Introduction Hyperlipidemia hyperlipoproteinemia Primary hyperlipidemia (Familial) Secondary hyperlipidemia (Acquired)
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2 Introduction Hyperlipidemia, or hyperlipoproteinemia, is the condition of abnormally elevated levels of any or all lipids and/or lipoproteins in the blood. Hyperlipidemias are divided in primary and secondary subtypes. Primary hyperlipidemia (Familial) is usually due to genetic causes (such as a mutation in a receptor protein), while Secondary hyperlipidemia (Acquired) arises due to other underlying causes such as diabetes mellitus, alcoholism, nephrotic syndrome, chronic renal failure, administration of drug. Also, hyperlipidemia may be idiopathic, that is, without known cause. Lipid and lipoprotein abnormalities are common in the general population, and are regarded as a modifiable risk factor for cardiovascular disease due to their influence on atherosclerosis. In addition, some forms may predispose to acute pancreatitis.
3 Classification Hyperlipidemias may also be classified directly into which types of lipids are elevated, that is hypercholesterolemia, hypertriglyceridemia or both in combined hyperlipidemia. Elevated levels of lipoproteins may also be classified as a form of hyperlipidemia.
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5 Lipoprotein Metabolism Lipids originate from two sources: Exogenous lipids, ingested and processed in the intestine. Endogenous lipids, synthesized in the liver. Over 93% of the fat that is consumed in the diet is in the form of triglycerides (TG). Dietary cholesterol and triglycerides are packaged into chylomicrons in the intestine, before passing into the blood stream via lymphatics. The liver synthesizes triglycerides and cholesterol, and packages them as VLDLs before releasing them into the blood.
6 Excess dietary carbohydrates are converted into triglycerides and also stored in adipose tissue.
7 Dietary intake supplies only about 20 25% of the cholesterol needed everyday to build cell membranes,
8 The other 75 80% of our daily need for cholesterol is synthesized in the liver. Saturated fats raise LDL cholesterol by decreasing the synthesis of LDL receptors.
9 The overall results are about the same, no matter which defect you consider, cholesterol is not removed from the circulation
10 Lipoprotein Metabolism LIPIDS, including LESTEROL () and TRIGLYCERIDES (TG), are transported in the plasma as lipoproteins, of which there are four classes: Chylomicrons transport TG and from the GIT to the tissues, where they are split by lipoprotein lipase (LPL), releasing free fatty acids. There are taken up in capillary of muscles and adipose tissue. Chylomicron remnants are taken up in the liver for disposal. Very low density lipoproteins (VLDL), which transport and newly synthetised TG to the tissues. Low density lipoproteins (LDL) with a large component of, some of which is taken up by the tissues and some by the liver, by endocytosis via specific LDL receptors High density lipoproteins (HDL): are also secreted from the liver and intestine, have the task of preventing lipid accumulation, absorb derived from cell breakdown in tissues and transfer it to VLDL and LDL
11 Lipoprotein Metabolism There are two different pathways for exogenous and endogenous lipids: THE EXOGENOUS PATHWAY: + TG absorbed from the GIT are transported in the lymph and than in the plasma as CHYLOMICRONS to capillaries in muscle and adipose tissues. Here, the core TG are hydrolysed by lipoprotein lipase, and the tissues take up the resulting FREE FATTY ACIDS is liberated within the liver cells and may be stored, oxidised to bile acids or secreted in the bile unaltered Alternatively it may enter the endogenous pathway of lipid transport in VLDL
12 Lipoprotein Metabolism EXOGENOUS PATHWAY ENDOGENOUS PATHWAY may be stored oxidised to bile acids secreted in the bile unaltered
13 ENDOGENOUS PATHWAY for lipids EXOGENOUS PATHWAY for lipids Fig.1a HEPATOCYTE GIT bile acids Bile duct bile acids Fat + + fatty acids ENDOGENOUS PARTHWAY chylomicr remn TG chylomicr TG Peripheral tissues Fatty acids (According to Rang, Dale 1999)
14 Lipoprotein Metabolism THE ENDOGENOUS PATHWAY: 1. and newly synthetised TG are transported from the liver as VLDL to muscle and adipose tissue, there TG are hydrolysed and the resulting FATTY ACIDS enter the tissues 2. The lipoprotein particles become smaller and progressively more dense and ultimetaly turn into LDL, which provides the source of for incorporation into cell membranes, for synthesis of steroids, and bile acids 3. While most of the resulting LDLs are taken up by the liver cells by endocytosis via LDL receptors that recognise LDL apolipoproteins for disposal, some circulate and distribute cholesterol to the rest of the body tissues. 4. can return to plasma from the tissues in HDL particles and the resulting cholesteryl esters are subsequently transferred to VLDL or LDL
15 ENDOGENOUS PATHWAY for lipids EXOGENOUS PATHWAY for lipids Fig.1b HEPATOCYTE GIT ACoA MVA bile acids Bile duct bile acids 3 LDL receptors 4 HDL LDL VLDL TG 2 1 lipase from cells Uptake of Fatty acids Peripheral tissues (According to Rang, Dale 1999)
16 Dyslipidemia The normal range of plasma total concentration < 6.5 mmol/l. There are smooth gradations of increased risk with elevated LDL-C conc, and with reduced HDL-C conc. Elevated concentrations of lipid (hyperlipidemia) can lead to the development of atherosclerosis and CAD. VLDLs and LDLs are atherogenic lipoproteins, whereas HDL concentrations are inversely related to the incidence of CAD. Hence, treatments for hyperlipidemia aim to reduce LDL levels and raise HDL levels.
