Cell injury

hi Venus I'm back here with some stuff related to general pathology so before going into this topic as we are humans every day we have challenges every day we have surprises can be a positive one or can be a negative one but you always should follow this theory the challenges are not supposed to paralyze you they are supposed to help you to discover who you are what you are capable of when you get a challenge in front of you then you will know the real capability of yourself only when you have tough tasks in front of you and if you achieve them you will really get to know what you are to the people around you so now you feel have any challenge in front of you that can be personal or professional let's take it let's fight for it let's let's it hear it then you will show yourself to the world what you are here for so please try to implement all these good aspects in your preparation so coming to today's topic that is Sellinger in the cell injury is something like the traumatic injury for us like when you when you have a stimulus something like a stress and when you are not able to bear the stress then you will start adapting to the stress even when the stress is too increased even then after in distress is English then you may cause some reversible damage and even then if it is more more of intensity then it may lead to some irreversible damage this is something similar like the situation to the human life so cell injuries can be basically due to modification in the internal or in the external environment but the cell responds to the stress so the cell responds to the external stress or the internal stress by the host factors or by the factors of the agent the agent which is causing the stress so either can a stress or can a pathological stimulus lead to following changes in the cell the change one is the adaptation the change two is irreversible or a reversible damaged and the end it may lead to the death of the cell so these are the changes which are based upon the intensity or the duration of the stimulus that can be physiological or a pathological so what happens in cell injuries so when the cells are getting injured there will be damage to the mitochondria as you know that the mitochondria is called as powerhouse of the cell which generates the ATP so whenever there is no mitochondria there will be drop in the ATP so whenever there is drop in the ATP okay and lysis of the mitochondria most of the cell contents which are present in the mitochondria the leech is outside so whenever there is drop in ATP or drop in the oxygen levels the cell leads to anaerobic and further leads to damaged by the release of the free radicals as you know I have already discussed about the reversible irreversible cell injury slide so reversible type of reversible how you can identify reversible irreversible by seeing and microscope this is a most commonly asked question which are the following is a reversible cell damage which would have fallen seen in a reversible cell damage so simple logical explanation simple way to handle the things is intensity means normal cell will become versed in reversible injury and will become too versed in irreversible injury intensity varies the second one easy to remember in most of the cases your reversible smelling your reversible cell injury there will be swelling okay there will be swelling swelling of all the articles you can see you can see the mitochondria the mitochondria there is swelling we can see in the cell membrane there is swelling and you can see in the rough endoplasmic reticulum or ribosomes there is swelling okay and next one is irreversible so you reversible damage is of more intensity in most of the cases it will be disturbed or disorganized you can see there will be apart from swelling which is there in reversible there will be lots of large densities accumulation okay large densities of the bodies are accumulated we can see these vacuoles and the large density of the bodies that are accumulated you can see there is disruption of the cell membrane apart from lysis which is of severe case there will be dispersed ribosomes the ribosomes are disorganized okay okay so all these are the basic differences you have to know the next comes it goes the same okay you will have disturbed you will have ruptured and of course t3 these three terms are very very important in examination different because we have seen n number of questions in these areas and the questions were passed recently Penna kosis okay is condensed form okay you can see the nuclear material is condensed okay is condemned excess is fragmentation you can see so many facts of nuclear membrane and of course you know the meaning of lysis which ruptures and the material will get lysis or to something called as dissolution okay so please do make a note about these three terms which are very very important the next comes is the Salinger right the cell injury cell injury can be either physical the theology can be physical the etiology can be chemical okay physical chemical or can be infections few infections lead to cell injury and in few cases it can be genetic because of genes also okay so these are the primary four causes for different categories of cell injury but the most common cause of cell injury is hypoxia okay as everyone knows the most common cause of cell injuries hypoxia hypoxia means hypo means less boxia means less oxygen okay less what sir wherever you have lack sources and what is going to happen so this can be given as a flow chart based questions on you okay so whenever you have less oxygen there will be decreasing in the ATP generation okay they will be decreasing in the ATP generation so what happens when there is decreasing in the ATP generation either the calcium which is present outside will increase that is cytosolic calcium linkage or when the