The document discusses various types of drugs used to treat angina pectoris. It describes nitrates, calcium channel blockers, and beta blockers. Nitrates are vasodilators that work by converting to nitric oxide and relaxing smooth muscles. Common nitrates include nitroglycerin. Calcium channel blockers block calcium channels, reducing calcium entry into cardiac and smooth muscle cells. Examples given are verapamil, diltiazem, and nifedipine. Beta blockers inhibit sympathetic stimulation by blocking beta receptors. They decrease heart rate and contractility. Propranolol, atenolol and metoprolol are beta blockers mentioned.
This document provides an overview of nitrates, beta-blockers, calcium channel blockers, and potassium channel openers used to treat angina. It describes their mechanisms of action, pharmacokinetics, adverse drug reactions, drug interactions, and uses. The drugs work to reduce cardiac workload and oxygen demand or increase myocardial blood flow. Their effects include vasodilation, reduced heart rate, contractility and blood pressure. Common side effects are headache, flushing, and hypotension due to vasodilation. Drug interactions and dependence are concerns, requiring gradual withdrawal from nitrates. The document references essential pharmacology textbooks for further information.
principle action of drugs,types of angina classification of drugs ,nitrates,calcium channel blockers pharmacological actions ,combination therapy and its sid effects
This document discusses beta blockers, including their mechanism of action, effects on different tissues, classification, and the properties of propranolol as a nonselective beta blocker. It describes how propranolol blocks beta-1 and beta-2 receptors, lowering heart rate and blood pressure. It also causes vasoconstriction and potential bronchospasm as side effects. The document outlines propranolol's uses for hypertension, angina, myocardial infarction, and migraine and notes potential metabolic and cardiac adverse effects. It provides contraindications and interactions for propranolol and discusses selective beta-1 blockers and alpha/beta blockers like labetalol.
This document discusses antiarrhythmic drugs used to treat irregular heart rhythms or arrhythmias. It describes the mechanisms that can cause arrhythmias such as enhanced pacemaker activity, after-depolarizations, and reentry. It then covers the major classes of antiarrhythmic drugs including class I sodium channel blockers, class II beta blockers, class III potassium channel blockers, and class IV calcium channel blockers. Specific drugs from each class are discussed, how they work, their therapeutic uses, and potential side effects. Common arrhythmias like atrial fibrillation, atrial flutter, and ventricular tachycardia are also defined.
Sulfonylureas for Diabetes: A deep insightRxVichuZ
This powerpoint presentation solely deals with Sulfonylureas, that come under Insulin secretagogues. Their complete pharmacological profile, with pharmacovigilance parameters, important catchpoints and mnemonics have been explained.
This document discusses anti-histamines, including H1, H2, H3, and H4 receptor types and their roles. It focuses on H1 anti-histamines, covering their mechanism of action as inverse agonists, classifications as first or second generation, and structure-activity relationships. First generation drugs readily cross the blood-brain barrier and can cause sedation, while second generation are less sedating. The document discusses various chemical groups of H1 anti-histamines and provides examples of drugs for each group along with notes on their potency and usage.
aminoglycosides medicinal chemistry short notes by sadhana dahal.pptxSadhana Dahal
This document provides information about various aminoglycoside antibiotics, including their members, chemistry, mechanisms of action, pharmacokinetics, and clinical uses. It discusses 8 major aminoglycosides - streptomycin, neomycin, kanamycin, amikacin, gentamicin, tobramycin, sisomycin, and spectinomycin - covering their structures, properties, mechanisms of action, and indications. The document is intended to help students understand aminoglycosides, their mode of action, and clinical applications.
This document provides an overview of nitrates, beta-blockers, calcium channel blockers, and potassium channel openers used to treat angina. It describes their mechanisms of action, pharmacokinetics, adverse drug reactions, drug interactions, and uses. The drugs work to reduce cardiac workload and oxygen demand or increase myocardial blood flow. Their effects include vasodilation, reduced heart rate, contractility and blood pressure. Common side effects are headache, flushing, and hypotension due to vasodilation. Drug interactions and dependence are concerns, requiring gradual withdrawal from nitrates. The document references essential pharmacology textbooks for further information.
principle action of drugs,types of angina classification of drugs ,nitrates,calcium channel blockers pharmacological actions ,combination therapy and its sid effects
This document discusses beta blockers, including their mechanism of action, effects on different tissues, classification, and the properties of propranolol as a nonselective beta blocker. It describes how propranolol blocks beta-1 and beta-2 receptors, lowering heart rate and blood pressure. It also causes vasoconstriction and potential bronchospasm as side effects. The document outlines propranolol's uses for hypertension, angina, myocardial infarction, and migraine and notes potential metabolic and cardiac adverse effects. It provides contraindications and interactions for propranolol and discusses selective beta-1 blockers and alpha/beta blockers like labetalol.
This document discusses antiarrhythmic drugs used to treat irregular heart rhythms or arrhythmias. It describes the mechanisms that can cause arrhythmias such as enhanced pacemaker activity, after-depolarizations, and reentry. It then covers the major classes of antiarrhythmic drugs including class I sodium channel blockers, class II beta blockers, class III potassium channel blockers, and class IV calcium channel blockers. Specific drugs from each class are discussed, how they work, their therapeutic uses, and potential side effects. Common arrhythmias like atrial fibrillation, atrial flutter, and ventricular tachycardia are also defined.
Sulfonylureas for Diabetes: A deep insightRxVichuZ
This powerpoint presentation solely deals with Sulfonylureas, that come under Insulin secretagogues. Their complete pharmacological profile, with pharmacovigilance parameters, important catchpoints and mnemonics have been explained.
This document discusses anti-histamines, including H1, H2, H3, and H4 receptor types and their roles. It focuses on H1 anti-histamines, covering their mechanism of action as inverse agonists, classifications as first or second generation, and structure-activity relationships. First generation drugs readily cross the blood-brain barrier and can cause sedation, while second generation are less sedating. The document discusses various chemical groups of H1 anti-histamines and provides examples of drugs for each group along with notes on their potency and usage.
aminoglycosides medicinal chemistry short notes by sadhana dahal.pptxSadhana Dahal
This document provides information about various aminoglycoside antibiotics, including their members, chemistry, mechanisms of action, pharmacokinetics, and clinical uses. It discusses 8 major aminoglycosides - streptomycin, neomycin, kanamycin, amikacin, gentamicin, tobramycin, sisomycin, and spectinomycin - covering their structures, properties, mechanisms of action, and indications. The document is intended to help students understand aminoglycosides, their mode of action, and clinical applications.
1) Aminoglycosides are a class of bactericidal antibiotics that interfere with protein synthesis in bacteria. They are effective against many gram-negative aerobic bacteria.
2) Their mechanism of action involves binding to the 30S ribosomal subunit and inducing misreading of mRNA, which breaks up polysomes.
3) Common toxicities include ototoxicity, nephrotoxicity, and neuromuscular blockade. Gentamicin and amikacin are more nephrotoxic while certain drugs like streptomycin and tobramycin exhibit both cochlear and vestibular ototoxicity.
