Rheumatic Fever | Etiology, Pathophysiology, Diagnosis | Retired

[Music] hi engineers in this video we are going to talk about acute rheumatic fever we're going to go into detail particularly on the pathophysiology of it we'll talk about some signs and symptoms and then we'll go into diagnostics all right so let's go ahead and get started so what is rheumatic fever rheumatic fever is a inflammatory condition that can be in response to streptococcal pharyngitis particularly group a beta hemolyticus streptococcal bacteria we'll get into more detail on this so let's say that somebody gets a strep throat whenever they get strep throat their body has a response to that they produce antibodies against the actual foreign bacteria mount the immune system and then try to destroy the bacteria however we're going to need antibiotics in response to that right so we need to treat with antibiotics now here's the thing 97 of the population respond properly to it by producing antibodies against the bacteria itself however in three percent of the population they can have this condition where they produce antibodies not against only the bacteria but against other tissues that have antigens or proteins that mimic the antigens of the actual bacteria so let's go ahead and start off with this whole process so what is the most common etiological bacteria that leads to strep throat that bacteria is called group a beta hemolyticus streptococcal bacteria but specifically streptococcal pyogenes streptococcus pyogenes literally means that it's pus forming now what does beta hemolyticus mean if you were to take this bacteria and you put it on a blood auger so microbiology right you have like a let's say here i have a blood auger plate and on this blood auger i have obviously what it says i have some red blood cells so here i'm going to have this all right here kind of highlighted here in this dark red i'm going to put some red blood cells there what i'm going to do is i'm going to take the group a beta hemolytic streptococcal bacteria and i'm going to put it in here on top of this bloodhocker what it would do is is you would go back and look after look at it after it's properly incubated and you would see these white spots what that means is is that the actual bacteria produced a protein and that protein is called strepto lysin and what streptolycin does is it causes the hemolysis of bacteria particularly what's called beta hemolysis so to understand this group a beta hemolytic streptococcal pyogenes is a bacteria that causes streptococcal pharyngitis strep throat what is this name coming from the beta hemolyticus is because if you take the bacteria you put it on a blood auger microbiology wise you let the bacteria incubate it'll start breaking down the red blood cells by producing an enzyme called streptolysin that breaks down the bacteria via beta hemolysis there is another process that's called alpha hemolysis but it doesn't really break the bacteria down you can think about it kind of like bruising or just beating up on the red blood cell but it doesn't completely lyse the actual red blood cell okay now what happens normally is we have this actual bacteria this bacteria has particular antigens on it okay these little blue antigens here we call m proteins they're called m proteins and these are the antigens on the streptococcal pyogenes that activates particularly our immune system now what happens is you'll have this bacteria he'll start producing tissue damage right so he'll start producing tissue damage when you damage the tissues what does it do it triggers an inflammatory response right so they'll be the production of leukotrienes they'll be the production of prostaglandins they'll even be the activation of mast cells so you know you have mast cells in the connective tissue those mast cells upon stimulation will release massive amounts of histamines and what will this do in response it'll increase the inflammatory response it'll cause the blood vessels in the area to dilate and to increase their capillary permeability so now you'll have more blood flow right so this is going to do two things increase blood flow and increase permeability the whole purpose of that is if we have more blood flow we have more white blood cells we have more complement proteins we have more uh immune system structures coming to the area if we have an increase in permeability that allows for a lot of our white blood cells and complement proteins and immune system molecules to leak out of the capillaries and into the tissue spaces to start breaking down that bacteria so that's the first thing that's going to happen now after we initiate this immune system response guess what white blood cell is going to come to the area this is going to be your macrophage so there's going to be the macrophage and there's another cell that comes to the area as well he's even more in concentration in this area and that is going to be your neutrophils okay neutrophils are they love to break down bacteria so what happens is your neutrophils and your macrophages will come out and they'll actually undergo phagocytosis of the actual streptococcal bacteria now once they undergo phagocytosis two things will happen if you guys have watched our inflammatory videos or videos on inflammation we've talked about how whenever the neutrophil will phagocytose the actual bacteria it'll take it in and it'll use a lot utilize what's called lysosomes those lysosomes will then break down the bacterial cell wall and then what it'll do is it'll exocytose all the remaining antigens so what it's going to do is it's going to break that bacteria down and through exocytosis it's going to release these antigens so it's going to release these antigens that freely circulate through the lymphatic circulation and into a regional lymph node okay within the throat the macrophage is a little bit different he's a little