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GIGU > Hepatobiliary Function (Lopez) > Flashcards

Hepatobiliary Function (Lopez) Flashcards

1
Q

What are the main functions of the liver?

A
  • bile production/secretion
  • metabolism of carbs, proteins, lipids
  • bilirubin production/excretion
  • detox of substances
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2
Q

What two capillary beds does the hepatic portal system connect?

A

1) that of abd and pelvic parts of gut from abd part of esophagus to lower anal canal, together w/ the pancreas, gallbladder, and spleen
2) the hepatic sinusoidal ‘capillary’ bed

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3
Q

What are the metabolic liver functions?

A
  • carbohydrate metabolism: gluconeogenesis, storage of glycogen, release of glucose
  • protein metabolism: synthesis of nonessential AAs, modification of AAs for use in pathways for carbs, synthesis of almost all plasma protein (e.g. albumin, clotting factors) (liver failure can lead to hypoalbuminemia > edema), conversion of ammonia to urea
  • lipid metabolism: FA oxidation, synthesis of lipoproteins, cholesterol, and phospholipids
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4
Q
  • chronic liver dz where nml liver cells are damaged and replaced by scar tissue
  • excessive alcohol intake is common cause due it leading to accum of fat within hepatocytes > fatty liver > steatohepatitis (fatty liver w/ inflammation) > scarring of liver > this condition
  • this condition can also lead to portal hypertension
A

cirrhosis

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5
Q

What is portal hypertension and what types of changes in venous circulation are a/w this condition?

A
  • portal htn: can be caused by cirrhosis; develops when there is resistance in portal blood flow which most often occurs in liver; nml hepatic sinusoidal pressure is 3-5 mmHg, but is >5 mmHg in this condition

changes in venous circulation (see image):

  • esophageal varices: swollen connection between systemic and portal systems at inferior end of esophagus
  • caput medusae: swollen connections between systemic and portal systems around umbilicus
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6
Q

How can liver dz lead to hepatic encephalopathy?

A
  • decreased hepatic urea cycle mblsm in context of liver cirrhosis or portosystemic shunting leads to accum of ammonia in systemic circ
  • ammonia readily crossses BBB and alters brain function
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7
Q

What is the composition and function of bile?

A
  • composition: bile salts (50%), bile pigments (2%, e.g. bilibrubin), cholesterol (4%), phospholipids (40%, e.g. lecithin), ions, H2O
  • function: vehicle for elimination of substances from the body, solves insolubility problem of lipids
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8
Q

How are bild acids/salts generally formed and what is the purpose of converting bile acids to salts?

A
  • primary bile acid synthesis (occurs in hepatocytes): cholesterol > (7α-hydroxylase) > cholic acid and chenodeoxycholic acid
  • secondary bile acid synthesis (occurs in lumen of SI): cholic and chenodeoxycholic acid > (7α-dehydroxylase from intestinal bacteria) > deoxycholic acid (from CA) and lithocholic acid (from CDA)
  • bile salt synthesis (occurs in liver): deoxycholic acid and lithocholic acid > (via conjugation) > glycodeoxycholic acid, taurodeoxycholic acid (from DA) and glycolithocholic acid, taurolithocholic acid (from LA)
  • purpose: bile salts form micelles w/ the products of lipid digestion (better at eliminating lipids)
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9
Q

What organs play a role in bile secretion?

A
  • liver
  • gallbladder/bile duct
  • duodenum
  • ileum
  • portal circulation
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10
Q

What is the mechanism of bile secretion and absorption of bile salts?

A

1) synthesis and secretion of bile salts from liver into circ
2) bile salts are stored/conc in gallbladder (absorption of ions/H2O)
3) CCK-induced gallbladder contraction and sphincter of Oddi relaxation

(bile salts synthesized in the SI via bacterial enzymes)

4) absorption of bile salts into portal circulation
5) delivery of bile salts to liver

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11
Q

What is the mechanism of bile secretion out of the liver?

A

two mechanisms:

  • almost all bile formation is drive by bile acids (bile acid-dependent)
  • small portion of bile is stimulated by secretin and is secreted from the ducts (bile acid-independent or ductular secretion)
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12
Q

How does bile flow during periods of digestion?

A
  • interdigestive period: gallbladder filled w/ bile and relaxed, sphincter of Oddi is closed
  • upon eating (food in duodeum): CCK is released, causing contraction of gallbladder and relaxation of sphincter of Oddi
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13
Q

How are bile salts recirculated back to the liver?

A

via enterohepatic circulation

1) bile salts are transported from ileum to portal blood
2) bile salts brought back to liver
3) synthesis of bile salts to replace amount that was lostx

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14
Q

How is the reuptake of bile salts in hepatocytes facilitated?

