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
2
Q
Endogenous opioids
A
- Endorphins
- Enkephalins
- Dynorphins
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
4
Q
Pros of opioid use
A
- Decrease pain
- Improve quality of life
- Increased exercise tolerance
- Increased therapy engagement
5
Q
Cons of opioid use
A
- Side effect profile
- Abuse potential
- Long term complications
6
Q
What are the 3 subclasses of opioid receptors
A
- Mu
- Kappa
- Delta
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
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
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)
10
Q
Where does opioid activity derive from
A
- derives from receptor binding & downstream (intracellular) mechanisms
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
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
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
14
Q
Opioid analgesic MOA on the PNS
A
- Decrease excitability of sensory neurons
- Exogenous opioids work in conjunction with endogenous opioids
15
Q
List strong opioid analgesic agonists
A
- Fentanyl*
- Hydromophone*
- Methadone*
- Morphine*
- Tramadol*
- Alfentanil
- Levorphanol
- Mederidine
- Oxymorphone
- Remifentanil
- Sufentanil
- Tapenadol
16
Q
List mild to moderate opioid analgesic agonists
A
- Codeine*
- Hydrocodone*
- Oxycodone*
- Propoxyphene
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
18
Q
List mixed opioid analgesic agonist-antagonists
A
- Buprenorphine*
- Butorphanol
- Nalbuphine
- Pentazocine
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
20
Q
List opioid analgesic antagonists
A
- Naloxone*
- Naltrexone*
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
