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sotalol toxicity

amiodorone toxicity

ibutilide toxicity

bretylium toxicity

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torsades

new arrhythmias, hypotension

torsades, excessive beta-block 

hypothyrodism/hyperthyrodism,

pulmonary fibrosis, hepatic toxicity,corneal deposits, skin deposits(photodermatitis), neurologic

defects, constipation, bradycardia,heart block, chf 

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what 3 tests to do before usingamiodarone?

what are class IV antiarrhythmicsused for

name 2 class IV antiarrhytmics

mechanism for class IVantiarrhythmics

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verapamil, diltiazem

blocks Ca channels; affect AV nodalcells, decrease conduction velocity,

incrase ERP, increase PR.

PFT, LFT, TFT

prevent nodal arryhtmias (SVT)

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what are 4 general side effects forclass IV

potassium function

bepridil toxicity

adenosine function

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torsades

hyperpolarizes cells by facilitating Kmovement out of cells. drug of choice in diagnosing/abolishing AV

nodal arryhtmias

constipation, flushing, edema, cv(chf, av block, sinus node

depression)

depress ectopic pacemaker, esp indig toxicity

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magnesium function

what is the first-line treatment of hypertension in pregnancy?

what are the adverse effects of nifedipine and verapamil? (5)

adverse effects of Diazoxide?

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dizziness, flushing, nausea(verapamil also has constipation and

AV block)

hypoglycemia - reduces insulinrelease

torsades and dig toxicity use

hydralazine with methyldopa

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what is the mechanism of minoxidil?

what is the mechanism of action of fenoldopam?

what is the toxicity of minoxidil?

what is the treatment for malignanthypertension?

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hypertrichosis, pericardial effusion

nitroprusside, fenoldopam anddiazoxide

K channel opener --> hyperpolarizesand relaxes vascular smooth muscle

Dopoamine D1 receptor agonist -->relaxes renal vascular smooth

muscle

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what is the mechanism of diazoxide?

what is the mechanism of action of the Statins?

what are the HMG-CoA reductaseinhibitors?

What effects do the statins have onLDL, HDL and TGs?

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lovastatin, pravastatin, simvastatin,atorvastatin

greatly decreases LDL, increasesHDL and decreases TGs

K channel opener --> hyperpolarizesand relaxes vascular smooth muscle

inhibit cholesterol precursor,mevalonate

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side effects of statins?

what effect do the Bile acid resinshave on LDL, HDL, and TGs?

What effect does Niacin have onLDL, HDL and TGs?

what is the mechanism of action of niacin?

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decreases LDL, increases HDL,lesser decrease in TGs

inhibits lipolysis in adipose tissue;reduces hepatic VLDL secretion into

circulation

reversible increase in LFTs andmyositis

decrease LDL, slight increase inHDL, slight increase in TGs

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what are the bile acid resins?

What effect does ezetimibe have onLDL, HDL and TGs?

what is the mechanism of action of cholestyramine and colestipol?

what are side effects of cholestyramine and colestipol?

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prevent intestinal reabsorption of bile acids; liver must use cholesterol

to make more

bad taste, causes GI discomfort,decreased absorption of fat-soluble

vitamins

cholestyramine, colestipol

decreases LDL; no effect on others

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what is the mechanism of action of ezetimibe?

what is the mechanism of action of the fibrates?

What are the Fibrates?

what effect do the fibrates have onLDL, HDL and TGs?

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gemfibrozil, clofibrate, bezafibrate,fenofibrate

mainly decrease TGs, lesserdecrease LDL and increase HDL

prevents cholesterol reabsorption atsmall intestine brush border

upregulate LPL --> increase TGclearance

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what are the side effects of fibrates?what Beta blockers are

contraindicated in angina and why?

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labetalol, pindolol and acebutolol,due to partial agonist effects

myositis, and increase in LFTs

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