[Music] H what's up Ninja nerds in this video today we're going to be talking about diabetes metis this is a monster lecture let's get right into it when we talk about the pathophysiology of diabetes meitus there is two there's type one and type two and the pathophysiology does differ somewhat so for type one the concept behind this is that it's usually in a younger individual usually want to think age less than 30 that's not always the case but it is most commonly going to be like this for your board exams the other important thing to
remember for this is that the pathophysiology is different in the sense that the beta cells the pancreatic beta cells that are ones that are responsible for producing insulin are being destroyed and because of that they're not going to be able to produce an adequate amount of insulin so there'll be a reduction or deficiency of insulin in these patients now with a reduction in insulin what leads to the downstream consequence here is that insulin won't be able to bind on to its appropriate receptors right so these insulin receptors aren't going to be activated as much what
do these do they're supposed to come down and tell this glucose transporter to allow for glucose to be brought easily into the cell and to be metabolized and undergo oxidation processes or glycogenesis Etc however since insulin isn't sending the signal appropriately glucose will not be taken up into the cell and instead it will remain in the bloodstream it'll develop something called hypoglycemia this is really the big pathophysiological difference now the question comes is what's leading to the destruction of the beta cells correct and it's usually an autoimmune attack of the beta cells so there has
been some Associated like autoimmune diseases like celiac disease maybe Hashimoto thyroiditis that have been linked and very commonly associated with type 1 diabetes the reason why is there's these certain types of like gene mutations in the HL drr3 and hr4 that may make the immune system a little bit more hyperactive than it should be what do I mean well let's say that a patient has these immune system cells they become exposed to an environmental agent of some particular etiology and what happens is this causes these immune system cells to inadvertently become hyperactive and produce lots
of cyto kindes that then stimulate plasma cells these plasma cells become stimulated in such a way that they start to make antibodies inappropriately and these antibodies that are produced they're going to start attacking proteins that unfortunately look like those environmental agents and these proteins that they're going to attack is going against be against the beta cells the cells that are producing insulin so you'll produce these antibodies like the anti-gad antibodies which is a very critical enzyme within the beta cells that helps with the production of insulin and these ones that actually go against the eyet
cells again the eyelet cells of langerhan the cells of the pancreas that are again responsible for producing hormones such as the beta cells and the alpha cells so again you're going to be destroying those cells leading to the reduction in insulin in comparison type 2 diabetes malius you want to think about this in a patient who is a little bit older usually the age is greater than 40 but it can happen in younger individuals especially in the more modern era what you really want to associate this with is more particularly uh metabolic syndrome so in
patients who are obese they may have kind of a transition into this adipokine process where their fatty tissue is releasing adipokines and causing a lot of alterations within some other metabolic parameters for example I may drop down my HDL I may increase my triglycerides to greater than 150 my BP might start trending up to greater than 130 over 85 my blood glucose may start kind of going up to greater than 100 my waist circumference may start exceeding 40 if I'm a male uh 35 of I'm a female and if I have at least three out
of five of these I have what's called metabolic syndrome so usually in patients who are a little bit older and have features of metabolic syndrome what we found is that these things alter the insulin receptors in other words it makes the insulin receptors less sensitive and more resistant to insulin so what the heck does that mean that means if these receptors are not responding to insulin then they're not going to be as good at being able to stimulate this receptor that's supposed to take glucose up into the cell and as a result glucose will build
up in the bloodstream this is referred to as hypoglycemia this high glucose will then tell the pancreatic beta cells hey dude glucose is pretty high here you want to do something about it and the beta cells will say okay I got you I'm going to release a lot of insulin and other types of molecules this insulin that's being released though you have to remember it's not going to work properly on these tissue cells because again these receptors are less sensitive why likely because of metabolic syndrome these particular factors that we just talked about above so
because of that again they're not going to take the glucose up into the cells it's going to build up and they start going to developing really bad high glucose levels the other thing that's really important to remember here in these patients is that whenever the beta cells are pumping out tons of insulin the other complication that we see here is that there's other proteins that are released called ameloid proteins ameloid proteins whenever you're releasing tons and tons of insulin you're releasing tons and tons of amalo proteins and these over time can lead to fibrosis and
destruction of the actual beta cells to the point where the beta cells die and they aren't able to produce enough insulin and so that's the difference over time is that initially in a patient who has Type 2 diabetes they'll have insulin resistance hypoglycemia and high insulin levels but over time with more amalo deposition their insulin levels will drop and they'll kind of start taking on the characteristics of a type 1 diabetic so metabolic syndrome is going to be one of the big features here but there's also been a lot of studies that have shown that
