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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
istradefylline (Nourianz) indication
new drug for PD
26
istradefylline (Nourianz) class
A2A receptor antagonist
27
istradefylline (Nourianz) MOA
blocks adenosine A2A receptor in the basal ganglia (region which controls movement) exact MOA is unknown
28
istradefylline (Nourianz) indication
used as add therapy to levodopa/carbidopa to treat "off" episodes
29
istradefylline (Nourianz) AE
worsening dyskinesia
30
what are the 2 aspects to MS treatment
1. disease modifying therapies | 2. symptom management
31
interferon B (IFN-B) indication
used submit or IM to treat relapsing MS to decrease exacerbations and delay accumulation of physical disability
32
interferon B (IFN-B) class
interferon
33
interferon B (IFN-B) MOA
unknown but typically is a protein produced by fibroblasts and has an impact on immune function
34
interferon B (IFN-B) AE
- 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
glatiramer acetate (Copaxone, Glatopa) class
miscellaneous biologic agent
36
glatiramer acetate (Copaxone, Glatopa) MOA
reduce autoimmune response to myelin by reducing T-cell response against myelin
37
glatiramer acetate (Copaxone, Glatopa) indiccation
subcut or IM in relapsing MS to decrease exacerbations and lesions on MRI may NOT slow progession
38
glatiramer acetate (Copaxone, Glatopa) AE
most common: injection site reaction other: rash, vasodilation, dyspnea, chest pain (typically resolves within a few mins)
39
S1P Receptor Modulator drugs
fingolimod (Gilenya)
40
S1P Receptor Modulator MOA
converted to active metabolite which blocks release of lymphocytes into CNS to decrease inflammation
41
S1P Receptor Modulator indication
PO daily to decrease exacerbations and overall disease severity
42
S1P Receptor Modulator AE
headache, increased LFTs rare AE: macular edema (vision changes), infection monitor for bradycardia (esp within first 24 hours of first dose)
43
dimethyl fumarate (Tecfidera) Class
fumaric acid derivative
44
dimethyl fumarate (Tecfidera) MOA
unknown in MA may have anti-inflammatory properties
45
dimethyl fumarate (Tecfidera) indication
PO BID to decrease exacerbations and overall disease severity
46
dimethyl fumarate (Tecfidera) AE
GI (n,v,d, abdominal pain and flushing) rare: hepatoxicity
47
monoclonal antibodies drugs
natalizumab (Tysabri) | ocrelizumab (Ocrevus)
48
monoclonal antibodies MOA
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
monoclonal antibodies indication
used to decrease exacerbations, decrease lesions on MRI and or slow disease progression
50
monoclonal antibodies AE
infusion release reactions, headache, fatigue, arthralgia monitor for infection
51
general treatment of AD mild approach
cholinesterase inhibitor
52
general treatment of AD moderate approach
cholinesterase inhibitor + memantine (more likely to delay progression)
53
general treatment of AD severe approach
consider if med will provide a benefit, possibly do a med-free trial
54
Colinesterase inhibitors for AD drugs
donepezil (Aricept)
55
Colinesterase inhibitors for AD MOA
inhibits acetylcholinesterase to increase ACh to help correct the deficiency
56
Colinesterase inhibitors for AD duration of benefit
3-24 months
57
Colinesterase inhibitors for AD AE
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
NMDA antagonist drugs
memantine (Namenda)
59
NMDA antagonist MOA
antagonizes NMDA receptor to decreases excitation and neuronal death
60
NMDA antagonist indication
used with cholinesterase inhibitor or as mono therapy may be used off-label bc not FDA approved
61
NMDA antagonist AE
usually well tolerated monitor for falls and dizziness
62
a2 agonist for spasticity drugs
tizanidine (Zanaflex)
63
a2 agonist for spasticity MOA
selectively binds a2 receptors in CNS to decrease excitability of postsynaptic neurons
64
a2 agonist for spasticity AE
drowsiness, dizziness, asthenia sedation within 30 mins of dose hypotension
65
a2 agonist for spasticity dosing
PO 2-3x a day, start at bedtime and titrate slowly may take with o with our food but must be consistent
66
central acting antispasmodics drugs
cyclobenzaprine (Flexeril)
67
central acting antispasmodics MOA
unknown may inhibit polysynaptic reflex in spinal cord also possible GABA and serotonin effects
68
central acting antispasmodics indication
vary from short term use to longer use of maintenance doses
69
central acting antispasmodics AE
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
Botulinum toxin indication
spasticity
71
Botulinum toxin MOA
blocks release of ACh into NM junction
72
Botulinum toxin drugs
botox
73
Botulinum toxin AE
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
direct acting agents for spasticity (Baclofen) MOA
inhibitory effect on alpha motor neuron through inhibition of excitatory neurons
75
direct acting agents for spasticity (Baclofen) boxed warning
abruptly stopping medication can lead to... | high fever, AMS, exaggerated spasticity and muscle rigidity, rare cases of rhabdo and organ system failure
76
direct acting agents for spasticity (Baclofen) indication
useful for spasticity caused by diseases like MA and conditions such as SCI
77
direct acting agents for spasticity (Baclofen) AE
CNS depressant, muscle weakness, in older adults and TBI - impaired memory and cognition
78
Baclofen: ITB
intrathecal baclogen - pump implanted into abdominal area - fewer systemic side effects
79
Baclofen: ITB indication
good for long term use used to treat severe spasticity unresponsive to oral medication

Pharmacology (11 decks)

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