Antiparkinson Medications Flashcards

1
Q

Parkinson disease

A

Chronic, progressive, neurodegenerative disorder

Affects dopamine-producing neurons in the brain

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2
Q

Parkinson disease is caused by an imbalance of two neurotransmitters?

Their actions?

A

ACh- excitatory
Dopamine- inhibits nerve actions (inhibitory)

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3
Q

Parkinson disease symptoms

A

Bradykinesia (slow, movement)

“TRAP”
Tremor
Rigidity- of muscle
Akinesia – no movement
Postural instability

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4
Q

Symptoms occur when about 80% of the dopamine stored in the ________ _____ of the basal ganglia is depleted. (20% left of dopamine- far along the disease before diagnosis)

Symptoms can be partially ________ as long as there are functioning _____ ______that can take up dopamine.

A

Symptoms occur when about 80% of the dopamine stored in the substantia nigra of the basal ganglia is depleted. (20% left of dopamine- far along the disease before diagnosis)

Symptoms can be partially controlled as long as there are functioning nerve terminals that can take up dopamine.

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5
Q

akinesia

A

absence of psychomotor activity- masklike facial expression

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6
Q

bradykinesia

A

slow movement

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7
Q

rigidity

A

cogwheel rigidity, resistance to passive movement

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8
Q

tremor

A

pill-rolling- the tremor of the thumb against the forefinger

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9
Q

postural instability

A

unsteadiness

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10
Q

Dyskinesia

A

Difficulty in performing voluntary movements

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11
Q

Two common types of Dyskinesia

A

chorea and dystonia

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12
Q

Chorea

A

irregular, spasmodic, involuntary movements of the limbs or facial muscles

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13
Q

Dystonia

A

abnormal muscle tone leading to impaired or abnormal movements

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14
Q

Parkinson disease

Rapid swings in response to levodopa occur. Called?

Parkinson’s disease (PD) worsens when too little ________ is present.

_________ occurs when too much dopamine is present.

A

Rapid swings in response to levodopa occur (“on–off phenomenon”)

Parkinson’s disease (PD) worsens when too little dopamine is present.

Dyskinesia (problem with movement) occurs when too much dopamine is present.

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15
Q

What is “Wearing-off phenomenon”

A

the drug is losing effectiveness

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16
Q

“on-off phenomenon”

A

variable response to levodopa, resulting in periods of good control and periods of poor control of PD symptoms

worsening of symptom near the end of the next dose

swings in the response of levodopa

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17
Q

On phenomenon

A

greater symptom control

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18
Q

Off phenomenon

A

less symptom control

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19
Q

PD is thought to be caused by an imbalance of _____ & _____ with a deficiency of _______ in certain areas of the brain.

A

PD is thought to be caused by an imbalance of dopamine and ACh with a deficiency of dopamine in certain areas of the brain.

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20
Q

Drug therapies are aimed at

A

at increasing the levels of dopamine or antagonizing(lowering) the effects of ACh.

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21
Q

Unfortunately, current drug therapy does not slow the progression of the disease but rather is used to

A

slow the progression of symptoms.

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22
Q

What type of drug is given first?

A

direct acting

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23
Q

Part of brain where dopamine deficit occurs?

A

substantia nigra
(destruction of substantia nigra by PD)

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24
Q

Dopamine depletion reults in

A

excessive unopposed ACh (cholinergic activity) due to lack of dopamine effects

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25
Q

diagnostic of PD

Lab tests

A

based on symptoms

CT/ MRI… to rule out other disease

No lab test to detect or confirm PD

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26
Q

end of dose wearing off

A

diminishing dopamine effect towards the end of the dose associated with increased loss of stored dopamine

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27
Q

direct-acting dopaminergic drugs- define:

2 subclasses

A

first-line agents

non dopamine dopamine receptors

dopamine replacement drugs

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28
Q

2 subclasses non dopamine dopamine receptors and give examples of each

A

ergot derivative (bromocriptine)

non-ergot drugs (pramipexole and ropini-
role).

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29
Q

Levodopa is the

A

Levodopa is a precursor of dopamine.

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30
Q

Blood–brain barrier does not allow _________ to enter but does allow ________.

A

Blood–brain barrier does not allow exogenously supplied dopamine to enter but does allow levodopa.

