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Uh, okay. So, as I said, this will be the topics I'll be covering. Um, so let's get started. So when you look at an abdomen, we can separate it into different quadrants, so you can see here. There's nine different quadrants on, but this is kind of a giveaway, but can let's start off with some interaction. So consider bumping into the chat what we can find in the right hypochondriac 100 region. So that's this one, um, clears in the diagram, but it's just to get people talking. So just put in the chat. So yeah, liver, what else can you find that gallbladder? So yet perfect. So in that order and we can find the liver and if you also find the right kidney, although it's not saying that, But just remember that what can you see in the umbilical region? Can anyone put in the chart what that would be? Yes. So I think people are putting stuff in the chat, so I'm gonna just put it up. So you have the stomach, the pancreas, the small intestine and the transverse colon. Here on finally, in the right iliac fossa. I was gonna put it. You just find the appendix. The K. Come on, Descending colon. If you look here, just this corner here. All contains deliver on. Just remember, the pancreas is here and here. So those is, um, keywords on one thing to remember if the kidneys are also quite high appearance. Well, okay, so, um, your sign of this slide let's quite played. But let's talk about the abdominal wall is So let's say you're a surgeon, so you've got your scalpel, and you want to cut through the step all the way down to the abdominal cavity here. So I just put some intestine there. What's the first layer that you'd have to cut through consumer in the chart if they know was the first layer after the skin that you would cut through, um, on your way. And so some said fashion perfect. Um, so you'd have campus fascia and Scarpa's flashes. So the's are superficial fashion layers on, and I've got diagrams will pop up a later, but one is fatty and the other is member nous. And then you go into the muscle layers, so skin fascia, and then you have three muscle layers, so you have the external oblique, which transitions into the externals dramatic fascia. You have the internal oblique, this transitions into the car master muscle on also fascia on you have the trans this abdominus, and then you have another layer of fascists of skin fascia muscle fresher. And then this is the transfers fashion that transitions to the internal spermatic fresher. And you have this extraperitoneal layer of fat and as the extra protein you layer of fat suggest it outside the parietal paratonia layer. So his, uh and then you reached abdominal cavity. So those are the legs you have to cut through, and here's a diagram. So, as I said, the superficial fascia, the campuses, coppers, scalpers campus is an adipose fat layer, whereas Scarpa's is this membranous layer. So just remember, that's how you distinguish between those on the way to remember what these transition into the muscles on the fascia. It would be tight turns to ice to transversalis fascia. It would be internal spermatic pressure, internal oblique we karma, Starik muscle and fascia on the external oblique could be the externals Martic fresher. Okay, so let's talk about hunger and satiety societies when opposite of hunger and you're just suppression of hunger. So it all begins in the ark. You a nucleus, right? Let's located in the hypothalamus. So let's talk about hunger first. So you're having almost senses that you need more food intake. So you get These are exogenesis Neurontin that stimulate the hunger center that's located in the lateral only place of the hypothalamus on the neurotransmitters would be growling neuropeptide y and kind of annoyed that would trigger the hunger sender to stimulate. Have appetite, so that would make you hungry. So Garland makes you gain weight. Some people remember as ghrelin makes your stomach go, girl. That's the way I tend to remember it. But now let's talk about, say, if you're feeling full, how do suppress hunger? So you have these anorex suggest IQ You're on so on your X is associated with not eating and satiety on. Then that goes the satiety center that's found in the ventral medial nucleus of the hospital. Ms Surround Hunger Center would be the lateral nucleus. Satiety Center is in the ventral medial necklace off the hospital. Um, it's on the neurotransmitters that you need to know, like leptin peptide, while I cystic a GLP and vagus nerve stimulation. And there's basically similar. It's entirety. Leptin makes you lose a ghrelin, makes you gain weight. Leptin makes you lose weight. So just remember that. So now I'm going to just talk about So now you've seen the food and you are hungry. That would trigger the cephalic phase, which was then lead on to the gastric phase. And finally the intestinal phase. These of the faces off digestion. So the cephalic phase. This is when you've seen the food you've smelled food on. It's tantalized those taste buds when you see it, and this basically stimulates the vagus snap. This then causes a seat. How Colin to be released into various cells in the summer that will go into later, such as GI cells that produce gas. Trinh on this stimulates parietal cells to produce hydrochloric acid and then she cells produce Pepcid, a gyn on the hydrochloric acid. I would convert this pepsin Pepcid a gyn, but we'll go into that later. But then, also in this space, you have stomach distention as well in gastric face. And in this in this stomach distension is you have these stretch receptors called chemo receptors, which trigger the short and long reflex. So the short is vial and Terek nervous system on that's due to chemo receptors on the long reflex is due to the from the vagus love, and that's due to stretch your sectors. So the short reflects is the enteric nervous system from chemo receptors on the long reflex is via the vagus nerve due to stretch for separatists, and it basically stimulates different cells in the gastric lines like gee cells, brighter cells and chief cells will go into that again later in more detail. Now we finally have the intestinal face with the food. Leave the stomach into the intestines, specifically the duodenum on day. This is basically you have the low pH of the duodenum and that triggers various different things to be released from the pancreas in the bile. So the protein products in the dude in, um, basically trigger the production off gas trend viaje cells on this basically up regulates the secretions of price all and also there's the production of CCK on CDK has various different functions. Don't worry if you don't memorize everything I say right now, I have, like, uh, diagrams a try and explain it in more detail. But basically, CCK generally inhibits do cells, triggers the contraction of the gallbladder and decrease this gastric emptying. And it also stimulates a sin ourselves in the pancreas to produce different enzymes and also relaxes the same thing. 2/80. But I'll go into that also later. But what is how I said low pH here that also true goes Sl's just decree secreted. And these Let's close them like diesels to produce a thing called some Artist Act in which basically inhibit had acid some secretion. So let's go on about absorption of different products of foods offer. It contains carbohydrates for doing the lipid on days that along the digestive tract are digestive in different ways. Carbohydrates tend to be digested either in the small intestine. On first board enzymes are, um, Elise in the mouth, the brushed your enzymes. This bone intestine would be super small trees. In that case, there's also proteins you have had a trips in, which is the end of today's, and this is activated. This is just the activity form of trips. To mention anything ended in in urgent is kind of like, um um, inactivated or Precose a form of something. So trips in, um is the activity form of trips religion by this and enter kindness and other pancreatic enzymes. Also, that just is he also have lipids deal by the drive by the gallbladder and the liver, and it contracts, which to create bile. And these basically and multiply make these droplets big. Um, um, most of the fact opposites they can see here you have a mean acid on down, so don't buy a second active transport through, you know, up. You know, part is that the proteins and small peptides as well have the protein part, and then you have passive diffusion of lipids on back. I'll, um, my constipation. A little transporters on. You also have the SGLT one the glucose and galactose on gluten for for this factors. Okay, so I'm gonna talk about when you eat something, you salivate. I'm going to go into the functions and saliva in the next slide. But first, I want you guys to be familiar with. I own movement in salivary glands. This is where we determine the osmolality off saliva. So this is just a schematic off a celebrate gland and you can see there's various different islands. But we'll go into that, um, in a second. So you see here you see this chlorine I ones. They basically moved into this. A sickness of the salary gland via you know, Porter. So it's just moving in on. Do you have this negative potential being generated Cause you can see here this chloride I want a negatively charged on these. This basically causes these positive sodium islands to enter into the Is Nece like that? Because of the negative potential being created that this basically generates on osmotic grace Grady in so osmosis is the diffusion of water particles from a ah high water potential to a lower. What potential on then you have the fluid from this isotonic to this high Protonix solution because of osteo says it would go from there is higher to hypo low Earth. So they have this flow off this fluid down this duct and then while so it's slowing down the duct, you have the exchange of chlorine chloride and sodium as well on also, you have the bicarbonate being exchanged chloride into the duct, making us alive basic, so it's more alkaline on 60 and sodium is also exchange for a task in here. So what I'm saying is because of this negative potential sodium moves in creating this isotonic saliva because it was, most says, because this bit more hypotonic the saliva goes down the duct and then you have the exchange for these islands at various different rates, depending on the rate of float belt. Talked about that in the next slide. So that's just the bicarbonate million. Okay, so, um, food and his mouth, like I said. And then this is where saliva is secreted on. There's different roles of saliva that we must be aware off. Saliva has floor main roles lubrication, defense, buffering on digestion, lubrication would be saliva contains These glycoprotein that have been used in his medicines are just a component of mucus that I kind of like like a protein, the main glycoprotein off Nukus. So just associate it with mucus and it basically you Procrit salivary glands and you have our food. I'm in so saliva conclude our food because of the mucus. You also have the defense role. So lysozyme have found it on sale over on this basically breakdown gram positive bacteria in our food, so it's protecting us. It buffers because of the bicarb and I on rays in the pH off saliva, and you also have the digestive aspect, the one that we're probably most familiar with. Or it contains different enzymes like salary. I'm lazy to break down. Start to Allegra Saccharide. So what are the contents off saliva. So it contains alpha amylase. Lingle, like pays on cal a crime on also in big on immunoglobulin. And how do we determine the osmolality off saliva just to make it clear? Osmolality of saliva when talking about saliva would be the concentration of particles, mainly electrolytes, her liter off saliva. So how do we determine the concentration of electrolytes? Carlita is what that say, so you can increase floor eight. That means, as the as I said in the earlier as it flows down the duct, Um, if it flows faster, there's less time in the ducks for things to move I/O. Those IRS to move I/O. So that's less time for doctor modification, because there's less exchange for sodium and chloride was just brushing through on this causes a higher osmolality, so this would be the most isotonic saliva. There's less time for that exchange, but if you have a slow flow rate, it's kind of going slower. You