The document discusses anticoagulant and thrombolytic drugs. It begins by describing haemostasis and the coagulation cascade. It then discusses various anticoagulant drugs including heparin, low molecular weight heparins, warfarin, and fondaparinux. It describes the mechanisms of action, pharmacokinetics, clinical uses, monitoring, and adverse effects of these drugs. Reversal of anticoagulation and contraindications are also covered. The target ranges for oral anticoagulants in different clinical conditions are provided. Finally, it lists some drug interactions that can potentiate or antagonize the effects of oral anticoagulants.
The document discusses disseminated intravascular coagulation (DIC), including its causes, clinical features, diagnostic testing, management, and complications. DIC results from excessive activation of coagulation pathways leading to microthrombi formation and bleeding. It is always secondary to an underlying condition like infection, malignancy, trauma, or obstetric complications. Management involves treating the underlying cause, monitoring for bleeding and organ dysfunction, and replacing clotting factors or administering anticoagulants depending on the clinical situation. Complications can be bleeding or thromboembolic in nature. The prognosis depends on the severity of DIC and underlying condition.
The document discusses disseminated intravascular coagulation (DIC), including its causes, clinical features, diagnostic testing, management, and complications. DIC results from excessive activation of coagulation pathways leading to microthrombi formation and bleeding. It is always secondary to an underlying condition like infection, malignancy, trauma, or obstetric complications. Management involves treating the underlying cause, monitoring for bleeding and organ dysfunction, and replacing clotting factors or administering anticoagulants depending on the clinical situation. Complications can be bleeding or thromboembolic in nature. The prognosis depends on the severity of DIC and underlying condition.
1) The document discusses various drugs that can cause bleeding disorders, including heparin, warfarin, thrombolytic agents, and anti-platelet drugs. It provides details on the mechanisms of action and risks of bleeding for each class of drugs.
2) Physiological deficiencies in coagulation factors in neonates can result in bleeding disorders. The pattern of bleeding seen in neonates is different from adults.
3) Minor bleeding from drugs like warfarin may be treated with stopping the drug, while severe bleeding requires vitamin K and clotting factor concentrates. Reversing heparin requires protamine sulfate.
This document provides an overview of anticoagulants and the blood clotting process. It discusses the four phases of blood clotting - vascular, platelet, coagulation, and fibrinolysis. It then describes various types of anticoagulants including heparin, low molecular weight heparins, direct thrombin inhibitors, vitamin K antagonists like warfarin, and new oral anticoagulants. The mechanisms of action, pharmacokinetics, uses, monitoring, and adverse effects of these anticoagulants are summarized. Recommendations for their use during regional anesthesia and general anesthesia are also outlined.
This document discusses drugs used for treating bleeding disorders and provides information on several types of anticoagulant and thrombolytic drugs. It begins by describing the normal coagulation process and then discusses various drugs that work by inhibiting coagulation factors or thrombin, including heparin and related drugs, lepirudin, bivalirudin, argatroban, and drotrecogin alfa. It also covers the oral anticoagulant warfarin, describing its mechanism of action by antagonizing vitamin K and inhibiting the regeneration of reduced vitamin K needed for coagulation factor synthesis.
1) The document discusses various tests of coagulation and platelet function, including bleeding time, activated partial thromboplastin time (aPTT), prothrombin time (PT), thrombin time (TT), and INR. These tests measure different parts of the coagulation cascade.
2) Disseminated intravascular coagulation (DIC) is described as a condition where excessive blood protease activity leads to widespread fibrin formation in blood vessels. Common causes include infection, cancer, trauma, and pregnancy complications. DIC can cause both bleeding and thrombosis.
3) Laboratory findings in DIC may include low platelet count, prolonged aPTT and PT, elevated D-dimer, and presence of
Thrombosis is the development of a ‘thrombus’(clot) consisting of platelets, fibrin, red cells and white cells in the arterial or venous circulation.
If part of this thrombus in the venous circulation breaks off and enters the right heart, it may be lodged in the pulmonary arterial circulation, causing pulmonary embolism (PE).
In the left-sided circulation, an embolus may result in peripheral arterial occlusion, either in the lower limbs or in the cerebral circulation (where it may cause thromboembolic stroke).
The document discusses anti-coagulants and fibrinolytic drugs. It covers the normal coagulation cascade and hemostasis. It then discusses various anti-coagulant drugs including heparin and low molecular weight heparins, which work by potentiating antithrombin. Oral vitamin K antagonists like warfarin are also covered. Fibrinolytic drugs discussed include tissue plasminogen activator, streptokinase and urokinase, which work by converting plasminogen to plasmin to lyse clots. The risks of bleeding are also summarized for anti-coagulant and fibrinolytic therapies.
The document discusses disseminated intravascular coagulation (DIC), including its causes, clinical features, diagnostic testing, management, and complications. DIC results from excessive activation of coagulation pathways leading to microthrombi formation and bleeding. It is always secondary to an underlying condition like infection, malignancy, trauma, or obstetric complications. Management involves treating the underlying cause, monitoring for bleeding and organ dysfunction, and replacing clotting factors or administering anticoagulants depending on the clinical situation. Complications can be bleeding or thromboembolic in nature. The prognosis depends on the severity of DIC and underlying condition.
