Computer generated transcript

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

OK, I think let's go for it. So my name is Olivia. I'm one of the IMT one s currently over at the Royal Brampton Hospital currently in respiratory medicine. But I have an interest in ONC, which is why I was asked to do this lecture in oncology and palliative care. I have kind of the lucky task of trying to summarize the whole of oncology and palliative care into a one hour lecture, which is pretty tricky. Um So I've just try to focus on kind of the learning objectives that were sent to me by your medical education team is kind of basically what you need to know in your exams because I'm sure that's all what your priorities are and I might as well teach you what you need to know. So the topics we are going to go through are firstly the common cancers, we obviously can't be able to go through all of them. We are going to dive through just the popular exam topics really within them. And we're going to have a quick look at oncology treatment as a whole and then a few oncology emergencies very briefly alongside that from the palliative care perspective. We're going to focus on some, um, end of life symptoms, medications that we use for them and their favorite exam topic question, which is on your opioid conversions. So I think it's always nice to start with a case. Um, so we've got Mr P here. He is a 78 year old male with a background of hypertension and diabetes. He came to the GP due to a history of back pain and lethargy. So he describes what sounds like a six month history of just some lumbar ache. Um and he cannot identify any trigger such as a fall or an injury that may have precipitated this alongside that he's lost a couple kilos in weight, which is completely unintentional from the end of the bed. He looks epic. You try to um on examination of his back, you can't reduce the pain, but the remaining examination is unremarkable. His bloods show a a mildly raised CP. His ALP is markedly raised and he's got some hypercalcemia. So hopefully that gets your brain thickened a little bit. So this is his X ray. I don't know if anyone wants to be brave and tender i on and see if they can tell me what they can see. If not. I'll let you know no takers. Ok? No worries. So I hope that you can see throughout this, there are a few bright white dots particularly on the lateral spine that don't look like they should be there. I don't know if you can see my cursor, but here, here, here, normally the vertebrae are quite homogenous and they shouldn't have this kind of polka dot appearance and the same thing with the pelvis here. So this was reported as multiple radio opaque lesions throughout the lumbar spine, sacrum and pelvis. So hopefully that gets you thinking about possible causes for these lesions and going on to that, I'm going to get you to or out your phones and either scan this or use the in to code and give me some ideas about what may be causing these findings. So if I go on to this, yeah, that is a good one. Try and be a little more specific if you can. Yeah, multiple myeloma is always a good suggestion when you think about bony lesions and the other causes for bony lesions that we thinking about METS that you can think of. Right. Nice. So we are thinking about parathyroid home and I think that should say RP production, which is really, really important. We will touch on that shortly. And sarcoid is another really good suggestion. So I'll stop it there and I'll go back to the presentation. So you were right in thinking that bony me was really our biggest concern here. And I guess the question really is what cancers are the most likely to metastasize to the bone. And that actually came up in my final exams and it's a really common question because it's just rote learning. So it's one that I would probably remember and I don't know about anyone else, but I find it really useful to learn mnemonics because they stick in my head a lot better. Um So the one I use for this is precious bone killed through lesions. And that is prostate breast, kidney, lung and thyroid, switch them around. And it's a really easy makes sense And the five top malignancies that often spread to bone. So if you're thinking about it in a kind of single best answer question, they are the five that you've got to go through with in terms of symptoms and see if they fit with the main stem of the question. So out of all of these, the one that we would probably think about most in a 78 year old gentleman with a kind of insidious history with no significant smoking history. Um We would think of our most common cancer in males, which is prostate cancer. So with all the cancers that we are going to go through, I've tried to do kind of just a little summary so that you can kind of remember the main points in terms of symptoms, investigations, markers if there are and treatment. So prostate cancer is the most common cancer in males. It often comes up in exams and it happens to one in eight men in their lifetime. We know the prostate is a gland that is located between the bladder neck and the urethral sphincter. And the section of the prosthetic urethra actually runs through the prostate, which becomes really important when we think about symptoms associated with both BPH and prostate cancer. So when we are looking at types of prostate cancer, there is only really one that you need to remember for your exams. And that's adenocarcinoma, which means it originates from the glandular tissue. And that is for over 95% of the types of prostate cancer. There are others like transitional cell, but they are very, very rare. When we look at risk factors, you're always going to do well by saying age and smoking. But other things specific to prostate cancer include a diet that is high in red meat and fat and also Afro Caribbean origin symptoms for these. So actually, as we kind of alluded to prostate cancer can be a very insidious asymptomatic almost onset and often it's found incidentally in people who have had their psa taken. But it's quite easy to work out what the other symptoms may be if you think about what is the cause of it. So if we are thinking about symptoms due to the hypertrophy of the prostate, which is BPH, but can sometimes happen in prostate cancer, you think of your lower urinary tract symptoms. So