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did you just start recording? Perfect. On the show. My screen. Okay, great. And I see, um, you will concede that. Uh huh. Great. So, hi, everyone. I'm Shree, and today will be covering some hiatal topics and restaurant in medicine. I will be doing the anatomy, histology some of the physiology aspect. And then Justine's going to take over and do some pharmacology and pathophysiology. Great. So, as usual, just to test our pre existing knowledge A few s p s o back if you could just launched a pole, please. Around 30 seconds for each question. Great, sir. I think I'll end the pulled there. Um, you guys, I should absolutely smash it. It is be the fourth rib second question again, if you could just long to pull these. That's fine. I'm gonna end the pole there again. Um, this one had more of a mix, but the right answer was be, um And then finally, just one more as baby before we start our lung and Anthony Amazing. So you guys absolutely fascia that one as well. That is, he eating two receptors. Great. So without further ado, let's do some long enough to me for a such a start off with our basics. We've got a right lung and the left lung. Now these lungs are divided into a few lobes. Both of them have a superior low. The right lung has a middle lobe of the left lobe, doesn't of the left lung doesn't and then both lungs haven't inferior lobe. So the way I like to remember that the right lung is divided into three lobes is that both right and three have the letter or in it, so just sort of reminds me that the right lung has three lobes. So then let's just talk about a few of the surfaces so the pop of the lung is referred to as the apex, and then the bottom is referred to as the base. We don't have a few fissures that we need to be aware of. So both lungs have an oblique fissure, which sort of runs diagonally. In the case of the right lung, that's going to divide the middle lobe in the inferior lobe. And for the left lung that's going to divide the superior Logan inferior low. Since the right lung has three lobes, it it's gonna have to fishers. So the additional fissure is referred to as the horizontal or transfers Fisher on. That obviously is just gonna run Horizonte. A few specialist it features of the left lung is one the cardiac knowledge. So the cardiac notches basically sort of an indentation of the left lung to accommodate for the heart. So we know that the heart is sort of displaced to the left side. So the cardiac notches an indentation just to accommodate for that large, pericardial peri cardio sac that the heart is placed in. We then have something known as a lingular, which is just sort of a tongue like projection of the left lung. Right, So now let's talk about the vasculature, the blood vessels. First, we'll talk about the D auction ated blood so that the auction a did blood is going to leave the heart and enter into the lungs by the pulmonary arteries, which is one of the great vessels. Obviously, the lungs main function is to oxygenate deoxygenated blood. So once that the auction a did blood and twist the lungs, it's gonna get oxygenated and re enter the heart by the pulmonary veins after oxygenation, Um, the heart is obviously gonna pump out the blood, the systemic circulation or the rest of the body on this is going to flow through the aorta. Now the pulmonary circulation differs from the systemic circulation in two main ways, the first one being that the arteries carried the auction ated blood like we just mentioned on the second one, being high poxy a induces vasoconstriction. So usually in the systemic circulation if we have high poxy A, which is when there's less oxygen supply to a tissue. What are body's tried to do is they try to base a dilate so that they can supply more blood and more oxygen to overcome that hypoxia. But in our pulmonary circulation, it's slightly different because when there's high poxy A, what happens is the blood vessel try to vasal constrictor in order to divert the blood to a better ventilated or better perfused area. When I talk about the insulation and profusion in the next few slides is gonna make a lot more sense. But those are the two main differences between pulmonary circulation and systemic circulation. Great. So now let's talk about the innovation of the lungs. Um, so we have a parasympathetic supply and a sympathetic supply for the person that X apply. It is going to be regulated by the vagus nerve on is going to bring about bronchoconstriction basal dilation and increase mucous secretion. Now, I've also detailed what the specific receptors do for each one. So if you guys want to go back to the slides and refer to it, um, you can do so let's just talk about the sympathetic supplied, um so the sympathetic supply is brought about by the pizza. Two adrenal receptors on a break. It brings about bronchodilation and basic constriction. Now, the easiest way I remember this is by thinking about fight or flight. So imagine were put in a dangerous situation, right? Imagine we're being chased by align or something. Um, that's obviously going to trigger are sympathetic system are synthetic reflexes on What's gonna happen is our heart rate is gonna increase via vasoconstriction. Um, obviously, when you're running, you want as much oxygen oxygen to the tissue as you can. So your airways are going to bronchodilate in order to allow for increase translation and increased perfusion to the tissue. So that's why sympathetic supply is going to bring about bronchodilation on basal constriction. On that, I just remember that the parasympathetic supply does the opposite, so it's going to control bronchoconstriction and basically relation. Um, there's also something known as the visceral Afrin. This is to do with the pain pathway. So if there's any pain that's felt, relays this information to the CNS for the central nervous system. Now, um, memory eight. For this to know which receptors are placed for the synthetic supply is that we have one heart. So it's going to have beetle one adrenal receptors in the heart, and we have two lungs, so there's gonna be beat. So two adrenal receptors in the lungs. Now the slide is quite wordy, Um, but it is quite a high yield slide, especially in surgical applications. When you want to know from the external aspect what actually lies within without actually cutting in, you want to know where the structures actually lie, but I have quite a good name on it That's worked for me, which is a 2468, 10 12. So these are the main landmarks in the service anatomy, where the pleura either diverge or convert or, like, go behind the ribs. So if we start off with the apex, that's where the pleura start. And then at the second rib, they're both going converged the midline. Then at the fourth rib. Like we mentioned the SBA, your your left sided tour is going to diverge slightly in order to accommodate for the heart on. Then the sixth rib at the 60 or the right tourist going to start diverging and then at the eighth rib deplores the floor on both sides have been across the midclavicular line. Which is it? The middle of the clavicle on. Then, at the 10 through, the Tora crosses the Midaxillary line, the middle of the armpit on and finally at the 12, and they sort of curl around the back and then meet a to posterior side of the 12 great Um, so now I'm moving onto the hilum. The Hilum is basically the lung route, or it's where structures either enter or leave the heart. Now it's quite important to know which structures comes superior Lee and then inferior Lee. So for the right hilum, it starts off with the Broncos superior early on in the pulmonary artery, and then the pulmonary veins on there for the left. Hilum. You have your pulmonary artery superior early with the bronchus and the pulmonary veins follow in them. So these are the other sort of contents you find in the hilum. The main ones I've listed, sort of on the slide, the way I like to remember which comes. Where is through this memory aids, right? Bronchus is superior. So Royal Bank of Scotland, they both have the same initial letters. So I remember that. Oh, yeah, the bronchus in the right hilum is situated superior early on, then followed by the arteries and then the veins. Okay, so for this one, I want some participation. For me, guys is the tricky and bronchial tree. It's quite a simple concept. So for the first one, this label can anyone in the chat tell me what it's pointing to? Yep. Tricky. Agree. I want is much participation from you guys as possible because we have been working for the sleds for a little really long time. So yeah, trachea. Tricky is main function is sort of to allow air to enter the actual respiratory system on. But what they have are these see shaped cartilaginous mornings made of highland cartilage on because when you're inhaling, inhaling and exhaling, there's going to be quite a few pressure differences in the actual drug Kia. And so to prevent collapse of the airway, these cartilaginous rings actually hold the trachea and to spend them open. Great. So now can anyone tell me what this next? Um, structure? Is it sort of bifurcate? It's someone, said the Korean uh so yeah, that is the point at which the drippy a bifurcate, But they bifurcate into the main bronchitis. That's right, then the main bronchitis, or then going to buy for Kate into what structures? So there's going to come just before the bronchioles. This might be a slightly harder one, so this is referred to as a segmental bronchus. And then finally, they're going to buy for kids into like you guys rightly, said the bronchioles. So we have