Pain Part 2 Flashcards
Strong agonists
Fentanyl
Hydromorphone
Methadone
Morphine
Tramadol
Mild-to-moderate agonists
Codeine
Hydrocodone
Oxycodone
Propoxyphene
Mixed Agonist-Antagonists
Buprenorphine
Butorphanol
Nalbuphine
Pentazocine
Buprenorphine duration of action
SL: 6-12 hours
IM: 6 hr
Antagonists
Naloxone (Narcan)
Naltrexone
Naloxone duration of action
IV: 30-120 min
Multimodal Pain Management
Utilize various mechanisms of action to target pain at different receptors
Goal: smallest possible doses = less adverse effects
Goal: reduce opioid requirement
Central effects of opioids
Drowsiness
Mental slowing
Euphoria
Respiratory depression
Orthostatic hypotension
peripheral effects of opioids
Constipation
Nausea/vomiting
Urinary retention
Bronchospasm
Opioid-Induced Hyperalgesia
Compensatory increase in glutamate pathways, which promotes pain responses by stimulating NMDA receptors
Patients simply may not respond to opioids even before tolerance develops
PCA loading dose
Establish analgesia
PCA demand dose
Self-administered dose
Can track “successful” vs total demands to determine if parameters areappropriate for patient
Successful = self-administered outside of lockout interval
Unsuccessful = dose attempted during lockout interval
PCA lockout interval
Required interval between doses
PCA interval limits
limits usually set for max amount of drug in a 1 or 4 hr period- is a safety feature but if not calculated correctly can lead to the patient being undertreated for a period of time
total dose per limit
PCA background infusion
Small, continuous dose maintains background analgesia
Useful when the patient is asleep or unable to activate the pump
May lead to over sedation and increased side effects
Epidural (PCEA)
Typically inserted in the epidural space at a certain level of the spinal cord
More effective (using less drug), but more difficult to place and manage than IV
Skeletal Muscle Relaxants
Used to treat various conditions associated with hyperexcitable skeletal muscle
Can work synergistically with rehabilitation to reduce muscle spasms and spasticity
Ultimately, the goal is to normalize excitability, to decrease pain, and improve motor function
Antispasm Drugs
These medications cause generalized CNS sedation, which leads to skeletal muscle relaxation, but also carries a risk for drowsiness and dizziness
Best used as an adjunct for short-term relief of spasms caused by acute musculoskeletal injuries
Long-term use can lead to tolerance and physical dependence issues that maymimic those of opioid users
Antispasm Drugs MOA
central acting medications,
Increase sedation in the CNS global decrease in CNS excitability generalized sedation muscle relaxation
Baclofen
Antispasticity drug,
Can be administered via intrathecal pump,
Fewer side systemic effects
- Greater efficacy with smaller doses due to localized administration
Tizanidine MOA
alpha 2 agonist, Decreases release of excitatory neurotransmitters resulting in decreased excitatory input to the alpha motor neuron
Baclofen adverse effects
Drowsiness (transient), generalized weakness
Elderly: Confusion and hallucinations
Abrupt withdrawal can cause withdrawal symptoms (dependence)
Tolerance risk (requiring increased doses for same effect)
Diazepam adverse effects
Use limited by sedative effects, generalized weakness
Tolerance risk
Tizanidine adverse effects
Sedation, dizziness
Commonly used anti-spasm drugs
Carisoprodol, cyclobenzaprine, diazepam, and methocarbamol, not long-acting drugs, have to be taken multiple times daily
