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
- Cardiovascular disease is the leading cause of death worldwide, with coronary heart disease being the main cause of death in CVD patients.
- High total plasma cholesterol, elevated LDL levels, and low HDL levels are important risk factors for coronary heart disease.
- Antidyslipidemic drugs are used to treat dyslipidemias and reduce the risk of cardiovascular disease by lowering LDL and triglyceride levels and raising HDL levels. These drugs include statins, fibrates, nicotinic acids, bile acid sequestrants, and ezetimibe.
This document summarizes different types of oral hypoglycemic agents (drugs used to lower blood glucose levels orally). It discusses sulfonylureas, biguanides, meglitinides, thiazolidinediones, and alpha-glucosidase inhibitors. For each class, it describes the mechanism of action, pharmacokinetics, adverse drug reactions, and examples of drugs from each class like glibenclamide, metformin, repaglinide, rosiglitazone, and acarbose. It also briefly mentions newer anti-diabetic drugs like SGLT-2 inhibitors, DPP-4 inhibitors, and GLP-1 receptor agonists that have been approved
A condition in which the heart is unable to pump sufficient blood
to meet the metabolic demand of the body and also unable to receive it back because every time after a systole.
This presentation discusses HMG-CoA reductase inhibitors, also known as statins. It begins with an introduction to hyperlipidemia and its risk factors. It then discusses atorvastatin as the prototype statin drug, and provides examples of other statins. The presentation explains that statins work by inhibiting the HMG-CoA reductase enzyme, which lowers cholesterol synthesis and raises LDL receptor levels, reducing LDL cholesterol. Adverse effects can include increased liver enzymes, myopathy, and interactions with other drugs. The presentation concludes by thanking the audience.
This document outlines information about the anticoagulant drug warfarin. It discusses that warfarin was discovered after cows ate spoiled clover and died of hemorrhaging. Warfarin works by inhibiting vitamin K epoxide reductase, preventing vitamin K from being reduced to its active form and inhibiting coagulation factors II, VII, IX, and X. It has a nearly 100% oral bioavailability and is highly protein bound. Warfarin is used to prevent thromboembolic disorders and is monitored through prothrombin time and INR levels. It can cause bleeding and interacts with many other drugs through pharmacokinetic and pharmacodynamic mechanisms. Overdose is managed by stopping the drug and administer
Sulfonylureas are oral hypoglycemic drugs that enhance insulin secretion from the pancreas. They work by blocking ATP-sensitive potassium channels in pancreatic beta cells, which leads to insulin release. Common side effects include hypoglycemia and weight gain. Examples include glibenclamide, glipizide, and glimepiride. Choice of sulfonylurea depends on factors like duration of action, renal function, and patient age. They are generally effective treatments for type 2 diabetes but require caution in elderly patients or those with kidney/liver problems.
This document discusses antihyperlipidemic drugs used to treat hyperlipidemia. It begins by defining hyperlipidemia and describing risk factors. It then covers the various classes of lipid-lowering drugs including HMG-CoA reductase inhibitors (statins), bile acid sequestrants, fibrates, nicotinic acid, cholesterol absorption inhibitors, and PCSK9 inhibitors. For each class, it provides examples of drugs, their mechanisms of action, therapeutic uses, and major side effects and drug interactions. The document concludes with recommendations on drug therapy and monitoring treatment effectiveness.
This document discusses oral hypoglycemic drugs and insulin used to treat diabetes. It describes the two main types of diabetes - type 1 caused by insulin deficiency and type 2 caused by insulin resistance. The document outlines several classes of oral hypoglycemic drugs including biguanides, sulfonylureas, meglitinides, thiazolidinediones, and alpha-glucosidase inhibitors. It provides details on the mechanism of action, pharmacokinetics, effects and side effects of drugs from each class.
- Cardiovascular disease is the leading cause of death worldwide, with coronary heart disease being the main cause of death in CVD patients.
- High total plasma cholesterol, elevated LDL levels, and low HDL levels are important risk factors for coronary heart disease.
- Antidyslipidemic drugs are used to treat dyslipidemias and reduce the risk of cardiovascular disease by lowering LDL and triglyceride levels and raising HDL levels. These drugs include statins, fibrates, nicotinic acids, bile acid sequestrants, and ezetimibe.
This document summarizes different types of oral hypoglycemic agents (drugs used to lower blood glucose levels orally). It discusses sulfonylureas, biguanides, meglitinides, thiazolidinediones, and alpha-glucosidase inhibitors. For each class, it describes the mechanism of action, pharmacokinetics, adverse drug reactions, and examples of drugs from each class like glibenclamide, metformin, repaglinide, rosiglitazone, and acarbose. It also briefly mentions newer anti-diabetic drugs like SGLT-2 inhibitors, DPP-4 inhibitors, and GLP-1 receptor agonists that have been approved
A condition in which the heart is unable to pump sufficient blood
to meet the metabolic demand of the body and also unable to receive it back because every time after a systole.
This presentation discusses HMG-CoA reductase inhibitors, also known as statins. It begins with an introduction to hyperlipidemia and its risk factors. It then discusses atorvastatin as the prototype statin drug, and provides examples of other statins. The presentation explains that statins work by inhibiting the HMG-CoA reductase enzyme, which lowers cholesterol synthesis and raises LDL receptor levels, reducing LDL cholesterol. Adverse effects can include increased liver enzymes, myopathy, and interactions with other drugs. The presentation concludes by thanking the audience.
This document outlines information about the anticoagulant drug warfarin. It discusses that warfarin was discovered after cows ate spoiled clover and died of hemorrhaging. Warfarin works by inhibiting vitamin K epoxide reductase, preventing vitamin K from being reduced to its active form and inhibiting coagulation factors II, VII, IX, and X. It has a nearly 100% oral bioavailability and is highly protein bound. Warfarin is used to prevent thromboembolic disorders and is monitored through prothrombin time and INR levels. It can cause bleeding and interacts with many other drugs through pharmacokinetic and pharmacodynamic mechanisms. Overdose is managed by stopping the drug and administer
Sulfonylureas are oral hypoglycemic drugs that enhance insulin secretion from the pancreas. They work by blocking ATP-sensitive potassium channels in pancreatic beta cells, which leads to insulin release. Common side effects include hypoglycemia and weight gain. Examples include glibenclamide, glipizide, and glimepiride. Choice of sulfonylurea depends on factors like duration of action, renal function, and patient age. They are generally effective treatments for type 2 diabetes but require caution in elderly patients or those with kidney/liver problems.
This document discusses antihyperlipidemic drugs used to treat hyperlipidemia. It begins by defining hyperlipidemia and describing risk factors. It then covers the various classes of lipid-lowering drugs including HMG-CoA reductase inhibitors (statins), bile acid sequestrants, fibrates, nicotinic acid, cholesterol absorption inhibitors, and PCSK9 inhibitors. For each class, it provides examples of drugs, their mechanisms of action, therapeutic uses, and major side effects and drug interactions. The document concludes with recommendations on drug therapy and monitoring treatment effectiveness.
