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PBT 3 Exam 2 > Epilepsy > Flashcards

Epilepsy Flashcards

1
Q

Seizure

A

episode causing movements or feelings patient cannot control. Electrical activity in the brain –> neurons fire at abnormally high rate

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2
Q

epilepsy

A

multiple seizures; group of disorders

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3
Q

What causes seizures

A

most are idiopathic; may also be caused by withdrawal from CNS depressant drugs (causes brain to rebound)

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4
Q

Two types of focal seizures

A

simple partial and complex partial

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5
Q

Two types of generalized seizures

A

primary and secondary

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6
Q

Where do focal seizures start

A

localized point in cortex –> agitates neighboring regions, but starts and stays in cortex

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7
Q

Where do secondary generalized seizures start

A

starts as focal –> activates thalamus –> causes all other regions to depolarize/fire abnormally

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8
Q

Thalamus

A

main relay station; connections to all other brain regions

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9
Q

Where do primary generalized seizures start

A

original seizure activity STARTS in the thalamus and leads to activation of both hemispheres

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10
Q

Describe simple partial seizures

A

WITHOUT altered mental state; patient stays awake; unexplained feelings of joy, anger, sadness, etc; ONLY time pt does not lose consciousness

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11
Q

Describe complex partial seizures

A

WITH altered mental status; loss of consciousness; repetitive behaviors; automatisms; lasts 30 seconds to 2-3 minutes

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12
Q

Absence seizure

A

Generalized. Very brief, often no symptoms, rapid blinking or nose rubbing, common in children –> often outgrow

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13
Q

Tonic seizure

A

Generalized. Bilateral increase in limb tone, arms curl inward

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14
Q

Clonic seizure

A

Generalized. Bilateral jerking of limbs –> rapid

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15
Q

Tonic-Clonic

A

Generalized. Bilateral increase in tone followed by bilateral jerking

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16
Q

Atonic

A

Generalized. Sudden loss of muscle tone and consciousness –> patient passes out

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17
Q

Myoclonic

A

Generalized. Brief, rhythmic jerks, lasts a few seconds

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18
Q

Tonic-Clonic (grand mal) description

A

Can be primary or secondary –> entire brain activated either way. Sensory aura often precedes seizure, followed by post-ictal state. Patient is unconscious and has no memory of event

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19
Q

Role of AMPA in Tonic stage

A

Sodium channel, open

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20
Q

Role of GABA in Tonic stage

A

Chlorine channel, open briefly at beginning

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21
Q

Role of NMDA in Tonic stage

A

Calcium channel, Opens after AMPA (AMPA must depolarize NMDA)

22
Q

Role of G-coupled Calcium channels in Tonic stage

A

open

23
Q

Role of AMPA in Clonic stage

A

Opens and closes

24
Q

Role of GABA in Clonic stage

A

Opens and closes opposite of AMPA - when one is open the other closes

25
Q

Role of NMDA in Clonic stage

A

closed - no role

26
Q

Role of G-coupled Calcium channels in Clonic stage

A

open

27
Q

Role of AMPA in Post-ictal stage

A

low level –> not much activity

28
Q

Role of GABA in Post-ictal stage

A

open on full power –> pt unconscious

29
Q

Role of NMDA in Post-ictal stage

A

no activity

30
Q

Role of G-coupled Calcium channels in post-ictal stage

A

On full-power –> tons of Cl- leads to CNS depression

31
Q

Status epilepticus

A

continuous seizure activity lasting more than 30 minutes OR two or more sequential seizures without full recovery of consciousness btwn seizures. Can lead to brain damage or death if not stopped.

32
Q

Causes of status epilepticus

A

sudden withdrawal of meds (remove CNS depressant get seizure activity), stroke, acute head trauma

33
Q

Sodium channel blockers

A 
thought to be more effective in treatment of focal and secondary generalized, but can be used in primary generalized.
Phenytoin (Dilantin)
Carbamazepine (Tegretol)
Lamotrigine (Lamictal)
Valproic Acid (Depakene)
34
Q

What do Sodium channel blockers do

A

Keep channels in refractory period for longer.
When refractory, no ions flow –> difficult to reopen
Blockers increase time in refractory period so no ions flow
AP dives below -70, making it harder to generate an AP (hyperpolarized).
No AP = harder to get abnormal neuron firing

35
Q

Phenytoin kinetics

A

Zero order (rare)
drug eliminated at constant, set rate regardless of concentration
system can become saturated
take more drug than body can clear –> build-up –> can lead to CNS depression

36
Q

Valproic Acid (Depakene)

A

not typical sodium blocker
also blocks calcium channels
increases GABA synthesis
Inhibits enzyme activity that degrades GABA

37
Q

Side effects of Penytoin

A

Rash, gingival overgrowth, confusion

At high doses: CNS depression, hypotension, hyperglycemia

38
Q

Side effects of Carbamazepine and Lamotrigine

A

Rash, constipation, N/V, dizzy. Can cause drowsiness or aplastic anemia

39
Q

Side effects of Valproic acid

A

alopecia, weight gain, back pain. Tremor, pancreatitis, hepatic failure, depression

40
Q

Calcium channel blockers

A

Ethosuximide (Zarontin)
Zonisamide (Zonegran)
Block Calcium - block NMDA - block tonic phase

41
Q

Calcium channel modulators

A 
Gabapentin (Neurontin) - modulator
Pregabalin (Lyrica) - modulator 
unknown mechanism of action
reduces clonic seizures
may induce GABA release
42
Q

Side effects of Ethosuximide (Zarontin)

A

sedation, headache, GI issues, rash

43
Q

Side effects of Zonisamide (Zonegran)

A

Fatigue, dizziness, confusion, kidney stones, weight loss

44
Q

Side effects of Gabapentin (Neurontin)

A

sedation, dizziness, ataxia, weight gain, blurred vision

45
Q

How do Benzo’s work to reduce seizures

A

Target GABA system
typically given IV during status epilepticus
inducess GABA release

46
Q

Vigabatrin (Sabril)

A

inhibits GABA transaminase –> leads to increase in GABA levels.
For seizures, NOT status epilepticus
Want LOTS of GABA in epilepsy

47
Q

Tiagabine (Gabitril)

A

GABA transporter blocker. Blocks reuptake from synapse, so increases synaptic levels of GABA

48
Q

Felbamate

A

Mixed mechanism

NMDA receptor antagonist –> antagonize, less calcium in so less depolarization –> less activity

49
Q

Rufinamide

A

Sodium channel blocker and metabotrophic glutamate receptor blocker

50
Q

Topiramate (Topamax)

A

Blocks sodium and calcium channels, enhances GABA and blocks AMPA/Kinate (prevents depolarization)

51
Q

Levetriacetam (Kepra)

A

disrupts vesicles to prevent release of neurotransmitters; blocks calcium channels, may increase GABA activity

PBT 3 Exam 2 (8 decks)

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