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IPAP 21-2 Soph Semester > Anticonvulsants > Flashcards

Anticonvulsants Flashcards

1
Q

What are the two broad categories of SZR

A
  1. Generalized: conceptualized as originating at some point within and rapidly engaging bilaterally distributed neural networks
  2. Focal (or partial):
    Involve only a portion of the brain, typically part of one lobe of one hemisphere

Can be associated with impairment of consciousness or awareness (previously called complex partial seizure) or no impairment of consciousness (previously called simple partial seizures)

Can evolve over seconds into a tonic-clonic convulsion, also referred to as a secondarily generalized seizure

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2
Q

What are the 5 phases tonic-clonic SZR

A

five phases of a primary tonic-clonic seizure:

(1) flexion
(2) extension
(3) tremor
(4) clonic
(5) postictal

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3
Q

What does tonic mean

A

Flexion or extension

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4
Q

What does clonic mean

A

Clonic: rhythmic, repetitive, jerking muscle movements

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5
Q

What does myoclonic mean

A

Myoclonic: brief, lightning-like jerking movements of the entire body or the upper and occasionally lower extremities

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6
Q

What is an atomic SZR

A

Characterized by a loss of muscle tone

Often described as drop attacks in which a patient loses tone and falls to the ground

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7
Q

What is an absence SZR

A

Typical seizures are brief and abrupt, last 10-30 seconds, and occur in clusters

Usually results in a short loss of consciousness, or the patient may stare, be motionless, or have a distant expression on his or her face

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8
Q

Define epilepsy

A

Epilepsy: condition characterized by 2 or more epileptic seizures that are unprovoked and have no identified cause

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9
Q

Define epileptic SZR

A

Epileptic Seizure: clinical manifestation presumed to result from abnormal and excessive discharge of a set of neurons in the brain that results in abnormal movements or perceptions

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10
Q

Define SZR

A

Seizure: a paroxysmal disorder of the CNS characterized by abnormal cerebral neuronal discharges with or without loss of consciousness

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11
Q

What is primary and secondary epilepsy

A

Primary Epilepsy: no specific anatomic cause
-Drug treatment (MAY) be for life

Secondary Epilepsy: reversible disturbances responsible for seizures

  • Tumors
  • trauma
  • hypoglycemia
  • alcohol withdrawal

Drug treatment is used until the primary cause of the seizure can be corrected

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12
Q

What is the non pharm approach to SZR/ epilepsy

A

Dietary Modifications: some data supports a low-carbohydrate, high fat diet (ketogenic diet)

Vagus Nerve Stimulator for difficult to manage partial seizures

Implanted stimulator delivers stimuli on a regular basis and patients can use “on demand” stimulation

Alternative Treatments: biofeedback, mega vitamins, and melatonin

Surgery

Driving Restrictions:
All states have restriction, refer to state restrictions
Some states require mandatory physician reporting to the state department of transportation

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13
Q

Since Lifelong SZR therapy in no longer the standard, when can therapy be withdrawn

A

May attempt withdrawal from therapy if:

  • Seizure free for 2-5 years
  • Single seizure type
  • Normal neurological exam and IQ
  • Normal electroencephalogram (EEG) with medication treatment

Withdraw medications slowly and one at a time if on poly-therapy

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14
Q

What is the MOA of anticonvulsants

A

anticonvulsants work by blocking the initiation or preventing the spread of electrical discharge by several mechanisms

  • Enhancement of GABAnergic transmission
  • Diminution of excitatory transmission (i.e. Glutamate)
  • Modification of ionic conductance (i.e. Calcium, Sodium)
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15
Q

What are the two narrow spectrum anticonvulsants used to treat absence SZR

A

Ethosuximide

Valproate (alternative)

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16
Q

What is the MOA of phenytoin

A

Sodium Channel blocker

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17
Q

Can you used phenytoin in absence SZR

A

NO !

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18
Q

is phenytoin a 1st line Tx for SZR

A

NO!

