Difference between revisions of "Hyperparathyroidism"
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− | + | [[Image:parathyroidadeoma.jpg|thumb|right|100px|Parathyroid adenoma. Image courtesy of Biomed Archive.]] | |
− | + | ===Primary=== | |
+ | * Primary hyperparathyroidism is caused by glandular hyperplasia or neoplasia. [[Image:parathyroidhyperplasia.jpg|thumb|right|100px|Parathyroid hyperplasia. Image courtesy of Biomed Archive.]] | ||
+ | * Rare. | ||
+ | ===Secondary=== | ||
+ | * Secondary hyperparathyroidism causes [[Bones Metabolic - Pathology#Hyperparathyroidism|fibrous osteodystrophy or "rubber jaw"]]. | ||
+ | * In secondary hyperparathyroidism, the gland is overactive due to another condition coexisting in the body, rather than a primary parathyroid gland defect. | ||
+ | * There are two common forms of secondary hyperparathyroisism: | ||
+ | *# [[Hyperparathyroidism#Nutritional Hyperparathyroidism|'''Nutritional Hyperparathyroidism''']] | ||
+ | *#* This includes [[Metabolic Bone Disease|Metabolic Bone Disease]]. | ||
+ | *# [[Hyperparathyroidism#Renal Hyperparathyroidism|'''Renal Hyperparathyroidism''']] | ||
+ | * Both forms result in increased osteoclastic resorption of bone and deposition of fibro-osteoid matrix that fails to mineralise. | ||
+ | ** Flat bones of the skull swell. | ||
+ | ** Fibrous tissue is seen around the tooth roots. | ||
+ | ** Bone softens in adult animals. | ||
+ | *** This is what gives rise to the term "rubber jaw". | ||
+ | *** Long bones become soft with thin cortices. | ||
+ | **** These fracture easily. | ||
+ | ====Nutritional Hyperparathyroidism==== | ||
+ | [[Image:secondaryhyperparathyroidism.jpg|thumb|right|100px|Secondary hyperparathyroidism - "rubber jaw". Image courtesy of Biomed Archive.]] | ||
+ | * Nutritional hyperparathyroidism is also known as nutritional osteodystrophy. | ||
+ | * This occurs most commonly in: | ||
+ | ** Young, fast-growing animals | ||
+ | ** Animals with a poor diet, for example: | ||
+ | *** Swine fed unsupplemented cereal grain | ||
+ | *** Dogs and cats fed all-meat diets | ||
+ | *** Horses fed bran | ||
+ | **** In this case, nutritional hyperparathyroidism is known as "bran disease". | ||
+ | =====Pathogenesis===== | ||
+ | * Pathogenesis follows low calcium/high phosphate diets. | ||
+ | ** These lead to decreased serum calcium levels, stimulating [[Calcium#Parathyroid Hormone (PTH)|PTH]] release. | ||
+ | ** The increase in PTH gives an increase in bone resorption, causing pathology. | ||
− | == | + | =====Pathology===== |
− | [[ | + | * '''Gross''' |
− | [[Image: | + | ** Severe cases may show: |
− | + | *** Maxillary and mandibular swelling | |
− | [[Image:Renal_osteodystrophy.jpg|thumb|right| | + | *** [[:Category:Teeth - Anatomy & Physiology|Teeth]] lost or buried in soft tissue |
− | + | *** Nasal and frontal bone enlargement, leading to dyspnoea | |
− | + | *** Long bone fracture | |
+ | *** Detatchment tendons and ligaments | ||
+ | ** Early or less severe cases are characterised by shifting lameness and ill thrift. | ||
+ | * '''Histological''' | ||
+ | ** Osteoclastic resorption | ||
+ | ** Fibrous replacement | ||
+ | =====Metabolic Bone Disease===== | ||
+ | * Metabolic bone disease affects lizards in captivity, particularly young green iguanas | ||
+ | * The condition is caused by: | ||
+ | ** Dietary deficiency of calcium and vitamin D | ||
+ | *** For example, due to poor lighting (which diminishes viatmin D production). | ||
+ | ** Dietary excess of phosphorus | ||
+ | ** Certain toxicities | ||
+ | ** Diseases of the kidneys, [[Liver - Anatomy & Physiology|liver]] or parathyroid | ||
+ | *** This aetiology is rare | ||
+ | * Clinical signs include: | ||
+ | ** Lethargy | ||
+ | ** Inability to support weight | ||
+ | ** Rounded skull | ||