17 Lipid-lowering drugs Drug therapy to lower plasma lipids is only one approach to treatment and is used in addition to dietary management and correction of other modifiable cardiovascular risk factors Several drugs are used to decrease plasma LDL-C
18 Pharmacotherapeutic options in hyperlipidemia I-Agents Targeting Endogenous Cholesterol: A. Statins B. Fibrates C. Nicotinic acid II-Agents Targeting Exogenous Cholesterol A. Cholesterol Uptake Inhibitors, e.g. ezetemibe B. Bile acid binding resins, e.g. colestipol & cholestyramine
19 ENDOGENOUS PATHWAY for lipids EXOGENOUS PATHWAY for lipids GIT Fig.1c HEPATOCYTE GIT STATINS ACoA STATINS FIBRATES MVA bile acids Bile duct bile acids FIBRATES LDL receptors VLDL TG FIBRATES Chylomikr remn TG v.portae Chylomikr RESINS fat + + fatty acids HDL LDL lipase TG from cells Uptake of Fatty acids Fatty acids Peripheral tissues (According to Rang, Dale 1999)
20 Statins Drugs: Simvastatin, atorvastatin, mevastatin, lovastatin, pravastatin and their derivatives Pharmacological effects: Apparently decrease plasma TC and LDL-C HMG-CoA (3-hydroxy-3-methylglutaryl-coenzyme A) reductase inhibitors. The reductase catalyses the conversion of HMG-CoA to mevalonic acid Several studies demonstrated positive effects on morbidity and mortality
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23 Statins Pharmacokinetics: well absorbed when given orally They are subjected to extensive first-pass metabolism by the liver. More than 95% of most of these drugs are bound to plasma proteins. All statins are taken orally at bedtime because of diurnal rhythm of cholesterol synthesis, except atorvastatin taken at any time because of its long half-life (14 hours). At the peak of the rhythm (between midnight and 3 a.m.) MVA concentrations were 3-5 times greater than (between 9 a.m. and noon).
24 Adverse effects: Statins - Nearly 10% patients suffer from mild gastrointestinal disturbances, insomnia, headache and rash - More serious adverse effects are rare but include Hepatotoxicity (increased serum transaminase), myositis (rhabdomyolysis) and angio-oedema - Myopathy (increased creatine kinase) especially when combined with: other lipid lowering drugs: i) Fibrates. ii) Niacin. other drugs that are metabolized by 3A4 isoform of cytochrome P450 e.g.: erythromycin, cyclosporine, verapamil, ketoconazole. Note: liver transaminases and CK must be regularly measured during therapy with statins
25 The most common symptoms of rhabdomyolysis include: dark urine (typically brown); swollen, tender muscles of the thighs, calves, and lower back.
26 Statins Contraindications 1. Pregnancy & lactation (Cholesterol is important for normal development, and it is possible that statins could cause serious problems). The effects of high cholesterol do not cause problems for many years or even decades. Therefore, if a woman does not take her statin or other cholesterol medications during breastfeeding, it will likely have only a minimal impact on her long-term risks. Therefore, it is best to wait until you have weaned your child before starting or resuming a statin medication 2. Active liver diseases.