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19
Q

Can you use phenytoin in pregnancy

A

No

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20
Q

What are the ADE of phenytoin

A

Non-dose-related adverse effects:

  • Sexual dysfunction
  • Hirsutism (excessive hair growth)
  • gingival hyperplasia (40-90%)
  • Long term use causes coarsening of facial features

Dose-related adverse effects:

  • Nystagmus (rapid eye movement)
  • ataxia
  • drowsiness
  • cognitive impairment

High Dose Indicators:

  • Blurred or double vision
  • Thick tongue
  • Dizziness

Less common: N/V, anemia, drowsiness, hyperglycemia and anti-arrhythmic activity

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21
Q

how does phynetoin affect the mouth

A

Gingival hyperplasia

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22
Q

What are the DDI for phenytoin

A

Multiple enzyme activity

Anticoagulants increase phenytoin concentration

Contraceptives, reduces efficacy of contraceptives

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23
Q

What is a common clinical error of phenytoin

A

Common clinical error is to increase the dosage directly from 300mg/day to 400mg/day
- toxicity frequently occurs

A decrease in protein (e.g. hypoalbuminemia) results in an increase in free drug concentration and same total drug concentration.

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24
Q

How does protein effect phenytoin

A

A decrease in protein (e.g. hypoalbuminemia) results in an increase in free drug concentration and same total drug concentration.

NEEDS CLOSE DRUG MONITORING

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25
Q

is phenytoin a 1st or zero order kinetic drug

A

Zero order, drug concentration changes with respect to time at a constant rate;

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26
Q

What is the MOA of fosphenytoin

A

prodrug for phenytoin; fast sodium channel blocker

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27
Q

What is the clincal use of fosphenytoin and what advantage does it have to phenytoin

A

Clinical Use:

  • Status epilepticus
  • Parenteral formulation for loading or maintenance dosing in place of phenytoin

Advantages over phenytoin:

  • Preferred when parenteral administration is needed (reduced extravasation, faster load)
  • Infusion can be up to 150mg of phenytoin equivalents per minute
  • Can be mixed in NS or D5W
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28
Q

1mg of phenytoin is equal to __ of fosphenytoin

A

1.5 mg

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29
Q

What is the MOA of Carbamazepine

A

Sodium Channel Blocker

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30
Q

What is the clinical use of Cabamazepine

A

Clinical Use:
-Only available orally

  • Primary generalized tonic-clonic, simple or complex partial
  • Newer anticonvulsants are beginning to displace it from this role

Other uses: trigeminal neuralgia and bipolar disease

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31
Q

What is the enzyme interaction of Carbamazepine

A

CYP3A4 inducer and auto inducer (self induction) for up to 1 month

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32
Q

What are the ADE of carbamazepine

A

Many adverse effects related to intermediate metabolite

RASH
WT GAIN
SIADH

Hypo NA 
Bone Marrow suppression 
SJS 
Necrosis 
Osteomalacia
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33
Q

Because of its ADE profile what must be monitored with carbamazepine

A

LFTs and CBC status at baseline then for 2-3 months and then every 1-2 years

Concern of aplastic anemia and agranulocytosis that can occur within the first 4 months

34
Q

Can carbamazepine be used in pregnancy

A

NO

35
Q

What are the DDI of Carbamazepine

A

Drug Interactions: CYP 3A4 substrates

Lamotrigine may also increase carbamazepine epoxide levels

Concomitant use of valproic acid can inhibit epoxide hydrolase and cause carbamazepine epoxide accumulation

Contraceptives: reduces efficacy of estrogen-containing contraceptives, oral progestin-only contraceptives, and the etonogestrel implant

36
Q

What genetic testing must be done for carbamazepine

A

Patients with HLA-B1502 and/or HLA-A3101 allele are at increased risk of hypersensitivity syndrome, aka Stevens Johnson Syndrome

Asians

37
Q

What is the MOA of oxcarbamazepine

A

Sodium channel blocker

38
Q

What is the clin use of Oxcarbazepine

A

Generalized tonic-clonic

Other uses: trigeminal neuralgia and bipolar disease

Reserve for patients who do not tolerate carbamazepine due to drug interactions or adverse effects

