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What is pain?
an unpleasant sensory + emotional experience associated with actual/potential tissue damage
What is pain the result of? (3)
a response to tissue injury
a symptom of pathology associated with a disease process
an altercation of the somatosensory system (how your body interprets pain)
What is the purpose of pain?
a protective response
What are the components of the nature of pain? (5)
physiological (transmission of nociceptive pain)
affective - emotions/suffering
behaviour - behavioural responses
cognitive - beliefs, attitudes, evaluations, goals
sensory - pain perception
What does unrelieved pain impact?
decreased personal autonomy
increased perception of vulnerability
dignity of human person is undermined
What is the pain pathway? (4)
transduction
transmission
perception
modulation
What is transduction? (1.1)
harmful stimuli causes cell damage with the release of sensitizing chemicals
these substances activate nociceptors = generation of action potential
What are the sensitizing chemicals released after noxious stimuli? (5)
prostaglandins
bradykinin
serotonin
substance P
histamine
What occurs after noxious stimuli stimulates nociceptors? (2)
chemical mediators release from site of injury - attach to nociceptor
after attachment - signals Na/K channels to open = action potential
What is transmission?
AP moves from site of injury → spinal cord → brainstem + thalamus → cortex for processing
What type of pain sensations do the different pain receptors transmit? (3)
c - dull ache/throbbing
non-mylinated
delta - fast sharp
beta - all other non-pain processing stimuli
What is the pathway of transmission for pain? (1.1)
sensory/stimuli → grey matter → white matter → brain
dorsal horn → thalamus (sorts stimuli) → midbrain (evaluates signals to see how much pain)
What is perception?
conscious experience of pain
What is modulation? (2)
sending the signal from the brain → spinal cord → back down
= releases substances that inhibit nociceptive impulses
What are enkephalins?
endogenous opioids
What are the types of pain? (2)
acute
chronic
What is acute pain? (1.1)
abrupt sudden onset pain; time limited
a SNS response
What is chronic pain? (1.1)
ongoing pain; >3 months or years
altered SNS response from over-activation
What are the classifications of pain? (4)
nociceptive pain
neuropathic pain
nociplastic pain
mixed
What is nociceptive pain?
normal pain - warns of actual/potential injury + starts SNS response
What are the types of nociceptive pain? (3)
somatic
visceral
referred
What is somatic pain?
pain from nerve receptors in skin/close to surface
sharp + well localized or dull and diffused
What is visceral pain?
from organs
What is referred pain? (1.1)
pain perceived in a distant area
common with visceral pain
What is neuropathic pain?
abnormal processing of sensory input as result of injury of peripheral or CNS
What are the types of neuropathic pain? (2)
centrally generated pain
peripherally generated pain
What is centrally generated pain?
deafferentation pain - injury to peripheral or CNS
sympathetically maintained pain association with dysregulation of ANS
What is peripherally generated pain? (2)
painful polyneuropathies - pain felt along peripheral nerves
painful mononeuropathies - associated w/ peripheral nerve injury
What is nociplastic pain?
pain from altered pain processing in nervous system without clear evidence of tissue/nerve damage - we dont know why it’s happening
What is mixed pain?
combination of nociceptive + neuropathic pain
What are dermatones?
area of skin supplied by a single nerve root
What is the goal of a pain assessment? (2)
describe patients sensory, affective, behavioural, and sociocultural response to pain
identify patient goals for therapy, resources, and strategies for self management
What is the primary role of the nurse in relation to pain?
advocate for patient by accepting reports of pain + acting quickly to relieve it while respecting values
What are the types of descriptive pain assessment tools? (3)
faces pain scale revised
pain assessment tool
wong-baker faces pain rating scale
What are potential challenges in assessing pain? (7)
critically ill
comatose/LOC
sedated
imminently dying
language/communication
developmental age
cognitively impaired
How do you observe the pt in relation to pain? (6)
position of comfort
guarding area of pain
facial expression
movement/gestures
behaviour
vital signs
What are patient related barriers to adequate pain management? (9)
fear of addiction
fear of tolerance
concerns about adverse effects
fear of injections
desire to be a good patient
forgetting to take analgesics
concern that pain = worsening disease
medication not working
don’t want to bother HC team
What are the assessment considerations for acute pain? (1.4 + 1.4)
subjective findings:
pain 4+
mild-moderate severity
should be able to identify how much they can tolerate
assess nausea, vomiting, pruritus
objective:
elevated vitals
respiratory changes
physical changes
gastrointestinal changes
What are assessment considerations for neuropathic pain? (1.2 + 1.3)
subjective
altered sensation
nocturnal flare ups
objective
skin + tissue inspection
trophic changes
secondary complications
What are the goals of care for chronic pain? (3)
controlled symptoms
functional independence
active support systems
What are the steps in the WHO step ladder? (1.4 + 1.6 + 1.6)
1 - mild (1-3) non-opioids
ASA
acetaminophen
NSAIDS
+adjuvants
2 - moderate (4-6) moderate opioids
A/codeine
A/hydrocodone
A/oxycodone
A/dihydrocodeine
tramadol
+ adjuvants
3 - severe (7-10) strong opioides
morphine
hydromorphone
methadone
levorphanol
fentanyl
oxycodone
What are pharmacological interventions for pain? (1.4)
analgesics
non-opioids
opioids
adjuvant analgesics
atypical analgesics
What are types of NSAIDS? (4.1)
acetylsalicylic acid
ibuprofen
naproxen
celecoxib
never take 2 together
What are NSAIDS not good for? (1.7)
the entire body
kidney problems
bleeding disorders
GI issues
asthma
CV
ASA not safe for kids
not safe for pregnancy
What is the MOA for NSAIDS?
