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Regulation ADH and the Syndrome of Inappropriate Antidiuretic Hormone Secretion (SIADH)

by Carlo Raj, MD
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    We are into a topic where students tend to have once again, problems with organization, but likely have done the entire time the more organized you are with your thoughts, the more methodically you can go through the material and the more number of times you do this, then it becomes part of your reflex and this brings us to the concentration of urine. And with this lecture series, we will be getting into issues of ADH either, too much or too little. At first, let us say that you have a patient that is deprived of water. The best thing to do before you go through all of these chronological order, you want to pay attention or predict as to what you can expect in your patient. Once you have done that, then you take a look at the chronology and all of it will make sense. You deprive your patient of water. What does that mean to you? It means that your plasma osmolarity is going to increase, doesn't it? Once your plasma osmolarity increases, then the osmoreceptors by the hypothalamus will be triggered and you will be releasing your ADH. That ADH then runs down to the collecting duct that works to then insert these aquaporins via V2 receptors so that you can reabsorb that water, so that you can bring the plasma osmolarity back down to normal, right? So in essence, it is exactly what this illustration is showing you. Deprivation of water, increased plasma osmolarity. What happens next? Operative word, stimulation of your osmoreceptors. Next, you increase ADH. That ADH will then run down to the collecting duct, they'll work through V2 receptors. It will then insert the aquaporins so that you reabsorb water purely. As you do so, it then causes the urine osmolarity...

    About the Lecture

    The lecture Regulation ADH and the Syndrome of Inappropriate Antidiuretic Hormone Secretion (SIADH) by Carlo Raj, MD is from the course SIADH. It contains the following chapters:

    • Response to Water Deprivation
    • Regulation of ADH Secretion
    • Volume vs. Osmolarity
    • Significance of Clearance of Water
    • SIADH

    Included Quiz Questions

    1. Increased activation of osmoreceptors in the anterior hypothalamus
    2. Decreased thirst
    3. Increased plasma osmolarity
    4. Decreased urine osmolarity
    5. Decreased activation of V2 receptors in the distal tubules
    1. Urine osmolarity
    2. Plasma osmolarity
    3. NaK2Cl cotransporter suppression
    4. Insertion of aquaporins on principal cells of the collecting duct
    5. Urine volume
    1. Urea
    2. Potassium
    3. Calcium
    4. Sodium
    5. Chloride
    1. The ability to concentrate and dilute urine is related to the concentration of urea in the interstitium.
    2. Increased activity of the NaK2Cl cotransport in the thick ascending limb decreases the corticopapillary osmotic gradient.
    3. All are correct.
    4. Bartter syndrome results in the loss of diluting capability only.
    5. A decrease in urea permeability increases water reabsorption.
    1. Plasma hyperosmolality
    2. Plasma hypovolemia
    3. Plasma hypervolemia
    4. Plasma hypo-osmolality
    5. Plasma renin activity
    1. Angiotensin II induced ADH release
    2. Activation of osmoreceptors in the hypothalamus
    3. Plasma hypervolemia
    4. Increased systolic blood pressure
    5. Increased activation of systemic baroreceptors
    1. ADH secretion is inhibited by plasma hypo-osmolality.
    2. Plasma volume is tightly regulated by ADH release.
    3. ADH is released from the anterior hypothalamus in response to decreased plasma osmolality.
    4. Under normal conditions, Angiotensin II is the most important regulator of ADH release.
    5. ADH release is triggered by activation of osmoreceptors in the anterior pituitary.
    1. Thirst
    2. Urine osmolarity
    3. V1 receptor activation
    4. Urine volume
    5. Plasma osmolarity
    1. 275 mOsm/L
    2. 250 mOsm/L
    3. 290 mOsm/L
    4. 320 mOsm/L
    5. 300 mOsm/L
    1. All are correct.
    2. A given plasma osmolality will result in a higher ADH concentration.
    3. Plasma ADH concentration will increase.
    4. Plasma Angiotensin II concentration will increase.
    5. The range of osmolalities that will activate hypothalamic osmoreceptors will decrease.
    1. Increased ADH activity
    2. Loop diuretics
    3. Urine is isotonic to plasma
    4. Clearance of free water is zero
    5. All are associated with isosthenuria.
    1. Free water must be generated in the thick ascending limb.
    2. Urine must be hypertonic compared to plasma.
    3. Sodium reabsorption must be impaired.
    4. The countercurrent multiplier must be impaired.
    5. Diluting ability of the kidney must be impaired.
    1. It represents positive free water clearance.
    2. It may be induced by elevated plasma ADH concentration.
    3. It may be induced by severe hypovolemia.
    4. Concentration of the urine relies on the countercurrent multiplier.
    5. It may be induced by water deprivation.
    1. It is impossible to know without knowledge of lab results.
    2. Central diabetes insipidus
    3. Diabetes mellitus
    4. Autonomous release of ADH
    5. Nephrogenic diabetes insipidus
    1. Plasma ADH concentration is low.
    2. Hypertonic urine is produced inappropriately.
    3. It may be induced by damage to the pituitary gland.
    4. It will present with negative free water clearance.
    5. It is a paraneoplastic syndrome associated with small cell lung cancers.
    1. Nephrogenic diabetes insipidus
    2. Central diabetes insipidus
    3. Hypovolemia
    4. Renal papillary necrosis
    5. SIADH

    Author of lecture Regulation ADH and the Syndrome of Inappropriate Antidiuretic Hormone Secretion (SIADH)

     Carlo Raj, MD

    Carlo Raj, MD


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