family history can be you know accompanied to this so there may be some type of genetic relationship here that causes an alteration in the sensitivity of the insulin receptors not just these factors themselves we know now that hypoglycemia is the common thread between type 1 and type two diabetes though right now often times this will lead to the classic 3p presentation polyurea polyphasia polydipsia how well hyperglycemia whenever this happens it actually is one of the solutes of our bloodstream so the it's going to lead to a change in What's called the osmolarity of the blood
with higher amounts of glucose comes a higher osmolarity it's a part of our normal osmolarity calculation so whenever our osmolarity goes up there's a couple things that happen one is it starts to activate the osmo receptors in the hypothalamus right the subicular organ the lamina terminalis and what happens is when they become stimulated they start causing an increase in our thirst so now we're going to start getting thirsty trying to drink tons and tons of water why the concept is that if we drink more water will then help to dilute down the amount of solutes
in our bloodstream and reduce the osmolarity all right but you're still going to have hypoglycemia that will persist the other concept is when patients have hypoglycemia that Sugar that's not getting taken into the cells will get filtered across the Glarus into the kidney tubules and what glucose is it's an osmotic molecule and it'll draw with it a ton of water and these patients can have massive what's called osmotic diuresis and pee out very large volumes of urine or they have to pee more frequently and this is called polyura problem with this is that now not
only is your sugar going up which is causing an increase in your hyperosmolarity but you're also getting rid of a ton of water and if I pee out a ton of water the amount of water I have in my bloodstream starts going down because I'm becoming dehydrated so now I have high glucose and low water that's going to make even more hyperosmolar and make me even more thirsty so it's a very vicious cycle the polyphasia one's very interesting and these patients they're not utilizing the main source of kind of fuel which is the carbohydrates so
because of that they start taing into alternative sources they start breaking down proteins in particular tissues and they start breaking down fats in other tissues because they need that to generate ATP so as I break down proteins and I break down lipids I start chewing through this metabolic kind of fuels and this could lead to a catabolic state that leads to increased hunger because as I start kind of breaking down all these molecules right I'm going to increase my metabolism increase my heat generation and this will start causing the people to be in much more
hungry right so this is another thing to also consider and usually in type 1 diabetics this hypercatabolic state can be so insane that they actually could be uh have weight loss so they actually can lose weight in type ones all right that's a lot of stuff to talk about with diabetes with the path of fiz but I think it really sets us up for the next part here which is what are some of the complications and the scary issues that can arise in patients with diabetes metis where they live with this very chronically high high
glucose or in the scary scenarios they have very acute rise of glucose so there's something that you really need to remember and this is called dka and HHS this is a part of our hyperglycemic crisis and a patient who has diabetes and they experience an infection maybe they have a myocardial infarction they have pancreatitis or they have some type of like surgical procedure of some sort what happens is that in the States you create a stress response that stress response will then increase the release of your catacol amines like norepinephrine and epinephrine via the sympathetic
nervous system and it'll also increase the release of cortisol both of these guys are Bad News Bears especially in a patient with diabetes you want to know why because they're going to increase glycogenolysis gluconeogenesis and they are going to lead to a very high glucose level and when you have a high glucose level and a patient already has diabetes you have a recipe for some disaster such as dka and HHS diabetic keto acidosis and hypoglycemic hyperosmolar syndrome now we have to differentiate between these two so let's talk about that so first one's dka I like
to remember more particularly that dka is going to be something that's more likely to be seen in type 1 diabetics it can be seen in type two diabetics but it's much more common in type ones the concept behind diabetic keto acidosis is that the pancreatic beta cells are not making insulin if you're not making insulin the concept behind this is that you're not going to be taking glucose up into the cells if you don't take glucose up into the cells your body has to start tapping into alternative source to generate ATP and that's usually starts
chewing through fats and it does this through a process called ketogenesis so what happens is you start breaking down lipids in your adapost tissue and in your liver what happens is those fatty acids get taken up into your liver and it starts chewing through them via a process called beta oxidation unfortunately when you take fatty acids and convert it into aeta you may be doing way too many of them that acetyl Co gets kind of built up and it can't go into the kreb cycle so what happens is it shunts into an alternative cycle which
is making Ketone bodies like beta hydroxy uate and acetoacetate these Ketone bodies are problematic the reason why is is that they can kind of cause especially the acetone which is one of the products of the Ketone bodies they can cause the breath to be very fruity the other thing is that they can actually release protons and when it releases protons it drops the pH of the blood and it can actually cause metabolic acidosis and these are kind of organic acids so they have the capability of causing an Anin Gap metabolic acidosis where the anine Gap
