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run a big kid. Guys, welcome to our renal session. As usual, we're going to short introduction. This is our finals. Easy. Ah, Siris Real. Next week we have hematology part one and two and we have neurology coming up. It's also please do stay tuned. Follow our socials on if any of your interested please do check into our pre clini sessions. We have some very interesting sessions coming up. We have pre medical student if you're if you have any connection with your yet 18 students were planning to go to medicine next year. Probably. Please do give ah given looked or instagram page three might Easy is very up and coming. A new branch which we've opened up and we help to begin to help loads of medical students and surgeries is something which will be coming up with next semester to keep an eye out for that as well we just move on, please. So, as you saw, this is one of our main sponsors medical protection services. 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It's been very, very, very interesting and a wonderful session. Please do enjoy. If at any point, if you have any questions, all of us that they're so please just use the chart function and yeah, over here a mont Yeah, thank you very much. Sorry for the slide, Elaine. Starting also, it's, uh we just we had to accommodate are stones is and you check them on their Wonderful. So we ask Easy. And today we're doing a finals. Easy session. Um, so I will be presenting. I'm Provan. Hello. Welcome to the session. Just a few things. A few few pointers. The question some of them can be slightly had. Some of them are on the easier side. Um, so don't get this heart. And if you do get the question right there, we're trying to make the questions slightly tougher. Do so that, uh, you guys can remember it, but also layering the questions so that different kind of aspects can be caught with just one question. So, yeah, today is a nephrology session. And so let's start off with our first question. Could someone lost launched a pole? So I think in in a few feet back forms. In the past, we have noticed that you guys said that you wanted a bit longer for the questions. So we're accommodating a bit around 50 seconds for the questions rather than our usual uh 40 right? So let's stop it there. Right, So majority of you have gone for hepatic and careful opathy and people have gone for alcoholic liver disease. 25% of people have gone psychotic liver disease, but the the topic that we're going to cover all that the arms up like this question is actually acute kidney injury. And I'll just explain to you why exactly. It's acute kidney injury of the woman. So firstly, there's pain on this abdomen and back, and this is significant off green. Oh, uh, bizarre, visceral renal pain. The second point is bruises and a PT Patricia, which is a phenomenon that you see an acute candy kidney injury because it can cause platelet dysfunction. So you get a microblade all around your body, which is bruises and petition. Nausea and vomiting is a common feature of acute kidney injury as well. Um, and, uh, being a, he's a heavy drinker off 14 units of alcohol. So I do understand that could be hepatic and careful. Ah, buddy. But the history points towards a cute can injury because of the legal urea, as well as confusion in a bit of asterixis seen. So the moment you see the what asterixis. You don't go directly to have panic and can flow pretty. And that's the main point that I wanted to bring about here because you remix syndrome as a result of acute kidney injury could cost and careful opathy as well. It's called a urine make and careful Oh, pretty. And that's why the asterixis is seen in the, uh in the in the patient here, so I hope that makes sense on. But I hope you understand why it is a acute kidney injury. Being a heavy drinker also could mean another kind of concept toe that points towards acute can take an injury. The person being a heavy drinker could mean that he's dehydrated, occasionally also trying to think about the multiple factors that can be brought about by the patient and stuff and then, uh, go on, go into answering the SBA. So the next question is the exact same same question, except that there's an extra line here, so the patient does not respond to the fluid to a fluid challenge. So what could the what could the diagnosis be? It is an acute kidney injury, but the patient now doesn't respond to a fluid challenge, so it has to be one of the other options. So so one of the common 14 units a week, pretty light, think drinker. But he's been drinking for a 30 years so it could. It could actually add up and cause I've seen people who drink under the limit also, but for a long extended period of time, on still present with liver cirrhosis due to alcohol, alcoholic fatty liver disease. So it's not something that you can just include just because they're on the dot it's what the images I recommend. Um, flu challenges basically IV fluids. Right, Let's call it there. So, majority, if you have actually gotten it right and the answer is the hepatorenal syndrome. So what exactly happens to cause the patient did not respond to a fluid challenge And this is really interesting, actually. So what happened? What? What is happening here is that because off. So it has been changed it to 25 minutes of alcohol. So the patient does have hepatic a call if I deliver disease and cirrhosis because of this. So when the patient has cirrhosis, it causes a portal hypertension, and this portal hypertension actually causes splanchnic arteries and veins to dilate a slack. Big arteries and veins are basically the arteries and veins that supply the supply the god pancreas, spleen. And it's just it's just a collective term to refer to all of those. So when when this, uh, arteries dilate, there's a There's a a decrease in systemic resistance, uh, in the in the blood and so That means a lesser amount of blood is being supplied to the kidneys now because the lesser amount of blood is being supplied to the kidneys. The fluids kind of my great, and it causes causes stuff like a demon because of the low BP that's that's being brought about demand stuff. So when you do do a flu challenge to this patient, what exactly happens is that the food goes in. But it doesn't get distributed to the kidneys because the bodies in a power saving more, gives it to only the heart and the brain on all the major organs. And so it just moves out into the third space. And that's why a fluid challenge doesn't really respond if the patient has a hepatorenal syndrome, right? So there are three main key points went diagnosing an acute kidney injury. The first one is the create that they need to be a creatinine creatinine rice off over 26 micromole up a little in greater than or in 48 hours. The 2nd 2nd important is that if there needs to be a 50% rise in Christian in the possible, it's more than a 26% 26 million micromole a decrease. And so you might think that what's happening is this patient is definitely not acute kidney injury. But you need to establish this based on, because that could be the normal for the patient, no matter what. So that's why it's very important. Established baseline and check based on this, and the way you check based on this is to look at past records in the energy assistance. That's usually a graph that shows past creating in values on. So that is usually something that you need to check out before seeing how how much the creatinine has right here. Isn't it right? So there is a a K classifications. It's not commonly used in the in the wards, but it is something that's commonly tested, So there's three different classifications. System stage is the stage one, Stage two in ST ST Creatinine rise of 1.5 to 1.9 off the baseline and a urine output of 0.5 mL per kilo per hour for 6 to 12 hours. A stage one stage two is to do 22223, about 2 to 3 off the baseline creatinine rice last lesson and 0.5 ml for greater than 12 hours. And finally, Stage three is, uh, creatinine rice off more than three. And you're in, uh, pulled off less than 0.3 mL for 24 hours. Or if the patient is an uric, that means they're not producing any urine that you're in a dull for 12 hours. It goes directly in the street, Stage three. Or, if the patient is on dialysis, they immediately go into Stage three. So that's really that's, um It is important to categorize this people which stage on that that would deduce the kind of amount of cat that they require in the world. So let's the management plan went, sending them home and and the duration off their state, too. So acute can injury now can be caused by three different features. We can if you If you see the anatomy here, you can see there's a ah, there's a descending aorta renal artery going to the, uh, left kidney here. So as it as it goes in, it could be a pre renal cause. Anything before this renal artery or inclusive off this renal artery, it could be a renal cause, which means that's an intrinsic problem inside. And if it is, if it's in the urethra, that