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Year 3 Pharmacology > Physiological Analgesia and Analgesic Drugs > Flashcards

Physiological Analgesia and Analgesic Drugs Flashcards

1
Q

Pharmacological strategies employed by analgesics to manage pain?

A

Reduce nociception by:

  • Acting at the site of injury to decrease nociceptor sensitisation in inflammation, e.g: NSAIDs
  • Blocking nerve conduction, e.g: local anaesthetics
  • Modifying transmission of nociceptive signals in the dorsal horn of the signal???? cord, e.g: opioids and some anti-depressants
  • Activating (or potentiating) descending inhibitory controls, e.g: opioids
  • Targeting ion channels up-regulated in nerve damage
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2
Q

Steps in the WHO analgesic ladder?

A

……..

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3
Q

Examples of drugs used in step 1?

A

NSAIDs, e.g: aspirin, dicllofenac, ibuprofen, indomethacin, naproxen

OR

Paracetamol

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4
Q

Examples of weak opioid drugs?

A

Codeine, tramadol, dextropropoxyphene

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5
Q

Examples of strong opioid drugs?

A

Morphine, oxycodone, hydromorphone, heroin, fentanyl

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6
Q

Difference between opiates and opioids?

A

Opiates - substances extracted from opium OR of similar structure to those in opium

Opioids - ANY agent, inc. endogenous peptides, that act upon opioid receptors

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7
Q

Describe segmental anti-nociception

A

Physiological analgesia occurring via the gate control theory

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8
Q

…………

A

…………..

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9
Q

Describe supraspinal anti-nociception

A

Physiological analgesia inv. descending pathways from the BRAINSTEM

The brain regions inv. with pain perception and emotion project back to the brainstem and spinal cord, in order to modify afferent inputs

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10
Q

Brain regions inv. with pain perception and emotion?

A

Cortex, amygdala, thalamus and hypothalamus

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11
Q

Important brainstem regions for analgesia?

A 
Periaqueductal grey (PAG) - excitation here, by ELECTRICAL STIMULATION, produces profound analgesia; other substances that cause excitation here:
• Endogenous opiods (enkephalins)
• Morphine and related compounds

Nucleus raphe magnus (NRM) - contains serotonergic and enkephalinergic neurones; substances that cause excitation here:
• Morphine

Locus coeruleus (LC) - contains noradrenergic neurones

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12
Q

How do the brainstem regions above allow analgesia?

A

PAG positively feeds into the NRM and LC

NRM stimulation inhibits 5-HT (serotonin) release

LC stimulation inhibits noradrenaline release

This leads to inhibition of nociceptive transmission in the dorsal horn of the spinal cord

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13
Q

………….

A

……………

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14
Q

………….

A

……………

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15
Q

Receptors mediating opioid action?

A

Mediated by G protein coupled opioid receptors, all of which couple, preferentially to Gi/o protein

This results in:
• Inhibition of opening of voltage-activated Ca2+ channels (pre-synaptic effect) - this suppresses excitatory NT release from nociceptor terminals
• Opening of K+ channels (post-synaptic effect) - suppresses excitation of projection neurones

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16
Q

Types of opioid receptors and their responsibilities?

A

μ (mu) - responsible for most of the analgesic action of opioids but also mediate major adverse effects, e.g: respiratory depression, constipation, euphoria, sedation, dependence

δ (delta) - contributes to analgesia but activation can be pro-convulsant

ORL1 - activation produces an anti-opioid effect

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17
Q

Mechanism of action of agonists as analgesics? Examples?

A 
Act mainly through prolonged activation of μ-opioid receptors:
• Morphine
• Diamorphine
• Fentanyl
• Burenorphine
• Pethidine
• Codeine 
• Tramadol
• Methadone
• Etorphine
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18
Q

Use of morphine?

A

Used in acute severe pain and chronic pain (step 3 of the WHO ladder)

For acute severe pain - IV, IM or SC administration

For chronic pain - oral administration is most appropriate:
• Oramorph (immediate relief)
• MST Continus (modified release)

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19
Q

Different between morphine and diamorphine?

A

Diamorphine is AKA 3,6-diacetylmorphine or heroin

More lipophilic than morphine

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20
Q

Use of diamorphine?

A

Rapid onset of action when administered IV, as it enters the CNS rapidly

Can be used for post-operative pain

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21
Q

Uses of fentanyl (an opioid)?

A

Administered IV to provide analgesia in maintenance anaesthesia

Suitable for transdermal delivery in chronic pain states but not in acute pain

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22
Q

Uses of buprenorphine?

A

Is a partial agonist

For chronic pain with patient-controlled injection systems; it can be given via injection or sublingually

Has a SLOW ONSET but LONG DURATION OF ACTION

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23
Q

Uses of pethidine?

A

Used for ACUTE pain, part. in labour; it has rapid onset of action, when given IV, IM or SC, but has a short duration of action (unsuitable for control of chronic pain)

24
Q

Contraindications with pethidine?

