by Carlo Raj, MD

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    What’s adrenal gland pathology? Our focus here will be aldosterone, hyper and hypo. I highly recommend that you go back and review your physio because I will go through this rather quickly, expect you to know the basic functioning of aldosterone so that we can walk through the path effectively. Our topic here is hyperaldosteronism. Before we begin, you automatically start thinking about what’s going on with your patient. There’s going to be increased reabsorption of sodium, doesn’t matter if it’s primary or secondary. In addition, there’s increased reabsorption of water, thus you’ll have increase in blood pressure. Next, what does aldosterone do with potassium? It gets rid of it, you secrete it. If there’s too much aldosterone, either primary or secondary, your patient is suffering from hypokalemia, your potassium level will be less than 3.5. Next, what do you do with hydrogen? Or what does aldosterone do with hydrogen? It secretes it, it gets rid of it. If you get rid of hydrogen, your PH is going to increase, your patient is in a state of alkalosis. What is primary and secondary? Well, primary hyperaldosteronism will be a specific tumour in the zona glomerulosa that is only producing aldosterone… welcome to Conn’s syndrome. What is it going to do to your blood pressure? It is going to increase it. Now, be careful, this blood pressure that you’re increasing, obviously called hypertension, is it primary or secondary, do you remember? Secondary. In the United States, a very common cause of secondary hypertension is primary hyperaldosteronism. Interesting, isn’t it? Do not ever forget that. Bilateral adrenal hyperplasia, what’s happening here? Well, here, you might have increased production of aldosterone by your adrenal cortex, specifically the zona glomerulosa. If you were to find increased levels of aldosterone primarily, what is its feedback...

    About the Lecture

    The lecture Hyperaldosteronism by Carlo Raj, MD is from the course Adrenal Gland Disorders.

    Included Quiz Questions

    1. Hyponatremia
    2. Hypertension
    3. Metabolic alkalosis
    4. Hypokalemia
    5. Decreased renin
    1. Renal ischemia
    2. Conn's syndrome
    3. Aldosterone producing adenoma
    4. Bilateral adrenal hyperplasia
    5. Adrenal carcinoma
    1. Edema
    2. Secondary hypertension
    3. Hypokalemia
    4. Alkalosis
    5. Hypernatremia
    1. Non-suppressed PAC after IV saline solution
    2. Non-suppressed 8 hour urine aldosterone after salt loading
    3. Non-suppressed PAC after diuretic loading
    4. Suppressed plasma renin activity over 20 ng/dL
    5. PAC over 15 ng/dL
    1. It antagonizes aldosterone
    2. It increases potassium excretion
    3. It decreases sodium excretion
    4. It decreases plasma renin
    5. It down regulates aldosterone receptors

    Author of lecture Hyperaldosteronism

     Carlo Raj, MD

    Carlo Raj, MD

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