Cox 1 and Cox 2 inhibition
What is the function of cox 1?
prostaglandin production
What do cox 1 prostaglandins help with? (3)
gastric mucosa protection
renal blood flow
platelet aggregation (clotting)
What do cox 2 prostaglandins help with? (3)
mediates inflammation (swelling/vasodilation)
sensitizes pain receptors
induces fever
What is the MOA for ibuprofen?
inhibits prostaglandin synthesis by blocking cox 1 + 2 = decreased inflammation
What are the indications of ibuprofen? (3)
inflammation
mild/moderate pain
fever reduction
What are the contraindications for ibuprofen? (4)
allergy to NSAIDS
renal or liver dysfunction
peptic ulcer
thrombotic events
What are the side effects of ibuprofen? (1.4 + 1.5 + 1.2 + 1)
CVS -
MI/stroke
HTN
edema
nephrotoxicity with high doses
GI
nausea
dyspepsia
GI pain
constipation
diarrhea
Hema
bleeding
platelet inhibition
steven johnson syndrome
What are the nursing considerations for ibuprofen? (3)
assess for S+S of Gi bleed, renal + liver function
use drug only as suggested
report - sore throat, fever, rash, itching, swelling, changes in vision, black/tarry stool
What is the MOA of acetylsalicylic acid?
inhibits the synthesis of prostaglandins - inhibits platelet aggregation
What are the indications of acetylsalicylic acid? (4)
mild to moderate pain
fever
reduced risk of recurrent stroke in males
MI prophylaxis
What are the contraindications for acetylsalicylic acid? (4)
allergy to salicylates, NSAIDS
conditions that increase the risk of bleeding, clotting, or deficiencies
surgery scheduled within a week
severe hepatic disease
What are the side effects of acetylsalicylic acid? (4)
irritation of GI tract
hepatotoxicity
hypersensitivity
tinnitus
What are the nursing conditions for acetylsalicylic acid?
assess: history, allergies, physical condition related to liver, kidneys,
reported ringing in ears, dizziness, confusion, abdominal pain, nausea, vomiting, bloody stool
What are the therapeutic effects of acetylsalicylic acid? (3)
reduction in pain
reduction in fever
reduces risk of heart attack + stroke (anti-platelet action via COX 1 inhibition
What is the MOA of acetaminophen? (2.1)
reduces fever by acting directly on hypothalamic heat regulating centre
analgesic mechanism: through inhibition of prostaglandins in CNS
not an inflammatory agent
What is the max dosage of acetaminophen in adults + geriatrics? (2)
4000 mg - adults
3000 mg - geriatric
What are the indications for acetaminophen? (2)
treatment of mild-moderate pain
reduction in fever
What are the therapeutic effects for acetaminophen? (2)
reduced pain
reduced fever
What are the contraindications for acetaminophen? (2)
allergy to acetaminophen
use cautiously with impaired hepatic function, chronic alcoholism
What are the side effects of acetaminophen? (3)
hypersensitivity; rash, fever
hepatotoxicity
renal damage
What are the nursing considerations for acetaminophen? (3)
assess history + physical condition related to liver + kidneys
monitor LFTs if concerned
avoid using multiple preparations with acetaminophen (scheduled + PRN)
What are the opioid strengths? (2)
hydromorphone 5x stronger than morphine
fentanyl 10x stronger than hydromorphone
Why are opioid analgesics used?
manges moderate-severe nociceptive pain
How do opioid analgesics produce effects?
