Hemostasis

Vasospasm caused by

is part of primary hemostasis

sympathetic stimulation: norepinephrine

immediate release of endothelin from damaged endothelial cells

release of thromboxane a2, adp, serotonin from activated platelets

platelet plug formation

primary hemostasis

derived from bone marrow megakaryocytes (reach between cells and release fragments called platelets or thrombocytes

stimulated by hepatic and renal thrombopoietin

known as platelets in their resting state

damaged endothelial cells release a glycoprotein known as von willebrand factor which bind to damaged cells and exposed collagen fibers

platelets then go through a confirmation change (along with degranulating) and exposes receptors for resting platelets → loose binding

then fibrinogen is used between platelets to make a more secure clot

platelet degranulation releases

ADP, Platelet activating factor, thromboxane A2, coagulation factors and calcium in preparation for secondary hemostasis

what cellular process mainly associates primary and secondary hemostasis?

platelet degranulation

what molecules prevent platelets from binding to healthy endothelium

prostacyclin

Rickettsial disease

von willlebrand disease

Rodenticide poisoning

main goal of secondary hemostasis

also known as coagulation stage

form a well attached and strong seal of the vessel injury site to stop bleeding until healing of the vessel wall has occurred several days after the injury which is accomplished through a fibrin clot

stages of coagulation

common pathway

coagulation factors and their half-lives

factor VII will disappear first after liver stops working

vitamin K dependent coagulation factors

1972

Tertiary hemostasis

fibrinolysis

DIC (disseminated intravascular coagulation)

greyhound bleeders

hyperfibrinolysis, significance of elevated FDPS= suggests the prsence of ongoing fibrinolysis and severity of DIC