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NAPLEX Review > Dyslipidemia > Flashcards

Dyslipidemia Flashcards

1
Q

What is the importance of cholesterol in the body?

A

Cholesterol is an important component of healthy cells and tissues, including the brain. Cholesterol is a structural component of cell walls, a precursor in hormone synthesis and is used in the production of bile acids

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2
Q

What is enterohepatic recycling?

A

Bile acids travel from the liver through the bile ducts (with free cholesterol and waste products) and into the small intestine, where they are needed to absorb fat. The acidic environment in the intestine converts bile acids into bile salts, which are recycled from the intestine and returned to the liver

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3
Q

What is the result if the absorption of free cholesterol is blocked in the intestine or the enterohepatic recirculation of bile salts is blocked?

A

The end result is a decrease in cholesterol

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4
Q

What is atherosclerosis?

A

Atherosclerosis is the formation of plaque from a buildup of fats, cholesterol and other substances on the inner walls of arteries

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5
Q

What complication does atherosclerosis lead to?

A

Atherosclerosis leads to atherosclerotic cardiovascular disease, which includes myocardial infarction, stroke/transient ischemic attacks, angina and peripheral arterial disease

*Different types of cholesterol protect from or contribute to ASCVD risk

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6
Q

What lipoproteins is included in total cholesterol?

A

Low-density lipoprotein (LDL), high-density lipoprotein (HDL) and very-low density lipoprotein (VLDL)

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7
Q

Describe HDL

A

HDL takes cholesterol from the blood and delivers it to the liver for removal from the body. High LDL lowers ASCVD risk

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8
Q

What does non-HDL include and what does it predict?

A

Non-HDL includes the lipoproteins that contribute to atherosclerosis: LDL, intermediate-density lipoproteins, VLDL, chylomicron remnants and lipoprotein(a). Non-HDL is a strong predictor of ASCVD

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9
Q

How is non-HDL calculated?

A

Non-HDL = TC - HDL

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10
Q

What is lipoprotein (a)?

A

Lipoprotein (a) is a genetic variant of LDL. High lipoprotein (a) indicates high risk of ASCVD

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11
Q

What is a complication that can occur with high triglycerides (TGs)?

A

High triglycerides or hypertriglyceridemia, are associated with high ASCVD risk. TGs > 500 mg/dL can cause acute pancreatitis

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12
Q

What is dyslipidemia?

A

Abnormal lipoprotein levels are called dyslipidemias

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13
Q

What is primary (familial) hypercholesterolemias?

A

Genetic defects that cause severe cholesterol elevations. FHs include heterozygous familial hypercholesterolemia (HeFH) and homozygous familial hypercholesterolemia (HoFH)

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14
Q

How can familial dyslipidemias be categorized by?

A

Fredrickson classification

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15
Q

What are most dyslipidemias due to?

A

Most dyslipidemias are due to poor diet and lack of physical activity that result in central adiposity

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16
Q

What are some medical conditions that can cause dyslipidemia?

A

Medical conditions that cause dyslipidemia include hypothyroidism and diabetes

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17
Q

What are some key drugs that increase both LDL and TG?

A

Diuretics, Efavirenz, Steroids, Immunosuppressants, Atypical antipsychotics, Protease inhibitors

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18
Q

What is a key drug that increases LDL only?

A

Fish oil (except Vascepa)

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19
Q

What are some key drugs that increase TG only?

A

IV lipid emulsions, propofol, bile acid sequestrants (~5%)

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20
Q

What are some conditions that can increase risk of dyslipidemia?

A

Obesity, poor diet, hypothyroidism, alcoholism, smoking, diabetes, renal/liver disease, nephrotic syndrome

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21
Q

When are lipid panels taken?

A

Lipid panels are taken after a 9-12 hour fast

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22
Q

How can LDL be calculated if it is not reported?

A

Friedewald Equation: LDL= TC - HDL - (TG/5)

*The formula is not used when the TGs are > 400 mg/dL

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23
Q

What can happen to TG level if lipid panels are not taken after fasting?