4) Examples include streptomycin, gentamicin, tobramycin, am
This document discusses various antiplatelet and antithrombotic drugs used to prevent thrombosis. It describes the mechanisms and indications for aspirin, clopidogrel, ticlopidine, cilostazol, abciximab, eptifibatide, tirofiban, terutroban, and dipyridamole. It also briefly mentions prasugrel and ticagrelor, newer P2Y12 receptor antagonists with more rapid onset of action than clopidogrel. The document lists common indications for antiplatelet therapy as myocardial infarction, unstable angina, coronary artery bypass grafts, prosthetic heart valves, venous thromboembolism, and transient ischemic
Sympathomimetic drugs mimic the actions of norepinephrine and epinephrine by binding to adrenergic receptors. They can be classified as direct-acting agonists like epinephrine, indirect-acting agonists like amphetamines, or mixed-action agonists like ephedrine. Common uses include pressor agents, cardiac stimulants, bronchodilators, nasal decongestants, CNS stimulants, and anorectics. Examples discussed in more detail include epinephrine, norepinephrine, dopamine, dobutamine, ephedrine, amphetamines, phenylephrine, and pseudophedrine.
This document summarizes fibrinolytics and antiplatelet drugs. It discusses the fibrinolytic system and lists fibrinolytics such as streptokinase, urokinase, alteplase, and newer recombinant tissue plasminogen activators. It also discusses their uses for conditions like myocardial infarction and mechanisms of action. The document then discusses antiplatelet drugs, focusing on mechanisms of platelet aggregation and inhibition. It lists classes of antiplatelet drugs like aspirin, dipyridamole, clopidogrel, and abciximab and their uses, mechanisms, and side effects. Finally, it lists common uses of antiplatelet drugs for conditions like coronary artery disease and angioplasty.
Neuromuscular blocking drugs are used during surgery to inhibit voluntary muscle tone and reflexes. They work by blocking neuromuscular transmission either through competition with acetylcholine or by depolarizing the motor end plate. Competitive blockers such as atracurium and cisatracurium are antagonized with anticholinesterases while succinylcholine is a depolarizing blocker that causes initial fasciculation before paralysis. Proper anesthesia is required when using neuromuscular blockers to ensure patient comfort and safety during paralysis.
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.
A diuretic is a chemical that increases urine production by inhibiting sodium reabsorption in the nephron at four major sites. The primary sites are the proximal tubule, thick ascending limb of Henle's loop, distal convoluted tubule, and connecting tubule/cortical collecting tubule. Diuretics work by blocking sodium transport mechanisms like cotransporters at these sites, causing increased excretion of sodium and water. The specific transport mechanisms and diuretic drug targets vary between nephron segments.
Sedatives calm without sleep, hypnotics induce sleep. Benzodiazepines like diazepam are commonly used sedative-hypnotics with high safety indices. They act by enhancing GABA inhibition. Newer drugs like zolpidem act similarly but with less residual effects. Barbiturates were widely used previously but are no longer preferred due to risks of overdose and dependence. The goal of treatment is to reduce anxiety, induce sleep, and have minimal daytime effects.
This document discusses anti-platelet drugs used to treat arterial thrombi, specifically newer P2Y12 receptor antagonists. It provides details on Clopidogrel, Prasugrel, and Ticagrelor which are widely used due to being more potent than Aspirin. Clinical trials including TRITON-TIMI 38, TRILOGY-ACS and PLATO compared the drugs and found Ticagrelor and Prasugrel superior to Clopidogrel in reducing ischemic events without increasing major bleeding risk. The document concludes the drugs have differences in efficacy against stent thrombosis and risk of bleeding.
1) There are several classes of anti-diabetic drugs that treat diabetes mellitus by lowering blood glucose levels, including insulin secretagogues, insulin sensitizers, alpha-glucosidase inhibitors, and DPP-4 inhibitors.
2) Insulin secretagogues like sulfonylureas stimulate insulin release from the pancreas. Insulin sensitizers like biguanides and thiazolidinediones improve target cell response to insulin without increasing secretion.
3) Alpha-glucosidase inhibitors prevent carbohydrate digestion and absorption, reducing post-meal blood sugar spikes. DPP-4 inhibitors prolong incretin hormone activity, increasing insulin release and reducing glucagon levels in response to meals.
This document discusses proton pump inhibitors (PPIs) which are a group of drugs that reduce gastric acid production. PPIs are used to treat common gastrointestinal issues like gastritis, dyspepsia, peptic ulcers, and gastroesophageal reflux disease (GERD). The causes, symptoms, and treatment approaches for each condition are described. Specifically, the document focuses on esomeprazole as a clinically used PPI and discusses its unique selling propositions and market share.
This document discusses the lincosamide antibiotics clindamycin and lincomycin. Clindamycin is a potent lincosamide antibiotic that inhibits protein synthesis by binding to the 50s ribosome. It has a similar spectrum of activity to erythromycin and is effective against most gram-positive cocci, diphtheria, nocardia, and actinomyces. Common side effects include rashes, diarrhea, and pseudomembranous colitis caused by C. difficile infection. Clindamycin is restricted to anaerobic infections and is used for Bacteroides fragilis infections of the abdomen, pelvis, and lungs. Lincomycin was the predecessor to cl
Hypolipidaemics pharmacology with a note on Statins /Fibrates/ Sterol absorption Inhibitors/ CETP Inhibitors / Lipoprotein Lipase activators and Bile acid sequestrants
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.
Antiarrhythmic drugs are classified into four classes based on their mechanism of action and effects on cardiac action potentials. Class I drugs like quinidine and procainamide are sodium channel blockers. Class II includes beta blockers like propranolol. Class III prolongs repolarization by blocking potassium channels, represented by drugs like amiodarone and bretylium. Class IV calcium channel blockers like diltiazem and verapamil slow conduction in the atrioventricular node. These drugs work to normalize abnormal electrical activity in the heart and treat arrhythmias of various origins.
This document summarizes different types of drugs used to treat diabetes mellitus. It discusses insulin, the main types of which include rapid-acting, short-acting, intermediate-acting, and long-acting insulins. It also discusses oral hypoglycemic drugs that help control blood sugar levels, including sulfonylureas that stimulate insulin secretion, biguanides that overcome insulin resistance, and others such as alpha-glucosidase inhibitors. New drug classes are also mentioned, like GLP-1 receptor agonists and DPP-4 inhibitors that enhance the body's own insulin response after meals. The document provides details on the mechanisms and examples of specific drugs within each class.
Blood coagulation involves a balance between procoagulants and anticoagulants that allows blood to clot normally after a vascular injury. Hemostasis is achieved through vascular constriction, formation of a platelet plug, and ultimately a blood clot. Coagulation disorders can result in too little or too much clotting. Anticoagulants like heparin and warfarin are used to treat and prevent thrombotic conditions by inhibiting different steps in the coagulation cascade, but also increase the risk of bleeding.
Fibrinolytics and anti platelet agents(easy)prithvilokesh
about platelet plug formation Fibrinolytic and anti platelet agents pathology, classes of drugs with mechanism of action , adverse effects uses and novel drugs..
This document discusses angiotensin receptor blockers (ARBs) which are used to treat hypertension and other cardiovascular conditions. It notes that ARBs work by competitively blocking the angiotensin receptor type 1, leading to vasodilation and other effects. Some examples of individual ARB drugs are provided like losartan, candesartan, and valsartan. The document compares ARBs to ACE inhibitors, noting that ARBs do not cause cough like ACE inhibitors. It concludes by discussing the theoretical rationale and benefits of combining ARBs with ACE inhibitors to more completely suppress the renin-angiotensin system.
