Abstract

A COMPARITIVE STUDY OF APPROACHES TO MODULATE THE PHARMACOTECHNICAL PROPERTIES OF BCS CLASS III DRUG

*Prashant Ramdas Kadam, Saddam Rashid Pathan, Rini Punathil, Dr. Akshay D. Meshram

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Abstract

Anticoagulants are medicines that facilitate stop formation of blood clots. They're given to individuals at a high risk of obtaining clots and to scale down their possibilities of developing serious conditions like strokes and heart attack. A blood clot acts as a seal created by the blood to prevent loss of blood from wounds. Whereas they're helpful in stopping bleeding, sometimes they may block blood vessels and reduce blood flowing to organs such as the brain, heart or lungs if they are generated within the wrong place. Anticoagulants work by interrupting the events concerned in the formation of blood clots. They're sometimes referred to as "blood-thinning" medicines, though they don't truly make the blood thinner. Though they're used for common purposes, anticoagulants differ completely from antiplatelet medicines, like low-dose Aspirin and clopidogrel. If flow of blood through a blood vessel is blocked by a clot, the affected part of the body will become short of oxygen and it will not work smoothly. Medical care involving use of anticoagulants is suggested within the case of stroke, deep vein thrombosis (DVT), pneumonic embolism, atrial fibrillation, etc. Treatment with anticoagulants could also be counselled if your doctor feels you're at an enhanced risk of developing one or more problems enlisted above. This may be as a result of your medical history of having blood clots within the past or a condition like atrial fibrillation may develop and trigger formation of blood clots. In case of vitamin K antagonists (VKA) like aspirin, warfarin dose is set on a personal basis (no fix dose), whereas novel Non-vitamin K oral anticoagulants (NOACs) are administered in fixed doses, except in case of individuals with impaired functioning of liver or kidney. NOACs lead to direct inactivation of thrombin (FIIa) and prothrombinase (FXa) and therefore also known as direct oral anticoagulants or target anticoagulants APX falls within the class of NOACs. Clotting is initiated once the integrity of the endothelium is breached. Factor VIIa and tissue factor (TF) lead to formation of complex of the TF– factor VIIa, that subsequently activates factor X and factor IX. Thrombin is then converted to thrombin by Factor Xa. The little quantity of thrombin produced amplifies coagulation by activating factor V, antihaemophilic globulin and platelets. Factor VIIIa & factor IXa get together to form the factor IXa–factor VIIIa– phospholipid complex – a key activator of factor X. Factor Xa binds to negatively charged lipoid surfaces (e.g. activated platelets), and along with factor Va forms the coagulation factor advanced the central coagulation factor activator that converts prothrombin to thrombin (Figure 1.2). Thrombin contains a central role within the natural process of clotting, as well as changing soluble coagulation factor to fibrin, activating platelets and activating clotting factor to induce fibrin cross-linking. Blood-borne TF has been known on microparticles derived from leukocytes and different cell varieties that are concerned in the initiation of coagulation once vessel injury is proscribed to activation of endothelial tissues.

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