Diabetes Mellitus | Type I and Type II Diabetes Mellitus

[Music] I ninja nerds in this video we're gonna talk about type 1 type 2 diabetes mellitus and the chronic complication so let's go and get started I envision air so the first thing that we need to know a type 1 diabetes mellitus that is extremely high yield is that it is autoimmune disease there's two components to an autoimmune disease the environmental component which we believe to be a virus we don't know exactly what the virus is what we think is that these viruses infects particular cells in our body and these viral proteins get expressed onto MHC one complex is on our cells then what happens is our cytotoxic T cells recognize this foreign antigen and generate an immune response against it now here's where the other part of the autoimmune disease comes in our immune system reacts inappropriately to this virus or this environmental factor because of what's called susceptibility genes particularly HLA susceptibility genes and there's two that are particularly high-yield here the first one is called HLA dr3 and the other is called HLA dr4 now when these genes lead to an inappropriate immune response our T cells release cytokines that stimulate plasma cells these plasma cells then in a response to that produce antibodies now these HLA susceptibility genes are not just polymorphic or mutated in diabetes but it can also be associated with other autoimmune diseases such as rheumatoid arthritis systemic lupus erythematosus celiacs disease in vitiligo now when these antibodies are produced they attack particular portions of cells and with respect to diabetes they attack what's called the pancreatic beta-cells now we're zooming in on a pancreatic beta-cell what happens in the beta cell is extremely important you know within a beta cell glucose is basically able to come into these cells via a glucose transporter then once taken inside of the cell it undergoes an aerobic metabolism and then aerobic metabolism to produce ATP these ATP molecules then bind to put I see insensitive channels that are sensitive to the ATP and when ATP binds they close now when these channels close potassium can't exit potassium builds up inside of these cells and creates a positive charge inside the cell that activates voltage-gated calcium channels these calcium channels open and calcium rushes into the cell and stimulates these vesicles that contain insulin and stimulate and so on release in addition to that there's also an enzyme called glutamic acid decarboxylase this enzyme converts glutamic acid into gaba and gaba is another molecule that is associated with the stimulation of insulin production as well as protective effects of these beta cells now let's apply the antibody concept here when antibodies attack our tissues they attack specific self antigens that are present on our pancreatic islet cells and these antibodies which is high-yield are called anti islet cell antibodies the second set of antibodies are targeted against this glutamic acid decarboxylase and these are high-yield called anti glutamic acid antibodies the last one is that there's antibodies directed against the insulin and these are called anti insulin antibodies now as these antibodies attack the beta cell or the proteins within it what happens to the beta cell activity well these antibodies start destroying the beta cells and as there's decreased number of beta cells what happens to their insulin production it starts dropping what's the problem with that that can lead to high blood glucose how if we look at the cellular level let's follow this insulin as it binds on to a particular cell insulin binds on to what's called insulin receptors and triggers an intracellular cascade that increases the expression of glucose transporters on the cell membrane and then what happens is that allows for glucose to come into the cell and effectively decrease blood glucose levels that's the effect to decrease the blood glucose levels but if this insulin production decreased what happens to the increased expression of glut transporters it drops if we decrease glucose transporter expression what happens to the glucose entry into the cell it's inhibited if glucose can't come into the cell what happens to the glucose levels in the blood as a response to that it starts to rise and that is the effect of type 1 diabetes art the next type of diabetes we have to talk about is type 2 now type 2 is a little bit different it's I'm an autoimmune disease what we believe to be responsible for it is what's called metabolic syndrome and this is extremely high yield what are some of the things that we see with individuals with metabolic syndrome well all you need is three or more of the following things that we're going to talk about here in order to be considered diagnosed with metabolic syndrome one is you have to have a fasting glucose level greater than or equal to a hundred milligrams per DL triglycerides greater than or equal to 150 milligrams per DL and HDL if you're a female less than or equal to 50 and a HDL less than or equal to 40 if you're a male the last thing is that the blood pressure has to be greater than or equal to 130 over 85 and lastly they have to have a high BMI female greater than or equal to 35 male greater than or equal to 40 metabolic syndrome through all of these associated activities are believed to be responsible for what's called insulin resistance the other component that you need to know is that there's even research six that suggests there's a genetic component to it two components one is if you have a high risk if you have a first-degree relative with diabetes and the second thing is certain ethnicities for me that's an example Pacific Islanders Hawaiians they're more prone why it comes to