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Hi guys. Uh sorry, just give me a moment and we'll get started. Oh, sorry. Ok. Um Sorry about that. So, um Hi, my name is Shruti. I have done some of the previous lectures as well. Um So today we're gonna be doing AK I and glomerulonephritis. Um So we're gonna start off talking about AK I um which is obviously um one of the commonly tested conditions. So AK I is an acute decrease in renal function. So it's basically acute renal failure. Um and it occurs because of an insult or something that's damaging the kidneys. Um And the main thing to remember is that it's an acute thing. Um So in the presentation, it can be asymptomatic, but when it uh does have symptoms, the main things are reduced urine output, which makes sense when you've got damage to the kidney, your um kidney function is gonna go down. And obviously, one of the main functions of the kidney is to produce urine. So your urine output goes down, you can get arrhythmias, you can get pulmonary peripheral edema and uh you can get uremia. All three of these are mainly because of um the things that build up when your kidneys aren't working. So the kidneys uh work to filter your blood and to remove um waste products. And when they build up, you can get these um symptoms and you can also get dehydration and nausea as a result. Um So it's a rapid reduction in G FR with or without. And so what that means is that the main difference between AK and CKD. So chronic kidney disease is that this is something that's rapid. They both have a drop in G FR but here it's something you know, when a patient is fine baseline and then suddenly their GG FR has dropped. Um Then that's an AKI. And the second main point to remember here is that it's with or without oliguria and you can have AKI without oli ura, maybe in the early stages. So risk factors are CKD. Now, that might be confusing. Basically, a patient can have CKD, they can have a chronic kidney disease and then they can have an acute factor that leads them to, to have an AKI. So you can have AKI on a background of CKD. Um So be careful of that. So the patient might be a long term renal patient anyway, but they can have an acute insult that damages the kidney and leads to an AKI, they might have another organ failing. It's usually like heart failure, liver disease, um which can predispose to, to getting an AKI as with a lot of things in medicine. Previous history of the same thing leads to an increased risk of getting it again. Um And drugs with nephrotoxic toxic potential. So these are things that can trigger the AKI. So nsaids aminoglycosides. Um so those are antibiotics like gentamicin within the last week. Um So these are certain drugs which can um attack the kidney and cause an AKI. Um These are quite important to remember because like in a, in a question, like generally, the patient would have been on an NSAID or on gentamicin. So that's like your trigger to think about AKI um use of iodinated contrast agents within the past week. So they might tell you that the patient had like a CT with contrast or, or something like that, which would make you think of that um older age and uh uria. Um So you've got prerenal causes intrinsic or renal causes and post renal causes. So things that are issues before the kidney in the kidney, after the kidney, which is actually a really easy way of remembering um what's going on. So we're gonna go through them one by one. So we'll start with prerenal causes. Basically, the main thing here is decreased kidney perfusion. So there's reduced blood supply to the kidneys and that's causing the AK I. So it's like with anything, if you've got reduced blood supply to the heart, you're gonna get heart. If you've got reduced blood supply to, you know, the bowel, you're gonna get bowel ischemia. So it's the same kind of thing. Um And basically you get shock, which can be hypovolemic. So due to um low blood volume, it can be cardiogenic or it can be distributive. Um and you can get hypovolemic, um you know, var disease. So hypovolemia usually um presents with a few symptoms. So one being tachycardia and the other one being hypotension. So, if you've got a low blood volume, obviously, your BP is low and then the tachycardia kind of tries to compensate for that. So, because your cardiac output is low, um if you increase your heart rate, then you're going to get a little bit more blood per minute. Um So the tachycardia is kind of like a compensatory measure. Um and you will have cool peripheries um because of reduced perfusion. Um So, yeah, and the causes are usually acute hemorrhage. So, blood loss, burns, diuresis gi losses, which are all like fluid losses, um and sepsis as well. And your management is fluid resuscitation. Um and basically, that should help treat the cause, which is decreased kidney perfusion. And so they should get better. Um vascular insults can be nsaids, ace inhibitors or Arbs contrast A CT and renal artery stenosis. So that's when the arteries and the the um supply, the, the kidneys are like narrowed. So you've got less blood supply. Basically. Now, renal causes. Um So basically the issue is like there's a problem with any one part of the kidney. So this could be a problem with the glomeruli as in acute glomerular nephritis. It could be a problem with the tubules of the kidney. So, acute tubular necrosis, it could be the interstitium of the kidney. So, acute interstitial nephritis, it could be that the renal vessels have been damaged. So you can get that in hemolytic uremic syndrome, which is the common one that comes up and you might have tumor lysis syndrome. Uh So if a patient is on chemo for like cancer or whatever else, um that can lead to tumor lysis syndrome and rhabdomyolysis, which is where your um your um you've got breakdown basically and that enters the blood. Um So, 35% of cases are due to intrinsic damage to the glomer renal bu or interstit of the kidneys themselves. Now, tubular renal causes, there's two main things that you need to remember. So there's ischemia and there's nephrotoxin and both can damage the tib. So firstly, let's go through the toxin. So this is a direct effect of a nephrotoxin something that's toxic to the kidneys acting on the tubular cells. Now, these can be myoglobin like in rhabdomyolysis. So, here you have breakdown of the muscles and that releases myoglobin and the sign that you'll see in the questions will be dark urine following um trauma or a crush. And that's because of the myoglobin that enters into the urine. You can have uric acid which can damage the kidneys. Um in the case of tumor lysis syndrome. Um So when the tumor like breaks down, um basically, it releases like uric acid potassium and some other things. So, a uric acid part of that can um can be toxic to the kidneys. And you've got monoclonal light chains, which is seen in multiple myeloma, which is a um cancer of the plasma cells. Um And again, that can also damage um the um tubules. Now, you've also got endo exogenous toxins, the things that you're taking in and usually the ones are aminoglycosides. So, antibiotics and radio contrast agents lead nsaids and CISplatin realistically in questions. It's gonna be immunoglycoside or nsaids most of the time. But you know, it's, it's good to be aware of the ones as well. Um And the other option is ischemia. Um and this is because of damage to the tubular cells as a result of prolonged ischemia. Now, this might get a little bit confusing because we said that pre renal AKI is caused by a drop in renal perfusion, which is true. So that's because we've got less blood supply coming into the kidney here. That ischemia is more kind of like, you know, on a, on a prolonged level when you've got low blood supply to each individual tubular cell. So we're not talking about the, the overall picture but more like each individual tubular cells and the tubular cells themselves die if that makes sense um and break down and you can get shock and sepsis as well causing this. So, features are firstly, you'll see raised urea and creatinine um and also potassium. So um creatinine is usually gonna be raised even in KD, but it's the same thing in, in AKI eye as well. Usually if there's a higher urea, then you're thinking more of a um of like an achy eye, like if the urea is a lot um higher than creatinine. Um and you get potassium because of the, you know, you're not excreting as much. So you, you get potassium retention, um and you'll see muddy brown casts in the urine. And so that's an MSU test that you do and that's just like a buzzword that you need to know. Um And it's like something that you see on his histology. Um But yeah, it's called Muddy brown casts. And stages are the oliguric phase, the polyuric phase and then the recovery phase. So l little urine too much urine and then you, you get recovery um.