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in UTI is, um, sorry. That's, you know, for a second. Okay, so just said an introduction about myself, that's what this into presentation with it. It's ah. Oh, I'm Dr Kotex. I'm an f y to equivalent, um, a gateway doctor. So that means that I'm equivalent to the foundation, your doctors, but I'm on a slightly different pathway on. That is to get my Crestor difficult signed off, which is certificate regiments of specialty training. And it's just basically signing off the same company competencies as the foundation doctors and getting myself ready for specialty training. I did this because I graduated from Bulgaria, and for me, it was the route that seemed to most appropriate for myself. I'm currently working in Birmingham Children's Hospital because I haven't interest in pediatrics and family medicine. So enough about me, let's get started. So initially I thought I'd just do a little slide on the Humira lists because that is the focus off these renal diseases that I'll be talking about. So go Mary less is Paul of the Nephron is the first part of our nephron. So we have our Ms Ngiam here on. We have capillaries that come into the gum area less to compel a reservist line with Understand your cells, and we also have epithelial cells with foot processes around them. Now these foot processes have given them the name of her sides. So the participants in the endothelium in the basement membrane all together Mexico Marylise basement membrane. Now this is basically like a filter. So if you think of a sieve on everything coming out of the capillaries into this glomerulus space and then into the proximal troubles, primary urine. So when there is damage that occurs to this basement member in these three layers that I mentioned ourselves that we have becomes a bit more of a colander and it has bigger gaps in it, bigger holes in it. And that's a lot more things through. So welcome aerialists. Usually it doesn't allow large proteins to be filtered through. It's usually smaller size proteins. However, when there's damage and our safest become a calendar, these large large proteins and other things are allowed to be faulted through and go into our urine, and this leads to some symptoms that we'll talk about. So let's start with Nephrotic syndrome with a big capital O just to help his remember things. So let's define a syndrome first, because it just helps me when I'm learning something new to break it down into little definitions that then come together to make her own clearer picture. So a syndrome is a collection of symptoms that occur together and that are associated with the specific condition. So where the definition of nephrotic syndrome is basically encapsulating the symptoms that would have but the pathophysiology and causes off them and the management is slightly different for each cause. So the definition of nephrotic syndrome is it the clinical syndromes us to find by massive protein urea greater than 40 mg per meter squared per hour on this leads to hypoalbuminemia hypoalbuminemia because because we're losing proteins and albumin faster that are liver could make it so we have less albumin in our blood on this, then in turn needs to. The loss of proteins leads to hyperlipidemia because if we think about upper lip proteins, they help us carry our lipids around the blood. And if they're not there, then we're just gonna have Nope, it's floating around. This is ah hyperlipidemia. Our Dema occurs because we don't have proteins in our blood. Well, less proteins in our blood on your proteins are usually there for the oncotic pressure, too. Then bring all the interstitial foods back into our vascular system. So if there's no oncotic pressure, the blood that's gone into our into cellulitis base, there's no pressure to bring it back into the vessels. So it just stays in this interstitial space, and this causes our edema, and there are other complications occur with Nephrotic syndrome, and this is also due to the loss of proteins. But we'll talk about that in a short while. So the reason I had the capital O is to highlight that Nephrotic syndrome is a syndrome that involves Dema oh Dema protein, urea and hypoalbuminemia. So if you remember that, remember these three things and that should kind of take you down your pathway of the understanding that syndrome. So we have an increased paraben it easy to damage to the, uh, Amaryl, a basement membrane. So while the path that it could be primary do two disease completely isolated to the kidneys, or it could be secondary due to some other kind of person going on in the body, that has now taken its toll of the kidneys. So we have congenital infections, diabetes, because we know that diabetes leads to some and organ damage is and the kidneys being one of them. This is known as diabetic nephropathy. We have, ah, systemic Lupus erythematosus. And this leads to Lupus. Uh, never apathy again with the proteins on, um, or two antibodies. I get two positive in the kidneys basement membrane. We have neo plays er so any lymphoproliferative diseases kidney to this is well on. Drug use is such as Ansaids on. We'll have, um, a low doses. So speak about these different types of nephrotic syndrome. So the first one I'll talk about is minimal change to see. So as the name suggests, it's very little