The document discusses disseminated intravascular coagulation (DIC), including its causes, clinical features, diagnostic testing, management, and complications. DIC results from excessive activation of coagulation pathways leading to microthrombi formation and bleeding. It is always secondary to an underlying condition like infection, malignancy, trauma, or obstetric complications. Management involves treating the underlying cause, monitoring for bleeding and organ dysfunction, and replacing clotting factors or administering anticoagulants depending on the clinical situation. Complications can be bleeding or thromboembolic in nature. The prognosis depends on the severity of DIC and underlying condition.
1) The document discusses various drugs that can cause bleeding disorders, including heparin, warfarin, thrombolytic agents, and anti-platelet drugs. It provides details on the mechanisms of action and risks of bleeding for each class of drugs.
2) Physiological deficiencies in coagulation factors in neonates can result in bleeding disorders. The pattern of bleeding seen in neonates is different from adults.
3) Minor bleeding from drugs like warfarin may be treated with stopping the drug, while severe bleeding requires vitamin K and clotting factor concentrates. Reversing heparin requires protamine sulfate.
This document provides an overview of anticoagulants and the blood clotting process. It discusses the four phases of blood clotting - vascular, platelet, coagulation, and fibrinolysis. It then describes various types of anticoagulants including heparin, low molecular weight heparins, direct thrombin inhibitors, vitamin K antagonists like warfarin, and new oral anticoagulants. The mechanisms of action, pharmacokinetics, uses, monitoring, and adverse effects of these anticoagulants are summarized. Recommendations for their use during regional anesthesia and general anesthesia are also outlined.
This document discusses drugs used for treating bleeding disorders and provides information on several types of anticoagulant and thrombolytic drugs. It begins by describing the normal coagulation process and then discusses various drugs that work by inhibiting coagulation factors or thrombin, including heparin and related drugs, lepirudin, bivalirudin, argatroban, and drotrecogin alfa. It also covers the oral anticoagulant warfarin, describing its mechanism of action by antagonizing vitamin K and inhibiting the regeneration of reduced vitamin K needed for coagulation factor synthesis.
1) The document discusses various tests of coagulation and platelet function, including bleeding time, activated partial thromboplastin time (aPTT), prothrombin time (PT), thrombin time (TT), and INR. These tests measure different parts of the coagulation cascade.
2) Disseminated intravascular coagulation (DIC) is described as a condition where excessive blood protease activity leads to widespread fibrin formation in blood vessels. Common causes include infection, cancer, trauma, and pregnancy complications. DIC can cause both bleeding and thrombosis.
3) Laboratory findings in DIC may include low platelet count, prolonged aPTT and PT, elevated D-dimer, and presence of
Thrombosis is the development of a ‘thrombus’(clot) consisting of platelets, fibrin, red cells and white cells in the arterial or venous circulation.
If part of this thrombus in the venous circulation breaks off and enters the right heart, it may be lodged in the pulmonary arterial circulation, causing pulmonary embolism (PE).
In the left-sided circulation, an embolus may result in peripheral arterial occlusion, either in the lower limbs or in the cerebral circulation (where it may cause thromboembolic stroke).
The document discusses anti-coagulants and fibrinolytic drugs. It covers the normal coagulation cascade and hemostasis. It then discusses various anti-coagulant drugs including heparin and low molecular weight heparins, which work by potentiating antithrombin. Oral vitamin K antagonists like warfarin are also covered. Fibrinolytic drugs discussed include tissue plasminogen activator, streptokinase and urokinase, which work by converting plasminogen to plasmin to lyse clots. The risks of bleeding are also summarized for anti-coagulant and fibrinolytic therapies.
Platelets play a key role in hemostasis. Disorders of platelets can be quantitative, involving too few or too many platelets, or qualitative, involving platelet function defects. Common causes of thrombocytopenia include decreased production, increased destruction, sequestration, or pseudothrombocytopenia. Immune thrombocytopenic purpura is an immune-mediated disorder treated with steroids, IVIG, or splenectomy. Thrombotic thrombocytopenic purpura involves a deficiency in ADAMTS13 treated with plasma exchange. Von Willebrand disease involves defects in von Willebrand factor.
This document discusses coagulation, anticoagulants, and fibrinolytics. It begins by describing the coagulation cascade and fibrinolysis system, which work to stop bleeding through platelet plug formation and blood clotting. It then discusses natural anticoagulants like prostacyclin and antithrombin III that prevent inappropriate clotting. Various coagulants and anticoagulants are outlined, including heparin and low molecular weight heparins, vitamin K, and newer oral anticoagulants. Adverse effects and clinical uses of different agents are also summarized.
The document provides an overview of anticoagulants and their clinical use. It discusses hemostasis and the mechanisms of coagulation. It then classifies anticoagulants as oral, parenteral or antiplatelets. The document focuses on warfarin and heparin, describing their mechanisms of action, dosing, and perioperative management considerations for patients receiving these anticoagulants. It emphasizes balancing the risks of bleeding and thromboembolism during the perioperative period.
DIC is one condition that always trouble patients and doctor, though its a nightmare for any clinician , its also a potent question in both UG and PG exams. I hope this will help you in answering those questions well.
Platelets are cell fragments that originate from megakaryocytes and play a key role in hemostasis. The normal platelet count is 150,000-450,000/L. Thrombopoietin regulates platelet production in the liver and spleen. When the endothelium is damaged, platelets adhere through von Willebrand factor and become activated, releasing granule contents that promote clot formation. Thrombocytopenia can result from decreased production, increased destruction, or sequestration and has various acquired and inherited causes. Disorders like immune thrombocytopenic purpura and thrombotic thrombocytopenic purpura involve autoimmune or inflammatory platelet destruction.
