The document discusses various anticoagulants and their mechanisms of action, including heparin, low molecular weight heparins, warfarin, and direct thrombin inhibitors. It also covers fibrinolytic agents and their role in dissolving blood clots. The key mechanisms discussed are how heparin activates antithrombin III to inactivate thrombin and factor Xa, how warfarin inhibits vitamin K to decrease production of coagulation factors, and how fibrinolytic agents activate plasminogen to break down fibrin clots. Monitoring and clinical uses of these drug classes are also summarized.
This document provides information on anticoagulants. It begins with an introduction to anticoagulants and how they differ from antiplatelets. It then defines anticoagulants and provides a classification including heparin and low molecular weight heparins, vitamin K antagonists, direct thrombin inhibitors, and factor Xa inhibitors. For each drug class, specific drugs are discussed along with their mechanisms of action, indications, dosages, side effects and nursing considerations.
Platelets and thrombin systems work together to form blood clots. Platelets become activated when bleeding occurs and begin sticking together. Activated clotting proteins engage in chemical reactions producing fibrin strands that stick to vessel walls, trapping red blood cells and forming clots. Anticoagulants prevent clotting by inhibiting factors in the coagulation cascade like thrombin and factor Xa. Heparin is a commonly used anticoagulant that activates antithrombin to inhibit coagulation factors. Newer direct thrombin and factor Xa inhibitors offer more consistent anticoagulation than warfarin with less drug interactions and monitoring requirements.
The document discusses anticoagulants and blood coagulation. It describes the intrinsic and extrinsic pathways of coagulation and the stages that form a blood clot. Natural anticoagulant mechanisms include prostacyclin, antithrombin III, and protein C. Common anticoagulants discussed are heparin, low molecular weight heparin, and oral agents like warfarin. The uses, mechanisms, benefits, and risks of various anticoagulants are summarized.
The document discusses anticoagulants and their use in preventing blood clots. It describes tests like PT, INR, and PTT that are used to monitor anticoagulant therapy and provides normal ranges. PT measures clotting factors while INR standardizes PT results between labs. PTT evaluates heparin therapy and clotting factors. Warfarin users should have an INR of 2.0-3.0 for basic needs or 2.5-3.5 if at high risk of clots.
Anticoagulants are drugs that prevent blood clotting and can be used to treat thrombotic disorders. Heparin is a commonly used anticoagulant that works by binding to antithrombin-III and inhibiting several clotting factors. Low molecular weight heparins provide the benefits of heparin with less monitoring requirements but less risk of thrombocytopenia. Oral anticoagulants like warfarin are vitamin K antagonists that are used for long-term anticoagulation therapy due to their longer half-lives. Anticoagulants are prescribed to prevent dangerous clots in conditions like deep vein thrombosis, pulmonary embolism, myocardial infarction, and
Dr. D. K. Brahma discusses antiplatelet drugs, which interfere with platelet function and are useful for preventing thromboembolic disorders. The document defines antiplatelet drugs and describes the role of platelets in thrombosis formation. It then discusses the mechanisms of various antiplatelet drugs including aspirin, dipyridamole, ticlodipine, clopidogrel, prasugrel, and GPIIb/IIIa receptor antagonists like abciximab. The uses of these antiplatelet drugs for conditions like heart attacks, strokes, angioplasty and stents are summarized.
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.
This document provides information on anticoagulants. It begins with an introduction to anticoagulants and how they differ from antiplatelets. It then defines anticoagulants and provides a classification including heparin and low molecular weight heparins, vitamin K antagonists, direct thrombin inhibitors, and factor Xa inhibitors. For each drug class, specific drugs are discussed along with their mechanisms of action, indications, dosages, side effects and nursing considerations.
Platelets and thrombin systems work together to form blood clots. Platelets become activated when bleeding occurs and begin sticking together. Activated clotting proteins engage in chemical reactions producing fibrin strands that stick to vessel walls, trapping red blood cells and forming clots. Anticoagulants prevent clotting by inhibiting factors in the coagulation cascade like thrombin and factor Xa. Heparin is a commonly used anticoagulant that activates antithrombin to inhibit coagulation factors. Newer direct thrombin and factor Xa inhibitors offer more consistent anticoagulation than warfarin with less drug interactions and monitoring requirements.
The document discusses anticoagulants and blood coagulation. It describes the intrinsic and extrinsic pathways of coagulation and the stages that form a blood clot. Natural anticoagulant mechanisms include prostacyclin, antithrombin III, and protein C. Common anticoagulants discussed are heparin, low molecular weight heparin, and oral agents like warfarin. The uses, mechanisms, benefits, and risks of various anticoagulants are summarized.
The document discusses anticoagulants and their use in preventing blood clots. It describes tests like PT, INR, and PTT that are used to monitor anticoagulant therapy and provides normal ranges. PT measures clotting factors while INR standardizes PT results between labs. PTT evaluates heparin therapy and clotting factors. Warfarin users should have an INR of 2.0-3.0 for basic needs or 2.5-3.5 if at high risk of clots.
Anticoagulants are drugs that prevent blood clotting and can be used to treat thrombotic disorders. Heparin is a commonly used anticoagulant that works by binding to antithrombin-III and inhibiting several clotting factors. Low molecular weight heparins provide the benefits of heparin with less monitoring requirements but less risk of thrombocytopenia. Oral anticoagulants like warfarin are vitamin K antagonists that are used for long-term anticoagulation therapy due to their longer half-lives. Anticoagulants are prescribed to prevent dangerous clots in conditions like deep vein thrombosis, pulmonary embolism, myocardial infarction, and
Dr. D. K. Brahma discusses antiplatelet drugs, which interfere with platelet function and are useful for preventing thromboembolic disorders. The document defines antiplatelet drugs and describes the role of platelets in thrombosis formation. It then discusses the mechanisms of various antiplatelet drugs including aspirin, dipyridamole, ticlodipine, clopidogrel, prasugrel, and GPIIb/IIIa receptor antagonists like abciximab. The uses of these antiplatelet drugs for conditions like heart attacks, strokes, angioplasty and stents are summarized.
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.
Here are some key drug and food interactions to consider with warfarin:
- Thyroid medications, metronidazole, fluconazole/azoles can increase INR. Monitor more closely.
- Certain antibiotics like 2nd/3rd gen cephalosporins, broad spectrum antibiotics can interact. Monitor INR.
- Alcohol in excess and amiodarone can potentiate warfarin's effects. Limit intake.
- Azithromycin, some statins, and omeprazole have been associated with interactions. Monitor INR.
- Phenytoin can decrease warfarin's effects. May require warfarin dose adjustment.
- Grapefruit juice
1. Antiplatelet drugs work by inhibiting platelet aggregation which is essential for forming blood clots. They are used to prevent thrombus formation in certain pathological conditions.
2. There are several classes of antiplatelet drugs including aspirin, clopidogrel, abciximab which work via different mechanisms such as inhibiting thromboxane A2, blocking ADP receptors, or inhibiting the glycoprotein IIb/IIIa receptor.
3. Fibrinolytics like streptokinase, alteplase work by activating plasminogen to plasmin to break down fibrin clots and are indicated for pulmonary embolism, myocardial infarction, and ischemic stroke. The major risks are bleeding complications.
A 50-year-old male patient is scheduled for open cholecystectomy and the surgeon is concerned about risk of deep vein thrombosis. The assistant professor is consulted to choose an appropriate anticoagulant. Coagulants promote coagulation for bleeding disorders while anticoagulants prevent clotting. Common anticoagulants discussed include heparin, low molecular weight heparin, warfarin, and newer oral anticoagulants. Given the patient's surgery, the assistant professor would likely recommend a low molecular weight heparin due to its advantages over unfractionated heparin in subcutaneous absorption and reduced bleeding risk.
This document discusses antiplatelet drugs used to treat arterial and venous thrombosis. It describes the role of platelets in arterial thrombosis, triggered by disruption of atherosclerotic plaque. Common antiplatelet drugs discussed include aspirin, clopidogrel, prasugrel, ticlopidine, dipyridamole, and glycoprotein IIb/IIIa inhibitors like abciximab and tirofiban. Their mechanisms of action, indications, and side effects are summarized. Clopidogrel resistance due to genetic factors is also mentioned.
