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So first we're gonna talk about what causes cell injuries. So, there are many different things that cause cell injuries, including hypoxia, which is low oxygen, um chemical agents and drugs, um infections, immune mediated processes, nutritional imbalances, genetics and trauma. Um So there are for hypoxia, there are different types. So there's hypoxemia. So, blood in the on low oxygen in the blood anemia, which is low oxygen carrying capacity or ischemia which is decreased blood flow. Um This causes an inhibition of oxidative phosphorylation. So the cell isn't able to make en get energy and, and get injury. Um for chemical agents and drugs, um they generate reactive oxygen species. Um And we just wanna remember that hydroxyl ions are the most dangerous to the cell. These also disable oxidative phosphorylation. For example, we know that cyanide disables oxidative phosphorylation. Um in immune mediated processes, they create endogenous self antigens that then destroy the cell. Um for nutritional imbalances, it's either excess or insufficiency. Um And in genetics, you either don't make the end product, make too much of the side product or you lack the enzymes to go through this. Um the the reaction and for trauma there's mechanical trauma, um extreme temperatures, radiation and other types of trauma that can cause damage to the cell. So this is a little pathway to see um after cell injury, if it'll go into necrosis or apoptosis or if the injury is reversible. Um So we'll talk about necrosis a little later, but it's a programmed cell death. Um It could be both physiological or pathological but it's controlled. Um whereas apoptosis isn't as controlled, but cell injury can also be reversible. So it doesn't mean that if the cells injure, they automatically die. So the changes that happen in cell injury. So it um the first change is reversible where there's swelling of the organelles and sorry, that's just say blebbing, not blabbing but blubbing of the plasma cells. So you get little blebs like little out pouches a bit and that's just ivers, I'm sorry. And the irreversible changes is that you then get a breakdown of the plasma membrane organelles and nucleuses nuclei. And um there's at least a constant leakage. And then the irreversible n nuclear change are um the first one is pyknosis. So then the nuclei condensed, then it leads into karyorrhexis. So then the nuclei fragment and then karyolysis, which is the dis dissolving of the nuclei. So there are some protective factors against cell injury. Um for example, heat shock proteins and they help maintain cell viability. Um They prevent aggregation, um protein aggregation and they label misfolded proteins for degradation for example, ubiquitin. So now we can talk about necrosis. Um So, the main processes in necrosis include denaturation of intracellular proteins and enzymatic digestion. Um And there are different types of necrosis. So there is coagulative necrosis, liquefactive necrosis, caseous necrosis, fat necrosis and fibrinoid necrosis. So, coagulative necrosis is the most common type of necrosis um and is due to protein denaturation. Um and you get a firm pale wedge. So essentially where there's that stop of blood flow, you'll have the tip and then where that blood flow was going, you'd have um a spread. So it essentially makes like a triangle shaped wedge. Um and then in softer tissues um or for example, like the brain or in infections were often in abscesses, you get liquefactive necrosis. Um and then this is also sorry from degradation of tissue enzymes and you get the presence of pus. So you'll have like this creamy yellow liquid and that is filled with neutrophils and caseous necrosis. This is oftentimes seen in tuberculosis and you'll have a case caseating center. Um and it's cheese like um so in the sun, you'll see like that. Kating um necrosis, fat necrosis is a little more rare. Um You'll see it in more like traumatic, for example, like in a car accident. Um the seatbelt can cause fat necrosis across the breast tissue or in delivery of a baby, you can get necrosis on the cheeks. Um If it was a bit of a complicated um delivery um and this is caused by destruction of the fat cells due to trauma um or the release of lipas. So you also see this in pancreatitis um and the fatty acids react uh with the calcium and form white deposits in fatty tissue. So, as mentioned, you see this in um the breast post car accidents in pancreatitis or neonatal labor and fibrinoid necrosis also isn't as common. Um but is seen in immune reactions in involving blood vessels. For example, you see it in vasculitis and you get deposit of immune complexes and fibrin in blood vessels. So, um on infarct, there are two different types of infarct, there's white infarct and red infarct. So um white infarct is seen in solid organs. And so it's usually when there's a blockage in the end artery and this is the wet shape I was talking about see at the point and then get