This document discusses hemostasis and mechanisms of coagulation, fibrinolysis, platelet function, and their regulation. It describes the roles of coagulation factors, fibrinolysis, endothelium, platelets, calcium, and vitamins in hemostasis. Direct and indirect acting agents that promote coagulation or inhibit fibrinolysis are discussed. Uses and side effects of heparin, warfarin, aspirin, streptokinase, and aprotinin are summarized.
Hypertension is a common cardiovascular condition caused by persistently high blood pressure that damages organs. Antihypertensive drugs work via different mechanisms like inhibiting the renin-angiotensin-aldosterone system, blocking calcium channels, promoting sodium excretion with diuretics, and reducing sympathetic nervous system activity. Common classes of antihypertensives include ACE inhibitors, angiotensin receptor blockers, calcium channel blockers, diuretics, sympatholytics, and vasodilators. Treatment involves beginning with certain drug classes based on patient characteristics and guidelines, and escalating treatment by adding other classes as needed to control blood pressure. Antihypertensive drug choice is also based on minimizing adverse effects and avoiding
This document discusses hypertension and its treatment. It defines hypertension as a systolic blood pressure over 140 mmHg or a diastolic blood pressure over 90 mmHg. It describes the types of hypertension as essential, secondary, and environmental. Treatment of hypertension is important to prevent damage to blood vessels and organs like the heart, brain, and kidneys. Several classes of antihypertensive drugs are discussed in detail, including ACE inhibitors, angiotensin receptor blockers, calcium channel blockers, beta blockers, and diuretics. The renin-angiotensin system and how ACE inhibitors work to treat hypertension by inhibiting the conversion of angiotensin I to angiotensin II are also
The document discusses calcium channel blockers (CCBs), which are a class of antihypertensive drugs. CCBs work by blocking calcium channels, thereby relaxing blood vessels and reducing blood pressure. They are classified into phenylalkylamines, dihydropyridines, and benzothiazepines. CCBs are effective antihypertensives and are also used to treat angina by dilating coronary arteries and reducing oxygen demand of the heart. Their adverse effects include headaches, dizziness, and hypotension. CCBs are contraindicated in conditions like heart failure and bradycardia.
Pharmacological management of heart failureNaser Tadvi
Heart failure is caused by decreased cardiac output and increased sympathetic discharge. Drugs used to treat heart failure include diuretics to reduce preload, ACE inhibitors to reduce afterload, beta blockers to attenuate sympathetic activation, and digitalis for its inotropic effects. Newer drugs target vasodilation and myosin activation to further increase cardiac efficiency while reducing energy demands. Combination therapy following an assessment of cardiac function and volume status provides the best approach for management of heart failure.
The document discusses various anticoagulants and their mechanisms of action, including heparin, low molecular weight heparins, warfarin, and direct thrombin inhibitors. It also covers fibrinolytic agents and their role in dissolving blood clots. The key mechanisms discussed are how heparin activates antithrombin III to inactivate thrombin and factor Xa, how warfarin inhibits vitamin K to decrease production of coagulation factors, and how fibrinolytic agents activate plasminogen to break down fibrin clots. Monitoring and clinical uses of these drug classes are also summarized.
This document discusses antiarrhythmic drugs, their mechanisms of action, classifications, and effects on cardiac electrophysiology. It covers 4 main classes of antiarrhythmic drugs - Class I agents which affect sodium channels, Class II agents which are beta blockers, Class III agents which affect potassium channels, and Class IV agents which affect calcium channels. Specific drugs from each class are described in detail including their indications, mechanisms, dosages, side effects, and drug interactions. The document provides an overview of the pharmacological treatment of cardiac arrhythmias.
Hypertension is a common cardiovascular condition caused by persistently high blood pressure that damages organs. Antihypertensive drugs work via different mechanisms like inhibiting the renin-angiotensin-aldosterone system, blocking calcium channels, promoting sodium excretion with diuretics, and reducing sympathetic nervous system activity. Common classes of antihypertensives include ACE inhibitors, angiotensin receptor blockers, calcium channel blockers, diuretics, sympatholytics, and vasodilators. Treatment involves beginning with certain drug classes based on patient characteristics and guidelines, and escalating treatment by adding other classes as needed to control blood pressure. Antihypertensive drug choice is also based on minimizing adverse effects and avoiding
This document discusses hypertension and its treatment. It defines hypertension as a systolic blood pressure over 140 mmHg or a diastolic blood pressure over 90 mmHg. It describes the types of hypertension as essential, secondary, and environmental. Treatment of hypertension is important to prevent damage to blood vessels and organs like the heart, brain, and kidneys. Several classes of antihypertensive drugs are discussed in detail, including ACE inhibitors, angiotensin receptor blockers, calcium channel blockers, beta blockers, and diuretics. The renin-angiotensin system and how ACE inhibitors work to treat hypertension by inhibiting the conversion of angiotensin I to angiotensin II are also
The document discusses calcium channel blockers (CCBs), which are a class of antihypertensive drugs. CCBs work by blocking calcium channels, thereby relaxing blood vessels and reducing blood pressure. They are classified into phenylalkylamines, dihydropyridines, and benzothiazepines. CCBs are effective antihypertensives and are also used to treat angina by dilating coronary arteries and reducing oxygen demand of the heart. Their adverse effects include headaches, dizziness, and hypotension. CCBs are contraindicated in conditions like heart failure and bradycardia.
Pharmacological management of heart failureNaser Tadvi
Heart failure is caused by decreased cardiac output and increased sympathetic discharge. Drugs used to treat heart failure include diuretics to reduce preload, ACE inhibitors to reduce afterload, beta blockers to attenuate sympathetic activation, and digitalis for its inotropic effects. Newer drugs target vasodilation and myosin activation to further increase cardiac efficiency while reducing energy demands. Combination therapy following an assessment of cardiac function and volume status provides the best approach for management of heart failure.
