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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
Q

What are the 2 aspects of MS treatment?

A
  • DMT (disease modifying treatment)

- Symptoms- lessen symptoms

26
Q

How long can it take to see results with DMT?

A

1 year

27
Q

What are the common treatments associated with MS?

A
  • Interferon B
  • Glatiramer acetate
  • S1P
  • Dimethyl fumarate
  • Monoclonal antibodies
28
Q

How does IFN-B work?

A

The exact MOA is unknown in MS. The goal of it is to decrease exacerbations and delay accumulation of physical disability.

29
Q

What is the most important AE to know with these drugs?

A

Flu-like symptoms (occurs in >50%)

30
Q

How does Glatiramer acetate work?

A

Reduces the autoimmune response to myelin by reducing T-cell response against myelin.

31
Q

What is the most important AE to know with these drugs?

A

Injection site reaction

32
Q

How do S1P (Sphingosine 1-Phosphate) receptor modulators work?

A

Converted to active metabolites which blocks release of lymphocytes from BBB to CNS which decreases inflammation.

33
Q

What drug is a S1P?

A

fingolimod

34
Q

What are the common AE associates with S1P?

A

Headache (15%), increased LFTs

35
Q

What should we monitor for within 24hrs of the 1st dose?

A

bradycardia

36
Q

How does dimethyl fumarate work?

A

MOA is unknown in MS but may have anti-inflammatory properties.

37
Q

What are the common AE associated with this class?

A

GI (N/V/D, ab pain) and flushing

38
Q

How do monoclonal antibodies work?

A

Antibodies that bind to lymphocytes, preventing them from crossing the BBB which results in decreased inflammation. Also impacts antigen presentation.

39
Q

What is important to know about monoclonal antibodies?

A

Monitor for infection due to increased risk.

40
Q

Generally speaking, all the common drugs used for MS are considered what?
All these drugs also act to reduce what?

A
  • Immunosuppressants

- Exacerbations

41
Q

What is PML (progressive multifocal leukoencephalopathy)?
What should we do if we have any suspicion of PML?
WHAT DRUGS CAUSE PML?

A
  • Demyelinating CNS disorder caused by reactivation of JCV.
  • Refer
  • monoclonal antibodies, dimethyl fumarate, and SP1 Receptor modulators
42
Q

What are the overall MS drug concerns?

A
  • FATIGUE- most common and disabling MS symptom
  • Corticosteroid drug treatment
  • DMT can have substantial AE including flu-like symptoms to immunosuppression
43
Q

What is Alzheimer’s Disease?

A

A progressive neurodegenerative disease that results in the gradual loss of memory and function.

44
Q

Alzheimers account for 60% of what?

A

Dimentia cases

45
Q

In Alzheimers, produce mistakes throughout the brain resulting what?

A

cell death which leads to decreased size of brain tissue

-specifically areas of memory and language

46
Q

Alzheimers is a dramatic reduction in what?

A

ACh, a loss of 60-90% of ACh activity results in memory impairment.

47
Q

What are the 2 types of drugs used to treat Alzheimer’s Disease?

A

Cholinesterase Inhibitors

NMDA antagonists

48
Q

How do cholinesterase inhibitors work?

A

Prevent the breakdown of ACh in the body.

49
Q

What is an example of a cholinesterase inhibitor?

A

donepezil (Aricept)

50
Q

What are the AE associated with cholinesterase inhibitors?

A
  • N/V
  • DUMBELLS
    • Diarrhea
    • Urination
    • Miosis
    • Bradycardia
    • Emesis
    • Lacrimation
    • Lethargy
    • Salivation
51
Q

Do we want to taper these meds off?

A

Yes

52
Q

How do NMDA antagonists work?

A

Stops excessive receptor activation by glutamate which decreases excitation and neuronal death.

53
Q

What is an example of an NMDA antagonist?

A

memantine (Namenda)

54
Q

What are the AE associated with NMDA antagonists?

A

Usually well tolerated but watch for falls.

55
Q

What should Alzheimers patients not be taking?

A

Anticholinergic drugs

56
Q

What are the overall Alzheimer’s Disease drug concerns?

A
  • 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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