Lectures

Introduction & Graves' Disease – Hyperthyroidism (Thyrotoxicosis)

by Carlo Raj, MD
(1)

Questions about the lecture
My Notes
  • Required.
Save Cancel
    Learning Material 2
    • PDF
      Slides HyperthyroidismGravesDisease EndocrinePathology.pdf
    • PDF
      Download Lecture Overview
    Report mistake
    Transcript
    Hypothyroidism is where we are. Think about your patient walking through the door. Anxious, palpitations, sweating, eating quite a bit of food, but yet is not gaining weight. What we’ll take a look at with hyperthyroidism and then differentials for you; in other words, thyrotoxicosis. Something’s causing your thyroid gland to increase production of T3, T4. Maybe Graves’, thyroiditis, iodine-induced, choriocarcinoma… why? Human chorionic gonadotropin replaces TSH. Pituitary tumour, what are you releasing? TSH. Struma ovarii, where are you? Ovaries. How is that causing hyperthyroidism? Struma ovarii, it’s part of a female teratoma in the ovaries producing directly T3, T4. Topic, hyperthyroidism… patient has too much T3, T4 for whatever reason… look at the differentials. Exogenous… absolutely, maybe of an athlete that was… wishes to increase his or her athletic performance. Why not take thyroid hormones or perhaps even you have a patient that has hypothyroidism taking synthroid excessively resulting in hyperthyroidic type of symptoms. We’ll begin our discussion by looking at Graves’. Let me set this up for you. On your left, you see that grey blob? Hahaha, well, that grey blob; in other words, that’s your thyroid gland and on your basolateral membrane, you have a TSH receptor. Do you remember that? And that TSH receptor regulates whom? That’s important known as your sodium-iodide symport. As long as everything’s perfectly normal, you have a proper feedback mechanism in place. The TSH will bind to the receptor and you will have increased production of one lightning bolt. What does that lightning bolt represent? T3,T4. Just right so you can maintain normal basal metabolic rate… BMR versus Graves’, what’s happening? Oh, the TSH is being replaced by whom? An immunoglobulin antibody known as TSI, thyroid stimulating immunoglobulin. When you have an immunoglobulin that is then attacking in this case, remember...

    About the Lecture

    The lecture Introduction & Graves' Disease – Hyperthyroidism (Thyrotoxicosis) by Carlo Raj, MD is from the course Thyroid Gland Disorders.


    Included Quiz Questions

    1. Radiation
    2. Grave's disease
    3. Choriocarcinoma
    4. Struma ovaril
    5. Iodine induced
    1. TSI acting on the TSH receptor
    2. Overproduction of TSH
    3. Overproduction of TRH
    4. Up-regulation of TSH receptor
    5. Increased deiodinase activity
    1. Suppress TSH
    2. Suppress TSI
    3. Increase TRH
    4. Increase TSH
    5. Increase TSI
    1. Heat intolerance
    2. Exopthalmos
    3. Pretibial myxedema
    4. Thyroid acropachy
    5. Thyroid bruit
    1. Iodine-dependent goiter
    2. More frequent in women
    3. Associated with HLA-DR3 and HLA-B3
    4. Diffuse toxic goiter due to autoimmune production of TSI
    5. Exopthalmos due to autoimmune function not related to hyper-functioning thyroid

    Author of lecture Introduction & Graves' Disease – Hyperthyroidism (Thyrotoxicosis)

     Carlo Raj, MD

    Carlo Raj, MD


    Customer reviews

    (1)

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