Transcript for:
Introduction to Pathology and Cell Injury

it's coming actually okay guys good evening everyone hope everyone is doing good so now I just want to tell you that we are going to start a series of lectures on pathology so that in the next 30 days in 30 classes I should say we'll be completing the entire pathology the entire pathology what is needed for your exams that will be done in the next 30 classes this is the class one so 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 if you go through these 30 classes 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 okay so hello everyone how are you elastis see me good afternoon everyone okay we are from which country here it is almost night good evening hope everyone is doing well now if you have any doubts you can all the time ask me in the chat session so having said that now our chapter is still 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 now let's maybe let me begin 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 where you are keeping yourself 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 the inner 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 cell injury happened but it's a little sir 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 so what exactly is this reversible cell injury cell is endured sir true but not much damaged till there is a chance that the silk will go back to its original state okay it will go back to its original so it's a 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 adapter apoptosis okay so irreversible cell injury will lead to what the irreversible cell injury can lead to cell death how many types of synthet 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 solids how many types of cylinderies are there so there are two types of cell injury reversible cell injury foreign that injury will be reversed irreversible cell injury there is no reversal the only fetish cell death cell is going to die for sure okay and now let's begin our topic with reversible cylinder research 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 YSL 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 hypoxia this is the stress hypoxes definitely 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 are because of some reason so there is ischemia that ischemia is leading to hypoxia now say 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 know it 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 then whenever the mitochondrial dysfunction happen do you think ATP will be produced no it's an 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 currencies are ATP now it's not there so what do 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 a 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 you 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 Divya Reddy 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 drinking two potassium into the cell Always by using the ATP okay by using the ADB sir what is the name of the sperm this is called as sodium foreign 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 at EPS is not going to function when the sodium potassium atpase is not functioning not functioning what will happen which I amps will 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 there is sodium water follows you know the basic thing now ATP is not there when ATP is not there this for pumps this pumps are going to fail when the pumps are failed this ionic balance is affected the sodium is going to get accumulate 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 is everything okay yeah the same thing I have shown here see decrease in the ATP okay ATP is decreased so the sodium potassium atpss are getting affected sir sodium potassium ATP is then the sodium potassium atps are affected they go what happened increase influx 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 swelled with the water now they are getting little obese or obeys 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 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 change water accumulation they go when more one more water is coming into the cell Now by getting like you know by just dissolve like you know why uh when more water comes into the cell this water because of this excessive water the cell organelles will start to swell cell so endoplasmic reticulum is also going to swell okay 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 hydropic change here McQ Plus or 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 microvilli 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 the cell is swelling what happened to this Villi the will I get now flattened okay now the cell will become something like this the Villi has lost sir because more water came into the cell so the loss of micro value will be seen okay so loss of microbial 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 live 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 now this is the Seltzer it is forming the same cell it is forming some small small protrusions okay so these are the blephs OK the cytoplasm 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 blips so these are the cytoplasmic lips okay so cytoplasmic webs are seen one thing there is a loss of microvilli second thing second thing endoplasmic reticulum is going to be solid the cell is also getting swollen so all these are because of what why are all these problems because of the failure of sodium potassium ATP exists why so sodium potassium ads are failed because of decrease in ATP why decrease in ATP mitochondrial dysfunction why mitochondrial dysfunction because of hypoxia why hypoxia ischemia okay so just I am trying to repeat as this is your first class so most of you guys are from your first year second year okay so you should be able to understand this okay I am just repeating it 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 myelin figures what are what exactly are they just look at it this is the image based question which can become in 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 like 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 or lamellations which you can see in the cytoplasm so these figures are called as a marine 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 so their cell membrane whatever is there okay their membrane the organs which are solved by their membrane even the membrane is getting distended membrane 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 sir now it is going to in the cytoplasm it will come and it will go into walls or lamellations 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 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 microvilli 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 now what happens there is clumping of Chromatin the chromatin material which is present