This document discusses drugs that affect hemostasis and those used for cardiovascular accidents. It covers the coagulation cascade and drugs that influence it, including antiplatelet drugs like aspirin, clopidogrel, and dipyridamole. It also discusses anticoagulants like heparin, warfarin, and newer agents. Thrombolytics that break up clots such as tPA and streptokinase are also reviewed. The document concludes with sections on cholesterol metabolism, dyslipidemia, and antihyperlipidemic drugs including statins.
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.
Antiplatelet agents such as aspirin and clopidogrel work by preventing platelet activation and aggregation to reduce clot formation. Anticoagulants like heparin and warfarin slow down the clotting process by inhibiting coagulation factors. These drugs are used to prevent conditions caused by clots such as heart attacks, strokes, and deep vein thrombosis. Common side effects include bleeding and gastrointestinal issues. The choice of antiplatelet or anticoagulant depends on the medical condition being treated.
The document discusses various drugs used in anticoagulation and antiplatelet therapy. It covers heparin and low molecular weight heparins, direct thrombin inhibitors like argatroban, oral anticoagulants like warfarin, and new oral anticoagulants like dabigatran and rivaroxaban. It also discusses antiplatelet drugs including aspirin, clopidogrel, and glycoprotein inhibitors. Fibrinolytic agents discussed include alteplase, tenecteplase, streptokinase and urokinase.
This document discusses drugs that affect hemostasis and cardiac pharmacology. It provides details on antiplatelet drugs like aspirin and clopidogrel, anticoagulants like heparin and warfarin, fibrinolytic drugs, and drugs for bleeding disorders. It also covers antihyperlipidemic drugs including statins, bile acid binding resins, niacin, and fibric acid derivatives. For each drug class and example drugs, it describes the mechanism of action, effects, indications, contraindications, and interactions.
This document discusses drugs that affect hemostasis and cardiac pharmacology. It provides details on antiplatelet drugs like aspirin and clopidogrel, anticoagulants like heparin and warfarin, fibrinolytic drugs, and drugs for bleeding disorders. It also covers antihyperlipidemic drugs including statins, bile acid binding resins, niacin, and fibric acid derivatives. For each drug class and example drugs, it describes the mechanism of action, effects, indications, contraindications, and interactions.
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.
Hemostasis, Thrombosis, Fibrinolysis, and Cardiovascular Disease - Copy.pptxJohn Smith
1) The document summarizes hemostasis, thrombosis, and their treatment. It describes the vascular endothelium, platelets, coagulation system, and fibrinolytic system which maintain hemostasis and how perturbations can lead to thrombosis.
2) Thrombosis can occur in arteries or veins and is treated using antiplatelet drugs like aspirin, anticoagulants like heparin and warfarin, and thrombolytic drugs.
3) Antiplatelet drugs inhibit platelet activation while anticoagulants inhibit thrombin generation; together they prevent clot formation and growth to treat thrombosis.
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.
Antiplatelet agents such as aspirin and clopidogrel work by preventing platelet activation and aggregation to reduce clot formation. Anticoagulants like heparin and warfarin slow down the clotting process by inhibiting coagulation factors. These drugs are used to prevent conditions caused by clots such as heart attacks, strokes, and deep vein thrombosis. Common side effects include bleeding and gastrointestinal issues. The choice of antiplatelet or anticoagulant depends on the medical condition being treated.
The document discusses various drugs used in anticoagulation and antiplatelet therapy. It covers heparin and low molecular weight heparins, direct thrombin inhibitors like argatroban, oral anticoagulants like warfarin, and new oral anticoagulants like dabigatran and rivaroxaban. It also discusses antiplatelet drugs including aspirin, clopidogrel, and glycoprotein inhibitors. Fibrinolytic agents discussed include alteplase, tenecteplase, streptokinase and urokinase.
This document discusses drugs that affect hemostasis and cardiac pharmacology. It provides details on antiplatelet drugs like aspirin and clopidogrel, anticoagulants like heparin and warfarin, fibrinolytic drugs, and drugs for bleeding disorders. It also covers antihyperlipidemic drugs including statins, bile acid binding resins, niacin, and fibric acid derivatives. For each drug class and example drugs, it describes the mechanism of action, effects, indications, contraindications, and interactions.
This document discusses drugs that affect hemostasis and cardiac pharmacology. It provides details on antiplatelet drugs like aspirin and clopidogrel, anticoagulants like heparin and warfarin, fibrinolytic drugs, and drugs for bleeding disorders. It also covers antihyperlipidemic drugs including statins, bile acid binding resins, niacin, and fibric acid derivatives. For each drug class and example drugs, it describes the mechanism of action, effects, indications, contraindications, and interactions.
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.
Hemostasis, Thrombosis, Fibrinolysis, and Cardiovascular Disease - Copy.pptxJohn Smith
1) The document summarizes hemostasis, thrombosis, and their treatment. It describes the vascular endothelium, platelets, coagulation system, and fibrinolytic system which maintain hemostasis and how perturbations can lead to thrombosis.
2) Thrombosis can occur in arteries or veins and is treated using antiplatelet drugs like aspirin, anticoagulants like heparin and warfarin, and thrombolytic drugs.
3) Antiplatelet drugs inhibit platelet activation while anticoagulants inhibit thrombin generation; together they prevent clot formation and growth to treat thrombosis.
1) The document discusses various drugs used to treat clotting disorders including anticoagulants, antiplatelets, and thrombolytics. Anticoagulants prevent clotting while antiplatelets inhibit platelet aggregation. Thrombolytics dissolve existing clots.
2) Common anticoagulants discussed are heparin, warfarin, and newer oral anticoagulants that inhibit thrombin or Factor Xa. Thrombolytics discussed include streptokinase, urokinase, anistreplase, and tissue plasminogen activators like alteplase.
