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Parmacology includes the study of... |
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1.Drugs and their * Interactions within the body * Medicinal purposes * Toxic characteristics * Social or recreational use |
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3 general properties of drugs |
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1.Drugs do not create a response in the body but modify the body's response. 2.Drugs exert multiple effects on the body rather than a single effect. 3.Drug action occurs as the result of an interaction of the drug with a molecule or structure in the body. |
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describes the drug using exact chemical nomenclature. |
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* Derived from chemical name. * First letter of the generic name not capitalized * Also known as nonproprietary name |
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* Provided by the manufacturer * First letter is capitalized * Also known as proprietary name or brand name. |
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Pure Food and Drug Act (1906) |
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* first major drug law * Provided consumers accurate information about the quality of drug products. * Designated the United States Pharmacopeia and the National Formulary as sources of the official standards for drugs. |
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* Amended the Pure Food and Drug Act * Prohibited labeling drugs with false therapeutic claims. |
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Federal Food, Drug, and Cosmetic Act (1938) |
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* Amended the Pure Food and Drug Act -Established the FDA |
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Food and Drug Administration (FDA) |
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* Center for drug evaluation and research. * Center for biologics evaluation and research. * Center for Food Safety and Applied Nutrition. |
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Kefauver-Harris Amendment (1962) |
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Tightened control on drug safety * authorized FDA to establish official names for drugs. |
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Dietary Supplement Health and Education Act of 1994. |
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* Regulate herbal products and dietary supplements. * FDA has power to remove a product that has significant risk. |
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Dietary Supplement and Nonprescription Drug Consumer Protection Act (2007). |
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* Contact information and contents required on labels. |
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Prescription Drug User Fee Act (1992). |
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* Yearly product user fees for drug and biologic manufacturers. * Decreased the time in the drug approval process. |
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Prescription Drug User Fee Act was reauthorized. |
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5 Phases of drug development |
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1. Preclinical testing. 2. FDA 30 day safety review 3. Clinical Testing in Humans 4. NDA review and approval 5. Phase IV: Postmarketing surveillance of the drug. |
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* Phase I---Small number of healthy volunteers that do not have the disease or ailment. * Phase II----Small number of volunteers with the disease or ailment. * Phase III----Large number of clients in research center. * Phase IV----Postmarketing surveillance of the drug. (this is where nurses are involved) |
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Used to treat rare and/or unusual diseases. -"orphans"-no one wants the cost of developing these meds. |
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Durham-Humphrey Amendments (1952) to the 1938 Act. |
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Legend drugs--Classified drugs as ones requiring a prescription.
Non legend drugs--over the counter |
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-diagnosis prior to taking med -Correct drug -Education on proper use of drug. |
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OTC:available to the public |
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-saves time and money. -serious adverse effects if instructions are not followed. |
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Harrison Narcotic Law (1914) |
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-Regulated habit forming narcotics' * Importation * Manufacture * Sale * Use |
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The Controlled Substance Act (1970) |
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Controlled drugs are categorized according to their abuse potential and medical usefulness. 1-5 |
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1. Right med 2. Right patient 3. Right tim 4. Right Route 5. Right Dosage 6. Right Documentation |
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Controlled by ANS =SNS: Constriction =PNS: Dilation |
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First line of immune defense |
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Mucus Defense cells -mast cells: contains histimine -basophils |
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-Inflammation of nasal mucosa -Symptoms =tearing, sneezing, congestion... |
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Allergic Rhinitis treatment |
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Drugs -Preventers =Antihistamines =Intranasal corticosteroids =Mast cell stabilizers -Relievers =Oral and intranasal decongestants |
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mimics sympathomimetic system |
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mimics parasympathomimetic system |
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blocks the parasympathomimetic reaction |
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blocks the sympathomimetic reaction |
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vasoconstriction "fight or flight" |
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Vasodilation "rest and digest" |
