Unit 3 - Blood PART E Flashcards
Hemostasis
Process of preventing blood loss (opposite of hemostasis is hemorrhage).
What are the 4 main steps of Hemostasis?
- Vasconstriction (vascular spasm)
- Platelet plug formation
- Coagulation (clot formation)
- Fibrinolysis (Clot dissolution)
- Vasconstriction (vascular spasm)
a. Damage to blood vessel wall activates local pain receptors. Which triggers an increase in SYMPATHETIC ACTIVITY causing vasoconstriction that reduces blood flow to the site of damage.
b. Platelets stick to exposed collagen fibers and release platelet factors (factors = ions/molecules/cytokines), some of which reinforce vasoconstriction including:
i. Serotonin
ii. Thromboxane A2
Platelets stick to exposed collagen fibers and release platelet factors (factors = ions/molecules/cytokines), some of which reinforce vasoconstriction including:
i. Serotonin (from secretory vesicles of platelets)
ii. Thromboxane A2 (from platelet membrane)
- also contribute to platelet aggregation (along with ADP & PAF)
- net result is a growing platelet plug that seals the damaged vessel wall
- Platelet Plug Formation
a. Platelet adhesion
b. Factors involved in platelet aggregation include:
i. Platelet Activating Factor (PAF).
ii. Serotonin
iii. Adenosine diphosphate(ADP)
iv. Thromboxane A2
c. Platelet plug formation cannot spread beyond the site of injury due to secretion of PROSTACYCLIN and NITRIC OXIDE (NO) from surrounding endothelial cells which blocks adhesion and aggregation.
Platelet adhesion
platelets stick to exposed collagen and release factors that attract other platelets to the site (POSITIVE FEEDBACK) that fill in damaged area forming a platelet plug.
Factors involved in platelet aggregation include:
i. PLATELET ACTIVATING FACTOR (PAF).
ii. SEROTONIN (from secretory vesicles of platelets)
iii. ADENOSINE DIPHOSPHATE (ADP) (from platelet mitochondria)
iv. THROMBOXANE A2 (from platelet phospholipids)
ii & iv are VASOCONSTRICTORS
Serotonin & Thromboxane A2 are…
VASOCONSTRICTORS
Platelet plug formation CANNOT spread beyond the site of injury due to what?
secretion of PROSTACYCLIN and NITRIC OXIDE (NO) from surrounding endothelial cells which blocks adhesion and aggregation.
Coagulation
complex process in which fluid blood forms a gelatinous clot
- Coagulation (Clot Formation)
a. Cascade/Network of factor interactions activated through two pathways almost simultaneously:
i. intrinsic Pathway (Contact Activation Pathway)
ii. Extrinsic Pathway (Cell Injury/Tissue Factor Pathway)
b. Each pathway results in activation of Factor X, whose
formation is the start of the common pathway.
c. Factor X combines with Ca2+, Factor V, and phospholipids to form PROTHROMBIN ACTIVATOR.
- Active factor X exerts positive feedback on the extrinsic pathway (activating more Factor VII and Tissue Factor III).
d. Prothrombin activator converts Prothrombin (a plasma protein) into Thrombin.
d. Thrombin acts on Fibrinogen (soluble clotting protein in plasma) to produce insoluble Fibrin polymers. These form a web of thread-like protein that covers the platelet plug and traps formed elements (RBCs).
- Thrombin exerts positive feedback on intrinsic pathway (activates more Factor XI = plasma thromboplastin)
e. ActiveFactorXIII(FibrinStabilizingFactor) converts fibrin into a cross-linked polymer, and stabilizes the clot.
Cascade/Network of factor interactions activated through two pathways almost simultaneously: (eventually merge into 1)
i. Intrinsic Pathway (Contact Activation Pathway)
- Initiated by factors in blood exposed to collagen (tissue factor XII)
ii. Extrinsic Pathway (Cell Injury/Tissue Factor Pathway)
- Initiated by factors in surrounding damaged tissues (Tissue Factor III = Tissue thromboplastin)
Intrinsic Pathway (Contact Activation Pathway)
Initiated by factors in blood exposed to collagen (tissue factor XII)
Extrinsic Pathway (Cell Injury/Tissue Factor Pathway)
Initiated by factors in surrounding damaged tissues (Tissue Factor III = Tissue thromboplastin)
Prothrombin activator converts Prothrombin (a plasma protein) into _____.
Thrombin
- the enzyme that converts FIBRINOGEN into insoluble FIBRIN polymers
- these fibrin fibers become part of the clot