3) Thrombolytics work by activating plasminogen to form plasmin,
This document provides an overview of hemostasis and antithrombotic drugs. It discusses the four phases of hemostasis - vascular, platelet, coagulation, and fibrinolytic. Antithrombotic drugs include antiplatelet drugs that inhibit platelet activation and aggregation, anticoagulants that inhibit fibrin formation, and fibrinolytic agents that degrade fibrin. The document focuses on antiplatelet drugs, describing their mechanisms of action, types including aspirin, clopidogrel, prasugrel, ticagrelor, and glycoprotein IIb/IIIa antagonists. Their uses, pharmacokinetics, adverse effects, and interactions are summarized.
Hyperlipidemia and coagulation disorders are discussed. Hyperlipidemia involves abnormal lipid levels that can lead to atherosclerosis and is treated through diet, supplements like omega-3, and medications like statins. Coagulation disorders disrupt the hemostatic balance between clot formation and dissolution and are treated with antiplatelet drugs, anticoagulants that indirectly or directly inhibit thrombin or factor Xa, and coumarin anticoagulants like warfarin. Various drug classes and their mechanisms and uses for treating hyperlipidemia and coagulation disorders are outlined.
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.
Antiplatelets thrombolytics and drugs for bleeding 2023.pptxBatMan752678
This document provides an overview of anticoagulants, antiplatelets, and thrombolytics. It discusses the coagulation cascade and platelet activation that leads to thrombus formation. It then summarizes various anticoagulant drugs including indirect inhibitors like heparin and fondaparinux, direct factor Xa inhibitors like rivaroxaban and apixaban, and direct thrombin inhibitors like hirudin, argatroban, and the oral drug dabigatran. It highlights their mechanisms of action, pharmacokinetics, uses, and adverse effects including bleeding risks. Reversal agents like protamine and idarucizumab are also mentioned.
Anticoagulants and antiplatelet agents work to prevent clot formation through different mechanisms. Anticoagulants like heparin and warfarin prevent clotting by inhibiting coagulation factors, while antiplatelets like aspirin prevent platelet aggregation. Platelets play a key role in hemostasis, initially forming a platelet plug through adhesion and aggregation at the site of vascular injury. This is later stabilized by the coagulation cascade forming a fibrin clot. Anticoagulants and antiplatelets are used to prevent thrombus formation in conditions like heart attacks, strokes, and deep vein thrombosis.
This document summarizes drugs used to treat blood dysfunctions related to thrombosis, bleeding, and anemia. It describes the formation of blood clots and the drugs used to regulate clotting, focusing on platelet activation and aggregation inhibitors like aspirin, clopidogrel, abciximab, eptifibatide, and tirofiban. It also discusses the coagulation cascade and anticoagulants like heparin and warfarin that inhibit coagulation factors to prevent unwanted clotting.
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 agents used to treat dyslipidemia. It describes the pathogenesis of various lipid abnormalities and how different drug classes work to lower LDL cholesterol, triglycerides, and raise HDL cholesterol through various mechanisms. The major drug classes covered are HMG-CoA reductase inhibitors (statins), resins, ezetimibe, niacin, and fibric acid derivatives. Each drug class' mechanism of action, clinical uses, and potential toxicities are summarized. Combination therapy is often required to achieve optimal lipid lowering goals.
This document discusses drugs used to treat disorders of blood clotting and bleeding. It describes three classes of anticoagulant drugs that reduce clotting: oral anticoagulants like warfarin that inhibit vitamin K-dependent clotting factors; injectable anticoagulants like heparin and hirudin that inhibit thrombin; and antiplatelet drugs like aspirin and clopidogrel that decrease platelet aggregation. It also discusses fibrinolytic drugs like tissue plasminogen activator that dissolve blood clots, and hematopoietic drugs used to treat anemia, such as iron supplements, folic acid, and vitamin B12.
This document discusses different types of anticoagulant, antiplatelet, and thrombolytic medications. It provides details on the mechanisms of action, indications, dosages, side effects and nursing responsibilities for some common medications in each category including enoxaparin sodium, heparin, clopidogrel, aspirin, streptokinase. It also includes some review questions related to managing adverse effects of these medications.
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 provides an overview of newer oral anticoagulants compared to traditional anticoagulants like warfarin. It discusses the mechanisms of action, indications, monitoring, side effects and management of bleeding for direct thrombin inhibitors like dabigatran and direct factor Xa inhibitors like rivaroxaban. It also covers considerations for using each drug depending on factors like kidney function and risk of gastrointestinal bleeding. The newer oral anticoagulants offer advantages over warfarin in terms of predictable dosing without monitoring, but also have some limitations and drug interactions that require careful management.
This document provides an overview of newer oral anticoagulants compared to traditional anticoagulants like warfarin. It discusses the mechanisms of action and indications for direct thrombin inhibitors like dabigatran and direct factor Xa inhibitors like rivaroxaban. These newer oral anticoagulants have predictable dosing without monitoring, fewer drug interactions than warfarin, and may cause less intracranial bleeding than warfarin. However, they increase risk of gastrointestinal bleeding. Guidance is provided on managing bleeding events and specific considerations for using each drug based on factors like kidney function and risk of gastrointestinal bleeding.
Anti thrombotic therapy in difficult clinical conditionsDrArpan Chouhan
This document discusses anti-thrombotic therapy in difficult clinical conditions. It summarizes various antiplatelet and anticoagulant drugs, difficult situations for their use including high ischemic or bleeding risk, and strategies for balancing thrombotic and hemorrhagic risks. Certain drugs like prasugrel and ticagrelor are preferred for high ischemic burden due to more potent platelet inhibition, while dose adjustments and shorter durations are recommended for high bleeding risk. Careful management is needed in situations like surgery, renal dysfunction, and pregnancy to minimize risks.
