hello everyone am i clearly visible audible to you guys kindly someone give me a thumbs up in the chat box if i'm clearly visible audible you have to give me a minute to confirm if i'm clearly visible audible i will start the lecture ahead you have to give me a minute just a second i hope it's working yes is it yes i hope it's working yes so welcome you all for today's session very very good afternoon to all of you so just a second so uh there's some icon coming on my face now you cannot you cannot see my video clearly right can you see my video clearly can you see my video clearly just a second yes i can see it now okay anyways i will continue just a second so yeah so i welcome you all for today's session uh a very very good afternoon to all of you this is episode three of renal system i am dr priyanka sajdevian and today morning um today morning i have i have started renal pathology so in renal pathology we have started the various type of glomerular nephritis studying the various type of glomerulonephritis in a comparative manner so in today morning we have already seen the pathogenesis of glomerulonephritis we have seen the anatomy of the kidney the anatomy of the nephron the structure of the glomerulus the structure of the filtration barrier we have seen the various type of pathogenesis of glomerular injury it can be antigen antibody mediated it can be cell mediated it can be complement pathway alternate pathway we have seen all of them now we have started the glomerulonephritis in the glomerulonephritis we know that there are nine type of primary glomerulonephritis which you have which we have started studying in the morning so the first one is the apgn which we have completed in the last lecture also known as psg and those who have missed please please watch the recording after this you can't afford missing that the second is the rpgn rapidly progressive glomerulonephritis that also we have completed in the last lecture so apgn also known as psgn we have completed in the last lecture rpgn is also completed the last lecture the third one is the mcd that we have completed in the last lecture and now i am starting from from membranous onwards so in this lecture i will start with membranous glomerulonephritis membrane of proliferative glomerulonephritis and the remaining one focal segmental globular nephritis glomerulous sclerosis ign after patching chronic so first i will be finishing these primary glomerulonephritis the remaining one and after that i will continue with the secondary globular nephritis and hereditary globular nephritis so what you are asking deepak please complete general pathology first please ma'am so i'm taking two courses deep one on the youtube and one on the special classes on special muscles i'm continuing with the general pathology on youtube i'm continuing with the systemic pathology so if you want to study general pathology stay connected on the special classes so on special classes of an academy more or less i will complete the entire general pathology and hematology youtube is specifically for systemic pathology you got your answer i guess you so let me continue with the primary glomerulonephritis first shall i continue give me a minute you have to give me a minute right okay and these are the secondary ones which i will finish the primary glomerulonephritis and in the secondary i will teach you lupus nephritis that is sle diabetic naturopathy amyloidosis good posture we have already competed in type 1 rpg and if you know and just for pura and in the heritage one i will be completing this so first i will help you again we will compare the first three glomerulonephritis that we have learned till now in the first five minutes of the lecture so that we have a overview that what we are going to do ahead so we have completed apgn rpgn and mc uh mcd till now and then we will continue with marina so just sachin i will require five minutes the revision and then i will continue ahead so give me a minute for that also [Music] let me move on the slide of the comparison directly keeping the first three global lunar practice that we have already completed okay i will be continuing with the third one again because mcqs of the third one are remaining we have not completed the mcqs of the third one i guess right so i will be continuing with the mcd so we have completed apgn we have completed rpg and we've completed mct also so etiology we have seen that apgn also known as posttreptococcal glomerulonephritis rpgn also known as crycentric glomerulonephritis and mcd minimal change disease also known as nil deposit disease or food processed disease first learn the other names given to these globular nephritis right after that coming on the etiology or retrieve pathogenesis of each of them apgn is due to antigen antibody immune complexes formation that is in c2 it is in c2 deposition of the antigen antibody complexes against a planted antigen who is the planted antigen here the planted antigen is the bacteria you know the name of the bacteria it is group a beta streptococcus bacteria that is known as gas bacteria you know the complete etiology i guess in rpg we have seen type 1 type 2 type 3 rpgn type 1 rpg is good pasture syndrome that is anti-gbm disease here also nc2 deposition is there but against a fixed antigen not the planted antigen in type 2 again it is psgn only so it is the planted antigen and in type 3 rpg and it is the possy immune disease so no antigen antibody complexes are there it is cell mediated immunity we came on the gross of each of the following so in apg and the cross is clear bitten kidney you already know that pre-orbit and kidney in rpgn the grass is large white kidney and in minimal change disease the grass is normal we have already discussed the normal pros in light microscopy electron microscopy and immunofluorescence microscopy we have to say three microscopy in light microscopy in apg and the size of the glomerulus is increased in rpg and also the size of the chloroplast is enlarged glomerulus is hyper cellular in both of them and most of the cells are inflammatory cells neutrophil and lymphocyte and glomerulus is proliferative in both of them hyper proliferative the only difference between rpg and epgn is that in rpgn crescent is the hallmark you already know what is present right in minimal change disease light microscopy is absolutely normal that's why it is known as minimal change disease minimal means there is minimum change on the light microscopy in electron microscopy we have already seen that here the deposits are epithelial deposits here in type 1 the deposits are intra membranous in type 2 against epithelial and in type 3 no deposits are there in minimum change disease it is flattening it is flattening which is seen flattening of the food processes we already know the meaning immunology and the composition is same everywhere igg plus c3 so i'm not repeating that so that is the summary gel number let me start the next one membranous and membrane of proliferative glomerulonephritis shall i continue with that give me a thumbs up so i am continuing with just a second membranous and membrane of proliferative globulin practice so i will take the next two together so first i will teach you membranous and then membrane proliferative and we will see the poles together both of them we will i will launch the poles together so what is the difference between membranous and membrane of proliferative i'm going to teach you in sequence now membranous glomerulonephritis membrane of proliferative glomerulonephritis what is the difference between the two what is the difference between the two as the name indicate in the membrane there is thickening there is thickening of the basement membrane glomerular basement membrane that is membranous the meaning of the membranous in membrane of proliferative membranous component is there so thickening of glomerular basement membrane is also there but the difference is proliferative so proliferation means hyper cellularity here hypercellularity is also a feature here cellularity is normal it is not hyper proliferative have you got the difference between membranous and lavender proliferative the name itself says its meaning in the membranous glomerulonephritis only membrane is the thicker thickening of the glomerular basement membrane is there and in membrane of proliferative along with the thickening of the glomerular basement membrane proliferation that is hyper cellularity is also there you got my point if you got my point give me a thumbs up have you got it have you got it so let me start the membrane as fast let me start the membranous first the membranous is also known as ep membranous epi membranous naturopathy and it is the most common cause of nephrotic syndrome in adults yes so geopathogenesis so i will tell you the idiopathogenesis here let me draw the basement membrane let me draw the filtration barrier in the filtration barrier this is the basement membrane you can see this is the basement membrane on one side we always have endothelium right and on other side we always have visceral podocytes these are the visceral protocytes right now visceral podocyte have a protein inside that that like the basement membrane is made up of type 4 collision i have taught you in type 1 rpg and this is the type 1 collagen type 4 collagen present in the glomerular basement membrane so in the same way the visceral podocytes the visceral photocytes have a protein in it the name of the protein is glycoprotein 330 gp330 glycoprotein 330 it is like a protein same as that of collision so it is a self protein normally body doesn't make antibodies against it but sometimes in some autoimmune diseases the immunity of the body becomes deranged the immunity of the body become mad and body start forming antibodies against the gp330 protein so what will happen this antigen is fixed antigen there it is not um planted here it is already present there so it is fixed antigen there it is fixed antigen now contrast compare and contrast this with psg and post structural glomerulonephritis in post-streptococcal uh glomerulonephritis in post-traumatic globular nephritis also we are having antigen on the podocyte but that antigen was a bacteria here the antigen is the protein gp330 that antigen was planted here and this antigen is fixed there so here also antigen antibody complexes will be formed so let me draw the antigen antibody complexes antibody will form the antibodies are auto antibodies so these auto antibodies will come and bind here and form antigen antibody complexes so here also in c2 antigen antibody complexes are