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Pharmacology > Exam 3 Neuro Part 2 & 3 Drugs > Flashcards

Exam 3 Neuro Part 2 & 3 Drugs Flashcards

1
Q

what are the three ways PD can be treated

A
  1. dopamine replacement therapy
  2. dopamine agonist therapy
  3. anticholinergic therapy
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2
Q

what are the different types of dopamine replacement therapy to treat PD

A
  1. levodopa-carbidopa (Sinemet)
  2. MAO-B Inhibitors
  3. COMT inhibitor
  4. Amantadine
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3
Q

what are the different types of dopamine agonists to treat PD

A
  1. Amantadine

2. dopamine agonists

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4
Q

what are the long term effects of dopamine replacement

A

MOVEMENT RELATED COMPLICATIONS

  • dyskinesia
  • motor fluctuations (wearing off phenomenon, on-off medication state)

as many as 84% have reported issues

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5
Q

what is the first like option of treatment for PD

A

levodopa-caribidopa (sine met)
and
dopamine agonists

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6
Q

what is the MOA of levodopa-caribidopa

A

levodopa: precursor to dopamine that can cross BBB and has CNS action
carbidopa: stops breakdown of 1-dopa to dopamine in periphery so more 1-dopa crosses BBB

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7
Q

levodopa-caribidopa AE

A
  • motor disturbances
  • end dose “wearing off” so stiffness and rigidity return
  • med not having an effect due to absorption issues
  • freezing
  • “on” period dyskinesia (must differentiate from PD tremors)
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8
Q

MAO-B inhibitors MOA

A

inhibits monoamine oxidase B which typically breaks dopamine thus increasing dopamine levels in CNS

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9
Q

Indication of MAO-B

A

usually used after levodopa-carbidopa and dopamine agonists for PD

both approved adjunct therapy to reduce end dose wearing off with 1-dopa

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10
Q

types of MAO-B inhibitors

A

selegiline PO and Rasagiline

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11
Q

COMT inhibitor MOA

A

inhibits COMT which intern decreases breakdown of 1-dopa

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12
Q

MAO-B inhibitors AE

A

Seleginine PO: has first pass metabolism and increases hallucinations, insomnia, jitteriness

Rasagiline: approved mono therapy but is less effective

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13
Q

COMT inhibitor AE

A

involuntary movements, nausea

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14
Q

COMT inhibitor indication

A

used as adjunct therapy to reduce end of dose wearing off with 1-dopa

but overall less commonly used

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15
Q

Amantadine MOA

A

unknown

possibly increases dopamine release or may have direct affect on dopamine neurons

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16
Q

Amantadine AE

A 
confusion
hallucinations
diziiness
dry mouth
constipation
lived reticularis
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17
Q

Amantadine indication

A

was previously used for flyu

usually in early disease management, younger people usually respond better

modest mono therapy benefit and adjust therapy to reduce dyskinesias with 1-dopa

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18
Q

dopamine agonists MOA

A

binds to and agonizes dopamine receptors

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19
Q

dopamine agonists drug

A

ropinirole (Requip)

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20
Q

dopamine agonists AE

A

nausea, drowsiness, dizziness, syncope

monitor for lightheadedness and postural hypotension, hallucinations, lower-extremity edema

less common: impulsive behavior, sleep attacks

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21
Q

dopamine agonist indication

A

first line treatment

used as mono therapy esp in younger pts and adjunct therapy to reduce end of dose wearing off with 1-dopa

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22
Q

anticholingeric therapy for PD MOA

A

antagonizes muscarinic receptors to prevent acetylcholine binding

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23
Q

anticholingeric therapy for PD AE

A

anticholinergic effects

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24
Q

anticholingeric therapy for PD indication

A

used as mono therapy or adjunct treatment specifically for tremor

limited use bc of AEs and modest benefit

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25
Q

istradefylline (Nourianz) indication

A

new drug for PD

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26
Q

istradefylline (Nourianz) class

A

A2A receptor antagonist

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27
Q

istradefylline (Nourianz) MOA

A

blocks adenosine A2A receptor in the basal ganglia (region which controls movement)

exact MOA is unknown

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28
Q

istradefylline (Nourianz) indication

A

used as add therapy to levodopa/carbidopa to treat “off” episodes

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29
Q

istradefylline (Nourianz) AE

A

worsening dyskinesia

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30
Q

what are the 2 aspects to MS treatment

A
  1. disease modifying therapies

2. symptom management

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31
Q

interferon B (IFN-B) indication

A

used submit or IM to treat relapsing MS to decrease exacerbations and delay accumulation of physical disability

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32
Q

interferon B (IFN-B) class

A

interferon

33
Q

interferon B (IFN-B) MOA

A

unknown

but typically is a protein produced by fibroblasts and has an impact on immune function

34
Q

interferon B (IFN-B) AE

A
  • flu like sx and injection site reaction
  • fatigue, depression, pain, abdominal pain, nausea, leukopenia, increase LFTs, myalgia, back pain, weakness, fever

monitor for neuropsychiatric changes, drug induced hypothyroidism, worsening cardiac function

35
Q

glatiramer acetate (Copaxone, Glatopa) class

A

miscellaneous biologic agent

36
Q

glatiramer acetate (Copaxone, Glatopa) MOA

A

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

37
Q

glatiramer acetate (Copaxone, Glatopa) indiccation

A

subcut or IM in relapsing MS to decrease exacerbations and lesions on MRI

may NOT slow progession

38
Q

glatiramer acetate (Copaxone, Glatopa) AE

A

most common: injection site reaction

other: rash, vasodilation, dyspnea, chest pain (typically resolves within a few mins)

