B/B: Reproduction, Embryogenesis, and Development MCAT Review

Hello guys and welcome to Grow Series and MCAT Review Podcasts. After a much needed break after finishing psychology and sociology, I want to go ahead and get as many episodes of bio and biochem done before I get really busy with med school again. I appreciate the support from the reviews to the emails, it means a lot and I'm glad you guys like the psychology and sociology part. As of now, I think I'm going to separate biology in biochemistry. I might focus on going over biology first then biochemistry or one episode than the other but there won't be episodes that intertwine a ton of biochemistry and biology together besides the concepts that are already naturally intertwined. So just like psychology and sociology, this podcast should not be your main source of content review. Take that from books, notes, whatever. This is more of a passive supplemental source of content. For when you're in your car on your daily commute or you're walking your dog, whatever you do, just like a passive supplemental source. So we're going to just run through concepts in your head so you can get more custom of them and you can get the score that you're aiming for come test day. Also another heads up, I'm human, I can make mistakes. If I do make a mistake, let me know via email but I do try my best to double and triple check my sources to make sure everything is correct for you guys. So in this episode, we'll be talking about reproduction, genetics and evolution. This is as you can see biology. We'll be going over topics like the cell, how baby does its baby stuff and becomes a baby and then touch on concepts like aging. Most of this episode is focused on the nitty gritty details so might be an episode you listen to a few times. So after a few months off, let's not waste any time, let's get right into it. All right, well most of this y'all have already probably gone over a thousand times through high school and undergrad, but it's all good. First thing is the cell cycle and mitosis. So each cell has 23 sets of chromosomes. We got 22 of the autosomes which are the normal body cells and the 23rd set of chromosomes are the sex chromosomes. The 2nd number is 46. So we have 46 chromosomes in a somatic cell, but the sex cells, those have 23 chromosomes. So sex cells kind of think of them as little kids. Their half is tall as a big adult body cells. Also, let's not confuse sex chromosomes with sex cells. Sex cells are the cells used to make babies. Sex chromosomes are the 23rd set of chromosomes which is xy for males and xx for females. Now the cell cycle and mitosis, the cell cycle for mitosis has four basic stages you got to know about. Four quarters of a pie. Three of those quarters are interface and as you can assume, since three fourths of stages is 75% of the stages, interface is the longest part of the cell cycle. So we have G1, S, G2 and M. The first three stages are interface. So G1, S and G2 are the interface stuff. Now a cell is chilling, wants to get that cell cycle going. They start off in that first step, which like I said is G1. Now imagine that cell goes, "Oh crap, definitely not ready to divide at this point. What would that cell do?" It would go into the G0 phase. So G0 is an offshoot of G1. The cell won't commit to the second, third and fourth step of the cell cycle, which is S, G2 and M. Without knowing, it's 100% prepared for that. It's like in who wants to be a millionaire when they settle with the money they earned or they can go further and answer more questions and risk the money they earned. The cell that chills in G0 are like, "You know, now I'm actually good. I'll say where I'm at." Also a little tidbit of information. A good way scientists can see if the interface is currently happening is that they look at the chromosomes themselves. If you can see the actual formed chromosomes that you're accustomed to seeing, then that's not interface. Interface is all less condensed chromatin. So, okay, more details about the steps themselves. G1, we call the presynthetic gap. It's the gap for synthesis. So in interface, we have a synthesis sandwich here, it goes G1, S and G2. Mytosis in the end is kind of like a dessert to the sandwich. Mytosis comes after all of it. So G1 is a presynthetic gap. Here, cells make organelles so they can make two things. Energy and protein. And with the production of both of those comes bigger size. So G1 has to pass a certain test before it can get into synthesis. And that is the restriction point. Here we make sure that everything is ready for launch into the important part. Just like people check a plane to make sure everything is ready for launch, G1 has to make sure the DNA is all correct and checks all the boxes. So G1, we have the cellular contents duplicated like basically everything but chromosomes. Chromosomes takes its own special stage and that's the synthesis stage. The synthesis stage is where the DNA gets synthesized. We replicate genetic info so that the daughter cells have a full set of chromosomes. Remember, we're talking about mytosis here. So we only want two daughter cells, not four like myosis. Anyways, yeah, so the chromosomes have two identical chromatids that are bound together at the centromere. Now, something that tripped me up all the time was the concept of ployd. What is ployd? That is the sets of chromosomes. So ployd doesn't change in s. Sure, we're doubling the DNA but the amount of chromosomes does not change. How does that make sense? We still have 46 chromosomes but 92 chromatids. See, there's tons of words here that can confuse you. So chromatin makes chromosomes. Chromatid is a duplicated chromosome that is formed after synthesis. So the amount of chromosomes stays the same. 46 chromosomes but we have double the chromatids because that is what chromatid is. It's just the duplicate chromosome but since it isn't individualized, since it's still connected to the same centromere as the original chromosome, it's not a fully mature chromosome yet. It's a little baby chromatid. So it gets a little confusing but basically think we have the same number of chromosomes but after the s stage, each chromosome has their buddy, the new chromatid that joins the squad. All right, so then we get into the last part of the synthesis sandwich, the G2 stage. So we have double the genetic material coming into G2 compared to G1 because we have 92 chromatids. But just like G1 where we had a passive checkpoint, G2 also has a checkpoint. Here we make sure there's enough organelles and cytoplasm to divide and see if DNA replication turned out okay. So G1 checkpoint, we see if the DNA is even able to replicate. G2, we see if the DNA replication turned out all right and if the organelles that we replicate in G1 also turned out all right. After all that, we got mitosis and mitosis's sidekick is cytokinesis which when mitosis is finished doing its thing splits that cytoplasm and organelles into their two daughter cells. So a good acronym for mitosis is go, Sally, go, make children. G1, go, S synthesis which is Sally, G2 which is go again, make children mitosis is make and cytokinesis is children. Go, Sally, go make children, G1, S, G2 mitosis and cytokinesis. All right, so before I go into mitosis itself, I want to emphasize the importance of these checkpoints. Now imagine we got a really weird looking cell, really wonky and then G1 and G2 checkpoints are like screw it let it pass. What might happen if these cells keep going through my toses and keep making new copies? We might get cancer. So with cancer, these weird looking cells not only have the confidence to grow through cell division, they actually increase the speed of cell division to make tumors. Not good, we don't vibe with that. So if the cancer gets crazy, it can metastasize and that's when it spreads through one of the two ways, bloodstream or the lymphatic system. That means it can spread to other organs pretty easily, which is pretty scary stuff. So how does that happen? How could a weird looking cell possibly get approved to go through the checkpoints? Well, one of the most common mutations for cancer is the mutation of the gene TP53. TP53, so what does that do? It makes P53. Well, what the heck is P53 then? Seems like a random letter in number. T53 is the star of these checkpoints in G1 and G2. So to remember, TP53, the quarantine showed us that if we're out of TP, toilet paper, we're kind of screwed, right? Well, without TP53, making P53, we're