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Adrenal

Adrenal gland: cortisol or cortisone and the mineralcorticoids like aldosterone are produced by the outer, or cortex area (shown at right).

Addison's disease, also known as hypoadrenocorticism, is a chronic condition in which the adrenal glands [1] produce insufficient cortisol. It is the opposite of Cushing's disease, where too much cortisol is produced. The adrenal glands produce two types of hormones; we're most familiar with the glucocortoid ones, such as cortisone.[2][3] Cortisol and other hormonal levels rise during anger or fear, stress or injury. The term "getting one's adrenalin going" in response to these situations applies to the natural response a healthy body has to them. Those with faulty adrenal glands don't produce enough cortisol to allow the body to respond properly.

The other adrenal hormones, known as mineralcorticoids, are what keeps the system in balance regarding proper amounts of salt, potassium,[4][5][6] and water in the body.[7] Imbalances of these keys to life can have grave consequences also. [8][3]

As in diabetes, the problem is not enough--not enough of the hormones the adrenal glands produce necessary for proper bodily function. Also like diabetes, Addison's is an endocrine disease, and its sufferers are at risk of developing neuropathy and some eye-related diseases.[9]

SymptomsEdit

Addison's Disease in Dogs

The symptoms range from poor appetite, lethargy. weight loss, and can include shaking and/or shivering, polyuria, [10][11] hypoglycemia, [12] diarrhea, [13] and vomiting. They are not always specific.[3] [14] Many are similar to those of other diseases, and are the reason why Addison's is known as "The Great Mimic" or "The Great Imitator".[3][15][6][16]

Untreated Addison's disease, like untreated diabetes, can be fatal. It is also like diabetes in the respect that the disease is often well-advanced by the time symptoms occur.

It is possible to see no symptoms of Addison's disease until 90% of the adrenal cortex is no longer functioning. [15][17][3]

Addisonian Crisis/Addisonian ShockEdit

Those with untreated Addison's disease are at risk for what's known as an Addisonian crisis, where, possibly under any stressful situation, they go into shock because of the lack of these hormones to regulate the body. This is a life-threatening situation. [18][19][20]

The diagnosis of about 35% of all canine Addison's patients begins when they are brought to the hospital or clinic in Addisonian crisis. In crisis, the shock symptoms mimic those of "classic" shock; Addisonian shock also includes a slow heart rate due to high potassium blood levels. [15]

While most commonly used steroids will compromise an ACTH test, dexamethasone[21][22][23][24] may be used in the case of a Addisonian emergency without alteration of the test results.[25]


CausesEdit

The cause(s) of Addison's are not always clear--most are attributed to an overactive immune system or are simply idiopathic--no cause able to be found.

Abrupt Withdrawal of Steroids [26]
Layer Produces
Zona glomerulosa Mineralcorticoids (aldosterone)
Zona fasciculata Glucocorticoids (cortisol)
Zona reticularis Sex steroids (androgens)

 Addison's can result when there has been long-term steroid  therapy and the medication is suddenly stopped. [15][27]

 Use of steroids means that the adrenal glands do not function fully during the course of the medication. The body senses  the levels of the exogenous steroids in the system and  therefore does not signal for additional production of it. [14]

During this time, the adrenal glands go into a type of "hibernation" because the steroid medication is literally doing  their work for them. In pets and people, the usual protocol for stopping steroid medications is not to eliminate them  suddenly, but to withdraw from them gradually in a "tapering off" process. Doses become less and less frequent prior to the planned cessation of the medication.[14]

This tells the body to signal the "hibernating" adrenal glands that it's time to go back to producing adrenal hormones. Simply put, the "sleeping" adrenal glands are not able to be "awakened" in cases like this, and the body will need to have its adrenal glucocorticoid hormones replaced by medication; the mineralcorticoids are not affected by this and do not need replacement therapy.[14][19]

There are times when the adrenal glands must either be removed or made to stop functioning with medication. This is sometimes neccessary in the treatment of Cushing's disease, which occurs when the adrenal glands are overactive. The loss of the adrenal glands means that the patient now has Addison's disease and must take medication to replace the hormones the adrenal glands formerly supplied. [28]

Typical and atypical Addison'sEdit

The adrenal outer layer, or cortex, has three layers; each produces a specific type of steroid.[14]

Adrenal Cortex Layers [26][28]
Layer Produces
Zona glomerulosa Mineralcorticoids (aldosterone)
Zona fasciculata Glucocorticoids (cortisol)
Zona reticularis Sex steroids (androgens)

In typical Addison's, all of these layers stop functioning; the problem is with the adrenal gland. But in atypical Addison's, the problem is not in the adrenal gland but in the pituitary gland. The gland produces a hormone, ACTH, (adrenocorticotropic hormone), that signals the Zona fasciculata and Zona reticularis to produce their steroids. When the pituitary is unable to produce ACTH, there is nothing to activate the Zona fasciculata and Zona reticularis and they stop production of their respective hormones. The Zona glomerulosa remains able to produce a normal amount of mineralcorticoids because it is not controlled by ACTH.[29] An atypical Addison's patient does not face the risk of an Addisonian crisis and only needs to have medication to replace the glucocorticoid steroid cortisol.[14][19]

Typical Addison's [14]
Layer Produces
Zona glomerulosa Mineralcorticoids (aldosterone)
Zona fasciculata Glucocorticoids (cortisol)
Zona reticularis Sex steroids (androgens)
Atypical Addison's [14]
Layer Produces
Zona glomerulosa Mineralcorticoids (aldosterone)
Zona fasciculata Glucocorticoids (cortisol)
Zona reticularis Sex steroids (androgens)


