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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
Q

Rare Fingolimod AEs

A
  1. macular edema (report vision changes immediately),
  2. infection
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26
Q

What AE warrants an immediate referral for somone on an S1P receptor modulator?

A

vision changes

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27
Q

Dimethyl fumarate Use

A

PO 2x/day to decrease exacerbations and disease severity

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28
Q

MOA of dimethyl fumarate

A

unknown in MS; may have anti-inflammatory properties

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29
Q

AEs of dimethyl fumarate

A
  1. GI (N/V/D, abdominal pain in 12-18%)
  2. flushing (up to 40%)
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30
Q

Rare AE for dimethyl fumarate

A

hepatoxicity

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31
Q

Monoclonal Antibodies drugs suffix

A

-mab

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32
Q

general MOA for monoclonal antibodies

A

decrease inflammation in CNS and autoantibody formation

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33
Q

Use of Monoclonal antibodies

A
  1. may decrease exacerbations
  2. decrease lesions on MRI and slow progression
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34
Q

Common AEs for monoclonal antibodies

A
  1. infusion related rxns
  2. HA
  3. fatigue
  4. arthralgia
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35
Q

What is PML?

A

Progressive Multifocal Leukoencephalopathy

demyelinating CNS disorder caused by reactivation of JCV

36
Q

Patients on which meds are at a higher risk of developing PML?

A
  1. Monoclonal Antibodies
  2. Dimethyl Fumarate
  3. SP1 receptor modulators
37
Q

Signs and Symptoms of PML?

A
  1. altered mental status (AMS)
  2. aphasia
  3. ataxia
  4. hemiparesis
  5. hemiplegia
  6. visual field disturbances (double vision, partial blindness)
  7. seizures
38
Q

Off-label trxs for relapsing/progressive MS

A
  1. Azathioprine
  2. Methotrexate
39
Q

Symptom trx for MS

A
  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
Q

Drug Concerns for MS patients

A
  1. Fatigue
  2. Corticosteroid drug treatment
  3. DMT drugs can have substantial AEs influcing flu-like symptpoms to immunosuppression
41
Q

Key features of Alzheimer’s Disease

A
  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
Q

What neurotransmitters are depleted in AD?

A
  1. Acetylcholine
  2. serotonin
  3. somatostatin
  4. NE
43
Q

General trx approach for AD

A
  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
Q

Cholinesterase Inhibitor Drug

A

Donepezil (Aricept)

45
Q

Cholinesterase Inhibitors pros

A

modest improvements in cognition and ADLs

benefits last ~3-24 months

46
Q

Cholinesterase Inhibitors MOA

A

inhibit acetylcholinesterase from breaking down acetylcholine =

increased ACh helps correct ACh deficiency in AD

47
Q

Primary AEs for Cholinesterase Inhibitors

A

SLUDGE

DUMBELLS

48
Q

T/F: Cholinesterase Inhibitors can exacerbate UTOs, asthma, and COPD

49
Q

T/F: Cholinesterase Inhibitors are on the Beers List?

50
Q

what class of drug is Memantine (namenda)

A

NMDA antagonist

51
Q

NMDA antagonist MOA

A

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

52
Q

When are NMDA antagonists used?

A
  1. monotherapy for moderate cases
  2. in conjunction with cholinesterase inhibitor in moderate cases
  3. Not FDA approved for mild cases
53
Q

NMDA Antagonists AE

A
  1. usually well tolerated
  2. monitor for falls
54
Q

Individuals with AD should not be taking what?

A
  1. Anticholinergic Drugs
  2. OTC antihistamines (Benadryl)
55
Q

AD drug concerns

A
  1. Cholinergic meds: GI issues (NVD) most common
  2. Memantine may cause dizziness, watch for falls
  3. Communicate behavioral issues to healthcare providers
56
Q

What should be taken into consideration when scheduling PT for patients with AD?

