Antiparkinson Medications Flashcards
(107 cards)
1
Q
Parkinson disease
A
Chronic, progressive, neurodegenerative disorder
Affects dopamine-producing neurons in the brain
2
Q
Parkinson disease is caused by an imbalance of two neurotransmitters?
Their actions?
A
ACh- excitatory
Dopamine- inhibits nerve actions (inhibitory)
3
Q
Parkinson disease symptoms
A
Bradykinesia (slow, movement)
“TRAP”
Tremor
Rigidity- of muscle
Akinesia – no movement
Postural instability
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.
5
Q
akinesia
A
absence of psychomotor activity- masklike facial expression
6
Q
bradykinesia
A
slow movement
7
Q
rigidity
A
cogwheel rigidity, resistance to passive movement
8
Q
tremor
A
pill-rolling- the tremor of the thumb against the forefinger
9
Q
postural instability
A
unsteadiness
10
Q
Dyskinesia
A
Difficulty in performing voluntary movements
11
Q
Two common types of Dyskinesia
A
chorea and dystonia
12
Q
Chorea
A
irregular, spasmodic, involuntary movements of the limbs or facial muscles
13
Q
Dystonia
A
abnormal muscle tone leading to impaired or abnormal movements
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.
15
Q
What is “Wearing-off phenomenon”
A
the drug is losing effectiveness
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
17
Q
On phenomenon
A
greater symptom control
18
Q
Off phenomenon
A
less symptom control
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.
20
Q
Drug therapies are aimed at
A
at increasing the levels of dopamine or antagonizing(lowering) the effects of ACh.
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.
22
Q
What type of drug is given first?
A
direct acting
23
Q
Part of brain where dopamine deficit occurs?
A
substantia nigra
(destruction of substantia nigra by PD)
24
Q
Dopamine depletion reults in
A
excessive unopposed ACh (cholinergic activity) due to lack of dopamine effects
25
diagnostic of PD
Lab tests
based on symptoms
CT/ MRI... to rule out other disease
No lab test to detect or confirm PD
26
end of dose wearing off
diminishing dopamine effect towards the end of the dose associated with increased loss of stored dopamine
27
direct-acting dopaminergic drugs- define:
2 subclasses
first-line agents
non dopamine dopamine receptors
dopamine replacement drugs
28
2 subclasses non dopamine dopamine receptors and give examples of each
ergot derivative (bromocriptine)
non-ergot drugs (pramipexole and ropini-
role).
29
Levodopa is the
Levodopa is a precursor of dopamine.
30
Blood–brain barrier does not allow _________ to enter but does allow ________.
Blood–brain barrier does not allow exogenously supplied dopamine to enter but does allow levodopa.
31
give 1 example of nondopamine dopamine receptor agonists
and its subclass
Ergot derivatives: bromocriptine
32
direct-acting nondopamine dopamine receptor agonists: mechanism of action
directly stimulate PRE and POST synaptic dopamine RECEPTORS in brain
33
Bromocriptine indications
Parkinson's disease
hyperprolactinemia
34
bromocriptine 1 mechanism of action
activates presynaptic dopamine receptors to stimulate more dopamine production
chief site of activity is D2 subclass of dopamine receptors
35
bromocriptine other mechanism of action
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
36
Bromocriptine contraindications
why?
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
37
bromocriptine may be used with levodopa to
decrease dose of levodopa
38
bromocriptine adverse effects
GI upset, dyskinesias, sleep disturbances
39
bromocriptine interactions
erythromycin
adrenergic drugs (increases hr, bp- vasoconstriction)
40
1 example of Dopamine replacement drugs
Levodopa
41
Levodopa is
biological precursor of dopamine required by the brain for dopamine synthesis
exogenous source
42
Levodopa mechanism of actions
stimulate presynaptic dopamine receptors to increase dopamine in brain
43
Levodopa is able to cross the ______, and then it is converted to _________.
Levodopa is able to cross the blood–brain barrier, and then it is converted to dopamine.
44
Large doses of ____ needed to get dopamine to the brain also cause adverse effects.
However, large doses of levodopa needed to get dopamine to the brain also cause adverse effects.
45
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 __________.
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
Levodopa is converted into?
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
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.
5 to 10 years
48
Route of dopamine/ levodopa
administered orally in order to cross blood-brain barrier
Levodopa cannot pass blood-brain barrier if given through IV
49
_______ is the biological precursor of dopamine and can penetrate into the ____.
Levodopa is the biological precursor of dopamine and can penetrate into the CNS.
50
Adverse effects of Levodopa (replacement drugs)
Adverse effects: confusion, involuntary movements, GI distress, hypotension, cardiac dysrhythmias
51
Levodopa indication
Note: critical care settings can give IV levodopa as
restore dopaminergic activity
Note: critical care settings given IV as pressor drug to raise BP and enhance kidney function
52
Levodopa- carbidopa contraindications
Used cautiously in patients with
angle-closure glaucoma, undiagnosed skin cancer
use cautiously in patients with open-angle glaucoma
vitamin B6 pyroxidine/ high protein
53
Levodopa- carbidopa adverse effects
Adverse effects: cardiac dysrhythmias, hypotension, chorea, muscle cramps, GI distress
54
Levodopa- carbidopa
Interactions
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
carbidopa treats?
What does it inhibit when given with levodopa?
adjunct to treat nausea associated with Sinemet
breakdown of levodopa in the periphery
56
Sinemet CR
Sinemet CR: increases “on” time and decreases “off” time- do not crush
57
Carbidopa–levodopa is best taken on an empty stomach; to minimize ________, it can be taken with food.
