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Fall 2 > Pain + Analgesia > Flashcards

Pain + Analgesia Flashcards

1
Q

Define Pain

A

The World Health Organisation define pain as “an unpleasant sensory or emotional experience associated with actual or potential tissue damage, or described in terms of such damage”

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2
Q

How is pain rated?

A
  1. Pain scales where patient is asked to indicate degree of pain in relation to extremes: Numerical scale and Visual Analogue Scale
  2. Rating scales: patient asked to indicate degree of pain: Word descriptor scale and Verbal scale
  3. Functional scale and Categorical scale. For young/disabled patient: Graphic scale
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3
Q

What are the different classes of pain?

A
  1. Nociceptive pain

2. Neuropathic pain

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4
Q

What is Nociceptive pain?

A

Noci = harm/injury
Peripheral visceral or somative pain due to direct activation of pain-sensing receptors (nociceptors) in response to a noxious stimulus that alerts the organism of impending tissue damage.

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5
Q

Give examples of Nociceptive pain? (5)

Duration of this pain?

A 
Inflammation
Fractures
Burns
Bumps
Bruises

Acute: lasting <3-6 months, desirable defence mechanism
Chronic: > 6 months, undesirable

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6
Q

What is Neuropathic pain?

A

Pain produced by damage to, or dysfunction of, nerves in the peripheral or central nervous system. e.g. Shingles, Stroke

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7
Q

Give examples of Neuropathic pain (4). How long does it usually last for?

A

Trigeminal Neuralgia
Nerve Trauma
Peripheral Neuropathy
Phantom limb pain

Tends to be chronic, but can be acute after surgery

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8
Q

Pain perception may be viewed as a 3 stage process. explain

A
  1. Detection of pain in the periphery. Noxious stimuli (to skin or subcutaneous tissue) activates sensory nociceptors
  2. Transmission of pain signals from the periphery to spinal cord, predominantly by C-fibres and A(delta sign) - fibres. Signals are amplified or inhibited by local neuronal circuits and descending inhibitory pathways from higher brain centers.
  3. Reception of signal by higher central brain centres, afferent activity generates a pain sensation and initiates an appropriate response.
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9
Q

Which two fibres predominantly transmit pain signals from the periphery to spinal cord?

A

C fibres and A(delta) fibres.

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10
Q

What are the characteristics of the AB fibres?

Function, Diameter, conduction velocity and myelination

A

Function: touch/pressure (mechanorecptors). likey target of TENS and acupuncture
Diameter: 5-10
conduction velocity: 30-70m/s
Myelination: thick

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11
Q

What are the characteristics of the A delta fibres?

Function, Diameter, conduction velocity and myelination

A

Function: sharp pain (nociceptors) touch
Diameter: 2-5
Conduction velocity: 5-30 m/s
Myelination: thin

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12
Q

What are the characteristics of the C fibres?

Function, Diameter, conduction velocity and myelination

A

Function: Dull, burning pain (nociceptors) Touch, Temperature Diameter: ~1
Conduction velocity: <1
Myelination: none

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13
Q

When and who proposed the Gate control theory of pain?

A

Melzack and Wall in 1965

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14
Q

What is the Gate control theory of pain?

A

Melzack and Wall proposed that perception of pain may be controlled by a ‘gate’.

The gate is formed by transmission neurones which supply the thalamus and are affected by small inhibitory neurones (substantia gelatinosa SG interneurones) and by nociceptive (C and Ad fibres) and mechanoreceptor (Ab) fibre input

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15
Q

How does the Gate Theory work?

A

SG (substantia gelatinosa) interneurones inhibit (close) the gate: reduce pain

Activation of C/Ad fibres open the gate (increase pain) by:
(i) direct excitation of the gate
(ii) inhibition of SG interneurones

Activation of Ab fibres close the gate by: excitation of SG interneurones

Descending inhibitory pathways from the CNS close the gate by:
(i) inhibition of the gate
(ii) direct activation of SG interneurones

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16
Q

Name 6 inflammatory mediators of peripheral pain and what do they activate?

A
  1. Bradykinin (produced from precursors in the vasculature) activates
    B2 receptors in nociceptive neurones
    B1 receptors: via the metabolite des-Arg9BK; ‘upregulated’ by inflammation
  2. Substance P: activate NKA (neurokinin) receptors in nociceptive neurones
  3. Adenosine triphosphate (ATP): activate P2X3 receptors
  4. Protons (H+): activate Acid-Sensing Ion Channels (ASICs)
  5. Endogenous activators of TRPV1 vanilloid receptors (endovanilloids, anandamide) also heat, target of capsaicin (active ingredient of peppers). TRPV1 upregulated by BK and Nerve Growth Factor (NGF)
  6. Prostanoids
    produced from precursors in cell membrane. In particular, PGE2 and PGF2 released in inflammation, greatly increase responses to bradykinin and 5-HT
    = sensitization
    Non-Steroidal Anti-Inflammatory Drugs (NSAIDs) such as aspirin block the cyclooxygenase enzyme
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17
Q

Non-Steroidal Anti-Inflammatory Drugs (NSAIDs) such as aspirin block the cyclooxygenase enzyme. Name 3 important neurotransmitters/

A
  1. Glutamate
  2. Substance P (peptide)
  3. Nitric Oxide
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18
Q

How does the neurotransmitter Glutamate work?