the spread. Um And so you'll oftentimes see this in the heart, the spleen and the kidneys um red infarct is when an organ has dual blood supply, do dual blood blood supply, sorry, or if it has multiple anastomoses. And um this is also known as hemorrhagic infarct, but you get that blockage and then there's hemorrhage in those other um vessels. And so you actually get like a dark red um hemorrhagic infarct. Um and this is seen in organs with loose um striatal tissue. Um And for example, like in the lungs. Um and so gangrene, this is also uh this is the um clinical term for the visible form of necrosis. And there are three types of gangrene. So there's wet gangrene, dry gangrene, and gas gangrene. So, in wet gangrene, this is necrosis modified by bacteria. Um So you'll see this in like bowel ischemia. For example, there's dry gangrene which is necrosis modified by air and then there's gas gangrene which is nec necrosis modified by gas forming bacteria. So, as you mentioned earlier, there is apoptosis which is an energy dependent cell death. Um and it's selective. So it's not random. So it's more controlled than necrosis and so on this one, there is no inflammatory response. Whereas in necrosis, there is an inflammatory response, excuse me. So this can be physiological or pathological. Um For example, as we develop, we have webbing between our fingers and through apoptosis that webbing goes away um or it can be pathological. So, um apoptosis is inhibited by growth factors, um extracellular matrix, sex steroids and others and it is induced by the withdrawal of those growth factors. The loss of that ex extracellular matrix attachment, um glucocorticoids and others. So, there are two main mechanisms for apoptosis. There's the external extrinsic pathway and the intrinsic pathway. The extrinsic pathway is by um external death receptors. So, um TNF tiss necrosis factor or pa receptors and the intrinsic um pathway is by the withdrawal of growth factors and then you will see macrophages and histiocytes will then um phagocytose apoptotic cells. So they come and essentially eat it up. So here is a comparison between necrosis and apoptosis. Um This is a good um like the differences is a good thing to know. Um And so there are different things that can accumulate in a cell. Um that includes water and electrolytes, lipids, carbohydrates proteins and pigments and they can damage the cell on to acute inflammation. So this is a rapid protective response of living tissue to injury. Excuse me, it tends to be short lived. It's innate and stereotyped, which means it's the same every time. Sorry, I'm just gonna take a break. So um what immune cell is predominant in acute inflammation. This is a question to you guys. So if you guys know what immune cell is most um common in acute inflammation, place it in the chat or you can turn your microphone off. It's up to you. I can't see the trap. So if joie wants to read it out, yeah, we've got majority saying neutrophils. Great good job. So yeah, it is indeed neutrophils. Um um and some clinical features of uh your in a I mean, sorry, your um acute inflammation, sorry. Um So there is your heat, your redness, your pain, I put heat twice um and your loss of function. Um Yeah. Um So some key feature features include the vascular reaction and the cellular reaction. So there are two things in the vascular reaction. So there's the um well, a few things in the vascular reaction. So at first, you actually get a transient vasoconstriction. So you actually get um transient blanching of the tissue. And then that is then followed by vasodilation um which increases blood flow to the injured area. And then you get exudation of fluid into tissue um due to increased permeable val um increased vascular permeability. And so there's hydrostatic pressure and osmotic pressure, the way I like to remember which is like which. So you have hs static. So it goes out and osmo in. So it pulls in. Um so it's essentially like a push and a pull. And then you also get vascular stasis and in the cellular reaction, you get infiltration of inflammatory cells, like you mentioned mainly neutrophil, neutrophils. And um you get oxidization of the cell, which is essentially coding of the cell marking it for phagocytosis. And this is done by C three B and IG GC three B being from the complement system and IgG being an immunoglobulin. So, um what's the difference between exudate and transudate? So, essentially exudate is high protein content and then transudate is low protein content. And in exudate, there are a few different types of exudate. So there is pent me um prevalent exudate which you'll see in meningitis, there's hemorrhagic um which you'll see in malignancies. Um there's serous, which you'll see in blisters and then fibrinous which you'll see in fibrinous pericarditis. So your serous is like, you're clearest, you're purulent is like you're yellowish and you're hemorrhagic is like, you're reddish and then your fibrinous is like your little like