this concept of insulin resistance let me explain same concept here happens in the beta cells glucose comes in through all of these prop processes we've talked about above it leads to insulin production insulin will then go and bind - these insulin receptors and the design is to increase glucose transport here's the thing these receptors they're stingy they don't like to respond to the insulin and so what happens is there's a decreased intracellular response and so because of that there's less stimulation of the glucose transporters that means less glucose gets into the cells now as less glucose gets into the cells what happens is that the glucose levels start to rise as they start to rise more of it starts to go back into the pancreatic beta-cells and as a result this continues to try to increase insulin production and this causes hyperinsulinemia the thought is that with high insulin levels we might somehow be able to get an increased activity inside of that cell to get some of the glucose in here's the problem over time so over time two things happen one is that these beta cells they have to crank out so much insulin so they start to get tired they start to decrease in their activity and as they start to Tucker out what happens to their insulin production it drops as the insulin production drops what happens we'll remember if you decrease insulin production you decrease glucose transporters and you decrease glucose entry that leads to hyperglycemia the second thing they associated with this is that whenever insulin is released there's another protein released called amylin and amylin when accumulated in this tissue space around the beta cells cause amyloid deposition and that starts to damage the beta cells decreasing the beta cell activity leading to decreased insulin production if there's less insulin you can't express more glucose transporters you can't move glucose into the cells and as a result the glucose levels rise now with all of that being said let's now talk about what are some of the clinical manifestations of these individuals now remember with high glucose levels when it comes to the glomerulus you know the capillaries within the kidney high glucose levels means that you're gonna have whenever you have that glomerular filtration process a lot of glucose is gonna get filtered into the kidney tubules whenever there's high amounts of glucose and the kidney tubules your kidney tubules can't tolerate these large volumes of glucose and so the ability to reabsorb as much of it as possible is diminished and so because of that more glucose is lost in the urine and that's called glycosuria now here's what I want you to remember one more glucose is lost in the urine glucose is osmotic aliy active that's extremely high yield what does that mean it means it pulls water with it so with a lot of glucose in the urine comes a lot of water in the urine and whenever you're peeing out these large volumes of urine we call that polyuria that's extremely high yield next thing as you urinate large volumes your blood volume starts to drop because you're peeing out tons of water and glucose but your glucose levels are still high so we call this whenever there's low water and high glucose in the blood hyperosmolar blood that hyperosmolar blood stimulates what's called Osmel receptors in the hypothalamus and they trigger an increase in thirst the thought behind that is if I drink more water or more fluids I'll replenish my blood volume and the water that I'm losing and this is extremely high yield because the symptom is called polydipsia when there's increased thirst the next thing you have to remember is that whenever we're not able to bring glucose into the cells so whenever glucose is not being utilized what happens is whenever there's decreased glucose utilization that means there's decrease ATP production because of that our body starts tapping into the other metabolic sources of fuel one is it taps into the fat and undergoes a process called lipolysis which is extremely high yield and proteolysis which is extremely high yield what are these concepts lipolysis as I'm breaking down triglycerides into free fatty acids and glycerol why is that important because I can shunt them into the cellular pathway to make energy because I have decrease ATP I have to counteract that proteolysis is on breaking down proteins and muscles making amino acids in hopes that I can use that for energy to compensate for the drop in ATP why is this important because with increased lipolysis and proteolysis you're breaking down fat and proteins in the body that leads to unexplained weight loss and because you're consuming so many calories your body has to respond to this increased caloric consumption by increasing your hunger so you can replenish those calories and this is an extremely high yield fact is that increased hunger is called polyphagia the next thing that you need to know with diabetes is how to diagnosis and this is extremely high yield why so what you do is you take some blood work from them and you can do what's called a fasting glucose when you take a fasting glucose they have to not eat for a certain period of time and you expect their blood glucose to be lower based on that but in individuals who have diabetes anything where the blood glucose is greater than or equal to 126 milligrams per DL fasting is positive and that's a sign of diabetes especially if they have symptoms in addition to that if we just took a glucose without them fasting and it's greater than or equal to 200 milligrams per DL plus the symptoms that they have that's diagnostic of diabetes another test that you can run just to remember for your exams is called a two-hour oral glucose tolerance test simple explanation I give them glucose it's