I don't know. Hello everyone! I'm alive. I'm visible. Audible. Give me a thumbs up in the chat box if I'm clearly visible and audible, and even from the audience, a very good morning to all of you. Hi Shalini, Arvind. Can you please confirm if I'm clearly visible, audible, everything is good to go? If people confirm, I will go ahead. I am still waiting for the confirmation. Good morning, good morning everyone. A very, very good morning. A refreshing morning, enthusiastic morning today. Yes, okay. So, am I clearly visible, audible? Thank you, thank you for confirmation. Thank you everyone. So, let me start the session. A very good morning to all of you. I am Dr. Priyanka Sachdev here, and today I am here to, you know, to take a crash course, uh, most important, high-yielding topics of General Pathology and Hematology. So, we have a two-day crash course. Today, we are going to finish complete General Pathology as well as Hematology, and tomorrow, we are going to take complete Systemic Pathology. So, today also, we are having a six to seven hour session. Tomorrow also, we are having a six to seven hour session. So, in this approx 14, 15 hour session, we are going to cover the most important, high-yielding topics of entire pathology in a crisp manner. So, I can challenge if you attend my this course, like 12 to 15 hour course completely, the 90 questions will hit from the syllabus only because we are going to cover most important, you know, repeatedly asked questions. Whatever exam you are targeting, if you are targeting FMG, if you are targeting NEET PG, if you are targeting NEXT, whatever exam you are targeting, now I am going to cover the most important topics here. Most of the students know my way of teaching. First, I will take a chapter, I will take a topic, I will teach you the concise theory related to that, and then we will solve the PYQs and, you know, most important MCQs which can be asked from that topic. So, in this way, the PYQs, the last three years PYQs from that topic will be completed. Not only this, if new questions are framed from that particular topic, you are prepared for that all also. So, can we go ahead? Are you people ready? Are you people ready? So, let's start super simplified course of pathology. Can we go ahead? Are you people ready? Can I start? Okay, so let's start with General Pathology. So, let's finish General Pathology in say, four or five hours, and after that, two to three hours of Hematology. Okay. So, again, I'm repeating, I am taking the most important topics of each chapter. You can also understand, completing entire pathology is not possible in 15 hours. If we want to complete entire pathology, it requires 80 hours, 60 to 80 hours, not 15 hours. Then, in 15 hours, what we can do? We can see the most high-yielding topics or most, uh, repeatedly asked topics from each chapter. Okay. So, let's start with chapter number one of General Pathology. Let's start with chapter number one, cell adaptation, cell injuries, cell death. Okay. So, let's start with the topic cell adaptation first. I will let you know what the cell adaptation, then cell injury, then cell death. In cell death, we will see two things: apoptosis as well as necrosis. I can challenge whatever exam you are targeting now, you will get one question from this topic. Okay. So, what is cell adaptation? Cell injury? Cell death? Are the three things related to each other? Are the three things related to each other? Listen, in human body, from head to toe, we all are made up of cells. You know, cell is the structural and functional unit of human life. So, we are completely made up of cells. Normally, all the cells are in homeostasis. Can you see a cell in this diagram? All the cells are in homeostasis. You can ask them, what is homeostasis? Homeostasis means a cell is performing a particular function with a particular structure. For example, the God has assigned particular function to particular cells. For example, the cells of the salivary gland, they do the function of secretion. The cell of the intestine, they do the function of absorption. The cell of the nervous system, they do the function of cognition and memory. So, they all are cells, but they are assigned different function because they have little bit structural differences between them. That is the meaning of homeostasis. But whenever any stress acts on the cell, whenever any stress acts on the cell, whether physiological or whether pathological, three things happen back to back. Number one thing is cell adaptation, in which the cell will try to adapt and survive, uh, the unfavorable condition. It will, it will, you know, try to survive the stress, overcome the stress. That is known as cell adaptation. But these are reversible. I mean to say, once you remove the stress, the cell will come to a homeostasis again. After that, if the stress is continued, continued, continued, the second thing takes place as cell injury. Again, cell injury, first there is reversible cell injury, followed by there is a point of no return. After that, there is irreversible cell injury. Reversible cell injury, it is reversible. Irreversible cell injury is actually cell death. It is irreversible. Once the cell is dead, it is not again alive, right? Now, please understand with the help of example. It was a theory part. Let me tell you, uh, the example. Okay, I'm coming, I'm coming on that. MD Islam, I'm coming. What is stress? Stress is anything which is not physiological. I mean to say, that is not normal. That is known as stress. Let me take an example. Okay, how many hours you study in a day? Can you tell me how many hours you study in a day? Normally, normally today, how many hours you will study? You will say, "Ma'am, four." Some students will say, "Ma'am, four." Or some will say, "Six hours." Okay. So, four to six hours normally you study every day. That is your homeostasis. You are in homeostasis. But what about the day before the exam? How many hours you study a day? One day before exam or on the day of exam, how many hours you study? You will say, "Ma'am, 12 hours." Some will say, "18 hours." Maybe "16, 17 hours." Impressive, right? So, what is this? What is this? So, exam is acting as a stress, and to overcome the stress, your body is doing the adaptation. So, instead of doing normal, you are doing something, uh, extraordinary, you know? So, instead of studying six hours, you are studying for 12 hours, 15 hours. So, that is adaptation, right? So, you will do. So, what about once the exam is over? How many hours you will study? How many hours you will study once the exam is over? Don't say, "Ma'am, I will not study zero hours." So, again, you will shift to the homeostasis. I mean to say, the once you remove the stress, now the adaptations are reversible. I, I want to explain this, but imagine the exams are continued for one month or two months. So, what will happen? Continuously, you will study for 12 to 15 hours for one month or two months. You will have certain diseases in your body, right? That is injury. That is injury. Again, up to a certain point, injury is reversible. Once you remove the stress, the exams are over, it is removable. It is reversible. I mean, but if exam continues forever, forever, you cannot study for 15, 16 hours or 20 hours, you know, you will have many disorders. This is the irreversible cell injury. You can have. So, this is just an example to understand. So, I mean to say, I mean to say, there are three things happen back to back. The first thing is adaptation, followed by reversible cell injury, and followed by irreversible cell injury, which is known as cell death. So, if the stress continued, continued, continued, these three things are the progressive one by one, they will happen. Okay. How many types? Let's talk about adaptation first, then we will come on injury, then cell death. Okay. The three things we have to cover. The first thing is the adaptation. How many, how many, uh, types of adaptations are there? There are five types of adaptations. What are the five types of adaptations? Hypertrophy, hyperplasia, atrophy, metaplasia, and dysplasia. Okay. What do you mean by that? Okay, first understand the word hypertrophy and hyperplasia. Okay, both are hyper. Hyper means more. Hypertrophy and hyperplasia. Okay. What is the difference between between them? Trophy means size. In pathology, the word trophy means size. And in pathology, the word plasia, the word plasia means number. Okay. Number. It's the number of the cell. Hyper means more or increase. So, increase in size of the cell is hypertrophy, and increase in number of the cell is hyperplasia. You got it? So, that is the meaning of hypertrophy. Trophy means increase in size of the cell. Plasia means increasing number of the cell. Can you see here? Can you tell me what is this? What is this? Can you see there? One cell. So, normally this cell was in homeostasis. Now the stress is acting on the cell because of the stress, the cell is doing certain adaptation. So, what does it? So, you can see the size of the cell here. You can see the exact same size of the cell here, but here one cell, here multiple cells. So, basically the number is increased, not the size. So, you can say it's hyperplasia. It's hyperplasia. Okay. Let me see. Okay, can we go ahead? Okay, okay. So, this that is hyperplasia, increase in number of the cell. And here you can see this cell is also in homeostasis. So, when stress is acting on this cell as a part of adaptation, this cell is same here. It is also one. Here it is also one. Number is not increased, but you can notice the size is increased. So, you can say this is hypertrophy. So, one is hyperplasia, one is hypertrophy. See the third here. The cell is in homeostasis. Now the stress is acting. Because of the stress, it decreases in size. Appreciate the size here. Appreciate the size here. It is decreasing in size. That is known as atrophy. That is known as atrophy. Give me a thumbs up. Yes, I will provide the PDF after the session. Don't make the notes. I will provide the PDF on the Telegram group. Okay. You can find the PDF on the Telegram group of the Pro-CRM. Okay. So, can we go ahead now? Give me a thumbs up. This is atrophy. Okay. Atrophy. Now, I taught you three things: hypertrophy, hyperplasia, and atrophy. Can you tell me a common example of all three? Hypertrophy is increase in size. Hyperplasia is increase in number. Atrophy is decrease in size. Can you tell me a common example of all three? Can you people please tell me the common example of all three? Yes. So, best example is the pregnant uterus, you know. So, during pregnancy, can you see the size of the uterus? Normally, this is the size of the uterus normally. But during pregnancy, to accommodate the fetus inside that, the size of the uterus increases. We all know. But how does the size of the uterus increases? In the uterus, there are three layers: endometrium, myometrium, perimetrium. Let's talk about the middle layer, myometrium. These are the cells of the myometrium. Okay. You can see the cells of the myometrium. So, basically, the hormones during the pregnancy, the estrogen and progesterone, they are acting as a stress. They are acting as a stress during pregnancy. The hormonal changes takes place now. So, they are acting as a stress. Because of this stress, the cells, can you see the cells in the uterus? These cells will increase in size as well as number. So, they increase in size, that is hypertrophy. They increase in number, that is hyperplasia. So, basically, pregnant uterus is an example of both. So, because of increase in size and number both of the cell, the uterus increases in size. The uterus increases in size because of increase in size as well as number of the cells in the myometrium. But what if after delivery? Now, the delivery of the fetus already took place. The delivery of the child, the fetus, the newborn already took place. Now, parturition, you know, during the next two, three months, uterus again becomes normal size. So, how does it become again shrink in the size? Because of atrophy of the cell. Now, these cells undergo reduction in size. Whatever cells they were increased, now they undergo reduction in size. And because of which, there is parturition. So, can I say uterus is coming in all three examples? Say yes, if you got it. So, during pregnancy, it's hypertrophy and hyperplasia, which is which is leading to increase in size of uterus. And after pregnancy, during parturition, after delivery, the reduction in the size of the uterus is due to atrophy. I want each of you to give me a thumbs up on this point if you got it. So, you can see three of the adaptation: hypertrophy, hyperplasia, and atrophy are coming in this, in this, the three, the three of them are coming in this. Can we go ahead? Okay. Yes, hypertrophy is the single best, you can say. Another, but all three are there. Okay. Can we go ahead? Okay. You can see here the gross and the microscopy of the uterus. You can see this is the normal uterus, non-pregnant uterus. And you can see this is the pregnant uterus. This is the pregnant uterus. Uh, see the appreciate the size. Appreciate the increase in the size grossly. Appreciate that. Now, make the slide of this. Make the slide of this. See the histopathology of both of them. The non-pregnant uterus. See the cells of the myometrium. And during pregnancy, see the cells of the myometrium. I appreciate the size of the cell is increased. And if you count the total number also, the size as well as number, both is increased. Give me a thumbs up if you got it. Yes, I'm, I'm going to cover important topics of the entire syllabus. Adil, I'm going to cover entire syllabus today. So, can we go ahead? So, we are done with three: hypertrophy, hyperplasia, atrophy. Coming on the fourth one. The fourth adaptation, what is the fourth adaptation? The fourth adaptation is metaplasia. What is metaplasia? Now, can you tell me what is metaplasia? It is transformation of one type of cell to another one type of mature cell is transformed to another type of mature cell. I mean to say, either the squamous cell converted into columnar, or the columnar cell converted to squamous. So, either squamous to columnar or vice versa, columnar to squamous. So, it is known as metaplasia. Basically, there are two types of metaplasia. Whenever the squamous cell converted to columnar, so finally columnar is formed. Now, this is known as columnar metaplasia. And whenever the columnar converted to squamous, it is known as squamous metaplasia. So, basically, you have to see finally what is formed. Finally, what is formed? Can you see here? In columnar metaplasia, finally columnar is formed. In squamous metaplasia, finally squamous is formed. So, yes, yes, another, absolutely right. It is the transformation of one type of epithelium to another type of mature epithelium. It's not increase in size, increase in number, decrease in size. It is transformation or replacement of one type of epithelium by another, either by squamous to columnar or columnar to squamous. If it is converted from squamous to columnar, it is known as columnar metaplasia. And if it is converted from columnar to squamous, it is known as squamous metaplasia. Okay. Can we give me a thumbs up? Yes, I am coming, Osama. I'm coming on the examples also. Okay. Give me one example which is common for both types of metaplasia. I mean to say, the columnar and squamous. As I have given you an example of uterus, uterus was a common example of hypertrophy, hyperplasia, and metaplasia, right? Now, I want you to give an example. Can you tell me the organ, the example which is common for columnar metaplasia as well as squamous metaplasia in one organ? Both of them takes place. Can you tell me the name of that organ? It's female cervix. The female cervix. Okay. Let me give you the basics. So, this is the uterus of a female. This is the cervix of a female. And this is the vagina of a female. Okay. Tell me the lining of the cervix. Okay. The uterus is lined by columnar epithelium, I guess we all know that. The uterus is lined by columnar epithelium. Okay. And the vagina is lined by the squamous epithelium. We all know that. So, this is the normal lining. Can you tell me the organ cervix, which is between them? What is the lining? What is the lining of the cervix? Can you tell me? So, yes, the cervix is having two portions. The cervix is having two portions. Let me divide the cervix. This is endocervix, and this is ectocervix. So, can I say endocervix is a continuation of uterus? That's why it's columnar? Common sense? Yes. The endocervix is. And can I say the ectocervix is a continuation of the vagina? So, it's the ectocervix is squamous? Yes. So, use your common sense. There is nothing rocket science in that. Do nothing, nothing to learn. So, if you have understood, so normally, the endocervix is columnar, and normally, the ectocervix is squamous. The cervix is an organ in which we find both the linings, right? So, basically, let's talk about the endocervix first. Imagine the uterus is connected with the pelvic cavity with the help of ligaments. Imagine if the tear, if there is a tear in the ligaments, what will happen? The uterus will prolapse. The uterus will prolapse like this. The uterus will prolapse. The uterus will prolapse like this. Now, this prolapse is acting as a stress for the endocervix. The prolapse is acting as a stress for the endocervix. Okay. Because of the stress, because of this stress, the endocervix, which was columnar, converted to squamous now. So, this is an example of squamous metaplasia. Finally, squamous is formed. See what is finally formed. Okay. Now, let's take the example of the ectocervix. In the ectocervix, during, during reproductive age, or during pregnancy, whenever there is increased estrogen and progesterone in the blood, that is acting as a stress. So, here, the stressor is the hormone. Whenever there is increased estrogen and progesterone in the female blood, during pregnancy, or during reproductive age, during puberty, at that time, at that time, the ectocervix converts, that cervix, which is normally squamous, from squamous, it converted to columnar. So, ectocervix is an example of columnar epithelium. Say yes. So, the two things are in front of you. So, have you got it? So, the cervix is coming in both examples. So, can I say the endocervix is an example of squamous metaplasia, in which columnar get converted to squamous? And can I say ectocervix is an example of columnar metaplasia, in which the squamous cell get converted to columnar? Everyone, give me a thumbs up. It was complicated, but I try my best to give you the concept. Learn the stressor is different in both of them. Please try to learn the stressor. In case of endocervix, the stressor is the uterine prolapse, the uterus prolapse. In case of ectocervix, the stressor is the estrogen present in the blood. Try to, you know, give me the thumbs up. Have you got it? So, please interact. It's an interactive session. It's a live session. It is not a recording you are watching. So, if you have any doubt, please ask. If you don't have any doubt, give me your gesture that you got it. How you can see me, but I cannot see you in front of me. There is only one camera. So, I can see your comments only. Okay. So, the comment is the only way we can interact with each other. So, give me a thumbs up. You got it. Can we go ahead? So, that is regarding the metaplasia. So, till now, we have seen four adaptations: hypertrophy, hyperplasia, atrophy, and metaplasia. The two types of the metaplasia, we have seen the example. We have seen one common example of these three, the uterus, you know, during pregnancy, its hypertrophy and hyperplasia. During parturition, etc., in the uterus. And we have seen a common example of the two types of the metaplasia, that is cervix. In endocervix, metaplasia takes place. And in ectocervix, its columnar. Am I right? Am I right? Yes, I guess I'm right. So, that is what we have learned till now. Let's continue. The last one is the dysplasia, and most important and difficult to understand. Most of the students have trouble in understanding what is dysplasia. Okay. I will make it super easy for you. What is dysplasia? If you want to give the definition of dysplasia, it's disordered development. What is dysplasia? It's disordered development. It is a pre-malignification. You can ask me, what do you mean by that? Okay. So, I will tell you seven features. If these seven features are present in any cell, that cell is known as dysplastic cell. That is a pre-malignant cell. So, let me explain you the seven features in a diagram instead of, you know, reading and learning, try to see them in the diagram. Try to see them in the diagram. The seven features, all seven, I will show you in one diagram. The one diagram is in front of you. Okay. This is the diagram. Okay. Now, see this one is the normal, normal epithelium. And this one is the dysplastic epithelium. We will notice the changes between them. The seven changes which are absent in normal and which are present in dysplasia. So, you will understand the definition of the dysplasia in this way. Okay. Listen. Now, normally, normally, you can see this is the cell. You can see these are the cells. Can you all see? Please have a look. These all are cells. Okay. This is the normal cell lining. You can see actually it is a cell lining of the endocervix of the female. It's a columnar lining. Now, see during dysplasia, what is happening? The first thing you can see, the number of the layers is increased. Here we can see one layer. Here we can see multiple layers. So, the first thing you can see, the number of layers is increased in dysplasia. On every point, please appreciate that. You got it? The first point is increase in number of layers. I guess everyone can notice here is one layer and here is multiple layer. We all can see. Number two, here you can see normally it's ordered arrangement. They are back to back, beautifully orderly with a pattern, like orderly arrangement. But here, you, you can see haphazard. They all are like half is it? Half is it? So, you can see the second point is disordered arrangement or haphazard arrangement. So, normally it's, I'm sorry, normally it's orderly arrangement, and here it's disorderly arrangement. That is the second point. Everyone can see in the same diagram. The third point, which is very important to understand, is the loss of basal polarity. What do you mean by basal polarity? Let me explain you. Let me explain the normal epithelium here. Normally, this is the epithelium lining. This is the basement membrane. You can see this is normal. I am drawing non-dysplastic and this is the basement membrane. This is the basement membrane. Where is the nucleus? Where is the nucleus of these cells? The nucleus is not in the center. Normally, the normally, the nucleus is towards the basement membrane. I'm saying towards the basement membrane. Mind my words. I am saying it is present towards the basement membrane. It is known as basal polarity. Basal means basement membrane. Polarity means, you know, North Pole, South Pole. So, it is pole, base, couple, basal polarity. It is present towards the basement membrane, right? Basal polarity is present normally. Normally, but see what is happening here. Um, in dysplasia, let me draw this plastic lining. And this plastic lining, it's haphazard. Let me draw multiple layers, not one layer. Let me draw. They all are haphazard. They all are disorderly arrangement. This is just plastic. Now, where is the nucleus? Here, nucleus is away from the basement membrane. It is not towards the basement membrane. Number one, nucleus is enlarged in size, and it is away. It is dark. It is condensed. And it is away, away from the basement membrane. So, can I say here the basal polarity is absent? Basal polarity is absent here. So, basically, I want to say the loss of basal polarity takes place in dysplasia. Say yes. Loss of basal polarity. Basal polarity. Presence of basal polarity is a normal thing. We all have this basal polarity in all our columnar epithelia. It's normal. But the loss of basal polarity is dysplasia. So, learn the third finding. Its loss of basal polarity. You can appreciate in this diagram also. See the normal diagram. All the nucleus towards the basement membrane. But in the second diagram, the nucleus is not towards the basement membrane. It's away or haphazardly arranged. Got it? The third point. Coming on the fourth point. Fourth point is pleomorphism. Pleomorphism. Uh, you can see all the cells. Normally, they all are same size, same shape. Normally, they all are same size, same shape. That is, they all are uniform. But in dysplasia, some are small, some are moderate, some are large. So, it is known as pleomorphism. Pleomorphism means variation in size of the cell. All the cells are of different size. So, normally pleomorphism is absent. But in dysplasia, the pleomorphism is present. Can I say it? Yes. The pleomorphism. The next is we will talk about three things of the nucleus. Okay. See the size of the nucleus, color of the nucleus, and mitosis in the nucleus. Compare three things in the nucleus, back to back. Normally also, in dysplasia also. See the size of the nucleus in both the diagram. Can you appreciate? Here nucleus is small, small. Okay. We will talk about the ratio known as NC ratio. Nucleus in the numerator and cytoplasm in the denominator. The size of the nucleus in the numerator, the size of the cytoplasm in the denominator. This is known as NC ratio. Okay. Okay. See the NC ratio here and see the NC ratio here. Can you please appreciate what is increasing? Numerator, denominator, what is happening? So, see, normally nucleus is small, cytoplasm is large. Appreciate nucleus is small, cytoplasm is abundant normally. So, numerator is small, denominator is more. Normally, but see dysplasia, reverse is happening. Can you appreciate the nucleus is big, cytoplasm is small? You know, so nucleus is increasing as compared to cytoplasm. So, basically, can I say in dysplasia, in dysplasia, NC ratio increases because numerator is increasing and denominator is decreasing? Can I say so? Overall NC ratio increases in dysplasia. So, here NC ratio is normal. But here, NC ratio increases because of increase in size of nucleus. Say yes, if you got it. Do you have any problem in understanding or you got it? The meaning of the NC ratio. NC ratio, the numerator is the size of the nucleus, and the denominator is the size of the cytoplasm. Normally, nucleus is small, cytoplasm is more. But during dysplasia, the nucleus increases in size as compared to cytoplasm. So, if you compare, you can say NC ratio increases during dysplasia. Say yes. Yes, very good Shalini, very good everyone. Can we go ahead? So, this is the NC ratio. The next is the color of the nucleus. You have seen the size. Now, let's appreciate the color of the nucleus. Here, nucleus is light color. And here, the chromatin inside the nucleus becomes condensed. Because of condensation, the nucleus becomes dark color. What is color in pathology known as? The color and pathology known as chroma. The meaning, the dictionary meaning of chroma's color. The color is increased in dysplasia now. So, say hyperchromatism. Hyper. Split the term. The meaning is in front of you. Hyper means more. Chroma means color. More color, dark color, because the nucleus is condensed. So, say hyperchromatism is not a normal picture. Hyperchromatism is present in dysplasia. Okay. And last is mitotic activity. Normally, we cannot see the mitosis. Normally, but here, if you can appreciate, you can see the spindle formation in some of the cells. Some of the cells are dividing. Mitosis is a common feature of dysplasia. Can you appreciate the seven features? We are done with dysplasia. What are the seven features? Please everyone with me. What are the seven features? See normalcy, dysplasia. I appreciate the seven features. Yes. Here the number of layers are normal. Here the number of layers are increased. Say yes. The second, here see the arrangement. Its orderly arrangement. Here they are disorderly arrangement. The figures are in front of you. Please appreciate the changes. Don't learn. See in the image. The third is the basal polarity. Normally basal polarity is present. In dysplasia, it is absent. In dysplasia, it is absent, right? Pleomorphism. Normally it is absent. Hyperchromatism. Normally it is absent. But in dysplasia, pleomorphism present. Hyperchromatism present. And the ratio. Normally it's normal. But in dysplasia, it is increased. Mitosis. Normally it's normal. But in dysplasia, mitosis also increased. So, you learn the seven points. It's the definition of dysplasia. We are done with topic number one, cell adaptation. Everyone, give me a thumbs up. We will solve some questions now. If you got the topic, I want you to answer the MCQs. Can we start? Are you people ready? I will give it 20 seconds to answer each. You have to write your answer from ABCD in the comment. Fast and accurate. You have to be fast. You have to be accurate. The first question is in front of you. Give the answer. Both hypertrophy and hyperplasia are seen in four examples: breast enlargement during lactation, uterus during pregnancy, skeletal muscle during exercise, and left ventricular hypertrophy during heart failure. So, what is the correct answer? ABCD may say, what is the correct answer here? Can you please give me the correct answer? Very good. Arthur is first to give me the correct answer, and rest all are also right. Very good, very good. Yes, very good Osama. Very good. Absolutely right. You have enumerated the seven features. I appreciate it. Very good everyone. Please everyone give me the answer. It's the easiest question I have asked you. Pregnant uterus is an example of both hypertrophy and hyperplasia. And instead of pregnant uterus, if I say the parturating uterus, parturating uterus, it is an example of atrophy. So, mind the words. Okay. So, yes, the correct answer is B, and you all are right. Very good. The next question: Transformation of one epithelium to another type of epithelium, what is it known as? Is it dysplasia? Is it hypertrophy? Is it neoplasia? Or is it metaplasia? What does it known as? Can you give me the answer? So, this is the definition of what? Yes, you all are right. Very good. Yes, yes, very good. So, it is the definition of metaplasia. Very good. The transformation of one type of cell to another type of cell. It is a definition of metaplasia. It is of two types: either squamous to columnar or columnar to squamous. Okay. So, I have given you an example that is cervix. It is an example coming in both. The next question is in front of you. All are true about metaplasia except. Don't miss the word except. Is it slow growing? Yes or no? Reversible back to normal with appropriate treatment? Yes or no? Is it irreversible? Yes or no? If persistent, it can convert into cancer? Yes or no? Tell me the correct answer. I mean, tell me what is there in the except. All are true regarding metaplasia except. Yes, what is the correct answer? You all are right. I told you all five adaptations are reversible. The definition of adaptation is reversible. Metaplasia is a type of adaptation. So, it has to be reversible. It cannot be irreversible. So, correct answer is C. The next question is in front of you. About hyperplasia, which of the following statement is false? Which of the following statement is false for hyperplasia? Is it increase in number of cell? Is it true or false? Increase in size of cell? Is it true or false? Endometrial response to estrogen is an example? Or all of the above? What is the correct answer? It's a tricky question. You don't get confused in the option. It's very easy but tricky. What is the correct answer? Hyperplasia. Plasia means number of the cell. It's increasing number of the cell, but not the size. And the endometrial response to estrogen is an example. The incorrect among them is B. They are asking the false statement, not the true. And they are asking about hyperplasia. I told you, don't get confused with the trick. Okay. Coming on the next question. It's very easy. All of them are cellular adaptation except. I told you there are five types of adaptation now. So, which of the following is not an adaptation? Hypertrophy, hyperplasia, necrosis, metaplasia. Which of the following is not an example of cell adaptation? Can you tell me the answer? Can you please tell me the answer? Yes, what's the correct answer? Can you please tell me? Yes, you all are right. Necrosis is not an example of adaptation. It's the type of cell death. Rest all are the examples. Decrease in cell size is known as. Is it atrophy? Metaplasia? Hyperplasia? Hypertrophy? Can you please give me the answer? I guess super easy question. Decrease in size of the cell. Yes, there is a little bit lag if I ask and you give me the answer. There is 10 second lag. So, I have to wait here. So, all are right. The correct answer here is, of course, A, atrophy. Atrophy is decrease in size. You all are right. The correct answer is A. Let me change the question. Increase is the correct answer here is atrophy. Instead of decrease, if I ask increase in size of the cell, what is your answer now? What is your answer now? Increase in size of the cell? Yes. So, what is the correct answer now? If I change the question a little bit? Yes, I'm waiting. Yes, very good. The correct answer here is D, yes, hypertrophy. And if I change the size to number, increase the number of the cell, what is the answer now? In that case, your answer will become C, hyperplasia. Do you know? So, that is the thing. So, let's come on the next topic. The two types of the cell death. So, I am going to cover two types of cell death now. One is apoptosis, one is necrosis. So, we will be covering two types of cell death, one by one: apoptosis and necrosis. So, why there are two types of cell death? These two types of cell death, the cell die by one of the method. So, you can compare apoptosis with the suicide, and necrosis with the murder. Yes, I will prove that. In the annual convince, the apoptosis is a suicide, and the necrosis like murder, you know. The two ways in both of them, the person will die. So, here also, the cell is dead, but there are two ways. The first point is that you may be thinking, "Ma'am, why there are two ways of the cell death?" I mean, if there is a choice given to the cell, you want to do suicide or you want to do the murder? I mean, why no, nobody wants to die. Another cell also do not want to die. So, why there are two different types of the cell death? I will explain you. Okay. So, let's start first with apoptosis. See the details of the apoptosis, then we will come on the necrosis, then we will see the differences between them. Let's start with apoptosis. The first point here, the first thing we will discuss is the apoptosis. In short, if you ask me the definition of apoptosis, it's cell suicide. In short, in short, it's cell suicide. Number one, learn the thing. It's cell suicide. Okay. Now, uh, let me define it properly. So, if you want to learn the definition, this is the definition. You cannot understand it directly if I read. Let me show you a diagram, then I will read the definition. Can you see a cell? Yes. Now, the point is that my question is again, why a cell want to do a suicide? Nobody wants to do a suicide. I do not want to decide. You do not want. Why a cell want to do a suicide? There are two reasons. Either this cell has performed its function in the body, and it is no more required. The function is already done, and this cell is no more required in this, in this human body, in this world. Number one. Number two, the cell DNA, the nucleus, or the DNA is damaged by some physical, chemical, or biological agent. Not DNA, not p53 will try to repair it fast, but the DNA damage is too much, and p53 is unable to repair it. It is beyond repair. So, in this way, this is a cancerous cell. Now, we do not want to keep it in the body. It is an abnormal cell. It is a damaged cell. So, we will ask the cell to commit suicide because you are damaged, the DNA is damaged. So, these are the two reasons by because of which we will ask the cell to commit suicide. Yes, the body will send the signal to the cell. Either the cell has already performed its function in human body and is no more required, or else its DNA is damaged beyond repair. In both of these situations, we will ask the cell to commit suicide. So, whenever the cell gets the signal that I have to commit the suicide, at that point, inside the cell, there are enzymes. The name of the enzyme is caspase. Please learn the name of the enzyme. Normally, these enzymes are inactive. It is present in all human cells. The caspases are present in all our cells, but they are inactive. They are inactive. Whenever the cell gets the signal that you have to commit the suicide, at that time, the caspase present in the cytoplasm get activated. Once the caspase become activated, what did, what they do inside the cell? There are three things. The cell have a nucleus. You will say, "Yes, ma'am." The cell have a nucleus. The cell have a cell membrane, and the cell have a cytoplasm. Three things are present in the cell. So, basically, the caspase divide the entire cell into multiple small, small apoptotic bodies. Each apoptotic body contains three things: small, small portion. So, nucleus get fragmented into multiple pieces. Each apoptotic body contains a small amount of nucleus. Each apoptotic body contains a small amount of cytoplasm, and each apoptotic body contains a small amount of cell membrane. And during this process, when the entire cell, you can see the entire cell get converted into multiple small, small apoptotic bodies, during this process, there is no leakage. During this process, there is no inflammation. No leakage, no inflammation is the hallmark of apoptosis, which differentiate apoptosis from necrosis. In necrosis, there is leakage. There is inflammation. Here, leakage, no. That's why I am comparing this, the apoptosis with suicide, you know. If someone want to commit suicide, it will be done in silence, you know. It is done personally, silence, in a closed room. It is not, the person will take loudspeaker and shout everywhere, "I am committing suicide! I am committing suicide!" It is done silently, you know. So, in this way, here also, the cell is committing suicide. So, silently, the cell will convert into multiple apoptotic bodies. There is no leakage, there is no inflammation. The inflammatory cell do not come to know that something is going wrong. No, it's silently, you know. And in the end, what will happen? A phagocyte will come, you know, what is a phagocyte? A phagocyte, it will engulf all the apoptotic bodies, and the cell disappeared from the world, disappeared from the from the from the human body. Say yes, if you got it. Say yes, if you got it. Okay. Yes, it is required in organogenesis also. Say yes. So, have you got it? Can we go ahead? So, this is the definition of apoptosis. So, what is apoptosis? Can you define now? You will say, "Ma'am, apoptosis is the type of cell death." Yes, it is one of the type of cell death. There are two types of cell death. Apoptosis is one of them. It is a tightly regulated intracellular program during which the cell which is destined to die, the cell which gets the signal for death, that cell activates an enzyme, the name of the enzyme is caspase. And caspase degrade the DNA and the cytoplasm into multiple apoptotic bodies. In the end, the apoptotic bodies are phagocytosed. During the entire process, no leakage, no inflammation. Highlight the negative findings. This is the definition of apoptosis. No need to learn, just understand. So, apoptosis is a type of cell death in which the cell which is destined to die, that will activate caspase. The caspase convert the cell into multiple apoptotic bodies. A phagocyte will come and engulf all the apoptotic bodies. No leakage, no inflammation. Give me a thumbs up. Got it? This is the definition of apoptosis. Now, you should ask me, "Ma'am, what is the mechanism?" In the mechanism, there are two pathways in the apoptosis. There are two pathways: extrinsic and intrinsic. What do you mean by extrinsic and intrinsic? Okay. So, this is the cell. This is the nucleus of the cell. The nucleus of the cell containing DNA. As I told you, the signal, the cell is receiving the signal to do the suicide. From where the signal is coming? Can you tell me? From where the signal is coming? The signal can come from the outside or the signal can come from the inside only. Okay. If the signal is coming from outside, it's known as extrinsic pathway. Extrinsic means outside. And if the signal is coming from inside, it is known as intrinsic pathway. Intrinsic means inside. Say yes. Okay. So, this is the meaning. Now, each of the pathway has two, two phases. So, in extrinsic also, in intrinsic also, there is initiation, there is execution. There is initiation, there is execution. Right? So, there are two, two phases in each of the pathway: extrinsic pathway and intrinsic pathway. In each of them, there are two, two phases. So, we will understand the mechanism of apoptosis. Are you people with me? Can I tell you the ultra important topic, the mechanism of apoptosis? I will tell you like a movie story, you know, in a fun manner. We will understand the entire complicated mechanism of apoptosis like this, like this, we will understand. Give me just three minutes. In three minutes, I will explain you the entire mechanism. Okay. So, I told you the meaning of the extrinsic and intrinsic. The meaning of the extrinsic and intrinsic. This is the cell. This is the nucleus of the cell. Now, this cell want to commit the suicide. This cell want to commit the suicide. Now, from where the signal is coming? If the signal is coming from outside, it's extrinsic pathway. And if the signal is coming from inside, it is known as intrinsic pathway. Okay. Now, each of them having two, two phases. The first, how, what is the sequence? I will teach you. First, I will let you know the initiation phase of extrinsic pathway. Then I will let you know the initiation phase of intrinsic pathway. And in the end, I will tell you execution of both of them together because execution is common for for both of them. So, I'm going to teach you three stories now. The first story is the initiation of extrinsic. The second story is the initiation of intrinsic. The third story will connect the two stories together, and it is the third story, that is execution, which is common for both of them. This is the sequence I will teach you like this. Say yes, if you got it. Say yes. Can we go ahead? Can we go ahead? Yes. So, let's start. So, let's start with the extrinsic pathway initiation phase. Okay. Now, can you see yourself? All human body cells have receptors on their surface. These are known as death receptors. What is it known as? Death receptors. There are two types of death receptors: Fas, which is known as CD95, one and the same thing. It is the name of receptor. The Fas receptor or CD95 receptor. It's a type of death receptor. And second is TNF, tumor necrosis factor. TNF. So, please appreciate the cell on the surface of the cell. Please appreciate the receptors. Can you appreciate these receptors? This one, this one. These are death receptors. It can be Fas, CD95. It can be TNF. Okay. So, these are the death receptors. They are inactive currently. They are inactive. I'm really sorry. I'm really sorry. So, these all are inactive. These are the death receptors present on the surface of the cell. Now, you can see here, this is the signal. This is the signal coming to the cell that this cell has to commit the suicide. The signal is coming. The signal is in the form of the ligand. It is in the form of the ligand. So, this signal is coming from outside or inside? You can see it is coming from outside. That's why it is extrinsic pathway. It is extrinsic pathway. I'm teaching you now. Extrinsic pathway, the signal is coming from outside. So, either the cell has performed its function, it is no more required. So, the signal is coming. Whenever the signal is coming, the ligand is coming, the ligand will come. So, let me zoom. So, I'm zooming the diagram. Okay. This ligand is coming and binding with the receptor. One of the receptor. So, ligand is coming, binding with one of the receptor. You can see once it will bind with one of the receptor, the receptor get activated. Once the receptor, the death receptor, the death receptor get activated, multiple death receptors come closer now. You can see a distance between them.

