Diabetes Insipidus
Picture
Picture
 Growth
Hormone
 Addison’s
Disease
 Hyperthyroidism
 Pheo - 
chromocytoma
 Hypothyroidism
 Diabetes
Mellitus
 Cushing’s
Disease
 Diabetes
Insipidus

QUESTIONS

  1.   Where are ADH & Oxytocin manufactured?
     
  2. What stimulates the release of ADH?
     
  3. Where in the nephron does ADH act?
     
  4. How does pyometra cause PU/PD?
     
  5. What would be a water consumption rate compatible w/PUPD?
     
  6. What is the difference between Osmolality, Osmolarity, & Osmotic Pressure?
     
  7. What is the Hickey-Hare test?
     
  8. How would you use pitressin tannate in oil to treat central DI?
     
  9. How would you use DDAVP to treat central DI?
     
  10. Humans w/central DI use Diapid nasal spray (Lysine 8 vasopressin).  Why don’t we use it for animals?




     

ANSWERS

  1. Did you think that ADH & Oxytocin were manufactured in the posterior pituitary gland?  Shame on you.  Both are manufactured in the supraoptic & paraventricular nuclei of the hypothalamus.  Neurophysins which are also made there bind them (a  different neurophysin for each hormone) & the whole complex is transported down nerve tracts.  When the nerve tracts are stimmulated, the complex is exocytosed, the neurophysin comes off & the hormone is on the road.




     
  2. The neurons carrying the neurophysin/ADH complex respond to osmolality changes & baroreceptor changes.  Osmolality changes as slight as 1% change can stimulate ADH release but this depends on what electrolytes are causing the change.  For example, sodium & mannitol work but glucose & urea don’t affect the neurons) 

    Baroreceptors are located in the atria & aortic arch & info ascends to the brain via the vagus & glossopharyngeal nerves.  This info also stimulates ADH release.

    (Note, some fibers from the hypothalamus carry ADH to other areas besides the post pit. We don’t know the full implications of this yet.)




     
  3. ADH acts on the distal tubule & collecting ducts.  We’ll go over the nephron in annoying detail when we get to the renal section of this course.




     
  4. E. coli endotoxin causes a reversible renal tubular insensitivity to ADH. Th is would be an example of secondary nephrogenic diabetes insipidus.  Cushings’ disease, acromegaly, hyperthyroidism, hypokalemia are all examples of secondary nephrogenic diabetes insipidus.




     
  5. Eddie Feldman’s book lists 100 cc/kg per day as in the definite PU/PD range.




     
  6. Okay, let’s go back to high school for a moment.  Osmosis is the process by which water moves across a membrane into a compartment containing a solute.  Osmotic pressure is the tendency of the solvent to cross the membrane. Osmotic pressure is the force drawing the solvent from the dilute side to the concentrated side.

    An osmole is an amount of solute which when dissolves in solvent dissociates into one mole of particles.

    Osmolarity is mOsm/L of solution
    Osmolality is mOsm/kg of solvent

    Tonicity describes osmotic pressure relative to plasma.  Hypertonic is more concentrated than plasma & hypotonic is less concentrated than plasma.

    Osmolality of plasma is increased in diabetes insipidus as water is being lost in a big way.




     
  7. The Hickey-Hare test is part of the screen test they use in the porno industry.  No, it isn’t.  It is a test for central DI that can be used when the water dep. test is not diagnostic.  It used to be the main test before the water dep. test came out.

    First, you give water by stomach tube  & then you collect urine over the next 30 min noting the urine production rate.

    Next,you give hypertonic saline & collect urine.  You ought to get a >25% reduction in urine volume after giving hypertonic saline if the pituitary/renal axis is OK.




     
  8. You gotta teach the owner how to give IM injections if you want to go this route.  The pitressin tannate must be warmed & shaken (not stirred :) & injections are given every 1-3 days.  The aqueous solution only lasts a few hours so you can’t really use it.




     
  9. DDAVP is desmopressin, a synthetic version of ADH.  It has no pressor activity & seems to actually have a greater affinity for the ADH receptor than does real ADH.  It is a nose drop but in animals you give in the eye.  A coupleof drops lasts 8-24 hours.




     
  10. It is $$$ & only lasts 2-6 hours.  Forget it. 
    (Though those who do Life Extension use Diapid as a memory enhancer - just a thought as we all study madly for the test.)