27 Statins Drug interactions Potentiate the action of oral anticoagulant and antidiabetic drugs (displacement from plasma protein binding sites). Clinical uses Secondary prevention of myocardial infarction and stroke Primary prevention of arterial disease
28 Fibric Acid Derivatives [Fibrates] Drugs: Clofibrate, gemfibrozil, bezafibrate, fenofibrate, ciprofibrate Pharmacological effects and mechanisms: to decrease TG, VLDL and to increase HDL Stimulate the beta-oxidative degradation of fatty acids Liberate free fatty acids for storage in fat or for metabolism in striated muscle Increase the activity of lipoprotein lipase, hence increasing hydrolysis of triglyceride in chylomicrons and VLDL particles reduce hepatic VLDL production and increase hepatic LDL uptake
29 Fibric Acid Derivatives [Fibrates] Adverse effects: Mild GIT symptoms, skin rashes, decrease in white blood count, hepatic dysfunction In patients with renal impairment myositis (rhabdomyolysis) myoglobulinuria, acute renal failure [Fibrates should be avoided in such patients and also in alcoholics]
30 Fibric Acid Derivatives [Fibrates] Drug interactions: 1. Increased risk of myopathy when combined with statins. 2. Displace drugs from plasma proteins (e.g. oral anticoagulants and oral hypoglycemic drugs). Contraindications: 1- Patients with impaired renal functions. 2- Pregnant or nursing women. 3-Preexisting gall bladder disease.
31 Fibric Acid Derivatives [Fibrates] Clinical uses: Mixed dyslipidemia (i.e. raised serum TG and ) Patients with low HDL and high risk of atheromatous disease (often type 2 diabetic patients) Patients with severe treatment- resistant dyslipidemia (combination with other lipidlowering drugs)
32 NICOTINIC ACID (NIACIN) Mechanism of action: 1. In adipose tissue: it binds to adipose nicotinic acid receptors, this will lead to decrease in free fatty acids mobilization from adipocytes to the liver resulting in TG and thus VLDL synthesis. 2. In liver: niacin inhibits hepatocyte diacylglycerol acyltransferase-2, a key enzyme for TG synthesis. Thus, it decreases VLDL production. 3. In plasma: it increases LPL activity that increases clearance of VLDL & chylomicron.
33 Nicotinic acid (Niacin) Adverse effects: Pruritus, rashes, flush acanthosis: The niacin flush results from the stimulation of prostaglandins D(2) and E(2). This flush is avoided by low dose aspirin 325 mg ½ h before niacin. Reactivation of peptic ulcer (because it stimulates histamine release resulting in increased gastric motility and acid production. Hepatic dysfunction Hyperglycemia which is believed to be caused by an increase in insulin resistance. Palpitations, Nausea and abdominal discomfort Hyperuricaemia
34 Nicotinic acid (Niacin) Contraindications 1. Gout. 2. Peptic ulcer. 3. Hepatotoxicity. 4. Diabetes mellitus. Therapeutic Uses Niacin is the most effective medication for increasing HDL cholesterol levels and it has positive effects on the complete lipid profile. Mixed dyslipidemias.
35 Ezetimibe Mechanism of action: Impairs dietary and biliary cholesterol absorption at the brush border of the intestines without affecting fat-soluble vitamins. Reducing the pool of cholesterol absorbed from the diet results in a reduced pool of cholesterol available to the liver. The liver in turn will upregulate the LDL receptor, trapping more LDL particles from the blood and result in a fall in measured LDL cholesterol. Pharmacokinetics Elimination half-life of ezetimibe approx. 22 h Long half-life: 1. Permits once-daily dosing 2. May improve compliance
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37 Bile acid binding resins Anion exchange resins Drugs : Cholestyramine, Colestipol Pharmacological effects: TC/LDL-C HDL MOA: When resins are given orally, they are not absorbed, they sequester bile acids in the GIT, prevent their reabsorption and enterohepatic recirculation. The r e s u l t is: decreased absorption of exogenous and increased metabolism of endogenous into bile acids in the liver increased expression of LDL receptors on liver cells increased removal of LDL from the blood reduced concentration of LDL-C in plasma
38 Bile acid binding resins Adverse effects: GIT symptoms: nausea, constipation or diarrhea abdominal bloating, Interfere with the absorption of fat-soluble vitamins and drugs (chlorothiazide, digoxin, warfarin) : These drugs should be given at least 1 hour before or 4-6 hours after a resin Use of these agents has declined since the introduction of the statins. They require very large doses and need to be taken with lots of water. C l i n i c a l u s e s: Heterozygous familial hypercholesterolemia: Hypercholesterolemia when a statin is contraindicated Uses unrelated to atherosclerosis, including: pruritus
39 Others Fish oil (rich in highly unsaturated fatty acids) to decrease TG, VLDL, LDL-C and to increase HDL-C Reduce plasma TG but increase ( is more strongly associated wih coronary artery disease) The effects on cardiac morbidity or mortality is unproven (although there is epidemiological evidence that eating fish regularly does reduce ischemic heart disease)
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