Anticoagulants are drugs that reduce the coagulability of blood. They can be used in vitro in laboratory settings or in vivo in patients. Common anticoagulants include heparin, low molecular weight heparins like enoxaparin, and oral anticoagulants like warfarin. Heparin works by binding to and activating antithrombin III, which then inhibits various clotting factors. Warfarin interferes with vitamin K dependent clotting factor synthesis. Both can cause bleeding as an adverse effect. Anticoagulants are used to treat conditions like deep vein thrombosis, pulmonary embolism, and acute myocardial infarction.
This document summarizes different types of antiplatelet drugs. It discusses how platelet aggregation occurs through interactions between collagen, platelet receptors, and release of substances like thromboxane A2 and ADP. It then categorizes main classes of antiplatelet drugs as aspirin, dipyridamole, P2Y12 receptor blockers like clopidogrel and prasugrel, and GP IIb/IIIa receptor antagonists like abciximab, eptifibatide, and tirofiban. For each drug, it provides information on mechanism of action, pharmacokinetics, clinical uses, and side effects. The overall document provides a concise overview of the mechanisms and classes of
Fibrinolytics such as streptokinase, urokinase, alteplase, reteplase, and tenecteplase activate the natural fibrinolytic system and lyse thrombi to recanalize occluded blood vessels. They are used to treat myocardial infarction, deep vein thrombosis, pulmonary embolism, and peripheral arterial occlusion. Antifibrinolytics like epsilon amino-caproic acid and tranexamic acid inhibit plasminogen activation and clot dissolution to prevent or control bleeding caused by fibrinolytics or surgical procedures. The timing of fibrinolytic administration is critical for heart attack treatment, with better outcomes seen within 1-3 hours of symptom onset.
Platelets play a key role in arterial thrombosis by sticking to damaged vessel walls and aggregating, releasing substances that promote further platelet activation and aggregation. Antiplatelet drugs target various steps in this process, including thromboxane A2 synthesis via aspirin; ADP receptors via drugs like clopidogrel and ticagrelor; the final common pathway of the glycoprotein IIb/IIIa receptor via abciximab; and thrombin receptors via vorapaxar. While effective for reducing thrombosis, all antiplatelet drugs increase the risk of bleeding to some degree.
- The document discusses anticoagulation and blood clotting. It describes how blood clots form and are broken down, as well as drugs that can regulate clotting such as heparin, warfarin, and dicoumarol. It provides details on the coagulation factors, classes of anticoagulant drugs, the blood clotting process, and coagulation disorders.
This document discusses fibrinolytics, which are agents that help dissolve blood clots through fibrinolysis. It describes the mechanisms of fibrinolysis and plasminogen activation. The main fibrinolytic agents discussed are streptokinase, urokinase, and tissue-type plasminogen activator. Their mechanisms of action and uses for conditions like myocardial infarction and pulmonary embolism are summarized. The document also discusses antiplatelet drugs, how they inhibit platelet aggregation, their classifications like aspirin and mechanisms of action. Adverse effects of various antiplatelet drugs are mentioned.
Drugs for coagulation, Antiplatelets, Fibrinolytics & AntifibrinolyticsBikashAdhikari26
Hemostasis is the process of stopping blood loss from damaged blood vessels. It involves vascular constriction, platelet plug formation, blood clotting, and fibrous tissue growth. Coagulants promote coagulation and are used to treat hemorrhagic states. Vitamin K is a necessary cofactor for the production of coagulation factors and is used to treat bleeding disorders caused by vitamin K deficiency or impaired coagulation factor synthesis. Antifibrinolytics like tranexamic acid and epsilon amino caproic acid inhibit fibrinolysis by blocking plasminogen and preventing clot dissolution, reducing bleeding in various conditions.
This document discusses various anticoagulant agents including heparin, low molecular weight heparins, synthetic heparin derivatives like fondaparinux and idraparinux, direct thrombin inhibitors like lepirudin and bivalirudin, and synthetic thrombin inhibitor argatroban. It provides details on their mechanisms of action, pharmacokinetics, therapeutic ranges, and comparisons between unfractionated heparin and low molecular weight heparins. Protamine sulfate is discussed as an antagonist for reversing heparin overdose.
Desmopressin
Lypressin
Terlipressin
Felypressin
Argipressin
ornipressin
Desmopressin: It is a selective V2-receptor agonist and is more potent than vasopressin as an antidiuretic. It has negligible vasoconstrictor action. It is administered by oral, nasal and parenteral routes. Lypressin: It acts on both V1- and V2-receptors. It is less potent but longer acting than vasopressin. It is administered parenterally. Terlipressin: It is a prodrug of vasopressin with selective V1 action. It is administered intravenously. Felypressin: It is a synthetic analogue of vasopressin. It is mainly used for its vasoconstrictor (V1 ) action along with local anaesthetics to prolong the duration of action. Felypressin should be avoided in pregnancy because of its oxytocic (uterine stimulant) activity.
The document discusses the four phases of hemostasis: vascular, platelet, coagulation, and fibrinolysis. It describes the coagulation cascade and the intrinsic and extrinsic pathways. Key components of coagulation like clotting factors, platelets, thrombin, and fibrinogen are explained. Common anticoagulants and antiplatelet drugs are also summarized, including heparin, warfarin, aspirin, and thrombolytic agents like tissue plasminogen activator. The mechanisms of action, uses, dosing, and side effects of these pharmaceutical agents are highlighted at a high level.
This document discusses anticoagulants, including heparin. It defines anticoagulants as drugs used to reduce blood coagulability and classifies them into those used in vivo and in vitro. It provides details on heparin, including its discovery, chemistry, mechanisms of action, pharmacokinetics, dosage, adverse effects, contraindications, and uses.
This document discusses various drugs that modify blood coagulation by affecting platelet function and the clotting cascade. It describes several classes of drugs: anticoagulants which prevent clot formation; antiplatelet drugs like aspirin which inhibit platelet aggregation; thrombolytic drugs which lyse existing clots; and hemostatic drugs which promote clotting. For each drug class, the document outlines mechanisms of action, indications for use, dosages, side effects and interactions.
Introduction to Anticoagulants
Coagulants, Local agents, Systemic agents, Anticoagulants, Heparin, Low molecular weight heparins, Heparinoids, Oral anticoagulants (Warfarin), Therapeutic uses
Presented by
N. Ramya
Department of Pharmacology
Hypertension is a common cardiovascular condition caused by persistently high blood pressure that damages organs. Antihypertensive drugs work via different mechanisms like inhibiting the renin-angiotensin-aldosterone system, blocking calcium channels, promoting sodium excretion with diuretics, and reducing sympathetic nervous system activity. Common classes of antihypertensives include ACE inhibitors, angiotensin receptor blockers, calcium channel blockers, diuretics, sympatholytics, and vasodilators. Treatment involves beginning with certain drug classes based on patient characteristics and guidelines, and escalating treatment by adding other classes as needed to control blood pressure. Antihypertensive drug choice is also based on minimizing adverse effects and avoiding
Anticoagulants work by interfering with the body's normal clotting mechanisms. There are several classes of anticoagulants that work at different stages of hemostasis - the process of forming blood clots. Antiplatelet drugs like aspirin and clopidogrel inhibit platelet activation and aggregation during primary hemostasis. Heparin and low molecular weight heparins like enoxaparin affect secondary hemostasis by inhibiting thrombin. Warfarin prevents the synthesis of clotting factors and affects secondary hemostasis. Fibrinolytics like tPA work during tertiary hemostasis by dissolving already formed clots. Patients on anticoagulants require regular monitoring of
Coagulation: In medicine, the clotting of blood. The process by which the blood clots to form solid masses, or clots.
More than 30 types of cells and substances in blood affect clotting. The process is initiated by blood platelets. Platelets produce a substance that combines with calcium ions in the blood to form thromboplastin, which in turn converts the protein prothrombin into thrombin in a complex series of reactions. Thrombin, a proteolytic enzyme, converts fibrinogen, a protein substance, into fibrin, an insoluble protein that forms an intricate network of minute threadlike structures called fibrils and causes the blood plasma to gel. The blood cells and plasma are enmeshed in the network of fibrils to form the clot.
Anti coagulationin patient with ckd Prof.Basset El Essawy MD ph DFarragBahbah
1. The document discusses physiology and pathways of coagulation, as well as antiplatelet drugs, anticoagulants, and thrombolytics used to treat coagulation.
