This document provides an overview of anticoagulants, including their uses, mechanisms of action, and history. It discusses how anticoagulants work to prevent blood clotting by interfering with coagulation factors. The major anticoagulant drugs covered are heparin, warfarin, and newer oral anticoagulants like dabigatran, rivaroxaban, and fondaparinux. The future of anticoagulant drugs lies in developing more targeted inhibitors of coagulation factors like factor Xa to replace warfarin.
This document provides an overview of anticoagulants, including their general use in preventing blood clotting, a brief overview of the blood coagulation process, and descriptions of several anticoagulant drugs both currently used and in development. It discusses the mechanisms of action and uses of heparin, warfarin, newer oral anticoagulants like dabigatran and rivaroxaban, and the future potential for anticoagulants that directly target specific coagulation factors such as factor Xa.
The document discusses anticoagulant drugs and their use, mechanisms, and side effects. It focuses on warfarin and heparin. Warfarin acts indirectly by interfering with vitamin K, lowering clotting factors. Heparin activates antithrombin III to inactivate coagulation factors. They are used to treat conditions involving blood clots and prevent clotting during procedures. Risks include bleeding as overdose is the most serious complication. Bridge therapy with heparin is used prior to surgery to reduce thromboembolism risk when discontinuing long-term anticoagulants.
Anticoagulants are used to treat and prevent blood clots that may occur in your blood vessels. Blood clots can block blood vessels (an artery or a vein). A blocked artery stops blood and oxygen from getting to a part of your body (for example, to a part of the heart, brain or lungs).
This document discusses perioperative bleeding and homeostasis. It begins with defining bleeding and describing different types. It then covers preoperative bleeding risk assessment, including medication and bleeding history, physical exam, and tools to evaluate risk. Methods of achieving homeostasis during and after surgery are outlined, including mechanical, thermal, pharmacological, and TEG monitoring. Predictors of postoperative bleeding in cardiac surgery and guidelines for assessing bleeding risk from British and European societies are presented.
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 various hematologic drugs used to treat conditions related to blood circulation. It covers the mechanisms, indications, contraindications, side effects and nursing considerations for different classes of drugs including anticoagulants, antiplatelets, thrombolytics, agents to treat bleeding, antihyperlipidemics, and antianemics.
The document discusses blood coagulation, anticoagulant and thrombolytic drugs. It provides details on the coagulation cascade and factors involved in coagulation. It also describes various anticoagulant drugs like heparin, warfarin and thrombolytic drugs like streptokinase, urokinase and tissue plasminogen activators; and discusses their mechanisms of action, uses, and adverse effects.
Coagulants and anticoagulants work in opposing ways to regulate blood coagulation. Coagulants such as vitamin K and plasma fractions help promote coagulation by activating clotting factors. Anticoagulants like heparin and warfarin inhibit coagulation factors or their production. Thrombolytics such as streptokinase and tissue plasminogen activator dissolve clots by activating plasmin. Platelet aggregation inhibitors including aspirin and clopidogrel prevent platelet activation and aggregation, which are key steps in clot formation. These drugs are used to treat and prevent thrombotic conditions.
This document provides an overview of anticoagulants, including their general use in preventing blood clotting, a brief overview of the blood coagulation process, and descriptions of several anticoagulant drugs both currently used and in development. It discusses the mechanisms of action and uses of heparin, warfarin, newer oral anticoagulants like dabigatran and rivaroxaban, and the future potential for anticoagulants that directly target specific coagulation factors such as factor Xa.
The document discusses anticoagulant drugs and their use, mechanisms, and side effects. It focuses on warfarin and heparin. Warfarin acts indirectly by interfering with vitamin K, lowering clotting factors. Heparin activates antithrombin III to inactivate coagulation factors. They are used to treat conditions involving blood clots and prevent clotting during procedures. Risks include bleeding as overdose is the most serious complication. Bridge therapy with heparin is used prior to surgery to reduce thromboembolism risk when discontinuing long-term anticoagulants.
Anticoagulants are used to treat and prevent blood clots that may occur in your blood vessels. Blood clots can block blood vessels (an artery or a vein). A blocked artery stops blood and oxygen from getting to a part of your body (for example, to a part of the heart, brain or lungs).
This document discusses perioperative bleeding and homeostasis. It begins with defining bleeding and describing different types. It then covers preoperative bleeding risk assessment, including medication and bleeding history, physical exam, and tools to evaluate risk. Methods of achieving homeostasis during and after surgery are outlined, including mechanical, thermal, pharmacological, and TEG monitoring. Predictors of postoperative bleeding in cardiac surgery and guidelines for assessing bleeding risk from British and European societies are presented.
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 various hematologic drugs used to treat conditions related to blood circulation. It covers the mechanisms, indications, contraindications, side effects and nursing considerations for different classes of drugs including anticoagulants, antiplatelets, thrombolytics, agents to treat bleeding, antihyperlipidemics, and antianemics.
The document discusses blood coagulation, anticoagulant and thrombolytic drugs. It provides details on the coagulation cascade and factors involved in coagulation. It also describes various anticoagulant drugs like heparin, warfarin and thrombolytic drugs like streptokinase, urokinase and tissue plasminogen activators; and discusses their mechanisms of action, uses, and adverse effects.
Coagulants and anticoagulants work in opposing ways to regulate blood coagulation. Coagulants such as vitamin K and plasma fractions help promote coagulation by activating clotting factors. Anticoagulants like heparin and warfarin inhibit coagulation factors or their production. Thrombolytics such as streptokinase and tissue plasminogen activator dissolve clots by activating plasmin. Platelet aggregation inhibitors including aspirin and clopidogrel prevent platelet activation and aggregation, which are key steps in clot formation. These drugs are used to treat and prevent thrombotic conditions.