inside the nucleus now this is a nuclear chromatin now the nuclear chromatin it will start to Clump pump 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 what other changes can be seen they go 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 the endoplasmic reticulums are getting swollen who is attached to endoplasmic reticulum I'm asking you who is attached itself to endoplasmic reticulum 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 sir now what will happen do you think protein synthesis 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 ah 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 come on guys is that clear trial expert seems that you are so active diversible cell injury all this is reversible cell injury right now we are all discussing about the reversible cell injury it's a reversible cell injury can happen in any initial it can happen in any cell when you are giving stress to a cell 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 first what will happen the sodium potassium ads will stop functioning so silver 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 function sir this the cell Will Survive OK 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 irreversible cell injury 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 damaged sir 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 cell can no longer undergo repairs 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 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 sir from outside calcium whatever the calcium is there okay calcium levels inside the cell is very very lesser this is also the fmg equation the question which was asked in the recent fmg exam question is Which ion concentration is maintained Less in the cell when compared to the other ions this calcium concentration the calcium concentration inside the cell is very less inside facilities less outside facility 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 Sir calcium what exactly is this the 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 dicer 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 then the phospholipids is they will break the cell membrane and break the mitochondrial payments of cell membranes mitochondrial membranes will be broken down and one more thing I want you to know is see this phospholipasis in the name itself is a phospholipase phosph they will break the phospholipids where phospholipids are there phospholipids are there in the membranes membrane cell membrane mitochondrial membrane you're right 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 so if they are present inside the cell it is no longer reversible cell injury it is now irreversible cell injury okay now McQ switch we're asking your exam calcium came into the cell 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 okay 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 OK 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 these large amorphous broccoli intensities what exactly are they they are nothing but calcium deposition in mitochondria McQ okay next time secure the large flocculent densities which are there in the mitochondria that the Hallmark of Watson Hallmark of AC unit okay large amorphous large amorphous flocculent densities that the Hallmark okay so they are the Hallmark of irreversible cell injury okay so that the Hallmark of irreversible cell injury sir so now let's just see the mcqs okay what are the mcqs which I want you to know is 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 large flocculent amorphous densities which are the high Mark 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 cell 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 nucleus 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 chromatin 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 okay hypnosis means condensation condensation carry your excess means fragmentation fragmentation and the last one carriolysis carriolysis carriolysis 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 salary lead to death now what kind of nuclear changes are seen hypnosis carrier axis 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 cylinder recommodates are irreversible cell injury is also completed in reversible cell injury simple important points failure of the sodium potassium adbs 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 what are 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 nucleus changes clumping of Chromatin clumping of Chromatin okay now here I want to add one McQ point so The Smiling figures are there right so the smiling figures are they going to be seen in reversible or irreversible they are seen in both sir this is modern figures they are seen in both reversible and irreversible they are seen both in reversible as well as irreversible cell injury okay migrant figures are seen both interversible as well as 0% engineering what is the nuclear change that is seen pumping of Chromatin now in irreversible salary what are the points which I want you to know what are the two things that decide that cell 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 6 and karyolysis with this irreversible cylinder is also completed reversible irreversible after reversible cylinder what happened cell will die cell will die sir okay now that I will discuss so is that clear so far guys is that clear so far a travel expert you are asking about what sir in McQ what we will choose clumping of Chromatin no clumping of Chromatin is seen in reversible reversible and that's it just your mother clumping off from Adam is in reversible cell engineering okay that's a nuclear change in irreversible cell injury what are the nuclear changes I have said you hypnosis carrier axis carriolysis okay okay next let's talk about the necrocessor 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 OK actually there are two types of cellulite one is necrosis and apoptosis first we will discuss about the necrosis say necrosis first point always a pathological set always pathological cell doesn't want to die they'll always want to live now in this condition still 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 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 will undergo 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 tissue cylindrical coagulative form of necrosis what is this are coagulating exploresis cell dead Okay cell is dead sir 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 cell 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 a 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 infarction this is a word they will use you most of the time infraction so because of the information what exactly is infarction you have cut down the blood supply the tissue is dead infarcted 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 is 