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5 Cards in this Set

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Familial Hypercholesterolemia: Clinical Presentation, Risk Factors, Etiology, Pathophysiology, Treatment
1. Clinical Presentation: asymptomatic, high LDL-C, achilles tendon thickening, xanthelasma, arcus cornealis
2. Risk Factors: French Canadian, South African, Lebanese
3. Etiology: heterozygote mutation of gene for LDL-receptor
4. Pathophysiology: LDL-C has a high concentration of cholesterol, in the endogenous pathway the liver produces VLDL which gets converted to IDL, then LDL and is then taken up by the liver via the LDL-R receptor. Since receptor is defective, LDL-C and cholesterol accumulate in blood.
5. Treatment: statins, ezetimibe
Treatment of Hyperlipidemia: Why Target LDL Cholesterol, Statin Mechanism of Action, Ezetimibe Mechanism of Action, 2009 Lipid Target Guidelines, Rule of 6, One-step vs 3-step lowering of LDL
1. Why target LDL-cholesterol: has a high cholesterol content and lowering has been shown to reduce risk of cardiovascular disease
2. Statin MOA: statin inactivates HMG CoA reductase in liver which is needed to breakdown LDL-C into cholesterol -> decreased liver cholesterol -> increased expression of LDL-receptor -> increased uptake of LDL-C into the liver (and out of the blood)
3. Ezetimibe MOA: blocks cholesterol uptake in gut -> decreases cholesterol content in chylomicron/exogenous lipid pathway -> decreased cholesterol gets to liver -> increased expression of LDL-R -> increased LDL-C uptake by liver
4. 2009 Lipid Target Guidelines: LDL-C <2 mmol/L or >50% reduction in LDL-C (moderate to high risk), >50% decrease in LDL-C (low risk)
5. Rule of 6: Every doubling of the dose of a statin decreases the LDL-C by an additional 6%
6. One-step vs 3-step lowering of LDL: one-step=add Ezetemibe to statin, 3-step=double statin dose 3x, both reduce LDL-C by 18%
Hypertriglyceridemia: Health Risks, Clinical Presentation, Pathophysiology,
1. Health Risks: acute pancreatitis (extreme elevation for TG), coronary heart disease (modest elevation of TG)
2. Clinical Presentation: pancreatitis, heart problems, lipemia retinalis, eruptive xanthoma
3. Pathophysiology: LPL is not functioning. LPL converts chylomicrons (exogenous pathway) and VLDL (endogenous pathway) into IDL. Chylomicrons and VLDL are high in TG and they accumulate in blood due to LPL impairment
Framingham Risk Score: Low Risk, Medium Risk, High Risk
1. Low Risk: FRS<10%, LDL-C>5.0
2. Moderate Risk: FRS 10-20%, LDL-C >3.5, TC/HDL-C>5.0
3. High Risk: FRS >20%, diabetes, atherosclerosis, PAD, CAD
Types of cholesterol: Measured Directly, Calculated
1. Measured: Total Cholesterol (TC), Triglycerides (TG), HDL-C
2. Calculated: LDL-C