change that because in the kidneys themselves, but it leads to Nephrotic syndrome. So this is the most common type of nephrology Children syndrome that will occur in the Children. So if a child comes to with a d. M. A protein urea, um, hypoalbuminemia is a presumptive diagnosis, and it's cost is minimal change disease. Until that there is proof for it to be something else. So in terms of the pathophysiology of Manimal Change disease. We just have fusion off the part asides, and that's some kind of immune dysfunction going on in the background, which is not very clear. But this disrupts our filtration barrier again, our self becomes out calendar on we have lots of loss of protein on in child in Children is the most common form of Nephrotic syndrome. Uh, also a cousin. Adults, you know, do two xs answer Do see, uh, lymphoproliferative disorder or syphilis, But this is very, very rare. Um on it's usually managed with prednisolone. So another type of nephrotic syndrome that we have is called focal segmental glomerulosclerosis. So, uh, sclerosis is, ah, word for scarring and glomerular obviously being a glomerulus. So we have scarring off focal or segments of all, um, very less in the kidneys. So this can be probably again idiopathic with circulating factors again. Not much is known about these, but it can be, you know, idiopathic primary, or it could be secondary. So if we have a process going on in our body, for example, for civilian beast or that's reflux nephropathy, uh, there's damage that occurs to our kidneys with this on the damn major cousin, the primary less and some of them then scar the ones that scar shrink in size. However, if many dumb aerialists have shrunken stopped working, others will have to take home that slack and they become hypertrophic. So we have scarring and scarring from a real eye. And then we have hypertrophic primary allies. Well, so this is a diagnosis that has made histologically by renal biopsy and, of course, our history and examination and things on other investigations that will do that. I'll speak about later. But for this one, specifically, it's a histological diagnosis on. You'll see focal areas of Scott, Primary Line and areas of hypertrophic primary Guy. If this kind of nephrotic syndrome occurs in Children, we then start looking for underlying genetic cause. So again, if it's primary and we don't know what the cause for it is, we give them prednisone that on glass of minus and another immunosuppressive. If it's second reserve there severely obese or there has been other damage to the kidney, we can treat the underlying cause, and they should help with the nephrotic syndrome. Uh, with that way, is it, uh, that any question civil? Okay, then we have membranous nephropathy. So this is an autoimmune condition that occurs and is due to antigens attacking the filtration barrier. So things that this pa p l a true receptor that is expressed our practice ides are antibodies are made against these on this causes damage to al filtration barrier on there's a secondary cause which again incidents, um, sle or a viral hepatitis is congenitally to nephrotic syndrome, prostate cancer. So this membranous nephropathy because there's no sending the proliferation of damage going on is thinking of the basement. So then we will look for auto antibodies against, um, these receptors that were mentioned on. We'll also do a renal biopsy to see the histopathological, um, parents of the kidneys to identify that is ideal even, um, member, that's nephropathy. Uh, primary will be self limited. It can be, um, different tics, injured one, and then they kind of get over it. However, certain people are at higher risk of disease progression. Um, on for these type of patients, we need to give them some kind of immune suppression because they're not able to limit the disease themselves. So we're not gonna have to stop there. System dampen it so that they can have, um no, no more nephrotic syndrome. No more nephropathy know Want to autoantibodies attacking their primary left on a one to have nephritis in drum. So then we go on to secondary. How do we treat? Second reason is it's been caused by and said SLE viral hepatitis cancer with to treat the underlying cause. Um, and lastly, in a frantic syndrome, we have ah, renal amyloidosis. So amyloid justices, deposits of these different types of pretty and then our body, so it can be a hell. So we have idiosyncrasy off the heavy and light chain and immunoglobulins. And when we have excessive like chains, they become, um they're resistant to degradation and they become insoluble, and then they become deposited from a type of unloaders. This is due to chronic inflammations. If there's a Cornick information going on in the background of the one of these condemn get deposited into the government's membrane as well. On this would lead to ask symptoms of nephrotic syndrome. So this is also diagnosed by renal biopsy and Congo red staining specifically, Um, but again, if there's a history of amyloid doses and we developed these and then you can cut of piece your picture together in that way and again, we treat the underlying cause of the amyloidosis. So what do we see? So we've spoken a little bit about the clinical picture, but here's a nice The pneumonic that spread spells up nephrologically instead of nephritis. Nephronic. Um and