+ | ** Spontaneous fractures | ||
+ | ** Adult animals also show signs of [[Hypocalcaemia|hypocalcaemia]] | ||
+ | * The skeleton shows reduced density on radiography. | ||
+ | ====Renal Hyperparathyroidism==== | ||
+ | * Renal Hyerparathyroidism is mostly seen in the dog as an expression of chronic renal disease. | ||
+ | =====Pathogenesis===== | ||
+ | [[Image:renalhyperparathyroidism.jpg|thumb|right|100px|Parathyroid hyperplasia in renal hyperparathyroidism. Image courtesy of Biomed Archive.]] | ||
+ | # Chronic renal disease results in reduced glomerular filtration. | ||
+ | # As glomerular filtration is reduced, phosphate is retained. Chronic renal failure also causes inadequate vitamin D production in the kidneys. | ||
+ | # Hyperphosphataemia develops due to phosphate retention. | ||
+ | #* Hypocalcaemia also occurs, as high levels of phosphate depress calcium levels. | ||
+ | # PTH is released in an attempt to maintain the correct blood calcium:phosphorous ratio. This can have several effects: | ||
+ | #* Parathyroid hyperplasia | ||
+ | #** I.e. '''renal secondary hyperparathyroidism'''. | ||
+ | #* Soft tissue mineralisation | ||
+ | #** Particularly seen in dogs | ||
+ | #** Calcium is commonly deposited in the subpleural connective tissue of the intercostal spaces. | ||
+ | #** Calcification also occurs in other sites, e.g. [[Monogastric Stomach - Anatomy & Physiology|stomach]] wall, lungs, kidneys. | ||
+ | #* Increased bone resorption | ||
+ | #** This causes fibrous osteodystrophy, or "rubber jaw". | ||
+ | =====Pathology===== | ||
+ | [[Image:Renal_osteodystrophy.jpg|thumb|right|100px|"Rubber jaw" in renal osteodystrophy. Image courtesy of Biomed Archive.]] | ||
+ | * Pathology seen in renal hyperparathyroidism is very similar to that seen in nutritional hyperparathyroidism. | ||
+ | * '''Gross''' | ||
+ | ** The major gross presentation is a fibrous osetodystrophy, or rubber jaw. | ||
+ | *** The maxillae and mandible appear swollen. | ||
+ | *** Radiographically, bone shows reduced density, and [[:Category:Teeth - Anatomy & Physiology|teeth]] hence appear embedded in soft tissue. | ||
+ | *** However, only a few cases of chronic renal disease show such severe bone lesions. | ||
+ | ** Other lesions may also be seen. | ||
+ | *** Intercostal muscles may be calcified. | ||
+ | *** Bone marrow lesions may cause anaemia. | ||
+ | *** The lung may show oedema, and have calcified alveolar walls. | ||
+ | * '''Histological''' | ||
+ | ** Osteoclastic resorption | ||
+ | ** Fibrous replacement | ||
− | |||
+ | ==From musculoskeletal== | ||
− | + | *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''''' | ||
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− | + | [[Category:Bones - Metabolic Pathology]] | |
− | + | [[Category:Parathyroid Glands - Pathology]] | |
− | + | [[Category:To Do - Clinical]] | |
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Revision as of 18:50, 27 February 2011
Primary
- Primary hyperparathyroidism is caused by glandular hyperplasia or neoplasia.
- Rare.
Secondary
- Secondary hyperparathyroidism causes fibrous osteodystrophy or "rubber jaw".
- In secondary hyperparathyroidism, the gland is overactive due to another condition coexisting in the body, rather than a primary parathyroid gland defect.
- There are two common forms of secondary hyperparathyroisism:
- Both forms result in increased osteoclastic resorption of bone and deposition of fibro-osteoid matrix that fails to mineralise.
- Flat bones of the skull swell.
- Fibrous tissue is seen around the tooth roots.
- Bone softens in adult animals.
- This is what gives rise to the term "rubber jaw".
- Long bones become soft with thin cortices.
- These fracture easily.
Nutritional Hyperparathyroidism
- Nutritional hyperparathyroidism is also known as nutritional osteodystrophy.
