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Pharmacology Exam 3 > Neurology Degenerative Conditions > Flashcards

Neurology Degenerative Conditions Flashcards

1
Q

What is Parkinson’s Disease?

A

Chronic, progressive disease characterized by movement deficits.

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2
Q

What are the clinical manifestations of Parkinson’s and what do each mean?

A
  • Akinesia- delayed initiation of movement
  • Bradykinesia- slow movement
  • Postural instability- impaired/absent postural responses
  • Rigidity- freezing episodes
  • Tremor- “pill roll” resting tremor often 1st sign
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3
Q

Parkinson’s is defined by the death of what in our body?

A

Dopamine producing neurons (dopamine)

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4
Q

What is the cause of Parkinson’s?

A

Unknown, but a combination of genetic and environmental factors.

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5
Q

What does medical management do to dopamine?

A
  • Dopamine replacement
  • Increasing dopamine stimulation
  • Modulation of nondopaminergic systems
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6
Q
  • What are the two scales used for Parkinson’s?
  • Which one divides Parkinson’s into 5 stages?
  • Which one is a measure to determine symptomatic relief from PD medications?
A
  • UPDRS (Unified Parkinson’s Disease Rating Scale)
  • Hoehn and Yahr Scale
  • UPDRS
  • Hoehn and Yahr Scale
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7
Q

What are the long-term effects of dopamine replacement?

A
  • MOVEMENT RELATED COMPLICATIONS
  • Dyskinesia- uncontrolled, involuntary movements
  • Motor fluctuations- “on off” medication states
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8
Q

What are the 3 dopamine replacement therapy drugs?

A
  • Levodopa-carbidopa (Sinemet)
  • MOA-B Inhibitors
  • COMT Inhibitors
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9
Q

How does levodopa-carbdopa (Sinemet) work?

A

Sinimet is a combination drop, l-dopa is a precursor to dopamine that CAN cross the BBB. Carbidopa acts to stop the breakdown of l-dopa into dopamine so we have CNS action.

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10
Q

What are the biggest AE associated with levodopa-carbidopa (Sinimet)?

A

Motor Disturbances

  • End of Dose “wearing off”- stiffness and rigidity return
  • Freezing- sudden inhibition of LE function
  • “On” period dyskinesia- involuntary movements
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11
Q

How does MOA-B Inhibitors work?

A

Inhibits MOA B, which usually acts to break down dopamine.

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12
Q

When are MOA-B inhibitors used?

A

After levodopa-carbidopa and dopamine agonists

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13
Q

How does COMT Inhibitors work?

A

Inhibits COMT, which usually acts to break down l-dopa.

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14
Q

How do dopamine agonists work?

A

Bind to and agonize dopamine receptors.

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15
Q

What are the main AE associated with dopamine agonists?

A
  • nausea
  • dizziness
  • drowsiness
  • syncope

less common-impulsive behavior and sleep attacks

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16
Q

How does anticholinergic therapy work?

A

Antagonizes muscarinic receptors to prevent ACh binding

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17
Q

What are the AE associated with anticholinergic therapy?

A
  • Cant see
  • Cant spit
  • Cant shit
  • Hot
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18
Q

What type of drug is amantadine?
What is it mainly used for?
What is a unique AE associated with it?

A

Dopamine agonist or dopamine replacement

  • Unknown MOA so classification is difficult.
  • Mainly used for dyskinesia.
  • livedo reticularis
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19
Q

What are the two first line treatments for Parkinson’s?

A
  • levodopa-carbidopa

- dopamine agonists

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20
Q

What are the overall Parkinson’s Disease drug concerns?

A
  • Timing of PT session with delivery of medications.
    • PT during “on” cycle can help with participation.
    • Also important to see patients during “off” cycles.
  • Effects of exercise on medication absorption.
    • Possibly improved L-dopa with aerobic activities.
  • Long tern medication use.
    • L-dopa dosage less effective over time.
    • More “off” cycles as disease progresses.
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21
Q

What is multiple sclerosis?

A

It is a chronic, progressive immune disease that attacks the CNS.

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22
Q

What are the clinical symptoms associated with MS?