could be a post renal cause. And they're few different reasons for prerenal, renal and post renal cause. It's says you can see here in terms of pre renal causes if you're having loss of fluids, which could include diarrhea, vomiting and burns. These are all causes of loss, of loss of fluids. You could get an A K I hemorrhage because of the loss of blood hypertension, because the kidneys are being less perfused. Insets, which caused a different artery, is a constriction. A centimeters, which caused an Efren artery raise. A dilation both efficiently, effectively reduces the E G F R, a distributive shop where fluids are not going to the kidneys but going to different, mainly the third space. That's when it's hard, hard failure, whether it is not being able to pump enough blood to the kidneys. Now, in terms of the renal causes off acute kidney injury that could be acute. Tubular injury, which is one of them, is known as acute tubular necrosis, not frosting and nephrotic syndrome, which we're gonna talk about in the next few slides. Basket like this, which is more of a systemic cause. Inflammation of the vessels. Lupus, which is also the inflammation of the vessel. Humility. Your remix syndrome, Uh, where there's high amount of urea and the kidneys are not able to cope to the secretion of this urea, which causes damage. So let's rhabdomyolysis, which is the breakdown of muscles again. The kidney is not able to cope with the rhabdomyolysis. Break down and release off it, so there's an acute kidney injury. Now, post renal are more likely than not. Obstructive causes, often acute kidney injury. One is kidney stones, and that's the main one in males, at least benign prostatic hyperplasia or prostate hypertrophy you to cancer and congenital abnormalities such as basically urinary reflux, where all the urine can just back up into the kidneys and eventually cause pyelonephritis. Um, and so what exactly do you do when you see a patient with a kidney injury? Uh, first thing you don't panic. You try to identify the cause what I mean by causes, whether it's a pretty renal renal or post renal cause on you, just you do this by doing investigations and tests while trying to order order the investigations and tests. You immediately stop any medication that could cost this, and we'll talk about all the medications that could cause a kidney injury in, I think two slides time on you. Treat them with fluids because any fluid, any amount of fluid, is gonna profuse the kidneys no matter what and allow it to go even in a renal stone. Little pill, because a higher pressure in the ureter is to at least attempted, push out the renal start depending on the size of the renal stone, so higher pressure could help Help help out. So this is what you do for in acute kidney injury. So let's go on to the second question here. Someone could launch the pool right? If you if you just stay till the and I'll explain the habit of renal syndrome again, right? It's been 50 seconds, and, um, it's a close one between 80 and he So this is This is a kind of a mean question, because it's something that, if you know it, you know what? If you don't, it's a bit hard to, uh, it's basically guesswork. So proteins Mirabilis is a type of pathogen that is associated with Strovite stones. And the reason why this happened is because protease mirror bliss in the urea ureter, and then you breathe ureter. Sorry. It causes the breakdown of urea into, um it causes the breakdown of urea on what happens? What happens when when your air breaks down, it allows for the protease marvelous to kind of have a non hostile environment to grow on. So this allows for a lot of sedimentation in that in the region. And it all just collects up and causes this time of Strovite stone, so Strovite. So if the stones are are, stones in general are causes of a post renal acute kidney injury, and they can be really, really painful. And the classic sign has seen in the previous slide is a low into growing pain on that side. Usually people complain of that, so let's, um, microscopic hematuria. I know they're different kinds of stones. Yeah, and, uh, it all varies depending on what type of stone and what the composition is. So there's a calcium oxylate stone, which is radio opaque, and it's cause of increased calcium in the urine calcium phosphate stone, which is cause of a high protein diet. And it's also radio Pick your it's done high amount of Furia, as it says in the name, and it's radio loosened cystine stones. Cystine stones are 16 is a type of amino acid, and when Sistine leaks into the urine, it causes a cystine stones, and it appears as a semi a P. And the reason why I put this open exam, your bacon and radio loosen is that it's all key words. And it could point to what the right diagnosis? No, as long as you hear the word and you guys will never forget it. Sometimes you hear the pathogen Proteus, Mirabilis. You know that it straight up a Strovite stone or even even then it's a stone. And finally zante in stone eyes. For those who cannot oxidize, uh, Santa into uric acid, so it remains is anti in, and the kidney has to excrete it out. Um, now, before we we just go to man the management of stones. Could someone tell me calcium oxylate stone. It's cause of increased calcium in the urine. What could potentially be given to people with the calcium oxylate stone to prevent it from getting bigger or prevented in the future. Anyone know a particular medication? Yeah, correct. So the eyes are dire. Your ethics can actually help with calcium stones because they increase the calcium optic in the convoluted two bills. And so it actually causes less amount of calcium to be excreted by the urine test. And so it can be used as a potential prevention measure or treatment measure. But but the treatment measure, as long as the patient is in pain, this is the treatment for a stone. So for pain management, use the end said called diclofenac. And it said to be really, really effective. But a caveat to that is I think Stranger just mentioned it to me today also is that as long as the patient is has an acute kidney injury, you can't give an answer. So you need to give some other type of management of pain relief, maybe go up the ladder in non contrast, CT in low dose because City city liquid, the and I that they use for city can be green atopic. Uh, and so a noncontrast CT with low does CDK you be needs to be done. The reason why it's non contrast is because the stone appears very bright on a city here you be. And so if we put contrast in, it will just mask the stone being present, because everything will be covered with contrast, which is bright also. So that's I use a non contrast. So once you have seen that there is a stone there, what you can do is if the stone is lesser than five mm millimeters, it'll most likely or not pass out smart spontaneously, so you could encourage the patient to drink more fluids and keep them in hunger. They feel that the the the stone has passed and the Penis reduced for stunted, a persistent or bigger than five millimeters a shock way truck wave lithotripsy can be used, so that's basically shockwaves. They put the machine on the exact kind of direction that the stone is in after calibrating it, and they send a shock waves to break down the stone. And if that still doesn't work, you can use a percutaneously. No, I never really told me, which is by the skin percutaneous the inside a kind of a device that helps exactly target and break down the stone. So those are the steps of management for it. Renal stone. All right, let's go on to the next question. This is a slightly tough question, but it's worth trying and learning about someone launched a pool. Okay, right. Thanks. So it seems to be quite an even split, with majority of you going for a which is the ramipril. So the correct answer here is actually clarithromycin. And let me try to explain why it is a bit of a tough concept. But if we if we if you look at a really tough SBA off this sort, you just need to break down the questions. And with the rule of elimination, you can actually get the get the answer. So, firstly, a 59 year old male presents to the GP with cramps in his hand and muscle spasm. The moment you hear cramps in your hand and muscle spasm, that means that, uh, you need to think of a electrolyte imbalance or neurological condition. But concerning the fact that this dispersed patient in the next line doesn't really show too much off a neurological sign, it shows more of a nephritic are enough. Nephrologically sign. Um, it's more more than not not likely to be hypocalcemia. So that is confirmed because this patient has long standing crank any disease where hypocalcemia is a predominant feature now it might not be as diabetic a ting as having cramps in the hand or muscle spasms and chronic kidney disease, So there must be some other sort of pathological cause that's causing such a low calcium level. Okay, fair enough. He has diabetes, hypertension and ischemic heart disease, and for that he is on ramipril, which is an ace