you think frequency urgency and terminal dribbling things like that. If you want to think about local invasion, then you think about what's around the prostate. So it's your rectum, your urethra and your vas ephrin. So that will give you things like urinary retention hematuria, hematospermia and erectile dysfunction. And then lastly, you think about symptoms due to distal metastases, we've already alluded to the fact that prostate cancer often spreads to bone and that's normally in the first place. Um So for that, alongside the liver, lung and lymph, the symptoms would be weight loss, anorexia, shortness of breath, bone pain, and pathological fractures. Investigations for prostate cancer is what we all know kind of first off that PSA is associated with prostate cancer, which I will also kind of dive into a little bit more later on. But it's our favorite examination first to begin with, which is the D and the things that you look in a dire is an asymmetrical nodular and injury to prostate. I've also put with blood to the ALP as well as the PSA because the ALP shows that there is damage to the bone. So if you had a, a rise in your PSA and a rise in your ALP is very suggestive of underlying prostate malignancy. So you see both of them in an exam question that's quite useful to pair them together. If you have concerns from either the dre or from the blood, then you would send them for a urology two week. Wait. And if there is high clinical suspicion after both a repeated D and a PSA to look at the trend, then they would undergo an MRI and the MRI is most sensitive to look at the prostate tissue itself that can contribute to forming your Gleason score, which is your scoring system for your prostate cancer. And it will show you the best way to really obtain tissue and that can be through transrectally or a transperineal approach. But the MRI will kind of guide you on where the tumor is sitting and where it would be easiest to kind of get it from treatment for prostate cancer is really kind of varied because it's such a varies malignancy. We all know that is a good cancer to have. In most cases, it grows very slowly. A lot of people die with it rather than die from it. So in the low grade reasons, we can kind of act one of two approaches. So either a watchful weight, this is often in people who are elderly who aren't fit for surgery or who just don't want any treatment. And that would be through regular PSAs and regular DRS. And if it were that the symptoms were worsening or the PSA shot up, then it would be suggestion about moving to a palliative approach rather than active treatment because this is what the patients have elected for active assailants. On the other hand, is still for low grade and it's for those who would consider treatment, but they are low enough that we can kind of watch and wait in the meantime. So they again would be regular DRS and PSAs, but they would also have a yearly prostate biopsy alongside that to make sure that the tissue isn't advancing any more than what we can see in the blood tests. If there is a higher grade or intermediate, really, then the first option is surgery almost always. And that would be through a radical prostatectomy and that can be open laparoscopic or urology, favorite robotic type. It's also one of the few prostate cancers that actually radiotherapy alone can be curative without treatment. So that's also an option or again, if someone is not fit for surgery, then we can go back to the watchful wait approach with the knowledge that this will be a palliative care pathway. And then lastly alongside the surgery and radiotherapy, we can have some hormonal treatment that's associated with that. So these are gonadotropin or LHRH agonists. And I don't know if you've heard of any of them called Goserelin or Galex. And we can use them in one of two ways if it's locally advanced and treatable, we use them kind of around surgery to try and reduce the tumor. So it's easier to resect or in our more elderly patients who aren't fit for surgery who have already metastatic disease. We put them on lifelong hormonal therapy kind of just to stunt the growth of the tumors. So psa screening, um, there isn't actually a nation nationwide kind of prostate cancer screening program. And that's because the PSA is so non sensitive and nonspecific and it's a little bit of a controversial topic, which is why I just put it in here. The nice kind of s guidelines are that we can inform the patients that they are able to request a PSA when they would like, but you have to kind of counsel them on the fact that this may well lead to false negatives, which are falsely reassuring and also false positives, which means they may go for invasive investigations when they actually had a normal prostate. So patients can request the PSAs in primary care, but there are risks associated with that, ok. A quick, quick snapshot of prostate cancer and we'll move on to the next one. This is Mrs B. She is unlike what the image suggests 32 years old and she has no past medical history. She attended the GB due to concerns of a breast lump. She feels systemically well and denies any additional symptoms. Her medications just includes the oral contraceptive pill. She has no known family history but she was adopted. So it's not too reassuring at the time. Um And she's a non smoker drinks, very minimal alcohol. Her examination uh on a breast exam showed a hard, irregular irregular mass, the upper outer quadrant but remaining examination was unremarkable. Her bloods were also unremarkable. So what we're going to look at next is a bit of our favorite pathophysiology. And I'd like to know if you can tell me the different types of breast cancer and it should be the same link and I hope I can make that work. Uh Yes, but no one can remember. Amazing. You don't need me. Yes. That's a really, really good response. And all of those are correct because we've even got pagets in there, which is a little bit rarer. A lot of ductal carcinoma, which is the most common. That's unsurprising. They're brilliant. So we move on. Um It's always best to kind of refer back to anatomy when we're looking at solid organ malignancies because that always again, lets us know what kind of symptoms that we may suspect when they metastasize or grow locally. So the breast anatomy