Welcome to chapter 4 and in this chapter we will be talking about the alterations in immunity. The learning objectives of this chapter is to describe the cellular components that includes lymphocytes, macrophages, antigen-presenting cells, and the adaptive immune response or processes. You want to be able to differentiate between the innate immune response and the adaptive immune response.
You want to be able to define the process of primary and secondary antibody Response in the development of immunity and you also want to outline those similarities and differences between T lymphocytes and active Cell mediated immunity we will talk about antibodies or immunoglobulins More specifically we'll talk about IgA IgD IgE IgG and IgM We'll compare and contrast the immune function associated with several types of alterations That'll be the host defense failure, hypersensitivity, autoimmunity, and alloimmunity. We'll also describe the interactions between cell-mediated and humoral immune response and what is necessary for mounting an effective immune response. And of course, we'll talk about different clinical models that are related to altered immunity. In order to start talking about immunity, we're going to backtrack a little bit and talk about the anatomy and physiology. And this is just a brief overview.
This is regarding the lymphatic system, and really the lymphatic system is responsible and important in establishing an effective immune response. So simply put, if your lymphatic system is not working, then you don't have as adequate of an immune response. You'll notice in this picture, there are several areas that are located in the human body for the immune response to start developing.
You have central organs such as the bone marrow and the thymus. And then you have different ancillary organs or your peripheral organs. You'll see the spleen.
You have lymph nodes and lymphoid tissue. All of these work together to help with the immune response. So the immune defense is characterized as the third line of defense. So all of chapter three was talking about that second line of defense, that inflammatory response. But now that inflammatory response has failed and we're moving into the third line of defense.
So that's when your actual immune response starts to develop and it starts to fight those harmful substances or pathogens that are trying to attack the body. So the immune response does help with the recognition and the neutralization of pathogens or foreign agents. And really what happens is that if you get exposed to that pathogen enough, the body wants to help remember. what that pathogen looks like just in case if you get infected again the immune response will know how to handle that so all of chapter four we'll be discussing that third line of defense and what happens when we have an adequate response and hopefully that will result in resolution versus if it does not work and we have alteration that results in disease spread here's a really good concept map regarding the normal immune response and the branches that are involved with the immune response. As you can see, we have two different branches.
You have the innate immunity and you also have adaptive immunity. Innate immunity is also characterized by being nonspecific. So all that means is that once an antigen is presented, if that same antigen is presented again, the body does not necessarily remember that it was exposed to it at a previous date and time versus adaptive immunity.
That actually is characterized by specific or it is specific to various antigens that have been presented to the body. So in this immune response, we have a memory component. The body remembers that it was exposed to this particular agent or harmful pathogen and the body mounts an even more detailed response as it relates to that pathogen.
It does involve lymphocytes, particularly those T lymphocytes and B lymphocytes. Those are also known as white blood cells. And again the body is remembering that there was an exposure so you normally see a more aggressive response by the body to help get rid of that antigen. So moving further into the adaptive immune response, this is the immunity response that we're talking about that is specific or has memory of different antigens or pathogens that have been presented to the body.
When we look at adaptive immunity, there are two different types. We have active immunity where the body is actively developing antibodies to those specific antigens. And it is normally achieved by having the disease prior or it is achieved by having a vaccination.
A good example of that is having a flu vaccine. So once you are injected with that flu vaccine for that year, if you are exposed to that same flu virus, the body normally recognizes it and it amounts a more specific response depending on the flu vaccine that you have received. Again, if you've already had a specific. disease such as the chicken pox. Normally, if you are exposed to the chicken pox again, the body does not, it remembers that you've been exposed to it and you do not receive the chicken pox again as a result.
Then we have passive immunity, and that is immunity that is transferred from a host to a recipient. And the best example of that is when we talk about embryos or infants. One example I can give you is that if a mother receives a vaccination, that vaccination, that immunity that is developed from that vaccination, it is actually passed on to that embryo.
Another example of that would be through breast milk. What the mother has as immunity for that period of time, that can be passed on to an infant through breast milk because breast milk does help with the... immune response and developing a baby's immunity system. So again, you have active immunity that falls up under that specific immune response, that adaptive immune response, and you have passive immunity, which also falls under that adaptive immune response.
