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crack on. Yeah, Okay. And it's like, now Okay. Righty ho. Um, so Hi, everyone. Um, yeah, down from the BMA here. I'm just gonna talk very quickly, just before, um, the guys going the way with the session. Um, so, yeah, you'll see. There's, um there's some text on the screen. There's a QR code. Um, yeah, I guess all you guys watching, obviously, finally is, uh, so it's a pretty pivotal time, uh, to join the b m a, um, with the ballot going on and what not? It would be very good if the sort of incoming F ones are strong in membership. So the current finally is because, um uh, well, we don't want it to, but it's part. It's possible that this rumbles on through into when you begin. Um, your F one. So yeah. So, basically, um, if you wanted to join today, um, it's 3 lbs and 25 a month. You guys, um uh it's, uh, animals in the vulture. If you join. Using this QR code we need to do is follow that QR code. Um, and then drop me an email after you signed up, and I'll get you, uh I'll get you a, uh, an Amazon voucher sent over. So that's sort of like covering. Fine. Doctor version, Um, not the student version. So that's included for finally. So, yeah, this isn't available online. It's only because of some sort of coming on the sponsor today, so, yeah, take advantage of it. You pay monthly. So, um, you sort of stays is always you want anywhere. You're not sort of fixed. Um, but yeah. Good. Good time to join. So just a little bit about membership. I'm sure you all members or you'd be members at some point, So you know a bit about what we do. Um, What you sort of get as part of membership as well. So it's a little bit of a refresher on hoping you might find something new as well. Um, so we're the trade union for for medicines and doctors in the UK, We act as the voice of the profession, so represent you on an individual, local and national basis on all the issues that affect you. Um, so, yeah, so we often often get the confusion with companies like M, M, D. U and MPs. So they're indemnity companies. They deal with things like patient complaints were your union. So that's why um, we're the ones sort of doing that. The balloting and what not? Not no. The indemnity companies like M. D u and MPs. Um, so, yeah, I could talk all night about this, but I'm sure you'll know what's going on at the moment. Um, in terms of, uh, the ballot for the juniors that opened last last Monday. Now, um, so Yeah. So since 2008, there's been a real terms pay loss of about 26%. Um, for junior doctors. Um, so that's taking into account the lack of lack of change of pay in line of interest rates. Um, so yeah, so we've called for for a full, um, full pay restoration. So 26% is what we're going for. The ballot at the moment is the ballot juniors on whether they they're happy to go to industrial Axion, um, to sort of pushing through because we've had no response. Um, from the government since since we start talking to them. Sort of middle of last year. Absolutely nothing. So that's why we were in this position. Now, um, I haven't gone too much. But the reason why we're only balloting, uh, the juniors is because we're just balloting people that are working. Um, and so anyone that's employed as a junior in a training scheme in the NHS um, it will be balloted. We obviously think the government thinks well, it will look unfair if we we ballot you guys because it won't necessarily impact your day to day, Um, as you won't have to strike against the job because you're not employed. Um, so that's why it's currently, um, just for juniors only, Of course. Um, if when you guys become F one in July, if there's a pay deal on the table, that's when we'll be, um, balloting again. Um, so say, say, we've got an offer of, you know, I'm picking a number out of the air here, but the barristers got 15% offer and they took it. Say we get 15% off for when you guys start and your f one's at this point, you will be asked, Do you accept this payoff or not? We're only going to accept what we agree as as a whole, as a as a union. Um so Yeah. So this this obviously is going to affect you guys massively being the juniors coming in and just about to begin. Okay, Don't say much more about it, but please keep up to date with what's going on. Sorry. Christ, because the the impact for for you guys is massive. Um, so, yeah, it's just a bit more about benefits. Uh, day to day stuff. So BMA library. We used to have a library service where we send our books and whatnot. Now it's all on. It's all virtual so you can access our e books and whatnot straightaway. BMJ learning is those original tools on there that you can you can access so really good for exams and whatnot. BMJ mentioned at the start. So now you're fine. On a year, you can get the BMJ delivered through the post, um, every Friday. So the doctors version, if you all remember, you're not getting that. Just give us a phone call on the on the phone number that you'll find anywhere on our website. Um, and just say I'm finally and I want to opt into that, um, and we'll send the paper version ultimately, um, if you don't want it. Um, you can still don't know the app. Um, and I access it, um, for your phone or laptop. Anyway, so you can save save on paper. Um, and yeah, we'll run a series of webinars about for the year. Um, we've got really good tool specially explore. Um, so this will give you a bit of a better picture of what specialty is to your best. So it's an online psychometric test. Takes about 20 minutes to complete and ask all sorts of work, like balance questions that will give you a detailed report. Listening tops, especially, is, um, according to the answers you've given, it is really, really thorough covers all specialties and and the analysis and all the graphs. You get the end of it. Um, yeah. Sort of show. Maybe so. Especially that you hadn't considered before are suitable to you. So worth doing. Worth doing? Uh, sort of now in six months time just to see how your your taste that will not change. Uh, we've got really well being service, so that's available to everybody. So regardless, if you remember or not so open 24 7. You have the choice to speak to a counselor or a peer support doctors Or someone's been through, um, what you've been through completely confidential, Of course. And yet, if you speak to us more than once, we'll try and make sure that you speak to the same person again. So So I just think about later in the year, um, our contract checking services is pivotal. Um, with F one's, Obviously, we negotiate the contracts. Um, you're