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Okay, everyone. So today we're going to be doing a little bit or physiology of of you eso It's really helpful when we come across his urology and home. So the teachers today, I'm gonna cover quite a few different organ systems and talking a little bit about how they work. Since in a level, I'm sure a lot of people get confused, for example, of gas exchange and the kidneys. And it's super super useful for you just to cover it and review again. Just a quick reminder for everyone who's watching the video, uh, feel. Please fill. Fill in the form that we sent out a couple days ago for, ah, data handling slash memes. Practical questions. Stuff do send that in. It's really helpful for our teachers to get some precession Malaysian or where, but you are a lot. Okay, so I think 100 to the teachers today for his old drove you. I, um I guess I'll go first. Since my topics are covered first in the year, my name is Jam a second year at Saint John's on I will be covering nerves action potentials on the muscles. So I'm gonna try and show my screen. I hope it works. I'm I'll do that now. You know, if can you see that just comes up. Oh, okay. So, um, the first thing is something probably not that exciting. Um, I need to cover some visits. Concepts, because some of you might have not done physics a level I didn't on go. There's one thing which I think we should all know about before we start on. That is about capacitors. Because I had never heard of a capacitor when I started. So, uh, what is a capacitor? Well, it could. Pastor is an electrical component that constable electrical charge on. If we think of it in its most simplest, um, form, we've got two parallel conductors within insulating material in between. And so because we've got an insulated material in between on one side, we can gather positive charge on one side, we can gather negative charge on. That's why it constricture arj because the two charges insulated from each other. So I've got a question here, Um, which I want you to think about and I give you just a few seconds. It doesn't really matter. Um, can you think off the biological example, that's really important. That could be compared to a pastor. So I'll just leave it 10 seconds, right? I hope you thought of it. Is our pastor membrane on day. So the membranes in Nurse Ailes are like one big, longer pastor running along the whole length of the nerve. So, um, the next point is our important equation. We have the capacity in, um, capacitance equals charge over, um, voltage. And so that's one equation you might have to remember that you might not have seen already on then. The final point that I will say is a capacitance off a certain something is that depending on it's area the distance between the two conducting plates and then the the insulated material between them. So, um, that this will be covered again later on in the year for you. But that's why a Miley my later neuron has a different capacitance, too. In that area has a different the president's to know my native neuron because off the distance between the two conducting areas inside and outside, then sell on also the material, it's insulated in between, which in this case, would be on one cells. Um, okay, so I think that's enough new physics for you. Next thing is some equations, which you might find useful in the first instance that you probably have seen before. First one is quite simple voltage, because current times resistance um, it's a nice and simple and come on which we should remember next one charge equals current times time. Um, you might not end up using these, but it's just it's important to understand them so that when your supervisors come to talk about them on bringing new equations, you understand the basics. Um, we've got our previous one. That capacitance is the charge of the voltage, and the final one is about resistance. And this becomes important when you're discussing the resistance of in your on on how quickly it's going to conduct a potential, Um, we have the resists. The resistance equals the rest resistive itty off that particular material multiplied bites area divided by its length. So that's four important question is that you should probably have already covered Okay, um, so now we'll move on to nerve impulses themselves. Um, so let's start with the resting potential because we may start out when the nervous doing nothing. So we have a resting potential, which is usually around minus 70 millivolts. I'm in a nurse. I'll especially from the always put it's minus 70. It's not, You know, you need to remember the minus, um, on. This is because there is an imbalance off sodium and potassium ions on either side, which were both questionably charged on. The polarization is where it here, which means so there is going to be more sitting on one side than the other. It's going to be more potassium on one side, the other. So this polarization causes a voltage across the membrane. Because if you remember from physics, a voltage is a potential difference, and there's a difference in the distribution of these two irons. So in general, interesting