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317 Cards in this Set
- Front
- Back
Parasympathetic preganglionic neurons release the neurotransmitter -------- which act on -------- receptors.
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Ach, nicotinic.
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Parasympathetic postganglionic neurons release the neurotransmitter -------- which act on ------- receptors.
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Ach, muscarinic.
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Sympathetic preganglionic neurons to sweat glands release the neurotransmitter ------- which act on ------- receptors.
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Ach, nicotinic.
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Sympathetic postganglionic neurons to sweat glands release the neurotransmitter ------- which act on ------- receptors.
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Ach, muscarinic.
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Sympathetic preganglionic neurons to glands, cardiac and smooth muscles release the neurotransmitter ------- which act on ------- receptors.
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Ach, nicotinic.
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Sympathetic postganglionic neurons to glands, cardiac and smooth muscles release the neurotransmitter ------- which act on ------- receptors.
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NE, alpha and beta
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Sympathetic preganglionic neurons to renal vascular smooth muscle release the neurotransmitter ------- which act on ------- receptors.
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Ach, nicotinic.
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Sympathetic postganglionic neurons to renal vascular smooth muscle release the neurotransmitter ------- which act on ------- receptors.
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Dopamine, D1
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Sympathetic preganglionic neurons to the adrenal medulla release the neurotransmitter ------- which act on ------- receptors.
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Ach, nicotinic.
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Sympathetic preganglionic neurons to the adrenal medulla synapse directly on ------- cells of the adrenal medulla.
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Chromaffin.
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Somatic neurons synapse directly on -------- muscle and release the neurotransmitter ------- which act on ------- receptors.
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skeletal muscle, Ach, nicotinic.
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Autonomic drugs: Ach is synthesized from acetyl-CoA and choline by the enzyme ---------.
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Choline acetyltransferase.
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Autonomic drugs: The transport of choline into the nerve terminal can be inhibited by --------.
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Hemicholinium.
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Autonomic drugs: The release of transmitter from vesicles in the nerve ending require the entry of ------ into the neuron.
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Calcium.
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Autonomic drugs: --------- inhibits the release of the stored Ach.
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Botulinum toxin.
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Autonomic drugs: The action of Ach in the synapse is terminated by its metabolism to acetate and choline by the enzyme ---------.
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Acetylcholinesterase.
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Noradrenergic:: In the noradrenergic nerve terminal, tyrosine is hydroxylated to -------, which is decarboxylated to --------, which is finally hydroxylated to NE.
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DOPA, dopamine.
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Noradrenergic:: Dopamine is transported into vesicles for hydroxylation to NE. This transport can be blocked by the drug --------.
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Reserpine.
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Noradrenergic:: The action of NE and DA is terminated by --------- and ----------.
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Reuptake, diffusion (different than for Ach).
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Noradrenergic:: --------- inhibits the release of the stored NE.
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Guanethidine.
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Noradrenergic:: The --------- drugs promote catecholamine release.
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Amphetamine.
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Noradrenergic:: The drugs --------- and ---------- inhibit the reuptake of NE.
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Cocaine, TCA.
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Noradrenergic:: The release of NE from a sympathetic nerve ending is modulated by ---------, --------- and ---------.
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NE, Ach, angiotensin II.
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Noradrenergic:: NE inhibits its own release at the noradrenergic nerve terminal through --------- receptors.
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Alpha 2.
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Noradrenergic:: Angiotensin II --------- (inhibits / stimulates) the release of NE from the noradrenergic nerve terminal.
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Stimulates.
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Noradrenergic:: Ach inhibits the release of NE from the noradrenergic nerve terminal by binding to --------- receptors.
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M1.
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What is the Clinical application and action of Bethanechol.
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Postoperative and neurogenic ileus and urinary retention. / Activates bowel and bladder smooth muscle.
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What are the Clinical application and action of Carbachol and Pilocarpine.
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Glaucoma. / Activates ciliary muscle of eye (open angle), pupillary sphincter (narrow angle); Xerostomia assoc with Sjorgens Syndrome (Pilocarpine)
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Clinical application / action of Neostigmine.
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Indirect Ach Agonists/ anticholinesterase; Postoperative and neurogenic ileus and urinary retention, myasthenia gravis, reversal of neuromuscular junction blockade (postoperative). / Increase endogenous Ach.
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Clinical application / action of Pyridostigmine.
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Indirect Ach Agonists/ anticholinesterase; Myasthenia gravis. / Increase Ach; increase strength.
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Clinical application / action of Edrophonium.
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Indirect Ach Agonists/ anticholinesterase;Diagnosis of myasthenia gravis (extremely short acting); differentiates between MG and cholinergic crisis/ Increase endogenous Ach.
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Clinical application / action of Physostigmine.
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Indirect Ach Agonists/ anticholinesterase; Glaucoma (crosses blood-brain barrier) and atropine overdose. / Increase endogenous Ach.
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Clinical application / action of Echothiophate.
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Indirect Ach Agonists/ anticholinesterase; Glaucoma. / Increase endogenous Ach; extremely long acting t1/2 = 100 hrs
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What are the Symptoms of cholinesterase inhibitor poisoning.
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Diarrhea, Urination, Miosis, Bronchospasm, Bradycardia, Excitation of skeletal muscle and CNS, Lacrimation, Sweating, Salivation (also abdominal cramping). "DUMBBELSS".
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Indirect agonists (anticholinesterases):: Cholinesterase inhibitor poisoning may be caused by ---------.
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Parathion and other organophosphates.
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What is the clinical use for Donepezil and Tacrine?
