quiz gecko.pdf

1. What are the ways that we can put the brakes on excitation? block or interfere with voltage-gated Na+ channels; block or interfere with voltage-gated Ca+ channels; interfere with synaptic vesicle machinery; block excitatory glutamate receptor signaling 2. What are the ways that we can put the gas...

1. What are the ways that we can put the brakes on excitation? block or interfere with voltage-gated Na+ channels; block or interfere with voltage-gated Ca+ channels; interfere with synaptic vesicle machinery; block excitatory glutamate receptor signaling 2. What are the ways that we can put the gas on inhibition? block GABA transporters; block GABA-transaminase; promote GABA-A activation 3. What are the most common AE of ASMs? CNS depressing/sedating effects 4. T/F. Suicidal ideation is noted with many ASMs. true 5. What is the additional warning for many ASMs? slow withdrawal due to increased risk of seizure recurrence 6. What is the MOA for voltage-gated Na+ channel blockers? reduce VGSC activity to reduce high frequency APs 7. Which VGSC blockers facilitate transition to inactivated state? phenytoin, fosphenytoin, lamotrigine 8. Which VGSC blockers prolong the inactivation state? lacosamide, valproic acid 9. What are the shared AE of VGSC blockers? drowsiness, dizziness, ataxia 10. What are some rare but serious AE of VGSC blockers? increased risk of arrhythmias or cardiac failure; blood dyscrasias; delayed hypersensitivity 11. What is the MOA of phenytoin? block voltage-gated sodium channels 12. What is phenytoin used for? seizures, status epilepticus 13. T/F. Phenytoin (Dilantin) has poor water solubility. true 14. Why is phenytoin (Dilantin) slightly acidic? due to electron withdrawing effect of the benzene rings 15. What is phenytoin (Dilantin) metabolized by? 2C9 and 2C19 16. What does phenytoin (Dilantin) induce? 3A and 2C19 17. What is the MOA of fosphenytoin? blocks voltage-gated sodium channels 18. What is the prodrug of phenytoin? fosphenytoin 19. What is fosphenytoin used for? seizures 20. T/F. Fosphenytoin is NOT water-soluble. false 21. What is fosphenytoin activated by? phosphatases 22. What is fosphenytoin metabolized by? 2C9 and 2C19 23. What does fosphenytoin induce? 3A and 2C19 24. What is the BBW with phenytoin (Dilantin) and fosphenytoin? CV risk with rapid infusion 25. What is the MOA of carbamazepine (Tegretol)? voltage-gated sodium channel blocker 26. What is carbamazepine (Tegretol) used for? seizures, neuralgia, bipolar disorder, neuropathic pain 27. T/F. Carbamazepine (Tegretol) is indicated for absence seizures. false 28. What is carbamazepine (Tegretol) metabolized by? 3A4 29. T/F. Carbamazepine (Tegretol) has an active metabolite. true 30. What does carbamazepine (Tegretol) induce? 3A, 2B6, 2C9 31. What are the BBW of carbamazepine (Tegretol)? HLA-B* 1502 allele dermatologic reactions; aplastic anemia, agranulocytosis 32. What is the MOA of oxcarbazepine (Trileptal)? voltage-gated sodium channel blocker 33. What is oxcarabazepine (Trileptal) used for?seizures, neuralgia 34. What is oxcarbazepine (Trileptal) metabolized by? 3A4 35. What is the active metabolite of oxcarbazepine (Trileptal)? lizcarbazepine 36. What is the MOA of eslicarbazepine acetate? voltage-gated sodium channel blocker 37. What is eslicarbazepine acetate used for? seizures 38. What is the prodrug of eslicarbazepine? eslicarbazepine acetate 39. Eslicarbazepine acetate is the ____-enantiomer of licarbezapine. S 40. What is eslicarbazepine acetate activated by? hydrolysis 41. What is the MOA of lamotrigine (Lamictil)? block voltage-gated sodium, voltage-gated calcium channels, and inhibits glutamate release 42. What is lamotrigine (Lamictil) used for? seizures, neuralgia, bipolar disorder 43. What is lamotrigine (Lamictil) metabolized by? glucoronidation 44. What is the BBW of lamotrigine (Lamictil)? skin rashes 45. What is the MOA of lacosamide? block voltage-gated sodium channels 46. What is lacosamide indicated for? seizures 47. What is the MOA of rufinamide? not fully clear but seems to prolong inactivation of voltage-gated sodium channels 48. What is rufinamide used for? seizures 49. What is rufinamide metabolized by? hydrolysis 50. What does rufinamide induce? 3A 51. What is the MOA of cenobamate (Xcopri)? voltage-gated Na+ channel blocker and GABA-A PAM 52. What is cenobamate (Xcopri) used for? seizures 53. What is cenobamate (Xcopri) metabolized by? glucoronidation and multiple CYPs 54. What is the MOA of primidone? voltage-gated Na+ channel blocker, plus active metabolite is GABA-A PAM 55. What is primidone used for? seizures, tremor 56. What is primidone metabolized by? 2C9 57. What are the 2 active metabolites of primidone? phenobarbital, PEMA 58. What does primidone induce? 