This document discusses treatment with anticoagulation drugs like warfarin and heparin. It provides details on their mechanisms of action, pharmacokinetics, drug interactions, and monitoring. Warfarin is a vitamin K antagonist that inhibits clotting factors. Its effects are delayed and it requires monitoring with an INR test. Heparin works by enhancing antithrombin, indirectly inhibiting thrombin and factor Xa. It has a risk of heparin-induced thrombocytopenia. Both drugs require careful dosing and monitoring due to their narrow therapeutic windows and variability between patients.
Managing Warfarin Therapy in Atrial Fibrilation)Dr Sukanta sen
The document discusses managing warfarin therapy in patients with atrial fibrillation. It describes warfarin as the recommended oral anticoagulant to prevent thromboembolic complications of atrial fibrillation. However, warfarin therapy is difficult to manage due to its narrow therapeutic window and drug interactions. The document provides guidance on indications for warfarin, initiating therapy, maintaining patients in the therapeutic INR range, addressing bleeding risks, and strategies like patient self-monitoring to improve outcomes. Regular monitoring and patient education are important for safe and effective long-term use of warfarin.
This document discusses anticoagulation during hemodialysis. It begins by explaining coagulation and anticoagulants. It then discusses how hemodialysis can activate coagulation pathways due to interactions with artificial surfaces. Unfractionated heparin is most commonly used for anticoagulation during dialysis due to its low cost and short half-life, though it carries bleeding risks. Low molecular weight heparins are also used and provide benefits like less bleeding risk. Anticoagulation is monitored during dialysis through tests like aPTT and ACT to prevent clotting while limiting bleeding risks.
Antiplatelets and anticoagulation in AMISCGH ED CME
1) Aspirin, P2Y12 inhibitors (ticagrelor, prasugrel, clopidogrel), and heparin are used to treat acute myocardial infarction. Aspirin and P2Y12 inhibitors prevent platelet aggregation while heparin inhibits thrombin.
2) Clinical trials have shown that aspirin reduces mortality and reinfarction rates compared to placebo. P2Y12 inhibitors like ticagrelor and prasugrel are more effective than clopidogrel but increase bleeding risk.
3) Fibrinolytics like tenecteplase can be used when primary PCI is not available within 120 minutes to reperfuse the infarcted area through
The document discusses using genetic testing to guide warfarin therapy. It explains that genetic polymorphisms affect individuals' responses to medications like warfarin. Variants in CYP2C9 and VKORC1 genes influence warfarin dosing, with clinical trials showing genotype-guided dosing results in faster stabilization of anticoagulation and less risk of bleeding events. The author proposes a study at UNC to incorporate pharmacogenomic guidance in initial warfarin dosing to improve outcomes.
This document provides an overview of pharmacogenomics and its clinical relevance. It discusses examples of how genetic variability can influence drug metabolism and response to drug targets. Variability in genes like CYP2C9, CYP2D6, TPMT, and beta-1/beta-2 adrenergic receptors can help predict drug efficacy and toxicity. Understanding these pharmacogenomic factors may help optimize dosing and select alternative therapies for individual patients. Challenges remain in fully explaining interindividual variability and implementing pharmacogenomics in clinical practice.
This document discusses atrial fibrillation (AF), including its classification, mechanisms, and management. AF is characterized by disorganized atrial electrical activity seen on ECG as irregular baseline undulations. The ventricular response rate is irregularly irregular between 100-160 bpm. AF can be classified as first detected, paroxysmal lasting <7 days, persistent lasting >7 days, or permanent lasting >1 year. The mechanism involves multiple reentrant wavelets propagating randomly through the atria. Management strategies include pharmacological or electrical cardioversion for acute termination, antiarrhythmic drugs to prevent recurrence, and rate control medications.
This document provides an overview of anticoagulants including their mechanisms of action, indications, dosing, and monitoring. It discusses normal hemostasis and coagulation factors. Unfractionated heparin, low molecular weight heparins, and factor Xa inhibitors are described as parenteral anticoagulants. Oral anticoagulants reviewed include warfarin, rivaroxaban, apixaban, and dabigatran. The roles of clinical pharmacists in managing anticoagulation therapy are also mentioned.
