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Neurologic & Psych > Antiseizure drug Pharmacology Dr. Pond > Flashcards

Antiseizure drug Pharmacology Dr. Pond Flashcards

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1
Q

What are the possible causes of seizures?

A

-disturbed levels of body water/electrolytes
-disturbed level of blood glucose
-altered blood gases
-raised body temperature
-altered sleep patterns
-hormonal changes
-Toxicity

excess excitation
lack of inhibition

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2
Q

Where in the brain are seizures thought to arise?

A

Cerebral cortex (outermost part of the brain)

partial seizures
generalized seizures

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3
Q

What is the difference between partial and generalized seizures?

A

-partial seizures: start a specific locus in the cerebral cortex

-generalized seizures: both hemispheres are involved in the onset

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4
Q

What differentiates a simple partial seizure from a complex partial seizure?

A

simple: consciousness is not impaired

complex: consciousness is impaired -> may have a simple partial-onset where patients are aware -> followed by loss of consciousness OR they are unconscious right away

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5
Q

Secondarily generalized seizures

A

-simple partial to generalized (start at on area and spread to both hemispheres)

-complex partial to generalized

-simple partial to complex partial to generalized

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6
Q

What is a synonym for secondarily generalized seizures?

A

tonic-clonic seizure?

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7
Q

What is the gyrus (bump) before the central sulcus called?

A

-precentral gyrus
-> Primary motor cortex Homunculus, frontal lobe

-> collateral control: left control right sight of the body
seizures in the left side of the motor cortex will affect the right sight of the body

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8
Q

Which structure is found behind the central sulcus?

A

Postcenter gyrus
-> Primary somatosensory cortex Homunculus

collateral: sensation on the right side of the body are received on the left side of the brain

seizures in this area can sometimes be perceived as a tingeling

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9
Q

In which lobe is the Primary somatosensory cortex Homunculus located?

A

Parietal lobe

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10
Q

How long does a simple partial seizure last?

A

20-60 seconds

consciousness is not impaired

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11
Q

What symptoms are expected when seizures occur in the motor cortex?

A

Tonic-clonic movements of the upper or lower limb

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12
Q

Other symptoms - seizure

A

Occipital lobe (eye): flashing lights
Temporal lobe (auditory): ringing, noises
Autonomic: sweating, flushing, pallor, or epigastric sensation

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13
Q

How long does a complex partial seizure last?

A

-30 seconds to 2 minutes

impairment of consciousness

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14
Q

Features of complex partial seizures

A

-blank stare
-funny face, grimaces
-chewing movements of the mouth

-bad or unusual smell before the seizure
-dysphasia (unable to speak)
-auditory hallucination
-visual hallucination

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15
Q

Symptoms of Generalized seizures: Absence

A

last less than 30 sec

-vacant stare
-eyes rolled upwards
-eyelids flutter
-cessation of activity
-lack of responses

-patients may be unaware that they are having a seizure and move on with what they have been doing before the seizure

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16
Q

How are muscles affected by seizures?

A

Myoclonic: sudden, shock-like contraction (<1sec)
-> often occur falling asleep or shortly after waking up

Tonic: muscle stiffening -> person falls to the ground

Clonic: repetitive muscle jerking and short post-ictal phase

Atonic: sudden loss of muscle tone, dropping of head or limb, possible fall to the ground

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17
Q

Characteristics Tonic-clonic seizure

A

Tonic phase: stiffening, epileptic cry, cyanosis, incontinence

Clonic phase: clonic jerks of limbs, body and head, salivary frothing (foam), eyes blinking, cyanosis

Post-ictal (time after the seizure): confusion, fatigue, drowsiness, hypotension, confusion, headache, nausea

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18
Q

Antiseizure drug MOA

A

-Sodium channel modulation (fast inactivation)
-Sodium channel modulation (slow inactivation)

-K+ channel opener
-Blockade of voltage-gated calcium channels

-> getting back to resting potential

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19
Q

What is the MOA of Levetiracetam/brivaracetam?

A

-Synaptic vesicle protein 2A modulation

hinder vesicle formation

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20
Q

What are MOAs that involve GABA?

A

-Prolongs chloride channel opening: GABA binds to Cl(-) channels -> inhibitory (IPSP): barbiturates and stiripentol
-Increased frequency of chloride channel opening: benzodiazepines, ganaxolone

-Inhibits GABA-transaminase
-Blocks synaptic GABA reuptake
-increases GABA: Valproate

-Glutamate antagonist (Glutamate is an excitatory NT -> blocking will have an inhibitory effect):
->AMPA/kainate: phenobarbital, lamotrigine, perampanel, topiramate
->NMDA: carbamazepine, valproate, felbamate, lamotrigine, oxcarbazepine,
eslicarbazepine

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21
Q

Which channels are affected by Phenytoin?