cell that said Well, in fact, at all times, the Sony in concentration will be higher on the outside. On the potassium, concentration will be higher on the inside off the cell. Um, so yeah, so like I mentioned the rest of attention that is maintained by the imbalance of violence on then they're selective permeability through the membrane. So there's iron channels all along the nerve membrane on. But it's more permeable, Teo. Um, but particular islands, the last people to others on said this partly helps get arrested potential down to within about five millivolts off arresting potential on. Then roughly the final five will be due to the stadium potassium pump. So if your supervisor says to you, what means be interesting potential? You don't say the sodium potassium pump. It makes a really, really small contribution. Um, it just take things over, really is actually the imbalance of the ions and they're selective. Permeability, ease. Um, next thing I'm a piece of useful very coverage that we talk about when we're talking about these irons flowing across this membrane. Is that electrochemical Grady int? So, um, remember that in diffusion, you have, um, I on slowing or any solute, I guess, flowing from our area of higher concentration to lower concentration. And that's gonna be the same for these sodium bones and the potassium miles. But the fact that they're charged means that there's gonna be extra portion from these positive islands to push them away from each other. So that might be down the concentration grade in, But also as things start to balance out, there's gonna be pushed back from the positive ions. So in the end, that's why the balance might not be exactly 50 50 on either side of the membrane due to the different positive, the different I'm charges on either side. So each eye on has its own electrochemical. Grady. It's It's not just it's comical. Grady in It's an electrical agreement as well. Because of that charge. Um ah, yes. And then the final point is the outside extracellular space in general is more positive than the inside. So we have our two electrodes, one inside the cell, one outside the cell on There's gonna be more positive islands outside, which is why our cell membrane gets the reading of minus 17 minute votes. Okay, that's a brief overview. What you have probably covered in biology level, um, for the resting potential. Now we move onto action potentials. So, um, can you see my cursory to serve comes up. Yeah. Cool. So, um, here we have a graph of an actual potential, and I've got it, um, unable so that we can try and have a look at it and maybe test yourself so See if you can remember Well, this is quite obvious part. This is arresting potential. So we've got no net for alot of ions from either side of the membrane. Then we've got this rising stage where there's some ions moving on to try and remember which aren't moving at this point. Then we've got this falling stage, which is when we're so this this upwards movement is called on depolarizing and then this downwards is called hyper polarizing. So we got going back down to being hyper polarized, and then it goes past the resting potential. Think why it does not see if you can try. Remember why it does that and then returned back. Tow arresting potential. Okay, now I'm going to move onto the next diagram, which is labeled on Explains it. So, um, we have the first depolarizations coming up here. There's an influx sodium ions due to the opening of voltage gated sodium channels. So when the actual potential rise voltage gated sodium channels open on, then rushing down there. Election coming. Radiant. Come this 30 miles. Next we have the report or is a shin, and that's even flux of potassium ions again. That's because they're voltage creative potassium channels were triggered that the same time. It's a certainly ones, but I just take slightly longer to open. They go down on the electric chemical. Great damage means out this out to the cell becomes more negative. Um oh, I might have got it wrong here, but I think it was actually more. Yeah, right. Me Polarization is right. I think, actually, polarization on then it's hot becomes hyper polarized here, which means that we're actually more polarized than the resting potential. And that's because more potassium ions they carried more charge out within your own than the side of your minds carried it. Um, because, uh, there are they're iron channels are not as fast it closing as well. And then we return back to arresting potential because the sodium on channels are shut the voltage gate of taxing mind. China's a shirt. And so we're back to just having are normal little channels all the way along. A little leak channels on back to a normal electric chemical, Grady in with our equilibrium, just like a resting potential. And so it gets back to normal again. On there's a small contribution from the sodium potassium pump, but again, It's not the sodium potassium pump which restores back to resting potential. So that's really important. Remember, the same testing doesn't do that. Um, also it's really important. Remember, in the girl and scheme of things that