So again, this is the branch that we're talking about is specific and the body is remembering those types of pathogens. So another word for adaptive immunity is humoral immunity and this is more specific to the development of antibodies against pathogens or antigens and humoral immunity is more focused on those B lymphocytes the development of those different antibodies or immunoglobulins as you can see that there are a plethora of immunoglobulins and we will talk about some of those in this lecture today but Those immunoglobulins are secreted from those B lymphocytes. And this whole process is through humoral immunity. And again, it is specific to the creation of antibodies. It's important to note that humoral immunity does fall under that adaptive immune response because there are immunoglobulins, there are antibodies that are being developed to help the body remember the said pathogen in order to have a more aggressive response.
If presented with this specific antigen again so we'll talk about two specific immunoglobulins as it relates to humoral immunity the first area I want to talk about is primary adaptive immune response and that is the activation of the immune response the adaptive immune response with the first recognition of a specific antigen so in this process the body has never seen this pathogen before so there is no pre exposure except for at that moment that the body has been exposed. The antibody that is initiated is called IgM. It is an immunoglobulin.
And for the purposes of this lecture, please understand that immunoglobulins are the same thing as antibodies, and I will use them interchangeably within this lecture. Now, IgM is the initial antibody that is initiated and circulating around the body to One, search and see what is the pathogen and what is it made of. It's not necessarily recognizing it, excuse me.
It is scanning to see what the pathogen is so that it can gather data so the body can start to remember what this pathogen or harmful agent is. Again, this is the primary adaptive immune response, and it only occurs when the body has never seen this pathogen before. Then we move into the secondary adaptive.
immune response and this is the reactivation of your immune response with the same antigen so there has to be a primary adaptive immune response and IgM has had to surveillance this pathogen first in order for there to be a reactivation in the secondary adaptive immune response at this point in time the body has seen this pathogen before and therefore IgM is no longer going to be surveillancing this pathogen. We have another immunoglobulin. called IgG that will mount a more specific and a more aggressive response.
So again when there's a secondary adaptive immune response the body has seen this pathogen before and therefore will mount a more aggressive response as a result. So again the immunoglobulin that is involved with this immune response is IgG. When it's the primary it is IgM.
This graphic helps explain that concept further when it comes to those antibodies, also known as immunoglobulins. As you can see, the green lines show IgM. This is your first exposure, and as you can see, there's not an aggressive response.
It takes its time. It's surveillancing this disease or this pathogen, and it takes about 28 days in order for that immune response to develop. and become active and eventually get rid of that that agent whereas when we have IgG that secondary response there is still a response but as you can see there is a more aggressive response you see that at that 28 day mark not it the curve is much higher and what this is showing is that the antibody titer that you may pull for this for this agent is more aggressive, it's circulating in the blood more frequently, more often. And again, we do see this more aggressive response by the body to protect and mount that immune response.
So again, when you have primary adaptive immune responses, IgM is involved. It's that initial surveillance to look at what the pathogen is. And then we have that IgG response.
where it's a more aggressive and greater response to what that specific pathogen is. Okay, we're going to continue our lecture. And yes, you can see my daughter here. She is going to be hanging out with me for a little bit. She wants to be held.
So here we are. But anyhow, we have active immunity. And when we discuss active immunity, I discussed that there's a type called humoral immunity.
So humoral immunity specifically deals with antibodies or immunoglobulins. Now, just know for the purposes of this lecture, if I use immunoglobulins versus antibody, that is a word that is being used interchangeably, and it actually means the same thing. So if you hear me say one word versus another, I'm talking about the same thing.
Now, when we talk about humoral immunity, we have a plethora of antibodies or immunoglobulins that we will discuss in this lecture. As you can see on this chart, there are five specific immunoglobulins that I want you to know for this class. The first two you've already kind of gotten exposed to already.
The first two are IgM and IgG. So IgM again is involved with that primary adaptive immune response and IgM again is involved with that initial circulation and surveillance for antigens or pathogens that are first presented to the body. IgM is also the first antibody produced by newborns as they're developing in their mother's placenta in the uterus. Now we have IgG. IgG is the most abundant class of antibodies, but we know that IgG, it helps yield a more intense secondary immune response.