is greater than 12 and the pH is very low less than 7.35 the other thing is because they're super acidotic this actually stimulates the peripheral chemo receptors and tells the patient to breathe faster to hopefully breathe off more CO2 and then by doing that hopefully you'll bring up the pH so often times as a result these patients are breathing very fast and we call this cous small breathing very deep and fast breathing going back to the problem with having less insulin is that you don't take glucose up into the cells and so their glucose goes
up as well and this glucose can be pretty high sometimes greater than like 250 uh in a patient with dka so if I have type 1 diabetes I have keto acidosis and H hyper glycemia that really kind of gives me the the recipe for a patient having dka other things that are really important to remember with these patients with dka that are complications is when you have very very high glucose it actually has the capability of kind of pulling potassium out of the cells and so you can get a really total body potassium depletion another
thing is that it's going to cause osmotic diuresis when you have lots of glucose into the bloodstream it gets filtered into the kidneys it's going to pull a ton of water with it and these patients can develop massive polyurea and dehydration now with that being said we go to HHS HHS is hyperglycemic hyperosmolar syndrome I want you to think type 2 diabetics now remember I told you that dka it is more common in type one you can see it in type two but it's usually at the end stage when the insulin levels pretty much dropped
and HHS I'm thinking early type 2 diabetics now in this particular scenario you pancreatic beta cells are still producing insulin it's just not a sufficient amount right but you're still producing to some some of this to some degree problem is is that it is enough insulin for your body to use some of the glucose but it's not it's not the problem enough where you'll actually start kind of tapping in to the Ketone body formation so that's the big difference they'll have enough insulin that they don't have to tap into the liver and start generating Ketone
bodies that's one huge difference between HHS and dka is that there is no ketogenesis so there's not going to be any cous small breathing there's not going to be an anap metabolic acidosis there's not going to be any Fruity breath but you are going to have all the other complications such as insulin resistance where they're not going to respond to the insulin they're not going to take the glucose simp into the cell it builds up in the bloodstream you pull potassium out of the cells and depletes your total body potassium you cause a lot of
water to be lost into the urine and cause polyera and dehydration the last thing that's really interesting here in these patients is that their glucose can be so high greater than 600 milligram sometimes to the point where it can cause the osmolality of the blood to start PR exceeding 320 and the problem with this is this starts causing encylopaedia altered with respect to their mental status and that's a really big difference here so you're not going to see this kind of effect as clear as you would see dka and you're not going to see keto
acidosis and HHS as well to really kind of recap this I think the big thing to remember here is in between these two is type one type two again when we're think thinking about DK it's more likely type one HHS more likely type two which one's gonna have more significant hypoglycemia HHS can get up into the 600s or greater dka can get up above greater than 250 dehydration HHS is going to be profound hypoglycemia that's going to cause significant osmotic diuresis polyura and profound dehydration DK they will be dehydrated but not as significantly keto acidosis
you're going to see that in dka because they don't have any insulin h s you get a little bit of insulin enough that you don't have to tap into the Ketone bodies hyperosmolarity you're going to see a very high hyperosmolarity almost G than 320 for patients who have HHS not as severe in patients with dka the other thing is dka is usually rapid so these patients they develop severe hypoglycemia keto acidosis dehydration Etc whereas HHS is more of a gradual slow Insidious onset all right that covers the hyperglycemic crisis which is one of the most
Terri terrifying complications of diabetes what about the more chronic like masro macrovascular complications that you can experience if a patient has chronic hyperglycemia so one of the big things to remember is if again your patient has like no insulin or they're having insulin resistance whatever this you know the issue is they're not taking glucose into the cell so they're living with hypoglycemia one of the problems with hypoglycemia is that it can actually trigger something called non-enzymatic glycation in other words you can take proteins and lipids and bind glucose onto them problem with this is is
that this really accelerates atherosclerosis whether it be Highline or basement membrane thickening you're really causing damage to the blood vessels the blood vessels become more thick and they become more high risk for atherosclerosis the problem with having atherosclerosis is now that this patient can have plaqued up vessels that supply their brain they end up with a Tia or a stroke they can end up with potentially coronary artery disease from pla up myocardial from pla up coronary arteries in severe cases they even have very high risk of myocardial infarction and on top of that they also
can pla up some of the vessels that supply their lower extremities and end up with peripheral artery disease in the form of claudication or sometimes severe ulcers that can even become infected and even chronic lisia these are what we call macrovascular complications so big things like Strokes Tia again myocardial infarction CAD pad critical osmia there's other vessels that can become atherosclerotic and they can cause injury but particularly more at the smaller microscopic level this this is going to be something that we call diabetic nephropathy and retinopathy so when patients have diabetic nephropathy you actually cause
