Brainscape's Knowledge GenomeTM

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


See full index

PMCOL 200 > Seizures > Flashcards

Seizures Flashcards

1
Q

what are seizures?

A

transient alteration in behaviour due to abnormally excessive and synchronous neuronal activity in brain

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

what is epilespsy?

A

disorder of brain function due to periodic and unpredictable seizures

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

what is the difference btwn symptomatic and asymptomatic brain seizures?

A

symp: occurs due to a known event (head trauma or cancer)
asymp: occurs due to genetics

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

what is the difference btwn provoked or unprovoked seizures?

A

provoked: by chemical or electrical stimulation
unprovoked: spontaneous (epilepsy)

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

t/f: everyone who experiences seizures has epilepsy

A

false

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

t/f: neurons normally fire asynchronously in the brain

A

true

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

what 2 factors inhibit the spread of elec. activity in neurons?

A
  1. refractory period (individual neurons)

2. surround inhibition (network of neurons)

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

what is surround inhibition?

A

physiological mechanism that focuses neuronal activity in CNS

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

t/f: primary afferent fibres will all produce APs w/ a stimulus

A

false, the afferents whose receptive field is closest to point of stimulation will produce more APs than those in periphery (surround inhibiton)

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

how is surround inhibition shown in second order neurons?

A

collateral inhibitory neurons project from central afferent neurons to inhibit peripheral second order neurons (focuses stimulus)

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

what are the 3 phases of a seizure?

A

initiation, propagation and termination

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

what 2 events occur in seizure initiation?

A
  1. high frequency bursts of APs (overcome ref. period)

2. hyper-synchronization of neuronal population (overcome surround inhibition)

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

how is neuronal depolarization sustained to produce a burst of APs?

A

AMPARs (Glu receptors) are activated and depol. cell (Na influx) which stimulates Mg release from NMDARs and additional influx of Na and Ca (importantly)

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

how is propagation of bursting activity normally prevented? (2)

A

refractory period (hyperpolarization) and surround inhibition

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

how does incr extracellular K cause propagation of neuronal activity?

A

K gradient is saturated (high extracellular [K] if incr previous APs) then neuron can’t hyperpolarize (overcomes refractory period)

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

what causes incr intracellular Ca in presynaptic terminal to allow propagation of neuronal activity?

A

opening of NMDA channels causes accumulation of intracellular [Ca] and incr NT release

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

how does depolarization-induced NMDAR activation cause propagation of neuronal activity?

A

allows further Ca influx and incr neuronal activation

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

what does incr extracellular K, incr intracellular Ca, and depolarization-induced NMDAR activation cause?

A

loss of surround inhibition and propagation of seizure activity

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

what 4 factors can terminate a seizure?

A

loss of ionic (Na) gradients, ATP depletion, NT (Glu) depletion, activation of inhibitory circuits (GABA)

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

t/f: seizures usually resolve spontaneously

A

true

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

what is status epilepticus?

A

seizure lasting longer than 5 min or >1 seizure in 5 min period

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

what is the postictal period?

A

5-30 min period after a seizure wherein individual is drowsy, confused, depressed/anxious, or psychotic (hallucinating/delusional)

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

what differentiates different types of seizures?

A

where in brain they initiate and how widely they propagate

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

what are the 3 types of seizures?

A

focal seizures, generalized seizures and non-convulsive (absence) seizures

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

what are focal seizures?

A

seizures in precise part of brain (don’t spread) that may include visual, psychic, autonomic, olfactory, or motor phenomena

26
Q

what is the difference btwn simple vs complex focal seizures?

A

simple: retain consciousness
complex: loss of consciousness

27
Q

what is a Jacksonian March?

A

propagation of a seizure in one body part to other/nearby body parts

28
Q

what are automatisms?

A

unusual activities that are not consciously created (smacking lips)

29
Q

t/f: focal seizures do not become generalized over time

A

false, focal seizures can become generalized over time

30
Q

what are generalized seizures?

A

seizures that begin in a precise part of the brain and spread to entire brain, are spontaneous and cause unconsciousness

31
Q

what is the difference btwn tonic-clonic and myoclonic generalized seizures?

A

tonic-clonic: sustained contraction (tonic) then convulsions of entire body (clonic) - grand mal seizures
myoclonic: brisk (~1s) contraction that can be localized or generalized (no convulsions)

32
Q

what is the difference btwn absence and atonic non-convulsive seizures?