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31
Q

give 1 example of nondopamine dopamine receptor agonists

and its subclass

A

Ergot derivatives: bromocriptine

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32
Q

direct-acting nondopamine dopamine receptor agonists: mechanism of action

A

directly stimulate PRE and POST synaptic dopamine RECEPTORS in brain

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33
Q

Bromocriptine indications

A

Parkinson’s disease

hyperprolactinemia

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34
Q

bromocriptine 1 mechanism of action

A

activates presynaptic dopamine receptors to stimulate more dopamine production

chief site of activity is D2 subclass of dopamine receptors

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35
Q

bromocriptine other mechanism of action

A

Also INHIBIT the production of the hormone PROLACTIN, which stimulates normal lactation

Can be used to treat women with excessive or undesired breast milk production (galactorrhea) and for treatment of prolactin-secreting tumours

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36
Q

Bromocriptine contraindications

why?

A

CAUTION: severe ischemic disease: peripheral vascular disease– due to its ability to stimulate dopamine receptors in peripheral tissues outside brain-vasoconstriction worsens PVD

adrenergic drugs due to cardiovascular risks of excess catecholamine activity

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37
Q

bromocriptine may be used with levodopa to

A

decrease dose of levodopa

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38
Q

bromocriptine adverse effects

A

GI upset, dyskinesias, sleep disturbances

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39
Q

bromocriptine interactions

A

erythromycin

adrenergic drugs (increases hr, bp- vasoconstriction)

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40
Q

1 example of Dopamine replacement drugs

A

Levodopa

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41
Q

Levodopa is

A

biological precursor of dopamine required by the brain for dopamine synthesis

exogenous source

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42
Q

Levodopa mechanism of actions

A

stimulate presynaptic dopamine receptors to increase dopamine in brain

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43
Q

Levodopa is able to cross the ______, and then it is converted to _________.

A

Levodopa is able to cross the blood–brain barrier, and then it is converted to dopamine.

44
Q

Large doses of ____ needed to get dopamine to the brain also cause adverse effects.

A

However, large doses of levodopa needed to get dopamine to the brain also cause adverse effects.

45
Q

Carbidopa is given with levodopa.

Carbidopa does not cross the________ and prevents __________ breakdown in the _________.

As a result, more levodopa crosses the _______, where it can be converted to __________.

A

Carbidopa is given with levodopa.

Carbidopa does not cross the blood–brain barrier and prevents levodopa breakdown in the periphery.

As a result, more levodopa crosses the blood–brain barrier, where it can be converted to dopamine.

46
Q

Levodopa is converted into?

A

dopamine

Levodopa is taken up by the dopaminergic terminal, converted into dopamine, and then released as needed

As a result, neurotransmitter imbalance is controlled in patients with early PD who still have functioning nerve terminals.

47
Q

As PD progresses, it becomes more difficult to control it with levodopa.

Ultimately, levodopa no longer controls the PD, and the patient is seriously debilitated.

This generally occurs between __ and __ years after the start of levodopa therapy.

A

5 to 10 years

48
Q

Route of dopamine/ levodopa

A

administered orally in order to cross blood-brain barrier

Levodopa cannot pass blood-brain barrier if given through IV

49
Q

_______ is the biological precursor of dopamine and can penetrate into the ____.

A

Levodopa is the biological precursor of dopamine and can penetrate into the CNS.

50
Q

Adverse effects of Levodopa (replacement drugs)

A

Adverse effects: confusion, involuntary movements, GI distress, hypotension, cardiac dysrhythmias

51
Q

Levodopa indication

Note: critical care settings can give IV levodopa as

A

restore dopaminergic activity

Note: critical care settings given IV as pressor drug to raise BP and enhance kidney function

52
Q

Levodopa- carbidopa contraindications

Used cautiously in patients with

A

angle-closure glaucoma, undiagnosed skin cancer

use cautiously in patients with open-angle glaucoma

vitamin B6 pyroxidine/ high protein

53
Q

Levodopa- carbidopa adverse effects

A

Adverse effects: cardiac dysrhythmias, hypotension, chorea, muscle cramps, GI distress

54
Q

Levodopa- carbidopa

Interactions

A

Interactions: pyridoxine( vitamin B6), nonselective MAOIs, benzodiazepines, antipsychotics, dietary PROTEIN

High protein food- meat, eggs, milk, fish (take 30 mins before). No high protein diet, amino acid related- interferes and slows absorption of medication

Drug interactions occur with tricyclic antidepressants and other drugs.

55
Q

carbidopa treats?

What does it inhibit when given with levodopa?

