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Pharmacology Final Content > Neuro Pt 1 (Epilepsy & ADHD) > Flashcards

Neuro Pt 1 (Epilepsy & ADHD) Flashcards

1
Q

What is epilepsy?

A

a chronic condition characterized by recurrent seizures

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2
Q

what are the types of epilepsy?

A

primary and secondary

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3
Q

Describe the cause of primary epilepsy

A

idiopathic (cause unknown)

>50% of all cases

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4
Q

Describe the cause of secondary epilepsy

A 
Children: 
- injury at birth
- metabolic disease
Adults:
- TBI
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5
Q

define seizure

A

a finite event resulting from excessive discharge of cerebral neurons, causing transient impairments or loss of consciousness

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6
Q

what is important to note about the symptoms of seizures?

A

they will depend on the location of injury

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7
Q

What are the types of seizures?

A

Partial

Generalized

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8
Q

define a partial seizure

A

occurs in one cerebral hemisphere with no loss of consciousness

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9
Q

define a generalized seizure

A

occurs in both hemispheres and pt will have a loss of consciousness

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10
Q

What are the types of generalized seizures?

A
  • tonic-clonic
  • tonic
  • clonic
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11
Q

what are the characteristics of a generalized tonic-clonic seizure?

A
  • rigid extensor spasm for 10-30s with LOC and stopped respiration
  • pt will poop, pee, or salivate
  • rhythmic flexor spasm for 2-4mins with continued LOC (alertness will slowly return)
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12
Q

what are the characteristics of a generalized tonic seizure?

A

rigid extensor spasm lasting a few seconds

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13
Q

what are the characteristics of a generalized clonic seizure?

A

rhythmic flexor spasm lasting a few seconds

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14
Q

Which type of seizure is most common?

A

Generalized tonic-clonic

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15
Q

describe the role of GABA in a seizure

A
  • the main CNS inhibitory transmitter
  • normally inhibits depolarization of the postsynaptic neuron
  • too little –> seizure
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16
Q

describe the role of Glutamate in a seizure

A
  • main excitatory neurotransmitter

- too much –> seizure

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17
Q

for what reason is CNS inflammation pertinent to seizures?

A

microglia may initiate a cycle of inflammation-induced seizures and seizure-induced inflammation

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18
Q

What are the steps of the excitatory pathway for seizures?

A
  1. Na+ and Ca2+ enter presynaptic neuron
  2. Ca2+ push glutamate vesicle to bind with presynaptic neural wall
  3. Glutamate opens AMPA to allow Na+, and NMDA to allow Ca2+ to enter the postsynaptic neuron
  4. T-type Calcium 2 Channels open to allow more Ca2+ into the postsynaptic neuron (making it more positive and facilitating the AP)
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19
Q

What are the steps of the inhibitory pathway for seizures?

A
  1. Na+ and Ca2+ enter presynaptic neuron
  2. Ca2+ push glutamate vesicle to bind with presynaptic neural wall
  3. GABA opens GABA-A channels to allow Cl- to enter the postsynaptic neuron making it harder for an AP to occur
  4. GAT-1 reuptakes GABA and is degraded by GABA-T
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20
Q

Where do anti-epilepsy excitatory drugs work?

A

inhibit GAT1 and GABA-T

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21
Q

Where do anti-epilepsy inhibitory drugs work?

A
  1. block Na+ and Ca2+ channels
  2. block glutamate release
  3. block glutamate binding
  4. prolong the opening of GABA-A channels
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22
Q

What are the types of treatment for Epilepsy

A

excitatory or inhibitory

  • antiepileptic drugs (AED)
  • antiseizure drugs (ASD)
  • anticonvulsants
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23
Q

What should be known about the 3 types of Epilepsy treatments?

A

They are used interchangeably

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24
Q

What does Epilepsy treatment depend on?