going on to, um and sadly, one in for the contracts we checked 2021. To be honest, 2020 has been the same. Um, were wrong. Um, so it's just too high number, um, and trust the slipping in extra things or changing wording that they shouldn't be doing. I mean, 25% is is not on. Um, what was the point of negotiating contract? And they're just going to change anyway. Um, so, yeah, don't let them breach terms. Send it to us before you sign it. Um, we'll check in of any issues we take up with the trust, but yeah, just anything work schedules will not send it to us first. Also, you can check your right of us um, so, yeah, that's it. Been as quick as possible. Um, yeah, I mentioned earlier. If you join using that QR code, you'll get a 10 lb Amazon voucher. So it sort of covers the first three months or so. Um, please. You pay monthly. So it's up to you when you when you stop. We want obviously membership to be as strong as possible at the moment, um, to give us a bigger cloud and getting or getting, um, pay restoration. Um, so, yeah, so I'd obviously encourage you to join. Um, and that's it. Um, enjoy the session, and thanks for listening. Thanks dot Thanks. Dan. Uh, do you want to present your slides now? Abby? Yeah. Just going to say thanks for joining us for that fourth session. Um, I'll hand over to Abby. He's gonna be teaching you all things renal. Hi, everyone. So, as live said, I'm Abby. I'm currently a doctor working in Manchester, and I'm doing I m t one. So my teaching session is gonna be on nephrology. Nephrology is a large topic, so I've tried to condense it as much as possible in the space in well, just under an hour and I think hopefully we touch a bit on everything that may come up in Europe Finals. Also just a big shoutout to Wesleyan and they sponsor our webinars and they support you throughout the foundation program and beyond. So just scan your QR code if you want to find out more so the outline of this session. So I'm going to start off with a bit of basic anatomy and physiology. The boring parts then split the session to AKI and CKD. A lot of it does overlap and then finish off with some SBS at the end. So as we all should probably know, we have two kidneys around Tencent meter in size are blood flow comes in through the affront arterial and exits through the f rinse so e n e f exit referent, it goes into the bones capital into the proximal convoluted tubule. The thing you need to remember about the proximal convoluted tubule majority of re absorption occurs here, so it's going back into our system. All amino acids or glucose is re absorbed here, majority of bicarb half of year sodium and your phosphate re absorption is controlled by a APTH You then go into your Lupron Penley. You've got your descending and your ascending. Your ascending is the one that's impermeable to water, and this is where your loop diuretics act. The act on the sodium potassium chloride channel. Just important if there's any pharmaco kinetics that come up in your exam, and then it goes through the proximal convoluted, tubule way Thiazide Zynga Spironolactone act and then through to the collecting duct. And this is where your ADH Jack so anti diuretic hormone produced by the pituitary. This is usually produced in a response to Hypovolemia. I always remember is anti anti. We anti diuretic, anti. We. I put slash lithium here because lithium can block the action of the ADH and causing nephrogenic diabetes insipidus, which is important to know for any patient who are started on lithium and they start to present with polyuria. And what are the main things you need to know with the physiology function of the kidney? I'm sure you've all heard of the acronym a wet bed. If you know how the kidney works, you know how they present and you can link the complications. So a is acid base balance, and this is your metabolic acidosis, so you've got a failure of re absorption of the bicarb is a failure to buffer the acidosis. You've got water removal. I'll go into more of it in more detail throughout the talk. But this is just a quick overview, so W is water removal. So you all here. When patient's presenting AKI, they present an uric, or they can be a dumb Otis. They're not passing urine efficiently. A referral oasis so your kidneys produce your endogenous e p o e. P o is in charge of making your red blood cells. These patient's who aren't producing it efficiently will then become fatigued. They'll be tired and they'll be anemic. Anemic anemia tends to presenting your CKD patient's rather than your A K eyes you've got. Then you've got your teeth A toxin removal, the most important being your ear. So when your your ear starts to rise, they become you get your your a mc toxicity. You can get pruritis pericarditis, confusion, seizures and you also get your remick flat, which is important in your I don't know if you call the mosque ease, but your practical exams at the end of finals be for BP control. Uh, kidneys produce the running. Running is important in the run running angio, uh, aldosterone activation system. And this can then lead to hypertension. Then electrolyte balance, the most important being potassium. Potassium is the one that's most life threatening in high doses, so this can lead to your arrhythmias. Always get an E C G and then vitamin D. So your kidney is responsible vitamin D activation. And if it's not been activated, you're not re absorbing your calcium. Your phosphate starts to rise, and this can lead to a secondary hyperparathyroidism. So the three main things you need to remember with a K I s is you get a quick decreasing your kidney function, a raising creatinine and reduced urine output. The stages 123. This was taken from K D. Goes definition, and I'm sure you've all heard of it before. Book. It's quite self explanatory. One stage one is 1.5 to 1.9 baseline to 2 to 2.933 and above. So it's 123123, and then urine output again, not less than 9.5 per kg per hour for stage one in 6 to 12 for Stage two. It's above 12 hours, and then Stage three is less than naught. 