Hyperlipidemia Flashcards
How is the atherosclerotic cardiovascular disease (ASCVD) risk calculated?
Using the Pooled Cohort Equations risk calculator.
When are children/young adults screened for dyslipidemia?
9 to 11 and then again 17 to 21.
For average/low risk patients, what is the interval for surveillance for dyslipidemia?
every 4 to 5 years
Males are screened for dyslipidemia starting at what age?
35 years old
Females are screened for dyslipidemia starting at what age?
45 years old
What are the risks of TAGs, LDL, and HDL?
Elevated levels of LDL are known to be atherogenic, while HDL is anti-atherogenic. Triglycerides do not have clear association with atherosclerosis, but at very high levels (> 1000) are associated with pancreatitis.
Hyperlipidemia increases the risk of … ?
Risk factor for coronary disease and stroke.
Lipid deposits can lead to … ?
“xanthelasma,” lipid deposit, commonly of tendon and eyelid.
Corneal arcus (lipid deposit in cornea).
What are the lifestyle modifications for all patients with hyperlipidemia?
- Healthy diet
- Exercise
- Quit smoking
What comorbid condition accelerates atherosclerotic cardiovascular disease (ASCVD) the worst?
diabetes > smoking > hypertension
What comorbid condition accelerates atherosclerotic cardiovascular disease (ASCVD) most commonly?
hypertension
Patients between 40 to 75 who are high risk (DM, smoking, HTN, family history) are managed for atherosclerotic cardiovascular disease by … ?
Getting a statin regardless of LDL levels.
What are the primary preventive measures for statin therapy?
LDL > 190 → High intesity statin
40 to 75 yrs old w/ DM → Mod./High intensity statin
ASCVD risk > than 7.5% to 10% → Mod./High statin
When a patient has known ASCVD (CAD, CVA, PAD) what is the measure to manage their dyslipidemia?
They will get a “Secondary Prevention,” which is a High intensity statin.
What are the current guidelines recommend in all patients aged 75 with known ASCVD for statin therapy?
Patients with established atherosclerotic cardiovascular disease (ASCVD) such as previous myocardial infarction require statin therapy. Patients with known ASCVD are at high risk for future cardiovascular events and death. Several randomized trials for secondary prevention of ASCVD have shown significant risk reduction in cardiovascular events and overall cardiovascular disease mortality in patients treated with statins.
What are the current guidelines recommend in all patients age older than 75 with known ASCVD for statin therapy?
For patients with ASCVD <75 years, risk assessment is not necessary, as the guidelines recommend statins universally for all with clinical ASCVD.
What are the high intensity statins?
High-intensity statins:
- Atorvastatin 40-80 mg
- Rosuvastatin 20-40 mg;
What are the moderate-intensity statins?
Moderate-intensity statins:
- Atorvastatin 10-20 mg
- Rosuvastatin 5-10 mg
- Simvastatin 20-40 mg
- Pravastatin 40-80 mg
- Lovastatin 40 mg
What is the MOA of statin therapy?
HMG-CoA inhibitor
Once starting statins, what must be done before initiation of treatment and is there a reason to monitor patients?
Obtain baseline LFTs and CK, but no need to screen for LFTs/CK unless symptomatic.
What is the effect of statin on LDL, HDL, and Trig?
Lowers LDL, increases HDL, Lowers Trig.
What are the adverse effects of statin therapy?
Myopathy (most common), rhabdomyolysis, and Hepatotoxicity (least common).
If a patient develops myalgias or transaminitis on statins, what is the first course of action?
stop drug, retry at lower dose.
If a patient develops myopathy and elevated CK, what is the best course of action?
Patients with symptomatic myopathy from statin use should discontinue therapy. In asymptomatic patients, a CK level >10 times the upper limit of normal range is considered an indication for discontinuation of statin therapy. Statin therapy is an effective treatment for hypercholesterolemia and is recommended for secondary prevention of cardiovascular events in all patients with known coronary heart disease. Statin-induced myopathy is the most common complication of statin use and can range from asymptomatic elevation of serum creatine kinase (CK) levels to rhabdomyolysis. Statins can also potentiate muscle injury with elevation of CK levels in patients with an episode of prolonged vigorous exercise.