have more time for Dr Modification. There's more exchange of sodium and chloride because it's going slower. This causes the osmolality to lower, so this is the most hypertonics. Just to be clear, a faster rate of secretion means less iron transfer out of the duct. That means the higher hospitality. And that means it's more hypertonics with more solid. And that makes saliva more similar to the plasma concentration. That's good. So autonomic nervous system controls what type of saliva and the volume of Survivor that's secreted. So you have these Parsons. You have the parasympathetic nervous system, which has acetylcholine, really, and acts on the M. Three receptors will hear about this pile off along the tractor, but empty receptors ones live bands, and they also act on empty receptors on the blood vessels to stimulate basal dilation. Um, so just remember, here, parasympathetic stimulation increases the synthesis and secretion of watery saliva where sympathetic increases isn't this synthesis in secretion of viscous saliva, parasympathetic rest and digest. So you want more watery saliva Okay, so I've got an SBA. Fenelon could launch Paul, So patient suffers from the brains of stroke. The war doctors are worried about his ability to swallow Which face is swelling is most likely affected. Um, so give it a go. It's anonymous. I'll go into, um, the answer later. Okay? I think I'll end the pole. That. Okay, so I think most of the went for fire in Jul phase. Um, Andi, that would be correct. So the fine Jill face the notice. Assess phases off swallowing, so I'll go into the face of swallowing next. So let's talk about the smaller reflex. So there's three faces off the sweater reflex. The first thing, the oral phase, and this is a voluntary. When you eat food, you choose to chew it. So that's why even say it's voluntary cause you are actively like selecting to chew food if you you know what I mean. So in this stays, the ball is off, food is masticated. In other words, shoot on the ball is's acted on by all the on saliva in our mouth. Remember how that's repeated earlier? But it's after on by the saliva, and then you have our tongue, which is here. It's much bigger than most people expect. But it's that giant pink structure in this diagram on it pushes it back to the hard palate, then to the parents. One thing we must know is the muscles of mastication. Rumba, Cranial, not five is the trigeminal nerve on this button. Braless Must her lateral terabytes on medial pterygoid? I don't know. I pronounce that right. But just remember these and then you have the involuntary face. So this is something that we don't have to consciously think about the pharyngeal face. This is when the ball is basically stimulates pressure receptors of the back of our next week where signals off a sent to the swallowing center in our brain. And it basically causes the soft palate to push the food upwards, um, by muscle blocking the bolus entering the nasopharynx. So this is why food doesn't go up our nose basically on it blocks the food entering laser pharynx. Then the ball ist is pushed down towards the Sophocles by the initiation off Paris Talis is is this kind of a wave of contractions? Um, but and it's a reflex by our pharyngeal constrictor muscles that kind of create a wave that pushes it down. Um, well, this happens. You have a phenomenon called degludec in apnea. This is just when our respiration is inhibited. Um, in this phase on, as the ball is continues to, the esophagus are larynx rises. So it's going down. And if you can see my 0.2 here, I'm going to point at a really important structure here. Called the Epiglottis. This is a flap like structure, so in this diagram, it's kind of if you can see my camera, it's propped up a tolerance prizes. As the food comes down, it closes off the trachea on. That's really important because we don't want food entering into the trick here. We wanted to go down into the esophagus, going down into the stomach so that epiglottis stops food entering our windpipe and actually makes the end to the gut pipe instead. On the upper stuff, a jewel sphincter opens in this phase. One clinical thing to remember is if someone's unconscious, What could happen is that you got is covers back trick. Yes, so they could actually, um, stop breathing as a result of best. But it's quite unlikely, but it could be something that happened that could lead to a medical emergency. So you also have, in the involuntary phase being controlled by lower points on the medulla. Remember that on the final phase. Is this off the jewels? Things This is involuntary. So the bolus moves down those off because by Paris tell says now, going back to the SBA, I asked about basically the connection to the brain and stroke. So the pharyngeal phase expected a by stroke on a condition called accolade A. That just, um, we're going to later. It's effect effects that was off the jewel days. Okay, so you're meeting. I went, Teo, but something. So in this there are different areas of the brain that control vomiting, the main area being the vomiting center, which lies within the medulla and contains muscular neck receptors. There's also a chemo receptive trigger zone that stimulates the vomiting center. This'll eyes in the medulla, and it contains opening to receptors on five ht receptors. You also have the vestibule I nuclei points which stimulates the chemoreceptor trigger zone. On the contents histamine. Two receptors on muscarinic receptors you have the higher is very much stimulate the vomiting center on the lower areas off the stomach that can stimulate the chemo receptive trigger zone. But just remember, the main one is the vomiting center, which lies within the medulla does annual can you know, this is kind of a link to the last case case five. Can anyone tell me why in the chat why, if you are traveling in a car or like, heights and stuff can make you feel sick like, um, car sickness and, um, traveling? How can that make you feel sick? Related in terms of the vomiting center, the motion. But how come How can it make you feel sick? Yes. Oh, someone said it. So they're vested vehicle clean. Your region is the vomiting center and our balance centers That can kind of make us feel sick. Okay, so let's just talk about the actual, um um, physiology of vomiting. So when the vomiting center is simulated, you get respiration being inhibited, the lowering surprising. So the up epiglottis closes off the trachea. You have the soft palate rising to prevent vomiting, entering on nose. Don't stick to come out of our nose, which is kind of gross things. So that's our self pilot rising to prevent that you have the stomach and I'll or extinct er relaxing to let the food go. And then you have reverse Palestine else is off the duodenum, so it doesn't go this way. It goes that it's a back up on the biologics power power. Expect a closes and they're softer. Jules, big too, relaxes. So food kind of goes back up to the esophagus and the dive on Diovan grabbed on the world contract and it kind of like pushes out upwards, and we project are moment, which I think is kind of gross topic. But basically, that's what happens with that explanation made sense. So the next talk about the mayor's of the GI tract. So you have, um, the advantage. Uh, when you go on an adventure, you go out, says the outermost layer, and then you cut. Coming in, you have the outer longitudinal, the sub mucosal in a circular. The muscular is because of the lamina propria, the epithelium and then the Lumen. So most of the GI tract is quite Luminal. You have their Sophocles, which is Luminal, the duodenum, all kind of circles of different sizes on diameters. Um, and the food kind of just troubles down it. So it's kind of the same structure throughout the external. Muscularis there is these two on the mucosa. Are these three just around the advantage of adventure out. But yeah. So the epithelium is important. This is Chris. Um, ends on hormones and digestive juices. The lamina propria contains plans blood vessels and in implanted vessels, the muscular hours mucosa as a layer of smooth muscle between the mucosa and the suddenly Koza that in a second layer is a big player of connective tissue. And it contains our major blood vessels and lymphatics and also contains the sub mucosal plexus. That could be a question. You get asked to remember the sub mucosal plexuses here you also have the flare is extend. It is important for the pack peristyle for a stylistic movements. And it also contains on myenteric plexus. And the cirrhosis is an intraperitoneal, and it continues with the vessel party. Um, remember, adventitia is retroverted to deal. Okay, so I'm gonna talk about the diaphragmatic hiatus. So, um, you might be asked to remember what layer levels go up, but first I'm going to just describe this image. So here you have the anterior side and here you have the posterior side, his spinal better breath for reference. And here's the sternum for reference. And this big sheet is the diet from And so the most interior one is the inferior vena Kaveh coming out from T eight. And then immediately you have this off against this is T 10 and then posteriorly you have the aortic hiatus here a t 12. A really good way to remember this is just count the number of letters. Savina Cable had eight letters, So t eight Asafa Ghous has 10 letters, So t 10 aortic hiatus has 12. 30 12. So this is a really good way off remembering what level they exit. Diaphragmatic hiatus from in terms of the esophagus, esophagus runs from C 62 t 11. Um, before it passes through the diet for diaphragmatic hiatus it before it passes the diaphragm above the diaphragm. We call it the thoracic esophagus on below the diaphragmatic hiatus before it passes. After it passes through the diaphragm. We call it the abdominal stuff ago. Okay, so I'm going to talk about this a focus a bit more. So we've gone from the mouth through the highest. Now we're nearly reaching our stomach. So the upper one third of the esophagus is striped ID muscle, and it's controlled by the brain stem. So remember, striated is the opposed to bed on the lower tooth beds. It's moved muscle controlled by the, uh yes, a soft ajeel. The smooth muscle is innovated by parasympathetic vagal. Trump's on sympathetic invasion from the cervical and thoracic. Um, sympathetic. Trump this up the Remember that the esophagus also gets its blood from the thoracic aorta and also the inferior thyroid artery. Both of these drain into the azygos and internal thyroid vein. Um, the abdominal I otezla is below the diaphragm is supplied by the left, the left gastric artery. So that's just a difference in blood supply that you must remember. So here we have this off for this coming down here, and it connects with the heart at the cardia level. So you see here you have a Z line on but separates the squamous muscle here on, but, uh, columnar muscle off the esophagus on it lies exactly at the point of the gastroesophageal junction. Just it will go into this later. But if you have a Z line shift So if the Squamocolumnar junction is no longer in line with the gastroesophageal junction, you have this squamous cells coming up the esophagus. You see pictures of it later, but that's when Barris is off. Suffocates would occur when the sea line moves away from the gastroesophageal junction. That make sense. Um, okay, so there's some fungus and is that the cardio here? Just remember that they're suffered. Goes, hasn't up her on the lower esophageal sphincter in the lower one is what's relevant to us right now. The lower has a right proves muscle, and it wraps around this off because basically, if this is weakening or damage off the right Christmas a while, it means that the stomach could exit through. Kind of kind of pushes out, and it's called herniation, and this could lead to reflux or dyspepsia. Now I want you guys to put in the chat. What you think this type of hernia is? There's two different types of hernia that we need to know about. What's this? But in the shop, um, this one, the first one here What do you think it is? The pneumonia? This is the one put rolling. That's the correct answer. So this is a rolling hernia, and this is a sliding hernia. You could just kind of see it kind of got a little role here. And this kind of looks like I don't know how to describe it is kind of slide down. Just remember, this has