Transcript for:
Overview of Hypersensitivity Types for Exams

Hypersensitivity has four different types and they each have their own unique mechanism or pathophysiology and they each have their own unique examples and all of this stuff is pretty high yield. Hypersensitivity does show up a lot on USMLE and COMLEX. So with that said, we're going to give you a mnemonic that's going to help you work through all of this. In today's video, we're going to go one at a time through each of these four types, paying attention to the normal pathophysiology, right? I'll always explain the normal science. And then I'll give you the mnemonic kind of overlaid on top of that so that you can easily learn this in this short video. So for just as a summary, here's everything that you need to know if you didn't watch this video. This is what is in first aid. This is what's in all the resources out there. There are four different types. There's type 1, type 2, type 3, and type 4. The mnemonic that you're going to use today is ACID. And the A goes with type 1, C with type 2, I with type 3, and D. D with type four. So just like there's four types, each of those letters corresponds to one of these types of hypersensitivity. So let's go through these one at a time. I'm going to explain the normal pathophys and I'm going to overlay the mnemonic at the end so that you better recall all of this information. So why don't we get started with type one hypersensitivity. So this one is referred to as allergic hypersensitivity. Basically what happens is that first an antigen binds to IgE. Then IgE and that allergen get cross-linked at the receptor. This cross-linking occurs at the Fc receptor. You don't need to know that for USMLE or COMLEX, but it does get tested if you're using this video to study for your class exam. After the cross-linking occurs, mast cells and basophils release vasoactive substances, and those vasoactive substances, they cause massive vasodilation. So this makes sense, right? In the context of an allergic reaction, or some type of anaphylaxis, you know that the end result is massive vasodilation. And that is why we give epinephrine when someone is undergoing anaphylaxis, because you have to stop the vasodilation. And of course, you know that epinephrine causes vasoconstriction. So basically, type 1 is allergic. And if I were to summarize type 1, I would say it's allergic, anaphylaxis, and allergy. Everything that begins with the letter A. So if you recall from our mnemonic, acid. type 1 goes with the letter A. So acid, allergic, asthma, allergy, anaphylaxis. Basically what you need to know besides the letter A's is that you get cross-linking with IgE and the allergen. So type 1, allergic, acid, allergy, anaphylaxis involving an IgE antibody and mast cells and basophils release vasoactive substances that cause vasodilation. All right that's type 1. Now we're going to move on to type 2. So type 2 is the C in our acid mnemonic and what does C stand for? Cytotoxic. So what you get here is that either IgG or IgM bind to an antigen and you're going to see this on all of these slides you're going to see what's actually happening in a little picture on the left. When IgG or IgM bind to the antigen into the cell receptor you get complement activation. You also can get natural killer cell activation but that doesn't always happen. What you get after that is the death of your self cells. So this is a type of hypersensitivity that results in the death of cells that are actually native to the human body. So type two is cytotoxic. And again, we're in our acid mnemonic. We're at the C because we're type two. So cytotoxic with the C in acid. And what you need to remember is that it's cytotoxic involving IgG or IgM and that it's smooth. And we're going to use the C in smooth. And you'll understand why after I explain type 3. So this is really high yield that it's smooth antibody deposition. So I'm going to slow down for a second. So far, we've talked about type 1 and type 2. Type 1 was allergic anaphylaxis, all the A's, right? The A in acid. And it involved IgE. Type 2 is cytotoxic, right? The C in acid. And it involves smooth with a C antibody deposition. So, so far, both type 1 and type 2 involve antibodies. Now we're going to go on to type 3. So type 3 is the I in our acid mnemonic. And what does that stand for? Immune complex. Okay, so IgG or IgM, we're talking about the same immunoglobulins here. They're going to bind to an antigen. And when they bind to the antigen, they're going to form these complexes. And the complexes are thick. They're like little globules of stuff. And that globule or that complex is going to deposit itself in various tissues. You write usually at the basement membrane. And it's this deposition of complexes that damage the tissues and cause complement to be activated, which then destroys those tissues. So in all of the diseases that are type 3 hypersensitivities, the