39 terms

Pain Meds (NSAIDs, Opiates)

Causes if Pain
Types of Pain
Chronic or Acute
Visceral, Somatic, Inflammatory, neuropathic
Drug that has actions similar to morphine
Opioid receptors
physical dependence, euphoria, analgesia, respiratory depression
Kappa: SAM
sedation, analgesia, miosis
Classification: Pure Opioid Agonist
activate mu and kappa
strong and moderate strong agonists
ie: percocet/vicodin
Classification: Agonist-antagonist
when given alone produce analgesia
when given with another agonist, they have an antagonist effect.
Given in L/D
Classification: Opioid antagonist
naloxone (narcan)= antidote
reversal agent for overdoses
Drugs: Strong Agonists
morphine, fentanyl, meperidine, hydromorphone (delaudid), methadone, heroin
Used for 8/9/10 pain
Drugs: Moderate Agonists
codeine, oxycodone, hydrocodone, propoxyphene
Drugs: Agonist-Antagonist
butophanol, nalbuphine, pentazocine
Morphine (Action/Use/Causes)
Action: mimics action of endorphins
Use: moderate to severe pain
Causes: analgesia, sedation, euphoria, anxiety reduction, respiratory depression, cough suppressoin, decrese bowel motility
Morphine PK
metabolized by liver excreted by kidnesy
large first pass effect with PO meds
Onset dependent on route
Avoid abrupt discontiuation of opioids
Morphine SE
sedation, orthostatic HYTN, cough supression, urinary retention, biliary colic, constipation, N/V, euphoria, miosis, neurotoxicity, itching, flushing
SE start with first does then go away slowly
Easing AE of Morphine
Constipation- treat early w/ stool softener, stimulatn laxatives
Sedation- eases with time-caffeine or amphetammines
N/V- treat w/ promethazine or ondasteron
Itching- antihistamine
Respiratory depression- naloxone
Cautions when using Opioids
hypersensitviity, head injury, acute asthma, decrease respiratory reserve, sleep apnea, biliary tract disease, chronic users, preg/labor, age extremes, live impairment, IBD, other resp dec drugs
Fentanyl IV (Sublimaze)
100x more potent than morphine
IV: conscious sedation / anesthesia
rapid onset / short duration
HIGH Abuse potential
Fentanyl (Duragesic, Actiq, Fentora)
Duragesic- patch slowly absorbed. Heat acceleartes
First patch takes 24hrs to become effective
Actiq-losenges on stick
Fentora- buccal tablets
Meperidine (demerol)
similar to morphine
use is in decline bc frequent dosing needed, interactions, toxic metabolites with long term use
Avoid with renal insufficiency
Rigers=the shakes when coming out of anesthesia
similar to morphine- longer duration and better bioavilabiliy
May prolong QT and lead to fatal dysrhythmias
Moderate-Strong agonists drugs/use
Codeine (tyleno #3)=pain, cough
Oxycodone (oxycontin, percocet) =pain, breakthrough
Hydrocodone (vicodin)= pain, cough
less effective for severe pain
kappa agonist, mu antagonist
less resp depression, no euphoria
can preciptate withdrawl and should not be given to pts who are physically dependent on pure opiods
Tramadol (ultram, ultracet)
Action: weak mu agonists, blocks reuptake of NE and serotonin (not opioid receptors)
Minimal potential for dependence, abuse, or respiratory depression (not controlled)
SE: rare, sedation, dizziness, headache, dry mouth, constipation, SEIZURES
Option for patient who cannot take NSAIDs
NSAIDs - how they work
block production of prostaglandins by inhibiting cyclooxygenase (COX) at the site of injury in the periphery, thus decreasing the formation of mediators of pain in the peripheral nervous system.
First Gen NSAIDs
aspirin/nonaspirin NSAIDs
Inhibit Cox-1 and Cox-2
alleviate mod/mild pain, suppress fever, relieve dysmenorrhea
Aspirin (ASA) AE
gastro effects (PPI may be used in high risk pts)
bleeding, renal impairment, salicylism, reye's syndrome, pregnancy, hypersensitivity rxn
Aspirin (ASA) Drug Interactions
anticoagulants: warfarin & heparin- increase risk of bleeding
Glucocorticoids: gastric ulcer
EtOH: gastric bleeding
Ibuprophen: reduce antiplatelet effect by binding site competition
ACE-I / ARBs: only when high dose ASA due to renal function impairment
Acute poisioning
NonASA 1st Generation
ibuprophen (every 4-6hrs)
naproxen (aleve) longer half life
NSAID interactions
anti-HTN meds
2nd Generation NSAIDs
Just as effective as traditional NSAIDs at suppressing inflammation and pain
Somewhat lower risk for GI side effects
Can impair renal function and cause hypertension and edema
Increase the risk for MI and stroke
celecoxib (celebrex)
fewer AE than first gen drugs.
CV risks= last choice drug for long term mgmt of pain
Uses: osteoarthritis, RA, acute pain, dysmenorrhea, FAP
celecoxib (celebrex) AE
dyspepsia, abdominal pain, renal toxicity
drug IA: May decrease diuretic effect of furosemide
May decrease antihypertensive effect of ACE inhibitors
May increase levels of lithium
acetaminophen (tylenol)
analgesic and antipyretic properties- but not anti-inflammatory.
drug of choice for kids, fever reduction
Does not cause gastric ulceration or suppresses platelet aggregation or cause renal impairment
Acetaminophen OD Tx
acetylcystine (mucomyst)
Acetaminophen toxic dose
max dose in grams is 3.325 in 24hrs
DMARD: methotrexate (rheumatrex)
1st choice for RA
works in 3-6wks
relatively safe, low cost, effective
SE: hepatic fibrosis, bone marrow suppression, ulceration, pneumonitis
watch liver, kidney, CBC labs!
etanercept (enbrel)
used for moderate to severe RA
AE: infection (serious), injection site rxn, TB, HF, Cancer, Live vacines
Hyperuricemia- uric acid = excess buildup or impaired excretion.
Stages: asymptomatic, acoute gouty attacks, intercritical, tophaceous
NSAIDS are first choice
inhibits leukocyte inflitration
Used for acute gouty arthritis, prophylaxis
SE: GI-N/V/D/pain occurs 80%
Precaution in elderly, cardiac, renal, GI, pregnacy
Allopurinol (Zyloprim)
inhibits uric acid production
Used for chronic tophaceous gout
SE: well tolerated, GI, neuro, cataracts; rarely hypersensitivity
Interactions: inhibits hepatic enzymes increasing on warfarin