This document discusses treatment with anticoagulation drugs like warfarin and heparin. It provides details on their mechanisms of action, pharmacokinetics, drug interactions, and monitoring. Warfarin is a vitamin K antagonist that inhibits clotting factors. Its effects are delayed and it requires monitoring with an INR test. Heparin works by enhancing antithrombin, indirectly inhibiting thrombin and factor Xa. It has a risk of heparin-induced thrombocytopenia. Both drugs require careful dosing and monitoring due to their narrow therapeutic windows and variability between patients.
Managing Warfarin Therapy in Atrial Fibrilation)Dr Sukanta sen
The document discusses managing warfarin therapy in patients with atrial fibrillation. It describes warfarin as the recommended oral anticoagulant to prevent thromboembolic complications of atrial fibrillation. However, warfarin therapy is difficult to manage due to its narrow therapeutic window and drug interactions. The document provides guidance on indications for warfarin, initiating therapy, maintaining patients in the therapeutic INR range, addressing bleeding risks, and strategies like patient self-monitoring to improve outcomes. Regular monitoring and patient education are important for safe and effective long-term use of warfarin.
This document discusses anticoagulation during hemodialysis. It begins by explaining coagulation and anticoagulants. It then discusses how hemodialysis can activate coagulation pathways due to interactions with artificial surfaces. Unfractionated heparin is most commonly used for anticoagulation during dialysis due to its low cost and short half-life, though it carries bleeding risks. Low molecular weight heparins are also used and provide benefits like less bleeding risk. Anticoagulation is monitored during dialysis through tests like aPTT and ACT to prevent clotting while limiting bleeding risks.
Antiplatelets and anticoagulation in AMISCGH ED CME
1) Aspirin, P2Y12 inhibitors (ticagrelor, prasugrel, clopidogrel), and heparin are used to treat acute myocardial infarction. Aspirin and P2Y12 inhibitors prevent platelet aggregation while heparin inhibits thrombin.
2) Clinical trials have shown that aspirin reduces mortality and reinfarction rates compared to placebo. P2Y12 inhibitors like ticagrelor and prasugrel are more effective than clopidogrel but increase bleeding risk.
3) Fibrinolytics like tenecteplase can be used when primary PCI is not available within 120 minutes to reperfuse the infarcted area through
The document discusses using genetic testing to guide warfarin therapy. It explains that genetic polymorphisms affect individuals' responses to medications like warfarin. Variants in CYP2C9 and VKORC1 genes influence warfarin dosing, with clinical trials showing genotype-guided dosing results in faster stabilization of anticoagulation and less risk of bleeding events. The author proposes a study at UNC to incorporate pharmacogenomic guidance in initial warfarin dosing to improve outcomes.
This document provides an overview of pharmacogenomics and its clinical relevance. It discusses examples of how genetic variability can influence drug metabolism and response to drug targets. Variability in genes like CYP2C9, CYP2D6, TPMT, and beta-1/beta-2 adrenergic receptors can help predict drug efficacy and toxicity. Understanding these pharmacogenomic factors may help optimize dosing and select alternative therapies for individual patients. Challenges remain in fully explaining interindividual variability and implementing pharmacogenomics in clinical practice.
This document discusses atrial fibrillation (AF), including its classification, mechanisms, and management. AF is characterized by disorganized atrial electrical activity seen on ECG as irregular baseline undulations. The ventricular response rate is irregularly irregular between 100-160 bpm. AF can be classified as first detected, paroxysmal lasting <7 days, persistent lasting >7 days, or permanent lasting >1 year. The mechanism involves multiple reentrant wavelets propagating randomly through the atria. Management strategies include pharmacological or electrical cardioversion for acute termination, antiarrhythmic drugs to prevent recurrence, and rate control medications.