two different room feels we have the terminal bronchioles, and then the respiratory bronchioles now or bronchial tree, can be divided into two main portions. One being are conducting portion, and in this portion there's actually no gas exchange occurs. It's mainly just the movement of air to the actual respiratory, bronchioles and alveola. And then so the conducting portion of the eternal bronchioles and then the respiratory portion of the bronchial tree includes of respiratory bronchioles and the alveolar. So in this area, obviously there's gonna be some gas exchange. So what happens is the capillaries that line next to the albuterol. I are going to have a carbon dioxide diffusing out of them on an oxygen diffusing back into them. Now, the LDL are really well adapted for their function because they have a large surface area to volume ratio. They have a really good blood supply. How they have really thin walls that are only one cell think one cell thick and made up of simple squamous epithelium. So obviously, because of the thing gas exchange barrier, that's going to increase the efficiency of gas exchange. Amazing. So, um, openings of the dye front. This is a really high your point on. I have sort of really easy way of remembering this. So just to know the cable highest occurs at the level of T eight on the way. I like to remember this. Is that the letter? Vienna vena cava has eight letters, so it occurs at the level of T eight. Through this perforation, we have the inferior vena cava and the terminal branches of the right phrenic nerve passing. Um, and then can anyone can anyone tell me the nerve roots of the diaphragm or the innovation of the diaphragm? C 345. Yes. C 345 keeps a diaphragm alive. Okay, so then we'll move on to the esophageal hiatus. Um, so this is where the esophagus, right and left vagus nerves. And the abdominal part of the esophagus is supplied by the left gastric brains or the left gastric arteries. Um, and the way I like to remember where this perforation occurs is at the letter. The word esophagus has 10 letters in it. So it occurs a p 10, and then finally, we have our aortic hiatus. So the word aortic hiatus has 12 letters, so the perforation occurs at the level of T 12. Um, so I hope that's sort of made it easier for you guys to remember the openings of the diaphragm. Great. So now we're just going to move on briefly to histology. Histology is another really high yield concept. They really like to ask about what? Everything they're found in which areas of the airway. So if we start off with our trachea and bronchus, I just find it really easy to relate structure to function to remember these things so tricky on bronchus have ciliated pseudostratified columnar epithelium. Now, why is that? What did the trick and bronchus actually do? Well, at the nasal cavity, we have warming humidification and filtration of the air that's being inhaled. But sometimes we can have that odd dust particle actually reached the level of the tricky on bronchus. So what the cilia do is they have, like, a 3 60 to be motion, and they try to walk away any mucous any dark from the actual respiratory system so that it doesn't affect things like the terminal bronchioles restrict your bronchioles and Albiol I, which are a lot more fragile structures. So the tricky on bronchus contain ciliated shooter, certified Columbia Epithelium. Then if we move on to our bronchioles, they contain ciliated kilometer again just walked away any of the mucus and dust particles. But then at the terminal bronchioles, the terminal bronchioles are too small to accommodate the cilia any longer. So they start to lose thesis here and then becomes simple columnar epithelium. Then we moved down to a respiratory bronchioles, which contains simple cuboidal epithelium. And if you guys remember, cuboidal epithelia are usually found in places that have a secretary function. So in this case, that's our car cells are Clara cells actually help secrete a portion of surfactant, which is something I'll get onto in a bit. And then finally, we have our Albiol. I, like I mentioned alveoli, are made about simple squamous epithelium. They're only one Celtic in order to increase the efficiency of diffusion and gas exchange. Now, it's also important to know what new besides do what. So are type of human sides of the one we always remember. It's the ones that secrete surfactant in order to reduce surface tension. Now, what exactly is the surface tension will surface Tension is basically the force exerted by the liquid in the thoracic cavity, so that we just like water molecules on the way. That's a fact Introduce the surface tension is that the surfactant absorb some of these water molecules on that's going to break some of the internal Acura forces between the water molecules and That's how it reduces the surface tension. Now, what time when you, besides are one that we never usually talk about, But they're equally as important, and what they do is they form the gas exchange barrier. Okay, now, this is a concept that took me a while to get my head around, so I sort of created an analogy that hopefully helps you guys shadow tissue injury from all ski. See, he's the one who sort of explained it to me this way. So let's start off with compliance. Compliance is first week in any one in the chat. Tell me what compliance actually is. Just a he's e way of remembering it. Okay, so we've got a few answers. Um, and they're sort of on the bright lines, so compliance is basically the ease at which an object stretches. In this case, it would be the lungs. So compliance is also calculated by change in volume over changing pressure. Now, let's talk about that beautiful. An allergy that I was on about. So, um, let's imagine. We have a metal balloon and we have a normal balloon and we're trying to inflate both these balloons. It's obviously gonna take a lot more force to inflate the metallic balloon down the normal balloon so the metallic balloon would demonstrate something known as low compliance. Between that, it's harder for it requires more force in order to allow that metallic balloon to stretch. It's less compliant because it isn't easily stretchable. Now, with our normal balloon, when we blow in, it's going to stretch easily, so it shows a high compliance. So on, Uh, um, sort of blowing up the balloon and inflating the balloon it's going to easily stretch on. It's going to be very compliant, which is what shows a high compliance. So in the case of the lungs, if a lung has a low compliance, that means it's harder. It takes more effort for the lungs, actually expand, whereas if along is highly compliant, which is what it should be in the normal situation. In a healthy situation, that means it doesn't require a much effort or forced to actually expand the lung. Now, last menses just a complete in verse or the complete opposite of that. So it would be the easier which an object be coils or returns to its original shape. Um, so in this case, if we take the metallic balloon, a normal balloon say it's already inflated. The metallic balloon is going to have a much harder time deflating down a normal balloon so the normal balloon would have a high last. Since the cause, it doesn't require much effort to return to its original shape, whereas for the metallic balloon it sort of retains its shape and takes a lot more effort to return to its original shape. So that would demonstrate lower lessons. I hope that was useful because that's the way I sort of think of it. Great. So now we have another SBA. If we could just get the pole launch, please. I think I'll end the pool there. So there is again, like a mixed bag of answers. But we're going to explain that in the next few slides, the answer was a so well, don't everyone who's had a carbon dioxide. So let's talk about the different receptors of the lung. First, we'll talk about the mechanic receptors, which detect strange Sorry, which detect, stretch or inflation are stretch receptors are involved in One of the reflex is known as a herring brewer reflects on that's when it's sort of terminates inflation after finding out that the mechanic receptors have actually stretched. So these are gonna be found in the smooth muscles of the airway or the lung parent timer. The lung parent calmer, basically the skeleton of the lungs. Then we have our J receptors, or a just a pulmonary aceptar is. These are more to do with the actual capillaries rather than the lungs, so they can find out if there's any blocks of the aorta because and that would cause distention of pulmonary capillary walls on. Then they will sort of detect that change and then really, really that back to the medulla oblongata to sort of cause relax a shin of the arteries. Then we have a return, receptors says in your allergic or a topic sort of reactions. This is when you inhale any dust particles, and that's what causes the ejection of air or even a sneeze. So that's what's going to expel any of the dust particles or foreign objects that come into contact with your respiratory system. And then finally, we have appropriate Septra. So are appropriate sectors actually have the complete opposite sort of effect. Uh, that are stretch receptors, so they actually stimulate. So what they realize when there's deflation and will stimulate inflation. So what they do is during expiration. Obviously, your lungs are going to start to deflate, and you don't want too much of that deflation occurring, so you're proprioceptor as well. Then detect that and then tell the medulla oblongata of blonde Girl said that there's too much deflation and it's going to allow