Diabetes Mellitus | Clinical Medicine

Summary

This 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

00:00

🔬 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.

05:00

💉 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.

10:01

🌡 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.

15:03

🏥 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.

20:05

🛠 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.

25:06

💊 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.

30:07

📈 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.

35:08

🏥 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.

40:09

🌟 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.

Keywords

💡Diabetes Mellitus

Diabetes Mellitus is a chronic metabolic disorder characterized by high blood sugar levels. In the video, it is the central theme, with a detailed discussion on its two main types, pathophysiology, and treatment approaches. The script mentions the distinction between Type 1 and Type 2 diabetes, emphasizing their different causes and management strategies.

💡Insulin

Insulin is a hormone produced by the pancreas that regulates blood sugar levels by allowing glucose uptake into cells. The script explains that in Type 1 diabetes, there is an insulin deficiency due to the destruction of insulin-producing beta cells, while in Type 2 diabetes, there is insulin resistance where cells do not respond effectively to insulin.

💡Autoimmune Attack

An autoimmune attack refers to the body's immune system mistakenly targeting and damaging its own tissues. In the context of Type 1 diabetes, the script describes how an autoimmune attack destroys pancreatic beta cells, leading to insulin deficiency.

💡Metabolic Syndrome

Metabolic Syndrome is a cluster of conditions that increase the risk of heart disease and type 2 diabetes. The script associates Type 2 diabetes with metabolic syndrome, highlighting factors such as obesity, high blood pressure, and abnormal cholesterol levels that contribute to insulin resistance.

💡Hyperglycemia

Hyperglycemia is a condition where there is a high concentration of glucose in the blood. The script discusses hyperglycemia as a downstream consequence of insulin deficiency or resistance, leading to glucose accumulation in the bloodstream and the associated clinical manifestations.

💡Polyuria, Polydipsia, Polyphagia

These terms describe the classic symptoms of diabetes: excessive urination (polyuria), excessive thirst (polydipsia), and increased hunger (polyphagia). The script explains how these symptoms arise due to the body's attempt to manage high blood sugar levels.

💡Diabetic Ketoacidosis (DKA)

Diabetic Ketoacidosis is a metabolic complication that occurs in diabetes, characterized by high levels of ketones in the blood. The script describes DKA as a potentially life-threatening condition more common in Type 1 diabetes, where the lack of insulin leads to the breakdown of fats for energy, resulting in acidic blood.

💡Hyperosmolar Hyperglycemic Syndrome (HHS)

Hyperosmolar Hyperglycemic Syndrome is a condition where there is severe dehydration and very high blood sugar levels without ketosis. The script differentiates HHS from DKA, noting its association with Type 2 diabetes and the absence of ketone body formation.

💡A1C

A1C, or glycated hemoglobin, is a measure of average blood sugar levels over the past 2-3 months. The script mentions A1C as a critical test for diagnosing diabetes and monitoring its control, with a value greater than 6.5% indicating diabetes.

💡C-Peptide

C-Peptide is a biomarker used to assess insulin production by the pancreas. The script refers to C-Peptide levels to differentiate between Type 1 and Type 2 diabetes, with lower levels typically indicating Type 1 diabetes due to the destruction of beta cells.

💡Neuropathy

Neuropathy is a type of nerve damage that can occur in people with diabetes, leading to pain, numbness, or tingling in the hands and feet. The script discusses diabetic neuropathy as a complication that can affect the quality of life and requires careful management.

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

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time