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Summary

Join F2 Doctor Nathaniel who has had experience across 33 surgical jobs for a comprehensive teaching session on general principles of Pain Management. This session is designed for final year medical students and foundation level doctors. In this talk, Nathaniel covers various aspects ranging from definitions of pain and the physiology of pain to discussing the WHO pain ladder and different kinds of pharmacological options. Dive deep into understanding NSAIDs, opioids, neuropathic pain agents, and how to handle pain in different scenarios. Plus, get to understand the broader implications of pain beyond the sensory neurons, exploring the emotional aspect of pain as well. This talk promises to offer thorough coverage of pain management and broadens the perspective to include emotional aspects and treatment options.

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Description

Discover the best methods to effectively manage patients' pain in this crucial session led by Dr Nathaniel Shatwell. Expand your knowledge on the core principles of pain management, comprehend different pain categories, evaluate potential treatments, and learn ways to deliver a balanced care approach - all designed to improve patient comfort and outcomes. Ideal for medical professionals who are eager to advance their expertise in pain management. Don't miss this opportunity to learn from Dr Shatwell's experience

Learning objectives

  1. Understand the definition and different types of pain, differentiating between acute and chronic, as well as nociceptive and neuropathic pain.
  2. Learn the physiology of pain and the process of going from stimuli to feeling pain, examining the roles of transduction, transmission, modulation and perception.
  3. Become familiar with the basic principles of the World Health Organization's pain ladder and its usage in clinical practice.
  4. Study the mechanism of action and side effects of NSAIDs in pain management, along with their contraindications in various health conditions such as asthma, renal disease, and heart failure.
  5. Enhance skills in managing pain in specific scenarios, including an in-depth understanding of the pharmacological treatment options available.
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Computer generated transcript

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The following transcript was generated automatically from the content and has not been checked or corrected manually.

Ok. Hello. So, um I'm, I'm Nathaniel. Um, I'm an F two, currently on GP um with interest in um, in anesthetics. Um, and welcome to our talk on general principles of pain management and this is part of a, a series of pain management talks that we're delivering along with, er, Charlie and, er, and Rachel who aren't here today. Um, and so, um, I've had about 33 surgical jobs so far and un easy jobs. I've had quite a lot of experience dealing with acute pain. Um, and so this talk is really aimed at, aimed at final year medical students, sort of finals level. Um, and also for, for foundation level doctors as well. Um, so what we're gonna cover, we're gonna go with some definitions. Um, we're just gonna have a, have a brief um, discussion about the physiology of pain. Um, we're going to talk about the wh O pain ladder and then different types of, er, of pharmacological, er, options that you've got. So, NSAID s opioids, neuropathic pain agents and then, er, we're just gonna go over some pain management and specific scenarios. So just to sort of go with some some definitions of pain then. So what is pain? So, pain is an unpleasant, sensory and emotional experience associated with or resembling that associated with actual or potential tissue damage. Um So the thing with pain is, is it doesn't just involve our sensory neurons, but there are many other factors including our emotions that change the way we perceive pain. Um So this is what makes pain different to nociception and it sort of has this concept of pain, having emotional er, um, aspects with it. Um, it helps us, er, work on treatment options later down the line, um, and acute pain. So that's classified as short pain. Um, that's less than 12 weeks in duration. And this is typically the, the pain that's er, in response to acute injury, illness or surgery and it should normally disappear once that trauma or, um, once that provoking factor has gone away, uh, chronic pain is continuous, long term pain of more than 12 weeks duration. And it can be al also be defined as a pain that persists after the time expected for the injury to have resolved. Um, and then we've got nociceptive pain. Um, so