inflation to occur once again. So our central chemoreceptor ear's are the main players of the game, so this is one that I want to spend a bit more time on. So what happens is when there is an increased amount of metabolic activity, or if there is a lot of physical activity that we're going through, the amount of carbon dioxide in our computer blood is going to increase. That's going to bind with water to form HTZ or three or bicarbonate acid. Now, the age to see other is going to disassociate to give HCO three and, um, hydrogen ion zar protons. The's protons actually worked two videos pH. But in the capillary blood, we have something known as plasma proteins, and these plasma proteins are going to buffer or neutralize the hydrogen ion. So an increase in carbon dioxide isn't going to cause a very immediate pH change because the's plaza proteins are gonna buffer up any of the hydrogen ion now each to see oh three. And the ions cannot actually pass a blood brain barrier because we know that the blood brain barrier is really specific and what it allows. So h 203 is too big of a molecule to pass the blood brain barrier on the three. And HDLs are two polar to cross the blood brain barrier. So the only molecule that can actually cross is carbon dioxide. So then the same reaction is going to occur in the CSF. Carbon dioxide is going to cross the blood brain barrier, and then it's going to, um, form. Hydrea is gonna form bicarbonate acid. Give the H one H c 03 and hydrogen islands on. Then these hydrogen ion is over here are actually going to cause a change in pH. Because our CSF don't consider those plasma proteins. So if these hydrogen I owns aren't locked up or if they're not buffered, then that's going to reduce the pH and that reduced pH is going to start stimulating the chemo receptors to start firing on. That's what's going to increase ventilation. Now. The increased ventilation is sort of a mechanism to expire as much carbon dioxide. It's possible because obviously you don't want your carbon dioxide levels to increase in your blood on. Then, once the carbon dioxide level's a reduced, you return back to a normal state. If you guys need me to repeat that, then just let me know in the chart. Now, what about our purple receptors? So we have our central receptors, and they're sort of located in the brain and the ventral actual surface of the medulla, and they're quite sensitive to the pH of CSF. However, they have a relatively slow response time, and the reason for that is because you saw those long cascades of reactions that needs to occur before the firing of the chemo receptors actually occur. So they have quite a slow response time. However, our peripheral human receptors, they're located in the carotids Sinuses and the aortic bodies on, so since her located quite perfectly, they can sort of, um, detect the chemical changes in the blood quite quickly, so they have a much faster response time on there. Also sensitive to the pH of capillary blood. Okay, now moving on to breathing cycles and lung function curves. So I am unsure you guys are quite familiar with breathing cycles, inspiration, expiration. What actually happens, so I won't spend too much time on this. What happens first, when we inspire, is that there's going to be the contraction of our diet from So are diaphragm is going to move down and out, and there's going to be contraction of our external intercostal muscles now. What that means is it's going to increase our thoracic cavity. So that means that there's gonna be an increased volume in the thoracic cavity, which will lead to a decrease in the intrapleural pressure that decreases going to lead to a decrease of alveolar pressure, which is they're deformed pressure, Grady, in where the pressure outside the lungs, um, is going to be greater than the pressure inside the lungs. So that's going to force air into the lungs. And that's what happens in inspiration and with expiration is just a complete opposite. So we're gonna have relax a shin of the diaphragm and relaxation of the intercostal muscles. So the diaphragm is going to move up and in so again that's going to decrease the volume of the thorax and bi boils. Law and degrees in volume is going to increase pressure on that. Increased pressure is going to form a pressure grade in where the pressure inside of the acid cavity is higher than the pressure in the atmosphere. So that's going to cause there's a flow out of the lungs, and that's going to cause recoil of the albuterol. So this is a graph that comes up a lot in exams, So let's just break down each value. Let's start off with our first one. Can anyone tell me what title volume is in the chart? Yeah, yeah, the voltage volume of normal breathing. So there's no effort whatsoever. It's just normal breathing and the inhalation and exhalation and that's involved in it. Next, we're gonna have functional residual capacity. So that is this value here on. That's just the amount of air remaining in the lungs after a normal X elation. So again, no effort is involved. It's just normal breathing. Then we have our vital capacity, so here. This is where there is maximum effort in our inhalation and exhalation, and that's going to be denote it by this value here. Then we have our inspiratory reserve volume. So this is the amount of air that can be inhaled with maximum effort. After a normal inhalation on an experience, areas are volume is just obviously the opposite of that. So this is when there's going to be, um, an amount of air that could be exhaled with maximum effort after again a normal breath on then finally, we have residual volume. So this is the amount of air that's remaining of the lungs. This is always gonna be there, so there's always gonna be some amount of air in the lungs. The only time this will change if is if there's like a perforation to the thoracic cavity, and that can obviously be quite fatal. Now, F E V one and FEC are two values that just is going to cover in a lot more detail, cause this is quite important for obstructive and restrictive conditions. FV one is basically a forced experience, revolting in one second, so that's the maximum amount of air you can exhale in one second. So that's with maximum effort on FEC is just a total amount of air exhaled with maximum effort in a maximum excellent shin. So f e c stands for forced vital capacity. Right? So another quick SBA before we talk about the insulation profusion looking at the polls launched. Great. So I'm just gonna end it there. Um, so most of you did get a bright well done. Everyone who said be the answer is wasted perfusion, which leads to a decreased translation profusion ratio. So let's talk a bit about ventilation and profusion. First, we have a few basic zones of the lung, so we have zone one zone two and zone three. And as we move down from the apex to the base, we have increasing ventilation and profusion. So what actually is ventilation? Well, ventilation is the flow of air into the alveola on why is that relation highest of the base of the lungs? Well, we know that the alveolar, the base of the lungs, are smaller than those of the apex, so they're going to occupy less space on what that means is there's going to be more space when expiration actually occurs. So when you actually inhale, what happens is there's gonna be more expansion of the base of the lungs rather than the apex. And so that's going to cause an increased volume on as we know from Boils law and increased volume is going to lead to a decreased pressure. So that's going to form a pressure Grady in so that there's less pressure at the base of the lungs. And so when you inspire, there's going to be preferentially blown to the base of the lungs, which is why we have a high amount of ventilation at the base now with our profusion. That's just basically the flow of blood to the alveoli. And it's a very simple reason as to why the profusion is highest of the base of the lungs, and that's gravity. So gravity obviously has a downward acting force, so that's going to cause blood to pull down in the base of the lungs or just trickle down to the base. Now they're going to be times where we have a ventilation profusion mismatch. So this is when there's either too much ventilation or too much perfusion. If we start off with wasted profusion, that's also known as shunting. So that's when we have perfect profusion. But we don't have ventilation. There could be three main reasons for this. One of them is an anatomic lesions. So far, I'm in a valley is basically when there's a hole in the heart, so that's going to do is that's gonna cause mixing of oxygenated and the auction. They did blood. So it's obviously going to reduce the overall oxygen saturation of the blood that's being pumped out of the heart. We can then have physiological and pathaphysiology culture ending, which is when there's either any diffusion deficits. So that's going to cause a poor gas exchange things like, um idiopathic pulmonary fibrosis or pneumonia. So pneumonia when there is, um, sort of fluid filling in the valve, your life that's gonna cause poor gas exchange because the alveolitis no longer participate in gas exchange. So when there's blood flowing past these alveolitis not going to participate in gas exchange, so there's gonna be this mixing of auction aided and deoxygenated blood, and that's gonna cause the shunting now with things like idiopathic pulmonary fibrosis that's gonna cause thickening of theatrical alveolar walls on That means that's going to increase the diffusion barrier, which is going to reduce the efficiency of gas exchange with wasted profusion. We