Hypolipidemic pharmacology outline
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pharmacology of hypolipidemic drugs with outline of lipid metabolism ...... it helps in easy understanding ... i have focused solely on mechanism and key features of each class of drugs..... each class of drugs has specific use , i didnt mention it in my presentation ..... post ur comments in case u want to add , edit or want more info abt the topic ...
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Antihyperlipidemic agents
This document summarizes several antihyperlipidemic agents including ezetimibe, bile acid sequestrants, HMG-CoA reductase inhibitors (statins), fibrates, and nicotinic acid. It provides details on their mechanisms of action, pharmacological effects, indications, adverse reactions, contraindications, and interactions. The key points are:
1. Ezetimibe works by inhibiting cholesterol absorption in the intestine and lowers LDL levels the most. Bile acid sequestrants work by binding bile acids in the intestine and lowering LDL levels.
2. Statins are the first line treatment as they lower cholesterol synthesis in the liver and have pleiotropic effects in
Antihyperlipidemics1
This document discusses various drugs used to treat hyperlipidemia. It describes how statins work by inhibiting cholesterol biosynthesis in the liver, leading to increased LDL receptor levels and lowered cholesterol. It also discusses other drugs like fibrates that lower triglycerides, bile acid sequestrants that lower cholesterol by increasing bile acid excretion, and niacin that reduces triglycerides and LDL while increasing HDL. The risks and mechanisms of these antihyperlipidemic drugs are summarized.
" Anti-Hyperlipidemic Agents/Drugs "
Hyperlipidemia is an excess of lipids in the blood, including cholesterol, triglycerides, and phospholipids. It is usually chronic and requires medication to control blood lipid levels. Antihyperlipidemic agents work to lower LDL cholesterol, triglyceride, and raise HDL cholesterol levels. Some common antihyperlipidemic agents include statins, fibrates, nicotinic acid, bile acid sequestrants, cholesterol absorption inhibitors, and PCSK9 inhibitors. Bile acid sequestrants like cholestyramine and colestipol work by binding bile acids in the intestine to reduce cholesterol absorption and increase excretion.
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Hyperlipidemia, or high lipid levels, is a common disorder that increases the risk of heart disease. It results from abnormalities in lipid metabolism or transport. The main causes are lifestyle factors like obesity and lack of exercise, as well as medical conditions like diabetes. Drugs used to treat hyperlipidemia work by inhibiting cholesterol biosynthesis, sequestering bile acids to reduce cholesterol absorption, altering cholesterol metabolism, or inhibiting absorption of dietary cholesterol. Statins are the most commonly used class that lower LDL cholesterol by inhibiting HMG-CoA reductase. Other drug classes include bile acid sequestrants, fibrates, and niacin. Combination therapies may be used for more severe or treatment-resistant cases of
Lipid metabolism and hypolipedemic drugs
This document discusses lipid metabolism and hypolipidemic drugs. It defines different types of lipids including triglycerides, cholesterol, and lipoproteins. It describes the normal metabolism of lipids and how elevated LDL and triglycerides can lead to conditions like atherosclerosis. The document then summarizes several classes of drugs used to treat hyperlipidemia including statins, bile acid sequestrants, cholesterol absorption inhibitors, and fibrates. It provides examples of drugs in each class and their effects on lipid levels as well as common adverse effects.
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This document discusses hypolipidemic drugs, which lower lipid and lipoprotein levels in the blood. It describes the mechanisms of lipid transport through lipoproteins like chylomicrons, VLDL, LDL, HDL, and how different drugs like statins, fibrates, bile acid sequestrants work to lower lipid levels. Statins competitively inhibit HMG-CoA reductase to lower cholesterol synthesis. Fibrates activate lipoprotein lipase and lower triglyceride levels. Bile acid sequestrants bind bile acids in the gut to increase their excretion. The document provides details on the classification, mechanism of action, synthesis, structure-activity relationships and uses of these major
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Hypolipidemic drug, also called lipid-lowering drug, any agent the reduces the level of lipids and lipoproteins (lipid-protein complexes) in the blood.
Class hypolipidemics
This document discusses hyperlipidemia and its treatment. It begins by explaining how elevated lipid levels can lead to atherosclerosis and coronary artery disease. It then outlines different drug classes for treating hyperlipidemia, including statins, fibrates, and niacin, describing their mechanisms of action and side effects. Combination therapies are discussed as being more effective for certain conditions like familial combined hyperlipidemia. The document provides an overview of hyperlipidemia management through pharmacological means.
