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Elevated levels of LDL-C, and high levels of HDL-C. Cigarette smoking, high blood pressure, obesity, diabetes and genetic/lifestyle factors all contribute.
What causes coronary heart disease?
Reduce LDL-C specifically.
What is the biggest goal of Hyperlipidemia treatment?
Lifestyle Modifications (exercise and low fatty diet)
What always comes with drug therapy for hyperlipidemia?
They inhibit cholesterol synthesis and increase LDL catabolism, forcing cells to use plasma cholesterol instead of making their own with LDL-C receptors
How does a HMG CoA reductase inhibitor work?
In patients homozygous for familial hypercholesterolemia. They don’t upregulate LDL-C receptors.
In what case is HMG CoA reductase inhibitors ineffective?
Liver dysfunction, myopathy/rhabdomyolysis, and teratogenic
Adverse HMG CoA reductase inhibitors effects?
Inhibit lipolysis in adipose tissue, meaning that the liver doesn’t have free fatty acids for triglyceride synthesis. VLDL production decreases, and so does LDL-C plasma concentration.
How does Niacin work?
Familial hyperlipidemia (lowers LDL-C by 10-20% and triglycerides by 20-35%)
What is Niacin especially useful for?
Administered orally, converted to nicotinamide and NAD+, and excreted in urine
Niacin Pharmacokinetics?
Intense flush/warmth, nausea, abdominal pain, hyperuricemia and hepatic dysfunction
Niacin adverse effects?
Lifestyle changes; HMG CoA reductase inhibitors (statins) are primary treatment
How do we treat hypercholesterolemia?
Diet and exercise (crucial), niacin and fibric acid derivatives, and Omega-3 fatty acids
How do we treat hypertriglyceridemia?
Binds to peroxisome proliferator-activated receptors (PPAR’s) which regulate lipid metabolism in the nucleus. PPAR’s increase the expression of lipoprotein lipase, decreases triglycerides and apo CII, and increase HDL with apo AI and apo AII expression.
How do Fibrates work?
They all end in “-statin”
What’s an easy way to identify HMG CoA reductase inhibitors?
Complete oral absorption, distributed widely and bound to albumin. Excreted in urine.
Fibrate pharmacokinetics?
Mild GI tract discomfort, possible gallstones, myositis, and myopathy.
Fibrate adverse effects?
It’s like a “speed check” for cholesterol synthesis, regulating how fast synthesis occurs.
What is HMG CoA reductase?
Lovastatin and simvastatin; these are prodrugs that need to be activated.
What two statins cannot be given to patients with liver dysfunction/failure?
Binds bile acids and salts in the small intestine, increasing their excretion and lowering bile acid concentration. The liver is forced to pull cholesterol from the plasma to make more bile acids. There are 3 of these.
How do bile acid-binding resins work?
Fenofibrate
What’s more effective between fenofibrate and gemfibrozil at lowering triglycerides?
Triglycerides
Fibrates mainly reduce—
Inhibits absorption of dietary cholesterol, lowering hepatic cholesterol and forcing clearance by the liver in the blood.
How do cholesterol absorption inhibitors work?
Lowers serum triglyceride by inhibiting its synthesis in the liver
How do omega-3 fatty acids help hyperlipidemia?
GI disturbances, impair absorption of many drugs and fat-soluble vitamins. Triglyceride levels may actually rise; this is strictly a cholesterol medication class.
Bile acid-binding resin adverse effects?
Ezetimibe
What is our one cholesterol absorption inhibitor?
Most cholesterol is made in the body; preventing absorption only lowers LDL-C by 17%
Why is ezetimibe always used in adjunct with other therapies?
Hepatic insufficiency
What is ezetimibe contraindicated with?
Patients with definitive ASCVD, 10 year risk pf ASCVD, or when statin therapy is ineffective.
When are hyperlipidemia drugs combined?
Liver and muscle toxicity
What are combination therapy risks?
Aspirin
What curbs the adverse effects of niacin?
Fenofibrate and Gemfibrozil (Fibrates)
What drugs are contraindicated with renal sufficiency?
Note 
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