have a ventilation profusion of zero because we have a value for profusion. But we don't have a value for zero for mental a shin. So fentanyl a shin is 00 divided by anything is going to give you a value of zero. Then if we move on to our base, a wasted ventilation that's also referred to as a dead space. So this is when we have Bentyl a shin, but we don't have any profusion. So this can be anything to do with damage to the actual blood vessel or blockages to the blood vessels. So imagine we have healthy alveolar. They're all able to partake in gas exchange. However, the actual capillaries that are running pasties, Albiol, I are either infarcted inflamed or damaged or even block. That means that blood can't actually flow through these blood vessels and so they can't partake in gas exchange, obviously. So that means that there's gonna be less less amount of blood or less amount of auction ated blood being pumped out of the heart, a dead space would lead to a ventilation profusion, uh, ratio of infinity because we have a value for rental a shin. But we don't have a value for profusion. So anything divided by zero is going to give us infinity. So, um, we have a few mechanisms to sort of, um, you know, contract this hypoc CIA that's caused by wasted ventilation and wasted profusion, one of them being the what I mentioned previously. Which is high pox. Yeah, India strays of constriction. Now you would think that if there was hypoxia, basal dilation would allow more oxygen and more blood to sort of, um, auction eight that area and overcome the hypoxia. But in the lungs, it's slightly different because the basal constriction is going to cause diversion of the blood to a better ventilated or better profuse area so they can actually participate in gas exchange and overcome the hypoxia. Or they can sort of give a higher oxygen saturation of the blood. So this mechanism usually works, and it's quite efficient. However, obviously when we have basic construction that's going to narrow the Lumen of our pulmonary vessels on what that means is it's going to increase pressure and It's also going to increase pulmonary vascular resistance. So again, our pulmonary vessels are quite smart, and they have a way to cope with this, one of them being distention. So distention is when the vessels will actually stretch or distend on. The Lumen is going to become larger in order to reduce the pulmonary vascular resistance and in order to sort of reduce the pressure of the blood flowing through it. We also have another coping mechanism. Notice recruitment. So this is when if there any blood vessels or any pulmonary vessels that aren't participating in gas exchange or sort of supply of the lungs, then they will be recruited to sort of take this blood. Take this blood so that there's an increased surface area that is being covered, and that's going to reduce the pulmonary vascular resistance and pulmonary pressure. Something in track. Okay, um, there's another SBA. If we could just get the pole launched, please. Okay. And I think I'll just end the pole there. Sorry. Um, so some of you got that one right before action? We're going to the next few slides. Someone asked me a question about whether emphysema would cause, um wasted ventilation or waste of profusion. So I'm just gonna move back to the slides to sort of explain it, right? Yes. So, um, with emphysema, that's basically going to be destruction of the alveolar walls. That would, I think, um and don't take me for this, but I think it would be wasted profusion on. The reason for that, it's is because it's actually damage to the L the older wall. So that means the actual algae, like, can't participate in gas exchange rather than damage the blood vessels, which would be wasted ventilation. So I think emphysema but actually cause wasted profusion, right? So let's quickly move on to our last few slides, which is respiratory failure. So the answer for this was COPD, and I'll cover that in the next few slides. Um, so before we talk about respiratory paler, let's talk about our normal range is the main ones that were concerned with is our partial pressure of carbon dioxide and oxygen. So a partial pressure of over six killer house scales is going to be termed as hyper Cap me A, which is basically a high carbon dioxide concentration and a partial pressure of oxygen that is lower than 10 points. It's killing. Pascal's is going to be high pox. Senior, Um, the difference between high box See A and hypoxemia is that high pox era is a reduced auction. Concentration for the tissue grows. Hypoc Sina is a reduced concentration of oxygen in the actual blood. So with Type one respiratory failure, it's also refer to as an oxygenation failure because this is when there is a low partial pressure of oxygen with a normal or low partial pressure of carbon dioxide. So the main sort of failure in this sort of type one respiratory failure is the actual oxygenation, so there's less auction being supplied. So what would actually cause less option to be supplied to the tissue and the blood first is our ventilation profusion mismatch like we previously mentioned? So we have things like, um, idiopathic pulmonary fibrosis. We have pneumonia. We have pulmonary embolisms that cause blockages of the blood vessels. So any of these things can either cause waste of ventilation or wasted profusion on overall Concordes. Hypoc seen yet because it's going to reduce the oxygen saturation of the blood. Then we have diffusion deficits, so deficient deficits or anything that sort of, um, reduce the efficiency of gas exchange that this could be things like thickening of the actual gas exchange barrier, like idiopathic pulmonary fibrosis. It could also be if there is a produced Sorry if there's an yeah, everything's surface area to volume ratio or if there is reduced blood supply that's going to, um, sort of reduce the efficiency of gas exchange. Then we have right to left shunting. So in things like for him in a valley where there is a hole in the heart, there's going to be mixing of oxygenated in the oxygenated blood. In some cases, thie uh, blood can actually bypass the lungs and won't even get oxygenated. So obviously, that's going to lead to a reduced oxygen saturation of the blood and cause high poxy mia. Then we have increased auction consumption paired with low auction content, so anything that sort of increases our demand for office. And so this could be if we are partaking in a lot of physical activity. If we're standing up for a long time during long operations or even in things that accepts is where there's a lot of infection on day so that would increase the demand for our oxygen. But in things like high altitudes, there's going to be a low option content in the atmosphere, so they sort of oxygen supply is not going to meet the oxygen demand. And that's going to lead to Hypoc senior. And then finally, we have hypoventilation. The hyperventilation is when the rate and the depth of breathing is reduced. And so, obviously, if you're bathing is too shallow. That means that there's not enough option being inhaled on it. Some cases there might also not be enough carbon dioxide being exhaled on. That's going to lead to something on this time to respect your failure. So Type two MS Victory failure is referred to as ventilation failure. So this is when there's high proxy me A with hyper capita. That's when there is a low partial pressure of oxygen with a high partial pressure of carbon dioxide. So hyperventilation is the main sort of cause of Type two respiratory failures on Let's Talk About Some a few causes of high blood insulation. One of them is a reduced ventilatory. Efforts of this could be if, with IV drug users on even in obesity. So if you can imagine when they're lying when people who are obese are lying down, there could be a lot of adipose tissue, sort of pressing on the thoracic cavity on. That's going to reduce the rate and depth of breathing. And we can have things like COPD. So COPD, like the SBA mentioned, is the main sort of severe chronic lung disease. That's sort of a cause of pack to mister tree failure, because what it does is it's going to lead to hyperventilation because there's going to be mucus buildup in the actual bronch bronch I and the bronchioles on what that means is, it's going to increase this sort of effort to ventilate the lungs. And so that's going to lead to reduce rate and depth of breathing, which means that less carbon dioxide is going to be expelled unless oxygen is going to be inhaled. And we have depression, depression of the respiratory center. So with things like stroke and drug overdose on D, this is a main one, which is the failure of anything that sort of lead service for two muscle weakness. So motor neuron disease, Gillian Bar Bar syndrome, Duchenne muscular dystrophy. So anything that weakens the's respiratory muscles means that the contract shin of external intercostal muscles during inspiration does not occur. And the relax a shin of external interventional muscles is going to be prolonged. And that's going to cause Hypo Bensel a shin on, then find the chest wall deformities. So anything that even effects the diaphragm or even things like obesity. What that means is the diaphragm is no longer able to contract properly. So if it doesn't contract, it's not gonna have that nice down and out movement. So that's not going to, like increase of their ass. A cavity like we mentioned on that's going to reduce the rate, end up the breathing on finding things like I focal uses, which is sort of an abnormal curvature of the spine, and then sort of, um, press