this is pain that arises from actual or threatened damage to non neural tissue and it's due to the activation of nociceptors. Um, so this is our sort of the typical pain that we might use to, er, we might use the nsaids or um opiates to, to treat. Um, and then we've got a neuropathic pain and this is pain caused by a primary lesion or dysfunction of the nervous system itself. Um So just a sort of a brief um description of the physiology of pain. Um So I'll, I'll keep it brief but just enough to get through the basic concepts. Um So, from the process of going from stimuli to feeling pain, there are four main steps to transduction, transmission, modulation and perception. So, um in terms of pain signals are transduced by um nociceptors. And there are er, they're unspecialised, free endings of er sensory neurons and they take three types of stimuli. So you've got mechanical stimuli, heat and chemical. So, chemical things that are being released by cell injury. So, bradykinin ATP potassium histamine. Um and then you've got your nociceptors here. Now there are no, the no receptors are interesting because they're, they're not a separate sense cell like you ha might have in other sensory organs. So say, for example, in the retina, you've got special sense cells, whereas the nociceptors are both the neuron and also the er the sensory receptor. Um and you've got two main types of nociceptor. So you've got a delta fibers. Um So these are thinly myelinated and they're responsible for what's known as your first pain. So this is the rapid acute localized pain. So, if you step on a nail, it's that first sharp pain you're gonna get and you, you experience that first because the A delta fibers are, are myelinated. So they're a bit quicker than the fibers. You see just below there, which are the C fibers and they're unmyelinated and they're responsible for what we call second pain. So that's the delayed, more diffuse, dull pain. Um, and then a, as you can see at the top there. Um, so there's also the um alpha beta, the A, a beta fibers which carry er, information for touch and they're a lot quicker than the er than the C and the er A delta fibers. Um So, tissue injury leads to disruption of the phospholipid cell membrane which then releases something called arachidonic acid. Now, arachidonic acid is then converted to prostaglandin. Now, prostaglandins themselves do not cause pain. But what they do is they decrease the activation threshold for the nociceptors. So, this is known as peripheral sensitization. And so peripheral sensitization also occurs as no seps themselves release substance P and uh something called calcitonin gene related peptide in response to pain. Um and that sensitizes the neighboring those receptors. Um So, a similar process occurs in the spinal cord by a different mechanism. Um and that's known as central sensitization. Um and so both peripheral and central sensitization may contribute towards pathological pain processes. Now, pain is modulated in many different places along the nervous system. Um So this is where the pain signals that reach the brain are altered. So, one of these um modulation pathways is known as the um mel zack and wall pain gate theory. So this occurs here. So if you might, if you see this, this sort of the initial red er line here is your um your your first order neuron and then this big blob at the bottom right hand corner here is imagine that being your spinal cord. So in the presence of noxious stimuli, um if the sensory, a beta fibers are also are stimulated at the same time. So for example, if you um if you rub your skin um after an injury, um the A beta fiber is faster than the A delta fiber, so it'll get to your spinal cord before the A delta fiber and then it will activate an in, in an inhibitor in neuron in the spinal cord. Um and then that inhibitory neuron will it release endogenous opioids such as enkephalin, which will then inhibit neurotransmitter release from the pain fibers from the er first order neuron and also hyper polarization of the second order neuron. And what this does is this results in interruption of the pain signal. And so that explains why we might rub the site of a painful injury. And it also explains why some non non pharmacological techniques might work such as tens machines. And there's also another mod er modulation pathway that's known as the descending modulation of pain. Er This theory 1st, 1st thought up um after doctors noticed that soldiers during er world war two who had serious injuries and they had limbs blown off and things like that and some of them, some of the soldiers didn't report any pain at all and didn't require any pain relief. Um, and so it's