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!!!!! Summer Pharm !!!!! > Opioids - Review, General info > Flashcards

Opioids - Review, General info Flashcards

1
Q

firing of a neuron that is not indicative of of physical damage, but is a pathalogical firing

A

Neuropathic pain

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2
Q

Pain out of proportion to noxious stimuli

A

Hyperalgesia

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3
Q

Pain evoked by a non-noxious stumuli

A

Allodynia

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4
Q

pain with no apparent stimuli - it is NERVE pain

A

spontaneous pain

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5
Q

Peripheral nociceptive neuron activated by intense noxious stimimuli (tissue damage) via

A

* Mechanical * thermal * chemical

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6
Q

slow conduction, dull, burning, diffuse

A

non-mylinated C fibers

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7
Q

fast conduction - sharp and well localized

A

A-delta fibers

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8
Q

nociceptiv impulse depends on the balance between

A

excitatory and inhibatory receptors

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9
Q

excitatory cation channel activated by: * Protons * heat * capsaisin * Endovanilloids

A

TRIP1

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10
Q

hyperpolarization related to opioid receptor activation

A

cells will need a stronger stimulus to fire

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11
Q

promotes depolarization and stimulates pain

A

Bradykinin and Prostaglandins

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12
Q

Area of dorsal horn that is very rich in opioid peptides and receptors

A

substantia geletinosa

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13
Q

Lamina for A delta fibers

A

Lamina I and V

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14
Q

Lamina for C fibers

A

Lamina II and III (substantia gelatinosa)

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15
Q

Located in lamina II and III

A

Substantia gelatinosa

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16
Q

where do opioids act at the brain level

A

pre and post synaptically to activate descending inhibatory pathways

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17
Q

where do opioids act at the spinal cord level

A

work directly on the dorsal horn of the spinal cord

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18
Q

where do opioids act at the periphery level

A

act on peripheral teminals of nociceptive neurons

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19
Q

why is the perception of noxious stimuli not the same as pain?

A

it is lacking the emotional component

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20
Q

Opioids can change patients ___ without necessarily changing the patients ability to _____ noxious stimuli

A

* tolerance of pain * perceive ie- they can still tell you where the wound is

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21
Q

The main use of opioids on anestehsia

A

Attenuate the SNS response to noxious stimuli- Laryngoscopy

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22
Q

opoids and inhaled anesthetics

A

act as an adjunct allowing for less use of inhaled agent

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23
Q

natrurally occuring drugs derrived from opium from the poppy plant

A

Opiate * Morphine * Codeine

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24
Q

Opioids produce analgesia without loss of

A

* Touch * Propioception * Conciousness

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25
Q

naturally occuring opioids

A

Morphine

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26
Q

semisynthetic: analogs of morphine

A

heroine dihydromorhone codeine

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27
Q

Synthetic Opioids

A

* Exogenous Has 4 classifications * agonist * partial aginist * mixed agonist/antagonist * antagonist

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28
Q

Synthetic antagonist

A

Narcan

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29
Q

can reach maximum eficacy on dose response curve their potency is what varries

A

Synthetic agonists (full)

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30
Q

will have a ceiling effect cannot reach maximum effect on dose response curve

A

Synthetic partial agnosts

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31
Q

Synthetic opioid agonist / antagonist

A

agonist at kappa receptors antagonist and mu receptors

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32
Q

if their is any potential you will need to switch to a full agonist you want to start with

A

a parial agonist and NOT an agonist / antagonist

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33
Q

Opioids - Mechanism of action

A

Activate stereo-specific G-protein coupled receptors and act post-synaptically to directly decrease neurotransmission by: increase K conductance (hyperpolarization) and Ca++ channnel inactivation (decreased NT release), inhabition of adenylate cyclase (decreased cAMP) Modulation of phospinositide- signaling cascade for phospholipase C increase MAP kinase which affects gene expression and increases phospholipase A2 (increase in leukotriens) and act Pre synaptically Decrease ACh, dopamine, norepi and Substance p release *anytime you hyperpolarize a membrane you decrease NT release*

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34
Q

anytime you hyperpolarize a cell you

A

decrease neurotransmitter release

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35
Q

Opioids PRE-synaptic mechanism of action

A

inhibits the release of excitatory neurotransmitters * ACh * Dopamine * Norepi * Substance P