This document discusses drugs used to treat gout, including colchicine, NSAIDs, corticosteroids, uricosuric agents like probenecid and sulfinpyrazone, and the uric acid synthesis inhibitor allopurinol. It provides details on the pathophysiology of gout, mechanisms of action, pharmacokinetics, indications, dosages and adverse effects of these drugs for both acute gout attacks and long-term treatment of chronic gout and hyperuricemia.
This document summarizes various classes of antihypertensive and antianginal drugs. It describes 11 classes of antihypertensive drugs including diuretics, ACE inhibitors, angiotensin receptor blockers, calcium channel blockers, beta blockers, and others. It also describes 5 classes of antianginal drugs including nitrates, beta blockers, calcium channel blockers, potassium channel openers, and others. Specific drugs are provided within each class with details on mechanisms of action, indications, dosages, and side effects.
The document discusses the use of organic nitrates and calcium antagonists to treat angina. It provides details on their mechanisms of action, pharmacological effects, and clinical uses. Specifically, it explains that organic nitrates act by relaxing smooth muscle and increasing cGMP, while calcium antagonists prevent the opening of voltage-gated calcium channels. Both drug classes are used to reduce cardiac oxygen demand and redistribute blood flow for the treatment of stable and unstable angina.
1) Aminoglycosides are a class of bactericidal antibiotics that interfere with protein synthesis in bacteria. They are effective against many gram-negative aerobic bacteria.
2) Their mechanism of action involves binding to the 30S ribosomal subunit and inducing misreading of mRNA, which breaks up polysomes.
3) Common toxicities include ototoxicity, nephrotoxicity, and neuromuscular blockade. Gentamicin and amikacin are more nephrotoxic while certain drugs like streptomycin and tobramycin exhibit both cochlear and vestibular ototoxicity.
4) Examples include streptomycin, gentamicin, tobramycin, am
This document discusses various antiplatelet and antithrombotic drugs used to prevent thrombosis. It describes the mechanisms and indications for aspirin, clopidogrel, ticlopidine, cilostazol, abciximab, eptifibatide, tirofiban, terutroban, and dipyridamole. It also briefly mentions prasugrel and ticagrelor, newer P2Y12 receptor antagonists with more rapid onset of action than clopidogrel. The document lists common indications for antiplatelet therapy as myocardial infarction, unstable angina, coronary artery bypass grafts, prosthetic heart valves, venous thromboembolism, and transient ischemic
Sympathomimetic drugs mimic the actions of norepinephrine and epinephrine by binding to adrenergic receptors. They can be classified as direct-acting agonists like epinephrine, indirect-acting agonists like amphetamines, or mixed-action agonists like ephedrine. Common uses include pressor agents, cardiac stimulants, bronchodilators, nasal decongestants, CNS stimulants, and anorectics. Examples discussed in more detail include epinephrine, norepinephrine, dopamine, dobutamine, ephedrine, amphetamines, phenylephrine, and pseudophedrine.
This document summarizes fibrinolytics and antiplatelet drugs. It discusses the fibrinolytic system and lists fibrinolytics such as streptokinase, urokinase, alteplase, and newer recombinant tissue plasminogen activators. It also discusses their uses for conditions like myocardial infarction and mechanisms of action. The document then discusses antiplatelet drugs, focusing on mechanisms of platelet aggregation and inhibition. It lists classes of antiplatelet drugs like aspirin, dipyridamole, clopidogrel, and abciximab and their uses, mechanisms, and side effects. Finally, it lists common uses of antiplatelet drugs for conditions like coronary artery disease and angioplasty.
Neuromuscular blocking drugs are used during surgery to inhibit voluntary muscle tone and reflexes. They work by blocking neuromuscular transmission either through competition with acetylcholine or by depolarizing the motor end plate. Competitive blockers such as atracurium and cisatracurium are antagonized with anticholinesterases while succinylcholine is a depolarizing blocker that causes initial fasciculation before paralysis. Proper anesthesia is required when using neuromuscular blockers to ensure patient comfort and safety during paralysis.
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.
A diuretic is a chemical that increases urine production by inhibiting sodium reabsorption in the nephron at four major sites. The primary sites are the proximal tubule, thick ascending limb of Henle's loop, distal convoluted tubule, and connecting tubule/cortical collecting tubule. Diuretics work by blocking sodium transport mechanisms like cotransporters at these sites, causing increased excretion of sodium and water. The specific transport mechanisms and diuretic drug targets vary between nephron segments.
Sedatives calm without sleep, hypnotics induce sleep. Benzodiazepines like diazepam are commonly used sedative-hypnotics with high safety indices. They act by enhancing GABA inhibition. Newer drugs like zolpidem act similarly but with less residual effects. Barbiturates were widely used previously but are no longer preferred due to risks of overdose and dependence. The goal of treatment is to reduce anxiety, induce sleep, and have minimal daytime effects.
This document discusses anti-platelet drugs used to treat arterial thrombi, specifically newer P2Y12 receptor antagonists. It provides details on Clopidogrel, Prasugrel, and Ticagrelor which are widely used due to being more potent than Aspirin. Clinical trials including TRITON-TIMI 38, TRILOGY-ACS and PLATO compared the drugs and found Ticagrelor and Prasugrel superior to Clopidogrel in reducing ischemic events without increasing major bleeding risk. The document concludes the drugs have differences in efficacy against stent thrombosis and risk of bleeding.
1) There are several classes of anti-diabetic drugs that treat diabetes mellitus by lowering blood glucose levels, including insulin secretagogues, insulin sensitizers, alpha-glucosidase inhibitors, and DPP-4 inhibitors.
2) Insulin secretagogues like sulfonylureas stimulate insulin release from the pancreas. Insulin sensitizers like biguanides and thiazolidinediones improve target cell response to insulin without increasing secretion.
3) Alpha-glucosidase inhibitors prevent carbohydrate digestion and absorption, reducing post-meal blood sugar spikes. DPP-4 inhibitors prolong incretin hormone activity, increasing insulin release and reducing glucagon levels in response to meals.
This document discusses proton pump inhibitors (PPIs) which are a group of drugs that reduce gastric acid production. PPIs are used to treat common gastrointestinal issues like gastritis, dyspepsia, peptic ulcers, and gastroesophageal reflux disease (GERD). The causes, symptoms, and treatment approaches for each condition are described. Specifically, the document focuses on esomeprazole as a clinically used PPI and discusses its unique selling propositions and market share.
This document discusses the lincosamide antibiotics clindamycin and lincomycin. Clindamycin is a potent lincosamide antibiotic that inhibits protein synthesis by binding to the 50s ribosome. It has a similar spectrum of activity to erythromycin and is effective against most gram-positive cocci, diphtheria, nocardia, and actinomyces. Common side effects include rashes, diarrhea, and pseudomembranous colitis caused by C. difficile infection. Clindamycin is restricted to anaerobic infections and is used for Bacteroides fragilis infections of the abdomen, pelvis, and lungs. Lincomycin was the predecessor to cl
Hypolipidaemics pharmacology with a note on Statins /Fibrates/ Sterol absorption Inhibitors/ CETP Inhibitors / Lipoprotein Lipase activators and Bile acid sequestrants
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.