thought that, er, on once a pain signal reaches the brain, it may trigger this, what's known as descending, er, modulation new pathway. Um, so you can see that that's that blue line there. Um, And that actually signals the endogenous opioid system to inhibit the signals coming from the spinal cord. Um And it's thought that this may have have evolved to allow an organism to function enough to respond to the pain. And then we've got perception. So finally, brain is the er pain is perceived um in multiple areas of the brain. Um So you've got the somatosensory cortex where pain is perceived and you've also got the insular cortex where the degree of pain is judged. So this is the wh o pain ladder that I'm sure you're all familiar with. Um So it was originally developed for cancer pain, but it can be used for most types of pain. And it suggests that you start er in most pain management, you should start with a simple analgesics like paracetamol and nsaids. Um And it's important to remember that you can skip steps um in acute pain. Um So I remember when I first started as an F one, I thought you had to be really strict with this and start with the paracetamol and then with the NSAIDS. But, er, if someone's screaming in pain, you are allowed to go straight to the, the IV morphine, um, and skip steps if, if someone's in, in serious pain. Um, so we're just gonna discuss each of these sort of sections of the wh O pa wh O pain Ladder in turn. Um, so moving on to nsaids, um, now, nsaids are more appropriate than paracetamol or um or opioid analgesics in inflammatory conditions. Um So, um how do they work? Um So, nsaids reduce inflammation and pain by preventing the release of prostaglandins at the site of nociception. Um So they, they inhibit two enzymes. You've got your cox two enzyme and your cox one enzyme. Er Now, both both of these enzymes are responsible for converting arachidonic acid er released by the um er phospholipid membrane in the cells um to er prostaglandins. Um Now, cox two is responsible for producing the prostaglandins responsible for the sensitization of nociceptors that cause pain. And cox one is broadly responsible for the um prostaglandins involved in protecting the gastric mucosa in renal perfusion and also in platelet aggregation. So broadly inhibition of the cox. One enzyme is responsible for the side effects of nsaids. So let's just sort of go through the side effects and some of the contra contraindications of some of the NSAIDS. Um So, um as mentioned earlier, er, prostaglandins are involved in inhibiting stomach acid secretion. Um and er, they also help to produce gastric mu mucus to protect the gastric mucosa. And this is all via the cox one enzyme. So, if you inhibit that um, that cox one enzyme, um then you're also gonna um, er, leave the gastric mucosa unprotected. Um And so people are more likely to get gastric irritation and ulcers. Um, and nsaids were also cautioned in asthma. So, around 10% of asthmatics are thought are thought to experience either broncho, bronchoconstriction or hay fever type symptoms after taking nsaids. Um So you might have heard of something called Samter's triad before and that's a triad of as of asthma, nasal polyps and sensitivity to aspirin. So well, specifically aspirin and Samter's triad, but um sensitivity to nsaids is also included. Um and it's thought be this is um er thought to happen um because blocking the cox one enzyme inhibits the antiinflammatory prostaglandins and also causes an excess of a bronchoconstrictive leukotrienes and some asthmatics are particularly sensitive to these leukotrienes. And so some asthmatics do get uh some bronchoconstriction with nsaids. Um And then we've also got renal disease. So, NSAID S are cautioned in renal disease. Um this is because they constrict the afferent arterial and reduce G fr that way. Er, so it's important to remember that. So, nsaids constrict, the afferent arterial. Um and then you've also got ace inhibitors that also affect the um the, the kidney, I know it's not related to pain, but they um cause dilation of the efferent arterial and that's how they worsen renal function. But nsaids cause constriction of the afferent arterial um and then just at the bottom there. Um NSAID should also be avoided in heart failure. Um So this is because inhibition of prostaglandins in the kidney may reduce G fr and so they may reduce the excretion of sodium and water. And that can therefore increase the risk of hyper hypervolemia and worsening heart failure. And then some nsaids are also contraindicated in ischemic heart disease, peripheral artery artery disease, and also stroke as well. So think about the choice of NSAID S. Now cos