A

If not fasting, the TG level can be falsely elevated, which can cause an incorrect LDL calculation

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24
Q

What is a desirable non-HDL level?

A

< 130

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25
Q

What is a desirable LDL level?

A

< 100

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26
Q

What is a very high LDL level?

A

> 190

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27
Q

What is a desirable HDL level in women?

A

> 50

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28
Q

What is a desirable LDL level in men?

A

> 40

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29
Q

What is a desirable triglycerides level?

A

< 150

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30
Q

What is a very high triglyceride level?

A

> 500

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31
Q

Which group provides guidelines for cholesterol management?

A

The American College of Cardiology and the American Heart Association

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32
Q

What is the ASCVD risk calculation used for?

A

The ASCVD risk calculation is used to provide an estimate of an individual’s risk of having a first cardiovascular event during the next 10 years. Healthcare providers use the estimated risk to determine whether they should prescribe risk-reducing treatments

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33
Q

What does a clinician input into the ASCVD calculator?

A
  • The patient’s gender, age (20-79 years) and race
  • TC and HDL
  • Systolic blood pressure, and whether antihypertensive treatment is used
  • The presence of diabetes and smoking status
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34
Q

How often should the ASCVD risk assessment be repeated?

A

Every 4-6 years in those found to be at a low 10-year risk (< 7.5%)W

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35
Q

How often should the ASCVD risk assessment be repeated?

A

Every 4-6 years in those found to be at a low 10-year risk (< 7.5%)

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36
Q

When is an ASCVD risk score not needed?

A

The risk score is not needed for patients with clinical ASCVD, diabetes or LDL > 190 mg/dL as all patients in these groups should be started on a statin

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37
Q

What are some risk-enhancing factors that can increase ASCVD risk?

A

Very high LDL, family history of premature ASCVD, metabolic syndrome, chronic kidney disease, history of preeclampsia or premature menopause, chronic inflammatory disorders, high CRP, high coronary artery calcium score (CAC) and abnormal ankle brachial index

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38
Q

What is the CAC measurement beneficial for?

A

The CAC measurement is helpful in deciding if statins should be initiated in those with 10-year ASCVD risk of 7.5-19.9%. A CAC score > 100 Agatston units indicates statins should be initiated

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39
Q

What are some lifestyle modifications that are an important part of management of dyslipidemia?

A
  • Consume a diet to maintain a healthy weight
  • Diet should be rich in vegetables, fruits, whole grains and high-fiber foods
  • Consume fish, especially fish with high-fat content
  • Limit intake of saturated fat, trans fat and cholesterol by choosing lean meats, non-meat alternatives and low-fat dairy products. Aim for 5-6% of calories from saturated fat
  • Limit intake of added sugars and salt
  • Engage in aerobic physical activity 3-4 times per week, lasting 40 minutes/session
  • Avoid tobacco products and limit alcohol consumption
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40
Q

What is a natural product that contains naturally occurring HMG-CoA reductase inhibitors?

A

Red yeast rice

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41
Q

What are some natural products that are effective in lowering LDL?

A

Plants stanols, sterols, fibrous foods (found psyllium, barley, oat bran) and a specific type of artichoke extract are each effective in lowering LDL

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42
Q

What is a product that can lower TG?

A

OTC fish oils can be used to lower TG, but some products can increase LDL

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43
Q

What is the purpose of statin-benefit groups?

A

Patients are classified into statin-benefit groups to determine the appropriate intensity of statin treatment

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44
Q

What is the drug of choice in treating high non-HDL and LDL?

A

Statins

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45
Q

What are some other cholesterol-lowering drugs that may be used that aren’t statins?

A

Ezetimibe and PCSK9 inhibitors

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46
Q

When should many cholesterol-lowering drugs not be used?

A

Many cholesterol-lowering drugs cause liver damage. These drugs should not be used if the AST or ALT is > 3 times the upper limit of normal

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47
Q

What are the different statin benefit groups?