a circular roll on. Then that's how you differentiate them. Now it's really important to know about the abdominal I OTA and it's by fixation. This is just a really good way to remember it. Remember, a key question that they could ask is what level does it by five k, and it would be helpful is by Fick a Shin is the effort for and buy for occasion for occasion. That's a way of remembering it on D like trunk I like to remember is to 12 here. So, um, 12 letters ciliate trunk on Superior messing a mesenteric artery comes off from al 11 is superior. Okay, um but just Yeah, I'm not going to go that much into this diagram, but it would be really good. Teo, land another question if anyone could launch the pole. A stomachs at the stomach. Arterial supply is predominantly from the branches off the celiac trunk. The greater couple jobs. Stomach is supplied by the left and right gastroepiploic arteries. Which major artery that the left caster apoplectic our tree branch off from? Remember, it's anonymously, you know, No seizures. Guess and the next slide will explain it. Um, um has been a few more. Okay. Think I'll end it, Dad. Okay, siding. Most people got that right. It's the Spanish car tree. So if my slide with discharge ago starting our trees, um, so I'm gonna talk about, um the blood supply off the stomach. And also the bifurcate ones are this splitting off the select trying so is adopted from knishes diagram, which he is really great. Last year when he told us that, um, I mean, the first talk about the anatomy of the stomach. So you have their soft because coming here, which enters at the cardia on one of the top of the stomach, which is the fund. It's of the body here that untrue, um, the pylorus. And then it leads into the small intestine, which is star is called the duodenum. So you have, unless a curvature of the smallest see on the greater curvature, the greater biggest see off the stomach on this will be really useful when they running about the blood supply. So you have the celiac trunk here, and it goes off to the common hepatic and the splenic arteries splaining going to the spleen hepatic whenever you had the with hepatic think liver, you'll be hearing the word hep on. Do that later on. But hepatic think liver so on this planet, or then branch off into the short gastric, which goes funders. And then, um then for the splits into the left. Gastroepiploic going on this, supplying this great culture aspect off the stomach and it splits and it turns into the right, um, gassed gastroepiploic As it comes back up on here, it splits off into the superior pancreatic Seiko duodenum artery on. Then the lesser curvature comes directly from the Selectra in the left gastric. And then the right last Rick Oh, and then following the common hepatic goes onto the proper hepatic and then leads off to the cystic into the gallbladder. Now, um, we're just gonna talk about stomach distention, so this is quite a heavy topic. So we're talking about the movement off the stomach so you have GI cells that release gastrin. So when you have a vasovagal response, the stomach basically relaxes to allow food and turkeys you want. It's kind of like opening in the bag, allowing to fill because food is coming from the esophagus after you've eaten. And this it was just relaxed. Allow food to enter. Then this relaxation. There's local stretch of a local stretch reflex VIAS. It'll coli that's basically vagal stimulation by the gas release impact on GRP. So there's an increase in constant concentration in parietal cells. On that, I'll go into the specific details of this later. But there's an increase in cousin concentration in practice cells and that basically causes an increase in potassium in proton concentration via the proton pump. Um, don't read. This will be much clearer later on in my closer up diagram of the parietal cell. But basically this works on Entocort stuff in like cells to release histamine by a hates to receptors, which increase I click MP. An increased activity off the proton pump on that basically increases the proton concentration. Um, you have, um, local structures Reflects why it's a chair, a swell, and they assimilation by the gas releasing peptide to RPI. So here you have the parietal cells increasing the proton concentration because of the release off. Um, hate cl. Does anyone know what else parietal cells release? Apart from her, um, gastric acids, hydrochloric acid intrinsic factor nailed it. So intrinsic factor is really important to know about so parietal cells. The only release are gastric acid Ph yell, but they also release intrinsic factor on intrinsic factor of binds to be 12, and it protects it protects our B 12, and the stomach from stomach acid on B 12 is then transported into the small intestine where it's absorbed. So just remember B 12 is absorbed in the small intestine and intrinsic factor kind of forms of bubble to protect it from my stomach acid. So the stomach distension also triggers college in Collin allergenic at Collin, a dentist activity from the vagus nerve on basically the acidic stomach conditions of the stomach, then on the gastrin and secreted is presence triggered. Chief cells to release pepsinogen on Pepsinogen basically is converted to pepsin as acidic condition created by the parietal cells activity. Perhaps image and remember in urgent is just a precursor to its active or pepsin pepsin know Jen on hep c l o activates it to form pepsinogen chief cells also release. Um, Simon Jen's a swell. Um, we're gonna talk about inhibition real quick. Doesn't even know what inhibits GI cells from releasing gastrin. There's two things CCK There's another one. Secretin. Yep. Perfect. So gi cells release. Um, if my slide move GI cells are stopped by CCK and secreted on parietal cells are so by somatostatin, which is relieved by diesels in the funders on prostaglandins. So CCK and secrete in for guest room in Samata Statin on prostaglandin Stop there. Sitting conditions off our stomach became, so I'm gonna move on to the next line. Okay, So, um, just to explain this diagram this is a blood vessel. This is the parietal cells in our stomach. On this is just the hollow gastric. Lumen, off stomach. So this is the gastric. Lumen, this is the price is all This is the blood. So there's water and go to in our parietal cells that combined by the action of carbonic anhydrase to form carbonic acid. This then dissociated into protons on, uh, carbonate ions. Here on, basically, you see this proton pump that the proton that's produced from the car bonnet acid enters our gastric. Lumen, increasing that city off the gastric juice. Um, but whilst this happens, you have on this bicarbonate here, and it basically goes through the bicarbonate chlorate exchanger, and it moves into our blood swapping itself for a chloride ion, and that moves into the parietal cells. We called us that alkaline tied because we know that this is alkaline. So this is an article. I'm tired. So now we have a chloride I on in the prior to sell, and it has two places. It could go because you can see there's two channels it could travel through. It could go through the chloride channel into the gastric. Lumen on it connects change itself. It can swap with potassium into the gastric. Lumen Um, so here it is, But you can see both the proton pump on the chloride channel, both the interaction of potassium so it's off, cycled through. You can see it's off, cycled through t allow protons to be pumped into the gastric. Lumen and chloride ion still be pumped into the gastric. Lumen. Now why do we want a clot? And I own here? Well, it's because his age see out is hard to click acid. And that's our stomach acids in a parietal sell. This is how, um, gastric acid is secreted. Uh, how you call it acid is secreted. I hope that was clear. But now let's talk about this proton pump specifically. So remember the proton pump from before. So just I've just simplified the hate for cll bed. But just remember, hate shell was one from that previous slide. But there's different things can that can regulate the action off the stomach acid. So you have prostate glands and so much statins and three other things that combined two receptors on our parietal cells to increase or decrease the stomach acid secretion. Does anyone know what binds to hate to receptors? Can they put it in the chop histamine? Yeah. So hey, hbh histamine. Uh, my slide with mute. Does anyone know what causes what binds to cytic it Two sectors isn't doing No. Um yes, Trinh. Yes. So gastrin binds to CCK two receptors on what binds to m three receptors. I said earlier, these popped up in the salary secretion spirits. Well, sch perfect. You guys know your stuff? So, um, if my side was just real, So Yeah, I see. Tell Coli. So, um, I'm gonna break down this diagram more specifically in the next few slides, but in summary, you have a cut a cycle it amp dependent pathway here on. Do you have a calcium dependent pathway here? G i G s is the cycling amp dependent pathway, and you have the GQ calcium dependent pathway. So, um, prostaglandins and somatostatin if you remember from my summary earlier, stop our parietal cells from secrete and gastric acid. And that's because they're part of the GI I i for inhibitory I remember. So person, Landon's and somatostatin inhibit cycling MP from acting on a proton pump from secretive thing hydrocodone grass. It's that they would decrease our stomach acid secretions. Whereas all of these, um, would increase, uh, stomach acid secretion. I'm going to quickly go into some quick summary of some pharmacology, but just in will explain this later on, when he specifically going goes into the pharmacology of the upper GI I but and said so and said would stop the action or prostaglandin because remember, prostate enzymes are involved in the pain pathway. And that's that's kind of remember we treat them when someone's like trying really painful. You give them and said, And they stopped that pathway. So, um, prostaglandins, um, this receptors inhibited by and sex so you wouldn't have the inhibition off the cycling MP pathway. Instead, it would continue because of this pathway, and you would get hard to college acid secretion into the Lumen so prostaglandins would stop. The inhibition off would stop us inhibiting this hydrochloric acid secretion, so therefore would increase hydrochloric acid. Secretion of that makes sense. I'm sorry if that was really complicated, but basically prostaglandins end up increasing his HDL, which, if you think about it, I'm explained stomach ulcers. But, um, we'll talk about that later on with Justin, but okay, we're gonna talk about histamine antagonised. So as you can imagine, if something stopping this such a similar to d. You stopped this pathway and hence decrease gastric contents secretion must You're in a receptor inhibitor. A trippin it would stop, are muscular in the receptor and the receptor. It also called, um, aspirin. Your receptor would stop that, and so it would decrease our gastric acid secretion on. If you have a proton pump inhibitor like a map result, then obviously you can't have any of these pathways because your proton pump itself is inhibited. And hence you wouldn't have your hydrocodone acid in the Lumen. I'm happy happy to explain this later if I didn't make that clear. But let's first focus on this pathway next. So it's not a simple as just going into high Be three, but I'll go into it a bit more. So this is the calcium dependent pathway. Gastrin and acetylcholine are involved in it. So you have this physical a two and then three receptors, activating the GQ pathway. The PLC forceful, IBC. It's activated on it. Basically, catalyze is the conversion off picture to Dag and I pee three. Dag basically, um, increases p k. C. And that acts on our proton pump to increase our hard for chronic acid secretion. And I pee three acts on a endoplasm. It was it was like ridiculous, um on basically allows calcium to be released from it many calcium combined to our proton pump, and it basically allows hard chronic acid to be secreted. So both of these increase gastric acid secretion. Now let's talk about the G I and the GS pathway. So this was the camp dependent, Probably the cycling MP dependent pathway. So both of these involved a dental cycle is G g s pathway, um, stimulates active. It's dental Psychlos. Where is the GI inhibitory pathway? Inactivated ml