CHAPTER 1 - HEMOSTASIS PART 2 Flashcards
retains the blood within the vascular system during periods of injury
(vasoconstriction)
localizes the reaction involved to the site of injury.
(platelet adhesion and aggregation)
repairs and re-establishes blood flow through the injured vessels.
(coagulation and fibrinolysis)
Three Hemostatic Components
1) Extravascular component
2) Vascular component
3) Intravascular component
Play a part in hemostasis by providing back pressure on the injured vessel through swelling and entrapment of escaped blood
Extravascular components
Extravascular components Depends on the:
bulk or amount of surrounding tissue
type of tissue
tone of the surrounding tissue (
Vascular components Depends on the:
Size of the blood vessels
Amount of smooth muscle within their wall
Integrity of the endothelial cell lining
Platelets and biochemicals in the plasma.
Intravascular components
Stages of Hemostasis
Primary Hemostasis
Secondary Hemostasis
Platelet Clot
Primary Hemostasis
Temporary
Primary Hemostasis
Fibrin Clot
Secondary Hemostasis
Permanent
Secondary Hemostasis
activated by desquamation of damaged endothelial cells from small tissue injuries
Primary Hemostasis
Activated by large injuries to the blood vessel, releasing tissue factor.
Secondary Hemostasis
Primary Hemostasis Steps involved:
a) Blood vessel constriction
b) Platelet function cascade
c) Product: Platelet plug formation
Secondary Hemostasis Steps involved:
a) Activation of coagulation proteins.
b) Stabilization of platelet plug.
c) Fibrinolysis.
Platelet function cascade
- Adhesion
- Activation
- Secretion
- Aggregation
Primary Hemostasis Characteristics:
Rapid, shortlived response.
Secondary Hemostasis Characteristics:
Delayed, long term
Regulation: Naturally occurring inhibitors block activated coagulation factors to avoid widespread coagulation.
Secondary Hemostasis
Primary Hemostasis Involves:
(1) Vasoconstriction
(2) Platelet function Cascade
Secondary Hemostasis Involves:
• activation of a series of plasma proteins in the coagulation system until fibrin clot formation
Activated by desquamation and small injuries to blood vessels
Primary Hemostasis
→ Procoagulant substances are exposed or released by damaged or activated endothelial cells
Primary Hemostasis
Activated by large injuries to blood vessels and surrounding tissues
Secondary Hemostasis
→ Tissue factor exposed on cell membranes
Secondary Hemostasis
Involves vascular intima and platelets
Primary Hemostasis
Involves platelets and coagulation system
Secondary Hemostasis
- Slow breakdown & removal of fibrin clot as healing of the injured vessel occurs
Fibrinolysis
lumen becomes small to ctrl blood flow to prevent blood loss
vasoconstriction
During injury, substances like collagen factor will call/attract hemostatic substances.
platelet adhesion and aggregation
bv exposes substances to attract hemostatic components
platelet adhesion and aggregation
collagen activators etc w/in bv
platelet adhesion and aggregation
platelet travels
platelet adhesion and aggregation
complete occlusion (clog)
coagulation and fibrinolysis
sealing plt clog
coagulation and fibrinolysis
a. Repairs -
Coagulation
b. Re-establish -
Fibrinolysis
- Sealer
Coagulation Factor
Vasoconstriction during injury due to surrounding tissues that swells until maipit ang blood vessel.
Extravascular components
(Fleshy part exerts more pressure unlike in the scalp)
bulk or amount of surrounding tissue
(Skeletal tissue: more effective than loose connective tissue = more vasoconstriction = less bleeding)
type of tissue
(“ Elasticity or Flexibility “ - lesser for varicose veins)
tone of the surrounding tissue
Extravascular cells that participates –
a. Fibroblasts
b. Smooth muscle cells
- All are highly pro-coagulant
- Temporary seals
a. Fibroblasts b. Smooth muscle cells
Size of the blood vessels.