39
Q

Which drug should be chosen by providers

Carbamazepine or phenytoin

A

Carbamazepine is first choice of many providers

  • Less sedating
  • Not associated with hirsutism (excess hair growth), acne, gingival hyperplasia
  • Phenytoin has reputation for causing functional impairment and learning problems
40
Q

What is the MOA of primidone and Phenobarbital

A

Increases GABA mediated chloride influx

41
Q

What is the clincal use of Phenobarbital

A

Generalized tonic-clonic seizures, simple or partial seizures

Refractory status epilepticus; tried for virtually every seizure type, especially when attacks are difficult to control

42
Q

Can phenobarbital be used in pregnancy

A

D, not advised

43
Q

What are the DDI of phenobarbital

A

Drug-interactions:

  • CYP Interactions
  • Ethanol: additive CNS and respiratory depression
  • Contraceptives: reduces efficacy of estrogen-containing contraceptives, oral progestin-only contraceptives, and the etonogestrel implant
44
Q

What is the MOA of Primidone

A

Increases GABA mediated chloride influx (inhibitory neurons)

Metabolized to phenobarbital and phenylethylmalonamide

45
Q

What is primidone Metz to

A

Metabolized to phenobarbital and phenylethylmalonamide

46
Q

What is the clin use of primidone

A

Alternate choice in generalized tonic-clonic seizures and used for essential tremor

May be used with carbamazepine and phenytoin

47
Q

What are the BXD commonly use to treat SZR

A

Most Commonly Used Drugs:
Diazepam (Valium)*
Lorazepam (Ativan)*
Clonazepam (Klonopin)

48
Q

What is the MOA of Gabapentin

A

Inhibition of α2δ subunit of voltage-dependent calcium channels

An analog of GABA, but does not directly impact GABA receptor

49
Q

What is the Clin Use of Gabapentin

A

Partial onset seizures

Neuropathic pain and post herpetic neuralgia pain

Spasmolytic

Diabetic neuropathy (off-label)

50
Q

What are the ADE of Gabapentin

A

Drowsiness, fatigue, dizziness, headache, weight gain, and tremor during initiation

Excreted renally, may need adjustments

51
Q

What is the MOA of Pregabalin

A

Inhibition of α2δ subunit of voltage-dependent calcium channels.

GABA derivative similar to gabapentin that binds pre-synaptically to the alpha-2-delta subunit of the voltage-gated calcium channel and blocks influx of calcium in hyper excited neurons

52
Q

What is the clin use of Pregabalin

A

Partial-onset seizure (adjunct)

Non-epileptic: neuropathic pain associated with diabetic neuropathy, restless leg syndrome, post-herpetic neuralgia, fibromyalgia, pain due to spinal cord injury, social phobia

53
Q

What are the ADE of pregablin

A

Adverse effects:

Sexual dysfunction, dizziness, weight gain, edema, angioedema, creatine kinase elevations

Insomnia, nausea, headache, diarrhea reported after abrupt discontinuation

54
Q

What is the DOC in an absent SZR

A

Ethosuximide

55
Q

What monitoring must accompany ethosuximide

A

CBC due to neutropenia and leukopenia

56
Q

What is the MOA of Valporic Acid

A

Blocks T-type calcium currents

Blocks sodium channels

Increases GABA production

Decreases GABA degradation

57
Q

What is the clinical use for Valporic Acid

A

Generalized non-convulsive seizures

2nd line agent in absence seizures to ethosuximide when the patient has concomitant generalized tonic-clonic attacks

Non-epileptic indications:
Manic episodes associated with bipolar disorder

Migraine prophylaxis

58
Q

What effect does valproic acid have with lamotrigine

A

Increases lamotrigine levels and risk of serious rash

Requires lamotrigine dose reduction

59
Q

What effect does Valporic acid have on carbamazepine

A

Exacerbates carbamazepine epoxide accumulation

60
Q

Effect of Valporic acid with ethosuximide

A

Inhibits the metabolism of ethosuximide

61
Q

What are the ADE of valproic ACid

A

Common:
alopecia, N/V, interferes with platelet aggregation, pancreatitis, sedation, weight gain (average of 2 kg after one year), rash

