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Yr 2 - Pharmacology > opiids and narcotic analgesics > Flashcards

opiids and narcotic analgesics Flashcards

1
Q

Which size/shape of axons have slower signal propogation?

A

Larger diameter

Unmyelinated

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2
Q

What underpins the gate control theory of pain in the dorsal horn?

A

Other sensory information (in greater amounts/ covering larger areas) such as touch and muscle joints) overrides pain due to modulation via inhibitory GABA pathways

N.B. The trigeminal pathway is still gated but in a different way

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3
Q

Which 7 types of drugs are used for analgesia?

A
  • Local anaesthetics
  • General anaesthetics
  • NMDA (glutamate) receptor antagonists
  • Voltage-gated calcium channel blockers (selective = into spinal cord) &
  • Anti epileptics (blocks overactive Ca channels)
  • NSAIDs - especially for low grade pain
  • Cannabinoid CB1 receptor agonists (animals)
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4
Q

What are NSAIDs used to treat? What is its method of action?

A

Inflammatory pain

Used to cleave cyclooxygenase (produces prostaglandins = pain, fever and inflammation)

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5
Q

What is an opiate?

A

Natural substance produced by opium poppy = binds and activates opioid receptors

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6
Q

What is an opioid?

A

Any drug (synthetic or natural) that binds and activated opioid receptors

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7
Q

What is a narcotic analgesic (narcotics)?

A

Any drug with the potential for abuse (traditionally opioids only) e.g. Cocaine

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8
Q

What are the 4 well defined classical opioid receptors?What are their classic names? (and their new names?)

A

μ (MOPr)

δ (DOPr)

κ (KOPr)

Opiod receptor like 1 ORL1 = (NOPr)

-> N.B. not relavent in analgesia

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9
Q

What type of receptors are opiod receptors?

A

GPCR

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10
Q

What is the principal transduction mechanism for Opioid receptors?

A

Gi/o= inhibits Ca= activates K= activates cAMP -> PKA = other mechanism (not the main pathway for analgesia)

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11
Q

What are the 3 consequences of opioid receptor activation?

A
  • Inhibit transmitter release
  • Inhibit neuronal firing
  • Disinhibition (removes inhibitory influence = excitation!)
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12
Q

What is the opioid structure similar to?

A

Tyrosine

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13
Q

What is the terminal Amino acid for most opioid peptides?

A

Tyrosine

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14
Q

Name two μ opioid receptor agonists:

A
  • DAMGO
  • Morphine (partial)
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15
Q

Name two μ opioid receptor antagonists:

A
  • CTOP
  • Naloxone (all types of receptors but strongest with μ)
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16
Q

Name a δ opioid receptor agonist:

A

DPDPE

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17
Q

Name two δ opioid receptor antagonists:

A
  • Naltrindole
  • Naloxone
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18
Q

Name a κ opioid receptor agonist:

A

Enadoline

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19
Q

Name two κ opioid receptor antagonists:

A
  • nor-binaltrophimine
  • naloxone
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20
Q

Give an example of a drug that show mixed activity

A

Pentazocine (μ antagonist & κ agonist)

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21
Q

What are the 4 behavioural effects of μ opioid receptor agonists:

A
  • Analgesia
  • Euphoria
  • Respiratory depression
  • Constipation
22
Q

What are the 4 behavioural effects of κ opioid receptor agonists:

A

Analgesia

Dysphoria/Hallucinations

No respiratory depression

Diuresis

23
Q

What are the 2 behavioural effects of δ opioid receptor agonists:

A

Analgesia

Antidepressant/proconvulsant

24
Q

What are the 5 desirable effects of opioids?

A
  • Analgesia
  • Euphoria
  • Constipation
  • Sedation (premed for surgery)
  • Cough suppression
25
Q

What is the other effect of opioids?

A

Pupil constriction

26
Q

What are the 8 undesirable effects of opioids?

A
  • Respiratory depression
  • Euphoria
  • Constipation
  • Sedation
  • Nausea and vomitting
  • Tolerance (need to increase dose over time)
  • Psychological dependence
  • Physical dependence
27
Q

Which two neurotransmitters are found in the 1st synapse for pain to the CNS (A delta/c fibres)?

A
  • Substance P
  • Glutamate
28
Q

Which membranes in the synapse are μ opioid receptors located?

A

On both the pre and post synaptic membrane

29
Q

What is the effect of opioids on presynaptic μ opioid receptors?

A

Reduces transmitter release

30
Q

What is the effect of opioids on postsynaptic μ opioid receptors?

A

Hyperpolarisation (activating potassium channels) = decreased size of action potential

31
Q

What happens in disinhibition?

A

A decrease in GABA release (by decreasing Ca) = hyper polarisation of inhibitory interneurone = less inhibition and increased activity in projection neurones

32
Q

In which pathways can disinhibition occur?

A

Descending inhibitory pathways

33
Q

What causes Euphoria in Opioid users?

A

Disinhibition in ventral tegmental area (VTA) = enhanced dopamine release in nucleus accumbens

34
Q

What are the 3 main problems with opioids?

A
  • side effects
  • Breakthrough pain (with chronic use)
  • Neuropathic pain (doesn’t treat all kinds of pain)
35
Q

Why are drug combinations used?

A

To reduce side effects

Possibly due to synergy (binding to other drug used)

36
Q

Which two drugs is co-codamol a mixture of?

A

Codeine

Paracetamol

37
Q

Which two drugs is co-codaprin a mixture of?

A

Codeine

Aspirin

38
Q

Which two drugs is co-proxamol a mixture of?

A

Dextroproxyphene

Paracetamol

N.B. this is not used as much now

39
Q

Which two analgesic drugs are recommended for mild pain in the WHO pain ladder?

A

Non opioid drugs (ibuprofen & paracetamol)

40
Q

Which analgesic drug is recommended for moderate pain in the WHO pain ladder?

A

Mild opioid e.g. codeine

41
Q

Which analgesic drug is recommended for severe pain in the WHO pain ladder?

A

Opioid e.g. morphine

42
Q

Which type of pain can be unresponsive to opioids?

A

Neuropathic pain

43
Q

Which drugs are used as an alternative to opioids in neuropathic pain?

A

Antidepressants e.g. amitriptyline

Antiepileptics e.g. gabapentin & Carbamazepine

44
Q

How does the anti epileptic drug gabapentine produce an analgesic effect?

A

Modulates Na and Ca Channels

45
Q

Which 6 inflammatory mediators are released following tissue damage?

A
  • Histamine
  • Bradykinin
  • 5-HT
  • Prostaglandin
  • ATP
  • Acidosis (H)
46
Q

What are collaterals?

A

Neurones that feedback to the area of tissue damage

47
Q

Which chemicals are released by collaterals?

A
  • Substance P
  • CGRP (Calcitonin gene related peptide)
48
Q

What effect does substance P have in the area of tissue damage?

A
  • Histamine release from mast cells (= pain and inflammation)
  • Vasodilation
49
Q

What effect does CGRP have in the area of tissue damage?

A

Vasodilation

50
Q

Which types of nerve fibres produce the sensation of pain?

A

Nociceptive fibres

51
Q

Where do nociceptive fibres first synapse in the spinal cord?

A

The dorsal horn

Yr 2 - Pharmacology (18 decks)

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