Inflammation - Vascular Events

Inflammation – Vascular Events



today we are going to discuss about the inflammation inflammation is one of the most important pathological process who will define inflammation for me you know doctors deal with inflammation every day every single day when they are practicing they are having the patience with inflammations so who will define what is inflammation anyone okay he says that whenever this swelling or this redness or there is heat some area is hot or red or swollen right and it is having loss of function so you think this is inflammation okay this is one way either some of the cardinal signs of information right I want to know what is inflammation it's a very basic process listen it's a very very basic process in which if anything injures your tissue listen now carefully anything which injures your vascular connective tissue tissue will response to the injury by producing inflammation I will explain in big detail what is inflammation first of all what is the basic concept related with inflammation inflammation is the response of vascular connective tissue towards injury that's it this is the simplest concept what is inflammation inflammation is a response of the vascular connective tissue towards injury regardless of whatever is the cause of injury whenever your tissue is damaged whenever your tissues injured inflammation is going to be there if your tissue is vascularized is there clear so again let's repeat what is inflammation inflammation is response of vascular connective tissue towards injury it means those tissues which are not vascular they want have inflammation but of course most of the tissue in our body are vascular so whenever any tissue in the body is injured now it is so important to understand any tissue in the body is injured and inflammation will be there it may be a central nervous system it may be a skin or it may be your GI T it may be kidney or any tissue in the body now any tissue in the body injured by any means injured by any mechanism or by any means will have inflammation if there's significant injury the cause of injury may be any type for example this is my hand you injure it physically or you for example you enjoy it but Rama physical trauma or you do some chemical trauma here the a three-door some strong alkali or you do trauma by the microbial invasion or you damage here by some immune process or you damage this tissue by radiation whatever the mechanism of injuries you choose to damage this tissue regardless of the cause of injury tissue will undergo a process of information now what is the whole purpose of inflammation white tissue undergoes and family response whenever it is injured actually inflammatory response is primarily beneficial to the organism the cause when a tissue is injured inflammatory response is one building up the defense against that cause of injury right for example lot of microbe enter here listen if there lot of microbes invading here and those microbe like Staphylococcus aureus Steph locust aureus if it enters here and produces toxins and damage the local tissue tissue will interview information now what will be the purpose of inflammation purpose of inflammation is to bring more blood to this area to bring more our defense mechanisms into this area especially for example inflammation will bring more plasma proteins in extrasolar fluid bring more blood more leukocytes to number one remove the cause of injury what further information is that either to remove the cause of injury or to neutralize the cause of injury or to wall off the cause of injury plus another purpose of information is that results of injury for example many cells due to injury are dead there another purpose of information is to remove those dead cells and pave the way for repair process so what is the whole purpose of inflammation inflammation is response of vascular connective tissue towards injury number one number two that inflammation inflammation process right is concerned with bringing over defense mechanisms at the focus of injury you know one of our major defenses are present in the blood complement 14 the present in the blood antibodies are present in the blood major defenses are your white blood cells they are present in the blood so tissue under cause inflammatory response so that blood vessels dilate microcirculation become more permeable and lot of plasma protein rich fluid goes into excess of fluid with lot of white cells go over there and there try to destroy the cause of injury or deluge the cause of injury or duval of the cause of injury plus information process helped to remove the injured tissues or remove the dead cell the necrotic cells so that they should open the way for repair process is that right now this inflammatory response is primarily divided into two types of inflammation inflammation is primarily of two types we say there is a huge information and there is yesplease chronic inflammation there's a cute inflammation and there is chronic inflammation acute inflammation is when due to injury vascular connective tissue develops a rapid response but transient response when the words the engineer to the tissue vascular connective tissue responses rapidly developing and it is short-lived so rapidly developing response to the injury and if response is short-lived we say there is acute inflammation so what is the cute 'information accurate information is rapidly developing inflammatory response which is of short duration opposed to that sometimes to certain in injury mechanisms and from military response last very long and when inflammatory response last very long we say that this is chronic inflammation so what is the real and primary difference in the acute and chronic inflammation primary differences the duration of inflammatory process if if there is injury to the tissue inflammation develops very rapidly and it is for short duration this should be