Download Free Medical Antidyslipidemic Drugs PowerPoint Presentation

Antidyslipidemic Drugs PowerPoint Presentation

DOWNLOAD MEDICAL POWERPOINT PRESENTATION

About This Presentation

Description : Check out this medical presentation on Pharmacology, which is titled "antidyslipidemic drugs", to know about antidyslipidemic drugs.

Tags : Pharmacology, antidyslipidemic drugs

Published on : Jul 18, 2021 | Views : 2174 | Downloads : 6

Shareable Url :

Embed Code :

Comment

Transcript

Slide 1-

Antidyslipidemic drugs (Summary) Assoc. Prof. Iv. Lambev E-mail: itlambev@mail.bg www.medpharm-sofia.eu
Slide 2-

CVD (cardiovascular disease) is the leading cause of death among the adult population in the world. CHD (coronary heart disease) is the main cause of death in patients with CVD. Total plasma cholesterol, high plasma levels of LDL, low levels of HDL are important risk factors for CHD.
Slide 3-

ppt slide no 3 content not found
Slide 4-

Free cholesterol Phospholipids Triglycerides Cholesterol esthers Apolipoproteins Structure of lipoproteins
Slide 5-

Chylomicrons Very low density lipoproteins (VLDL) Intermediate density lipoproteins (IDL) Low density lipoproteins (LDL) High density lipoproteins (HDL) Classification of lipoproteins according to their density
Slide 6-

They are the main protein ingredient of lipoproteins with the following functions: (1) Facilitate lipid transportation (2) Activate main enzymes in lipid metabolism – lecithin cholesterol acetyltransferase – lipoprotein lipase – liver triglyceride lipase (3) Connect to receptors on the cell surface Apolipoproteins
Slide 7-

After LDL oxidation free radicals and active oxygen species are formed and they activate macrophages.
Slide 8-

Activated macrophages produce inflammatory cytokines (IL-6, TNF alpha), which damage endothelium and initiate atherogenesis.
Slide 9-

Hypertriglyceridemia can predict CHD risk independently to HDL.
Slide 10-

Phenotype I IIa IIb III IV V Lipoprotein increased Chylomicrons LDL LDL and VLDL IDL VLDL VLDL and Chylomicrons Atherogenity NO +++ +++ +++ + + Rate Low High High Medium High Low Plasma cholesterol Normal to Normal to Normal to Plasma triglycerides Normal Adapted from Yeshurun D, Gotto AM. Southern Med J 1995; 88 (4): 379–391 Fredrickson classification of dyslipidemias (WHO)
Slide 11-

Notes 1. The Fredrickson classification does not take into account HDL-C (cholesterol in HDL), whose low plasma level has a significant atherogenic role. 2. Homocysteine (normal 5–15 mmol/l) is produced in methionine metabolism. Increased plasma levels of homocysteine is an independent risk factor for the development of atherosclerosis and CVD, even in normal lipid status. High homocysteine plasma levels are reduced by folic acid (vitamin B3), pyridoxine (vitamin B6), and vitamin B12.
Slide 12-

I. Drugs inhibiting cholesterol and lipoprotein synthesis Statins Fibrates Nicotinic acids
Slide 13-

 Statins HMG-CoA reductase inhibitors) – p.o. CYP 3A4 substrates Atorvastatin Lovastatin Simvastatin CYP 2C9 substrates Fluvastatin Rosuvastatin CYP450 substrate Pravastatin ARs: CPK, myositis, rabdomyolysis, hepatotoxicity
Slide 14-

As a result of meta-analyses of many years of clinical studies on statins FDA (2012) makes the following findings: Due to the their extremely rare hepatotoxicity it does not recommend frequent routine monitoring of liver enzymes. (2) Long-term therapy with statins is associated with increases in fasting serum glucose levels and glycosylated hemoglobin and increses te risk for incident DN in 9 to 13%; in rosuvastatin-treateted patients this risk is higher.
Slide 15-

(3) Statins, though rare, can cause reversible symptoms of cognitive impairment (memory loss, amnesia, some confusion) requiring discontinuation of therapy. (4) Lovastatinat is a substrate of P450 3A4 with proven in vivo sensitivity to this class isoenzymes. Comedication with strong inhibitors of P450 3A4 (anti-retroviral drugs, etc.) significantly increases the risk of serious ADRs (myopathy and/or rhabdomyolysis) in therapy with lovastatin. This may require its replacement with another statin or reduce DD. The risk is much greater in liver function and alcoholism.
Slide 16-

 Fibrates – p.o. (inhibit lipolysis in adipocytes) – Ciprofibrate – Clofibrate – Fenofibrate  Nicotinic acid inhibits secretion of VLDL and reduces production of LDL: – Niacin (Vitamin B3)
Slide 17-

II. Drugs enhancing cholesterol and lipid metabolism (ARs: constipation, decreased GI absorption of many other drugs)  Bile acid sequestrants inhibit bile acid enterohepatic recirculation – p.o. : Colestipol, Colestyramine  Phytoproducts (p.o.): Pectin Pectivit C® (pectin/vitamin C)
Slide 18-

III. Drug, inhibiting intestinal cholesterol absorption: Ezetimibe – p.o. IV. Drugs containing polyunsaturated essential omega-3-fatty acids: Escimo-3® Omacor®
Slide 19-

Control of total serum cholesterol < 5,2 mM 5,2–6,2 mM  6,2 mM Normal levels Bordeline levels High levels Control in 5 years Control in 12 months + diet In CHD or/and risk factors – lipid status analysis, diet, and antidyslipidemic treatment Control in 6 months with lipid status analysis, diet, and antidyslipidemic treatment
Slide 20-

BMI >30: >>> saturated fatty acids > >>salt and >>> sugar >>> (or <<<) alcohol <<< fruits and vegetables Smoking Lipid status Stress Diabetes mellitus Metabolic syndrome Sedentary life style 2/3 of the risk Risk factor for CVD Homocysteine >15 mmol/l 
Slide 21-

Metabolic syndrome – high risk for CVD (European Guidelines, 2003) presence of ≥ 3 risk factors: •Waist > 102 cm in men and > 85 cm in women •Triglycerides ≥ 1,7 mmol/l •HDL-cholesterol < 1 mmol/l in men or < 1,3 mmol/l in women •Arterial hypertension > 130/85 mm Hg •Glucose ≥ 6,1 mmol/l Patients with hypertension and concomitant CVD have increased risk for diabetes mellitus. 
Slide 22-

ATP 3’, 5’-AMP cAMP Lipolysis (–) AC PD Cholesterol synthesis Caffeine > 300 mg/d: 5–6 coffee cups daily (+) (+) Hypercholesterolemia
Slide 23-

Patient’s compliance 200 ml/24 h Quantum therapy device  treatment (+ 1 to 2 measure of BP) non-pharmacological treatment physical activity dietary regimen 8–9 h of sleep avoidance of risk factors