Primary Hemostasis Flashcards
Steps of primary hemostasis
Vasoconstriction > Platelet Adhesion > Platelet Aggregation > Platelet Secretion
T/F: Primary hemostasis happens simultaneously
TRUE
Constriction or narrowing of the (lumen) diameter of blood vessel to decrease blood flow
Vasocontriction
What is the purpose of vasoconstriction?
To decrease blood flow to prevent continuous bleeding
This substance reside in the connective tissue will activate platelets
Collagen
Bring deoxygenated blood from body tissues to heart
Veins
Where the gas exchange happen, when venous and arterial blood components are found
Capillaries
Brings oxygenated blood from heart to body tissues
Arteries
Structure of blood vessel: outer most layer
Vascular adventitia
Structure of blood vessel: Middle layer
Vascular media
Structure of blood vessel: Inner most layer
Vascular intima
Made up of simple squamous epithelium cells which are involved in clotting process by producing and storing clotting
Endothelia lcells (endothelium)
The internal elastic lamina the supports the endothelial cells is composed of
Elastin and collagen
Veins are composed of
Collagen and fibroblast
Arteries are composed of
Collagen, Fibroblast and Smooth muscles
This cells produces majority of the collagen
Fibroblast
This matrix regulates the permeability of the inner vessel wall
Connective tissue matrix
Highly active metabolically; involved in clotting process by producing or storing clotting components
Endothelium
A reversible process where platelets stick or bind to the endothelial cells or to a non-platelet surfaces
Platelet Adhesion
A membrane receptor that would expose when platelets are activated
GP Ib
GP Ib will bind to the endothelium (sub-endothelial collagen) with the help of
Von Willebrand Factor (vWF)
This promotes platelet adhesion
vWF
Important components in Platelet adhesion
vWF and Glycoprotein membrane
- Absent: GP IB/IX/V Platelet membrane receptor
- Characterized by giant platelet (giant bernie)/macrothrombocyte
Bernard-Soulier Syndrome (BSS)
- VWF is absent of defective
- Bleeding tendencies/risk *the first lining will not be processed in the injured site
vWF disease
An irreversible process where platelet stick or bind together
Platelet Aggregation
Important components in Platelet aggregation
GP IIb/IIIa receptor, fibrinogen, calcium
When platelets are activated, a change in GP IIb/IIIa receptor allows binding of fibrinogen as well as VWF and fibronectin which result to
Platelet clumping
Fibrinogen is one of the coagulation factor known as
Factor I
Act as glue for GP IIb/IIIa receptors but with the presence or help of calcium
Fibrinogen
Is also one of the coagulation factor also known as FACTOR IV but preferred to be called by its chemical name
Calcium
- Absence of GP IIb/IIIa platelet membrane recepto
- Problem with the aggregation process
Glanzmann thrombasthenia
Lack of fibrinogen
Afibrogenemia
Low levels of normal fibrinogen (functional but decrease in concentration
Hypofibrogenemia
Dysfunctional or defective fibrinogen (normal in count but dysfunctional)
Dysfibrogenemia
An irreversible step where platelets release alpha and dense granules
Platelet secretion
Platelet a-granules (Large Molecules) examples
- B-thromboglobulin
- Factor V
- Factor XI
- Protein S
- Fibrinogen
- VWF
- Platelet Factor 4
- Platelet-derived Growth factor
Platelet Dense Granules (small molecules) examples
- Adenosine diphosphate (activates neighboring platelets)
- Adenosine triphosphate
- Calcium (Ca++)
- Serotonin (vasoconstrictor)
During activation ADP and Ca2+ activates
Phospholipase A2
Phospholipase A2 converts membrane phospholipids to
Arachidonic acid
Cyclooxygenase converts arachidonic acid to
Prostaglandin endoperoxidase
In platelet : Thromboxane synthetase > prostaglandins to
Thromboxane A2
- Caused ionized calcium to be released
- Promoted platelet aggregation
- Promotes vasoconstriction
Thromboxane A2
If this phenomena, it will permanently inactivates cyclooxygenase
Aspirin Acetylation/Aspirin Light Effect
Blocks thromboxane A2 production
Aspirin
Key surface for coagulation enzyme-cofactor-substrate complex formation
Plasma Membrane