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blocks NMDA channel, thus inhibiting the opening and depolarization |
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blocks NMDA channel, thus inhibiting the opening and depolarization |
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inhibits the GABA transaminase enzyme (which causes higher levels of GABA,which reduces membrane excitability) and is use to inhibit seizures |
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GABA-A Competitive agonist (binds at same site as GABA)
Increase Cl- content within the cell |
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GABA-A Antagonist
(pro-convulsants) decrease the opening frequency and mean open time of the Cl- channel |
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GABA-B receptor agonist (reduce spasticity associated with motor disorders, Huntingtons Chorea)
reduces voltage Ca++ gated conductance, and increases K+ conductance out of the cell |
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GABA-B receptor antagonist (experimental) |
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Glycine receptor antagonist
causes massive excitation and soon after death (pesticide) |
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presynaptic alpha 2 agonist, reduces NE lowers blood pressure |
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selective NE reuptake inhibitor at presynaptic cleft, used to treat (ADHD) |
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inhibit NET, which prolongs and potentiates the effects of NE |
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5-HT3 receptor (excitatory ionotropic receptors)antagonist used in preventing and treating vomiting caused by radiation therapy in cancer patients |
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5-HT1a agonist used to treat anxiety (decrease cAMP resulting in neuronal inhibition) |
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Alzheimer's disease treatment cholinesterase inhibitor, mild to moderate AD may also act as a nicotinic and muscarinic (M1) agonist |
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Alzheimer's disease treatment cholinesterase inhibitor, mild to moderate AD |
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Alzheimer's disease treatment cholinesterase inhibitor, mild to moderate AD |
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N-methyl D-aspartate (NMDA) antagonist
For treatment of moderate to severe AD.
Because NMDA antagonists work very differently from cholinesterase inhibitors, the two types of drugs can be prescribed in combination. |
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Definition
Metabolic precursor to Dopamine. Tyrosine hydroxylase is normally the rate limiting enzyme, for L-Dopa formation, thus giving L-dopa directly bypasses the rate limiting step, leading to increased dopamine synthesis. L-dopa is taken up by remaining dopamine neurons in the brain if it can get there. The major problem with L- Dopa, is that it is significantly metabolized in GI and peripheral tissues. L-Dopa can be converted to dopamine by dopa-decarboxylase in the periphery and then degraded peripherally by peripheral enzymes (MAO), thus preventing L-Dopa from getting where it needs to go (the brain). To prevent this problem, L-Dopa is given with Carbidopa. |
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Dopa decarboxylase inhibitor
Does not cross the BBB, thus it inhibits L-Dopa from being converted to dopamine in the periphery and ensures L-Dopa gets into the brain. Since it doesn’t cross the BBB, dopa decarboxylase in the brain can convert L-Dopa into dopamine. Diminishes metabolism of Levodopa. Reduces dosing concentration side-effects, as you no longer have to give tons of L-dopa in order to get it into the brain. |
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mixed preparation of L-Dopa and Carbi-dopa |
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D2 dopamine receptor agonist
Little response in patients who do not respond to L-dopa
Parkinson's disease treatment drug that mimics dopamine activity D2 dopamine receptor agonist |
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Parkinson's disease treatment drug that mimics dopamine activity D1/D2 dopamine receptor agonist |
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Parkinson's disease treatment antiviral
Less potent than L-dopa, but has fewer side-effects. Mechanism of action in helping PD is poorly understood. |
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Parkinson's disease treatment MAOi-B |
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a COMT inhibitor (not a dopamine eplacement drug): reduces breakdown of dopamine formed from L-Dopa, thus prolonging its effect |
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mixed preparation of L-Dopa and Carbi-dopa and Entacapone |
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Parkinson's disease treatment muscarinic acetylcholine receptor antagonist
Muscarinic acetylcholine receptors exert an inhibitory effect on dopaminergic nerve terminals, suppression of which compensates for a lack of dopamine. |
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Parkinson's disease treatment muscarinic acetylcholine receptor antagonist
Muscarinic acetylcholine receptors exert an inhibitory effect on dopaminergic nerve terminals, suppression of which compensates for a lack of dopamine. |
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Huntington's disease treatment dopamine antagonist |
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Prednisolone (i.e. a corticosteroid) |
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Definition
Corticosteroids work by decreasing immune system antibody production and by reducing myelin swelling and inflammation (multiple sclerosis treatment) |
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Interferon-Beta (e.g. Avonex, Betaseron, Rebif) |
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Definition
multiple sclerosis treatment regulates immune system |
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Glatiramer acetate (Copaxone®, formerly known as copolymer-1) |
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Definition
first non-interferon, nonsteroidal medication that effectively reduces new brain lesions
thought to stimulate T cells in the body’s immune system to change from harmful, pro-inflammatory agents to beneficial, anti-inflammatory agents that work to reduce inflammation at lesion sites |
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Mitoxantrone (Novantrone®) |
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Definition
antineoplastics (i.e. cancer-drugs)
It acts in MS by suppressing the activity of T cells, B cells, and macrophages that are thought to lead the attack on the myelin sheath |
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Potent anesthetic (inhaled)
Weak analgesic
Bradycardia and potental cardiac arrhythmias
Hypotension (phenylephrine: vasoconstriction)
Heavily metabolized in the liver, to toxic hydrocarbons with repeated use not hepatotoxic in children, and has pleasant odor, so used with kids
Malignant Hyperthermia (excessive Ca++ release from sarcoplasmic reticulum skeletal muscle) results in acidosis, muscle contraction, and increased body temp |
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neuromuscular blocker, blocks calcium channels (inhaled)
hyerthermia |
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Similar to Halothane (less potent, faster induction and recovery, less toxicity) (inhaled)
Can cause seizures and Malignant hyperthermia |
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Similar to Halothane and Enflurane but even low side-effect profile (less potent, fast induction and recovery, less toxicity, no-seizure effect) (inhaled)
Most widely used |
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Rapid induction and recovery (i.e. low blood-gas coefficient) (inhaled)
Weak general anesthetic (but low anesthetic potency, must be coadministered often with a volatile anesthetic)
Strong Analgesic
Can cause a transient diffusion hypoxia (retards oxygen uptake), but this is usually only important with patients with respiratory conditions |
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(barbiturate) Intravenous anesthetic
CNS depressant
very lipid soluble but short acting (thus used as an induction agent)
Poor analgesic
Anesthetic action stops due to redistribution to other organs |
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(non-barbituate) Intravenous anesthetic
Similar to thiopental
Thought to act via GABA-A
Used only as an induction agent
Does not induce cardiac and respiratory depression
Frequent involuntary muscle movements |
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(Intravenous anesthetic)
Very rapidly metabolized, thus rapid recovery
Used for induction or maintenance of anesthesia
Poor analgesia (thus requires coadministration of opioids)
Lowers intracranial pressure |
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Short acting non-barbituate (Intravenous anesthetic)
Provides “Dissociative Anesthesia” with sensory loss, sedation, amnesia, and immobility (also patient may appear awake but does not feel pain or remember)
Increases blood-flow, blood-pressure and cardiac out-put
Used mostly in children due to enhanced hallucinations in adults |
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Lidocaine Procaine Bupivicaine |
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