ch 47 - lipid lowering agents

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34 Terms

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antihyperlipidemic agents

general term used for drugs used to lower lipid levels in the blood

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bile acids

cholesterol-containing acids found in the bile that act like detergents to break up fats in the small intestine

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cholesterol

waxy, fat-like substance found in all cells of the body, essential for the formation of cells and hormones, but can contribute to health issues when levels are too high.

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chylomicron

carrier for lipids in the bloodstream, consisting of proteins, lipids, cholesterol, and other component

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High-density lipoprotein (HDL)

good cholesterol

loosely packed chylomicron-containing fats, able to absorb fats and fat remnants in the periphery and deposit into liver for excretion; thought to have a protective effect, decreasing the development of atherosclerotic cardiovascular disease

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hydroxymethylglutaryl-coenzyme A (HMG-CoA) reductase

enzyme that regulates the last step in cellular cholesterol synthesis

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hyperlipidemia

excessive amounts of lipids in the blood

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low-density lipoprotein (LDL)

"bad cholesterol"

it carries cholesterol to cells but can deposit excess cholesterol in arteries, leading to atherosclerosis and increased risk of cardiovascular disease.

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ASCVD

Atherosclerotic cardiovascular disease, a condition characterized by the buildup of fatty deposits in the arteries, leading to reduced blood flow and increased risk of heart attacks and strokes.

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ASCVD risk factors

LDL>100, HTN, smoking, sedentary lifestyle, unhealthy diet, diabetes, gout, family history of premature ASCVD

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what can cause high cholesterol?

  • genetics

  • high fat diet

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causes of hyperlipidemia

Excessive dietary intake of fats

Genetic alterations in fat metabolism leading to a variety of elevated fats in the blood

Lack of exercise

Smoking

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treating ASCVD

dietary modification, exercise, medications

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lipid-lowering agents

bile acid sequestrants, HMG-CoA reductase inhibitors (Statins), a cholesterol absorption inhibitor, and PCSK9 inhibitors

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bile acid sequestrants

Cholestyramine, colestipol, colesevelam

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actions&indications for bile acid sequestrants

Reduce serum cholesterol in patients with primary hypercholesterolemia by binding to bile acids in the intestines, preventing reabsorption in the liver and promoting cholesterol excretion

Cholestyramine: pruritus associated with partial biliary obstruction

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contraindications to bile acid sequestrants

allergy, bile obstruction, abnormal intestinal function

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adverse effects to bile acid sequestrants

constipation/ nausea/ aggravation of hemorrhoids(Gi effects)

heartburn

headache, drowsiness/ fatigue

increased bleeding time due to decreased absorption of vitamin K, Vitamin A and D deficienciesproblems with fat soluble vitamins

Rash

Muscle aches and pains

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nursing considerations when administering bile acid sequestrants

Inspect the abdomen for distention and auscultate bowel sounds for changes in GI motility.

Assess bowel elimination patterns, including frequency of stool passage and stool characteristics, to identify possible constipation and fecal impaction.

Monitor the results of laboratory tests, including serum cholesterol and lipid levels, to evaluate the effectiveness of drug therapy.

Educate pt not to chew, crush, or cut tablets

Take med before meals; administer other meds 1 hour before or 4-6 hours after these meds

Encourage pt to increase fluid intake and dietary fiber to prevent constipation

Small frequent meals help nausea

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HMG-CoA Reductase Inhibitors (Statins)

atorvastatin, simvastatin

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actions&indications for statins

block cholesterol production, decreasing LDL levels and slightly increasing HDLs

Most effective

indications: increased cholesterol, triglycerides, and LDL unresponsive to dietary restrictions; slows progression of ASCVD, assist with prevention of MI, stroke, revascularization procedures in patients with multiple ASCVD risk factors

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contraindications and cautions Statins

allergy, active liver disease

history of or chronic liver impairment, renal impairment, impaired endocrine function

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adverse effects to Statins

GI/CNS effects, hepatotoxicity(cholesterol is made in liver), rhabdomyolysis(breakdown of muscle tissue), muscle pain

**avoid grapefruit juice and alcohol

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nursing considerations for Statins

- Assess baseline lipid panel, liver function tests, and creatine kinase levels before administering therapy

- Assess for muscle pain, weakness, or tenderness

- Assess for signs and symptoms of liver dysfunction (jaundice, dark urine, right upper quadrant pain)

  • Take with evening meals

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Cholesterol Absorption Inhibitor

Ezetimibe (Zetia).

Take 1 hour before or 4 hours after other antilipemics. Risk of liver damage increased when combined with statins.

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actions and indications of cholesterol absorption inhibitor

Inhibits the absorption of cholesterol secreted in the bile and from food —- prevents absorption in small intestine / bloodstream. Often used in combination with other antilipemic medications.

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adverse effects of cholesterol absorption inhibitor

- mild abdominal pain and diarrhea

- headache, dizziness, fatigue, upper resp tract infection, back pain, muscle aches and pain, hepatotoxicity

- hepatitis (rare)

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drug-drug interactions: cholesterol absorption inhibitor

- bile acid sequestrants

- statins

- cyclosporine and fibrates

- fenofibrate

- warfarin

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what levels increase in a patient taking ezetimide?

warfarin

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fibrates

fenofibrate, gemfibrozil, fenofibric acid

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fenofibrate actions

- increases lipolysis and elimination of triglycerides

- increases uric acid production

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gemfibrozil actions

- inhibits peripheral breakdown of lipids

- reduces production of triglycerides and LDLs

- increases HDL concentrations

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Vitamin B3 (Niacin) actions

inhibits the release of free fatty acids from adipose tissue, increases the rate of triglyceride removal from plasma, and generally reduces LDL and triglyceride levels and increases HDL levels.

increases uric acid--> may lead to gout

often combined with bile sequestrants

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Vitamin B3 adverse effects

GI upset, flushing, muscle pain, hepatotoxity, hyperglycemia, gout