00:01
Secondary, what does this mean to you?
You’re developing hyperglycemia due to other
endocrinopathies.
00:10
What does Cushing’s mean to you?
Too much cortisol.
00:13
What is that going to do?
It’s going to increase gluconeogenesis and
it will then impair peripheral utilization
resulting in hyperglycemia.
00:23
What’s the hormone in acromegaly?
A growth hormone.
00:26
What does that do?
It brings about anti-insulin like effect,
decreased peripheral utilization.
00:34
What if you had a patient that has MEN type
I and has prolactinoma, has hypercalcemia
and also has… have the skin issues maybe
down in the legs and such known as necrolytic
migratory erythema, a glucagonoma.
00:49
All of these are hyperglycemic secondary type,
there was an underlying issue that resulted
in secondary diabetes mellitus.
01:00
Down syndrome is a big one, genetically that
you want to keep in mind… trisomy 21.
01:06
Hemochromatosis… now, completely all the
different organs that are commonly affected
in hemochromatosis - pancreas obviously; number
two skin, bronzing; number three liver, fibrosis…
gone.
01:25
Patient may die of heart disease… hemochromatosis.
01:29
Topic here, however, secondary diabetes mellitus
being caused by hemochromatosis.
01:37
Chronic pancreatitis, pancreatic carcinoma…
Earlier we had a discussion of pancreatic
islet cell tumours.
01:48
Is that what this is?
No.
01:51
So, when you do pancreas, forever more you
divide it into endocrine and exocrine… endocrine,
exocrine.
01:59
You divide it so that you can understand the
physiologic aspects of endocrine-exocrine.
02:04
You divide this so that you understand the
pathologic effects.
02:07
Now, granted we’re doing endocrine pathology,
but if your patient, for example, you know
of Steve Jobs.
02:15
He died of pancreatic cancer.
02:17
He died however of pancreatic adenocarcinoma.
02:22
When we did our islet cell tumours of the
pancreas, what were they again?
Insulinoma, glucagonoma, VIPoma, somatostatinoma…
completely different discussion.
02:33
This is pancreatic adenocarcinoma, this is
the one that you know and which we have our
tumour marker called CA 19-9.
02:42
You know about the molecular mechanism called
KRAS?
Ah, are bells ringing?
I hope so.
02:49
In diabetes mellitus could be a presenting
sign because of extensive pancreatic damage
in pancreatic adenocarcinoma.
02:57
In gestational diabetes, now initially, gestational
pregnancy, there’s going to be a hormone
that the placenta releases.
03:07
It’s called human placental lactogen.
03:11
That human placental lactogen works like your
growth hormone, it decreases the peripheral
utilization of glucose.
03:16
Therefore, there should be high levels of
glucose during pregnancy in the mother, no
doubt.
03:23
That glucose from the maternal circulation
is passing through the placenta to the foetus,
therefore the baby’s growing… the foetus
is growing.
03:33
Now, you’re in third trimester… third
trimester and you find hyperglycemia in your
pregnant woman in addition ultrasound of the
pregnant woman shows a large foetus, why?
Macrosomia, why?
Because now the mother, the pregnant woman
has all these glucose that’s being constantly
fed, fed, fed, fed, fed to the foetus.
04:01
May I ask a question?
Is the foetus capable of producing its own
insulin?
Oh, absolutely.
04:08
What kind of hormone is the insulin, anabolic
or catabolic?
Why does an athlete perhaps take insulin or
glucagon?
Anabolic, right?
All that anabolism taking place in the foetus…
macrosomia.
04:23
Now, this is the problem, if that hyperglycemia
continues in the pregnant woman, the delivery
of the child takes place and that’s not
our discussion right now, but that will be
another discussion later.
04:38
But, understand that with gestational diabetes
mellitus, it predisposes that mother to type
II diabetes years down the road.
04:50
Increased birth weight, associated hyaline
membrane disease.
04:53
We don’t really call it this anymore, we
call what’s known as neonatal respiratory
distress syndrome NRDS, we’ll talk about
that later.
05:03
That’s because with all that insulin, that
might be present in that foetus that you might
be releasing… decreasing the cortisol and
therefore, the lecithin which is a surfactant
is not being produced properly, may result
in NRDS.
05:20
You need to put things together here, these
are not just bullet points.
05:24
A lot of important things going on.
05:26
The infant that’s being born here with all
that insulin, wow, the number one step that
you’re worried about is with all that insulin
that just… that newborn just came out of
the vaginal canal is going to suffer from
hypoglycemia especially when you cut off
the umbilical cord because now the glucose
is no longer being fed to the foetus or the
newborn and with all that insulin that the
newborn has, you’re worried about hypoglycemia
in that newborn called rebound effect… big
time.
05:59
Very important section here with gestational
diabetes, we will revisit all these, don’t
worry.
06:05
A few times in pulmonology, we’ve seen it
and in female reproductive pathology.