and we know that this is found, the breast tissue itself is found anterior to the pectoralis muscle and it's made up of a network of lobules and ducts. The lobules are the secretory units and they are made up of el ace and I which line the lobules and they all connect into these series of ducts which eventually form the lactiferous ducts and which is a lot of words to say in one sentence. And then these eventually drain onto the surface of the nipple. The breast itself is supported by some fatty tissue, adipose tissue and some fibrous connective tissue. And it's got an extensive network of lymphatic vessels which is why we get obsessed about kind of lymphatic drainage and the armpit axilla when we look into breast examinations and pathology. So we've kind of touched on this. We all did a brilliant job, but we're looking at the different types of breast cancer. So this will kind of be classified into two different types, which is invasive and noninvasive. The noninvasive includes ductal carcinoma in situ and lobular carcinoma in situ or DCIS and LCIS. And these are kind of classed as pre malignant because they've not invaded the basement membrane. Uh D CS unsurprisingly involves the ductal tissue as lobular is uh coming from the ana cells within the lobule where um they differ that DCIS is almost always unilateral but it is more common. Whereas um L CS can be and often is bilateral and this has a high risk of progressing to invasive lobular carcinoma. Then we'll be looking at our invasive causes. We've got invasive ductal carcinoma and invasive lobular carcinoma and this is where the tumor cells have invaded the basement membrane. There are rarer causes of breast cancer, which we kind of touched on there, which is an inflammatory breast cancer in Paget's disease of the nipples, important thing that I always kind of highlight with pagets is the differentiation in kind of other mimics or benign conditions compared to the underlying elis. So in pagets, your red flags are that if you have thickening of the skin and dryness, that is just associated to the nipple itself and not to the surrounding tissue because that would be in contrast to what you'd expect of eczema, for example, which would be very dry, thickened scaly skin around the breast tissue itself, but should not affect the nipple. So it's a good way to kind of differentiate between red flags. Ok. So again, we are just doing kind of a little bit of a summary on breast cancer itself. Um So we've gone through the types. So we think about risk factors. These are all linked to increased exposure to estrogen. So you've got things like early menarche, late menopause, nar HRT. These can all be explained by your increasing either the length of time that you've been exposed to estrogen or the amount of estrogen that you've been exposed to. For example, in HRT. Alongside this, we know that we've got some genetic risk factors which are really heavily associated with breast cancer. And they include the BRCA one and two mutations, symptoms can really vary. Um and they can be quite misleading alongside that the most common symptoms was really asymptomatic and they are found through the regular breast screening program. But also commonly is a woman who has come in, found a painless lump when in the shower and she wants to get it checked out. There are also specific breast changes that make us really worry and would warrant a kind of more urgent two week weight, a referral they include nipple changes, such as retraction, discharge, scaling, or thickened nipples or skin changes such as the classic po orange or skin puckering or erythema, which is a bit misleading unfortunately, because it's really suggestive in inflammatory breast cancer of active disease. But it also can be mimicked as a breast abscess or a cellulitis or a mastitis. So that one can be a little bit of a delayed prognosis diagnosis because of the ability to have it mimicked by other conditions. Um investigations. Hopefully some of you will have attended these amazing triple assessment clinics and they are kind of a one stop clinic that looks into the history and examination and then you go undergo imaging at the same time and then plus or minus. But usually unless they are very well kind of reassured, you would have a biopsy alongside that. The important thing to remember for your exams is that women under the age of 40 sometimes 35 but normally 40 do not undergo mammograms because their breast is too dense. They would have an ultrasound. Whereas the older generations will have a mammogram. In terms of biopsy, we always try and get a core biopsy because it gets more tissue and it has a higher yield. But if it's a kind of a small cystic structure that is more difficult to kind of get to, then we can do an FNA but it's less reliable sites of Mets. Um pretty similar actually to the previous and that's lung, liver, bone, brain and adrenals. Um And when we think of symptoms kind of further down the line, they may be associated to spread to these areas in terms of treatment. Uh, surgery is usually always the mainstay of treatment. And there's two options really. So we can do a wide local excision if it's a small isolated breast cancer. Um but often people undergo more radical mastectomies for larger or multifocal cancers. The axilla always needs to be investigated when we look into these cancers because as we mentioned, the extensive lymphatic drainage into the axilla and they often do this to something called a sentinel node biopsy where it's very clever. Actually, they put blue dye and radioactive technetium into the nipple and it drains into the first node which they can detect both by looking at it because it will go blue and also through kind of a monitor that can pick up the radioactive substance, they will take a biopsy of that sentinel node. And if there is any evidence of malignancy and then they will do a full axillary node clearance, which is kind of a radical clearance of the whole of the armpit. So in touching on what I've kind of mentioned here, which is hormonal treatment and biologics. These are targeting specific oncogenes within the breast cancer itself. So her two is an oncogene that kind of has a significant role in proliferation and cell differentiation. So obviously if we've got a mutation in that, that can be very