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25 Cards in this Set
- Front
- Back
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List first-generation AEDs:
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PHT
CBZ Diazepam PB VPA |
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List second-generation AEDs:
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FBM
GBP LTG TPM TGB OXC ZNS LVT PGB |
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Why aren't we all seizing all of the time?
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brain maintains homeostasis by balancing GABA and glutamate
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What are the two main excitatory NTs in the brain?
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glutamate, aspartate
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What is the main inhibitory NT in the brain?
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GABA
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Where is the big money at in AEDs?
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neuromodulators (regulate the modulatory system)
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What are the main targets for controlling seizures?
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Na channels
Ca channels GABAergic transmission glutamatergic transmission |
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How can sodium channels be altered to decrease seizure frequency?
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Decreasing the action potential frequency will prevent hyperexcitation
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What are the three types of Ca channels, and what can each do to decrease seizure frequency?
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T-type--decrease thalamocortical reverberations (decreased swings in thalmus regulation)
L-type--decrease cortical excitation N-type--decrease neurotransmitter release |
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What are the four targets of GABAergic transmission, and how does each affect seizure control?
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increase GABAa receptor activity
increase GABA synthesis and release decrease GABA reuptake increase serotonin release all of this increase inhibtion |
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What are the two targets of glutamatergic transmission, and what effect does each have?
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--inhibit glutamate receptors
--decrease glutamate synthesis and release both decrease excitation |
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Where do Ca and Na modulations take place?
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presynaptically
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Which drugs affect sodium channels?
How do they work? |
PHT
CBZ PB VPA LTG? prolongs inactivated state of sodium channels, but it is concentration dependent |
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Which drugs affect t-type calcium channels?
How do they work? |
ethosuximide
valproate --only effective for absence seizures --slows flux of Ca2+ through channel |
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Which drugs have a presynaptic effect on glutamine release?
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--adenosine (caffeine, theophylline antagonize this, makes seizures worse)
--GABA agonists (baclofen) --BZDs PHT CBZ LTG |
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What are the three types of glutamate receptors?
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NMDA, AMPA, Kalnate
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Describe the action of GABA:
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interacts post-synaptically which causes Cl- permeability which causes hyperpolarization which causes inhibitory post-synaptic potential
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Which enzyme breaks down GABA?
What problems can you have with too much GABA? |
--GABA transaminase
--narrowing of visual field |
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How does tiagabine work?
How do BZDs work? |
GABA reuptake inhibitor
keep Cl- channels open and increase hyperpolarization |
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What is the main difference between first generation and second generation AEDs?
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first generation AEDs are one trick ponies
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How does LTG work?
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Na channel inactivation prolongation
inhibits NT relase (glutamate and GABA) |
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What is different about OXC and CBZ?
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OXC goes through reduction, does not cause autoinduction
CBZ goes through oxidation and causes autoinduction bind onto different sodium and calcium channels |
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How does Gabapentin work?
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binds onto calcium channels (does not act like GABA like it was designed to)
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How does LTG work?
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decreases neuronal activity (presynaptic modulation)
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How does TPM work?
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blocks Na channels
modeulates kainate and ampa receptors enhances GABA receptor activity |
