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Summary

In this on-demand teaching session, Jasmine, a second-year medical student discusses infections. Throughout the talk, Jasmine covers a breadth of topics including the immune system, specific pathogens, how infections are fought, and system-specific infections (i.e. gi tract, S ti sepsis, hepatitis, and the respiratory tract). Jasmine describes the different roles of the innate and adaptive systems in immunity, the variety of cells and receptors involved, and gives a detailed breakdown of how the complement system works. In addition, the importance of T cells and B cells in adaptive immunity are discussed. The session also covers different types of infections, essential definitions, and structures of bacteria and viruses. She highlights key concepts such as exotoxins and endotoxins in bacterial defence mechanisms. The session wraps up with a detailed presentation on sepsis, a critical condition that requires immediate attention.
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Description

Join us for an insightful talk on "UKMLA Guide: Infection" by Jezne Sfarijani, an essential session for all aspiring medical professionals preparing for the UK Medical Licensing Assessment. This talk will delve into critical infection-related topics, offering a comprehensive overview aligned with the UKMLA content map. Attendees will gain valuable insights into diagnosing, managing, and preventing infections, ensuring readiness for clinical practice in the UK. Don't miss this opportunity to enhance your knowledge and ace your exams with expert guidance from Jezne Sfarijani!

Learning objectives

1. To understand the structure of the immune system, including its innate and adaptive components and how they function together in the body's response to infections. 2. To be able to explain the process of pathogenesis, focusing on the mechanisms used by different types of pathogens including bacteria and viruses to cause disease. 3. To understand the phenomenons of gram staining in identifying bacterial infections and the roles of exotoxins and endotoxins in the progression of disease. 4. To gain a comprehensive understanding of sepsis, its pathophysiology, its risk factors and its diagnosis and management in the context of clinical medical practice and patient care. 5. To understand the roles of T cells and B cells in adaptive immunity and how they provide long term immunity against re-exposure to the same pathogen.
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Computer generated transcript

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The following transcript was generated automatically from the content and has not been checked or corrected manually.

That's all right. Hi, everyone. I'm Jasmine. I'm a second year medical student as Farah mentioned earlier. Um, today I'll be talking about infections and this is something that, um, we previously went through last year in time two. So I'll be going through high. Um, everything that I think is high yield and of importance clin clinically and academically. So, um, so the topics that I'll be going through is the immune system, pathogens, infections, fighting infections and system specific infections. So, to do with the gi tract S ti sepsis, hepatitis and the respiratory tract. So I'll start off with the immunity. So the immune system consists of the innate system and the adaptive system. The innate system is just immediate response of your body to nonspecific um particles and antigens um and antimicrobials. So your body will literally just respond straight away to what is presented to them. And then the adapter system is just a humoral response with B cells and um T cells. So it's more adaptive as it says in the name and more specific um in to be specific, the adapter system is slower. Um, the innate system is faster, the adaptors, the adapter systems al also to do with memory and learning. So once you've been exposed to the certain condition or the disease or any sort of particles, your body will remember due to the adaptive system. And like I said, this involves T cells and B cells. So we'll start with the A um immunity. So there's a cellular response and the humor, humoral response um within the humoral response is the complement system. And the complement system just includes a, a bunch of serum proteins and cyto kinds. So, with the innate immune system, there's a bunch of receptors and cells that are involved. So we have on the left, as I've mentioned, we have the natural killer cells, mast cells, basophils, neutrophils and some others. And it starts off with the detection of pathogens. So we have these pattern recognition receptors that can identify pathogen associated molecular patterns and damage associated molecular patterns. These are all um molecules and particles that can be released by the bacteria. The damage associated molecular patterns are released when um a cell is dying or they're damaged. And this just triggers the innate immune system to get rid of it, to remove it from the body as it no longer needs to be there. Um There, there are different types of path uh pattern recognition receptors. We have um tor 2345 and seven and these are toll like receptors. And I've put a table of what PMS. So pa and associated molecular patterns they do recognize and the group that they do belong to. Um So the compa the complement system, your complement system activates the proteins that work with your immune system. So it basically just enhances the effect of your immune system. And it can work hand in hand with the innate immune system and the adaptive