This document discusses oral hypoglycemic drugs and insulin used to treat diabetes. It describes the two main types of diabetes - type 1 caused by insulin deficiency and type 2 caused by insulin resistance. The document outlines several classes of oral hypoglycemic drugs including biguanides, sulfonylureas, meglitinides, thiazolidinediones, and alpha-glucosidase inhibitors. It provides details on the mechanism of action, pharmacokinetics, effects and side effects of drugs from each class.
This document discusses antihyperlipidemic agents used to treat hyperlipidemia, a condition of high lipid levels in the blood. It begins by defining hyperlipidemia and describing its causes such as diet, genetics, and medical conditions. It then covers the main classes of antihyperlipidemic drugs like HMG CoA inhibitors, fibrates, bile acid sequesterants, and their mechanisms and examples like lovastatin, atorvastatin, clofibrate, and cholestyramine. The document concludes by explaining how these drugs work to lower lipid levels through inhibiting cholesterol synthesis and absorption or increasing lipid catabolism.
This document discusses various drug classes used to treat type 2 diabetes, including their mechanisms of action, pharmacokinetics, and side effects. It describes sulfonylureas, metformin, thiazolidinediones, meglitinide analogues, DPP-4 inhibitors, GLP-1 receptor agonists, alpha-glucosidase inhibitors, amylin analogues, and SGLT2 inhibitors. For each class, it provides details on representative drugs, how they work, considerations around use, and common adverse effects. The document aims to comprehensively cover oral and injectable pharmacologic options for managing hyperglycemia in type 2 diabetes.
Hypolipidemic agents, also known as cholesterol-lowering drugs or antihyperlipidemic agents, are a diverse group of pharmaceuticals that are used in the treatment of high levels of fats (lipids), such as cholesterol, in the blood (hyperlipidemia). They are also called lipid-lowering drugs.
Macrolides are a class of antibiotics derived from Saccharopolyspora erythraea (originally called Streptomyces erythreus), a type of soil-borne bacteria.
This document discusses various immunosuppressant drugs, including their mechanisms of action and uses. It describes how immunosuppressants work by inhibiting T cell activation through mechanisms such as blocking co-stimulatory signals, inhibiting cytokine production or action, and inhibiting purine or pyrimidine synthesis. Common immunosuppressants mentioned include calcineurin inhibitors like cyclosporine and tacrolimus, mTOR inhibitors like sirolimus, corticosteroids, purine synthesis inhibitors like mycophenolate mofetil and azathioprine, co-stimulation inhibitors like abatacept, and antibodies against T cell surface molecules. The document provides details on the mechanisms, uses, and side effects of these
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.
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 body fluid compartments and their compositions. It notes that total body water makes up 60% of body weight, with two thirds located intracellularly and one third extracellularly. The extracellular fluid consists of interstitial fluid and blood plasma. Key electrolytes like sodium, potassium, calcium, and chloride are discussed along with their concentrations in plasma, interstitial, and intracellular fluids. Various volume expanders used to increase blood volume are also described, including crystalloids like saline and lactated Ringer's, as well as colloids like albumin, dextrans, gelatin, hydroxyethyl starch, and polyvinylpyrrolidone. Their mechanisms of action, properties, uses,
Autacoids - pharmacological actions and drugs related to them. SIVASWAROOP YARASI
Autacoids or "autocoids" are biological factors which act like local hormones, have a brief duration, and act near the site of synthesis. The word autacoids comes from the Greek "autos" (self) and "acos" (relief, i.e. drug).
These are antibiotics having a macrocyclic
lactone ring with attached sugars. Erythromycin
is the first member discovered in the 1950s,
Roxithromycin, Clarithromycin and Azithromycin
are the later additions. Antimicrobial spectrum is narrow,
includes mostly gram-positive and a few gramnegative
bacteria, and overlaps considerably with
that of penicillin G. Erythromycin is highly active
against Str. pyogenes and Str. pneumoniae, N.
gonorrhoeae, Clostridia, C. diphtheriae and
Listeria, but penicillin-resistant Staphylococci
and Streptococci are now resistant to erythromycin
also.
All cocci readily develop resistance
to erythromycin, mostly by acquiring the
capacity to pump it out. Resistant Enterobacteriaceae
have been found to produce an erythromycin
esterase. Alteration in the ribosomal binding
site for erythromycin by a plasmid encoded
methylase enzyme is an important mechanism of
resistance in gram-positive bacteria. All the above
types of resistance are plasmid mediated. Change
in the 50S ribosome by chromosomal mutation
reducing macrolide binding a
Fibrinolytics such as streptokinase, urokinase, alteplase, reteplase, and tenecteplase activate the natural fibrinolytic system and lyse thrombi to recanalize occluded blood vessels. They are used to treat myocardial infarction, deep vein thrombosis, pulmonary embolism, and peripheral arterial occlusion. Antifibrinolytics like epsilon amino-caproic acid and tranexamic acid inhibit plasminogen activation and clot dissolution to prevent or control bleeding caused by fibrinolytics or surgical procedures. The timing of fibrinolytic administration is critical for heart attack treatment, with better outcomes seen within 1-3 hours of symptom onset.
1) Peptic ulcers are caused by an imbalance between aggressive factors like gastric acid and protective factors in the stomach and duodenum.
2) Anti-ulcer drugs work by decreasing gastric acid secretion, enhancing mucosal protection, or eradicating the H. pylori bacteria responsible for many ulcers.
3) Common classes of anti-ulcer medications include H2 receptor antagonists, proton pump inhibitors, antacids, and anti-H. pylori drugs. H2 receptor antagonists and proton pump inhibitors reduce acid by blocking histamine and the proton pump, while antacids neutralize existing acid.
This document discusses antiarrhythmic drugs used to treat irregular heart rhythms or arrhythmias. It describes the mechanisms that can cause arrhythmias such as enhanced pacemaker activity, after-depolarizations, and reentry. It then covers the major classes of antiarrhythmic drugs including class I sodium channel blockers, class II beta blockers, class III potassium channel blockers, and class IV calcium channel blockers. Specific drugs from each class are discussed, how they work, their therapeutic uses, and potential side effects. Common arrhythmias like atrial fibrillation, atrial flutter, and ventricular tachycardia are also defined.
This document summarizes different drugs used for treating diabetes. It discusses the types of diabetes, mechanisms and types of insulin preparations including rapid-acting, intermediate-acting, and long-acting insulins. It also covers oral antidiabetic drugs like sulfonylureas, meglitinides, DPP-4 inhibitors, metformin, thiazolidinediones, alpha-glucosidase inhibitors, and SGLT-2 inhibitors; describing their mechanisms of action, pharmacokinetics and adverse effects. It concludes by listing common oral hypoglycemic agents and their usual daily doses and frequencies.