considered acute inflammatory response opposite to that when tissues injured and primarily response develops gradually right and lasts very long we say then from it early responses chronic inflammation this is it clear now let's talk about acute inflammatory process okay let's suppose this is a tissue and in this tissue we'll see how inflammatory response develops again let's suppose in this area some bacteria have entered right and they are proliferating ends and producing toxins and damaging the local tissue and this tissue is going to develop acute inflammatory response to that microbial challenge so a piece of that tissue I have put on the board and we'll see what's really going on inside here again to start inflammation any type of injury may be there that may be physical injury it may be chemical engineer it may be radiation injury it may be thermal injury it may be microbiological engineer it may be immune mediated injury it may be a piece of necrotic tissue right and it of injury to any tissue in the body which is vascular will result into inflammation this is that right now let's suppose there's a piece of tissue here I've removed it from this area to which microbiological agents are doing injury we will see how then firmly responds develop right you already know that what will happen to the tissue the cardinal signs of inflammation you know it already everyone knows what are the cardinal signs of inflammation number one that there is there is pain is there right okay write it down here the cardinal signs of information first the cardinal signs of information is yes there's pain there is redness tissue become red and it become hard right wrong and it becomes yes swollen you should become swollen and there's a loss of function these finds five features right they are called the cardinal science or Cardinal features of inflammation especially acute inflammation now we'll discuss later the pain developed due to swelling plus it develops due to some chemical mediators are produced at the site of inflammation which irritates the nerve endings right we'll discuss about redness there due to arterial or dilatation increased blood is coming in to injured area and that produces redness and more blood increases the temperature locally and that is responsible for local area which is warmed and local tissue swell up because a micro circulation will become increasingly permeable and that will produce as excessive escape of fluid from micro circulation into local extra vascular area or interstitial area and eventually injured tissue because local cells are injured they don't perform the normal function so we see this loss of function another term which is used for this thing is pain is called also dollar it is not that dollar which you dream to our dollar redness is called ruber very good this temperature increases that is calor and swelling is called humor and of course this is not that tumor we are afraid of right if neoplastic growth produces tumor that is a different situation but in old times any swelling was called tumor and loss of function is called functio okay you know I don't remember spelling write it like this function lasya that function is lost of course if your hand is injured you do you think hand will function well no so this loss of function means this is that right now so these are just basic Cardinal features but we have to see what really goes in that tissue now we are going to study the real underlying mechanisms that when a tissue is injured why the pain develop why redness develop or temperature locally increase why there is swelling why there's loss of function right what are the underlying mechanisms when a tissue is injured and inflammatory process has been started so we'll study now as I told you that here's injury microbiological injury and we are removing a piece of tissue from here and I'm going to make a diagram related with that tissue right number one like all tissue this t-shirt should have arterioles coming to it is their right arterioles must be there should be vascular input this is arterioles coming to it and arterioles are breaking up into capillaries am i right these are capillaries I haven't lied this area so that so these are the capabilities which are with the arterial side then there are triple is in between then there are ends of such abilities towards the venous side which are also called win youth right when use which eventually drain into venous system so in this diagram I'm showing you the wasp her pattern of the tissue that there's arterial import there is microcirculation microcirculation represented by this black area and this is a venous drainage from the tissue is that right Plus this tissue is having parenchymal cells Paran as all tissue has parenchyma cells what are parenchymal cells you know a British was parenchyma cells and stromal cells what our parent camel cells yeah there are some special cells in every tissue which are specially functional cells of that tissue those special functional cell to any tissue archive parenchymal cells for example in the brain parenchyma Felda neurons in the liver parenchymal cells or hepatocytes is the right in the kidney parenchymal zelda nephron cells right in the skin parenchymal zelda epidermal cells every tissue as special specific functional cells which are called parenchymal cells plus in every tissue there are other cells which are supporting the parenchymal cells right and those cells which support the parenchymal cells and make the connective tissue within that tissue those cells are called the supporting cells are called stromal cells every tissue has two types of cells it has parenchymal cells then it has stromal cells parenchyma cell de the unique cells in a tissue which are specifically doing a function to that tissue and stromal cells are the cells which are just supporting the parenchyma cells for example in central nervous system neurons are