Antiarrhythmic drugs are classified into four classes based on their mechanism of action and effects on cardiac action potentials. Class I drugs like quinidine and procainamide are sodium channel blockers. Class II includes beta blockers like propranolol. Class III prolongs repolarization by blocking potassium channels, represented by drugs like amiodarone and bretylium. Class IV calcium channel blockers like diltiazem and verapamil slow conduction in the atrioventricular node. These drugs work to normalize abnormal electrical activity in the heart and treat arrhythmias of various origins.
This document summarizes different types of drugs used to treat diabetes mellitus. It discusses insulin, the main types of which include rapid-acting, short-acting, intermediate-acting, and long-acting insulins. It also discusses oral hypoglycemic drugs that help control blood sugar levels, including sulfonylureas that stimulate insulin secretion, biguanides that overcome insulin resistance, and others such as alpha-glucosidase inhibitors. New drug classes are also mentioned, like GLP-1 receptor agonists and DPP-4 inhibitors that enhance the body's own insulin response after meals. The document provides details on the mechanisms and examples of specific drugs within each class.
Blood coagulation involves a balance between procoagulants and anticoagulants that allows blood to clot normally after a vascular injury. Hemostasis is achieved through vascular constriction, formation of a platelet plug, and ultimately a blood clot. Coagulation disorders can result in too little or too much clotting. Anticoagulants like heparin and warfarin are used to treat and prevent thrombotic conditions by inhibiting different steps in the coagulation cascade, but also increase the risk of bleeding.
Fibrinolytics and anti platelet agents(easy)prithvilokesh
about platelet plug formation Fibrinolytic and anti platelet agents pathology, classes of drugs with mechanism of action , adverse effects uses and novel drugs..
This document discusses angiotensin receptor blockers (ARBs) which are used to treat hypertension and other cardiovascular conditions. It notes that ARBs work by competitively blocking the angiotensin receptor type 1, leading to vasodilation and other effects. Some examples of individual ARB drugs are provided like losartan, candesartan, and valsartan. The document compares ARBs to ACE inhibitors, noting that ARBs do not cause cough like ACE inhibitors. It concludes by discussing the theoretical rationale and benefits of combining ARBs with ACE inhibitors to more completely suppress the renin-angiotensin system.
This document discusses drugs used to treat gout, including colchicine, NSAIDs, corticosteroids, uricosuric agents like probenecid and sulfinpyrazone, and the uric acid synthesis inhibitor allopurinol. It provides details on the pathophysiology of gout, mechanisms of action, pharmacokinetics, indications, dosages and adverse effects of these drugs for both acute gout attacks and long-term treatment of chronic gout and hyperuricemia.
This document summarizes various classes of antihypertensive and antianginal drugs. It describes 11 classes of antihypertensive drugs including diuretics, ACE inhibitors, angiotensin receptor blockers, calcium channel blockers, beta blockers, and others. It also describes 5 classes of antianginal drugs including nitrates, beta blockers, calcium channel blockers, potassium channel openers, and others. Specific drugs are provided within each class with details on mechanisms of action, indications, dosages, and side effects.
The document discusses the use of organic nitrates and calcium antagonists to treat angina. It provides details on their mechanisms of action, pharmacological effects, and clinical uses. Specifically, it explains that organic nitrates act by relaxing smooth muscle and increasing cGMP, while calcium antagonists prevent the opening of voltage-gated calcium channels. Both drug classes are used to reduce cardiac oxygen demand and redistribute blood flow for the treatment of stable and unstable angina.
- Antianginal drugs are used to treat different types of angina pectoris including classical, variant, and unstable angina. The drugs work by reducing oxygen demand on the heart muscle, relaxing blood vessels to improve blood flow, or inhibiting calcium channels.
- The main classes of antianginal drugs are nitrates, beta-blockers, calcium channel blockers, and newer drugs like nicorandil and ranolazine. Nitrates rapidly relax blood vessels to relieve chest pain during angina attacks. Beta-blockers and calcium channel blockers are used for long-term prevention of angina by reducing heart rate and oxygen demand.
- While these drugs can relieve symptoms, they do not treat the
The document discusses various types of angina and treatments for restoring the balance between oxygen supply and demand in the heart. It describes 3 main types of angina - chronic stable angina, unstable angina, and vasospastic angina. The goal of antianginal drug therapy is to increase blood flow to the heart and decrease myocardial oxygen demand. The major antianginal drug classes discussed are nitrates, beta-blockers, calcium channel blockers, and potassium channel openers. Specific drugs within each class are also named and their mechanisms and uses summarized within 3 sentences.
This document discusses various drugs used to treat angina pectoris, which is chest pain due to myocardial ischemia. It describes several classes of antianginal drugs that work by either increasing oxygen supply to the heart or decreasing oxygen demand. These include organic nitrates like glyceryl trinitrate, beta-blockers, calcium channel blockers, and ACE inhibitors. The document provides details on the mechanisms and sites of action of these drug classes as well as their adverse effects. Alternative treatment methods for ischemic heart disease like rotational atherectomy are also mentioned.
This document summarizes drugs that affect the cardiovascular system. It describes the components of the cardiovascular system and classifies drugs as cardiotonics, anti-anginals, or antihypertensives. Cardiotonics like digoxin are used to increase heart contractility in heart failure. Anti-anginal drugs like nitrates and beta-blockers treat angina by improving blood flow or decreasing oxygen demand. Antihypertensive drug classes include diuretics, adrenergic inhibitors, calcium channel blockers, and angiotensin inhibitors which are used to lower blood pressure.
Antianginal drugs unit-II by Dr. Monika Singh as per PCI syllabus 2020Monika Singh
The document discusses various drugs used for the treatment of angina pectoris, including nitrates, beta blockers, calcium channel blockers, and others. Nitrates work by reducing preload and afterload on the heart, thereby decreasing oxygen demand. They act by converting to nitric oxide which increases cGMP levels to cause vasodilation. Beta blockers decrease heart rate and contractility to lower myocardial oxygen consumption. Calcium channel blockers inhibit calcium influx into cardiac and vascular smooth muscle to produce vasodilation and reduce workload on the heart. The document provides details on the mechanisms, uses and adverse effects of these major classes of antianginal medications.
Antianginal ppt brief description and informationDevoratsingh1
This document discusses drugs used to treat angina pectoris, a chest pain syndrome caused by inadequate blood flow to the heart. It describes two main types of angina - classical, brought on by exertion and relieved by rest, and variant which occurs at rest. Nitrates like glyceryl trinitrate are first-line treatments that work by dilating blood vessels and reducing workload on the heart. Beta-blockers also lower heart rate and workload while calcium channel blockers and nicorandil relax blood vessels. Other options include isosorbide dinitrate, trimetazidine, and dipyridamole. All work to prevent or terminate angina attacks by increasing oxygen supply or decreasing demand
This document discusses antianginal drugs used to treat angina pectoris. It describes the three main types of angina and the mechanisms of four classes of antianginal drugs: nitrates, beta-blockers, calcium channel blockers, and potassium channel openers. Nitrates like nitroglycerin and isosorbide are first-line treatments that work by dilating blood vessels to reduce cardiac preload and afterload. Proper administration and storage of nitrates is important to avoid side effects like headaches. Nurses monitor patients and educate them about safe use of antianginal medications.