A
  1. Patient specific factors
  2. Type of seizure
  3. Response to previous medications
25
What are the treatment goals for Epilepsy?
1. eliminate seizures 2. experience no AEs 3. improve quality of life
26
What are the AEs of antiepileptic drugs?
1. neurotoxicity (SEDATION, ATAXIA, confusion, dizziness, blurred vision) 2. weight gain/loss 3. hypothyroidism 4. rash - stevens-johnson syndrome
27
What are the differences between acute and chronic AEs of antiepileptic drugs?
Acute: may be concentration dependent or idiosyncratic Chronic: due to duration of use
28
Who are the "at risk populations" for AEs related to antiepileptic drugs?
- Women - Pregnant women - Children - Elderly
29
Why are women at risk when taking AEDs?
changes in hormone levels during the menstrual cycle can change the efficacy of the drugs - sometimes require supplemental meds at highest risk
30
Why are pregnant women at risk when taking AEDs?
stress | hormones
31
Why are children at risk when taking AEDs?
hepatic/renal activity changes | - requires increased drug monitoring and dose adjustments
32
Why are the elderly at risk when taking AEDs?
1. change in body mass changes volume distribution and half-life of drug 2. hypoalbuminemia (increased free drug in plasma) 3. greater sensitivity to neurocognitive effects 4. hepatic/renal changes (monitor/dose changes) 5. polypharmacy --> DDIs
33
What are the therapeutic considerations of AEDs?
1. some are NTI drugs 2. Watch for sedation, dizziness, and ataxia 3. Rashes 4. Bone marrow depression 5. Vitamin K deficiency 6. MUST ask about seizure activity and know how to appropriately respond to a seizure
34
What are therapeutic considerations specific to women and AEDs?
1. decreased ovarian function 2. infertility 3. PCOD - polycystic ovarian disease 4. weight gain
35
What is ADHD?
a series of behavioral disorders
36
What does ADHD stand for?
Attention-Deficit/Hyperactive Disorder
37
What are the subtypes of ADHD?
1. inattentive 2. hyperactive-impulsive 3. combined
38
What are the causes of ADHD?
- multifactorial: environment, genetics, biologic factors | - pre/perinatal exposure to cigarettes/alcohol increase risk 2-3x
39
What are the main treatments for ADHD?
1. Stimulants | 2. atomoxetine
40
What are the alternative medications for ADHD?
1. alpha-2 adrenergic agonists 2. Bupropion 3. Lithium 4. Antipsychotics
41
What is the general MOA of stimulants?
block dopamine and norepinephrine reuptake and increase dopamine and NE release
42
What are the different ways stimulants are taken?
IR (immediate release) | XR (extended release)
43
What are the characteristics of IR stimulants?
- 15-30min onset - 2-6hr duration - multiple daily doses
44
What are the characteristics of XR stimulants?
- 8-12hr duration
45
What should be considered when taking stimulants with food?
there is a slower onset and decreased absorption BUT it may decrease some AEs
46
What are common AEs of stimulants?
1. decreased apetite/weight loss 2. stomachache 3. insomnia 4. HA 5. irritability/jitteriness
47
What are some rare AEs of stimulants?
1. dysphoria 2. zombie-like state 3. tics/abnormal movements 4. HTN, HR fluctuations 5. Hallucinations 6. Hypopigmentation from the patch
48
What are the stimulant drugs on the drug list?
- Ritalin/Concerta (methylphenidate) | - Adderral (mixed amphetamine salts)
49
What are the BOXED WARNINGS for stimulants?
- CV risk | - abuse potential
50
What class is atomoxetine (Strattera) in?
Selective Norepinephrine Reuptake Inhibitors (SNRI)
51
What is the MOA of atomoxetine (Strattera)?
selectively inhibits norepinephrine reuptake
52
T/F: atomoxetine (Strattera) takes effect immediately
False; 2-4wk onset, 6-12wk before full benefits
53
What are the AEs associated with atomoxetine (Strattera)?
1. more fatigue, sedation, and dizziness than stimulants | BOXED WARNINGS
54
What are the BOXED WARNINGS for SNRIs (atomexatine)?
increased risk for suicidal ideation | - must monitor mood changes
55
How are alpha-2 adrenergic agonists used to treat ADHD?
as an adjunct tx to decrease disruptive behaviors, control aggression, or increase sleep in youth
56
When is Bupropion appropriate?
if a patient has concomitant depression
57
When is Lithium appropriate?
- if a patient has bipolar disorder | - to control aggression or explosive behavior
58
When are antipsychotics used?
for refractory cases of severe aggression
59
What are the Therapeutic Concerns regarding ADHD medications?
- monitor vital signs - be aware of loss of appetite or insomnia - monitor behavior and attention span

Pharmacology Final Content (2 decks)

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