Von Willebrand Disease (VWD)
- Blood disorder where blood does not clot properly
How has Von Willebrand Disease relate to evolution?
Propagation
Identified by Erik Adolf Von Willebrand in 1924
In 1960s, combined with factor FVIII and plasma responsible for platelet adhesion
In 1970s, found Ristocetin to induce platelet aggregation
Selective Breeding
Symbiosis between humans and dogs
Breeding Dogs
Spontaneous hemorrhages
Doberman Pinscher
Scottish Terriers
Shetland Sheepdogs
Learning to increase VWF
Treatments
Desmopressin (1977)
Hormonal injection that stimulates body to create more VWF in blood vessels
VWF infusions
Receive regular VWF infusions
Antifibrinolytics
Drugs that blood clots to breakdown
Inheritance
Equal Chance of Male/Female carrying VWD
Receiving VWD Allele from parent
Types A, B, AB blood have higher levels of the VWF
Directional Selection
Type O blood with lower levels of VWF
Mutations
Harmful Mutation
Mutation on chromosome 12
Pseudogene duplicated on chromosome 22
Lack of Von Williebrand Factor (VWF)
Inability to make proper blood clots
Types
Autosomal Dominant
Type 1
Mildest, most common
Autosomal Recessive
Type 3
Rarest, most severe
Lack of Von Willebrand Factor
Glycoprotein
Platelet adhesion
Symptoms
Bruises
Excessive bleeding (Nose, gums, menstral)