formed against a fixed antigen and it is an autoimmune disease you got my point what is the fixed antigen there the fixed antigen is glycoprotein 330 it is a component of the podocyte what is the location of the deposit siddhika sachin motion what does the um what is the location of these deposits is it intra membranous is it sub epithelial it is sub endothelial yes it is sub epithelial it is sub epithelial in the same way as that of psgn everyone give me a thumbs up everyone have you got it first give me a thumbs up have you got it so this is the pathology this is the pathogenesis the draw flow chart what i have explained you draw the flow chart so immune complexes are formed so the the podocyte the podocyte have a protein the name of the protein is glycoprotein 330 right because it is 330 kilodalton in weight that's why it is known as glycoprotein 330 right it is located on the podocytes the body form antibodies against this it is a fixed antigen in the autoimmune diseases that's why nc2 antigen antibody complexes are formed and these are absolutely right these are sub epithelial machines sachin absolutely it is sub epithelial in location so this is the flow chart so antigen here is gp 330 which is a component of photoside that's why it is a fixed antigen so antibodies are formed against it antibodies are formed against it and these antibodies will form antigen antibody complexes against the fixed antigen and that will lead to acute renal failure this is the diagram now same diagram i have shown you in psg and also post rectifical glomerulonephritis you can see the podocytes on the photoside here the red colored antigen here is gp 330 which is a fixed antigen and if i talk about psg and the red color antigen here this diagram is same but the red color antigen is the bacteria group a beta streptococcus bacteria now this this is planted antigen and this is fixed antigen you want my point so till now what i have taught you the first glomerulonephritis i taught you is psgn or apgn one and the same thing post streptococcal globular nephritis or acute proliferative globular nephritis then i taught you rpgn rapidly progressive glomerulonephritis type one then i taught you type two then i taught you type three after that i taught you minimal change disease and after that now i am teaching you membrano proliferative glomerulonephritis i want to compare idiopathogenesis till now of all the glomerulonephritis i taught you till now have you got it have you got it yes have you got it so you tell me so what is happening you tell me so in psgn or apgn a bacteria is coming the name of the bacteria is gas bacteria group a beta-streptococcus bacteria that is coming that is causing tonsillitis or skin infection so imagine a person is having tonsillitis or a skin infection of group a beta streptococcus from the tonsil and skin the bacteria is going in the blood right from the blood the bacteria is going in the kidney in the kidney it get deposited on the podocyte it get deposited that's why this antigen is planted antigen this antigen is planted antigen no body will form antibodies against it and antigen antibody complexes will be formed in c2 against a planted antigen this is the complete story in type 1 here the antigen was group a beta streptococcus antigen here the antigen is type 4 collision which is a component of basement membrane that's why it is an autoimmune disease so type 4 collision of the basement membrane alpha 3 chain and c1 domain is the exact antigen body will form antibodies against it which are actually auto antibodies right so antigen antibody complexes formed here also but this antigen is fixed antigen it is not planted it is initially present here only so it is a fixed antigen so antigen antibody complexes here formed again in c2 but against a fixed antigen not the planted see here also in c2 antigen antibody complex formation here also in c2 but here the antigen is planted and here the antigen is fixed that is the difference between the two type 2 is same as that of this so another name given to psg and is type 2. so same story is repeated here right so same story is repeated of apgn is the type 2 rpg and only in type 3 there are no deposit because it is cell mediated cell mediated knees t lymphocytes cd4 cd8 lymphocyte will cause the damage to the filtration barrier if you talk about mcd again it is cell mediated so no anticipation antibody complexes are there not coming on amp gm in ampgan what is the antigen antigen is glycoprotein 330 which is a component of podocyte again it is the fixed antigen not the plantation one it is a fixed antigen it is already present there and body is forming auto antibodies against it so these outer antibodies are going to the antigen and antigen antibody complexes are formed so these antigen antibodies complexes are formed in c2 against a fixed antigen which is present on the photosite everyone give me a thumbs up have you got the complete picture what i want to explain you so in psgn here since the bacteria got deposited on podocyte so antigen antibody complexes on podocytes so deposits are some epithelial in type 1 since the antigen is type 4 collagen which is a component of basement membrane that's why the deposits are intra membranous or epi membranous in type 2 again it is sub epithelial because it is same as that of psgn type 3 no deposit mct no deposit in mpgn the deposits are against the epithelial the deposits so you can see the subway epithelial deposit in apg and pspn and mpg and both have you got it no one will explain you with such a clear concept have you got it say yes or no have you got it till now so now i'm drawing two filtration barriers in front of you i am drawing the first filtration barrier of psgn in which the deposits will be sub-epithelial and then i will draw the filtration barrier of mpgn again the deposits will be sub-epithelial but how to differentiate the two type of deposits then so here see the two diagram you will understand what i mean to say so this is psg and i am drawing or apgn whatever you say post traffic global unified is the first one and here i am drawing mpg not mpg and i'm sorry mgn last maybe many share the mpg and bullet i have it was by mistake i'm teaching you membranous globular nephritis mgl it is not amputeen right now draw the filtration barrier so in the center this is the basement membrane okay on one side of the basement membrane this is the endothelial cell okay so these are the endothelial cell on other side of the basement membrane these are the visceral podocytes can you appreciate the podocytes say yes if you can appreciate the polar side please say yes right you can appreciate like this right now here this is bacteria i'm drawing so this is group a beta streptococcus bacteria i'm drawing on the podocyte that's why this is a planted antigen right this is the planted antigen and here i am drawing gp330 this is the 330 here the antigen is gp330 see the location of both of them is same this one i'm drawing is gp3 turning glycoprotein 330. so this is a fixed antigen so that is the difference first you see the difference between them everyone give me a thumbs up so body is forming antibodies against the antigen so these are the antibodies formed here so antigen antibody complexes are formed sub epithelial right and here also the antigen antibody complexes are formed sub epithelia right so in c2 formation of in both of them the antigen antibody complexes are formed in c2 and the deposition is sub epithelial the deposition is sub epithelial here also here also so what is the only difference here the antigen is planted which is the bacteria here the antigen is fixed which is the integral component of the border side till now if you got it give me a thumbs up sachin siddhika motion i can't see the name of others have you got it if you got it one more thing now the deposits in both of them is sub epithelia now see how to differentiate the deposits on electron microscopy yeah everyone see everyone see here i'm drawing again psgn or apgn right and here i'm drawing mgn membranous glomerulonephritis so as i have told you in both of them this is the basement membrane in both of them this is the endothelial cell and in both of them by drawing again there is a reason behind it and this is the visceral podocyte in both of them right you already got the atrial pathogenesis i'm not repeating the ego pathogenesis i'm directly drawing the deposits now i will draw the deposits with blue color now you yourself appreciate the shape of the deposit so this is the deposit it is the epithelial okay let me fill the color also it is sub-epithelial in location these are the deposits i'm drawing the sub-epithelial only you know how they are formed i'm not repeating the geopathogenesis how the bacteria is coming and forming it you already know so this is the psgl appreciate the shape the location is up epithelial i'm not saying but the shape will be different so this is the shape of the deposit in psgn or apgn now i'm drawing the same deposit the sub epithelial deposit in mpgn see the shape see the shape i guess you can appreciate the difference in the shape let me fill the color in few of them so that you can appreciate the shape these are spikes i'm drawing the spikes the pointed shape is known as spike have you appreciated no one will tell you with such a beauty with such a detail i'm really doing a hard work for you people just to you you you get the concepts right i'm covering medicine also here the renal pathology will be covered from pathology as well as medicine so you can see the deposits here are some epithelial the deposits here also sub-epithelia right both of them are same but the shape of the deposit here are lumpy bumpy humpy deposits if you remember the hump of a camel have you seen a camel they are looking the hump of a camel and here the deposits are like the spikes so these are the small small clues that you have to take in the question here the bacteria uh group a beta structures bacteria that is a planted antigen and here the antigen is gp 330 which is a fixed antigen so these are the differences between them you can see everyone give me a thumbs up chutney audience with me thumbs up have you got it shall i proceed ahead shall air procedure ahead so you can see here the deposits will be formed here also in both of them in psgn and in mgm uh in c2 complexes are formed but it is the fixed antigen on the podocyte it is membranous glomerulonephritis it is the planted antigen on the uh podocyte that is a bacteria so it is psgn everyone give me a thumbs up so both of them in c2 complexes are