A

Should not be used in conjunction with MAO inhibitor; this would cause excitement, convulsions, hyperthermia

25
What is norpethidine?
A neurotoxic metabolite of pethidine
26
Uses of codeine and dihydrocodeine?
These are weaker opioids used in mild/moderate pain; they undergo hepatic metabolism to morphine and dihydromorphine Administered ORALLY, not IV
27
Mechanism of action of tramadol?
Weak μ-receptor agonist It likely exerts significant analgesic action by potentiating the following descending systems: • Serotonergic (from nucleus raphe magnus, NRM) • Adrenergic (from locus coeruleus, LC)
28
Use of tramadol?
Oral administration
29
Contraindications to tramadol use?
AVOID in patients with EPILEPSY
30
Mechanism of action of methadone?
Weak μ-receptor agonist with additional actions at other sites in the CNS, inc: • K+ channels • NMDA receptors • Some 5-HT receptors
31
Uses of methadone?
Mainly used to assist in withdrawal from strong opioids, like heroin It is not a cure but helps by reducing the very serious risks assoc. with self-injection and illegal activity to support strong opioid drug habits Administered orally and has a long duration of action (plasma 1/2-life of >24 hours)
32
Uses of etorphine?
Used in veterinary, NOT HUMAN, practice; it is 1000x more potent than morphine and is useful in sedation of large animals It is even incorporated into a dart, pellet, etc, to down a large animal
33
How to reverse the action of etorphine?
Diprenorphine is a weak partial agonist that reverses the action of etorphine
34
Which drug agents are more addictive?
Generally, agents with abuse potential that have a short 1/2-life are more addictive than those with a long 1/2-life
35
Examples of opioids that are antagonists?
* Naloxone | * Naltrexone
36
Uses of NSAIDs?
Reduce mild/moderate inflammatory pain They have analgesic, anti-pyretic and anti-inflammatory actions
37
Mechanism of action of NSAIDs?
Inhibit synthesis and accumulation of PGsby COX1 and COX2 enzymes
38
Normal processes mediated by COX1 and COX2?
Phospholipase A2 turns phospholipids into arachidonic acid; this is turned into endoperoxides by COX1 and COX2 Endoperoxides are acted on by various enzymes, resulting in different products and actions: • Prostagladin isomerase acts on endoperoxidases to form PGs, causing hyperalgesia • Thromboxane synthase acts on endoperoxidases to form thromboxane A2, causing platelet aggregation and vasoconstriction • Prostacyclin synthase acts on endoperoxidases to form prostacyclin (PGI2), causing platelet disaggregation and vasodilatation
39
Types of NSAIDs?
``` Non-selective NSAIDs - inhibit both COX1 and COX2 enzymes: • Aspirin • Ibuprofen • Naproxen • Diclofenac • Indometacin ``` COX2 selective inhibitors ('coxibs': • Etoricoxib • Celecoxib • Lumiracoxib
40
When are COX1 and COX2 active?
COX1 is constitutively active COX2 is induced in inflammation, i.e: therapeutic benefit is derived via inhibition of COX2
41
How does GI toxicity occur?
Via inhibition of COX1
42
Action of PGE2?
Most cells generates this in response to mechanical, thermal or chemical injury PGE2 sensitises nociceptive neurones and causes hyperalgesia
43
Side effects of long-term administration of non-selective NSAIDs?
GI damage, as PGE2, produced by COX1, protects against the acid/pepsin environment NOTE - paracetamol does not have this adverse effect
44
Side effects of selective COX2 inhibitors?
PROTHROMBOTIC (this limits their use)
45
Why is paracetamol not classed as an NSAID?
AKA acetaminophen It lacks anti-inflammatory activity and only weakly inhibits COX isoenzymes
46
Mechanism of the analgesic effect of paracetamol?
Due to its metabolities, e.g: N-acetyl-p-benzoruinoneimine; this is also responsible for hepatotoxicity in overdose
47
Conditions assoc. with neuropathic pain?
``` Severe and debilitating pain occurring in: • Trigeminal neuralgia • Diabetic neuropathy • Post-herpetic neuralgia • Phantom limb pain ```
48
Features of neuropathic pain?
DOES NOT respond to NSAIDs Relatively insensitive to opioids, unless given in high doses
49
Drugs used in treatment of neuropathic pain?
Gabapentin and pregabalin (anti-epileptics as well) Tricyclic anti-depressants (TCAs), e.g: amitriptyline, nortryptiline, desipramine Carbamezapine
50
Mechanism of action of gabapentin and pregabalin?
Do NOT act via the GABAergic system; they reduce cell surface expression of a sub-unit of some voltage-activated Ca2+ channels, which are up-regulated in damaged sensory neurones The theory is that these decreased NT release, e.g: glutamate, substance P, from the central terminal of nociceptive neurones
51
Uses of gabapentin?
Migraine prophylaxis
52
Uses of pregabalin?
Painful diabetic neuropathy
53
Mechanisms of action of TCAs?
Act centrally by decreased noradrenaline uptake
54
Uses of SSRIs (selective serotonin reuptake inhibitors)?
E.g: duloxetine, venlafazine decreased reuptake of 5-HT but they DO NOT PROVIDE ANALGESIA
55
Mechanism of action of carbamazepine?
Blocks sub-types of voltage-activated Na+ channel, which are upregulated in damaged nerve cells
56
Uses of carbamazapine?
1st line for control of pain intensity and frequency of attacks in trigeminal neuralgia

Year 3 Pharmacology (5 decks)

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