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Pharmacology > Antiepileptics > Flashcards

Antiepileptics Flashcards

1
Q

Epilepsy (2)

A
  • manifests by seizures caused by the asynchronous discharge of neurons
  • seizures can also be caused by trauma, infections, surgery, tumors
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2
Q

Types of epilepsy

A
  1. Partial - simple or with generalization
  2. Generalized - tonic-clonic, myoclonic, absence
  3. Status epilepticus
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3
Q

Partial seizures (5)

A
  • involves a part of brain (depends on the part affected)
  • involuntary muscle contractions
  • abnormal sensory experiences
  • affects mood and behavior
  • simple (with conscious), complex (without consciousness)
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4
Q

Generalized seizures (4)

A
  • involves the whole brain
  • tonic-clonic: strong contraction of whole muscle (1min), rapidly contracts and relaxes (2-4min), still unconscious for a few min (defecation, micturition, salivation is possible), fell “ill” after recovery
  • myoclonic: short muscle twitches
  • absence: thalamus is responsible, calcium channels are important. Abrupt “disconnection”, patient doesn’t know what happened
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5
Q

Status epilepticus (5)

A
  • continuous uninterrupted seizures
  • lasts for more than 5 min
  • several episodes of seizures during this period
  • usually tonic-clonic
  • life threatening
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6
Q

Anti-epileptic drugs mode of action (4)

A
  • imbalance between excitatory and inhibitory processes in the brain
  • too much excitation or too little inhibition
  • main goal: decrease neuronal excitability or increase neuronal inhibition
  • main mediators: glutamate (excitation), GABA (inhibition)
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7
Q

Anti-epileptics names (9)

A
  1. Phenytoin
  2. Carbamazepine
  3. Valproate
  4. Ethosuximide
  5. Phenobarbital
  6. Benzodiazepines
  7. Lamotrigine
  8. Topiramate
  9. Gabapentin
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8
Q

Channels blocked by phenytoin and carbamazepine

-pharmacokinetics of phenytoin

A

Sodium channel in pre-synaptic neuron

-metabolism is non-linear, zero-order at moderate to high doses

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9
Q

Channels blocked by valproate

-pharmacokinetics

A
  • sodium channel in pre-synaptic neuron
  • low voltage calcium channel in post- synaptic neuron (T-type)
  • GABA transaminase (GATA-T)

-compete with phenytoin for plasma binding proteins, hepatotoxicity, inhibit –> carbamazepine, phenobarbital, ethosuximide, lamotrigine, phenytoin

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10
Q

Channels blocked by ethosuximide

A

-low voltage calcium channels in post-synaptic neuron T-type)

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11
Q

Channels blocked by barbiturates and benzodiazepines

A
  • they act on GABA A receptors on the post- synaptic neuron
  • benzodiazepines - increase the frequency of channel opening
  • barbiturates - increase the duration of channel opening
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12
Q

Channels blocked by lamotrigine

-pharmacokinetics

A
  • sodium channel in pre-synaptic neuron
  • high voltage calcium channel in pre-synaptic neuron

-eliminated via hepatic glucuronidation

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13
Q

Channels blocked by gabapentin, pregabalin

-pharmacokinetics

A

-high voltage calcium channel in pre-synaptic neuron

  • eliminated by the kidneys (uncharged form), no drug-drug interactions
  • only used for partial seizures because it partially blocks the calcium channels binding to alpha and delta sub-unit
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14
Q

Channels blocked by topiramate

-pharmacokinetics

A
  • sodium channel in pre-synaptic neuron
  • high voltage calcium channel in pre-synaptic neuron
  • block AMPA receptor in post-synaptic neuron
  • stimulate GABAA receptor in post-synaptic neuron

-both hepatic and renal elimination (uncharged form)

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15
Q

Anti-epileptic drugs choice in:

  1. Partial Seizures
  2. Generalized
  3. Status epilepticus
A
  1. for both simple and generalized: valproate, topiramate, carbamazepine, phenytoin, gabapentin, lamotrigine
  2. absence –> ethosuximide, valproate
    myoclonic –> valproate, lamotrigine, topiramate
    tonic- clonic –> valproate, lamotrigine, topiramate
  3. diazepam
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16
Q

Other indications of anti-epileptic drugs

A
  1. Depression: lamotrigine, topiramate
  2. Bipolar disorder: valproate, carbamazepine, lamotrigine, topiramate
  3. Migraine: valproate, topiramate
  4. Neuropathic pain: carbamazepine, gabapentin
17
Q

Anti-epileptic drugs of choice in pregnancy

A
  1. Lamotrigine
  2. Topiramate

***Contraceptives could also affect anti-epileptic drugs and vice-versa

18
Q

Anti-epileptic’s pharmacokinetics (6)

A
  • used for long periods of time
  • well absorbed, good bio-availability
  • many are metabolized by hepatic enzymes
  • resistance –> increase expression of transporters at the level of blood-brain barrier
  • many of these drugs are strong inducers or inhibitors of liver enzymes that metabolize other drugs –> drug interaction!!!!!
  • ex: rifampin –> induce hepatic enzymes and may decrease the anti-epileptic effects of some drugs
19
Q

Anti-epileptic drugs - unwanted effects

-only main ones

A
  1. Phenytoin –> gum hypertrophy, hirsutism, megaloblastic anemia, fetal malformation
  2. Carbamazepine –> leucopenia, cardiotoxicity
  3. Phenobarbital –> sedation, depression
  4. Benzodiazepines –> sedation, withdrawal syndrome
  5. Ethosuximide –> may exacerbate tonic-clonic seizures
  6. Lamotrigine –> Stevens-Johnson syndrome (severe allergic reaction)
  7. Gabapentin (Pregabalin) –> sedation, ataxia
  8. Topiramate –> metabolic acidosis, kidney stones
  9. Valproate –> fetal malformation, liver damage

general: sedation, ataxia

20
Q

Parkinson’s disease

  • characteristics (5)
  • symptoms
A
  • chronic, progressive, neuro-degenerative disorder
  • dopamine deficiency
  • neurons connecting substantia nigra and striatum progressively degenerate
  • affects coordination and movement
  • exact cause still unknown
  • 4 cardinal symptoms: resting tremor, rigidity, postural instability, bradykinesia
  • also cognitive impairment
21
Q

Pathogenesis - Parkinson’s disease (5)

A
  • degenerative disease of basal ganglia
  • idiopathic –> may follow stroke, virus infection, drug induced
  • early degeneration of dopaminergic nigrostriatal neurons, followed by general neurodegeneration
  • dopaminergic neurons in substantia nigra –> inhibit GABA neurons in striatum –> less dopamine, more GABA –> increased inhibition of thalamus and less excitation to motor cortex
  • dopaminergic neurons in susbtantia nigra –> inhibit excitatory cholinergic neurons in striatum –> increased production of acetylcholine = impaired mobility
22
Q

Diagnosis - Parkinson’s disease (3)

A
  • there are no definitive tests
  • neurological exams or medical history/ symptoms
  • other tests (ex: blood, brain scans…) only made to exclude other causes
23
Q

Treatment - Parkinson’s disease

  • drugs act by…
  • name of the drugs and their function? (5)
A

-counteracting dopamine deficiency in the basal ganglia or blocking muscarinic receptors

  1. Levodopa + carbidopa (inhibit peripheral dopa decarboxylase) or entacapone (inhibit cathecol-o-methyltransferase)
  2. Bromocriptine (dopamine agonist)
  3. Selegiline (inhibit monoamine oxidase B)
  4. Amantadine (enhance dopamine release)
  5. Benztropine (muscarinic receptor antagonist)
24
Q

Why is Levodopa given with another drug?

A
  • Levodopa is dopamine’s precursor.
  • Dopamine cannot cross the blood-brain barrier, so instead Levodopa is used (it is able to cross it).
  • Another drug is necessary to prevent peripheral metabolism of Levodopa.
  • After it crosses the blood-brain barrier, it is converted to dopamine
25
Q

Levodopa

  • characteristics (2)
  • unwanted effects (4)
  • benefits of levodopa with carbidopa
A
  • “Gold standard”- most effective for motor symptoms
  • given 2-4 times daily
  • “on-off” effects due to rapid plasma concentration fluctuations, nausea, anorexia, psychological effects (schizophrenia like syndrome), postural hypotension
  • reduce dose by about 10-fold and minimize side effects
26
Q

Bromocriptine

  • characteristics (4)
  • unwanted effects (6)
A
  • dopamine agonist, longer duration of action, less tendency to causes “on-off” effects and dyskinesia, inhibits release of prolactin
  • nausea, anorexia, confusion, delusions, peritoneal fibrosis, sleep disturbances
27
Q

Benztropine

  • characteristics (1)
  • unwanted effects (8)
A
  • muscarinic receptor antagonist
  • dry mouth, urinary retention, constipation, memory and cognitive problems, hallucinations, confusion, sedation, blurred vision
28
Q

Selegiline

  • characteristics (3)
  • unwanted effects (8)
A
  • monoamino oxidase B inhibitor, mild anti-depressant activity, less tendency to cause “cheese reaction”
  • nausea, dizziness, confusion, hallucinations, nightmares, headache, heartburn, dry mouth
29
Q

Pathogenesis - Alzheimer’s disease

A
  • Cholinergic hypothesis - lack of acetylcholine due to loss of central cholinergic neurons
  • Amyloid hypothesis - accumulation of beta-amyloid proteins (induce neuroinflammation)
  • Tau hypothesis - abnormal accumulation of tau proteins (form neuro-fibrillary tangles in the brain)
30
Q

Alzheimer’s disease

  • risk factors (3)
  • protective factors (4)
A
  • advancing age, modifiable (mid-life obesity, diabetes, smoking, hypertension, dyslipidemia), non-modifiable (genetics)
  • education, diet, exercise, social and cognitive engagement
31
Q

During Alzheimer’s disease, in which part of the brain we have a problem?

A
  • cholinergic neurons
  • hippo-campus
  • frontal cortex
32
Q

Features of Alzheimer’s disease (3)

A
  • appear gradually and eventually leads to irreversible ability to reason, remember and learn
  • cognitive impairment –> memory loss, inability to learn new things, language impairment, disorientation, difficulty in performing familiar tasks
  • non-cognitive impairment –> irritability, agitation, anxiety, aggression, sleep disturbances, depression
33
Q

Diagnosis - Alzheimer’s disease (2)

A
  • clinical features and patho-histological confirmation by brain autopsy or biopsy
  • 3 key patho-histological features: cortical atrophy, b-amyloid neuritic plaques, neuro-fibrillary tangles
34
Q

Treatment - Alzheimer’s disease (2)

A
  1. Cholinesterase inhibitors –> inhibit cholinesterase enzymes, increase the levels and duration of acetylcholine
    - donepezil, rivastigmine, galantamine
  2. NMDA receptor antagonists –> B-amyloid proteins cause an abnormal rise in glutamate, which bind to NMDA receptors and over stimulate them = excessive influx of Ca2+. Receptors need to be blocked
    - memantine
35
Q

Cholinesterase inhibitors and NMDA receptors antagonists - side effects

A
  1. Cholinesterase inhibitors –> GI effects (nausea, vomiting, diarrhea), bradycardia, loss of appetite, weight loss
  2. NMDA receptor antagonists –> headache, insomnia, diarrhea

Pharmacology (29 decks)

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