damage to the particularly to the Glarus and a lot of injury to the Glarus Glarus sclerosis starts to occur and as a result these patients have difficulty being able to excrete waste products um and also they lead to a lot of loss of albumin due to damage to their nephrons so you'll see these patients will have significant increased risk of developing chronic kidney disease and we'll see that based on an increase in their GFR as well as a very significant loss of albumin in their urine retinopathy is another one they can really cause a lot
of damage to the blood vessels and plaque these puppies up so these patients can start off with maybe like Little microaneurysms they can cause hard exudates which are these kind of like little lesions that kind of occur outside of the vessels and the the retinal tissue they can cause flame hemorrhages and cotton wool spots but the worst case scenario is when they start having to form new blood vessels to get around the damaged blood vessels and that's called proliferative or neovascularization so this is a type of proliferative retinopathy and all of these are nonproliferative retinopathy
these patients can start to come in with visual changes and that's pretty bad all right so watch out for patients who start having a bump in their GFR an increase in their alumin watch out for any evidence of macrovascular complications such as neurological deficits angen and St changes and potentially troponin elevations claic ulcers and then again retinopathy with vision changes another complication that could be very significant is neuropathy this is actually really interesting the concept behind this is that glucose whenever it's in really high amounts it gets into your cells and what it does is
it can actually increase the amount of sorbitol now sorbitol the problem with this thing is that it can loves to pull water into the cells as you pull a lot of water into the cells via its osmotic kind of PR practic um its osmotic characteristics it can lead to these cells dying because of the osmotic damage when that happens the cells that are really kind of being affected by this is the Schwan cells which are significant to your actual peripheral nervous system so often times these patients can develop what's called neuropathy peripheral neuropathy that's called
diabetic neuropathy now ways that this can present is that it Alters The Sensation from the lower extremities and they can develop paresthesias and sometimes in the worst case scenarios they lose all complete sensation to their lower extremities usually in what's called a stock and glove type of pattern the problem with this is if you lose sensation to your lower extremities and as a patient who goes around maybe you step on something you hit your leg against something you start getting sores or ulcers that form on your foot you may not even know that they're there
the problem with this is that these diabetic foot ulcers are very high risk for infection especially in a patient who has diabetes why because diabetes accelerates the risk of pad so if a patient has peripheral artery disease they won't give good oxygen to their tissues they have increased risk of ulcers and now this thing can become infected and even potentially progress to gangrenous uh necrosis and that's a very important thing to remember the other concept here is that it also Alters the neurons that Supply the stomach and so these patients may have difficulty being able
to generate enough profound contraction of their stomach and empty the contents of their stomach and so because of that they may present with what's called gastroparesis so they may present with nausea vomiting stomach dilation um and this is potentially common as well the last one is what's called orthostatic hypotension this one's due to um kind of an autonomic nervous system neuropathy so you kind of demate some of the autonomic neurons and so what happens is is your sympathetic nervous system is supposed to provide Vaso constriction to your veins and to your arteries if a patient
is not getting enough good venoc constriction they're not going to be able to squeeze their veins and return enough blood to their right heart maintain a good Venus return stroke volume blood pressure and they won't be able to profuse their brain as well so because of that if you have a patient who has some type of autonomic neuropathy because you demyen their sympathetic neurons they won't give good venal contriction they won't have good Venus return they won't have a good stroke volume cardiac output blood pressure and they could end up with Syncopy or they could
end up whenever they stand up they start getting lightheaded and pre synple so this is very common complications in patients with diabetes we talked a lot about the complications right I think the next thing to go to is okay I have a patient comes in polyurea poly dipsia polyphasia maybe they come in with a hyperglycemic crisis like dka HHS they have common atherosclerotic cardiovascular dis maybe they had a TIA a stroke maybe they also had a heart attack or OC cardial infarction is the proper term maybe they have pulon um they have peripheral artery disease
um on top of that they coming in with neuropathy so they have sensory losses they have ulcers on their foot um maybe they have kidney disease so they're having an increased GFR a lot of abum loss um they're having visual changes and now they're having blurry vision and maybe even complete vision loss or retinal detachments in these particular scenarios it's important to consider diabetes as the cause so what we'll do is for these patients is we'll look for findings of hypoglycemia so if they have the polyurea the poly dipsia and the polyphasia or do they
