pain meds Flashcards

1
Q

Ketorolac/Toradol class

A

NSAID

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2
Q

Ketorolac/Toradol MOA

A

blocks cyclooxygenase 1&2 inhibiting prostaglandin synthesis causing anti-inflammatory effects and analgesia effects

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3
Q

Ketorolac/Toradol PK

A

99%PB, onset 10min, peak 2-3 hours, e1/2 5HR- prolonged 5-8hr with elderly.liver conduction and 60% renal excretion unchanged

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4
Q

Ketorolac/Toradol Se

A

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

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5
Q

Ketorolac/Toradol CI

A

asthma, RF, ASA allergy, liver failure, GIB, coagulation problems, 3rd trimester, BLACK BOX- do not use post CABG

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6
Q

Ketorolac/toradol dose

A

30mg IV x1 or q6hr (daily max 120mg), don’t give longer then 5 days, decrease dose for elderly to 15mg

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7
Q

Acetaminophen/Tylenol class

A

antipyretic, analgesic, antiprostaglandin cenrally acting NSAID

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8
Q

Acetaminophen/Tylenol MOA

A

NMDA receptor blocker in CNS, blocks substance P in SC; desensitizes TRPA channels which transmit CA2+ and NA. lacks peripheral effects

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9
Q

Acetaminophen/Tylenol PK

A

c-max 15min, PO peaks 30-60min, conjugated and hydroxylated in the liver with little excreted unchanged in the urine

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10
Q

Acetaminophen/Tylenol SE

A

renal toxicity bc metabolites can acculate; od= liver failure, ulcers, can impair platelet function

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11
Q

Acetaminophen/Tylenol CI

A

liver and renal disease, decrease dose for alcoholic cirrhosis,

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12
Q

Acetaminophen/Tylenol dose

A

ig IV over 15 min q 4-6hr, 325-650mg PO-

4G max per day

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13
Q

opioid MOA

A

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.

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14
Q

Hydromorphone/Dilaudid- class

A

opioid agonist that is derivative of morphine that is 5x more potent than morphine

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15
Q

Hydromorphone/Dilaudid SE

A

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

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16
Q

Hydromorphone/Dilaudid CI

A

allergy, severy respiratory depression- COPD, asthma, wooden chest syndrome, decrease dose in elderly and/or hypovolemia

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17
Q

Hydromorphone/Dilaudid dose

A

1-4mg IV a4-6hr

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18
Q

Hydromorphone/Dilaudid PK

A

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

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19
Q

Morphine class

A

natural opioid agonist

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20
Q

Morphine PK

A

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.

21
Q

Morphine SE

A

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

22
Q

Morphine ci

A

respiratory depression, asthma/COPD, allergy, bronchospasm, decrease dose or give only 1 dose to RF pts bc the metabolites accumulate

23
Q

Morphine dose

A

1-5mg IV q2-5min

24
Q

Meperidine/Demoral class

A

phenyl-piperidine synthetic opioid agonist

25
Q

Meperidine/Demoral Pk

A

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

26
Q

Meperidine/Demoral Se

A

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

27
Q

Meperidine/Demoral CI

A

fatal interaction with MAOi’s, metabolite accumulates in renal disease; watch for CV disease, watch in neuro disease, allergy, sz history

28
Q

Meperidine/Demoral dose

A

12-.5- 50mg IV

max dose 1gm/day

29
Q

Fentanyl class

A

phenyl piperidine synthetic opioid agonist

30
Q

Fentanyl PK

A

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

31
Q

Fentanyl SE

A

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;

32
Q

Fentanyl CI

A

liver disease, watch in renal disease, head trauma, gallbladder disease, brady arrhythmias

33
Q

Fentanyl dose

A

bolus 15-50mcg; initial 1-3mcg/kg; infusion 0.01-0.05 mcg/kg/min

34
Q

sufentanil class

A

phenyl-piperidine synthetic opioid agonist= most potent opoid

35
Q

sufentanil PK

A

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

36
Q

sufentanil SE

A

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

37
Q

sufentanil CI

A

asthma, allergy, airway obstruction, decrease dose in elderly and hypovolemia

38
Q

sufentanil dose

A

initial 0.1mcg/kg; infusion- 0.001mcg/kg/mi

39
Q

alfentanil class

A

tetrazole fentanyl derivative that is a synthetic opid agonist

40
Q

alfentanil PK

A

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

41
Q

alfentanil SE

A

slows eeg, increases ICP, respiratory depression, no change to SVR, CO. SOO, pruritus, N/V/C, skeletal muscle rigidity

42
Q

alfentanil CI

A

untreated parkinson’s, increased ICP, respiratory depression, allergy

43
Q

alfentanil dose

A

initial 10-20mcg/kg; infusion 0.25–.75mcg/kg/min

44
Q

Remifentanil class

A

phenyl-piperidine synthetic opioid agonist with ester link

45
Q

Remifentanil PK

A

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

46
Q

Remifentanil SE

A

N/V/C delayed gastric emptying, SOO, dose dependent decrease hr bp; respiratory depression, dizziness, pruritus

47
Q

Remifentanil cI

A

do not use in epidural/spinals; need plan for post op pain control; allergy, respiratory depression

48
Q

Remifentanil dose

A

initial 1-2mcg/kg; infusion 0.05-0.25mcg/kg/min