Let’s talk about type I, epidemiology: early
Remember when I say early, we’re not talking
just infants, huh?
Even 20, 22, 24, young.
With type I, insulin or non-insulin dependent?
Good, insulin dependent.
Weight usually normal, they won’t be obese;
genetic predisposition, 50 percent amongst
HLA, definitely know about DQ, also know about
DR3 and 4, those links you definitely want
to know; pathophysiology, ah, autoimmunity.
So, apart from genetic, which could be a component,
What if you have autoimmune disease of the
thyroid, what’s that called?
I’m sorry, I can’t hear you.
Autoimmune disease of the adrenals, what’s
Autoimmune disease of the pancreas, what’s
Type I diabetes.
Put those together, give me diagnosis… polyglandular
endocrinopathies… do not forget that.
poly - many glands, these three… thyroid,
pancreas, adrenal pathology… endocrinopathy.
Carbohydrate intolerance with hyperglycemia.
Clinical PPP… polyphagia, polyuria, polydipsia;
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
Theoretically, if there was a time in which
you can actually measure your autoimmunity,
you’d find the phenomenon in type I diabetes
Some immunologists will call type I diabetic
a type II hypersensitivity.
Many immunologists will call type I diabetic
a type IV hypersensitivity.
Destruction of pancreatic beta cells resulting
in complete lack of insulin… insulitis.
It’s a reaction that’s occurring early
on, an autoimmune destruction of your beta
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.
Often detectable antibodies directed against
pancreatic islet cells.
You tell me what kind of hypersensitivity
That’s a type II.
And here, the anti-islet cell antibody here,
you must know the exact detail, a glutamic
acid decarboxylase 65… auto antibodies.
Patient require insulin at all times to prevent
hyperglycemia and therefore, not present with
That’s your patient, the bottom line, coming
through that door.
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.
In pathology, I will refer to type II hypersensitivity
against glutamic acid decarboxylase.
Which one of these is diabetic, which one
of these is not and what are we looking at?
On your left is non-diabetic.
You notice here in the pancreas and islet
cells, it’s all filled with these little
vesicles that contain insulin.
On the right, we got a diabetic.
You don’t find the same abundance of insulin,
No, you do not.
Welcome to diabetic on the right with decreased
concentration of insulin; on your left, non-diabetic
with normal amounts of insulin.
Where are you in the body?
In the pancreas.