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pharm hell test 1
parasym. drugs
| Question | Answer |
|---|---|
| what is the purpose of the sympathetic nervous system | Its general action is to mobilize the body's resources under stress; to induce the fight-or-flight response,regulate body temp, regulate the cardiovascular system. |
| What is the purpose of the parasympathetic nervous system. | The parasympathetic system specifically is responsible for stimulation of "rest-and-digest" activities that occur when the body is at rest. sexual arousal, salivation, tears, focusing the eye for near vision urination, digestion and defecation |
| How do neurons regulate other cells? | 1. conductionof an action potential along the axon of a neuron. 2. release of neurotransmitter molecules form and axon of the neuron. 3. binding of trinsmitter to receptor of postsynaptic cell. |
| What are the two ways a drug can alter the basic neuronal activities? | axonal conduction and synaptic transmission |
| What is axonal conduction? | The process of conducting an action potential down the axon of the neuron. |
| What is synaptic transmission? | the process by which information is carried across the gap between teh neuron and the postsynaptic cell. This requires a the release of the transmitter from axon to receptor |
| Most neuropharmacologic agents act by altering what type of transmission | synaptic-because they are highly selective. |
| What is an example of axonal conduction? | local anesthesia-not very selective. |
| No matter what its percise mechanism of action a neuropharmacologic drug ultimately works by: | Influencing receptor activity on target cells. |
| When a drug influences receptor functions what are the two things that can happen | it can enhance receptor activation or it can reduce receptor activation |
| Transmitter synthesis what are the 3 different effects that drugs are know to have on transmitter synthesis | increase transmitter synthesis, decrease transmitter synthesis or cause the synthesis of trasmitter molecules that are more effective than the natural transmitter itself. |
| drugs that interfere with transmitter storage will cause receptor activation to decrease why? | Because disrupton of storage depletes vesicles of their transmitter content, thereby decreasing the amount of transmitter available for release. |
| Transmitter release-drugs can either ... | promote or inhibit transmitter release |
| What are the three actions of receptor binding | bind to receptors and cause activation bind to receptors and thereby block receptor activation by other agens bind to receptor components and thereby enhance receptor activation by natural transmitter at the site. |
| What is the exampleof a drug that binds to receptor site and henhances the acton of a natural transmitter | benzodiazepines |
| cholinergic drugs promote the action of what neurotransmitter | acetylcholine |
| The two major classes of cholinergic drugs are | cholinergic agonist-mimic the action of neurotransmitter acetylcholine Anticholinesterase drugs-work by inhibiting the destruction of acetylcholine at the cholinergic receptor site. |
| Bethanechole is an example of | a cholinergic drug that works on muscarinic receptors |
| How does bethanechole work | it binds reversibly to muscarinic cholinergic receptors. |
| What are the effects of bethanechole | elicits all of the respones typical of suscrinic receptor activation |
| What are the common results of cholinergic agonist | salivaton, bradycardia, dilation of blood vessles, constriction of pulmonary bronchioles, increasd activity of GI tract, increased ton and contraction of bladder muscles, constriction of puplis |
| How are cholinergic agonist used | urinary retention where it relaxes the ruirnary sphincter and increases voiding pressure |
| What is contraindication of cholinergic drugs like bethanechol | latent or active asthma, gastric ulcers, intestional obstruction, recent bowel surgery |
