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− | [[Image:parathyroidadeoma.jpg|thumb|right|100px|Parathyroid adenoma. Image courtesy of Biomed Archive.]]
| + | Also Known As – '''''Parathyroid hyperplasia – Parahyroid adenoma - Fibrous Osteodystrophy – Grain Overload – Bran Disease – Bran-head Disease ''''' |
− | ===Primary===
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− | * Primary hyperparathyroidism is caused by glandular hyperplasia or neoplasia. [[Image:parathyroidhyperplasia.jpg|thumb|right|100px|Parathyroid hyperplasia. Image courtesy of Biomed Archive.]]
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− | * Rare.
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− | ===Secondary===
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− | * Secondary hyperparathyroidism causes [[Hyperparathyroidism|fibrous osteodystrophy or "rubber jaw"]].
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− | * In secondary hyperparathyroidism, the gland is overactive due to another condition coexisting in the body, rather than a primary parathyroid gland defect.
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− | * There are two common forms of secondary hyperparathyroisism:
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− | *# [[Hyperparathyroidism#Nutritional Hyperparathyroidism|'''Nutritional Hyperparathyroidism''']]
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− | *#* This includes [[Metabolic Bone Disease|Metabolic Bone Disease]].
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− | *# [[Hyperparathyroidism#Renal Hyperparathyroidism|'''Renal Hyperparathyroidism''']]
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− | * Both forms result in increased osteoclastic resorption of bone and deposition of fibro-osteoid matrix that fails to mineralise.
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− | ** Flat bones of the skull swell.
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− | ** Fibrous tissue is seen around the tooth roots.
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− | ** Bone softens in adult animals.
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− | *** This is what gives rise to the term "rubber jaw".
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− | *** Long bones become soft with thin cortices.
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− | **** These fracture easily.
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− | ====Nutritional Hyperparathyroidism====
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− | [[Image:secondaryhyperparathyroidism.jpg|thumb|right|100px|Secondary hyperparathyroidism - "rubber jaw". Image courtesy of Biomed Archive.]]
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− | * Nutritional hyperparathyroidism is also known as nutritional osteodystrophy.
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− | * This occurs most commonly in:
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− | ** Young, fast-growing animals
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− | ** Animals with a poor diet, for example:
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− | *** Swine fed unsupplemented cereal grain
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− | *** Dogs and cats fed all-meat diets
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− | *** Horses fed bran
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− | **** In this case, nutritional hyperparathyroidism is known as "bran disease".
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− | =====Pathogenesis=====
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− | * Pathogenesis follows low calcium/high phosphate diets.
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− | ** These lead to decreased serum calcium levels, stimulating [[Calcium#Parathyroid Hormone (PTH)|PTH]] release.
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− | ** The increase in PTH gives an increase in bone resorption, causing pathology.
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− | =====Pathology===== | + | ==Introduction== |
− | * '''Gross'''
| + | 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)]]. It occurs in many veterinary species and can be primary or secondary. |
− | ** Severe cases may show:
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− | *** Maxillary and mandibular swelling
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− | *** [[:Category:Teeth - Anatomy & Physiology|Teeth]] lost or buried in soft tissue
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− | *** Nasal and frontal bone enlargement, leading to dyspnoea
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− | *** Long bone fracture
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− | *** Detatchment tendons and ligaments
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− | ** Early or less severe cases are characterised by shifting lameness and ill thrift.
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− | * '''Histological'''
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− | ** Osteoclastic resorption
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− | ** Fibrous replacement
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− | =====Metabolic Bone Disease=====
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− | * Metabolic bone disease affects lizards in captivity, particularly young green iguanas
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− | * The condition is caused by:
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− | ** Dietary deficiency of calcium and vitamin D
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− | *** For example, due to poor lighting (which diminishes viatmin D production).
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− | ** Dietary excess of phosphorus
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− | ** Certain toxicities
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− | ** Diseases of the kidneys, [[Liver - Anatomy & Physiology|liver]] or parathyroid
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− | *** This aetiology is rare
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− | * Clinical signs include:
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− | ** Lethargy
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− | ** Inability to support weight
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− | ** Rounded skull
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− | ** Spontaneous fractures
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− | ** Adult animals also show signs of [[Hypocalcaemia|hypocalcaemia]]
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− | * The skeleton shows reduced density on radiography.