side, please. So this pathway wouldn't occur. But say we had histamine on this part. There was activated. If I don't know, cyclists activated. It would convert ATP to psych like MP and hence would would because prospect first kind of a to work on our proton pump to increase drastic ask secretion. But if a dental cyclades is inhibited by our GI I pathway, none of this would occur on a gastric acid wouldn't be secreted. I hope that made sense. This is just a big summary off. Um, um, what I just talked about, but I'm going to skip it because I would talked about it earlier, but you want to come back to it. Um, I'm happy to go through it later. So let's talk about the rolls off gastric acid. So, uh, gastric acid delays gastric emptying. If acid is getting into the duodenum at two higher rate that's feedback mechanism, which reduce the rate of stomach emptying so that acid itself is involved in feedback, control off the rate of emptying process is, and also it solidifies, is that they're for improves absorption off calcium and iron and helps to release. It may be 12 from food. It also activates Pepcid Jin's and destroys any microbes. That's why the five second rule tighten clean isn't really because even if it's been on the ground for more than five seconds, you have these microbes in our stomach to, like help destroy anyway. But I don't. You feel from the world anyway, um, so now food's getting into our intestine. Now we finished our stomach phase were going into an intestinal secretions. So you have acidic time, or Kym that basically activator are cells to release, secrete in and secrete in. Um also allows bicarbonates to be really, and you also have bicarbonates relief from ductal cells in the pancreas. I'll go into the specific physiology off this later, but this basically It's an alkaline, um, basic solution which neutralizes are acidic time. The fatty acids in the low behaves can also trigger I cells to release cholecystectomy. I mean, which does two things. It's, um it allows the gallbladder to contract on, which means that vial connector the duodenum. But it also allows digestive enzymes to be released from pancreatic, a Sinus allergy, which I'll go into later on. These at these enzymes of the families, like pears and trips vision, which is really important for digestion. These all would then enter. I do it in a by the sphincter body into the duodenum, so I'll show you other is in this slide. Say, see, here, this is the sphincter off body, and it's basically connects everything and allows everything to enter the duodenum. So, um so in the intestinal faced my leads to trigger off some secretion of secreted and CCK, what do these do? CCK triggers the garden to contract secretin's demyel eight. The bile to secrete deliver to secrete bile on secreted also causes the ductal cells in our pancreas to release bicarbonate um, cystic and 60 because 18 ourselves to release those enzymes that mentioned earlier on all of these joints, these enzymes come into the duodenum buyer this victor OD, which relaxes because of Susie case. So I said can tell These are really important in the intestinal face. Specifically looking at the pancreas. I'm gonna just talk about what's happening inside these islets of Langerhans. So that sounds like a really fancy name. But basically, the pancreas has these ducks at the end of these ducts, there of these islands of land, A hands which kind of look like this. So these florals, the's floor like structures are a sinner Cells on. Do you have beta cells? Delta cells and alpha cells, The most important one to just remember in terms of these cells are big beta cells because they're really important in insulin production. So the pancreas is heavily involved in that. But I won't get into that in this case, but I just want the beta cells are involved. Incident secretion. So we're gonna be focusing on the ace in the cells on the ducks of the ace. In the cells of these is no cells have a kind of like a hole in the middle on. They are like a duck that connect into the but assist the ducks. Basically. So you have a chloride kind of just going in here a swell. So does anyone know what enzyme acts on the ace and are cell I mentioned earlier? Which two ends are not enzymes? What, out to hormones? Act on the ace and ourselves. So did someone just say CTK? Yes, Ck Yeah, that's correct. One ball CCK. And we'll act on the ace and ourselves So a lot of people are saying secreted, but that doesn't act on the ace in ourselves. Um, I'll just say it. So you have CC cake on a seat. I'll curly, I have my slide. Um, with the assistance CK and a CT colonography on the estate on the ace and ourselves don't even know what acts on the duck cells. Um, no, you guys said earlier secrete insulin secreted acts on the duck cells. I have my slide would just move that you get so just from the ace and ourselves CCK and ACTH depth cells secrete in see secure message trigger enzyme chloride rich secretions on duck cells are produced, um carbonate ions secretions. So the fact is that determine the bike out of the carbonate iron in pancreatic juice would be the rate of the when the Raiders there's more exchange. I was about okay. Lasting. Okay, The 60 age, he's a PCR. So if you were, um, on there is that increase osmolality of the pantry patients. It's the, um, ability of water Denham. And it's really important in him secretion regulation. And then, basically, do you do you know, by the whole 0.5 it will come out and secreted SBA. If anyone could lungs coli in and do prophy collie angiography off the military and adjacent structures, What does the letter C represent? Well, you guys getting this, um, be familiar with labeling the rest off them too. Um hum, maybe just practice going out to me and they bring this, but for time, I'll stop it. That so the answer is actually he said most of you about that, right? If my slide, it changes the common hepatic duct here. So I'm gonna talk about the liver in terms of liver and act to me. I'd say definitely learned that, actually, but in terms of time, I would be covering that today. But in terms of functional and at me that a Sinus is the smallest functional unit off deliver, and basically it has three sons and basically three concentric cycles. A zone one is closer to our hepatic triad here. So that's the portal vein in the portal arterial on the portal duct. And, um, his own one is the closest, so it's really, well oxygenated. But Zone three is poorly oxygenated, cause it's further away from this triad here, Um, some when you look at some histology on, be familiar with labeling. Are triads here from on the A Sinus, but some may show some cup for cells on. There's basically just macrophages that engulf old red blood cells and bacteria and any fun guy. And they basically maintained normal liver function are protecting the liver from any infection on the infections that you might hear about later in part two of the talk. So bio productions of bile production. There's a really good table out really good flow Child made later that will explain this slightly back to the in summary. Hemoglobin is broken down by macrophage is to build. I didn't and hence but ribbon, um binds two albumin and is transported to the liver, the liver consecrates it by gluconica acid on the enzyme Any to those GT, but I'll go into that later in her pacified on basically secreted out as mild. Now I want some more engagement. So can someone suggest what deliver said? That liver has former infections, synthesis, metabolism, storage on the top two toxifications What might deliver synthesize. So if you could just put any suggestions you have. Okay, Um, most of you got it. So was really quick, So hopefully my slide changes So Glucose kit and body's plasma proteins courting factors definitely fatty acids and bile. Um, what does it metabolize? What's what type of metabolism is the liver involved in? Um, I would just put the answer out. So I think some people have been saying it's a glucose metabolism. Fat metabolism, protein metabolism on bilirubin metabolism. What does the liver store? Yes, and most people going for like a shin. That's what it's famous for, obviously, the liver cells, glycogen, fat soluble vitamins, iron. Remember iron on copper on. I'll just quickly go through this. It also is involved in the cytochrome people. 50 system with the breakdown of ethanol, so alcohol, constipation, of bilirubin. Too late. Trump will talk about how this pathway that can go wrong. I also have really are interesting question to ask most you. So what? So we mentioned clotting factors and sisters? Anyone know what courting factors are actually made in the liver? Okay, um, I think most people are saying it. So you have fibrinogen profound. Been a factor. 5 to 7 factor and nine factor 10 factor 11, in fact, 12 as well as protein C and s on anti thrombin. I don't know why I asked. Um, I should have asked. What does it know? Um synthesized that most are clotting factors are actually in the liver, if you can see the point of most of them are in the liver. But the early ones that I'm no would be factored three tissue from the plastic. In fact, of four calcium and factor eight, which is actually in the liver, Sinus, Sinus surgery, endothelial cells and that basically those produce factor eight, which is our one will do brand Wilder brand factor. Okay, so obviously the liver is really important. Now, I'm just going to talk about red blood cell metabolism and this will be our final topic, that I'm going to talk about the fire handover. So, um, in circulation you have red blood cells. They travel after 120 days into a macrophage in our liver. Selena, Burma, on they die because red blood cell death. So when the red blood cells are broken down by five cytosis Ah, hemoglobin is broken down into a globin, which is recycled into amino acids and then gets reused for protein synthesis elsewhere. So that's a pathway one off the life over red blood cell. But it constipates lit into him, um, in my voice. But also he's bitten to him, which basically troubles out of the cell by transferring him. I just remember transferring transfers that iron in him into the liver where it's 13, and it's transported out of the liver by transfer and again. So in the letter travels is transferring into the bone, and then you have the bone process of end end right for police s. So just remember iron at globin, add vitamin B 12 and write the potent all trigger and rice the police is, which then forms a red blood cell and makes it travel in our circulation again. So that's pathway to off the life off the blood of a red blood cell. On the third option is this him serum. It can split into iron. Or a poor friend, Ray um, which is an organic him component which then the poor for Imran gets broke and down into build their dinner, which is agree on bilirubin, which is yellow, and this basically binds to Albany. Albumin on was transported to the liver sinusoids, and then here would associate and enter the space off this into hepatitis I cell where it gets conjugated by blue chronic acid. Remember, the ends on catalyze is that is you GT enzyme and it's capitalized by UTI and zone where it's made water soluble. So this conjugated bilirubin is that excreted as bile on down in the small intestine. You have bacteria, um, in the gut here, where basically modifies are bilirubin to form your ability gyn so bilirubin is modified by bacteria in the gut to from your village, in which is colorless. I couldn't really create that on this diagram, but remember, it's colorless on then. This has two choices. It could either be re absorbed into the liver or the kidneys where it cleaned. What if I didn't to further into urine? All it It could be further modified into stir kobilinsky, which is brown and then excreted a species. So that's the third option to the life cycle of a red blood cell. It can either become a red blood cell again. It could become, um, and, um, you know, acids. And then eventually a protein or it could be excreted out either a species or urine. So those are the three choices off our red blood cell. So hope that made that clear up. And that's the end of my part of the talk. I hope that was helpful. If anyone has any questions, I'm happy to answer them in the chart. Oh, I'll stop sharing now. Okay. I'm not the best technology s. Oh, here we go, Case, except the physiology of their