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Indirect Ach agonists used to treat Alzheimers dz
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Indirect agonists (anticholinesterases):: Mechanism of action of Pralidoxime.
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Regenerates active cholinesterase, chemical antagonist, used to treat organophosphate exposure. It acan be used as an antidote for cholinesterase inhibitor poisoning
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Cholinoreceptor blockers:: Clinical uses of the muscarinic antagonist Atropine.
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Dilate pupils, decrease acid secretion in peptic ulcer disease, decrease urgency in mild cystitis, decrease GI motility, reduce airway secretions, and treat organophosphate poisoning. "Blocks SLUD: Salivation, Lacrimation, Urination, Defecation."
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Cholinoreceptor blockers:: Side effects of Atropine.
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Increase body temp, rapid pulse, dry mouth, dry/flushed skin, disorientation, mydriasis with cycloplegia, and constipation. "Atropine parasympathetic block side effects: Blind as bat, Red as a beet, Mad as a hatter, Hot as a hare, Dry as a bone."
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Cholinoreceptor blockers:: Hexamethonium (ganglionic blocker) blocks -------- receptors.
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Nicotinic.
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What are some other drug categories with Anti Muscarinic activity?
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Anti histamines Anti psychotics tricylic Anti depressants Anti arrythmics amantadine Meperedine
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antimuscarinic drugs: "tropi" are anti-muscarinic
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while vacationing in the tropics you lie on a beach and your muscles waste away!
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antimuscarinic drugs: benztropine acts on the ____, and is used to treat
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CNS, Parkinson's disease
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antimuscarinic drugs: scopolamine acts on the _____, and is used to treat
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CNS, motion sickness
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What three antimuscarinics that act on eye and what is their MOA?
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atropine, homatropine, tropicamide they all produce mydriasis and cyclopegia
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what is the mechanism of ipatropium and what is it used to treat
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its and antimuscarinic used to treat asthma, COPD
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neuromuscular blocking drugs: neuromuscular blocking drugs are used for
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muscle paralysis in surgery or mechanical ventilation
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neuromuscular blocking drugs: name a depolarising neurmuscular blocking drug
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succinylcholine
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neuromuscular blocking drugs: name 6 nondepolarizing neuromuscular blocking drugs
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tubocurarine
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neuromuscular blocking drugs: *mnemonic -- the "cur" drugs are all _________ neuromuscular blocking agents
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nondepolarizong
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neuromuscular blocking drugs: what is tubocurarine used for
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nondepolarizing neuromuscular blockade
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neuromuscular blocking drugs: what agents are used to reverse neuromuscular blockade by succinylcholine?
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cholinesterase inhibitors in phase II (ex -- neostigmine)
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neuromuscular blocking drugs: what phase of succinylcholine neuomuscular bloackade is reversible?
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phase II (repolarized but blocked)
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neuromuscular blocking drugs: what agents are used to reverse pahse I neuromuscular blockade by succinylcholine?
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phase I Succinylcholine neuromuscular blockade cannot be reversed
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neuromuscular blocking drugs: what phase of succinylcholine neuomuscular bloackade is irreversible?
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phase I Succinylcholine neuromuscular blockade cannot be reversed
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neuromuscular blocking drugs: what is atracurium used for
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nondepolarizing neuromuscular blockade
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neuromuscular blocking drugs: what is the effect of cholinesterase inhibitors on succinylcholine neuromuscular blockade?
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phase I: cholinesterase inhibitors potentiates the blockade phase II: cholinesterase inhibitors reverse the blockade
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neuromuscular blocking drugs: what cholinesterase inhibitor is used to reverse phase II of succinylcholine neuromuscular blockade?
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neostigmine
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neuromuscular blocking drugs: what is mivacurium used for
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nondepolarizing neuromuscular blockade
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Dantrolene: what is dantrolene used for
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treat malignant hyperthermia
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Dantrolene: what causes malignant hyperthermia
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use inhalation anesthetics and succinylcholine together
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Dantrolene: what inhalation anesthetic DOES NOT cause malignanat hyperthermia?
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N2O
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Dantrolene: what is dantrolene used for
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neuroleptic malignant syndrome
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Dantrolene: what is neuroleptic malignant syndrome
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a toxicity of antipsychotic drugs
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Dantrolene: what drug is used to treat malignant hyperthermia
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dantrolene
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Dantrolene: what is the mechanism of dantrolene
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prevents release of Ca++ from saarcoplasmic reticulum of skeletal muscle
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Sympathomimetics: the 5 catecholamines
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EPI, NE, Isoproterenol, dopamine, dobutamine
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Sympathomimetics: what receptors does epinephrine act on and what is used for?
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alpha-1, (alpha-2), beta-1, beta-2 adrenergics anaphylaxis, open-angle glaucoma, asthma, hypotension
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Sympathomimetics: what receptors does NE work on and what is it used to treat?
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alpha-1, (alpha-2), beta-1 adrenergics hypotension (but decreases renal perfusion)
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Sympathomimetics: what receptors does isoproterenol work on and what is its clinical application?
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beta-1 = beta-2 adrenergics AV block
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Sympathomimetics: what receptors does dopamine work on and what is it used to treat?
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D1 = D2, D1 and D2 more than beta, beta more than alpha shock with renal failure, heart failure
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Sympathomimetics: what receptors does dobutamine work on and what is it used to treat?
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beta-1 > beta-2 shock, heart failure
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Sympathomimetics: what is the action of amphetamine and what are its clinical applications?
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indirect general adrenergic agonist, releases stored catecholamines narcolepsy, obesity, attention deficit disorder
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Sympathomimetics: what is the action of ephedrine and what are its clinical applications?
