| Term 
 
        | Example of HMG-CoA reductase inhibitor. |  | Definition 
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        | Term 
 
        | Mechanism of action of HMG-CoA reductase inhibitor. |  | Definition 
 
        | Statins inhibit the enzyme (HMG-CoA) that synthesizes cholesterol and increases the # of LDL receptors on liver cells; therefore, decreasing LDL levels. Can also increase HDL levels and lower TGs- effect unknown. |  | 
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        | Term 
 
        | Indication of HMG-CoA reductase inhibitor. |  | Definition 
 
        | Hypercholesterolemia and mixed dyslipidemias; elevated LDL cholesterol that cannot be controlled via diet and exercise; pts w/high risk of CV events, post MI, diabetes. |  | 
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        | Term 
 
        | Contraindications of HMG-CoA reductase inhibitor. |  | Definition 
 
        | Pts w/ viral or alcoholic hepatitis and pregnant woman. Caution in pts w/nonalcoholic fatty liver disease, those who drink alcohol excessively, those taking fivrates or ezetimibe or agents that inhibit CYP3A4. |  | 
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        | Term 
 
        | Serious adverse effects of HMG-CoA reductase inhibitor. |  | Definition 
 
        | Hepatotoxicity (can injure liver, but jaundice and further signs are rare); rabdomyelysis (breakdown of skeletal muscle- release of chemicals into bloodstream); Myopathy (can rarely cause muscle injury, mechanism unknown); peripheral neuropathy. |  | 
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        | Term 
 
        | Common adverse effects of HMG-CoA reductase inhibitor. |  | Definition 
 
        | Side effects uncommon. Dizziness, insomnia, chest pain, weakness, headache, rhinitis, blurred vision, rash, and some GI disturbances (abdominal cramps, flatulence, constipation)- all usually mild and transient. |  | 
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        | Term 
 
        | Preadministration assessment of HMG-CoA reductase inhibitor. |  | Definition 
 
        | Baseline lipid profile, full cholesterol profile, LFT and CKs, pregnancy test, dietary Hx (for fat consumption) |  | 
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        | Term 
 
        | Monitoring of HMG-CoA reductase inhibitor. |  | Definition 
 
        | Cholesterol levels should be monitored monthly (serum cholesterol); liver function tests for hepatotoxicity, if unexplained muscle pain, CK level should be measured- if > 10X ULN, statin should be withdrawn. |  | 
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        | Term 
 
        | Patient education of HMG-CoA reductase inhibitor. |  | Definition 
 
        | Take lovastatin w/ evening meal, all others can be taken w/out regard to food- all statins should be taken in the evening (body makes more cholesterol at night); inform PCP if muscle pain or tenderness developes. Promote diet, exercise, and lifestyle changes. |  | 
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        | Term 
 
        | Example of Bile-acid sequestrants. |  | Definition 
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        | Term 
 
        | Mechanism of action of Bile-acid sequestrants. |  | Definition 
 
        | Reduces LDL cholesterol by binding to bile salts, preventing reabsorption. Increases receptors on hepatocytes. Body picks up more LDL to make more bile salts, so less LDL in body. Often used in combo w/statin. Doesn't raise HDL, may raise TGs. |  | 
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        | Term 
 
        | Indication of Bile-acid sequestrants. |  | Definition 
 
        | High LDL cholesterol and hyperglycemia in diabetic patients. |  | 
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        | Term 
 
        | Contraindication of Bile-acid sequestrants. |  | Definition 
 
        | Genetic inability to increase synthesis of liver LDL receptors. |  | 
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        | Term 
 
        | Serious adverse effects of Bile-acid sequestrants. |  | Definition 
 
        | The drug remains in the GI tract, so there are no systemic effects. |  | 
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        | Term 
 
        | Common adverse effects of Bile-acid sequestrants. |  | Definition 
 
        | GI tract- constipation, bloating, nausea, indigestion. Some older forms of the drug can inhibit vitamin absorption. |  | 
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        | Term 
 