inhibitor. And remember, ramipril. And being an ace inhibitor actually causes different artery race, a dilation and in chronic kidney disease, it's actually said to be renal protective. The reason for this is because there's different artery dilation, which you might think actually reduces the G f r. But remember one thing. The ramipril is actually always titrated to the patient's dose so that the E G F does not lower down go go too low. But the reason why it's really a renal protective and have been some papers on this suggesting that this is that if you increase the EEG EFR too high, it might cause, ah, high amount of protein loss, which could cause a decrease in bone cortic pressure and lead to loads of a Dema and a faster progression off the chronic kidney disease. Because of this, because of hypo believe me and stuff. And so that's right, a ramipril in the right dose. All the dose is said to be renal protective, so in this case, it can be ramipril metformin. Now his EEG EFR is 40 and the reason why I put 40 is because metformin causes lactic acidosis, but it needs to be stopped only with an e jafar of lesser than 30. And that's nice guidelines. So, um, it can it can really be metformin. In this case, Vitamin D Tablet is, I would say, it's quite harmless. You can you probably can overdose on vitamin D tablet, but it doesn't have too many complications. And vitamin D tablets are prescribe because this person has chronic kidney disease, so it it usually wouldn't cause a hypocalcemia. It'll be, it'll be more too. Help correct. The calcium levels now in the indapamide is a ties. I like diuretic, and it causes absorption of calcium in the kidneys so that, as I mentioned earlier, so it shouldn't really cause a hypocalcemia. No, this is actually a drug to drug interaction. Clarithromycin can never be given with atorvastatin statins and close your eyes and can be given or azithromycin as well. And that's because they cost rhabdomyolysis. It's a confirmed and 100%. It's a contraindication because it really can be given. And so because of that, um, the first sign of rhabdomyolysis is actually hypocalcemia. And Saturday I said, It's it's slightly harder to interpret, but that's what it's leading is his to step hypocalcemia and causing this cramps and and muscle spasms, I hope. I hope that was easy to understand. So that's why the on testicles from myself now. So we move onto chronic kidney disease. Chronic kidney disease can be categorized into five stages, and it can be it is done with the E G f r. So can some Can anyone tell me what are the four components off the e g f I that you look for and how what affects the e g f r. Basically, yeah, So the pneumonic is actually cage creatinin age, gender and ethnicity, and these are the four factors that affect easier Far, and it's older to every single, every single patient based on their background and stuff. So a patient with less than 90 sorry greater than 90 with mild Ah, little kid kidney damage is in stage. One UH 60 to 89 with my loss of kidney function is stage 2 30 to 59 moderate kidney damage is stage three. Severe loss of kidney function 15 to 29 is stage four, and this is the This is a reason that you need to stop metformin, and Stage five is less than 15 e Jeff, And more likely than not this. Patients are on hemodialysis dialysis, which we'll talk about in the in the next few slides. So there's some drugs that can cause acute kidney injury and chronic any disease exacerbations on. These are all the drugs that we need to know. Just know that as I mentioned a centimeters, I I mentioned the the the pathology and the mechanism and said also have mentioned furosemide because of fluid uptake and as well as potassium. Sorry, sodium, it absorbs. It keeps the sodium in the it releases the sodium so it can cause lots of fluid loss. Um, and it can impair kidney function. Trimethoprim trimethoprim is actually a kind of a paradoxical, paradoxical drug. It causes a fault, uh, false exacerbation, which means that it falsely raises the creatinine level that stored in the body. You can read all about the few papers regarding that CT contrast as well as American trust. Both of them actually cause, um ah, this exacerbation gentamicin Lithium gentamicin is used in care of the elderly. More to treat diseases. Lithium issues for bipolar affective disorder as a mood stabilizer as well as metformin and metformin is it causes lactic acidosis. So I need to be stopped at the g r g f o g fro off less than 30. So these are refused drug side effects. I wouldn't go into detail. I'll let you guys read, read it at your own time, But just I'll just highlight the salient point points here if you just remind people don't really know. But it causes a lot of toxicity and everything else. I just remember it's hypo Know spirinolactone hyperkalemic antagonised. And another side effect is gynecomastia Dyazide or thighs. I like diuretics. Can cause hypercalcemic, as we mentioned earlier. It helps with calcium stones. And finally, a Sinemet is that the main two side effects are cough. The usual classic presentation of person comes with a dry cough on an ace inhibitor. What do you do? You change to an ARB or as a periorbital edema. Enjoy the mail around the around the lips. That's the usual thing. And to contrast this with calcium channel blockers, calcium channel blockers caused, people must. Now how do you manage a chronic kidney disease patients? Chronic kidney disease? Obviously, there's a conservative medical and surgical management as every good medical student they start in there in all the words. So you start off with lifestyle and diet modification. You give a seen a better in early in the disease. As I mentioned the reason now the kidney helps to produce vitamin D. It it helps it. One of the steps in metabolic metabolic eyes ing vitamin D and vitamin D has the same ah, hormonal function as the parathyroid hormone, which means it helps absorb calcium in the kidneys and helps secrete phosphate in the kidneys. Know if, with, um, India is not being secreted that means that the patient has hypocalcemia and so you need to give you calcium replacement. And if it, um, India is not being produced, the patient has a high amount of force fit, so phosphate binders need to be applied. And obviously this is based on checking the patient's blood levels, blood, phosphate and blood calcium. And of course, you need to first things first. You need to stop the g f l West Wing drugs, as we mentioned in the previous slide as well as vitamin the replacement. Now let's go to the next question. Yeah, right. This is the big baby coming to Nephrotic Nephritic syndrome and all the stuff in between the wonderful diseases, right? It seems to be stagnant now, so that's yeah. So majority 38% off. You have got any correct. So the answer here is actually cramming granulomatosis with polyangiitis. Now, the reason why it is grandma doses with Poly Poly angiitis also formally known it's wetness disease is because he mentioned that he complains of blood in his urine. He doesn't really mention too much off protein, so it's hematuria only. So it must be looking at the hematuria column. So it's a nephric take central. So once you identify that, it's an effort. Six in Drum. What are the other extra renal manifestations here is that he has a recurrent nose nose irritations, and this is quite a quite a pattern ammonic for sinusitis or epistaxis epistaxis. But he doesn't really say bleed. So no secretations sinusitis on had 12 days ago. Um, that's just a red herring because I wanted to trick a few people into thinking that it's Iga Nephropathy, which we will go through in the next few slides. And he has no other past medical history. And the reason why I put that is that he has No, he's no Felix features. So as long as he has no, even if you like features, it can't really. 