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| − | ===Pituitary===
| + | #REDIRECT[[:Category:Bones - Metabolic Pathology]] |
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| − | *Growth hormone
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| − | **Secreted by the anterior pituitary
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| − | **Influences the size of the skeleton and soft tissue
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| − | ====[[Congenital Panhypopituitarism|Pituitary dwarfism]]====
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| − | ====Pituitary gigantism ([[Acromegaly]])====
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| − | ===Thyroid===
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| − | *Thyroid hormones affect maturation of growth of cartilage
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| − | ====[[Hypothyroidism]]====
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| − | ====[[Hyperthyroidism]]====
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| − | ===[[Gonadal Effect on Bones]]===
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| − | ===Adrenal glands===
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| − | *[[Hyperadrenocorticism]]
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| − | ===[[Hyperparathyroidism|Hyperparathyroidism]]===
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| − | ===Rickets===
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| − | [[Image:Rickets in dog.jpg|right|thumb|100px|<small><center>Rickets in dog (Image sourced from Bristol Biomed Image Archive with permission)</center></small>]]
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| − | *Essentially the same disease as osteomalacia
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| − | *Caused by Vitamin D and phosphorus deficiency
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| − | *In young animals
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| − | *Failure of:
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| − | **Mineralisation of osteoid at sites of membranous growth
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| − | **Cartilage vascularisation and mineralisation at sites of endochondral ossification
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| − | *Osteoid and catilage build up at those sites
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| − | *Histologically:
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| − | **Lines of hypertrophic cartilage cells are lenghtened and disorganised
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| − | **Ossification at metaphysis is poor
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| − | **Persisting osteoid and cartilage -> shaft modelling failure
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| − | **Thuckened physes due to normal chondrocyte proliferation but defective removal
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| − | *Ends of bones enlarge -> club-like thickening of metaphysis + compression of epiphysis
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| − | **Most affected:
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| − | ***Proximal humerus
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| − | ***Distal radius
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| − | ***Ulna
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| − | ***Ribs
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| − | ****Enlargement of costochondral junction - called 'rachitic rosary'
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| − | *Weight bearing leads to:
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| − | **Thickening of the physis and
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| − | **Flaring of the excess matrix at the metaphysis
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| − | *Histological lesions heal whn diet corected
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| − | *Minor deformities correct but major deformities remain
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| − | *Occurs after weaning because:
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| − | **''In utero'' and in milk - adeqaute nutrients obtained at expense of dam
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| − | *In Foals
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| − | **Rare - long nursing period and relatively slow rate of growth
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| − | *In Calves and lambs
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| − | **When diet deficeint of phosphorus and poor exposure to sunlight
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| − | *In Puppies, Kittens and Piglets
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| − | **Rapid growth, weaned early -> fulminating rickets if poor exposure to sunlight and lack of vitamin D in diet
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| − | [[Category:Bones - Metabolic Pathology]]
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| − | ===Osteomalacia===
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| − | *Failure of mineralisation of osteoid / softening of the bones
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| − | *Active resorption of bone replaced by excess osteoid on trabeculae, endosteum of cortices and [[Bones - Anatomy & Physiology#Bone Remodeling|Haversian canals]]
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| − | *Decreased resistance to tension -> osteoid build-up at tendon insertions
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| − | *In advanced disease
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| − | **Bones break easily and become deformed
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| − | **Tendons may separate from bones
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| − | *Caused by prolonged phosphorus and Vitamin D deficiency
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| − | **Vitamin D maintains normal plasma levels of calcium and phosphorus through acting on the intestines, bones and kidneys
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| − | *In mature animals
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| − | *Mainly grazing ruminants following gestation and lactation
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| − | **Sunlight is important for production of vitamin D in the skin of ruminants
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| − | **Vitamin d is also present in sun-dried hay
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| − | **Mostly seen where there is long grass growing season with poor sunlight
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| − | [[Category:Bones - Metabolic Pathology]] | |
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| − | ===Hypovitaminosis A===
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| − | *Vitamin A is essential for normal bone growth in foetus and neonates
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| − | *Hypovitaminosis from dietary deficiency of dam -> teratogenic in pigs and large cats
