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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
Polysynaptic inhibitors
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
26
Botulinum Toxin
-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
27
Clinical uses of BTX
FOCAL DYSTONIAS SPASTICITY INVOLUNTARY MUSCLE ACTIVITY NYSTAGMUS CHRONIC PAIN urinary incontinence Lots of off label uses, like LBP and neck pain, cosmetic use
28
Uses and Limitations of BTX
Results in paralysis of injected muscle, uninjected are unaffected Repeated injections necessary limited # of muscles that can be injected misinjections
29
Drugs used for muscle spasticity
GABA receptor agonists gabapentin alpha adrenergic receptor agonist peripheral acting drugs
30
Baclofen (GABA agonist)
Pharmacodynamics: binding causes neuron hyperpolarization by increasing K flow out of cell. Results in inhibition of alpha motor neuron
31
Clinical uses of Baclofen
on label: spasticity, for SCI and MS off label: LBP, trigeminal neuralgia, cluster headache
32
Routes of Administration for Baclofen
oral: systemic ADRs that are limiting intrathecal: fewer systemic ADRs. Predominantly for LE spasiticty . Limits bending and twisting
33
ADRs of Baclofen
muscle weakness or hypotonia transient drowsiness confusion and hallucinations Tolerance MAY occur with larger , constant doses
34
Gabapentin
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
Clinical uses of gabapentin
partial seizures, spasticity with SCI also used for neurologic pain, but many stop it because of the ADRs
36
Tizanidine (Alpha 2 agonist)
-CNS receptor agonist used for spasticity due to spinal lesions ADRs: muscle weakness, sedation, dry mouth
37
Centrally acting skeletal muscle relaxants and PT
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
Phsyiological effects of NSAIDs
Antiinflammatory Analgesia Antipyresis Antiplatelet (effect is dependent on dosage)
39
NSAIDs and Inflammation
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
COX Enzymes
COX 1 = housekeeping. Mediates normal cell function, like protecting the stomach COX2 = mediates processes in injured cells
41
COX 2 Selective inhibitors
(-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
Which NSAID is best?
no clear evidence that any NSAID is more effective than aspirin lots of patient variability. no best for all.
43
Acetaminophen
MOA: weak inhibitor of COX1 and COX2 Pharmacodynamics: not considered an anti-inflammatory or inhibit platelet function. WOrks as analegesia and antipyresis
44
ADRs of acetaminophen
Hepatotoxicity
45
NSAIDs and PT
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
Opioids
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
Mu Receptor Activation
causes analgesia, respiratory depression, sedation, addiction
48
Kappa Receptor Activation
analgesia w/out respiratory depression, psychotropic effects, sedation, constipation
49
Clinical Uses of Opioids
analgesia, indicated for moderate to severe pain cough suppression severe diarrhea acute pulmonary edema
50
Clinical use of opioids for analgesia
for treatment of constant pain oral tried before parenteral regular dosing is better produce altered pain perception
51
Opioids administration
Enteral: Oral Parenteral: injection, Transdermal, Intranasal
52
Opioid drug classes
1. Strong agonists 2. Moderate agonists 3. Mixed agonist-antagonists 4. Opioid combo drugs 5. Antagonists
53
Strong opioid agonists
Mu receptors, high affinity and efficacy used for moderate to severe pain morphine and fentanyl
54
Black Box warning for fentanyl transdermal
only for opioid tolerant patients with severe chronic pain high potential for addiction abused and misuse respiratory depression
55
Moderate Agonists
Mu and Kappa moderate affinity and efficacy used for moderate to severe pain, codeine or oxycontin
56
Mixed agonist and antagonists
Kappa agonist and mu antagonist used for moderate to severe pain less addictive and fewer ADRs less pain relief, more psychotropic effects
57
Opioid combo drugs
used for moderate-moderately severe pain tramadol--> binds to opioid receptors usually a combo between one pain med and opioid
58
Antagonists Opioid Drugs
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
Tolerance
higher dose to achieve the same effect
60
Addiction/abuse potential
seeking out additional drug for pleasurable effect
61
Dependence
physical dependence abrupt cessation of drug in chronic user result in withdrawal syndrome definitive end point
62
Addiction
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
Physical Withdrawal S/S
aching, fever, insomnia, irritability, nausea
64
Guidelines to decrease use/abuse of opioids
Try other treatments first Assess risk for abuse Keep expectations realistic Start with short term trial Weight potential harms and benefits
65
Are opioids effective for chronic noncancer pain?
There is weak evidence that pts who are able to continue opioids long term experience clinically significant pain relief
66
Rehab Relevance w/Opioids
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
Cannabiniods
1. THC, responsible for the high that is felt 2. CBD, responsible for decreasing pain, antiseziure effects
68
Indications of cannabinoids
nausea/vomiting anorexia/weight loss
69
FDA Approved Cannabinoids
1. Dronabinol --> chemo therapy nausea 2. Cannabidiol --> used for seizures
70
Are cannabinoids effective for chronic pain?
moderate quality evidence supporting use of cannabinoids for treatment of chronic pain and apsticity increased risk of short term ADRs
71
Drugs for Migraine
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
Rehab and TRIPTANS
Common ADRs: altered sensations, dizziness, weakness PT: postpone PT, dim lights, passive modalities for pain
73
Drugs for Fibromyalgia
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
Rehab and Fibromyalgia drugs
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
Uses for glucocorticoids
Allergic reactions, collagen vascular disorders, GI diseses, bone/joint inflammation, neuro disorders, organ transplants, asthma, dermatitis
76
Glucocorticoids used for inflammation
Hydrocortisone, predinose, triamcinolone usually oral, can be topical or intra articular.
77
Effects of exogenous systemic glucocorticoids
benefits of use vary major ADRs result from hormonal actions must be tapered off slowly to avoid impact on adrenocortical systems
78
Rehab and Glucocorticoids
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
Viscosupplementation
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
Effectiveness of viscosupplementation
Comparable efficacy to NSAIDs and intraarticular glucocorticoids more beneficial when given in earlier stages of OA

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