The document discusses proton pump inhibitors (PPIs) which inhibit gastric acid secretion by blocking the hydrogen-potassium ATPase pump in the stomach. PPIs are converted to sulfoxide derivatives that covalently bind to cysteine residues on the pump, preventing it from pumping protons into the stomach lumen. Common PPIs mentioned are omeprazole, pantoprazole, rabeprazole, and lansoprazole. Each drug is used to treat various acid-related gastrointestinal conditions such as heartburn, GERD, and ulcers. The mechanism of action involves the covalent inhibition of the proton pump through binding of activated PPIs to the pump.
5-Hydroxytryptamine & it’s Antagonist is a Topic in Pharmacology which will defiantly Help You in pharmacy field All information is related to pharmacology drug acting and it's effect on body. it is collage project given by our department i would like to share with you.
This document discusses various drugs used to lower lipid levels. It begins by listing the main classes of lipid-lowering drugs: statins, fibric acid derivatives, niacin, and bile acid sequestrants. It then provides details on the mechanisms and effects of specific drugs. Statins work by inhibiting HMG-CoA reductase and increasing LDL receptor expression. Fibrates activate lipoprotein lipase. Ezetimibe inhibits cholesterol absorption. Bile acid sequestrants bind bile acids in the gut. Niacin stimulates a receptor on adipocytes that decreases free fatty acid release from fat cells and lowers triglyceride and LDL levels while increasing HDL. All work to ultimately lower
This document discusses volume of distribution (Vd), which is the apparent volume required to achieve a desired drug concentration in the body. It provides examples of calculating Vd based on drug dose and desired concentration in a fish tank or human patient. Factors that influence Vd include drug properties, patient characteristics, and physiological/pathological conditions. Vd can be single or multiple compartments, and its clinical significance includes determining loading doses and differences between pediatric/adult or obese/normal dosing. Special tissue compartments and redistribution are also discussed. In conclusion, understanding Vd aids in dosing drugs that require loading doses or are affected by protein binding and tissue storage.
Phytochemical screening and evaluation of aphrodisiac and antihyperlipidemic ...Srota Dawn
This document discusses a dissertation submitted to Vels University in partial fulfillment of the requirements for a Master of Pharmacy degree. The dissertation involves phytochemical screening and evaluation of the aphrodisiac and antihyperlipidemic activities of a polyherbal extract containing Daucus carota sativus seeds, Musa paradisiaca sapientum stem, and Cucumis melo peel. It provides background on the plants and certificates from the dissertation guide and university directors.
This document discusses animal models used to study obesity. It begins by defining overweight and obesity according to BMI thresholds set by WHO. It then describes the pathophysiology of obesity and various animal models used to study it, including diet-induced, hypothalamic, virus-induced, genetic, transgenic, and in vitro models. Specific details are provided about procedures and parameters examined for several models, such as how diet-induced and hypothalamic models work. Genetic models discussed include yellow mouse, Zucker rat, and transgenic knockout models. In vitro models described aim to study metabolic activity in brown adipose tissue, beta-3 agonism, neuropeptide Y, and the role of leptin.
This document discusses antihyperlipidemic agents used to treat hyperlipidemia, a condition of high lipid levels in the blood. It begins by defining hyperlipidemia and describing its causes such as diet, genetics, and medical conditions. It then covers the main classes of antihyperlipidemic drugs like HMG CoA inhibitors, fibrates, bile acid sequesterants, and their mechanisms and examples like lovastatin, atorvastatin, clofibrate, and cholestyramine. The document concludes by explaining how these drugs work to lower lipid levels through inhibiting cholesterol synthesis and absorption or increasing lipid catabolism.
This document discusses various drug classes used to treat type 2 diabetes, including their mechanisms of action, pharmacokinetics, and side effects. It describes sulfonylureas, metformin, thiazolidinediones, meglitinide analogues, DPP-4 inhibitors, GLP-1 receptor agonists, alpha-glucosidase inhibitors, amylin analogues, and SGLT2 inhibitors. For each class, it provides details on representative drugs, how they work, considerations around use, and common adverse effects. The document aims to comprehensively cover oral and injectable pharmacologic options for managing hyperglycemia in type 2 diabetes.
Hypolipidemic agents, also known as cholesterol-lowering drugs or antihyperlipidemic agents, are a diverse group of pharmaceuticals that are used in the treatment of high levels of fats (lipids), such as cholesterol, in the blood (hyperlipidemia). They are also called lipid-lowering drugs.
Macrolides are a class of antibiotics derived from Saccharopolyspora erythraea (originally called Streptomyces erythreus), a type of soil-borne bacteria.
This document discusses various immunosuppressant drugs, including their mechanisms of action and uses. It describes how immunosuppressants work by inhibiting T cell activation through mechanisms such as blocking co-stimulatory signals, inhibiting cytokine production or action, and inhibiting purine or pyrimidine synthesis. Common immunosuppressants mentioned include calcineurin inhibitors like cyclosporine and tacrolimus, mTOR inhibitors like sirolimus, corticosteroids, purine synthesis inhibitors like mycophenolate mofetil and azathioprine, co-stimulation inhibitors like abatacept, and antibodies against T cell surface molecules. The document provides details on the mechanisms, uses, and side effects of these
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.
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 body fluid compartments and their compositions. It notes that total body water makes up 60% of body weight, with two thirds located intracellularly and one third extracellularly. The extracellular fluid consists of interstitial fluid and blood plasma. Key electrolytes like sodium, potassium, calcium, and chloride are discussed along with their concentrations in plasma, interstitial, and intracellular fluids. Various volume expanders used to increase blood volume are also described, including crystalloids like saline and lactated Ringer's, as well as colloids like albumin, dextrans, gelatin, hydroxyethyl starch, and polyvinylpyrrolidone. Their mechanisms of action, properties, uses,
Autacoids - pharmacological actions and drugs related to them. SIVASWAROOP YARASI
Autacoids or "autocoids" are biological factors which act like local hormones, have a brief duration, and act near the site of synthesis. The word autacoids comes from the Greek "autos" (self) and "acos" (relief, i.e. drug).
These are antibiotics having a macrocyclic
lactone ring with attached sugars. Erythromycin
is the first member discovered in the 1950s,
Roxithromycin, Clarithromycin and Azithromycin
are the later additions. Antimicrobial spectrum is narrow,
includes mostly gram-positive and a few gramnegative
bacteria, and overlaps considerably with
that of penicillin G. Erythromycin is highly active
against Str. pyogenes and Str. pneumoniae, N.
gonorrhoeae, Clostridia, C. diphtheriae and
Listeria, but penicillin-resistant Staphylococci
and Streptococci are now resistant to erythromycin
also.
All cocci readily develop resistance
to erythromycin, mostly by acquiring the
capacity to pump it out. Resistant Enterobacteriaceae
have been found to produce an erythromycin
esterase. Alteration in the ribosomal binding
site for erythromycin by a plasmid encoded
methylase enzyme is an important mechanism of
resistance in gram-positive bacteria. All the above
types of resistance are plasmid mediated. Change
in the 50S ribosome by chromosomal mutation
reducing macrolide binding a
Fibrinolytics such as streptokinase, urokinase, alteplase, reteplase, and tenecteplase activate the natural fibrinolytic system and lyse thrombi to recanalize occluded blood vessels. They are used to treat myocardial infarction, deep vein thrombosis, pulmonary embolism, and peripheral arterial occlusion. Antifibrinolytics like epsilon amino-caproic acid and tranexamic acid inhibit plasminogen activation and clot dissolution to prevent or control bleeding caused by fibrinolytics or surgical procedures. The timing of fibrinolytic administration is critical for heart attack treatment, with better outcomes seen within 1-3 hours of symptom onset.
