Term
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Definition
| Acts as an Excitatory (nicotinic, M1, M3 receptors) and as an inhibitory (M2, M4 receptors) neurotransmitter |
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Term
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Definition
Major inhibitory NT present in the CNS; found in brian interneurons, especially in the amygdala region
Binding of GABA to the GABA receptor results in an increase in the inward movement of chloride ion |
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Term
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Definition
| antagonist of GABA action |
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Term
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Definition
| inhibitory NT found in interneurons of the spinal cord; similar to GABA |
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Term
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Definition
excitatory NT present at high concentrations in the brain
AMPA, Kainate, NMDA Receptors |
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Term
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Definition
catecholamine NT located in the basal ganglia and other regions of the limbic system
Excitatory - D1, D5
Inhibitory - D2 |
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Term
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Definition
catecholamine NT located within the hypothalamus, in the limbic system, and at the sympathetic effector synapses
Excitatory - Alpha1, Beta
Inhibitory - Alpha2 |
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Term
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Definition
NT located in the midbrain and pons and extending to all CNS regions
Excitatory - 5-HT2, 5-HT3
Inhibitory - 5-HT1 (subdivided into 5 subtypes: A,B,D,E,F) |
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Term
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Definition
colorless gas; nonflammable, non-irritating to the respiratory tract; produces little systemic toxicity; rapid induction and emergence; no muscle relaxant activity, but does produce analgesia
Use: adjunct to halothane and other volatile anesthetic agents, used solely for brief procedures |
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Term
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Definition
Advantages: moderately potent; rapid induction and emergence properties; non-flammable and non-irritating to the respiratory tract; los incidence of post-operative nausea and vomiting; causes bronchodilation
Disadvantages: produces little analgesia, suppression of visceral reflexes, or skeletal muscle relaxation; relaxes uterine smooth muscle
CV effects: causes hypotension by direct myocardial depression and by depression of baroreceptor reflexes (decrease CO); sensitizes the myocardium to catecholamines ( increases chance of arrythmias)
CNS effects - increase cerebral blood flow; respiratory depression which usually necessitates supplemental ventilation
Metabolism: P450 (15-20%)
Use - maintenance agent for surgical anesthesia |
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Term
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Definition
CV: hypotensive actions similar to those of halothane; less likely to sensitize the myocardium to catecholamine
CNS: may induce seizures of short duration; increases cerebral blood flow similar to halothane; depresses respiration
Effects on muscle - produces more skeletal muscle relaxation that halothane; potentiates the actions of neuromuscular blockers; relaxes bronchial and uterine smooth muscle
Biotransformation- 2-10%
Use - Maintenance of anesthesia |
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Term
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Definition
Advantages to Halothane: more rapid induction and emergence; less likely to sensitize myocardium to catecholamines; does not reduce CO; less likely to increase intracranial pressure; less metabolism (0.2%), with no reported hepatic or renal toxicity
Effects on muscle: produces skeletal muscle relaxation and potentiates the actions of neuromuscular blockers; bronchodilates similar to halothane
NO SEIZURES
Disadvantages: respiratory depression, hypotension and uterine relaxation
Use: most widely utilized inhalational anesthetic for maintenance of surgical procedures |
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Term
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Definition
General: least soluble inhalational agent; considerably more potent than N20; very rapid induction and emergence properties; at higher concentrations, it is irritating to the respiratory tract
CV: produces hypotension, but no significant effect on CO; does not sensitize the myocardium to ventricular arrythmias
Respiration similar to that of halothane
Effects on muscle: some skeletal muscle relaxation; potentiates the muscular relaxation of neuromuscular blockers
Biotansformation - 0.02%
Use: outpatient procedures for rapid recovery |
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Term
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Definition
Advantages to desflurane: non-irritating to respiratory tract; more effective bronchodilation; less CV effects
Disadvantages to desflurane: lower volatility; higher extent of metabolism (3%)
Use: Outpatient therapy, particularly in children |
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Term
| Barbiturates - thiopental (pentothal; most common), methohexital, thiamylal |
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Definition
MOA: potentiation of the action of GABA at GABAa; CNS depression, in polysynaptic circuits at which GABA is the NT
Metabolism: Liver; thiopental is metabolized slowly; methohexital is metabolized more rapidly, resulting in the formation of metabolites that may produce side effects
Admin: single or intermittent I.V. injections or continuous infusion; after a single injection of thiopental, consciousness is lost in 10-20 sec and regained in 20-30 min.
