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Neuro 2 Exam 2 > DSA 34 Drugs for Motor Disease and Muscle Spasticity > Flashcards

DSA 34 Drugs for Motor Disease and Muscle Spasticity Flashcards

1
Q

which drugs are used for dopamine replacement therapy?

A

levodopa, carbidopa

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2
Q

which anti-Parkinson’s drugs are direct agonists?

A

pramipexole, ropinirole

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3
Q

which anti-Parkinson’s drug is a COMT inhibitor?

A

entacapone

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4
Q

which anti-Parkinson’s drugs are antimuscarinics?

A

biperiden, trihexyphenidyl, benztropine

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5
Q

which anti-Parkinson’s drugs are MAO-B inhibitors?

A

selegiline, rasagiline

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6
Q

what is the mechanism of action of amantidine?

A

increases dopamine availability by increasing dopamine release and decreasing dopamine reuptake

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7
Q

which drugs used to treat myasthenia gravis are immunosuppressants?

A

azathioprine, cyclosporine, intravenous immunoglobulin

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8
Q

which drugs used to treat myasthenia gravis are anticholinesterases?

A

pyridostigmine, neostigmine

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9
Q

list the CNS spasmolytics.

A

baclofen, diazepam, tizanidine, riluzole, gabapentin, metaxalone

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10
Q

what class of drug is dantrolene?

A

PNS spasmolytic

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11
Q

which class of anti-Parkinson’s drugs primarily help with tremors but not bradykinesia?

A

anti-ACh agents

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12
Q

what is thought to cause the symptoms of Parkinsonism?

A

loss of dopamine inhibition → cholinergic excitation → symptoms of Parkinsonism

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13
Q

what primarily occurs in Huntington’s chorea?

A

GABAergic loss in the indirect pathway → loss of inhibition of thalamic activity

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14
Q

fill in the blank: ACh __ (>/<) DA → Parkinson’s. akinesia, tremors, rigidity.

A

ACh > DA

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15
Q

fill in the blank: ACh ___ DA (>/<) → Huntington’s. dyskinesia, choreiform movements

A

ACh < DA

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16
Q

what is the intended target for drug therapy in Parkinsonism?

A

nigrostrial system

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17
Q

what is the mechanism of action of antipsychotics? result of this action?

A

block DA receptors, can produce Parkinsonism and/or dystonias

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18
Q

why is L-DOPA not initially used in the treatment of Parkinson’s?

A

it has about a 5 year window of effectiveness

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19
Q

what is the typical strategy for the treatment of Parkinson’s?

A

start with MAO-B inhibitor and/or dopaminergic agonist

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20
Q

what is the primary isoenzyme responsible for the degradation of DA in the striatum?

A

MAO-B

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21
Q

what is a benefit of MAO-B inhibitors not affecting degradation of catecholamines in other brain regions or in the periphery?

A

little risk of hypertensive crisis due to accumulation of peripheral NE

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22
Q

what causes insomnia as a side effect for MAO-B inhibitors?

A

amphetamine and methamphetamine metabolites

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23
Q

identify: this drug’s best documented use is as an adjunctive agent to improve response to levodopa.

A

selegiline

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24
Q

why should selegiline not be given to patients taking TCAs or SSRIs?

A

danger for serotonin syndrome (profound sympathetic activity with hyperthemia)

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25
Q

why should non-selective MAOIs not be used in Parkinsonism?

A

would lead to hypertensive crisis when combined with L-DOPA therapy

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26
Q

explain how dopamine agonists have nausea/vomiting as significant untoward effect.

A

they stimulate D2 receptors

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27
Q

identify: dopamine agonist that affects D3 receptors.

A

pramipexole

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28
Q

what is the mechanism of action of anticholinergics?

A

centrally-acting competitive inhibitors of muscarinic cholinergic receptors

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29
Q

which symptom(s) of Parkinson’s is not improved by anticholinergics?

A

bradykinesia

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30
Q

what are classic side effects of anticholinergics?

A

dry mouth, urinary retention, constipation

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31
Q

what are contraindications for the use of anticholinergic agents?

A

prostatic hyperplasia

obstructive GI disease

glaucoma

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32
Q

identify: giving this class of drug will worsen dementia in patients with age- or Parkinson’s-related dementia.

A

anticholinergics

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33
Q

what are side effects of amantidine?

A

insomnia, restlessness, depression, GI disturbances, ataxia, livedo reticularis

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34
Q

what are contraindications for amantidine?

A

seizures disorders, congestive heart failure

35
Q

explain the relationship between catecholamine neurons and L-DOPA.

A

L-DOPA can be converted to dopamine in catecholamine neurons via dopa decarboxylase

36
Q

why is therapy with L-DOPA necessary?

A

dopamine itself does not penetrate the CNS

37
Q

what is the function of carbidopa?

A

it does not cross the BBB. inhibits peripheral DA formation → allows levodopa dose to be lowered while increasing its availability to the CNS

38
Q

how is L-DOPA administered?

A

always in combination with carbidopa

39
Q

what is the benefit of giving carbidopa with levodopa?

A

carbidopa gets into the peripheral system and blocks transformation of some of the L-DOPA into DA. this will then limit the side effects of levodopa

40
Q

what can be used to control the behavior disturbances induced by L-DOPA?

