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culture
past experiences
meaning
attention, anxiety
suggestion and placebo
feelings of control
factors n fluencing pain experience [6]
believe person’s self report
establish cause of pain
initiate appropriate treatment
principles of pain management [3]
Ask about pain regularly/assess pain systematically
believe the patient and family reports of pain and what relieves it
choose pain control options appropriate for the patient, family, and setting
deliver interventions in a timely manner
empower patients to control their treatment to the greater extent possible
Pain management strategy (ABCDE)
adjuvants
drugs that can be used for pain management but are not in anagelsic class
Pain pathway
always consider how pain management strategies work in relation to what?
nociceptors
small nerve endings of a-delta and c fibres
histamine
bradykinin
prostaglandins
substance P
serotonin
leukotrienes
tissue injuries release which chemical(s): [6]
dorsal hornw
relay station and sensory processing area in substantia gelatinosa
cerebral cortex
where muscle response is initiated in pain pathway
thromboxanes and prostaglandins
release of COX1 and COX2 results in the release of what? [2]
Cox-1
cyclo-oxygenase for house-keeping duties: protection of gastric mucosa, support renal function, and promotes platelet aggregation, stimulates uterine conractions
COX-2
cyclo-oxygenase for synthesis of prostaglandins associated with pain and inflammation
Acts by inhibiting COX-2 which blocks the synthesis of prostaglandins.
NSAID MOA:
Aspirin
First generation NSAID
first generation drug
NSAID that blocks both COX-1 and COX-2
Second generation
NSAID that targets cox-2
Celecoxib (Celebrex)
second generation NSAID prototype
Irreversible inhibition (3-5 days) of COX1 and 2
Acetylsalicylic acid (ASA) MOA:
7 days
stop taking aspirin how many days before surgery?
absorbed rapidly in GI tract
Highly bound to plasma protein
excreted in kidneys
Aspirin pharmacokinetics: [3]
GI upset
bleeding
renal dysfunction
ASA (aspirin blocks COX-1, so it will have which adverse effects?
Salicylism
Too much aspirin, causes tinnitus, sweating, and headache
warfarin is an antigoaculant
aspirin decreases platelet aggregation
risk of severe bleeding
Aspirin and warfarin drug interaction
Glucocorticoids act like cortisol. increases gastic secretions.
exaccerabates effects of aspirin
aspirin and glucocorticoids drug interaction
Alcohol increases bleeding risk
aspirin causes bleeding
Alcohol and aspirin drug interaction:
hepatotoxicity
renal toxicity
visual changes
alergic reactions
bleeding
It is important patients taking aspirin be educated to report signs of what? [6]
dark urine
claycoloured stool
yellow skin/sclera
itching
abdominal pain
Signs of hepatotoxicity[5]
Ibuprofen (advil, motrin)
First generation NSAID that is an anti-inflammatory, analgesic, antipyretic. Preferred drug now for inflammation over ASA, also has milder side effects
inhibits COX-1 and COX-2 but is reversible
Ibuprofen (Advil) MOA
Acetaminophen (Tylenol)
Drug for mild to moderate pain without anti-inflammatory properties
Inhibits prostaglandin synthesis in CNS to reduce pain and fever
Tyelenol MOA:
Competes for metabolism sites in the liver.
Tyelenol and alcohol drug interaction
causes warfarin to stay around longer
Tylenol and warfarin drug interaction
easily distributed
half-life of 2 hours
excretion: metabolites in urine
Tylenol pharmacokinetics [3]
Opioid agonist
Drug that attaches to opioid receptor and causes something to happen
Opioid agonist/antagonist
Drug that attaches to opioid receptor and works as an agonist in some ways and an antagonist in others:
In the CNS, not an anti-inflammatoryM
where does tylenol work?
morphine
opioid agonist prototype
binds to opioid receptors
inhibits neurotransmitter release
decreases firing rate and excitability
decreases transmission of impulses
decreased perception of pain and emotional response
triggers histamine release from mast cells
Morphine MOA:
It causes histamine release from mast cells, causing itching
Why does morphine cause iching?
well absorbed
widel distributed
half-life: 2-3 hours with significant (25%) hepatic first pass effect
90% appears in urine in 24 hours
Opioid pharmacokinetics: [4]
Mu receptors
opioid receptors in limbic system, thalamus, brainstem, dorsal horn, gut
Kappa
opioid receptors in cerebral cortex, spinal cord
Delta
Opioid receptors in the bowel, no much interaction
analgesia
euphoria
sedation
respirator depression
nausea
decreased GI motility
restlessness, confusion
pupil ocnstriction
peripheral vasodilation
itching
cough suppression
effects of opioids [11]
less than 8 breaths per minute
respiratory depression rate
patients with compromised respiratory system (ex: COPD)
patients with head injuries, respiratory centre in medulla could be compromised
patients with what conditions should be cautioned about using opioids due to them causing respiratory depression [2]
always start a bowel regimen (laxatives) when giving opioids
Nursing care for opioids and constipation
offer anti-emetics to start; nausea will disappear in time unless sensitive
nursing care for opioids and nausea
observe for over-sedation; remove/be cautious with any other drugs with sedating effect
nursing care for opioids and sedation
Around the clock (ATC). Manage pain before it can “break through”
when should opioids be given? (schedule-wise)
Hydromorphone (Dilaudid)
Opioid 5X more potent than morphine
codeine
opioid that has the most constipation as a side effect
Meperidine (Demerol)
opioid that should only be given 600mg per day because it has a toxic metabolite that can build up with long term use. half life is 18 hours.
Percocet
combination opioid wit 5mg oxycodone and 325mg tylenol
Tylenol #3 or #4/Atasol 30 or 60
combination opioid with codeine, tylenol, and caffeine
patient-controlled analgesia (PCA)
pump that delivers opioid when patient pushes button
a certain amount per hour maximum
a lock-out period
Safety features of PCA:
Intrathecal morphine
“spinal” morphine, with or without anesthetic. Usually administered during a procedure in the OR. The effects can last up to 24 hours
clocks access of opioid agonists to the opioid receptors
reverses opioid actions and side effects
bumps opioid molecules out of receptor
Naloxone (Narcan) MOA:
Naloxone (Narcan)
strucurally like morphine. is a competitive antagonist
0.4mg IV; repeat at 2-3 minute intervals
Narcan dosing:
severe N+V with cheotherapy
loss of appetite and weight with cancer and/or HIV/AIDS
muscle spasms
palliative/end of life care
when is medical cannabis prescribed?
causes drowsiness
Cannabis and drugs that slow CNS interactions
other anti-depressants
certain heart meds
certain antibiotics
antiretroviral drugs (HIV)
caution with psychoactive drugs
Medical cannabis should not interact with what? [5]
it is individualized and titrated to effect. Usually no more than 3 grams per day (dried)
Medical cannabis dosing:
drowsiness
lightheadedness
disorientation
confusion
side effects of medical cannabis [4]
responds poorly to opioids but much better with adjuvant analgesics
treatment for neuropathic pain:
antidepressants (imipramine)
Anti-convulsants (Carbomazepine)
Local anaesthetics (lidocaine)
examples of adjuvant analgesics for opioids: [3]
the brain to support and augment endorphins
opioids
relaxation
imagery
distraction
enhance control
meditation
targeting the brain for pain relief for neuropathic pain and examples [6]
opioids via epidural
nerve blocks
peripheral stimulation through massage / TENS
methods for pain relief that interrupt spinal cord messages: [3]
Use effective doses on a regular schedule
combine with alternative therapies
should not deter use if needed
Clinical implications for pain relief: [3]