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There is a set rule because it's a set rule, right? One strand will always be complementary to the other strand. And that's what makes DNA so unique and so useful in storing genetic information. Because if you've got G A on one strand, you have to have CTG on the other strand because they're complementary to each other. Um And nucleotides are then covalently linked together in that chain. I've spoken about that with the phosphodiester. So this, this picture shows you the, the, the structure of the phosphodiester bond. You've got this three prime carbon uh on the sugar molecule on the top and the five prime carbon on the sugar molecule at the bottom. And they, they are on both sides of the phosphodiester, right? So I've spoken about the four types of bases and I've spoken about how they bind. Now DNA is a double standard structure, which is a double helix. So how do you form the double helix? Now that you've got the double standard DNA, you've got the binding, the DNA. Now just twists around itself to then form a double helix. And it's important to remember that both these plans are and de parallel to each other, right. So next DNA replication, this is what happens during the s phase of the interphase. And the main enzyme that runs this entire process is known as DNA polymerase. Like there are other enzymes involved as well. Like you've got helicase and stuff like that DNA ligase. But the main enzyme which runs this entire process is DNA polymerase. And essentially what it does is it, it unzips the he he uh helix and it uses both the strands, both the strands as a template to form the complementary strand. And because DNA is complementary, you end up by the end of it, you end up with two DNA strands because it uses each strand as a template to then make two sets of DNA. So DNA keeps adding nucleotides complemented to what it's reading. And I made this nice um flow of events which occur which we can go through. But the one important thing which I wanted to talk about is the DNA polymerase always adds nucleotides to three to, to the three prime end of a growing DNA strand. So if we use the picture on the bottom left, you've got two strands of DNA, you've got the blue and the red. Now the blue strand conveniently goes from three prime to five prime. And that is very convenient for DNA Premera because it always adds nucleotides to the three prime. And so it's adding nucleotides in the same direction as the DNA is unzipping the death strand. However, it's unfortunate because it's running antiparallel. So it's running five prime to three prime. So the DNA polymerase now has to add new new nucleotides in the opposite direction to which the whole unit of the replication is moving. So say if the whole unit of replication is unzipping the DNA to the left DNA Premera on the lagging strand is adding nucleotides to the right. So what it then has to do is it has to add new nucleotides in the right and then go back to the left with the whole unit. So it's, it's adding stuff in a discontinuous manner and that's what it's called the lagging line. And these fragments with it adds in a discontinuous manner, are known as Okazaki fragments. So that's the difference in DNA polymerase on the continuous and the discontinuous strand. So up next, you've got RNA. So you'll be spoken about DNA and how it's uh stored for genetic information. Um RNA on the other hand, is different in terms of its biochemistry, but it's also got different functions. So uh RNA is ribonucleic acid, whereas DNA is the oxy tronic acid and the one of the major differences is that the pento sugar is different in RNA and DNA. Um and RNA, there are different types of RNA A, you've got messenger RNA transfer, RNA, ribosomal, RNA and micro RNA. And another key difference between RNA and DNA is the, is the nitrogen bases. So we've spoken about DNA, you've got adenine, thymine, uh cytosine and guanine. But in RNA, you've got uracil instead of thymine. So you don't have thiamine in RNA, you've got uracil instead. But the major rules of, of uh nitrogen binding still remain the same. So, adenine will bind to uracil and cytosine will bind to guanine and w while DNA solely functions as an inflammation. So, RNA has some structural regulatory and catalytic catalytic roles in the body as well. So Mrna is very important during transcription and translation of, of DNA. And that's essentially when DNA is used to then form proteins, which is what they're used for. Um Another um so M RN acts as the blueprint for the ribosome to then used to then form the protein. Another form of RNA is transfer RNA and it's, it's very important to know this because it's, it, it will be useful during translation. So the Trna as a structure, it's got two important sides. One side has the anticodon which has three nucleotides uh complementary to the nucleotides on the M RN. And these anticodons then match the codon stones on the RNA and they have the amino acid linked to those codons on, on the other end of its attachment site. So it's, it's basically like an adaptor molecule which connects to Mrna in the ribosome to then allow amino acids to then bond to the growing peptide chain in the ribosome. Um So if you have a look at um transcription, so this is when Mrna is formed. So during transcription, essentially happens is RNA polymerase um does essentially what DNA polymerase does. But instead of forming another DNA stent, it's forming an M RNA strand. And RNA polymerase does not use both the DNA strand, just uses one of them as a template to form the M RN. And then this MNA undergoes some modification. Um It, then it enters the cytosol and then it then goes to the ribosome for translation. So this is a nice picture explaining how R RNA polymerase work. So it unzips, the DNA uses one of the strands and then forms the MRNA molecule. Uh So what happens after transcription? So RNA M RN undergoes modification. So what sort of modification you've got, you've got removal of the introns and you've got addition of caps and now what are introns? Interns are basically sequences of M RN which don't actually code for genes or they don't code for proteins. They just sequences which don't code for any protein. And those are introns, you've got exons as well. Now exons are sequences of M RN which actually code for protein. So they are very important. So they, they remain the way they are. So you've got splicing and removal of introns and you've got addition of these methyl caps on the M RN which make the M RN molecule very stable. And then the M RN then leaves the nucleus through the pore in the nuclear membrane and then enters the cytosol goes to the ribosome and then translation occurs with TNA. Now, before we go on to translation, we need to know what a codon is, what the genetic code is. So a codon is essentially a N A nucleotide sequence of three nucleotides and three nucleotides from one codon and one codon codes for one amino acid. So if you look at this table on the right, very important, you'll notice that U UA U CCU CCU A and cu all code for one amino acid leucine. So what you've noticed is multiple sequences of codons can code for the same amino acid. So the TNA molecule like I mentioned earlier, it got this one side which has the anti codon strand. So say the M RN strand had U UA as one of its codons. The TNAS, the TN molecule having um TT TT U will have a leucine amino acid attached on the other end of it. And it will match, match that to the M RN in the ribosome and release the leucine to then bind to the polypeptide. So that's essentially how translation occurs. We there's a picture on the next slide and that's why codon is so important because a codon is essentially a sequence of three nucleotides that codes for one amino acid. And the Trna has the anticodon, which is complementary to the codon that you want So the ribosome has three attachment sites, the AP and side and essentially the T TNA comes in onto the A side. Um It matches its anti codon to the codon on the M RN and releases the amino acid, which I was talking about. And it allows an amino acid to form the peep peptide bond to the polypeptide that's already growing. And now this polypeptide will undergo further modification, folding, tertiary structure, folding, stuff like that to form the protein that you want. So that's essentially what happens during translation. We've completed the first part of my presentation. So we've got the first SBA. So if we can get the poll up um and you guys can try this SBA out. So what type of chromosome does the image below show you've got telocentric Acrocentric Metacentric submetacentric and centro centric, right? So I think the majority of you guys have got this right. Um The answer is b so um yeah, it's Acrocentric. And um yeah, I think it's important for you guys to know the different types of um chromosomes because when you go on the case seven and year two, you'll, you'll notice that a lot of chromosomal abnormalities or genetic abnormalities often can arise from Acrocentric chromosomes. So it's just important to know what these chromosomes look like and what their classifications are. So, moving on to the next part of the presentation, you've got the abdomen when we talk about the anatomy of the abdomen first. So what are the boundaries of the abdomen? So, you've got, superiorly, you've got the diaphragm, um inferiorly, you've got the pelvic cavity of the perineum. Uh anteriorly, you've got the parietal peritoneum and the anorectal abdominal wall with the rectus abdominis, stuff like that. And then posteriorly, you've got the posterior abdominal muscles on the posterior abdominal wall. Um So along with the boundaries, it's