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→Introduction
Also Known As – '''''Parathyroid hyperplasia – Parathyroid adenoma - Fibrous Osteodystrophy – Grain Overload – Bran Disease – Big Head Disease – Millers Disease - Rubber Jaw – Metabolic Bone Disease'''''
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Also Known As: '''''HPT — Parathyroid Hyperplasia — Parathyroid Adenoma — Fibrous Osteodystrophy — Grain Overload — Bran Disease — Big Head Disease — Millers Disease — Rubber Jaw — [[Metabolic Bone Disease]]'''''
==Introduction==
==Introduction==
[[Image:parathyroidadeoma.jpg|thumb|right|200px|Parathyroid adenoma. Image courtesy of Biomed Archive.]]
[[Image:parathyroidadeoma.jpg|thumb|right|200px|Parathyroid adenoma. Image courtesy of Biomed Archive.]]
[[Image:secondaryhyperparathyroidism.jpg|thumb|right|200px|Secondary hyperparathyroidism - "rubber jaw". Image courtesy of Biomed Archive.]]
[[Image:secondaryhyperparathyroidism.jpg|thumb|right|200px|Secondary hyperparathyroidism - "rubber jaw". Image courtesy of Biomed Archive.]]
[[Image:renalhyperparathyroidism.jpg|thumb|right|200px|Parathyroid hyperplasia in renal hyperparathyroidism. Image courtesy of Biomed Archive.]]
[[Image:renalhyperparathyroidism.jpg|thumb|right|200px|Parathyroid hyperplasia in renal hyperparathyroidism. Image courtesy of Biomed Archive.]]
[[Image:Renal_osteodystrophy.jpg|thumb|right|200px|"Rubber jaw" in renal osteodystrophy. Image courtesy of Biomed Archive.]]
[[Image:Renal_osteodystrophy.jpg|thumb|right|200px|"Rubber jaw" in renal osteodystrophy. Image courtesy of Biomed Archive.]]
[[Image:Renal osteodystrophy.jpg|right|thumb|200px|Renal osteodystrophy (Image sourced from Bristol Biomed Image Archive with permission)]]
[[Image:parathyroidhyperplasia.jpg|thumb|right|200px|Parathyroid hyperplasia. Image courtesy of Biomed Archive.]]
Hyperparathyroidism is an '''[[Endocrine System - Anatomy & Physiology|endocrine]] disease''' caused by overactivity of the [[Parathyroid Glands - Anatomy & Physiology|parathyroid gland]] and consequent '''raised body levels of [[Calcium#Parathyroid Hormone|parathyroid hormone (PTH)]]'''. This in turn results in chronic hypercalaemia. It occurs in many veterinary species and can be primary or secondary.
<big>'''Primary hyperparathyroidism'''</big> originates within the parathyroid gland itself and can be due to '''glandular hyperplasia or [[Neoplasia - Pathology|neoplasia]]'''. It is most commonly due to a '''solitary benign [[Adenoma|adenoma]]''' of either the [[Parathyroid Glands - Anatomy & Physiology|internal or external parathyroid gland]].<ref>Merck Veterinary Manual, '''Primary Hyperparathyroidism''', accessed online 25/07/2011 at http://www.merckvetmanual.com/mvm/index.jsp?cfile=htm/bc/40407.htm</ref>
'''Secondary hyperparathyroidism''' can be either renal or nutritional in origin:
<big>'''Secondary hyperparathyroidism'''</big> is usually diffuse hyperplasia of the parathyroid glands due to relative hypocalcaemia and can be either renal or nutritional in origin:
Secondary '''renal hyperparathyroidism''' is a complication of '''chronic renal failure'''. This is due to '''hyperphosphataemia developing as a result of impaired glomerular filtration rate'''. Renal production of [[Calcium#Calcitriol|calcitriol]] is also reduced, exacerbating the resulting hypercalcaemia.
Secondary '''renal hyperparathyroidism''' is a complication of '''chronic renal failure'''. This is due to relative '''hyperphosphataemia developing as a result of impaired glomerular filtration rate'''. '''Reduced vitamin D''' synthesis or absorbtion is also thought to contribute to low serum calcium levels and subsequent stimulation of the parathyroid gland. Renal production of [[Calcium#Calcitriol|calcitriol]] (active Vitamin D3) is also reduced, exacerbating the resulting [[hypercalcaemia]].
Secondary '''nutritional''' hyperparathyroidism is caused by excessive '''phosphorus intake''' causing a total or relative calcium deficiency by '''binding calcium in the gut and decreasing its absorption'''. This category encompasses '''bran disease in horses and also [[Metabolic Bone Disease|metabolic bone disease]] in reptiles'''.
Secondary '''nutritional''' hyperparathyroidism is caused by excessive '''phosphorus intake''' causing a total or relative calcium deficiency by '''binding calcium in the gut and decreasing its absorption'''. This category encompasses '''bran disease in horses and also [[Metabolic Bone Disease|metabolic bone disease]] in reptiles'''.
'''Serum PTH''' levels may be useful in diagnosing '''primary hyperparathyroidism''', but only in animals with normal renal function, i.e., those with normal creatinine and blood urea nitrogen. A '''high PTH assay along with high creatinine and blood urea nitrogen is indicative of possible renal secondary HPT'''.