This document provides an overview of anticoagulants including their mechanisms of action, indications, dosing, and monitoring. It discusses normal hemostasis and coagulation factors. Unfractionated heparin, low molecular weight heparins, and factor Xa inhibitors are described as parenteral anticoagulants. Oral anticoagulants reviewed include warfarin, rivaroxaban, apixaban, and dabigatran. The roles of clinical pharmacists in managing anticoagulation therapy are also mentioned.
Anticoagulants and antiplatelets and hyperlipidemia drugsAreej Abu Hanieh
Blood dysfunctions can cause thrombosis, bleeding, and circulation problems. Thrombotic disorders like heart attacks and strokes are treated with anticoagulants and fibrinolytics. Platelets play a key role in thrombosis by aggregating to form clots. Anticoagulants and antiplatelet drugs are used to treat and prevent thrombosis. Anticoagulants inhibit coagulation factors while antiplatelet drugs inhibit platelet aggregation. These drugs have benefits but also risks like bleeding that require monitoring.
Anticoagulants help prevent blood clotting. They are classified as those used in vivo (parenteral or oral) and those used in vitro. Parenteral anticoagulants include indirect and direct thrombin inhibitors like heparin and direct factor Xa inhibitors like fondaparinux. Oral anticoagulants include coumarin derivatives like warfarin and newer direct thrombin and factor Xa inhibitors. Anticoagulants are used to treat conditions involving blood clots like deep vein thrombosis, pulmonary embolism, and atrial fibrillation. Newer anticoagulants have advantages over warfarin like fewer drug and food interactions and less monitoring requirements.
This document discusses pharmacogenetics and how genetic differences can influence drug response. It introduces key concepts like the human genome project, pharmacogenomic effects on drug metabolism and transport, and how genetic testing can help determine who will respond to or be toxic to specific drugs. The goal is to develop personalized medicine where a person's genetic makeup is used to optimize drug selection and dosing for safety and effectiveness.
This document discusses atrial fibrillation (AF), including its characteristics, prevalence, types, management, and pathophysiological mechanisms. Some key points include:
- AF is characterized by uncoordinated atrial activation and deterioration of atrial function. Prevalence increases with age, affecting over 8% of those over 80 years old.
- Types include paroxysmal, persistent, and permanent AF based on duration and frequency. Management may involve rate control, cardioversion, or rhythm control strategies.
- Pathophysiological mechanisms involve atrial fibrosis, dilation, and inflammation promoting reentrant wavelets within the atria leading to the uncoordinated activation seen in AF.
The document discusses drugs affecting blood and their mechanisms of action. It describes agents that stimulate or inhibit erythropoiesis, such as iron supplements or vitamin B12/folic acid deficiencies respectively. It also covers platelet aggregation inhibitors like aspirin, anticoagulants like heparin, and thrombolytic drugs like streptokinase used to treat thrombosis. Growth factors that stimulate leukopoiesis and chemotherapy drugs that inhibit it are also mentioned.
A comprehensive approach to Atrial Fibrillation. Everything you need to know about Atrial fibrillation. Including recent 2014 AHA guidelines of management.
1. Atrial fibrillation (AF) is a common arrhythmia where abnormal electrical signals in the atria cause an irregular heartbeat.
2. AF increases the risk of stroke by 5 times and is associated with increased mortality, hospitalization, and reduced quality of life.
3. Management involves rate or rhythm control as well as anticoagulation to prevent stroke, with treatment tailored based on the pattern and burden of AF and individual patient factors.
This document discusses coagulants and anticoagulants. It describes how thrombosis occurs via venous and arterial pathways and the process of hemostasis. Coagulation involves a balance between procoagulants and anticoagulants. Common coagulation factors and pathways are outlined. Vitamin K and other coagulants like fibrinogen and antihemophilic factor are discussed. Anticoagulants include heparins, oral anticoagulants like warfarin, and other agents. Mechanisms, uses, and adverse effects of various coagulants and anticoagulants are summarized.
This document summarizes drugs used to treat three blood dysfunctions: thrombosis, bleeding, and anemia. It discusses anticoagulant and thrombolytic drugs used to treat thrombosis. Anticoagulants like heparin and warfarin prevent clotting through different mechanisms. Heparin enhances antithrombin inhibition of coagulation factors. Warfarin inhibits vitamin K-dependent clotting factor synthesis. Thrombolytics like plasmin dissolve clots by activating plasminogen. The document also covers the mechanisms, uses, and toxicities of various anticoagulant and thrombolytic drugs.