very, very, very small amount of the islands that I found on either side of the membrane or actually moving, Um, so the concentration grade it's is still the on. That's an advantage because that means that the same, no one can fire more than once without, um without having to kind of restore concentration graded on Detrol Chemical radiance all over again. So in the grand scheme of things, barely barely any irons are moving. Um, hence why? It's just millivolts. Okay, last thing, Speed of action potentials. So you would have covered the fact that the presence or absence of mile in chief can increase well, minor sheet will increase the speed of action potentials. Um, there are a few reasons, but the main one that you probably would have covered is that you can achieve salted saltatory conduction, which means that, um, the kind of actual attention bounces between the gaps in the myeloma chiefs rather than having to activate all the little channels along the way. Um, we also have the diamond off the axon. Greater diameter means less resistance, which means the action potential control after a long finally the temperature. If we have a high temperature up to a certain threshold, that is. But we have a high temperature, and all of the little lions have more energy is they can diffuse a lot faster and cause a little local circuits on. Move along and propagate along the nerve. Um, okay, Next we have a sign apathetic transmission. So this is just a kind of flow of events that happens. I'm leading to, um, a sign of transmission. So action potential arrives at the end off the presynaptic neuron on that causes voltage gated calcium channel strip, and so casting channels are present at the end of on you're on. Um, so that means that Carson Russia's things it's got a really strong electrical company radiant to enter the cell, cast him with them, cause fusion of synaptic, be schools filled with a seat on currency. You would have covered the ones that he took a colonos check sign ups. It is probably already so physicals containing settle. Curlin then traveled to the pre Semitic membrane fuse. And then all that see tycoons released into the sign Optic Left, which is this little gap here. And then they're still tickling, travels across and binds to receptors on the person active membrane on sodium on channels. Um, in fact, actually, that they're not selective, really, to sodium or potassium, but it's just there's a stronger great in pursuit in to enter. But I think I think about it. You probably would have learned that is actually said in my arms. Um, finally, all their sodium ions entering the Postsynaptic cell will cause the polarization off the second membrane, and that's how it started on. I'm okay now on two muscles. The second part. Um, so here's some of the recovery we have the sun kilometer on the stock present particularly, um, Sarcolemma is just a fancy muscle name for the membrane rather than the president membrane. We see the sarcoma. I think that's right. I know known that to myself on then. We also have the cycle plasmid particular. That's instead of our usual and a pleasant particular um, so if you hear, there's where's that's what they mean, So here we have the structure of muscle. Um, with an electron microscope. So try on. Remember what each of the parts are before I reveal it. Um, I'm going to give you 15 seconds and try to remember them. Sorry for your silence. Lovely. Okay. And now we'll look at the label, that one. So here are the important tens unit. Remember, we have Zadvydas six, which will anchor our active filaments on. We have our M line, which is the middle of your mycin filaments on. Then we have acting coming along here. Onda, um, reaching across on the bits where the overlap. It's not labeled here, but that's what the age plans to the bits where the to filaments over like it's for the age brand. And then we have the A band, which is this length. So the whole length and that's the whole interview mycin filaments. And then the i bond. Which of the bits without the, um, my Sinus. It's just acting on these bits on then. Our sarcomere length is the length between two discs. So when you talk about muscles contracting, the actual bits that short tern are your eye band well, your eyebrows will get shorter because there's more. Overlap it for my synaptic in. But your A band will stay the same length because the mice in itself doesn't get shorter. I'm in. Here you go. Here's some more. If you want to pause this one and have a look at this side, it might be a good thing if you're watching a recording. But there's no point going through all those times now, Um so briefly the structure of muscle we have myofibril, which made from thick and thin film that thick and thin filaments, the thick filaments, what we call Miocene on the thin filaments are acting. And we have to add two molecules twisted together, Um, which form the kind of active filament on we have minds in, which is a wheeze. Little projections coming off that we call heads that bind to the actor enjoying contraction. Um, okay, excitation contracting company. So how does the muscle know that it's needs