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Neurology 2 > Pharm - ET and PD > Flashcards

Pharm - ET and PD Flashcards

1
Q

First line agents to treat essential tremor

A
  • Propranolol (and other BB)

- Primidone, an anticonvulsant

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2
Q

Second line agents to treat essential tremor

A

Anticonvulsants:

  • Gabapentin
  • Topiramate
  • Benzodiazepines

Alcohol

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3
Q

What are the two benzodiazepines used to treat ET?

A
  • Alprazolam (Xanax)

- Clonazepam (Klonopin)

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4
Q

When should intermittent therapy be used for ET?

A

Mild ET with situational exacerbations of tremor

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5
Q

Whens should continuous therapy be used for ET?

A

persistent functional or psychological disability (including embarrassment or anxiety)

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6
Q

What is the expected clinical effect of either propranolol or primidone?

A
  • Reduced tremor magnitude by 50%

- Response rate of 50%

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7
Q

ADRs of propranolol

A
  • Bradycardia
  • Lightheadedness
  • Fatigue
  • Impotence
    • these are more LT effects
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8
Q

Propranolol contraindications

A
  • heart block
  • asthma/bronchospasm
  • DM (can mask hypoglycemia)
  • unstable heart failure
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9
Q

ADRs of primidone

A

ADRs generally more severe at tx initiation (** Dr. Letassy mentioned out loud)

  • Nausea
  • Ataxia **
  • Confusion **
  • Sedation **
  • Drowsiness
  • Fatigue
  • Depression
  • Vomiting
  • Malaise
  • Dizziness
  • Unsteadiness
  • Vertigo
  • Acute toxic reaction
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10
Q

Primidone contraindication

A
  • no response after titration to 250 mg ea night
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11
Q

What is the onset of action of Propranolol

A
  • Normal release is pretty quick, can use within one hour of situation where need therapeutic effect.
  • Extended release lasts longer and is sometimes preferred dt its daily dosing
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12
Q

What is the onset of action of Primidone

A

slower onset of action than propranolol (sometimes limits its utility)

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13
Q

What is indication for use of both primidone and propranolol to treat ET?

A
  • ET is resistant to mono therapy with either alone

- they have different MoAs…

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14
Q

Place in ET therapy for gabapentin

A
  • Can be used as a 2nd line monotherapy to reduce limb tremor
  • If failed both propranolol and primidone, unlikely gabapentin will work
  • More often used if can’t tolerate propranolol or primidone
  • Also used as adjunct to propranolol and/or primidone
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15
Q

Place in ET therapy for Topiramate

A
  • 2nd line to reduce lib tremor

- very effective but bad ADR!

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16
Q

Place in ET therapy for Benzodiazepines

A
  • 2nd line option
  • Consider if tremor is aggravated by anxiety (bc these drugs lower anxiety)
  • Caution for abuse, sedation, cognitive/behavioral changes
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17
Q

What ET patient would benefit most from botulinum toxin type A therapy

A

Inadequate response or poor toleration of first and second line oral drug therapies

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18
Q

botulinum toxin type A ADR when used to treat ET

A
  • When used to treat voice tremor: breathiness, hoarseness, swallowing difficulty
  • Also: injection site pain, stiffness, cramping, hematoma, paresthesias
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19
Q

What three PD drugs have the potential to cause orthostatic hypertension?

A
  • Levodopa
  • Dopamine agonists
  • COMP inhibitors
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20
Q

Goals of therapy in PD treatment

A
  • Improve motor and non-motor sx to maintain best quality of life
  • Preserve ability to perform activities of daily living
  • Improve mobility
  • Minimize ADR, treat complications
  • Improve non-motor features (cognitive impairment, depression, fatigue, sleep disorders)
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21
Q

What is the pharmacologic class for L-dopa (carbidopa/levodopa)

A

Levodopa

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22
Q

What is the pharmacologic class for Pramipexole

A

Dopamine agonist

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23
Q

What is the pharmacologic class for Ropinirole

A

Dopamine agonist

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24
Q

What is the pharmacologic class for Apomorphine

A

Dopamine agonist

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25
Q

What is the pharmacologic class for Bromocriptine

A

Dopamine agonist

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26
Q

What is the pharmacologic class for Rotigotine

A

Dopamine agonist

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27
Q

What is the pharmacologic class for Seligiline

A

MAOB Inhibitor

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28
Q

What is the pharmacologic class for Rasagiline

A

MAOB Inhibitor

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29
Q

What is the pharmacologic class for Trihexyphenol

A

Anticholinergic

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30
Q

What is the pharmacologic class for benzotropine

A

Anticholinergic

31
Q

What is the pharmacologic class for Amantadine

A

Antiviral

32
Q

What is the pharmacologic class for Entacapone

A

COMT inhibitor

33
Q

What is the pharmacologic class for Tolcapone

A

COMT inhibitor

34
Q

Levodopa MoA

A
  • Immediate precursor of dopamine
  • Crosses blood brain barrier (dopamine cannot)
  • Is decarboxylated to dopamine in the substantia nigra par compacta (SNc)
  • Converted dopamine is stored in presynaptic SNc neurons until released into the synaptic cleft
35
Q