- This occurs most commonly in:
- Young, fast-growing animals
- Animals with a poor diet, for example:
- Swine fed unsupplemented cereal grain
- Dogs and cats fed all-meat diets
- Horses fed bran
- In this case, nutritional hyperparathyroidism is known as "bran disease".
Pathogenesis
- Pathogenesis follows low calcium/high phosphate diets.
- These lead to decreased serum calcium levels, stimulating PTH release.
- The increase in PTH gives an increase in bone resorption, causing pathology.
Pathology
- Gross
- Severe cases may show:
- Maxillary and mandibular swelling
- Teeth lost or buried in soft tissue
- Nasal and frontal bone enlargement, leading to dyspnoea
- Long bone fracture
- Detatchment tendons and ligaments
- Early or less severe cases are characterised by shifting lameness and ill thrift.
- Severe cases may show:
- Histological
- Osteoclastic resorption
- Fibrous replacement
Metabolic Bone Disease
- Metabolic bone disease affects lizards in captivity, particularly young green iguanas
- The condition is caused by:
- Dietary deficiency of calcium and vitamin D
- For example, due to poor lighting (which diminishes viatmin D production).
- Dietary excess of phosphorus
- Certain toxicities
- Diseases of the kidneys, liver or parathyroid
- This aetiology is rare
- Dietary deficiency of calcium and vitamin D
- Clinical signs include:
- Lethargy
- Inability to support weight
- Rounded skull
- Spontaneous fractures
- Adult animals also show signs of hypocalcaemia
- The skeleton shows reduced density on radiography.
Renal Hyperparathyroidism
- Renal Hyerparathyroidism is mostly seen in the dog as an expression of chronic renal disease.
Pathogenesis
- Chronic renal disease results in reduced glomerular filtration.
- As glomerular filtration is reduced, phosphate is retained. Chronic renal failure also causes inadequate vitamin D production in the kidneys.
- Hyperphosphataemia develops due to phosphate retention.
- Hypocalcaemia also occurs, as high levels of phosphate depress calcium levels.
- PTH is released in an attempt to maintain the correct blood calcium:phosphorous ratio. This can have several effects:
- Parathyroid hyperplasia
- I.e. renal secondary hyperparathyroidism.
- Soft tissue mineralisation
- Particularly seen in dogs
- Calcium is commonly deposited in the subpleural connective tissue of the intercostal spaces.
- Calcification also occurs in other sites, e.g. stomach wall, lungs, kidneys.
- Increased bone resorption
- This causes fibrous osteodystrophy, or "rubber jaw".
- Parathyroid hyperplasia
Pathology
- Pathology seen in renal hyperparathyroidism is very similar to that seen in nutritional hyperparathyroidism.
- Gross
- The major gross presentation is a fibrous osetodystrophy, or rubber jaw.
- The maxillae and mandible appear swollen.
- Radiographically, bone shows reduced density, and teeth hence appear embedded in soft tissue.
- However, only a few cases of chronic renal disease show such severe bone lesions.
- Other lesions may also be seen.
- Intercostal muscles may be calcified.
- Bone marrow lesions may cause anaemia.
- The lung may show oedema, and have calcified alveolar walls.
- The major gross presentation is a fibrous osetodystrophy, or rubber jaw.
- Histological
- Osteoclastic resorption
- Fibrous replacement
From musculoskeletal
- 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
Primary hyperparathyroidism
- This is increased production of PTH not related to calcium or phosphorus levels
- Due to parathyroid neoplasia or bilateral idiopathic parathyroid hyperplasia
- Rare
Secondary hyperparathyroidism
- 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
- Renal hyperparathyroidism
- Pathogenesis:
- Chronic renal failure
- -> Retention of phosphate (due to reduced glomerular filtration) and inadequate production of vitamin D by kidneys
- -> 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
- -> Increased bone resorption
- -> Increased PTH output
- -> Hyperphosphataemia and hypocalcaemia (high P depresses Ca)
- -> Retention of phosphate (due to reduced glomerular filtration) and inadequate production of vitamin D by kidneys
- Chronic renal failure
- 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) +/- osteomalacia
- Pathogenesis:
- 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
- -> Increased PTH
- -> Parathyroid gland stimulated (may become enlarged)
- -> Decreased calcium levels in serum
- Low calcium / high phosphate diets
- 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