immune system. The complement system consists of a wide variety of proteins and it just mainly involves the destruction of the bacteria and the viruses and any other sort of um particles that are damaging to the body. Um They are always present in your body at low levels and they are activated after the cleavage which takes place during um the innate and adaptive um immunity. So I've put a picture that just summarizes the pathway of the complement system. I do want to highlight the main um cytokines that you do need to remember. And that is C three ACC five B and C three B. So C three A and also C five A, they're both involved with information. So the complement system will release these cytokines when there is an inflammatory um response and C five B. So cytokine five B will be released when um the cell is dying and it there needs to be activation of these cytokines and then C three B is involved with phagocytosis. So, the engulfment of the bacteria. So now adaptive immunity, um I want you to remember that the two main cells involved in adaptive immunity is are T cells and B cells. So we'll start off with T cells. T cells are cell mediated responsive cells and they are activated by dendritic cells. We have two types of um T cells that we do learn about. And that is CD eight plus and CD four plus CD four plus are known as T cells. CD eight plus are T cells that recognize the anti the antigen and they release grand enzymes or porphyrin to induce apoptosis, which is just cell mediated death. So that cell that is exposed to these enzymes will be will die. And um the CD four plus cells, the T helper cells, they activate other immune cells um to carry on the process of immunity and to attack the cells, they activate cells such as B cells, antibodies, macrophages and they also activates um CD eight plus T helper cells. Just a quick note, CD eight plus T helper cells are what is attacked in HIV um later on in the presentation, I will go further into this. Um with B cells, they are antigen presenting T cells. So they present the antigen to the T helper cells. Once this is done, they are then matured um due to activation of by the T helper cells. And once they are mature, they can um they will become either plasma cells or memory b cells. Plasma cells are just cells that produce antibodies specific to the bacteria that they are fighting. And memory b cells, as I mentioned earlier is what makes adaptive immunity an adaptive process. So once you've been exposed to this certain bacterial particle, um it will be an initiate rapid response the next time you are exposed to it again. Ok. So we have different types of infections, viral, bacterial parasitic fungal s. Um I will be going into these in more depth. So we'll start off with um the definitions that you do need to remember. So we have a pathogen, an organism that causes death to the host. We have uh violence which is the degree of pathogenicity and toxogen, which is the ability to produce toxins. So, with bacteria I have on the right, the general structure of a bacteria and I would say the most important to remember or necessarily the easiest is the capsule flagellum ribosomes and just the cell wall and obviously the DNA within it. Those are general ones that are easy to remember and the associated functions when we do talk about bacteria. Obviously, there are there are different types and there's this process called gram staining. And this is just to differentiate the different types of bacterias and with gram positive and gram negative negative bacteria, cells, there are a huge difference. Gram positive cells have a thick pepto pepto glycan layer which is just the outer layer of the bacteria. And when this is stained, it stains as um blue or purple when gram negative cells are stained, they do have a thinner wall. So they stain as red or pink, which is something that you do need to remember as this is a very um high yield question that they could ask. OK. So with viruses, um obviously they are very different to bacteria. Um But there's two structurally different types of viruses. So we have a naked virus and an envelope virus Above, I have a, I have put an image of their structure and um or what they look like in general. So um it is bounded by a capsid and that forms a nuclear capsid and these are derived from protomers. And below, I have um attach the image of the process of um what how viruses basically um attack the host cell. And this is just in general, obviously depending on the disease and condition. It's uh there are other steps involved, but this is a general generally what takes place. So um factors have a, a lot of defense mechanisms which and the main one that we do learn are toxins. So we have exotoxins and endotoxins. I'll start off with exotoxins. Exotoxins are released from the bacteria into the environment. So the toxin basically damages the surrounding environment that it is um around. So this is secreted by both gram positive and gram negative bacteria and we have different types of um exotoxins. Um I would just, we have type 12 and three. And type one is what is involved in toxic shock syndrome. And I have um put the general involvement for each one. So now we have endotoxins. This I um these are within the bacterial cell wall and it is released when the bacterial cell just disintegrates and basically dies. And this is released by gram, gram negative bacteria. It's a part of the cell wall as I did mention earlier and this is um recognized by P RRS which are pattern recognition receptors and specifically toll like receptors. Four, because this is um not a substance that is recognized by your