0.2 with the diagnosis off is not filling Grandma doses with Polyangiitis, which is also known as Chuck Straws disease. So it needs to be granulomatosis with polyangiitis now, Output syndrome would have more of a year, and then I involvement. Good passions will also have a pulmonary involvement as well as in moment. You see something like hemoptysis and that kind of features Arjuna properties usually two days after a infection. Oh, our any idea? Kind of, um, a phenomenon. So it can't really It doesn't really show in the history. So that's why the answer is Grand Grand Mama Tosis with polyangiitis. Now, the difference between NEPHROTIC and the critics syndrome is is listed here. Nephrotic syndrome is gross or microscopic hematuria seen in the urine analysis, renal insufficiency. And as a team, Yeah. Wasn't uremia um no, not frantic syndrome. The key difference between arthritic syndrome antibiotic syndrome is that Nephrotic syndrome has protein urea, more than 3 g of protein. In theory, hypoalbuminemic, Albany mia, which is low amount of protein, a low amount of blood. So, uh, the the kind of urination off this protein is causing a low amount of protein in the blood blood and because there's a low amount of fluid in it, put in the blood. There's a loan on chronic pressure, so the fluid can really stay in the vascular space. And so it leaks out into the third space, which causes period orbital edema. Now two added features off the nephrotic syndrome is hyperlipidimi a and hypercoagulable hypercoagulable coagulopathy The reason why I have a lipidemia happens is because the there is a hypoallergenic mia, and so the liver is working extra time to kind of produce this new amount of albumin that's being deficient here. And so as the liver produces albumin, it has to it kind of in the in the process of producing albumin producers. Ah, large amount of lipids. Also. Now, the reason why it has a Hypercoagulopathy. It's because it there's a loss of coagulation factors in the, uh, renal in the urine as well because of the renal insufficiency, but at the same time, the levels that produces a high amount off renal factors just like the lipid factors on. So there's a Hypercoagulopathy right? So this is the kind of classifications of nephrotic and if nephrotic syndrome and syndromes in between. So let's take a look at nephrotoxic drum first, so there are few kinds of nephrotic syndrome. Alport syndrome is a excellent dominant, and usually in a history you notice hematuria protein, urea And, as as I mentioned earlier, they'll be sharing loss. Our lung manufacture manifestations on. They'll be a family history because it's excellent. Dominant on. The reason why output syndrome happens is because it there are antibodies against anti the glomerular basement membrane and type for collagen. And so all the regions where you kind of see this kind of stuff will be affected. You seen lenticonus also on that. That is a manifestation of myopia. It's more prevalent in males, and that could be deduced from the excellent dominant feature. And you need a transplant for that. Now, Chuck Straws disease, also known as you know, fill it granulomatosis with polyangiitis eyes. That association off P Anca and Myeloperoxidase enzymes. Um, it is a autoimmune condition, And it there are other a topic features like hay fever, asthma on stuff that you see with check shows disease, you see a granuloma in the affected region and UTI rash. In addition, also there you see a small amount of peripheral neuropathy, and it can be used to distinguish between checks, trust and witness. This is also known as crawling Potosi's with Polyangiitis on the way that you treat it is with high dose cortical steroids. And if that doesn't work as it open now, the way to distinguish choke stroke from another condition, which is a microscopic polyangiitis, is that the is only by the Association said it It has. So a microscopic polyangiitis would not have an ankle association. It will only have a M P o association. Uh, together with peripheral neuropathy. Um, if I if I remember correctly, Yeah. Now, Grandma doses of polyangiitis is a rapidly progressing grand grandma glomerular nephritis. I'm sorry. All these words are really a mouthful on, because is recurrent recurrent Sinus Sinus infections and no splits. Um, so that is the key presentation in the history. Recruiting low speeds up. It's taxes and recurrent Sinus infections. With sinusitis. You find a difficulty breathing because of this, and you tend to cough up blood, too, and and, uh, finally step. The kind of way that he managed it is steroids and immune modulators. Now post streptococcal glomerular nephritis is caused by a streptococcus pyre. Genes upper respiratory infection, and it's usually happens about 1 to 2 weeks after the infection. And that's the classic history on the reason why it's so specific. That is 1 to 2 weeks after it's because there's another condition in the middle off nephrotic, and it protects and rub. It has both features called iga nephropathy, which presents usually want to do this after an infection, you notice ah, bit of fruit in the area. Not too much for you to be classified as a nephrotic syndrome. There are low complement levels and see see three. The position in the glomerular. Finally, in the in the category of nephrotic syndrome, you have good passions disease, which is also an anti GB um antibodies. Similar dial put um, and what it causes it because it'd to activate the complement system and cause inflammation. So there's a leaner deposition off this IgE Indy in the basement membrane, causing it to degenerate. Um, and it's also against the type for college in Alveolar College. And that's why you get just manifestations, because this antibodies going bind in the kidneys as well and go straight into the chest as they go into the system executive in the way to diagnose most of this is a kidney biopsy and, like microscopy off the kidney biopsy itself. And if she gets serious enough, you have to do hemodialysis and offer steroids. Um, and if that still doesn't work, you can offer this drug called cyclophosphamide, which is an immune modulator to help out. No, when I say one caveat to that point. They need a biopsy point. Is that when when they're small, small conditions that don't last too long and our self resolving you don't really need to do about kidney biopsy and put the patient through that. So the moment you feel that in the history it it kind of has enough like it's 1 to 2 weeks after a a upper respiratory infection. It's posttraumatic agreement. Glomerulonephritis. You're more likely than not would just kind of monitor, observe, give fluids and stuff rather than go for a kidney biopsy, because the potential harm caused by the beginning biopsy is higher than the potential benefit to the patient. So I always look at the clinical picture when you kind of try to manage this patients. So let's go to the next next question. I've had a bit of, um, neurology here. That's one of my favorite topics. All right, right. Let's Let's stop it there. No, this is this question is actually based on the point that I made earlier. The right answers actually membranous glomerulonephritis and the reason why it's members come from the mirror and Fridays is because all these conditions are nephric takes in rooms, and this is the only one which is in Nephrotic syndrome. So you'd be able to get it by the mechanics of elimination and the reason why it is it has to be in a frantic syndrome. It's because Nephrotic syndrome, as I mentioned earlier, causes hypercoagulability on. So this hypercoagulable itty actually, what it happens, What has happened here is that a clot as form and gone and cost cost a stroke. And so that's that's what exactly has happened here. And so that's an important point to remember when you notice a difference with the nephrotic and the free take syndrome, too, they're. Here's another question. This is slightly tough. Um, but let's try to power through it. Someone launched a pool again. Uh huh. Right. Let's stop it there. Yeah, so majority of you have actually got in the question right? And the correct answer is actually minimal change from pathy. Um, Now there are few indications that it's minimal change on the property. Earlier, I put a a 44 year old female and a few of my D members said that that's a bit too mean because it's really hard to get the diagnosis because 90% of the cost of minimal change is idiopathic. Um, now a 17 on it is usually seen in young females a minimal change. The property. Now the reason why it's minimal change. The property is because, um, she presents with pain on urination and orange and red urine. Why would it? Why would the urine be orange and read? Can you Can someone put it put in the chart By what exactly? Yeah, right. So, um, refund person causes orange less red here in, and I put another another kind of point in the in the history that indicates that this this patient is on Remember seeing, which is that she had she had Cuba close is 1.5 months, and she's receiving treatment for it. So the refund person, I think I believe that it's given until two months and then four months later it's reviewed and a few other drugs are added in our changed. So that's why 1.5 months this patient is still on refund person and reforms. It actually causes 10% off minimal change. Nephropathy. It's not always that it causes, but 10%. It's accommodated for reform person news. And so if 90% of idiopathic with this kind of presentation of a 70 year old female other 10% is it's via the refund person cause. And so it's not. I'm not saying that she has to get minimal change the property. But if she does get a kind of a disease in the in the and in her kidneys, it's mostly likely they're not gonna be minimal. Change their property? No. So we moved over to the Nephrotic syndrome, and I just seen the chat that someone has asked what's difference between the fronting and then predict syndrome. So if we just we just go back to the that kind of categorization that I I brought about. This is the difference between a frantic in the fridge. It syndrome where Nephritic syndrome mainly presented hematuria while Nephrotic syndrome mainly presents with protein