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36
Q

Opioid receptors

A

* Mu (agnoist binding site) * Kappa (antagonist binding site) * Delta

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37
Q

All endogenous and exogenous opiois agonists work at these receptors

A

Mu-1 and Mu-2

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38
Q

May actually cause immunosupression and accelerate some types of cancer

A

Mu-3

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39
Q

Mu receptors location

A

* brain- supraspinal * spinalcord * periphery

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40
Q

Mu 1 site of analgesia

A

Supraspinal is thought to be the principal site of action but also works at spinal cord in a lesser degree (and periphery)

41
Q

Mu-1 receptor activation causes

A

cardio - bradycardia no respiratory effects CNS effects: euphoria, sedation, prolactin release, hypothermia, catalepsy, indifference to environmental stimuli Pupil - miosis no Gi effects GU - urinary retention no pruritus low abuse potential

42
Q

Mu-2 receptor activation effects

A

cardio - bradycardia respiratory - depression ->hypoventilation CNS: euphoria, pruritus, dopamine turnover, possible growth hormone release pupils - miosis GI - inhibition of peristalsis (constipation), nausea, vomiting GU - urinary retention Physical dependence

43
Q

Mu 2 analgesia

A

principal site of action is the spinal cord (but also has some supruaspinal action as well)

44
Q

kappa receptor analgesia

A

supraspinal, spinal

45
Q

kappa receptor endogenous agonists

A

dynorphins

46
Q

Kappa receptor activation effects

A

no cardio effects respiratory - possible depression ->hypoventilation CNS: sedation, dysphoria, hallucinations, delirium pupils - miosis GU - diuresis (inhibition of vasopressin release) Low physical dependence (low potential abuse)

47
Q

Delta receptor endogenouas ligand

A

enkephalin

48
Q

delta receptor analgesia

A

supraspinal, spinal modulates mu receptor activity

49
Q

Delta receptor activation

A

no cardio respiratory - depression ->hypoventilation no CNS effects GI - minimal inhibition of peristalsis (some constipation) GU - urinary retention Pruritus Physical dependence

50
Q

Located on Chromosome 6q24-q25

A

Mu opoid receptor

51
Q

aspartated in place of asparagine 10-20% of the population

A

* Nucleotide 118 polymorphism * Gene Effects agonist binding to Mu receptor

52
Q

valine in place of alanine 1-10% of population

A

* Nucleotide 17 polymorphism * Gene Effects agonist binding to Mu opioid receptor

53
Q

Codine has unpredictable pharmacokinetics and half lives due to

A

CYP2D6 gene polymorphisms

54
Q

Opioid least likely to be impacted by genetic variability. Predictable pharmacokinetics.

A

Fentanyl

55
Q

side effect rate can be influenced by ….

A

The rate of metabolism

56
Q

Ultra-rapid metabolizers are at risk for

A

PONV

57
Q

Opioids and Perioperative cardiovasucular effects (4)

A

Minimal impairment of CV function but has additive effect with other analgesics profound vasodilation/ decrease SVR- most evident in patients with hypovolemia Dose dependant bradycardia- via vagal stimulation (nuclei in medula) and Direct SA/AV nodal depression Impairmennt of SNS response and baseline tone orthostatic hypotension that is pronounced with hypovolemia

58
Q

morphine and meperedine and cardiovascular effects

A

Have a dose dependant histamine release * risk more vasodilation - decreased BP and SVR * risk bronchospasm

59
Q

Why is meperidine an exception to the CV effects of opioids

A

It will cause tachycardia - due to its atropine like structure

60
Q

When a large dose of opioids are given and the BP drops what is it likely due to?

A

Hypovolemia with vasodilation it is NOT likely a contractility isusse, Opioids are pretty cardiac stable

61
Q

Opioids and HR

A

Dose dependant bradycardia * Central vagal stimulation * act directly on SA/AV nodal depression

62
Q

Opioids and vasculature

A

Vasodilation/ Decreased SVR * decreased SNS response and baseline tone decreased CO and venous pooling = orthostatic hypotension * Pronounced effect on vasculature

63
Q

What opiods do we want to avoid in astmatics? Why?