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An organic nitrogen compound involved in local immune responses as well as regulating physiological function in the gut and acting as a neurotransmitter. |
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"Histamine antagonist" is a pharmaceutical drug that inhibits the action of histamine by blocking it from attaching to histamine receptors; or may inhibit the enzymatic activity of histidine decarboxylase, catalyzing the transformation of histidine into histamine. |
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fluticasone (Flonase, Veramyst...) |
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nasal spray, is a synthetic corticosteroid. Used to treat seasonal and perennial allergic rhinitis. |
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-Beneficial: dry mucous membranes -Adverse: excessive dry mucous membranes. Dry mouth, urinary hesitancy |
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activated by; or sensitive to; releasing; resembling the effect produced by; |
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of or relating to drugs that mimic the effects of the sympathetic nervous system. |
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the acetic acid ester of choline released and hydrolyzed during nerve conduction and causing muscle action by transmitting nerve impulses across synapses. |
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of or pertaining to; made of; like; |
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Relating to a neuron or axon that is activated by or is capable of releasing acetylcholine when a nerve impulse passes. The nerve ending of the parasympathetic NS are cholinergic. |
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opposing the physiological effects of stimulation of the sympathetic nervous system. |
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Sympathetic nervous system |
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The part of the autonomic nervous system that tends to act in opposition to the parasympathetic nervous system, as by speeding up the heartbeat and causing contraction of the blood vessels. It regulates the function of the sweat glands and stimulates the secretion of glucose in the liver. The sympathetic nervous system is activated especially under conditions of stress. Compare parasympathetic nervous system. |
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Parasympathetic Nervous System |
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parasympathetic nervous system n. The part of the autonomic nervous system originating in the brain stem and the lower part of the spinal cord that, in general, inhibits or opposes the physiological effects of the sympathetic nervous system, as in tending to stimulate digestive secretions or slow the heart. |
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what do you worry about with nasal decongestants |
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Vasoconstriction=high blood pressure
It mimics the Adrenergic system-Vasoconstriction |
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Intranasal corticosteroids |
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SABA Short acting Beta agonists (rescue drugs) |
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-pirbuterol (Maxair) -terbutalin (Brethine) -albuterol (Proventil) -levalbuterol (Xopenex) |
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LABA Long acting Beta Agonists (treatment drugs) |
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-salmeterol (Serevent) -arformoterol (Brovan) -formoterol (Foradil, Perforomist) |
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-Are the safest of all asthmas treatments. -Not for acute asthma -Sting or burning sensation -Short half life: administer 4-6times per day. |
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What is the number 1 cause of COPD? |
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Beta Agonists(used the most) -SABA-rescue -LABA-Solmeterol Anticholinergic-ipratropium Methylyanthines-theopollyne -PO, narrow therapeutic index, sever side effects |
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Inhaled Corticosteriods (use spacer, thresh risk) -Raised cortisol-systemic -Glucose-diabetes -Bleclomethesone Leukotriene modifiers -Zafirlukast, montelukast, sielutan Mast Cell Stabilizer-Cromelyn |
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Primary use for beta-adrenergic blockers |
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adverse affects of beta-adrenergic blockers |
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fatigue, decreased libido, erectile dysfunction. |
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Primary use of alpha1-adrenergic antagonists |
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adverse effects of alpha1-adrenergic antagonists |
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orthostatic hypotension, dizziness, nausea, nervousness, fatigue |
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mechanism of action of alpha1-adrenergic antagonists |
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to block sympathetic receptors in arterioles leading to vasodilation. |
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Primary use of alpha2-adrenergic agonists |
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adverse effects of alpha2-adrenergic agonists |
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sedation, dizziness, abnormalities in sexual function. |
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Alpha2-adrenergic agonists drugs |
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clonidine (catapres); methyldopa (Aldomet |
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Alpha1-Adrenergic Antagonists drugs |
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Primary use of direct vasodilators |
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for severe hypertension and hypertension crisis. |
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Adverse effects of Direct Vasodilators |
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reflex tachycardia, sodium and fluid retention |
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Direct Vasodilators mechanism of action |
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to cause vasodilation by direct relaxation of arterial smooth muscle |
