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Endocrinology Exam 2 > Antihyperlipidemics > Flashcards

Antihyperlipidemics Flashcards

1
Q

Dyslipidemic states

A

Hypercholesterolemia
Hypertriglyceridemia
Familial combined (mixed) hyperlipidemia
Familial hypercholesterolemia
Elevated Lp(a)
Familial chylomicronemia syndrome (FCS)
Other rare genetic conditions

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2
Q

LDL-C treatment goal for extreme risk category

A

<55

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3
Q

LDL-C treatment goal for very high risk category

A

<70

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4
Q

LDL-C treatment goal for high risk category

A

<100

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5
Q

LDL-C treatment goal for moderate risk category

A

<100

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6
Q

LDL-C treatment goal for low risk category

A

<130

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7
Q

How often should lipids be checked when treating LDL-C to Goal?

A

every 3 months or more frequently where necessary

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8
Q

TG goal for all ASCVD risk categories is

A

<150

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9
Q

Five general recommendation categories for Lifestyle recomendations in CV risk patients

A

Nutrition
Physical activity
Sleep
Mental health
Smoking

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10
Q

If someone is determined to be low risk for ASCVD, what is the first step?

A

No risk factors
Lifestyle change

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11
Q

If someone is determined to be moderate risk for ASCVD, what does this mean and what is the first step?

A

<2 risk factors and 10-year risk <10%
Lifestyle + moderate intensity statin

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12
Q

If someone is determined to be high risk for ASCVD, what does this mean and what is the first step?

A

> 2 risk factors and ASCVD risk 10-20%
Diabetes or CKD >3 with no orther risk factors

Start lifestyle + moderate intensity statin

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13
Q

If someone is determined to be very high risk for ASCVD, what does this mean and what is the first step?

A

Established ASCVD or recent hospitalization for ACS, or 10 year risk >20%
Diabetes with >1 risk factors
CKD >3 with albuminuria
HeFH

Start Lifestyle + High intensity statin

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14
Q

If someone is determined to be extreme risk for ASCVD, what does this mean and what is the first step?

A

Progressive ASCVD including unstable angina
established ASCVD plus diabetes or CKD >3 or HeFH
History of premature ASCVD (<55 years male or <65 years female)

Start Lifestyle + High intensity statin

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15
Q

Measure Lp(a) in patient sin the following settings

A

Family history of previous ASCVD risk
All patients with premature or recurrent ASCVD despite LDL-C lowering

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16
Q

CAC scoring

A

Coronary Artery Calcium scoring:
Type of heart CT (not the same as a regular CT, must order CAC scan)
Can predict ASCVD risk (in conjunction with other risk scoring)

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17
Q

Who do we scan with CAC scoring?

A

Selected asymptomatic, nondiabetic adults 40+ w/ 10-year ASCVD risk intermediate to high (7.5-20%)
Sometimes borderline risk (5-7.4%)

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18
Q

CAC score ≥ 100 or >75 percentile for age, sex, and race

A

Use statin if LDL-C between 100-190 mg/dL
Daily aspirin too if CAC ≥100

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19
Q

CAC score 1 to 99 or <75th percentile for age, sex, and race

A

Consider statin if LDL-C between 100-190 mg/dL

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20
Q

CAC of zero

A

No statin unless major risk factors (eg, diabetes, active smoking, hypertension, family history of premature coronary artery disease, etc.)

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21
Q

STATINS

A

Simvastatin (Zocor)
Atorvastatin (Lipitor)
Rosuvastatin (Crestor)
Lovastatin (Altoprev, Mevacor)
Pravastatin (Pravachol)

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22
Q

Statins MOA

A

HMG CoA Reductase is an enzyme that mediates the first step in cholesterol synthesis
Statins inhibit this enzyme, thereby reducing biosynthesis of cholesterol.
Leads to increased number of hepatic LDL receptors (decreasing LDL-C in circulation), small increase in HDL and decrease in TGs.

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23
Q

Statins are associated with _____

A

plaque stabilization and decreased inflammation in the arterial walls

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24
Q

Statins effect on LDL-C, HDL-C and TGs

A

Can decrease LDL-C by 18-50%!
Can increase HDL-C by 5-15%.
Can decrease plasma Triglycerides by 10-25%.