it is, uh, sodium retention hour and a I'll be mandating to hypoalbuminemia protein urea more than 3.5 g a day. Hyperlipidemia renal vein thrombosis A demand due to the lack of on cottage pressure that we have with our Dema, uh, thromboembolism infection on a collectibility. We can also get a CT. He's on pleural effusions as long we don't usually get pulmonary edema with nephrotic syndrome. And that's because, um, the through it going back into the blood vessels is not due to oncotic pressure in in the of your life. It's true to hydrostatic pressure, and that's not affected by the loss of the proteins. So we get pleural effusion and the CT is a swell. Can anyone think of why we might get sodium retention in? Um, nothing sticks. Andrew can't seem to get the chapter open. Sorry, guys? Yeah. Don't. I can tell you if anyone replies. Okay, um, I will tell you then because we have lost off volume intravascular volume because become so a dermatitis. Our kidneys trigger the rest system so and the rest system obviously leads to surgery retention to try and increase celebrate lost so much pressure in from the loss of our proteins. So that's why we get sodium retention and the hyper I'll be minimal was due to a loss of proteins and not being able to replace the loss. I quickly protein urea, which we know about the hyperlipidemia, which I spoke about as well on from Versus is also complication increased risk of infections because we're losing a lot. These proteins that are going to help us fight these infections and increase collectibility. So how are we going to diagnose this? So we get a patient who comes in who's very a definite it's has had, you know, um, a two week history of, you know, noticing increased a Dema pitting edema. Um, no other real background. So one. The easiest thing to do that is gonna guide our diagnosis is to do a urine dip. So get them to pee and do a urine dip. And on a urine dip, we should see 33 plus two full plus proteins. So now we consider this protein urea. There will be no hematuria. Nothing else really will be seen. It will just be the protein urea on. We will then take some protested. That's your guide us towards the Nephrotic syndrome initially. And then we must do, of course, blood tests to see what else is going on. Because there are other causes of a Demers. Well, so after rule things out. So we'll look at I'll be red. Which one? Of course below we can see of the renal profile. There usually isn't a disrupted kidney function unless it's leading to end stage renal disease. But usually Reno function is maintained will also check out cholesterol levels, which and triglyceride levels which will be increased. Uh, and we will look at serologies to find the cool. Why is this happening? Is an autoimmune condition. Is it due to an underlying fired infection? We will also do ultrasonography to look at, um, kidney structure and other imaging as well. To see you know, is that, um a, uh anatomical problem with the kidney itself is enlarged. Is it shrunk? Er, just to see ah, full of picture on. We can do a renal biopsy as well, because this diagnosis of exactly which type off, uh, Nephrotic syndrome it is is done by renal biopsy. Because although you might have noticed there are similar causes for a lot of them, the histopathology looks slightly different. The pathophysiology of it is slightly different, and how is affecting the kidneys might be slightly different, so we then move on to management. So in all Children, because it's always thought women, um, or change disease. And that's proven otherwise. They all get steroid therapy and a lot of on a frantic syndrome treated with steroids. Or if you would have seen prednisolone in the management columns of all of them. So this is Ah, we give 60 mg per meter, squared once a day for four weeks, and then we do a winning regimen, so we slowly slowly decrease the prednisolone dose until they're a level where they're on alternate days and then they can stop. We can also, if they can't have steroids. For whatever reason, all the steroids are no longer effective we can give them a monoclonal antibody is rituximab. Um, if again the steroids, um or no or helping. But they're not completely taking away the symptoms we can add in immunosuppressive therapy such as Zack, Possible Minds actress Warren and things like that. Um and then we need to treat the symptoms as well. So the beauty of demodex No one wants to your party like that. So we would give them diarrhetics to help them lose all this extra fluid that they've been retaining on the statins to help with the hypercholesterolemia. And if it's diabetic nephropathy specifically, then we treat them with a sin hip bitters or angiotensin receptor blockers. So that is enough Rogic syndrome on. We have different stagings of nephrotic syndrome. So once we have, uh, no protein urea for three consecutive mornings, that child is then in or the adult is then in remission so that, you know, the Nephrotic syndrome occurs in as any kind of autoimmune condition. My current cousin flares to have to control the flare, get them into remission. Sometimes they have relapses where the urine albumin goes back up to three plus or four plus on This has to occur for three consecutive mornings for it to be a relapse and have to previously been in remission. So they had no argument in the