30.3. So there's all your threes. Three times baseline, less than 9.3 per kg per hour, and that's for 24 hours. Or you can be, um, uric or they've been started on renal replacement therapy. So we split our causes of our okay into three different sections. Prerenal intrinsic and post renal prerenal, as it says in the name is anything before the kidney. So all your hypervolemia your shock, the sepsis that all fits in your prerenal intrinsic again what we'll talk about in more depth shortly. Your intrinsic is anything that's damaging the kidneys. So you've got intrinsic damage. You can affect your interstitial, you tubules or your grandma, Really, and those against that are further into different diseases. And then your post renal is anything further down the renal trap that's blocking urine output, urine flow. So that's anything. Usually males. It's the prostate or malignancy or renal stones. So prerenal is the important one, because that is 65% of all a K I s and majority of patient's tend to be septic as the primary course, you can either get absolute fluid loss where you're big. You're physically losing the fluid through hemorrhaging burns or G eye loss. It can be relative in your heart failure. Patients'. Your fluid is third spacing, so it's not in your intervascular space. Or you can get renal artery obstruction so you can get stenosis or your medications, like your insides can affect your afferent arterial. And once this, when the kidneys are panicking, they're not getting the blood flow that they need. The running, uh, angiotensin aldosterone activation system kicks off, so they they start to produce a running the running, then produces your aldosterone. And then this, then acts on the collecting ducks and your sodium and water then reabsorbed back into the system because they're not providing enough well through blood supply to the kidneys. You want to re absorb more water to increase the volume and increase your BP and so on. This obviously would also activate your anti diuretic hormones, and like we said, anti diuretic anti we So you're holding onto the water. You're not wearing it out, so your urine concentration is going to increase you know, reduced amount of urine, and the most important thing to look at is the urinary sodium. This is important in differentiate between your intrinsic and your prerenal, because sometimes prolonged prerenal can then lead to intrinsic AKI. You need to look at the urinary sodium, so the question stem will give you a urine, urine, sodium sample. And if it's low, think prerenal. If it's high, think intrinsic. So this is an overview to intrinsic Greenland parents. So this there's multiple causes of intrinsic renal impairment, and this is just a quick summary of each of the following. Like I said before, you can split it into tubules, interstitial and Gomorrah line, so the tubules would be acute tube in your interstitium. Sorry would be interstitial nephritis, and you can Merrill. I then splits into you nephritic and you nephrotic syndrome again highlighted below, which we'll discuss a little bit more shortly. So what happens with the entrance that the epithelial cells become damaged? You get impaired re absorption and secretion in the kidneys, and this can then, like I said before, the importance of the urinary sodium can only to increase urinary sodium because it's not being reabsorbed efficiently. So we'll start by talking about cute glomerulonephritis so glomerulonephritis, this isn't the diagnosis. This is almost like the umbrella term. The histology findings. This is when the antigen antibody complexes deposit in your glomerular tissue. You get inflammation and loss of the filtration barrier, and this is when it starts become leaky. So this is where your bigger proteins can start to leak through, and also your red blood cells. So this common causes a good pastures, Lupus and HSP. This is around 15% of all your A K eyes. Symptoms will be depending on what the presenting disease is, what the condition is. And the main thing to remember with acute glomerular nephritis is that buzz words in the exam if they give you a biopsy, will show inflammatory Crescent. So be a crescent. Eric Picture now your rapid progressive glomerulonephritis. So there's three different types, as as it says in the name, it's rapidly progressive. It comes on very quickly. So this, then is further subtyped into 12 and three. Type one is your anti glomerular basement membrane. So this is your good pastures disease, So good pastures should be a good question. to come up. It's if you just think of the triad of pulmonary hemorrhage, anti GBM antibodies and glomerulonephritis. So the question stem might be a someone's presented to E. D with hemoptysis iss, and they've also they do the blood and the show. They've got an AKI. So any patient with a K I and apoptosis think good pastors first, because this is a glomerulonephritis. The histology will show you crescent Eric, and they also have a buzzword of linear i g deposition. So with anti G b m, it's a G B m four letters. You might have your own way of remembering remembering it, but it's it activates on the type for collagen, So anti G b m type for pulmonary hemorrhage and a K. I think when this comes up in the questions, then think good pastures we manage these patient's with plasmapheresis You want to get rid of the antibiotic is to prevent this disease progressing any further. Type two is your Indian complex, so the most common being post strep suppose strep is the questions. Then would be a lady presents, Um, two g. P. She's Two weeks ago, she had an upper respiratory tract infection. She's now presented feeling still, feeling a bit rubbish, bit fatigue and G. P does bloods and notice she's got a raging AKI. So from the history, it's important to look at the history so they wouldn't mention that she had an infection two weeks ago if it wasn't relevant. So if it's normally around 1 to 2 weeks, that's how you differentiate it from IGA NEPHROPATHY, which we'll talk about shortly. But that tends to be naught to three days, whereas post strep is 7 to 14 days post infection, and then you've got your Lupus and Lupus will have your typical characteristic history of joint pains rash. They would probably they would most likely definitely give you the antibody. So your antidouble, uh, stranded DNA and your histology buzzwords is wire loop appearance. So I'm trying to give you the buzz words for each an exam question, because we don't have time to talk about them all completely in depth. But if you do have any questions, feel free to ask. But so good pastures, your pulmonary hemorrhage, your type for collagen anti gbm membranes. You post strep to two for 1 to 2 weeks. Post infection and then your Lupus, you've got your antibodies and then your wire loop appearance on histology and type three. This is your vasculitis. So your vasculitis there is, uh we tend to put into to you got your sea anchor and anti pr three, which pair together and that produces your G p a. C granulomatosis with polyangiitis. So this question's them would normally present with a patient with respiratory