The document discusses various anticoagulants and their mechanisms of action, including heparin, low molecular weight heparins, warfarin, and direct thrombin inhibitors. It also covers fibrinolytic agents and their role in dissolving blood clots. The key mechanisms discussed are how heparin activates antithrombin III to inactivate thrombin and factor Xa, how warfarin inhibits vitamin K to decrease production of coagulation factors, and how fibrinolytic agents activate plasminogen to break down fibrin clots. Monitoring and clinical uses of these drug classes are also summarized.
This document discusses antiarrhythmic drugs, their mechanisms of action, classifications, and effects on cardiac electrophysiology. It covers 4 main classes of antiarrhythmic drugs - Class I agents which affect sodium channels, Class II agents which are beta blockers, Class III agents which affect potassium channels, and Class IV agents which affect calcium channels. Specific drugs from each class are described in detail including their indications, mechanisms, dosages, side effects, and drug interactions. The document provides an overview of the pharmacological treatment of cardiac arrhythmias.
1. Antiplatelet drugs work by inhibiting platelet aggregation which is essential for forming blood clots. They are used to prevent thrombus formation in certain pathological conditions.
2. There are several classes of antiplatelet drugs including aspirin, clopidogrel, abciximab which work via different mechanisms such as inhibiting thromboxane A2, blocking ADP receptors, or inhibiting the glycoprotein IIb/IIIa receptor.
3. Fibrinolytics like streptokinase, alteplase work by activating plasminogen to plasmin to break down fibrin clots and are indicated for pulmonary embolism, myocardial infarction, and ischemic stroke. The major risks are bleeding complications.
This document provides information on anticoagulants. It begins with an introduction to anticoagulants and how they differ from antiplatelets. It then defines anticoagulants and provides a classification including heparin and low molecular weight heparins, vitamin K antagonists, direct thrombin inhibitors, and factor Xa inhibitors. For each drug class, specific drugs are discussed along with their mechanisms of action, indications, dosages, side effects and nursing considerations.
This document discusses antihypertensive drugs. It begins by defining hypertension and describing the types and outcomes of hypertension. It then covers the normal blood pressure regulation mechanisms. The document classifies antihypertensive drugs into several categories including diuretics, ACE inhibitors, angiotensin receptor blockers, calcium channel blockers, beta blockers, and others. For each drug class, it provides examples, discusses the mechanism of action, desirable properties, and drawbacks. It concludes by discussing the current treatment approaches and guidelines for selecting antihypertensive drugs.
This document provides an overview of antihypertensive agents (blood pressure medications). It discusses the types and classes of antihypertensives, including diuretics, ACE inhibitors, angiotensin receptor blockers, calcium channel blockers, beta blockers, and alpha blockers. It describes the mechanisms of action, therapeutic uses, and potential side effects of each class. The document is intended to teach healthcare providers about selecting and utilizing different antihypertensive drugs to treat hypertension.
The document discusses anticoagulants and blood coagulation. It describes the intrinsic and extrinsic pathways of coagulation and the stages that form a blood clot. Natural anticoagulant mechanisms include prostacyclin, antithrombin III, and protein C. Common anticoagulants discussed are heparin, low molecular weight heparin, and oral agents like warfarin. The uses, mechanisms, benefits, and risks of various anticoagulants are summarized.
This document discusses drugs that act on blood components to prevent clotting. It covers anticoagulants like heparin and warfarin that prevent clot formation, fibrinolytics like streptokinase that break down existing clots, and antiplatelets like aspirin and clopidogrel that inhibit platelet aggregation. The stages of coagulation and fibrinolysis are described. Specific drugs are explained including their mechanisms of action, clinical uses, and potential side effects.
1. ACE inhibitors work by inhibiting the angiotensin converting enzyme and reducing angiotensin II levels, leading to vasodilation and sodium excretion.
2. Common ACE inhibitors include lisinopril, enalapril, ramipril, and benazepril. They are used to treat hypertension, heart failure, myocardial infarction, and diabetic nephropathy.
3. Potential side effects include dry cough, hypotension, hyperkalemia, angioedema, and renal dysfunction. ACE inhibitors can also cause fetal harm during pregnancy.
This document discusses lipid-lowering drugs used to treat hyperlipidemia and prevent cardiovascular disease. It covers the main classes of drugs including statins, fibrates, bile acid sequestrants, and niacin. Statins work by inhibiting cholesterol synthesis while fibrates activate lipoprotein lipase. Bile acid sequestrants bind bile acids in the gut. The document reviews the mechanisms, effects, uses, and side effects of these drug classes and emphasizes the importance of lifestyle modifications and managing hyperlipidemia.
This document discusses cardiac electrophysiology and arrhythmias. It begins by describing the cardiac pacemaker and sinus rhythm, then details the phases of the cardiac action potential. Various types of arrhythmias are described caused by abnormalities in automaticity, ectopic foci, reentry pathways and conduction blocks. Classes of antiarrhythmic drugs are introduced and specific examples are explained regarding their mechanisms and effects on the action potential and use in treating arrhythmias. Side effects and considerations for various drugs are also mentioned.
Adrenergic agonists and antagonists act on adrenergic receptors. Agonists like epinephrine and norepinephrine directly stimulate receptors, whereas antagonists like prazosin competitively block receptor activation. These drugs have widespread effects throughout the body due to the sympathetic nervous system's role in functions like heart rate, blood pressure, bronchodilation and uterine contraction. Care must be taken with certain drugs that can cause severe side effects like hypotension or bronchospasm.
