- Antiplatelet drugs work by interfering with platelet function and are used to prevent thromboembolic disorders. They act on platelet receptors and inhibit the release of substances like thromboxane A2 and adenosine diphosphate that promote platelet activation and aggregation.
- Aspirin is one of the most commonly used antiplatelet drugs. It works by irreversibly inhibiting the enzymes cyclooxygenase-1 and thromboxane synthase, suppressing the formation of thromboxane A2. This reduces platelet aggregation. It is used long-term after heart attacks and strokes to lower the risk of recurrence.
- Other antiplatelet drugs include dipyridamole, ticlopid
This document summarizes information about statins, including their uses, mechanisms of action, types, interactions, and safety considerations. It discusses how statins are used to prevent heart disease by lowering LDL cholesterol and discusses their four proposed mechanisms of action, including improving endothelial function and maintaining plaque stability. It also provides comparisons of different statin medications and identifies atorvastatin and simvastatin as producing the greatest LDL reduction, as well as pravastatin and fluvastatin as having fewer drug interactions.
Statins are a class of drugs that lower cholesterol by inhibiting its production in the liver. They have been shown to significantly reduce risks of cardiovascular events. While generally safe and effective for primary prevention when LDL is over 190 mg/dL, statins can cause side effects like muscle pain and cognitive issues. They work best when started before or after CABG to improve graft patency. Rosuvastatin and atorvastatin may provide the greatest benefits for postoperative CABG patients by allowing LDL to be lowered below 100 mg/dL. Maintaining LDL at this level can nearly double venous graft patency rates.
Calcium channel blockers are useful treatments in the management of hypertension. In this presentation by Dr Vivek Baliga, we look at the added benefits of newer types of CCBs in treating high blood pressure. Read more from Dr Baliga here - http://drvivekbaliga.net
This document summarizes various drugs used to treat dyslipidemia. It discusses statins including various types and their mechanisms and effects. It also discusses other drug classes like ezetimibe, bile acid sequestrants, fibrates, niacin, PCSK9 inhibitors, lomitapide, mipomersen and CETP inhibitors. It provides details on the mechanisms, effects, dosages and adverse effects of these drugs. It also discusses the use of combination drug therapies for treating different types of dyslipidemia.
Cilnidipine is a dual-acting calcium channel blocker that blocks both L-type and N-type calcium channels. It is used to treat hypertension. Studies have shown that cilnidipine is as effective at lowering blood pressure as amlodipine, but it does not cause reflex tachycardia and has a lower risk of side effects like ankle edema. Combining cilnidipine with drugs that inhibit the renin-angiotensin-aldosterone system provides improved blood pressure control and reduces cardiac remodeling compared to other calcium channel blockers. Cilnidipine's unique dual blocking properties also help regulate leptin secretion, reducing atherosclerosis risk in obese hypertensive patients
Dyslipidemia, or abnormal lipid levels in the blood, increases the risk of atherosclerosis and cardiovascular disease. The document discusses the definition and causes of dyslipidemia as well as screening recommendations. It also summarizes the roles of different lipids like LDL, HDL, and triglycerides in atherosclerosis. The treatment approaches for different lipid abnormalities are outlined, including lifestyle modifications and medications like statins, fibrates, bile acid sequestrants, nicotinic acid, and ezetimibe.
1. Metformin was introduced in 1957 and is effective for lowering blood glucose levels as monotherapy or in combination with other agents.
2. It works by decreasing hepatic glucose production and increasing insulin sensitivity. Common side effects include gastrointestinal issues.
3. Metformin is recommended for preventing type 2 diabetes in prediabetic patients and is the first-line treatment for type 2 diabetes.
The document discusses various types of oral hypoglycemic agents (OHAs) used to treat type 2 diabetes mellitus (T2DM). It describes the classifications of OHAs including biguanides like metformin, sulphonylureas, meglitinides, thiazolidinediones, and others. For each class, it provides details on mechanisms of action, pharmacokinetics, dosing, side effects, and contraindications. Metformin and sulphonylureas have been used the longest and remain first-line treatment options, though each class has advantages and disadvantages discussed in the document.
This document summarizes information about statins, including their uses, mechanisms of action, types, interactions, and safety considerations. It discusses how statins are used to prevent heart disease by lowering LDL cholesterol and discusses their four proposed mechanisms of action, including improving endothelial function and maintaining plaque stability. It also provides comparisons of different statin medications and identifies atorvastatin and simvastatin as producing the greatest LDL reduction, as well as pravastatin and fluvastatin as having fewer drug interactions.
Statins are a class of drugs that lower cholesterol by inhibiting its production in the liver. They have been shown to significantly reduce risks of cardiovascular events. While generally safe and effective for primary prevention when LDL is over 190 mg/dL, statins can cause side effects like muscle pain and cognitive issues. They work best when started before or after CABG to improve graft patency. Rosuvastatin and atorvastatin may provide the greatest benefits for postoperative CABG patients by allowing LDL to be lowered below 100 mg/dL. Maintaining LDL at this level can nearly double venous graft patency rates.
Calcium channel blockers are useful treatments in the management of hypertension. In this presentation by Dr Vivek Baliga, we look at the added benefits of newer types of CCBs in treating high blood pressure. Read more from Dr Baliga here - http://drvivekbaliga.net
This document summarizes various drugs used to treat dyslipidemia. It discusses statins including various types and their mechanisms and effects. It also discusses other drug classes like ezetimibe, bile acid sequestrants, fibrates, niacin, PCSK9 inhibitors, lomitapide, mipomersen and CETP inhibitors. It provides details on the mechanisms, effects, dosages and adverse effects of these drugs. It also discusses the use of combination drug therapies for treating different types of dyslipidemia.
Cilnidipine is a dual-acting calcium channel blocker that blocks both L-type and N-type calcium channels. It is used to treat hypertension. Studies have shown that cilnidipine is as effective at lowering blood pressure as amlodipine, but it does not cause reflex tachycardia and has a lower risk of side effects like ankle edema. Combining cilnidipine with drugs that inhibit the renin-angiotensin-aldosterone system provides improved blood pressure control and reduces cardiac remodeling compared to other calcium channel blockers. Cilnidipine's unique dual blocking properties also help regulate leptin secretion, reducing atherosclerosis risk in obese hypertensive patients
Dyslipidemia, or abnormal lipid levels in the blood, increases the risk of atherosclerosis and cardiovascular disease. The document discusses the definition and causes of dyslipidemia as well as screening recommendations. It also summarizes the roles of different lipids like LDL, HDL, and triglycerides in atherosclerosis. The treatment approaches for different lipid abnormalities are outlined, including lifestyle modifications and medications like statins, fibrates, bile acid sequestrants, nicotinic acid, and ezetimibe.
