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Hyperlipidemia > Medication > Flashcards

Medication Flashcards

1
Q

Drugs that inhibit cholesterol absorption

A

Bile Acid- Binding Resins and cholesterol absorption inhibitors

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2
Q

Bile acid binding resins: MOA

A

bind to the bile acids prevention reabsorption thereby the availability of cholesterol and triglycerides in the liver; bile acids are the source of 75% of cholesterol in the intestine.

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3
Q

Bile acid binding resins: Warning

A

Use cautiously in pts with hypertriglyceridemia because of the upregulation of cholesterol and triglyceride synthesis.

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4
Q

Bile acid binding resins: Colesevelam

A

lowers glycated hemoglobin and fasting plasma glucose; is approved as add-on tx for glycemic ctrl in select patients with type 2 diabetes

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5
Q

Cholesterol Absorption Inhibitors: MOA

A

block the intestinal absorption of cholesterol of dietary and biliary origin as well as plant sterols do (plant sterols aka phytosterols are available via plants)

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6
Q

Cholesterol Absorption Inhibitors: Ezetimibe

A

Inhibits cholesterol absorption which increases expression of hepatic LDL receptors and enhances clearance of LDL from circulation; reduces LDL by 15-20%; it is indicated as adjunctive tx to diet for reduction of cholesterol, LDL, and ApoB in those with PH; is synergistic with statins can lower LDL by additional 25% than statins alone.

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7
Q

Effects

A

Reduces cholesterol absorption by 50%; unlike bile acid binding resins it does not prevent absorption of triglycerides or fat-soluble vitamins.

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8
Q

Vytorin

A

Is a combo drug made of ezetimibe and simvastatin

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9
Q

Cholesterol Absorption Inhibitors: AE

A

URI, sinusitis, diarrhea, arthralgia; pain in an extremity

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10
Q

Drug Interactions

A

Cyclosporine, cholestyramine and fibrates; use of ezetimibe with a statin is CA in pts with active liver disease or unexplained persistent elevated transaminases as well as pregnant/nursing women

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11
Q

Fibrates: MOA

A

Activation of lipoprotein lipase which lowers triglycerides and VLDL; inhibition of Apo C-III synthesis in the liver, preventing the inhibitory action of Apo C-III on lipoprotein lipase activity; and stimulation of Apo A-I and Apo A-II expression which increases HDL levels

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12
Q

Fibrates: Pharmacology

A

The removal of triglycerides from chylomicrons alters the size and composition of LDL from small, dense particles to large, buoyant and less atherogenic particles that have a greater affinity for LDL receptors and are rapidly cleared from the plasma

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13
Q

Fibrates: Types

A

Fenofibrates, gemfibrozil, and bezafibrate

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14
Q

Fibrates: Effectiveness

A

Decrease triglyceride levels by 20-50%, increase HDL 10-20% and lower LDL by 5-15%

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15
Q

Fibrates: Indications for use

A

Treatment of hypertriglyceridemia and dysbetalipoproteinemia and in individuals with moderately elevated triglyceride levels (150-400), as sign often associated with metabolic syndrome. Prevention of pancreatitis in patients with severely high triglyceride levels (>1,000)

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16
Q

Fibrates: Adverse Effects

A

GI: N/D, dyspepsia, and abdominal pain. Skin rash, myalgias, headache and impotence

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17
Q

Fibrates: Drug Interactions

A

Myositis occurs in up to 5% of patients taking a fibrate who are also being treated with statins. when combined with statins, fenofibrate is the preferred drug because it has less risk of rhabdomyolysis compared with gemfibrozil. Fibrates potentiate the effects of oral anticoagulants as they compete for their binding sites to albumin. fibrates also increase cholesterol excretion onto the bile, leading to a risk of cholelithiasis. D/C fibrate if gallstones occur

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18
Q

Statins: MOA

A

the most effective and the most prescribed class of lipid-lowerin drugs

19
Q

Statins: MOA

A

Selectively inhibit HMG CoA to mevalonate, the rate-limiting step in cholesterol synthesis in the liver. Inhibition of HMG CoA reductase leads to increased expression of the hepatic LDL receptor and increased clearance of LDL from the circulation

20
Q

Statins: Types and effectiveness

A

Rosuvastatin, atorvastatin, and simvastatin have the highest drug efficacy. Others - lovastatin, pravastatin, fluvastatin.

