Transcript for:
Understanding Cell Injury and Death

in this class one we are going to start with the basics we are going to start the general pathology and what general pathology starts with the basic chapter there is a cell injury right so I will be covering all the important topics that will be coming in your exam mainly I am going to teach you keeping exam in mind I will be giving you the clinical examples also wherever the clinical examples are needed wherever the clinical questions need to be integrated that will be done in the classes having said that without any further late let's begin the class so having said that now our chapter is cell injury right so what happens if their cells are injured and how many types of cell injury are there reversible cell injury and irreversible cell injury okay and how many types of cell death are there there's a necrosis and apoptosis everything will be covered in this class okay so let's begin our topic see this is our poor cell which got injured okay so let's look at here this is your normal cell okay imagine there is a normal cell which is under homeostasis everything is perfectly all right everything is perfectly all right sir now when you try to give some stress to it okay when you are trying to give some stress to it some kind of microbiological stress or radiological stress or doesn't matter you are stressing the cells okay now when you are stressing the cell even you are keeping yourself in stress environment environment first cells will try to undergo adaptation okay so usually when I am giving you excessive for example you are working under me imagine the superintendent is giving excessive work for the interns okay so whenever there is so much of work what you will try to do first you will try to adapt yourself to the environment even the cells will do the same thing cells will try to adapt okay for the stress if the stress is still coming the stress is increasing day by day now the cells will give up okay now the cells are getting injured okay so when cell adaptation fails inability to adapt okay failure to adapt will cause cell injury okay cell injury sir now do you think what do you think about the cell injury immediately the cells are going to die with the cell injury no if there is a little cell injury which can be reversed so injury happened but its Littles are not too much not much damage the cell membranes are not damaged the nucleus is not damaged the mitochondria are not damaged much so still there is a chance that you can take back this cell to normal back to the homeostasis to the normal level so the cell injury can be of two types what are they first one is called as a reversible cell injury but what exactly is this reversible cell injury cell is endured so true but not much damaged till there is a chance that the silk will go back to its original state okay you will go back to its original states are normal homeostasis but if the damage is so severe the cell is severely damaged so the stress is so much it cannot adapt it is so much of damage that's happening now this is called as irreversible cell injury okay now the cell is having only one way that is it have to die okay it have to die either by the process of necrosis or adopted apoptosis okay so irreversible cell injury will lead to what the irreversible cell injury can lead to cell death how many types of cell death are there a cell can die by two ways first one is called as a necrosis and second one is called as apoptosis so now tell me normal sulcer you are stressing it when you are stressing it it will start to adapt but if it's failed to adapt it's failing to adapt you are increasing the stress it's failing to adapt it's not adapting sir so what will happen first initially reversible cell injury will happen reversible now there is a still chance that the cell can go back to its original normal function but there is an irreversible cell injury the amount of stress that you are giving is so much that cell will go into irreversible cell injury so that the only fate of the cell is now it's a cell death by either necrosis or apoptosis just tell me sir how many types of cell death are there two types of so not cell deaths how many types of cell injuries are there so there are two types of cell injury reversible cell injury foreign now let's begin our topic with reversible cell injuries a reversible cellular what happens what happens now look here always let's begin with this sir what is the most common cause of cylindering why acid is getting injured reversible cell injury only sir why cell is getting injured look here the most common cause of cylinder is hypoxia so what is hypoxia right hypoxia means decrease oxygen oxygen is not there for the cell now what is the cause of hypoxism this is a stress hypoxes definitely a stress Okay so hypoxia now what is the right first is the most common cause of cell injury is the most common cause of cell injury then what is the most common cause of hypoxia why hypoxia is happening why there is no oxygen availability for the cell the most common cause of hypoxia is ischemia okay what is this ischemia means decrease in blood supply okay so decrease in blood supply the blood vessel might be occluded because of a thrombus the blood vessel is occluded because of thrombus and atherosclerosis because of some reason so there is ischemia that ischemia is leading to hypoxia now see whenever there is a hypoxia inside a cell the cell May hypoxia okay whenever there is a hypoxia in the sulcer which organelle is going to be most commonly affected OK which common which organ is going to be most commonly affected versus the mitochondria will be affected sir because mitochondria loves Oxygen by taking the oxygen it causes you know it you know oxidative phosphorylation ATP production you're right right so first organelle that will be affected is mitochondria is going to be affected sir mitochondrial dysfunction now whenever there is no oxygen mitochondria is not functioning properly so whenever the mitochondrial dysfunction happen do you think ATP will be produced no sir ATP production decreases so oxidative phosphorylation will be affected OK the process of oxidative phosphorylation in the electron transport chain it will be affected sir so ATP production decreases ATP decreased so the cell the cell currency sir ATP now it's not there so what you have what you have done you have given the stressor now you are giving the stress stress in the form of hypoxia hypoxia is going to cause the mitochondrial dysfunction this is the first cellular change okay first change in cell injury so what is the first change in the cell injury the first change that happened in the cell injury is mitochondrial dysfunction that's McQ okay sir ATP decreased ATP not there so what happens see on each and every cell you know one thing okay let me show here sir actually on all our body cells there is a universal pump present what is that pump can you tell me come on travel expert DVR ID can you tell me what is this pump which is bringing two potassium into the cell it is taking out three sodium out of the cell do you know what is this pump it is throwing three sodium out of the cell and bringing two potassium into the cell Always by using the ATP okay by using the ADB server what is the name of this pump this is called as sodium this is sodium potassium atps three sodium potassium atps requires ATP for the movement of sodium out of the cell and to bring the potassium into the cell now Miracle just just tell me sir so when the ATP is not there okay now the cell is not having the ATP cell now do you think this pump will function the sodium potassium ATP ISS which has present not all our cells now this cell also the cell which is getting injured so the sodium potassium atps is not going to function when the sodium potassium atpase is not functioning not functioning what will happen which I am should start to accumulate inside the cell there see they go sodium ions are getting accumulated inside the cell okay so there is accumulation of the sodium ions now tell me sir wherever there is sodium water follows wherever there are wherever the sodium water follows you know the basic thing now ATP is not there when ATP is not there this pumps this pumps are going to fail when the pumps are failed this ionic balance is affected the sodium is going to get accumulated inside the cell wherever there is sodium this sodium will try to drag the water so more water will come into the cells more water okay now water is coming into the cell okay there they go the same thing whatever we have discussed the same thing the same thing I have shown here see decrease in the ATP okay ATP is decreased so the sodium potassium 80 phases are getting affected sir sodium potassium ATP is then the sodium potassium atps are affected they go what happened increase in flux of water I have explained you why more water is coming because of the accumulation of the sodium ion sodium ions are more inside the cell accumulation of the water now tell me sir now more water is coming into the cell so can I call this as a hydropic change cellular swelling right hydropic changer okay so this is the first morphological visible change in reversible cell injury okay so cellular swelling cells are getting swilled with the water now they are getting little obesity water is coming into them now they are little swell swollen okay so this is called as right hydropic swelling okay hydropic swelling now right what is McQ for your exams especially for all the board exams any exams the first morphological change the first morphological change that is visible now if they ask you what is the first change in cell injury the first change in cell injuries mitochondrial dysfunction and what is the first morphological change that you can see under the microscope it's the cellular swelling or hydropic change hydropic changes water accumulation when more one more water is coming into the cell Now by getting like you know by just deserve like you know why ah when more water comes into the cell this water because of this excessive water the cell organelles will start to swelter so endoplasmic reticulum is also going to swell OK there is swelling of endoplasmic reticulum not only endoplasmic reticulum all these organelles will start to swell okay so this is seen in a reversible cell injury hydraulic change McQ class of microbializer what is this normally just look at here sir imagine normally this is one cell okay now the cell is having this microglide so micro value are there now tell me when more water is coming into the cell in order to accommodate this water the more water is coming right in order to accommodate with water now cell is swelling now when a cell is swelling what happened to this Villi the will I get now flattened okay now the cell will become something like this The Villa has lost sir because more water came into the cell so the loss of microvilli will be seen okay so loss of microvilli is seen in reversible cell injury true and Aki what are these envelops these are the cytoplasmic blood cell now more water is coming into the cell now cell what it is trying to do cell doesn't like this cell is still trying to control it want to it want to live sir it want to leave but more and more water is coming into it you know what it will do see now the cell in order to accommodate this extra water okay in order to accommodate this extra water cell there they go now this is a Seltzer it is forming the same cell it is forming some small small protrusions okay so these are the blips okay the cytoplasmic uh the cytoplasm is getting the volume of the cytoplasm is getting expanded because of the excessive water so the cytoplasm sorry not the cytoplasm this cell membrane now cell membrane is forming this little blephs extra water so these are the cytoplasmic glyphs okay so cytoplasmic webs are seen one thing there is a loss of microorganic second thing second thing endoplasmic reticulum is going to be solid the cell is also getting swollen so all these are because of what these are all these problems because of the failure of sodium potassium ATP exists price because of decrease in ATP why decrease in ADP mitochondrial dysfunction y mitochondrial dysfunction because of hypoxia why hypoxia ishemia okay so cytoplasmic blips are also going to form extra pouch small small pouches to accommodate the water okay and myelin figures so what are the smile in figures okay Milan figures what are what exactly are they just look at it this is the image based question which can be coming your exams okay so this is electron microscopic image okay what this myelin figures especially can be seen this is a feature of electron microscopic it's an electron microscopic feature not just the light microscopic feature look are you able to appreciate this laminated appearance these are like a laminate laminated appearances okay so this structure is concentric walls are laminations which you can see in the cytoplasm so these figures are called as a minor figures so what exactly are they or they are made up of listen the cell is getting water more and more water is going into the cell the cell is getting swollen small and swollen swollen even a cell organelles are getting swollen cell now tell me one thing cell is made up of the cell is covered by what cell membrane which is made up of phosphor lipids lipids which are hydrophobic okay and even your cellular organelles like endoplasmic reticulum mitochondria Golgi complex even they are also surrounded by the membranes right even organelles are also surrounded by their own membranes now whenever the too much water is coming this water is distending the organelles making them swollen so during this process during this process some amount of cell membrane damage will occur some amount of cell membrane damage will occur not severe just some amount of cell membrane damage okay the cellular organelles also they go endoplasmic reticulum also it is getting swollen swollen swollen so their cell membrane whatever is there okay their membrane the organs which are covered by their membrane even the membrane is getting distended membrane distant distant distance and there will be a small damage so some phospholipate some membrane is going to be teared away so these cell membrane this phospholipid membrane okay which is hydrophobic cell now it is going to in the cytoplasm it will come and it will go into walls or Revelations so very important point is myelin figures which are nothing but look here they are what exactly are they they are membranous walls are laminated Aggregates of phospholipids what they are made up of they are made up of phospholipids derived from there derived from damaged membranes of mitochondria or endoplasmic reticulum or cell membrane okay so this is the question that they will ask you in your exam they are made up of what they are made up of phospholipids they are mainly made up of phosphere but other components are there like calcium but they are mainly made up of phospholipids okay next so far let's recap what we have seen sir come on guys let's see we have started with the reversible cell injury reversible okay we have started with the reversible cell injury now in reversible cell injury what happens there is a decrease in the ATP okay there is decrease in the ATP now when the ATP is going down what happens sodium potassium 80 bases failed more water is coming into the cell so hydropic change that's the first morphological change endoplasmic reticulum is filling loss of microbial are seen cytoplasmic bleeps are seen and myelin figures are seen myelin figures are made up of what phosphor lipids next sir next what happens so whenever the ATP is not there oxygen is not there sir okay is not there do you think aerobic respiration is going to be possible aerobic respiration needs oxygen now oxygen is not there hypoxia the patient the cell is having hypoxia so now the respiration will shift into anaerobic pathway anaerobic respiration will start to happen inside the cell so whenever anaerobic respiration occurs what happens lactic acid is going to be produced you know lactic acid is the product of anaerobic respiration now inside the cell lactic acid levels are going to increase lactic acid acidosis now what will happen because of this acidic environment see acidosis sir now what happens there is clumping of Chromatin the chromatin material which is present inside the nucleus now this is a nuclear chromatin they go now the nuclear chromatin it will start to Clump come together clumps okay so why this is happening this is the nuclear change what is the nuclear change McQ nuclear change nuclear change okay so what is the nuclear change that is seen in the reversible cell injury it is a clumping of Chromatin okay next up whatever changes can be seen now I have said you one thing the endoplasmic reticulum because of this hydropic changes the more and more water is coming into the cell the endoplasmic reticulum is getting swollen no the endoplasmic reticulums are getting swollen who is attached to endoplasmic reticulum I'm asking you ribosomes right ribosomes are attached now because of the swelling of the endoplasmic reticulum those ribosomes will undergo Detachment the ribosomes will start to detach now what will happen do you think protein senses will happen now protein synthesis will stop so there is decrease in the seed there is ribosomal Detachment leading to decrease in the protein synthesis so these are the three main events that happens in the reversible cell engineering okay these are the three main events that happens in the reversible Synergy what are three main events which I want you to know are cellular swelling second thing is clumping of the chromatin and third one is decrease in the protein synthesis okay is it clear guys so far is it clear it's a reversible cell injury can happen in any initial it can happen in any cell when you are giving stress to SL first it will undergo reversible cell injury see now try to understand like this okay try to understand like this any of your body cell if you stop oxygen to it you don't give oxygen to it so cellular swelling will happen clumping of Chromatin will happen decrease protein synthesis will happen myelin figures are same but still if you just leave the cell if you take out the stress from the cell okay just remove the stress from the cell still the cell will go back to its normal functions are the the cell Will Survive okay there is no cellular death till here this is reversible cell injury still the cell can move if you remove the stress the still the cell can go back to its normal function okay then let's begin the topic of irreversible cell injury sir okay now they go when can we say that the cells are irreversibly damaged so beyond repair now there is no repressor Beyond repair the cell is damager you know what is that one thing there is severe membrane damage if the cell membrane the cell membrane of the cell it is severely damaged the silken no longer undergo you cannot repair the cell okay now it is no longer reversible cell injury now