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Pharmacology Test 3 > Neural System 2: PD, MS, and Alzheimers > Flashcards

Neural System 2: PD, MS, and Alzheimers Flashcards

1
Q

what is multiple sclerosis (MS)?

A

a chronic, progressive disease of CNS - axonal damage and demyelination

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2
Q

what is the etiology of MS

A
  1. autoimmune process
  2. genetic predisposition
  3. environmental exposure
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3
Q

what are the clinical symptoms of MS?

A
  1. weakness, poor endurance
  2. sensory impairments
  3. balance impairments
  4. ataxia
  5. UMN signs
  6. blurred vision, nystagmus
  7. dysarthria
  8. autonomic dysfunction
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4
Q

what are UMN signs in MS?

A
  1. spasticity
  2. hyperreflexia
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5
Q

What are some outcome measures used to determine trx effectiveness in MS?

A
  1. MRI - visualize lesion
  2. relapse rate
  3. expanded disability severity scale (EDSS)
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6
Q

how is the Kurtzke EDSS scored?

A

0-10 (0 = normal, 10 = death)

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7
Q

what are the major aspects of MS treatment?

A
  1. Disease modifying therapies
  2. symptom management
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8
Q

what do DMTs lessen?

A
  1. # of new lesions that form/keep existing from getting larger
  2. lessen # of relapses
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9
Q

name 5 DMT drugs

A
  1. Interferon B
  2. Glatiramer acetate
  3. Sphingosine 1-Phosphate Receptor Modulator
  4. Dimethyl fumarate
  5. Monoclonal antibodies
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10
Q

MOA for Interferon-B

A

exact MOA is unknown. Impacts immune function

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11
Q

Administration route for Interferon-B

A

subcut or IM

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12
Q

Indications for Interferon-B

A
  1. relapsing MS 2. decrease exacerbations and delay accumulation of physical disability
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13
Q

AE for >50% Interferon-B

A
  1. flu-like symptoms
  2. HA
  3. injection site rxn
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14
Q

AE for >20% Interferon-B

A
  1. fatigue
  2. depression
  3. pain
  4. abdominal pain
  5. nausea
  6. leukopenia
  7. increase LFTs
  8. myalgia
  9. back pain
  10. weakness, fever
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15
Q

*monitor Interferon-B for __________

A
  1. Neuropsychiatric changes
  2. drug-induced hypothyroidism
  3. worsening cardiac function in HF
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16
Q

MOA of Glatiramer acetate

A

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

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17
Q

Administration route for Glatiramer acetate

A

subcut or IM

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18
Q

Indication for Glatiramer acetate

A

relapsing MS, decreasing exacerbation and lesion on MRI

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19
Q

Most common AE for Glatiramer acetate

A

injection site rxs

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20
Q

other common AE for Glatiramer acetate

A
  1. rash
  2. VD
  3. dyspnea
  4. chest pain
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21
Q

what drug is a S1P receptor modulator?

A

Fingolimod

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22
Q

Fingolimod MOA

A

coverts to active metabolite which blocks release of lymphocytes into CNS = decrease in inflammation

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23
Q

Fingolimod use

A

PO daily to decrease exacerbation and overall disease severity

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24
Q

Fingolimod >15% AE

A

headache, increased LFTs

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25
Rare Fingolimod AEs
1. macular edema (report vision changes immediately), 2. infection
26
What AE warrants an immediate referral for somone on an S1P receptor modulator?
vision changes
27
Dimethyl fumarate Use
PO 2x/day to decrease exacerbations and disease severity
28
MOA of dimethyl fumarate
unknown in MS; may have anti-inflammatory properties
29
AEs of dimethyl fumarate
1. GI (N/V/D, abdominal pain in 12-18%) 2. flushing (up to 40%)
30
Rare AE for dimethyl fumarate
hepatoxicity
31
Monoclonal Antibodies drugs suffix
-mab
32
general MOA for monoclonal antibodies
decrease inflammation in CNS and autoantibody formation
33
Use of Monoclonal antibodies
1. may decrease exacerbations 2. decrease lesions on MRI and slow progression
34
Common AEs for monoclonal antibodies
1. infusion related rxns 2. HA 3. fatigue 4. arthralgia
35
What is PML?
Progressive Multifocal Leukoencephalopathy demyelinating CNS disorder caused by reactivation of JCV
36
Patients on which meds are at a higher risk of developing PML?
1. Monoclonal Antibodies 2. Dimethyl Fumarate 3. SP1 receptor modulators
37
Signs and Symptoms of PML?
1. altered mental status (AMS) 2. aphasia 3. ataxia 4. hemiparesis 5. hemiplegia 6. visual field disturbances (double vision, partial blindness) 7. seizures
38
Off-label trxs for relapsing/progressive MS
1. Azathioprine 2. Methotrexate
39
Symptom trx for MS
1. **Spasticity -- baclofen** 2. ambulation and mobility impairments -- dalfampridine 3. **Upper extremity tremor -- botulinum toxin type A** 4. **Central neuropathic pain -- gabapentin** 5. Psudobulbar dysfunction -- combo dextromethorphan/quinidine sulfate 6. Urinary symptoms -- oxybutynin 7. depression/anxiety -- antidepressants
40
Drug Concerns for MS patients
1. Fatigue 2. Corticosteroid drug treatment 3. DMT drugs can have substantial AEs influcing flu-like symptpoms to immunosuppression
41
Key features of Alzheimer's Disease
1. Progressive neurodegenerative disease 2. Gradual loss of memory and function leading to total dependence on caregivers 3. Eventual inability to recognize family/friends/self
42
What neurotransmitters are depleted in AD?
1. Acetylcholine 2. serotonin 3. somatostatin 4. NE
43
General trx approach for AD
1. Mild case 1. cholinesterase inhibitor 2. Moderate case 1. cholinesterase inhibitor + memantine (delays progression) 2. address behavioral and pyschological symptoms 3. Severe case 1. consider if meds will be beneficial 2. may continue cholinesterase inhibitor
44
Cholinesterase Inhibitor Drug
Donepezil (Aricept)
45
Cholinesterase Inhibitors pros
modest improvements in cognition and ADLs benefits last ~3-24 months
46
Cholinesterase Inhibitors MOA
inhibit acetylcholinesterase from breaking down acetylcholine = increased ACh helps correct ACh deficiency in AD
47
Primary AEs for Cholinesterase Inhibitors
SLUDGE DUMBELLS
48
T/F: Cholinesterase Inhibitors can exacerbate UTOs, asthma, and COPD
TRUE
49
T/F: Cholinesterase Inhibitors are on the Beers List?
TRUE
50
what class of drug is Memantine (namenda)
NMDA antagonist
51
NMDA antagonist MOA
antagonise NMDA receptor = stops excessive receptor activation by glutamate = decreases excitation and neuronal death
52
When are NMDA antagonists used?
1. monotherapy for moderate cases 2. in conjunction with cholinesterase inhibitor in moderate cases 3. Not FDA approved for mild cases
53
NMDA Antagonists AE
1. usually well tolerated 2. monitor for falls
54
Individuals with AD should not be taking what?
1. Anticholinergic Drugs 2. OTC antihistamines (Benadryl)
55
AD drug concerns
1. Cholinergic meds: GI issues (NVD) most common 2. Memantine may cause dizziness, watch for falls 3. Communicate behavioral issues to healthcare providers
56
What should be taken into consideration when scheduling PT for patients with AD?
1. lots of structure to help reduce behavioral issues 2. reduce behavioral issues related to sundowning 3. utilize time of day when pateint most alert
57
Characterizations of Parkinson's Disease
1. Akinesia 2. Bradykinesia 3. Postrual instability 4. Rigidity (freezing episode) 5. Tremor (pill-roll)
58
Pathophysiology of PD
1. progressive death of dopamine-producing neurons in basal gangali 2. reduced communication with Thalamus 3. results in loss of voluntary movement, especially automatic movements
59
Etiology of basal ganglia neurotransmitter imbalance
Overall unknown, possible impact of 1. genetics 2. environmental factors
60
Medical management of PD
1. Dopamine replacement 2. Dopamine agonist therapy 3. Anticholinergic therapy
61
Overall goal of pharmacologic treatment Parkinson's Disease
Restore neurochemical balance
62
Name of Parkinson's Disease Scales
1. Unified Parkinson's Disease Rating Scale (UPDRS) 2. Hoehn & Yahr Scale
63
PD, dopamine replacement therapy drugs
Levodopa-carbidopa (L-dopa) MAO-B inhibitors COMT Inhibitor Amantadine (both agonist and replacement therapy)
64
PD, dopamine agonist therapy
Amantadine Ropinirole (Requip)
65
Anticholinergic Therapy Drugs for PD
1. Benztropine (Cogentin) 2. Trihexyphenidyl
66
benefits of Levodopa-carbidopa
1. improves movement velocity 2. may reduce tremor 3. reduce rigidity 4. improves force production & coordination of anticipatory postural task
67
What are the long-term effects of dopamine replacement therapy
1. Movement-related complications 2. Dyskinesia 3. Motor Fluctuations
68
how does dopamine impact cholinergic response?
without dopamine the cholinergic response is uninhibited
69
what is the 1st line trx and most effective treatment for PD patients?
Levodopa-carbidopa (Sinemet)
70
carbidopa MOA (why is it combined with l-dopa)?
stops breakdown of l-dopa to dopamine in periphery so more l-dopa crosses BBB
71
AE of Levodopa-carbidopa (Sinemet)
1. End of dose "wearing of" 2. "Delayed on" or "no on" 3. Freezing 4. "on" period dyskinesia
72
MOA for MAO-B inhibitors
inhibit monoamine oxidase (MAO) B which breaks down dopamine = increased dopamine levels in CNS
73
what PD treatment has a risk for serotonin syndrome?
Selegiline (a type of MAO-B inhibitor) when combined with serotonergic meds
74
MOA of COMT inhibitors
Inhibit COMT which in turn decreases breakdown of l-dopa
75
when are COMT inhibitors used?
Adjunct used to reduce end of dose wearing off with l-dopa
76
AE of COMT Inhibitors
\>10% = involuntary movements, nausea
77
what has Amantadine been used to treat in the past?
Influenze
78
MOA of Amantidine
Unknown possibly increases dopamine release
79
Amantadine AE
1. confusion 2. hallucinations 3. dizziness 4. dry mouth 5. constipation 6. livedo retiularis
80
T/F: Dopamine agonists can be a 1st line option for trx PD?
TRUE
81
Dopamine Agonist Drug
ropinirole (Requip)
82
ropinirole (Requip) AE
1. nausea 2. drowsinee 3. dizziness 4. syncope
83
what to monitor for on a pt on ropinirole?
1. light-headedness 2. postural hypotension 3. hallucinations 4. lower-extremity edema
84
less common AE of ropinirole
1. impulsive behavior 2. sleep attacks
85
when might ropinirole be used?
as a monotherapy adjunt therapy to reduce end of dose wearing off with l-dopa
86
Anticholinergic Therapy for PD MOA
antagonzie muscarinc receptors to prevent acetylcholine binding
87
PD Drug concerns
1. Timing of PT session with delivery of meds 2. Effects of exercsie on med absorption, utilization, and motor effects 3. Long-term meds use and disease progression

Pharmacology Test 3 (10 decks)

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