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NEURO PHARM > Epilepsy > Flashcards

Epilepsy Flashcards

1
Q

What is a seizure?

A
  • high frequency of bursts of APs (influx of Ca and activation of Na channels or a decrease in inhibitory interneurons) or hypersynchronization
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2
Q

what are the 3 main MOAs for for anticonvulsants?

A
  1. blockade of voltage-gated Na channels (AP generation) - used for partial and secondarily generalized tonic-clonic seizures
  2. enhancement of principal inhibitory neurotransmitter in the CNS (GABA) - used for partial and secondarily generalized tonic-clonic seizures
  3. inhibition of voltage-activated T-type Ca channels - used for absence seizures
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3
Q

What are the Na channel blockers

A 
Carbamazepine
Phenytoin
Topiramate
Lamotrigine
Valproate
Zonisamide
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4
Q

Where do the anti-seizure drugs act in the GABA pathway?

A
  1. benzos and barbiturates - act on post-synaptic side

2. Valproate works at pre-synaptic side by inhibiting GABA metabolism and increasing quantum yield release of GABA

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5
Q

What is the net effect of the Ca channel blockers

A

to reduce activity of pacemaker currents that underlies the thalamic rhythm in spikes and waves

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6
Q

What is a major ADE for anti-convulsants?

A

Suicidal ideation (1-24 weeks after starting drug) - educate patients, minimally effective drug levels should be used to manage epilepsy

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7
Q

How should we treat epilepsy?

A

Monotherapy, switch if it doesn’t work, then consider polypharamcy
- adverse effects vary from minimal impairment to death from aplastic anemia or hepatic failure

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8
Q

MOA of carbamazepine, Lacosamide, lamotrigine, phenytoin

A

block Na channels

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9
Q

MOA of clonazepam

A

GABA allosteric agonist – shift dose reponse curve for GABA to left.

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10
Q

MOA of ethosuximide

A

block T-type Ca channel

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11
Q

MOA of felbamate

A

inhibit NMDA, activate GABA

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12
Q

MOA of Gabapentin and Pregabalin

A

inhibit alpha 2 delta1 subunit of Ca channel

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13
Q

MOA of oxcarbazepine

A

inhibit Na channel, possibly increase K channel and decrease Ca channel

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14
Q

MOA of topiramate

A

inhibit Na channels, activate K current, activate GABA, decrease glutamate activity

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15
Q

MOA of Valproate

A

activate GABA, inhibit Na chanel

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16
Q

MOA of Zonisamide

A

inhibit N and T-type Ca channel

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17
Q

ADMA summary of anti-convulsants

A
  1. oral
  2. limited protein binding -except phenytoin and valproate
  3. hepatic metabolism w/ urinary elimination
  4. CYP interactions
  5. long half lives
  6. slow release products facilitate adherence - fewer doses/day
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18
Q

Which anti-convulsants don’t have hepatic metabolism

A
  1. gabapentin
  2. Pregabalin
  3. minor topiramate
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19
Q

Which anti-convulsants is eliminated in stool

A

phenytoin

20
Q

Which anti-convulsants have no CYP interaction?

A

Gabapentin, Levetiracetam, pregabalin, topiramate

21
Q

Which anti-convulsants have CYP activity that does it’s own hepatic metabolism?

A
  • this leads to a drug decrease due to increased rate of hepatic metabolism
    Carbamazepine, phenytoin
22
Q

Which anti-convulsants need routine drug levels?

A

Carbamazepine, ethosuximide, gabapentin, phenytoin, valproate

23
Q

What is a concern w/ topiramate and zonisamide?

A

they are weak carbonic anhydrase inhibitors –> leads to renal bicarb loss –> metabolic acidosis and may promote stone formation by reducing urinary citrate excretion and increasing urinary pH

24
Q

What is abrupt discontinuation a problem w/ anti-convulsants?

A

can precipitate status epilepticus, increase the frequency of seizures and lead to various neurologic issues

25
Q

What anti-convulsant has 0 order elimination

A

phenytoin - elimination of time and concentration

26
Q

ADE effects of Phenytoin

A
  1. CNS effects - nystagmus, ataxia, headache
  2. Gingival hyperplasia
  3. SJS, TEN, DRESS, hypertrichosis or hirsutism
27
Q

ADE of carbamazepine

A
  1. CNS especially during initial treatment phase - Dizziness, drowsiness, ataxia, blurred vision
  2. BBW for agranulocytosis. Aplastic anemia
  3. rash to severe derm problems
  4. Constipation or dry mouth, N/V
28
Q

When is the incidence of SJS higher when taking anti-convulsant drugs?

A

Asians who carry a SNP change in HLA-B 1502. Can determine w/ whole blood EDTA testing

29
Q

ADE of Valproic acid

A
  1. CNS effects related to infusion rate - somnolence, dizziness, paresthesias, asthenia, headache
  2. Thrombocytopenia, prolonged BT
  3. Rare rashes
  4. Nausea, diarrhea, hepatotoxicity more commonly in kids
30
Q

ADE of clonazepam, gabapentin

A

somnolence, ataxia/dizziness/fatigue

31
Q

ADE of ethosuximide

A

somnolence, ataxia/dizziness/fatigue, GI upset

32
Q

ADE of felbamate

A

BBW for aplastic anemia, bone marrow suppression, and hepatic dz.
N/V, constipation

33
Q

ADE of Lacosamide

A

dizziness, headache, diplopia, N/V

34
Q

ADE of lamotrigine

A

BBW for serious rash

Dizziness, diplopia, ataxia, blurred vision, rhinitis

35
Q

ADE of levetiracetam

A

headache, URTI, somnolence

36
Q

ADE of oxcarbazepine

A

Dizziness, diplopia, headache, N/V, nystagmus, somnolence, ataxia

37
Q

ADE of pregabalin

A

Dizziness, somnolence, peripheral edema

38
Q

ADE of topiramate

A

dizziness, fatigue, ataxia, paresthesias, abnormal vision, psychomotor slowing

39
Q

ADE of zonisamide

A

somnolence, anorexia, dizziness

40
Q

What anti-convulsants are cat C?

A

lamotrigine

41
Q

What anti-convulsants are cat D?

A

carbamazepine, phenytoin, topiramate, phenobarbital

42
Q

What anti-convulsants are Cat X?

A

Valproate

43
Q

DOC for partial and secondary generalized seizures

A

Lamotrigine
Carbamazepine
Levetiracetam
Oxcarbazepine

44
Q

DOC for primary generazlied tonic-clonic seizures and atypical absence/myoclonic/atonic seizures

A

Valproate
Lamotrigine
Levetiracetam

45
Q

DOC for absence seizures

A

Ethosuximide

Valproate

46
Q

Treatment for status epilepticus

A

initially give a benzodiazepines (lorazepam-IV) then add other anti-convulsants

47
Q

How do barbiutrate act on GABA receptors

A

they prolong opening time of Cl- channel

NEURO PHARM (10 decks)

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