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 the 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 fragility 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 what is this sir come on guys tell me this is your brain now see this area of the brain is getting infarcted 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 right the scene in brain okay brain and also pancreas sir brain and pancreas so these tissues what is something special about them so 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 death 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 look 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 cases necrosis is actually a combo it's a composer It's a combination of both coagulative it's an example of both coagulative Plus liquefactive penis little misbehaving okay no issue it's an example of both coagulative 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 okay she's 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 it's also because of some fungal infections fungal infections like histoblasmosis anyone anyone travel expert it's seen in thank you Angus and India so you teach us is very nice thank you very much so this is the first class that we'll go we'll gradually in 30 classes let's complete the entire pathology what is needed for you okay I'm just teaching especially keeping exams in mind what they will ask you in your exam okay so a TV May is condition TB histoblasmosis and coccidiomaicosis one more conduction one more condition so TB histoblasmosis coccidiomycosis 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 May processor 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 ditzer adipocyte death the death of the adipocytes now some important exam important points are there they go see this fat Negroes is 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 root traffic accident because of some abuse or because of some like you know injury like in a fall now there is ah damage that is happening to the breast cell breast tissue damage is happening now the breast inside the breast the liposites 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 is 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 saponification so calcium binding with the fatty acids now we will start to see in the area of necrosis in that particular area of necrosis we will start to see white white white deposits 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 come on Buddies guys can you tell me what is this Argon English Sun all the best for your net page exam hope you will clear your exam with flying colors so this argon this is a pancreas okay a pancreasa it's a pancreasa now you know you already know it's a pancreas will undercover which type of necrosis pancreas will undergo pancreas cylindrical liquefactory 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 parent chyma will undergo liquefacture 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 it's process 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 chalky white appearance okay next cell especially this is very much important for your nitpage exams also look fibrinoid necrosis fibrinoid means to bring 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 in which conditions you will see fibrino and necrosis what are the examples okay example seen in vasculitiser okay especially autoimmune like an immune mediated immune Myriad vasculitis like polyarthritis nodosa so the polyartrite is known as an example of what what happens in polyartrate is nodosa polyarthritis they'll be 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 sir how can you say this is a 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 509 necrosis okay so fibrino necrosis is synonym polyartride is known as a and 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 will undergo necrosis which are called as astronaut bodies Ash of Bodies Okay the astronaut bodies which are pathognomic they are pathognomic of rheumatic heart disease in 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 an example of what this ash of bodies are again example of the fibrino necrosis 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 gaseous 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 a 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 against 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 allow to go into deposit in that fatty acid area wherever the fatty acids are there now the calcium will start to reposit in that area okay and fibrino necrosis seen in the vessels vasculitis condition then now after this some important types of necrosis are there important types some little special so what is this diabetic patients you know diabetic patients especially they will be having the gangreneur 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 water and a drag anger is nothing but coagulative necrosis it's a type of coagulative necrosis okay in that area what happened why glad your 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 coagulative necrosis okay so just look here important mcqs which you need to know for your exams concentrate there are two types of ganglion 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 and green 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 mainly it's in the bubbles red gangrene is in the bubbles in the limbs no why why do I ganglion sir diagram is because of the main arterial occlusion the artery is applying this area that's blocked when the arterial occlusion happens no blood flow hypo ischemia hypoxia stress reversible cell injury irreversible cell injury gone coagulating necrosis okay so due to the arterial occlusion dragon this vatic gangrene is more of venous blockage okay more commonly venous occlusion the veins are occluded OK 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 necross Square creative necrosis sir look here so this is more it's not looking dry so it's not looking right 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 infections will start sir 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 okay there is no growth of bacteria that I will show you whether they go looks are here now see the line of demarcation in dry ganglion present okay so the line of demarcation means healthy tissue 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 because of the arterial occlusion with gangrene is because of the VR seclusion next after this the next question that we ask that will come in your exam is zincers degeneration what is this zinc or degeneration or zincers necrosis so this zincers 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 this 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 zynga's degeneration skeletal muscles are dying undergoing necrosis death why see necrosis of skeletal muscles in which condition in acute infectious conditions 