track symptoms so you can have saddlenose nasal discharge. Hemoptysis ISS and the this and good pastures would be the only two patient's that would present with hemoptysis. So when you're not quite sure this patient presents with the pharmacist and make a I, it can either be the vasculitic picture, or it can be good pastures if to differentiate between them both. Look at the bloods. They'll give you the bloods. They'll give you the antibodies. They'll be anchor positive and and with good pastures, they'll have anti G B M antibodies. So look at the antibodies to differentiate between them both. Then this church Strauss and start your e g p a u eosinophilic. So you're in this one you have raised as NFL's. It's not common that a question stem would tell you the Eosinophil count. So it's given it you use. It means it's use. It's there for a reason. If they've got raised as NFL's think, check Strauss and this would have positive P Anca and anti M M p O. They also have quite another characteristic. Part of the questions then would be this patient would have a history of asthma, so it might present in the past medical history or the drug history they'd be on asthma medications. So if you get the classic triad of positive anchor antibodies, asthma and raised his inner fills, think jerk Strauss. There's also microscopic polyangiitis, which again tends to protect with positive P anca and anti MPO. But these patient's wouldn't get your typical asthma and raised his inner fills their just your general symptoms. So that's how you would differentiate between them. Three. That's a quick summary slide of them all. Feel free to take a pic or whether live we can send these slides out later, and you can have a look at them. It's an acute tubular necrosis, so this is the one where I think it's most important with the urinary sodium because acute tubular necrosis can be caused by prolonged hyperperfusion, So the questions then can be very similar to that other pre renal AKI. So it could be also a septic patient. There's other multiple other causes, like nephrotoxic sins rhabdomyolysis, so the long like patient's. But they have a very similar presenting history. A lot of the time and how you would then differentiate between acute tubular necrosis and prerenal is you Look at the urine sodium, so prerenal low your knee, sodium intrinsic, high urinary, sodium it. This tends to happen when you're tubular cells and crows. They then break off and block the tubules. Lumen. This can present quite nastily. It's not easily reversible, and the management is supportive. So get all the fluids in them. And also a common description would be that the urine looks and muddy brown color, especially when presenting with the rhabdo patient's acute interstitial nephritis. So when this one is mainly due to the medication, so they will give you a list of the medication that the patient's on and you notice around, some nephrotoxic is this is most likely what the cause is going to be. This is another AKI, where it will present with raised as enough pills. So it's a characteristic AKI, and they're on a nephrotoxin drug, and they've got raised as in a fills. This is almost like an allergic reaction, its hypersensitivity reaction. So look at the medications. There are other causes, like infection, but this is the main course. Drugs are the main cause of acute interstitial nephritis. So now we've got two causes with raised as NFL's, so with rather thinking church Strauss or acute interstitial nephritis. Question. Stems vary. They'll get positive anchor in your church Strauss, and you'll get their drug hissed. You'll probably still get the drug history on the other one, but just focus more when there's no when there's either got raised as NFL's and did not mention the antibodies. Look at what medication they're on. If this is prolonged or the patient's taken a while to present, they can present in renal papillary necrosis. So this is basically if a queue in traditional arthritis has been left quite a while and these patient's will be quite sick, they'll have quite severe pain, and they'll have visible hematuria. A typical I've just mentioned there quickly is if they've had analgesia abuse. So save the patient's been taking a lot of analgesia for a long time, where they've got a history of chronic pain and the characteristic histology for analgesic um in traditional right is the cup and spill, So that would be how they describe it. Don't ask me what it means. That's just the characteristic words you tend to use diagnosed with the look at the NFL's management. Stop the drug supportive. So fragile. Fluids, whatever support they need, if there's any complications occurring, and then steroids now your nephrotic v nephritic. So this is the glomerular disease. I've discussed a few earlier on your protein. Your ear is with the nephrotic and just actually minimal change. FSGs membrane is that your hematuria's associated with you nephritic? And that's your anti GBM post strep and your vasculitis. How do we tell the difference so nephrotic it has pro innit? Nephrotic nephrotic and protein your ear. So that's how we figure out which one's got. The protein area, which one's got. The hamachi area tend to be above 3.5 g to 4 g in 24 hours. These patient's are very edematous. They have reduced oncotic pressure, so the album is third spacing. They tend to have high cholesterol. They're very coachable because of the loss of Antithrombin three, and they tend to have frothy urine. If they do describe what the urine looks like, then you Nephritic syndrome is your hematuria your high BP red cell casts. So I put Red Cell cast to it because hematuria there are still a lot of other causes. That doesn't mean it's in a critic syndrome if they've got hematuria. So it can be your UTIs menstruation malignancy, So it doesn't mean necessarily You've got nephritic syndrome. Where is your red cell casts? Or from the kidney directly itself. So that would suggest be more suggestive of the Nephritic syndrome. And then you would also get your classic crescent seen on histology like we discussed earlier with the glomerulonephritis so very quick summary slightly view Nephrotic syndrome. So minimal change. These tend to be younger Children, very edematous. So think of a puffy child and it's very steroid, responsive. So with the hence the name minimal change. Nothing is seen on like microscopy, but electron microscopy get parasite. Basement also could be called foot effacement so look out for those but buzzwords when thinking minimal change. Yeah, FSGS. So this is actually