parenchymal cells and glial cells are Sports stromal cells of supporting cells in the liver if you talk about parasites of parenchymal cells and in the liver all the wasp ler cells and plus macrophages in the liver and other fibroblasts all of them are stromal cells is the right in the same way in the skin epidermal cell er parenchymal cells but dermis is supporting the epidermal cell that is consisting of stromal cells emmaclaire now so in the same way in this diagram I have put a tissue here whether its arterial input where there's micro circulation we with venous drainage plus output here these black Zelda parenchymal cells and here there are stromal cells what could be the stromal cells stromal cells maybe mast cells stromal cells maybe some mass cells or stromal cells maybe some resident lymphocyte or promote stromal cells maybe some resident macrophages in this particular tissue right stromal cells now let's suppose this tissue injured then what will happen when a tissue is injured how the process of inflammation start right let me tell you whenever a tissue is injured it means whatever the cause of injury let's suppose these are bacteria here right and these bacteria are damaging this they are producing the toxic substances these toxic substances are damaging the parenchymal cells as well as they're damaging the stromal cells so what will happen from the membranes of parenchymal cells the stromal cells prostaglandins will be released now listen carefully when you damage my my hand the injured cells within the cell membranes of the injured cells special enzymes are activated and the start producing prostaglandins the start producing Luca trains when mast cells are injured by any mechanism listen mast cells may be injured by any mechanism they will start releasing preformed histamine they start releasing proteome proteolytic enzymes mast cell membranes will start releasing prostaglandins mast mast cell membranes will start releasing leukotrienes they will start releasing platelet activating factors and even when stimulation of the mast cell all macrophages resident macrophages or lymphocyte is there these cells will start releasing cytokines the start synthesizing interleukin 1 they will start synthesizing tumor necrotic factor is the right so what really happens what I'm trying to tell you that whenever you injure any tissue by any mechanism the local cells in the tissue start producing chemical substances which will mediate different steps of information so it means injury to the human cells either to the parenchymal cells injury or to the stromal cell injury whatever the mechanism of injury these cells start producing mediators of inflammation right what are these mediators of inflammation I have just spoken few of them that if these these are the bacteria which are multiplying they are damaging the parenchymal cells they are damaging the stromal cells and these injured cells start releasing chemical substances which will mediate the inflammatory response you are getting here so prostaglandins concentration in the injured tissue become high histamine leukotrienes concentration in injured tissue become high right histamine concentration in injured tissue become high and gradually cells stromal cells specially mast cells in tissues and macrophages and lymphocytes which are resident cells they also start producing tumor necrotic factors and interleukins so what really happens that at the site of injury from the injured cell membrane prostaglandins and leukotrienes are released platelet activating factors are released from mast cells preformed histamines are released and nuclear machinery is activated in the injured cells and specially stromal in yourself start producing interleukin and to manic rhotic factors these are right in the same time as we will discuss later when lot of complements will come into this area they will leak from the blood to this area those complements are broken down into active product which can also mediate certain steps of inflammation is that right so what really happens that at the site of injury from the cell membranes of the injured cell from the granules of the injured cells and from the nuclear activation of the injured cells and also some plasma derived proteins all these factors produce lot of chemical substances which will mediate different steps of inflammation so we simply we can say that these chemical substances which will control and mediate the different steps of inflammation is a broad category such chemical substances are called chemical mediators of information what are these chemical substances called chemical mediators of information so I dare to repeat it once again you injure because it's worth it all your life you will deal with information either you become any speciality you will have some tissue which is injured and you are dealing with that is that right again even if you become radiologist and you are doing some radiotherapy to a patient you will produce information yes because the radiation can damage the tissue as well anyway let's come back in a nutshell what we have discussed a very simple thing and I don't know how to emphasize it further but I will repeat it once you damage any tissue by any mechanism right the vascularized connective tissue response will be inflammation what is the purpose of inflammation purpose of inflammation is to remove the cause of inflammation cause of injury or to dilute the cause of injury or to contain a wall of the cause of injury and remove the injured and dead cells and pave the way for repair this is right this is the whole purpose of information another way to state the purpose of information is that because of our major defenses are in the blood what are our major defenses certain proteins in the blood like complement proteins are present in the blood and immunoglobulins are present in the blood right plus major defenses are your white blood cells