They are inactive. There is a distance between them. These are the death receptor, CD95 receptor, Fas receptor, one and the same thing. CD95 is one and the same thing. It's not different. These are synonyms, okay?

Now, once the ligand binds with the receptor, multiple receptors come closer like this. Can you see multiple receptors coming closer like this? And they are forming a domain. It is known as the death domain. It is known as Fas-Associated Death Domain (FADD). So, it's not my mnemonic; it is given in Robbins also. FADD. So, Fas-Associated Death Domain is formed, right?

Because of the formation of this domain, what will happen now? Now, in the cytoplasm, caspases are present. I told you now, the main enzymes here are the caspases, okay? There are many types of caspases: caspase number 1, 2, 3, 4, 5. So, because of the formation of FADD, the first caspase which is activated is caspase number 8. The inactive caspase 8 is converted into active caspase 8. The story is over. I will continue this. This is an intermission of this story. I will continue the story in the execution phase. This is the initiation phase, you got it? Initiation phase.

So, same thing whatever I have drawn you in this sketch diagram, the same is shown here. So, can you see the cell membrane? So, this is the cell membrane, you can see. Can you see these are the receptors? Let me show you. These are the death receptors, okay? On the death receptor, this is the ligand. The coming signal is coming and binding. So, multiple death receptors coming closer and because they are coming closer, this is FADD formation. Because of FADD formation, the caspase 8 is converted into active form. Active caspase 8 is formed, and that will lead to apoptosis. I will let you know how it is.

So, Fas receptor, Fas ligand is coming, binding with the Fas receptor. Multiple Fas receptors coming closer, and FADD is formed. FADD leads to conversion of pro-caspase 8 to active caspase 8. Sometimes caspase 10 also gets converted to active caspase 10. So, learn to caspase 8 and 10. Do they get converted from inactive to active form? So, this is over. This is over. And leaving it to caspase 8 and 10 activation, what will happen after this? I will continue here in the execution phase, but later on. Let me first tell you the initiation phase of the intrinsic pathway also. Then I will tell you the two execution phases together. Say yes if you got it, right? So, let me start. You know, you just learn the endpoint here. I will continue later on.

Let me tell you the initiation of the intrinsic pathway. Intrinsic pathway. Intrinsic, what do you mean by intrinsic here? The signal will come from inside the cell, okay? So, here, can you see a cell in front of you? Yes, you all can see a cell. Inside the cell, you can see the nucleus, and inside the nucleus, you can see the DNA. This is the DNA. It is intact. Now, there is no problem. It's a healthy DNA. You can see the mitochondria, the two membranes of the mitochondria, the inner membrane, the outer membrane. Between the two membranes of the mitochondria, there is a protein known as cytochrome C. So, cytochrome C is present between the two membranes of the mitochondria. Cytochrome C never comes in the cytoplasm. Once it comes in the cytoplasm, it will cause the apoptosis, right? Currently, it is present inside the two membranes of the mitochondria. This is normal. This is normal.

Now, let me zoom it. Now, you should ask me, "Ma'am, you are saying cytochrome C is present between the two membranes of the mitochondria, but mitochondria have a door? Now, the transit? This is the door, the door or the transit in the mitochondria." You should ask me, "Ma'am, why is cytochrome C not leaking out of this transit? Transit method?" So, why is it not coming out? Because the three guards are present. The three guards are present, you know, they are like guards. They prevent the cytochrome C to come out. The name of the three guards is Bcl-2, Bcl-x, and Mcl-1. So, these are preventing the apoptosis. Since cytochrome C is not coming in the cytoplasm, they will not cause the apoptosis, right? So, these three proteins are known as anti-apoptotic proteins. These three, the anti-apoptotic proteins, prevent the cytochrome C from coming out. Normally, in all of our cells. So, currently, in all of our cells, these three guards are preventing the cytochrome C to come out.

But imagine the DNA is damaged. Now, the DNA is damaged. The p53 will try to repair it, but it is beyond damage, beyond repair. p53 is unable to repair it. So, this will give the signal to the mitochondria that "I am gone. The nucleus is giving the signal to the mitochondria that "I am gone. I am damaged. I cannot be repaired. Commit suicide." It's not suicide. Who is giving the signal? The nucleus to whom it is giving? The nucleus is giving the signal to the mitochondria. So, from where the signal is coming? Is it coming from outside? No, no. It is not coming from outside. The signal is coming from inside only. So, that's why it's intrinsic pathway. Please appreciate intrinsic. The signal is coming from inside only. So, that basically the nucleus is giving the signal to the mitochondria. So, nucleus is asking the mitochondria to start the suicide, to commit the suicide. How does the mitochondria will do so? The mitochondria will replace the three guards with four other guards that will open the door. These were the three guards that closes the door, that that inhibit the transit. But it is replaced by another guard. The name of another guard is Bax, Bak, Bim, Bad. They are ultra important. They will open. They will open the transit, and cytochrome C will leak out. They cause the apoptosis. So, these were anti-apoptotic proteins. These are pro-apoptotic proteins. So, basically, on receiving the signal, the mitochondria replaces the anti-apoptotic protein by pro-apoptotic proteins. Proteins are replaced by pro-apoptotic proteins. Anti-apoptotic proteins close the door. They prevent apoptosis, and pro-apoptotic proteins open the door. They cause the leakage of cytochrome C. So, anti is replaced by pro. You can see cytochrome C is coming out. One cytochrome C comes out, the first caspase it activates is caspase-9. So, caspase 9 is the first caspase which is activated here. And caspase 8 and 10 were the first caspases which were activated in extrinsic pathway. Here, caspase 9 is activated. The story is over. The story is over. The story is over. Okay.

So, whenever the stimulus is given, the stimulus is the DNA damage. On DNA damage, receiving the signal, the mitochondria replaces replaces the anti-apoptotic protein with pro-apoptotic protein. So, basically, the anti-apoptotic proteins are replaced by pro-apoptotic proteins. On receiving the signal, the pro-apoptotic proteins open the door. So, cytochrome C leaks out. After coming out, it activates caspase-9. Say yes if you got it. So, we are done with this also. So, till now, I taught you the initiation of both of them. Can you tell me the endpoint here? The endpoint was activation of caspase 8 and 10. Here, the endpoint is activation of caspase 9. You will see my bots ahead. Here, the death receptors were required. Here, mitochondria and cytochrome C were required.

Okay, now what's ahead? So, let me tell you the execution phase of both of them together. The execution is common for both of them. So, in execution phase, which is a convergence point for both of them, in extrinsic pathway, the first caspase activated is 8 and 10. And in intrinsic pathway, the first caspases are activated. You know what happens? All the caspases will convert the cell into multiple apoptotic bodies. So, multiple apoptotic bodies are formed. In the end, a phagocyte will come and engulf all the apoptotic bodies. The cell will disappear from the world. No leakage, no inflammation. This is the mechanism. Say yes if you got it.

So, I taught you the two mechanisms, the extrinsic pathway, the intrinsic pathway. In both of them, I taught you two phases: the initiation and the execution. Initiation is different in both of them, but execution is a common feature for both of them. I want all of you to appreciate that you got it. Kindly write down "you got it" or if you have any doubt, please ask it or give me a thumbs up. Can we go ahead? Okay.

So, let me tell you the next thing. The next thing is the morphological changes on apoptosis. There are seven morphological changes in apoptosis. You have to learn the sequence. During extrinsic or intrinsic, whatever pathway, seven things take place one by one. Let me tell you the seven features. Let me tell you the seven features of apoptosis. Can you see a normal cell? This is a normal cell. Now, this cell is receiving the signal either from outside or from inside that it has to commit suicide, right? So, it is starting the suicide. So, the first thing happens is cell shrinkage. Please appreciate cell shrinkage. The first thing, the cell reduces in size. It's a very important question. The earliest feature of apoptosis is cell shrinkage, repeatedly asked PYQ, okay? You can see the cell is decreasing in size.

After that, you know, inside the cell, is present in the cytoplasm. You will see mitochondria, endoplasmic reticulum, ribosomes, multiple cell organelles are present. If the cell reduces in size, the multiple cell organelles, they will come closer, closer, closer. Because of the multiple cell organelles coming closer, the cell cytoplasm become more pink in color. Can you see the cytoplasm become more pink in color? It is known as eosinophilia. So, second thing is the eosinophilia because of the shrinkage. So, the first thing is the shrinkage and second thing is eosinophilia. Learn the sequence. The sequence of the seven is important. The earliest is the cell shrinkage. And you can imagine the cell is shrinking, so the cell organelles are coming closer, so cytoplasm looks more pink. It's known as eosinophilia, okay?

After that, coming on the nucleus. See, the nucleus become more compact. The nucleus become more compact, more dense. It is known as pyknosis. Pyknosis is compactness of the nucleus. After that, the nucleus, nucleus fragments into multiple pieces. The conversion of the one nucleus into multiple pieces, it is known as karyorrhexis. Pyknosis and karyorrhexis takes place in the nucleus first. It gets condensed, then it gets fragmented. So, that is the third feature. The two we will take together, the nuclear features. So, first is shrinkage, then eosinophilia, and then nuclear features, that is pyknosis and karyorrhexis.

After that, on the cell surface, multiple blebs are formed. Multiple blebs are formed because of the cell injury. The fourth feature is the bleb formation, right? Now, caspases are activated. If it is extrinsic pathway, caspase 8 is activated. If it is intrinsic pathway, caspase 9 is activated. And now, in execution phase, all the caspases are activated. Caspases convert the cell into multiple apoptotic bodies. So, apoptotic body formation is the fifth feature. In the end, a phagocyte will come and engulf all the apoptotic bodies. That is the sixth feature.

Can you please enumerate? Mirza, Nikhil, Jewel, Shake, Sachin, Shalini, everyone. I cannot read all the names. So, can you tell me the six features? The sequence of the apoptosis, please. One, two, three, four, five, six. Six sequence. Yes, the first thing is yes, the cell shrinkage. Very good. It's shrinkage. Now, this is a very important feature. The earliest feature that differentiates apoptosis from necrosis. In necrosis, the cell swells. Here, the cell is shrinking. Okay? Cell shrinkage is there. The second is the eosinophilia. Eosinophilia is due to compactness, due to the multiple cell organelles are coming closer, okay? That is the eosinophilia. The cytoplasm looks more pink. What is the third feature? The nuclear feature. The two nuclear features. Nucleus becomes compact and it becomes fragmented. Compactness is known as pyknosis, and fragmentation is known as karyorrhexis, okay? That is the third feature. After that, blebs are formed on the surface. Then apoptotic bodies are formed. And in the end, phagocytosis takes place. Say yes. So, these are the six features.

Now, let me ask you two questions here. Two questions, two answers. Who will answer the two questions? The first, tell me the earliest feature of apoptosis. Of course, everyone can see. Earliest feature of apoptosis. It's a PYQ. And tell me the characteristic, characteristic feature of apoptosis. Two different questions, two different answers. Don't get confused. What is the earliest feature? What is the earliest feature? Very good, Osama. Very good, Saya. Yes, very good. You have enumerated all the six features very correctly. Yes, the earliest feature is the cell shrinkage. Everyone knows. Everyone knows it is visible. But what is the characteristic feature? I mean to ask, the characteristic or the pathognomonic feature. The characteristic or the pathognomonic feature is its nuclear features, the pyknosis and karyorrhexis. So, read your question very, very carefully in your exam. What they are asking? If they are asking earliest feature of apoptosis, go, go with cell shrinkage. If they are asking characteristic or pathognomonic or specific feature, go with the nuclear feature, pyknotic and karyorrhexis. So, please read your question very carefully. Can we go ahead? Yes, yes.

So, you can see the same thing. Cell shrinkage is the earliest feature. Can you see in this diagram? This cell which is marked with an arrow, this cell which is marked with an arrow, I have highlighted the cell with blue color. It is smaller than the rest of the cells. See this cell. It is smaller than the rest of the cells. It is more pink than the rest of the cells. See this cell. It is smaller as well as more pink than the rest of the cells. So, cell shrinkage is also visible, and cell eosinophilia is also visible. Pyknosis, you can see. See the cell. See the nucleus. See the nucleus. It gets condensed. Condensation is known as pyknosis, and fragmentation into multiple pieces is known as karyorrhexis. That is the most specific or pathognomonic feature. A pathognomonic feature. See the bleb formation. Appreciate the bleb formation. The normal cell. See the apoptotic cell in electron microscopy. You can appreciate the blebs are formed. So, multiple blebs are formed on the surface.

Okay, after that, multiple apoptotic bodies are formed. Phagocytosis. Yes. No leakage, no inflammation is the hallmark. The last thing in the apoptosis. Tell me the diagnosis of apoptosis. How to diagnose apoptosis? Tell me two features. Two, two features. There is a marker for apoptosis. Just suppose I am giving you this slide and I am asking, "Can you identify an apoptotic cell?" You will say, "Ma'am, the cell which is smaller, the cell which is pink, the cell whose nucleus is condensed, that cell is an apoptotic cell." But still, you have confusion. "Ma'am, this is looking like others only. I am not very much trained to pick it up." So, the marker is available in the market. Don't worry. The name of the marker is Annexin V. And Annexin V is the name of the marker. It's a liquid. Brown color liquid. Spread it on the slide. Spread it. Leave it for some time. Wash it. Only apoptotic cells will pick the marker. It will become brown color and it will be highlighted. Other cells will not pick that marker. Say yes.

So, what is the name of the marker? It's very important PYQ. Annexin V. You should ask me a question, "Ma'am, why Annexin V is picked only by the apoptotic cell, not by other cells? What is the principle behind that?" Please ask the questions. More and more questions arise in your mind. You know, retention power you will have. Okay? So, apoptotic marker Annexin V is there, that is highlighting the apoptotic cell. But why? The question is why? Let me draw a diagram for you. This is a normal cell, okay? And this is an apoptotic cell with bleb formation. It is converting into an apoptotic cell. Normal cell has a protein, a phospholipid, which is present on the inner surface of the cell membrane. The name of that phospholipid is phosphatidylserine. During apoptosis, during apoptosis, there is flip-flop. I am using the word flip-flop. During which the phosphatidylserine is coming on the outer surface. The phosphatidylserine is coming on the outer surface. Now, Annexin V binds with phosphatidylserine. So, it will not bind with the normal cell. It will bind only with the apoptotic cell. So, the answer is phosphatidylserine. Say yes. Phosphatidylserine is the answer. Phosphatidylserine. You can see it is present normally on the inner surface. This is a normal cell. And during apoptosis, there is a flip-flop. During this flip-flop, it is coming on the outer surface. That's why Annexin V is not binding here. It is binding here. This is the first way.

The second way of the diagnosis of apoptosis is agarose gel electrophoresis. Do you know what is electrophoresis? Let me draw a normal cell. Let me draw an apoptotic cell. See the nucleus. This is the nucleus of the normal cell. And this is the nucleus of the apoptotic cell. Am I right? Have I drawn it rightly? Correctly? You will say, "Yes, ma'am, because in apoptosis, the nucleus undergoes fragmentation, which is known as karyorrhexis." We know that, right? So, if I do the electrophoresis here, in this, so let's do the electrophoresis. So, here the DNA is continuous, right? We will get one band. The DNA is continuous. But here, the DNA is like this. We will get multiple bands, you know? So, on electrophoresis, we can identify whether the DNA is continuous, single band, or it is multiple bands. The multiple band DNA, it is looking like a stepladder. See, see. It is known as stepladder appearance. Stepladder. It's a PYQ. Stepladder appearance. It is yes, very good. Andhra, very good. It is the stepladder appearance.

So, this is the stepladder appearance. The fragmentation of the nucleus is caused by an enzyme, endonuclease. You can see here. It's continuous. Here, it's continuous or it is discontinuous also. So, big, big pieces are there normally. But here, small, small pieces. It is looking like a stepladder. So, this is an apoptotic cell. These all are normal cells. Say yes. You got it. So, we are done with this also. So, we are done with apoptosis, everyone. Give me a thumbs up. Everyone. Do you have any doubt till now? Can I tell you the differences between apoptosis and necrosis? The differences between apoptosis and necrosis. Please consider apoptosis as suicide, and I am going to teach you the next topic, necrosis, that's like murder. Apoptosis takes place of a single cell. Necrosis takes place of a group of cells. If someone is committing suicide, he will do it alone. Now, suicide is done alone. It is not the complete town is doing the suicide or complete family is doing the suicide, right? You can consider like that, just for learning purposes. A single cell. But murder can be done of multiple persons at one time, okay? So, here, the necrosis, like murder, it's a group of cells. Here, cells shrink. Cells swell. So, here, cells shrink in size. Cells swell in size, right? Here, nuclear features are common in both of them. Here also, pyknosis, karyorrhexis. Here also, pyknosis and karyorrhexis. But here, cell membrane is intact. So, no inflammation, no leakage. Here, cell membrane disrupts. The cell bursts, right? So, inflammation is present. Leakage is present. Here, inflammation and leakage are absent. So, please learn. Please learn the differences between them like this. We will solve some MCQs on apoptosis and move on to the next topic, very quickly, necrosis. So, you have to be fast. You have to give me the answer. What's the correct answer here? Please tell me. CD95 is a marker of. Is it intrinsic pathway, extrinsic pathway, monocyte, or leukocyte? CD95. Just now I told you. Okay, let me give you a clue. CD95 is the other name of the Fas ligand. What is the correct answer now? CD95 is a marker of. Yes, yes, very good, very good. CD95, Fas, or TNF, these are the death receptors which are which are present in extrinsic pathway, not in intrinsic pathway. And you all are right. Very good, very correct, very intelligent, very good.

The next question. The following is an example of anti-apoptotic proteins. I told you three anti-apoptotic proteins and four pro-apoptotic proteins. I told you during intrinsic pathway. So, is it Bax, Bak, Bcl-x, or Bim? What is the correct answer here? Yes. So, I told you anti-apoptotic proteins are the proteins which uh closes the door, and pro-apoptotic proteins open the door, okay? Here, I told you three examples: Bcl-x, Bcl-2, and Mcl-1. And here, I told you four examples: Bax, Bak, Bim, Bad. Okay? Yes, you all are right. The correct answer is Bcl-x here. The remaining three are from pro-apoptotic. It is a very important MCQ.

The next. Everyone knows the earliest change in apoptosis. I guess everyone knows the answer. Earliest change in apoptosis. So, is it cell shrinkage, pyknosis, formation of apoptotic bodies, or fragmentation of the cell? What is the correct answer? I'm asking the earliest. Mind members. Earliest feature of apoptosis. What is the correct answer? Yes. So, there are two different questions. Earliest is different, and most specific and characteristic or pathognomonic is different. You all are right. The earliest is the cell shrinkage. But if I change the question from the earliest to the pathognomonic, what is your answer? No, pathognomonic feature or specific feature. In that case, your answer will become B, pyknosis, right? In that case, pyknosis and karyorrhexis.

Answer coming on the next question. The last question. All of the following are the features of apoptosis except. I am using the word except. Can you tell me the answer? Cell swelling. Is it a feature? Yes or no? Nucleus becomes compact. Yes or no? Cell membrane is intact. Yes or no? And cytoplasmic eosinophilia takes place. Yes or no? So, what do not take place? You have to tell me what do not take place. I'm using the word except. What is the correct answer? Yes, very good. The correct answer here, very good, is A, cell swelling. Swelling takes place in necrosis, never in apoptosis, right?

The next question. Annexin V is a marker of. I guess each and every one of you know the answer. Is it apoptosis, necrosis, atherosclerosis, or inflammation? Now, the question looks very simple to you because just now I taught you apoptosis. I am putting this question. But once you finish all 19 subjects, now the same question looks difficult to you. So, please learn. And Annexin V is a marker of apoptosis. It's a repeatedly asked question.

So, we are done with apoptosis. Coming on the next, necrosis. Okay, necrosis is another type of cell death. That is the murder. We are done with apoptosis. Now, I'm coming on necrosis. So, chapter one will be done. Then we will move on to the next chapter, that is inflammation. Can I start? Are you people there? So, let's start with necrosis. Let's start with necrosis. What is necrosis? The necrosis is also a type of cell death. But here, the cell will undergo bursting, and the cytoplasmic leakage is there. Because of which, inflammation is present. Inflammation is present. So, basically, there are five types of necrosis. I'm going to teach you now. The differences between coagulative, liquefactive, caseous, fat, fibrinoid. The liquefactive also known as colliquative. So, you can learn a mnemonic: Triple C, double F. The five types of necrosis. The five types of necrosis. What are the five types of necrosis? There are five types of necrosis. What are the five types of necrosis? Triple C and double F. The five types of necrosis: coagulative, liquefactive, caseous, fat, and fibrinoid. The five types of necrosis.

So, basically, all of them are cell death. All of them are murder. In all of them, the inflammation is present. Okay? Then you will ask them, "Why are there five types? Come on, they are all cell death." So, how can death be of five types? Yeah, there can be five different types of death. In all of them, the cell is bursting, the cytoplasm is leaking out, the inflammation is present in all of them. But still, there is some, some, some, some minor difference between them. I want to highlight those differences to understand you the differences between the five types. Give me a thumbs up. Give me a thumbs up. You got it? You got it? So, let me explain you the five different types. I want all my dear students to make this comparative table with me. Otherwise, I am providing the notes. Anyways, if you don't make it, it's good. But if you make it, it will fit in your permanent memory, okay? So, I request you to make this table in which in the introduction, write down the definition of all five necrosis. Then causes, gross and microscopy. Draw the microscopy. So, you will never do a wrong question on necrosis, okay? So, let's start with the first one, coagulative. Before that, before coming on the five types of necrosis, let me tell you something. Can you see a cell in front of your screen? Yes, you all can see a cell in front of your screen. You can see yourself. The cell has a particular shape. The shape of the cell is known as architecture. Architecture or the outline. It is the shape of the cell. The shape of the cell is known as architecture. Inside the cell, cytoplasm is present. Now, see the color of the cytoplasm. See the amount of the cytoplasm. Is it scanty or abundant? See the granularity. Whether the granules are present or absent. And see the nucleus. The nucleus. See the location. Is it central or eccentric? See the color. Is it dense or see its composition? So, based on the three details, you can identify a cell. How many types of cells are present in the human body? You will say, "Ma'am, we have hundreds or thousands of types of cells." Few of them are in front of your screen. So, can you identify the different types of cells? You will say, "Yes, ma'am, we can identify. Is it a muscle cell, stem cell, intestine cell, liver cell, blood cell? We can identify." You can identify any cell because of the three features. See their architecture, I mean shape. See their cytoplasmic color. See their nucleus. Based on that, you can identify what type of cell it is. So, if you want to identify any cell of the human body, there are many cells now. You have to see for three details. You have to look for architectural detail, cytoplasmic detail, and nuclear detail. By architecture, I mean the outline or the shape of the cell. Give me a thumbs up. Got it, right? So, please appreciate. Go on appreciating that you got it, okay? So, this is the thing. Now, let's start the necrosis.

The first type of the necrosis, I am starting is coagulative necrosis. In coagulative necrosis, uh, non-necrosis takes place of a group of cells. Can you see here? A group of four cells. All of them are alive. See the forces. Not four, I mean, they are multiple cells. They are alive. See the three details. See their outline. See their shape. See their cytoplasm. See their nucleus. Okay? And see they undergo death. They are coagulative now. So, you will say, "Ma'am, what two things are changing?" Your cytoplasm is changed, okay? You can see the cytoplasm is changed. Okay? You can see the nucleus has also become pyknotic and karyorrhectic, or it disappears. The nucleus is also changed. The only thing which is same here also is the shape. The shape is still same, right? So, in coagulative necrosis, the architectural details are maintained, but cytoplasmic and nuclear details are lost. This is the definition of coagulative necrosis. No one will teach you with such a simplicity in such a short duration of time. The coagulative necrosis, how will you define it? You will say, "Ma'am, the architectural details are maintained, but cytoplasmic and nuclear details are lost." Such and necrosis is known as coagulative necrosis. Say yes. Got it? Got it? This is the most common type of necrosis among the five. Among the five, this one is the most common. Write down the definition here in the introduction. Architecture present, but cytoplasmic and nuclear details are lost. So, okay.

Here, architectural outline persists, but the cytoplasmic and nuclear details are lost. It is known as coagulative necrosis. Since out of the three details, at least one of them is still present, it is still present, we can identify the cell. Identified because at least the shape you can see. Now, you cannot see the cytoplasm, not the nucleus, but at least the shape you can see. Have you seen a ghost? Have you seen? I have never seen. But the ghosts have only outline. It doesn't have inner detail. So, can I say the cells in the coagulative necrosis? Can I compare the cells in the coagulative necrosis with the ghosts? Because ghosts also have outline only, no inner detail. Or else, have you seen a tombstone? What is a tombstone? It is a stone which is present over the graveyard, okay? So, it is also having only outline. No inner detail. No inner detail. Can I compare the cells in coagulative necrosis with ghosts and tombstones? Yes. Both of them, the meaning is same. Only outline persists. I want to highlight the thing. The outline persists, and the cytoplasmic and nuclear details are lost. But the outline persists. That's why the cells are known as ghost cells or tombstone cells. Say yes. Learn this terminology, okay? So, that is the coagulative necrosis. Definition. Coming on the causes. You know, human body from head to toe, we are supplied with blood. Each and every organ has blood supply. What happens if any organ or any cell do not get the blood? You will say that organ will die because of necrosis. So, which necrosis takes place because of ischemia? It's the coagulative necrosis. So, in any organ of the human body, if blood supply is not there, if there is ischemia, ischemia means no blood supply, that organ will die because of coagulative necrosis, except brain. Learn the exception, that's brain. So, ischemia and all organs leads to coagulative necrosis, but ischemia and brain leads to liquefactive necrosis. The second type, liquefactive necrosis. Okay? The second, uh, ischemia and brain leads to liquefactive necrosis. If you have burns anywhere, just suppose I am having a small burn here, or multiple burns are there. In burns, the cells of that portion undergo death because of coagulative necrosis. And Zenker's degeneration is also an example. Please learn. Grossly, the organ is pale. Microscopically, all the cells look tombstone or ghost appearance. Now, compare in this diagram. You can see a kidney here. You can see a kidney here. You can see this is normal kidney, and you can see this is coagulative necrotic kidney. Compare. And at the junction, you can see the inflammation. Let me show you. You can see the junction. It contains the inflammatory cells. It contains the lymphocytes. So, in all necrosis, inflammation is a hallmark. Inflammation is present at the junction. Now, see the cells here. See the cells here. Compare the cells. So, you can see, "Ma'am, the outline is exactly same." You can see the outline is exactly same. These are the cells. Now, outline is same, but the cytoplasmic and nuclear details are lost. But outline is same. So, the cells are looking like tombstone or ghost. So, this is the diagram. Can we go ahead? Can we go ahead? Uh, Andhra, brain is not spared. I am saying in ischemia of the brain, it's liquefactive necrosis, not the coagulative one. Because brain has multiple hydrolytic enzymes, in which the liquefactive necrosis will take place. I mean to say, the entire necrotic tissue will convert into a gel-like material, which is liquefied. I am coming on the second one after that, you will understand your point. Can we go ahead? Yes, yes. Mohit, absolutely right.

The second type is the liquefactive, also known as colliquative necrosis. Why is it known as liquefactive? Because after necrosis, the necrotic tissue is semi-fluid, like a gel, like a gel, jelly, gel. That's why it is known as liquefactive. It's looking like liquid. So, what is the difference? See here, a group of alive cells. Can you see this architecture? You will say, "Yes." Can you see the cytoplasm? Can you see the nucleus? Yes. But when it undergoes necrosis, everything disappears. Architecture detail is lost. Cytoplasm is lost. Nucleus is also lost. So, all three details are lost. In contrast, coagulative necrosis, we are at least architecture was maintained. Cytoplasmic and nuclear details were lost there also, but at least architecture was maintained there. But here, architecture is also lost, and the cells are converted, a group of cells converted into a gel-like material, liquefied. That's why known as liquefactive necrosis. Say yes. So, here the architecture is maintained. That's why known as ghost cell or tombstone appearance. Here, the group of cells get converted into a liquid, a gel-like material. That's why known as liquefactive. See the two diagrams. See the contrast between them. Appreciate. Appreciate it. And if you have appreciated, let me know. Okay?

So, here the architecture, cytoplasmic, nuclear, all three details are lost. That is liquefactive necrosis. Okay? Causes. One of the cause you already know. It's ischemia of the brain. Ischemia of all organs is coagulative, but ischemia of brain is liquefactive. Okay? And if you have pyogenic, pus-forming bacterial infection in any body, any body organ, so it also leads to liquefactive necrosis. Grossly, you can see this is the brain. This is the diagram of the brain. Intentionally, I put a diagram of the brain to learn you that in brain, there is liquefactive necrosis. See the cavity formation. And inside the cavity, appreciate the gel, the liquid. It's liquefactive necrosis, right? Microscopically, this is the diagram. Again, a diagram of the brain. Okay? Let me show you. This is a normal brain. This side is normal. Okay? And this side, it's liquefactive necrosis. And I appreciate the junction. At the junction, it is all inflammation. Inflammation with granulation tissue. It's all inflammation. Junction is inflammation. There is nothing in that. Compare the normal with the necrotic site. Okay? Let me show you. Normally, I can see the neurons. See the outline. See the cytoplasm. See the nucleus. I can see all three details, right? But see when it converted to necrotic tissue. I can see nothing. What I can see is dot, dot, dot, dot, dot. This is all liquid material. So, neither architecture, nor cytoplasm, nor nuclear details. Say yes. Appreciate the diagram. Okay? This is liquefactive necrosis.

The third one is the caseous. You know the word caseous. It's a Greek word. It means cheese. You like cheese? I love cheese. You know, I like cheese. So, you see this is cheese. It's looking white. It is known as caseous necrosis because grossly, it looks like cheese. How does the cheese look? You'll say, "Ma'am, the cheese is white or yellow in color. It's granular in appearance." Granular. I'm using the word granular. It's dry, dry, granular, white cheese. It is cottage cheese. The necrosis looks like that, okay? That's why it is known as caseous necrosis, right? What is the definition now? So, this is the meaning. Because it is looking like cheese, what's the definition now? See the three types of. See the three types of necrosis in front of you. So, in caseous necrosis, here the architecture, cytoplasmic, nuclear, all three details are lost. So, you will say, "Ma'am, the same three details were lost in liquefactive also." Then what is the difference between liquefactive and caseous? You are saying here also all three details are lost. So, the difference is that here, in liquefactive, if all three details are lost, and the group of cells converted into a gel or liquid-like material, here the group of cells converted into granular debris. Solid granular debris, not liquid. Solid granular debris like cheese, you know? So, that is the difference. And in coagulative, you know, the architecture is maintained, but the cytoplasmic and nuclear details are lost. That's why giving a ghost or tombstone appearance. See the three things in front of you. See I appreciate my hard efforts behind all this. You can appreciate the alive cell have all three details: architecture, cytoplasmic, and nuclear. Now, you have to see which details are lost, and accordingly, you can decide the type of the necrosis. Appreciate. Appreciate it. Yes, yes. Can you? Can you got it? Do you got it? Give me a thumbs up if you got it. The three types of necrosis. No one will teach you with such a super simplicity. The three types of necrosis. Define them. Coagulative necrosis, liquefactive necrosis, caseous necrosis. Have you understood the differences between them? Now, can I come on the examples of the caseous? In caseous, there are two bacteria, two fungus. So, the two bacteria are TB and syphilis. And the two fungus is Histoplasma and Coccidioidomycosis. So, learn the two bacteria, learn the two fungus. The four causes of the liquefactive necrosis, right? Are caseous necrosis. Grossly, it looks like cheese. I told you, it looks like cheese. And microscopically, this is the diagram. It is a diagram of the lymph node. You all can see a diagram of the lymph node in which you can see this is the normal lymph node. This section is normal. In all the necrosis, one is normal, one is necrotic tissue. This is necrotic tissue. And at the junction, you can appreciate the inflammation. At the junction, please appreciate the inflammation. This is the inflammation at the junction, right? At the junction, I'm not interested in inflammation, but here the inflammation is a special inflammation. It's chronic granulomatous inflammation. I can see the giant cells, epithelioid cells. The inflammation is special. It's granulomatous inflammation. And see the normal cells. The normal cells, they have this architecture. These are the lymphocytes. You can see the shape, size. You can see the cytoplasm, nucleus. But here, you can see nothing. A pink color material, the debris, the granular material. This is caseous necrosis. It is looking like cheese, the dry, the granular. Say yes. Got it or didn't got it? So, that is the third type.