A

Glutamate (excitatory amino acid) acts at:
AMPA receptors mediate acute pain (fast response, sets baseline)
NMDA receptors (delayed response)

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19
Q

How does the neurotransmitter Substance P work?

A

Substance P (peptide) acts at NK1 (NKA) receptors to enhance NMDA action (hypersensitivity). Often CGRP (peptide) is co-released; leading to…..

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20
Q

How does the neurotransmitter Nitric Oxide work?

A

Nitric oxide (NO) release which enhances further transmission of pain signal (hyperalgesia)

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21
Q

What two ways is Neuropathic pain generated?

A

(i) Sodium channel clustering
Redistribution of sodium channels to areas of nerve damage can set up ectopic (out of place) firing

(ii) Sympathetic NS-mediated pain
Upregulation of a-adrenoceptors means that NA release causes pain

22
Q

What is the usually therapy for Nociceptive pain?

A

non-opioid (paracetamol, aspirin and other Non-Steroidal Anti-Inflammatory Drugs (NSAIDs)) and opioid analgesics are the main drugs used to treat pain.

Non-opioids are limited by ceiling effect (dose above which there is no further pharmacological action)

23
Q

What is the usually therapy for Neuropathic pain?

A

antidepressants, anticonvulsants, and other CNS-active drugs may also be used and are first-line therapy for some conditions

24
Q

What is the mechanism of action of Aspirin?

A 
Aspirin mechanism
Blocks cyclooxygenase (COX) enzymes: COX-1 (constitutive form) and COX-2 (induced at the site of damage) isoforms

COX-1 associated with gastroprotection, therefore COX-2-selective drugs (‘coxibs’) sought

25
Q

Uses for NSAIDs?

A
  • acute mild to moderate pain
  • chronic disease accompanied by pain and inflammation

NSAIDs also widely used to prevent blood clots and as anti-pyretic (reduce fever) and anti-inflammatory agents

Dose used to treat inflammation is typically higher and time-course is longer (up to 3 weeks) compared to analgesia (~ 1 week)

26
Q

Why is it sometimes that other NSAIDs are recommended rather than aspirin?

A
  • due to gastric irritant effects (via COX-1 block) and anti-platelet effects ( via TXA2 effect)
27
Q

Name and Give examples of the 2 subgroups of non-selective NSAIDs

A
  1. Indoles e.g. diclofenac or indomethacin

2. Propionic acid derivatives e.g. ibuprofen, naproxen and ketoprofen

28
Q

Why were COX-2 selective NSAIDs - Rofecoxib (Vioxx), Valdecoxib (Bextra) and Lumiracoxib withdrawn?

A

Rofecoxib (Vioxx) and Valdecoxib (Bextra) due to cardiovascular side effects.
Lumiracoxib due to hepatotoxicity problems,

29
Q

What are Celebcoxib and Etoricoxib licensed for in the UK and what warning sign do they carry?

A

Used for Osteoarthritis and rheumatoid arthritis and ankylosing spondylitis.

Etoricoxib is also licensed for the relief of pain from acute gout.

All carry a warning for cardiovascular risk

30
Q

What is Nefopam and when can it be used?

A

Non-opioid analgesic. used for persistant pain if NSAIDd are not effective.

Causes little or no respiratory depression (associated with opioids), but can have sympathomimetic and antimuscarinic side-effects.

31
Q

How does Paracetamol work?

A

work by reducing the production of prostaglandins in the brain and spinal cord

Lacks anti-inflammatory effects and so is not an NSAID (also lacks anti-platelet action and does not cause gastric irritation)

Mechanism of action: TRPA1 mediates spinal antinociception induced by acetaminophen and the cannabinoid Δ9-tetrahydrocannabiorcol.

32
Q

Other pain therapy include the use of Compound analgesic preparations. Give examples

A

Co-codamol 8/500
P medicine

Co-codamol 30/500
effective in more severe pain, but accompanied with opioid side effects
POM medicine

Also co-dyramol: paracetamol with dihydrocodeine tartrate

33
Q

What are opioid receptor agonists? When mostly used?

A

Opioids are morphine-like drugs whose effects are blocked by naloxone, act spinally and supra-spinally to produce analgesia in moderate to severe pain (post-operative, cancer pain)

34
Q

Name 4 therapeutic agonists that act on the mu receptor?

A

Morphine
Codeine
Fentanyl
Pethidine

35
Q

What are the 4 opioid receptor subtypes?

