Blood 2

platelets

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