Levodopa ADR

A

MANY

  • common early: Nausea*, somnolence, dizziness, HA
  • serious: orthostatic hypotension, confusion, hallucinations, delusions, agitation, psychosis
36
Q

Levodopa Place in therapy for PD

A
  • most effective drug for symptomatic tx of PD
  • Effective for management of bradykinetic symptoms (when intrusive, troublesome, uncontrolled by other anti-PD drugs)
  • Also work for tremor and rigidity but less effective on postural instability
  • Usually used first in patients who are ≥ 65
37
Q

Dopamine agonist MoA

A
  • Directly stimulate dopamine receptors
  • Do not require metabolic conversion
  • Longer duration than most forms of levodopa
38
Q

Dopamine agonist ADRs

A
  • ADR similar to levodopa (nausea, vomiting, orthostatic hypertension, confusion, vivid dreams, psychoiss) except:
  • May impair impulse control
  • Dopamine agonist withdrawal syndrome
39
Q

Some differences between dopamine agonist and levodopa ADRs

A

dopamine agonist:

  • Lower risk of dyskinesias, “wearing off”, and “on-off” fluctuations
  • Higher risk of hallucinations, sleepiness (caution about driving), edema
40
Q

Dopamine agonist withdrawal syndrome

  • sx
  • how to tx
A
  • Resembles cocaine withdrawal: anxiety, panic attacks, depression, sweating, nausea, pain, fatigue, dizziness, drug craving
  • Only way to treat is resume dopamine, refractory to other anti-PD meds
41
Q

Dopamine agonist place in therapy for PD

A
  • Monotherapy in early, mild-moderate PD, esp in pts <65 yo
  • Adjunct therapy with levodopa to reduce motor fluctuation symptoms, reduce frequency of off periods, may allow reduction in levodopa dosage, and can help manage dyskinesias due to levodopa
  • Not as effective as levodopa
42
Q

True/false dopamine agonist is a good alternative for a patient unresponsive to levodopa

A

FALSE

dopamine agonists are ineffective in patients who show no response to levodopa

43
Q

MOAB inhibitors MoA

A

Inhibits MAO-B, a mitochondrial enzyme that terminates the activity of intracellular dopamine, prolonging the action of dopamine

44
Q

MOAB inhibitor ADRs

A
  • Hallucinations or orthostasis
  • Nausea, insomnia
  • May worsen dyskinesias when used with levodopa or other dopaminergics
  • Many drug interactions due to MAO inhibition
45
Q

MOAB inhibitor place in therapy for PD

A
  • Mild to moderate benefit for pts with early PD
  • Selegiline and rasagiline can be used as first line therapy
  • modest benefit as monotherapy
  • Can be added to levodopa to reduce off time
  • May have antidepressant effects
46
Q

Anticholinergic MoA

A
  • Inhibits acetylcholine

- ACh activity is increased in PD due to dopamine depletion, contributes to tremor symptoms

47
Q

Anticholinergic ADRs

A
  • Anti-SLUD
  • Memory impairement, confusion, hallucinations, esp in elderly population*
  • Caution in pts with prostatic hypertrochy or closed-angle glaucoma
48
Q

Place in therapy for anticholinergics in PD

A
  • Can be used as monotherapy or adjunct, esp if tremor is main symptom (no bradykinesia or gait disturbance) and patient is young
  • Works best for tremor and dystonic symptoms
  • Use is limited due to intolerable side effects
49
Q

What sort of patient is the use of anticholinergic meds strongly discouraged?

A
  • older/demented patients

- those without tremor

50
Q

Amantadine MoA

A
  • Antiviral agent
  • MoA uncertain, known to increase dopamine release, inhibit dopamine reuptake, stimulate dopamine receptors, and possibly exert anticholinergic effects
  • Contains N-methyl-D-aspartate (NMDA) receptor antagonist properties that may account for therapeutic effect by interfering with excessive glutamate in basal ganglia
51
Q

Amantadine ADRs

A
  • Confusion, cognitive impairment, dry mouth, insomnia, hallucinations, nightmares
  • More common when used in combo with other antiPD drugs in older patients
52
Q

Place in therapy of Amantadine for PD

A
  • Monotherapy to target tremor or adjunct to levodopa in later disease for dyskinesias
  • Most useful in treating younger patients with early or mild PD
  • provides symptomatic benefit for tremor, rigidity, bradykinesia
53
Q

COMT Inhibitors MoA

A
  • Inhibition of COMT reduces peripheral and central methylation of levodopa and dopamine
  • Increases plasma half-life of levodopa
54
Q

COMT inhibitors ADRs

A
  • Symptoms of increased dopamine
  • Dyskinesia, hallucinations, confusion, nausea, orthostatic hypertension
  • Diarrhea that is poorly responsive to antidiarrheal meds
  • Hepatotoxicity (tolcapone), monitor ALT/AST
  • Entacapone can cause orange urine
55
Q

Place in PD therapy for COMT inhibitors

A
  • Always adjunct, never monotherapy
  • Tx pts with motor fluctuations who are experiencing end-of-dose “off” periods
  • No apparent advantage to use in patients without motor complications
56
Q

When use Levodopa (vs. dopamine agonist)?