there's there's lots of nsaids available. So how do you choose um which patients go? Which nsaids? So there's a big variation in how people respond to nsaids. Um And about 40% of patients don't respond to the first NSAID. They try. Um But there's a good chance that they will respond to a different one. Um So in general, um Ibuprofen is the safest NSAID at lowest dose at low doses and it has the fewest side effects um but it might not be that good for inflammatory conditions. Um And then you've got naproxen. So naproxen is the, is the second safest NSAID after Ibuprofen um and its effects last slightly longer than Ibuprofen. Um And it may also be slightly stronger. So it may work slightly better. Um And so they're classed as the nonselective nsaids and so they act on both cox one and cox two other nonselective there. So you've got indomethacin. So that may be slightly better than, than your naproxen, er, and korac that you might have seen in, er, in theaters, er, that's typically given IV, and it's good for postoperative pain. Um, so then you've got diclofenac. Er, so that's classed as a nonselective NSAID and it's got preference for cox two for the cox two enzyme. Um but it is one of the most dangerous um nsaids for heart failure and arterial er arterial diseases. So your ischemic heart disease and your peripheral artery artery disease. So, um because part of the risk, part of the side effects from nsaids are caused by the um the cox two, the cox one enzyme. Um So um pharmacologists thought, oh, well, if we um make selective um er, selective cox two enzy er nsaids, um then we might stop all the issues with having side effects from nsaids. Um So there are 22 cox selective enzymes, er, er cox active er NSAID. Sorry. So you've got Celecoxib and Etoricoxib. Um Now all these are good for, these are good for uh patients that are high risk of er, gastrointestinal disease. Um So they're safer in gi bleeding. However, um unfortunately, they haven't, er, managed to eliminate all of the er, side effects of um and contraindications for um nsaids. And the, in fact, the cox two inhibitors are um, have a higher risk in heart failure and also in, er, in ischemic heart disease and peripheral artery disease as well. Um along with diclofenac. So, um back to the wh O pain. I know again. So now we've covered paracetamol nsaids. If they aren't really helping your pain, then what you want to move on to is, is your opioids. Um So let us sort of talk about, about opioids. Um So how do opioids work? Well, the human body releases its own endogenous opioids in response to pain. So, you've got your opioids, enkephalins, dinos and endocrines, endorphins. So, there are um opioid receptors on the presynaptic neuron. Um and the other, the first or neuron. Um and also in the postsynaptic um head of the second order neuron. And these, these are receptors are found across the brain ac ac across the brain and the spinal cord. Um and er the opioids um prevent the release of neurotransmitters from the presynaptic neuron. Um and they also hyperpolarize the postsynaptic neuron. Um And so they prevent the release of neurotransmitters by closing these voltage gated calcium channels on the, on the er presynaptic terminal. So, there are three types of opioid receptor. So you have your Mu delta and Kappa. So on, on this er table here is mop cop and, and dop and that just stands for er mu opioid peptide or opioid peptides. Um Now, each receptor has a different activity on the body. So for example, the mu receptor is primarily responsible for the analgesic properties of opioids. Whereas the Kappa receptor is responsible for some of the hallucinogenic effect of opioids. Now, each different opioid has a different affinity for the receptors. So some are strong agonists at one receptor, but then they, they might be weaker agonists at another re er receptor. Also different patients have different amounts of these types of receptors in their body. Um So this explains firstly why some opioids have different side effects and also why some patients can tolerate some opioids but not others. Um So I'm just gonna talk through different types of opioids now. And so when you might want to consider using each one, so you've got your codeine and morphine and these are natural opioids from er made from, made from the poppy seed. Um and then the other opioids that we've made are synthetic opioids. Um So general side effects of opioids. So um they affect the medulla. So they affect resp, they can cause respiratory depression. Um they can cause papillary constriction by because they activate the um aing of SV nucleus in the brainstem, it can cause constipation, um itching from histamine