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Thiazide Diuretics
Mechanism of action Therapeutic uses Side Effects/ precautions Interactions Nursing/ Patient teaching Common drugs Block reabsorption of sodium and chloride, prevent reabsorption of water. (but in a different site than loop diuretics) often first choice medication for HTN, edema and mild heart failure, liver and kidney disease same as loop diuretics, these are also not potassium sparing Same as loop diuretics same as loop diuretics hydrochlorothiazide (Hydrodiuril) most commonly referred to as HCTZ, chlorothiazide (Diuril) Note: a lot of these end in azide
Osmotic Diuretics
Mechanism of action Therapeutic uses reduce intracranial pressure and intraocular pressure by raising serum osmolality, and drawing fluid back into vascular and extravascular space prevent renal failure in causes of hypovolemic shock and hypotension, decrease intracranial and intraocular pressure, promote sodium retention and water excretion caution with patients with heart failure furosemide contributes to overall effect by promoting excretion of the fluid that is drawn into the vascular space daily I&O and serum electrolytes, signs for dehydration mannitol (Osmitrol)
All of the above generally used for hypertension, some for angina and heart failure Cardiac Glycosides
Mechanism of action Therapeutic uses Side Effects/ precautions Interactions Nursing/ Patient teaching Common drugs positive inotropic effect: increased force of myocardial contraction (improving cardiac ouput), negative chronotropic effect: decreased heart rate (giving ventricles more time to fill with blood) heart failure, dysrhythmias dysrhythmias, cardiotoxicity:such as weakness, fatigue, anorexia (levels should be 0.8 to 2.0 ng/ml), GI upset, CNS effects (weakness) with diuretics may lead to hypokalemia, ace inhibitors may lead to decreased effects of glycoside, quinidine increases toxicity monitor digoxin levels closely, avoid OTC medications, observe for symptoms of hypokalemia digoxin
Adrenergic Agonists
Variety of drugs that includes: Epinephrine: increases BP, treatment of AV block during cardiac arrest, bronchodilator, vasocontrictor Dopamine: treatment for shock and heart failure, renal blood vessel dilator, vasoconsrtictor Dobutamine: treatment for heart failure, increases heart rete, myocardial contractility
Cardiac Glycosides/ Adrenergic Agonists above generally used for heart failure Nitrates
Mechanism of action Therapeutic uses Side Effects/ precautions Interactions dilation of veins, decreases venous return (preload) which decreases oxygen demand acute angina attack, or prophylaxis for chronic angina h/a, orthostatic hypotension, tolerance additive hypotensive effect with alcohol, and other antihypertensives, contraindication with Viagra
sublingual tablets for rapid onset, sustained release tabs for long onset, during angina attack instruct patient to stop activity, patient can take up to three doses in five minute intervals Nitrostat, Isordil, isosorbide (Imdur)
Antidysrhythmic Medications
variety of drugs are used, most of them already discussed above, book goes into great deal of detail Sodium channel blockers: Lidocaine (Xylocaine) Beta blcokers: propanolol (discussed above) Potassium channel blockers: amiodarone (Cordarone) Calcium channel Blockers: verapamil (Calan) (discussed above)
Fibrates
Mechanism of action Therapeutic uses Side Effects/ precautions Interactions Nursing/ Patient teaching Common drugs decrease triglyceride levels, increase HDL levels reduction of triglycerides, increase HDL GI upset, myopathy (muscle pain), hepatotoxicity concurrent use with coumadin increased risk for bleeding, bile acid sequestrants interfere with absorption take meds 30 min prior to breakfast and dinner gemfibrozil (Lopid), fenofibrate (TriCor)
bile acid sequestrants interfere with absorption instruct client to report muscle aches and pain, discontinue if CK levels are elevated Zetia. This is the only one according to ATI
Antiplatelets: prevents platelets from sticking together Aspirin clopidogrel (Plavix) Thrombolytic Medications: dissolve clots that have already been formed, by conversion of
plasminogen to plasmin which destroys fibrinogen and other clotting factors, treatment for acute MI, PE, DVT, stroke streptokinase (Streptase) alteplase (tPA)