Dr. D. K. Brahma discusses antiplatelet drugs, which interfere with platelet function and are useful for preventing thromboembolic disorders. The document defines antiplatelet drugs and describes the role of platelets in thrombosis formation. It then discusses the mechanisms of various antiplatelet drugs including aspirin, dipyridamole, ticlodipine, clopidogrel, prasugrel, and GPIIb/IIIa receptor antagonists like abciximab. The uses of these antiplatelet drugs for conditions like heart attacks, strokes, angioplasty and stents are summarized.
This document provides an overview of anticoagulants and the blood clotting process. It discusses the four phases of blood clotting - vascular, platelet, coagulation, and fibrinolysis. It then describes various types of anticoagulants including heparin, low molecular weight heparins, direct thrombin inhibitors, vitamin K antagonists like warfarin, and new oral anticoagulants. The mechanisms of action, pharmacokinetics, uses, monitoring, and adverse effects of these anticoagulants are summarized. Recommendations for their use during regional anesthesia and general anesthesia are also outlined.
This document discusses coagulants and anticoagulants. It defines coagulants as substances that promote coagulation and are used to treat hemorrhagic states. Anticoagulants delay blood clotting and are given to prevent conditions like strokes and heart attacks. Specific coagulants and anticoagulants discussed include heparin, warfarin, vitamin K, and factors I-XIII involved in coagulation. The mechanisms, uses, and side effects of heparin and warfarin are summarized.
This document discusses antihypertensive agents used to treat hypertension. It describes different categories of agents including adrenergic agents, ACE inhibitors, angiotensin II receptor blockers, calcium channel blockers, diuretics, and vasodilators. For each category, the document outlines mechanisms of action, examples of medications, therapeutic uses, and potential side effects. It emphasizes the importance of monitoring blood pressure during therapy and avoiding abruptly stopping medications.
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.
Drugs for coagulation, Antiplatelets, Fibrinolytics & AntifibrinolyticsBikashAdhikari26
Hemostasis is the process of stopping blood loss from damaged blood vessels. It involves vascular constriction, platelet plug formation, blood clotting, and fibrous tissue growth. Coagulants promote coagulation and are used to treat hemorrhagic states. Vitamin K is a necessary cofactor for the production of coagulation factors and is used to treat bleeding disorders caused by vitamin K deficiency or impaired coagulation factor synthesis. Antifibrinolytics like tranexamic acid and epsilon amino caproic acid inhibit fibrinolysis by blocking plasminogen and preventing clot dissolution, reducing bleeding in various conditions.
This document summarizes anticoagulants and their uses. It discusses the coagulation cascade and how anticoagulants work to prevent unwanted clotting. Several classes of anticoagulants are covered, including unfractionated and low molecular weight heparins, vitamin K antagonists like warfarin, and direct acting anticoagulants. Indications, dosages, monitoring, and adverse effects are provided for many of the discussed anticoagulants. The document also addresses perioperative management of anticoagulation and treatments for bleeding or over-anticoagulation.
Platelets are small cell fragments that help the blood clot. Several drugs target platelets to prevent excessive clotting. Aspirin and clopidogrel inhibit platelet aggregation by blocking thromboxane A2 and ADP receptors. Heparin enhances the effects of antithrombin III to inhibit coagulation factors Xa and IIa. Low molecular weight heparins have fewer side effects than unfractionated heparin and do not require monitoring.
Fibrinolytics such as streptokinase, urokinase, and alteplase work by activating the natural fibrinolytic system to dissolve blood clots and recanalize occluded vessels. Streptokinase obtains plasminogen to form a complex that activates plasminogen but is non-specific, antigenic, and destroyed by antibodies. Urokinase is non-antigenic and not destroyed by antibodies. Alteplase is fibrin-specific, non-antigenic, rapid-acting, and more potent but also more expensive. Fibrinolytics are used for conditions like myocardial infarction, deep vein thrombosis, and pulmonary embolism. Antifibrinolytics
1. Antiplatelet drugs work by inhibiting platelet aggregation which is essential for forming blood clots. They are used to prevent thrombus formation in certain pathological conditions.
2. There are several classes of antiplatelet drugs including aspirin, clopidogrel, abciximab which work via different mechanisms such as inhibiting thromboxane A2, blocking ADP receptors, or inhibiting the glycoprotein IIb/IIIa receptor.
3. Fibrinolytics like streptokinase, alteplase work by activating plasminogen to plasmin to break down fibrin clots and are indicated for pulmonary embolism, myocardial infarction, and ischemic stroke. The major risks are bleeding complications.
This document provides information on anticoagulants. It begins with an introduction to anticoagulants and how they differ from antiplatelets. It then defines anticoagulants and provides a classification including heparin and low molecular weight heparins, vitamin K antagonists, direct thrombin inhibitors, and factor Xa inhibitors. For each drug class, specific drugs are discussed along with their mechanisms of action, indications, dosages, side effects and nursing considerations.
This document discusses antihypertensive drugs. It begins by defining hypertension and describing the types and outcomes of hypertension. It then covers the normal blood pressure regulation mechanisms. The document classifies antihypertensive drugs into several categories including diuretics, ACE inhibitors, angiotensin receptor blockers, calcium channel blockers, beta blockers, and others. For each drug class, it provides examples, discusses the mechanism of action, desirable properties, and drawbacks. It concludes by discussing the current treatment approaches and guidelines for selecting antihypertensive drugs.
This document provides an overview of antihypertensive agents (blood pressure medications). It discusses the types and classes of antihypertensives, including diuretics, ACE inhibitors, angiotensin receptor blockers, calcium channel blockers, beta blockers, and alpha blockers. It describes the mechanisms of action, therapeutic uses, and potential side effects of each class. The document is intended to teach healthcare providers about selecting and utilizing different antihypertensive drugs to treat hypertension.