destructive by causing high cell turnover. If a woman has her two positive receptors on her tumor, then this can be treated with trastuzumab or Herceptin, which hopefully you've heard of the other receptors that we look for are estrogen receptor or progesterone receptor. And if these are positive, they can be treated in the same way with either tamoxifen or aromatase inhibitors. And they both work by reducing estrogen levels. If a woman is triple negative, that means that her, her two and estrogen receptor and progesterone receptors are all not present so negative. And unfortunately, this does limit treatment options and it means that the cases are often have a poorer prognosis. So we'll go on to our last case. Um And this is Mr apologies for all the rubbish images and he is a 49 year old with a background of hypertension diverticulitis and BPH. And he's come to Ed this time because his wife has brought him as she was concerned that he was more confused than usual. She reports he's been unwell for the last one week with general aches, constipation and nausea. And then in the last 48 hours, he's become acutely confused. He's usually really fit and well. Um he lives with his wife, he's independent and all his ADLs. So this is very out of character. He does have a heavy smoking history of 50 pack years. Um But doesn't drink too much any 10 to 12 units of Largo a week. So, what would you like to do next? I don't know if anyone again, can I attempt someone to have a think about what they would like to do if they were seeing this patient in an themselves? Ok. Oh, very shy. Ok. Well, we'll do the basics, won't we? So we'll do examination and blood to start off with. So, our examination from top to toe, um, positive findings were that he had some reduced air entry at the right base. Um, but otherwise the chest was clear, his abdomen was soft and generally a bit discomfort, a bit of discomfort, but no peritonism, normal bowel sounds. And his gcs was 14 because he was confused. His bloods show an elevated CRP of 22 which isn't too exciting but isn't normal. Um, and quite a high calcium of 2.99. So our next step we often do and we've got a gentleman that is confused. He's got abdo pain. He's got hypercalcemia and reduced air entry at the right base. We're probably going to think about some imaging to try and find out why they are so basics. First, we'll do a chest X ray. I'm going, I would ask if someone would be brave enough to interpret that for me. But I think from track history, it's probably not going to happen. And then we would also like to do an ABDO X ray due to the abdominal pain. And then in, in a young gentleman that's acutely confused, they'd always earn themselves as a CT head. So if we go through the findings for these imagings, hopefully you can see them properly and have a bit of a go yourself as what you think is going on. But this chest X ray, yeah, I've somehow cut off the writing from that, but this shows that there's, I don't know if you can see here, there's a small little meniscus. So instead of having your kind of um usual diaphragmatic curve down here, it's going up. So it shows that we probably have a small right sided pleural effusion. And also I don't like the look of this. So I think hopefully you can appreciate from looking at this lung field to this, that we've got quite kind of high radiopaque density in the right hilar region, which makes me worried, especially because it's kind of got this almost speculated pattern if you can see. So already concerned about that, the ABDO X ray, I don't know if everyone can see just this speckled material here. So that's just really fecal loading. So he's got a whole load of poo all the way up here, ascending colon and descending and into the rectum too with very little air, but no signs of kind of dilated bar loops that we'd worry about obstruction. And the CT obviously, this is just a screenshot, but I can just tell you that it's normal s we have in summary, a 49 year old gentleman, so relatively young with new confusion, abdominal pain and constipation, he's got hypercalm on his bloods and a right hilar mass and chest X ray. Can you piece that altogether for me and tell me what you think is going on. There's always a hint in these initials as well. So you've got some very correct answers. I'm very impressed. Um others that we could probably explain. But um as with everything in your kind of single best answers, you always want to think about the option that will most um most easily fit with the with the history of symptoms there, some really good answers there. So we'll go through what we think might be going on then. So a real brief touch on hypocalcemia before we talk about the underlying diagnosis. So I don't know if anyone can remember. Again. I like pneumonics. I like easy ways to kind of remember things for exams. And I always remember for hypocalcemia, the classic stones, bones, abdominal bones, and psychic groans. This is part of a hypercalcemia kind of picture of what the classic symptoms are. So we've got stones for kidney stones and that's because the calcium is, there is a part of a kidney stone. I was going to say ingredients is probably not the right word. But so the increased calcium means that you are more likely to form these stones themselves, bone pain, constipation, nausea, and vomiting as we saw in the ABDO X ray and depression and confusion. So these are kind of classic hypercalcemia symptoms. And when we think about calcium, again, it's a really common exam topic. We've got to think about what it's closely linked to and it's regulated by both phosphate and parathyroid hormone. So, difficulties in renal problems like CKD where your phosphate is managed, that can cause hypercalcemia along with the parathyroid hormone in hyperparathyroidism. So, the common causes are, as we said, hyperparathyroidism and it really closely linked to malignancy. So this can be either directly through destruction of bone. So you've got bony metastases and you've got increased osteoclast activity and then you break down the bone and you've got a big store of calcium there that is released into the serum. So you get a hypocalcemia but also which someone really, really greatly alluded to in the ment is from tumors themselves, producing something called PTHRP. So that is a substance