formed antigen antibody mediated yes or no yes or no that is the thing grossly the kidneys and large pale nothing important coming on microscopy what is the name of the disease what i'm teaching you right now i'm teaching you membranous glomerulonephritis so as the name indicate on light microscopy the membrane will be thicker so there is diffuse thickening of the glomerular basement membrane in the diagram you see the diagram in this diagram can you see this is this is the glomerulus can you appreciate the glomerulus yes you all can appreciate the globalist inside this this glomerulus i can see multiple capillaries one two three multiple capillaries are there i can see if i zoom i can see the uh on the inner side of the capillary if you can appreciate you can appreciate some flattened cell i can't zoom the image you yourself try to zoom it and see the flattened cells are the endothelium very flattened cells are and on the outer side epithelial cells are there on the outer side the visceral epithelial pods are there if you can appreciate zoom the image can you appreciate the spikes here if you can appreciate the spike i have drawn the spikes here the spikes are the deposit so because of this deposit the membrane become thickened so it is it is the diffuse thickening of the glomerular basement and brain the only finding the only finding on light microscopy rest everything is normal right now it the basement membrane is thickened so much that it looks like there are two basement membrane but actually it is one only it is known as duplication of the basement it is not duplicated it but is it is not double it is a single membrane only it is looking that it is duplicated one more thing that you should notice here here cellularity is normal it is not hypersolution i cannot find the cells inside that right i can't find abundant of neutrophils and lymphocytes inside that i can find only one finding thickening of the basement membrane so only one finding is thickening of the basement membrane that's why it is known as membrane-ness globular so membranous means thickening of the basement membrane the thickening of the basement membrane is better seen on a silver stain so or do a pastel let me see this is this is a pasting in the past ten appreciate the thickening of the basement membrane thickening these all our capillary loops this is the glomerulus i appreciate the basement membranous difference right rest all is normal on light microscopy now i am coming on electron microscopy you already know the location of the deposit it is sub epithelial like psgn only but the shape is different the shape is spike not humpy you can appreciate this is the basement membrane everyone appreciate this is the basement membrane please appreciate inner is that the endothelial please appreciate these are podocytes can you appreciate now see the pink color deposits can you see these are the deposits so these are stuff epithelial and they are spike in shape more or less their spike in shape right here also you can appreciate the spikes here also you can appreciate they are spikes and shape and they are sub epithelial have you appreciated on immunofluoroscopes the composition is to be said the composition is again igg plus c3 nothing important it's igc plus c3 granular deposits are there that's it clinical finding it is nephrotic syndrome in contrast to psgn which was nephrited who will help me in filing this table anyone among you and even among you we have completed membranous globular nephritis right after that i am teaching you membrane of proliferative liberal nephritis right membrane it is in c2 formation of antigen antibody complexes against a fixed antigen the fixed antigen is gp30 gp330 that is present a protein on the podocyte roughly the kidney is large nothing important right light microscopy only one finding glomerular basement membrane got thicker the only one finding thickening of the basement membrane it looked so thick and that it looks the duplicated it looks duplicated here such an absolutely right on electron microscopy the deposits are sub epithelial but the shape is spike on immunofluorescence the composition is igg plus c3 like others now let me complete one more mpg and then i will make a comparative table between them right amputee and a chord pulled again right now we have studied just now we have studied mgm and now i'm teaching you mpgm can you first tell me the full form can you this is membranous glomerulonephritis this is membrane of proliferative globulin nephritis so in membranous membrane nephritis only one finding is membrane that is thickening of the base membrane here jbm get thicker we have already seen the diaphragm here two findings will be there one is membrane membrane or proliferative material gbm thickening will be there but proliferation is hyper cellularity is also a feature which differentiate which differentiate mgn from amplitude and we have seen earpiece singularity was normal in in membranes have you got it i'm coming on mpgn that is memory no proliferative globular nephritis right it is also known as misangio capillary glomerulonephritis you have a two findings will be there beginning of the gbm and increased cellularity of the glomerulus and the mesangium right if your pathogenesis is a gain of three type type one type two type three don't go in details it is of three types just learn it is of three types type one two three like rpg and only grossly they keep nothing important that kidney is pale and appearance but not important light microscopy this is the diagram now you will tell me what you will appreciate in this diagram you are appreciating two things number one see the glomerulus substitute globalistic see the glomerulus now inside the glomerulus see try to see the two findings where are the capillaries these are the loop of the capillary c on the inner surface they are an endothelial cell no problem in the endothelial cell no problem in the endothelial cell see two findings number one the basement membrane got thickened basement membrane got thickened and number two there is increased cellularity also you can find most of the cells are lymphocytes and neutrophils so two findings are there thickening of the basement membrane and hypercellular hypercellularity that's why known as membrane no proliferative glomerulonephritis it is not only membranous see the thickening of the basement membrane is best appreciated appreciated on silver state now compare the two everyone compare the two no one will give you such a beautiful comparison see this is a diagram of mgn and this is a diagram of mpgn now you yourself decide what is the difference between them in both of them one thing is fine common thickening of the basement membrane is the common finding here also and here also because membrane is a component of c don't only learn see the basement membrane is thickened here also in all of them and here also in all of them the basement membrane is thicker but one thing which differentiates the two is cellularity is normal cellularity is hyper cellular compared to cellularity can you see uh the inflammatory cells here no no neutrophils no lymphocyte and i can find abundance of neutrophils and neutrophils and lymphocytes here everyone give me a thumbs up give me your audience with me thumbs up everyone give me a thumbs up let me see your chat give me a minute so give me a thumbs up have you got it shall i proceed ahead shall i proceed ahead so that is the comparison that is the comparison between membranous and membrane oh proliferative the light microscopy uh in membranous as i have told you the membrane is so thickened that it looks like duplicated that's where known as duplication of the base membrane in membranous globular nephritis but in membrane or proliferative also the basement membrane has thickened too much just a second where is it i'm going ahead i'm sorry give me a minute those midnight is thickened so much that it is known as double contour double contoured basement membrane it is known as double contour basement membrane or splitting or trom track appearance you know the meaning of tran track what is the meaning of the trans track some track means two parallel lines so the basement membrane is splitted from the between because there are lymphocytes and neutrophils in between so it is known as strong track appearance so we are done with these two have you got it coming on electron microscopy you have to learn the features in type 1 it is sub endothelial first time we are saying sub endothelial deposit in type 1 it is sub endothelial deposit in type 2 in type 2 it is intra membranous it is intra membranous and in type 3 it can be anywhere it can be anywhere there is no fixed location type 1 2 3 the type of mpgn in type 1 it is sub endothelial in type 2 it is intra membranous and in type 3 it is antivirus have you got it and it can present with nephritic as well as nephrotic syndrome it can be nephritic it can be nephrotic so would you like to revise till now we are done with five type of glomerulonephritis still no till now four more to go so i will complete the remaining four also but can you help me in the revision of these five till now can you help me so start with apgn also known as psgn here in c2 deposition of antigen antibody complexes against the planted antigen the planted antigen is the bacteria that is gas bacteria in arpeggian you already know type 1 2 3 type 1 type 2 type 3 type 1 again it is in c2 but against a fixed antigen the fixed nitrogen is the collision in type 2 again it is same as that of psgn and in type 3 no no deposits minimal change when no deposits it is the flattening of the food processors right in membranous and membrane of proliferative in membranous deposits are sub epithelial right uh like the uh here the uh antigen is gp 330 antigen is three gb 338 which is the fixed antigen on the polar side and then membrano proliferative again it is of three type but don't go in the details of the pathogenesis of each of them right we have seen the important features in the grass also only draws of clear bitten kidney is important rest of the cross here it is not important here gross is normal that is important in mcd and here gross are not important in all of them the kidneys and touch that's it light microscope is important for all of them what is the light microscopy of apgn so the glomerulus is the last hyper cellular hypertrophy rpg also enlarged hypercellular but along with christians along with christians in mcd the grosses the light microscope is normal in membranes only one finding thickening of gbm gbm got thickened