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P2 Spring: PHRM 845 > Exam 3: Seizures (Yang) > Flashcards

Exam 3: Seizures (Yang) Flashcards

(54 cards)

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1
Q

What does focal onset of seizures mean?

A
  1. aware and impaired awareness
  2. motor and non-motor onset
  3. may progress from focal to bilateral tonic-clonic
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1
Q

what does generalized onset of seizures mean?

A
  1. motor (clonic or other motor)
  2. non-motor (absence seizures)
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2
Q

what does unknown onset of seizures mean?

A
  1. motor (clonic or other motor)
  2. non-motor
  3. unclassified
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3
Q

What is the MOA of a focal seizure? how does it progress to bilateral?

A
  1. spreads from one part of brain (neocortex)
  2. progress to secondary generalized via projections to the thalamus
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4
Q

What is a primary generalized seizure?

A

Propagate via diffuse interconnection between thalamus and cortex (no discrete focus). Earliest clinical sign show both brain hemispheres

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5
Q

What is the EEG activity of a focal wave?

A

only one hemisphere and very normal but some tight temporal activity

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6
Q

what is the EEG activity of the generalized (tonic-clonic) wave?

A

all over the place and huge lines; involves both hemispheres

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7
Q

What is impaired awareness? What goes on within this seizure?

A
  1. most common among focal seizures
  2. clouding of consciousness
  3. aura is common
  4. postictal state due to impaired awareness
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8
Q

What is an absence: typical or atypical seizure? What goes on within this>

A
  1. brief loss of consciousness
  2. may not realize until after seizure
  3. no convulsions, aura, or postictal period
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9
Q

What seizure causes an aura?

A

focal to bilateral

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10
Q

What drugs aggravate or increase risk of seizures?

A
  1. alcohol
  2. theophylline
  3. CNS stims
  4. bupropion
  5. oral contraceptives
  6. withdrawal from depressants
  7. clozapine
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11
Q

what occurs during hyperpolarization of PDS?

A

influx of cl- resulting in GABAA receptor activation

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12
Q

In the PDC (paroxysmal depolarizing shift), what neurons are involved?

A
  1. Inhibitory Interneuron (GABAergic)
  2. Excitatory pyramidal neurons (glutamatergic)
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13
Q

What happens in the depolarization phase of PDS?

A

Activation of AMPA and NMDA by glutamate and Ca+ leading to influx of Ca2+

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14
Q

What happens in the hyperpolarization phase of PDS?

A

activation of GABA leading to influx of Cl- and efflux of K+

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15
Q

What is neuronal signaling?

A

depolarization; dampened by feed forward and feedback inhibition. Disrupted E/I balance

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16
Q

What is the MOA of anticonvulsant drugs?

A

stabilize and reduce neuronal excitability (reduce E/I balance)

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17
Q

How can we use the MOA of anticonvulsants? What drugs?

A
  1. enhance GABA-mediated neuronal inhibition (vigabatrin, tiagabine, benzos)
  2. antagonism of excitatory transmitters (glutamate)
  3. other targets (kepra)
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18
Q

What drug leads to non-linear PK? How is it eliminated?

A
  1. Phenytoin
  2. it is elimination kinetics are dose-dependent
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19
Q

What drug interactions are there with phenytoin?

A
  1. displaced from plasma proteins by other drugs
  2. induces P450s
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20
Q

what are the side effects of phenytoin?

A
  1. arrhythmia
  2. visual
  3. ataxia
  4. GI symptoms
  5. gingival hyperplasia, hirustism (hair growth)
  6. hypersensitivity reactions (skin rash)
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21
Q

What drug is phenytoin?

22
Q

what drug is “azepines”?

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A

iminostilbenes

23
Q

What is the MOA of oxcarb and carb?

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A

binds and stabilizes the inactivated state of Na+ channels

24
what is the drug drug interactions of oxcarb and carb?
CYP P450
25
what toxicity is there with oxcarb and carb?
1. Blurred vision 2. ataxia 3. GI disturbances 4. sedation at high doses 5. serious skin rash (SJS) 6. DRESS
26
what drugs are barbiturates?
phenobarbital and primidone
27
what is the drug of choice in infants up to 2 months of age ?
phenobarbital
28
what is the MOA of phenobarbital?
binds to allosteric regulatory site on the GABAA receptor increasing Cl- duration opening channels and thus enhancing signaling
29
what drug interactions are there with phenobarb?
CYP P450
30
what toxicity is there with phenobarb?
1. sedation 2. pysical dependence
31
What drugs are benzos?
diazepam and clonazepam
32
what is the MOA of benzos?
binds to allosteric regulatory site on the GABAA receptor increasing Cl- duration opening channels and thus enhancing signaling
33
what is clonazepam useful for?
for acute tx of epilepsy and absence seizures
34
what is diazepam useful for? How is it admininstered?
tonic-clonic seizures; often admin as rectal gel for acute control of seizure activity
35
what SEs do benzos have?
1. sedation 2. physical dependence 3. not useful for chronic tx
36
what is Vigabatrin?
irreversible inhibitor of GABA-T, the enzyme responsible for degrading GABA
37
what are the SEs of vigabatrin?
1. sedation 2. depression 3. visual field defects
38
what is the MOA of tiagabine?
inhibits GAT-1
39
what are the SEs of tiagabine?
1. sedation 2. ataxia
40
what are pre-synaptic targets in the GABAergic response?
GAT-1 and GABA-T
41
what are post synaptic targets in the GABAergic repsonse?
GABAA
42
what is the MOA of felbamate?
NMDA antagonist
43
what are the SEs of felbamate?
severe hapatitis
44
what is the MIA of topiramate?
AMPA and kiainte antagonist
45
what are the SEs of topamax?
1. confusion 2. cognitive dysfunction 3. sedation 4. vision loss
46
what is the class of ethosuximide?
succinimides
47
what is the MOA of ethosuximide?
blocks T-type CA2+ channels in thalamic neurons
48
what are the SEs of ethosuximide?
1. GI distress 2. sedation
49
what are T-type Ca2+ channels thought to be involved in generating?????? What signaling?
1. rhythmic discharge of an absence attack 2. thalamocorticol signaling
50
what are the presynaptic targets in the excitatory (glutamatergic) synapse?
NA+ and Ca2+
51
what are the post synaptic targets in the excitatory (glutamatergic) synapse?
NMDA and AMPA
52
what is the MOA of levetiracetam?
binds the SV2A and thus interferes with synaptic vesicle release and neurotransmission
53
Where does keppra also appear to interfere and why is it unique in this was for treatment of status epilepticus?
1. interfere with Calcium entry thru Ca2+ channels & with intraneuronal calcium signaling 2. it is a candidate for this for refractory cases

P2 Spring: PHRM 845 (10 decks)

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