Coagulants and anticoagulants work in opposing ways to regulate blood coagulation. Coagulants such as vitamin K and plasma fractions help promote coagulation by facilitating the production and function of clotting factors. Anticoagulants like heparin and warfarin inhibit coagulation factors or their production. Thrombolytics like streptokinase and tissue plasminogen activator dissolve clots by converting plasminogen to plasmin. Platelet aggregation inhibitors such as aspirin and clopidogrel prevent platelet activation and aggregation to inhibit clot formation. These drugs are used to treat or prevent conditions involving abnormal blood clotting.
Hematologic drugs are used to treat various blood disorders like thrombosis, bleeding, and anemia. The document discusses several classes of drugs including anticoagulants, antiplatelets, thrombolytics, agents to treat bleeding, antihyperlipidemics, and antianemics. Specific drugs within each class like heparin, warfarin, aspirin, streptokinase, iron, and erythropoietin are explained in terms of their mechanisms of action, indications, adverse effects and nursing considerations.
Drugs acting on Haemopoietic system - Anticoagulants.pptxLogeshtharanD
The document discusses various topics related to haemopoietic system pharmacology including thrombosis, anticoagulants, and coagulation factors. It describes how venous thrombosis can lead to pulmonary embolism and arterial thrombosis is associated with atherosclerosis. It also summarizes the mechanisms of heparin and warfarin as anticoagulants, their clinical uses, monitoring, and toxicity. Low molecular weight heparins mainly inhibit factor Xa while heparin inhibits both factor Xa and thrombin. Warfarin is an oral anticoagulant that acts as a vitamin K antagonist by inhibiting the epoxide reductase enzyme.
Direct-acting anticoagulants like heparin work directly in the blood to inhibit coagulation factors. Heparin is extracted from pig intestines and bovine lungs. Indirect anticoagulants called oral anticoagulants or vitamin K antagonists inhibit coagulation factor synthesis in the liver. Coumarin derivatives like warfarin and dicoumarol are commonly used oral anticoagulants that act by inhibiting vitamin K and decreasing prothrombin synthesis. Warfarin is effective for treating deep vein thrombosis while dicoumarol has fallen out of favor due to side effects and unpredictable response. Anticoagulants must be closely monitored to prevent bleeding complications.
Drugs that help prevent the clotting (coagulation) of blood
Coagulation will occur instantaneously once a blood vessel has been severed.
Blood begins to solidify to prevent the excessive blood loss and to prevent invasive substances from entering the bloodstream.
USED IN VIVO
A. PARENTRAL ANTICOAGULANTS
B. ORAL ANTICOAGULANTS
USED IN VITRO
A.HEPARIN
B.CALCIUM COMPLEXING AGENTS
PARENTRAL ANTICOAGULANTS
1. INDIRECT THROMBIN INHIBITORS
Heparin, Low molecular weight heparins, Fondaparinux,Donaparoid
2. DIRECT THROMBIN INHIBITORS
Lepirudin, Bivalirudin, Argatroban
ORAL ANTICOAGULANTS
1. COUMARIN DERIVATIVES
Bishydroxycoumarin (dicumarol), Warfarin sod, Acenocoumarol,
(Nicoumalon), Ethylbiscoumacetate
2.INDANDIONE DERIVATIVES
Phenindione
3.DIRECT FACTOR Xa INHIBITORS
Rivaroxaban
4.ORAL DIRECT THROMBIN INHIBITOR
Dabigatran, etexilate
USED IN VITRO
1.HEPARIN
2. CALCIUM COMPLEXING AGENTS
SODIUM CITRATE
SODIUM OXALATE
SODIUM EDETATE
Heparin is a non uniform mixture of straight chain mucopolysaccharides with molecular weight 10000 to 20000
It contains polymers of two sulfated diasaccharide units
D –glucosamine-L-iduronic acid
D-glucosamine-D-glucoronic acid
Heparin
It is present in all tissues containing mast cells, richest sources are lung, liver and intestinal ,mucosa
Clinically Important DRUG INTERACTIONS OF ANTICOAGULANTS:Naina Mohamed, PhD
The document discusses clinically important drug interactions of various anticoagulants including warfarin, dabigatran, heparin, with other medications, supplements, foods and diseases. It provides details of potential mechanisms of interactions that can increase bleeding risk like additive anticoagulant or antiplatelet effects, or decrease anticoagulant effectiveness by affecting drug metabolism. Close monitoring of anticoagulant effect and bleeding signs are recommended when using certain interacting agents together due to the risk of bleeding complications or reduced thrombosis prevention.
the all the content in this profile is completed by the teachers, students as well as other health care peoples.
thank you, all the respected peoples, for giving the information to complete this presentation.
this information is free to use by anyone.
This document discusses drugs that modify blood coagulation. It begins by describing two case scenarios involving bleeding during tooth extraction. It then outlines the key learning objectives for medical students regarding drugs that achieve and prevent coagulation. The rest of the document provides details on the mechanisms, pharmacokinetics, uses, and adverse effects of various anticoagulant and coagulant drugs, including heparin, warfarin, vitamin K, fibrinolytics, antiplatelet drugs like aspirin, and dipyridamole.
