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pharmacology 4810 > opioids MT1 > Flashcards

opioids MT1 Flashcards

1
Q

this is an unpleasant sensory and emotional experience with actual or potential tissue damage or described in terms of such damage

A

pain

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2
Q

the absence of pain

A

analgesia

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3
Q

this type of pain is caused by tissue damage

A

nociceptive pain

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4
Q

this type of pain is caused by nerve damage

A

neuropathic pain

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5
Q

these are nerve endings that detect damaging mechanical, thermal and chemical stimuli. they are found on the skin, on internal surfaces such as the periosteum, joint surfaces and in some internal organs

A

nociceptors

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6
Q

this is a physiological process by which stimuli that are associated with tissue damage activate neural pathways. the nervous systems processing information received by nociceptors

A

nociception

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7
Q

what are the four stages of the nociceptive circuit

A
  • transduction
  • transmission
  • modulation
  • perception
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8
Q

following an injury, a variety of chemicals are released and act on nociceptors. these chemicals include

A
  • bradykinin
  • serotonin
  • histamine
  • prostaglandins
  • leukotrienes
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9
Q

noxious stimuli is received via a nociceptor and transducer into electrical signals that are transmitted to the spinal cord. ____________ and _____________ are excitatory neurotransmitters found at these synapses and are released. from there the stimuli travels up the spinal cord to the thalamus and other various cortical structures (somatosensory cortex, insula, anterior cingulate cortex, or the prefrontal cortex)

A

glutamate and aspartate

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10
Q

from the cortical structures, descending modulatory signals project downward and modulate the signal at the level of the dorsal root ganglion and spinal cord. _________ and _______ are key inhibitory neurotransmitters found at the supra-spinal and spinal level. the net effect of this pathway produces an individuals perception of pain and their overall pain experience

A

GABA and glycine

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11
Q

this is when innocuous stimuli are detected as painful; pain due to a stimulus that does not normally provoke pain (e.g. a light feather touch causing pain)

A

allodynia

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12
Q

this is an exaggerated response to noxious stimuli (e.g. feeling intense, excruciating pain when touching a recently burned area of skin or a hangnail)

A

hyperalgesia

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13
Q

the site of action of these medications is (peripheral, supraspinal or spinal)
- lidocaine
-oxcarbazepine
-capsaicin
-anti-ngf
-anti-cgrp
-nsaids
-BoNT-A

A

peripheral

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14
Q

the site of action of these medications is (peripheral, supraspinal or spinal)
- gabapentin/pregabalin
- opioids
- NMDA blockers
- TCAs
- SNRI
- clonidine

A

spinal

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15
Q

the site of action of these medications is (peripheral, supraspinal, or spinal)
- gabapentin/pregabalin
- opioids
-TCA
-SNRI

A

supraspinal

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16
Q

this is an analgesic that affects the GABA receptor

A

pregabalin/gabapentin

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17
Q

what is the MOA of pregabalin/gabapentin

A

modulates hyper excited neurons
- drug binds to presynaptic neuron at the alpha2-delta subunit of the voltage gated calcium channels
- when the drug binds = reduced calcium influx
- less calcium PREVENTS DEPOLARIZATION = less release of excitatory neurotransmitters (e.g. glutamate, substance P, noradrenaline)

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18
Q

What are some side effects of pregabalin/gabapentin

A

drowsiness, dizziness, dry mouth, headache, constipation, nausea, difficulty concentrating, weight gain

19
Q

what is the MOA of both TCA’s and SNRI’s

A

block the reuptake of serotonin and NE in the synaptic cleft (mechanism of pain relief is unknown)

20
Q

the brainstem centers that provide noradrenic input are thought to be pain inhibitory. the ____________ contains the greatest amount of noradrenergic neurons in the brain and is described as a pain suppressor. the noradrenic neurons of this project to the spinal dorsal horn, release NE to inhibit pain transmission

A

locus ceoruleus (LC)