Use: induction of anesthesia, which is subsequently maintained by inhalational anesthetic; used solely to provide anesthesia for short procedures with minimal pain
Disadvantages: minimal analgesia; induces cough, laryngospasm, and bronchospasms relatively frequently; does-related respiratory depression; no effective antidote for overdose; contraindicated in patients with variegate or acute intermittent porphyria |
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Term
Neurolept analgesic-anesthetic
Droperidol-Fentanyl |
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Definition
Actions of droperidol - state of reduced anxiety, reduce motor activity, and apathy to the surroundings (neuroleptic state)
Actions of fentanyl - analgesia nd loss of consciousness
Side effects: moderate hypotension, bradycardia, marked respiratory depression, and extrapyramidal side effects (in 1% of pts) |
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Term
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Definition
MOA - antagonism of the actions of glutamate at NMDA receptors
Side effects - skeletal muscle tone may be increased and excessive movements may occur in reaction to sensory stimuli; respiratory depression is minimal; blood pressure and heart rate are often increased; emergence in adults may be delayed and may be accompanied by nightmares and hallucinations; incidence of these effects can be reduced by prior administration of benzo
Use - diagnostic or minor surgical procedures that do not require skeletal muscle relaxation, particularly in children |
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Term
Benzodiazepines -
Diazepam
Lorazepam
Midazolam |
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Definition
MOA - potentiates the action of GABA at GABAa
Effects - induce amnesia and loss of consciousness; minimal analgesia or muscle relaxation; minimal respiratory and CV depression
Use - sole agent in short procedures unaccompanied by pain; induction of anesthesia which is maintained by inhalational anesthetics |
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Term
Propofol
chemically unrelated to other i.v. anesthetics |
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Definition
MOA - potentiates the action of GABA at the GABAa
Effects - induces anesthesia within 1-3 minutes after administration; emergence is more rapid with propofol than with thiopental (rapid metabolism)
Use - brief procedures, particularly in out-patients |
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Term
Opioid anesthetics
fentanyl
sufentanil
alfentanil
remifentanil |
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Definition
MOA- agonism at Mu opioid receptos
Effect - produce potent analgesia that is rapid in onset
Side effects - respiratory depression, bradycardia, hypotension, and muscular rigidity
Use - fentanyl utilized for all phases of anesthesia: pre-oeprative, induciton maintenanc, and post-operative; others for induction or maintenance; for maintenance, co-administerd with muscle relaxants and N2O or small doses of volatile anesthetics; of particular benefit in cardiac surgery |
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Term
Benzodiazepinzes;1/2 life; use
Chlorazepate: 2; anxiety
Traizolam: 3; insomnia
Oxazepam: 8; Anxiety
Chlordiazepoxide: 10; anxiety
Estazolam: 10-24; insomnia
Alprazolam: 12; Anxiety
Lorazepam: 14; anxiety
Temazepam: 11; insomnia
Quazepam; 39; insomnia
Diazepam: 43; Anxiety
Flurazepam: 74; Insomnia |
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Definition
General - utilized as sedative-hyponotic agents since 1961
Clinical uses -
Insomnia - sleep induction (agents with shorter half-lives; sleep maintenance (agents with longer half-lifes)
Anxiety - generalized anxiety disorders and severe anxiety disorders associated with panic attacks; more effective in the therapy of acute anxiety reactions |
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Term
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Definition
MOA - Pharmacological antagonist of the actions of benzos; i.v. administration blocks effects of therapeutic doses of BZs within 1-2 min and of overdoses within 5-15 min
Side Effects - nausea, vomiting, pain at the injection site, and agitation' administration to a patient dependent on BZs may precipitate withdrawal seizures
Use - reversal of BZ-induced anesthesia and BZ overdosage (including zolpidem, zaleplon, and eszopiclone); does not antagonize the action of other drugsw that bind to GABA receptors such as barbiturates, alcohol, and general anesthetics |
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Term
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Definition
MOA - uncertain; partial agonist at 5-HT1a receptors (inhibitory)
Effects, relative to BZs - lacks anticonvulsant actions and skeletal muscle relaxation; minimal interactions with CNS depressants; less sedative; produces no detectable tolerance or physical dependance
Absorption/Metabolism - well-absorbed after oral administration; highly bound to plasma proteins; extensively metabolized in the liver (4% bioavailability)
