Pathogenesis of Diabetes Mellitus – Hyperglycemia

by Carlo Raj, MD

Questions about the lecture
My Notes
  • Required.
Save Cancel
    Learning Material 2
    • PDF
      Slides HyperglycemiaDiabetesMellitus EndocrinePathology.pdf
    • PDF
      Download Lecture Overview
    Report mistake

    00:02 Let’s talk about the pathogenesis.

    00:05 This is the most important called non-enzymatic glycosylation.

    00:08 What does that mean? With all that glucose that’s circulating, it will then bind to protein.

    00:14 It will cause and wreak havoc up and down the body through depositing in the capillary membrane.

    00:21 When it does so, it will cause arteriolosclerosis.

    00:24 If it’s in the capillary, it will then cause non-enzymatic glycosylation therefore compromise proper exchange of nutrients.

    00:35 Altered carbohydrate metabolism and a second pathogenesis here is that you want to know about sorbitol and that’s because with all that glucose instead of going through the glycolytic pathway, might end up going through what’s known as aldose reductase.

    00:51 With that aldose reductase and sorbitol, specifically in the lens, remember what I told you? If you start a patient with diabetes over long period of time, what colour could that lens be? In Greek, cataract means waterfall.

    01:04 When you take a look at the waterfall, what colour is that water when it’s falling over the cliff? Opaque and white, that’s what cataract means in Greek, you find whiteness over the lens.

    01:17 That’s because sorbitol accumulating in the lens is going to cause waterfall, ha-ha, into the lens.

    01:23 In other words, increased osmotic pressure.

    01:27 Unregulated glucose intake by these tissues partially explains why these are the main diabetes mellitus targets.

    01:37 The increased glucose metabolized by the enzyme aldose reductase to sorbitol.

    01:43 That’s an important point, make sure you pay attention to that enzyme.

    01:48 Two major pathogeneses that I just walked you through.

    01:52 The most important would be non-enzymatic glycosylation neg or you might have heard of AGE, advanced glycosylate end-product, one and the same; capillary membrane destruction.

    02:04 Remember the arteriolosclerosis that you find with diabetes, that’s called hyaline arteriolosclerosis and do not forget about the sorbitol pathogenesis.

    02:15 Quickly, type I versus type II, a brief, beautiful summary of things that we’ve looked at.

    02:21 In your head now, you should have a firm understanding as to why these things are taking place.

    02:26 Type I weight please… normal or thin; type II overweight.

    02:32 First step of management type II diabetic, lose the weight.

    02:37 Age type I… young; by young we mean still less than 20 or 30 about 22, 23, but usually younger, but you never know.

    02:49 Remember the other differential that you want to keep in mind called unconventional or MODY in which is called Maturity Onset of Diabetes in Young, in which I told you to focus upon a deficiency in your glucokinase gene.

    03:02 If it’s type II a little bit older, 30, obese, insulin resistance.

    03:09 Type I with glycaemic pattern all over the place because of insulin pump; type II less variable.

    03:18 Insulin sensitivity… in type I, perfectly normal hence the insulin pump; in type II, if the receptors are not working, how in the world is insulin even being properly responded to? Insulin sensitivity reduced in type II.

    03:35 What about oral agents? Only effective in type II.

    03:41 Antibody status… in type I, remember the topic insulitis? I told you about your glutamic acid decarboxylase, a type II hypersensitivity, that’s autoimmunity, so antibody status positive in type I, negative in type II.

    04:00 Remember the autoimmune disease within the thyroid, the pancreas, the adrenal… polyglandular endocrinopathy.

    04:08 C-peptide level undetectable in type I.

    04:12 When would you see C-peptide level be high in type II, early or late disease? Early will be high, late undetectable or very, very slightly detectable.

    04:26 What does C-peptide mean to you? Endogenous production of insulin.

    04:32 Family history… strong family history in type II.

    04:37 Other autoimmune disorders for sure in type I and I walked you through all of these, your patients here tend to be more of females.

    About the Lecture

    The lecture Pathogenesis of Diabetes Mellitus – Hyperglycemia by Carlo Raj, MD is from the course Pancreatic Disease & Diabetes.

    Included Quiz Questions

    1. Aldose reductase
    2. Insulin
    3. Glycosylation
    4. Lactate dehydrogenase
    5. Glucose oxidase
    1. Unregulated glucose uptake by nerves leading to increased sorbitol
    2. Capillary basement membrane thickening
    3. Arteriosclerosis
    4. Decreased levels of of aldose reductase
    5. NEG
    1. Highly variable glycemic patterns
    2. Insulin resistance
    3. Obesity
    4. High C-peptide levels
    5. A first degree relative with the disease

    Author of lecture Pathogenesis of Diabetes Mellitus – Hyperglycemia

     Carlo Raj, MD

    Carlo Raj, MD

    Customer reviews

    5,0 of 5 stars
    5 Stars
    4 Stars
    3 Stars
    2 Stars
    1  Star