Diabetes Mellitus | Clinical Medicine
Summary
TLDRThis video delves into the pathophysiology, types, and treatment of diabetes mellitus. It covers the differences between type 1 and type 2 diabetes, the role of insulin, and the complications associated with the disease. The lecture also discusses the management of diabetic ketoacidosis (DKA) and hyperglycemic hyperosmolar syndrome (HHS), emphasizing the importance of fluid and electrolyte balance, insulin therapy, and monitoring.
Takeaways
- 🧬 Diabetes Mellitus is divided into Type 1 and Type 2, each with distinct pathophysiological mechanisms.
- 🔍 In Type 1 diabetes, the body's immune system attacks and destroys pancreatic beta cells, leading to insulin deficiency.
- 🛡️ Autoimmune diseases such as celiac disease and Hashimoto thyroiditis are often associated with Type 1 diabetes due to genetic mutations that hyperactivate the immune system.
- 👨🦳 Type 2 diabetes typically affects older individuals and is associated with metabolic syndrome, characterized by obesity, high blood pressure, and abnormal cholesterol levels.
- 🔄 Insulin resistance in Type 2 diabetes results in the body's inability to use insulin effectively, causing high blood sugar levels.
- 💉 Treatment for Type 1 diabetes involves insulin replacement therapy, while Type 2 diabetes may be managed with lifestyle changes and anti-diabetic medications.
- 🚨 Diabetic ketoacidosis (DKA) and hyperosmolar hyperglycemic state (HHS) are severe complications of diabetes that require immediate medical attention.
- 🌡️ DKA is more common in Type 1 diabetes and is characterized by high blood sugar, ketosis, and metabolic acidosis.
- 🌡️ HHS is more prevalent in Type 2 diabetes and presents with severe dehydration and hyperglycemia without ketosis.
- 🏥 Chronic hyperglycemia can lead to macrovascular and microvascular complications, including cardiovascular disease, kidney disease, and neuropathy.
- 📈 Monitoring and managing blood glucose levels, along with regular check-ups for complications, are crucial for the health of individuals with diabetes.
Q & A
What are the two main types of diabetes mentioned in the script?
-The two main types of diabetes mentioned are Type 1 and Type 2 diabetes.
What is the primary cause of Type 1 diabetes according to the script?
-Type 1 diabetes is primarily caused by the autoimmune destruction of pancreatic beta cells, which are responsible for producing insulin.
What is the typical age range for individuals with Type 1 diabetes?
-Type 1 diabetes is usually seen in younger individuals, typically those under the age of 30.
How does insulin resistance in Type 2 diabetes affect the body's ability to regulate glucose?
-In Type 2 diabetes, insulin resistance leads to the body's inability to effectively use insulin, resulting in high blood glucose levels as cells do not take up glucose efficiently.
What is the role of adipokines in the development of Type 2 diabetes?
-Adipokines, released by fatty tissue in obese individuals, cause alterations in metabolic parameters that can lead to insulin resistance and the development of Type 2 diabetes.
What are the common autoimmune diseases associated with Type 1 diabetes?
-Autoimmune diseases such as celiac disease and Hashimoto thyroiditis have been linked and are commonly associated with Type 1 diabetes.
What is the term used to describe the condition where the body cannot effectively use glucose due to insulin deficiency?
-The condition is referred to as hypoglycemia, which is characterized by high blood glucose levels because glucose is not being taken up into the cells.
What are the classic symptoms of hyperglycemia known as?
-The classic symptoms of hyperglycemia are known as the 3Ps: polyurea (frequent urination), polydipsia (increased thirst), and polyphagia (increased hunger).
What is Diabetic Keto Acidosis (DKA) and what type of diabetes is it more commonly associated with?
-Diabetic Keto Acidosis (DKA) is a condition where the body, lacking insulin, starts breaking down fats for energy, leading to the production of ketone bodies that can cause metabolic acidosis. It is more commonly associated with Type 1 diabetes.
What is the difference between DKA and Hyperglycemic Hyperosmolar Syndrome (HHS) in terms of ketone body production?
-In DKA, ketone body production is present due to the lack of insulin, whereas in HHS, ketone body production is not a feature as the body still produces some insulin, preventing the shift to ketone body formation.
What are the chronic complications of diabetes that can affect the cardiovascular system?
-Chronic complications of diabetes that affect the cardiovascular system include macrovascular complications such as stroke, TIA (transient ischemic attack), coronary artery disease, myocardial infarction, and peripheral artery disease.
How does hyperglycemia contribute to the development of atherosclerosis?
-Hyperglycemia can trigger non-enzymatic glycation, which accelerates atherosclerosis by causing damage to blood vessels, leading to thickening of the basement membrane and increasing the risk of plaque formation.