kind of screwed as well. Now we got other things too, like the cycling dependent kinases. So basically, cyclans are these things that increase or decrease in concentration, depending where the cell is at in the cell cycle. Cyclans are just proteins, right? So the kind of swing between high and low concentration, depending on where you are in the cell cycle. So these cyclans, aka cell cycle proteins, bind to the CDK to make active complexes. So the binding makes this fancy bigger machine, which phosphorylates transcription factors. So the joining of CDKs and cyclans is basically the flag that says, all right, transcription factors, you're good to go. The transcription factors then go ahead and finish the job by promoting the transcription of genes for that next stage of the cell cycle. But P53 is like the star quarterback for these checkpoints. When the star quarterback goes down, usually no matter how good the rest of the players are, the season is basically lost. All right, so we clearly talked about how important those checkpoints are and who the key players are, but we made it 75% the way through the cell cycle. You know, we got those three easy parts that make up interface. Now let's get to the big guy, mytosis. Mytosis is a process in which two identical daughter cells are made from a single cell. So interface, We got everything ready, made sure all the boxes were checked, and mytosis had the proper ingredients to do its magic. Now mytosis has to actually do it. Mytosis here only occurs in somatic cells, so those are cells that aren't used in sexual reproduction. The stuff down there uses myosis. So with mytosis, we got the four steps. Prophase, metaphase, anaphas and telephase. Then of course, you can't forget the sidekick we mentioned, sideokinesis, which is all the way at the end. The best way to remember mytosis is the mnemonic p on the mat. Prophase is p, metaphase, anaphas, telephase are the mat part. Of course, to keep this podcast pg, the p on the mat is simply the letter p, right? Definitely not talking about the other p. So you got that weirdo sidekinesis who's kind of washing some person p on the mat at the end there, and you got that prophase, metaphase, anaphas, telephase. Perfect. So prophase, first step in mytosis here, loss going on, and it's kind of the most confusing honestly. So first, we condensed that chromatin into chromosomes. Remember chromatin is just what makes up chromosomes. Don't confuse it with chromatids. Then once the chromosomes are nice and dense, the centrile pairs that makes up the centrizone splits and goes to the opposite size of the cell. Now before I get any further, you might be like, oh, centrizone, yeah, you talked about that earlier with chromosomes. No, I did not. You're wrong. Centrizomes are different from centriomers. Centriomers are merely where the chromatids are bound together with chromosomes. See what I did there? Centriomers merely. Centrizomes are an organ out that consists of centrioles. So to understand it, centrizomes have some centrioles in it. Nothing to do with centriomers. Anyways, yeah. So centrioles from the centrizone go ahead and move to the opposite sides of the cell, and their job is to make sure that DNA is correctly divided. The centrioles are anchors. They're the muscle that lets the spindle fibers tug and rip on the chromosomes later on in mitosis. So it's basically like preparing for tug-a-war. In tug-a-war, you're strongest persons in the back. They're the anchor. The centriole is the anchor here. So he or she's in the back and spindle fibers connect to that centriole and get ready to pull on that chromosome. Alright, the nuclear membrane dissolves and the protective halo the chromosome have disappears. Their exposed genetic information and the spindle fibers are about to pull. So we got one side of the spindle fibers that is attracted to the centrioles, but spindle fibers can't touch the genetic information bare-handed. They need the equivalent of oven mitts, and those are kinetic cores. Kinetic cores are protein structures that are attachment points for some spindle fibers, but they don't just sit there waiting for spindle fibers. They make their own fibers to help out. So in pro-phase, we condensed the chromatin, we had centrioles go to the opposite sides, had the spindle fibers begin forming, and then right at the end, the nuclear membrane dissolves and the genetic information is right there exposed to the world. Then we have metaphase. Here, centriole pairs are at the opposite ends of the cell, and the kinetic core fibers are finally interacting with the spindle fibers at the chromosome to really get everything aligned. This is another step of organization, getting everything straight, but like literally straight. The lining chromosomes at the metaphase plate, so the name metaphase means "after appearance", and that can kind of help you out. So in pro-phase, that nuclear membrane dissolves, and the genetic information is exposed to the world, it appears. Metaphase is post-appearance. So we got everything straightened out, we have anaphase. Anaphase is chaotic. Centromeres, the middle section of those chromosomes, split, and the sister chromatids are pulled towards opposite pulls. So remember, there were 96 chromatids after the S-phase. We're splitting those into the two opposite sides of the cell, so you can kind of see what's going on here. By the end of it, we want 46 chromatids on each side. Finally, we have telaphase and cytokinesis. Telaphase is the opposite of pro-phase. The spindle apparatus we had going on goes ahead and disappears. That nuclear membrane reforms. Nuclear lire reappeared and the chromosomes uncoyle into chromatin. Finally, the curtain closes with cytokinesis, separating cytoplasm and the organelles so that the daughter cells have sufficient supplies and everything is dandy. So boom, that's a cell cycle with mitosis, lots of action, lots of drama, riveting story. Now we got myosis. The important and obvious differentiation here is that it only occurs in germ cells, cells that make gametes. So in men, the gametes are sperm and females, they're eggs. One thing you got to know about germ cells though, they don't only do myosis. Germ cells do myosis and mitosis. Easy thing to slip on, you know, thinking somatic cells are only mitosis and germ cells are only myosis, but that is wrong. Germ cells do both mitosis and myosis. But since myosis is so unique to them, let's talk about it. So what is the difference? Well myosis makes four daughter cells, meanwhile myosis only makes two, but both mitosis and myosis have one round of replication. Myosis has two rounds of division instead of one, just like myosis. So myosis is one round of replication, two rounds of division and mitosis, the one we just went over is one round of replication and one round of division. Another difference is that mitosis wants to make two exact daughter cells. So if you got a liver cell that's undergoing mitosis, you want to have two of the exact same types of cell come out for mitosis. Myosis is different. With making babies, we want some uniqueness, some diversity, something that might help humanity evolve. So when we make our four daughter cells at the end of myosis, they aren't identical copies to the parent cells, they're all unique. So sex cells are considered N and somatic cells, aka body cells are considered 2N. So sex cells have one set of chromosomes, body cells have two. And that makes sense. If sex cells of a female and a male come together, we want a human, not something with double the amount of chromosomes and one plus one equals two. One set of chromosomes from the mom, one set of chromosomes from the dad, two sets of chromosomes for the kid, just like the body cells of you and I. So myosis one, here we have haploid daughter cells from the homologous chromosomes being separated. So we're going to skip all the interface stuff by the way, we're going to jump into the steps themselves. Now remember with mitosis, there were stages of mitosis that go P on the mat, prophase, metaphase, anaphase, and telophase, same thing with myosis. So prophase one and myosis, just like prophase and mitosis has lots of stuff going on. And some of the actions are similar, some of them are a little different. So in prophase one, chromatid condenses into chromosomes, spindle fibers form, and the nuclear membrane disappears. That's all identical to mitosis. What's unique is the concept of synapsis and crossing over. Synapsis is when homologous