Hemostasis and Coagulopathies (copy)

Composition of blood

-Plasma

-Blood Cells

-Thrombocytes(platelets)

-Leukocytes

plasma proteins

immune systems

Erythrocytes

RBCs

4

#of oxygen hemoglobin carry

platelets

help with clotting

leukocytes

white blood cells

pluripotent stem cells

-makes multiple cell types

-master cells

-make blood cells from 3 types of body tissue

*can self renew

myeloid stem cells

circulate in blood

Hemostasis

ability to clot blood

*specifically the lining of a blood vessel

platelet storage

spleen

megakaryocytes

large fragment in bone marrow responsible for creating platelets

thrombopoetin

platelet production

place of platelet formation

liver, kidney, smooth muscle, bone marrow

Plasma protiens

-circulate as inactive procoagulation factors

-most synthesized by liver

-von Willebrand factor made by megakaryocytic and endothelium

calcium factor

works with other clotting factors as a co clotting factor

vWF

platelet adhesion

ADP, TXA2

platelet aggregation

calcium

coagulation cascade

COX-1

catalyzes production of thromboxane A2

-present in most tissues in the body especially GI tract protects from digestive juices

COX-2

catalyzes production of prostacyclin

-sites of inflammation

anticoagulant

-prevents clots

*not break down clots

vessel spasm

restricts blood flow to prevent blood loss

allows epithelial later to start healing

formation of platelet plug

*platelets arrive quickly

-von Willebrand factor is released by epithelial lining

-bind to receptors on collagen fibers to form plug

blood coagulation

prothrombin→ thrombin turns fibrinogen→ fibrin

interinsic factor

-begins in circulation

*initiated by C12

extrinsic pathway

-release mediators when agitated

clot retratction

-repair epithelial lining

-fibrin threads will be stretched and will squeeze plasma out of wounds

plasminogen

forms within clot while clot forms

Clot lysis

Plasminogen activators will turn plasminogen→ plasmin which will digest fibrin

hypercoagulation

-extreme blood clot

-overcoagulation

thrombocytopenia

decrease production

increased destruction

platelets used up in formed clots

coagulation disorder

impaired platelets functions

von willebrand diesease

decrease platelets adhesion

disseminated intravascular coagulation

unregulated thrombin explosion

-too much tissue factor

-leads micro vascular thrombosis and target organ damage

platelets disorder

bleeding diesease