that mimics or acts exactly like PTH and PTH is what we use in the parathyroid gland to increase our calcium. But this is an exogenous production of PTH, which can be produced from the tumors itself. And that causes the same, same kind of subsequent events that you would do. If you release PTH, you get increased calcium absorption in the intestine and the kidneys and you get increased bone turnover and breakdown to release calcium into the serum, but it's just caused from this PTHRP, which kind of mimics the PTH itself. So hopefully, from that mentality, we all saw that we're thinking about a lung cancer in this situation. And I would stress um that with lung cancers, this, this is a really, really common topic and I think the most important things to learn really are how you can differentiate. For me. I think if you learn every single bit of kind of histology, you're a better student than I am. But what I was focused on is what could be present in the stem, which will immediately bring me to the diagnosis. And these are the things that I've put in red, but we'll go through it all in the beginning. Um So first, you always think about location and I like to think of the s for central kind of approach. So the squamous cell in small cells are always more central in origin. Whereas the adeno and the large cells are more peripheral lesions, the squamous cell is the only cancer that grows slowly, but it also grows in the wrong places. So it grows within the bronchi, which means that people get symptoms really early on. So it's actually a pretty good one to have as lung cancers go because it won't spread as rapidly. And also you get symptoms pretty early, which means it's detected much earlier than something like a large cell, which is rapidly progressive and normally extensively metastasized before you get the diagnosis. In terms of the key features. This is the main thing to remember. So, squamous cell think hypercalcemia, the squamous cell tumors are very well known to produce PTHRP, which causes as we've just discussed hypercalcemia. So if you've got a stem of a question that says alludes to a lung cancer and no calcium is up, this is almost always the answer. Adenocarcinoma sets them apart from the fact that it's actually not significantly linked to smoking. Um So again, if it alludes to the fact that this patient has, doesn't have a smoking history, it's probably going to be the one that you're going to choose. And your single best answer, large cell of the defining features, it's most commonly associated with gynecomastia compared to the others. And then small cell itself or the previous or the non small cell, small cell lung cancer is linked to a paraneoplastic syndrome where act or ADH can be produced or both sometimes. So the ACTH, if you can remember from your endocrine pathology that, that an increase in ACTH will give you a Cushing's disease. So then you think about things like a Buffalo hump stry, facial plethora hypertension diabetes and ADH will give you a syndrome of inappropriate ADH exclusion. So you get hyponatremia, hypervolemia and we'll move on to treatment in a second. So again, just a really brief overview into lung cancer as we don't have lots of time to delve very deeply. Um, risk factors hopefully are well kind of drilled into at this time is smoking really is by far the predominant risk factor for some of the rarer cancers like asbestos, asbestosis and mesothelioma. Then you've got to think about other environmental exposures. But other than that, we really want to think about smoking and smoking prevention in the long term. If you are diagnosed with the lung cancer, increased age, family history and rad on gas exposure are also other risk factors. In terms of symptoms. There are other classical symptoms such as shortness of breath, cough, weight loss, hemoptysis. But I kind of try to bring you through this case to show you that people can present really atypically. So this was just a man with abdominal pain and confusion and I'm sure none of us when he first walked through the door would have estimated immediately that he would have had a lung cancer diagnosis. So sometimes they can be more of an insidious onset and not as kind of typical as we think as with anything in medicine. Unfortunately, in terms of sites of metastases, again, it's very similar to the previous breast and prostate in that they metastasize to the bone or the liver, brain lymph and adrenal glands. In terms of investigations. As with everyone, we would get our baseline bloods and chest X ray. But we're really looking forward to get a high resolution CT chest, which can help us with staging and also identify the location and most likely cause of the tumor because these lung cancers are so different in their growth and location. It is quite often able to diagnose lung cancer purely and CT findings. And then you just get a biopsy for reassurance. Before you start treatment, the biopsies can be done in multiple ways. The gold standard is an EBUS, which is an endobronchial ultrasound. So you actually do a bronchoscopy, put a tube, put a camera down the bronch and you would take a biopsy through the bronchial wall. Obviously, if the tumor is peripheral, then you are not able to do that. So you would think about either going in and just doing a pneumonectomy or a lobectomy and looking at the tissue under histology afterwards, or sometimes you can do kind of percutaneous approaches through the chest wall, but they don't come with their own risks. Uh in terms of treatment. Unfortunately, all except the squamous cell carcinoma, they are rapidly growing cancers and they have a pretty poor prognosis if they are surgically receptible. This is gold standard, but there is quite a high kind of criteria for this to be curative. And that is that it can spread to the other lung, it can spread to the lymph nodes. It has to be a certain size. It can't spread cross fishes. So it's very unlikely that these cancers unfortunately can be totally cured by surgical resection in addition to surgery, we can think about other adjunctive treatments. So you can have adjuvant or neo adjuvant chemotherapy or radiotherapy, which are often used. Uh quite excitingly in oncology. There are some new treatments coming out in terms of immunotherapy and targeted therapy, which