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Anaesthetics > Pain and Analgesia > Flashcards

Flashcards in Pain and Analgesia Deck (29)
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1
Q

When would you consider giving paracetamol for pain?

A

Mild to moderate pain. Often used by anaesthetists both intra and post-operatively as part of the patient’s analgesic regime

2
Q

What is the WHO pain ladder?

A

Structured approach to pain management, starting off with non-opioads, preogressing to weak opiods, then strong opiods

3
Q

What is the definition of acute pain?

A

Pain of recent onset and probable limited duration, and is usually the result of a clearly defined cause such as an injury.

4
Q

What is the definition of chronic pain?

A

Pain that lasts for >3 months

5
Q

What are the pain conducting fibres in peripheral tissue?

A
  • A-delta fibres
  • C-fibres
6
Q

Which type of fibre conducts pain signals faster?

A

A-delta

  • Aδ = small myelinated (5-30m/s) cold, “fast” pain, pressure
  • C = unmyelinated fibres (0.5-2m/s) warmth, “slow” pain
7
Q

What tracts do pain fibres travel in in the spine?

A

Lateral spinothalamic tracts

8
Q

Where do pain fibres cross to enter the spinothalamic tracts?

A

Same level as where the fibres enter, or a few levels above point of entry

9
Q

How many nerve fibres are there in the afferent nerve fibre tracts for pain?

A

3 nerve fibres

10
Q

Which order neuron crosses at the level of entry?

A

2nd order neuron

11
Q

What types of nerve endings are nociceptors?

A

Free nerve endings in the skin whose ion channels are sensitive to a variety of chemical, mechanical and thermal stimuli

12
Q

What is the gate control theory of pain?

A

Aβ fibers carrying sensory information about mechanical stimuli help block pain transmission. These synapse on the inhibitory interneurons and enhance the interneuron’s inhibitory activity.

If simultaneous stimuli reach the inhibitory neuron from the Aβ and C fibers, the integrated response is partial inhibition of the ascending pain pathway so that pain perceived by the brain is lessened.

The gate control theory explains why rubbing a bumped elbow or shin lessens your pain: the tactile stimulus of rubbing activates Aβ fibers and helps decrease the sensation of pain

13
Q

What descending pathways are involved in pain modulation?

A

Descending pathways from the peri-aqueductal grey matter and nucleus rapheus magnus

14
Q

What is the theory behind referred pain?

A

Visceral pain is often poorly localized and may be felt in areas far removed from the site of the stimulus e.g. pain of cardiac ischemia may be felt in the neck and down the left shoulder and arm due to multiple primary sensory neurons converge on a single ascending tract.

When painful stimuli arise in visceral receptors, the brain is unable to distinguish visceral signals from the more common signals arising from somatic receptors. As a result, it interprets the pain as coming from the somatic regions rather than the viscera

15
Q

What are the different classifications of pain?

A
  • Somatic
  • Visceral
  • Neuropathic
  • Cancer pain
16
Q

When assessing pain, what are the key things to think about (and ask)?

A
  1. How long has the patient has had pain? - Acute vs Chronic
  2. What is the cause? - Cancer vs non-cancer
  3. What is the mechanism? - nociceptive,neuropathic,visceral
  4. What is the intensity of pain?
17
Q

What is somatic pain?

A

Pain is initiated by activation of nociceptors in the skin or other superficial tissue, and is sharp, well-defined and clearly located. Can also be deep, due to activation of nociceptors in ligaments and tendons

18
Q

What is visceral pain?

A

Visceral structures are highly sensitive to stretch, ischemia and inflammation, but relatively insensitive to other stimuli that normally evoke pain in other structures, such as burning and cutting.

Visceral pain is diffuse, difficult to locate and often refers to a distant, usually superficial, structure. It may be accompanied by nausea and vomiting and may be described as sickening, deep, squeezing, and dull.

19
Q

What is the function of somatic pain?

A

Protective function

20
Q

What is neuropathic pain?

A

Abnormal processing of pain signal due to nervous system damage or dysfunction. A variety of mechnisms can lead to neuropathic pain, including:

  • Increased receptor numbers
  • Abnormal sensitisation of nerves - Peripheral +/- Central
  • Chemical changes in the dorsal horn
  • Loss of normal inhibitory modulation
21
Q

What are examples of causes of neuropathic pain?

A
  • Nerve trauma
  • Diabetic pain
  • Fibromyalgia
  • Chronic tension headache
22
Q

How would someone typically describe neuropathic pain?

A
  • Burning, shooting ± numbness
  • Pins and needles
  • Not well localised
23
Q

How would someone describe visceral pain?

A
  • Cramping
  • Dull
  • Tightening
  • Bloated
24
Q

How would someone typically describe somatic pain?

A
  • Sharp
  • Throbbing
  • Knife-like
  • Well-localised
25
Q

What are examples of simple analgesics?

A
  • Paracetamol
  • NSAID’s
26
Q

What are examples of mild opiod drugs?

A
  • Codeine
  • Dihydrocodeine
  • Tramadol
27
Q

What are examples of strong opioids?

A
  • Morphine
  • Diamorphine
  • Fentanyl
  • Pethidine
  • Methadone
28
Q

How would you manage neuropathic pain?

A

Offer a choice of amitriptyline, duloxetine, gabapentin or pregabalin as initial treatment for neuropathic pain

If the initial treatment is not effective or is not tolerated, offer one of the remaining 3 drugs, and consider switching again if the second and third drugs tried are also not effective or not tolerated

29
Q

Rank all analgesia in terms of strength of analgesia

A