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 the processor 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 entry 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 rectus Abram is what exactly is this muscle rectus abdominus rectus abdominance is the 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 started in cell death I have also done the necrosis and different types of necrosis is that clear mode sriraj is that clear okay okay guys now after this let's continue with the apoptosis very simple topic it will complete this in next 15 minutes let's try to complete the apoptosis 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 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 link the contents we leak the similar 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 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 or cell death by using ATP okay we are making everything by using ATP 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 caspasis 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 and it's an active process and it's a caspase dependent some caspases 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 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 have a group of cells because of the stress not one single cell a group of tissue because of arterial occlusion that wedge-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 optosis like suicide during suicide you will die our others are also going to die 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 increases cellular swelling will happen OK 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 cell size 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 cellular contents are not leaking out so no inflammation okay now yeah this is the last one see they go 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 pathology 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 body is good like it will happen which 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 stumpster one single stump okay now actually during embryosis the fingers are not there okay the digits 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 of the cells in this area will create the spaces so that digits are formed okay it's 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 for endometrium harendo material 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 three reposites for example see there is this one telymphocyte 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 self-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 till 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 embryogenesis 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 Infosys 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 chain viral hepatitis now and not only this I am going little fast now not only this just by heart so sell our tubers 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 apopt 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 though 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 induced by radiation radiotherapy all these examples of apoptosis okay so tell me what are the three pathological examples of apoptosis pathological apoptosis tumor cells and giving anti-cancer drugs killing the cells okay these are the three pathological uh examples of our process and what the physiological examples of upper process physiological processor during embryogenesis second one is elimination of self reactive lymphocytes and endometrium endometrium shading 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 now last five minutes sir how about process is happening there is something program right program or 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 the cell 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 a timerization 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 cross Associated depth domain foreign the death receptor is activated the timerization of death receptors will happen OK three death receptors will fuse and they will activate the fat okay this first 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 Casp phases caspase these are the enzymes these enzymes are getting activated just note till here no till here okay so extrinsic pathway purposes 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 Casper spaces are there so this inactive Pro Cast space 8 10 to 10 are converted into active 8 and 10 okay now they are ready these caspases are the first initial Cash basis right 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 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 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 detected sir 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 row 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 the apoptosis means they will inhibit the children they will they are anti-apoptosis so what are the pro upper process again FMJ McQ and as well as need PG McQ in each and every cell there are proposing factors present what are the 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 antibiotic 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 cell cell now stress is going to activate what stress sensors Bim 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 property 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 inner 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 low 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-apoprotic factors so now look here what happened sir putting table to series okay but anyway now look here this BCL two 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 of one now this combo this 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 it's a reason 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 Bim bit backs knocks of Puba they detect the stress whenever the stress on the cell is increasing they will inhibit the anti-apopodic 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 forming apoptosome now what is this a purpose I'm doing an apoptosome is converting Pro Cast space 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 path pressure 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 caspasis 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 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 till death apoptosis so this caspase number three six seven they activate what phospholipases inside the cell once phospholipids 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 activate the enzyme is 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 kill the that cause the damage to the the phospholipases 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 caspase is eight ten the caspase means C for 16. okay these enzymes contain 16 amino acids cysteine 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 aspartated every aspartate residues okay so cysteine as