Side effects - dizziness, nervousness, headache, tachycardia, GI tract disturbances, dose-dependent pupillary constriction
Use - generalized anxiety disorder (equi-effective with diazepam); less effective for acute disorder (anxiolytic effects require 1 week of therapy) |
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Term
| Zolpidem - chemically unrelated to BZs |
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Definition
Mechanism - potentiation of the actions of GABA at GABAa
Effects, relative to BZs - lacks muscle relaxant and anticonvulsant actions (interacts with only a subset of the GABAa receptors); minor effects on REM sleep; slower onset of tolerance and dependance
Absorption/Metabolism - rapidly absorbed after oral administration; short duration of action (t1/2 = 3 hr); extensively metabolized in the liver and the metabolites are excreted in the urine
Side effects - modest daytime drowsiness, dizziness, and gastrointestinal disturbances
Use - widely used for short-term treatment of insomnia |
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Term
| Zaleplon - ultra-short acting hypnotic agent |
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Definition
MOA - potentiation of the actions of GABA at GABAa
Effects - very rapid onset of sleep; exhibits muscle relaxant and anticonvulsant actions; low abuse potential; minimal daytime drowsiness; t1/2 = 1 |
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Term
| Eszopliclone - newer hypnotic agent |
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Definition
MOA - potentiation of the actions of GABA at the GABAa
Effects - t1/2 = 6 hours; minimal daytime drowsiness; low abuse potential
Side Effects - bitter taste, dry mouth, nausea, somnolence
Use - induction of sleep |
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Term
| Ramelteon - novel hypnotic agent |
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Definition
MOA - agonist at melatonin receptors
Effects - reduced sleep latency; no effect on REM sleep; no abuse potential; t1/2 = 2-5 hours; lower effectiveness than GABAa receptor modulators
Side effects- dizziness, somnolence, fatigue
Use - induction of sleep |
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Term
Barbiturates - lipid solubility, protein binding, and metabolism in order from low to high
Phenobatbital - long acting (6-12 hours); anticonvulsant
Amobarbital - Intermediate acting (4-6 hours); sleep sustainer
Secobarbital - short acting (3-4 hours) sleep inducer
Thiopental - ultra short acting (<2 hours); anesthetic |
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Definition
MOA - dose dependent; at low doses potential of acitons of GABA to produce inhibition; at higher doses, direct activation of GABA receptor (GABA agonist); contributes to the non-selectivity of these agents - general neuronal depressants
Liver - induction of the synthesis of P450 enzymes after chronic administration; increase their own metabolism; induces ALAS, which increases porphyrin synthesis; results in an increase in heme required for P450 enzymes
Contraindicated in patients with variegate and acute intermittent porphyria who have defects in the heme biosynthetic pathway
Absorption/Excretion - well-absobed; binding to plasma proteins dependent upon the lipid solubility (increased binding with increased solubility); distribution dependent upon tissue blood supply and upon lipid solubility (the higher the solubility, the more rapid the distribution to the brain and the greater the redistribution to other tissues, such as fat); renal excretion dependent upon lipid solubility (increased lipid solubility results in increased reabsorption); metabolism by the liver results in the formation of more polar metabolites, which are excreted in the urine more efficiently
Side effects - drug hangover (residual CNS depression), paradoxical excitement (geriatric patients), hypersensitivity, and drug interactions (other CNS depressants, numerous drugs and endogenous biochemicals)
Acute intoxication - more lipid soluble the more toxic and more potent than the polar barbiturates
Tolerance and dependence
tolerance: due to decreased barbiturates binding at the GABA receptor and to increase metabolism of barbiturates (induce P450); occurs more readily to the sedative and hypnotic actions than to the anticonvulsant and respiratory depressant actions
physical dependence may occur after chronic administration of high doses
Use - to reduce pre-operative anxiety; to antagonize the effects of CNS stimulants (amphetamines, theophylline); in the emergency treatment of convulsions; in the induction of general anesthesia |
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Term
| Phenytoin, diphenylhydantoin |
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Definition
MOA - stabilization of neuronal membranes; delayed recovery of Na+ channels after depolarization; reduction in spread of electrical discharge from a focus; neither general depression nor sedation
Absorption/Metabolism - slowly absorbed; variable biovailabiltiy; extensively bound to plasma proteins; metabolized by p450