This document discusses antiplatelet drugs used to prevent thromboembolic events. It describes how different drugs act on platelets by inhibiting receptors like P2Y1, P2Y12, GP IIb/IIIa. Aspirin, clopidogrel, prasugrel, ticagrelor, and GP IIb/IIIa inhibitors like abciximab are described in detail. It outlines their uses in conditions like coronary artery disease, acute coronary syndromes, cerebrovascular diseases, and venous thromboembolism to reduce thrombotic risks while minimizing bleeding risks. Combination antiplatelet therapies are recommended for high-risk situations like angioplasty and stent placement.
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.
IRON METABOLISM & MICROCYTIC HYPOCHROMIC ANAEMIAS.pptxparisdepher
Abigail was diagnosed with iron deficiency anaemia (IDA) at KNUST Hospital. On her follow up visit after 3 months of iron fersolate treatment, her iron profile results are expected to show:
1. Increased serum iron and transferrin saturation levels as the treatment replenishes her iron stores.
2. Normal serum ferritin levels as the treatment addresses the iron deficiency.
3. Potentially normal or increased sTFR-1 levels depending on whether her increased iron levels meet erythropoietic demand, since sTFR-1 reflects iron availability for red blood cell production.
The treatment is expected to correct the iron deficiency underlying Abigail's IDA
The document discusses the benefits of exercise for mental health. Regular physical activity can help reduce anxiety and depression and improve mood and cognitive functioning. Exercise boosts blood flow, releases endorphins, and promotes changes in the brain which help regulate emotions and stress levels.
1) The document discusses various drugs used to treat clotting disorders including anticoagulants, antiplatelets, and thrombolytics. Anticoagulants prevent clotting while antiplatelets inhibit platelet aggregation. Thrombolytics dissolve existing clots.
2) Common anticoagulants discussed are heparin, warfarin, and newer oral anticoagulants that inhibit thrombin or Factor Xa. Thrombolytics discussed include streptokinase, urokinase, anistreplase, and tissue plasminogen activators like alteplase.
3) Thrombolytics work by activating plasminogen to form plasmin,
This document provides an overview of hemostasis and antithrombotic drugs. It discusses the four phases of hemostasis - vascular, platelet, coagulation, and fibrinolytic. Antithrombotic drugs include antiplatelet drugs that inhibit platelet activation and aggregation, anticoagulants that inhibit fibrin formation, and fibrinolytic agents that degrade fibrin. The document focuses on antiplatelet drugs, describing their mechanisms of action, types including aspirin, clopidogrel, prasugrel, ticagrelor, and glycoprotein IIb/IIIa antagonists. Their uses, pharmacokinetics, adverse effects, and interactions are summarized.
Hyperlipidemia and coagulation disorders are discussed. Hyperlipidemia involves abnormal lipid levels that can lead to atherosclerosis and is treated through diet, supplements like omega-3, and medications like statins. Coagulation disorders disrupt the hemostatic balance between clot formation and dissolution and are treated with antiplatelet drugs, anticoagulants that indirectly or directly inhibit thrombin or factor Xa, and coumarin anticoagulants like warfarin. Various drug classes and their mechanisms and uses for treating hyperlipidemia and coagulation disorders are outlined.
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.
Antiplatelets thrombolytics and drugs for bleeding 2023.pptxBatMan752678
This document provides an overview of anticoagulants, antiplatelets, and thrombolytics. It discusses the coagulation cascade and platelet activation that leads to thrombus formation. It then summarizes various anticoagulant drugs including indirect inhibitors like heparin and fondaparinux, direct factor Xa inhibitors like rivaroxaban and apixaban, and direct thrombin inhibitors like hirudin, argatroban, and the oral drug dabigatran. It highlights their mechanisms of action, pharmacokinetics, uses, and adverse effects including bleeding risks. Reversal agents like protamine and idarucizumab are also mentioned.
Anticoagulants and antiplatelet agents work to prevent clot formation through different mechanisms. Anticoagulants like heparin and warfarin prevent clotting by inhibiting coagulation factors, while antiplatelets like aspirin prevent platelet aggregation. Platelets play a key role in hemostasis, initially forming a platelet plug through adhesion and aggregation at the site of vascular injury. This is later stabilized by the coagulation cascade forming a fibrin clot. Anticoagulants and antiplatelets are used to prevent thrombus formation in conditions like heart attacks, strokes, and deep vein thrombosis.
This document summarizes drugs used to treat blood dysfunctions related to thrombosis, bleeding, and anemia. It describes the formation of blood clots and the drugs used to regulate clotting, focusing on platelet activation and aggregation inhibitors like aspirin, clopidogrel, abciximab, eptifibatide, and tirofiban. It also discusses the coagulation cascade and anticoagulants like heparin and warfarin that inhibit coagulation factors to prevent unwanted clotting.
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 agents used to treat dyslipidemia. It describes the pathogenesis of various lipid abnormalities and how different drug classes work to lower LDL cholesterol, triglycerides, and raise HDL cholesterol through various mechanisms. The major drug classes covered are HMG-CoA reductase inhibitors (statins), resins, ezetimibe, niacin, and fibric acid derivatives. Each drug class' mechanism of action, clinical uses, and potential toxicities are summarized. Combination therapy is often required to achieve optimal lipid lowering goals.
This document discusses drugs used to treat disorders of blood clotting and bleeding. It describes three classes of anticoagulant drugs that reduce clotting: oral anticoagulants like warfarin that inhibit vitamin K-dependent clotting factors; injectable anticoagulants like heparin and hirudin that inhibit thrombin; and antiplatelet drugs like aspirin and clopidogrel that decrease platelet aggregation. It also discusses fibrinolytic drugs like tissue plasminogen activator that dissolve blood clots, and hematopoietic drugs used to treat anemia, such as iron supplements, folic acid, and vitamin B12.
