00:01
Let’s talk about type I, epidemiology: early
age.
00:05
Remember when I say early, we’re not talking
just infants, huh?
Even 20, 22, 24, young.
00:12
With type I, insulin or non-insulin dependent?
Good, insulin dependent.
00:19
Weight usually normal, they won’t be obese;
genetic predisposition, 50 percent amongst
twins.
00:28
HLA, definitely know about DQ, also know about
DR3 and 4, those links you definitely want
to know; pathophysiology, ah, autoimmunity.
00:41
So, apart from genetic, which could be a component,
autoimmune disease.
00:45
What if you have autoimmune disease of the
thyroid, what’s that called?
I’m sorry, I can’t hear you.
00:53
Good, Hashimoto.
00:54
Autoimmune disease of the adrenals, what’s
that called?
Addison’s.
00:59
Autoimmune disease of the pancreas, what’s
this called?
Type I diabetes.
01:03
Put those together, give me diagnosis… polyglandular
endocrinopathies… do not forget that.
01:11
Polyglandular?
poly - many glands, these three… thyroid,
pancreas, adrenal pathology… endocrinopathy.
01:23
Carbohydrate intolerance with hyperglycemia.
01:26
Clinical PPP… polyphagia, polyuria, polydipsia;
acute complication…
DKA.
01:35
Now, with the autoimmune disease, I told you
that for the most part, your patient walking
through that door with type I diabetes doesn’t
have insulin.
01:46
Theoretically, if there was a time in which
you can actually measure your autoimmunity,
you’d find the phenomenon in type I diabetes
called insulitis.
01:59
Some immunologists will call type I diabetic
a type II hypersensitivity.
02:06
Many immunologists will call type I diabetic
a type IV hypersensitivity.
02:14
Destruction of pancreatic beta cells resulting
in complete lack of insulin… insulitis.
02:17
It’s a reaction that’s occurring early
on, an autoimmune destruction of your beta
islet cells.
02:24
Immune-mediated process, type II, type IV,
they will not have you choose between the
two, but usually, you-you’ll be referring
to type IV.
02:33
Often detectable antibodies directed against
pancreatic islet cells.
02:36
You tell me what kind of hypersensitivity
that is.
02:38
That’s a type II.
02:41
And here, the anti-islet cell antibody here,
you must know the exact detail, a glutamic
acid decarboxylase 65… auto antibodies.
02:54
Patient require insulin at all times to prevent
hyperglycemia and therefore, not present with
DKA.
03:01
That’s your patient, the bottom line, coming
through that door.
03:05
Theoretically, what happened prior… an autoimmune
destruction of a beta islet cell, what do
we call this?
Insulitis, either type IV or type II hypersensitivity.
03:15
In pathology, I will refer to type II hypersensitivity
against glutamic acid decarboxylase.
03:26
Which one of these is diabetic, which one
of these is not and what are we looking at?
On your left is non-diabetic.
03:35
You notice here in the pancreas and islet
cells, it’s all filled with these little
vesicles that contain insulin.
03:42
Hmm.
03:43
On the right, we got a diabetic.
03:45
You don’t find the same abundance of insulin,
do you?
No, you do not.
03:50
Welcome to diabetic on the right with decreased
concentration of insulin; on your left, non-diabetic
with normal amounts of insulin.
04:00
Where are you in the body?
In the pancreas.