in mpgn2 findings along with thickening of the gbm you will find hyper proliferation or hypercellularity also so see the difference you yourself see the difference between membranous and membrane productivity everyone give me a thumbs up everyone shall i proceed ahead shall i proceed ahead hyper cellularity is also a feature of psgn but only hyper cellularity will be there gvm thickening is not there in psgn here in apigee and gbm is also thicker you got my point now an electron microscope p you tell me the location of the deposits here the location of deposits in apgn it is it is sub epithelial but the shape is hump you know the shape is lumpy bumpy humpy right here in rpg and type 1 it is intra membranous type 2 it is again sub epithelial humpy sub epithelial because it is psgn only in type 3 no deposits in minimal change no deposits but flattening flattening of the food processor is there in membranous the deposits are against sub epithelial like psgn but the shape is pipe but the shape is pipe in amputeen again type 1 2 3 type 1 type 2 type 3 in type 1 the deposits are sub-endothelial the only glomerulonephritis in which the endothelial deposits are there in type 2 it is intra membranous and in type 3 it can be ndpr it can be anywhere and composition everywhere is same it is igg c3 so i'm not discussing separately apart from it everyone gave me a thumbs up i cannot uh simplify more than this these are the height these are the heights give me a minute just a second now okay okay i cannot open it right okay anyways so can i proceed ahead can i proceed ahead i cannot see your chat actually so can i proceed to the next one yeah now i can see so yeah so i am proceeding to the next one now next two i will take together the next two i will take together fsgn and fsgs it's very easy before that i would like to launch few poles are you ready for the poles i would like to launch few poles now which you have to learn the ah prognosis yeah one more column you have to add here is the clinical features dismantle critique is minotake so in apgn it is nephritic in rpg and also it is nephritic in minimum minimal change it is nephrotic right here in membranous it is also nephrotic it is also nephrotic and in ampugn it can be nephritic it can be nephrotic so you have to learn which of them are nephritic which of them are nafta everyone give me a thumbs up this is the most simplified version i can tell you i cannot simplify more than this these are the heights now i'm coming on the next two before that there are few polls for you this is the first question can you help me in solving it which of the following is the characteristic feature which of the following is the characteristic feature of mpgl you tell me characteristic feature of mpgn just now i taught you you tell me the characteristic feature of the mpgn can you tell me the characteristic feature of mpgn yes anyone anyone among you so is it sub epithelial deposit is it foamy cells is it splitting of the glomerular basement membrane or is its endothelial deposit right so you will say amping gene is of three type type one two three in type one such endothelial deposits are there in type two intra membranous are there in type three anywhere can be there so sub epithelial can be there right so these are not the characteristic feature the characteristic feature is the c right that is splitting off ruler basement membrane which give tram track appearance i've told you this appearance known as strong track appearance give me a thumbs up so correct answer here you see the correct answer here is the right lenient deposits along the glomerular basement membrane are seen in i am seeing along the glomerular basement membrane i am asking for intra membranous deposits so you already know till now we have seen intra membranous deposit at two locations intra membranous here rpg and three type type one two three one two and three i have taught you mpg and also of three type right type one two three right yes or no so who will tell me the location of deposit in each of them in type one rpg and it is good posture so answer is intra membranous yes siddhika the answer here is intramembranous in type 2 in type 2 it is sub epithelial same as that of psgn in type 3 no deposits are there that was the summary of arpeggian in ampign type 1 it is sub endothelial and type 2 it is intramembranous and type 3 it can be anywhere it can be anywhere that is the summary of deposits in ampga now see what i have why i have written this c intra membranous coming there so can i say type 1 rpgn is intra membranous and type 2 and pgn of intra membranous say yes or no so everyone give me a thumbs up everyone yes here the correct answer is sachin you are right siddhika you are right here the correct answer here is a because here again intra membranous deposits are asked linear deposits along the glomerular basement membrane that is intra membranous so answer is type 1 rpg and another name of type 1 rpg is good posture so i will go with it if the option contain type 2 mpg and also i will go with that also so that i want to tell you have you got it the location of the deposit in each of them is very peculiar you have to learn you have to learn now tell me where we are all subvitiliar present is it mpgn is it membranous is it minimal change or is it diabetic diabetic method deposits i will teach you diabetes later on in secondary glomerulonephritis in mgn minimal change disease mcd there are no deposits there is flattening of the food process there is flattening of the food process right but in membranous yeah there are sub epithelial deposits and the shape of that depositor spikes i have told you particularly so go with a go with on answer b in a if you say some students can argue mpgn is of three type right type one type two type three type one is the endothelial so of course type one is not the answer type two is intra membranous that is also not the answer but type three can be anywhere as i have told you it can be anywhere so it can be sub-epithelial also it can be so i agree partially in this option is also correct the type three month mpg and type 3 can be anywhere like in membranous is always tube epithelial now so best is to go with b i've got so the best is to go with b you've got my point siddhika sachin you got my point so best is to go with b yes the correct answer here will be right the next question you already know the answer ep membranous deposits are so epic two answers will be correct two answers what two answers will be correct give me two answers which are correct so one is good posture that is type one rpg type one rpgn that is intra membranous or epi membranous or mpgn type 2 amp type 2 right so a and c both are correct don't know my intro membranos yes absolutely right right the answer manigault click right it is not epi memory yeah a and c are the correct answer you got my point you got my point now you okay this is a repeat one okay you tell me sub endothelial deposit sub endothelial cell glomerulonephritis now only one glomerulonephritis have sub endothelial deposit can you tell me sachin sindhika the name of that can you tell me the name of that yes or no what is the correct answer here who will tell me the correct answer who will tell me the correct answer what is the correct answer yes so the correct answer is type 1 rpg type 1 rpgn it is the sub endothelial deposit the correct answer is right so in this way based on deposits many question can come many question can come till now we have seen many type of glomerulonephritis now i'm coming on the next two that is i'm taking next to focal segmental focal segmental one is focal segmental glomerulonephritis one is focal segmental glomerulosclerosis what do you mean by that the two type of focal segmental focal segmental glomerulonephritis and focal segmental glomerulosclerosis what is the meaning of the two what is the meaning of the two okay first one is one of those processes understand the meaning of focal and segmental what do you mean by focal what do you mean by segmental for that i would like to draw a slide can you see in the slide this is a slide of kidney i'm drawing multiple glomerulus so imagine this these all are glomerulus these all are glomerulus now some of the glomerulus have disease just suppose this one is the disease this one is the diseased and some of them are healthy so the disease is known as focal what do you mean by focal now you tell me in focal out of multiple marulas some are involved some are not involved if all of them are involved the disease is known as diffuse the disease is known as diffuse but if some are involved some are not involved some are diseased some are healthy it is the disease is known as focal have you got the meaning of the focal sachin siddhika have you got the meaning of the focal now i'm coming on the meaning of segmental what do you mean by the meaning of segmental here let me another draw another slide in which i am drawing another multiple glomerulus now that all of them are diseased imagine all of them are diseased but in the disease the partially they are diseased and partially healthy the disease is not involving the complete glomerulus have you got it so this portion is diseased this is healthy so this disease is known as segmental you got my point what i mean now i will draw the two together to explain you the difference between focal and to explain you the meaning between segmental so draw a slide here draw a slide here right you can see the two slides you can see multiple glomerulus here and you can see multiple glomerulus here also right in the first slide you can see this one is disease this one is diseased and these are healthy right in the second slide you can see half is diseased half is healthy half is diseased half as healthy so this condition is known as that focal number of nephritis is there and this condition is known as segmentation at anyone anyone if in any one half is diseased and half is healthy it is segmented so for commenting on focal you have to see all the globulars for commenting on segmental you have to see individual individual glomerulus have you got it have you got it now i am going to teach you two diseases right focal segmental focus both of them are focal also segmental also but one is glomerular nephritis and one is glutamine no sclerosis you got my point now see the two slides the two slides in front of you okay let me explain you the two slides first let me explain you can you see this is a slight of focal segmental glomerulonephritis and this is the slide of focal segmental glomerulosclerosis now both of them