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1. Ezetimibe works by inhibiting cholesterol absorption in the intestine and lowers LDL levels the most. Bile acid sequestrants work by binding bile acids in the intestine and lowering LDL levels.
2. Statins are the first line treatment as they lower cholesterol synthesis in the liver and have pleiotropic effects in
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This document discusses various drugs used to treat hyperlipidemia. It describes how statins work by inhibiting cholesterol biosynthesis in the liver, leading to increased LDL receptor levels and lowered cholesterol. It also discusses other drugs like fibrates that lower triglycerides, bile acid sequestrants that lower cholesterol by increasing bile acid excretion, and niacin that reduces triglycerides and LDL while increasing HDL. The risks and mechanisms of these antihyperlipidemic drugs are summarized.
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Hyperlipidemia is an excess of lipids in the blood, including cholesterol, triglycerides, and phospholipids. It is usually chronic and requires medication to control blood lipid levels. Antihyperlipidemic agents work to lower LDL cholesterol, triglyceride, and raise HDL cholesterol levels. Some common antihyperlipidemic agents include statins, fibrates, nicotinic acid, bile acid sequestrants, cholesterol absorption inhibitors, and PCSK9 inhibitors. Bile acid sequestrants like cholestyramine and colestipol work by binding bile acids in the intestine to reduce cholesterol absorption and increase excretion.
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Hypolipidaemic drugs
This document discusses hypolipidemic drugs, which lower lipid and lipoprotein levels in the blood. It describes the mechanisms of lipid transport through lipoproteins like chylomicrons, VLDL, LDL, HDL, and how different drugs like statins, fibrates, bile acid sequestrants work to lower lipid levels. Statins competitively inhibit HMG-CoA reductase to lower cholesterol synthesis. Fibrates activate lipoprotein lipase and lower triglyceride levels. Bile acid sequestrants bind bile acids in the gut to increase their excretion. The document provides details on the classification, mechanism of action, synthesis, structure-activity relationships and uses of these major
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Hypolipidemic drug, also called lipid-lowering drug, any agent the reduces the level of lipids and lipoproteins (lipid-protein complexes) in the blood.
Class hypolipidemics
This document discusses hyperlipidemia and its treatment. It begins by explaining how elevated lipid levels can lead to atherosclerosis and coronary artery disease. It then outlines different drug classes for treating hyperlipidemia, including statins, fibrates, and niacin, describing their mechanisms of action and side effects. Combination therapies are discussed as being more effective for certain conditions like familial combined hyperlipidemia. The document provides an overview of hyperlipidemia management through pharmacological means.
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Hyperlipidemia refers to elevated levels of lipids or lipoproteins in the blood. It is caused by disorders involving elevations of lipoproteins such as low-density lipoprotein (LDL), very low-density lipoprotein (VLDL), and triglycerides. This puts one at risk for complications like atherosclerosis and pancreatitis. Treatment involves medications that lower LDL and triglyceride levels such as statins, resins, fibrates, and nicotinic acid. Each work by different mechanisms but commonly decrease lipid synthesis or increase lipid clearance to normalize lipid profiles and reduce cardiovascular risk. Side effects depend on the specific drug but may include gastrointestinal issues or myopathy.
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This document discusses various types of drugs used to treat hyperlipidemia. It begins by defining hyperlipidemia as a common disorder involving abnormal lipid metabolism that is a major cause of heart disease. It then describes several classes of antihyperlipidemic drugs, including HMG-CoA reductase inhibitors (statins), fibric acid derivatives, bile acid sequestrants, LDL oxidation inhibitors, and pyridine derivatives. For each class, examples of drugs are provided along with their mechanisms of action and effects on lipid levels.
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This document provides an overview of lipid metabolism and hypolipidemic drugs. It discusses lipids, lipoproteins, lipoprotein classification, lipid metabolism pathways including exogenous and endogenous pathways, atherogenesis, and drug therapy. The endogenous pathway can be separated into the atherogenic apo-B100 lipoprotein system and the antiatherogenic apo-A1 lipoprotein system. The document provides details on the structure and function of lipoproteins, their classification based on density and electrophoretic mobility, and the roles of apolipoproteins.
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The document discusses hyperlipidemia and the metabolic syndrome. It defines hyperlipidemia as abnormal lipid levels in the blood and metabolic syndrome as a clustering of conditions including obesity, high blood pressure, and abnormal cholesterol and blood sugar levels. The document outlines the causes, effects, diagnosis, and treatment of hyperlipidemia as well as the diagnostic criteria and resulting conditions of metabolic syndrome.