1) Peptic ulcers are caused by an imbalance between aggressive factors like gastric acid and protective factors in the stomach and duodenum.
2) Anti-ulcer drugs work by decreasing gastric acid secretion, enhancing mucosal protection, or eradicating the H. pylori bacteria responsible for many ulcers.
3) Common classes of anti-ulcer medications include H2 receptor antagonists, proton pump inhibitors, antacids, and anti-H. pylori drugs. H2 receptor antagonists and proton pump inhibitors reduce acid by blocking histamine and the proton pump, while antacids neutralize existing acid.
This document discusses antiarrhythmic drugs used to treat irregular heart rhythms or arrhythmias. It describes the mechanisms that can cause arrhythmias such as enhanced pacemaker activity, after-depolarizations, and reentry. It then covers the major classes of antiarrhythmic drugs including class I sodium channel blockers, class II beta blockers, class III potassium channel blockers, and class IV calcium channel blockers. Specific drugs from each class are discussed, how they work, their therapeutic uses, and potential side effects. Common arrhythmias like atrial fibrillation, atrial flutter, and ventricular tachycardia are also defined.
This document summarizes different drugs used for treating diabetes. It discusses the types of diabetes, mechanisms and types of insulin preparations including rapid-acting, intermediate-acting, and long-acting insulins. It also covers oral antidiabetic drugs like sulfonylureas, meglitinides, DPP-4 inhibitors, metformin, thiazolidinediones, alpha-glucosidase inhibitors, and SGLT-2 inhibitors; describing their mechanisms of action, pharmacokinetics and adverse effects. It concludes by listing common oral hypoglycemic agents and their usual daily doses and frequencies.
The document discusses proton pump inhibitors (PPIs) which inhibit gastric acid secretion by blocking the hydrogen-potassium ATPase pump in the stomach. PPIs are converted to sulfoxide derivatives that covalently bind to cysteine residues on the pump, preventing it from pumping protons into the stomach lumen. Common PPIs mentioned are omeprazole, pantoprazole, rabeprazole, and lansoprazole. Each drug is used to treat various acid-related gastrointestinal conditions such as heartburn, GERD, and ulcers. The mechanism of action involves the covalent inhibition of the proton pump through binding of activated PPIs to the pump.
5-Hydroxytryptamine & it’s Antagonist is a Topic in Pharmacology which will defiantly Help You in pharmacy field All information is related to pharmacology drug acting and it's effect on body. it is collage project given by our department i would like to share with you.
This document discusses various drugs used to lower lipid levels. It begins by listing the main classes of lipid-lowering drugs: statins, fibric acid derivatives, niacin, and bile acid sequestrants. It then provides details on the mechanisms and effects of specific drugs. Statins work by inhibiting HMG-CoA reductase and increasing LDL receptor expression. Fibrates activate lipoprotein lipase. Ezetimibe inhibits cholesterol absorption. Bile acid sequestrants bind bile acids in the gut. Niacin stimulates a receptor on adipocytes that decreases free fatty acid release from fat cells and lowers triglyceride and LDL levels while increasing HDL. All work to ultimately lower
This document discusses volume of distribution (Vd), which is the apparent volume required to achieve a desired drug concentration in the body. It provides examples of calculating Vd based on drug dose and desired concentration in a fish tank or human patient. Factors that influence Vd include drug properties, patient characteristics, and physiological/pathological conditions. Vd can be single or multiple compartments, and its clinical significance includes determining loading doses and differences between pediatric/adult or obese/normal dosing. Special tissue compartments and redistribution are also discussed. In conclusion, understanding Vd aids in dosing drugs that require loading doses or are affected by protein binding and tissue storage.
Phytochemical screening and evaluation of aphrodisiac and antihyperlipidemic ...Srota Dawn
This document discusses a dissertation submitted to Vels University in partial fulfillment of the requirements for a Master of Pharmacy degree. The dissertation involves phytochemical screening and evaluation of the aphrodisiac and antihyperlipidemic activities of a polyherbal extract containing Daucus carota sativus seeds, Musa paradisiaca sapientum stem, and Cucumis melo peel. It provides background on the plants and certificates from the dissertation guide and university directors.
This document discusses animal models used to study obesity. It begins by defining overweight and obesity according to BMI thresholds set by WHO. It then describes the pathophysiology of obesity and various animal models used to study it, including diet-induced, hypothalamic, virus-induced, genetic, transgenic, and in vitro models. Specific details are provided about procedures and parameters examined for several models, such as how diet-induced and hypothalamic models work. Genetic models discussed include yellow mouse, Zucker rat, and transgenic knockout models. In vitro models described aim to study metabolic activity in brown adipose tissue, beta-3 agonism, neuropeptide Y, and the role of leptin.
This document discusses hyperlipidemias, which are elevated lipid levels in the blood. It defines the different types of hyperlipidemias, including familial forms caused by genetic defects and those related to lifestyle. Consequences of hyperlipidemia include heart disease. The document outlines normal lipid levels and describes the six main types of hyperlipidemias in terms of their causes and treatments. It concludes by classifying common drugs used to treat hyperlipidemias.
This document discusses screening methods for anti-obesity drugs using animal models. It outlines the need for new anti-obesity drugs given the growing obesity epidemic and lack of new FDA-approved drugs. Ideal animal models replicate human obesity pathophysiology through representative genetics, environment, and behaviors. No single model exists, so different models are used including diet-induced, genetic, viral-induced, and transgenic models. Parameters assessed include food intake, weight, adipose tissue, and metabolic markers. In vitro assays also study targets like uncoupling proteins and neuropeptides using cell and tissue samples. Animal models provide insights despite limitations but human clinical trials remain necessary.
The document discusses OECD Guideline 423 for acute oral toxicity testing. It outlines that the guideline uses a stepwise testing process with only 3 animals per step to classify chemicals according to their toxicity while minimizing animal use. The testing involves observing animals for signs of toxicity after administering chemical doses and determining subsequent dose levels based on mortality responses. The goal is to classify chemicals according to the globally harmonized system to improve knowledge of hazardous chemicals.
This document discusses corticosteroid hormones including their classification, mechanisms of action, effects, therapeutic uses, and adverse effects. It covers mineralocorticoids such as aldosterone and fludrocortisone, glucocorticoids such as cortisol and synthetic derivatives, their effects on metabolism, inflammation, and more. Precautions for glucocorticoid therapy and drug interactions are also summarized.