A

-blocking voltage-gated Na-channels (presynaptic - preventing action potential, postsynaptic)
-blocking Ca2+ channels -> prevent Glutamate (excitatory NT) release

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22
Q

Kinetic features of Phenytoin

A

-Elimination of phenytoin is dose-dependent (1st order), -> metabolism is saturable - changes to 0 order when accumulating

-Fosphenytoin: prodrug, more soluble, less alkaline -> less skin irritation

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23
Q

Phenytoin: Adverse Effects

A

-Drowsiness
-Involuntary movement of the eyes, double vision
-Loss of muscle coordination (ataxia)
-Gingival hyperplasia (20% of chronic therapy)
-Hirsutism
-Pregnancy risk !!!
-Stevens-Johnson Syndrome (SJS)/Toxic epidermal
necrolysis (TEN)
-> Immune-complex–mediated hypersensitivity complex

-Purple Glove Syndrome (IV) – must be
administered slowly

24
Q

What is a common Phenytoin IV complication?

A

-Purple Glove Syndrome
Skin necrosis and gangrene may develop

25
Q

Which channels are affected by Carbamazepine?

A

-Inactivation of Na+ channels
-High threshold Ca2+ channel blocker
-Inhibit NMDA receptors

-Autiinduction of its own metabolism (CYP 3A4), higher dose needed with continuous therapy

26
Q

ADE/BBW of Carbamezapine

A

ADE:
-drowsiness, dizziness, double vision & ataxia (poor muscle control), rash, nausea/vomiting

-Pregnancy risk!!!

BBW:
-agranulocytosis (low number of neutrophils)
-aplastic anemia (number of blood-building stem cells goes down)
-SJS, TEN

27
Q

Which channels are affected by Lamotrigine?

A

-Inactivation of Na+ channels
-Increase GABA neurotransmission
-Low threshold Ca2+ channel blocker
-Inhibits AMPA, kainate, and NMDA receptors (Glutamate receptors)

28
Q

Adverse effects of Lamotrigine

A

-drowsiness, dizziness, blurred vision,
headache

-rashes, SJS !!!

-Most evidence for safe use in pregnancy

29
Q

Which channels are affected by Valproate/Valproic acid?

A

-Inactivation of Na+ channels
-Low threshold Ca2+ blocker

-Increased GABA levels possibly through increasing synthesis and/or decreasing degradation of GABA
-Inhibit NMDA receptors (Glutamate receptor)

30
Q
A
31
Q

Adverse effects of Valproate

A

-drowsiness, dizziness, weight gain, hair loss,
polycystic ovarian syndrome, blurred vision, headache, tremor

-hepatotoxicity – hyperammonemia (drunken-like behavior), pancreatitis

32
Q

Which channels are affected by Topiramate?

A

-Inactivation of Na+ channels
-Activates/enhances GABAA receptor currents
-inhibits AMPA/Kainate receptors
-carbonic anhydrase inhibitor
-high threshold Ca2+ channel blocker

33
Q

ADE of Topiramate

A

-Drowsiness, dizziness, weight loss,
metabolic acidosis, paresthesia, impaired concentration,
schizophreniform disorder

34
Q

Which antiseizures may be used in pregnant patients?

A

Lamotrigine

risk: Phenytoin, Carbamazepine, Valproate/Valproic acid (BBW), Primidone, Phenobarbital, Ethosuximide, Benzodiapenes

35
Q

Which channels are affected by Zonisamide?

A

-Inactivation of Na+ channels
-high threshold Ca2+ channel blocker
-increased GABA neurotransmission
-carbonic anhydrase inhibitor (change pH -> anticonvulsant)
-Low threshold Ca2+ channel blocker

36
Q

ADE of Zonisamide

A

-drowsiness, cognitive impairment,
rarely SJS and TENS, schizophreniform disorder

37
Q

Which channels are affected by Rufinamide?

A

-Inactivation of Na+ channels

ADE:
-dizziness, drowsiness, headache, nausea, fatigue
-shortened QT interval (common) !!

38
Q

Which channels are affected by Primidone?