to contract? Well, there needs to be some sort of electrical signal, so usually depolarizations off the muscle. I think the oh goodness. What's it called? The The Junk Neuromuscular Junction. There we go. I got it in the hand out of your own musculature junction because, um, the song prosom it particular to release casting my own's into, um, that's awesome of the muscle were standby in two molecules. Put proponent and troponin usually stops the mice and heads for binding to act in. But when cancer in buys, they move up way, move off the binding site on appetite in on allow myself and connect on defy custom remains available. The cycle, which I'm about to show you the cycle off prosperous cycling is allowed to continue because the my son has been keeping on joining on. So here is a, um, image I got from a textbook. Um, so yeah, so you can see the crossbridge. Forms here, Um, which causes, um, long acting to be bound to my eyes. Um, so this is so this what this complicated thing is trying to tell you on. Then we have our power stroke, which causes ATP on Peter be released. Then if there's enough ATP which usually I mean, I always will be for your life. Um, AIDS people join, which allows the act in on my centered associate from each other and then we can start the cycle again on where the at in binds that the mice and had a lot of hydrolyzed ATP, which then allows it to bind to the acting again. And we have the cross which form again. So this cycle goes run around around on what it mentions here, so there's no ATP. The reason why dead bodies will go stiff initially is because there's no ATP to release. There's mice and head, so they're all stuck. And so all the muscles become, um, really, like tightens. So that's what regulated is is on normally in our life. Um, the cycle, we'll just stop here because it's unbound on, but it doesn't need to be bound on, but it's it's ready to go when it needs to. I'm okay. I got this feeling about four side, but I think it's best to do it at the end. So, um, it's my turn to stop. Um, okay. Thank you. I'm great. I'm gonna present a bit about hemoglobin and the heart. I'll just share my screen okay on D that we get a community that. All right, uh, so this should be mostly things that you might have seen a A level or equivalent, but there might be a couple of new things as well. So hemoglobin. It's a large critter know restructure with full polypeptide chains. Andi, each polypeptide chains has a huge group on each finger. It contains an iron iron on do the oxygen associate with the iron. So in total, each hemoglobin structure can carry for oxygen molecules. So here I'm gonna show you the oxygen association curve. You can see that's this s shaped curve this sigmoid or curve on. This means that the affinity off hemoglobin for oxygen varies depending on the partial pressure of oxygen. And this happens because after the first oxygen binds, you get this confirmation of change, which then makes it easier for the next oxygen to find. So the affinity of hemoglobin for oxygen essentially increases. Um, I'll just point out here we have peace 50 which is the partial pressure of oxygen at which 50% off the hemoglobin is saturated. On here, you can see the systemic arterial blood, which is a healthy person, almost 100% hemoglobin saturation. Um, so here we have this reversible reaction. Hemoglobin and oxygen makes oxyhemoglobin on D. The direction of the reaction depends on the conditions, so ah, high partial pressure of oxygen. Such a Zen the lungs means that we get oxyhemoglobin being made. So this is important to pick up the oxygen in the lungs on a low partial pressure of oxygen. Such a zen respire ing tissues. You get oxygen being released from the oxyhemoglobin. So here we have the ball shift on. You can see here we have the curve that shifted to the right. So when um Carbondioxide is present for any given partial pressure of oxygen, the presented saturation of the hemoglobin is lower, so misfiring tissues they produce carbon dioxide's on dcaa. Open dioxide combines of water to make carbonic assets on. This is catalyzed my carbonic anhydrase on. Come on a casted, it associates into hydrin irons on bicarbonate irons on. Do the hydrogen irons lower the pH, which decreases the oxygen affinity off hemoglobin on get. This is important because if hemoglobin has a lower affinity for oxygen, it means it more ready more readily releases the oxygen so it facilitates the unloading of oxygen at the actively respire ing tissues. So the oxygen's going where it needs to go, Um, and again, this facilitates the uptake of carbon dioxide so it could be removed from these tissues. Fetal hemoglobin is another interesting sigmoid, a little curve, but here you can see you have a left shift. So for any given partial pressure of oxygen, the percentage saturation off fetal hemoglobin is higher than for maternal hemoglobin on. But that's important because the oxygen saturation off maternal hemoglobin in the percenter is lower because the mothers used up some of the oxygen in her respire in tissues. So the fetal hemoglobin must have, ah, higher affinity for the oxygen in