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Hi guys. Can you hear me? Hello? Ok, perfect. So sorry about all of these um technical difficulties we've been having. Um It's been a bit stressful, but hopefully we should be all fine now. Um So just give me one second. I've got my friend who's going to be doing the slides for us today. Um But yeah, so we'll get started in about a minute or so. Ok, so, hi guys, I'm Shreya. Um I'm one of the third years and today I'm going to be talking to you about um disorders of pregnancy and parturition and the biology of aging. So you can see my email is there. So if you have any questions about the session at all, please do email me. Um We're here to help. Ok, so can we go to the next slide, please? Thank you. Uh So, so these are some of the Tylo's we'll be covering today. Um And next slide my shot. Thank you. Um So yeah, we'll be covering fetal growth and placentation pathophysiology, um preeclampsia. We'll be covering small gestational age, uh intrauterine growth restriction and some stuff on the biology of aging. Next slide. Thank you. So, basically, um there are two stages of nutrition for the fetus. Uh Histiophryne histiotypic nutrition basically starts um in the first trimester. And it's when the fetus takes nutrition from the uterine gland secretions and the breakdown of endometrial tissue. And um this is appropriate because there's not much fetal demand on the mother at this point. However, when we get to the start of the second trimester, so around week 13, the fetus has a higher demand. So then it begins to de depend on the maternal blood supply directly through a hemochorial type placenta. And by hemochorial will basically mean a placenta which has direct contact with the maternal blood and the fetal membranes. And this is done via the chorionic villi. Next slide. So yeah. So the first trimester, the nutrition that's used by the placenta is hist atrophic, which as we said is appropriate because of the low fetal demand on the placenta. And it's mainly dependent on two processes. So, the breakdown of endometrial tissue and uterine gland secretions and the two major cell populations which are involved in his terrific nutrition are the cytotrophoblast and the syncytiotrophoblasts, which you can see in the diagram here. And so the cytotrophoblast essentially break down into the syncytiotrophoblasts. And those are the two cell types responsible for providing the fetus with nutrition in the first trimester via breaking down those endometrial tissues and um using those uterine gland secretions. OK. And also if you have any questions please do put them in the chat or feel free to interrupt. Um So yeah. OK. Um Next slide. So then hemo terrific nutrition, as we said is the second nutrition stage and that starts in the uh second trimester at the beginning. And in the hemotropic nutrition, we use uh a placenta and um the placenta helps the fetal membranes come into direct contact with the maternal blood supply. And this, as we said is done by the chorionic villi, which you can see in the diagram here. And these are basically finger like extensions of the cytotrophoblast which undergo lots and lots of branching to help provide a very substantial surface area to make um gas exchange, nutrient exchange as um efficient as possible. Next slide. So you can see here the structure of the placenta. So this is just something that you have to remember. So you've got your, your fetal veins, your fetal arteries all in the umbilical cord. Then you can see they branch off into your chorionic villi which are suspended in these intervillar spaces which are lacunae, which are basically filled with the uh maternal blood. And this is the whole placenta um as a structure next side. So yeah, so there are two sort of main parts which are involved in nutrient exchange within the placenta. So you have your maternal spiral arteries and you have your fetal chorionic villi. OK. So your spiral arteries um basically feed blood into the intervillar spaces. So the lacunae which the chorionic villi are embedded in and then the chorionic villi help to exchange nutrients and gas with the intervillar spaces. So that's where the exchange occurs between the fetal membranes and the maternal blood flow. Um And obviously, the branching of the chorionic villi which increases throughout pregnancy is very, very important because it helps to increase the area for exchange and sort of make it as efficient as possible. And then we will now move on to um the Coron Villa and how they develop next side. Thank you. Um So, yeah, initially, they are just outgrowths of the cytotrophoblast. Um And then in the secondary phase, what they ha but what they start to do is they start to grow into primary villa. And in the last stage, you get the growth of the umbilical artery and the vein into the venous uh villous mesoderm which then provides vasculature. And you can see here that the um microstructure of the terminal villus, it's quite a convoluted uh knot of vessels and there's a lot of dilation of the vessels going on as well. And what this does is it basically helps to slow the blood flow, which means that you get as much exchange as possible between the maternal and the fetal blood and you can't see it here, but usually the terminal villus is coated by a trophoblast. And in terms of the changes of the chorionic villi from early pregnancy to late pregnancy. So one thing, there are three things that happen. Um So your vili become much smaller in diameter, you get less separation distance between the capillaries and the maternal blood. So the vessels move closer to the vili, which again helps you increase the exchange and the trophoblast layer. So the outer coating, it gets thinner and thinner with gestational age. So all of these three factors and these three changes in the terminal villa microstructure essentially helps to um make the exchange as quickly, as quick and efficient as possible next side. So we've ta ta talked about um the fetus and its corona villi um within the placenta. But there's also the other part which is the maternal spiral arteries within the endometrium. So the spiral arteries undergo remodeling in the placenta. And this is really, really important because this basically turns the very, very like tightly wound spiral arteries into a high capacity, low pressure conduit for maternal blood flow. So, again, getting as much maternal blood into the intervillar spaces as possible. So that means we have as many nutrients as many things available for exchange with the chorionic villi of the fetus. And so if we look at spiral artery remodeling and how it happens. So, um the corona villus is essentially coated in these trophoblasts. Um so they're called extravillous trophoblast cells. And you can sort of see this in the top diagram on the right and these E VT cells. So these extravillous trophoblast cells coating the chorionic villi will then begin to invade into the spiral arteries and they begin to line the inside of the spiral arteries forming something called endovascular evt and then the endovascular evt basically triggers all of the spiral artery remodeling. So one, it triggers the um endo it triggers the endothelium of the spiral arteries to start releasing things called chemokines, which then attract and recruit a bunch of immune cells which help to dilate the spiral arteries and make them much um much sort of bigger, not as like convoluted, uh like a convoluted bunch of vessels. Um The endovascular evt also helps to disrupt the vessel walls and essentially break down the smooth muscle uh lining the er spiral artery. And it also um replaces the spiral arteries, uh normal vessel extracellular matrix with something called fibrinoid. So basically this all results in the um changing of the spiral artery into a low pressure.