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5 Ortho > L6 Pain Medicine > Flashcards

L6 Pain Medicine Flashcards

1
Q

Meds for muscle spasms and spasticity

A

skeletal muscle relaxants

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2
Q

Meds for pain

A

NSAIDs, opioids, acetaminophen, cannabinoids

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3
Q

Meds for pain and inflammation

A

NSAIDs and glucocorticoids

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4
Q

Meds for OA and RA

A

NSAIDs, acetaminophen, opioids, SAIDs, DMARDs, viscosupplmentation

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5
Q

Pharmacodynamics

A

effect of the drug on the body

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6
Q

Pharmacokinetics

A

effects of body on the drug

Absorption, Distribution, Metabolism, Excretion, Elimination

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7
Q

Intracellular nuclear receptors

A

directly affects gene function
slowest

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8
Q

Metabotropic receptors

A

activates a second messenger system

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9
Q

Ionotropic receptors

A

opening an ion channel and changing membrane permeability or membrane potential
fastest

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10
Q

Affinity

A

amount of attraction between drug and receptor

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11
Q

Selective

A

drug only binds to 1 receptor subtype and produces a single response
no drug is perfectly selective

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12
Q

Agonist

A

drug binds to receptor and produces change in cell function (affinity and efficacy)

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13
Q

Partial agonist

A

less efficacy, varying levels of affinity

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14
Q

Full agonist

A

high efficacy, high affinity

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15
Q

Antagonist

A

drug binds to receptor but produces no change in cell function
only affinity, no efficacy

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16
Q

Spasticity

A

result of UMN lesion
increased muscle tone, hyperactive velocity dependent stretch reflex, clonus

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17
Q

Spasms

A

results of local musculoskeletal injury
nociceptive stimuli eventually leads to increased tonic muscle contraction

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18
Q

Skeletal muscle relaxants and CNS

A

all but two relaxants ultimately decrease neural excitability at the “final common pathway”

most muscle relaxers work upstream, having impacts on the CNS that controls the muscle

causes decreased excitability of all neurons with GABAA receptors. causes a general slowing of the CNS, or sedation

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19
Q

Antispasm agents

A

Benzodiazepines (BZDs)
Polysynaptic inhibitors
Botulinum toxin

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20
Q

Benzodiazepines (BZDs)

A

agonists at GABAA ion channel receptor complex

after it binds to the receptor, CL flow through channel increases, hyperpolarizing the neuron

Receptors for BZDs are present throughout the CNS

causes muscle relaxation and decreased arousal

also used for insomnia and anxiety

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21
Q

ADRs and Interactions of Benzos

A

ADRs: muscle weakness, ataxia, drowsiness, confusion, dependency, abuse

Interactions: Alcohol and other depressants. Grapefruit juice

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22
Q

Tolerance

A

higher dose required for same effect

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23
Q

Withdrawal

A

occurs with abrupt discontinuation
irritability, insomnia, muscle cramps

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24
Q

Benzos and Half Lives

A

can have up to a 30 to 60 hour half life (diazepam/valium)

would be about 150-300 hours to be eliminated from the system

half lives can increase in adults that are older

usually prescribed for short term use

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25
Q

Polysynaptic inhibitors

A

includes cyclobezaprine
exact MOA is not well understood

all drugs in this group decrease alpha motor neuron stimulation

all produce general CNS depressant effect

onset of action is usually 30 to 60 min, and lasts up to 24 hours

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26
Q

Botulinum Toxin

A

-produced by bacteria
-when injected into a muscle, it blocks AcH release at NMJ
-paralysis is dose related and transient
-recovery occurs when new nerve terminals regenerate at injection site. Takes about 3 months

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27
Q

Clinical uses of BTX

A

FOCAL DYSTONIAS
SPASTICITY
INVOLUNTARY MUSCLE ACTIVITY
NYSTAGMUS
CHRONIC PAIN
urinary incontinence

Lots of off label uses, like LBP and neck pain, cosmetic use

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28
Q

Uses and Limitations of BTX

A

Results in paralysis of injected muscle, uninjected are unaffected

Repeated injections necessary
limited # of muscles that can be injected
misinjections

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29
Q

Drugs used for muscle spasticity

A

GABA receptor agonists
gabapentin
alpha adrenergic receptor agonist
peripheral acting drugs

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30
Q

Baclofen (GABA agonist)

A

Pharmacodynamics: binding causes neuron hyperpolarization by increasing K flow out of cell. Results in inhibition of alpha motor neuron

