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MLA - Pharmacology Revision > Pharmacology of Pain Control > Flashcards

Pharmacology of Pain Control Flashcards

1
Q

What is the principle of pain relief?

A

By the mouth, by the ladder and by the clock.

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2
Q

Which drugs can be given at the following levels of the analgesic ladder:

Step 1 - Mild Pain (1-3)

Step 2 - Moderate pain (3-6)

Step 3 - Severe pain (7-10)

A

Step 1 - Paracetamol, NSAIDs

Step 2 - Codeine, dihydrocodeine, tramadol (+ laxative)

Step 3 - Morphine, diamorphine, fentanyl (+ laxative + antiemetic)

At each step you can give non-opioid analgesics and adjuvants.

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3
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7
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8
Q

Why is paracetamol toxic in overdose?

A

In overdose - the conjugation mechanisms are saturated and glutathione stores are depleted.

Therefore the NAPQI metabolite binds to proteins instead - this disrupts cellular function, damages tissues and organs and causes liver failure.

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9
Q

What is the treatment for paracetamol OD?

A

NAC (N-acetylcysteine). This is a glutathione precursor.

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15
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16
Q

What are adjuvant analgesics?

A

Adjuvant analgesics represent a diverse group of drugs that were originally developed for a primary indication other than pain. Many of these medications are currently used to enhance analgesia under specific circumstances.

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17
Q

What adjuvant analgesics can you recall?

A
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18
Q

What is the mechanism of action of duloxetine?

A

SNRI - prevents reuptake of 5HT and NOR.

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19
Q

What is duloxetine used for in terms of analgesia?

A

Neuropathic pain in adults

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20
Q

What are the potential adverse effects of duloxetine?

A
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21
Q

What is serotonin syndrome?

A

Serotonin syndrome: occur with concomitant use of other serotonergic agents (including SSRIs, tricyclic antidepressants), with agents that impair metabolism of serotonin. Serotonin syndrome symptoms may include mental status changes (e.g., agitation, hallucinations, coma), autonomic instability (e.g., tachycardia, labile blood pressure, hyperthermia), neuromuscular aberrations (e.g. hyperreflexia, incoordination) and/or gastrointestinal symptoms (e.g., nausea, vomiting, diarrhoea).

Happens when your body has too much serotonin in it.

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22
Q

What is the mechanism of action of amitriptyline?

A

TCA - prevents reuptake of 5HT and NOR - therefore increased 5HT levels.

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23
Q

What is the difference between TCAs and SNRIs?

A

TCAs are considered “first-generation” antidepressants, and SSRIs are considered “second-generation” antidepressants. They’re both effective in improving the symptoms of major depressive disorder. But healthcare providers more commonly prescribe SSRIs than TCAs because TCAs cause more significant adverse side effects.

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24
Q

What is amitriptyline used for?

A

Neuropathic pain in adults
Prophylactic tx of migraine

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25
Q

What are the adverse effects of amitriptyline?

A
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26
Q

What drug interactions should you beware of when prescribing amitriptyline?

A

Other depressants - inc ethanol, benzos and opioids.

Drugs which prolong the QT interval (quinidine) - inc likelihood of ventricular arrythmias when taken with TCAs.

CYP2D6 inhibitors

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27
Q

What is the mechanism of action of gabapentin?

A

Gabapentin decreased the excitation of voltage-gated nerve channels in neurons - and therefore reduces release of excitatory NTs.

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28
Q

What is gabapentin used for?

A

Tx of neuropathic pain - e.g. diabetic neuropathy and post-herpetic neuralgia.

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29
Q

What are the adverse effects of gabapentin?

A
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30
Q

Which drug interactions do you need to be aware of when prescribing gabapentin?

A

Morphine
Antacids - decreases bioavailability if they contain Al and Mg

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31
Q

What is the mechanism of action of lidocaine?

A

Blocks nerve conduction of sensory impulses via Na channel inhibition

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32
Q

What is lidocaine used for?

A

Neuropathic pain

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33
Q

What are the adverse effects of lidocaine?

A
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34
Q

What are the drug interactions to be aware of when prescribing lidocaine?

A

Acebutolol = severe cardiac toxicity
Anxiolytics and opioids - can cause CNS depression
Antipsychotics = can cause inc risk of ventricular arrythmias

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35
Q

What is the mechanism of action of NSAIDs?

A

Reversible competitive inhibitors of COX enzymes
- reduces prostaglandin production (these stimulate nociceptors)

Aspirin = irreversible inhibition of COX

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36
Q

What effects do NSAIDs have?

