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GIGU - Week 2 > 20- Hepatobiliary Function > Flashcards

20- Hepatobiliary Function Flashcards

1
Q

This organ is ideally located to receive absorbed nutrients and to detoxify drugs/toxins. Its main functions include the following:

    • Bile production and secretion
    • Metabolism of carbohydrates, proteins, and lipids
    • Bilirubin production and excretion
    • Detoxification of substances
A

Liver

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2
Q

The ________ ________ _________ connects the following two capillary beds:

1) That of the abdominal and pelvic parts of the gut from the abdominal part of the esophagus to the lower anal canal, together with the pancreas, gallbladder, and spleen.
2) The hepatic sinusoidal ‘capillary’ bed.

A

Hepatic Portal System

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3
Q

What are the carbohydrate metabolism functions of the liver?

A
    • Gluconeogenesis
    • Storage of glucose as glycogen
    • Release of glucose
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4
Q

What are the protein metabolism functions of the liver?

A

– Synthesis of nonessential AAs

– Modification of AA for use in biosynthetic pathways for carbohydrate

– Synthesis of almost all plasma proteins (i.e., albumin and clotting factors)

– Conversion of ammonia to urea

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5
Q

Liver failure can result in hypoalbuminemia, which may lead to _________.

A

Edema

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6
Q

What are the lipid metabolism functions of the liver?

A
    • FA oxidation

- - Synthesis of lipoproteins, cholesterol, and phospholipids

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7
Q

This is a chronic liver disease in which normal liver cells are damaged and replaced by scar tissue. Excessive alcohol intake is a most common cause.

A

Cirrhosis

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8
Q

Alcohol abuse leads to accumulation of fat within hepatocytes. Fatty liver leads to ___________, which is fatty liver accompanied by inflammation. This leads to scarring of the liver and cirrhosis.

A

Steatohepatitis

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9
Q

Cirrhosis can cause _________ _________, which develops when there is resistance to portal blood flow, and most often occurs in the liver.

A

Portal Hypertension

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10
Q

This change to the venous circulation associated with portal hypertension is due to a swollen connection between systemic and portal systems at the inferior end of the esophagus.

A

Esophageal Varices

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11
Q

This change to the venous circulation associated with portal hypertension is due to swollen connections between systemic and portal systems around the umbilicus.

A

Caput Medusae

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12
Q

Decreased hepatic urea cycle metabolism in the context of liver cirrhosis or portosystemic shunting leads to accumulation of ammonia in the systemic circulation (hyperammonemia). Ammonia readily crosses the BBB and alters brain function and can cause __________.

A

Encephalopathy

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13
Q

This is produced and secreted by the liver, and is a vehicle for elimination of substances from the body. It also solves the insolubility problem of lipids.

A

Bile

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14
Q

What is bile composed of?

A
    • Bile Salts (50%)
    • Bile Pigments (20%; i.e., bilirubin)
    • Cholesterol (4%)
    • Phospholipids (40%; i.e., lecithin)
    • Ions
    • Water
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15
Q

In the hepatocytes of the liver, cholesterol reacts with 7a-hydroxylase to form the two primary bile acids. These acids are…

A

Cholic Acid

Chenodeoxycholic Acid

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16
Q

In the lumen of the small intestine, the two primary bile acids will react with 7a-dehydroxylase to form the two secondary bile acids. These acids are…

A 
Deoxycholic Acid (from Cholic Acid)
Lithocholic Acid (from Chenodeoxycholic Acid)
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17
Q

In the liver, the secondary bile acids will be conjugated to form bile salts. What are these bile salts?

A

Glycodeoxycholic Acid
Taurodeoxycholic Acid
Glycolithocholic Acid
Taurolithocholic Acid

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18
Q

Bile salts form _________ with the products of lipid digestion.

A

Micelles

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19
Q

Bile secretion results from the concerted actions of biliary system’s organs. These organs are…

A 
Liver
Gallbladder and Bile Duct
Duodenum
Ileum
Portal Circulation
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20
Q

Bile acids and electrolytes are secreted from the liver via the bile duct. Bile is stored in the gallbladder between meals, but otherwise is taken to the _________ for emulsification and digestion of fats.