A

adjunct to treat nausea associated with Sinemet

breakdown of levodopa in the periphery

56
Q

Sinemet CR

A

Sinemet CR: increases “on” time and decreases “off” time- do not crush

57
Q

Carbidopa–levodopa is best taken on an empty stomach; to minimize ________, it can be taken with food.

A

GI ADVERSE EFFECTS

58
Q

1 EXAMPLE OF INDIRECT ACTING DOPAMINE RECEPTOR AGONISTS

A

MAO Inhibitors

59
Q

2 MAO Inhibitors

A

Selegiline

Rasagiline

60
Q

Indirect acting: MAO Inhibitors mechanism of actions

What are MAO enzymes?

A

MAOIs improve the effect of levodopa by preventing its breakdown

MAO enzymes break down catecholamines in the CNS, primarily in the brain.

61
Q

Selegiline hydrochloride and rasagiline mesylate (Azilect®) are

A

are SELECTIVE MAO-B inhibitors.

62
Q

Selegiline & Rasagiline action

A

Cause an increase in levels of dopaminergic stimulation in the CNS

63
Q

Does Seligine & Rasagiline (MAO INHIBITORS) cause CHEESE EFFECT?

What causes cheese effects?

A

Do not elicit the “cheese effect” of the nonselective MAOIs used to treat depression (if 10 mg or less is used)

ONLY NON SELECTIVE MAOIs cause cheese effect

64
Q

What does the cheese effect cause?

What food/ beverages cause the cheese effect?

A

Hypertension

TYRAMINE FOODS: cheese, red wine, beer

65
Q

Selegiline and Rasageline (selective MAOIs) mechanism of action

Relationship with levodopa?

Adjuct with?

A

increase levels of dopaminergic stimulation in the CNS, because it inhibits MAO enzymes form breaking down dopamine

used with levodopa> allow the dose to be reduced

adjunct with levodopa, can prolong levodopa

66
Q

rasagiline and selegiline contraindications

A

meperidine-opiod

67
Q

rasagiline and selegiline adverse effects

A

DIZZINESS,

insomnia, hallucination, depression, somnolence, headache

ataxia (without coordination), paresthesia, dyskinesia

68
Q

1 example of Dopamine modulator (indirect acting)

A

amantadine hydrochloride

69
Q

INDIRECT ACTING: amantadine hydrochloride mechanism of action (4)

and result of the mechanism of action

A

Has anticholinergics effects

Antiviral

Causes the release of dopamine and other catecholamines from their storage sites in the presynaptic fibres of nerve cells

Blocks the reuptake of dopamine into the nerve fibres

Result: higher levels of dopamine in the synapses between nerves and improved dopamine neurotransmission between neurons

70
Q

amantadine used in

effective for only

treats _____ associated with carbidopa-levodopa

A

early course of the disease

6 to 12 months

Used to treat dyskinesia associated with carbidopa–levodopa

71
Q

amantadine adverse effects

A

MILD and include dizziness, insomnia, and nausea.

72
Q

amantadine interactions

A

increased ANTICHOLLINERGIC adverse effects when given with anticholinergic drugs

73
Q

amantadine indications

A

early stages of PD/ moderate/ advanced stages

74
Q

1 example INDIRECT ACTING: Catechol ortho-methyltransferase Inhibitors (COMT inhibitors)

A

entacapone

75
Q

COMT-I mechanism of action

A

Block catechol ortho-methyltransferase (COMT), the enzyme that catalyzes the breakdown of the body’s catecholamines

WORKS PRESYNAPTICALLY

76
Q

COMT-I relationship with levodopa

A

Prolong the duration of action of levodopa; reduce wearing-off phenomenon

manages wearing off effect of levodopa

77
Q

COMT-I adverse effects

A

gastrointestinal (GI) upset, urine DISCOLORATION; can worsen dyskinesia that may already be present.

78
Q

COMT- I works _____, and cannot cross________

A

works presynaptically

peripherally and cannot cross blood brain barrier

79
Q

COMT-I interactions

NEEDS to be taken with_____, why?

A

NON SELECTIVE MAO-Is due to cardiovascular risk (because of decreased catecholamine metabolism)

80
Q

COMT-I contraindication

A

Liver disease

81
Q

COMT-I onset of action

COMT: entacapone- give an hour to 2 hours before_____

A

Rapid therapeutic effect compared to others

levodopa

82
Q

Anticholinergic drugs

action?

treats which symptom?