The document discusses anticoagulants and blood coagulation. It describes the intrinsic and extrinsic pathways of coagulation and the stages that form a blood clot. Natural anticoagulant mechanisms include prostacyclin, antithrombin III, and protein C. Common anticoagulants discussed are heparin, low molecular weight heparin, and oral agents like warfarin. The uses, mechanisms, benefits, and risks of various anticoagulants are summarized.
This document discusses drugs that act on blood components to prevent clotting. It covers anticoagulants like heparin and warfarin that prevent clot formation, fibrinolytics like streptokinase that break down existing clots, and antiplatelets like aspirin and clopidogrel that inhibit platelet aggregation. The stages of coagulation and fibrinolysis are described. Specific drugs are explained including their mechanisms of action, clinical uses, and potential side effects.
1. ACE inhibitors work by inhibiting the angiotensin converting enzyme and reducing angiotensin II levels, leading to vasodilation and sodium excretion.
2. Common ACE inhibitors include lisinopril, enalapril, ramipril, and benazepril. They are used to treat hypertension, heart failure, myocardial infarction, and diabetic nephropathy.
3. Potential side effects include dry cough, hypotension, hyperkalemia, angioedema, and renal dysfunction. ACE inhibitors can also cause fetal harm during pregnancy.
This document discusses lipid-lowering drugs used to treat hyperlipidemia and prevent cardiovascular disease. It covers the main classes of drugs including statins, fibrates, bile acid sequestrants, and niacin. Statins work by inhibiting cholesterol synthesis while fibrates activate lipoprotein lipase. Bile acid sequestrants bind bile acids in the gut. The document reviews the mechanisms, effects, uses, and side effects of these drug classes and emphasizes the importance of lifestyle modifications and managing hyperlipidemia.
This document discusses cardiac electrophysiology and arrhythmias. It begins by describing the cardiac pacemaker and sinus rhythm, then details the phases of the cardiac action potential. Various types of arrhythmias are described caused by abnormalities in automaticity, ectopic foci, reentry pathways and conduction blocks. Classes of antiarrhythmic drugs are introduced and specific examples are explained regarding their mechanisms and effects on the action potential and use in treating arrhythmias. Side effects and considerations for various drugs are also mentioned.
Adrenergic agonists and antagonists act on adrenergic receptors. Agonists like epinephrine and norepinephrine directly stimulate receptors, whereas antagonists like prazosin competitively block receptor activation. These drugs have widespread effects throughout the body due to the sympathetic nervous system's role in functions like heart rate, blood pressure, bronchodilation and uterine contraction. Care must be taken with certain drugs that can cause severe side effects like hypotension or bronchospasm.
Dr. D. K. Brahma discusses antiplatelet drugs, which interfere with platelet function and are useful for preventing thromboembolic disorders. The document defines antiplatelet drugs and describes the role of platelets in thrombosis formation. It then discusses the mechanisms of various antiplatelet drugs including aspirin, dipyridamole, ticlodipine, clopidogrel, prasugrel, and GPIIb/IIIa receptor antagonists like abciximab. The uses of these antiplatelet drugs for conditions like heart attacks, strokes, angioplasty and stents are summarized.
This document provides an overview of anticoagulants and the blood clotting process. It discusses the four phases of blood clotting - vascular, platelet, coagulation, and fibrinolysis. It then describes various types of anticoagulants including heparin, low molecular weight heparins, direct thrombin inhibitors, vitamin K antagonists like warfarin, and new oral anticoagulants. The mechanisms of action, pharmacokinetics, uses, monitoring, and adverse effects of these anticoagulants are summarized. Recommendations for their use during regional anesthesia and general anesthesia are also outlined.
This document discusses coagulants and anticoagulants. It defines coagulants as substances that promote coagulation and are used to treat hemorrhagic states. Anticoagulants delay blood clotting and are given to prevent conditions like strokes and heart attacks. Specific coagulants and anticoagulants discussed include heparin, warfarin, vitamin K, and factors I-XIII involved in coagulation. The mechanisms, uses, and side effects of heparin and warfarin are summarized.
This document discusses antihypertensive agents used to treat hypertension. It describes different categories of agents including adrenergic agents, ACE inhibitors, angiotensin II receptor blockers, calcium channel blockers, diuretics, and vasodilators. For each category, the document outlines mechanisms of action, examples of medications, therapeutic uses, and potential side effects. It emphasizes the importance of monitoring blood pressure during therapy and avoiding abruptly stopping medications.
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.
Drugs for coagulation, Antiplatelets, Fibrinolytics & AntifibrinolyticsBikashAdhikari26
Hemostasis is the process of stopping blood loss from damaged blood vessels. It involves vascular constriction, platelet plug formation, blood clotting, and fibrous tissue growth. Coagulants promote coagulation and are used to treat hemorrhagic states. Vitamin K is a necessary cofactor for the production of coagulation factors and is used to treat bleeding disorders caused by vitamin K deficiency or impaired coagulation factor synthesis. Antifibrinolytics like tranexamic acid and epsilon amino caproic acid inhibit fibrinolysis by blocking plasminogen and preventing clot dissolution, reducing bleeding in various conditions.
This document summarizes anticoagulants and their uses. It discusses the coagulation cascade and how anticoagulants work to prevent unwanted clotting. Several classes of anticoagulants are covered, including unfractionated and low molecular weight heparins, vitamin K antagonists like warfarin, and direct acting anticoagulants. Indications, dosages, monitoring, and adverse effects are provided for many of the discussed anticoagulants. The document also addresses perioperative management of anticoagulation and treatments for bleeding or over-anticoagulation.
Platelets are small cell fragments that help the blood clot. Several drugs target platelets to prevent excessive clotting. Aspirin and clopidogrel inhibit platelet aggregation by blocking thromboxane A2 and ADP receptors. Heparin enhances the effects of antithrombin III to inhibit coagulation factors Xa and IIa. Low molecular weight heparins have fewer side effects than unfractionated heparin and do not require monitoring.