2. Standard heparin and low molecular weight heparins are compared, noting differences in molecular weight, bioavailability, monitoring needs, and clearance.
3. New oral anticoagulants are discussed as alternatives to warfarin, noting their benefits of fixed dosing, limited drug interactions and food effects, and lack of routine monitoring needs. However, concerns remain regarding a lack of monitoring methods and proven antidotes.
Here are some key drug and food interactions to consider with warfarin:
- Thyroid medications, metronidazole, fluconazole/azoles can increase INR. Monitor more closely.
- Certain antibiotics like 2nd/3rd gen cephalosporins, broad spectrum antibiotics can interact. Monitor INR.
- Alcohol in excess and amiodarone can potentiate warfarin's effects. Limit intake.
- Azithromycin, some statins, and omeprazole have been associated with interactions. Monitor INR.
- Phenytoin can decrease warfarin's effects. May require warfarin dose adjustment.
- Grapefruit juice
1. Antiplatelet drugs work by inhibiting platelet aggregation which is essential for forming blood clots. They are used to prevent thrombus formation in certain pathological conditions.
2. There are several classes of antiplatelet drugs including aspirin, clopidogrel, abciximab which work via different mechanisms such as inhibiting thromboxane A2, blocking ADP receptors, or inhibiting the glycoprotein IIb/IIIa receptor.
3. Fibrinolytics like streptokinase, alteplase work by activating plasminogen to plasmin to break down fibrin clots and are indicated for pulmonary embolism, myocardial infarction, and ischemic stroke. The major risks are bleeding complications.
A 50-year-old male patient is scheduled for open cholecystectomy and the surgeon is concerned about risk of deep vein thrombosis. The assistant professor is consulted to choose an appropriate anticoagulant. Coagulants promote coagulation for bleeding disorders while anticoagulants prevent clotting. Common anticoagulants discussed include heparin, low molecular weight heparin, warfarin, and newer oral anticoagulants. Given the patient's surgery, the assistant professor would likely recommend a low molecular weight heparin due to its advantages over unfractionated heparin in subcutaneous absorption and reduced bleeding risk.
This document discusses antiplatelet drugs used to treat arterial and venous thrombosis. It describes the role of platelets in arterial thrombosis, triggered by disruption of atherosclerotic plaque. Common antiplatelet drugs discussed include aspirin, clopidogrel, prasugrel, ticlopidine, dipyridamole, and glycoprotein IIb/IIIa inhibitors like abciximab and tirofiban. Their mechanisms of action, indications, and side effects are summarized. Clopidogrel resistance due to genetic factors is also mentioned.
Anticoagulants are drugs that reduce the coagulability of blood. They can be used in vitro in laboratory settings or in vivo in patients. Common anticoagulants include heparin, low molecular weight heparins like enoxaparin, and oral anticoagulants like warfarin. Heparin works by binding to and activating antithrombin III, which then inhibits various clotting factors. Warfarin interferes with vitamin K dependent clotting factor synthesis. Both can cause bleeding as an adverse effect. Anticoagulants are used to treat conditions like deep vein thrombosis, pulmonary embolism, and acute myocardial infarction.
This document summarizes different types of antiplatelet drugs. It discusses how platelet aggregation occurs through interactions between collagen, platelet receptors, and release of substances like thromboxane A2 and ADP. It then categorizes main classes of antiplatelet drugs as aspirin, dipyridamole, P2Y12 receptor blockers like clopidogrel and prasugrel, and GP IIb/IIIa receptor antagonists like abciximab, eptifibatide, and tirofiban. For each drug, it provides information on mechanism of action, pharmacokinetics, clinical uses, and side effects. The overall document provides a concise overview of the mechanisms and classes of
Fibrinolytics such as streptokinase, urokinase, alteplase, reteplase, and tenecteplase activate the natural fibrinolytic system and lyse thrombi to recanalize occluded blood vessels. They are used to treat myocardial infarction, deep vein thrombosis, pulmonary embolism, and peripheral arterial occlusion. Antifibrinolytics like epsilon amino-caproic acid and tranexamic acid inhibit plasminogen activation and clot dissolution to prevent or control bleeding caused by fibrinolytics or surgical procedures. The timing of fibrinolytic administration is critical for heart attack treatment, with better outcomes seen within 1-3 hours of symptom onset.
Platelets play a key role in arterial thrombosis by sticking to damaged vessel walls and aggregating, releasing substances that promote further platelet activation and aggregation. Antiplatelet drugs target various steps in this process, including thromboxane A2 synthesis via aspirin; ADP receptors via drugs like clopidogrel and ticagrelor; the final common pathway of the glycoprotein IIb/IIIa receptor via abciximab; and thrombin receptors via vorapaxar. While effective for reducing thrombosis, all antiplatelet drugs increase the risk of bleeding to some degree.
- The document discusses anticoagulation and blood clotting. It describes how blood clots form and are broken down, as well as drugs that can regulate clotting such as heparin, warfarin, and dicoumarol. It provides details on the coagulation factors, classes of anticoagulant drugs, the blood clotting process, and coagulation disorders.
This document discusses fibrinolytics, which are agents that help dissolve blood clots through fibrinolysis. It describes the mechanisms of fibrinolysis and plasminogen activation. The main fibrinolytic agents discussed are streptokinase, urokinase, and tissue-type plasminogen activator. Their mechanisms of action and uses for conditions like myocardial infarction and pulmonary embolism are summarized. The document also discusses antiplatelet drugs, how they inhibit platelet aggregation, their classifications like aspirin and mechanisms of action. Adverse effects of various antiplatelet drugs are mentioned.
Drugs for coagulation, Antiplatelets, Fibrinolytics & AntifibrinolyticsBikashAdhikari26
Hemostasis is the process of stopping blood loss from damaged blood vessels. It involves vascular constriction, platelet plug formation, blood clotting, and fibrous tissue growth. Coagulants promote coagulation and are used to treat hemorrhagic states. Vitamin K is a necessary cofactor for the production of coagulation factors and is used to treat bleeding disorders caused by vitamin K deficiency or impaired coagulation factor synthesis. Antifibrinolytics like tranexamic acid and epsilon amino caproic acid inhibit fibrinolysis by blocking plasminogen and preventing clot dissolution, reducing bleeding in various conditions.
This document discusses various anticoagulant agents including heparin, low molecular weight heparins, synthetic heparin derivatives like fondaparinux and idraparinux, direct thrombin inhibitors like lepirudin and bivalirudin, and synthetic thrombin inhibitor argatroban. It provides details on their mechanisms of action, pharmacokinetics, therapeutic ranges, and comparisons between unfractionated heparin and low molecular weight heparins. Protamine sulfate is discussed as an antagonist for reversing heparin overdose.
Desmopressin
Lypressin
Terlipressin
Felypressin
Argipressin
ornipressin
Desmopressin: It is a selective V2-receptor agonist and is more potent than vasopressin as an antidiuretic. It has negligible vasoconstrictor action. It is administered by oral, nasal and parenteral routes. Lypressin: It acts on both V1- and V2-receptors. It is less potent but longer acting than vasopressin. It is administered parenterally. Terlipressin: It is a prodrug of vasopressin with selective V1 action. It is administered intravenously. Felypressin: It is a synthetic analogue of vasopressin. It is mainly used for its vasoconstrictor (V1 ) action along with local anaesthetics to prolong the duration of action. Felypressin should be avoided in pregnancy because of its oxytocic (uterine stimulant) activity.
The document discusses the four phases of hemostasis: vascular, platelet, coagulation, and fibrinolysis. It describes the coagulation cascade and the intrinsic and extrinsic pathways. Key components of coagulation like clotting factors, platelets, thrombin, and fibrinogen are explained. Common anticoagulants and antiplatelet drugs are also summarized, including heparin, warfarin, aspirin, and thrombolytic agents like tissue plasminogen activator. The mechanisms of action, uses, dosing, and side effects of these pharmaceutical agents are highlighted at a high level.
This document discusses anticoagulants, including heparin. It defines anticoagulants as drugs used to reduce blood coagulability and classifies them into those used in vivo and in vitro. It provides details on heparin, including its discovery, chemistry, mechanisms of action, pharmacokinetics, dosage, adverse effects, contraindications, and uses.
