| 04/04/2006 11:09 FAX 435 797 2805
UT VET DIAGNOSTIC LAB raJ 002/01 UVDL Accession#: L06-1262 Date received: 3/30/2006 Final Report Utah Veterinary Diagnostic Laboratory 950 East 1400 North . Logan. UT 84322-5700 Phone: (435)797-1895 Fax: (435)797~2805 Website: http://www.usu.eduluvdl Client ID: NORTH_OGDEN Attention: Dr. Wynlee Decker VeterinarianlSubmitter: NORTH OGDEN ANIMAL HOSPITAL 1580 NORTH WASHINGTON BLVD OGDEN, UT 84404 Owner's Information: (801)737-4289 Michael Chandler 505 East 1700 North North Ogden UT 84412. Date specimens received: 3/30/2006 Specimens received by: Courier Client Phone: (801)782-4401 Client Fax: (801)782-9864 Animal ID: Cindy Sex: Spay Age: Species: Canine Breed: Greyhound. Tests Requested: Necropsy & Cremation with ashes returned Specimens Submitted: Entire Animal 11 Years . LABORATORY TEST STATUS Cremation (cremains returned) Necropsy Report CURRENT STATUS Completed 4/4/2006 Summary: 1. Lymphangiectasia, moderate to severe, smal1 intestine 2. Herniated intervertebral disk, C6 - C7 3. Adrenal cortical nodular hyperplasia, multifocal, adrenal glands 4. Adrenocortical atrophy, bilateral, moderate 5. Dennatopathy characterized by epidermal, follicular and sebaceous gland atrophy 6. Hepatopathy, vacuolar, diffuse, moderate to severe 7. Myelopathy, cervical spinal cord, mild 8. Biventricular hypertrophy, with the left ventricle significantly more affected 9. Aortic valvular dilation 10. Splenic congestion Although intestinal lymphangiectasia is the most conunon cause of protein-losing enteropathy in dogs, its underlying cause (infiltrated neoplasm, intlammatOt)' thrombosis, sclerosis of lymphoid channels, postsurgical scarring, etc.) is rarely evident. Unfortunately. this is the case in this particular animal- the lymphangiectasia is evident but its cause is not. The herniated disk explains the reported neck pain, and occasional axonal tracks in the spinal cord are degenerate, suggesting cord compression. Hyperplastic nodules in the adrenal glands are common in aging dogs and have been associated with functional abnormalities. Hence, the dermal changes, which are strongly suggestive of hyperadrenocorticism, may be due to excess cortisol from the hyperplastic nodules or exogenously administered corticoSteroids. The adrenocortical atrophy reflects this hyperadrenocorticism, as do hepatic changes. Bivcntricular hypertrophy is evident, which is far more significant on the left side. Left ventIjcular hypertrophy is attributcd to aortic valvular dilation and subsequent insufficiency. Cause of right ventricular hypertrophy is not evident. Absense of hemosiderin accumulation in alveolar septal macrophages suggests that cardiac similar albeit smaller masses replace the zona fasciculata and reticularis, and extend into the central med1,111a. In both glands, the zone fascicula.ta in regions away from the masses is uniformly thin (atrophied). Skin: The epidermis is less than three layers thick (atrophic) and is diffusely and moderately hyperkeratotic (orthokeratosis). Hair follicles are severely reduced in number and those present arc small (atrophic) and it's telogen or catagen phase; virtually no anagen bulbs are identified. Sebaceous glands are uniformly smaIl and/or absent (severely atrophic). Liver: Virtually all hepatocytes are dilated and have lacy vacuolated cytoplasm Sinusoids are uniformly congested and contain clusters of hemosiderin-laden Kupffer cells. Cervical spinal cord: Rare myelin sheaths in the ventral funiculi are dilated and lack central axons. Spleen: Congestion is moderate. No significant microsCopic abnormalities are noted in sections of stomach, large intestine, trachea, lung, heart, kidney, urinary bladder and brain. End of Report |