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− | ====Renal Hyperparathyroidism====
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− | * Renal Hyerparathyroidism is mostly seen in the dog as an expression of chronic renal disease.
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− | =====Pathogenesis=====
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− | [[Image:renalhyperparathyroidism.jpg|thumb|right|100px|Parathyroid hyperplasia in renal hyperparathyroidism. Image courtesy of Biomed Archive.]] | |
− | # Chronic renal disease results in reduced glomerular filtration.
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− | # As glomerular filtration is reduced, phosphate is retained. Chronic renal failure also causes inadequate vitamin D production in the kidneys.
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− | # Hyperphosphataemia develops due to phosphate retention. | |
− | #* Hypocalcaemia also occurs, as high levels of phosphate depress calcium levels.
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− | # PTH is released in an attempt to maintain the correct blood calcium:phosphorous ratio. This can have several effects:
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− | #* Parathyroid hyperplasia
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− | #** I.e. '''renal secondary hyperparathyroidism'''.
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− | #* Soft tissue mineralisation
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− | #** Particularly seen in dogs
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− | #** Calcium is commonly deposited in the subpleural connective tissue of the intercostal spaces.
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− | #** Calcification also occurs in other sites, e.g. [[Monogastric Stomach - Anatomy & Physiology|stomach]] wall, lungs, kidneys.
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− | #* Increased bone resorption
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− | #** This causes fibrous osteodystrophy, or "rubber jaw".
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− | =====Pathology=====
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− | [[Image:Renal_osteodystrophy.jpg|thumb|right|100px|"Rubber jaw" in renal osteodystrophy. Image courtesy of Biomed Archive.]]
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− | * Pathology seen in renal hyperparathyroidism is very similar to that seen in nutritional hyperparathyroidism.
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− | * '''Gross'''
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− | ** The major gross presentation is a fibrous osetodystrophy, or rubber jaw.
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− | *** The maxillae and mandible appear swollen.
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− | *** Radiographically, bone shows reduced density, and [[:Category:Teeth - Anatomy & Physiology|teeth]] hence appear embedded in soft tissue.
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− | *** However, only a few cases of chronic renal disease show such severe bone lesions.
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− | ** Other lesions may also be seen.
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− | *** Intercostal muscles may be calcified.
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− | *** Bone marrow lesions may cause anaemia.
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− | *** The lung may show oedema, and have calcified alveolar walls.
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− | * '''Histological'''
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− | ** Osteoclastic resorption
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− | ** Fibrous replacement
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| + | Primary hyperparathyroidism originates within the parathyroid gland itself and can be due to glandular hyperplasia or [[Neoplasia – Pathlology|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 name=Merck1>Merck Veterinary Manual, '''Primary Hyperparathyroidism''', accessed online 24/07/2011 at http://www.merckvetmanual.com/mvm/index.jsp?cfile=htm/bc/40407.htm</ref> |
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− | ==From musculoskeletal== | + | ==Signalment== |
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− | *Can arise in a number of ways but single common factor is elevated PTH
| + | ==Clinical Signs== |
− | *Results in increased resorption of bone and replacement by fibrous connective tissue
| + | The main effect of hyperparathyroidism is [[Hypercalcaemia|hypercalcaemia]] which causes a range of clinical signs. Polydipsia, polyuria, anorexia, lethargy and depression are the most common signs but animals may also be constipated, weak, stiff-gaited, shivering and vomiting. Mild hypercalcaemia may not generate any overt clinical signs. |
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− | =====<u>'''Primary hyperparathyroidism'''</u>=====
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− | *This is increased production of PTH not related to calcium or phosphorus levels
| + | ==Diagnosis== |
− | *Due to parathyroid neoplasia or bilateral idiopathic parathyroid hyperplasia
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− | *Rare
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− | =====<u>'''Secondary hyperparathyroidism'''</u>=====
| + | Electrolyte imbalances on blood biochemistry profiles are highly suggestive. Hypercalcaemia with a normal to low serum phosphorus and a low urine specific gravity are fairly consistent findings. |
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− | *Regardless of pathogenesis, the result is:
| + | 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. |
− | **Increased osteoclastic resorption of bone and deposition of fibro-osteoid matrix that fails to mineralise
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− | **Flat bones of the skull swell, including maxillary and nasal bones
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− | **Long bones become soft with thin cortices which fracture easily