A

Duodenum

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21
Q

After emulsification and digestion of fats in the duodenum, there is micelle formation and fat absorption in the ________. After this, there is active absorption of bile acids via the ________, which then takes the bile acids back to the liver via the portal circulation.

A

Jejunum

Ileum

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22
Q

Put the following steps of the mechanism of bile secretion and absorption of bile salts in order:

A. Absorption of bile salts into the portal circulation.

B. CCK-induced gallbladder contraction and sphincter of Oddi relaxation.

C. Delivery of bile salts to the liver.

D. Synthesis and secretion of bile salts.

E. Bile salts are stored and concentrated in the gallbladder (absorption of ions and water).

A

1) D.
2) E.
3) B.
4) A.
5) C.

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23
Q

Together with newly synthesized bile acids, the returning bile acids are secreted into the ________ ________. This bile is then secreted by ductule cells in response to the osmotic effects of anion transport.

A

Bile Canaliculi

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24
Q

Secretion of bile acids is accompanied by the passive movement of _______ into the canaliculus.

A

Cations

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25
Q

Canalicular bile is primarily an ultrafiltrate of ________.

A

Plasma

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26
Q

_________ stimulates the secretion of HCO3- and H2O from the ductile cells, resulting in a significant increase in bile volume, HCO3- concentration, and pH and a decrease in the concentration of bile salts.

A

Secretin

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27
Q

Almost all bile formation is driven by bile acids (bile acid-dependent). A small portion of bile is stimulated by ________ and is secreted from the ducts (bile acid-independent or ductular secretion).

A

Secretin

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28
Q

In between meals, what happens to bile?

A

The gallbladder is relaxed and fills with bile, and the Sphincter of Oddi is closed.

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29
Q

During meals, what happens to bile?

A

CCK stimulates contraction of the gallbladder to release bile and causes relaxation of the Sphincter of Oddi.

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30
Q

Bile salts are transported from the Ileum to the portal blood and taken back to the liver via __________ circulation. There is synthesis of bile salts to replace the amount that was lost.

A

Enterohepatic

31
Q

Bile salts uptake (from portal blood) across the basolateral membrane of the hepatocytes is mediated by two type of systems, which are…

A

– Na+-dependent transport protein, NTCP (Sodium Taurocholate Cotransporting Polypeptide)

– Na+-independent transport protein, OATPs (Organic Anion Transport Proteins)

32
Q

These systems transport bile acids from hepatocytes to the bile canaliculi via the use of ATP.

A

BSEP (Bile Salt Excretory Pump)

MRP2 (Multidrug Resistance Protein 2)

33
Q

This system transports bile acid from biliary excretion into the small intestine (enterocytes).

A

ASBT (Apical Sodium-Dependent Bile Acid Transporter)

34
Q

This system transports bile acid from the small intestine (enterocytes) into the portal circulation.

A

OST-a
OST-ß

(Organic Solute Transporter alpha-beta)

35
Q

This system transports bile acid from the portal circulation back into the liver (hepatocytes).

A

NTCP (Sodium Taurocholate Cotransporting Polypeptide)

36
Q

The enterohepatic circulation of bile acids is carried out by both active and passive transport processes. The ileal transport process is highly efficient, delivering more than ______ of the bile acids to the portal blood. Only a small proportion of bile acids, _______, are excreted into the feces.

A

90%

3-5%

37
Q

State whether active or passive transport occurs in each of the following:

    • Jejunum
    • Ileum
    • Colon
A

Jejunum – Passive transport

Ileum – Active and Passive transport

Colon – Passive transport

38
Q

Increased bile secretion normally increases the rate of return of bile acids to the liver via portal blood, which exerts a negative feedback on synthesis. _________ _________ is inhibited by bile salts. Interruption of the enterohepatic circulation can increase synthesis to values > 10-fold higher than normal.