pharmacology as well. So these other kind of talk isn't covering it right into it. So starting with kind of we're looking like yourself a guess to stomach and then go into the liver. But obviously started with a question while of questions. I know it's quite late into the evening hours, but I want every everybody to engage. So could we get the poles up a swell, please? Um, as that there is no I can't totally anonymous, So please do give it a go. But amazing. A lot of you guys got the right answer, which is so great to see, um, they give a few seconds. Maximum participation is all right. So have did look into this a little bit, and I think we'll end it there. That's okay. So look, you guys went for be on. The answer is very well done. Be the bud. Big sign. So, look, we're going to start off with some stuff. It'll motility disorders, looking at accolades. You first. So what is actually easier. So at least it's just his red. It's order. It's characterized by this inadequate relaxation of that Lower soft your sphincter. The lowest suffer you think is usually contracted and relaxes for what we eat in in. The difference is that perhaps talked about is caused by degeneration, inhibitory neurons. So, as I said, it usually is contracted. And without this inhibitory neurons, it can't relax on. But the thing that the most important thing Yes, in stone is how to recognize it on a, um, kind of a nimit Eso from a barium swallow is we can see the characteristics are things persistently narrowed region at the end of the esophagus of the theme Lower esophagus on. Then you see this kind of dilated esophagus above the narrow region. And so this is that bird beak sign about a little elevation just so you guys get idea. It does look like a big, um looking at diffuse or so for your spasms. Eso the cause for this isn't very well understood it it basically is a condition characterized by uncoordinated contractions. So we know the esophagus contracts with from With Paracels, the story process is just this wave like muscle contraction that helps the food moved down the digestive tract. It's when the food bolus is pushed through. But in does I guess, diffuse in these spasms. What we get is this uncoordinated kind of contraction on the cracked. A characteristic that image is that corkscrew esophagus It can see there. So it's just important to be able to notice these different signs. And b it's characterized. So moving forward. I've got another question as well. Sorry if you could hear my, um, fact, it's not that loud, but here we go. So second question SBA Sorry. Okay, Late. Because we that could we get be poles up again. Guys. Totally anonymous. Does not matter if you get it wrong at this stage. The point is that you guys get good, stab it it you're gonna have to ask your gonna have to answer every question exam. So give a good guess. But guys, honestly, it very well done. A lot of you guys get the right answer. So it's so good to see that, um, few more seconds on, I think we'll close it there, if that's okay. So you guys went for D on. The answer is very well done. The Medical Asia. A suffer job because I'm going to see what that's about. Coming up. So gas s so Gord God's disease or that this disease is, um, multi fact. It is caused by different factors, So it must be different factors, but it's usually characterized by that neuro soft. You'll speak to a weakening eso rather than being contracted. It's kind of relaxed. There's a lot of things involved in it, including the including changing pressure as well. The diagnosis of this is when your acid reflux twice a week or you get the information of yourself, suffer Guess which is a sulfa jointness. What you get with this stinks of weakening is a reflux of lose it. Everything's acid bile, perhaps in a lot of things that can damage your epi, Um, on. But what you get to see is this's what you get is just a a lot, a lot of different kind of effectively. Heartburn. Pain in the esophagus. Pain beating. The main finding is heartburn. Yet after meals, you get it lying down, bending forward. You also get these other complications, strictures and gas. Esophagus. We're looking about coming up. Strictures are basically an area of narrowing on. This could be caused by inflammation or computers. You're healing tissue that's been replaced by scar tissue, with management and risk factors that kind of come in hand in hand, a list of the risk factors there for you. Um, on. We've talked about few of these before, like high tech hates hernia, but I think the key thing I'm laying goes with this. But the key thing I want to get sick from This is with any kind of management I wanted. You get to learn a C. M s. So CMS is conservative, medical and surgical. So that's kind of how our group, the management, they're the kind of this is just a way for you're the future. Any time when you're explaining management, get kind of gives you a structure, a tool to follow. And so a Z could see there. I've the conservative kind of management options are weight, last mechanization and dietary modification. So anything that is causing the gored include includes, like, stresses, well, so dealing with stress and stuff like that. Medically, we've looked at PPI eyes and we're gonna look a little bit more people is an option. And then I just know that a surgical options well, and this and frontal fundoplications this is just basically a surgery that involves taking funders off the stomach, kind of wrapping around the lower self against on that kind of creates this kind of tight, and I think, oh, it tightens the sphincter. And so, yeah, that that this is kind of God. But what's very important with Gore is Barrett's so coming up. It's barrettes. What is it so far, it is just a condition that causes it would pass the condition that's characterized by this. The flat pink lining of the esophagus become damaged by acid reflux on it causes it to be replaced with a thick and red kind of tissue. The thing that you you guys need to know is that, um the normal karate non correct. And I stratified squamous epithelium gets replaced with Colombia. Epithelium in on an endoscope. What you can see is this advancing Squama Columnar junction have talked about that said line. So what you can see and the images How does it look like? It looks like this and said So what you get is this advancing kind of thicken inbred band kind of progresses up yourself against and that's by itself. Focus. Um, also, what you need to know is that there is an increased risk of adding a carcinoma on. This is the histology as well. I'll let you guys go through that, but what you can what you should be able to see is a metaplasia from the normal stratified squamous epithelium to the stick and damaged and kind of messy Columbia apathy. Um, but yes, I think just a quick side. Now see, this is just a little bit, but that's how I kind of learned thinking. Two different cases a case for it on remembers thesis. Vicks, the epithelial lining of the cervix actually follows the same person as yourself because eso the inner kind of thing. So the outer kind of epithelial is simple columnar a billion, uh, contrast with the kind of sorry, The yes, the inner inner kind of cervix is Columbia epithelium, whereas the outer cervix is stratified squamous the BD um So it can it comes hand hand when you come to revise Just so you know these things moving forward quickly. Peptic ulcer disease eso peptic ulcer disease Quite straightforward. It's just basically to get this imbalance between you're damaging forces against your definite defense mechanisms. So your defense mechanisms are that mucus layer, um, and bicarbonate that is secreted by the stomach and intestines as kind of covered. The clinical features are as follows you get was epigastric pain dyspepsia, which is just indigestion, pain and disk discomfort. When you're eating food on heartburn, we have listed some causes here and we're gonna be looking at that coming up. But I think the thing I wanted you guys to know, very importantly, is the difference between Giardino else. Those vest is gastric else is so do do you know ulcers are more common on the characteristic future is that there is pain relief after a meal on, but what you commonly see is weight gain on gastric ulcers is kind of the direct opposite, but this is obviously less common. Pain is pain is really during food during a meal on Did you character characteristically see weight loss? And so the way I like to remember this is not very straightforward, but duodenum. Intestines are involved in food like food absorption and a vitamin, so option. So with the absorption of food, you're gonna gain weight. And so that's a way to remember it. And then gastric kind of stomach breaks down food. And so you're losing, I guess where it lost its kind of way. I like to remember, but that's weakness. Remember, duty? No. Ulcers versus gastric else is so looking more specific about the causes of peptic ulcer disease. We're looking at hate glory, a trial or is quite straightforward. It colonizes in the stomach. Different parts of stomach on what effectively causes is, um, acid secretion says, increase acid secretion but also decreased acid neutralization. On top of that, there's a disruption of the mucus, um, mucosal barrier. All of this combined. You get damaged. That CD, um, on what this causes do deal and gastric ulcers. So again, it's It's a question before, but the things you need to know about HPV Laurie is what a little bit about bacteria so that it's gram negative and spiral shape. It's transmitted fecal orally on the gold standard Diagnosis is a stool antigen test. I recently I recently found out that you can't take a stool sample from just within the toilet you because toilet water can't kind of the only a sample. So don't get me started on how you get it. Collect thie sample. That's for another time. The other thing you need to know about HPV Laurie management at this important and PT and s one is well is the 123 s. So you give for one week, two a day, three different medications, that is a PPI amoxicillin, and either tourism I said, or Metro Metronidazole. So you just give either of those depending on what is best tolerated. I'm sorry about that. Um, there. That's hpai nori path. Kind of cover this a little bit so and said sort of the chronic use of and said We know that effectively decreases prostaglandin e to census with decrease muscle. I mean, each census, you get decreased mucus secretion decreased bicarbonate secretion indicates blood flow again. All of this put together kind of increases mucous damage on empty lot observation. The other cause of peptic ulcer disease that you need to know is Zelen a Salinger else and syndrome on britches, just a gastrin secreted in tumor. So with increased gastrin secretion, as we saw in the physiology, you get an increased you get increased acid secretion on this. Then later on, of course, is Pepcid ulcers on chronic gastritis says as you can see that eso it's not. It's a peptic ulcer, that is. It all comes down to the kind of same thing. You get increased acid secretion and you get this increased acid neutral, the neutralization and a disruption that music it mucosal layer. So again, if you think about those balancing forces. You get increased damage without with decrease in defense. Effectively. On this is a quite quickly just looking at the pharmacology again, there's only kind of foot kind of students have any kind of three drugs or three classes that you need to know. PPI eyes on Do hate receptors kind of come hand in hand Together, they kind of work in the same way. BP eyes obviously irreversibly inhibits the acid. Potassium ATPase hate to receptor antagonists competitively inhibit age receptors. This both combined come together, decreases acid secretion, and I've given you some examples of each their the important that you need to know on a result on soliciting. I've put some side effects that as well, and the third type the use those antacids on antacids are just a week base, so based acid neutralizer stomach acid on. That is how you would treat acid AST problems in the stomach are put some examples. They're a swell, so I think I'm speeding through. It's a little bit just to get onto a little bit of the later pathophysiology is, but the key thing here is trying to link it. Teo. The normal facility as have very nicely detailed out there if