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Pharmacology > AED > Flashcards

AED Flashcards

1
Q

Difference between seizure and epilepsy?

A

Seizure - rapid, synchronized, and uncontrolled spread of electrical activity in the brain (may result in loss of consiousness, involuntary movements, abnormal sensory phenomena, increased autonomic activity, and a variety of psychic disturbances)

Epilepsy - individual has a tendency toward recurrent seizures

A seizure is not necessarily epilepsy: may be isolated: either high/low sodium/glucose or alcohol withdrawal

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2
Q

Classifications:

  1. What is a simple partial seizure?
  2. What is a complex partial seizure?
  3. What is a partial seizure with secondary generalization?
A

Classifications:

  1. Simple partial - no alteration in consciousness
  2. Complex partial - alteration in consciousness
  3. Partial with secondary - spread from one focal area to multiple brain regions resulting in loss of consciousness and possibly a tonic-clonic seizure
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3
Q

Classifications:

Primary generalized:

  1. What is a tonic clonic seizure?
  2. What is an absence seizure? EEG pattern?
  3. What is a myoclonic seizure?
A

Classifications:

Primary generalized:

  1. Tonic clonic - abrupt loss of consciousness without warning, followed by tonic contraction of all muscle groups (arched back/estensor posturing) followed by rhythmic jerk of arms and legs
  2. Absence - brief lapses of attention w/o loss of consiousness or town. 3-Hz spike and wave EEG
  3. Myoclonic - brief contraction of muscles, no loss of con.
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4
Q

Classifications:

Status epilepticus:

  1. What is a tonic clonic status?
  2. What is an absence status?
A

Classifications:

Status epilepticus:

  1. Tonic clonic - continuous or recurrent without the individual regaining consciousness between seizures
  2. Absence - prolonged or continuous lapses of consciousness associated with continuous 3Hz spike an wave activity in the EEG
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5
Q

2 strategies for AED therapy?

A

2 strategies for AED therapy:

a. Decrease discharge at seizure focus
b. Decrease discharge spread

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6
Q

Partial seizure:

  1. Results from?
  2. Targets of AEDs?
A

Partial seizure:

  1. Results from rapid, uncontrolled neuronal firing and loss of surround inhibition
  2. GABA, Na+ channels, HVA Ca++ channels, and glutamate receptors
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7
Q

Absence seizure:

  1. Cause?
  2. Drugs target?
A

Absence seizure:

  1. Caused by a self-sustaining cycle of activity generated between thalamic and cortical cells
  2. Drugs target GABAa in reticular thalamic nucleus and T-type Ca++ channels
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8
Q

AEDs facilitate GABA how? (4)

A

AEDs and GABA:

a. Bind directly to GABA-A receptors
b. Blocking presynaptic GABA uptake
c. Inhibiting metabolism by GABA transaminase
d. Increasing the synthesis of GABA

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9
Q

Drugs that are general hepatic inducers?

A

General hepatic inducers:

a. Carbamazapine
b. Phenytoin
c. Phenobarbital
d. Primidone

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10
Q

Drugs that are CYP3A inducers? (3)

A

CYP3A inducers:

a. felbamate
b. Topiramate
c. Oxcarbazine

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11
Q

AEDs with NO CYP effect? (6)

A

NO CYP effect:

a. Gabapentin
b. Lamotrigine
c. Pregabalin
d. Tiagabine
e. Levetiracetam
f. Zonisamide

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12
Q

Calcium channel blockers:

T type vs HVA inhibitors? And examples?

A

Calcium Channel Blockers:

T-Type: “pacemakers” of normal rhythmic brain activity, especially in the Thalamus (and in regards to absence seizures); Ethosuximide and valproate

HVA (high-voltage-activated) - Control entry of calcium into presynaptic terminal; Gabapentin

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13
Q

Sodium channel blockers:

  1. Blockade causes?
  2. Should not be used when?
A

Sodium Channel Blockers:

  1. Blockade causes stabilization of neuronal membranes, prevents posttetanic potentiation, limits development of maximal seizure activity, and reduces the spread of seizures
  2. Should NOT be used for absence seizures - makes the worse
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14
Q

Sodium channel blockers:

Drugs? (9)