ATP is dropped down there will be more oxygen free radicals available in the or the ADP generation for synthesis of phospholipids the synthesis of phospholipids will decrease because phospholipids are the primary contents of your cell memory of all the cell memories whenever you there is a decreasing in the phospholipids there will be no membranes so when there is decreasing in the synthesis of phospholipids okay okay so there will be no proper memory information on the cell because phospholipid is the primary content that leads to cell memory and darkness okay so that is one side right the second side when there is increasing in the cytoplasmic calcium levels these cytoplasmic calcium levels will cause increasing in the calcium in the mitochondria so most of your pathological changes or cell injuries are associated with an ion this is again a question iron which is responsible for most of the cell injuries or any type of cell injury is primarily the catcher primarily the calcium the answer for this is cancer so whenever you have increasing in the cytoplasmic calcium levels as well as mitochondrion calcium levels this calcium is going to activate phospholipid s and Gen or it's going to activate protease enzymes it's going to activate all the enzymes so whenever these enzymes are active is going to activate protease enzyme is going to break the protein structures phospholipid s is going to break the phospholipid so it's going to break and and cause damage to the membrane cause damage to the lipid production cause damage to the cytoskeleton leading to the cell membrane damage has already discussed that the whenever there is oxygen radicals okay so oxygen radicals are going to cause damage to the DNA as well as the lipid peroxidation aiding to the cell membrane damage so finally the end product of hypoxia is after lots of pathophysiological changes it's leads to memorandum s so that membrane damage can be any of areas so whenever the membrane is damaged all these enzymes which are present inside the cells to come out and they will be increasing in the serum and gem estimation okay so most of the enzymes serum and gem estimation can be done most of the enzymes they increase think is because there will be liberation of intracellular in chips okay so they may lead to the cell that because the membrane is damaged the cell death or the nuclear membrane is damaged there will be the nuclear changes this is the basic pathophysiology outline pathophysiology of Hoppus on the next comes is as I was telling that adaptation okay the first change first stress to the cell is adaptation so all these categories that comes under adaptations one is it tropi okay one is a trophy second one is hypertrophy hypertrophy means there will be increasing in the size of the cell hyperplasia there will be increasing in the number of cells okay metaplasia there will be change in the shape of the Sun okay you can see this is a normal cell because of some stimulus there is changing in the type and the shape of the cell that is called as metaplasia but of course you know this dysplastic changes of dysplasia okay few examples you have to make a note ll regularly they may ask you simple definition of what is hypertrophy what is hyperplasia but they may ask an example based questions okay so these are the examples which have a little bit of controversy but you need to conclude with these answers so regularly a pregnancy uterus comes under which category okay it comes under hypertrophy it has hyperplasia but it is very very minimal hypertrophy okay the breast tissue of a woman during pregnancy and puberty okay it comes both both okay sorry it's not drug it is during pregnancy and puberty it comes both okay it is an example of both hypertrophy as well as hyper plane but if you are talking only about the lactating tissue of the breast during the pregnancy or gross pregnancy it is only hypertrophic so please do make a note about three examples because these are the examples which are regularly asked as a controversial things rest on I hope you can easily madness the next comes as I was stressing you more that okay these are the comments sequences right so so metaplasia is the exchange of normal epithelium for other epithelium okay and preferably the key word is it is reversible because means once the stimulus is given it is something like your reversible pulpitis wondersteam once the stimulus is given there will be pal paddles once the stimulus is removed there will it reverse back to the normal condition means once the stimulus is there the epithelium changes to a different type once the stimulus is removed the epithelium come back student so it is called as a reversible metaplasia is called as reversible so some key points and notices that you need to add related to manipulation metaplasia is something like a normal cell okay modifies into a different cell this is called as metaplasia if a cell converts like this to this visitors also called as metaplasia but it is basically reversible means it reverses back after the removal of the stimulus similarly like your reversible vampiress so key points to bed at point one metaplasia is thought to arise by reprogramming of stem cells to differentiate along a new pathway rather than a phenotype exchange of already differentiated cells okay the key word and this is reprogramming of the same stones is a question which was previously asked okay it's a direct line that is taken from the text of it okay so reprogramming of the stem cells is is nothing but this is nothing but the metaplasia and of course it's a question that is asked in few exams that is it is a reversible condition okay so what happens if metaplasia stimulus is for longer duration of time for example your reversible pulpitis stimulus is for longer duration of time then it will be converted into irreversible