What are the common treatments for Type 1 diabetes?
-Treatments for Type 1 diabetes include the administration of insulin, which can be rapid-acting, short-acting, intermediate-acting, or long-acting, depending on the patient's needs.
What is the typical first-line medication for treating Type 2 diabetes?
-Metformin is typically the first-line medication used to treat Type 2 diabetes.
What are the common treatments for diabetic ketoacidosis (DKA)?
-Treatments for DKA include fluid replacement, electrolyte correction (especially potassium), insulin therapy to reduce ketone production, and monitoring and managing acid-base balance.
How is the management of hyperglycemic hyperosmolar syndrome (HHS) different from DKA?
-HHS management focuses on fluid and electrolyte replacement, insulin therapy to address hyperglycemia, and careful monitoring of osmolarity to prevent rapid shifts that could worsen the condition, unlike DKA, which emphasizes ketone body reduction.
Outlines
🔬 Introduction to Diabetes Mellitus
The video begins with an introduction to diabetes mellitus, focusing on the pathophysiology of type 1 and type 2 diabetes. Type 1 diabetes is typically seen in younger individuals and is characterized by the destruction of pancreatic beta cells, leading to insulin deficiency. This deficiency results in reduced insulin receptor activation, hindering glucose uptake by cells and causing hyperglycemia. The destruction of beta cells is often due to an autoimmune attack, associated with conditions like celiac disease and Hashimoto's thyroiditis. Type 2 diabetes, more common in older individuals, is linked to metabolic syndrome and involves insulin resistance, where cells do not respond effectively to insulin, leading to high blood glucose levels. The lecture emphasizes the importance of understanding these differences for effective management.
💉 Complications of Diabetes and Pathophysiology
This paragraph delves into the complications associated with diabetes, particularly the metabolic changes that occur due to high glucose levels. It discusses how beta cells, when overworked, release amyloid proteins that can lead to fibrosis and destruction of these cells, eventually causing insulin deficiency. The video also covers the classic symptoms of diabetes, such as polyuria, polydipsia, and polyphagia, which result from hyperglycemia. The osmotic effects of glucose in the bloodstream lead to increased thirst and urination, and the breakdown of alternative energy sources like proteins and fats can cause weight loss and increased hunger. The paragraph concludes with a discussion on the acute complications of diabetes, such as diabetic ketoacidosis (DKA) and hyperglycemic hyperosmolar syndrome (HHS), which can arise from stress responses and the release of hormones like cortisol and catecholamines.
🌡 Differentiating DKA and HHS in Diabetes
The video script clarifies the differences between diabetic ketoacidosis (DKA) and hyperglycemic hyperosmolar syndrome (HHS). DKA is more common in type 1 diabetics and is characterized by the absence of insulin, leading the body to break down fats for energy, resulting in ketone body production and metabolic acidosis. Symptoms include fruity breath, rapid breathing, and high glucose levels. In contrast, HHS is more prevalent in type 2 diabetics and involves insulin resistance rather than insulin deficiency. This condition is marked by high blood glucose without ketosis, leading to severe dehydration and potential mental status changes due to hyperosmolarity. The paragraph emphasizes the importance of recognizing these conditions and their distinct management approaches.
🏥 Managing Acute Complications of Diabetes
This section of the video script discusses the treatment of acute complications in diabetes, specifically focusing on DKA and HHS. The primary goal in managing these conditions is to address severe dehydration through fluid replacement, typically with half normal saline or LR solution. For DKA, insulin therapy is crucial, starting with an insulin infusion and monitoring the anion gap to adjust the infusion rate. Potassium levels must be normalized before initiating insulin therapy to prevent hypokalemia. In cases of severe acidosis, bicarbonate may be administered. For HHS, the focus is on treating hyperglycemia and hyperosmolarity with insulin infusions, closely monitoring glucose levels and osmolarity, and ensuring potassium supplementation to counteract the effects of insulin-induced shifts in potassium.
🛠 Chronic Complications and Management of Diabetes
The video script highlights the importance of managing chronic complications of diabetes, such as retinopathy, nephropathy, neuropathy, and atherosclerosis. Annual eye exams are recommended to detect and prevent retinopathy, with treatments like VEGF inhibitors and laser photocoagulation considered if necessary. Nephropathy is managed through annual urine albumin and creatinine ratio tests, with ACE inhibitors or ARBs used to reduce albuminuria and slow CKD progression. Neuropathy management involves annual foot exams and treatments for neuropathic pain, such as gabapentin or duloxetine. Atherosclerosis prevention includes annual lipid panel checks and the use of statins and aspirin for patients at high risk of cardiovascular disease. The script emphasizes the need for proactive management to reduce the long-term impact of diabetes.
