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Pharmacology > Principles Opioids 3 > Flashcards

Principles Opioids 3 Flashcards

1
Q

Most abundant alkaloid in raw opium

A

morphine

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2
Q

sedation before analgesia

A

morphine

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3
Q

Morphine- histamine release from mast cells causes:

A

local itching, redness, hives

enough histamine –> Decrease SVR/BP, tachycardia

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4
Q

Doesn’t undergo 1st pass pulmonary uptake

A

morphine

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5
Q

Morphine metabolite thats 100x more potent than morphine, mu receptor agonist

A

M6G

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6
Q

Morphine CV side effects

A

Brady then reflex tachy, direct depressant of SA node, hypotension from histamine release, decreases sympathetic venous tone of peripheral veins

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7
Q

N20 and morphine together

A

decrease CO, hypotension

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8
Q

Morphine and benzos together

A

decrease SVR, hypotension

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9
Q

Stim of mu 2 receptors affect ventilatory centers, decreased response to C02 (right shift and down)

A

morphine

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10
Q

Cough supression, decrease CBF, skel muscle rigidity

A

morphine

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11
Q

direct stimulation of CTZ, s. Oddi/biliary/GI smooth muscle spasm, constipation, decrease detrusor tone, increase spincter tone, cutaneous vessels dilate

A

morphine

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12
Q

Demerol (meperidine)– what receptors? structure resembles?

A

mu and kappa receptor agonist

resembles atropine

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13
Q

Well absorped from GI tract, hepatic metabolism, urinary excretion is pH dependent

A

Demerol

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14
Q

Demerol’s metabolite

A

Normeperidine (1/2 as potent) accumulates causes CNS excitation, seizures, delirium

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15
Q

suppress shivering by stimulating kappa receptors, high doses = neg cardiac inotropic effects and histamine release, does NOT block cough

A

demerol

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16
Q

Associated with orthostatic hypotension, causes MYDRIASAS

A

demerol

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17
Q

Serotonin syndrome:

A

Demerol with MAOIs and SSRIs,

HTN, tachycardia, hyperpyrexia, convulsions

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18
Q

Fentanyl is a derivative of what

A

phenylpiperidine

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19
Q

Fentanyl times/dose

A

Onset 2-5 min
Peak 20-30 min
Duration 30m-1hr
Dose: 2-150mcg/kg

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20
Q

75% of initial dose undergoes first-pass pulmonary uptake, rapid? redistribution into inactive tissues

A

fentanyl

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21
Q

Peripheral becomes saturated with prolonged infusions, increase context sensitive T1/2 d/t metabolized drug replaced by tissue reservoir drug

A

fentanyl

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22
Q

Prolonged T1/2 in elderly d/t to (fentanyl)

A

decreased hepatic blood flow, decreased albumin production

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23
Q

Not a cardiac depressant, no histamine release, suppresses stress response to surgery

A

Fentanyl advantages

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24
Q

Fentanyl patch

A

24 hrs for blood conc to stabilize, subQ must be saturated before absorbed into blood, once removed… 17 hour T1/2

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25
Q

Secondary peaks in fentanyl d/t

A

ion trapping (acidic gastric fluid), washout from lungs as VQ relationships resume

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26
Q

Modest increase in ICP despite unchanged C02, usually with decreases in MAP and CPP, decreases cerebral metabolism

A

Fentanyl side effects

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27
Q

Sufentanil vs fentanyl potency and cont-sens T1/s

A

Sufentanil 5-10X more potent than fentanyl

CST1/2 less than fentanyl and alfentanil for infusions up to 8 hours

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28
Q

60% of initial dose goes through first pass pulmonary uptake

A

sufentanil

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29
Q

Sufentanil has smaller Vd d/t

A

extensive protein binding (92%)

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30
Q

Sufentanil excretion

A

metabolites excreted almost equally in urine and feces

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31
Q

Alfentanil onset and peak

A

immediate.. d/t low pKa and 90% being non-ionized

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32
Q

Renal failure does not alter clearance, cirrhosis prolongs half life, 10% initial dose first pass pulmonary uptake

A

alfentanil

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33
Q

Effects prolonged with erythromycin use, alterations in P450 slow metabolism, smaller Vd, longer CST1/2, decreases dopamine transmission

A

Alfentanil

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34
Q

peripheral distribution is not a contributor to decrease in plasma conc after D/C

A

alfentanil

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35
Q

Alfentanil…..

A

15mcg/kg blunts BP and HR response to intubation, 30mcg/kg blunts catecholamine resposne

36
Q

Remifentanil- what receptor?

