Difference between revisions of "Bones Metabolic - Pathology"

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===Pituitary===
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#REDIRECT[[:Category:Bones - Metabolic Pathology]]
 
 
*Growth hormone
 
**Secreted by the anterior pituitary
 
**Influences the size of the skeleton and soft tissue
 
 
 
====Pituitary dwarfism====
 
 
 
*Rare in animals, reported in German Shepherd Dogs
 
*Deficiency of growth hormone
 
*Proportionate dwarfism
 
*Growth plates remain open for up to 4 years
 
*Disorganised proliferating chondrocytes
 
 
 
====Pituitary gigantism (Acromegaly)====
 
 
 
*Occurs in humans with pituitary adenoma
 
*Due to [[Acromegaly|pituitary hyperfunction]]
 
*Overgrowth of cranial bones, chin, hands and feet
 
*Reported in dogs '''?(and cats)?'''
 
 
 
 
 
===Thyroid===
 
 
 
*Thyroid hormones affect maturation of growth of cartilage
 
 
 
====Hypothyroidism====
 
 
 
*In young animals
 
*Retardation of growth and development of endochondral bone
 
*Stunted growth
 
*Skeletal abnormalities
 
*In neonatal foals, Giant Schnauzers and Scottish Deerhounds
 
 
 
====Hyperthyroidism====
 
 
 
*In young animals causes accelerated maturation of growth plate
 
*In adults causes [[Bones Degenerative - Pathology#Osteoporosis (Atrophy)|osteoporosis]]
 
 
 
 
 
===Gonads===
 
 
 
*Oestrogen and androgens
 
**Affect growth of skeleton
 
**Accelerate epiphyseal closure
 
*Oestrogen
 
**Stimulates [[Bones - normal#Normal structure|osteoblasts]] to produce matrix
 
**Inhibits [[Bones - normal#Normal structure|osteoclasts]]
 
*'''Hypogonadism''' in growing skeleton -> delayed epiphyseal closure and skeletal maturation
 
 
 
 
 
===Adrenal glands===
 
 
 
*[[Adrenal Glands - Pathology#Adrenal Hyperfunction|Hyperadrenocorticism]]
 
**Causes [[Bones Degenerative - Pathology#Osteoporosis (Atrophy)|osteoporosis]]
 
**Reported in dogs with Cushing's disease
 
 
 
 
 
===[[Parathyroid Glands - Pathology#Hyperparathyroidism|Hyperparathyroidism]]===
 
 
 
*Can arise in a number of ways but single common factor is elevated PTH
 
*Results in increased resorption of bone and replacement by fibrous connective tissue
 
 
 
=====<u>'''Primary hyperparathyroidism'''</u>=====
 
 
 
*This is increased production of PTH not related to calcium or phosphorus levels
 
*Due to parathyroid neoplasia or bilateral idiopathic parathyroid hyperplasia
 
*Rare
 
 
 
=====<u>'''Secondary hyperparathyroidism'''</u>=====
 
 
 
*Regardless of pathogenesis, the result is:
 
**Increased osteoclastic resorption of bone and deposition of fibro-osteoid matrix that fails to mineralise
 
**Flat bones of the skull swell, including maxillary and nasal bones
 
**Long bones become soft with thin cortices which fracture easily
 
[[Image:Renal osteodystrophy.jpg|right|thumb|100px|<small><center>Renal osteodystrophy (Image sourced from Bristol Biomed Image Archive with permission)</center></small>]]
 
*'''Renal hyperparathyroidism'''
 
**Pathogenesis:
 
***[[Kidney Renal Failure - Pathology#Chronic|Chronic renal failure]]
 
****-> Retention of phosphate (due to reduced glomerular filtration) and inadequate production of vitamin D by kidneys
 
*****-> [[Kidney Renal Failure - Pathology#Uraemia|Hyperphosphataemia]] and hypocalcaemia (high P depresses Ca)
 
******-> Increased PTH output
 
*******-> Increased bone resorption
 
********-> '''Fibrous osteodystrophy''' - increased osteoclastic resorption of cancellous and cortical bone + proliferation of fibrous tissue
 
**Mainly in dogs
 
**Affects whole skeleton but mainly skull
 
**Bones soft and pliable
 
**Canine teeth easily removed - rubber jaw
 
**Microscopically - ''Osteodystrophia fibrosa'' (above  = fibrous osteodystrophy) +/- [[Bones Metabolic - Pathology#Osteomalacia|osteomalacia]]
 
