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PSYC3030 > Narcotic Analgesics > Flashcards

Narcotic Analgesics Flashcards

1
Q

All of the following are effects of the class of drugs called narcotic analgesics except

a. relaxation
b. euphoria
c. pain reduction
d. diarrhea

A

d. diarrhea

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2
Q

The nociceptin/orphanin FQ receptor (NOP-R)

a. is genetically related to the classical opioid receptors, mu, delta, and kappa
b. produces euphoria when activated
c. has a high binding affinity for the endogenous opioids
d. is found only in limbic areas and the spinal cord

A

a. is genetically related to the classical opioid receptors, mu, delta, and kappa

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3
Q

The effects of analgesics on pain are difficult to study because

a. the results depend on the specific technique being used to produce pain
b. it is impossible to obtain subjective reports of pain
c. humans refuse to participate in the research
d. ethical guidelines prohibit the application of painful stimuli to animals

A

a. the results depend on the specific technique being used to produce pain

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4
Q

What is first/early pain?

A

Immediate, sensory component of pain.

Signal is carried by myelinated Adelta neurons, which conduct action potentials rapidly.

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5
Q

What pathway does first/early pain follow?

A

Transmitted from spinal cord via spinothalamic tract to PVL nucleus of thalamus to somatosensory cortex.

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6
Q

What is second/late pain?

A

The emotional component of pain carried by slower thin, unmyelinated C fibers.

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7
Q

What pathway does second/late pain follow?

A

Also goes to thalamus, but gives off collaterals to limbic structures and anterior cingulate cortex.

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8
Q

How can chronic pain be treated?

A

Electrical stimulation of PAG.

Tolerance often occurs with repeated use, and cross-tolerance with injected morphine occurs

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9
Q

How can pain be measured?

A

Subjective pain rating can be monitored while simultaneously recording magnetic fields on surface of skull using magnetoencephalography

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10
Q

Activation of which areas are related to first pain?

A

Primary somatosensory cortex and secondary somatosensory cortex

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11
Q

Second pain is related to activation of which areas?

A

Anterior cingulate and secondary somatosensory cortex

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12
Q

When was morphine isolated?

A

Early 1800s

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13
Q

What is opium? What does it contain?

A

Extract of poppy plant. Main ingredient is morphine but also contains codeine, thebaine, narcotine, etc.

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14
Q

What is heroin?

A

Made by adding 2 acetyl groups to morphine, making it more lipid soluble so it reaches brain faster and is more potent.
Dramatic euphoric effects

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15
Q

What are partial opioid agonists?

A

Pentazocine, nalbuphine, buprenorphine

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16
Q

How do pure antagonists compare to opioid agonists?

A

Are structurally similar but have no efficacy. Can prevent/reverse effect of opioids

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17
Q

What are 2 examples of pure opioid antagonists?

A

Naloxone or nalorphine

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18
Q

What routes of administration are utilized for opioids?

A

Intramuscularly, orally, smoking, snorting, subcutaneous

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19
Q

Does morphine cross barriers?

A

Only a small fraction of morphine crosses BBB, but easily crosses placenta so newborns can suffer withdrawal symptoms

20
Q

How long does opioid excretion take?

A

After metabolism, most metabolites are excreted in urine within 24 hours

21
Q

What kind of receptors are opioid receptors?

A

Metabotropic receptors linked to inhibitory G proteins, inhibiting adenylyl cyclase and reducing cAMP production

22
Q

Describe mu receptors.

A

High affinity for morphine. Analgesia (in medial thalamus, periaqueductal gray, median raphe, spinal cord), feeding and positive reinforcement (NAcc), cardiovascular and respiratory depression, cough control, nausea and vomiting (brainstem), sensorimotor integration (thalamus, striatum)

23
Q

Describe delta receptors.

A

Predominantly in forebrain structures.
Modulates olfaction, motor integration, reinforcement, cognitive function.
Overlap with mu receptors suggest modulation of both spinal and supraspinal analgesia

24
Q

Describe kappa receptors.