also important to know the regions and the divisions of the abdomen. Because uh clinically, if a patient walks in with abdominal pain or any lesion in the abdominal uh a abdomen, um it's important for you to localize where that pain is. And after localizing it on, on the first look, it's important for you to kind of get a gist of where the problem might be. So if a patient walks in with right upper quadrant pain, you need to know what structures there are in the right upper quadrant or say if a patient walks in with right iliac fossa pain with fever, you kind of need to know what structures are in that region for you to then figure out what the possible problem could be. So this this slide here, I think uh I have used it a lot. It was very helpful for me because it, it told me or helped me revise which organs are in which region of the body. So you need to know if there's, if patient comes in with epigastric pain that could be a problem in the stomach, the liver, the pancreas or the right to left kidney. Um So, very interestingly, your gi tract is embryologically divided into the for gu med gut and the hind gut. And why this is so interesting to me is because the fut, the midgut of the hind guard individually have a major vascular supply which is different from each other. So the full guard is from your esophagus down to your second part of the duodenum. And all these structures have a major arterial supply of the celiac trunk, which is a branch of the abdominal aorta, the mid guard, which is from the second part of the duodenum all the way up to the two thirds of the transverse colon. Uh that's supplied by the superior mesenteric artery. And the hind guard is from the 21 3rd of the transverse colon down your back passage. That's the inferior mesenteric artery. So, the peritoneum, you've heard of the pericardium, the pleura and they're all double wall membranous sacs that surround the organ and give it protection. And the same thing is applied to the abdomen as well. So you've got these organs which are surrounded by these double walled membranous sacs. And that's the peritoneum and certain organs in the body have peritoneum associated with it and they have separate names for it. So, for example, the peritoneum which surrounds the stomach is known as the omentum. You've got the greater omentum and the lesser omentum. And that's according to the peritoneum attached to the lesser curvature of the greater curve of the stomach. So the lesser, the lesser omentum connects the lesser curvature to the liver. And the portal triad runs through the lesser omentum. The greater omentum is the peritoneum hanging down from the greater curvature of the stomach. So it's like an apron which surround like which covers the abdomen when you open it from the front. Um and the gated omentum interestingly is also known as the policeman of the abdomen. And why it's so interesting is because if there's any inflammation in the abdomen. So for example, a patient walks in with cholecystitis which is inflammation of the gallbladder. Um When you, when, when there is surgery, you'll notice that the greater omentum goes and wraps itself around that inflamed gallbladder. And that is in order to prevent the inflammation from spreading. Similarly, even during appendicitis, the the greater omentum moves towards the appendix and surrounds it. Um And then similarly, you've got the mesentery and the mesocolon, which is like the peritoneum associated with the small intestine and the large intestine. So you, you've got organs that can be intraperitoneal or retroperitoneal. So, intraperitoneal organs are organs which are surrounded by the peritoneum and retro peritoneal organs are the organs that sit in the retroperitoneal space which is behind the peritoneal cavity. And a good pneumonic for you to remember these are, is the side and I've not come up with this Pneumonic, but uh it's just, I just found it very helpful and you've got all these structures in this Pneumonic, which are Apera. And I'd, I'd advise you to remember this Pneumonic because a lot of questions and your examinations in the S one formative exams, they do like to ask what organs are retroperitoneal and retroperitoneal organs usually come up with a particular type of characteristic diag um sign. So if you've got pancreatitis, which is a retroperitoneal organ, a patient will come in with pain, which he feels along his back. And it's important to know that because then that's how you can spot certain certain is conditions which are, you know, characteristic. Um So the posterior abdominal wall, you've got the quadratus lumborum, um the psoas major and the iliacus and the Iliacus and the soas major together from the iliopsoas. And if you see the attach, the attachment site of this muscle is on the femur, so what this muscle helps you out with is hip flexion. And the thing is this muscle runs very close to the appendix. So when you've got an inflamed appendix, contraction of this muscle might cause a bit of irritation and that can be used as a sign to die. Like, figure out if a patient has got appendi appendicitis. Um and that's called a zine. Another important aspect of the abdomen is the inguinal canal. And I essentially think of it as a tunnel and this tunnel is formed by the abdominal anterolateral abdominal wall muscles, like the external oblique, the internal oblique and the openings of this canal are essentially defects in the anterolateral a wall. And these defects are the deep inguinal ring and the superficial inguinal ring. And what passes through this channel is different in males and females. So, in females, you've got the round ligament of the uterus which is being transmitted. And in males, it transmits the spermatic cord and the gonadal vessel. Um but obviously because of the defects, it is prone to herniation. And you've got two types of hernias, you've got the direct hernia and the indirect hernia. So the direct hernia is in the is the intestine that goes through the deep inguinal ring but does not go through the superficial inguinal ring and instead the abdominal wall. So the a abdominal contents, they push against the abdominal wall inside this area known as the heel back strangle. Um And the direct hernia always pops out immediately to the inferior epigastric artery. Whereas in an indirect hernia, the abdominal wall contents go through the deep inguinal ring and the superficial inguinal ring down to the scrotum. So the abdominal contents pass later to the inferior epigastric. And both of these types of hernias can be checked using something known as the valsalva maneuver. So the Hassleback strangle is this green space here and the boundaries of are the inferior epigastric artery. The rectus abdominis medially and the inguinal ligament inferiorly. So, up next, you've got the biliary tree. Um, personally, the biliary tree is very interesting to me. And I think if you learn it now you k six or K six, which you will come across at the end of the year and most of the upper gi pathologies, you will understand a lot better if you understand the biliary tree fully. Right. I can, um, let's let's go through this together. So you've got the right hepatic duct, the left hepatic duct, which which which carries bile produced by the liver, it goes down into the common hepatic duct. Now, the gallbladder, as you know, also stores some bile. So the gallbladder releases its bile through the cystic duct and joins the common hepatic duct from the common bile duct. The common bile duct then joins the main pancreatic duct which carries exocrine secretions of the pancreas and forms this common hepatopancreatic duct which empties into the duodenum. Now, the point where this attaches to the duodenum, there's also something known as the hepatopancreatic ampulla of water. Now, this joining, I think in some textbooks is also also demarcates the the the the the the distinction between the f gut and the mid gut. And then you've got the Juju and the ilium which are the other parts of the small intestine. So the juju is precedes the ileum. So it's more subject to acidic content. So which is why it's got thicker walls, wild lumen and it's packed with pli circularis. Uh It's, it, it has longer vasa, which are these blood vessels which are straight in line and they have fewer arcades. The ileum however, has thinner walls, narrow lumen, uh short of acid Acta and it's 2/5 of the small intestine. The juin is bigger than the ileum. Uh When I say the ileum does not face as much acidic content. I don't mean it faces no acidic content. It still faces acidic content, but the content is less as acidic. In comparison to the juna, you've got three unpair branches of the abdominal aorta, the celiac trunk, superior mesenteric and the inferior mesenteric. It's important for you to know where each of these branch out of the abdominal aorta. Again, a very common question in your sbs. So the celiac trunk branches are t 12, superior mesenteric L1 and inferior mesenteric L4. The celiac tongue individually, it branches out thrice right. It has three important branches. The left gastric, the common hepatic and the splenic artery. The left gastric supplies mainly the lesser curvature of the stomach. The common hepatic moves to the right of the body and it gives off this hepatic artery proper, which goes to the liver and the gastroduodenal artery which then goes off and supplies the duodene and the pancreas and the greater part of the, the, the greater curvature of the stomach. Um The splenic artery is a bit tortuous and it runs posterior to the stomach and it goes and supplies the spleen. It also gives off the short gastric artery that supplies the fundus of the head of the stomach. Right? So