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49 Cards in this Set
- Front
- Back
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Nicotinic N receptor |
In all ganglion of PNS and SNS Promotes ganglionic transmission at all ganglia of SNS and PNS Promotes release of epi |
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Nicotinic M receptor |
Found in all skeletal muscles in the SNS Contractions of skeletal muscles |
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Muscarinic receptor |
Target organs of PNS Increase glandular secretions, contraction of smooth muscles, slowing of heart rate |
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Alpha 1 receptor |
All SNS, eyes, arterioles, veins, male sex organs, bladder, prostate Dilates pupils, vasoconstriction, ejaculation, bladder and prostate capsule contraction, activation of epi and norepi |
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Alpha 2 |
Presynaptic nerve terminals Inhibit transmitter release epi |
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Beta 1 |
Heart and kidneys Increase HR, force on contraction, conduction velocity, release renin and epi |
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Beta 2 |
Bronchi, arterioles, uterus, liver Dilate arterioles, bronchi, relax uterus, glycogenolysis, enhanced skeletal muscle contraction |
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Dopaminergic |
Only responds to dopamine, and found within kidneys |
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Acetylcholine (ACh) |
Found in all pre and postganglionic neurons that responds to action potentials and all motor neurons to skeletal muscles |
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Acetylcholine (ACh) |
Found in all pre and postganglionic neurons that responds to action potentials and all motor neurons to skeletal muscles |
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Norepinephrine |
Practically all postganglionic neurons of SNS Is the preform of epinephrine Is either uptake into vesicles for reuse or deactivated with monoamine oxidase (MAO) |
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Acetylcholine (ACh) |
Found in all pre and postganglionic neurons that responds to action potentials and all motor neurons to skeletal muscles |
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Norepinephrine |
Practically all postganglionic neurons of SNS Is the preform of epinephrine Is either uptake into vesicles for reuse or deactivated with monoamine oxidase (MAO) |
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Epinephrine |
Released by adrenal medulla in SNS Norepi is changed into epi Stored in vesicles Activates adrenergic receptors Termination by hepatic metabolism and is not uptake by nerves |
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Bethanechol |
Binds with muscarinic receptors and causes them to stimulate Helps relieve urinary retention, especially in post-op patients, postpartum, and those with GERD Activates PNS decrease in HR, stimulate GI function and secretion of glands, promote bowel and bladder elimination, contract pupils, constrict bronchioles, vasodilate Contradictions Bradycardia, obstructions, blurry vision, asthma, hypotension |
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Bethanechol |
Binds with muscarinic receptors and causes them to stimulate Helps relieve urinary retention, especially in post-op patients, postpartum, and those with GERD Activates PNS decrease in HR, stimulate GI function and secretion of glands, promote bowel and bladder elimination, contract pupils, constrict bronchioles, vasodilate Contradictions Bradycardia, obstructions, blurry vision, asthma, hypotension |
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Cholinergic crisis |
Over-stimulation as a neurotransmitter junction due to an excess of ACh d't inactivation of AChE |
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Atropine |
Muscarinic antagonist Blocks activation of ACh Increases HR, decrease GI motility, decrease secretion of glands, decrease bowel and bladder elimination, dilate pupils and bronchioles, vasoconstriction Contradictions Acute muscarinic poisoning, glaucoma, tachycardia, CHF, CAD, chronic lung condition d/t dried secretions, formation of mucus plugs, impairs airways, BPH, bladder neck obstruction , gastric ulcers, GERD, GI infection |
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Atropine |
Muscarinic antagonist Blocks activation of ACh Increases HR, decrease GI motility, decrease secretion of glands, decrease bowel and bladder elimination, dilate pupils and bronchioles, vasoconstriction Contradictions Acute muscarinic poisoning, glaucoma, tachycardia, CHF, CAD, chronic lung condition d/t dried secretions, formation of mucus plugs, impairs airways, BPH, bladder neck obstruction , gastric ulcers, GERD, GI infection |
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Side effects of atropine |