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25
First line agents in the management of hyperlipidemia
Statins
26
Contraindications for Statins
Pregnancy! Statins cause birth defects. Liver disease - this is NOT absolute. Muscle disease - case by case (myopathy). Caution with concomitant Coumadin (may increase INR).
27
Side Effects of Statins
Typically well tolerated Headache Arthralgias/Myalgias (without CK changes) Very mild myositis? Occurs in about 10% of patients Fatigue Flu-like symptoms
28
Adverse reactions of statins
Hepatotoxicity (very rare) Myositis and Rhabdomyolysis
29
Follow Up and Monitoring of statins
All are Pregnancy Category X and unsafe in lactation! Check Creatinine and LFTs at baseline
30
Statins are also known as
HMG CoA Reductase Inhibitors
31
Fibric Acid Derivatives
Gemfibrozil (Lopid) Fenofibrate (Tricor)
32
Fibric Acid Derivatives MOA
These bind to gene promoters which transcriptionally upregulate production of certain proteins. Increased expression of lipoprotein lipase (which does what again?) Increased expression of apoproteins found in High Density Lipoproteins
33
Taking a Fibric Acid Derivative Results in decreased plasma triglycerides by about ____%.
30
34
Function of Fibric Acid Derivatives
Results in decreased plasma triglycerides by about 30%. Decreases circulating levels of VLDL Increases circulating levels of HDL ( by ~9%).
35
Fibric Acid Derivatives Indication
Essentially used for Hypertriglyceridemia. Fenofibrate can be added to Statin therapy if there is significantly elevated Triglycerides
36
Contraindications of Fibric Acid Derivatives
Gemfibrozil should NOT be used in combination with Statins
37
Side Effects of Fibric Acid Derivatives
GI side effects (N/V, dyspepsia) are common Associated with development of Cholelithiasis
38
Adverse Effects of Fibric Acid Derivatives
Myositis and Rhabdomyolysis (rare) - More common if combined with Statins - Rosuvastatin + Fenofibrate = Safest combo option Pancreatitis (MOA is largely unknown)
39
Follow Up and Monitoring of Fibric Acid Derivatives
Both are pregnancy category C; contraindicated during breastfeeding. Creatinine and LFTs at baseline and then periodically.
40
Niacin (Niacor, Niaspan) MOA
Decreases rate of HDL break down, resulting in 15-35% increase in HDL. Prevents lipolysis in adipocytes, decreasing free fatty acid circulation, decreasing VLDL (and LDL) levels.
41
Niacin (Niacor, Niaspan) Indication
Most effective agent for increasing HDL levels (NO DATA for benefit though). Modestly effective at decreasing LDL and serum Triglycerides. Decent 3rd or 4th line option in patients who do not tolerate Statins and in whom you have tried ezetimibe and/or PCSK9i. Pellagra (Niacin deficiency).
42
Contraindications of Niacin
Hepatic disease Gout Peptic Ulcer Disease
43
Side effects of Niacin
Flushing and Pruritus- very common Hyperuricemia and gout attacks Hyperglycemia due to impaired glucose tolerance
44
Adverse Reactions of Niacin
Myositis and Rhabdomyolysis NOT SEEN when Niacin is used alone!
45
Niacin Follow Up and Monitoring
- You want to start at a low dose and increase gradually to 1500-3000 mg daily over 2-3 months (Or 1g ER dose at night). - Check LFTs at baseline, then again after 6-8 weeks, and again after 6-8 weeks on max dose. - Fasting glucose and uric acid level at baseline and again after 6-8 wks. - Pregnancy category C and lactation safety unknown.
46
Cholesterol Absorption Inhibitor
Ezetimibe (Zetia)
47
Cholesterol Absorption Inhibitor MOA
Selectively inhibits absorption of dietary and biliary cholesterol in the small intestine. Decreases circulating LDL cholesterol by about 15-20%. Very small increase in HDL levels.
48
Indication for Cholesterol Absorption Inhibitor
Hypercholesterolemia - Consider Ezetimibe 2nd line therapy.
49
Contraindications of Cholesterol Absorption Inhibitor (Ezetimibe)
Hepatic dysfunction
50
Side Effects of Cholesterol Absorption Inhibitor
URI and Flu-like symptoms are common Myalgias (without increasing CK) Diarrhea is common
51
Adverse Reactions of Cholesterol Absorption Inhibitor
Myositis and Rhabdomyolysis (rare, highest risk when combined with statin – ARE YOU SEEING A PATTERN HERE?) Drug-induced hepatitis Acute Pancreatitis Thrombocytopenia