roughish, essentially. Um So neutrophil extravasation. So, there are four steps um to this, I would remember this, this came up on my exams. Um And this includes marginalization where it essentially all goes to like the edge rolling adhesion and diapedesis or extra, which is actually um a migration which is actually the leading of the neutrophils. So, what immune cells are associated with viral infections? You guys can put in the chart and mute up to you lymphocytes. We've got a oh yeah, we've got majority saying lymphocytes perfect. Yeah. So it is indeed lymphocytes. So it's good to remember acute or neutrophils. Lymphocytes is I mean also like bacterial infections or neutrophils. And then viral infections are lymphocytes and then chronic infections, macrophages, but we'll get to that later. So, um killing mechanisms. Um so there is oxygen dependent or oxygen dependent um killing mechanisms. Um So essentially free radicals are released into phagosomes and then there is a respiratory burst um in oxygen dependent and then in oxygen independent, this is done by enzymes which include lysozyme proteases and lyes. And essentially you wanna um punch a hole into the bacterial wall and then this causes um everything to like leak out, I guess. And um gram negative tends to have more pressure than gram, gram positive tend to have more pressure than gram negative um bacteria. Um So here are some anti-inflammatories. Um So there's aspirin, antihistamines, corticosteroids, leukotriene antagonist, nsaids M TNF alpha. I remember it by ACL um doesn't really mean anything but it's just the way it's stuck for me. Um So yeah, if that works for you perfect. But yeah, no few anti-inflammatories and so on to chronic inflammation. So this may take over from acute inflammation. Um It may also arise gradually with an obvious acute phase or it may not. And it like like I mentioned earlier, this tends to come um contain macrophages. Macrophages are extremely important because they're essentially the maximizes of chronic inflammation. And so they phagocytose um cells which is again like eating it and then they're also antigen presenting presenting cells. So for um uh for our immune system and they also control other cells. So this is a little um I guess like pathway ish for comparison of acute to chronic um inflammation. Um So there are two types of cells. We like two types of things we see happen with macrophages. We have giant cells and we have granulomas. Um So giant cells are essentially fused macrophages. And with this, we have different types of um giant cells. We have like han giant cells which you see in tuberculosis. Um not Langer hand. I used to always call it, lay your hand. It's L hand. Uh we also have foreign, that's just a body, sorry, foreign body type, um giant cells, which you'll see when there's a foreign body um implanted into the body. And there's two to type giant cells um which are seen as xanthoma or fat necrosis. Um and then there's granulomas which are modified macrophages. Um And th so these ones are epithelioid, so slipper shaped and um there's immune granulomas, caseating granulomas, different types of granulomas. So, um the effects of chronic inflammation include fibrosis. Um So you'll see this um in things like for example, like chronic um chronic cholecystitis. Um and for that, we know like our five f so fat female fare 40 for fertile 40. Um So those are like the five, I guess like risk factors of people that tend to get chronic cholecystitis. So people that are obese, um people if there are skin um women um in their fertile age, younger women and in women in their forties. Yes. Um And then there's impaired function, for example, in liver cirrhosis or in IBD, um there can be increased function as well, for example, with thyrotoxicosis, um and graves disease and um you can have atrophy, so, autoimmune gastritis, for example, shows atrophy or you can have an inappropriate stimulation of the immune response. Um excuse me, um for example, an atopic disease which we know is a combination of asthma, eczema and hay fever. Um So, onto wound healing, the principles of wound healing is you want to close the gap um and rec um repair with a scar and as we know, the smaller the better. So there are a few processes involved. So there's hemostasis, um inflammation um and regeneration or repair, preferably, I mean regeneration or repair. So there's primary intention or secondary intention. Um So in primary intention, you get complete resolution, whereas in secondary with um intention, you don't get that complete um resolution. Um So usually primary intention will be like clean like surgical wounds um that don't have to bring in them. Um And they are brought together, for example, like with stitches or sometimes glue. Um and then in secondary intentions, um intention, you'll have wounds that like where like for example, like in excision wounds, where there's a lot more tissue damage or um infected wounds, wounds that have had de um debris in them. Yeah. Um