Q: What is hyperlipidemia?
A: A condition where there are elevated levels of lipids (cholesterol, triglycerides, or both) in the blood and low HDL
TG(increase risk to BV and tissue deposition)
low HDL(they remove fat/cholestrol from tissues)
high LDL (deposits of TC + TG on BV cuz atherosclertic plaques
Q: What lipoproteins are involved in atherosclerosis?
A:
LDL-C (Low-Density Lipoprotein) – major contributor to plaque
VLDL & Triglycerides – also atherogenic
HDL-C (High-Density Lipoprotein) – protective (removes cholesterol)
Q: Why is high LDL dangerous?
A: LDL particles deposit cholesterol in arteries → atherosclerotic plaque → ↑ risk of MI, stroke, PAD
Statins (HMG-CoA Reductase Inhibitors)
Q: MOA?
Q: Indications?
A: Inhibit HMG-CoA reductase → ↓ cholesterol synthesis → ↑ LDL receptors → ↓ LDL
increase synthesis of HDL
First-line for high LDL, ASCVD prevention, post-MI/stroke
Diabetes patients age >40 with risk factors
STATINS
Q: Monitoring?
Q: Counseling Points?
LFTs (AST, ALT) every 6 months
Lipid profile after 4–12 weeks
Watch for myopathy → monitor CK(creatinin kinase) if muscle pain=rhabdomyolysis
Ezetimibe (Cholesterol Absorption Inhibitor)
Q: MOA?
Q: Indication?
A: Inhibits cholesterol absorption at intestinal brush border
Add-on to statin if LDL target not met
Used in statin-intolerant patients
Ezetimibe
Q: Monitoring?
Q: Counseling?
Lipid profile
Liver enzymes if used with statins
Fibrates (e.g., fenofibrate, gemfibrozil)
Q: MOA?
Q: Indications?
A: Activate PPAR-alpha → ↑ lipolysis → ↓ triglycerides, ↑ HDL
Severe hypertriglyceridemia (>5.6 mmol/L or >500 mg/dL)
Prevention of pancreatitis
Fibrates
Q: Monitoring?
Q: Counseling?
a.Triglycerides
Liver and renal function
Risk of rhabdomyolysis with statins
b.Take with meals
Avoid combination with statins unless necessary
Watch for muscle pain
Niacin (Vitamin B3)
Q: MOA?
Q: Indications?
A: ↓ hepatic VLDL synthesis → ↓ LDL and triglycerides, ↑ HDL
B.Used in mixed dyslipidemia
No longer first-line due to side effects
NIACIN
Q: Side Effects?
Q: Counseling?
A.Flushing, hepatotoxicity, hyperglycemia, hyperuricemia
B.Take aspirin 30 min before to reduce flushing
Take with food
Monitor for blood sugar and uric acid
Bile Acid Sequestrants (e.g., cholestyramine)
Q: MOA?
Q: Indications?
Q: Side Effects?
Q: Counseling?
A: Bind bile acids in intestine → excreted → liver uses cholesterol to make more
B.Adjunct for high LDL
May help in pruritus due to bile acid excess
Cholestsis of pregnancy
C.GI issues: constipation, bloating
May reduce absorption of fat-soluble vitamins (A, D, E, K)
D.Take other meds 1 hour before or 4–6 hours after ie digoxin
Mix with plenty of water
PCSK9 Inhibitors (e.g., alirocumab, evolocumab)
Q: MOA?
Q: Indications?
Q: Monitoring?
Q: Counseling?
A: Monoclonal antibodies block PCSK9 → ↑ LDL receptors → ↓ LDL
B.Familial hypercholesterolemia
ASCVD not controlled on statins
C.Lipid panel
Injection site reactions
D.Administer via subcutaneous injection
Store in fridge
Expensive
Targets & Monitoring Goals (2024 AHA/ESC)
Risk Category LDL Goal
Low Risk < 3.0 mmol/L
Moderate Risk < 2.6 mmol/L
High Risk (e.g. DM, CKD) < 1.8 mmol/L
Very High Risk (ASCVD) < 1.4 mmol/L (or <1.0 in some)
Additional Counseling Tips for All Patients
Combine with lifestyle: diet, exercise, smoking cessation
Emphasize adherence – lipid control = lifelong
Encourage regular lipid checks
Be cautious with polypharmacy (especially in elderly)
ASCVD 10 year risk ie stroke,MI
SAD CHF
Smoking
Age greater than 45M,55F
Daibetes
High TC
HTN
Family Hx
Indication for statin therapy
1.ASCVD(CAD,CVA,PAD) less than 7.5-moderate statin else high intensity
2.LDL greater than 190
3.LDL greater than 70 =40-75yr =DM
4.ASCVD greater than 7.5 = 40-75yr = ldl greater than 70