This document discusses screening methods for anti-obesity drugs. It outlines the need for new anti-obesity drugs due to the growing obesity epidemic. Both in vivo and in vitro models are used to screen drugs. In vivo models include diet-induced obesity in rodents, hypothalamic lesions, virus-induced obesity, and genetic models like yellow obese mice. Parameters assessed include food intake, body weight, adipose tissue analysis, and blood biomarkers. In vitro assays study metabolic pathways in adipose tissue and cell lines. While no single model captures all aspects of human obesity, together these methods aim to better understand obesity pathophysiology and identify new drug targets.
This document provides an overview of toxicity testing methods for acute, subacute, and chronic toxicity studies. It discusses the importance and history of toxicity testing, as well as standard methods and guidelines established by organizations like OECD and EPA. A variety of in vivo and in vitro toxicity tests are described, including acute, repeated dose, genotoxicity, carcinogenicity, and local toxicity studies. The document also addresses the large number of animals used annually for toxicity testing globally and the regulatory framework for animal testing in India.
Hypolipidaemics pharmacology with a note on Statins /Fibrates/ Sterol absorption Inhibitors/ CETP Inhibitors / Lipoprotein Lipase activators and Bile acid sequestrants
Antihyperlipidimic drug therapy-current and noval approaches.pptxMohammedObaidMohiudd
This document outlines a seminar presentation on current and novel approaches for treating dyslipidemia. It discusses the relationship between different lipids like LDL, HDL, and triglycerides and cardiovascular disease risk. It then summarizes the current drug therapies for dyslipidemia which lower LDL cholesterol through statins, bile acid sequestrants, ezetimibe, and nicotinic acid. Novel drug targets and approaches being researched are also highlighted, including monoclonal antibodies against PCSK9 to further lower LDL, as well as strategies to increase HDL through CETP inhibitors, vaccines, and HDL mimetics. The conclusion emphasizes the need for new biomarkers and trials to monitor progression of atherosclerosis with these novel therapies.
Hyperlipidemia , dyslipidemia , and drug therapy
also Fat transport and metabolisim and pathophysiology of lipoprotein
clincal importance of
1. Hypertriglycredemia
2. Hypercholesterolemia
3.Combined hyperlipidemia
4. Some other lipoprotein disorders
Including disorder of HDL_C
This document summarizes key aspects of lipid metabolism and hyperlipidemia management. It defines lipids and lipoproteins, describes their normal roles and abnormalities. Mechanisms and examples of different drug classes for treating hyperlipidemia are provided, including statins, fibrates, bile acid sequestrants, nicotinic acid, ezetimibe, and PCSK9 inhibitors. Their mechanisms, therapeutic uses, side effects and drug interactions are concisely outlined. Non-drug management including lifestyle changes and therapeutic lifestyle counseling are also mentioned.
This document provides information on hypolipidemic drugs used to treat dyslipidemia and cardiovascular disease. It discusses the classification and mechanisms of action of major drug classes, including statins, bile acid sequestrants, fibrates, nicotinic acid, ezetimibe, and newer drugs. Adverse effects and guidelines for use are also summarized. The document aims to inform readers about lipid-lowering pharmacotherapy and lipid level targets for reducing cardiovascular risk.
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.
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.
This document summarizes different classes of hypolipidemic drugs used to lower lipid levels in the blood. It discusses statins, bile acid sequestrants, nicotinic acid, fibrates, and other drugs. Statins are the most effective and best tolerated class, lowering LDL cholesterol by inhibiting HMG-CoA reductase. Bile acid sequestrants lower cholesterol indirectly by interrupting bile acid reabsorption. Nicotinic acid is unique in its ability to significantly raise HDL cholesterol levels in addition to lowering triglycerides and other lipid levels. Fibrates primarily work by activating lipoprotein lipase to break down triglyceride-rich lipoproteins.
This document discusses hypolipidemic agents used to treat high cholesterol and triglycerides. It begins by describing cholesterol and lipoproteins, then covers atherosclerosis and its causes. Various drug classes are explained in depth, including HMG-CoA reductase inhibitors (statins), bile acid sequestrants, fibrates, nicotinic acid, and ezetimibe. Combination drug therapies are also used. Statins are generally the preferred first-line treatment due to their ability to significantly lower LDL cholesterol levels. Special considerations include drug interactions and contraindications of the various hypolipidemic agents.
The bile salts such as cholic acid contain a hydrophobic side and a hydrophilic side, thus allowing bile salts to dissolve at an oil-water interface, with the hydrophobic surface in contact with the non-polar phase and the hydrophilic surface in the aqueous medium. This detergent action emulsifies fats and yields mixed micelles, which allow attack by water-soluble digestive enzymes and facilitate the absorption of lipids through the intestinal mucosa. Mixed Micelles also serve as transport vehicles for those lipids that are less water-soluble than fatty acids, such as cholesterol or the fat-soluble vitamins A, D, E, and K. Thus, efficient absorption of lipids depends on the presence of sufficient bile acids to solubilize the ingested lipids.
This document summarizes recent therapeutic approaches for dyslipidemia. It discusses lifestyle changes like smoking cessation, weight loss, improved diet, and increased physical activity. It also discusses pharmacological management including ATP III guidelines, novel therapies that block lipoprotein output or increase clearance like PCSK9 inhibitors. Therapies to raise anti-atherogenic lipoproteins by promoting ApoA1 production or cholesterol efflux are also covered, as well as therapies slowing HDL removal and dual PPAR agonists. Surgical modalities like partial ileal bypass and liver transplantation are mentioned for severe dyslipidemia cases.
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.
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.
Drugs for Hyperlipidemia for BAMS studentsRemya Krishnan
Lipid-lowering drugs work to lower cholesterol and triglyceride levels through various mechanisms. Statins inhibit cholesterol synthesis in the liver, increasing LDL receptors to clear LDL from the blood. Resins bind bile salts in the gut to lower cholesterol absorption and increase clearance. Fibrates boost fatty acid breakdown and clearance of triglyceride-rich particles. Together, these drugs lower risk of atherosclerosis and cardiovascular events by modifying lipid profiles. Adverse effects include gastrointestinal issues and, rarely, muscle damage.
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.
This document discusses the treatment of hyperlipidemias. It outlines the main risk factors for coronary heart disease including high LDL cholesterol, low HDL cholesterol, smoking, hypertension, obesity and diabetes. The primary treatment goal is reduction of LDL levels through lifestyle changes and medication. Main drug classes for treatment include statins, bile acid sequestrants, cholesterol absorption inhibitors, niacin, and fibric acid derivatives. The document provides details on the mechanisms of action, pharmacokinetics, therapeutic uses and adverse effects of these drug classes.
This document discusses drugs used to treat hyperlipidemia. It describes several classes of drugs including statins, fibrates, niacin, bile acid sequestrants, cholesterol absorption inhibitors, PCSK9 inhibitors, and omega-3 fatty acids. Statins are first-line treatment as they lower LDL cholesterol and risk of cardiovascular events by inhibiting HMG-CoA reductase. Other drug classes lower triglycerides, raise HDL cholesterol, or inhibit cholesterol absorption to treat different lipid abnormalities. Lifestyle modifications such as diet and exercise should always accompany drug therapy for hyperlipidemia.
low birth weight presentation. Low birth weight (LBW) infant is defined as the one whose birth weight is less than 2500g irrespective of their gestational age. Premature birth and low birth weight(LBW) is still a serious problem in newborn. Causing high morbidity and mortality rate worldwide. The nursing care provide to low birth weight babies is crucial in promoting their overall health and development. Through careful assessment, diagnosis,, planning, and evaluation plays a vital role in ensuring these vulnerable infants receive the specialize care they need. In India every third of the infant weight less than 2500g.