chromosomes come together and intertwine. So the chromosomes from the mom and the chromosomes from the dad join together and intertwine. Now if you've seen how a chromosome looks, you notice that there are two chromatids on each chromosome that are hanging together by that centromere. So we have a dad chromosome with two sister chromatids and a mom chromosome with two sister chromatids. Total that means four chromatids. That's called a tetrad. So synapsis is when the chromatids get to know each other. They touch tips, not like that, and then we get into crossing over where chromatids after that touching with each other decide to switch places. So crossing over is when chromatids break at the chiasma and switch pieces of DNA with each other. Chiasma is just a fancy way to say the point of contact between two chromatids and a homologous pair. So essentially, it's like if I shook hands with someone and we decided to just cut our hands off and switch them with each other. We both ended up with two hands, but one of our hands is kind of different. It's the other person's hand just on our body. That's good for the chromosomes because more genetic variation is great. If the chromatids can be unique, then we have a less chance of scary complications occurring because of genetic similarity. Then we get metaphase one. This is pretty similar to what happens in mitosis, but instead of the chromosomes aligning at the metaphase plate, aka the middle, we instead have the homologous pairs, aka the tetrads, align at the middle. Now since we have four chromatids on each spot, we don't have to rip the chromatid off at the middle part. That middle part being the centromere, what we ripped off in mitosis. Then anaphase one comes in. The homologous pairs are put on the opposite poles, and that separating to different poles is called disjunction. The word disjunction isn't used just in meiosis. We actually use that word in mitosis too. So disjunction is when you put the genetic information on opposite ends. Telaphase one comes in and the nuclear membrane reforms around the nucleus, and then we have two daughter cells by cytokinesis. Sometimes the cell takes a little breather at that point, and that's called intercanesis. So okay, at this point, we had the first myotic division finished, and we have two cells. Each of them have the same number of chromatids as a parent cell, because all we did was just duplicate the information like we did in mitosis, and we split them into two different cells. So this is kinda like mitosis in a way, just that we had that crossing over going on, and we had that tetrad formation where they aligned at the metaphase plate as four chromatids, and we split the genetic information in a different way. Mitosis pulls at the centromere, but here we separated the homologous chromatids. Now mitosis two, this is called chromatid separation. So mitosis one was reduction division. Mitosis two is chromatid separation. Here it's important to know in prophase two, the homologous chromatids. Dometids don't duplicate. They just separate. So we don't have that loading phase of interface again where we duplicate the information. Now here we just go right back into it and dissolve the nuclear envelope, get centrioles and migrate to the poles and get the spindle apparatus to form. Metaphase 2, same thing as before, chromatids line up at the metaphase plate, nothing too crazy. Antaphase 2, we split their chromatids at the centromere. So like my toses where we pulled at the centromere, in anaphase 2 of myosis, we split at the centromere. And remember this is happening in both of the daughter cells we made at the end of myosis 1. So essentially we're getting four daughter cells. Then telephase 2 happens with cytokinesis, the same old nuclear membrane reforming stuff happens and boom, done with myosis 2. So now that that's all over, let's get into reproductive anatomy. So moving on from the cell cycle jazz, basically what you got to know is biological sex is determined by the 23rd pair of chromosomes, which is why they're called the sex chromosomes. X, Y's male, X, X's female and the ovum for females only carries the X chromosome, but the sperm can carry X or Y. So the sperm differentiates the sex of the child. That makes sense so far. So the X chromosome, it carries a law of genetic information. If someone is hemizigus, means they only have one copy of a gene. So guess what, since males are X, Y, they're hemizigus. They got half of the X chromosomes as females who are X, X. This means that they have a higher risk for some diseases, since a disease carrying a leal can't be suppressed by having a second chromosome, which is normal. So because of that, females express sex linked disorders way less than males, but they can be a carrier because they can have a sex linked disorder that's just chilling on one X chromosome, but it isn't showing itself because they have another X chromosome that's telling the dysfunctional one to chill. The Y chromosome for males, not as cool, doesn't have much genetic information besides the sex determining region Y. We call the S, R, Y. So S, R, Y, sex determining region Y. So let's talk about males and sperm first, and then we'll get into females. So the actual anatomy of the males starts with the testes. The primary gonads develop into testes, which have two functional components. The semenifers tubules and the interstitial cells of laidic, aka the laidic cells. The testes themselves hang in the scrotum, which is the external pouch that hangs below the penis. The semenifers tubules are the sites of germination, maturation, and transportation of the sperm cells within the male testes. And the laidic cells are found next to the semenifers tubules in the testicle. They make testosterone when luteinizing hormone aka LH is present. So sperm is made in those semenifers tubules, but they get nourished by serotonly cells. So their home is the semenifers tubules, but their energy source are serotonly cells. So all right, the sperm is growing. It passes through this checkmark. We call the epididimus. And the epididimus is a place that gives the flagella motility. If you've seen a sperm before, you kind of know it has flagella. It's kind of the most distinctive aspect of the sperm. So they give the flagella motility. And after that, they're stored until ejaculation. So the sperm are kind of bored until ejaculation comes. ejaculation comes. All right. Yeah. So the sperm, they travel through the vast deference to the ejaculatory duct. And that ejaculatory duct is at the posterior end of the prostate gland. And then after that, they finally come out through the urethra. So a good mnemonic for the sperm pathway is seven up, pretty popular mnemonic. So the first letter of each part of the pathway corresponds to the mnemonic. So seven semenifers tubules, epididimus, vast deference, ejaculation tract, and then the n in seven up is nothing. And then the up part is urethra and penis. So seven up, semenifers tubules, epididimus, vast deference, ejaculation tract, nothing urethra and penis. So when sperm passes through the reproductive tract, it mixes with seminal fluid. This seminal fluid is made by the seminal vesicle, prostate gland, and the bubble urethral gland. So three components to seminal fluid. The seminal vesicle, it just makes the fructose to nourish the sperm on its journey. The seminal vesicle here is kind of like sertoli cells in the semenifers tubules, except the sertoli cells help nourish the sperm when they're being matured. And the seminal vesicle helps to nourish the sperm on their way out during ejaculation. The prostate gland plus the seminal vesicle help give sperm alkaline properties. Then finally, the bubble urethral gland makes this clear viscous fluid that cleans out the track before the sperm. Cleanse out any remnants of urine and gives it some lubrication. Kind of weird, but if you've ever seen the sport of curling, the people who brush the ice in front of the stone reminds me of the bubble urethral gland, lubricating and cleaning on the journey. So semen is the end component of sperm and seminal fluid. And the seminal fluid is made by the seminal vesicle, the prostate gland, and finally, the bubble urethral gland. All right, so we talked about the journey of the sperm. Let's talk about the sperm itself. Spirum are made from meiosis as we discussed. Jerm cells make sperm, and that occurs in the semenifers tubules. So let's go through meiosis and talk about the wording of the