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indirect general adrenergic agonist, releases stored catecholamines nasal decongestion, urinary incontinence, hypotension
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Sympathomimetics: name three sympathomimetic drugs used to treat hypotension
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epinephrine, norepinephrine, ephedrine
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Sympathomimetics: what is the action of phenylephrine and what is it used for?
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adrenergic agonist, alpha-1 > alpha-2 pupil dilator, vasoconstriction, nasal decongestion
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Sympathomimetics: what is the action of albuterol and what is it used to treat?
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adrenergic agonist, beta-2 >beta-1 asthma
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Sympathomimetics: what is the action of terbutaline and what is it used to treat?
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adrenergic agonist, beta-2 >beta-2 asthma
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Sympathomimetics: what is the MOA of methoxamine and what is it used to treat?
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alpha-1 paroxysmal atrial tachycardia, thru the vagal reflex
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Sympathomimetics: what is the mechanism of cocaine and what are its actions?
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indirect general adrenergic agonist, catecholamine uptake inhibitor it causes vasoconstriction, local anesthesia
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Sympathomimetics: what is the mechanism of clonidine
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centrally acting alpha-adrenergic agonist, decreases central adrenergic outflow
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Sympathomimetics: what is the mechanism of alpha-methyldopa
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centrally acting alpha-adrenergic agonist, decreases central adrenergic outflow
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Sympathomimetics: what are clonidine and alpha-methyldopa used to treat
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hypertension, especially in renal disease because they do not decreased blood flow to the kidney
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Sympathomimetics: what sympathomimetic is used to treat urinary incontinence
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ephedrine
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Sympathomimetics: what sympathomimetic is used to treat attention deficit disorder and narcolepsy?
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amphetamine
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What is Epiniephrine Reversal?
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use of an alpha 1 blocker to reverse HT to HYPOtension in a patient receiving too much epinephrine
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alpha-blockers: what is the mechanism of phenoxybenzamine
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nonselective irreversible alpha blocker
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alpha-blockers: what is the mechanism of phentolamine
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nonselective reversible alpha blocker
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alpha-blockers: what are phenoxybenzamine and phentolamine used for?
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pheochromocytoma
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alpha-blockers: what are the side effects of nonselective alpha blockers
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orthostatic hypotension, reflex tachycardia
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alpha-blockers: name 3 alpha-1 selective adrenergic blockers
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prazosin, terazosin, doxazosin the " -sin" drugs
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alpha-blockers: what are alpha-1 selective adrenergic alpha blockers used for
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hypertension, urinary retention in BPH
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alpha-blockers: what are the side effects of alpha-1 blockers
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first dose orthostatic hypotension, dizziness, headache
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alpha-blockers: what are the side effects of terazosin?
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orthostatic hypotension, dizziness, headache
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alpha-blockers: what selective alpha blockers cause orthostatic hypotension
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phenoxybenzamine, phentolamine, terazosin, prazosin, doxazosin
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alpha-blockers: name an alpha-2 selective adrenergic blocker and what is it used for?
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yohimbe
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alpha-blockers: what is yohimbine used for
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impotence (effectiveness controversial)
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alpha-blockers: what alpha blockers are used to treat pheochromocytoma
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phenoxybenzamine, phentolamine
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What are some Pharmacological uses for Propanolol?
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migraine prophylaxis, performance anxiety, essential tremor, Thryotoxicosis (blocks T3/T4 conversion; inhibits deiodinase activity)
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beta-blockers ("lol"s): name some beta-blockers
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propranolol, metoprolol, atenolol, nadolol, timolol, pindolol, esmolol, labetalol
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beta-blockers ("lol"s): what are beta-blockers used to treat
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hypertension, angina, MI, SVT, CHF, glaucoma
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beta-blockers ("lol"s): how do beta blockers treat hypertension
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decrease cardiac output, decrease renin secretion
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beta-blockers ("lol"s): how do beta blockers treat angina
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decrease heart rate, decrease cardiac contractility, decreased O2 consumption
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beta-blockers ("lol"s): why are beta blockers used to treat MI
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decrease MI mortality
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beta-blockers ("lol"s): how do propanolol and esmolol treat SVT
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decrease AV conduction velocity
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beta-blockers ("lol"s): how do beta blockers used treat CHF
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used to slow progression of chronic failure
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beta-blockers ("lol"s): which beta blocker is used to treat glaucoma and how does it work?
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timolol; decrease secretion of aqueous humor
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beta-blockers ("lol"s): what are the toxic effects of beta blockers
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impotence, exacerbation of asthma, CV adverse efx (bradycardia, AV block, CHF) CNS Adverse efx (sedation, sleep alterations); use with caution in diabetes b/c they block glycogenolysis and gluconeogenesis; some may INC LDLs, TGs
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beta-blockers ("lol"s): what are the cardiovascular toxic effects of beta blockers
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bradychardia, AV block, CHF
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beta-blockers ("lol"s): what are the CNS adverse effects of beta blockers
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sedation, sleep alterations
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beta-blockers ("lol"s): which beta blockers are beta-1 selective
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acebutolol, betaxolol, esmolol, atenolol, metaprolol (those that start with A-M)
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beta-blockers ("lol"s): which beta-1 blocker is short-acting
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esmolol
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beta-blockers ("lol"s): which beta blockers are non-selective
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propanolol, timolol, pindolol, nadolol, labetalol
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beta-blockers ("lol"s): which beta blocker also blocks alpha receptors
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labetalol (all others are spelled "olol")
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What is Open Angle Glaucoma?
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DEC reabsorption of aqueous humor causing an INC in IOP; P/W progressive PAINless visual loss; Treate with Beta blockers and Muscarinic activators
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What is Closed Angle Glaucoma?