So tissue regeneration. So there are different types of tissues, um different classifications of tissue. So you can either have a labeled tissue, stable tissue or permanent tissue. Um And this would um determine whether um the extent essentially uh regeneration. Um So labile tissue essentially constantly replicating, for example, like um hemato tissue, sorry. Um So for example, like bone marrow constantly making blood um and then they're stabile and a stable, sorry. And this is only when necessary, for example, like the liver parenchyma um as we know this can regenerate um but it's not constantly, it's just when we need it and then there's permanent. So these I don't have the ability to regenerate. So, for example, like neural tissue, cardiac tissue, these ones is like what we have is what we have. Um So the difference between regeneration versus fibrous repair. So in regeneration repair is complete. Um this happens in um tissues that are either labile or stable. Um And in tissues where the damage is not extensive. However, in fibrous repair, um we get the formation of a scar um and this is um healing by secondary intention and this is when there's significant tissue loss or if permanent tissue is injured, we get a scar. Um So, here's again, a little, little, little pathways. Um So here's a little pathway of whether you'll get regeneration or um a fibrous scar, like fibrous repair. So, onto granulation tissue, this is not a granuloma. Um uh And this, you get this in essentially in healing of tissue. Um It's made up of capillaries, fibroblasts, myofibroblast and inflammatory cells. So, the capillaries for nutrients, blood oxygen, all that kind of stuff. Fibroblasts and myofibroblasts essentially put on the myofibroblasts contract, pull the edges together um and inflammatory cells as well for the i immune process. And so this is to fill the gap. Um As we said, the capillaries provide oxygen nutrients. As we said, the myofibroblasts and fibroblasts pull the edges together and fill the wound essentially. Um And the cells involved include inflammatory cells, endothelial cells and fibroblasts and myofibroblasts. So, if you guys can name me a few fla factors that influence healing. There are quite a few for you to pick from. Uh we've got enters like wound size, wound location, nutrition, uh blood supply. Oh If there's a good blood supply. Um Yeah, absolutely. You guys are on it. Great job. So there's the type of wound, the size of the wound, the location of wound, you guys essentially got it in my order. That's crazy. Um The blood supply if there's an infection, um the healing won't be as, as well as good. Um If there are foreign bodies if um age, so the older they are, the worse, the healing will be um obesity, diabetes, drugs, um vi vitamin deficiencies, those are all factors I can, can influence healing. Good job guys. So there are a few complications of fibrous repair. Um So there's um for example, inefficient, insufficient fibrosis. So that means that the edges actually won't come together. Um So typically, if you wanna bring the edges together in 24 hours, the shorter the period, the better but with insufficient fibrosis, the wound will actually stay open and the edges won't come together. This can be for different reasons. Um But yeah, and then there's also formation of adhesions. Um We know this um happens often with um for example, like surgeries and stuff you like internal surgeries, you can get adhesions and then this leads can lead to a loss of function or you can have loss of function on its own. For example, as we mentioned, uh the heart um tissue is permanent tissue. Um So it doesn't have the ability for regeneration. So you get a fiber scar instead. And so that fiber scar doesn't have the ability to work like heart cells like heart tissue. And so you get that loss of function, um you can also get over the overproduction of a fiber of fiber scar tissue. Um This is called a keloid. So you get a really, really big scar. Um It's not anything really like, it doesn't really hurt your health other than mental health. Um um but this is uh more common in people with darker skin. Um and excising the keloid can actually result in a bigger keloid, which is why you also typically will give steroids to prevent a further keloid. And you can also get excessive scar contraction. Um This can be seen in, for example, um burn victims. Um And so they'll have like excessive scar con contraction and they'll, this will also lead to um decreased function as well. So um we on to bone healing, uh there are the four stages of bone healing. I know we've heard this a million times. Um but there is the initial hematoma and then you get the soft callus um in the soft callus, there's no calcium, which is why when you take take an X ray, you actually like, you don't see anything there cause there's no calcium in it. Um And it's made of cartilage that woven bone forms in and then it moves on to the hard callus and then there's a remodeling phase which is when