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The high risks of lipids and its relevance towards the development of different cardiovascular diseases has been known to all where this present slide focuses on that only along with the different treatment procedures,.
Antihyperlipidemic drugs
Lipids such as cholesterol and triglycerides are transported in the blood by lipoproteins including LDL and HDL. High LDL and low HDL are risk factors for atherosclerosis, where plaque builds up in the arteries. Several genetic disorders and secondary causes can lead to hyperlipidemia and abnormal lipoprotein levels. Treatment focuses on lowering LDL and triglycerides while raising HDL to reduce cardiovascular risk. Statins are commonly used drugs that lower cholesterol by inhibiting HMG-CoA reductase.
Antihyperlipidemic drugs
Hyperlipidemia is a common disorder caused by abnormalities in lipid metabolism or transport. It results in high levels of lipids like cholesterol and triglycerides in the blood. Hyperlipidemia is classified based on the abnormal lipid levels and is primarily treated through lifestyle changes and medications that lower lipid levels. Common drug classes used to treat hyperlipidemia work by inhibiting cholesterol synthesis, breaking down fats, or blocking lipid absorption.
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Statins like simvastatin and atorvastatin work by inhibiting HMG-CoA reductase and lowering cholesterol production in the liver. Bile acid sequestrants such as cholestyramine and colestipol bind bile acids in the gut. Ezetimibe decreases intestinal cholesterol absorption while statins lower endogenous production. Niacin can cause flushing and other side effects. Fibric acid derivatives like gemfibrozil and fenofibrate lower triglycerides and raise HDL levels but have potential side effects as well. Together, these classes of hypolipidemic drugs act through different mechanisms to lower cholesterol and lipid levels.
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Hyperlipidemia refers to elevated levels of lipids or lipoproteins in the blood. It is caused by disorders involving elevations of lipoproteins such as low-density lipoprotein (LDL), very low-density lipoprotein (VLDL), and triglycerides. This puts one at risk for complications like atherosclerosis and pancreatitis. Treatment involves medications that lower LDL and triglyceride levels such as statins, resins, fibrates, and nicotinic acid. Each work by different mechanisms but commonly decrease lipid synthesis or increase lipid clearance to normalize lipid profiles and reduce cardiovascular risk. Side effects depend on the specific drug but may include gastrointestinal issues or myopathy.
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This document discusses various types of drugs used to treat hyperlipidemia. It begins by defining hyperlipidemia as a common disorder involving abnormal lipid metabolism that is a major cause of heart disease. It then describes several classes of antihyperlipidemic drugs, including HMG-CoA reductase inhibitors (statins), fibric acid derivatives, bile acid sequestrants, LDL oxidation inhibitors, and pyridine derivatives. For each class, examples of drugs are provided along with their mechanisms of action and effects on lipid levels.
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This document provides an overview of lipid metabolism and hypolipidemic drugs. It discusses lipids, lipoproteins, lipoprotein classification, lipid metabolism pathways including exogenous and endogenous pathways, atherogenesis, and drug therapy. The endogenous pathway can be separated into the atherogenic apo-B100 lipoprotein system and the antiatherogenic apo-A1 lipoprotein system. The document provides details on the structure and function of lipoproteins, their classification based on density and electrophoretic mobility, and the roles of apolipoproteins.
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The high risks of lipids and its relevance towards the development of different cardiovascular diseases has been known to all where this present slide focuses on that only along with the different treatment procedures,.
Antihyperlipidemic drugs
Lipids such as cholesterol and triglycerides are transported in the blood by lipoproteins including LDL and HDL. High LDL and low HDL are risk factors for atherosclerosis, where plaque builds up in the arteries. Several genetic disorders and secondary causes can lead to hyperlipidemia and abnormal lipoprotein levels. Treatment focuses on lowering LDL and triglycerides while raising HDL to reduce cardiovascular risk. Statins are commonly used drugs that lower cholesterol by inhibiting HMG-CoA reductase.
Antihyperlipidemic drugs
Hyperlipidemia is a common disorder caused by abnormalities in lipid metabolism or transport. It results in high levels of lipids like cholesterol and triglycerides in the blood. Hyperlipidemia is classified based on the abnormal lipid levels and is primarily treated through lifestyle changes and medications that lower lipid levels. Common drug classes used to treat hyperlipidemia work by inhibiting cholesterol synthesis, breaking down fats, or blocking lipid absorption.