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blockade of the canal of Schlemm causing an INC in IOP; Acutely PAINful; Tx with Cholinomimetics, Carbonic Anhydrase Inhibitors, and Mannitol
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What drugs are CONTRAINDICATED in the Tx of CLOSED angle glaucoma?
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Antimuscarinics, and alpha 1 agonists
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How are Pilocarpine and Echothiophate used to treat Glaucoma and what are the Side Efx?
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Closed Angle; INC the outflow of the AH; contract the ciliary muscle to open the trabecular meshwork; Side Efx miosis and cyclopegia
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glaucoma drugs: what classes of drugs are used to treat glaucoma
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alpha agonists, beta blockers, cholinomimetics, diuretics, prostaglandins (*mnemonic -- treating glaucoma is easy as ABCD)
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glaucoma drugs: what is the effect of epinephrine in glaucoma
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increase outflow of aqueous humor
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glaucoma drugs: what are the side effects of epinephrine treatment in glaucoma
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mydriasis, stinging
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glaucoma drugs: what glaucoma should epinephrine NOT be used for
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closed-angle glaucoma
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glaucoma drugs: what is the effect of brimonidine in glaucoma
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decreased aqueous humor synthesis
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glaucoma drugs: what are the side effects of brimonidine treatment in glaucoma
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no pupillary or vision changes
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glaucoma drugs:What Beta blockers are used to treat Glaucoma and what is the effect?
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Timolol, (betaxolol, carteolol); decrease aqueous humor secretion
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glaucoma drugs: what is the effect of cholinomimetics in glaucoma
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ciliary muscle contraction, opening of trabecular meshwork, increase outflow of aqueous humor
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glaucoma drugs: what is the effect of diuretic treatment in glaucoma
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inhibition of carbonic anhydrase --> decrease HCO3 secretion --> decrease aqueous humor secretion
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glaucoma drugs: what is the effect of prostaglandin (latanoprost) treatment in glaucoma and what are the Side Efx?
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increase outflow of aqueous humor; darkens color of iris (browning)
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glaucoma drugs: which drugs used to treat glaucoma increase outflow of aqueous humor
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cholinomimetics, prostaglandin, epinephrine
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glaucoma drugs: which glaucoma drugs decrease aqueous secretion
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beta blockers, diuretics
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L-dopa/carbidopa: what is the mechanism of action of L-dopa/carbidopa and what are they used to treat?
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increase dopamine level in brain; Parkinson's disease
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L-dopa/carbidopa: how does L-dopa differ from dopamine?
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L-dopa can cross the blood-brain barrier, dopamine cannot
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L-dopa/carbidopa: what happens to L-dopa after it crosses the BBB
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converted to dopamine by dopa decarboxylase
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L-dopa/carbidopa: what enzyme convertes L-dopa to dopamine
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dopa decarboxylase
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L-dopa/carbidopa: what is the function of carbidopa
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peripheral decarboxylase inhibitor
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L-dopa/carbidopa: why is carbidopa given with L-dopa
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increase L-dopa availability in CNS by inhibiting decarboxylase in periphery, also limits peripheral side effects
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L-dopa/carbidopa: what are the side effects of L-dopa.carbidopa treatment
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arrhythmias due to peripheral efx, dyskinesias due to excess dopamine stimulation
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Parkinson's disease drugs: what classes of drugs are used to treat Parkinson's disease
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dopamine agonists, MAO inhibitors, antimuscarinics
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Parkinson's disease drugs: specifically, which drugs are used to treat Parkinson's
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Bromocriptine, Amantadine, Levodopa, Selegiline, Antimuscarinics (BALSA)
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Parkinson's disease drugs: which dopamine agosts are used to treat Parkinson's
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L-dopa/carbidopa, bromocriptine, pramipexole, ropinirole, amantadine
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Parkinson's disease drugs: what is the action of bromocriptine in Parkinson's
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ergot alkaloid, partial dopamine agonist
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Parkinson's disease drugs: what is the action of amantadine in Parkinson's
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enhances dopamine release
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Parkinson's disease drugs: what is the mechanism of selegiline
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selective MAO type B inhibitor
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Parkinson's disease drugs: what is the effect of benztropine in Parkinson's
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improves tremor, rigidity, little effect on bradykinesia
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Sumatriptan: what is its MOA and what is it used for?
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5-HT1D agonist; acute migraine, cluster headache attacks
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Sumatriptan: what is the half life of sumatriptan, what are some Side Efx?