it is irreversible cell injury okay so what is that thing which differentiate reversible cell injury for irreversible cell injury it's a severe membrane damage okay so now let's see here imagine this is one cell where the membrane of the cell is damaged sir in many places say for example in this place the membrane is damaged in this place also the membrane is damaged cell membrane is damaged okay now where the cell membrane is damaged just tell me so from outside calcium whatever the calcium is there okay calcium levels inside the cell is very very lesser this is also the fmg question the question which was asking the recent fmg exam question is Which ion concentration is maintained Less in the cell when compared to the other ions the calcium concentration the calcium concentration inside the cell is very less inside facilities less outside acid is more outside the cell it is more so now tell me when the cell is damaged the cellular membrane when the membrane is damaged now this calcium will start to come into the cell now I hope you already know from your first year of mbbs so calcium what exactly is this a calcium calcium is enzyme activator okay calcium is the enzyme activator it activates all the enzymes are multiple enzymes okay now let's see what happens there is severe membrane damage so that it is increase in the calcium influx into the cell from outside the calcium is going to come into the cells okay now what this calcium will do see calcium is going to activate certain enzymes which enzymes are phospholipases now it is decided cell membrane is damaged there is no chance of repair now the cell have to undergo death for sure irreversible no so still have to die sir so if the cell have to die the you have to break the cell membrane you have to break the nucleus you have to break the proteins inside the cell okay so this calcium it activates inside the cell the calcium activates the phospholipases the phospholipases are going to be activated okay now what happens now they go that the phospholipids is they will break the cell membrane and break the mitochondrial membrane sub cell membranes mitochondrial membranes will be broken down and one more thing I want you to know is see this phospholipases in the name itself is the phospholipase phosph they will break the phospholipids where phospholipids are there phospholipids are there in the membranes membrane cell membrane mitochondrial membrane you know it right so now the cell membrane is getting damaged the mitochondrial membrane is also getting damaged the membrane around the mitochondria is also getting damaged sir now this is also very important once the mitochondrial is damaged this is also an indication if the mitochondria are damaged that's also an indication that it is irreversible cell injury sir what are the two things which will say this is irreversible cell injury that is severe membrane damage cell membrane damage as well as mitochondrial damage if they are present inside the cell it is no longer reversible cell injury it is now irreversible cell injury okay now McQ switch for asking your exam calcium came into the Seltzer calcium is activating what calcium is activating the phospholipasis the cell membranes are getting damaged mitochondrial membranes are getting damaged now they go what happens do you know calcium now will enter into the mitochondria calcium rate is going calcium is going into the mitochondria ok so now this calcium which is going into the mitochondria it is called as large flocculent densities okay so this is the question they go now imagine this is your mitochondria now mitochondrial membrane is damaged now now in some places in some places mitochondrial membrane is also damaged sir now this is your mitochondria right now see here now calcium it will go into the cell and it will start to deposit in the mitochondria now this green color thing imagine it as a calcium okay so these are the calcium deposits okay so this calcium deposits are called as large amorphous flocculent densities okay large amorphous flocculent densities are seen in which organelle can you tell me large amorphous focaline densities are seen in mitochondria so what exactly are this large amorphous broccolin densities what exactly are they they are nothing but calcium deposition in mitochondria McQ okay next McQ the large flocculent densities which are there in the mitochondria then the Hallmark of Watson Hallmark of OK large Mr first large amorphous flocculent densities than the Hallmark so they're the Hallmark of irreversible cell injury okay so now let's just see the mcqs okay what are the mcqs which I want you to know is sir calcium is coming into the cell now where this calcium is going that the calcium is going inside the mitochondria and the calcium is getting deposited in the mitochondria so this calcium is called as a larger flocculent amorphous densities which are the Hallmark of irreversible cell injury irreversible cell injury okay next so the calcium whatever is coming in calcium is coming in right so this calcium not only activating the phospholipases which breaks the cell membrane it will also activate the proteases in the cell all the proteins will be broken down so the cytoskeletal proteins okay the cytoskeletal proteins they will be broken down so again causing damage to the cell okay so cell membranes are getting damaged the proteins in the cells are getting damaged and the last one the calcium it will start to activate the nucleuses inside the cell okay phospholipases are activated proteases are activated and the nucleuses are activated once the nucleuses are activated what they will do nuclease breakdown of the nucleus the nucleus will be broken down sir okay so the nuclear DNA it is going to be damaged the nuclear damage is going to be broken down once look at here guys now here I am showing you the normal cell this is the normal cell with the normal chromatin and the nucleus nucleus and the nuclear chromatic but once the cell decided it's decided irreversible cell injury now the cell is undergoing death sir okay now do you know what happens the nucleus all this nucleus will shrink in size become condensed this is condensation of the nucleus is called as hypnosis okay so the condensation of the nucleus is called as thicknesses after condensation look at the nucleus what is happening what's happening to the nucleus the nucleus is getting broken down into small small pieces this is called as Cario rexis hypnosis means condensation condensation carrierxis means fragmentation fragmentation and the last one carriolysis carolysis carolysis means what lysis dissolved dissolution okay dissolution so what are the nuclear changes this is the question sir they will ask you in an order what are the nuclear changes that are seen in irreversible cell injury if the cell is undergoing irreversible damage once it is decided irreversible cell injury lead to death now what kind of nuclear changes are seen hypnosis carrier access carriolysis order is important condensation condensation fragmentation dissolution okay these are the nuclear changes okay so this is uh what I want you to know the reversible cylindricary completed sir irreversible salinity is also completed in reversible cell injury simple important points failure of the sodium potassium at basis cellular swelling hydropic change myelin figures are seen swelling is going to be seen cytoplasmic blips are going to be seen microvilli loss is going to be same okay these are some important points which I want you to know and one of the nuclear changes that you will see here in reversible cell inducer in reversible cell injury what is the nuclear change that is seen the nuclear change is clumping of Chromatin clumping of Chromatin okay now here I want to add one McQ point so this myelin figures are there right that is myelin figures are they going to be seen in reversible or irreversible they are seen in both sir this is Myron figures they are seen in both reversible and irreversible they are seen both in reversible as well as irreversible cell injury okay mind triggers are same both in reversible as well as the reverse special engineering what is the nuclear change that is seen clumping of Chromatin now in irreversible salary what are the points which I want you to know what are the two things that decide that certainly is irreversibly damaged one is cell membrane damage and mitochondrial damage presence of large flocculent mitochondrial densities is the Hallmark of irreversible cell injury and that's because of the calcium deposition is in the mitochondria okay and what are the nuclear events that are same this is important nuclear events are condensation of nucleus hypnosis followed by carrier axis and karyolysis that so with this irreversible cylinder is also completed reversible Cell Energy irreversible after reversible cylinder what happened cell will die cell will die sir okay now talk about the neck processor cell death cell dead cell dead how many types of cells do you have there are multiple organs are there multiple tissues are there in our body there are different different tissues are there different different simple try to understand like this different different tissues different different cells so different different cells will undergo different types of cell deaths are okay actually there are two types of cell one is necrosis and apoptosis first we will discuss about the necrosis say necrosis cost Point always a pathological set always pathological cell doesn't want to die they'll always want to live now in this condition so you want to live but some stress from outside stress there is reversible cell injury irreversible cell injury now it is causing the death of the cell so necrosis is always always pathological it's always pathological okay it's always pathological necrosis is it active or passive so it's a passive processor what does I mean by passive sir during this process the cell is dying no no ATP is involved there is no ATP no program nothing because of some external stress it is killing the sulcer okay I used to remember necrosis more like a murder okay the cell doesn't want to die but some stress from outside is actually killing the cell okay different types of tissues we learned about different types of necro system so what you should know for your exam the most common type of necrosis is coagulative necrosis most of our body tissues coagulative form of necrosis but if you put under the microscope still you can identify the cell architecture ah sir this is a cardiac myocyte ah this is a nephron so this is a renal tubule still the architecture cell is dead but still the architecture is preserved okay so this is called as coagulative necrosis which is the most common type let's once look at here here I am showing you the kidney this is the kidney now because of the occlusion of the artery because of the occlusion of the artery see there is wedge shape necrosis so this part of the kidney have undergone necrosis coagulate your necrosis okay so now one by one one by one coagulative necrosis this is the image based question which was many times tested in the exam many times tested in the exam first tell me what happened to the tissue architecture what happens preserved so still you can say ah sir this is cardiac myocyte or this is like this is hepatocyte or this is a nerenal tubule you can still identify the structure even after the death of the cell so this type of cell death is called as coagulative necrosis okay now it is seen in that it is seen in heart myocardial infarction is an example of what myocardial infarction is an example of coagulative necrosis the tissue did but still structure is preserved the cell structure architecture the boundaries outline it is still preserved okay so under the microscope you can identify it okay heart and kidneys spleen and most of the solid organs ok most of the solid are bonds so because of infraction this is a word they will use you most of the time infarction so because of the information what exactly is infarction you have cut down the blood supply the tissue is dead in fact infarcted area okay so now you can say that this is the infarcted area you have cut down the blood supply that area is dead so that's an example of coagulative necrosis now it is due to what in coagulative necrosis still you are saying I am saying you that still architecture is preserved why architecture is preserved because of a process called as denaturation of proteins denaturation of proteins okay so the proteins will undergo denaturation and because of this process because of the denaturation of the process because of this process denaturation still the architecture is preserved okay next so what are these ghost cells this is also McQ which was asked from this area ghost cells are seen in now tell me this is a normal healthy sensor with a nucleus in the center normal healthy cells with the nucleus in the center okay now when a cell is undergoing depth cell is dying sir now inside the cell okay cell is dead already dead inside the cell can you see the nucleus the nucleus is not there so now there is an empty cell so these empty cells without the nucleus still the architecture is preserved the outlines boundaries are there but inside the cell there is nothing deserted no one is there nothing is inhabited so you use the word deserted cities right deserted ghost towns okay ghost towns ghost towns means what no one is inhabiting over there nothing is there okay just empty houses in the same way now in the cells Nothing Is there empty cells okay so these cells are called as ghost cells so ghost cells are seen in which type of necrosis they are saying in coagulative necrosis okay and coagulation denaturation of proteins are coagulation of proteins will be seen coagulation of proteins will cause the preservation of the architecture denaturation or the coagulation of the proteins will cause the probability necrosis completed sir now image based question which was tested in fmg exams and PG exams Indian exams this question was asked and even in the mle exams board exams also these questions will come now what is this which I am showing you right now this is your brain now see this area of the brain is getting infected gone okay I shouldn't say but anyway this area of the brain is getting damaged dead sir now if you take small tissue from here just take a small tissue from here put it under the microscope and look at it you cannot say anything the tissue architecture you cannot say that this is a neuron the tissue architecture is not preserved sir okay so the entire that area there is liquefacture necrosis happening totally it's getting dissolved liquefication okay so now these tissues okay these type of tissues necrosis so which tissues so first write the scene in brain okay brain and also pancreas sir brain and pancreas so these tissues what is something special about them the brain and pancreas they have lots of enzymes okay lots of enzymes Q2 presence of hydro enzymes okay so when these cells are undergoing depth due to the presence of high amount of hydrolytic enzymes within them these enzymes will start to totally dissolve the cell architecture cell so what happened to the tissue architecture the tissue architecture is not preserved the tissue architecture is not going to be preserved so then the image based question very important okay now after that look at this this is your lung tissue actually this is your lung tissue now in this lung tissue there is this area they go so this area how it is looking like it's looking like a cottage cheese it's looking like a Cheesy appearance cheesy appearance waxy cheesy appearances so this lung tissue is undergoing necrosis okay and because of this necrosis just morphologically not another microscope just by look morphology itself gross morphology itself is showing you Cottage cheese-like appearance so that's it's called as Cassius necrosis means cheese like okay so mcqs which were asked are the Cassius necrosis is actually a combo it's a composer It's a combination of both it's an example of both coagulative Plus liquefactive spin is little misbehaving okay no issue is an example of both coagulated and liquefactive necrosis so it's both combo both are happening okay now appearance how it is appearing so this tissue is dead and how it is appearing like you know grossly cottage cheese like she's like which is like appearance It's associated with which condition especially this type of necrosis will be associated with infections okay infections like TB mainly it's a TB because of the mycobacterium tuberculosis organism and is also because of some fungal infections fungal infections like histoblasmosis so a TBA is conditioned TB histoblasmosis and coccidiod or mycosis one more conduction one more condition so TB histoblasmosis coccidiydomycosis I'm not writing it uh it's a lengthy name so TB histoblasmosis coccidihydomycosis in these conditions if you have this infections in your lung yeah lung parenchyma is dying lung is dying no doubt but after death it will look like a cheese capacious necrosis okay now fat necrocessor what is this fat necrosis now wherever there is fat in your body fat and in some places there is fat cell if this fat is undergoing necrosis that is called as fat necrosis fat edit sir adipocyte death the death of the adipocytes now some important exam important points are there they go see this fat necrosis first where it is sensor where more fat is there in your body the fact is mainly present in your breast in females breast tissue fat hair is buttocks okay buttocks way okay so in these areas very much fat is there very very high amount of fat is there now imagine there is a trauma trauma to the breast okay some road traffic accident because of some abuse or because of some like you know injury like in a fall now there is a damage that is happening to the breast cell breast tissue damage is happening now the breast inside the breast the reposites whatever were there now they are undergoing death okay now they are undergoing that's a necrosis is going to happen now this necrosis as well as a fat necrosis important points are once the fat is dead okay there adipocytes are dead now the fatty acids are going to be released okay fatty acids are going to be released sir is fatty acids love to bind with the calcium okay this fatty acid slow to bind with the calcium okay so fatty acids are buying are binding with the calcium sir ah okay now what is this process called is this process is called as a saponification so calcium binding with the fatty acids now you will start to see in the area of necrosis in that particular area of necrosis we will start to see white white white deposits so this is called as chalky white appearance okay okay right appearance so chalky white appearance is seen which type of necrosis fat necrosis just look at here sir so can you tell me what is that argon so this argon this is a pancreas okay a pancreasa it's a pancreasa now you know you already know it's a pancreas you don't know which type of necrosis pancreas pancreas cylindrical liquefacture