- Arteries – thicker & larger
- (?)– harder to seal
-(?) – easier to seal
Thicker
Thinner
(does not easily clot; with strong pressure causing excessive bleeding; with many sm)
Arteries - larger and thicker
(compare the walls of the arteries from that of the veins and capillaries)
Amount of smooth muscle within their wall
have higher amount of SM
Arteries
- Platelet affects endothelial cell lining and make the cessel strong
Integrity of the endothelial cell lining
- arteries have thick walls, but can be a cause of death due to difficulty to seal (longer clotting)
Integrity of the endothelial cell lining
: coagulation factor
Biochemicals
Less important systems:
complement system (inflammation)
kinin system (bradykinin)
serine protease inhibitors
- controls heart beat during hemostais
kinin system (bradykinin)
– regulate clotting, inhibits coagulation, fibrinoloysis; proteins from the liver
serine protease inhibitors
endothelial lining shedding
desquamation
tissue factors and collagen is released from the damaged endothelium
small tissue injuries
Platelet function Cascade:
a. Platelet adhesion
b. Attraction
c. Secretion
d. Aggregation
– change their shape
b. Attraction
– secretes granules and these granules attracts more platelet.
c. Secretion
Activation of coagulation - (?) (proenzyme ) inactivated enzymes
Zymogens
Zymogens Example :
Fibrinogen – inactivated fibrin Factor 10 (inactivated) – Factor 9 (inactivated to Activated form
- assembly area for coagulation factors (in the cell membrane)
Platelet phospholipid
Primary Hemostasis Ends with
(3) platelet plug formation
: These substances work against the coagulation process, preventing blood coagulation.
ANTICOAGULANTS
: initiates the process of fibrinolysis or blood clot degradation.
FIBRINOLYTIC
: substances that keep the blood vessels from narrowing or contracting.
VASODILATOR
Warfarin is an example of this.
ANTICOAGULANT
It causes the blood vessel’s interior (lumen) to widen.
VASODILATOR
: substances that tighten or shrink the blood vessels.
VASOCONSTRICTOR
It causes the blood vessels’ lumen to be smaller.
VASOCONSTRICTOR
: a substance that is necessary for the coagulation of blood to occur.
PROCOAGULANT
These promote/stimulate coagulation, hence known as “hemostatic agents.”
PROCOAGULANT
Examples of these are Tissue factor and FXa.
PROCOAGULANT
• Stimulates vasodilation
Prostacyclin (PGIz)
• Inhibits platelet activation
Prostacyclin (PGIz)
Prostacyclin (PGIz)
Anticoagulant
Heparan sulfate
Anticoagulant
Thrombomoduli n (Endothelial protein C receptor)
Anticoagulant
Fibrinolytic
Tissue factor pathway inhibitor (TFPI)
Anticoagulant
Tissue plasminogen activator (tPA)
Fibrinolytic
Reduces blood flow rate
Adenosine
Adhesion molecules
Procoagulant
von Willebrand factor (VWF) (Weibel-Palade bodies)
Procoagulant
• Coats the endothelial cell surface and weakly enhances activity of antithrombin-III
Heparan sulfate
• Endothelial surface receptor for thrombin (binds and inactivates thrombin)
Thrombomoduli n (Endothelial protein C receptor)
• Enhances anticoagulant and fibrinolytic action of protein C
Thrombomoduli n (Endothelial protein C receptor)
• Controls activation of the extrinsic pathway
Tissue factor pathway inhibitor (TFPI)
• Stimulates vasodilation
Prostacylin
Adenosine
• Required for platelet adhesion to site of vessel injury
von Willebrand factor (VWF) (Weibel-Palade bodies)
• P-selectin; Intercellular adhesion molecules (ICAMs)
Adhesion molecules
• Platelet endothelial cell adhesion molecules (PECAMs)
Adhesion molecules
- help cells stick to each other and to their surroundings.
• Platelet endothelial cell adhesion molecules (PECAMs)