1. Metformin was introduced in 1957 and is effective for lowering blood glucose levels as monotherapy or in combination with other agents.
2. It works by decreasing hepatic glucose production and increasing insulin sensitivity. Common side effects include gastrointestinal issues.
3. Metformin is recommended for preventing type 2 diabetes in prediabetic patients and is the first-line treatment for type 2 diabetes.
The document discusses various types of oral hypoglycemic agents (OHAs) used to treat type 2 diabetes mellitus (T2DM). It describes the classifications of OHAs including biguanides like metformin, sulphonylureas, meglitinides, thiazolidinediones, and others. For each class, it provides details on mechanisms of action, pharmacokinetics, dosing, side effects, and contraindications. Metformin and sulphonylureas have been used the longest and remain first-line treatment options, though each class has advantages and disadvantages discussed in the document.
This document discusses antidiarrheal agents including opioid agonists like loperamide, bile salt-binding resins like cholestyramine, and octreotide. Opioid agonists increase colonic transit time through inhibition of nerves in the colon wall. Bile salt-binding resins bind excess bile salts in the colon that cause diarrhea. Octreotide is a synthetic somatostatin analogue that reduces intestinal secretion and slows motility, making it effective for treating diarrhea from various causes like short bowel syndrome or dumping syndrome. Potential side effects include changes in pancreatic function, gallbladder sludge, and alterations in blood sugar.
This document discusses the pharmacotherapy of dyslipidemia. It begins by defining dyslipidemia as disorders of lipoprotein metabolism that result in abnormal cholesterol and triglyceride levels, and describes lipoproteins. It then discusses the treatment of dyslipidemia, including lifestyle modifications and various drug therapies such as statins, fibrates, bile acid sequestrants, nicotinic acid, ezetimibe, PCSK9 inhibitors, and other newer therapies. It provides details on the mechanisms of action, uses, dosing, and side effects of these different drug classes.
Diabetes is the leading cause of end-stage renal disease (ESRD), accounting for over 50% of new ESRD cases. Strict control of blood pressure, blood sugar, cholesterol, and protein in the urine can help prevent or delay kidney damage in patients with diabetes. For patients with diabetes and existing chronic kidney disease, careful management of medications, diet, anemia, bone disease, and other comorbidities is needed. Dialysis or kidney transplantation may be required as kidney function declines.
This document discusses cardiovascular disease (CAD) in South Asians and a clinical trial on the use of statins. It contains the following key points:
1) South Asians have a higher prevalence of CAD than other ethnicities due to genetic and environmental/lifestyle factors such as metabolic syndrome and central obesity.
2) The JUPITER trial found that treating individuals with low LDL cholesterol but high C-reactive protein with rosuvastatin reduced cardiovascular events like heart attack and stroke by 44% compared to placebo, showing statins can benefit those not currently eligible for treatment.
3) Rosuvastatin was well-tolerated in JUPITER and showed no increase in side effects even when LDL
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
This document discusses statins, which are lipid-lowering drugs used to treat high cholesterol and reduce the risk of cardiovascular events. It describes the physiology of lipoproteins such as LDL and HDL cholesterol. Statins work by inhibiting HMG-CoA reductase and reducing cholesterol production in the liver. Common side effects include muscle pain and elevated liver enzymes, while rare side effects include rhabdomyolysis (muscle breakdown). The document provides guidance on using statins for primary and secondary prevention of cardiovascular events and cautions about drug interactions and monitoring for side effects.
Rifaximin treatment in hepatic encephalopathyPratap Tiwari
Rifaximin treatment significantly reduced the risk of hepatic encephalopathy episodes and hospitalizations over a 6-month period compared to placebo. In the study, 22.1% of patients taking rifaximin experienced a breakthrough hepatic encephalopathy episode, compared to 45.9% of patients taking placebo. The incidence of adverse events was similar between the two groups. The study demonstrates that rifaximin is effective for maintaining remission from hepatic encephalopathy in patients with cirrhosis.
This document discusses cardiovascular disorders, specifically hyperlipidemia and coronary heart disease. It covers the pathophysiology of lipid metabolism and atherosclerosis, conditions that can cause angina, distinguishing characteristics of chronic stable angina versus unstable angina, and treatments including lifestyle modifications, pharmacotherapy, percutaneous coronary intervention, and coronary artery bypass graft surgery. The goal of treatment is to prevent acute coronary events and death, alleviate acute ischemic symptoms, prevent recurrent ischemia, and minimize adverse effects of treatment.
This document summarizes a presentation on statins and their pleiotropic effects. It begins with an overview and introduction on statins. It then discusses cholesterol synthesis and statins' mechanism of action in inhibiting HMG-CoA reductase to lower cholesterol. The document outlines various pleiotropic effects of statins including improving endothelial function, providing plaque stability, anti-inflammatory effects, and effects on other organs. It summarizes several research articles on topics like statins' effect on CRP and the association between statins and vitamin D.
ARBs (Angiotensin receptor blockers) are the most widely used anti hypertensive throughout the world. A solid knowledge related to ARB will make our practice more patients friendly & benefit will be maximum.
Fibrates - class, effects, side effects, drugs interactions, main indications...OlgaGoryacheva4
My student Niraj Maheshwari had presented this topic in our 22nd Student Scientific Society Conference in the department of Propaedeutic of Internal Diseases No.2
The document discusses drugs used to treat dyslipidemia. It begins by defining dyslipidemia as disorders of lipoprotein metabolism resulting in abnormal lipid levels. It then covers the classification, mechanisms of action, effects, and indications for various drug classes including statins, bile acid sequestrants, ezetimibe, fibrates, and niacin. Statins are highlighted as the most effective and best tolerated first-line treatment for lowering LDL cholesterol. Fibrates and niacin are discussed as second-line options for lowering triglycerides and raising HDL cholesterol.
This document discusses thyroid conditions and their treatments. Hypothyroidism can cause constipation while hyperthyroidism can cause diarrhea. Medications used to treat hyperthyroidism include propylthiouracil, methimazole, and carbimazole which inhibit thyroid hormone production. Iodine and radioactive iodine can also be used. Less potent treatments include thiocyanate, perchlorate, and nitrates. Propylthiouracil has a shorter half-life and crosses the placenta less than methimazole. Beta blockers, calcium channel blockers like diltiazem and verapamil, and medications to bind thyroid hormone in the gut were also historically used but are
This document discusses management strategies for nonalcoholic fatty liver disease (NAFLD). It begins by outlining lifestyle changes like weight loss through diet and exercise as the foundation for treatment. Weight loss of at least 3-5% is associated with histological improvement. The document then reviews current pharmacologic options, noting that pioglitazone and vitamin E are the only FDA-approved therapies. Surgical management through bariatric surgery can also improve clinical parameters and resolve fibrosis. Emerging investigational therapies discussed include elafibranor, obeticholic acid, and cenicriviroc, though pioglitazone remains the most effective option based on clinical trials to date.
