Type 1 Diabetes Mellitus – Hyperglycemia

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.