So what that means is that once IgM has surveillance and allowed the body to start recognizing what those pathogens are, If exposed to that pathogen again, that IgG antibody is now the one that's circulating and that's the one that yields a more aggressive and a tits response to that same pathogen. We'll move on to IgA. And this one is more involved with passive immunity. And you'll see IgA floating, especially when there's a newborn and a mother. IgA is the immunoglobulin that's involved with antibodies.
pass from newborn well from mother to newborn we have igd and that one's more specific to the stimulation of b lymphocytes and we'll discuss what b lymphocytes are in a little bit but igd is more closely associated with b lymphocytes and developing them into plasma cells we have ige and ige is more related to anaphylaxis and the inflammation response you normally have ige detected when there's some sort of allergic hypersensitivity reaction. And ultimately, it does trigger the release of histamine in these reactions. So from the last slide, it's important to know the different types of immunoglobulins or antibodies because they have different purposes in the body. So I do want you to understand and know what they are and how they function in the body.
Now we're going to move on to the cellular components of adaptive immunity. And we have two different types of cells that we'll discuss. And under those cells, there are more cells that are developed. So the first set of cell types will... discuss our B lymphocytes.
B lymphocytes are lymphocytes, white blood cells that are originating in the bone marrow. So we call them B lymphocytes for bone marrow B. Now B lymphocytes are more specific to humoral immunity and I believe I mentioned earlier in this lecture that humoral immunity is the immune response that develops your antibodies that produces those immunoglobulins that circulate through the body. But how do they do that? They do that through the stimulation of B lymphocytes.
So when B lymphocytes are activated, they're circulating through the body, they actually proliferate more or develop into plasma cells. And from that, plasma cells are the ones that produce the immunoglobulins and antibodies in the body. Now, we'll move on to the second type of cell component. And this is more involved with what we call cell-mediated immunity.
So again, humoral immunity associated with antibodies. T lymphocytes, however, which are originated in the thymus, T lymphocytes, thymus, this is a cell immune response. So T lymphocytes actually develop into three different types of cells. B lymphocytes, they develop into more B cells and plasma cells, whereas these T lymphocytes, they turn into what we call cytotoxic T cells. They turn into helper T cells.
suppressor T cells and what's really cool about these T lymphocytes is that the name kind of tells you what their function in the body is so we have cytotoxic T cells that directly destroy antigen carrying cells so when the immune response occurs those antigens are engulfed and then the cytotoxic T cells come in and they destroy those antigen carrying cells or the pathogens And that can be a virus, that can be a bacterium, that can be a fungi, anything that is not supposed to be a body and the body recognizes as foreign, that's what these cytotoxic T cells will come in and destroy. Then we have what we call helper T cells. Helper T cells help enhance the humoral and cell-mediated response.
So helper T cells help stimulate more B lymphocytes in the humoral response. And they also help stimulate more T lymphocytes, which thus turn into more cytotoxic T cells, helper T cells, and suppressor T cells. So helper T cells help enhance the whole immune response.
Now, we'll have suppressor T cells. Suppressor T cells are, well, their function is to inhibit the humoral and cell-mediated response. So after the body has fought off the infection and has done so successfully,... these suppressor T cells start to inhibit that response and starts to scale it back. You want to have suppressor T cells that scale the response back because you don't want that overproduction of the immune response.
Again, that's bad and that's called an alteration. So when the body is working, these suppressor T cells come in and they help suppress that immune response and ultimately helps drive the body towards resolution with the immune response. So here we're going to be more detailed with the T lymphocytes and the cell-mediated immunity. And again, it results in the recognition and destruction of cells that carry antigens or pathogens.
Those cytotoxic T lymphocytes, again, are involved. We have those helper T cells that are involved, and then eventually the suppressor T cells that are involved that help inhibit that response. Now, there are differentiation cells.
called clusters of differentiation CDs that help with this response and the CD8 they help determine the specific function and response of the T cells so cytotoxic T cells are more closely related to the CD8 cells whereas helper T cells or T lymphocytes they're closely associated with CD4 so all you have to remember here is that cytotoxic T cells have CD8s with their surface molecules, whereas helper T lymphocytes have CD4s as their surface molecules. And then there is another cell type called the MHC cell, or major histocompatibility complex, and that helps with the presentation of the portion of a foreign body. So what this particular cell does is that it helps present, it basically tags what is foreign to the body.
breaks it up and it's presenting these parts throughout the body so we could recognize what is what is not a part of the response or what is not a part of the body what is foreign so again you have different types of these you have MHC class 1 which are presented with those CD8 cells which means that MHC class 1 is related to those cytotoxic T cells whereas MHC class 2 modules there are molecules, they are associated with CD4. And again, that means they are associated with helper T lymphocytes. So just remember cytotoxic T cells, CD8 cells, MHC class 1. We remember helper T cells, CD4, MHC class 2. So we discussed a lot about what the immune response is supposed to do and the different variations and levels of that immune response.