Fibrinolytics such as streptokinase, urokinase, and alteplase work by activating the natural fibrinolytic system to dissolve blood clots and recanalize occluded vessels. Streptokinase obtains plasminogen to form a complex that activates plasminogen but is non-specific, antigenic, and destroyed by antibodies. Urokinase is non-antigenic and not destroyed by antibodies. Alteplase is fibrin-specific, non-antigenic, rapid-acting, and more potent but also more expensive. Fibrinolytics are used for conditions like myocardial infarction, deep vein thrombosis, and pulmonary embolism. Antifibrinolytics
Fibrinolytics such as streptokinase, urokinase, and alteplase work by activating the natural fibrinolytic system to lyse thrombi and recanalize occluded blood vessels. They activate plasminogen to plasm in order to dissolve blood clots through the process of fibrinolysis. Streptokinase is the least expensive but also the least specific and can cause allergic reactions. Urokinase is non-antigenic and adverse effects are rare. Alteplase is fibrin-specific, rapid-acting, and has a lower risk of bleeding but is more expensive. Fibrinolytics are used to treat conditions like myocardial infarction, deep vein thrombosis, and pulmonary
Coagulants and anticoagulants work to maintain a balance in the coagulation system. Coagulants such as fresh whole blood and factors promote clotting, while anticoagulants like antithrombin and the fibrinolytic system inhibit clot formation and maintain blood fluidity. Vitamin K is essential for the production of coagulation factors and warfarin is an oral anticoagulant that works by inhibiting vitamin K. Heparin is commonly used as an injectable anticoagulant that prevents clotting by binding to antithrombin. Newer oral anticoagulants directly inhibit thrombin or factor Xa.
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.
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.
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.
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 blood and blood forming organsUrmila Aswar
This document discusses drugs that act on blood and blood forming organs. It covers topics like hemostasis, coagulation factors, coagulation pathways, anticoagulants like heparin and warfarin, fibrinolytics, and antiplatelet drugs. Key points include that hemostasis is the process by which bleeding stops, coagulation involves intrinsic and extrinsic pathways, and anticoagulants prevent clotting through various mechanisms like inhibiting thrombin formation. Common anticoagulants discussed are heparin, low molecular weight heparins, warfarin, and fibrinolytics like streptokinase that lyse clots. Antiplatelet drugs like aspirin are also covered.
This document 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.
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
Haemostasis is the physiologic system of competent blood vessels, endothelial cells, platelets and numerous plasma proteins that act in a finely controlled manner to preserve blood vessel integrity and prevent pathologic hemorrhage or thrombosis.
Haemostasis is achieved by :-
Vascular constriction
Formation of platelet plug
Formation of blood clot
Growth of fibrous tissue into the clot
This document discusses various drugs that affect blood fluidity and the hemostatic system. It describes anticoagulants like heparin and warfarin that prevent blood clotting through different mechanisms. It also covers antiplatelet drugs like aspirin and clopidogrel that inhibit platelet aggregation. Thrombolytics like tissue plasminogen activator and streptokinase are discussed as agents that lyse blood clots. The causes and treatments of anemia are summarized, including iron deficiency and megaloblastic anemias related to vitamin B12 and folate deficiencies.
This document discusses various coagulants and anticoagulants. It describes vitamin K and its uses including in newborns and for overdose of oral anticoagulants. It also discusses other coagulants like fibrinogen, antihemophilic factor, and desmopressin. The document then covers oral anticoagulants like warfarin including its dosing, effects, interactions and newer oral anticoagulants. It provides details about parenteral anticoagulants including heparin, its uses, pharmacokinetics, administration and adverse effects. Low molecular weight heparins and direct thrombin inhibitors are also summarized.
Antiplatelet new and anti coagulants : Dr Rahul Kunkulol's Power Point Prese...Rahul Kunkulol
This document discusses hemostasis and platelet function. It begins by defining hemostasis as the cessation of blood loss from damaged blood vessels. It then describes the role of platelets in normal hemostasis and thrombosis. Specifically, it explains how platelets adhere to sites of vascular injury and aggregate to form a platelet plug that stops bleeding. It also discusses how platelet activation is mediated by various agonists like collagen, thrombin, ADP, and thromboxane A2. The document summarizes the targets of various antiplatelet therapies such as aspirin, ADP receptor antagonists, and glycoprotein IIb/IIIa receptor antagonists.
Anesthesia for non obstetric patient in pregnancyAgrawal N.K
This document discusses anesthesia considerations for non-obstetric surgery during pregnancy. It covers topics such as placental transfer of anesthetic drugs, teratogenic risks, and techniques to ensure maternal and fetal safety. Regional anesthesia is preferred when possible to minimize drug exposure. General anesthesia requires careful maintenance of oxygenation, ventilation, hydration and avoiding hypotension. Fetal monitoring may be needed depending on gestational age. Postoperative monitoring and analgesia techniques aim to prevent preterm labor. Overall the goals are maternal safety, maintaining the pregnancy, and achieving the best fetal outcome.
This document discusses monitoring protocols for obstetric patients. It outlines the importance of clinical monitoring and equipment monitoring to help make treatment decisions and ensure better patient outcomes. It describes how to monitor various vital systems clinically including cardiovascular, respiratory, nervous and metabolic systems. It provides guidance on monitoring blood loss, recovery from procedures, and specific conditions like diabetes, thyroid disorders, anemia and preeclampsia/eclampsia. Target parameters for vitals and fluid management are presented to guide care.
The document outlines potential complications during and after anesthesia and intubation. It discusses intraoperative complications that can arise from laryngoscopy and endotracheal tube insertion such as aspiration, hypoxia, hypotension/hypertension, and hypothermia/hyperthermia. Postoperative complications include trauma to lips, teeth, tongue, tonsils, epiglottis or vocal cords, as well as injury to the trachea or blockage of the endotracheal tube. The document provides guidelines for monitoring patients' oxygen levels, end-tidal carbon dioxide, blood pressure, blood sugar, fluid intake and output, and temperature during and after the procedure.