have shown promising effects but aren't really rolled out fully into the kind of the oncology hospital guidelines. Yet the difference just to touch on between targeted therapy and immuno and chemotherapy. Sorry is that targeted therapy targets cancer specific genetic changes and helps to slow the cancer growth. Whereas chemotherapy targets any fast growing cell, which means that you unfortunately get the side effects associated with chemotherapy because there is a much less specific approach, right? So that was a really brief overview of some of the common cancers. Um So I'm going to really briefly, unfortunately touch on some of the oncological emergencies. There's so many that I could talk about oncology. Patients are one of our sickest in the hospital. We all know the classic neutropenic sepsis. Um Someone coming into ed with neutrophils, not, not one and really unwell and septic, but there are some other more obscure ones which I thought would be more important to touch on because we probably talk about them less and they were also listed in the med list of learning objectives that were sent to me prior to this lecture. So really briefly malignant spinal cord compression. So this is basically when the spinal cord or the CHD quina is compressed due to malignancy. And that can be from a few different ways. So it can be from direct compression. So you have a spinal met that directly compresses either the spinal cord or the Cordner and grows and invades that area or it can often be through vertebral collapse. So if you get osteolytic lesions, so things like multiple myeloma are really common for this and you kind of degrade the integrity of the bone, then these are much more likely to collapse. And when a vertebra collapses, it can cause it then direct compression or instability. So the symptoms we want to think about and always think about with middle and spinal cord compression are back pain, but particularly nocturnal. That's our red flag and it will be back pain, that's not reproducible on examination in terms of our neurology. And we always think about what's below the level of the compression. So below the level, we'd have limb weakness below the level, we'd have sensory loss, we'd have hypertonia. If it's specifically affecting the CHD, then it was a classic Chro syndromes. You'd have urinary retention and fecal incontinence for these patients. Kind of, it's the same as stroke in that time as tissue. So we have to act really, really quickly to prevent kind of irreversible paralysis. So gold standard is actually that they have an Mr within three hours, but often in hospital guidelines, we look at this within a 24 hour period. And not only are we looking at the, at the level of the spinal cord obstruction or compression, but also looking at the underlying disease process because this may be the first presentation in someone. And he wasn't known to have an underlying malignancy prior management as soon as they come in, as soon as you have a suspicion, really, you start them on dexamethasone, high dose eight mg BD minimum. And then you're looking at your directed referral to a neurosurgeon, which can kind of come one of three outcomes. The most common as per neurosurgery. Sorry, any budding neurosurgeons is not for surgical management. And unfortunately, that means that it would be a palliative care approach. But often if there is a large tumor and they feel like that they can get at it and reduce it and give these people a little bit of a better quality of life, then they can be convinced. Uh We also look at other things like radiotherapy again to just reduce the tumor size by the time it has spread to a point where you are at malignant spinal cord compression. These are almost never curative um diseases, which is a shame because of the poor prognosis. From this point onwards, it's a very brief touch. Um And then next, we'll look at SBC obstruction. So we know that our SVC is a vein that basically drains all the blood is returning to the heart from the head, thorax and upper limb. So if we think about it, from that perspective, then we can kind of think about why we get our symptoms. The reason why we would obstruct the SVC can be through to external pressure of the SVC itself. You can have a thrombus in it or you can have malignant infiltration. So the cancer actually spreads into the SVC itself. You wouldn't necessarily prevent present with bleeding because it's a venous system rather than arterial. So you can actually have almost complete occlusion and infiltration, which I've seen previously in someone before they present with facial swelling, which I find it quite hard to get my head around. Um So as I said, the, the symptoms are all related onto the fact that you're kind of stopping the venous return from the head and the arms. So for that reason, you get a really swollen plethoric, sometimes even blue face. Um You can also get some significant edema associated with that, but it won't be pitting. Uh You can get distended neck and chest veins and I don't know if you can see on this gentleman to the left though, he's gotten gorged veins all the way down the chest wall. I mean, that's just due to backflow really and pressure and then on occasion, it can be a real emergency and the fact that the swelling can compress the airway itself, you would get signs like hoarseness, which could lead to strider and sometimes respiratory arrest. So, investigations, we want to find out what's causing the spc obstructions. So really they are going to go straight to CT and that should hopefully tell us what the obstruction is due to. Sometimes we can have infective obstructions like a blood THS angina. So it will have a different approach to something like a malignancy. So we want to find out what the underlying cause of the obstruction is. And we can also use things like Doppler because it's a moving image. Sometimes it's better looking at things like Thrombus inside the vessel compared to that of CT, our management is really dependent on the cause. Obviously, if it's an infection, then we want to give them really strong antibiotics. If there's an airway emergency, these patients are going to get intubated and then go straight to it so that we can protect that airway while we can manage the obstruction. Otherwise, we are just looking at steroids