This document discusses different types of anticoagulant, antiplatelet, and thrombolytic medications. It provides details on the mechanisms of action, indications, dosages, side effects and nursing responsibilities for some common medications in each category including enoxaparin sodium, heparin, clopidogrel, aspirin, streptokinase. It also includes some review questions related to managing adverse effects of these medications.
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 provides an overview of newer oral anticoagulants compared to traditional anticoagulants like warfarin. It discusses the mechanisms of action, indications, monitoring, side effects and management of bleeding for direct thrombin inhibitors like dabigatran and direct factor Xa inhibitors like rivaroxaban. It also covers considerations for using each drug depending on factors like kidney function and risk of gastrointestinal bleeding. The newer oral anticoagulants offer advantages over warfarin in terms of predictable dosing without monitoring, but also have some limitations and drug interactions that require careful management.
This document provides an overview of newer oral anticoagulants compared to traditional anticoagulants like warfarin. It discusses the mechanisms of action and indications for direct thrombin inhibitors like dabigatran and direct factor Xa inhibitors like rivaroxaban. These newer oral anticoagulants have predictable dosing without monitoring, fewer drug interactions than warfarin, and may cause less intracranial bleeding than warfarin. However, they increase risk of gastrointestinal bleeding. Guidance is provided on managing bleeding events and specific considerations for using each drug based on factors like kidney function and risk of gastrointestinal bleeding.
Anti thrombotic therapy in difficult clinical conditionsDrArpan Chouhan
This document discusses anti-thrombotic therapy in difficult clinical conditions. It summarizes various antiplatelet and anticoagulant drugs, difficult situations for their use including high ischemic or bleeding risk, and strategies for balancing thrombotic and hemorrhagic risks. Certain drugs like prasugrel and ticagrelor are preferred for high ischemic burden due to more potent platelet inhibition, while dose adjustments and shorter durations are recommended for high bleeding risk. Careful management is needed in situations like surgery, renal dysfunction, and pregnancy to minimize risks.
This document discusses antiplatelet drugs used to prevent thromboembolic events. It describes how different drugs act on platelets by inhibiting receptors like P2Y1, P2Y12, GP IIb/IIIa. Aspirin, clopidogrel, prasugrel, ticagrelor, and GP IIb/IIIa inhibitors like abciximab are described in detail. It outlines their uses in conditions like coronary artery disease, acute coronary syndromes, cerebrovascular diseases, and venous thromboembolism to reduce thrombotic risks while minimizing bleeding risks. Combination antiplatelet therapies are recommended for high-risk situations like angioplasty and stent placement.
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.
IRON METABOLISM & MICROCYTIC HYPOCHROMIC ANAEMIAS.pptxparisdepher
Abigail was diagnosed with iron deficiency anaemia (IDA) at KNUST Hospital. On her follow up visit after 3 months of iron fersolate treatment, her iron profile results are expected to show:
1. Increased serum iron and transferrin saturation levels as the treatment replenishes her iron stores.
2. Normal serum ferritin levels as the treatment addresses the iron deficiency.
3. Potentially normal or increased sTFR-1 levels depending on whether her increased iron levels meet erythropoietic demand, since sTFR-1 reflects iron availability for red blood cell production.
The treatment is expected to correct the iron deficiency underlying Abigail's IDA
The document discusses the benefits of exercise for mental health. Regular physical activity can help reduce anxiety and depression and improve mood and cognitive functioning. Exercise boosts blood flow, releases endorphins, and promotes changes in the brain which help regulate emotions and stress levels.
IRON METABOLISM & MICROCYTIC HYPOCHROMIC ANAEMIAS.pptxparisdepher
This document discusses microcytic hypochromic anemias, including iron deficiency anemia, anemia of chronic diseases, and thalassemias. It covers iron metabolism, the causes and symptoms of anemia, the development of different types of microcytic hypochromic anemia, and their laboratory diagnosis and treatment. Specifically, it outlines iron's role in the body, how the body regulates iron levels, the causes and signs of iron deficiency, and how excess iron can be toxic. It also discusses the adaptive responses to anemia and the diagnostic markers used to identify different types of microcytic hypochromic anemia.
This document provides an overview of medical entomology, which is the study of the relationship between arthropods like insects and arachnids, and their ability to transmit pathogens or parasites that cause disease in humans. It discusses how arthropods can directly cause issues like allergic reactions, annoyance, or myiasis. Additionally, it explains how some arthropods act as vectors, undergoing part of the life cycle of a pathogen and transmitting it between hosts. Knowing the taxonomy, biology and ecology of vectors is important for developing control strategies. As medical professionals, understanding insect-human contact and identifying common vectors can help in treating patients and controlling diseases.
The document discusses literature reviews and how to search for relevant literature. It defines a literature review as an extensive search of available information on a topic that results in a list of references. Literature can come from various sources like books, journals, reports, and online resources. Primary sources contain first-hand accounts while secondary sources describe and summarize information from other sources. Effective searching involves using keywords, synonyms, Boolean operators like AND and OR, and searching databases like PubMed, Google Scholar, CINAHL, and EMBASE that contain medical and scientific literature. The goal of a literature search is to gather information to define problems, review past work, and support research.
This document provides information about alanine aminotransferase (ALT), including that it catalyzes the conversion of amino acids to keto acids, higher activity is in the liver but also in other organs, and elevated levels can indicate organ damage. It also notes that an AST:ALT ratio greater than 2 suggests alcoholic liver disease. The document then provides details on the test principle, reagents, specimen collection, procedure, calculations, linearity, sensitivity, normal values, and references for the ALT test.
This document discusses purine metabolism, including the biosynthesis and catabolism of purines. It covers several key points:
- Nucleotides are composed of a nitrogenous base, pentose sugar, and phosphate groups, and are building blocks for DNA and RNA. They also participate in energy production and carbohydrate metabolism.