the most common cause of Nephrotic syndrome. In adults, you can either have primary, which is idiopathic or secondary, which is your HIV patient's or your heroin patient's. So the question stem might be an IV D. U user, and they've got protein your ear. Very edematous. What is the most likely diagnosis? Think focal segmental glomerulosclerosis Again, These title's normally based on the histology, not the actual diagnosis, but this. In this case, it would be the diagnosis. So just think. You don't have to worry too much about, um, you know, like the title's like the camera nephritis. Think of the cause and what potentially might be causing it and then think of that as an umbrella term rather than the diagnosis itself, then your diabetic nephropathy. This is the most common cause of end stage renal disease worldwide, and the classic histology finding is Kinnel still Will Wilson nodules. They used to like that in our exams. I don't know what all the use like. That's a very common histology findings with diabetic nephropathy the questions them would otherwise be very obvious of diabetes. They've got irregular BMS, you know, erratic. BMS raised. So just look at the questions, then tends to give it away majority of the time. Then membrane is good. Maryland fright. It's This is idiopathic 70% of the patient's rather positive anti fossil lipid A two and histology would say a spike and don't pattern. So these are all the common words that you're looking for in the questions them positive for antiphospholipid a to think membrane iss uh, they give the histology patterns bike and, um, again think membrane ISS and these patient's are also very thrombotic. So think about your anti coagulation and then potential side effects that are patient might present with. So in a pretty quick summary overview slides, you've got your hypertension at AKI, your hematuria and then nephritic syndrome. We've discussed a few. So your vascular, your vasculitis, your ankle positives, your G p A. Yeah, check Strauss and MPA. Remember G p. A. Respiratory symptoms. See Anca pr three. Check Strauss, your asthma raised as in the pills and m p o N P. Anca. Then you've got your post strep two weeks following infection and your Lupus your characteristic Lupus history with positive DS double stranded D N A. Antibodies urg in a property, which I'll talk about in the next slide, and then you could put good pastures. Think you're hemoptysis and you're type ball collagen and your antibody. Anti GM antibodies. So ajamie and complex disease. This is you nephrotic syndrome. You hate just peeing your IGA nephropathy. These are both basically the same ones for Children once for adults. So, like I said earlier, this would present a lot quicker than your post strep. So you may still present with an upper respiratory tract infection, but they will present within a few days, potentially 48 to 72 hours following the infection with them deranged kidney function, H S B. You get. The characteristic rush on the legs is seen in the picture, and kids can have joint pains. They tend to present between the ages of four and 11, and then your IGA Nephropathy also called Berger's disease. This is the adult version, but it does only affect the kidneys, and they won't get the characteristic rash. Now your post renal causes. This is just any cause of obstruction to urine outflow you get your extrarenal and your intrarenal causes. You've got your chain measure malignancy, retroperitoneal, fibrosis, your BPH and then intrarenal. You've got your renal stones for pillory necrosis or even a blood clot. If these patient's present acutely, this will be very painful. Their bladder will be distended. They'll be in a lot of pain, even with complete obstruction, even if it's unilateral. They still are and uric as they get such intense afferent basal constriction of the opposite kidney. But they still don't produce urine diagnoses. Patient's ultrasound them quickly or CT. KB them if sometimes you can't get a CT as quickly. But ultrasound again is user dependent, so scan these patient's as quickly as possible. And treatment depends on whereabouts that the obstruction is but catheterize these patient's. They'll have instant relief. Well, thank you for it. Percutaneous nephrostomy nephrostomy and or endoscopy extend extending. This is normally pending surgical correction. I don't think, you know need to know much about the management in this situation, but just a lot of the time they probably ask you for scans and what's most important initial investigation or diagnostic investigation. So, investigations. If you're doing your Osti again I call it a Noski, but you might call it something else. So your practical exams and they're asking you how do you investigate this patient? Always split it into bedside blood's imaging and special tests. It impresses the Examiner. Every turn your bedside of we've we've pretty much covered all of these, but urine dip is important. And your p c r a c R u M c s for infection all your bloods imaging ultrasound C t k b being the most important. If you, um, want to Doppler them if you're thinking a renal artery stenosis and special tests, if they ever ask for a gold standard, what is the gold standard investigation? 99% of the time, it will be a biopsy. So always pick the biopsy option, if ever in doubt management. So we tend to manage the complications in a k. I s stop all the nephrotoxic drugs. Most important, look at the patient or the overloaded or the dry replace or diaries. Hypochelemia is a complication. It's quite serious complication. We need to treat that quickly and efficiently. So when we get these patient's with high potassium, get the E. C G ace up, and we should all know how to. I'm sorry. So we all should know how to manage high potassium, and you want to protect the heart, give you calcium gluconate, stabilize my guardian, increased Sell your potassium uptake uptake. Give your insulin decks and your salbutamol, and you can also give diuretics, which is often forgotten about that can get rid of your potassium, your pulmonary edema. Diaries. These patient's the metabolic acidosis, both of them with the sodium bicarb. If nothing's working, all these patient's are very sick. Dialyze them. Speak to I see you get them on the renal replacement therapy. We're still not very good at managing AKI. Prognosis is still not great, so it's important to get the management in quickly now onto CKD. So again there's another. That picture is not very clear. Actually, it isn't for me, but this 1 to 5 staging, and it tends to go down in