Methotrexate is a folate antagonist antimetabolite drug that works by inhibiting the enzyme dihydrofolate reductase, depleting tetrahydrofolate cofactors needed for DNA synthesis. It is used to treat cancers like acute lymphocytic leukemia, breast cancer, and rheumatoid arthritis. 5-Fluorouracil and capecitabine are pyrimidine antagonist antimetabolites that inhibit the enzyme thymidylate synthase, blocking DNA synthesis. They are used for cancers like colon cancer. Cytarabine is also a pyrimidine antagonist that incorporates into DNA, inhibiting its synthesis, and is used for acute leukemias. 6-Mercap
Vymada Tablet (ARNI: Angiotensin Receptor Neprilysin Inhibitor) is an anti-hypertensive drug used in combination with Sacubitril & Valsartan to reduce the risk of cardiovascular events in patients with chronic heart failure (NYHA Class II-IV) and reduced ejection fraction.
Dyslipidemia refers to abnormalities in lipoprotein metabolism that result in high total cholesterol, high LDL cholesterol, low HDL cholesterol, and high triglycerides. The prevalence of dyslipidemia varies but is estimated to affect over 100 million Americans. Dyslipidemia is caused by both genetic factors like familial hypercholesterolemia as well as secondary factors such as diabetes, hypothyroidism, and certain medications. It is a major risk factor for cardiovascular disease.
Recent Advances in Obesity PharmacotherapyShreya Gupta
This document summarizes recent advances in obesity, including potential new drug targets. It discusses drugs currently in development like tesofensine, setmelanotide, semaglutide, and velneperitide that act on targets such as serotonin-norepinephrine-dopamine reuptake, melanocortin receptors, GLP-1 receptors, and neuropeptide Y receptors. The document also mentions exploring cannabinoid type 1 receptor blockers with limited brain penetration to avoid the psychiatric side effects that led to previous drugs being withdrawn.
Dipeptidyl peptidase-4 (DPP-4) inhibitors are a class of drugs for treating diabetes that work by blocking the DPP-4 enzyme, allowing glucagon-like peptide-1 (GLP-1) to remain active. GLP-1 stimulates the pancreas to release more insulin and less glucagon in response to food intake, lowering blood sugar levels. There are currently three DPP-4 inhibitors approved for use: sitagliptin, saxagliptin, and vildagliptin. DPP-4 inhibitors are effective at lowering blood sugar while having a low risk of hypoglycemia and not causing weight gain.
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.
This document discusses antidiarrheal agents including opioid agonists like loperamide, bile salt-binding resins like cholestyramine, and octreotide. Opioid agonists increase colonic transit time through inhibition of nerves in the colon wall. Bile salt-binding resins bind excess bile salts in the colon that cause diarrhea. Octreotide is a synthetic somatostatin analogue that reduces intestinal secretion and slows motility, making it effective for treating diarrhea from various causes like short bowel syndrome or dumping syndrome. Potential side effects include changes in pancreatic function, gallbladder sludge, and alterations in blood sugar.
This document discusses the pharmacotherapy of dyslipidemia. It begins by defining dyslipidemia as disorders of lipoprotein metabolism that result in abnormal cholesterol and triglyceride levels, and describes lipoproteins. It then discusses the treatment of dyslipidemia, including lifestyle modifications and various drug therapies such as statins, fibrates, bile acid sequestrants, nicotinic acid, ezetimibe, PCSK9 inhibitors, and other newer therapies. It provides details on the mechanisms of action, uses, dosing, and side effects of these different drug classes.
Diabetes is the leading cause of end-stage renal disease (ESRD), accounting for over 50% of new ESRD cases. Strict control of blood pressure, blood sugar, cholesterol, and protein in the urine can help prevent or delay kidney damage in patients with diabetes. For patients with diabetes and existing chronic kidney disease, careful management of medications, diet, anemia, bone disease, and other comorbidities is needed. Dialysis or kidney transplantation may be required as kidney function declines.
This document discusses cardiovascular disease (CAD) in South Asians and a clinical trial on the use of statins. It contains the following key points:
1) South Asians have a higher prevalence of CAD than other ethnicities due to genetic and environmental/lifestyle factors such as metabolic syndrome and central obesity.
2) The JUPITER trial found that treating individuals with low LDL cholesterol but high C-reactive protein with rosuvastatin reduced cardiovascular events like heart attack and stroke by 44% compared to placebo, showing statins can benefit those not currently eligible for treatment.
3) Rosuvastatin was well-tolerated in JUPITER and showed no increase in side effects even when LDL
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
This document discusses statins, which are lipid-lowering drugs used to treat high cholesterol and reduce the risk of cardiovascular events. It describes the physiology of lipoproteins such as LDL and HDL cholesterol. Statins work by inhibiting HMG-CoA reductase and reducing cholesterol production in the liver. Common side effects include muscle pain and elevated liver enzymes, while rare side effects include rhabdomyolysis (muscle breakdown). The document provides guidance on using statins for primary and secondary prevention of cardiovascular events and cautions about drug interactions and monitoring for side effects.
Rifaximin treatment in hepatic encephalopathyPratap Tiwari
Rifaximin treatment significantly reduced the risk of hepatic encephalopathy episodes and hospitalizations over a 6-month period compared to placebo. In the study, 22.1% of patients taking rifaximin experienced a breakthrough hepatic encephalopathy episode, compared to 45.9% of patients taking placebo. The incidence of adverse events was similar between the two groups. The study demonstrates that rifaximin is effective for maintaining remission from hepatic encephalopathy in patients with cirrhosis.
This document discusses cardiovascular disorders, specifically hyperlipidemia and coronary heart disease. It covers the pathophysiology of lipid metabolism and atherosclerosis, conditions that can cause angina, distinguishing characteristics of chronic stable angina versus unstable angina, and treatments including lifestyle modifications, pharmacotherapy, percutaneous coronary intervention, and coronary artery bypass graft surgery. The goal of treatment is to prevent acute coronary events and death, alleviate acute ischemic symptoms, prevent recurrent ischemia, and minimize adverse effects of treatment.