Coming on the fourth type. The fourth type is the fat necrosis. It's a special necrosis which occurs in fat-rich locations in human body. Tell me three fat-rich locations in human body. Three locations. Number one, female breast. The female breast have abundant of. Female breast have abundant of fat. Number one. Number two, pancreas, okay? And number three, mesentery. Number three, mesentery, okay? These are the three fat-rich locations. So, they contain adipocytes. They contain adipocytes. Adipocytes are the fat cells. So, death of adipocytes is known as fat necrosis. So, basically, fat necrosis takes place in three organs, right? Female breast, pancreas, and mesentery. Inflammation. These are the causes because of which the adipocytes undergo death, leading to fat necrosis. Basically, fat necrosis, death of the adipose cells. The three causes I told you: female breast, pancreatitis, and mesentery inflammation, because of which grossly it looks like chalky white. Can you see chalky white due to saponification? You can see the chalky white deposits or yellowish deposits. Grossly, and microscopically, it is having a cloudy appearance. Take the word cloudy. Cloudy. Can you see cloudiness? Appreciate the cloudiness. I want to highlight the cloudiness. If you are getting the word cloudy in your question, they are talking about fat necrosis because they contain fat. Now, the fat is cloudy in appearance, right? So, that is cloudiness. That's it.

The last one is the fibrinoid. The last one is the fibrinoid necrosis. Okay? The fibrinoid necrosis, it is a special type of necrosis. Takes place in the wall of the blood vessel. You know, blood vessel have three layers. The innermost is the intima. The middle layer is the media. And the outermost is the adventitia. These are the three layers. In the media, in the media, a pink color, fibrin-like material is formed. Let me show you the diagram. Can you see this? It is a wall of the blood vessel. See the innermost layer, this one, this one is the lumen containing the blood. It is intima. And this is all media. In the media, I can see the inflammation. Along with the inflammation, I can see a pink color material, a fibrin-like, a ribbon-like, eosinophilic structure, less material. It is fibrinoid necrosis. The fibrinoid necrosis takes place in the wall of the blood vessel due to vasculitis. Due to vasculitis. That's it. Nothing important. We are done. We are done with the five types of necrosis. The master table is in front of you. If you have understood it correctly and completely, you can revise the necrosis hardly in two minutes with this table. Can you please revise with me? Everyone, everyone. Can you please revise with me? The first thing is to learn the name of the five types of necrosis. The mnemonic is Triple C, double F. There are five types of necrosis. The first one is the coagulative. The second is the liquefactive. The third is the caseous. Then fat, then fibrinoid. The five types of necrosis. Tell me the definition. Come on, everyone. Tell me the definition. So, in coagulative, the architecture is maintained, but cytoplasmic and nuclear details are lost. That's why it is known as ghost or tombstone appearance. In liquefactive, all three details are lost. Here also, in caseous, all three details are lost. But in liquefactive, it's gel-like formation. And in caseous, it's the debris, granular formation. The fat necrosis takes place at fat-rich locations. You know the three fat-rich locations: the female breast, pancreas, and omentum or mesentery, one and the same thing. And fibrinoid necrosis takes place in the wall of the blood vessel. So, first learn the definition. First learn that. Then learn the examples. So, ischemia for all organs except brain is coagulative necrosis. Ischemia of brain with pyogenic infection is liquefactive necrosis. Caseous, you know the bacteria and parasites. Fat and fibrinoid, I told you. Grossly, I have given you the microscopy. I have given you the diagram for all of them. So, in all of them, on one side there was normal, on one side there was necrotic tissue, and at the junction, there was inflammation. Can we go ahead? Can you solve the MCQs now? Are you ready for solving the MCQs? Can we solve it right now? Are you people ready? If you people are ready, ready, give me a thumbs up. You have to be fast, huh? Very fast. You have to match your speed with me. Are you are you ready? Can we start? Okay.

So, this is the first question in front of you. We are done with necrosis also. Necrosis. Which cell body is retained as ghost cell? It is seen in which necrosis? Coagulative necrosis, liquefactive necrosis, caseous necrosis, or none? What is the correct answer? Yes. So, I am asking about the ghost cell or tombstone appearance. I told you in which type of cell this is seen? The type of necrosis in which the architecture is maintained, but the inner detail, cytoplasmic and nuclear details are lost. So, yes, the correct answer here is the coagulative necrosis. You all are right. I guess everyone is right. The correct answer is coagulative necrosis. Very good.

The next question is in front of you. All of the following organs likely to undergo coagulative necrosis except. Very repeatedly asked question. Tell me one organ in which never, never coagulative necrosis takes place, but liquefactive necrosis takes place. Is it spleen? Is it heart? Is it kidney? Or is it brain? Yes. What's the correct answer? I told you one exception. Ischemia of all organs except one in which coagulative necrosis never takes place, but liquefactive necrosis takes place. Yes, brain is the exception. In brain, coagulative necrosis never takes place. Can we go ahead? Yes.

So, we are done with chapter number one. We are done with chapter number one. Let's start chapter number two, inflammation. Are you people ready? Can I start? Chapter two, inflammation. Okay. So, first let me start with acute inflammation. Then I will be coming on chronic inflammation. Before starting the inflammation, you should understand what is inflammation. What is inflammation? You know, there are four types of microbes that can enter the human body: bacteria, virus, fungus, and parasite. And they all, after entering the human body, what do they cause? They cause ill effects. They cause ill effects. I mean, they cause disease. They cause disease. But the human body does not want to have disease. So, the body has a defense mechanism for them. The body does not want it. The body wants to defense the the ill effects caused by them. And that defense mechanism is known as inflammation. Okay? And what is inflammation? Inflammation is the body's defense mechanism. Infection is the harmful effect caused by the microbes, and inflammation is the protective response against them. So, inflammation is useful for us. That is the meaning of inflammation. So, you can understand inflammation is the defense mechanism. Or anything which is foreign for the human body, it can be bacteria, virus, fungus, or parasite. You can learn like, every country has an army. Now, every country and you also have an army. Every country has an army. So, army is the defense for that country, right? So, whenever any foreign terrorist, harmful foreign, like the terrorist enters the human, enters the country's territory, the army gets activated. So, there is a fight between the army and the terrorist. Who wins? Depending on who wins.

What is the result if the Army wins, that is WBC wins? It is inflammation. And if the terrorist wins, I mean the bacteria, when it's the infection. So, in our body, infection or inflammation, what is taking place? That will result. Decide the fact. Give me a thumbs up. You got it? You got it.

What is inflammation? So, there are two types of inflammation: the acute inflammation and the chronic inflammation. Acute inflammation: Take the example of tonsillitis. Take the example of tonsillitis. Chronic inflammation: Take the example of TB. Okay? Both of them are caused by bacteria. Tonsillitis is caused by bacteria, Streptococcus pyogenes. TB is also caused by bacteria, Mycobacterium tuberculosis. Both of them are caused by bacteria.

So, here, as soon as to have tonsillitis, of course, I guess everyone has had tonsillitis till now. So, from childhood, we have multiple episodes of tonsillitis. Now we are aware what is tonsillitis. So, as soon as bacteria enters inside the human body, within a few hours, the symptoms appear. So, onset is very fast here. But in TB, the bacteria enters the lung, remain there for years or months, and when the immunity drops, then the patient has symptoms. So, here, onset is very slow.

Once the person has tonsillitis, it will residency. It will, you know, the person will become normal in 7 days, whether he takes treatment or does not take treatment. But TB lasts for one year, two years, six months. So, here, duration is short. Duration is long. Okay? So, here, onset is fast. Your onset is late. Here, duration is short. Here, duration is long. Your edema is always present. Here, granuloma is also always present. The hallmark features: edema. Here, the hallmark feature is granuloma. Your main cells are neutrophils. Here, main cells are macrocytes or monocytes. Give me a minute. Okay?

So, please learn the differences between acute and chronic. Understand the example. Now, for acute, there are five cardinal signs. Acute inflammation takes place from head to toe, at any part of the body. Acute inflammation can take place in any part of the body, from head to toe. Acute inflammation can take place in any organ. Whenever acute inflammation takes place, five things happen one by one. The five things always happen one by one. Okay? Example, I will always tell you tonsillitis to learn the example of tonsillitis because we can understand it better, right? Not only in tonsillitis, in all organs, acute inflammation, these five things take place. These are known as the cardinal signs.

So, that organ turns red in color. You can see the tonsils become red in color. That organ temperature is more as compared to surrounding temperature. That is increased local temperature. That organ swells up. You can see the swelling. The organ swells up. In that organ, there is pain. There is pain. In that organ, we have tonsillitis, we have pain. Okay? And there is temporary loss of function of that particular organ. Temporary. Okay? So, that is the five signs. You don't have to learn the five signs in English language. I taught you in English. Now, do you know Latin? I don't know Latin. But in the exam, you have to learn these five cardinal signs in Latin language. It's an important answer cube.

So, redness in Latin language is known as rubor. Increased temperature in Latin language known as calor. Have you heard the calorimeter instrument? The instrument used to measure the heat. Calor. Okay? Then swelling is known as tumor. Don't get confused. Okay? Don't get confused. Tumor is not English. It is not cancer. Tumor, I am asking tumor in Latin language. In Latin, the tumor is the swelling. Pain is known as dolor. And loss of function is known as functional laesa. The five enumerate the five features: rubor, calor, tumor, dolor, functional laesa. Rubor, calor, tumor, dolor, functional laesa. So, rubor means redness. Calor means increased temperature. Tumor means swelling. Dolor means pain. And functional laesa is temporary loss of function. So, please learn the five cardinal signs of acute inflammation. It's a very important MCQ.

Let's start acute inflammation. Okay? In acute inflammation, there are five vascular, six cellular, total 11 events. I am going to teach you all 11 events in one diagram. So, these are the five vascular events. I will, I am not reading it. I will directly explain you. These are the six cellular events. I am not reading directly. I will explain you. At the end, after 5 or 10 minutes, in 10 minutes, I will explain all 11 events. After that, you will be able to say all the events. We will revise all 11 events in the end. Okay? All 11 events. I am going to explain in one diagram. The master diagram. Everyone here on the screen, please concentrate. Now, on your gadgets. Everyone. It's a very important topic. I am going to explain you all 11 events in one diagram. If you don't understand this diagram, you cannot understand the acute inflammation. This is my sketch diagram, my way of teaching. Okay?

Can you see this master diagram? In this master diagram, can you see the yellow line here? I have drawn a yellow line. Okay? Just a second. You can see this is the yellow line. Imagine this is the skin. The human skin. Imagine this is the skin of this portion. Okay? Now, some bacteria have entered the human body. It can be bacteria, it can be virus, it can be fungus, it can be anything. It can be the injurious agent. So, let's take an example, bacteria. I will call it a terrorist. It is a foreign material. Now, I will call it the terrorist. Okay? You can see the blood vessel just below that. There is a blood vessel. This is the endothelial lining of the blood vessel. And inside the blood vessel, we have three types of cells: RBC, WBC, platelet. Currently, I am interested in WBC, which is the Army, the defense mechanism. These are the Army. These are WBC. This is the Army, right?

Now, there is a terrorist. There is Army. You can see the terrorist. You can see the Army. The terrorist causes the disease, and the Army protects us. You got my point? But there is a, they should fight with each other. If the terrorist wins, then infection takes place. If the Army wins, inflammation takes place. Let them fight. Let's see who is learning, who is more powerful. Let's see. And that will decide the fate whether the person has infection or inflammation. That will decide after the fight. But there is a problem. There is a problem. A small problem for which we have to conduct the 11 steps. What's the problem? Can you see what is the problem? Huh? You all can see. You will see, ma'am, the terrorist is extravascular. I mean, the bacteria is extravascular, and the Army is intravascular. So, how they can fight? They cannot meet. No. One is extravascular, one is intravascular. They cannot meet with each other. If they cannot meet, how they can fight with each other?

So, you will see them. There are two ways. Either, either, either, uh, take, I'm sorry, either take the bacteria inside the blood vessel. If you take the bacteria inside the blood vessel, they will meet and they will fight, right? They will meet and they will fight. But it's a bad idea. If you take the bacteria inside the blood vessel, there is sepsis. There is sepsis. No. So, the other way around. We will take the Army out. Yes, it's a good idea. Take the WBC out and let them fight. So, for taking WBC out, we have to do 11 steps. So, that is the motto. Why we are doing 11 steps? Everyone learns the 11th struggle. At the five vascular, the six cellular, even students don't know why it is happening. What is the purpose? Why we are performing all this tedious exercise? We want to take the WBC out so that it can fight or it can do the phagocytosis of the bacteria and bacteria is dead. This is the purpose. Say yes, everyone. With me? You got it?

So, I will tell you the 11 steps one by one. Among the 11 steps, the five are vascular events, and six are cellular events. The last event in which the WBC will do the phagocytosis of the bacteria. Can I start? Are you people with me? If you say yes, then only I will start. Okay? So, this is the master diagram in which I'm going to explain you all 11 events. Okay? Let me start with the five vascular events first, then I will come on cellular. In the five vascular events, the first event is the vasoconstriction, transient vasoconstriction. See the diagram. See the diagram. Can you see this is the, uh, bacteria or a terrorist, whatever you say? So, the blood vessel just below that undergo vasoconstriction, you know, sympathetic stimulation. So, that portion undergo vasoconstriction. But it is transient. It is only for few seconds, hardly, hardly for few seconds. So, say the word transient vasoconstriction. The first event. Transient vasoconstriction. The first event.

So, as soon as, so, just suppose this is my skin, and just below that, I am having a blood vessel. So, if some injury is here, so the blood vessel just below this injurious agent, the blood vessel in that segment, not the complete blood vessel, blood vessel in that segment undergoes constriction transiently. So, transient vasoconstriction is the first event. It is only for few seconds or minute. Appreciate it. The first event, transient vasoconstriction. I am teaching you the 11 events of acute inflammation. The five vascular, the six cellular. The first is over. The second is vasodilation. Now, after that, the same portion which was initially undergo vasoconstriction, it's also dilated now, and it is persistent. It's not transient. So, say the second event is vasodilation, and it's persistent. Okay?

Now, imagine again, this is the portion. This is the point where the bacteria is entering. So, the blood vessel just below this portion of the skin, this is undergoing, this portion, not the complete blood vessel, only this blood vessel portion which is below this section, it is undergoing vasodilation. What do you mean by vasodilation? You will see my ambassador. Vasodilation means more blood. So, this portion has more blood. So, if I see from above, this portion looks red to me. Yes, obviously. Hannah? So, it is explaining the rubor. I told you the five cardinal signs. Now, one is explained. If I ask you, what is the reason for rubor? You can answer, ma'am, it is the second step, that is persistent vasodilation leading to rubor. And if I touch this portion, as compared to surrounding temperature, it's more hot because it is having more blood. More blood, more hotness, as compared to more warm, I mean, as compared to surrounding area. So, rubor and calor can be explained because of this. So, second step, step number two, that is persistent vasodilation, is explaining the two. Can be explained because of persistent vasodilation. We are done with two features till now. The first is vasoconstriction. The second is vasodilation. The vasoconstriction is transient in nature. The vasodilation is persistent in nature. Vasoconstriction leading to nothing. Vasodilation leading to two features: rubor and calor. Everyone? Yes? Everyone, give me a thumbs up. Everyone. Can we go ahead?

Yeah, coming on the third. Third feature. The third feature for understanding the third, uh, step, you have to understand Starling's Law. What is Starling's Law? Starling's Law says that in a blood vessel, in a capillary, two types of pressure always operate. One is outward, that is hydrostatic pressure, and one is inward, that is osmotic pressure. Hydrostatic is always outward. Osmotic is always inward. Hydrostatic, as the name says, hydro, hydro, water, that is the pressure due to water. The water is leading to this pressure. And osmotic or oncotic is due to protein. It's always inward. And normally, they are equal and opposite. So, whatever coming out is going back. There is no fluid, no edema. This is normal. Starling's Law. I guess, um, like you all have, have read this thing in the physiology. Okay? So, can we go ahead?

Okay, yes. So, this is the two types of the pressure. Now, you tell me, because of the last step, the second step was vasodilation, which pressure will increase? Is it hydrostatic or oncotic? Is it hydrostatic or oncotic? Which pressure will increase? Can you please tell me? Which pressure will increase? Common sense. We will say, ma'am, vasodilation means there is more blood, more blood in this section, in the section. More blood, more blood means more water. More water means hydrostatic pressure. The hydrostatic pressure will increase. So, outward is more, inward is less. Outward is more, inward is less. Since outward is more, inward is less, there is an imbalance. The imbalance because of the imbalance, the fluid will come out. The fluid will come out, leading to edema. It will accumulate here and leading to edema. Leading to edema. Say yes. This is step number three. So, step number three, leading to edema, because of the edema, there is swelling. This portion will swell out. This portion will just suppose I am having an injury. Yes, it can be insect bite, Arthur. Yes, it can be any injury, bacteria, virus, insect bite, whatever. So, that portion will swell out. Do you have a mosquito bite anytime? Of course, we all have experienced that. So, we have a swelling, focal swelling at that point. Now, where the mosquito is biting or any insect is biting, the swelling is due to this step. So, the third step is explaining the swelling or the tumor out of the five cardinal features. Yes. So, this is the thing. Can you have you got it? Have you got it?

The fourth step. Till now, we have studied three steps: one, two, three. The one was vasoconstriction, which was transient. The second is vasodilation, which is persistent. Which is persistent. And third is increase hydrostatic pressure. The fourth step. The fourth step. The fourth step is increase vascular permeability. You must ask me, ma'am, what do you mean by vascular permeability? Have you seen a blood vessel? In the blood vessel, these are the endothelial cells. These are the endothelial cells. They are continuous, one behind the other. They are continuous, one behind the other. There is no gap in them. I'm using the word gap. There is no gap. You can see. Okay? But now, the increased vascular permeability means the gaps will be created. The gaps will be created. Creation of gap. Can you see the gaps now? These are the gaps. Creation of gaps is known as increased vascular permeability. You must be thinking, ma'am, by the gaps, you are creating the gaps. I want to take WBC out. Now, what is my ultimate purpose? I want to take this WBC out and make a fight between the bacteria and the WBC. If there is no gap, how the WBC will come out? Ultimately, we have to create the gap, and from that gap, we have to take the WBC out. So, that is creation of gap. The creation of the gap is known as increased vascular permeability. And this step is the hallmark. Out of the 11 steps, this step is the most important. Okay?

Now, the gaps are created. You can see these are the gaps. These are the gaps. The gaps are created. From this gaps, the protein will also leak out. Protein will also leak out. Fluid was already there. Now, protein also leaks out. So, edema will increase. And this edema is exudate. Okay? Let me explain you. You can see here, the first diagram. In the first diagram, see the wall of the blood vessel. See the endothelial cells. They are continuous. There is no gap. I appreciate. There is no gap in the first diagram. And see the two pressure, outward is equal to inward. So, everything was normal. Everything was normal. In the second diagram, you can see the gap is still not there. It's continuous. It's continuous. Okay? There is no gap. Okay? But the outward pressure is more, and inward is less. So, because of the imbalance, only fluid came out. Can you see the fluid is coming out? See the background blue color. I appreciate the background blue color here, which is accumulating. So, only fluid is accumulating. So, this is known as transudate. Transudate contains only fluid. Now, see the third diagram. In the third diagram, this is endothelial cell. This is the endothelial cell. This is endothelial cell. Now, at the junction, you can see the gaps. You can see the gaps at the junction. From this gaps, the protein is going out. The protein is also going out. Now, the fluid along with protein is known as exudate. Initially, only fluid was there. So, there are two types of edema. What are the two types of edema? Transudate and exudate. Transudate contains only fluid. Exudate contains fluid plus protein. So, here, among the six steps, or five steps, I am telling you the third step, that is increase hydrostatic pressure, leading to transudate. And the fourth step, increase vascular permeability, leading to exudate. That is my point to explain you both of them, leading to edema. Both of them causing the swelling. So, initially, the swelling contains only fluid. After that, the swelling contains fluid with the protein. That is pus formation. Say yes. So, you got my point? You got my point? That is the thing. So, transudate followed by exudate. The reason for the transudate is increase hydrostatic pressure. The reason for exudate, increase vascular permeability. Say yes. You got it? Everyone?

So, let's revise the fourth step. Till now, we have studied the fourth step. Then I will come on the fifth one. Can you please tell me the four steps? Anyone from the audience? Anyone from the audience? Can you tell me the four steps, please? I am teaching you the vascular, vascular steps. The first step is the vasoconstriction. The second is the vasodilation. The vasoconstriction is transient. The vasodilation is the persistent. Okay? The third is increase hydrostatic pressure. The fourth is increased vascular permeability. Increased vascular permeability is the hallmark step. Increase hydrostatic pressure leads to edema. Increase vascular permeability also leads to edema. But increase hydrostatic pressure, only fluid came out. That's why edema's transudate in nature. And increase vascular permeability, along with fluid, protein also came out. That's why edema's exudate in nature. So, till now, I taught you this. Anyone having any confusion in that? Anyone having any confusion in that? Can we go ahead to the last step?

Okay, don't go in the mechanisms. There are five mechanisms of creating the gaps. You must know the name, but don't go in the detail. The five mechanisms of creating the gaps. We can skip of creating the gaps. Okay? And, yeah, the last and the fifth step is the slowing, the slowing, like stasis of the blood. Now, the fluid also came out, the protein also came out. So, what remains now in the lumen of the blood vessel, in this section, only cells are present. So, there is stasis of blood. So, the fifth and the last step is the stasis. We are done with five vascular steps. Yes, everyone? Yes? You all are genius. Good. Great. And very happy. Good, good, everyone. Everyone. Yes. Okay. So, namin, you have, you have a trouble in understanding exudate? Can I repeat? You got it? Or you are asking? So, there are two types of edema. I mean, there are two types of edema. There is transudate and there is exudate. Okay? In transudate, only fluid comes out of the wall of the blood vessel. And in exudate, along with the fluid, protein also comes out. This also leads to edema. This also relates to edema. But this is a watery edema. Only fluid is there. And this is pus, thick, along with the fluid, it contains protein and cell also. It looks like pus, white, thick pus. So, that is the two types of the edema, right? So, whenever the wall of the blood vessel is continuous, now it's like this, so only fluid can come out. Only fluid can come out. But whenever the gaps are present in the wall of the blood vessel, along with the fluid, protein also comes out. So, whenever there is increased hydrostatic pressure, it's only fluid coming out. But whenever there is increased vascular permeability, the protein also comes out. You got it? I hope you got it now, right?

Okay, so stasis. There is nothing to understand in stasis. Stasis is just, you know, the fluid and the protein is already leaked. Whatever remaining is the stasis. So, that's the stasis. There is nothing to learn in stasis. So, the fight, the five, you should learn the vasoconstriction, which is transient. Vasodilation, which is persistent. Increase hydrostatic pressure. Increase vascular permeability. And stasis. Please learn. And among them, the hallmark feature is the increase vascular permeability. And you know the consequences of each of them. Yes. Give me a thumbs up. You got it? Can we go ahead?

So, we will solve some questions on these five. And then I will command the six cellular events. In this way, all 11 will be done. So, please solve some MCQs. The first question is in front of you. Can you give the answer, please? Can you tell me the sequence of the events in acute inflammation? I told you the vascular events. You can read the four options. I told you the five events. Can you tell me the sequence? Is it vasodilation followed by stasis followed by transient vasoconstriction or permeability? Read the four options. I'm not reading the four options. Please read the four options and tell me the correct sequence of the vascular events of acute inflammation. Who will tell me the correct sequence, please? What is the correct sequence of vascular events in acute inflammation? Yes. What is the correct sequence, please? Yes. Very good. Very good. No matter, it's not C. Read again. Read again. Others, you all are right. Correct answer is D. The first is vasoconstriction, followed by vasodilation. Increase hydrostatic pressure is not given the third. The fourth is increased vascular permeability. And then last one is the stasis. So, out of the five, four are given. But you have to arrange them in a sequence, right? It is a very commonly asked PYQ. Okay?

The next question is in front of you. Can you tell me the first step in acute inflammation? The first is it vasodilation or construction? Is it increased vascular permeability or decreased vascular permeability? The first step. The first step. Yes. Hydrostatic is missing, Mohit, right? What's the first step? Yes. You all are right. I guess the question is very easy. The first step is vasoconstriction. Although it's transient, but don't miss it. Although it's transient and only for few seconds, only for few minutes, but please don't miss it. Although it's transient, but don't miss it. So, correct answer here is B. Yes, everyone is right. You all are right.

So, going to the next question. All of the following vascular changes are observed in acute inflammation except. In your question, there are many questions having the word "except". Don't miss the word "except". What are the four options which do not take place in acute inflammation? Vasodilation takes place? Yes or no? Stasis takes place? Yes or no? Increase vascular permeability takes place? Yes or no? Decreased hydrostatic pressure takes place? Yes or no? So, tell me what is the correct answer? What is the correct answer here? Yes. Yes. You all are. Osama, absolutely right. And everyone else is also right. The correct answer here is D, because it's not decreased hydrostatic pressure, it's increased hydrostatic pressure. And rest all the three options are right. You all are right. So, correct answer here is D. We are done with vascular events. Coming on the cellular events, very quickly. Can I start the cellular events? Yes. We should start quickly.

Now, the cellular events of, uh, acute inflammation. So, till now, tell me the summary. First, tell me the summary of these five vascular events. We have done the five vascular events: vasoconstriction, vasodilation, increase hydrostatic pressure, increase vascular permeability, and stasis. What is the summary? The last summary diagram is this. Till now, what we have done in the vascular events of acute inflammation? We have created a gap. We have already created a gap. Now, it's time to take WBC out of that gap. You will see them. Take it out. Now, why you require six steps? It is not that easy. We require six steps to take WBC out, right? These six events are cellular events in which the cell will come out. The cell is the WBC, the Army. You know, this is the terrorist. You can see the microbe is the terrorist. It's still present. And the Army is still inside. But we are, you know, arranging, arranging a channel, arranging a, yeah, a promise. We will take the Army out and take it towards the terrorist and let them fight. We will do the phagocytosis by the Army to the terrorist, right? So, this is ultimately what we want. So, we have already created a gap. We have already created a gap. But now we want to take WBC out of that gap. That is cellular events. So, what is the problem? Have you read Bernoulli's Theorem when you were a kid? I mean, in physics, in your sixth, seventh, eighth standard? Bernoulli's Theorem. What is Bernoulli's Theorem? So, this is a pipe, you know, a luminated pipe. Whenever fluid travels in a pipe, the heavy portion travels at the center, and the light portion travels at the periphery. This is the statement of Bernoulli's Theorem. Let's apply Bernoulli's Theorem on a blood vessel. Blood vessel is also a luminated pipe now, right? In which we are having four things: we are having RBC, WBC, platelet, and, uh, the plasma. So, which is the heaviest one? The heaviest will travel at the center. I told you now, the heaviest is the WBC. The WBC travels at the center. And after that, there is RBC. So, this is all RBC. Surrounding the WBC, there is RBC. Okay? After that, there is platelet. So, surrounding that, there is platelet. And most lightest one, the lightest one is the plasma. So, this is the plasma, the lightest one, presented the plasma at the most periphery. Now, there is a gap. Imagine this is my gap, right? I want to take WBC out. I do not want to take RBC and platelet and plasma out. I want to take WBC, which is present at the center. So, how can I take it directly from the gap? It is present at the center. Now, first, I have to take it at the periphery. Then only I can take it out. It was a fun when it, it was very easy when the WBC already presented the periphery. But it is not the case in all of our blood. The WBC present in the center. So, during inflammation, we have to take it to the periphery so that we can take it out of the gap. You got my point? Normally, when the WBC travels at the center, right? It is known as axial blood flow. Axial blood flow. So, basically, we want to convert axial to reverse axial. Axial to reverse axial, in which we want to take the WBC from the center to the periphery. Say yes. So, this is the thing.

So, let me tell you the six steps now. So, this is the summary. These are the six steps. See here, everyone here on the screen. Can you see this is a WBC? I'm drawing this one. See, this is the WBC present at the center. Say yes, right? The first step, taking the WBC from the center to the periphery. This is known as margination. Margin. You are taking the WBC from the center to the margin. That's why known as margination. Okay? Margination also known as pavementation. After that, where is the gap? This is my gap. So, gap is not immediate. Gap is not immediate. We have to take it a distance. It is so, WBC have to travel that distance to reach the gap. Okay? So, for that, WBC will do rolling. You know, WBC is rolling like a tire on a road, like a tire on a road. Who's the tire? WBC. Who's the road? It is the endothelial lining. Say yes. It's very important to understand. So, here, you can see the tire is the WBC, and the road is the endothelial lining. So, the tire is rolling on a road, road, road. This step is known as rolling. So, the second step is the rolling. After that, just before the gap, it stops. Stoppage is known as adhesion. The third step is adhesion. First margination, then rolling, then adhesion. It stopped. After that, it comes out. Ultimately, WBC comes from intravascular space to extravascular space. Ultimately, it's known as transmigration. What is it known as? It's known as transmigration. In which WBC comes from intravascular space to extravascular space. It's transmigration. Okay? Transmigration also known as diapedesis. That diapedesis is very important step. Yes. It's diapedesis. It's coming out. Okay?

Now, WBC don't have eyes. Whereas the bacteria, it's a three-dimensional space. In the three-dimensional space, how does WBC recognize that bacteria is in this direction? And in a three-dimensional space, I have to move this, not there, not there. WBC don't have eyes to see where is the bacteria or here is the bacteria. I have to move here, not here. So, it is due to the chemical. How does it takes place? The bacteria secrete some chemical, and that chemical attracts the WBC. So, this step is known as chemotaxis. Chemo means chemical. Axis means chemical oriented movement. So, WBC will move towards the chemical. That is the fifth step. And lastly, you can see WBC is phagocytosing the bacteria. The last, phagocytosis. Enumerate the six steps, please. What are the six steps? Can you tell me the same six steps from a book diagram? You can see this is my sketch diagram. Okay? You can see that WBC at the center. WBC leave the center and come at the periphery, margination. After that, rolling, rolling, rolling. Just before the gap, it stops, that is known as adhesion. After that, it is coming out, that is transmigration or diapedesis. Diapedesis. Okay? After that, it moves towards the bacteria because of chemical, it's chemotaxis. In the end, it will perform phagocytosis. It will perform phagocytosis. Absolutely right. Absolutely right, Naveen, Osama. Very good. Very good.

So, these are the six steps. Among them, I will, no margination. You already got it. To convert the axial blood flow into reverse axial. Please learn this definition. The definition of margination. Now, I will explain you how does rolling, adhesion, and transmigration and chemotaxis takes place. The details of them. So, let me take the rolling, adhesion, and transmigration together. How does it takes place? How does rolling takes place? How does adhesion? How does? So, can you see for rolling, it's rolling on the surface of the wall of the blood vessel. So, with the help of the receptors, everything in pathology is like receptors. It's like receptors. So, can you see here? The receptors are present on the surface of the WBC. The corresponding, I am using the word corresponding, the corresponding receptors are present on the, on the wall of the blood vessel. So, because of which interaction of these receptors, the rolling takes place. So, the receptors are present on the surface of the WBC. The corresponding receptors are present on the wall of the blood vessel. So, the receptor between the road and the, and that, you know, this is a road, and this is a tire. So, because of the receptors, the bond is formed. It's very transient. It breaks, then it moves, then again the bond is formed, then again it breaks, then again the bond is formed. In this way, the rolling takes place. And for adhesion, the bonds are formed. It stops, right? So, tell me the name of the corresponding. Tell me the name of the corresponding receptors. It is known as complementary adhesion molecules, CAMs. Complementary adhesion molecules. There are six pairs. You have to learn the six pairs. And these are pairs. You cannot change. No, these are pairs. Exactly. So, you have to learn which member present on the road, which member present on the tire. This is road. I always call endothelium as a road. I always call WBC as a tire. So, you will have a better imagination. What is road? What is tire? So, what is present on the road? Correspondingly, what is present on the tire? And what is the pair? What is the pair? You have to learn it. So, don't worry. I'm having a super simplified diagram for you. Super duper simplified. Nowhere it is given else in the world. In none of the book, this diagram is given. It is, I have drawn this diagram for you. Right? You have to understand the six pairs. The six pairs are drawn in front of you. I will write their names in front of you to make the pair. You have to learn the pairs. So, this is a diagram of complementary adhesion molecules, the CAMs. Okay? These pairs. You can see this is tire, uh, the WBC. Okay? This is WBC. You can see this is road, the endothelial lining, the road. Now, I appreciate the receptors, corresponding receptors between them. Let's write. Let's write. Okay? So, the first is the P and E selectin. First pair. Okay? Let me write. This is P selectin present on the tire. And this is E selectin again present on the tire. I mean, on WBC. They form bond. What is present on the road? On the endothelium, P and E is selectin. They form bond with Sialyl Lewis X. Both of them form bond with Sialyl. So, first pair is P selectin with Sialyl Lewis X. The second pair is E selectin with Sialyl Lewis X. You have to learn the name of the pairs. I'm sorry, but you have to learn. I'm trying to simplify it. Okay? The third selectin. P and E selectin present on the, I'm sorry, I'm sorry, I'm sorry. Let me erase it. I have done reverse. By mistake. Uh, how to erase it? Okay. We'll try. Done. Okay. Okay. So, we will try again. Okay. I'm sorry. It was my mistake. So, here, P is selectin and E selectin is present. I mean, to say, P selectin and E selectin is present here. They form bond with Sialyl. You cannot reverse it. They form bond with Sialyl Lewis X only. But the P and E selectin present on the endothelium, and Sialyl Lewis is present on the WBC. The third selectin is L selectin. Present on the WBC. Alpha leukocyte. Leukocyte, WBC. So, L selectin present on the leukocyte. Okay? It forms bonds with GlyCAM. It forms bonds with GlyCAM. It forms bonds with Integrins. It forms bonds with Integrins. So, this is beta 2 integrin. This is beta 1 integrin. Please learn it. I know it's difficult. I know. But you have to learn the five pairs. So, the first pair is in front of you: P selectin with Sialyl Lewis X. The second is E selectin with Sialyl Lewis X. The third selectin is L selectin. It is present on WBC. It forms bonds with GlyCAM. It forms bonds with Integrins. So, this is beta 2 integrin. This is beta 1 integrin. So, learn the pairs. It's not very tough. I tried. Okay? You can see. And the last, how does diapedesis takes place? WBC don't have isq. There is a gap. Just fall down. It doesn't happens like this. Just fall down and go out. No, it's not like that. Again, it is with the help of receptors only. So, what is the receptor for diapedesis? So, you can see these are the receptors. Only one receptor which is present on both, which is present on WBC also, which is present on endothelium also, the road also, the tire also. So, the name of that receptor is PECAM. You're also here also. It's PECAM. Known as CD31. PECAM. It's the only receptor which is common in the road and the tire. And that leads to transmigration or diapedesis. Ultra important MCQ. Say yes, if you got it.

So, can you try the pairs? Can we write it? Can you help me? Tell me what is present on the road? Tell me what is present on the tire? Tell me the pairs. Can you please help me try it out? At least try it out. The first pair is P selectin and E selectin. Okay? P and E selectin. So, P and E selectin, they form bond with Sialyl Lewis X. Sialyl Lewis X. The third selectin is L selectin. It is present on WBC. It forms bonds with GlyCAM. It forms bonds with Integrins. So, this is beta 2 integrin. This is beta 1 integrin. So, learn the pairs. It's not very tough. I tried. Okay? You can see. And the last, ultra important, super duper important pair, you cannot afford missing, is also PECAM. Also known as CD31. Learn other name also. And this one is responsible for transmigration or diapedesis. So, say yes. Say yes.

