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(OMS1) GIGU Exam > Lecture 19: Hepatobiliary Function > Flashcards

Lecture 19: Hepatobiliary Function Flashcards

1
Q

What are the main functions of the liver?

A

-bile, billirubin, metabolism of carbs/lipids/proteins, detoxification

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2
Q

What are the metabolic functions of the liver?

A 
carbohydrate metabolism (make/release glucose storing clycogen)
protein metabolism (AA and plasma protein synthesis and modification, ammonia conversion)
lipid metabolism (FA oxidation, lipid synthesis)
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3
Q

If protein metabolism is impaired due to liver dysfunction, what happens?

A

Hypoalbuminemia > loss of oncotic pressure in capillary so fluid leaks out > edema/ascites

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4
Q

Describe the blood flow system serving the liver

A

2 capillary beds connected by hepatic portal system:
Abdominal/pelvic bed > hepatic portal vein (all GI blood passes through liver sinusoidal bed

Hepatic artery feeds liver with oxygenated blood

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5
Q

How can liver dysfunction cause bruising?

A

-lack of coagulation factors synthesized by liver

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6
Q

What is cirrhosis and how does it happen

A

-liver cells are damaged & replaced with fibrotic tissue

major cause is alcohol > fat accumulation in hepatocytes > fatty liver > steatohepatitis (fat + inflammation) > scarring

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7
Q

What is portal hypertension and what causes it?

A

-hepatocytes are dysfunctional and can’t drain the venous blood well > turbulence at HPV > blood is shunted to other veins causing them to distend

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8
Q

Clinical manifestations of Portal HTN

A

esophageal varices - swollen vessels at inferior esophagus

caput medusae - swollen vessels by umbilicus

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9
Q

What is hepatic encephalopathy and what causes it?

A
  • alteration of brain function due to NH3+ buildup

- impaired urea cycle in liver > NH3+ accumulates and is able to cross the BBB

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10
Q

What is the importance of bile?

A

basically “opens” lipid cluster so enzymes can digest it

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11
Q

Be able to draw the synthesis of bile (also from Zaidi’s lecture)

A

Ok

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12
Q

Where are primary bile acids synthesized?
Where are secondary bile acids generated?
Where is bile conjugated?

A

liver
Small intestine
liver

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13
Q

What are the relative amounts of the four bile acids in the body?

A

cholic > chenodeoxycholic > deoxycholic > lithocholic

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14
Q

What happens to bile at these locations?
duodenum
jejunum
ileum

A
  • bile emulsifies
  • bile aggregates and forms micelles and recruit lipases to break down lipids
  • bile and b12 reabsorbed/recycled
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15
Q

What is the mechanism of bile secretion and absorption?

A
  1. canalicular bile formed @ liver (isotonic to plasma)
  2. some of the final bile formed from secretions of HCO3, Na and H2O by secretin
  3. storage @ gallbladder and release in bile duct
  4. Sphincter of Oddi opens in response to CKK > bile released to duodenum
  5. bile salts and b12 reabsorbed in ileum
  6. return to canaliculi via portal circulation
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16
Q

How much bile does the liver produce?

A

As much as it lost/excreted

17
Q

What happens at the biliary system during these periods of digestion?
Interdigestive
Eating

A
  1. ) Bile fills gallbladder (relaxed), sphincter of Oddi is closed contracted
  2. ) CCK stimulates = signals food, gallbladder contracts, Sphincter of Oddi opens and relaxes to release the bile
18
Q

What are two transport mechanisms for recycled bile to return to the hepatocyte?

A

Na dependent: Na taurocholate cotransporting polypeptide
Na independent: organic anion transport proteins

-both located on the basolateral side of the hepatocyte

19
Q

What transporters allow bile to enter the canaliculi from the hepatocyte?

A

BSEP and MRP2 (active transport)

*located on the canalicular membrane

20
Q

What transporters allow bile to be reabsorbed at the ileum?