sperm at each step, because for some reason they decided to throw a ton of vogue about you about sperm. So spermatogonia are the diploid cells and males, and through mitosis they make diploid primary spermatocytes. Then after meiosis one, we get secondary spermatocytes. Then after meiosis two, we get spermatids. And remember at the end of meiosis two, they're haploid. So spermatids with time become spermatuzowa. So spermatogonia is gonna become sperm gonia gunna. I don't know, that's a stretch, but you can kind of connect that spermatogonia is early and it's diploid. And remember that germ cells can undergo mitosis and meiosis. So after mitosis, they become spermatocytes. And we know with mitosis that it produces identical daughter cells. So that means the daughter cells are also diploid. So these daughter cells are called diploid primary spermatocytes. Then after that we do meiosis. The first division occurs and we get some secondary spermatocytes. And then meiosis two occurs and we get spermatids, which are haploid. Finally the spermatids with time become spermatuzowa. So essentially the word spermatogonia is before mitosis and meiosis. Spirmatocytes is during mitosis and meiosis. Spirmatids is after mitosis and meiosis. And with time spermatids become spermatuzowa. A good mnemonic to remember this is gonna see the zoo, but the sea is the letter C. So let's take the different sperm wardings we have here. Spirmatogonia, spermatocytes, spermatid, and spermatuzowa. Now let's notice that the first half is always the same, right? It always starts with sperma, but the second half is different. So the first phase is gonia, spermatogonia. And that corresponds with gunna and the mnemonic gunna see the zoo. The second word is site, spermatocyte. So that corresponds to the sea, gunna see the zoo, spermatocyte. Third word is tib, spermatid. So that's the part of the mnemonic gunna see the zoo. And the last part is zowa, spermatuzowa, that corresponds with zoo. So if you break this down, gunna see the zoo, spermatogonia, spermatocyte, spermatid, spermatuzowa, you're golden. The actual anatomy of sperm includes the head, which has the genetic information. And in acrozone cap that's needed to penetrate the ovum. Then we have the mid-piece that's filled with mitochondria used to make ATP from the fructose. Remember the seminal vesicle gives the sperm fructose on its journey. And finally we have the flagellum, which is used for movement. Alright, so we're all down with males. Let's get into females. The female reproduction tract has all the organs inside. The gonads are known as ovaries, and those make both estrogen and progesterone. Only one egg is ovulated per month, and the immature ova is surrounded by these follicles that are there to nourish them and protect them. The uterus is the site of the fetal development, and the lower end is a cervix, and it's connected to the vaginal canal. Finally, the vulva is the external female anatomy. So with oogenesis, aka the production of female gametes, it's a lot of moving parts, and there are a set amount of ogonia a woman has. That's made during the fetal development of a girl. So by the time a girl is born, all their ogonia has undergone DNA replication, and they're considered primary oocytes. They're all deployed, and they all stay in that prophase-one section. Remember, prophase-one of myosis is when the homologous chromosomes get to know each other, crossing over-happens, all that fun, unique myosis stuff. So primary oocytes stay all throughout primary school. That's a good way to remember the timing. Secondary oocytes come at the first menstrual cycle. At that point, one at a time, the primary oocytes complete myosis-one, make a secondary oocyte and a polar body. So remember, myosis-one makes two daughter cells. In this case, one cell is a secondary oocyte, and the other cell is a polar body. In myosis, we aren't trying to get identical daughter cells like mitosis, so having two different daughter cells here makes sense. The difference between a polar body and the secondary OSI is the amount of cytoplasm. The polar body gets almost no cytoplasm but the secondary OSI gets plenty. So with all that real estate that the secondary OSI has, it has way more space to divide and so it will. Meanwhile the polar body will not. The secondary OSI goes ahead, does pro phase 2 and then it gets stuck in metaphase 2. So if you remember metaphase 2, the chromatids are all lined up at that metaphase plate. If fertilization happens, we advance if not, it gets disintegrated and released in menstruation. So OSI's are surrounded by two layers. First layer is the zona pelicita. It surrounds the OSI itself and the zona pelicita is just a mix of glycoproteins for protection and sperm binding. Then outside of that we have the corona radiata, which is outside the zona pelicita and the sperm break down this layer with these enzymes in their acryzome, which if you remember the acryzome is a part of the head region of the sperm. Alright, so let's say it's a couple lucky day and the secondary OSI does get fertilized. The sperm goes through both of these layers, the corona radiata and the zona pelicita and then the secondary OSI breaks down into yet another polar body. Plus the big ol mature ovum. The mature ovum is thick with two C's. It's that big because it has to give all of its organelles, cytoplasm and physical space for the zygote, as well as half of the DNA and RNA that the zygote needs. The sperm kind of just chills there and gives the other half. So we finally say myosis two finishes when the haploid sperm and the ovum nuclei join together and we get that diploid zygote. Okay, so before we get deeper into the craziness that happens once that zygote is made, let's talk about sexual development. So when we're little kids, the hypothalamus restricts the production of gonatotropin releasing hormones aka GNRH. It tells that GNRH chill before puberty. Once the gonatotropin releasing hormones starts pumping after puberty, we get the anterior pituitary gland in the brain to make and release two hormones, the follicle stimulating hormone and the luteinizing hormone. Those two hormones are key factors for sexual development. So basically post puberty, GNRH, gonatotropin releasing hormone, makes LH, luteinizing hormone and FSH, follicle stimulating hormone. With males, we have that fancy Y chromosome which makes us produce antigens when we're in the fetus. But, antigen production is low during childhood. Just ahead's up, antigens are basically just male sex hormones. So testosterone, that's an antigen. And so the two hormones that GNRH release hormone produces which are a follicle stimulating hormone and b, luteinizing hormone, those go ahead and they produce mature sperm and produce testosterone. So FSH, it makes sirtoly cells mature this sperm and LH makes the lady cells make testosterone. Females, they also get some changes because of FSH and LH. Estrogen is made as a response to FSH. It develops and maintains the female reproductive system. So in the embryo, it stimulates the development of the reproductive tract and in adults, it thickens the lining of the uterus in what's called the endometrium. It does that each month when it prepares for the zygote. Estrogen, that's secreted by the corpus luteum initially. The corpus luteum is the remnant of the follicle that stays after ovulation. So progesterone is controlled by luteinizing hormone, aka LH. This is also important for the development and maintenance of the endometrium but not the creation of the endometrium. So estrogen is used for the creation of endometrium. Progesterone is used for the development and maintenance of it. When we get later in the first trimestery, we switch the source of progesterone from the corpus luteum to the placenta. So basically, FSH makes estrogen. Estrogen thickens the endometrium every month in preparation for the zygote and LH makes progesterone. That helps maintain the endometrium but it doesn't make the endometrium like estrogen does. Alright so the menstrual cycle. There's basically three stages to start and if fertilization occurs, we go down the pregnancy path. If it doesn't, we go down the menstruation path. The first stage is the follicular stage. This starts when the menstrual flow starts. Mensural flow is the shedding of the uterine lining aka the endometrium. So essentially gonadotropin releasing hormone, GNRH that we talked about is secreted from the hypothalamus when a woman has decreased concentrations