urine and then three mornings in a row, that go argument in the urine. So then they need to go back onto that, um, doses of prednisolone that helps with the management. Uh, there can be frequent relapses so true or more relapses in six months or more than four in 12 months. We have steroid dependence. So two consecutive relapses while they're on alternate days therapy. So they take Percocet and Wonder and they just the other. And sometimes this is maintenance therapy. So this is what keeps them in their remission, but instead no achieving remission on that, their steroid dependent that they continuously did that. Steroids to stay in remission, um, steroid resistance. So even if they're on daily therapy, they're still getting these symptoms on the studio, in your in, in their protein, in the urine. So this means it's resistant to steroid. So in this case, is you Would you move on to your immunosuppressive or your monocle monoclonal antibodies on. We have a congenital type of Nephrotic syndrome that occurs as well. And this occurs within the first three months of life, and it's usually due to a genetic condition. It's not very common. So that is not practicing drum. Does anybody have any questions about that at the moment? Yeah, there is. One question was, why is there increased Cargill itty in practice syndrome? Why's the increased coagulability? It does seem, um, almost counterintuitive. But there is increased collectibility because we've got, um, one of our our blood flow becomes becomes. So we've lost all our proteins in the urine with no got as much pressure in our vessels because again, we're quite a Demetrius. So if you think of the triad, it's due to the Stasis off the blood. So, you know, you have, um, you have under cereal damage and you of human spaces. And there's another one that contributes to the triad of collectibility. So this is due to the state says do to decrease Well, you designs your question. Yeah. She said Yeah. Yeah. Okay. So, um, let's move on to Nephrotic syndrome, and then I'll ask a question, um, about a patient who comes in early in trying to side whether it's nephric tickle nephronic syndrome. But this is not critics syndrome with a capital I and I stands for inflammation. So what is different? Tick syndrome? So it's a syndrome present again. Another syndromes. It's a collection of symptoms that occur due to an underlying pathology. Do two different causes. So, um, this nephritis Androgel is present as hematuria, too. Micro microscopic blood in the urine, elevated BP, decreased urine output. So renal insufficiency and a Dema so they both have a d. Mother's. The one thing that's joining these two, um, syndromes together, and this is due to a get another line pathology off inflammation ongoing in the glomerulus. So why do we think we get Hematuria's in Nephrogenic syndrome, but not enough? Roddick's in drum, and I will tell you it's because if you think about information, we have a lot off. Um, laser dilation that occurs on your blood vessels become leaky. So if there's inflammation going on and in the good Mary less those blood vessels have become leaky on, they'll then gonna see you in. Then there's gonna let you read blood cells person to through the filtrates into the urine. So that's where we get our him actually a front so the allergy can be primary. I select the kidneys, or it could be a systemic disorder. And this is another table, too. Break up. I like learning and tables because it puts on my information in one place, you know? So that's why I suspect it up like this. On the plastic was a critic syndrome number one. Sorry, the first one last week about is acute proliferative glomerulonephritis, so this could be post infectious. So after uninfected or it could be infection associates occur at the same time. So this is, um, Post streptococcal Go Maryland a fright. It's the G M stands for governor, and Fridays is the most common type off America, Fridays and Children. So this occurs after uninfected with streptococcus, and this could be strep throat or in potato, a skin infection. So if it's a throat infection, the glomerular nephritis will usually cut 10 days afterwards. Uh, and if it's a strip throat that sorry if it's strep throat, it will be 10 days afterwards. If it's impetigo between 23 weeks after the infection on the causative agent is group maybe to him a little structure caucus. It can be infectious infection associative. So different infections could be meningococcus. See me a fill? A coca infection. And the card itis pneumococcal infections. Hepatitis is mumps, HIV, varicella, HPV, toxoplasmosis or malaria. So you can see that there are a lot of different infections that can lead to nephrotic syndrome. So if we talk about just streptococcal post streptococcal Romeril enough right is this occurs because of something called molecular mimicry. So the structure caucus. Um, bacteria has something called an M protein on it. And we have similar structure proteins in our kidneys. Another person, the body. It could be the heart as well. Uh, but what happens is we make antibodies against the M protein antigens. But this can also, um, has a similar structure the proteins found in the kidney so that these antibodies that are supposed to fight the infection than going to file gonna marinus eso What this needs to is immune complex