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finals > Chapter 21: Neuromuscular Medications > Flashcards

Chapter 21: Neuromuscular Medications Flashcards

1
Q

what are neurodegenerative diseases?

A

progressive, irreversible loss of neuron function in the brain and/or spinal cord

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2
Q

what is a common problem with many neuromuscular diseases?

A

depression

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3
Q

what is parkinsons disease?

A

progressive, neurodegenerative disorder characterized by abnormal motor movement

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4
Q

what are initial signs of parkinsons?

A

fatigue, slight tremour, slow movement (bradykinesia)

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5
Q

what is the mean age for parkinsons and who does it affect more?

A

40-70, men

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6
Q

what are the cardinal signs of parkinsons?

A

-tremor: hands and head develop a palsy-like, continuous motion or shaking at rest, and pill rolling (thumb and forearm rub together in circular motions)
-muscle rigidity: resistance to passive movement of arms and legs, can resemble arthritis, rigidity of facial muscles, and uncontrollable drolling
-bradykinesia: slowed down movement and speech, difficulty chewing/swallowin/speaking, shuffled gait
-postural instability: stooped over, hard to maintain balance, and frequent stumbling

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7
Q

what is Parkinsons caused by?

A

Decrease in dopamine which is produced by substantial nigra. Also causing Ach to have a more dramatic effect (neurotransmitter for PNS)

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8
Q

what is the goal and how long does it take to see results from parkinson meds?

A

to balance dopamine and ach, 2-3 weeks

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9
Q

what is wearing off effect, on/off syndrome, and extrapyramdial symptoms?

A

-wearing- off: when a pt takes a med for a prolonged period, the drugs effectiveness wears off closing to the end of the dosing interval
-on/off: pt alternates between symptom-free peroids and times when the drug stop working briefly
-extrapyramidal: adverse effects that develop from a deficiency of dopamine, not causes by parkinson, usually by antipsychotic meds

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10
Q

what 2 types of drugs are used for Parkinsons?

A

dopamine agonists and anticholinergic drugs

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11
Q

what is the most effective dopamine replacement drug?

A

levodopa

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12
Q

what does levodopa do?

A

It enters the blood-brain barrier (because dopamine is a polar molecule, and the BBB blocks polar molecules), and enzymes in the brain convert levodopa into dopamine

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13
Q

what is levodopa taken with?

A

Carbidopa
-together they’re called Sinemet
-carbidopa inhibits the metabolism of levodopa, causing a greater portion of levodopa to cross the BBB
-carbidopa allows for more of levodopa to be increased
-it also allows for a lower dosage of levodopa perscribed for the pt

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14
Q

what is the prototype drug for dopamine replacement?

A

levodopa and carbidopa

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15
Q

what are the adverse effects of levodopa?

A

GI: n/v, flatulence, abdominal distress, dysphagia, anorexia
CNs: anxiety, confusion, agitation, headache, nightmares, insomnia,
MSKL: hand tremors, involuntary movements, twitching, numbness, choreiform
Anti-cholinergic: urinary retention, dry mouth

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16
Q

what are the serious ADR for levodopa?

A

leukopenia, agranulocytosis, hemolytic anemia

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17
Q

what are contraindications for levodopa?

A

-hypersensitivity
-acute psychosis
-severe psychoneuroses
-narrow angle glaucoma
-use of MAOIs within 2 weeks

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18
Q

what are nursing considerations for levodopa?

A

-take on an empty stomach
-do not take with multi-vit
-have a low protein diet
-monitor VS (rr, hr, and bp)
-no alcohol
-monitor liver and kidney
-monitor for safety with ambulation due to dizziness
-watch for mood or behaviour changes

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19
Q

when can dopamine agonists be used?

A

as a monotherapy during early stages or as adjuncts to levodopa in advanced stages

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20
Q

what do dopamine agonist do?

A

activate dopamine receptors without increase dopamine

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21
Q

are dopamine agonist more or less effective than levodopa?

A

less effective, but have less adverse side effects like no toxic metabolites, no need for low protein diet, lower risk for dyskinesia (involuntary uncontrollable muscle movements) and lower incidence of wearing off effect

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22
Q

what are the two classifications of dopamine agonist?