necrosis because of enzyme Rich pancreas have lots and lots of enzymes okay pancreas have pancreatic lipase School lipase tipsinogen chemotrypsinogenase so many so many enzymes are there inside the pancreas so pancreatic parenchyma will undergo liquid fracture necrosis no doubt but now I am talking about the peripancreatic fat okay around the pancreas also fat is there now this is the fat I am talking about now in this condition sir are you able to look the peripancreatic fat is undergoing necrosis and whenever fat necrosis happens their calcium will start to deposit their calcium is starting to deposit so this process is called as saponification okay so this is called as what saponification sir so giving you which kind of appearance chaki white appearance okay now the questions will be something like this this kind of questions will come in your exam acute pancreatitis the patient is having acute pancreatitis so what kind of necrosis will happen in the pancreas inside the pancreatic parenchyma pancreatic parenchyma will undergo liquefacture necrosis but the peripancreatic fat will undergo fat necross is giving you charging weight appearance okay next step especially this is very much important for your nippy's exams also look fibrinoid necrosis fibrinoid means brain deposition necrosis is happening there in the area of necrosis you will see pink color fibrin like material pink color glossy material is going to be same where it is same in which conditions you will see fibrino necrosis what are the examples okay example seen in vasculitiser okay especially autoimmune like you know immune mediated us are not a very immune mediate vasculitis uh like polyarthritis nodosa so the polyartrite is known as this it's an example of what what happens in polyartrate is necrotizing vasculitis the vessels are undergoing necrosis vessels are dying because of immune mediated damage now if you look at the vessel this is absolutely a bit whistle sir how can you say this is the Lumen where blood cells are seen now this is the wall of the blood vessel which is undergoing necrosis but look here in the wall there is a pink color fibrin like material present so this type of necrosis where pink color material is getting deposited this is called as fibrinoid necrosis okay so fibrino necrosis is cinnamon polyartride is known as a not only that one more heart condition sir which is called as rheumatic heart disease in rheumatic heart disease again in the heart there is some areas where undergo necrosis which are called as the astronaut bodies Ash off Bodies Okay the astral bodies which are pathognomic they are pathognomic of rheumatic heart disease and cardiovascular system again I will teach you there but for now just trust me sir in a condition called as rheumatic heart disease you will see Ash of bodies this ash of what is our example of what this ash of bodies are again example of the fibrinid processor okay so with this the important types of necrosis are completed just you look what are the important types of necrosis coagulative necrosis liquefacture necrosis coagulated necrosis in all the solid organs like heart kidneys plain all solid solid organs next liquefactory necrosis in those organs where enzymes are more present like brain and pancreas next cases necrosis in infections fungal infections and TB infections in the lung with a Cheesy material development next fat necrosis in the breast for example the question will be something like there is this one female she is driving the car now she met with the road traffic accident now because during this road traffic accident now she had a trauma to her breast that steering wheel the steering wheel now her breast is getting compressed again is the steering wheel now which type of necrosis will happen in her breast fat necrosis will happen okay which process will happen saponification will happen calcium will stop allow to go into deposit in that fatty acid area wherever the fatty acids are there now the calcium will start to deposit in that area okay and fibrino and necrosis seen in the vessels vasculitis condition nah now after this some important types of necrosis are there important types some little special same the weather so what is this diabetic patients you know diabetic patients especially they will be having the ganglines or gangrene so this is the dry gangrene okay Dragon green where you can see a very clear demarcation this is the word which is important sir okay so this area is dead which is looking like a mummy mummified totally dry area totally mummified there is no bacteria growing in that area okay so what exactly is happening dragon is what sir are a drag anger is nothing but coagulative necrosis it's a type of coagulated necrosis okay in that area what happened coagulative necrosis happen okay now you cut down the blood supply to that area slowly gradually gradually you have cut down the let's apply to that area so that area is dead coagulated necrosis okay so just look here important mcqs which you need to know for your exams concentrate there are two types of gangrene dry gangrene wet gangrene okay so dry gangrene is most commonly seen in it's a dry gangrene is going to be say in the limbs upper Limbs and lower limbs but vertical gangrene it is seen more in the bubbles or intestines okay mainly seen in the intestines okay it doesn't mean it is seen in the other extremities yes it can also be seen even in the limbs also but mainly it is seen in the limb it is mainly it's seen in the bubbles red ganglines in the bubbles in the limbs now why why vertical angle in white dragon so diagram is because of the main arterial occlusion the artery supplying this area that's blocked when the arterial occlusion happens no blood flow hypoxemia hypoxia stress reversible cell injury irreversible cell injury gone coagulative necrosis okay so due to the arterial occlusion dragon this vatic gangrene is more of venous blockage OK more commonly venous occlusion the veins are occluded okay the venous drainage is blocked so the venous drainage is blocked congestion will happen no new blood is coming to that area no new blood is coming to that area venous congestion is there so tissues will tissues will die okay but in your exam for example point of view sir I do not want to remember all these things tell me something which will come in your exam is image based question see when you see a clear demarcated line and if it's looking like a mummified appearance a dry mummified appearance that's a dry gangrene it's an example of what it's an example of coagulate your necrosis okay Square creative necrosis sir look here so this is more it's not looking dry cell it's not looking dry it's not looking mummified but here also tissues are dying tissue death is happening but it's more like liquidy okay here most of the time infection still starts are here infections will start okay so this is more of liquefacture necrosis necrosis along with the infections usually infections will develop here okay in dry gangrene usually infections are not developed OK there is no growth of bacteria that I will show you whether they go look sir here now see the line of demarcation in dry ganglion present okay so the line of demarcation means healthy ratio dead tissue present at the junction between healthy and gangliness part but in gangrene cases that line of demarcation is not clear okay line of demarcation is McQ line of demarcation is seen in Dragon green it is not seen in the weight gangrene next bacteria I have said you where bacteria will grow so in Dragon grain bacteria will not grow bacteria fail to survive in vertigang green area May liquefactory necrosis along with infection superimposed infection will cause the liquefacture necrosis okay so these are the some questions which I want you to know for your exam dragon is coagulated necrosis when ganglion is lift Factor necrosis is not same okay drag angle is because of the arterial occlusion with gangrene is because of the VR seclusion next after this the next question that will ask that will come in your exam is zincers degeneration what is the zinc or degeneration or zincerosis so this zincus degeneration is also called as hyaline necrosis ironic processor where this necrosis is happening necrosis of skeletal muscles okay so very important especially for the neat pH exam which is severe glassy glassy looking like glassy shining glassy or waxy hyaline degeneration they are the same things waxy they will use the word waxy degeneration that is happening in the skeletal muscles what exactly is it zenger's degeneration skeletal muscles are dying undergoing necrosis death why see necrosis of skeletal muscles in which condition in acute infectious conditions an acute infectious conditions because of the production of the toxins these toxins are going to give the stress to the muscles and the muscles are going to die okay so skeletal muscles are going to die so this type of skeletal muscle death is called as zincers degeneration okay so this younger degeneration it's which type of necrosis skeletal muscle is dying which type of necrosis again coagulative okay coagulative necrosis okay coagulating negrocessor see one thing sorry whenever you see the word coagulate in a process imagine my skeletal muscles my skeletal muscles are undergoing necrosis now I am saying it's an example of coagulated necrosis which means if you take a tissue and if you put it under the microscope and if you look at it the tissue architecture is preserved okay tissue architecture is preserved so it's still which type of infection zincus degeneration seen in which type of infection especially typhoid typhoid and not only in typhoid it's also serene's hepatitis also but typhoid said typhoid is also called as intric fever because of which organism salmonella Type e okay so which skeletal muscles are going to most commonly undergo this zincus degeneration with skeletal muscles so skeletal muscles here are rectus abdominis rectus abdomination okay so rectal supplement is what exactly is this muscle rectus abdominance rectus abdominance is a six-pack muscle that muscle okay we will have to go degeneration so with this all important types of necrosis are completed okay reversible cell injury irreversible cell injury after that cell death we have studied in cell death I have also done the necrosis and different types of necrosis is that clear okay guys now after this let's continue with the apoptosis very simple topic sir first you tell me you just name me sir apoptosis apoptosis is it physiological or pathological tell me necrosis is always always pathological every time necrosis is pathological cell does not want to die but someone from outside is killing the cell okay apoptosis is sometimes physiological and sometimes pathological cell both it's both physiological as well as pathological sometimes the cell have to die our body cells have to die sometimes I will explain you so it's both physiological as well as pathological so this is a programmed cell death okay everything is properly planned it's not like necrosis it's not like murder it's like a suicide sir okay everything is properly planned by using ATP we are killing the cells so it's a programmed cell death is called as apoptosis and one thing I want you to know is that after necrosis the cells are dying the cell membranes are ruptured and the cellular contents are leaking out after necrosis one thing very important point is after necrosis cell damage will leak the contents we leak The Cellar contents outside so that inflammation will start after necrosis there will be inflammation but here after a pop process there is no inflammation I will explain you later why why there is no inflammation because cellular contains the cell membrane is not damaged okay cell membrane is not damaged sir the cellular contents are not leaking out so no inflammation no neutrophils will come no recruitment of the neutrophils nothing will happen so no inflammation it's a program Itself by using ATP okay we are making everything by using at Pizza everything is programmed because we are using ATP okay ATP is used in this process and this apoptosis it is caspase dependent so caspases are the enzymes there are certain enzymes involved in this process of cell death okay what are those enzymes caspases so caspase is will kill the cell okay so what are some important points about the power process physiological and pathological okay it's a program cell death there is no inflammation okay no inflammation after the cell death and it's an active process and it's a caspase dependent some caspase as enzymes are involved in killing the cell now just look at here this is something which I find in the Internet it's very simple very interesting also see necrosis versus support process necros is always pathological upper processes may be physiological may be pathological most of the time in necrosis okay most of the time in necrosis sir many cells will die a group of cells because of the stress not one single cell a group of tissue because of arterial occlusion that veggie shaped area you have seen a little extra tissue more tissue is getting dead Okay so effects many number of cells adjacent cells surrounding cells will also be affected but this is apoptosis of purposes like suicide during suicide you will die and others are also going today no only one person one person is committing the suicide so affects very less number of cell single cells usually single single cells okay now during necrosis the cell size increases the cell size actually increaser cellular swelling will happen Okay water is coming into the cell reversible cylinder first initially cellular size is going to be increased and burst away okay and in apoptosis further later in next 15 minutes I will tell you salsa is actually become small with the time cell size is getting smaller and smaller the cell size is getting strong can okay now it's a necrosis is a passive process no use of any ATP apoptosis is active a for a apoptosis is active after necrosis there is inflammation seen McQ after necrosis there is no inflammatory reaction I have said you after necrosis cell membrane is damaged during necrosis cell membrane is damaged the cellular contents will leak out leading to inflammatory trigger inflammatory reaction in necrosis the cell membranes are intact cell membranes are not damaged similar contents are not leaking out so no inflammation okay now yeah this is the last one see Nico see in necrosis I have said you plasma membrane of cell membrane is a disrupted in apoptosis cell membrane is intact McQ all these are the McQ trust me for in this entire class this one single slide is the most most most important before going to the exam one should go through this okay just normal fmg exam this will be another this one single slide will be enough but if you are aiming for the need PG exams like a higher level of exams you need to have little more knowledge okay now sir tell me apoptosis is it physiological or pathological I said you apoptosis is both physiological as well as pathological what are the physiological conditions in which conditions physiologically cells will commit suicide in my body some cells they will commit suicide sir and it is good only for good for God is good it like it will happen each condition see physiological examples of apoptosis during embryogenesis okay when you are an embryo many many cells in your body will undergo apoptosis okay actually the classical example which they give you is your hand will be something like this it's like a stem cell one single stump okay now actually during embryogenesis the fingers are not there okay the dishes are not formed it's like a one single stem cell now here in this area whatever the cells were there in this area okay it's like a one single stump it's like one pad of tissue okay now whatever the cells which are filling in this area they will all undergo apoptosis so death car this cells in this area will create the spaces so that digits are formed okay this is a classical example okay so separation of digits okay so separation of digits during limb development one examples second example hormone dependent evolution in female we know every month once in a month or endometrium her endometrial cells will shed out okay why progesterone comes down whenever position is not there automatically the endometrial cells will undergo involution and death so how these are the cells their survival the cell survival depends on the progesterone if progesterone is not there they will commit suicide physiological this is not something pathological this is something normal ah whenever position is not there by physiology Itself by female physiology itself the endometrial cells will undergo death and shading will occur so this is again example of upper process endometrial shading during menstruation is an example of physiological apoptosis okay and deletion of Auto reactive T cells okay self-reactive lymphocytes are normally in your thymus thymus actually the T cells they will they are going actually it's like a school set the T cells they will learn there what is self tissue what is foreign tissue whom to attack whom should not be attacked the T cells maturation will happen in the thymus during that maturation what will happen they will differentiate they will know to differentiate which is self and which is non-self which is self and which is foreign antigen okay now during this process if a p lymphocytes for example say there is this one t lymphocyte it is recognizing the self it is recognizing the self antigen as a foreign antigen now is that good a lymphocyte have to recognize a non -self antigen okay it have to attack a foreign antigen it have to attack the bacteria not my own cells for example one lymphocyte it is identifying myself antigens as foreign and it's trying to attack means sulfur reactive these lymphocytes are attacking me only now what the cell should go I have to undergo the cells have to undergo apoptosis we don't want the cells so by physiology Itself by physiology itself these cells will undergo upper process they will die they will commit suicide okay so deletion of self reactive teal lymphocytes is an example of physiological apoptosis now for example if it is not happening failure okay you do not eliminate you haven't eliminated the self-reactive lymphocytes not eliminated sir they're still present in our body what they will cause they will cause autoimmune diseases okay they will cause what autoimmune diseases next so physiological hypothesis examples I have given you embryo Genesis hormone dependent conditions like evolution of the endometrium when you remove the progesterone every month once in a month and the deletion of the self-reactive lymphocytes elimination of the self-reactive lymphocytes is also an example of physiological about process now favorite question in the need PG exam and fmg exam sir councilman bodies okay councilman bodies what are they sir councilman bodies these are nothing but dying hepatocytes the hepatocytes which are infected with the virus okay so what are these consonant