bit nicer he's more polite what he does is he engulfs the bacteria right breaks it down with the lysosomes and then it activates the gene on chromosome number six to produce mhc2 molecules and what will happen as a result of this is it'll activate the hla2 genes or the mhc2 genes on chromosome number six and cause it to produce a protein called an mhc2 molecule and that mhc2 molecule that it's going to produce is going to harvest a particular molecule on top of it so let's do this one here and brown so here we're going to have this protein like this and this is going to be called the mhc2 molecule presenting onto that we're going to present that antigen that comes from the bacteria and we'll present this here in that bluish color so now it's going to have the antigen presented with the mhc2 complex this is our macrophage so neutrophils exocytosis macrophages are going to engulf it and present to with the mhc2 complex and the antigen now what will happen you have some really important cells that are located within your lymph nodes these are called t cells our t cells are really important because they have specific proteins that allow for them to recognize that mhc2 molecule that specific protein molecule is called cd4 so it has a cd4 molecule which helps to be able to react with the mhc2 it has another molecule which is specific to react with this foreign antigen and this is called a tcr a t cell receptor now based upon this interaction as well as co-stimulatory reactions between b7 and cd28 there's a massive amount of cytokines being released we're not going to go over all the cytokines in detail it's not necessary but what i want you to know is there is going to be the massive release of cytokines by these t cells if you really want to know interleukin-1 is what stimulates this actual t cell and the t cell will produce many many different cytokines interleukin 2 interleukin 4 interleukin 5. the whole purpose of this is that these cytokines are then going to go and activate specific cells located in this actual lymph node and this is going to be our b cells so here we're going to have our b cells so right here we're going to have the macrophage right so this is our macrophage this is our t cell our t helper cell and then again this is going to be our neutral fill these interleukins they stimulate the b cells right and what happens is these b cells when they're hit with all of these different types of cytokines what it does it tells the b cells to start proliferating so they undergo clonal expansion and then it triggers them to differentiate what does that mean it means that they turn into what's called plasma cells plasma cells are really really important cells they have a lot of rough endoplasmic reticulum because they're protein-producing factories and whenever these guys are differentiated and they're also going to be stimulated by the cytokines so let's actually draw an arrow there these cytokines will also stimulate not just proliferation and differentiation but it'll also stimulate antibody production so now this plasma cell is going to start producing antibodies and these antibodies are designed to do what well they're designed to go and attack this actual antigen and then tag it for what to enhance phagocytosis of the macrophages to activate the natural killer cells to enhance the complement proteins to produce membrane attack complexes and to elicit more inflammation to bring more white blood cells more complements more inflammatory mediators to this area to break down the bacteria that's the overall goal and 97 percent of the population will properly respond to this however three percent of the population unfortunately will have these antibodies directed to other tissues for reasons we're not completely sure of the only thing that we've been able to elicit out of this is that it might be related it's specific in children that's one thing so one of the things that we've been able to elicit for the reasons why this can occur is it's specifically common in children peak age of 5 to 15 years old is usually the average age range another thing is we've seen it in situations of poverty and in areas of where there's overcrowding populations so these are the common theoretical reasons of why we believe that this three percent reaction occurs but now guess what happens these antibodies we said that they're designed to be able to attack what the proteins on the group a beta hemolytic is streptococcal bacteria however those proteins in our body we have proteins that mimic that actual protein on these bacteria in other words it looks very similar so our antibodies will love to attack those different areas that have proteins that mimic it what do we call this it's very simple it's called molecular mimicry so what's going to happen is in that three percent reaction we have this thing called molecular mimicry in other words it just means that if i have a tissue cell here and let's say that i draw that bacteria just a crude diagram here all right so here's my tissue cell and here's the bacteria i might have an antigen present on this group a beta hemolytic of streptococcal bacteria that is very very similar to an antigen that i have on my own host cell that's the problem so where are these actual tissues and what are these proteins that are maybe mimicking the bacterial proteins well one is in the skin and what is the main protein in the skin keratin so one of the big things that you'll see is is that these antibodies will deposit and actually have an interaction with the keratin right it'll interact with the keratin within our keratinocytes within our skin cells that's going to produce specific skin lesions and we'll talk about what skin lesions will see when we go over the different target tissues in more detail the next thing is it can target proteins with inside of our actual central nervous system you know there's these really