Principles Opioids 3 Flashcards by Stacey Vernon

Most abundant alkaloid in raw opium

morphine

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sedation before analgesia

morphine

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Morphine- histamine release from mast cells causes:

local itching, redness, hives

enough histamine –> Decrease SVR/BP, tachycardia

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Doesn’t undergo 1st pass pulmonary uptake

morphine

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

M6G

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Morphine CV side effects

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

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N20 and morphine together

decrease CO, hypotension

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Morphine and benzos together

decrease SVR, hypotension

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

morphine

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Cough supression, decrease CBF, skel muscle rigidity

morphine

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

morphine

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Demerol (meperidine)– what receptors? structure resembles?

mu and kappa receptor agonist

resembles atropine

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

Demerol

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Demerol’s metabolite

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

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

demerol

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Associated with orthostatic hypotension, causes MYDRIASAS

demerol

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Serotonin syndrome:

Demerol with MAOIs and SSRIs,

HTN, tachycardia, hyperpyrexia, convulsions

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Fentanyl is a derivative of what

phenylpiperidine

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Fentanyl times/dose

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

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

fentanyl

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

fentanyl

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

decreased hepatic blood flow, decreased albumin production

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

Fentanyl advantages

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Fentanyl patch

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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Secondary peaks in fentanyl d/t

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

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

Fentanyl side effects

Sufentanil vs fentanyl potency and cont-sens T1/s

Sufentanil 5-10X more potent than fentanyl | CST1/2 less than fentanyl and alfentanil for infusions up to 8 hours

60% of initial dose goes through first pass pulmonary uptake

sufentanil

Sufentanil has smaller Vd d/t

extensive protein binding (92%)

Sufentanil excretion

metabolites excreted almost equally in urine and feces

Alfentanil onset and peak

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

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

alfentanil

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

Alfentanil

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

alfentanil

Alfentanil.....

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

Remifentanil- what receptor?

selective mu agonist

potency similar to fentanyl, BBB equil similar to alfentanil

remifentanil

Structure makes it susceptible to hydrolysis by esterases to inactive metabolites

remifentanil

Remifentanil times

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

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

remifentanil

Remifentanil metabolism

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

Remi CST1/2

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

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

Remifentanil

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

remi

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

remi

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

codeine "methylmorphine"

Codeine metabolism

Liver, to MORPHINE... excreted by kidneys

Codeine clinical uses

15mg- antitussive | 60mg- max analgesia

Why isn't IV codeine recommended?

Profound histamine release

Dilaudid is a derivative of what?

Morphine (5x more potent than morphine)

More sedation with less euphoria

Dilaudid compared to morphine

Oxymorphone (numorphan)

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

Methadone (dolophine) classification

synthetic opioid agonist

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

methadone

Methadone side effects:

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

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

Propoxyphene (darvocet)

Propoxyphene side effects

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

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

heroin

centrally acting analgesic, low affinity for mu receptors

tramadol

Tramadol analgesic effects

inhibits NE and serotonin neuronal uptake (facilitates serotonin release)

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

tramadol

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

partial agonist

Talwin (pentazocine) is a derivative of

benzomorphan

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

talwin

Talwin...

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

Miosis does not occur with

Talwin (pentazocine)

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

Stadol (butorphanol)

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

Stadol

Stadol eliminated in

bile

Most common side effect of Nubain

sedation

Nubain good for heart pts because...

does not increase BP, HR, PAP

Nubain withdrawal symptoms:

>pentozacine (talwin) but

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

Nubain

Buprenex (Buprenorphine) classification

agonist-antagonist

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

limits cephalad spread and delays resp depression

Respiratory depression from this drug may be resistant to narcan

buprenorphine

pulmonary edema can be precipitated by what drug?

buprenorphine

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

Nalorphine

Dalgon (dezocine)....

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

Pure mu opioid antagonists

naloxone, naltrexone, nalmephene

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

narcan

Narcan side effects

n/v, increased SNS, PULM EDEMA, VFIB

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

Naltrexone (Revia)

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

Nalmefene (revex)

Opioid agonist decrease MAC by

50-60%

opioid agonist-antagonist decrease MAC by

8-20%

Depends on dermatome that organ developed from

referred pain

Principles Opioids 3 Flashcards

(87 cards)