This document discusses various drugs that modify blood coagulation by affecting platelet function and the clotting cascade. It describes several classes of drugs: anticoagulants which prevent clot formation; antiplatelet drugs like aspirin which inhibit platelet aggregation; thrombolytic drugs which lyse existing clots; and hemostatic drugs which promote clotting. For each drug class, the document outlines mechanisms of action, indications for use, dosages, side effects and interactions.
Introduction to Anticoagulants
Coagulants, Local agents, Systemic agents, Anticoagulants, Heparin, Low molecular weight heparins, Heparinoids, Oral anticoagulants (Warfarin), Therapeutic uses
Presented by
N. Ramya
Department of Pharmacology
Hypertension is a common cardiovascular condition caused by persistently high blood pressure that damages organs. Antihypertensive drugs work via different mechanisms like inhibiting the renin-angiotensin-aldosterone system, blocking calcium channels, promoting sodium excretion with diuretics, and reducing sympathetic nervous system activity. Common classes of antihypertensives include ACE inhibitors, angiotensin receptor blockers, calcium channel blockers, diuretics, sympatholytics, and vasodilators. Treatment involves beginning with certain drug classes based on patient characteristics and guidelines, and escalating treatment by adding other classes as needed to control blood pressure. Antihypertensive drug choice is also based on minimizing adverse effects and avoiding
Anticoagulants work by interfering with the body's normal clotting mechanisms. There are several classes of anticoagulants that work at different stages of hemostasis - the process of forming blood clots. Antiplatelet drugs like aspirin and clopidogrel inhibit platelet activation and aggregation during primary hemostasis. Heparin and low molecular weight heparins like enoxaparin affect secondary hemostasis by inhibiting thrombin. Warfarin prevents the synthesis of clotting factors and affects secondary hemostasis. Fibrinolytics like tPA work during tertiary hemostasis by dissolving already formed clots. Patients on anticoagulants require regular monitoring of
Coagulation: In medicine, the clotting of blood. The process by which the blood clots to form solid masses, or clots.
More than 30 types of cells and substances in blood affect clotting. The process is initiated by blood platelets. Platelets produce a substance that combines with calcium ions in the blood to form thromboplastin, which in turn converts the protein prothrombin into thrombin in a complex series of reactions. Thrombin, a proteolytic enzyme, converts fibrinogen, a protein substance, into fibrin, an insoluble protein that forms an intricate network of minute threadlike structures called fibrils and causes the blood plasma to gel. The blood cells and plasma are enmeshed in the network of fibrils to form the clot.
Anti coagulationin patient with ckd Prof.Basset El Essawy MD ph DFarragBahbah
1. The document discusses physiology and pathways of coagulation, as well as antiplatelet drugs, anticoagulants, and thrombolytics used to treat coagulation.
2. Standard heparin and low molecular weight heparins are compared, noting differences in molecular weight, bioavailability, monitoring needs, and clearance.
3. New oral anticoagulants are discussed as alternatives to warfarin, noting their benefits of fixed dosing, limited drug interactions and food effects, and lack of routine monitoring needs. However, concerns remain regarding a lack of monitoring methods and proven antidotes.
Anticoagulant, antiplatelet, and thrombolytic drugs work to prevent and treat blood clots in different ways. Anticoagulants like heparin and warfarin prevent clot formation. Antiplatelet drugs like aspirin and clopidogrel inhibit platelet aggregation. Thrombolytics such as streptokinase and tPA promote fibrinolysis to dissolve newly formed clots. While these drugs are effective, they also carry risks of excessive bleeding and require careful monitoring and management of drug interactions to be used safely.
This document provides information about drugs used in hematology, including anticoagulants, antiplatelet agents, and thrombolytic agents. It begins with learning outcomes and an outline of topics to be covered, including disorders of inappropriate blood clotting that these drugs treat. The document then discusses the normal coagulation process and thrombosis. It describes the two main types of thrombus and how anticoagulants, antiplatelet agents, and thrombolytic agents work to prevent and treat them. Specific drug classes are covered in more depth, including heparin and low molecular weight heparins, warfarin, and fibrinolytic agents. Clinical uses and guidelines for these drugs are also summarized.
A 25-year-old woman presents with shortness of breath, leg swelling and pain. Her family has a history of blood clots. Examination shows leg erythema and edema. The document discusses anticoagulants including heparin, low molecular weight heparins, oral anticoagulants like warfarin, and their mechanisms, pharmacokinetics, uses and comparisons.
This document discusses haemostasis (arrest of blood loss), thrombosis (pathological formation of blood clots), and factors that influence clotting. It also outlines different types of clots and emboli. Three main ways drugs can affect clotting are by impacting blood coagulation, platelet function, and fibrin removal. Specific drugs are highlighted that impact the coagulation cascade, platelet activation, and fibrinolytic system. These include heparins, warfarin as blood thinners, antiplatelet drugs like aspirin, and fibrinolytic drugs like streptokinase and tissue plasminogen activator. Their uses, mechanisms of action, properties and monitoring are described.
The document discusses various blood disorders that affect red blood cells, including different types of anemia. It describes iron-deficiency anemia, which can be caused by low iron intake or blood loss. Anemia of chronic disease is common in people with kidney disease or other chronic illnesses. Pernicious anemia results from a vitamin B12 deficiency due to problems absorbing the vitamin. Aplastic anemia occurs when the bone marrow does not produce enough red blood cells or other blood cells.
Diseases involving blood clotting factors can be inherited or acquired. The coagulation cascade involves several clotting factors that work together as enzymes to form a blood clot. Deficiencies or defects in these clotting factors can result in bleeding disorders. Some of the major clotting factor deficiencies include hemophilia A caused by factor VIII deficiency, hemophilia B caused by factor IX deficiency, von Willebrand disease caused by von Willebrand factor deficiency, and fibrinogen deficiencies that cause bleeding issues. Diagnostic tests evaluate clotting factor levels and clotting times. Treatment focuses on replacing the deficient clotting factor through blood products or concentrates.
PC of Blood and Blood forming agents.pdfRAMDAS BHAT
This document provides an overview of drugs acting on blood and blood forming agents. It discusses coagulants that promote coagulation like calcium salts and vitamin K. It also discusses anticoagulants that prevent coagulation, including heparin, low molecular weight heparins, direct thrombin inhibitors, factor Xa inhibitors, and vitamin K antagonists like warfarin. The document provides details on the mechanisms of coagulation, platelet function, fibrinolysis, and conditions requiring treatment with coagulants or anticoagulants.
This document summarizes various blood clotting factor disorders. It begins with an introduction to hemostasis and blood coagulation. It then discusses the history of discoveries in coagulation factors. There are 13 coagulation factors involved in the intrinsic and extrinsic pathways that activate enzymes in a cascade to form a fibrin clot. Inherited disorders can result from mutations in the genes for various coagulation factors. Diagnostic tests evaluate coagulation factors and inhibitors. Specific disorders are discussed, such as hemophilia A and B resulting from factor VIII and IX deficiencies respectively. Symptoms and inheritance patterns are provided for deficiencies of several coagulation factors.
Platelets are small cell fragments that help the blood clot. Several drugs target platelets to prevent excessive clotting. Aspirin and clopidogrel inhibit platelet aggregation by blocking thromboxane A2 and ADP receptors. Heparin enhances the effects of antithrombin III to inhibit coagulation factors Xa and IIa. Low molecular weight heparins have fewer side effects than unfractionated heparin and do not require monitoring.
This document provides an overview of haemostasis and coagulation. It defines haemostasis as the arrest of bleeding and describes the two stages as primary haemostasis involving platelet plug formation and secondary haemostasis involving fibrin clot formation via the coagulation cascade. Key aspects of both the intrinsic and extrinsic pathways are summarized. Common coagulation factor deficiencies and disorders are also mentioned.
This document discusses secondary haemostasis, or blood coagulation. It begins with an overview of how platelet plug formation in primary haemostasis is followed by fibrin clot formation via the blood coagulation cascade. The coagulation factors involved in this cascade are then described. The document outlines the intrinsic and extrinsic pathways, as well as the common pathway where they converge to generate thrombin and form a fibrin clot. Finally, it discusses the natural inhibitors that regulate coagulation to prevent excessive clotting, including antithrombin III, protein C/S, tissue factor pathway inhibitor, and others.