Now, learn the first pair is responsible. First and third is responsible for rolling. Fourth is responsible. Fourth and fifth for adhesion. But the second pair is responsible for both. Second pair, that is E selectin and Sialyl Lewis X, responsible for both rolling as well as adhesion. And the last one, we all know, is for diapedesis. So, this is the thing. Can you see here? Here also, you can see the first. Let me write. The first and the third responsible for rolling. Rolling. The fourth and the fifth responsible for adhesion. Adhesion. And the second pair responsible for rolling and adhesion. It's a PYQ. Okay? And the last one, PECAM with PECAM, it is responsible for transmigration or diapedesis. You get many MCQs on this. No one will teach you this complicated topic with such simplicity. You can see in front of you. You can appreciate the pairs. Give me a thumbs up.

So, the next is the chemotaxis. I told you the bacteria. This is the bacteria. It is secreting the chemicals. It is secreting the chemicals, and chemicals is attracting the bacteria. Attracting the WBC. So, this WBC travels towards the bacteria because of the chemical. It is known as chemotaxis. Which is a unidirectional motion. Unidirectional chemical oriented motion. Say unidirectional motion or movement because of the chemical gradient. Okay? Name the chemical. Name the four chemicals. What are the four chemicals here? Can you name them? One is leukotriene. One is interleukin. And two are complement. Learn the numbers. Leukotriene is B4. Okay? Interleukin is 8. Okay? And the two complement are C3a and C5a. The four chemicals, please learn. So, these are the chemicals. The four chemicals secreted by the bacteria that attracts the WBC. So, that WBC moves towards the bacteria. And a three-dimensional space. Do not go anywhere else. B4, interleukin 8, complement C3a, complement C5a. Say yes. Okay? So, can you see these are the four, uh, chemicals? So, you have among them, C5a is most potent. C5a is most potential. There are multiple time PYQs on that. We are done with all. And lastly, there is phagocytosis. So, we are done with cellular events also. Congratulations. We are done with acute inflammation.

So, do you want to solve some MCQs? Or shall I skip this MCQs? Or you want to solve it? Okay. So, the first question is in front of you. Can you please give me the answer? What's the correct sequence in exposition of the WBC? Tell me the sequence for, uh, cellular events. I told you the six cellular events. Now, arrange them in a sequence. Can you please arrange them in a sequence for me? You know the six events. Read the four options. If you know the sequence, you can tell me. Yes. What is the correct answer? Okay. So, is it margination followed by rolling, adhesion, or transmigration? Or transmigration followed by margination, rolling, adhesion? We can read the options and tell me what is the correct answer. Yes. Absolutely right. Absolutely right. The correct answer here is A. So, it's margination followed by rolling, followed by adhesion, followed by transmigration. Chemotaxis and phagocytosis is not given here. The next two. So, out of the six, four are given. Yes, you all are right. The correct answer is A. The next question is, most important for diapedesis. What is diapedesis? The transmigration. Tell me the receptor responsible for that. Is it PECAM? Is it one of the selectin? Is it integrin? Or is it mucin-like glycoprotein? What is the correct answer? What is the correct answer, please? Yes. Yes. Margination and pavementation is same, Metroid. It's same. Yes. You all are right. The correct answer here is PECAM. Ultra important question. PECAM. And if I change the question, instead of diapedesis, it's rolling, answer will become selectin. Please selectin. And if I change it to adhesion, answer selectin and integrin, both. So, that's how we can change the question according to, we can change the answer according to the question. So, the next question is in front of you. Chemotaxis is mediated by. I told you the chemicals for the chemotaxis. Now, I told you one leukotriene, one interleukin, and two complement. You have to learn the numbers. And you have to match it here. Is it histamine? Is it leukotriene B4 and C5a? Is it leukotriene C4 and C3a? Or bradykinin? If you know the numbers, you can answer it very correctly and very easily. So, let me help you. Let me help you. So, leukotriene is B4. Interleukin is 8. And the two chemicals are C3a and C5a. Now, match it correctly. Match it correctly. Among the options, leukotriene B4 is given. And C5a is also given. If you see the option number C, C3a is correct, but leukotriene C4 is not there. So, yes, you all are right. The correct answer here is B. Very, very good. Excellent. Excellent. And most potent among them is C5a. Okay? So, correct answer here is B. We are done with acute inflammation.

The next thing is the chronic inflammation. Another 10 minutes, 10 or 15 minutes, we will be done with chapter two also. Inflammation. I have to teach you five important chapters in general. The two will be done. I mean, the first chapter was important cell adaptation, cell injury, cell death. And inflammation was also important. After that, we will come on hemodynamics. After that, we will come on neoplasia. The next, we will come on genetics. And lastly, we will see something on immunopathology. Right? So, these are the four, five, five, six important topics in general. After that, we have to see hematology related disorders. Okay? So, let's finish chronic inflammation quickly.

So, what is chronic inflammation? Chronic inflammation is a prolonged duration in which inflammation, injury, and attempts to repair takes place simultaneously. Before understanding the chronic inflammation, you have to understand a concept. Let me explain you. You know, where are the blood cells formed in human body? Where does the blood cells formed? The all the blood cells are formed in bone marrow. In the bone marrow, the first cell is always hematopoietic stem cell. This is the first cell. The hematopoietic stem cell. From the hematopoietic stem cell, RBCs are also formed. WBC, platelets are also formed. There are five types of WBC. What are the five types of WBC? Neutrophil, eosinophil, basophil, monocyte, and lymphocyte. I am interested in monocyte because I am teaching you chronic inflammation. Now, I am interested in monocyte. So, from the hematopoietic stem cell, monoblasts are formed. Monoblasts. And this is the blood vessel. From the monoblast, monocytes are formed. So, these monocytes will come in the blood. So, in the, in the bone marrow, these are known as monoblast. In the blood vessel, these are known as monocyte. Right? After that, once the monocyte comes out of the blood vessel, in the tissue. This is any tissue. Once it comes out of the blood vessel, these are known as macrophages. These are known as macrophages. Macrophages get modified. They get modified. They become, become bigger. Nucleus become bigger. These are known as epithelioid cells. Epithelioid cells are nothing. They are modified macrophages. Epithelioid cells are the modified macrophages. Okay? And multiple epithelioid cells fuse with each other, and they form giant cells. They form giant cells. To learn the sequence, I mean to say, so they all are same, one behind the other, they are forming. So, tell me the sequence. The first cell is monoblast in the bone marrow. It gave rise to monocyte in the blood. Monocyte in the tissue is known as macrophage. Macrophage become modified, known as epithelioid cell. And epithelioid cell fuses with each other and they form the giant cell. Give me a thumbs up if you want it. So, the same thing is seen here. Monoblast giving rise to monocyte, giving rise to macrophage, giving rise to activated macrophage, known as epithelioid cell. You can see. And epithelioid cell fuses with each other and form the giant cell. The same thing. You can see the bone marrow, hematopoietic stem cell, monoblast. This is monocyte. This is epithelioid cell. Same thing is changed.

Let's start chronic inflammation. Are you people with me? Can I tell you the steps of chronic inflammation? Acute inflammation have 11 steps. The five.

Vascular and six cellular chronic division have only three steps. It's small; it's not as big as acute inflammation. So, the chronic inflammation has only three steps.

The chronic inflammation is also known as granulomatous inflammation because, uh, because, uh, it is, uh, here the granulomas are formed. I will send you the notes now after the session. Yes, definitely after the session, I will send the notes on the group, on the Telegram group of the Pro CM. You will get it, okay?

The granulomatous inflammation, also known as chronic inflammation, here granulomas are formed. The Anderson is granuloma; it's Type 4 hypersensitivity reaction. I will draw all the three steps in one diagram. Everyone, here on the screen, see the diagram. This is the antigen entering the human body. The specialty of this antigen is it's non-digestible. It is non-degradable, like the TB bacteria, like the talcum powder, right? They are non-degradable antigens. Once they enter the human body, the first cell they interact with is the antigen-presenting cell. The antigen-presenting cell engulfs the antigen, tries to degrade it, but is unable to degrade it because the antigen is non-degradable.

So, what does the antigen-presenting cell do? This antigen-presenting cell will take the antigen to the T lymphocyte, the helper T lymphocyte, helper TH1 lymphocyte to be specific and precise. Helper TH1 lymphocyte will get activated. The helper TH1 lymphocyte, on activating, will secrete three cytokines. On the tip of your tongue, the three cytokines. There, it will secrete three cytokines that will lead to the formation of granuloma. The first is interferon gamma. Please learn it. The first is interferon gamma. Please learn each. Interferon gamma, the second is TNF alpha, okay? And the third is interleukin, interleukin one and two. Multiple interleukins are there, right?

What do the three cytokines do now? See, this is a blood vessel. From the blood vessel, they will take one, one cell out of the blood vessel. Let me tell you the name of the cell, okay? So, let's talk about interferon gamma. Interferon gamma takes the monocyte out. Let's take the monocyte out. Monocytes, after coming out, they convert into macrophages, okay? So, basically, it causes accumulation of the macrophages. And not only this, it modifies the macrophages, and the macrophages convert into epithelioid cells. Epithelioid cells. Not only this, epithelioid cells fuse with each other and it leads to the formation of giant cells. So, macrophage, epithelioid cell, giant cell are all due to interferon gamma. Interferon gamma, okay?

Coming on the next, the next, TNF alpha. What does it do? TNF alpha takes the fibroblast. Fibroblast out. Fibroblast out. And fibroblast will do the collagen formation or fibrosis. And last one, the interleukins. Interleukin. Now, interleukins, they will take the T lymphocyte out. T lymphocyte out. So, they will cause the proliferation of the T lymphocyte. Now, at last, we have three types of cells. What are the three types of cells due to the three types of cytokines? Can you tell me what are the three types of cells with the three types of cytokines? Please. We have epithelioid cells and giant cells because of interferon gamma. We have fibroblast because of TNF alpha. We have T lymphocyte because of interleukin one and two. Please learn which, which cytokine is leading to which type of cell.

Now, these cells will arrange themselves. This one, this will form the center. This will form the middle zone, and this will form the outermost zone. And this is known as granuloma. On the next page, I will draw a granuloma for you. You got it? Let me draw a granuloma. In the granuloma, in the center, epithelioid cells are present, which are slipper-shaped, like this. Epithelioid cells. Some of them fuse with each other and they form the giant cell. Some of them, not all. So, in the center, there is epithelioid cell and giant cell. It is surrounded by T lymphocyte. It is surrounded by T lymphocyte. And outermost, it is surrounded by fibroblast. Outermost, it is surrounded by fibroblasts, like this. And fibroblasts secrete collagen and do the fibrosis. So, most outermost is the fibrosis. This is granuloma. People don't understand what is granuloma. This is the most simplified version of granuloma I have made for you. Say yes.

So, how does a granuloma form? In the granuloma, there are three types of cells. The central epithelioid cells and giant cells are due to interferon gamma. The middle T lymphocytes are due to interleukin one and two. And the outermost fibroblasts are due to TNF alpha. Are you people there, or everyone is gone? Are you still there? Give me a thumbs up if you got it. This is the diagram of a granuloma. The well-structured diagram. How does the granuloma form? This is chronic inflammation, step by step. You have to tell me what is chronic inflammation. Say yes if you got it. Everyone, just a second. Everyone got it. What is inflammation? The chronic inflammation.

Now, there are two types of granuloma. Sometimes, just a second. You can see just a granuloma. There is no necrosis at the center. It is known as a hard tubercle or hard granuloma. Sometimes, at the center, there is caseous necrosis. I told you five types of necrosis. Now, the third type, the caseous necrosis at the center, the cheese-like. It is known as soft granuloma. This is known as soft granuloma. This is how a granuloma is formed. This is chronic inflammation. Can you tell me the steps of the chronic inflammation, please? The first, antigen will come in the human body. The antigen is non-degradable. It will go to APC. APC will try to degrade it but unable to degrade it. APC will take it to TH1 cell, helper TH1 cell. Helper TH1 cell, on stimulation, secrete three cytokines. Name the three cytokines. You cannot miss that. You cannot miss interferon gamma, the most important. Okay? After that, interleukin one and two. Okay? And after that, TNF alpha. After that, TNF alpha. Now, they will take one, one cell from the blood out. The interferon gamma takes the monocyte out and converts them to macrophage, converts them to epithelioid cell, and fuses some of them to form giant cells. Yes. Lymphocytes out. Okay? And I'm sorry, interleukin takes the lymphocyte. And TNF alpha will take the fibroblast out. They will arrange themselves and they form a granuloma. This is the center. This is the middle zone. And this is the outermost zone. Just arrange them. Center, middle, outer. A granuloma is in front of you. Okay? It is as simple as that. Thank you. Thanks for the compliment. It's as simple as that. So, please learn the steps. You know, it should be crystal clear in your mind, step by step. It's Type 4 hypersensitivity. The antigen is poorly digestible. The same thing is shown here. Whatever I have drawn for you, let me show it here also. Can you all see antigen? Yes, it is entering the human body. This cell is APC. APC is capturing it, engulfing it. See, trying to degrade it, but unable to degrade it. So, that's why taking it to the next cell. The next cell is what? It is helper TH1. It is not helper TH2. You will get helper TH2 also in your option. It's helper TH1 cell. On stimulation, it will secrete three types of cytokines. The interferon gamma, TNF alpha. They are taking one, one cell out. And in this way, a granuloma is formed. The granuloma is in front of you. Same thing is written. The antigen is coming. Macrophage, APC is engulfing it, trying to destroy it, but unable to destroy it, fail to digest it. That's why it is taking it to the helper TH1. The helper TH1 will get activated and secrete the three, secrete the three cytokines. The three cytokines will do one, one thing. The interleukins will take the T lymphocyte. Interferon gamma takes the macrophages and converts them into epithelioid cell and giant cell. TNF alpha takes the fibroblast out. They will rearrange themselves, and this is granuloma. Everyone on the screen, this is granuloma. You can see the central purple colored cells. These are epithelioid cells. Some of them fuse and form the giant cell. The epithelioid cells and the giant cells are due to interferon gamma. I'm repeating again and again. The middle zone, the red colored cells, can you see the middle zone? The red colored cells. These are T lymphocytes. These are due to interleukin one and two. And outermost, you can see the fibroblast, the spindle-shaped fibroblast. These are due to TNF alpha. We are done. We are done. Okay? Let me tell you the types of the giant cells in патологический inflammation also. Okay? How many types of giant cells you know? This is how granuloma is formed. Now you understand what is acute inflammation. In acute inflammation, in chronic inflammation, acute inflammation, chronic inflammation. In acute inflammation, we have 11 events, the five vascular, the six cellular. I guess you know the sequence. In chronic inflammation, we have only three events. Ah, what are the three events? The first event is the engulfment of the antigen by the APC and unable to destroy it. The second is activation of helper TH1 cell. And third is secret, secretion of the three cytokines, which is taking one, one cell out and forming them. That's it. But here we have five vascular and six cellular events. You know the detail. So, this is how acute and chronic inflammation differ from each other. You got it?

Now, let me tell you the types of the giant cells. There are four types of giant cells. Foreign body giant cells, Langhans giant cell, Touton giant cell, it's not Trotter, it's Touton, and giant cells and tumor. Let me explain you all. Giant cells have multiple nuclei. You know, 20 to 100 nuclei in one cell, that is a giant cell. See the foreign body. See, first, the foreign body giant cell. In the foreign body, can you see this is a foreign body? Whereas the nucleus, the nucleus is present haphazardly throughout the cytoplasm. There is no sequence. In foreign body, the nucleus is present haphazardly throughout the cytoplasm. Okay? But in Langhans, the nucleus is not haphazard. It is present at the periphery. It is present at the periphery, forming a two-third ring. A two-third ring. It is known as horse, horse-shoe ring, horse-shoe ring. Or as the nucleus is present at the poles, the North Pole and the South Pole, right? This is known as Langhans. Now, see the difference. The foreign body, the Langhans. Please appreciate the foreign body and the Langhans. In the foreign body, the nuclei are present haphazardly, right? Right? And in the Langhans, the nucleus is present either at the poles or in the form of the horseshoe. Langhans examples are important. TB is a common example of both types. In TB, both types, foreign body as well as Langhans giant cells are seen. It's very important PYQ. Along with TB, in foreign body, the second example you have to learn is sarcoidosis. And along with TB, the second example in Langhans you have to learn is leprosy. It's leprosy. Please learn the examples. The third is the Touton. In Touton, where is the nucleus? Where is the nucleus? The nucleus is present at the center, not at the periphery. The nucleus, multiple nuclei are forming a ring. Multiple nuclei forming a ring. And not only this, in the cytoplasm, you can see the, you can see the vacuoles. The vacuoles in the cytoplasm is very important. It's Touton type. Only one example, xanthoma. See the diagram. You can get an image-based question very frequently. See the definitions, I mean, where is the, what is the arrangement of the nucleus, and see the examples in each of them. Yes, say. So, the three types of the giant cells, the three important types. The first is the foreign body, then Langhans, then Touton. I'm coming on the tumor giant cells also. Okay? These three. First, in the foreign body giant cells, the nucleus is scattered throughout the cytoplasm. Example, uh, you have to learn here is the TB, leprosy, foreign body. The second is the Langhans. I told you reverse, I guess, examples here. In Langhans, the example is TB and sarcoid. Leprosy and sarcoid. I told you reverse, but learn this one. In Langhans, the nucleus is present. The nucleus is present either at the periphery in the form of the horseshoe ring, or they are clustered at the two poles. Right? And you can see here, please appreciate this diagram and this diagram. See where is the nucleus? Haphazard throughout the cell. See where is the nucleus? In the form of the horseshoeing, two-third ring. This is foreign body, and this one is Langhans. Say yes, got it? The third one is the Touton. In Touton, the nucleus is present. You can see a real diagram. They are formed. They are present at the center and they are forming a ring. They are forming a ring. See the cytoplasm is vacuolated. Learn example is xanthoma. Learn the example. Foreign body, Langhans. We will revise. Foreign body, nucleus present haphazard throughout the cytoplasm. Example TB, example leprosy. The second, Langhans, the nucleus is present at the periphery, horseshoeing, or at the poles. Example TB, example sarcoid. Okay? And Touton, the nucleus is present forming a ring. The last one, the last type of the giant cells, sometimes in tumors they are present, but not important at your level, you know. Read Sternberg cell. You know, in Hodgkin's lymphoma, today only I will teach you. It is a type of giant cell. And other tumors also have that. So, we are done with the various types of the giant cells.

Now, there is a special type of granuloma known as stellate granuloma. What do you mean by stellate? The star. The meaning of the stellate is star. The meaning of the stellate is star. Can you see here the granuloma? The shape of the granuloma is looking like a star, you know, how does a star? It's like this. The granuloma is like a star. That's why known as stellate. Very commonly asked PYQ in your exam. Learn the two examples of the stellate granuloma. On the tip of your tongue. Star-shaped granuloma. It is the only granuloma in which the center has the neutrophil. Normally, granuloma don't have neutrophil. You know the three types of the cells. The center has epithelioid cells and giant cells, surrounded by T lymphocyte, and outermost is the fibroblast. But it is an exception where the center has the neutrophils. Example is cat scratch disease and LGB lymphogranuloma. Two to learn the two examples. Cat scratch and LGB. These are the two examples where stellate-shaped granulomas are seen.

Lastly, before ending this chapter, let me tell you the examples. How many examples of granuloma you know? Can you tell me? Millions? Anyone? Anyone? I cannot read the names. Anyone? Can you tell me how many examples of granuloma you know? Examples, just examples. I know every one of you will guess more examples. How many examples you know? I want you to tell me at least 18, 20 examples, right? How many of you know? Okay, let me tell you. There are eight bacterial causes. Can you see the eight bacterial causes of granuloma? There are four fungal. Eight plus four, twelve. And there is one parasitic, thirteen. And there are four miscellaneous, fourteen, fifteen, sixteen, seventeen, eighteen causes of granuloma. Eighteen. Sarcoid is right. TB, everyone knows. Shalini, apart from that, I am asking. Okay, let me tell you. Learn the eight causes of the bacteria. One is TB, that everyone knows. TB is a granuloma. Granulomatous disease. Leprosy. Syphilis. You should learn also, right? Granuloma inguinale. Brucella. Cat scratch. My cat scratch disease. And glanders. Learn the eight. TB, leprosy, syphilis, granuloma inguinale, brucella, cat scratch, tularemia, and glanders. If you don't learn it's also okay, but have a look on the examples so that in MCQ, you can pick it up. These are the eight bacteria. Learn the causative organism also. TB is caused by Mycobacterium TB. Leprosy is caused by Mycobacterium leprae. So, these are the eight bacterial causes. There are four fungal causes. One is actinomycosis, blastomycosis, cryptococcosis, coccidioidomycosis, right? You know the causative organism. Please learn the fungal causes. Parasitic, maybe only one parasite from granulomas. Only one. Schistosoma. Schistosomiasis. Okay? The Schistosoma is the parasite. And in miscellaneous, there is sarcoid, Crohn's disease, silicosis, foreign body granuloma. So, please, these are the examples. Yes. In malaria, there is drug granuloma. Absolutely right. It is also a specialized form of granuloma in which plasmodium calcifies, forming the granuloma. The granulomas filled with the parasite. Plasmodium. Durex granuloma. Very good. So, we are done with chronic inflammation also. We will solve some MCQs and pack this chapter also.

So, the first question is in front of you. Can anyone try? The first question is in front of you. Can you try, please? What's the correct answer? The macrophages are converted to epithelioid cells by which cytokine? By which cytokine? Is it interleukin 2? Is it interferon gamma? Is it TNF alpha? And is it TGF beta? What is the correct answer? So, I told you, macrophages are converted into a specialized epithelioid cell by which cytokine? And then the same cytokine, um, causes the fusion of multiple epithelioid cells and converts them to giant cells. Yes, absolutely right, Nikhil. Everyone else is also right. No, no, no. Answer is not C. What is the correct answer? Yes, the answer is B, not C. It's interferon gamma, which converts the macrophages to epithelioid cells. Interferon gamma. Interferon gamma. Some of you are saying TNF alpha. No, TNF alpha is responsible for the fibroblasts. Interferon gamma is there.

The next question is in front of you. The epithelioid cells and multinucleated giant cells, these are giant cells of granulomatous inflammation, are derived from basophil or eosinophil or T lymphocyte or monocyte macrophage. So, what does, what does epithelioid cells and multinucleated giant cells are derived from? Have you understood the question? I have told you the entire sequence now. What is the correct answer here? What is the correct answer? Is it? So, the epithelioid cells and multinucleated giant cells are derived from which cells? From the blood, which cells is coming out and converted into epithelioid cells and multinucleated giant cells? Yes, you all are right. The correct answer here is D. I told you the sequence. In the bone marrow, it's monoblast. Once it goes in the blood, it is known as monocyte. Once it comes out of the blood, it is known as macrophage. Once the macrophage is modified, it is known as epithelioid cell. And epithelioid cells fuse with each other and are known as giant cell. So, in the question, they are asking for epithelioid and giant cells. So, basically, they are derived from monocyte and macrophage. You all are right. The correct answer here is D.

Okay, the next question is not a characteristic feature of granuloma. Not, tell me one feature which is not characteristic of granuloma. What is the correct answer? Is it chronic inflammatory infiltrate? Is it epithelioid cell? Is it giant cell? Or is it PMN with fibrinoid necrosis at the center? PMN means neutrophil. What is not seen in granuloma? Tell me, which thing is not seen in granuloma? Very easy question. If you know the composition of granuloma, you can answer it very easily. Which thing is not seen in granuloma? Yes, yes, you all are right. The correct answer is never contain neutrophil. No, it's not contained. Epithelioid cells are present. Giant cells are present. Chronic inflammation is there. But neutrophils are not present. And it's not fibrinoid necrosis. It's caseous necrosis. Both the things are wrong. And PMN is seen only in one type of granuloma, stellate granuloma. That is an exception. That is an exception. Answer is not B. Caseous. Answer is D. Epithelioid cells are present. Now, they are asking, not a characteristic feature. So, PMN are not present, right?

The next question is in front of you. Seen in which two diseases? I told you the two examples. What is the correct answer here? Yes, star-shaped granuloma. Beautiful granuloma. The exception of granuloma where the center contains the neutrophil. What is the correct answer? Yes, you all are right. The correct answer here is the cat scratch disease. The correct answer here is the cat scratch disease.

We are done with inflammation also. Till now, we are done with two chapters. The third chapter, hemodynamic, we will start after a break. So, let's take a break. Let's say currently it's 11:30. Now, so we will start again at 11:50. Let's take a 20-minute break. Let's take a 20-minute break. Okay? 30 to 40, 40 to 50. It's 11:50. Please everyone back. I'm not ending the session. The session is on. I only. I will mute and, you know, the camera will be off. The same link you have to join. In this link only, we will be back at 11:50. Okay? If you got it, give me a thumbs up. Everyone, give me a thumbs up. So, we are taking a break just for 20 minutes. Appreciate it. Give me a thumbs up. 11:50, I will be back here and we will start with hemodynamics, followed by neoplasia, followed by genetics and immunopathology. So, uh, before lunch, we will finish the general. We will take a lunch break for 30 minutes or 45 minutes. After that, in the evening, I mean, after two o'clock, we will be taking the hematology. So, hematology, I will teach you few anemias and leukemias, okay? Thank you. Hello everyone. I'm alive. I'm a visible. I'm audible. Give me a minute to confirm if I'm clearly visible, audible. I will start the session. You can write in the chat box. I can see your chat. We will wait for a few seconds. I'm just waiting for the confirmation if I'm clearly visible, audible. I will start the session. I guess there is a little bit lag. Okay, can you write down in the chat box if I'm clearly visible, audible? Okay, okay, okay. Thank you. Thank you for confirming. Give me a minute. Okay, I guess yes, it's working now. Okay, so let's continue the session and welcome for this, uh, session. Uh, so after the break, let's continue the session. Let's start with hemodynamic disorders. Okay? In the first session, we have already completed the general pathology, cell adaptation, cell injury, cell death, acute inflammation, chronic inflammation. Now, I am starting with hemodynamic disorders. Here, basically, I would like to discuss four disorders. I would, I would like to discuss edema, thrombosis, embolism, and shock in detail. And after that, we will move on to the next chapter quickly, okay? So, let's start with hemodynamic disorder. Let's start with edema. What is edema? How will you define edema? Does anyone know what is edema? What is edema? So, in Hindi, if you say edema, in layman language, it's swelling. Swelling on any portion of the body. Swelling, you know, that is the edema. You know, human body is made up of cells, from head to toe. We all are made up of cells. All our organs are made up of cells. The cells are like this in the organ. The space between the cells is known as interstitial space. Can you see the space? The space between the cells is known as interstitial space. Can you see the space? Yes, it's interstitial space. It is all interstitial space. Normally, interstitial space is dry. There is no fluid in that. But if fluid accumulates in the interstitial space, it gives rise to edema. Can you see here? It's edema. Edema is the accumulation of the fluid, abnormal and excessive accumulation of the fluid involved in interstitial space. But students have trouble in understanding what is interstitial space. Interstitial space is the space between the cells. If fluid is accumulating here, the fluid is accumulating, it is known as edema. So, please learn the definition of the edema. There is a related term known as effusion. Effusion and edema are same. The pathophysiology is same. Here also, the fluid gets accumulated. The abnormal and excessive fluid accumulation is there. But where? Not in the interstitial space, in the body cavities. We know that we have few cavities in our body, like the lungs are surrounded by pleural cavity. You can see the heart is surrounded by pericardial cavity. So, if there is fluid in pleural cavity or pericardial cavity, it is known as effusion. So, can anyone define edema and effusion for me? What is edema and effusion? The pathophysiology of both of them is same. That's why I'm taking the two topics together, edema and effusion. So, what is edema? What is effusion? In both of them, edema and effusion, there is abnormal and excessive, abnormal and excessive accumulation of fluid. Here, in edema, in interstitial space. But in effusion, it is accumulated in the cavities, like pleural cavity, pericardial cavity, whatever cavity. So, edema and effusion, that is the definition. Now, for understanding the pathophysiology of edema and effusion, you have to understand the Starling's law. The normal fluid exchange. Ah, you know, human body, from head to toe, we have cells, we have organs. All the organs receive blood. We all know all the organs receive blood. Why all the organs receive blood? Why blood is required for all the organs? For all the cells? All the tissues? Why? Because of supply of oxygen. Basically, organs do not require blood. Oxygen requires oxygen, or organs require oxygen from the blood, you know. So, let me draw an organ. Imagine this is any organ of the human body. These are the cells of the organ. These are the cells of the organ. This is the blood supply. This is the blood supply. So, this is the pure blood. This is the artery. The pure blood, or oxygenated blood, is coming here. See the arrow. It is coming towards here. Here, exchange takes place, and it converts. This is capillary. And here, it is converted to green in the vein. It is deoxygenated blood. So, how does the oxygenated blood converts into deoxygenated blood? Have you ever thought? Can you tell me how oxygenated blood converts into deoxygenated blood? How does it happen? How does? So, basically, at cellular level, exchange takes place. So, at cellular level, the fluid comes out. Those, the exchange, the oxygen is given to the cell, and carbon dioxide is taken from the cell. So, after the exchange, whatever fluid comes out, the same fluid goes back. And that's why the tissue is dry. There is no edema. The tissue is dry. Only for exchange purpose, the fluid is coming out momentarily. The fluid is coming out, doing the exchange, going back. The fluid is coming out, doing the exchange, going back. So, this happens normally, physiologically, at arterial end, fluid comes out. At venous end, fluid goes back in the capillary. So, basically, you can see a capillary. So, basically, there is a capillary. Let me draw a capillary for you. This is a capillary. So, capillary has two ends. This is the arterial end of the capillary. This is the venous end of the capillary. This is a capillary. So, at arterial end, the oxygenated blood enters. And at venous end, the deoxygenated blood takes out. So, what is happening in between? In between, this is happening. The oxygenated blood comes out, does the exchange, and then at venous end, it goes back. Give me a thumbs up if you got this basic concept. So, this is the fluid exchange. We will talk. So, for this fluid exchange, you have to understand the pressure. How does the pressure acts? Normally, there are two types of pressure. Let me draw a capillary. There are two types of pressures acting. The one is the hydrostatic pressure. The pressure due to water. It's outward. Look at the arrow. It is always outward. It is due to the water. The second is osmotic pressure. It is due to protein. You know, the protein, the albumin present in the blood. It is always inward. Look at the arrow. To learn the basics, hydrostatic pressure is outward. Osmotic pressure is inward. So, learn these two things right now. You can tell me the values of hydrostatic and osmotic pressure at the arterial end and at the venous end. Again, this is a capillary. This is a capillary. This is the arterial end. This is the venous end. Please tell me hydrostatic pressure, osmotic pressure here. And please tell me the values of the hydrostatic pressure and osmotic pressure here. Right? Osmotic pressure is always same. It's always 25, 25 mm. 25 mm. It's throughout. There is no problem in that. There is no change in that. Protein is throughout same. Whatever protein present here, the same protein present here. That's why it's always 25. But see the values of the hydrostatic pressure. At arterial end, the hydrostatic pressure is 38. Because water is more. After that, water will leave, so hydrostatic pressure will fall because water is leaving, right? And it is falling. It is falling up to 12 here. It becomes 12 mm, right? Now, see the change. The change in the hydrostatic pressure. You have to learn the values. Come on. You have to learn the values, right? Hydrostatic is outward. Osmotic is inward. You know the basics, okay? Now, tell me at arterial end, what is the net? Net, which is more? So, you will see my net is 38 minus 25. Can you do the calculations? Yes, it's 13 mm. 13 mm outward or inward? Which is more? 38 is more or 25 is more? Of course, 38 is more. Hydrostatic is more. So, net 13 is outward. So, with 13 mm, fluid goes out. And do the calculation at the venous end. At the venous end, it's 25 minus 12. Again, it's 13. But this time, it's inward. This time, it's inward. So, with the same 13, the fluid comes back. You got my point? So, basically, at high, at arterial end, you can see 38 minus 25, the fluid is going out with 13 mm. Lose the exchange. By exchange, I mean two things. I mean two things. The fluid is giving oxygen to the cell, taking carbon dioxide from the cell. And after all the exchange, at venous end, it is coming back. So, with 13 mm, it is going out. With 13 mm, it is coming back. So, whatever is going out, it is same coming back. So, there is no balance. There is no balance here. That's where the tissue is dry. After that, at the end, the tissue is, the tissue is dry. You got my point? So, at arterial end, the fluid goes out. At venous end, it is coming back. So, the tissue is dry. The tissue is dry. At the end, with 13 mm, the fluid is going out. With the same 13 mm, the fluid is coming in. Give me a thumbs up, everyone. Give me a thumbs up, everyone. Give me a thumbs up. Kindly don't spam. Medical Nepal, please don't spam. Sending the same, same message again and again, okay? So, this is the thing, okay? So, with whatever pressure, the values you have to learn the values, okay? Now, any change in pressure? If the output is more, imagine a condition, outward pressure is more, or inward is less, what will happen? More fluid will come, but less will go. So, what will lead? It will lead to accumulation of the fluid. And accumulation of the fluid is in, is known as edema. The accumulation of the fluid is known as edema, okay? So, hydrostatic pressure is the outward pressure. Osmotic pressure is the inward pressure. So, osmotic pressure is always 25. But hydrostatic pressure at arterial end is 38. At venous end is 12. You have seen the values. You do the calculation at both. Here also, you do the calculation. Answer is 13 mm. Here, the calculation answer is 13 mm. But this 13 is outward. This 13 is inward. So, there is a balance. Whatever goes out, you can see here, with the same pressure, it is coming in. So, tissue is dry. Insist the word dry. There is no edema. There is no edema. When the edema will occur? When, whenever come more and go less, so there is accumulation of the fluid, right? This is very complicated. Is it really means when I, I read it for the first time, now, when I was in second draft, I was really wondering. This is operating in my body constantly. I'm not aware of it. At every moment, whether we are aware or don't aware, this all mechanics is applied in our body in each and every capillary. This is automatically taking place. We don't have to take care of it. We don't have to take care of it. Like, what is my hydrostatic pressure? What is my osmotic pressure? We don't have to take care of it, right? It is taking place automatically, okay? So, that is the hydrostatic pressure, osmotic pressure balances take place. Now, what happens? Even a small change, just suppose instead of 13, it is 14. Just suppose instead of 38, maybe 12. So, what happens? A little bit accumulation. Who does take care of it? So, God has given a backup. The name of the backup is the lymphatic. The name of the backup is the lymphatic. We all have lymphatics. So, whatever a small amount of fluid is accumulated here, now it is taken away by the lymphatic. At the end, the tissue is dry. We don't have edema. I don't have edema. The healthy human don't have edema because God has given this mechanics inside us. This is the pressures operating at our capillary. That's why we don't have edema. Even a little bit edema is there, that is taken care of by the lymphatic. So, tell me the causes. So, normally, there is a balance between the outward and the inward pressure. Even after the balance, a small amount of the fluid is there, it is taken care of by the lymphatic. If you got it, let me know, okay? Okay, if you got it, let me know, okay? So, this is how normally we don't have edema. This is the reason for that. Now, you tell me the causes of edema. If you have understood this, you can tell me three causes of edema out of five. You can tell me from three from this diagram. Can you tell me? You will see him. I'm the first reason. It can be their outward pressure is more. It can be the reason. I mean, hydrostatic pressure is more. Oncotic pressure is less. Oncotic pressure is less. Inward is less. So, if outward is more, or inward is less, or both of them, it leads to edema. Yes, agree or do not agree? Outward. So, there is accumulation of fluid. So, increase hydrostatic pressure, decrease osmotic pressure, and the third reason is lymphatic obstruction. Lymphatic, if lymphatics get obstructed, this also leads to edema. So, these are the three main reasons of the edema in front of you. If you understand the Starling's law, there is no need to learn. You can yourself tell me the three, three reasons for the edema, okay? So, increase hydrostatic pressure, decrease osmotic pressure, and lymphatic obstruction. These are the three main causes of edema. Learn these three. Increase hydrostatic pressure, decrease oncotic, osmotic pressure, encoding, and osmotic is same, okay? And lymphatic obstruction. The fourth one you have to learn, sodium water retention. I will explain. And fifth is increased vascular permeability. In inflammation, we have seen. I will explain. So, there are five causes of edema, out of which the three can be understood from the Starling's itself, okay? Now, let me give you the causes or examples of each of them. Now, the patient, you are a doctor. Now, of course, you are a doctor. And the patient will come to you. Doctor, I am having swelling. I am having swelling. Now, the cause of the swelling can be anything. Swelling can be any, any part of the body. No, it can be due to increased hydrostatic pressure. It can be due to decreased osmotic pressure. It can be due to lymphatic obstruction. It can be due to sodium and water retention. And it can be due to increased vascular permeability. It can be affecting different organs, different physiology. So, treatment is different. Prognosis is different. So, for patient, it's only swelling. But being a doctor, swelling has all these differentials. So, let me give you the examples of each category. Let me give you the first, increase hydrostatic pressure. Do you know some example of increase hydrostatic pressure edema? There are two examples. The first is the cardiac left heart failure or right heart failure. Let me do right heart failure. Imagine the right ventricle is not pumping. What will happen? Common sense. What will happen? The right ventricle is not pumping. What will happen? The blood will not go ahead in the lungs for the purification. The lungs, the blood will not go ahead. It will go backward. The right ventricle is not pumping. Now, right heart failure. So, blood will go backward. From the backward, from the left, right ventricle, it will go to the right auricle. From the right auricle, it will go to SVC, IVC. From SVC, IVC, it will go to all organs. All organs. Veins. So, more blood, more blood is going because of the backward flow. More blood means more water. More water means more hydrostatic pressure. More hydrostatic pressure. So, all organs will have edema. So, in right heart failure, patients have another, all, this is the reason. This is the reason. So, heart failure can be the reason. Or second, postural edema. Especially seen in the persons who are standing, like traffic policemen and all. So, you can see the person is standing. So, you know, gravity is operating all the time. Newton has given gravity, you know, he discovered gravity, I mean. So, gravity is operating all the time. So, because of the gravity, most of the blood is present in the leg veins. So, out of the five liters of the blood in the body, most of the blood is in the leg veins because of the gravity. More blood means more water. More water means more hydrostatic pressure. So, this person will have edema of the legs and the foot. So, this is known as postural edema. To learn two examples. Cardiac edema and postural edema are due to increased hydrostatic pressure. Give me a thumbs up if you got it. Everything is very conceptual. If you understand now, there is nothing to learn in pathology. Just understand it. It will be forever, you know, and it will be like fun, okay? So, please learn. Please learn the two things. The cardiac edema and the postural edema are due to increased hydrostatic pressure. You have seen this diagram. You can see right heart failure. At the backward pressure, more blood, more water, more hydrostatic pressure, leading to edema. Such edema in all organs is due to heart failure. It's hydrostatic pressure. And edema in the person who is standing. Not only traffic havaldar, only, uh, all the persons whose job is like more and more standing, because of the standing, because of the gravity, more blood is in the leg veins. More blood, more water, more hydrostatic pressure, leading to edema, right?