Disseminated intravascular coagulation (DIC) is a syndrome characterized by widespread activation of coagulation that can occur as a result of various underlying conditions. It results from an imbalance between coagulation and anticoagulation processes in the body. DIC can be acute, with bleeding and shock being dominant symptoms, or chronic, where thrombosis and clotting may predominate. The most common triggers of DIC are infectious diseases, cancer, obstetric complications, and severe tissue injury. Diagnosis involves identifying symptoms of bleeding and thrombosis, abnormal laboratory coagulation test results, and ruling out other conditions. Treatment focuses on treating the underlying cause, replacing coagulation factors, platelets, and fibrinogen, and
Blood coagulation involves a balance between procoagulants and anticoagulants that allows blood to clot normally after a vascular injury. Hemostasis is achieved through vascular constriction, formation of a platelet plug, and ultimately a blood clot. Coagulation disorders can result in too little or too much clotting. Anticoagulants like heparin and warfarin are used to treat and prevent thrombotic conditions by inhibiting different steps in the coagulation cascade, but also increase the risk of bleeding.
This document discusses anticoagulation and neuraxial anesthesia. It begins by introducing some risks of anticoagulation like bleeding. It then focuses on the risks of spinal and epidural hematoma formation during regional anesthesia when patients are anticoagulated. It provides recommendations from ASRA on the timing of regional blocks for various anticoagulants like heparin, LMWH, warfarin, antiplatelets, and newer anticoagulants. It also briefly discusses peripheral nerve blocks and herbal therapies. The recommendations aim to balance thrombosis prevention with bleeding risks from regional anesthesia.
Anticoagulant, antithrombotic and anti platelet drugsraj kumar
The document discusses various anticoagulant, antithrombotic and antiplatelet drugs. It notes that deep vein thrombosis and pulmonary embolism affect millions of people annually and cause tens of thousands of deaths. It then covers the indications for antithrombotic therapy for conditions like venous thromboembolism, arterial thromboembolism and disseminated intravascular coagulation. The document also discusses specific drugs for treating these conditions, including heparin, warfarin and newer anticoagulants. It provides details on the mechanisms of action, monitoring and side effects of these pharmaceutical agents.
Heparin and low molecular weight heparins are anticoagulants used to prevent blood clots. Heparin was discovered in 1916 and works by enhancing the activity of antithrombin III, which inhibits coagulation. Adverse effects include bleeding and heparin-induced thrombocytopenia, an immune reaction that increases the risk of blood clots. Protamine sulfate can reverse the anticoagulant effects of heparin in an overdose. Monitoring coagulation parameters is important when using heparin to balance its benefits and risks.
This document discusses anticoagulant drugs including unfractionated heparin, low molecular weight heparins, warfarin, and novel oral anticoagulants. It covers the mechanisms of action, indications, monitoring, perioperative management, and reversal of anticoagulation for bleeding events. Key points include how unfractionated heparin acts by inhibiting thrombin and other clotting factors, how warfarin inhibits vitamin K to reduce clotting factor production, and advantages of novel oral anticoagulants over warfarin in terms of pharmacokinetics and indications.
This document provides an overview of thrombocytopenia (low platelet count). It defines thrombocytopenia as a platelet count below 150,000/microL and describes the degrees of severity. The causes of thrombocytopenia include decreased platelet production in the bone marrow, increased platelet destruction, and dilution of platelets. Specific conditions that can cause thrombocytopenia like immune thrombocytopenia, disseminated intravascular coagulation, thrombotic thrombocytopenic purpura/hemolytic uremic syndrome, and drug-induced thrombocytopenia are discussed in more detail. Evaluation and management of thrombocytopenia in pregnancy and neonates is also reviewed.
Anticoagulants help prevent blood clotting by interfering with the coagulation phase. Heparin is an indirect thrombin inhibitor that works by accelerating the inactivation of clotting factors. It is administered parenterally and monitored with aPTT. Warfarin is an oral anticoagulant that acts by inhibiting vitamin K dependent clotting factors and is monitored with PT/INR. Both can cause bleeding and have specific contraindications and protocols for use during procedures.
Drugs acting on blood and blood forming organsUrmila Aswar
This document discusses drugs that act on blood and blood forming organs. It covers topics like hemostasis, coagulation factors, coagulation pathways, anticoagulants like heparin and warfarin, fibrinolytics, and antiplatelet drugs. Key points include that hemostasis is the process by which bleeding stops, coagulation involves intrinsic and extrinsic pathways, and anticoagulants prevent clotting through various mechanisms like inhibiting thrombin formation. Common anticoagulants discussed are heparin, low molecular weight heparins, warfarin, and fibrinolytics like streptokinase that lyse clots. Antiplatelet drugs like aspirin are also covered.
This document provides an overview of anticoagulants including their mechanisms of action, indications, dosing, and monitoring. It discusses normal hemostasis and coagulation factors. Unfractionated heparin, low molecular weight heparins, and factor Xa inhibitors are described as parenteral anticoagulants. Oral anticoagulants reviewed include warfarin, rivaroxaban, apixaban, and dabigatran. The roles of clinical pharmacists in managing anticoagulation therapy are also mentioned.