you understand the normal physiology and you just know that if there is increased acid secretion and how that can come up kind of can happen. You you know where to target these drugs. So PPI, eyes and hate do it receptor antagonist directly inhibit the cause is of gastric gas a gastric acid secretion on that antacids work by neutralizing it. So all kind of comes together quite nicely. And that's why I'm gonna move forward to the pathophysiology of the liver. The first thing I look at is the alcohol and the liver. And how is metabolized? There's to make it. That's two mechanisms of alcohol metabolism. The first day and the most prominent is alcohol Dehydrogenase s. So this is This takes about 25% of the metabolism, and the other 25% is by cytochrome p 4 50 cytochrome, so you would have seen them before. They're just a group off phase one. Enzymes. Metabolism is kind of split into phase one. Phase two. These phase one end times allow the metabolism off drugs and alcohol, but problem with cytochrome enzymes are that they have a lot of toxic by products that we don't want to be made. So with the alcohol dehydrogenase on such people 50 What you get is a seat aldehyde being made. See how the height is then further broken down into acetate on You can see that is, by another dehydrogenase quickly. The thing I want you to note here is the abundance off any hates molecules being made our these reactions. So just know that with alcohol it goes down. It's broken down in this kind of way. And there is, uh, an increased NADH kind of creation with acetate. What you get is a fatty acid, a production so acidy it becomes a seat Elko A which is then which is then used to synthesize fatty acids on. So what you get is, um, yes, with that you get fatty acids on this Kaletra. Only Teo increased, Um, a fatty alcoholic, uh, liver eso The thing that we need to there here is this is how normal alcohol metabolism works. The problem with increasing excessive alcohol consumption is your dehydrogenase enzymes get saturated on. So then the CIA, the scientific enzymes are then utilized, and they're they're kind of the need for them are increased. And so the problem with that is you get increased toxic byproducts being made, including be active oxygen species and radicals. Um so this kind of this, as well as a seat aldehyde being produced, adds on to the inflammatory part of alcoholic disease due to liver diseases. Alcohol. So on top of that, what you get is increased fatty acid production as well. And so remember I told you, NADH, there's an abundance of NADH being made on. The problem with acetylcholine A and 80 HBO made is that there isn't a lot of fast acid breakdown. And so you get increased fatty acids insist, but also not you get a decrease in fatty acid base oxidation, as that's what happens with increased alcohol intake as you can kind of see already the problem of. So that's kind of alcohol in shorts. And I'll see alcohol like just a heavy night one night. Our it's not gonna cause you any problems. Yes, you're going to get kind of get, um, inflammatory process as well as improving fatty acid. Um, fat fatty acid production. But the liver usually is is good at, um, handling this over a chronic period of, uh, over a long time, what you get is increased. You get increased fatty acid production, which leads to a liver damage as well as hepatit. Sorry, hepatitis is, well, alcohol except hepatitis, which is severe inflammation of the liver. Thing to know is alcoholic fatty liver is also down the stair Tosis, and so with. Even at this point, Theofanis are reversible, the point that it doesn't get reversed, it becomes irreversible, is known, has cirrhosis, and so how, and the liver kind of goes into alcoholic double disease is you have a healthy liver through excessive alcohol consumption you get you get fatty liver disease, which is stage ptosis on. Then your liver gets damaged, which causes liver fibrosis on Then, from there you get increased access scarring, which leads to cirrhosis, which is that reversible. Remodeling off the liver on the things that I know about cirrhosis is that there's two types. There's compensate and decompensated on. But most important things is the common symptoms and kind of signs that you can see on so you can see a curriculum with these so reduce clotting factors. We're gonna look about a little bit more coming up. We have joined. This is well, Look at that. And cephalopod the which is the poor detoxification of ammonia is increasing Moughniyah on we're not. The liver isn't able to detoxify that causes encephalopathy. Onda, just aside, know seeing a gastric examine you. You can see this with a handful and I don't see I can't see myself in the camera that uti, a hand flapping sign can get a scientist and also viruses. Well, a size is is just fluid collected in the abdominal cavity is and viruses can just increase our kind of these bold is that due to the increased portal pressure? What the complication with viruses that you guys need to know is that it can cause GI I bleeds s so you can get blood and vomit. Or melena, which is kind of like this dark, tired like blood in the in your stools. The diagnosis of alcoholic liver disease is a liver biopsy, and the treatment is obviously the best treatment. It's stopping the course on supporting liver, but also considering them for transplant. So I hope that was I hope that's clear in sense, that it's very simply alcohol you get with increased alcoholic consumption over excessive period time. You get alcoholic fatty liver on top of this in from inflammation of the liver as well. Those two things put together. You get increased damage of the liver, causing fibrosis increase over over a long period of time. The fibrosis that becomes kind of irreversible scarring, just cirrhosis. Eyes are Call it liver disease. I've listed out quite a few different metabolic liver disease that you need to know. I'm just I'm kind of giving you the most important things that you guys need. A note here. Eso Non alcoholic liver disease is the most is one of the most common cause of chronic liver disease. It's very strongly Associated Teo Metabolic syndrome is a metabolic syndrome is just a class trip. Conditions that cause that increased risk of heart disease, stroke and type two diabetes is includes I BP, hyper blood sugar, excess fat around your waist and so on. Brings along those lines hemachromatosis eso increased or excessive iron deposition. There's many different causing from ranging from congenital toe viral hepatitis C. Just know that it it can be an auto from auto soma recessive disorder. Um, with Wilson's disease, you get increased copy deposition, copper increase of deputies. Your deposition in the liver causes again fibrosis that could lead to cirrhosis. Scarring of the liver Alpha one antitrypsin. You should have seen that in case three for respiratory case. Alpha one antitrypsin is just a protein that acts to protect your lungs from damage when the immune system is kind of clearing different kind of pathogens. But after one trips in deficiency and then cause lung damage, which is seen a COPD, especially in young patients but in the liver leader to protein build up, which will then again cause fibrosis that can lead to cirrhosis. Um, but those are just some of the metabolic liver diseases, and the key things have lists out some hepatic about a biliary disease as well. Um, again, just the most important things to know Goldstone's or credulous see cysts before risk factors. The four f Sorry, The four big risk factors for Goldstone's females over the age of four. See our our overweight, obese on the first of all is when they've had one or more Children. You just you see your seem to have a higher risk because there's increased Easter gyn after pregnancy and or around pregnancy, which increases your risk of Goldstone's on. I'll let you guys read about thie. Other two just gonna move forward because of time. You guys are gonna get these slights but to move before we go into acute liver failure. A question. So do you mind if we could Yeah, the, um, call up, please. Okay. Eso again? I I I want you guys to have Ah, good guess at this, um, the same. Like I guess, and let you get the other. My answer is a very well known guys. Um, please, you stay with me. Uh, I still got its cover. Um, okay, I think we'll call it their, um So what additional finding would you find? That confirms your diagnosis. And it is the protime at increased problem. Been tough prothrombin time. So you look about now. So acute liver failure. So cute. Liver failure is characterized by three things that you need. Three main things. Join this which we will look at coming up several avi on coagulopathy. So that's why the increase prothrombin time would have bean. You're kind of final diagnosis of cute liver failure. Um, because we're checking for the coagulation factors you describe that a little bit coming up. There are just too many calls. Is that the two big causes of cute liver failure that I need to get, you know, on the first, pass it on toxicity or kind of any 100 drugs? Because liver liver damage on a second is viral hepatitis. The first up, we're going to get a little bit of viral hepatitis, but obviously a question. Because I know you like you guys love. SBA is so again, um, could get the whole up. Please. And please do give a good guess. Giving you some serology results on. Just want us. Interpreter. Has it doing good yesterday. A very good sign. You get maximum participation. Guys would love to see all of you guys give it a good Okay. She was a, um okay. And we'll school it there. Please s Oh, yes. A lot of you guys got my answer. It is d I'm gonna look at why that is coming up. Say a table. I'm sorry, guys. I just thought the best thing for you is right now. Especially so close. Exactly. is in everything you need and one table. You got it. You guys are gonna get this the slides coming up. But I just want to highlight a few things to some important things for us. A note about the hepatitis is so acute hepatitis is obviously when the immune system can clear the virus within a few weeks or months, acute acute time period is less and six months. This is commonly seen with hep A and B. We'll also be, um, I grew up and eat together because they don't tend to be chronic. The common symptoms that you see are malaise, fever, nausea, vomiting and diarrhea. Some signs that you can see are jaundice and in large liver. And so that's why when you're investigating, emphasizes yes, you do the LFTs. We'll look at that as well. You look a bilirubin again, going to describe that coming up, But you also do an ultrasound on a hepatitis serology. We're gonna look at that as well. But yeah, those are signs for acute hepatitis with chronic hepatitis. The immune system can clear. The virus within kind of lingers around on. So chronic is more than six months and so the common common hepatitis that cause chronic hepatitis is is A B and C. That's about 80% of cases on the complications that you see with chronic hepatitis is live fibrosis and for leading on to cirrhosis and also cause about a cellular carcinoma but also leads to end stage liver failure. This could be due to pull hypertension or selfish self. Your virus is a swell, um, the things to know a swell are that vaccines are available for hep A and B, and don't quote me on this. I think there are some unlicensed about vaccines as well, but the ones that you need to know is that as vaccines for A and B So again I've given you the table. I'll let you guys read through it all the efficiently. It is there a little bit on serology. The thing is that the PSA staying off again, I think it's animated tries animated at work again. Another table. I'm very sorry, but I'm gonna be going to go through this a little bit when you understand what each of those each of these markers and solid Gee, I mean, it kind of makes it easier to interpreter Serology result Start from the top page s H. B s antigens. So hepatitis B surface antigen is a surface antigen on is indicative off infection. So having the surface antigens means there is an infection. But at this point, we don't know if it's acute or chronic. Hep B e antigen is indicative off infectivity, but also replication. But mainly, in fact, it is he. So I like to remember it is be for you. So they're infectious on. So that's how I remember