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Also known as '''''Cushings disease'''
 
Also known as '''''Cushings disease'''
 
==Introduction==
 
==Introduction==
Hyperadrenocorticism is a common disease of adrenal hyperfunction.
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Hyperadrenocorticism is a common disease of adrenal hyperfunction that is seen most commonly in the dog. There are three known causes of the adrenal hyperfunction: dysfunction of the pituitary gland, dysfunction of the adrenal glands and iatrogenic administration of corticosteroids.
 
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==Pituitary Dependant Hyperadrenocorticism==
 
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[[Image:Chromophobe adenoma.jpg|right|thumb|150px|<small><center>'''Chromophobe Adenoma'''. Courtesy of A. Jefferies</center></small>]]
Most often seen in the dog.
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80-85% cases of Cushings disease show bilateral adrenal hyperplasia due to excess stimuation by ACTH.  There is a failure of the negative feedback mechanism at the level of the pituitary and so ACTH is produced in an unregulated fashion. This is thought to occur due to a functional chromophobe cell (Produces ACTH and MSH) neoplasia, although visible macroadenomas are only found in 10-15% cases with this aetiology.  Most cases are therefore thought to be microadenomas and may be visualised by histopathological staining of the pituitary.
====Pituitary Dependant====
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[[Image:Nodular hyperplasia.jpg|left|thumb|150px|<small><center>'''Adrenal Nodular Hyperplasia'''. Courtesy of A. Jefferies</center></small>]]
[[Image:Chromophobe adenoma.jpg|right|thumb|125px|<small><center>'''Chromophobe Adenoma'''. Courtesy of A. Jefferies</center></small>]]
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80-85% cases show bilateral adrenal hyperplasia due to excess stimuation by ACTH.  There is failure of negative feedback at the level of the pituitary and so ACTH is produced in an unregulated fashion.
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Thought to be due to a functional chromophobe cell (Produces ACTH and MSH) neoplasia, although visible macroadenomas are only found in 10-15% cases with this aetiology.  Most cases are therefore thought to be microadenomas and may be visualised by histopathological staining of the pituitary.
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[[Image:Nodular hyperplasia.jpg|left|thumb|125px|<small><center>'''Adrenal Nodular Hyperplasia'''. Courtesy of A. Jefferies</center></small>]]
      
Grossly the adrenals have an irregular surface with protruding nodules of cortical tissue; the hyperplased zona fasciculata cells.
 
Grossly the adrenals have an irregular surface with protruding nodules of cortical tissue; the hyperplased zona fasciculata cells.
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====Adrenal Dependant====
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==Adrenal Dependant Hyperadrenocorticism==
[[Image:Adrenal neoplasia.jpg|right|thumb|125px|<small><center>'''Adrenal Neoplasia'''. Courtesy of A. Jefferies</center></small>]]
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[[Image:Adrenal neoplasia.jpg|right|thumb|150px|<small><center>'''Adrenal Neoplasia'''. Courtesy of A. Jefferies</center></small>]]
 
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Approximately 15% all cases of Cushings disease fit into this category, which is primarily a neoplastic abnormality of the adrenal glands; approximately 50% are benign and 50% are malignant.
Approximately 15% all cases of Cushings disease.  Of the adrenal neoplasia approximately 50% are benign and 50% are malignant.
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====Iatrogenic====
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==Iatrogenic Hyperadrenocorticism==
 
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This is created by the administration of parenteral corticosteroids.In these cases adrenal atrophy is induced as the administered steroids have a negative feedback effect on the pituitary and normal ACTH release is inhibited.
Due to excessive administration of parenteral corticosteroids.
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In these cases there will be adrenal atrophy as the administered steroids have a negative feedback effect on the pituitary and ACTH release is inhibited.
      
===Pathophysiology===
 
===Pathophysiology===
   
The clinical signs of Cushings disease are brought about by excess glucocorticoids, particularly cortisol.   
 
The clinical signs of Cushings disease are brought about by excess glucocorticoids, particularly cortisol.   
[[Image:Cushings alopecia.jpg|right|thumb|125px|<small><center>'''Cushings Alopecia'''. Courtesy of A. Jefferies</center></small>]]
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[[Image:Cushings alopecia.jpg|right|thumb|150px|<small><center>'''Cushings Alopecia'''. Courtesy of A. Jefferies</center></small>]]
    
*'''[[Liver - Anatomy & Physiology|Liver]]''': Cortisol induces enzymes to increase gluconeogenesis leading to '''hyperglycaemia''' in Cushings patients.  The [[Pancreas - Anatomy & Physiology|pancreas]] attempts to maintain normal blood glucose by producing increasing amount of insulin.  Eventually the [[Pancreas - Anatomy & Physiology|pancreas]] is exhausted inducing a diabetic state.
 
*'''[[Liver - Anatomy & Physiology|Liver]]''': Cortisol induces enzymes to increase gluconeogenesis leading to '''hyperglycaemia''' in Cushings patients.  The [[Pancreas - Anatomy & Physiology|pancreas]] attempts to maintain normal blood glucose by producing increasing amount of insulin.  Eventually the [[Pancreas - Anatomy & Physiology|pancreas]] is exhausted inducing a diabetic state.
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