| Whate are other muscarinic agonist(cholinergic drugs) | pilocarpine (eyedrops) acetylcholine (eyes) Muscarine ( |
| Adverse effects of Muscarinic Agonist | rare with PO, more common in SQ, hypotention and bradycardia, |
| What is the antidote for muscarinic agonist | atropine (will increase heart rate, and bp) |
| Muscarinic antagonist | competitively black the actons fo ACh at muscarinic receptors |
| Atropine is the muscarinic prototype | it turns off cholinergic responed through competitive blockade |
| What are Atropine(muscarinic antagonist)effects | low dose: decreases slivary glands, sweat glands broncheal secretions High doese: increased heart rate, mydriasis, urinary interference, intestine decreased tone, lung dilation of bronchi, stomach decreased acid secretion. |
| How can I remember bethanechole: | Better bring extra panties-you might pee yourself, or have atropine on hand |
| Toxicology of Muscarinic agonist | eating certain mushrooms, direct acting muscarinic agonist, and cholinesterase inhibitors |
| Symptoms of toxic muscarinic antagonist | profuse drooling, tearing, visual disturbances, bronchospasm, diarrhea, bradycardia and huypotension |
| Treatment of toxic muscarinic agonist | administer atropine-by blocking access of muscarinic agonist to their receptors, atropine can reverse most signs of toxicity |
| Adverse effect of muscarinic antagonist | dry mouth, blurred vision, IOP, urinary retention tachycardia asthma |
| toxicology of muscarinic antagonist | atropa bella donna, datura stramonium, atropine, antihistimines phenothiazines, tricyclic antidepressants DEATH RESULTS FROM RESPIRATORY DEPRESSION |
| What is the antidote for muscarinic antagonist | physostigmine(inhibits acetycholinesterase) |
| OAB (over active bladder) tx with anticholinergic drugs | Oxybutynin (ditropan) and tolterodine (detrol)block muscarinic receptors on the detrusor thereby inhibiting bladder contractions and the urge to void. |
| What side effects will you see with anticholinergic drugs | dry mouth, constipation, ritnary retention, blurred vision(dialated pupils) photophobia, tachycardia, and confusion |
| Cholinesterase inhibitors what do they do | they perven the degradation of ACH by acetylcholinesterase. |
| Cholinesterase inhibitors are highly selective or nonselective? | they have limited therapeutic application due to lack of selectivity. |
| What are cholinesterase inhibitors also known as | anticholinesterases |
| Reversible cholinesterase inhibitors | two catagories reversible(moderate duration) & irreversible (long lasting) |
| Mechanism of Action for Neostigmine and other reversible (moderate duration) cholinesterase inhibitors | binds with acetylchonliesterase(ChE)and prevents the breacke down of acetylcholine (Ach) |
| What are the effects of Neostigmine | Cant intensify transmission at vertually all junctions where ACh is transmitter. |
| Pharmacokinetics | PO-in large doese, or by injection-SQ,IM, IV can not cross BBB |
| What are uses for Neostigmine | Myasthenia gravis |
| Adverse effects of Neostigmine | EXCESSIVE muscarinic stimulasiton, neuromuscular blockade |
| Precaustions and contrindications with Neostigmine(cholinesterase inhibitor) | obstruction of the GI tract, obstruction of urinary tract, peptic ulcer disease, asthma coronary insufficiency and hyperthyroidism |
| Drug interactions of neostagmine | muscarinic antagonist-because its the opposite they will reverse each other. |
| Toxicity of neostagmine (cholinesterase inhibiotr) | causes excessive muscarinic stimulation and respiratory depression |
| Antidote for Neostagmine is | Atropine |
| Irreversible chlinesterase inhibitors (long acting) | nerve gas |
| Action of irreversible cholinesterase inhibitors | binds to the active center of chilinesterase adn thereby preventing the enzyme from hydrolizying ACh(will split off but extremely slow) |
| Use for irreversible cholinesterase inhibitors | glaucome-the only indication |
