360 - Iron & Bilirubin Flashcards

1
Q

The majority of the body’s iron, approximately 94% is distributed in…

A

hemoglobin, ferritin, and hemosiderin

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2
Q

Less than 0.1% of the body’s iron is present in plasma as…

A

transferrin

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3
Q

a plasma protein that transports ferric iron (Fe3+) from one organ to another

A

apotransferrin

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4
Q

Normally, approximately ___ of the iron binding sites of transferrin are occupied by iron

A

1/3

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5
Q

Plasma iron levels are highest in the ___________ and progressively ______ over the day

A

morning; decline

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6
Q

causes of increased serum iron

A

hemochromatosis

iron meds

hormonal contraceptives

aplastic anemia

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7
Q

causes of decreased serum iron

A

IDA

hemorrhage

menstruation

medication

anemia of chronic disease

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8
Q

TIBC

A

total iron binding capacity

  1. serum iron is measured as described
  2. ferric iron (Fe3+) is added in excess to the sample to saturate the binding sites on transferrin

excess iron is removed by either a silica or anion exchange column, or by the addition of magnesium carbonate; serum iron assay performed after to compare to first measurement

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9
Q

increased TIBC

A

IDA

pregnancy

oral contraceptives

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10
Q

decreased TIBC

A

chronic inflammatory disease

malignanacy

hemochromatosis

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11
Q

major storage form of iron

A

ferritin
- acute phase protein
- found in BM, liver, spleen
- detected by immunoassay

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12
Q

increased ferritin

A

malignancies

chronic infections

hemochromatosis

chronic inflammatory diseases (SLE)

hepatitis (eg. viral)

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13
Q

decreased ferritin

A

IDA

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14
Q

where is apotransferrin produced?

A

produced by the liver and carries ferric iron in the blood; the iron/apotransferrin complex is known as transferrin

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15
Q

how can we measure apotransferrin?

A

immunoturbidimetry

immunonephelometry

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16
Q

increased transferrin

A

pregnancy

administration of estrogen

iron deficiency

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17
Q

decreased transferrin

A

negative AP: rxn to inflammation, malignancy

decreased synthesis: chronic liver disease, malnutrition

protein loss: nephrotic syndrome

18
Q

fecal immunochemical testing (FIT)

A

detects hemoglobin in feces
screening test for colorectal cancer
recommended for 50y/o; test every 2 years

19
Q

FIT test reaction

A

monoclonal or polyclonal Ab + Hb => Ab-Ag product

20
Q

a degradation production of heme

21
Q

main sources of heme

A

aged red blood cells, myoglobin, cytochromes, and peroxidases

22
Q

how is bilirubin transported in blood

A

bound to albumin

23
Q

what happens to bilirubin in the liver?

A

it is conjugated to produce bilirubin monoglucuronide and diglucuronide

both products excreted into intestine with bile

intestine = bilirubin monoglucuronide is hydrolyzed and reduced to form urobilinogen => may further degraded to urobilin

24
Q

method for measuring total bilirubin

A

diazo method (modified Jendraski-Grof method)

Bilirubin + Diazotized sulfanilic acid -> azobilirubin

25
this is used as an accelerant in diazo method as it frees unconjugated bilirubin from albumin
caffeine-benzoate-acetate
26
which wavelength is used to measure bilirubin?
530 nm
27
interefernece in measuring bilirubin
- lipemia = false INCREASE - hemolysis = false DECREASE - exposure to light = false DECREASE
28
Direct spectrophotometry for Unconjugated Bilirubin
- exclusively used for newborn children - [bilirubin] directly determined at 454 nm - bichromatic measurement is used to eliminate interference from oxyhemoglobin > absorbance at 454 nm minus the absorbance at 540 nm equals the true bilirubin absorbance
29
interference of direct spectrophotometry for unconjugated bilirubin
carotenoids absorb at 454 nm, but newborn children do not have carotene
30
neonatal jaundice
- immature livers cannot conjugate bilirubin = cannot synthesize proteins - HbF = increased catabolism of Hb - neonates, intestinal flora not fully developed = conjugated bili does not get reduced to urobilinogen for excretion - hemolytic disease of newborns = increased Hb catabolism - may be treated with UV light therappy
31
Critical levels of unconjugated bilirubin may cause THIS which can result in brain damage (neonatal jaundice)
KERNICTERUS
32
critical balue of total bilirubin in children <30 days old
>300 umol/L
33
pre-hepatic jaundice
Hemolytic anemia may produce more bilirubin than the liver can process
34
hepatic jaundice
Damage to the hepatocytes, or inherited disorders result in the inability to conjugate or excrete conjugated bilirubin, or inability to take up unconjugated bilirubin for conjugation and excretion
35
post-hepatic jaundice
cholestasis - gallstones, spasms, or neoplasms may prevent bilirubin-glucuronide from reaching the intestine
36
inherited disorders of bilirubin metabolism (hepatic jaundice)
Crigler-Najjar Syndrome Type I " Type II Dubin-Johnson Syndrome Rotor Syndrome Gilbert Syndrome Lucey-Driscoll Syndrome
37
Crigler-Najjar Syndrome Type I
complete absence of UDP-glucuronyltransferase, resulting in very high concentrations of unconjugated bilirubin autosomal recessive Kernicterus results in severe brain damage and usually results in death
38
Crigler-Najjar Syndrome Type II
autosomal dominant disorder is the result of a partial deficiency in UDP-glucuronyltransferase. Normal life is expected with phenobarbital administration
39
Dubin-Johnson Syndrome
- autosomal recessive condition with jaundice - elevated levels of conjugated bilirubin with only a slight increase in unconjugated bilirubin - problem involves the excretion of conjugated bilirubin from the hepatic microsomes into the canaliculi
40
Rotor Syndrome
similar to Dubin-Johnson Syndrome.
41
Gilbert Syndrome
probably autosomal recessive with mild unconjugated hyperbilirubinemia. No treatment is required
42
Lucey-Driscoll Syndrome
- caused by an inhibitor of bilirubin conjugation - unconjugated bilirubin levels are increased - occurs in the early neonatal period lasting about 2 -3 weeks post-delivery