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Direct vasodilators prototype drug |
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The patient is on two antihypertensive drugs. The nurse recognizes that the advantage of combination therapy is.. |
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There will be fewer side effects and greater patient compliance. |
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Systemic vascular resistence |
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Alpha1-Adrenergic Antagonists drugs |
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Primary use of direct vasodilators |
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for severe hypertension and hypertension crisis. |
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Adverse effects of Direct Vasodilators |
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reflex tachycardia, sodium and fluid retention |
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Direct Vasodilators mechanism of action |
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to cause vasodilation by direct relaxation of arterial smooth muscle |
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Direct vasodilators prototype drug |
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The patient is on two antihypertensive drugs. The nurse recognizes that the advantage of combination therapy is.. |
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There will be fewer side effects and greater patient compliance. |
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Systemic vascular resistence |
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chest pain in heart region. It is a symptom of a myocardial infarction. |
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interruption of blood supply to a part of the heart causing cells to die. |
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-Acute chest pain due to insufficient O2 to myocardium.
-Accompanies physical exertion or emotional excitement.
-Cuases increased myocardial oxygen demand. |
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for lowering myocardial oxygen demand. |
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hypotension, dizziness, headache, flushing of face, rash |
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Nitrates mechanism of action |
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relax both arterial and venous smooth muscle; dilate coronary arteris. |
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nitroglycerin (Nitrostat) |
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Beta-Adrenergic Blockers primary use |
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for prophylaxis of stable angina |
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Beta-Adrenergic Blockers adverse effects |
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fatigue, insomnia, drowsiness, impotence, bradycardia, confusion. |
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Beta-Adrenergic Blockers mechanism of action |
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to reduce the cardiac workload by slowing heart rate and reducing contractility. |
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Beta-Adrenergic Blockers prototype drug |
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Calcium Channel Blockers primary use |
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for lowering blood pressure; bring more oxygen into myocardium |
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Calcium Channel Blockers Adverse effects |
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hypotension, bradycardia, heart failure, constipation, headaches, dizziness, edema, |
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Calcium Channel Blockers mechanism of action |
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to reduce cardiac workload by relaxing arteriolar smooth muscle; dilate coronary arteries. |
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Calcium Channel Blockers prototype drug |
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Reduce Myocardial Demand for O2 by... |
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-slowing heart rate -reducing preload -reducing contractility -lowering blood pressure (reduce afterload) |
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the breakdown of blood clots |
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used in myocardial infarction to clear a blocked artery and avoid permanent damage to tissue. |
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Thrombolitics primary use |
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for restoring circulation to myocardium |
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Thrombolitics adverse effects |
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Thrombolitics prototype drug |
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Thrombolitics mechanism of action |
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to dissolve clots obstructing coronary arteries. |
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Adjunct drugs for myocardial infarction |
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* Nitrates -Diagnosis of MI; arterial venous dilation; relieve coronary artery vasospasm
* Beta-Adrenergic Blockers -Reduce myocardial oxygen demand; slow impulse conduction through the heart.
* ACE Inhibitors -Increased survival for those MI patients administered captopril (Capoten) or lisinopril (Prinivil, Zestoretic) |
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Nitrates are potent what? |
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isosorbide dinitrate (Isordil), isosorbide mononitrate (Imudur), nitroglycerin (Nitrostat) |
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Beta-Adrenergic Blockers do what? |
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Calcium Channel Blockers do what? |
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Reduce cardiac workload and dilate coronary arteries |
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types of drugs for Heart Failure |
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-ACE Inhibitors -Diuretics -Beta adrenergic blockers -Cardiac Glycosides -Phosphodiesterase Inhibitors |
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Inability of ventricles to pump enough blood for body's needs.