        | Preadministration assessment of Bile-acid sequestrants. |  | Definition 
 
        | Baseline cholesterol levels (LDL, HDL, and THs/VLDLs). Identify CHD risk factors (smoking, obesity, age, family Hx, and high BP). |  | 
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        | Term 
 
        | Monitoring of Bile-acid sequestrants. |  | Definition 
 
        | Monitor cholesterol levels and for GI side effects. |  | 
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        | Term 
 
        | Patient education of Bile-acid sequestrants. |  | Definition 
 
        | Vitamin supplements may be needed. To reduce constipation, increase fiber and fluids. Take other meds 1hr before or 4hrs after to minimize absorption problems. |  | 
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        | Term 
 
        | Mechanism of action of Nicotinic acid. |  | Definition 
 
        | Decreases productin of VLDLs by inhibiting lipolysis, causing LDL #s to fall as well. |  | 
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        | Term 
 
        | Indication of Nicotinic acid. |  | Definition 
 
        | For pts w/high LDL #s and low HDL #s, especially for those at risk of pancreatitis. |  | 
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        | Term 
 
        | Contraindications of Nicotinic acid. |  | Definition 
 
        | Pts w/active liver disease or those w/sever or recurrent gout. Caution in pts w/DM, asymptomatic hyperuricemia, mild gout, and peptic ulcer disease. |  | 
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        | Term 
 
        | Serious adverse effects of Nicotinic acid. |  | Definition 
 
        | Hepatotoxic- more likely w/slo-niacin (long acting formulation) especially if in high doses or when used w/a statin. Hyperglycemia, gouty arthritis. |  | 
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        | Term 
 
        | Common adverse effects of Nicotinic acid. |  | Definition 
 
        | Flushing, itching (occurs in almost all pts, will diminish in several weeks), GI rxns are also common |  | 
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        | Term 
 
        | Preadministration assessment of Nicotinic acid. |  | Definition 
 
        | Baseline cholesterol levels (LDL, HDL, and THs/VLDLs). Identify CHD risk factors (smoking, obesity, age, family Hx, and high BP); liver function tests to check liver condition. |  | 
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        | Term 
 
        | Monitoring of Nicotinic acid. |  | Definition 
 
        | Monitor cholesterol levels, liver function tests to make sure liver isn't being damaged, blood lipid levels should be continually monitored. |  | 
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        | Term 
 
        | Patient education of Nicotinic acid. |  | Definition 
 
        | Advise pts to use immediate-release formulations or ER, not long-acting (slo-niacin). Take w/meals to reduce stomach upset. Diet modification counseling. Flushing can be lessened if aspirin is taken before, also if taking ER form. |  | 
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        | Term 
 
        | Mechanism of action of Ezetimibe. |  | Definition 
 
        | Inhibits cholesterol absorption by acting on cells of brush border of the small intestine to inhibit cholesterol absorption. Reduces LDL, TG, total cholesterol, and might slightly increase HDL. Blocks dietary and bile cholesterol. |  | 
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        | Term 
 | Definition 
 
        | Reduce total cholesterol and apolipoprotein B (transports fat to nonhepatic tissue) w/diet modicigation. Greater effect when used w/a statin. |  | 
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        | Term 
 
        | Contraindications of Ezetimibe. |  | Definition 
 
        | Hepatic disease/hepatic insufficiency, severe allergy |  | 
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        | Term 
 
        | Serious adverse effects of Ezetimibe. |  | Definition 
 
        | Drug-drug interactions, gall stones, myopothy |  | 
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        | Term 
 
        | Common adverse effects of Ezetimibe. |  | Definition 
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        | Term 
 
        | Preadministration assessment of Ezetimibe. |  | Definition 
 
        | Total cholesterol levels (TG, LDL, HDL), know other drugs being taken at the same time. |  | 
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        | Term 
 | Definition 
 
        | Drug levels of Ezetimibe, liver damage (indicated by transaminase levels), liver function tests |  | 
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        | Term 
 
        | Patient education for Ezetimibe. |  | Definition 
 
        | Talk to provider before beginning other drugs because of drug-drug interactions. Lower dietary cholesterol. |  | 
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        | Term 
 
        | An example of Fibric acid derivatives. |  | Definition 
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        | Term 
 