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31
Q

Clinical uses of Baclofen

A

on label: spasticity, for SCI and MS

off label: LBP, trigeminal neuralgia, cluster headache

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32
Q

Routes of Administration for Baclofen

A

oral: systemic ADRs that are limiting

intrathecal: fewer systemic ADRs. Predominantly for LE spasiticty . Limits bending and twisting

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33
Q

ADRs of Baclofen

A

muscle weakness or hypotonia
transient drowsiness
confusion and hallucinations

Tolerance MAY occur with larger , constant doses

34
Q

Gabapentin

A

MOA is unclear, as it does not bind to GABA a or b receptors

decreases release of glutamate and may increase GABA in brain

also called pregabalin

35
Q

Clinical uses of gabapentin

A

partial seizures, spasticity with SCI

also used for neurologic pain, but many stop it because of the ADRs

36
Q

Tizanidine (Alpha 2 agonist)

A

-CNS receptor agonist

used for spasticity due to spinal lesions

ADRs: muscle weakness, sedation, dry mouth

37
Q

Centrally acting skeletal muscle relaxants and PT

A

Common ADRs impact rehab, like weakness, decreased muscle tone, etc

make sure to coordinate PT sessions according to peak action of drug.

Focus techniques on disrupting spasms so that they can decrease meds

Pt education about neuroscience

38
Q

Phsyiological effects of NSAIDs

A

Antiinflammatory
Analgesia
Antipyresis
Antiplatelet

(effect is dependent on dosage)

39
Q

NSAIDs and Inflammation

A

inhibit both COX1 and COX2, Most all NSAIDs have this function

COX2 inhibitors (celecoxib or Celebrex) will only stop COX2.

will inhibit the production of arcadonic acids

40
Q

COX Enzymes

A

COX 1 = housekeeping. Mediates normal cell function, like protecting the stomach

COX2 = mediates processes in injured cells

41
Q

COX 2 Selective inhibitors

A

(-coxibs)

Advantages: decrease sysnthesis of proinflammatory prostaglandins, spare the prostaglandins required for normal function. Decrease risk of peptic ulcers

Disadvantage: May increase risk of MI and VA because it inhibits PGI2 which does vasodilation and anticlotting

42
Q

Which NSAID is best?

A

no clear evidence that any NSAID is more effective than aspirin

lots of patient variability. no best for all.

43
Q

Acetaminophen

A

MOA: weak inhibitor of COX1 and COX2

Pharmacodynamics: not considered an anti-inflammatory or inhibit platelet function. WOrks as analegesia and antipyresis

44
Q

ADRs of acetaminophen

A

Hepatotoxicity

45
Q

NSAIDs and PT

A

Common ADRs: GI toxicity may impact PT, impacts on clotting, impacts on liver/kidney/GI

PT should educate the patient about S/S of gastric irritation, taking on full stomach, referral of pain. Avoid taping, consistently monitor VS, incorporate resistance

46
Q

Opioids

A

most powerful drug available to treat pain. Treat both affective and sensory aspects of pain

high potential for dependence and abuse

3 different receptors in our body for them. Mu, Kappa, Delta

47
Q

Mu Receptor Activation

A

causes analgesia, respiratory depression, sedation, addiction

48
Q

Kappa Receptor Activation

A

analgesia w/out respiratory depression, psychotropic effects, sedation, constipation

49
Q

Clinical Uses of Opioids

A

analgesia, indicated for moderate to severe pain
cough suppression
severe diarrhea
acute pulmonary edema

50
Q

Clinical use of opioids for analgesia

A

for treatment of constant pain
oral tried before parenteral
regular dosing is better
produce altered pain perception

51
Q

Opioids administration

A

Enteral: Oral
Parenteral: injection, Transdermal, Intranasal

52
Q

Opioid drug classes

A
  1. Strong agonists
  2. Moderate agonists
  3. Mixed agonist-antagonists
  4. Opioid combo drugs
  5. Antagonists
53
Q

Strong opioid agonists

A

Mu receptors, high affinity and efficacy

used for moderate to severe pain

morphine and fentanyl

54
Q

Black Box warning for fentanyl transdermal

A

only for opioid tolerant patients with severe chronic pain

high potential for addiction abused and misuse

respiratory depression

55
Q

Moderate Agonists

A

Mu and Kappa moderate affinity and efficacy

used for moderate to severe pain, codeine or oxycontin

56
Q

Mixed agonist and antagonists

A

Kappa agonist and mu antagonist

used for moderate to severe pain
less addictive and fewer ADRs
less pain relief, more psychotropic effects