A

Bind to ketocyclazocine, which produces hallucinations and dysphoria.
Found in striatum and amygdala, hypothalamus and pituitary.
May participate in regulation of pain, gut motility, and dysphoria.

25
Q

Describe NOP-Rs.

A

In CNS and PNS.
High concentration of them in the cerebral cortex, limbic areas, thalamus, raphe nuclei, spinal cord.
Involved in analgesia, feeding, learning, motor function, and neuroendocrine regulation.

26
Q

How do opioids modulate pain?

A

Modulate pain directly in spinal cord by small inhibitory interneurons and by regulating descending pain inhibitory pathways ending in the spinal cord and originating in the periaqueductal gray, and at higher brain sites (emotional/hormonal aspects)

27
Q

What are the effects of low to moderate doses of opioids?

A

Pain relief, constricted pupils, drowsiness, inability to concentrate, dreamy sleep, anxiety relief, aggressiveness, feelings of inadequacy

28
Q

What are the effects of higher doses of opioids?

A

Elation or euphoria, can lead to unconsciousness (body temp and BP fall, constricted pupils, and respiratory failure)

29
Q

What are the adverse effects of opioids?

A

Dysphoria, restlessness and anxiety, nausea and vomiting (via area postrema)

30
Q

How do opioids affect the GI tract?

A

Opium and morphine treat diarrhea and stop fluid loss in severe bacterial and parasitic diseases.
Loperamide is commonly used because it does not cross BBB

31
Q

How does opioid reinforcement occur?

A

Opioids increase DA cell firing.

Dynorphin acts on kappa receptors on DA neuron terminals and can reduce release of DA by similar mechanisms.

32
Q

Which opioid receptors are implicated in development of tolerance?

A

Mu-delta heteromer-mediated functions

33
Q

How long does withdrawal occur for morphine?

A

36-48 hours after last use

34
Q

How long does withdrawal for methadone last?

A

Gradual increase over several days and decrease over several weeks

35
Q

How do withdrawal symptoms for longer lasting opioids differ?

A

They are milder (e.g., buprenorphine)

36
Q

How can opioid dependence be treated?

A

Treatment by detoxification, behavioural and social therapy, and pharmacotherapy (methadone, buprenorphine, naltrexone, naloxone)

37
Q

Which four large propeptides are processed into the smaller, active opioids?

A

Prodynorphin, POMC, proenkephalin, and pronociceptin/orphanin FQ

38
Q

Which 2 methods were used to map endogenous opioid pathways?

A

In situ hybridization and immunohistochemistry

39
Q

Where are the propeptide opioid precursors find?

A

Brain, spinal cord, autonomic nervous system (concentrated in areas related to pain and mood)

40
Q

Which endogenous opioids bind the mu receptor?

A

Endomorphins, endorphins (POMC)

41
Q

Which endogenous opioids bind the delta receptor?

A

Enkephalin (proenkephalin), endorphins (POMC)

42
Q

Which endogenous opioids bind the kappa receptor?

A

Dynorphins (prodynorphin)

43
Q

Which endogenous opioids bind NOP-R?

A

Nociceptin/orphanin FQ (pronociceptin/orphanin FQ)

44
Q

Describe postsynaptic inhibition by opioids.

A

Receptors activate a G protein that opens K+ channels to hyperpolarize postsynaptic cells, reducing firing rate

45
Q

Describe axoaxonic inhibition by opioids.

A

Receptors activate G proteins that close Ca2+ channels, reducing release of neurotransmitters

46
Q

Describe the function of presynaptic opioid autoreceptors.

A

Activate G proteins and reduce release of a co-localized neurotransmitter

47
Q

What are the functions of endogenous opioids?

A

Pain suppression, reward, motor coordination, endocrine function, feeding, body temp and water regulation, and response to stress

PSYC3030 (12 decks)

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