The second cause of the edema is decrease osmotic pressure. Decrease osmotic pressure means due to decreased protein content. The protein content is less. Decrease osmotic pressure is decreased protein content. Which protein? The main protein here is the albumin. The main protein here is the albumin. And albumin is the main protein, okay? The main protein here is the albumin. Uh, we have albumin also, globulin also. But when, when total protein, what's the normal protein in our blood? Normal protein is six to eight gram per deciliter. You, me, all healthy individuals have this level. If it is below five, it will lead to edema. Please learn the values. If it is below five gram per deciliter, it will lead to edema. Main protein which leads to edema, the decrease is the albumin. Give me the causes. Examples from where the protein comes in the blood, blood vessel. Simple question, simple answer. Do you know from where protein comes in the blood? Osama, Shalini, Kuldeep, Sage, The Pumpkin, anyone? Do you know from where protein comes in the blood? There are two sources. Number one, whatever protein we eat in the diet. Do you eat protein? Of course, the pulses, soya bean, egg, meat, whatever we eat, veg, non-veg, contains protein. So, the protein is absorbed and from the GIT, it is coming. Number one. Number two, liver also synthesizes protein. So, it is coming from the liver. So, here it is coming by absorption. Here it is coming by synthesis, okay? In the blood, it is coming. Thus, protein excreted in the urine via kidney? No. Normal human don't have protein in the urine. Normally, healthy individual don't excreted, don't excreted. Now, there can be three causes for fall of protein in the blood. Either the absorption is less, there is problem in the intestine, like malabsorption. Or the synthesis is less, there is problem in the liver, like cirrhosis and stage disease or cirrhosis. Or absorption is normal, synthesis is normal, but the excretion is more, right? The kidney, kidneys are defective. In the kidney, there is glomerular nephritis or some disease. Nephrotic syndrome is there, leading to more and more excretion. So, there can be three causes. The three causes of decrease oncotic pressure. You know, in malabsorption, patients have edema. In liver cirrhosis, patients have edema. In glomerulonephritis, nephrotic syndrome, patients have edema. But the reason for all these three edema is same, decrease oncotic pressure. Give me a thumbs up if you got it. So, patient will come to you. Doctor, I am having edema. So, you have to look for the albumin level, protein level. If the protein level is low, there can be three organ problems. Problem in the kidney, problem in the liver, or problem in the intestine. So, you have to look for that. For liver, you will do LFT. You will do imaging. For kidney, you will do RFT and imaging. For intestine, you will do endoscopy, you will do biopsy, you can do some imaging, whatever. So, based on that, you will make the diagnosis. You will treat the disease. So, for patient, it's very simple swelling. But being a doctor, there are multiple differentials. You got it? Say yes. So, there are three reasons for decrease, decrease oncotic pressure or decrease protein. Number one, problem in the intestine, decrease absorption, that is malabsorption. There is problem in the synthesis, decrease synthesis, that is liver disease or cirrhosis. Or increased excretion, problem in the kidney, that is nephrotic syndrome. You got it? Everything is conceptual. If you get it.

So, you can see, decrease absorption, decrease synthesis, or increase excretion. The three causes of decrease oncotic pressure leading to edema. Coming on the third, third cause is the lymphatic obstruction. What do you mean by lymphatic obstruction? Can you give me the example when lymphatic obstruction leads to edema? At least give one example. At least give one important example of lymphedema. The edema due to lymphatic obstruction is lymphedema. Why God has given us lymphatics? The lymphatics are the backup. Now, I told you, right? Imagine a lady is coming to you. Doctor, I am having a lump in the breast. A lump in the breast. Okay? So, you are doing the biopsy, and it's a cancer. It's malignant cancer, not benign one. It's malignant. So, what is the treatment? Of course, the treatment is surgery. You will ask the lady to get it operated. It's a malignancy. It can do metastasis. So, in operation, we don't remove only cancer. We remove the auxiliary lymphatics also, right? Because these are the regional lymphatics, and tumor can spread via the lymphatics, you know that. Every teacher, neoplasia also, right? So, we will remove the tumor. We will do the lumpectomy, mastectomy, and we will remove the lymphatics also. It is necessary to prevent the metastasis. But these were not vestigial organs. The lymphatics. God has given the lymphatics as a backup. So, after the surgery, this lady will present like this. Edema of that particular limb, right or left. Edema of that lymph. So, it is the breast surgery with auxiliary lymph node removal. It is the post-surgery morbidity. So, if we don't do it, the patient will have metastasis. And if we are doing it, the patient is having lifelong morbidity. There is the most common example of lymphedema. Number one. Number two, there is a parasite known as Wuchereria bancrofti. The name of the parasite. It's a nematode, okay? What does it do? It blocks the lymphatic. The adult form lives in the lymphatic and you see the worm, the male and the female worm, they are blocking the lymphatic. Once the lymphatics are present, but they are blocked, they are non-functional, it leads to edema of the leg. It is known as elephantiasis. You see the leg is looking like an elephant. That's why known as elephantiasis. Elephantiasis, got it? And third is Milroy's disease. You know, congenital. God has given the de facto lymphatics or absent lymphatics. It is Milroy's disease. To learn the three examples. Removal of the axillary lymph node after breast cancer, obstructing the lymphatics, known as elephantiasis. And number three, Milroy's disease, hereditary lymphedema. You got it? So, these are the three examples. The fourth cause is the sodium water retention. So, you know, sodium, wherever there is a sodium, there is a water. So, due to any reason, either due to renal failure or due to heart failure, there is sodium water retention in the body. And all the pressures are normal. Hydrostatic pressure is normal. Oncotic pressure is normal. Still, the patient can have edema. And this is due to sodium water retention. Okay? And last is increased capillary permeability. Have I told you this diagram in, in inflammation chapter? You can see the blood vessel here. The endothelial lining is continuous, okay? The endothelial lining is continuous. You can see the blood vessel here. You can also see the blood vessel. But here, the endothelium lining is not continuous. There are gaps in between. See the gaps. The gaps are present in between. So, I told you when the endothelial lining is discontinuous and the gaps are present, the gaps are known as increased vascular permeability. When the endothelial lining is continuous, only fluid goes out. But when the gaps are present, along with the fluid, protein also goes out. So, this edema is exudative edema. Basically, it's pus. It's acute edema. It's acute edema, right? So, whenever there is the inflammation, I told you the five vascular events. Now, the fourth event is the increased vascular permeability that leads to acute type of edema. Now, learn two things. The edema can be generalized throughout the body. Throughout the body. It is known as anasarca.

Anasarca throughout the body. Edema, and it can be focal, localized, mosquito bite, or an insect bite. So it can be focal, it can be generalized. So these are the five causes of the edema. Can you please enumerate? Can you please enumerate? Increase hydrostatic pressure, pressure, lymphatic obstruction, sodium retention, and inflammation or increased vascular permeability. Learn the examples. The examples are important. So increase hydrostatic pressure is cardiac failure, right heart failure, leading to edema of all organs, postural edema, and traffic policemen. Okay. Decrease osmotic pressure, three causes: decrease absorption from the intestine, decrease synthesis from the liver, and increase excretion in the kidney. Right. Lymphatic obstruction, again, three examples: after breast surgery, auxiliary lymph node removal, leading to elephantiasis, and Milroy disease. Okay. Sodium retention, heart failure, renal failure, and inflammation. May acute inflammation, basically acute inflammation. Everyone give me a thumbs up. At least I try giving you the causes of the edema. These are the causes as well as pathogenesis of the edema. Yes, yes. Can we go ahead? Can we go ahead? How many types of edemas there? How many of you know the meaning of the transudate, exudate? Diagram is in front of you. See everyone here. Concentrate here on your gadgets. See the lining of the endothelium. It's continuous. It's continuous here. It's continuous. And the pressure is equal. Outward pressure is equal to inward pressure. No edema. See the background is clean. See the background. It's clean. There is no edema. See the second diagram. Here also the lining is continuous. You will see, ma'am, the lining is continuous here also. I cannot see the gap. Yes, the lining is continuous. There is no problem. But see this arrow is thicker than that arrow. So I mean to say the outward pressure is more as compared to inward pressure. Either the outward pressure increases or the inward decreases. So only fluid comes out. Can you see the background? In the background, I appreciate the blue color. Fluid is accumulating in the background. The only fluid is coming out. And this edema is known as transudate edema, which contains only fluid, only fluid. See the third diagram. In the third diagram, this is endothelial cell. This is endothelial cell. This is now you can see the gaps between them. Oh, there are gaps. From these gaps, the protein will come out, the cell will come out, protein and cell. So along with fluid, there is protein and there is cell. This edema is known as exudate edema. The exudate edema. You got it? So transudate edema, can I say transudate is low protein or low cell? So can I say transudate edema's protein poor, cell poor? No protein, no cell. But exudate is protein rich, cell rich, because the gaps are present. Can I say this is non-inflammatory edema? It doesn't occur in inflammation. And this is inflammatory edema. This occurs in inflammation because of increased vascular permeability, the gaps formation. Say yes. So as I told you, here protein is less, cells are less. Specific gravity is also less. Since protein and cells are high, the specific gravity is also high. Okay. And LDH is also low. LDH is also high. So four things are low: protein, cell, specific gravity, and LDH. And all four things are high there. The only thing which is opposite is the pH. Here pH is high, and here pH is low. You have to learn. Okay. So that you have to learn the differences between transudate and exudate. Does anyone have any difficulty in understanding the transudate and exudate? The two types of the edema. Can you please tell me? So your protein is less, cells are less, specific gravity is less, and LDH is less. All the three, four things are more there. Okay. But here pH is more than 7.3. Is it discount? I guess it is connected now. I guess it is connected now. Okay. So increase accumulation of fluid in the interstitial space is known as, is it edema, effusion, transudate, or exudate? What is the correct answer? Please highlight the word interstitial space. Increase accumulation of fluid in the interstitial spaces known as what is edema? Very good. You all are right. Absolutely right. Shalini, what about others? Please answer. It is everyone answer it. The correct answer here is okay. Very good, very good. If I change the question instead of interstitial space, I say the word cavities. What is their answer now? Usama, would you like to change the answer? Dr. Parveen Islam, anyone? Would you like to change the answer now? Yes, in this case, the answer will change. Instead of edema, we will say effusion. I told you the definition is very correctly. The next question, edema occurs when plasma protein level is below what? What's the normal plasma protein in blood? Six to eight gram per deciliter. Six to eight gram per deciliter. When it is below what, it will lead to edema? When it is below what? I told you the value. When it is below five. When it is below five, then it will lead to edema. So correct answer is five. Correct answer is five. Yes. So coming to the next question, all of the following are included in the pathogenesis of edema except. Don't miss the word except. I told you the five causes of edema. Decrease hydrostatic pressure. Is it a cause or does it is not a cause? Decrease osmotic pressure, lymphatic obstruction, and increased vascular permeability. So tell me which is not a cause of edema? Not. I'm asking not. You people are getting confused. You people are getting. Why you are saying C? You are saying C for which option? Easily. Yes, the correct answer is A. It is decrease. It is not never decrease osmotic pressure. The increase, uh, I'm sorry, increase hydrostatic pressure leads to edema, not decrease. So incorrect among them is A. The remaining three are correct. And now decrease osmotic pressure also leads to edema. Lymphatic obstruction also leads to edema. And increased vascular permeability also leads to edema. The correct answer is A. Okay. You're getting confused. I guess the question is about accept. Got it? Can I move ahead? Yes. Moving to the next topic, thrombosis. What is thrombosis? Can I move to the next topic? What is thrombosis? Imagine I have a cut here. What will happen? Of course, I will bleed. Everyone bleeds. Whenever we have injury at any portion of the body, we start bleeding. How long we bleed? We bleed for the next few seconds, same next few minutes. After that, the bleeding stops automatically. Why does the bleeding stop automatically? Because of the clot formation. So here, at the site of the injury, the blood vessel is sealed. There is injury in the blood vessel. It is sealed with the help of a clot. So let me draw a diagram for you. Imagine this is the blood vessel and this is the site of the injury. Okay. Here the endothelial lining is continuous and here it is discontinuous. So this is the site of the injury. This is the site of the injury. You can see, imagine. So here the person is bleeding. Whenever we have injury, so first the platelet will come and form a clot here, the primary clot. The platelet will seal it, stop the bleeding temporarily, and after that it is stabilized by fibrin, by coagulation cascade, the fibrin. So secondary clot is formed. So basically, this site is sealed and patients stop bleeding. You will say, yes, ma'am, we all know that this is known as clotting. This is known as clotting, right? So this is the normal physiological clotting. It is not a disease. It is known as hemostasis. Hemo means blood, bleeding. Stasis means stoppage. Stasis, stasis means stoppage to bleeding. Stoppage whenever we have cut anywhere, we don't think, we see, okay, we just press it for few seconds, it stops automatically because it is a physiological phenomenon given by the God in all human body. It is hemostasis. It is not a disease. It is a useful physiological phenomenon. Tables. Yes, we can understand hemostasis. But how does you are teaching us thrombosis right now? Now, how does thrombus? Thrombosis is related to this? Why you are teaching this here? Because thrombosis is the same as that hemostasis without injury. If the same thing occurs without injury itself, it's a disease. If it occurs after injury, it's physiological, it's useful. But if it occurs with just imagine, I don't have injury anywhere on the body and still inside my blood vessel, small, small clots are formed. They are not known as clots now. They are known as thrombus because they are without injury. They are they are not useful. They are harmful. They are causing obstruction in the flow of the blood. Now, this, this, um, it's this is the blood vessel, artery supplying to some organ now. So this organ can have ischemia because of the obstructed blood flow. So it is harmful to have thrombus. So with injury, it is known as hemostasis, it's physiological, it's useful. Without injury, clotting is known as thrombus, and it's harmful and it's a disease. Say yes if you got it. Yes, I am coming on with children, but you got it. What is thrombus? So thrombus is the clotting without injury. In short, what is thrombus? It's the clotting. Same as the tough clotting like hemostasis, but the glitch here, the glitch to be taken here is without injury. Without it is occurring without injury in an intact blood vessels. Okay. The formation of a blood clot in unruptured blood vessel. And rupture means uninjured. So that is the glitch you have to take here. That is thrombosis. It is the pathological form of intravascular fibrin platelet. Two things are there now in the clot. First, platelet come and they form a clot. Then it is stabilized by a thread like material that is fibrin. So it is also made up of the same thing. It is also made up of the same thing. And it is known known as thrombus. It is known as thrombus. You can see in the intact blood vessel, how does the clot is forming in the intact blood vessel? You can see these are the platelet. You can see these are the RBCs. These are the platelet and the thread like material. And you see the thread like material, it is fibrin. So this is the thrombus. This is a thrombus. So the same thing is written. Hemostasis, thrombosis. Hemostasis after the injury, thrombosis without injury. Right. So please understand the differences. One is hemostasis, one is thrombus. This is after injury, this is without injury. This is useful, physiological. This is harmful, causing ischemia. Everyone say yes. Everyone say yes. Got it? Got it. Coming on the pathophysiology. Now you may be thinking, why without injury the clot is formed? Why without injury the clot is formed? There can be three causes which are known as Virchow's Triad. The three causes. What are the three causes? So imagine this is the blood vessel. This is the endothelial lining of the blood vessel. Endothelial lining is injured by some toxin or something present in the blood. But bleeding is not there. Still the blood vessel is intact. So because of the endothelial lining injury, the clot can be formed here in an intact blood vessel, which is not bleeding. Now it is not hemostasis. It is thrombus. So the first cause is the endothelial injury. Say yes. The first cause is endothelial injury. Number two, I said you this is the blood vessel. I told you Bernoulli's Theorem now, I guess I told you now in the last, uh, first session. What is Bernoulli's Theorem? The the heavy thing travels at the center. So basically, the WBC and the RBC travel at the center. And in the periphery, there is plasma. The WBC, RBC is at the center. And in the periphery, there is plasma. And this blood flow is known as axial blood flow. Axial blood flow. So till the blood is flowing in all of us, the heart is pumping continuously, the blood is flowing continuously. It is never stopping. The blood is flowing continuously. This is axial blood flow. Imagine for a few seconds, the blood's blood flow stopped due to any reason. There is stasis of the blood. Like in inflammation, the last step was stasis. So blood is not flowing into stasis. So due to the gravity, the RBC will fall down. The platelet will fall down. You know, the revolution will fall down. You know, because of the gravity. And they form a clot there. They form a clot there. So stasis can lead to formation of clot. Altered blood flow, that is stasis or turbulence. The second cause. And third cause, hypercoagulability. Now, in a blood, in a blood, God has given two things, the procoagulant and the anticoagulant. What are procoagulant? They promote coagulation. They cause coagulation. Anticoagulation coagulants inhibit coagulation. So basically, we all have a balance. We all have a balance. In my blood, procoagulants are equal to anticoagulants. So they neutralize each other. They balance each other. But due to any condition, if procoagulants are more and anticoagulants are less, so such a blood is known as hypercoagulable blood. Hypercoagulable blood. And that leads to clot formation even without injury. So the third cause is the hypercoagulability. So can you tell me the three causes? Please Osama, Sage, Deep, Mohit, Debanjan, anyone? Can you tell me the three causes of the thrombosis? The Virchow's Triad. What are the three causes? The first one is the endothelial injury. Okay. The second one is the stasis of the blood or, um, the stasis or the turbulence of the blood. And the third one is the, what is the third one? I told you, hypercoagulability. Hypercoagulability. Please write down the three causes. Ultra important PYQ. The three causes of the thrombus. Okay. Now coming on the types of the thrombus. Ultra important. Where does the thrombosis present? If the thrombus is present in the artery or vein? Both are intact. No injury. No injury. Where is the thrombus? So if the thrombus is formed in the artery, it's arterial thrombus. If it is formed in the vein, it's venous thrombus. Both are intact. There is no injury. Without injury, it is forming. So basically, it is of two types: arterial thrombus, venous thrombus. There are two types of thrombi: arterial and venous. See this diagram. I've drawn this diagram for you. Everyone here on the screen, can you see? This is an artery. See the blood flow. See the direction of the blood flow. Can you see? This is a vein. See the direction of the blood flow. Can you see? The arterial thrombus, I have drawn yellow color intentionally. It is white thrombus. It is having more platelet. That's why it is yellow, Asian color, yellowish or whitish. But the venous thrombus contains more RBC. That's why it's red in color. So firstly, the arterial one is the white. The venous one is the red. Please learn the color because of the composition. The arterial one, can you see here? It's partially obstructing. And the venous one is completely obstructing. Can you see here? The venous one is completely obstructing. The arterial one is partially obstructing. The venous one is completely obstructing. So partial obstruction is known as mural. Complete obstruction is known as occlusive. So arterial ones are partially obstructive. The venous ones are complete obstructive. Please learn that. The third one, in the arterial one, the lines of Zahn are present. Alternate light, dark, light, dark, light, dark lines are present. These are known as lines of Zahn. In the venous one, the lines of Zahn are absent. The lines of Zahn are absent. There are no lines of Zahn in the venous one. They are absent. Okay. In the arterial one, okay, you tell me, what does the artery do? It's a nice pure blood to this organ. Now, because of the thrombus, the limited blood is coming to the organ. It is leading to ischemia. This is the effect of arterial thrombus. But what does a vein do? It carries impure blood away. The pure blood is coming, but impure is not leaving. Impure blood is accumulating in the organ because of the venous thrombus. And it will lead to edema of the organ. It will lead to edema of the organ. Can you tell me the arterial and the venous one? Arterial and venous one more difference. One more difference, please. See the differences. One more difference. So the last difference you can see here, let me show you here. This is the point of the origin of arterial thrombus. After that, where does it grow? Please see. It is growing in opposite direction as compared to blood flow. And venous one, it is growing in the same direction as compared to blood flow. So arterial one is growing in retrograde direction, opposite direction to that of blood flow. And venous one growing in the same direction, antegrade direction of the blood flow. Give me a thumbs up if you got it. Give me a thumbs up. You got it? Yes. Or some are lines of Zahn are alternate light or dark bands. Can you see here? Alternate light, off. So these are the, the dark bands are made up of RBC. And the light bands are made up of platelet and fibrin. So basically, the, the RBC is then platelet, fibrin, then RBC, then platelet, fibrin. So it occurs in arterial thrombus. But in venous thrombus, they all are mixed match. And basically, there are more RBCs. That's why it is red in color. So that's why lines of Zahn are absent in venous one. But in arterial one, the alternate light, dark, light, dark bands are present. Let me show you. So you can see, Osama, this is a thrombus. So here also you can see the alternate light, dark, light, dark. And if I cut and make a slide, you can see the light, bright, dark, light, dark. These are known as lines of Zahn, which are present in arterial but not in venous. You got it? Say yes or no. You got it? If you got it, can we go ahead? Okay. So yes. So these are the differences between arterial and venous. Better to understand them in a diagram. So don't learn the table, students used to learn the table like arterial, venous, this, that. Why you are learning? Come on. Have a look on the diagram. Everything is crystal clear. Everything is crystal clear. Only here, okay, see the arterial thrombus. See the venous thrombus. Can you see? The arterial one is white color, yellow color. Venous one is red color. You know the reason. Okay. Arterial one is partially obstructing. The venous one is completely obstructing. The arterial one, the lines of Zahn are present. In the venous one, the lines of Zahn are absent. Most important point. Arterial one leads to ischemia. Why you are learning? Come on. If the arterial blood supply is obstructed, what the organ will have? Organ will have ischemia, of course. And if the venous one is obstructed, the vein is obstructed. So impure blood will not leave and accumulate in the organ leading to edema. Arterial one growing in opposite direction, retrograde. The venous one growing in the same direction, antegrade. So please have a look on the diagram and enumerate. Enumerate the differences. Don't try to learn that. So these are the differences between arterial and venous. We are done with thrombosis. In the thrombosis, I told you the causes and the two types of the thrombosis. The causes of the thrombus, we have seen the Virchow's Triad. And the two types, arterial and venous. Everyone give me a thumbs up. Can I move ahead? Can I move ahead? Can we go ahead? Yes. So this is the first question in front of you. With Virchow's Triad or thrombosis include all except. The question includes except. Please tell me the answer. What is the correct answer? The question includes the except. Which Triad do not include? So you know the three things in the Virchow's Triad. Give me a minute. The three things in the Virchow's Triad: stasis, is there or not there? Endothelial injury, there or not there? Hypercoagulability and platelet thrombus. So platelet thrombus is not there. The remaining three are the three points of the Virchow's Triad. You have to learn. Okay. Now the answer is not a Kushma. The answer is D, right? They are asking the except. Correct answer here is D. So next topic, I am coming is embolism. What is embolism? What is embolism? Can you define embolism? The embolism is anything solid, liquid, or gas. Anything solid, liquid, or gas mass moving in the blood. The point of origin is something else. Okay. So here in the diagram, have a look. See this is the blood vessel. In the blood vessel, this is the thrombus. Just now I taught you what is thrombus. Till it is attached to the wall, it is thrombus. Once it gets detached, not as no more thrombus. It is moving freely. So we will call it the embolus. The embolus are moving freely. Moving mass. It is not attached with the wall of the blood vessel. So imagine if the wall of the blood vessel, this is the thrombus. Without injury, it is formed. The clot without injury, it's a thrombus. So till it is attached, it is known as thrombus. Once it gets detached and start freely moving here, it is no more thrombus. Now I will call it an embolus. So what is embolus? What is embolus? What is embolus? Embolus can be solid, can be liquid, can be gaseous mass. It can be any mass moving freely in the blood from one point to another. This is known as embolus. One of the embolus is made up of thrombus. It is one of the type, thromboembolus. But there can be other types also. The thromboembolism, one is the solid one. But there can be liquid and gaseous also. You got it? So what is embolism? It can be solid, it can be liquid, it can be gaseous mass. Say yes. So it can be any mass moving freely in the blood. Yes. When the thrombus migrates, so move it. When the thrombus migrated, it is one of the embolus. The embolus is not always thrombus originated. It can be some other origin also. It is one of the example I had given you. So it is not the definition. The definition is solid, liquid, or gaseous mass moving freely, moving freely, carried to other organs. It is known as embolus. Okay. There are four types of classification of embolus. The first depends whether it is solid or liquid or gas. In the solid, I have given you an example. The solid embolus is the thrombus embolus. The thrombus, once it detaches, it is a solid embolus. Now, so it is thromboembolus. The solid example is the thromboembolus. In the liquid, see amniotic fluid, amniotic fluid embolus is the liquid embolus. Or fat embolus is also liquid embolus. And in the gas, air embolus can be there. So it can be solid, it can be liquid, it can be gas. It can be of three types. I will give you examples of all of them. The second classification, whether it is infected or not. Whatever embolus are there, does it contain bacteria inside them? Or does they are sterile? If they are sterile, they are bland. If they are infected with bacteria, they are septic. They can be of two types. Where they are present? They are present in artery or vein. If they are present in artery, they are arterial type. If they are present in vein, these are the venous types. Right. Now I would like to explain you something here. Just a second. Can you see this diagram? I guess everyone can see this diagram. Where are the organs? These are the organs. You can understand the cardiac cycle. I am not explaining to that. These are the organs. You can see the arterial supply to the organ via aorta. Aorta supplying pure blood. And venous drainage of the organ to SVC, IVC. Impure blood is carried by the vein. Where is the embolus? Embolus can be present at two places. It can be present in the artery. It can be present in the vein. Listen everyone here on the screen. Imagine if the embolus is present in any artery, what will happen? Common sense. No knowledge is required. I'm asking common sense. We will see, ma'am, the arterial blood flow is obstructed because of the embolus. The organ will not get the pure blood because the artery is obstructed. It will lead to ischemia. Yes, it will lead to ischemia of that organ. If the embolus is present in artery. If the embolus is present in artery, streaming of that organ. If the organ is heart, it's MI. If the organ is the brain, it's stroke. If the organ is the leg, it's gangrene. It can be intestinal gangrene. So depending on organ to organ, basically it's, it's, um, basically it's ischemia. But what happens if the embolus is present in vein? Who will tell me? Who will tell me? Kuldeep, Shalini. So what happens if the embolus is present in vein? Not in the artery, what will happen? What is the consequence? I'm waiting for your reply. What happens if the embolus is present in vein? I told you what happens if the embolus presented the artery. The pure oxygenated blood is obstructed. The organ will not get the blood. So it will lead to ischemia of that organ, depending on organ to organ, it can be MI, it can be stroke, temporary gangrene. But what happens if the or embolus is present in the vein? What is the consequence? I want to ask. Yes, yes. I was waiting for this. So most of you are saying congestion or edema. Okay. No, it is not congestion or edema. If it was a fixed one and completely obstructing the lumen, it can lead to congestion or edema. But it is freely moving now. Edema will not be there. No congestion will not be there. You are wrong. Because it is freely moving, it is not obstructing it completely. So blood is accumulating in that. Here it is not complete. Like it is freely moving from here and there. So blood flow is not obstructed here completely. I mean to say. So no, it will not. Yes, Shalini, absolutely right. So Shalini is right. So here the embolus will go in the vein. It will keep on moving, keep on moving, keep on moving, all the veins. Where does it go? Any vein of your human body. All. So the embolus will move to SVC, IVC. From SVC, IVC, it will move to the right article, right side of the heart. From the right side of the heart, it will move to the right ventricle. From the right ventricle, the embolus will go in pulmonary artery. From the pulmonary artery, it will go to pulmonary capillary and block there. So basically, it will cause pulmonary edema. So all venous embolus leads to pulmonary edema. You can see the root. All arterial leads to infection, ischemia. And all venous leads to pulmonary edema. Give me a thumbs up on this point. It was a very big point I explained you. All arterial embolus, what is the consequence? All venous con embolus, what is the concept? Whatever embolus it is, whether it is thromboembolus, fat embolus, amniotic fluid. If it is present in artery, whatever it is, solid, liquid, gas. If it is present in artery, it will lead to ischemia and infarction of that organ. And if it is present in vein, it will lead to pulmonary edema. It will lead to pulmonary edema. You got it? So this is a basic concept you must know. Now we will see the various types of embolus one by one. So the same thing is written. All the arterial one lead to ischemia and infarction of that organ. In the lower limbs, it leads to gangrene. In the heart, MI. In the brain, it needs to stroke and sudden death. So it is ischemia and infarction. But venous one will lead to pulmonary embolism, pulmonary thromboembolism. Okay. The same root. So here it will start from here. It will keep on moving, moving, moving, moving, like this, right side of the heart, right article, right ventricle, pulmonary artery, and finally lungs. So any vein, it will go to SVC, IVC. From there to right article. From there to right ventricle. From there to pulmonary artery. And from there it will lead to pulmonary thrombolis. So whatever vein is there, it will lead to pulmonary thrombolis. Now I am going to discuss four embolus one by one. The thromboembolus, which is a solid one. The two liquid, I will discuss fat and amniotic fluid. And I will discuss the gas embolism. Thromboembolism, you already know how does it formed by detachment of thrombus. Still the clot is attached, it is known as thrombus. Once it gets detached, it is no more thrombus, it is known as embolus. So out of all the embolus, the 90% are thromboembolus. The most common type. Most common source? Deep vein thrombosis, DVT. Deep vein thrombosis leads to embolism. Most common. Second is fat. Okay, we got it from where the thrombus is coming. But from where the fat will come? Imagine this is a blood vessel. In the lumen of the blood vessel, from where the fat is coming? The fat embolism. What is the source? I mean to ask, what is the source of this fat embolism? From where it is coming? Fat embolism. From where this fat is coming? Can anyone tell me? Do you know from where this fat is coming? The fat embolism. From where this fat is coming? The fat embolism. Yes, from where this fat is coming? There can be two causes. Listen. We all know, we all have bone marrow. In the bone marrow, there are two types of marrow, the red marrow and the yellow marrow. The yellow marrow contains the fat. Okay. The yellow marrow contains the fat. Now imagine this person has a fracture. From here, the bone is cracked. There is a fracture of the bone. So the yellow marrow is leaking out. The yellow marrow is leaking out of the fracture and entering in the blood and forming a fat embolus. So this is how fat embolus is formed by fracture. This is known as traumatic cause. Traumatic cause means because of the fracture, the yellow marrow is leaking and coming and forming embolus, moving here and there. Number one. Number two, without fracture also, sometimes we can see it is present in the blood without fracture. So this is non-traumatic cause. This can be the non-traumatic cause. In the non-traumatic cause, um, like lipid profile can be altered. Like in the blood, we have LDL, we have VLDL, chylomicrons, and all. So if all these are increased, they will accumulate and form a fat embolus. That can be the non-traumatic cause. Okay. So fat embolism. Here the fat globules are formed. Can you see the lumen of the blood vessel containing a fat globule? It is a fat globule. The embolus is formed by the fat globule. There can be two causes, the traumatic and non-traumatic. In the traumatic, I told you it is the injury or the fracture to the bone. And in non-traumatic, it can be any cause which can alter the lipid profile. So that can be the two causes. Now imagine a scenario. You are an orthopedician. And even if you want to become orthopedician, you want to become orthopedician. Orthopedics is a very, you know, fascinating branch. Most of the students wanted, yes, especially the boys. Huh? It's a very good branch. Yes, orthopedics. Imagine you are an orthopedician. And a 25-year-old boy who was driving, having a road traffic accident, right? And he is having the fracture of, say, tibia. He is having fracture of tibia. And he is on your clinic, on your hospital, whatever. And he is having a fracture of the tibia. It will say, it's okay. It's a simple fracture of the tibia. Let's fix it. We have fixed the fracture. If the stent is required, you have put the standing is done. You have done the surgery. You have fixed the fracture. And you have put the cast for two months. There is a cast. The patient is still admitted in the hospital. In a day or two, in a day or two, you got a call from your nurse. The doctor, the patient, the 25-year-old boy you operated is dead. What happened? What happened? It was a simple case of fracture. Oh my God. It was a shocking. It was a shocking news. What may have happened? Can you correlate? No. What may have happened? So you asked, what is the cause of the death? He was having some breathing difficulties. All of a sudden, he has dyspnea, he has respiratory distress, and suddenly he is dead. So what may have happened? What may have happened to this boy? Can you tell me? So yes, he is having fracture. From this fracture, the yellow marrow may have leaked. That may have formed the fat globule, the fat embolism in the vein. All venous embolus, they are where, where does they go? They go in the lung. And he may have pulmonary thromboembolism. And that is the cause of the death. The cause of the death can be pulmonary thromboembolism because of the venous obstruction, you know, the venous embolus caused by the fat embolism. So yes, it's a typical case scenario. You will get typical. This case maybe the values, the age, and this scenario may be different. But ultimately, after injury, after fracture, the patient is dead or the patient is having respiratory difficulty. So it's a typical case of the fat embolism, right? Now, what will happen? You are in trouble now. You are an orthopedician in this case. So the family will sue you. You are under medical legal case. That why the boy is dead? Is there some negligence? Medical negligence from your side? Or it is simple fat embolism? You will ask for autopsy. The postmortem of the dead body. The autopsy. The autopsy is supposed. I am the doctor performing the autopsy right now. I will hear the complete history. What is the problem? Why the autopsy is performed? The autopsy will be performed by the forensic team. Okay. The medical legal team. So they will perform the autopsy and they will take extra care of the lung. They will take the lung out, especially the pulmonary capillaries out. They will cut the lung, make a slide, and they will look for fat embolism. If the fat embolism is found, it will be a proven case that the cause of the death is fat embolism. And there is no negligence of the doctor. You got my point? So here autopsy has a main role in the autopsy. So same thing is written. So after the fracture of the bone, if there is a sudden death, so on autopsy, we will see the lungs, especially in the lungs, we will apply special stain for the fat. You know, there are two special stains for the fat. Sudan black and oil red. They will highlight the fat. Right. Sudan black gives black color. Oil red gives red color to the fat, to the adipocytes. So if these are found in the lung, either this or this, it is found in the lung. So it is a typical, it is a typical case of the, uh, it is a typical case of the fat embolism. There is no prevention or thrust. You have to be vigilant. But yeah, I, I don't know if exactly some prevention is taken by the orthopedicians, you know, but yeah, it is a typical case. You should understand. So from MCQ point of view, if after the fracture, if sudden death is given, so pulmonary edema or pulmonary embolism is the cause. Okay. Now coming on the next, amniotic fluid embolism. How does it is formed? What is amniotic fluid? What is amniotic fluid? Whenever there is a pregnancy, this is a pregnancy. Okay. The lady is pregnant. This is the fetus inside the pregnant uterus. So the fetus is surrounded by amniotic membranes containing the amniotic fluid. So the fetus are surrounded by the, in the gestational sac, the fetus are surrounded by the amniotic fluid. Right. Now, just suppose it is the time of the labor. It is the time of the labor. The lady is in labor pain. During labor, the uterus contracts vigorously. The uterus contracts vigorously like this during labor. I'm saying, okay? So there are tears. There can be the tears in the myometrium. There can be. And this is the umbilical vein. Let me draw the umbilical vein. This is the umbilical vein of this mother. Vein. Umbilical vein of the mother. Okay. So because of the tear in the uterus and vigorous contraction, the amniotic fluid can enter via tears into the umbilical vein. And all veins go where? All veins go in SVC, IVC. So this embolus is amniotic fluid embolus. It is a liquid embolus. It will reach the lung, leading to pulmonary edema. It can lead to sudden death during labor or just after delivery of the mother. So imagine a mother, she was absolutely, mother needs a pregnant lady. Imagine a pregnant lady who is absolutely normal, healthy. And during labor, she is dead. Or just after the delivery, she is dead. So what can be the cause? The cause can be the amniotic fluid embolism. So here again, we will order the postmortem, the autopsy. In this case, again, the lung, we will see very carefully. We will make the slide of the lung section. And in the lung, we will find the amniotic fluid. Say yes, if you got the complete scenario. So this is the amniotic fluid embolism. It is very serious, unpredictable. It is very serious, unpredictable, unpreventable cause of maternal mortality. Just a second. Okay. And during labor or immediate postpartum, due to vigorous contraction, the amniotic fluid can enter the uterine vein. Sorry, not umbilical vein. It's the uterine vein. And it will reach the right side of the heart, causing pulmonary embolism in the pregnant lady and can cause. So if you are making the slide, you will get the amniotic fluid in the lung. The amniotic fluid in the lung is a typical scenario here. The next and the last is the gas embolism. Got it? The next and the last is the gas embolism. How does the gas embolism occur? How does the gas can can present inside the blood vessel? So you give injections to your patients. IV injections. So when we give IV injection, we fill the injection with the medicine, whatever the liquid medicine is there. And we take the air out. If you have seen, first we take the air out. We take the medicine up to the tip of the needle. And then we inject. If we don't take the air out, air is also injected. And that can cause air embolism. So that can be the one of the cause. One of the causes. But not very much because most of the time we take the gas out. But sometimes it can lead to air embolism where air is introduced in the vein or the artery. Us. This can be one of the causes. Okay. One of the causes. Just direct injection, IV infusion of the. Or second cause, just suppose you are a head surgeon, head and neck surgeon. You are operating on your patient on the head and neck area. And by mistake, you have cut the jugular vein or any major vein in the neck. So what will happen? The air present in the environment during surgery can enter inside the vein. Or you are an obstetrician. Uh, and during some surgery, you're a gynecologist. During some surgery, some major vein is traumatized in the pelvic area. Again, the environmental air can enter. So operation on head, neck, or operation of the obstetrics. It can lead to accidental opening of the major vein like jugular. And accidental opening of the air. So that can happen. So this is the air embolism. Again, air embolism can also be venous. The venous is dangerous. It is always leading to the pulmonary embolism. You can see the pulmonary embolism. That's all about it. That's all. Right. What does you do in this case? Imagine there is a patient. And you're a head neck surgeon. You are operating on the patient. And by accidental incision, the jugular vein is open. So the environmental air will enter inside. And it will form the air embolism. It's a vein. Where does all the veins go? All the veins, the blood will go in the pulmonary circulation. So the air embolism will leave the pulmonary circulation. And patient is suddenly dead. Just imagine. Again, we will perform the autopsy. In this case also, we will take the lungs out. So what do you want to see in the lung? In the fat embolism, you look for fat. In the amniotic fluid embolism, you look for amniotic fluid. How does you see the air? Air is not visible. Air is not visible. If you give the cut, it will evaporate like this. You know, if you give a cut here, where is the air embolism? If you give a cut here, it will, you know, it will just go out. You cannot capture the air on a slide. How you will prove that it's a typical case of air embolism? I'm asking you. Does anyone know the answer? Does anyone know the answer? So what we will do in such case? So we perform the autopsy. We take the lungs out. We try to figure out the pulmonary capillary. And we take the pulmonary capillary and give a cut, under the water. Under the water. Under the water. You got my point? So we will give the cut under the water. In the water, bubbles will come out. If the bubbles are coming out in the water, it means the air was present in the pulmonary capillary. You got my point? So give the cut underneath water. Not in the air. And openly in the air, you cannot notice that. Say yes, if you got my point. Say yes, you got my point. Yes. In the water, like have you seen how a tire puncture is repaired? How the tire puncture person who's repairing the tire puncture, he finds out what is the site of the tire puncture? We take the entire tire, put it in a water and see where the leakage of the air is there. In the same way, we do it under water. So same thing is written. We open it in situ water. We so open the pulmonary artery in situ water. Right. This is how we see that. So we are done with embolus also. We are done with embolus also. Embolism. We will solve some questions and we will move on the last topic, shock, of hemodynamics. Okay. So the first question is in front of you. Can you please tell me the answer? The most common source of embolism. What is the most common source of embolism? Please. Is it DVT, trauma, infection, or surgery? The most common cause of embolism. I told you 90% of the embolus are thromboembolus. They are made up of thrombus. Once the thrombus gets detached, it leads to embolism. The 90% of them. So what is the most common cause of thromboembolism? Now I had given you a clue. Can you tell me the answer? Yes, DVT. Because in deep veins, most common site of thrombus is the deep vein. And this is the origin of the embolus. Yes. The next question is in front of your typical case scenario question. Please pay attention. Take the clues. There is a 58-year-old man having a road traffic accident. Okay. Came to the hospital. He had multiple fractures in lower limb, in the ribs, in the lung contusion. Ultimately, he succumbed to his injury. He's dead. We cannot save him. Unfortunately, the person is dead. Now, at autopsy, the lung is showing the following slide. Typical slide given to you. You can see something in the lung. Can you see? What are these? These cells, white colored cells, cluster of white cells. These are adipocytes in the lung. You can see the fat. The fat in the lung. What is the correct answer? Yes, it's a typical case of fat embolism. So see the slide also. It's a, you can do the special stains also. The Sudan black, the oil red. I have told you. So sometime you can get the question on the special stain. So it can be typical case scenario based question. It can be image based question. You know, it can be handy question. Like if you know the concept, you can make it out. We are done. We are done. The last thing here, I will tell you, the shock. Right. So hemodynamics is also done. And after that, we will move on the last topic, neoplasia, genetics and neoplasia. Two more are left in the general. Okay. You want me to take him out also today? Now you want me to take him out also? Right. Okay. Okay. So let's continue with shock. Let's continue with shock. Does anyone know what is shock? What is shock? How you will define shock? Don't read here. Just tell me what is shock. If shock is the disease of one organ? No. It is a disease of multiple organs. In shock, multiple organ failure takes place in human body. From head to toe, we are supplied with multiple organs made up of multiple cells. We require blood supply to all these cells. Why? Why all the cells require blood? Why all the cells are requiring blood? Can you tell me the answer? Why all the cells require blood? Because it contains oxygen. All the cells require pure oxygen. That's why all the cells. So this is known as perfusion. You know. So all organs require perfusion because of the oxygen. If oxygen is not supplied, the organs or the cells will undergo ischemia and infarction. So ischemia and infarction can be there. So, uh, if all the organs simultaneously do not get the perfusion, if all the organs, not only one organ, all the organs of human body do not get proper perfusion, do not get proper blood supply, what will happen? First, the cells will start dying. The cells will start dying. Then.