A

block the effects of Ach.

Used to treat muscle tremors and muscle rigidity associated with PD (which are caused by cholinergic activity due to lack of dopamine)

reduce cholinergic activity in the brain (increase ACh in PD- causes overstimulation of cholinergic excitatory pathways)

83
Q

Anticholinergic drugs do not relieve ________

A

Does not relieve bradykinesia (extremely slow movements).

84
Q

What does cholinergic or ACh promote? (5) hint: acronym

A

SLUDGE

increased salivation,
lacrimation (tearing of the eyes) urination,
diarrhea,
increased GI motility
emesis (vomiting)

85
Q

What are antichollinergic efects?

A

dry mouth or decreased salivation
urinary retention
decreased GI motility (constipation)
dilated pupils (mydriasis)
smooth muscle relaxation (dilation)

86
Q

antichollinergics can cross? and can reach?

A

blood brain barrier, can reach substantia nigra

87
Q

1 example of anticholinergics

A

benztropine

antihistamine, diphenhydramine

88
Q

benztropine 2 indication

A

Parkinson’s disease

antipsychotic

89
Q

benztropine caution and contraindication

A

Caution during HOT WEATHER or exercise because it may cause hyperthermia

avoid alcohol- increase drowsiness

90
Q

benztropine interactions

A

anticholinergic drugs- can cause anticholinergic syndrome (amantadine, tricyclic antidepressant)- increase anticholinergic effects

91
Q

benztropine adverse effects

A

tachycardia, confusion, disorientation, toxic psychosis, urinary retention, dry throat, constipation, nausea, vomiting

92
Q

What 2 types of antiparkinsonian cause postural hypotension?

A

amantadine (Dopamine modulator)

entacapone (COMT-I

93
Q

Which antiparkinsonian drug has a rapid effect?

A

entacapone

94
Q

Which antiparkinsonian drug should not be taken with other medications?

A

antichollinergic

95
Q

Thorough assessment includes: (2)

A

nursing history
medication history

96
Q

Ask about this system when administering antiparkinsonian drugs.

A

CNS
GI and genitourinary (GU) tracts
Psychological and emotional status

97
Q

Assess signs and symptoms of PD such as (5)

A

Masklike expression
Speech problems
Dysphagia
Rigidity of arms, legs, and neck
Shuffling gait

98
Q

Anti Parkinson medication and their contraindications

A

(levodopa- glaucoma, vitamin B6, high protein)

(PVD- bromocriptine)

(nonselective MAOIs- tyramine foods)

(selective MAOIs/ selegiline/ rasagiline- meperidine/ opioids)

(Amantadine- anticholinergic drug because it has antichollinergic properties- blocks ACh)

(COMT- liver diseases)

(Antichollinergic/ benztropine- antichollinergic drugs> increase effects, avoid alcohol> increase drowsy/ dizzy)

99
Q

Nurisng Implications

A

Administer drugs as directed by manufacturer.

Provide patient education regarding PD and the medication therapy.

Inform the patient not to take other medications with PD drugs unless the patient checks with the physician.

100
Q

Nurisng Implications

A

When starting dopaminergic drugs, assist patient with walking, because dizziness may occur.

Administer oral doses with food to minimize GI upset.

Patient should be taught not to discontinue antiparkinsonian drugs suddenly> worsen symptoms

Teach patient about expected therapeutic and adverse effects with antiparkinsonian drug therapy.

101
Q

Encourage patient to take in at least _____ mL of fluids per day (unless contraindicated).

A

3 000

102
Q

Taking levodopa with non selective MAOIs may result in?

A

Hypertensive crisis.

103
Q

What medication may darken a patient’s urine and sweat?

A

Entacapone

104
Q

Therapeutic effects of ______ _______ may be noticed within a few days; it may take weeks with other drugs.

A

COMT inhibitors (entacapone)

105
Q

Monitor for response to drug therapy.

A

Improved sense of well-being and mental status

Increased appetite

Increased ability to perform activities of daily living, to concentrate, and to think clearly

Less-intense parkinsonian manifestations, such as less tremor, shuffling gait, muscle rigidity, and involuntary movements

106
Q

What medication prompts you to assess for dizziness and syncope?

Which medications causes dizziness?

A

Levodopa/ cabidopa

amantadine and entacapone

107
Q

Which medication should be taken several hours before bedtime to reduce insomnia?

A

anticholinergic