A

Morphine and meperidiene- dose and infusion rate dependant histamine release causes more vasodilation and BRONCHOSPASM

64
Q

Do opioids produce amnesia

A

No

65
Q

Opioids and patients with increased ICP

A

*minimal decrease in ICP * Must have ventilations controlled prior to giving opioids * Hypoventilation and Increased CO2 will cause cerebral vasodilation and increased ICP

66
Q

Opioids and urination

A

Increased Uregency and reduced ability to void * Increased tone and peristaltic activity of ureter * incresed tone of detrusor

67
Q

Why do opioids cause nausea and vomiting

A

* decreased gastric emptying * stimulation of chemoreceptor zone of the 4th ventricle * balanced depression of medulary vomiting center

68
Q

Puritis and Opioids

A

cause is unknown, could be the histamine release with morphine and meperidine, but fentanyl it is unknown (fentanyl nose itch)

69
Q

drugs that cause adverse affect: muscle rigidity in chest, abdomen, jaw and extremeties

A

* Fentanyl * Sufentanyl * Hydromorphone (Dilaudid)

70
Q

issues with adverse affect: muscle rigidity from opioids

A

High airway pressures from increased intrathoracic pressure and decreased veonus return difficult/impossible to ventilate only releived my non-depolarizing muscle relaxant glottic rigidity and closure reported

71
Q

Smaller dose of opioids - respiratory effects

A

Increased Tidal voume and decreased RR Increased CO2 and decrease O2

72
Q

Larger dose of opioids

A

Decreased TV and Decreased RR

73
Q

ventilatory effects of opioids

A

Dose dependant respiratory depression Decreased chest wall compliance constriction of pharyngeal and laryngeal muscles cough suppression Dramatically decreased response to hypercarbia and hypoxia

74
Q

Factors that increase the magnitude and duration of opioid induced respiratory depression

A

higher doses Intermittent boluses have higher degree of respiratory depression than contiuous infusion Speed of injection Concurrent admin with other anesthetics Decreased clearance (active metabolites build up) Age - older and younger alkalosis - opioid are weak bases secondary peaks in plasma levels from reuptake from muscle, fat, lung and intestines

75
Q

Morphine active metablolite

A

morphine-6-glucuroninde

76
Q

prodrug- active form is morphine

A

Codeine (3-methylpmorphine)

77
Q

Long plasma half life 8-59 hours or 13-100, sources vary * High variability among individuals

A

Methadone

78
Q

How long does it take to develop tolerance to opioids?

A

48 hours - need to taper

79
Q

effects of tolerance

A

reduction of adverse effects (less respiratory, nausea and CNS side effects) shorter duration of analgesia decrease in effectiveness does not work

80
Q

What side effect dies NOT go away with tolerance

A

Constipation - a stimulant laxative w/ or without stool softener should be started early in treatment

81
Q

Neuralaxial analgesia (diffusion)

A

Cross the dura onto mu receptors to the substantia geletinosa difuses into the vasculature to get systemic effect

82
Q

given neuroaxial: very lipid soluable

A

fentanyl

83
Q

Given neuroaxial: very water soluable - will circulate with CSF

A

Morphine

84
Q

Opioids in the epeidural space may diffuse into * _______ * _______ * _______

A

* fat * systemic absorbtion (vasculature) * CSF

85
Q

Cephalad movemnt of opioid in CSF depends on ____________.

A

Lipid solubility

86
Q

lipid solubility and migration of neuroaxial opioids

A

more lipid soluble = limited migration, penetrates the dura more readily and has quicker peak in CSF/systemic concentration; resp depression seen immediately or early on Less lipid soluble = will remain in CSF for transfer to cephalad location; resp depression not seen until hrs later

87
Q

Why is the dose for an epidural 5x higher than that for a spinal?

A

Because the spinal is directly at the site

88
Q

side effects with neuraxial opioids

A

ventilatory depression pruritus N/V urinary retention

89
Q

This can be given to treat muscle rigidity from opioids

A

NDMRs

90
Q

What should you do if you see a localized reaction at the site of morphine injection?

A

DON’T PANIC Morphine causes histamine release, so this is a common reaction

91
Q

These meds can be used to relieve sphincter of oddi spasm

A

Glucagon, nubain, and NTG

92
Q

Opioids are weak (acids/bases)

A

Bases

93
Q

Vd is related to

A

Lipid solubility and protein binding

94
Q

A large Vd will equate to a long or short DOA?

A

Long

95
Q

Do opioids produce amnesia?

A

NO

96
Q

How do opioids produce bradycardia?

A

Vagal stimulation and inhibition of the SA node

97
Q

The bradycardia and ventilatory depression caused by opioids are

A

dose dependent

98
Q

Where do agonists/antogonists work?

A

They are Mu antagonists and full or partial kappa agonists

!!!!! Summer Pharm !!!!! (17 decks)

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