First, cells will not function. It will show ischemia, then cell death, then particular organ death, then multiple organ death, then death of the person. So, it's a syndrome, one by one. So, if all the organs do not receive enough perfusion of the blood, the pure blood, because the cell will not function of multiple organs, then cell death of multiple organs, then organ death of multiple organs, multiple organ failure leading to the death of the person. This is shock. This is shock. It's a syndrome. One by one, the things take place. It's a syndrome. So, for cell death, then organ failure, then multiple organ failure, and then the death of the person. This is shock.

Now, you may be thinking, why multiple organs are not receiving the blood at the same time? So, there are three types of shock having three different reasons: hypovolemic, cardiogenic shock, septic shock. I request all my dear students to make a comparative table between them once for all: hypovolemic shock, cardiogenic shock, septic shock. So, I will tell you the causes of each of them, pathogenesis, how each of them leads to decreased perfusion, and the symptoms of each of them. So, treatment of each of them is different, you know. So, let's start with the first shock, hypovolemic shock, as the name indicates, okay?

How many liters of blood you have in your body? All the adult humans, they have five liters of blood. I am having five liters of blood. You are having. All adults have approx. 5 liters of blood in our body. That is our fluid. That is our fluid balance, right? We all know we have five liters of fluid in our body, five liters of blood in our body, right? If you imagine someone is having some accident, road traffic accident, or there is a major surgery, or there is abundant vomiting, or there is diarrhea, or there are burns. In burns, the fluid evaporates. All these reasons lead to less than five liters of blood in the body. So, less than five liters of the blood, so bloody night. So, all the organs are receiving less blood. If I'm having enough blood, I'm having five liters, so my five liters is distributed. My brain is getting, my heart is getting, my kidneys, my liver, my all organs are receiving a proportion of five liters. That is fixed and that is sufficient for them. But if, if some person is having less than five liters of blood, it can be four liters, three liters, two liters, depending on the blood losses, how much, right? So, whatever blood is left, so all the organs are receiving less blood. All the organs. And that shock is known as hypovolemic shock. So, all the organs undergo multiple organ failure. That will that is known as hypovolemic shock. So, the name itself indicates hypovolemic. Hypo means less, volumic means less volume of the blood. So, out of the three types of the shock, this is the most common type of the shock. Hypovolemic shock is the most common type of the shock. It is the most common type of the shock in which there is decreased volume of the blood. In which there is decreased volume of the blood. What are the causes? It can be acute hemorrhage. It can be, you know, acute hemorrhage like RTA, road traffic accident, surgery, dehydration, vomiting, diarrhea, burns. In burns, everything evaporates. The use of the diuretics, right? Uh, okay.

You can see what is the pathogenesis. If the blood in the body is less, see in hypovolemic shock due to the hemorrhage, road traffic accident, surgery, trauma, burns, dehydration, vomiting, diarrhea, less blood is present. Less blood, less venous return, less venous return means less cardiac output. Less cardiac output, less blood will go in aorta, less blood will be distributed to all the organs. All the organs have anoxia, and that will lead to shock. Give me a thumbs up if you got it. Give me a thumbs up if you want it. Okay. What is hypovolemia? What should I say about hypovolemia? Tej deep, it is related to hypovolemia, not hypervolemia. Hypovolemia is less than five liters of blood leading to the shock, okay?

Now, what will be the symptoms? As soon as the blood supply to all the organs is less, the heart will try to compensate and increases the rate, right? So, all the organs are not receiving enough blood. So, heart will try to compensate by increasing the heart rate, I mean, increasing the pumping, increasing the rate of the pumping. So, heart rate is more. That is tachycardia. Since there is less blood in all the arteries, it will lead to low blood pressure. So, blood pressure is less than 120 by 80, and heart rate is more than 100. So, tachycardia with hypotension. The typical, typical two things which occurs in the typical two symptoms in the shock. So, all the organs are receiving less blood. Kidney also receives less blood. It will lead to oliguria. The brain also receives less blood. It is leading to confusion and lethargic, and you know, coma, death can be there. That is hypovolemic shock. Got it?

Now, it is of three types. How much blood is lost? You, you told me that there are, there is five liters of blood. So, if 20, 20, 80 percent is lost, 20 is only one liter. 20 to 40 percent means two liters. And more than two liters, how much it is lost? If only one liter or less than one liter has lost its height, might hypovolemic shock stage one. If two liters is lost at stage two. If more than two liters is lost at stage three. Say yes if you got it. That is hypovolemic shock. That is the first cause.

Second, cardiogenic shock. Here, normally five liters of the blood is present. You will sit. Then why organs are receiving less blood? Because heart is not pumping. The left ventricle is not pumping. So, there is some problem in the muscle of the left ventricle, you know, the muscle of the left ventricle. The muscle of the left ventricle is ischemic. It is cardiomyopathy, or some problem is there. So, that it is not pumping. So, although five liters of the blood, five liters of the blood is present, but since it is not pumping properly, it is not ejecting the blood in the aorta. So, all the organs are receiving less blood. This is known as cardiogenic shock. Here, the problem is in the heart. So, here the blood is normal, but the problem is in the pumping of the heart. Inadequate pumping of the heart. Okay. So, when at least 40 percent of the left ventricle is destroyed by some disease, then inadequate pumping takes place, right? It can be MI, cardiomyopathy, rupture of the heart, cardiac arrhythmia, cardiac tamponade. It can be any cause. The basic problem is in the heart. That is known as circulatory failure. But here, the volume is normal. It's normal volumic shock. It's a shock with five liters of the blood. The blood is five liters. In contrast to hypovolemic shock, still patient is in shock. The problem is in the circulation. I mean, the problem is in the heart. Say yes.

So, in hypovolemic shock, the blood was less. Total blood is less than five liters. That's why cardiac output was less. In cardiogenic shock, blood is five liters, normal five liters, but since the heart is not pumping, that's why cardiac output is less. So, cardiac output is ultimately less here also, here also cardiac output is less. Here it is less because blood is less. It is not five liters. That's why it is there. But left ventricle cannot eject it. The cardiac output is less. Less blood will go in aorta. All the organs receive less blood, less oxygen, leading to anoxia, or leading to shock. Say yes. Say yes. Got it?

So, here the symptoms are same. Here also exactly same symptoms are there. All the organs will receive less blood. Kidney receives less blood, having oliguria and anuria. Brain receives less blood, again confusion, lethargy, coma, death. But one symptom is additional. Can you tell me what is the additional symptom here which was not there in hypovolemic shock? Here also tachycardia is there. Hypotension is there. Here, backward flow of the blood is there. That is not moving forward. The left ventricle is not pumping. So, blood is not moving forward. It is going backward. So, left ventricle, the blood is going backward from left ventricle to left atrium, from left atrium to pulmonary vein, and from pulmonary vein to the lungs. It is accumulating in the lungs. It is accumulating in the lungs and leading to dyspnea, pulmonary edema, leading to dyspnea. So, dyspnea has an additional symptom here, which was not there in uh, the dyspnea was not there in hypovolemic shock. But dyspnea is there in this shock, cardiogenic shock.

The last and most difficult shock to understand is people awaken or still there? Kindly interact in between, right? Don't keep the session as monotonous. So, Shalini is awakened. What about others? Others are sleeping or listening to me? Huh? Are you there? Okay, give me a thumbs up everyone. Give me a thumbs up. Can we go ahead? The third type of the shock, the septic shock. Okay. The third type of the shock is septic shock. Here, due to the bacterial infection, the gram-positive or the gram-negative bacteria leads to the shock. How infection can lead to the shock? Infections can lead to shock. I'm asking you, how does infection lead to the shock? How does the infection lead to the shock? Yes. So, gram-positive bacteria and gram-negative bacteria, how does they lead to the shock? Can you tell me? So, let me tell you, it's a difficult mechanism, but I will try. Okay, listen. The gram-positive bacteria, I'm sorry, then gram-negative bacteria have lipopolysaccharide on their cell wall, and gram-positive bacteria have lipoteichoic acid on their cell wall. I will draw it also for you. So, in the blood vessel, whenever gram-positive or gram-negative bacteria, whatever entering, it will go to the macrophage and stimulate the macrophage. Lipopolysaccharide through CD14 receptor, and lipoteichoic acid through TLR2 receptor. Macrophages on activating secrete interleukin-1 and TNF alpha. Okay, let me draw it. Okay, let me draw a blood vessel. In the blood vessel, these are the macrophages. Imagine this is a gram-positive bacteria, and imagine this is a gram-negative bacteria. The gram-positive bacteria, the gram-positive bacteria have lipoteichoic acid on their cell wall, and gram-negative bacteria have lipopolysaccharide on their cell wall, right? So, here lipoteichoic acid, here lipopolysaccharide. It will stimulate the macrophage. On the macrophage, specific receptors are present. Acid TLR1 receptor is present, and for lipopolysaccharide, CD14 receptor is present. If you want to learn the name of the receptors. So, ultimately, macrophage is activated. On activating, macrophage secretes TNF alpha and interleukin-1. That causes two things. Please understand, it's difficult. These two will cause two things. Number one, it causes vasodilation. Number one, it causes vasodilation. This is our artery supplying blood to some organ. It is causing vasodilation in the artery. What do you mean by vasodilation? By vasodilation, there is more blood supply to this organ. You are saying shock is due to decreased blood supply, but you are saying here there is more blood supply? Yes, it's a unique shock. It's a unique shock in which initially there is hyperdynamic circulation, instead of hypodynamic. So, there is more blood supply to this organ. In contrast to hypovolemic and cardiogenic shock, I taught you two shocks till now. In both of them, there was less blood supply to the organ. In hypovolemic shock, the blood is less, less blood supply. And cardiogenic shock, the heart is not pumping properly, that's why there is less blood supply. But in septic shock, I am saying there is more blood supply to the organ. You got my point? There is more blood supply. There is more, uh, blood supply to the organ. Okay, there is more blood supply to the organ. So, it's a hyperdynamic situation initially. But later on, the vascular permeability is also increased. After vasodilation, vascular permeability means gaps will be formed. The gaps will be formed. So, what will happen? You can see the gaps are formed here. The gaps are formed. From this gaps, the fluid will leak out. Fluid will leak out, leading to edema, leading to edema. So, less fluid will remain in the blood, and now it will lead to shock. So, there are two stages in septic shock. First, hyperdynamic stage, and later on, in hypodynamic stage, that leads to shock. Hyperdynamic stage is due to vasodilation, and later on, increased vascular permeability, permeability leading to the shock. Say yes if you want it. Everyone. So, this is the mechanism. This is the mechanism of the shock, the septic shock. Gram-positive bacteria, gram-negative bacteria, both of them can lead to shock. The vasodilatation leads to hyperdynamic circulation, which is in contrast to other two shocks, right? And increased vascular permeability later on leads to edema. I tried at least appreciate my efforts. You got the mechanism of the septic shock. Septic shock has two stages: early hyperdynamic stage, in which there is more blood. So, if you touch the extremities, the palms and the soles of the patient, in cardiogenic and hypovolemic shock, they are very cool because of less blood supply. But here, initially, they are warm. Warm extremities. When the patient is in shock with warm extremities, it's a typical clue given to you in the question. The warm extremities which show it's septic shock. But later on, the patient have increased vascular permeability, leading to the shock. Say yes if you got it. We are done with three types of shock. You want me to explain it again? The third type of the shock, septic shock? You got it?

So, in all the shock, whether it is hypovolemic shock, whether it is cardiogenic shock, or whether it is septic shock, in all of them, one thing is common: decreased perfusion. All the organs are receiving less blood supply. Less blood supply means less oxygen, less oxygen means anoxia. Multiple organs have anoxia, leading to multiple organ failure and leading to death. So, this is common for all of them, but the reason is different. Here, less perfusion, the reason is less blood, less volume of the blood, less than five liters of the blood is present due to accident, surgery, vomiting, diarrhea, burns, diuretics, whatever. In cardiogenic shock, the left ventricle is not pumping. That's why this is the reason. And in septic shock, either gram-positive or gram-negative bacteria, first leading to hyperdynamic circulation, that is increased perfusion, and later on, because of increased vascular permeability, decreased perfusion and decreased perfusion leading to the shock. So, that is the thing. So, yes, I hope you all got it. Yes. Can we go ahead? Kindly everyone respond.

So, you can see this is the master table of the shock. This is the master table of the shock. Here you can see. So, hypovolemic shock, cardiogenic shock, septic shock. See the causes of hypovolemic shock. See the causes of cardiogenic shock. See the causes of septic shock. Septic shock is due to gram-positive, gram-negative bacteria. See the pathogenesis. Hypovolemic shock: decrease volume of the blood, less than five liters. Cardiogenic is due to left heart failure, right? And septic shock is due to bacteria, right? See the symptoms here. Increase heart rate, decrease BP, decrease urine output, altered mental status. Unique, right? And here, inflammatory edema is unique because of the increased vascular permeability. We are done with shock. We are done with shock. Are you ready for the MCQs? Can we try some MCQs now?

The first question is in front of you. Perioperative shock is an example of which type of shock? Perioperative, like during surgery, during surgery or after surgery, which type of shock the patient have? Hypovolemic, septic, cardiogenic, or neurogenic? I'm asking you, what's the correct answer? So, during surgery, the patient can bleed. Sometimes the patient can bleed too much because of the bleeding, the volume of the blood will be less than five liters. Yes, absolutely right. And this will lead to hypovolemic shock. Is it right? Why people, you are not answering? Is it right? The perioperative shock is hypovolemic shock? Let me see. Yes, yes, very good.

In shock, what is the characteristic feature which is present in all shock? Tell me one feature which is present in all types of shock, whatever type of shock it is. Tell me one feature. Is it cardiac failure, overperfusion, cyanosis, or edema? So, is it cyanosis, edema, cardiac failure, or poor tissue perfusion which is present in all type of shock? Tell me one feature. Yes, you all are right. The correct answer is poor perfusion. Decrease blood supply to all the organs, whether it is hypovolemic shock, cardiogenic shock, or septic shock, it occurs in all of them. The hallmark feature of the shock. The correct answer is B, and you all are right. So, we are done with hemodynamics also. Got it? Can we go ahead? Say yes if you can go ahead. Can we go ahead? Yes, yes.

So, coming to the next chapter, very quickly, genetics. And after that, we are left with one more chapter, neoplasia. Okay? So, general will be done. All the important topics are general is done. General is very vague, but yeah, most of the important topics I'm trying to compile in a short span of time. So, let's start with genetics. In genetics, let me tell you, the genetic inheritance of single gene disorders: autosomal dominant, recessive, X-linked disorder, X-linked recessive. If you are an FMG student, or you always get one question on genetic inheritance of this. But in other exams also, directly or indirectly, there can be integrated questions on this. But in FMG, always there is a question, right? So, let me tell you, genetics is the study of the genes. You know, what is chromosome? What is human karyotype? In humans, how many chromosomes are present in each cell, in each nucleus, diploid nucleus? How many chromosomes are present in humans? I'm asking, how many chromosomes are present in humans? The 46 chromosomes. Either say 46 chromosomes or say 23 pairs. So, if we arrange all 23 pairs, pair number one, pair number two, three, likewise till 23, so it is known as karyotype. Karyotype is the arrangement of all 23 pairs according to their length. See, it is the largest one. See this one is the smallest one. So, according to their descending order of their length, of the length of the chromosome, okay? So, this is known as karyotype. You can see the karyotype. Out of the 23 pairs, the 22 pairs, you can see these one, these one till here, it is common in all. It is common in all. But the last pair is known as sex chromosome, right? These are known as allosomes or sex chromosome. These are different in male and female. We all know it's, it's a male, it's XY, and if it is a female, it's XX. The last pair is different according to the gender. The males have XY, and the females have XX. We all know that. But the first 22 pairs is common in all of them, right? We all, we all know that. Yes, the first 22 pairs. Absolutely right, Shalini. It's autosome, and the last pair is the sex chromosome. Absolutely right.

Now, let me discuss some genetic inheritance, single gene disorders with you. Genetic inheritance, single gene disorders: autosomal dominant, autosomal recessive, X-linked dominant, X-linked recessive. Let's start with autosomal dominant. Autosomal dominant. Can you see this is the pedigree? Now, it is not related to sex. You can see the males, the square is a male, I guess everyone knows, and the circle is a female. To learn the basic sign, I know. So, the, the filled one, the dark is the diseased, and the empty one or the healthy, I guess everyone knows that. So, male and female both can transmit the disease. So, it is not related to the sex, okay? You can see there is no skip of the generation. There is no gender bias. You can see in this generation, in this generation, in this generation, all the generations, the diseased persons are there. So, no generation skip, no gender bias. You can see the male is also transmitting to the next generation, and here you can see the female is also transmitting to the next generation. The female is also transmitting. There is no gender bias also, and it is having variable onset, variable. Right? Learn the examples. Autosomal dominant. What is the example? I am having a mnemonic for you for the four inheritance. I am going to give you four mnemonics, okay? Yes, I'm giving you four mnemonics. So, the mnemonic is disease. Familial is familial adenomatous polyposis. Neurofibromatosis one and two. A is for achondroplasia. T is for tuberous sclerosis. And H is for Huntington's disease and hereditary spherocytosis. So, please learn the full form. Try to learn the full form. I know it's not very easy, but at least with the full form, you can apply in the exam and Google out some options. Try to say the full form. It's not very difficult if you try. B for bone, brittle bone disease. F for familial hypercholesterolemia. H's I have to see. Hypercholesterolemia. A is adult polycystic kidney disease. D for dystrophic myotonica, osteogenesis imperfecta, Marfan syndrome, intermittent porphyria, neurofibromatosis type 1 and 2, achondroplasia, tuberous sclerosis, Hutchinson's disease. Maybe I have missed something or I am wrong, but at least that's right. So, write down the mnemonic and try like this. These all are autosomal dominant.

Coming on the next one, autosomal recessive. Autosomal recessive. See the generation skip. So, the first generation has, the second don't have, third don't have, then the fourth has. So, generation skip is very common here. Generation skips are there. Again, both sexes are involved. There is no gender bias, right? And it is early onset. That was variable in onset. This one is early onset. See the examples. The example is A, B, C, D, E, F, G, H, S, P, W. A stands for albinism. B stands for beta-thalassemia. C stands for cystic fibrosis. D for Dubin-Johnson and deafness, sensory neural deafness. E stands for enzyme deficiency, especially G6PD deficiency. F for Friedreich's ataxia, Fanconi anemia. G for galactosemia. H for hemochromatosis, Hurler. S for sickle cell anemia, very commonly asked. P for phenylketonuria. W for Wilson's disease. W for Wilson's. So, please try to say A, B, C, D, E, F, G, H, S, P, W.

The next is the X-linked dominant. X-linked dominant disorders, right? Here you can see the gender variation is there. Everyone, here on the screen, say here the female is affected. The mother is affected, but the father is healthy. So, when they get married, out of the four children, the mother is giving. Out of the four children, you can see the four children: one, two, three, four. So, out of the two sons, one is affected. Out of the two daughters, one is affected. So, basically, 50% of the sons, 50% of the daughters are affected. The affected mother is giving it to 50% sons, 50% daughters. She is not doing any variation. But this is the affected father. The father is affected here. The mother is normal. If they get married, the father is very partial. The father is giving disease to 100% daughters, not the sons. So, 100% daughters are affected, not the sons. The point is that the male gives the disease to 100% daughters, and the female gives the disease to 50% sons, 50% daughters. It's just a mnemonic to learn, okay? So, you can learn. So, this is X-linked dominant pattern. Say yes. Say yes. It is X-linked dominant pattern. Please say yes. So, typically looking at the pattern, you can see, see the mother, see the father, you can typically see the pattern based on that, you can answer. It's X-linked dominant only. Four diseases are X-linked dominant. The mnemonic is FAIR. F is for fragile X syndrome. A is for Alport syndrome, very important. I is for incontinentia pigmenti. And R is for rickets, vitamin D resistant rickets. Okay?

And the next is X-linked recessive. You can see females are always carriers. They don't have the disease, and males are the males have the disease. Males are the cases. Females are the carriers, right? Males are because it is X-linked recessive now. So, if both the X's are involved, then only the disease is there. If one of them is involved, patients don't have disease, and females have double X. Males have only one X. So, males will express it, but females will never express. So, the mnemonic is GRAHAMBELL. G-R-A-H-A-M-B-E-L. So, please read the full form. G for G6PD deficiency. R for retinitis pigmentosa. A for androgen insensitivity. H for hemophilia, very important. P for pyruvate kinase deficiency. Q for ??. Hemophilias are X-linked recessive. A for ??. M for ??. B for ??. E for ??. L for ??. So, I know it's difficult. I know, I know. Still, I insist you to learn. There are four patterns. If you don't learn the pedigree, it's okay, but learn the mnemonics. Learn the full form. So, there are four patterns. We will revise. We will revise the mnemonics of all of them. Let's see. Let's see who will answer. Let's see who will answer. Tell me the mnemonics. Kiran, Habib, Nikki, Osama, HD, anyone can answer? Want to try to tell me the mnemonics? At least full form, I will say, but trying to say the mnemonics. Autosomal dominant hypercholesterolemia. Autosomal dominant. D-O-M-I-N-A-N-T. Dominant. Head. This is the mnemonic. The second mnemonic. I guess it's connected again. I guess it's connected again. I guess it's connected again. Let's wait. I'm waiting for. Okay, connected? No. Okay, okay.

So, see, I have told you the mnemonics. The four mnemonics. If, if the four mnemonics you know, you can have half the job done. You know, you have to just say the full form. And at least if you are confused in the full form also, you can rule out some options. You will always get a question on these or direct or indirect clues can be there. So, please learn the four mnemonics as well as their full form. Can we go ahead? Can we go ahead? Let me show you some questions based on that.

The first question is in front of you. Can you tell me the type of inheritance in tuberous sclerosis? In which mnemonic it was coming? Tuberous sclerosis. Can you please give me the answer? In which mnemonic it was coming? The mnemonic was FAIR. Familial, Adenomatous Polyposis, Neurofibromatosis, Achondroplasia, Tuberous Sclerosis. So, yes, in which mnemonic it is coming? It is coming in the mnemonic of autosomal dominant. So, correct answer here is autosomal dominant. The correct answer here is autosomal dominant.

The next question is in front of you. Type of inheritance in Wilson disease. In which mnemonic it is coming? Just apply all four mnemonics and tell me where W was coming. SPW. Where it was coming? It is a mnemonic of autosomal recessive. You can see W is for Wilson. In none of the others, it is coming. So, correct answer here is B. You got it? This is how the mnemonics will help you. Many questions are there on this. Which of the following is an X-linked recessive disease? X-linked recessive disease. So, what's the mnemonic? FAIR. X-linked recessive. GRAHAMBELL. Apply the mnemonic and look for the option which option is coming in this mnemonic. As I can see, G is coming only. So, G is G6PD deficiency. This is how the mnemonics will be useful for you. Okay?

This is the next is on the pedigree analysis, right? Look at the pattern of the pedigree and tell me the answer. Which type of inheritance is it? So, I will see for male and female. There is no generation skip. I can see. I can see the male can transmit the disease to daughter, daughter, daughter. But the female transfer getting the disease to 50% sons, 50% daughters. 50% sons, 50% daughters. It's a typical pattern of X-linked dominant. I told you, it's a typical pattern of X-linked dominant, okay? So, the correct answer here is D. So, based on the pedigree, I have told you the pedigree of all four. I have told you the pedigree of all four, right? You got it?