this picture very important. It might not be as important during pcs. But I think some case six, I think you'll have to learn all the supplies to the upper gi very important. Um, moving on. So you've got the superior mesenteric which then gives off the genital ileo colic, right colic, middle colic. But remember, the superior mesenteric will only supply two thirds of the transverse colon because the other parts are supplied by the inferior mesenteric, which gives out the left colic and the rectal arteries. Now, the venous blood coming from the gi tract does not go directly to the heart, right? It goes through this portal system which empties into the portal vein, portal vein empties the blood into the liver, the liver sinusoids, and then the some of the blood is then absorbed, uh whatever is absorbed from the gi tract then like processed by the liver. And then all of that blood is then emptied into the hepatic vein which empties into the inferior vena cava, which then enters the systemic circulation. So this bottom left image here gives you a flow of blood from through the two capillary beds and then to the heart. So the blood does not go directly from the gi tract to the heart, it goes via the liver. And there are three primary tissues where blood can also drain into the portal system, but can also drain into the cable veins. And these are the distal esophagus, rectum and superficial abdomen. And the reason why these are so important is because say if you've got a occlusion of the portal vein, you've got portal hypertension, a thrombus which is occluding the portal vein blood over here. Now will s will notice that the blood will i it's tougher to go through the portal veins. The blood will now start pulling up in these three tissue areas because remember the blood can go in either direction, can either go through the portal vein or it can go through the cable veins. And because it's tougher to go through the portal vein, the blood will start redirecting itself to these three areas. And in situations like portal hypertension, liver fibrosis, stuff like that. You'll get pooling of blood in these areas and and say pooling of blood in the distal esophagus can lead to esophagus, esophageal ulceration. You can have hemorrhoids. You can have uh these veins which run over the abdomen, which is called caput medusa. So it's important to know how these come up. And then lastly, you've got abdomen, histology. So abdomen histology, you look at the epithelium first. So the epithelium of the gi tract starts off with nonkeratinized stratified squamous in the esophagus. And then the moment you read the stomach, the epithelium becomes simple col columnar. And how this helps is it increases the surface area but also allows the ce uh the cells to be able to release enzymes, mucus fluid important. And then the layers of the gi tract, you've got the mucosa submucosa muscularis and the cirrhosa. And within these layers, you've got the enteric nervous system and you've also got the uh submucosal plexus and the muscularis and the muscularis plexus. So, so the muscularis is where the um gi motility occurs and the submucosa is where the secretions occur. Right. So, I've, I've gone through the anatomy of the abdomen, the histology of the abdomen. I've got a few last four or five sbs for you guys to give a shot at. Um Most all of these are related to the abdomen. So, if we can have the pulse up, you guys can answer these questions. So a patient presents to his GP with the right iliac fossa pain. The GP notices that the pain is exacerbated when he asks the patient to flex his hip on abdominal palpation of the left iliac fossa. The patient also complains of pressure like pain on the right hand side. What is the most likely diagnosis? Right. So I think most of you again have got it spot on. Um The answer is appendicitis. So left, right and left fossa pain is an right and left fossa pain exacerbated by flexion of hip. And if if he has a temperature, it's very likely to uh appendicitis. So because you've, you, he's got the ileo, the patient has got the ileo sign and palpation and pressure on the left. And the left fossa is another sign known as Robin sign. And both of these give you a brief idea of it might be or a differential of it might be appendicitis, right? So the next question, what are the contents of the portal triad? So II mentioned that the portal triad runs through the lesser omentum or what runs through the portal triad, right? So again, most of you have got this one or this one, right? But it the the the the spread of results isn't as convincing. So the correct answer is e so you've got the portal vein, the hepatic artery and the bile duct which run through the portal th and if, if you remember the triad later in case six, it will also help you understand the histology of the liver because a majority of the vessels in the liver, they all run in the same fashion. So they all form a portal triad which then branches off into smaller portal triads is how I'd like to put it. So the next question, his water supply is the greater curvature of the stock. So I mentioned the left gastric is a branch of the celiac trunk. OK. Interesting. So majority of you guys have chosen a but that's the wrong answer. Because the left and right gastric arteries, they supply the lesser curvature of the stomach. The greater curvature of the stomach is supplied by left and right gastroepiploic arteries. That's, that sounds a be. So if you can go back to the picture that I've put up on the slides and if you can have a look at the, the branching of the hepatic artery, right, the common hepatic, which gives off the gastroduodenal. That is where you'll find that the greater curvature of the stomach is applied by the left and right gastroenteric. So again, I think, I think an opportunity for all of us to learn and I think this was a good s pa. So at what level does the trunk branch out of the abdominal aorta? We went through this right now. So hopefully it shouldn't be that tough. Yeah, you guys have slashed it. Yeah. DD is the correct answer right. Next question. A patient presents with right upper quadrant pain. What structures of the abdomen are most likely to have a lesion? Yeah. It's important to know what o what organs are and what regions of the abdomen. And it's very common uh for patients to present with right upper quadrant pain. So and in the clinical scenario, right, upper quadrant pain is very common. So if you if you guys can remember this, it can be helpful in future years as well. Yeah, again, 90% of you guys have got this right the answer would be because you've got liver and the gallbladder that sit right up on the right side of the upper quadrant of the abdomen. Um Right. I think, I think this is the last question, which of the following is a rep peritoneal structure. So again, if you, if you go back to the sad pucker, the pneumonic and then work your way around that, you should find a structure which is retroperitoneal. OK. Right. So the correct answer is the infective Vena Cava. So again, if you just have a look at the side of Pneumonic, it, this, this, this should be an easy on, easy question. Yeah. So yeah, that's about it for me. I hope you guys enjoyed. Um I will now pass on to Nada OAD and um they can carry this forward. Hi um Dev mother. Can you, can you hear me? Uh Yes, I great. OK. So sorry, I share my screen. Yeah. Uh Can you get, can you guys see my screen? Yeah. Do you wanna take um just a five minute break for everyone to kinda get a drink or something? Yeah. Sure. Sure, definitely. Yeah. So um should we come back at five past? Yeah, perfect. Yeah, great. All right guys, if you wanna um grab a drink or um take a short little break. Um Thank you. That, that was a really good presentation and a lot of really high yield stuff guys to make sure to kind of go through the, um, powerpoint in your exam season. Um, and yeah, we'll see you at five past, um, for presentation. Ok. So hopefully you guys have come back from your break. Um, I'm gonna pass it on to Sad for his presentation on nutrition, digestion. Um, I'm gonna send a feedback form at the end. Um, so do stay so you can get the catch up content. Hi. Hello, everybody. Um, my name is Sad and I'd first like to say thank you. Um to everybody who's attending. I know it is a Sunday evening and the, the session was scheduled to finish at six. So I'll try my best to finish before then. Uh Another thing I like to add was dev's presentation was um full of information. It was, it was very um high yield. But I like I just wanted to add if anybody um wasn't familiar with some of the content there, especially on the DNA, the cell cycle, then don't worry, I was in that position last year. Uh It's normal and if anybody is looking is a bit stuck for the revision for F one or F two, I'd highly recommend focusing it on uh systems, for example, cardiac anatomy, cardiac physiology, uh respiratory anatomy, respiratory physiology, repre anatomy, rep, predictive physiology. But the best thing would be to um and get through all your lectures which you've had this year. I know pcs can be quite busy. So uh without further ado, let's get started. I'd also just like to add that today's session is full of um, very important topics. However, in the grand scheme of things, um, on, um, test wise, um, they do tend to come up quite infrequently. I wouldn't spend a lot of, a lot, a lot of time, especially on DNA, cell cycle, nutrition, um, nutrition, digestion. These questions do come up but, um, definitely, um, try and manage your, um be smart with your revision. So let's get started on nutrition and digestion. So today I want to cover um today, I want to cover nutrition, digestion, vitamins, uh