💊 Treatment Approaches for Type 1 and Type 2 Diabetes
The video script outlines the treatment strategies for type 1 and type 2 diabetes. For type 1, insulin therapy is essential, with different types of insulin like rapid-acting, short-acting, intermediate-acting, and long-acting used based on meal times and basal needs. A basal-bolus regimen is commonly used, involving long-acting insulin for baseline coverage and rapid-acting insulin for mealtime control. Type 2 diabetes treatment starts with lifestyle changes and metformin, with additional anti-diabetic medications added if A1C goals are not met. These may include GLP-1 agonists, SGLT2 inhibitors, DPP-4 inhibitors, and insulin, depending on the patient's specific needs and risk factors. The script emphasizes the importance of individualized treatment plans based on patient history and metabolic parameters.
📈 Monitoring and Adjusting Diabetes Treatment
This paragraph discusses the importance of monitoring and adjusting diabetes treatment plans based on A1C levels and other clinical factors. For type 2 diabetes, if A1C remains above target after three months on metformin, additional anti-diabetic medications are considered. The choice of second and third line agents depends on the patient's underlying conditions, such as coronary artery disease, CKD, or weight loss goals. Insulin therapy may be initiated if A1C remains above 9.5% despite multiple anti-diabetic medications. The script underscores the need for regular A1C testing and medication adjustments to achieve optimal glycemic control and reduce the risk of complications.
🏥 Hospital Management of DKA and HHS
The final paragraph of the video script focuses on the in-hospital management of DKA and HHS. It emphasizes the need for aggressive fluid replacement, potassium monitoring, and insulin therapy. For DKA, regular insulin infusion is used to reduce ketosis, with the rate adjusted based on the anion gap. If the patient becomes hypoglycemic, dextrose is added to the IV fluids to maintain blood glucose levels. For HHS, the primary focus is on treating hyperglycemia and hyperosmolarity, with insulin infusions adjusted based on hourly glucose levels. Potassium supplementation is crucial to prevent hypokalemia, and the script concludes with a reminder of the importance of comprehensive care in managing these acute diabetic complications.
🌟 Conclusion and Final Thoughts on Diabetes Management
The video concludes with a summary of key points and a reminder of the importance of comprehensive diabetes management. It emphasizes the need for regular monitoring, appropriate medication adjustments, and proactive management of both acute and chronic complications. The script encourages viewers to apply the knowledge gained in the lecture to improve patient outcomes and manage diabetes effectively. The presenter expresses hope that the information was clear and helpful, and signs off with a reminder to stay informed and engaged in diabetes care.
Mindmap
Keywords
💡Diabetes Mellitus
💡Insulin
💡Autoimmune Attack
💡Metabolic Syndrome
💡Hyperglycemia
💡Polyuria, Polydipsia, Polyphagia
💡Diabetic Ketoacidosis (DKA)
💡Hyperosmolar Hyperglycemic Syndrome (HHS)
💡A1C
💡C-Peptide
💡Neuropathy
Highlights
Introduction to diabetes mellitus, covering both type 1 and type 2.
Explanation of pathophysiology differences between type 1 and type 2 diabetes.
Description of how beta cell destruction leads to insulin deficiency in type 1 diabetes.
Discussion on the role of autoimmune attacks in type 1 diabetes.
Insulin receptor function and its impact on glucose metabolism.
Development of hyperglycemia due to insulin resistance in type 2 diabetes.
Link between metabolic syndrome and type 2 diabetes.
Importance of family history and genetic factors in type 2 diabetes.
Clinical presentation of diabetes including polyuria, polydipsia, and polyphagia.
Differences between diabetic ketoacidosis (DKA) and hyperglycemic hyperosmolar syndrome (HHS).
Risk factors and management of DKA in type 1 diabetes.
Characteristics and treatment of HHS, typically seen in type 2 diabetes.
Chronic complications of diabetes, including macrovascular and microvascular issues.
Importance of monitoring and managing diabetic nephropathy.
Strategies for managing diabetic retinopathy and its progression.
Approach to treating diabetic neuropathy and its associated symptoms.
Diagnosis of diabetes through fasting plasma glucose, oral glucose tolerance test, and hemoglobin A1c.
Treatment strategies for type 1 diabetes, emphasizing insulin therapy.
Management of type 2 diabetes, including lifestyle changes and anti-diabetic medications.
Treatment protocols for hyperglycemic crises in diabetes, focusing on fluid and electrolyte management.
Prevention and management of long-term complications in diabetes, emphasizing annual screenings and appropriate therapies.
Transcripts
[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
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