This document discusses angina pectoris, including its causes, risk factors, classifications, and treatments. Angina is chest pain due to an imbalance between myocardial oxygen demand and supply. It is classified into four types based on triggers and severity. Treatment includes short-acting nitrates for acute attacks and long-acting options like nitrates, calcium channel blockers, and beta-blockers for prophylaxis. Additional therapies discussed are potassium channel openers, fatty acid oxidase inhibitors, and antiplatelets/anticoagulants. Combination drug regimens and surgical options are also outlined for management of angina.
These slides contain detailed description of antianginal drugs including : Introduction, Definition of Angina, Types of Angina, Classification of antianginal drugs - nitrates, beta adrenergic blockers, calcium channel blockers, potassium channel openers, ( with their classification, pharmacological action, mechanism of action, available forms, therapeutic uses, pharmacokinetics, adverse effects, and contraindications ) Nursing responsibility, Summary.
This document discusses antianginal drugs used to treat angina pectoris, or chest pain caused by reduced blood flow to the heart. There are three main classes of drugs used: organic nitrates, beta-blockers, and calcium channel blockers. Organic nitrates like nitroglycerin work by dilating blood vessels to increase blood flow to the heart and reduce its workload. Beta-blockers lower the heart rate and force of contraction to decrease oxygen demand. Calcium channel blockers inhibit calcium entry into heart and blood vessel cells to relax vessels and reduce workload. Each drug class is described in more detail regarding mechanisms, effects, pharmacokinetics, uses, and side effects.
Nitroglycerin is a vasodilator used to treat angina pectoris, heart failure, and myocardial infarction. It works by relaxing blood vessels, reducing the workload on the heart. It is rapidly absorbed through the skin or oral mucosa and has a quick onset of action within 1-3 minutes. Nitroglycerin is administered sublingually for acute angina attacks or before exertion. It can also be given intravenously to treat heart attacks or control blood pressure during surgery. Common side effects include headaches, dizziness, and hypotension.
Anti anginal drugs ppt by anjali kotwalanjali kotwal
This document discusses various anti-anginal drugs used to treat angina pectoris. It describes three main classes of drugs: nitrates, beta-blockers, and calcium channel blockers. Nitrates work by dilating blood vessels to increase oxygen supply and decrease oxygen demand. Beta-blockers lower heart rate and contractility to reduce myocardial oxygen consumption. Calcium channel blockers inhibit calcium entry into cardiac and vascular muscle to produce vasodilation and reduce myocardial work. Combination therapy using drugs from different classes is often most effective for treating angina due to their additive effects on myocardial oxygen balance.
This document discusses the classification, treatment, and management of angina pectoris. Angina is chest pain caused by an imbalance between myocardial oxygen supply and demand. It classifies angina into exertional, variant, and unstable types based on symptoms and etiology. Treatment involves short-acting nitrates for acute episodes and long-acting nitrates, calcium channel blockers, beta-blockers, or potassium channel openers for prophylaxis. Combination drug therapy and surgical options like balloon angioplasty or bypass surgery may also be used in severe cases.
This document provides information on the treatment of angina pectoris, including the types of angina and agents used. It discusses the main strategies for treating angina as reducing oxygen demand and increasing oxygen delivery. The key agents discussed are nitrates, calcium channel blockers, and beta blockers. Nitrates act by releasing nitric oxide to cause vasodilation and reduce preload and afterload. Calcium channel blockers block calcium channels to reduce contraction. Beta blockers reduce cardiac work and oxygen demand by lowering heart rate and contractility. All three are effective prophylactically for different types of angina.
Nitrates work by relaxing smooth muscle in blood vessels via the production of nitric oxide. This leads to vasodilation and reduced preload and afterload, lowering oxygen demand on the heart. Common side effects include headaches and hypotension. Tolerance develops with chronic use and can be prevented through intermittent dosing schedules and adjunctive treatments that replenish nitric oxide stores. Nitrates are available in various oral, topical, and intravenous formulations for use in angina and heart failure.
Ischemic heart disease occurs when coronary arteries become narrowed by atherosclerosis, reducing blood flow to the heart muscle. Angina, myocardial ischemia, and myocardial infarction can result. Myocardial infarction is caused by sudden blockage of a coronary artery and leads to cell death in the affected region. Treatment focuses on pain relief, oxygenation, volume maintenance, acidosis correction, and preventing/treating arrhythmias. Drugs like nitrates, beta blockers, and calcium channel blockers aim to reduce oxygen demand and increase supply.
Anti-Angina & Anti arryhthias Drugs .pptssuser504dda
This document discusses drugs used to manage angina and arrhythmias, and current guidelines for managing acute coronary syndrome (ACS). It describes the classification and pathophysiology of angina, then focuses on pharmacological management including nitrates like nitroglycerin, calcium channel blockers like nifedipine, beta blockers like atenolol, and alpha/beta blockers like carvedilol. It provides details on their mechanisms of action, indications, interactions, and side effects in treating conditions like angina, heart failure and ACS.
This document discusses different methods for delivering fluorides, including topical and systemic methods. It focuses on topical fluoride delivery methods which are applied directly to teeth. Topical fluorides can be divided into professionally applied and self-applied products. Professionally applied products contain higher fluoride concentrations and include neutral sodium fluoride, acidulated phosphate fluoride, and stannous fluoride solutions, gels, pastes, and varnishes. Application techniques for professionals include the paint on and tray methods. Stannous fluoride and sodium fluoride are discussed in more detail regarding their preparation, mechanisms of action, advantages, and application procedures. Repeated topical fluoride treatments over time help strengthen tooth enamel and reduce the risk of dental caries.
Megaloblastic anaemia . And all anout anaemia, pernicious anaemia,GaurishChandraRathau
Megaloblastic anemia is a type of deficiency anemia characterized by abnormally large nucleated red blood cell precursors called megaloblasts in the bone marrow. It is most commonly caused by vitamin B12 or folic acid deficiencies, which lead to defective DNA synthesis. The pathophysiology involves an imbalance between the cytoplasm and nucleus in red blood cells due to improper nucleoprotein synthesis. Laboratory diagnosis shows macrocytic anemia with large red blood cells, hypersegmented neutrophils, and giant platelets in peripheral blood smears.
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Leukemia is a cancer that affects the blood and bone marrow. It causes the body to overproduce immature white blood cells that do not function properly. There are four main types of leukemia - acute lymphocytic leukemia (ALL), chronic lymphocytic leukemia (CLL), acute myelogenous leukemia (AML), and chronic myelogenous leukemia (CML). The document discusses the definition, causes, signs and symptoms, diagnosis, treatment approaches which may include chemotherapy, targeted therapy and stem cell transplant, and management of the different types of leukemia.
Removable partial dentures (RPDs) replace missing teeth and are part of prosthodontic treatment. RPDs are designed to provide support from teeth and tissues, retention to prevent displacement, and stability to resist lateral forces. They are made of biocompatible materials and connected by major connectors like lingual bars that provide cross-arch support and stability. RPDs are classified based on location of missing teeth to aid in proper design of retainers, rests, and other components.