have lots of foot ulcers infections um do they have any atherosclerotic cardiovascular disease factors all those things that we talked about if they don't and it's more Insidious then it's kind of important to obtain three particular tests you want to get a fasting plasma glucose level a 2hour oral glucose tolerance test this one's a little bit more specific for gestational diabetes but we'll talk about it and then lastly the most clear test is the hemoglobin A1c from these this will give you an idea if the patient has diabetes or not if the fasting plasma glucose
level is greater than or equal to 126 milligrams per deal that means that they're living with a high glucose pretty much without any food in them so that's definitely diagnostic if the blood glucose is greater than equal to 200 after you give them a little bit of sugar that's definitely indicative of diabetes and then lastly if their A1C is greater than or equal to 6.5% that tells me that they're living with a high sugar pretty decently high sugar that you can extrapolate over a period of 3 months and that's one of the benefits of A1C
it's a little bit better at being able to tell you the longterm effect or at least a three-month time frame of what their sugars have looked like if they have these you have diabetes right you can go further if you want to say I want to see if it's type one or type two oftentimes you can gain that from history but if you want to go the length of determining if it really is type one type two you contain something called a c peptide and antibodies before we talk about that though let's let's say that
we have a patient who comes in with polyurea polyphasia polydipsia or other concerning findings that suggest diabetes from that you can get a random plasma glucose and if the random plasma glucose on at least two occasions is greater than or equal to 200 milligrams per DL plus symptoms it's likely diagnostic of diabetes now I'll say that you you're not sure is it type one type two again history usually can elucidate this but if not you can obtain the C peptide often times the antibodies the anti-gad anti-et those are going to be present in type one
you're not going to see that really in type two the other thing is the C peptide levels those should be lower generally in a patient who has Type 1 diabetes also look at the history are they less than 30 greater than 40 that also May provide some effect this would suggest more of a type one in the other scenario where I think the patient has type two the antibodies should technically be negative they're going to have more of the characteristics of metabolic syndrome so obesity um low HDL high triglycerides High BP high sugar uh increased
waste circumference and often times their C peptide in the initial periods are going to be high so C peptide is kind of like one of the molecules that gets released with insulin and patients who have type two diabetes they release a lot of insulin it's just they are insulin resistant so if they release a lot of insulin they'll release a lot of C peptide if you don't release a lot of insulin you don't release a lot of C peptide all right how do we treat diabetes Well type one they're just not making insulin so you
got to give them insulin that's pretty straightforward for this one so there's different types of insulin we'll go through this briefly there is what's called rapid acting insulin in the form of lisbo and aspar lisbo is the more commonly utilized one the duration for these are pretty short so because of that if they're very very short acting the best time to give them is usually um for meals so whenever a person's going to be eating breakfast or lunch or dinner we should be giving it around those times to help them to control that Sugar Spike
whenever they eat so again this is best for whenever their patient is going to about to eat the other one is a short acting insulin so this one's going to be the regular insulin its duration is a little bit longer not significantly longer but it's a little bit longer problem with this is it's a little bit too long for a patient you know eating um and it's not long enough that it's going to last an entire day for their basil insulin so really the only time where we really use short acting insulin is in a
hypoglycemic crisis um so this is going to be more fitting for a patient who's going to be on an infusion that we can titrate every single hour and so for patients who come in with dka or HHS are very very difficult to control um type 1 diabetes metis we may put them on an insulin infusion to get a a little bit more better control and then we can extrapolate how much insulin they're on on that infusion and then switch them over to a rapid acting and a long acting insulin there's another one it's a little
bit cheaper and it's more commonly utilized because of that it's called intermediate acting insulin also known as NPH um and this one humin it can have a little bit of a longer period in comparison to the regular insulin problem is it's not going to last 24 hours so this can be used as a basil insulin meaning that you're going to give it and it may give you a pretty good extent of time where the sugars are relatively stable however you're going to have to give probably two doses of it so you may need it twice
a day so it's not commonly utilized U but it is a little bit cheaper these are going to be the more commonly utilized one which is the long acting ones garene and damir garene is probably the more one that you'll see um these have no peak they're pretty stable and as you can see here it's kind of got a plateau phase that it's pretty good and it can last a decent amount of time so about 24 hours so to give you a full day length of insulin that's kind of like your Baseline and if you
think about this this would be really good for insul that you can give maybe at the end of the night or maybe you can give it around lunchtime around 12:00 and this should give you a very long coverage of the entire 24-hour period so this may seem like a lot you're like okay what am I supposed to to do with this to treat them I don't know I know that if they got really high glucose I'll put them on an insulin Fusion I know that this is I give with the meals I know I could