into the grass a cavity and reduce the volume of it. And that's going to increase chest wall resistance, which will overall lead to hyperventilation. Great. So I hope that was helpful. Um, we'll take sort of a five minute break before Justin starts his talk. Just, um right, So So for this SBA, the answer was COPD because it asks what is the most common pathologic Cool cause of type of this type of respiratory failure. So, yeah, you'll be right. Hyperventilation is the most common cause of type two respiratory failure. But COPD is the most common pathological cause of type 2% failure. So I hope that helps again. If you guys have any questions, just put it in the chat on. Guys should get to do it. Um, someone just asked me to go to a type one and type two respiratory failure just in. You don't need to record this. I don't think I'll just quickly go through it. Uh, okay. So if that's okay with everybody, hope of runs back. This is a second part to be a case three session, so I'll be covering a beauties. Obstructive restrictive lung disease is on a little bit of pharmacology as well. So I get right into it. Arterial blood glasses. I know tree kind of mentioned this a little bit, but we're gonna get right away with a little bit of a question. I just see where everything's at. They should They should be a nice leading from she's first half. If I could ask the maximum participation. There's nothing more that I love to see. People just given estaba like it doesn't matter if you get it wrong, all right? We can see who's answering, so just give it a good, good guess. We'll get you into it. Can't give it a few seconds. The long read Amazing. Just as much participation, it's possible, would be amazing. Okay, I think we'll end it there so very well done. Treatment really did it nicely. It is C types of respiratory failure, and so we'll get into a while. I so maybe geez, um, arterial blood gases, this is the normal range is and actually mentioned it. It's just just let us know. It's good to know them. You are gonna give it give be, given the reference values, but it's always just nice to know them just from the top of your head. Just be able to recognize them easier, but looking at, um, a little bit more specifically. So we know that pH is the acidity of the blood that ranges from 7.35 to 7.45. Um, she mentioned a pa Oh, to pee a coatue. The partial pressure's off. The gas is in the blood. Just a little side. Note. P a p with a with a capital A Is the partial pressure off the gas in the alveolus on P A. With a little A is the participation in the arteries, so that's just a little slight side note for the best. Remember, this is just a measure of how well is just a measure of how well oxygen it's moving from on to the blood from the lungs. Eso fox, Joan for have how well it's moving from the lungs. Blood on for a carbon dioxide, How well it's being moved out of the body. Bicarbonate is an electrolyte made by just a byproduct from the body's metabolism on they work, but by having it works in the kidneys to regulate pH, this's by a result, resolving it and excreting it on. It also brings blood, brings by computer lungs, be XL. That, too, but we got a little bit more specifically like a base excess. You might be giving this. You might not be giving this, but basic stress is just the amount of acid required to restore the blood to normal. PH so hi Basics s indicates a higher than normal amount of a bicarbonate in the blood. So there are some necessary times that you want to take a a B G. They're the first one being peri arrest. So Perry arrest Is this recognize period of time just before or just after a full cardiac arrest? There's a period time when the patient's condition is unstable on must be taken to prevent progression over aggression off the full of a full cardiac arrest. There's lots of other indications, but the main thing to know is that they can be painful. And so when you do get into wars and when you first try these out, do be wary of this. So looking at that, looking at acid regulation. So I know she mentioned this with regards to the blood, the blood brain barrier. But with regards to ask as a regulation in the lungs and the kidneys, this's is the reaction that you should know. Overregulation can be seen as a reversible reaction, so I'm gonna need you guys to tap into a level knowledge. I know that's a traumatic time for everybody, but just understanding reversible reactions and equilibrium reactions just remember that bicarbonate is a base. So I put a note there to see her fingers to remember on that so two is acidic, so when one goes up, the compensation mechanisms is to increase the other. So it's an example. If he increased you to, it's counteracted by increasing bicarbonate. So this makes sense if you to is acidic. How you want to contract is by increasing the base to neutralize it. And so the base is by coming in the sense. And as we said, there's a regulated in the kidneys and lungs. So looking at a BG interpretation S o, there's this. This is just a bit of a rough form that I put for you guys, that there are different ways that people say you should be looking at a veggies. But if you have no idea, that's probably best way to look at it. I think the thing to note here is the in any kind of illness. Clinical scenario. When you do start doing our skis, you could always start with confirming the name and date of birth on a patient. That's just the best. If I could give you, you should always just just make sure that you're talking about and talking to the right patient. So that's the first thing you should do on. Then have to put some side notes about respiratory conversation. It's immediately eso. Obviously, when you're breathing, that's That's, uh, You want to compensate respect through respiratory when you bring that that reaction immediate or metabolically, it's a metabolic conversation could take a few days and then a little note on type one and type two respiratory failure. But looking at evidence of interpretation says we said a pH. We first with the age Well, actually, first confirm the name of the spur on the pH. So the Ph is low. Guys noticed acidemia. If the pH is high, that is known as alkalemia, so I'll Gilenya alkalosis. You might have heard of both. Or neither. Alka Alkalemia is the blood pH or seven page when it's greater than 7.45, whereas alkalosis is thie physiological process, causing out colli accumulation or acid acid loss. So, uh, with acidemia, if you had low bicarbonate, this would be known as metabolic acidosis with out leave me if you had a high bicarbonate. This is known as metabolic alkalosis, so you can already see that it's It's the physiologic process, not just their being low, low acid in the blood or past in the blood. And then when we look at if there was high pH go to if there was a lot of high carbon dioxide in the blood, this would be known as respiratory acidosis on low PC or two would be known as respiratory ankylosis. And so that that is just a basic idea or basic concepts that I hope you guys understand it with a BeeGees. I think the best thing I can tell you is just look at it as many babies you can on to practice trying to understand them because there are low loads. Very particular scenario is we will look at. But I just want to give you guys just a general idea. On another thing that you have to know is about compensation. So comes a compensation mechanisms of quite easy because it's basically the opposite off what is going on? So if there's metal like a so says the compensation mechanisms would be respiratory alkalosis, and so I put them there, and so that's a that's a nice little things that you guys remember, so I'll give you some examples. These are questions I just want to I'm going to leave these here and you guys are getting it slides later. But just just to give you an idea of how so, Okay, be genes and what they mean And what you what you can use, maybe use four. The first example. We've got four year old lady post surgery, and it's been playing a shortness of breath. So, as you can see as you might, um, I might be able to know this is type one respiratory failure. We have no oxygen and low See a two. So there is low. See a to another thing that you need to know about Type one respiratory failure is that Type one is hyper. It's low to on normal to low low, too. Type two is when you go to exceeds 6.6 Pascal's. And so there's alkalosis here, but here's most likely to to the patient blowing off. So too, on a Z said, when you when you're losing so two, you're losing that acidity off the blood, almost so that causes the alkalosis with this particular scenario that likely differentials are probably apartment number embolism blocking the blood supply. You can have pneumonia. Common postoperative infection, asthma pony at your pulmonary edema. Onda, um s said that's what this case with the next case we have a 67 year old man presents with history of peptic ulcer disease on has a persistent vomiting. So, as you can see here, there is that high, high pH so alkalosis again, um, with normal partial pressure values. But ah, high bicarb candy. So this is metabolic alkalosis a said high pH of high bicarbonate Valley. So things you know about here is that the compensation would be respiratory acidosis on. So it took me a while to understand this concept, and so do you take your time with this, But it does make sense if you think about it logically. So we've got metabolic acidosis, and the conversation, as we said, is the reverse. So when this to Robert's is a metabolic acidosis, what would happen is there would be an increase in