In this discussion,
we'll talk about Insulin Dependent Diabetes Mellitus Type 2.
What we previously referred to as adult onset diabetes.
With the American obesity epidemic, we're seeing more and more of this in children.
So the definition of Type 2 Diabetes is a metabolic hyperglycemia
resulting from increased insulin secretion
and in the face of increased insulin resistance.
So two phenomenon: more secretion, more resistance.
The age of diagnosis of this problem is bimodal,
where we're seeing more and more children
between the age of 10 and 18 years developing the condition
and then also we're seeing it in older people.
Generally, all of these people have a problem
with excessive weight, although some do not.
So this has a prevalence of about
currently 0.4% of children in the United States.
It is strongly associated with obesity.
All ethnicities have a rate of Type 2 Diabetes but some more than others.
So there is a genetic predisposition
in addition to the environmental one that we see in this condition.
Females are 5 times more likely to have Type 2 Diabetes than males
and 75% of diagnosed children have a first or second degree
relative with Type 2 Diabetes.
So, the pathology of Type 2 Diabetes is complex and confusing
and a little bit different than Type 1.
So I'd like to go through it carefully with you now.
The hallmark of this problem is a peripheral insulin resistance.
In other words, insulin at the level of the cell
is not having a strong signal and telling that cell what to do as well.
This can be as a result of prolonged glucose exposure
and high insulin exposure and these cells are downregulating their response
or it can also be a result of training very early in life
of how those insulin receptors will respond to the presence of insulin.
Nonetheless, what happens is with this decreased insulin response,
one of those insulin receptors is found in the liver
and so that liver is not seeing the negative feedback loop
telling it to slow down in gluconeogenesis.
The liver continues to make more and more sugar
and thus these patients will have a high glucose level.
There are other tissues involved, too, though.
The fat cells also will have less of an insulin response.
This causes less fat storage and more production of free floating fatty acids
that are going through the blood.
These in turn, can cause damage and in particular,
cause damage to the pancreas and as they damage the pancreas,
they actually damage the pancreas's ability to secrete more insulin.
So you can see there's becoming a feedback loop
where there's less insulin responsiveness
but the damage is causing in the pancreas
an inability to create more insulin to overcome that insulin resistance.
Simultaneously, muscle cells are also getting damaged
and their less responsive nature to insulin
is causing them to have more protein breakdown
and more materials for which the liver can manufacture
an inappropriate quantity of glucose.
So it's a combination of decreased insulin presence from the pancreas
and a decreased insulin resistance.
All of these leads to hyperglycemia which is the hallmark of the disease.
So, risk factor for Type 2 Diabetes are obesity,
ethnicity, a family history of Type 2 Diabetes.
Maternal gestational diabetes can cause a baby to be large for gestational age or LGA
and those children are at risk for developing Type 2 Diabetes decades later.
So our children who have rapid weight gain in the first year of life
and those typically are the premature infants
or the small for gestational age babies.
This is really interesting
because what it implies is that during that first year of life,
children's insulin receptors are being somehow programmed
in terms of how responsive they would be to insulin.
If they're exposed to excessive amounts of insulin,
they're at increased risk for eventually
developing Type 2 Diabetes far down the road.
So what are the signs and symptoms of a child
who's presenting with early Type 2 Diabetes.
First off, because of the hyperglycemia, they will have the polys,
an increased risk of urination because of the osmotic effect of the sugar
and subsquently an increased thirst.
They may develop some weight loss.
This is from fat and protein catabolism that's happening.
These patients, remember, are overweight
and they start experiencing some weight loss.
We may see acanthosis nigricans.
This is a heralding skin finding of the metabolic syndrome.
I'll show a picture a little bit later on in the talk.
If they present later in disease after a prolonged period of hyperglycemia,
they have may have more substantial symptoms.
These can be irritability from the hypergylcemia.
Again, they can have polyuria but now in the phase of dehydration.
They may develop significant dehydration.
This can lead to altered mental status.
This can be confusing.
Remember, these are Type 2 Diabetes patients, not Type 1 Diabetes patients,
but nonetheless, they can present in diabetic ketoacidosis.
This is because, remember, they're having pancreatic cell damage
and they're making less insulin.
So they can totally present DKA and about a third of them will.