A

Sodium channel blockers:

a. Carbamazepine, Oxcarbazepine, and Eslicarbazepine
b. Phenytoin
c. Lamotrigine
d. Zonisamide
e. Lacosamide
f. Rufinamide
g. Primidone

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15
Q

Carbamazepine:

  1. First line therapy for?
  2. Other uses?
  3. Drug of choice for?
A

Carbamazepine:

  1. First line: focal seizures w/ or w/o secondary generalization and generalized tonic-clonic seizures (DOC)
  2. Other - BPD, ADD, ADHD, schizophrenia, phantom limb, and paroxysmal extreme pain disorder
  3. DOC - trigeminal neuralgia
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16
Q

Carbamazepine:

  1. Primary MOA?
  2. Also decreases? Blocks what receptors? And blocks reuptake of?
  3. Action results in action potential ____ AND?
A

Carbamazepine:

  1. Stabilize voltage-gated axonal Na+ channels in the inactivated conformation (increases refractory period)
  2. Also decreases voltage gated Ca++ channels; blocks adenosine receptors; and blocks reuptake of NE
  3. Action potential propagation AND increased seizure threshold
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17
Q

Carbamazepine:

  1. Given IV, IM, or subcutaneously for?
  2. Role in CYP450 enzymes?
A

Carbamazepine:

  1. IV/IM/SQ - for status epilepticus
  2. POTENT INDUCER OF CYP450
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18
Q

Carbamazepine:

  1. Potent inducer increasing metabolism of?
A

Carbamazepine:

  1. Inducer: increasing its own metabolism (autoinduction) as well as other AEDs (met in the liver), oral contraceptives, warfarin, theophylline, and protease inhibitors
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19
Q

Carbamazepine:

Side effects:

  1. CNS? Due to?
  2. Systemic?
A

Carbamazepine:

Side effects:

  1. CNS - _nystagmus, blurred vision, diplopia, ataxia, lethargy, _drowsiness and HA; due to hyponatremia
  2. Systemic - N/V, diarrhea, rash, pruritis, and fluid retention
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20
Q

Carbamazepine:

Rare side effects?

A

Carbamazepine:

Rare SE:

a. BM suppression: agranulocytosis, leukopenia, aplastic anemia, and thrombocytopenia
b. Steven johnson - esp with HLA-B allele and asian
c. Teratogenic - NT tube defects (abnormal facial features, spina bifida etc)

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21
Q

Carbamazepine:

  1. Contraindications?
  2. Increases metabolism of?
  3. What decreases its metabolism? This results in?
A

Carbamazepine:

  1. Contraindications - hypersensitivity
  2. Increase met: AEDs, oral contraceptives, warfarin
  3. Macrolides, cimetidine, and Ca++ channel blockers decrease its metabolism leading to raised carbamazepine levels
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22
Q

Carbamazepine:

  1. Can increase toxicity of?
  2. Monitor what levels?
A

Carbamazepine:

  1. Increase toxicity of lithium
  2. Monitor renal, hepatic, and hematologic levels
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23
Q

Oxcarbazepine (OXC):

  1. First line monotherapy for?
  2. May aggravate?
A

Oxcarbazepine (OXC):

  1. First line: partial and generalized seizures
  2. May aggravate: myoclonic and absence seizures
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24
Q

Oxcarbazepine (OXC):

  1. OXC does not produce the ____ metabolite, which is largely responsible for what with carbamazepine?
  2. Common side effects?
A

Oxcarbazepine (OXC):

  1. Doesnt produce epoxide metabolite responsible for SE with carbamazepine
  2. SE: sedation, HA, dizziness, vertigo, ataxia, diplopia, rash, hyponatremia, wt gain, GI disturbances, and alopecia
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25
Q

Oxcarbazepine (OXC):

  1. Severe side effects?
  2. Interactions?
  3. Contraindications?
A

Oxcarbazepine (OXC):

  1. Severe SE: Stevens-Johnson
  2. Reduces the effectiveness of hormonal contraceptives
  3. NOT to be used in combination with eslicarbazepine (active metabolite of OXC)
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26
Q

Eslicarbazepine:

  1. Use?
  2. MOA?
  3. SE?
  4. Contraindications?
A

Eslicarbazepine:

  1. Focal onset seizures
  2. MOA: active metabolite of OXC - blocks Na+ channels in rapidly firing neurons
  3. SE: dizziness, sedation, HA, vertigo, ataxia, blurred vision, and tremor
  4. Contraindications: OXC or patients with severe liver impairment
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27
Q

Phenytoin:

  1. First line monotherapy/adjunctive for?
  2. Also used for?
A

Phenytoin:

  1. First line: focal and generalized seizures
  2. Also: Lennox-Gastaut syndrome, status epilepticus, and childhood syndromes
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28
Q

Phenytoin:

  1. What is Lennox-Gastaut syndrome?
  2. Contraindicated for?
  3. No longer used for what kind of seizures?
A

Phenytoin:

  1. LG = frequent seizures of different types accompanied by retardation and behavioral problems seen in children
  2. Contra - absence seizures
  3. No longer used for alcohol withdrawal or toxin induced seizures
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29
Q

Phenytoin:

MOA:

  1. Primary MOA?
  2. Also inhibits? Limits fluctuation of neuronal ___ gradients via?
  3. Effects on ___ and other ___ ___ systems.
  4. Action results in? Does NOT?
A

Phenytoin:

MOA:

  1. Primary - Na+ blocker in inactivated conformation
  2. Also inhibits voltage-gated Ca++ channels; limits fluctuation of ionic gradients via Na+/K+ ATPase
  3. Effects on calmodulin and other 2nd messenger systems
  4. Action results in decreased AP propagation (size and spread) but DOES NOT increase seizure threshold
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30
Q

Phenytoin:

  1. Kinetics?
  2. Protein binding?
  3. Strong _____ of hepatic enzymes.
A

Phenytoin:

  1. Dose-dependent zero order kinetics (smaller change in dose leads to BIG change in [plasma])
  2. Highly bound (90%) but free is active
  3. Strong inducer of hepatic enzymes
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31
Q

Phenytoin:

  1. Induction of hepatic enzymes results in?
  2. Common CNS side effects?
  3. Systemic side effects? ___ ____ can reduce incidence of?
A

Phenytoin:

  1. Induction results in increased metabolism of other liver metabolized AEDs, oral contraceptives, warfarin, theophylline, and protease inhibitors
  2. CNS: horizontal gaze nystagmus, loss of smooth pursuit eye movements, diplopia, confusion, ataxia, slurred speech, neuropathy
  3. Systemic: gingival hyperplasia and hirsutism; Folic acid can reduce the gingival hyperplasia
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32
Q

Phenytoin:

Serious side effects?

A

Phenytoin:

Serious side effects: osteomalacia, bleeding problems, megaloblastic anemia, teratogen, seizures, drug-induced lupus, steven-johnson syndrome, toxic epidermal necrolysis, rash and severe allergic reactions

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33
Q

Phenytoin:

  1. Osteomalacia due to?
  2. Bleeding problems due to?
  3. Megaloblastic anemia due to?
A

Phenytoin:

  1. Osteomalacia: interference with Vit D metabolism –> bone softening
  2. Bleeding - interference with Vit K
  3. Megaloblastic anemia - due to reduction in folic acid
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34
Q

Phenytoin:

  1. Teratogenic result? Resembles?
  2. What occurs with parenteral administration? Why? How to avoid?
  3. Has one of the most problematic ____ _____ profiles.
A

Phenytoin:

  1. Teratogen: craniofacial anomalies, cardiac defects, and mild retardation; resembles Fetal Alcohol Syndrome
  2. Parenteral: skin necrosis and cardiac arrhythmias because the drug is VERY insoluble in H2O and the dilutant is toxic; avoid by administering fosphenytoin
  3. Most problematic drug interaction profiles
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35
Q

Phenytoin:

  1. Increased phenytoin metabolism by?
  2. Decreased metabolism of phenytoin by?
A

Phenytoin:

  1. Increased phenytoin MET by carbamazepine and phenobarbital
  2. Decreased phenytoin met by cimetidine
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36
Q

Phenytoin:

  1. Phenytoin accelerates metabolism of?
  2. Autoinduction?
  3. Protein binding?
A

Phenytoin:

  1. Accelerates metabolism of other liver metabolized AEDs, theophylline, warfarin, protease inhibitors, and oral contraceptives
  2. Minimal autoinduction
  3. Highly protein bound, other highly bound drugs can interfere with binding and leads to increased free phenytoin levels
37
Q