order to get enough oxygen on. But that's important for growth in normal development. So just remembering. We have the left shift for the he's fetal hemoglobin and then the right shift for the boar effect. So that's everything on hemoglobin. I'll talk to you about the heart now, so here we have a nice diagram of the heart. We can see we got our ventricles. We've got our Atria on. We've got vows, which you learn a lot about in anatomy. But I won't really talk about now. Um, the blood comes in the deoxygenated blood comes into the right atrium by the vena cava and then goes into the right ventricle, where it leaves by the pulmonary artery and goes through the pulmonary circulation to be oxygenated. And then it comes back into the heart via the left atrium via the pulmonary vein before going into the left ventricle and leaving via the aorta to supply the rest of the body. Um, just wanted to draw your attention to the difference. In sickness of the walls. You can see that the left ventricle has a thicker war than the right ventricle on. This is because you might know already the right ventricle only pumps to the lungs on the left, compensable pumps to the whole body, so it requires a higher pressure because it has to pump further. As I mentioned, we've got valves, and they're important for preventing backflow, which means the blood only flows through the heart in one direction. Onda. That's important to prevent turbulent flow because if you get turbulent flow, you're at a higher risk of getting from this formation, which is what you might have heard called clots before. Onda obviously clots if they get lodged in your circulation in your brain you can have a stroke on. There are many other consequences, so that's not good. Um, again, just this important equation. Cardiac output equals heart rate times straight. William. You'll probably come across that a lot. Invest Year Nice. The cardiac cycle. I probably won't go through this in detail cause you'll go through it more in more detail in first year, and I don't think it's particularly interesting. But, um, this just shows the direction the blood's coming through so into the atria, down into the bench, coz and then out. And this is just something you probably haven't seen before. But we came across in first year, and it's quite interesting. It just shows that in the heart you have sometimes what's caused, cooled and I've all you metric contraction, and it just it's shown nicely on this graph. That means that the pressure changes, but the volume doesn't so you can see here the volume on the X access because like that, so we're no changing volume, but we are changing pressure, but that's not really that relevant. You'll cover that in first year, so don't worry. Here, I'll just do an overview off the notes. You have your sign of atrial note in the wall of the right atrium. So this means that you're right and your left atrium contracts at the same time. And you also have this band off non conducting College and fibers are really important because if you didn't have them, the, um, impulse would go straight to the ventricles, and then you'd have your atria and your ventricles contracting at the same time so you wouldn't get a coordinated contraction. So you have that non conducting college and fiber. Then the impulse travels to the Aviane earthy atrioventricular node. And then from here, there's a slight delay to make sure that the atria have fully emptied before moving onto the ventricles. Um, so it goes down the bundle of hiss along the back injury fibers, and then that causes the contraction of the ventricles from the bottom to the top, in sort of a squeezing motion. Here we have a little overview off the E C. G. So here we have our P wave, which is the depolarizations off the atria. Here we have our QRS complex, so it's much bigger than the P wave on That's the depolarizations of the ventricles. And then here we have our T wave, which is the repolarization off the ventricles on. If you're wondering sort of where the repolarization off the atria happens, it's somewhere in this curious complex. It's kind of masked, so we can't see it on. Just know that bigger wave means stronger contraction. So the curious complex, because it involves the ventricles is much bigger than the P wave. And here we just have some clinical applications of the EKG. So here we can see we put these curious complexes on the Our point is that the top of the QRS complex is so here we have a normal heart, our interval. So that's a healthy heart. Here we have a decreased our our interval. So that means that the heart beats faster on this can be called tachycardia. So too fast heart rate. And then here we have an increased our our interval. So the heart rate is slower and that's bradycardia down here. We can see that we have what looks like normal cure rest complexes. But just this squiggly line in between the QRS complex is there's no clear p wave, so the atria aren't contracting properly. So this is atrial fibrilation where the atria just sort of contracting really, really fast without any rhythm or coordination. And this is important because it can result in