This document discusses homeostasis and coagulation. It begins by describing how platelets adhere to injured blood vessels to form clots during homeostasis. It then discusses thrombosis and how clots can block vessels. It details the coagulation process and factors involved. It describes the intrinsic and extrinsic coagulation pathways. It discusses substances that promote coagulation like calcium and vitamin K. It also covers anticoagulants like heparin and oral anticoagulants. Finally, it summarizes fibrinolytics like streptokinase that are used to break up clots.
GP IIb/IIIa inhibitors are a class of drugs that block the GP IIb/IIIa receptor on platelets to prevent aggregation. The three main GP IIb/IIIa inhibitors are abciximab, eptifibatide, and tirofiban. They are used during percutaneous coronary interventions and for acute coronary syndromes to reduce complications by inhibiting the final common pathway of platelet aggregation. While generally well-tolerated, bleeding is a common side effect due to their antiplatelet effects.
The document discusses blood clotting and drugs that affect the clotting process. It describes the four phases of clotting - vascular, platelet, coagulation, and fibrinolytic. It then covers classes of drugs that prevent clotting, dissolve clots, prevent bleeding, and treat clotting deficiencies. Specific drugs discussed include heparin, warfarin, aspirin, streptokinase, tissue plasminogen activator, vitamin K, and factors VIII and IX for treating hemophilia. The mechanisms, effects, preparations and administration of these drugs are outlined.
This document discusses various anticoagulants and antiplatelet drugs. It describes how anticoagulants prevent the formation of blood clots through different mechanisms like inhibiting vitamin K, heparin activating antithrombin III, and direct factor Xa inhibitors. Common anticoagulants mentioned include heparin, warfarin, and rivaroxaban. The document also discusses fibrinolytics which lyse blood clots, and antiplatelet drugs like aspirin, dipyridamole, and clopidogrel which prevent platelet aggregation. Monitoring of anticoagulant therapy and drug interactions are also summarized.
This document discusses sedative-hypnotic drugs. It defines sedatives as drugs that decrease excitement and cause drowsiness without sleep, while hypnotics induce and maintain sleep. Different stages of sleep are described, along with the effects of sedative-hypnotics on sleep architecture. Benzodiazepines and barbiturates are provided as examples of sedative-hypnotic drugs and their mechanisms of action, effects, uses, and adverse effects are summarized. Non-benzodiazepine hypnotics such as zolpidem and zopiclone are also mentioned.
Iron deficiency anemia is the most common type of anemia seen in clinical practice. It is characterized by a decrease in hemoglobin and oxygen-carrying capacity due to low iron levels. Oral iron supplements are usually the first line treatment, with ferrous sulfate being a commonly used and inexpensive option. Parenteral iron is considered when oral iron is not tolerated or absorbed. The document provides details on causes of iron deficiency anemia, distribution and absorption of iron in the body, classification of anemias, oral and parenteral iron preparations and their administration, and indications and adverse effects of iron therapy.
The document discusses cardiac glycosides and their use in treating congestive cardiac failure (CCF). It describes the mechanism of action of digoxin, noting that it increases myocardial contractility and reduces heart rate. Adverse effects and management of digoxin toxicity are also summarized. The document outlines the therapeutic uses of digoxin in CCF and arrhythmias like atrial fibrillation.
Anticholinergic drugs act as competitive antagonists at muscarinic receptors. They block the effects of the neurotransmitter acetylcholine (Ach) and thus reduce parasympathetic nervous system activity. Key points:
- Atropine and scopolamine are examples of naturally occurring anticholinergic drugs. Synthetic muscarinic antagonists include benztropine, hyoscyamine, and oxybutynin.
- They have therapeutic effects in the eyes (mydriasis, cycloplegia), gastrointestinal tract (reducing motility), respiratory tract (reducing secretions), and central nervous system (treating extrapyramidal side effects).
- Potential adverse effects include dry
Parasympathomimetic or cholinergic drugs act on cholinergic receptors in the parasympathetic nervous system to produce effects similar to parasympathetic stimulation. They have two types of activities: muscarinic and nicotinic. Examples include direct-acting drugs like acetylcholine and indirect-acting anticholinesterases. Anticholinesterases inhibit the enzyme cholinesterase, leading to accumulation of acetylcholine at receptor sites. They are used to treat conditions like glaucoma, myasthenia gravis, Alzheimer's disease, and organophosphate poisoning.
Teriparatide (brand name Forteo) is a form of parathyroid hormone that stimulates new bone formation. It is the only osteoporosis drug approved to build new bone.
The document discusses how teriparatide works by activating osteoblasts through intermittent exposure to parathyroid hormone. This leads to increased bone mineral density, especially in the spine and hip. Clinical trials showed teriparatide reduced the risk of vertebral fractures by 65% and nonvertebral fractures by 53% compared to placebo.
Teriparatide is recommended for patients with severe osteoporosis who have failed or cannot tolerate bisphosphonate therapy. It may also be used off-label to
Mechanism of action of drugs can occur through various pathways including biochemical, physiological, physical, chemical, enzymatic, and receptor-mediated actions. Drugs can act through membrane-bound receptors by binding with varying affinity and efficacy, and can cause effects as agonists, antagonists, partial agonists, or inverse agonists. Factors like dosage, drug potency, efficacy, interactions, tolerance, and individual patient characteristics influence a drug's effects.
This ppt discusses pharmacological actions, toxic effects and clinical applications of corticosteroids. It also mentions precations to be taken while using steroids
This document provides information on anti-anemic drugs, focusing on iron and vitamins B12 and folate. It defines different types of anemia based on red blood cell size and describes the manifestations and causes of megaloblastic anemia from deficiencies in B12 or folate. It outlines the dietary sources, absorption, transport, storage and excretion of iron as well as indications, preparations, dosages and adverse effects of oral and parenteral iron therapy for iron deficiency anemia. The roles and therapeutic uses of vitamins B12, folate and erythropoietin in various clinical conditions are also summarized.
There are four types of malaria parasites that infect humans. Plasmodium falciparum causes the most serious form of malaria. The parasites are transmitted via the bites of infected female Anopheles mosquitoes. Several anti-malarial drugs are discussed, including chloroquine, quinine, primaquine, artemisinin derivatives, mefloquine, and combinations of sulfadoxine and pyrimethamine. Treatment regimens vary depending on the parasite species and drug resistance patterns. Malaria prevention includes suppressive prophylaxis with drugs like chloroquine, mefloquine, or doxycycline.
This document provides information about anti-tuberculosis therapy. It begins by listing the learning objectives, which include describing primary and secondary anti-tuberculosis drugs, the phases of TB treatment, mechanisms of action and side effects of drugs, defining multi-drug resistant TB, and the role of vaccines in prevention. It then discusses specifics of TB as a global health problem, treatment regimens, first and second-line drugs, mechanisms of action of isoniazid and rifampin, and side effects of isoniazid. The document aims to educate about best practices for treating TB through use of combination drug therapy.
This document discusses beta-lactam antibiotics, including penicillins and cephalosporins. It provides details on their chemistry, mechanisms of action, mechanisms of bacterial resistance, classifications, kinetics, uses, and adverse effects. Penicillins are the original beta-lactam antibiotics and were discovered from the fungus Penicillium. Cephalosporins are structurally similar but were derived from the fungus Cephalosporium. Both classes inhibit bacterial cell wall synthesis but bacteria can develop resistance through various mechanisms.
This document discusses the principles of antimicrobial therapy including:
- Classifying antimicrobials and their mechanisms of action such as inhibiting cell wall synthesis or protein synthesis
- Key concepts like bactericidal vs bacteriostatic activity, minimum inhibitory concentrations, and pharmacokinetic/pharmacodynamic principles
- Factors that influence antimicrobial selection including the infection site, patient characteristics, safety, and antimicrobial spectrum and properties
- Strategies for antimicrobial use including prophylaxis, empirical vs directed therapy, and preventing resistance
- Adverse effects and toxicities of different antimicrobial classes
This document discusses the principles of antimicrobial therapy. It begins by outlining objectives related to classifying antimicrobials, understanding pharmacokinetic and pharmacodynamic principles, microbiology, and factors that influence antimicrobial selection. It then covers specific topics like the mechanisms of different antibiotic classes, natural and acquired resistance, strategies to prevent resistance, management of superinfections, and uses of antimicrobial combinations. The document emphasizes selecting the appropriate antimicrobial based on the infection site, patient factors, safety, and cost considerations. It also addresses empirical therapy and reasons therapy may fail.