bicarbonate on That means an increase in base, and this is gonna be contacted by increasing acid. And so remember what we said the acid in the blood is. And so by retaining Syria, too, we can increase Theus. It easy of the blood and how they retain See it in the blood. It's by breathing less or it's hyperventilation. So if you decrease the response rate, you effectively keep more oxygen in the blood on. That causes respite That that because the compensation mechanisms respiratory acidosis on that counteracts the metabolic alkalosis. So that is most likely why the part of pressures are normal. Uh, or he will be compensating coming up. But I just thought I was created concept when I first understood it. And I hope you understand that as well. So moving forward, looking at lung diseases. I've got a few questions for you guys again, eh? So forget the pull up, Please. Again, I just want maximum participation. I'm not looking at forget that's right or wrong right now. I just want to see I don't want you guys have a good staff. But this uh huh, as the other bit of a rough throat. So if I keep coughing really sorry. Um, but yeah. So again, it doesn't matter if you know, if you don't know, it just get a really good guess. There's a bit of a bonus question there. I'm not looking for anyone. Aunts were just just have it in your mind. Um, so given this information, what is the most likely diagnosis and what does the CT show gang? Varying answers. And I think we will close it there, please. Thank you so much for people went with a E. The answer is actually be, and we'll look at that. But quickly before we move on to the next question is a little bit about the bronchiectasis. So one second you know we have about put bronchiectases what the CT is showing. So it's good a little radio, radiological images, but on being able to pick out specific things. But if you're able to describe it using medical terminology, you'll you'll progress very well on. It is very important for your medical career. So with this we're looking at actual CT on this reveals dilated and thickened airbase eso. You might be able to see that that there's abnormally widened and thinking airway on, uh, where there is an irregular wall as well. Certain signs that you can see in bronchiectasis and this is quite important to know if you can. If you're able to name them, it's basically just name it. We can see. So some people might say that they can see Trump tracks sometimes my safe Bunches of grapes, but the one I like is signature in a signature ring sign. So signal ring is just bring with on emblem or sign or some of the initials so you'll see a ring with a bit of a body on. So if you look, you can see these rings with a little protrusion, and that is a signature ring Sign on that is common for bronchiectosis. It's moving on to the next question. Create a whole up again. Please. It can give a good guess. Much participation as I can. Here be amazing to see just It just shows that you guys are still around Still, listen to me, mazing. I got a few more people and I think will close it there. Thank you very much. So people have got d The answer is probably fibrosis. Very well, don't you look at what that is? Pressure full is the final one again. Thank you for the whole um so I told that spirometry chases. Do you know what they are going to be? Not never there. And she mentioned about the one that we see. So the war is What is it showing what is the most likely diagnosis? So just a few more seconds and s okay on. I think we're close it there. Think very well done. Diversity. It is C COPD. So moving forward. Well, look at lung disease is on day. Could be split into obstructive on destructive obstructive lung disease is when there is a aircraft in the lungs and so it makes it difficult Expire or get the extra out or the air out. Sorry on D. Looking at the lung respiratory spirit spirometry trace. What we can see is f e V one produced. So remember what she said about fever One is the forced experience. Volume in the 1st 2nd on FEC is the functional the functional vital capacity. So with the obstructive lung disease is f e V one is reduced. FEC is normal or slightly reduced onda ratio. FEG wonder fbc ratio is also reduced. And so this does make sense because it is, um it's difficult to get that out on, but the total vital capacity is hasn't changed on. So that's why that 1st 2nd is it's, it's reduced. But overall, the vital capacity should be normal to same, um, with restrictive lung spirometry. As you can see what restrictive lung disease is, something is preventing full expansion of the lungs, and that is causing the causing it a difficulty to inspire to get the oxygen in. Um, and so, as you can see F E V one s so that ratio F E V one FEC ratio looks normal, so normal is greater than 0.7 a week or two separate seven. The reason it looks normal is the amount of air being expelled out of the lung. The vital capacity percent of the percentage of air being expelled in the 1st 2nd is relative to a normal trace. But when we look at the specific values we can see, F E V one is reduced. FEC is reduces well, so actively, when they're both reduce, the ratio or percentage almost looks like a normal trace. But when you look at the individual values can see that they're if they're both reduced. That's clear pathology on so the clinical definition or produce would be 80% of it's predicted value. So when you look at the spirometry chase, you can see that the bypass see and the the F E V one is massively reduced. And so, again recapping on that instructive, everyone is reduced. The FEC is normal, almost no, whereas in restrictive the F E V one and FEC is both reduced. So, looking at restrictive lung disease again, we we told my restrictive lung disease. It's It's, uh, it's the pathology. It's hard to get the oxygen in difficult inspiration ventilation. We're gonna talk about some of these in a little bit more detail coming up, but it's a few things to know. So festival restrictive lung disease connects plane to subcategories, almost pulmonary and extra pulmonary. So these are some pathologies. I come under a partner in a extra problem. It's a few things I want you to know before we go into a few specific details. A Dema partner demon is fluid in the lungs, and this is usually due to severe underlying systemic pathology that's gonna be heart failure or volume overload cook pleural effusion. It has been mentioned in the extra pulmonary is fluid in that pleural space, As you should know from she's talk pleural space that the lining of the lung on detains it contains fluid. But when there's an increased amount of fluid, that's pleural effusion. I wanted to go on trust this with pneumonia, sodium a fluid in the lungs, but you Monje, is when there is an infectious pathology. So we're gonna look at that coming up a little bit. There's a mention of at, uh, like electricity. I always try. I struggle with that collect. This is This is when there is partially collapsed lung. When the air enters the pleural space, this's could be contracted with pneumothorax with the total collapse of the land on. But that is a surgical emergency medical emergency. Sorry, we've also got lung resection there, and that is a removal of a part of a lung, and that is a surgical removal. I think the reason I'm telling you these things are is t the easiest way to learn and understand these things by under the war they are on what effect they have, and then you'll see why it's restrictive Again. Restrictive is the difficult of getting getting oxygen or air into your lungs on, so the's pathologies would are expecting. Restricting your lung from it's from It's maximum potential looking at the extra pulmonary pathologies. Just a quick note. So she mentioned kyphoscoliosis Kyphoscoliosis. There's two parts. It's the kyphoplasty. Okay, first spit, which is an abnormal curvature of the spine, which which is almost like a Ford. Benjamin is you hunt back parents on scoliosis is a sideways bends. When you look at it in a hard to talk to, you can see um, that that there's an abnormal curvature. So both put together. You get this, you get this. But you get this kind of scoliosis. What effectively does is it almost cramps. The lung is best second tier, and it effectively causes along to be restricted, and it stops it from expanding to its full potential for oh, it's normal, normal level. And then we've got mention of your muscle diseases that you should know on obesity, which we're gonna look at coming up eso there's no that. So first off, looking at it here. Perfect partner Fibrosis. So fibrosis fibrosis is, um, lung tissue that has become scarred or damaged on this causes a thickened or stiffened tissue on this effectively makes it more difficult in hell air and hence that restrictive on pathology. So the lung tissue that we're talking about is the interstitial was always indecision is just just this extra long material. Besides, so it's everything besides the to being in the vasculature. It's everything that makes up the lung, so its its role is to be elastic, and it should allow good lung movement. But with, um, the with idiopathic or apartment fibrosis, you get fibroblast entering on, producing collagen on also extracellular matrix. What this causes scars in your lungs and scar tissue to informed on this reduces the efficiency of your breathing on scarring makes your lung stiffer on defectively less elastic. So we talked about that, the less elastic, and it's less able to move. And so the ability taking oxygen is compromised on that restricted pathology that we talked about. And so you can see