give one of these two potentially with you know once a day or twice a day I don't really understand Zach how do I do this I got you the basic concept here is we use something called a basil blls regimen so we're putting them on an infusion we just monitor this every hour and we titrate to their glucose for these we're going to more commonly base it off of their weight um and their A1C so in a Bas of bus regimen you're going to take their weight and you're going to multiply by a factor this
factor is variable so a patient who's like you're just starting them on insulin 3.5 is okay if a patient is has really high A1C you may need a 7 or one and that's something that really depends from Patient to Patient but let's say that you start off with this when you do this this will give you a number that tells you the total amount of insulin that you can give them for a day all right so it's a total daily dose so what I'm going to do is I'm going to split this into two parts
the one that I'm going to give them that's going to last them 24 hours and the one that I'm going to give them that'll last for particularly whenever they eat so I'm going to split this in half when I split it in half half of it's going to be the glargine dose that's my long acting insulin that'll give me the entire 24-hour period then I'm going to take the other half and that's going to be my lispro dose that's my rapid acting that I'm going to give them with the meals but I have about three
meals a day maybe I'm going to eat breakfast lunch and dinner I'm going to take this dose and I'm going to split it up over three meals so maybe it was a total of like yeah I don't know 12 units I'm going to divide that by three and and you know four units at breakfast four units at lunch four units at dinner and then for this one I'm going be going to give 12 units I'll give it around 12:00 and that's going to last me until 12:00 the next day that's the concept behind this the
important thing to remember is when you start them on this you should kind of track their glucoses maybe again at breakfast at lunch at dinner and right before you go to bed to make sure that they're appropriately within a good range and you don't have to modify these a little bit but this is how we would treat type 1 diabetes again the alternative is I could say instead of me using garene I could use NPH here it's just I would have to potentially give it twice a day rather than once a day all right what
about type two diabetes well they're still making insulin so I don't need to give them insulin there is a couple exceptions where I could but often times we just need to try to improve insulin resistance so often times it is changing up the lifestyle right trying to treat the metabolic syndrome losing weight reducing caloric intake Etc but unfortunately with these patients they're going to require anti-diabetic medications to some degree the most common one that we'll start off with is a biguanide it's metformin It's usually the first line medication so we'll start them on that and
then three months what we'll do is we'll get an A1C because it's going to tell me where their sugars have been for at least a 3-month period remember greater than or equal to 6.5% is considered diabetes right at this point I want to just know if they're being better controlled so I'm going to use an arbitrary number such as 7% this is what we've been shown in the the guidelines if a patient gets that A1C though and I see that after I put them on Metformin for three months their A1C is greater than 9.5% there's
not a chance in heck that if I put them on a second anti-diabetic medication I'm going to get them from 9.5 down to like less than seven so at this point if it's greater than 99.5% just start them on basil insulin so you're going to put them on something like garene or you're going to put them on something like DLC or NPH potentially and this is going to give you a little bit more extended coverage to try to bring that glucose down and have a basil control of their sugar if the A1C is greater than
7% it means okay I know that I started met foran I'm still not less than 7% I want to get less than 7% That's my goal if I'm not there yet I got to add on a second agent all right so if I'm I'm greater than seven but I'm still less than 9.5 I'm gonna add on a second anti-diabetic all right what's that one there's a lot of them and it's really based upon the patient's underlying diseases are what they're trying to do so let's say that the patient has coronary artery disease they have a
history of a Tia or a stroke they have peripheral artery disease in these particular scenarios there is a couple drugs that actually may help with that glyp one agonis stide lorag these potentially can provide a lot of benefit there sglt2 Inhibitors like your flosin these can also be potentially beneficial the other one is if a patient has underlying CHF if a patient has ch HF we have seen that particularly sglt2 Inhibitors are very very effective and they can be a part of what's called your guideline directed medical therapy the one that you should never give
to a patient with CHF because it's been shown to potentially worsen it is thadine diones so stay away from those if a patient has CKD we know that sglt2 Inhibitors and glip one Agonist are pretty good for these patients if they are looking to lose weight we know that SGL t2s glip 1es and DPP four Inhibitors have been shown to be good for weight loss so if your goal is to treat your Arro or the atherosclerosis related diseases these should be initiated if it's CHF these well this one sorry if it's CKD this one and
if it's weight loss it's this one so you notice a trend the most commonly utilized ones here as a second line agent is glyp one agonists or sglt2 Inhibitors and maybe a dpp4 inhibitor the other one is if you don't want to have a lot of periods of hypoglycemia because these can cause like neurog glyc pic symptoms you can become diaphoretic you can actually go into a comose state from severe hypoglycemia so it's important to be able to give drugs that you want to do to reduce that risk glip one agonists are really good at