meta meta uh metabolism in a fed state and metabolism in a fasted state. So let's get started. So nutrition. So as we know the essential carbohydrate, the essential components um of our food, of our diet involve carbohydrates, they involve proteins, they involve lipids and we also have vitamins and minerals. And we also have the gly, the glycemic index. So what is the glycemic index? I wouldn't worry too much about the glycemic index, but what the glycemic index is is it's a way of assessing how good or bad a particular source of carbohydrate is. So, what we do is we have a certain amount of a certain carbohydrate. So that could be, for example, Pisa and we could compare that with um pasta. And what we do is we'd see which form of carbohydrate would give us the quickest um blood glucose uh measurement. And what is uh what ha what scientific cities have seen is that the, the, the compound which gave the carbohydrate, which gives the highest spike, um and the highest spike which stays up for a long period of time and then comes suddenly crashing down those types of foods. Carbohydrates are more associated with type two diabetes. And the carbohydrates that we eat. The most digestible one is actually starch and the least digestible one is are called non starch polysaccharides. And the interesting thing about nonstarch polysaccharides is we can't actually digest these to obtain glucose, but they are very, very important because they're useful as fiber and in gut health. And a very important fact is most carbohydrates are absorbed in the small intestine. So the glycemic index, this was just a picture. So as you can see, the red shows uh a carbohydrate with a high glycemic index. So when we eat it, the blood glucose levels go up quite rapidly. And as you can see, they fall down quite rapidly as well. And when they fall down, that can lead to feelings such as cravings, it can lead to like a sugar crash or something. Whereas with this low um glycemic index, carbohydrate, we can see that the blood glucose increase is quite small, it's gradual and it doesn't go down as quick as the high glycemic index food. So basically low glycemic index. So what I'm trying to get at here is that low gly glycemic index, foods are healthier in the long term and high glycemic index foods have a higher risk of causing type two diabetes and um heart disease as well. So, moving on to proteins and carbohydrates, um proteins are polymers of amino acids. We know we have 20 amino acids and these are split into essential amino acids, non essential amino acids and conditional amino acids. So very quickly, essential amino acids are ones that we can't synthesize ourselves. So we have to obtain them from our diet. Non-essential amino acids are those acids which we can synthesize uh by ourselves and conditional amino acids. These are quite um these are quite unique because we don't need them in a day to day scenario. However, in certain situations such as disease, such as illness, these can become essential and now we move on to the function of lipids. So, lipids have three main functions. These are instillation, protection and storing energy. And I just want to mention here and this was something I didn't realize was that we had two types of cholesterol. We had LDL cholesterol and that's the bad type of cholesterol. So we don't really want um LDL cholesterol in our diet. But LDL HDL cholesterol, that's the good type of cholesterol and that lowers the risk of coronary artery disease. And in terms of fatty acids, saturated fatty acids. So, a saturated fatty acid is a fatty acid which has no carbon to carbon double bonds. Those are quite bad for our health, whereas poly and saturated fatty acids. So those which are seen in, for example, fish, those are quite good for our health and lipids are also uh separated into essential um fatty acids and nonessential fatty acids. And Ara Ara Arachidonic acid is an essential fatty acid. A fatty acid which becomes crucial in linoleic acid deficiency. So I definitely wouldn't recommend learning the whole 20 amino acids. But what I would recommend is if you have time would be to learn the essential amino acids. And there is a Pneumonic um called PVT Tim Hall. And that can help you er, in your revision, learning the essential amino acids. So, because this, these topics tend to be quite um not f focus much on um I've included a lot of SBA S and a lot of the SBA S I've included. But actually questions that uh I had in my F one and F two. So the question is uh a patient goes to the GP complaining about dry skin and joint discomfort. A blood test shows that the patient is very low in essential fatty acids. The patient is adamant that they have a high fatty diet regularly using corn and soybean oils in cooking and eating buttered bread. The GP decides to refer the patient to a nutritionist who investigates the problem and recommends that the patient eats two portions of oily fish a week. So what is the potential reason for the patient's symptoms despite having, uh, high fatty diet? So, it is quite a big question. There's a lot of words here. So I'll give you guys around 30 to 40 seconds and, um, please do have a go, the polls are anonymous and it'll be very good. Um, a allow the concept to stick, um, a bit more in your, in your mind. We gained quite a lot of responses which is um uh very encouraging. We'll give you about five more seconds once it's coming through. So if you can end the poll there, please. Um Great. So the answer was the patient had a high diet in Omega, six fats, but low in Omega three fats. And we'll go back to why. Um In a second, I've got another SBA and this SBA actually came up in uh our last year's uh F one. So Lewis is a first year medical student who is passionate about body building. After bulking throughout the summer holidays, Lewis is considering cutting. So reducing his calorie intake to reduce body fat whilst maintaining muscle mass. Lewis is unsure about the recommended calorie intake for men. Can you help him out? So what is the calorie intake for an adult male? I give you guys around 20 seconds. Love answers are coming in which is uh very good. Five more seconds. And uh if we could end the pull that, please. Um So the answer was D so it was 2500 calories. And now we'll go through the answers to both of the mnemonics. So to be honest, both of these are quite niche facts which um I would recommend, I would recommend learning. So the smaller topics tend to, whenever they are examined upon, they tend to be quite niche. So for example, um the question here, the second question was the recommended intake for men and women. So for men, it was 2500 koc calories and for women, it was 2000 koc calories. And I've also included the basal metabolic uh metabolic rates there as well for both genders. And then I've also included the cal the equation to calculate BMI I so BM I is weight over height and the basal metabolic rate is basically the energy that our body needs to perform a basic day to day tasks, basic life functioning activities. So the first question, if I could just remind you guys of the first question was, was this? So the patient comes in and he's got dry skin, he's got joint discomfort. So they are eating a high fatty diet. Um And for example, they're using corn, they're using soybean oils and they also have uh joint joint discomfort and dry skin. So the reason why it was due to the omega six to Omega three ratio is this is quite common in the in western diets. And the reason why is omega six to the ideal omega six to omega three ratio should be around um 2212421. However, in a western diet, in a, in the average western diet, the omega six to omega three ratio is 6 to uh 15 to 1 approximately. And having this high of a ratio can lead to increased mortality from cardiovascular disease. So, inflammation which was what a patient had there. He had joint pain and it can lead to increased risk of breast cancer. So that's the answer um for that first question. So I hope it makes sense if it doesn't, please do type in the chart. So moving on, moving on to digestion and absorption. So this is something which I would say is um you perhaps might not find it particularly important or you might find it a bit confusing at the moment. But hopefully by the time you come to K six, you'll be quite familiar with this. So another SBA so after completing medical school, you decide to pursue a career as a GPA patient comes to your practice and presents you with an image on their phone of their bowel contents. You quickly discern that it is steatorrhea, meaning they have a lot of fat in their stools. So where are fats primarily um absorbed? So if you could launch the poles, please, we'll give you um 10 more seconds. Great. And if you could end the polls there, please. So uh the answer to this question was the Judum. Sorry was the judging and we'll talk more about that. Uh In the next slide, another S pa so Marriam is learning the enzymes involved in protein digestion due to erratic sleeping schedule. She falls asleep halfway through the osmosis videos. When she wakes up a few minutes later, the narrator mentions the enzyme responsible for the breakdown of peptones into amino acids. Uh What enzyme is the narrator referring to? So, what enzyme is responsible for the breakdown of peptones into amino acids? Sweet. But we'll keep you guys another 10 seconds. And if you could and the post that please, so it was quite a lot of people chose a, quite a few people chose B as well and a few people chose e so the correct answer here was ie so it was Erepsin and we'll talk through um that now. So first of all, we talk about carbohydrate digestion. So what, what, how are carbohydrates