Side effects/toxicity - nystagmus, vertigo, ataxia, behavioral changes, increased frequency of seizure, GI tract disturbances, gingival hyperplasia, osteomalacia, megaloblacstic anemia, hirsutis, hypersensitiby reactions, blood dyscrasias, potential teratogenicity
Drug interactions - competition for plasm protein binding; induction of 2C and 3A CYP families; inhibits the p450 metabolism of other drugs (e.g., warfarin)
Use - generalized tonic-clonic, partial seizures, including those that become secondarily generalized |
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Term
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Definition
MOA - potentiation of the actions of GABA
Effects - elevation of seizure threshold and reduction in spread of discharge from a focus; anticonvulsant actions occur at doses below those for hypnotic actions
Absorption/Distribution/Metabolism - complete but slow; 40-60% bound to plasma proteins; metabolized by p450 enzymes
Side effects - sedation, nystagmus, vertigo, ataxia, hypersensitivity reactions, hyperactivity in children, osteomalacia, megaloblastic anemia, numerous drug interactions (induces 2C, 3A CYP families); abuse potential
Use - alternative agent for generalized tonic-clonic seizures and partial seizures; first-line for neonatal seizures |
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Term
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Definition
Anticonvulsant Effects - similar to those phenobarbital; less potent in elevating the seizure threshold
Metabolism - metabolized to phenobarbital by p450 enzymes
Side effects - sedation, nystagmus, vertigo, ataxia, hypersensitivity reactions, megaloblastic anemia, osteomalacia, blood dyscrasias, acute psychotic reactions
Use - similar pheobarbital |
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Term
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Definition
MOA - inhibiiton of the recovery of Na+ channels after depolarization; reduction in spread of seizure activity from a focus (phenytoin-like mechanism)
Absorption/Metabolism - slow absorption; 75% bound to plasma proteins; metabolized by P450; induction of P450 upon chronic administration (2C9 and 3A CYP families)
Side effects - drowsiness, ataxia, increased frequency of seizures, blurred vision, GI tract disturbances, hypersensitivity reactions, blood dyscrasias, water retention; drug interactions
Use - primary drug for the treatment of all seizures except absence seizures |
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Term
| Oxcarbazepine - analog of carbamazepine |
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Definition
MOA - rapid and extensive metabolism to a monohydroxy derivative, the active metabolite; much less induction of p450 than carbamazepine (induction of 3A4/5 CYPs)
Side effects - sedation, headache, dizziness, hypersensitivity reactions, ataxia, nausea, diplopia, and mild hyponatremia; 25-30% of patients exhibit cross-reactivity between carbamazepine and oxcarbazepine
Use - monotherapy or adjunctive therapy for partial seizures in adults; adjunctive therapy for partial seizures in children |
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Term
| Gabapentin - derivative of GABA |
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Definition
MOA - increase in synaptic concentration of gABA by interaction with a pre0-synaptic receptor; not a GABA agonist
Absorption/Metabolism - well-absorbed; not metabolized
Side Effects - sedation, dizziness, ataxia, nystagmus; antacids reduce bioavailability by ~20% |
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Term
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Definition
MOA - stabilization of neuronal membranes by blocking Na+ channels (phenytoin-like mechanism); other actions: inhibition of the release of glutamate into the synapse
Absorption - rapid and complete absorption; 98% bioavailability
Side effects - dizziness, ataxia, somnolence, diplopia, blurred vision, nausea and vomiting, hypersensitivity reactions (may be life-threatening)
Use 0 adjunct therapy in the treatment of partial and generalized seizures in adults; may have utility in absence seizures |
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Term
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Definition
MOA - inhibition of reuptake of GABA into nerve terminals; increase in availability of GABA for binding to the post-synaptic receptor
Absorption/Metabolism - rapid, near-complete absorption; 96% bound to plasma proteins; extensively metabolized by CYP 3A4
Side effects - dizziness, asthenia, somnolence, nausea, nervousness, irritability, tremor, abdominal pain, and difficulty with concentrations or attention; drug interactions: tiagabine is eliminated more rapidly in patients receiving carbamazepine, phenytoin, primidone and pheobarbital
Use - adjunct therapy of partial seizures, with or without secondarily generalized seizures |
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Term
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Definition
MOA- prolonged inactivation of Na+ channels; potentiation of the action of GABA on Cl- channels; reduction of actions of excitatory NTs