Weakening of heart muscle due to aging or disease. |
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If a patient has hyperkalemia they can develope an... |
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Normal potasium level is... |
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Normal blood glucose level is... |
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ACE Inhibitors prototype drug |
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lisinopril (Prinivil, Zestril) |
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ACE Inhibitors mechanism of action |
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to enhance excretion of sodium and water. |
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ACE Inhibitors primary use |
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to decrease blood pressure and reduce blood volume; dilate veins |
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ACE Inhibitors adverse effects |
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first dose hypotension, cough, hyperkalemia, renal failure |
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Diuretics mechanism of action |
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to increase urin flow, reducing blood volume and cardiac workload. |
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to reduce edema and pulmonary congestion. |
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Diuretics adverse effects |
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dehydration, electrolyte imbalance, hypotension, ototoxicity. |
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Cardiac Glycosides prototype drug |
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Cardiac Glycosides mechanism of action |
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Definition
to cause more forceful heartbeat, slower heart rate. |
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Cardiac Glycosides primary use |
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to increase contractility or strength of myocardial contraction. |
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Cardiac Glycosides adverse effects |
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neutropenia, dysrhythmias, digitalis toxicity. |
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Beta-Adrenergic Blockers for heart failure prototype drug |
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Metroprolol (Lopressor, Troprol XL) |
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Beta-Adrenergic Blockers for heart failure mechanism of action |
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block cardiac action of sympathetic nervous system to slow heart rate and B/P, reducing workload of heart. |
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Beta-Adrenergic Blockers for heart failure primary use |
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to reduce symptoms of heart failure and slow progression of disease |
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Beta-Adrenergic Blockers for heart failure adverse effects |
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fluid retention, worsening of heart failure, fatigue, hypotension, bradycardia, heart block |
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Vasodilators for heart failure prototype drugs |
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hydralazine (Apresoline); isosorbide dinitrate (Isordil) |
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Vasodilators for heart failure mechanism of action |
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Vasodilators for heart failure primary use |
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Vasodilators for heart failure adverse reactions |
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reflex tachycardia, orthostatic hypotension |
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Vasodilators are used for clients who cannot take what? |
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Hemostatics prototype drug |
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aminocaproic acid (Amicar) |
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Hemostatics mechanism of action |
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to prevent fibrin from dissolving |
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to prevent and treat excessive bleeding from surgical sites |
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Hemostatics adverse effects |
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may cause hypercoagulation with concurrent use of estrogen and oral contraceptives |
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Hemostaics prevent formation of what? |
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Clots -Inhibit removal of fibrin |
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1.Fluid volume 2.electrolytes, 3.acid-base balance -they do more than just those three. |
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1.Renin-for blood pressure regulation 2.Erythropoietin-to stimulate blood cell production. 3.Calcitrol-active form of vitamin D for bone hemeostasis |
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most common cause of acute renal failure is what? |
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Beta-Adrenergic Blockers (Class II) prototype drug |
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Beta-Adrenergic Blockers (Class II) mechanisim of action |
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Definition
to block beta receptors, which reduces automaticity and slows conduction velocity across myocardium. |
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Beta-Adrenergic Blockers (Class II) primary use |
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to treat atrial dysrhythmias associated with heart failure. |
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Beta-Adrenergic Blockers (Class II) adverse effects |
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bradycardia, hypotension with dizziness and fainting. |
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Potassium channel blockers (Class III) prototype drug |
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Potassium channel blockers (Class III) mechanism of action |
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Definition
to block potassium-ion channels in myocardial cells, which prolongs refractory period of heart. |
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Potassium channel blockers (Class III) primary use |
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to treat resistant ventricular tachycardia, atrial dysrhythmias with heart failure. |
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Potassium channel blockers (Class III) adverse effects |
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Definition
blurred vision, pneumonia like syndrome, bradycardia, hypotension |
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