This document summarizes a presentation on statins and their pleiotropic effects. It begins with an overview and introduction on statins. It then discusses cholesterol synthesis and statins' mechanism of action in inhibiting HMG-CoA reductase to lower cholesterol. The document outlines various pleiotropic effects of statins including improving endothelial function, providing plaque stability, anti-inflammatory effects, and effects on other organs. It summarizes several research articles on topics like statins' effect on CRP and the association between statins and vitamin D.
ARBs (Angiotensin receptor blockers) are the most widely used anti hypertensive throughout the world. A solid knowledge related to ARB will make our practice more patients friendly & benefit will be maximum.
Fibrates - class, effects, side effects, drugs interactions, main indications...OlgaGoryacheva4
My student Niraj Maheshwari had presented this topic in our 22nd Student Scientific Society Conference in the department of Propaedeutic of Internal Diseases No.2
The document discusses drugs used to treat dyslipidemia. It begins by defining dyslipidemia as disorders of lipoprotein metabolism resulting in abnormal lipid levels. It then covers the classification, mechanisms of action, effects, and indications for various drug classes including statins, bile acid sequestrants, ezetimibe, fibrates, and niacin. Statins are highlighted as the most effective and best tolerated first-line treatment for lowering LDL cholesterol. Fibrates and niacin are discussed as second-line options for lowering triglycerides and raising HDL cholesterol.
This document discusses thyroid conditions and their treatments. Hypothyroidism can cause constipation while hyperthyroidism can cause diarrhea. Medications used to treat hyperthyroidism include propylthiouracil, methimazole, and carbimazole which inhibit thyroid hormone production. Iodine and radioactive iodine can also be used. Less potent treatments include thiocyanate, perchlorate, and nitrates. Propylthiouracil has a shorter half-life and crosses the placenta less than methimazole. Beta blockers, calcium channel blockers like diltiazem and verapamil, and medications to bind thyroid hormone in the gut were also historically used but are
This document discusses management strategies for nonalcoholic fatty liver disease (NAFLD). It begins by outlining lifestyle changes like weight loss through diet and exercise as the foundation for treatment. Weight loss of at least 3-5% is associated with histological improvement. The document then reviews current pharmacologic options, noting that pioglitazone and vitamin E are the only FDA-approved therapies. Surgical management through bariatric surgery can also improve clinical parameters and resolve fibrosis. Emerging investigational therapies discussed include elafibranor, obeticholic acid, and cenicriviroc, though pioglitazone remains the most effective option based on clinical trials to date.
Methotrexate is a folate antagonist antimetabolite drug that works by inhibiting the enzyme dihydrofolate reductase, depleting tetrahydrofolate cofactors needed for DNA synthesis. It is used to treat cancers like acute lymphocytic leukemia, breast cancer, and rheumatoid arthritis. 5-Fluorouracil and capecitabine are pyrimidine antagonist antimetabolites that inhibit the enzyme thymidylate synthase, blocking DNA synthesis. They are used for cancers like colon cancer. Cytarabine is also a pyrimidine antagonist that incorporates into DNA, inhibiting its synthesis, and is used for acute leukemias. 6-Mercap
Vymada Tablet (ARNI: Angiotensin Receptor Neprilysin Inhibitor) is an anti-hypertensive drug used in combination with Sacubitril & Valsartan to reduce the risk of cardiovascular events in patients with chronic heart failure (NYHA Class II-IV) and reduced ejection fraction.
Dyslipidemia refers to abnormalities in lipoprotein metabolism that result in high total cholesterol, high LDL cholesterol, low HDL cholesterol, and high triglycerides. The prevalence of dyslipidemia varies but is estimated to affect over 100 million Americans. Dyslipidemia is caused by both genetic factors like familial hypercholesterolemia as well as secondary factors such as diabetes, hypothyroidism, and certain medications. It is a major risk factor for cardiovascular disease.
Recent Advances in Obesity PharmacotherapyShreya Gupta
This document summarizes recent advances in obesity, including potential new drug targets. It discusses drugs currently in development like tesofensine, setmelanotide, semaglutide, and velneperitide that act on targets such as serotonin-norepinephrine-dopamine reuptake, melanocortin receptors, GLP-1 receptors, and neuropeptide Y receptors. The document also mentions exploring cannabinoid type 1 receptor blockers with limited brain penetration to avoid the psychiatric side effects that led to previous drugs being withdrawn.
Dipeptidyl peptidase-4 (DPP-4) inhibitors are a class of drugs for treating diabetes that work by blocking the DPP-4 enzyme, allowing glucagon-like peptide-1 (GLP-1) to remain active. GLP-1 stimulates the pancreas to release more insulin and less glucagon in response to food intake, lowering blood sugar levels. There are currently three DPP-4 inhibitors approved for use: sitagliptin, saxagliptin, and vildagliptin. DPP-4 inhibitors are effective at lowering blood sugar while having a low risk of hypoglycemia and not causing weight gain.
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.
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 provides an overview of hemostasis and antithrombotic drugs. It discusses the four phases of hemostasis - vascular, platelet, coagulation, and fibrinolytic. Antithrombotic drugs include antiplatelet drugs that inhibit platelet activation and aggregation, anticoagulants that inhibit fibrin formation, and fibrinolytic agents that degrade fibrin. The document focuses on antiplatelet drugs, describing their mechanisms of action, types including aspirin, clopidogrel, prasugrel, ticagrelor, and glycoprotein IIb/IIIa antagonists. Their uses, pharmacokinetics, adverse effects, and interactions are summarized.
9. NSAIDS.pptxNSAIDS inhibit the enzyme cyclooxygenase (COX) types 1 and 2, w...samiyamohammed284
Renal
Renally produced prostaglandins (PGE2 and PGI2) are essential
in maintaining adequate renal perfusion when the level of circulating vasoconstrictors Platelets
Impaired platelet function (reduced aggregation).
as a result of decreased thromboxane A2 (TXA2) production.
TXA2 is present in large amounts in activated platelets and acts locally as a chemo-attractant for other platelets, leads to the formation of a platelet plug and induces localized vasoconstric
This document discusses different types of drugs used to modulate clotting, including antiplatelet drugs, fibrinolytics (thrombolytics), and antifibrinolytics. It provides details on specific antiplatelet drugs like aspirin and clopidogrel, fibrinolytic drugs like streptokinase and tissue plasminogen activator, and antifibrinolytics like epsilon amino caproic acid and tranexamic acid. It also outlines their mechanisms of action, dosages, clinical uses, and contraindications in treating conditions like heart attacks, DVTs, and excessive bleeding.