they're also circulating in the blood so purpose of inflammation is that inflammation should bring more blood to the injured area bring more leukocyte into injured area and poor these blood and leukocyte into at the focus of injury to remove or deal with the injurious cause and to pave the way for repair next step how the information start inflammation start the whenever tissue is injured injured parenchyma cells injured stromal cell right injured stromal cell may be mast cells may be resident macrophages injured stromal cell may be your resident lymphocyte injured stromal cell may be injured endothelial cells right there are also stromal cells so injured parenchyma cells plus injured stromal cells they start producing chemical substances right plus the plasma proteins which are coming there they also break down into certain chemical substances right all these chemical substances which are / derived from the injured cells and derived from the plasma all these chemical substances which are mediating the different steps of inflammation as a group they are called chemical mediators of information right let me tell you why it occurs in every tissue for example if I asked you where in our body mast cells are present yes please your irene is going to tell me where in your body mast cells are concentrated excellent mast cells are specially they are present all over in the connective tissue number one point and all the tissues in the connective tissue mast cells are present for Marcelle mast cells especially concentrated around the blood vessels around the nerves and under there all external lining of the body and under the all internal lining of the body under the skin mass cells are there under all the mucosal lining the lot of mast cells so what these mast cells are doing whenever you will enjoy the tissue the mast cells which are around the blood vessels or under the linings of the body they will be irritated and mast cells are very very sensitive whatever the mechanism of injury to them they will start pouring out and synthesizing and releasing chemical mediators of inflammation is that right we'll have a full lecture on chemical mediators of inflammation later the only purpose was this that engineers there and chemical mediators are produced now we will see what the chemical mediators of information will do they will control two major right steps and inflammation we can say the whole mechanism of acute inflammation whole mechanism of acute inflammation can be divided into to expand be explained by two mechanisms number one vascular changes vascular changes and number two white white blood cells events again tissues enjoyed chemical mediators are produced their chemical mediators will produce vascular events in the inflamed tissue there will be vascular events and there will be cellular event rather we should say cellular events in old times we should use to say white blood cell event but now I know in inflammation and all serious cells play a lot of role in inflammation your platelets play a role an inflammation mass cells play a role right so in a nutshell acute inflammatory process should have vascular changes and it should have cellular events especially white blood cell event now first I will explain the vascular events and then I will explain the cellular event which will occur in to this tissue after the injury is that right no first of all you know that these are deal input to the tissue arteriole they have lot of smooth muscles amirite arteriole the blood of smooth muscle and are the you know smooth muscle tone control the blood flow to any tissue is there right now at the injured side you need more blood or less blood you need more blood you want to bring more white cells there you want to bring more antibodies there you want to bring more complement there so chemical mediators of inflammation which are produced these chemical mediators number one will act on vascular smooth muscle sometimes after injury there is very transient with a constriction followed by prolonged with the relation this transient way the constriction is due to neurogenic mechanism which produces a little bit looser construction but usually after a few second whether dilation dominates right so what really happens that after the transient initial transient neurogenic visual construction right there is prolong significant visual dilation or arteriolar dilation why this arterial dilation is there because medical chemical mediators like histamine yes histamine prostaglandin e2 nitric oxide just to mention few are produced at the site of injury and these are strong or smooth muscle relaxer for the arterioles so arteriolar dilation will be there again let me tell you let's suppose if this is one smooth muscle here right this smooth muscle will have receptors for histamine it will have receptors for prostaglandins it will have receptors for nitric oxide okay let me make the smooth muscle here so this is a smooth muscle but actually it is circular smooth muscles right it will have receptor for histamines what kind of receptor the histamine salmon pass receptors which are covered with interest early with the G proteins prostaglandin receptors are what type of receptors yes please there are also seven pass receptors which are coupled with intracellular G proteins and nitric oxide receptor is the intracellular go in a lile cyclase so what really happen histamine or prostaglandins of nitric oxide activate certain receptors in the smooth muscles of vessels and those smooth muscle undergo relaxation when these smooth muscles will relax now you look if there was a major this was a this is a major artery here and this was the arteriole here when the this major artery may have many smaller arteries and arterioles because this area is injured so this arterioles will relax so more blood will be shifted towards this area because local resistance to the blood flow is decreased in injured