release and also urinary retention. And they're broadly um side effects of all the opioids. Um some er cause the side effects worse than others. Um So starting with codeine and dihydrocodeine. So these are prodrugs and they need to be converted by the liver to morphine and dihydromorphine. About 10% of Caucasians lack the C YP two D six enzyme to metabolize the um, codeine and dihydrocodeine to morphine. Um, so some patients won't receive any effect from these medications. Um, and the main, the main, uh, side effect of uh, codeine and dihydrocodeine is, is constipation. Uh, so codeine a little bit more constipating than dihydrocodeine. Um, interestingly you can't give codeine, um, or dihydrocodeine intravenously. Er cos it can cause a severe reaction similar to anaphylaxis um mediated by histamine release. It's not an allergy but it's AAA severe reaction similar to an allergy. Um And then we've got traMADol. So, traMADol, traMADol is a synthetic analog of codeine. So, uh in addition to working on opioid receptors, it also acts on serotonergic and adrenergic pathways. Um So you need to be aware of serotonin syndrome. Um if you're prescribing traMADol for someone, especially if they're on SSRI s already. Uh traMADol can also lower the lower the seizure threshold. So you don't want to be given traMADol in patients that have uncontrolled epilepsy, um is possibly less constipating and maybe causes less respiratory depression than um then um er the other opiates. Um but a lot of patients seem to say that they go, they go wacky on traMADol and they seem to have uh some s hallucinations and things like that. Um And then you've got morphine, which is the, the, the opioid, which most of these opioids are based off um and oxyCODONE. So, oxyCODONE is twice as strong as morphine, er potentially causes less, less nausea, vomiting and hallucinations than morphine. Er but it also depends on the patient really. Um And then it's worth mentioning buprenorphine and buprenorphine is interesting because it's both an agonist and an antagonist um at the opioid receptors. Um So this means that if you've got a patient on high dose buprenorphine patches, um the opiates to give them might not work. Um And this is the reason why buprenorphine is, is used in opioid dependence cos it's harder to overdose on it. Ok. So treatment for opioid overdose, um I'm sure most of you will probably know this. So it's naloxone. Er so it doesn't really need to be given unless the respirate is less than eight. So you typically like to monitor the respirate rather than consciousness level er as as to decide whether to give er naloxone or not. Um but you need to be really careful in the palliative care patients because you don't want to completely take the pain relief away and have them wake up in a lot of pain. Ok. So the neuropathic pain agents. So there are four neuropathic pain agents that um nice suggests that you use. Um and um so these are, these are useful for things like phantom limb pain, er compression neuropathies, um and pain after stroke. So, in general, um amitriptyline is the er is the most well tolerated and least risky of, of all the um the neuropathic pain agents and should normally be trialed first, followed by gabapentin, pregabalin and then DULoxetine. Um although DULoxetine can be used first line in uh diabetic neuropathy, um and then you can also use traMADol for neuropathic pain as well as a last resort while you're waiting for a pain specialist. So, talking about amitriptyline then, so amitriptyline is quite a dirty drug cos it affects lots of different receptors. Um, so it's a tricyclic antidepressant and it works by inhibiting neuronal reuptake of serotonin and noradrenaline from the synaptic cleft. Um this means that you can't give it with er, monoamine oxidase inhibitors. Um because er, y you risk um serotonin syndrome, er, now because it acts on all the different receptors. Um, so it blocks er, muscarinic receptors that has anticholinergic side effects. Um So your anti, your classic um, anticholinergic side effects, uh being unable to urinate. So urinary retention, um you can have blurry vision. So it, it worsens glaucoma. Um you have a dry mouth and you also can't, you also, er, can become constipated. Um, so there's use for a ha a handy er, rhyme for that and that's can't pee, can't sit, can't spit, can't shit. So that's the for the muscarinic side effects of um, of amitriptyline, it also blocks histamine receptor. Um, so that causes er, sedation and er, weight gain. Um, it blocks alpha adrenergic er, receptors that can cause hypotension. Um and then it also blocks dopamine receptors so that can cause sexual dysfunction and extrapyramidal