Birth period, socioeconomical status, nutritional and intrauterine environment are the factors influencing low birth weight
Travel Clinic Cardiff: Health Advice for International TravelersNX Healthcare
Travel Clinic Cardiff offers comprehensive travel health services, including vaccinations, travel advice, and preventive care for international travelers. Our expert team ensures you are well-prepared and protected for your journey, providing personalized consultations tailored to your destination. Conveniently located in Cardiff, we help you travel with confidence and peace of mind. Visit us: www.nxhealthcare.co.uk
Cell Therapy Expansion and Challenges in Autoimmune DiseaseHealth Advances
There is increasing confidence that cell therapies will soon play a role in the treatment of autoimmune disorders, but the extent of this impact remains to be seen. Early readouts on autologous CAR-Ts in lupus are encouraging, but manufacturing and cost limitations are likely to restrict access to highly refractory patients. Allogeneic CAR-Ts have the potential to broaden access to earlier lines of treatment due to their inherent cost benefits, however they will need to demonstrate comparable or improved efficacy to established modalities.
In addition to infrastructure and capacity constraints, CAR-Ts face a very different risk-benefit dynamic in autoimmune compared to oncology, highlighting the need for tolerable therapies with low adverse event risk. CAR-NK and Treg-based therapies are also being developed in certain autoimmune disorders and may demonstrate favorable safety profiles. Several novel non-cell therapies such as bispecific antibodies, nanobodies, and RNAi drugs, may also offer future alternative competitive solutions with variable value propositions.
Widespread adoption of cell therapies will not only require strong efficacy and safety data, but also adapted pricing and access strategies. At oncology-based price points, CAR-Ts are unlikely to achieve broad market access in autoimmune disorders, with eligible patient populations that are potentially orders of magnitude greater than the number of currently addressable cancer patients. Developers have made strides towards reducing cell therapy COGS while improving manufacturing efficiency, but payors will inevitably restrict access until more sustainable pricing is achieved.
Despite these headwinds, industry leaders and investors remain confident that cell therapies are poised to address significant unmet need in patients suffering from autoimmune disorders. However, the extent of this impact on the treatment landscape remains to be seen, as the industry rapidly approaches an inflection point.
Know the difference between Endodontics and Orthodontics.Gokuldas Hospital
Your smile is beautiful.
Let’s be honest. Maintaining that beautiful smile is not an easy task. It is more than brushing and flossing. Sometimes, you might encounter dental issues that need special dental care. These issues can range anywhere from misalignment of the jaw to pain in the root of teeth.
Nano-gold for Cancer Therapy chemistry investigatory projectSIVAVINAYAKPK
chemistry investigatory project
The development of nanogold-based cancer therapy could revolutionize oncology by providing a more targeted, less invasive treatment option. This project contributes to the growing body of research aimed at harnessing nanotechnology for medical applications, paving the way for future clinical trials and potential commercial applications.
Cancer remains one of the leading causes of death worldwide, prompting the need for innovative treatment methods. Nanotechnology offers promising new approaches, including the use of gold nanoparticles (nanogold) for targeted cancer therapy. Nanogold particles possess unique physical and chemical properties that make them suitable for drug delivery, imaging, and photothermal therapy.
How to Control Your Asthma Tips by gokuldas hospital.Gokuldas Hospital
Respiratory issues like asthma are the most sensitive issue that is affecting millions worldwide. It hampers the daily activities leaving the body tired and breathless.
The key to a good grip on asthma is proper knowledge and management strategies. Understanding the patient-specific symptoms and carving out an effective treatment likewise is the best way to keep asthma under control.
Summer is a time for fun in the sun, but the heat and humidity can also wreak havoc on your skin. From itchy rashes to unwanted pigmentation, several skin conditions become more prevalent during these warmer months.
Osteoporosis - Definition , Evaluation and Management .pdfJim Jacob Roy
Osteoporosis is an increasing cause of morbidity among the elderly.
In this document , a brief outline of osteoporosis is given , including the risk factors of osteoporosis fractures , the indications for testing bone mineral density and the management of osteoporosis
8 Surprising Reasons To Meditate 40 Minutes A Day That Can Change Your Life.pptxHolistified Wellness
We’re talking about Vedic Meditation, a form of meditation that has been around for at least 5,000 years. Back then, the people who lived in the Indus Valley, now known as India and Pakistan, practised meditation as a fundamental part of daily life. This knowledge that has given us yoga and Ayurveda, was known as Veda, hence the name Vedic. And though there are some written records, the practice has been passed down verbally from generation to generation.
Kosmoderma Academy, a leading institution in the field of dermatology and aesthetics, offers comprehensive courses in cosmetology and trichology. Our specialized courses on PRP (Hair), DR+Growth Factor, GFC, and Qr678 are designed to equip practitioners with advanced skills and knowledge to excel in hair restoration and growth treatments.
Are you looking for a long-lasting solution to your missing tooth?
Dental implants are the most common type of method for replacing the missing tooth. Unlike dentures or bridges, implants are surgically placed in the jawbone. In layman’s terms, a dental implant is similar to the natural root of the tooth. It offers a stable foundation for the artificial tooth giving it the look, feel, and function similar to the natural tooth.
2. ANTIHYPERLIPIDEMIC AGENTS
1. Inhibits cholesterol absorption in the intestine Ezetimibe
2. Sequester bile acids in the intestine Exchange resins
1. Inhibits synthesis of cholesterol Inhibitors of hydroxymethylglutaryl coenzyme A reductase
(HMG-COA Reductase)
2. Alter relative levels & patterns of different plasma LPs Fibrates, Nicotinic acids
ADJUVANT AGENTS
Omega-3-Fatty Acids, Stanols
1 CHD: Coronary Heart Disease
Targeting Exogenous Pathways:
1. Inhibition of Cholesterol Absorption in Intestine
Selective C Transporter Inhibitors; Ezetimibe
2. Sequester Bile Acids in Intestine
Ezetimibe
Is a selective C absorption inhibitor
Mechanism Blocks sterol transporter (NPC1L1) pool of cholesterol
available to the liver upregulate LDL receptor (which collect
cholesterol from the circulation)
Pharmacological
action (don’t memorize the
numbers just know what
which drug work best on
what)
LDL 20% (54% of intestinal cholesterol + phytosterol absorption are blocked)
TG 8%
HDL 1-4%
To sum up it works more on cholesterol and LDL
(no effect on steroids, lipid-soluble vitamins, bile a)
Pharmacokinetics Absorbed & conjugated in intestine to active
glucuronide (> potent )
Reaches peak blood level in 12–14 hours
Its half-life is 22 hours
Undergoes enterohepatic circulation (prolong action
of drug)
80% of the drug is excreted in feces
N.B. Drug level if with statins & if with
cholystyramine (Bile Acid Sequestrant)
Indications Monotherapy:
Pry prevention of low
risk of CHD1 (need
modestLDL)
Statin-intolerant
patients
Combination Therapy:
-With statins; synergistic
In moderate/severe LDL.