Now, coming on the next chapter, the chromosomal disorder. The last chapter in the genetics. After that, we will start the neoplasia, right? So, uh, chromosomal disorder. The next is the chromosomal disorder. In chromosomal disorder, I will tell you Down, Patau, Edward, Turner, their karyotype, only the symptoms. I will give you diagrams. The five diagrams I will give. Based on the diagram, the important, important symptom, sign, you have to learn. You don't have to learn all the symptoms and signs. Only the important symptoms, signs, you have to learn. But you have to learn the karyotype. So, among them, you know, the normal karyotype of a male and female. So, during, uh, gamete formation, I mean, so what is the male? Male is 46. Female is also 46. But in male, the last pair is XY. In female, the last pair is XX. So, in male, when the sperms are formed, it's 23X and 23Y. Two types of sperms are formed. Two types of sperms are formed. But in females, when the ova are formed, when the gametes are formed, both are same. Both are 23X, 23X. I guess everyone knows this. There is no need to say, right? What I mean to say, now what I mean to say, if the female is more than 35 years of age at the time of the pregnancy, so sometimes there can be some problem which is known as non-disjunction. What it is known as? Non-disjunction. So, in increased or older females, that's why it is said that first pregnancy or pregnancy should be before 35 years of age in females. Male age hardly matters, but female age matters, right? Because in females, what is the problem? After 35 years of age, when the gametes form, see what, what is the distribution? It is 23+1 in one of them, and in other gamete, it is 23-1. So, here in one of the ovum, it will be 24. In one of the ovum, it will be 22. So, it will, it will, it will fuse with one of the normal, both of them will fuse with one of the normal sperm. So, total count will be in the fetus either 47 or 45. It's not 46. So, the fetus which is formed because of the fusion of the defective ovum with normal sperm, I am repeating, the defective ovum and the normal sperm, the ovum is defective, either having one more chromosome or one less. The reason is the non-disjunction. What is the reason? The reason is the non-disjunction. Due to the non-disjunction, the two ova are formed. They are not same, right? They are they are abnormal. When the fuses with the sperm, it will lead to monosomy, trisomy. So, the fetus which is born with 47 and 45, now, so 47 is known as trisomy. It is having one extra chromosome. And the fetus with 45 is known as monosomy. So, monosomy and trisomy can happen. You got my point? So, this is the meaning of the monosomy and trisomy. So, this is known as aneuploidy. And aneuploidy is of two types: monosomy, trisomy. In monosomy, 45 chromosomes are there. Trisomy, 47 are there. You got my point? So, the same thing is shown to you, okay?

Now, the three disorders: Down, Patau, and Edward. They occur due to autosome involvement. And the last two, that is the Turner and Klinefelter, they occur due to sex chromosome, the last pair involvement. In Down, there is trisomy of 21. But how is trisomy of 13? And Edward's trisomy of 18? So, all of them have 47 chromosomes instead of 46. Normal humans have 46, but these patients have 47 chromosomes. In all, this is out of the 47. So, I told you now, the chromosomes are in pairs. So, this is pair number one, pair number two, pair number three, pair number four, likewise. So, here, pair number 21, not two chromosomes, three chromosomes. Pair number 13, not two chromosomes, three chromosomes. Pair number 18, not two chromosomes, three chromosomes. So, this is the main thing you have to understand here. So, Down syndrome is the most common chromosomal abnormality among all. Most common is Down. See, see the karyotype. Can you see the karyotype? Now, identify the disorder, please. Identify the disorder. See, this is the abnormality. This is one pair. This is one pair. One pair. Count the. If you count total, it's 47, not 46. Subscribe. If you count, if you have the time, please count now. See, which is the triplet? All of them are pair, pair, pair, pair. One is triplet. So, 21 is the triplet. It's trisomy 21. So, that's my answer is. Don't give me a thumbs up if you got it. But don't learn the symptoms and signs. Have a look on the diagram. This is a Down baby. Down syndrome baby, right? So, basically, the face, broad, flat faces there. The eyes are far away from each other, having the epicanthic fold in between. Okay? The hands, there is a single palmar crease, single palmar crease on the hand, okay? In the heart, there are congenital heart abnormalities, especially VSD, okay? And hernias are very common, umbilical hernia, especially very common. So, I request you, I'm not reading all the symptoms. Have a look on the diagram. Mentally, the child is mentally retarded. So, have a look on the diagram and learn main features. In the complication of the Down, the most important complication is VSD, I told you. In the heart, there is ventricular septal defect. And all type of leukemias may occur, okay?

Now, coming on the Patau. The Patau is trisomy 13. Can you see here? If you count it, total, the total are 47 again, not 46. But what is a triplet? This is a pair. This is a pair. This is a pair. I can say 13th number is a triplet. So, there is trisomy of 13, that is trisomy 13. The most, most typical feature is the cleft lip and cleft palate, very unique feature. Apart from that, many things are there, but most important is cleft lip and cleft palate, right? And polydactyly. You know, if you see the hands, it is not visible. More than five fingers are there. Polydactyly is very unique feature, right? So, please learn it. Right? You can see all the features. And the next one is the Edward. Here you can see the Edward. Again, if you count again, it's 47. But this time, you can see the triplet is 18. It's 18 trisomy, right? The typical feature here is rocker bottom foot. Have you seen your foot? So, the normal human foot is like this. It's like this. I appreciate the arch. I appreciate the arch. And see the foot here. It's opposite. It's opposite. This foot is known as rocker bottom foot. And opposite arch. This is rocker bottom foot. It is very unique feature for Edward. Rocker bottom foot. Other features are also there. There is a typical, this thing also, the fist. Please do a fist. Fist, we can do it normally. Now, here you can see if you ask the baby to make a clenched fist, the digit number two and five are overlapping. Three and four. You can see two and five are overlapping. Three and four. This is two. This is five. They are overlapping. Three and four. So, it is always like this, like yay. This is digit number one, I guess everyone knows. This is two, three, four, five. Count the. Counting starts from the thumb. So, digit number two and five is on the, I'm sorry, one and five. No, no, no. Two and five is on three and four. It's like this. It's always like this. Very unique thing. So, it is Edward. Say yes. It is Edward, okay? Edward syndrome. Ah, yes. It's Edward. Okay? So, we are done with the three disorders here. Down, Patau, Edward. Trisomy 21, Trisomy 13, Trisomy 18. I told you unique, unique feature. Learn the unique feature. Don't learn all the features, okay?

Coming on the sex chromosome. In the sex chromosome, I will tell you one disorder in male, one in female. In the female, in the male, it's Klinefelter. In female, it's Turner. So, see the Klinefelter. The total, total chromosome are 47. What is additional? Additional is the sex chromosome. Normal male have XY. Here, one additional X is present. It's XXY. The normal male is XY, but here the male, it's male only. Male having XXY, right? So, one extra X chromosome will give the female like picture. Access female chromosome. It will give female like feature in the male. So, the male will have atrophic testes, feminization, lack of secondary sexual characters. The breast is enlarged in male like females. It is gynecomastia. I know. So, that can be the thing. You can see. But the male is tall looking. The male is tall looking. The bones are tall. Then intelligence is normal. I know. Such a male are usually get married. And after marriage, when they cannot conceive, then they come and notice that their clinical presentation. And they have normal intelligence. They are tall looking. The only thing they don't have beard. They don't have mustache. The testes are atrophic. The external genitalia are extra atrophic. And the pubic hairs are not there, or the hair distribution is like females. So, small testes, wide hip, narrow shoulders, poor beard, right? So, these are the features of the Klinefelter. Say yes.

The next is the Turner. The Turner is a female, right? Normal female support is what is the chromosome? She is having 45. So, which one is missing? One of the X is missing. So, X0, right? Normal female have two X. No, it's only one X. This is known as X0. X0. The total, if you count total, it's 45. That's a monosomy. It's a monosomy. It's 45X. Monosomy X. So, such a female again, she is having atrophic ovaries. She is having edema over the neck, short neck, and edema over the neck, right? And she don't have menstruation. Don't have breast enlargement. Don't have secondary sexual characters. She cannot conceive like that. And she's short stature. But mental status is normal. So, these are the symptoms. Give me a thumbs up if you got it. So, we have discussed five disorders: Down, Patau, Edward, Klinefelter, Turner. Say yes. Okay, okay. Turner. So, Down is trisomy. Let's try trisomy 21. This is trisomy 13. And this is trisomy 18. So, tell me the total number of the chromosomes. The total chromosome: 47, 47, 47. Says they are trisomy. But here, the pair number 21 is triplet. Here, pair number 13 is triplet. Here, pair number 18 is triplet, right? What about Klinefelter and Turner? Klinefelter and Turner involve the sex chromosome. So, Klinefelter is also trisomy, but of the sex chromosome. And this one is a monosomy of the sex chromosome, right? Klinefelter is a male. Turner is a female. Tell me the karyotype here. It's 47. Normal male is XY. It's XXY. One additional X. And here it is 45. Normal female is XX. Here it's X0. So, here one X is additional. Here one is missing, right? And you know, main, main symptom. So, this is the, this is the crux. You have to learn the crux, okay? And learn one, one, one, one, one main symptom in all of them. Please everyone, appreciate my efforts. Please give me a thumbs up. We are done with genetics. Congratulations.

Can you please answer this question? What is Patau syndrome? What is syndrome? What is Patau syndrome? Please. Yes, you all are right. The Patau syndrome is trisomy 13. Yes, correct answer here is trisomy 13. I guess everyone of you is right. Everyone of you is right. Okay, yes. Instead of Patau, if I ask Down, the answer will become A. And instead of Down, if I ask Edward, the answer will become B. Very commonly asked question. Can we go ahead?

Down syndrome is most commonly caused by what? Maternal non-disjunction or paternal? Maternal is mother, paternal is father, or translocation, or mosaicism. So, what is the most common cause of the Down? Not only Down, all these genetic disorders. Most common cause is maternal non-disjunction. Normally, mother is 46XX. If the age of the mother, as I told you, is more than 35 years, or some other problems are there, so the two ova are formed. They are not equal. One of the ovum contain 23+1, one of the ovum contained 23-1. Normal ovum 23, 23. And both of them are XX. So, here, this is known as maternal non-disjunction. This is the cause of these disorders.

In Turner, what is the number of chromosomes? Turner. What is Turner? Turner is a female. So, what is the number of chromosomes? Is it a monosomy? Trisomy? 45? 47? 46? 42? What is the total number of chromosomes in a Turner female? You all are right. It's 45. The Turner female is XO. I'm not O, X zero, I mean, right? So, one of the X is missing. So, that's why it's 45, right?

Let me read one more question for you. There is a male. The biggest clue given in the question is a male. Sexually underdeveloped. The sex, sex organs are not developed. Rudimentary testes are there. Prostate gland is also rudimentary. Sparse pubic hair, facial hair is not there, beard is not there. More stack. But the male is long, long, tall, right? Large hands, large feet. So, can you tell me the diagnosis and the genetic makeup? So, of course, based on the symptoms, they are talking about the Klinefelter syndrome. You can make it out. The male is with normal intelligence, long, tall. The only thing the beard, mustache is missing. The pubic hair is missing. And atrophic testes are there. So, what is Klinefelter? It's 47 XXY. Yes, you all are right. The correct answer, you see, it's a very repeatedly asked question. They can change the, you know, symptom signs, but ultimately, the crux of the question is that you have to make the diagnosis and tell the genetic makeup. Yes. We are done. Okay, so we are done here also.

So, what's now? Just a second. I will share the annotated version of PPT with you on the group after completing the session. Give me a minute. Okay, so now I am moving on to neoplasia. The next chapter to be discussed here is the neoplasia. Just a second. Can we where it is? The last chapter which I will discuss here in the general pathology is the neoplasia. So, let's start neoplasia. You people there? Can I start neoplasia? So, let's start neoplasia. What is neoplasia? Neoplasia. Neoplasia means new growth. Neoplasia, the new growth which is known as tumor. Tumor. The study of the neoplasia is known as oncology. So, what is neoplasia? How you will define a neoplastic cell? How the neoplastic cell is different from the normal cell? Normal cell is different from the neoplastic cell. How can you tell me the answer? How does the normal cell is different from the neoplastic cell? Can you see this is a normal cell? I have drawn for you. In this cell, there is a growth factor coming, binding with a growth receptor. The red color is the growth receptor. The growth factor is coming, binding with the growth receptor, and because of which, the mitosis takes place. So, the cell division takes place. The two cells are formed out of the cell. So, mitosis takes place only when growth factor or stimulus is coming. So, mitosis is under physiological control, okay? Now, see a neoplastic cell. See this is not a normal cell. This cell I have drawn here is a neoplastic cell. Why does a neoplastic cell? Here, the growth factor is absent. Here, the growth factor is absent. The stimulus is absent. Even in absence of growth factor, it is doing the mitosis. To such a cell in which the mitosis, the cell division is uncontrolled, it's uncoordinated, even on cessation of growth stimulus, it is going on dividing. So, this cell will go on dividing, go on dividing, go on dividing. It will form a mass of cells, and that mass of cells is known as neoplasm or cancer. The only problem in the neoplastic cell is that their mitosis or cell division is uncontrolled. It's unregulated. They keep on dividing, keep on dividing, uncontrolled growth. Yes, absolutely right. More they have uncontrolled growth, and uncontrolled growth leads to the neoplasm. So, that is the thing. So, what is neoplasia? It is the new growth. New growth. The new growth is the neoplasm, okay? So, when the growth is excess, uncoordinated, and even it occurs even after the cessation of the stimulus, it is known as neoplasia, right? Or neoplasm. Now, there is a special type of cancer. You know, the human body is made up of three germ cell layers during embryology. You may have read the three germ cell layers: the ectoderm, the mesoderm, and the endoderm. All the germ cell layers lead to some organs. Like our blood vessels, our circulatory system is formed from the mesoderm. The nervous system is formed from the ectoderm. So, I don't know exactly, but yeah, all the organs are made up of some or other germ cells. So, one organ contains one germ cell. So, whenever cancer occurs in one organ, it is arising from one germ cell. The cancer.

Of that organ having one germ cell, but there are certain cancers which arise from totipotential. What are totipotential? They can give rise to all the three germ cell layers: the ectoderm, the mesoderm, and the endoderm. So, basically, the tumor containing all three germ cells. Such a tumor which contains is a tumor which contains all three germ cell layers. Normal tumors contain one germ cell layer, but teratomas are derived from totipotent cells and they contain all three germ cell layers, all three germ cells. So, inside them, anything can present. So, usually, they occur in ovaries or testes. Now, if you take out the tumor, you can find teeth in them, you can find hair, you can find gelatin, you can find cartilage, you can find bone, you can find brain inside the tumor. We can find pancreas, adipose tissue, technically anything, anything. So, teeth, hair, bone, muscle, anything can be present. It is a teratoma. Say yes. So, that is the meaning of the teratoma. So, please learn the special tumor that is teratoma.

Now, I would like to, before coming on the main chapter of neoplasia, I would like to highlight two things: hamartoma and choristoma. What is hamartoma and what is choristoma? Both of them, these terminologies, they look like tumor, but they are not tumor. They look like tumor. You can see the suffixes -oma and -oma. So, you can confuse that it is a tumor, but they are not tumor. Let me explain you both. What is hamartoma? What is choristoma? Let me explain. Let me read the definition. I will explain. Don't be confused.

So, when the tissue is normal, but the site is abnormal, it's choristoma. But when the tissue is abnormal, but the site is normal, it's hamartoma. You will see, "Ma'am, what does it mean? What does it mean?" Let me explain you. Let me explain you. Let me come on the hamartoma. Can you see here? So, this is lung. Inside the lung, you can see this is the cartilage. This is the cartilage. So, does normal lungs have cartilage? Yes, normal lungs have the tracheal rings here and the cartilage in the bronchi. We know. So, normal lungs have cartilage. But the only thing here, so the site is normal. The site is normal and have cartilage. But the only thing, the cartilage becomes malformed. It becomes underdeveloped. Malformation is there, right? It's not cancer. If you cut it, it's not dysplastic. It's not anaplastic. It's not cancer. The only thing, it is disorganized. The cartilage becomes disorganized. It becomes malformed. It is known as hamartoma. So, hamartoma, the site is normal, but the tissue is abnormal. The tissue is abnormal, that is malformed. That is hamartoma. See the second example is spleen. You know, in spleen, there is red pulp and there is white pulp. In the spleen, this is normal spleen. You can see it here. This is the normal spleen. Inside the normal spleen, you can see abundant red pulp. The red pulp is normally present. The only thing, it becomes malformed. It becomes, uh, it becomes malformation or a developmental mild development is there. So, but here the site is normal. Site is normal. Tissue is abnormal. It is a developmental abnormality. The tissue becomes disorganized. The tissue becomes malformed. Okay. The tissue becomes malformed. Okay. So, hamartoma of the lung and hamartoma of the spleen. Hamartoma of the lung contains the cartilage. Hamartoma of the spleen contains the red and the white pulp. The site is abnormal. Tissues, tissue, site is normal. Tissues abnormal.

The next is the choristoma. In choristoma, reverse happens. Can you see this is the tongue? In the tongue, can you see the cartilage and the bone? Normal tongue doesn't have cartilage and bone here, right? So, if you cut this cartilage, bone, it's absolutely normal. It's not malformed. The only thing is site. Site is abnormal. The tissue is normal, but the site is abnormal. The site is abnormal. That is osteocartilaginous mass of the lung. Here also, you can see we are doing the endoscopy of the stomach. In the stomach, we found a mass that is pancreas. Pancreas doesn't present inside the stomach normally. It's absolutely normal pancreas. The only thing, the site is abnormal. So, say the thing. Say the two things what we have learned. What we have learned? Say about the tissue. Say about the site. Tissue and site. Say about the tissue. Say about the site. What do you say? What is normal? What is abnormal? So, say if the tissue is normal, but the site is abnormal. Site is abnormal means ectopic. Site is abnormal. What is this known as? Or say the tissue is abnormal. Abnormal means it's not cancer, mind it. It is malformation. Tissue is abnormal, but the site is normal. Site is normal of that organ only. What is it known as? Can you tell me the answer? When the tissue is normal, site is ectopic, it is known as choristoma. Okay. And when the tissue is abnormal, but site is normal, it's known as hamartoma. How you will learn? I don't know, right? Okay. You have to learn this. There is no mnemonic for that. Okay. If you know Hindi, "site is normal," you can learn like that. It's a small mnemonic if you understand Hindi. My own. So, site is normal. It's normal site, but tissue is abnormal. And you can make the reverse for the choristoma if you want a mnemonic at all. Okay. So, can we go ahead? Yes, yes, absolutely right. There are something different. You have got it. Okay. So, can we go ahead? So, please get many questions on that. So, what we have learned, let's summarize. They are not tumors. Neither choristomas tumor, nor hamartomas tumor. Both are tumor-like lesions, but they are not tumor. Choristoma: the tissue is normal, but the site is not abnormal, that is ectopic. Hamartoma: the tissue is abnormal, but the site is normal. Site is normal, but the tissue is abnormal. I hope everyone got it. Okay, okay. Can we get it? Go ahead. Okay, yes, yes. You can learn. He means to say that, I guess. So, it's a good one. So, choristomas. Chori, you know, stealing something. If we steal something, so this, the site is abnormal. The site is abnormal. It's a good one. Thank you, thank you. Good one. So, Kush has given a good mnemonic, "Chori, kamal." Okay. So, you can learn like that. Good one. So, can we go ahead? So, we have learned the two things. The summary is in front of you. Both of them, none of them is tumor. Both of them are tumor-like lesions, but none of them is real tumor. So, one is choristoma. So, the site is ectopic, but the tissue is normal. Hamartoma: the tissue is abnormal, but the site is site is normal, but the tissue is abnormal. I hope you got it. Can we go ahead? Can we go ahead? We will solve some MCQs now based on that. So, the first question is in front of you. Tumor containing cells of all three germ cell layers. I guess everyone knows the answer. I guess everyone knows the answer. What is the correct answer here? Please. Tumor containing cells of all three germ layers. What is the correct answer? What is the correct answer? Yes, tell me the answer. Yes, of course. The correct answer is. I don't know why you people are not writing the answer. Yes, yes, very good. So, all three germ layers, the teratoma. Only tumor. What is hamartoma? Can you define? Is it malignant tumor? Is it metastatic tissue? Is it developmental malformation? Or is it hemorrhage in the vessel? Very easy question. Can you tell me what is hamartoma? Who will tell me what is hamartoma? Is it malignant tumor? Malignant tissue? Developmental malformation? Or hemorrhage in the vessel? Yes, I'm waiting for the answer. So, of course, the correct answer is C. It's a developmental malformation. It's not malignant. You neither malignant nor metastatic, not hemorrhage. The correct answer is. The next question is in front of you. Ectopic rest of the normal tissue. I mean to say, the tissue is normal, but the site is abnormal. The site is abnormal. The tissue is normal, but the site is abnormal. What it is known as? Choristoma, hamartoma, pseudotumor, pseudotumor, or lymphoma. What is the correct answer? Yes, you all are right. The correct answer is A. That ectopic site but the normal tissue. What is hamartoma? The next question. What is hamartoma? Is it proliferation of the cell in the foreign site? Proliferation of the native cell in the tissue? Malignant condition? Acquired condition? It's neither acquired. It's neither malignant. Now, tell me the answer from A and B. Is it proliferation of the cell at foreign site? Or is it faulty proliferation of the native cells of the same site in other tissue? So, what do you say? Yes, the correct answer here is B. It's the native cell. The site is normal. The same site. The tissue is abnormal. So, the word native is very important here. Yes, the correct answer here is B. So, we are done with this also. The next topic is benign versus malignant tumors. Okay. So, what are the differences? You know, there are two types of tumors: the benign and the malignant. How to differentiate between benign and malignant tumor? What are benign tumors? What are malignant tumors? How to differentiate between the two? How you can differentiate the benign tumor from the malignant tumor? Can you please tell me how you can differentiate the benign tumor from the malignant tumor? Yes, how you can differentiate the benign tumor from the malignant tumor? Based on the five features, we can differentiate based on their rate of growth, clinical features, gross microscopy, and most important is the spread of the tumor. So, the benign tumor and malignant tumor. Let me show you here only. The benign tumors are slow growing. The malignant tumors are fast growing. This is based on their rate of growth. Based on the clinical features, benign tumors are usually asymptomatic. Usually, exceptions are there. And malignant tumors are usually symptomatic. Again, exceptions are there. Gross features: the benign tumors, they are well circumscribed. They are well circumscribed. They are encapsulated. They are circular, oval. Malignant: they are irregular. They don't have capsule. They are infiltrating. The benign compress the tissue. The malignant infiltrates inside, invades the tissue. Okay. Microscopic features: I will explain you. I will explain the 10 features. The 10 features of the dysplasia which makes the differences between benign and malignant. And most important, the last one is the spread of the tumor. Benign tumors do not do any spread. No metastasis, no local invasion. Malignant, you must do both. So, based on these features, we can differentiate the benign tumor from the malignant tumor. Yes, based on the gross finding, Shalini, based on the size also, we can differentiate. Okay. So, let me discuss the five points one by one. Let me start. Let me start the characteristic of the tumor. So, benign tumor, the rate of the growth here, they are slow growing. The malignant ones are fast growing. Clinical features: the benign tumors, the benign tumors, they are asymptomatic, usually, except some like meningioma, they can produce seizures and various symptoms. Malignant tumors, usually rapidly growing. Usually, they rapidly grow. They rapidly grow. They can ulcerate on the surface and they can do the systemic features also like weight loss, anorexia, anemia. Usually, they are symptomatic. Gross features: benign tumors are small, spherical, capsule present, well circumscribed. Malignant tumors are irregular. You can see here. Both of them are breast tumors. This one is benign. This one is malignant. Both are breast tumors. Here you can see the benign tumor is well circumscribed. The malignant tumor is irregular. It is invading inside, right? So, based on the gross, we can identify. And the most important feature to differentiate benign and malignant tumor is the microscopic feature. The microscopic feature is the anaplasia. Can you see? These are the 10 points of the anaplasia based on which we can define whether it is a benign tumor or a malignant tumor. Let me discuss the 10 points of the anaplasia. Can you see? This is a normal or benign. And this one is the malignant tumor. So, see, first is the basal polarity. In the morning, I explained you what is basal polarity. Basal polarity means the nucleus is present towards the basement membrane. So, basal polarity is present in benign, but it is lost in the malignant. The first feature is loss of basal polarity. Second, pleomorphism. Here, all the cells are of the same size. Here, some cells are small, some are moderate, some are large. So, here pleomorphism is absent. Here, it's present. The presence of pleomorphism is anaplasia. NC ratio. Here, NC ratio, you can see small nucleus and more cytoplasm. Here, you can see the nucleus is big and cytoplasm is less. So, your NC ratio is high, right? Anisokaryosis is the size of the nucleus. All the nuclei here, same size. Here, some are small, some are large. So, here, no anisokaryosis. Here, anisokaryosis is present. You can see the nuclear chromatin. Here, it's normal. Here, dark color nucleus is there. So, hyperchromatism is there inside the nucleus. I appreciate the nucleoli. Here, there are no nucleoli. Your nucleoli is present here. There is no mitosis. Here, mitosis is present. Here, you can see no giant cells. Here, some of the cells having multiple nuclei, that is giant cells are present. So, these are the features basically you have to learn differentiating between the benign and the malignant tumors. You got my point? So, just to let me go. And the next point is the spread of the tumor. There are two types of spread. Let me explain you after that, we will take a lunch break. Okay. So, just five minutes more. So, you can see this is a patient. This is a patient. Just imagine she's having any tumor. Just suppose breast tumor. Okay. So, if it is growing, growing, growing and involving the pectoralis major, involving the ribs, involving the surrounding tissue, it is known as local invasion. Local means in continuity. It is growing. Local invasion means it is continuity involving other organs. Apart from that organ, involving other organs also in continuity. But the second option is that the tumor cells are going in the blood vessel or lymphatic vessel and by a blood vessel, it is reaching in multiple organs of the body and involving multiple secondaries and multiple organs which are discontinuous with the primary. Discontinuous. This is known as distant spread. Distance spread is known as metastasis. Metastasis. The what to be picked here is the discontinuous multiple secondaries. So, there are two types of spread: local and distant. You got it? If you got it, give me a thumbs up. What are the two types of spread? Local spread, distance spread. Distance spread is known as metastasis. The local spread occurs in continuity and distance metastasis, it is the discontinuous multiple secondaries are formed. Both of them are absent in benign and both of them are present in malignant. You got it? You got it? So, same thing is shown to you. Can you see here? This is a tumor. What is going on? Involving the surrounding tissue and continuity. In continuity. This is local invasion. After that, it is moving to the blood. One of the cell is going to the blood. Via blood, it is going to multiple other organs and forming multiple secondaries here. So, this is metastasis. This is local invasion. This is metastasis. I hope you got it. I hope you got it. Now, please understand. Benign tumor: absent. Neither local invasion nor metastasis. But malignant: please, please. Okay. So, I told you the five. Now, please, I'm enumerating everyone here on the screen. So, I have told you the five differences to differentiate the benign and the malignant tumor. Okay. Benign tumor, malignant tumor. Help me in filling. So, based on rate of growth, these are slow growing. These are fast growing. Okay. Based on clinical features, these are asymptomatic. Exceptions are there. These are symptomatic. Exceptions are there. Based on the gross finding, these are circular, oval, spherical, numbers, um, capsule is there. These are irregular, no capsule is there. They based on microscopy, I told you the features of the anaplasia. So, here the polarity is present. Here the basal polarity is lost. Um, here hyperchromatism is present. Pleomorphism is present. Anisokaryosis is present. I mean, all of them are absent in benign and present in malignant. So, please learn those 10 features. The last one I told you, the local invasion and distant invasion. Both are absent in benign. Both are present in malignant. Both are present. Now, these are the differences. Everyone here, everyone here on the screen. Which is the shortest sign of malignancy out of the five? Purest, most reliable sign which differentiate benign versus malignant. One sign. The shortest one. Purest, most reliable sign to differentiate benign or malignant. It is known as shortest sign of malignancy. Can you tell me the answer? The shortest sign. Charter sign. What is the shortest sign of malignancy? The most reliable one. The most reliable one is the metastasis. Number one. So, if metastasis is present, it has to be malignant. There is no exception. There is no exception. Okay. The second most shortest is the local invasion. Again, if it is present, it has to be malignant. Third most is the microscopy. Right? Rest all are just clues. They will not give you sure. Okay. So, most shortest sign is metastasis. Okay. Please learn. It's a very important MCQ. So, surest sign, most reliable sign is the metastasis. Second most reliable sign is the local invasiveness. Same thing is written in front of you. You got it? So, that is the benign versus malignant tumors. I told you we will solve some MCQs and we are done till now. Just a second. MCQs are not very important here. We can be. So, let's take a break. Let's say a lunch break. After that, what topics are left? Let me tell you. Okay. So, from neoplasia, metastasis is left, right? So, I will tell you the three roots of the metastasis. I will tell you the tumor markers. I will tell you the carcinogenesis. The physical, chemical, and biological. Yeah, these are the important topics from neoplasia. We are packing with general. So, I guess I was having more 30-40 minutes. I can pack general before lunch. But yeah, I am lacking. First, I will take the lunch. In the next, after lunch, 30 minutes, I will try or 40 minutes, I will try to complete general, right? After that, in hematology, we have few anemias, leukemias, and platelet disorders. I will take only important ones here, not the detail. In anemia, I would require one hour. In leukemias, I would require one hour. Right? Platelet disorders, I will tell you only classification. And hemophilia is not important one here. So, I will take, I guess, two and a half hour session more here. Let me plan how we can do after the lunch. Okay. So, let's take a lunch. Currently, it's 2 o'clock. So, let's connect again at, what, how many, how much time you require for lunch? Let me know. How much time you require for lunch? Uh, let's connect at after 45 minutes, 2:45. Okay. At 2:45, we will connect and we'll try to compile till 4 o'clock, 4:30 maximum. 4 or 4:30, I will try to finish it up. Okay. So, let's come back at 2:45. Lunch break. Give me a thumbs up if you got it. Okay, okay. So, please come back at 2:45 sharp. I'm ending it right now. Hello everyone. Am I back? Am I visible? Am I audible? Give me a minute to check if everything is good. I will start the session. End. Am I clearly visible? Audible? You can write in the chat box. Okay. Thank you. Thank you, Kush, for confirming. Thank you so much. So, can we continue the session ahead? Can we continue the session? Yes. So, let's continue the session. Okay, okay. Thank you, Osama. Thank you, Farhad. Thank you. Thank you. So, you people are still there. Thank you. So, let's start ahead. We were studying the general pathology. In general pathology, we have covered most of the topics. The last topic is the neoplasia. We are taking on. We have already seen cell adaptation, cell injury, cell death, acute inflammation, chronic inflammation, apoptosis, necrosis. We have already covered. Um, after that, hemodynamics, right? Thrombosis, embolism, shock, edema. We have already covered the genetics. And now we have started neoplasia. So, neoplasia, uh, just a second. Give me a minute. So, I would like to continue neoplasia with the topic carcinogenesis. Give me a minute. Let me start with carcinogenesis and tumor markers. These two topics are important here. Still in neoplasia. After that, the general pathology is done. The important topics are done. After that, we will move on hematology. So, let's start with carcinogenesis. Okay. What is carcinogenesis? First, understand what is carcinogens. What is carcinogenesis? First, understand that. Okay. Carcinogenesis is the mechanism of induction of tumor. Can you see here? Okay. Let me show you. Can you see two cells in front of you? In the first cell, you can see the growth factor is coming. This is the growth factor. It is binding with a growth receptor. When the growth factor comes, binds with the growth receptor, the cell divides. In the second cell, you can see no growth factor is coming. In absence of growth factor, cell does not divide, right? Now, what are the genes which are leading this? Like the growth factor. In presence of growth factor, there is a gene known as proto-oncogene, which gets stimulated and causes the cell division. In absence of growth factor, there is another gene known as tumor suppressor gene inside the nucleus, in the DNA. These are the names of the genes. Tumor suppressor gene gets stimulated and it inhibits cell division, causes mitosis. Tumor suppressor gene inhibits mitosis. Normally, in all of us, in me, in you, in all normal individuals, the cell division is caused by proto-oncogene in presence of growth factor, and cell division is inhibited by tumor suppressor gene. Learn the names of the two genes: the proto-oncogene and tumor suppressor gene. One is causing the stimulation of cell division, other is causing the inhibition of the cell division. Please understand. So, can I say proto-oncogenes like the accelerator? Have you driven any vehicle like car or any vehicle? So, if you want to increase the speed, what do you do? Of course, you will apply the accelerator. If you want to decrease the speed or stop the car, what do you do? Of course, you will apply the brake. So, can I say the proto-oncogene is like accelerator? It is causing the stimulation of the cell division or increasing the rate of cell division. Can I say tumor suppressor genes are the like the brakes? They inhibit or stop the cell division. Can I say this? Say yes or no. Say yes or no. Can I say this? So, these are the accelerator. These are the brakes. So, imagine I am driving a car. I want to increase the speed, I will apply the accelerator. I want to decrease the speed or stop the car, I will apply the brake. So, speed is balanced. This is known as balance. The same occurs in human body. The God has provided the molecular accelerator and the molecular brake with us. We have a molecular accelerator. We have a molecular brake. Okay. So, but imagine an unfortunate condition. If the brake is failed, you are driving a car, or anyone is driving a car, the brake is failed, or the accelerator got stuck at the highest speed, you cannot reduce the accelerator. What will happen? The speed increases drastically. Imagine if the same occurs in human body. In the human body, the proto-oncogenes get overstimulated. These are the accelerators. They got stuck at the highest speed. They are overstimulated. Or the tumor suppressor genes, they are inhibited because of the mutation. So, what will happen? The one which causes cell division is overstimulated. The one which stops cell division is inhibited. It will lead to uncontrolled cell division. It will lead to cancer. So, this is how the cancer takes place in human body. Cancer takes place because of two reasons. There are two reasons for cancer: overstimulation of proto-oncogene, inhibition of tumor suppressor gene. So, you can see the two types of the genes. The accelerator got overstimulated, and the brakes got inhibited. The brake is failed, and accelerator is stuck at the highest speed. What will happen? Uncontrolled speed. Uncontrolled cell division. Uncontrolled cell division leads to cancer. Give me a thumbs up. This is the simplified version how you can understand the molecular mechanism of the cancer. You got it? Now, the point is that you must ask me, "Ma'am, by the proto-oncogene get overstimulated?" They are present in me. You all have the individual. But we have normal version. If they get mutated and get overstimulated, or if they get mutated and get inhibited, then they are abnormal and lead to cancer. You got my point? You must suppress a gene and proto-oncogene. They are not abnormal. Normally, they are normal only. But once they get, they get mutated, they are abnormal. So, who is causing the mutation? Who is causing the mutation? The mutation can be caused by one of the three agents: either the physical, or chemical, or biological. And that is known as carcinogenesis. You got it? That is known as carcinogenesis. So, what is known as carcinogenesis? It is the mechanism of induction of mutation inside the cell. And the agents, the physical, chemical, or biological agents are known as carcinogens. So, basically, there are three types of carcinogens. They all cause mutations. Mutation of the two genes: either they cause mutation of proto-oncogene, that is gain of function mutation, that is they get overstimulated, or they can cause mutation of tumor suppressor gene, that is loss of function mutation, they got inhibited. So, these mutations are caused either by the physical agent, or chemical agent, or biological agent. And this is known as carcinogenesis. First, understand what is carcinogenesis. Have you got it? Now, let's start with physical carcinogenesis. What is physical carcinogenesis? The physical carcinogenesis is, you know, radiation induced carcinogenesis. So, there are rays in the environment where we are living now. We are surrounded with multiple rays. You know, UV and IR rays are mainly. They can induce the cancer. We will discuss them one by one. UV and IR. The source of them. The cancers they cause. And the mechanism. The source. Let's start with UV light. What's the source of the UV light? From where we get the UV light? We get the UV light from sunlight. Imagine this is the Earth and this is the sun. Let me draw the sun. This is the sun. We get sunlight from the sun. And it falls on the Earth. There are three UV rays present in the sunlight: UV A, B, C. Three UV rays are coming from the sunlight. C never reaches the Earth because C is filtered by the ozone. We know the Earth is surrounded by ozone. So, C is filtered by ozone. Only A and B are coming on the Earth. A is coming. B is coming on the Earth. Learn B for bad. B for bad. B is bad for humans. B for bad, right? So, A does not cause the cancer. B causes cancer. It's a very important question. B can cause cancers. UVB. You can learn the wavelength if you wish. The wavelength of A, B, C. C gets filtered by the ozone, not reaching the Earth. B is the carcinogenic among A, B, C. B is carcinogenic. Never, never forget. Which cancers it causes? It causes only skin cancer. On the skin, it can cause squamous cell carcinoma, basal cell carcinoma, and melanoma. The three types of cancers in the skin. So, squamous cell carcinoma, basal cell carcinoma, and melanoma. Among them, the most common is basal cell carcinoma, right? What is the mechanism? Imagine this is a skin cell. It is a skin cell of human, the keratinocyte. This is the nucleus. Inside the nucleus, this is the DNA containing multiple genes. Now, this UVB is coming. UVB is coming from the sunlight. Once it comes, now, you know, normal Watson and Crick model of the DNA. You have read this in biochemistry. So, purine forms bonds with pyrimidine, right? Adenine forms bonds with cytosine. I'm sorry, thymine. And cytosine bonds form bonds with guanine. We know that purine forms bonds with pyrimidine. I guess everyone knows that. If the UV, UVB is falling on the cell, because of UVB on the DNA, there is pyrimidine-pyrimidine bond formation. I repeat my words. There is pyrimidine-pyrimidine bond formation. Pyrimidine forms bonds with pyrimidine. Pyrimidine-pyrimidine dimers are formed, which leads to mutation. And this mutation leads to cancer. The mutation can be in proto-oncogene or tumor suppressor gene that leads to cancer. Say yes. You got it? So, what is the mechanism? Due to UV light, pyrimidine-pyrimidine dimers are formed. Pyrimidine forms bonds with pyrimidine. Pyrimidine-pyrimidine dimers are formed. That leads to mutation. That leads to cancer. The mutations are two types, you know, either proto-oncogene gain of function or tumor suppressor gene loss of function. Say yes. Are you people there? Are you understanding? The topic is difficult, but I'm trying my best. So, this is the mechanism, right? Let me come on the next rays. The next rays. The IR rays. IR rays are present in sunlight? No, no. UV rays are present in sunlight. But IR rays are not present in sunlight. The IR rays are present in X-rays, gamma rays, beta rays. It can present. That many cancers it causes? It causes all types of leukemia. How many types of leukemia? You know, it is acute myeloid leukemia, acute lymphoid leukemia, chronic myeloid leukemia, chronic lymphoid leukemia. There are four types of leukemia. IR causes three of them. Not the fourth one. So, which one it doesn't cause? It never causes CLL. IR. It's a very important PYQ. IR, IR means ionizing radiation. Ionizing radiation never causes CLL. Apart from CLL, it causes all leukemia. Say yes. So, it causes all leukemia except, except, except, mind the exception. Please mind the exception. Exception is CLL. It never causes CLL. Number one. Number two, it causes all thyroid cancer. There are four types of thyroid cancer: follicular, papillary, anaplastic, medullary. It causes all of them. Most common is papillary, but it causes all of them. Right? So, that is the thing. That is the thing. And CLL is never caused by IR. What is the mechanism? Imagine either this is a WBC, bone marrow cell, or it is a thyroid cell. It is having the DNA. And IR is falling. This time, UB is not falling. The IR is falling on the cell. So, when ionizing radiation is falling on the cell, you know, in the cytoplasm, the cell is having water. Of course, all cells have water. What is water? What is H2O? When IR rays fall on the water, water forms the free radicals. OH negative. Water forms a free radical OH negative. And this OH negative will cause the mutation. To form the mutation here, it is due to the formation of the free radical from the water. This is the mechanism. You got it? So, exposure to ionizing radiation dislodges ions from the water and it will form the free radical that causes mutation that leads to cancer. You got it? So, we are done. Listen, listen. First, I will write for you. Then you will tell me the answers. So, tell me UV rays, IR rays, the two types of the physical carcinogenesis. Okay. You have to tell me the source of each of them. Number one. You have to tell me the cancers they are causing in which organ. And you have to tell me the mechanism in one or one line, not in detail. That's it. So, what is the source of UV? Who will tell me? What is the source of UV? Of course, it's sunlight. There are three UV: UV A, B, C. Which is bad? Default bad. UVB is bad. It is carcinogenic. C never reaches the Earth. And A is good. A is healthy, right? So, IR. The sources: X-ray, Alpha, Beta ray, Gamma ray. Which cancers does it cause? Here, UV rays cause skin cancer. The three types of skin cancer: squamous cell carcinoma, basal cell carcinoma, and melanoma. Okay. And here, it causes either thyroid cancer or blood cancer. Thyroid cancers are four types: papillary, follicular, medullary, anaplastic. And blood cancer, all leukemia, but never CLL, right? Mechanism. You have to tell me for both of them. What is the mechanism here? The mechanism is pyrimidine-pyrimidine dimer formation, which leads to mutation. Here, the mechanism is formation of free radical, which leads to mutation. Say yes. So, you get many MCQs based on the physical carcinogenesis. Answers. We are done with physical. Let's start chemical. Can I? Can I? Okay. So, there are many chemicals which can cause cancer. There are two types of chemicals: direct, indirect. We are surrounded with chemicals in the air, in whatever we eat, whatever we drink, it contains many pesticides, many chemicals, you know. So, pollution contains the chemicals. And some of the chemicals causes cancer. The best example you can take, not only like this, you can take the smoking. What does the smoke contain? We all know. We all know smoking leads to lung cancer. What does the smoke contain? Smoke contains tar. And tar leads to cancer. So, tar is the chemical present inside the smoke that leads to lung cancer. So, there are two types of chemicals: the direct and the indirect. Direct carcinogens and indirect carcinogens. Two types of chemicals are present: direct and indirect carcinogens. Okay. What do you mean by direct? They are directly going in the body and they induce mutation. They go to the target organ and induce mutation. Indirect ones are inactive ones. First, they go in the liver. They become activated inside the human body. After that, they go to the target organ and they cause the cancer, right? Now, what are the steps? How does the chemical induces cancer? Like, what are the stages in chemical carcinogenesis? So, there are three stages. What are the three stages? You can see its initiation, promotion, and progression. In the initiation itself, there are four steps: metabolic activation, reactive electrophile, mutation, and initiate itself. I will show you all. Rather, I will draw it for you. Okay. Let me draw a rough diagram of human body. So, I'm drawing a rough sketch diagram. So, don't laugh, okay? It's a rough sketch diagram just to explain you. Imagine this person is exposed to some chemical, right? Now, the chemical is present in the blood. Let me draw the blood vessel. Okay. Let me draw the liver. Let me draw the target organ. Let's say the target organ is lung. It can be anyone, right? The chemical is present in the blood. So, if the chemical is direct, it will go directly to the target organ. But if the chemical is indirect, first it will go to the liver. In the liver, hepatocytes are present. Inside the hepatocytes, there is an enzyme known as cytochrome P450. Then cytochrome P450 converts the inactive to active, inactive chemical to active chemical. That is the first step. So, let's start initiation. In the initiation, the first step is metabolic activation. The metabolic activation takes place in the liver. So, indirect chemical goes in the liver. The liver converts it from indirect to direct, inactive to active, and again it will go in the blood. After becoming active, it will go in the blood. So, first step is over. The metabolic activation. Say yes. After that, after that, we are going to the target cell. We are going to the target cell. I mean, the chemical will go to the target cell. In the target cell, imagine the target cell. This is the nucleus of the target cell. Imagine it is a cell. So, in the cytoplasm, it will lose electron. Let me draw a target cell. This is a target cell. The nucleus of the target cell. The DNA of the target cell. This is the chemical which is already active. Which is already active. If it is direct, it is directly coming here. Indirect, first go in the liver and then come here. Okay. Now, this chemical will lose electron and form the electrophile. Electrophile here, lose the electron and become positively charged. It will in the cytoplasm of the target cell. Now, nucleus is negatively charged. We all know nucleus is negatively charged. And by losing electron, it becomes positively charged. The negative attracts positive. So, because of that, it will go in the nucleus and hit the DNA. I'm using the word hit. It will hit the DNA. It will hit the DNA, right? Because of which it will produce the cancer. Right? So, first electrophile formation, then it hits the nucleus and causes mutation. And because of the mutation, the cell will divide and form the initiated itself. So, these are the steps of initiation. You got it? So, in initiation, there are four steps. I have explained you. So, first, the metabolic activation, it occurs in liver. It is required only by indirect chemical, not direct chemical. Then electrophile formation. Electrophile formation takes place in the target organ cells. In its cytoplasm. Then mutation. Mutation. Mutated cell is formed. And initiated cell is formed. Then promoter is required. That causes clonal proliferation of the mutated itself. So, this cell goes on dividing, goes on dividing, from one to two, two to four, or two eight, eight to sixteen, sixteen to thirty-two, thirty-two to sixty-four, likewise. And it will form a bunch of cells known as cancer. So, this is known as promotion. So, initiation, different chemical is required. Promotion, different chemical is required. The chemical required for initiation is initiator. The chemical required for promotion is promoter. Right? And for a cancer, both are required, right? Initiator causes mutation. It is mutagenic. And promoter causes proliferation of already mutated cell. Please appreciate my efforts. Come on. You got it? So, initiator chemical causes the mutation. And promoter chemical causes the proliferation of the mutated itself. And finally, the cancer occurs, right? This is known as progression. You got it? The promoter is required. It does not damage the DNA. It does not produce the mutation. It causes proliferation of the mutated itself. Okay. So, initiator should be followed by promoter. Promoter should not be followed by initiator. Then only cancer will occur. If only initiator is present, there is no cancer. If only promoter is present, see the triangles are the promoter. Green triangles. Then also no cancer is present. If initiator, if promoter is followed by initiator, again no cancer is present. Cancer occurs only if initiator is followed by promoter, whether in continuity or whether after a gap. Say yes. So, it is a diagram from Robbins. And I hope you all can understand very well now. Okay. So, initiator should be followed by promoter. Promoter should not follow that initiator. Promoter. What does the promoter will do? Mutated. First, initiators should come, cause the mutation. Then promoter should come, and it should cause the proliferation of the mutated itself. Okay. And finally, just suppose we are talking of the lung cancer. The initiator is the tar. It will produce the cancer. The promoter is also tar. Sometimes the same chemical acts as both. Okay. It is also causing the front. But the patient doesn't have cough. Patients don't have dyspnea. So, genotypically, the patient has cancer. But we know typically, you know, phenotype. Phenotype is the expression. When the cancer is expressing, it is known as progression. The progression is the phenotypic expression of the malignancy. You got it? So, these are the steps: initiation, promotion, progression. In the initiation, there are four steps. Say yes. How does a chemical carcinogenesis occurs? Who will tell me? How does the chemical carcinogenesis occurs? There are three steps. First, initiation is required. Then promotion is required. And then progression, that is phenotypic expression. In the initiation, there are four steps. First, metabolic activation. It occurs in liver. It is required only by indirect chemical, not direct chemical. Then electrophile formation. Electrophile formation takes place in the target organ cells. In this cytoplasm. Then mutation. Mutation. Mutated cell is formed. And initiated cell is formed. Then promoter is required. That causes clonal proliferation of the mutated itself. And then progression is the phenotypic expression of the cancer. Say yes. So, I hope you got it, right? So, is there any test to prove the chemical carcinogenesis? Explain to you the chemical carcinogenesis. You should not believe me. You should ask me, "Ma'am, is there any proof that whatever you are saying is right? Chemical causes cancer." There is some test which can prove that chemical causes cancer. Yes, there is the test. So, the name of the test is Ames test. Very important PYQ. Ames test. First, learn Ames test is proving that chemical can cause cancer. Let me explain the test. It's a very easy test. Take a bacteria in a test tube. Take the bacterial suspension. The name of the bacteria is Salmonella typhimurium. What is the name of the bacteria? It's Salmonella typhimurium. It's the name of the bacteria. Salmonella typhimurium. It is already mutated. We are taking already mutated strain. You know, what is the mutation? Salmonella typhimurium cannot grow without histidine. Histidine is given, then only it will do banner efficient. Otherwise, it will not grow. It's a unique property. This is the mutated strain that cannot synthesize histidine. In the body. So, if you give from outside, then only the bacteria will grow. Otherwise, it will not grow because it is a mutated strain. It cannot synthesize histidine. Okay. Now, you put one drop of this bacteria, bacterial suspension, mix it with the chemicals in a jar, right? Now, if the chemical is carcinogenic, the chemical will cause the mutation in this bacteria. But you will see, "Mom, it's already mutated." It's already. So, basically, they will reverse the mutation. You got my point? The bacteria is already mutated, right? And the chemical will cause the mutation. So, you know, minus minus is equal to plus in mathematics. So, basically, the mutation will reverse. Because of the chemical, the mutation, the already mutated cell, the mutation will reverse. It will cause mutation over mutation to reverse the mutation. I mean to say, now, if you try to grow this bacteria on histidine-free media, the bacterial colonies can be seen. This is only occurring when the mutation is reversed. Say yes. Say yes. Can we go ahead? Can we go ahead? Okay. So, this is Ames test. This is Ames test. You can see the list of the chemicals and the corresponding cancers they cause. I request all my dear students, I will provide the notes. Please have a look on this list. Like alkylating agents cause AML. Androgens cause prostate cancer. Dyes cause bladder cancer. Arsenic causes cancer of the lung and the skin. Asbestos causes cancer of lung, pleura, mesothelium. Like this. Or there is a already asked question PYQ on the vinyl chloride, on benzene, on aflatoxin. Vinyl chloride causes angiosarcoma of the liver. Benzene, benzene causes leukemia. And aflatoxin causes liver cancer. So, please learn this list. It's very important. We are done. We are done with the chemical carcinogenesis also. Can you tell me the answer? The question is in front of you. A simple bacterial test for mutagenic carcinogenesis is it Ames test? Redox test? Bacteriophage? Or gene pricing? What is the correct answer? The simple bacterial test for mutagenic carcinogenesis for mutagenic carcinogens. One test. Single bacterial test to prove that. Here's the correct answer is Ames test. Just now I told you for mutagenic carcinogens. Okay. So, correct answer is A. You all are right. Okay. Uh, rest questions you can see by yourself. The last thing here in neoplasia, I would like to.