Absorption/Metabolism - rapid, complete absorption; minimal metabolism
Side Effects - psychomotor slowing, difficulty with concentration and speech, somnolence
Use - adjunct therapy in the treatment of partial seizures in adults |
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Term
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Definition
MOA - binds to a synaptic protein; thought to inhibit the release of glutamate and increase the release of GABA
Absorption/Metabolism - rapid, complete absorption; minimal metabolism
Side Effects - most frequent: somnolence, asthenia, infection, and dizziness; minimal drug interactions with other anti-epileptic drugs
Use - adjunct therapy int he treatment of partial onset seizures in adults |
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Term
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Definition
MOA - prolonged inactivation of Na+ channels
Absorption/Metabolism - rapidly, completely absorbed; no active metabolites; minimal drug interactions
Side effects - dizziness, headache, nausea, diplopia
Use - adjunctive therapy in treatment of partial onset seizures in adults |
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Term
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Definition
MOA - inhibition of voltage-activated Ca++ channels in thalamic neurons; inhibition of the recovery of Na+ channels (phenytoin-like mechanism)
Absorption/Metabolism - nearp-complete absorption; excreted primarily as unmetabolized drug
Side effects - somnolence, ataxia, anorexia, fatigue; 1% of patients develop renal calculi
Use - adjunct therapy in the treatment of partial and generalized tonic-clonic seizures |
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Term
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Definition
MOA - inhibition of voltage activated Ca++ channels in thalamic neurons; elevates seizure threshold
Absorption/Distribution/Metabolism - complete absorption; no significant binding to plasma proteins; metabolized by p450 enzymes
Side effects - GI tract disturbances, headache, drowsiness, euphoria, Parkinson-like syndrome, photophobia, hypersensitivity reactions, apalastic anemia
Use - primary treatment of absence seizures |
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Term
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Definition
MOA - inhibition of the recovery of Naa+ channels after depolarization (phenytoin-like mechanism); at higher doses, inhibition of voltage-activated Ca++ channels in thalamic neurons; elevation of seizure threshold and suppression of the spread of seizure activity
CNS effects - minimal sedation and ataxia
Absorption/Distribution/Metabolism - rapid and complete absorption; highly bound (90%) to plasma proteins; inhibits 2C9 CYP
Side effects GI tract disturbances, clotting, abnormalities; adverse - potential teratogenicity, fulminating hepatitis (rare but frequently fatal); contraindication - history of hepatitis or jaundice
Use - primary treatment of absence, myoclonic, and complex partial seizures; also for generalized seizures, if an absence seizure is involved |
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Term
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Definition
MOA - inhibition of voltage-activated Ca++ channels in thalamic neurons; elevation of seizure threshold
Absorption/Distribution/Metabolism - rapid absorption; no significant binding to plasma proteins; metabolized by p450 enzymes to dimethadione (anticonvulsant actions)
Side effects - sedation, hemeralopia, potential teratogenicity, myasthenia-like syndrome; adverse- exfoliative dermatitis, blood dyscrasia, hepatitis, nephrosis
Use - adjunct therapy for absence seizures |
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Term
| Benzodizaepines - potention of actions of GABA; inhibition of the spread of seizure activity from a focus |
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Definition
Clonazepam and clorazepate
Side effects - sedation, ataxia, hypotonia, behavioral disturbances in children, withdrawal reactions after chronic use, interactions with CNS depressants
Use - adjunct therapy of absence and myoclonic seizures; tolerance develops rapidly to anticonvulsant actions
Diazepam
Absorption/Distribution - highly-lipid soluble; extensively bound to plasma proteins
Use - drug choice for status epilepticus |
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Term
Antimuscarinics (including antihistamines)
Trihexyphenidyl - prototype
procyclidine
biperiden
ethopropazine
benztropine
diphenhydramine - well-tolerated; less efficacious |
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Definition
supportive therapy for minimal disease; improve the rigidity, bradykinesia, and tremor; less peripheral anticholinergic efffects
symptoms - cycloplegia, dry mouth, urinary retention, constipation |
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Term
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Definition
Dopamine releaser: indirect-acting sympathomimetic