| Toxicology of irreversible cholinesterase inhibitors | usually by insecticides. Causes a state of cholinergic crisis |
| Treatment for irreversible cholinesterase inhibitors | 1. ventilation, 2. atropine for muscarinic stimulation, 3. pralidoxime to reversie inhibition of ChE and 4. diazepam (atavan) to decrease seizures. |
| Neuromuscular blocking agents | prevents ACh from activating nicotinic M receports on skeletal muscles and causes muscle relaxation. |
| neuromuscular blocking agents in two classes | a. nondepolarizing neuromuscular blockers b. depolarizing neuromuscular blockers |
| nondepolarizing blockers do what | cause muscle relaxation, hypotention-paralysis in minutes and lasts for hours |
| What is the prototype | Tubocuraine (oldest) used by native americans on the tips of arrows for paralyzing the muscles of respiration. |
| uses for nondepolarizing neuromuscular blockers | surgery, mechanical ventilation, endotracheal intubation, and electroconvulsive therapy, can be give iv or im |
| adverse effects of nondepolarizing neurmuscular blockers | respiratory arrest, cardiovascular-precautions with MG and electrolyte imbalances, cholinesterase inhibitors can decrease effects. |
| durg interactions of nondepolarizing neuromuscular blockers | general anesthetics and some antibiotics can intensify effects of neuromuscular blockers. |
| Toxicology of nondepolarizing neuromuscular blockers | prolonged apnea, massive histamine relase, cardiovascular collapse |
| Depolarizing neuromuscular blockers | Succinylcholine-ultra short acting only on in clinical use |
| What is the action of Deporlaizing neuromuscular blocks | bins to incotinic M, remains bound, preventing the end plate from repolarizing, mantains constant depolarizations Paralysis persists until levels decline |
| What are the effects of depolarizing neuromuscular blocks | muscle relaxation, CNS effects |
| How can depolarizing neuromuscular blocks given | IV or IM-plaralysis peaks in 1min, fades in 1-10mins |
| Uses for depolarizing neuromuscular blockers | endotracheal intubation, electorconvulsive therapy, endoscopy and other SHORT PROCEDURES |
| Adverse effects of depolarizing neuromuscular blockers | prolonged apnea in those with low pseudocholinesterase activity, malignant hyperthermia, postoperative muscle pain, hyperkalemia |
| What are the drug interactions for depolarizing neuromuscular blockers | chilinesterase inhibitors enhance effects of sussinycholine, some anitbiotics enhance effects. |
| Toxicology | there is no antidote, you are purely supportive. |
| Can a person given suxxinylcholine loose consciousness or feel pain | yes they feel pain and they do NOT loose consciousness |
| What is speudocholinesterase | an enzyme that is present in plasma that degrades succinylcholine |
| Ganglionic stimulating agents | no therapeutic use |
| Ganlionic stimulating agent is | nicotine |
| What are nicotine's effects | heart, GI, CNS= vasoconstriction increases memory, alertness, cognitive funct. reduces aggression, suppresses appetite, activates please sense. |
| Ganglionic stimulating agents acute poisoning | hightly toxic, insecticides. |
| is there an antidote for nicotine | no just supportive therapy |
| Ganglionic blocking agents are | drugs that lack selectivity, limited use, used tolower BP in special circumstances. |
| What is the only ganglionic blocking agent used in the US | Mecamylamine (Inversine) |
| What are the actions of Mecamylamine | interrups impulse transmission through anglia of the ANS. Competes with ACh for binding to Nicotinic N receptors in autonomic ganglia. Blocks transmission of all autonomic ganglia, can shot down entire ANS. |
| What are the effects of Mecamylamine | MOST RESPONSES RESEMBLE THOSE PRODUCED BY MUSCARINIC ANTAGONIST lowers BP by causing dilation of arterioles and veins due to blocking SNS stimulation to vascular smooth muscle. |
| Adverse effects of Ganglionic blocking agents | antimuscarinic effects, hypotentions, CNS |