urea. No. So we were on the slide, and obviously there's some conditions in the middle, which we'll talk about in the next few slides, which present as both nephrotic and Nephrotic syndrome. So let's talk about Nephrotic syndrome on. There are a few different causes off Nephrotic syndrome and a frantic syndrome as I mentioned, is categorized by protein urea. Uh uh, Protein your eyes. Well, it's low amount of help. You mean in the blood? Um, and Peter edema. So the first one here is focal segmental group glomerulonephritis. And what it? What that actually means is that there are certain segment in the in the renal biopsy that shows that the only that but has been affected and enjoyed us a specified segment that is affected. And that's what's called focal segment of glomerulonephritis is usually in young adults, and you have to do a renal biopsy for this. The reason why it's cost is still unknown. It's usually caused by idiopathic reasons on steroids. Respond well to this. The next one is glomerular nephritis. Membranous gram Primary a nephritis. If you remember the first question, this was the answer on. It's caused by the thickening off this basement member basement membrane because of immune the position here. So I just take thickens. And as you can see here because is that there's kind of a hood on top off the chicken basement membrane, and that's what is called a spike in dorm appearance. That's what it looks like a spike and a dorm appearance here and for these patients and a centimeter, or an ARB understands and receptor blocker should be given as therapeutics and the kind of mean anybody that's affected. Uh, here is the anti ple two antibodies that's causing this kind of the position in the member. Now diabetic nephropathy is the most common cause of Nephrotic syndrome. It is the most common cause off renal disease as well, and it's the most common cause off, uh, peripheral neuropathy as well. So the first symptom of diabetic diabetic now on the property is protein in the urine and usually check the urine albumin to creatine in your ratio, and this would be raised because there's a high amount of albumin. The way to manage this is again a conservative, which is glycemia control as well as lifestyle modifications and a centimeter as we mentioned. It could be renal protected, as these patients could rapidly progress the chronic kidney disease, a statin because of the hyperlipidimi that could be caused and could affect the patient's heart together with with a high amount of glucose, which is a important oxidizing agent, which causes vascular changes. And so a statin must be started immediately. And one feature that you notice it's really hard to see. Here is the Kimmel Wilson nodules. So when you guys do get the site just zooming into this arrows, it's just so it's really, really small nodules that they're never gonna ask you to identify it. But you see, see it in a question. Chemo, pills and audios is diabetic nephropathy. Now I'm a lower dose is is a. It happens in different different parts of the body. Happens in the brain happened to the heart, but again, it happens in the kidneys to It's a deposition of, um, a lot of proteins, and the only thing that we need to know about it is that on a Congo red stain that it causes an apple green by fringes. And this is the kind of Apple Green bye friend wants to DC on this Congress stain minimal change. The property, as we saw in the earlier question, majority off the populace. Majority of it happens in the younger individuals. It's caused by a diesel or cytokine mediated glomerular basement member and damage. Or it's postulated that this is what causes it on the fusion of foot processes off the board of sites. So we see here that he said, the kind of put it put aside, the foot processes kind of fuse here. So it's not really a spike in the appearance, but rather the future of this foot processes cause happened in a minimal general property. It is really reactive to prednisolone on. In severe cases, the road of resistant cases. Cyclophosphamide is useful. So let's go on to the next question. We have 10 questions today. So about three more questions left. So could someone launch the pool? So remember, we talked about, um, Nephrotic syndrome of doctor about nephric take syndrome, and we need to talk about what's in the middle. And that's what seen by a mixture of protein and he material without giving too much away. Okay, right. Uh, let's stop it there. Um Okay, So majority of you guys went for sle, which unfortunately, isn't the right answer. The right answer here is I g n a from pathy on. Let me try to break it down for you. So first and foremost, it is a a ah, mixed picture. So it's either in Africa is both. Come back combined the nephrotic and, uh, nephrotic syndrome. Uh, that that being said, um that that does that doesn't mention that the this patient has computer crashes that came and went in her childhood. And what exactly? So I understand why you guys went for SLE, but SLE would have more than one manifestation if that makes sense. Ah, popular rashes are not really seen. The necessarily because these are dermatologically. Ishan is more of a vascular, the condition sle. And so this popular crashes are seen in this kind of condition called He knocks alone Pop Your, uh and he national popularized Very, uh, very possible in this in this in this patient, because induction popular is also cost about GI deposit in an extra renal manifestations that that causes this peak petition purpuric rashes all across the body. And so this is actually based on a case that I've seen on this the same patient presented as a few years later because of this IGA deposition in the basement membrane off off the, uh, glomerulus on it was diagnosis and iga nephropathy after a a biopsy was done eventually. Unfortunately, she had a. By that time, she had stage five chronic kidney disease as it as it had progressed. So that's the kind of rationale behind purpuric rashes and the mixed presentation off protein euros. We'll see Materia. So let's talk about the stuff in the middle. Remember, no Gram member in a proliferative glomerulonephritis SLE and iga nephropathy. So a combination of nephrotic and nephrotic syndrome first on this membrane a project proliferative glomerulonephritis and it really shows that you have a kind of a poor prognosis because the membrane is proliferating could be considered a type of cancer. But it's not really exactly put, uh, put and placed Marcus a cancer because it's just a membrane proliferating without a stop. Now what? You can see the trump track appearance because of the to kind of, uh, edges off the, uh, remember it. Does anyone else know where where else to be used this term Trump track as just a kind of separate question. It's not really related to, uh, Reno Physiology. Wells is the term try and track used. Yes, yeah, lungs. So bronchiectasis is one of the conditions that you use here so bronchiectases because it's to try. Try that appearance, but maybe in your free time. You could do a bit of reading. It's It's It's done. It's caused by couch calcifications in the skull as well, as well as meningiomas with expressing on optic optic nerve. So the's do these two of manifestations also cause a tramp appearance in their respective places. They have no relevance to the the kidney at the moment. So let's go back that the three different types off a membrane a proliferative glomerulonephritis Um, the first type one. There's no need to know the different three different types. But just consider this month you see a rapidly progressing in Africa and Nephrotic syndrome Picture, as you can see here, that's intramembranous deposit and submental endothelial deposits, which are different types of this membrane proliferative. Well, um, area nephritis. Now, SLE uh, Lupus is the most common cause of a diffuse proliferative glomerulonephritis. And classically, you see a wire loop ng baton, which, which it's a lesion that kind of loops around. If you if you zoom in when you get the slides, you can you can see that why I kind of looping around. And it has many other systemic kind of presentations to, uh, and the picture would not be just off a renal manifestations. It would be more of a systemic manifestations two. And the way you treat it is with corticosteroids. And you do immunosuppression, right? The final one is iga nephropathy, and it is a macroscopic in material that you see an idea nephropathy It can be associated with this condition, as I mentioned earlier enough in action on pop your, uh which is also an IGA extra renal manifestations. But it could have intrarenal manifestations. Two. It's caused by IgE the position in the MS and, um And it's usually shortly after upper respiratory infection and that the classic history presentation is about 1 to 2 days after the operation. Which way that tract infection, as we saw in the earlier uh, nephronic syndrome, we saw that, um um, the streptococcal post trip glomerulonephritis is one that presents about 1 to 2 weeks after, and