A

ergot and non-ergot alkaloids

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23
Q

what is the prototype drug for non-ergot alkoids?

A

pramipexole (mirapex)

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24
Q

what are adverse and serious effects of pramipexole?

A

adverse: hallucinations, drowsiness, dizziness, insomnia, orthostatic hypotension, dyskinesia, nausea, agitation
serious: sleep attacks, and the 3 from levodopa

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25
Q

what are considerations for pramipexole?

A

-assess for baseline vitals and symptoms of Parkinsons
-assess mental status
-monitor for orthostatic hypotension
-monitor for tardive dyskinesia (invol repetitive movements)
-alert pt and family about sleep attacks
-ensure family knows PD treatment does not cure but may help with symtoms for a period of time

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26
Q

what are some adjuncts to levodopa therapy?

A

-amantadine (symmetrel): increase release of dopamine by the storage sites
-COMT inhibitors: prevent destruction of levodopa, adjuncts to levodopa, eg. entacapone (comtan), and tolcapone (tasmar)
-monoamine oxidase b inhibitors: selegilene (eldepryl), may slow down the progression fo PD but effectivness not clearly established

27
Q

what are anticholinergic drugs for?

A

oldest of the antiparkinsons, and are effective are reducing tremor not bradykinesia

28
Q

how do anticholinergic drugs work?

A

restore balance between ach and dopamine by blocking muscarinic receptors in the striatum, inhibiting effects of Ach

29
Q

what is the prototype drug for anticholinergics for parkinsons?

A

Benztropine (cogentin)

30
Q

what are the adverse effects of benztropine (cogentin)? (7)

A

CNS: blurry vision, sedation, confusion
GI/GU: constipation, urinary retention, dry mouth
decreased sweating

31
Q

what is a serious adverse effect of benztropine (cogentin)?

A

paralytic ileus

32
Q

what is a major contraindication of benztropine (cogentin)?

A

alcohol

33
Q

what is the treatment for overdose of benztropine (cogentin)?

A

physostigmine, 1-2mg SQ or IV to reverse s/s of anticholinergic intoxication

34
Q

with benztropine (cogentin), what drugs are for additive toxicity, sedative effect and slow down GI/decrease absorption?

A

-additive toxicity: MAOIs, antihistamine, tricyclic antedepressants, phenothiazines , quinidine
-additive sedative: alcohol, CNS depressants
-slow Gi motility/decrease absorption: antidiarrheals

35
Q

what is the most common type of dementia?

A

alzheimers

36
Q

what is dementia?

A

chronic, degenerative disorder characterized by progressive memory loss, confusion, inability to think or communicate effectively

37
Q

what is an early sign of dopamine?

A

loss of short term memory

38
Q

what are drugs used for alzhemiers?

A

cholinesterase inhibitors, cholinesterase breaks down acetycholine, but in alzhemiers there is already not enough acetycholine

39
Q

what neurotransmitter is deficient in alzhemiers?

A

acetylocholine, meaning dopamine has a more drastic effect = bear

40
Q

what is the goal of alzheimer medications?

A

to improve ADLS, behaviour, cognition

41
Q

what are side effects of cholinesterase inhibitors?

A

mostly GI like n/v, diarrhea and the liver

42
Q

what do reversible cholinesterase inhibitors do?

A

-raise acet concentrations in the brain
-side effects are typically GI related
-serious side effects include a fib, sinu bradycardia, and seizures

43
Q

what is the prototype drug for reversible cholinesterase inhibitors?

A

Donepezil (aricept)

44
Q

what are adverse and serous side effects of donepezil?

A

adverse
-GI: n/v/d and anorexia
MSKL: muscle cramps, joint pain, bruise
CNS: fainting, fatigue, headache, abnormal dreams/ hallucination

serious
-life threathening dysrhythmias (a fib, and sinus bradycardia)
-seizures
-renal failure or hepatotoxity

45
Q

what is txt of overdose for donepezil (aricept)

A

anticholinergic drugs

46
Q

what are nursing considerations for donepezil (aricept)

A

-determine safety and cognitive functioning
-obtain baseline lab test esp liver and renal
-determine s/s of alzheimer
-ensure family knows to monitor pt for abnormal heart beat or if the pt feels “butterflies” in their chest
-avoid alcohol
-encourage participation in support group and include family
-evaluate need for alternative living arrangements

47
Q

what is multiple sclerosis?