in the CT in the X ray story that started you that we can see the the cloudy nature of it. And if we look at some causes, the main causes idiopathic so idiopathic is, um, we just don't know, unfortunate. That is the most common course. The other other causes Are there some groups that you should know? So there are environment pollutants. I can cause fibrosis. Uh, probably for over a cyst. So starches, asbestos and silicosis, It could be drug induced. So certain drug you should know is, um, you're drawing. So this will come in your cardiac a saw in second day. You should know more about this, but it's just a good night. Um, your urine is an anti arrhythmic drug on go can cause, probably fibrosis. There are some connective tissue diseases on interested strong disease. They should Marin's well, because progresses. So there are some symptoms that I have noted that as well I'll let you read through those. But the main one is that gradual and progressive cough, uh, with, um and there's a So there's a gradual progressive cough, which was a destiny year or shortness of breath. But it's a dry cough. Should be No, nothing produce double nothing coming up. And I mentioned my algebra on day after I got out there. My older is muscle pain and authority as joint pain or aching. Yeah, I know you guys gonna have? Look at these slides later on. So a lot of is content. It's there for you to look at moving forward. We have pneumonia. The new earlier is an infection that inflames effects. Eso there is a breakdown with. Normally, there's a breakdown of the natural body defenses, and there's actually allows germs invade and multiply eso already. This the lung is a warm, moist environment so perfect for jobs to grow. But with no, you get white blood cell on battery accumulation on. This causes restriction in the air sacs on the main thing to know about pneumonia. It's going to see that in the X ray. Main thing to know is, that is, there's two types of causes. Are two groups. Of course they should know. So there's a community acquired on the main bacteria there. Streptococcus pneumonia. But you should know that you know you could be caused by a bacteria. Bacteria like organized organisms, fun guy or viruses. Onda Hospital acquired Is the gram negative bacillus on? But then there are some symptoms, so classic flu cold symptoms, but the importance know, are the nausea, vomiting, diarrhea on there's chest. There's just pain on breathing or coughing. So when you look at symptoms, when it comes a respiratory, they'll they'll they'll come together. All they're all quest similar. But it's the specifics that you should also testing for what kind of bacteria is. That's how you differentiate pneumonia from anything else. Looking at a chest X rays. How you'd understand it. It's bronchiectasis. Or if it's if it's probably fibrosis off anything else. So it's a it's a little necessarily things, but I've noted everything down for you to look back at later. So now, looking at an extra pulmonary, um, restrictive lung disease. Obesity. So, as most of you would know, obesity that increased adipose tissue everywhere but also around the thoracic cavity increasing increased adipose tissue can make it harder to breathe. It can make it harder for the lungs expand fully. It's at restrictive nature of a little game. Well, the main thing to know, uh, I think you know it's very about obesity is that it can cause obstructive sleep apnea. And so this is basically when there is increased adipose tissue around your neck, and as you sleep, your muscles relax on. But the excessive pressure that causes your airway to collapse almost on this causes stimulation of the brain on because you're not getting any area in this waste with endless effectively wakes you up on allows you to read it in that muscle tone and control. But you can see that is this destructive condition that you have When you're sleeping and you can become more tired, you can lose on sleep. But I just actually thing that come from obesity. Moving forward. Looking at obstruct obstructive lung disease is again is important for us to to relate the condition to the classification, and it will be it'll help you to understand what is involved in the pathology and how how is obstructive and they'll be easy if you just learn. We've talked about obstructive lung disease is when the lung the tubes obstructed, impairing ventilation on expression. And so there's a few ones that I'm gonna talk about and then a few ones are a little specifically. We had mentioned bronchiectasis, and how we would have it looks like on a CT bronchiectasis is is this abnormal dilatation off the bronch I have brown bronchioles, and it causes extra extended airways as well as mucous things. Chronic overproduction, mucus. Um, you diagnose it clinically with a clinical history. And with the CT scans we saw on, Do you get this classic triad of symptoms? So it's It's the what if you heard that you wouldn't know what it is. But classic Triad is that cough the sputum and a recurrent infection. So certainly we should should note you to be looking at bronchiectasis, another obstructive lung pathology. Cystic fibrosis. You may have heard of this in your level, but what we're talking about it a little bit more. Cystic fibrosis is a mutation in the CFTR gene CFTR gene codes for the channel that regulates normal movement off fluoride island and sodium ions. I/O of the apathy, a process of remembering in out of the mucous in the lungs mutation can cause decreased clearance off the mucus by causing it, causing the mucus to be sticking on thicker on. As you can already see, it's it's the same pathology. It is the toe. The mucus increases and come straight sticky and accumulate on obstructs the airways. On top of that increases the risk of infection as well, because you have mucus collecting pathogens and airway from from the environment, and it causes it to grow in this began, warm and moist environment. So we're going to look a little a few more specifically so that asthma and COPD and under COPD comes chronic bronchitis and emphysema. Saying off with Asper eso asthma is this chronic inflammation disorder of the airways mediated by IgE production. So quiet things that are gonna understand what is Break it down a little bit. So after physiology off aspirin walk first year is this inhaled allergen. So this is a topic asthma. This is the most common kind of ask for. We get inhaled allergen, which activates the dendritic cells. Allergen gets into your lungs, and it's taken by the cells on dendritic cells and get activated. This then activates T helper of type two T helper cells. The thing to know about T Helper cells is that there's two types. Most common is th one on. This is, uh this goes information by a cell mediated immunity, but ask for you get activation of Sorry, th two on this goes information by a human, um immunity so antibody release. And that's why I g e gets released so I d e antibody production then causes increase and GI antibody production idea either by by instant, Marcello's within the lungs with a long cells on because the release of histamine prostaglandins leucotrienes on. So all of this together causes bronchial smooth muscle constriction eso with asthma. That's technically three things that you should be looking out for this bronchoconstriction airway inflammation and extra mucus production. And I'm gonna look at how we can manage that coming up. But those are I guess they try out of symptoms that you see or the trial of things that you'd be looking out for. So I know it down here some histological things that you should be looking out for. I let you read that in your in time, but again, coming back to this is where we this where it again, I'm going to give you guys a hint of a tip. The most important thing is to learn normal pathology, its normal physiology, normal anatomy, and then link it to this pathology. You go straight into the pathology of pathophysiology, you're gonna get confused s again. She talked about seven histological site of the certain history histology of lung Um and then I don't know some symptoms there as well. Once again, it's that shortness of breath with asthma. You get trying a drying, irritating cough. That's what you should be noted forward looking at chronic obstructive pulmonary disease, COPD COPD is actually capped clinically characterized by two pathologies, which is chronic bronchitis and emphysema. So what is correct? Tightness? Cobra Bronchitis is this hyper tree of sub mucosal glands. So what you get is an increase in bublitz cells. So you might seem previously, goblet cells secrete mucus into the into the lungs. Well, you can get you can get, um, increase in goblet cells. Or it can be a Macos celery ciliary dysfunction. So dysfunction in the cilia move mucus out. So what? You should be looking at eso what again? It's a classic. That's the classic. Guess is your path of pathology of you get this increased mucus, hyper secretion and retention with chronic bronchitis. This blocks the airway. Increases in risk of infection leads to a greater in a greater inflammation on the bronchial tube in gets thicker and narrower so we can see clinically is cough on dispute. Um, on most days with emphysema you get an abnormal and permanent dilatation of air space due to the loss of elastic report on the basis of the on this is caused by it can be caused by the lack of that, the main commonly. So you get so you get back from smoking on that contains nicotine and reactive oxygen species. This causes a tissue damage by an activating antidepressant eases on. This increases neutrophils. So