 
 
 
 
 
 
*'''Nutritional hyperparathyroidism''' (nutritional osteodystrophy)
 
**Also called '''fibrous osteodystrophy, “rubber jaw”''' or '''“bran disease”'''
 
**More common in young, fast-growing animals
 
**Pathogenesis:
 
***Low calcium / high phosphate diets
 
****-> Decreased calcium levels in serum
 
*****-> Parathyroid gland stimulated (may become enlarged)
 
******-> Increased PTH
 
*******-> Increased bone resorption
 
**Caused by poor diet
 
***Cattle and sheep - usually mild disease
 
***'''Swine''' fed un-supplemented cereal grain, usually mild disease
 
***'''Dogs/cats''' fed all-meat or offal diets (Ca:P often as high as 1:20)
 
****Few weeks after weaning
 
****Provision of calcium alone correct the problem
 
****Very brittle bones -> sponataneous fractures
 
****Extreme porosity of the whole skeleton on radioghraphs
 
***'''Horses''' fed bran
 
****Very susceptible to high phosphorus diet
 
****Any time after weaning, susceptibility declines after seventh year
 
****Early signs:
 
*****Mild changes of gait
 
*****Stiffness
 
*****Transient shifting lameness
 
****Advanced signs:
 
*****Swelling of mandible and maxilla - 'Big head'
 
*****Dyspnoea caused by swelling of nasal and frontal bones
 
*****Teeth lost or buried in softened jaw
 
*****Fractures from mild trauma
 
*****Detached tendons and ligaments
 
*****Histologically:
 
******Marked loss of bone
 
******Replacement by proliferative tissue
 
****Often called '''''Osteodystrophia fibrosa'''''
 
 
 
===Rickets===
 
[[Image:Rickets in dog.jpg|right|thumb|100px|<small><center>Rickets in dog (Image sourced from Bristol Biomed Image Archive with permission)</center></small>]]
 
*Essentially the same disease as osteomalacia
 
*Caused by Vitamin D and phosphorus deficiency
 
*In young animals
 
*Failure of:
 
**Mineralisation of osteoid at sites of membranous growth
 
**Cartilage vascularisation and mineralisation at sites of endochondral ossification
 
*Osteoid and catilage build up at those sites
 
 
 
*Histologically:
 
**Lines of hypertrophic cartilage cells are lenghtened and disorganised
 
**Ossification at metaphysis is poor
 
**Persisting osteoid and cartilage -> shaft modelling failure
 
**Thuckened physes due to normal chondrocyte proliferation but defective removal
 
*Ends of bones enlarge -> club-like thickening of metaphysis + compression of epiphysis
 
**Most affected:
 
***Proximal humerus
 
***Distal radius
 
***Ulna
 
***Ribs
 
****Enlargement of costochondral junction - called 'rachitic rosary'
 
 
 
*Weight bearing leads to:
 
**Thickening of the physis and
 
**Flaring of the excess matrix at the metaphysis
 
*Histological lesions heal whn diet corected
 
*Minor deformities correct but major deformities remain
 
*Occurs after weaning because:
 
**''In utero'' and in milk - adeqaute nutrients obtained at expense of dam
 
*In Foals
 
**Rare - long nursing period and relatively slow rate of growth
 
*In Calves and lambs
 
**When diet deficeint of phosphorus and poor exposure to sunlight
 
*In Puppies, Kittens and Piglets
 
**Rapid growth, weaned early -> fulminating rickets if poor exposure to sunlight and lack of vitamin D in diet
 
 
 
 
 
===Osteomalacia===
 
 
*Failure of mineralisation of osteoid / softening of the bones
 
*Active resorption of bone replaced by excess osteoid on trabeculae, endosteum of cortices and [[Bones - Anatomy & Physiology#Bone Remodeling|Haversian canals]]
 
*Decreased resistance to tension -> osteoid build-up at tendon insertions
 
*In advanced disease
 
**Bones break easily and become deformed
 
**Tendons may separate from bones
 
*Caused by prolonged phosphorus and Vitamin D deficiency
 
**Vitamin D maintains normal plasma levels of calcium and phosphorus through acting on the intestines, bones and kidneys
 
*In mature animals
 
*Mainly grazing ruminants following gestation and lactation
 
**Sunlight is important for production of vitamin D in the skin of ruminants
 
**Vitamin d is also present in sun-dried hay
 
**Mostly seen where there is long grass growing season with poor sunlight
 
 
 
