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Pharmacology > Pain & Opioids - EMILY > Flashcards

Pain & Opioids - EMILY Flashcards

1
Q

What is pain?

A

An unpleasant sensory and emotional experience associated with actual or potential tissue damage or described in terms of such damage

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2
Q

How is pain perceived?

A

Nociception

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3
Q

What is anti-nociception?

A

Absence of response to a normally painful stimulus

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4
Q

What is analgesia?

A

Absence of pain in response to a stimulation which would normally be painful

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5
Q

What is general anesthesia?

A

Drug-induced unconsciousness characterized by controlled but reversible depression of the CNS and perception

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6
Q

How is pain classified (4)?

A

-Duration
-Pathogenesis
-Location
-Severity

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7
Q

What are the 3 types of pain?

A

-Nociceptive pain
-Inflammatory pain
-Neuropathic pain

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8
Q

What do inflammatory mediators (prostaglandins, leukotrienes) activate?

A

They activate silent (high threshold) nociceptors and nociceptor sensitization

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9
Q

What do antidepressants target?

A

Perception of pain in the cerebral cortex

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10
Q

What do opioids target?

A

Perception of pain in the cerebral cortex and modulation of pain in the spinal cord

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11
Q

What do alpha-2 agonists target?

A

modulation of pain in the spinal cord

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12
Q

What do local anesthetics target?

A

Transmission of pain through sensory (afferent) nerves

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13
Q

What is spinal facilitation of pain (wind up)?

A

High frequency action potentials train the second order neurons in the spinal cord to respond more vigorously to subsequent stimulation

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14
Q

Does general anesthesia prevent nociception?

A

No, so pre-emptive analgesia is needed to stop spinal facilitation of pain

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15
Q

What is the difference between pain and nociception?

A

Pain has a conscious component while nociception does not

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16
Q

Why is it important to provide analgesia before surgery?

A

Because general anesthetics are not analgesics

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17
Q

What are descending inhibitory pathways?

A

Decrease neurotransmitter release from primary afferents and reduce excitability of secondary neurons

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18
Q

What endogenous molecules are produced to cause descending inhibition?

A

-Serotonin
-Norepinephrine
-Dopamine
-GABA
-Opioids
-Cannabinoids

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19
Q

What are 3 physiological pain inhibition mechanisms?

A

-Endogenous opioid agonists
-Upregulation of peripheral opioid receptors at site of injury
-Migration of opioid-producing leukocytes to site of injury

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20
Q

What are the 4 possible sites of analgesia?

A
  1. Block Peripheral nociceptors
  2. Prevent transmission to spinal cord
  3. Prevent transmission to brain
  4. Enhance descending inhibitory pathways
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21
Q

What is the most effective way to prevent and treat pain?

A

Affect all the different levels of pain conduction (balanced or multimodal approach)

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22
Q

What are the 3 major types of opioid receptors?

A

-Mu
-Kappa
-Delta

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23
Q

Where are opioid receptors expressed?

A

-CNS/PNS
-Intestinal tract
-Immune cells

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24
Q

Opioid receptors are ___-protein coupled receptors

A

G

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25
Q

What is the MOA for opioid receptor activation?

A

-Decreased cAMP formation and adenylyl cyclase inhibition
-Inhibition of Ca2+ channels in presynaptic neurons (reduced NT release)
-Increased K+ outflow in postsynaptic neurons (hyperpolarization)

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26
Q

What does activation of Mu receptors do?

A

-Analgesia, sedation, euphoria**
-Respiratory depression
-Increased vagal (parasympathetic) tone
-Increased locomotor activity in horses

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27
Q

What does activation of kappa receptors do?

A

-Mild analgesia, sedation, dysphoria**
-Diuresis

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28
Q

What does activation of delta receptors do?

A

Mild analgesia

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29
Q

Which receptor agonist would you pick for a severely painful patient?

A

Mu agonist

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30
Q

Which drugs are full Mu agonists?

A

-Morphine
-Hydromorphone
-Fentanyl
-Methadone
-Etorphine

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31
Q

Which drugs are partial Mu agonists?

A

-Buprenorphine
-Tramadol
-+/- butorphanol

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32
Q

Which drugs are full kappa agonists?

A

-Etorphine
-Butorphanol

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33
Q

Which drug is a partial kappa agonist?

A

Morphine

34
Q

Which drug is a full delta agonist?

A

Etorphine

35
Q

What to opioid receptors do when activated in primary afferent neurons?

A

Inhibit calcium inflow leading to decreased NT release

36
Q

What are some clinical uses of opioids?

A

-Analgesic
-Sedative
-Antitussive
-Antidiarrheal

37
Q

Which opioids would you select for a patient in severe pain?

A

-Morphine
-Methadone
-Hydromorphone
-Fentanyl

38
Q

Which opioids would you select for a patient in mild/moderate pain?

A

-Buprenorphine
-Butorphanol
-Tramadol

39
Q

When could you give opioids for a patient that is undergoing surgery?

