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Pharmacology II Exam 1 > Parkinson's > Flashcards

Parkinson's Flashcards

1
Q

What is the primary pathology of Parkinson’s Disease that leads to the gradual onset of voluntary motor dysfunction?

A

Degeneration of nigrostriatal dopaminergic neurons

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2
Q

What is the normal function of nigrostriatal dopaminergic neurons (the ones that degenerate in PD)?

A

Inhibit GABA neurons in the corpus striatum, initiating voluntary movement (cholinergic neurons activate GABA neurons and provide counterbalance)

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3
Q

How is PD diagnosed?

A

Neuropathologic exam and response to drug therapy

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4
Q

What neuropathologic findings indicate PD?

A

Bradykinesia + tremor or rigidity

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5
Q

What is the response to drug therapy that is indicative of PD?

A

Improved UPDRS score 1 hour after challenge with levodopa

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6
Q

Rank the prominent symptoms of PD in the order of usual onset: tremor, bradykinesia, rigidity, postural instability

A

Bradykinesia
rigidity
tremor
postural instability

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7
Q

Which symptom is the most responsive to levodopa therapy?

A

Bradykinesia (and major cause of disability!)

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8
Q

Increased resistance to passive movement

A

Rigidity (2nd onset symptom)

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9
Q

Which symptom is least responsive to levodopa therapy?

A

Postural instability (usually appears late in the disease)

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10
Q

Prophylactic, curative, abortive, symptomatic: which goal of pharmacotherapy is the treatment for PD?

A

Symptomatic (restore/maintain motor function so patients can have a higher QOL and live longer)

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11
Q

Generally what is PD therapy directed towards? (3 ideas)

A

Restoring DA to physiologic levels, providing an exogenous D2 receptor agonist, blocking muscarinic receptors to bring the SNc motor system back into balance

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12
Q

The initial stage of PD treatment is identified when the patient has developed a disability (bradykinesia) that requires drug therapy. What is the treatment goal here?

A

Control symptoms while minimizing side effects

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13
Q

What defines the second stage of PD treatment and what are its treatment goals?

A

Patient develops dyskinesia related to the usage of levodopa; reduce motor fluctuations but preserve motor function

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14
Q

MOA: prodrug metabolized in the brain to DA by aromatic L-amino acid decarboxylase in neurons & glial cells - restores DA levels in the substantia nigra

A

Levodopa (DA synthesis adjuvant)

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15
Q

T/F: The additional dopamine that the administration of levodopa brings about is used at that time only.

A

False (taken up and stored in presynaptic vesicles so more can be released in response to neuronal action potentials)

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16
Q

PK of levodopa: how is it administered/absorbed?

A

Orally (in GI tract)

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17
Q

PK of levodopa: how is it transported, if at all, across the BBB?

A

By the neutral L-amino acid transporter (fun fact: dopamine is NOT a substrate because it’s not an amino acid duh)

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18
Q

T/F: Amino acids from proteins in the diet can compete with levodopa for absorption from the GI tract and for transport across the BBB.

A

true

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19
Q

PK of levodopa: What reaction/interaction increases the severity of peripheral side effects and diminishes the amount of levodopa that reaches the CNS?

A

Metabolism by peripheral DOPA decarboxylase

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20
Q

MOA of carbidopa

A

Inhibitor of peripheral DOPA decarboxylase (also doesn’t cross the BBB so we good there)

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21
Q

What percentage of levodopa reaching the brain is increased by the administration of carbidopa? Can there be a dose reduction because of this? If yes, how much?

A

2% to 10%; yes 75% dose reduction

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22
Q

How many times is carbidopa/levodopa taken per day? Why?

A

3-4 times daily; half-life 1.5 hours (beneficial effects last about 6-8 hours)

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23
Q

T/F: Levodopa (+/- carbidopa) is the most effective PD drug, especially for bradykinetic symptoms, but it does NOT increase lifespan.

A

False- yes most effective, but DOES increase lifespan AND quality of life

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24
Q

2 uses for levodopa

A

PD, restless legs syndrome (off-label)

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25
Q

Levodopa has peripheral & central side effects. What are the 3 GI side effects noted?

A

Nausea, vomiting, anorexia (activation of chemoreceptor trigger zone? What does that mean idk moving on…)

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26
Q

Levodopa has peripheral & central side effects. What are the 2 cardiovascular side effects noted?

A

Orthostatic hypotension (common), arrhythmias

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27
Q

T/F: Carbidopa improves the percentage of levodopa that reaches the CNS, but it does not minimize peripheral side effects.

A

False (it does minimize them)

28
Q

Levodopa has peripheral & central side effects. Generally, what are the central side effects, which, by the way, are worsened by carbidopa?

A

Psychiatric (hallucinations, impulsive behavior, depression, somnolence, insomnia), neuroleptic malignant syndrome with abrupt withdrawal

29
Q

Madeline has been on levodopa/carbidopa since 2008 for advanced PD. What complication are you MOST concerned with?

A

Motor fluctuations (on-off phenomenon) and dyskinesia (associated with long term use ~10 years & advanced disease

30
Q

DDI of levodopa (1)

31
Q

4 contraindications of levodopa

A
  • Psychotic disorders (can use quetiapine, psychosis central ADEs!)
  • CV disorders (orthostatic hypotension, arrhythmias are ADEs)
  • Narrow angle glaucoma
  • Melanoma
32
Q

Describe the on-off phenomenon.

A

Striatal neurons become increasingly dependent on the peripheral availability of levodopa, which results in a pulsatile stimulation of DA neurons; dyskinesia (involuntary movements) occurs at peak blood levels

33
Q

MOA: D2 receptor agonist

A

Pramipexole

34
Q

PK of pramipexole: How is it administered?

