Week 6 Hemostasis - Lecture notes 24-28 PDF

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Summary

Professor Eckfield...

Description

Hemostasis - (clotting) disorders and medications

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Homeostatic action to prevent bleeding out from blood vessels -

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By action of clot

Make sure that normal blood vessels are clot-free and have normal cv function

Definition: arrest of bleeding, or prevention of blood loss after blood vessel injury (platelets, clotting factors; clotting proteins) -

When inadequate: bleeding

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Excessive: clotting/ thrombosis, embolus (too many clots/ clots too big)

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Injury to vessel -

Forming foundation layer w/ platelet layer -

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Leads to fibrin clot

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Tunica intima = Endothelial cells secrete endocrine = helps vasoconstriction

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Tunica media = (smooth muscle) help vessel contract/ dilate

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Tunica externa = (connective tissue) initiates platelets to start clumping together

Platelets = major component of blood/ blood clot -

Stick to walls of blood vessel

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Secrete substances to call more platelets to site

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Platelets to stick together to clot

Stages of clotting (temporary/ overlapping stages)

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Primary hemostasis -

Immediate vasoconstriction to minimize blood loss

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Platelet aggregation

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Formation of platelet plug

Secondary hemostasis -

Activation of clotting factor cascade through intrinsic and extrinsic pathway to produce complete fibrin clot

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Common pathway factor x to Xa for formation of Fibrin (insoluble strands)

Final stage (fibrinolysis or thrombolysis to dissolve clot) -

Clot retraction

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Activation of plasmin to dissolve clot

Primary hemostasis - (vasoconstriction/ platelet aggregation) -

Exposure to collagen (enothelin from endothelial cells)

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Immediate vasoconstriction to minimize blood loss

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Platelet aggregation

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Serotonin (secretary granules)- recruit cells to clot site

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Adp (secretary granules)

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Thromboxane A2 (secretary granules)

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Von Willebrand factors (vWF) - found in endothelium

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Platelet degranulation

How platelets cells get activated -

Change shape, become granules and become sticky

Platelet function -

Collagen-containing sub-endothelial tissue is exposed

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Platelets are attracted to vessel injury site (15-20 sec)

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Platelets beginning to fill endothelial gaps

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Platelets degranulate (release granules: ADP, thromboxane A2)

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Von willebrand factor = from endothelial tissue -

Secreted when there’s injury to blood vessel

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Purpose: join platelets together (bridge between platelets and membrane)

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Important for production of Clotting Factor VIII

Platelet degranulation products for platelet aggregation -

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Serotonin and histamine -

Immediate vasoconstriction

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Promotes platelet degranulation

Thromboxane A2 -

Vasoconstriction

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Promote platelet degranulation

Adp -

Stimulate platelet aggregation by causing their plasma membranes to be ruffly and sticky -

Promote nearby platelets to degranulate

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GPIIb/IIIA receptors -

Primary mediators of platelet aggregation

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Found in surface of plasma membrane

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Purpose: to bind to fibrinogen & membranes (vWF)

Platelet factor 3 -

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Stimulate coagulation cascades

Platelet factor 4 -

Heparin neutralizing factor

Formation of hemostatic plug -

Tissue injury

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Platelet adhesion (exposed to collagen) - releases substances to activate platelets

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Shape of platelets change

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Platelet aggregation

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Secretion of granules (ADP, etc) - to call other platelets

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Form hemostatic plug

Process of hemostasis -

Blood coagulation factors -

Factors II (prothrombin), VII, IX, X, protein C and S are dependent on vitamin K for synthesis

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Antithrombin III and protein C promote anticoagulation -

Heparin enhances antithrombin III

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Protein S assists protein C in binding to phospholipase and stimulate the release of tissue plasminogen activation, initiating fibrinolysis

Clotting factor activation -

Intrinsic (XII, XI, IX, VIII)

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Extrinsic (VII) -

Vitamin K dependent

Clotting activation factor -

coumadin - decrease clotting factor

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Vitamin k - to increase clotting factor...