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IPAP 21-2 Soph Semester > Anticonvulsants > Flashcards

Anticonvulsants Flashcards

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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
is phenytoin a 1st or zero order kinetic drug
Zero order, drug concentration changes with respect to time at a constant rate;
26
What is the MOA of fosphenytoin
prodrug for phenytoin; fast sodium channel blocker
27
What is the clincal use of fosphenytoin and what advantage does it have to phenytoin
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
28
1mg of phenytoin is equal to __ of fosphenytoin
1.5 mg
29
What is the MOA of Carbamazepine
Sodium Channel Blocker
30
What is the clinical use of Cabamazepine
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
31
What is the enzyme interaction of Carbamazepine
CYP3A4 inducer and auto inducer (self induction) for up to 1 month
32
What are the ADE of carbamazepine
Many adverse effects related to intermediate metabolite RASH WT GAIN SIADH ``` Hypo NA Bone Marrow suppression SJS Necrosis Osteomalacia ```
33
Because of its ADE profile what must be monitored with carbamazepine
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
Can carbamazepine be used in pregnancy
NO
35
What are the DDI of Carbamazepine
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
What genetic testing must be done for carbamazepine
Patients with HLA-B*1502 and/or HLA-A*3101 allele are at increased risk of hypersensitivity syndrome, aka Stevens Johnson Syndrome Asians
37
What is the MOA of oxcarbamazepine
Sodium channel blocker
38
What is the clin use of Oxcarbazepine
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
Which drug should be chosen by providers Carbamazepine or phenytoin
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
What is the MOA of primidone and Phenobarbital
Increases GABA mediated chloride influx
41
What is the clincal use of Phenobarbital
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
Can phenobarbital be used in pregnancy
D, not advised
43
What are the DDI of phenobarbital
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
What is the MOA of Primidone
Increases GABA mediated chloride influx (inhibitory neurons) Metabolized to phenobarbital and phenylethylmalonamide
45
What is primidone Metz to
Metabolized to phenobarbital and phenylethylmalonamide
46
What is the clin use of primidone
Alternate choice in generalized tonic-clonic seizures and used for essential tremor May be used with carbamazepine and phenytoin
47
What are the BXD commonly use to treat SZR
Most Commonly Used Drugs: Diazepam (Valium)* Lorazepam (Ativan)* Clonazepam (Klonopin)
48
What is the MOA of Gabapentin
Inhibition of α2δ subunit of voltage-dependent calcium channels An analog of GABA, but does not directly impact GABA receptor
49
What is the Clin Use of Gabapentin
Partial onset seizures Neuropathic pain and post herpetic neuralgia pain Spasmolytic Diabetic neuropathy (off-label)
50
What are the ADE of Gabapentin
Drowsiness, fatigue, dizziness, headache, weight gain, and tremor during initiation Excreted renally, may need adjustments
51
What is the MOA of Pregabalin
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
What is the clin use of Pregabalin
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
What are the ADE of pregablin
Adverse effects: Sexual dysfunction, dizziness, weight gain, edema, angioedema, creatine kinase elevations Insomnia, nausea, headache, diarrhea reported after abrupt discontinuation
54
What is the DOC in an absent SZR
Ethosuximide
55
What monitoring must accompany ethosuximide
CBC due to neutropenia and leukopenia
56
What is the MOA of Valporic Acid
Blocks T-type calcium currents Blocks sodium channels Increases GABA production Decreases GABA degradation
57
What is the clinical use for Valporic Acid
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
What effect does valproic acid have with lamotrigine
Increases lamotrigine levels and risk of serious rash | Requires lamotrigine dose reduction
59
What effect does Valporic acid have on carbamazepine
Exacerbates carbamazepine epoxide accumulation
60
Effect of Valporic acid with ethosuximide
Inhibits the metabolism of ethosuximide
61
What are the ADE of valproic ACid
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
Can Valporic acid be used in pregnancy
Pregnancy Category: D X for migraine prophylaxis Substantial increase in the incidence of spina bifida
63
What drug can be used in valproic acid OD
Naloxone may reverse CNS depressant effects, theoretically it can have a convulsant effect
64
What is the MOA of lamotrigine
Decreases glutamate and aspartate release Delays repetitive firing of neurons Blocks fast sodium channels
65
What is the clincal use of Lamotrigine
Generalized tonic-clonic seizures Lenox-Gastaut: specific pediatric onset epilepsy Non-epileptic: maintenance treatment of bipolar I mood disorder
66
What are the ADE of lamotrigine s
SJS! Slowly ti trate this drug! VALPROIC ACID INCREASES RISK
67
What is the MOA of Topiramate
Fast sodium channel blocker Enhances GABA activity Antagonizes AMPA/kainase activity Weak carbonic anhydrase inhibitor
68
What is the Clin use of Topiramte
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
What are the ADE of Topiramate
memory impairment Met. Acidosis Encephalopathy
70
What DDI does Topiramate have
Contraceptives
71
How are febrile SZR tx
Treat fever with acetaminophen (Tylenol) and treat status epilepticus if required Prolonged febrile seizures may be treated with phenobarbital or diazepam
72
What are the emergency meds for epilicticus
Lorazepam, Diazepam, midazolam
73
What are the urgent medications for Status epilepsy
Fosphenytoin Phenytoin Phenobarbital Off Label: Valproic Acid Levetiracetam (Keppra) Lacosamide
74
What medications can be used in refractory status epilepsy
Pentobarbital (must be on ventilator) Propofol (must be on Vent) Midazolam
75
What are the effects of geriatric SZrs on medications
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
What are the DOC for eclampsia
Mag,. Sulfate
77
What drug prevents neural tube defects
Folic acid supplementation
78
WHich drugs absolutely should be avoided in pregnancy
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
Which drugs have they highest and lowest risk of sexual dysfunction
Highest incidence of sexual dysfunction: carbamazepine, phenobarbital, phenytoin, pregabalin, topiramate, and zonisamide Improved sexual functioning: lamotrigine and oxcarbazepine
80
Which drugs have most effect on bone suppression and increase fx
Risk is increased with carbamazepine, clonazepam, phenobarbital, phenytoin, and valproic acid

IPAP 21-2 Soph Semester (20 decks)

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