to reduce the inflammation diuretics. So if you are offloading the right side of the body, and then that means that there is less backflow of fluid, which means the swelling gets better. And often they go for endovascular stents, which is basically just putting a really stiff stent in the SPC, which means that it can't collapse with the weight of the obstruction. You can also do things like radiotherapy again to reduce the tumor mass. As with the MSCC, it's a really poor prognosis in someone that has got SVC obstruction because at this point, you are looking at a significant amount of neck vessels that have been invaded or surrounded and the chances of that being then resectable are very low, unfortunately. Ok. Um, rapid fire on to the next subject. And this is um taken actually directly from your learning objectives. So just thought I'd really briefly touch on it and it's looking at the different treatment modalities in oncology. And I know that actually this was a question last year in your exam. Um but it's one of those just learn it and you know it and it's a pretty easy after that. So you looking at the kind of different treatment goals in different oncology, treatment modalities. So first we look at curative approach and that's as easy as it sounds. We are looking at getting rid of the underlying malignancy. We are looking at improving prognosis, improving and prolonging life. And our aim is to completely eradicate through surgery, chemotherapy or radiotherapy or both adjuvant chemotherapy often, but sometimes it can be adjuvant radiotherapy is given after surgery. So your goal there is to prevent cancer recurrence. So they will have had the surgical resection and then you have adjuvant chemotherapy. So, adjuvant aid after and that's basically just trying to mop up or clear any of the remaining cancer cells so that you can make sure or be as confident as possible that you've got as much of the disease as you can. Whereas neoadjuvant is given prior to surgical procedures and that's often for the surgeon's benefit because some of these tumors can be really nasty, can be huge, can be encapsulating vessels. And by giving some neoadjuvant chemotherapy, it makes them more likely to be resectable. And then in turn, gives a better prognosis. And then lastly, I'm sure you all know what palliative is. But palliative treatment, we would look at addressing the symptom management without kind of expecting to reduce or get rid of any of the cancer or prolong or improve prognosis. So that leads me nicely onto our palliative section. A very brief palliative section. Um when I was looking at your learning objectives, the it kind of fell into three main categories. So the first was the different teams that are involved with palliative care. Um And that topic is kind of one that you can probably uh decipher on your own in a spa because it's just looking at things like million nurses and hospice care and palliative care consultants. So just have a think about all the people you get involved in the MDT. But I think it, it is easier to be able to guess correctly than some of the other points within palliative care. So I thought I'd prioritize them in terms of topics. So first, we are looking at end of life symptoms. So this is a really common question that I found at least in my finals. Anyway, was looking at what symptoms we can expect when a patient unfortunately does progress to the end of their life and what treatment, what we call anticipatory medications we use to help these, the end of life symptoms are actually relatively predictable. And with new palliative care input, we have ended up being pretty good at being able to manage these. So if we go through these constipation is never underestimate constipation, I'd say I've seen on the ward a million times where people are in agony, even if they are not obstructed. And if someone is nearing the end of their life, all we are focusing on is comfort. So it's important to be able to get these symptoms under control. So for constipation, we'd usually use a stimulant and a softening laxative such as senna and lactulose. That's my favorite combo. And we really just load them up with as much as they can tolerate to make sure that their bowels are moving. Because when you're near the end of your life, everything seems to slow down slightly. But that does include your gastric motility. So they can really, really quickly fall into severe constipation, which obviously can be quite uncomfortable and promote nausea as well, which we'll touch on next breathlessness. So, terminal breathlessness is a really common end of life symptom and it actually doesn't seem to distress the patient that much, but it can really distress the relatives. So if they are having these apnic episodes and then really panting and look like they can't catch a breath and family feel like they are, they are almost drowning or gasping for air and it's really distressing to watch. So more for their benefit, we give things like Oramorph or we can also give Midazolam as a sedative which will help slow that down in terms of agitation. The most commonly used medication is haloperidol. And I think that's mostly because it is also a brilliant antiemetic. So it's often one that we put in a syringe driver, which will help with both the agitation and nausea alongside that. But we can also use something called levopromazine as well. In terms of nausea, everyone's favorite antiemetic is always on Dansetron. But actually, we really rarely use that in an end of life setting because it can cause such significant constipation. And the palliative care team hate it. So it's really good for chemotherapy related nausea. So if there's ever a question about what antiemetic you would use within chemotherapy related symptoms, then always go for Dan. But otherwise I would say stay clear and again, kind of look at haloperidol as your first line option. If someone has got some real problems with gastrostasis, then metoclopramide is a prokinetic drug so that can help kind of move things along a little bit. So sometimes we use that instead and then secretions. This can be really troublesome, particularly in people like MND patients who have problems with their swallow. So we look at different type of antimuscarinic agents which help dry up those secretions. And the