In some dogs with atypical (secondary) Addison's, the disease progresses to the point where mineralcorticoid replacement is necessary (making them typical or primary Addison's patients), while others retain their ability to continue production of mineralcorticoids for years, requiring glucocorticoid replacement only.[30][31]

False test reportsEdit

Dog breeds whose origin is in the Pacific Rim, such as the Akita, normally have elevated potassium levels found during blood testing; ACTH testing results should be within normal ranges if the patient does not have Addisons.[14]

Whipworm infections can produce a syndrome that appears to be an Addisonian crisis. Just as with Addison's, blood tests will also show abnormalities in sodium and potassium levels. ATCH testing will be within normal ranges.[14]

TreatmentEdit

Diagnosis is through testing, with ACTH testing being the gold standard.[19][3] Treatment is by replacing or augmenting the insufficient or absent hormones. [32][3] Addison's disease patients will need this treatment for the rest of their lives and can lead normal ones, as long as they are given proper treatment for their deficiency.[19][3][15][33]

Dogs [34] with diagnosed and treated diabetes but undiagnosed/untreated Addison's disease may have reduced insulin needs. I16

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ReferencesEdit

  1. Adrenal gland. Wikipedia.
  2. Adrenal Steroids. School of Veterinary Medicine-Colorado State University.
  3. 3.0 3.1 3.2 3.3 3.4 3.5 3.6 3.7 Stafford, Debbie (September 1999). The Great Mimic:Addison's Disease. Veterinary Technician.
  4. Mineralcorticoids. School of Veterinary Medicine-Colorado State University.
  5. Potassium Toxicity & Addison's Disease. Pet Education.com.
  6. 6.0 6.1 Addison's Disease. New Hope Animal Hospital.
  7. Wortinger, Ann (February 2001). Electrolytes, Fluids and the Acid-Base Balance. Veterinary Technician.
  8. Nussey, SS., Whitehead, SA. (2001). Endocrinology-an Integrated Approach-Aldosterone. National Institutes of Health (US).
  9. Plummer, Caryn E., Specht, Andrew, Gelatt, Kirk N. (December 2007). Ocular Manifestations of Endocrine Disease. Compendium.
  10. Diabetes Mellitus. Petplace.com.
  11. Lunn, Katharine F., James Katherine M. (2007). Normal and Abnormal Water Balance: Polyuria and Polydipsia. Compendium.
  12. Hypoglycemia in Dogs. Petplace.com.
  13. Steiner, Jörg (2001). Chronic Diarrhea. WSAVA.
  14. 14.0 14.1 14.2 14.3 14.4 14.5 14.6 14.7 14.8 14.9 Brooks, Wendy C.. Addison's Disease-Hypoadrenocorticism. Veterinary Partner.
  15. 15.0 15.1 15.2 15.3 15.4 Addison's Disease. Southpaws Veterinary Center.
  16. Meeking, S. (2007). Treatment of acute adrenal insufficiency. Clinical Tech-Small Animal Practice.
  17. Klein, Susan C., Peterson, Mark E. (January 2010). Canine hypoadrenocorticism: Part I. Canadian Veterinary Journal.
  18. Durkan, Samuel (2008). Endocrine Emergencies. DVM 360.
  19. 19.0 19.1 19.2 19.3 19.4 Klein, Susan C., Peterson, Mark E. (February 2010). Canine hypoadrenocorticism: Part II. Canadian Veterinary Journal.
  20. Schaer, Michael (2005). Acute Adrenocortical Insufficiency. 30th World Congress of the World Small Animal Veterinary Association.
  21. Dexamethasone--Azium. 1-800PetMeds.com.
  22. Generic Dexamethasone Injection. Medi-Vet.com.
  23. Dexamethasone Sodium Phosphate--Generic Label Photo. Moore vet. Archived from the original on 2013-06-24.
  24. Dexamethasone Tablets--Generic Package Label. Moore vet. Archived from the original on 2013-06-24.
  25. Guide to Endocrinology. Axiom Vet Lab.
  26. 26.0 26.1 Overview of Adrenal Histology. School of Veterinary Medicine-Colorado State University.
  27. Maddison, Jill (2009). Corticosteroids: Friend or Foe?. WSAVA.
  28. 28.0 28.1 Peterson, Mark E., Kintzer, Peter P. (2006). Hypoadrenocorticism (Addison's Disease) in Dogs-page 20. OSU Endocrinology Symposium.
  29. Hypoadrenocorticism (Addison's Disease). Merck Veterinary Manual.
  30. Gaydos, Christine A., DeClue, Amy E. (1 Jun 2008). Updates on hypoadrenocorticism. DVM 360.
  31. Thompson AL, Scott-Moncrieff JC, Anderson JD. (2007). Comparison of classic hypoadrenocorticism with glucocorticoid-deficient hypoadrenocorticism in dogs: 46 cases (1985-2005).. Journal of the American Veterinary Medical Association.
  32. About Percorten-V-Treatment for Canine Addison's Disease. Novartis Animal Health.
  33. Church, David B. (2009). Management of Hypoadrenocorticism. WSAVA.
  34. Greco, Debra (March 2001). Canine Diabetes & Addison's Disease. District of Columbia Academy of Veterinary Medicine.


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