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20003 > opioids and analgesics > Flashcards

opioids and analgesics Flashcards

1
Q

what is pain

A

unpleasant sensory and emotional experience associated with actual or potential tissue damage

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2
Q

what are the stages of the ascending pain pathway

A
  1. neurotransmitters released by stimuli
  2. action potential created on the nerve terminal
  3. this is conducted along the sensory neurone from periphery to spinal neurone
  4. sodium channels open causing depolarisation
  5. impulse reaches nerve terminal and nociceptor neurotransmitters are released
  6. communicated with 2nd order neurone by activating their receptors
  7. synapse then communicates with 3rd order neurone in cortex
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3
Q

what are the fibres in the first order pain afferents

A
  • a-delta fibres
  • c fibres
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4
Q

what is the dull pain pathway called

A

palaeospinothalamic pathway

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5
Q

what is the sharp pain pathway called

A

neospinothalamic pathway

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6
Q

what are the properties of a fibers

A
  • high conduction speed
  • transmit proprioception, stretch, touch, pain, mechanical stimuli
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7
Q

what are the properties of c fibers

A
  • slow conduction speed
  • respond to thermal stimuli
  • unmyelinated
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8
Q

what are the properties of a alpha fibers

A
  • myelinated
  • proprioception
  • fastest a fibre conduction
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9
Q

what are the properties of a beta fibres

A
  • myelinated
  • stretch
  • skin touch
  • pain
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10
Q

what are the properties of a delta fibers

A
  • myelinated
  • slowest of a fibre conduction
  • acute pain and pressure
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11
Q

what are the 2 modulations of pain transmission

A
  • gate control system
  • descending inhibitory neurones
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12
Q

how does the gate control system work

A
  • sensory stimuli to the spinal cord, primary afferent pathway
  • mechanical stimuli to primary afferent
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13
Q

how is mechanical stimuli transmitted

A
  • stimulate inhibitory interneuron
  • these inhibit impulse from higher primary afferent neurones
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14
Q

how does the descending inhibitory neurones modulate pain

A
  • release inhibitory neurotransmitters
  • noradrenaline
  • serotonin
  • encephalins
  • endorphins
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15
Q

what is hyperalgesia

A

noxious stimuli pt reacts in a very exaggerated manner

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16
Q

what is allodynia

A

a reaction to a non-noxious stimulus

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17
Q

what is somatic pain

A
  • from skin, skeletal muscle and bone
  • due to stimulation of mechanical, thermal or chemical
  • well localised
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18
Q

what is visceral pain

A
  • from injury to viscera
  • less localised
  • dependent on organ
  • referred pain
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19
Q

what is neuropathic pain

A
  • from damage to pain fibres
  • hypersensitivity to stimuli
  • persistent perception of pain
  • pins and needles
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20
Q

how does peripheral sensitisation happen

A
  1. peripherally released sensitizing agents (PGE, bradykinin)
  2. activation of signal transduction
  3. enhancement of ion influx from noxious stimuli
  4. reduction of activation thresholds of Na channels
  5. increased sensitivity of peripheral nerve terminal
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21
Q

how does a change in sodium channel threshold affect pain sensitsation

A

more easily activated channels means the pain is transmitted faster so you feel the pain faster

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22
Q

what is central sensitzation

A

repetitive synaptic transmission that activates intracellular signal transduction cascade that enhances the response to subsequent stimuli

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23
Q

how does glutamate affect central sensitisation

A
  • activates AMPA-R and NMDA-R
  • activation causes depolarisation causing a sodium influx
24
Q

how does the activation of the signal transduction cascade affect centralsenstisation

A
  • substance P, NK1 and glutamate trigger the cascade
  • causes short and long term sensitisation
25
Q

what are the stages of central sensitsation

A
  1. action potential at primary sensory neuron central terminal
  2. ca2+ influx
  3. synaptic vesicles released
  4. glutamate, substance P and BDNF released
  5. triggers activation of signal transduction cascade
  6. altered gene expression - long term sensitisation
  7. phosphorylation of postsynaptic proteins - short term sensitisation
26
Q

what is the pathophysiology of neuropathic pain

A
  • inflammatory cytokines increase gene transmission of Na channels
  • faster pain transmission
  • Schwan cells secrete nerve growth factor upregulating gene expression of sodium
27
Q

what happens to the injured nerve fibres in neuropathic pain

A
  • loss of neurotrophic support
  • heightened pain sensitivity and continued pain perception
  • loss of C fibres allows regenerated Ab fibres which synapse with spinothalamic tract
28
Q

what is the pathophysiology of inflammatory pain

A
  1. damage to phospholipid bilayer
  2. arachidonic acid released
  3. COX2 site
  4. PGG2
  5. Peroxidase site
    6.PGH2
    PGE2
29
Q

how does prostaglandins affect peripheral sensitisation

A

decreased activation threshold at peripheral terminals or primary afferent nociceptor neurons