in this case, usually steroids are not useful. As a matter of fact, steroids only useful for very, very severe iga nephropathy just cause it doesn't, it doesn't help. It actually causes a more rapid progression. So I generally is the one that you don't use steroids right eight question. We just have 89 and 10 left. No, right around the other question I asked you if you could explain why a Sinemet is a useful in diabetic nephropathy. A centimeters are useful in desperate, so 18 impetus actually help reduce the systemic. And so a reduction in the systemic BP actually boards well for the patient because it not only produces and only reduces the cardiovascular risk, but it also reduces the renal risk because a high pressure in the in the renal systems could actually cost loads off. Um, bloating pretends to be lost because of the chronic kidney damage that's already occurred because of diabetes. So you don't want too much protein leaking, too, because off a small amount of damage it's caused. So a Sinemet has helped with that. I have them explain to you, right? Shall we stop it there? So majority of you have actually gone for acute tubular necrosis that, unfortunately, the cancer is strenuous exercise? Um, no. So let's let's break it down. First and foremost, the patient who is a 54 your male male, as it is found to have highly and casting in microscopy now no matter what their only three courses of highland costs. One is in the normal state. You could be producing highland costs. Number two. It's furosemide. I'm sorry. Therefore causes number two is furosemide. Number three is dehydration and number for strenuous exercise. No, I've added the the point that he was recently diagnosed with heart failure and he was recently started on a drug that improves his prognosis. So, um, many people would have gone for furosemide because it is a drug that they use in heart failure. But it's only for symptomatic management as covered by moving in our cardiology station or cardiology lecture. So it can't be furosemide here because the drug that has been started on it's actually spirinolactone. Serena. Reluctant is one of the main drugs in heart failure that helps improve the prognosis. So if it can be furosemide and there's no dehydration, it has to be strenuous exercise. So that's why the concept of kind of eliminating at the right answer and I will talk about what, exactly what type of costs and frantic syndrome, which is a fatty cast. The cuticle on a crisis, which is a brown cost and chronic kidney disease, which is a waxy brown cost. Uh, it's all covered in the next light, so there we go. These are the different types of cost that are produced in pathology. Red blood cell cast in glomerulonephritis, white blood cell casts and interstitial nephritis, or pyelonephritis. This is more of an infection type of picture brown or black sea costs in chronic renal failure, highly in cost and exercise. Diuretic such as furosemide and concentrated urine, which could be caused by a different Dehydration are different. Different factors fatty costs are in a frantic syndrome. As we said, there's hyperlipidemia and find a brown money cost. An acute problem across is because all the cells that are necrosis all combined with the byproducts off the stuff that's being excreted by the kidneys and just go straight through. So that's why it's brown money costs. All right, let's go onto the pen. Ultimate question. Now a bit of stepping on knishes Toto's because he's doing the end of crime section of things. But I thought that this might be a really, really interesting and important topic to cover in the renal concept off things possible to launch the pool yes or someone asked why spirinolactone any increased problems is It's just based on studies that have been done. Um, spironolactone is instead to increase the prognosis, basically increase the life span, and that's that's based on epidemiology. There's another study that's being done. Uh, now, which is the Iron Man study that I'm sure my friends would be able to test the devil. Seen it, Uh, which is in heart failure, where the IV iron makes a difference in pregnancies two. So there's a few things of you assist evidence based medicine kind of things that come into play. But, yes, spironolactone is the one that helps with the prognosis. Remember, in their medical therapy for chronic carpet, the spironolactone is the one that's sort of third line. Furosemide is only used for symptomatic relief or sort of acute. A demon acute Dema Good. Yeah, right. Uh huh. The polls doing okay. Uh, let's stop the poultry. It's a majority of you guys have gone for B, which is, uh, nephrogenic diabetes insipidus and 30% off you have gone for a which is cranial diabetes. Insipidus. The right answer here is cranial diabetes, insipidus and, uh and I put I put lithium there because, like them a mood stabilizer for bipolar affective order as a kind of a red herring. Because the woman you seen lithium, everyone just goes for nephrogenic diabetes in separatists. But there's more to this question. So a 60 66 year old female presented the need do constantly urinate. Now that means that she is a fluid over overloaded or she is having a lot of loss of water because of some pathology in the kidney. More likely than not, it's it's a kidney in this case because this is a kidney session, Um, but she was diagnosed with bipolar effective disorder and started on lithium. Lithium actually is a cause off nephrogenic diabetes insipidus, and this is a known fact. It just interferes with the ADH Medical is, um, are antibody binding effect on because it's less amount of aquaphor is to be to be produced now. The reason why I added that she had a postpartum hemorrhage year when she gave us the first child is because there is this. Actually, I'll ask you guys, Do you know any syndrome that this could lead to exactly she had syndrome, so she and syndrome is where this ischemia to the picture to clan, not pituitary gland, is the one that produces 80 hitch. And because that's a scheme you to this pituitary gland. The pituitary gland is not producing ADH. I've added it in the next sentence that the water depravation test is conducted on her urine. Osmolality increases a stuff the desmopressin and a desperate person face know desperate president is. It's in that idiot, and when that is given, as long as the kidneys are working, it's It should be able to absorb as much water as possible so it can be a kidney cause off diabetes insipidus. But it needs to be a cranial cost because a. D. H is not being produced because there's a response to 80 inch so that also gives it away, that it is cranial D. I that was talking about the next three and the next light. So the difference within cranially I and Nephrogenic idea the I, as I mentioned earlier, is that cranial the brain can produce the pituitary gland can can produce water on because of the known what has been collected back but never cardiogenic. The the brain is producing what 80 88. Sorry, ADH normally, but then it's not able to bind in the kidneys and cause water reabsorption. And so that's That's how that's how that's pathogenesis there so that the ways to manage this is synthetic idiots just as decimal person or nephrogenic DEA eyes to stop the causative agent. Does anyone know what other condition could use? That's one person. That's one major condition that you can use the small person for us. Well, yeah, that's right. One willebrand's factor disease disease Uh, desmopressin is cost. And the reason why I ask this question is it's just a desire for the next session, which is hematology, and I'm sure it'll be covered in the next session next week. Tuesday? Yeah. So nephrogenic diabetes insipidus can be can be reversible. If, for example, if you stop you stop the lithium, it should be easily reversible. Yeah, um, the reason why it presents much later after the post partum hemorrhage is because it could be a kind of a slow, pathological cause, um, are are things like that. We have actually seen this being this happening, and sometimes you just don't know why it's presenting so much later Maybe the body accommodates until it's a point that it can't accommodate anymore. So the water depression test is done for cranial and nephrogenic d I. The water deprivation test is basically eight hours off, stopping fluids for the patient. And then, after that desperate presidents in ISS, it's is given, and you see the the urine osmolality go up or stay the same. Now, if it's I'll just talk about three normal condition. Cranial, die and nephrogenic die in a normal response. Askew fluid. Restrict the your urine osmolality goes up because there's less amount of water going into the urine and after desmopressin face, because the body is normal that it still remains the same. Now with cranial eso complete nephrogenic uh, the eye, which is the green line here when you when you want to deprive, nothing really happens because the patient is just extreme and and the same amount. And when the ADH is given, it's not being able