A
  • Secondary prevention: clinical ASCVD
  • Primary prevention: primary elevation of LDL > 190 mg/dL, diabetes and age 40-75 years with LDL between 70-189 mg/dL, age 40-75 years with LDL between 70-189 mg/dL
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48
Q

What is the patient criteria for secondary prevention of clinical ASCVD?

A

Includes CHD, stroke, TIA or peripheral arterial disease thought to be of atherosclerotic

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49
Q

What is the recommended statin treatment for those with clinical ASCVD?

A

High-intensity

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50
Q

What is the statin treatment for those with primary elevation of LDL > 190 mg/dL?

A

High intensity

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51
Q

What is the statin treatment for those with diabetes and age 40-75 years with LDL between 70-189 mg/dL?

A
  • Multiple ASCVD risk factors: High-intensity

- Regardless of 10-year ASCVD risk: Moderate-intensity

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52
Q

What is the recommended statin treatment for someone age 40-75 years with LDL between 70-189 mg/dL?

A
  • 10 year ASCVD risk > 20%: High intensity

- 10 year ASCVD risk .5-19.9% + risk-enhancing factors: moderate-intensity

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53
Q

What are considered high intensity statins?

A
  • Atorvastatin 40-80

- Rosuvastatin 20-40

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54
Q

What is considered moderate intensity statins?

A
  • Atorvastatin 10-20
  • Rosuvastatin 5-10
  • Simvastatin 20-40
  • Pravastatin 40-80
  • Lovastatin 40
  • Fluvastatin 40 BID/80 XL
  • Pitavastatin 2-4
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55
Q

What is considered a low intensity statin?

A
  • Simvastatin 10
  • Pravastatin 10-20
  • Lovastatin 20
  • Fluvastatin 20-40
  • Pitavastatin 1
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56
Q

What is the most important adverse effect of statins?

A

Muscle damage

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57
Q

How does muscle damage present after the use of statins?

A

This generally presents as muscle soreness, tiredness or weakness that is symmetrical in large adjacent muscle groups in the legs, back or arms

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58
Q

When do symptoms of the adverse effect of muscle damage typically occur?

A

Symptoms usually occur within 6 weeks of starting treatment, but can develop at any time

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59
Q

How can the severity of muscle damage be presented?

A
  • Myalgias: muscle soreness and tenderness
  • Myopath: muscle weakness +/- CPK elevations
  • Myositis: muscle inflammation
  • Rhabdomyolysis: muscle symptoms with very high CPK (>10,000) + muscle protein in the urine (myoglobinuria), which can lead to acute renal failure
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60
Q

What are some strategies to reduce the risk of myalgias with statins?

A
  • Avoid drug interactions, including OTC products
  • Do not use simvastatin 80 mg/day
  • Do not use gemfibrozil + statin
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61
Q

How do you manage myalgias from statins?

A
  • Hold statin, check CPK, investigate other possible causes
  • After 2-4 weeks; re-challenge with same statin at same or decrease dose. Most patients who did not tolerate a statin will tolerate it when re-challenged, or will tolerate a different statin
  • If myalgias return, discontinue statin. Once muscle symptoms resolve, use a low dose of a different statin; gradually increase dose
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62
Q

What are some examples of statins?

A

Atorvastatin (Lipitor), Fluvastatin (Lescol), Lovastatin (Mevacor), Pitavastatin (Livalo), Pravastatin (Pravachol), Rosuvastatin (Crestor), Simvastatin (Zocor)

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63
Q

What are some contraindications of statins?

A
  • Do not use in pregnancy, breastfeeding
  • Do not use strong CYP3A4 inhibitors with simvastatin and lovastatin
  • Do not use with liver disease, including any unexplained increases LFTs
  • Do not use with cyclosporine with pitavastatin
64
Q

What are some warnings associated with statins?

A
  • Muscle damage: myopathy/rhabdomyolysis with increased CPK +/- acute renal failure, higher risk with higher dose, advanced age (> 65 years), niacin, fibrates, CYP3A4 inhibitors, hypothyroidism (uncontrolled), renal impairment
  • Diabetes: increases A1C/FBG; benefit of statin outweighs risk
  • Hepatotoxicity, with increased LFTs (rare), immune-mediated necrotizing myopathy (IMNM)(rare)
65
Q

What are some warnings specific to Rosuvastatin?