A

atypical antipsychotics (e.g. olanzapine)

41
Q

why can L-DOPA not be used with MAO-A inhibitors?

A

intense peripheral vascular effects of excess DA

42
Q

what are adverse effects of levodopa?

A

mood change, hallucinations, sleep disturbance, arrhythmia, N/V, dyskinesia

43
Q

what are 3 ways in which levodopa therapy can fail?

A
  1. ) response fluctuations
  2. ) end of dose failure
  3. ) on-off phenomena
44
Q

what is the clinical benefit of COMT inhibitors?

A

the “capones” may smooth response to levodopa and may permit lowering of levodopa dose

45
Q

where is entacapone active?

A

only in the periphery

46
Q

what is the mechanism of action of azathioprine?

A

converted to mercaptopurine, interferes with purine nucleic acid metabolism

47
Q

what are the toxicities of azathioprine?

A

bone marrow suppression (leukopenia), GI signs (diarrhea, vomiting) typical of high dose

48
Q

what is the mechanism of action of cyclosporine?

A

inhibits production of helper T cells

49
Q

what are the toxicities of cyclosporine?

A

nephrotoxicity and hypertension

50
Q

what is the benefit of IV Ig over azathioprine or cyclosporine?

A

much faster than either, used for immediate improvement in MG patients

51
Q

what are side effects of IV Ig?

A

during: headache, muscle aches, chills

post-infusion: fatigue, fever, nausea

52
Q

what is a main use of plasmapheresis?

A

relieve myasthenic crisis

53
Q

identify: these drugs are quarternary salts. as such, permanently charged and cross membranes very poorly.

A

pyridostigmine and neostigmine

54
Q

what are the benefits of quarternary salts as treatment for MG?

A

do not penetrate CNS → no intoxication/seizure problem

penetrate ganglia poorly → little effects on blood pressure

55
Q

identify: when using these drugs, you must also use an antimuscarinic to block excess ACh in the parasympathetic nervous system.

A

anticholinesterases

56
Q

how does the tensilon test differentiate between myasthenic crisis (under dose of AChE) and cholinergic crisis (overdose of AChE)?

A

by adding short acting anticholinesterase, the situation will get better (patient was under dose) or worse (patient was overdosed)

57
Q

what is the mechanism of action of baclofen?

A

GABA-B receptor agonist → inhibits release of excitatory amino acids and substance P from IA neurons themselves

58
Q

when is baclofen more effective?

A

spinal injury and MS

59
Q

what are the untoward effects of baclofen?

A

drowsiness, lassitude, ataxia

muscular weakness

constipation, urinary retention

60
Q

fill in the blank: diazepam is not effective in the treatment of _______.

A

ALS

61
Q

what is the mechanism of action for diazepam?

A

increases GABAergic neurotransmission → enhanced presynaptic inhibition (internuncial neurons)

62
Q

how do GABA-B receptors cause hyperpolization?

A

stimulation of GABA-B receptors increases K+ conductance

63
Q

how do GABA-A receptors cause hyperpolarization?

A

excitation of GABA-A receptors increases Cl- conductance

64
Q

identify: this drug is particularly used in peripheral neuropathies for pain reduction.

A

gabapentin

65
Q

what is the mechanism of action for gabapentin?

A

increases GABA release

66
Q

what are the toxicities/contraindications for gabapentin?

A

somnolence, dizziness, ataxia, headache, tremor

67
Q

what drug has the same side effects as gabapentin?

A

metaxalone

68
Q

identify: this drug is marketed for the relief of muscle spasm.

A

metaxalone

69
Q

what adverse effects are seen with use of tizanidine?

A

alpha2 agonist effects → hypotension, drowsiness

70
Q

what are the adverse effects of riluzole?

A

GI hemorrhage, sepsis, convulsions, neoplasm

71
Q

what is the contraindication for riluzole?

A

lactation

72
Q

identify: this drug is a skeletal muscle relaxant that interferes with release of Ca2+ from SR.

A

dantrolene

73
Q

what are the uses for dantrolene?

A

cerebral spasticity (not ALS), malignant hyperthermia, external sphincter hypertonicity

74
Q

fill in the blank: avoid use of dantrolene in ______ patients

A

ambulatory–it causes muscle weakness

75
Q

in what other CNS area will anticholinergic treatment most likely produce significant unwanted effects?

A

hippocampus

76
Q

what are the criteria for beginning L-DOPA therapy?

A

age >65

debilitating Parkinson’s

77
Q

how does selegiline improve Parkinson’s symptoms?

A

blocks DA metabolism presynaptically

78
Q

what is mechanism of action of ropinirole?

A

dopamine D2 receptor agonist

79
Q

what is the most likely untoward effect of trihexyphenidyl?

A

dry mouth

80
Q

selegiline or rasagiline are less likely than other drugs to enhance dietary effects of?

A

tyramine

81
Q

entacapone may be started with carbidopa/L-DOPA because?

A

reduces rate of metabolism of L-DOPA in the periphery → longer half-life and more even uptake of the L-DOPA

82
Q

to minimize unwanted side effects of pyridostigmine, it may be necessary to also administer?

A

muscarinic antagonist

83
Q

mechanism by which anticholinesterases cause worsening of muscle strength in cholinergic crisis?

A

excess ACh binding at nicotinic receptors

Neuro 2 Exam 2 (16 decks)

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