University:
Glendale Community College
Course:
BIO160 | Introduction to Human Anatomy and Physiology
Academic year:

2019
Views:

310

Pages:

8
Author:

Jamison Bradshaw

Hemostasis 1) Vascular Spasm: Vasoconstriction reduces bleeding 2) Platelet Plug Formation: platelets adhere to exposed collagen fibers 3) Blood Clotting: RBCs and more platelets become enmeshed in fibrin threads 1) Vascular Spasm • Prompt constriction of a broken blood vessel • Triggers for a vascular spasm: – some pain receptors directly innervate smooth muscle surrounding the blood vessel • lasts only a few minutes – injury to smooth muscle • longer-lasting constriction – platelets release serotonin which is a chemical vasoconstrictor 2) Platelet Plug Formation • Normal endothelium is very smooth and is coated with prostacyclin (an ecosanoid that repels platelets) • Broken vessel exposes rough surfaces of collagen • Platelet plug formation: – platelet pseudopods stick to damaged vessel and other platelets – pseudopods contract and draw walls of vessel together forming a platelet plug – platelets degranulate releasing a variety of substances • serotonin is a vasoconstrictor • thromboxane, an eicosanoid that promotes aggregation and degranulation of platelets and vessel vasoconstriction • Positive feedback cycle is active until break in vessel is sealed 3) Blood Clotting (Coagulation) • Clotting is the most effective defense against bleeding – conversion of soluble plasma protein fibrinogen into insoluble fibrin threads that form the framework of a clot • Clotting Factors are always present in the plasma and in tissues – activating one factor will activate the next to form a reaction cascade • Factors released by damaged blood vessel tissues cause the extrinsic cascade pathway to begin. • Factors found only in the blood itself causes the intrinsic cascade pathway to begin (platelet degranulation). • Both cascades normally occur together and lead to a fibrin clot. Colorized scanning electron micrograph of a blood clot removed from the coronary artery of a patient with acute myocardial infarction showing he fibrin meshwork (brown) with trapped red blood cells and a cholesterol crystal (yellow). Science Vol 335 February 10, 2012 Coagulation Pathways • Extrinsic Pathway – Factors released by damaged tissues cause the extrinsic cascade pathway to begin which usually lasts about 15 seconds. • Intrinsic Pathway – Factors released by platelets start the intrinsic cascade pathway which usually lasts about 3-6 minutes. • Calcium is required for both pathways. Completion of Coagulation • Both the intrinsic and extrinsic pathways lead to production of Factor X. • Factor X produces key enzymes for activating Thrombin which converts soluble fibrinogen into an insoluble fibrin polymer. • Thrombin also feeds back on the system to amplify its own production. Coagulation Disorders • Unwanted coagulations: – Thrombosis = abnormal clotting in unbroken vessel • most likely to occur in leg veins of inactive people • clots can travel from veins to lungs producing a pulmonary embolism • death can occur from hypoxia – Embolism: abnormal clot traveling in a blood vessel • Infarction, or tissue death, may occur if clot blocks blood supply to an organ – Myocardial Infarction (MI) – Stroke (brain clot or bleed) – 650,000 Americans die annually of thromboembolisms