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Drug Action III > Epilepsy (Physiology) - Block 1 > Flashcards

Epilepsy (Physiology) - Block 1 Flashcards

1
Q

How many lobes are in the brain?

A

5: frontal, parietal, occipital, temporal, insula

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2
Q

What is cerebral white matter?

A

Myelinated fibers bundled into large tracts

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3
Q

What is the decussation of the pyramids?

A

Where fibers cross over to the opposite side before contnuing into the spinal cord which is the crossover point
* Each hemisphere controls the opposite side of the body

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4
Q

What is an ambulatory EEG?

A

Records brain waves continuously for up to 72 hrs

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5
Q

What is a seizure?

A

Discrete clinical event of abnormal electrical discharge from neurons in the cerebral cotex leading to involuntary movement and/or behavior and sensory alterations

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6
Q

What age group are seizures more common?

A

Children
* first seizure is expereinced before 20 for most people

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7
Q

What is epilepsy?

A

Chronic disorder of recurrent discharges from neurons due to a CNS disorder/disruption

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8
Q

How are seizure classified?

A
  1. Clinical sx
  2. EEG activity
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9
Q

What are the 2 classes of seizure disorders?

A

Focal (partial): Limited to 1 hemisphere and discretely localized or widely discributed
Generalized: Bilaterally distributed networks
Epileptic spasms

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10
Q

What is an idiopathic seizure?

A

Cause is unknown

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11
Q

What are some known causes of seizures?

A
  1. Metabolic derangement
  2. Infection
  3. Tumors
  4. Drug abuse
  5. Vascular lesions
  6. Congenital deformities
  7. Brain injury
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12
Q

List some of the theories that can cause abnormal brain activity?

A
  1. Alterations in cell permeability or distribution of ions
  2. Decreased inhibion of cortical or thalamic neuronal activity (excitiability of neurons)
  3. Neurotransmitter imbalances
  4. Genetic mutations (channelopathy)
  5. Immunopathogenesi
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13
Q

Describe some of the neurotrasmitter imbalances associated wit seizures?

A
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14
Q

What is the normal function of VGNCs?

A
  1. Progresses from closed to open states
  2. Largetransient Ns influx (INaP)
  3. Small percentage of Na influx persists at steady state
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15
Q

What is channelopathy?

A

Point mutation that impairs inactivatio of the VGNC -> increased INaP and excessive sodium influx at steady state

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16
Q

Describe the 5 anticonvulsant targets?

A
  1. Enhance GABAergic neural activity (Na+ channel inactivation)
  2. Inhibit glutamatergic neural activity (Cl- channel activation)
  3. Inhibition of Ca2+ current (Ca2+ channel inhibition)
  4. Potentiate GABAergic signaling at inhibitory presynaptic nerve terminals (Promotes IPSPs)
  5. Inhibit glutamate signaling at excitatory presynaptic nerve terminals (Prevents EPSPs)
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17
Q

WHat is the most common type of seizure among newly diagnosed cases?

A

Focal (partial)

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18
Q

Describe the Immunopathogenesis of seizure disorders?

A
  1. Elevated levels of immune mediators
  2. Neurons, glia, and endothelial cells of the blood-brain barrier (BBB) take part in inflammatory processes
  3. Elevated cytokine levels in serum and brain tisse
  4. IL-1b, IL-6, TNF-a are most common
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19
Q

What are the types of focal sz?

A
  1. Simple partial: without impairment of consiousness, memory, awareness
  2. Complx partial: memory impairment or behavior changes
20
Q

Sz with observable motor or autonomic components?

A

Simple partial sz (focal motor and autonomic)

21
Q

Sz subjective sensory or psychic phenomena only?

A

Aura

22
Q

What are the clinical manifestations of focal without impairment?

A

Abnormal neural discharge corresponds to location of onset on the contralateral side of the body:
Motor area: motor movement
Sensory area:
* Somatic sensoy disturbance: tingling, crawling
* Special sensory disturbances: visual, auditory, gustatory, olfactory

23
Q

How does abnormal cortical discharge affect the ANS?