turbulent flow. And like I mentioned before, that increases your risk off from this formation. So now I'm gonna move on to a problem solving exercise which hopefully you can work out with some of the knowledge you already have. Um and I'll just give you some time to think about each thing. So imagine you have a patient who has a hole in their heart on Did you learn all about these in first year? But the most common is, uh, ventricular septal defect. So hole between the ventricles on. But there are many other holes in the heart. Think about which way with the blood flow if this patient had a hole in their heart, so from right to left or from left to right, so it would cause blood flow A from left to right. So this is a left to right shunt. This is because the left centrist ventricular wall is thicker than the right, as I mentioned before, because it has to pump blood to the whole body rather than just through the pulmonary circulation. So you've got the blood in. There is a higher pressure because it's being stored in a smaller volume. On day fluids flow from high pressure, too low pressure, so that flows from the left to the right ventricle. But what can happen is your right ventricle is coping with, ah, higher volume of bloods than it normally would. So it's over working. So the right ventricular will consider um, or hypertrophy on. Do the pressure inside the right ventricle can build up on eventually. In some cases, the pressure in the right ventricle can actually be bigger than the pressure in the left ventricle so it can shift. Um, so then you get this right election so the shot reverses on this is called Eyes and Mangus syndrome. You'll probably learned about this in first year, but it's very rare. 1 to 6% off adults born with a heart defect will go on to develop eyes and make a syndrome, so it's not common at all. I meant just what symptoms do you think these patients might have thinking about soul, which brought this mixing that sort of thing. So the symptom I really want. So, like, highlight is the cyanosis. So these patients might appear to be actually a bit blue. Um, and this is because you have your deoxygenated blood in the right side of the heart that can just go straight into the left side of the heart without going through the pulmonary circulation to be oxygenated. So you get this mixing off oxygenated and deoxygenated blood on that's then pumped around the body so the patients can appear bit blue, and they're not getting sufficient oxygen. Hence why they probably have the dizziness and fatigue on Ben. The pulmonary hypertension is because remember, the blood's coming at start from the left to the right side of the heart. So then it gets pumped around the pulmonary circulation, but more of it's being pumped around. So there's a higher pressure in that circulation. But yet that's all I have for you today. I'll pass it on to you. Thanks for listening. Hi. I even a surge. Um, attic up teo 100. It'll take you a bit about, um, Espirito re on. But renal physiology, um, I think is my screen Shit. Yep. Yeah. Thank you. Alright. Going to start with, uh, respiratory physiology? Um, was it to begin with? I'm gonna just discuss bridge them. How do we get a I/O of the loans before we even talk about gas exchange? So for eight of low, we need to pressure difference. So that means the pressure is like the lens needs to be different to the pressure in the atmosphere. Remember, product them. They will always flow from high pressure to a local pressure. Okay, So, inspiration, We need the pressure in the lungs to be lower for 18 of insulins on for expiration. We need the pressure, um, in the lens to be higher for a two out. A little point to remember is that inspiration is active. So this involves muscle contraction. Where is normal? Expiration is passive, So the muscles just relax on the lungs on the chest wall. Just recall you. You can get active expiration a swell. You force air out. But usually expiration is passive on the pleural space. This is the space between the thoracic wall onda the lungs. So the gap between that is very, very important for the briefs. The mechanisms of breathing. Um, it's really important to generate pressure. Difference is, um, in the lungs on do along here to flow. So inspiration, as the diagram showed, was well stopped with muscles contracted by muscles contracting. I mean, the diaphragm was left in, uh, creating more space in that thoracic in the pleural space onda, the intercostal muscles will contract on. They'll move your thoracic cage sort of up, and do you increase in the volume off the clear old space? So if you increase the volume of the space between your thoracic cage on your lungs, um, the pressure is going to drop the drop in pressure. Then I was the lungs to expand on. If you get a bigger lung volume, the pressure in the lens also drops. So now you've got a lower pressure in the lungs than in the atmosphere on a controller. Wind billons. So that's an active poor service. Because the diaphragm from the muscles have contracted on, the pressure has dropped. Allowing a to flow in expiration is just the opposite. Remember, it's