the osteo class come and eat away the excess and fix stuff. Um So for hemostasis, um on hemostasis, there's um this is essentially the complex that stops bleeding um through our lovely coagulation cascade. Um So, there are three stages, there's the unstable platelet plaque, plaque plug, sorry. And then there um that's um platelet plug will get stabilized by fibrin and then there's dissolution. Uh You want the solution, it's very important. And in the unstable platelet plug, um platelets will adhere to von Willebrand factor um which is in the subendothelial structures and then they aggregate to form a plug and then it gets held together by fibrin. Um So, the things that help essentially um include the vessel wall, um platelets, um the coagulation system and a very important fibrin fibrinolytic system because you do wanna break that clot down. Um So, the um coagulation cascade, um there's the intrinsic and the extrinsic pathway. Um So, the intrinsic pathway is essentially when you get damage to endothelial lining of blood vessels and this activates tissue 12. Um So it's like the 12 to 12, 8, 11 to 11 A, skip, 10, go to 9 to 9 A and then go back to 10 and then you get prothrombin to thrombin, fibrinogen to fibrin. Um And um like factor 10 onwards is your common pathway and then your gens are pathway is um there's the um trauma which leads to the release of tissue factor three. It's a lot faster. Um And then you get your 7 to 7 A and then 10 to 10 A. Um Yeah. And so the things that inhibit coagulation include antithrombin three. So this inhibits um thrombin and factor 10 A um protein C which um cleaves factor five A and A A which are cofactors. Um And then there's also protein s so for fibrinolysis, um there you can use those TPA streptokinase or urokinase. Um So these will get um given potentially when there's a clot um to break down that clot. And so any hemophilia, um you get some internal spontaneous, you get some spontaneous internal bleeding. Um and there's different types of hemophilias. But um the main one is an in inherited f deficiency of factor eight. And then you'll oftentimes also get like bleeding around the joints, um which can cause joint pain and decreased function as well. Uh So, there are a few tests that we do to test hemostasis. Um There's testing the extrinsic pathway or the intrinsic pathway. And so for the extrinsic pathway, it's your pt um your prothrombin time. And so this is essentially tests factor 257, 10 and fibrinogen and um So you have your A PTT, so your activated partial thromboplastin time, which tests your interns or pathway. So this test your factors 2589, 1011 and fibrinogen. And so um Warfarin is a drug which is essentially a blood thinner. Um And this is a Vitamin K antagonist um because Vitamin K helps the coagulation cascade. So this essentially prevents the coagulation. Um And so it inhibits factors 279 and 10. The way that I remember this is by the year 1972. So you do 10 plus nine and then you're seven and year two. And so if you do start leaning while on Warfarin, um they can either give Vitamin K or they can give prothrombin complex concentrates. So thrombosis, uh this is the formation of a solid mass of blood clot um in the circulatory system. And um there's verse triad um which is actually explains a prothrombic states. And so there is either in the venous system or the arterial system. So, in the venous system, if there's blood stasis and depend on blood constituents. So, for example, like increased platelets, um you're more likely to form a clot in the venous system and, and the arterial system, if the blood constituents and the vessel wall um can essentially put you in a prothrombic state. So if someone wants to um tell me what a, let's say what a VTE is a, you know, thromboembolism, what is it, what what does it comprise of? Hence, there are two things. Uh we've got a thrombus that breaks off into the vein, um close. So it's essentially the term for a DVT and a PE is a combined term. Um So DVT is a deep vein thrombosis and a pe is a pulmonary embolism. So kind of a combination of that. Um Yeah, so risk factors for VTE. Um, there are quite a few so age, um, having a previous one. the oral contraceptive pill or, um, HRT hormone replacement therapy. Um, smoking is a really big one. obesity immobility, um, POSTOP. Um, you have, um, POSTOP like operative, you, um, are at higher risk for having a VTE. Um, so if someone after like you, so something you like, oftentimes wanna ask is like, if they've, um, like in a history is if they've recently had surgery, um, if they've recently had a long haul travel, um, cause they'll probably be sitting for many hours and then they'll get a DVT and then it'll break off and then it can become a pe. Um, and so they'll get that short, um, that shortness of breath, that pleuritic chest pain. Um, so you really wanna ask if they smoke if they're POSTOP, if they've, um, been immobile for a long period of time, if they're on the pill or on HRT, those are very important