deposition in and around the glomerular basement member, and see if we've got immune complexes that this is gonna activate the information inflammatory processes in locally, around and in the camera. This so we have the deposit in and around the Premarin basement. We have activation of the compliment cascade. Then we get these cells coming in, plasma cells coming in and macrophages coming in. So this is organ it to Ah, lot of inflammation in the glomerulus on the coagulation Cascade gets affected as well. And all this leads to, um, increase probability of the blood cells theca pillories to little these cells in and this'll or gets voted into the blood into the urine. Sorry. And then this, um that's just for the structure, Coco. But a similar kind of, um pathaphysiology occurs with these other infections as well. It's not due to molecular mimicry again. It's due to these inflammatory processes are going on elsewhere in the body, getting moved around the body and then attacking our kidneys. So to diagnose post streptococcal Okay, Maryland nephritis. We could do something called a rescue. Oh, titers, which are antistreptolysin of titers. And this just tells us that there was an infection going on, Um uh, by streptococcus. That was ongoing. And that has led to this. So we just continue with a course of antibiotics, penicillin, or if the penicillin allergic, we give them a referral mycin and with the others. It's just about managing and treating the infection that's going on on. Also managing on treating the symptoms are occurring because of it. So another form off nephritic syndrome is rapidly progressive. Go Maryland on Fridays. So this can be due to, um, many different things that are listed here. So we have antidiarrheal a basement membrane antibodies, and this is known as good Pastor syndrome. So there's no only only, uh, these antibodies attacking our kidneys, but they also attack cells in the lvot lie of the lungs. So we will have known enough retic syndrome, but they can present with hepatitis. It's a swell. Um, we have Lupus nephritis again with SLE post infectious can kind of hear a swell r g a nephropathy because so where we have a lot of iga immunoglobulins and they go in a tackle kidneys and lead to information there, uh, head actually in poor again occurring after an infection. This usually a cousin killed Ren's. So this is a type of vasculitis that occurs after on ongoing infection that has occurred. So they come out in a palpable potpourri rush. Um, uh, they also have symptoms of Nephrotic syndrome as well. Um policy Immune associate ID with vasculitis that this is a kind of autoimmune condition occurs on. It leads to vasculitis again. Information of the blood vessels. Information of blood vessels specifically in the kidneys in the glomerulus is going to lead to Nephrotic syndrome. So with these kind of conditions, there's with rapidly progressive grammarian and a fright. It's we have hatred. Yeah, Leo's which all associate it. So we have the or 14 Indian or four and good pastor syndrome. We have the auto antibodies against, um, collagen. Four on It's the non collagenase portion of the collagen, so her not sure and put pour a HSP usually occurs after operas prior tree tract infection. So we have our GI a, um, antibodies that go into the Mazon Geom at least a cellular proliferation on white blood cell recruitment. And we have also ankle antibodies occur which is associated with um, or term in destruction on systemic question litis. So we get our symptoms and then we have to find out why that's why this is occurring and find out cause entry Alacort so to diagnosis that we would obviously do our your in deplete would give us a matter of some protein urea as well. Um, a patient will be hypertensive, um, and we will then have to go in and to further investigation. So in the form of blood tests. So we will look for auto antibodies like the, um, primarily based basement membrane. Antibodies will look a compliment levels as well. We'll look at some history off epitope itis. We can also do some protein. Electrophorous is to look out for the SLE and rheumatoid factor also. So in terms of nephric take syndrome Well, giving cortico steroids like we did in a frantic syndrome. And again, we're treating he symptoms that occur. So we give them and top tenses to help with the hypertension diuretic, Stop the Dema. And if the rapidly progressing got married and nephritis can if untreated Lee to, uh, renal dysfunction on and stayed renal disease. And if physicals and the patient will require dialysis. Okay, so how does, uh, no for ticks syndrome manifest. So we have on the morning, they'll have periorbital edema because I've been lying down and we've got a deeper of our face. And then as the day goes on this edema because people dream. Also, we can see on our own cause, and it always be pitting edema. We also have hematuria. This can be micro microscopic. It's usually microscopic on it will be a Coca Cola colored urine. And when we put it under the microscope, we'll see three red blood cells in a high powered field. Um, protein urea, but not as severe as we saw in the frantic syndrome. Hypertension, uh, renal insufficiency. So we'll see a decrease in their urine output, a liquor era and again in good posture. Or Wegmans granulomatosis, which is a type of vasculitis. We