the passive well, so the muscles relaxed to the diet from left on the thoracic cage will relax. The move down again on this will decrease the volume of the bureau space so that space between the grass EKG on the lens will get smaller. Well, you increased the pressure around Dylan's in the pleural space. We'll decrease the volume of the lens. And if you've got a low of about lung volume, the pressure in the lungs is gonna be higher. The pressure in the lung is that higher than the atmosphere, and they come off with high pressure. Millan's out into the atmosphere, get expiration. So that's how we move in an active the lens. And I, um I'm going to explain to you just a little bit about the anatomy of the lungs themselves. And I'm sure you've seen this. We have you trickier, which comes on your neck on splits into left and right Name. Bogguss on this keeps bruncheon and they get narrower and narrower. More numerous cetera like a tree on the end. And I'll be with me like I'm sure you know, Um, the purpose of all this bruncheon is to warm the atmospheric. It will be cooler than body temperature, so we want to warm this a 12 body temperature and humidify it. So when add some water, basically that another very important property of all this of the sort of the airways themselves just to filter the air coming in. So we want to trap any dust particles and pathogens sort of anything coming in to stop thumb. Um, reaching out. I'll be only, um, to do this. We have some mucus stuff, sticks to the mucus and have cilia to move it up. The airways. Okay, um, the pulmonary circulation than just a Cialis, uh, spoke about earlier is thie. Blood that passes through the lens is coming from the right ventricle around the lens on back into the left atrium before it's bumped. The body is a really important circulation. This is the blood that's in the lens gets oxygenated. So when we talk about blood in the lens, this is it. On a little brunch on Keep punching into capillaries. So these capillaries, then we'll surround the alveoli is you can see in the diagram and they come into very, very close proximity with the alveoli is a very, very similar and bring between the capillary on the alveoli themselves, allowing a very thin diffusion barrier for gases to exchange between the allergy Only on the pill, every themselves there's loads and loads of I'll be only in the lungs. So this creates a huge surface area for exchanging the higher the surface area. The more gas exchange you're gonna get, you know, in the same amount of time on it brings the gas in the A m. Sorry. The gas in a on the blood in very close proximity. Um, but they don't, you know, they don't touch for the exchange of gas is to take place. Um, right now, moving on to gas exchange. So explain how we get into the lens on now. We actually need the gases to swap between the alveoli and the blood. There's something I want you to remember about that the gas exchange happens twice. It happens once in the lungs between the atmospheric, you on the blood on happens and gain at the tissues, so the blood will give some glasses to the tissues and the tissues for the blood. I always used to forget that it happened. The tissues is that I only ever thought breast rations about the surgery was about lens. So happens twice. Onda just like earlier when I described. We need a higher pressure on a lower pressure for you to float done. It's pressure Great again. This is true for individual gas is a swell. So they moved down there. Partial pressure, greedy int. So that means that, for example, oxygen an area with higher oxygen pressure Um, I am. If you've got a lower oxygen pressure in another area is gonna flow to the lower partial pressure of oxygen. So in the case of us breathing, the partial pressure of oxygen in the atmosphere is higher than that of blood. So oxygen comes down. It's partial partial pressure. Greedy int into blood on the partial pressure grade and of oxygen in the blood is hiding that of the tissues so oxygen could move down that Brady and then into the tissues on, if you'd expect it's just the opposite for carbon dioxide, which is our waste cans. So our partial pressure of carbon dioxide is higher in the tissues and it is in the blood, so it come from the tissues to the blood on. Then it's higher in the blood in the atmospheres were coming back out again, so I hope that's given a very brief overview off spirit topics. Um, I didn't fast sort of too easy to difficult. I didn't do a level. Got allergies. I'm not quite sure what you know. Now I'm going to talk a little bit about renal physiology. I start with just describing the kidneys because I think it's quite hard in Reno physiology to actually picture the anatomy of what's going on. So as you can see in the diet ground, we have a court act, which is the doctor bit of the kidney on the medulla, which is the in a bit of the kidney. So should we appeared of nephrons. I never realized that they sort of start in the cortex on D and in the medulla. Um, they're very small on. It's like a small unit within the kidney, so the kidneys contain not to lots of that from's, um, we have then the