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10 Cards in this Set
- Front
- Back
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Atorvastatin
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+Lipitor, Caudet*
+HMG-COA reductase inhibitor +Primary prevention of CHD, dyslipidemias (FH, HeFH) +PC: X MOA:Inhibitor of 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase, the rate-limiting enzyme in cholesterol synthesis (reduces the production of mevalonic acid from HMG-CoA); this then results in a compensatory increase in the expression of LDL receptors on hepatocyte membranes and a stimulation of LDL catabolism |
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Rosuvastatin
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+Crestor
+HMG-COA reductase inhibitor +Hyperlipidemia, mixed dyslipidemia, hypertriglyceridemia, primary dysbetalipoproteinemia, slowing progression of atherosclerosis +PC: X MOA: Inhibitor of 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase, the rate-limiting enzyme in cholesterol synthesis (reduces the production of mevalonic acid from HMG-CoA); this then results in a compensatory increase in the expression of LDL receptors on hepatocyte membranes and a stimulation of LDL catabolism |
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Niacin
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+Niaspan, Slo-Niacin
+Antilipemic agent, vitamin +Hyperlipidemia, pellagra +PC: A/C Enter Breast Milk +MOA: Component of two coenzymes which is necessary for tissue respiration, lipid metabolism, and glycogenolysis; inhibits the synthesis of very low density lipoproteins (VLDL) and low density lipoproteins (LDL); may also increase the rate of chylomicron triglyceride removal from plasma. |
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Ezetimibe
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+Zetia, Vytorin*
+Antilipemic Agent, 2-Azetidinone +Hyperlipidemias, sitosterolemia +PC: C +MOA: Inhibits absorption of cholesterol at the brush border of the small intestine via the sterol transporter, Niemann-Pick C1-Like1 (NPC1L1). This leads to a decreased delivery of cholesterol to the liver, reduction of hepatic cholesterol stores and an increased clearance of cholesterol from the blood; decreases total C, LDL-cholesterol (LDL-C), ApoB, and triglycerides (TG) while increasing HDL-cholesterol (HDL-C). |
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Fenofibrate
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+Tricor
+Antilipemic agent, fibric acid +Hypertriglyceridemia, hypercholesterolemia or mixed hyperlipidemia +PC: C +MOA:Fenofibric acid, an agonist for the nuclear transcription factor peroxisome proliferator-activated receptor-alpha (PPAR-alpha), downregulates apoprotein C-III (an inhibitor of lipoprotein lipase) and upregulates the synthesis of apolipoprotein A-I, fatty acid transport protein, and lipoprotein lipase resulting in an increase in VLDL catabolism, fatty acid oxidation, and elimination of triglyceride-rich particles; as a result of a decrease in VLDL levels, total plasma triglycerides are reduced by 30% to 60%; modest increase in HDL occurs in some hypertriglyceridemic patients. |
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Omega-3 polyunsaturated
Fatty acids |
+Lovaza
+Antilipemic agent +Hypertriglyceridemia, tx of IgA nephropathy (unlabeled use) +PC: C +MOA: Possible mechanisms include inhibition of acyl CoA:1,2 diacylglycerol acyltransferase, increased hepatic beta-oxidation, a reduction in the hepatic synthesis of triglycerides, or an increase in plasma lipoprotein lipase activity. |
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Furosemide
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+Lasix
+Loop Diuretic +Edema, heart failure, acute pulmonary edema, hypertension, refractory heart failure +PC: C +MOA: Inhibits reabsorption of sodium and chloride in the ascending loop of Henle and distal renal tubule, interfering with the chloride-binding cotransport system, thus causing increased excretion of water, sodium, chloride, magnesium, and calcium +BB Warning: a potent diuretic which, if given in excessive amounts, can lead to a profound diuresis with water and electrolyte depletion |
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Hydrochlorothiazide
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+HydroDIURIL*
+Diuretic, thiazide +Hypertension, edema +Inhibits sodium reabsorption in the distal tubules causing increased excretion of sodium and water as well as potassium and hydrogen ions +PC: C |
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Spironolactone
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+Aldactone
+Potassium sparing diuretic, selective aldosterone blocker +Edema, hypokalemia, hypertension, heart failure +PC: C/D +Spironolactone has been shown to be a tumorigen in chronic toxicity studies in rats. Use spironolactone only in those conditions for which it is indicated. Avoid unnecessary use of this drug. |
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Clonidine
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+Catapres, Catapres-TTS
+Alpha-2 adrenergic agonist +Mild-to-moderate hypertension +Stimulates alpha2-adrenoceptors in the brain stem, thus activating an inhibitory neuron, resulting in reduced sympathetic outflow from the CNS, producing a decrease in peripheral resistance, renal vascular resistance, heart rate, and blood pressure; epidural clonidine may produce pain relief at spinal presynaptic and postjunctional alpha2-adrenoceptors by preventing pain signal transmission; pain relief occurs only for the body regions innervated by the spinal segments where analgesic concentrations of clonidine exist +PC: C |