This document provides an overview of anticoagulants. It discusses the history of anticoagulant development beginning in the late 19th century. Common anticoagulants used for blood collection and storage are described, including their mechanisms of action and uses. EDTA, citrate, and heparin are highlighted. The coagulation cascade and numbered coagulation factors are also summarized. Changes that occur in stored blood over time are reviewed at both the physical and biochemical levels. Finally, therapeutic uses of anticoagulants like heparin and warfarin are mentioned.
The document provides an overview and learning module on coagulation and hemostasis created by a medical student at the University of Vermont College of Medicine. It begins with definitions of key terms and an overview of primary and secondary hemostasis. It then reviews the components of the coagulation cascade including the extrinsic, intrinsic, and common pathways. It discusses pharmacologic considerations and the roles of the endothelium and subendothelium. Finally, it provides a detailed review of coagulation and hemostasis in a series of slides for students to test their knowledge.
The document discusses several advances in future medicine including pharmacogenomics, regenerative medicine, molecular medicine, and robotic surgery. Pharmacogenomics allows prediction of drug response based on a person's genetics and aims to improve drug safety and effectiveness. Regenerative medicine focuses on stimulating the body's ability to repair itself using stem cells, genes, and biomaterials. Molecular medicine utilizes genetic testing for improved disease diagnosis and detection of predispositions.
Personalized medicine involves the prescription of specific therapeutics best suited for an individual based on their genetic or proteomic profile. This talk discusses current approaches in drug discovery/development, the role of genetics in drug metabolism, and lawful/ethical issues surrounding the deployment of new health technology. I highlight some bioinformatic roles in the drug discovery process, and discuss the use of semantic web technologies for data integration and knowledge discovery..
Deep venous thrombosis is the formation of a blood clot in the deep veins, usually in the legs. It can progress and cause a pulmonary embolism, a potentially life-threatening blockage in the lungs. Risk factors include prolonged bed rest, obesity, older age, and inherited or acquired hypercoagulable states. Diagnosis involves ultrasound, venography or MRI. Treatment is usually blood thinners to prevent clot extension and embolism.
Anticoagulant, antithrombotic and anti platelet drugsraj kumar
The document discusses various anticoagulant, antithrombotic and antiplatelet drugs. It notes that deep vein thrombosis and pulmonary embolism affect millions of people annually and cause tens of thousands of deaths. It then covers the indications for antithrombotic therapy for conditions like venous thromboembolism, arterial thromboembolism and disseminated intravascular coagulation. The document also discusses specific drugs for treating these conditions, including heparin, warfarin and newer anticoagulants. It provides details on the mechanisms of action, monitoring and side effects of these pharmaceutical agents.
Deep vein thrombosis (DVT) is a blood clot that forms in the deep veins, usually of the legs. It can be asymptomatic or cause leg pain, swelling, warmth, and redness. Risk factors include prolonged bed rest, surgery, cancer, and inherited or acquired hypercoagulable states. Diagnosis involves the Wells criteria for pre-test probability followed by D-dimer testing and duplex ultrasound imaging of the legs. Treatment aims to prevent pulmonary embolism and includes bed rest, leg elevation, compression stockings, and anticoagulation medications like heparin or warfarin. Differential diagnoses include cellulitis, arthritis, and peripheral edema from other causes.
Anticoagulants and antiplatelets and hyperlipidemia drugsAreej Abu Hanieh
Blood dysfunctions can cause thrombosis, bleeding, and circulation problems. Thrombotic disorders like heart attacks and strokes are treated with anticoagulants and fibrinolytics. Platelets play a key role in thrombosis by aggregating to form clots. Anticoagulants and antiplatelet drugs are used to treat and prevent thrombosis. Anticoagulants inhibit coagulation factors while antiplatelet drugs inhibit platelet aggregation. These drugs have benefits but also risks like bleeding that require monitoring.
