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Pharmacology > Pain Management Part II > Flashcards

Pain Management Part II Flashcards

1
Q

Background of opioid analgesics

A
  • partially occurring & semisynthetic opioid analgesics are derived from the opium poppy
  • Opium contains about 20 biologically active compounds including morphine & codeine
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2
Q

Endogenous opioids

A
  • Endorphins
  • Enkephalins
  • Dynorphins
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3
Q

Background of morphine

A
  • It is the prototypic opioid agonist
  • Named after the Greek god of dreams, Morpheus
  • Remains the standard in comparing opioid analgesics in terms of potency & efficacy
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4
Q

Pros of opioid use

A
  • Decrease pain
  • Improve quality of life
  • Increased exercise tolerance
  • Increased therapy engagement
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5
Q

Cons of opioid use

A
  • Side effect profile
  • Abuse potential
  • Long term complications
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6
Q

What are the 3 subclasses of opioid receptors

A
  • Mu
  • Kappa
  • Delta
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7
Q

What opioid receptors has the most effect on analgesia

A
  • Mu receptors found within the CNS have seemingly the most effect on analgesisa
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8
Q

What opioid receptor is more linked to respiratory and the receptor more linked to sedation

A
  • Mu receptors more linked to respiratory depression and abuse potential
  • Kappa receptors linked to sedation
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9
Q

Mechanism of action for opioid analgesics

A
  • Inside the cell opioid receptors linked via G proteins causing: calcium channel inhibition (decrease neurotransmitter release), potassium channels open (postsynaptic K efflux & decreases excitability), & signaling pathways (decreases cAMP synthesis & decreases excitability)
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10
Q

Where does opioid activity derive from

A
  • derives from receptor binding & downstream (intracellular) mechanisms
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11
Q

Mechanism of action of opioid analgesics in the CNS/Spinal

A
  • Pre-synaptic: inhibit neurotransmitter release into the synapse
  • Post-synaptic (achieved by hyper polarization): decrease excitability & transmission of pain signals
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12
Q

What excitatory neurotransmitter is mainly affected (opioid MOA on the CNS/Spine)

A
  • Glutamate is the main one affected
  • Acetylcholine, norepinephrine, serotonin, & substance P. are also affected
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13
Q

MOA of opioid analgesics in the CNS/Brain

A
  • Binding within midbrain to effect descending efferent pain pathways by the release of norepinephrine & serotonin to further inhibit synapses
  • Decrease ascending afferent pain transmission
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14
Q

Opioid analgesic MOA on the PNS

A
  • Decrease excitability of sensory neurons
  • Exogenous opioids work in conjunction with endogenous opioids
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15
Q

List strong opioid analgesic agonists

A
  • Fentanyl*
  • Hydromophone*
  • Methadone*
  • Morphine*
  • Tramadol*
  • Alfentanil
  • Levorphanol
  • Mederidine
  • Oxymorphone
  • Remifentanil
  • Sufentanil
  • Tapenadol
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16
Q

List mild to moderate opioid analgesic agonists

A
  • Codeine*
  • Hydrocodone*
  • Oxycodone*
  • Propoxyphene
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17
Q

Difference between strong agonists and mild to moderate agonists

A
  • Mild to moderate agonists have good analgesic effect but have less affinity & efficacy in comparison to strong agonists
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18
Q

List mixed opioid analgesic agonist-antagonists

A
  • Buprenorphine*
  • Butorphanol
  • Nalbuphine
  • Pentazocine
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19
Q

Describe Buprenorphine

A
  • It’s a mu receptor agonist but weak antagonist at kappa & delta receptors
  • this class of medication can produce adequate analgesia while limiting risk of respiratory depression & fatal overdose
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20
Q

List opioid analgesic antagonists

A
  • Naloxone*
  • Naltrexone*
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21
Q

Describe opioid analgesic antagonists

A
  • Greater affinity towards mu receptors than kappa or delta
  • Pure antagonist effect useful in reversal of opioid overdose
  • Short duration of action in comparison to pure opioid agonists may require multiple administrations when in response to opioid overdose
22
Q

Clinical use of opioid analgesics

A
  • Helpful for constant moderate to severe pain & lesser for intermittent & sharp pain
  • Oral opioid administration is preferred for pain management due to convenience as tolerated
  • Appropriate pillar to multimodal pain management with non-opioid alternatives
  • Scheduled opioids may be more effective than as needed but could lead to over medication
23
Q

Central side effects of opioid analgesics

A
  • Drowsiness
  • Mental slowing
  • Euphoria
  • Respiratory depression
  • Orthostatic hypotension
24
Q

Peripheral side effects of opioid analgesics

A
  • Constipation
  • Nausea/Vomiting
  • Urinary retention
  • Bronchospasm
25
Q

What other negative effects can occur from inappropriate prescribing/use of opioid analgesics

A
  • Addiction
  • Tolerance
  • Physical dependence
26
Q

Define addiction

A
  • typically refers to when an individual repeatedly ingests certain substances for mood-altering & pleasurable experiences
27
Q

Define tolerance

A
  • is defined as the need to progressively increase the dosage of a drug to achieve a therapeutic effect when the drug is used for prolonged periods
28
Q

Describe tolerance effects from prolonged use of opioid analgesics

A
  • Down-regulation (quantity of receptors)
  • Desensitization (sensitivity of receptors)
  • Endocytosis (location of receptors)
  • Disruption of Opioid and G protein communication
29
Q

Describe tolerance

A
  • Tolerance may begin after the first opioid dose
  • Noticeable effect after 2-3 weeks
  • Tolerance effect lasts around 1-2 weeks after last opioid dose
30
Q