Lamotrigine:

  1. Adjunctive therapy for?
  2. Initial therapy in?
  3. Preferred choice of treatment for who? Why?
A

Lamotrigine:

  1. Adjunct to focal seizures (2yrs old+), generalized tonic-clonic seizures, and Lennox-Gastaut syndrome
  2. Initial therapy in newly diagnosed focal epilepsy and absence seizures in kids
  3. Elderly, children, and pregnancy –> due to excellent SE profile and lack of CNS toxicity
38
Q

Lamotrigine:

  1. Primary MOA?
  2. Secondary moa? (inhibits what 3 things)
A

Lamotrigine:

  1. Primary MOA: Na+ stablization and blocks repetitive firing
  2. Secondary: inhibits glutamate and aspartate release and T-type Ca++ currents
39
Q

Lamotrigine:

  1. Lamotrigine clearance increases in ____
  2. CNS side effects?
  3. Main concern? Due to?
A

Lamotrigine:

  1. Increases clearance in pregnancy
  2. CNS - ataxia, dizziness, diplopia, and somnolence
  3. Main concern = rash, due to rapid titration (minimize by starting drug slowly)
40
Q

Lamotrigine:

  1. Children taking ____ ___ may cause the rash to develop to?
  2. What increases lamotrigine clearance (other than pregnancy)
A

Lamotrigine:

  1. Children taking valproic acid may cause formation of steven-johnson’s syndrome
  2. Hormone replacement therapy and hormonal contraceptives increase clearance of lamotrigine
41
Q

Lamotrigine:

  1. Half life of lamotrigine is decreased by?
  2. Half life of lamotrigine is increased by?
A

Lamotrigine:

  1. Half life is decreased by carbamazepine and phenytoin
  2. Half life is increased by valproic acid
42
Q

Zonisamide:

  1. Adjuvant treatment for? in who?
  2. Also approved for?
  3. MOA: an oral _____ similar to ____ and ___ and it inactivates what two things?
A

Lamotrigine:

  1. Adjuvant for partial and generalized seizures in adults and kids, also myoclonic seizures
  2. Also approved for migrane prevention
  3. MOA: an oral sulfonimide similar to phenytoin and carbamazepine and it inactivates voltage-gated Na+ channels and T-type Ca++ channels
43
Q

zonisamide:

  1. Metabolism?
  2. Common side effects?
  3. Interactions?
A

zonisamide:

  1. Liver by CYP and non-cyp transformations
  2. SE - somnolence, ataxia, dizziness, psychomotor slowing, fatigue, and weight loss
  3. Drugs that affect CYP3A4 may alter serum concentrations
44
Q

Zonisamide:

  1. Serious side effects?
  2. Rare serious side effects?
  3. Contraindications?
A

Zonisamide:

  1. Aplastic anemia, metabolic acidosis, and kidney stones
  2. Rare: reduced sweating (can cause hyperthermia), depression, and psychosis
  3. Contraindicated in pregnancy (serious risk to fetus) and those with renal insufficiency
45
Q

Lacosamide:

  1. Adjunctive therapy for?
  2. MOA?
  3. Stabilizes? and inhibits?
A

Lacosamide:

  1. Adjunctive for partial onset seizures
  2. MOA (not completely known) - modulation of Na+ – selective enhancement of slow inactivation without interaction with fast inactivation gating
  3. Stabilizes neuronal membranes and inhibits repetitive neuronal firing
46
Q

Lacosamide:

  1. Metabolism: does not affect?
  2. Common side effects?
  3. Rare side effects?
  4. Contraindications?
A

Lacosamide:

  1. Metabolism: does NOT affect hepatic enzymes
  2. SE - diplopia, blurred vision, dizziness, ataxia, and N/V
  3. Rare: prolongs PR cardiac interval
  4. Contra: severe hepatic impairment
47
Q

Rufinamide:

  1. Adjunctive for? May have efficacy in?
  2. MOA?
  3. Weak inhibitor of ____ and a weak inducer of ____.
A

Rufinamide:

  1. Adjunctive for Lennox-Gastaut (4 yrs old+); may have efficacy in focal epilepsy
  2. MOA: prolongs Na+ channels in inactivated state
  3. Weak inhibitor of CYP2E1 and a weak inducer of CYP3A4
48
Q