- Purines are synthesized through de novo and salvage pathways. De novo synthesis builds the purine ring from simple precursors, while salvage pathways recover purines from nucleic acid breakdown.
- Adenine and guanine are formed through a series of reactions adding carbon and nitrogen atoms to ribose-5-phosphate. IMP is converted to AMP and GMP, which
This document provides an overview of the course Engl 264: Introduction to Prose which focuses on studying prose works in the second semester. Six short stories and one novel will be analyzed as part of the course. The specific prose works that will be studied this semester are then listed. The document then provides definitions and explanations of key concepts related to prose including the definition of prose, types of prose (nonfictional, fictional, heroic, prose poetry), types of fiction (short story, novella, novel), elements of prose (plot, setting, character, point of view, theme, style), and an analysis of styles of prose.
Ama Ata Aidoo's short story "The Girl Who Can" is about 7-year-old Adjoa who lives in a village in Ghana. Adjoa struggles as her society believes women should only be wives, mothers, and serve their families. Despite having legs considered too thin for childbearing, Adjoa wins trophies in running competitions, proving women's abilities aren't limited. Her grandmother Nana, initially skeptical of Adjoa due to her legs, becomes proud of her accomplishments. The story examines themes of fighting for women's rights and identities beyond motherhood.
This document provides an overview of decalcification in histopathology. It discusses the need to decalcify bony tissue specimens to make them thin enough for microscopic examination. The key aspects of decalcification covered include the criteria for good decalcifying agents, factors that affect the process, common techniques and decalcifiers used, potential artifacts, and assessing the endpoint of decalcification. The techniques described aim to remove calcium from bone while minimizing damage to tissue morphology and antigenicity.
William Faulkner was an American novelist and short story writer who was awarded the 1949 Nobel Prize for Literature. He was born in Mississippi in 1897 and set many of his most famous novels, like The Sound and the Fury and As I Lay Dying, in the fictional Yoknapatawpha County in Mississippi. Faulkner often wrote in a stream-of-consciousness style and explored complex social and psychological issues in the American South through characters ranging from slaves to aristocrats. He served as a writer-in-residence and professor at the University of Virginia later in his life until his death in 1962 in Mississippi.
CELLS OF THE IMMUNE SYSTEM SAS 2021 RR [Autosaved].pptparisdepher
Here are the answers to the study questions:
a. False. Macrophages express class II MHC molecules, not class I, to present antigen to CD4+ T cells.
b. False. Not all lymphoid cells have antigen-specific receptors. For example, macrophages and dendritic cells do not have antigen-specific receptors.
c. False. Follicular dendritic cells cannot process or present antigen. They retain antigen-antibody complexes on their surface for B cell recognition but do not process or present antigen.
Eosinophil is phagocytic cell important in the body’s defense against parasitic organisms.
Neutrophil is generally first cell to arrive at site of inflammation
This document provides a table summarizing blood group antigens organized into 72 different systems. The table lists the antigen numbers within each system and the total number of antigens in that system. Some examples of major systems listed include:
- The ABO system containing antigens A, B, and 4 total antigens.
- The RH system containing the D, C, E, and c antigens among 56 total antigens.
- The MNS system containing the M, N, S, and s antigens among 50 total antigens.
1) Fixation is a process that preserves tissues using chemical fixatives to prevent decay. It terminates biochemical reactions and may increase mechanical strength.
2) There are several types of fixatives including cross-linking (e.g. formaldehyde, glutaraldehyde), precipitating (e.g. alcohol, picric acid), and oxidizing (e.g. osmium tetroxide) fixatives. Each works through different mechanisms like cross-linking proteins or denaturing and coagulating them.
3) The quality of fixation is influenced by factors like duration of fixation, size of specimens, temperature, concentration, and pH/buffers to allow for deep and even penetration while preserving tissue
Local Advanced Lung Cancer: Artificial Intelligence, Synergetics, Complex Sys...Oleg Kshivets
Overall life span (LS) was 1671.7±1721.6 days and cumulative 5YS reached 62.4%, 10 years – 50.4%, 20 years – 44.6%. 94 LCP lived more than 5 years without cancer (LS=2958.6±1723.6 days), 22 – more than 10 years (LS=5571±1841.8 days). 67 LCP died because of LC (LS=471.9±344 days). AT significantly improved 5YS (68% vs. 53.7%) (P=0.028 by log-rank test). Cox modeling displayed that 5YS of LCP significantly depended on: N0-N12, T3-4, blood cell circuit, cell ratio factors (ratio between cancer cells-CC and blood cells subpopulations), LC cell dynamics, recalcification time, heparin tolerance, prothrombin index, protein, AT, procedure type (P=0.000-0.031). Neural networks, genetic algorithm selection and bootstrap simulation revealed relationships between 5YS and N0-12 (rank=1), thrombocytes/CC (rank=2), segmented neutrophils/CC (3), eosinophils/CC (4), erythrocytes/CC (5), healthy cells/CC (6), lymphocytes/CC (7), stick neutrophils/CC (8), leucocytes/CC (9), monocytes/CC (10). Correct prediction of 5YS was 100% by neural networks computing (error=0.000; area under ROC curve=1.0).
share - Lions, tigers, AI and health misinformation, oh my!.pptxTina Purnat
• Pitfalls and pivots needed to use AI effectively in public health
• Evidence-based strategies to address health misinformation effectively
• Building trust with communities online and offline
• Equipping health professionals to address questions, concerns and health misinformation
• Assessing risk and mitigating harm from adverse health narratives in communities, health workforce and health system
- 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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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.
Osteoporosis - Definition , Evaluation and Management .pdfJim Jacob Roy
Osteoporosis is an increasing cause of morbidity among the elderly.