A

Flushng, tachy, diaphoresis, hypo and hypertension, pupillary changes

24
Q

What are the warning signs of impending seizure activity?

A

Prodrome and aura

25
Q

What is aura?

A

Sx that may occurs before seizure (visual changes, bright lights, zigzags)

26
Q

What are the manifestations of focal with impairment?

A

Focal seizures envolving to a bilateral convulsive seizures (complex partial sz)
* Impairment of consciousness
* Often arise from temporal lobe

Sx: psychomotor seizures with automtisms and postictal state

27
Q

What are automatisms?

A

Repetitive, purposeful activates such as lip smacking, grimacing, patting, rubbing clothing

28
Q

What is postictal state?

A

COnfusion after seizure

29
Q

What are generalized sz? Categories?

A

Effects both hemispheres at onset
1. Tonic-clonic
2. Absence
3. Myoclonic
4. Clonic
5. Tonic
6. Atonic

30
Q

What are the phases of a tonic clonic seizure?

A

Tonic: vague warnings with sharp tnic contraction f the muscles
* Pupil fixed and dilated
* Incontinence of bladder and bowel
* Hypoxia, skin pallor, cyanosis
* 15-60 seconds

Clonic:
* Alternating periods of muscular contraction and relaxation
* 60-90 sec

Postictal:
* Level of consciousness is decreased

31
Q

What are typical absence sz?

A
  1. Non-convulsive epileptic events
  2. Disturbances in consciousness
    3, Petit mal
32
Q

What are the automatisms of absense sz?

A
  1. Lip smacking
  2. Mild clonic motion
  3. Increased or decreaed postural tone
  4. Autonomic phenomena
  5. few seconds
33
Q

What are atypical absence sz?

A

Similar to typical absence seizures except for greater alterations in muscle tone and less abrupt onset and cessation.

34
Q

What are myoclonic sz?

A

Involves brief involuntary muscle contractions induced by stimuli or cerebral origin (bilateral jerking of muscles)

35
Q

What are clonic sz?

A

Begin with a loss of consciousness and sudden hypotonia (limb jerking)

36
Q

What are tonic sz?

A

Sudden onset of increased tone, which is maintained in the extensor muscles (falling)

37
Q

What are atonic sz?

A

Sudden, split second loss of muscle tone leading to slackening limbs (drop attacks)

38
Q

What are status epilepticus?

A

Acute symptomatic sz that is a medical emergency
Duration: >30 minutes

39
Q

What are febrile sz?

A

Seizures that occur as a result of a rapid body temperature rise above 102.2°F, often in association with an acute illness.

Most common in 6 months to 5 yrs old

40
Q

What are intractable sz?

A

Seizures that are refractory

41
Q

What is the Pharmacokinetic Hypothesis?

A

: Overexpression of drug efflux transporters in peripheral organs decreases ASD plasma levels, reducing the amount of ASD available to enter the brain and reach the epileptic focus.

42
Q

What is the neuronal network hypothesis?

A

: Seizure-induced degeneration and remodeling of the neural network suppresses the brain’s seizure control system and restricts ASDs from accessing neuronal targets.

43
Q

What is the intrinsic severity hypothesis?

A

Common neurobiological factors contribute to both epilepsy severity and pharmacoresistance.

44
Q

What are gene variant hypothesis?

A

Variations in genes (e.g., metabolic enzymes, ion channels, and certain neurotransmitter receptors that are targets for ASDs) associated with ASD pharmacokinetics and pharmacodynamics cause inherent pharmacoresistance.

45
Q

What are target hypothesis?

A

Alterations in the properties of ASD targets such as changes in voltage-gated ion channels and neurotransmitter receptors (e.g., GABAA receptor) result in decreased drug sensitivity and lead to refractoriness.

46
Q

What are transporter hypothesis?

A

Overexpression of ASD efflux transporters at the blood–brain barrier in epilepsy leads to decreased ASD brain uptake and ASD resistance.

Drug Action III (23 decks)

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