Anticoagulants help prevent blood clotting. They are classified as those used in vivo (parenteral or oral) and those used in vitro. Parenteral anticoagulants include indirect and direct thrombin inhibitors like heparin and direct factor Xa inhibitors like fondaparinux. Oral anticoagulants include coumarin derivatives like warfarin and newer direct thrombin and factor Xa inhibitors. Anticoagulants are used to treat conditions involving blood clots like deep vein thrombosis, pulmonary embolism, and atrial fibrillation. Newer anticoagulants have advantages over warfarin like fewer drug and food interactions and less monitoring requirements.
This document discusses pharmacogenetics and how genetic differences can influence drug response. It introduces key concepts like the human genome project, pharmacogenomic effects on drug metabolism and transport, and how genetic testing can help determine who will respond to or be toxic to specific drugs. The goal is to develop personalized medicine where a person's genetic makeup is used to optimize drug selection and dosing for safety and effectiveness.
This document discusses atrial fibrillation (AF), including its characteristics, prevalence, types, management, and pathophysiological mechanisms. Some key points include:
- AF is characterized by uncoordinated atrial activation and deterioration of atrial function. Prevalence increases with age, affecting over 8% of those over 80 years old.
- Types include paroxysmal, persistent, and permanent AF based on duration and frequency. Management may involve rate control, cardioversion, or rhythm control strategies.
- Pathophysiological mechanisms involve atrial fibrosis, dilation, and inflammation promoting reentrant wavelets within the atria leading to the uncoordinated activation seen in AF.
The document discusses drugs affecting blood and their mechanisms of action. It describes agents that stimulate or inhibit erythropoiesis, such as iron supplements or vitamin B12/folic acid deficiencies respectively. It also covers platelet aggregation inhibitors like aspirin, anticoagulants like heparin, and thrombolytic drugs like streptokinase used to treat thrombosis. Growth factors that stimulate leukopoiesis and chemotherapy drugs that inhibit it are also mentioned.
A comprehensive approach to Atrial Fibrillation. Everything you need to know about Atrial fibrillation. Including recent 2014 AHA guidelines of management.
1. Atrial fibrillation (AF) is a common arrhythmia where abnormal electrical signals in the atria cause an irregular heartbeat.
2. AF increases the risk of stroke by 5 times and is associated with increased mortality, hospitalization, and reduced quality of life.
3. Management involves rate or rhythm control as well as anticoagulation to prevent stroke, with treatment tailored based on the pattern and burden of AF and individual patient factors.
This document discusses coagulants and anticoagulants. It describes how thrombosis occurs via venous and arterial pathways and the process of hemostasis. Coagulation involves a balance between procoagulants and anticoagulants. Common coagulation factors and pathways are outlined. Vitamin K and other coagulants like fibrinogen and antihemophilic factor are discussed. Anticoagulants include heparins, oral anticoagulants like warfarin, and other agents. Mechanisms, uses, and adverse effects of various coagulants and anticoagulants are summarized.
This document summarizes drugs used to treat three blood dysfunctions: thrombosis, bleeding, and anemia. It discusses anticoagulant and thrombolytic drugs used to treat thrombosis. Anticoagulants like heparin and warfarin prevent clotting through different mechanisms. Heparin enhances antithrombin inhibition of coagulation factors. Warfarin inhibits vitamin K-dependent clotting factor synthesis. Thrombolytics like plasmin dissolve clots by activating plasminogen. The document also covers the mechanisms, uses, and toxicities of various anticoagulant and thrombolytic drugs.
This document provides an overview of anticoagulants. It discusses the history of anticoagulant development beginning in the late 19th century. Common anticoagulants used for blood collection and storage are described, including their mechanisms of action and uses. EDTA, citrate, and heparin are highlighted. The coagulation cascade and numbered coagulation factors are also summarized. Changes that occur in stored blood over time are reviewed at both the physical and biochemical levels. Finally, therapeutic uses of anticoagulants like heparin and warfarin are mentioned.