Now we're going to talk about those alterations and there are four specific alterations to the immune response that we'll talk about in this lecture. They are hypersensitivity, host defense failure, autoimmunity, and alloimmunity. So here we have hypersensitivity reactions and under those hypersensitivity reactions we have four different types of reactions.
We have hypersensitive reaction type 1 which is an immediate allergic reaction and those immunoglobulins that are associated with that is IgE. And remember, I told you there's a plethora of immunoglobulins that are associated with the inflammation and allergic response. So this table describes where those fall in their function.
So again, type one is an immediate hypersensitivity response, allergic reaction, and it is IgE mediated. The injury is allergic reaction, which is a local site. area that could be in the tongue that could be just hives on the Different areas of the body whereas you can have a more severe reaction Which is life-threatening when we have a type 1 that is severe and life-threatening. We call that anaphylactic Reaction that's where we have maybe the closing of the throat We have airway that are compromised things of that nature then we have type 2 And this is a hypersensitivity reaction where the body cannot recognize itself versus what's foreign. So type 2 hypersensitivity reactions is a case of mistaken identity.
And the immunoglobulins antibodies that are involved are IgM and IgG, which makes sense because IgM is related to the first exposure in the first presentation of a pathogen, whereas IgG is related to the second exposure of that pathogen. And the... What's happening here is that the body can't recognize what is itself versus what's foreign.
It confuses that first exposure of what's foreign as itself, so the body doesn't attack. Or the reverse, the body attacks itself and mounts this more severe response as a result. Now we have the reaction against the cell and we have the opsonization or AKA the killing or lysis of cells as a result.
So this is a hypersensitivity reaction type 2. We have type 3 where we have antibody complexes that are not soluble. They can't react so again this is an IgM and IgG mediated reaction. And then we have a type 4 which is generally a delayed reaction and this is more so T cell mediated. So the first three are related to B cell mediation because that's a part of humoral immunity so type 1 type 2 type 3 fall under humoral immunity because there are immunoglobulins involved type 4 is the only one where there is T cells T lymphocyte mediation and it does lead to an inflammatory response that leads to cell death or cell lysis So here we'll talk about the secondary way to alter immune function and this is called host defense failure and what this is is that it is the failure of the host to defend against infection and there are three different ways that this can occur.
You have antigenic variation which means that there are multiple variations of that antigen with multiple presentations or variations of that antigen it makes it very difficult for those T lymphocytes and B lymphocytes to circulate and recognize that the antigen is foreign. We have viral latency where viruses enter a period of inactivity, so they're not actively being replicated, they just remain undetected in the immune system until they proliferate enough in order to infect that host organism. And then we have immunodeficiency, and we have two different types of immunodeficiency. We have that where the individual is born through genetic mutation. that impairs the immune response.
And normally this is seen in young children, that's how it's diagnosed as primary. Whereas secondary immunodeficiency is the result of another disease. So an example of this would be AIDS. HIV would be one part of the disease that causes AIDS, and eventually there's that immunodeficiency that is developed from that.
As far as your genetic mutation, you have lupus as an example of that. Lupus is normally detected in young children, and you have signs and symptoms of lupus. And that's where they would diagnose that this is some sort of genetic mutation. That's where that immunodeficiency derives from.
Next, we'll talk about alloimmunity. And this is when the immune response is activated as a result of the presence of other cells from a different individual and it must be from a person of the same species so you see this a lot when there are blood or plasma transfusions or transplants so what is occurring is that the body is rejecting it although it is coming from an individual of the same species so you'll see graft rejection where the body does not tolerate a transplant that could be from an organ or different part of the body that has been donated or given to this individual. And then we have something that we call graft versus host disease. And it commonly results from the transplantation of hematopoietic cells. And when we talk about hematopoietic cells, those are cells that differentiate into healthy blood cells.