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− | [[Image:Renal osteodystrophy.jpg|right|thumb|100px|<small><center>Renal osteodystrophy (Image sourced from Bristol Biomed Image Archive with permission)</center></small>]]
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− | *'''Renal hyperparathyroidism'''
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− | **Pathogenesis:
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− | ***[[Chronic Renal Failure|Chronic renal failure]]
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− | ****-> Retention of phosphate (due to reduced glomerular filtration) and inadequate production of vitamin D by kidneys
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− | *****-> Hyperphosphataemia and hypocalcaemia (high P depresses Ca)
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− | ******-> Increased PTH output
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− | *******-> Increased bone resorption
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− | ********-> '''Fibrous osteodystrophy''' - increased osteoclastic resorption of cancellous and cortical bone + proliferation of fibrous tissue
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− | **Mainly in dogs
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− | **Affects whole skeleton but mainly skull
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− | **Bones soft and pliable
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− | **Canine teeth easily removed - rubber jaw
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− | **Microscopically - ''Osteodystrophia fibrosa'' (above = fibrous osteodystrophy) +/- [[Osteomalacia|osteomalacia]]
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| + | Exploratory surgery of the cervical region may identify enlarged parathyroid glands if no other test is available or confirmatory. |
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| + | ==Treatment== |
| + | Treatment for primary hyperaparathyroidism usually required surgical excision. |
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− | *'''Nutritional hyperparathyroidism''' (nutritional osteodystrophy)
| + | ==Control== |
− | **Also called '''fibrous osteodystrophy, “rubber jaw”''' or '''“bran disease”'''
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− | **More common in young, fast-growing animals
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− | **Pathogenesis:
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− | ***Low calcium / high phosphate diets
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− | ****-> Decreased calcium levels in serum
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− | *****-> Parathyroid gland stimulated (may become enlarged)
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− | ******-> Increased PTH
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− | *******-> Increased bone resorption
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− | **Caused by poor diet
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− | ***Cattle and sheep - usually mild disease
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− | ***'''Swine''' fed un-supplemented cereal grain, usually mild disease
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− | ***'''Dogs/cats''' fed all-meat or offal diets (Ca:P often as high as 1:20)
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− | ****Few weeks after weaning
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− | ****Provision of calcium alone correct the problem
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− | ****Very brittle bones -> sponataneous fractures
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− | ****Extreme porosity of the whole skeleton on radioghraphs
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− | ***'''Horses''' fed bran
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− | ****Very susceptible to high phosphorus diet
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− | ****Any time after weaning, susceptibility declines after seventh year
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− | ****Early signs:
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− | *****Mild changes of gait
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− | *****Stiffness
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− | *****Transient shifting lameness
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− | ****Advanced signs:
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− | *****Swelling of mandible and maxilla - 'Big head'
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− | *****Dyspnoea caused by swelling of nasal and frontal bones
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− | *****Teeth lost or buried in softened jaw
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− | *****Fractures from mild trauma
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− | *****Detached tendons and ligaments
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− | *****Histologically:
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− | ******Marked loss of bone
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− | ******Replacement by proliferative tissue
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− | ****Often called '''''Osteodystrophia fibrosa'''''
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| + | {{Learning |
| + | |flashcards = [[Hyperparathyroidism Flashcards]] |
| + | }} |
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− | [[Category:Bones - Metabolic Pathology]]
| + | ==References== |
| + | <references/> |
| + | Lavoie, J-P., Hinchcliff, K. W (2008) '''Blackwell’s Five-Minute Veterinary Consult: Equine 2nd ed'''. ''Wiley-Blackwell, Oxford'', pp. |
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− | [[Category:Parathyroid Glands - Pathology]]
| + | Haskell, S (2008) '''Blackwell’s Five-Minute Veterinary Consult:Ruminant'''. ''Wiley-Blackwell, Oxford'', pp. |
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− | [[Category:To Do - Clinical]] | + | [[Category:To Do - Manson review]] [[Category: Diseases - Horse]] [[Category:]] |
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− | [[Category:To Do - Steph]] | |