pertases caspasis means their enzymes they contain 16 amino acid and what they will do they will break the protein set as part 8 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 plates 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 these Casper is activated the phospho phospholipases proteases endonucleases the one cell now it is fragmented into small small fragments okay now still one above prediction first it will shrink now it is going to be broken down into small small pieces with the intact cell membrane remember with the intact cell number 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 small pieces so 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 these 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 HP signal okay so this is nothing but they go it's a eat me signal whenever this apoptotic bodies are expressing these molecules on their surface now the phagocytic cells the macrophages will come and eat the apocratic bodies clear the upper product Bodies Okay so the it may signal what is the 8B signal what are these green color molecules so this green color molecules are nothing but phosphatidyl serine and thrombosponding so mainly phosphoryl serums are the phosphoridal serine is now expressed outside the cell it is externalized actually it is inside normal in healthy cells the phosphoidal Serene molecules are inside but in apoptotic cells now this phosphoidal serine molecules are exposed out it's like eat me signal okay it's like eat me signal set so whenever a macrophage series password also in macrophage will come and clear this apoptotic bodies so the upper body products 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 pathway of properties apoptosis because of the depth 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 probability factors inhibiting the anti-apoprotic 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 they still 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 upper process 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 equation 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 acrosis and apoptosis and question sir what is the stain used by staining by staining method can you differentiate apoptosis and 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 strain 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 so my thing is completed now you are part mcqs just M6 I will show you the mcqs just answer it what is zinker's degeneration just tell me the answer a b c d can you tell me what is zenger's degeneration come on travel expert I will definitely I will definitely come to Kazakh again okay to the cash pin definitely I love that place can you tell me what is answer ABCD travel expert can you sir zenkers I said you so zenkers is yes it is hyaline waxy hyaline 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 so this is degeneration option number say excellent excellent 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 requests and difficulty speaking a 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 paradoxical atrial fibrillation is Atria fibrillating now you know when especially okay I don't know whether you can know it or not especially when you do your medicine then you will understand this whenever your A3 are undergoing fibrillation there is a chance that in Atria clots will form sir mural 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 these clots will do this 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 lateral 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 key word whenever you see this keyword irregularly regular parts that's the 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 a 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 okay hemis 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 his symptoms are not coming to normal failed 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 brain is some part of the brain is dead now tell me what is answer A B C or D uh most of the students have already gave the answer what is answer a b c r d see definitely the answer here is D sir okay D why because brain and pancreas are rich in enzymes hydrolytic enzymes which type of negro says liquefactory necrosis so hydrolytic enzyme inducer tissue degradation that is an example of liquefactory necrosis okay so here answer is D now answer this a 46 year old man present to your office with slowly growing neck mass is having slowly growing neck mass the mass is Stony heart and palpation it's a Stony hardship the neck mass is Tony hard on pulpation and seems to be fixed to the adjacent tissues it is fixed to the addition 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 C 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 okay in apoptosis what will happen the cytochrome C is going to leak out of the sulcer okay intrinsic pathway cytochrome is going to leak out of the cell binds with epiph1 forming apoptoso right so which of the following substances released from the mitochondria most likely trigger the cellular changes what is answer who is going to be leaked out thank you OMC thank you thank you I'll definitely meet you again in ksma okay again I will do the patho there okay in highly integrated more integrated way for your next exam okay so the answer is cytochrome 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 a 65 year old woman sorry yeah sorry 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 he's 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 diaphrotic 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 wedge-shaped I said when the arteries are blocked then the veggies say whenever you see the word wedge shape perfusion defect veggie 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 the problem he is having say membranous nephropathy okay membranous nephropathy you should know again I will teach you this again in uh 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 enforter real blood vessels are blocked bed shaped infant so one step of necrosis which type of neck processor 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 so with this all the important topics in this class okay the class one of cellular cell injury is completed tomorrow let's discuss about the cellular adaptations and the miscellaneous topics whatever they're in this leftover in this topic will continue tomorrow okay guys today class is completed hope the video is helpful for you okay the entire PDF will be the PDF will be shared in your in the SARS telegram group answer siligram group the entire PDF will be shared so this is how we are going to discuss every day first we are going to see the normal topic with the image based questions and the previous year questions and for your next exam we will do the clinical cases also clinical case approach also will be done okay okay guys see you good night