A

Mu
Delta
Kappa
Nociceptin/Orphanin FQ (N/OFQ)

36
Q

Describe the spinal action of opioids

A

Activate pre-synaptic m > d receptors to reduce transmitter release

37
Q

Describe the supra-spinal action of opioids

A

Opioid action at mu (d and k) receptors enhance descending inhibitory pathway in brain stem/midbrain involving NA and 5-HT release (by blocking GABA inhibition

38
Q

True or False

All opioid agonists act on the mu receptors?

A

False. All EXCEPT Pentazocaine which acts on the K (Kappa) receptor.

39
Q

What is used as gold standard to which all opioids are compared to ?

A

Morphine

40
Q

What is Morphine?

A
  1. reduces the affective component of pain
  2. metabolised to potent analgesic morphine-6-glucuronide
    3, dose typically titrated against amount of pain relief
  3. commonly given IV or orally as morphine sulphate tablets (MST)
41
Q

What is Fentanyl used for?

A

very potent, short-duration, often used as a transdermal patch

42
Q

What is Pethidine used for?

A

used during labour (due to lack of effect on uterine contraction)

43
Q

What is Oxycodone used for?

A

used primarily for control of pain in palliative care.

44
Q

What is Codeine used for?

A

low efficacy, orally effective drug. Not addictive, so widely used for mild pain such as back-, head- and toothache
- causes constipation with long-term use

45
Q

What is Dihydrocodeine used for?

A

similar efficacy to codeine

- can cause more nausea and vomiting

46
Q

What is Diamorphine (Heroin) used for?

A

metabolised to morphine, high lipid solubility means rapid action and also higher efficacy (important in the emaciated patient in palliative care)

47
Q

What is Tramadol used for?

A

weak opioid and an inhibitor of the noradrenaline uptake/transport system

48
Q

What is Buprenorphine?

A

A partial agonist. Long duration and can be given sublingually

49
Q

Describe the side effects of Opioid agongists.

A
  1. Respiratory depression: reduces sensitivity of respiratory centre; most common cause of death from overdose with street use of opioids; treated with naloxone. Side-effects reduced with d and k agonists
  2. Euphoria: action on reward pathway in the brain to increase dopamine release (likely related to dependence); however, little euphoria in pain.
    For k agonists (pentazocine) side-effects are dysphoria (nightmares, hallucinations) rather than euphoria
  3. Cough suppression (anti-tussive): can be therapeutically useful
  4. Nausea: activate the chemoreceptor trigger zone (which in turn activates the vomiting centre) - anti-emetics typically co-prescribed
  5. Constipation: due to maintained contraction of smooth muscle
    (Kaolin & Morphine used as an anti-diarrheal agent)
50
Q

What are the therapeutic options for neuropathic pain? as they are different to nociceptive pain

A
  1. Antiepileptic drugs e.g.
    Carbamazepine, phenytoin (sodium channel blockers) and gabapentin, pregabalin (via effects on calcium channels)
  2. Tricyclic antidepressants e.g.
    Duloxetine (selective serotonin- and norepinephrine-reuptake inhibitor) and imipramine/amitriptyline (tricyclic antidepressants) effective in conditions such as in diabetic neuropathy
  3. Ketamine
    Analgesic (due to block of NMDA receptors)
  4. Lidocaine or bupivacaine
    Local anaesthetics which block sodium channels (= nerve block) when injected close to a sensory nerve (also effective epidurally)
  5. Ziconotide
    First of new generation calcium channel blockers; administered intrathecal infusion (spinally) to treat neuropathic pain
  6. Cannabinoid agonists
    Sativex (mixture of 2 cannabis extracts THC/CBD) licenced in UK to treat pain in multiple sclerosis patients. Mechanism of action not fully known but THC is a cannabinoid receptor agonist
51
Q

Describe the WHO pain ladder

A
  1. Pain - Non-opioid + adjuvant
  2. Persisting pain - OPioid for mild to moderate pain + adjuvant + nonopioid
  3. perissiting pain - opioid for moderate to severe pain + adjuvant + nonopioid
52
Q

Which analgesic would you use for each scenerio:

  1. Musculoskeletal and dental pain, period pain
  2. Mild, inflammatory pain (sprains)
  3. Severe, acute pain treated by strong opioid IV
  4. . Severe, chronic pain treated by oral, intrathecal or subcutaneous strong opioid (patient-operated infusion also common)
  5. Neuropathic pain generally unresponsive to opioids treated with tricyclic antidepressants or anticonvulsants
A
  1. Ibuprofen
  2. Co-codamol, codeine, dihydrocodeine
  3. Morphine, fentanyl
  4. Oral, intrathecal or subcutaneous strong opioid Morphine, fentanyl (patient-operated infusion also common)
  5. Amitripyline, Pregabalin

Fall 2 (33 decks)

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