really important structures with inside of our central nervous system called the basal ganglia they're really important specifically for being able to coordinate movements specifically preventing overshooting and undershooting of the motor movement dampening the motor movements they're really important with that well they have proteins very similar and they call these proteins ganglioside proteins ganglio sides the particular one is called lysoglioside proteins and this can produce what's called we'll talk about in a second but they call this cindenhams chorea and we'll go over what this means the next thing is you have proteins and the heart tissue one of the serious tissues that is affected here is it can affect the endocardium the myocardium and the pericardium all three layers so they call that pancarditis but there's many different proteins here so some of them to name a few is laminin laminin is a really important protein also what's the proteins of the muscle cells so you're going to have tropomyosin is a big one tropo myosin um myosin maybe even actin troponin we can have some of these proteins being attacked and that's going to lead to what kind of situation we call this when it affects all three layers we call it pancarditis pan carditis the last one is it can affect the proteins particularly within our actual synovial joints particularly the large joints which have a protein in it which is called vimentin so it's called vimentin and whenever this antibody attaches to the vimentin within the synovial joints it produces what's called poly arthritis and particularly migratory polyarthritis and we'll go over that okay so we should really understand what happens again with this whole path of physiology bacteria has the opportunity to damage the tissue right it starts damaging the tissue triggers an inflammatory response increases blood flow permeability more white blood cells more compliments come to the area what specific white blood cells are going to be in this area in high concentrations macrophages and neutrophils macrophages and neutrophils engulf the bacteria neutrophils they just undergo exocytosis of the remaining antigens because they under they break it down with the lysosome and reactive oxygen species macrophage engulfs it breaks it down with lysosomes and presents it on the cell membrane with the mhc2 complex and then it takes it to a regional lymph node where it presents it to a t helper cell interacts via the mhc2 cd4 tcr antigen interaction and releases a massive amount of cytokines that turn b cells into plasma cells and stimulate the plasma cells to produce antibodies those antibodies are directed against the antigens the m proteins with inside of the respon for the actual streptococcal bacteria but there's other antigens in some situations three percent of the population and children impoverished areas and overcrowded populations where those antibodies can attack proteins or within our tissues that mimic the actual proteins on the bacteria such as keratin within the skin the ganglioside proteins like lyso ganglioside proteins and our basal ganglia the laminin tropomyosin myosin actin all these proteins within a heart tissue and then the vimentum within the actual joints and this is called molecular mimicry okay now what we need to do is is we need to talk about a little bit more about this tissue damage go over these in a little bit more detail and then after that i want to talk about what's called the jones criteria of how you'd be able to diagnose rheumatic fever all right so let's go ahead and move on now to the heart all right so like i said it damages the heart tissue here's the thing when those antibodies are directed against our heart tissue 50 to 60 percent of the symptoms that arise from rheumatic fever in response to streptococcal sore throat or streptococcal pharyngitis is with respect to carditis so again just remember that 50 to 60 percent is usually going to be presenting within the symptoms of the heart disease and this is actually one of the big ones because what can happen is rheumatic fever over consistent and recurrent attacks can lead to what's called rheumatic heart disease which is no bueno not a good thing you don't want it okay and we'll talk about why so let's go through here we said that it affects the uh all the three layers well if you guys go back to your anatomy what do we have we have the pericardium first so the first layer is going to be the pericardium now just a little bit on your anatomy what are the two layers of the actual pericardium there's the visceral and then there is the parietal layer now what happens is is in between so here you're going to have this pink layer here that's going to be our parietal layer they're going to have that baby blue there that's going to be the visceral layer what's in between in between is actually going to be serous fluid there's going to be serous fluid and the serous fluid is called the pericardial fluid what can happen is whenever there is actually going to be inflammation of the visceral and the parietal pericardium it's going to lead to these layers becoming inflamed and whenever these two layers become inflamed whenever the card is going through systole contracting and diastole relaxing those two layers are rubbing up against one another and producing some intense inflammation a really stabbing chest pain that we can feel called a pericardial friction rub so one of the big things that i want you guys to remember here is that whenever these two layers rub up against one another it produces a very important thing called a pericardial friction rub and one of the important things about a pericardial friction rub is you can hear this upon auscultation so if you're auscultating and you're listening to the heart you'd be able to hear that scratchy sound of a pericardial friction rub okay so that's one thing is it's going to