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GI > Jaundice Jigsaw > Flashcards

Jaundice Jigsaw Flashcards

1
Q

The liver’s cells (hepatocytes) excrete bile into

A

Canaliculi

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2
Q

Intercellular spaces between the liver cells

A

Canaliculi

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3
Q

These canaliculi drain into the right and left hepatic ducts, after which bile travels in the common hepatic duct and into the

A

Gallbladder

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4
Q

Has a capacity of 50 mL and concentrates the bile 10 fold by removing water and stores bile until a person eats

A

Gallbladder

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5
Q

Supplies the gall bladder

-a branch of the right hepatic artery 90% of the time

A

Cystic Artery

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6
Q

Venous return is carried either through small veins that enter directly into the liver or, rarely, to a large cystic vein that carries blood back to the

A

Portal vein

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7
Q

An imaging procedure that helps track the production and flow of bile from your liver to your small intestine

A

Hepatobiliary Scintigraphy (HIDA Scan)

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8
Q

Creates pictures of your liver, gallbladder, bile ducts, and small intestine

A

HIDA scan

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9
Q

Technetium-99m-labeled iminodiaceticacid analogues are a new class of organic anions taken up and secreted by hepatocytes into

A

Hepatic Bile

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10
Q

The only mechanism the body has to eliminate cholesterol

A

Bile acids in their feces

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11
Q

The primary bile acids differ from cholesterol in being composed of

A

24 carbon atoms

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12
Q

The mixture of primary and secondary bile acids and salts circulates between the liver and the small intestine, with storage in the

A

Gall bladder

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13
Q

If more cholesterol enters the bile than can be excreted, cholesterol may precipitate/crystallize in the gallbladder, leading to

A

Gallstone disease (cholelithiasis)

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14
Q

Gallstones are caused by a decrease of

A

Bile acids in bile

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15
Q

Gallstone disease can be caused by gross malabsorption of bile acids from the intestine, as seen in patients with severe

A

Ileal disease

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16
Q

Obstruction of the biliary tract, interrupting the enterohepatic circulation, can result in

A

Gall stones

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17
Q

An excessive feedback suppression of bile acid synthesis as a result of an accelerated rate of recycling of bile acids can cause

A

Bile acids

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18
Q

What percentage of patients with asymptomatic gallstones develop symptoms within 10 years

A

Only 25%

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19
Q

Generally indicated in patients who have experienced symptoms or complications of gallstones

A

Removal of Gallbladder (Cholecystectomy)

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20
Q

Drainage of pus from the gallbladder, which may be preferred in some cases to allow stabilization and later cholecystectomy

A

Cholecystostomy

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21
Q

If surgical removal of common bile duct stones is not immediately feasible, we can use

A

Endoscopic, retrograde sphincterotomy

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22
Q

Can prevent gallstone formation

A

Ursodeoxycholic acid (UDCA) treatment

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23
Q

Used in the treatment of cholestatic liver diseases, gallstone dissolution, and for patients with hep C

A

UDCA

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24
Q

UDCA is used in patients with hepatitis C virus infection to ameliorate elevated

A

Alanine aminotransferase levels

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25
Q

A bile acid with fewer hepatotoxic properties than endogenous bile acids

-competes with endogenous bile acids for absorption in the terminal ileum

A

Ursodeoxycholic acid (UDCA)

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26
Q

Ursodeoxycholic acid (UDCA) competes with endogenous bile acids for absorption in the

A

Terminal ileum

27
Q

Appears to promote the endogenous secretion of bile acid and reduce the cytotoxic potential of endogenous bile acids

A

UDCA

28
Q

Alters and reduces inflammatory cytokine production, protects cell membranes from disruption, and reduces the display of aberrant HLA antigens

A

UDCA

29
Q

Breaks one of the methynyl bridges holding the four part ring together, releasing the green pigmented biliverdin, iron, and CO

A

Heme oxygenase

30
Q

The products of heme oxygenase are shown to be

A

Cytoprotective

31
Q

Biliverdin is a substrate for biliverdin reductase, producting the red-orange colored

A

Bilirubin

32
Q

In the liver, adds two molecules of glucuronic acid to bilirubin, making the more water-soluble bilirubin diglucuronide

A

Bilirubin glucuronyl transferase

33
Q

Bilirubin diglucuronide is secreted into the bile ducts and stored in the gall bladder until they are released into the

A

Intestine

34
Q

Bacteria in the gut hydrolyze bilirubin and reduce it to a colorless

A

Urobilinogen

35
Q

Gives urine its yellow color

A

Urobilin

36
Q

May result due to excess hemolysis of red blood cells

A

Jaundice

37
Q

Thallasemia, sickle cell anemia, G-6-P dehydrogenase deficiency, etc. may lead to

A

Jaundice

38
Q

A plasma glycoprotein that binds extracorpuscular hemoglobin (Hb) in a tight noncovalent complex

A

Haptoglobin

39
Q

Approximately 10% of hemoglobin that is degraded each day is released into the circulation and is thus

A

Extracorpuscular

40
Q

Too large to pass through the glomerulus

A

Hemoglobin0haptoglobin complex

41
Q

Low levels of haptoglobin are found in patients with

A

Hemolytic anemias

42
Q

This is because the Hb-Hp complex has a short

A

Half-life

43
Q

Thus, during hemolytic anemia when lots of RBC are breaking down and releasing Hb into plasma, we have low levels of

A

Haptoglobin

44
Q

A condition characterized by yellow discoloration of the skin, conjunctivae, and mucous membranes as a result of widespread tissue deposition of the pigmented metabolite bilirubin

A

Jaundice

45
Q

Stems from a mechanical obstruction of the bile duct, preventing the “draining” of conjugated bilirubin into the intestines

A

Obstructive jaundice

46
Q

Both the liver uptake of bilirubin and the conjugation of bilirubin can be affected by

A

Hepatocellular Jaundice

47
Q

Defect due to the complete absence of the EDP-GT gene

A

Criggler-Najar syndrome: Type I

48
Q

What is the extent of jaundice in Criggler-Najar syndrome: Type I?

A

Severe, causing Kernicterus in the brain of the newborn

49
Q

Defect due to a mutation in the UDP-GT gene

A

Criggler-Najar syndrome: Type II

50
Q

What is the extent of jaundice in Criggler-Najar syndrome: Type II?

A

Benign

51
Q

Defect caused by the reduction in transcription of UDP-GT due to a mutation in the promoter region

A

Gilbert Disease

52
Q

What is the extent of Jaundice in Gilbert Disease?

A

Mild jaundice with physiological stress

53
Q

Common and affects 2-10% of the population

-appears during or after adolescent years

A

Gilbert Disease

54
Q

Defect due to a mutation in MRP2 resulting in diffuse deposition of coarse granular, dark brown pigment in hepatocytes

A

Dubin-Johnson

55
Q

Appears during adolescence or early adulthood and is more common in iranian and moroccan jews

A

Dubin-Johnson

56
Q

Jaundice is the only symptom of

A

Dubin-Johnson

57
Q

Defect due to biallelic mutations in OAT1B1 and OAT1B3

A

Rotor

58
Q

Rotor occurs shortly after

A

Birth or in childhood

59
Q

What is the extent of jaundice in Rotor?

A

Mild conjugated and unconjugated hyperbilirubinemia

60
Q

The jaundice seen in Rotor is

A

Intermittent

61
Q

Low haptoglobin means

A

Intravascular Hemolysis

62
Q

If direct levels of bilirubin are high

A

Obstructive Jaundice

63
Q

Increased levels of unconjugated bilirubin

A

Hepatocellular Jaundice

GI (59 decks)

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