Lipids Hyperlipidemia

Hyperlipidemia. Elevated lipid levels in the blood. Hypertension. Elevated blood pressure. 

Nicotinic acid is used in the treatment of hyperlipidemia. It causes various changes in lipid and lipoprotein metabolism when administered in high doses (up to 5 g/d) ... 

In many individuals, hyperlipidemia has no symptoms and the disorder is not discovered until laboratory tests reveal elevated cholesterol and triglyceride levels, elevated LDL levels, and decreased HDL levels. Often, these drags are initially prescribed on an outpatient basis, but initial administration may occur in the hospitalized patient. Seram cholesterol levels (ie, a lipid profile) and liver functions tests are obtained before the drugs are administered. 

TOMEO A c, GELLER M (1995) Antioxidant effect of tocotrienols in patients with hyperlipidemia and carotid stenosis. Lipids, 30 1179-83. 

Hyperlipidemia has not clearly been established as a risk factor for stroke, although it is a modifiable risk factor for coronary heart disease. Recent studies show that statin use may reduce the incidence of a first stroke in high-risk patients (e.g., hypertension, coronary heart disease, or diabetes) including patients with normal lipid levels. A recent meta-analysis showed a 25% risk reduction for fatal and non-fatal strokes with statin use.4 Patients with a history of MI, elevated lipid levels, diabetes, and... 

Bexarotene—causes severe hyperlipidemia in majority of patients treated may require concomitant lipid-lowering therapy... 

Primary or genetic lipoprotein disorders are classified into six categories for the phenotypic description of dyslipidemia. The types and corresponding lipoprotein elevations include the following I (chylomicrons), Ha (LDL), lib (LDL + very low density lipoprotein, or VLDL), III (intermediate-density lipoprotein), IV (VLDL), and V (VLDL + chylomicrons). Secondary forms of hyperlipidemia also exist, and several drug classes may elevate lipid levels... 

A complete history and physical examination should assess (1) presence or absence of cardiovascular risk factors or definite cardiovascular disease in the individual (2) family history of premature cardiovascular disease or lipid disorders (3) presence or absence of secondary causes of hyperlipidemia, including concurrent medications and (4) presence or absence of xanthomas, abdominal pain, or history of pancreatitis, renal or liver disease, peripheral vascular disease, abdominal aortic aneurysm, or cerebral vascular disease (carotid bruits, stroke, or transient ischemic attack). 

Many patients treated for primary hyperlipidemia have no symptoms or clinical manifestations of a genetic lipid disorder (e.g., xanthomas), so monitoring is solely laboratory based. 

Side effects of thiazides include hypokalemia, hypomagnesemia, hypercalcemia, hyperuricemia, hyperglycemia, hyperlipidemia, and sexual dysfunction. Loop diuretics have less effect on serum lipids and glucose, but hypocalcemia may occur. 

Unlike the previously discussed compounds, which inhibit MTP in both liver and intestine, an intestine-selective orally-active MTP inhibitor JTT-130 (structure not yet disclosed) has been reported to decrease plasma cholesterol and TG in guinea pigs with no hepatic lipid accumulation [16]. Although further studies in human are needed, inhibitors that selectively target intestinal MTP might be a safer alternative as a treatment for hyperlipidemia than the liver-targeting MTP inhibitors. 

B Chronic hyperlipidemia and chronic infection potentiate inflammation and lipid oxidation. An increase of lipid oxidation might inhibit tbe immune system and thus facilitate a chronic infection and a rise in oxLDL-mediated apoptosis. 

Excess lipid in the blood can result from primary genetic deficiencies, most of which are rare, or as a secondary consequence of another disease. Two primary hyperlipidemias, type I hypertriglyceridemia and type IIA hypercholesterolemia, are summarized in Table 1-15-2. 

As noted above, obesity is a health problem. It is associated with both elevated mortality and morbidity. More specifically, obesity is a risk factor for cardiovascular disease, including heart attack and stroke, and for high blood pressure (hypertension), diabetes, and hyperlipidemia (elevated levels of lipids in the blood, a risk factor for atherosclerosis and its sequelae), and for cancer. 

Other- Liver disease with impaired hemostasis severe renal disease. Hyperlipidemia Heparin may increase free fatty acid serum levels by induction of lipoprotein lipase. The catabolism of serum lipoproteins by this enzyme produces lipid fragments that are rapidly processed by the liver. Patients with dysbetalipoproteinemia (type III) are unable to catabolize the lipid fragments, resulting in hyperlipidemia. 

Lipid metabolism Raloxifene lowers serum total and LDL cholesterol by 6% to 11 % but does not affect serum concentrations of total HDL cholesterol or triglycerides. Take these effects into account in therapeutic decisions for patients who may require therapy for hyperlipidemia. 

Monitoring Pretreatment and annual exams should include blood pressure, breasts, abdomen and pelvic organs, including Papanicolaou smear. Perform preventative measures and screening, which should include total and HDL cholesterol within 5-year intervals. Advise the pathologist of OC therapy when relevant specimens are submitted. Do not prescribe for more than 1 year without another physical exam. Lipid disorders Closely follow women taking OCs who are being treated for hyperlipidemias. 

Treatment of hyperlipidemia is based on the assumption that lowering serum lipids decreases morbidity and mortality of atherosclerotic cardiovascular disease. 

The cornerstone of treatment in primary hyperlipidemia is diet restriction and weight reduction. Limit or eliminate alcohol intake. Use drug therapy in conjunction with diet, and after maximal efforts to control serum lipids by diet alone prove unsatisfactory, when tolerance to or compliance with diet is poor or when hyperlipidemia is severe and risk of complications is high. Treat contributory diseases such as hypothyroidism or diabetes mellitus. 

Monitor patients who are administered sirolimus for hyperlipidemia using laboratory tests. If hyperlipidemia is detected, initiate subsequent interventions such as diet, exercise, and lipid-lowering agents, as outlined by the National Cholesterol Education Program guidelines. 

Unless contraindicated, lipid lowering with HMGCoA reductase inhibitors (statins) should be used to treat hyperlipidemia for prevention of cardiovascular complications and are effective and well tolerated in those at least up to 80 years with coronary disease. 

Prazosin may be particularly useful when patients cannot tolerate other types of antihypertensive agents or when blood pressure is not well controlled by other drugs. Since prazosin does not significantly influence blood uric acid or glucose levels, it can be used in hypertensive patients whose condition is complicated by gout or diabetes meUitus. Prazosin treatment is associated with favorable effects on plasma lipids. Thus, it may be of particular importance in managing patients with hyperlipidemia. 

Hyperlipidemia, dyslipidemia PO 5 to 40 mg/day. Usual starting dosage is 10 mg/day, with adjustments based on lipid levels monitor q2-4wk until desired level is achieved. Maximum 40 mg/day. 

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