to go on a match. Its function. And so it just remains the same, however, for cranial diabetes Insipidus, which is labeled as complete, complete central d I. It remains the same for the dehydration face and then when you give the idiots, the osmolality goes up because more water is being absorbed by the synthetic ADH. And that's the whole concept of water. The provision test. Now there are few other conditions that can bring about this type of state or similar type of state. SIADH also syndrome off appropriate the edge, which causes a high amount of release of 88. So it's the opposite of diabetes insipidus. So because of hae months of age being being produced, more water is being reabsorbed. No. Do you see that more water is being reabsorbed? But given that more what is being absorbed, the patient is still in a euvolemic state. And the reason why this basically that the euvolemia basically happens is that a whirl Over the course of time when the patient has a side, the itch, the th actually is released by the pituitary gland. It goes into the into the nephron and binds into the ADH receptor. Once this ADH receptors activated, it causes the synthesis off Aquaphor is to absorb. Initially, when high amount of experience are being produced. Because of the large amount of 80 it's being present that as a state of hyperbole, Mia. But over time, the kind of that cell that produces a copper and gets used to the higher amount of 80 which has anything with our body tries to it tries to achieve hemostasis hemostasis home used a sensory, and it causes a normal amount of, um, normal amount off razor presents to be produced a copper Inspra produce. Sorry. And so, uh, it it becomes a state of you've anemia. Yeah, but then at the same time, why is the serum sodium low? You might think now, because high amounts of what is being absorbed back in the initial stages there is a higher amount. That's a hypovolemia in the in, the in the blood. It's a high amount of blood volume. What happens is that now, because that's high amount of blood volume, the heart has to contract and work harder to come A larger amount of blood volume. Now this put the pressure on the heart and causes the release off. Can you say the chart? What, What is released exactly and B and B and B so anti natural, aging, naturally Hepatitis A and B M p. And so what? This causes is naturally cysts, as it says in the name, naturally says, is the release of sodium. And so it causes a low serum sodium, and that's right as the low serum sodium. But over time it is a state of you've Alinia if that makes sense now, primary politics CIA is that there is a low serum off course osmolality because as a continues to drinking off water by the patient, it's more considered as a psychiatrist disorder, and so that the patient should try to can seek seek help. If they're, they're negative effects based on this pseudo hyponatremia, which is a low amount of a fake low amount of sodium. It's caused by, uh, different different reasons. But it could be because just of the test, because if there's a higher amount of lipid, it could cause a false positive. The the machine actually notes high amount of lipids as normal serum, so it combines the Lipitor with the serum as well and compassion a sodium sodium with the lipid lipids also, and so it shows that there's a pseudo hyponatremia, although up the the kind of sodium levels are normal, so that particular serum level many dollars a can, cause, um, hope on the tremor and ah, bladder irritation, actually, also, um, yeah, man, it all is is kind of used in, uh, states off high intracranial pressure. So this is kind of a flow chart flow chart that I made up for the, um, damage. So some some people are asking, Why is there not hypovolemia? So let me let me just try to expend again. Sorry. Some people, some people are not getting it. Just try to expend. Okay, So initially there is a high amount of 80. It's being produced. And because high amount of idiots is being produced, there's a lot of water being re absorbed by the kidneys, and this causes a hyperbole. Mia, because of this hyper of Olympia, it was. It put a lot of stress on the heart and B and BNP, which is atrial, natural, natural tick pepdite and be in peace released on because this amp and bmp bmp a release because naturally, cysts, as it says in the name naturally says, is basically the loss off sodium. Now, over time, the body accommodates and kind of gets used to the higher amount of 80 hitch ADH is Remember, 88 is the end of crime agent. That kind of works on receptors to produce higher amount of like a parents. So once it gets kind of get used to it, ah, high amount of ADH would still come and produce the same amount of a lesser amount of aquaporin as it's meant to be producing, because off the homeostatic drive off the body to kind of natural eyes, everything. And so this consistent high amount of 80 it's being produced causes the same amount of vasopressin as before to be produced. That's our number. Is a person a copper in to be produced, causing a euvolemia in a row for time, if that makes sense. Event. Someone asked me a similar thing. So in the sed it you technically do get free water, excessive free water absorption. But you call it euvolemic because I couldn't. Clinically, they have no states or fluid overload off or hyperperfusion zit issues. Okay, so it's basically on the clinical fluid status assessment euvolemic. Okay, that's why you say beside the age, they usually, um it cause off hyponatremia. I think I think I mentioned the kind of the pathophysiology off it also. Yeah. Yeah. So this this is how the part of his village. But what version works, too? Yeah. So this is This is the kind of flow chart that you know how to assess. If it's if someone is hyponatremia, I let you guys read on your on your own time. And if you guys don't understand, do email us off messages and we'll be more than happy to help. It's just a simple quick guideline. So this is the last question If someone could launch the pool, right? Shall we call it there? People are still putting. Okay, right. Let's Let's stop it there. It's been about one minute. Okay, Cool. So majority of you guys have gone for see here? Uh, the right answer here is actually a which is low pH. Little PCR doing low bicarbonate. And the reason why this is is actually the second question why we mentioned about Hepatorenal syndrome? It's a similar presentation to there, but this is actually uremia. So this patient has been brought into the emergency room for progressively was worsening confusion. So you missed this last dialysis so it could mean that he is overloaded with electrolytes. or maybe even urea. So that's something that should go into your head. And he has a past medical history of chronic in front kidney disease, so it's not able to simply the cereal electrolytes properly. Auscultation you can hear heart sounds and rub can be heard. Our Oscal Station of heart Heart sounds you can you can hear a rub. So more likely than not, it's pericarditis. Now Uremia has many manifestations, and this kind of points towards the diagnosis of uremia because of the confusion because of the pericardial rub your remake pericardial. But remember regarding this as well as the Mist dialysis appointment now what happens in Uremia is that there's a high amount off a hitch plus that's being released. So how much of which plus would put you in Acidotic. State because it causes metabolic acidosis acidosis so it would cause a low pH? No, because there is a metabolic acidosis, they'll be respiratory compensation because by the lungs. And so this respiratory compensation would cause a low amount of PC or two. And a feature of metabolic acidosis is is that there will be low bicarbonate because majority of the bicarbonate has been converted to hedge to see or three for buff in terms of the buffering system, because the body has a has an internal trash, a little buffer acid, and so then stents. That's the presentation. That's why a low pH know PCO toe and nobody carbonate is the right answer there. Now there are a few features for uremia and uremia is one of your emails. One of the features for an urgent dialysis and the features of urgent dialysis can be, uh, not in a pneumonic 80. I owe you right over here. So is for acidosis. Be so acidosis in terms of lactic acidosis or even your remake acidosis or metabolic acidosis in the urgent hemodialysis for especially for a metabolic acidosis unit agent. You know human Dallas is based on a clinical features electrolytes. If that's high amount of electrolytes intoxication such as drugs and stuff, the last line is actually hemodialysis. If if stuff a medical management, whole conservative management doesn't work. If there's a fluid overload, usually need a human Alice And finally uremia, which is what this patient had because you had missed one of his dialysis. So once the urgent dialysis is completed, you need to reassess the patient, to review the investigations and call for help. So the reason why we put the