dyslipidemia Flashcards
5 major lipoproteins
VLDL, IDL, LDL, HDL, chylomicrons
HMG CoA reductase inhibitors
patients who benefit
- Adults with DM
- PTs with ASCVD
- 10 year risk of ASCVD greater than 7.5%
- LDL cholesterol greater than 190 mg/dL
HMG CoA reductase MOA
inhibition of HMG-COA reductase decreases cholesterol synthesis,
this results in increased LDL receptors on hepatocytes for increased uptake/degradation
↓ cholesterol → liver ↑ receptors → receptors grab more LDL → cleans the blood → ↓ circulating LDL
When during the day should your patient take the statin? Why?
Statins should be taken at night.
Spike of cholesterol is made at night duh
Results of taking a statin
Therapeutic Effects
1. ↓ cholesterol synthesis
2. ↑ hepatic LDL receptors
3. ↓ circulating LDL cholesterol level by 50% or more at the HIGHEST doses
also slight ↑ HDL, ↓ triglyceride, ↓ high-sensitivity CRP
What percentage do statins reduce circulating LDL?
High-intensity = 50%
(recent cardiac event)
Moderate-intensity = 30-49%
(if they can tolerate low-intensity)
Contraindications of statins
- PREGNANCY duh
- severe hepatic dysfunction
- extreme ↑ CPK within a matter of days after starting a statin = severe muscle damage
Which statin intensity is the longest-acting and has the longest half-life?
High intensity:
- atorvastatin
- rosuvastatin
Statins with _____ intensity have less side effects and work all day long on the body
low-intensity
What is the most common side effect of statins? When would you expect to see the onset?
Statin-associated Muscle Symptoms (SAMS)
- muscle aches with normal serum creatine kinase levels
- onset = within 4-6 weeks of initiation OR dose increase
In severe cases, starting someone on a statin can lead to the development of ______
myositis or rhabdomyolysis
- CPK >10 times the upper limit
DO NOT use statins moving forward
What Increases the risk of severe adverse effects of taking statins?
Co-administration with CYP450 inhibitors (niacin, fibrate, erythromycin, antifungals, nefazodone, cyclosporine)
Your patient started a statin and is experiencing cognitive symptoms including memory loss, forgetfulness, and confusion. What is the next step for this patient?
Discontinue statin
Reversible - depending on how long symptoms started
Symptoms typically resolve around 3 wks
With statins, there is a small increased risk of ….
DM II
3 statins that inhibit CYP3A4
simvastatin, atorvastatin, lovastatin
= higher risk of rhabdo
Adverse effects of statins
- rhabdo
- elevated liver enzymes
- cognitive symptoms
- DM II
After 4-12 wks of starting a statin, what lab should you run?
Fasting lipid panel (FLP)
- check FLP for anticipated clinic response (e.g. high intensity > 50% LDL decrease)
- if LESS than anticipated, verify adherence, lifestyle, secondary causes
- consider lower statin dose if 2 consecutive LDL <40 mg/dL
What class does ezetimibe (Zetia) belong to?
absorption inhibitors
MOA of ezetimibe (Zetia)
inhibits cholesterol transporters → inhibits intestinal absorption of dietary + biliary cholesterol across intestinal wall → ↓ LDL cholesterol 15-20% when used as monotherapy
When is ezetimibe (Zetia) preferred?
best as adjunct with statins IF LDL doesn’t improve by 70 mg/dL
What should you avoid ezetimibe (Zetia) with?
- moderate-severe liver dysfunction
- skeletal muscle effects (when taken with statin)
- pregnancy
- CHOLELITHIASIS when taken with fibrate
MOA of PCSK9 Inhibitors
prevents degradation of LDL receptors so they continue to take up LDL
increase removal of LDL in circulation by liver
PCSK9 lowers cholesterol levels by ______ %. Best for what type of pts?
Lowers by 50-60%
Best for young pts and extremely high LDL levels
How often do you inject PCSK9?
every 2-4 weeks
What drug in combo with a statin causes a 15-20% reduction in CV death, MI stroke, hospital admission for unstable angina, or coronary revasc?
Evolocumab
MOA for bile acid-binding resins
bind bile acid in GI → forces body to take up more cholesterol → take cholesterol from the reserves
thank u for ur service
Dyslipidemia Rx safe for pregnancy
bile-acid binding resins
Adverse effects of PCSK9 inhibitors
- flu-like symptoms
- cognitive issues
- local injection site rxn
Cut off for bile acid-binding resins is a triglyceride level of _____
> 500 mg/dL
Drug class associated with a lot of GI side effects
Bile acid-binding resins
Vitamin deficiency may be a consideration with what drug class
Bile acid-binding resins
Fibric acid derivatives mostly do what
lower triglycerides by 40%
MOA of fibrates
PPAR (peroxisome proliferator-activated receptor-alpha agonists)
genes or whaTeva
Gemfibrozil considerations
Avoid with any dose of any statin (myopathy)
Fenofibrate Considerations
avoid with high intensity statin
Fibric Acid Adverse effects
Dyspepsia, SCr increase, Cholelithiasis, Myopathy, Hepatotoxicity (increase ALT)
Fibric acid drug interaction potential
Resin: separate dosing
Warfarin: increase INR
Ezetimibe: increase cholelithiasis
Colchicine: increase myopathy
Fibrates________ in all statin-treated patients with CVD or diabetes
have not been shown to reduce CV events
Niacin MOA
Reduce production of VLDL particles (LDL precursor), secondary decrease in LDL and increase in HDL cholesterol levels
↓ VLDL, ↓ LDL, ↑ HDL → ↓ cholesterol
Niacin adverse effects
flushing + skin shiitake
…..
skin flushing
dyspepsia/abdominal pain
nausea, vomiting, diarrhea
pruritus
skin rash/hypersensitivity
hyperglycemia
increased uric acid
dry eyes
myalgia
hepatotoxicity
Niacin considerations (how to take/ what to avoid)
avoid spicy/hot food
avoid alcohol
take with food
aspirin 30 minutes before dose
Omega-3 fatty acid do what
lower triglycerides by up to 30%
Omega-3 fatty acid preparations
Lovaza: DHA and EPA
Vascepa: EPA
Epanova: DHA and EPA
Omega-3 fatty acid warnings
Hypersensitive to fish or shellfish
Pregnancy/ lactation
Omega-3 fatty acid adverse effects
GI disturbances: belching, dyspepsia; taste perversion
skin: pruritus, rash
Arthalgia/ joint pain
increased bleeding risk
Omega-3 fatty acid monitoring
ALT+AST
LDL increase (not with EPA only ie vascepa)
afib/ flutter
Vascepa (Icosapent ethyl) is the only preparation shown to
reduce CV death, nonfatal MI/ stroke, coronary revascularization, unstable angina 25%
Diet therapy goal
reduce total fat to 25-30%, saturated fat to <7% of calories, no trans fat
LDL-C > 190 mg/dl
high intensity statin; no risk assessment
DM and age 40-75
moderate statin, risk assessment for high intensity
age>75
clinical assessment
0-19y/o
lifestyle mod, familial hypercholesterolemia
age 20-39
lifetime risk assessment/ modification
consider statin with family Hx
40-75y/o
LDL-C >70 and <190, PT doesn’t have DM
10 year ASCVD assessment
low risk
<5%
borderline risk
5-7.5%
intermediate risk
> 7.5 to <20%, reduce LDL-C by 30-49%
high risk
> 20%, reduce LDL-C by >50%