Vitamin K acts as a cofactor in the liver's synthesis of coagulation proteins, and a daily intake of 50-100 micrograms is usually sufficient. Coagulants like plasma fractions containing coagulation factors VIII and IX are used to treat deficiencies that cause bleeding disorders. Anticoagulants prevent thrombus formation and embolism by reducing fibrin formation; they include heparin and low molecular weight heparins, warfarin and related oral anticoagulants, and newer direct factor Xa and thrombin inhibitors. Monitoring of anticoagulant levels is important when they are used to treat conditions involving deep vein thrombosis, pulmonary embolism, myocardial infarction and others.
This document summarizes the development of newer anticoagulants, including direct thrombin inhibitors and factor Xa inhibitors. It discusses the limitations of older anticoagulants like heparin, warfarin, and low molecular weight heparins. Newer oral anticoagulants like dabigatran, rivaroxaban, apixaban and edoxaban directly inhibit thrombin or factor Xa and have improved properties over warfarin such as fewer drug and food interactions and more predictable dosing without monitoring. Clinical trials found these newer anticoagulants to be as effective or more effective than warfarin or enoxaparinux for preventing strokes in atrial fibrill
Anticoagulants, commonly referred to as blood thinners, are chemical substances that prevent or reduce coagulation of blood, prolonging the clotting time.
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 discusses haemorrhage and haemostasis in dentistry. It defines haemorrhage as the escape of blood from blood vessels. The mechanisms of primary and secondary haemostasis that work to stop bleeding are described. Common bleeding disorders like hemophilia A and B, von Willebrand's disease, and those caused by vitamin K deficiency or liver disease are outlined. Methods for managing bleeding during dental procedures and treating bleeding disorders are provided. The roles of public health dentists and dental hygienists in addressing bleeding disorders are also mentioned.
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.
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.
- Oral anticoagulants like warfarin and dicoumarol work indirectly by inhibiting the synthesis of vitamin K-dependent clotting factors in the liver.
- Heparin is a direct-acting anticoagulant that works by activating antithrombin III, which inactivates coagulation factors and prevents clot formation.
- Anticoagulants are used to treat and prevent dangerous blood clots caused by conditions like deep vein thrombosis, pulmonary embolism, and atrial fibrillation.
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.
PARENTERAL anticoagulants, fibrinolyticsKarthiga M
1) Parenteral anticoagulants like heparin and low molecular weight heparins work by binding to clotting factors to inactivate the intrinsic pathway and prevent further clot formation.
2) Direct thrombin inhibitors like hirudin, argatroban, and dabigatran directly bind and inhibit thrombin to prevent clot development and extension.
3) Thrombolytic drugs such as streptokinase, urokinase, and alteplase activate plasminogen and convert it into plasmin to enzymatically degrade existing clots.
Drug interactions of Low Molecular weight Heparins (LMWHs)Naina Mohamed, PhD
This document discusses drug interactions of low molecular weight heparins (LMWHs), which are a class of anticoagulants. It notes that LMWHs can interact with various prescription drugs, supplements, foods and herbs to increase the risk of bleeding. Specifically, it finds that LMWHs combined with warfarin, heparin, other anticoagulants, antiplatelet agents, fibrinolytics, NSAIDs, SSRIs, SNRIs, St. John's Wort, ginkgo, garlic, papaya, chamomile and various other supplements can have additive anticoagulant effects and increase bleeding risk. It advises close monitoring of patients if these drugs are coadmin
This document provides information on peripheral nerve blocks of the wrist. It discusses the anatomy and techniques for blocking the radial, ulnar, and median nerves. It describes identifying landmarks for each nerve and injecting local anesthetic. Potential complications are also reviewed, along with signs and treatment of local anesthetic systemic toxicity. Proper technique and avoiding excess volumes are emphasized to prevent issues like nerve injury or gangrene.
Coagulants and anticoagulants work in opposing ways to regulate blood coagulation. Coagulants such as vitamin K and plasma fractions help promote coagulation by facilitating the production and function of clotting factors. Anticoagulants like heparin and warfarin inhibit coagulation factors or their production. Thrombolytics like streptokinase and tissue plasminogen activator dissolve clots by converting plasminogen to plasmin. Platelet aggregation inhibitors such as aspirin and clopidogrel prevent platelet activation and aggregation to inhibit clot formation. These drugs are used to treat or prevent conditions involving abnormal blood clotting.
Hematologic drugs are used to treat various blood disorders like thrombosis, bleeding, and anemia. The document discusses several classes of drugs including anticoagulants, antiplatelets, thrombolytics, agents to treat bleeding, antihyperlipidemics, and antianemics. Specific drugs within each class like heparin, warfarin, aspirin, streptokinase, iron, and erythropoietin are explained in terms of their mechanisms of action, indications, adverse effects and nursing considerations.
Drugs acting on Haemopoietic system - Anticoagulants.pptxLogeshtharanD
The document discusses various topics related to haemopoietic system pharmacology including thrombosis, anticoagulants, and coagulation factors. It describes how venous thrombosis can lead to pulmonary embolism and arterial thrombosis is associated with atherosclerosis. It also summarizes the mechanisms of heparin and warfarin as anticoagulants, their clinical uses, monitoring, and toxicity. Low molecular weight heparins mainly inhibit factor Xa while heparin inhibits both factor Xa and thrombin. Warfarin is an oral anticoagulant that acts as a vitamin K antagonist by inhibiting the epoxide reductase enzyme.