A

selective mu agonist

37
Q

potency similar to fentanyl, BBB equil similar to alfentanil

A

remifentanil

38
Q

Structure makes it susceptible to hydrolysis by esterases to inactive metabolites

A

remifentanil

39
Q

Remifentanil times

A

onset and peak = 1 min
duration 5-10 min
T1/2 = 6 min

40
Q

Small Vd, rapid clearance with low variability, less accumulation, great for kidney/liver pts

A

remifentanil

41
Q

Remifentanil metabolism

A

Nonspecific plasma and tissue esterases to inactive metabolites that undergo renal excretion

42
Q

Remi CST1/2

A

independent of duration of infusion, 4 min, short d/t lack of accumulation

43
Q

Less risk of respiratory depression, not given neuraxial, profound anes for transient use, wake up test

A

Remifentanil

44
Q

No change in ICP or intraocular pressure, decrease CBF similar to other opioids

A

remi

45
Q

large doses or rapid IVP can cause skel muscle rigidity….. n/v, resp depression, hypoT, brady

A

remi

46
Q

Limited first pass hepatic metabolism– substitution of methyl group for hydroxyl group

A

codeine “methylmorphine”

47
Q

Codeine metabolism

A

Liver, to MORPHINE… excreted by kidneys

48
Q

Codeine clinical uses

A

15mg- antitussive

60mg- max analgesia

49
Q

Why isn’t IV codeine recommended?

A

Profound histamine release

50
Q

Dilaudid is a derivative of what?

A

Morphine (5x more potent than morphine)

51
Q

More sedation with less euphoria

A

Dilaudid compared to morphine

52
Q

Oxymorphone (numorphan)

A

10x potency of morphine, more n/v and dependence

53
Q

Methadone (dolophine) classification

A

synthetic opioid agonist

54
Q

20mg IV can produce p/o analgesia for 24 hours

A

methadone

55
Q

Methadone side effects:

A

vent depression, miosis, constipation, biliary spasm, less euphoria and sedation than morphine

56
Q

Structurally similar to methadone, does not possess antipyretic, anti-inflammatory or antitussive effects, T1/2 is 14 hours

A

Propoxyphene (darvocet)

57
Q

Propoxyphene side effects

A

vertigo, sedation, n/v, IV use damages veins, OD resp depression/seizures

58
Q

Synthetic opioid, acetylation of morphine, rapid entrance into CNS d/t lipid solubility and chem structure… lack of nausea, greater dependency than morphine

A

heroin

59
Q

centrally acting analgesic, low affinity for mu receptors

A

tramadol

60
Q

Tramadol analgesic effects

A

inhibits NE and serotonin neuronal uptake (facilitates serotonin release)

61
Q

high n/v, chronic pain, no tolerance/addiction, seizures?

A

tramadol

62
Q

binding affinity same for both drugs but max response is significantly less

A

partial agonist

63
Q

Talwin (pentazocine) is a derivative of

A

benzomorphan

64
Q

Opioid agonist effects on delta and kappa…and weak antagonist effects

A

talwin

65
Q

Talwin…

A

can cause dependence, well absorbed PO or IV, extensive 1st pass metabolism, dysphoria

66
Q

Miosis does not occur with

A

Talwin (pentazocine)

67
Q

Resembles talwin, agonist effects are 20xgreater, antagonist effects 10-30x greater
Low affinity for mu receptors to produce antagonism

A

Stadol (butorphanol)

68
Q

Moderate affinity for kappa receptors.. analgesia and antishivering
Minimal affinity for sigma (dysphoria is low)

A

Stadol

69
Q

Stadol eliminated in

A

bile

70
Q

Most common side effect of Nubain

A

sedation

71
Q

Nubain good for heart pts because…

A

does not increase BP, HR, PAP

72
Q

Nubain withdrawal symptoms:

A

> pentozacine (talwin) but <morphine

73
Q

antagonist effects at mu receptors could help reverse lingering resp depression while still managing analgesia

A

Nubain

74
Q

Buprenex (Buprenorphine) classification

A

agonist-antagonist

75
Q

Buprenorphine in epidural: high lipid solubility and affinity for opioid receptors….

A

limits cephalad spread and delays resp depression

76
Q

Respiratory depression from this drug may be resistant to narcan

A

buprenorphine

77
Q

pulmonary edema can be precipitated by what drug?

A

buprenorphine

78
Q

equally potent as morphine, not used d/t high incidence of dysphoria

A

Nalorphine

79
Q

Dalgon (dezocine)….

A

comparable to morphine, elim through urine, has ceiling effect: resp depression, high affinity for mu1 and moderate affinity for delta receptors

80
Q

Pure mu opioid antagonists

A

naloxone, naltrexone, nalmephene

81
Q

Promptly reverses analgesia and respiratory depression, use gtt for neuraxial opioids

A

narcan

82
Q

Narcan side effects

A

n/v, increased SNS, PULM EDEMA, VFIB

83
Q

Has sustained antagonism for 24 hours, highly effective PO, good for tx addicts

A

Naltrexone (Revia)

84
Q

Equal potent to narcan but longer duration, metabolized by hepatic conjugation

A

Nalmefene (revex)

85
Q

Opioid agonist decrease MAC by

A

50-60%

86
Q

opioid agonist-antagonist decrease MAC by

A

8-20%

87
Q

Depends on dermatome that organ developed from

A

referred pain

Pharmacology (3 decks)

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