In this document , a brief outline of osteoporosis is given , including the risk factors of osteoporosis fractures , the indications for testing bone mineral density and the management of osteoporosis
3. Drugs that affect Coagulation
■ Thrombosis may occur in both arteries and veins
■ Arterial thrombi cause disease by obstructing
blood flow which can result in tissue ischemia or
death
■ Venous thrombosis is associated with venous
stasis. A venous thrombus is less cohesive than
an arterial embolus so venous emboli more
prevalent
4. Hemostasis
■Hemostasis is the prevention or stoppage of
blood loss from an injured blood vessel.
■Process involves vasoconstriction, formation
of a platelet plug, activation of clotting factors
and growth of fibrous tissue into the blood
clot making it more stable.
5. Antiplatelet Drugs
■ Arterial thrombi are composed primarily of platelets
■ Antiplatelet drugs act by inhibiting platelet
activation, adhesion, aggregation, or procoagulant
activity.
■ Include drugs that block platelet receptors for
thromboxane, ADP, glycoprotein IIb/IIIa and
phosphodiesterase inhibitors
6. Platelet Inhibitors
■ Inhibit the aggregation of platelets
■ Indicated in progressing MI, TIA/CVA
■ Side Effects: uncontrolled bleeding
■ No effect on existing thrombi
7/17/23 6
7. Thromboxane A2 Inhibitors
■ Work by inhibiting synthesis of prostaglandins. TA
inhibitors work by acetylating cyclooxygenases, the
enzyme in platelets that synthesizes thromboxane A2
(which causes platelet aggregation).
■ ASA (aspirin) is example. It affects the platelets for the
life of the platelet.
■ NSAIDs not so useful as action wears off as drug
wears off
8. Adenosine Diphosphate Receptor
Antagonists
Ticlopidine
■ Inhibit platelet aggregation by preventing ADP-
induced binding between platelets and fibrinogen.
This reaction inhibits platelet aggregation irreversibly
and persist for the lifespan of the platelet (9-10
days)
■ Indicated in TIAs
■ Adverse effects-neutropenia, diarrhea, skin rashes
9. Adenosine Diphosphate Receptor
Antagonists
Clopidogrel
■ Fewer side effects than ASA or Ticlopidine
■ indicated for patients with atherosclerosis
for reduction of MI, stroke and vascular
death
■ Does not need reduction in those with renal
problems
10. ■ Used with aspirin and heparin and is contraindicated in
clients who have recently received oral anticoagulants or
IV dextran.
■ Other contraindications include active bleeding,
thrombocytopenia, history of stroke, surgery or trauma
within past 6 weeks, uncontrolled hypertension or
hypersensitivity.
11. Miscellaneous
■ Dipyridamole inhibits platelet aggregation, but
mechanism is unclear
■ Used for prevention of thromboembolism after
cardiac valve replacement and is given with
Coumadin
12. Anticoagulants
■ Interrupt clotting cascade at various points
– No effect on platelets
■ Heparin & LMW Heparin (Lovenox®)
■ warfarin (Coumadin®)
7/17/23 12
13. Heparin
■ Endogenous
– Released from mast cells/basophils
■ Binds with antithrombin III
■ Antithrombin III binds with and inactivates excess
thrombin to regionalize clotting activity.
– Most thrombin (80-95%) captured in fibrin mesh.
■ Antithrombin-heparin complex 1000X as effective as
antithrombin III alone
7/17/23 13
14. Heparin
■ Measured in Units, not milligrams
■ Indications:
– MI, PE, DVT, ischemic CVA
■ Antidote for heparin OD: protamine sulphate.
– MOA: heparin is strongly negatively charged.
Protamine is strongly positively charged.
7/17/23 14
15. Low Molecular Weight Heparins
■ Given subcutaneously in abdomen and do not
require close monitoring of blood coagulation tests
■ Still should follow platelet counts
■ Dalteparin
■ Enoxaparin
16. warfarin (Coumadin®)
■ Prothrombin (II), Proconvertin (VII), Christmas factor
(IX) and Stuart-Prower factor (X) all require vitamin
K dependent enzymes for their synthesis.
■ Warfarin competes with vitamin K in the synthesis
of these enzymes.
■ Depletes the reserves of clotting factors.
■ Delayed onset (~12 hours) due to existing factors
7/17/23 16
17. Warfarin
■ Dosage reduction in patients with biliary tract
disorders, liver disease, malabsorption syndromes,
and hyperthyroidism. These conditions increase
anticoagulant drug effects by reducing absorption of
vitamin K or decreasing hepatic synthesis of clotting
factors
■ Has multiple, multiple drug interactions
■ Counteract with vitamin K
18. Other anticoagulants
■ Danaparoid — low molecular weight, heparin-
like drug. Used in management of hip surgery,
ischemic stroke or in those who cannot take
heparin. Does not contain heparin.
■ Lepirudin — used as heparin substitutes
■ Fondaparinux –binds to clot bound factor Xa,
inhibits thrombin productions
20. Thrombolytics
■ Given to dissolve thrombi
■ Stimulate conversion of plasminogen to plasmin, an
enzyme that breaks down fibrin (the framework of a
thrombus)
■ Used in severe thromboembolic disease such as MI,
PE and ileofemoral thrombosis
21. Thrombolytics
■ Goal is to re-establish blood flow and prevent tissue
damage
■ Also used to dissolve clots in arterial or venous cannulas or
catheters
■ Must obtain baseline INR, aPTT, platelet count and
fibrinogen
■ Will monitor labs 2-3 hours after thrombolytic treatment is
instituted to determine efficacy
22. Thrombolytics
■ Directly break up clots
– Promote natural thrombolysis
■ Enhance activation of plasminogen.
■ Reduce mortality from MI
■ Less systemic bleeding risk with Alteplase and other
newer thrombolytics as compared with Streptokinase.
■ However, haemorrhagic stroke risk with Alteplase is
higher than Streptokinase.