This document provides information on drugs used to treat depression. It begins by classifying various types of antidepressants including tricyclic antidepressants (TCAs), selective serotonin reuptake inhibitors (SSRIs), serotonin-norepinephrine reuptake inhibitors (SNRIs), and monoamine oxidase inhibitors (MAOIs). It then describes the pharmacological actions and side effects of these different classes of antidepressants. Finally, it discusses the clinical uses and limitations of antidepressant therapies in managing conditions like depression, anxiety disorders, and bipolar disorder.
Basavarajeeyam is a Sreshta Sangraha grantha (Compiled book ), written by Neelkanta kotturu Basavaraja Virachita. It contains 25 Prakaranas, First 24 Chapters related to Rogas& 25th to Rasadravyas.
Recomendações da OMS sobre cuidados maternos e neonatais para uma experiência pós-natal positiva.
Em consonância com os ODS – Objetivos do Desenvolvimento Sustentável e a Estratégia Global para a Saúde das Mulheres, Crianças e Adolescentes, e aplicando uma abordagem baseada nos direitos humanos, os esforços de cuidados pós-natais devem expandir-se para além da cobertura e da simples sobrevivência, de modo a incluir cuidados de qualidade.
Estas diretrizes visam melhorar a qualidade dos cuidados pós-natais essenciais e de rotina prestados às mulheres e aos recém-nascidos, com o objetivo final de melhorar a saúde e o bem-estar materno e neonatal.
Uma “experiência pós-natal positiva” é um resultado importante para todas as mulheres que dão à luz e para os seus recém-nascidos, estabelecendo as bases para a melhoria da saúde e do bem-estar a curto e longo prazo. Uma experiência pós-natal positiva é definida como aquela em que as mulheres, pessoas que gestam, os recém-nascidos, os casais, os pais, os cuidadores e as famílias recebem informação consistente, garantia e apoio de profissionais de saúde motivados; e onde um sistema de saúde flexível e com recursos reconheça as necessidades das mulheres e dos bebês e respeite o seu contexto cultural.
Estas diretrizes consolidadas apresentam algumas recomendações novas e já bem fundamentadas sobre cuidados pós-natais de rotina para mulheres e neonatos que recebem cuidados no pós-parto em unidades de saúde ou na comunidade, independentemente dos recursos disponíveis.
É fornecido um conjunto abrangente de recomendações para cuidados durante o período puerperal, com ênfase nos cuidados essenciais que todas as mulheres e recém-nascidos devem receber, e com a devida atenção à qualidade dos cuidados; isto é, a entrega e a experiência do cuidado recebido. Estas diretrizes atualizam e ampliam as recomendações da OMS de 2014 sobre cuidados pós-natais da mãe e do recém-nascido e complementam as atuais diretrizes da OMS sobre a gestão de complicações pós-natais.
O estabelecimento da amamentação e o manejo das principais intercorrências é contemplada.
Recomendamos muito.
Vamos discutir essas recomendações no nosso curso de pós-graduação em Aleitamento no Instituto Ciclos.
Esta publicação só está disponível em inglês até o momento.
Prof. Marcus Renato de Carvalho
www.agostodourado.com
TEST BANK For Community Health Nursing A Canadian Perspective, 5th Edition by...Donc Test
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Promoting Wellbeing - Applied Social Psychology - Psychology SuperNotesPsychoTech Services
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Histololgy of Female Reproductive System.pptxAyeshaZaid1
Dive into an in-depth exploration of the histological structure of female reproductive system with this comprehensive lecture. Presented by Dr. Ayesha Irfan, Assistant Professor of Anatomy, this presentation covers the Gross anatomy and functional histology of the female reproductive organs. Ideal for students, educators, and anyone interested in medical science, this lecture provides clear explanations, detailed diagrams, and valuable insights into female reproductive system. Enhance your knowledge and understanding of this essential aspect of human biology.
8 Surprising Reasons To Meditate 40 Minutes A Day That Can Change Your Life.pptxHolistified Wellness
We’re talking about Vedic Meditation, a form of meditation that has been around for at least 5,000 years. Back then, the people who lived in the Indus Valley, now known as India and Pakistan, practised meditation as a fundamental part of daily life. This knowledge that has given us yoga and Ayurveda, was known as Veda, hence the name Vedic. And though there are some written records, the practice has been passed down verbally from generation to generation.
- Video recording of this lecture in English language: https://youtu.be/kqbnxVAZs-0
- Video recording of this lecture in Arabic language: https://youtu.be/SINlygW1Mpc
- Link to download the book free: https://nephrotube.blogspot.com/p/nephrotube-nephrology-books.html
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ABDOMINAL TRAUMA in pediatrics part one.drhasanrajab
Abdominal trauma in pediatrics refers to injuries or damage to the abdominal organs in children. It can occur due to various causes such as falls, motor vehicle accidents, sports-related injuries, and physical abuse. Children are more vulnerable to abdominal trauma due to their unique anatomical and physiological characteristics. Signs and symptoms include abdominal pain, tenderness, distension, vomiting, and signs of shock. Diagnosis involves physical examination, imaging studies, and laboratory tests. Management depends on the severity and may involve conservative treatment or surgical intervention. Prevention is crucial in reducing the incidence of abdominal trauma in children.
Rasamanikya is a excellent preparation in the field of Rasashastra, it is used in various Kushtha Roga, Shwasa, Vicharchika, Bhagandara, Vatarakta, and Phiranga Roga. In this article Preparation& Comparative analytical profile for both Formulationon i.e Rasamanikya prepared by Kushmanda swarasa & Churnodhaka Shodita Haratala. The study aims to provide insights into the comparative efficacy and analytical aspects of these formulations for enhanced therapeutic outcomes.
Here is the updated list of Top Best Ayurvedic medicine for Gas and Indigestion and those are Gas-O-Go Syp for Dyspepsia | Lavizyme Syrup for Acidity | Yumzyme Hepatoprotective Capsules etc
Muktapishti is a traditional Ayurvedic preparation made from Shoditha Mukta (Purified Pearl), is believed to help regulate thyroid function and reduce symptoms of hyperthyroidism due to its cooling and balancing properties. Clinical evidence on its efficacy remains limited, necessitating further research to validate its therapeutic benefits.
4. • Mechanism of blood coagulation
• Hemostasis: Spontaneous arrest of
bleeding from damaged blood vessels.
first thing to happen is precapillary
constriction.
04/11/19 PATKI 4
5. • Injured blood vessel
• subendothelial collagen exposure
• platelets adhere to exposed collagen
fibrils at glycoprotein receptor release of
granules from platelets including ADP
• Activation of intrinsic pathway
04/11/19 PATKI 5
10. • Anticoagulants:
In vitro:
Sodium oxalate 10mg
Sodium Edetate
Sodium citrate,
EDTA
Heparin
150U ----- 100 ml blood
Used in blood taken
For investigations
04/11/19 PATKI 10
11. • Anticoagulants:
In vivo anticoagulants:
Parenteral :
In direct thrombin inhibitors:
Heparin, Foundaparinux
Direct thrombin inhibitors
hirudin, lepirudin,
Bivalirudin, Argatroban
Danaparoid
04/11/19 PATKI 11
12. • Anticoagulants:
In vivo anticoagulants:
Oral
coumarin derivatives
e.g. Warfarin,
Bishydroxycoumarin
Indandione derivatives
e.g. Phenindione
Anisindione04/11/19 PATKI 12
13. HEPARIN
• Heparin was discovered by McLean.
• Naturally occurring substance.
• It is found in the metachromatically
staining granules of mast cells.
Mainly in lung, liver, intestinal mucosa
• Commercial Heparin obtained from
bovine lung and porcine intestinal
mucosa.
04/11/19 PATKI 13
14. • It is a mucopolysaccharide.
• It is composed of D- glucosamine and
D-glucuronicacid .
• It is a strongest organic acid in the body.
• Strongly electronegative compound.
• Two types:
Unfractioned Heparin
( 10,000- 30,000)
Low molecular weight Heparin
(4000-6500)04/11/19 PATKI 14
15. • Action of unfractioned Heparin:
AT III IIa AT III II a
+ + + + +
- - - - - - - - - - -
heparin
AT III X a
04/11/19 PATKI 15
16. Mechanism of action:
It increases the activity of antithrombin III
Heparin combines with Antithrombin III
Heparin induces conformational changes in
antithrombin III to expose its interactive sites.
