Anticoagulant, antiplatelet, and thrombolytic drugs are used in the prevention and management of thrombotic and thromboembolic disorders. Thrombosis involves the formation (thrombogenesis) or presence of a blood clot (thrombus) in the vascular system. Blood clotting is a normal body defense mechanism to prevent blood loss. Thus, thrombogenesis may be lifesaving when it occurs as a response to hemorrhage;however, it may be life threatening when it occurs at other times, because the thrombus can obstruct a blood vessel and block blood flow to tissues beyond the clot. When part of a thrombus breaks off and travels to another part of the body,it is called an embolus.
Atherosclerosis is the basic disease process that often leads to pathologic thrombosis. It begins with accumulation of lipidfilled macrophages (ie, foam cells) on the inner lining of arteries. Foam cells develop in response to elevated blood lipid levels and eventually become fibrous plaques (ie, foam cells covered by smooth muscle cells and connective tissue).Advanced atherosclerotic lesions also contain hemorrhages,ulcerations, and scar tissue.Atherosclerosis can affect any organ or tissue, but often involves the arteries supplying the heart, brain, and legs.Over time, plaque lesions become larger and extend farther into the lumen of the artery. Eventually, a thrombus may develop at plaque sites and partially or completely occludean artery. In coronary arteries, a thrombus may precipitate myocardial ischemia (angina or infarction) in carotid or cerebral arteries, a thrombus may precipitate a stroke; in peripheral arteries, a thrombus may cause intermittent claudication (pain in the legs with exercise) or acute occlusion. Thus, serious impairment of blood flow may occur with a large atherosclerotic plaque or a relatively small plaque with superimposed vasospasm and thrombosis. Consequences and clinical manifestations of thrombi and emboli depend primarily on their location and size.Normally, thrombi are constantly being formed and dissolved (thrombolysis), but the blood stays fluid and flow is not significantly obstructed. If the balance between thrombogenesis and thrombolysis is upset, thrombotic or bleeding disorders result. Thrombotic disorders occur much more often
than bleeding disorders and are emphasized bleeding disorders may result from excessive amounts of drugs
that inhibit clotting. To aid understanding of drug therapy for thrombotic disorders, normal hemostasis, endothelial functions in relation to blood clotting, platelet functions, blood coagulation, and characteristics of arterial and venous thrombosis are described.
HEMOSTASIS:
Hemostasis is the process that stops bleeding in a blood vessel. Normal hemostasis involves a complex
process of extrinsic and intrinsic factors.The coagulation cascade is so named because as each factor is activated it acts as a catalyst that enhances the next reaction, with the net result being a large collection of fibrin that forms a plug in the vessel.Fibrin is the insoluble protein that is essential to clot formation.
THROMBOSIS:
Thrombosis is the formation of a clot. A thrombus may form in any vessel, artery, or vein when blood flow is impeded. For example, a venous thrombus can develop as the result of venous stasis (decreased blood flow), injury to the vessel wall, or altered blood coagulation. Venous thrombosis most often occurs in the lower extremities and is associated with venous stasis. Deep vein thrombosis (DVT) occurs in the lower extremities and is the most common type of venous thrombosis. Arterial thrombosis can occur because of atherosclerosis or arrhythmias, such as atrial fibrillation. The thrombus may begin small, but fibrin, platelets, and red blood cells attach to the thrombus, increasing its size and shape. When a thrombus detaches itself from the wall of the vessel and is carried along through the bloodstream, it becomes an embolus. The embolus travels until it reaches a vessel that is too small to permit its passage. If the emboli goes to the lung and obstructs a pulmonary vessel, it is called a pulmonary embolism (PE). Similarly, if the embolus detaches and occludes a vessel supplying blood to the heart, it can cause a myocardial infarction (MI). The anticoagulant drugs are used prophylactically in patients who are at high risk for clot formation
Mechanism of Action
All anticoagulants interfere with the clotting mechanism of the blood. Warfarin and anisindione interfere with the manufacturing of vitamin K-dependent clotting factors by the liver. This results in the depletion of clotting factors II (prothrombin), VII, IX, and X. It is the depletion of prothrombin , a substance that is essential for the clotting of blood, that accounts for most of the action of warfarin.