bodies they are dying hepatocide same okay these are the hepatocytes they are undergoing what they are undergoing apoptosis why they are undergoing apoptosis they are committing suicide why because inside them there is a virus it's CV virus okay hepatitis virus is there inside them now they have decided let's commit suicide right because the virus is there the cell is still alive the virus will replicate and more number of copies are going to be produced now this will spread to the surrounding healthy tissue also so now this hepatocyte have decided let me commit suicide so this dying hepatocyte is called as the councilman body seen in viral hepatitis okay the continent bodies are seen in the viral hepatitiser Okay so right here seen in viral hepatitis genital hepatitis now and not only this I am going literally fast now not only this just by heart so sell our tumors if you are having a tumor okay there is a tumor so there is a mass now most of the tumor cells they are not normal cells most of the tumor cells will undergo death the process so this is again a power processor most of the tumor cells they will die by which process apoptosis that's a pathological apoptosis tumor is not something normal viral hepatitis is not something normal the cells are dying in some pathology but in a more programmed way they are deciding that they are terminating themselves okay by programmed cell deaths so councilman bodies and sell within a tumor tumor conditions cell death in tumors and whenever you use anti-cancer drugs okay whenever you use anti-cancer drugs that will kill the cancerous cells so that's also because of apopt processor cell death inducer by anti-cancer drugs are celled at inducer by radiation radiotherapy all these examples of hyper process okay so tell me what are the three pathological examples of apoptosis pathological apoptosis and giving anti-cancer drugs killing the cells okay these are the three pathological uh examples of upper process and what the physiological examples of upper process physiological during embryogenesis second one is elimination of self-reactive lymphocytes and endometrium endometrium shedding during menstruation so 100 question will come from this area okay this is the one thing which is very important and after this is the second thing and most of the time in exam this was the question asked this is the question asked during embryogenesis the separation of digits is an example of physiological apoptosis the cells are committing suicide okay sir how about process is happening there is something program right program cell death Casper is a dependent okay so what exactly is happening in the support processor look at here there actually there are two ways by which a cell will commit suicide two ways sir okay now see now there is this one cell now it is simply sitting like this now a signal is coming from outside a signal is coming from outside telling that we still have to die this will have to die so there is an extrinsic pathway okay an extrinsic pathway from outside signal is coming to terminate the cell now the cell will undergo death so this is called as extrinsic pathway now you will understand don't worry the extrinsic pathway of apoptosis so what is this extrinsic pathway of our process see now this is your sensor this is one cell okay now on the cell on most of yourself there is this one receptor present this receptor is called as cd95 okay our death receptor okay there is 3095 depth receptors present now this this that this death receptor okay now if it gets a signal C from outside this this ligand is called as a fast ligand a phase okay fast ligand now this fast ligand is coming and binding with the death receptor now it's a signal now it's a signal that this cell have to undergo death okay this cell have to autocodile signal is coming from outside that this cell now it have to undergo that now you should die now you should die something like that okay now fossil again is binding with the death receptor that is CD 95 now what happens they go once this receptor is activated this is a death receptor actually primerization like a three death receptors will come from a fuse OK there is something called as a primerization of the receptor you know not that much important but once the cd95 receptor is activated it will activate intracellularly it will activate something called as fad do you know what is fat fast associated fast Associated depth domain foreign the death receptor is activated the timerization of death reciprocal will happen Okay three death receptors will fuse and they will activate the fat okay this fast Associated depth domain is going to be activated now what this fat will do now what is fat will do sir gas phases now they are coming same now they will activate Pro Cast phase number 8 under 10. okay now these are the processes they're sleeping now that the inactive Casper system now this inactive caspasis are going to be converted into active caspases caspase these are the enzymes these enzymes are getting activated just no till here no till here okay so extrinsic pathway purpose is what is happening the extrinsic Pathways is signal is coming from outside the fast ligand is going to bind with the death receptor that is cd95 death receptor is activated primerization of receptor will occur that activates the fat pass Associated the domain is activated now is fast associated with domain will convert the inactive caspasis inside this in each cell inactive casabases are there so this inactive Pro Cast space 8 10 to 10 are converted into active 810 okay now they are ready these Casper is are the first initial Cash basis rate okay these are the initial cash bases so these eight and ten are called as the initiator caspasis initiator caspasis okay there is one more initial caspase I will explain you but just for now ah 8 and 10 are the initial cases now they are activated I am ready now what is intrinsic pathway extrinsic pathway well and good now what is intrinsic pathway of upper processor no signal is coming from outside there is nothing coming from outside now still cell is under stress system now the cell is having more and more stress now cell is getting more and more stressor now cell will decide this is not the time I should leave okay I should not live in this stressful environment now do you know what happens the intrinsic pathway means okay do you know what happens see actually in each and every cell okay in our salesman okay in our cells there are some stresses sensors present okay in our cells this stress sensors are present McQ okay fmg PG McQ these are the stress sensors they were all the time since the stress inside the cells if there is more stress less stress is everything good or not then all the time sensing what are the strength sensors Puma these are the stress sensors they will sense the stress everything normal or not normal or not normal or not now whenever there is more stress on the cell okay microbiological stress are immunological stress or radiation on the cell stress is increasing sir now they are detected now there is more stress now they detect itself now do you know what they will do now they go so this stress sensors they will activate the pro apoptotic factors now they will activate certain Pro apoptotic factors Pro means what they will do the apoptosis now the stress sensors they are activating the pro apoptotic factors in each and every cell see in my every cell there are two sets of practice person two two sets of like you know these factors present one is pro apoptotic factors anti-apocratic factors means it will cause the apoptosis and tap operas means they will inhibit the children they will they are anti-apoptosis so what are the pro upper process again FMJ McQ and as need PG McQ in each and every cell there are pro upper processing factors present what are they back backs BCL XL p53 so these are the populism they will kill the cell they will kill the Cell Pro apoptosis but in each and every cell there are anti-apoptosis factors also what they will do they will prevent the cell death what are they bcl2 MCL BCL XL these are the anti-apocratic factors normally normally the probability factors anti-appropriate factors there is a balance factors there is a balancer but right now right now what is happening look there is more stress okay now there is stress on the sensor now stress is going to activate what stress sensors been bit bad North some Puma now they are activated now what distress sensors will do they will activate the property factors they increase the number of four appropriatic factors and this anti-apoprotic factors are inhibited they are inhibited sir anti-apocratic factors are inhibited okay now tell me now tell me what happens sir this concentration their concentration increases their concentration decreases do you know what happens intrinsic pathway okay an intrinsic pathway normally what is this organelle can you tell me what is this organelle sir this is the mitochondria this is the mitochondria now sir can you tell me what are this can you tell me what is this sir in the inner mitochondrial membrane in between actually outer mitochondrial remember inner mitochondrial membrane in that space that inter membrane space there is a substance present do you know what is the substance called as Sir this is called as cytochrome C which is the dangerous substance the dangerous substance in the sensor cytochrome C so the cytochrome C actually it is present on the inner mitochondrial membrane it's present on the inner mitochondrial membrane okay now it will never ever it will never leak into the cell so normally it will never come into the cytoplasm never but right now the cells are under stress the stress sensors are activated now what they will do now they will inhibit they will decrease the anti-apoptotic factors look okay just look at here sir they go normally do you know what is this red color thing which I have shown here these are bcl2 molecules where you have studied bcl2 so the important molecule bcl2 bcl2 is anti-apoptosis it will inhibit the apoptosis no cell death no cell death but now same in stressful conditions this stress sensor do you know what they will do stress sensors they are decreasing they are inhibiting they are decreasing the number of anti-apropriatic factors so now look here what happened sir according to able to series okay but anyway now look here this BCL 2 molecule it's gone the bcl2 molecule now it is not there when you remove the bcl2 molecule now what happens cell cytochrome C is going to leak into the cell so the cytochrome c is now leaking into the cell cell now what the cytochrome C will do now cytochrome see once if it comes into the cell the cell will die for sure the cell is going to die for sure sir so the cytochrome see it is going to bind with a substance called as a path one a path one and do you know what is apoptosis apoptosis activating Factor 1 F1 cytochrome is going to bind with the a path one now this combo is the cytochrome c and a power 1 is called as apoptosome is formed okay now what you are left with one thing I want you to know so easily any signal coming from outside in this pathway any signal is coming from outside no signal no signal is coming from the outside it's the stress sensors dim bit backs knocks of Puba they detect the stress whenever the stress on the cell is increasing they will inhibit the anti-apopotic factors they will increase the probability factors so because of that bcl2 is gone now cytochrome C is going to leak into the cytoplasm cytochrome C binds with a path1 bombing apoptosome now what is this a purpose I'm doing an apoptosome is converting pro-cast phase number nine in two caspase number nine Pro Cast space means inactive caspase this is active caspase So Pro Cast Space Nine is converted into active caspase number nine so at the end of the day so what we have seen we have seen extrinsic pathway because of the depth receptor death receptor pathway sir cd95 information is coming from outside signal is coming from the outside the cell should die see eight and nine caspases are activated because of the extrinsic pathway because of the intrinsic pathway caspase number nine is activated so this 8 9 and 10 they go eight n here 8 and 10 here 9. so what are this eight nine and ten take a small node so this 8 9 and 10 car spaces these are the First Cash bases which are activated 8 and 10 are activated in the extrinsic pathway nine is activated in the intrinsic pathway nine is activated in the intrinsic pathway so these eight nine and ten are called as initiator the other initiator cast phases now initiator caspians are activated once eight nine ten are activated that's its cell will die simple now initiation completed now what is the final thing execution initiator cash processor activated now you know it say they go caspase number eight and ten separately I am writing why I am writing separately because 8 and 10 are activated because of extrinsic pathway extrinsic pathway this caspase number nine is activated because of intrinsic pathway doesn't matter whether it's extrinsic path where intrinsic pathway once if 8 and 10 are activated and once if nine is activated what they will do they will activate the executory caspases these are the real heroes here these are the real heroes who are they before the real caspases three six and seven so caspase number three six and seven these are executionary executionary Casper this so what are the executing sir what are they executing final thing cell death apoptosis so this Casper is number three six seven they activate what phospholipases inside the cell once phosphorables are activated cell membrane damage organelles are organal membranes are going to be damaged proteases once the proteases are activated the cell cytoskeleton the entire cell cytoskeleton the actin filaments intermediary filaments breakdown okay and this caspase is a very very important McQ Casper this are also activated the enzymes called as endonucleases endonucleases are going to cause the fragmentation of the DNA the DNA is going to be chopped into small small pieces so done so phospholipids is kill the that cause the damage to the the phosphoryl images will cause the damage to the membranes okay the membranes especially not the outer memory not the cell membrane uh it will it will cause the damage to the membranes of the argonals okay and proteases once the proteins are activated the cytoskeleton is going to be damaged and endonuclease ones that have once they are damaged the DNA material is going to be damaged so that's it once this happens cell will dicer cell will die now for your exam okay neat pH exam what you should know is sir what are like you know what exactly these caspasis are doing caspase look this is some important McQ or what is the full form of this cash Pacer this enzyme Casper is eight ten the caspase means C for 16. okay these enzymes contain 16 amino acids 16 caspase means 16 ASP for aspartate aspartate they'll cleave they will cleave the proteins at aspartate residues they will break down the proteins at aspartate in every aspartate residues Okay so cysteine aspartacus caspasis means their enzymes they contain 16 amino acid and what they will do they will break the protein set aspartate residues okay that's why that's why that's what I want you to know so as per it every aspartate residue the protein will be breaked and endonucleases that is endonucleus is what they will do they will cut down the DNA at every 200 base period after every 200 base pairs one cut will be there sir okay they are going to make a chop after every 200 base pairs okay now at the end of the day just that they go because of the apoptosis okay because of the apoptosis what happened to the cell now because of the caspase of this caspase is activated the phosphor phospholipases proteases endonucleases the one cell now it is fragmented into small small fragments okay now still one upper protect cell at first it will shrink now it is going to be broken down into small small pieces with the intact cell membrane remember with the impact cylinder still the cell membrane is intact the cellular contents are not leaked out the cellular contents are not leaked out sir so this one cell is divided into small small small small pieces these pieces are called as pop toe tick bodies okay apoptotic bodies okay now in this upper product bodies what do you feel what do you see so in this apopotic bodies some cell organelles with the cytoplasm so cytoplasm will be there and some cell organelles are going to be there the one cell is driven into small small pieces cell now tell me so this apoptotic bodies should we leave them just like that no we have to clear it right we have to clear the entire debris now here is a lot of mess there is a lot of debris we have to clear it now how can we clear it McQ sir these apoptotic bodies these apoptotic bodies they will Express they are expressing something on their cell surface this is called as the 8B signals are actually this is called as a 8B signal okay so this is nothing but they go it's a 8 me signal whenever this apoptotic bodies are expressing these molecules on their surface now the phagocytics are the macrophages will come and eat the apoprotic one is clear the upper product Bodies Okay so the it may signal what is 8 me signal what are these green color molecules so this green color molecules are nothing but phosphatidyl serine and thrombosponding so mainly phosphodel settings are the phosphorididal serine is now expressed outside the cell it is externalized actually it is inside normal in healthy cells the phosphoidal saying molecules are inside but in apoptotic cells now this phosphodylserine molecules are exposed out it's like eat me signal okay it's like eat me signal set so whenever a macrophage see this password also in macrophage will come and clear this apoptotic bodies so the upper body produce are going to be cleared away so with this completed apoptosis is completed sir okay so in our properties what we have seen the extrinsic Pathways apoptosis because of the death receptor path the signal is coming from outside where Pro cap space number eight and ten are activated and intrinsic pathway because of the stress sensors activating the pro apocratic factors inhibiting the anti-apocratic factor the cytochrome C is leaked at the end of the day caspase number nine is activated so finally execution sir caspase number eight nine ten activates caspase number three six seven so this caspase is these are the enzymes they will actuate proteases endonucleases as well as the phospholipases they will break the cell into small small fragment which are called as a upper product parties and they will be clear they will be cleared Away by the macrophages okay because of this it may signal that is nothing but the phosphoridil serine okay now final thing how to differentiate between okay how to differentiate between apoptosis and necrosis you have two I gave you two dead cells two dead cells sir I gave you I am asking you whether this will have undergone apoptosis or necrosis now do STD