are focal first we will concentrate on the word vocal form in the first light i can see two glomerulus glomerulus number one and glomerulus number two can you see out of the two granules i can find this glomerulus is uninvolved it is absolutely normal this one this is healthy this is healthy and involved i can see it is a normal glomerulus but yeah this glomerulus i can find the more cellularity here this area is having increased cellulity so this one is the diseased right so one glomerulus is healthy one is diseased so can i say the disease is focal right yes or no such and right yes or no can i say the disease is focal because one of the glomerulus is healthy and one is diseased right so diseases focal now concentrate on the want segmental segmental see the diseased one don't see both glomerulus see only diseased one in the diseased one the disease is only partially involving the globulus half of it is hypercellular half of it is normal cellular so the disease is segmental also so can i say the disease is focal also segmented also one glomerulus no intentionally the author just may be a book like the author have given you two glomerulus in the diagram without which we cannot explain the meaning of focal and segmental you got got my point so out of the two glomerulus one is healthy and one is diseased we can see this one is healthy this one is disease so disease is focal and the diseased one may half is healthy and half is uh showing the disease so that is known as segmental you got my point coming on the second diagram in the second diagram also you can see two glomerulus here also glomerulus number one glomerulus number two can you see this one this one is absolutely healthy normal globulus but see this glomerulus in this glomerulus i can find out some abnormal area here in this portion this area is clarissed this area is absolutely sclerosed so again the disease is focal one is involved one is not involved so disease is focal and the involved one may half is involved half is not involved so disease is segmental so actually both the diseases are focal both the diseases are segmental but the disease is different what is the disease now the see the beauty in the first diagram the disease is hypersolution this portion of the glomerulus is hyper solute that's why known as nephritis and this portion of the globulus is clairost it is not hypercellular that's why known as dominosclerosis everyone give me a thumbs up no one will explain you with such a beauty again everyone give me a thumbs up have you got it do you have any doubt in that can you see the two diagrams in front of you can you say this is focal segmental this is also focal segmental so two more modulus here two glomerulus here one is involved one is an involved one is involved so that's why the disease is focal the involved one is half involved half not involved so that's why the disease is segmental but here the disease is glomerular nephritis because this is the hyperstimularity of the glomerular glomerulus that is the disease here sclerosis is there that is sclerosis of the glomerulus is the problem so see the change in the disease you have a disease hyper cellularity hyper proliferation or you have a disease of sclerosis everyone give me a thumbs up have you got it these are the two next diseases i am going to first let's study focal segmental glomerulonephritis msgn also known as messenger proliferative glomerulonephritis right here the disease is focal and the disease is segmental you explain me the meaning focal means not all some of the global rulers are involved some are not involved and segmental means may involve a portion is involved a portion is not involved right this you can see here and the disease is only once hyper cellularity increase proliferation you see increased cells here what all cells are these these all are messenger cells hypersolidarity of the messenger cell that is the disease give me a thumbs up give me a thumbs up here deposits are there first time deposits are coming in the messenger i taught you four locations of the deposit what are the four locations of the deposit let me draw a filtration barrier so this is the basement membrane on one side you can notice endothelium on other side you can notice visceral podocytes visceral epithelium and these are the messenger cells can you notice these all are messenger cells so what is the location of the deposits the deposits can be intra membranous so intra membranous deposit till now we have seen at two locations uh i guess rpg and type one and mpg and type 2. am i right cytika rpgn1 or ampegn2 right the second type of depositor endothelial endothelium type 1 yes and sub epithelial sub epithelial we have seen in psgn the first one and mpgn and we have seen the comparison one is lumpy and one is pipe right now i'm coming on messenger deposit so in fsgn the deposits are messenger in fsg and the deposits are miss and gl right okay so ashish you want full pharmacology course on an academy definitely ashish i will launch the full again uh pharmacology free course on the an academy but i should show you on telegram if you are on telegram please tag me a personal message on the group please tag me uh i will help you with the links of the last wedge so i will definitely take the live classes but meanwhile don't waste your time if you want the free links of complete pharmacology i can give you the free links of youtube and um special classes upon academy only of the last batch so meanwhile start watch the recording start watching the recordings only and after some time few days i will launch the pharmacology crash course also let me first finish pathology right ashish so please check me on the telegram if you want the free link of the last wedge i can send you all failings of the last patch the only thing these are not live lectures that will be the recordings that you can see right okay anyways and the composition is same composition is igg or c3 yoga i'm done with fsgs fngn now i am coming on fsgs i am coming on fsgs in fsgs you can see in fsgs again the disease is focal and segmental that is some global rulers are involved some are not involved and the glomerulus which are involved they are partially involved and partially not involved right right and what is the problem the problem is not hyper proliferation the problem is solidification or sclerosis i can see this portion of the glomerulus this one is solidified or this one is clarisse in contrast to fsgn where this portion of the glomerulus is hypercellular so this is fsgn this is fsgs you can see the disease you can see the difference between them here also in the in effigy and two globalists are there this is healthy this is disease so one is involved one is not involved here also two glomerulus are there this is healthy this is diseased so one is involved one is not involved so both the diseases are focal because some globulars are involved some are not involved right the involved one see the involved one here see the involved one here the involved one is half involved half not involved here also half involved half not involved so the disease is segmental in both of them because the involved glomerulus is partially involved partially not involved so basically both the diseases are focal and both the diseases are segmental but the disease is different what is the disease here the disease is proliferation and here the disease is solidification proliferation is global nephritis appreciate the hyper cellularity and most of the cells are messenger cells and appreciate the solidification sclerosis is here so that's why this is known as globular nephritis and this is known as glomerulous sclerosis so everyone give me a thumbs up ashish siddika sachin others give me a thumbs up have you got it the difference between them so here electron microscopy again diffuse loss of food processes like mcd that is the feature minimum change minimal change disease it is not the uh immune complexes immune complexes will not be there and composition is same igg plus c3 so we are done till here till here we all are done so two more are left two more are left last two are left ig naturopathy and chronic you want me to complete that also and then we will take a comparative analysis of all the ruling fractions till now yes or no so let me take two more iga naturopathy and chronic globulin refractive so first i am taking chronic chronic glomerulonephritis chronic glomerulonephritis is also known as end stage kidney disease or chronic kidney disease ckd so one and the same thing these are the other names given to that right now there is no fixed um um uh diagram for that it can result in rpg and actually all the till now how many i have taught you i have taught you apg and the first one i have taught you rpgn the second one then i taught you mcd then i taught you mgn and mpgn together these two together then i taught you fsgn and fsgs together these two together all of them listen my point all of them ultimately result in ckt right so secret is the end result of all of these you got my point so ckd is the ends result of all of these significant if treated they will stop but if not reject the end result of all of them is secretly so most rapidly among all of them will convert like in the speed of conversion is different most rapidly conversion occurs in rpgn that's why the name is rpgn rapidly progressive glomerulonephritis within few weeks it will convert into security that's why prognosis is very poor and you have to treat very abruptly you got my point others also convert into ckt but gradually and slowly you got my point so rpgn in ninety percent of the cases convert into ckg membrane was also convert in fifty percent cases membrane of proliferative also convert in fifty p percent cases fsgs also convert ign nephropathy apg and apg and only one percent chance of converting into ctd so apgn have best prognosis everyone give me a thumbs up if you got it so ultimately all of them are converting into ckd in ckd it's the only glycologist in which kidney becomes small grossly kidney contracted rest all kidney expand in all of them i taught you kidneys in large kidneys and large kidneys and large but in ckd it is the ant kidney kidneys as small as 50 gram as small as a very small kidney 50 gram and the surface of the kidney is granular can you appreciate the granularity the granularity granular surface is very important and the cortex is narrow cortex is narrow at profit and you can see uh the cortex is narrow and retrofit that's it for the light microscopy this is the diagram you see where are the glomerulus it's very easy