side effects. Now, amitriptyline is dangerous in overdose. Um So in overdose, you might see um anticholinergic side effects. So if you, if you sort of think the way I always like to think of it is um, yeah, cholinergic is, er, er, is, er, the um, so acetylcholine is al always involved in the, in the um er parasympathetic nervous system. So, if you turn that off, you're activating the, the um sympathetic nervous system. So you've got pupil dilation, tachycardia. Um So there you know, classic signs of um of the overdose there. Um And then you've also, you can see uh central nervous system depression um and also respiratory depression as well. And the classic finding, especially in terms of exams is broadening of the QR S interval. And that can indicate that convulsions and ventricular arrhythmias are about to occur. And the treatment for that is er with sodium bicarbonate. Um and that's the thought to work by making the blood more alkaline. And so the amitriptyline becomes more protein bound, so it can't affect the heart. Um and also it may work because um the er er sodium and the sodium bicarbonate may help to reverse the sodium channel blocking effect to amitriptyline. So that's most things you need to about amitriptilina voltage gated, um calcium channels. Um Now, the reason why they probably use slightly less, um, amitriptyline is because they're, they're drugs of abuse. Um, and, er, there's also, you can also get increased suicidal, um, ideation after starting the medications. Um, they do have relatively few side effects, especially when you compare them to other anti epileptics. Um, and their classic side effects include drowsiness, dizziness, dizziness, um, and ataxia, um, pregabalin is licensed for both, er, peripheral and central pain. Er, central pain, pain being the pain from stroke and multiple sclerosis. Um, and er, it's also licensed for anxiety as well. Um, and then pregabalin is, is er, for er, peripheral pain. Um, ok. So now we've got DULoxetine. So d DULoxetine is a selective um, noradrenaline and er, serotonin, um, and noradrenaline reuptake inhibitor and it's specifically licensed for the treatment of diabetic neuropathy. Um, ok. So now we're gonna talk about analgesia in specific situations. So, one particular situation that I've come across a lot, um, we, uh, cos I've, especially since I've had quite a lot of surgical jobs, um, is patients that are nail by mouth. So say, for example, a patient might have had er, surgery on her bowel and they've got an anastomotic leak and so they're literally not allowed to have anything at all. Um, so your options are to give things in intravenously, intramuscular and subcutaneously. Er, so we typically like to give things intravenously. So, intramuscular is quite painful. Um, sub subcutaneous isn't as painful as intramuscular, but um, er, it, it is far easier given intravenously. Um, now here's the problem is that you can give IV paracetamol, but as I mentioned earlier, you can't give IV codeine and dihydrocodeine. So your options here are IV traMADol. Um, and then above that, in terms of your strong analgesics, your, your strong opioids, you have your oxyCODONE and your morphine. Um, so if this is the ward situation, um, the ward don't usually like to give IV um morphine or IV um oxyCODONE because that normally needs to be given in high dependency areas where the patient can be monitored, um, where they can, uh have their BP monitored closely. So, um IV, er, bolusing IV morphine can cause hypotension because of the release of histamine when you bolus it. Um, so, um, they're usually only given in, in, uh, in the emergency department. Er IV morphine. So you can't really bolus that in a patient, what you can do is you can give them something called patient controlled analgesia. So that's where um, a specific mix of, er, of the opiate and um, uh a um, something to dilute it is, is made up. Um, and then the patient can have a, they have a little clicker that they can press, um, and that goes through into the vein. Um, and the benefit of that is, it gives them a very small amount of, um, amount of opiate. Um, and um, if they become too sedated, then it means they can't click the button anymore. So patient controlled analgesia is really good. Um, a thing for, it's handy to know for F ones I think is, um, patient controlled analgesia needs fluids going at the same time. So sometimes a nurse might ask you to put up a bag of fluids so that the, the PCA can run through. Um, and in that, in that case, you can just run a really slow bag of fluids, 12 hour bag of fluids will do. Um. Ok. So a specific situation here for back pain and sciatica. So interestingly, um, er, nice, doesn't