A

Orally or transdermally

35
Q

Which of the following is NOT true concerning pramipexole (and really all D2 receptor agonist)?
A. Needs to be stored and released by nerve terminals (similar to levodopa after it is metabolized)
B. Does not require metabolism
C. All given orally or transdermally except apomorphine (SQ)
D. Not affected by amino acids for uptake

A

A (doesn’t need this)

36
Q

Specific use of pramipexole (D2 receptor agonist) for PD: (2)

A

Monotherapy in early PD patients < 65 years old OR used in combination with levodopa for advanced PD

37
Q

How do you start a patient on pramipexole?

A

Start with a low dose and titrate up to minimize side effects (similar ADEs to levodopa)

38
Q 
What other use, besides PD, can pramipexole (D2 receptor agonist, Mirepex™️) be used for?
A. Seizures
B. Bipolar disorder 
C. Depression
D. Restless legs syndrome
39
Q

Motor fluctuation “rescue” drug

A

Apomorphine

40
Q

How do you start a patient on apomorphine?

A

First, pre-treat with an antiemetic for 3 days, inject SQ, then continue antiemetic for 2 months

41
Q

Use of apomorphine:

A

Treats hypo-mobility (can’t move, can’t swallow) “off” episodes in advanced PD

42
Q

Apomorphine has a more reliable & rapid onset than oral D2 agonists, ___, and its duration is ___.

A

4-12 minutes, 60 minutes

43
Q

How do the ADEs of dopamine receptor agonists compare to levodopa’s? (Remember: GI & CNS…na/v, anorexia, hypotension, arrhythmias, psychiatric, etc.)

A

Similar to levodopa, but less dyskinesia and more impulsive behavior

44
Q

MOA: selective irreversible inhibitor of MAO-B - therefore, inhibiting the degradation of endogenous dopamine in the CNS & prolonging the effects of levodopa

A

Selegilene

45
Q

Uses (2) of selegilene:

A

Monotherapy in early PD (disease-modifying????), combination with levodopa-carbidopa to reduce motor fluctuations

46
Q

3 most common ADEs of selegilene (although usually well-tolerated)

A

Headache, insomnia, dizziness (MAO-B inhibitor)

47
Q

What can giving levodopa with selegilene cause?

A

Increased dyskinesia due to levodopa (increases the dose the reaches the CNS!!)

48
Q

DDI selegilene (1)

A

SSRIs (serotonin syndrome)

49
Q

T/F: At normal doses, selegilene is not associated with tyramine HTN crisis (wine/cheese effect).

50
Q

MOA: reversible inhibitor of COMT in the periphery - enhances/prolongs the effect of levodopa because levodopa can be metabolized by COMT to 3-OMD, which competes for uptake into the brain

A

Entacapone

51
Q

Use/benefit of entacapone

A

Used in combination with levodopa-carbidopa to enhance/prolong action (COMTI); reduces off episodes (hypo-mobility)

52
Q

T/F: MAOIs (like selegilene) are effective when given alone

53
Q

T/F: COMTIs (like entacapone) are effective when given alone.

54
Q

3 side effects of entacapone

A

Increases side effects of levodopa (dyskinesia, nausea, confusion), delayed diarrhea, urine discoloration orange/brown

55
Q

What is the general rationale & efficacy of using anticholinergics in PD?

A

Too little dopamine stimulation in PD allows ACh action on muscarinic receptors to predominate (which, I think, causes impaired voluntary movement/immobility), so blocking muscarinic receptors should improve symptoms BUT only tremor is significantly improved

56
Q

MOA: blocks muscarinic receptors in CNS

A

Trihexyphenidyl

57
Q

Use of trihexyphenidyl in PD (hint: fairly specific…)

A

In patients < 70 years old with disturbing tremor (ok kinda mean??) but no significant bradykinesia

58
Q

ADEs of trihexyphenidyl

A

Anticholinergic; cognitive dysfunction

59
Q

MOA: uncertain, but may antagonize glutamate-NMDA receptors

A

Amantadine (anti-influenza agent)

60
Q

What is the use (2) and relative efficacy of amantadine for PD?

A

Short term monotherapy in early PD (improves bradykinesia/rigidity), drug-induced dyskinesia; weak, temporary efficacy

61
Q 
3 ADEs= cognitive impairment
Livedo reticularis (zetus lapetus!- purplish discoloration of the skin)
Ankle edema
A

Amantadine (anti-influenza, antagonist of glutamate-NMDA receptor maybe)

62
Q

T/F: Benefits of dopamine therapy diminish with time, while CNS side effects increase.

63
Q 
Which of the following could you use in a younger PD to begin therapy?
A. Trihexyphenidyl
B. Amantadine
C. Pramipexole
D. Selegilene
A

All but C (DA receptor agonists used with disease progression)

64
Q 
With disease progression, what can be used in PD therapy in older patients?
A. Levodopa-carbidopa
B. Amantadine
C. Pramipexole
D. Selegilene
A

A (preferred initial treatment in older patients)

65
Q 
With disease progression, what can be used in PD therapy in patients < 65 years?
A. Levodopa-carbidopa
B. Amantadine
C. Pramipexole
D. Selegilene
A

C (DA receptor agonist)

66
Q 
Long-term complications of levodopa therapy are managed with all BUT the following:
A. Trihexyphenidyl
B. Entacapone
C. Apomorphine
D. Selegilene
A

A (anticholinergic for tremor but not significant bradykinesia)

Pharmacology II Exam 1 (9 decks)

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