This document outlines recommendations for pre-operative patient evaluation by an anesthesiologist. It recommends that the anesthesiologist visit with the patient the day before surgery to plan anesthesia and assess the patient's medical fitness. During the visit, the anesthesiologist should evaluate the patient's cardiopulmonary, hepatorenal, endocrine and central nervous systems, and confirm normal vital organ function or delay surgery if abnormalities exist. The evaluation also includes checking the patient's pulse, blood pressure, blood sugar, temperature, respiration, kidney, liver and nervous system. Finally, the anesthesiologist should provide night orders to the patient regarding fasting, medications and any other specific instructions.
The document defines anesthesia as an "induced, controlled, reversible, painfree state of sleep, which makes an individual, non responsive to noxious stimulus." It explains that patients are induced with intravenous, inhalational, or local anesthetics. The induced state is controlled through drug dosages and is mostly reversible. The goal is for patients to be painfree irrespective of the type of anesthesia. The induced state is described as a sleep-like state where patients are arousable rather than unconscious and non-responsive to painful surgical stimuli.
Assesment of lung parenchymal damage with arterial bloodAgrawal N.K
This document presents a study assessing lung damage at the alveolar level using arterial blood gas (ABG) analysis. It describes how gas exchange occurs between alveoli and blood capillaries, noting factors like surface area, membrane thickness, and gas pressure that affect diffusion. Patients with lung conditions have changes in these factors. The document introduces equations incorporating FiO2 and atmospheric pressure to calculate the expected versus measured PaO2 from ABG results. This is used to quantify lung damage in two patient cases in intensive care and pre-operation. The study concludes ABG reports should account for FiO2 and pressure to assess lung function and prognosis.
This document discusses endotracheal intubation, including what it is, its indications, required equipment, techniques, confirmation, ventilation, complications, and extubation. Endotracheal intubation involves placing a tube into the trachea to secure the airway and provide oxygen or ventilation support during procedures like general anesthesia, CPR, or ICU care. The document outlines sizes of tubes for different age groups and describes how to properly position and intubate a patient while visualizing the vocal cords using a laryngoscope.
1. Perioperative management of diabetes requires tight glucose control to prevent hyperglycemia and hypoglycemia.
2. Patients should be optimized before surgery with HbA1c <7% and preoperative blood glucose between 100-140 mg/dl.
3. During surgery, blood glucose should be monitored hourly and maintained between 100-200 mg/dl through insulin drips or oral medications depending on the patient's regimen.
4. Postoperative monitoring and management continues to prevent hyperglycemic or hypoglycemic complications.
This document discusses benzodiazepines (BDZs), including their discovery, mechanism of action, effects, and examples like diazepam and midazolam. It notes that BDZs bind to GABA receptors in the brain to have sedative, anxiolytic, hypnotic, amnestic, and anticonvulsant effects. Their onset and duration of action depends on lipid solubility. While generally safe, they can cause respiratory depression, especially in high doses or with pre-existing lung conditions. Their effects are reversed by the antagonist flumazenil. Midazolam is water-soluble and shorter-acting than diazepam. It is metabolized in the liver
The document discusses the properties and characteristics of various intravenous anesthetic agents. It provides details on propofol, thiopental, etomidate and ketamine. Some key points mentioned are that an ideal IV agent should have a short duration of action, not cause pain on injection, maintain hemodynamic stability and have minimal side effects. Propofol acts rapidly, has a short half-life and no accumulation. Thiopental dosage needs to be carefully monitored. Etomidate provides hypnosis without affecting ventilation or hemodynamics. Ketamine provides sedation, analgesia and sympatholysis when used in low doses.
This document discusses the composition and distribution of fluids in the human body. It notes that 60% of the body is fluid, with 40% being intracellular fluid and the remaining extracellular fluid distributed between interstitial fluid and intravascular fluid. It provides details on fluid requirements, losses, electrolyte concentrations in different compartments, and types of intravenous fluids including crystalloids and colloids. The document emphasizes the importance of fluid balance and maintenance of adequate hydration and outlines factors to consider for fluid management in pre-operative, intra-operative, and post-operative settings.
Muktapishti is a traditional Ayurvedic preparation made from Shoditha Mukta (Purified Pearl), is believed to help regulate thyroid function and reduce symptoms of hyperthyroidism due to its cooling and balancing properties. Clinical evidence on its efficacy remains limited, necessitating further research to validate its therapeutic benefits.
TEST BANK For Basic and Clinical Pharmacology, 14th Edition by Bertram G. Kat...rightmanforbloodline
TEST BANK For Basic and Clinical Pharmacology, 14th Edition by Bertram G. Katzung, Verified Chapters 1 - 66, Complete Newest Version.
TEST BANK For Basic and Clinical Pharmacology, 14th Edition by Bertram G. Katzung, Verified Chapters 1 - 66, Complete Newest Version.
TEST BANK For Basic and Clinical Pharmacology, 14th Edition by Bertram G. Katzung, Verified Chapters 1 - 66, Complete Newest Version.
TEST BANK For Basic and Clinical Pharmacology, 14th Edition by Bertram G. Katzung, Verified Chapters 1 - 66, Complete Newest Version.