'''Serum PTH''' levels may be useful in diagnosing '''primary hyperparathyroidism''', but only in animals with normal renal function, i.e., those with normal creatinine and blood urea nitrogen. A '''high PTH assay along with high creatinine and blood urea nitrogen is indicative of possible renal secondary HPT'''.
'''Exploratory surgery''' of the cervical region may identify enlarged parathyroid glands if no other test is available or confirmatory.
'''Exploratory surgery''' of the cervical region may identify enlarged parathyroid glands if no other test is available or to confirm the diagnosis.
Animals with '''secondary renal hyperparathyroidism''' may demonstrate signs of bone loss radiographically. The bones of the '''jaw''' are affected first - with loss of the '''lamina dura, interdental and interradicular regions'''. Eventually bone loss generalises and widespread radiographic signs can be seen.
In cases of '''nutritional hyperparathyroidism, serum calcium is normal or low''' compared to high in other pathogeneses. '''Urinary excretion of phosphorus is markedly increased''' and serum PTH high. Radiographs will identify bony resorption and pathological fractures with fibrous tissue calluses.
In cases of '''nutritional hyperparathyroidism, serum calcium is normal or low''' compared to high in other pathogeneses. '''Urinary excretion of phosphorus is markedly increased''' and serum PTH high. Radiographs will identify bony resorption and pathological fractures with fibrous tissue calluses.
'''MBD''' is usually identified by '''clinical signs and radiographic evidence''' of a poorly mineralised skeleton.
'''[[Metabolic Bone Disease|MBD]]''' is usually identified by '''clinical signs and radiographic evidence''' of a poorly mineralised skeleton.
==Treatment==
==Treatment==
Treatment for '''primary hyperparathyroidism''' usually required '''surgical excision'''. Hypocalcaemia is a known post-operative complication and supplementation may be required in the short or long term management. If the hypercalcaemia persists, metastatic disease should be suspected and investigated.
Treatment for '''primary hyperparathyroidism''' usually requires '''surgical excision'''. [[Hypocalcaemia]] is a known post-operative complication and supplementation may be required in the short or long term management. If the hypercalcaemia persists, metastatic disease should be suspected and investigated.
Renal secondary HPT therapy is directed at '''control of the renal disease by way of specialised diet and rehydration along with supplementation of calcitriol and phosphorus binders'''.
Renal secondary HPT therapy is directed at '''control of the renal disease by way of specialised diet and rehydration along with supplementation of calcitriol and phosphorus binders'''.
'''Horses with bran disease should be confined until radiographs show normal bone density'''. Diet should be rectified if inadequate, and '''calcium: phosphorus ratio maintained at 1:1-3:1 for the first 2-3 months''' followed by a normal ration. If horses have also been feeding on plants high in oxalates (which can also bind calcium in the intestine) then these should be removed from the diet and limestone can be added to the diet to prevent or treat any associating signs.
'''Horses with bran disease should be confined until radiographs show normal bone density'''. Diet should be rectified if inadequate, and '''calcium: phosphorus ratio maintained at 1:1-3:1 for the first 2-3 months''' followed by a normal ration. If horses have also been feeding on plants high in oxalates (which can also bind calcium in the intestine) then these should be removed from the diet and limestone can be added to the diet to prevent or treat any associating signs.
Horses with colic as a result of '''grain engorgement''' require '''aggressive fluid therapy and analgesia, and a nasogastric tube''' should be passed to alleviate any reflux. Measures should also be taken to try and prevent [[Laminitis - Horse|laninitis]] such as specialised shoes.
Horses with colic as a result of '''grain engorgement''' require '''aggressive [[:Category:Fluid Therapy|fluid therapy]] and analgesia, and a nasogastric tube''' should be passed to alleviate any reflux. Measures should also be taken to try and prevent [[Laminitis - Horse|laninitis]] such as specialised shoes.
{{Learning
{{Learning
|flashcards = [[Hyperparathyroidism Flashcards]]
|flashcards = [[Hyperparathyroidism Flashcards]]<br>[[Small Mammals Q&A 19]]<br>[[Veterinary Dentistry Q&A 12]]
}}
}}
Merck Vet Manual, '''Nutritional Diseases''', accessed 25/07/2011 at http://www.merckvetmanual.com/mvm/index.jsp?cfile=htm/bc/182606.htm&word=nutritional%2csecondary
Merck Vet Manual, '''Nutritional Diseases''', accessed 25/07/2011 at http://www.merckvetmanual.com/mvm/index.jsp?cfile=htm/bc/182606.htm&word=nutritional%2csecondary
Verstraete, F. J. M. (1998) '''Self-Assessment Colour Review - Veterinary Dentistry''' ''Manson''
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[[Category:Endocrine Diseases - Dog]] [[Category: Endocrine Diseases - Cat]] [[Category:Bones - Metabolic Pathology]] [[Category:Parathyroid Glands - Pathology]] [[Category:Colic in Horses]][[Category:Endocrine Diseases - Horse]]
[[Category:Expert Review]]