Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

GIGU > Hepatobiliary Fxn > Flashcards

Hepatobiliary Fxn Flashcards

1
Q

What capillary beds does the hepatic portal system connect?

A

1) hepatic sinusoidal capillaries

2) portal vein (abd organs from lower esophagus to anal canal)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What organs are drained via portal vein to liver?

A 
Pancreas
Gallbladder
Spleen
SI and LI--> anal canal
Lower esophagus
Stomach
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What is the function of the liver in carb metabolism?

A

Makes glucose
Stores glucose as glycogen
Releases glucose

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What is the function of the liver in protein metabolism?

A
  • Synthesizes non-essential AA
  • Modifies aa so it can feed into glucose metabolism
  • Synthesizes plasma proteins
  • Converts ammonia–>urea
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What results in liver failure?

A

Hypoalbuminemia

–>low albumin because liver can’t make it–>EDEMA

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What is the function of the liver in lipid metabolism?

A
  • fatty acid oxidation

- synthesis of lipoproteins, CHOLESTEROL, phospholipids

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

How does impaired liver fxn results in hepatic encephalopathy?

A

Decreased urea cycle metabolism in liver (d/t cirrhosis or shunting)—> accumulation of AMMONIA

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

How does impaired liver fxn results in ascites?

A

can’t make plasma proteins, decreased osmotic pressure and portal HTN–>fluid flows out of blood into tissue

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Describe cirrhosis

A

Chronic liver disease–> normal liver cells damaged and replaced by SCAR TISSUE

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What is the most common cause of cirrhosis?

A

excessive alcohol

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

How does impaired liver fxn results in bruising?

A

can’t make coagulation proteins–>increased bruising d/t easy bleeding

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What is steatohepatitis?

A

fatty liver with inflammation–> leads to scarring of liver (cirrhosis)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What can cause portal HTN?

A

cirrhosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Why does portal HTN develop?

A

there is resistance to portal blood flow d/t scarring

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What changes in venous circulation are associated with portal HTN?

A

Esophageal varices

Caput medusae

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What are examples of portosystemic shunting d/t portal HTN?

A

esophageal varices

caput medusae

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

How does ammonia cause hepatic encephalopathy?

A

increased ammonia (d/t impaired urea cycle in liver) crosses blood-brain barrier and alters brain fxn (toxic)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

How does ammonia cause hepatic encephalopathy?

A

increased ammonia (d/t impaired urea cycle in liver) crosses blood-brain barrier and alters brain fxn (toxic)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

What composes bile?

A 
bile salts (50%)
bilirubin
cholesterol
phospholipids (40%)
ions
water
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

What is the fxn of bile?

A

solubilizes lipids in intestines

vehicle for elimination of substances from body

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Where is bile produced and secreted?

A

liver

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Examples of primary bile acids

A

cholic acid

chenodeoxycholic acid

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Examples of secondary bile acids

A

deoxycholic acid

lithocholic acid

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Examples of bile salts

A

acids + glycine or taurine (lower pKA)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

What are the relative amounts of bile acids?

A

cholic acid> chenodeoxycholic acid> deoxycholic acid> lithocholic acid

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

What are the relative amounts of bile acids?

A

cholic acid> chenodeoxycholic acid> deoxycholic acid> lithocholic acid

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

Where are primary bile acids synthesized?

A

hepatocytes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

Where are secondary bile acids found?

A

lumen of SI

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

Where are bile salts conjugated?

A

liver

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

What form micelles with products of lipid digestion?

A

bile salts

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

What are the biliary system organs?

A 
Liver
GB
Bile duct
Duodenum
Ileum
Portal circulation
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

What are the biliary system organs?

A 
Liver
GB
Bile duct
Duodenum
Ileum
Portal circulation
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

What agent activates ion and water addition to bile in the bile duct?

A

secretin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

Where are ions and water absorbed to concentrate bile salt?

A

Gallbladder

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

What agent stimulates the contraction of the gallbladder AND relaxation of the sphincter of Oddi (pancreas)?

A

CCK

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

What happens to the bile salts after release into duodenum?

A

Form micelles–> absorbed into PORTAL circulation–> back to liver

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

What happens to bile salts when they are returned to the liver via portal circulation?

A

secreted into bile canaliculi along with newly formed bile acid–> ductule cells in response to anion transport (osmotic effects)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

What drives bile-acid dependent bile formation?

A

Bile acids

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

What stimulates bile acid-independent/ ductular bile secretion?

A

secretin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

What accompanies the secretion of bile acids into canaliculi?

A

passive movement of cations

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

What is the fxn of secretin in bile secretion?

A

Stimulates:

  • secretion of bicarb and water from ductile cells
  • sig increase in bile volume and pH
  • decrease in concentration of bile salts
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

When is CCK activated?