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less than 2 hours; chest discomfort, mild tingling
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Sumatriptan: what are the contraindications for sumatriptan
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patients with CAD or Prinzmetal's angina
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Epilepsy drugs: which drugs are used for simple and complex partial seizures
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phenytoin, carbamazapine, lamotrigine, gabapentin, topiramate, phenobarbital
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Epilepsy drugs: what types of seizures is phenytoin indicated for
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simple and complex partial, tonic-clonic, status epilepticus
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Epilepsy drugs: what types of seizures is carbamazepine indicated for
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simple and complex partial, tonic-clonic
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Epilepsy drugs: what types of seizures is lamotrigine indicated for
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simple and complex partial, tonic-clonic
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Epilepsy drugs: what types of seizures is gabapentin indicated for
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simple and complex partial, tonic-clonic
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Epilepsy drugs: what types of seizures is topiramate indicated for
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simple and complex partial
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Epilepsy drugs: what types of seizures is phenobarbital indicated for
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simple and complex partial, tonic-clonic
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Epilepsy drugs: what drugs can be used for tonic-clonic seizures
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phenytoin, carbamazapine, lamotrigine, gabapentin, phenobarbital, valproate
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Epilepsy drugs: what drugs can be used for absence seizures
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valproate, ethosuximide
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Epilepsy drugs: what drugs can be used for status epilepticus
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phenytoin, benzodiazapines (diazepam, lorazepam)
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Epilepsy drugs: what types of seizure is valproate indicated for
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tonic-clonic, absence
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Epilepsy drugs: what types of seizure is ethosuximide inidcated for
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absence
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Epilepsy drugs: what type of seizure are benzodiazepines indicated for
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status epilepticus
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Epilepsy drugs: other than anti-seizure, what else is phenytoin used for
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class 1B anti-arrhythmic
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Epilepsy drugs: how should a patient taking carbamazepine be followed
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monitor LFT's weekly
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Epilepsy drugs: which seizure drugs have adjunct use
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gabapentin, topiramate
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Epilepsy drugs: which seizure drug is safest in pregnant women
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phenobarbital
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Epilepsy drugs: which seizure drug is used in Crigler-Najjar II
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phenobarbital
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Epilepsy drugs: what are the advantages of phenobarbital
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can be used in pregnant women, Crigler Najjar II
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Epilepsy drug toxicities: what are the side effects of benzodiazepines
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sedation, tolerance, dependence
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Epilepsy drug toxicities: what are the side effects of carbamazepine
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diplopia, ataxia, CYP induction, blood dyscrasias, liver toxicity
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Epilepsy drug toxicities: what are the side effects of ethosuximide
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GI distress, lethargy, headache, urticaria, Stevens-Johnson syndrome
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Epilepsy drug toxicities: what are the side effects of phenobarbital
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sedation, CYP induction, tolerance, dependence
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Epilepsy drug toxicities: what are the side effects of phenytoin
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nystagmus, diplopia, ataxia, sedation, ginigival hyperplasia, hirsutism, anemias, teratogenic
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Epilepsy drug toxicities: what are the side effects of valproate
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GI distress, rare by fatal hepatotoxicity, neural tube defects (spina bifida)
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Epilepsy drug toxicities: what are the side effects of lamotrigine
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life-threatening rash, Stevens-Johnson syndrome
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Epilepsy drug toxicities: what are the side effects of gabapentin
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sedation, movement disorders
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Epilepsy drug toxicities: what are the side effects of topiramate
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sedation, mental dulling, kidney stones, weight loss
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Epilepsy drug toxicities: which anti-epileptic drug is teratogenic
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phenytoin
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Epilepsy drug toxicities: which anti-epileptic drug can cause dependence
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benzodiazepines, phenobarbital
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Epilepsy drug toxicities: which anti-epileptic drug can cause neural tube defects
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valproate
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Epilepsy drug toxicities: which anti-epileptic drugs can cause GI distress
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valproate, ethosuximide
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Epilepsy drug toxicities: it is necessary to check LFT's with which anti-epileptic drugs
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carbamazepine, valproate
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Epilepsy drug toxicities: which anti-epileptic drugs cause CYP induction
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phenobarbital, carbamazepine
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Epilepsy drug toxicities: which anti-epileptic drugs can cause blood problems
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carbamazepine, phenytoin
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Epilepsy drug toxicities: which anti-epileptic drugs can cause Stevens-Johnson syndrome
|
lamotrigine, ethosuximide
|
|
Epilepsy drug toxicities: which anti-epileptic drugs can cause diplopia
|
carbamazepine, phenytoin
|
|
Phenytoin: what is the mechanism of phenytoin action
|
use-dependent blockade of Na+ channels
|
|
Phenytoin: what is the clinical application of phenytoin
|
grand mal seizures
|
|
Phenytoin: what are the toxicities of phenytoin
|
nystagmus, ataxia, diplopia, lethargy
|
|
Phenytoin: what are the chronic toxicities of phenytoin
