L6 Pain Medicine Flashcards
Meds for muscle spasms and spasticity
skeletal muscle relaxants
Meds for pain
NSAIDs, opioids, acetaminophen, cannabinoids
Meds for pain and inflammation
NSAIDs and glucocorticoids
Meds for OA and RA
NSAIDs, acetaminophen, opioids, SAIDs, DMARDs, viscosupplmentation
Pharmacodynamics
effect of the drug on the body
Pharmacokinetics
effects of body on the drug
Absorption, Distribution, Metabolism, Excretion, Elimination
Intracellular nuclear receptors
directly affects gene function
slowest
Metabotropic receptors
activates a second messenger system
Ionotropic receptors
opening an ion channel and changing membrane permeability or membrane potential
fastest
Affinity
amount of attraction between drug and receptor
Selective
drug only binds to 1 receptor subtype and produces a single response
no drug is perfectly selective
Agonist
drug binds to receptor and produces change in cell function (affinity and efficacy)
Partial agonist
less efficacy, varying levels of affinity
Full agonist
high efficacy, high affinity
Antagonist
drug binds to receptor but produces no change in cell function
only affinity, no efficacy
Spasticity
result of UMN lesion
increased muscle tone, hyperactive velocity dependent stretch reflex, clonus
Spasms
results of local musculoskeletal injury
nociceptive stimuli eventually leads to increased tonic muscle contraction
Skeletal muscle relaxants and CNS
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
Antispasm agents
Benzodiazepines (BZDs)
Polysynaptic inhibitors
Botulinum toxin
Benzodiazepines (BZDs)
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
ADRs and Interactions of Benzos
ADRs: muscle weakness, ataxia, drowsiness, confusion, dependency, abuse
Interactions: Alcohol and other depressants. Grapefruit juice
Tolerance
higher dose required for same effect
Withdrawal
occurs with abrupt discontinuation
irritability, insomnia, muscle cramps
Benzos and Half Lives
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
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
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
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
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
Drugs used for muscle spasticity
GABA receptor agonists
gabapentin
alpha adrenergic receptor agonist
peripheral acting drugs
Baclofen (GABA agonist)
Pharmacodynamics: binding causes neuron hyperpolarization by increasing K flow out of cell. Results in inhibition of alpha motor neuron
Clinical uses of Baclofen
on label: spasticity, for SCI and MS
off label: LBP, trigeminal neuralgia, cluster headache
Routes of Administration for Baclofen
oral: systemic ADRs that are limiting
intrathecal: fewer systemic ADRs. Predominantly for LE spasiticty . Limits bending and twisting
ADRs of Baclofen
muscle weakness or hypotonia
transient drowsiness
confusion and hallucinations
Tolerance MAY occur with larger , constant doses
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
Clinical uses of gabapentin
partial seizures, spasticity with SCI
also used for neurologic pain, but many stop it because of the ADRs
Tizanidine (Alpha 2 agonist)
-CNS receptor agonist
used for spasticity due to spinal lesions
ADRs: muscle weakness, sedation, dry mouth
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
Phsyiological effects of NSAIDs
Antiinflammatory
Analgesia
Antipyresis
Antiplatelet
(effect is dependent on dosage)
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
COX Enzymes
COX 1 = housekeeping. Mediates normal cell function, like protecting the stomach
COX2 = mediates processes in injured cells
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
Which NSAID is best?
no clear evidence that any NSAID is more effective than aspirin
lots of patient variability. no best for all.
Acetaminophen
MOA: weak inhibitor of COX1 and COX2
Pharmacodynamics: not considered an anti-inflammatory or inhibit platelet function. WOrks as analegesia and antipyresis
ADRs of acetaminophen
Hepatotoxicity
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
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
Mu Receptor Activation
causes analgesia, respiratory depression, sedation, addiction
Kappa Receptor Activation
analgesia w/out respiratory depression, psychotropic effects, sedation, constipation
Clinical Uses of Opioids
analgesia, indicated for moderate to severe pain
cough suppression
severe diarrhea
acute pulmonary edema
Clinical use of opioids for analgesia
for treatment of constant pain
oral tried before parenteral
regular dosing is better
produce altered pain perception
Opioids administration
Enteral: Oral
Parenteral: injection, Transdermal, Intranasal
Opioid drug classes
- Strong agonists
- Moderate agonists
- Mixed agonist-antagonists
- Opioid combo drugs
- Antagonists
Strong opioid agonists
Mu receptors, high affinity and efficacy
used for moderate to severe pain
morphine and fentanyl
Black Box warning for fentanyl transdermal
only for opioid tolerant patients with severe chronic pain
high potential for addiction abused and misuse
respiratory depression
Moderate Agonists
Mu and Kappa moderate affinity and efficacy
used for moderate to severe pain, codeine or oxycontin
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
Opioid combo drugs
used for moderate-moderately severe pain
tramadol–> binds to opioid receptors
usually a combo between one pain med and opioid
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
Tolerance
higher dose to achieve the same effect
Addiction/abuse potential
seeking out additional drug for pleasurable effect
Dependence
physical dependence
abrupt cessation of drug in chronic user result in withdrawal syndrome
definitive end point
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
Physical Withdrawal S/S
aching, fever, insomnia, irritability, nausea
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
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
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
Cannabiniods
- THC, responsible for the high that is felt
- CBD, responsible for decreasing pain, antiseziure effects
Indications of cannabinoids
nausea/vomiting
anorexia/weight loss
FDA Approved Cannabinoids
- Dronabinol –> chemo therapy nausea
- Cannabidiol –> used for seizures
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
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
Rehab and TRIPTANS
Common ADRs: altered sensations, dizziness, weakness
PT: postpone PT, dim lights, passive modalities for pain
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
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
Uses for glucocorticoids
Allergic reactions, collagen vascular disorders, GI diseses, bone/joint inflammation, neuro disorders, organ transplants, asthma, dermatitis
Glucocorticoids used for inflammation
Hydrocortisone, predinose, triamcinolone
usually oral, can be topical or intra articular.
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
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
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
Effectiveness of viscosupplementation
Comparable efficacy to NSAIDs and intraarticular glucocorticoids
more beneficial when given in earlier stages of OA