Eltrombopag for management of chronic immune thrombocytopenia finalDr.Goutham Valapala
The document discusses thrombocytopenia (low platelet count) and the use of eltrombopag to treat chronic immune thrombocytopenia. Eltrombopag is an oral thrombopoietin receptor agonist that stimulates platelet production. A 6-month study of 135 patients treated with eltrombopag found that 79% responded well with platelet counts between 50,000-400,000, with few serious bleeding events or thromboembolic risks compared to placebo. Transient increases in liver enzymes were reported in some patients treated with eltrombopag. The conclusions are that eltrombopag seems beneficial for patients who do not respond to other treatments for chronic immune thrombocytopenia, but further studies
Coagulants and anticoagulants work to maintain a balance in the coagulation system. Coagulants such as fresh whole blood and factors promote clotting, while anticoagulants like antithrombin and the fibrinolytic system inhibit clot formation and maintain blood fluidity. Vitamin K is essential for the production of coagulation factors and warfarin is an oral anticoagulant that works by inhibiting vitamin K. Heparin is commonly used as an injectable anticoagulant that prevents clotting by binding to antithrombin. Newer oral anticoagulants directly inhibit thrombin or factor Xa.
1. The document discusses laboratory investigation of hemorrhagic disorders and covers topics like primary and secondary hemostasis, inherited and acquired bleeding disorders, diagnosis of bleeding disorders through history, clinical examination and laboratory tests.
2. Key laboratory tests discussed are platelet count, bleeding time, tests for platelet function like PFA-100, screening tests for coagulation like PT, APTT and tests for specific coagulation factor deficiencies.
3. Causes, interpretation and clinical relevance of prolongation of various coagulation tests are explained. Inherited and acquired bleeding disorders of platelets, vessels and coagulation factors are summarized.
quick lecture about DIC, I used textbook sources and some online references hope you find what you are looking for.
in this presentation, you will find practical guidance for DIC management which you can depend on in managing your patients
8 Surprising Reasons To Meditate 40 Minutes A Day That Can Change Your Life.pptxHolistified Wellness
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Platelets play a key role in hemostasis. Disorders of platelets can be quantitative, involving too few or too many platelets, or qualitative, involving platelet function defects. Common causes of thrombocytopenia include decreased production, increased destruction, sequestration, or pseudothrombocytopenia. Immune thrombocytopenic purpura is an immune-mediated disorder treated with steroids, IVIG, or splenectomy. Thrombotic thrombocytopenic purpura involves a deficiency in ADAMTS13 treated with plasma exchange. Von Willebrand disease involves defects in von Willebrand factor.
This document discusses coagulation, anticoagulants, and fibrinolytics. It begins by describing the coagulation cascade and fibrinolysis system, which work to stop bleeding through platelet plug formation and blood clotting. It then discusses natural anticoagulants like prostacyclin and antithrombin III that prevent inappropriate clotting. Various coagulants and anticoagulants are outlined, including heparin and low molecular weight heparins, vitamin K, and newer oral anticoagulants. Adverse effects and clinical uses of different agents are also summarized.
The document provides an overview of anticoagulants and their clinical use. It discusses hemostasis and the mechanisms of coagulation. It then classifies anticoagulants as oral, parenteral or antiplatelets. The document focuses on warfarin and heparin, describing their mechanisms of action, dosing, and perioperative management considerations for patients receiving these anticoagulants. It emphasizes balancing the risks of bleeding and thromboembolism during the perioperative period.
DIC is one condition that always trouble patients and doctor, though its a nightmare for any clinician , its also a potent question in both UG and PG exams. I hope this will help you in answering those questions well.
Platelets are cell fragments that originate from megakaryocytes and play a key role in hemostasis. The normal platelet count is 150,000-450,000/L. Thrombopoietin regulates platelet production in the liver and spleen. When the endothelium is damaged, platelets adhere through von Willebrand factor and become activated, releasing granule contents that promote clot formation. Thrombocytopenia can result from decreased production, increased destruction, or sequestration and has various acquired and inherited causes. Disorders like immune thrombocytopenic purpura and thrombotic thrombocytopenic purpura involve autoimmune or inflammatory platelet destruction.
Disseminated intravascular coagulation (DIC) is a syndrome characterized by widespread activation of coagulation that can occur as a result of various underlying conditions. It results from an imbalance between coagulation and anticoagulation processes in the body. DIC can be acute, with bleeding and shock being dominant symptoms, or chronic, where thrombosis and clotting may predominate. The most common triggers of DIC are infectious diseases, cancer, obstetric complications, and severe tissue injury. Diagnosis involves identifying symptoms of bleeding and thrombosis, abnormal laboratory coagulation test results, and ruling out other conditions. Treatment focuses on treating the underlying cause, replacing coagulation factors, platelets, and fibrinogen, and
Blood coagulation involves a balance between procoagulants and anticoagulants that allows blood to clot normally after a vascular injury. Hemostasis is achieved through vascular constriction, formation of a platelet plug, and ultimately a blood clot. Coagulation disorders can result in too little or too much clotting. Anticoagulants like heparin and warfarin are used to treat and prevent thrombotic conditions by inhibiting different steps in the coagulation cascade, but also increase the risk of bleeding.