A

Analgesia
Anti-inflammatory
Antipyretic

37
Q

What do the COX enzymes in the body do?

A
38
Q

How can you avoid the gastric side effects of NSAIDs?

A

Prescribe PPIs
Use selective COX2 inhibitors - BUT - they have ADRs. The COXIBs.

39
Q

Which opioids are:-
- Naturally occuring
- Semi synthetic
- Synthetic?

A

Naturally occurring = morphine, codeine
Semi-synthetic = diamorphine
Synthetics = fentanyl

40
Q

What are the three main opioid receptors?

A

Mu, δ and kappa - all couple to Gi protein channels.

41
Q

How do opioids work?

A

2 fold mechanism = strong effect

(1). Activate Gαi = inhibitory effect
Gαi - inhibit AC - decreases cAMP - inhibits Ca channels - decreases release of NTs.

(2). Opioids also bind to the post-synaptic cell and activate K+ channels - means the post-synaptic cell is hyper polarised and no signalling can take place.

42
Q

Which opioid is deemed to be a weak opioid?
Why?

A

Codeine

Is a pro-drug - is metabolised into morphine which is why the effect is weaker - there is a lower dose of morphine after metabolism.

Codeine also has a ceiling dose.

43
Q

The effects of codeine are subject to a degree of genetic variability. What are the different levels of codeine metabolisers?

A

Poor metaboliser
Intermediate metaboliser
Extensive metaboliser
Ultra-rapid metaboliser

43
Q

What is codeine metabolised by?

A

CP450 family - in the liver CYP2D6 metabolises.

44
Q

How is morphine excreted?

A

Renally - so beware Ps with renal impairment

45
Q

What are the adverse effects of opioids?

A
46
Q

What is the reversal agent for opioids?

A

Naloxone

47
Q

What drugs can be used for sedation?

A
48
Q

Which is the
- main excitatory
- main inhibitory
NT in the nervous system of humans?

A

Excitatory = glutamate
Inhibitory = GABA

49
Q

How do GABA receptors work in the brain?

A

Opened by GABA binding - allows the flow of Cl- ions - making the surrounding hyper polarised and less excitable. Therefore depressive effects.

50
Q

How do benzos, Z-drugs and barbiturates work?

A

Benzos & Z-drugs (Zopiclone) - bind to GABA receptor sites and modulate them (can’t work independent of GABA). Make the channel open more times in the presence of GABA = greater depressive effect.

Barbituates - keep the channel permanently open - therefore have an extremely depressive reaction is easy to kill the P on these drugs.

51
Q

What are the adverse effects of taking Benzos or Z drugs?

A
52
Q

What are the two main types of pain?

A

Adaptive and Pathological

53
Q

What are the types of adaptive pain?

A

Nociceptive (from viscera or somatic source) and Inflammatory

Adaptive pain is protective - stops you doing something as something is wrong in the body)

54
Q

What are the types of pathological pain?

A

Neuropathic (central and peripheral) and Dysfunctional

55
Q
A
56
Q

There are three types of nociceptors - how does each type differ and what effect does this have?

A

Differ in diameter and degree of myelination.

Affects speed of transmission - the larger the diameter and the more myelinated = faster transmission.

57
Q

Which nociceptors when activated cause -
- Sharp pricking pains
- Slow dull ache / burning sensation?

A

Sharp pricking = Aδ fibres
Slow ache / burning = C fibres

58
Q

Why does visceral pain not have a sharp sensation?

A

Because they do not have Aδ fibres - only C fibres

59
Q

What stimuli do nociceptors respond to?

A

Most are polymodal - will respond to pressure, temperature and chemical stimuli.

60
Q

How is inflammation sensed by nociceptors?

A

Inflammation causes there release of inflammatory cytokines and chemicals - these cause excitation of nociceptors which result in the feeling of pain.

61
Q

What is hyperalgesia?

A

Noxious stimuli produce an exaggerated pain response

62
Q

What is allodynia?

A

Non-noxious stimuli produce a painful response

63
Q

Why do we get pain hypersensitivity?

A

If one nociceptor is activated by inflammation - it releases substances that cause vasodilation and activation of mast cells.

The mast cells release histamine which cause inflammation and result in further inflammation and activation of other nociceptors.

This causes pain hypersensitivity = which helps healing by ensuring that contact with the injured tissue is minimised until healing is complete.

64
Q

Which tract do nociceptors run in?

A

The spinothalamic tract (form the tract of Lissauer in there)

65
Q

What is the main mode of action of NSAIDs therapeutic effect?