Factor IIa combines with Antithrmbin III and
Heparin.
Inactivation of Factor IIa.
But factor Xa combines with only
antithrombin III.
Inactivation of factor Xa.
04/11/19 PATKI 16
18. • Monitoring of Heparin therapy:
Whole blood clotting time:
which should be kept at 2-3 times the normal
Activated partial thromboplastin time: (APTT)
which should be kept at 11/2 - 2 times normal
04/11/19 PATKI 18
19. Pharmacological actions:
1. Blood Coagulation:
2. Activation of Lipoprotein lipase
3. Antiplatelet action
Pharmacokinetics:
Orally not effective
should not be injected IM
subcutaneous route ( action after 60min
IV ( immediate action )
Does not cross BBB, Placenta
Metabolized by Heparinase04/11/19 PATKI 19
20. • PREPARATIONS:
1) Low fixed dose SC regimen:
5000 u every 12 hrs
2) Dose adjusted SC regimen:
15,000- 20,000 every 12 hrs
3) IV intermittent regimen:
5000-10,000 every 4-6 hrs
4) IV infusion: 0.5u/kg /min
04/11/19 PATKI 20
23. • ADVANTAGES:
1) Better subcutaneous bioavailability 70-90%
2) Longer duration of action
once daily administration
3) PTT, clotting time are not prolonged
Laboratory monitoring is not needed
Predictable anticoagulant effect
4) Dose is given in mg and calculated on body
weight basis
5) Less thrombocytopenia
6) Less antigenic04/11/19 PATKI 23
24. • Mechanism of action of L.M.W Heparin:
AT III Xa AT III X a
LMW Heparin
04/11/19 PATKI 24
26. • Enoxaparin:
2000 units SC 2hrs before surgery
then 2000 units every 24 hrs for 7-10 days
• Dalteparin :
2000 units SC 2hrs before surgery
then 2000 units every 24 hrs for 7-10 days
• Tinzaparin:
3500 units SC 2hrs before surgery
then 3500 units every 24 hrs for 7-10 days
04/11/19 PATKI 26
27. INDICATIONS:
• Prevention and treatment of deep venous
thrombosis and pulmonary embolism
• Myocardial Infarction
• Rheumatic heart disease
• Cerebrovascular disease
04/11/19 PATKI 27
29. • Heparin antagonists:
Protamine sulphate
1mg for 100 units of heparin
obtained from salmon sperm
> 50-100 mg ----
itself produces some anticoagulant activity
Histamine liberator:
hypotension ,bradycardia, flushing, bronchosasm
trongly basic compound, which neutralizes
trongly acidic Heparin weight by weight.
04/11/19 PATKI 29
30. Fondaparinux:
Synthetic pentasaccharide
Inactivation of factor X
Long half-life 15days
SC, once daily dosing
Prevention & treatment of venous
thromboembolism
Alternative anticoagulant in heparin
induced thrombocytopenia.04/11/19 PATKI 30
32. Oral anticoagulants
Warfarin:
In vivo anticoagulant
Oral anticoagulant
Coumarin derivative
Synthetic
Delayed onset of action ( 1-3 days )
Duration of action 3-6 days
04/11/19 PATKI 32
33. WARFARIN: MECHANISM OF ACTIONWARFARIN: MECHANISM OF ACTION
Inactive factors II,
VII, IX, and X
Proteins S and C
Active factors II,
VII, IX, and X
Proteins S and C
Vitamin K epoxide
Vitamin K reduced
WARFARIN
Prevents the reduction of vitamin K, which is essential forPrevents the reduction of vitamin K, which is essential for
activation of certain factorsactivation of certain factors
Has no effect on previously formed thrombusHas no effect on previously formed thrombus
Epoxide reductase
Inactive
II, VII, IX, X
Active
II, VII, IX, X
Warfarin
Warfarin mechanism of action
04/11/19 PATKI 33
34. Mechanism of action:
It inhibits the synthesis of vit K
dependent clotting factors in the liver by
inhibiting Epoxide reductase enzyme.
This enzyme is essential for formation of
reduced vitK.
This reduced VitK activates clotting
factors II,VII, IX, X.
Monitoring of Warfarin therapy:
Prothrombin Time
04/11/19 PATKI 34
35. The commercial preparation is mixture
of R( Dextro, less potent ) &
S ( Levo, more potent)
99% protein bound
It crosses Placenta
Undergoes enterohepatic Circulation
Excreted in urine
Dose: 5-10mg/day
04/11/19 PATKI 35
37. Treatment of Warfarin toxicity:
Withhold the anticoagulant
fresh blood transfusion
Antidote vit K1
04/11/19 PATKI 37
38. Drug Interactions:
Increases the Warfarin effect:
Malnutrition, malabsorption
Enzyme inhibitors: Cimetidine
Drugs which displace the Warfarin
from protein binding site: Phenytoin
drugs inhibits the gut flora: antibiotics
Liquid paraffin
Drugs causing Hypoprothrombinaemia
Cephalosporins
04/11/19 PATKI 38
39. Drug Interactions:
Decreases the Warfarin effect:
Enzyme inducers: Barbiturates
Drugs that inhibits absorption
Cholestyramine
Drugs that increases the synthesis of
clotting factors: Oral contraceptives
04/11/19 PATKI 39
40. Mucopolysaccharide
Bovine lung
Binds with antithrombin III &
Inactivates factor IX a & xA
Immediate action
Duration 6 hrs
PT
Indicated in pregnancy
No drug interactions
Protamine antidote
Monitored by APTT
HEPARIN
Parenteral
In vitro & in vivo
5-7 days
Vit K antidote
Drug interactions
Not indicated
WARFARIN
After 1-3 days
Inhibits the epoxide reductase
Inactvates II, VII,IX, X
Synthetic
Coumarin derivative
Oral
In vivo
04/11/19 PATKI 40
41. FIBRINOLYTIC AGENTS
These are the drugs used to lyse
Thrombi / clot recanalize the
occluded blood vessels
04/11/19 PATKI 41
46. Lytic activity:
Streptokinase > Urokinase > rt- PA
Disadvantage:
Mainly for treatment not for prophylaxis
Venous thrombi better than arterial thrombi
Do not distinguish between fibrin of
a thrombus and fibrin of a
haemostatic plug04/11/19 PATKI 46
47. Streptokinase:
beta hemolytic streptococci group C
Half-life: 15-20min
Dose: 1.5 million units IV over one hour
Bind with the free plasminogen in circulation
more bleeding
Allergic reactions & hypotension are common
Indirect plasminogen activator
No fibrin specificity
04/11/19 PATKI 47
48. Urokinase:
• Cultured human renal cells
• Half-life: 15-20min
• Dose: 1.5million units IV bolus then
1.5 m.units IV over one hour
Direct plasminogen activator
It lacks fibrin specificity
Non antigenic: no allergic reactions
No hypotension
04/11/19 PATKI 48
49. • Alteplase:
recombinant tissue plasminogen activator
Always combine with heparin
10mg IV 1-2min f.by 50mg IV 1 hour
40 mg IV next 2 hours
It activates only fibrin bound plasminogen
( avoids activation of systemic plasminogen)
no bleeding
It is a short half-life 4-8min
rethrombosis
04/11/19 PATKI 49
50. STREPTOKIN
ASE
Urokinase Anistreplase Alteplase
Plasma half
life-min
15-25 15-25 50-90 4-8
Fibrin
specificity
minimal moderate minimal maximum
Plasminogen
binding
indirect direct indirect direct
allergy yes no yes no04/11/19 PATKI 50
51. • Uses:
1) MI:
indications:
with in 6 hours of onset
minimum duration of pain 30min
ST elevation in two leads
< 75 years age
Streptokinase 1.5 million units over one hour
2) Stroke
3) pulmonary embolism
4) DVT
5) peripheral arterial occlusion04/11/19 PATKI 51
54. • ARVIN: It is a enzyme
venom of malayan pit viper( agkistroden
rhodostoma)
Mechanism of action:
Converts the fibrinogen to imperfect fibrin
Dose: 2units /kg every 12 hours IV
Resistance to IM administration ( antibody formation)
Mainly for venous thrombosis
adv: no bleeding
Adverse reactions:
urticaria, unilateral vision impairment
04/11/19 PATKI 54
55. • Mechanism of action of HEPARIN
• Name LMW Heparins
• Advantages of LMW Heparins
• Antidote for Heparin
• Warfarin mechanism of action
• Name direct thrombin inhibitors
• Antidote for warfarin
• Name fibrinolytic agents
• Streptokinase dose in MI
04/11/19 PATKI 55
57. MRK
What happens when the vessel is damaged?