Therapeutic effect - increase in release of ddopamine from functional dopaminergic neurons that remain in the nigrostriatal pathway
Sid effects - insomnia, dizziness, lethargy, slurred speech, livedo reticularis
Use - as a single agent, more efficacious than anticholinergics but less efficacious than L-Dopa; actions are synergistic in combination with L-Dopa |
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Term
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Definition
Synthesis enhancers
Therapeutic effect - elevation of dopamine levels in the CNS
L-Dopa is a pro-drug of dopamine
L-dopa crosses the blood-brain barrier (dopamine cannot)
L-Dopa is concerted to dopamine by L-amino acid decarboxylase in the CNS and teh periphery
Dopamine is tored in dopaminergic neurons in nigrostriatal pathway
Actions are those of dopamine
CNS - decreased bradycardia, rigidity, tremor; increase alertness; decreased prolactin secretion
periphery - cardiac stimulation, orthostatic hypotension
Absorption/Metabolism: rapidly absorbed from small intestine by an amino acid transport system; affected by rate of gastric emptying, gastric pH, amino acid concentration; 95% decarboxylation in periphery; metabolites excreted in urine
Adverse reactions/Side effects - early -GI disturbances, hypotension, cardiac arrhythmias
LONG - TERM - abnormal involuntary movements (dyskinesias), fluctuations in efficacy ("on-Off" Phenomena), psychiatric disturbances (anxiety, paranoia, hallucination, mania)
Precautions - cardiac disease, affective disorders, major psychoses
Drug interactions
pyridoxine - increases peripheral metabolism of L-Dopa
Phenothiazines - inhibit the actions of dopamine at its receptor
nonselective MAO inhibitors - decrease metabolism of dopamine
anticholinergics - delay gastric emptying
Use - agent of choice; generally utilized in combination with metabolic inhibitors |
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Term
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Definition
Metabolic inhibitor - inhibits the peripheral metabolism of L- Dopa
MOA - inhibition of the activity of L-amino acid decarboxylase in the periphery (inhibits decarboxylation of L-dopa in the periphery); carbidopa cannot cross the blood-brain barrier; increases L-Dopa in the CNS, leading to an increase in dopamine in the CNS
Effects - reduces dose of L-Dopa by 75%; reduces peripheral side effects of L-Dopa (less oncersion to dopamine); counters effects of pyridoxine
Side effects - due to L-Dopa
Use - therapy of choice (L-Dopa + carbidopa) |
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Term
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Definition
Metabolic inhibitor
MOA - inhibition of the activity of catechol-O-methyltransferase in the brain and periphery; decreases formation of 3-O-methyldopa from L-Dopa; 3-O-methyldopa (major metabolite of sinamet)
Effects - increase bioavailability of L-Dopa by 3 to 4 fold
Side effects (in combo with Sinemet) - dyskinesias, sleep disorders, dystonia, GI tract disturbances, muscle cramps, syncope, hallucination, confusion; elevated liver function (6 weeks - 6 mos; 1-3%) |
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Term
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Definition
Metabolic inhibitor
MOA - more selective for SOMT in the periphery (penetrates the CNS poorly)
Actions, relative to tolcapone - shorter duration of action; no evidence of hepatotoxicity
Side effects (combo) - dyskinesias, GI tract disturbances, fatigue, shortness of breath, dizziness, confusion, muscle cramps, anxiety |
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Term
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Definition
Metabolic inhibitor
MOA inhibition of MAOb in the CNS; MAOb activated MPTP to toxic metabolites that destroy dopaminergic neurons
Effects - maintenance of dopamine levels; protection of dopaminergic neurons; reduces the dose of L-Dopa by 10-30%; delays the need for L-dopa by 9 mos.
Side Effects - at therapeutic doses, side effects are minimal; causes no hypertensive crisis in the presence of L-Dopa or foods that contain tyramine
Use - delay progression of disease (single therapy); therapy of parkinsonism in combination with L-Dopa |
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Term
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Definition
First generation DA agonist
MOA - long-acting dopamine agonism at the dopamin receptor; binds to dopamine receptors in CNS, CV system, GI tract
Absorption/metabolism - rapid, partial absorption; Rapid metabolism (t1/2 = 3 hours)
Side effects - Gi tract disturbances, postural hypotension, hallucination, livedo reticularis
Use - monotherapy - early disease; adjunct to L-Dopa in patients with excessive involuntary movements |
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Term
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Definition
Second generation DA agonists
MOA - agonism at D2 receptors
Side effects - syncope, nausea, somnolence
Use - monotherapy - early disease; in combination with L-dopa for advanced disease |
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