| Adrenergic agonist-aka | sympathomimetics |
| These drugs activat by 4 basic mechanisms | 1. direct receptor binding 2. promotion of NE release, 3. inhibition of NE uptake 4. inhibitionof NE inactivation |
| Chemical Classification 2 types | catecholamines and noncatecholamines |
| Catecholamines are | epinephrine, norepinephrine, isoprotereol, dopamine, and dobutmine and they are inactiviated rapidly by MAO and COMT. |
| How are catecholamines given | by infusion, inactivate PO can not cross BBB |
| Noncatecholamines are | ephedrine, phenylephrine, and terbutaline |
| How are noncatecholamines given | Can give PO longer half lives can cross BBB |
| Alpha 1 | theraputic effect:hemostasis, nasal decongestion, adjunct to local anesthesis, elevation of BP, Mydriasis (dilation) |
| adverse effects of Alpha 1 | HYpertention, necrosis , bradycardia |
| Alpha 2 | therapeutic no applications in periphery, in CNS reduces sympathetic outflow to heart and blood vessels |
| Beta1 | therapeutic-cardiac arrest, heart failure, shorck, atrioventricular heart block |
| Adverse effects of beta 1 | altered heart rate or rhythm, angina pectoris |
| Beta 2 | therapeutic asthma delay of preterm labor (relaxes uterin muscles) |
| Adverse effects of beta 2 | hyperglycemia tremor |
| Dopamine | activation of dopamine receptors causes dilation of the vasculature of the kidneys. This is used in tx of shock, by dilating renal blood vessels you inprove renal perfusion and can reduce the resik of renal failure. it also enhances cardiac performance. |
| Epinephrine | prototype of adrenergic agonist |
| What receptor does epinephrine work with | alpha 1, beta 1, beta 2 |
| How is epinephrine given | toical, injectin, inhalation=Not PO |
| Adverse effects of epinephrine | hypertensive crisis, dysrhythmias, angina, necrosis (vasodilation) , hyperglycemia |
| Nursing interventions for epinehprine | check does, monitor constatly if IV, watch site |
| Norepinephrine | differs from epinephrins in taht it does not activate beta 2 receptors therefore it does not help the lungs |
| Norepinephrine activates what receptors | Alph1, alpha 2, and beta 1 |
| Whw is norepinephrine used for | hypotensive states, and cardiac arrest |
| Isoproternol works on what receptors | Beta 1 beta 2 it is the prototype of beta selective adrengergic agonist |
| What are the uses of isoproternol | cardiovascular , asthma |
| Drug interactions of isoproternol | MAOI's, tricyclics, beta blockers |
| Dopamine | is dose dependent |
| uses for dopamine | shock heart failure |
| adverse effects of dopamine | tachycardia, dysrhythmias, angina, necrosis |
| Drug interactions of dopamine | MAOI's tricyclics, genral anesthetics |
| Dobutamine Beta 1 | used for heart failure adverse effect is tachycardia |
| Phenylephrine alpha 1-remember this one by wayne hartley | used local for nasal congestion parenterally to increase BP, and dyriasis |
| terbutaline beta 2 | Ephedrine alpha 1, 2 and beta 1,2 mixed acting drug used for nasal congestion narcolepsy adverse effects hypertensive crisis dysrhythmias, angina, necrosis, hyperglycemia. diet pills, cold pills |
| Adrenergic antgonist- | cause direct blockade of adrenergic receptors. Display a hight degree of receptor specificity=good |
| A dosage of 24mg has been ordered. the solution strength available is 12.5mg in 1.5ml | 2.9 mL |
| a 40ng in 2.5 mL soultion will be used to prepare a 30mg dosage | 1.9 mL |
| prepare 0.3mg from a solution strength of 0.6 mg in 0.8 mL | 0.4mL |
| a 36mg per 2mL strength solution is used to prepare 24mg | 1.3 mL |
| A dosage of 52 mg is to be prepared from a 78mg in 0.9 mL solution | 0.6mL |
| A dosage of 150mg has been ordered. The solution strenght is 100mg per mL | 1.5mL |
| Apha adrenergic antagonist are used for | essential hypertension, reversal of toxicity from alpha 1 agonist, BPH, pheochromocytoma, Raynaud's disease |
| What are the adverse effects of alpha1 drenergic antagonist | Alph 1: orthostatic hypotention, reflex tachycardia, nasal congestion, inhibition of ejaculation, sodium retention. |