This document discusses drugs used to treat deep vein thrombosis (DVT). It outlines platelet aggregation inhibitors, anticoagulants, and thrombolytic drugs - their mechanisms of action, uses, and adverse effects. Platelet aggregation inhibitors work by inhibiting cyclooxygenase-1 or blocking platelet receptors. Anticoagulants like heparin and warfarin prevent clotting by suppressing clotting factors. Thrombolytic drugs dissolve blood clots by activating plasminogen to form plasmin, which breaks down fibrin in clots. While these drugs can effectively treat DVT, they may increase bleeding risk as a side effect.
- Platelets play an important role in blood clotting by clumping together to form blood clots, which stop bleeding from cuts or wounds. However, blood clots inside arteries can block blood flow and damage tissues.
- Antiplatelet drugs like aspirin work by preventing platelets from clumping together. Aspirin is commonly used after CABG surgery and procedures like angioplasty to prevent new blood clots from forming and reduce the risk of future heart attacks.
- While aspirin is generally safe, concerns remain about how soon after surgery it can safely be given to balance preventing clots versus risks of bleeding complications. Studies found low dose aspirin given within 48 hours of CABG was not
This document discusses various drugs used to treat angina pectoris. It begins by defining angina and describing its causes as inadequate blood flow through the coronary arteries. It then discusses the different types of angina - stable, unstable, and Prinzmetal's variant angina. The main drugs used to treat angina are described - nitrates, beta-blockers, calcium channel blockers, and newer drugs like ranolazine. Nitrates work by dilating blood vessels to reduce preload and afterload. Beta-blockers reduce heart rate and contractility. Calcium channel blockers inhibit calcium entry to arteries and heart muscle. Ranolazine inhibits sodium channels to reduce oxygen demand. Combinations of these drugs
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 discusses various drugs that modify blood coagulation by affecting platelet function and the clotting cascade. It describes several classes of drugs: anticoagulants which prevent clot formation; antiplatelet drugs like aspirin which inhibit platelet aggregation; thrombolytic drugs which lyse existing clots; and hemostatic drugs which promote clotting. For each drug class, the document outlines mechanisms of action, indications for use, dosages, side effects and interactions.
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 discusses drugs used for angina pectoris. It defines angina as chest pain caused by insufficient oxygen to the heart muscle. Angina has underlying causes like coronary heart disease and atherosclerosis. The document outlines four types of angina and discusses the mechanisms and pathophysiology of atherosclerosis. It then summarizes various drug classes used to treat angina, including nitrates, beta blockers, calcium channel blockers, nicorandil, aspirin, and clopidogrel. Specific drugs within each class are mentioned along with their mechanisms of action, indications, and side effects.
This document summarizes several drugs used to treat hyperlipidemia and cardiovascular conditions. It describes the mechanism of action, clinical use, and side effects of statins, ezetimibe, bile acid resins, niacin, fibrates, and fish oil for treating hyperlipidemia. It also summarizes nitrates, ranolazine, and hydralazine used for angina, as well as beta-blockers, calcium channel blockers, aspirin, ADP receptor inhibitors, and GP IIb/IIIa inhibitors used for antiplatelet and anticoagulant therapy.
Aspirin in Myocardial Infarction by Pharm Jimmy AidenJimmy Potter
This document discusses the use of aspirin in the management of myocardial infarction. It begins with an overview of myocardial infarction and the platelet mechanisms involved in clot formation. It then discusses aspirin, including its introduction, mechanism of action inhibiting platelet activation, and indications for use in acute myocardial infarction and long-term management. The document outlines aspirin's pharmacokinetics, dosage, adverse effects, interactions, and concludes that aspirin's irreversible inhibition of platelet thromboxane synthesis provides cost-effective prevention of reinfarction.
The document discusses various antithrombotic agents, including antiplatelet drugs that inhibit platelet adhesion and aggregation, anticoagulants that target the coagulation system, and fibrinolytic agents that lyse thrombi. It provides details on the mechanisms and targets of common antiplatelet drugs like aspirin, clopidogrel, prasugrel, and ticagrelor. Indications, dosages, interactions, and adverse effects are described for optimal use of these antiplatelet therapies.
TEST BANK For Community Health Nursing A Canadian Perspective, 5th Edition by...Donc Test
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These lecture slides, by Dr Sidra Arshad, offer a quick overview of the physiological basis of a normal electrocardiogram.
Learning objectives:
1. Define an electrocardiogram (ECG) and electrocardiography
2. Describe how dipoles generated by the heart produce the waveforms of the ECG
3. Describe the components of a normal electrocardiogram of a typical bipolar lead (limb II)
4. Differentiate between intervals and segments
5. Enlist some common indications for obtaining an ECG
6. Describe the flow of current around the heart during the cardiac cycle
7. Discuss the placement and polarity of the leads of electrocardiograph
8. Describe the normal electrocardiograms recorded from the limb leads and explain the physiological basis of the different records that are obtained
9. Define mean electrical vector (axis) of the heart and give the normal range
10. Define the mean QRS vector
11. Describe the axes of leads (hexagonal reference system)
12. Comprehend the vectorial analysis of the normal ECG
13. Determine the mean electrical axis of the ventricular QRS and appreciate the mean axis deviation
14. Explain the concepts of current of injury, J point, and their significance
Study Resources:
1. Chapter 11, Guyton and Hall Textbook of Medical Physiology, 14th edition
2. Chapter 9, Human Physiology - From Cells to Systems, Lauralee Sherwood, 9th edition
3. Chapter 29, Ganong’s Review of Medical Physiology, 26th edition
4. Electrocardiogram, StatPearls - https://www.ncbi.nlm.nih.gov/books/NBK549803/
5. ECG in Medical Practice by ABM Abdullah, 4th edition
6. Chapter 3, Cardiology Explained, https://www.ncbi.nlm.nih.gov/books/NBK2214/
7. ECG Basics, http://www.nataliescasebook.com/tag/e-c-g-basics
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.
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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.
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2. PLATELETS
• Platelets, also called thrombocytes, are a component of blood whose function (along
with the coagulation factors) is to react to bleeding from blood vessel injury by clumping,
thereby initiating a blood clot
• Platelets have no cell nucleus; they are fragments of cytoplasm that are derived from
the megakaryocytes of the bone marrow which then enter the circulation.
• Circulating unactivated platelets are biconvex discoid (lens-shaped) structures, 2–3 µm in
greatest diameter.
• Activated platelets have cell membrane projections covering their surface.
• Lifespan of platelets is about 10 days
• Normal platelet count is 150000 to 400000 cells/microlitre of blood
4. PLATELETS
• Under normal conditions platelets circulate freely without significant interaction with other platelets
or healthy vascular endothelium.