Vasospasm (immediate response)
Platelet adhesion
Platelet aggregation
Viscous metamorphosis (gelatinous mass)
PLATELET PLUG
Fibrin reinforcement (activation of coagulation)
58. Antiplatelet drugs:
These drugs interfere with platelet function
Useful in prophylaxis of thromboembolic
disorders.
Cyclooxygenase inhibitors: Aspirin
Phosphodiesterase inhibitors: Dipyridamole
ADP antagonists : Clopidogrel, Ticlopidine
Gp II b | III a antagonists: Abciximab
Eptifibatide, Tirofiban
04/11/19 PATKI 58
61. Aspirin: Aspirin is NSAID
Antiplatelet dose of Aspirin: 75-150mg
Mechanism of antiplatelet action:
It acetylates & inhibits the cyclo-oxygenase I
Irreversibly in portal circulation
So it inhibits the production of
thromboxane A2 till fresh platelets are formed.
> 325mg it inhibits the production of
prostacycline and thromboxane A2.
other NSAIDs reversible inhibition04/11/19 PATKI 61
62. MRK
AspirinAspirin
Platelets – major COX product is TXA2
– platelet aggregation & vasoconstriction.
Aspirin – Ecosprin75, 150mg tab
Irreversibly inhibits COX
160 mg/day complete inactivation of platelet COX
Antithrombotic effect dose 160-320 mg/day
At low doses TXA2 formation selectively suppressed
Higher doses > 900mg/d may ↓ both TXA2 & PGI2 production
Other NSAID’s –short lasting inhibition of P function
63. Dipyridamole:
It is a vasodilator
It inhibits the phosphodiesterase
blocks the uptake of adenosine
Finally it increases the cyclic AMP which
potentiates the PG I2& interferes with
platelet aggregation.
DOSE: 150-300mg | day
04/11/19 PATKI 63
64. Ticlopidine
Theinopyridine
Mechanism of action:
alters the surface receptors on platelets and
inhibits the ADP induced platelet aggregation.
It binds with the Gi coupled purinergic
receptors, so it blocks the ADP action.
Finally it increases the cyclic AMP levels and
interferes with the platelet function.
04/11/19 PATKI 64
66. CLOPIDOGREL
Newer congener of Ticlopidine
Mechanism of action, efficacy similar
to Ticlopidine but better tolerated
Lower frequency of neutropenia and
thrombocytopenia
Dose: 75 mg OD
04/11/19 PATKI 66
67. Glycoprotein IIb| IIIa receptor
antagonists:
• Glycoprotein IIb| IIIa receptor
antagonists blocks the platelet
aggregation induced by all platelet
agonists through Glycoprotein IIb/IIIa
receptor.
Abciximab
Eptifibatide
Tirofiban04/11/19 PATKI 67
68. ABCIXIMAB:
It is a monoclonal antibody against
Glycoprotein IIb| IIIa receptor.
It is given along with Aspirin & heparin in
PCI.
It reduces the incidence of restenosis
Dose: 25mg|kg
Adverse reactions:
hemorrhage, thrombocytopenia,
arrhythmias
04/11/19 PATKI 68
71. HEMOSTATIC AGENTS:
These are the substances used to control the bleeding
from local & approachable site
Natural: contraction of blood vessels
platelet aggregation
fibrin deposition
Physical methods:
manual pressure, tourniquet, cold, cautery
04/11/19 PATKI 71
72. Locally acting agents:
Thrombin ( bovine plasma , dry powder )
Thromboplastin ( rabbit brain)
Fibrin ( human plasma )
Gel foam
Oxidized cellulose
Microfibrillar collagen
left in situ these materials are absorbed in 1-4 weeks
Transfusional agents:
fibrinogen
Antihaemophilic globulin
plasma or blood04/11/19 PATKI 72
73. Non- transfusional agents:
VIt K
antifibrinolytics:
Epsilon amino- caproic acid
Tranexaemic acid
Aprotinin
Vit C
Ethamsylate
Desmopressin
Conjugated estrogens04/11/19 PATKI 73
74. • Vit K:
Fat soluble vitamin
Essential for synthesis of clotting factors
( II, VII, IX. X activation )
Vit K1( phytonadione): from foods
Vit K2 : colonic bacteria
Vit K3 : ( Menadione ) synthetic ( water soluble)
Deficiency:
liver disease
jaundice, malabsorption
long term antimicrobial therapy04/11/19 PATKI 74
75. Uses:
1) Over dose of oral anticoagulants
phytonadione 10mg IM
2)Treatment of bleeding in Vit K deficiency states
3) Premature infants:
Phytonadione 1 mg IM after birth
5mg IM 4-6 hours before delivery
Menadione not indicated in newborn, pregnancy
& warfarin induced bleeding:
it induces hemolysis( increases bilirubin load)
competitive inhibition of glucuronidation of
bilirubin
04/11/19 PATKI 75
76. Epsilon amino - caproic acid:
Plasminogen
Plasmin
Uses:
prmary menorrhagia
after prostatic surgery
upper GI bleeding
dental extraction
50mg/kg 6th
hourly04/11/19 PATKI 76
77. Tranexamic acid:
Aprotinin:
• It inhibits the plasmin
• It inhibits the coagulation & fibrinolysis
Ethamsylate:
500mg four times a day
It corrects the abnormal platelet adhesion
04/11/19 PATKI 77
78. Sclerosing agents:
these are irritants
they cause inflammation, coagulation & fibrosis
They are useful only for local injection
into the hemorrhoids and varicose veins
Phenol in almond oil
Ethanolamine oleate
Sodium tetradecyl sulphate
Sodium linoleate
Sodium morrhuate04/11/19 PATKI 78
79. • Name four antiplatelet drugs
• Antiplatelet dose of Aspirin
• Why other NSAIDs are not antiplatelet drugs
• Mechanism of action of HEPARIN
• Name LMW Heparins
• Advantages of LMW Heparins
• Antidote for Heparin
• Warfarin mechanism of action
• Name direct thrombin inhibitors
• Antidote for warfarin
• Name fibrinolytic agents
• Streptokinase dose in MI
• Name antifibrinolytic drugs04/11/19 PATKI 79
81. ANTIFIBRINOLYTICS:
• Epsilon amino caproic acid :
• combines with lysine binding sites of
plasminogen and plasmin so latter is not
able to bind fibrin and lyses it
• Specific antidote for fibrinolytic agents
used in hyper plasminemic states
associated with excessive
intra vascular fibrinolysis.
04/11/19 PATKI 81
82. USES:
• To prevent recurrence of subarachnoid and GI
haemorrhage .
• Abruptio placentae
• PPH
• menorrhagia
• Traumatic surgical bleeding
• haemophilics
• Dose-
• 5g oral / IV followed by 1g hourly
04/11/19 PATKI 82
83. • Trenexaemic acid
• It binds to lysine binding site on plasminogen
prevents combination with fibrin. Seven times
more potent
• USE:
• Over dose of fibrinolytics
• After cardiopulmonary by pass surgery
• Tooth extraction in hemophiliacs
• Menorrhagia due to IUCD
• Recurrent epistaxis
• ocular trauma
• bleeding peptic ulcer
• Dose 10 to 15 mg / kg Day
04/11/19 PATKI 83
84. APROTININ:
• Polypeptide isolated from bovine tissue.
polyvalent protease inhibitory activity
• It inhibits Trypsin, chymotrypsin, kallikrein.
• USES:
• Beginning of cardio pulmonary by pass
surgery – reduces blood loss
• Acute pancreatitis
• Fibrinolytic states
• prostatic surgery
• carcinoid afford symptomatic relief04/11/19 PATKI 84
85. • Adverse effects :
Renal toxicity
MI
Stroke
• Dose
5 lac KIU followed by 2 lac KIU every
4hr slow IV infusion
04/11/19 PATKI 85