Direct-acting anticoagulants like heparin work directly in the blood to inhibit coagulation factors. Heparin is extracted from pig intestines and bovine lungs. Indirect anticoagulants called oral anticoagulants or vitamin K antagonists inhibit coagulation factor synthesis in the liver. Coumarin derivatives like warfarin and dicoumarol are commonly used oral anticoagulants that act by inhibiting vitamin K and decreasing prothrombin synthesis. Warfarin is effective for treating deep vein thrombosis while dicoumarol has fallen out of favor due to side effects and unpredictable response. Anticoagulants must be closely monitored to prevent bleeding complications.
Drugs that help prevent the clotting (coagulation) of blood
Coagulation will occur instantaneously once a blood vessel has been severed.
Blood begins to solidify to prevent the excessive blood loss and to prevent invasive substances from entering the bloodstream.
USED IN VIVO
A. PARENTRAL ANTICOAGULANTS
B. ORAL ANTICOAGULANTS
USED IN VITRO
A.HEPARIN
B.CALCIUM COMPLEXING AGENTS
PARENTRAL ANTICOAGULANTS
1. INDIRECT THROMBIN INHIBITORS
Heparin, Low molecular weight heparins, Fondaparinux,Donaparoid
2. DIRECT THROMBIN INHIBITORS
Lepirudin, Bivalirudin, Argatroban
ORAL ANTICOAGULANTS
1. COUMARIN DERIVATIVES
Bishydroxycoumarin (dicumarol), Warfarin sod, Acenocoumarol,
(Nicoumalon), Ethylbiscoumacetate
2.INDANDIONE DERIVATIVES
Phenindione
3.DIRECT FACTOR Xa INHIBITORS
Rivaroxaban
4.ORAL DIRECT THROMBIN INHIBITOR
Dabigatran, etexilate
USED IN VITRO
1.HEPARIN
2. CALCIUM COMPLEXING AGENTS
SODIUM CITRATE
SODIUM OXALATE
SODIUM EDETATE
Heparin is a non uniform mixture of straight chain mucopolysaccharides with molecular weight 10000 to 20000
It contains polymers of two sulfated diasaccharide units
D –glucosamine-L-iduronic acid
D-glucosamine-D-glucoronic acid
Heparin
It is present in all tissues containing mast cells, richest sources are lung, liver and intestinal ,mucosa
Clinically Important DRUG INTERACTIONS OF ANTICOAGULANTS:Naina Mohamed, PhD
The document discusses clinically important drug interactions of various anticoagulants including warfarin, dabigatran, heparin, with other medications, supplements, foods and diseases. It provides details of potential mechanisms of interactions that can increase bleeding risk like additive anticoagulant or antiplatelet effects, or decrease anticoagulant effectiveness by affecting drug metabolism. Close monitoring of anticoagulant effect and bleeding signs are recommended when using certain interacting agents together due to the risk of bleeding complications or reduced thrombosis prevention.
the all the content in this profile is completed by the teachers, students as well as other health care peoples.
thank you, all the respected peoples, for giving the information to complete this presentation.
this information is free to use by anyone.
This document discusses drugs that modify blood coagulation. It begins by describing two case scenarios involving bleeding during tooth extraction. It then outlines the key learning objectives for medical students regarding drugs that achieve and prevent coagulation. The rest of the document provides details on the mechanisms, pharmacokinetics, uses, and adverse effects of various anticoagulant and coagulant drugs, including heparin, warfarin, vitamin K, fibrinolytics, antiplatelet drugs like aspirin, and dipyridamole.
Vitamin K acts as a cofactor in the liver's synthesis of coagulation proteins, and a daily intake of 50-100 micrograms is usually sufficient. Coagulants like plasma fractions containing coagulation factors VIII and IX are used to treat deficiencies that cause bleeding disorders. Anticoagulants prevent thrombus formation and embolism by reducing fibrin formation; they include heparin and low molecular weight heparins, warfarin and related oral anticoagulants, and newer direct factor Xa and thrombin inhibitors. Monitoring of anticoagulant levels is important when they are used to treat conditions involving deep vein thrombosis, pulmonary embolism, myocardial infarction and others.
This document summarizes the development of newer anticoagulants, including direct thrombin inhibitors and factor Xa inhibitors. It discusses the limitations of older anticoagulants like heparin, warfarin, and low molecular weight heparins. Newer oral anticoagulants like dabigatran, rivaroxaban, apixaban and edoxaban directly inhibit thrombin or factor Xa and have improved properties over warfarin such as fewer drug and food interactions and more predictable dosing without monitoring. Clinical trials found these newer anticoagulants to be as effective or more effective than warfarin or enoxaparinux for preventing strokes in atrial fibrill
Anticoagulants, commonly referred to as blood thinners, are chemical substances that prevent or reduce coagulation of blood, prolonging the clotting time.
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 discusses haemorrhage and haemostasis in dentistry. It defines haemorrhage as the escape of blood from blood vessels. The mechanisms of primary and secondary haemostasis that work to stop bleeding are described. Common bleeding disorders like hemophilia A and B, von Willebrand's disease, and those caused by vitamin K deficiency or liver disease are outlined. Methods for managing bleeding during dental procedures and treating bleeding disorders are provided. The roles of public health dentists and dental hygienists in addressing bleeding disorders are also mentioned.
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.
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.
- Oral anticoagulants like warfarin and dicoumarol work indirectly by inhibiting the synthesis of vitamin K-dependent clotting factors in the liver.
- Heparin is a direct-acting anticoagulant that works by activating antithrombin III, which inactivates coagulation factors and prevents clot formation.
- Anticoagulants are used to treat and prevent dangerous blood clots caused by conditions like deep vein thrombosis, pulmonary embolism, and atrial fibrillation.
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.