generally normally supposed to stimulate insulin production insulin should push glucose into the cells but in diabetics they don't have that insulin or their insulin resistant so because of that their glucose levels will still be high greater than or equal to 200 milligrams per deal on two tests is positive and positive for diabetes the last thing which is you live utilize not just a diagnose but to monitor their glucose control over a period of three months this is extremely high yield is called hemoglobin a1c anything greater than or equal to six point five percent is considered diagnostic very quickly what is this hemoglobin a1c whenever you have high glucose levels in the blood they love to conjugate to the Hema and whenever they conjugate to the hemoglobin they make a glycated hemoglobin that's what we measure and it gives us three months because what's the lifespan of a red blood cell approximately three months what's inside of a red blood cell hemoglobin the next thing you can add on in a diagnostic if you truly want to is take into consideration those antibodies that we talked about the anti gad anti-islanding insulin antibodies but take into consideration their age and their risk factors are the next thing we have to talk about in this video is the chronic complications associated with diabetes now what happens is whenever there's high levels of glucose into the blood they love to conjugate with two types of molecules proteins and lipids when they conjugate with them via process with no enzyme it's called non enzymatic glycation now whenever glucose binds to these proteins and lipids it creates very inflammatory molecules very potent inflammatory molecules these potent inflammatory molecules can cause inflammation to occur within the blood vessels and as a result a lot of LDL deposition to that tissue leading to what's called atherosclerosis this is extremely high yield the other thing is that some of these protein deposits can occur in the vessel and around the basement membrane and this is called hyaline arteriolosclerosis and this is extremely high yield the combination of these two effects leads to decreased blood flow distal to these plaques as well as the arterioles and it decreases gas exchange across the tissues because the basement membrane is thickened now with these two effects this leads to the physical manifestation of particular types of diseases what are the diseases that are associated with this non enzymatic location well atherosclerosis that develops within the walls of the vessels in the heart can lead to coronary artery disease and potentially myocardial infarction if it develops within the vessels that are in the lower extremities this can lead to peripheral artery disease but 10 presenting with claudication and decreased blood flow to the tissues leading to ulcers it can decrease the blood flow getting to the nervous tissue potentially leading to a ischemic stroke that's some of the things that we can see here with the a thorough attic process now another thing is that this can affect the vessels within the retina and lead to it's called retinopathy and three high-yield things that are classified what diabetic retinopathy is microaneurysms as we can see here cotton wool spots which we can see here and flame hemorrhages which we can see here and these affect vision now the next thing that you want to know is that this Highland arteriosclerosis which is extremely important can occur in the vessels of the glomeruli and whenever these proteinaceous deposits occur within the glomerular it can damage the glomeruli and lead to increased filtration of proteins like albumin and this Abuna can enter into the urine and we call this albumin that is in the urine microalbuminuria now as this occurs over time the concern is that with consistent microalbuminuria this can lead to chronic kidney disease and this is the most common cause of chronic kidney disease now another high-yield fact is that these proteinaceous deposits are nodules that form within the glomeruli are given a very specific name that is extremely high-yield called camel Steele Wilson nodules the next thing that we have to talk about what your potential complications now in certain cells of the body what happens is glucose gets get taken up into the cell with more glucose what happens is this glucose gets converted into what's called sorbitol via an enzyme called aldo reductase now sorbitol then gets converted into fructose with an enzyme called sorbitol dehydrogenase this is important because in certain particular tissues certain tissues don't have this enzyme and because of that you can't convert sorbitol into fructose why is that important schwarber tal is extra namely osmotically active and what that does is that pulls water into the cells that don't have the sorbitol dehydrogenase and causes osmotic cell death this is extremely high yield and what tissues do we not have this enzyme in this effect occurs one is in the lens of the eye and if that occurs in the limbs of the I guess what it can lead to cataracts if this osmotic cell death occurs within the proximal convoluted tubule cells or other tubular cells it can again lead to the progression of nephropathy the other one is Schwann cells and this is extremely high yield what damage of Schwann cells this leads to what's called demyelination this demyelination is going to affect peripheral nerves if it's the peripheral autonomic nerves it affects the nerve supplying the stomach the stomach can't contract properly this can lead to gastroparesis inability of the stomach to contract and push time into the duodenum the other thing is if they don't have the nerves to supply the bladder and the bladder can't contract they have neurogenic bladder and they are urine