Exam 1 - Dyslipidemia (Jasmine) - Longer Cards Only Flashcards
What are non-modifiable risk factors of dyslipidemia?
Genetics
Race
Hypothyroidism
Increasing age
Pregnancy
PCOS
Obesity
Sex (male > female)
(Green + Red HIPPOS)
what are modifiable risk factors of dyslipidemia?
Excessive alcohol use
Anorexia
Diet (excess carbs, high saturated fats)
Obesity
Weight gain
(Eat A Dick, Old Woman)
what meds can increase both LDL-C and TGs?
Glucocorticoids
Diuretics
Tacrolimus
Atypical antipsychotics
Cyclosporine
Oral estrogen & progestin
Beta blockers
(God Damn TACO Bell)
What is the clinical presentation of dyslipidemia?
Mostly asymptomatic, may present w/ primary event initially
Prothrombotic or proinflammatory state
Elevated total cholesterol, LDL, TGs
Decreased HDL
Many patients have at least one of the following:
- Abdominal obesity
- Atherogenic dyslipidemia
- HTN
- Insulin resistance/glucose intolerance
What is included in clinical ASCVD?
Coronary or other arterial revascularization
PAD (includes aortic syndrome)
Acute coronary syndrome (includes Hx of MI)
Stable/unstable angina
Stroke or TIA
(C = PASS)
Metabolic syndrome is diagnosed by the presence of 3 of the following 5 risk factors:
Reduced HDL
Elevated waist circumference
Elevated serum TGs
Elevated BP
Elevated fasting glucose
what pharmacologic agents are used for dyslipidemia?
HMG CoA reductase inhibitors (statins)
Fibrates
Bile binding sequestrants
Fish oil (omega 3 FA)
PSK-9 inhibitors
Ezetimibe (zetia)
(Huge Fucking Boobs Feel Pretty Evil)
what are major ASCVD events?
Recent acute coronary syndrome
Hx of MI
Hx of ischemic stroke
Symptomatic PAD
what are high risk conditions?
CKD
HTN
Age ≥ 65
DM
Hx of prior CABG or PCI outside major ASCVD
Hx of CHF
Current smoking
Persistently elevated LDL
Heterozygous familial hypercholesterolemia
(CHAD Hates His Cute Puppy Hank)
what are the AEs of HMG CoA reductase inhibitors?
Increased liver function tests
CNS effects
Myalgias
Increased blood glucose & A1C
Rhabdomyolysis
(I Can’t Make It Right)
what levels of CPK are cause for concern?
CPK > 10,000 IU/L
CPK . 10x the ULN plus an elevation in SCr or medical intervention w/ IV hydration therapy
what are the risk factors for developing myopathy/myalgias during statin therapy?
Increased statin concentrations
Uncontrolled hypothyroidism
Concomitant fibrate or niacin
Cocaine and alcohol abuse
Age > 65
Asian ancestry
(In Usual Cases, Cats Are Awesome)
what drugs interact w/ atorvastatin
Itraconazole
Macrolides (not azithromycin)
Fenofibrate
Cyclosporin
Niacin
Gemfibrozil
(I’m Making Fried Cod, Not Goldfish)
what drugs are contraindicated for use w/ simvastain?
Gemfibrozil
Protease inhibitors
Itraconazole
Ketoconazole
Erythromycin
Clarithromycin
Cyclosporine
(Get PIKE County Coal)
statin equivalency
Pitavastatin 2 mg
Rosuvastatin 5 mg
Atorvastatin 10 mg
Simvastatin 20 mg
Lovastatin 40 mg
Pravastatin 40 mg
Fluvastatin 80 mg
(Pharmacists Rock At Saving Lives & Preventing Flu)
what are AEs of zetia?
GI complaints (diarrhea)
Arthralgias
URTIs (non-serious)
Mild increase in serum transaminases when used w/ a statin
(GUAM)
what is the MOA of evinacumab (evkeeza)
Angiopoietin like protein 3 (ANGPTL3) inhibitor
ANGPTL3 inhibits LPL and endothelial lipase, which are responsible for breaking down fats in the body
Increases lipid metabolism
Decreases LDL, HDL, and TGs
what AEs can be seen with BASs?
Increased TG
Bloating
Constipation
Abdominal pain
Gas
Cramping
(I’m Being Careful And Getting Cooch)
what AEs can be seen w/ fibrates?
Enhanced gallstone formation
Arthralgia/myalgia
Transient transaminase level elevation
GI complaints
(EAT Grass)
What AEs can be seen w/ niacin?
Hepatotoxicity
Flushing/itching
Hyperuricemia (gout)
Increased blood glucose
GI upset
(Happy Frogs Hop In Grass)
how can you reduce AEs of niacin?
Titrate slowly
Avoid spicy food & alcohol
Take aspirin 325 before dose
Take w/ food
Use ER
(TATTU)
Special populations: hispanic/latino
Greater prevalence of:
- High TG
- Obesity
- T2DM
- Low HDL
- Metabolic syndrome
(HOT Like Me)
special populations: African American
ASCVD risk higher, but less driven by dyslipidemia
Lower metabolic syndrome incidence
Lower TG
Higher HDL
Higher T2DM incidence
special populations: Asian ancestry
more likely to have reduced ABCG2 polymorphism
Leads to increased crestor concentrations
special populations: american indian and alaska native
Higher ASCVD prevalence
Obesity
Metabolic syndrome
DM
Smoking
special populations: HIV
Increased ASCVD risk
Newly diagnosed pts should have lipid screening before and after ART initiation
Statins are 1st line
Caution for drug interactions w/ protease inhibitors
(IN SC)
special populations: rheumatoid arthritis
Increased ASCVD risk
Lipid panel may not be reliable during flare
Statins are 1st line
