Lipid Disorders

hyperlipidemia

hyperlipidemia

A syndrome in which measured serum lipid components (TC, LDL, HDL, cholesterol, TGs) deviate from optimal levels

genetic predisposition (mutation in the gene encoding the LDL receptor protein)

Primary hyperlipidemia is due to

lifestyle, weight gain, DM, renal, thyroid disease

Secondary hyperlipidemia is due to

LDL 500+, tendon xanthomas, xanthelasma, cornal arcus, family hx, childhood raised LDLs, no response to treatment

What are some red flags for familial hyperlipidemia?

genetic testing

How do you diagnose primary hyperlipidemia?

familial combined hyperlipidemia

primary hyperlipidemia with both elevated TG and LDL; linked to early CAD?

Lp(a)

What is a risk factor for CAD and Stroke because it is thought to be atherogenic?

obesity, DM, hypothyroidism, corticosteroids, progestin, anabolic steroids, liver disease, renal disease, ethanol use/abuse, pregnancy

What are some causes of secondary hyperlipidemia?

lower HDL levels

Why do peeps of asian descent have a increased ASCVD risk?

Socioeconomic status, DM (disproportionally present)

Why do hispanics have a increased ASCVD risk?

increased prevalence of DM and HTN

Why do black women have an increased risk of ASCVD?

family history (young peeps with MIs), history of ASCVD, cholesterol lowering therapy, DM, when was the last screening, overweight, obese, HTN, smoke, metabolic syndome, are statins C/I (history of rhabdo)

Concerning hyperlipidemia, what do you want to find out in you history?

vitals, cardiovascular exam, whatever else is indicated

Concerning hyperlipidemia, what is included in the exam (usually flat normal)?

Fasting lipids (SKAGGS JAM), CRP (if the patient wants), ALT/AST, hemoglobin A1c, glucose, CK, CBC, UA/microalbumin

Concerning hyperlipidemia, what labs are we ordering?

men over 35, women over 45

For peeps with LOWER cardiovascular risk - when we screening?

males between 25-30, females 30-35

For peeps with HIGHER cardiovascular risk - when we screening?

HTN, DM, smoking, family hx of CHD

What are some red flags for higher cardiovascular risk?

total cholesterol, HDL

What levels does you screening panel have to have, like which ones are completely necessary?

total cholesterol:HDL (5.0 = average for males, 4.4 = average for females)

What is the cholesterol ratio

coronary artery calcium scoring (CAC)

What looks at the atherosclerosis in your heart and see’s how far along you are in brewing that blockage?

ur good (no identifiable disease)

0 Agaston units on CAC

mild disease

1-99 Agaston units on CAC

moderate disease

100-399 Agaston units on CAC

severe disease (call the cath lab)

400+ Agaston units on CAC

atorvastatin, rosuvastatin

What are the high intensity statins?

atorvastatin, rosuvastatin, simvastatin, pravastatin, lovastatin, fluvastatin XL, fluvastatin, pitavastatin

What are the moderate intensity statins?

simvastatin, pravastatin, lovastatin, fluvastatin

What are the lower intensity statins?

LFTs

Concerning statins, what labs do we need to check on the reg?

myalgias, rhabdo (rare), LFT elevations, hepatic failure

ADRs associated with statins?

ezetimibe

For patients who do not meet cholesterol goals with dietary modification and we’ve maxed out the statins, what can we add to the mix

Bempedoic acid

What is recommended for patients with maximally tolerated statin therapy and includes hyperuricemia, gouty arthritis, myalgia, muscle spasms, and increase AST as ADRs?

PCSK9 inhibitors (evolcumab, alirocumab)

What is a new kid on the block that can be used to treat primary hyperlipidemia because it is a fully humanized mab that binds free plasma PCSK9?

fibrates

What drug is effective in lowering TGs but not as good in lowering LDL and raising HDL?

Nicotinic acid

Which drug raises HDL but there is currently no evidence for improved outcomes in recent trials - no longer used because it has an ADR of massive flushing and ITCHY, ITCHY skin?