call as DNA gel electrophoresis if a cell is undergoing necrosis it will show smear pattern smearing so this is a smearing pattern okay the DNA is going like in one smear okay it's like a smear sir so smearing pattern is seen But if a cell have undergone apoptosis we know in apoptosis endonucleases are activated they will chop the DNA at every 200 base pairs so what you will see is see here step ladder pattern is seen okay so stepladder pattern is seen in the upper process of course the platter pattern is also seen in necrosis that's a different question okay stepladder pattern is in both necrosis as well as our purposes but mainly if you have to select one single option one single option the platter pattern is same necrosis then this is one thing how to differentiate between necrosis and apoptosis and question sir what is the stain used by staining by staining method can you differentiate a population necrosis so there is a stain called as a tunnel stain so this tunnel stain it is positive only in apoptosis this tunnel stain the cells will get like you know there will be positive cells are going to be positive for the tunnel stain and necrosis there is a negative tunnel stain is going to be negative and necrosis positive in apoptosis so with this the entire topic all Integrations whatever need to be done whatever you should know for your exam I have completed sir okay M6 I will show you the mcqs just answer it what is zincer's degeneration just tell me the answer a b c d it is highly in waxy highly in degeneration our necrosis are the skeletal muscle in acute infections like typhoid which muscles is going to be emotionally affected rectus abdominis rectus abdominis is going to be affected okay next so this kind of clinical integrated questions will come in your exam okay it's just a general pathology sir what if you are going to give the next exam clinical integrated so once look at this a 73 year old man comes to the emergency department due to right sided weakness and difficulty speaking he's having right side Recreation difficulty speaking the patient woke up with symptoms an hour before arriving but felt when he went to the went to bed last night he has a history of paroxysmal sorry he has a history of paroxysmal atrial fibrillation Ah that's it here is the key is having what paroxysmal atrial fibrillation is Atria fibrillating okay his Atria fibrillating now you know whenever your ATR undergoing fibrillation there is a chance that in Atria clots will form sir neural thrombosis will occur clots will start to form in that fibrillating Atria now clots so this is the one thing you should know clots now what this clots will do these clots will go into the systemic circulation will occlude the blood vessels now they go so what's happening so the patient is having a paroxysmal atrial fibrillation but is not adherent with the medical therapy he's not taking any therapy his body temperature is okay normal blood pressure is 130 by 70 almost normal and pulses 110 per minute pulses irregularly irregular see whenever you see the word irregularly irregular pulse that is atrial fibrillation so that's a keyword whenever you see this keyword irregularly regular parts that's atrial fibrillation so now he is having atrial fibrillation okay so atrial fibrillation patients are ready to risk of remember atrial fibrillation patients are at risk of stroke or stroke thrombus will form in the Atria the thrombus will go into the cerebral blood vessels and will cause a stroke cell okay now physical examination physical examination shows right side hemiplegia stroke came paralysis stroke a okay hemisensory loss sensory losses are there Aphasia cannot talk properly despite of appropriate treatment a patient symptoms fail to improve okay whatever you're doing is symptoms are not coming to normal fail to improve means something damage permanent damage occurred okay over the next one week which of the following processes they have given an entire medical case and what they are asking which of the following process is most likely to be affected in the brain region ah atrial fibrillation stroke hair so brain is have undergoing infarction brain cell brain is some part of the brain is dead now tell me what is answer see definitely the answer here is diesel okay D why because brain and pancreas are rich in enzymes hydrolytic enzymes which type of negrosis liquefactory necrosis so hydrolytic enzyme inducer tissue degradation that is an example of X Factor necrosis okay so here answer is D now answer this a 46 year old man present to your office with slowly growing neck Mass he's having slowly growing neck mass the mass is Tony hard on palpation it's a Stony hardship the neck mass is totally hard on pulpation and seems to be fixed to the adjacent tissues it is fixed to the adjacent tissues after initial evaluation see after initial evaluation combination chemotherapy is prescribed you are prescribing him combination chemotherapy okay you detected you diagnose that it's some cancer okay you are doing the chemotherapy several weeks later the mass significantly decreases in size and biopsy determinates many shrunken eosinosphynic cells with in the tumor okay within the tumor which of the following see I have said you tumor cells will die by giving anti-cancer drugs if you give anti-cancer drug cells will die by apoptosis the cells will die by apoptosis in apoptosystem mean okay in apoptosis what will happen cytochrome C is going to leak out of the sulcer okay intrinsic pathway cytochrome is going to leak out of the cell binds with epf1 forming apoptoso right so which of the following substances released from the mitochondria most likely trigger the cellular changes cytochrome C is going to leak out remember one thing tumor cells die via apoptosis if you give anti-cancer drugs that anti-cancer drugs kills the cancer cells via apoptosis now answer this x 60 year old man comes to the emergency department due to acute onset okay acute answered right flank pain right side flank pain okay nausea and vomiting for the past her okay his medical condition includes prostate cancer is already having prostate cancer and membranous nephropathy okay blood pressure is 148 by 60 and pulse is 95. on physical examination the patient appears to be moderately distressed due to pain and a diaphoretic means he is having little pain and his diaphoretic means waiting is there there is right cost overtebral angle tenderness right side right side Coastal vertebral okay vertebral angle tenderness is there urine analysis shows hematuria okay contrast enhanced CT reveals wedge-shaped perfusion see veggie shaped I said when the arteries are blocked then the weight just say whenever you see the word wedge shape perfusion defect wedge-shaped in farts blood vessel is blocked okay see now when you go into your second year third year then you will understand see what is a problem he is having say membranous nephropathy okay membranous nephropathy you should know again I will teach you this again in renal pathology those patients whoever have membranous nephropathy they'll more likely to develop the renal artery blocks green Lottery will be the real Lottery will be blocked sir because of the clots nephropathy is one of the most important risk factor for the blocks in the renal arteries now same thing happened here there is a clot that happened blocking the artery leading to the wedge-shaped infarct wedge-shaped infarction real blood vessels are blocked wet shaped in fact so one step of necrosis which type of necrocessor answer is coagulative necrosis okay see the affected renal tissue is most likely to develop which of the following histological changes over the next several over the next several days coagulative necrosis the tissue architecture is preserved ghost cells okay denaturation of the protein so coagulation of the proteins is going to cause the architecture preservation okay now completed till apoptosis right necrosis and apoptosis are completed now let's do other side other types of silt okay the other types of cell death now the other types of silhouette are say necroptosis necroptosis the questions which were asked in the exam these are the topics which were very important like our process in necroptosis what exactly is it is it apoptosis or is it necrosis see necroptosis is a combination of both okay it's a combination of both necrosis as well as apoptosis so necra process what exactly is it necra process is both a combination of necrosis and apoptosiser so something related to necrosis and something related to apoptosis happens here in the micro process okay now so this is also called as programmed necrosis program it's mainly a necrosis okay it's mainly necrosis why we are calling it as necrosis at the end you will understand okay at the end you will understand so necroptosis is also called as a program necrosis in the name itself it's a necro necro stands for necrosis and ptosis what is this apoptosis so necrosis and apoptosis now this necroptosis yes it is a caspase independent caspase independent cell death why we are not calling it as apoptosis complete apoptosis right because the caspase is no cash spaces are involved Celtic is happening but yes it is programmed it is programmed but the caspases are not involutely stress class we have discussed caspase number eight nine ten three six seven caspasis okay those caspases are not involved in necroptosis okay now is it an active processor yes of course it's an active process just like apoptosis is also active next is it physiological or pathological it's both physiological and pathological just like apoptosis apoptosis is physiological and pathological here also this necroptosis is again physiological and pathological just recap what are the important things which you should know necroptosis is also a type of cell dip just like necrosis and apoptosis necroptosis is also a special type of cell death sir is it necrosis are apoptosis that is combination of both both the necrosis as well as apoptosis certain features of necrosis are seen and certain features of apoptosis are same okay why we are calling it as apoptosis what is something related to apoptosis here it is programmed okay it's a program selected okay it's an active process yes true and it is also physiological as well as pathological both now as we are saying it this is both physiological Electro processes in both in physiological conditions as well as pathological conditions now let's see what are the physiological examples of necroptosis physiologically necroptosis happens in our body do you know where sir the growth splay the growth plate formation for your exams is very important okay we are again and again every morning we are all the doctors have okay we are not going to be like you guys are not going to be a pathologist you are going to be doctors so you should know necroptosis is physiological and pathological what are the physiological examples and what are the pathological examples mainly concentrate on them okay for your exams okay so they are going to be both physiological and pathological physiological example is during the growth plate formation okay during the growth plate formation in your bones certain cells will undergo necroptosis it is physiologically okay this is physiological and what are the pathological examples of necroptosis where you will see pathological uh necroptosis in pancreatitis condition in fatty liver fatty liver main cystiatosis you know it right straight or hepatitis the fatty liver whenever the person is suffering with fatty liver that's definitely pathology pancreatitis definitely pathology okay and cytomegaloviral infection CMV if the virus if this virus enters into our cell if this virus enters into a cell that particular cell will undergo necroptosis if you commit necrop processor okay and neurodegenerative disorders like parkinsonism and Alzheimer's okay in these conditions in parkinsonism and in Alzheimer's the neurons okay parkinsonism is pathological Alzheimer's is pathological so in this conditions neurons will undergo necroptosis okay so now tell me necrop process important points it's both physiological as well as pathological It's a combination of necrosis as well as upper process why I am saying this as necrosis and apoptosis later you will understand we will understand okay but tell me what are the physiological examples of necroptosis growth plate formation mammalian growth plate formation and what are the pathological examples in pancreatitis in yesterday's class I have discussed in pancreatitis acute pancreatitis there is a liquefacture necrosis Peri pancreatic fat will undergo fat necrosis okay but some are the cells in pancreatitis will undergo necroptosis also okay necroptosis so fatty liver and neurodegenerative disorders like parkinsonism and viral infections like cytomegalovirus infections so in this conditions a special type of cell death will occur and that special cell death is NECA processor ok now what is a pathway I have said you it's a programmed program okay it's not happening just like that okay there is a sequence sequence of events are going to happen okay see the pathway of necroptosis is now first tuber necrosis Factor the tuber necrosis factor is going to come and act on a cell okay for example imagine this is the cell that's going to undergo the necroprocess now first the tumor necrosis Factor Alpha it's going to come and bind with this cell first it will go and come and act on the cell so the tuber necrosis factor I will show in the image also so this is the tuber necrosis Factor they go it is going to bind with its receptor tumor necrosis factor receptor okay tuberculosis factor is coming and binding with the tumor necrosis factor receptor so what happens now this tumor necrosis factor receptor it's going to activate certain proteins inside the cell certain enzymes I should say certain enzymes inside the cell called as a rip Kinesis so tnf tnf is going to bind with its receptor binding of this activation of this TNS tnf receptor is going to activate the rip Kinesis okay so now this rip kinases there are two types of rip Kinesis repair is one and two there are two rip Kinesis this ripokinases what they will do now they will activate something called as mlkl or milk no need to remember the full forms Ok mlkl Okay rip Kinesis are going to activate which structure inside the cell mlkl that rip kindness kinase kinase is what they will do kinases will do the phosphorylation right so this rip kinases are going to do the phosphorylation of this mlkl so once the MLK is phosphorylated once it is activated that's it sir now it is going to cause the cell membrane damage and now the cell membrane will be damaged the cell like you know water will enter into cells cell will become swollen okay see cell membrane damage is occurring inflammation will occur cell will swell and it will die it will die so there is a pathway sir there is a pathway okay there is a program like you know there is a blueprint this is how it should happen so that's why we are calling it as apoptosis okay that's why we are calling it as apoptosis okay then y t is called as a necrosis say at the end of the day the cell membrane damage is happening normally in our property see normally in apoptosis cell shrinkage will happen the cell membrane is not going to be damaged but here in necroptosis and then they go and the end results are morphologically the cell is getting damaged and this damage looks like necrosis okay after the cell damage even inflammation will start sir because the cell membrane is getting damaged the cellular contents will leak out once the cellular contents are leaking out that will trigger the inflammation that will recruit the neutrophils inflammation will start sir Okay so let's look at here sir this is the cell okay imagine now this is the cell membrane now on the cell membrane who is that tnf is that tumor necrosis factor receptor when the tnf when the tuber necklace is Factor binds with the dnf receptor now what it will do I said you it's going to activate the rip kinases three now what the strip Kinesis will do sir this ripkinesis are going to phosphorylate mlkl okay so now what this MLK will do now it will cause the cell membrane damage and lead to depth of the cell okay so necrosis like you know that at the end of the day the morphologically the morphologically the cell that looks like neck crosses because after the cell death inflammation will follow up so looking like necrosis right okay that's it even here this is little a more detailed diagram of an acroprocess what exactly happens same even same events the tnf is going to bind with its receptor tuber negrosis factor receptor now when the tuber necrosis factor receptor is activated they go what is happening the rip coin is a strip coin is one three this rib crisis are activated these rip kinase is what they will do so these rip kinases of course here one point I want you to know here caspase is involved which caspase is not active caspase inactive caspase okay inactive caspase number eight other pro caspase eight is involved here okay now you can ask me sir you said this is caspase independent cell death necroptosis so you said that it is caspase independent is caspase independently independent only but here see they go it's a inactive caspase eight okay not active caspase this is broadcast space okay Pro Casper is 80 is involved row caspase it is involved so now what happens sir these three things rip kinase one ripkind S2 along with this Pro caspase they will cause phosphorylation they call phosphorylation of mlkl once the mlkl is activated what happens that will cause necroptosis the mechanism I also have explained you now in your exam in your exam what they will ask you is Rip Kinesis are involved in Ripken is one Bitcoin S3 mlkl they're all involved in the necroptosis necroptosis pathway okay initiation is from that human necrosis Factor human ecosis factor activates the tumor request factor receptor and all the events you already know it so after necroptosis inflammation is seen yes cell damage cellular swelling cell damage followed by inflammation inflammation will be sensor McQ okay this mcqmc inflammation is seen in necroptosis true next continue with the pyroposis necroppers is completed next one is what pinoptosis so what exactly is this type of cell death this is also a type of cell death necrosis apoptosis the next type of cylinder that I am going to discuss is called as a pyroplosis in this spiral process as a doctor going for the exams what you should remember is they go pyro here stands for a pyrogen okay pyrogen what is the pyrogen the pyrogen is the one is a chemical which is going to cause a fever okay so after this cell death in this type of cell death or I should say after this cylinder the patient is going to the person is going to experience the fever sir okay so Pyro pyro means it's a like you know the the agent which use the fever the one which causes the fever okay so what is that pyrogen in this case here the pyrogen that pyrogen in this case is interleukin one okay interleukin