pain meds Flashcards
Ketorolac/Toradol class
NSAID
Ketorolac/Toradol MOA
blocks cyclooxygenase 1&2 inhibiting prostaglandin synthesis causing anti-inflammatory effects and analgesia effects
Ketorolac/Toradol PK
99%PB, onset 10min, peak 2-3 hours, e1/2 5HR- prolonged 5-8hr with elderly.liver conduction and 60% renal excretion unchanged
Ketorolac/Toradol Se
no respiratory or CV depression, impaired bone healing, GI bleed, ulcers, bonchospasm (increased leukotrines), ARF, increased bleeding time, can inhibit platelet function, chronic use increases likely hood for MI and stroke
Ketorolac/Toradol CI
asthma, RF, ASA allergy, liver failure, GIB, coagulation problems, 3rd trimester, BLACK BOX- do not use post CABG
Ketorolac/toradol dose
30mg IV x1 or q6hr (daily max 120mg), don’t give longer then 5 days, decrease dose for elderly to 15mg
Acetaminophen/Tylenol class
antipyretic, analgesic, antiprostaglandin cenrally acting NSAID
Acetaminophen/Tylenol MOA
NMDA receptor blocker in CNS, blocks substance P in SC; desensitizes TRPA channels which transmit CA2+ and NA. lacks peripheral effects
Acetaminophen/Tylenol PK
c-max 15min, PO peaks 30-60min, conjugated and hydroxylated in the liver with little excreted unchanged in the urine
Acetaminophen/Tylenol SE
renal toxicity bc metabolites can acculate; od= liver failure, ulcers, can impair platelet function
Acetaminophen/Tylenol CI
liver and renal disease, decrease dose for alcoholic cirrhosis,
Acetaminophen/Tylenol dose
ig IV over 15 min q 4-6hr, 325-650mg PO-
4G max per day
opioid MOA
activates g-coupled protein receptors on Mu1, Mu2, Kappa and Delta receptors located on the peripheral ends of primary afferent neurons to directly decrease transmission or inhibit the release of neurotransmitters increasing the pain threshold, altering pain perception and inhibiting ascending pain pathways. They mimic endogenous substances such as endorphins, enkephalins, and dynorphins at the opioid receptor resulting in presynaptic receptors to decrease neurotransmitter release such as ePI, NE, ACh, and substance p; postsynaptic effects include hyper polarization of the neuron because increase K conductance out of the cell and Ca2+ channel inactivation.
Hydromorphone/Dilaudid- class
opioid agonist that is derivative of morphine that is 5x more potent than morphine
Hydromorphone/Dilaudid SE
provides analgesia, euphoria, sedation, and no histamine release; can cause N/v/C, pruritus, dry mouth, respiratory depression, urinary retention, bradycardia, decrease sVr (dose dependent), tolerance with prolonged use
Hydromorphone/Dilaudid CI
allergy, severy respiratory depression- COPD, asthma, wooden chest syndrome, decrease dose in elderly and/or hypovolemia
Hydromorphone/Dilaudid dose
1-4mg IV a4-6hr
Hydromorphone/Dilaudid PK
8-19%PB, onset <30min IV, Peak 5-10min, DOA 4-5h, e1/2 1-3hr, significant 1st pass metabolism in liver with 95% metabolized to Hydromorophone-3-glucuronide (inactive) and excreted in the urine
Morphine class
natural opioid agonist