digested? So, first of all, we begin with starch or Glycogen and then that is acted upon by the alpha amylase enzymes present in our saliva and in our pancreatic secretions that then turns into maltose and then maltose is then broken down by maltase in the fresh border um of the small intestines and that then becomes glucose which is then absorbed and which is then absorbed. And then we can also have these following enzymes such as maltase sucrase and lactase and maltase breaks down maltose into glucose and lactose, sucrase breaks down sucrose into glucose and fructose and lactase breaks down lactose into glucose and galactose. So, this is quite important. This is where the majority of these nutrients are absorbed, um where they're absorbed in the small intestine. So, the carbohydrates are primarily absorbed in the duodenum proteins are primarily absorbed also in the duodenum fats. So that was what the second question here was referring to, that's absorbed in the jejunum and bile acids are absorbed in the ileum and cobalamin, which is another important uh mineral um uh vitamin, sorry, that's also absorbed in the ileum as well. And protein digestion. This was um the question referring to the er aips for the peptones into amino acids. So, in the stomach, we have the enzyme pepsin and that breaks down proteins into polypeptides. In the small intestine, we have trypsin and that breaks down polypeptides into peptones and we have risin which breaks down peptones into amino acids. So these are um this is a table of the transporters. So I would, I would recommend learning um these transporters and just having a rough idea of where they're located and what, what, what, what are their characteristics. Um For example, SGL T one is located in the enterocytes on the Luminal side of the intestinal epithelium. And that's important for glucose absorption. Um And definitely I in your own, in your own time, go through all of these transporters and see um how many you can er remember. So, moving on to Vitamin D and calcium absorption. So first of all, we start off with vitamin D2 and vitamin D3. So vitamin D2 is derived from plants. Vitamin D3 is derived from animal source foods and sunshine. So basically, Vitamin D it improves the calcium absorption within our bodies. But before vitamin, in this case, D2 and vitamin D3 can have that effect on calcium. Uh because they are currently inactivated, they need to be activated. So these forms of Vitamin D are not activated and we need to activate them er to really ob um obtain the full effects of Vitamin D on calcium absorption. So what happens is this Vitamin D uh vitamin D2 and vitamin D3 will travel to the liver and then in the liver, it will become calcifiable and then calcidol will travel to the kidney where it become the active form of calcitriol. And this will then increase calcium absorption and normal calcium absorption. Uh you need to have a functioning liver and the kidney. And the reason why is that these enzymes, 25 hydroxylase, one hydroxylase are in the liver and kidneys respectively. I think this is um this is this would be quite important to have a look at. Um because there are sometimes they do try and catch you out with the location of the enzymes. For example, there might be a question um asking where one hydroxylase is located and maybe what it converts er what into. So, in this case, it converts calciol into calcitriol. Um moving on, we have fat soluble vitamins and water solu soluble vitamins and it's really important to know the difference between them. So, fat soluble vitamins are vitamins, ad E and K and water soluble vitamins tend to be the B vitamins and we also have Vitamin C er in there as well. So here is another SB eight. So Michael is having difficulty memorizing the fat and water soluble vitamins to aid his learning, he decides to go on to peer wise and complete some questions. So the question reads, what vitamin is involved in electron transport, choose from the following options. So this was um a similar question was asked this last year um where it asked to uh focus on the vitamin, which was uh involved in electron transport. So have a go and um we'll see uh have a go. It's anonymous and uh hopefully you get it right. Oops, sorry. So we'll give um five more seconds there because uh I accidentally pressed the next button. Yeah. So if you could end the pole back. So um a lot of you put D which is correct. So D riboflavin also known as B2 is involved in electron transport as well as um B3, which is niacin. So, niacin and riboflavin are both involved in electron transport and we'll explore that here. So this is, I've included some information about fat soluble vitamins. Uh, Vitamin A, Vitamin D vitamin E and Vitamin K you don't need to learn all of it, but I would definitely focus on Vitamin A, um, Vitamin K and Vitamin D So Vitamin A, where is it found? Vitamin A can be found in carrots. And this is if you, and there's also, uh, an interesting fact to me is if you eat too many carrots, you can actually turn yellow. So they involve in the formation of redoxin which are the low light photoreceptors. Um excess Vitamin A like I mentioned can be toxic and deficiency Vitamin A can lead to blindness. Vitamin D Its name is 125 dihydroxy Cec Calciferol. It controls the absorption of calcium in the gi tract like we discussed previously. And it's recommended during pregnancy and a deficiency of Vitamin D can lead to rickets moving on to Vitamin E. This is not the, I wouldn't say this is the most important vitamin out of all the fat soluble vitamins. Um But nevertheless, it's, it's worth learning. So Toso uh topher is found in nuts and, and plant oils and it protects unsaturated fatty acids. And finally, we have Vitamin K its name is called phyto mona mona monodion. Um It's found in Greef, green leafy vegetables. So that's probably an important fact is that Vitamin K is found in green leafy vegetables and it's involved in the synthesis of prothrombin in the coagulation cascade. If you haven't done the, if you haven't done homeostasis yet, don't worry too much about that. But um it's definitely worth remembering once you've done homeostasis and it's antagonized um with Warfarin. So now we move on to the water soluble vitamins and I've mentioned the four water soluble vitamins, which I felt were the most important at this stage. So thiamine plays a role in energy metabolism by a thiamine pyrophosphate and alcohol also inhibits the absorption of thiamine. And there's certain um syndromes um which can be caused by uh alcohol consumption. And one of those is a thymine deficiency and also we can have a deficiency in thymine and that can lead to another disease called beriberi disease. Um riboflavin and nicene, we mentioned these previously, both are important as electron carriers. Um B2 is important in FM and, and F ad while B3 is important in NAD D and N ADP um in glycolysis um in the in the Krebs links to the Krebs cycle. Folic acid is particularly important during pregnancy. And again, uh like Vitamin K is found in green leafy vegetables. It's important in an RNA and DNA synthesis and is recommended in pregnancy to avoid neural tube defects such as spina bifida. And finally, we have B12 called valamin, which we'll touch on uh in the next couple of slides. This is found in yogurt and cheese. It's important in DNA synthesis and an important fact, is folic acid can compensate for B12. However, b12 cannot compensate for folate. So that's, that's worth remembering. Is folic acid can compensate for B12. However, it doesn't occur the same way round B12 can't compensate for folate. So looking at kalimin, this is a um uh mineral which they do like to test um where it's absorbed et cetera. What does it bind to during which stages of its digestion? So, cobalamin is bound to haploid. So in the saliva, uh cobalamin is bound to haptor and that protects the vitamin from the acidic environment of the stomach. Then we have intrinsic factor which is secreted by the parietal cells. And then these bind to um cobalamin in the duodenum. And then once that B12 has entered the internal site, it dissociates from er the pa the parietal factor intrinsic factor and it binds to transcobalamin two and, and then it's transported into the portal blood and taken up by the liver. And this is very, very important B12 is absorbed in the ileum. So now moving on to the hormones of appetite. So I purposely chose to mention the hormones of appetite before the hormones of digestion because I think the hormones of appetite are just much easier to remember than the hormones of digestion. They can get quite confusing, er and it, it gets confusing very, very quickly. So with the hormones of appetite, it's quite simple, they divide it into orexigenic hormones and these are hormones which increase your appetite and anorexigenic hormones. And these are hormones which decrease your appetite. So, for example, the hormones which increase your appetites could be Krein. Um and that's released from the D one cells in the fundus of the stomach and orexin, which is released from the neurons in the lateral hypothalamus leptin um is an anorexigenic hormone. So that would decrease appetite and that's released from adipose cells. P YY is also um an anorexigenic hormone as well as CCK. And a little um trick memory aid would be ghrelin makes you gain weight. So it would increase your appetite and leptin makes you lose weight. So it makes you um reduce, have a reduced appetite. Now, moving on to the hormones of appetite, there are many hormones of appetite and at this point um for students studying at college, university, um I've included the four main ones. I haven't included all the main