• In the presence of endothelial disruption or activation, whether from vascular injury, rupture of an
atherosclerotic plaque or maladaptive signals, a chain of events ensues that leads to platelet-rich
clot formation.
• Depending on the initiating event, this may represent protective hemostasis, a vital step toward
vascular repair, or pathologic vascular thrombosis causing an acute coronary syndrome or ischemic
stroke.
• The causative events represent a complex series of integrated biochemical and cellular processes
that
• can be divided into five functional categories: Translocation (tethering), activation, secretion,
adhesion, and aggregation
6. INTRODUCTION
• Antiplatelets are drugs which interfere with platelet function and are useful in the prophylaxis of
thromboembolic disorders.
• Platelets express several glycoprotein (GP) integrin receptors on their surface.
• Reactive proteins like collagen are exposed when there is damage to vascular endothelium, and
they react respectively with platelet GPIa and GPIb receptors. This results in platelet activation and
release of pro-aggregatory and vasoconstrictor mediators like Thromboxane A2 (TX A2), Adenosine
diphosphate (ADP) and 5-Hydroxytryptamine (5HT)
• The platelet GPIIb/IIIa receptor undergoes a conformational change favouring binding of fibrinogen
and vonWillebrand factor (vWF) that crosslink platelets inducing aggregation and anchorage to
vessel wall/other surfaces.
• Thus, a ‘platelet plug’ is formed. In veins, due to sluggish blood flow, a fibrinous tail is formed which
traps RBCs ‘the red tail’. In arteries, platelet mass is the main constituent of the thrombus.
Antiplatelet drugs are, therefore, more useful in arterial thrombosis, while anticoagulants are more
effective in venous thrombosis.
7. ANTIPLATELET DRUGS
• Prostacyclin (PGI2), synthesized in the intima of blood vessels, is a strong inhibitor of platelet
aggregation.
• A balance between TXA2 released from platelets and PGI2 released from vessel wall appears to
control intravascular thrombus formation.
• Various drugs act on different targets to interfere with platelet function. And when given
together, their actions are synergistic.
The clinically important antiplatelet drugs are
• Aspirin
• Dipyridamole
• P 2 Y 12 receptor blockers-Ticlopidine, Clopidogrel, Prasugrel, Ticagrelor
• Glycoprotein IIb IIIa receptor antagonists – Eptifibatide, Tirofiban, Abciximab
8. Biosynthesis of Cycloxygenase, prostaglandins (PG), Thromboxanes and leukotrienes (LT).
Less active metabolites are shown in italicsTX—Thromboxane, PGI—Prostacyclin;
HPETE—Hydroperoxy eicosatetraenoic acid (Hydroperoxy arachidonic acid);
HETE—Hydroxyeicosatetraenoic acid (Hydroxy arachidonic acid);
SRS-A—Slow reacting substance of anaphylaxis
9. ASPIRIN
Aspirin is acetylsalicylic acid.
It is rapidly converted in the body to salicylic acid which is responsible for most of the actions.
Other actions are the result of acetylation of certain macromolecules including Cyclo-oxygenase
(COX).
It is one of the oldest analgesic-and anti-inflammatory drugs.
10. ASPIRIN
• Thromboxane A2 (TXA2), is a major arachidonic acid product produced by platelets, is a potent inducer
of platelet aggregation and release reaction. It also causes vasoconstriction.
• On the other hand, Prostacyclin (PGI2) generated by vascular endothelium is a potent inhibitor of platelet
aggregation. Generally all prostaglandins are vasodialaors.
Mechanism of action of Aspirin :
• Acetylatation and inhibition of the enzymes Cyclo-oxygenase 1 (COX1) and Thromboxane synthase (TX-
synthase)—inactivating them irreversibly.
1. TXA2 is the major arachidonic acid product generated by platelets and its formation is suppressed at very
low doses and till fresh platelets are formed.
2. Aspirin inhibit synthesis of both proaggregatory (TXA2) and antiaggregatory (PGI2) prostanoids, but
effect on platelet TXA2 (COX-1 generated) predominates, hence it inhibits platelet aggregation: bleeding
time is prolonged.
3. Aspirin inhibits the release of ADP from platelets and their sticking to each other
• Aspirin induced prolongation of bleeding time lasts for 5–7 days.
• Effect of daily doses cumulates and it has been shown that doses as low as 40 mg/day have an effect on
platelet aggregation.
• Maximal inhibition of platelet function occurs at 75–150 mg aspirin per day.
• Daily maintenance dose 75 to 150 mg per day.
11. USES OF ASPIRIN
• Post Myocardial infarction and stroke- Large studies have demonstrated that aspirin 60–100
mg/day reduces the incidence of myocardial infarction (MI) and it is routinely prescribed to
post-infarct patients. Aspirin reduces ‘transient ischaemic attacks’ and lowers incidence of
stroke in such patients.
• As analgesic – for headache, bodypain, joint pains, toothache, neuralgia. It is effective in low
doses (0.3–0.6 g 6–8 hourly)
• As antipyretic Aspirin is effective in fever of any origin; dose is same as for analgesia.
However, paracetamol, being safer, is generally preferred.
• Acute rheumatic fever -Aspirin is the first drug to be used in all cases for acute rheumatic
fever with arthritis. In a dose of 4–5 g or 75–100 mg/kg/day brings about marked
symptomatic relief in 1–3 days. Dose reduction may be started after 4–7 days and
maintenance doses (50 mg/kg/day) are continued for 2–3 weeks or till signs of active
disease (raised ESR) persist. Withdrawal is done gradually over the next 2 weeks.
12. Precautions and contraindications for Aspirin
• Contraindicated in people with Hypersensitivity to Aspirin and peptic ulcer
• Bleeding tendencies is seen in children suffering from chicken pox or influenza. Due to risk of
Reye’s syndrome pediatric formulations of aspirin are prohibited in India and the UK.
• Cautious use in chronic liver disease: cases of hepatic necrosis have been reported.
Aspirin should be stopped 1 week before elective surgery.
Given chronically during pregnancy it may be responsible for low birth weight babies.
13. Dipyridamole
• It is a vasodilator that was introduced for angina pectoris
• It inhibits phosphodiesterase as well as blocks uptake of adenosine to increase platelet cAMP which
in turn potentiates PGI2 and interferes with aggregation.
• Levels of TXA2 or Prostaglandin I (PGI2) are not altered, but platelet survival time reduced by
disease is normalized.
• Dipyridamole alone has little clinically significant effect, but improves the response to warfarin,
along with which it is used to decrease the incidence of thromboembolism in patients with prosthetic
heart valves.