Increase intraocular pressure > blurred vision, photophobia Tachycardia Drying and thickening of bronchial secretions Urinary retention Constipation Absence of sweating, potential for over heating |
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Neostigmine |
Reversible inhibitor ChE splits neostigmine more slowly than ACh > drug remains attached to center on ChE and prevents it from catalyzing breakdown of ACh Increase force of muscle contraction Adverse effects Excessive muscarinic stimulation > excessive salvation, increase tone and motility of GI tract, urinary urgency, bradycardia, sweating , miosis |
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Myasthrnia gravis |
Antibodies attack nicotinic m receptors Neostigmine is used to cure/ help this disease |
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Depolarizing blocking agents |
Depolarizes muscles and prevents repolarizing > muscle relaxation Shorter than non-depolarizing Binds to nicotinic M receptors and cause depolarization > transient muscle contractions State if constant depolarization Much shorter duration of paralysis
Adverse effects: malignant hyperthermia- muscle rigidity associated with profound elevation of body temperature (d/t excessive and uncontrolled metabolic activity in muscles) Muscle aches |
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Non-depolarizing |
Keeps the muscles relaxed Binds with nicotinic M receptors and prevent attachment of ACh> cannot contract>paralysis
Adverse effect: respiratory depression, apnea |
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Alpha 1 receptor activation |
Uses: vasoconstriction, hemostasis, nasal congestion, adjunct to local anesthesia, elevated blood pressure, mydeiasis Adverse effect: hypertension, necrosis, bradycardia Should not be on MAOI's d/t them metabolizing epi while alpha 1 receptors activate with epi |
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Alpha 1 receptor activation |
Uses: vasoconstriction, hemostasis, nasal congestion, adjunct to local anesthesia, elevated blood pressure, mydeiasis Adverse effect: hypertension, necrosis, bradycardia Should not be on MAOI's d/t them metabolizing epi while alpha 1 receptors activate with epi |
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Beta 1 receptor activation |
Uses: heart failure, shock, AV heart block, cardiac arrest cause by asystole Adverse effect: altered heart rate or rhythm > overstimulation of beta 1 receptors, monitor for development of arrhythmias, angina > cardiac oxygen supply insufficient to meet needs |
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Alpha 1 receptor activation |
Uses: vasoconstriction, hemostasis, nasal congestion, adjunct to local anesthesia, elevated blood pressure, mydeiasis Adverse effect: hypertension, necrosis, bradycardia Should not be on MAOI's d/t them metabolizing epi while alpha 1 receptors activate with epi |
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Beta 1 receptor activation |
Uses: heart failure, shock, AV heart block, cardiac arrest cause by asystole Adverse effect: altered heart rate or rhythm > overstimulation of beta 1 receptors, monitor for development of arrhythmias, angina > cardiac oxygen supply insufficient to meet needs |
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Beta 2 receptor activation |
Uses: asthma, delay of preterm labor Adverse effect: hyperglycemia, tremors |
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Dopamine receptor activation |
Uses: to treat shock (improves renal blood flow), reduces the risk of renal failure, evaluate urine output for effectiveness |
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Epinephrine |
Activates all 4 adrenergic receptors Bronchodilates during anaphylaxis Uses: delays absorption of local anesthetics, controls superficial bleeding, elevate BP, overcome AV heart block, restore cardiac function in asystole, bronchodilation Adverse effects: hypertensive crisis, dysthymia, angina pectoris, necrosis, hyperglycemia Interactions: MAO-Is - drug effect will be prolonged d/t blockers Alpha/beta- can stop or prolong process |
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Epinephrine |
Activates all 4 adrenergic receptors Bronchodilates during anaphylaxis Uses: delays absorption of local anesthetics, controls superficial bleeding, elevate BP, overcome AV heart block, restore cardiac function in asystole, bronchodilation Adverse effects: hypertensive crisis, dysthymia, angina pectoris, necrosis, hyperglycemia Interactions: MAO-Is - drug effect will be prolonged d/t blockers Alpha/beta- can stop or prolong process |
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Alpha blockers |
Vasodilation, reduce contraction of smooth muscle in prostatic capsule and bladder neck Adverse effects: orthostatic hypotension > dizziness, lightheadedness, syncope, reduced muscle tone in veins Reflex tachycardia via baroreceptor reflex, nasal congestion, inhibition of ejaculation |
