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29 Cards in this Set
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Levodopa
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Tx for PD
Ldopa is converted into DA after the rate-limiting step (tyrosine hydroxylase). Is effective in reducing all sx of PD (esp. bradykinesia) - best results in first few years of usage. Has intense side effects (peripheral and central) and does not slow progression of the disease. Will exacerbate psychosis. Drug interactions with MAO A inhibitors or non-specific MAOIs. |
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Carbidopa
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Peripheral decarboxylase inhibitor that prevents Ldopa from being converted to DA in the periphery (doesn't cross the BBB); important in prevention of side effects
For tx of PD - coadministered with Ldopa |
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Entacapone
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Peripheral COMT inhibitor used to increase the amount of Ldopa that reaches the brain (by preventing it's breakdown by COMT in the periphery).
Used to tx PD - coadministered with Ldopa |
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Bromocriptine
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D2 agonist (DA receptor agonist); shuts down the indirect pathways
Often used as: -monotherapy prior to L-Dopa -to lower the dose of L-Dopa -reduce on/off syndrome |
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Rasagaline
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MAOB selective inhibitors; MAO B metabolizes DA, and inhibitors block conversion of MPTP to MPP+ and decrease free radicals generated by DA metabolism.
Is nontoxic and may slow progression of the disease. Ldopa interacts with MAO A inhibitors and non-specific MAOIs |
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Selegeline
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MAOB selective inhibitors
-Limited efficacy -poor bioavailability -converted into methamphetamine |
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Phenelzine
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Nonselective MAO Inhibitor
L-DOPA interacts with MAOA or nonselective MAO inhibitors |
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Amantadine
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Antiviral agent that also blocks NMDA receptors.
-Effects are very short-lived (weeks). -May function by preventing excitotoxicity or by altering the activity of the basal ganglia (decreasing activation of the indirect pathway) |
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Carbamazepine
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For tx of all seizures except absence seizures
-Limits repetitive firing by prolonging the inactive state of sodium channels following an action potential. **Note: it does not alter spontaneous activity of a neuron Side effect: Leukopenia |
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Valproate
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Tx for absence, myoclonic, partial and tonic-clonic seizures; reserved for the treatment of serious seizures
MOA: -Prolongs the inactive state of voltage-gated sodium channels -Produces small reductions in current from T-type calcium channels -Increases GABA synthesis, inhibits GABA transporters, inhibits GABA metabolism Side effect: Hepatotoxicity |
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Ethosuximide
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First-line drug for treating absence seizures.
MOA: blocks T-type calcium channels that underlie absence seizures |
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Phenobarbital
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Tx for partial and tonic-clonic seizures and status epilepticus; may worsen absence seizures
MOA: primary site of action is GABA-induced influx of chloride via GABAA receptors; also inhibits sodium channels, AMPA receptors Side effects: long-term use can cause drowsiness/lethargy or hyperactivity in children |
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Lamotrigine
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Tx for partial seizures, tonic-clonic seizures, absence seizures
MOA: prolong the inactive state of voltage-gated sodium channels and inhibits glutamate release **Only drug that can be used to tx an absence seizure that does not target T-type Ca channels.** |
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Clonazepam
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Benzodiazepine used for tx of absence seizures
MOA: GABA-induced influx of chloride via GABAA receptors and inhibits T-type calcium channels Side effects: long-term use results in tolerance, drowsiness, and lethargy or paradoxical hyperactivity in children *Best for acute administration - tx of status epilepticus* |
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Lorazepam
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Benzodiazepine used for tx of status epilepticus.
MOA: primary site of action is GABA-induced influx of chloride via GABAA receptors *Best used for acute administration - long term use can result in tolerance, drowsiness, lethargy or paradoxical hyperactivity in children* |
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Haloperidol, Thorazine
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1st generation anti-psychotics
MOA: block D2-like DA receptors; effects take weeks to emerge Effective in tx of positive sx of schizophrenia - can reduce frequency and severity of subsequent psychotic episodes. Side effects: Parkinson's-like syndrome, extrapyramidal side effects (acute dystonias, akathisia, tardive dyskinesias), autonomic and endocrine effects, and neuroleptic malignant syndrome (possible) |
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Clozapine
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Prototype for 2nd Generation (Atypical) Antipsychotics
MOA: block D2-like and 5-HT receptors w/ quicker dissociation constant Effective in treating positive AND negative sx of schizophrenia (even in resistant individuals) - higher efficacy than haldol. Side effect: agranulocytosis (still has lower mortality rate due to decrease in suicide rates with clozapine) |
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Olanzapine
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2nd generation antipsychotic; less effective than clozapine (compliance to olanzapine is not greater than compliance w/ 1st generation anti-psychotics)
MOA: block D2-like and 5-HT receptors w/ quicker dissociation constant Effective in treating positive AND negative sx of schizophrenia Side effects: fewer extrapyramidal side effects; metabolic syndrome |
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Lidocaine
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Amide anesthetic (short-acting)
-most commonly used local anesthetic (safe for children and inexpensive) -Metabolized by cytochrome p450 system in liver = increased duration of action (because duration of action depends on how long it takes for the drug to diffuse away from the site of action) -Most local anesthetics relax (dilate) blood vessels, preventing retention of the drug at the site of administration, so they must be administered w/ a vasoconstrictor -Less allergenic than ester anesthetics |
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Mepivacaine
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Amide anesthetic (intermediate-acting)
-exhibits the least vasodilation and can be administered w/o a vasoconstrictor |
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Prilocaine
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Amide anesthetic (short-acting)
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Bupivacaine
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Amide anesthetic (long-acting)
-Can be used as an epidural anesthetic but is rarely used because it seems to be more cardiotoxic than ropivacaine when delivered systemically |
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Articaine
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Amide anesthetic (intermediate-acting)
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Ropivacaine
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Amide anesthetic (long-acting)
-commonly used as an epidural anesthetic: produces regional nerve block, in many cases with an opiate analgesic Has a lower risk of cardiotoxicity than bupivacaine. |
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Cocaine
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Ester anesthetic and indirect-acting sympathomimetic
-produces local anesthesia and vasoconstriction = longer duration of action |
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Benzocaine
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Ester anesthetic
-Tend to have higher PKAs than amides = slower onset of action -Rapidly hydrolyzed by esterases in the blood = decreased duration of action -Metabolized into PABA derivatives (highly allergenic) |
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Procaine
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Ester anesthetic
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Tetracaine
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Ester anesthetic
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Epinephrine, Levonordefrin, Phenylephrine
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Vasoconstrictors coadministered with local anesthetics.
Administered to: - Prolong the duration anesthesia by preventing diffusion from the site of action - Limit systemic toxicity of local anesthetics - Reduce blood loss for surgical procedures Caution: ALPHA-1 adrenergic receptor agonists are HYPERTENSIVE AGENTS and should be used with caution in patients with cardiovascular disease |