===Hypovitaminosis A===
 
 
 
*Vitamin A is essential for normal bone growth in foetus and neonates 
 
*Hypovitaminosis from dietary deficiency of dam -> teratogenic in pigs and large cats
 
*More commonly, deficiency in neonates (puppies, kittens, calves, piglets) on vitamin-deficient diets
 
*Dietary deficiency -> failure of [[Bones - normal#Normal structure|osteoclastic remodelling]] resulting in bone overgrowth and nerve compression
 
*Optic nerves particularly affected
 
 
 
 
 
===Hypervitaminosis A===
 
[[Image:Hypervitaminosis A.jpg|right|thumb|100px|<small><center>Hypervitaminosis A (Image sourced from Bristol Biomed Image Archive with permission)</center></small>]]
 
*Main lesions:
 
**Injury to growth cartilage -> [[Bones - normal#Physis (Growth plate)|premature closure of growth plate]]
 
**[[Bones Degenerative - Pathology#Osteoporosis (Atrophy)|Osteoporosis]]
 
**'''Exostoses'''
 
**[[Musculoskeletal Terminology - Pathology|Osteophyte]] formation in prolonged exposure
 
*In cats fed bovine liver for prolonged periods
 
**Rich in vitamin A in grazing animals
 
**Vertebrae fuse with each other due to bone proliferation - '''cervical spondylosis''' ('''ankylosing exostosis''' of the vertebral column), especially in the neck
 
*Can also be teratogenic, especially in pigs ([[Cleft Palate|cleft plate]] and abortions)
 
 
 
 
 
===Hypervitaminosis D===
 
 
 
*May be of dietary or iatrogenic origin (has narrow safety margin)
 
*Key features are hypercalcaemia with metastatic calcification of soft tissues
 
*'''Acute poisoning'''
 
**In dogs and cats often from rodenticides containing cholecalciferol
 
**Grossly:
 
***Gastrointestinal haemorrhage
 
***Foci of [[Myocardial Mineralisation|myocardial discoloration]]
 
**Microscopically:
 
***Mucosal haemorrhage
 
***Necrosis of crypts
 
***Focal myocardial necrosis
 
***Mineralisation of intestinal mucosa, [[Arterial Calcification#Medial calcification|blood vessel walls]], [[Pulmonary Calcification|lungs]] and kidneys
 
*'''Chronic poisoning'''
 
**Grossly:
 
***Intense [[Bones - normal#Normal structure|osteoclastic activity]] -> active resorption of bone, especially [[Bones - normal#Bone organisation|trabecular]]
 
**Microscopically:
 
***Excessive production of [[Bones - normal#Normal structure|osteoid]] - appears both eosinophilic and basophilic in different places
 
***Marrow cavity may be obliterated
 
***Mineralisation of soft tissues, especially [[Arterial Calcification|blood vessel walls]]
 
**Due to inhibition of [[Bones - normal#Bone resorption|PTH]] and increase of [[Bones - normal#Bone resorption|calcitonin]]
 
 
 
 
 
===Fluorine poisoning===
 
 
 
*F is widespread in nature
 
*Pastures may be contaminated by industrial processes (e.g. brick manufacture)
 
*'''Acute poisoning''':
 
**Gastroenteritis
 
**Nephrosis
 
*'''Chronic poisoning''':
 
**''Dental abnormalities''
 
***Intoxication during teeth development
 
***Foci of poor enamel formation - yellow, dark brown/black, chalky
 
***Irregular wear of teeth, chip easily
 
**''Osteodystrophy = Fluorosis''
 
***Generalised skeletal disturbance
 
***Most affected are metatarsals and mandibles
 
***Periosteal hyperostosis + endosteal bone resorption -> thickened bones with enlarged marrow cavities
 
 
 
 
 
===Lead poisoning===
 
 
 
*Lead can bind to mineral portion of bone and cartilage
 
*In young animals ingesting large dose at once
 
** -> Lead induced malfunction of osteoclasts
 
** -> Transverse band of increased density on radiographs of metaphysis = "lead line" = [[Bones Developmental - Pathology#Retention of elongated primary trabeculae|growth retardation lattice]]
 
 
 
[[Category:Musculoskeletal System - Pathology]]
 

Latest revision as of 19:07, 27 February 2011