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Pharmacology > Parkinson's Disease > Flashcards

Parkinson's Disease Flashcards

1
Q

Pathophysiology of Parkinson’s

A

loss of dopaminergic neurons, decreased cortical activation, sysmptom severity correlates with nigrostriatal dopamine loss, environmental? MPTP

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2
Q

Loss of dopaminergic neurons causes

A

increased GABA, increased relative cholinergic activity

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3
Q

Drug induced Parkinson’s

A

associated with drugs that disturb the DA/ACh balance and usually only at high doses, it is reversible

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4
Q

Drugs associated with drug induced Parkinson’s

A

Antipsychotic agents, Metoclopramide, Misc anticonvulsants, TCAs

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5
Q

Complications associated with Advanced disease

A

Motor and dyskinesias (TRAP), neuropsychiatric manifestations, sleep disturbances, autonomic dysfunctions, falls

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6
Q

TRAP

A

Tremor, muscular rigidity, Akinesia, bradykinesia, postural/gait defects

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7
Q

Goals of therapy

A

provide maximal function, individualize treatment to minimize ADRs, manage long-term disease progression&subsequent symptoms, restore NT balance (minimize disturbances in movement and balance)

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8
Q

Non-pharm therapy

A

Exercise, PT/OT, nutrition (fiber, increased fluid intake), procedures, support, education

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9
Q

Pharmacotherapy

A

Carbidopa/Levodopa (Sinemet), COMT inhibitors, anticholinergics, dopamine agonists, amantadine (Symmetrel), Monoamine oxidase B inhibitors

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10
Q

Stages of PD progression

A

Honeymoon-meds work well at low dose, middle stage- meds effective but PT/OT more influential, late- meds lose effectiveness, battle loss of function vs ADRs, consider brain stimulation

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11
Q

Levodopa

A

most effective drug for PD, dec morbidity/mortality, ALL pts will respond, if not question diagnosis, never monotherapy

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12
Q

MOA of Levodopa

A

precursor to DA, crosses BBB, converted by DDC in periphery and CNS to dopamine

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13
Q

Carbidopa MOA

A

inhibits peripheral DDC, prevents l-dopa metabolism here, more drug crosses BBB, carbidopa doesn’t cross BBB

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14
Q

How much carbidopa do you need for L-dopa to cross BBB

A

75 mg

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15
Q

Carbidopa/Levodopa (Sinemet)

A

Gold standard, pt need>1000 mg prob won’t benefit, try to hold off adding until needed,

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16
Q

Benefit of Sinemet

A

dec bradykinisia/rigidity

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17
Q

Dosage forms of Sinemet

A

IR (10mg carbidopa/100 Ldopa-25mg carbidopa/250 ldopa), CR (25mg carbidopa/100mg ldopa, 50 mg cdopa/200mg ldopa), oral disintegrating

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18
Q

Sinemet IR dosing

A

inc dose no sooner than every 3 days, use lowest possible to control sx, take an hour before or after eating to avoid drug food interactions

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19
Q

Sinemet ER dosing

A

initial dose CR 50/200 mg BID, inc 1/2-1 tab every 3 days, slower onset than IR

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20
Q

Drug-Drug interactions

A

antacids, oral iron, isoniazid, dopamine receptor antagonists, metoclopramide, phenytoin

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21
Q

ADRs of levodopa

A

N/V, anorexia, arrhythmias, orthostatic hypotension, sedation, insomnia, dyskinesia, cog impairment, psychosis, choreiform movements

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22
Q

What is the most rate limiting ADR of sinemet

A

choreiform movements, dyskinesias

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23
Q

Contraindications of Sinemet

A

non-selective MAO-I in previous 14 days, narrow-angle glaucoma

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24
Q

Precautions w/ sinemet

A

orthostatic hypotension, hx depression/psychosis, hx of PUD, renal impairment, may inc liver enzymes

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25
Q

Complications of long term use of sinemet

A

dramatic improvement intially, after 5 y 50-90% develop motor issues, wearing off after 4 hrs, delayed ON or no ON response, no response, unpredictable off, freezing, suboptimal response, diphasic, dystonia

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26
Q

How to manage wearing off of sinemet

A

manipulate LD dose, Cr for early stages or overnight use, add dopamine agonist, add COMT-I, SQ apomorphine for severe off episodes