physiological actions, but I've, I've included the main physiological actions. For me. What I struggled with was I didn't know what cells um which hormones came from which cells. So after scrolling through numerous book, I found um I found this uh I had a friend tell me this pneumonic and it's the pneumonic is called sick G. And basically the purpose of this pneumonic is that if we write out the cells in terms of, in terms of the pneumonic. So si kg. So we have S cells, I cells K cells and G cells. So the S cells are secreting. So S and S is quite easy to remember. Secreting is secreted by the S cells. And if you also remember G so gastrin is secreted by the G cells. So now we're left with the cells and the K cells. And what you need to remember is that the eye and K are flipped. And what I mean is the eye cells um they produce CCK. So CCK has got K in it and that's produced by the eye cells and the K cells produce gi. So I personally find this pneumo quite helpful because I tend to get confused about what what hormone came from which cells now looking further into the physiological act action of the hormones secretin has got an in at the end and that I in my mind, it, it just helps me remember that it inhibits gastrin. And the first three, all all have a um an action where they are inhibiting gastrin or they're not in favor of gastrin secretion. So, so secretin inhibits gastrin CCK causes gallbladder contraction. It stimulates pancreatic secretion and it also inhibits gastric secretion. G IP um reduces the gastric acid secretion and intestinal motility. And gastrin is the last hormone uh from this list and that is in pro favor er of gastric um acid secretion. So it stimulates the secretion of gastric acid and intrinsic factor from prior cells and it promotes gastric and intestinal motility. So I'd just like to add that I haven't included all of the hormones, but I think at this stage, uh these hormones should suffice. Um At this point, once you get to K six, obviously, um I'd recommend learning all of the hormones and their full um actions. So another SBA so ali is researching into the hormone um CCK. So he finds out that it is involved in stimulating pancreatic secretions, gallbladder contractions and that it inhibits gastric secretion. So what cells produce CCK? So hopefully, um if you want to try, you can use the Pneumonic to help you remember um what cells secrete CC but hopefully you guys um should, should, should be getting this right. Oops, but I'll give you guys 10 more seconds and if you could end the poles there, please. Great. So a lot of people wrote I cells, so CCK has got K in it. Opposite is I and that it is correct. So, very well done to everybody who got that correct. And now moving on to metabolism during fed and fasted states. So I just want to give everyone a warning that metabolism during fed and fasted states, it tends to be quite dry. It's it's difficult to find images and pictures to explain this quite well. So what I've done is I've written um a large uh a large section of a large paragraph explaining both of these sections. So there are three energy states of the body absorptive. So that's once we've eaten, that's just right after we've eaten where we're, um, digesting and absorbing all of those nutrients. Um, in our meal post, absorb, this is where it's been, it's been a few hours after our meal, maybe, perhaps we've gone to sleep and during our sleep in a post absorbtive state and finally, the prolonged fasting state is where we haven't had, um, uh, a meal in, in a few, in a lot, in a quite a substantial period of time. And there are three major fuels of the body. So the body has three major fuels. So the first one is carbohydrates. The second one is lipids and the third is proteins. And this is something I really want to kind of drill within you guys is that regardless of which state we're in the main, the aim of all of these states is to make sure that we have sufficient glucose in our bloodstream um for the brain because the brain, it requires glucose as a source of energy. So we always want to make sure that we have enough glucose in our blood to make sure that the brain has uh sufficient energy. And I've got this table showing the concentrations of the substrates here. So glucose lactate, I wouldn't worry too much about that. If you are going to memorize any of these values, I'd recommend you memorizing glucose and it, I'd encourage knowing what circulating form each of these substrates are in for the fed state of metabolism. So uh prepare yourself guys with a lot of information. And I've also noticed that these tend, I've, I've never seen a question asking the fed state of fasting state and metabolism, but it is worthwhile knowing it. So after eating a meal, we have an increase in glucose, we have an increase in proteins and we have an increase in fats. So the pancreas will sense that increased glucose and it'll secrete insulin. And hopefully, that's nothing new to you guys. So that insulin will cause the glucose to be converted into glycogen. Because at the moment, our blood glucose are quite high after we've eaten a meal and we want to reduce our blood glucose. So we um package that glucose into glycogen in the levels in our muscles. And we also have increased glycolysis. Glycolysis is breaking down that glucose um into pyruvate. So, and, and this, this process basically allows us to produce ATP and the ATP produced allows us to undergo anabolism. So we can the amino acids that we've ingested in our meal, we can build them up to proteins, the triglycerides, the uh the fatty acids, the, the fatty acids and glycerol that we digest in our meal, we can build them up into uh triglycerides. And, but eventually there comes to a point where the glycogen stores in our liver, they get filled up. So the glycogen stored in our liver get filled up. However, we still have glucose in our blood which we want to remove. So the remaining glucose will then undergo glycolysis and then that will form acetyl coa and that acetylcoa will undergo fatty acid synthesis synthesis to form triglycerides. So basically that extra glucose which can't be stored in our liver as glycogen that will undergo fatty acid synthesis and it will form triglycerides. And those triglycerides will then be stored in our adipose tissue. And the amino acids in the meal are used to build and replace existing proteins excess. So, if we have excess amino acids, um they will then undergo fatty acid synthesis and they will then be transferred um into the adipocytes as triglycerides. So that is a lot of writing, I think if you break it down, it's not that hard and it is not that complicated and it is quite straight forward and the same is goes with the fastest state of metabolism. So if we haven't eaten naturally, the blood glucose concentration will decrease and the pancreas that decrease in blood glucose concentration and it secretes glucagon. So the effects of glucagon are, it wants to act on the liver to break down that glycogen that we store during the fed states. So when we, during our uh feeding states and where we store that extra glucose in our blood as glycogen, what Glucagon wants to do? It wants to break that glycogen down and use that glucose to make sure that there's enough glucose in the blood um to maintain that the brain has enough glucose to use. So what the uh glucagon does is it acts on the liver, it breaks down the glycogen and then we use the glucose from that broke down glycogen. It also instructs the liver to start gluco neogenesis. So, gluconeogenesis is the process where we form new glucose. And as we know, forming new glucose, uh anabolism requires ATP it requires energy. So where do we get the energy from? And so there's two questions here. So where do we get that energy from? And where do we get the carbons from? Because pyruvate is a three carbon structure, whereas glucose is a six carbon stricture. So we need three more carbons. So where do we get those carbons from? So, gluconeogenesis requires carbons and we obtain these carbons from lactate amino acids, glycerol. Um and the ATP which we need um to undergo um anabolism to create that gluconeogenesis that's obtained by breaking down fats. So uh the adipose tissue, we break down the adipose tissue in a process called lipolysis. And that allows us to use ATP to then form glucose. So we mentioned that we're using amino acids, we're using lactate and we are using glycerol and the amino acids that we use here, they come from skeletal muscle. So I want you to think that in the short term, it's good that we can use amino acids from a skeletal muscle, but that's not something we want to be doing long term. And the glycerol comes from adipocytes. Um and there's not, there's not really a harm in using glycerol comes from adipocytes, adipocytes. Um We, we tend to use them in the long term uh when we're in a prolonged fasting state. So the fatty acids produce from like policy. So when we break down those adipocytes, when we break down that fat, we produce fatty acids, they go through beta oxidation, they create that ATP which can then be created, which which can then be used to create new glucose. And the process of beta oxidation leaves behind acetyl coa. And the body is so clever that it uses the acetyl coa to in ketone genesis to create basically new ketone bodies. And that ketone body rep repla it doesn't replace, but it all in the ketone bodies are used as fuel by um other organs within the body. So, like I mentioned before, amino acids, we can use them uh in the short term for gluconeogenesis, but we don't want to be using them in the long term as they are required as elsewhere. However, ketones can be used. So how do we get