A

when eating

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

When is the GB relaxed and sphincter of Oddi closed?

A

between digestion/eating

44
Q

How are bile salts recirculated to liver?

A

enterohepatic circulation

–> ileum-portal blood- liver- synthesize what was lost

45
Q

What mediates uptake of bile salts via basolateral membrane of hepatocytes?

A
  • NTCP= sodium taurocholate cotransporting polypeptide (Na+ dependent transport protein)
  • OATPs= organic anion transport proteins (Na+-independent transport protein
46
Q

What is cholesterol 7 alpha-hydroxylase inhibited by?

A

bile salts

47
Q

What increases synthesis of bile acids 10 fold higher than normal?

A

interruption of the enterohepatic circulation

48
Q

What does bile secretion normally increase?

A

increases rate of return of bile acids to liver via portal blood

–> negative feedback synthesis==== inhibits 7alpha hydroxylase

49
Q

Why do some infants have jaundice?

A

UDP glucuronyl transferase (conjugates bilirun) slowly synthesized after birth

50
Q

What gives stool dark color?

A

urobilin

stercobilin

51
Q

Where is bilirubin conjugated?

A

liver via UDP glucuronyl transferase

52
Q

What happens to urobilinogen in terminal ileum?

A

Urobilinogen from conjugated bilirubin either:
- converted to urobilin and stercobilin–>feces

  • back to liver via enterohepatic circulation–>urine
53
Q

What are the characteristics (makeup) of saliva?

A

High bicarb and K+

hypotonic

alpha amylase and lingual lipase

54
Q

What factors increase secretion of saliva?

A

PNS (predominant) and SNS

55
Q

What factors decrease secretion of saliva?

A

sleep
dehydration
atropine

56
Q

What are characteristics (makeup) of gastric secretions?

A

HCL

Pepsinogen

Intrinsic factor

57
Q

What factors increase gastric secretions?

A

Gastrin

ACh

Histamine

PNS

58
Q

What factors decrease gastric secretions?

A

H+ in stomach

Chyme in duodenum

Somatostatin

Atropine

Cimetidine

Omeprazole

59
Q

What are characteristics (makeup) of pancreatic secretions?

A

High bicarb

Isotonic

Pancreatic lipase, amylase, proteases

60
Q

What factors increase pancreatic secretions?

A

Secretin

CCK (potentiates secretin)

PNS

61
Q

What factors decrease pancreatic secretions?

A

N/A

62
Q

What are characteristics (makeup) of bile?

A

Bile salts

Bilirubin

Phospholipids

Cholesterol

63
Q

What factors increase bile secretions?

A

CCK (contract GB, relax sphincter of oddi)

PNS

64
Q

What factors decrease bile secretions?

A

ileal resection

65
Q

What is a sign of hyperbilirubinemia?

A

Icterus/Jaudice

66
Q

What is icterus?

A

Yellow discoloration of the sclera, skin and mucous membranes

67
Q

What shows in a quantitative jaundice test (bilirubin test)?

A

Direct (conjugated)

Indirect (unconjugated)

Total bilirubin

68
Q

Describe the pathway of RBC breakdown to passage of bile

A 
RBC Breakdown-->
Unconjugated bilirubin->
Uptake to liver-->
Conjugated bilirubin-->
Secretion to bile-->
Passage of bile
69
Q

What stages of RBC breakdown can be involved in unconjugated jaundice?

A

RBC breakdown–>
Unconjugated bilirubin->
Uptake to liver–>
Conjugated bilirubin

70
Q

What can cause increased bilirubin?

A

hemolytic anemia

71
Q

What can cause decreased delivery of bilirubin to liver for conjugation?

A

Heart failure

72
Q

What parts of the RBC breakdown pathway does Gilber’s syndrome affect?

A

Can’t:

Uptake of bilirubin to liver

conguated bilirubin

73
Q

What part of the RBC breakdown pathway does Crigler-Najjar syndrome affect?

A

Can’t:

Conjugate bilirubin in liver

74
Q

What part of the RBC breakdown pathway does Dubin-Johnson syndrome affect?

A

Can’t:

Secrete conjugated bilirubin to bile

75
Q

What part of the RBC breakdown pathway does Rotor syndrome affect?

A

Can’t secrete conjugated bilirubin to bile

76
Q

What part of the RBC breakdown pathway does a biliary tree obstruction affect?

A

Can’t pass bile

77
Q

What parts of the RBC breakdown pathway correspond to conugated jaundice?

A

Secretion of bilirubin to bile and passage of bile

78
Q

What are the 5 known hereditary defects in bilirubin metabolism?