get him up pieces and dyspenea. So when we see our patient there might look, um, pale and name. It will take the BP and it's gonna be raised. They're going to look a bit overloaded. There might have some Dema dead regular Valium might be disciplined, distended if it's good pastures or Wagner's. If we have a listen to the lungs, we might have some calls, which is also gonna turns out that's a fluid buildup in the lungs. Um, it can be a new heart murmurs that this will tell us that this under carditis going on. And, like I said earlier with the post streptococcal with the molecular mimicry, the M protein has a You can always have the similar protein in the heart. So that's what would lead to the undercard. Itis on the palpable Popo might be seen in SLE or hatred. Pia's Well, so no, only do we look at the urine dip when we have to look at the clinical examination of the patient is well on what we see on like Nephrotic syndrome. We can deline in eight a lot easier. What kind of nephrotoxin driven is as opposed to with Nephrotic syndrome, where there's not much else going on a lot from the edema on the protein urea. So, um, if we so we have a patient who comes in a little case study to, then you can try and decide. Is it nephritis or nephrotic syndrome? So we have a eight year old male patient who comes in on the the little boy is looking quite a Demetrius, um, Onda. He's coming into any on what kind of things would you want to know? Just based on the a diva on the age of the child. Is there anything specifically that you would want to ask from the history to help you decide which way you're going on? What is the first thing that you would do in terms of investigations to help you with your decision in which is it? Never taken a frantic. So is there anything specifically that you would like to investigate? A very simple investigation that could be done within seconds. And this will already take it towards your diagnosis on anything specific that you'd want to note from their history. Someone's just see? Just said a urine dipstick. Yep. You're in dipstick. So you dip. Say you're in on we see, um, my old protein urea about a one plus two. A two plus on we see him at your ear is well, it's called a colored urine. And on a dip, we can see red blood cells as well. So already this kind of going away, Which of the two is, um, but is there anything else you'd want to specifically ask? So okay. From this urine dip that you've seen, which one of the two do you think it is? They're suggesting to ask for any kind of recent infections and recent respiratory infections. Far Bs. So you ask him about his recent respiratory infections. And he said he had the operation tract infection. Um, a few days ago on, that should kind of take you to your kind of final. Is it nephrotic? Is it nephrotic? Yeah, people are saying nephrotoxic someone stress It could be idea. So if there's any rushes Yeah, there's no rush is. But just the history of operas Prior tree tract infection. Those of us have the critic That's absolutely correct. It is never tick syndrome. And he had a strep throat infection a few days ago about oh, a week to 10 days ago. So this would take you to your ultimate diagnosis off. Never did say, Yep, never tick syndrome. And it would be the acute streptococcal post post streptococcal glomerulonephritis. We're done. So, um, glad it makes a bit of sense. So then, if we take a break from all the syndrome and we forget about it now, let's move on to our third discussion, which is polycystic kidney disease. Now there's a lot more to this condition than I have written about, because there's a few different types, but I had just broken about or two. So more dominant, so polycystic kidney disease. So this is a multi systemic and progressive disease that leads to cyst formations at the system. Little kidney enlargement and other organs could be involved of the organs being liver, pancreas since clear. Like I said already, it hasn't gone to their more dominant inheritance pattern. So this means that it's no excellent linked. It's gonna cut in an equal distribution in in male and female. So it's autism or dominant, found in males and females equally, there's two genes that means that are involved, and there's that means the true variants. So we have PKD one, which is the most common. And this is due to, um, kind of genetic mutation that because in 16 p 13.32 chromosome 60 the segment pee 13.3 on this Kurds for polycystic one. And this is the most severe type of polycystic kidney disease, and we also have PKD two, which occurs in 15% of the cases, and it could for polycystic to so on these these all expressed on the cells in the kidneys and they interact with each other, and they regulate cell cycle, the cell cycle and division of the cells on also intracellular calcium transport so polycystic one and two belong to a transient receptor potential channels, and these are mechanical receptors that sends food flow through the tubules, and they transport intracellular calcium accordingly. So what they have found that is in polycystic kidney disease is they haven't increased off the interest. Cellular Messengers associate AM PM PK on this and handsome south proliferations of the cells and of derived from this genetic mutation. So the polycystic kidney disease. So let's get proliferated more and more