        | Mechanism of Fibric acid derivatives. |  | Definition 
 
        | Interacts w/specific receptor subtypes to decrease VLDL production by liver, so lowers plasma TG levels. Can slightly raise HDL levels pts w/normal TG levels, can reduce LDL to minor extent. If TG levels are high, can actually raise LDL levels. |  | 
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        | Term 
 
        | Indication of Fibric acid derivatives. |  | Definition 
 
        | Used to reduce TGs, not very effective at lowering LDL, may be used to raise HDL. Principal indication is hypertriglyceridemia. |  | 
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        | Term 
 
        | Contraindications of Fibric acid derivatives. |  | Definition 
 
        | Pts w/liver disease, severe renal dysfunction, and gallbladder disease. Also those on warfarin. Caution w/those on statins. |  | 
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        | Term 
 
        | Serious adverse effects of Fibric acid derivatives. |  | Definition 
 
        | Gallstones, Myopothy, liver disease (may disrupt liver function) |  | 
        |  | 
        
        | Term 
 
        | Common adverse effects of Fibric acid derivatives. |  | Definition 
 | 
        |  | 
        
        | Term 
 
        | Preadministration assessment of Fibric acid derivatives. |  | Definition 
 
        | Baseline cholesterol levels (LDL, HDL, and THs/VLDLs). Identify CHD risk factors (smoking, obesity, age, family Hx, and high BP); pre-existing muscle pain; liver function. |  | 
        |  | 
        
        | Term 
 
        | Monitoring of Fibric acid derivatives. |  | Definition 
 
        | Monitor blood lipids, liver function, muscle pain. |  | 
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        | Term 
 
        | Patient education for Fibric acid derivatives. |  | Definition 
 
        | Take 30 minutes before morning and evening meals. Inform pts of gallbladder symptoms, notify PCP if noticed. Also signs of muscle injury. Promote diet, exercise, and lifestyle changes. |  | 
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        | Term 
 
        | Mechanism of action of Nitrates |  | Definition 
 
        | Vasodilates smooth muscles, acts mostly on veins, only slightly on arterioles. Stable Angina- decreases pain by decreasing oxygen demand (dilate veins leading to reduced venous return leading to reduced ventricular filling leading to reduced preload leading to reduced oxygen demand)  Varient angina- relaxes/prevents spasm in coronary arteries leading to increased oxygen supply, not reduction in oxygen demand) |  | 
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        | Term 
 
        | Indications for Nitrates. |  | Definition 
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        |  | 
        
        | Term 
 
        | Contraindications for Nitrates. |  | Definition 
 
        | Use w/sildenafil (viagra) or other PDE5 inhibitors (erectile dysfunction drugs); very important to ask- BOTH men and women. |  | 
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        | Term 
 
        | Common adverse effects of Nitrates. |  | Definition 
 
        | Headace- will lessen over first few weeks of treatment, use aspirin or tylenol. Orthostatic hypotension. Tachycrdia- b/c BP is lower, HR will increase to make up for it (pretreat w/a beta blocker or Ca channel blocker). |  | 
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        | Term 
 
        | Preadministration assessment for Nitrates. |  | Definition 
 
        | Baseline for frequency, intensity, location, and triggers of angina attacks. Monitor BP before and after each dose. |  | 
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        | Term 
 | Definition 
 
        | Sublingual- under tongue, wait 5 min and call 911 if not relieved, can take 2 more in next 10 min. SR- taken daily to avoid attacks. Transdermal/Topical- on skin, covered, to protect against attacks. Translingual- spray into mouth for termination of attack. Transmucosal- between gums and upper lip, dissolves in 3-5 hrs, to terminate attacks. IV- used in ICU/ER when SL isn't working |  | 
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        | Term 
 
        | Patient education for Nitrates. |  | Definition 
 
        | Tell pt to sit/lie down in case of orthst hypotens. Promote wt reduction, exercise, smoking cessation, avoid alcohol. Tolerance can develope rapidly, use lowest dose able on an intermittent schedule (drug-free for at lest 8 hrs). Needs to be discontinued slowly. |  | 
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