ketones by breaking down uh fats uh using lipolysis, we can do that because um they come from adipocytes and they're not really needed compared to um the uh availability and the urgency of amino acids and how they needed. And after a period of time, the brain can use ketone bodies as a source of fuel. And one thing I forgot to add here is that if we're using ketone bodies for a long time, so if we are fasting for, if a person is fasting for quite a long time, then the key, the fats will eventually run out and that person will eventually use the proteins from the organs which is uh critical and we don't want that to happen. So the final SBA uh on this uh on this powerpoint um is when glu blood glucose is very low. Glucagon is released by the pancreas into the bloodstream. Uh What are the effects of Glucagon? You apologize guys every time II click the next slide comes up. So try your best. And if you did see the slide, try and figure out why that happens. So we'll give um another 10 seconds for the pole. And also thank you to the person who pointed out that my, the BM equation was wrong. Um I must have um misread it when I was writing it down. But thank you so much for uh pointing that out. So if you can end the post there, please. Great. So II think I a lot of people, I think it was a quite easy question. So if our blood glucose is low and Glucagon is released, Glucagon wants to downregulate glycolysis and it wants to upregulate gluco neogenesis. We want to, we want to be producing um more glucose and we don't want that glucose being broken down into pyruvate. So that is the end of this presentation. I have one more presentation on the kidney. And hopefully this won't take long and we can finish uh before six o'clock and you guys can have an early evening. So this is on the kidney. So the kidney is quite important. Uh I wouldn't say it's the most important stricture out there, but it's definitely something which um I definitely recommend um trying to revise or learn uh before um before, before your exams. Uh Can I just check if my screen is recording as well if my screen is showing? Uh Yes, it is. Oh, are you? You're on the question? Uh My other question. Uh Can you say now? No, not yet. Uh Does it say that it's paused at the top? It does say it's paused. Yeah, if you click on it, it should I think if I stopped showing for a second and then I start showing again. So if I share my screen again, if I can find the bottom. Shereen, sorry about this guys. Uh Sure. Can you see it on my screen now? Yeah, perfect. Great. So, uh we're going on to the kidney. So I'm just going to touch a kidney anatomy, ultrafiltration, absorption and secretion, secretion, uh hormones, affecting reabsorption and a few SBA s dotted throughout. So this is the anatomy of the kidney. So can anybody tell me and feel free to write it in the chat? What this top structure uh is if anyone's brave. Um you can type in the chart. If not, then I can show it. Um I showed uh oops, I showed the first one. Sorry, the second stricture then. Yeah. Uh Very good Jack. Yeah. Cortex. Um The next one. Then you, I wanna have an idea of the next stricture. All right, keep up um cortex. Uh I think that was for the previous one. I think I'll go through it just for the sake of time. But this would be quite important once you receive the slides to just um copy I, what I tend to do is I copy and paste any uh pieces of the slides I like and put it into my notes. So if you guys are interested in, I'd recommend doing that. But I think it's very important, especially for uh people studying in Cardiff and elsewhere as well that you can identify the strictures in the kidney. And it is quite common um for those people, people um who are staying at Cardiff that in the F one and F it's in the F two in the anatomy center, they do have specimens which you are required to label. And last year a question did come up, I believe um on the kidney. So I would definitely recommend learning the main structures of the kidney. Um And if you have a system to it, it's not that difficult. So here we have the renal cortex on the outside. We have the renal medulla on the inside. There we have the renal pyramids. You can see the triangular shaped, we have the renal artery which is more posterior. We have the renal vein which is more anterior. We have the renal papilla where these renal um pyramids um kind of drain the urine out into and then that forms the minor calyx which then forms a major Calyx and all that urine is then eventually drained into the ureter. So this is some information about the kidneys. So, the kidneys are situated between t 12 to L3. The right kidney is lower than the left kidney due to the presence of the liver and the renal vein is more anterior and the renal artery is more posterior. So, if you ever see a specimen and you and the, and the ask you um and the uh the question regarding a vessel of the um kidney, then you know that the renal vein is more anterior and the renal artery is more posterior because sometimes looking at a uh CAA image, they both tend to look quite similar. Um or to me, they do. So this is a question. So jake a first year medical student learns that the kidney is a retro peritoneal organ. He assumes that adrenal glands, glands are also retroperitoneal. However, he has no idea what other glands are retroperitoneal um from the following strictures which are not retroperitoneal. So you guys should be pros at this, um, def included this in these slides, um, as well. So hopefully you guys should be getting the correct answer and I try my best not to show the answer. Um, before all the ads had to go, I'll give you roughly around 10 seconds, five more seconds try and have a go. Um And you never know you, you, you'd be right. Um And if you could end the pole there, please. Great. So a lot of people put down the pancreas and it was quite mixed between the other two. So, unfortunately, um so the question was, which are not retroperitoneal. So if the question was, which was retroperitoneal, then the pancreas would have been correct. Uh I saw would have been the others. The actual answer was the spleen. So the spleen is an e retroperitoneal organ. So, like I mentioned, the pneumonic is sad PCA. So s would stand for the suprarenal glands or basically the adrenal glands. A would be the aorta and inferior vena cava D would be the 2nd and 3rd parts of the duodenum B would be for pancreas, U for ureter, C for colon, the ascending and descent parts only K for kidney, E for esophagus, R for rectum. And here we have an image showing a retroperitoneal organ and we have an image showing the uh visceral peritoneal organ. So we can see that the retroperitoneal organs tend to be just wrapped by some visceral peritoneum. Whereas the intraperitoneal organs tend to be wrapped fully by visceral and parietal protein. Now, key facts worth remembering for the kidneys, there is a little bit of mass with the kidneys. So and this is quite important. So I definitely, if you take nothing away from the lecture, this um presentation today, one thing I would take away is that the kidney receives 22% of cardiac output. And we'll do a question and SBA later on, but that is a quite an important fact to um memorize and the human body is made up of one third of extracellular fluid and two thirds of intracellular fluid and women have a slightly um have slightly less fluid than men and that is due to adipose tissue. So, moving on to that SBI was talking about so on the urology placement, you are ambushed by Doctor Miller, the consultant nephrologist. So he hands you a table and asks you to calculate the renal flow. So the figures are end diastolic volume is 100 and 60 mL. End systolic volume is 40 mL and the heart rate is 73 BPM. What is the renal flow and try and remember what I said about the percentage of cardiac output, which is um which goes to the kidneys. So this is a math question. I understand. Um some of you guys, uh, might have access to a calculator. So, um, I'll give you guys a minute for this question. So, do have a go. Um And if you get it correct, that's great. If you don't, then, um, you can learn, um, from where you went wrong. So I'll give you guys, um, 40 40 50 seconds for this one. Do you have a go? It's, uh, it's all anonymous, but we will have another 20 seconds, 10 seconds. And if we could end the pole there, please. So we got uh a lot of people saying C and quite a few people went a so they were the two big majorities. So a was 1.22 L per minute and C was 3.4 L per minute. So um before I uh an uh show the answer, um it's just good to have a rough idea of figures in your head. I don't expect you any of you guys to know. Um But renal flows typically tends to be between 1.2 to 1.3 L per minute. So, um and that would be incorrect, but we'll go through it mathematically. So to calculate renal flow, renal flow is cardiac output times naught 0.22. So that naught 0.22 is 22% of the cardiac output goes to the kidneys. So we start with calculating to what ideally, what we need to cut is just cardiac output and multiply that by 0.22. But for that, you need to know the equation for cardiac output. So cardiac output is stroke volume. So how much heart, your volu your how much uh so the volume of blood that your heart pumps out in a minute times your heart rate. So to calculate the stroke volume, you need to do end diastolic volume minus the end systolic volume. And that would be 160 minus 40 then you'd multiply by 73 BPM to give you a cardiac output of 5.54 L per minute. And then you would then need, you would then need to multiply that by no 0.22 to leave you with a renal flow of 1.22 L per minute. So this is the overview of the Nephron. And I personally