PARENTERAL anticoagulants, fibrinolyticsKarthiga M
1) Parenteral anticoagulants like heparin and low molecular weight heparins work by binding to clotting factors to inactivate the intrinsic pathway and prevent further clot formation.
2) Direct thrombin inhibitors like hirudin, argatroban, and dabigatran directly bind and inhibit thrombin to prevent clot development and extension.
3) Thrombolytic drugs such as streptokinase, urokinase, and alteplase activate plasminogen and convert it into plasmin to enzymatically degrade existing clots.
Drug interactions of Low Molecular weight Heparins (LMWHs)Naina Mohamed, PhD
This document discusses drug interactions of low molecular weight heparins (LMWHs), which are a class of anticoagulants. It notes that LMWHs can interact with various prescription drugs, supplements, foods and herbs to increase the risk of bleeding. Specifically, it finds that LMWHs combined with warfarin, heparin, other anticoagulants, antiplatelet agents, fibrinolytics, NSAIDs, SSRIs, SNRIs, St. John's Wort, ginkgo, garlic, papaya, chamomile and various other supplements can have additive anticoagulant effects and increase bleeding risk. It advises close monitoring of patients if these drugs are coadmin
This document provides information on peripheral nerve blocks of the wrist. It discusses the anatomy and techniques for blocking the radial, ulnar, and median nerves. It describes identifying landmarks for each nerve and injecting local anesthetic. Potential complications are also reviewed, along with signs and treatment of local anesthetic systemic toxicity. Proper technique and avoiding excess volumes are emphasized to prevent issues like nerve injury or gangrene.
Dengue fever is a viral disease spread by the Aedes mosquito. The document discusses what dengue fever is, its symptoms, the characteristics and life cycle of the Aedes mosquito, how it transmits diseases like dengue, and how to prevent the spread of dengue fever. It also provides tips for what dengue patients should and should not do, and includes a quiz.
The document discusses Dengue Awareness Day and provides information about dengue fever, the Aedes mosquito, and how to prevent the spread of dengue. It notes that the Aedes mosquito has black and white stripes and bites during the day. It lays its eggs in clean, stagnant water and can transmit dengue virus to humans. The document also includes three quiz questions that test understanding of why the Aedes mosquito is dangerous, steps to wipe out dengue mosquitos, and things to do before going on holiday to prevent dengue.
Dengue fever is a mosquito-borne disease caused by the Aedes mosquito. The document discusses what dengue fever is, its symptoms, the characteristics and life cycle of the Aedes mosquito, how it transmits diseases, ways to prevent the spread of dengue fever, dos and don'ts for dengue patients, and includes a quiz. The document aims to raise awareness about dengue fever on Dengue Awareness Day through providing information on the disease and its causes.
Basics of echo Cardiac Structure, Chamber quantifications & Artifacts.pptxmuhammadshoaib578
This document discusses an echocardiogram procedure including indications, objectives, cardiac structures, chamber quantifications, and artifacts. It describes assessing the size and function of the left ventricle, valves, vessels, and other structures. Doppler techniques are outlined for evaluating pressures, velocities, and shunts. Guidelines are provided for measuring chambers like the left atrium and aortic root. Methods to minimize aliasing artifacts in echocardiograms are also reviewed.
Nutritional deficiency Disorder are problems in india.
It is very important to learn about Indian child's nutritional parameters as well the Disease related to alteration in their Nutrition.
Dr. Tan's Balance Method.pdf (From Academy of Oriental Medicine at Austin)GeorgeKieling1
Home
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Academy of Oriental Medicine at Austin
Academy of Oriental Medicine at Austin
Academy of Oriental Medicine at Austin
About AOMA: The Academy of Oriental Medicine at Austin offers a masters-level graduate program in acupuncture and Oriental medicine, preparing its students for careers as skilled, professional practitioners. AOMA is known for its internationally recognized faculty, award-winning student clinical internship program, and herbal medicine program. Since its founding in 1993, AOMA has grown rapidly in size and reputation, drawing students from around the nation and faculty from around the world. AOMA also conducts more than 20,000 patient visits annually in its student and professional clinics. AOMA collaborates with Western healthcare institutions including the Seton Family of Hospitals, and gives back to the community through partnerships with nonprofit organizations and by providing free and reduced price treatments to people who cannot afford them. The Academy of Oriental Medicine at Austin is located at 2700 West Anderson Lane. AOMA also serves patients and retail customers at its south Austin location, 4701 West Gate Blvd. For more information see www.aoma.edu or call 512-492-303434.
Milan J. Anadkat, MD, and Dale V. Reisner discuss generalized pustular psoriasis in this CME activity titled "Supporting Patient-Centered Care in Generalized Pustular Psoriasis: Communications Strategies to Improve Shared Decision-Making." For the full presentation, please visit us at www.peervoice.com/HUM870.
TEST BANK For Brunner and Suddarth's Textbook of Medical-Surgical Nursing, 14...Donc Test
TEST BANK For Brunner and Suddarth's Textbook of Medical-Surgical Nursing, 14th Edition (Hinkle, 2017) Verified Chapter's 1 - 73 Complete.pdf
TEST BANK For Brunner and Suddarth's Textbook of Medical-Surgical Nursing, 14th Edition (Hinkle, 2017) Verified Chapter's 1 - 73 Complete.pdf
TEST BANK For Brunner and Suddarth's Textbook of Medical-Surgical Nursing, 14th Edition (Hinkle, 2017) Verified Chapter's 1 - 73 Complete.pdf
This presentation gives information on the pharmacology of Prostaglandins, Thromboxanes and Leukotrienes i.e. Eicosanoids. Eicosanoids are signaling molecules derived from polyunsaturated fatty acids like arachidonic acid. They are involved in complex control over inflammation, immunity, and the central nervous system. Eicosanoids are synthesized through the enzymatic oxidation of fatty acids by cyclooxygenase and lipoxygenase enzymes. They have short half-lives and act locally through autocrine and paracrine signaling.