|
gingival hyperplasia in children, peripheral neuropathy, hirsutism, megaloblastic anemia, malignant hyperthermia (rare)
|
|
Phenytoin: should pregnant women take phenytoin
|
NO -- teratogenic
|
|
Phenytoin: why does phenytoin cause megaloblastic anemia
|
causes decreased vitamin B-12
|
|
Barbiturates: name 4 barbiturates
|
phenobarbital, pentobarbital, thiopental, secobarbital
|
|
Barbiturates: what is the mechanism of barbiturate action
|
increase duration of Cl channel opening --> decreased neuron firing --> facilitate GABA-A action
|
|
Barbiturates: how do barbiturates facilitate GABA-A action
|
increase duration of Cl channel opening which decreases neuron firing (Barbidurate increases duration
|
|
Barbiturates: is barbiturate action on the CNS stimulatory or inhibitory
|
inhibitory
|
|
Barbiturates: what is the clinical application of barbiturates
|
sedative for anxiety, seizures, insomnia, anesthesia induction (thiopental)
|
|
Barbiturates: which barbiturate is used for anesthesia induction
|
thiopental
|
|
Barbiturates: what are the side effects of barbiturates
|
dependence, additive CNS depression effects with alcohol, respiratory or CV depression (death), drug interactions due to CYP induction
|
|
Barbiturates: what should you find out before giving a patient barbiturates
|
what other medications they take, because of CYP induction and many drug interactions
|
|
Barbiturates: what happens if you give barbiturates to a patient in alcohol-induced coma or DT's
|
they might DIE!! Because of additive effect of barbiturates and alcohol --> respiratory depression
|
|
Barbiturates: when are barbiturates contra-indicated
|
porphyria
|
|
Barbiturates: can barbiturates cause dependence
|
YES
|
|
Barbiturates: My friend Barb was very anxious so her doctor gave her barbiturates to increase the duration of the time she could speak in public without freaking out and having a seizure. She became so dependent on it that she recommended it to her friend Portia who couldn't take it because of porphyria. One day Barb drank too much alcohol and took her barbiturates and never woke up! THE END
|
clinical pharmacology made ridiculous. Period
|
|
Benzodiazepines: name a bunch of benzodiazepines
|
diazepam, lorazepam, triazolam, temazepam, oxazepam, midazolam, chlordiazepoxide (all have ZZZ in them)
|
|
Benzodiazepines: what is the mechanism of benzodiazepines
|
increase frequency of Cl channel opening --> facilitate GABA-A action (Frenzodiazepines increase frequency)
|
|
Benzodiazepines: which GABA receptors are facilitated by barbiturates and bezodiazepines
|
GABA-A
|
|
Benzodiazepines: what are the clinical applications of benzodiazepines
|
anxiety, spasticity, status epilepticus (diazepam), detoxification (alcohol withdrawal, DT's)
|
|
Benzodiazepines: which benzodiazepine can be used for status epilepticus
|
diazepam
|
|
Benzodiazepines: what drugs can be used to treat alcohol withdrawal
|
benzodiazepines
|
|
Benzodiazepines: which benzodiazepines are short-acting
|
TOM thumb: Triazolam, Oxazepam, Midazolam
|
|
Benzodiazepines: what are the toxic effects of benzos
|
dependence, additive CNS depression effects with alcohol
|
|
Benzodiazepines: how are benzos better than barbiturates
|
less respiratory depression and coma risk
|
|
Benzodiazepines: how do you treat benzo overdose
|
flumazenil
|
|
Benzodiazepines: what is flumzenil used for
|
benzo overdose
|
|
Benzodiazepines: how does flumazenil work
|
competitive antagonist at GABA receptor
|
|
Benzodiazepines: can a patient become benzodiazepine dependent
|
YES
|
|
Benzodiazepines: are barbiturates or benzodiazepines used for alcohol withdrawal
|
benzodiazepines
|
|
Antipsychotics (neuroleptics): what is another name for antipsychotics
|
neuroleptics
|
|
Antipsychotics (neuroleptics): name 4 antipsychotic drugs
|
thioridazine, haloperidol, fluphenazine, chlorpromazine
|
|
Antipsychotics (neuroleptics): how do you keep benzos straight from antipsychotics
|
Benzos help 3rd year Jon Kazam be less anxious around patients: Shazam Kazam! Without antipsychotics patients talk like a crazy 'zine (well, not perfect, but I'm working on it)
|
|
Antipsychotics (neuroleptics): what is the mechanism of most antipsychotics
|
block dopamine D2 receptors
|
|
Antipsychotics (neuroleptics): what is the clinical application of antipsychotics
|
schizophrenia, psychosis
|
|
Antipsychotics (neuroleptics): what are the side effects of antipsychotics
|
extrapyramidal side effects (EPS), sedation, endocrine, muscarinic blockade, alpha blockade, histamine blockade
|
|
Antipsychotics (neuroleptics): what is a long-term effect of antipsychotic use
|
tardive dyskinesia
|
|
Antipsychotics (neuroleptics): what is neuroleptic malignant syndrome
|
a side effect of antipsychotics; rigidity, autonomic instability, hyperpyrexia
|
|
Antipsychotics (neuroleptics): how do you treat neuroleptic malignant syndrome
|
dantrolene, dopamine agonists
|
|
Antipsychotics (neuroleptics): what is tardive dyskinesia
|
side effect of neuroleptics; stereotypic oral-facial movements, may be due to dopamine receptor sensitization
|
|
Antipsychotics (neuroleptics): what is the "rule of 4" with EPS side effects from antipsychotic drugs
|
evolution of EPS side effects: 4 hours -- acite dystonia, 4 days -- akinesia, 4 weeks -- akasthesia, 4 months -- tardvie dyskinesia
|
|
Antipsychotics (neuroleptics): is tardvie dyskinesia reversible
|
often irreversible
|
|
Antipsychotics (neuroleptics): what is fluphenazine used for
|
schizophrenia, psychosis
|
|
Atypical antipsychotics: name 3 atypical antipsychotics
|
clozapine, olanzapine, risperidone
|
|
Atypical antipsychotics: what type of antipsychotic is clozapine
|
atypical
|
|
Atypical antipsychotics: what type of antipsychotic is olanzapine
|
atypical
|
|
Atypical antipsychotics: what type of antipsychotic is risperidone
|
atypical
|
|
Atypical antipsychotics: what is the mechanism of atypical antipsychotics
|
block 5-HT2 and dopamine receptors
|
|
Atypical antipsychotics: what is the mechanism of clozapine
|
block 5-HT2 and dopamine receptors
|
|
Atypical antipsychotics: what is the mechanism of olanzapine
|
block 5-HT2 and dopamine receptors
|
|
Atypical antipsychotics: what is the mechanism of risperidone
|
block 5-HT2 and dopamine receptors
|
|
Atypical antipsychotics: what is the clinical application of clozapine
|
schizophrenia positive and negative symptoms
|
|
Atypical antipsychotics: what is the clinical application of olanzapine
|
schizophrenia positive and negative symptoms, OCD, anxiety disorder, depression
|
|
Atypical antipsychotics: what is the clinical application of risperidone
|
schizophrenia positive and negative symptoms
|
|
Atypical antipsychotics: how are atypical antipsychotics different from classic ones
|
atypicals treat positive and negative symptoms of schizophrenia, fewer extrapyramidal and anticholinergic side effects than classic antipsychotics
|
|
Atypical antipsychotics: which antipsychotics should be used to treat positive and negative symptoms of schizophrenia
|
atypical ones -- clozapine, olanzapine, risperidone
|
|
Atypical antipsychotics: which antipsychotics should be used for fewer side effects
|
atypical ones -- clozapine, olanzapine, risperidone
|
|
Atypical antipsychotics: what is a potential toxicity of clozapine
|
agranulocytosis
|
|
Atypical antipsychotics: which antipsychotic drug can cause agranulocytosis
|
clozapine
|
|
Atypical antipsychotics: what test must be done weekly on patients taking clozapine
|
WBC count because of potential agranulocytosis
|
|
Lithium: what is the mechanism of action of lithium
|
unknown; may be related to inhibition of phosphoinositol cascade
|
|
Lithium: what is the clinical application of lithium
|
mood stabilizer for bipolar disorder
|
|
Lithium: how does lithium help people with bipolar disorder
|
prevents relapse and acute manic episodes
|
|
Lithium: what are the side effects of lithium
|
tremor, hypothyroidism, polyuria, teratogenic
|
|
Lithium: is it OK for women taking lithium to get pregnant
|
NO -- teratogenic
|
|
Lithium: what does lithium cause polyuria
|
ADH antagonist --> nephrogenic diabetes insipidus
|
|
Lithium: AUTHOR
|
Hina Talib
|
|
Antidepressants: What do the following drugs inhibit: 1. MAO inhibitors, 2. Desipramine/maprotilline, 3. Mirtazapine and 4. Fluoxetine/trazodone?
