hemostasis lecture Flashcards
(24 cards)
platelets contain
- actin & myosin
- cell contraction
- empty vesicles*
- mitochondria (ATP & ADP*)
- remnants of the ER (Ca++ storage)
- Cyclooxgenase (COX1)
- thromboxane A2
- Fibrin stabilizing factor (clot stability)*
- Platelet-derived growth factor (repair)*
- Serotonin (5-HT)
platelet cell membranes express
• Glycoproteins • when activated, sticky • Phospholipids • including platelet factor 3 • Important in activation of clotting cascade
• Receptors for collagen
four steps of hemostasis
- vascular spasm
- formation of a platelet plug
- formation of a blood clot
- repair of damage
primary causes of vascular spasm
- myogenic
- platelet factors: serotonin, thromboxane A2
- neuronal reflex is not necessary or sufficient
Step 2 - Formation of a platelet plug
•collagen exposed
•platelets will bind to collagen (2 step
process)
Von Willebrand Factor
- Plasma protein
* bind between collagen and platelet (receptor).
platelet activation
after intigrin receptor binds collagen platelet becomes activated
- swells
- extends podocytes
- contraction
- granules leave platelet
- platelet sticks to vessel wall and each other
thromboxane A2 and ADP
- cause platelets to stick to vessel wall and each other
Step 3 Blood coagulation
Clot Retraction •get rid of excess fluid within clot •solidify clot •platelets required •bind fibrin polymer together •actin and myosin in platelet - contraction •also requires calcium
Step 4 - Repair of damage
Secreted by platelets: •Platelet-derived Growth Factor • stimulate fibroblast to grow into area. • Fibroblasts differentiate into smooth muscle, etc... to close the hole.
Plasminogen
•made by liver
•floating in plasma
•not active form
- breaks up clots
what activates plaminogen to plasmin?
•Tissue plasminogen activator
•released by damaged tissue
- by protein C inactivating TPA inhibitor
Preventing Clotting
1) smooth surface
2) membrane proteins (glycocalyx)(thrombomodulin)
3) protein C
How did his atherosclerosis increase his
risk for a clot?
Exposing platelets to an atherosclerotic plaque will cause the platelets to rupture, triggering activation of circulating platelets and initiating the clotting cascade as well.
vit k dependent factors
II, VII, IX, X
vit k deficiency
coagulation becomes impaired due to decreased function of factors
factor 13a
stabilizes fibrin monomers by crosslinking
aPTT
screen for intrinsic and common pathway
XII, HMWK, prekallekrein, XI, IX, VIII (von willebrand disease), X, V, II, Fibrinogen (I)
PT
screen for extrinsic and common pathway
VII, X, V, II, fibrinogen (I)
heparin therapy
anticoagulant inhibits factor IIa, IX, Xa
hemophilia A
def factor VIII
hemophilia B
def factor IX
coumadin (warfarin therapy)
inhibits pathway for vit K utilization necessary for factors II, VII, IX, X
vit k deficiency
decreased levels of factors II, VII, IX, X