think in education prior to coming to university, the Nephron tends to be quite rushed and a lot of students including myself and I was quite confused about the Nephron. So if we just go through um the main structures of the Nephron, so I'll go through in order. So let's say blood is coming up into here. So that would be the renal artery, um that would be the renal vein and then blood goes into here. So what would this structure be here? So um this structure, I just to answer the questions. Um If you guys can just think about it in your head. That would be great. So the stricture here would be the glomerulus and the glomerulus is located within the bowman's capsule. And then from here, um the filtrate would then move up into the proximal combined tubule, then move down into the descending limb of the loop of Henley, then up the ascending limb of the loop of Henley and finally in not, well, not finally but into the distal combined tubule and then, and then finally into the collecting duct. So that's um a very basic overview of the anatomy or the stricture on the Nephron. I definitely recommend learning that. Um and now we'll move on to the process of uh essentially uh producing urine and filtering waste products. So the first step occurs here in the Bowman's capsule and this step is called ultra filtration. So what happens in ultrafiltration? So, in ultrafiltration, there's a barrier and it's a three layer barrier, the first barrier. So we're going here inward. So if we look at from here into that, the first barrier is actually the glomerular capillary endothelium. And this has more pore and this blood cells because we don't want our blood cells being excreted um in our urine. So this has pore big enough to allow um proteins and big molecules through and but not big enough to allow red blood cells to. So the basement membrane, this is the membrane which surrounds the capillary endothelium and it retains those plasma proteins. Um We definitely don't want to be excreting proteins. Um And that would be a sign of kidney damage if someone is. And finally, we have these um specialized cells called podocytes and they have filtration slits. Um and they prevent large molecules from entering into the bones culture and becoming a part of the filtrate. All three days have a negatively charged uh glycoproteins and and they only allow positively charged molecules through and ultra filtration is due. So why is this called ultra filtration and not filtration? That was something that I was quite confused with for, for quite a while. And the reason I II figured out was the, the reason it's called ultrafiltration because the pressure within the bone of the capsule is really, really, really high. And the reason um it's high is the afferent arteriole. So the art which is bringing in blood into the bones capsule that is really wide. So imagine you have a really wide hosepipe. So a lot of water is moving through the hosepipe at the end of that hose pipe. Um, at the end of the bones capsule, the efferent arteriole that is really, really small. So we have a lot of water coming in but very little water or blood in this case, er leaving um, or filtrate. And that suggests that the pressure is really high. We have lots of fluid going in there, very fluid that's coming out. That means we have filtration and the pressure, hence the name ultrafiltration. And this creates a pressure gradient and hopefully the glomerular filtration rate that's starting to move, make sense. Now, so we mentioned that the glomerular filtration rate was uh 125 mL per minute. And that means 125 mL filtered through that BS capsule. Um um Yeah. So 100 and 25 Millers fluid is filtered. So hopefully starting to make a little bit of sense now. So Jake has his glomerular filtration rate measured using inulin. So the findings indicate that his G fr his glomerular filtration rate is too high, which of the following mechanisms would decrease his G fr but basically what the question he's trying to ask is that the pressure within the BS capsule is really high. And from the following options, which one would if um implemented would reduce the G fr uh inulin and creatinine are two measurements which we can do to um measure G fr inulin being the gold standard. But creatinine tends to be used um in a clinical setting. So I'll give you guys about 15 seconds for this one if we could end the pole that please. So looking at the answers, a lot of people went with D and a lot of people went with E So it was quite narrowed down. So the answer is D. So if we increase the diameter of the efferent arterial, that allows more blood to leave more fluid to er that allows more blood to leave through the efferent arterial, therefore, reducing the pressure uh within the bone's capsule. And therefore, um leading to a decrease in that G fr so nearly finished. Now, we have the absorption and secretion. So, reabsorption and secretion are two terms which I would suggest that you become familiar with. Um I was quite confused what they meant until actually looked into it. But reabsorption is the movement of water and solute from the Nephron into circulation, from, from the Nephron into those arteries, capar surrounding uh those the Nephron secretion is the movement of solutes and water from the circulation into the nephron. So the main, the main one I would remember and is would be the proximal convoluted tubule because the proximal convoluted tubule, reabsorbs all of the glucose and reabsorbs all of the amino acids. So, if we have any glucose in our urine amino acids in our urine, that means something is wrong at the proximal convoluted tubule, it also absorbs 65% of our water, our sodium, our potassium and our chloride ions and creatinine is secreted. So, creatinine moves from the circulation into the Nephron um and that's secreted into the G fr at the proximal convoluted tubule, the descending limb of er limb of the limb of Henley of the, the descending limb of the loop of Henle. Sorry. Um That's involved in water reabsorption. The ascending limb is not involved in water reabsorption. And that is because the ascending limb is impermeable to water. And that's involving sodium chloride and potassium absorption. The distal convoluted tubule in is involved in selective reabsorption. So, depending on how much irons, how many irons and the concentration of irons being absorbed up until the distal convoluted tubule. The distal convoluted tubule will then decide whether it wants to abs reabsorb sodium, potassium chloride, calcium and all of these minerals um depending on the ph of our blood and I the concentration of rons within our blood. So distal, so the disal tubule is quite lucky in that sense that he gets to handpick what he wants and what he doesn't want and the collecting duct would then reabsorb uh the sodium chloride urea and water. So nearly there. So these are just a few hormones which would be, which I think are very important um on the, on, on, on reabsorption. So the main one being a DH. So ADH acts on the distal convoluted tubule and it acts on the collecting duct and the effects of a DH is water reabsorption, aldosterone and angiotensin. I don't think you'll have covered that yet. This yet. You will cover this when you do the um renin angiotensin aldosterone system system. And if any, if any of you guys are really keen, then you can look into that because that is a very, very important system uh within the kidneys and within the heart as well uh maintaining BP. But aldosterone acts on the collecting D and it in and it basically allows for sodium chloride um and sodium chloride and um water to be reabsorbed. And it also allows for potassium secretion from uh the circulation into the Nephron angiotensin. Two acts on the proximal tubule and the ascending limb of Henley um loop of Henle, sorry, and it acts on um water absorption and uh hydrogen secretion. And finally, I believe this would be the last SBA of today. So, a DH I believe is quite an easy one. So, a DH plays a key role in water reabsorption, uh inhibition of A DH due to alcohol consumption leads to excess urination and dehydration. Where is a DH produced? Is it produced in the anterior pituitary, posterior pituitary, zona fasciculata, zona glome, Losa and or the zona reticularis. I'll give you guys around 1010, 20 seconds for this one you try is the last SBA of today. And um a lot of the F ba s um of today were, were if not questions from F one or F two were generally high, high questions which are, are tend to come up often uh year after year. So I hope you guys did enjoy um the SBA from today. But if we could end the poll there, please. And we can see what people wrote. So, 67% of people wrote the anti pituitary and 33% of people wrote the po um chose the posterior pity. So it's great that we managed to narrow it down with the pituitary. Unfortunately, um to most people, the answer was actually the posterior pituitary. So the posterior pituitary produces um a um a DH. But the other strictures which I am glad to chose um would be the strictures within the um adrenal glands. So that would be the z glomerulosa, zona fasciculata, zona reticularis um and the adrenal medulla. So the zona glomerulosa is involved in aldosterone production. Zona fasciculata is involved in secreted cortisol. Zona reticularis is involved in the secretion of sex hormones such as estrogen and testosterone. And the adrenal medulla is involved in adrenaline and nor adrenaline and that is the end of my presentation uh Right on the dot At six o'clock. Um I hope you guys can enjoy. It would mean um It would mean so much to myself and Dave if you guys could fill out the feedback form and uh I hope you guys did enjoy uh the presentation.