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Pharm 716 > Week 13/14 Neuro > Flashcards

Week 13/14 Neuro Flashcards

1
Q

what is main CNS inhibitory neurotransmitter?

A

GABA

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2
Q

what is main CNS excitatory neurotransmitter?

A

Glutamate

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3
Q

what is a focal (partial) seizure?

A

localized in one cerebral hemisphere

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4
Q

what is generalized seizure?

A

involves both cerebral hemispheres

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5
Q

AE of antiepileptic

A
  • neurotoxicity, sedation, ataxia, confusion, dizziness,

- many DDI

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6
Q

therapeutic concerns with epileptic drugs

A
  • sedation, dizziness, ataxia
  • skin rashes - massage may exacerbate
  • bone marrow depression and Vit K deficiency - check for bruising/bleeding
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7
Q

3 subtypes associated with ADHD

A

inattentive, hyperactivity, and impulsivity

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8
Q

stimulant medication MOA

A

block re-uptake of NE, dopamine, or both

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9
Q

atomoxetine (Strattera) MOA

A

SNRI - selective NE reuptake inhibitor - blocks NE reuptake

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10
Q

methylphenidate (Ritalin, Concerta) MOA

A

stimulant - blocks dopamine and NE reuptake

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11
Q

amphetamine (Adderral) MOA

A

stimulant - blocks dopamine and NE reuptake

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12
Q

common AE of stimulants

A

decreased appetite/weight loss, stomachache, insomnia, HA, rebound symptoms, jitteriness

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13
Q

boxed warning of stimulants

A

safe if no baseline CV disease

report signs of abuse/dependence

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14
Q

atomoxetine (Strattera) AE

A

similar to stimulants (decreased appetite/weight loss, stomachache, insomnia, HA, rebound symptoms, jitteriness) but more fatigue, sedation, and dizziness
- monitor mood changes

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15
Q

Parkinson’s is related to a decrease in what?

A

dopamine

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16
Q

what is dyskinesia

A

uncontrolled, involuntary movements

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17
Q

levodopa-carbidopa MOA

A

Parkinson’s
l-dopa is a precursor to dopamine and can cross BBB and carbidopa stops the breakdown of l-dopa in the periphery so more l-dopa can cross BBB to be converted to dopamine

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18
Q

levodopa-carbidopa AE

A

Parkinson’s

motor disturbances, end dose wearing off, delayed on, freezing

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19
Q

MAO-B inhibitor MOA

A

Parkinson’s

inhibit monoamine oxidase B (MAO B) which breaks down dopamine

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20
Q

MAO-B inhibitor AE

A

Parkinson’s

serotonin syndrome, watch for DDI

21
Q

COMT inhibitor MOA

A

Parkinson’s

inhibit COMT which breaks down l-dopa

22
Q

COMT inhibitor AE

A

Parkinson’s

involuntary movements, nausea

23
Q

dopamine agonists MOA

A

Parkinson’s

bind to and agonize dopamine receptor

24
Q

dopamine agonists AE

A

Parkinson’s

drowsiness, dizziness, syncope

25
Q

2 options for MS treatment

A

DMT - disease-modifying therapies and symptom management

26
Q

Interferon B AE and what needs to be monitored

A

MS

  • flu-like symptoms, HA, injection site reaction
  • fatigue, depression, pain, nausea, increase LFT, myalgia
  • monitor for neuropsychiatric changes, drug-induced hypothyroidism, worsening cardiac function
27
Q

Glatiramer acetate MOA

A

MS

reduce autoimmune response to myelin by reducing T-cell response against myelin

28
Q

Glatiramer acetate AE

A

MS

injection site reaction, rash, vasodilation, dyspnea, chest pain

29
Q

Sphingosine 1-Phosphate (S1P) receptor modulator MOA

A

MS

decrease inflammation

30
Q

Sphingosine 1-Phosphate (S1P) receptor modulator AE and what should you monitor

A

MS
HA, increase LFT (liver function tests), macular edema, infection
- monitor bradycardia

31
Q

dimethyl fumarate AE

A 
MS
GI (N/V/D, abdominal pain) and flushing - usually improve with time
32
Q

common ending for monoclonal antibodies

A

-mab

33
Q

monoclonal antibodies MOA

A

MS

decrease inflammation in CNS

34
Q

monoclonal antibodies AE and what should you monitor

A

MS
infusion-related reactions, HA, fatigue, arthralgia
- monitor for infection

35
Q

serious risk associated with monoclonal antibodies (-mab), dimethyl fumarate, and SP1 receptor modulators

A

PML - progressive multifocal leukoencephalopathy

36
Q

PML s/sx

A

altered mental status (AMS), aphasia, ataxia, hemiparesis, hemiplegia, visual disturbance, seizures

37
Q

what is the most common and disabling MS symptom

A

fatigue

38
Q

what neurotransmitter is depleted with Alzheimer’s

A

ACh

39
Q

cholinesterase inhibitor MOA

A

Alzheimer’s

- inhibits AChesterase which breaks down ACh = increase ACh

40
Q

cholinesterase inhibitor AE

A

Alzheimer’s
cholinergic AE
- nausea, vomiting
- SLUDGE

41
Q

NMDA Antagonists MOA

A

Alzheimer’s

antagonizes NMDA receptor = stops activation by glutamate = decreases excitation and neuronal death

42
Q

NMDA Antagonists AE

A

Alzheimer’s

- usually well tolerated; monitor for falls

43
Q

what should Alzheimer patients not be taking?

A

anticholinergic drugs

44
Q

tizanidine MOA

A

a2 agonist for spasticity

- bind to a2 receptors in CNS to decrease the release of excitatory neurotransmitters

45
Q

tizanidine AE

A

drowsiness, dizziness, asthenia (weakness)

46
Q

Flexeril AE

A

spasticity

  • sedation and dizziness
  • Beer’s list
47
Q

Baclofen MOA

A

spasticity

- inhibit effect on alpha motor neurons through inhibition of excitatory neurons

48
Q

Baclofen AE

A

spasticity

  • abruptly stopping med can lead to: high fever, altered mental status, rebound spasticity, rhabdo
  • CNS depressant (sedation, CV depression), muscle weakness, TBI in older adults
49
Q

therapeutic concerns with antispasticity/muscle relaxant drugs

A

sedation and weakness

Pharm 716 (10 decks)

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