immune system automatically, this induces an immune response and then inflammation. So we'll move on to sepsis. Um sepsis is very important and the reason why it's so important is because it is a life threatening organ dysfunction which can take place due to an infectious pathogen or general dys dysregulation of systems that can occur to a number of reasons. Septic shock is a type of sepsis. And this is just when all systems are in your body. Cellular metabolic. Um circularity are all abnormal due to compensatory mechanisms that are overwhelmed um in sepsis. There's decompensated and compensated uh mechanisms decompensated. It's when the mechanisms do not work and therefore your BP is low compensated. Comp um mechanisms is when your BP is normal. And the me um the mechanisms have worked. I want to highlight when during sepsis. And just any any general condition or disease. The ultimate goal is to maintain perfusion. So it prevents organ ischemia and hypoxia. And to do this, generally, the body will increase your heart rate, your stroke volume and um your overall vascular resistance. And the reason why this takes place is because if the e the way I remember is the BP equation, which is to do with overall perfusion of your body. And that is heart rate, time, stroke, volume, times systemic vas vascular resistance. So, if you remember that equation, you will remember during sepsis, the way your body will maintain perfusion is by increasing heart rate, increasing the stroke volume and increasing the systemic vascular resistance, which will overall increase your BP and maintain perfusion. Um So the pa there's a pathophysiology with um sepsis. Uh The main five points that I do want you to remember is vasodilation, vasocon, then vasoconstriction of your vessels and then papillary, leakage, reduced venous return and reduced vital organ peru perfusion with vasodilation of the vessels. And there's an increased vessel di dial which reduces your overall systemic vascular resistance. But because there is um an increase in your vessel diameter, your body wants to compensate for that. So it increase the heart rate and that causes tachycardia. So your heart will pump more blood around your body and then um so on so forth with the rest vasoconstriction, completely leakage, reduce venous return and reduce vital organ per perfusion. Um So with sepsis six. And like I said earlier, it is a very important condition that if it is um acknowledged in a patient, you need to um 10 to them within the first hour. So there's three things you need to give and there's three things you need to take. So you need to give IV fluids, antibiotics, um bloods and o and oxygens and oxygen, sorry. And you need to monitor the um urine output and just the overall state. But I have put an image there to summarize everything. Now, moving on to gi infections. So I have um split everything up. So we have here first is um c dia diarrhea. These are all the diseases that can cause that. So we'll start off with cholera, food poisoning and tr travelers diarrhea. I have put the organisms that do cause these diseases and the main symptom is um usually watery diarrhea for all three of these diseases. And um I've also put the pathophysiology of what happens with the diseases on the right. But in general, they just um and they just colonize the intestinal cells and they release toxins that are damaging to these cells and that um can disrupt the overall balance of your um gi tract and can cause watery diarrhea. Um Then we have inflammatory diarrhea and on the. So we have the three diseases on the left that causes inflammatory diarrhea to do. So, if you think of inflammatory diarrhea it's an inflammation. So we associate with this with bloody diarrhea. So, dysentery, salmonella and diarrhea, um caused by a Colostri difficile is called causes symptoms such as bloody diarrhea because it's an inflammatory um disease. On the right. I have included her pathophysiology of this. Again and again, it's to do with the colonization of the gi tract and the um intestinal wall cells. Um I have put an image here and it's just all the dis um organisms that can cause um diarrhea in general. Ok. So now I'm going to talk about gastroenteritis. We have um a viral causes and bacterial causes here. I've put the viral causes. So we have rotaviruses, novovirus, poliovirus and enteric adenoviruses. Um in general, all of them can be asymptomatic. But if it's not, they will um present with for poliovirus, sore throat, fever, tiredness and an enteric is vomited, mild fever and water diarrhea. The pathophysiology for all four is that they just um infect the intestinal epithelial cells. They replicate and they just impair the absorption which can cause vomiting and diarrhea. Uh These are the organisms that can cause bacterial gastroenteritis. So, we have uh five listed here. C difficile Campylobacter cholera. These are all different types. Um for the most um frequent organisms seen to cause gas, bacterial gastroenteritis is colosi difficile. So I will talk about those symptoms. So it does stick into your head. It causes watery diarrhea. It can also be bloody, but generally um watery. Um it causes painful tummy cramps, you feel sick, you're dehydrated, you have a fever, loss of appetite and weight loss. Obviously, depending on the patient, these can um fluctuate in terms of your symptoms, but these are generally what takes place. And on the right again, I have put the path for physiology of all the organisms um mainly for clo diff and cholera as those are what are going into DL. So now we have respiratory infections. I have summarized all the