reason that your self-native human tissue is being destroyed is because you're... you're accidentally activating complement because there's little complexes stuck in these tissues. So going back to our acid mnemonic, we're now at the third letter because we're type three. And the third letter was I for immune complex. And what you need to remember here is the I for immune complex, but the I in lumpy, bumpy, or lump I, bump I. So lumpy, bumpy is the way that antibody complexes, immunoglobulin complexes are deposited in the tissues. Now let's slow down for one second because this is the highest yield part of this entire video. I told you in type 2 that you needed to remember smooth with a C, smooth linear deposition. Contrast that to type 3, it's lumpy bumpy or globular or thick deposition. So what does that mean and why does that matter? What this means is that there are two different types of renal pathologies that can exist secondary to hypersensitivity reactions. You can either have Goodpasture syndrome or Poststreptococcal glomerulonephritis. So let's pay attention to that now. Goodpasture syndrome is a type 2 hypersensitivity. Poststreptococcal glomerulonephritis is a type 3 hypersensitivity. Because in type 2 the antibodies are deposited smooth, you get a linear deposition and you see that picture at the top. Notice how the deposition in the basement membrane is smooth. However, in type 3, in post-strep glomerulonephritis, you get complexes being deposited, right? Because type 3 is immune complex mediated. And because it's a complex, which is a little ball of stuff, those little balls are spaced out in the basement membrane. So instead of being linear, like smooth, it's lumpy, bumpy. And these are buzzwords. They are very high yield. So if you're taking your exam and they show you a picture like this and they use either linear or lumpy bumpy, you already need to train your brain to think good pasture versus post-trep glomerulonephritis and type 2 versus type 3 hypersensitivity. This is, without question, the highest yield piece of information in this whole lecture. And I think that you can appreciate the difference between the two pictures here. One is very smooth and the other is very lumpy bumpy or globular, if that's even a word. But this is high yield. Spend some time on this slide. The way that you can remember this is that good pasture is two words, but PSG for post-stripteous glomerulonephritis is three letters, and they go with type 2 and type 3. But at the end of the day, if you remember lumpy bumpy versus smooth, you'll understand immune complex versus linear and type 2 versus type 3. Again, very high yield. I cannot stress that enough. Know this slide. We're going to end with type 4 hypersensitivity. And type 4... corresponds to the D in our acid mnemonic. And what does the D stand for? Delayed. So what's happening here? An antigen is going to sensitize a Th1 CD8 plus cell and that cell is going to release cytokines that are going to activate macrophages. And those macrophages directly remove target cells, right? They phagocytize the cell and kill the cell. This is delayed because it takes time to occur. The antigen first has to sensitize your cell and then later on a kind of like a repeat insult, so to speak, the cell releases the substances that then activate macrophages. So just know that it's delayed. It doesn't happen immediately. And again, D, delayed acid, is our mnemonic. And what you need to remember here is that it's delayed. And this is what's occurring with type 1 diabetes. This is what's occurring in a contact dermatitis. And this is how you... diagnose tuberculosis. So the TB test that you get in your skin, the reason that you have to come back after you've gotten that little shot under your skin to see if there's any induration is because it's delayed, right? It doesn't happen right away. So anybody who's gotten a TB shot knows that you don't just get injected under your skin and get it red right there and then. Rather, you got to come back 48 hours later to get it red because it's a delayed reaction. So if it's going to be positive, it won't be positive until two days later. So that's type 4 hypersensitivity, D delayed, diabetes, dermatitis, and diagnosing tuberculosis. So here is again the summary of everything that you need to know. We talked about the mnemonic, we talked about A for allergy, C for cytotoxic, I for immune complex, and D for delayed. I tried my best to fit in the clinical examples with the letters. Again, make sure you understand the difference between good pasture and post-strap glomerulonephritis in that good pasture type 2 is smooth or linear deposition, whereas type 3 is immune complex or lumpy bumpy deposition. That's super, super high yield and that shows up all the time on your exams. But know this chart and I hope that I was able to simplify this really complex topic for you guys. Best of luck.