So these are cells that are supposed to be injected or given to another individual, and they're supposed to proliferate into cells that produce healthy. blood cells. The T lymphocytes that are already present in the individual that is the recipient recognize the donor as being foreign and those darned donors tend to detect antigens in the recipient's tissue and then they attack.
This is generally a delayed reaction, also known as a type 4 hypersensitivity reaction, and it's oftentimes fatal. The last alteration that we'll talk about is called autoimmunity and this is simply the failure to distinguish the self from non-self. So the body is literally attacking itself and it does cause proliferative damage. It can cause damage to specific organs, tissues, or it could cause damage to the entire organ system and would be perfused throughout the body.
Again, one of these would be lupus, systemic lupus, and you will see normally in individuals with lupus that Their entire body systems different areas are affected due to the body attacking itself We will discuss this later in this chapter So we study the four different ways of alterations with the immune response to help develop goals again The goal of pathophysiology is to develop ways that we could stop these pathological processes from affecting the human body, so first goal would be the first level of prevention and that is Prevention, right? So you want to use vaccines that help the body develop more antibodies to help further protect against those antigens that can cause these maladaptive responses. Another goal is to have immunosuppression for those that have the overreaction of the immune response, particularly those that have autoimmune disorders. We want to provide ways that we can have immunosuppression because their immune system is overactive. It keeps working and working and more specifically working against itself.
So we have anti-inflammatory drugs available to Help with that. They're normally corticosteroids or steroid drugs. You have cytotoxic drugs We have bacteria and fungal derivative drugs all of these would help with immunosuppression in that area And then another goal would be with cancer specifically.
Well, we have a whole chapter about cancer But just understand that one of the goals is to recognize and destroy those altered cells without destroying normal cells. So you may have radiation, some types of radiation therapies, but the type of radiation therapy that they would use is hopefully ones that are specific to what is altered in the body. Sometimes you cannot avoid that with that type of therapy, but that is the goal.
So again, we want to help. with the maladaptive responses by manipulating what the immune response will do. Again, the immune response is overactive a lot of times, and by suppressing the immune system, by preventing it from working overly well, then we allow healing for individuals that are affected by these immune disorders.
Okay, so here are our clinical models that we'll be discussing as it relates to alterations in the immune response. Make sure you complete your disease cards as it relates to these four different clinical models, and feel free to fill them out as we're discussing them in our lecture today. The first disease that we'll talk about today is the AIDS disease or acquired immunodeficiency syndrome. And a lot of you may have heard of this syndrome already, and it's more closely related to HIV. So we see HIV and AIDS paired together, but we're talking specifically about HIV.
about the AIDS portion of that condition. And the pathophysiology is that there is an altered host defense resulting from secondary immunodeficiency. And when we discuss secondary immunodeficiency, then it's primarily caused by HIV. HIV is where the individual is infected with this virus, that viral load increases, and then it thus progresses into AIDS. So that's where we are at this particular portion.
So the infection of CD4 helper T lymphocytes are infected with the human immunodeficiency virus. This virus is literally inside of the T lymphocytes, so it remains undetected until it gets to a level where it proliferates so much where the infection now explodes inside of the individual. And now this virus is circulating, causing the immunodeficiencies that we see in AIDS. So. It does result in the loss of cell-mediated and humoral immunity because we are losing those T lymphocyte cells.
Those T lymphocytes have been taken over and they're no longer their purest form. So now they are infected with that HIV virus and now they do not work functionally. You have clinical manifestations that are system-wide. We will be looking at that in the next slide. But just understand that once AIDS has progressed, you see these system-wide effects across different body systems.
You have diagnostic criteria. Of course you have to be diagnosed with a health care provider. They are looking at your risk factors and different signs and symptoms or those clinical manifestations that we'll talk about in a few minutes. And then you have laboratory analysis. Now I want you to pay attention to this portion because this is how HIV is detected.
