Edema

hello everyone this is dr. Marjorie from Team MBS conquer I'm going to discuss about the edema in this video so this edema means the abnormal and excessive accumulation of free fluid in the interstitial tissue even in the spaces and serous cavities is called as a edema and in the Greek terminology the edema means the swelling there are two things here that is free fluid in the body cavities and free fluid in the industrial space okay free fluid in the body cavities is commonly called as an effusion whereas free fluid in the interstitial space is termed as a edema then coming to the classification it is of two types localized Eddy minor and generalized edema and then generalized edema is also called as a Ana Sarkoja dropsy and depending upon the fluid composition the edema may be of a transudate and the exudate now we will see the differences between the transudate and the exudate and here the translate means the filtrate of the blood plasma without any changes in the endothelial permeability whereas in the x-ray there is the increased vascular permeability translate is a non-inflammatory whereas x-ray it is an inflammatory protein content is very low this point is very important protein content is less than one gram in the trans date whereas high that is 2.5 to 3.5 gram per decilitre in xr8 glucose content is same as in class now whereas accelerated is low that is less than 60 mg specific gravity is low your ex rate it is high pH is greater than 1.3 for trans date less than 7.3 for ex rate le H is low whereas exudate is in it is high a fusion of ndh or serum at this ratio is less than 0.6 whereas here in the x-rated is greater than 0.6 cells will be few cells only present like mainly mesothelial cells and cellular debris but as many inflammatory cells as well as parenchymal cells can be seen in the exudate an example in edema in the consistory cardiac failure is your translate whereas purulent exudate such as puss-puss is the example of the purulent exudate this table is very very important then the coming to the pathogenesis of edema this edema may be because of six reasons that is decreased the plasma oncotic pressure so that is decreased in plasma oncotic pressure may be you can see in the edema in renal disease or a ascites liver or a edema due to hyper protein india hypo protein emia so these are the renal disease ascites and hypo protein emia on because of decreased plasma oncotic pressure if you see the second one that is increased capillary hydrostatic pressure okay this capillary hydrostatic pressure is the is the force that normally tends to drive the fluid through the capillary wall I mean this pressure will drive the fluid through the capillary one okay this increased capillary hydrostatic pressure may be seen in edema of cardiac diseases or in a ascites pass you congestions and postural edema all these are the examples of this increase the capillary hydrostatic pressure then coming to the lymphatic obstruction lymphatic obstruction is mainly because of in the examples include lymphedema like removal of axillary lymph nodes or inflammation of the lymphatics and one important term is there it is Milroy disease will mi l ar-15s min rise disease that is it is called as a hereditary it is a hereditary lymphedema then coming to them tissue factors like sorry this is the tissue factors like increased oncotic pressure of interstitial fluid and decreased tissue tension then increase the capillary permeability and the sodium and water retention so these are the pathogens I mean of edema then you can see here in the picture is the norm fluidics chains whereas here you can see the decrease the plasma osmotic pressure here you can see the decreased plasma osmotic pressure then increase the capillary pressure also he leads to the more amount of fluid into this extracellular space is leadings to the edema find lymphatic flow obstruction causes lymphedema and the tissue factors and the increased capillary permeability also causes the edema then this is the pathology Amalek pathogens is showing the sodium and water retention so this involves like extra renal that is hormonal intrinsic renal or a deist mechanism so if there is a hypovolemia it causes the renal ischemia this causes a decrease in the sodium in renal tubules which causes angiotensin or gen substrate and this hypovolemia will will act on the baroreceptors at the vasomotor center and it activates the sympathetic outflow and even in if there is hypovolemia there is increase in the ABS production in the posterior pituitary gland so all these things and in Nanji attention this angiotensin will convert angiotensin 1 is committed to angry dancing do finally there is a I lost it on release so this causes increase the sodium and water retention and the sympathetic flow will cause renal ischemia decreased drum roll filtrate rate and decrease the excretion of sodium and finally the sodium and water retention and also the finally the production of ADH causes increased retention of water and finally the sodium and water retention so this sodium and water retention increase the residence in an atomizer so these are the results of sodium and water retention and these are the differences between the nephrotic edema in Ephrata Kadima and here the nephrotic edema the important thing to be is proteinuria it is heavy here it is moderate there is protein content it is high here where it is low mechanism is decreased plasma oncotic pressure and sodium and water retention and this is nephrotic this is because of sodium and water retention degree of edema will be severe and generalize wear a smile in the freighting distribution subcutaneous tissues as well as visceral organs whereas here the loose tissues mainly nephrite academy that is face i isn't anchors genitalia okay so if they float academy is there you can see the swelling of this whereas nephrotic edema you can see the swelling of face remember this thing okay this is important then this is speaker this is the pathogens of cardiac edema that is in congestive heart failure you will see the increase the central venous pressure or a decreased cardiac output or a chronic hypoxia these three things you will see so because of the increased central venous pressure there is a increased capillary hydrostatic pressure and because of the back pressure hypothesis cardiac atomized seen and because of the decreased cardiac hype output there is a hypovolemia and because of this we have seen right previously that hypovolemia may be extra renal and because of hollister are intrinsic is because of GFR and the ADH production the PT during all these leads to water retention sodium and water retention cardiac edema and this chronic hypoxia will needs to increase the capillary permeability and because of the forward pressure hypothesis it causes the cardiac edema then coming to this thing you can see the pathogenesis of the pulmonary edema this is because of the increased in the hydrostatic pressure you can see the annular ad my here I need this thing because of the increased permeability so increase in the pulmonary hydrostatic pressure and increase in the permeability are the two things which make the pulmonary edema and in the cerebral edema the mechanism here it differ differs from the other because there is no draining the lymphatics in the brain so the function of fluid electrolyte exchange is performed by the blood brain barrier located in the theatres and so the function of fluid and electrolyte exchange is performed by the blood-brain barrier here remember in the cerebrum the cerebral edema may be it is of vasogenic or a cytotoxic and uh industrial types and if you see the hepatic edema you there is a hyper protein Linea portal hypotension failure on inactivation of aldosterone and the secondary stimulation of graining and your tension mechanism so these four things are there which we can see in the hepatic edema then in the nutritional edema mainly the nutritional deficiency of proteins likewise your a prolonged starvation and vitamin deficiencies and chronic alcoholism all these may be - the edema and finally the mix edema this is due to the deposition of glycosaminoglycans on the industries iam and remember this is important that if it appears as basophilic mucopolysaccharides in the when seeing microscopically so that is regarding the edema so the important thing to be remembered in the idem is your transudate and exudate and also the difference between the nephrite taken the nephrotic edema okay well work hard steepest you and lower learning with MDS conquer