A

Proteinuria, hematuria - usually transient

66
Q

What are some warnings specific to Atorvastatin?

A

Hemorrhagic stroke (if recent stroke or TIAs); benefit of statin outweighs risk

67
Q

What are some side effects of statins?

A

Generally well-tolerated, can cause myalgia/myopathy

68
Q

What are some baseline/routine monitoring parameters of statins?

A

Lipid panel (TC, LDL, HL, TGs) 4-12 weeks after starting treatment and then every 3-12 months (usually annually), LFTs

69
Q

What are some monitoring parameters for someone who is symptomatic?

A
  • Myalgia/myopathy: check CPK
  • Little/no urine: check SCr/BUN for acute renal failure due to rhabdomyolysis
  • Abdominal pain or jaundice: check LFTs for possible hepatotoxicity
70
Q

What are some notes about statins?

A
  • Can take Crestor, Lipitor, Livalo, Lescol XL and Pravachol at any time of day
  • FloLipid is taken on an empty stomach
  • For CrCl < 30 mL/min, use lower starting doses of lovastatin, simvastatin and rosuvastatin
  • For eGFR < 60 mL/min, use lower starting dose of pitavastatin
  • Rosuvastatin exposures are 2 times higher in Asian parents (consider 5 mg starting dose)
71
Q

What are the lipid effects of statins?

A
  • Decreased LDL ~ 20-55%
  • Increased HDL ~5-15%
  • Decreased TG ~10-30%
72
Q

Which statins are CYP3A4 substrates?

A

Atorvastatin, lovastatin and simvastatin

73
Q

Which statins have less drug interactions?

A

Rosuvastatin and pravastatin

74
Q

Can you use statins with Gemfibrozil?

A

Fibrates and niacin can increase the risk of myopathies and rhabdomyolysis. Do not use statins with gemfibrozil

75
Q

What statins can Amlodipine increase the concentrations of?

A

Amlodipine can increase the concentration of atorvastatin, lovastatin and simvastatin

76
Q

What is the max daily dose of simvastatin with concomitant use of Amlodipine?

A

Max daily dose of 20 mg/day

77
Q

What are the significant drug interactions with statins?

A

Grapefruit, Protease inhibitors, Azole antifungals, Cyclosporine/Cobicistat, Macrolides (except Azithromycin), Amiodarone, Non-DHP CCBs

78
Q

Which medications should not be taken with the use of simvastatin or lovastatin?

A

Grapefruit, protease inhibitors, azole antifungals, cyclosporine/cobicistat, macrolides

79
Q

What is the max daily dose of Rosuvastatin with cyclosporine?

A

5 mg

80
Q

What is the max daily dose of Atorvastatin with Cobicistat?

A

20 mg

81
Q

What is the max daily dose of simvastatin and lovastatin with use of Amiodarone?

A
  • Simvastatin 20 mg/day max

- Lovastatin 40 mg/day max

82
Q

What is the max daily dose of Simvastatin and Lovastatin with non-DHP CCBs?

A
  • Simvastatin 10 mg/day max

- Lovastatin 20 mg/day max

83
Q

What are some options for a non-statin add on treatment?

A

Ezetimbie, PCSK9 inhibitors, bile acid sequestrants

  • Fish oils and fibrates are used to target high triglycerides
84
Q

What is the preferred add-on treatment for patients who are very high-risk, statin at max dose & LDL remains > 70 mg/dL OR primary hypercholesterolemia (LDL > 190 mg/dL), statin at max dose & LDL remains > 100 mg/dL?

A

Ezetimibe (preferred) or PCSK9 inhibitors

85
Q

What is the MOA of Ezetimibe?

A

Inhibits absorption of cholesterol in the small intestine

86
Q

What are contraindications of Ezetimibe?

A

Vytorin: statin contraindications apply; active liver disease (including any unexplained increase in LFTs), pregnancy/breastfeeding

87
Q

What are some warnings about Ezetimibe?