Antilipemic Drug -Pharmacology ppt
This document summarizes several classes of antilipidemic drugs used to treat elevated blood lipids. It discusses bile-sequestering drugs like cholestyramine which bind to bile acids in the intestines. Fibric acid derivatives like fenofibrozate and gemfibrozil are used to reduce triglycerides and LDL. Statins like HMG-CoA reductase inhibitors block cholesterol production to lower LDL and increase HDL slightly. Ezetimibe inhibits cholesterol absorption from the intestines. Nicotinic acid lowers LDL and triglycerides while raising HDL but causes flushing as a side effect. All work in combination with lifestyle changes to reduce cardiovascular risks from high lipids.
Hypolipidemic drugs MBBS and PG Dr. Resu Neha Reddy
This PPT contains hypolipidaemic drugs explanation with all recent drugs and with lots of pictures, for better understanding of MBBS and PG students
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Lipids originate from either endogenous or exogenous sources. Dietary lipids are packaged into chylomicrons in the intestine and transported through the lymphatics and bloodstream. Chylomicrons are broken down by lipoprotein lipase, releasing fatty acids. Chylomicron remnants are taken up by the liver. The liver synthesizes and packages triglycerides and cholesterol into VLDLs, which circulate and release fatty acids. VLDLs become progressively denser LDLs that distribute cholesterol. HDLs remove cholesterol from tissues and transfer it back to the liver for disposal.
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Hypolipidaemic drugs
Dr. Nutanbala Goswami,
Associate proffecer,
Pharmacology Department,
Govt. medical college, Bhavnagar.
Fibrates - class, effects, side effects, drugs interactions, main indications...
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
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This document summarizes several herbal drugs that have anti-hyperlipidemic properties. It discusses artichoke, prosopis cineraria bark, and fenugreek. Artichoke contains sesquiterpenes and sesquiterpene glycosides that were found to suppress serum triglyceride elevation and inhibit gastric emptying, contributing to its anti-hyperlipidemic effects. Prosopis cineraria bark contains bioactive compounds and was shown to lower blood glucose and maintain lipid profile parameters in diabetic mice. Fenugreek contains fiber, saponins, and protein that are believed to contribute to its ability to significantly reduce total cholesterol, triglycerides, and LDL cholesterol in hyperlip
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This document discusses lipids and hyperlipidemia. It begins by explaining how chylomicrons, LDL, and HDL transport lipids between the intestines and cells. High levels of oxidized LDL can lead to atherosclerosis. Hyperlipidemia is characterized by abnormally high levels of fats and lipids in the blood. It causes atherosclerosis and conditions like heart disease. Various drugs are used to treat hyperlipidemia including statins, fibrates, niacin, bile acid sequestrants, and omega-3 fatty acids. The document explains the mechanisms of these drug classes.
Hypolipidemic agents
This document summarizes hypolipidemic agents used to treat various dyslipidemias and reduce cardiovascular risk. It discusses the physiology of lipid metabolism, pharmacological targets for lowering lipids, individual drug properties and combinations. Key drugs include statins, bile acid sequestrants, ezetimibe, niacin, fibrates and fish oils. The document also reviews use of these agents in special populations like children, women and diabetics.
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lipid metabolism, LDC-C targets level, treatment of dislipidemia, pathogenesis of dislipidemia, diagnosis of dislipidemia
Class hypolipidemics
This document discusses hyperlipidemia and its treatment. It begins by explaining how elevated lipid levels can lead to atherosclerosis and coronary artery disease. It then outlines different classes of drugs that target endogenous and exogenous cholesterol, including statins, fibrates, nicotinic acid, ezetemibe, and bile acid sequestrants. The mechanisms of action, indications, and adverse effects are described for each drug class. Combination therapies are also discussed.
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16.hypolipidemics
Statins like simvastatin and atorvastatin work by inhibiting HMG-CoA reductase and lowering cholesterol production in the liver. Bile acid sequestrants such as cholestyramine and colestipol bind bile acids in the gut. Ezetimibe decreases intestinal cholesterol absorption while statins lower endogenous production. Niacin can cause flushing and other side effects. Fibric acid derivatives like gemfibrozil and fenofibrate lower triglycerides and raise HDL levels but have potential side effects as well. Together, these classes of hypolipidemic drugs act through different mechanisms to lower cholesterol and lipid levels.