produce pericarditis pericarditis by causing inflammation of the visceral and the parietal epithelial tissue that isn't going to be making up the pericardium leading to inflammation rubbing up against one another producing friction that leads to the pericardial friction rub and this is a stabbing pain very very painful the next and the most serious one is the next layer here this muscle layer that cardiac muscle tissue called the myocardium so the myocardium is really important and the reason why is it is the the the pump of the heart it's responsible for contracting and ejecting blood out of the heart what happens is is those antibodies again can start damaging the tissue of the myocardium and you can imagine that whenever it produces this damage it produces a specific type of necrosis you know what they call that they call this fibrinoid necrosis fibrinoid necrosis there's a lot of fibrinogen deposited into the area but another thing is there's a lot of inflammatory cells into the area what you'll actually see is you'll see what's called if you take a slide you'll have what's called ascio bodies okay so let's say i took a slide here and i looked at the slide what i would have histology wise is i would have this area of fibrinoid necrosis so let's say that here is going to be this area of fibrinoid necrosis so we're going to have a lot of fibrinogen deposited into this area here okay the next thing you'll have here is you're going to have these things called initial bodies and knit shell bodies or knit shell cells and all these are are like these caterpillar-like uh uh macrophages so you're gonna have these caterpillar-like macrophages and those are called your init sow shells uh knit a knit chow cells another thing you'll have in areas you're gonna have a lot of t cells in the area so you're going to have a lot of t cells so what is this whole thing here called this entire fibroid necrosis which consists of a lot of fibrinogen some t cells and some initial cells which is going to be these large caterpillar-like macrophages this is called ash off bodies this is called ash off bodies okay why is this very serious because imagine if you produce a lot of fibrous tissue with a lot of this inflammatory mediators in the area a lot of the actual immune system cells is this tissue able to contract no so what's going to happen if it starts becoming more widespread it's going to lead to the myocardium not being able to contract enough what does that mean then remember when we talk about cardiac output that you have what's called preload so preload is the degree of stretch well you're going to have a lot of fibrous tissue it's going to decrease the stretch now your contractility is going to decrease because now you're losing a lot of the actual myocardial cells as a result of that that's going to decrease the stroke volume if you decrease the stroke volume you decrease the cardiac output why is this dangerous because over time if it continues it can lead to congestive heart failure and that is no bueno right we don't want that and that is the the severe really problematic thing here with the myocardium okay so myocardium you get fibonaccis with ash off bodies over time it can lead to a decrease in the preload which is a decrease in the stretch a decrease in the contractility because of loss of myocardial cells a decrease in the stroke volume decreasing the cardiac output and then eventually over time it can lead to just complete deficiency in the pump adequacy and that can lead to congestive heart failure the last thing is it can affect the endocardium so it can also affect the endocardium now the endocardium is the inner lining of the heart one of the big things is is it loves to attack the valves okay it loves to attack the valves so what does it do to the valves let's pretend here i have like a um a drawing here of the valve so i'm going to kind of put a valve right here all right and then we're going to put a valve right here what happens is and you have this thing connecting the two you have an annulus fibrosis ring so here is going to be a ring this is going to be the annulus fibrosus ring and i'm taking a section i'm taking a section here of the heart valves so here's our heart valves what happens over time and here we'll have our chordae tendineae what happens over time is that these valves start getting what's called rheumatic vegetations okay rheumatic vegetations and a lot of inflammatory cells into this area so this actual valve is going to become swollen it's going to have a lot of edema so the valve will become swollen so there's going to be edema consisting of a lot of inflammatory infiltration t cells macrophages right you're going to have these things called rheumatic vegetation so what are these things here they're called rheumatic vegetations another thing is over time these valves as the inflammation occurs it activates particular cells you know we have these things called fibroblasts and our fibroblasts when stimulated love to produce a lot of collagen and fibrous tissue what happens is this collagen starts actually causing this actual valve to become thicker so now we have the valve becoming inflamed we have vegetations we have a lot of inflammation and now we're activating fibroblasts to thicken the valves and here's where it gets really bad it can get to the point where if this is recurrent recurrent recurrent episodes of rheumatic fever where this actual fibrous tissue in this uh collagen bob thickening can lead to stenosis of the valve okay so what can happen with this it can actually over time lead to stenosis and and also it can lead to regurgitation right now what valves are primarily affected within the endocardium it's specifically the left heart what is this valve right here the mitral valve right what is this valve right here the aortic valve so what you'll notice over time is that it's going to