Heparins and Heparin-Induced Thrombocytopenia

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Nowadays, there are many ways to be used to prevent deep vein thrombosis and the development of pulmonary embolism. Heparin is one of the well-known blood thinners that could be used to treat problems with blood and myocardial infarctions. Though heparin is not actually an anticoagulant, it performs the function of a catalyst in plasma antithrombin III (Little, Falace, Miller, & Rhodus, 2012). It is important to know its pathophysiology and recognize its forms to make the correct choice.

Pathophysiology of Heparin

The peculiar feature of heparin is that it has to be taken parentally only because of its inability to be absorbed through the gut. It could be injected under skin frequently because it has a short biologic life. Therefore, it is necessary to give enough Heparin that may include 1400 units/h (DeLoughery, 2014). In the body, heparin is used to make anti-thrombin (AT), a serine protease inhibitor, a better inhibitor for proteases that are activated by each other in the coagulation cascades (Hoffman, 2010). Negatively charged molecules of heparin are bound with positively charged molecules of AT. This connection causes changes that result in the inactivation of thrombin. Heparin-induced thrombocytopenia (HIT) is one of the most serious side-effects of heparin observed in people. HIT pathophysiology is dynamic and complex because it depends on the way of how activated platelets, coagulation proteins, and monocytes behave (McKenzie & Sachais, 2014). The formation of an immune complex occurs that could be recognized as a foreign substance in the organism and the necessity to form an antibody against it. As soon as the antibody is formulated, it destroys platelets and promotes thrombocytopenia.

Common Conditions of Heparin

Stroke

In many hospitals, heparin is used intravenously in order to reduce stroke damage or stroke risks that are usually connected with the formation of thrombus in leg veins and artery blockage in lungs. Strokes are directly associated with the creation of blood clots. It is necessary to scan the brain of a stroke patient and clarify if there are the cases of bleeding. If no bleeding is discovered, heparin could be offered. However, heparin may not dissolve the already present blood clots but just prevent their growth and reduce the possibility of stroke. At the same time, heparin could be the reason for another stroke in case bleeding begins.

Blood Clots

The analysis of heparin proves that this medication helps to prevent the formation of new blood clots and the growth of the already existing clots in the blood. Heparin has a possibility to inactivate thrombin and prevent the creation of fibrin clots. It should be slowly injected into a vein, never in muscle, six or even more times per day. Much attention should be paid to the use of heparin in mesenteric ischemia and the creation of an embolus that usually occurs in the superior mesenteric artery (SMA). It is necessary to remove the embolus in a short period of time and reduce the possibility of its development, heparin could be used through a catheter that is placed in the SMA.

Work of Heparin in the Drip Form

Heparin drip is usually prescribed after surgeries in order to avoid the possibility of stroke risks and thrombosis. The drip form helps to avoid unexpected outcomes and achieve the required results with ease reverse and absent renal dosing.

References

DeLoughery, T.G. (2014). Heparins and heparin-induced thrombocytopenia. In T.G. DeLoughery (Ed.), Hemostasis and thrombosis (pp. 111-116). New York, NY: Springer.

Hoffman, M. (2010). Heparins: Clinical use and laboratory monitoring. Laboratory Medicine, 41(10), 621-626.

Little, J.W., Falance, D., Miller, C., & Rhodus, N.L. (2012). Dental management of the medically compromised patient. St. Louis, MO: Elsevier Health Sciences.

McKenzie, S., & Sachais, B.S. (2014). Advances in the pathophysiology and treatment of heparin-induced thrombocytopenia. Current Opinion in Hematology, 21(5), 380-387.

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