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GIGU Midterm > Biliary Secretion: Hepatobiliary Function > Flashcards

Biliary Secretion: Hepatobiliary Function Flashcards

1
Q

Why is the location of the liver ideal?

A

it can receive absorbed nutrients and detoxify drugs/toxins

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2
Q

what can hypoalbuminemia lead to?

A

edema

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3
Q

what does the liver convert ammonia to?

A

urea

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4
Q

what does alcohol abuse lead to?

A

accumulation of fat within hepatocytes

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5
Q

what does fatty liver lead to?

A

steatohepatitis

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6
Q

what is steatohepatitis?

A

fatty liver accompanied by inflammation, which leads to scarring of the liver and cirrhosis

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7
Q

what can cirrhosis cause?

A

portal hypertension

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8
Q

when does portal hypertension develop?

A

when there is resistance to portal blood flow

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9
Q

what is associated with portal hypertension?

A

changes to the venous circulation

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10
Q

what are esophageal varices?

A

swollen connection between systemic and portal systems at the inferior end of the esophagus

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11
Q

what is caput medusae?

A

swollen connection between the systemic and portal systems around the umbilicus

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12
Q

what else is associated with portal hypertension besides the venous changes?

A

spleenomegaly and porto-systemic collaterals

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13
Q

how does liver dysfunction lead to hepatic encephalopathy?

A

the decreased hepatic urea cycle metabolism leads to the accumulation of ammonia in the systemic circulation; ammonia readily crosses the BBB and alters brain function

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14
Q

where is bile produced and secreted from?

A

the liver

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15
Q

where does the synthesis of the primary bile acids occur?

A

liver

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16
Q

where does the synthesis of the secondary bile acids occur?

A

lumen of small intestine

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17
Q

where does the conjugation of the bile acids occur?

A

liver

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18
Q

what are the components of the biliary system?

A

the liver, gallbladder and bile duct, duodenum, ileum, and portal circulation

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19
Q

how is bile concentrated in the gallbladder?

A

by the absorption of water and ions

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20
Q

when chyme reaches the small intestine, what is secreted?

A

Cholecystokinin (CCK)

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21
Q

what are the two separate by coordinated functions of CCK?

A

it stimulates the contraction of the gallbladder and the relaxation of the sphincter of Oddi (this causes the stored bile to flow from the gallbladder into the lumen of the duodenum)

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22
Q

what happens when lipid absorption is complete?

A

the bile salts are recirculated to the liver via the enterohepatic circulation

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23
Q

where does the absorption of bile salts take place?

A

in the ileum

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24
Q

how is the bile rediluted?

A

secretin stimulates the production of ions (HCO3-) and H2O in the bile duct

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25
Q

bile in the liver (both new and recycled) is secreted into where?

A

bile canaliculi

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26
Q

bile secretion occurs via two mechanisms. what are they?

A
  1. bile-acid dependent 2. by secretin and it is then secreted from the ducts (bile acid-independent)
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27
Q

what is the secretion of bile acids accompanied by?

A

the passive movement of cations into the canaliculus

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28
Q

bile salts are recirculated to the liver via what?

A

enterohepatic circulation

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29
Q

how do the bile salts move from the lumen of the ileum into the enterocyte?

A

via the apical sodium dependent bile acid transporter (ASBT)

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30
Q

how do the bile salts move into the basolateral side of the enterocyte?

A

via the organic solute transporter alpha/beta (OST-alpha or OST-beta)

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31
Q

how do the bile salts move from the portal circulation into the hepatocytes?

A

either via the Na+ Tauroholate Co-transporting polypeptide (NTCP) or the organic anion transporter protein (OATPs)

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32
Q

how do the bile salts get from the hepatocytes into the bile canaliculi?

A

either the bile salt excretory pump (bsep) or the multidrug resistance protein 2 (mrp2)

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33
Q

how does the liver “know” how much new bile acid to synthesize daily?

A

bile-acid synthesis is under negative-feedback control by the bile salts

34
Q

what is the rate limiting enzyme in the biosynthetic pathway and what is it inhibited by?

A

7-alpha- hydroxylase, inhibited by bile salts

35
Q

what processes senescent red blood cells?

A

the reticuloendothelial system

36
Q

what happens when hemoglobin is degraded by the RES?

A

one of the byproducts is biliverdin (green-color)

37
Q

what is biliverdin converted into?

A

bilirubin (yellow-color)

38
Q

what is bilirubin bound to in the blood stream and where does it travel to?

A

it is bound to albumin and it travels to the liver to be taken up by hepatocytes

39
Q

once in the liver, in hepatic microsomes what happens to the bilirubin?

A

it is conjugated with glucuronic acid via the enzyme UDP glucuronyl transferase

40
Q

why do some newborns develop jaundice?

A

because the UDP glucuronyl transferase is synthesized slowly after birth

41
Q

what could be said about the solubility of conjugated bilirubin?