that, Um on this is a surgeon in the virus. And so obviously, if you have a lot of my wrist, you're getting a lot of repetition a lot release of this antigen and that's how you get checked up. And then we have antibodies. So I know it's kind of amusing with a Z and antigens and antibodies, but antibody their hep B C antigen. So that's what that means. You get two types, you get me a musical. Billions Um um hum bill in g m g on go. Each of those kind of indicate time period I am indicates more of an acute infection on IDG indicates more of a chronic infection or a result infection. I'm going to see that coming up the antibody for hate to be e kind of. Obviously in the at the antibody hate to be even indicates decreased infectivity eso again if we know that is for you Infectious, There's just reduced infectivity on. Then finally, the one that you'd want to look out for antibody hate for hep B surface antigen, The last one indicates immunity. So this could be resolved by infection. Will vaccination. So another big table And you might see this on our instagram? Uh, no. Yeah, no, I meant sorry. Every day is another big table. It's got everything you need and I know it's a little confusing and I kind of don't want I don't want to tell you got to learn it through this table But I've detailed out what the serology results for Each of these scenarios would look like. It's obviously a healthy person that no exposure vaccine would be negative for all of this. That's very straightforward thing. I don't want you guys looking at this and try to memorize this as a table, but I want you to understand what each of those markers men, and then it will help you kind of. It'll help you understand what kind of what the story is helping you actively. So obviously, if there's an acute infection or chronic infection, we're gonna have that surface antigen that that's always going to be positive. If you're immune, that's not gonna be there, Um, for things like active infection beginning, we're going to see, um, infectivity. So we're going to see that he antigen. But if it's inactive, if it's an inactive but acute chronic infection, you'll see that the surface antigen is there. But there are no antigens effectively antibodies for you on. But with immunity or immunity due to due to prior infection, what you're going to see is you might see an active infection. So they're they have an active infection that is, that that is causing them. Teo, that that is causing the immunity. That's kind of known as a window period, but don't worry about that. But you can also get immunity to vaccination so you wouldn't see any other kind of androgen. You would just see antibodies for that surface antigen, that main antigen that causes the infection. I can give you as a question. I just I will. I'll let you guys answer it. You guys have got great grip on it. So I'm not worried that you guys don't understand what's going on, but can we uphold up a swell? So not that 26 year old patient returns to you? Um, they, uh, having the new problems. So they were treated for their gram. Negative diplococcus bacterial infection. And so there was a bonus question. If people can put in the comment section What that grand negative, Difficult. A bacterial infection is brownie points to you guys. Um, but yes, I think a lot of you guys are getting it on. I'm glad. Please, guys, Everybody Aunts on a C c a. Full. Yeah. Just isn't on a message. Give a good stop. Big time out would be amazing again. Please answer those questions in the chapel. I can't see the chat, so I'm assuming you got to get it. If not, we'll send out. So can you close it there, please? So you guys want to see on. So again, if we're going through it one by one. There is a surface antigen, so it is obviously an acute or chronic infection. There is an active infection. Oh, there is an infection. Sorry. The e antigen is present as well. So it is a active infection. There is, um there aren't antibodies for the surface antigen. And there aren't antibodies for the B antigen either, so it hasn't has been cured. So that last from the first one kind of out the picture on We know it's chronic because off the I'd I g antibodies, I'll be made. And so you guys are right. It is. See, on that bonus answer was gonorrhea. And so this is just something everybody for anyone should know, but kind of students especially. I'm sure you'll be tested on it. Gonorrhea is a gram Negative. Diplococcus bacteria. Just learn it like poetry. That is the best thing I could tell you. Gonorrhea is a grand negative. Difficult, but I'm very I'm glad to say I'm sure you guys getting it, But as I said, just try and read it one by one. So see if they're antigen, is it? What antigens are there? What antibodies are They're on kind kind of create a picture, try and say it out yourself. Rather learning tables and minuses and plus is just try and understand serology and that. And I hope I hope you can refer back that table later. But moving forward another question. My bad. Just before we got power. Sensible toxicity. I want to see what you guys know. So you get a pole up. Please, Just giving us pays off SPL is I hope you guys like it again. Please, everybody answer. I love to see back from participation. Um, So, yes. What is the toxic byproduct that causes liver damage and paracetamol overdose guys. Very well done. I don't know. I'm doing it. Yes, You guys get the answers. So I'm very glad we'll call it there. Thanks. Thank you guys. Um so you guys went for D at on the answer 50. So, looking at your assessment. Psoriasis itchy. So we got, like, a a normal metabolism on. So what we see is possible. Um, the The scenario here is just is there a 0.5 g? Because passes tablets are given in 500 microgram kind of tablets You commonly take two adults complicate to Well, he What you get is you GT ends. It's a powder kind of mentioned a little bit. Ugt enzymes directly glucon right. Eighth paracetamol on this produces a a inactivated water soluble compound called Paracetamol Blue Clone or a ride, which is excreted easily and safely. And so that is the majority off paracetamol metabolism again. Unfortunately, where there is a hero, there's always a villain was, well, MMC X. There is no damage to liver about sites, unfortunately or fortunately, you need you need a wheeze. Reckon is, um's there is a second kind of record. Is, um so the main the main part is through the UTI enzymes, but there are cytochrome enzymes are listed there. That embolden process more metal is, um's well, they create they form. I'm not even gonna try and say that, not becue. I know how I pronounce it. But that toxic byproduct on this, thankfully, can be deactivated but binding to hepatic glutathione on. So when it's deactivated, it causes no damage to the never have passed sites, and this is in normal metabolism. And so that's one thing. If you have to know in this kind of slide, is that, uh, you did the enzymes kind of metabolized past. That's mold, mainly creating paracetamol Glucon ride again excreted safely passes mall is given in separate 5 g tablets on in the UK you can't buy more than two to kind of like packets of Paris is more for sale. On the kind of figures to know is that for more, for more than like a healthy dose is it varies between people, person to person and healthy adults and Children. But for a healthy adult, the maximum daily dose recommended is 4 g, 4 to 6 toxic and then over 12 can be lethal. Um, but yes. So in a scenario where someone has, um, no, the animation hasn't come through, But in a scenario where someone has taken more than 4 g, what occurs is the UTI enzymes get saturated, so it's kind of the same. It's the same story, just like how we were talking about previously, where enzymes exaggerated What we get is the's ugt enzyme saturated and so passive smoke glucon ride Combinator. And so then what happens is the cytochrome metabolism is kind of useless. If there's an increased need before it on, then as you kind of salt before you get massive amounts of that toxic by product they made, then the problem is hepatic glucose diet is rapidly depleted. There's only, um there's kind of only a certain capacity for the liver. Teo excludable the activate this toxic by product on where you get from that is significant about aside injury. And so Okay, so, yeah, that, as I said, the key things to know is that kind of pathway of metabolism. So you have that the main face to metabolism, That's that's the key thing to know that you have the basal metabolism, which is those usually tea enzymes. But you also get these Phase one enzymes is phase one metabolism, the cytochrome enzymes that cause this kind of toxic byproduct to be made on, um, effectively in an overdose situation. You get, uh, you get a range off kind of symptoms present with Paris is more overdose. But the key thing to know is that raticide injury. Um, but I think yes, moving forward. We have another question. So we get, um, if we could get pull up, please. Thank you. I'll let you guys, we don't want to read over it. The top of you guys say exciting stuff going on. So November lefties. Okay, um, I will take too much of the time again. Guys give it could stop. Get a good guess. It was like and if we could end it there a little bit more. Very. But the most of you are getting it very well done. It is C a L t is the best indication of damage. I'm going to see why Another table? Sorry, guys. I'm very sorry. Um, but again, I've kind of listed it all in one slightly here, but we're going to talk about just a few things coming up on. So the key things I know about a lefty's are the's individual markers on what they kind of show. So the top to the first two are the Trans am amazes thie a little and see So we said a lot is thie specific kind of liver marker because it's purely made by the liver issues also made by muscle. So they are indicated off kind of damage to those muscles and the liver in it also indicates m i s t a c also kind of take it, um I as well I mean the liver damage. I've noted some ratios of a little and ST that you need to kind of be able to recognize. So as we said, SGLT ratio should be around one. That's normal if Ailton is increased. What that is indicative of his chronic liver disease on the way I like to remember is a l l is for long time liver. So long time liver problems ST is greater in cirrhosis. So, um, if you can, there's yeah, so there's no better way to remember it other than just kind of recognizes. The lt is that long time liver problems Chronic liver disease is on a ST is seen a cirrhosis of the S for cirrhosis. Thea Other thing that you guys should be able to recognize is that if the ratio is two or greater, that is very strongly indicative off alcoholic hepatitis A S T A. L T. Ratio on then, if either of a lot to your risk is greater than 1000 into that's international unit or units per liter. That's indicative off as we talked about paracetamol overdose, but also ischemic hepatitis, so it's given. Hepatis is commonly caused by a portal vein thrombosis, which is usually secondary to portal hypertension on this is known as body Chiari syndrome, but that is that is where you see a SGLT rates so it's important to a Z is important. To know where these markers are made is also important to understand what those ratios kind of means. I've noted that there for you moving forward, we have LP and GT. They are strongly indicative off post hepatic kind of problems so you can see they're LP is made by the new system. But it is also made by bone placenta so as well as it being an indication of current Stasis. So when there is a mild problem about obstruction, it is also indicated with bone breakdown and you going to see that next year, hopefully near, too, with the bone with with kind of bone, and have to recognize that GGT involving to know is that it's indicated off Billary epithelium damage, but also by old flow obstruction so kind of Stasis. A Z well, all women is made in the liver has a lot of you guys 100 before. The thing to know about Algren is that yes is a measure of synthetic function of liver. But the thing to do is that has a long half life. So if Alvin is, if there's change, the albumin is indicative off chronic liver problems or chronic liver damage. We talked about PT eso. The prothrombin time profile minutes is one of the several coagulation factors that is made by the liver. Um, I saw