Hyperlipidemias

Hyperlipidemia is a condition characterized by the presence of elevated lipoprotein levels in the blood. The term hyperlipidemia encompasses a number of different conditions, but it most often refers to high levels of cholesterol in the form of low-density lipoprotein (LDL). LDL cholesterol is often called bad cholesterol. High-density lipoprotein (HDL) is the good form of cholesterol. High LDL and/or low HDL levels are widely believed to be linked to increased heart disease risk. Because of the prevalence of hyperlipidemia in developed nations, antihyperlipidemic drugs are in high demand. 

Hyperlipidemia is known to be one of the most potent factor associated with the premature development of atheromatous arterial disease. Thus an increased serum cholesterol level is frequently found in patients with ischemic heart disease and myocardial infarction, and hypercholesterolemic patients have a high incidence of coronary artery disease. Therefore, because cholesterol is partially eliminated from the body as bile acids (see Section VB), it would be important to know the role of bile acid metabolism in the development of different types of hypercholesterolemia. 

It has been reported that fecal elimination of bile acids correlates negatively (62,90) with the serum cholesterol level in patients with familial hypercholesterolemia, suggesting that in this condition conversion of cholesterol to bile acids is defective and that this defect contributes to the development of hypercholesterolemia. A low average fecal output of bile acids has been repeatedly detected in this condition (11,62,63,90). The detailed relationship of fecal bile acids to obesity and sex based on 69 subjects with familial hypercholesterolemia is presented in Table II. 

The negative correlation between fecal bile acids and serum cholesterol was of low degree for the total series (r = —0.24) and for nonobese patients (r = —0.27), the correlation being positive with the serum cholesterol pool (r = 0.28). Fecal bile acids also correlated positively with body weight (r = 0.52), relative body weight (r = 0.31), and body surface (r = 0.53). 

Another group of hypercholesterolemic (type II) patients, indicated in Table II by the term essential hypercholesterolemia, was also studied. These patients differed from familial hypercholesterolemia patients in that the family history was less clear, serum cholesterol was less elevated, and xanthomata were not present. Hypercholesterolemia may be primarily caused by environmental, primarily dietary, factors. Bile acid production in this group is less significantly reduced than in the familial group, and the relative catabolism of cholesterol by way of bile acids is within normal limits. Sodhi (151) observed in this type of hypercholesterolemia a markedly low fecal bile acid excretion. 

In agreement with the findings presented above, the turnover of cholic acid has been reported to be low in patients with hypercholesterolemia (73, 152). Production of cholic and chenodeoxycholic acids has also been shown to be markedly lower in hypercholesterolemic than in triglyceridemic patients, the former subjects exhibiting a smaller cholic but not chenodeoxycholic acid pool than the latter ones (69). 

Dyslipidemia is defined as elevated total cholesterol, low-density lipoprotein (LDL) cholesterol, or triglycerides a low high-density lipoprotein (HDL) cholesterol or a comhination of these abnormalities. Hyperlipoproteinemia describes an increased concentration of the lipoprotein macromolecules that transport hpids in the plasma. Abnormalities of plasma lipids can result in a predisposition to coronary, cerebrovascular, and peripheral vascular arterial disease. 

Cholesterol, triglycerides, and phosphohpids are transported in the bloodstream as complexes of lipid and proteins known as hpoproteins. Elevated total and LDL cholesterol and reduced HDL cholesterol are associated with the development of coronary heart disease (CHD). 

Repeated injiuy and repair within an atherosclerotic plaque eventually lead to a fibrous cap protecting the underlying core of lipids, collagen, calcium, and inflammatory cells such as T lymphocytes. Maintenance of the fibrous plaque is critical to prevent plaque rupture and subsequent coronary thrombosis. 

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), Ila (LDL), Ilb (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 dmg classes may elevate hpid levels 

The primary defect in familial hypercholesterolemia is the inability to bind LDL to the LDL receptor (LDL-R) or, rarely, a defect of internalizing the LDL-R complex into the cell after normal binding. This leads to lack of LDL degradation by cells and unregulated biosynthesis of cholesterol, with total cholesterol and LDL cholesterol (LDL-C) being inversely proportional to the deficit in LDL-Rs. 

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

Diuretics Frequent urination, hyperuricemia, hyperglycemia, hyperlipidemia... 

Hyperlipidemia. Bile acid binding resins such as cholestyramine sequester bile acids in the intestine,... 