pulpitis so the stimulus is of longer duration of time it is going to convert it into the next level that is displaced yeah and there are two types of multipliers one is epithelial and mesenchymal but if you compare the conditions epithelial matter places are more common epithelium matter places are more out of epithelial matter places columnar cell converted into squamous cell is more calm regularly they may ask you which is most common epithelial my top lashes are most common in epithelial metaplasia s-- the conversion of a column inner cell to that of the squamous cell is the most common okay so we'll learn some some examples which are mainly conserved or mainly mainly ask for the dental students okay so as already told there two types of metaplasia s-- one is epithelial and mesenchymal so coming to the epithelial metaplasia okay so regularly occurrence of this epithelial metaplasia like the squamous changes again that occur in the respiratory epithelium of the smokers okay respiratory epithelium of the smokers normally you will have your columnar epithelium with the cilia in the in the respiratory system but due to smoking this is going to convert it into squamous epithelium okay the columnar epithelium is going to convert into squamous epithelium okay so that's that that's an important example of a person who is smoking okay so so you can see here the normal bronchial epithelium so the normal bronchial epithelium is is columnar epithelium with the cilia which is going to convert it into the squamous epithelium after few days and which is further going to convert it into carcinoma that is with the dysplastic changes this is the best example of squamous metaplasia so other other example of squamous metaplasia I will will be having some textbook reading related to this slide is vitamin A related stuff that can be a the deficiency or excess of vitamin A lead to squamous metaplasia either excess or deficiency because this is again a most commonly asked question related to your vitamins which vitamin deficiency or excess may causes metaplasia squamous metaplasia the answer is vitamin A and of course we we have learned okay that is Barrett's esophagus so Barrett's esophagus regularly in the use of fakirs okay so in the ease of a goes you have your squamous epithelium okay you have your squamous epithelia but due to secretion of assets the squamous epithelium is being replaced by the columnar epithelium okay so you can see this bio this is a biopsy often lower okay particle this is I get a question lower half of the esophagus only will show this Barrett's esophagus with a chronic grd it shows columnar epithelium that is columnar metaplasia which is called as Barrett's esophagus and of course it contains the glowblade cells okay okay so regularly what is what is the epithelium the squamous epithelium is typically of normal use of aegisub regularly we used to have squamous epithelium but due to acid secretion in that area to protect the cells from the acid secretion because glowblade cells are the responsible for secretion of mucus and which acts as a protection from acid so the squamous epithelium which is original they will be converted into the columnar epithelium so this is the best example you can see is the lower part of the esophagus regularly line by the squamous epithelium but due to acid secretion to protect the cells this has been replaced by the columnar epithelium and this area of lower esophagus which has been replaced from the squamous epithelium to the columnar epithelium is called as the Diocese of Vegas and the same goes with many other areas okay so there are many other areas your urinary bladder is again an example of the squamous metaplasia okay so squamous metaplasia anyway will have a textbook reading of examples they may not go very deep into the concept things may be they may ask a depth oriented question related to Barrett's esophagus okay or maybe maybe apathy liam of the metaplasia they can ask but mostly they may not ask you the urinary system okay but most of these metaplasia will lead to carcinomas in the future okay it can be your Barrett's esophagus which will be converted into high risk of converting into adenocarcinoma fees of haggis or you can see this particular type of metaplasia which can lead to squamous cell carcinoma in future so as already said like epithelial metaplasia and the second one is nice and common metaplasia epithelial metaplasia are more common okay so in epithelial metaplasia you have squamous metaplasia and columnar metaplasia okay so as far as metaplasia is the example is chronic smokers okay and and if you want you can add this vitamin A deficiency or excess may lead to squamous metaplasia okay so that's that's again a most commonly asked question for the dental students okay and if you want you can add this uterine okay you can add this squamous metaplasia can be seen a new trained endo cervix particular in the case of prolapse or in the old individuals it is going to get replaced the original it is lined by simple columnar epithelium later it is going to replaced by the squamous epithelium the next comes is the columnar metaplasia okay when compared to scram is metaplasia the column in our metaplasia is going to be less common so the best examples of columnar metaplasia are yes I have already discussed that is the Barrett's esophagus okay the Barrett's esophagus is one smoking it is promised metaplasia whereas chronic bronchitis is a columnar metaplasia okay so if you want you can add this examples but the highlighted one are the most commonly asked questions the next one we are done with the epithelial metaplasia s' the next part is nice and caramel meta pleasures okay the mesenchymal meta places are of two types one is osseous metaplasia and cartilaginous metaplasia s' so if you want you can add these