one is going to be released and so pyroptosis pyro completed and again see ptosis is there what is the ptosis apoptosis okay so pyroptosis is a combination of pyrogen and apoptosis spiroptosis so why I am using the word apoptosis here the reason why I am using the word apoptosis is because again this is program cell death okay this is program celled itself so you can see a sequence of events okay sequence of events are going to occur here okay Shall We Begin same now this pionoptosis listen here see there is an antigen now antigen might be bacteria Salmonella bacteria okay it was actually discovered with those algorithms so antigen let's take a bacteria okay the bacterial antigens okay now this bacterial antigen is going to come and bind with this receptor on the cell who recognizes this antigens all like receptor tlr stands for tall like receptor okay so this bacterial antigen it's going to bind with the tall like receptors Now The stall-like receptors are activated sir first or like receptors are activated okay now the stallic receptors what they will do now once if you activate them they are going to convert the pro caspase 11 4 and 5 mainly here important is 11 Pro Casper is 11 okay Pro Cast space number 11 4 and 5 will be converted into active caspases active caspase number 11 4 and 5. now you should look here see gas prices are getting involved or not yes sir casparates are getting involved then why we are not calling it as just like apoptosis why this is not just apoptosis why it is called as pyroptosis because yes of course this is apoptosis but the caspases which are involved here in this spiroptosis are different these are the different caspases in apoptosis then the intrinsic pathway in extrinsic pathway instead as class I have discussed in apoptosis which caspases are involved in apoptosis sir caspase number three six seven and even the Casper is never initiated caspase is like the caspase number eight nine ten they are involved but here look at the caspasis these are Casper's number 11 4 5 these are different caspases which are getting involved okay so now just tell me what is happening in this panoptosis in this pyroptosis this pyroposis actually it is a pyrogen involved here there is a pyrogen involver what is that pyrogen I will discuss OK and what's happening antigen binds with tall like receptor so the Pro Cast spaces are going to be converted into active gas phases now they go sir now once this cash phases are active now they are going to activate something called as gsdmd so do you know what is this jsgmd so this jsdmd for gas dermin okay something called as gas dermin is getting activated now what is this gas damager I will explain you okay I will explain you in this diagram I will explain you but for now look at here caspase number 11 caspase number four and caspase number five are activated now they are going to activate and they are going to produce this something called as gas damage now this gas statement do you know what it will do sir now it is going to cause the cell membrane damage actually it will put porcessor it will put pores okay it's gas there mainly it's going to put holes into the cell membrane causing the cell membrane damage first cell will start to swell cell membrane damage will occur followed by inflammation against inflammation is going to be there okay cellular swelling will occur cell membrane damage and inflammation so even it is looking like necrosis right yes even this type of cell death inflammation will be there okay even in this type of cell death inflammation will be there sir okay so this gstmd is going to be produced just tell me sir bacterial antigens are going to bind with the Tor like receptors the tall like receptors are going to be once they are activated they will convert the procast-based number 11 into active caspase number 11 act caspase number 11 is most important now this caspase number 11 is going to activate the gas German gas Dam mean what it will do it is the one which causes the cell membrane damage so this is one half of the story one half of the story sometimes do you know what happens sometimes the antigens can directly enters into the cell the bacterial and antigens can directly enter into the cell once they directly enters into the cell now they go they are going to bind with a not like receptors okay now they are not like receptors ok now they are binding with not like receptors antigen binding with not like receptors so antigen is going to bind with the not like receptors now this complex this complex is going to activate something called as inflammozome okay so inflammosome is activated in iraptosis this inflammosome is activated sir I will show you in the image also okay so inflammosomes are activated now what happens what this inflammosome will do set this inflammazone they go it will activate Pro Cast phase number one okay Pro Cast space number one this is the most important sir on this side broadcast phase number 11 is important and this side Pro caspase number one is important so this Pro Cast space number one these are the enzymes so these are the very dangerous enzymes caspases they will cause the death of the cell the Pro Cast space number one is convert converted into caspase number one now this caspase number one what it is doing so now is caspase number one is again going to produce gas damage again going to activate the gas German so no you know it once the gas German is produced it is going to put the holes inside the cell cell membrane damage cell depth okay and not only that not only that so this Casper is number one is going to activate is going to activate Pro interleukin 1 into interleukin one okay what I'm what I'm telling you this caspase number one sir what it will do it will convert the pro interluke in one means inactive one inactive okay inactive Pro interleukin one into active interlooking one and interleukin 18. so caspase number one it is going to help in production of each interleukins interleukin one and interleukin 18. in this hydroptosis now tell me there are two Pathways there are two pathways by which the gas by which the gas element can be produced what are the two Pathways one thing is when antigen binds with look when antigen binds with tall like receptors the Tor like receptors are going to convert the pro case number 1145 into active caspase number 1145 these active casparas are going to activate the gas dermin gas dermin is going to cause a cell Damage Done not only that if a bacterial antigen if it enters into the cell if it enters into the cell now this additions can be recognized by the not like receptors now antigen antibodies sorry not antigen antibodies antigens are going to bind with the not like receptors now they will activate a structure called as inflammosome now the inflammosome once it is activated they will convert the procast phase number one into active caspase number one the caspase number one again is going to produce the gas German again it's going to produce a gas German gas German do the cell death Point number one is the pro the caspase the caspase number one is going to help in production of each interleukins interleukin one and interleukin 18 so this is the point this interleukin one it comes out of the cell this interleukin one is the one which causes the fever so this is the pyrogen interleukin one is called as a pyrogen so pyrogens are produced at the end that will cause the fever cell Okay so what else you should know please look here so this caspase 11 okay important one the Casper is 11 4 5 okay this caspase 11 mainly so what it is doing it is also directly activating the inflammozome okay so it is also activating what inflammozome okay so inflamazoo is activated by this not like receptors and these are not like receptors as well as this Casper is number 11 can also activate the inflammosome now whatever we have seen let's look it in the pathway okay this is simple diagram which I have drawn now let's look the pathways let's look at this pathway okay now look at look at here see now this is the bacterial antigen lipopolysaccharides bacterial antigensor now this bacterial antigen where it's going to bind with it is going to bind with tall like receptor once the tall light receptors are activated now tell me what they will do they will convert the Pro Cast basic Pro Cast space number four Pro Cast space number five and procast space number 11 into active caspase number four five and eleven so these caspases are produced the acute casparates are produced now what these caspases will do I have explained so this caspase is they will produce this as German so what is gasoline will do so this gas determin C gas dermine poor formation is going to form the pores in the cell membrane cell membrane damage the fluid will come into the cell fluid will like no cellular swelling will occur cell damage will occur okay cell membrane damage and cell death will occur followed by the cell death Okay so this is one half and not only that you can also see here see these antigens they can directly enters into the cell okay these antigens they can directly enters into the cell now after entering into the cell they binds with not like receptors now once they bind with non-like receptors they will activate what they will activate inflammosome these inflammosomes what I have to do they will convert procast space number one to active caspase number one now what this active Casper is number one will do they call this active Casper is number one say again it is activating the gas domain now gas statement what it will do it will put holes in the cell membrane kills the cell okay and not only that this caspase number one what it is doing it is converting the pro interleukin one and pro interleukin 18 Pro means inactive so this caspase number one is converting the Pro interleukin-1 and interleukin 18 into active interleukins say interleukin one and interleukin 18 is released out of the cell they are coming out of the cell and they are responsible for the fever interleukin one is responsible for the fever mainly okay so with this pyroptosis is also completed apocalypse is completed pyrup process is also completed I have said you this caspase number 11 say they can directly activate the inflammozome this is called a secondary inflammasome activation okay so this caspase number 11 can directly activate the inflammation have shown here okay say caspase number 11 it can directly activate the inflammosome I have shown you okay with this necrosis apoptosis necroptosis and pyroptosis all are completed okay we have seen the four important types of necrosis apoptosis necroprosis paraprosis most of the students majority of the students they know necrosis apoptosis but you should know you are a special student so you should know that what is necroptosis and what is a pine optosis okay what's that Pathways MLK is activated in necroptosis are activated in necroptosis gas phase number caspase number 11 caspase number one are activated in find our process interleukin-1 is produced in fibroptosis fever is seen in pyroposis okay now after this the next topic that we are going to start is cellular adaptations very simple topic now let me ask you what exactly is the cellular operation what exactly cellular operation sir see when you are stressing yourself when you are giving stress to the cell the cell will try to adapt to that stress okay if I am giving you more and more work so initially we will try to adapt to the environment so even cells will try to adapt to the stress so this is called a cellular adaptation okay so for example simple example I will give you if you are going and doing exercise every day you are putting stress on your muscles right you are putting stress on your muscles so what your what happened to your muscle in order to encounter that stress in order to weigh the like you know to have the power to lift the weights now your muscle cell will undergo hypertrophy your muscle cells are becoming bigger so that they can help you in the work okay adaptation the cells are getting adapted to the stress so how many types of cell adaptations are there sir Cellar operations include hypertrophy hyperplasia metabolasia atrophy okay we'll discuss about them one by one okay first type of cellular adaptation is hypertrophism what is what exactly is this hypertrophy now imagine there is this one cell okay normally this is the size of the cell now with this cell if it increases in the size if it becomes this much big okay if it becomes this much bigger so now what have happened hyperplasia hypertrophy hypertrophic cell so hypertrophy means increase in the size of the cell okay the size of the cell is increased okay the size of the cell is increased the increase in cell size why cell size is getting increased now what is the reason what is the primary reason why the cell size is getting increased because in that cell when you are giving stress in that cell protein synthesis is increased increased in the amount of protein synthesis protein synthesis increased that's why the cell is increasing in size okay next now example point of view what you should know that when hypertrophy is happening that proteins are getting more and more right more and more protein synthesis is happening so the cell size is also increasing the proteins are helping in the formation of the cytoskeleton so the cell size is increasing now in the cells what you will find what you will observe sir in the cells the transcriptional factors OK transcriptional factors are increased so what are transcription factors transcription factors are the ones which helps in the protein production so this transcriptional factors okay so transcription factors they will cause first transcription followed by translation proteins will be produced okay you know it right from the DNA first transcription occur followed by translation at the end of the day DNA is going to be produced so in this cell in that particular cell which is undergoing hypertrophic a if you check the transcriptional factor levels are more which transcriptional factors are these transcription factors are called as geta 4 and fat in fat and meth2 see these are the transcription factors which are increased in the cells when those cells which are undergoing hypertrophy these transcription factors are increased elevated memory is elevated sir okay is that clear now after this let's discuss about the examples OK where you will see the hypotrophism in which conditions you will see the hypertrophic they go sir when you do go for the exercise okay when you go for the exercise so exercise they go exercise whenever you do exercise what happened to the muscles muscles will undergo hypertrophy right okay muscle cylinder go hypertrophy whenever you do exercise muscles will undergo hypertrophy that's one example next outro tract obstruction so what is this outro tract obstructions and the cases of outflow tractor obstruction again the organ the Argon the Argon will undergo hypertrophy one example I will give you look here now imagine this is your left ventricle I am drawing here the left ventricle only the left ventricle now this is the outflow from the left ventricle what is this this is iota now imagine this is the left ventricle this is the Iota now what is this wall which is present over here the valve it's the iotic wall now in this condition imagine the iotic wall is still lost okay the iotic valve stenos that is iotic stenosis the patient is now having iotic stenosis then the patient is having iotic stenosis in order to push the blood into the Iota okay now this left material how to push the blood into the Iota right so what happened to the left ventricular size and now this left ventricular myosides they will undergo hypertrophy so now we are going to have a very big heart sir very big heart big size heart the hypertrophied heart is going to be seen okay so whenever there is an obstruction the proximal part will undergo hypertrophy okay now this is one example and apart from that especially for your exams especially for the board exams FMJ examinate exams these questions will be asked sir best henna breast tissue here so breast is going to increase in size the breast tissue is going to increase in size in which condition during puberty it will increase during pregnancy it will increase now why the breast tissue the breast size is increasing is it because of hypertrophy or hyper pressure yes both because of hypertrophic hyperplasia so during puberty and during pregnancy in both the conditions both the hyperplasia and hypertrophy will occur both will occur but hyperplasia is more prominent than the hypertrophy hyperplasia is more so more prominent than the hypertrophic okay same way uterus also uterus or uterus during puberty and during pregnancy it will increase in the size the uterine size will increase okay the uter size will be increased why this there is this increase in the size why sir it is increase in the size is again because of both hypertrophy as well as hyper pressure both hypertrophy occurs as well as hyper pressure occurs but hypertrophy is the best answer these are the already asked questions okay in breast hyperplasia breast hyperplasia is more than hypertrophy and in uterus in uterus the hypertrophy is more than the hypoplasia okay so the what are the four examples of the hypertrophy I have given exercise imagines outflow track obstruction rest during pregnancy and puberty and uterus during pregnancy and puberty investment breast there is more hypoplasia and in uterus there is more hypertrophy okay more hypertrophy than hypoplasia and tell me hypertrophy means what increase in the cell size because of what because of the increase in the transcription because of the increase in the protein synthesis by the transcription factors which are transcription factors are going to be elevated the transcription factors are here the data for nfat and mf2 now after this let's discuss about the next cellular adaptation there is adaptations here okay that is hyperplasia the next cellular adaptation which we are going to discuss here is a hyperplasia so what exactly is hyperplasia hyperplasia means one cell it is dividing into many cells OK the number of cells one cell will divide into two two will divide into four four will divide into eight cells okay so what is hyperplasia hyperplasia means increase in the number of the cells one cell dividing into two cells these two cells dividing into four cells means due to the mitosis due to the mitosis the number of cells are getting increased so increase in cell number okay now here regarding hyperplasia I want to ask you some questions sorry is this hyper pressure is it dangerous is it going to cause cancer increase in the more number of cells so cancer is also the same thing right more and more and more and more divisions more and more divisions so here is this hyperplasia does it increases the risk of cancer yes of course certain types of hyperplasia increase the risk of cancer what is the example see especially in the post menopausal females they will let they will get a tumor sir they will get a tumor in