thirties. One being above 92 62 93 is split between A and B, and that's Harbin thirties. To go down by 15 and 15, and then four and 54 is 15 to 30 and five is less than 15. So they are the patient. You need to start thinking about dialysis, about they with CKD. The important thing to remember is they need an abnormality of the kidney function or structure, so you will get your elderly patient with an egfr of 60 for longer than three months. And don't instantly assume that they have CKD because these patient's probably have very low muscle mass. And the egfr equation isn't doesn't take that into account, so make sure that presenting you have to find a cause. So look for protein your ear, him at urea. Scan the kidneys. There has to be a physical abnormality of the kidney for it to be CKD. So common causes diabetes being the most common glomerulonephritis hypertension, your infections, your polycystic kidneys, which would be very visible on ultrasound scan. And very and your own common causes your analgesia, hereditary disorders, your rare causes and your renal tumor's. So this is just a quick overview again like we discussed before when discussing the function of the kidneys. Think of the function. Think of the complications. The complications are more likely to occur at the presentation. Sorry, that's more likely to occur and CKD or symptoms from your anemia or your rise in your toxic waste your eyes and your your ear, and so your and the big majority because they're anemic. So how do we differentiate CKD from a K? I get your imaging. CKD Patient's tend to have smaller kidneys unless it's polycystic kidney disease, then that will be the only exception. They they're anemic. They can have their secondary hyperparathyroidism, so they've got the high phosphate, the low calcium. With these CKD patient. They tend to be very tolerant of a severe uremia, so you can get a CKD patient presenting with a your ear of 30 35 40 and they will be a symptomatic, whereas you could get an AKI patient with your ear of 25 they could be severely symptomatic, so they have a much better tolerance than your AKI patient's. They also have a best tolerant with potassium as well, so you can get patient's who sit with a potassium of around 6.8. Well, these patient's will be on dialysis, but they will be again, be a symptomatic with it. So investigations, same as before, your blood, you, your analysis, your ultrasounds your CTS MRI. Do you think in malignancy and your gold standard biopsy? Like I said before, creating, can be falsely low in low muscle mass or they're malnourished and liver failure. So just always take that into account when they give you the questions than so complications. So we had a quick run overview, and I'll discuss some of them in more depth. But the Commons being fluid overload and sodium retention So you've got to sodium restrict these patient's dietary advice is really important in CKD and diaries and get rid of the fluids. A lot of them tend to be on high dose fruits might. Despite it's been an effort toxin. It is required in CKD potassium exclusion. Treat your potassium so normally, like I said before, these patient's tolerate high potassium. So normally we advise diet restriction, and we can give potassium binders, which you can have long term, and normally, if they're on dialysis, this will remove it anyway. You must have, like acidosis, your sodium bicarb, your high phosphate and low calcium. See your secondary hyperparathyroidism that results. Think of your phosphate binders and then you've got your throw. Police is to get any anemic. Replace E P O and give iron. Always check the iron, so anemia of CKD doesn't tend to present till the region far is minimum below 45 sometimes a lot lower. It's a lack of endogenous CPO that's being produced by the kidneys. Risk factors that make them more prone to this anemia is patient's tend to have a low dietary intake. The Urania, which sometimes people forget your ear, actually has a toxic effect on bone marrow itself, so that also reduces the production of red blood cells. And any hemodialysis patient is not great for red blood cell survival either. Always replace the iron first. The iron needs to be normal before starting the PPO replacement. Because E P. O replacement isn't always a safe option, it comes with its complications. Like these Patient's were already hypertensive as it is. So when we started on E. P o. This further increases their BP and make some very high risk of strokes and from Bostic events and just a point to always try avoid transfusions in patient's you are potentially for transplant to prevent our sensitization for the future renal osteodystrophy. So this is your bone disease that results of CKD so you can you can ease a responsible of act for activating the vitamin D. So if you've got reduced active vitamin D, you get reduced calcium reabsorption. This reduced calcium reabsorption then affects the parathyroid dance. This stimulates the production of P. T. H. You get a rise in phosphate, and all these together can cause bone disease and a secondary high parathyroid picture. It can actually eventually lead to territory hyperparathyroidism, but that's a secondary talking itself. So you've got your high phosphate to look at the phosphate. It's got high phosphate starting on the binders, low calcium, low vitamin D Start them on the vitamin D. So you get stimulation of E p T H, which leads to the secondary hyperparathyroidism. These have end organ effects, so bones, the most common think of but it actually also really affects the heart and can cause left ventricular failure. You can get acidosis as well. No, sorry, the acidosis can increase the bone disease as well. So how do we treat these? Patient's prevention is better than cure. So the minute we get our CKD CKD patient's and you see they've got a rise in phosphate. Start them on the binders. Give them dietary advice, the vitamin D. And most likely, these patient's will be requiring dialysis if it's very resistant and dialysis still isn't working, you can do a parathyroidectomy so management. Identify the cause and treat so causes, like discussed earlier, you most likely going to need a biopsy. If you're not aware, it's not something obvious, like diabetes or hypertension, and treat the cause. Control of BP is imperative. Control the BP. These patient's already thrombotic as it is, so we need to reduce the BP. And surprisingly, we do give a sin him bitters in CKD patient. So we are told a lot when we get our AKI patient stop, the nephrotoxin ace inhibitors being one of them, but a