and more on it inhibits the normal kidney cortex to proliferate, so we have more and more cystic cells that we do no more Selves. We also have a reduced endothelial visit dilations that there's a reduction in nitric oxide. Sendai's on. This leads to hyper hypertension because there's no phase a dilation that occurs. So we get we become hypertensive. So this manifest in ically as hypertension on. If we were to dip the urine, we may see microalbumin EMEA protein. You re re a and hematuria. We also have renal enlargement. Now this leads to a lot of our symptoms that we have, so this will lead to the pain. This would lead to the renal impairment because it's not the kidney that's getting larger. It's the cysts themselves and the system functional. We've got enlargement of non functional parts of the kidney. It's not going to be able to do its job as well as it would have, so this leads to the renal impairment. This can be seen as a lingering on eventually gets worse and west. It can lead to formation of renal stones. So if we think about cysts on the way we get kidney stones, it will form in the same way, because there's a lot of fluid that's there. And the fluid isn't just pure fluid. It has things that can crystallize, and then these then go on to form stones. We can have hemorrhage of the cysts on. We can get recurrent UTI as well, so we take all history and examinations that this they come with flat pain, which would be the most common cause of them come into the hospital so they might have a lot of flight pain on. We take a full history examination and it can only tell us so much. So we don't go on to do our imaging so we can do an MRI, a CT or an ultrasound scan on you. With this kind of condition, the older the person gets, the more cysts you'd expect them to have. So it's a progressive condition. So from the ages from about 15 to 29 you'd have two or more cysts in one kidney from the ages of 30 to 50. Have two or more cysts in each kidney on by the time you're over 60 you should have four more cysts in each kidney On the way to confirm the diagnosis is through genetic testing to see exactly which type is because, as I mentioned, there are other times there's a lot of them are recessive pattern of inheritance. There's acquired polycystic kidney disease as well, so we need to do some genetic testing to figure out exactly which type of polycystic kidney disease this is so management. So the patient may cramp commend you to flank pain, so the flank pain is usually due to a non going infection that's occurring within the cyst or a UTI due to the formation of the stone, or it can be due to muscle effect as well. So if we have a really large cyst, it can, you know, portion on to other structures. And this can cause pain, too. So if it's due to one large cyst, then we just aspirate the cyst. If there's many cysts that we can do, a surgical fenestrations of this is basically just filling. They fill them in almost, you know, remove them. And, um, I think it's about putting in a kind of, um, some kind of mechanism that stops the cysts form again. We can have hemorrhage of the system well, so this can be a self limiting episode, and if it is, then they just need some bed rest, some analgesia and increase the fluid intake. Make sure that their kidneys of being rushed out well, if it's severe and the patient becomes a huma dynamically unstable, this will require a transfusion on admission to the hospital. So if we have a cyst and UTI, so we have to treat this immediately because the sister filled with fluid and this condemned to further infection off the upper. You're in a retract and the kidneys. Um, And if the fever possessed for 1 to 2 weeks after the antibiotic therapy and you have to drain the infected cyst, uh, we have a stone formation as well, and we treat that with potassium citrate, and the hypertension is treated with a sin Hypotears and angiotensin receptor blockers. So the complications this conclude to end stage renal disease need to hypertension again. Like I said, other other organs can become involved and this could be the levels so we can end up with a policy stick. Clever. We can have cerebral aneurysms, renal stones and infections, and that is all I have about polycystic kidney disease. So again, there is a bit more information out there on it. But I fought for the purpose of this talk. It would be best just to do a little bit of an introduction into one of thumb. So now I'm going to speak about UTI is on UTI is is one of the really easy ones in renal disease because I feel like a nephrology can be quite tricky. But you t i z a very simple and easy nice topic. So I thought I'd end in that with the information overload I did at the beginning, just something quite quick and snappy. So for the UTI, so we have It can be uncomplicated, so it's just a bacterial infection of the bladder on the lower urinary tract. Infection of the bladder is called cystitis. So if you were to test someone's urine with just to your in depth the way you know that they have bacteria in there is true too positive nitrites. And that's because the bacteria breaks down, think and releases nitrides due to their own kind of mechanism going on. Um, the most common cause is a colitis on. Um, just because if you did the urine and you see the nitrates doesn't mean that they you have a UTI, they