interacts with opioid receptor sites throughout body ; binds to receptor sites to produce analgesia + unwanted side effects
What are facts about moderate opioid analgesics? (7)
second on the pain ladder
most effective + primary drugs for moderate to severe pain
they’re weak opioids with acetaminophen
can cause sedation, euphoria, constipation, respiratory distress, urinary retention
tolerance can develop
ceiling effect
can result in physical dependence
What is the MOA for codeine phosphate? (2)
binds to opioid receptors in CNS + alters perception + response to painful stimuli while depressing CNS
codeine metabolized to morphine = lots of the analgesic effect
What are the therapeutic effects of codeine phosphate? (3)
relieves mild-moderate pain
suppresses cough
mild antidiarrheal effect
What are the indications for codeine phosphate? (3)
relief of mild-moderate acute + chronic pain
antitussive for nonproductive cough
sometimes used for diarrhea
What are the contraindications for codeine phosphate? (6)
hypersensitivity to codeine/other opioids
respiratory depression
acute/severe asthma
paralytic ileus
children <12 years - risk of fatal respiratory depression
breastfeeding
What are the side effects of codeine phosphate? (7.3)
CNS depression (drowsiness, sedation, dizziness)
respiratory depression
constipation
nausea
vomiting
sweating, pruritus
potentially fatal:
severe respiratory depression
collapse
anaphylaxis
What are the nursing considerations for codeine phosphate? (6)
assess pain, respiratory rate, level of sedation before + during therapy
keep naloxone available
encourage fluids, fiber, and possible stool softeners
educate pt on not driving + operating machinery
avoid alcohol + other CNS depressants
monitor for signs of misuse or dependence
What are strong opioid analgesics?
pure opioid agonists
What are characteristics about strong opioid analgesics? (2)
no ceiling effect - increased dose = increased relief
can adjust on pain severity
What is the MOA for strong opioid analgesics? (2)
binds to mu-type opioid receptors in CNS = altered perception + response to painful stimuli
also produces generalized CNS depression
What are the potencies for morphine, hydromorphone, and fentanyl? (3)
morphine - 1x (standard)
hydromorphone - 4-7x more potent vs morphine
fentanyl - 100x more potent vs morphine
What are the dosing units for morphine, hydromorphone, and fentanyl? (3)
morphine - mg
hydromorphone - mg
fentanyl - mcg
What are the indications for morphine? (4)
moderate-severe pain relief
MI chest pain
acute pulmonary edema
palliative dyspnea
What are the indications for hydromorphone? (3)
moderate-severe pain relief
severe breakthrough pain
palliative dyspnea
What are the indications for fentanyl? (4)
severe chronic/cancer pain
surgical anesthesia
procedural sedation
acute pain
What is the relation between morphine + renal impairment?
use with caution/avoid because causes accumulation of active metabolites = neurotoxicity/sedation
What is the relation between hydromorphone + renal impairment?
preferred over morphine - fewer metabolites = safer in moderate renal dysfunction
What is the relation between fentanyl + renal impairment?
safest choice in severe renal impairment/dialysis - no active neurotoxic metabolites
What are the nursing responsibilities when administering strong opioid analgesics? (3)
monitor baseline + ongoing pain rating, spO2, sedation score
monitor for hypotension
keep naloxone nearby
What are the adverse effects of strong opioid analgesics? (7)
sedation
constipation
nausea/vomiting
urinary retention
respiratory depression
dizziness
itching
What are the contraindications for strong opioid analgesics? (7)
severe acute respiratory depression
acute/severe asthma
COPD exacerbation
paralytic ileus
severe head injury
increased intracranial pressure
acute alcoholism
What is the adjuvant therapy for those on the 2nd step of the WHO ladder?
acetaminophen
anti-inflammatory meds
both
What is the adjuvant therapy for those with chronic pain? (5)
anticonvulsants
antidepressants
benzodiazepines
other opioids
cannabinoids
How do cannabinoids affect the body?
affects all cell receptors in the body
What is multimodal therapy?
using 2+ classes of analgesics or interventions to target different pain mechanisms in PNS or CNS
purposeful combination of pain meds to maximize relief + prevent gaps in treatment
Where do opioid antagonists work?
at mu and kappa receptors
What is tolerance?
effect where prolonged use requires a higher dose to produce an effect
What is physical dependence?
needing a medication to maintain function
What is addiction?
intense cravings, loss of control, and compulsive behaviour to obtain the substance
What are non-pharmacological interventions? (8)
heat/ice
massage
TENS
physiotherapy
imagery
distraction
deep breathing
cultural practices
What is the gate-control theory? (1.1)
non-pain sensations override/alter the pain response from pain stimuli
large nerve A-beta fibers excite inhibitory neurons = closes gate to block pain signals