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This document provides information on hyperlipidemic drugs. It begins with an introduction to hyperlipidemia and its causes. It then discusses various drug classes for treating hyperlipidemia, including their mechanisms of action, effects on lipid levels, pharmacokinetics, therapeutic uses, adverse effects and interactions. The major drug classes discussed are HMG-CoA reductase inhibitors (statins), bile acid sequestrants, fibrates, and niacin. For each class, specific drugs are highlighted and their properties compared.
Hypolipidaemic drugs
Biochemistry, physiology and pathology of lipid metabolism in brief and its applied pharmacotherapeutics in details
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This document discusses various drugs used to treat hyperlipidemia. It describes how statins work by inhibiting cholesterol biosynthesis in the liver, leading to increased LDL receptor levels and lowered cholesterol. It also discusses other drugs like fibrates that lower triglycerides, bile acid sequestrants that lower cholesterol by increasing bile acid excretion, and niacin that reduces triglycerides and LDL while increasing HDL. The risks and mechanisms of these antihyperlipidemic drugs are summarized.
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This document outlines guidelines for screening and treating dyslipidemia. It discusses lipid handling in the body and pathophysiology of atherosclerosis. Current drug treatments include statins as first-line therapy, with bile acid sequestrants, nicotinic acid, fibrates, ezetimibe, and omega-3 fatty acids as alternatives. Newer drugs that inhibit PCSK9 are also mentioned. Treatment goals depend on risk level, with lifestyle changes recommended initially before adding drug therapy for higher risk patients.
Ppt hyperlipidimic
This document discusses lipid and cholesterol-lowering agents. It begins by defining hyperlipidemia and introducing lipid-lowering drugs, which lower lipid and lipoprotein levels in the blood to prevent cardiovascular disease. It then categorizes and describes different types of hyperlipidemia and the mechanisms of various drug classes, including HMG-CoA reductase inhibitors (statins), fibric acid derivatives, bile acid sequestrants, and nicotinic acid. Biological evaluation methods are outlined, such as inducing hyperlipidemia in rats and collecting blood and liver samples to analyze lipid parameters after treatment.
Hypolipidemic drugs
This document discusses hypolipidaemic drugs and plasma expanders. It begins by introducing cardiovascular diseases and dyslipidemia as major causes of morbidity and mortality. It then describes the classification, metabolism, and disorders of lipoproteins. The main sections discuss the pharmacotherapy of hyperlipidemias including statins, fibrates, nicotinic acid, ezetimibe, and other agents. Adverse effects and guidelines for use are provided. Management of shock includes types of shock and treatment approaches for hypovolaemic, cardiogenic, septic, anaphylactic, and neurogenic shock. Ideal properties and examples of plasma expanders like dextran are also summarized.
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This document discusses drug therapies for treating hyperlipidemia and dyslipidemia. It describes five major classes of drugs: statins, fibrates, niacin, bile acid sequestrants, and ezetimibe. Statins lower cholesterol by inhibiting the enzyme HMG-CoA reductase. Fibrates lower triglycerides and increase HDL by modulating lipid metabolism through PPAR receptors. Niacin lowers lipids by inhibiting lipolysis in adipose tissue. Bile acid sequestrants lower bile acid levels, increasing cholesterol conversion to bile acids. Ezetimibe lowers cholesterol absorption in the small intestine by inhibiting sterol transporters. The document provides details on the
Statins
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.
Anti hyperlipidemic agents
This document summarizes various lipid lowering drugs. It discusses the classification of these drugs and provides details about the mechanism of action, structure-activity relationships and synthesis of various classes of drugs. The main classes covered are HMG-CoA reductase inhibitors (statins), fibric acid derivatives, bile acid sequestrants, LDL oxidation inhibitors, nicotinic acid, plant sterols, and hormone replacement therapy. Key structural features and enzymes/pathways targeted by different drug classes are discussed.
Atorvastatin
Atorvastatin is a statin drug used to lower cholesterol and prevent cardiovascular events. It works by inhibiting HMG-CoA reductase in the liver to decrease cholesterol production. It is well absorbed orally but has low bioavailability. The liver metabolizes atorvastatin through CYP3A4 enzymes and excretes it primarily in bile. Grapefruit juice and certain other drugs can interact with atorvastatin metabolism. Its medical uses include treating various dyslipidemias and preventing heart attacks and strokes in those with risk factors like diabetes. Side effects may include muscle pain or weakness.
