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16 Cards in this Set

  • Front
  • Back
what is the relationship between VW factor and blood type
lowest levels with type O
highest levels with AB
what is the defect in VWD type 2B
dominant GAIN of function
the HMW mulitmers bind spontaneously to platelets and are subsequently removed from the circulation (which is why there can be thrombocytopenia with this type)
what is the difference in pathophysiology between type 1 and type 2 vWD
type 1: quantitative
type 2: qualitative
what differentiates type 2 A vWD from type 2b on aggregation studies
2A - get virtually no aggultination with ristocetin
2B get increased agglutination comared to normal
what treatment is contraindicated in type 2B vWD
DDAVP
lab findings in type 1 vWD
normal PT, PTT, platelets
vWF antigen, ristocetin cofactor and f8 all tend to be decreased in parallel
treatment for type 2a vWD
DDAVP
clotting factor concentrates containing f8 and vwf (but not cryo b/c no viral inactivation)
why is DDAVP contraindicated in type 2B vWD
DDAVP causes the release of additonal vWF which is then spontaneously bound to platelets and cleared from the system - worsening the thrombycytopenia
what is the treatment for type 2B vWD
clotting factor concentrates containing both f8 and vWF
what is the defect in type 2N vWD
vWF molecule does not bind factor 8
which types of vWD have decreased levels of F8
type 2N
in this type VWF does not bind F8 and the unbound F8 is rapidly cleared from the system
type 3 - levels are virtually undetactable
potential misdiagnosis in type 2N vWD
hemophilia
who gets type 2N vWD
compund heterozygotes with type 1 VWD or
recessive inheritance
what is the defect in type 2M vWD
abnormal binding site on vWF for platelet GP Ib resulting in reduced ristocetin cofactor activity
how does type 2M vWD differ from other type 2s in terms of multimeric pattern
normal multimeric pattern
(other type 2s have decreased large size multimers)
what are the lab findings in type 3 vWD
virtually no detectable vWF:Ag and markedly decreased f8