diagram funny diagram can you see this is the global rulers this is the glomerulus this is the i can see three or four glomerulus here i guess right inside the globules i cannot see anything the glomerulus is completely converted into a cellular mass a cellular hyaluronized glomerulus the glomerulus is completely converted into a cellular mass that is highly nice stuff glomerulus converted into highly nice stuff i can't see capillary i can't see endothelium on one side epithelium on the other side no complete glomerulus are gone they converted into a cellular eosinophilic hyalinized mass everyone gave me a thumbs up that's all about the blue mirrorless right let's count the glimmer let's reduce in numbers convert into highly nice mass that is about the glomerulus in the tubules also people's you will find a trophy and highline droplets where are the tubules let me show you the tributes these all are pct loop of hanley dct collecting that these all are tubules so tributes are at profit you can see small small tributes so we have seen the glomerulus we have seen the tubules see the blood vessels one of the blood vessels is shown here you can see this is one of the blood vessels the blood vessel is showing what does it showing the blood vessel is thickened because it is showing arteriosclerosis there is atherosclerosis in the blood vessel arteriosclerosis and the last one see the background interstitium the background the background can you see in the background these cells what are these cells this cluster of cell this cluster the cells present in the background are lymphocytes no neutrophil mind there is no neutrophil so chronic inflammatory infiltrate so comment on the four things comment on four things in this diagram comment on glomerulus comment on blood vessel comment on tubules and comment on interstitium who will comment on the four things one by one glomerulus may write down one thing they converted into acellular masses can you see this one this one they are hyalinized right blood vessel may show they show arteriosclerosis atherosclerosis arteriosclerosis the ball is thickened triples means they are at profit you can see small small tubules and interstitium a background like chronic inflammation not acute that is only lymphocyte not neutrophil everyone give me a thumbs up so that is the summary of chronic glomerulonephritis the chronic memory learning is done i'm coming on the last one ig naturopathy everyone give me a thumbs up the last one the ninth one is iga naturopathy the last one then i will do a comparative analysis of all nine the last one is the iga naturopathy idea nephropathy also known as berger's disease also known as ig nephropathy it is the most common type of globular nephritis throughout the world so out of the nine type of glutamate is this is this was first time described by a physician known as berger the name is badger so that's why it is known as bursar's disease and it is the most common global nephritis it always occur after tonsillitis after either tonsillitis that is upper respiratory tract infection tonsillitis pharyngitis or after gastrointestinal infection now compare the first one sdn psgn or apgn the first one and the last one the last one i am teaching you is ig naturopathy the first and the last compare both of them are after infection the psdn or apgn is after respiratory or skin infection i told you the person is either having tonsillitis or the skin infection this one is after respiratory or git infection so see the difference so this also occurs this also occur this occurs seven to ten days after infection and this occurred four to five days after infection so see the incubation period period is different here exact mechanism is not known why it is happening exact mechanism is not known some people say it is due to antigen antibody complexes formation so what is the problem white is known as ig and nephropathy why it is known as c i have not uh put the pathogenesis here i will draw it for you i forgot to put the slide uh what is ig nephropathy what is happening here here uh the b lymphocytes become abnormal these are b lymphocytes these are b lymphocytes they become mutated they become abnormal right they become abnormal so the plasma cells formed out of it b cell converts into plasma cells so plasma cell will become abnormal right so plasma cell will form antibody the antibodies iga antibody this one antibody there are five type of antibodies not gambling igg iga so this one is iga in contrast to all others you have a composition right this antibodies ig listen listen this is abnormal ig not normal ig this ig is abnormal listen so it is acting as the foreign material for the blood you got my point this is antibody but this is the abnormal antibody that's why it is acting as an antigen so body is forming antibody against antibody you got my point so body will form antibody against this ig antibody so antigen antibody complexes will be formed in the antigen antibody complexes who is the antigen who is the antibody who will tell me the antigen is iga antibody and the antibody against antibody this antibody can be igg can be ige this can be anything but it is formed against ig antibody which is abnormal due to the abnormal b cells and abnormal plasma cells have you got the point so antigen antibody complexes are formed and these complexes get deposited exclusively in mesangium mesangia they will deposit deposit only in mesangium not intra membranous not sub epithelial not the endothelial in the miscentrium that's why this is messenger disease ign nephropathy because iga is abnormal that is the antigen here give me a thumbs up if you watch it everyone give me a thumbs up this is the pathogenesis shall i repeat again or have you got it so here ga become abnormal body will form antibodies against the ig right so iga antigen antibody complexes will be formed and that will be deposited in the misagen to draw a flowchart like that right in the light microscopy there is no fixed pattern there is no diagram it can look like fsg and fsgs membranous membrane or really rpg and there is no fixed pattern so don't clone the diagram electron microscopy deposits only at one place mesangio you see these messenger deposits deposits will be in the mesangium in the misangium you got it immunofluorosense is important and the composition is iga with or without igg okay antibody against antibody can be igg but main antibody to antigens so that is the hallmark of this disease immune fluorescence give me a thumbs up give me a thumbs up it can be nephritic it can be neptune right so see the differences between post streptococcal glomerulonephritis the first one and ig nephropathy the last one post streptococcal occurs after seven to twenty one days after the infection this one is occurring after one to four days after the infection here recurrences are very common vapid occurrences were rare right so these are the differences between them i'm not launching the poles right now i am done with the nine type of globular nephritis are you people with me are you people with me we are done with the nine type of glomerular nephritis now now i want to make a comparative analysis between the nine type of globular nephritis you want to realize with me do you want to revise with me so just a second let me see the people if you want to revise with me i will help you with the revision okay here is the table you can see this table so in this table you can see the nine names given here nine type of glutatal nephritis i have covered all the most important feature you have to learn here is the three type of microscopy right so you have to tell me that deposits the location of deposit composi okay let me start with the three type of microscopy okay let me start with the mirror fluorescence the easiest one so only thing i would like to say in ig naturopathy immune fluorescence contain iga apart from it everyone else contain igg plus c3 only iga have iga with or without igg so that is the summary of immunofluorescence are you agree with this summary imminent resistance is done answer the same igg plus t3 it contains ig along with with or without igg i have told you yes iggy plus c3 absolutely so that is the first thing you must learn in all of them right the second thing which i would like to tell you is the electron microscopy of all of them we are done with immunofluorescence right now i am teaching you the electron microscopy of all of them please tell me the location in each of them siddhika would you tell me others would you tell me such a video tell me apga location the location was sub epithelial and the shape is hum location and shape you tell me rpg in type 2 again it is sub epithelial in type 3 no deposits no deposits right coming on minimal change the third one minimal change who will tell me the minimal change for summary minimum change minimal change there are no deposits but there is fusion fusion or there is a fusion of the podocytes or flattening of the podocyte fusion or flattening of the buddha site absolutely right sidhika yes right coming on the membrane membrane and membrane proliferative first let's talk about the membranous membrane rpgn type one type two type three the three types of ampign you can see the three type of amplitude so type one it is sub endothelial sub endothelial please learn it type two is intra membranous and type 3 can be anywhere it can be anywhere right fsgn or fsgs may you can skip this portion because there are no deposits right ig and nephropathy deposits are typically in messaging and chronic again deposits are not important so see the summary of the deposits now split them which of them are intra membranous which of them are 73 sub epithelial sub endothelial and messenger so please split them into four components everyone give me a thumbs up so i am done with the summary of immunofluorescence i am done with the summary of electron microscopy light microscopy i will show you nine images one by one and you will take a summary of each of them so apgross is important it is kidney it is clear and kidney the rest all grows the kidneys enlarged yapi kidney is normal in minimal change the kidney is normal otherwise kidney is enlarged enlarged enlarged enlarged enlarged only in chronic the kidneys small contracted with granular surface so this that is the important point about the gross i would like to comment so question yeah your chronic pain from gross otherwise gross is not important for this everyone give me a thumbs up everyone give me a thumbs up so till now what we have completed we have completed we have completed immunofluorescence summary we have completed electron microscopy summary we have complicated gross summary etiopathogenesis you already know in which of them what is nature pathogenesis i have discussed the flowcharts of all of them right now let me discuss the light microscopy the nine diagrams the first diagram i'm showing right now is apgn so what is the summary of apgn so apgn this is the diagram apgn also known as psgn it is post tractor vocal glomerulonephritis or acute proliferative glomerulonephritis you can see this is the diagram in this diagram this is the glomerulus i can find three findings the glomerulus is enlarged in size the glomerulus is increased in cellularity hyper cellularity and increase in proliferation hyper proliferation the cells are both acute and chronic so inside this diagram i can find out neutrophils also and i can find out lymphocytes also if you zoom you can see multi-lobated as well as single nucleus right so cellularity is acute and chronic so that is the summary of apgn would you be able to draw shall i proceed ahead and this is the light microscopy electron microscopy you already know the sub-epithelial deposits and immunofluorescence you already know right rpgn is of three types so the light microscopy here this is the summary of light microscopy of rpgn coming on the second type of glomerulonephritis rpg in rpgn you can find out there is a can you say this is the global plus inside this numerals appreciate the crystalline can you appreciate this crescent this christian i'm talking about this is the chrysant right this is this christian is compressing the remaining liberalism the remaining globalist is increased in size increase in cellularity and increase in proliferation exactly same as that of psgn you can see the cells are both again they are neutrophils also and they are lymphocytes also the only feature which differentiate rpgn from psgn as the christian formation and present is the hallmark here in rpgn it is the pathognomatic feature and the number of reasons is important for the prognosis so that is rpgm right we are done with the of rpg and also the light microscopy coming on the third glamorough neptune is mct can you tell me the diagram of mct minimal change disease light microscopy is normal there is no problem with so absolutely normal glucose absolutely there is no problem in the glomerulus it's absolutely normal in normal abnormality that you miss the disease on light microscopy so on light microscopy you cannot pick the disease give me a thumbs up on electron microscopy you will find the fattening of the podocytes the flattening of the podocytes is seen on electron microscopy not on light microscopy coming on the next two membrane gluconeonephritis and membrane proliferative glomerulonephritis so what is the difference between them the difference between them membrane you will find only one thing bbm thickening gb of thickness gbm thickness right but here it is the only feature here proliferation also there so gbm hyper cellularity is also there here cellularity is normal have you got it gbm is thickened in both of them so different appearances there here thickening of the gvm is known as duplication of gbm it looks like it is doubled but actually it is not doubled here thickening of the gpm is known as strong track appearance tran track appearance so learn the appearances are different give me a thumbs up no one will give you such a crystal clear view of the global lunar fighters this is the diagram of membranous if you appreciate the chromium less inside the nominals only one finding all the gbm you can appreciate there is spike shaped uh uh sub epithelial deposits and they are thickened they are thick and they are looking duplicated that's the only finding but there are no cells inside there are no cells that's why security is normal see this diaphragm mpgn you can see again a glomerulus inside which two findings are there if the glomerulus membranes are thickened that is the first finding and you can appreciate the cells neutrophils lymphocyte both so two findings are there hyper cellularity and thickening of the gbm which is known as strong track or splitting give me a thumbs up give me a thumbs up coming on the next two sg and fsgs focal segmental glomerulonephritis focal segmental globular sclerosis you already know the two diagrams just now i have explained you the two diagrams in both the diagrams in both of them this is a diagram of fsgn this is a diagram of fsgs focal segmental the disease is focal the disease is segmental here two glomerulus are there here also two globulars are there what do you mean by focal one glomerulus is healthy one is diseased here also one is healthy one is disease so can i say the disease is focal pure formulas are involved you are not involved in both of them so that's why the disease is focal coming from the meaning of the segmental the involved glomerulus so this one is disease now so half is diseased half is normal here also this one is disease now so half is diseased half is normal so the disease is segmental in both of them so the disease normally a part of it is involved a part of it is not involved so the disease is focal the disease is segmental but the disease is different here problem is hyper cellularity that is glomerulonephritis that is proliferation and most of the cells are messenger cells which are getting hyper proliferated and here the problem is sclerosis half of the glomerulus gets solidified it is hyalinized and sclerosed so the problem is glubrillosclerosis so that's why it is glamorous nephritis it is normal sclerosis you're not giving the thumbs up are you getting all these points yes or no it is going bounce bouncer for you you getting it the next one eighth one is chronic chronic this is the diagram of chronic you see you have to comment on four things here what four things spent on globalists comment on tributes comment on blood vessels and comment on interstitium can you see these are the glomerulus globalist one global rule is two global all of them inside them they convert into a cellular mass that is they are hyalinized so all the globulars are hyalinized see the tribute can you see the tributes these are the tributes all the tributes are small they are atrophic so all the tubules are at profit right see the blood vessel i can see one blood vessel so the blood vessel is showing thickening of the wall that is it is showing arterial arterial sclerosis right and see the interstitium can you see the background the interstitium in the industry and see the collection of cells now please they say because all these cells are only chronic that is their lymphocyte they are not neutral so chronic inflammation so that is the summary of chronic chronic glomerulonephritis the last one is ig necromancy there is no diagram of it any of the diagram can work there is no fixed diagram only one finding the deposits will be messenger the deposits will be messenger exclusive deposit will be misangel here all the deposits will be sent that is the primary glomerulonephritis i am done with all primary globulin titles the nine type of primary globulin arthritis everyone give me a thumbs up first do you have an any doubt in that till now till now do you have any doubt in that we have covered the nine type of primary global nephritis in a beautiful comparative manner from today morning this is my fifth hour i guess i'm taking the lecture yes or no so those who are attending my lecture from the morning so they all know that i have covered all nine in a comparative manner those who have missed my past uh the last lectures episode one and two i request them they are available on the youtube please go and see the recording please everyone see the recording have a look on the recording you yourself will realize how important topic it is and we have covered the nine type in a comparative manner in a comparative manner now any question either from pathology or any question from medicine the glomerulonephritis question you can crack it the question can be one liner the question can be image-based the question can be big clinical question if you have knowledge of all the glutamate especially their pathogenesis and the three type of microscopy you are able to solve all the questions based on glomerulonephritis that is my challenge to you still you try it out you try it out you figure it out still if you find any difficulty that man this question doesn't fit from your notes i have watched your lecture still i cannot find this question i cannot answer this question kindly get back to me i will help you in solving that so i can challenge any question based on primary global neuropractice you can technically solve it now if you have watched my lectures attentively yes or no so now it's time to start the secondary nephritis so let me start the secondary glomerulonephritis now let's start the secondary one we are done with the nine primary one the nine primary one are over now i am coming on the secondary globular nephritis in secondary glomerulonephritis what is the problem there is some other systemic disease there is some other secondary disease not the primary so glomerulus is involved secondarily so here most important i am going to teach you diabetes diabetes here after that we will start hearing also and secondary glomerulonephritis i am teaching you diabetic naturopathy the name indicate the main disease here is the diabetes japanese is very common especially in developing countries like india so there are two type of diabetes type 1 type 2 we all know that i'm not teaching you diabetes here i'm going to teach you the effect of diabetes on the kidney that is diabetic naturopathy so how diabetes results in damage of the global rulers so that is diabetic naturopathy or diabetic glomerulopathy and muscle so that is a type of secondary glomerulonephritis here main disease is not involving the kidney main disease is something else that is diabetes and hyperglycemia and the diabetes results in naturopathy that is glomerulonephritis that's why it is secondary it is more common in type 1 diabetes as compared to type 2 diabetes so we can understand that right so okay uh i will tell you three things here what three things first i will tell you the effect on the glomerulus then i will tell you the effect on the blood vessel then the effect on the tubules effect on tributes effect on blood vessel effect on glomerulus let's first talk about glomerulus so glomerulosclerosis is there again globular nephritis is not there in diabetes glomerulosclerosis is there i will tell you the reason right and glomerular nephrosis