Now, you know I'm a sucker for physiology, so before we go any further in this lecture,
we've got to breakdown what goes on with diabetes and the pregnancy,
and it gets a really fancy name called diabetogenic effect.
I think they should name that a dance, like right?
Diabetogenic effect, okay? So let's talk about what it is.
So, what you'll see here is that we have a placenta that's producing hormones,
and specifically, we're thinking about estrogen, cortisol, human placental lactogen.
Now, human placental lactogen is also known as HCS,
or Human Somatomammotropin, another word,
I don't have a dance for that, but it does work here.
So those products are going to be produced by the placenta.
They have a lot of responsibilities.
So what do those hormones do in terms of gestational diabetes?
Well, the baby doesn't have a 24-hour McDonald's in-utero
so they're dependent on the glucose from the maternal bloodstream to go through the placenta,
come into the fetal bloodstream so they have something to eat, you know, like an extra large fry.
So, what happens when we release HCS and cortisol and estrogen,
is that it causes some insulin resistance in the pregnant person.
That way the cells don't use up all the glucose and there's some left for the baby.
Now, the problem is, is that when we do that and the insulin isn't working well
and we have some insulin resistance from the cells, if it overshoots,
then there'll be too much glucose left in the maternal bloodstream
and that will make the maternal bloodstream really hyperglycemic, so that's the diabetogenic effect.
So let's superimpose what's going on with our insulin needs during the pregnancy
so we know what the diabetogenic effect is. So, let's look at our needs.
So on this graph, what you see is the level of insulin
and the insulin requirements over the duration of pregnancy, so over the weeks.
So you can see on this data points that we're looking at the time
from conception all the way to after delivery,
so you see that's represented by the dots, and the orange line shows how the insulin needs change.
So at conception, during that first trimester which ends at the end of 12 weeks,
you see the insulin needs actually drop,
and then after 12 weeks you start to see the insulin needs increase
all the way to about 36 weeks where it levels off.
And then watch what it does after delivery - it just drops almost straight down like a cliff.
This is going to be really important as we get through the lecture
so make sure you sort of have this seared in your brain.
So, now, if we have someone who has normal insulin resistance,
that's a normal part of pregnancy, so that the baby has glucose, then our graph looks like this.
Now, if we have someone with gestational
diabetes and they have an impairment, then
this is what their graph looks like.
Ok. So you can see that the change is
absolutely affected by the pregnancy and the
gestation. So let's summarize again what the
effects of pregnancy are on diabetes.
So an altered carbohydrate metabolism is
exactly what the diabetes effect is.
So that's put a little more simply.
We also have to remember that we have
impaired insulin action.
So the insulin remember that's the key that
lets the glucose go into the cell is
slightly altered as an effect of the
pregnancy. A lot of that is normal.
When we get to gestational diabetes, it
overshoots, which makes it pathologic and a
complication. Remember what that graph
showed? The insulin requirements increase as
the pregnancy advances, so that happens at
the end of the first trimester, all the way
up to about the time of delivery, around 36
So let's talk about some of the other
effects of the pregnancy on diabetes.
So when we think about someone who might
have a pre-existing disease, we know that
vascular damage is something that can happen
Pregnancy actually accelerates those
So someone who might have pre-existing
diabetes actually can find that those
consequences are sequelae happen a little
faster while they're pregnant.
Also, we have a situation where we have
Now this is diabetic ketoacidosis or DKA,
and we're going to talk about that a lot
more in just a second.
And finally, when we think about someone who
has diabetic ketoacidosis, it can cause more
complications than just on the person with a
diabetes because we have Clitus inside the
body and so we can also have fetal
complications as a result of that.
So I want to spend some time breaking down
this accelerated starvation and reminding
you of what DKA looks like.
So I have a slide for that and let's work
through it. So when we think about DKA, we
know that the pancreas is responsible for
That's our key.
So our glucose is actually floating through
our vessels and the insulin is going to
allow that glucose to enter the cell.
Well, someone with diabetes, whether it's
pre-existing or whether it's gestational
onset, they're going to have an issue with
getting the glucose into the cell.
So remember, we have insulin resistance and
some degree of change in our ability of our
insulin to open up the cells.
So how does the body respond?
It's starving, right?
It needs energy, so it's going to use the
And so when it uses the fat cells, it needs
a little bit of help.
And that help comes from the liver.
So the liver is actually going to convert
those glucose cells that are floating around
in abundant supply into ketones.
And so those ketones are acidic.
So it's actually going to change the acidity
of the blood.
And that's not so great.
And that leads to acidosis, which is almost
like filling the bloodstream full of poison.
So too many ketones can actually lead to a
coma or even death.
So that's DKA.