main ones are Hyo or glycopyrronium. These can be put on as patches, but often I put IV or subcu alongside that, all these medications actually will just touch on our available IV. But when it comes to a patient nearing the end of their life, we normally put a subcut infusion in which we can bolus these medications through. If we don't think that's controlling their symptoms, then you can put up something called a syringe driver, which is a 24 hour infusion. And that will continuously give the drug and we can change the composition of that based on if their breathlessness isn't managed, the secretions aren't managed, it's really based on their symptoms, then we can alter it accordingly. And then lastly, um, the most difficult one really is pain. So relatives find that they obviously really want to spend time with their family within these kind of last hours to days. And unfortunately, we load them with significant amounts of pain relief. It can be really difficult because we can knock them off. So it's finding a comfortable balance where people can spend time with their loved ones, but also making sure that they are not uncomfortable. So the way we normally do this is through a moderate release morphine and then a short release PRN and we use hopefully, you have seen before this calculation if this works. Sorry. Um So what we'll do is we'll put them on some morphine for 24 hours. We'll do the modified release morphine and then the PRN alongside that. And then after that 24 hour period, we'll add up in M GS the whole total daily morphine dose. That's PRN and the regular doses and then we will divide that by two. So if they have not used any PRN, then the dose won't change. But if they've used say seven or eight PRN, then we are incorporating that into the modified release dose. And we are dividing by two because we normally give half in the morning and half in the evening to calculate your PRN dose alongside that, then it's just 1/6 of the total daily morphine dose. So if you just think divide by two, that means morning and afternoon of your long acting and that's your baseline level of pain relief and then you breakthrough pain or you are short acting, then you want to give short acting morphine standard relief and that will be divided by six. So, and that one leads us nicely onto, I think, what is the last slide? Um So the first thing that when they sent me in your learning objectives that came up was the or an opioid conversion table. And I always think it's a bit of an ugly table and I always think that they expect you to learn lots, but only one thing really comes up, which is your morphine conversions and particularly your oral to IV subcut. So I've popped up this slide because I thought it was quite easy to picture. But, and I've also got this downloaded on my phone for when I'm on the ward myself. But I mean, I think you can just learn it whatever way you find most comfortable. But the most important thing to know is that 10 mg of oral morphine is the equivalent to half the amount of IV or a subcut. And that, that can be tested frequently, even more insidiously in an exam question. So I would say just try and learn that fact alongside that you've got things like codeine, which is the power of 10. Um I think they are frequent, less frequently asked. So I would say even take a picture of that and just remember, remember your morphine conversions and hopefully that will get you through. Um So to finish, sorry, I've been talking for a very, very long time. Um We're just going to test your knowledge. I think I ended up only doing a few of these questions, but we'll see what we've got. So back to M for the last um and we'll see how much you are listening. Yeah, pretty good. Um So if we remember back to that table, uh we think about the one main important fact to remember from each type of lung cancer and our small cell lung cancer is associated with a paraneoplastic syndrome that produces ACTH, which means that we get a Cushingoid appearance. I would, the only thing I would put with a caveat to that is that if it's really acute. Um, so if it's a cancer that has grown more rapidly, um, sometimes you wouldn't get these kind of stria and Buffalo hump pictures because they, they are often ones that develop over months to years. So, depending on how long the lung cancer is, you might have a more acute presentation with kind of still swollen face, moon face hypertension, but you might not have all these typical feature that they suggest. Remember you're pneumonic. Yeah. Well, um so remember always remember precious bone killed through lesions. So, prostate breast, kidney, lung and thyroid brain is actually uh not very commonly associated with um spread to any sort of solid viscera is normally through the CNS. Um So things like spreading to the spine and I think this may be the last one we talked about it 10 minutes a day. So hopefully everyone. Amazing. We nailed it. You are listening. Um Yeah, that's great. So top fat you're gonna take away from the opioid conversion is 10 mg of oral morphine is 5 mg of subcut or IV. So 0.5 to one. And I think that is it. Uh yeah. So thanks so much for joining me. I mean, I'm very happy to take any questions, but I'm not sure if you've already assumed that I am definitely not an oncology specialist. So I, if anything doesn't, something that I can't answer, I can find out the right answer for you or drop me a message later down the line. I put my email up on the screen at the beginning, but I hope you enjoyed. Thank you so much, Olivia. That was really good, especially the, um, the stuff on the conversions. It's really useful to like go through that because it's, it's really easy to forget. Um I've put the feedback form in the chart, everybody. So please just make sure you fill that in cos Olivia has taken, you know, a large chunk of her time out of the day to give us a really good lecture. Um And again, if anyone has any questions, like now is your time, like stick your hand up or just fire away? All right, I don't think there's anything. So, um thank you very much for attending everyone and thank you Olivia. So that's the last um med, final year's revision series talk. So hopefully everyone's enjoyed and uh have a good Christmas everyone. Thank you. Thank you. Thanks everyone. All right. Take care now.