The document discusses the anatomy and histology of the gingiva. It defines gingiva as the part of oral mucosa that surrounds the teeth. Macroscopically, it describes the three types of gingiva: marginal, interdental, and attached gingiva. Microscopically, it explains that gingiva contains stratified squamous epithelium, the epithelium-connective tissue interface, and connective tissue. It details the layers of the epithelium, the cells present, and their roles in keratinization and immune response.
This document discusses megaloblastic anemia, which is caused by deficiencies in vitamin B12 or folic acid. It describes the history and discoveries regarding B12 and folic acid, including their roles in DNA synthesis and hematopoiesis. The document covers absorption, transport, functions and deficiencies of B12 and folic acid, as well as their treatment and uses. It also briefly discusses erythropoietin and drugs used to treat neutropenia.
This document provides an overview of the Russel's Periodontal Index and the CPITN (Community Periodontal Index of Treatment Needs). It discusses the scope, procedure, scoring criteria, and calculation methods for both indices. The Russel's Periodontal Index was developed in 1956 to estimate the prevalence and severity of periodontal disease on a scale of 0-8. The CPITN was developed in 1982 by the WHO and FDI to survey and evaluate periodontal treatment needs, examining six index teeth in each sextant and assigning codes from 0-4 based on probing depth and other factors. The document reviews the advantages, limitations, and modifications of these two common indices used in epidemiological studies of periodontal health.
This document discusses the history and development of dentin bonding agents across 7 generations from the 1950s to 2000s. It describes the ideal requirements for bonding agents and challenges bonding to dentin like the smear layer. The roles of conditioners, primers, and adhesives are explained. Critical factors for bonding like moisture control and the hybrid layer formation are also summarized.
This document provides an overview of dental casting procedures and defects. It discusses the history of casting, the lost wax technique, and steps in the casting process including investing, wax burnout, alloy casting, and cleaning. Key aspects covered are sprue formation, crucible and ring usage, investing materials, and factors that influence dimensional changes like wax and alloy shrinkage. Causes of common casting defects are also mentioned but not described in detail.
The document discusses the role and importance of adhesive dentistry. It describes the different generations of dentine bonding agents from the early phosphoric acid-based systems to newer self-etch adhesives. Key challenges in dentine adhesion are the structural differences between enamel and dentine such as dentine's high water content and presence of a smear layer. Conditioning with acid or chelators is needed to remove the smear layer and expose collagen fibers for bonding to occur. Current adhesive systems are classified as etch-and-rinse or self-etch and involve either two or three step application processes.
This document discusses denture base materials, specifically acrylic resins. It begins by defining denture base and classifying denture base resins into categories such as metallic vs. non-metallic, temporary vs. permanent, and ANSI/ADA classifications. It then discusses the ideal requirements for dental resins and their various uses. The document goes on to explain key terms like polymer, monomer, copolymer, polymerization, and cross-linking as they relate to denture base materials. It also discusses composition, curing techniques, and important considerations for both heat cure and self-cure acrylic resins.
Cellular adaptations occur through atrophy, hypertrophy, hyperplasia, metaplasia, and dysplasia in response to environmental stresses. Atrophy is a decrease in cell size or number, hypertrophy is an increase in cell size, and hyperplasia is an increase in cell number. Metaplasia is the reversible change of one adult cell type into another. Dysplasia involves disordered cellular development accompanied by metaplasia and hyperplasia.
This document summarizes the key properties and characteristics of different elastomeric impression materials, including polysulfide, condensation silicone, addition silicone, and polyether elastomers. It describes the composition, setting reactions, available consistencies, and mechanical properties of each material. Properties like viscosity, working and setting times, dimensional stability, hardness, tear strength, and detail reproduction are compared between the different elastomers. The document also discusses techniques for mixing and using impression materials, as well as their wettability and hydrophilicity.
The document discusses cell injury and its causes, pathogenesis, and morphology. It defines cell injury as stress encountered by cells due to changes in their internal or external environment. Cell injury can be caused genetically or acquired through various external factors like hypoxia, physical or chemical agents, microbes, immunological reactions, nutritional imbalances, aging, and psychological stress. The pathogenesis of cell injury depends on the type of cell, extent of injury, and underlying biochemical processes. Reversible cell injury causes changes like hydropic swelling, fatty changes, and hyaline changes. Irreversible injury leads to autolysis, necrosis, apoptosis, or gangrene.
Neoplasia refers to abnormal tumor growth. Benign tumors are non-invasive and localized, while malignant tumors are invasive and spreading. Tumors are named based on the tissue of origin, such as carcinomas arising from epithelial tissue and sarcomas from connective tissue. Well-differentiated tumors resemble normal cells, while poorly-differentiated tumors have primitive, undifferentiated cells. Malignant tumors exhibit features like irregular growth, invasion, increased size and mitosis, and lack of differentiation. Dysplasia refers to disordered cell growth showing abnormalities but remaining in situ.
Pathological calcification involves the abnormal deposition of calcium salts in tissues other than bone. There are two main types: dystrophic calcification occurs in dead or damaged tissue with normal calcium levels, while metastatic calcification affects normal tissues and is caused by high calcium levels in the blood (hypercalcemia). Dystrophic calcification is seen in areas of necrosis, atherosclerosis, and infarcts. Metastatic calcification is associated with disorders that cause hypercalcemia like hyperparathyroidism and bone destruction. The deposits appear histologically as basophilic intracellular and extracellular calcium salt accumulations.
Amyloidosis is a condition characterized by the abnormal deposition of amyloid protein fibrils in tissues and organs. The fibrils form when normally soluble proteins misfold and aggregate extracellularly. Amyloidosis has many subtypes classified by the precursor protein involved, pattern of organ involvement, and hereditary versus inflammatory causes. Diagnosis involves tissue biopsy with Congo red staining to identify the apple-green birefringence of amyloid under polarized light, as well as immunohistochemistry to determine the subtype. Advanced imaging and molecular PET can also detect amyloid plaques in neurodegenerative diseases like Alzheimer's.
This document discusses various types of cellular adaptations, including atrophy, hypertrophy, hyperplasia, and metaplasia. It also discusses pathologic calcification. The main types of cellular adaptation are a decrease in cell size and number through atrophy, an increase in individual cell size through hypertrophy, an increase in cell number through hyperplasia, and the replacement of one cell type with another through metaplasia. Pathologic calcification can occur through either dystrophic or metastatic calcification and results in the abnormal deposition of calcium salts in tissues.
The document discusses various methods of sterilization including physical agents like heat, radiation and filtration, as well as chemical agents. It defines sterilization as a process that eliminates all microorganisms, while disinfection only destroys pathogenic organisms. Several sterilization techniques are described in detail, such as moist heat methods using steam under pressure in an autoclave, dry heat methods using hot air ovens, and chemical agents like alcohols, aldehydes, and dyes. The ideal properties of chemical disinfectants are also outlined.
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5. Nitrates are vasodilators.
Nitrates act directly on smooth muscles and
produce relaxation.
Commonly used nitrate is nitroglycerine
(GTN).