area is that right so first was floor event is yes first was floor event is arteriole or dilation arteriole Oh dilation is the right now what will happen with arterial ooh deletion there will be change in the different forces which control the which control the fluid exchange here you know starlings forces hydrostatic pressure and osmotic pressure we'll see what happens there first I will explain normal then I will tell you during inflammation what changes occur due to arterial or dilation normally what happened that in these this is arterial side of capillaries and that is venous side of cappellas or venules right now what happens hydrostatic pressure here hydrostatic pressure here is how much when our diesel side of capillary hydrostatic pressure is about 35 millimeter of mercury as blood moves normally I am talking about normal now then I will tell you how pathology changes normally when blood is moving through micro circulation blood enters and most of the micro circulation in the body with the pressure off with the pressure of 75 35 millimeter of mercury and as blood is moving forward right the hydrostatic pressure is decreased up to maybe 15 millimeter of mercury so what really happens that pressure in the microcirculation or arterial side is high and as normally blood moves through the what is this blood moves through the capillaries right as total jerk you can say diameters of circulation become more so pressure within the micro circulation drop maybe up to 15 is that right but osmotic pressure which is exerted by the plasma proteins that is approximately 28 that is approximately 28 millimeter of mercury normally in a healthy tissue it remains stable from arterial end of the crippled way up to the venous end of the Occulus osmotic pressure remains stable this is the right now due to this mechanism on this early part of the capillary suppose from here up to here hydrostatic pressures are more and osmotic pressure less because hydrostatic pressures are you know they are responsible they are pulling the hydrostatic pressures are pushing the fluid outward and osmotic pressure they're trying to retain the fluid within the hospital compartment is that right plasma proteins did produce colloid osmotic pressure and they're try to retain the fluid within circulatory system hydrostatic pressure is pushing the fluid outward am i clear to everyone now what is happening first normal on arterial side is the crippled way hydrostatic pressure is more and osmotic pressure is let's – so net force for the fluid movement is outward but and this fluid which is coming out will bring oxygen for the tissues and carbon and bring the glucose and other nutrients for the tissues but as you move towards the venous end of the cripple raised hydrostatic pressure has progressively fallen down now osmotic pressure is more and hydrostatic pressure is less for example osmotic pressure is suppose still 28 in word but hydrostatic pressure is now only maybe 15 Outworld so now the net pressure is in world what really happens that in healthy micro circulation from arterial side is accelerate fluid is gradually coming out right and providing the tissue with the oxygen and other nutrients and from venous side of the capillaries fluid is gradually going back to the circulatory system so whatever the amount of fluid seeps out goes back an interstitial fluid volume does not change even though from one side fluid is coming out but from other side fluid is going back so interstitial fluid amount normally does not change and some proteins very little proteins may leak out they are drained by lymphatics these are right this is normal micro circulation now we will see then what happens to micro circulation during inflammation first normal micro circulation has also endothelial cells and these endothelial cells are connected you know they are edge to edge you don't have any signal can normal healthy microcirculation does not have inter endothelial gaps because they are not significant in turn endothelial gaps so there is not protein plasma protein cannot leak out and become out from vascular compartment to extra muscle compartment normally now we see what happens during inflammation as I told you during inflammation chemical mediators produce arteriole or dilation so blood flow in the tissue increases when blood flow in the tissue increases then hydrostatic pressure will go up because in micro circulation more blood is coming so hydrostatic pressure will move up so look at it this will moved up maybe rather than 35 it becomes 65 so we see hydrostatic pressures are up so this is the hydrostatic pressures in micro circulation of inflamed acutely inflamed tissue it has moved upward so micro circulation has higher pressure within it at the top Heather will tell you later that endothelial cells develop inter endothelial gaps they develop in Turandot finial gaps and inflamed tissue I will explain later why that in micro circulation of injured tissue and up see the cells shrink an inter endothelial gaps appear due to those inter and ethereal gaps some proteins may leak out and when these proteins leak out the colloid osmotic pressure will go up or down when plasma proteins are leaking out and inflamed tissue in injured tissue right not only does increase blood flow into that tissue but in the micro circulation inter endothelial gaps appear right and due to those gaps some of the plasma protein leak out from wasö compartment to interstitial compartment so concentration of proteins within vast or compartment is slightly less and when that is less than osmotic or colloidal osmotic pressure within the vas flow compart within the microcirculation is more or less less which means this will drop down for example it become on average 20 now this is the change in the Starling forces in injured tissue that an injured tissue hydrostatic pressure has gone up and colloid osmotic pressure has gone down