their ovaries ovarian tumor they will get this ovarian tumor so what is the name of this ovarian tumor this ovarian tumor is called as a granulosa cell tumor see granular cells you know granulosa cells are the cells which produce the estrogens in the females granulosa cells so these granules are cells they are producing excessive amount of the estrogens because of the presence of excessive high levels of estrogens now what happens now whenever ATM will start to grow much more more and more so more and more endometrium is growing that is nothing but endometrial hyperplasia okay so in this tumor condition glandular cell tumor condition more estrogens are there so this Centro this estrogens they can lead to endometrial hyper pressure so this endometal hyper pressure now in post menopausal females now she is at a risk of developing endometrial cancer so this endometrial hyper pressure it may turn into not every time it may turn into endometrial cancer okay endometrial cancers okay so endometal cancer even the topic of endometrial cancer I have explained this OK so you can find the endometrial cancer video on the YouTube in the search channel there I have explained endometal hypoplasia can increase the risk of endometrial cancer next let's discuss about about other type of hyperplasia in males there is something called as benign prostatic hyperplasia benign prostatic hyperplasia in the name itself it's there they go benign condition this PPH benign prostatic hyperplasia it does not increase the risk of cancer usually hyperplasias can increase the risk of cancer true but which hyperplasia do not process the risk of cancer benign prostatic hypoplasia okay now something related uh to pharmacology which you should know is Sir for the endometrium for the endometrium what is the food what is the stimulus for endometrium it is the estrogens cell tumors are producing more and more estrogens that estrogen is stimulating the endometrium to grow much more in males in males the prostate for the prostate what is the food serve what is the stimulus for the prostate to grow it's not the testosterone testosterone in males it will be converted into five dihydro testosterone okay the DHT sulfide Hydro testosterone dihydro testosterone okay so the testosterone is getting converted into dihydro testosterone testosterone will be converted into dihydro destruction with the help of enzyme five Alpha reductase with the help of this five Alpha erectase testosterone is getting converted into the hydro testosterone this dihydrotestosterone will stimulate the prostate to grow is a one which stimulate the prostate to grow causing a leading to benign prosthetic hyperplasia now how to treat this condition which drugs are used in benign prostatic hyperplasia I have taught you there is a dihydrotestosterone which is the stimulus for the prostate to grow so we can inhibit this enzyme five Alpha reductase let's inhibit the five Alpha reductase so dihydrotestosterone levels will decrease so who are the five Alpha rectus Inhibitors in Asteroid and neutral asteroid okay so this drugs if an asteroid and uterus stride these are the five Alpha erectase Inhibitors so they will decrease the dihydro testosterone levels when the dihydrotestration level decreases brain prostatic hyperplasia will be controlled okay will be control set the rate of growth will be controlled so now tell me important points about the hyperplasia sir hyperplasia is increasing the number of cells hyperplasia it's a precancerous condition yes it increases the risk of cancer now example of hyper pressure is endometrial hyperplasia okay which is seen in post menopausal females because of granulosis tumor now it increases the risk of cancer true and in males there is something called as a benign prostatic hyperplasia but it never increases the risk of cancer it does not increase the risk of cancer but the growth of this prostate what is the stimulus it's not the testosterone it's a dihydrotestosterone testoster is converted into Hydro testosterone this dihydro testosterone gives the stimulus for the prostate to grow now how to decrease the dihydrotestosterone levels by inhibiting this enzyme called as 5 Alpha reductase by inhibiting five Alpha reductase you can decrease the DHT levels and the drugs are ferocyte and due to asteroid now after this let's discuss about atrophisser atrophy so what exactly is this atrophy so can you tell me what exactly is this atrophy atrophy is decreased in the size okay increase in the size is hypertrophy okay increase in the size is called as hypertrophy decrease in the size of an argon is called as atrophy why there is decrease in the size of an argon why argon size is getting decreased because in that argon both the number of cells and the size of the cells the size of the cells are decreasing as well as the number of the cells are also decreasing okay right so decrease in the size of an argon or tissue the size of a tissue is getting decreased okay so both the decrease in the size of the cells as well as number of the cells why sir what is a mechanism hypertrophy is because of increase in protein synthesis hyperplasia is because of the mitosis more number of Divisions and atrophy do you know because this is because the size the tissue size is decreasing because now in this cells a pathway will occursor which is called as ubiquitin proteosome degradation pathway okay ubiquitin proteosome degradation pathway it's happening it's going to it is going to destroy the seller component sir The Unwanted cellular components the proteins everything is going to be destroyed so the cell number and cell size decreases so the Argon will undergo atrophy so as a student what you should know is Sir atrophy is due to decrease in both number as well as the size of the cells why the cell number and why the cell size is decreasing in those cells which pathway is activated ubiquitin proteosome degradation pathway that's activated sir okay now what are the examples examples of atrophy examples of atrophy are diffuse atrophy are wasting atrophy okay wasting atrophy for example if you don't use the muscles maybe in lower motor neuron regions okay in lower motor neurologists that is for example simple ah let's let's put it this way not the lower motor literal region I will give you the example in another place sir you are not using a muscle everything is okay but you are not using a muscle for example you had an accident you had an accident a person is having an accident and during that accident there is a fracture there is a fracture the patient is having a fractures the patient is having fractures now he's totally bread written he's totally bedridden okay now he's totally better in for six months for example so he is not using his muscles he's not using his back muscles he's not using his thigh muscles so what these muscles will undergo as you are not using them their size will decrease so wasting the muscles are getting wasted away okay the measles are getting wasted away so that is one example of atrophy the wasting or diffuse atrophy are not using it you are not using them so the size is getting decreased next malnutrition atrophy you are not giving a proper nutrition to the cells if you are not giving proper nutrition to the cells more catabolism inside the cells the cells will start to become small in size okay so that is small nutrition atrophy no nutrition the cell size will decrease okay tissue size will decrease next so what exactly is this is you have decreased the blood supply to the tissue okay so you have decreased the blood supply to that tube when you decrease the blood supply to the tissue ischemia so automatically the tissue size decreases wasting atrophy or diffuse atrophy malnutrition atrophy no proper nutrition atrophy will occur what exactly is ischemic atrophy ischemic atrophy means you have blocked the blood vessel there is a thrombus occlusion in the blood vessels so there is a decrease in blood flow blood flow decreases atrophicular curve okay next denervation atrophy so what is denervation atrophy denervation atrophy means can you anyone tell me what is denial atrophy anyone in the chart section can you tell me what is denervation atrophy denervation atrophy means let me tell you okay denaration atrophy means all your muscles okay all your muscles they are innervated by the neurons okay especially the Alpha motor yours the lower motor neurons called as Alpha motor neurons they will come to your muscles and they are the ones which are causing the contraction of your muscles because of some reason like pinpolio in polio the Alpha motor neurons are damaged the lower motor neurons are damaged when the lower motor neurons are damaged now denervation so do these muscles the nerve Innovation is gone okay lower motor neuron regions so now tell me can you use this muscle no you cannot use this muscle okay so the lower motor neurons which are coming to this muscle they will actually cause the contraction now what you should do is this lower motor neurons which are coming the lower motor neurons are the Alpha motor neurons which are coming they will give the trophic nutrition they will give the electrophic nutrition to the muscles if there is a deleervation the traffic effect is lost okay so that will cause atrophy of the muscles so that is called as a denervation atrophy so tell me what exactly is atrophy atrophy is decrease in the size decrease in the size of the tissue why there is decrease in the size of the tissue because both the decrease in the size of the cells as well as the number of the cells what is the pathway that's running in them ubiquity integration ubiquitin proteosome degradation pathway what are the examples if you use a trophy malnutrition atrophy ischemic atrophy and denervation atrophy completed uh this is me in that YouTube video I have explained sir atrophy listen when a patient is having say they go endometrial hyperplasia endometrial hyperplasia now she is going to have type 1 endometrial cancer I have said you endometrial hyperplasia can lead to endometrial carcinoma the increases the risk which type of cancer see endometrial hyperplasia this is very important for the exams if there is endometal hyperplasia in a postmenopausal female it will cause type 1 endometrial cancer type of endometrial cancer but sometimes do you know what happens endometrial actrophy endometrium is undergoing atrophisser okay endometrial atrophy so this endometrial atrophy right now our topic atrophy so if there is endometrial atrophy it will cause type 2 endometrinal cancer carcinoma type 2 endometrial carcinoma so type 2 endometrial carcinoma is associated with atrophy type 1 endometrial carcinoma is associated with endometrial hyperplasia that's also something important especially for your exams ok I have done this video I have already recorded this video in the YouTube you can watch the lecture if you want you can go through the endometrial cancer okay video now after this let's talk about the other cellular adaptation the next cellular adaptation cell which is called as metaplasia okay metabolasia so what is metabolism what you should know for your exam okay so metabolasia means change in one cell type okay one cell type is going to change into other cell type totally different cell type so change of one cell type into other type is called as okay metaplasia why it is changing because of the stress okay because of the stress what is the mechanism underlying here again for hypertrophy increase protein synthesis for hyperplasia it's the mitosis for atrophy or atrophy it is a ubiquitin proteosome regulation pathway and for metabolicia say there is something called as stem cell reprogramming so stem cell reprogramming will occur so because of this yes because of the stem cell reprogramming one cell type will change into the other cell type the stem cells program the program of the stem cells is changed now they are forming different sense now they are forming different types of cells I will give you examples I will give you examples examples are most important the questions which were asked in the FMJ exam and neat PG exam and even in the board exams your civil exams the question which will come is which vitamin deficiency can lead to metabolicia which vitamin deficiency vitamin A deficiency OK vitamin A deficiency can lead to metaplasia why because for epithelial differentiation vitamin A is very important so very important but if there is vitamin A deficiency that will lead to metaplasia examples this is from here these are the important points which you should know there is something called as Barrett's esophagus so what is Barrett's esophagus normally let me draw here imagine this is your esophagus and here is your stomach okay this is your stomach now when acid is reflexing okay yeah that's why we'll give retinoic acid is trial expect you are true retinoic acid vitamin A okay uh later I'll explain about the retinoic acid vitamin A but for now just listen here sir acid when it was supposed to be present where acid was supposed to be present in the stomach now with this acid if it is regurgitating into the esophagus if the acid is coming back into the esophagus is that good is that good definitely not good sir so normally esophagus is lined by which epithelium the esophagus is lined by square ah the esophagus is lined by stratified squamous epithelium esophagus it is lined by the stratified squamous epithelium now because of this insult because of the stress continuous stress as it is coming acid is coming do you know what happens now now in the esophagus the epithelium is changed into columnar type of epithelium the squamous epithelium is replaced by the columnar type of epithelium because of the stress especially in the lower one third of the esophagus so yes in the lower one third of the esophagus spamaseptidium is gone replaced by columnar epithelium so along with this columnar epithelium important Point even you can see goblet cells OK goblet cells even along with this column epilium goblet cells are same this is the McQ okay which cells are seen goblet cells goblet cells are same in his behaving okay so goblet cells are same why goblet cells are sincere why goblet cells have occurred like you know why they came into the esophagus do you have any idea why goblet cells are coming into the esophagus normally in the esophagus there are no goblet cells goblet cells are not seen in the esophagus okay now why the goblet cells are coming the goblet cells are going to now produce the mucus okay now they are going to produce the mucus in the esophagus why mucus acid is regurgitating back no there is gastro yeast of agile reflexity is a GRT so the patient is suffering with what g e r d gastroesophageal reflex disease the acid is getting reflected back into the esophagus okay so what happened squamous epithelium they call the squamous epithelium is replaced by along with the goblet cells the goblet cells are now going to produce the MU sin there mucus over there okay so this is one example barrex isophagus now just tell me say in which condition barrettes esophagus seen in GE or the gastroesophageal reflex disease and what you will see over there I have explained you sir what you are going to see in Balance esophagus there is columnar columnar metaplasia okay there is columnar metablasia which type of columnar metabolism intestinal type of carbon metabolasia why I am using the word intestinal type of calmer meta pressure why because goblet cells are seen in the intestines not in the stomach not in the esophagus now you are having the goblet cells also so it is called as intestinal type of carnal metabrasia and that's a McQ okay that's the McQ next what else are the examples of metaplasia that's a myositis occipants myositis occipants means what for example whenever you are having a trauma sometimes when you are having trauma now in the muscles after some days now you will feel hard lump or mass which is nothing but the bone sir now a bone formation is happening in the muscles bony tissue who is growing inside the muscles after trauma which means one type of tissue the recent camel tissue one type of the the muscle tissue is changing into bone type material so this is called as a myositis so myositis means inflammation of the inflammation within the muscles because of the trauma at the end bone formation ossificans bone-like growth is happening so myositis is an example of metabolism and smoker's lung so normally in your lungs columnar epithelium is there ciliated columnar ethylene this is the most common type of metabolism this is McQ the most common type of metabolicism what is that squamous meta pressure do you know what is happening now normally in the lungs ciliated columnar epilium is there okay ciliated columnar epsilium is there in the lungs do you know what is happening now see the ciliated columnar epithelium when the person is smoking continuously smoking smoking smoking now because of the smoke the ciliated carbon epithelium is converted into squamous epithelium okay so this is an example ciliated common epithelium converted into squamous epithelium so this is called as squamous meta pressure okay normally inside the lungs what do you have you have ciliated columnar ciliated columnar epsilium when the person is smoking continuously there is a stress cell so the ciliated columnar epithelium OK is going to be converted into squamous epithelium so end result is what the squamous epithelium it's getting changed into squarebocythelium so it is called as squamous metablature and one more example so small are zaskar's disease Okay small are the scar disease in smokers in smoking females okay in smoking females actually this type of metaplasia is seen in the breast okay so squamous metaplasia of lactiferous ducts mold means s-m-o-l-d s m o l d means small means squamous metaplasia see metabolasia is happening they will ask you smold is an example of which type of cellular adaptation mold is an example of metaplasia smooth means squamous metaplasia of lactivarus ducts lactiferous ducts in the breast tissue they will undergo metaplasia okay so this is also one more example so what we have seen what are the examples of metal pressure we have seen parrot cesophagus okay cylinder grd myocyte is ossificants smokers lung and Jessica's disease all these are the examples of beta pressure and metaplasia what is that keyword so in metabrasia this is because of stem cell reprogramming where one cell type is getting changed into other cell types okay next so lastly dysplasia let me ask you something about the dysplasia okay so dysplasia is it a cellular adaptation sir hypertrophy is a cell adaptation hyperplasia is cellular operation atrophysic cellular operation metabolism but dysplasia is not a similar adaptation sir dysplasia is not a solid adaptation and remember one more thing all the cellular adaptations whatever I have discussed all the similar adaptations are reversible okay if you take out the stress if you remove the stress atrophy metaplasia hypertrophy hypoplasia everything will be reversed everything is reverse so now