Hezb are here is because it is very commonly used and in our future or skis the sessions. We'll definitely cover the S bar station. So there's one question that says, Why does uremia uremia cause acidosis? So your email can can cause if I correct me if I'm wrong? Mention. But you're American cause the release of uric acid also, um, but also it in him. For you know, you're a cast that uric acid is different image for can associate the form to produce a proton. Just hedge plus, um, so it can cause acidosis, right? So there are few indications for hemodialysis, peritoneal, dialysis and renal transplant. Human dialysis usually takes about three every 3 to 43 to 3 to 5 hours, three times a week on eight weeks before hemodialysis started, an AB fistula needs to be started. I need to be done. That's just the merging off a artery and vein. It's really, really obvious on the patient's wrists, the region, and usually that's where it's done. You can see because off the high pressure artery going to a vein, the vein just completely extends and becomes really big. You'd be able to clearly see that on the patient's for so the complications that hemodialysis could have is that it could have hypertension, which would cause arrhythmia because you're taking loads of fluid out and then pushing it back in. That could be our ambulance in by the air bubble that goes straight in. And this thing called it this equilibrium equilibrate in syndrome, which is basically that the fact that the machine takes too much electrolytes and leave you with two little electrolytes and this causes a fluid shift into the space. And this fluid shift is basically really, really, really pathological when it goes into the brain and cause a cerebral edema. And so that's why I think Equilibrating syndrome shouldn't be. Shouldn't be. A complication should be something that should be avoided. And this kind of help the renal diet hemodialysis machine looks like the next time is a peritoneal dialysis, which is through the abdomen. The dialysis liquid is injected. All the stuff are allowed to diffuse into the dialysis liquid, and then you just remove the dialysis liquid that The only caveat to this is that it takes a while to do this. And so there's a high risk off infections, a risk of malnutrition, because nutrition could also come into the kind of dialysis fluid because it's in the peritoneum. Um, and you could have a certain certain features are certain complications of this could be constipation, fluid retention and catheter blocks. So that's why hemodialysis is the most common. We use kind of more of dialysis, at least in the UK And finally, if all of this doesn't work, you do a renal transplant. It could be either from a live or a deceased donor, and you because you're putting a new new kind of kidney. There, you need lifelong immunosuppressive because it's from a different person. Obviously you do actually matching, And they are. They are matching also, um, actually, India Magic. Yeah, um, I believe initially it was 6 20 the antigens that needed to be matched, but nowadays they don't want to do indigents matching on the offer. Strong immunosuppressants. It can last for about 12 to 15 years and the old kidney, surprisingly, the old kidney is not removed because it has a high risk of bleeding, infection and stuff. So they keep the old kidney there, and they actually put it attached a new kidney to one of the branches of the iliac artery. So it's actually a day on the left or right peritoneum region that you would be able to feel so don't miss it out in our ski when you're kind of, uh, palpating. And if you feel like a solid mass, it's probably a a renal transplant that the patient has had. So there are a few things that can happen with, uh, renal transplant. If it happens, really, really quickly, that could be a hyper curing, very rejection. And this is when antigens against the blood type or Hatchell antigens kind of going attack the new kidney. And it causes a Type two hypersensitivity reaction. And this only management of this is immediate removal off the new kidney. The second type of, uh, complication is an acute grand failure, and this happens about six months. Ah, bit lesser than six months into the into the renal transplant, and that's that's the kind of measure that they do. And it's cause of cytotoxic T cells that attacked a graph, and this can be treated with immunosuppressants. Now, if it's more than six months and recurrence off the disease that cost a renal transplant itself, it's called a chronic graph ailure, and what you can do in this is you can eat a transplant, the same kidney again, to maybe a different side of. So you remove this kidney and transplant a new kidney and or you do the If it's in the early stages, it's a disease. Management protocol are symptomatic management protocol. That's not too much that you can do in that case. So this is our final few slides. We're just gonna talk about renal cancer. Renal cancer has a try it. It's called renal cell Cancer, and it's known as an adenocarcinoma. It's more more predominant in males than females and presents with the classic triad of hematuria line pain and renal mass. And the way you do it is you do a CT tap, correct Salberg abdomen and pelvis with staging and reading. So I'm sure those who are doing oncology in your block would have heard of stating in staging and grading and t one lesions are kind of treated with partial nephrectomy. Where's d? Two lesions are treated with radical nephrectomy d one meaning on the tnm spreading Get grading scale. Um, it's do one, which is kind of small. Look more contained ones partial nephrectomy. And nowadays, these procedures are done hands free as a by the the robot Robotic surgery. So it's really cool to see if if anyone has seen uh, no. There's one thing that I wanted to ask you guys, Uh, what is the kind of difference that you might see in renal cancer presenting in the meals versus females? Yes. The patient will have three kidneys in total. What is what is Yeah, so yeah, very cost you that. That that's right. Um, and varicocele is basically the kind of, um, expansion off the veins in the testes in the mail. Now, the reason why this happens is because off an anatomical kind of structural, think that the mail has the testicular artery actually started this testicle, a vein from the testes goes straight into the IV, see on the right side, barbarous, it goes straight into the renal vein on the left side. Now the renal vein, the way the the place where it attaches the renal vein. The testicular pain to the renal vein is actually quite approximately towards the kidneys, and so it grows. Could compress on that and cause kind of fluid overload in the test is causing this varicocele. So that's the battle pathology to DC now in the probe. That blast, um, also called a Wilms took tumor is usually a mass that you feel any child's abdomen a song. You see a mass in the child's abdomen. You go for Wilms tumor. It presents very early on. It's usually an asymptomatic abdominal mass. You get hematuria with it on. If you do it early enough, rectum me, you can actually prevent it from metastases. Now I've I've said that there's metastases to the lungs. Can anyone tell me what is the most common type of metastases? That that the term that basically it's called when it metastasizes to the lungs there's a specific dumb that it happens? So it's called Cannonball Mets. I didn't include a radiological figure, but, uh, it's called Cannonball Meds because it looks like a small, small round balls all around the chest, and that is quite commonly because of the translocation off human cells from the renal renal pelvis toe all the way straight into the lungs. So let's just quickly talk about pain management in renal disease, chronic kidney disease and acute kidney disease. Well, so conservatively, you'd ask the patient to rest and refer to pain specialist in terms of in terms of medical management. This is the normal kind of a step wise approach that you take has based on the who ladder. But this is the kind of step wise approach that you take in chronic kidney disease. So you started with Tramadol, then you go into oxycodone. Fentanyl blueprint, orphan. Her fentanyl on this is because these things substances are not medical ized by the kidneys. And so it can. There's no chances are it collecting up in the system now? Anyone know a rather common I wouldn't take common but a side effect of Tramadol. Does anyone know a possible side effect of tramadol that you need to be kind of concerned about? Yeah, so it's kind of Yeah, Ryan, you're right in saying it's serotonin to know it causes causes mood, mood changes, mood disturbances, actually, um, and it can cause certain syndrome because it has a type of SSRI property in the tramadol. So that's something that you can look out for if the patient is already in a s s Are are I or a Maui, my mommy inhibitor. Um, then that is potential for the patient to develop serotonin syndrome. Right? So I think that concludes my presentation. Sorry.