As described in the previous section, bile acids have evolved over the last years from regulators of bile acid homeostasis to general metabolic integrators. It is therefore not too surprizing that a number of bile acid-activated signaling pathways have become attractive targets for the treatment of gallstones and other metabolic diseases, such as obesity, type 2 diabetes, hyperlipidemia, and atherosclerosis. 

LRP6 Missense mutation (familial, autosomal dominant) Autosomal dominant early coronary artery disease (hyperlipidemia, hypertension, diabetes)... 

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) ... 

Hyperlipidemia, particularly elevated serum cholesterol and LDL levels, is a risk factor in the development of atlierosclerotic heart disease. Other risk factors, besides cholesterol levels, play a role in the development of hyperlipidemia. Additional risk factors include ... 

In general, the higher the LDL level and the more risk factors involved, the greater the risk for heart disease. The main goal of treatment in patients with hyperlipidemia is to lower the LDL to a level that will reduce the risk of heart disease ... 

These drugs, alongwith a diet restricted in saturated fat and cholesterol, are used to treat hyperlipidemia when diet and other nonpharmacologic treatments alone have not resulted in lowered cholesterol levels. 

While the fibric acid derivatives have antihyperlipidemic effects, their use varies depending on the drug. For example, Clofibrate (Atromid-S) and gemfibrozil (Lopid) are used to treat individuals with very high serum triglyceride levels who present a risk of abdominal pain and pancreatitis and who do not experience a response to diet modifications. Clofibrate is not used for the treatment of other types of hyperlipidemia and is not thought to be effective for prevention of coronary heart disease. Fenofibrate (Tricor) is used as adjunctive treatment for the reduction of LDL, total cholesterol, and triglycerides in patients with hyperlipidemia. 

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. 

The nurse takes a dietary history, focusing on the types of foods normally included in the diet. Vital signs and weight are recorded. The skin and eyelids are inspected for evidence of xanthomas (flat or elevated yellowish deposits) that may be seen in the more severe forms of hyperlipidemia. 

Because hyperlipidemia is often treated on an outpatient basis, die nurse explains die drug regimen and possible adverse reactions. If printed dietary guidelines are given to die patient, die nurse emphasizes the importance of following these recommendations. Drug dierapy usually is discontinued if the antihyperlipidemic drug is not effective after 3 months of treatment. 

A patient in the medical clinic is taking cholestyramine (Questran) for hyperlipidemia. The primary health care provider has prescribed TLC for the patient. The patient is on a low-fat diet and walks daily for exercise. His major complaint at this visit is constipation, which is very bothersome to him. Discuss how you would approach this situation with the patient. What information would you give the patient concerning his constipation ... 

Which of the following points would the nurse include when teaching a patient about drug and diet therapy for hyperlipidemia ... 

The most common adverse reaction associated with the administration of fat emulsion is sepsis caused by administration equipment and thrombophlebitis caused by vein irritations from concurrently administering hypertonic solutions. Less frequently occurring adverse reactions include dyspnea, cyanosis, hyperlipidemia, hypercoagulability, nausea, vomiting, headache flushing, increase in temperature sweating, sleepiness, chest and back pain, slight pressure over the eyes, and dizziness. 

Loading of the Liver With Fructose May Potentiate Hyperlipidemia Hyperuricemia... 

Alcoholism leads to fat accumulation in the liver, hyperlipidemia, and ultimately cirrhosis. The exact mechanism of action of ethanol in the long term is stiU uncertain. Ethanol consumption over a long period leads to the accumulation of fatty acids in the liver that are derived from endogenous synthesis rather than from increased mobilization from adipose tissue. There is no impairment of hepatic synthesis of protein after ethanol ingestion. Oxidation of ethanol by alcohol dehydrogenase leads to excess production of NADH. 

Nicotinic acid has been used to treat hyperlipidemia when of the order of 1—6 g/d are required, causing dilation of blood vessels and flushing, with skin irritation. Intakes of both nicotinic acid and nicotinamide in excess of 500 mg/d can cause liver damage. 

Phytochemicals have little nutritional value and do not get absorbed in the body, but they seem to turn on certain switches in the biochemical mechanisms, which signal the beneficial pathways to maintain health, and to turn off the switches which proceed to adverse biochemical pathways. Rice bran products have demonstrated significant benefits as nutritional therapies in diabetes, hyperlipidemia, cancer, fatty liver, hypercalcuria and heart disease. There is experimental and clinical evidence for the beneficial health effects of the following bioactives of rice bran ... 

RUKMINI c, REDDY SASTRY c, MCPEAKP, LYNCH I (2000) Method for treating hypercholesterolemia, hyperlipidemia, and atherosclerosis. US Patent 6,126,943. 

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