This document discusses anticoagulation and neuraxial anesthesia. It begins by introducing some risks of anticoagulation like bleeding. It then focuses on the risks of spinal and epidural hematoma formation during regional anesthesia when patients are anticoagulated. It provides recommendations from ASRA on the timing of regional blocks for various anticoagulants like heparin, LMWH, warfarin, antiplatelets, and newer anticoagulants. It also briefly discusses peripheral nerve blocks and herbal therapies. The recommendations aim to balance thrombosis prevention with bleeding risks from regional anesthesia.
Anticoagulant, antithrombotic and anti platelet drugsraj kumar
The document discusses various anticoagulant, antithrombotic and antiplatelet drugs. It notes that deep vein thrombosis and pulmonary embolism affect millions of people annually and cause tens of thousands of deaths. It then covers the indications for antithrombotic therapy for conditions like venous thromboembolism, arterial thromboembolism and disseminated intravascular coagulation. The document also discusses specific drugs for treating these conditions, including heparin, warfarin and newer anticoagulants. It provides details on the mechanisms of action, monitoring and side effects of these pharmaceutical agents.
Heparin and low molecular weight heparins are anticoagulants used to prevent blood clots. Heparin was discovered in 1916 and works by enhancing the activity of antithrombin III, which inhibits coagulation. Adverse effects include bleeding and heparin-induced thrombocytopenia, an immune reaction that increases the risk of blood clots. Protamine sulfate can reverse the anticoagulant effects of heparin in an overdose. Monitoring coagulation parameters is important when using heparin to balance its benefits and risks.
This document discusses anticoagulant drugs including unfractionated heparin, low molecular weight heparins, warfarin, and novel oral anticoagulants. It covers the mechanisms of action, indications, monitoring, perioperative management, and reversal of anticoagulation for bleeding events. Key points include how unfractionated heparin acts by inhibiting thrombin and other clotting factors, how warfarin inhibits vitamin K to reduce clotting factor production, and advantages of novel oral anticoagulants over warfarin in terms of pharmacokinetics and indications.
This document provides an overview of thrombocytopenia (low platelet count). It defines thrombocytopenia as a platelet count below 150,000/microL and describes the degrees of severity. The causes of thrombocytopenia include decreased platelet production in the bone marrow, increased platelet destruction, and dilution of platelets. Specific conditions that can cause thrombocytopenia like immune thrombocytopenia, disseminated intravascular coagulation, thrombotic thrombocytopenic purpura/hemolytic uremic syndrome, and drug-induced thrombocytopenia are discussed in more detail. Evaluation and management of thrombocytopenia in pregnancy and neonates is also reviewed.
Anticoagulants help prevent blood clotting by interfering with the coagulation phase. Heparin is an indirect thrombin inhibitor that works by accelerating the inactivation of clotting factors. It is administered parenterally and monitored with aPTT. Warfarin is an oral anticoagulant that acts by inhibiting vitamin K dependent clotting factors and is monitored with PT/INR. Both can cause bleeding and have specific contraindications and protocols for use during procedures.
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This document discusses drugs that act on blood and blood forming organs. It covers topics like hemostasis, coagulation factors, coagulation pathways, anticoagulants like heparin and warfarin, fibrinolytics, and antiplatelet drugs. Key points include that hemostasis is the process by which bleeding stops, coagulation involves intrinsic and extrinsic pathways, and anticoagulants prevent clotting through various mechanisms like inhibiting thrombin formation. Common anticoagulants discussed are heparin, low molecular weight heparins, warfarin, and fibrinolytics like streptokinase that lyse clots. Antiplatelet drugs like aspirin are also covered.
This document provides an overview of anticoagulants including their mechanisms of action, indications, dosing, and monitoring. It discusses normal hemostasis and coagulation factors. Unfractionated heparin, low molecular weight heparins, and factor Xa inhibitors are described as parenteral anticoagulants. Oral anticoagulants reviewed include warfarin, rivaroxaban, apixaban, and dabigatran. The roles of clinical pharmacists in managing anticoagulation therapy are also mentioned.
Eltrombopag for management of chronic immune thrombocytopenia finalDr.Goutham Valapala
The document discusses thrombocytopenia (low platelet count) and the use of eltrombopag to treat chronic immune thrombocytopenia. Eltrombopag is an oral thrombopoietin receptor agonist that stimulates platelet production. A 6-month study of 135 patients treated with eltrombopag found that 79% responded well with platelet counts between 50,000-400,000, with few serious bleeding events or thromboembolic risks compared to placebo. Transient increases in liver enzymes were reported in some patients treated with eltrombopag. The conclusions are that eltrombopag seems beneficial for patients who do not respond to other treatments for chronic immune thrombocytopenia, but further studies
Coagulants and anticoagulants work to maintain a balance in the coagulation system. Coagulants such as fresh whole blood and factors promote clotting, while anticoagulants like antithrombin and the fibrinolytic system inhibit clot formation and maintain blood fluidity. Vitamin K is essential for the production of coagulation factors and warfarin is an oral anticoagulant that works by inhibiting vitamin K. Heparin is commonly used as an injectable anticoagulant that prevents clotting by binding to antithrombin. Newer oral anticoagulants directly inhibit thrombin or factor Xa.
1. The document discusses laboratory investigation of hemorrhagic disorders and covers topics like primary and secondary hemostasis, inherited and acquired bleeding disorders, diagnosis of bleeding disorders through history, clinical examination and laboratory tests.
2. Key laboratory tests discussed are platelet count, bleeding time, tests for platelet function like PFA-100, screening tests for coagulation like PT, APTT and tests for specific coagulation factor deficiencies.
