Difference between revisions of "Muscles Developmental - Pathology"

Revision as of 17:29, 3 March 2011

Caused by a deficiency of an enzyme
See general pathology
Type II glycogenosis
- Deficiency of acid maltase
- In Shorthorn cattle
- Muscular weakness and incoordination
- Glycogen stored in skeletal muscle, heart and CNS
- Type I and II muscle fibres contain glycogen vacuoles
Type III glycogenosis
- Deficiency of debranching enzyme
- In dogs
- Causes hypertrophic cardiomyopathy and hepatomegaly
- Glycogen in skeletal and cardiac muscle, neurons nad hepatocytes

Acquired
- Autoimmune disease
  - Antibodies directed against acetyl choline receptors
- Associated with thymomas, megaoesophagus and dysphagia
- In adult dogs
Congenital
- Inherited deficiency in acetyl choline receptors
- Rare
- Newfoundland, Jack Russel Terrier, Springer Spaniels – genetic predisposition
- In dogs – 4 DLA genes recognized: DLA-12, DLA-88, DLA-79 and DLA-64
- Associated with HLA gene in humans
- No antibodies against acetyl choline receptors in serum
- Non-specific muscle disuse atrophy and fibrosis or no changes on histology
Both forms manifest as weakness which worsens on exercise

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 ===[[Myofibrillar Hypoplasia]]===
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-===Muscular dystrophies===
+===[[Muscular Dystrophy]]===
-*Inherited group of degenerative muscular diseases
-*Progressive muscle weakness and wasting
-*Usually due to a genetic fault -> muscular protein deficiency
-**Duchenne MD in humans due to dystrophin deficiency also present in some animals
-**Dystrophin gene mutations reported in the Golden Retriever, Rottweiler, German shorthaired pointer and Irish terrier ''etc.''
-*Inadequate [[Muscle Regeneration - Anatomy & Physiology|regeneration]], [[Muscles Hyperplastic and Neoplastic - Pathology#Hypertrophy|compensatory hypertrophy]]
-*More about [[Muscular dystrophy]]
-[[Category:Muscles - Developmental Pathology]]