A
  • VISION PROBLEMS, nystagmus
  • Weakness, poor endurance
  • Sensory and balance impairments
  • UMN signs (spasticity, hyperreflexia)
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23
Q

What are the outcome measures to determine treatment effectiveness?

A
  • MRI
  • Relapse Rate
  • Expanded Disability Severity Scale
24
Q

What can the frequency of exacerbation/relapses tell us?

A

Can show us disease progression.

25
What are the 2 aspects of MS treatment?
- DMT (disease modifying treatment) | - Symptoms- lessen symptoms
26
How long can it take to see results with DMT?
1 year
27
What are the common treatments associated with MS?
- Interferon B - Glatiramer acetate - S1P - Dimethyl fumarate - Monoclonal antibodies
28
How does IFN-B work?
The exact MOA is unknown in MS. The goal of it is to decrease exacerbations and delay accumulation of physical disability.
29
What is the most important AE to know with these drugs?
Flu-like symptoms (occurs in >50%)
30
How does Glatiramer acetate work?
Reduces the autoimmune response to myelin by reducing T-cell response against myelin.
31
What is the most important AE to know with these drugs?
Injection site reaction
32
How do S1P (Sphingosine 1-Phosphate) receptor modulators work?
Converted to active metabolites which blocks release of lymphocytes from BBB to CNS which decreases inflammation.
33
What drug is a S1P?
fingolimod
34
What are the common AE associates with S1P?
Headache (15%), increased LFTs
35
What should we monitor for within 24hrs of the 1st dose?
bradycardia
36
How does dimethyl fumarate work?
MOA is unknown in MS but may have anti-inflammatory properties.
37
What are the common AE associated with this class?
GI (N/V/D, ab pain) and flushing
38
How do monoclonal antibodies work?
Antibodies that bind to lymphocytes, preventing them from crossing the BBB which results in decreased inflammation. Also impacts antigen presentation.
39
What is important to know about monoclonal antibodies?
Monitor for infection due to increased risk.
40
Generally speaking, all the common drugs used for MS are considered what? All these drugs also act to reduce what?
- Immunosuppressants | - Exacerbations
41
What is PML (progressive multifocal leukoencephalopathy)? What should we do if we have any suspicion of PML? WHAT DRUGS CAUSE PML?
- Demyelinating CNS disorder caused by reactivation of JCV. - Refer - monoclonal antibodies, dimethyl fumarate, and SP1 Receptor modulators
42
What are the overall MS drug concerns?
- FATIGUE- most common and disabling MS symptom - Corticosteroid drug treatment - DMT can have substantial AE including flu-like symptoms to immunosuppression
43
What is Alzheimer's Disease?
A progressive neurodegenerative disease that results in the gradual loss of memory and function.
44
Alzheimers account for 60% of what?
Dimentia cases
45
In Alzheimers, produce mistakes throughout the brain resulting what?
cell death which leads to decreased size of brain tissue | -specifically areas of memory and language
46
Alzheimers is a dramatic reduction in what?
ACh, a loss of 60-90% of ACh activity results in memory impairment.
47
What are the 2 types of drugs used to treat Alzheimer's Disease?
Cholinesterase Inhibitors | NMDA antagonists
48
How do cholinesterase inhibitors work?
Prevent the breakdown of ACh in the body.
49
What is an example of a cholinesterase inhibitor?
donepezil (Aricept)
50
What are the AE associated with cholinesterase inhibitors?
- N/V - DUMBELLS - Diarrhea - Urination - Miosis - Bradycardia - Emesis - Lacrimation - Lethargy - Salivation
51
Do we want to taper these meds off?
Yes
52
How do NMDA antagonists work?
Stops excessive receptor activation by glutamate which decreases excitation and neuronal death.
53
What is an example of an NMDA antagonist?
memantine (Namenda)
54
What are the AE associated with NMDA antagonists?
Usually well tolerated but watch for falls.
55
What should Alzheimers patients not be taking?
Anticholinergic drugs
56
What are the overall Alzheimer's Disease drug concerns?
- Be aware of potential AE with meds - Cholinergic meds: GI issues (NVD) most common - memantine may cause dizziness, watch for falls - Communicate behavioral issues to healthcare provider - Timing of PT

Pharmacology Exam 3 (10 decks)

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