-Or If must statin dose
because of side effects.
-Or With other lipid lowering
drugs; As fibrates
ADRs & Interactions Not common.
GIT disturbance, headache, fatigue, artheralgia & myalgia.
Seldom reversible impairment of hepatic function
Sequestrants; Colestipol, & Cholestyramine, Colesevelam
The doctor said
only memorize the
first two
3. Targeting Endogenous Pathways:
Inhibits synthesis of cholesterol
Inhibitors of hydroxymethylglutaryl coenzyme A reductase (HMG-COA Reductase)
Alter relative levels & patterns of different plasma LPs
Fibrates, Nicotinic acids
Bile Acid Sequestrants (Cholestyramine, Colestipol)
Are polymeric cation exchange resins
Mechanism Bind bile acids [BA]preventing their enterohepatic recycling &
fecal excretion (10 folds). ”so in liver BA C absorption & its
hepatic breakdown” compensatory LDL Receptors LDL
Pharmacological
action
LDL 15-30%
HDL 3-5%
TG & VLDL
( initial & transient ) but show marked in type IIb
Hyperlipoproteinemia “Mixed hyperlipidemia”
Indications A. In Hyperlipidemia
1- Monotherapy:
Seldom given
Only if statin is contraindicated & LDL & TG
levels are not too high
2- Combination: with statins in type IIa
Hyperlipoproteinemia.
Statins acts in synergism to
LDL Receptors + LDL levels
N.B.
Resins must be taken with meals / lack
effect if between meals
B. Other Indications:
Pruritus due to
biliary stasis
Digitalis
poisoning
ADRs GIT bloating, diarrhea, constipation, dyspepsia
Absorption of fat soluble vitamins ( A, K, E, D) ‘’أكيد (you have
prescribe these vitamins to your patient)
Dry flaking skin
Contraindications Type IIb Hyperlipoproteinemia WHY? Because of transient
increase of TG and VLVL.
Biliary obstruction.
Diverticulitis
Chronic constipation.
Severe hypertriglyceridemia (the cause is the same as 1st
contradicted)
Interactions absorption of some drugs;Digoxin, Thiazides, Frusemide,
Propranolol, Warfarin, L-thyroxin, …
N.B. So these drugs must be taken 1 hr before or 4 hrs after
sequestrantes
The doctor said
only know the
first
contraindication
4. Diabetes mellitus lipid profile :( ↑ TG + normal LDL + ↓ HDL )
2 FFA: Free Fatty Acids
3 LPL: Lipoprotein lipase
NICOTINIC ACID
Is known as Vit B3. Its amide derivative nicotinamide has no lipid lowering effects
Mechanism
Bind to a specific receptors in adipose tissue (reverse effect of b-AR
stimulation) cAMP PKA -ve TGs breakdown FFA2 to liver (it
decrease the mobilization of free fatty acid to the liver)
TGs hepatic synthesis & VLDL formation
This eventually LDL & HDL
In plasma: LPL3 activity VLDL & CMs clearance (in other way VLDL &
CMs)
Pharmacological
actions
LDL 5-25% LP(a) “Lipoprotein A = atherogenic lipoprotein”
HDL 15-30% Fibrinogen
TG & VLDL 20-50% Tissue plasminogen activator
Nicotinic acid works o ALL the lipid profile
Indications Type IIa hypercholestrolemia
Type IIb hypercholesterolemia & any combined hyperlipidemia
Patient with hypertriglyceridemia & low HDL-C ?? (If the patient
wasn’t diabetic)
Hyperchylomicronemia.
ADRs Sensation of Warmth &
Flushing
(prostaglandin induced /
-ve by aspirin ½ h before
niacin).
N.B Slow release
formulations incidence of
flushing !!!
Pruritus, rash, dry skin
Dyspepsia: nausea, vomiting,
reactivation of peptic ulcer ( if taken
after meal).
Reversible liver enzymes
hepatotoxicity.
Impairment Of Glucose Tolerance
Overt Diabetes
Uric Acid
Contraindications Gout.
Peptic ulcer. (Because of the prostaglandin)
Hepatotoxicity.
Diabetes mellitus WHY? Bcoz it Impairment Of Glucose Tolerance
5. Fibrates: act as Nuclear Transcription Factors
(PPARα Agonist)
- When fibrates bind with Linoleic Acid (α receptor), it’s activated and acts on nuclear
transcription factors. (They don’t reduce Cholesterol very much)
Mechanism:
Bind and activate PPARα Receptor
Dimerize with RXR
Expresses Gene Transcription, and represses other Gene Transcription.
mRNA Translation.
Protein formation, that is responsible for:
It represses other proteins. The most imp. is LDL.
Fibrates:
Fenofibrate (F)
Gemfibrozil (G)
Clofibrate (not used nowadays) it cause: Gall stones/ Cancer
Pharmacological Actions:
- LDL 5-20%
- HDL 10-20% > (G)
- TG & VLDL 20-50%
- Fibrinogen
- Vascular inflammation > (G)
- Improve glucose tolerance > (F)
*metabolic syndrome: metabolic syndrome is pt. has 3 of these:
1- obesity 2- hyperlipidemia 3- hyperglycemia 4- hyperuricemia 5- hypertension so Fenofibrate
is good for n 2, 3 and 4
TG (Most imp)
VLDL by liver
HDL
RCT (reverse
cholesterol transport)
Used for; 1- Gout + Metabolic Syndromes* -> (because it has
uricosuric action”help In excretion of uric acids”)
2- Diabetes
3- Hyperuricemia
Extra Information:
- (F) & (G): mostly used to decrease TG.
- Metabolic Syndromes, such as Insulin
Syndrome, are pre-diabetic. This means
there is an increase in TG & a decrease in
HDL in fatty acid circulation because of
obesity which can lead to diabetes. With
or without an increase in cholesterol.
6. Indications:
Monotherapy > (G)
Hypertriglcyredemia; Type IV lipoproteinemia
Combined Therapy with Statins:
1. Mixed dyslipidaemia; i.e type IIb
2. . In decrease in HDL and increase in TG + risk of atherothrombosis [type 2 Diabetes].
Combined therapy with other lipid lowering drugs:
in severe treatment-resistant dyslipidaemia.
ADRs:
1. G.I.T upset, headache, fatigue, weight gain
2. Rash, urticaria, hair loss
3. Myalagia, Myositis, Rhabdomyolysis, which may cause Acute renal failure, that Occurs in
alcoholics. Due to combination with lipophilic statins or impaired Renal function.
Contraindications:
Renal or hepatic impairment.
Pregnant or nursing women.