A
  • Avoid use in moderate or severe hepatic impairment

- Skeletal muscle effects (e.g. myopathy, rhabdomyolysis), risk increases when combined with a statin

88
Q

What are some side effects of Ezetimibe?

A

Myalgias, diarrhea, URTIs, arthralgias, pain in extremities, sinusitis

89
Q

What are some monitoring parameters of Ezetimibe?

A

When used with a statin and/or fibrate, obtain LFTs at baseline and as clinically indicated thereafter

90
Q

What are the lipid effects with ezetimibe monotherapy?

A
  • Decreases LDL 18-23%
  • Increases HDL 1-3%
  • Decreases TG 5-10%
91
Q

What are some significant Ezetimibe drug interactions?

A
  • When Ezetimibe and cyclosporine are given together, the concentration of both can increase; monitor levels of cyclosporine
  • Concurrent bile acid sequestrants decreases ezetimibe; give ezetimibe two hours before or four hours after bile acid sequestrants
  • Can increase risk of cholelithiasis when used with fenofibrate and gemfibrozil. Do not use with gemfibrozil
92
Q

What is the MOA of PCSK9 inhibitors?

A

Proprotein convertase subtilisin kexin type 9 (PCSK9) is an enzyme that increases LDL receptor degradation. The PCSK9 inhibitors, alirocumab and evolocumab, are monoclonal antibodies that block the ability of PCSK9 to bind to the LDL receptor. They dramatically decreases LDL cholesterol and reduce the risk of cardiac events. They are costly and given by SC injection

93
Q

What are the two PCSK9 inhibitors?

A

Alirocumab (Praluent), Evolocumab (Repatha)

94
Q

What are some warnings associated with PCSK9 inhibitors?

A

Allergic reactions

95
Q

What are some side effects of PCSK9 inhibitors?

A

Injection site reactions, nasopharyngitis, influenza, URTIs, UTI, back pain (evolocumab), increased LFTs (alirocumab)

96
Q

What are the monitoring parameters of PCSK9 inhibitors?

A

LDL at baseline and at 4-8 weeks to assess response

97
Q

How should PCSK9 inhibitors be stored?

A
  • Store in the refrigerator in the original carton to protect from light
  • Can be kept at room temperature for up to 30 days; discard after 30 days if stored at room temperature
  • Prior to administration, allow prefilled pen to warm to room temperature and inspect for particulate matter and discoloration
  • Expensive: ~$14,000/yr
98
Q

What are the lipid effects of PCSK9 inhibitors?

A
  • Decreases LDL ~60%
  • Decreases non-HDL ~35%
  • Decreases apoB ~50%
  • Decreases TC ~36%
99
Q

What is the MOA of bile acid sequestrants?

A

The drugs bind bile acids in the intestine, forming a complex that is excreted in the feces. This non-systemic action results in a partial removal of the bile acids from the enterohepatic circulation, preventing their reabsorption

100
Q

What are some examples of bile acid sequestrants?

A

Cholestyramine, Colesevelam (Welchol), Colestipol (Colestid)

101
Q

What are some contraindications of cholestyramine?

A

Complete biliary obstruction

102
Q

What are some contraindications of Colesevelam?

A

Bowel obstruction, TG > 500 mg/dL, history of hypertriglyceridemia-induced pancreatitis

102
Q

What are some contraindications of Colesevelam?

A

Bowel obstruction, TG > 500 mg/dL, history of hypertriglyceridemia-induced pancreatitis

103
Q

What are some warnings associated with bile acid sequestrants?

A
  • Cholestyramine “light” formulations and colesevelam granules contain phenylalanine and should not be used in patients with PKU
  • Increased bleeding tendency due to vitamin K deficiency
104
Q

What are some side effects associated with bile acid sequestrants?

A

Constipation (may need dose reduction or laxative), abdominal pain, cramping, bloating, gas, increased TG, dyspepsia, nausea, esophageal obstruction

105
Q

When are bile acid sequestrants not recommended?

A

Not recommended when TG are > 300 mg/dL

106
Q

What is a note about cholestyramine packets?