Atorvastatin
The SPARCL trial investigated whether high-dose atorvastatin (80 mg daily) could reduce the risk of fatal or non-fatal stroke in patients who had a stroke or transient ischemic attack 1-6 months prior and no history of coronary heart disease. The double-blind randomized controlled trial assigned 4731 eligible patients to atorvastatin or placebo groups. After a median follow-up of 4.9 years, treatment with atorvastatin reduced the risk of fatal or non-fatal stroke by 2% compared to placebo, with a number needed to treat of 53. Atorvastatin also reduced the risk of major cardiovascular events by 18% compared to placebo.
Statin
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.
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This patient presents with multiple metabolic risk factors including obesity, elevated triglycerides and fasting blood glucose, and a family history of diabetes. While she does not meet the criteria for metabolic syndrome, her 10-year risk of heart disease is elevated. Her LDL cholesterol goal according to NCEP guidelines is less than 160 mg/dL. Fasting glucose would be most influential in determining her treatment plan given her risk factors.
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This document discusses hyperlipidemia and cholesterol. It defines important acronyms like HDL, LDL, VLDL and cholesterol levels. It lists major risk factors for high cholesterol like smoking, family history, age and obesity. It discusses therapeutic agents to treat high cholesterol like statins, fibric acids, niacin and bile acid resins. It provides an overview of their mechanisms of action, dosages and side effects. It emphasizes the importance of dietary changes like reducing fat and alcohol intake and increasing fiber for overall cholesterol management.
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Management Strategies for Dyslipidemia & Sitosterolemia: Summarized Catchpoin...
This work mainly deals with cholesterol transport mechanisms, the various types of hyperlipoproteinemias, and the drugs used to combat cholesterol excess.
A very precise insight into drugs, their mechanisms, efficacy & adverse effects have been explained.
A separate section on NEWER DRUGS for hypercholesterolemia(including drugs in clinical trials) have also been mentioned.
A separate category on SITOSTEROLEMIA, their effects & management has been mentioned too.
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10 lipoprotein metabolism 2015
Lipoproteins are spherical complexes of lipids and proteins that transport lipids in the bloodstream. They are classified based on composition, density, and electrophoretic mobility into chylomicrons, very low density lipoproteins (VLDL), low density lipoproteins (LDL), high density lipoproteins (HDL), and free fatty acid-albumin complexes. Chylomicrons transport exogenous triglycerides from the intestine to tissues, VLDL transports endogenous triglycerides from the liver, LDL transports cholesterol to tissues, and HDL transports cholesterol from tissues back to the liver. Disorders in lipoprotein metabolism can result in hyperlipoproteinemias or hypolipopro
antihyper lipidemia & plantcons
This document discusses hyperlipidemia and various plant constituents that can help treat it. It begins by defining hyperlipidemia and listing some common causes. It then discusses the lipid regulation pathway and how various conditions like diabetes, hypothyroidism, and alcohol use can disrupt this pathway and cause hyperlipidemia. The document focuses on various polyphenolic compounds found in plants that have been shown to help treat hyperlipidemia by modulating the AMPK pathway and SREBP transcription factor to lower cholesterol synthesis and increase excretion. Specific polyphenols discussed include catechins, EGCG, and the Bergamot Polyphenol Fraction.
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Lecture-8.-Dyslipoproteinemias-and-Fatty-Liver.pptx
Lipid associated disorders include obesity, metabolic syndrome, fatty liver, atherosclerosis, and coronary heart diseases. They can be caused by nutritional imbalances, lifestyle habits, genetic abnormalities, or secondary to other diseases. Disorders are classified based on abnormal lipid concentrations, including hyperlipoproteinemias which have increased lipids and hypolipoproteinemias which have decreased lipids. Fatty liver disease occurs when excess lipids accumulate in liver cells, known as steatosis, and can progress to inflammation and fibrosis and even cirrhosis with repeated damage over time.
Hyperlipidaemia
Hyperlipidemia is high levels of lipids in the blood. The document discusses hyperlipidemia including types of lipids in the body, lipoproteins, causes of hyperlipidemia, diagnosis, and management. Specifically, it covers primary and secondary causes, Frederickson classification of lipid disorders, diagnostic tests and criteria, physical signs, lifestyle management including diet and exercise, and drug therapies such as statins, fibrates, nicotinic acid, and bile acid sequestrants.
