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Pharm > Lecture 19: Opioids II > Flashcards

Lecture 19: Opioids II Flashcards

1
Q

What drugs are used to manage severe acute pain?

A

Opioids

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2
Q

Why are Opioids not the best to treat chronic pain?

A

Because of their side effects

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3
Q

Why are opioids such good drugs at blocking pain?

A

Because opioid receptors are distributed along the entire neural axis that transmits pain to the brain and processes pain into an experience

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4
Q

What neurons are mu, delta and kappa opioid receptors located on?

A

Primary and secondary afferents in the skin and spinal cord

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5
Q

How does agonist binding to opioid receptors affect pain transmission?

A

Agonists binding to opioid receptors inhibit pain transmission from skin to brain

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6
Q

What are nociceptors?

A

Primary afferent neurons that are specifically tuned to the detection of pain

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7
Q

What do opioid receptors localized in the brainstem (rostroventral medulla) do?

A

Increase diffuse noxious inhibitory control

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8
Q

Which part of the brain is important in controlling the endogenous pain system?

A

The rostroventral medulla

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9
Q

What is the diffuse noxious inhibitory control?

A

The endogenous pain system of the body that dampens the experience of pain

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10
Q

When is the diffuse noxious inhibitory control activated?

A

When pain fibers are activated in the skin. Basically when there are pain signals being transmitted from the skin to the brain

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11
Q

What is the diffuse noxious inhibitory control comprised of?

A

Descending excitatory and inhibitory neurons in the medulla that inhibit or activate pain synapses in the spinal cord

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12
Q

What can the excitatory and inhibitory neurons in the diffuse noxious inhibitory control system do?

A

The can amplify or inhibit the transmission of pain from the primary to secondary afferent

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13
Q

What are the On cells in the diffuse noxious inhibitory control system?

A

The descending neurons that project from the rostral ventral medulla to the spinal cord

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14
Q

What does activation of the On cells in the diffuse noxious inhibitory control system do?

A

Amplify pain

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15
Q

What are the On cells in the rostral ventral medulla under the control of?

A

Neurons that express opioid peptide

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16
Q

What receptors do the on cells of the rostral ventral medulla express?

A

Mu opioid receptors

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17
Q

What does the release of opioid peptides on the rostral ventral medulla on cells do?

A

Inhibits the activity of On cells and reduces the signals of nociceptive signals reaching the brain

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18
Q

What is Dopamine involved in?

A

Motivated behavior and reward

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19
Q

where are dopamine neurons located primarily?

A

In the ventral tegmental area (VTA)

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20
Q

What are Mu opioid receptors in the VTA located on?

A

Inhibitory GABAergic interneurons

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21
Q

What do Mu opioid receptors on GABAergic neurons do?

A

They inhibit activation of GABA neurons which stops them from releasing GABA which is an inhibitory neurotransmitter onto dopamine neurons causing dopamine neurons to produce more dopamine (disinhibition)

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22
Q

What are the two ways opioid receptors inhibit pain?

A
  • Decreasing nociception at the level of the nociceptor, in the spinal cord, and in the brain step
  • Decreasing the emotional and cognitive aspects of pain (make the pain bother you less)
23
Q

Which opioid receptor do most opioid agonists use to target pain?

A

Mu receptors

24
Q

What are examples of drugs that for pain that are mu agonists?

A
  • Morphine
  • Fentanyl
  • Codeine
  • Oxycodone
25
Q

What are Delta agonists being developed for?

A

Chronic migraines

26
Q

Why was development of delta agonists initially limited?

A

Because of severe side effects (seizures)

27
Q

Why has enthusiasm been renewed with delta agonists?

A

Because the analgesic effects can be isolated through biased agonism that activates the G protein pathway and not the beta arrestin pathway

28
Q

What is an example of a biased delta opioid agonist?

A

TRV250

29
Q

Why haven’t kappa agonists that penetrate the brain been developed for pain?

A

because of dysphoria/hallucinogenic effects

30
Q

What don’t peripherally restricted kappa agonists not do?

A

Cross the BBB

31
Q

What do kappa agonists do?

A

Bind to kappa receptors in the skin and inhibit pain transmission while avoiding CNS adverse events

32
Q

What is an example of a kappa agonists?

A

CR845

33
Q

What are the effects of CR845?

A
  • Potent analgesic
  • Anti-inflammatory
  • Anti-itch properties with little CNS effect
34
Q

What is Tolerance?

A

Decrease response to the effects of a drug, requiring even larger doses to achieve the same effect

35
Q

What does opioid tolerance develop to?

A

The analgesic, euphorigenic, sedative and respiratory effects of the drugs

36
Q

What causes Tolerance?

A

Following agonist binding and G-protein signalling, Beta arrestin is also recruited to shit off signalling and pull the receptor off the membrane leading to less receptors on the membrane

37
Q

When does Physical dependance develop?

A

Following chronic opioid use and is revealed following abrupt discontinuation of drug as withdrawal

38
Q

What are the symptoms of acute withdrawal?

A
  • Rhinorrhea (runny nose)
  • Lacrimation (tearing eyes)
  • Chills
  • Muscle aches
  • Diarrhea
  • Yawning
  • Anxiety
39
Q

What is addiction?

A

A brain disease driven by disfunction in reward, motivation, memory circuitry

40
Q

What is addiction characterized by?

A
  • Inability to abstain consistently
  • Impairment of behavioral control
  • Drug craving
  • Diminished recognition of significant problems with one’s behaviors and interpersonal relationships
  • Dysfunctional emotional response
41
Q

How are physical barriers a treatment for opioid use disorder?

A

Physical barriers prevent chewing/crushing of oral tablets for intravenous/intranasal drug use

42
Q

How are chemical barriers a treatment for opioid use disorder?

A

They can be added to resist extraction of the opioid by common solvents like water/alcohol

43
Q

How are Agonists/Antagonist combination be barriers a treatment for opioid use disorder?

A

An antagonist can be added to an agonist to interfere with euphoria associated with abuse. The antagonist is only release when oral tablet is tampered with (crushed, injected)

44
Q

What is Agonist Replacement therapy?

A

A comprehensive treatment approach including maintenance on an opioid agonist and cognitive behavioral therapy

45
Q

What are the advantages to agonist replacement therapy?

A
  • Reduced drug cravings
  • Better participation in addiction treatment since withdrawal symptoms aren’t a distractions
  • Improved social functioning
  • Reduction in infectious disease/death associated with illicit drug use
46
Q

What drugs are used in agonist replacement therapy and why?

A

Methadone and Buprenorphine because they have a longer half life

47
Q

What is Methadone?

A

A long-acting full agonist at the mu opioid receptor used in agonist replacement therapy

48
Q

What is the disadvantage to methadone?

A

It is a full agonist so overdose is still possible

49
Q

Which receptors do Buprenorphine work on?

A

It is a partial agonist at the mu opioid receptor and an antagonist at the kappa and delta opioid receptor used for agonist replacement therapy

50
Q

What is Buprenorphine marketed as?

A

Suboxone and is mixed with naloxone

51
Q

Why does Buprenorphine have a safer agonist profile?

A

Because it is a partial agonist

52
Q

What is Injectable opioid therapy (iOAT)?

A

When clients are prescribed specific doses of injectable opioids and are expected to self administer them at the iOAT clinic

53
Q

What is Naloxone?

A

A non-selective competitive opioid receptor agonist

Pharm (31 decks)

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