respiratory infections that um are of importance here when it comes to respiratory tract infections. There's the upper respiratory tract in the lower respiratory tract. It is important to remember what is involved in the upper respiratory tract. And the lower respiratory tracts will have put an image on the side, on the left that just shows you the structures in both um sectors. So I've included the common cold influenza, um tuberculosis and pneumonia. Um And then I've put the organisms that cause these diseases. Um in general uh for the common cold influenza, you do get high fever, congestion, cough chills and then pneumonia, you get confusion, cough, fatigue and fever. And then for tuberculosis, um a symptom that does stand up for tuberculosis to, to differentiate from the others is um a bloody cough that is also persistent with weight loss, night sweats and so on and so forth. On. The right. I have included the pathophysiology of um the of these diseases. But I do want to mention that because they are respiratory tract infections. It, the pathophysiology will state how there is um infiltration of the respiratory tract in epithelium which then causes inflammation and so on and so forth. Ok. So now we have STIs s so um the reproductive system um I when it comes to S ti si split them into um bacterial viral and um others. So we'll start off with the main AOP. So we have bacterial vaginosis. F and pa pa pa cyst. These are not bacterial and these are not um viral and these are not transmitted sexually. So sorry that um I mean, the, I don't mean that they're not b bacteria viral. I mean that they're not transmitted sexually with bacterial vaginosis. The organism that causes that is gel vagin uh vaginalis and there's an overgrowth of this fascia is candida albicans and Bartholin cyst is e coli. I have put the symptoms for uh for each of them as they are very different. And I've also included the pathophysiology of um those three on the right, the bacterial diseases of um the rep reproductive system is chlamydia, gonorrhea and syphilis. Um chlamydia and gonorrhea are usually asymptomatic so it can be missed. Um And on the right, I have put the pathophysiology of syphilis. Um They are there, there are stages to the symptoms which I have included in this um in this table and on the right, I have put the pathophysiology. Um And now we have viral diseases of the reproductive system. So we have HPV. HSV. And then, um HIV, HPV. HPV is the herpes. Um, sorry, not, it's not the herpes simplex virus. That's HSV. My mistake that HPV is the human papilla virus. And symptoms include painless warts which um can be discomfort, um uncomfortable and can cause irritation with HPV. It can be asymptomatic. Um HSV, which is a herpes simplex virus is caused by um which is just herpes in general can cause small blisters that are red and can be, can leave open sores around the genitals. And with women, um you can have abnormal vaginal discharge and pain when you pass urine on the right eye included the pathophysiology of that. Ok. So with um HIV, we do have the primary infection and then the chronic infection uh with HIV, as I mentioned earlier, it's they infiltrate and affect the um T helper cells. They replicate very rapidly and your body can produce um molecules and particles to fight this. But because it is viral and it is, it does replicate within the T helper cells. It's very hard to um manage and there is no cure for this with the chronic infection. This take, this takes place after several years and this is when there's a very low T helper cell count and you're very much so asymptomatic. Whereas in the primary infection, you have flu like symptoms and fever and muscle joint, uh muscle joint pains and with HIV, it does progress into AIDS, which is just overall immunosuppression and your body is just not able to fight the overall disease anymore. Um I have put the overall cycle of HIV. Um as I said, it binds to the CD four receptors, T helper cells and it then replicates within these cells using reverse transcriptase to convert H IVR N to HIV DNA. Once it's done this, it will use integrase enzyme to then, to then integrate the O DNA into the cell replicate and then burst the cell to um basically take over the whole system. Ok. Now, moving on to hepatitis, there are different types of hepatitis. We have hepatitis ABCD and E A&E are very similar and then HBC and D um are also um have similar symptoms and overwhelm um presentation with HAV and H um H EV. It's fecal, it's an fecal oral spread. And the symptoms include nausea, fever, vomiting. And I have put the, if they are chronic or if they're not chronic and the overall complications of them on the right HP BV and HCV, as well as H DV, are transmitted sexually and they do have similar symptoms such as joint pain, loss of appetite, nausea and vomiting. All three of these are, can be chronic, which is something that you do need to remember and something that makes them different to HIV and H EV. Um complications can be liver failure and liver psoriasis with all three. So they are taken very seriously. Oh um Now on to crowns. So, prions are just in general, they are misfolded proteins. Um And these misfolded proteins can cause neurodegenerative diseases. Um because it causes proliferation of astrocytes and microglia and they also cause amyloid plaque, build up on the bottom. Right. I have included an image that shows um what, what disease it causes and what area of the brain due to these misfolded proteins with PS, we do have normal PS in our body already and these are P RPC variants of PS where the reason why these neurodegenerative