Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

control > L20 - epilepsy > Flashcards

L20 - epilepsy Flashcards

1
Q

what is a seizure

A

Clinical manifestations of abnormally excessive and hypersynchronous activity of neurones located predominantly in the cerebral cortex

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

ionic cause of excitation

A

inwards Na+ and Ca2+ currents

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

neurotransmitters for excitation

A

glutamate, aspartate

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

ionic cause of inhibition

A

insufficient inward current of Cl- or outward current of K+

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

neurotransmitter for inhibition

A

insufficient release of GABA

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

what synapses onto the excitatory neurone

A

inhibitory neurone

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

what % of neurones are interneurones

A

10-20%

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

role of inhibitory neurones

A

to keep neurone activity tightly focussed as it flows through the brain - prevents it spreading sideways

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

mechanism of a seizure

A

localised hyper excitability spreads into surrounding neuronal networks and involves more and more neurones (activity spreads sideways), resulting in a seizure

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

how to measure excitation

A

intracellular calcium levels

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

anticonvulsant

A

a drug decreasing the frequency/severity of seizures in people with epilepsy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

measurement of calcium levels to measure excitation:

A
  • brain slides bathed in Mg2+
  • free artificial CSF leads to recurrent spontaneous seizures
  • after removing Mg2+, there is a transition period where the tissue behaves as if it were expecting surges of activity, which are then overcome by inhibitory neurones
  • normal background behaviour in the network is followed by a sudden collapse of inhibition
  • strong excitatory signals dominate cellular responses and these produce step-like waves of local excitation at the network level
  • this is observed in Ca imaging
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

what do anti epileptic drugs do

A

treat symptoms of seizures, not the underlying epileptic condition

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

modes of action of anticonvulsants

A
  • suppress action potential
  • enhance GABA transmission
  • suppress excitatory transmission
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

how do AED suppress action potentials

A
  • sodium channel blocker or modulator

- potation channel opener

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

how do AED enhance GABA transmission

A
  • GABA uptake inhibitory

- GABA mimetrics

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

what are GABA mimetrics

A

drugs which have the same effects as GABA

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

how do AED suppress excitatory transmission

A

glutamate receptor antagonist

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

most widely used AED

A

valproic acid

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

febrile seizures

A

seizures in infants

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

main inhibitory neurotransmitter in CNS

A

GABA

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

what % of synapses is GABA found at

A

30%

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

GABA receptors

A

GABAa and GABAb

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

GABAa receptor

A

ligand-gated chloride channel receptor

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

GABAb receptor

A

G protein-couples receptor

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

which GABA receptor is most relevant in seizures and epilepsy

A

GABAa

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

GABAa receptor binding site and action

A

when GABAa receptor is activated through binding, it forms a chloride channel, allowing chloride ions to enter the cell

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

GABA enhancement

A

benzodiazepines or barbiturates (have binding sites for GABA) –> resulting in an influx of chloride ions

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

which drugs can be used to inhibit GABA uptake back into the presynaptic neurone

A

vigabatrin

tiagabine

30
Q

methods of enhancing GABA action

A
  • enhancing action of GABAa receptors
  • inhibiting GABA transaminase
  • inhibiting GABA uptake by pre-synpatic neurone
31
Q

barbiturate drug which enhances action of GABAa receptors

A

phenobarbital

32
Q

barbiturate

A

CNS depression drug

33
Q

benzodiazepines drug which enhances action of GABAa receptors

A

clonazepam

34
Q

benzodiazepines

A

sedatives

35
Q

examples of benzodiazepines

A

clonazepam
clorazepate
diazepam (valium) and lorazepam

36
Q

clonazepam

A

Effective in generalized tonic-clonic, absence and partial seizures

37
Q

Clorazepate

A

Effective against partial seizures

- Used in conjunction with other drugs

38
Q

Diazepam (Valium) and lorazepam

A

Effective against status epilepticus when given i.v.