suggest that you use paracetamol for back pain. It suggests that you use nsaids first line. Um, and then after that codeine and then you can add in paracetamol. Um, if, if that's not helping, um, now neuropathic agents aren't recommended in back pain. Um, and then you've got sciatica. So there's shooting pain to be starting in the buttock and going, working down towards the leg. Um, so again, you can use the er lower back pain medications here. So, nsaids, not paracetamol. Um, and then codeine. Um, now, nice specifically suggests that you don't use gabapentino its um for sciatic pain. Um, but they don't make any recommendation on whether you should use any of the other neuropathic pain agents. Er, but they say from, they say there's not enough evidence to suggest that using amitriptyline or D or DULoxetine works, but from their experience. It does. So, I think if your, if someone's pain isn't controlled on nsaids or codeine, then you can try either amitriptyline or DULoxetine. Um, if you have a patient with back pain and sciatica, you can use something called the start back tool and that works out their risk of progressing from acute back pain to chronic back pain. If they've got a moderate risk, then you can offer them other things such as physiotherapy, er, CBT, er, group exercise therapy and if those things don't work, um, then there's a, er, an intervention called radiofrequency denervation. Um, and that's good for facet joint dysfunction, dysfunction in the back. Um, and then you can also offer surgery as well for sciatica, trigeminal neuralgia. So, can anyone think of there's a specific pain medication that's first line for trigeminal neuralgia. Although trigeminal neuralgia is a, a, uh, um type of um, neuropathic pain. Um, those four agents aren't the ones that we use. So we use carBAMazepine, um renal colic. So, er, there's one, particular medication that works very well for renal colic. Um, and that is pr diclofenac. Um, so it's stocked in most SA us in, in hospitals acro around, around the UK. Um, it works particularly well. Er, be partially because it, it, there's also a local effect of um, of the, er, NSAID going from the rectum and can, may poten, there is thought that it may potentially be able to make its way the, er, anti-inflammatory effect over to the ureters. Um, so the nsaids also work there, er, very well because, er, er, as well as reducing um, pain and inflammation, um, by acting on the prostaglandin pro prostaglandins. Um, it can also inhibit the um, um, contraction of the ureteric muscle and you've got muscle spasms. Um, so there's two particular medications that you can use here that are quite good. So, diazePAM and Baclofen. So, Baclofen is typically used in um, stroke or er, MS. And then you've got gastrointestinal spasm, so high C and Butyl bromide, um that can also be used for um, er, um ureteric spasm as well. Um, and then mebeverine. So they're both very good for patients that have um IBS type symptoms or nonspecific spasmodic type pain. So let's go through a, through a case. So Jean's a 50 year old lady who sprained her ankle five days ago. She's in a lot of pain and she's taking paracetamol and er P RN codeine, which is not helping. She's got gord and mild heart failure. So I'll give you a few minutes just to think which medication, which NSAID might be the best for this sort of pain. So, the best sort of pain, man, the best NSAID in this situation would be Naproxen. Um, so Ibuprofen isn't on there. You'd probably try Ibuprofen first. Um, but she can't have the Celecoxib um, or the Etoricoxib because she's got heart failure. Um, and she can't have the diclofenac because of the heart failure as well. Um And then ketorolac that's, er, used for the postoperative pain. Uh soap proxen is the best, the best shout there. So, Bob is a 70 year old man who struggled with radicular pain. So, er, neuropathic type pain in his right arm from C seven nerve impingement for five months. So he's taking regular paracetamol, er P RN Ibuprofen and codeine, which aren't helping. He's got severe heart failure and he's taking phenolax for depression. So, what's the most appropriate analgesia regimen here? So, I'll, I'll give you a little bit to think. So, the best option here would be a, would be uh gabapentin. So he can't have the amitriptyline because he's taking phenazine, which is a monoamine oxidase inhibitor. Um And then the um he's got er severe heart failure so he can't take diclofenac or Ator. Um and then traMADol. So traMADol, traMADol can be used for neuropathic pain, but it's only used um in situations where um uh you've tried everything and you're waiting for a specialist pain management. So that