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Summary

This document describes coagulation factors, the coagulation cascade, and clot prevention methods. It covers topics such as intrinsic and extrinsic pathways, and different types of anticoagulants. The document discusses the causes and prevention of blood clots.

Full Transcript

Coagulation factors are primarily produced in the liver ○ Then go to site of injury and go through coagulation cascade The liver synthesizes most of the proteins involved in blood coagulation Factor III (tissue factor- cofactor) and factor IV (calcium ions- calcium in cells ar...

Coagulation factors are primarily produced in the liver ○ Then go to site of injury and go through coagulation cascade The liver synthesizes most of the proteins involved in blood coagulation Factor III (tissue factor- cofactor) and factor IV (calcium ions- calcium in cells are the “microchip” in a computer), are produced by other cells in the body, such as endothelial cells and platelets Coagulation cascade Occurs at the site of injury [“a” is the activated form] ○ Intrinsic pathway: activated by damage to the blood vessel and exposure of collagen Dominated primarily by thromboplastic ○ Extrinsic pathway: triggered by tissue factor (factor III) released from damaged tissues ○ Common pathway: both pathways coverage @ X to produce factor Xa, leading to the conversion of prothrombin (factor II) into thrombin (factor IIa), which in turn converts fibrinogen (factor I) into fibrin Xa is what causes the “Clot” Activated partial thromboplastin time (APTT) ○ Reflects the intrinsic pathway ○ Isolated prolongations of APTT may occur due to deficiencies in factor VIII, IX, XI, or XII Prothrombin time (PT) ○ Reflects the extrinsic pathway ○ Isolated prolongations are commonly due to factor VII deficiency Common pathway ○ Deficiencies in factors V, X, thrombin and fibrinogen prolong both the APTT and the PT Thrombin clotting time (TCT) ○ Measure of the final step in the coagulation pathway ○ Conversion of fibrinogen to fibrin via the action of thrombin ○ Prolongation is due to deficiencies in fibrinogen and direct and indirect thrombin inhibitors Classes and drugs use ○ Factor Xa and direct thrombin inhibitors can be taken home but not heparin and vitamin K antagonists Clot prevention ○ They do not dissolve clots ○ Prevent clots from forming They stop an existing clot from becoming worse; they do not break an existing clot ○ Thrombus: a blood clot that forms abnormally within the blood vessels ○ Embolus: a blood clot becomes dislodged from the vessel wall and travels through the bloodstream (breaks off and travels upstream) People at risk for forming blood clots ○ Artificial heart valves ○ Atrial fibrillation (AF) ○ Acute coronary syndrome (ACS) ○ Deep-vein thrombosis (DVT) ○ Pulmonary embolism (PE) Heparin Endogenous heparin ○ Produced by basophils and mast cells Allergic conjunctivitis with a red eye: mast cells break off and heparin is released = vasodilation ○ Prevents formation and extension of blood clots ○ Does not disintegrate clots that have already formed ○ Permits physiological fibrinolysis

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