Jaundice Jigsaw Flashcards

(63 cards)

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
A bile acid with fewer hepatotoxic properties than endogenous bile acids -competes with endogenous bile acids for absorption in the terminal ileum
Ursodeoxycholic acid (UDCA)
26
Ursodeoxycholic acid (UDCA) competes with endogenous bile acids for absorption in the
Terminal ileum
27
Appears to promote the endogenous secretion of bile acid and reduce the cytotoxic potential of endogenous bile acids
UDCA
28
Alters and reduces inflammatory cytokine production, protects cell membranes from disruption, and reduces the display of aberrant HLA antigens
UDCA
29
Breaks one of the methynyl bridges holding the four part ring together, releasing the green pigmented biliverdin, iron, and CO
Heme oxygenase
30
The products of heme oxygenase are shown to be
Cytoprotective
31
Biliverdin is a substrate for biliverdin reductase, producting the red-orange colored
Bilirubin
32
In the liver, adds two molecules of glucuronic acid to bilirubin, making the more water-soluble bilirubin diglucuronide
Bilirubin glucuronyl transferase
33
Bilirubin diglucuronide is secreted into the bile ducts and stored in the gall bladder until they are released into the
Intestine
34
Bacteria in the gut hydrolyze bilirubin and reduce it to a colorless
Urobilinogen
35
Gives urine its yellow color
Urobilin
36
May result due to excess hemolysis of red blood cells
Jaundice
37
Thallasemia, sickle cell anemia, G-6-P dehydrogenase deficiency, etc. may lead to
Jaundice
38
A plasma glycoprotein that binds extracorpuscular hemoglobin (Hb) in a tight noncovalent complex
Haptoglobin
39
Approximately 10% of hemoglobin that is degraded each day is released into the circulation and is thus
Extracorpuscular
40
Too large to pass through the glomerulus
Hemoglobin0haptoglobin complex
41
Low levels of haptoglobin are found in patients with
Hemolytic anemias
42
This is because the Hb-Hp complex has a short
Half-life
43
Thus, during hemolytic anemia when lots of RBC are breaking down and releasing Hb into plasma, we have low levels of
Haptoglobin
44
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
Jaundice
45
Stems from a mechanical obstruction of the bile duct, preventing the "draining" of conjugated bilirubin into the intestines
Obstructive jaundice
46
Both the liver uptake of bilirubin and the conjugation of bilirubin can be affected by
Hepatocellular Jaundice
47
Defect due to the complete absence of the EDP-GT gene
Criggler-Najar syndrome: Type I
48
What is the extent of jaundice in Criggler-Najar syndrome: Type I?
Severe, causing Kernicterus in the brain of the newborn
49
Defect due to a mutation in the UDP-GT gene
Criggler-Najar syndrome: Type II
50
What is the extent of jaundice in Criggler-Najar syndrome: Type II?
Benign
51
Defect caused by the reduction in transcription of UDP-GT due to a mutation in the promoter region
Gilbert Disease
52
What is the extent of Jaundice in Gilbert Disease?
Mild jaundice with physiological stress
53
Common and affects 2-10% of the population -appears during or after adolescent years
Gilbert Disease
54
Defect due to a mutation in MRP2 resulting in diffuse deposition of coarse granular, dark brown pigment in hepatocytes
Dubin-Johnson
55
Appears during adolescence or early adulthood and is more common in iranian and moroccan jews
Dubin-Johnson
56
Jaundice is the only symptom of
Dubin-Johnson
57
Defect due to biallelic mutations in OAT1B1 and OAT1B3
Rotor
58
Rotor occurs shortly after
Birth or in childhood
59
What is the extent of jaundice in Rotor?
Mild conjugated and unconjugated hyperbilirubinemia
60
The jaundice seen in Rotor is
Intermittent
61
Low haptoglobin means
Intravascular Hemolysis
62
If direct levels of bilirubin are high
Obstructive Jaundice
63
Increased levels of unconjugated bilirubin
Hepatocellular Jaundice