now the net force which will move the fluid right outward that has been increased the net force which is going to move the fluid outward that has been increased for example look here before inflammation this tissue had hydrostatic pressure pressure of let's post 30 and osmotic pressure at this point was 28 so what was the difference before inflammation 30 and 28 right or even you say it's 35 and 28 so what was the difference 7 so under the pressure of 7 fluid was leaking out after inflammation this has gone to 55 and this has dropped to 20 now difference is too much right so fluid will come out in excessive amounts and it will not go back at all if there's weather information because throughout the length of microcirculation hydrostatic pressure may remain far higher than the osmotic pressure because hydrostatic pressure has increased due to increased blood flow and smoting pressure has dropped due to slight escape of plasma proteins to the ditch interstitial tissue due to increase permeability of the micro circulation so micro circulation will lose normal amount of fluid outward or excessive amount of fluid excessive amount of your secondly the food inflammation attention please before inflammation whatever fluid was lost from this point up to this point was pulled back during last part of the micro circulation before inflammation but after inflammation all the micro circulation from beginning up to the end is excessively losing the fluid and it is not absorbing any significant amount of fluid so fluid is appearing here with a lot of proteins because endothelial cell def shrunken and there is increased permeability of microcirculation so there's a lot of fluid which is coming out with lot of proteins or we say from vascular compartment there is massive escape of protein rich fluid to the interstitial compartment all to the body cavities if there is some body cavity nearby for example if the Schiphol is in the pleura then pleural cavity will be having protein rich fluid here it is interstitial area because my hand doesn't have pleural cavity remember that right so let's come back so what was happening here that two changes have shown that when tissues inflamed right tissues injured chemical mediators are produced chemical mediators number one produce arteriolar dilation and bring more blood into injured tissue of course that increasing blood ulcer is responsible for redness of the tissue and also responsible for high temperature of the inflamed tissue secondly chemical mediators act on the endothelial cells and increase the permeability of micro circulation these two things result into what higher hydrostatic pressures and lower osmotic pressure so the difference between the forces with pushing the fluid out and the forces which are trying to retain the fluid that difference increases and micro circulation loses excessive amount of fluid from the vascular compartment to interstitial compartment and this fluid which is coming out it has lot of proteins also and this protein rich fluid which is coming out is called exuded later on we'll learn that to dis exudate lot of white blood cells will be added as well so what is absolute Asian we say at the point of inflammation accurate information there's a lot of excitation what is X audition as audition is excessive escape of protein rich fluid from the washer compartment from micro circulation to the interstitial area or body cavities and then flame inflammatory zone is that right of course now this is al rotation here I want to point out one very point those you must know the difference between translation and exultation absolutely it is protein-rich fluid coming from wastrel compartment to interstitial compartment that is episode 8 and as you did as a high specific gravity due to presence of proteins or white blood cells absolutely at a specific gravity always more than one point zero two zero ever did but sometimes listen carefully sometimes hydrostatic pressure unduly increase in microcirculation and colloidal osmotic pressure may decrease but if permeability of micro circulation is normal again listen if for example if I put a rubber band here arterial blood will go to my arm but venous blood cannot drain well then hydrostatic pressure will increase in my micro circulations of the hand but do you think permeability of micro circulation of hand will change no that excessive hydrostatic pressure will force excessive fluid to move from vastrel commitment to interstitial compartment but that fluid will be protein poor because plough permeability of micro circulation is not increased so when ever do to increase hydrostatic pressure or do to decrease osmotic pressure in micro circulation lot of fluid escape from the wastrel compartment to interstitial compartment right but if micro circulation permeability is normal there is no increase in micro circulation permeability there is no increase in leakiness of the micro circulation then only fluid which is coming out is protein rich or protein poor that is protein poor so whenever you to disturbed Starlin forces but with normal permeability of the capillaries protein pore fluid escape from the Wasco compartment to interstitial compartment or to the body cavities such fluid is called transudate that is such kind of fluid is called trans you did transit it is essentially a process of ultra filtration it is simply I filtration so let's talk about that here is excitation here is transportation as the date is when excessive protein-rich fluid leaks into interstitial area or body cavity translation is protein pore fluid from Vassar compartment coming to the interstitial areas or body cavities elderly it has not only disturbed a relation occur not only due to disturb Starling forces but they will also increase micro circulation permeability for excitation perfect translation micro circulation permeability is normal only Starling forces are disturbed right another