of estrogen and progesterone. So GNRH, it makes the luteinizing hormone and the follicle stimulating hormone and those to make progesterone and estrogen respectively. So when estrogen and progesterone are low, which happens at the end of a menstrual cycle, the body goes out crap, let's get these up again. So gonadotropin releasing hormone increases that FSH, which starts working together to make several ovarian follicles. When the ovarian follicles are made, they start making estrogen themselves. So when the parts downstairs start doing their thing, the part upstairs can go ahead and shale out for the rest of the time. Gnato-Tropin releasing hormone relaxes and the LH and FSH from the anterior pituitary in your brain starts to level off, not decline but level off. The estrogen from these follicles then re-grows the endometrial lining by vascularization and glanduralization. It basically increases the blood flow and starts rebuilding what was lost with menstruation. So the follicular phase starts with the help of GNRH in the brain, but then the star of this phase is unsurprisingly the ovarian follicles. Follicular phase. After that we have ovulation. Abulation is actually late in the follicular phase. The follicle secrete really high concentrations of estrogen at this point and that hits a threshold which spikes the upstairs hormones. Gnato-Tropin releasing hormone, follicle stimulating hormone and luteinizing hormone. The important hormone for ovulation is the luteinizing hormone. The spike in LH makes ovulation occur. The ovum sees that spike and it jumps out of the ovary and gets into the peritonial cavity. So then we get into this third part here and that's the luteal phase. We mentioned the corpus luteum before. It's the remnant follicle that remains after ovulation. LH is the reason the corpus luteum is made from those remnant follicles. That corpus luteum's main role is to secrete progesterone and the progesterone levels increase while estrogen is still super high. So progesterone is high and that tells upstairs hormones, GNRH, LH and FSAs to chill and not accidentally ovulate multiple eggs. We just want one at this time. So at this point the three phases are done. Radar crossroads depending on if fertilization occurs or not. Now the menstrual cycle is confusing. There's lots of different hormones going up and down so it's hard to get a good grasp on it. I'll go over it one more time but I highly suggest looking at a diagram as well. So in fast forward the follicular phase starts when the endometrium starts shedding. The gonadotropin releasing hormone from the hypothalamus causes a spike in estrogen and progesterone and this causes two things. The regrowth of the endometrial lining as well as the development of ovarian follicles. The development of the follicles causes gonadotropin releasing hormone, luteinizing hormone, and follicle stimulating hormone to chill and level off. Then at the end of the follicular phase we have ovulation. Here follicles that we made in the follicular phase start working independently. They start secreating estrogen themselves and that causes a spike in the upstairs hormones. The gonadotropin releasing hormone, luteinizing hormone, and follicle stimulating hormone. The spike in LH, luteinizing hormone, makes the ovum release from the ovary. So at this point we went from GNRH in the brain releasing FSH and LH which produced in ovarian follicle which makes estrogen which spikes LH which causes ovulation. Pretty confusing. Finally after ovulation we get the luteal phase. The spike in LH causes the production of the corpus luteum which increases progesterone. Progesterone crashes the party and makes gonadotropin releasing hormone, luteinizing hormone, and follicle stimulating hormone to chill out so we don't get multiple eggs ovulated. Alright so we went from GNRH in the brain releasing follicle stimulating hormone and luteinizing hormone which produced in ovarian follicle which makes estrogen. And spikes that luteinizing hormone which causes ovulation. Then that spike in luteinizing hormone causes the corpus luteum to come out and make progesterone. That progesterone from the corpus luteum then tells the gonadotropin releasing hormone, luteinizing hormone, and follicle stimulating hormones to go back home. So GNRH makes FSH and LH, FSH and LH makes estrogen, estrogen makes LH, LH makes progesterone, dcreses GNRH, LH and FSH. Wow alright so finally we come to the crossroads of menstruation and pregnancy. Submanceration is when implantation does not occur. The corpus luteum which remember was made from the ruptured follicle, that starts losing stimulation. That loss of stimulation then lowers the progesterone levels and the uterine lining is shed off. And at this point you can see how the cyclore repeats. The GNRH says, "Oh snap, the progesterone that kicked us out is leaving, let's go back in." If pregnancy does occur we get a new hormone invited to the party. As I go develops into a blastocyst that implants into the endometrium and secrete human chorionic gonadotropin or HCG. This human-chorionic gonadotropin is basically the same thing as LH, and remember LH was used to develop the corpus luteum to make progesterone. So the HCG is basically LH's twin and tells everyone downstairs that the party isn't over, and the corpus luteum makes sure the endometrium doesn't shed by making estrogen and progesterone. And some pregnancy tests use HCG to see if you're pregnant, since that hormone is only present after implantation, if HCG is detected then you got a fun nine months ahead of you. Alright, so then we have menstruation. As you age your ovaries become less sensitive to luteinizing hormone and follicle stimulating hormone. They don't get as excited when the upstairs neighbor has come downstairs, and that causes ovarian atrophy or ovarian degeneration. And the endometrium starts to atrophy as the estrogen and progesterone starts to drop. Menopause then means that there is high LH and FSH in the blood, but the ovaries aren't really vibing with it. So that's that, but let's get a little deeper on pregnancy and embryogenesis and then we'll call this episode a wrap. So fertilization occurs in the fallopian tube, and the OSI can be fertilized for up to 24 hours. You got that 24 hour window for fertilization, and if you miss it, then it's mission failed, or mission succeeded I guess it kind of depends on if you want a baby or not. So the fallopian tube has three parts, and the second part which is also the longest is the ampula. The ampula dilates, and that's where fertilization is most likely to occur. So the sperm meets a secondary OSI in the ampula, says what's up, and then releases acrozoamal enzymes. These enzymes help the sperm penetrate those two layers we talked about earlier, the corona radiata and the zona pelocita. So when the sperm penetrates the cell membrane, we get what's called a cortical reaction. That's an influx in calcium ions. So when you hear cortical, think calcium. Calcium goes ahead and depolarizes the membrane and increases the metabolic rate of the zygote that just formed. The zygote is a diploid cell made from the fusion of two haploid gametes, the sperm and the secondary OSI. Once that reaction happens, the cell membrane of the egg is impossible to penetrate. It's called the fertilization membrane. It's kind of like a halo field. It's depolarized and no other sperm can crash the party. Now if you think about twins, you know, those can also occur at this stage. If it's fraternal twins, aka dyes, I got it, then two different eggs are fertilized by two different sperm. If you're an identical twin or monozygotic, then it's a single zygote that splits into two. So fraternal twins is two different eggs getting fertilized, and identical twins is the same egg that gets fertilized splitting into two when it's a zygote. Now the scar with identical twins is conjoined twins. So if that zygote split isn't complete, then they could possibly grow as conjoined twins. The number one thing to know here is that no variation of twins has two sperm going for one egg. That's impossible due to the cortical reaction. So the zygote at this point is moving down from the floping tube to the uterus, and as it does, it starts to really rapidly divide. A zygote is a single celled organism. When it starts to divide, it's classified as an embryo. So this embryo keeps getting more cells, but the actual size doesn't change. Instead, there are just more cells in that area. So let's