examples to your notes they can be given as a questions so next level of metaplasia is already discuss that is dysplasia dysplasia clearly gives this disorganized disorganized self development is called as dysplasia sometimes it is also called as atypical hyperplasia hyperplasia we know but hyperplasia is an organized one but here it is atypical hyperplasia it's not normal hyperplasia it is an abnormal hyperplasia and of course the characteristic features that are seen in the cells or in the epithelium are very very important there will be increasing in the number of layers of epithelium the number of cells increase the number of layers increase disorganized arrangement of cells from the basal layer to the superficial layer can be seen loss of basal polarity of course you know this is a trademarked feature of carcinoma lots of basal priority means the nucleus move away from the basement membrane okay there will be cellular and nuclear pleomorphic some different nucleus different cells are of different shape different nucleus of different shape of course this is a star trademark question okay in this plastic features there will be increasing in the nuclear cytoplasm ratio there will be nuclear hypo chromaticism strain different strains for different nucleus of different cells increasing in the mitotic activity so all these are the futures which are seen in the dysplastic cells and it is a very very important area to be focused the next comes is the difference between the metaplasia and displaced you have learned so much related to metabolization dysplasia now just make a note about difference metaplasia is reversible metaplasia is changed from one cell to other type of cell whereas dysplasia is the extinction of metaplasia when your stimulus is extended more than it will be dysplasia okay so the simple definition change of one cell epithelium or mesenchymal cell to others and is called as metaplasia disorganized cell development may be accompanied after hyperplasia or metaplasia is called as dysplasia metaplasia is of two types that is epithelial metaplasia and mesenchymal metaplasia epithelial metaplasia is more common when compared to the maze and common metaplasia whereas dysplasia is only epithelial type there is no me sand camel type only epithelial tissue is most commonly affected you can write down the examples okay the next one cellular changes there will be matured cellular development okay here everything is disorganized cell development glioma fit some nuclear hypo chromatids of mitosis loss of basal power all are disorganized here they're well organized because there's they're giving it try to save the system right so it's reversible once the stimulus is removed it is reversible okay so it will progress to the next level I think these are the simple differences okay which are very very important in examination point of view the next comes I'm going to talk about necrosis in detail we'll have some rapid fire and discussion in our respective groups but this is completely a solidly textbook based analysis so simple I hope you know the definition necrosis can be defined as localized area of death of tissue followed by disintegration of cells by hydrolytic enzymes that is important hydrolytic is important so there are five types of of course there even special types of necrosis but there are five types of necrosis that is the coagulative necrosis liquefaction necrosis Katia's necrosis fat necrosis fibrin or necrosis so out of which the coagulative necrosis is is the most common most common type of necrosis is quiet or necrosis okay the most common type of necrosis followed by irreversible focal injury most commonly due to hypoxia this coagulate or necrosis is most commonly due to hypoxia that is the cell injury okay and it is less often because of bacteria or the chemical agent it's the most often due to hypoxia the organs which are affected by this are heart kidney and spleen okay so this example is very very important heart kidney and spleen next one is the liquefaction necrosis so liquefaction necrosis occurs most commonly by an ischemic injury or bacterial or fungal infection converted into semi solid fluid like material and you can write down the examples that is the brain infection of a brain and abscess cavity or the best example of liquefaction necrosis next one is cassius necrosis so Katia's necrosis you can most commonly seen in the case of tuberculosis we'll learn about that okay you'll learn how soft Chebarkul hodcha burcu what is difference between soft and hard tubercle all these are regularly asked questions in your ug as well as in the entrance examination so cassius necrosis is most commonly related to the TB and it is a combination of both coagulant or and liquefaction necrosis the next comes is the fact necrosis means fat necrosis occurs in the tissues or in the bodies or in the areas where there is more fat so it is a special form of cell death which is mainly concerned with fat rich anatomical areas - traumatic fat necrosis of the breast because that breast is an area of more amount of fat okay and pancreatic a crude acute pancreas you can see FAK necrosis of breast necrosis and fact nickel bang cleared acute pancreas are the best example of fat necrosis the last comes is fibroid fibroid is something like a material it's more like a material fiber no it is casting by deposition of fibrin like material which has the staining properties of fibrin okay so where does they come most of the immune complex mediated reactions like autoimmune diseases all these diseases hypertension and practicals are the examples of the fiber out necrosis most commonly they will ask you the examples of each type of necrosis as a question the next comes we are done with the necrosis ok I'll be posting another video related to apoptosis okay at the sequence of