3. Causes, interpretation and clinical relevance of prolongation of various coagulation tests are explained. Inherited and acquired bleeding disorders of platelets, vessels and coagulation factors are summarized.
quick lecture about DIC, I used textbook sources and some online references hope you find what you are looking for.
in this presentation, you will find practical guidance for DIC management which you can depend on in managing your patients
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Anticoagulants and thrombolytic drugs.ppt
1. ANTICOAGULANTS AND THROMBOLYTIC DRUGS
Haemostasis
Vascular injury results firstly in vasoconstriction and formation of platelet plug at
the site of injury (primary haemostasis).
The platelet plug is then stabilized by the formation of a fibrin meshwork,
resulting from activation of the coagulation cascade.
Fibrin is eventually cleared through digestion by fibrinolytic enzymes.
2.
3. Primary Haemostasis
When endothelial integrity is breached, platelets adhere to exposed subendothelial
collagen. The adherent platelets become activated and result in;
1) Exposure of fibrinogen receptors, allowing fibrinogen to bind and cross-link
adjacent platelets. The process is known as platelet aggregation. The
platelet fibrinogen receptor consists of a complex of glycoproteins IIb and
IIIa on the platelet membrane.
2) Release of contents of secretory granules including substances such as
adenosine diphosphate (ADP) which promote further platelet activation.
3) Synthesis of thromboxane A2 which also acts to promote further platelet
activation and vasoconstriction.
4. Activation of the coagulation cascade;
The coagulation cascade can be divided into three parts;
1) The common pathway consists of those reactions subsequent to the
generation of factor Xa, culminating in the cleavage of fibrinogen by thrombin,
with subsequent polymerization of fibrin monomers into fibrin strands. Factor
Xa may be generated either by the extrinsic pathway or by the intrinsic
pathway.
2) In the extrinsic pathway, tissue factor is expressed by cells or released
following tissue injury. Binding of tissue factor to factor VII greatly accelerates
the activation of factor VII and also the action of factor VIIa in the activation of
factor X..
3) The intrinsic pathway is initiated by the action of factor XII by contact of blood
with a ‘foreign’ surface. In vivo, this is usually the subendothelial tissues. A
sequence of reactions then results in activation of factor X. most coagulation
factors are synthesized in the liver, and the synthesis of the pro-coagulant
forms of factors II, VII, IX and X is dependent on the availability of vitamin K.
5. Fibrinolysis
The fibrinolytic system, just like the coagulation cascade, also consists of a series
of enzymatic steps, this time resulting in the breakdown of polymerized fibrin by
plasmin into degradation products (FDP). Plasmin is generated from the plasma
protein plasminogen by the action of tissue plasminogen activator (tPA), which is
most efficient in the activation of plasminogen, when it is bound to fibrin.
6. Pathophysiology
Thrombosis is haemostasis in the wrong place.
When haemostasis proceeds unchecked within a blood vessel, thrombosis
occurs and vascular occlusion may result. Thrombi may also break up into
small pieces and lodge at distant points within the circulation system
(embolism).
7. The process of thrombosis in a blood vessel is promoted by one or more of
three underlying pathological events referred to as Virchow’s triad i.e.;
1) Abnormality of the vessel wall
2) Abnormalities of flow within a vessel wall (Stasis)
3) Abnormality of blood constituents
Thrombosis in arteries usually result from rupture of an atheromatous plaque,
and arterial thrombosis usually consists initially of platelets and subsequently
of fibrin. Venous thrombosis usually occur in the context of stasis of blood flow
e.g. during periods of immobility or during pregnancy when pressure from
gravid uterus may impede venous return.
8. ANTICOAGULANT DRUGS
HEPARIN
Anticoagulation can be achieved very rapidly with heparin, and it is therefore
the anticoagulant of choice in many acute thrombotic states such as treatment
of deep venous thrombosis (DVT) or pulmonary embolism and in severe
unstable angina in which it has an additive effect to aspirin.
9. Chemistry and pharmacology
Unfractionated heparin is a mixture of naturally occurring glycosaminoglycans with
polysaccharide chains of length and molecular weights ranging from 5000 to
30,000.
Low molecular weight heparins are manufactured from unfractionated heparin to
produce materials with an average molecular weight of 4000 – 6500.
All heparins exert their anticoagulant activity by binding to and greatly accelerating
the action of Antithrombin as an inhibitor of thrombin (factor IIa), factor Xa and
other serine protease coagulation factors.
10.
11. All heparins must be given parenterally either by the intravenous route or by the
subcutaneous route.
The half-life of standard heparin following intravenous route is 45-60 minutes.
Heparins however have complex kinetics depending on the dose, molecular
weights and route of administration.
Low molecular weight heparins demonstrate less to cells and to heparin
neutralizing proteins than the unfractionated heparin. This leads to improved
bioavailability and to a longer half-life. These properties allow a more predictable
anticoagulant response and once daily dosing subcutaneous administration and
there is no need to monitor therapeutic doses with anticoagulation time assays.
12. Clinical use of unfractionated heparin
Heparin is used in;
o DVT and pulmonary thromboembolism. In this situation, standard
practice has been to administer 5000 IU unfractionated heparin
intravenously as a loading dose, followed by a continuous infusion of
30,000 IU over 24-hours, and to monitor anticoagulant effect.
o Unstable angina and in myocardial infarction to prevent coronary re-
occlusion following thrombolysis, and in the treatment and prevention of
mural thrombus.