A

Cholesterol 7a-hydroxylase

39
Q

Bilirubin is conjugated via _______ _______ _______, which is synthesized slowly after birth. Some newborns develop jaundice because this hasn’t developed yet.

A

UDP Glucuronyl Transferase

40
Q

_______ and _______ give stool its dark color.

A

Urobilin

Stercobilin

41
Q

This is a sign of hyperbilirubinemia. It causes yellow discoloration of the sclera, skin, and mucous membranes.

A

Jaundice (Icterus)

42
Q

T/F. Measurement of the total serum (bilirubin) allows quantitation of jaundice. Bilirubin test results are expressed as direct (conjugated), indirect (unconjugated), or total bilirubin.

A

True

43
Q

This is a form of anemia due to hemolysis. Any cause of this could lead to increased production of bilirubin. Increased bilirubin levels can overwhelm the liver’s capacity to produce conjugated bilirubin, resulting in increased conjugated bilirubin.

A

Hemolytic Anemia

***Unconjugated Jaundice

44
Q

This is caused by increased unconjugated bilirubin in the blood during the 1st week of postnatal age. Some infants may be tired and feed poorly.

A

Neonatal Jaundice

45
Q

Neonatal jaundice has 2 main causes, which are…

A

1) Bilirubin production is elevated because of increased breakdown of fetal erythrocytes (shortened lifespan of fetal erythrocytes)
2) Low activity of UDP glucuronyl transferase

46
Q

This disease is caused by a mutation in the gene that codes for UDP glucuronyl transferase (UGT1A1). Its activity level is about 30% of normal. Additional factors that interfere with the glucuronidation process may be necessary for the development of the condition. For example, the movement of bilirubin into the liver, where it would be glucuronidated, may be impaired.

A

Gilbert Syndrome

***30% of people have no signs or symptoms of the condition

47
Q

Gilbert Syndrome can result in increased levels of (CONJUGATED/UNCONJUGATED) bilirubin in the blood. Can be relatively mild, and is usually recognized during adolescence. If people with this condition have episodes of hyperbilirubinemia, these episodes are generally mild and typically occur when the body is under physiological stress.

A

Unconjugated

48
Q

This disease is caused by mutations in the gene that code for UDP glucuronyl transferase. This results in increased levels of unconjugated bilirubin in the blood, and can cause nonhemolytic jaundice.

A

Crigler-Najjar Syndrome

49
Q

This type of Crigler-Najjar Syndrome is very severe and starts earlier in life. Jaundice is apparent at birth or in infancy. In this type there is no function of UDP glucuronyl transferase. Can lead to death of patients by kernicterus before phototherapy is available, or they survived until early adulthood with clear neurological impairment.

A

Crigler-Najjar Syndrom Type 1

50
Q

This is a form of brain damage caused by the accumulation of unconjugated bilirubin in the brain and nerve tissues.

A

Kernicterus

51
Q

This is a permanent neurologic sequelae of bilirubin-induced neurologic dysfunction. It develops during the 1st year postnatal, and features include cerebral palsy, sensorineural hearing loss, and gaze abnormalities.

A

Kernicterus

52
Q

This type of Crigler-Najjar Syndrome is less severe and starts later in life. There is less than 20% function of UDP glucuronyl transferase and the patient is less likely to develop kernicterus. Most affected individuals survive into adulthood.

A

Crigler-Najjar Syndrome Type 2

53
Q

This is a treatment for Crigler-Najjar Syndrome, and is needed throughout a person’s life. In infants, this is done using bilirubin lights (‘blue lights’). Does not work as well after age 4, and thickened skin blocks the light.

A

Phototherapy

54
Q

This is a treatment for Crigler-Najjar Syndrome that may help control the amount of bilirubin in the blood.

A

Blood Transfusions

55
Q

This is a treatment for Crigler-Najjar Syndrome that is used to form complexes with bilirubin in the gut.

A

Oral Calcium Phosphate and Carbonate

56
Q

This is a treatment for Crigler-Najjar Syndrome that can be done in some people with Type 1.

