Brainscape's Knowledge GenomeTM

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


See full index

physiology and pharma > L16 - epilepsy > Flashcards

L16 - epilepsy Flashcards

1
Q

list the types of epilepsy

A
  1. generalised seizure (grand mal) -> tonic clonic seizures
  2. generalised seizures (petit mal) -> absent seizures
  3. partial seizures ( jacksonian epilepsy)
  4. status epilepticus
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

describe generalised seizure (grand mal)

A

tonic clonic seizure
sustained contraction of muscles (often along with respiration cessation) followed by waves of synchronous contractions

consciousness resumes after several minutes

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

describe generalised seizure (petit mal)

A

most common in children

absent seizures

not assoicated with motor fucntions but involves loss of attention for short period of time

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

describe partial seizures

A

muscle spasm in one digit / limb / side of body often spreading from one location to others

can be conscious

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

describe status epilepticus

A

when a grand mal seizure continus or repeats for a long period of time (30 mins)

can be life threatening due to repeated cessation of respiration

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

what is the EEG

A

a measure of summated changes in extracellular voltage caused by activity of many axons and synapses

recorded by attaching electrodes to scalp

measures brain activity in seizures

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

what can cause epilepsy

A

brain injury -> stoke / trauma can provide epileptic focus

infection -> can cause inflammation which provides epileptic focus

tumours

autoimmune disease -> can cause encephalitis which provides epileptic focus

idiopathic (most common)

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

explain the kindling experimental model foe epilepsy

A
  1. repetitive electtical / chemical stimulation of a small region of the brain (in an animal model)

initially the stimulation only excites the local area, but after repeating the stimulation several times the excitation spreads across the entire brain similarly to an epileptic fit

useful in studying anti-epileptics

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

what are the two main classes of drugs to treat epilepsy?

A
  1. drugs that enhance GAGA activity (BZDs, barbiturates, valproic acid, KBr)
  2. drugs that block VG Na/Ca channels in a use dependant manner - so that only repetitive nerve activity is blocked
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

where do barbiturates bind?

A

to inner foldings of the GABA(A) receptor pore (allosteric site)

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

function of barbiturates

A

bind to the allosteric site of GABA(A) opening the channel, and hold the channel open for longer allowing more Cl- to flow through

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

how is tolerance possible for Barbiturates?

A

upregulation of excitatory receptors

upregulation of CP450 enzymes in liver

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

where do BZDs bind

A

between the a and y subunit on GABA

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

explain mechanims of action of BZDs

A

positive modulators that increase agonist binding

  1. bind between the a and y subunits of GABA and increase the receptors affinity for GABA, increasing GABA binding and channel opening
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

when stage of epilepsy are BZDs given

A

during status epilepticus

usually too sedative for epilepsy prophylaxis

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

in epilepsy what is the route of administration of BZDs

A

anal suppositorys / IV

17
Q

what are limitations of barbiturates in epilepsy

A
  1. low therapeutic index and can act in the absence of GABA - overdose could be fatal
    suicide risk
  2. tolerance through upregulation of excitatory receptors and P450 enzymes
18
Q

limitations of BZDs in epilepsy

A

often too sedative for epilepsy prophylaxis

19
Q

what effect does picrotoxin have?

A

blocks the GABA channel soo Cl- cant flow

promotes seizures

20
Q

where does ethanol act

A

to enhance GABA(A) action

explains sedative effects of alcohol

21
Q

explain use of KBr in epilepsy

A

bromide is more permeable through the GABA(A) channel than Cl-, and so enhances the inhibitory effect

KBr no longer used in humans due to its toxicity

first successful anti-epileptic

22
Q

give examples of BZDs

A

diazepam

midalozam

23
Q

give an example of a barbiturate

A

phenobarbital

24
Q

describe the overall mechanism of use dependant Ca and Na channel blockers

A

in an inactivated state, part of the channel (inactivation gate) will bind to the open channel, blocking it

  1. use dependant channel blcokers can only bind to the channel when its open (as they bind within the channel)
  2. occasional APs and openings of the channel dont give the blocker much opportunity to enter and block the channel
  3. however repetitive APs and repetitive openings of the channel gives the drug many opportuities to enter the channel and block it

so the channel is only blocked with repetitive activity of the channel

25
Q

give some examples of use dependant Na channel blockers

A

carbamazepine

phenytoin

26
Q

how can tiagabin be used in epilepsy treatement

A

it is a GAT blocker, inhibiting GABA reuptake so increasing its concentration in the cleft and increasing receptor activation

27
Q

how can vigabatrin be used as an anti-epileptic

A

it inhibits GABA aminotransferase, reducing GABA breakdown in the cleft

so increases [GABA] in cleft and increases GABA(A) activation

28
Q

what two anti-epileptic drugs may trigger absent seizures in children

A

vigabatrin

tiagabin

29
Q

what type of seizures do class 1 epileptics treat

A

tonic clonic
partial
temporal lobe seizures

30
Q

what are the class 1 anti-epileptics

A

BZDs
barbiturates
Tiagabin
vigabatrin

31
Q

what are the class 2 anti-epileptics and what type of seizures do they treat

A

use dependant VG Na / Ca blockers

tonic clonic
partial
temporal lobe seizures

32
Q

what types of sezures are treated by the class 3 anti-epileptics

A

absent seizures only

33
Q

give an example of a type 3 anti-epileptic and its mechanism

A

ethosuxamide

mechanism unknown, thought to be due to blockade of T-type VG Ca channels in thalamic neurones

(important in generation of rhythmic activity)

34
Q

what types of seizures are class 4 anti-epileptics used to treat

A

tonic clonic and absent seizures

35
Q

give 2 examples of class 4 anti-epileptics and their function

A

lamotrigine - use dependant Ca2+ blocker

sodium valproate -> mechanism not fully understood
combines weak use dependant Ca block and weak GABA transaminase block

36
Q

what are the class 5 anti-epileptics

A

drugs that work by other mechanisms as anti-epileptics

37
Q

give an example of a class 5 anti-epileptic

A

gabapentin -> interact with Ca2+ channel (in a different manner to blockers) inhibiting the channels activity and release of excitatory NTs

physiology and pharma (18 decks)

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