A
  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
Q

Characterizations of Parkinson’s Disease

A
  1. Akinesia
  2. Bradykinesia
  3. Postrual instability
  4. Rigidity (freezing episode)
  5. Tremor (pill-roll)
58
Q

Pathophysiology of PD

A
  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
Q

Etiology of basal ganglia neurotransmitter imbalance

A

Overall unknown, possible impact of

  1. genetics
  2. environmental factors
60
Q

Medical management of PD

A
  1. Dopamine replacement
  2. Dopamine agonist therapy
  3. Anticholinergic therapy
61
Q

Overall goal of pharmacologic treatment Parkinson’s Disease

A

Restore neurochemical balance

62
Q

Name of Parkinson’s Disease Scales

A
  1. Unified Parkinson’s Disease Rating Scale (UPDRS)
  2. Hoehn & Yahr Scale
63
Q

PD, dopamine replacement therapy drugs

A

Levodopa-carbidopa (L-dopa)

MAO-B inhibitors

COMT Inhibitor

Amantadine (both agonist and replacement therapy)

64
Q

PD, dopamine agonist therapy

A

Amantadine

Ropinirole (Requip)

65
Q

Anticholinergic Therapy Drugs for PD

A
  1. Benztropine (Cogentin)
  2. Trihexyphenidyl
66
Q

benefits of Levodopa-carbidopa

A
  1. improves movement velocity
  2. may reduce tremor
  3. reduce rigidity
  4. improves force production & coordination of anticipatory postural task
67
Q

What are the long-term effects of dopamine replacement therapy

A
  1. Movement-related complications
  2. Dyskinesia
  3. Motor Fluctuations
68
Q

how does dopamine impact cholinergic response?

A

without dopamine the cholinergic response is uninhibited

69
Q

what is the 1st line trx and most effective treatment for PD patients?

A

Levodopa-carbidopa (Sinemet)

70
Q

carbidopa MOA (why is it combined with l-dopa)?

A

stops breakdown of l-dopa to dopamine in periphery so more l-dopa crosses BBB

71
Q

AE of Levodopa-carbidopa (Sinemet)

A
  1. End of dose “wearing of”
  2. “Delayed on” or “no on”
  3. Freezing
  4. “on” period dyskinesia
72
Q

MOA for MAO-B inhibitors

A

inhibit monoamine oxidase (MAO) B which breaks down dopamine = increased dopamine levels in CNS

73
Q

what PD treatment has a risk for serotonin syndrome?

A

Selegiline (a type of MAO-B inhibitor) when combined with serotonergic meds

74
Q

MOA of COMT inhibitors

A

Inhibit COMT which in turn decreases breakdown of l-dopa

75
Q

when are COMT inhibitors used?

A

Adjunct

used to reduce end of dose wearing off with l-dopa

76
Q

AE of COMT Inhibitors

A

>10% = involuntary movements, nausea

77
Q

what has Amantadine been used to treat in the past?

78
Q

MOA of Amantidine

A

Unknown

possibly increases dopamine release

79
Q

Amantadine AE

A
  1. confusion
  2. hallucinations
  3. dizziness
  4. dry mouth
  5. constipation
  6. livedo retiularis
80
Q

T/F: Dopamine agonists can be a 1st line option for trx PD?

81
Q

Dopamine Agonist Drug

A

ropinirole (Requip)

82
Q

ropinirole (Requip) AE

A
  1. nausea
  2. drowsinee
  3. dizziness
  4. syncope
83
Q

what to monitor for on a pt on ropinirole?

A
  1. light-headedness
  2. postural hypotension
  3. hallucinations
  4. lower-extremity edema
84
Q

less common AE of ropinirole

A
  1. impulsive behavior
  2. sleep attacks
85
Q

when might ropinirole be used?

A

as a monotherapy

adjunt therapy to reduce end of dose wearing off with l-dopa

86
Q

Anticholinergic Therapy for PD MOA

A

antagonzie muscarinc receptors to prevent acetylcholine binding

87
Q

PD Drug concerns

A
  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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