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33 Cards in this Set
- Front
- Back
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T or F: DNA for the ABO blood groups codes for an enzyme.
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True
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T or F: Types A, B, and O blood group antigens are alleles - expressed from the same gene.
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True
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What is required for the ABO alleles to be expressed?
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The H antigen
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What is front and back typing?
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Blood banks want to know what antigen is on the RBC and what is in the plasma
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What antibodies do each of the ABO groups make?
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Group A = anti-B Ab
Group B = anti A Ab Group AB = none Group O = anti A and anti B Abs |
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The difference between the A and B genes is how many nucleotides, and what what does that result in?
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7 nucleotides
Results in 4 amino acid substitutions *Only 1 difference between A and O |
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Which amino acid is most important in making an A an A, or a B a B?
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Amino acid #268
Glycine - A Alanine - B Codes for specificity of enzyme pocket, which differs between A and B in what they can add to the H Ag |
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T or F: Recombination between an O allele with part of a B allele can produce an A allele.
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True
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Which blood type is the universal donor? Universal recipient?
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Type O is donor
Type AB is recipient |
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What is the Bombay phenotype?
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Normally, genotype is HH or Hh for the H antigen
Bombay phenotype results when person is hh for H antigen, so they are blood type O regardless of presence of A or B enzymes *Causes problems at the blood bank |
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If the father is type O and has the Bombay phenotype, the mother is AO, and the son is AB, what must be true of the father?
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He must have a B allele even though he is type O
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What is another unique feature of those with the Bombay phenotype and what must these people do?
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They are the universal rejectors
Patients must donate their own blood to the blood bank for later use |
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T or F: Blood type does not vary by race.
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False!
Most type A is in Alaska/Canada, while there is none in South America Type B is Central Asia Type O almost all in South America |
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Describe the RH antigens.
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Glycoprotein
43 antigens determined by 2 genes Gene for the RhD antigen Gene for the RhC and RhE antigens |
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How do we get Rh+ and Rh-?
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Recombination leads to the loss of the RHD gene and the "d" phenotype
+ = RHD and RHCE - = RHCE |
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What is hemolytic disease of the newborn?
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RH incompatibility - potentially severe
Rh+ man marries an Rh- woman During first pregnancy mom can become sensitized to Rh antigen and make anti-Rh antibodies Second child, if Rh+, can get hemolytic disease from the Rh antibodies from mom |
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How is hemolytic disease of the newborn prevented?
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Rhogam
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What two proteins compete for binding sites at TFR1?
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HFE and transferrin
Transferrin binds TFR1 better |
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What happens when HFE binds TFR2?
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Stimulates hepcidin expression
Happens when there is too much Fe** |
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What does hepcidin do?
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Down regulates transport of Fe out of enterocytes by destroying ferroportin
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Too little HFE can cause what? And how?
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Hereditary hemochromatosis
Decreased HFE means less binding to TFR2, resulting in less hepcidin, leading to increased Fe transfer out of enterocytes |
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What is hereditary spherocytosis?
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A hemolytic anemia characterized by spherical and fragile RBCs that lyse and release hemoglobin
Caused by mutations in genes for the erythrocyte membrane skeleton |
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How does hereditary spherocytosis present?
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Hemolysis, anemia, splenomegaly
Ranges from mild to severe anemia and can be fatal |
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What does the erythrocyte membrane skeleton do and what is it made of?
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Confers property of durability and stability to the RBCs
Spectrin |
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What test can help diagnose hereditary spherocytosis?
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Osmotic fragility test - used to measure RBC resistance to hemolysis
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What is hereditary elliptocytosis (stats, overview)?
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Autosomal dominant
1 in 2000-4000 All races, more common in blacks Mutation in spectrin Asymptomatic Lab findings: Elliptocytosis, no anemia, no hemolysis, normal osmotic fragility |
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What is hereditary spherocytosis (stats, overview)?
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Autosomal dominant
1 in 5000 but 1:2000 More common in northern European descent Mutation in spectrin Asymptomatic to moderate/severe anemia, splenomegaly Lab findings: reticulocytosis, spherocytosis, increased osmotic fragility |
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What is hereditary pyropoikilocytosis?
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Autosomal recessive
Rare Predominantly in blacks Mutation in spectrin Splenomegaly, aplastic crises Lab findings: severe hemolysis, poikilocytes, microspherocytes, increased osmotic fragility |
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Describe the G6PD cascade.
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Starts with H2O2, which can be removed by glutathione peroxidase by donating an electron to form H2O
The now oxidized glutathione is reduced by NADPH, forming NADP G6PD can generate NADPH from glucose metabolism |
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What happens if you have a G6PD deficiency?
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Cannot regenerate NADPH from glucose metabolism, so you are unable to rid the body of H2O2 and the result is hemolytic anemia
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What is methemoglobin?
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Formed by interaction of Hb with H2O2 and free radicals
It is unable to bind oxygen |
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What are "Heinz bodies" and "bite cells"?
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Heinz bodies are an erythrocytic inclusion from methemoglobin precipitate - stains purple
Bite cells are cells that have the Heinz bodies removed by macrophages in the spleen |
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There is one gene, two alleles for G6PD. What are they and what's the difference?
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G6PDA+/- is self limiting and not life threatening since the enzyme has 10-20% activity
G6PDB+/- causes acute hemolysis and is life threatening (fava bean induced hemolysis) due to barely detectable enzyme activity |