imagine a box that we throw a ping pong ball in. With more ping pong balls that we throw in, the box isn't getting bigger, but the amount of ping pong balls in that box increases. So each ball is a cell, and with increased ping pong balls in that box, there's more surface area. If I throw water in the box, the water can cover more surfaces of the ping pong balls. Then if there were just one ball in the box. So surface area increases, box size stays the same. So volume is constant, and therefore we can conclude that the nuclear decidoplasm ratio and the surface area to volume ratio are both getting higher and higher. That's important because there's more area for nutrient and gas exchange. Then we get to blastulation. So after enough ping pong balls gets placed in that box, it becomes pretty dense, almost like a solid mass. That's known as a morola. So we went over fertilization with psychology and sociology back in the earlier episodes, and I think I did a pretty good job there. So I'm just going to go ahead and hit the trusty old copy and paste real fast and run through that again. So the cells start dividing in that zone of pellicita until you have 32 cells. We call these 32 cells the morola. A good way to remember that the morola is a product of cell division to go from one to 32 cells. Think of morola being a product of more cell divisions. The morola is important because this is what then differentiates into the trophoblasts and the embryoblasts. The trophoblasts is on the outside and it makes the placenta and nourishes the baby later on. But the embryoblast is the VIP because of embryoblast helps form the fetus. Alright, so that embryoblast, right? That does a bit more. It's involved in blastulation. So the embryoblast gets a little tighter and makes two things. In inner cell mass and a hollow cavity, we call the blastosial. So you might be wondering why it's called blastylation and where blastosial comes from. They're both Greek. So the intercell mass is the fun part that hangs around on one side while the hollow cavity hangs around on the other side of the zygote. The intercell mass makes three layers, the amniotic cavity, the epiblasts and the hypoblasts. The amniotic cavity is a hollow cavity. So the inner cell mass is the fun part that hangs around on one side while the hollow cavity hangs around on the other side of the zygote. The inner cell mass makes three layers, the amniotic cavity, the epiblasts and the hypoblasts. The amniotic cavities at the top, the epiblasts are at the middle, which is the layer over the hypoblasts just like A is before the letter E and the letter E's before the letter H. So we have the amniotic cavity, the epiblasts and the hypoblasts. So in summary with blastylation, the morala's embryoblasts makes an inner cell mass and a hollow cavity called a blastosial. And then the inner cell splits even further into the amniotic cavity at the top, the epiblasts in the middle and the hypoblasts on the bottom, kind of an alphabetical order from top to bottom. So after blastylation, there's implantation, but during implantation two stages occur, gas relation and neuralation. So after blastylation, we have gas relation. Now you might be wondering where the word gas relation came from, well, gas row means stomach because originally they thought this stage was just about the formation of the gut, but it's actually more about the formation of the trilaminer embryo, which is basically the three germ layers. The germ layers are the ectoderm on the top, the mesoderm in the middle, and the endoderm on the bottom. To remember what is where, just know the ectoderm is the only one with the letter T in it. So it makes sense that this germ layer is on the top. The mesoderm starts with the letter M, so it's in the middle, and the endoderm you can kind of fill in the rest, you know it's on the bottom. Finally, there's neuralation where the core in the mesoderm becomes a nodal cord. And a great nomonic for this is my baby grows nicely. So the first letter of each word corresponds to a phase. My is for morla, baby is for blasula, grows for gastrola nicely for a neuralation. So morla, blasula, gastrola, and neuralation, my baby grows nicely. All right, so back to the implantation, that's when the endometrium beefs up while the zona pelucita of the zygote starts breaking down. They're getting ready to land on the endometrium and form a connection so they can hit the next phase of growth. Now remember earlier we talked about the trophoblasts, how the morla splits into a trophoblasts and an embryoblasts, while we put a lot of attention on the embryoblasts, but an implantation, the trophoblasts really shines. It makes a few transformations and then it's able to fuse blood vessels with the endometrium to become the bridge between mother and child, transporting nutrients and waste. This whole web of blood vessels that the trophoblast formed is called the placenta. So at this point in psychology and sociology, we stopped, but let's get a bit more in the weeds for now. All right, so that whole placenta is being made and the zygote is forming roots in the endometrium. But while that's happening, the gas relation stage is happening simultaneously. Remember we said the layers of gas relation are the ectoderm, which is on the top, the mesoderm which is on the middle, and the endoderm which is in the bottom. The ectoderm makes all the quote-unquote outer stuff like the outer layers of your skin and sweat glands paired with the nervous system. Both central and peripheral nervous systems. The mesoderm makes the inner layers of the skin, it makes the muscles, the bones, kidneys, bladder, and sexual organs. The endoderm lastly makes things that have to do with digestion and the lungs, so that means the endoderm makes the GI tract, the liver, the pancreas, and the lungs. So all right, fast forward a bit and we're at the fetus stage. With the fetus, the placenta is where it's at. It's a place where nutrient, gas, and waste exchange occur between the fetus and the mother. Diffusion runs along the oxygen gradient and the fetal hemoglobin has a higher affinity to oxygen than adult hemoglobin. So the placenta is also homie because it gives you immune protection. Antibodies they cross over in order to protect the fetus from exposure to stuff in utero. In utero just means in the uterus but it's also a nirvana album, not sure what you can do with that information, but yeah. So there's two ways of transmission. There's the umbilical arteries and the umbilical veins. Now in a normal adult, arteries go away from the heart, which means it carries that rich oxygenated blood. Artery equals away. But in the fetus, we flip it. Umbilical arteries carry blood away from the fetus. Yeah. So artery always does equal away. But the fetus at this point isn't pumping its own oxygen. oxygenated blood. The lungs in the liver don't serve important functions for their fetus until birth. So at this point, the fetus is using up that oxygen and nutrients. So umbilical arteries actually are carrying away used blood to the placenta. And the umbilical veins carry fresh blood with oxygen and nutrients towards the fetus from the placenta. There's three shunts you need to know about. Shunts are used to actively draw blood away from the organs and a fetus that aren't used when the blood pressure gets too high. So the three shunts are the foramen ovale, the ductus arteriosus and the ductus venus. But good news, these are pretty low yield terms. I'd rather you spend time looking up other things and memorizing what these shunts do. Just know that the fetus has three shunts and shunts are used to actively direct the blood away from certain organs like the liver and the heart. So at this point, you need to know the three trimesters. But that's also not incredibly high yield. Major organs develop in the first trimester. The second trimester is known for tremendous amounts of growth and a more human appearance. And the third trimester is also known for more growth and more brain development until the end where the growth rate slows down. The third trimester is known for the amount of antibodies that are also transported. So with birth, it's done by rhythmic movements of the smooth uterine lining, which is controlled by prostate glandins and the peptide hormone known as oxytocin. There's positive feedback with oxytocin during birth. So there's a uterine contraction and then a bigger one because of the last, it gets bigger and bigger and bigger and