Serious:
Thrombocytopenia
Multi-organ hypersensitivity
Black box warning for hepatic failure fatalities
Monitor LFTs
Very Rare (<0.002% and most are in children under 10)

62
Q

Can Valporic acid be used in pregnancy

A

Pregnancy Category: D

X for migraine prophylaxis
Substantial increase in the incidence of spina bifida

63
Q

What drug can be used in valproic acid OD

A

Naloxone may reverse CNS depressant effects, theoretically it can have a convulsant effect

64
Q

What is the MOA of lamotrigine

A

Decreases glutamate and aspartate release

Delays repetitive firing of neurons

Blocks fast sodium channels

65
Q

What is the clincal use of Lamotrigine

A

Generalized tonic-clonic seizures

Lenox-Gastaut: specific pediatric onset epilepsy

Non-epileptic: maintenance treatment of bipolar I mood disorder

66
Q

What are the ADE of lamotrigine s

A

SJS!

Slowly ti trate this drug!

VALPROIC ACID INCREASES RISK

67
Q

What is the MOA of Topiramate

A

Fast sodium channel blocker
Enhances GABA activity
Antagonizes AMPA/kainase activity
Weak carbonic anhydrase inhibitor

68
Q

What is the Clin use of Topiramte

A

Clinical Use:

Primary generalized tonic-clonic seizures, simple or complex partial with or without generalization

Absence seizure (adjunct)

Lenox-Gastaut

Non-epileptic: migraine prophylaxis

Pregnancy Category: D

69
Q

What are the ADE of Topiramate

A

memory impairment
Met. Acidosis
Encephalopathy

70
Q

What DDI does Topiramate have

A

Contraceptives

71
Q

How are febrile SZR tx

A

Treat fever with acetaminophen (Tylenol) and treat status epilepticus if required

Prolonged febrile seizures may be treated with phenobarbital or diazepam

72
Q

What are the emergency meds for epilicticus

A

Lorazepam, Diazepam, midazolam

73
Q

What are the urgent medications for Status epilepsy

A

Fosphenytoin
Phenytoin
Phenobarbital

Off Label:

Valproic Acid
Levetiracetam (Keppra)
Lacosamide

74
Q

What medications can be used in refractory status epilepsy

A

Pentobarbital (must be on ventilator)
Propofol (must be on Vent)
Midazolam

75
Q

What are the effects of geriatric SZrs on medications

A

Seizure medications with renal elimination must be adjusted according to the CrCl value

Carbamazepine: decreased clearance

Phenytoin: decreased protein binding if hypoalbuminemic or in renal failure

Valproic acid: decreased protein binding

Diazepam: increased half-life

Lamotrigine: decreased clearance

76
Q

What are the DOC for eclampsia

A

Mag,. Sulfate

77
Q

What drug prevents neural tube defects

A

Folic acid supplementation

78
Q

WHich drugs absolutely should be avoided in pregnancy

A

Avoid or limit the dose of the following agents:

Phenytoin: Risk of cleft palate, Risk of poor cognitive functions

Carbamazepine: risk of posterior cleft palate

Benzodiazepines

Phenobarbital:
Risk of cardiac malformations
Risk of poor cognitive functions

Valproic acid: risk of major congenital malformation

Topiramate: risk of major congenital malformation

79
Q

Which drugs have they highest and lowest risk of sexual dysfunction

A

Highest incidence of sexual dysfunction: carbamazepine, phenobarbital, phenytoin, pregabalin, topiramate, and zonisamide

Improved sexual functioning: lamotrigine and oxcarbazepine

80
Q

Which drugs have most effect on bone suppression and increase fx

A

Risk is increased with carbamazepine, clonazepam, phenobarbital, phenytoin, and valproic acid

IPAP 21-2 Soph Semester (20 decks)

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