Giloy in Ayurveda - Classical Categorization and SynonymsPlanet Ayurveda
Giloy, also known as Guduchi or Amrita in classical Ayurvedic texts, is a revered herb renowned for its myriad health benefits. It is categorized as a Rasayana, meaning it has rejuvenating properties that enhance vitality and longevity. Giloy is celebrated for its ability to boost the immune system, detoxify the body, and promote overall wellness. Its anti-inflammatory, antipyretic, and antioxidant properties make it a staple in managing conditions like fever, diabetes, and stress. The versatility and efficacy of Giloy in supporting health naturally highlight its importance in Ayurveda. At Planet Ayurveda, we provide a comprehensive range of health services and 100% herbal supplements that harness the power of natural ingredients like Giloy. Our products are globally available and affordable, ensuring that everyone can benefit from the ancient wisdom of Ayurveda. If you or your loved ones are dealing with health issues, contact Planet Ayurveda at 01725214040 to book an online video consultation with our professional doctors. Let us help you achieve optimal health and wellness naturally.
The biomechanics of running involves the study of the mechanical principles underlying running movements. It includes the analysis of the running gait cycle, which consists of the stance phase (foot contact to push-off) and the swing phase (foot lift-off to next contact). Key aspects include kinematics (joint angles and movements, stride length and frequency) and kinetics (forces involved in running, including ground reaction and muscle forces). Understanding these factors helps in improving running performance, optimizing technique, and preventing injuries.
Congestive Heart failure is caused by low cardiac output and high sympathetic discharge. Diuretics reduce preload, ACE inhibitors lower afterload, beta blockers reduce sympathetic activity, and digitalis has inotropic effects. Newer medications target vasodilation and myosin activation to improve heart efficiency while lowering energy requirements. Combination therapy, following an assessment of cardiac function and volume status, is the most effective strategy to heart failure care.
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Storyboard on Skin- Innovative Learning (M-pharm) 2nd sem. (Cosmetics)MuskanShingari
Skin is the largest organ of the human body, serving crucial functions that include protection, sensation, regulation, and synthesis. Structurally, it consists of three main layers: the epidermis, dermis, and hypodermis (subcutaneous layer).
1. **Epidermis**: The outermost layer primarily composed of epithelial cells called keratinocytes. It provides a protective barrier against environmental factors, pathogens, and UV radiation.
2. **Dermis**: Located beneath the epidermis, the dermis contains connective tissue, blood vessels, hair follicles, and sweat glands. It plays a vital role in supporting and nourishing the epidermis, regulating body temperature, and housing sensory receptors for touch, pressure, temperature, and pain.
3. **Hypodermis**: Also known as the subcutaneous layer, it consists of fat and connective tissue that anchors the skin to underlying structures like muscles and bones. It provides insulation, cushioning, and energy storage.
Skin performs essential functions such as regulating body temperature through sweat production and blood flow control, synthesizing vitamin D when exposed to sunlight, and serving as a sensory interface with the external environment.
Maintaining skin health is crucial for overall well-being, involving proper hygiene, hydration, protection from sun exposure, and avoiding harmful substances. Skin conditions and diseases range from minor irritations to chronic disorders, emphasizing the importance of regular care and medical attention when needed.
Breast cancer :Receptor (ER/PR/HER2 NEU) Discordance.pptxDr. Sumit KUMAR
Receptor Discordance in Breast Carcinoma During the Course of Life
Definition:
Receptor discordance refers to changes in the status of hormone receptors (estrogen receptor ERα, progesterone receptor PgR, and HER2) in breast cancer tumors over time or between primary and metastatic sites.
Causes:
Tumor Evolution:
Genetic and epigenetic changes during tumor progression can lead to alterations in receptor status.
Treatment Effects:
Therapies, especially endocrine and targeted therapies, can selectively pressure tumor cells, causing shifts in receptor expression.
Heterogeneity:
Inherent heterogeneity within the tumor can result in subpopulations of cells with different receptor statuses.
Impact on Treatment:
Therapeutic Resistance:
Loss of ERα or PgR can lead to resistance to endocrine therapies.
HER2 discordance affects the efficacy of HER2-targeted treatments.
Treatment Adjustment:
Regular reassessment of receptor status may be necessary to adjust treatment strategies appropriately.
Clinical Implications:
Prognosis:
Receptor discordance is often associated with a poorer prognosis.
Biopsies:
Obtaining biopsies from metastatic sites is crucial for accurate receptor status assessment and effective treatment planning.
Monitoring:
Continuous monitoring of receptor status throughout the disease course can guide personalized therapy adjustments.
Understanding and managing receptor discordance is essential for optimizing treatment outcomes and improving the prognosis for breast cancer patients.
Selective alpha1 blockers are Prazosin, Terazosin, Doxazosin, Tamsulosin and Silodosin majorly used to treat BPH, also hypertension, PTSD, Raynaud's phenomenon, CHF
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Understanding Atherosclerosis Causes, Symptoms, Complications, and Preventionrealmbeats0
Definition: Atherosclerosis is a condition characterized by the buildup of plaques, which are made up of fat, cholesterol, calcium, and other substances, in the walls of arteries. Over time, these plaques harden and narrow the arteries, restricting blood flow.