bigger. Oxytocin has positive feedback. All right, let's get into cell specialization, which is the last part here, but it's an important part of development. Let's talk about differentiation. So differentiation occurs after determination and includes changing the structure, function, and biochemistry of the cell to match that cell type. Stem cells are cells that haven't differentiated. They're still free. And there's different types of stem cells varying in their freedom and what they can become. So totipotent cells have the greatest potency and they include embryonic stem cells. They can literally differentiate into any cell type. Totipotent cells are totally free. Pluripotent cells are pretty free. They can differentiate into anything, but those found in the placental structures. And then multi potent, they're free, but they can only differentiate into the certain types of cells within a group. So the bone marrow of an adult has multi potent cells. They're great. They can turn into whatever type of blood cells they want, but they're restricted to only being blood cells, nothing else. Then we have cell to cell communication. There are autocrine signals. Those are signals that act on the same cell that secreted it in the first place. It releases it, then grabs its own signal. Parachrine signals act in that local area. Juxocrine signals aren't diffused. They're like a cell directly stimulating receptors of an adjacent cell. Thing, Juxocrine equals just in, because Juxocrine signals are just in a certain specified cell. And then finally endocrine signals. Those are involved in the secretion of hormones through the bloodstream. So that's like really traveling, you know? And then a few other terms, cell migration, cell death, regeneration, cell migration is when a cell can disconnect and migrate to the right location. Cell death is known as apoptosis, and it's needed at certain stages of development. But necrosis, that's when a cell dies because of injury and internal substances are leaked. Finally, regeneration is how well you can regrow certain parts of your body. Humans have incomplete regeneration. If you cut your arm off, you're not growing it back. But salamanders, on the other hand, have some of the highest regenerative capacities. They can fully regrow limbs when needed. Complete regeneration like that requires stem cells to migrate to the right part of the body and start that regrowth. So finally, in that category of stuff, we have senescence and aging. Senescence is like the biological aging. With cells, that is like their inability to divide normally after 50 divisions. But that might just be due to short and telemiers. Telemiers are the caps on the ends of chromosomes, and they help the DNA from unraveling. But every time we synthesize DNA as we undergo mitosis, the caps get a little shorter. There's an enzyme, though, called telomerase that can make new ends of the chromosomes. And that's actually part of the reason why cancer cells not only survive, but they flourish and they replicate so well in this human body. All right, so at this point, we are done with the content for the episode. Interesting topics on this episode, but they're definitely pretty far in the weeds. Lots of small things to remember. So go over this podcast a few times, check it out in a book, whatever you do. If you're listening on Apple Podcast app, I would love if you could rate or review this. If you're listening at all at this point, please follow for more MCAT content or subscribe, I guess the wording just depends on what app you're using. As I've been doing lately, I'll give a high yield summary of concepts that I personally found important here. So we started off talking about the cell cycle and mitosis. With the cell cycle, there are four stages you have to know about, G1, S, G2, and M. The first three are interface, so G1, S, and G2 are the interface stuff. Along with that, we learned a good way to see if interface is happening is they look at the chromosomes. If there are visibly formed chromosomes, then it's not interface. And a quick demonic for mitosis is go-saly-go make children, G1, S, G2, mitosis, cytokinesis. During G1, the cells make organelles and basically make two things, energy and protein. There's a check at G1 to see if we can replicate and at the end of it, we basically have all cellular contents besides the chromosomes duplicated. During synthesis, DNA gets synthesized. We replicate genetic information, the 46 chromosomes gets duplicated. And at the end of synthesis, there are still 46 chromosomes, but they're in this X shape. G2 happens and it basically checks the C of replication turned out okay, looking at both chromosomes and organelles. The checkpoints are necessary and we learned about an important protein called P53, which is the guardian of the genome. Then we got the big boy, the last stage of the cell cycle, which is mitosis. The demonic we use for mitosis is P on the mat, prophase, metaphase, anaphase and telephase. Prophase, we condense the chromatin into chromosomes, the nuclear membrane dissolves and spindle fibers start reaching for that genetic material. Metaphase aligns the chromosomes to the equator and the spindle fibers attached to the sister chromatids. In anaphase, the chromatids separate after the centromere splits, the spindle fibers shore in and pull the chromosome to opposite poles of the cell and the chromatids are now considered as separate chromosomes. Lastly, in telephase, the chromosomes unwind into chromatin, the nuclear membrane reforms, the nucleolus reappears and the centrials and spindle fibers disappear. So that's everything for mitosis. We talked about meiosis as well and how it's pretty similar. Know that germ cells can do both mitosis and meiosis and that meiosis makes four daughter cells with two rounds of division and mitosis makes two daughter cells with one round of division. Mytosis and meiosis both have one round of replication though. The unique concepts of meiosis start with prophase I where we have crossing over and the concept of synapses which is when homologous chromosomes come together and intertwine. In metaphase I of meiosis, homologous pairs aka the tetrads align at the middle. Anaphase I and telephase I happens and sometimes the cell chills in the stage called intercanesis. Meiosis I is called reduction division. Meiosis II is called chromatid separation. The important part of meiosis II to know is that in prophase II, the homologous chromatids don't duplicate they just separate. After that, we moved on to the reproductive anatomy. We learned that males are more likely to express sex linked disorders because they're hemisigus. They have one X chromosome and one Y chromosome. This makes females more likely to be carriers and men more likely to actually suffer from those sex linked disorders. With males, we also learned about seven up, the sperm pathway. Seminiferous tubules, epididymus, vast deference, ejaculation tract, the end stands for nothing, urethra and penis, seven up. The seminiferous tubules are the site of germination, maturation and transportation of the sperm cells within the male testes. Lating cells are found next to the seminiferous tubules in the testicle. They make testosterone with luteinizing hormone is present. Along with that, we learned that the seminofluid is made by the seminovestical, the prostate gland, and the bulboyurethral gland. The seminovestical here is kind of like serotonly cells in the seminiferous tubules, except these serotonly cells help nurse the sperm when they're being matured, and the seminovestical helps nurse the sperm on their way out during ejaculation. The prostate gland and the seminovestical help give sperm alkaline, which is basic properties. Finally, the bulboyurethral gland makes this clear, viscous fluid that cleans out the track before the sperm. We also talked about the wording of sperm and the best way to remember that is the mnemonic gonna see the zoo, the sea being the letter C here. So, spermatagonia, spermatocyte, spermatid, and spermatizoe are the four stages. The first half of every stage starts with the word spermo, so let's ignore that. The second half of the phrase is what we're focusing on. The first stage is gonia, you know, spermatagonia, so that corresponds to the gunna in the mnemonic. The second word is site, spermatocyte, so that corresponds to the sea. Remember their letter C, spermatocyte, there you go. Third word is tid, spermatid, so that's the part of the mnemonic gonna