■ alteplase (tPA®, Activase®)
■ streptokinase (Streptase®)
■ anistreplase (Eminase®)
■ reteplase (Retevase®)
■ tenecteplase (TNKase®)
7/17/23 22
23. Drugs Used to Control Bleeding
■ Aminocaproic acid and tranexamic acid are used to
stop bleeding caused by overdoses of thrombolytic
agents
■ Aprotinin indicated in patients undergoing CABG .
Inhibits breakdown of blood clotting factors.
24. Cholesterol Metabolism
■ Cholesterol important component in membranes and as hormone
precursor
■ Synthesized in liver
– Hydroxymethylglutaryl coenzyme A reductase
– (HMG CoA reductase) dependant
■ Stored in tissues for latter use
■ Insoluble in plasma (a type of lipid)
– Must have transport mechanism
7/17/23 24
25. Cholesterol
■ Risk of Coronary artery disease linked to LDL levels
■ LDLs are deposited under endothelial surface and
oxidized where they:
– Attracts monocytes -> macrophages
– Macrophages engulf oxidized LDL
■ Vacuolation into ‘foam cells’
– Foam cells protrude against intimal lining
■ Eventually a tough cap is formed
– Vascular diameter & blood flow decreased
7/17/23 25
26. Overview of cholesterol panel
Total cholesterol
Desirable-less than 200
Borderline high—200-239
High—240 or greater
LDL
Desired <100
Above optimal—100-129
Borderline high—130-159
High-160-189
Very highà190
27. Overview cont.
HDL
■ High >60
■ Low <40
Triglycerides
Normal—less than 150
Borderline high—150-199
High--200 to 499
Very high—500 or above
28. Dyslipidemia
■ Associated with atherosclerosis and numerous
pathophysiologic effects
■ Elevated total cholesterol, high LDL and low HDL are
all risk factors for CAD
■ TG indicated excessive caloric intake; excessive
proteins and carbohydrates are converted to TG and
obesity
30. Dyslipidemia cont.
■ High dietary intake also increases the conversion of
VLDL to LDL cholesterol, and high dietary intake of
TG and saturated fat decreases the activity of LDL
receptors and increases synthesis of cholesterol.
31. Types of Lipoproteins
■ LDL—unfavorable type. Transports 75% of serum cholesterol
to peripheral tissues and the liver. High levels are
atherogenic
■ VLDL—contains 75% TG and 25% cholesterol. Transports
endogenous TG to fat and muscle cells.
■ HDL—favorable type. This LP transports cholesterol back to
the liver for catabolism and excretion.
33. Drug Therapy
■ Based on the type of dyslipidemia and its severity
■ Classes of agents include: HMB-CoA reductase
inhibitors or “statins”, fibrates, bile acid
sequestrants and niacin in different forms
■ Lovaza (omega-3 fatty acid)
■ Ezetimibe (Zetia®)
35. ■ Statins [Atorvastatin, Rosuvastatin, Simvastatin]
Compete to inhibit HMG-CoA reductase, rate limiting enzyme in the de novo
synthesis of cholesterol
■ Bile acid-binding resin [Cholestyramine, Colestipol]
– Increases bile acid excretion. Lowers LDL
■ Fibrates [Clofibrates, Gemfibrozil]
– Inhibits peripheral lipolysis, decreases hepatic uptake of free fatty acids;
lowers secretion of VLDL
■ Niacin
– niacin inhibits the lipolysis of TG by hormone-sensitive lipase
■ Ezetimibe
– Inhibits cholesterol absorption
7/17/23 35
36. HMG-CoA reductase inhibitors or “statins”
■ Inhibit an enzyme (hydroxymethylglutaryl-coenzyme
A reductase) required for hepatic synthesis of
cholesterol
■ Decrease serum cholesterol, LDL, VLDL and TG
■ Reach maximal effects within about 6 weeks
37. Statins cont.
■ Drugs also reduce C reactive protein, associated
with inflammation and development of CAD
■ Undergo extensive first pass metabolism
■ Metabolism occurs in liver
38. Statins cont.
■ Adverse effects include diarrhea, rashes,
headaches, constipation, hepatotoxicity and
myopathy.
■ Should obtain baseline LFTs and then at 6 and 12
weeks after starting then every 6 months
■ If serum aminotransferases increase to more than
3x normal, should be reduced.
39. Statins cont.
■ Do not take with grapefruit juice
■ Pregnancy category X
■ Examples: Lipitor (atorvastatin), Pravachol
(pravastatin), Zocor (simvastatin), Lescol
(Fluvastatin)
40. Bile Acid Sequestrants
■ Bind bile acids in the intestinal lumen. This causes
the bile acids to be excreted in feces and prevents
their being recirculated to the liver. Thus, the liver
will use cholesterol to produce bile acids thus
decreasing serum levels.
41. Bile Acid Sequestrants
■ Especially lower LDL
■ Examples are: Questran (cholestyramine) and
Welchol (colesevelam)
■ Often used with patients already on a statin
■ Long term use can affect absorption of folate,
Vitamins A,D,E,K
42. Fibrates
■ Tricor (fenofibrate)
■ Lopid (gemfibrozil)
■ These drugs increase oxidation of fatty acids in liver
and muscle tissue thus decreasing hepatic
production of TG, VLDL and increase HDL.
■ Most effective drugs for reducing TG.
43. Fibrates cont.
■ Can cause hepatotoxicity
■ Main side effects include diarrhea, GI discomfort,
cause gallstones, interact with Coumadin
44. Niacin (nicotinic acid)
■ Decreases both cholesterol and triglycerides
■ Bottom line—decreases hepatic synthesis of TG and
secretion of VLDL (which leads to decreased
production of LDL)
■ Need high doses for efficacy
45. Niacin
■ Side effects include flushing, pruritus, gastric irritation. May
cause hyperglycemia, hyperuricemia, elevated hepatic
aminotransferase enzymes and hepatitis.