USES:
Warfarin is used for:
• Prevention (prophylaxis) and treatment of DVT
• Prevention and treatment of atrial fibrillation with
embolization
• Prevention and treatment of PE
• As part of the treatment of MI
• Prevention of thrombus formation after valve
replacement
In most situations, warfarin is the drug of choice, with anisindione reserved for those who are unable to
take warfarin.
ADVERSE REACTIONS:
The principal adverse reaction associated with warfarin is bleeding, which may range from very mild to
severe. Bleeding may be seen in many areas of the body, such as the bladder, bowel, stomach, uterus, and
mucous membranes. Other adverse reactions are rare but may include nausea, vomiting, alopecia (loss of hair), urticaria (severe skin rash), abdominal cramping, diarrhea, rash, hepatitis (inflammation of the liver), jaundice (yellowish discoloration of the skin and mucous membranes), and blood dyscrasias (disorders).
CONTRAINDICATIONS:
Warfarin is contraindicated in patients with known hypersensitivity to the drug, hemorrhagic disease,tuberculosis, leukemia, uncontrolled hypertension, gastrointestinal (GI) ulcers, recent surgery of the eye or central nervous system, aneurysms, or severe renal or hepatic disease, and during pregnancy and lactation.Use during pregnancy (Pregnancy Category X) can cause fetal death.
PRECAUTIONS
Warfarin is used cautiously in patients with fever, heart failure, diarrhea, malignancy, hypertension, renal or
hepatic disease, psychoses, or depression. Women of childbearing age must use a reliable contraceptive to
prevent pregnancy.
INTERACTIONS:
The effects of warfarin may increase when administered with acetaminophen, NSAIDs, beta blockers, disulfiram,isoniazid, chloral hydrate, loop diuretics, aminoglycosides, cimetidine, tetracyclines, and cephalosporins. Oral contraceptives, ascorbic acid, barbiturates, diuretics, and vitamin K decrease the effects of warfarin. Because the effects of warfarin are influenced by many drugs, the patient must notify the nurse or the primary health care provider when taking a new drug or discontinuing use of any drug, both prescription and over-the-counter preparations.
Atherosclerosis is the basic disease process that often leads to pathologic thrombosis. It begins with accumulation of lipidfilled macrophages (ie, foam cells) on the inner lining of arteries. Foam cells develop in response to elevated blood lipid levels and eventually become fibrous plaques (ie, foam cells covered by smooth muscle cells and connective tissue).Advanced atherosclerotic lesions also contain hemorrhages,ulcerations, and scar tissue.Atherosclerosis can affect any organ or tissue, but often involves the arteries supplying the heart, brain, and legs.Over time, plaque lesions become larger and extend farther into the lumen of the artery. Eventually, a thrombus may develop at plaque sites and partially or completely occludean artery. In coronary arteries, a thrombus may precipitate myocardial ischemia (angina or infarction) in carotid or cerebral arteries, a thrombus may precipitate a stroke; in peripheral arteries, a thrombus may cause intermittent claudication (pain in the legs with exercise) or acute occlusion. Thus, serious impairment of blood flow may occur with a large atherosclerotic plaque or a relatively small plaque with superimposed vasospasm and thrombosis. Consequences and clinical manifestations of thrombi and emboli depend primarily on their location and size.Normally, thrombi are constantly being formed and dissolved (thrombolysis), but the blood stays fluid and flow is not significantly obstructed. If the balance between thrombogenesis and thrombolysis is upset, thrombotic or bleeding disorders result. Thrombotic disorders occur much more often
than bleeding disorders and are emphasized bleeding disorders may result from excessive amounts of drugs
that inhibit clotting. To aid understanding of drug therapy for thrombotic disorders, normal hemostasis, endothelial functions in relation to blood clotting, platelet functions, blood coagulation, and characteristics of arterial and venous thrombosis are described.