3A 59. What is the MOA of valproate (Depakote)? enhances inactivation by suppressing rapid Na+ currents, blocks NMDA-R, increases GABA 60. What is valproate (Depoakote)? seizures, bipolar disorder, migraine prophylaxis, status epilepticus 61. What is valproate (Depakote) metabolized by? glucoronidation 62. What is the BBW of valproate (Depakote)? hepatotoxicity; pancreatitis; fetal neural tube defects; enhanced toxicity in patients with mitochondria disease 63. What is the MOA of zonisamide? t-type voltage-gated calcium channel blocker, voltage-gated Na+ blocker, and weak inhibitor of carbonic anhydrase 64. What is zonisamide metabolized by? 3A4 65. What is the MOA of ethosuximide? t-type voltage-gated calcium channel blocker 66. What is ethosuximide metabolized by? 3A4 67. What is the MOA of methsuximide? t-type voltage-gated calcium channel blocker 68. What is methsuximide metabolized by? 3A4 69. What is the active metabolite of methsuximide? N-desmethsuximide 70. What happens when you inhibit T-type calcium channels? currents serve as 'pacemaker' in thalamic neurons that are thought to be responsible for some absence seizure attacks 71. What happens when you inhibit the alpha-2 delta subunit of P/Q and N-type calcium channels? reduce channel conductance and membrane trafficking to reduce neurotransmitter release 72. What is the MOA of gabapentin (Neuontin)? binds alpha-2 delta voltage-gated Ca+2 calcium channel 73. What is gabapentin (Neurontin) used for? seizures, neuralgia, anxiety disorder, neuropathic pain, fibromyalgia, restless leg disorder, alcohol use disorder 74. T/F. Gabapentin (Neurontin) interacts with GABA-R.false 75. What is the MOA of gabapentin enacarbil? binds alpha-2 delta voltage-gated Ca+2 calcium channel 76. What is the prodrug to gabapentin? gabapentin enacarbil 77. What is gabapentin enacarbil used for? neuralgia, restless leg disorder 78. What is gabapentin enacarbil activated by? hydrolysis 79. What is the MOA of pregabalin (Lyrica)? binds alpha-2 delta voltage-gated Ca+2 calcium channel 80. What is pregabalin (Lyrica) used for?seizures, neuralgia, anxiety disorders, neuropathic pain, fibromyalgia, restless leg disorder 81. Pregabalin (Lyrica) __________ channel conductance and inhibits channel trafficking. reduces 82. Pregabalin (Lyrica) is marketed as _____-enantiomer. S 83. What is the MOA of levetiracetam (Keppra) and brivaracetam? bind SV2A and disrupt excytosis 84. What is levetiracetam (Keppra) used for? seizures, status epilepticus 85. Levetiracetam is the ____-enantiomer of etiracetam. S 86. What is brivaracetam (Briviact) used for? seizures 87. What is brivaracetam (Briviact) metabolized by? 2C19 88. What is the 4-propyl analog of levetiracetam? brivaracetam 89. What are the glutamate receptor blockers? perampanel (Fycompa), topiramate (Topamax), felbamate 90. What is the MOA of topiramate (Topamax)? antagonize AMPA and KA-R 91. What is topiramate (Topamax) used for? seizures, migraine prophylaxis, cluster headaches, alcohol use disorder, binge eating disorder 92. What is the sulfamate-substituted fructose derivative? topiramate (Topamax) 93. What is the MOA of perampanel? highly selective, non-competitive AMPA antagonist 94. What is perampanel used for? seizures 95. What is perampanel metabolized by? 3A 96. What is the BBW of perampanel? serious psychiatric and behavioral reactions (hostility and anger) 97. What is the MOA of felbamate? NMDA-R blocker; specifically antagonizes the glycine binding site; also potentiates GABA-A receptor response 98. What is felbamate used for? seizures 99. What is felbamate metabolized by? 3A4 and 2C19 100. What does felbamate inhibit? 2C19 101. What is the BBW of felbamate? aplastic anemia, hepatic failure 102. What is the MOA of tiagabine (Gabitril)? selectively inhibits GABA transporter GAT-1 103. What is tiagabine (Gabitril) used for? seizures 104. What is tiagabine (Gabitril) metabolized by? 3A4 105. What is the MOA of vigabatrin (Sabril)? irreversible inhibitor of GABA-transaminase 106. What is vigabatrin (Sabril) used for? seizures 107. T/F. Vigabatrin (Sabril) has a REMS program. true 108. What is the BBW of vigabatrin (Sabril)? permanent vision loss 109. What are the barbiturates used for seizures? phenobarbital, pentobarbital 110. What are the BZDs used for seizures? lorazepam (Ativan), midazolam, diazepam (Valium), clonazepam (Klonopin), clobazam (Onfi) 111. What is the cannabinoid isolated from hemp? epidiolex 112. What is epidiolex metabolized by? 3A4 113. What is epidiolex used for? childhood forms of epilepsy: Lennox-Gastaut and Dravet Syndromes and Tuberous Sclerosis