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
Morphine PK
pKa=7.9, 23% unionized, 30%PB, low lipid solubility; IV Peak 15-30min, redistributes in 3 min; DOA 3 hours, e1/2 3-4h, liver metabolism to morphine-3-glucoronide (less active) and morphine-6-glucoronide(active metabolite that is 650x’s more potent than parent) and excreted in the urine 1-12%unchanged and excreted in bile.
Morphine SE
Histamine release, decreases HR, BP, SVR, CO (these 4 are dose dependent), CBF, ICP, CO2 response curve and shifts to the right. Miosis. inhibits SA/AV node can lead to bradycardia, delayed respiratory depression in epidurals and spinals bc hydrophilic and takes a longer time to diffuse to the respiratory center in the brain. urinary retention, pruritus, N/V/C; increased risk of dependence and tolerance- Class 2 drug. SOO
Morphine ci
respiratory depression, asthma/COPD, allergy, bronchospasm, decrease dose or give only 1 dose to RF pts bc the metabolites accumulate
Morphine dose
1-5mg IV q2-5min
Meperidine/Demoral class
phenyl-piperidine synthetic opioid agonist
Meperidine/Demoral Pk
60%PB, fast onset, nonionized 10%, DOA 3h, low lipid solubility, redistributes in 4-16min, e1/2 3-5h, liver metabolism to normeperdine (e1/2 15h and 1/2 potency of parent and can cause sz, confusion, hallucinations, myoclonus), and excreted in urine, 65% pulmonary 1st pass effect
Meperidine/Demoral Se
histamine release, decreases shivering; increases HR and direct cardiac depression, increases ICP, dry mouth, urinary retention, N/V/C, increased risk of tolerance and dependence
Meperidine/Demoral CI
fatal interaction with MAOi’s, metabolite accumulates in renal disease; watch for CV disease, watch in neuro disease, allergy, sz history
Meperidine/Demoral dose
12-.5- 50mg IV
max dose 1gm/day
Fentanyl class
phenyl piperidine synthetic opioid agonist
Fentanyl PK
80%PB, nonionized <10%; highly lipid soluble- Vd=4L/kg, effect site 6.4min; redistributes in 13min, short DOA 1hr, e1/2 3-6h, liver metabolism that is dependent on HBF and excreted in the urine, 75%pulmonary 1st pass effect, long context sensitive 1/2 time
Fentanyl SE
respiratory depression, sz, wooden chest syndrome, delayed gastric emptying, ADH release, SOO spasm, N/V/C, pruritus, dose dependent decrease in HR, BP, CO, SVR;
Fentanyl CI
liver disease, watch in renal disease, head trauma, gallbladder disease, brady arrhythmias
Fentanyl dose
bolus 15-50mcg; initial 1-3mcg/kg; infusion 0.01-0.05 mcg/kg/min
sufentanil class
phenyl-piperidine synthetic opioid agonist= most potent opoid
sufentanil PK
93%PB, highest lipid solubility; 20%nonionized, effect site 6.2min, short DOA- 30min, redistributes in 17min, e1/2 2.5h, liver and SI metabolism, excreted in urine 1%unchanged, 75% pulmonary 1st pass effect
sufentanil SE
hypotension, brady, cardiac arrest, potent respiratory depression, bronchospasm, wooden chest syndrome, muscle ridgidity, SOO, N/V/C, good for cardiac surgery; urinary retention, pruritus, dose dependent decrease in HR, BP, SVR, and CO; can cause dependence and tolerance
sufentanil CI
asthma, allergy, airway obstruction, decrease dose in elderly and hypovolemia
sufentanil dose
initial 0.1mcg/kg; infusion- 0.001mcg/kg/mi
alfentanil class
tetrazole fentanyl derivative that is a synthetic opid agonist
alfentanil PK
90%PB, 90%unionized, onset 1-2min, effect site 1.4min, short DOA 30-60 min, e1/2 90min, high lipid solubility so little accumulates in the tissues; metabolized in the liver and SI and leaves the plasma in 30min
alfentanil SE
slows eeg, increases ICP, respiratory depression, no change to SVR, CO. SOO, pruritus, N/V/C, skeletal muscle rigidity
alfentanil CI
untreated parkinson’s, increased ICP, respiratory depression, allergy
alfentanil dose
initial 10-20mcg/kg; infusion 0.25–.75mcg/kg/min
Remifentanil class
phenyl-piperidine synthetic opioid agonist with ester link
Remifentanil PK
80%PB, 67%non-ionized, high lipid solubility, onset 1-3min, very short DOA 10min, effect site 1.4min, metabolized by tissue plasma esterase’s- not affected by cholinesterase deficiency
Remifentanil SE
N/V/C delayed gastric emptying, SOO, dose dependent decrease hr bp; respiratory depression, dizziness, pruritus
Remifentanil cI
do not use in epidural/spinals; need plan for post op pain control; allergy, respiratory depression
Remifentanil dose
initial 1-2mcg/kg; infusion 0.05-0.25mcg/kg/min