in the chart I don't know anybody else saw, but the clotting factors. The liver produces a lot of clotting factors, but the main ones that you kind of do need to be able to recognize being to 79 and 10. There the vitamin K dependent or vitamin K derived clotting factors. So the prothrombin time is just a measure of how long it takes for a clot to form in a blood sample. On the iron are is thie is the IT international normalized ratio, and it's a type of calculation based on the PT, and so again, is a measure off the liver synthetic function. And then, as of those that their plate this is just indicated Officer OSIs having low platelets is that's what that means, So a Z conceive have not noted bilirubin, but that's coming up now. But before bilirubin question. So this is my last question. We're going onto the last bit overly have physiology talk. Okay. So again, um, you guys know what S t a l t kind of indicators? Yes. Liver damage, but want want to be looking at here again? You have a few seconds, guys do give it a good guess. Uh, if your second alright, we'll stop it there. Eso Yes. A lot of you guys are together, right? Answer. There is a little bit variation, but very well done. Um, well, some of that Yeah. Okay. Eso The answer is a her Patrick conjugated Hyperbilirubin amia on. What is that? We're gonna like that coming up now. So then I think you have no jaundice. This is the yellowing of skin. It is also the elegance. The sclera, because of the high lasting content that's lower is the first we affected. It occurs due to the accumulation of bilirubin on. Obviously, we looked up Billy Ruben on rebel itself. Kind of break down and how it gets reused. We're gonna look at what happens when a little bit isn't cleared properly. Uh, but the thing is, you know, is that also causes Porisis. Which is it? Your skin. But that's just due to the accumulation of bile salts. So pounds. How slide on this was a much better indication of the bilirubin physiology, but I just kind of kind of formatted it in this way for credit tenish for how he presents itself last year. This is just a way of you guys able to be to be able to understand what kind of parts of being affected so that macrolide the macrophage a stage and that's the that kind of side, including blood, is nose prehepatic, or it's more humility jaundice. But that's what that's when the regular cells have worked out to heme of the human process into the unconscious gated bilirubin that is water insoluble. So obviously that's why it needs to be bound albumin to be transporting the blood and then, um, uncomplicated bilirubin. Is that compared? It conjugated opens everything before then, is prehepatic on any kind of jaundiced is not a bureaucratic. Obviously, anything of the liver is hepatic causes of jaundice on. So about a cellular that is known as on then post hepatic is that the talk that we had about is everything in the biliary system on Do anything afterwards, obviously. So again, Please do refer back the power slide of this. But this is just a diagrammatic representation. Just give you an idea. We'll be I'm gonna be looking out of the different types of jaundice is on. But again, I'm sorry. It's a big table, and this table is the worst is well, but I just said the best thing for you guys on exam season. It's just everything in one kind of table. Um, So the first of all looking at is Patrick. The time to do once is on the first one is hepatic or more humanistic, John. So there is a variety. Of course. Is that list of the If you do, you need to know all of them. Not particularly, but is good to be able to recognize them. Um, s so I kind of group them in. I've kind of group them in these different categories. So obviously, get these deficiencies, you get a congenital or inherited kind of problems. But the underlying underlying idea of humanistic jaundice is just increased hemolyzes. It could be intervascularly or extravascular e. Um, It can also be drug or infection mediated on. But that's how I grew out for you there. The main things are not allowed. Findings is that there is decrease hemoglobin on an increased unconjugated bilirubin. And so again, if you refer back to the diagram, you should know that if there is, if there's something causing increased red blood cell breakdown, you're gonna see a decreased hemoglobin. But obviously and increased unconjugated bilirubin in either the spleen and the liver in blood on do Another indication is increase your ability in in a bit below engine in urine on. Um, obviously we weigh have kind of mentioned your oh belligerent bill. It didn't affect religion on going quickly. Give us an idea of that as well. So yes, conjugated bilirubin excreted in vialed and enters the intestines on. But she did say you can get you can get your ability and excreted in the urine as you're a billion. That kind of gives thie that gives thie. It gives you in that yellow color, um, and then the other the it most of your ability gyn is excreted a sterile Seroquel billion, which gives your stools that brown color. And I'm giving, um, kind of a firm mass. This for a particular reason. So these are things that you need to be able to recognize, so in Prehepatic. So I didn't like that, right? Prehepatic jaundiced or humility? Jaundice. You you get an increased breakdown of blood, but their liver function is normal. And so you're kind of conjugated. Your conjugated bilirubin is levels are normal and kidney function should be normal is well on. So you wouldn't see any any kind of changes in your urine or stool, which is what I've indicated down there. But you would see increased your ability engine in the urine. Um, moving forward. Hepatic John, this is kind of broken down into two. So what you get is one type is impaired conjugation. So the two kind of causes the two main causes that you get. I need us. Recognize is Gilbert syndrome on a cruise, Crigler and syndrome as well. Gilbert is where there is a decreased amount of you Deep e. So you DPA is the enzyme that converts gates uncomplicated bilirubin in the liver, as if there's increased decreased. You tp you get this kind of transient joint this it's going to blow on by stress infection on fasting as well. On that's Gilbert in the the quit Crigler Nausea syndrome. You do pee. It's just absent. And so this is common. Seen any neonatal jaundice? Eso There just isn't any conjugation off bilirubin main lab findings here obviously would be uncontradicted bilirubin if the room is not conjugated, that's the main thing you'd see. You might see increase a little and ST as well. On the thing to note here is the dark urine as well. On the reason for that is, um, the reason for that is, um, there is increased. So there is increased unconscionable Ruben on that bilirubin albumin complex in the blood on this then causes increased bilirubin to be in the blood on the bilirubin is what causes three urine. It leaks into urine, which causes the urine to be darker. So again, it's your ability that causes urine to be yellow. And if there isn't again, if it's a half a problem, you're not getting constipated bilirubin. You're going to be missing out on that yellow urine. But on top of that, you're getting bilirubin that is leaking into the blood on that into the urine, because is the dark urine. Yeah, the other type is hepatic thing. Other type of passage on days is hepatocellular. Uh, so this is where you are getting conjugation, but thie liver is failing. Teo is failing to transport that congregate that so it is kind of failing to, um, process the conjugated bilirubin. So what you get is conjugated bilirubin, so it's going conjugated, but it's not getting process properly on, so it leaks into the blood, and so that's the main finding it. See that you also see increased LDL ST because obviously, it's a perfect problem. Um, you'd also see dark urine. This is, well, upset makes sense, but normal stools cause the steroid circa Kobel in in intestines. There's no problem in that kind of metabolism in that kind of process. So again, uh, kind of reviewing that little bit? Where you get is in impaired conjugation you're not. You're you're missing out on that conjugation conjugating enzyme that you dpt or there's decreased amounts, or there's a problem in that day, increased unconjugated bilirubin in the blood. Um, Andi. For that reason, you get dark urine in a patio problem where you are getting congregation, but it's not getting process properly. You get increased conjugated bilirubin in the blood, but also uncomplicated as well. So you see a lease markets kind of raised, and so that is indicated off Patrick, her Pacis cellular problem. And finally, you get posthepatic jaundice, known as obstructive jaundice. Remember that diagram? It's a problem in that biliary system. And for this, if it's a problem of the biliary system as we talked about FT's, the main finding would be a really increased A, l E and GGT. You might see a creased a little and ST later in later stages, but the main finding is helping to to be massively increased. The important thing here is the dark urine and the pale stools a swell, so I like to think of it as like if it's prehepatic your urine, annual stores of fine with have had it. The first thing to go or less thing to be affected is your urine and the post hepatic. Both your urine and your stools are being affected on, so here the problem is you're getting you're getting you're getting the breakdown of human globin your gang uncomplicated little ruby and transported the liver in the liver. It's getting conjugated. It's getting processed. But then, when it comes to being excreted on transfer, transported into the intestines, there's a problem on this. Could be due to of right, of course, is that I have, um, elicit that. A lot of the curly problems. A lot to college, I says, Um, the thing to note here again, eso with the reason for the pill stools is the fact that your ability gyn isn't also congregate. Bilirubin is not being transported into intestines, and it can get processed on. For that reason, they just know your ability or stare ago, Bill in em in the in your intestines, being processed on. So for that reason, you get dark urine, impaled stools and again, the second marker of the second kind of lab findings that need to be aware of is that massively increased conjugated bilirubin in the blood and in the urine because it leaks, it kind of leaks back into the bird. It leaks out into the urine as well. So that is, um, each of the different types of Jonah says again, I've given you a big table, and I kind of letting us revise it in your own way. But the key thing to know is know the normal process is and how what kind of happens in if there's a problem in each stage. So there's a pre about it problem. I kind of understand what that means on then, if you know if you know that problematic as a humanistic problem. But the liver's liver's find you should know that there is no problem in the congregation side or the transport is either processing side on. So that's why you get those kinds of our findings. If there's a hepatic problem, you kind of see two different kind of side. You know you can get the conjugation problem with the on impaired constipation problem on with post hepatic. It's quite it's quite straightforward. The obstructive problem. The problem is that everything's been process. Everything's bean conjugated. Everything you need to be done is right, but it's just not being transported to intestine properly on. So you get those kind of clinical findings with the urine and stool that was quite faster. Whistle tour. You guys are going to get these slides afterwards, and if you have any questions, please do that at the Put it in the chat, but that's me. Done all the best with your exams. Guys. I know that you guys got special. You guys getting so many other questions about you guys got the key concepts down. So I'm not worried that you guys aren't understanding the concepts. But I hope you guys, I wish you guys the best for you against coming up. And thanks for attendance. Yeah. Guys, good luck for your exams. Don't get too nervous. Don't get too stressed. Um, but based off of your answers for the revision sessions, I think you're on track. So, Justin, also, there's a few questions, so I was really sure and that he did, Uh, okay, if you just want to stop the recording and, um, on one second, okay, so