• Dipyridamole has also been used to enhance the antiplatelet action of aspirin. This combination
may additionally lower the risk of stroke in patients with transient ischaemic attacks (TIAs), but trials
have failed to demonstrate additional benefit in prophylaxis of MI.
• Dose: 150–300 mg/day. PERSANTIN 25, 100 mg tabs,
• Combination tablets with aspirin : Dipyridamole 75 mg + aspirin 60 mg, Dipyridamole 75 mg +
aspirin 40 mg
14. TICLOPIDINE
• Ticlopidine It is the first thienopyridine which alters surface receptors on platelets and inhibits ADP
as well as fibrinogen-induced platelet aggregation.
• The Gi coupled P2Y12 type of purinergic receptors which mediate adenylyl cyclase inhibition due to
ADP are blocked irreversibly by the active metabolite of ticlopidine. As a result, activation of
platelets is interfered.
• Fibrinogen binding to platelets is prevented without modification of GPIIb/IIIa receptor.
• There is no effect on platelet TXA2, but bleeding time is prolonged and platelet survival in extra-
corporeal circulation is increased.
• Because of different mechanism of action, it has synergistic effect on platelets with aspirin. Their
combination is a potent platelet inhibitor.
• Ticlopidine is well absorbed orally, is converted in liver to an active metabolite, and is eliminated
with a plasma t½ of 8 hours.
• Because of irreversible blockade of P2Y12 receptors, the effect on platelets cumulates; peak
platelet inhibition is produced after 8–10 days therapy, and the effect lasts 5–6 days after
discontinuing the drug.
15. • Side effects: Diarrhoea, vomiting, abdominal pain, headache, tinnitus, skin rash. Serious adverse
effects are bleeding, neutropenia, thrombocytopenia, haemolysis and jaundice.
• Several fatalities have occurred.
• Dose: 250 mg BD with meals; effect persists several days after discontinuation;
• Ticlopidine has produced beneficial effects in stroke prevention, TIAs, intermittent claudication,
unstable angina, PCI, coronary artery bypass grafts and secondary prophylaxis of MI. Combined
with aspirin, it has markedly lowered incidence of restenosis after PCI and stent thrombosis.
• Because of its potential for serious adverse reactions, use of ticlopidine has markedly declined in
favour of clopidogrel
16. CLOPIDOGREL
• A potent congener of ticlopidine, has similar mechanism of action, ability to irreversibly inhibit
platelet function and range of therapeutic efficacy, but is safer and better tolerated
• Clopidogrel recipients to have a slightly lower annual risk of primary ischaemic events than aspirin
recipients. Combination of clopidogrel and aspirin is synergistic in preventing ischaemic episodes,
and is utilized for checking restenosis of stented coronaries.
17. CLOPIDOGREL
• Like ticlopidine, clopidogrel is also a prodrug.
• About 50% of the ingested dose is absorbed, and only a fraction of this is slowly activated in liver by
CYP2C19, while the rest is inactivated by other enzymes.
• It is a slow acting drug; antiplatelet action takes about 4 hours to start and develops over days.
• Since CYP2C19, exhibits genetic polymorphism, the activation of clopidogrel and consequently its
antiplatelet action shows high interindividual variability. Some patients are nonresponsive.
• Omeprazole, an inhibitor Of CYP2C19, reduces metabolic activation of clopidogrel and its
antiplatelet action.
• The action of clopidogrel lasts 5–7 days due to irreversible blockade of platelet P2Y12 receptors.
• Adverse effects : The most important adverse effect is bleeding. Addition of aspirin to clopidogrel
has been found high risk stroke patients
• Neutropenia, thrombocytopenia and other bone marrow toxicity is rare.
• Side effects are diarrhoea, epigastric pain and rashes.
• Dose : 300mg loading dose in ACS and prior to coronary angioplasty followed by 75 mg OD.
18. PRASUGREL
• Prasugrel is the most potent and faster acting P2Y12 purinergic receptor blocker,
• Prasugrel is being used in acute coronary syndromes (ACS) and when strong antiplatelet action is
required.
• It is a prodrug, but is more rapidly absorbed and more rapidly as well as more completely activated,
resulting in faster and more consistent platelet inhibition.
• Though CYP2C19 is involved in activation of prasugrel as well, genetic polymorphism related
decrease in response, or interference by omeprazole treatment has not been prominent.
19. TICAGRELOR
• Orally acting
• Reversible inhibitor of P2Y12 receptor
• Rapid and consistent onset of action and quicker offset of action
• Plasma half life is 12 hours
• Dose : 180 mg loading dose in ACS and prior to coronary angioplasty
90mg 12th hourly maintenance dose
• Adverse effects-bleeding risk, dyspnoea, increased frequency of
ventricular pauses, asymptomatic increase in uric acid levels. , caution
is required in advanced SA node disease or second/third degree AV
block unless already treated with permanent pacemaker.
20. PRASUGREL
• Because of rapid action, prasugrel is particularly suitable for use in STEMI. It is the preferred
thienopyridine for ACS to cover angioplasty with or without stent placement.
• The TRITON trial compared prasugrel with clopidogrel in STEMI and NSTEMI.
• There was 19% greater reduction in death from cardiovascular causes in the prasugrel group.
Superior clinical outcomes and reduction in stent thrombosis have been obtained with prasugrel.
• Bleeding complications are also more frequent and more serious.
• Patients with history of ischaemic stroke and TIAs are at greater risk of intracranial haemorrhage.
• Prasugrel is contraindicated in such patients.
• DOSE; a loading dose of 60 mg followed by daily maintenance dose of 10 mg OD
In elderly or those <60 kg body weight 5 mg OD
21. Glycoprotein (GP) IIb/IIIa receptor
antagonists
• GP IIb/IIIa antagonists are a newer class of potent platelet aggregation inhibitors which act by
blocking the key receptor involved in platelet aggregation.
• The GPIIb/IIIa is an adhesive receptor (integrin) on platelet surface for fibrinogen and vWF through
which agonists like collagen, thrombin, TXA2, ADP, etc. finally induce platelet aggregation. Thus,
GP IIb/IIIa antagonists block aggregation induced by all platelet agonists.
22. Abciximab
• It is the Fab fragment of a chimeric monoclonal antibody against GP IIb/IIIa, protein, but is relatively
nonspecific and binds to some other surface proteins as well.
• Given along with aspirin + heparin during PCI, it has markedly reduced the incidence of restenosis,
subsequent MI and death.
• After a bolus dose platelet aggregation remains inhibited for 12–24 hr, while the remaining antibody is
cleared from blood with a t½ of 10–30 min.
• It is expensive, but is being used in unstable angina and as adjuvant to coronary thrombolysis/PCI with
stent placement.