Bile acid sequestrant

Which causes significant GI side effects, no evidence for improved outcomes rarely used - low compliance because nobody wants to drink a “slurry”

lose weight, regular exercise, avoid food/drinks with lots of sugar, avoid red meat, butter, fried foods, cheese, oils/nuts, limit alcohol, quit smoking

What patient education measures do we need to for hyperlipidemia?

individual with clinical ASCVD, individuals with severe primary hypercholesterolemia, Individuals 40-75 old with DM, individuals 40-75 y/o with LDL-c 70-189 and an estimated 10-year ASCVD

What are the 4 statin benefit groups?

acute coronary syndromes, History of MI, stable/unstable angina, coronary/arterial revascularization, stroke, TIA, peripheral artery disease

How is clinical ASCVD defined?

lower LDL by 50%+

What is target #1 for for statin group one (Individuals with ASCVD)?

LDL below 70

What is target #2 for for statin group one (Individuals with ASCVD) or for peeps that are VERY high risk?

ezetimibe

If we can’t hit target 2 with statins alone we add

PCSK9 inhibitor

If we can’t hit target 2 with statins and ezetimibe, we add

continuation or initiation of a statin is reasonable (they’ve made it this long)

For patients above the age of 75 with mild risk of ASCVD, what’s our game plan?

Begin high intensity - target is 100 LDL

For peeps with severe primary hypercholesterolemia (group II) what is our game plan?

Reduce LDL by 50%+ using a high intensity statin

For statin group III (adults 40-75 with high LDL and DM) what is the game plan?

reduce LDLs by 30%

For statin group IV (adults 40-75 with high LDL and an estimated 10 year ASCVD risk of 7.5%) what is the game plan if risk is between 7.5-19.9%?

reduce LDLs by 50%+

For statin group IV (adults 40-75 with high LDL and an estimated 10 year ASCVD risk of 7.5%) what is the game plan if risk is 20% or higher?

4-12 weeks (Skaggs likes 6 week) at first, 3-12 after that

After we start statins when should we follow up?

STOP THE STATIN, work up for rhabdo (CK, creatinine, UA)

Billy (56 y/o male) presents to the clinic with unexplained SEVERE muscle pain and fatigue. He states that he’s been taking his statin like he’s supposed to. What do you want to do?

stop the statin, evaluate for other conditions that affect the muscles

Bob (65 y/o male) presents to the clinic for a check up. While doing your super thorough history he reports unexplained moderate muscle pain and fatigue. He states that he’s been taking his statin like he’s supposed to. What do you want to do?

restart on the OG/lower dose on the OG statin or start a new one on a low dose and gradually increase

So Bob starts feeling better and comes back to see you, what do you want to do about the statin?

multiple/serious comorbidities, history of previous statin intolerance, concomitant use of drugs affecting the metabolism, impaired renal/hepatic function, unexplained ALT elevations (3x normal), 75+ years old

What predisposes individuals to statin ADRs

garlic, red yeast rice, artichoke, guggul, reducing saturated fats, reducing cholesterol intake, increasing fiber, adding plant sterols, moderate EtOH usage, stop smoking

What are some COMPLIMENTARY therapies for hyperlipidemia since statins are the BOMB (as of rn)?

No (are you dumb)

Should we take patients off their statins or titrate the dose if we meet our goals?

hypertriglyceridemia

What is associated with elevated TGs and is commonly seen in combination with obesity, DN, renal disease, metabolic syndrome, estrogen usage, and hypothyroidism?

pancreatitis

Levels of TGs at 1000 mg/dL is a risk factor for

fix secondary cause - stop smoking and dranking, increase exercise, lose weight, low carbs, low fats, fibrates (if super high), fish oils

What is the treatment for hypertriglyceridemia?

abdominal obesity, high TGs, low HDL, HTN, elevated fasted glucose

Clinical identification of the metabolic syndrome includes 3 of any of:

wrong drug choice, wrong dose, patients needs a combo treatment, patient is non-compliant (figure out why - ADRs)

Metabolic syndrome is the result of what failures?

Get that buy-in, check/address BMI, talk about nutrition and health, ask family history, treat aggressively if you find it

How do we prevent metabolic syndrome?