have back to really have a presence of bacteria in the urine where they don't have the symptoms off urinary tract infection. And those symptoms are dysuria. So pain on urination, the increased frequency. So you're going to the toilet way more often. Um, hesitancy. So when you do sit down to go to the toilet, it doesn't, um, you have difficulty with initiating the voiding. I didn't see, you know, you feel like you need to go absolutely straight away on some people in a bit more severe infections can present with him at your ear is Well, um, what else might do you think? Except from the nitrites that you would see in a urine dip or other things that we look for in the urine? What else might we see in there if there's an infection going on some people's? Yes, a big sites. Yeah, most, Yeah. What blood cells. Which is another thing we'll see. Um, Andi, if it goes untreated or treated. But the treatment isn't effective. It can lead to an open your injury tract infection. So this is then involvement of the kidneys. This is known as planned on Fridays, and this can manifest with initially starting as a UTI. And then progress is to have a few beers, right? Horse nausea on back pain, flank pain. Um, one thing that again, having graduated in Bulgaria, we got talk is to do the renal punch test, which I don't think we really do here. But it's basically you place your hand on the under on the flank Aspect on, you kind of punch your hand, and this should kind of juggle around the kidneys and if because there's an infection going on, that kind of causes pain in that region, So that's a test that they do that. But I don't think going to in England Um So again, like we spoke about, we will do a urine dip or CR positive nitrides. We'll see your white blood cells on. We might see some red blood cells as well. So we always in a hospital setting. Anyway, if there is a UTI, you treat them. But we also send out for your analysis. So we're gonna send out to get cultured and get sensitivities. So we're going to see what kind of infection is going on on. Do, um, what is this bacteria sensitive, too. So a normal, uncomplicated basic. Um, UTI is usually treated with the natural for in tone and it, you know, just 5 to 7 day course, and it kind of watch quite well. We can also use a tremendous reprime penicillin, and then a lot of the Children we use with severe urinary tract infections. You suffer Lexan as well. So in terms of kind of presidents, UTI occur more often in females and redo than they do in men. And this is because of the shorter you're into that we have Onda. If we get a UTI in the mail, this is not just a simple UTI. Automatically get classes to complicate to Duty II, and you have to do further investigations to find the cause. And it could be signs of, um, quest years and things like that as well. Um, on I think that is all I have again. It can become a pilot nephritis when it becomes pilot in the Fridays, we have to move on to a stronger antibiotic, um, with um with a slightly longer course, but again with a good set of antibiotics. And if you maintained that if you do the course for however longest specified 5 to 7 days, it usually is quite self resolving, it doesn't come with many complications. Um, people who are at risk of UTI is again people, the elderly again, women on anyone who has a long term indwelling catheter I increased risk on there are increased risk of a more kind of complicated UTI kind of bacteria that won't occur. It's not usually due to recall. I can be due to a four bedroom. Um off bacterias on on. That is what I have for you guys today. Do you guys have any questions? Yes, There is one question regarding the treatment for you through and they're asking out all the spots. Export factory away, the antibiotics. A broad, broad spectrum. Yeah, Usually they are broad spectrum, but then it depends if there's no resolution and the m CNS constructs with something slightly different that there's another kind of bacteria going on and then they have to become a bit more narrow spectrum and specific as to what you're treating. But usually they're quite broad spectrum. Any more questions? Nothing so far. Or everyone that has a phone they can use. The QR code us up there for the feet that form on I If if you don't, I will Just put the QR code on the shot is a link. Ah, chatted in just a moment on. But yeah, if you do want to catch up on any of the previous events estrogen, part one. Oh, if you to invade. But this one you can head It was met out on a low the catch ups materials on that. Uh, does anybody have questions for those first? If no, I will. Just a second. But the link. What about phones, right? Can't really see the length. Nope. Sorry about this. About stuff is so funny. He always says about now. Seven. See you now. Yeah, I think so. No, that's great. Uh, next week, we have got scars up again who be doing at the endocrinology? Rector, Be sure to join us for that on. Yeah, if you do have any more questions or if you have any questions that you think of later on, I'm sure you can write to us or you can write it out. Scores back. Oh, you can say that for next week. Yep. I will be back. And thank you for having me here. And thank you for filling this out. No worries. There's no other questions on. We will see you guys next week. Lovely. Thank you. Bye, everybody