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Bile & Bile Salts Flashcards

0
Q

What is produced when heme oxygenase acts on hemoglobin?

A

Iron, CO, and biliverdin.

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1
Q

What is the primary source of bilirubin in the body?

A

Senescent RBCs (80%).

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2
Q

Where is heme oxygenase most plentiful?

A

Reticuloendothelial cells in the spleen.

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3
Q

How is bilirubin conjugated?

A

Once transported into the hepatocyte, UDP glucoronosyltransferase conjugates two glucoronides in the ER.

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4
Q

What are the organic components of bile, in order?

A

(1) bile salts
(2) phospholipids
(3) cholesterol
(4) protein
(5) bilirubin

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5
Q

How is bilirubin typically seen in the blood?

A

Unconjugated and bound to albumin by weak hydrogen bonds.

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6
Q

What are protective mechanisms against unconjugated bilirubin, a neurotoxic lipid?

A

(1) binding to albumin
(2) blood-brain barrier
(3) conjugation
(4) excretion in bile

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7
Q

What is delta bilirubin?

A

Conjugated bilirubin that is covalently bound to albumin. It is large, preventing passage into urine.

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8
Q

What does the presence of delta bilirubin indicate?

A

The protracted presence of conjugated bilirubin in the serum.

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9
Q

Describe what happens when bacteria in the gut encounter bilirubin.

A

(1) The bilirubin is converted to urobilinogen, a colorless, water-soluble substance.
(2) Some urobilinogen is absorbed (and can be excreted in urine).
(3) Alternatively, bacteria can further act on urobilinogen to produce pyrroles, which give stool its color.

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10
Q

What’s another term for jaundice?

A

Icterus.

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11
Q

How high must bilirubin levels be in the serum so that jaundice is seen?

A

At least twice normal.

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12
Q

Match:
Conjugated and Unconjugated:
Direct and Indirect.

A 
Conjugated = Direct
Unconjugated = Indirect
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13
Q

Which type of hyperbilirubinemia produces tea-colored urine?

A

Direct or conjugated.

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14
Q

Simply, what are the possible causes of unconjugated hyperbilirubinemia?

A

(1) overproduction of bilirubin
(2) reduced uptake of bilirubin by liver
(3) defects in bilirubin conjugation

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15
Q

What are causes of reduced hepatic uptake of bilirubin?

A

(1) altered circulation (portal systemic shunting, right heart failure, etc.)
(2) drug effects (rifamycin)

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16
Q

What are causes of overproduction of bilirubin?

A

(1) hemolysis
(2) extravasation into tissue
(3) ineffective erythropoiesis

17
Q

What are causes of defective conjugation of bilirubin?

A

(1) Gilbert’s syndrome
(2) Crigler-Najjar syndrome types I and II
(3) drug effects (testosterone, novobiocin)
(4) chronic hepatitis (Wilson disease)
(5) hyperthyroidism

18
Q

Why is jaundice common in newborns?

A

(1) immature transport and conjugation of bilirubin

(2) increased hemolysis

19
Q

How is jaundice treated in newborns?

A

Phototherapy.

20
Q

Why is phototherapy effective in treating some cases of jaundice?

A

Light exposure breaks the internal hydrogen bonds in unconjugated bilirubin, exposing the propionic acid groups and making it more water-soluble.

21
Q

What is Gilbert’s syndrome?

A

An autosomal recessive disorder in which there is a defect in the promoter gene for glucoronosyltransferase leading to decreased activity. Unconjugated bilirubin is slightly elevated (especially during fasting), but the disease is benign.

22
Q

How is Gilbert’s syndrome diagnosed?

A

It is a diagnosis of exclusion: unconjugated hyperbilirubinemia with no other cause.

23
Q

What are causes of conjugated hyperbilirubinemia?

A

(1) inherited secretory defects
(2) disease of hepatocytes (necrotizing hepatitis, chronic hepatitis, cholestasis)
(3) biliary obstruction

24
Q

What are the notable inherited defects of bilirubin secretion?

A

(1) Dubin-Johnson syndrome
(2) Rotor syndrome

LFTs are normal as is secretion of bile salts. In Dubin-Johnson, the liver may have black pigmentation.

25
Q

What are symptoms of cholestasis?

A

(1) jaundice
(2) pruritus
(3) vitamin deficiencies
(4) hypercholesterolemia

26
Q

What are signs of vitamin A malabsorption?

A

Night blindness.

27
Q

What are signs of vitamin D malabsorption?

A

Osteomalacia.

28
Q

What are signs of vitamin K malabsorption?

A

Impaired prothrombin synthesis.

29
Q

What are signs of vitamin E malabsorption?

A

Cerebellar and peripheral nerve disorder.

30
Q

What is a xanthelasma?

A

Deposits of cholesterol in tissue, particularly around the orbit.

31
Q

What are extrahepatic causes of cholestasis?

A

(1) gallstones
(2) strictures
(3) pancreatitis
(4) cancer of the pancreas, bile duct or gallbladder

32
Q

What are 3 predisposing factors for gallstones?

A

(1) supersaturation
(2) stasis
(3) nucleation factors

33
Q

How do gallstones form?

A

When cholesterol or bilirubin precipitate out in bile.

34
Q

How are gallstones detected?

A

Primarily by ultrasound.

35
Q

What can the color of a gallstone indicate?

A

Pale: primarily cholesterol

Black: primarily unconjugated bilirubin, formed in gallbladder

Brown: primarily unconjugated bilirubin, formed in bile ducts

36
Q

What profile is at increased risk of gallstones?

A

An obese female over thirty that doesn’t exercise, eats a Western diet, and has multiple children.

Rapid weight loss, estrogen, somatostatin, and TPN can also contribute.

37
Q

What is needed for a gallstone to be visible on X-ray?

A

Higher concentration of calcium salts.

38
Q

What is a precursor “lesion” for gallstones?

A

Sludge.

39
Q

What can be used to dissolve cholesterol gallstones?

A

(1) ursodeoxycholic acid
(2) chenodeoxycholic acid

Not effective for pigment stones.

40
Q

What type of gallstone is most easily seen on X-ray?

A

Black pigment stones (and calcium-rich cholesterol stones).

41
Q

What additional contents are seen in brown pigment stones?

A

Bacteria and fatty acids.

GI (39 decks)

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