HEMOSTASIS:
Hemostasis is the process that stops bleeding in a blood vessel. Normal hemostasis involves a complex
process of extrinsic and intrinsic factors.The coagulation cascade is so named because as each factor is activated it acts as a catalyst that enhances the next reaction, with the net result being a large collection of fibrin that forms a plug in the vessel.Fibrin is the insoluble protein that is essential to clot formation.
THROMBOSIS:
Thrombosis is the formation of a clot. A thrombus may form in any vessel, artery, or vein when blood flow is impeded. For example, a venous thrombus can develop as the result of venous stasis (decreased blood flow), injury to the vessel wall, or altered blood coagulation. Venous thrombosis most often occurs in the lower extremities and is associated with venous stasis. Deep vein thrombosis (DVT) occurs in the lower extremities and is the most common type of venous thrombosis. Arterial thrombosis can occur because of atherosclerosis or arrhythmias, such as atrial fibrillation. The thrombus may begin small, but fibrin, platelets, and red blood cells attach to the thrombus, increasing its size and shape. When a thrombus detaches itself from the wall of the vessel and is carried along through the bloodstream, it becomes an embolus. The embolus travels until it reaches a vessel that is too small to permit its passage. If the emboli goes to the lung and obstructs a pulmonary vessel, it is called a pulmonary embolism (PE). Similarly, if the embolus detaches and occludes a vessel supplying blood to the heart, it can cause a myocardial infarction (MI). The anticoagulant drugs are used prophylactically in patients who are at high risk for clot formation
Mechanism of Action
All anticoagulants interfere with the clotting mechanism of the blood. Warfarin and anisindione interfere with the manufacturing of vitamin K-dependent clotting factors by the liver. This results in the depletion of clotting factors II (prothrombin), VII, IX, and X. It is the depletion of prothrombin , a substance that is essential for the clotting of blood, that accounts for most of the action of warfarin.
USES:
Warfarin is used for:
• Prevention (prophylaxis) and treatment of DVT
• Prevention and treatment of atrial fibrillation with
embolization
• Prevention and treatment of PE
• As part of the treatment of MI
• Prevention of thrombus formation after valve
replacement
In most situations, warfarin is the drug of choice, with anisindione reserved for those who are unable to
take warfarin.
ADVERSE REACTIONS:
The principal adverse reaction associated with warfarin is bleeding, which may range from very mild to
severe. Bleeding may be seen in many areas of the body, such as the bladder, bowel, stomach, uterus, and
mucous membranes. Other adverse reactions are rare but may include nausea, vomiting, alopecia (loss of hair), urticaria (severe skin rash), abdominal cramping, diarrhea, rash, hepatitis (inflammation of the liver), jaundice (yellowish discoloration of the skin and mucous membranes), and blood dyscrasias (disorders).
CONTRAINDICATIONS:
Warfarin is contraindicated in patients with known hypersensitivity to the drug, hemorrhagic disease,tuberculosis, leukemia, uncontrolled hypertension, gastrointestinal (GI) ulcers, recent surgery of the eye or central nervous system, aneurysms, or severe renal or hepatic disease, and during pregnancy and lactation.Use during pregnancy (Pregnancy Category X) can cause fetal death.
PRECAUTIONS
Warfarin is used cautiously in patients with fever, heart failure, diarrhea, malignancy, hypertension, renal or
hepatic disease, psychoses, or depression. Women of childbearing age must use a reliable contraceptive to
prevent pregnancy.
INTERACTIONS:
The effects of warfarin may increase when administered with acetaminophen, NSAIDs, beta blockers, disulfiram,isoniazid, chloral hydrate, loop diuretics, aminoglycosides, cimetidine, tetracyclines, and cephalosporins. Oral contraceptives, ascorbic acid, barbiturates, diuretics, and vitamin K decrease the effects of warfarin. Because the effects of warfarin are influenced by many drugs, the patient must notify the nurse or the primary health care provider when taking a new drug or discontinuing use of any drug, both prescription and over-the-counter preparations.
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Unknown - Wednesday 15 December 2010