Importance: This condition is a major contributor to cardiovascular diseases, including coronary artery disease, carotid artery disease, and peripheral artery disease. Understanding atherosclerosis is crucial for preventing these serious health issues.
Overview: We will cover the aims and objectives of this presentation, delve into the signs and symptoms of atherosclerosis, discuss its complications, and explore preventive measures and lifestyle changes that can mitigate risk.
Aim: To provide a detailed understanding of atherosclerosis, encompassing its pathophysiology, risk factors, clinical manifestations, and strategies for prevention and management.
Purpose: The primary purpose of this presentation is to raise awareness about atherosclerosis, highlight its impact on public health, and educate individuals on how they can reduce their risk through lifestyle changes and medical interventions.
Educational Goals:
Explain the pathophysiology of atherosclerosis, including the processes of plaque formation and arterial hardening.
Identify the risk factors associated with atherosclerosis, such as high cholesterol, hypertension, smoking, diabetes, and sedentary lifestyle.
Discuss the clinical signs and symptoms that may indicate the presence of atherosclerosis.
Highlight the potential complications arising from untreated atherosclerosis, including heart attack, stroke, and peripheral artery disease.
Provide practical advice on preventive measures, including dietary recommendations, exercise guidelines, and the importance of regular medical check-ups.
2. Outline
General Overview of Anticoag
ulants
Overview of Blood Coagulation
Anticoagulant Drugs
History of Anticoagulant Drugs
Use of Anticoagulants Today,
Prevention
Future Outlook
3. Anticoagulants – General Overview
Drugs that help prevent the clotting (coagulat
ion) of blood
Coagulation will occur instantaneously once
a blood vessel has been severed
Blood begins to solidify to prevent
excessive blood loss and to prevent
invasive substances from entering
the bloodstream
4. A Blood Clot
Consists of platelets
meshed into fibrin
A web-like accumulati
on of strands with RB
Cs
There are two major f
acets of the clotting m
echanism – the platel
ets, and the thrombin
system
5. Platelets
Tiny cellular elements, made in the bone mar
row, that travel in the bloodstream waiting for
a bleeding problem to develop
When bleeding occurs, chemical reactions ch
ange the surface of the platelet to make it act
ivated and become “sticky”
These activated platelets begin adhering to t
he wall of the blood vessel at the site of blee
ding
6. Thrombin System
Calcium ions must be present for
the thrombin system to begin
The thrombin system consists of s
everal blood proteins that activate
when bleeding occurs
The activated clotting proteins en
gage in a cascade of chemical re
actions that finally produce a subs
tance called fibrin
Fibrin strands stick to the expose
d vessel wall, clumping together a
nd forming a web-like complex of
strands
Red blood cells become caught u
p in the web, causing a clot
7. Coagulation Factors
Factor Name
I Fibrinogen
II Prothrombin
III Tissue Factor or
thromboplastin
IV Ca++
V Proaccelerin
VII Proconvertin
VIII Antihemophilic A
factor
IX Antihemophilic B
factor or Christmas
factor
Factor Name
X Stuart or Stuart-
Prower factor
XI Plasma thomboplastin
antecedent
XII Hageman factor,
contact factor
XIII Fibrin stabilizing factor
Prekallikrein factor
High-molecular-weight
kininogen
8. Heparin
Heparin is a naturally-occurring anticoag
ulant produced by basophils and mast ce
lls to prevent formation and extension of
blood clots
Heparin does not disintegrate clots that h
ave already formed. It permits the body's
natural clot lysis mechanisms, i.e. fibrinol
ysis, to work normally to break down pre
viously formed clots
As the thrombokinase is released, it neut
ralizes the action of heparin to allow clotti
ng to occur
9. Anticoagulant Use
Anticoagulant drugs help prevent the development of
harmful clots in the blood vessels by lessening the bl
ood's ability to cluster together
The function of these drugs is often misunderstood b
ecause they are sometimes referred to as blood thin
ners; they do not in fact thin the blood
These drugs will not dissolve clots that already have
formed, but it will stop an existing clot from becoming
worse and prevent future clots
10. Anticoagulant Drugs
Heparin and warfarin are the two traditional anticoagula
nts
Anticoagulants are used for acute coronary syndromes,
deep-vein thrombosis (DVT), pulmonary embolism (PE)
, and heart surgery
Thrombus - A blood clot that forms abnormally within th
e blood vessels
Embolus - When a blood clot becomes dislodged from t
he vessel wall and travels through the bloodstream
It is also given to certain people at risk for forming bloo
d clots, such as those with artificial heart valves or who
have atrial fibrillation (AF)
11. Warfarin
Warfarin is an oral medication
It is a synthetic derivative of co
umarin, a chemical found natur
ally in many plants -- it decrea
ses blood coagulation by interf
ering with vitamin K metabolis
m
It stops the blood from clotting
within the blood vessels and is
used to stop existing clots from
getting bigger (as in DVT) and
to stop parts of clots breaking
off and forming emboli (as in P
E)
12. Warfarin
The most common side effects of warfarin are bleedi
ng and bruising
The bleeding can be in the form of prolonged bleedin
g from cuts; bleeding that does not stop by itself
Treatment is monitored by regular blood testing usin
g the International Normalized Ratio (INR), which is
a measure of how much longer it takes the blood to c
lot when oral anticoagulant drug is used
13. Warfarin
Warfarin inhibits the effective synthesis of biologically acti