the events that takes place video will be posted immediately but this is the basic difference between the necrosis and apoptosis apoptosis is a programmed cell death it's it's made programmed cell death whereas this is a disintegration by hydrolytic enzymes okay the causative the most common cause for necrosis as of course the quality necrosis is hypoxia whereas here it can be due to a pathological change or a physiological change which leads to the programmed cell death okay so morphological differences are most important whereas in the necrosis you can see inflammation is present whereas apoptosis is a programmed one there is no inflammation there is no activation of inflammation in necrosis there will be death of HSN cells also which are surrounding but there will be death of only single cell which is programmed the programmed cell only dies there will be cell string case here whereas in the necrosis because of inflammation everything atom and every formation there will be cell swelling initially okay there will be cytoplasmic blebs on the memory which leads to the breakage right and here the cytoplasm is totally disturbed there it is just will have blurbs so you can see a pop talking bodies can be seen here damaged cell organelles can be seen here the nuclear membrane or the nuclear material is condensed here it is totally disturbed phagocytosis of the hope TOC bodies occurs by macrophages here okay here the Deborah's is removed by the macrophages so molecular changes are already discussed because I will be discussing all these changes in another video please do have have a quickly look or this differences which can be asked as a question for you so the next comes is the gangrene okay you need to learn something about gangrene there are two types of pathological changes - gangrene and second one is pathological calcification okay so we'll try to learn about the basic definition of Kangaroo some pathophysiological changes in the gangrene and types of Gagarin's so gangrene is a necrosis of a tissue associated with superadded purification most commonly followed by coagulative necrosis means lack of blood supply it's just an extension of it then it crosses the process the coagulative necrosis process okay so I mean this this fortification can be primarily initiated by the bacteria which can resulting in Masuda to necrosis so there different types of example even your normal canker Morris and everything comes under gangrenous status around the mouth there is there is something called as gangrenous appendicitis so all these comes out together like it's it's necrosis forward by necrosis the battery additional will lead to the Putra fication of the particular area lead to the formation of a ganglion so coming to the dry gangrene okay dry gangrene this is a form of gangrene which begins in the distal part of the limp which is most commonly seen in the distal part of the limb and the very important aspect about this dry gangrene there will be line of demarcation okay a line of demarcation is formed at the point between the gangrenous part and the viable part you can see the line of demarcation okay and you will you can see some black color right this Blackard is basically due to hydros and disulfide the hydrogen dry sulfide produced by the bacteria will react with the iron that is present in the blood to form iron sulfate which is dark in color okay the next comes is the vet ganglion pack gangrene occurs naturally in the moist Eastridge and organs such as pole or organs such as lungs mouth cervix and everything okay the two other examples of bad gangrened clinically are diabetic foot in diabetes you can see both the get both wet as well as try but diabetic foot exclusion is a wet gangrene example T so this wet gangrene is basically due to hide Lucas content okay which allows the growth of bacteria so bacteria will grow because at the end after necrosis gap gangrene is something like which allows the bacteria to grow in that particular area and you can see bed suppose the patient who are like bedridden for a longer duration of time due to the pressure of the sites like sacrum buttock and heel there is chances of occurrence of bad kangaroo so wet gangrene dollars basically due to the due to the blockage of the venous returns okay due to the block is of the venous returns okay so and followed by the wet gangrene okay the next comes is the gas can grab the third one is gas kangaroo gas gangrene is a special type of wet gangrene it's again a tire itself it's a wet gangrene but special type of wet gangrene which is produced only by the gas forming bacteria this gas forming back to the best example is Clostridium okay so I hope you remember your gas gangrene in your general surgery also right so gas gangrene is mainly concerned with the Clostridium so they can ask you one is first one is dry second one is wet and third one is gas gas is nothing but it's a type of wet gangrene so the most common sight the most commonly seen in the limbs and extremities it is most commonly seen in the wet areas that is well okay so it's most commonly due to the arterial occlusion its most formally dodol occlusion of both mainly by the venous Freitas blockage of the venous writtens macroscopically the organ is dry shunkan and black here the organ is moist soft Solem wrote and dark both are dark here it is black here it is dark a purification is limited to a very little blood supply it's limited due to a very little blood supply his mark due to snuffing of organ with the blood and if you see the line of demarcation present clearly present no clear line of demarcation in the case of red kangaroo bacteria failed to survive in this area because of lack of oxygen or limitation so the supply of blood here the bacteria will be numerous okay so this this particular node was added basing upon talking about