|
1. MAO 2. NE reuptake 3. Alpha 2-R 4. 5HT reuptake
|
|
Antidepressants: All of the above actions are ------synaptic
|
PRE
|
|
List the Tricyclic Antidepressants: What are the three C's of their toxicity?
|
Convulsions, Coma, Cardiotoxicity (arrythmias). Also respiratory depression, hypyrexia.
|
|
List the Tricyclic Antidepressants: How about toxicity in the eldery?
|
confusion and hallucinations due to anticholinergic SE
|
|
List the Tricyclic Antidepressants: What is the mechanism of TCA?
|
block reuptake of NE and 5HT
|
|
List the Tricyclic Antidepressants: What is the clinical uses of TCAs?
|
Endogenous depresion. Bed wetting - imipramine. OCD- clomipramine.
|
|
List the Tricyclic Antidepressants: How are tertiary TCA's different than secondary in terms of side effects?
|
Amitriptyline (tertiary) has more anti-cholinergic effects than do secondary (nortriptyline). Desipramine is the least sedating.
|
|
List the Tricyclic Antidepressants: what are the SE of TCAs?
|
sedation, alpha blocking effects, atropine-like anti cholinergic side effects (tachycardia, urinary retention)
|
|
List the Tricyclic Antidepressants: Fluoxetine, sertraline, paroxetine, citalopram are what class of drugs?
|
pg 311 SSRI's for endogenous depression
|
|
List the Tricyclic Antidepressants: How long does it take an anti-depressant to have an effect?
|
2-3weeks
|
|
List the Tricyclic Antidepressants: How does the toxicity differ fromTCA's and what are they?
|
Fewer than TCA's. CNS stimulation - anxiety, insomnia, tremor, anorexia, nausea, and vomiting.
|
|
List the Tricyclic Antidepressants: What toxicity happens with SSRI's and MAO inhibitors given together?
|
Seratonin Syndrome! Hyperthermia, muscle rigidity, cardiovascular collapse
|
|
List the Tricyclic Antidepressants: What are heterocyclics?
|
pg 312 2nd and 3rd generation antidepressants with varied and mixed mechanisms of action. Used major depression.
|
|
List the Tricyclic Antidepressants: Examples of heterocyclics?
|
trazodone, buproprion, venlafaxine, mirtazapine, maprotiline
|
|
List the Tricyclic Antidepressants: Which one is used for smoking cessation?
|
Buproprion. Mechanism not known. Toxicity - stimulant effects, dry mouth, aggrevation of pyschosis
|
|
List the Tricyclic Antidepressants: Which one used in GAD?
|
Venlafaxine - inhibits 5HT and DA reuptake. Toxicity - stimulant effects
|
|
List the Tricyclic Antidepressants: which one blocks NE reuptake
|
maprotiline
|
|
List the Tricyclic Antidepressants: Which one increases release of NE and 5HT via alpha 2 antagonism?
|
mirtazapine. Also potent 5HT Rantagonist. Toxicity - sedation, increase serum cholesterol, increase apetite
|
|
List the Tricyclic Antidepressants: What is trazodone and it' SE?
|
primarily inhibits seratonin reuptake. Toxicity - sedation, nausea, priapism, postural hypotension
|
|
Give 2 examples of MAO: Mechanism and Clinical Uses?
|
non selevtive MAO inhibition. Atypical antidepressant, anxiety, hypochondriasis
|
|
Give 2 examples of MAO: What is the toxicity with tyramine ingestion (in foods) and meperidine?
|
Hypertensive crisis
|
|
Give 2 examples of MAO: Other toxicities?
|
CNS stimulation, contraindicated with SSRI's or B-agonists
|
|
What is the mechanims of selgiline (deprenyl)?: what is the clinical use and toxicity?
|
adjunctive agent to L-dopa for Parkinsons. May enhance adverse effects of L-dopa
|
|
General principles: What is the significance of drugs with decreased solubility in blood?