57
Q

Opioid combo drugs

A

used for moderate-moderately severe pain

tramadol–> binds to opioid receptors

usually a combo between one pain med and opioid

58
Q

Antagonists Opioid Drugs

A

Have affinity and no efficacy

primarily mu receptor used for opioid overdose and addiction treatment

Naloxone: reversal of opioid overdose
Naltrexone: treatment of addiction

59
Q

Tolerance

A

higher dose to achieve the same effect

60
Q

Addiction/abuse potential

A

seeking out additional drug for pleasurable effect

61
Q

Dependence

A

physical dependence

abrupt cessation of drug in chronic user result in withdrawal syndrome

definitive end point

62
Q

Addiction

A

psychological dependence

craving and inability to abstain consistently, problems with ones behaviors/relationships

no definitive end point

strongest and most consistent predictor for opioid abuse is a personal or family history of abuse

63
Q

Physical Withdrawal S/S

A

aching, fever, insomnia, irritability, nausea

64
Q

Guidelines to decrease use/abuse of opioids

A

Try other treatments first
Assess risk for abuse
Keep expectations realistic
Start with short term trial
Weight potential harms and benefits

65
Q

Are opioids effective for chronic noncancer pain?

A

There is weak evidence that pts who are able to continue opioids long term experience clinically significant pain relief

66
Q

Rehab Relevance w/Opioids

A

Common ADRs: sedation, hypotension, respiratory depression, delayed response

PT: schedule with peak time in mind, respiratory response may be blunted, reduce activities that require high amounts of attentiveness

67
Q

Cannabiniods

A
  1. THC, responsible for the high that is felt
  2. CBD, responsible for decreasing pain, antiseziure effects
68
Q

Indications of cannabinoids

A

nausea/vomiting
anorexia/weight loss

69
Q

FDA Approved Cannabinoids

A
  1. Dronabinol –> chemo therapy nausea
  2. Cannabidiol –> used for seizures
70
Q

Are cannabinoids effective for chronic pain?

A

moderate quality evidence supporting use of cannabinoids for treatment of chronic pain and apsticity

increased risk of short term ADRs

71
Q

Drugs for Migraine

A

Patho: involves trigeminal nerve distribuition, arteries, and release of NTs

First line therapy for acute severe migraines. -TRIPTAINS. Several doses may be required, ADRs limit daily dosage

72
Q

Rehab and TRIPTANS

A

Common ADRs: altered sensations, dizziness, weakness

PT: postpone PT, dim lights, passive modalities for pain

73
Q

Drugs for Fibromyalgia

A

Patho: cenral sensitivity syndrome characterized by abdnormal pain processing in CNS

TX: education, CBT, exercise, pharmacotherapy

medicine is aimed at increasing serotonin and decreasing excitatory NTs. Antidepressants and Anticonvulsants

74
Q

Rehab and Fibromyalgia drugs

A

ADRs: drowsiness, dizziness. Depends on medication. Altered cardiovascular

PT: limit activities that require attentiveness and concentration. Minimize fall risk in clinic. MOnitor vital signs

75
Q

Uses for glucocorticoids

A

Allergic reactions, collagen vascular disorders, GI diseses, bone/joint inflammation, neuro disorders, organ transplants, asthma, dermatitis

76
Q

Glucocorticoids used for inflammation

A

Hydrocortisone, predinose, triamcinolone

usually oral, can be topical or intra articular.

77
Q

Effects of exogenous systemic glucocorticoids

A

benefits of use vary
major ADRs result from hormonal actions
must be tapered off slowly to avoid impact on adrenocortical systems

78
Q

Rehab and Glucocorticoids

A

ADRs: increased risk of infection, fragile skin, decreased endurance, increased risk of CV dysfunction, increased risk of fractures, hyperglycemia, necrosis of hip

PT: Educate patient about infections, avoid taping, incorporate exercise w/vital sign monitoring

79
Q

Viscosupplementation

A

intra-articular injection of fluid to supplement thinning and less elastic synovial fluid in joints with mild to moderate OA

large sugar molecules tangle with synovial fluid to act as a shock absorber

hyalgan, synvisc

used in the KNEE

80
Q

Effectiveness of viscosupplementation

A

Comparable efficacy to NSAIDs and intraarticular glucocorticoids

more beneficial when given in earlier stages of OA

5 Ortho (14 decks)

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