Rufinamide:

  1. Common side effects? NO?
  2. Rare?
A

Rufinamide:

  1. Common: HA, dizziness, somnolence, N/V with NO visual effects
  2. Rare - rash
49
Q

Rufinamide:

  1. Interactions: may make what less effective?
  2. Contraindications: Rufinamide reduces the ___ ___. Patients with a history of ____ ____ ___ syndrome should NOT be treated. Also, use caution with other drugs that ___ the ____ _____.
A

Rufinamide:

  1. May make hormonal contraceptives less effective
  2. Contraindication: Rufinamide reduces the QT interval. Patients with a history of Familial Short QT syndrome should NOT be treated. Use caution with other drugs that shorten the QT interval
50
Q

Primidone:

  1. Use?
  2. Second line agent - why?
  3. Side effect profile similar to?
  4. Also useful in treatment of ____ ____ at low doses.
A

Primidone:

  1. Partial onset and 2ndary generalized seizures
  2. Second line - Side effects
  3. SE profile similar to phenytoin
  4. Also useful in the treatment of essential tremor at low doses
51
Q

Ethosuximide:

  1. Indications?
  2. MOA?
  3. Ethosuximide metabolism can be increased by?
A

Ethosuximide:

  1. For ABSENCE seizures, including children
  2. MOA: blocks low-threshold T-type Ca++ currents
  3. Ethosuximide metabolism can be increased by carbamazepine, phenytoin, and phenobarbital (all enzyme inducers)
52
Q

Ethosuximide:

  1. Common side effects?
  2. What decreases ethosuximide clearance (and thus increases serum levels)?
  3. ____ can alter seizure ____ in patients treated with ethosuximide.
A

Ethosuximide:

  1. SE: N/V, sleep disturbances, hiccups, anorexia, rash, Lupus syndrome
  2. Valproic acid decreases clearance of ethosuximide
  3. Haloperidol can alter seizure pattern
53
Q

Benzodiazepines:

  1. Indications?
  2. MOA?
  3. Adverse reactions?
A

Benzodiazepines:

  1. Status epilepticus, generalized epilepsy, Lennox-Gastaut
  2. MOA: enhances binding of GABA to GABAa channels
  3. Adverse RXN: sedation, respiratory depression, addiction
54
Q

Benzodiazepines:

  1. Diazepam and lorazepam for?
  2. Clonazepam is used for?
  3. Interactions?
A

Benzodiazepines:

  1. D/L: prolonged generalized seizures or tonic-clonic status epilepticus
  2. Clonazepam: absence, myoclonic, and atonic seizures
  3. Minimal interaction with other AEDs but alcohol increases CNS depressive effects
55
Q

Phenobarbital:

  1. Indication?
  2. May be used for treatment of ____ seizures, but can depress _____ function.
  3. Why is it a second-line drug?
  4. Containdicated in? Why?
  5. Also used in what other kinds of seizures?
A

Phenobarbital:

  1. Generalized tonic-clonic and simple partial seizures
  2. Febrile seizures, but can depress cognitive function
  3. Second line due to sedation
  4. Contraindicated in absence - increases T-type Ca++ channel activity
  5. Also used in alcohol/drug withdrawal seizures
56
Q

Phenobarbital:

  1. Primary MOA? Result?
  2. Also blocks? and has inhibitory action on?
A

Phenobarbital:

  1. Primary MOA: binds to allosteric site on GABA and prolongs opening time for Cl-; limits seizure spread and elevates threshold
  2. Blocks N-type Na+ channels and inhibitory action on AMPA-type glutamate transmission
57
Q

Phenobarbital:

  1. Metabolism?
  2. Can develop _____.
  3. Adverse reactions?
A

Phenobarbital:

  1. Hetapic enzyme inducer and competitively inhibits the metabolism of other drugs (including itself)
  2. Can develop tolerance
  3. Adverse - somnolence, ataxia, nystagmus, depression, behavioral problems, hyperactivity, rash, lupus, and mental slowing
58
Q

Phenobarbital:

  1. What can occur with discontinuance?
  2. Long term use may be associated with ____ of ____ features, ____, and _____ contractures.
  3. Rare SE?
A

Phenobarbital:

  1. Discontinuance - rebound seizures
  2. Long term use associated with coarsening of facial features, osteomalacia, and dupuytren contractures (thickening of tissue on hands)
  3. Rare SE: folate deficiency (supplement), megaloblastic anemia, and idiosyncratic skin reaction
59
Q

Phenobarbital:

  1. Increases the metabolism of?
  2. Why should blood levels be monitored when given with ______?
  3. What decreases phenobarbital metabolism?
A

Phenobarbital:

  1. Increases metabolism of AEDs, oral contraceptives, warfarin, theophylline, and protease inhibitors
  2. Blood levels monitored when given with phenytoin because the effect of the metabolisms together are NOT predictable
  3. Valproic acid and sodium valproate decrease phenobarbital metabolism
60
Q

Tiagabine:

  1. Indication?
  2. MOA?
  3. Common side effects?
A

Tiagabine:

  1. Adjuvant for refractory partial seizures w/ or w/o secondary generalization
  2. MOA: reversibly inhibits GABA transporter, GAT-1 (on presynaptic membrane), and reduces GABA reuptake
  3. SE: dizziness, somnolence, tremor, confusion, depressed mood
61
Q

Tiagabine:

  1. Tiagabine has been associated with what serious side effects? In who?
  2. Half life decreases when given in conjunction with?
  3. Contraindications?
A

Tiagabine:

  1. New onset seizures and status epilepticus in patients withOUT epilepsy
  2. Increased metabolism in presense of carbamazepine, phenytoin, or phenobarbital
  3. Contraindication: shouldnt be used in absence or partial epileptsy with generalized spike wave because it can worsen control or cause status epilepticus. It is also possibly teratogenic (not for preggers)
62
Q

Vigabatrin:

  1. Indication?
  2. MOA?
  3. FDA black box warning? Thus is only available as part of?
A

Vigabatrin:

  1. INFANTILE SPASMS and adjunctive for refractory seizures
  2. MOA: irreversible inhibitor of GABA-transaminase (inhibits GABA breakdown)
  3. Black box warning: loss of vision in 30-50% of patients; it is only available as part of the SHARE program (docs must be registered: Support Help And Resources for Epilepsy)
63
Q

Felbamate:

  1. Indications?
  2. MOA?
  3. SERIOUS side effects?
A

Felbamate:

  1. For refractory partial and secondary generalized seizures and Lennox-Gastalt syndrome
  2. MOA: inhibits glutamate NMDA receptors as well as potentiates those to GABA
  3. causes aplastic anemia and heptatitis
64
Q

Perampanel:

  1. Adjunctive treatment for?
  2. MOA?
  3. Common side effects?
  4. Black box warning?
A

Perampanel:

  1. Adjunctive for focal-onset seizures with or without secondary generalized seizures
  2. MOA: glutamate AMPA receptor antagonist
  3. SE: dizziness, somnolence, HA, fatigue, and irritability
  4. Black blox: serious psychiatric and behavior issues (aggression, hostility, irritability, anger, and homocidal ideation)
65
Q

Valproate:

  1. Drug of choice for?
  2. Also approved for what seizures?
  3. Treatment for what non-seizure related illnesses?
A

Valproate:

  1. DOC: primary generalized epilepsy, idiopathic generalized seizures, and juvenile myoclonic epilepsy
  2. Also: partial seizures, absence epilepsy, photosensitive epilepsy, lennox-gastaut syndrome, and infantile spasm (second choice - to vigabatrin)
  3. migrain headache prevention and alternative to lithium in BPD
66
Q

Valproate:

MOA:

  1. Blocks what channels?
  2. Slows rate of what channel recovery?
  3. Increases what effects? How?
A

Valproate:

MOA:

  1. Blocks T-type Ca++ channels
  2. Slows rate of Na+ channel recovery from the inactivated state
  3. Increases GABAeffects by facilitating glutamic acid decarboxylase (enzyme for GABA synthesis) and inhibits metabolism of GABA at high levels (GAT inhibitor)
67
Q

Valproate:

  1. Metabolized in liver and is a potent inhibitor of both _____ and ______ and increases plasma levels of?
  2. Common side effects?
A

Valproate:

  1. Metabolized in liver and is a potent inhibitor of both oxidation and glucuronidation and increases plasma levels of other AEDs.
  2. SE: GI complaints, weight gain, hair loss, and tremor
68
Q

Valproate:

Rare side effects:

  1. _______, which can lead to brain damage
  2. Idiosyncratic ____ that is frequently fatal. Seen in who?
  3. Acute ______ toxicity, especially in ____
A

Valproate:

Rare side effects:

  1. hyperammonemia, which can lead to brain damage
  2. Idiosyncratic hepatitis that is frequently fatal usually in children or with polytherapy
  3. Acute hematological toxicity, especially in kids
69
Q

Valproate:

Rare side effects:

  1. What adverse endocrine effects? What can this lead to?
  2. What else?
  3. Black box warning?
A

Valproate:

Rare side effects:

  1. Endocrine: insulin resistance and change in sex hormone levels –> causing anovulatory cycles, amenorrhea, and polycystic ovary syndrome
  2. Pancreatitis and thrombocytopenia
  3. Black box: avoided in women of childbearing age unless essential for mania of BPD or seizures. Teratogenic
70
Q

Valproate:

  1. Inhibits the metabolism of?
  2. May increase serum levels of? How?
  3. Also decreases the clearance of?
A

Valproate:

  1. Inhibits metabolism of phenobarbital and carbamazepine
  2. May increase serum levels of other AEDs via displacement from plasma proteins (like phenytoin)
  3. Valproate also decreases the clearance of antidepressants amitryiptyline and nortriptyline
71
Q

Topiramate:

  1. Adjuvant treatment for?
  2. Initial therapy for?
  3. Monotherapy for?
  4. Also for?
A

Topiramate:

  1. Adjuvant for partial and generalized seizures 2 years +
  2. Initial therapy for newly diagnosed partial and mixed siezure disorders
  3. Monotherapy for refractory generalized tonic-clonic seizures and partial seizures
  4. Lennox-Gastaut and migraine prevention
72
Q

Topiramate:

  1. Reduces ____ currents.
  2. Activates ____ currents leading to _____
  3. Enhances postsynaptic _____ ____ currents
  4. Limits activation of what receptors?
A

Topiramate:

  1. Reduces Na+ currents
  2. Activates K+ currents leading to hyperpolarization
  3. Enhances postsynaptic GABA receptor currents
  4. Limits activation of glutamate AMPA and kianite receptors
73
Q

Topiramate:

  1. How is there metabolic acidosis?
  2. Common side effects?
A

Topiramate:

  1. Metabolic acidosis: CAI: produces HCO3- loss
  2. SE: cognitive deficits, fatigue, nausea, parasthesia, mood alteration, and dose releated weight loss and metabolic acidosis
74
Q

Topiramate:

  1. Rare side effects (3)?
  2. Reduces effectiveness of?
  3. May increase ____ concentrations.
A

Topiramate:

  1. Rare SE: increased occurance of kidney stones, decreased sweating and thus hyperthermia, and vision problems (acute myopia associated with secondary angle closure glaucoma)
  2. Reduces effectiveness of contraceptives
  3. May increase phenytoin concentration
75
Q

Topiramate:

  1. Concomitant administration with ____ ____ has been associated with _____ with or without encephalopathy
  2. Contraindications?
A

Topiramate:

  1. Administration with valproic acid has been associated with hyperammonemia with or w/o encephalopathy
  2. Contra = pregnancy
76
Q

Gabapentin and Pregabalin:

  1. Adjunctive for?
  2. Gabapentin widely used to relieve?
  3. Pregabalin used for?
A

Gabapentin and Pregabalin:

  1. Adjunctive refractory partial seizures
  2. Gabapentin: neuropathic pain (diabetic neuropathy, shingls) and restless leg syndrome
  3. Pregabalin: chronic pain, neuropathic pain, and fibromyalgia
77
Q

Gabapentin and Pregabalin:

  1. Useful in what patients? Why?
  2. Primary MOA?
  3. Pregabalin also modulates release of several ________ like?
A

Gabapentin and Pregabalin:

  1. Useful in patients with hepatic diseases and on multidrug regimens bc lacks drug interaction, protein binding, and liver metabolism
  2. MOA: inhibition of HVA Ca++ channels in cortical and spinal neurons that decrease inward Ca++ currents
  3. Pregabalin: modulates release of several NTs like glutamate and NE
78
Q

Gabapentin and Pregabalin:

