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NEURO > Anti-Convulsants (4-3-14) > Flashcards

Anti-Convulsants (4-3-14) Flashcards

1
Q

what mutations cause tonic-clonic?

A

Na channels
K channels
N cholinergic receptor

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2
Q

what mutations cause absence?

A

T-type VGCC

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3
Q

MELAS (Myoclonic seizure)

A

Mitochondrial Encephalopathy,
Lactic Acidosis,
Stroke

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4
Q

MERRF (Myoclonic seizure)

A

Myoclonic Epilepsy,
Ragged Red Fibers

involves anything concerning mitochondrial function: oxidative phosphorylation, ETC

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5
Q

Pentylenetetrazol toxicity? MOA?

A

used as a respiratory stimulant
high doses –> seizure
MOA = inhibit GABAa + opens Ca channels

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6
Q

drugs to counteract Pentylenetetrazol induced seizure?

A
  1. Ethosuximide (blocks Ca channels)
  2. Valproate (increases GABA, block Na channels)
  3. Benzodiazepines (Clonazepam)** = opens Cl channels
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7
Q

drugs to counteract Electroshock induced seizure (used to treat suicide)

A
  1. Phenytoin
  2. Carbamazepine
  3. Lamotrigine
    note: Benzodiazepines NOT effective
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8
Q

length of Aura in Tonic-Clonic seizure? What happens during this time?

A

seconds

hallucination, dysmensia (Deja vu, Jamais vu), visceral aura

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9
Q

length of tonic state in Tonic-Clonic seizure?

A

< 1 min
body rigidity
gasp

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10
Q

length of clonic state in Tonic-Clonic seizure? What happens in this stage?

A

< 3min
jerking –> tongue biting
Autonomics = incontinence, tachycardia, HTN, hypersalivation, pupillary dilation

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11
Q

length of flaccid coma in Tonic-Clonic seizure?

A

hours

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12
Q

what seizure are you conscious for?

A

simple partial

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13
Q

what seizures are you unconscious for?

A

complex partial

generalized onset epilepsy

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14
Q

what is an interictal spike? What does it mean?

A

sharp EEG wave during symptom-less period

sign patient has epilepsy

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15
Q

benzodiazepine can block ____-induced seizures but not ____-induced seizures

A

blocks phenylenetetrazol-induced seizures

cannot block electroshock-induced seizures

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16
Q

what are the 3 major classes of anticonvulsants?

A

Na channel blockers
Ca channel blockers
GABA agonists

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17
Q

What drugs act on Na channels?

A 
old = carbamazepine, phenytoin, valproic acid 
new = lamotrigine, topiramate, zonisamide
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18
Q

carbamazepine S/E

A

Agranulocytosis, aplastic anemia (low WBCs)
hepatoxicitiy
CNS effects: nystagmus, diplopia, tired, vertigo, headache

19
Q

carbamazepine MOA

A

Na+-channel inactivation

20
Q

Phenytoin MOA? What seizure can it NOT be used for?

A

Na+-channel inactivation

do not give for absence seizures, give ethosuximide

21
Q

Fosphenytoin sodium. When do you use it?

A

water soluble, phosphatases convert to phenytoin.
I.V./I.M. administration, no phlebitis
arrhythmias.
Used in status epilepticus

22
Q

Phenytoin S/E

A 
painful phlebitis
lymphadenopathy***
osteomalacia 
gingival hyperplasia
excessive hair growth 
megaloblastic anemia (low folic acid)
double vision 
increased hepatic degradation of glucocorticoids
ataxia/nystagmus
23
Q

Valproic Acid MOA

A

a. Prolongation of Na+-channel inactivation
b. more GABA synthesis, less GABA breakdown
c. T-type calcium channel blockade

24
Q

Valproic Acid S/E

A

GI distress = Acute pancreatitis, Hepatotoxicity
Thrombocytopenia
Alopecia
Ataxia

25
Q

Valproic Acid C/I

A

Pregnancy: folate antagonist –> NTD –> meningocele/spina bifida
Bleeding disorders
Hepatic disease

26
Q

LAMOTRIGINE S/E

A

a. Dizziness
b. Diplopia
c. Sedation
d. Ataxia
e. Headache
f. Skin rash
g. Stevens-Johnson syndrome

27
Q

GABA Agonists

A

Benzos: LORAZEPAM, DIAZEPAM, CLONAZEPAM
Barbituates: PHENOBARBITAL, PRIMIDONE
TOPIRIMATE

28
Q

Synthesis of GABA is increased by:

A

VALPROIC ACID

VIGABATRIN

29
Q

GABA release increased by:

A

GABAPENTIN
PREGABALIN
-do not bind to GABA receptors, but increase release
-block membrane insertion of a2d subunit of T-Type Ca channel in glutamatergic neurons

30
Q

GABA transporter inhibitor

A

TIAGABINE

31
Q

topirimate S/E

A

paresthesia
kidney stones (don’t give w/ CA inhibitors)
weight loss
fatigue, sedation, psychomotor slowing
glaucoma
speech or language problems
hypohidrosis (decreased sweating in response to stimuli)

32
Q

phenobarbital S/E

A

sedation
respiratory depression
nystagmus, ataxia
megaloblastic anemia -> Rx = folate

33
Q

primidone use? S/E?

A

primidone metabolized to phenobarbital!!!
effective in all seizures EXCEPT ABSENCE
same SE as phenobarbitol = sedation

34
Q

drug for absence epilepsy

A

ethosuximide

Block T-type Voltage Gated Ca2+-channels

35
Q

ethosuximide C/I?

A

hepatic dx

renal dx

36
Q

ethosuximide adverse effects?

A

Bone marrow suppression  can’t make as many blood cells = Leukopenia, Thrombocytopenia, Aplastic anemia

Skin reactions, SLE, urticaria, pruritus
Ataxia, lethargy, headache

37
Q

Step 1 in treatment for status epilepticus

A

Coma Cocktail

  • dextrose
  • thiamine
  • naloxone
38
Q

Step 2 in treatment for status epilepticus

A

1) Benzos: Lorazepam, diazepam (not for longterm Rx)
2) fosphenytoin
3) now refractory status epilepticus –> phenobarbital
4) if still out, give general anesthesia

39
Q

Rx for focal epilepsy

A

carbamazepine
lamotrigine
phenytoin

40
Q

Rx for tonic-clonic

A

valproic acid
topiramate
lamotrigine

41
Q

Rx for absence

A

ethosuximide*

valproic acid

42
Q

Rx for myoclonic atypical absence atonic

A

valproic acid
topiramate
lamotrigine

43
Q

what happens during simple partial seizure?

A 
conscious*
Motor signs
Somatosensory or special sensory symptoms
Autonomic signs
Psychic symptoms
44
Q

what happens during complex partial seizure?

A 
Aura  = epigastric, limb numbness, vertigo 
Automatisms = hand-waving, lip-smacking 
Other motor (tonic posturing)

NEURO (18 decks)

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