ve forms of the vitamin K-dependent clotting factors: II, VI
I, IX and X, as well as the regulatory factors protein C, pr
otein S and protein Z
14. Dabigatran etexilate
It was developed by Boehringer Ingelheim
Dabigatran etexilate is a new oral direct thro
mbin inhibitor and the prodrug of dabigatran
Dabigatran is a small molecule that reversibl
y inhibits both free and clot-bound thrombin b
y binding to exosite 1 and/or the active site of
thrombin
15. Rivaroxaban
Developed by Bayer
Rivaroxaban is an orally available, small-molecul
e, active site-directed factor Xa inhibitor
There are no significant interactions between foo
d, antacids, digoxin, aspirin, naproxen and rivaro
xaban have been noted suggesting that dose adj
ustment of rivaroxaban would not be required wh
en these agents are concurrently administered
16. Anisindione
Anisindione (brand name Miradon) is a synth
etic oral anticoagulant and an indanedione d
erivative
Reduces the prothrombin activity of the blood
It prevents the formation of active procoagula
tion factors II, VII, IX, and X, as well as the a
nticoagulant proteins C and S, in the liver by i
nhibiting the vitamin K–mediated gamma-car
boxylation of precursor proteins
17. Dicumarol
It is a potent oral anticoagulant that acts by inhibiting
the synthesis of vitamin K-dependent clotting factors
(prothrombin and factors VII, IX and X) in the liver; it i
s starting to largely replace warfarin
Dicumarol is produced naturally by conversion of no
ntoxic coumarin in moldy sweet clover hay, lespepez
a hay or sweet vernal hay
It is used especially in preventing and treating throm
boembolic disease
Formerly called bishydroxycoumarin
18. Heparin
Heparin is given by injection or drip into a vein
(intravenously) or by injection under the skin
(subcutaneously) for treatment and prevention
It is derived from porcine intestinal mucosa, standardized fo
r anticoagulant activity
Heparin works by inhibiting the three major clotting factors (t
hrombin, thromboplastin, and prothrombin)
It slows the process of thromboplastin synthesis, decelerate
s the conversion of prothrombin to thrombin, and inhibits the
effects of thrombin on fibrinogen, blocking its conversion to f
ibrin
The agent also causes an increase in the number of negativ
ely charged ions in the vascular wall, which helps prevent th
e formation of intravascular clots.
19. Low-molecular weight heparin
Low-molecular weight heparin is gradually re
placing heparin for treatment of most patients
with venous thromboembolism and acute cor
onary syndromes because it has more conve
nient and cost-effective
It has similar results to heparin
Administered by subcutaneous
injection
LOVENOX® is an example
20. Fondaparinux
Fondaparinux is given via injection once daily
It is licensed for initial treatment of deep vein thr
ombosis (DVT) and pulmonary embolism (PE) a
nd for venous thromboembolism prevention in p
atients undergoing surgery for hip fracture or hip/
knee replacement
21. History of Anticoagulants
In 1960, DW Barritt and SC Jordan performe
d the first randomized trial showing the effica
cy of anticoagulant therapy in the treatment o
f venous thromboembolism. Since then, impo
rtant therapeutic advances have been made i
n the treatment of deep venous thrombosis a
nd pulmonary embolism.
22. History of Anticoagulants
Warfarin has been the drug of choice for the
prevention and treatment of arterial and veno
us thrombotic disorders for more than 40 yea
rs
It was initially marketed as a
pesticide against rats and mice,
and is still popular for this purpose
23. History of Anticoagulants
Ximelagatran was the first oral direct thrombin inhibit
or and had proven efficacy for prevention and treatm
ent of VTE, stroke prevention with AF and recurrent
coronary events after acute myocardial infarction
It was initially approved for short-term VTE preventio
n in patients undergoing orthopedic surgery in Europ
e
It was withdrawn by AstraZeneca in 2006 due to lab
works confirming significant damage to the liver
24. The future for anticoagulants
Limitations of warfarin have fostered a great i
nterest in the development of novel anticoag
ulants for oral use to potentially replace warf
arin
The design of specific inhibitors against mole
cular targets that play a pivotal role in the co
agulation cascade are in development
25. The future for anticoagulants
Molecular targets are factor IIa (thrombin) an
d factor Xa
The two candidate compounds, one direct thr
ombin inhibitor (dabigatran etexilate) and one
direct factor Xa inhibitor (rivaroxaban) are ho
ping to be approved as new oral anticoagula
nts in the near future
26. The future for anticoagulants
Factor Xa is an attractive
target for the design of n
ew oral anticoagulants b
ecause of the unique role
factor Xa plays in the coa
gulation cascade as a co
nnection between the ext
rinsic and intrinsic pathw
ays
27. The future for anticoagulants
Factor Xa also regula
tes thrombin generati
on via binding to fact
or Va followed by acti
vation of prothrombin
to thrombin
28. The future for anticoagulants
It is hypothesized tha
t anticoagulants targe
ting factor Xa might b
e more effective than
those targeting coagu
lation factors located
lower down in the cas
cade, such as thromb
in
29. The future for anticoagulants
This concept has bee
n partially proved whe
n the first indirect fact
or Xa inhibitor, fondap
arinux, received FDA
approval for the preve
ntion and treatment of
VTE.
http://scit.us/~reed/clotting_system.png
The enzyme thrombokinase is secreted by the damaged tissues and blood platelet
The target of anticoagulants are the different factors in the cascade of chemical reactions
intravascular coagulation of the blood in any part of the circulatory system, as in the heart, arteries, veins, or capillaries