13. o Prevention of clotting in extracorporeal circulations such;
Renal dialysis circuits
Cardiopulmonary bypass
Flushing of indwelling catheters.
o Perioperative; to reduce incidence of venous thrombosis and pulmonary
embolism following;
General or orthopaedic surgery
Acutely ill or immobile medical patients
o It is given subcutaneously at low doses of 5000 IU b.d. for prophylaxis.
14. Clinical use of low molecular weight heparin
Prevention of venous thrombosis in patients at risk including;
o DVT and pulmonary thromboembolism
o Patients undergoing general and orthopaedic surgery
o High risk medical patients
They have been shown to have similar efficacy to unfractionated heparin in all
these situations.
They however have the advantage of;
o Convenient once daily dosing making their use attractive and allows
savings on hospitalization costs.
o Less bleeding incidence in medical patients.
15. Monitoring heparin
Administration of therapeutic doses of unfractionated heparin must be monitored
in the laboratory.
A prolongation of the activated partial thromboplastin time (APPT) and the
thrombin time are observed.
APPT which tests the intrinsic and the common pathways of coagulation is the
test usually chosen for therapeutic heparin monitoring.
For thrombosis treatment, aim for an APPT of 2 - 3. An alternative is to measure
plasma heparin levels that are based upon plasma anti-Xa activity.
It is not usually necessary to monitor heparin given in low doses for prophylaxis
as such regimens do not lead to prolongation of the APPT.
APPT is insensitive to the effects of low molecular weight heparins. These may
be measured by anti-Xa assays (e.g. in renal failure) but monitoring is usually
unnecessary because of the predictability of the responses.
16. Adverse effects
Bleeding;
o A major hazard.
o Not entirely predictable by the APTT and patient related factors are also
important.
Heparin induced thrombocytopenia;
o Occurs in approximately 3% of patients given full-dose unfractionated
heparin. Mildly early thrombocytopenia may be common and of no clinical
significance.
o Thrombocytopenia occurring 4-14 days following heparin exposure is of
greater significance as potential life-threatening thrombosis occurs in
such patients.
17. o The thrombocytopenia is induced by a heparin-dependent antibody
that causes platelet aggregation.
o Heparin –induced thrombocytopenia can occur with any dose or
preparation of heparin. Although it appears to be much less common
with low molecular weight heparin, antibody cross-reactivity has been
documented.
o It is mandatory to monitor platelet count during heparin therapy and
prophylaxis from day 5 onwards; a baseline platelet count is useful.
o If heparin-induced thrombocytopenia is suspected, heparin should be
withdrawn immediately.
18. Osteoporosis;
o Reduction in bone density and bone fractures has been described
following prolonged use of heparin (usually greater than 20-weeks).
People at risk include pregnant women on prolonged anticoagulation
therapy.
o The mechanism is poorly understood. There appears to be a relationship
with dose and duration of treatment, but individual susceptibility is also
likely to be important.
o Monitoring of bone density may be considered in high risk patients.
Hypersensitivity;
o Local injections at injection sites have been reported and much more
rarely anaphylactoid reactions.
19. Reversal of anticoagulation with heparin
Because of the short half-life of heparin, in the absence of bleeding, it is
reasonable simply to withhold therapy temporarily if over anticoagulation has
occurred.
In the presence of haemorrhage, protamine should be administered
intravenously.
Protamine 1mg neutralizes the effects of 100 IU of unfractionated heparin.
protamine should never be given in doses greater than 50mg and should always
be administered slowly to avoid hypotension and bradycardia.
20. Contraindications to heparin
1) Uncorrected major bleeding
2) Uncorrected major bleeding disorder, e.g. thrombocytopenia, haemophilia.
3) Active peptic ulcer, oesophageal varices, aneurysm, proliferative retinopathy or
organ biopsy.
4) Recent surgery; especially neurosurgery or ophthalmic surgery.
5) Severe renal or hepatic impairment (not including patients on renal dialysis)
6) Recent stroke, intracranial or intraspinal bleed.
7) Severe hypertension
8) Previous heparin-induced thrombocytopenia or thrombosis.
9) Documented hypersensitivity.
21. HEPARANAOIDS AND HIRUDINS
These do not cross-react with heparin-dependent antibodies; hence they can be
used in heparin-induced thrombocytopenia.
Danaparoid is a heparanoid.
Desirudin and lepirudin are recombinant hirudins, the natural anticoagulant of the
medicinal leech.
FONDAPARINUX
This is a pentasaccharide which selectively inhibits factor Xa. It is effective in
prevention and treatment of DVT, but more expensive than heparin.
22. WARFARIN
In practice, warfarin a derivative of 4-hydroxycoumarin is by far the most
extensively used oral anticoagulant and is the drug of choice.
Acenocoumarol (nicoumalone) and phenindione are also available but are
rarely used.
All these drugs act as vitamin K antagonists and share the same
pharmacological principles.
23. Pharmacology
The coagulation factors II, VII, IX and X require gamma carboxylation on glutamic
acid residues in order to bind calcium during coagulation reactions.
Vitamin K is required for this carboxylation reaction, which is essential for
procoagulant activity.
Whilst acting as a cofactor, vitamin K is converted to vitamin K epoxide. The
epoxide is then recycled via reductase reactions to active forms of vitamin K.