A

Crigler-Najjar syndromes (1 and 2)

Gilber’s syndrome

Dubin-Johnson syndrome

Rotor syndrome

79
Q

How does hemolytic anemia lead to increased unconjugated bilirubin?

A

Increased bilirubin level overwhelmes liver’s capacity to produce conjugated bilirubin

80
Q

What are 2 causes of physiological neonatal jaundice?

A
  • elevated bilirubin production d/t increased breakdown of fetal RBCs
  • low activity of UDP glucuronyl transferase
81
Q

What syndrome is implicated in a mutation of UDP glucuronyltransferase (UGT1A1)?

A

Gilbert syndrome

82
Q

Describe Gilbert Syndrome

A
  • increased unconjugated bilirubin
  • mild, adolescence. mild cases of hyperbilirubinemia in times of stress
  • 30% no sx
83
Q

Is Type 1 or 2 Crigler-Najjar syndrome more severe?

A

Type 1

84
Q

What syndrome causes increased levels of unconjugated bilirubin d/t nonhemolytic jaundice?

A

Crigler-Najjar syndrome

–>also d/t mutation in UDP gene

85
Q

Describe Type 1 Crigler-Najjar syndrome

A
  • earlier in life with jaundice at birth/infancy
  • NO FXN of UDP glucuronyltransferase
  • TMT using phototherapy (most did not survive before this)
  • Kernicterus form of this
86
Q

Is Kernicterus d/t type 1 or 2 Crigler-Najjar syndrome?

A

Type 1

87
Q

Define Kernicterus

A

Permanent brain damage d/t accumulation of unconjugated bilirubin in brain and nerves

–> CP, sensorineural hearing loss, gaze abn

88
Q

Define Type 2 Crigler-Najjar syndrome

A

later in life, most survive into adulthood

less than 20% fxn of UDP

-not likely to develop kernicterus

89
Q

What are the possible treatments for Crigler-Najjar Syndrome?

A
  • phototherapy throughout life (doesn’t work well after age 4 d/t thick skin)
  • blood transfusions
  • oral calcium phosphate and carbonate to form complexes with bilirubin in gut
  • liver transplant
  • phenobarbitol to treat TYPE 2 (conjugates bilirubin)
90
Q

Define Dubin-Johnson syndrome

A
  • increased conjugated bilirumin without elevation of liver enzymes

—> defect of ability to secrete into bile

  • mild jaundice after puberty or adulthood
  • liver is black but fxn normal
91
Q

What is the function of multidrug resistance-associated protein 2?

A

transports bilirubin out of liver cells into bile

–> MUTATED in Dubin-Johnson syndrome

92
Q

What worsens jaudice in Dubin-Johnson syndrome?

A

alcohol, birth control pills, infection, pregnancy

93
Q

Define Rotor syndrome

A

Buildup of both conj and unconj bilirubin in blood, but majority is conjugated

–>similar to Dubin-Johnson, except mutations lead to nonfxnl OATP1B1 and OATP1B3 proteins

-liver not pigmented

94
Q

What are the fxns of OATP1B1 and OATP1B3 proteins?

A

transport bilirubin from the blood into liver to be cleared from body

–>MUTATED in Rotor syndrome

95
Q

How does phototherapy work on bilirubin?

A

Isomerization: trans bilirubin to water-soluble cis bilirubin isomer

96
Q

What is cholecystitis?

A

Inflammation of GB d/t obstruction of cystic duct from cholelithiasis

97
Q

What is choledocholithiasis?

A

Gallstones occlude common bile duct–> jaundice, conjugated hyperbilirubinemia

98
Q

What is cholangitis?

A

Infection of the distal bile duct

99
Q

Are liver function tests direct measures of liver fxn?

A

no, vary and can be abnl in patietns with nml liver fxn

100
Q

Elevated plasma aminotransferases are primarily the result of ?

A

Hepatocyte injury

101
Q

Elevated alkaline phosphatase in plasma are primarily the result of?

A

bile duct injury (cholestasis)

102
Q

What are liver enzymes measured in serum?

A

Aminotransferases (alanine and aspartate: ALT and AST)

Alkaline phosphatase

103
Q

What are abnml function tests seen in impaired hepatic synthetic fxn?

A

serum bilirubin, albumin, prothrombin time

104
Q

What does bilirubin function test measure r/t liver?

A

liver’s ability to detoxify metabolites, transport organic anions into bile

105
Q

Severe impairment of hepatocyte fxn likely to _______ level of albumin in plasma

A

reduce

106
Q

Is hypoalbuminemia specific for liver disease?

A

No, can be seen in kidney glomerular disease

107
Q

What does the prothrombin time function test reflect?

A

degree of hepatic synthetic dysfunction

–> increases as liver decreases clotting factor synthesis

–> worsening coagulation= severity of hepatic dysfunction

GIGU (37 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions