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Neuropharmacology > Drugs for Epilepsy > Flashcards

Drugs for Epilepsy Flashcards

1
Q

What is epilepsy?

A

a disorder of the brain characterised by repeated/recurrent seizures

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2
Q

What is a seizure?

A

an episodic/single sudden abnormal excessive and synchronous discharge of a group of neurons in the brain

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3
Q

What does abnormal electrical activity across the brain result in?

A
  • loss of consciousness
  • abnormal movements
  • atypical or odd behaviour
  • distorted perceptions
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4
Q

What are causes of epilepsy?

A
  • genetic
  • developmental defects/congenital abnormalities
  • infection
  • trauma/injury
  • degenerative diseases
  • pregnancy (eclampsia)
  • psychogenic seizures
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5
Q

What are symptoms of epilepsy?

A
  • sudden falls
  • uncontrollable jerking movements
  • strange sensations and emotions
  • loss of consciousness and awareness
  • staring
  • aura
  • confusion
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6
Q

What are the types of epileptic seizures?

A

focal/partial and generalised

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7
Q

What are the symptom types of focal seizures in the different lobes of the brain?

A
  • frontal - movement, emotions, memory, language, behaviour and personality
  • temporal - hearing, speech, memory and emotions
  • parietal - bodily sensations
  • occipital - processing vision
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8
Q

What are focal seizures divided into?

A

simple and complex

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9
Q

What is a simple focal seizure?

A

abnormal activity confined to a single locus in the brain, does not spread and presents as abnormal activity of single muscle or limb

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10
Q

What is a complex focal seizure?

A

complex sensory hallucinations and mental distortion that presents as motor dysfunction e.g. chewing mvts, diarrhoea and urination

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11
Q

What do generalised seizures involve?

A

abnormal electrical discharge throughout the brain (can be convulsive or non-convulsive with immediate loss of consciousness)

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12
Q

What are the 5 types of generalised seizures?

A
  • generalised tonic-clonic
  • absence seizures
  • generalised-myoclonic
  • febrile seizures
  • status epilepticus
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13
Q

How can epilepsy be diagnosed?

A
  • neurological examination (physical signs)
  • EEG
  • MRI
  • PET
  • SPECT
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14
Q

What are the neural mechanisms of epilepsy associated with?

A
  • enhanced excitatory neurotransmission
  • impaired inhibitory neurotransmission
  • abnormal electrical activity of affected cells
  • several susceptibilities of genes encoding neuronal ion channels
  • excitotoxicity
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15
Q

In an epileptic brain, what is the imbalance?

A

more excitation than inhibition

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16
Q

What are the 2 main mechanisms involved in epilepsy?

A
  • EPSP in the brain by sodium and calcium channel functions and glutamate and AMPA/NMDA receptor neurotransmission
  • IPSP in the brain by GABA neurotransmission
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17
Q

What causes generalised seizures?

A

prolonged neuronal excitability

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18
Q

What 2 mechanisms cause prolonged neuronal excitability?

A
  • dysfunction in sodium channels
  • abnormal potassium channels slowing the rapid efflux of potassium
19
Q

What do antiepileptic drugs aim to do?

A

inhibit neuronal discharge by decreasing excitation in the brain

20
Q

What are the main mechanisms of anticonvulsant drugs?

A
  • inhibition of voltage gated sodium and calcium channels
  • increased activity of voltage gated potassium channels
  • inhibition of neurotransmitter release
  • inhibition of AMPAR
  • increased activity of GABA receptor
21
Q

What are all first generation antiepileptic drugs metabolised by?

A

cytochrome P450

22
Q

What is the MOA of phenobarbital?

A
  • increases duration of bursts of GABA A receptor mediated current
  • enhances GABA action
23
Q

What are the side effects of phenobarbital?

A

respiratory depression, Vitamin D and folic acid deficiency

24
Q

What is the MOA of phenytoin?

A
  • blocks sodium channels
  • prevents repetitive firing by slowing the rate of recovery of voltage activated sodium channels from inactivation
25
Q

What are side effects of phenytoin?

A

gingival hypertrophy, hepatitis, hirsutism, folic acid deficiency, osteomalacia, SJS

26
Q

What are clinical uses of phenytoin?

A

all kinds of seizures except absence seizures

27
Q

What is the MOA of ethosuximide?

A
  • reduce T-type calcium currents in the thalamus
  • blocks synchronised thalamic firing
28
Q

What are side effects of ethosuximide?

A

nausea and vomiting, headache, dizzinesss, drowsiness, behaviour changes

29
Q

What are clinical uses of ethosuximide?

A

absence seizures

30
Q

What is the MOA of carbamazepine?

A

blocks sodium channels which slows their rate of recovery after inactivation

31
Q

What are side effects of carbamazepine?

A

neurotoxicity, hypersensitivity, hepatitis, agranulocytosis

32
Q

What are clinical uses of carbamazepine?

A

all seizures except absence, trigeminal neuralgia and bipolar disorder

33
Q

What is the MOA of valproate?

A
  • increases CNS GABA levels by increased synthesis and reduced catabolism
  • blocks T-type calcium current
  • enhances sodium channel inactivation
34
Q

What are side effects of valproate?

A

hair loss, tremors, weight gain, hepatotoxicity

35
Q

What are clinical uses of valproate?

A

all seizures and bipolar disorder

36
Q

What is the MOA of barbiturates?

A
  • act on a subset of GABA A receptors and increase frequency of opening of chloride channels
  • GABA potentiation
37
Q

What are clinical uses of barbiturates?

A

status epilepticus (not used for acute treatments of seizures)

38
Q

What do newer antiseizure drugs target?

A

synaptic release

39
Q

Which second/third generation antiseizure drugs decrease excitatory synaptic activity?

A

felbamate, topiramate, levetiracetam

40
Q

What does lacosamide do?

A

block sodium channels to allow neurons to recover from prolonged depolarisation

41
Q

What does retigabine do?

A

cause hyperpolarisation and stabilisation of resting membrane potential by potassium channel activation

42
Q

Which second/third generation antiseizure drugs enhance GABA neurotransmission?

A

gabapentin and vigabatrin

43
Q

What are screening methods for new antiseizure drugs?

A
  • enhancement of GABA transmission
  • diminution of excitatory transmission
  • modification of ionic conductance

Neuropharmacology (12 decks)

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