was a, a whistle stop tour of er, the general principles in, in pain management. Um So our next sessions and we're gonna be talking about pain management with patients with deranged user, deranged LFT S, er, pain management in palliative care, er, chronic pain and non pharmacological pain methods. Um and then also pain management in the trauma patient. So, um does anyone have any, any questions at all? I don't know if I can see the, uh, the, the chat. Hi, Miss. Yeah. Uh, thanks for speaking. I think there was a few questions on the message chat box. So that was the first one from, so you did ask about the form of medications in terms of formulation and its side effect profile. So, for example, diclofenac gel. Mm. Yes. Yeah. Um, so, um, diclophenac gel um works very well along with the Ibuprofen gel. Um So you can use them both for um musculoskeletal type pain. Um So the systemic absorption isn't really too much. So you can use that in patients with um with uh heart failure and uh and and gastrointestinal disease um because it shouldn't really as long as they don't apply, apply loads. Um then um things like dicopac gel can really help. Yeah. So the second question is from what he um he did ask if amitriptyline C for heart failure and ischemic heart disease, if, if Ami Triptans, what sorry is safe in heart failure, safe in heart failure. Um I'm not quite sure actually, I probably just have to double check. I I'm not, I'm not aware of any um any glaring contraindications with, with heart failure and uh and amitriptyline. Um I've seen a few patients with heart failure, amitriptyline before um I can have a quick look um off the top of my head. I think it will be just electrolyte imbalance as well as the hyperkalemia, I think potentially can cause issues with the drug. Yeah, of slides. Uh we can send the slides out. So, um, after you fill up the feedback form, you get a certificate and we can send out the slides later as well. Um, any other questions or anything else to share uh from your end? Yeah. No, I don't think so. I hope, I hope you all enjoyed it. It was just very, uh, very quick, um, er, overview of all the different, er, all, all the different ways that you can manage pain. Um, pharma with a focus on pharmacology. Really. Um, so our, our next sessions can focus more on, er, non pharmacological, er, pain management methods and if you'd like the slides, we can, we can send those out for you and, uh, any other questions you can? Yeah, we're happy to happy to take an email two. Oh, I think there was one more question from Darryl. Um, I think he did ask specifically if there is, um, Im codeine and also whether it's frequently stopped. If it's what? Sorry if it's like stopped in hospitals? Im codeine. Im codeine. I've never, I've never seen Im codeine before. It's a good question. Cos you can't, you can't give it. IV. Um, I've never seen Im, I, in fact I've never seen, um, any pain medications given I am. Um, I generally because, um, er, because it's painful to give things I am. Um, and with, for mo most drugs you've got the option of, er, subcutaneous. Um, so if someone can't take any oral medications, typically we'll go to, if you're trying to control acute pain in a ward situation where you can't use, um, IV morphine or oxyCODONE, we typically use, um, subcut morphine or oxyCODONE. I've never seen, uh, Im used. Oh, so they are saying that, um, he has seen it been being given in his hospital and just wondering if it's useful in the acute setting? II am. Hm. Um, I'm, I'm not quite sure, to be honest. Um, I've, I've never seen it, I've never seen it given myself, so I'm not, I'm not sure if it, uh, I'm not sure how well it, how well it works. Um, it's interesting that you've, you've, you've seen it at one of your hospitals? Um, I've never, er, er, in the game my colleagues have seen either. So that's, er, an interesting use. Um, I think typically in, in acute pain, um, you would, er, you would go for the IV options, um IV morphine. Um, in the, er, if you, if you're able to have access to a high dependency setting, er, but I'm not too sure about that. Um, Im Coding I'd have, I'd have to look up. Yeah. Can I see much of it from my end as well? Uh Pia Diclofenac is also quite commonly used. Um, yeah, we usually try paracetamol. And the IV morphine and also Diclofenac. Mhm. Any other questions from the group? Ok. Mhm. No. All right. I think we'll probably end it there. So, um we'll have the recordings uploaded to youtube um soon, maybe the next week or two. And also we'll appreciate if you can fill up any uh feedback form as well. Thanks so much for joining it. Ok. Thanks guys. See you later, you know. Yeah, it's, it's, it's not.