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Oh OK. Um What did I, where did I get up to before it? Uh You were up to class switching? Oh OK. Fine. OK. Can you see my screen? Uh Yeah, hopefully everyone else should be able to see. I don't know what happened there, but you should be fine. Yeah. Um Yeah, so class switching. So we said that IgM is sort of the default antibody produced by our immature B cells once they've been released from the bone marrow and that germinal center reaction between the T cells and the B cells is necessary to get them to undergo that process called somatic hypermutation in order to produce specific IgG G A&E. Um So that condition, remember hyper IgM is actually a problem with the T cells and it's a problem with the receptor that's necessary for the germinal center reaction called CD 40 L. And essentially because we can't undergo the class switch, we're going to get really, really high levels of IgM because that's the default setting. Um But we're not going to have any IgG A or E because we can't undergo the general center reaction. And again, here is just um a small recap of that reaction, which we already talked about. And again, here is, um, a summary slide again, just test yourself on it, um, um, as part of your vision. Um, and then we're just getting on to sort of the last bits of immune deficiencies. Um, so just in terms of investigations, so I have seen a couple of past paper questions where they ask about, um, investigations or they'll give you investigations and you have to determine the immune deficiency from that. Um, but it is pretty self explanatory. So obviously, the first thing you'd want to do is you want to check the white cell count, um, and get a differential cell count. So you have a look at the neutrophils, the B cells T cells and figure out which cells are low, which cells are high. Then within the white cells on the lymphocytes, you want to look at CD four and CD eight. And then after that, um, if you think it's a problem with the B cells, you could do immune globulins and protein electrophoresis to determine levels of antibody and that will kind of guide you with, um, what immune, what the immune deficiency actually is. Ok. Um I've got this question. I think this actually was a past paper question. Um, and I remember when I saw it last year, I thought it was really rogue and didn't really get it. Um, so I'll leave it on the screen for a bit and then I will check the chart. Ok. Um Let's see. I want to see does someone wanna explain why they think it's c convulsion due to hypocalcemia? Exactly. Yeah. Um So obviously this is a ridiculous question. Um But it's kind of very, very typical for the exam. Um Just remember in the exam, they're never gonna include anything that you don't need to use when determining your answers. So I always think, OK, why you put this in there? Um So yeah, obviously convulsion, hypocalcemia, we know from cath that can cause convulsions. Um and recurrent infection, it's gonna be immune deficiency and we know Digeorge syndrome um can give you hypoparathyroidism. Um So yeah, this is just a good example of sort of how all the different disciplines within path are linked in some of the questions. OK. Um Now sort of on to complement deficiencies. Um We have not too much left. We've kind of got about two thirds of the way through it. Um After complement deficiencies, do we want a small break? Like a five minute break? Um Because I'm aware that this is quite heavy content. Um If we put in the chart, whether you guys wanna do that or if you'd rather just kind of get it all done at once. Um We can also do that too. Yeah. Don't need a break. Nice. OK. OK, cool. We'll just let's keep going. Ok. Nice. Um So now complement deficiencies. Um So as we said, complement deficiencies are kind of, um we said complement is sort of an adjunct to the immune system. So, complement deficiencies aren't gonna be quite as severe as sort of the other deficiencies that we have talked about. But they are just important to have a basic understanding of um for some reason this comes up. So, so, so you may catch your cells out with complement deficiencies and also high postlens or if someone's had a splenectomy, you get an increased susceptibility to encapsulated organisms. Um And there's the really, really, really easy pneumonic to remember them, which is just NHS and for Neisseria, H for hemophilias as for streptococcus, just learn those complement deficiencies, more susceptible to encapsulated organisms and just remember NHS, it comes up so much and I don't know why, but just make sure you guys learn it. Um And again, similar, um we're gonna talk about the diagram and basically a block in any step is gonna cause an immune deficiency. Um Before I just kind of talk a little bit about the classical pathway, um a really, really good thing for a vision is to just make sure you can almost sketch out those diagrams. Um whilst looking at nothing, just grab a blank piece of paper, sketch out the diagrams and then it will really help you visualize what's going on with the immune system um at different points. OK. Um So now onto the classical pathway. So we said that the classical pathway acts on antigen antibody complexes and involve C one C two and C four. So any time you've got a deficiency of C one C two or C four, you're not gonna be able to um activate complement on the antigen antibody complexes. Um C two is the most common and um the clinical phenotype is gonna be anyone with C two deficiency is gonna have systemic lupus erythematosus. Um you can get severe skin disease and you can get of course an increased number of infections because it is an immune deficiency. Now, can anyone in the chart tell me why anyone with C two deficiency is gonna have systemic lupus erythematosus. I'll give you guys like 30 seconds. These are hard questions. I'm asking you guys and you guys are doing really well, so well done. Yeah, exactly. That reduced clearance of immune complexes. So the whole problem with lupus is that you get these immune complexes um depositing in tissues all over the body. Um and that then causes inflammation or causes the symptoms. Lupus. So they deposit the kidneys, the skin, the kind of gi tract anywhere. Basically. So if you're, if you have a CT deficiency, you can't clear the imine complexes. And as a result, you're gonna get massive deposition of these complexes everywhere, which is basically just what Lupus is. Um OK. And then deficiency of the mannose binding lectin pathway. Um Essentially you get, it's very, very m it's a very, very minor immune deficiency. Um It's basically almost ok, like if you have mannose binding lectin deficiency, you're kind of fine. Um but it will only kind of cause problems for you if you have another cause of immune deficiency. So for example, if you're premature, if you're undergoing chemotherapy, if you have HIV or if you have an antibody deficiency or something more severe, then the mannose binding um leptin pathway is gonna affect you. And then of course, the alternative um again, just wrote on this deficiency factors bi or P um And like all other complement deficiencies, you're gonna get um an increased susceptibility to encapsulated organisms. Um And then, yeah, finally, um if you have a deficiency of C three C five C nine, you're not gonna be able to form the membrane attack complex. Um And then again, of course, you're gonna have increased susceptibility to your NHS organisms, which is your encapsulated organisms. Um Can someone tell me um why, why there is increased susceptibility um to these encapsulated organisms? Yeah, I'll be, that's correct. So that.