|
rapid induction and recovery times . Ie. N20
|
|
General principles: What is the significance of drugs with increased solubility in blood?
|
increased potency = I/ MAC. Ie. Halothane
|
|
Inhaled Anesthetics: list them
|
halothane, enflurane, isoflurane, sevoflurane, methoxyflurane, nitrous oxide
|
|
Inhaled Anesthetics: What is good about lower solubility?
|
the quicker the anesthetic response, and the quicker the recovery
|
|
Inhaled Anesthetics: What are these drug's effects?
|
myocardial depression, respiratory depression, nausea/emesis, increase cerebral blood flow
|
|
Inhaled Anesthetics: What toxicity mactches the following drugs 1. Halothane 2. Methoxyflurane 3. Enflurane 4. Rare
|
1. Hepatotoxcity 2. Nephrotoxicty 3. Proconvulsant 4. Malignant hyperthermia
|
|
IV anesthetics: What do barbituates, benzodiazepines, arylcyclohexylamines and narcotic analgesics have in common?
|
they are IV anesthetics
|
|
IV anesthetics: What the pharmacokinetics and uses of thiopental?
|
high lipid solubility, rapid entry into brain. Used for induction of anesthesia for short surgical procedures. Terminated by redistribution from brain. Decreased cerebral blood flow
|
|
IV anesthetics: Give an example of a benzo and what is this class's shortcoming?
|
midazolam used for endoscopy. Used with gaseous anesthetics and narcotics. May cause severe post-op respiratory depressio and amnesia
|
|
IV anesthetics: What does Ketamine (PCP analog and an arylcyclohexylamine) do?
|
dissociative anesthetic. Cardiovascular stimulant. Causes disorientation, hallucination, bad dreams. Increases cerebral blood flow.
|
|
IV anesthetics: How are narcotic analgesics used? Examples?
|
Morphone and fentanyl are used with CNS depressant during general anesthesia.
|
|
IV anesthetics: What is the advantage of propofol
|
used for rapid anesthesia induction and short procedures. Less post-op nausea than thiopental
|
|
Local anesthetics: Name some esters?
|
procaine, cocaine, tetracaine,
|
|
Local anesthetics: Name some amides?
|
lidocaine, bupivacaine, (amides have two I's in name!)
|
|
Local anesthetics: What is the mechanism and clinical use?
|
bind receptor and block Na channels. Tertiary amine local anesthetics penetrate membrane in uncharge form, then bind charged form. Use for minor surgical procedures, spinal anesthesia.
|
|
Local anesthetics: How do you decide to use ester or amides?
|
if allergic to esters, give amides
|
|
Local anesthetics: what is the toxicity
|
CNS excitation, severe cardiovascular toxicity (bupivacaine), hypertension, arrhythmias (cocaine)
|
|
Local anesthetics: In infected ________ tissue, anesthetics are charged and cannot penetrate membrane. Therefore, ______ anesthetics are needed.
|
acidic; more
|
|
Local anesthetics: What is the order of nerve blockade for size and myelination? Which factor predominates?
|
small diameter> large diameter. Myelinated fibers> unmyelinated fibers. Size factor predominates
|
|
Local anesthetics: what is the order of loss of sensation?
|
pain first, then temp, then touch, then pressure
|
|
Local anesthetics: Why would you give these drugs with vasoconstrictors?
|
to enhance local action
|
|
Opiod analgesics: List as many as you can.
|
morphine, fentanyl, codeine, heroin, methadone, meperidine, dextromethorphan
|
|
Opiod analgesics: Mechanism: They act as _____ for opiod receptors to modulate synaptic transmission
|
agonists
|
|
Opiod analgesics: which drugs act at the mu, delta, kappa receptors?
|
morphine enkephalin, dynorphin
|
|
Opiod analgesics: Clinical use?
|
pain, cough supression (dex), diarrhea (loperamide), acute pulmonary edema, methadone maintenance programs
|
|
Opiod analgesics: What are the major toxicities?
|
addiction, respiratory depression, constipation, miosis, additive CNS depression wth other drugs
|
|
Opiod analgesics: Tolerance does not develop to __________and ______
|
miosis and constipation
|
|
Opiod analgesics: How would you treat toxicity?
|
naloxone, naltrexone (opiod R antagonist)
|
|
Other NSAIDS: List three NSAIDS?
|
ibuprofen, naproxen, indomethacin
|
|
Other NSAIDS: What is their mechanism?
|
reversibly inhibit COX 1 and 2. Blocks PG synthesis
|
|
Other NSAIDS: What is their clinical use (3As)?
|
Antipyretic, analgesic, anti-inflammatory. Indomethacin is used to close a PDA.
|
|
Other NSAIDS: What are common toxicities?
|
renal damage, aplastic anemia, GI distress, ulcers
|
|
COX 2 Inhibitors: Where is cox2 found?
|
in inflammatory cells and mediates inflammation and pain
|
|
COX 2 Inhibitors: Why is cox2 inhibition better than cox1?
|
cox1 helps to maintain gastric mucosa, thus, should not have the corrosive effects of other NSAIDs on the GI lining (less incidence of ulcers and bleeding)
|
|
COX 2 Inhibitors: Clinical Use?
|
RA and osteoarthritis
|
|
Acetaminophen: What is its mechanism and where does it work?
|
reversibly inhibits cox, mostly in CNS. Inactivated peripherally.
|
|
Acetaminophen: What are its 2 As?
|
antipyretic, analgesic but NOT anti-inflammatory.
|
|
Acetaminophen: Overdose effects?
|
hepatic necrosis, acetaminophen metabolites depletes glutathine and forms toxic tissue adducts in the liver
|