They also develop a problem that Type 1 Diabetes patients typically do not
which is Hyperglycemic Hyperosmolar Nonketotic Coma or HHNK.
This is a condition that's specific to Type 2 Diabetes.
Here's acanthosis nigricans.
This is a darkening of the skin that is seen typically over the back,
in the armpits and perhaps between the two breasts
which is commonly seen in patients
with the metabolic syndrome or
How do we diagnose Type 2 Diabetes?
First off, we can obtain a random glucose.
Any glucose level over 200 with signs or symptoms of Diabetes
such as polyphagia and polyuria, you've made a diagnois.
If you wish, you could do a more formal glucose challenge
with a fixed amount of glucose and then 2 hours later, obtain a glucose level.
If that glucose level is still high in patient
where you're concerned about diabetes,
it's entirely possible they have less insulin
and less ability to take care of the glucose problem
or alternatively, any glucose level in a fasting patient
that's over 126 is abnormal especially if you find it on more than 2 samples.
Lastly, because these patients do present later on,
you may simply measure a hemoglobin A1C
and that will be already elevated,
showing that this patient has for a long period of time
been exposed to high levels of glucose in the blood.
How do we manage Type 2 Diabetes?
First off and foremost, weight loss counseling and dietary help is indicated.
If patients can lose substantial amount of weight,
their diabetes improves markedly.
The first choice in children is different than the first choice in adults.
Some of the medicines in adults aren't even certified for use in children.
So our first choice in children is metformin.
If patients aren't responsidng to metformin,
we will move on to other therapies.
Metformin acts by increasing peripheral insulin sensitivity.
It also decreases hepatic glucose production
again through improving the sensitivity of those insulin receptors.
If patients are more severe, we will move on to insulin as well
especially if they are not producing enough insulin.
So, let's look carefully at the differences betweed diabetic ketoacidosis
which we see in Type 1 Diabetes or Type 2 Diabetes
and HHNK which we see in Type 2 Diabetes.
Remember, both of these conditions can happen in these patients with Type 2.
In DKA, they have a shortage of insulin.
This causes an increase in their ketones and dehydration is common.
These patients need an insulin infusion 0.1 units/kilo/hour.
In HHNK, they will develop severe dehydration
and their high glucose levels will be very high often higher than in DKA.
However, these patients do not have ketones. Remember it's nonketotic.
This may be caused by an underlying infection or some other problem.
What's key to keep in mind with HHNK is that it has a high mortality.
This is a very serious conditon and has to be maintained carefully.
So if you see a patient who has an altered mental status,
is profoundly dehydrated and they have Type 2 Diabetes,
it's the ketones or lack of ketones
this is gonna driving how you're gonna manage this patient
because you'll think of them as these two different presentations.
So let's review complications of Type 2 Diabetes.
We have acute complications, things that can happen right off the bat.
Examples are cerebral edema from diabetic ketoacidosis,
HHNK which can be life threatening or if they overtake their therapy,
for instance, they start on their insulin and take too high of a dose,
they may develop hypoglycemia and require resuscitation from that standpoint.
There are chronic complications that can happen as well
and these typically don't happen until adulthood.
Examples include nephropathy or kidney damage,
retinopathy or eye damage,
extremity infections such as the diabetic foot and a peripheral neuropathy.
We don't need to track these children with this disease
as carefully as adults do because these chronic complications
usually happen over years of exposure to high sugar levels.
So we do not need to send a 12-year-old with diabetes
to the eye doctor every year
but certainly we would do that for the older patient.
So, management of Type 2 Diabetes.
There're several key things to remember.
Your prognosis depends directly on your glycemic control.
If you can get that patient on a weight loss diet
and get their sugars under control, their long term prognosis is much better.
Follow their hemoglobin A1C to measure compliance
to continue conversations with them about how they're doing.
We want to see a low hemoglobin A1C level at their check-up visits.
Weight loss is a huge part of therapy and should be encouraged.
Get them eating better and get them to the gym
and in extreme cases, we may even consider weight loss surgery
which is a newly developing field in adolescent medicine.
People are looking more and more towards bariatric surgery
for certain categories of patients who fit very strict criteria for therapy.
That's all I have for you today about diabetes, Type 2 Diabetes in children.
There's another talk on Type 1 Diabetes which you can enjoy as well.
Thanks for your attention.