sin him. Bitters are actually renal protective in the long run. So in CKD, we do still use a sin. Him bitters. Not all the time. It still suggested it first line, but we use a lot of doctors Zosyn or calcium channel blockers first and then go on to the ace inhibitors depending on their potassium etcetera. So reduce the protein, your ear dietary modification so they need very low salt, phosphate, potassium. They're given a full list of what they can and can't eat. It's actually not a nice list, either a lot of good food or in there. They need very high calorie intake, and they just need a normal protein, normal protein diet, a lot of match. You tend to have very low protein diets, so dieticians are very heavily involved. So your anemia iron and europeo replacement your phosphate binders lokelma. That's a potassium binder. And think about a risk of cardiovascular disease. You need to reduce this risk. These patient's are very high risk of cardiovascular disease, so get on board with the statins and also the new upcoming SGLT two inhibitors are used very heavily and dialysis and transplant is your final resort. So when do we do dialyze? So we've got your A. I owe you, which I'm sure we've all heard of that acronym. So you've got your acidemia electrolyte disturbance intoxication edema, uremia. So an absolute indications egfr less than 15 in clinical practice is actually a lot lower than that. But for your exams, remember 15 p h. Less than 7.1. These patient's very acidotic they, you remick and got associate complications. Why the pericarditis? Urine. Careful, opathy. They're very overloaded to struggling to breathe. They potentially requiring oxygen the hyperkalemic. And it's resistant to your normal management. You can use it to remove drugs and drug intoxication is that only some medications on drugs work with dialysis, so it's good to check which ones do. And if you've got severe electrolyte disturbance, you're very high phosphate again. Resistance. Get them onto dialysis. So is peritoneal and hemodialysis. Just quickly hemodialysis three times a week for four hours. It's in hospital. It's not very nice. The patient. It's a lot of time taken out of their data, especially if they don't drive. And your elderly patient, you've got to get taxis. Hospital. It's all a lot fat for the patient, and you got your peritoneal dialysis, which is more common in younger Patient's. Um, it's at home. They can do it as they can do it overnight, or they can do it separate throughout the day. Um, and this is through the peritoneum instead of catheter. The problem with peritoneal dialysis it doesn't last as long. Unfortunately, you can probably get maybe 23 years out push and then transplants Quick overview, but best going for a living donor, which thinks for itself explanatory. They also can come following brain death or cardiac death. It's not an option for everyone. Is not everyone's fit enough or able to tolerate the surgery? And also these patient's need to run lifelong and, you know, suppression, which comes with complications in itself. So that was a very quick run through of AKI and CKD, and I understand I probably spoke very quickly. Um, I've tried to emphasize the buzz, buzz words and what's important in exam questions and exam stems. So if you do have any questions, feel free to ask. But I'm now going to start with some S P A s. So I'll put this on the slide, and I think lives done a poll, and she's kindly and put it into the questions then. So Mister Roberts is a 25 year old body builder who presents her GP for a routine medical. He's got rise in creatinine, but your ears normal and all these other bloods are normal, but not normally urine output. What investigations should you do? So I'll give you a few seconds. So I think Majority view, I've got this right. Okay. So yeah. So these patient's like I said, creatinine is not a reliable marker for E g f R. So this is a 25 year old body builder. They're going to have very heavy muscle mass. So their creatinine is going to be a lot higher than your average little old lady who presents two g p. So this with these patient's, we can reassure there's all his blood. Restless. Blood's normal. His urine output's normal. He's got no urinary symptoms. So we're not worried about this chap at all. So next question a 60 year old lady is, uh, is admitted with severe gastroenteritis. She's clinically dehydrated and has not passed any urine for several hours. Her baseline bloods are taken. She's got creating a 4 50 Your ear of 16 normal sodium and potassium is 6.5. What should your first should be? Your first actions. So what should you do initially? The first thing you do when you notice these bloods. Yeah. Okay. So I think again, majority of got this one. Right? So this is you've got to look at basically what's going to kill your patient first, so this potassium is 6.5. This is a six year old, so it's an acute. You had some gastroenteritis. It's the first time presenting there's an AKI, and they presented with a very high potassium. This patient is very high risk of arrhythmias, and this needs to potentially be treated asap. Another very important treatment of an AKI is giving fluids. Fluids is also something we need to get in as soon as possible. But we do need to treat the potassium first, as that's what's going to kill them first. I know it's really depressing, but next question So a 34 year old female presents the GP with a routine set of blood and has has a routine set of bloods. She's been feeling unwell recently with nausea and has not been going to the toilet as she normally does. The results come back as followed, so she's got increase. Slight increase in your ear. Increase in creating sodium is 143 potassiums 4.4 and egfr is 36. What is the most likely diagnosis for this patient? Okay, so this is most likely going to be an AKI. So looking at this patient, this is a 34 year old female, so most likely your average females. They present feeling unwell recently with nausea. So this is something she's been unwell recently. She has got very low egfr, but because the fact that there's no other other evidence of any renal abnormalities, there's nothing in the question stem of any imaging results. And there's nothing such as any signs of, uh, they would mention it as well in the questions them or any imaging or like raised phosphate or anemia. There's no signs of this being a CKD picture. If it was a CKD, it would be Stage three. So now it's between AKI and none. So given the fact that she has been unwell and they told you that she's been unwell and she's got reduced urine output, there's most likely still something wrong with her kidney function. So this is going to be an A K i. If the patient the questions, them was more. This patient's just come for routine bloods, but she's been very well in herself. Nothing else. No other symptoms. Then you would start to think there's nothing wrong this is just her e g f r. So next question. 