3. Peters - Hyperlipidemia Flashcards
(39 cards)
Signs and Symptoms of Hyperlipidemia
- Typically asymptomatic until a CV events occurs
- Pancreatitis: directly related to high TGs, >500
- Chest pain: clot in chest, MI or angina
- Shortness of breath: clot moves into lungs
- Speech or movement impaired: clot in brain (stoke)
What is Dyslipidemia?
- A combination of elevated TC, elevated TGs, elevated LDL cholesterol, and low HDL
What are the risk equivalents for coronary heart disease?
Hint, there’s 5
- Diabetes
- PAD
- CAD - MI or angina
- Abdominal aortic aneurysm (triple A syndrome)
- Framingham risk >20%
What are some major CV risk factors?
Hint, there’s 5
- Cigarette smoking
- Hypertension, BP >140/90
- Low HDL
- Family history of premature CHD
- Age, men >45 and women >55
What are the target numbers based on ATP III?
TC: 40 mg/dL
TGs:
Non-Pharm Therapy for Hyperlipidemia
- Diet counseling
- Weight management
- Increased physical activity
- Smoking cessation
- Hypertension treatment
Peters - MOA of statins
- HMG-CoA Reductase inhibitor
- Decrease cholesterol synthesis, lowers intracellular cholesterol which stimulates up regulation of LDL receptors increasing the intake of LDL, and lowering circulating LDL levels
Pleiotropic effects of statins
Help decrease plaque and clot formation
What are the two high intensity statins and what are their available strengths?
- Atorvastatin, 40-80mg
2. Rosuvastatin, 20-40mg
What are the 3 main statin drug interactions to avoid?
- CCB (nondihydropyridines)
- Gemfibrozil
- Grapefruit juice
What are the main adverse effects of statins?
- Headache and GI intolerance
- Myalgia, which can lead to myopathy and/or rhabdomyolysis
- New onset diabetes
- Potential increase in LFTs
Managing statin therapy - how to determine if a pt is “intolerant”
Try 3 statins, 3 different times, at three different strengths.
If a pt does not respond, then they are considered statin intolerant
Peters - Fibrates and their MOA
Fenofibrate and Gemfibrozil
- Agonist of proliferator-activated receptor-alpha
- inhibit TG synthesis, increase LPL activity, increase breakdown of VLDL and increase HDL synthesis
What is the net effect of statins?
Decreased TC
Decreased LDL
What is the net effect of Fibrates?
Significantly decreased TGs –> main effect
Decreased TC
Decreased LDL
Increased HDL
What are the main adverse effects of Fibrates?
- GI complaints
- Changes in LFTs
- Hypoglycemic effects in pts on sulfonureas
- Renal dysfunction
MAIN: Gemfibrozil inhibits break down of statins
Examples of Bile Acid Sequestrants and their MOA
Cholestyramine, colestipol, colesevelam
MOA: Block the reabsorption of bile acids back into the liver, allows for easy excretion out through feces
What is the net effect of bile acid sequestrants?
Decreased TC
Decreased LDL
What are the main adverse effects of bile acid sequestrants?
- GI distress
- Potential increase in TG, should not be taken when pt >300 mg/dL
- Impaired fat soluble vitamin absorption
- Reduced bioavailability of other meds, separated dosing is needed
What is Niacin’s MOA?
Decreased hepatic production of VLDL and LDL
What is Niacin’s net effect?
BIG EFECTS:
- Decreased TGs, decreased LDL, and increased HDL
What are Niacin’s main adverse effects?
- Flushing, but tolerance will develop over time
- P.U.D
- Exacerbate gout
- Exacerbate diabetes
- Hepatotoxicity w/ ER formulation
How should we monitor niacin?
Base line labs including: liver function tests, A1C and uric acid levels
- Labs should be repeated every 6 months
What is Ezitimibe’s MOA?
Block cholesterol absorption by inhibiting NPC1L1 receptor at the brush boarder