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27
Q

How to manage delayed ON or no ON response of sinemet

A

increase LD dose, administer on empty stomach or add agent that inc GI motility, add dopamine agonist, add COMT-I

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28
Q

How to manage no response of sinemet

A

dose above 1000mg and still no response, Pt may have atypical PD and be unresponsive to this therapy

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29
Q

How to manage Freezing w/ sinemet

A

inc LD dose if off period, dec DA drug if on period, nonpharm techniques

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30
Q

how to manage Suboptimal response w/ sinemet

A

gradually inc dose of LD, start low dose DA agonist, COMT-I+ldopa

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31
Q

How to manage diphasic w/ sinemet

A

overlap multiple doses of LD/CD at intervals just enough to preclude the development of dyskinetic phase at end of each cyle, switch form CR to IR, SQ apomorphine

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32
Q

how to manage dystonia w/ sinemet

A

if from PD give bedtime dose of CR LD, if from LD dec size of individual dose, add DA agonist

33
Q

Counseling pts of CD/LD

A

do not d/c abruptly, IR can be split, crushed or chewed, but CR can only be split, changes in diet and meds may affect absorption, morning dose of CR has delayed onset, body fluids amy be discolored

34
Q

Advantages of CD/LD

A

most symptomatically efficacious, virtually all pts respond intially

35
Q

Disadvantages of CD/LD

A

most develop ADRs, sedation, does not treat freezing. postural instability, autonomic dysfunction, or dementia, does not stop disease progression, potentially harmful metabolites

36
Q

Catechol-O-methyltransferase inhibitors

A

increase efficiency of LD, Entacapone (Comtan), Tolcapone (Tasmar)

37
Q

entacapone (comtan) MOA

A

inhibits peripheral COMT from metabolizing DA- no central inhibition because doesn’t cross BBB

38
Q

Tolcapone (Tasmar) MOA and pearl

A

inhibits peripheral and central COMT, not used often because of hepatoxicity, last line

39
Q

Advantages of COMT-I

A

inc LD bioavailability and plasma T1/2 by 50%, dec “off’ time association w/ wearing-off phenomenon

40
Q

Dosing COMT-I

A

dec LD by ~30% when starting, entacapone-200 mg w/ every LD dose

41
Q

ADRs of COMT-I

A

Entacapone is very well tolerated, may cause diarrhea, orange urine, dyskinesia, dystonia, nausea, cramps, tolcapone causes liver toxicity and explosive diarrhea

42
Q

COMT-I advantages

A

no titration, easy admin, dec off time, inc on time, enhanced motor responses in pt w/ LD motor fluctuation

43
Q

Disadvantages of COMT-I

A

dopaminergic ADR, urine discoloration

44
Q

Anticholinergic MOA

A

antagonize excitatory neurotransmitter acetylcholine in substantia nigra to minimize the relative increase in cholinergic sensitivity

45
Q

Use of anticholinergics

A

mostly beneficial for tremor, early in disease, initial tx for mild-moderate disease, adjunct to dopaminergic agents in mod to severe disease, for younger pts w/ tremores and preserved cog function, dec efficacy in eldely

46
Q

Stavelo

A

compo carbidopa, levodopa, and entacapone

47
Q

ADRs of anticholinergics

A

dry mouth, blurred vision, constipation, urinary retention, confusion, sedation, hallucinations, memory impairment

48
Q

Benzropine (Cogentin)

A

dose 1-3 mg PO BID, start low, titrate slowly

49
Q

Trihexyphenidyl (Artane)

A

dose 1-5 mg TID, start low and titrate slowly

50
Q

Anticholinergics used

A

Benztropine (Cogentin), Trihecyphenidyl (Artane), Diphenhydramine (Benadryl)

51
Q

Anticholinergic advantage

A

efficacy for tremors, peripherally acting agents useful for sialorrhea

52
Q

Anticholinergic disadvantage

A

relatively ineffective for more advanced PD, cognitive ADR, muscarinic ADR

53
Q

Dopamine Agonists

A

Ropinirole (Requip), Pramipexole (Mirapex), Bromocriptine (Parlodel), Apomorphine (Apokyn)

54
Q

Dopamine agonist MOA

A

direct stimulation of striatal dopamine receptors

55
Q

Place for DA agonists in therapy

A

1st line monotherapy for symptomatic pts if younger than 70, adjunct to dec response fluctuation w/ CD/LD, permits reduction in LD, decreases dyskinesias