GI ADVERSE EFFECTS
58
1 EXAMPLE OF INDIRECT ACTING DOPAMINE RECEPTOR AGONISTS
MAO Inhibitors
59
2 MAO Inhibitors
Selegiline
Rasagiline
60
Indirect acting: MAO Inhibitors mechanism of actions
What are MAO enzymes?
MAOIs improve the effect of levodopa by preventing its breakdown
MAO enzymes break down catecholamines in the CNS, primarily in the brain.
61
Selegiline hydrochloride and rasagiline mesylate (Azilect®) are
are SELECTIVE MAO-B inhibitors.
62
Selegiline & Rasagiline action
Cause an increase in levels of dopaminergic stimulation in the CNS
63
Does Seligine & Rasagiline (MAO INHIBITORS) cause CHEESE EFFECT?
What causes cheese effects?
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
What does the cheese effect cause?
What food/ beverages cause the cheese effect?
Hypertension
TYRAMINE FOODS: cheese, red wine, beer
65
Selegiline and Rasageline (selective MAOIs) mechanism of action
Relationship with levodopa?
Adjuct with?
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
rasagiline and selegiline contraindications
meperidine-opiod
67
rasagiline and selegiline adverse effects
DIZZINESS,
insomnia, hallucination, depression, somnolence, headache
ataxia (without coordination), paresthesia, dyskinesia
68
1 example of Dopamine modulator (indirect acting)
amantadine hydrochloride
69
INDIRECT ACTING: amantadine hydrochloride mechanism of action (4)
and result of the mechanism of action
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
amantadine used in
effective for only
treats _____ associated with carbidopa-levodopa
early course of the disease
6 to 12 months
Used to treat dyskinesia associated with carbidopa–levodopa
71
amantadine adverse effects
MILD and include dizziness, insomnia, and nausea.
72
amantadine interactions
increased ANTICHOLLINERGIC adverse effects when given with anticholinergic drugs
73
amantadine indications
early stages of PD/ moderate/ advanced stages
74
1 example INDIRECT ACTING: Catechol ortho-methyltransferase Inhibitors (COMT inhibitors)
entacapone
75
COMT-I mechanism of action
Block catechol ortho-methyltransferase (COMT), the enzyme that catalyzes the breakdown of the body’s catecholamines
WORKS PRESYNAPTICALLY
76
COMT-I relationship with levodopa
Prolong the duration of action of levodopa; reduce wearing-off phenomenon
manages wearing off effect of levodopa
77
COMT-I adverse effects
gastrointestinal (GI) upset, urine DISCOLORATION; can worsen dyskinesia that may already be present.
78
COMT- I works _____, and cannot cross________
works presynaptically
peripherally and cannot cross blood brain barrier
79
COMT-I interactions
NEEDS to be taken with_____, why?
NON SELECTIVE MAO-Is due to cardiovascular risk (because of decreased catecholamine metabolism)
80
COMT-I contraindication
Liver disease
81
COMT-I onset of action
COMT: entacapone- give an hour to 2 hours before_____
Rapid therapeutic effect compared to others
levodopa
82
Anticholinergic drugs
action?
treats which symptom?
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
Anticholinergic drugs do not relieve ________
Does not relieve bradykinesia (extremely slow movements).
84
What does cholinergic or ACh promote? (5) hint: acronym
SLUDGE
increased salivation,
lacrimation (tearing of the eyes) urination,
diarrhea,
increased GI motility
emesis (vomiting)
85
What are antichollinergic efects?
dry mouth or decreased salivation
urinary retention
decreased GI motility (constipation)
dilated pupils (mydriasis)
smooth muscle relaxation (dilation)
86
antichollinergics can cross? and can reach?
blood brain barrier, can reach substantia nigra
87
1 example of anticholinergics
benztropine
antihistamine, diphenhydramine
88
benztropine 2 indication
Parkinson's disease
antipsychotic
89
benztropine caution and contraindication
Caution during HOT WEATHER or exercise because it may cause hyperthermia
avoid alcohol- increase drowsiness
90
benztropine interactions
anticholinergic drugs- can cause anticholinergic syndrome (amantadine, tricyclic antidepressant)- increase anticholinergic effects
91
benztropine adverse effects
tachycardia, confusion, disorientation, toxic psychosis, urinary retention, dry throat, constipation, nausea, vomiting
92
What 2 types of antiparkinsonian cause postural hypotension?
amantadine (Dopamine modulator)
entacapone (COMT-I
93
Which antiparkinsonian drug has a rapid effect?
entacapone
94
Which antiparkinsonian drug should not be taken with other medications?
antichollinergic
95
Thorough assessment includes: (2)
nursing history
medication history
96
Ask about this system when administering antiparkinsonian drugs.
CNS
GI and genitourinary (GU) tracts
Psychological and emotional status
97
Assess signs and symptoms of PD such as (5)
Masklike expression
Speech problems
Dysphagia
Rigidity of arms, legs, and neck
Shuffling gait
98
Anti Parkinson medication and their contraindications
(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
Nurisng Implications
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
Nurisng Implications
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
Encourage patient to take in at least _____ mL of fluids per day (unless contraindicated).
3 000
102
Taking levodopa with non selective MAOIs may result in?
Hypertensive crisis.
103
What medication may darken a patient's urine and sweat?
Entacapone
104
Therapeutic effects of ______ _______ may be noticed within a few days; it may take weeks with other drugs.
COMT inhibitors (entacapone)
105
Monitor for response to drug therapy.
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
What medication prompts you to assess for dizziness and syncope?
Which medications causes dizziness?
Levodopa/ cabidopa
amantadine and entacapone
107
Which medication should be taken several hours before bedtime to reduce insomnia?
anticholinergic