Gall-bladder disease & morbid obesity
In hypoalbuminaemia
In alcoholics
They metabolism of lipophylic not hydrophilic statins -> toxicity %myalgia,
myositis, .......etc. Give lower doses
Interactions:
- They displace warfarin from their protein binding sites, which increases the tendency for
internal bleeding. Therefore, anticoagulant dose must be adjusted. (Warfarin ).
- They metabolism of lipophylic not hydrophilic statins -> toxicity %myalgia, myositis,
.......etc. Give lower doses
Very IMPORTANT Note:
In combination of fibrates with lipophilic statins (that interact with
cytochrome P450) we best use (F). Because (G) also interacts with CYT
P450, so if it’s combined with lipophilic statins toxicity will occur which
may lead to [myositis & rhabdomyolysis.]
7. Statins
(HMG CoA Reductase Inhibitors)
specific, reversible, competitive
- It stops Cholesterol (C) synthesis, so LDL will have to take more (C) which decreases
(C) in our circulation.
Mechanism:
HMG CoA Reductase: One of the enzymes in cholesterol synthetic pathways that controls
the rate limiting step of conversion to mevalonate.
1. Lipid lowering effect in the Liver:
Decreases hepatic (C) synthesis which decreases hepatic intracellular (C) that results in:
1. Synthesis of LDL receptors which clearance of LDL
2. Secretion of VLDL & uptake of non-HDL-(C)
2. PLEIOTROPIC ANTIATHEROGENIC effects in Vessels:
Because it blocks cholesterol synthetic pathway, it also blocks signaling molecules
responsible for progress of inflammation, vulnerability & athrothrombosis. This is the
2ndry effect of statins to excess C accumulation in periphery.
This results in:
- Improve endothelial function (NO).
- Decrease vascular inflammation
- Stabilization of atherosclerotic plaque
- decrease platelet aggregability
- Antithrombotic actions
- Enhanced fibrinolysis ...etc
**** So Statins are the drug of choice for Atherogenic Hyper-lipidemia. Because, they
decrease (C) Synthesis & Block Signaling Molecules.
8. Classification of statins:
Simvastatin
Fluvastatin [Weak] Lipophilic
Atorvastatin [Strong]
Lovastatin
Pravastatin Hydrophilic (Not obliged with the rule of (G))
Rosuvastatin [Super/Mega] Partial (It’s the best statin, reduces (C) by 60%).
Pharmacokinetics:
o Absorption varies (40-70%), fluvastatin almost completely
o Absorption enhanced if taken with food, except pravastatin
o All have high first-pass extraction by the liver, except pravastatin
o Simvastatin, Lovastatin, Atorvastatin are the most metabolized
o Metabolized variably
o By CYP3A4 Simvastatin, Lovastatin, Atorvastatin
o By CYP2C9 Fluvastatin, Rosuvastatin
o By sulphonation Pravastatin
o Excreted in bile & 5–20% is excreted in urine, except pravastatin 80-90% urine.
o t½ (V.imp):
- If short duration (1-3 hrs). Such as, Simvastatin, Lovastatin, Fluvastatin. Then, it’s
taken only in the evening, because cholesterol synthesis increases at night.
- If long duration (14 hrs). Such as, Atorvastatin. Or (19 hrs). Such as, Rosuvastatin.
Then it is taken any time.
Indications:
As Monotherapy:
2ndry prevention: at all times:
In all ischemic insults [, stroke, ACSs up to AMI, .....etc. So given from1st day of ischemic
attack%stabilize plaques + help to limit ischemic zone & to salvage preferential tissues
Primary prevention:
- 1. Patients with hyperlipidemia and with other risks for ischemic insults.
- 2. Type IIa Hyperlipoprotinemia.
9. As Combined Therapy:
1. Mixed dyslipidaemias; added to fenofibrates or niacine if necessary.
2. In diabetics and patients with insulin resistance *metabolic syndrome+. Even if there isn’t any
increase in LDL levels (just low HDL). Because they will already have small dense LDL with
endothelial dysfunction and increased thrombotic profile. So we must take Statins
Contraindications: In pregnancy and cautiously under age of 18 years
ADRs:
- increase serum transaminase can progress to evident hepatotoxicity So lab
investigations recommended every 6 month if level increase up to 3 folds at any time, statin
must be stopped then dose adjusted.
- Increase CK activity (index of muscle injury): Measured only if there are symptoms such as,
myalgia or myositis. If it increases up to 3-5 folds statins must be decreases/change to
hydrophilic statin / omit combination with fibrates......
- But, if there was severe elevation with blood in urine, this indicates Rhabdomyolysis
renal failure could be fatal, and dialysis is needed.
Interactions:
- Simvastatin, Atorvastatin. Which are metabolized by CYP3A4 show:
Decrease efficacy with INDUCERS (Phenytoin, Rifampin, Barbiturates, TZDs...).
Increase toxicity with INHIBITORS (Macrolides, Cyclosporine, Ketoconazole...).
- Fluvastatin & Rosuvastatin. Which are metabolized by CYP2C9 show:
Increase toxicity with INHIBITORS (Amiodarone, Cimetidine…)
10. Adjuvants in hyperlipidemia
*TARGETING DYSLIPIDEMIA & * TARGETING BEYOUND is just for reading if you
would like.
Omega-3-FA
found in fish oils
containing highly
unsaturated fatty acid.
Mechanism &
Pharmacological effect:
- Reduces TG
synthesis.
- Increases β
oxidation of FFA.
- Prolongation of
bleeding time.
- Reduction of plasma
fibrinogen
- Anti-inflammatory
effects
β-Sitosterol
Found in plants with structure similar
to (C).
Mechanism & Pharmacological
Effects:
Compete with dietary & biliary (C)
absorption to decrease LDL levels
+ and – 10%
Indications: Given as food supplement
before meal in hypecholestrolemia
11. MMCCQQ
Choose the ONE best answer.
1. Which one of the following is the most common side effect of antihyperlipidemic drug therapy?
A. Elevated blood pressure.
B. Gastrointestinal disturbance.
C. Neurologic problems.
D. Heart palpitations.
2. Which one of the following hyperlipidemias is characterized by elevated plasma levels of
chylomicrons and has no drug therapy available to lower the plasma lipoprotein levels?
A. Type I.
B. Type II.
C. Type III.
D. Type IV.
3. Which one of the following drugs decreases de novo cholesterol synthesis by inhibiting the
enzyme 3-hydroxy-3-methylglutaryl coenzyme A reductase?
A. Fenofibrate.
B. Niacin.
C. Cholestyramine.
D. Lovastatin.
.
4. Which one of the following drugs causes a decrease in liver triacylglycerol synthesis by limiting
available free fatty acids needed as building blocks for this pathway?
A. Niacin.
B. Fenofibrate.
C. Cholestyramine.
D. Gemfibrozil.
5. Which one of the following drugs binds bile acids in the intestine, thus preventing their return to
the liver via the enterohepatic circulation?
A. Niacin.
B. Fenofibrate.
C. Cholestyramine.
D. Fluvastatin.