things that you wanna ask. Um, so some risk factors for arterial thrombosis, very similar age, smoking. And then there's actual, uh, there's also atherosclerosis. Um, this is when, because we'll talk about it later. But when the plaque, um, fissures it's, um, it can, it's more likely to get a clot. Um, also hypertension, hypercholesterolemia and diabetes are also risk factors for a arterial thrombo thrombosis. So, um, how would your leg look if you had a DVT versus an arterial thrombosis? Do you guys wanna put that in the chart or we've got um A DVT would be red, swollen and feel hot uh in a DVT. Would there be varicose veins? Oh, yeah, good. So, um A DVT was exactly hot, red and painful. Um However, in an arterial thrombosis, um it would be cold and pale. So, varicose veins are actually from a failure in the valve. Um So you get backflow in those veins. So I don't, I don't know exactly that um specifically that arterial thrombosis would cause that. But if the venous valves fail maybe, but I'm not sure. Um So, um there are a few possibilities um that can happen post thrombosis. So you can get propagate propagation um lysis, which is actually the breakdown embolism. Uh So this is essentially going to a distal place. Um So embolism can be uh the blockage of a vessel, vessel by liquid solid or gas at a site distant from its origin. Um However, most embolisms are thromboemboli um and this can lead to ap ea pulmonary embolism. And so it's just like other classifications essentially. So there's your massive pe major pe minor pe and recurrent pe. So your massive pe is when there's a greater than 60% reduction in blood flow. Um Here, they will be hemodynamically um compromised and this is an emergency because they will die from this. Um Your major pe is when there's um a blockage in your medium size vessels. Um And from this, you'll get your shortness of breath, your ple chest pain. So it'll hurt more on inspiration and they can get hemoptysis, which is essentially um they'll like when they cough, they'll cough up some blood, excuse me. And then there's your migraine P ES um which are um blockages of your small peripheral p pulmonary arteries. Um This can either be asymptomatic or they can have a minor shortness of breath, but they won't be anything crazy. And um if you get recurrent peds, this can actually lead to pulmonary hypertension. Another outcome of pro um of sorry thrombosis includes organization and recanalization. So essentially you get like a hole made through, I guess. So you can still have flow um onto atherosclerosis. Um This is the thickening, narrowing and hardening of the walls of small um of large sorry and medium size arteries due to atheroma. Um And an atheroma is an accumulation of lipids in the intima and media of large and medium size arteries. So, there are the three steps of development of atherosclerosis. So, as your fatty streak, your simple plaque and then your complicated plaque. So um your fatty streak, um this can actually be seen in Children. Um and they, there is some debate on the implication of the fatty streak in atherosclerosis um being a associated um with atherosclerosis. Um but this is essentially lipid deposit in the tunica intima. Um and there's no that I have to say media but there's no di disruption to blood flow. Um And this is slightly raised. Um uh And then there's your simple plaque and this is also raised, it's about a centimeter in diameter. Um And this is oftentimes seen around branch poison vessels. So your osteo um and this can impinge on vessel lumen and then there's your complicated plaque. Um And then this one will see calcification, ulceration, thrombosis and hemorrhage. So, on the micro appearance of atherosclerosis, there are some early changes and then um some later changes. Um So the early changes include the accumulation of foam cells. So, foam cells are essentially made from a combination of smooth muscle cells, macrophages and fat cells. Um and and then there's a proliferation of smooth muscle cells, um extra lipid extracellular lipid deposits, sorry, and um some scattered T lymphocytes and then later on, you'll see some fibrosis, necrosis, calcifications. Um You'll see some disruption of the internal elastic lamina, um some damage going into the media um and then um fissuring and rupture of the plaque, which um like I mentioned earlier, um is more likely to result in a clot. And this um atherosclerosis also weakens the walls of blood vessels. And so you can get aneurysms and ruptures. Um for example, like the AAA like abdominal um aorta aneurysm. And so, essentially, an aneurysm is a ballooning of the vessel wall. Um And then this is like a weak because the wall has weakened and then this is gonna actually rupture and then you get a major bleed and you die. I don't know if they do something about it. Um So some cellular this um events leading up to atherosclerosis. Um So there's um chronic endothelial injury, um leading to endothelial dysfunction, there's smooth muscle immigration