Studied by 2 peopleplatelets
fragments of megakaryocytes, age quickly and have a short life cycle
platelet functions
form temporary platelet plug that helps seal breaks in blood vessels
Nitric oxide (NO)
keeps circulating platelets inactive and mobile
normal platelet count
150,000-400,000 platelets/ml of blood
hemostasis
fast series of reactions for stoppage of bleeding, requires clotting factors
3 steps of hemostasis
vascular spasm, platelet plug formation, coagulation (blood clotting)
vascular spasm
vessel constricts in response to endothelial cell injury (direct injury to vascular smooth muscle and chemicals released by endothelial cells and platelets), most effective in smaller blood vessels and can significantly reduce blood flow until other mechanisms kick in
platelet plug formation
platelets stick to collagen fibers (connective tissue) that are exposed when vessel is damaged
ADP effect on platelet plug formation
causes more platelets to stick and release their contents
Serotonin and thromboxane A2 effect on platelet plug formation
enhance vascular spasm (constriction) and platelet aggregation
platelet positive feedback cycle
as more platelets stick, they release more chemicals, which cause more platelets to stick and release more chemicals
coagulation (blood clotting)
reinforces platelet plug with fibrin threads, blood is transformed from liquid to gel, coagulation occurs in 3 phases
Coagulation phase 1
initiated by one or both of 2 pathways (intrinsic and extrinsic), eventually leading to factor X (factor 10) to form prothrombin activator
intrinsic pathway
clotting factors are present within the blood, relatively slower than extrinsic
extrinsic pathway
factors needed for clotting are located outside the blood, triggered by exposure to Tissue factor (TF), relatively faster than intrinsic
Coagulation phase 2
prothrombin activator transforms prothrombin to thrombin
coagulation phase 3
thrombin turns fibrin into the gel-like mesh
anticoagulants
factors that normally dominate in blood to inhibit coagulation
clot retraction
actin and myosin in platelets contract, contraction pulls on fibrin strands and draws ruptured blood vessel edges together
platelet derived growth factor (PDGF)
released by platelets, stimulates division of smooth muscle cells and fibroblasts to rebuild blood vessel wall
vascular endothelial growth factor (VEGF)
stimulates endothelial cells to multiply and restore endothelial lining
fibrinolysis
breaking down fibers, process where clots are removed after repair is completed
thrombus
clot that develops and persists in unbroken blood cells, typically not fully blocking off a blood vessel
embolus
a thrombus that freely floats in the bloodstream
embolism
embolus obstructing a vessel, can lead to a hypoxic environment for cells and later non functioning tissue
anticoagulant drugs
aspirin, heparin, warfarin
thrombocytopenia
deficient number of circulating platelets, platelet count less than 50,000 platelets
hemophilia
most common is type A (factor 8 deficiency), hereditary
Blood types
A, B, AB, O
AB blood
no antibodies, universal recipient
B blood
anti-A
A blood type
anti-B
O blood types
anti-A and anti-B, universal donor
hemolytic disease of newborn (erythroblastosis fetalis)
first pregnancy: Rh- mom gets exposed to Rh+ blood of fetus causing mom to synthesize anti-Rh antibodies, no illness/disease
second pregnancy: mom’s anti-Rh antibodies cross placenta and destroy RBCs of Rh+ baby