A

-Pre-anesthetic
-Intra-operative
-Post-operative

40
Q

What is the effect of giving opioids in combination with sedatives or anesthetics?

A

Causes additive/synergistic sedative and analgesic effects

41
Q

What are some formulations of opioids that aren’t injectable?

A

-Morphine sustained-release tablets
-Fentanyl patch
-Buprenorphine (buccal transmucosal)
-Butorphanol tablets
-Tramadol tablets
-Hydrocodone liquid

42
Q

What is the most problematic adverse effect of opioids?

A

Respiratory depression leading to apnea, especially during anesthesia and in neonates

43
Q

What is another clinically important adverse effect of opioids?

A

Constipation/ileus. This is especially important to consider in horses since it can make them colic at high doses

44
Q

What are some other adverse effects of opioids that are less significant?

A

-Severe pruritus
-Histamine release leading to vasodilation and hypotension
-CNS excitation/dysphoria/seizures

45
Q

Why should a horse undergoing a head procedure not be given butorphanol?

A

Butorphanol can cause twitches which makes doing the procedure difficult

46
Q

What are some pharmacokinetic considerations of opioids?

A

-Many opioids undergo high first pass metabolism resulting in poor oral bioavailability
-Metabolized by liver and excreted by kidneys, can be affected by hepatic or renal disease

47
Q

Why are non-injectable forms of opioids limited?

A

Because of the high first pass effect and poor bioavailability. Better to give as an injection or as a CRI

48
Q

What is opioid receptor expression upregulated by locally?

A

Inflammatory cytokines

49
Q

Which opioid receptor primarily gets upregulated by inflammatory cytokines?

A

Mu > kappa > delta

50
Q

Which two types of patients would the use of opioids not be recommended in?

A

-Patients with chronic kidney disease
-Pregnant patients

51
Q

What is considered the “gold standard” opioid? Why?

A

Morphine. It’s safe, effective and cheap

52
Q

Morphine is a Mu _______ and kappa partial ________

A

Agonist; agonist

53
Q

Hydropmorphone is a Mu _________

A

Agonist

54
Q

What is another use of hydropmorphone?

A

It is an emetic

55
Q

Methadone is a Mu ________, an NMDA _________, and a NE and serotonin reuptake ________

A

Agonist; antagonist; inhibitor

56
Q

What is a benefit of using methadone instead of other mu agonists?

A

It causes fewer CNS effects and less vomiting, especially in cats

57
Q

What are some other benefits of methadone?

A

-More effective against chronic pain
-Doesn’t cause histamine release when administered

58
Q

Fentanyl is a synthetic Mu ________

A

Agonist

59
Q

Fentanyl is 100x more potent than morphine. What does this mean for its reversal?

A

It has very high receptor affinity, meaning that reversal may be more difficult

60
Q

Fentanyl has a wide safety margin in dogs, but what can happen with a large overdose?

A

Fatal apnea

61
Q

Buprenorphine is a partial Mu _______ and a kappa ________

A

Agonist; antagonist

62
Q

What will happen if buprenorphine is given with other opioids?

A

It will displace them and anti-nociceptive effects won’t be as strong

63
Q

Can buprenorphine be fully reversed by naloxone?

A

Not completely

64
Q

Butorphanol is a kappa _______ and a Mu _________ (or partial agonist)

A

Agonist; antagonist

65
Q

What does butorphanol provide effective analgesic for?

A

Mild/moderate pain

66
Q

What does a low dose of butorphanol cause?

A

Sedation

67
Q

What does a high dose of butorphanol cause?

A

Analgesia

68
Q

Should you give butorphanol with a Mu agonist?

A

Probably not cause it can reduce the Mu agonists effects

69
Q

What else is butorphanol?

A

-Antiemetic
-Antitussive

70
Q

Tramadol is a multimodal analgesic. What are its functions?

A

-Mu agonist
-Serotonin reuptake inhibitor
-NE reuptake inhibitor
-Muscarinic antagonist

71
Q

Why is tramadol not recommended to be used as the sole analgesic in dogs?

A

It is a pro-drug that has to be metabolized to function. Individual differences in metabolic activity in dogs drastically alter its effectiveness as an analgesic

72
Q

Which species is better at metabolizing tramadol more consistently?

A

Cats

73
Q

The reversal of opioids occurs via:

A

Competitive opioid receptor antagonists

74
Q

What is the most commonly used opioid reversal drug?

A

Naloxone

75
Q

Naloxone is a competitive antagonist of all opioid receptors, but greatest for which one?

A

Mu

76
Q

Naloxone is a GABA _________. What can this cause?

A

Antagonist. Can cause seizures

77
Q

How should naloxone be given?

A

Small doses IV every 1-3 mins to reverse respiratory depression. IM/SQ will have slower onset of action

78
Q

Which opioid is not ideal for use in cats?

A

Morphine

79
Q

Which opioids can only be given as an injectable?

A

-Morphine
-Hydromorphone
-Methadone

80
Q

What is an important consideration when dispensing opioids?

A

They are drugs of abuse and must be tracked with a TPP

Pharmacology (11 decks)

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