A

it is water soluble, and therefore a portion of it is excreted in the urine

42
Q

what happens when the conjugated bilirubin that is secreted into bile reaches the terminal ileum and colon?

A

it is deconjugated by bacterial enzymes and metabolized to urobilinogen

43
Q

what is urobilinogen converted into?

A

urobilin and stercobilin- which are excreted in the feces

44
Q

what gives stool its dark color?

A

urobilin and stercobilin

45
Q

what is jaundice a sign of?

A

hyperbilirubinemia

46
Q

how can you determine the quantitation of jaundice?

A

measurement of the total serum {bilirubin}

47
Q

how are bilirubin test results expressed as?

A

direct (conjugated), indirect (unconjugated) or total bilirubin

48
Q

any cause of hemolytic anemia could lead to what?

A

an increase in production of bilirubin

49
Q

in hemolytic anemic patient’s, the increased bilirubin level overwhelms the liver’s capacity leading to what?

A

the liver cannot produce conjugated bilirubin- results in high unconjugated bilirubin levels

50
Q

what is another reason why some newborns can have high levels of unconjugated bilirubin levels during their first week of life?

A

bilirubin production is elevated because of increased breakdown of fetal erythrocytes

51
Q

what kind of bilirubin levels would you find in a patient with Gilbert’s syndrome?

A

increased levels of unconjugated bilirubin in the blood

52
Q

when do episodes of gilbert syndrome typically occur?

A

when the body is under physiological stress

53
Q

what causes gilbert’s syndrome?

A

a mutation in the UGT1A1 gene- the gene that codes for the UDP glucuronyl transferase enzyme

54
Q

why is gilbert’s syndrome mild?

A

because the UGT1A1 gene still has about 30% activity

55
Q

what kind of bilirubin levels would you find in a patient with Crigler-Najjar syndrome?

A

increased levels of unconjugated bilirubin in the blood

56
Q

what causes crigler-najjar syndrome?

A

mutations in the gene that codes for the UDP glucuronyl transferase enzyme

57
Q

what are the two types of crigler-najjar syndrome?

A

Type 1: very severe; Type 2: less severe

58
Q

what would crigler Najjar syndrome Type 1 cause in patients before the availability of phototherapy?

A

kernicterus, which is a form of brain damage caused by the accumulation of unconjugated bilirubin in the brain and nervous tissue

59
Q

what are the major clinical features of kernicterus?

A

cerebral palsy, sensoryneural hearing loss, and gaze abnormalities

60
Q

what kind of bilirubin levels would you expect to see in a patient with dubin-johnson?

A

high levels of conjugated bilirubin in the serum without elevation of liver enzymes

61
Q

what is dubin johnson syndrome caused by?

A

a defect in the ability of hepatocytes to secrete the conjugated bilirubin into the bile

62
Q

what gene mutation is involved in Dubin-johnson syndrome?

A

mutations for the gene that encodes the MRP2 drug

63
Q

what does the liver look like in dubin-johnson syndrome?

A

it is black, which is the result of an intracellular melanin-like substance

64
Q

what kind of bilirubin levels would you expect to see in a patient with rotor syndrome?

A

there will be a build up of unconjugated and conjugated bilirubin in the blood, but mostly conjugated

65
Q

what causes rotor syndrome?

A

gene mutations that lead to abnormally short and nonfunctional OATP1B1 and OATP1B3 proteins or an absence of these proteins

66
Q

what does the liver look like in Rotor syndrome?

A

it is normal

67
Q

what is the primary treatment in neonates with unconjugated hyperbilirubinemia?

A

phototherapy

68
Q

how does phototherapy work?

A

through a process of isomerization that changes trans-bilirubin into the water-soluble cis-bilirubin isomer

69
Q

when do gallstones occur?

A

when there is excess of either pigment of bilirubin breakdown or excess cholesterol

70
Q

what could contribute to pigmented stones (black stones)

A

hemolysis aka hemolytic anemia

71
Q

what is the medical term for gallstones?

A

cholelithiasis

72
Q

what is choledocholelithiasis?

A

gallstones occluding the common bile duct

73
Q

what would you expect to find in a patient with choledocholelithiasis?

A

jaundice and conjugated hyperbilirubinemia

74
Q

what is cholangitis?

A

infection of the bile duct

75
Q

what is a patient at risk of developing if a stone is impacted in the distal bile duct?

A

cholangitis

76
Q

what would elevated levels of aminotransferases point to?

A

hepatocyte injury

77
Q

what would elevated alk phos point to?

A

this is primarily due to a bile duct injury (cholestasis)

78
Q

what would abnormal serum bilirubin, albumin, and or PT point to?

A

impaired hepatic synthetic function

79
Q

what do decreased levels of albumin point towards?

A

severe impairment of hepatocyte function

80
Q

what does PT point to?

A

it is going to increase as the ability of a cirrhotic liver to synthesize clotting factors diminishes

GIGU Midterm (19 decks)

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