Tell you is the biological carcinogenesis. So let's start biological carcinogenesis. In biological carcinogenesis, I would like to tell you three types of carcinogenesis: viral, bacterial, and parasitic. What do you mean by biological carcinogenesis? Some biological agent is causing the cancer. So, how many viruses are there? Six viruses. There is one bacteria and four parasites. Total 11 organisms in this world are carcinogenic; they can cause cancer. So, you should know the first thing you should know: the list with six viruses. How many of them are DNA viruses? How many of them are RNA viruses? So, you should know the list of the viruses. You should know the list of the bacteria and list of the parasite. Okay, so let's start with the viruses. Okay, so you can see the list. These are the six viruses I am telling you they are carcinogenic. You can read: HPV (human papilloma virus), Epstein-Barr virus, Hepatitis B, Hepatitis C virus, HIV, HTLV, and HHV. So, you know these. So, you should know which cancer each of them is causing. Which cancer? Only one bacteria is carcinogenic, which can cause cancer. The name of the bacteria is Helicobacter pylori. It causes two stomach cancers: the gastric cancer, the adenocarcinoma of the stomach, and MALToma, the lymphoma or the MALToma of the stomach. Both are of the stomach. Only one is adenocarcinoma, one is MALToma. And there are four parasites which cause cancer: Schistosomiasis, Clonorchis sinensis, Opisthorchis, and Fasciola hepatica. Very important PYQ. Learn the list, learn the name of the six viruses, one bacteria, and four parasites which are oncogenic. Your 90% job is done. Then the most important among them, I will explain in detail. Okay, so the six viruses, out of the six viruses, are you can see how many of them are DNA? Four of them are DNA, and two of them are RNA. Which four are DNA? It is Hepatitis B virus, I'm really sorry, Human Herpesvirus 8, Human Papilloma virus, Epstein-Barr. And which are RNA viruses? HTLV and HCV. So, please learn them differently. Among them, I will give you details of only two. Which two? So, I will give you detail of HPV and EBV, how they cause cancer. I cannot give you the detail of all of them now, how they cause cancer. The most important which are important from some point of view, we will see.

So, how does HPV cause cancer? HPV, there are many types of HPV. Some cause benign cancer, some cause malignant. So, 16 and 18 most commonly cause malignant cancer; they are high risk. In the HPV, there are two proteins: E6 and E7. E6 causes mutation of p53, and E7 causes mutation of retinoblastoma gene, and because of which the person has cancer. HPV causes genital cancer. By genital cancer, I mean cervix cancer in females, and I mean penis cancer in males. You got it? Give me a minute, please. I'm really sorry. Let me draw it for you. Instead of reading, we will draw it. So, you can see here, I am drawing any cell, like either the skin cell or the genital cell of human. You can see I am drawing the nucleus, I am drawing the DNA. Okay, this is HPV virus. HPV virus enters inside the cell, and here it forms two proteins, E6 and E7. Among them, both of them will go in the nucleus. E6 causes mutation of p53, and E7 causes mutation of retinoblastoma gene, and because of which this cell becomes immortal, and it will lead to cancer, various types of cancer. This is the mechanism. So, E6 and E7 you have to learn. And Epstein-Barr virus most commonly it causes Burkitt lymphoma. It causes other cancers also, but most commonly it causes Burkitt lymphoma. So, that's all about it. That's all. So, please read the list: the viruses, the bacteria, and parasite. Bacteria and parasite, there is no mechanism; you have to learn the list. So, that's all about it. I guess we are done with the general pathology. We should start the hematology. I would like to take a small break for, say, 10 minutes only, and we will start the hematology. I will take one hour session for hematology right now after a break of 10 minutes. So, currently it's 3:20. I will start at 3:30. Okay, at 3:30, come back at 3:30, start hematology. Okay.

Hello everyone. Am I visible? Am I audible? Kindly confirm. From clear, divisible, audible. I will continue. Give me a minute. Let me check. So, if you can see and hear me, kindly write down in the chat box. I'm waiting. Yes. Okay. Okay. Thank you, Osama. Thank you for confirming. So, let me continue with hematology. So, we have done the most important topics in general pathology, and let's start with hematology. In hematology, we will start with anemias. So, what is the definition of anemia? How can you define anemia? Do you know what is anemia? Can you define anemia for me? What is anemia basically? So, anemia, how many RBCs? Humans have RBCs, WBC, and platelets in the blood. The normal count of RBC is 4.5 to 5.5 million per deciliter. This is the normal count, right? So, anemia is reduction in RBC mass. Reduction in RBC mass, but measuring RBC is difficult. And all the RBC contain hemoglobin inside them. We know how what is the RBC? RBC is a cell which is non-nucleated. It doesn't have the nucleus. At the periphery, hemoglobin is present. So, RBC is a non-nucleated cell which contains hemoglobin. All the RBC contain hemoglobin. So, whenever the RBC reduces in number, the hemoglobin also reduces in number because RBC is directly proportional to hemoglobin. So, indirectly, instead of measuring RBC, we can measure the hemoglobin. So, basically, anemia is reduction in total RBC mass. But in practice, measurement of RBC mass is difficult. That's why instead of measuring RBC mass, we measure the hemoglobin. So, nowadays, we define anemia as reduction of hemoglobin below what? Reduction of hemoglobin below what? Below the normal, normal limit, normal lower limit of hemoglobin for that individual. So, what is the normal limit for hemoglobin for individuals defined by the WHO? For males, it's 13.6 grams per deciliter. If any male having hemoglobin less than 13.5 grams per deciliter, it is anemic. The male is anemic. In females, it's 12 grams per deciliter. And in newborns, it's 15 grams per deciliter. So, it depends on the age of the person. It depends on the gender of the person. Let me ask a question. Let me ask a question. The question is: a person is having hemoglobin, ah, 12.5. Is the person anemic or not? Is the person anemic or not? My question to you is, is the person anemic or not? Do you know? Can you answer it? You should not answer it. You should ask me the age and you should ask me the gender. If I say the age is adult and if I say the gender is male, the male is anemic because for male, the cutoff is 13.6, and it is less. So, the male is anemic. But if I say the female, the female is non-anemic because for female, the cutoff is 12.00, is more than that. It is more than that. You got it? So, male and female. For male, it's anemic. The male is normal. For female, it's anemic. You got my point? I'm sorry. For male, it's anemic. For female, it's normal. So, the age and the gender is important to define anemia. That is my point. Oh, so let me come on the classification of the anemia. For understanding classification of anemia, you should understand the morphology of the RBC. In the RBC, see two things. Number one, okay, see the shape of the RBC. What is the shape of the RBC? RBC, if you see from front, it's circular. It's circular like a coin. And if you see it from side, it's biconcave. If you see from the side, it's biconcave. If you see from the front, from the top, it's circular. And if you see from the side, it's biconcave, right? The diameter of the RBC is 7.5 micrometers. The diameter of the RBC is 7.5 micrometers. Please learn this dimension: 7.5 micrometers. It's a circle. So, the diameter, you have to learn this. This is normal RBC. You have seen the shape. Now, is it nucleated? No, RBC is a non-nucleated cell. It contains hemoglobin. And wherever it contains hemoglobin, it is having the pink color. So, the hemoglobin is present at the periphery. See, I'm marking it. It is present at the periphery, not at the center. The central one-third is empty. The central one-third is empty. It is known as pallor. It is known as central one-third pallor. So, please learn two things for the RBC: number one, its size; number two, its color. Size and color. See the size from the top. Say, man, size is 7.5 micrometers. Please learn that. And what's the color? If you ask me about the color, the color is present at the peripheral two-thirds, not at the central one-third. The peripheral two-thirds is colored, but central one-third is empty. It's pallor. It's pink color. Okay, so this is the color. Learn central one-third is pallor, empty portion is. So, this is normal size, normal color. If you know the normal size, normal color, you can understand now ahead, like the classification of the anemia. So, normal size is 7.5 micrometers, and central one-third pallor. The lifespan of RBC is 120 days. Everyone knows that. Now, based on the size, RBCs are of three types. Based on the color, RBCs are of three types. First, talk about size. In pathology, size is known as "cytic." Please learn the word "cytic." "Cytic" is size. The "tic" is size. Okay, so normal size is 7.5 micrometers, okay, right? RBCs can be normal size, can be larger size, can be smaller size. Okay, normal, larger, smaller. The size, okay? So, this one is known as normocytic. This one is known as macrocytic, and this one is known as micro-microcytic. Okay, this "acidic," "acidic," "acidic." So, that is "cytic." "Cytic" means size. Please learn that. Based on the size, RBCs are of three types. So, they are in front of you: normocytic, macrocytic, microcytic. See the suffix, suffix "cytic." Normocyte, macrocyte, microcyte. Based on now, how you measure the size? Okay, let me tell you color also. Okay, first finish size. How you measure the size? Just suppose I'm giving a slide in front of you. There are three slides. Now, you measure the size of the RBC. You don't have a scale in the microscope, right? You don't use a scale to measure whether the RBCs are 7.5 micrometers, smaller than that, bigger than that. How you measure? We don't use a scale now. So, there is a way, you know, in the slide, we have WBCs also. One of the WBCs is lymphocyte. The size of lymphocyte is also 7.5 micrometers, and it is fixed. RBC can be smaller, can be larger, but the lymphocyte is always 7.5 micrometers. So, we compare the size of the RBC on a peripheral smear with a lymphocyte. See here, the RBCs are same size as that of lymphocyte. That's where it is normocytic. See in the second slide, the RBCs are smaller as compared to lymphocyte. These are microcytes. And in the third size, in the third slide, the RBCs are larger. The RBCs are larger than the lymphocyte. It is macrocytes. So, normal size, it's microcyte, and macrocyte. Based on the size, you can divide the RBC into three categories. Yes, we have to compare it with a small lymphocyte. So, that is the thing. Based on the color, RBCs are of two types only, right? Not three types. Color in pathology is known as "chromic." Color, color is known as "chroma." Chroma means color. If the RBC is there, in the RBC, if the peripheral two-thirds is colored, you can see peripheral two-thirds color, central one-third is an empty, it is known as normal chromic, normochromic. Okay? But if the color is present only at the periphery, central one-third pallor is more, and peripheral two-thirds ring is less, it's like this, hardly any color is present at the periphery, it is known as hypochromic. Hypo means less. There is no condition like hyperchromic. Hyperchromic, it doesn't exist. So, basically, normochromic, the central one-third pallor is there. And here, the pallor is more than one-third. The pallor is more than one-third. The color is less. So, this is based on the color. So, what we have learned? What we have learned? Can you please summarize? Based on the size, how many types of RBC? Based on the color, how many types of RBC? Based on the size, that is known as "cytic." How many types of RBC? Based on the color, that is "chroma." How many types of RBC? Can you please tell me? Based on the size, three types of RBCs: normal. Okay. Based on the color, there are two types of RBCs: normal, normal chromic. The suffix is important. The suffix is "cytic" and "chromic." Say that. And hypo, hypochromic. Hypo. There is no hyperchromic. Now, let me classify anemia. Everyone with me? Everyone? So, first type of anemia is normocytic, normochromic. The size is normal, the color is normal. Still, the person has anemia. Such anemia is normochromic. The second type of anemia is microcytic, hypochromic, in which RBCs are less than size, less than color, and the patient has anemia. It is known as microcytic hypochromic anemia. And the third type of anemia, macrocytic, but there is no hyperchromic, no corresponding. So, macrocytic, normochromic. So, tell me the three types of anemia. What are the three types of anemia? Normocytic, normochromic. Microcytic, hypochromic. Macrocytic, normochromic. You got it? So, based on the size, based on the color, we have three types of anemia: normocytic, normochromic; microcytic, hypochromic; and macrocytic, normochromic. Everyone give me a thumbs up if you got this basic concept. This is the basic classification of anemia, known as morphological classification of anemia. For measuring the size, you require a lymphocyte on the smear. For color, you don't require any lymphocyte. Give me a thumbs up, everyone. Are you people there? You got it? It's a normochromic and hypochromic. We got it. Can you see the RBCs here in the slide? In the slide, they are normochromic. See the central one-third pallor. See the central one-third pallor is there in all of them. Central one-third is pallor, right? See the second slide. In the second slide, you can hardly see any color. Maximum slide is pallor only. Hardly any color is present. Maximum is pallor. So, this is normochromic. This is hypochromic. Granted. Can we go ahead? Two more terminologies you have to learn here. Two more terminologies. One, two more terminologies. I want to tell you: anisocytosis and poikilocytosis. Now, can you see here? Some RBCs are small, some are normal, some are large. So, variation in size is known as anisocytosis. Some are small, some are normal, some are large. But variation in shape. Can you see this is tear shape, this is helmet shape, this is oval, this is circular? So, variation in shape is known as poikilocytosis. Poikilocytosis. So, variation in size is anisocytosis, and variation in shape is poikilocytosis. These are the basics. If you learn, okay, if you know the basics, learning the concepts are very easy. So, let's classify anemia now. You can very easily understand the classification of the anemia. There are two important anemias. More for two important classifications of anemia: morphological and etiological. Okay, morphological and etiological. So, morphological classification, I already told you: normocytic, normochromic; microcytic, hypochromic; macrocytic, normochromic. That is the three types of anemia, the morphological classification. And okay, coming on the etiological classification. Now, in etiological classification, what is the cause of the anemia? You have to learn the cause of the anemia. Okay, what is the cause of the anemia? So, the anemia can be due to three causes: number one, blood loss. Like someone is having surgery, someone is having an accident, acute blood loss, or someone is having hemorrhoids, peptic ulcer, menstruation, menorrhagia, chronic blood loss can be there. So, blood loss can lead to anemia. The two more important causes of anemia: where does the RBC produced? The RBCs are produced in the bone marrow. This is the bone marrow. This is the blood vessel. The RBCs are produced in the bone marrow from the cell, hematopoietic stem cell, which is the precursor of all cells. It gave rise to the RBC, and RBC finally formation, it comes in the blood like this. This is the RBC. RBC comes in the blood after formation. Okay, after formation in the bone marrow from the precursors, the normoblast, early, intermediate, late, right? Now, for anemia, there are two causes: either there is a problem in the bone marrow, and there is decreased production of RBC, or the production is normal, there is a problem in the peripheral blood vessel, there is increased destruction of RBC. So, these are the two main causes of the anemia. Please understand: decreased production. So, the problem is in the bone marrow, or increased destruction, the problem is in the peripheral blood vessel. What is the problem? Okay, so either there is decreased production or there is increased destruction. The two causes. The anemia due to increased destruction is known as hemolytic anemia. Hemolytic anemia. Hemolytic anemia is the anemia due to increased destruction of RBC. That's it. So, there are two main types of anemia: decreased production, increased destruction. So, what is the cause of decreased production? Now, why the production is less? The production can be less, you know, in the bone marrow. How does the production takes place? Let me tell you the precursors. So, what is erythropoiesis? How does the precursors of the RBC are there? The first cell is hematopoietic stem cell, then pronormoblast, early normoblast, intermediate normoblast, late normoblast, reticulocyte, and finally RBC is formed. After formation, it comes in the blood vessel. Okay, now in all these precursors, let me draw the precursors. These all are there. They all are there. Now, the cytoplasm contains the hemoglobin. They all have hemoglobin in the cytoplasm, and they all have nucleus. Nucleus, but nucleus is extruded at at late normoblast stage. The last reticulocyte and RBC don't have nucleus. They are non-nucleated cells. The nucleus is extruded at late normoblast stage. You got my point? So, basically, decreased production can be due to two reasons: either there is a problem in the cytoplasm, or there is a problem in the nucleus. The problem in the cytoplasm means hemoglobin is not there. Either heme is not there or globin is not there. Heme is not there, it is iron deficiency anemia, cytoplasmic anemia, anemia of chronic disease. And globin is not there, it is thalassemia or sickle cell anemia. Or else, there is a problem in the nucleus for the synthesis of nucleus, vitamin B12 and folic acid are required. It is megaloblastic anemia. Or there is a problem in the stem cell, that is aplastic anemia. So, these all are the various classifications of the anemia. You must understand. You got it? Give me a thumbs up if you got it. Give me a thumbs up. So, can we continue? Okay, so let's start hemolytic anemia. In the hemolytic anemia, I will be discussing a few more anemias. Just a second. Okay. Okay, so we will be discussing one more topic: hemolytic anemia. After that, I will end the session. The remaining RBC, few more anemias are important. Remaining and all WBCs, I mean all the leukemias, I will be discussing tomorrow along with the systemic. Tomorrow also, we are having the same session. The session tomorrow. Okay, so let me finish it now only because it is a fresh topic. If I start now and leave it in the between, and tomorrow, so there will not be a link of continuity. So, let me end the session now. Tomorrow, 9:00 AM in the morning till again 4:00 or 4:30, we will be having the session. We will be having a lunch break in between, that's it. So, we are having the session. I request all of you, don't miss tomorrow's session. Tomorrow, I will first start with systemic. In the systemic, I am going to cover 10 important systems. I have enumerated the 10 systems. You can see in tomorrow's link. So, we will start with the blood vessels, then we will move on CVS, then CNS, then, you know, one by one, we will take the systems like GIT, hepatobiliary, endocrine, and which is respiratory, musculoskeletal. So, we are going to take all these systems one by one. Tomorrow's session, the most important topics in them, not the complete systems, of course. Then blood vessels, I am going to teach you the important atherosclerosis, aneurysm, aortic dissection. In CVS, I will teach you MI, endocarditis. In CNS, I will teach you meningitis. In GIT, I will teach you gastritis. I will teach you gastric ulcer, just like the important, important topics we are going to cover in the entire systemic pathology. Right? And after that, so I will try to finish it till 2:00 o'clock. And after lunch, I will take hematology tomorrow directly. Hematology. So, the remaining anemias and WBC, I will cover it tomorrow. Will it work for you? Will it work for you? So, tomorrow, it's already today, it's already late now. So, tomorrow, we can continue. Okay, so how was the session? Can you give me the feedback? Do you find it useful? Do you find it useful? So, you want tomorrow session also? The systemic pathology? Any special request? I am going to cover the important topics on the import, entire systemic pathology according to me, whatever is important in entire systemic pathology, I will definitely cover. So, today we have covered the general. In the same way, we will cover systemic tomorrow, and hematology, we will continue. Okay, so tomorrow, sharp 9:00 AM, I will start with CVS. So, don't dare to miss it. If you miss the initial half now, you will lose the grip. Okay, so thank you so much. Thank you for being with me. Yes, it is more than enough for the FMG. If you study this much of pathology, I can guarantee all the questions in your exam will be from this section only. I will provide the notes on the Telegram group. Okay, I will provide it to the team, and the Pro CM team will share with share it with you on the Telegram channel. Okay, so the same notes I'm providing you. Thank you so much, and uh, tomorrow we will continue the session. Thank you so much. Bye-bye.

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Super Simplified Pathology by Dr Priyanka Sachdev || General Pathology & Hematology - Rapid revision

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