A

uptake across the basolateral membrane of hepatocytes is mediated by 2 types of systems:

  • Na+-dependent transport protein, sodium taurocholate cotransporting polypeptide (NTCP)
  • Na+-independent transport protein, organic anion transport proteins (OATPs)
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15
Q

What type of transport recycles bile acids?

A
  • both active and passive transport processes
  • ileal transport is highly efficient, delivering >90% of bile acids to portal blood
  • only small portion of bile acids (3-5%) are excreted into feces
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16
Q

Enterohepatic circulation of bile acids: big picture

A
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17
Q

How is bile acid synthesis and secretion regulated?

A
  • increased bile secretion normally increases rate of return of bile acids to liver via portal blood, which exerts a negative feedback on synthesis (cholesterol 7α-hydroxylase is inhibited by bile salts)
  • interruption of enterohepatic circulation can increase synthesis to values > 10-fold higher than nml
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18
Q

What is the mechanism of bilirubin production/secretion?

A
19
Q

saliva

  • characteristics:
  • factors that increase secretion:
  • factors that decrease secretion:
A

saliva

  • characteristics: high HCO3-, high K+, hypotonic, α-amylase, lingual lipase
  • factors that increase secretion: PNS (prominent), SNS
  • factors that decrease secretion: sleep, dehydration, atropine
20
Q

gastric HCL secretion

  • characteristics:
  • factors that increase secretion:
  • factors that decrease secretion:
A

gastric HCL secretion

  • characteristics: HCL
  • factors that increase secretion: gastrin, ACh, histamine
  • factors that decrease secretion: H+ in the stomach, chyme in duodenum, somatostatin, atropine, cimetidine, omeprazole
21
Q

gastric pepsinogen secretion

  • characteristics:
  • factors that increase secretion:
  • factors that decrease secretion:
A

gastric pepsinogen secretion

  • characteristics: pepsinogen, intrinsic factor
  • factors that increase secretion: PNS
  • factors that decrease secretion: n/a
22
Q

pancreatic HCO3- secretion

  • characteristics:
  • factors that increase secretion:
  • factors that decrease secretion:
A

pancreatic HCO3- secretion

  • characteristics: high HCO3-, isotonic
  • factors that increase secretion: secretin, CCK (potentiates secretin), PNS
  • factors that decrease secretion: n/a
23
Q

pancreatic enzymes secretion

  • characteristics:
  • factors that increase secretion:
  • factors that decrease secretion:
A

pancreatic enzymes secretion

  • characteristics: lipase, amylase, proteases
  • factors that increase secretion: CCK, PNS
  • factors that decrease secretion: n/a
24
Q

bile secretion

  • characteristics:
  • factors that increase secretion:
  • factors that decrease secretion:
A

bile secretion

  • characteristics: bile salts, bilirubin, phospholipids, cholesterol
  • factors that increase secretion: CCK (contraction of gallbladder, relaxation of sphincter of Oddi), PNS
  • factors that decrease secretion: ileal resection
25
Q
  • yellow discoloration of sclera, skin, and mucous membranes
  • sign of hyperbilirubinemia
  • measurement of total serum bilirubin allows quantitation of condition: bilirubin tests results are expressed as direct (conjugated), indirect (unconjugated), or total bilirubin
A

jaundice (icterus)

26
Q

What are the 5 known conditions due to hereditary defects in bilirubin metabolism?

A
  • Crigler-Najjar syndrome (types 1 and 2)
  • Gilbert’s syndrome
  • Dubin-Johnson syndrome
  • Rotor syndrome
27
Q
  • anemia due to hemolysis of RBC
  • any cause of this condition could lead to increased bilirubin
  • increased bilirubin level overwhelms liver’s capacity to prod conjugated bilirubin, resulting in increased unconjugated bilirubin
A

hemolytic anemia

28
Q
  • increase in unconjugated bilirubin in blood during 1st week after birth
  • 2 main causes: bilirubin prod is elevated b/c of increased breakdown of fetal erythrocytes, or low activity of UDP glucuronyl transferase
  • infants may be very tired and feed poorly
A

physiological neonatal jaundice

29
Q
  • increased unconjugated bilirubin in blood
  • relatively mild, usually recognized during adolescence, episodes of of hyperbilirubinemia are generally mild and typically occur under stress
  • cause: mutation in gene that codes for uridine diphosphate glucoronosyltransferase (UDP glucoronyltransferase), the activity of UGT1A1 is 30% of nml, additional factors that interfere w/ glucuronidation process may be necessary for development of this condition (e.g. movement of bilirubin into liver, where it would be glucuronidated, may be impaired)
  • ~30% of people w/ this condition have no signs or sx
A

Gilbert syndrome

30
Q
  • increased unconjugated bilirubin in blood
  • causes nonhemolytic jaundice
  • caused by: mutations in gene that codes for UDP glucuronyltransferase
  • two types: 1 is severe and 2 is less severe
A

Crigler-Najjar syndrome

31
Q

caused by: mutations in gene that codes for UDP glucuronyltransferase, no function of this enzyme at all