| What are the adverse effects of alpha2 andrenergic antagonist | reflex tachycardia |
| Prazosin (minipress) | blocks alpha 1 only |
| Prazosin uses | hypertension, BPH (not approved for this use) |
| Terazosin (Hytrin) used for | Hypertension, and BPH |
| Doxazosin (cardura) | Hypertention, and BPH |
| Tamsulosin (flomax) | BPH only |
| Nonselective prototype | phentolamine (regitine) it is used for prevention of necrosis from inflitration of alpha 1 mediated vasoconstricion |
| Phenoxybenzamine | is a noncompetitive receptor antagonist and therefore nonreversible used for pheochromocytoma only |
| Beta adrenergic antagonist are used for | angina pectoris, HTN, cardiac dysrhythmias, MI, heart failure, hyperthyroidism, migraine, stage fright, phenchromocytoma, glaucoma |
| Adervse effects of Beta 1 | bradycardia, reduced cardiac output, precipitationof heart failure, atrioventricular heart block, rebound cardiac excitation. |
| Adverse effects of Beta 2 | bronchoconstriction, inhibition of glycogenolysis. |
| Nonselective beta andrenergic antagonist Propranolol (inderal) | prototype blocks beta 1 and beta 2 |
| Uses for Propranolol | HTN, angina pectoris, cardia dysrhythmias, MI, migraine, stage fright |
| Adverse effects of Propranolol | depression, insomnia nightmares, hullcinations |
| precautions with propranolol | sever allergy (reduces the effects of epinephrine) diabetes, cardiac, respiratory, psychiatric |
| Drug interactions of propranolol | excessive cardiac suppression in combowith calsium channel blockers |
| Selective beta andrenergic antagonist Metoprolol (lopressor, Toprol XL) | blocks beta 1. Not likely to cause bronchoconstriction or suppression of glycogenolysis. |
| Why is metoprolol perfered for pts with asthma and diabetes | because there is no beta 2 activation, but can block beta 2 at higher doses. |
| Uses for metoprolol | HTN angina MI |
| Adverse effects of metoprolol | brady cardia, reduced cardiac output, HTN, cardiac dysrhythmias, MI,heart failure |
| Indirect acting antiadrenergic agents | prevent stimulation of periperal adrenergic recepotors by mechanisms that do not involve direct interaction with peripheral receptors. |
| Reserpine | action: delpetion of NE from postganglionic sympathetic neurons, decreasing the stimulation of practicall all adrenergic recpetors |
| Reserpine effects | Slows heart rate, reduces cardiac output, promotes vasodilation= decrease in BP. Produces sedation and indifference to environment, can cause depression |
| Reserpine uses | HTN, make take a week to obtain and effects lst several weeks after |
| Adverse effects of reserpine | severe depression, suicide, bradycardia orthostatic hypotension, nasal congestion |
| Centrally acting alpha 2 agonist do what | act in the CNS, their effects are like those of the direct-acting adrenergic recptor blockers |
| Clonidine (catapres) | action: alpha2 adrenergic agonist that causes selective stimulation of alpha 2 receptors in the cns,specifically in the brainstem areas associated with autonomic regulation of the CV system-reduces sympathetic outflow to blood vessls and heart. |
| Clonidine effects | bradycardia, decreases in cardiac output, vasodilation = decreased BP |
| Clonidine uses | HTN and relief of sever pain-admin. via epidual to CA pts. |
| Adverse effects of clonidine | drowsiness, xerostomia, rebound HTN with abrupt withdrwal, contraindicated in pregnancy |
| methyldopa and Methyladopate (aldomet) | Action similar to clonidine but not an alpha 2 agonist. Must be taken up in brainstem neurons na dconverted to methylnorepinehprine, a compund that is an effective alpha 2 agonist, Reduces BP by vasodilation. |
| Methyldopa and methyldopate uses | HTN |
| Adverse effects of methyldopa and methyldopate | positive coombs test and hemolytic anemia hepatotoxicity. |
Created by:
dlovelylisa
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