as the duration has high specific gravity due to presence of lot of proteins but crown to date has low specific gravity this is the right what is edema I think it's point to that we should make the terms clear the lecture is not meant to confuse you what is edema do you think atomizer or how you will define a Dima for me yes Ronald you look like Dima specialist what is there Dima know what is there Dima he has excessive fluid where I look at the lemon and fluid come excessively in my mouth is it edema no what is the Dima what is there Dima and body cavities why you forget that whenever there is excessive fluid present into interstitial areas and body cavities we say there's edema this fluid may be exuded or maybe translate the point which I want to put in your mind that edema is just excessive fluid in an interstitial area this may be also date or it may be transit date is that right am i clear to everyone right so of course during inflammation the edema which is formed and then flame tissue is due to process of degradation when inflamed tissue develops edema right of course inflamed tissue as excessive fluid in interstitial area due to excessive fluid shifting from plasma to interstitial area but this fluid is rich in proteins because there's increased permeability of microcirculation so an inflamed issue the edema which is formed is due to process of observation that is due to the process of observation am i clear to everyone now so you know very clearly that another way to define exit is extra vascular and flam every fluid present in interstitial area or body cavities or rather than going into such type of complicated statement there's extra vascular inflammatory fluid present in interstitial or body cavities this called as a jet simply you say f zu d it is escape of protein rich fluid from the Wasco compartment to the interstitial compartment and body cavities that's so simple and wild addition occur because there's increased hydrostatic pressure there decreased osmotic pressure in the area of attitudinal formation and of course there's increased permeability as well so all this process brings more fluid here and more proteins here and excitation again this is that clear now let's come back yes so we were talking about these are the endothelial cells of course right now up to now we have just discussed that shoe has been injured significantly and local cells in the tissue and some product from the blood they have produced chemical mediators of information chemical mediators up to now what they have done in our discussion that they produced arteriolar dilation so there was increase the blood coming into microcirculation of inflamed tissue this is that right there is no problem of to this and that increase input of the blood has done two things number one it has made the area red that is responsible for ruber red is ruber I think sure okay and also has made the tissue swollen oh sorry Vaughn and that is color and with that I said chemical mediators are also acted upon the endothelial cells and increase the permeability and protein which fluid has come out and due to this excitation tissue has been swollen now and we say there is no explanation for the tumor is that right why the fluid came out because hydrostatic pressures are high higher than normal and because in theory there is increased permeability in micro circulation so throats little bit protein escape reduces osmotic pressure here so higher hydrostatic pressure and lower osmotic pressure right increases the net force which drives the fluid outward and in turn to thin gap allow the proteins along with that that is whole explanation of oxidation later on we'll talk about that white cells will also shift over there any question up to this there is no question yes we'll talk about that I'm going to talk about dr. Sergio was very worried that I did not talk about cytokines I'm going to talk about right because he is you know cytokine specialist right so now we are going to talk about that histamine prostaglandins the nitric oxide what is this nitrous oxide or nitric oxide yeah it is night it is not nitrous oxide nitrous oxide is and – oh please don't confuse that with nitric oxide and inflamed tissue nitric oxide is produced by endothelial cell then nitric oxide is produced by the macrophages not nitrous oxide nitrous oxide is the gas which is given by doctors to the patience for it purpose during the anaesthesia this is also called laughing gas I doubt some of restaurants produced this themselves right so never confuse nitrous oxide with the nitric oxide this is nitric oxide those are right now we come to the next step we have discussed about the arterial or dilatation now we will talk about how the increase permeability occurs right during the inflammatory process what are the chemical mediators and what are the mechanisms of increasing the permeability of micro circulation what are the mechanisms and right what are the processes which make the micro circulation more leaky right of course the world-famous chemical mediator histamine right histamine and what really happened endothelial cells also have receptors for chemical mediators of inflammation right and because endothelial cells have receptors for chemical mediators of inflammation right so first of all I will tell you that an inflamed area this formation of inter endothelial gaps this formation of inter and Atheneum gaps now look here I am showing the endothelial lining in a tissue which is not inflamed here endothelial lining does not have any significant inter endothelial gaps but once once this tissue is injured chemical mediators will act on endothelial cells chemical mediators will act on endothelial cells for example histamine I'll put three important chemical mediators here's histamine bradykinin which is derived from some proteins in the blood and there is leukotrienes

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