Hyperlipidemia excess lipid
This document discusses hyperlipidemia, or high lipid levels, in various animal species. It defines hyperlipidemia and describes the most common form as postprandial, occurring after eating a meal high in fat. It explains that lipids are transported in the blood by lipoproteins, and the main classes of lipoproteins are chylomicrons, VLDLs, LDLs, and HDLs. Causes of hyperlipidemia in dogs include physiological responses, genetic factors, hypothyroidism, pancreatitis, Cushing's disease, and nephrotic syndrome. Symptoms in dogs range from no clinical signs to vomiting, diarrhea, and eye or neurological disorders. Feline fasting hyperlip
HDL
This document discusses lipoproteins and lipid profiles. It describes the different types of lipoproteins including HDL, LDL, VLDL, and chylomicrons. HDL is described as "good cholesterol" that removes cholesterol from the body, while LDL is described as "bad cholesterol" that deposits cholesterol in tissues and increases disease risk. Normal ranges for HDL and LDL are provided. Factors that influence lipid profiles like smoking, alcohol, medications, and medical conditions are also summarized.
Unit 4.ppt
Lipids are diverse molecules that include fatty acids, triglycerides, phospholipids, and steroids. They are insoluble in water due to their nonpolar characteristics. Lipids serve important structural and energy storage functions in cells. The main types of lipids are fatty acids, triglycerides, sterols like cholesterol, and phospholipids. Fatty acids can be saturated, monounsaturated, or polyunsaturated depending on the number of double bonds in their hydrocarbon chains. Triglycerides are composed of fatty acids esterified to a glycerol backbone and serve as long-term energy stores. Cholesterol is an important steroid lipid involved in membrane structure and synthesis of hormones and vitamins. Atheros
lipoprotein
Lipoproteins are biochemical assemblies that contain both lipids and proteins. They transport lipids through the blood and differ based on their density. The main types are LDL, HDL, chylomicrons, VLDL, and IDL. LDL transports cholesterol from the liver to tissues, while HDL transports excess cholesterol from tissues back to the liver in reverse transport. Chylomicrons transport dietary lipids from the intestine. VLDL transports endogenous lipids made by the liver. IDL forms from the degradation of VLDL and can convert to LDL. Each lipoprotein type plays a critical role in lipid metabolism and transport throughout the body.
LIPID_METABOLISM.pdf
Lipids are non-polar organic compounds that serve important structural and energy storage functions in living organisms. They are classified as simple or complex lipids and can be synthesized within cells or absorbed from digestion. The major sites of lipid metabolism are the liver, which synthesizes fatty acids and lipoproteins, and adipose tissue, which stores triglycerides for energy.
lipoprotein metabolism.pptx HDL METABOLISM, LDL METABOLIS, VLDL METABOLIS, C...
Lipoprotein introduction, their general characteristics, exogenous and endogenous metabolism focusing on chylomicron and vldl metabolism, ldl metabolism and HDL metabolism , reverse cholesterol transport.
Vbspu prabhakar singh first sem_ biochem unit iii_ lipids
Vbspu prabhakar singh first sem_ biochem unit iii_ lipidsDepartment of Biochemistry, Veer Bahadur Singh Purvanchal Univarsity, Jaunpur
This document provides information on lipids including fatty acids, phospholipids, sphingolipids, cerebrosides, steroids, bile acids, prostaglandins, waxes, terpenes, lipoamino acids, lipoproteins, proteolipids, and lipopolysaccharides. It discusses their structures, properties, functions, classification, and quantitative and qualitative estimation methods. Specific lipid types like fatty acids, glycerophospholipids, sphingolipids, bile acids, sterols, lipoproteins, and proteolipids are described in further detail including their production, roles in disease, and catabolism.Lipoprotein disorders and metabolic syndrome
Lipoprotein disorders and metabolic syndrome : obesity diabetes hypertension glucose tolerance statins weight insulin resistance
Medovahasrotodusti - Dyslipidemias
The document discusses dyslipidemia and lipid metabolism. It defines dyslipidemias as disorders of lipoprotein metabolism characterized by abnormal levels of cholesterol, triglycerides, or both. It then describes the different classes of lipoproteins involved in transporting lipids in the blood and the pathways of lipoprotein metabolism. The document further discusses classifications of dyslipidemias and various genetic and acquired causes that can lead to elevated or reduced levels of lipoproteins. Clinical features and management aspects are also briefly covered.