see the zoo, and the last part is zoa, spermatizoe, and that corresponds with zoo. So if you break that down, gonna see you next time. see the zoo, spermatic gonia, spermatic site, spermatid, and spermatizoa, you're good. If you look at the sperm itself, the head has all the genetic information and an acrozone cap that's needed to penetrate the ovum. The mid piece is filled with mitochondria to make ATP from the fructose, and finally we have the flagellum which is used for movement. We went pretty in depth with females and I won't lie this part is confusing because there's so many hormones moving up and down. When a female is born, all their oagonia have undergone DNA replication and they're considered primary oesites. They're all deployed and they all stay in that prophase one section. Remember prophase one of myosis is where the homologous chromosomes get to know each other, crossing over happens, all that fun, unique myosis stuff. So primary oesites stay all throughout primary school. Secondary oesites come at the first menstrual cycle at that point one at a time. Primary oesites complete myosis one, make a secondary oesite and a polar body. So to remember myosis one makes two daughter cells. In this case one cell is a secondary oesite, the other is a polar body. The difference between the polar body and the secondary oesite is the amount of cytoplasm. The polar body gets almost no cytoplasm, but the secondary oesite gets plenty. The secondary oesite goes ahead and does prophase two and then it gets stuck in the metaphase two. So if you remember metaphase two, the chromatids line up at the metaphase plate. If fertilization happens, we advance if not, then it's disintegrated and released in menstruation. The oesite itself has two layers, the zona polucida and the corona radiata. The zona pellucida is the closest to the oesite. The corona radiata is on the outside of the zona pellucida. Then we got into the hormones and that's something I highly suggest looking at diagrams for. When we're little kids, the hypothalamus restricts the production of gonadotropin releasing hormone, aka GNRH. The hypothalamus tells that GNRH to chill before puberty and once that hormone starts pumping after puberty, we get the anterior pituitary gland in the brain to make and release two hormones, the follicle stimulating hormone and the luteinizing hormone. We learn about the interaction of FSH, LH, estrogen and progesterone and females. Basically, FSH makes estrogen, estrogen thickens the endometrium every month in preparation for the zygote and LH makes progesterone and that helps maintain the endometrium but it doesn't make the endometrium like estrogen does. With a menstrual cycle, there are three stages. First is the follicular stage. Second is ovulation and lastly is the luteal stage. The follicular stage is where menstrual flow is going on and let's just think about this logically what is menstrual flow. It's a shedding of the endometrium lining right? So what happens when that gets shed? We want to remake it. So that's basically what the female body does every month. There's no baby, we restart the process and it goes on over and over again. So that shedding of the endometrium is going on and that gets our FSH and LH up which gets to making ovarian follicles. Hence why this stage is called the follicular stage. Ovarian follicles start making estrogen themselves and start re-growing the endometrial lining. So ovulation that's just later in the follicular stage. The follicles are pumping that estrogen like crazy at this point. So much so that it hits a threshold and the brain goes you know that's it let's spike the FSH and LH. So ovulation is a crazy time because everything is going up. The ovum sees all the hormone spiking and goes yo this is crazy I'm out of here. Leaves the ovary and gets in the peritoneal cavity. The luteal phase is like the chill out phase. The body just went in crazy mode and now we got a comet down. So here the follicles realize the OSI is gone and folds into itself making the corpus luteum. This structure starts releasing progesterone along with small amounts of estrogen. This combination of hormones maintains the thickened lining of the uterus waiting for a fertilized egg to stick to it. If we get that successful implantation of a fertilized egg we start pumping in hormones to maintain the corpus luteum and the corpus luteum again is basically a rehash version of the ovarian follicle. These are the hormones we pump include human corionic gonadotropin and fun fact pregnancy tests are looking for this hormone. Human corionic gonadotropin because if you do have it then it has some mean and egg was implanted successfully. The corpus luteum keeps producing the raised levels of progesterone that are needed to maintain that thickened lining of uterus. On the other hand if we don't get an implanted fertilized egg the corpus luteum withers and dies and that causes this huge drop in progesterone levels causing the lining of the uterus to fall away and we know that as menstruation. Now before we summarize fertilization and pregnancy let's talk about menopause. With aging your ovaries become less sensitive to luteinizing hormone and follicle stimulating hormone they don't get as excited when the upset neighbors come downstairs and that causes ovarian atrophy which is ovarian degeneration. The endometrium starts at atrophy as the estrogen and the progesterone start to drop. So how do we see if there's menopause? If we have high levels of LH and FSH in the blood but ovaries are like no I'm good. With fertilization we talked about how the ampula of the phylopean tubes is where the fertilization is most likely to occur. We also talked about what sperm do when they meet up with the egg. They shake hands then cause a cortical reaction that's like an influx in calcium ions and I could actually see a test question like that you know like which ion is increased during fertilization and it would be calcium. Calcium goes crazy depolarizes the combined zygote that we just made. That's like a halo shield that stops other sperm from crashing the party. Anyways the zygote starts moving down the phylopean tube and divides like crazy at which point we call it an embryo. The embryo has a higher surface area but the same volume and there's more area for nutrient and gas exchange. Then we went over a blastulation just a heads up the morala is made of a tropha blast and an embryo blast. So in summary with blastulation the morala's embryo blast makes an inner cell mass and a hollow cavity called the blastocel. And then the inner cells splits even further into the amniotic cavity at the top the epi blast in the middle and the hypoblast on the bottom in alphabetical order from top to bottom. We have gas relation and neuralation gas relation is the formation of the three germ layers and neuralation is the formation of the nodocord. A great numonic for this is my baby grows nicely. My for morla baby for blastula grows for gastrola nicely for a neuralation. So morla blastula gastrola neuralation my baby grows nicely. The other part of the morla which we've been ignoring so far the tropha blast I mentioned that does its job during implantation. It becomes the bridge between the mother and the child aka the tropha blast is the placenta. So fast forward a bit we get to the fetus stage. The placenta is really the MVP here because it does all the heavy lifting immune protection nutrient exchange, waste exchange, all that. Just a heads up the umbilical arteries and veins arteries usually carry blood away from the heart to the rest of the body but umbilical arteries carry blood away from the fetus. It carries used up blood to the placenta and the umbilical veins carry fresh oxygenated blood from the placenta to the fetus. We talked about birth with birth we have positive feedback, oxytocin increases and increases causing bigger and bigger contractions and I'll conclude this summary with totipotent pluripotent and multipotent. Totipotent has total freedom, pluripotent is pretty free and multipotent is just kind of free. So the bone marrow of an adult has multipotent cells. So that's it, thank you guys for listening. It's been a long time since I've done this but I appreciate all the support. I'll try my best to keep blasting these out but of course with med school it gets a little tough with the timing and all that. But yeah good luck on your MCAT whenever you guys are taking it and I'll see you guys on the next episode. [BLANK_AUDIO]