not having a lot of hypoglycemia um dpb4 Inhibitors sglt2 Inhibitors and thadine Dion so with that being said the one that does have a risk of hypoglycemia and you probably don't want to actually take is sanas the benefits of sulani uras are they a little they are a little bit more cheaper um so that's going to be one one of the reasons why that they could be considered so gide and glide all right so let's say that I start the second antidiabetic and I base it upon one of these particular factors you're seeing a trend
though that sglt 2s and glip 1es are really the best in a lot of scenarios here so I start them on one of those I get an A1C in three months and then I check if my A1C is greater than 9.5 there's not a chance that adding a third anti-diabetic is going to get me that love to bring the A1C less than 7% start the basil insulin all right get a little bit more Baseline control of their sugars if it is still greater than seven but less than 9.5 I can be a little bit more
aggressive and I can add on a third anti-diabetic so I say I started the m at foran A1C is still greater than 7% after 3 months start them on a glip one Agonist A1C still greater than 7% after 3 months start them on an sglt2 inhibitor if after that in 3 months I check it and their A1C is still greater than 7% you got to then then add on an another uh you got to add on insulin so that's what we would do in this particular scenario of treating a patient with type 2 diabetes start
off with metformin go to a second anti-diabetic if you're not meeting your goal then a third anti-diabetic if you're not meeting your goal and then insulin if you haven't met your goal with three anti-diabetics if along any point in that time frame your A1C is greater than 99.5% start them on basil insulin all right the last thing here is treating the complications of diabetes m there is a lot of these but the most concerning ones is dka and HHS so let's talk about how do we treat this well first thing is these patients are severely
dehydrated from the osmotic diuresis so because of that you want to replace their their volume losses and often times these are patients that can require like three to four liters of fluid so they should be seen in an ICU often times we start them on an infusion we may give them like a bolus of fluid maybe one or two liters like an a Bolis and then we'll start them at a very high maintenance rate maybe 120 150 milliliters an hour the two choices I'd say that are best is half normal saline and LR the only
reason why is that normal saline itself can cause a little bit of a normal anti-ap metabolic acidosis and if a patient's already acidotic from dka you can worsen their acidosis so you're going to start giving them some boluses and then start them on a maintenance rate to re replace their actual dehydration the next thing is you have to ask yourself the question I'm about to start insulin for this patient Well's their pottassium so get a BMP check what their pottassium is the reason why is you can't start the insulin infusion unless their po potassium is
normal so if I check it and the pottassium is low give them potassium first replace that then after the potassium is normalized then you can go ahead and initiate an insulin infusion and again the type of insulin is not going to be the rapid acting it's not going to be the intermediate the long acting it is the regular insulin all right so in this particular scenario if I start them off on regular insulin here's what we do this for because often times I think there's a misconception of how we give them insulin when we start
the insulin infusion we started off at at a particular portion and we're going to continue to up titrate the insulin not to glucose we're titrating it to the Ann Gap so you're going to be monitoring these patients BMP like every two hours so they're going to be getting frequent lab draws you start the insulin infusion their anine Gap is like 20 you get the insulin you check in two hours their anine gap's 18 all right you're kind of bringing the an gap down but if the Ann Gap is still present you need to then increase
increase the insulin infusion rate so that you can keep bringing down the anine Gap because insulin is going to start kind of shutting down the ketogenesis process so if the an Gap closed great you don't need to have them on regular in insulin infusion anymore you can just put them over onto the basil bolus and stop the infusion but if their insulin um if their uh anine Gap is still potentially present say that you went from 20 to 18 you have to keep them on the insulin infusion you might even have to increase the rate
now if I increase the rate of the insulin I also have to bolish them with more insulin so again start off with fluids check their potassium if it's normal start the insulin infusion check their anine Gap via their BMP every two hours if I check it and it completely normalized it's less than 12 you can stop the infusion you're good and you can just treat them with basil Bolis if you do it and the BMP shows that your an Gap is still elevated you have to increase the rate of your insulin infusion and then rebol
them with insulin keep checking their BMP every two hours during that time frame you should also consider maybe getting abgs or vbgs if a patient is severely acidotic a pH less than seven that's really bad and that can actually start altering a lot of problems that can lead to a lot of problems it can lead to you know poor responsive to poor response to vase oppressors it can even worsen a lot of your potassium derangements and so in this situation if the pH is less than seven you should give this patient bicarbonate and that's the
only time the other thing is you have to kind of think about this in a patient who has diabetic keto acidosis you're giving them a lot of insulin a lot of insulin that's going to start bringing down their glucose that's not what you're doing it for you're doing it to bring down their keto acidosis but unfortunately it may take some time to bring their keto acidosis down so as you're bringing down their keto acidosis their glucose may be really low and you need to keep giving them more insulin and the problem with that is if
