AntiCoag Flashcards
Finely regulated dynamic process of maintaining fluidity of
the blood, repairing vascular injury, and limiting blood loss while avoiding vessel occlusion (thrombosis) and inadequate perfusion of vital organs
Hemostasis
inactived if there are no injuries and because
of the intrinsic presence of anticoagulants
Platelets
Common causes of dysregulated hemostasis
○Hereditary or acquired defects in the clotting
mechanism
○ Secondary effects of infection or cancer
designed to stop bleeding at the site of vascular injury
through complex interactions between the vascular endothelium, platelets, procoagulant proteins, anticoagulant proteins, and fibrinolytic proteins
Coagulation System
THREE LAYERS OF BLOOD VESSELS
Endothelin
Subendothelium
Smooth Muscle
Endothelin produces
Nitric Oxide and Prostacyclin
Layer of the bv that heparin sulfate and thrombomodulin
Endothelin
A Natural coagulant
Heparin sulfate
Once bound, clotting factors II, IX, X will be
inactivated
Heparin sulfate
Heparin sulfate attracts and binds _________
antithrombin III
Composed of fibroblasts with abundant elastic and collagen fibers
Subendothelium
Changes vessel diameter to regulate blood flow and blood pressure
Smooth Muscle
Primary Hemostasis
Vascular constriction
Primary platelet plug formation
Secondary hemostasis
○ Clot propagation through fibrin formation ○ Coagulation cascade
○ Clot retraction/ repair
○ Fibrinolysis
The initial phase of the blood coagulation process is ____________
vascular constriction
T/F: Activation of platelets is absolutely required for hemostasis to proceed.
True
Platelets become activated by ___________
thrombin
Platelets clump by binding to ___________ that becomes exposed following rupture of the endothelial lining of vessels.
collagen
To ensure the stability of the initially loose platelet plug, a _____________ mesh (also called the clot) forms and entraps the plug.
fibrin
_____________ will bind to the smooth muscle and will
cause contraction
Endothelin
Pain is felt because of the
nociceptors
T/F: Nitric oxide and prostacyclin will not be released because of the injury therefore, platelets will be activated
True
Damaged endothelium layer will secrete
Von Willebrand Factor (VWF)
This exposes platelets to collagen thus a change in the shape of collagen can be obserbed
Von Willebrand Factor
activates phospholipase A2 (PLA2) which will be used in the synthesis of arachidonic acid (AA).
Calcium
Arachidonic acid requires ____________ in order to metabolize to form thromboxane.
cyclooxygenase (COX)
The end of the platelet plug will provide a __________ environment that will allow the coagulation cascade to proceed
negative
Intrinsic
12 -> 11 -> 9 -> 8 ->
Extrinsic
3 -> 7
Common Pathway junction
Intrinsic : 8 (with help of 3 and Ca) will activate X
Extrinsic: after 7a, PF4 and Ca will complex and activate X
will attach to Factor X and will activate Prothrombin (II) and Thrombin (Ila)
Factor 5
T/F: Prothrombin III is not too strong so Fibrinogen is needed
True
Activated form of Fibrinogen
Fibrin
activates Fibrinogen (I) to Fibrin (Ia)
Thrombin
insoluble to blood and provides the “jelly” structure of the blood.
Fibrin
In Clot retraction/repair Platelets will release
myosin and actin
contractile proteins that allow
contraction between spaces and connection of both
ends of endothelial tissues
Myosin and Actin
to regenerate cells -> Stimulate the production of endothelial cells and signal mitosis
VEGF (Vascular Endothelial Growth Factor
to regenerate smooth muscle
PDGF (Platelet Derived Growth Factor)
T/F: only VEGF signlas mitosis
False
Irreversible inhibits of Cyclooxygenase
Aspirin
T/F: When taking Aspirin, platelets are permanently inhibited
True
In Aspirin, replacement platelets restore overall function in
3-7 days
T/F: Patient canundergo a surgical procedure within 7 days of aspirin intake
False
dose of aspirin as antiplatelet effect
80 - 160 mg
Aspirin should not be taken with
NSAIDS
T/F: Aspirin should be taken with food
True
Glycoprotein IIb/IIIa Inhibitors
EPTIFIBATIDE, TIROFIBAN