A

Mix powder with 2-6 oz. water or non-carbonated liquid; sipping or holding the resin suspension in the mouth for prolonged periods may lead to changes in the surface of the teeth resulting in discoloration, erosion of enamel or decay; good oral hygiene should be maintained

107
Q

What is a note about colesevelam packet?

A

Empty 1 packet into a glass; add 8 oz. of water, fruit juice or a diet soft drink and mix well

108
Q

What is a bile acid sequestrant that is an option in a pregnant patient?

A

Colesevelam

109
Q

What is a note about Colestipol packet?

A

Empty 1 packet into at least 3 oz. of liquid and stir until completely mixed

110
Q

What are the lipid effects of bile acid sequestrants?

A
  • Decreases LDL ~10-30%
  • Increase HDL ~3-5%
  • No change or increased TG ~5%
111
Q

What is an administration counseling point of the bile acid sequestrants?

A

For cholestyramine or colestipol, take all other drugs at least 1-4 hours before or 4-6 hours after the bile acid sequestrants

112
Q

What are some key drug interactions of bile acid sequestrants?

A
  • With warfarin, monitor INR frequently during initiation and after a dose change
  • The following medications should be taken four hours prior to colesevelam: cyclosporine, glimepiride, glipizide, glyburide, levothyroxine, olmesartan, phenytoin, and oral contraceptives containing ethinyl estradiol and norethindrone. Colesevelam increases levels of metformin ER
  • Bile acid sequestrants can decreases absorption of fat-soluble vitamins (A, D, E, K), folate and iron. A multivitamin may be needed, but separate administration time from the bile acid sequestrant
113
Q

What is the MOA of fibrates?

A

Fibrates are peroxisome proliferator receptor alpha (PPARa) activators, which upregulate the expresion of apolipoprotein C2 (apoC-II) and apolipoprotein A1 (apoA-1). ApoC-II increases lipoprotein lipase activity leading to increased catabolism of VLDL particles. This will decrease TG significantly

114
Q

What are examples of fibrates?

A

Fenofibrate, Fenofibric Acid, Gemfibrozil

115
Q

What are some contraindications of fibrates?

A
  • Severe liver disease, including primary biliary cirrhosis
  • Severe renal disease (CrCl < 30 mL/min)
  • Gallbladder disease
  • Breastfeeding (fenofibrate derivatives)
  • Concurrent use with repaglinide or simvastatin (gemfibrozil only)
116
Q

What are some warnings associated with fibrates?

A
  • Myopathy, increased risk when coadministered with a statin, particularly in the elderly, diabetes, renal failure or hypothyroidism
  • Cholelithiasis
  • Reversible increased SCr (> 2 mg/dL); clinical significance unknown
117
Q

What are some side effects of fibrates?

A

Dyspepsia (gemfibrozil), increased LFTs (dose-related), abdominal pain, increases CPK, URTIs

118
Q

What are some monitoring parameters of Fibrates?

A

LFTs, renal function

119
Q

What are some notes about fibrates?

A

Reduce dose if CrCl 31-80 mL/min (fenofibrates)

120
Q

What are the lipid effects of fibrates?

A
  • Decreases TG ~20-50%
  • Increases HDL ~15%
  • Decreases LDL ~5-20% (can increase LDL when TG are high)
121
Q

What are some significant fibrate drug interactions?

A
  • Fibrates (especially gemfibrozil) can increase the risk of myopathies and rhabdomyolysis. Gemfibrozil should not be given with ezetimibe or statins
  • Colchicine can increase the risk of myopathy when coadministered with fenofibrate
  • Gemfibrozil is contraindicated with repaglinide as it can increase hypoglycemic effects
  • Fibrates can increase the effects of sulfonylureas and warfarin
122
Q

What is the MOA of Niacin?

A

Niacin decreases the rate of hepatic synthesis of VLDL (decreases TG) and LDL and can also increase the rate of chylomicron TG removal from plasm. It alerts the binding of HDL particles to scavenger receptor B-1 in the liver, which removes the cholesterol insides, but does not take up the HDL particle, which leaves it free to return to the circulation for reverse cholesterol transport

123
Q

What are some contraindications of Niacin?