let me write here all cellular adaptations are reversible Loadout let's take a note somewhere very important note all cellular adaptations are reversible okay all cellular adaptations they are reversible circuit so the question which was asked in the exam is meta pressure are the direct schizophagus the patient is balanced esophagus is it reversible absolutely absolutely reversible okay so metabrasia is reversible sir next so what is dysplasia dysplasia is not a cellular adaptation now the total disorganized growth of the cells now there is so much there's so much stress cells are trying to adapt there is one stage they gave up they gave up and the total totally they are growing in abnormal fashion so now they are going in abnormal fashion now you can't even identify the cell disorganized the growth of the cells you can't even identify what type of cell this is okay so dysplasia is not a cellular adaptation it's not a cellular adaptation so what exactly is happening in dysplasia keywords disorganized growth of the cells loss of differentiation you cannot identify whether it's a cardiac myosite whether it's hepatocyte whether it's a renal tubule it's you cannot identify itself disorganized growth okay and is it reversible all cellular adaptations are reversible but this is irreversible once dysplasia is there it is not reversible so it is ever irreversible it is irreversible irreversible and it is a pre-cancerous stage almost going into the cancer almost the cells are going into cancer cell Okay so with this for topic cellular adaptations is also completed okay I have given you important examples examples are the key examples are the important things okay so benign prostatic hyper pressure endometrial hyper pressure type of endometal cancer is a type 1 or type two okay and what are the transcription factors geta for nfat and meth2 so everything whatever I have written over here is an McQ in the previous year questions now after this let's discuss about topic which is called as a cellular intracellular accumulations okay in certain conditions in certain pathological conditions certain substances will start to accumulate inside your cells for example like iron accumulation copper accumulation glycogen accumulation calcium accumulation so in certain pathological conditions in different different pathological conditions different different substances will start to accumulate inside your cells so that's our topics are intracellular accumulation okay so here first I am going to discuss about the pigment normals are normally normal healthy cells also which pigment is there in our skin in our skin in the basal most layer so for example you can see here sir you see are you able to see this black color this black color which is present in the Deep layers of the skin not on The Superficial layer in the Deep layer of the skin cell there's a stratum basic layer of the skin are you able to look then the stratum Bay sale you can see the melanin pigment melanin pigment that's one that's the one which gives the color to our skin okay so melanin is a pigment yes it will accumulate in our cells okay it's going to accumulate in Source itself so matter and where it is there it is there in the skin okay but not only there in central nervous system also look here so what is this area can you tell me that this black color area which I have highlighted over there that's called as a substantial okay substantia so this is healthy midbrain okay this midbrain this actually mid brain cell this is a healthy midbrain so in this midbrain ah see they go what happened to the substantial aggressor the substantia it became pale pale substantial can you tell me what is this condition this condition is actually Parkinson's yes one more you are true this is Parkinson's so in parkinsonism actually what happens is the dopaminergic neurons okay from here right the dopa the open energy neurons are damaged the dopaminergic neurons in the substantial Agra they are damaged when the dopaminergic neurons are damaged look dopamine dopa dopamine is the raw material for melanin dopamine is the raw material for melanin normally here this black color is because of the melaninism because of the melanin the black color is there now in parkinsonism what happened the dopaminergic neurons are gone dopamine is not there when dopamine is not there melanin synthesis cannot happen sir when melanin synthesis is not there see it became pale okay so pale substantial aggression in parkinsonism due to loss of dopaminergic neurons dopamine is not there when dopamine is not there melanin is not produced okay so that's the point which I want you to know so melanin it's a pigment it is there in our skin stratum basal layer of our skin as well as substantia questions that will come in your exam is direct pathological questions or pathology related questions what are the stains what is the stain for this pigment sir stay in for melanin is Mason Fontana right Mason Fontana is the stain small stain Mason Fontana small stain and immunohistochemical strain is there which is called as a HMV 45 this is McQ which was asked in exam so hmb 45 is the immunohistochemical stain is also a type of stain okay immunohistochemistry chemistry to stain to look at the melanin this is the stain used hmb 45 Mason Fontana small stain and what is this THC enzyme histochemistry in enzyme histochemistry the stain which is used is called as a dope oxerase so tell me to stay in melanin to look at melanin under the microscope what are the four stains which are used there are four different types of strains which you can use one is small stain Mason Fontana hmb 45 and dopa oxidase dopa oxidase these are the stains which are used next now let's talk about the pathological conditions there is a pathological condition in which the iron will start to accumulate inside our cells iron is starting to accumulates inside our tissues what is that condition hemociderosis are hemochromatosis hemochromatosis now hemociderin is getting accumulated okay hemosted means what iron accumulation inside the tissues seen in which condition hemochromatosis in this condition hemochromatosis you can see Iron accumulation inside our cells so how to identify the iron look at here sir this is a tissue actually what is this issue can you identify so this tissue is nothing but your renal tubules these are renal tubules so reality fuel cell so inside the renal tubules are you able to appreciate this blue blue like dots so those blue color this is nothing but iron okay inside the renal tubules iron is getting accumulated okay actually this is seen in a condition called as peroxisible nocturnal hemoglobinuria where the hemoglobin is going to leak out in the urine now in this particular condition now iron will start to deposit inside the kidneys OK iron will start to deposit inside the kidneys renal tubules okay now this is called as a blue kidney okay this is called as a blue kidney now question is how to look at the iron what is the stain used the stain used is Pearl stain or Prussian Blue iron will look in blue color iron is going to look in blue color ok so what is the stain for iron well stain are Prussian Blue already asked McQ in the exams next copper accumulation if copper is getting accumulated inside your tissues in which condition which disease sir Wilson disease there is a disease called civil Center disease in this disease ATP 7B Gene is mutated question which was previously tested so ATP 17 mutation ATP 7 BG mutation leading to the Wilson disease now in this this is what happens now copper will start to accumulate inside our body this is the image based question which was asked you know are you able to see it so this is the copper deposition okay in the eyes copper deposition in the icer you know what is this called as what is this so these are the anyone KF Rings Kaiser Fletcher Rings okay so k for example we'll call it as kfrings okay so kfings are seen in which condition Wilson disease due to what copper deposition why Wilson disease ATP 7 between mutation okay 80 percentage in mutation copper excess excess copper in the body will cause we'll send this is copper efficiency I have explained copper deficiency will cause which disease copper excess will cause the Wilson disease excessive amount of copper in the body will cause the Wilson disease right now I am talking about copper deficiency proper deficiency remember especially important for your exams Indian exams that is main key disease main case disease is due to deficiency of the copper now tell me so what are the stains for the copper how to identify the copper cell so the stains which are used are rubionic acid okay rubyaric acid okay these are the two strains which are important rubionic acid and rhodonine next after this so what is celluloplasmid celluloplasmin celluloplasmin what is cytoplasmin it's a plasma protein which will bind with the copper so copper binding protein is called as a celluloplasmin now this is also just I am trying to integrate here it's a celluloplasmin if you want to stay in the cellular plasma not the copper if you want to stay in the ceruloplasmin then the stain which is usually is called as arsene stain okay Arsen stain is the stain for ceruloplasmin and there is this one more thing one more pigment which is called as a homogenesic acid okay it's an acid it's homogenic acid now even we are talking about the intracellular accumulations right now there is a condition called as alcaptainuria okay in all capital urea which substance will start to deposit inside our tissues which is substance will accumulate inside our tissues is called as a homogenesic acid okay now they go when homogeneous acid is getting accumulated now there will be blackish color discoloration now you can clearly see here in the ears this is the image based question that will give you this light black to bluish color discoloration that is saying this is condition is called as acronosis okay so acronosis is due to accumulation of its substance iron copper melanin emocidrine no homogenesic acid accumulation will cause acronosis seen in all caponeuria okay let's discuss about one more pigment cell one more pigment accumulation inside our tissues see this pigment very much important especially for the Indian exams and board exams the pigment name is called as a lipofusion or lipochrome when we are getting older and older okay when we are getting older and older inside our cells okay inside our cells this pigment will start to deposit as we are getting older and older ourselves are going to have more and more free radical damage in ourselves more and more free radical damage will occur now due to the free radical damages free radicals they will cause do you know what this free radicals will do these free radicals will cause lipid peroxidation inside our cells the lipid peroxidation when the lipids are getting like when lipid peroxidation occurs then these pigments are going to be producer due to lipid peroxidation this lipochrome is going to be produced okay so one by one sir what is this lipochroma lipofusion this is a wear and tear pigment it's a wear and tear pigment means with the time with usage with time with repeated damages with time this tissue is uh uh pigment is going to start accumulating inside our cells now where it is seen sir it is in the brown atrophy of the heart okay this old patient 80 year old patient now he's dead 80 year old patient he's dead now when you look at the tissue when you look at the biopsy you can see this brownish color depositions this brown color pigment deposition around the nucleus this brown colored pigment is nothing but the like poke room or lipofusion it's a brown color pigment it's a brown color pigment okay next now why why this lipochroma life official I have explained you it is because of the free radical injury free radical injury causing lipid peroxidation when the lipids are undergoing peroxidation that will produce lipochromar lipo Fusion now where it is going to be accumulated it's going to accumulate around the nucleus a perinuclear brown pigment deposition if this is a keyword wherever you see this word perinuclear perinuclear brown pigment is a scene that is nothing but lipochromark lipofusion due to free radical damage now what is the stain so what is the stain used for this lipochroma liposition you can very clearly see here this brown pigment around the nucleus even here this is the nucleus this is electron microscopic image where you can see the lipochrome okay lipochrome is seen around the nucleus now what are the stains the stains for this lipochromat lipofusion is oil red bow are the Saints used for the lipochrome are lipo Fusion next let's talk about the lipids pigment accumulation completed iron accumulation copper accumulation uh pigment accumulation like lipochrome completed sir now let's see lipids there are certain conditions where even lipids this lipids extra amounts of fats will start to accumulate inside yourself do you know any such condition livers are fatty liver fatty liver okay so fatty liver is the most common okay so lipids are going to be accumulated and the most common argon2 for the lipid accumulation is the fatty liver is a liver causing fatty liver if the more and more fats will start to accumulate inside the hepatocytes that will cause the theaters or fatty liver now one more condition you can very clearly see here so can you tell me what is this argon that's a gallbladder there is a gallbladder okay gallbladder now even in the gallbladder you can see these are all the cholesterol deposits all these other cholesterol deposits now gallbladder it's looking like a strawberry okay this is called as a strawberry gallbladder so it's strawberry carburetor what is happening it's a cholesterol that's getting deposited okay so this condition is called as cholesterolosis okay cholesterol losses are strawberry gallbladder what is happening is a lipid accumulation inside the sex okay lipid accumulation now how to identify the lipids are okay for lipids see whenever you look at the cell C all these vacuoles are there right these are nothing but the spaces where previously lipid is there previously here lipid is there right now the lipid is washed away now all these are the spaces where lipids are there okay now how to identify the lip itself what is the stain for the lipids if you want to look at the lipids what is the stain used the stain used is oil red oh okay so oil Red O now where we have just look at here the same oil red bow we have seen here oil red bow is used for lipofusion also the iron radio mainly it is used for the lipid set lipids important not only oil soda and black B Sudan 4 and osmium tetoxide all these are the stains mcqs previously and mcqs oil red rose so done black B Sudan four osmium tetroxide these are the stains used for lipids okay are the fats now look here all this red red color Okay red red color like here what you can see these are nothing but the lipids these are all the lipids lipids are going to come in red color okay the appearance of lipids in light microscopy left one this one is oil Red O and right one is Sudan black four okay see in Sudan black stains the lipids are going to take which color the lipids are going to take the black color Okay limits will be having black color sir Okay so what is the stain they can give you image based questions and they can ask you the stain is eyelid wo and this is Sudan black four okay so lipids also completed look at this this is a strawberry gallbladder or cholesterolosis where excessive lipids are getting deposited inside the tissues when you are suffering with hypercholesterolemia lipids will start to deposit okay next and we are at the end glycogen cell glycogen is getting deposited inside the tissues okay we have seen copper deposition iron deposition fat deposition brown pigment deposition okay homogenic acid deposition ok but there are certain diseases where now glycogen will start to deposit inside the tissues do you know any such thing diabetes mellitus or in diabetes mellitus okay look in diabetes mellitus what happens more and more glucose is getting filtered into the nephrons more and more glucose now this glucose will be reabsorbed in the proximal convoluted tubules now what is happening in diabetes mellitus more and more glucose is getting filtered into the nephrons now this glucose will be reabsorbed by the proximal convoluted tubular epithelial cells now in the PCT the glucose is stored now in the PCT the PCT epithelial cells are storing the glucose converting the glucose into glycogen and now they are showing the glycogen okay so now this PCT cells now this epithelial cells which are storing this glycogen they are called as Armani Epstein cells okay McQ Armani Epstein cells are seen in diabetes mellitus where that that's Electro diabetic nephropathy I should say diabetic nephropathy more and more glucose is filtered that glucose is stored in the PCT in the form of glycogen those cells are called as harmonic abstain cells you can very clearly see here see these look here let me show you see often referred as Armani Epstein change or Armani Epstein cells so what exactly are these harmonic abstain cells this Armani Epstein cells they are nothing but OK this harmonic abstain cells they are nothing but the cells which are storing the glycogen inside them so what is this OK these are the all the Armani abstinence cells they are storing the glycogen within them okay next what I want you to know is what is the stain for this glycogen how to stay in the glycogen cell so the state for the glycogen is that's Boston okay periodic acid shift stain okay periodic acid shift chain so pass pass stain is the stain for glycogen per iodic acid shift stain is the stain for glycogen okay and one important point about the glycogen is Sir glycogen yes it will take the past 10 it will take it will come pink it will come pink in the stain okay wherever there is glycogen where if you put pastain the glycogen will be coming in pink color it will come in pink colors but this glycos and one thing you should know for uh understanding the other concept later so this glycogen it is a diastase is a sensitive so dashed is an enzyme it's an enzyme when you put Dash stays over there the glycogen will be dissolved glycogen will be going out of that area Okay so glycogen is a past positive but Dash stays a sensitive okay glycogen so with this glycogen is also completed so tell me in which condition glycogen will start to accumulate inside the cell one thing I have explained your diabetes mellitus that's the Armani Epstein cells in the proximal convoluted tubule and not only that here there are glycogen storage disorders right in Biochemistry would have said glycogen storage disorders the glycogen is getting accumulated inside the cell now in all those conditions glycogen is accumulated inside the cell how you can know whether it's glycogen or not put pastain if the cells are taking past 10 which means inside them there is glycogen glycogen vacuoles are there okay so with this intracellular accumulations is also completed