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| − | *More commonly, deficiency in neonates (puppies, kittens, calves, piglets) on vitamin-deficient diets
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| − | *Dietary deficiency -> failure of [[Bones - Anatomy & Physiology|osteoclastic remodelling]] resulting in bone overgrowth and nerve compression
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| − | *Optic nerves particularly affected
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| − | [[Category:Bones - Metabolic Pathology]]
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| − | ===Hypervitaminosis A===
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| − | [[Image:Hypervitaminosis A.jpg|right|thumb|100px|<small><center>Hypervitaminosis A (Image sourced from Bristol Biomed Image Archive with permission)</center></small>]]
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| − | *Main lesions:
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| − | **Injury to growth cartilage -> [[Bones - Anatomy & Physiology|premature closure of growth plate]]
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| − | **[[Bones Degenerative - Pathology#Osteoporosis (Atrophy)|Osteoporosis]]
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| − | **'''Exostoses'''
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| − | **[[Musculoskeletal Terminology - Pathology|Osteophyte]] formation in prolonged exposure
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| − | *In cats fed bovine liver for prolonged periods
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| − | **Rich in vitamin A in grazing animals
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| − | **Vertebrae fuse with each other due to bone proliferation - '''cervical spondylosis''' ('''ankylosing exostosis''' of the vertebral column), especially in the neck
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| − | *Can also be teratogenic, especially in pigs ([[Cleft Palate|cleft plate]] and abortions)
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| − | [[Category:Bones - Metabolic Pathology]]
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| − | ===Hypervitaminosis D===
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| − | *May be of dietary or iatrogenic origin (has narrow safety margin)
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| − | *Key features are hypercalcaemia with metastatic calcification of soft tissues
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| − | *'''Acute poisoning'''
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| − | **In dogs and cats often from rodenticides containing cholecalciferol
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| − | **Grossly:
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| − | ***Gastrointestinal haemorrhage
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| − | ***Foci of [[Myocardial Mineralisation|myocardial discoloration]]
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| − | **Microscopically:
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| − | ***Mucosal haemorrhage
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| − | ***Necrosis of crypts
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| − | ***Focal myocardial necrosis
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| − | ***Mineralisation of intestinal mucosa, [[Arterial Calcification#Medial calcification|blood vessel walls]], [[Pulmonary Calcification|lungs]] and kidneys
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| − | *'''Chronic poisoning'''
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| − | **Grossly:
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| − | ***Intense [[Bones - Anatomy & Physiology|osteoclastic activity]] -> active resorption of bone, especially [[Bones - Anatomy & Physiology|trabecular]]
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| − | **Microscopically:
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| − | ***Excessive production of [[Bones - Anatomy & Physiology|osteoid]] - appears both eosinophilic and basophilic in different places
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| − | ***Marrow cavity may be obliterated
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| − | ***Mineralisation of soft tissues, especially [[Arterial Calcification|blood vessel walls]]
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| − | **Due to inhibition of [[Calcium|Parathyroid Hormone (PTH)|PTH]] and increase of [[Calcium#Calcitonin|calcitonin]]
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| − | [[Category:Bones - Metabolic Pathology]]
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| − | ===Fluorine poisoning===
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| − | *F is widespread in nature
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| − | *Pastures may be contaminated by industrial processes (e.g. brick manufacture)
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| − | *'''Acute poisoning''':
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| − | **Gastroenteritis
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| − | **Nephrosis
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| − | *'''Chronic poisoning''':
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| − | **''Dental abnormalities''
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| − | ***Intoxication during teeth development
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| − | ***Foci of poor enamel formation - yellow, dark brown/black, chalky
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| − | ***Irregular wear of teeth, chip easily
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| − | **''Osteodystrophy = Fluorosis''
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| − | ***Generalised skeletal disturbance
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| − | ***Most affected are metatarsals and mandibles
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| − | ***Periosteal hyperostosis + endosteal bone resorption -> thickened bones with enlarged marrow cavities
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| − | [[Category:Bones - Metabolic Pathology]]
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| − | ===Lead poisoning===
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| − | *Lead can bind to mineral portion of bone and cartilage
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| − | *In young animals ingesting large dose at once
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| − | ** -> Lead induced malfunction of osteoclasts
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| − | ** -> Transverse band of increased density on radiographs of metaphysis = "lead line" = [[Retention of Elongated Primary Trabeculae|growth retardation lattice]]
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| − | [[Category:Bones - Metabolic Pathology]]
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| − | [[Category:Musculoskeletal System - Pathology]]
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