A

Do not use with active liver disease, active PUD or arterial bleeding

124
Q

What are some warnings of Niacin?

A
  • Rhabdomyolysis with niacin doses > 1 gram/day combined with statins
  • Hepatotoxicity
  • Lab abnormalities: increases BG, increases uric acid, decreases phosphate
  • Use with caution in patients with unstable angina or the acute phase of an MI
125
Q

What are some side effects of niacin?

A

Flushing, pruritus (itching), vomiting, diarrhea, increases BG, hyperuricemia (or gout), nausea, cough, orthostatic hypotension, hypophosphatemia, decreased platelets

126
Q

What are some monitoring parameters of Niacin?

A

Check LFTs at the start (baseline); every 6-12 weeks for the first year and then about every 6 months, blood glucose (if diabetic), uric acid (if gout history), INR (if on warfarin), lipid profile

127
Q

What are some notes about Niacin?

A
  • IR niacin has poor tolerability due to flushing/itching
  • CR/SR have less (but still significant) flushing but more hepatotoxicity
  • The best clinical choice is ER Niaspan, with less flushing and less hepatotoxicity (compared to CR/SR formulations), but it is the most expensive
  • To reduce flushing: taking aspirin 325 mg (or ibuprofen 200 mg) 30-60 minutes before the dose; take with food, but avoid spicy food, alcohol and hot beverages (which can worsen flushing)
  • Formulations of niacin (IR vs. ER) are not interchangeable
  • Flush-fre niacins (inositol hexaniacinate or hexanicotinate), niacinamide or nicotinamide or not effective
128
Q

What are the lipid effects of Niacin?

A
  • Decreases LDL 5-25%
  • Increases HDL 15-35%
  • Decreases TG 20-50%
129
Q

What are some significant Niacin drug interactions?

A
  • Monitor for other concurrent drugs that are potentially hepatotoxic
  • Take niacin 4-6 hours after bile acid sequestrants
130
Q

What is the MOA of fish oils?

A

The mechanism is not completely understood; it may reduce hepatic synthesis of TG. These are indicated as an adjunct to diet when TG > 500 mg/dL

131
Q

Who is Vascepa recommended for?

A

Icosapent ethyl (Vascepa) is recommended for ASCVD risk reduction in select patients (age > 45 years and clinical ASCVD or age > 50 years with type 2 diabetes and additional risk factors) with triglycerides that are 135-499 mg/dL despite maximally tolerated statin

132
Q

What are examples of fish oils?

A

Omega-3 Ethyl Esters (Lovaza), Icosapent ethyl (Vascepa)

133
Q

What are some warnings associated with fish oils?

A
  • Use with caution in patients with known hypersensitivity to fish and/or shellfish
  • Lovaza can increase levels of LDL; monitor
  • Monitor LFTs (in patients with hepatic impairment) and LDL periodically during therapy
  • There is a possible association between Lovaza and more frequent recurrences of symptomatic atrial fibrillation or flutter in patients with paroxysmal or persistent atrial fibrillation, particularly within the first months of initiating therapy
134
Q

What are some side effects of fish oils?

A

Eructation (burping), dyspepsia, taste perversions (Lovaza), arthralgias (Vascepa)

135
Q

What are some notes about fish oils?

A
  • Many OTC omega-3 fatty acid products are marketed as dietary supplements; only prescription medications Lovaza and Vascepa are FDA-approved for TG lowering, in addition to diet, when TG > 500 mg/dL
  • Stop prior to elective surgeries due to increased risk of bleeding
136
Q

What are the lipid effects of fish oils?

A
  • Decreases TG up to 45%
  • Increases HDL ~9%
  • Can increase LDL (up to 44% with Lovaza, no increase seen with Vascepa)
137
Q

What are some key fish oil drug interactions?

A

Omega-3 fatty acids can prolong bleeding time; use with caution with other medications that can increase bleeding risk. Monitor INR if patients are taking warfarin at dose initiation or dose change

138
Q

What are other drugs that can help treat dyslipidemia?

