction?

A

Chlorpromazine

Erythromycin

59
Q

What are the pregnancy conditions that can cause hepatocellular dysfunction?

A

Preeclampsia

Toxemia

60
Q

What are the two most common types of bile obstruction?

A

Gallstones

CA of the head of the pancreas

61
Q

What are the ssx of cholestasis? (skin x2, stool, urine, bones)

A 
Pruritus
Jaundice
Clay-colored stool
Dark urine
Osteoporosis
62
Q

True or false: xanthomas can occur with cholestasis

63
Q

What happens to hepatocytes and kupffer cells with cholestasis?

A

Packing with bile

64
Q

What are the three outcomes of cholestasis in the liver?

A

Inflammation
Cirrhosis
Fibrosis

65
Q

Feathery degeneration of hepatocytes is manifested by what?

A

hydropic swelling, diffuse impregnation with bile pigment and a reticulated appearance

66
Q

What are bile lakes?

A

extravasation of a large amount of bile in extrahepatic obstruction

67
Q

What are the histological characteristics of cholestasis?

A

Neutrophils in the walls of the bile ducts and focally filling the lumen of ducts, often dilating or destroying them

68
Q

What are the three main causes of cirrhosis?

A

Viral
EtOH
Obesity

69
Q

What is the pathogenesis of cirrhosis?

A

Hepatocyte necrosis

Progressive fibrosis

70
Q

What happens when hepatocytes repair themselves from insult that can lead o cirrhosis?

A

Abnormal vascular connections

Disruption of function

71
Q

What causes the fibrosis of the liver?

A

Stellate cells convert to fibroblasts

72
Q

What are the factors that are released by macrophages to cause fibrosis?

A

PDGF
TNF
TGF-beta

73
Q

What is the space of Disse?

A

Area between a hepatocyte and a sinusoid. It contains the blood plasma. Microvilli of hepatocytes extend into this space, allowing proteins and other plasma components from the sinusoids to be absorbed by the hepatocytes

74
Q

Micronodular cirrhosis is usually caused by what insult to the liver?

75
Q

What is the main cause of macronodular cirrhosis?

A

Metabolic disorders

76
Q

What is the stain for collagen?

77
Q

What are the two types of cirrhosis?

A

Compensated

Decompensated

Gastrointestinal (42 decks)

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