we're gonna look, we can see really have that little bit more. But effectively, what you get is lung damage, a lung scarring, and it causes this pathologically it causes. This lasted a gradation, hyperinflation and destruction destruction off the albuterol and clear rules. But clinically, you may see a skinny or malnourished patient eso I've listed for you guys that causes against comes right on top. But there can also be a genetic factors and bolt. So alpha one antitrypsin is thie anti proteins that we talked about that prevents too much too many reactive oxidants, reactive oxygen species with the lung. But it regulates that neutral be active oxygen species species, uh, control or regulate. Sit. Um but there are some other causes. Well, and then looking at symptoms and signs again, I'll let you read through them. It's a classic progressive breathlessness and fatigue and weight loss, but I think the ones I wanted a note to you guys was again with emphysema. You can see you get you going to see you might see a very skinny and malnourished patient. And so the cause of that is that loss of muscle mass. This is known as Catch Xia. You will also see changes in breathing s so you'll see them breathing more quicker. They'll be use of respiratory accessory muscles at eight, breathing to allow more center, get in or help a lot more. You'll see personal it breathing so it's almost as a parting, and allowing this is kind of controlled. Flow off oxygen, and you'll also see a prolonged experience. Your phase because again obstructive it's the blockage of the tubes, and it's harder to get that oxygen out and again. Site. There's just remember, just a note. Remember about F E V one. That's why everyone is greatly reduced. You can't get that air out of your lungs, and that's that's a prolonged expert to face that we're talking about. So these are just certain signs and symptoms just look out for So, uh, I think three for this is a a nice summary slide that actually produce for our back to school at Siris. But I'll let you guys look through that. Just keeps saying key things there, but we're gonna move forward. I hope everyone still with me. I haven't seen any. I wasn't any questions to me. I I hope Yeah, everyone was okay. If there are any questions, let me know. And I look, I look through them at the end. We're gonna move on to respiratory pharmacology. So one of my favorite bits, actually with, um aspiratory. So signing off for the question that always on create the pole up. Thank you. Thank you. So again, guys, I don't know that you guys are still with me. Just if you could just give it a good start, even if you don't know it. But it looks like you guys are doing quite well. That's very nice. Keep up. Yeah. Okay. Um, I think we'll close it there. Thank you very much. So you guys are going to see that is the right answer. Very well done. So we'll look at that a little bit more detail. But first off, a little note. So she did cover this, but just a little bit more again, once once again and say, If you learn the normal physiology, the normal have asked me. The normal process is it'll be easier to relate them to pathology as well as pharmacology. So no, no on autonomic control. Passive That hasn't hasn't nerves me. Action by Moscow Rennick receptors. And this brings about bronchoconstriction raise a dilation on sympathetic nerves mediated by a beta receptors. Bring about bronchodilation and basic instruction. There's not really an easy way to learn this, other than just knowing it like this, but you can already see. So if I wanted to dilate the the bronchus or in the airway, I would need to I need to uh, preg You ate almost all the best one, but I guess I don't know the sound. We need beta two agonist so and so that would allow dog dilation. But similarly, if we blocked muscular neck receptors, we would stop bronchoconstriction, and this will allow bronchodilation. So that's just a baby. Just a quick tease. The trailer for the drugs that we're looking at. But with the especially drugs, we can classify them into the duration or the length of time that they use that they they act for. So we have acute situation, drugs, salbutamol, petroleum. So these are short duration bronchodilators and they use for acute asthma and COPD episodes. We have long term trade drugs. Such a cell natural and tear drop. The, um they're used for a slightly different condition. So for moderate to severe asked when you do some natural, but for COPD management, you'd use tear topia on. Then we have a both but a drug that you would use in both kind of scenarios on Do is fluticasone, which is a potent anti inflam in anti inflammatory steroid. And so this is you, uh, it's usually used in conjunction with these other drugs. So a little heads up. The slight is does look very heavy, and it's becoming a lot of words on there. But bear with me. I'm gonna break it down a little bit little So, uh, thankfully, it especially ones aren't too hard to remember because they kind of group together quite nicely. They got salbutamol and salmeterol eso again why we grew up in those two drugs. They're known a Sabas Sabbath and lab. So Sabir being short acting. But be a on the lab, the long acting drug. And so what are they? So the mechanism action for salmeterol salbutamol Star matter all is that they're a selective beta two adrenoreceptor agonist. So again, we talked about sympathetic innovation. If we can activate the beta two adrenal receptors using agonists, we will increase a rule cause Bronco dilator in that is through it's c A c A m p. Uh, CMP mediated through that for that pathway. And so again, as I said it, it dilates the bronchial with hypertropy a and tear tropia. They are Sammer and Lamott drugs or a short acting muscular neck drum antagonised or long acting must run it antagonist. So they are seeing healthcare acetylcholine receptors on. So they blocking these would allow bronchodilation and this is this's through reducing CGM pee again A quick note. So for the beta two adrenal receptor agonists where it's by a CMP on through the master tonic antagonised is CGM pee again. They both work by effectively brought, causing bronchodilation. It's just important. Note that uh, the muscarinic receptor in the lung is the M three receptor, and that's the most common one in the lung. They're looking at fluticasone. It is a steroid glucocorticoid receptors complex, awake or so again for flu. Fluticasone is a steroid that causes this complex, this steroid blue go to don't receptor complex. And again, if you don't move with me with my pieces three sessions, we'd know that steroids at transcription regulators on what they effectively do is strongly reduce the inflammation so acts on it, goes into the nucleus and acts on transcription directly on. It causes this really strong response, and it is by up regulating anti inflammatory proteins and down regulating inflammatory mediators on so producing that strong response. So look with, along with drugs, you need to know their address drug reactions on contraindications. And again, that's a lot of words on the slide, but I'll break it down for you. Most important thing to know are these non steroid drugs are the contraindications are commonly cardiac stuff or cardiac problems, and with steroid with any kind of steroid drug, the biggest problem is long term use on again. As we said, several drugs act directly on transcription Transcript regulates transcription on even though they take longer there, I guess longer time to take effect. The time they the time they have an effect on is so you live. It may take longer to take effect. They work for longer on so long term. Use wood and course, and problems aside mentioned that it can cause immune suppression on pushing syndrome or even osteoporosis. So they're contraindicated for immunocompromised patients. It's already again how I bring it down to you how I hope you guys will learn drugs in the future. It's by knowing that anyway, and how they act of grouping these drugs together and help you learn them. Advise thumb. But also learning common contraindications can help you remember these in future revision purposes. But, as I said, these labs will be will be given to you so you can take a look at them on. That brings me to a clues that my references on. But I do want to thank you guys very much a sticking around with me. Ah, hold That was a lot of high your content from both me and tree like thank you guys once again and please fill out feedback form. A lot of people ask me in the comments. How are you gonna get? I'm getting We have a lot of new people. You fill out the about form, make a metal account, and you'll be able to access the certificate. This recording on down on the slides. Pleased to give us a real nice feedback. It really helps us to improve our sessions. So thank you. Thank you, guys. Sell it for coming. Just one more thing. If you guys could let us know whether you we did put this in the chat. But if you guys prefer SBA is before, yeah, she covered the content to see to test your, like, old reprieve, existing knowledge. Or if you guys prefer the SBA is after we cover the topic. Um, if you could just let us know on the feedback for more here, Um, just so we could improve the sessions for you guys, But thank you for coming. Graner's asking on cactuses is an obstructive restrictive disease is destructive. Um, once again, it it's It's that inflammation and that chronic production mucus in the bronchus and the bronchioles, So again, stricter is obstructing air from leaving and entering. Well, just don't stop the recording. Thank you. Um, yeah,