39
Q

status epilepticus

A

a life-threatening condition in which the brain is in a state of persistent seizure
(more than 30min continuous seizure or two or more sequential seizures without full recovery between)

40
Q

actions of benzodiazepines

A
  • sedatives
  • hypnotic
  • anxiolytic
  • anticonvulsant
  • muscle relaxant
  • amnesic
41
Q

mechanisms of action of benzodiazepines

A

increase affinity of GABA for its receptor

  • increase Cl current
  • strengthens surrounding inhibition (preventing spreading)
  • raising action potential threshold
42
Q

unwanted effect of benzodiazepines

A

sedation - respiratory depression
tolerence
dependence

43
Q

what to give in case of overdose of benzodiazepines

A

flumazenil
BC-site antagonist
prevents BC binding to GABAa receptor

44
Q

most frequent drugs which inhibit Na channels

A

phenytoin
carbamazepine and oxcarbamazepine
lamotrigine

45
Q

voltage gated sodium channels at resting potential

A

closed

46
Q

voltage gated sodium channels when inactivated

A

Brief period after activation, channel does not open in response to a new signal

47
Q

voltage gated sodium channels when sodium enters the cell

A

open

48
Q

why action potentials jump down axons

A
  • myelination prevents AP from leaking out of axon
  • charge spreads alone axon until it reaches the Node of Ranvier, where there is no myelination
  • this is packed with Na+ channels
  • here, AP jump down the axon
49
Q

what happens when Na+ channels are inhibited

A

AP cannot arise in next neurone and signal is inhibited

50
Q

action of phenytoin

A

binds to the inactivated state of the Na+ channel and slows down its recovery - meaning membrane takes longer to repolarise when inactivated

51
Q

when does phenytoin bind

A

when sodium channels have recently opened (inactivated channels)

52
Q

what type of block is phenytoin

A

use dependent block

53
Q

use dependent block

A

the more channels which have been opened, the more in the inactivated state hence the more available to be targeted to phenytoin

54
Q

tonic blockage

A

When there are long intervals between impulses, the level of inhibition of each impulse is the same

55
Q

phasic blockage

A

When intervals between impulses is short, the level of inhibition increase with each impulse

56
Q

pharmacokinetics of phenytoin

A

taken orally

well absorbed

57
Q

consequence of free phenytoin (if other drugs have bound these so cannot be taken up)

A

increases hepatic clearance of the drug so effects can be unpredictable

58
Q

metabolism of phenytoin in the liver

A

95% metabolised to an inactive meyabolite

59
Q

phenytoin half life and metabolism

A

half life increases as dose increases

  • as we increase dose, rate of metabolism cannot keep up
  • small increase in dose can lead to a large increase in plasma concentration
60
Q

unwanted effects of phenytoin - mild

A

vertigo
ataxia
headache

61
Q

unwanted effects of phenytoin - severe

A 
confusion
hyperplasia in gums
megaloblastic anaemia
hypersensitivity and rashes
foetal malformations (cleft palate)
hepatitis
62
Q

foetal hydantoin syndrome clinical features

A

intrauterine growth restriction with microcephaly, resulting in dysmorphic features in face and lumps and growth and mental retardation

63
Q

foetal hydantoin syndrome

A

A group of defects caused to the developing foetus by exposure to the teratogenic effects of phenytoin or, more rarely, carbamazepine

64
Q

valproate

A
  • Not related chemically to the other classes of anti-epileptics
  • Unusual in that it is effective against both tonic-clonic and absence seizures
  • Can also be useful in bipolar depressive illness as a mood stabiliser
65
Q

how is valproate taken and absorbed

A

orally - well absorbed in GI tract

66
Q

foetal valproate syndrome

A

There is a 6-9% risk of congenital malformations in infants exposed to VPA prenatally, compared to 2-3% in the general population

67
Q

mechanisms of valproate

A
  • inhibits Na channels (weaker than phenytoin)
  • decreased GABA turnover
  • blocks neurotransmitter released by blocking T-type Ca2+ channels
68
Q

how does valproate decrease GABA turnover

A

Inhibition of succinic semialdehyde dehydrogenase, thereby indirectly inhibiting GABA transaminase
- May lead to increased synaptic GABA levels (in the synaptic cleft)

69
Q

why may valproate cause genetic disabilities

A

it is an inhibitor of histone deacetylase (HDAC)

70
Q

normal deacetylation of chromatin

A
  • chromatin becomes closed so transcription factors can’t bind
  • genes cannot be transcriped
71
Q

consequences of valproate inhibiting HDAC

A

hyperacetylation of chromatin

- increased transcription of gene

control (38 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions