9571647
Beschreibung
Karteikarten von Kate Parvey, aktualisiert more than 1 year ago
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Erstellt von Kate Parvey
vor mehr als 7 Jahre
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| Frage | Antworten |
| WHAT ARE THE 5 ADRENERGIC RECEPTORS? | Alpha 1 & Alpha 2 Beta 1 & Beta 2 Dopamine |
| ACTIVATION OF ALPHA 1 RECEPTORS | Alpha 1 Activation= Vasoconstriction: 1. Delay absorption of local anesthetics 2. Control superficial bleeding 3. Elevate blood pressure Adverse effects: hypertension, tissue necrosis with intravenous (IV) extravasation, and bradycardia. |
| ACTIVATION OF ALPHA 2 RECEPTORS | Activation of peripheral alpha2 receptors: no therapeutic applications. |
| ACTIVATION OF BETA 1 RECEPTORS | Heart- positive inotropic effect (+) heart rate and force of contraction, (+) cardiac output = (+) tissue perfusion. Enhancing impulse conduction through the atrioventricular (AV) node Restore cardiac function in cardiac arrest Adverse effects of beta1 activation: altered heart rate or rhythm and angina pectoris. |
| ACTIVATION OF BETA 2 RECEPTORS | Beta 2 Activation Bronchodilation FOR: asthma and delay of preterm labor adverse effect: hyperglycemia (mainly in diabetic patients) and tremor |
| EPINEPHRINE Uses & MOA | For: Management of cardiac arrest , control superficial bleeding, delay anesthetic absorption *Treatment of choice for anaphylactic shock MOA: Activation of all four adrenergic receptors: alpha 1, alpha 2, Beta 1, Beta 2 receptors |
| EPINEPHERINE Adverse Effects | Hypertension (severe) Cardiovascular effects: Anginal pain, tachycardia, Dysrhythmia Angina- increased cardiac work and oxygen deman Necrosis, Hyperglycemia |
| EPINEPHERINE Nursing Considerations | Use with caution in pt with hyperthyroidism, cardiac dysrhthmias, heart disease, or hypertension, angina pectoris, diabetes |
| NOREPINEPHERINE Uses & MOA | For: Hypotensive states and Cardiac arrest MOA: Activation of 3 adrenergic receptors: alpha 1, alpha 2, Beta 1 receptors ***Similar to epinephrine BUT, does NOT activate B2 receptors |
| NORPEPINEPHERINE Adverse Effects | Hypertension (severe) Cardiovascualr effects: anginal pain, tachycardia, dysrhythmias Angina- increased cardiac work and demand Necrosis |
| NOREPINEPHERINE Nursing Consideraions | Use with caution in pt with hyperthyroidism, cardiac dysrhthmias, heart disease, or hypertension, angina pectoris. |
| DOPAMINE Uses | Shock- B1 in heart receptors increase cardiac output, improve tissue perfusion. Dope Kidney receptors dilate renal blood vessels, improve renal perfusion. Alpha1 receptors- vasoconstriction may decrease renal perfusion, overriding dopamine activation. Thus monitoring urine output essential Heart Failure- B1 alleviate symptoms of reduced perfusion and reduced CO. increases myocardial contractility. |
| DOPAMINE MOA | Dose Dependent Receptor specificity: Dopamine, Beta1 and at high doses Alpha1 Low dose= dopamine only Mod dose= dopamine + Beta1 High dose= dopamine + Beta1 + alpha 1 |
| DOPAMINE Adverse EffectsTS | AE: tachycardia, dysrhythmias, anginal pain (from B1 activation) |
| DOBUTAMINE Use and MOA | BETA 1 AGONIST For: improvement of hemodynamic status in patients with heart failure MOA: selective activation of Beta 1 adrenergic receptors |
| DOBUTAMINE AE & Contraindications | AE: Tachycardia & dysrhythmias. GREAT caution in patients with heart disease, hyperthyroidism, tachydysrhythmias, hypertension. Caution w/ angina pectoris, tricyclic antidepressants, general anesthetics. |
| PHENYLEPHRINE | NON-CATECHOLMINE MOA: selective ALPHA 1 AGONIST Use: Elevate blood pressure |
| NAME THE ANTI-DYSRHYTHMIC DRUGS | 1) AMIODARONE Class III: - potassium channel blocker 2) ADENOSINE Class IV: - calcium channel blocker |
| AMIODARONE Therapeutic Uses | ANTIDYSRHYTMIC For: Atrial & Ventricular Dysrhythmias Class III: - Prolong action potential duration and delays repolarization |
| AMIODARONE Adverse Effects | ANTIDYSRHYTHMIC Cardiac: sinus bradycardia, dcereased contractility; Ophthalmic, smurf skin, photosensitivity TOXICITIES: thyroid, pulmonary, cardiac, liver, dermatologic |