21
Q

Statin: effects

A

Selective inhibition of hepatic HMG-CoA reductase initiates a cascade of events that results in decreases synthesis of cholesterol; decreased liver release of VLDL; and activation of the transcription factor SREBP2, which upregulates the LDL receptor and consequently increases the clearance of plasma LDL. As 60-70% of serum cholesterol is synthesized in the liver by HMG-CoA reductase, inhibition of the enzyme drastically lowers circulating LDL

22
Q

Statins: Additional pleiotropic effects

A

Modulation of endothelial function, decrease in vascular inflammation, neuroprotection, and immunomodulation by inhibition of major histocompatibility complex II expression, which is upregulated in patients with myocarditis, MS and rheumatoid arthritis. Statins have been linked to a reduction in he risk of developing Alzheimer disease

23
Q

Statins: choice of therapy

A

initial dosaage should be based on LDL percentage reduction (table 5)

24
Q

Statins: combination therapy

A

The combination of simvastatin with ezetimibe lowers LDL by an additional 18-20%; Administration of statins with bile acid-binding resin produces 20% to 30% greater reduction

25
Q

Statins: warnings

A

Stains are well absorbed through eh GI system and are metabolized by the liver by cytochrome P450. metabolites are eliminated through the bile and excreted in the feces and, to a lesser extent, the kidneys. These drugs should not be used in patients with active liver disease and should be used cautiously at lower does in patients with kidney disease

26
Q

Statins: Adverse effects

A

Dizziness, diarrhea, N/V and abdominal cramps. Associated with hepatotoxicity and elevated transaminases in 1-2% of patients. Rarely causes liver injury. Myopathy (muscle pain, weakness and grossly elevated creatine kinases levels - > 10xs the upper limit of normal) See Table 6 for management of side effects

27
Q

Statins: Drug Interactions

A

Drugs that inhibit their metabolism and increases their bioavailability such as CYP2CP inhibitors (azole antifungals, erythromycin, protease inhibitors, amiodarone, grapefruit) and CYP2C9 inhibitors (NSAIDs, phenytoin, warfarin); as well as drugs that potentiate stat’s therapeutic and AE (fibrates, niacin). These interactions increase statin toxicity

28
Q

Statins: clinical use

A

Lower LDL by 20-55%. Are also effective in the treatment of hypertriglyceridemias when levels are > 250, although fibrates remain the drug of choice for that use. When elevation of HDL is required, niacin remains the drug of choice, although combo tx may be considered in pts who also have elevated LDL

29
Q

Clinical pearls

A

Co-administration of statins and niacin, fibrates or ezetimibe increases the lipid lowering benefit but also increases risk of AR; if a fibrate is necessary it is safer to use fenofibrate

30
Q

Nicotinic Acid Derivatives: MOA

A

Niacin, aka nicotinic acid or vitamin B3, is a water-soluble vitamin. it is available in normal or extended-release formulation as well as in conjunction with lovastatin (Advicor)

31
Q

Niacin: Dosage

A

1,500-3,000 mg/day is required to gain lipid lowering effects; normal vitamin dose in 50 mg/day

32
Q

Niacin: Recommended Use

A

Specific Clinical Situations: (1) Triglycerides > 500 mg/dL, (2) a patient who is not able to achieve desired responses, or (3) is intolerant to other therapies. Not recommended by AHA/ACC guidelines

33
Q

Fish Oil Derivatives

A

Omega 3 polyunsaturated fatty acids are essential fatty acids because our bodies are unable to synthesize them

34
Q

Types of Fish Oil

A

Eicosapentaenoic (EPA), Docosahexaenoic acid (DHA) are derived from linolenic acid (ALA) and dietary supplementation is the only physiologically reelvenet source

35
Q

Sources of EPA and DHA

A

fatty fish (salmon, mackerel, sardines, trout, herring), other seafood sources, walnuts, canola, flaxseed and linseed oil

36
Q

Function of EPA and DHA

A

reduce the synthesis and secretion of VLDL and increase triglyceride removal from VLDL and chylomicrons through the upregulation of lipoprotein lipase

37
Q

Other benefits of Omega 3

A

anti-arrhythmic, antihypertensive, anti-atherogenic, and antithrombotic

38
Q

Effectiveness of Omega 3

A

primary and secondary prevention of CHD, reduce the risk of sudden cardiac mortality, and overall mortality; lower triglycerides. Can be used alone or in conjunction with medications

39
Q

Supplements

A

may also contain unwanted cholesterol or fats or toxins or oxidized fatty acids

40
Q

Prescriptions

A

900 mg of ethyl esters of Omega-3 (500mg EPA and 400 mg DHA) ; (2) 1,000 mg of omega 3 in free fatty acid form (contains 500-600 mg EPA, 150-250 mg DHA, and 150-320 of other omega 3. Dosage is 4g either once daily or 2 g BID; (3) icosapent ethyl as an adjunct for adults with triglycerides > 150, CVD and/or DM, and at least 2 other risk factors

41
Q

DHA and EPA

A

may be considered for trigykcerise levels > 1,000 and may be used alone or in conjuction with HMG-CoA

42
Q

Warnings: contamination and toxicty

A

There is a risk of mercury and other contaminants but in 2009, the FDA posted a warning regarding the ethyl ester formulations reporting anaphylactic or severe allergic rxs, and hemorrhagic diathesis

43
Q

Adverse effects

A

Minor GI: fish burps, eructation, diarrhea

44
Q

Drug Interactions

A

Anticoagulants: it has been recommended that bleeding times during 1st 3-6 months be monitored

Hyperlipidemia (7 decks)

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