I give more insulin I'm going to cause them to become hypoglycemic so if the blood glucose drops to less than 200 and your anine Gap is still not completely closed I have to give them sugar in order for me to give them insulin so what you're going to do is you already have them on like 125 or 150 of LR or half normal add D5 into it and that'll help to increase their sugar so that you can give them more insulin to bring down their keto acidosis and close their anion gap I know that's a
lot of stuff I hope that part made sense for HHS you're actually not going to do an insulin infusion for the keto acidosis you're doing it directly for the patient's hypoglycemia and hyperosmolarity but the same thing these patients are severely volume dehydrated give them IV fluids in the form of LR half normal give them a couple boluses and then start them on an infusion again insulin infusion is for hyperglycemia you actually are going to tight treated every hour off of their glucose level and then the other thing is you're going to check their osmolarity to
make sure that you're not dropping them down too quick and then again make sure that you're giving them pottassium because as you give insulin again insulin will cause the shifting of potassium into the cells which can worsen their hypokalemia that's why you never start an insulin infusion if they are hypocam because then we'll start becoming super tacac cardic the other thing that you want to manage for these patients is the more chronic complications such as retinopathy it's more prevention right so you're going to do annual eye exams looking to see if they have any evidence
of you know microaneurysms flame hemorrhages hard exat cotton wool spots proliferative Neo proliferative neovascularization and if you do catch that you should actually start again controlling their glucose but more specifically doing things that can prevent further injury because that neovascularization can cause hemorrhaging so oftentimes we'll do VF Inhibitors which will inject right there into the into the actual eye and that's been shown to potentially reduce the proliferation process sometimes you can do phaser laser photocoagulation if the VF is not an option another one is nephropathy we want to be able to catch a patient developing
nephropathy um and so if a patient has diabetes you want to do annual urine album and creatinine ratios to see if their alumin is really becoming high in their urine and then check their BMP to see if their GFR is really starting to decline because in these situations we should actually start them on drugs that can protect them from alumin area protect them from CKD and maybe even control their blood pressure so there's two drugs ACE inhibitors or ARB is one of them what they do is they actually help to kind of promote this change
in the eperen arterial they actually cause eperen arterial Vaso dilation so they stop constriction and they help to reduce the intraglomerular pressure reduce the GFR and that helps to reduce a lot of the albumin loss unfortunately though if you drop the GFR you can worsen their kind of kidneys a little bit and cause a bump in their creatinine but it's something that you have to use because it has been shown to be nephroprotective reduce albuminuria reduce the progression in CKD and also can treat a patient who has hypertension all right the goal that you're trying
to do here is you're trying to make sure they're not dumping enough protein into the urine so the goal is to get that urine abum and cattiny ratio less than 30 you don't want it from 30 to 300 you definitely don't want it greater than 300 the neuropathy is all about again making sure that they are very aware of their Sensations so doing annual foot exams with a licensed podiatrist would actually be very good to see if there is any kind of like diabetic ulcers um to also examine to see do they have diabetic ulcers
from from neuropathy or do they also have concominant pad that's also caused some ulcers because you want to be able to recognize those before the patient starts having problems the other thing is that they can cause a lot of pain and so for the pain that they have often times gabapentin and cabalin can be alternatives to treat the neuropathic pain um but if they also have concominant depression tcas or snris can be utilized if they have concominant depression atherosclerosis is again a very very important thing because the diabetes has a very high rate of atherosclerosis
so because of this the macrovascular complications are really important to prevent so what we should be doing for these patients is getting an annual lipid panel to make sure that we're screening for any incidents of high LDL low HDL and making sure that if we recognize that we start them in the appropriate therapy one of the reason why is again the indication for statins come from the literature that saying if a patient does have diabetes um they are 40 to 75 and they have an atherosclerotic cardiovascular disease risk that's greater than you know 10% they're
high risk for atherosclerosis and they should probably started be on be started on a Statin the concept here is you just really want to reduce this type of process but also you want to reduce the risk of this plaque rupturing a platelet sticking to it causing a clot on top of that so the other question is is do they have indications for aspirin if a patient has any clinical risk of atherosclerotic cardiovascular disease and you're trying to prevent them from having that aspirin could be a potential indication here but again statins is really something that
you have to have a very low threshold to start in a patient with diabetes because again the goal is to try to prevent plaque thrombosis and the complications like a stroke an MI and critical lisia often times if they're 40 greater than that they have diabetes and their atherosclerotic cardiovascular disease risk is greater than 10% you should start them on a stattin and also consider aspirin all right my friends that was a monster lecture on Diabetes I hope it made sense I hope that you guys really did enjoy it love you thank you and as
always until next [Music] time