| ADENOSINE Use & MOA | ANTIDYSRHYTHMIC For: Supraventricular Tachycardia - decreases automaticity in the SA Node and slows conduction through the AV node Prolongs PR Interval MOA: Inhibits cAMP induced calcium influx= suppresses calcium- dependent action potentials in the SA & AV Nodes |
| ADENOSINE Adverse Effects | ANTIDYSRHYTHMIC Minimal b/c rapidly cleared from blood. AE last less than 1 min. * must be given IV Sinus bradycardia, dyspnea (from bronchoconstriction), hypotension, facial flushing (from vasodilation) |
| ATROPINE Use & MOA | MUSCARINIC ANTAGONIST 1) Heart: Increase HR ; Treats symptomatic bradycardia 2) Exocrine Glands: Decrease secretions of exocrine glands 3) Smooth muscle relaxation myadriasis (pupil dilation) MOA: competitive blockade at muscarinic receptors. All responses are from preventing receptor activity by endogenous Acetylcholine |
| ATROPINE Adverse Effects | MUSCARINIC ANTAGONIST- ANTICHOLINERGIC AE: Dry mouth, blurred vision, photophobia, intraocular pressure, urinary retention, constipation, antihydrosis, tachycardia, asthma. |
| ATROPINE Drug-Drug Interactions | Drug-Drug Interactions: Antihistamines other muscarinic antagonists High risk patients: glaucoma, UT obstruction, tachycardia |
| MUSCARINIC RECEPTORS: Locations | Heart, Arterioles GI Tract, Gallbladder Lungs, Liver Urinary Bladder, Penis Lacrimal Glands, Eye |
| WHAT TYPES OF DYSRHTHMIAS MIGHT PHARMACEUTICALS TREAT? | SUPRAVENTRICULAR - Atrial fibrillation/ flutter Sustained SVT VENTRICULAR - sustained VT - ventricular fibrillation PVC Torsde de Pointes |
| NIACIN Use & MOA | ANTILIPIDEMIA Prophylaxis for Atherosclerotic Cardiovascular Disease MOA: Reduces LDL & TG levels and increases HDLs. Acts in liver and adipose tissue to inhibit synthesis of TGs , thus decreasing LDLs. |
| NIACIN Adverse Effects | HEPATOTOXICITY (severe liver damage) hyperglycemia, hyperuricemia= (+) uric acid GI distress Skin: intense flushing and itching. (take aspirin 30 min before dose) * slow titration up on dose due to adverse effects NEVER use w/ chronic liver disease, gout Caution w/ diabetes, peptic ulcer disease |
| ATORVASTATIN Therapeutic Use | Treat Hyperlipidemia/ Dyslipidemia, Hypercholesterolemia, Prevention of CV events, MI & stroke prevention in DM2, Increase HDLs |
| ATORVASTATIN MOA | MOA: Inhibition of HMG-CoA Reductase - enzyme pivitol to cholesterol synthesis Outcome= reduction of LDL & TG, Increase in HDL |
| ATORVASTATIN Adverse Effects | Pregnancy Category X Hepatotoxicity Myopathy/Rhabdomolysis |
| ATORVASTATIN Patient Education | Most effective when given at night. If meds stopped serum levels will return to pretreatment levels within weeks. - Life long treatment. Diet modification and exercise enhance therapeutic effects. |
| CLOPIDOGREL Therapeutic Indications | ANTIPLATELET prevention of atherothrombotic events in patients with ACS , unstable angina or MI. prevent blockage of coronary artery stents, reduce thrombotic events (MI, stroke, vascular death). |
| CLOPIDOGREL MOA | P2Y12 ADP RECEPTOR ANTAGONIST Prevents ADP stimulated platelet aggregation - irreversible antiplatelet effect platelet function and bleeding time return after 7-10 days after last dose |
| CLOPIDOGREL Adverse Effects | Bleeding Thrombotic thrombocytopenic purpura (TTP) neurologic renal dysfunction fever |
| ASPIRIN MOA | Blocks Thromboxane A2 which normally stimulates activation of new platelets and platelet aggregation. - Causes irreversible inhibition |
| ASPIRIN Therapeutic Indications | Ischemic stroke, transient ischemic attacks, acute MI, previous, MI, Chronic stable angina, unstable angina. |
| ASPIRIN Adverse Effects | bleeding risks, GI bleeds, Renal impairment, tinnitis, salicylate toxicity |
| DESCRIBE SALICYLATE TOXICITY | salicylate toxicity --> respiratory acidosis, metabolic acidosis, renal failure, altered mental status |
| ASPIRIN Contraindications | NO Pediatrics patients!!!! d/t risk for Reyes syndrome, Encephalopathy, and fatty liver degeneration |
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