21
Q

the two functions of increasing levels of this neurotransmitter are
- inhibits neuropathic pain through the alpha-adrenergic receptors
- acts on the LC and improves the function of an impaired descending noradrenergic inhibitory system

A

norepinephrine

22
Q

what are some adverse effects of TCAs

A

blurred vision, drowsiness, dry mouth, nausea, orthostatic hypotension, weight gain, cognitive impairment, constipation, urinary retention, arrythmias (antihsitamine and anticholinergic effects)

23
Q

what are some adverse effects of SNRI

A

drowsiness, insomnia, nausea, dry mouth, dizziness, constipation, excessive sweating

24
Q

this is a hormone like chemical in the body that contributes to inflammation, pain and fever by raising temperature and dilating blood vessels, which causes redness, swelling in the place where they are released

A

prostaglandins

25
Q

NSAIDs block _______ which plays a key role in makings prostaglandins thus NSAIDs help relieve pain

A

COX-1 and/or 2

26
Q

what are some adverse effects of NSAIDs

A

GI (ulceration, bleeding, dyspepsia) - more common in nonselective NSAIDs
hypertension
kidney damage
increased risk of MI/stroke (celecoxib)

27
Q

when NSAIDs inhibit _____, platelet aggregation is decreases and increases risk of bleeding

A

COX 1

28
Q

this NSAID has less GI bleeding risk than non selective NSAIDs

A

celecoxib (COX2 selective)

29
Q

this is any compound that binds to opiate receptors

A

opioid

30
Q

opioids attach to ________ on nerve cells in the brain, spinal cord, gut and other parts of the body: this blocks pain messages sent from the body through the spinal cord to the brain

A

G-protein coupled opioid receptor

31
Q

G-protein-coupled opioid receptors also bind endogenous opioid peptides known as ________ which ar einvolved in pain modulation

A

endorphines

32
Q

this type of opioid receptor is responsible for analgesia

A

mu receptor

33
Q

what is the MOA for analgesia for opioids

A
  • opioids inhibit adenylyl cyclase (decreases cAMP)
  • activate potassium efflux (increased post synaptic potassium)
  • suppresses calcium conductance (decreased presynaptic calcium)
  • inhibits neurotransmitter release (substance P0

overall it causes hyper polarization of the neuron making it LESS sensitive to excitatory neurons

34
Q

this class of opioid fully activates the opioid receptor, higher doses produce greater activation in a dose-dependant matter (e.g. morphine, oxycodone, methadone)

A

full agonist

35
Q

this class of opioid has low intrinsic activity with a ceiling on agonist activity. increasing the dose will only increase the effects to a certain level and further doses do not increase the effect (e.g. buprenorphine)

A

partial agonist

36
Q

this class of opioid occupies the receptor but does not activate, can reverse the effect of mu opioid agonists (naloxone, naltrexone)

A

antagonist

37
Q

what opioids have relatively long half lives

A

methadone and buprenorphine

38
Q

true or false: opioid receptors are widely distributed in both CNS and PNS

A

true

39
Q

what are some side effects of opioids

A
  • constipation
  • drowsiness/dizziness
  • headache
  • N/V
  • flushing/sweating
40
Q

this occurs when an opioid is used on a regular basis, and the brain adjusts so the effects of the same amount of drug become less over time

A

tolerance

41
Q

what are the two theories that explain tolerance

A
  1. opioid receptors may become less sensitive to the drug
  2. neurons may remove opioid receptors from the cell wall thus less receptors available for binding
42
Q

this is a neurobehavioral disorder characterized by a repeated compulsive seeking or use of an opioid medication. it is accompanied by well-described physical dependance with a withdrawal syndrome and tolerance

A

dependance

43
Q

why does someone become dependant with opioids

A

opioids increase dopamine in the reward pathways of the brain by inhibiting the release of GABA (inhibitory neurotransmitter)

44
Q

what are some symptoms of withdrawal

A
  • N/V/D
  • sweating
  • tremor
  • shivering
  • anxiety

pharmacology 4810 (12 decks)

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