A

Liver Transplant

57
Q

This is a treatment for Crigler-Najjar Syndrome that is sometimes used to treat Type 2 to aid in the conjugation of bilirubin. There is no response to this treatment for patients with Type 1.

A

Phenobarbitol

58
Q

This disease is caused by a defect in the ability of hepatocytes to secrete conjugated bilirubin into the bile. There is a mutation for the gene that encodes the MRP2 (Multidrug Resistance-Associated Protein 2). This is what transports bilirubin out of liver cells and into bile. Results in increased conjugated bilirubin in the serum without elevation of liver enzymes.

A

Dubin-Johnson

59
Q

Dubin-Johnson presents as mild jaundice throughout life. It may not appear until puberty or adulthood, and is usually the only symptom. It can be made worse by alcohol, birth control pills, infection, or pregnancy. The liver also has a ________ pigmentation, which is a result of an intracellular melanin-like substance but is otherwise histologically normal.

A

Black

60
Q

This disease results in a buildup of both conjugated and unconjugated bilirubin in the blood, but the majority is conjugated. Caused by gene mutations that lead to abnormally short, nonfunctional OATP1B1 and OATP1B3 proteins or an absence of these proteins. These proteins normally transport bilirubin and other compounds from the blood into the liver so that they can be cleared from the body. Liver cells are not pigmented.

A

Rotor Syndrome

61
Q

Any newborn with a total serum bilirubin of _________ should receive phototherapy. Works through a process of isomerization that changes trans-bilirubin into the water-soluble cis-bilirubin isomer.

A

> 21 mg/dL

***Phototherapy is the primary treatment in neonates with unconjugated hyperbilirubinemia!

62
Q

These can occur when there is excess in either pigment of bilirubin breakdown or cholesterol.

A

Gallstones (Cholelithiasis)

63
Q

This is inflammation of the gallbladder, most commonly due to obstruction of the cystic duct from cholelithiasis.

A

Cholecystitis

64
Q

This is the term for when gallstones are occluding the common bile duct. Patients may have jaundice and conjugated hyperbilirubinemia.

A

Choledocholithiasis

65
Q

This is the term for an infection of the bile duct.

A

Cholangitis

66
Q

The term ________ ________ ________, although commonly used, is imprecise since many of the tests reflecting the health of the liver are not direct measures of its function. Commonly, used liver biochemical tests may be abnormal even in patients with a healthy liver.

A

Liver Function Tests (LFTs)

67
Q

The biochemical test for liver enzymes is commonly measured in the serum. The things measured are…

A
    • Serum Aminotransferases (ALT and AST)

- - Alkaline Phosphate

68
Q

The pattern of test abnormalities for liver enzymes may suggest the underlying cause of the patient’s liver disease. For example, elevated __________ are primarily the result of hepatocyte injury and elevated ________ ________ is primarily the result of bile duct injury (i.e., cholestasis).

A

Aminotransferases

Alkaline Phosphate

69
Q

T/F. Abnormal serum bilirubin, albumin, and/or prothrombin time (PT) may be seen in the setting of impaired hepatic synthetic function.

A

True

70
Q

________ in part measures the liver’s ability to detoxify metabolites and transport organic anions into bile.

A

Bilirubin

71
Q

In cases of hyperbilirubinemia, it is important to determine whether it is predominantly _________ or _________ hyperbilirubinemia. Increased in unconjugated results from overproduction, impairment of uptake, or impaired conjugation of bilirubin.

A

Direct

Indirect

72
Q

Severe impairment of hepatocyte function is likely to reduce the level of ________ in the plasma. This is synthesized exclusively in the liver, and its levels fall as the synthetic function of the liver declines with worsening cirrhosis.

A

Albumin

73
Q

Important to consider: __________ is not specific for liver disease, it may also be seen in kidney glomerular disease.

A

Hypoalbuminemia

74
Q

_______ reflects the degree of hepatic synthetic dysfunction. It increases as the ability of a cirrhotic liver to synthesize clotting factors diminishes. Worsening coagulopathy correlates with the severity of hepatic dysfunction.

A

PT (Prothrombin Time)

GIGU - Week 2 (10 decks)

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