specifically target two valves one is the mitral valve or the bicuspid valve and the other one is going to be the aortic semilunar valve now again what we know the severe thing with this is that it becomes swollen or atomacious valves they can actually start causing rheumatic vegetations there's a lot of immune cell infiltration there's fibroblast activation which is going to produce fibrous tissue that is actually going to thicken the valves make them more stenotic particularly the aortic valve and the mitral valve it can produce mitral valve stenosis or regurgitation or aortic valve stenosis and regurgitation another really bad thing is it produces these types of fibrosis that we call commissural fusion it can literally cause the actual valves if you kind of imagine it like this let's say i draw kind of a upper view of a valve so here i'm going to have let's say here is one valve flap and here's another valve flap right here and here's the hole between the two what can start happening is this is supposed to be the actual hole where the actual blood is flowing through but over time because of that fibrosis it can start producing fusion here at the edges and that is called commissural fusion so this can lead to what's called commissural fusion now you can imagine how serious this can be they can lead to the point where the valve does not even open and that is not good another thing that can happen over time if there's repeated bouts of rheumatic fever is it can lead to what's called subacute bacterial endocarditis so here's the big big thing that i want you to remember to take away from this for the rheumatic condition is that over time the thing that you worry about is sub-acute bacterial endo this is the scary scary thing with this condition because over time with repeated inflammation and attacks it's going to lead to the valve becoming so damaged that eventually it starts leading to actual septic vegetations bacterial vegetations that can then break off lodge within the pulmonary vessels lodged within the cerebral vessels and become extremely dangerous and and fatal okay so that's why when we talk about management we'll talk about prophylaxis to if there is recurrent attacks to prevent subacute bacterial endocarditis because that's our fear okay so that's how we can affect the actual heart so that's the pancarditis effect the next one is how does it affect the actual central nervous system so if you remember inside of the central nervous system we have a couple different areas right we're not going to go into crazy detail but if you know we have a specific area here which is going to be really really important and this is going to be called the lentiform nucleus so you know you have what's called the linty form nucleus and the lentiform nucleus is made up of two things the putamen which is this outer part here i'll highlight that in this um bluish color here so the outer part here is the putamen and then this inner part here is broken into two layers that's called the globus pilitis so the globus pellitus externus is this green one and then the globus pelitus internis is this most inner one these are really really crucial part of the actual basal ganglia it's called the lentiform nucleus another important structure here is going to be what's called the caudate nucleus so another one is going to be what's called the caudate nucleus so caudate nucleus and another important area here is going to be just below the thalamus let's put my thalamus here is going to be called the subthalamus so that's another really really important structure here right below the thalamus is going to be what's called the sub thalamus now we already said that there's proteins like the ganglioside proteins that the antibodies come in and attack so they attack the lentiform nucleus the caudate nucleus the subthalamus all of these are important with being able to control what's called our direct and indirect pathways which help to prevent the overshooting of the movement the undershooting of the movement and help to provide smooth motor movements right well if we frack that up it's going to start really messing with our movements now they're going to be what's called really jerky because what happens is they helped mainly they helped to play a role within preventing like unwanted motor movements so now what we're going to have is we're going to have damage to these areas and that produces a condition that we refer to as sending hams chorea and this affects three percent this is about three percent of the symptoms that have rise from uh rheumatic fever now what this characterizes is it controls its uncontrolled kind of jerky movements uncontrolled jerky movement so what is that let's write this down here uncontrolled rapid jerky movements and particular areas of the body one is the face also the tongue and the upper limbs okay so it's going to produce these uncontrolled jerky rapid movements of the upper limbs the tongue and the face so one more thing i want to make sure that i mention before we move on to the joints is i wanted to come back to the heart remember we told you we said that there was this stenosis possible stenosis regurgitation from all of the stuff what we already mentioned i just wanted to make sure that we don't forget another thing that can happen over time is this chordae tendonite can become really thickened and that also can become a problem with contractility as well as the valvular function so over time what can happen is this can lead to chordae tendineae thickening so let's write that down there the chordae tendon a thickening and again this is just going to add on to the fact of the mitral valve issues particularly with the stenosis or regurgitation just adding on to that fact okay all right so the next thing we know is we said that it could actually attack the joints this is the really really important one some of the first