Dose : 0.25 mg/kg Intravenous. 10–60 min before PCI, followed by 10 μg/min for 12 hr.
• After a bolus dose platelet aggregation remains inhibited for 12–24 hr, while the remaining antibody is
cleared from blood with a t½ of 10–30 min.
Complications :
• Haemorrhage,
• Thrombocytopenia is another complication. It should not be used second time, since risk of
thrombocytopenia increases.
• Constipation,
• Arrhythmias can occur.
23. Eptifibatide
• It is a synthetic cyclic peptide that selectively binds to platelet surface GPIIb/IIIa receptor and
inhibits platelet aggregation. Though its plasma t½ (2.5 hours) is longer than that of abciximab,
platelet inhibition reverses in a shorter time (within 6–10 hours) because it quickly dissociates from
the receptor. Infused i.v.,
Eptifibatide is indicated in:
• Unstable angina 180 mcg/kg i.v. bolus, followed by 2 mcg/kg/min infusion upto 72 hours.
• Coronary angioplasty 180 mcg/kg i.v. bolus, immediately before procedure; followed by 2 mg/kg/min
for 12–24 hours.
• Aspirin and Heparin are given along with Eptifibatide.
• Adverse effects : Bleeding and thrombocytopenia are the major adverse effects.
• Rashes and anaphylaxis are rare.
24. Tirofiban
• This is a nonpeptide but specific
• GPIIb/IIIa antagonist that is similar in properties to eptifibatide. Its plasma t½ is 2 hours, and it
dissociates rapidly from the receptors. The indications and adverse effects are also similar to
eptifibatide.
• Acute coronary syndromes: 0.4 mcg/kg/min for 30 min followed by 0.1 mg/kg/min for upto 48 hours.
If angioplasty is performed, infusion to continue till 12–24 hours thereafter
25. USES OF ANTIPLATELET DRUGS
• The aim of using antiplatelet drugs is to prevent intravascular thrombosis and embolization, with
minimal risk of haemorrhage. The intensity of antiplatelet therapy is selected according to the
thrombotic influences present in a patient. For indications like maintenance of vascular
recanalization, stent placement, vessel grafting, etc. potent inhibition of platelet function is required.
This is achieved by combining antiplatelet drugs which act by different mechanisms.
• Indications for antiplatelet drugs
1. Coronary artery disease-ACS- STEMI, NSTEMI, Unstable angina
2. Cerebral vascular disease
3. Peripheral artery disease
4. Venous thromboembolism
5. Prosthetic heart valves
6. Arteriovenous shunts
26. ACUTE CORONARY SYNDROME (ACS)
• The coronary obstruction in UA and NSTEMI is partial, while that in STEMI is total. UA and NSTEMI
are differentiated on the basis of absence or presence of laboratory markers of cardiac myocyte
necrosis (myoglobin, CK, troponin I, etc.).
• The ischaemic status is often dynamic and the patient may rapidly shift from one category to the
next.
• Soluble aspirin (325 mg oral) and a LMW heparin (s.c.) are given at presentation to all patients with
ACS.
• 1. Unstable angina Aspirin reduces the risk of progression to MI and sudden death. Clopidogrel is
generally combined with aspirin, or may be used as alternative if aspirin cannot be given. For
maximum protection the antiplatelet drugs are supplemented with heparin followed by warfarin. The
‘Clopidogrel in unstable angina to prevent recurrent events’ (CURE) trial has found that addition of
clopidogrel to aspirin further reduced cardiovascular mortality, nonfatal MI and stroke by 20%.
• 2. NSTEMI - Patients of NSTEMI who are managed without PCI/thrombolysis are generally put on a
combination of aspirin + clopidogrel, which is continued upto one year and later continued on single
antiplatelet agent.
27. Antiplatelets in STEMI
• Primary PCI with or without stent placement is the procedure of choice for all
• STEMI as well as high risk NSTEMI patients presenting within 12 hours.
• Prasugrel or Ticagrelor+ aspirin is the antiplatelet regimen most commonly selected for patients
who are to undergo PCI.
• Prasugrel acts rapidly and more predictably than clopidogrel.
• Prasugrel is also perferred over clopidogrel in diabetics.
• The GPIIb/IIIa antagonists are the most powerful antiplatelet drugs; are combined with aspirin for
high risk patients undergoing PCI.
• Abciximab/eptifibatide/tirofiban infused i.v. along with oral aspirin and s.c. heparin markedly reduce
incidence of restenosis and subsequent MI after coronary angioplasty.
• The GPIIb/IIIa antagonists are infused for a maximum of 72 hours.
28. Antiplatelets in STEMI
• Aspirin and/or clopidogrel are routinely given to ACS patients treated with thrombolysis.
• Coronary artery bypass surgery is also covered by intensive antiplatelet regimen including aspirin +
GPIIb/IIIa antagonists/prasugrel.
• The patency of recanalized coronary artery or implanted vessel is improved and incidence of
reocclusion is reduced by continuing aspirin+ clopidogrel/prasugrel almost indefinitely.
• Dual antiplatelet therapy is recommended after stent placement.
• Prasugrel or Ticagrelor is used when stent thrombosis occurs during clopidogrel treatment.
29. Cerebrovascular disease
• Antiplatelet drugs do not alter the course of stroke due to cerebral thrombosis.
• However, aspirin has reduced the incidence of TIAs and of stroke in patients with TIAs.
• Occurrence of stroke is also reduced in patients with persistent atrial fibrillation and in those with
history of stroke in the past. Aspirin or clopidogrel is recommended in all such individuals.
• Combination of dipyridamole with low dose aspirin is synergistic in secondary prevention of stroke.
30. Prosthetic heart valves and arteriovenous
shunts
• Antiplatelet drugs, used with warfarin reduce formation of microthrombi on artificial heart valves and
the incidence of embolism.
• Aspirin is clearly effective but increases risk of bleeding due to warfarin.
• Dipyridamole does not increase bleeding risk, but incidence of thromboembolism is reduced when it
is combined with an oral anticoagulant.
• Antiplatelet drugs also prolong the patency of chronic arteriovenous shunts implanted for
haemodialysis and of vascular grafts.
31. Venous thromboembolism and PVD
• Venous thromboembolism Anticoagulants are routinely used in DVT and PE. Trials have shown
antiplatelet drugs also to have a prophylactic effect, but their relative value in comparison to, or in
addition to anticoagulants is not established; they are infrequently used.
• Peripheral vascular disease Aspirin/ clopidogrel may produce some improvement in intermittent
claudication and reduce the incidence of thromboembolism.