Dyslipidemia
Clinical Overview and Exam Mastery Guide covering LDL-centered risk reduction, statin-first treatment, non-statin escalation, and hypertriglyceridemia strategy.
Atherosclerosis Context
LDL-driven plaque formation underpins dyslipidemia-related ASCVD risk.
1. What Is Dyslipidemia?
Dyslipidemia refers to abnormal lipid levels that increase atherosclerotic cardiovascular disease risk.
2. Pathophysiology
LDL to ASCVD Pathway Diagram
3. Risk Assessment
Use ASCVD Risk Estimator to guide statin need and treatment intensity.
Assess
- 10-year ASCVD risk
- Need for statin therapy
- Intensity of treatment
High-Risk Groups
- Clinical ASCVD
- LDL at least 190 mg/dL
- Diabetes age 40 to 75
- Elevated 10-year ASCVD risk
4. First-Line Therapy: Statins
Statins are the cornerstone of dyslipidemia treatment.
| Intensity | Common Regimens | Typical Use |
|---|---|---|
| High-intensity | Atorvastatin 40 to 80 mg, Rosuvastatin 20 to 40 mg | Very high risk, LDL at least 190, secondary prevention |
| Moderate-intensity | Lower atorvastatin/rosuvastatin doses, simvastatin, pravastatin | Diabetes, intermediate risk, statin initiation in many primary settings |
A. Statins
- MOA: inhibit HMG-CoA reductase and lower hepatic cholesterol synthesis
- Increase LDL receptor expression and LDL clearance
- Benefits: lower LDL, reduce cardiovascular events, reduce mortality
- Major side effects: myopathy, rare rhabdomyolysis, elevated liver enzymes, rare new-onset diabetes
- Contraindications: active liver disease, pregnancy, breastfeeding
5. Non-Statin Therapy
Use when statin intolerance exists, LDL remains above goal, or risk is very high.
B. Ezetimibe
- MOA: inhibits NPC1L1 transporter and lowers intestinal cholesterol absorption
- Benefit: LDL reduction, especially as statin add-on
- Side effects: usually mild GI symptoms
- Contraindication: severe liver disease when combined with statin
C. PCSK9 Inhibitors (Alirocumab, Evolocumab)
- MOA: inhibit PCSK9 and prevent LDL receptor degradation
- Benefits: large LDL reduction and lower CV events
- Side effects: injection-site reactions, flu-like symptoms
- Contraindication: hypersensitivity
D. Bempedoic Acid
- MOA: ATP-citrate lyase inhibition upstream of statins
- Benefit: LDL lowering, useful in statin intolerance
- Side effects: hyperuricemia, rare tendon rupture
- Contraindication/caution: gout history
E. Fibrates (Fenofibrate, Gemfibrozil)
- MOA: PPAR-alpha activation increases lipoprotein lipase activity
- Primary use: severe hypertriglyceridemia
- Side effects: myopathy risk (higher with statins), gallstones
- Contraindications: severe liver disease, severe renal impairment
F. Omega-3 Fatty Acids
- MOA: reduce hepatic triglyceride synthesis
- Use: high triglycerides
- Side effects: GI upset, fishy taste
6. Hypertriglyceridemia
When TG at least 500 mg/dL
- Pancreatitis risk increases
- Treat with fibrates or omega-3 therapy
ASCVD Context
- Statins still required for overall ASCVD prevention
7. Treatment Strategy Summary
Management Recap Drill
Visual Algorithm Placeholder
[Insert Dyslipidemia Treatment Algorithm Flowchart Here During UI Integration]
Guideline References
ACC/AHA Guideline on Blood Cholesterol Management
https://www.acc.org/guidelinesImage Attribution (Wikimedia Commons)
- Atheroma illustration - Blausen.com staff, CC BY 3.0
8. Common Exam Traps
9. Quick Revision Summary
Must Remember
- LDL is the primary treatment target
- Statins reduce mortality and events
- Add ezetimibe before PCSK9 in common escalation pathways
- TG at least 500 means pancreatitis prevention priority
- Monitor liver-related symptoms and adverse effects clinically
Practice Questions Placeholder
- Topic: Dyslipidemia
- Subtopics: statins, non-statin agents, ASCVD risk, hypertriglyceridemia, treatment intensification