A

Lomitapide, Evainacumab-dgnb (Evkeeza) and Bempedoic acid (Nexletol)

139
Q

What is the MOA of Lomitapide?

A

Lomitapide is a specialty drug that decreases apoB, the main component of LDL and VLDL (the precursor to LDL). Lomitapide binds to and inhibits microsomal triglyceride transfer protein (MTP), which prevents the assembly of apoB containing lipoproteins

*Approved for use in homozygous familial hypercholesterolemia

140
Q

What is the MOA of Evinacumab-dgnb (Evkeeza)?

A

A novel treatment approved for HoFH which blocks the function of angiopoietin-like 3 (ANGPTL3), a protein involved in lipid metabolism

141
Q

What is the MOA of Bempedoic acid (Nexletol)?

A

Inhibits cholesterol synthesis in the liver by inhibiting adenosine triphosphate-citrate lyase (ACL). It is approved for use in HeFH and ASCVD requiring additional LDL lowering

142
Q

What is a boxed warning of Lomitapide?

A

Hepatotoxicity (increased LFTs, steatosis)

143
Q

What are contraindications of Lomitapide?

A
  • Active liver disease (including unexplained increased LFTs), moderate or severe hepatic impairment
  • Pregnancy
  • Do not use with moderate or strong CYP3A4 inhibitors
144
Q

What are some side effects associated with Lomitapide?

A

N/V/D, dyspepsia, abdominal pain, constipation, flatulence, increased LFTs, chest pain, back pain, fatigue, weight loss, influenza, nasopharyngitis

145
Q

What are some monitoring parameters of Lomitapide?

A

LFTs (including total bilirubin), alkaline phosphatase, lipids, pregnancy test in females of reproductive potential at baseline

146
Q

What are some notes about Lomitapide?

A
  • Drug interactions involving CYP3A4 and P-glycoprotein

- Expensive: > $500,000/yr

147
Q

What is a key counseling point of all cholesterol medications?

A

Follow lifestyle recommendations, including heart-healthy eating habits and exercise

148
Q

What are some key counseling points of statins?

A
  • Take simvastatin and fluvastatin IR, if taken once daily, in the evening, lovastatin IR with the evening meal and lovastatin ER at bedtime. Other statins can be taken at any time of day
  • Can cause: muscle damage, liver damage
  • Avoid grapefruit
  • Avoid in pregnancy (teratogenic)
149
Q

What are some key counseling points of ezetimibe?

A

Can cause muscle damage and liver damage

150
Q

What are some key counseling points of PCSK9 inhibitors?

A
  • Subcutaneous injection. Inject into the thigh, abdomen or upper arm
  • Can cause allergy/anaphylaxis or injection site reaction
  • Store in the refrigerator. Allow to warm to room temperature before injecting. Can be kept at room temperature for 30 days
151
Q

What are some key counseling points of bile acid sequestrants?

A
  • Take at mealtimes with plenty of water or other liquid
  • Can cause constipation
  • Reduces ADEK absorption
152
Q

What are some key counseling points of fibrates?

A
  • Fenoglide and Lipofen: take with food
  • Lopid: take twice daily, 30 minutes before breakfast and dinner
  • Can cause muscle damage, liver damage, cholelithiasis (e.g. gallstones); contact prescriber for severe abdominal pain, nausea or vomiting, pancreatitis
153
Q

What are some key counseling points of Niacin?

A
  • Niaspan: take at bedtime after a low-fat snack
  • Other niacins: take with food
  • Can cause hyperglycemia, liver damage, flushing (may subside after several weeks of consistent use)
  • To reduce flushing, take aspirin 325 mg (or 200 mg of ibuprofen) 30-60 minutes before the dose. Taking with food and avoiding drinking alcohol or hot beverages or eating spicy foods around niacin administration can help reduce flushing
154
Q

What are some key counseling points of fish oil?

A
  • Vascepa: take with food

- Can cause dyspepsia (all fish oils), burping or abnormal sense of taste (Lovaza) or joint pain (Vascepa)

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