the diabetic things more in concern because I've seen many questions related to a diabetic kangaroo okay so gang gram the foot is the most common location for tissue necrosis okay the foot is the most common location for occurrence of the gangrene and foot gangrene is 50 times more prevalent in diabetics compared with non diabetics individual more chances that not too particularly above 40 year or face so they can ask you a case based question okay a patient with this necrosis of a foot again they may give you a is of over 40 years or 50 years so the diagnosis is the diabetic foot or the patient is diagnosed with the diabetes because more they have more chances of occurrence of the diabetic foot okay well the dry form is caused by the dry form that is dry gangrene from is caused by the large results block is due to sclerosis dry is due to sclerosis okay try is due to the sclerosis because we have already known dry is basically due to arterial occlusion and what is believed to be a late manifestation what is believed to be laced manifestation of microangiopathic I hope you remember that diabetic complications like after which is one of one of which is Angela this micro ng over this so diabetic patients will have both dry as well as but if they ask in specific go for the vet because it's a late complication but you can see dry gangrene in diabetic patient also but dry gangrene in diabetic patient is mainly due to the three roses both see this both may occur in diabetics but very but a small vessel disease is more common and it's directly associated with the diabetic vascular D arrangements dry gangrene occurs mostly in diabetic patients with sclerosis whereas wet gangrene's develop basically acid late complications okay so if they specifically asked diabetic foot go for wet gangrene if they ask diabetic the chances that both dry as well as but canvasing but if you ask if they ask the etiology of red kangaroo and diabetic patient the answer is sclerosis okay the answer is sclerosis and wet gangrene it's normal okay so please do make a note about these difference because this is an area of controversy again so last but not the least is calcifications i hope you're very good at calcification so regularly what they do is they may ask you the difference between metastatic and dystrophic calcification so easy to remember dystrophic has D word okay so it is DNA so dystrophic calcification the calcifications which are occurring in the dead and degenerated okay when an individual is dead when the individual is not working the calcium metabolism is normal when the calcium metabolism is normal the serum levels are the calcium are normal everything is normal and when the individual or a cell is dead it is generally irreversible so all are interlinked dystrophic can be seen and dead and degenerated dystrophic is seen when the calcium metabolism is normal and the serum levels of the calcium is normal as it is in the dead and degenerated it is irreversible you cannot you cannot make a dead cell normal right so that is disturbing calcification so remember only dystrophic matter static is opposite so metastatic calcification can be seen in normal tissues there will be tea arranged disorganized or change calcium metabolism there will be increasing in the calcium levels and probably it will be reversible so all dead and degenerated examples will come under dystrophic very easy dead end degenerated because already said it is dead and already all live examples okay you can see adenoma is a live cell okay you can see hyper hypervitaminosis D is a live cell metastatic carcinoma is a live one so most of these syndromes and everything are live ones where as you can see here all are dead dead parasites in fact dead necrosis dead thrown by dead certain tumors which are dead so most of the examples easy to identify the examples most of disturbing examples are dead examples and most of the metastatic 8 examples are conditional examples which are live cells so apart from this I just want to add a note about our dental related stuff related to this calcifications so of course you I hope you remember your pulp stones the different types of bulbs true bulbs fall so anyway we're going to learn this either in the histology or either in the inner orbits but there will be some pulp cells pulp cells which are dead okay so when there is accumulation of calcium in these pulp cells which are that has already discussed dystrophic calcification is seen the tendon degenerated and some pulp cells are dead the calcifications that are curse in those pulp cells are called as dystrophic calcification which are nothing but pulp stones okay which are nothing but pulp stones how you can see them they are not inner calcified masses they can be seen either in the coronal part or in the radicular part okay and they down up into two that appears quite normal in their architecture externally but on radiography you can see this dystrophic or calcifications are the pulp stones okay the next comes is a little bit application part of the pulp related necrosis so in most of the cases the pulp necrosis is coagulative necrosis because lack of blood supply or damage to the blood supply or trauma to the dead zone because if you see a least class 4 which is a necrotic pulp due to trauma in his class 4 is a necrotic pulp due to trauma is basically due to the loss of blood supply the blood supply is lost whenever the blood supply is lost there will be huh foxier let's call the squag later necrosis but pulp shows both the types of necrosis that is liquefaction and coagulate oh but most 4 - the coagulate or necrosis yes thank you - I'll try my best to post another video related to the mechanism of apoptosis because I feel like that is the most trickiest area and this particular show ok stay positive stay blessed stay at home work hard