TEST BANK For An Introduction to Brain and Behavior, 7th Edition by Bryan Kol...rightmanforbloodline
TEST BANK For An Introduction to Brain and Behavior, 7th Edition by Bryan Kolb, Ian Q. Whishaw, Verified Chapters 1 - 16, Complete Newest Versio
TEST BANK For An Introduction to Brain and Behavior, 7th Edition by Bryan Kolb, Ian Q. Whishaw, Verified Chapters 1 - 16, Complete Newest Version
TEST BANK For An Introduction to Brain and Behavior, 7th Edition by Bryan Kolb, Ian Q. Whishaw, Verified Chapters 1 - 16, Complete Newest Version
Adhd Medication Shortage Uk - trinexpharmacy.comreignlana06
The UK is currently facing a Adhd Medication Shortage Uk, which has left many patients and their families grappling with uncertainty and frustration. ADHD, or Attention Deficit Hyperactivity Disorder, is a chronic condition that requires consistent medication to manage effectively. This shortage has highlighted the critical role these medications play in the daily lives of those affected by ADHD. Contact : +1 (747) 209 – 3649 E-mail : sales@trinexpharmacy.com
Here is the updated list of Top Best Ayurvedic medicine for Gas and Indigestion and those are Gas-O-Go Syp for Dyspepsia | Lavizyme Syrup for Acidity | Yumzyme Hepatoprotective Capsules etc
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
8 Surprising Reasons To Meditate 40 Minutes A Day That Can Change Your Life.pptxHolistified Wellness
We’re talking about Vedic Meditation, a form of meditation that has been around for at least 5,000 years. Back then, the people who lived in the Indus Valley, now known as India and Pakistan, practised meditation as a fundamental part of daily life. This knowledge that has given us yoga and Ayurveda, was known as Veda, hence the name Vedic. And though there are some written records, the practice has been passed down verbally from generation to generation.
Promoting Wellbeing - Applied Social Psychology - Psychology SuperNotesPsychoTech Services
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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.
11. When injury occurs, the platelets adhere to
the injury site
Exposure of sub endothelial matrix protein
like Collagen, vWF, glycoprotein leads to
adhesion of platelets
20. THROMBIN –
ACTIVE COMPOUND OF COAGULATION
SYSTEM WHICH HELP IN ARREST OF BLEEDING
FROM SMALL VESSELS
MAY BE USED TOPICALLY OR I.V.
FIBRINOGEN-
NON ACTIVE COMPOUND USED FOR BLEEDING
FROM BIGGER VESSELS
21. CALCIUM GLUCONATE AND CHLORIDE –
USED TO STIMULATE ACTIVATION FACTORS
GELATINA MEDICANILIS-
STABLIZES VESSEL WALL,
INCREASES VISCOSITY,
USED FOR BLEEDING FROM BIGGER VESSELS
22. SYNTHETIC WATER SOLUBLE VIT K
INDIRECT ACTING
MAY BE GIVEN ORALLY, IM, IV
ACTION IN 12- 18 HOURS
TAKES PART IN SYNTHESIS OF CLOTTING
FACTORS IN LIVER
23. USED IN REPEATED BLEEDING DISORDERS,
LIVER DISEASES, CHRONIC BLEEDING
RADIATION SICKNESS
OVERDOSE OF ANTI COAGULANT
24. DIRECT ACTING- (vivo and vitro )
HEPARIN
FRAXIPARIN
SODIUM CITRATE
27. NATURAL OCCURING SUBSTANCE
PRODUCED BY MAST CELLS
HIGH CONCENTRATION IN LUNGS AND WALLS
OF INTESTINE
IS A ACIDIC MUCOPOLYSACCHRIDE
28. CAN BE GIVEN IV, IM, SC OR TOPICALLY
IV –IMMEDIATELY 4-6 HRS
IM-15-30 MIN 6-8 HRS
SC-30-60 MIN 8-12 HRS
METABOLISED IN LIVER
EXCRETED IN URINE
29. Heparin binds to anti-thrombin III " conformational
change " rapid inactivation of
thrombin and inhibition of fibinogen conversion to
fibrin.
Heparin has negative charge "is absorbed on blood
cells " increase in negative charge
on platelets " decrease in platelet aggregation and
adhesion.
Heparin releases lipoprotein lipase from endothelial
cells
30. strong rapid decrease in all stages of blood
coagulation
decrease in platelet aggregation
improve of microcirculation and coronary
circulation
decrease in lipids concentrations in blood
serum
decrease in inflammation
decrease in immunity
31. increase in synthesis of surfactant in lungs
decrease in blood pressure (in higher doses)
decrease in glucose level in blood serum (in
higher doses)
increase in diuresis (in higher doses)
32. 1. - Acute thrombosis and thrombo embolism
2. - Myocardial infarction
3. -Ischemic insult
4. - Prevention of thrombus formation after
surgeries
5. - During haemodialysis or blood transfusion
6. - Thrombophlebitis
33. - Syndrome of disseminated blood coagulation
- Atherosclerosis
- Autoimmune diseases
- Chronic non-specific diseases of lungs
- Paradontitis, stomatitis (topically)
The time of bleeding or the time of blood
coagulation should be controlled
34. 1. Bleeding
2. Hematomas
3. Micro and macro hematuria
4. Thrombocytopenia
5. Allergy
6. Osteoporosis
7. Silvering of the hair
8. Severe diseases of liver and kidney
36. It is low molecular weight heparin
is administered SC once a day; has bigger
bioavailability, longer duration of action
less binding with plasma proteins
depress activated Stuart-Prauers factor more
than prothrombin
is used for treatment of thromboflebitis,
prevention of thrombus formation after surgery
37. Vitamin k epoxide reductase
Half life-40 hrs
Peak - 72-96 hrs
Antidote- vit K
38.
39. It is indirect acting anticoagulant, cumarine
derivative
40. . is administered orally
· is absorbed in GI tract
· is bound with proteins in plasma
· is metabolized in liver
41. begins to act 2-3 hr after administration
· maximal action after 12-30 hr after
administration
· action lasts up to 48 hours after the end of
treatment
· is excreted by urine
42. Mechanism of action of Neodicumarinum,
warfarin and other indirect-acting
anticoagulants is
block of epoxide reductase in the liver " block
of creation of active form of vitamin K “
inhibition of synthesis of clotting factors.
