QUESTIONS

1. What is the difference between primary & secondary hypoadrenocorticism?
    
2. Which layer of the adrenal cortex produces aldosterone?
    
3. What organs besides the kidneys does aldosterone act on to promote Na+ retention & K+ excretion?
    
4. The renal area that reads volume depletion is called the _______________.
   
   Cells in this area release _______________ which causes the liver to release _______________.
   
   This substance is converted to _______________ in the lungs.  This last substance is a strong stimulator of aldosterone release & a powerful vasocontrictor.
    
5. True or False:  Higher levels of K+ stimulate aldosterone release.
    
6. What CBC changes might one expect in hypoadrenocorticism?
   
7. What EKG changes are associated with hyperkalemia?
    
8. Why might a patient with hypoadrenocorticism have unconcentrated urine?
    
9. The usual clinical picture of the Addisonian patient is:
   a) greater than 8 yrs old or less than 8 yrs old?
   b) male or female?
    
10. What diagnositc tests might be alternatives to the ACTH stim test in the diagnosis of hypoadrenocorticism?
     
11. What is the most common endocrinopathy to accompany
    hypoadrenocorticism?
     
12. What does DOCP stand for?
    
    
    
    
     

ANSWERS

1. In primary Addison's the pituitary is normal & the adrenal cortex (usually all layers) is destroyed.  Usually, the adrenal cortex is destroyed by a lymphoplasmacytic infiltration.
   
   In secondary Addison's, the pituitary is not secreting ACTH due to some primary pituitary disease.  8-10% of Addisonians fit into this group.  Since the renin-angiotensin system is OK, you will not see electrolyte imbalances in these animals.
   
   There is also "secondary iatrogenic" Addison's, which comes in two flavors:  OP'ddd administration & exogenous corticosteroids.  In the former, the adrenal cortex is destroyed utterly & you get signs similar to primary Addison's.  In the latter, you should still get ok electrolytes because the zona glomerulosa can still respond to the renin-angiotensin system.
   
   
   
   
    
2. Aldosterone comes from the zona glomerulosa.  I find it easier to remember which comes from what layer in a very silly manner which I will now share.  "Glomerulosa" sounds like something that would affect the kidney so that must be the layer that goes with the mineralocorticoids.  "Reticularis" means network pattern, which is probably evident histopathologically or something -I'm guessing how it got its name.  Anyway, reticularis is the innermost later & it produces sex steroids.  I imagine sexy underwear with a network print pattern & in this way I can associate sex, inner-most (underwear is one's innermost clothing layer)  & reticularis. Fasiculata is the leftover one.
   
   
   
   
    
3. Aldosterone mostly acts on the proximal & distal convoluted tubules.  It also acts on the salivary gland, the intestinal mucosa, & the sweat glands.
   
   
   
   
    
4. The juxtaglomerular apparatus, renin, angiotensin I & angiotensin II.  Child's play for any one who can keep fT4, rT3, etc straight.
   
   
   
   
    
5. True.  Aldosterone is released in response to elevated K+ independently of ACTH or the renin-angiotensin sytem.
   
   
   
   
    
6. 30% of Addisonians have normocytic normochromic anemia (apparently cortisol facilitates hematopoesis) but this is frequently masked by dehydration.  Another clue is the lack of a stress leukogram in an obviously distressed patient.  Eosinophilia & leukocytosis also are reported.
   
   (Just a note to be stuck in somewhere, 30% of Addisonians have hypercalcemia)
   
   
   
   
    
7. a) Bradycardia (in 35% Addisonian dogs & 20% Addisonian cats)
   b) Mild elevations of K+ - tented T wave
   c) Shortened Q-T interval
   d) Moderate elevations of K+ - prolonged P-R interval
   e) Widened QRS
   f) Severe elevations of K+ - loss of P wave (like > 7.5)
   g) Dropped ST segment
   
   Other EKG abnormalities can be seen that have nothing to do with hyperkalemia.
   
   
   
   
    
8. Urine might not be concentrated for many reasons.  Addisonians are often PU/PD  & thus could have a medullary wash out.   They sure could have chronic Na+ depletion & impaired water reabsorption,too.  And renal blood flow will be reduced.
   
   
   
   
    
9. Classical clinical picture = female dog less than 8 yrs.  In cats, there is no sex predisposition & the disease has been reported in about all ages.  The standard poodle may be predisposed & one should note that the female predisposition is typical of immune-mediated disease.
   
   
   
   
    
10. Other tests (if you want to punish yourself) are:
    urinary 7-hydroxycorticosteroid determination (you need a 24 hour urine collection)
    OR
    endogenous ACTH level which is a very sensitive test & many labs don't even run it.  Cortisol levels are stable at room temp for up to 5 days so I think the ACTH stim will be popular for a while yet.
    
    The way endogenous ACTH works here is that in primary hypoadrenocorticism, ACTH will be very very high as it tries to turn on a non-responsive adrenal cortex.  In secondary hypoadrenocorticism, ACTH will be low or non-existant (as this is a pituitary problem.)
    
    
    
    
     
11. The most common accompanying endocrinopathy is hypothyroidism.  These multi-endocrine problems are thought to be related to a common under-lying autoimmune problem.
    
    
    
    
     
12. DOCP= deoxycorticosterone pivalate.