The document provides an overview and learning module on coagulation and hemostasis created by a medical student at the University of Vermont College of Medicine. It begins with definitions of key terms and an overview of primary and secondary hemostasis. It then reviews the components of the coagulation cascade including the extrinsic, intrinsic, and common pathways. It discusses pharmacologic considerations and the roles of the endothelium and subendothelium. Finally, it provides a detailed review of coagulation and hemostasis in a series of slides for students to test their knowledge.
The document discusses several advances in future medicine including pharmacogenomics, regenerative medicine, molecular medicine, and robotic surgery. Pharmacogenomics allows prediction of drug response based on a person's genetics and aims to improve drug safety and effectiveness. Regenerative medicine focuses on stimulating the body's ability to repair itself using stem cells, genes, and biomaterials. Molecular medicine utilizes genetic testing for improved disease diagnosis and detection of predispositions.
Personalized medicine involves the prescription of specific therapeutics best suited for an individual based on their genetic or proteomic profile. This talk discusses current approaches in drug discovery/development, the role of genetics in drug metabolism, and lawful/ethical issues surrounding the deployment of new health technology. I highlight some bioinformatic roles in the drug discovery process, and discuss the use of semantic web technologies for data integration and knowledge discovery..
Deep venous thrombosis is the formation of a blood clot in the deep veins, usually in the legs. It can progress and cause a pulmonary embolism, a potentially life-threatening blockage in the lungs. Risk factors include prolonged bed rest, obesity, older age, and inherited or acquired hypercoagulable states. Diagnosis involves ultrasound, venography or MRI. Treatment is usually blood thinners to prevent clot extension and embolism.
Anticoagulant, antithrombotic and anti platelet drugsraj kumar
The document discusses various anticoagulant, antithrombotic and antiplatelet drugs. It notes that deep vein thrombosis and pulmonary embolism affect millions of people annually and cause tens of thousands of deaths. It then covers the indications for antithrombotic therapy for conditions like venous thromboembolism, arterial thromboembolism and disseminated intravascular coagulation. The document also discusses specific drugs for treating these conditions, including heparin, warfarin and newer anticoagulants. It provides details on the mechanisms of action, monitoring and side effects of these pharmaceutical agents.
Deep vein thrombosis (DVT) is a blood clot that forms in the deep veins, usually of the legs. It can be asymptomatic or cause leg pain, swelling, warmth, and redness. Risk factors include prolonged bed rest, surgery, cancer, and inherited or acquired hypercoagulable states. Diagnosis involves the Wells criteria for pre-test probability followed by D-dimer testing and duplex ultrasound imaging of the legs. Treatment aims to prevent pulmonary embolism and includes bed rest, leg elevation, compression stockings, and anticoagulation medications like heparin or warfarin. Differential diagnoses include cellulitis, arthritis, and peripheral edema from other causes.
7. 評估指標
• Mean time in therapeutic range (TTR)
• Thromboembolic & major hemorrhagic
complications)
• ED visits and hospital admissions
• Patients’ knowledge of anticoagulants
• Compliance of medication and INR test
8. Comparison of pharmacist managed
anticoagulation with usual medical care
in a family medicine clinic
Young et al. BMC Family Practice 2011, 12:88
9. Quality of Anticoagulation Care in Patients
Discharged from a Pharmacist-Managed
Anticoagulation Clinic After
Stabilization of Warfarin Therapy
Pharmacotherapy. 2008 Jan;28(1):20-6.
10. Conclusions—In a population of patients
with AF, two-thirds were on ≥5 medications.
Increasing medication use was associated
with higher risk of bleeding but not stroke.
Rivaroxaban was tolerated across complex
patients on multiple medications.Circulation. 2016 Jan 26;133(4):352-60.
13. Warfarin-drug interactions: An emphasis on
influence of polypharmacy and high doses of
amoxicillin/clavulanate.
Young et al. BMC Family Practice 2011, 12:88
14. Warfarin-drug interactions: An emphasis on
influence of polypharmacy and high doses of
amoxicillin/clavulanate.
Young et al. BMC Family Practice 2011, 12:88