Nephrotic Syndrome – Types and pathology

Nephrotic Syndrome – Types and pathology

                                                                                         Welcome to another make cram lecture we’ll talk about in frolic verses nephrotic syndrome now these are both syndrome types that occur in the kidney the questions of what’s the difference between them and why did they happen in the first place. And I understand that we really need to get into the pathophysiology of how these syndromes are different so what we have here is a picture of a cross-section of the capillaries in a kidney and what we have here is the endothelium. Stay in the filial cell. And it completely surrounds. The lumen of the vasculature universe that there are little slits here that allow things to get through but not the red blood cells typically then this blue line represents the basement membrane which is permeable to a number of things and then finally on the outside is this epithelial cells melt the epithelial cell has little foot process sees that you see here that look like little triangles around the edge and basically these former very tight serve which allows only very small things to get through typically not even proteins are allowed to get through here proteins are too large and these what we call photo sites are helpful for that so if you want to imagine that we’ve got. Fluid okay leaving.

                                                     And when that fluid leaves the vasculature lumen and goes through the slits in the endothelium and the basement membrane and comes out even though the portal sites of the epithelial cells in the kidney what we’re left with here is basically Bowman’s space. This is a Bowman’s capsule of course. And all of this fluid eventually unless it gets reabsorbs is good to go. Down into the toilet okay.Flushes down. So basically anything that gets outside this area is good eventually end up in the urine I think that’s a very important thing to remember if you can remember the schematic of what a glomerulus looks like you remember that you’ve got a vasculature that comes in and then leaves and you’ve got a Bowman’s capsule here that picks that up that’s what we’re looking at here. In this picture. And that gets picked up goes into the proximal convoluted tubule. Down the descending loop of Hamley up the A. sending loop into the distal convoluted to bill and then into the collecting ducks and then out again.To the toilet. So once again this is a. Epithelial cell. And this is a. Endothelial cell. So what I’d like to do is I’d like to divide this picture if you well into two. And on this site, we’re gonna talk about the nephrotic syndrome. And this site will talk about the Frick syndrome.

                                                                So the fried egg syndrome is fairly straightforward it’s a process where for some reason these poto sites are all connected to the epithelial cell. Aren’t working or they get lost or the receipt or they include something makes them disappear and as a result of that. They’re not able to keep the protein in. And so as a result of that there is loss of protein. And it’s quite substantial and facts on the order of three and a half grams of protein. For day can be lost. Now this tremendous loss of protein has its consequences. One of the first symptoms that you’ll see is that the urine is ray frothy. Close frothy urine is caused by protein in the are now don’t get alarmed if your urine is frothy because there’s a certain amount of protein that’s in there naturally I guess there are some surfactants and another type of chemicals that’ll make naturally your urine frothy but if it’s especially frothy think about protein in the urine now as a result of this you’re also losing proteins so if there’s not enough protein in your intravascular space you’re not gonna be able to keep that fluid in the intravascular space and you’re gonna have more leakage of fluid and so this is what we see in patients with loss of protein is they become a damage to us and we’ll have a DM up just about all over their bodies the orbital the even in their legs and sometimes even in their lungs. Probably the main loss of protein is albumin.I’ll be me as the major protein that keeps fluid in the blood vessels now when albumen goes down because of its loss the liver has to compensate and when the liver compensates we get increased lipids in the blood this is another sign of nephrotic syndrome there’s also another protein that’s Los called antithrombin three now antithrombin three is a very important anticoagulant, in fact, it’s the same protein that heparin utilizes to exert it’s a fact. So the point is is that if antithrombin three is also going down in the situation the patient is going to have a hyper collectible state and since this protein is lost here in the front exedra because these portal sites are not working very well the renal vein this is the blood going back after it’s lost is going to be especially poor in antithrombin three and that’s where we tend to see thrombosis manifests thrombosis in the real thing this could amble lies and you could get blood clots to the length so you should think of DVDs.

                                                                                          And pulmonary embolisms are peas in patients with the fraud X. intro so to review a product syndrome it’s basically a problem with the portal sites or even the basement membrane anything that allows. Protein to sift through here causing frothy urine decreased albumen increased lipids both in the serum. And also in the urine okay you’ll see antithrombin three being reduced that leading to a hyper collectible state. Typically there are about three and a half grams of protein lost per day now there are diseases that are not of the kidney which can cause the fraud X. syndrome these are called secondary causes of the products in from and there are diseases which specifically affect the kidney which can cause nephrotic syndrome these are called primary the Friday diseases will talk about those in another lecture now on the different Exide completely different mechanism of action for causing the fatigue syndrome worse before there was a problem with the loss of poto sites in the frig syndrome what we have is immune complexes. So an antibody meeting up with another antigen and complex and. This type of an immune complex will lodge itself. In the capillary.As seen here and it will list set an immune response against these capillaries and against these antigens now as a result of this a number of white cells are recruited as strong here there will be many more white cells.As a result of this inflammatory response to these immune cells. These areas will become inflamed break down and it will allow red blood cells.

                                                                                         To pour through these openings. Not only that but also white blood cells to come through. And of course, since these openings are big enough for whole cells to get through. There’s also very. Usually allowed for protein to come through as well. And so very often even though the patient may have the fatigue syndrome they may also have what we call the frolic range proteinuria so the protein may also be high in for X. syndrome and leading to all the things that we saw over here in the front X. intro but in addition to that there’s something that’s very very different remember we said all of the stuff on the outside eventually goes into the urine and so what do you think we would expect to see in the urine in addition to protein isn’t just mention we would also expect to see. Blood in the urine.

Settlements in the urine because of this breakdown product and also what we call hi urea or white cells in the urine as well and so as a result of this there are few symptoms that we see in this new Frick syndrome the first thing we see is hematuria. That’s blood in the urine the next thing that we’ll see is all the curia or low urine output and that’s because the glomerulus is being damaged and so it can’t filter as much because this immune deposition here is not going to allow the free filtration of filtrate it’s going to become inflamed and the glomerulus is gonna start to shut down that causes a low GFR the other thing that you’ll see is high blood pressure because of that lack of filtration so hypertension. Plus you’ll see is granular casts. So this is the main difference between the frantic and fraud acct usually there’s more inflammation on then for Exide. There’s less on the nephrotic side typically if you just see an increase in protein in the urine at very high levels like three and a half grams a day and nothing else there’s no active settlement as what they would say then think of nephrotic syndrome if, on the other hand, you see a lot of cells debris settlements and inflammatory cells think of the Frick syndrome. Now just in the fraud X. syndrome where there are primary and secondary diseases that can cause nephrotic syndrome, there are also primary and secondary diseases that can cause the for X. intro and we’ll discuss that in upcoming lectures.

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