signs they usually appear rheumatic fever can usually appear about one to four one to five weeks post streptococcal pharyngitis usually the first signs to arise is a fever rheumatic fever and joint pain now one of the big things about 75 of the cases 75 of the symptoms that usually develop is going to be via this polyarthritis so one of the big things that you'll see here is what's called poly arthritis so it's going to produce a lot of tissue damage here right we said that it has the um the vimentin that it's very similar to so it's going to cause inflammation of the synovial joints which synovial joints particularly the larger synovial joints so obviously this would be your hips your shoulders those are going to be some of the ones that are really really affected here another situation is is in here let's put it down so it can really affect the hip joint and it can also affect the shoulder joint another thing is that it's migratory okay so it's migratory it can spread now this is important to realize that polyarthritis is different from the normal just kind of like arthralgia that we feel right this is going to evolve a lot of large synovial joints it's going to be migratory it's not just going to be pain over the joint all right so that's really important to realize so 75 of the symptoms usually develop with this polyarthritic pain of large synovial joints hips shoulder and it can be migratory all right all right so now we know that they can develop the tender you know joints to polyarthritis large hip joints migratory the last one that i want to talk about for the major criteria here is for the skin lesions now it can affect the epidermis and the dermis what it does is it leads to this really like interesting rash this rash is called an erythema marginatum so we call this erythema marginatum it's kind of like a annular concentric ring like rash okay what do they call this they call this erythema marginatum and this can appear on the skin so it's a skin lesion and it particularly occurs on the extremities extremities so upper and lower extremities and it can appear on the trunk of the body okay so the trunk of the body and then the upper upper and lower extremities the next thing is is you can also develop this collagen deposits so you can develop these collagen deposits particularly around the area of the subcutaneous tissue so now you're going to get these collagen deposits and these things are really really interesting they are called subcutaneous nodules so there are a lot of collagen deposits going to can attach to the fascia and the underlying bone tissue and again these are called sub cutaneous nodules and they usually appear on the extensor surfaces of our body so like the back of the wrists they can appear on the elbows usually on the side of the elbow is another common area so the elbows and the knees but in general you can find these in a lot of places sometimes they can be really superior severe and appear on the actual vertebral column okay so these are some of the big big signs that you'll see here okay so just uh it's going to see your skin lesions erythema marginatum it's going to appear in the extremities in the trunk the subcutaneous nodules which are going to be collagen deposits that can be attaching to the fascia underlying bone back of the wrist elbows knees your polyarthritis is another important one which you can affect the larger synovial joints hip shoulder and again remember that it's migratory all right so the last thing is we've already been able to notice how this actual the pathology all plays out i think we beat that like a dead horse so now what we need to do is we need to kind of get into how we would diagnose it just based upon our clinical understanding okay so what we do is we follow the specific criteria they call it a jones criteria let me write this over here for a second so we have to follow this thing called a jones criteria and what this criteria says is that in order for us to kind of be able to make a diagnosis we need an option we have an option we have two options here one is we need two major criteria or we need one major criteria plus two minor criteria and i'll explain what's that what that means okay all right so here's a nice little way of being able to remember this there's all these special ways out there now that we can kind of figure things out so jones jones kind of tells us our actual major criteria so here's what i want you to remember jones j for joints what's that polyarthritis that's one of the big big signs so oh if you can kind of think about it it kind of is myocardium it's the heart so for the o we're going to really kind of go to myocardium another thing i've also heard is that if you look at the o if you put a little dimple into it it can look like a heart so you can also think here myocardial right so that's another important one but in general don't just remember that it's just the myocardium it's all the heart layers so this helps you to identify this part but remember that it's really pan carditis the next one is n in for nodules and the nodules is going to be particularly the subcutaneous nodules e for erythema marginatum which is that skin lesion that we saw an s for sindenham's chorea as for cindenhams chorea okay so the jones joints o for myocardium kind of looks like a heart if you make a little dimple pan carditis nodules for subcutaneous nodules e for ethema marginatum sindin hams or s for sin and hands chorea this all of these are our major criteria so all we would need is two of these and we could diagnose dramatic fever so some of the minor criteria that we want to possibly consider is remember it can produce fever it can activate our hypothalamic area right the hypothalamus and trigger the actual resetting of our body's thermostat so fever is a really really important one another one is going to be arthralgia which is just kind of your