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PMCOL II > Anti-Seizure > Flashcards

Anti-Seizure Flashcards

1
Q

What are seizures

A

Transient (Short time) alteration of behaviour caused by excessive and synchronous neuronal activity

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2
Q

What is epilepsy

A

Disorder of brain function characterized by periodic and unpredictable seizures

Occurs spontaneously and unprovoked

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3
Q

What’s the difference between epilepsy and seizures

A

You can have seizures without epilepsy

But epilepsy is characterized by seizures

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4
Q

What is symptomatic epilepsy

A

Epilepsy that occurs due to a known event (blunt trauma)

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5
Q

What is asymptomatic epilepsy

A

Epilepsy that occurs due to poorly defined genetic factors

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6
Q

How do neurons normally fire

A

Asynchronously

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7
Q

What is surround inhibition

A

The primary afferent stimulated will produce more action potentials than those on the periphery

The peripheral neurons are strongly inhibited

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8
Q

What are the three steps of a seizure

A

Initiation
Propagation
Termination

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9
Q

What are the two events of seizure initiation

A

High frequency bursts of action potentials
High synchronization of neuronal population

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10
Q

What can overcome the barriers preventing bursting neuronal activity

A

Increasing extracellular potassium (Efflux of potassium is unfavoured and hyperpolarization does not occur)

Increasing calcium in presynaptic terminals will lead to enhanced neurotransmitter release

Activating NMDA receptors will cause more calcium influx and a greater neuronal activation

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11
Q

How does potassium flow in hyperpolarization

A

High potassium inside cell flows out of cell

Loss of positive ions inside the cell causes the cell to be more negative and thus, harder to depolarize

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12
Q

What are the likely reasons why seizures resolve

A

Loss of ionic gradients
Depletion of ATP
Depletion of neurotransmitters (Glutamate)

Activation of inhibitory circuits (GABA)

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13
Q

What is status epilepticus

A

Seizures that last more than 5 minutes or more than 1 seizures within a 5 minute period

Can be life threatening

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14
Q

What is postictal period

A

The period 5-30 minutes after a seizure, characterized by drowsiness, depression, and psychosis

Occurs because of increased inhibition the neurons perform in response to the increased excitatory activity they just experienced

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15
Q

What are the 3 types of seizures

A

Focal Seizures
Generalized Seizures
Non-convulsive (absence) seizures

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16
Q

What are focal seizures

A

Occur in one particular spot, can spread wider across cortex and result in a generalized seizure

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17
Q

What are Automatisms

A

Unusually activities that are not consciously created, like smacking the lips

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18
Q

What are simple seizures

A

Retain consciousness during focal seizure

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19
Q

What are complex seizures

A

Loss of consciousness during focal seizure

20
Q

What is Jacksonian March

A

Jerking activity that starts in specific muscles and spreads to surrounding muscle groups

21
Q

What are generalized seizures, and what are the different types

A

Seizures that effect a wide area, always involve loss of consciousness and happen without warning

Tonic-clonic and Myoclonic

22
Q

What are tonic-clonic seizures (Grand mal seizures)

A

Generalized seizure

Sustained contractions (tonic) of muscles alternating with periods of relaxation (clinic)
Occurs throughout the body

23
Q

What are myoclonic seizures

A

Generalized seizure

Brief 1 second shock-like contractions of muscles
Can be localized or generalized

24
Q

What are non-conclusive seizures

A

Absence and atonic seizure

25
Q

What are absence seizures (Petit mal seizures)

A

Loss of connection with environment

Abrupt impairment of consciousness, slight head turn or staring

Person does not fall over and can return to normal after a few seconds

There may be a period of postictal disorientation

26
Q

What are atonic seizures

A

Disconnect from body

Sudden loss of muscle strength. Person usually maintains consciousness but may fall down

27
Q

What is the mechanism of anti-seizure drugs

A

Blocking ionic conductance (sodium, calcium, and potassium)
Blocking neurotransmitter release
Inhibiting excitatory postsynaptic neurons or activating inhibitory postsynaptic neurons

28
Q

Benzodiazepines

A

Positive allosteric modulators at GABA type A receptors
Enhance the activity of GABA

GABA needs to be present for benzodiazepines to work

29
Q

Mechanism behind benzodiazepines

A

Increases the frequency GABA type A receptors open
(Increases potency of GABA)

Not as much GABA is needed for stronger effect as benzodiazepines are aiding in opening GABA receptors

30
Q

Barbiturates

A

Positive allosteric modulators at GABA type A receptors
Enhance the activity of GABA

GABA does not need to be present, barbituates can act as GABA agonists instead at higher concentrations

31
Q

Mechanism behind Barbiturates

A

Increases the duration of the GABA type A receptors opening
(Increases efficacy of GABA)

Channel is open for longer, more flow of Cl- leading to a stronger GABA effect and increasing the maximum possible effect,

Barbiturates can function as GABA and open the receptor

32
Q

Benzodiazepines and Barbituates have a risk of overdose, which one is riskier

A

Barbiturates because they can directly gate the GABA receptor, works without GABA easier to overdose

33
Q

What are the symptoms of Benzodiazepines and Barbiturate overdose

A

Slughisness, incoodination, faulty judgement, and death

34
Q

Benzodiazepines and Barbiturate should not be taken with what kind of drug

A

CNS depressants like alcohol and opioids
Increases overdose chances of opioids/alcohol

Additive risk

35
Q

Vigabatrin

A

Inhibits GABA aminotransaminase (GABA-T)

GABA-T degrades GABA, which would lead to less inhibition

36
Q

Tiagabine

A

Inhibits GABA transporter (GAT-1 located in neurons and Gila)

Prolongs action of neurotransmitters by lowering clearing of GABA

37
Q

Carbamazepine

A

Block voltage-gated sodium channels

38
Q

Mechanism behind Carbamazepine

A

Causes a conformational change of red I (the inactivation gate) which then blocks the sodium channel

Block prioritizes neurons with a higher level of neuronal discharge

Propagates the inactivated state of thee sodium channel and the refractory period of the neuron

39
Q

Gabapentin

A

Looks like GABA with cyclohexane attach and can cross BBB

However, does not bind to GABA receptors and instead inhibits voltage-gated calcium channels

40
Q

Mechanism behind GABApentin

A

Binds to a2σ subunit of calcium channel

Does not directly block, but disrupts the regulatory function of the a2σ subunit

Reduces the effect of glutamatergic neurons

41
Q

Perampanel

A

Non-compeitive antagonist at AMPA receptor

Blocks excitation driven by glutamate binding to AMPA and NMDA

Causes serious psychiatric and behavioural changes

42
Q

Why is homeostasis of glutamate important? What happens if this is not maintained

A

Important in how our brain functions

Too much glutamate: Psychiatric, hallucinations
Too little glutamate: Depression, death

43
Q

How often are anti-seizure drugs usually used

A

Used for long periods of time to prevent recurrence of seizures, thus, interactions with other drugs must be considered

44
Q

Anti-seizure drugs have what pharmacokinetic properties

A

Well absorbed, good bioavailability, and cross BBB

45
Q

What is the extraction ratio of anti-seizure drugs

A

Liver extracts a very low amount, can be long-acting in body

Lots of possible drug-drug interactions

PMCOL II (10 decks)

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