So HIV is detected because there are antibodies that have been developed to HIV. So we'll see increase in the antibodies in the detection and we will also see an increase in HIV viral load and this is where they actually determine if you are progressing into HIV AIDS well more so AIDS or not it's depending on that viral load and then they also look at the T helper lymphocyte counts because that's the type of cell that HIV attacks and proliferates in as far as your treatment you have anti retro viral therapy, ART therapy, and what it's structured to do is to suppress that viral load, that HIV viral load, is to help preserve immune function or help restore it if you catch it in enough time, and it hopefully reduces morbidity and mortality as it relates to AIDS. So again, in order to progress to AIDS, HIV has to develop and it has to proliferate so much, and then it develops into AIDS. As I've mentioned before, there are system-wide effects. On our slide here, you'll notice that there are different areas of the body that are affected.
You can see neurologically there's memory loss, disorientation. You may see some meningitis when it progresses further, headaches. You may see some encephalitis, which is the swelling and infection of the brain.
As far as your head, neck, and throat, eyes, you may see some White patches on the tongue, swollen nymph nodes in the armpits, growing area in the neck. You may see thrush or candidasis on the tongue, and you may see individuals with herpes simplex on the mouth. You may see an individual with AIDS progress to pulmonary tuberculosis and pneumonia, and normally this is a disease that they're unable to fight off on their own and ultimately results in their demise.
You have weight loss, loss of appetite. chronic diarrhea you have malignant lymphomas night sweats Kaposky's sarcoma which are the splotches that are developed on the skin and sometimes they're purple or dark in color on the skin and as far as musculoskeletal you see fatigue and muscle weakness so again these are clinical manifestations across different body systems and they're wide ultimately you do see immunosuppression which causes all of these signs and symptoms You do have the risk of getting an opportunistic infection. Sometimes it's fungal, sometimes it's that pneumonia or tuberculosis that I was telling you about.
Sometimes it's that cryptococcal meningitis and toxoplasmosis encephalitis. So you have different opportunistic infections that would affect the individual with AIDS and again this ultimately would result in their demise. Next we'll talk about anaphylaxis and again this is that allergic reaction that is life-threatening and it is characterized by an exaggerated systemic immune response due to a type 1 hypersensitivity reaction.
The triggers include insects, things, food allergies, drug allergies, anything that would be considered not normally infectious or detrimental to an individual would be considered a trigger. When exposed to any of these triggers they are considered antigens at that point. And they stimulate IgE-mediated responses. Again, when we're talking about anaphylaxis, this is an IgE-mediated response. And again, it is an exaggerated immune response.
Ultimately, you do see the degranulation of mast cells and basal fields that cause systemic and local responses. You have the dilation of vascular smooth muscle, which means that the blood pressure is going down. You have the constriction of the bronchial, which is in the lungs, smooth muscles. So that means that your lungs are constricting.
That's an airway problem. And then you see an increase in vascular permeability, which you will see that swelling in an individual. So again, all three of these things would lead to a life-threatening emergency.
And it does need to be taken care of and treated immediately because of that. So here are your clinical manifestations. And again, you have two different phases where you'll see this occur. Phase one normally results in difficulty breathing. You're still flushing and itching, and you have angioedema.
And then phase two, it moves more into that severe hypotension or that blood pressure drop that we mentioned in previous slides. You will see severe edema. And again, as far as your clinical manifestations, they are severe enough to notice that an individual is in a life-threatening emergency, and these do need to be treated as soon as you notice the symptoms. As far as your diagnostics, you will have to have a history and physical examination, but in the emergent state, you immediately see that a person has these signs and symptoms and you want to treat them appropriately. If the person has not had a life-threatening emergency or not actively in anaphylactic shock, you may see them go get allergy testing if they have had a severe reaction before.
And this allergy testing helps determine if there's potential for any other substances that are similar to affect the person to get anaphylactic shock. So after those diagnostics, you do want to treat. Again, symptomatic treatment is immediate. You want to give drugs that relax the bronchial smooth muscles and constrict that vascular smooth muscle.
So you want something to help the lungs open up and you want something to help those blood vessels. constrict to help bring that blood pressure up and to also help with breathing. You also want to have drugs that help limit inflammation so you'll most likely see drugs like epinephrine being used with an individual with anaphylactic shock. You may also see steroids in the less acute stage to help with the inflammation and edema that that person may be experiencing.