A

-autoimmune disease caused by the demyelinated secondary to inflammatory response
-exact cause not known
-leading cause of neurologica disability in 20 to 40 age group
-symptoms include: difficulty maintaining balance, muscle weakness and cold sensitivity

48
Q

what drugs are used for MS?

A

-immunomodulators: drugs that impact the immune response, either stimulate or inhibit response
-used to prevent exacerbations

49
Q

what is amyotrophic lateral sclerosis/lou gehrig disease?

A

-most common degenerative disease of the motor neurons
-characterized by weakness and atrophy of muscles of the legs, forearm and hands , which eventually spread to all muscles of the body
-death in 2-3 years from resp failure or pneumonia
-the only approved drug is riluzole (rilutek) for ALS, reduces degeneration of neurons, may also treat symptoms with muscle relaxants and anticholinergics

50
Q

what are muscle spasm vs muscle spasticity?

A

spasm: involuntary contractions most commonly caused by injury or overuse of skeletal muscles
spasticity: caused by neuromuscular disorders

51
Q

what are the two types of muscle spasms?

A

-spasms are involuntary contraction specific to a muscle group
-two types are: tonic (single and prolonged) and clonic (rapidly repeating)

52
Q

what are causes of muscle spasm?

A

-skeletal muscle overuse/injury
-dehydration
-electrolyte imbalance/hypokalemia
-related pathologies
-MS, epilepsy, muscular dystrophy, fractures, chronic low back pain

53
Q

what are meds you can take for muscle spasms?

A

-NSAIDS: relieve pain + inflammation, eg, aspirin, naproxen, ibuprofen
-muscle relaxants: for moderate to severe spasms, relax tight contracted muscles, can be used with NSAIDS
-centrally acting muscle relaxants

54
Q

what is the prototype drug for centrally acting muscle relaxants?

A

-cyclobenzaprine (amrix, flexeril)
-increases NE to produce anticholinergic effect

55
Q

what are nursing considerations for cyclobenzaprine?

A

-VS and physical assessment, history
-baseline neurological status
-assess for pain
-protect from injury related to falls from drowsiness
asses for rash, ithcing, hives
-inform pt not to drive

56
Q

what is methocarbamol (relaxin, robaxin)

A

-a drug similar to cyclobenzaprine
-its an adjunct to physical therpay interventions
-don’t drive

57
Q

what is Metaxalone (skelaxin)

A

-a drug similar to cyclobenzaprine
-ineffective txt in spasticity-related neurological disorders

58
Q

what is orphenadrine (banflex, myophen, norflex) ?

A

-a drug similar to cyclobenzaprine
-anticholingeric drug of the antihistamine class: it is closely related to diphenhydramine

59
Q

what is tizandine (zanaflex)

A

-a drug similar to cyclobenzaprine
-spasticity related to the brain or spinal cord injury of MS

60
Q

what is muscle splascity?

A

-continuous state of contraction
-pain is more intense than spasms and causes greater impairment
-irritable deep tendon reflexes
-fixed joint movement
-not a disorder itself but rather causes by neuromuscular diseases

61
Q

what is the prototype drug for muscle spasticity?

A

dantrole (dantrium), which directly relaxes splastic muscles

62
Q

what are nrsg considerations for dantrolene?

A

-history and prescription
-baseline pain and neurological status
-assess vitals during iV admin
-assess for cardiopulmonary changes
(monitor breath and heart sounds)
-do liver function tests, report signs of jaundice, avoid alcohol
-do not drive

63
Q

what is a drug similar to dantrole?

A

botox, inhibits release of ach paralyzing the muscle

64
Q

what are nonpharmalogical therapies?

A

-physical therapy: increase movements, and prevents contractures
-herbal remedies: black cohosh, castor oil packs, capsaicin - wear with gloves (all topic)
-b complex vits, specifically B6

finals (12 decks)

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