Another languishing LO. My feelings about this were “Ugh” and I wasn’t going to touch it either until I was looking through Acute Pain Management:Scientific Evidence, for another reason, and saw that there was a figure with that exact title – yippee!!
All statements relate to the figure (Fig 1.2 pg 26) and the surrounding text
Pain results in an decrease in activity of the parasympathetic nervous system T/F
Increased insulin sensitivity occurs in response to pain T/F
Cortisol levels are elevated by pain T/F
Activation of nociceptors results in changes in gene coding and protein synthesis T/F
In the post-operative setting it can be hard to separate the effects due to tissue damage from those caused by pain T/F
There have been quite a few of posts on topics related to this one, but generally looking at how blockade of the PG pathway causes analgesia (ie. the effects of NSAIDs). I marked an SAQ on the effect of NSAIDs a couple of years ago. Candidates were much better at describing how these drugs produced their adverse effects rather than their beneficial ones.
So, how is it that prostaglandin production results in the experience of pain? Let’s investigate.
Although it is a pharmacology textbook, Katzung’s Basic and Clinical Pharmacology has an excellent chapter on prostaglandins (Ch 18). All of these statements are taken from that chapter. For those of you without access to the textbook, the beginning of this article has a good summary of how prostaglandins can produce pain.
BT_PM 1.23 Describe the prostaglandin pathways and their physiological role in the production of pain
COX 1 isoenzyme has a greater role to play in pain production compared with the COX isoenzyme T/F
Tissue damage releases cytokines which induce the COX-2 enzyme T/F
Arachidonic acid (the precursor of all prostaglandins) is induced by tissue damage T/F
PGE2 is involved in the sensitisation of peripheral nerve endings to painful stimuli, by reducing the threshold for neural transmission T/F
PGE2 has a role at the level of the dorsal horn to promote central sensitisation T/F
Hyperaemia in damaged tissues results from increased vascular permeability mediated by prostacyclin T/F
Hyperaemia enables increased delivery of inflammatory mediators to the area of tissue damage, resulting in further prostaglandin release T/F
I think this is another LO where you what you learn should be directed towards how it affects function rather than just memorising in detail the intricacies of the receptor itself.
The top 4 statements are core. The last one is the most interesting (I’ll try to find a good concise article on it for those who are interested and will update the post when I have). You will find the answers to the rest in, you guessed it, Hemmings and Egan 2e. There is also a nice summary article in BJA Educationhere.
T/F multimodal analgesia involves the use of a combination of analgesic drugs which each have a different mode or site of action
T/F multimodal analgesia can: (i) improve the quality of analgesia, and (ii) reduce opioid use, thereby limiting opioid induced side effects
T/F an opioid is always needed for multimodal analgesia to be effective
T/F The concept of pre-emptive analgesia involves giving analgesic drugs prior to skin incision. This emerged from animal studies which showed that this technique minimised dorsal horn changes associated with central sensitisation. However, in clinical studies, there are conflicting outcomes when comparing “pre-incisional” and “post-incisional” interventions.
T/F epidural analgesia is one intervention which has a clear pre-emptive analgeic effect
T/F The concept of pre-emptive analgesia has largely been replaced by the concept of preventive analgesia. This refers to interventions which can reduce peripheral and central sensitisation, and thereby reduce the intensity and duration of post-operative pain (compared with other interventions, or no intervention). Preventive analgesia is not defined by the timing of the intervention.
T/F preventive analgesic effects can be produced by – local anaesthetics (regional and neuraxial), ketamine, and gabapentin
A few weeks ago I ran a series of posts on this LO.
I ran out of steam before reaching the last of the bullet points. This was partly because the area has held so much hope from a theoretical mechanistic viewpoint but there is little strong scientific evidence to support benefit from particular clinical practice – how disappointing….
I thought it might be timely to revisit now, just before the written exam. I wish there were a rapidly acting pre-emptive analgesic, I could prescribe, to make tomorrow less painful for those of you about to sit. However, the best prescription, to make the day easier, is to have studied well and practised lots – which I am sure all of you who read this blog will have done. BEST WISHES!!
In the protracted series on this LO, today we have made it to the brain. Again a complex area, but one where it is important to have some fundamentals sorted in your minds.
I thought you might need something beautiful today as an antidote to all the pain… Here is the inverted dome ceiling of the Palau de la Musica in Barcelona. The whole building is amazing and the ceiling even more sublime in person
BT_PM 1.3 Describe the basic physiological mechanisms of pain including:
• Central processing of pain
Nuclei in the lateral thalamus mediate the processing of the sensory and discriminative aspects of pain TRUE/FALSE
The amygdala is involved placing pain within an emotional context, which may enhance to inhibit the pain experienced TRUE/FALSE
The primary somatosensory cortex is involved with both sensory and emotional processing of pain TRUE/FALSE
Nuclei in the medial thalamus have projections to areas involved with the affective experience of pain TRUE/FALSE
At the level of the brainstem, and through associated neural networks, there is modulation of the autonomic response to pain TRUE/FALSE