A

-Metabolized into phenobarbital (and PEMA)

-Primidone itself: prolonged inactivation state of Na+ channel

-Phenobarbital: GABA(A)
modulator

39
Q

ADE of Primidone

A

-half life 6-8 hours, but phenobarbital half-life is 4-5 days

-Pregnancy risk

-Adverse effects: dizziness, drowsiness, ataxia, nausea

40
Q

MOA of Lacosamide

A

-newer drug

-Increased number of Na+ channels in the
SLOW inactivation state (occurs with prolonged neuronal activity)
-> long-term regulation of sodium channel availability

-Adverse effects: dizziness, headache, double vision,
nausea, fatigue (less drowsiness)

41
Q

MOA of Ezogabine

A

-opening KCNQ channels (specific K channels) -> K moves out (inhibitory)

42
Q

ADE of Ezogabine

A

-drowsiness, dizziness, fatigue
-urinary retention/symptoms
-prolonged QT interval
-retinal abnormalities
-skin discoloration

43
Q

What are drugs that inhibit low threshold Ca channels (T-type)?

A

-ethosuximide

-also zonisamide, valproate, lamotrigine

useful in Absence seizure

44
Q

Drugs inhibiting high threshold Ca2+ channels

A

-gabapentin, pregabalin
-lamotrigine, Levetiracetam
-carbamazepine, oxcarbazepine
-phenobarbital, phenytoin
-topiramate, zonisamide, felbamate

45
Q

How do drugs enhance the activity of GABA?

A

GABA -> inhibtory

GABA recycle (conversion to Glutamate in glial cells)
-on GABA transporter: tigabine
-on GABA-T enzyme: vigabatrin, valproate
-on succinic dehydrogenase: valproate

-on GABA receptors (postsynaptic): barbiturates (phenobarbital, primidone), benzodiazepines

46
Q

MOA of Benzodiapenes

A

Increase frequency of GABA(a) receptor channel opening -> increasing amplitude of IPSP

-pregnancy risk
-ADE: Sedation, tolerance, dependence, withdrawal

47
Q

MOA Phenobarbital

A

-increase duration of GABAA receptor channel opening -> increasing duration of IPSP

-At high concentrations: prolongs inactivation state of Na+ channels
-high threshold Ca2+ channel blocker
-GABA receptor agonist
-AMPA antagonist (Glutamate, excitatory)

-long half-life: 4-5 days

48
Q

MOA of Vigabatrin

A

-Irreversible inhibitor of GABA aminotransferase (GABA-T), the enzyme that degrades GABA

-ADE: permanent visual field defects !!
fatigue, dizziness, confusion, skin rash, weight gain

49
Q

MOA Tiagabine

A

-inhibitor of GABA uptake (both neurons and glia)

50
Q

Which receptors are involved in the MOA of Cannabidiol?

A

GPR55

-it antagonizes LPI -> so LPI (lipid
lysophosphatidyl-inositol (LPI) cant work on GPR55

-…

-Effects of food: Increased Cmax 5-fold; increased AUC 4-fold
-CYP and UGT inducer/inhibitor

51
Q

Which receptors are involved in the MOA of Stiripentol?

A

-GABA(a) receptor -> allosteric modulator:
↑ duration of GABA IPSPs

-Prefers GABAA receptors with α3 subunits, highest in immature brain* (Dravet syndrome - epilepsy at a young age)

-used with Clobazam
-CYP inhibitor/inducer - may increase levels of clobazam and its metabolite (Ndesmethylclobazam)

52
Q

Which receptors are involved in the MOA of Cenobamate?

A

-GABA(a) receptor
-> enhances GABA(a) receptor neurotransmission

-Inactivation of Na+ channels (persistent current blocked, not voltage-dependent channels), causes hyperpolarized state

53
Q

Drugs acting on Glutamate receptors

A

-AMPA receptor antagonists: perampanel, topiramate, lamotrigine, phenobarbital

-NMDA receptor antagonists: felbamate,
carbamazepine, valproate, lamotrigine, oxcarbazepine

54
Q

MOA of Perampanel

A

-Non-competitive AMPA receptor antagonist

-ADEs:
Aggression, hostility, irritability, anger & homicidal
ideation and threats
drowsiness, dizziness, fatigue, gait problems, some weight gain

55
Q

MOA of Felbamate

A

-blocks use-dependent NMDA receptor
-Inactivation of Na+ channels
-inactivation of high threshold Ca2+ channel blocker

-ADE: Causes aplastic anemia* and severe hepatitis

Neurologic & Psych (37 decks)

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