■ Can reduce flushing by starting with low doses, taking dose
with meals, and taking ASA 325mg thirty minutes before
taking dose
■ More effective in preventing heart disease when used in
combination with another dyslipidaemic agent such as a
bile acid sequestrant or a fibrate.
46. Others
■ Ezetimibe (Zetia) Inhibits absorption of cholesterol
from small intestine
■ Don’t give with cholestyramine (Questran)
47. Important reminders
Risk factors for thromboembolism
1. Obesity
2. MI
3. Atrial fibrillation
4. Prosthetic heart valves
5. Atherosclerotic heart disease
6. Oral contraceptives/Hormone replacement therapy
7. History of DVT or PE
8. Cigarette smoking
9. Immobility
49. ■ Stroke occurs when the supply of blood to the brain is either interrupted or
reduced.
■ There are three main kinds of stroke; ischemic, hemorrhagic and Transcient
ischaemic attacks.
■ Ischaemic stroke- caused by blockages or narrowing of the arteries that
provide blood to the brain, resulting in ischemia. Most common (in 80%).
■ Hemorrhagic stroke is caused by arteries in the brain either leaking blood or
bursting open.
– Hypertension, trauma, blood-thinning medications and aneurysm
(weaknesses in blood vessel walls).
■ TIAs are different from the aforementioned kinds of stroke because the flow
of blood to the brain is only briefly interrupted. TIAs are similar to ischemic
strokes in that they are often caused by blood clots or other debris.
7/17/23 49
50. Types of stroke
Intracerebral haemorrhage
(30%)
Ischaemic (65%) Subarachnoid
haemorrhage (5%)
• This type of stroke is
caused by a blockage in an
artery that supplies blood to
the brain
• The blockage reduces the
blood flow and oxygen to
the brain, leading to damage
or death of brain cells
• An emergency condition in
which a ruptured blood
vessel causes bleeding
inside the brain.
• High blood pressure and
trauma are two leading
causes.
• Bleeding in the space
between the brain and the
tissue covering the brain.
• Subarachnoid haemorrhage,
a medical emergency, is
usually from a bulging blood
vessel that bursts in the
brain (aneurysm).
51. Risk Factors of Stroke among West Africans
ISCHEMIC STROKE
■ Hypertension
■ Dyslipidaemia
■ Diabetes Mellitus
■ Raised Waist-to-Hip ratio
■ Cardiac Disease
■ Physical Inactivity
■ Stress
■ Table added salt
■ Regular Meat consumption
■ Low consumption of green leafy
vegetables
HAEMORRHAGIC STROKE
• Hypertension
• Dyslipidaemia
• Diabetes Mellitus
• Cigarette smoking
• Stress
• Table added salt
• Regular Meat consumption
• Low consumption of green
leafy vegetables
52. Management of Ischemic Stroke
■ Supportive Care
■ Management of BP (<180/110 mm Hg)
■ Fluid –0.9% Saline (to maintain hydration and electrolyte balance; in excess can cause
brain swelling. 5% dextrose or half NS avoided due to increased ICP risk)
■ Hyperglycaemia(> 40% of cases) (can be managed with insulin to prevent worsening
clinical outcome and increased mortality)
■ Fibrinolysis with rTPA
■ Acute angioplasty/stenting
■ Management of complications – DVT, sepsis
■ Rehabilitation
■ Citicoline (Somazina) believed to improve clinical outcome following
ischemic stroke (Decreases death rate and disability post-CVA)
53. Management of Ischemic Stroke
Antiplatelet/Anticoagulant therapy
■ Aspirin 300mg for 15 days or 150 mg for 30 days followed by 75 mg
for life
■ Clopidogrel if intolerant of Aspirin
■ Aspirin + Dipyridamole
■ Aspirin + Clopidogrel combination for TIA or mild strokes
■ Anticoagulant therapy for Cardioembolic strokes (Atrial fibrillation)
54. Management of Ischemic Stroke
Acute Thrombolytic Therapy
■ IV tissue Plasminogen Activator: 0.9 mg/kg (with caution)
Criteria for thrombolysis:
■ < 3 hr from onset
■ Intracerebral haemorrhage excluded by imaging
■ SBP < 185; DBP < 110 mm Hg
■ Platelets > 100,000
■ Patient not on anticoagulants, no recent surgery or GI bleeding; no seizures at onset
55. Management of Intracerebral Haemorrhage
■ Rapid neuroimaging
■ Intubation if necessary (CPR)
■ Emergency haematoma evacuation
■ External ventricular drainage
■ Management of raised ICP
■ BP and hyperglycaemia management
■ Reversal of coagulopathy
56. Management of Subarachnoid haemorrhage
■ Clipping
■ Endovascular coiling to limit blood flow into aneurysm
■ Use of Tranexamic Acid/Aminocaproic acid to prevent rebleeding in the
acute phase (<72 hrs.)
■ Management of raised ICP
■ BP management
■ Anticonvulsants to relieve pain and seizures
■ Prevention of vasospasms (e.g. Nimodipine, Clazosentan)
■ Simvastatin and Mag. Sulphate are contraindicated (no benefits in
decreasing incidence of vasospasm)
57. DVT Prophylaxis after ischaemic stroke
■ SC administration of anticoagulants is recommended for
treatment of immobilized patients to prevent DVT
■ Use of intermittent external compression devices is
reasonable for treatment of patients who cannot receive
anticoagulants
58. DVT Prophylaxis after haemorrhagic stroke
■ After documentation of cessation of bleeding, low-
dose subcutaneous LMW Heparin is probably safe in
patients with ICH
■ It may be considered on an individual basis for
patients with hemiplegia after 3 to 4 days of stroke
onset