What transporters allow bile to travel from the enterocyte in the ileum back to portal circulation?

A

ASBT (with reabsorbed Na)

OSTa/B

21
Q

What type of transport is utilized by bile at these regions?
Jejunum
Ileum
Colon

A
  • passive
  • active and passive, absorbs most bile
  • passive
22
Q

Is the bile that makes it to the ileum conjugated or unconjugated?

A

Conjugated, so needs to be actively reabsorbed at the ileum

-unconjugated bile passively diffuses proximal to the ileum

23
Q

What happens to bile synthesis during ….
ileal resection
bile acid feeding

A
  • ileum gone so most bile isn’t reabsorbed > increase in bile synthesis
  • lots of bile secreted so lots of bile coming back from the ileum > decrease in bile synthesis
24
Q

How is bile synthesis inhibited?

A

returning bile feedbacks and inhibits 7a hydroxylase > inhibits bile synthesis, not secretion

*secretion is triggered by food

25
Q

Draw the pathway of bilirubin excretion including locations in the GI tract

A

Ok

26
Q

Jaundice

How would you determine if jaundice is unconjugated or conjugated?

A

defect @ pathway up to liver > unconjugated jaundice

after liver > conjugated jaundice

27
Q

Hemolytic anemia

Physiological neonatal jaundice

A
  • RBC destruction > unconjugated bili buildup
  • UDPGT activity not up to speed at birth > unconjugated bili from fetal Hgb breakdown builds up, treat with phototherapy to avoid brain damage
28
Q

Crigler Najjar syndrome
Cause
Clinical

A

-UDPGT enzyme mutations, Type 1 (complete absence) more sever than Type 2 (decreased activity)
-Type 1: manifests in infancy, leads to kernicterus
Type 2: later onset, less likely to lead to kernicterus, less than 20% activity of UDPGT

29
Q

Gilbert syndrome:

A
  • UDPGT mutation > UGT1A1 activity 30% of normal

- usually asymptomatic

30
Q

Kernicterus
Cause
clinical

A
  • unconjugated bilirubin buildup in brain (yellow brain

- cerebral palsy, gaze abnormalities, sensorineural hearing loss

31
Q

Treatment for Crigler-Najjar syndrome

A 
phototherapy 
blood transfusion
phenobarbitol (type 2 only)
liver transplant (type 1)
oral phosphate and carbonate
32
Q

Dubin Johnson syndrome
cause
clinical

A
  • MRP2 transporter mutation > can’t transport conjugated bilirubin into bile
  • black liver (due to melanin buildup), mild jaundice
33
Q

Rotor syndrome
cause
clinical

A
  • OSTPB1/B3 mutations that transport bilirubin from ileum to portal circulation
  • conjugated bilirubin buildup, non-pigmented liver
34
Q

How does phototherapy work?

A
  • converts trans bilirubin to soluble cis bilirubin

- used to treat infants with > 21 mg//dL bilirubin

35
Q

Cholelithiasis:

A

-caused by cholesterol buildup in bile, too much absorption of bile acids from bile or epithelium inflammation

36
Q

Cholecystitis
Choledocholithiasis
Cholangitis

A
  • cystic duct obstruction by stone > gallbladder inflammation
  • common bile duct occlusion > jaundice or conjugated hyperbilirubinemia
  • bile duct infection
37
Q

What do biochemical tests evaluate?

Examples?

A

test liver enzyme function
-ALT, AST: elevated in hepatocyte injury
Alkalinephosphatase: elevated in bile duct injury

38
Q

If albumin is reduced, what does this mean about liver function?

If PT is elevated, what does this mean about liver function?

A
  • albumin is made in the liver, so if it is reduced there is something wrong with hepatic function
  • longer clotting time means liver isn’t producing enough clotting proteins, synthetic ability is impaired

(OMS1) GIGU Exam (40 decks)

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