Lipoprotein
Lipoproteins are biochemical assemblies that transport hydrophobic lipid molecules in water and blood. They consist of a phospholipid and cholesterol outer shell with apolipoproteins embedded that stabilize the complex and determine its function. The main types of lipoproteins are chylomicrons, VLDL, IDL, LDL, and HDL, which differ in size, density, and lipid and protein composition. They enable the transport and metabolism of triglycerides, cholesterol, and other lipids throughout the body.
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Hypolipidemic pharmacology outline
- 2. EZETIMIBE 1. IN FOOD WE CONSUME CHOLESTEROL AND TG 2. IT IS ABSORBED IN INTESTINE, TAKEN BY LACTEALS 3. FROM LACTEALS CHOLESTEROL AND TG TAKEN THROUGH THORACIC DUCT TO BLOOD VESSEL WITH HELP OF CHYLOMICRONS 4. IN BLOOD VESSEL , LIPO PROTEIN LIPASE TG FATTY ACID + GLYCEROL FATTY ACID TAKEN UP BY ADIPOSE CELLS AND GETS CONVERTED TO TG AGAIN FIBRATES
- 3. 5. REMANANT CHYLOMICRON ENTERS THE LIVER 6. LIVER SECRETE TG AND CHOLESTEROL INTO BLOOD VESSEL AS VLDL 7. THIS TG AGAIN GETS METABOLISED IN BLOOD VESSEL BY LPL 8. THUS NOW VLDL NOW CHANGES TO IDL TAKEN BACK TO LIVER IDL CONVERSION TO LDL CONTAINING ONLY CHOLESTEROL AND DISTRIBUTED TO VARIOUS TISSUE LPL
- 4. 9. HDL CARRIES CHOLESTEROL FROM PERIPHERY TO LIVER 10.CHOLESTEROL IS EXCRETED IN BILE IN FREE FORM AND AS BILE SALTS 11.BILE SALTS UNDERGO ENTEROHEPATIC CIRCULATION BILE ACID BINDING RESINS
- 5. • STATINS – INHIBIT HMG CO-A • NIACIN – INHIBIT LIPOLYSIS IN ADIPOSE TISSUE .
- 6. DRUGS • STATINS ( LDL ) • BILE ACID BINDING RESINS • INTESTINAL CHOLESTEROL ABSORPTION INHIBITORS - EZETIMIBE • FIBRATES (TG) • NIACIN (HDL)
- 7. HYPER LIPOPROTEINEMIA • PRIMARY • SECONDARY
- 8. TYPE 1 – FAMILIAL LIPOPROTEIN LIPASE DEFICIENCY TYPE 2A – FAMILIAL HYPER- LDL CHOLESTROLEMIA TYPE 2B – FAMILIAL COMBINED- VLDL , LDL HYPERLIPIDEMIA TYPE 3 – FAMILIAL DYSBETA- Mutation LIPOPROTEINEMIA TYPE 4 –FAMILIAL VLDL HYPERTRIGLYCERIDEMIA TYPE 5 – FAMILIAL MIXED VLDL , CM HYPERTRIGLYCERIDEMIA
- 9. STATINS • MECHANISM • DRUGS – PRAVASTATIN , ATORVASTATIN • PHARMACOKINETICS – ORALLY, M-LIVER , E- KIDNEY • USES – PLEOTROPIC EFFECT , PRAVASTATIN FIBRINOGEN LEVEL • A/E – HEPATOTOXITY , MYOPATHY AND RABDOMYOLYSIS ( PRAVASTATIN )
- 10. BILE ACID BINDING RESINS • MECHANISM • DRUGS – CHOLESTYRAMINE , COLESTIPOL • PHARMACOKINETICS – ORALLY , EXCRETED IN FAECES • A/E- FLATULENCE AND CONSTIPATION
- 11. INTESTINAL CHOLESTEROL ABSORPTION INHIBITOR • MECHANISM • DRUGS - EZETIMIBE • PHARMACOKINETICS – ORALLY , EXCRETED IN BILE
- 12. FIBRATES • MECHANISM • DRUGS – GEMFIBROZIL , FENOFIBRATE • PHARMACOKINETICS – ORALLY , M- LIVER , E –URINE • USE –FIBRATES PLASMA FIBRINOGEN , HYPERURICEMIA • A/E – MYOPATHY
- 13. NIACIN • MECHANISM • PHARMACOKINETICS – ORALLY , M- LIVER , E -URINE • A/E – FLUSHING , HYPERURICEMIA , HEPATOTOXITY
- 15. THANKYOU…..