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Beta blockers |
Most likely to use beta blocker 1 with cardiac issues Uses: reduce HR, reduce force of contraction, reduce velocity of impulse conduction through AV node, angina, HTN, cardiac dysthymias, MI, HF, hyperthyroidism, migraine prophylaxis, stage fright, glaucoma |
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Adverse effects of beta 1 blockers |
Bradycardia, reduce CO, precipitation of HF, AV heart block, rebound cardiac excitation |
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Adverse effects of beta 2 blockers |
Bronchoconstriction, hypoglycemia |
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Adverse effects of beta 2 blockers |
Bronchoconstriction, hypoglycemia |
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Adverse effects of non-selective beta blockers |
Can block both beta 1 and 2 receptors, bradycardia, AV heart attack, HF, rebound cardiac excitation, bronchoconstriction, inhibition if glycogenolysis, CNS effects: depression, insomnia, nightmares, hallucinations |
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Adverse effects of beta 2 blockers |
Bronchoconstriction, hypoglycemia |
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Adverse effects of non-selective beta blockers |
Can block both beta 1 and 2 receptors, bradycardia, AV heart attack, HF, rebound cardiac excitation, bronchoconstriction, inhibition if glycogenolysis, CNS effects: depression, insomnia, nightmares, hallucinations |
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Adverse effects of selective beta blockers |
Specific to beta 1 receptor, clinical use that same as non-specific beta blockers, safer for patients with diabetes and asthma |
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Parkinson's disease |
Cause: progressive, chronic neurological disorder. Dopamine deficit in area of cerebral cortex called substantia nigra > impacts motor function, posture, muscle tone, smooth muscle activity. ACh from higher centers then dominate, leading to uncoordinated movement S/S: TRAP Tremor that is one sided and noticeable at rest Rigidity or stiffness of the muscles Akinesia or absence of spontaneous movement and bradykinesia is the slowness of movement Postural instability or impaired gate and sense of balance |
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Levodopa and carbidopa |
Levodopa + carbidopa enhances therapeutic effects Works: levodopa increases the synthesis of dopamine and is the traditional therapy for Parkinson's disease Enters the brain via active transport > stimulates presynaptic dopamine receptors to increase brain levels of dopamine Carbidopa prevents peripheral conversion of levodopa in the intestines and peripheral tissues Higher levels of levodopa in the brain d/t carbidopa is unable to cross BBB Reduce production of dopamine in periphery > reduced CV response to levodopa Reduced N&V |
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Levodopa and carbidopa |
Levodopa + carbidopa enhances therapeutic effects Works: levodopa increases the synthesis of dopamine and is the traditional therapy for Parkinson's disease Enters the brain via active transport > stimulates presynaptic dopamine receptors to increase brain levels of dopamine Carbidopa prevents peripheral conversion of levodopa in the intestines and peripheral tissues Higher levels of levodopa in the brain d/t carbidopa is unable to cross BBB Reduce production of dopamine in periphery > reduced CV response to levodopa Reduced N&V |
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Side effects of levodopa |
Dyskinesia - abnormal voluntary movements GI- nausea, vomiting , loss of appetite, dry mouth CV- postural hypotension, dysrhythmias Reacts with 1st generation antipsychotic d/t blockage of dopamine receptors |
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Levodopa and carbidopa |
Levodopa + carbidopa enhances therapeutic effects Works: levodopa increases the synthesis of dopamine and is the traditional therapy for Parkinson's disease Enters the brain via active transport > stimulates presynaptic dopamine receptors to increase brain levels of dopamine Carbidopa prevents peripheral conversion of levodopa in the intestines and peripheral tissues Higher levels of levodopa in the brain d/t carbidopa is unable to cross BBB Reduce production of dopamine in periphery > reduced CV response to levodopa Reduced N&V |
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Side effects of levodopa |
Dyskinesia - abnormal voluntary movements GI- nausea, vomiting , loss of appetite, dry mouth CV- postural hypotension, dysrhythmias Reacts with 1st generation antipsychotic d/t blockage of dopamine receptors |
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Nursing implications for levodopa |
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