Introduction to Cortisol and Hypercortisolism – Adrenal Gland

by Carlo Raj, MD

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    The topic is hypercortisolism, a very important topic for us. A very important topic because Prednisone, a type of cortisol, is administered excessively in practice. But, before we get into any of that though, we will first take a look at the normal functioning of your cortisol so that when we take a look at the pathology, it will all come together. The normal effects physiologically of cortisol on metabolism as a stress hormone, we’ve talked about this plenty, is to make sure if one is in a state of fasting that cortisol will do everything in the power to increase the amount of glucose in circulation. If it comes down to what is happening to uptake of glucose by a tissue, understand that cortisol decreases the uptake of glucose, thus [Inaudible 00:00:56] glucose in circulation. If you are thinking about the balance in biochemistry between glycolysis and gluconeogenesis, it obviously will lean towards gluconeogenesis resulting in more of a “hyperglycemic state”. Next, cortisol, it permits for redistribution of fat from the legs to the trunk. Doesn’t it sound like an awful lot like Cushing, which we will get into later on in our discussion, where you have heard of trunk obesity and you have heard of wasted extremities in Cushing? Well, cortisol seems to-seems to do that on a physiologic basis, visceral adiposity. Cortisol causes bone demineralization. In other words, it is going through a move, your hydroxyapatite from the bone, bone reabsorption resulting in excessively look for, once again, long term corticosteroid use resulting in premature osteoporosis. Immunologically, cortisol has interesting effects. It could attenuate immune response. Now, this is rather confusing to some, but will bring clarity here, huh! If it is cortisol and you are dealing with acute inflammation, it causes demargination of your neutrophils. What...

    About the Lecture

    The lecture Introduction to Cortisol and Hypercortisolism – Adrenal Gland by Carlo Raj, MD is from the course Adrenal Gland Disorders.

    Included Quiz Questions

    1. Decreased gluconeogenesis
    2. Hyperglycemia
    3. Visceral adiposity
    4. Bone resorption
    5. Decreased glucose uptake into cells
    1. Lymphopenia
    2. Increased neutrophilic response
    3. Increased plasma cell differentiation
    4. Autoantibody production
    5. Leukocytosis
    1. Serum cortisol levels peak in the morning and decrease during the day
    2. Serum cortisol levels increase slowing during the day
    3. Serum cortisol levels decrease slowly during sleep
    4. Serum cortisol levels sharply decrease from a peak at midday
    5. Serum cortisol levels peak in the morning and in the middle of the day
    1. Cortisol binds to it's receptor on the nuclear membrane in order to enter the nucleus
    2. Lipid soluble- diffuses across membrane
    3. Activation of cytoplasmic cortisol receptors involving release of a heat shock protein
    4. Binds to hormone response element of DNA
    5. Transcription factors are produced that are translated into proteins that effect cell function

    Author of lecture Introduction to Cortisol and Hypercortisolism – Adrenal Gland

     Carlo Raj, MD

    Carlo Raj, MD

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