Define physical dependence

A
  • is usually defined as the onset of withdrawal symptoms
31
Q

Symptoms of physical dependence

A
  • Fever
  • Insomnia
  • Loss of appetite
  • Body aches
  • Sneezing
  • Sweating
  • Yawning
  • Runny nose
  • Gooseflesh
  • Irritability
  • Nausea/Vomiting
  • Diarrhea
  • Stomach cramps
  • Tachycardia
  • Weakness
  • Shivering
32
Q

Describe physical dependence

A
  • Can occur as quickly as 6-10 hours after last opioid administration
  • Peak side effects occur within 2-3 days from the stop of medication
  • Physical withdrawal symptoms last for up to 5 days but the desire for opioids may last for months to years after abstinence
33
Q

Describe hyperalgesia

A
  • Compensatory increase in glutamate pathways which promotes pain responses by stimulating NMDA receptors
  • “decreased pain tolerance”
34
Q

Opioid effects that may interfere with rehabilitation

A
  • Sedation, mental slowing, & drowsiness
  • Hypoxia/hypercapnia & blunted exercise potential due to respiratory depression
  • Diffuse muscle aches & pains due to opioid withdrawal
35
Q

Solutions to potential opioid effects that can interfere with rehabilitation

A
  • Opioids may allow for increased pt participation
  • Time therapy at peak levels to maximize analgesic effects for patients in acute pain
  • If unable to tolerate therapy work with providers to discuss analgesic alternatives that may allow for more therapeutic interventions
  • Be aware of abuse potential & help patient cope during acute withdrawal by using alternatives (heat, electrotherapy, massage, & relaxation techniques)
36
Q

Describe patient controlled analgesia (PCA)

A
  • Pt self-administers small & frequent doses to optimize pain relief
  • Can be administered IV or into the spinal canal
  • Emerging literature showing great benefit post-op or in other settings of chronic pain
  • PCA allows patients to maintain therapeutic levels of pain control while matching individual patient needs
37
Q

Describe PCA pharmacokinetics

A
  • Goal of pCA is to remain within a narrow therapeutic window to minimize over-sedation & untreated pain
  • PCA achieves more effective pain control with less side effects
38
Q

PCA (patient controlled self-administered) terms

A
  • Loading dose: establish analgesia
  • Demand dose: self-administered dose; can track successful vs total demands to determine if parameters are appropriate for patient (successful = self-administered outside of lockout interval; Unsuccessful = dose attempted during lockout interval)
  • Lockout interval: required interval between doses
  • Interval limits: total dose per limit
  • Background infusion: small continuous dose maintains background analgesia; useful when the pt is asleep or unable to activate the pump; may lead to over sedation & increased side effects
39
Q

What is a typical lockout interval for PCA

A
  • lockout intervals will vary slightly with patient/dose
  • Frequently 5-10 minute intervals
40
Q

Types of PCA analgesics

A
  • Opioids: common agents - morphine, fentanyl, hydromorphone
  • Non-opioids: common additive agents- ketorolac, ketamine, naloxone, or droperidol; local anesthetics may be used to block sensory afferents; many strategies to help implement on “opioid sparing technique”
41
Q

Describe a PICA (patient controlled intravenous administration)

A
  • injected in the peripheral vein (useful for short term)
  • most common PCA due to simplicity & convenience
  • longer durations require central line
42
Q

Describe a PCEA (patient controlled epidural administration)

A
  • typically inserted in the epidural space at a certain level of the spinal cord
  • more effective (using less drug) but more difficult to place & manage than IV
43
Q

Describe potential PCA benefits

A
  • Allows patient to control their own pain management
  • Associated with shorter hospitalizations & quicker return to ambulation in certain chronic pain populations
  • Reduced incidence of troublesome side effects: sedation, pruritic, nausea, vomiting
44
Q

Describe skeletal muscle relaxants

A
  • Used to treat various conditions associated with hyper excitable skeletal muscle
  • Can work synergistically with rehabilitation to reduce muscle spasms & spasticity
  • Ultimately the goal is to normalize excitability to decrease pain & improve motor function
45
Q

Describe spasticity

A
  • Caused by an injury to the CNS or the brain
  • Sustained effect secondary to a decreased control of stretch reflex & alpha motor neuron excitability
  • Defined as not in itself a disease but rather the motor sequela to the pathologies
46
Q

Describe spasms

A
  • Caused by a musculoskeletal injury or inflammation
  • Sudden & involuntary with multiple possible explanations on the exact pathophysiology
47
Q

Describe anti-spasm drugs

A
  • These medications cause generalized CNS sedation which leads to skeletal muscle relaxation but also carries a risk for drowsiness & dizziness
  • Best used as an adjunct for short term relief of spasms caused by acute musculoskeletal injuries
  • Long term use can lead to tolerance & physical dependence issues that may mimic those of opioid users
48
Q

Most commonly seen in practice anti-spasm drugs

A
  • Carisoprodol
  • Cyclobenzaprine
  • Diazepam
  • Metaxalone
  • Methocarbamol
49
Q

Most commonly seen in practice anti-spasticity drugs

A
  • Baclofen
  • Diazepam
  • Gabapentin
  • Tizanidine
50
Q

Physical therapy implications related to muscle relaxants

A
  • Skeletal muscle relaxants can be used alongside thermal, electrotherapeutic, & manual techniques to get through initial acute phase of a musculoskeletal injury causing spasms
  • Long term effects should be avoided which further strengthens the need for aggressive physical therapy
  • Physical therapists are critical in supporting patients who need to adapt to sudden changes in muscle excitability

Pharmacology (12 decks)

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