30
Q

what are the WHO guidelines on analgesic administration

A
  • oral dosing where possible
  • around the clock administration
  • prescribed according to pain level
31
Q

TWEED SASH - non pharmacological interventions

A

psychological
- Therapeutic touch
- Warn about painful interventions
- Explain what is happening
- Establish eye contact
- Defend pt dignity
physical
- Stabilise fracture
- Apply dressing to burns
- Soft surface
- Hypothermia avoidance

32
Q

what is multimodal analgesia

A

multiple pharmacological agents acting via different mechanisms

33
Q

what are some benefits of using multimodal analgesia

A
  • a synergistic effect
  • less incidence of side effect burden
34
Q

fentanyl usage

A
  • trauma
  • rapid on set of action
  • greater analgesic potency
  • less cardiovascular depression lacks unwanted histamine release
  • IV, oral, transdermal, intransally
35
Q

what receptors mediate opioids

A
  • mu
  • delta
  • kappa
36
Q

what do mu receptors mediate in opioids

A
  • analgesia - supraspinal, spinal, peripheral
  • respiratory failure
  • pupil constriction
  • euphoria
  • physical dependence
37
Q

what do delta receptors mediate in opioids

A
  • analgesia - spinal
  • respiratory failure
38
Q

what doe kappa receptors mediate in opioids

A
  • analgesia - spinal and peripheral
  • pupil constriction
  • dysphoria and hallucinations
39
Q

what occurs at the supraspinal analgesia with opioids

A
  • release endogenous opioid peptides
  • enhance descending pathway
  • alter brain perceptions of pain
40
Q

what occurs at the spinal analgesia with opioids

A

inhibit transmission of nociceptive impulses through the dorsal horn

41
Q

what occurs at the peripheral analgesia with opiods

A

inhibit discharge of nociceptive afferent terminal in the periphery

42
Q

how do supraspinal analgesia work

A
  • inhibit the descending pathway
  • block GABA (morphine)
43
Q

how do spinal analgesia work

A
  1. presynaptic activated - effects calcium influx and calcium blocked
  2. vesicle can’t release content
  3. postsynaptic activated - effects potassium channel by opening it
  4. potassium efflux, hyperpolarisation
44
Q

how is codeine metabolised

A
  • into morphine in the liver by CYP enzyme
  • then slowly metabolised
45
Q

what are additional mechanisms of action for opioids

A

block the reuptake in synaptic cleft stopping the action potential (tramadol, tapentadol)

46
Q

what are additional pharmacological actions of opioids

A
  • nausea
  • hypotension
  • pinpoint pupil
  • respiratory depression
  • suppression of cough
  • euphoria
  • bronchoconstriction
  • urticaria
  • dependency
  • tolerance
47
Q

why do opioids cause pinpoint pupils

A
  • stimulation of Edinger-Westphal nucleus of oculomotor nerve
  • enhances para-sympathetic stimulation of the eye
48
Q

why do opioids cause respiratory depression

A

reduce sensitivity of respiratory centre neurones to CO2

49
Q

why do opioids suppress a cough

A

direct inhibition of cough centre

50
Q

why do opioids cause urticaria and bronchoconstriction

A

histamine release

51
Q

why do opioids cause nausea

A

from CTZ stimulation

52
Q

what are opioid contraindications

A
  • acute respiratory failure
  • coma
  • head trauma
  • raised ICP
  • paralytic ileus
  • biliary colic
53
Q

what CNS depressants do opioids interact with

A
  • alcohol
  • benzodiazepines
  • z drugs
  • MOAI
54
Q

what are the signs and symptoms of opioid overdose

A
  • tachycardia
  • hypotension
  • respiratory depression
  • miosis
  • decreased level of consciousness
55
Q

what is the management of opioid overdose

A
  • supportive management eg airway
  • IV or IO naloxone every 5 mins

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