39
Q

S1P Receptor Modulator drugs

A

fingolimod (Gilenya)

40
Q

S1P Receptor Modulator MOA

A

converted to active metabolite which blocks release of lymphocytes into CNS to decrease inflammation

41
Q

S1P Receptor Modulator indication

A

PO daily to decrease exacerbations and overall disease severity

42
Q

S1P Receptor Modulator AE

A

headache, increased LFTs

rare AE: macular edema (vision changes), infection

monitor for bradycardia (esp within first 24 hours of first dose)

43
Q

dimethyl fumarate (Tecfidera) Class

A

fumaric acid derivative

44
Q

dimethyl fumarate (Tecfidera) MOA

A

unknown in MA may have anti-inflammatory properties

45
Q

dimethyl fumarate (Tecfidera) indication

A

PO BID to decrease exacerbations and overall disease severity

46
Q

dimethyl fumarate (Tecfidera) AE

A

GI (n,v,d, abdominal pain and flushing)

rare: hepatoxicity

47
Q

monoclonal antibodies drugs

A

natalizumab (Tysabri)

ocrelizumab (Ocrevus)

48
Q

monoclonal antibodies MOA

A

natalizumab MOA: antibody that binds to lymphocytes, preventing them from crossing BBB, decreases inflammation in CNS

ocrelizumab MOA: bind CD20 on mature B cells which impacts antigen presentation and autoantibody formation

49
Q

monoclonal antibodies indication

A

used to decrease exacerbations, decrease lesions on MRI and or slow disease progression

50
Q

monoclonal antibodies AE

A

infusion release reactions, headache, fatigue, arthralgia

monitor for infection

51
Q

general treatment of AD

mild approach

A

cholinesterase inhibitor

52
Q

general treatment of AD

moderate approach

A

cholinesterase inhibitor + memantine (more likely to delay progression)

53
Q

general treatment of AD severe approach

A

consider if med will provide a benefit, possibly do a med-free trial

54
Q

Colinesterase inhibitors for AD drugs

A

donepezil (Aricept)

55
Q

Colinesterase inhibitors for AD MOA

A

inhibits acetylcholinesterase to increase ACh to help correct the deficiency

56
Q

Colinesterase inhibitors for AD duration of benefit

A

3-24 months

57
Q

Colinesterase inhibitors for AD AE

A

primarily cholinergic AE
most common: nausea, vomiting

others: SLUDGE, DUMBELLS, decrease appetite or weight, dizziness, tremor

Beer’s list: avoid if hx of syncope that may be related to bradycardia

58
Q

NMDA antagonist drugs

A

memantine (Namenda)

59
Q

NMDA antagonist MOA

A

antagonizes NMDA receptor to decreases excitation and neuronal death

60
Q

NMDA antagonist indication

A

used with cholinesterase inhibitor or as mono therapy

may be used off-label bc not FDA approved

61
Q

NMDA antagonist AE

A

usually well tolerated

monitor for falls and dizziness

62
Q

a2 agonist for spasticity drugs

A

tizanidine (Zanaflex)

63
Q

a2 agonist for spasticity MOA

A

selectively binds a2 receptors in CNS to decrease excitability of postsynaptic neurons

64
Q

a2 agonist for spasticity AE

A

drowsiness, dizziness, asthenia

sedation within 30 mins of dose

hypotension

65
Q

a2 agonist for spasticity dosing

A

PO 2-3x a day, start at bedtime and titrate slowly

may take with o with our food but must be consistent

66
Q

central acting antispasmodics drugs

A

cyclobenzaprine (Flexeril)

67
Q

central acting antispasmodics MOA

A

unknown

may inhibit polysynaptic reflex in spinal cord

also possible GABA and serotonin effects

68
Q

central acting antispasmodics indication

A

vary from short term use to longer use of maintenance doses

69
Q

central acting antispasmodics AE

A

long term or excessive use may contribute to tolerance and physical dependence

sedation, dizziness

Beer’s list: sedation, fractures, some anticholinergic effects, limited efficacy

70
Q

Botulinum toxin indication

A

spasticity

71
Q

Botulinum toxin MOA

A

blocks release of ACh into NM junction

72
Q

Botulinum toxin drugs

73
Q

Botulinum toxin AE

A

can develop antibodies after long term use

boxed warning: rare cases of spread to distal tissues

muscle weakness, diplopia, blurred vision, urinary incontinence, swallowing and breathing difficulties

risk is likely highest in kids treated for spasticity

74
Q

direct acting agents for spasticity (Baclofen) MOA

A

inhibitory effect on alpha motor neuron through inhibition of excitatory neurons

75
Q

direct acting agents for spasticity (Baclofen) boxed warning

A

abruptly stopping medication can lead to…

high fever, AMS, exaggerated spasticity and muscle rigidity, rare cases of rhabdo and organ system failure

76
Q

direct acting agents for spasticity (Baclofen) indication

A

useful for spasticity caused by diseases like MA and conditions such as SCI

77
Q

direct acting agents for spasticity (Baclofen) AE

A

CNS depressant, muscle weakness, in older adults and TBI - impaired memory and cognition

78
Q

Baclofen: ITB

A

intrathecal baclogen

  • pump implanted into abdominal area
  • fewer systemic side effects
79
Q

Baclofen: ITB indication

A

good for long term use

used to treat severe spasticity unresponsive to oral medication

Pharmacology (11 decks)

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