What is the main cause of NSAIDs gastric adverse reactions? How can you prevent these?

A

Inhibition of COX2

Inhibition of COX1
Prescribe PPIs at the same time.

66
Q

What effect do prostaglandins have on the afferent arteriole?

A

Are vasodilators - increase renal blood flow and GFR = greater tubular flow and more secretion of K+

67
Q

Why don’t we give aspirin to children?

A

Potential for Reyes syndrome - hepatic failure in children.

68
Q

How do NSAIDs achieve the following:
- Anti-inflammatory effects
- Analgesic effects
- Antipyretic effects

A

Anti-inflammatory - reduce prostaglandins - this reduces vasodilation and oedema.

Analgesic - decreased prostaglandins = less stimulation of nociceptive nerve endings. (Headaches - pain relier if probably as a result of reduced vasodilation as well)

Antipyretics - Prostaglandins can eleveate the hypothalamic set point for temp control - thus causing fever. Inhibition of prostaglandins mean that this doesn’t occur.

69
Q

Production of which prostaglandins protect gastric mucosa and renal homeostasis?

A

PGE2
PGI2

Both decrease acid production and increase mucus production in the stomach. Stops damage to the mucosa.

70
Q

Why is rate of AKI higher in NSAID users?

A

Prostaglandins are inhibited.
Therefore vasodilation of afferent arteriole is prevented = reduced BF to the glomerulus.

Reduced BF -> ischaemia + Na & H20 retention

71
Q

What moderates vasoconstriction of the efferent arteriole?

A

ATII

72
Q

What can some patients get with NSAIDs that affects the kidneys (apart from AKI)

A

Acute interstitial nephritis = inflammatory lesions in the interstitial tissue of the kidney - mechanism for this is unknown.

73
Q

What cardiovascular adverse effects can be caused by NSAIDs?

A

Increased BP (don’t know why)

74
Q

What can NSAIDs cause in 10% of asthmatic Ps?

A

Bronchospasm

75
Q

How can we prevent NSAIDs adverse events?

A

Do they need an NSAID? Could you give other drugs?
Consider RFs - renal impairment, age, previous peptic ulcer disease, other medications
Avoid or dose adjust in renal impairment
Consider using PPIs as well

76
Q

Name a COX2 Inhibitor

A

Etoricoxib
Celecoxib
Parecoxib

77
Q

What are the pros and cons of COXIBs?

A
78
Q

The therapeutic actions of corticosteriods are achieved in majority by which type of receptor?

A

Cytoplasmic / Nuclear receptors

Corticosteriods are super soluble and cross the membrane easily.

79
Q

What are some of the side effects of corticosteroids?

A

Skin thinning
Bruising
Infection rate increased
Psychosis
Weight Gain
Cushings
Osteoporosis

80
Q

What are endogenous glucocorticoids responsible for?

A

Carb and protein metabolism
Fluid and electrolyte balance (mineralcorticoids)
Lipid metabolism
Psychological effetcs
Bone metabolism
Profound modulate of immune response

81
Q

What exogenous corticosteriods can you name?

A

Methylprednisolone
Prednisolone
Hydrocortisone
Beclametasone

82
Q

What is the mechanism of action of corticosteriods?

A

Cross cell membrane
Bind to glucocorticoid receptors (GR) - releases heat-shock protein which travels to the nucleus.
This binds to DNA - causes increased or decreased production of mRNA = inc or dec protein expression.

83
Q

What role do corticosteroids play in inflammation?

A

Suppress inflammatory genes = less cytokines, inflammatory enzymes (COX2) and adhesion molecules. Induce anti-inflammatory molecules.

84
Q

What anti-inflammatory effects to corticosteroids have?

A

Really powerful anti-inflammatories…

85
Q

How long does it take before endogenous production of glucocorticoids is stopped when taking exogenous corticosteroids?

A

Within 1 week

Prolonged use - adrenal cortex begins to atrophy and endogenous production can take some time to recover upon cessation.

86
Q

What can happen if there is abrupt withdrawal of steriods after prolonged use?

A

Adrenal crisis

Must carry a warning card and decrease any dose slowly over time.

87
Q

What are the two types of endogenous steroids? Where in the body are they both produced?

A

Glucocorticoids
Mineralcorticoids

Glucocorticoids are chiefly produced in the zona fasciculata of the adrenal cortex, whereas mineralocorticoids are synthesized in the zona glomerulosa.

MLA - Pharmacology Revision (17 decks)

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