A

absence: abrupt impairment of consciousness (can be subtle and not cause falling) - petit mal seizures
atonic: sudden loss of muscle strength (conscious but falls down)

33
Q

when are antiseizure drugs typically used?

A

chronically to prevent seizure in ppl w/ epilepsy (can be used to prevent seizures after neurosurgery/brain injury or during status epilepticus)

34
Q

how do antiseizure drugs typically work?

A

incr inhibitory GABAergic neurotransmission or decr excitatory Glutamatergic neurotransmission

35
Q

what are 3 mechanisms of antiseizure drugs?

A
  1. decr ion conductance (Na, Ca, K)
  2. block NT release (Glu)
  3. inh/act postsynaptic memb
36
Q

t/f: one drug may have multiple targets to decr seizures but depends on conc.

A

true

37
Q

what are benzodiazepines and barbiturates?

A

positive allosteric modulators of GABAa receptors

38
Q

at what GABA conc do benzodiazepines and barbiturates work?

A

benzo: when GABA is present (DON’T work wo/ GABA)
barb: can work wo/ GABA (usually at higher conc)

39
Q

what are GABAa receptors?

A

GABA-gated Cl-channels (hyperpolarize postsynaptic cell-inhibit)

40
Q

do benzodiazepines vs barbiturates incr potency or efficacy of GABA? how

A

benzo: incr potency (incr f of GABAa receptor opening)
barb: incr efficacy (incr t GABAa receptor is open)

41
Q

what is a risk of benzodiazepines vs barbiturates? which one is riskier?

A

both can overdose; barbs are riskier bcse direct gating at GABAaR and benzo require GABA to work

42
Q

what are 4 symptoms of benzodiazepines or barbiturates overdose?

A

sluggishness, incoordination, faulty judgement, and death

43
Q

t/f: risks of benzodiazepines and barbiturates are not affected by other CNS depressants such as alcohol or opioids

A

false

44
Q

what is vigabatrin/what does it do?

A

inhibits GABA aminotransferase (GABA-T) in presynaptic cell; decr GABA breakdown which incr GABA activity (incr inhibitory action)

45
Q

what is GABA aminotransferase (GABA-T)?

A

enzyme that breaks down GABA in presynaptic cell

46
Q

what is tiagabine/what does it do?

A

inhibits GABA transporter (GAT-1) which prolongs activity of GABA (incr inhibitory action)

47
Q

where is GABA transporter (GAT-1) located?

A

neurons and glia

48
Q

what does carbamazepine do?

A

block V-gated Na channels

49
Q

how does carbamazepine block Na conductance?

A

causes conf. change in inactivation gate (blocks channel)

50
Q

t/f: drugs that block Na conductance (carbamazepine) are rate dependent

A

true, blockage incr w/ incr activity of neuron (avoids blocking entire brain activity)

51
Q

t/f: drugs that block Na conductance (carbamazepine) result in a prolongation of inactivated state of Na channels and refractory period

A

true

52
Q

what is the general structure of gabapentin?

A

GABA molecule w/ cyclohexane ring (lipophilic)

53
Q

why was gabapentin developed?

A

GABA agonist that can cross BBB (lipophilic)

54
Q

what does gabapentin actually do? (not initial intent)

A

inhibits V-gated Ca channels (has little activity at GABA receptor) to reduce NT release (Glu)

55
Q

which subunit of Ca channel does gabapentin bind to?

A

a2∂ subunit (not direct block but alters regulatory function)

56
Q

what is perampanel?

A

non-competitive antagonist at AMPAR

57
Q

what are 2 Glu receptors that anti-seizure drugs can act as antagonists for? (decr Glu activity)

A

NMDARs and AMPARs

58
Q

what are risks of perampanel? (AMPAR antagonist)

A

psychiatric/behavioural changes such mood disorders and suicidal/homicidal ideation (not selective for active neurons-blocks all brain activity)

59
Q

why is it important to consider pharmacokinetics of antiseizure drugs?

A

to avoid toxicity and drug interactions

60
Q

what are the general pharmacokinetic properties of anti-seizure drugs? (3)

A

well-absorbed, good bioavailability, can cross BBB, low extraction ratios (long acting)

61
Q

t/f: since antiseizure drugs have a low extraction ratio/are long acting, they are less likely to have drugs interactions

A

false, are more likely to have drugs interactions

62
Q

what are side effects of most antiseizure drugs?

A

depression of CNS (depression, suicidal thoughts, death)

PMCOL 200 (27 decks)

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