6. Short acting nitrates
Used to terminate acute attack of angina
Eg: Nitroglycerin (GTN)
Long acting nitrates
Used to prevent an attack of angina
Eg: isosorbide dinitrate, isosorbide
mononitrate, pentaerythritol tetranitrate
7. In the smooth muscles nitrates are converted to
nitric oxide.
This nitric oxide activates vascular guanylyl
cyclase (GC) which in turn increases the
synthesis of cGMP (Cyclic guanosine
monophosphate).
This cGMP causes sequestration of Ca2+ , which
is responsible for relaxation of the smooth
muscles.
Results in vasodilation.
8. Vasodilation
Relax vascular smooth muscle
Relaxation of smooth muscles
cGMP causes sequestration of Ca2+
Increases the synthesis of cGMP
Activates vascular guanylyl cyclase
Nitrates converted to nitric oxide
9.
10. 1. Reduction of preload
2. Reduction of afterload
3. Coronary dilation
4. Other actions
1. Dilation of other vasculature
2. Relaxation of other smooth muscles
3. Effects on platelets.
11. Nitrates are vasodilators.
1. Reduction of preload
Venodilation reduces
venous return to the heart
thereby reduce preload.
2. Reduction of afterload
Arteriolar dilation reduces
vascular resistance thus
decrease afterload
3. Coronary dilation
Nitrates cause coronary vasodilation, thus relieves
vasospasm and increases coronary blood flow.
As both preload and afterload are reduced,
workload of the heart is decreased, thereby
reducing oxygen requirement of the heart.
12. 4. Other actions
Dilation of other vasculature
• Dilation of blood vessels in
skin results in flushing.
• Dilation of meningeal
vessels results in headache.
Relaxation of other smooth
muscles
Nitrates relax the bronchial,
gastrointestinal and
genitourinary smooth muscles
for a short period.
Effects on platelets
Nitric oxide from nitrates inhibits platelet aggregation.
13. Nitrates are available for oral, Sublingual, spray
parenteral, ointment and transdermal patch.
Nitrates are well-absorbed orally, but they
undergo extensive first pass metabolism.
So the oral bioavailability of nitrate is poor.
Sublingual route is preferred in case of
emergency for rapid absorption and better
bioavailability.
Sublingual tablets acts within 1-2 minutes
whereas Sublingual spray acts faster than tablets.
16. Headache (common)
Flushing of face
Nausea and vomiting
Sweating
Tachycardia
Palpitation
Weakness
Postural hypotension
Rashes
Contact dermatitis
Local hypersensitivity reaction
for topical use
17. Exertional angina
Acute anginal attacks :
▪ Sublingual nitroglycerin
▪ Drug of choice for acute anginal attacks.
▪ Relieves pain in 2 to 5 minutes.
▪ If the pain is not relieved, the dose is repeated-upto 3 tablets in 15
minutes.
Prophylaxis of angina
▪ NTG can be used for chronic prophylaxis.
▪ Longer acting nitrates are preferred.
▪ Nitroglycerin ointment orTransdermal patch may be used.
18. Vasospastic angina
Unstable angina
Acute coronary syndrome
Cardiac failure
Myocardial infarction
Cyanide poisoning
Nitrates are life saving in cyanide poisoning.
Amylnitrite is given by inhalation and sodium
nitrite by IV injection (10 ml of 3% solution). Then
Sodium thiosulphate is given IV (50 ml of 25%
solution).
19. Role of nitrates in cyanide poisoning.
Nitrates (Amylnitrite and sodium nitrite) convert
hemoglobin into methemoglobin, which has high
affinity for cyanide and forms cyano-
methemoglobin.
Cyano-methemoglobin reacts with Sodium
thiosulphate to form thiocyanate which is easily
excreted by the kidneys.
20. Relieve esophageal spasm
Sublingual NTG is taken just before meals to
counter the spasm.
Relieve biliary colic
Sublingual NTG is also useful as a spasmolytic.
21. Monitor BP before and after administration.
Nitroglycerine is sensitive to light, heat and
moisture, so stored in tightly closed amber
colored glass bottles.
Give sublingual preparations under the tongue
or in the buccal pouch.
Nitroglycerine IV preparation is mixed in 5%
Dextrose Injection or 0.9% Sodium Chloride.
Instruct the patient that a sublingual dose may
be repeated in 5 minutes if pain is not relieved,
for a total of 3 doses.
22.
23. Calcium channel blockers (CCBs) are the
drugs that disrupt calcium movement by
blocking voltage-dependent Ca2+ channels
used to treat angina and supraventricular
tachydysrhythmias as well as hypertension.
Also known as calcium antagonists.
25. Decrease myocardial contraction, Decrease heart rate and AV conduction
velocity, also cause Vascular smooth muscle relaxation
Decrease calcium entry into cardiac and smooth muscle cells
Block L-type calcium channels
Calcium channel blockers
26. Cardiac and smooth muscle
cell contraction depends
upon the activation of
calcium channels in the
cardiac myocytes. For
depolarization of cardiac and
other smooth muscles cells,
entry of calcium into the cells
occurs through these calcium
channels. This calcium
triggers the release of
intracellular calcium from
sarcoplasmic reticulum.
27. On vascular smooth muscles and Coronary
circulation
On other smooth muscles
On heart
29. Dihydropyridine CCBs have prominent effect
on blood vessels.
Nimodipine crosses the blood brain barrier
and relaxes the cerebral blood vessels.
On other smooth muscles
Relax GI and bronchial smooth muscles
Relax uterus, so used in premature labor.
32. CCBs are well-absorbed orally but undergo
extensive first pass metabolism.
They are metabolized in the liver.
Excreted through kidneys.
Onset of action is in 30-60 minutes after oral
administration while on IV use the action is
quick.
33. 1. Verapamil
Decrease heart rate (negative chronotropic effect)
Decrease force of myocardial contraction (negative
ionotropic effect)
DecreaseAV conduction
Vasodilator effect of verapamil is less potent.
Used in arrhythmia and angina.
Dose: 40-160 mgTDS orally and 5 mg by slow IV
inj.
Adverse effects
Nausea
Constipation
Bradycardia
Heart block
Hypotension
Skin rashes
34. 2. Diltiazem
Decrease heart rate (negative chronotropic
effect)
Decrease force of myocardial contraction
(negative ionotropic effect)
Vasodilator effect is less potent.
Dose: 30-60 mgTDS orally.
Adverse effects –same as verapamil.
35. 3. Nifedipine
Potent vasodilator and causes a significant fall in
BP and evokes reflex tachycardia.
Myocardiac depressant effect is weak
It can be given orally or sublingually. Patches also
Dose: 5-20 mg BD
Adverse effects
Headache
Flushing
Palpitation
Dizziness
Fatigue
Hypotension
Leg cramps
Ankle edema
Long-term use : gum hypertrophy
36. 3. Nimodipine
Crosses the blood brain barrier and relaxes
the cerebral blood vessels.
Used in haemorrhagic stroke and
subarachnoid haemorrhage.
Dose: 30-60 mg QID.
37. 4. Amlodipine, felodipine, nitrendipine,
nicardipine
High vascular effects.
Long acting CCBs.
Can be given once daily.
Useful HTN.
38. Angina pectoris
As prophylaxis for exertional angina
▪ Verapamil and diltiazem for prophylaxis
Variant angina
Vasospastic angina
▪ Verapamil and amlodipine are preferred
Unstable angina
▪ Verapamil is used
Dihydropyridine CCBs like amlodipine with beta
blockers for long term management.
40. Peripheral vascular disease
Nifedipine, felodipine and diltiazem can be used in
Raynaud's disease.
Migraine
Prophylaxis- verapamil is useful
Hypertrophic cardiomyopathy
Verapamil is useful
Subarachnoid hemorrhage and haemorrhagic
stroke
Nimodipine is useful.
Preterm labor
Nifedipine is useful.
41. Verapamil and diltiazem should be avoided
in patients receiving beta-adrenergic blockers
because the myocardiac depressant effects
get added up.
Verapamil can precipitate digoxin toxicity by
increasing digoxin levels (verapamil reduces
digoxin excretion).
42.
43.
44. Beta blockers are the drugs that block beta
receptors thereby inhibiting the actions of
sympathetic stimulations (catecholamines).
Beta antagonist.
46. 1. Nonselective
Blocks both β1 and β2 receptors.
2. Cardioselective (β1)
Blocks cardiac specific β1 receptors. β2 receptor
blockade is weak.
3. Partial agonists
Have some sympathomimetic action due to partial β
agonist property.
4. With additional alpha blocking property
Blocks both α and β (β1 and β2) receptors.
5. β1 blocker β2 agonist
Blocks only cardiac specific β1 receptors.
48. Reduce cardiac workload
Reduce myocardial O2 demand
Decrease heart rate, Decrease force of contraction,
Decrease cardiac output, Decrease BP, Delay AV conduction
Inhibit sympathetic (catecholamines) stimulations
Blocks beta receptors
49.
50. CVS
Act as cardiac depressant
Decrease heart rate (negative chronotropic effect)
Decrease force of contraction (negative ionotropic effect)
Decrease cardiac output
Decrease BP
Delay AV conduction (negative dromotropic effect)
Reduce myocardial O2 demand
Reduce cardiac workload.
Improve exercise tolerance in angina patients.
51. Respiratory tract
Blockade of B2 receptors in the bronchial smooth
muscle causes increase in airway resistance.
May precipitate acute attack in asthmatics.
Eye
Reduce intraocular pressure by decreased secretion of
aqueous humor.
Metabolism
β-antagonists block lipolysis & glycogenolysis – cause
rise in plasma free fatty acid and triglyceride.Also
interfere with recovery from hypoglycemia in diabetics
52. Well absorbed orally.
Given intravenously in emergencies.
Low oral bioavailability due to extensive first
pass metabolism.
Highly lipid soluble, so crosses blood brain
barrier.
Metabolized in the liver.
Excreted through kidneys.
53. Bradycardia (common)
CCF
Acute pulmonary edema
Cold extremities (in patients with peripheral vascular
disease)
Acute asthmatic attack (in asthmatics)
CNS
Insomnia
Depression
Halluçination (rare)
Fatigue, weakness
Decrease exercise capacity
Rebound hypertension and anginal attacks
Due to abrupt withdrawal of B-blockers after prolonged use.
54. Hypertension
As first line drugs in mild to moderate hypertension
Used alone or with other antihypertensives.
Angina pectoris
Long term prophylaxis of exertional angina and
classical angina.
Cardioselective drugs are preferred than non
selective drugs.
Have to take on regular basis.
Cardiac arrnythmias
For both supraventricular & ventricular arrhythmias
55. Myocardial infarction
Given IV infusion in acute MI to limit the size of
infarct.
Long-term treatment prolongs survival.
Congestive cardiac failure
Obstructive cardiomyopathy
Pheochromocytoma
Propranolol is given before surgery to control
hypertension.
56. Thyrotoxicosis
Propranolol controls palpitation, tremors and affords
symptomatic relief in thyrotoxicosis.
Used as adjuvant.
Also useful in thyrotoxic crisis.
Glaucoma
Timolol is used topically in open angle glaucoma.
Migraine
As prophylaxis.
Propranolol is used.
Anxiety
Propranolol prevents the acute panic symptoms
58. Atenolol
Cardioselective
Longer acting-given once daily
Less lipid soluble-does not cross BBB-hence no CNS
side effects
No side effects on lipid profile. Hence very
commonly used
Dose: 25-100 mg daily.
IV (5-10 mg over 5 minutes) reduce short term
mortality in MI and lowers incidence of arrhythmias.
59. Esmolol
Cardioselective
Ultra short acting - t½ - 8 minutes.
Used IV.
Safer in critically ill patients and in emergencies.
Metoprolol
Cardioselective
Well-absorbed but undergoes first pass metabolism
Given twice daily
Dose: 50-200 mg
Used in hypertension and angina pectoris.
60. Acebutolol
Cardioselective
Used in hypertension and arrhythmias.
Celiprolol
β1 blocker and β2 agonist
Safer in asthmatics
Used in hypertension.
61. Propranolol
Nonselective
Dose: oral 10 mg BD to 160 mgTID.
First line drugs in mild to moderate hypertension
Used in HTN, angina, arrhythmias, migraine
62.
63. Potassium-channel openers are drugs that
activate (open) ATP-sensitive K+ channels in
vascular smooth muscle and results vascular
smooth muscle relaxation.
64. Potassium channel openers
Open ATP-sensitive K+ channels in vascular
smooth muscle
Enhance K+ efflux
Membrane Hyperpolarization
↓ Ca 2+ entry
Reduced intracellular calcium
Smooth muscle relaxation
65.
66. Nicorandil is an arterial and venous dilator.
MOA
Nicorandil
Open ATP-sensitive Act as nitric oxide
K+ channels donor
Enhance K+ efflux
Membrane Hyperpolarization
↓ Ca 2+ entry
Reduced intracellular calcium
Smooth muscle relaxation
Decrease preload and afterload, increase coronary blood flow
67. Use
Resistant angina
In combination with other drugs
Dose: 10-20 mg twice daily.
Adverse effects
Headache
Flushing
Palpitation
Dizziness
Hypotension
68. Similar to nicorandil.
Uses
Angina
Hypertension
69.
70. Coronary vasodilator
But it is not used in angina as it diverts blood
from ischemic zone to non ischemic zone.
It inhibits platelet aggregation for which
it is used in post-MI and post-stroke patients
tor prevention of coronary and cerebral
thrombosis.
Dose 25-100 mgTID.
71. Long-term administration of low dose
aspirin is recommended to prevent myocardial
infarction.
Inhibits platelet aggregation.
Dose: 75-100mg
72. Anti-anginal action through inhibition of fatty
acid metabolism, also known as fatty acid
oxidation inhibitor.
Used in post MI patients.
Dose: 20 mgTID.
73. Recently introduced trimetazidine congener.
MOA
Prevents calcium overload in the myocardium during
ischemia and reduces myocardial O2 demand.
Uses
Prevention of angina as add on therapy.
Dose : 500 mg sustained release tablets twice daily.
Adverse effects
Weakness
Postural hypotension
Dizziness
Headache
Constipation
74. Nitrates + β blockers
Nifedipine + β blockers
Nitrates + CCB
Nitrates + β blockers+ CCB
If not controlled by 2 drug combination.