What medication can be used to bind fats in the GI for hyperlipidemia?
Bile Resins such as Cholestyramine or Colestipol.
What effect doest Cholestyramine or Colestipol have on LDLs, HDLs, and Trig?
These will lower LDL, raise HDL, but have no impact on trigs.
What are the adverse affects of Cholestyramine or Colestipol?
GI necrosis, malabsorption, GI disturbances, and drug malabsorption.
When can ezetimibe be considered for patients with hyperlipidemia?
If patient extremely high risk and LDL remains > 70-100 mg/dL.
What is the MOA of ezetimibe?
Inhibits cholesterol absorption (NPCILI).
What effect does ezetimibe have on LDLs, HDLs, and Trig?
Only lowers LDL.
What is the major adverse reaction with ezetimibe therapy?
Diarrhea
Gemfibrozil and Fenofibrate are fibrates that … ?
upregulate LPL and activate PPAR-a
When are Gemfibrozil and Fenofibrate indicated?
High TGs (>1000) when the risk of pancreatitis is elevated.
Gemfibrozil and Fenofibrate have on LDLs, HDLs, and Trig?
These will incresae HDL and decrease trigs.
What are the significant adverse reactions of fibrates?
First, these can’t be given with statins.
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They increase the occurance of gallstones.
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Gemfibrozil is known to cause myositis.
Niacin has what MOA?
Inhibits lipolysis
What effect does niacin have on LDLs, HDLs, and Trig?
Lowers LDL, raises HDL and Lowers Trigs.
Does niacin improve the overall cardiovascular outcomes, especially for patients who have experienced a previous MI?
Niacin (ie, nicotinic acid) is effective in increasing HDL levels and has modest effects in reducing LDL levels. However, despite the favorable effects on lipid profile, niacin has not shown improvement in cardiovascular outcomes in patients with known ASCVD.
What are the adverse reactions with use of niacin?
Flushing (use ASA), Hyperglycemia, uricemia
What is the MOA of Omega-3 fatty acids for hyperlididemia?
Decreases hepatic fat secretion.
What effect does Omega-3 have on LDLs, HDLs, and Trig?
raises HDL and lowers LDL.
When can PCSK-9 inhibitors (Evolocumab or Alirocumab) be considered for patients with hyperlipidemia?
If patient extremely high risk and LDL remains > 70-100 mg/dL.
What is the MOA of PCSK-9 inhibitors (Evolocumab or Alirocumab)?
Prevents LDL-R uptake/breakdown
What effect do PCSK-9 inhibitors (Evolocumab or Alirocumab) have on LDLs, HDLs, and Trig?
Lowes LDL, raises HDL, lowers trigs
What is the main adverse reactions of PCSK-9 inhibitors (Evolocumab or Alirocumab)?
Reaction at injection site.
When triglycerides are elvated (in isolation), what is used to drive management?
Whether TGs are between 15 to 500 mg/dL or above 500 mg/dL.
LPL deficiency is caused by an autosomal _________ genetic cause for hyperlidemia?
autosomal recessive
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Class I dyslipemia (Hyperchylomicronemia)
LPL deficiency leads to an increase of …. ?
Increases TG → Pancreatitis
LDL-R deficiency is caused by an autosomal _________ genetic cause for hyperlidemia?
autosomal dominant
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Class IIa dyslipemia (Hypercholesterolemia)
LDL-R deficiency leads to an increase of …. ?
Increases LDL → Severe atherosclerosis
APO-E mutation is caused by an autosomal _________ genetic cause for hyperlidemia?
autosomal recessive
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Class III dyslipemia (Dysbetalipoproteinemia)
APO-E mutation leads to an increase of … ?
Choesterol and TGs → Premature CAD
VLDL overproduction is caused by an autosomal _________ genetic cause for hyperlidemia?
autosomal dominant
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Class IV dyslipemia
VLDL overproduction leads to an increase in … ?
Increases TG and VLDL → Premature CAD