joint pain all right so arthralgia another one and this one's really kind of interesting is because it can affect the heart right the pancarditis it can alter with the electrical system the conduction system of our heart and what it can do is is it can produce a prolonged pr interval so prolonged pr interval so if you know here you have your p wave right at the beginning of the p wave you have here at the end of the p wave you go here pr segment and then from here we go qrs wave and then t wave so the pr interval is from here all the way till here that segment there is going to be prolonged so there's a prolonged pr interval here's another really good one remember we told you that over time it can start to cause valvular dysfunction so another big issue here so we have fever arthralgia prolonged pr interval another one is it can start to produce valvular dysfunction particularly what valves again mitral and aortic semilunar valve and what's another big one whenever there is inflammation this kind of inflammatory condition our liver responds to that by producing two things one is it produces what's called c-reactive peptide it's a it's a acute marker for non-specific types of inflammation it can be slightly specific for myocarditis or for fevers bacterial infections and things of that nature but it is going to be a marker of acute inflammation so crp levels would be elevated okay so if we did a lab if we did some labs right we would find that their crp levels would be elevated another thing is the liver also makes a protein called fibrinogen what happens is when we do a test we do what's called the erythrocyte sedimentation rate so what you do is is you take red blood cells actually let me go ahead and explain this to you so how this erythrocyte sedimentation rate works really quickly so imagine i take red blood cells i take a test tube all right here's my test tube i take some red blood cells right and when i take these red blood cells i'll put them in a test tube and i'll let them fall to the bottom of the test tube by gravity in situations like an acute inflammation our liver produces a protein called fibrinogen what happens is fibrinogen actually causes a lot of these platelets to start sticking together and these these i'm sorry not platelets red blood cells these red blood cells start sticking together and they kind of make like this little linear like tube like they stack up on top of one another this is called a rouleaux formation now why is that important because as this fibrinogen is actually causing a lot of these to stick together to form this reload now look at the density of this it's going to have a lot of proteins weighing on it it's more aerodynamic it can actually fall a lot faster so because of this that is actually going to fall to the bottom of the test tube a lot faster than normal the rate at which the red blood cells fall to the bottom of the test tube is called the erythrocyte sedimentation rate but if you increase the number of fibrinogen molecules based upon inflammation right so inflammation stimulates this produces fibrinogen causes the fibrinogen to stick to the red blood cells for meru drops down to the bottom what happens to the esr it goes up so that'll show us that there is some signs of inflammation so if we detect if we did like a test like that we would find that they would have an elevated erythrocyte sedimentation rate now this is our minor criteria so all we would need to be able to come up with the suspicion of possibly having rheumatic fever is two major criteria or one major criteria and two minor criteria other things that you can do to help with the diagnosis of this is you can do some tests because another thing actually one more thing i forgot and this is really important i'm going to put it over here on the side is you have to have evidence of post strep infection right because we said that this is most commonly due to strep throat so you need evidence of this so what would you do to determine that well you could do what's called a rat a rapid antigen test and all it does is you just do a quick test where you determine to see if there is any of the antigens present on the streptococcal bacteria that should be positive so you should have a positive rapid antigen detection test another thing is you should have a positive culture and sensitivity so you should culture do a culture if you get a culture you'll find that they'll have a positive culture and sensitivity another thing that we can do is we can test their anti strepto lysin o titers so we'll look to see that they're positive or have elevated anti-streptolysin o titers okay anti-streptolysin o antigen tighter elevation these are some of the things that we'll actually do look at okay so again two major criteria or one major and two minor criteria and one of the big big minor criteria is usually you need to have evidence of the poststreptococcal infection by doing either a rabbit rabbit antigen detection test positive culture and sensitivity and looking at their titers for the anti-streptolysin o antibodies okay if you guys like this video please hit that like button comment down in the comment section and please subscribe also go check out our facebook our instagram even our patreon account if you guys can actually donate a dollar we would truly appreciate that also go check 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Channel: Ninja Nerd

Views: 268,608

Keywords: Ninja Nerd Lectures, Ninja Nerd, Ninja Nerd Science, education, whiteboard lectures, medicine, science, rheumatic fever, rheumatic heart disease, fever, pathophysiology, etiology, acute rheumatic fever, usmle step 1, rheumatic fever symptoms, what is rheumatic fever, rheumatic fever pathology, Jones criteria, rheumatism, medical specialty, pathology, rheumatic, health, lecture

Id: aun61Xq8G3g

Length: 47min 35sec (2855 seconds)

Published: Tue Jan 05 2021