Barrier Function of Inflammation Part 2 5_6 USMLE

Barrier Function of Inflammation  Part 2 5_6 USMLE



so within the 40 of inflammation cells exchange with chemical signals which they produce themselves it is self regulation and this self regulation is based on several groups of outer codes you cause I know it's cytokines cell adhesion molecules step proto lytic activators stepwise proteolytic activators like complement like fibrinolysis and so on biogenic amines and polysaccharide mediators step by step in our next lectures we'll talk about each group of them but in general let me emphasize that these regulators are ruling inside that limited zone inside inflammatory focus in typical norm allergic cause of acute inflammation or art of logo uses the inflammatory outer coil act within the 4c of inflammation but only very small amounts of them spread across the inflammatory barriers into systemic circulation as a result of that norm inflammation is accompanied by minimal manifestations of systemic action of inflammatory out of codes these are leukocytosis because some cytokines spread to bone marrow and stimulate their buccal poisonous this can be fever because some inflammatory mediators in flu hypothalamus and change the body temperature regulation this can be also so called acute phase response or change of blood plasma protein fractions with increase of erythrocyte sedimentation rate and all that belongs to norm energy cause of events but sometimes very large amounts of inflammatory mediators may transgress the barrier and spread into systemic circulation in severe multiple falsey of inflammation for example in very very big percentage of skin burned the total area the total border of inflammation tara zone is so huge that the border Guardians cannot execute properly this barrier function if you just burnt your finger or two fingers that is not dangerous for your life but if for example 35% of total skin surface are burned in that case the border is so huge that very large amount of inflammatory outer coats would spread systemically this may cause systemic action of inflammatory mediators over respiration circulation systemic blood clotting and other vitally important functions and organs and tissues which are not primarily damaged would be involved in that let me say Wi-Fi field of inflammatory programs no one never used the Organa's – to designate this complication we designate the complication of severe excessive systemic action of inflammatory mediators we designate that with the word shock it causes acute car acute circulatory failure acute circulatory insufficiency and hypoxia of many different organs because of hypoperfusion so the consequence of this transgressing of barriers for the organism as a whole is very very harmful person may enter into various kinds of shock as a result of excessive systemic action of inflammatory mediators depending on situation dr. will call that infectious shock allergic shock pseudo allergic shock or for example traumatic shock but nevertheless regardless of the primary reason of tissue damage if the barrier mechanisms of inflammation did not function properly if they did not keep this huge storm of outer coils inside the inflammatory area this would destroy the systemic vitally important functions and this would cause shock which may result in huge litera T so two very important conclusions conclusion one systemic excessive action of inflammatory mediators may cause shock traumatic durn allergic septic toxic and many other kinds of this severe disorder but it means that inflammation per se as far as it is able to keep barriers is anti-shock mechanism not every inflammation results in shock only those cases which violate the barrier function and another conclusion is that in damaged or diseased organism we have not won at a logic process we have several pathological processes of different level developing in parallels and influencing each other in trauma locally inflammation starts and at the same time systemically stress starts and these pathological processes are interacting and look at this scheme when damaging agent acts on organism it can produce several lines of effects nonspecific effect resulted in stress flow genic effect and up optogenetic effect resulted in liberation and activation of inflammatory outer codes and inflammatory process and at the same time every agent has its specific side its specific action for example if it is a toxin it may cause poisoning if it is for example some immune League and like outer antibody it may cause out immune disorder it may block some receptor or vice versa stimulated if the damaging agent was a germ it has its own biological life within organisms with some consequences and the mosaic of all that constitutes the whole picture of disease so although fluorosis or normal normal allergic inflammation and you stress which means non excessive properly regulated acute stress they both are two natural mutually sustaining anti-shock mechanisms it means that inflammation is bad but as soon as you have normal Eirik inflammation keeping its barrier function you would not have shock stress is also unpleasant but as soon as you have properly regulated stress you would not have shock without barrier function of inflammation and without stress every serious damage would cause systemic Circulator insufficiency would cause shock with all its severe consequences the balance between stress and inflammation with its barrier function this balance does not allow after local damage fall into steady multi-organ hypoxia that is very essential if this rule is violated it means if barrier function of influen is unsuccessful in that case organism develops multi-organ hypoxia insufficiency and this is very serious complication of shock the last thing about the mechanisms of anti-shock and anti-inflammatory action of stress look at this picture glucocorticoids the main hormones of stress they both suppress the components of inflammation and at the same time they are applied in a resuscitation in anti-shock surgery and they serve in emergency medicine as important anti-shock drugs so the same drug adrenocortical hormones glucocorticoids the same drugs are both potent anti-inflammatory and potent anti-shock this is very essential detail please notice speed it means that inflammation and stress interact and mutually balance each other in order to prevent shock informational influences of hormones in the 40 of inflammation are limited they are limited by slowing of blood flow by slowing of hormone delivery into the 40 of inflammation but moreover we may remember that many inflammatory outer codes can partially block their transmission of hormonal signals good example is tumor necrosis factor alpha which is a potent antagonist of insulin on the post receptor level so because of that permissive interaction within the inflammatory 40 there is a predominance of local regulators and beyond the inflammatory 40 in normal aging inflammation in ortho fluorosis we have predominance of stress and other systemic anti inflammatory drivers look at this picture these are two persons who understood the anti-shock and anti-inflammatory role of stress hormones this hans selye who discovered stress and fred hinge who introduced glucocorticoids into broad medical practice shalyah non occasionally compared in his books the inflammation and stress although they contradict each other stress hormones are anti-inflammatory inflammation mediators can elicit and increase stress but nevertheless according shelley he even called inflammation local stress in one of his papers of 1959 of course it was just figurative expression but in fact both of these nonspecific responses to injury they are united in their final goal to avoid the shock if we regulate inflammation properly we avoid the shock after trauma if we regulate stress properly we avoid the shock attuma and in fact both inflammation and stress serve as natural anti shock barriers balancing each other thank you for attention my next lecture would be about mediators of inflammation

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