56
Q

DA agonist advantages

A

may delay need for LD for 4-5 years, may delay development of motor functions, may be neuroprotective

57
Q

DA agonist disadvantages

A

eventually will need LD, does not prevent LD complications, should provide better response than they do, complicating titrating dose

58
Q

Ropinirole (Requip) and pramipexole (Mirapex) MOA, Benefits

A

non-ergot derived, stimulate D2/D3 receptor site, more effective than bromocriptine at reducing motor sx, reduces off time associated w/ wearing off, may reduce LD requirement

59
Q

Ropinirole (Requip) dose, DI

A

low dose (.5 mg ish but complex titration), hepatically metabolized, DI- inhibits CYP1A2, induces CYP1A2, may switch from IR to similar dose ER

60
Q

Pramipexole (Mirapex) dose, Di

A

low dose (.25 mg ish, but complex titration), renally excreted (dec if CrCl

61
Q

Bromocriptine (Parlodel)

A

ergot derived dopamine agonist, stimulates D2 and antagonizes D1, not used much

62
Q

Apomorphine (Apokyn)

A

derived from morphine, sub-cut injection, stimulates D1/D2, adjunct/supp to LD in advanced disease, use for acute intermittent tx of hypomobility off episodes associated w/ wearing off/ on-off episodes

63
Q

Apomorphine (Apokyn) adrs, dosing, contraindications

A

2-6mg sq during acute, max dose 6 mgx5/day, sig N/V, skin nodules at injection, contra w/ sulfite allergy, 5GT3 receptor blockers, hypotension and syncope

64
Q

DA agonists class ADRs

A

nausea, orthostatic hypotension, confusion, hallucinations, light-headedness, lower edema, sleep attacks, psychosis, compulsive behaviors

65
Q

Advantages of DA agonists

A

efficacy as monotherapy, dec risk of LD related motor complications, NO oxidative metabolites, potentially neuroprotective

66
Q

disadvantages of DA agonists

A

neuropsychiatric ADRs, do not treat all PD features (freezing, postural inability, dementia), does not stop progression

67
Q

amantadine (Symmetrel)

A

antiviral, improvement in trmor, rigidity, akinesia, unknown MOA, augments DA release form presynaptic nerve terminals, inhibits reuptake, stimulates releases, anticholinergic effects, NMDA-I

68
Q

Amantadine in therapy

A

initial monotherapy in early disease, delays LD time, limited by rapid development of tacyphylaxis, possible use in late stage, adjunct, synergist w/ CD/LD

69
Q

Amantadine contraindications, ADRs

A

CHF, seizure disorder, other CNS stimulants, adjust dose in renal, do not abrupt w/drawal, cause edema, CHF, seizures, hallucinations, orthostatic hypotension, dizziness, confusion

70
Q

Amantadine advantages

A

some antiparkinson efficacy, may have antidyskinetic effect, possible neuroprotective

71
Q

Amantadine disadvantage

A

antiparkinson effects limited, tolerance can develop, cog SE

72
Q

Monoamine Ocidase B inhibitors

A

Selegiline (Eldepryl, Zelapar), Rasagiline (Azilect)

73
Q

MAO-B I MOA

A

irreversibly and selectively inhibits MAO-B, prevents breakdown of DA in CNS, can be monotherapy for neuroprotection, adjunct in all stages

74
Q

Selegiline (Eldepryl)

A

as dose inc MAO-I specificity is lost, dec LD at initiation

75
Q

Selegiline (Zelapar)

A

Oral disintegrating tab, dose 1.25 mg daily x 6 weeks then 2.5 mg, bypasses 1st pass metabolism, dec SE, dec off time by 2 hrs, do not swallow medication immediately

76
Q

Rasagiline (Azilect)

A

monotherapy in early PD, adjunct to LD in late stages, greater potency MAO-B inhibition, 1 mg daily, w/ LD- .5 mg daily, avoid tyramine rich foods

77
Q

Rasagiline (Azilect) and selegiline (Eldepryl) DIs

A

opiates, SSRIs, SNRI, TCAs, lithium, dextromethorphan, linezolid, ephedrine, phenylephrine, pseudoephedrine

78
Q

Rasagiline (Azilect) ADRs

A

wt changes, balance difficulties, bp changes, edema, dizziness, hallucinations, sleep changes

Pharmacology (61 decks)

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