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  1. Barbiturates: Phenobarbital, pentobarbital, thiopental, secobarbital.

    Facilitate GABAA action by inc duration of Cl− channel opening, thus dec neuron firing (barbidurates inc duration). Contraindicated in porphyria.
  2. Barbiturates toxicity
    Respiratory and cardiovascular depression (can be fatal); CNS depression (can be exacerbated by EtOH use); dependence; drug interactions (induces cytochrome P-450).Overdose treatment is supportive (assist respiration and maintain BP).
  3. Benzodiazepines:  Diazepam, lorazepam, triazolam, temazepam, oxazepam, midazolam, chlordiazepoxide,alprazolam

    • Facilitate GABAA action by inc frequency of Cl− channel opening. dec REM sleep. Most have long half-lives and active metabolites(exceptions: Alprazolam, Triazolam,Oxazepam, and Midazolam are short actingŽ higher addictive potential).
    • ATOM
    • “Frenzodiazepines”inc frequency. Benzos, barbs, and EtOH all bind theGABAA receptor, which is a ligand-gated Cl−channel..
  4. Benzodiazepines Treat overdose with
    flumazenil (competitive antagonist at GABA benzodiazepine receptor).
  5. Nonbenzodiazepine hypnotics are
    Zolpidem, Zaleplon, esZopiclone. “All ZZZs put you to sleep.”
  6. Anesthetics—generalprinciples
    CNS drugs must be lipid soluble (cross the blood-brain barrier) or be actively transported.Drugs with  dec solubility in blood = rapid induction and recovery times.
  7. Anesthetics—generalprinciples 
    Drugs with inc solubility in lipids = inc potency = 1/MAC

    MAC = Minimal Alveolar Concentration (of inhaled anesthetic) required to prevent 50% of subjects from moving in response to noxious stimulus (e.g., skin incision). Examples: nitrous oxide (N2O) has low blood and lipid solubility, and thus fast induction and low potency. Halothane, in contrast, has  high lipid and blood solubility, and thus high potency and slow induction.
  8. halothane toxicity
  9. methoxyflurane toxicity
  10. enflurane toxicity
  11. malignant hyperthermia tx
  12. Local anesthetics Esters
    procaine, cocaine, tetracaine
  13. Local anesthetics Amides—
    lIdocaIne, mepIvacaIne, bupIvacaIne (amIdes have 2 I’s in name).
  14. Local anesthetics
    Block Na+ channels by binding to specific receptors on inner portion of channel. Preferentially bind to activated Na+ channels, so most effective in rapidly firing neurons.
  15. 3°  amine local anesthetics moa
    penetrate membrane in uncharged form, then bind to ion channels as charged form.
  16. bupivacaine toxicity
    severe cardiovascular toxicity
  17. cocaine toxicity
  18. benzocaine toxicity
  19. Neuromuscular blocking drugs 

    Succinylcholine—strong ACh receptor agonist; produces sustained depolarization and prevents muscle contraction
  20. Neuromuscular blocking drugs Depolarizing
    Reversal of blockade:
    • ƒƒ-Phase I (prolonged depolarization)—no antidote. Block potentiated by cholinesterase inhibitors.ƒƒ
    • -Phase II (repolarized but blocked; ACh receptors are available, but desensitized)—antidote is cholinesterase inhibitors.
  21. Neuromuscular blocking drugs Depolarizing 
    include hypercalcemia, hyperkalemia, malignant hyperthermia.
  22. Neuromuscular blocking drugs 

    Tubocurarine, atracurium, mivacurium, pancuronium, vecuronium, rocuronium
  23. Tubocurarine, atracurium, mivacurium, pancuronium, vecuronium, rocuronium

    competitive antagonists—compete with ACh for receptors.
  24. Neuromuscular blocking drugs Nondepolarizing

    Reversal of blockade
    neostigmine (must be given with atropine to prevent muscarinic effects suchas bradycardia), edrophonium, and other cholinesterase inhibitors
  25. Dantrolene moa
    Prevents release of Ca2+ from the sarcoplasmic reticulum of skeletal muscle.
  26. Dantrolene use
    Malignant hyperthermia and neuroleptic malignant syndrome (a toxicity of antipsychotic drugs).
  27. Baclofen moa
    Inhibits GABAB receptors at spinal cord level, inducing skeletal muscle relaxation.
  28. Baclofen use
    Muscle spasms (e.g., acute low back pain).
  29. Cyclobenzaprine moa
    Centrally acting skeletal muscle relaxant. Structurally related to TCAs, similar anticholinergic side effects.
  30. Cyclobenzaprine use
    Muscle spasms.
  31. Parkinson disease drugs
    • Dopamine agonists
    • inc dopamine availability
    • inc L-DOPA availability
    • Prevent dopamine breakdown
    • Curb excess cholinergic activity
  32. Curb excess cholinergi cactivity for Parkinson disease  with
    Benztropine (Antimuscarinic; improves tremor and rigidity but has little effect on bradykinesia).   Park your Mercedes-Benz.
  33. Selegiline— moa
    blocks conversion of dopaminein to 3-MT by selectively inhibiting MAO-B.
  34. Entacapone, tolcapone—moa
    prevent peripheral L-dopa degradation to 3-O-methyldopa (3‑OMD) by inhibiting COMT.
  35. Levodopa (l-dopa)/carbidopa— moa
    • inc l-DOPA availability
    • carbidopa blocks peripheral conversion of l-DOPA to dopamine by inhibiting DOPA decarboxylase.
    • Also reduces side effects of peripheral l-dopa conversion into dopamine(e.g., nausea, vomiting).
  36. Amantadine
    MOA, use  and toxicity
    • (inc dopamine release and dopamine reuptake); also used as an antiviral against influenza A and rubella;
    • toxicity =ataxia, livedo reticularis.
  37. Dopamine agonists 

  38. Bromocriptine
  39. Dopamine agonists  

    Non-ergot (preferred)—
    pramipexole, ropinirole
  40. Parkinson disease drugs
    • BALSA:
    • Bromocriptine
    • Amantadine
    • Levodopa (with carbidopa)
    • Selegiline (and COMT inhibitors)
    • Antimuscarinics
  41. l-dopa (levodopa)/carbidopa toxicity
    Arrhythmias from inc  peripheral formation of catecholamines. Long-term use can lead to dyskinesia following administration (“on-off” phenomenon), akinesia between doses.
  42. Alzheimer drugs
    • Memantine
    • Donepezil, galantamine, rivastigmine, tacrine
  43. Memantine moa and toxicity
    NMDA receptor antagonist; helps prevent excito toxicity (mediated by Ca2+).

    toxicity: Dizziness, confusion, hallucinations
  44. Donepezil, galantamine, rivastigmine, tacrine
    moz and toxicity
    • AChE inhibitors.
    • TOXICITY : Nausea, dizziness, insomnia.
  45. Neurotransmitter changes in Huntington
    dec GABA, dec ACh, inc dopamine.
  46. Huntington disease tx
    Tetrabenazine and reserpine

    receptor antagonist.
  47. Tetrabenazine and reserpine— moa
    inhibit vesicular monoamine transporter (VMAT); limit dopamine vesicle packaging and release.
  48. Triptans : Sumatriptan   moa
    5-HT1B/1D agonists. Inhibit trigeminal nerve activation; prevent vasoactive peptide release;induce vasoconstriction.
  49. Triptans : Sumatriptan toxicity
    Coronary vasospasm (contraindicated in patients with CAD or Prinzmetal angina),mild paresthesia

Card Set Information

2015-07-26 05:04:00
nuro page 497-502
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