diseases do take place is because these are converted to prion, scrappy variants of prions. And these are the um abnormal proteins. They are, they proliferate abnormally. They can cause um um cellular death. A new a neuron death. And the overall symptoms for prions and any type of prion disease is um anxiety, ataxia, memory loss and dystonia. I do want to mention though that these symptoms are not the usual case. It's usually asymptomatic, but it can present with these other symptoms here. Um So overall treatment when talking about infections in general, so we'll start off with a antibiotics when it comes to antibiotics. They do have general purposes. So they will either target the cell wall, the ribosomes, the enzymes or the cell membrane. When it does target the cell wall, it will inhibit cell wall synthesis. If this is inhibited, um there will be a disruption of the pep that glycan cross links. So there won't be a cell wall and then the bacterial will die as there's no protection with the vs pro there's sim um inhibit of protein s synthesis um with enzymes and G DNA and RNA synthesis is is inhibited as well as other metabolic pathways. And when with the cell membrane, it's disrupted which can cause um leakiness as or sometimes holes can be punctured as well. So the contents of the bacteria will leak and it will die. Um So I have made a table and it just includes some antibiotics on the left, the different types. And I've put an example for each of them. Um It is important to just remember these and remember as much as you can, the more you look at it, the easier it is to remember and just remember the overall target as they are, they do have different. Um They do target different parts of the bacteria. For example, penicillin, it ba it targets the bacterial cell wall um prevents the bacterial glycan cross links from being produced. So the cell will, will disintegrate. Oh um So when it comes to antibiotics, there is a concept called antibiotic stewardship. And this is just uh when the optimal selection dosage or duration of antimicrobial treatment that results in the best clinical outlet for the treatment or prevention of infection. And this has to take place with minimal toxicity to the patient and m minimal impact on subsequent resistance with good stewardship. The basic principles include the um encouraging the treatment of narrow spectrum drugs and limiting, limiting the side effects that can take place. Um So I have included an image that just talks about the overall immunity um that takes place when um a vaccination is administered um with vaccines, they, their general role is to just train your immune system to create antibodies. And it's done this, it does this when you are then exposed to the disease later on if that does happen. Uh So I've included a table which just summarizes um the different types of vaccinations. Um There are four main types of vaccinations and that includes attenuated vaccines, Toxoid vaccines subunit and recombinant um vaccines. They all have different roles that generally links to the name of the vaccine. So attenuated vaccines, they are just um a weakened form of the pathogen. And I've included advantages and disadvantages. So an advantage of this vaccine is that only one dose is required as the immunity is strong and it lasts for a long period of time. Um The disadvantage of this though is that it's not um suitable for immunocompromised patients and it can cause a form of resistance. As at the end of the day, it is a foreign particle to your body. So it can cause um an unwanted immune response with Toxoid vaccines. It's in it's mm sorry about that. Sorry, I'm sorry. That's just um with to uh toxin vaccines. It just within these vaccines. It just includes the toxin of that specific bacteria that is released from it. Um and this will just allow your body to get used to that v uh toxin to reduce the um required molecules for that. The advantages advantages of this is that it can be used with other vaccines to just boost your immune system. However, you do require a large, a large dose of this. As at the end of the day, it's not targeting the bacteria itself. It's just targeting the toxins produced from the bacteria. Um Subunit vaccines are just inactivated vaccines that contains antigens of the pathogen. And a disadvantage of this is that they, if it is de denatured by the immune system, it doesn't have um an oval, it doesn't have an overall point of being in your system anymore. It's no longer useful. Um And then with recombinant vaccines, the role of this is that it has the pathogens genes in the vaccine. And the advantage of this is that it can be produced in large quantities and the risk of it being harmful is very low and with, with a, it just enhances the immune response to the vaccines. OK. Thank you. That's a summary of infections. If you do have any questions, um you can put them in the chart. Thank you very much Jasna for your presentation. Um Does anyone have any questions for Jasna at the moment? If you do, you can pop them in the chat or you can unmute yourself and ask? Uh Yeah, you will be getting the powerpoints. Uh Where would you be uploading that? Um So they will all be available on metal, both the powerpoint and the recording for this session as well. So we'll be posting that later today or tomorrow, but by the end of the weekend, for sure, Jasmine, I'll be staying online for a little while to, uh, discuss with you and give you some feedback if that's ok by you. Yeah, that's fine. So, has the, uh, session closed yet or? Um, the, uh, I'm not sure. I can't see, you can't see me. I can see you. I don't see.