43. . Decrease in blood coagulation
· Increase in fibrinolysis
· Decrease in lipids concentration in blood
44. - Acute thrombosis (together or after of heparin’s
usage)
- Myocardium infarction
- Ischemic insult
- Thrombo-embolism
- Thrombophlebitis
- Prevention of thrombus formation after
surgeries
Index of prothrombin should be controlled !
45. Side-effects/ Contraindications
1. Bleeding
2. Formation of hematomas
3. Haematuria
4. Dyspepsia
5. Suppression of liver function
6. Allergy
7. Bleeding gums and petechia in mucous
membrane of oral cavity
46. 1. Haemorrhage
2. Hemorrhagic diathesis
3. Gastric ulcer
4. Malignant diseases
5. Diseases of liver and kidney
6. Pregnancy
For treatment of overdose – Vikasolum !
47. · It is indirect-acting anticoagulant; indandione
derivative
· mechanism of action is the same of
Neodicumarinum
· start of action is slower, duration of action is
more
· may cause pink colour of urine resulting from
excretion of drug and its metabolites
49. ANTI-PLATELET ACTION OF ASPIRIN
Aspirin irreversibly inhibits platelet cyclooxygenase-
1"prevention of synthesis of thromboxane A
2 " decrease in platelet aggregation.
This effect occurs in lower doses ( less than 0.5gm
per day) and last more than 48 hr.
In higher doses aspirin also inhibits synthesis of
prostacycline.
50. ANTI-PLATELET ACTION OF DIPYRIDAMOLE
Dypiridamole inhibits adenosine desaminase
and phosphodiesterase in platelets “
increase in cAMP concentration in cells "
inhibition of thromboxane A2 synthesis “
decrease in platelet aggregation. It also
increases prostacycline level.
51. ANTI-PLATELET ACTION OF TICLOPIDINE
Ticlopidine irreversibly blocks purinergic
receptors for ADP in platelet membranes
Inhibition of ADP-induced expression of
glycoprotein (GP)IIb/ IIIa receptors in platelet
membrane decreases platelet aggregation.
52. INDICATIONS TO ANTI-PLATELET DRUG USAGE
- prevention of thrombosis and re-thrombosis
(as discontinuation of anticoagulant therapy)
- prophylaxis of myocardial infarction and insult
- prophylaxis of thrombosis after surgeries
- angioplasty
- prevention of thrombosis in patients with
prosthetic cardiac valves
- thrombophlebitis
53. Classification
1.Fibrinolytic drugs
a) direct-acting
Fibrinolysin
b) indirect-acting (activators of profibrinolysin)
non-selective
Streptokinase
Streptoliase
selective
Alteplase
55. It is protein from donors’ plasma, the active
factor of fibrinolysis
is administered by IV infusion
has direct action on fibrin and dissolves
fibrin clot in the first hours after thrombosis
is used for treatment of acute thrombosis,
acute myocardial infarction.
56. thrombophlebitis
may cause bleeding resulting from increase in
fibrinolysis, allergy, anaphylaxis, arrhythmia,
hypotension
contraindications:
bleeding, cerebral vascular accident, recent
trauma of brain surgery, uncontrolled
hypertension.
57. It is the proteolytic enzyme from haemolytic
streptococcus.
It acts indirectly, inhibits the conversion of
plasminogen to plasmin " degradation both
of fibrin and fibrinogen " systemic activation of
fibrinolysis and dissolving of thrombus.
Plasma half-life is 23 min; is administered by IV
infusion (intracoronary infusion in
myocardial infarction).
It is more active than fibrinolysin, does not
cause arrhythmia
58. ALTEPLASE (ACTILISE)
is tissue plasminogen activator, product of
biotechnology
half-life is 5 min, is administered by IV
infusion
has high affinity for fibrin and selectively
acts only on plasminogen, bound with
thrombus
59. INHIBITORS OF FIBRINOLYSIS
CONTRICAL (Aprotinin)
is direct acting inhibitor of fibrinolysis and
proteolysis
is administered IV slowly or by IV infusion
binds with plasmin and inactivates it, inhibits
activity of trypsin and kallikrein
60. inhibits fibrinolysis and decreases bleeding
caused by activation of fibrinolysis; inhibits
proteolysis and inflammation
INDICATIONS: bleeding resulting from activation
of proteolysis, myocardial infarction, acute
pancreatitis, prophylaxis of proteolytic
complications after surgeries on pancreas,
thyroid glands, prevention of proteolysis
activation after the surgery on bigger salivary
glands;
paradontitis (topically)
SIDE-EFFECTS: allergy, nausea, vomiting,
hypotension, tachycardia
61. is indirect-acting inhibitor of fibrinolysis
is administered orally and by IV infusion, acts
during 4-6 hr, is not metabolized
excreted with urine
62. interacts with plasminogen and inhibits its
transformation into plasmin, particularly
inhibits plasmin; inhibits proteolytic enzymes
and kallikcrein
inhibits fibrinolysis and decreases bleeding
caused by the activation of fibrinolysis
63. inhibits fibrinolysis and decreases bleeding
caused by the activation of fibrinolysis;
oppresses proteolysis, decreases
inflammation, has anti-allergic action,
stimulates
antitoxic function of the liver
indications are similar to the same to
contrykal and also syndrome of disseminated
64. intravascular coagulation, obstetrics
pathology (ablation placenta, uterine
haemorrhages), liver diseases, hypo plastic
anaemia
in dentistry, it is applied topically to treat
parodontitis and to stop bleeding from dental
root channels
SIDE-EFFECTS: dizziness, hypotension,
bradycardia, arrhythmia, skin rash, vomiting
and nausea