is of two type diffuse and nodular now listen diffuse and nodular i will show you the diagram uh this is the diagram of diffuse this is the diagram of diabetic number one sclerosis of two types what i'm teaching you i'm teaching you diabetes the first one is the diffuse and second one is the nodule the name itself indicate its meaning right let me first explain you the diffuse diffuse right this is the diagram of the diffuse in this diagram of the diffuse can you see this is a glomerulus appreciate only glomerulus don't see tubules blood vessels and interstitium c only glomerulus inside this glomerulus high line what is high line high line is pink color eosinophilic acellular structureless mass pink color that is eusynophilic structure less acellular homogeneous mass the highlight get deposited four places that's what is known as diffuse so let me show you the four location highline number one can you see the pink color mass at the center this is mesangium so high line is deposited in the misangium miss angel matrix number one have you appreciated yes you all can see the messenger deposits number two can you see the multiple blood capillaries here these one these all are blood capillaries inside the globalist right appreciate the blood capillaries see the lining of the blood capillaries that is boom basement membrane so the uh highlight is deposited in the basement membrane also so basement ribbon got thickened right so hyaline is deposited in the basement membrane thickened basement membrane number two in the basement membrane of the capillaries right number three is deposited in the form of the cap of the capillary as a capillary in a topia it is known as the cap cap of the capillary let me show you can you see this portion it is like the cap of a capillary see this portion cap of a capillary see this portion cap of a capillary so it is deposited in the form of the cap of the capillary number three number three and last it is deposited in the bowman's capsule can you see here in parietal layer of the woman's capsule right this is known as capsular drop so at four places this high line is deposited and that's why the disease is known as diffuse everyone give me a thumbs up everyone what are the four places for use one is more common first let me teach you diffuse diffuse my high line is deposited in four places one two three four so what are the four places high line is deposited four places it is deposited in nissan gm it is deposited in glomerular basement membrane it is deposited in capillary wall the cap of a capillary and it is deposited in bowman's capsule that is capsular drop first everyone give me a thumbs up so can you appreciate yes please it is the more common as compared to nodular here island is deposited in all the parts basically all parts so the most common and earliest in the basement members appreciate at the four parts i have shown you so this is diffuse one the second one is the nodular one here also high line will be deposited but not everywhere not everywhere see the diagram first where is the high line where is the glomerulus this is the glomerulus in this diagram hyaline is not deposited everywhere it is deposited in the form of the circles in the form of the nodule so hyaline is basically forming small small nodule it is not deposited in the woman's capsule the capillary the basement membrane no it is forming small small nodules that's why known as noodles give me a thumbs up so it is not diffused this one is modular that is the only difference deposition a pair in the form of multiple materials give me a thumbs up which is more common diffused one but which is more specific nodular one there is one more name given to nodular nodular globular sclerosis of the diabetes it is known as kw kidney mcq arthur repeated many times in your exams it is known as kimmelston wilson kidney what does it known as it is known as kimbel's stun it is known as kim wilston wilson kidney kw kidney and it is the most specific or prothogmatic feature so compare the two have i done the comparison yes compare the two can you compare the two type of chemical universes sclerosis and the diabetes please do the comparison everyone here everyone so can you see a glomerulus here yes you can see and can you see a glomerulus here yes you can see in both of them the high line what is highlight first say what is highlight it is pink eosinophilic structure less homogeneous mass so that is deposited in both of them here in diffuse it is deposited at four places let me show you number one mistand gm number two basement membrane glomerular basement membrane number three capillary cap the wall of the capillary capillary cap and number four women's capsule so that's why it is known as diffuse in number two in nodular one highland is deposited in the form of the nodules not at multiple places so it is deposited in the form of circular oval tube circular overloading so you can see the difference everyone give me a thumbs up now if a question comes which is more common more common answer is this question which is more specific answer is this nodular voila another name is given kimmelston wilson kidney it is known as kw kidney based on the scientist who has discovered it give me a thumbs up everyone give me a thumbs up that is about the glomerular changes now coming on the blood vessel now see the blood vessel in both of them in both of them one one blood vessel is shown can you see this is a blood vessel here the ball is thicker and showing higher line deposition can you see a blood vessel here the wall is thickened showing high line high line deposition so highlight thickening of the arteriole is a common feature involved that is not different glomerulus in blood vessels blood vessels changes same so in the blood vessel the same changes there high line arteriosclerosis hyaline artery sclerosis the last is the tributes fuels without please notice the tubules here and here here i can see these are the tubules these are the tubules and here i can see these are the tubules see the cells of the tubules can you see the cells of the tubules inside the cells of the tubules you can see the tubes you can see the vacuoles can you appreciate i cannot zoom it inside the cells of the tubules please appreciate the vacuoles are there this is known as armani its condition the name of the scientist only armani is is also common in both of them we got it so i am done with diabetes diabetic glomerulosclerosis then it is of two type diffuse and not you learn in both of them only glomerulus is different right glomerular findings are different right glomerular finding is different in both of them but blood vessel and tubular finding is same in both of them have you got it so can you tell me the summary what is the glomerular finding here also highline deposited here also highlight deposit but here four places that's why diffuse here only nodules that's why nodular give me a thumbs up here four places is basement membrane ruler basement membrane misangium capillary cap and bowman's capsule that is capsular drop right so that's why if you ask me which is more common this is more common if you ask me which is more specific this is more specific it is also known as kwkd coming on blood vessel blood vessel of both of them show hyaline artery sclerosis hyaline artery sclerosis typicals of both of them show vacuums that is known as armani installation armani is transition that is the summary of diabetes i am done with diabetes i am done with secondary glomerulonephritis and that is diabetes free one give me a thumbs up everyone here i would like to stop now right i would like to stop now let me declare my next lectures tomorrow's lecture then you people can go right so tomorrow morning i will again start i guess at seven o'clock i will start morning seven o'clock and continuously i will take six hour lecture right the free lectures on the youtube only so seven to nine will be the first nine to eleven will be the second and eleven to one will be the third so two r two r two our total six hour lectures will be there on the renal system only right so in the first lecture i will continue with secondary glomerulonephritis and hereditary globular nephritis first right so i will teach you diabetes we will revise once again we will start with diabetes revise diabetes the secondary one job then we will do sleep we will do hs we will do other then we will do the four type of harry potter global and francisco global new nephritis will be over right after that we will do we will do pyelonephritis we will do to below interstitial diseases that is atm acutabilion across us we will do obstructive uropathy that is calculus right that is in the second lecture in the third lecture exclusively i will teach you renal tumors the malignancies of the kidney the wrinkle tumors in adults also in children also in children i will continue with the welsh tumor and we will do some image based and clinical question practice in the end so tomorrow again three lectures renal pathology will be packed so today three and tomorrow three total six lectures complete renal pathology any question any any any any any question from any exam whatever is the exam whether it is clinical non-clinical whatever question you can be able to solve that question after attending my six lectures of pathology renal pathology right so don't forget to continue on youtube the same youtube channel of unacademy and academy live where you are attending right now tomorrow morning right now a few announcements for you uh on the an academy new batch is launched for the 2023 neat pg that is for freshers also for repeaters also so if you are um if you are uh having that i mean if you want to attend these batches you can take the subscription today at seven in the evening uh in the evening i'm talking about morning tomorrow morning at 7 00 a.m in the morning i will start call morning saturday we are having six hour class not today not today right and these are the various 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so thank you very much for being with me sadika i can send you the notes on the telegram ask on the telegram right so thank you for being with me thank you for giving your precious time to me and i request you to come again tomorrow morning and we will continue with renewal pathology finish renewal pathology after renal pathology we will move to other systemic pathologies cbs cns recipe git hepatobiliary bone soft tissue male genital female genital breast we will continue all chapters of systemic pathology one by one right bye bye see you study hard all the best