retentive if they have no nerves going through the blood vessels to promote vasoconstriction of the blood vessels when they go from seated to stand it and they need blood to get up to the right side of the heart they can become lightheaded and dizzy and this is called ortho stasis that's the effect on the autonomic nervous but if we jack up the Schwann cells that are affecting on the peripheral nerves for example the most common one which is high-yield here is the third cranial nerve oculomotor nerve he normally helps to control extra ocular movement if he is affected because of Schwann cell demyelination it causes the eye to move laterally and downward but the pupil dilation is not happening so the pupils are spared high yield next thing the other nerves that are affected are the somatic nerves but particularly the somatic sensory nerves that are supplying the distal extremities bilaterally now if you lose the ability of the sensory nerve a function you lose sensation and they also can have burning and tingling sensations as well burning is called dis Theseus and some tingling sensation is called paresthesias the problem with this is that over time if someone bangs their foot up against an object and they get a wound then what happens is if they have sensory deficits they might not be aware of that wound and hyperglycemia impairs wound healing so what can this progress to foot ulcers and that's extremely high yield the last thing I want to talk about is the treatment of type 1 type 2 diabetes in their chronic complications the first thing that you want to remember with type 1 diabetics they don't make insulin so give them insulin and we'll have another video on the different types of insulin the next thing is would type 2 diabetes there metabolic syndrome people right so they're obese they have bad diets so if we change that up and promote weight loss through exercise and dietary changes that's gonna make a difference but they might need some extra help and that's where certain diabetes medications might come into play to help a lot of these processes and we'll discuss each one of these in more detail in another video but the biggest most Hiab fact that I want you to remember is that type 2 diabetes medications the most high yield and first-line one is metformin there's multiple others that we'll go into more detail in another video like GLIP one agonist DT dpp-4 inhibitors sglt2 inhibitors the Izola deand ions so funny areas glucose I taste inhibitors Emlyn Kalitta knives the last thing is if sometimes individuals who are type 2 diabetic who are on multiple diabetes medications and are still not getting their hemoglobin a1c less than 7 sometimes we might have to add insulin the next thing that I want you to remember is how to treat conic chronic complications because this goes into play with diabetes treatment with that neuropathy if we decrease a lot of the pain the paresthesia is the numbness and the tingling to treat that we can use drugs like gabapentin and pre gabilan those are your first line medications and the other thing is you want to do yearly podiatry visits for overall foot care foot like fittings and trimming the nails all of those things the next thing is nephropathy we want to try to treat the nephropathy and decrease that protein area and the most effective drugs with that is ACE inhibitors and a arby's the other thing is monitor their kidney function because this can lead to chronic kidney disease check their BMP look to see if they have an elevated creatinine and elevated but be a blood urea nitrogen the other thing is checked that microboom and present in the urine the next thing is their retinopathy now with retinopathy things that we can do is we can give them drugs that are going to help in this process such as vag F inhibitors vascular endothelial growth factor inhibitors we can do laser photocoagulation you can even do what's called a vitrectomy but the big thing that I want you guys to remember which is high-yield is for them to get yearly optometry visits the next thing is because this can lead to atherosclerosis it doesn't hurt to give the patient a baby aspirin in addition if they're a thorough sclerotic cardiovascular disease risk is very high maybe it's greater than or equal to 7.5% when you put that in the calculator that may put you in a desire to want to check their lip the panel and maybe even put them on a statin to reduce the risk of CA D am i right as well as stroke and other peripheral artery disease effects the last thing I want to talk about is glucose control so whenever someone's coming in to the primary care office or whatever office you check their hemoglobin a1c and it's less than or equal to 7% that's good that's what we're wanting now diagnostic is 6.5 right greater than that but if we can get this seven or less that's doable and that's good for a diabetic now if it is uncontrolled so it's greater than 7% then you might want to check their hemoglobin a1c every six months I'm sorry every three months but if it's actually well controlled you're keeping it around seven maybe even lower then you can check it every six months [Music] [Music] you

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Keywords: Diabetes, What is diabetes, what is diabetes mellitus, what is difference between type I and type II diabetes, type 2 diabetes, diabetes mellitus, diabetes drugs, type 1 diabetes, Ninja Nerd Science, how to use insulin, what is insulin, pathophysiology of diabetes, diabetes, diabetes treatment, what is diabetic neuropathy, what is diabetic nephropathy, diabetes symptoms, what are the symptoms of diabetes, diabetes medications, diabetes nursing, diabetes diagnosis, insulin

Id: -axOMKLkLLQ

Length: 24min 55sec (1495 seconds)

Published: Wed Apr 22 2020