52
Follow Up and Monitoring of Cholesterol Absorption Inhibitor
Pregnancy category C and unknown safety with lactation. Check LFTs at baseline and periodically
53
Bile Acid Sequestrants
Cholestyramine (Questran, Prevalite) Colestipol (Colestid) Colesevelam (Welchol)
54
Bile Acid Sequestrants MOA
- These Resins bind negatively charged Bile Acids in the small intestine. - The Resin-bound Bile Acids cannot be reabsorbed. - Because bound Bile Acids are not reabsorbed, the liver is forced to make more Bile Acid than normal by metabolizing LDL-C
55
Indication of Bile Acid Sequestrants
Hyperlipidemia Interesting off-label uses for Colestipol and Colesevelam:
56
Contraindications of Bile Acid Sequestrants
GI obstruction
57
Side effects of Bile Acid Sequestrants
GI symptoms- Nausea, bloating, constipation, flatulence.
58
Bile Acid Sequestrants Adverse reactions
Decreased absorption of fat soluble vitamins (A, D, E, K) Drug interactions- Cholestyramine and Colestipol can interfere with absorption of many drugs
59
Bile Acid Sequestrants follow up
Cholestyramine and Colestipol are Pregnancy category C. Colesevelam is Pregnancy category B. Seem to be safe with lactation. No routine lab tests recommended.
60
Omega-3 Fatty Acids include
EPA: eicosapentaenoic acid (icosapent ethyl, Vascepa) EPA/DHA: Eicosapentaenoic/Docosahexanoic acid (Lovaza)
61
Omega-3 Fatty Acids MOA
Evidence suggests that Omega-3’s decrease TGs by… - Reducing VLDL production by the liver. - Accelerating chylomicron and VLDL elimination from blood. Can result in up to 25-30% reduction in circulating TGs.
62
Omega-3 Fatty Acids Indication
Hypertriglyceridemia >500 (prescription strength)
63
Contraindications with Omega-3 Fatty Acids
Caution if hepatic impairment Caution if allergic to fish or shellfish
64
Side Effects of Omega-3 Fatty Acids
“Fishy” taste in mouth Dyspepsia Nausea, vomiting Mild AST, ALT increase
65
Adverse Reactions of Omega-3 Fatty Acids
Anaphylaxis observed in people with fish or shellfish allergy.
66
T/F Dietary Omega-3 Fatty Acids supplement forms are monitored by FDA
F
67
ATP-Citrate Lyase (ACL) Inhibitors
Bempedoic acid (Nexletol) Bempedoic Acid +Ezetimibe (Nexlizet)
68
ATP-Citrate Lyase (ACL) Inhibitors MOA
Inhibits cholesterol synthesis Inhibits ATP-citrate lyase (upstream of HMG-CoA reductase) Upregulates LDL receptors to reduce LDL-C
69
ATP-Citrate Lyase (ACL) Inhibitors Indications
Heterozygous familial hypercholesterolemia Atherosclerotic cardiovascular disease Usually used w/ max tolerated statin
70
ATP-Citrate Lyase (ACL) Inhibitors Contraindications
Pregnancy or breastfeeding Caution w/ age >60, renal disease, gout hx, tendon disorder hx
71
Side effects of ATP-Citrate Lyase (ACL) Inhibitors
URI Muscle spasms *Hyperuricemia/Gout Back pain or extremity pain Abdominal pain Elevated LFTs BPH
72
Adverse reactions of ATP-Citrate Lyase (ACL) Inhibitors
Tendon rupture
73
ATP-Citrate Lyase (ACL) Inhibitors follow up
Check lipid panel and LFTs 8-12 weeks after starting Watch for signs of hyperuricemia and test as needed Monitor for signs/symptoms of tendinopathy or tendon rupture (eg, joint pain, swelling, inflammation).
74
PCSK9 inhibitors* (PCSK9i)
Monoclonal Antibodies (mAB) - Evolocumab (Repatha) - Alirocumab (Praluent) siRNA - Inclisiran (Leqvio)
75
Mechanism of Action for PCSK9 inhibitors* (PCSK9i)
Monoclonal Antibodies (mAB) Bind circulating PCSK9 and prevent it from degrading LDL receptors. SQ injection 1-2 x per month siRNA Blocks synthesis of PCSK9 SQ injection every 3 months for 2 doses, then every 6 months
76
PCSK9 inhibitors* (PCSK9i) Indications
Indications (Evolocumab, Alirocumab): Primary hyperlipidemia Heterozygous or homozygous familial hypercholesterolemia Clinical ASCVD event risk reduction *Typically used w/ statin Indications (Inclisiran): Primary hyperlipidemia Heterozygous familial hypercholesterolemia *Typically used w/ statin
77
Side Effects of PCSK9 inhibitors* (PCSK9i)
* >10% Nasopharyngitis (4-10.5%) URI (2.1-9.3%) Influenza (1.2-7.5%) Back pain (2.3-6.2%) Injection site reactions (3.2-5.7%) Cough (1.2-4.5%)

Endocrinology Exam 2 (4 decks)

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