And then you have preventative treatment. You don't want to keep exposing an individual to what triggers a life-threatening emergency. and there may be areas where they desensitize the individual to the allergen. Next we'll talk about lupus or systemic lupus erythematosus, SLE for short.
And this is a type 3 hypersensitivity reaction. This is also known as an autoimmune response. And it is a chronic systemic disease due to a persistent antigen. The body continues to attack itself. So this is where we call this an autoimmune response.
It does act. those B cells that produce antibodies against itself and the activation of T cells which keeps producing inflammation responses within the body those antibodies that are developed against the body by those B cells are called auto antibodies and they are targeted against those cell membranes cytoplasm and nucleus of the body now as far as your clinical manifestations we will discuss those further on the next slide but just know that again you have these system wide effects as a result of this type 3 hypersensitivity reaction. Of course, you have to be diagnosed by a healthcare provider, and you have different laboratory tests that determine if you have lupus. They'll detect your antibodies. They may look at inflammatory markers.
They may look at your complement activities, C3 and C4. There are different areas that they will assess to determine if you have systemic lupus or not. Then as far as treatments you want to have anti-inflammatories You may see DMARDS and immunosuppressants used in the treatment of these individuals As I've mentioned lupus has a plethora of system-wide effects that you'll see there are local Manifestations which is in one general area in the skin. You may see it in the lungs and the kidneys musculoskeletal just in those generalized areas.
And then you may see systemic manifestations, which include the neurological areas. Again, pulmonary, if it's diffuse enough, circulating in the blood hematologically, and you may also see cardiac disease. As far as specific signs and symptoms, you have seizures and psychosis.
You have butterfly rash. That is the rash that appears on the face, generally on the cheeks and the bridge of the nose. that's also known as discoid lupus.
You have the respiratory system where you see pleuritis, which is an infection in the lung area. You have cardiac where you have endocarditis or myocarditis in the outer layer of the heart or in the muscle of the heart. You have anemia, leukopenia, thrombocytopenia. In the kidneys, you may see glomerulonephritis.
Lymphatic system, you may see lymphedema. nonopathy you may see arthritis try to say that word several times fast but anyway you have different clinical manifestations throughout the body and again these are diffused in system wide and it's important to know that lupus is an autoimmune disorder and this is where it presents okay so the final disease that we'll talk about today is rh isoimmunization or the rh factor disease And this is caused by a type two cytotoxic antibody mediated reaction. So there is a reaction between two different individuals.
Normally it occurs in mothers versus a fetus. And often the mother is Rh negative and Rh is the antigen that is presented in this disease process. So normally the mother is Rh negative. And that fetus... They normally have an Rh positive and this Rh positive is presented as an antigen to the mother.
So then the mother recognizes this as foreign and then begins to attack. So it does cause different clinical manifestations as it relates to the fetus but it can be life-threatening for the fetus if it's not caught in enough time. So as far as diagnostics, you of course have to have a physical examination by a health care provider.
You have to have different screening tests that are occurring, so the identification of the D antigen and anti-D antibodies from your laboratory work. And then they'll do aminosynthesis to measure your bilirubin, and they'll also do fetal blood sampling. As far as the treatment you want to prevent, if the mother is known to be Rh negative, then that's when you'll see that RhoGAM shot or the Rh immunoglobulin. that is given to the mother to desensitize the fetal positive Rh antigen. And as far as other treatments, you may see some transfusion to replace the lysed blood cells with the healthy ones within the fetus and the mother.
So Rh should be discovered earlier than later. The longer that you allow this process to go on, the more at risk the fetus is within the body. As far as your clinical manifestations, as far as your fetal, you'll see anemia. You may see some fluid buildup or edema in the fetus, or you may even see death. And as far as infants, once they are born, you may see some bilirubin deposits in the brain.
This is called conicturus. You may see lethargy. hearing loss, cerebral palsy, and learning problems.
So again, fetal effects would be in utero or in the womb, whereas infant effects you'll see presented after the fetus is born. And again, this is after the fact. So this is the end of our lecture today. Make sure you complete your guided learning questions. Make sure you read the textbook, look at your disease cards, make sure you study your case studies, and do your...
activities associated in class. Make sure you review everything thereof and check your understanding and make sure you ask questions and as always I'm available by email or you can see me after class. Thank you and have a great day.