  • starts earlier in life, jaundice is apparent at birth/infancy
  • kernicterus: form of brain damage caused by accum of unconj bilirubin in brain/nerve tissues
  • before phototherapy tx, patients died of kernicterus or survived into early adulthood w/ neurologic impairment
A

Crigler-Najjar syndrome type 1

32
Q
  • permanent neurologic sequelae of bilirubin-induced neurologic dysfunction
  • develops during 1st year of infants life
  • clinical features: cerebral palsy, sensoryneural hearing loss, gaze abnormalities
A

kernicterus

33
Q
  • caused by: mutations in gene that codes for UDP glucuronyltransferase, less than 20% function of this enzyme
  • starts later in life
  • less likely to develop kernicterus
  • most individuals survive into adulthood
A

Crigler-Najjar syndrome type 2

34
Q

What are the treatments for Crigler-Najjar syndrome?

A
  • phototherapy: needed throughout individual’s life; in infants, bilirubin (blue lights) are used; does not work as well after age 4 due to thickened skin blocking light
  • blood transfusions: may help control amnt of bilirubin in blood
  • oral calcium phosphate and carbonate: form complexes w/ bilirubin in the gut
  • liver transplant: can be done in some people w/ type 1
  • phenobarbitol: sometimes used to tx type 2 to aid in conjugation of bilirubin; no response to tx in individuals w/ type 1
35
Q
  • increased conjugated bilirubin in serum w/o elevation of liver enzymes
  • caused by: defect in the ability of hepatocytes to secrete conj bilirubin into bile; mutations for gene that encodes the multidrug resistance-associated protein 2 (MRP2) which transports bilirubin out of liver cells into bile
  • mild jaundice throughout like, may not appear until puberty/adulthood, usually only sx
  • can be made worse by: alcohol, BCP, infection, pregnancy
  • liver has black pigmentation, result of intracellular melanin-like substance but is otherwise histologically nml
A

Dubin-Johnson syndrome

36
Q
  • buildup of both unconj and conj bilirubin, but majority is conjugated
  • caused by: gene mutations that lead to abnormally short, nonfunctional OATP1B1 and OATP1B3 proteins or absence of these proteins; these proteins normally transport bilirubin and other compounds from blood into liver for excretion
  • similar to Dubin-Johnson syndrome, except no black liver
A

Rotor syndrome

37
Q

What is the primary treatment in neonates w/ unconjugated hyperbilirubinemia?

A

phototherapy

  • any newborn w/ total serum bilirubin <21 mg/dL should receive phototherapy
  • works through process of isomerization that changes trans-bilirubin into water-soluble cis-biliruin isomer
38
Q
  • occur when there is excess in either pigment of bilirubin breakdown or cholesterol
  • causes: too much absorption of water from bile, too much absorption of bile acids from bile, too much cholesterol in bile, inflammation in epithelium
  • pigment stones: hard, formed of bilirubin polymers, hemolytic anemia could contribute to formation of these types of stones
  • cholesterol stones: too much cholesterol in bile
A

gallstones (cholelithiasis)

(see image for probability of stones blocking certain ducts)

39
Q

What does elevated aminotransferases (ALT and AST, biochemical tests) usually suggest?

A

primarily the result of hepatocyte injury

40
Q

What does elevated alkaline phosphatase (biochemical test) usually suggest?

A

primarily result of bile duct injury (e.g. colestasis)

41
Q

What is the importance of bilirubin liver function tests?

A
  • abnormal serum bilirubin, albumin, and/or prothrombin time (PT) may be seen in setting of impaired hepatic synthetic function
  • bilirubin in part measure liver’s ability to detox metabolites and transport organic anions into bile
  • in cases of hyperbilirubinemia, it is important to determine whether it is direct or indirect (e.g. increase in unconj results from overproduction, impairment of uptake, or impaired cong of bilirubin)
42
Q

What is the importance of albumin liver function tests?

A
  • abnormal serum bilirubin, albumin, and/or prothrombin time (PT) may be seen in setting of impaired hepatic synthetic function
  • albumin: severe impairment of hepatocyte function is likely to reduce albumin in plasma
  • synthesized exclusively in the liver, levels fall as synthetic function of liver declines w/ worsening cirrhosis
  • important to consider: hypoalbuminemia is not specific for liver dz (e.g. it may also be seen in kidney glomeurlar dz)
43
Q

What is the importance of prothrombin time (PT) liver function tests?

A
  • abnormal serum bilirubin, albumin, and/or prothrombin time (PT) may be seen in setting of impaired hepatic synthetic function
  • PT: reflects degree of hepatic synthetic dysfunction
  • increases as ability of cirrhotic liver to synthesize clotting factors diminishes, worsening coagulopathy correlates w/ severity of hepatic dysfunction

GIGU (23 decks)

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