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29 Cards in this Set

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Levodopa
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.
Carbidopa
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
Entacapone
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
Bromocriptine
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
Rasagaline
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
Selegeline
MAOB selective inhibitors

-Limited efficacy
-poor bioavailability
-converted into methamphetamine
Phenelzine
Nonselective MAO Inhibitor

L-DOPA interacts with MAOA or nonselective MAO inhibitors
Amantadine
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)
Carbamazepine
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
Valproate
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
Ethosuximide
First-line drug for treating absence seizures.

MOA: blocks T-type calcium channels that underlie absence seizures
Phenobarbital
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
Lamotrigine
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.**
Clonazepam
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*
Lorazepam
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*
Haloperidol, Thorazine
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)
Clozapine
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)
Olanzapine
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
Lidocaine
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
Mepivacaine
Amide anesthetic (intermediate-acting)
-exhibits the least vasodilation and can be administered w/o a vasoconstrictor
Prilocaine
Amide anesthetic (short-acting)
Bupivacaine
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
Articaine
Amide anesthetic (intermediate-acting)
Ropivacaine
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.
Cocaine
Ester anesthetic and indirect-acting sympathomimetic

-produces local anesthesia and vasoconstriction = longer duration of action
Benzocaine
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)
Procaine
Ester anesthetic
Tetracaine
Ester anesthetic
Epinephrine, Levonordefrin, Phenylephrine
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