from the media to the intima cause the smooth muscle is um located in the tunica media. Um The production of foam cells, which like I mentioned is those macrophages, smooth muscles and fat made into like formed into one combined in one um smooth muscle proliferation in response to cytokines and growth factors. Um the um collagen and matrix depositions and neovascular neovascularization. So, cells involved include endothelial cells, platelets, smooth muscle cells, macrophages, um and less to a lesser um extent lymphocytes and neutrophils. So, some risk factors for atherosclerosis include age. Again, the older you are, the more likely you are to get um to develop atherosclerosis. Um gender. So, women are actually protected um from atherosclerosis until menopause. So, there is a theory that estrogen might place something into uh the prevention of atherosclerosis. Um Also women on HRT are less likely to develop it but HRT shouldn't be given to prevent it. Um hyperlipidemia um is a risk factor. Um Smoking again, another big big one. honestly on exams, one in doubt risk factor, smoking, smoking, obesity, usually um hypertension, alcohol, another big one and diabetes. Um so some type, the types of cellular adaptation um include um regeneration, hyperplasia, hypertrophy, atrophy, metaplasia, aplasia, and um and yeah, and metaplasia. Sorry. Um uh So for regeneration, this is the replacement of cells lost by identical cells. Um So the tissue um size actually stay the same, it doesn't grow, it doesn't shrink, stay the same. Um and then under this called reconstitution, which is the replacement of a lost part in the body. So this is pretty minimal in mammals. But as we know, the liver, for example, can um to some extent there is reconstitution that can happen in the liver. Um And then there's hyperplasia. Um and so increase the in tissue or organ size due to the increase in cell numbers. So the cell size stay the same but there's just more of those cells. Um and then there's hypertrophy which is on the other side of it, which the size still increases. But it's because the size of the cells get bigger. So you have the same amount of cells but the cells are bigger and then there's atrophy, which is the opposite of the two, um which is the shrinkage of tissue. Um, or, or in size because there's either a decrease in cell size or cell number. Um And so there are a couple of causes of atrophy. There's denervation atrophy, for example, post um spinal cord injury. Um and there, or there could be disuse atrophy. So we have to say use it or lose it. So essentially, if you don't use it, you'll lose it, you'll get some atrophy and then metaplasia, this is a reversible change of um a different a differentiated cell type to another. Um And uh so, um and this can lead to dysplasia. So I have a hard time wrapping my head around metaplasia and dysplasia. So, metaplasia is normal cell to like normal cell to normal cell and then dysplasia is normal cell to abnormal cells. So, for example, you'll see metaplasia, excuse me in there's esophagus, um which is essentially people with GERD tend to get this and um your epithelium goes from esophageal epithelium, which is your stratified squamous nonkeratinized to your gastric epithelium, which is your simple columnar. Um And this is a protective mechanism because when you have um your gastroesophageal reflux disease, you oftentimes get stomach acid going up and um so to protect, protect the tissue, uh your lining essentially turns to that gastric tissue. Um This is also seen in smokers, um where the, where the change will go from simple squamous to stratified squamous. Um again, protective change. Um But in dysplasia, this is like your one that can lead to cancer. Um And then there's also aplasia and this is a complete failure of um a specific tissue or organ to develop. So you completely don't have it. But then there's hypoplasia which you get some development, but it's underdevelopment um or incomplete development of a tissue or organ. It's also important. Um And then, yeah, so then, and then there's dysplasia which is um abnormal maturation of cells in a tissue. And it's important to know that there are different definitions for dysplasia and pathology. Um Yeah. So I guess that completes my presentation. Are there any questions? I know this was super quick. I know we have a long day ahead of us. Um But yeah, if there are any questions, please shoot them my way. I'm more than happy to answer and thank you so much for um coming to this. I really appreciate it. And yeah, there's the feedback form. Oh yeah, thank you everyone uh for joining this meeting. Uh We really do appreciate it. Uh Thank you so much KJ. Um I'm sure many people found it very helpful and if uh everyone can fill out the feedback form below, uh that way she can include it into uh her portfolio as well. Uh uh The link I just put into the chat just now. Um Thank you. So much KJ. If you wanna linger for a second, actually, I'm gonna stop the recording now.