A
  • Levodopa is the most effective drug for symptomatic tx of PD
  • First drug of choice if symptoms (esp. related to bradykinesia) are intrusive or troublesome
  • patient is ≥ 65
57
Q

When use dopamine agonist (vs. Levodopa)

A
  • monotherapy or in combo with other drugs (can think of as breakthrough adjunct)
  • Ineffective in patients who show no response to levodopa
  • Patient is <65
58
Q

Pharmacokinetic differences between IR and CR carbidopa /levodopa

A
  • Peak clinical effect of controlled release is less than the immediate release formulations – the controlled release formulations reach the brain more slowly over time. (Lower peaks reduce dyskinesias)
  • Controlled release absorption is about 70% the amount of the immediate release formulation, requires 30% higher dose of controlled release to achieve similar response as immediate release
    • both appear to maintain similar levels of symptom control
59
Q

Which formulation of carbidopa /levodopa is best to use at first in PD treatment?

A

Begin therapy with immediate release, titrate dose to desired response; once response is stable, can switch to controlled release product if desired

60
Q

What is the role of carbidopa when used in combo with levodopa to treat PD

A
  • Peripheral decarboxylase inhibitor
  • Blocks conversion to dopamine in systemic circulation and liver (prior to crossing BBB), allowing more to cross into the brain
  • Also helps prevent nausea, vomiting, orthostatic hypotension
61
Q

Measure to manage nausea with carbidopa/levodopa

A
  • When taking for the first time, take with a meal or snack to avoid nausea
  • Small starting doses combined with decarboxylase inhibitor TID are MORE likely to cause nausea due to inadequate amt of carbidopa → add supplemental dose of carbidopa or use antiemetics
62
Q

What causes parkinsonism-hyperpyrexia syndrome?

A
  • Stopping levodopa or dopamine agonist suddenly
  • Life threatening neurologic emergency… do NOT run out of this medication!!!
  • Can’t regulate basic homeostatic functions such as body temperature, blood pressure, etc.
63
Q

List the motor complications of levodopa

A
  • motor fluctuations, aka “end-of-dose wearing off effect”
  • “Delayed on” or “no on” response (Delayed or absent)
  • Start hesitation “freezing”
  • Peak-dose dyskinesia
  • “Off-period” dystonia

** Increase with younger age at PD onset and higher levodopa doses

64
Q

What are motor fluctuations (“end-of-dose wearing off effect”)

A

Decreased length of time levodopa is effective in symptom control

65
Q

What is start hesitation or “freezing”

A
  • Sudden, episodic inhibition of LE motor function
  • Interferes with walking, fall risk
  • Difficulty taking step or making a turn
  • Exacerbated by anxiety or anticipating obstacles
66
Q

What is peak-dose dyskinesia

A

Involuntary choreiform movements usually in the neck, trunk, LE/UE

67
Q

What is “off-period” dystonia

A
  • Sustained muscle contractions, commonly in distal LE such as clenching toes or involuntary turning of foot
  • Usually occurs in early morning hours before medication
68
Q

What is best treatment/intervention for End-of-dose “wearing off” effect

A
  • Increase frequency of levodopa/carbidopa

- Add either COMT inhibitor, MOA B inhibitor, or dopamine agonist

69
Q

What is best treatment/intervention for “Delayed on” or “no on” response

A
  • more common when taken with food
  • Give levodopa/carbidopa on an empty stomach
  • Use levodopa/carbidopa oral dissolving tablet
  • Avoid levodopa/carbidopa controlled release, use apomorphine SC instead
70
Q

What is best treatment/intervention for start hesitation “freezing”

A
  • PT and sensory cues are more helpful than medication
  • Increase levodopa/carbidopa dose
  • Add dopamine agonst or MAO-B inhibitor
71
Q

What is best treatment/intervention for peak dose dyskinesia

A
  • Smaller doses of levodopa/carbidopa

- Add amantadine

72
Q

What is best treatment/intervention for “Off period” dystonia

A
  • Take medication (in am)
  • Bedtime administration of long acting dopamine agonist
  • SR levodopa/carbidopa
  • Focal injections of botulinum toxin type A or B
73
Q

What is the role of low-dose estrogen in the treatment of post-menopausal women with PD

A
  • Adjunct therapy
  • Postmenopausal women with motor fluctuations on antiPD meds
  • In one study, improved “on” time and motor control
  • No evidence that it works on dopamine receptors, benefit may be to overall well being
  • Concerns about ADRs associated with long-term use may limit its use

Neurology 2 (21 decks)

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