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.