ureter, which collects the urine and carries off to the bladder. And we have a renal after, um, they will. Blood comes in and after the kidneys, we've got blood coming into the kidney lead. Leaving on your leaving is well, so the function of the kidneys eyes to regulate body fluids. So, um, is very easy to associate kidneys with urine. And yes, they produce. Um, but I think it's important to remember that their job is to regulate the composition of our blood. Extracellular few. It's a swell. So they regulate the volume. So how much fluid we have in our body? It's osmolality and its composition. So tweak the levels of a lot different ones are blood, um, to go well of our fluids on do, uh um, and is produced as a waste. So rather than thinking, kidneys produce urine, think from us regulated horse in our blood in straddle I I think that's quite helpful way off thinking about being on physiology. So, um, now the nephron. This is a small unit off the kidney when we have a glomerulus, which is up in the cortex, um, ways. Blood comes in, uh, the to the kidney on, but we have it ends in a collect in duct, which leaves through the medulla into renal pelvis and act into the ureter. See, also, we have a path along the nephron. If you if you're not sure you have a primary less approximate convoluted tubule, but big loop with heavily in middle, a distal convoluted tubular which ends in the collecting duct. And around the nephron, we have, um, capillaries sort of know what part of it is known as the visit Rector, if you hear that, but these capillaries in very close proximity the nephron and allow exchanges to occur between the blood on do the nephron itself. So, um, computer, it's something. You go back over the the nephron. Has three main courses is occurring within it. We have filtration. We have reabsorption on. We have secretions, or filtration is happening in the glomerulus that initial bit way. Um, blood enters through the Afrin tart iria well, circulates in a network of capillaries on, then leaves really different of, um, different arterial. Um, in that network of capillaries, uh, it's quite high pressure, and it's forces water and solute out into the bones caps. You're ready to go around the rest of the nephron. So the is a little bit weird. Usually and often you really would become a capillary which would become a van. You asked someone, but in this case, it isn't. We have to arterials will complete a reason between on just a nisi way to remember the Afrin to me from doctor really is just automatically is before he in half about to the Afrin arterial was first s o water and solute are filtered out. Is an ultra filtrate, um, into the nephron. So that's filtration. And that happens in the primary less, um, a little bit, but I don't know if you would have done this. A level is something called your g f r, which is your glomerular filtration rate. And this is the rate which that filter it is forced from the capillaries into the nephron. Um, and it's altered essentially by the pressure within that, that network of capillaries. So if you have a high pressure more filter, it is gonna be forced out to your G f R is going to be higher on that. Could be altered by change in the diameter of those Afrin and different after year olds. And it's quite a logical thing once you've got your head around it. But you'll get talked a lot, uh, about how to, you know, well, this out. But I just assume example, if the Afrin's off two year old I'll. It's more blood is going in on the e front. Arterial constricts just that much harder to get the blood out on the pressure inside that network of capillaries is gonna be quite high. So I'm always gonna be full stopped into the nephrons. You're gonna have a high IgE Romeril, a filtration it and thats up, then the GFI quite clinically relevant. Okay, Now I want to re absorption So that number two in this diet ground. So it's the transport off solute some water from within the nephron back into the capillaries. And it's really, really important, because when we have this filtration Lourdes and Ordell's them of stuff is filtered into the neck from we can't afford to lose it all. So we need to regret them, re absorbed most of it to avoid excess doses. You know, we could we couldn't survive if we lost everything. Last proven by the fact that 65% of water assault on potassium is reabsorbed it pick the proximal convoluted to go just up again. And bit of that for me. Reabsorb all of that on in the beginning. Bit of natural. A swell we re absorbed. But we'll glucose on all the, um, you know, acids on Finally done secretion, which is number three in the diagram on last transport off, uh, molecules from the capillaries into the nephron. And that tends to be more regulatory. Come for Ph, for example. So we'll move acids and bases in the nephron. Um, and also stuff I drugs and top seems to make sure we get rid of them to You hear about these processes in a lot more depth, but I hope that just gives you a reminder off your, um, level content. I lost me. Done, huh? If if I'm hunted black over to Marquis Yeah, Wonderful. Thank you, guys. Let me just stop the recorder.