  1. Gabapentin side effects?
  2. Pregabalin side effects?
  3. Pregabalin serious side effect?
A

Gabapentin and Pregabalin:

  1. Gabapentin: sedation, dizzy, blurred vision, uncontrolled eye movements
  2. Pregabalin: dissines, somnolence, ataxia, tremor, headache, wt gain, lightheadedness, and mild nausea
  3. Pregabalin: NEW ONSET MYOCLONUS
79
Q

Levetiracetam:

  1. Adjuvant in treatment of?
  2. MOA?
A

Levetiracetam:

  1. Adjuvant of partial seizures and primary generalized tonic-clonic seizures (esp in kids)
  2. MOA: interacts with synaptic vesicle protein SV2A to modify release of glutamate AND gaba
80
Q

Levetiracetam:

  1. Drug interactions?
  2. Common side effects?
  3. Rare but serious side effects?
A

Levetiracetam:

  1. No significant interactions bc its excreted unmetabolized
  2. SE: somnolence, HA, weakness, dizziness, aggression, anger, and pins/needles sensation in extremities
  3. Rare SE: rash and teratogenic
81
Q

Levetiracetam:

  1. Helpful in what patients? Why?
  2. One of the preferred AEDs in _____ patients.
A

Levetiracetam:

  1. Good for pts with hepatic or renal insufficiency and thos on concomitant meds because it has NO drug interactions
  2. Preferred AED in ELDERLY patients
82
Q

Ezogabine:

  1. Adjunctive treatment for?
  2. MOA: enhances transmembrane _____ currents mediated by the ______ family of ion channels and is though to do what 2 things?
A

Ezogabine:

  1. Adjunctive treatment for adult partial-onset seizures
  2. MOA: enhances transmembrane K+ currents mediated by the KCNQ family of ion channels and is thought to stabilize the resting membrane potential and reduce brain excitablity
83
Q

Ezogabine:

  1. Metabolism?
  2. Common side effects?
  3. FDA BOX warning?
A

Ezogabine:

  1. Liver by glucuronidation and acetylation
  2. SE: dizziness, somnolence, confusion, fatigue, tremor, vertigo, decreased urination, psychiatric (psychosis, hallucination), cardiac arrhythmias (QT prolongation)
  3. FDA box warning: blue skin discoloration and eye abnormalities characterized by pigment changes in retina and potential vision loss
84
Q

Carbonic Anhydrase Inhibitors:

  1. Inhibition of enzyme CA increases the concentration of ____ ions _____ and ___ the pH –> ___ ions shift to the ______ compartment to buffer –> results in ____ and an increase in seizure threshold.
  2. Drug example?
A

CAI:

  1. Inhibition increases the concentration of H+ ions intracellularly and decreases the pH –> K+ ions shift to the extracellular compartment to buffer–> results in hyperpolarization and increase in seizure threshold
  2. Drug: acetazolamide
85
Q

CAI:

  1. Used as adjunctive therapy in?
  2. What are also weak inhibitors of carbonic anhydrase? (this doesnt really affect much)
A

CAI:

  1. Adjunctive therapy in refratory seizures with catamenial pattern (seizure clutering around period)
  2. Topiramate and zonisamide are also weak inhibitors
86
Q

Risk of seizures versus AEDs to the fetus?

A

Risk of seizure is WORSE than the risk of AEDs. Seizure threshold is lowered during pregnancy (due to increased volume of distribution) and stillbirths occur twice as often in women with epilepsy who have a seizure during pregnancy as in women with epilepsy who do NOT have a seizure.

Neural tube defects for women on meds extend to 2% risk.

87
Q

Risk to newborn?

A

Risk to newborn:

  1. Increase risk of bleeding by carbamazapine, phenobarbital, phenytoin, primidone, OXC, felbamate, and topiramate (these are ALL ENZYME INDUCERS)
  2. Congenital malformations
88
Q
  1. DOC status epilepticus?
  2. What given after DOC to provide longer duration of control?
  3. What to give if DOC not effective?
  4. Give _____ ____ in highly resistant cases.
A
  1. DOC status epilepticus: diazepam or lorazepam
  2. Given after: phenytoin/fosphenytoin
  3. If benzo doesnt work: phenobarbital
  4. General anesthetics in highly resistant cases

Pharmacology (24 decks)

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