49 year old woman with type one diabetes presents to GP with lethargy, nausea over some weeks her GP um her g p run some blood tests which come back as a following. So she's got very hot, very high creatinine a LPs 45 calcium 2.6, hemoglobin's 135, potassium 6.5 and phosphate is 1.8. So which of these results support the diagnosis of CKD? Okay, so if you have gone potassium, a few have gone for phosphate. So the answer to this one is, um phosphate. So phosphate and potassium can happen in a K as it happens a lot more acutely, but phosphate takes a while to gradually increase. It doesn't happen acutely. It wouldn't. You wouldn't often see a as in. You wouldn't see a raise phosphate in your AKI as these your phosphate takes a while for you know, your secondary hyperparathyroidism picture to come in. So this would be a late complication. So this is the one that's more likely to be a sign of your CKD. Other pointers would be, if the question sam said the you know, they had a small kidney on imaging or they were HB was low and they were severely anemic. Um, and then again, the raised phosphate potassium would also be high, but it wouldn't support the diagnosis of CKD. It could also be in AKI, so you won't be able to differentiate between them both. So next question, 58 year old man with known stage four D k. D. Comes to G P with headaches, nausea and severe confusions. It's got known CKD Stage four. His G p takes a set of blood. These are the results as followed. So it's got an age of Rs 16.5. Creatinine is 4 80 your ears 62. So do 1 40 potassium 6.1. So which of the following is the correct next step in management? Yeah. Okay, so I think majority again have got that one right with prepare for hemodialysis. So this man is already known stage four CKD. So he should have already had the diet restriction advice given he's very confused. So this means he's now decompensating on his stage four, so he's no longer tolerating the very high your ear of 62. He's now starting to come in in cattle pathic. This patient needs to in his Egypt Forest 16, he's heading towards dialysis. Another thing that we obviously worry about is the high potassium and potassium binders. One work a lot slower to reduce your potassium, so it's not something we do acutely. And so the way we'd reduce potassium quickly is for dialysis. So this way we'll get a line in the patient and start dialyzing them as soon as fluid. Restriction would also be something we do with our dialysis patient, because these patient's are basically an uric, So any fluid we put in come straight off dialysis. They'll tend to be on a 1 to 1.5 restriction antiemetics. I'll probably still give it them, but it's not the correct next step. And it's not the most important, so smaller print 23 year old woman this lady presents to a GP with headaches. She has a new onset hypertension. Your analysis shows her mature ear and protein your ear. She was admitted to am you with query course. His hemoglobin's normal creatinine high, and it's still rising. She's no significant past medical history apart from the fact that two miscarriages her a n a. Is positive and it's complement levels low. She's got negative All the above, Uh, but a positive antidouble stranded DNA. The biopsy shows no no presents, no sclerosis. But we've got positive immunofluorescence. What is the most likely diagnosis? I'm just aware of time. We've got one more question after this, but you are majority of a ride with Lupus and arthritis. So there's a lot in that questions then and a lot of it. It doesn't really matter what you read. Just look for the important. So this look at the history. This patient had two previous miscarriages, and they've also got high BP. She's antidouble stranded DNA positive. Just with that in itself. You can get the answer from the question to them and all the a renal biopsy was irrelevant because we've seen before that she's antidouble stranded DNA positive. So if you're looking at the options of the answers, the anti G b M questions them. They'd have hemoptysis anti G b m antibodies, and they were negative in this situation. So e g p A. So this is your church Strauss. It have raised, as in Aviles, most likely in the question and possibly a history of asthma. And they'd have positive anchor and your g p a would be the same. They'd have probably a history of hemoptysis iss. You have respiratory symptoms and you have your positive bankers. And same with the microscopic polyangiitis. The only remaining option left is the Lupus nephritis again. Which majority you got right? And I think this is the last question. So this is a 53 year old man with history of nasal crusting an episode of red eyes and skin rash. His creatinine was 1 80. Got him a diarrhea and 800 mg of protein. Normal complement. Negative A an A and anti double stranded d n a. They've got positive PR three anchor kidney biopsy showed focal necrotizing glomerulonephritis, and he's suddenly developed significant hemoptysis iss Think I've pretty much given you the answer previously, but what is the most likely diagnosis? So think of the buzzwords we said before hemoptysis iss positive pr three anchor. So this is most in keeping with g p a granulomatosis with polyangiitis g p a p r. Three. Anca see Anca and mopped Asus all very consistent with G p A. And your is an affiliate would have raised is enough pills and asthma symptoms. So just remembering them buzzwords that I've mentioned previously will help you very much with diagnosing from a question stamp. So thank you all for listening. Um, I hope I didn't bore you too much, and I hope it was useful. And the next obsession is respiratory with Doctor Hannah booze. And that will be on the 24th of January. Please scan the QR code for feedback, and it's always appreciated. You've got any questions? Feel free to email the final year at mind. Mind the bleep dot com. Thank you. Thanks, Abby. That was really useful. Can everybody, um, scan the QR code or on the link in the chat to provide Abbey with feedback? Um, it'll be helpful for her portfolio and also feedback for future sessions. And And make sure you sign up to the next session, which is respiratory next week. Thanks, Abby. Thank you all