| Question |
 |
|
| Answer |
|
|
| sotalol toxicity |
torsades, excessive beta-block |
| ibutilide toxicity |
torsades |
| bretylium toxicity |
new arrhythmias, hypotension |
| amiodorone toxicity |
hypothyrodism/hyperthyrodism, pulmonary fibrosis, hepatic toxicity, corneal deposits, skin deposits (photodermatitis), neurologic defects, constipation, bradycardia, heart block, chf |
| what 3 tests to do before using amiodarone? |
PFT, LFT, TFT |
| name 2 class IV antiarrhytmics |
verapamil, diltiazem |
| mechanism for class IV antiarrhythmics |
blocks Ca channels; affect AV nodal cells, decrease conduction velocity, incrase ERP, increase PR. |
| what are class IV antiarrhythmics used for |
prevent nodal arryhtmias (SVT) |
| what are 4 general side effects for class IV |
constipation, flushing, edema, cv (chf, av block, sinus node depression) |
| bepridil toxicity |
torsades |
| adenosine function |
hyperpolarizes cells by facilitating K movement out of cells. drug of choice in diagnosing/abolishing AV nodal arryhtmias |
| potassium function |
depress ectopic pacemaker, esp in dig toxicity |
| magnesium function |
torsades and dig toxicity use |
| what are the adverse effects of nifedipine and verapamil? (5) |
dizziness, flushing, nausea (verapamil also has constipation and AV block) |
| adverse effects of Diazoxide? |
hypoglycemia - reduces insulin release |
| what is the first-line treatment of hypertension in pregnancy? |
hydralazine with methyldopa |
| what is the mechanism of minoxidil? |
K channel opener --> hyperpolarizes and relaxes vascular smooth muscle |
| what is the toxicity of minoxidil? |
hypertrichosis, pericardial effusion |
| what is the treatment for malignant hypertension? |
nitroprusside, fenoldopam and diazoxide |
| what is the mechanism of action of fenoldopam? |
Dopoamine D1 receptor agonist --> relaxes renal vascular smooth muscle |
| what is the mechanism of diazoxide? |
K channel opener --> hyperpolarizes and relaxes vascular smooth muscle |
| what are the HMG-CoA reductase inhibitors? |
lovastatin, pravastatin, simvastatin, atorvastatin |
| What effects do the statins have on LDL, HDL and TGs? |
greatly decreases LDL, increases HDL and decreases TGs |
| what is the mechanism of action of the Statins? |
inhibit cholesterol precursor, mevalonate |
| side effects of statins? |
reversible increase in LFTs and myositis |
| What effect does Niacin have on LDL, HDL and TGs? |
decreases LDL, increases HDL, lesser decrease in TGs |
| what is the mechanism of action of niacin? |
inhibits lipolysis in adipose tissue; reduces hepatic VLDL secretion into circulation |
| what effect do the Bile acid resins have on LDL, HDL, and TGs? |
decrease LDL, slight increase in HDL, slight increase in TGs |
| what are the bile acid resins? |
cholestyramine, colestipol |
| what is the mechanism of action of cholestyramine and colestipol? |
prevent intestinal reabsorption of bile acids; liver must use cholesterol to make more |
| what are side effects of cholestyramine and colestipol? |
bad taste, causes GI discomfort, decreased absorption of fat-soluble vitamins |
| What effect does ezetimibe have on LDL, HDL and TGs? |
decreases LDL; no effect on others |
| what is the mechanism of action of ezetimibe? |
prevents cholesterol reabsorption at small intestine brush border |
| What are the Fibrates? |
gemfibrozil, clofibrate, bezafibrate, fenofibrate |
| what effect do the fibrates have on LDL, HDL and TGs? |
mainly decrease TGs, lesser decrease LDL and increase HDL |
| what is the mechanism of action of the fibrates? |
upregulate LPL --> increase TG clearance |
| what are the side effects of fibrates? |
myositis, and increase in LFTs |
| what Beta blockers are contraindicated in angina and why? |
labetalol, pindolol and acebutolol, due to partial agonist effects |
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