Warfarin inhibits the reductase enzymes involved in the recycling of vitamin K,
thus leading to the deficiency of procoagulant forms of factors II, VII, IX and X.
24. Because some of these cofactors have prolonged half-lives, anticoagulation is
not achieved for several days after initiating warfarin therapy. In acute situations,
it is necessary to overlap heparin and warfarin therapy.
Warfarin is rapidly absorbed from the gut and is extensively bound to plasma
albumin.
Elimination of warfarin is by oxidative metabolism in the liver, with a half-life of
15-50 hours.
25. Monitoring warfarin therapy
Warfarin therapy is monitored by the prothrombin time (PTI) which assesses the
extrinsic and the common pathways of coagulation.
Standardization is achieved by calibrating laboratory reagents used for
measuring the prothrombin time against an internationally sensitive index (ISI) to
each reagent. This allows the prothrombin time of each patient on treatment to
be converted to an international normalized ratio (INR).
The INR is the ratio of the patient’s prothrombin time over the mean value in a
normal reference population determined using the same batch of reagent and
corrected for the ISI of the reagent.
The development of the INR system of monitoring oral anticoagulation has
allowed comparability of results between laboratories.
26. Clinical use of oral anticoagulants
Venous Thromboembolism; prophylaxis, treatment and maintenance.
Atrial fibrillation (high risk patient)
Valvular heart disease and prosthetic valve replacements, cardiomyopathy
Mural thrombus.
27. Warfarin use in pregnancy
Warfarin crosses the placenta barrier and is contraindicated in the first trimester
of pregnancy because of teratogenicity, and in the last few weeks of pregnancy
because of fatal bleeding at delivery.
Placental passage of warfarin leads to fetal anticoagulation at any stage in
pregnancy, and so warfarin is not generally recommended in the management
and prevention of venous thromboembolism during pregnancy.
Because of the high risk and potentially catastrophic consequences of
embolization from artificial valves, warfarin is still the anticoagulant of choice
from 12-36 weeks of pregnancy in patients with mechanical prosthetic valve.
28. How to initiate anticoagulation with warfarin
Because of the kinetics considerations described, anticoagulation with warfarin
is not achieved for several days after initiating therapy.
In acute thrombosis, loading doses are given at the start of the treatment;
usually 5-10mg warfarin on two consecutive days and to check the INR on the
third day.
Lower doses are used in;
o Congestive cardiac failure
o Presence of abnormalities of the liver function
o Prolongation of baseline prothrombin time
o Elderly
o Familial protein C or protein S disfunction
29. A baseline coagulation screen should be checked prior to initiating treatment.
Maintenance doses usually lie between 3 and 9mg of warfarin (2.5 – 5.0mg
depending on the warfarin preparation). Daily or alternate-day monitoring of the
INR should be carried out until steady values are achieved within the target
range.
When overlapping heparin with warfarin, it is important to continue heparin until a
therapeutic INR is achieved with warfarin.
30. Target ranges for oral anticoagulants
INR Clinical condition
2.0 – 2.5
Prophylaxis of DVT
Pulmonary embolism
2.0 – 3.0
Treatment of DVT
Prophylaxis in atrial fibrillation and other cardiac sources of
embolism
Bioprosthetic heart valves
Post-myocardial infarction
3.0 – 4.5
Mechanical prosthetic heart valves
Recurrent thrombosis in patients with antiphospholipid
syndrome
31. Drug Potentiation Antagonism
Analgesic (NSAIDs) Azapropazone
Phenylbutazone
Aspirin
Ketorolac
Antibiotics Co-trimoxazole
Metronidazole
Ampicillin
Cephalosporins
Erythromycin
Aminoglycosides
Tetracycline
Miconazole
Rifampicin
griseofulvin
Cardiovascular drugs Amiodarone
Fibrates
Spironolactone
Cholestyramine
Endocrine agents Corticosteroids
Thyroxine
Tamoxifen
Anabolic steroids
Glucagon
Gastrointestinal drugs Cimetidine
Omeprazole
CNS Drugs Barbiturates
Antihistamines
Tricyclic antidepressants
Chlorpromazine
Carbamazepine
Phenytoin
Others Allopurinol
Alcohol
Vitamin K
Drug Interactions with
warfarin
Drugs either potentiate or
antagonize the effects of
warfarin;
32. Adverse effects
Bleeding;
o This is the most common adverse effect encountered in patients on oral
anticoagulant.
o Bleeding is usually related to prolongation of the INR above the
therapeutic range. Underlying causes should be sought if bleeding occurs
at therapeutic levels.
Alopecia
Skin rash; skin reaction seen a lot more with phenindione.
Skin necrosis susceptibility in patients with protein C or S disfunction
33. Treatment of haemorrhage and reversal of oral anticoagulation
For elective situations such as surgery including tooth extractions, warfarin
should be stopped at least 48-hours in advance of the procedure and the INR
monitored, with the option of substituting with heparin if there is high risk of
thrombosis e.g. mechanical valves.
Vitamin K takes 6-hours to have any effect and in an emergency fresh frozen
plasma or coagulation factor concentrate must be administered to provide an
immediate source of vitamin K dependent factors.
Small doses of phytomenadione i.e. vitamin K (0.5 – 2mg) are sufficient for the
reversal of warfarin effects in all but the most extreme cases. Administration of
large doses of vitamin K e.g. 10mg makes further use of oral anticoagulation
impossible for several weeks.