Difference between revisions of "Diabetes Mellitus"
Jump to navigation
Jump to search
m |
|||
| Line 1: | Line 1: | ||
<center><big>[[Pancreas|'''BACK TO PANCREAS''']]</big></center> | <center><big>[[Pancreas|'''BACK TO PANCREAS''']]</big></center> | ||
| − | <center><big>[[Pancreas - | + | <center><big>[[Endocrine Pancreas - Pathology|'''BACK TO PANCREAS - ENDOCRINE''']]</big></center> |
='''Diabetes mellitus'''= | ='''Diabetes mellitus'''= | ||
| Line 7: | Line 7: | ||
*Occurs in most species, most commonly in dog and cat | *Occurs in most species, most commonly in dog and cat | ||
*Predisposed to [[Pancreas - inflammatory|pancreatitis]] and may also have [[EPI|pancreatic insufficiency]] | *Predisposed to [[Pancreas - inflammatory|pancreatitis]] and may also have [[EPI|pancreatic insufficiency]] | ||
| − | *Persistent [[Pancreas - | + | *Persistent [[Endocrine Pancreas - Pathology#Glucagonoma|increase in glucagon]] may cause hyperglycaemia |
*More common in mature dogs, twice as common in females than in males | *More common in mature dogs, twice as common in females than in males | ||
===Aetiology=== | ===Aetiology=== | ||
Can be caused by | Can be caused by | ||
| − | *Absolute deficiency of insulin due to [[Pancreas - | + | *Absolute deficiency of insulin due to [[Endocrine Pancreas - Pathology#Degenerative pathology|degenerative changes]] in beta cells (Miniature poodles, Dachsunds,Terriers seem to be predisposed) |
*Antagonism of insulin by hormones from the adrenal and thyroid glands, anterior pituitary causing high levels of blood glucose (e.g. progesterone may initiate postoestrus DM in the bitch, hyperadrenocorticism) | *Antagonism of insulin by hormones from the adrenal and thyroid glands, anterior pituitary causing high levels of blood glucose (e.g. progesterone may initiate postoestrus DM in the bitch, hyperadrenocorticism) | ||
*Complication of pancreatic fibrosis | *Complication of pancreatic fibrosis | ||
Revision as of 10:44, 31 July 2008
Diabetes mellitus
- Clinically significant glucose intolerance
- Chronic disease caused by absolute or relevant deficiency of insulin and therefore disorders of carbohydrate metabolism
- Occurs in most species, most commonly in dog and cat
- Predisposed to pancreatitis and may also have pancreatic insufficiency
- Persistent increase in glucagon may cause hyperglycaemia
- More common in mature dogs, twice as common in females than in males
Aetiology
Can be caused by
- Absolute deficiency of insulin due to degenerative changes in beta cells (Miniature poodles, Dachsunds,Terriers seem to be predisposed)
- Antagonism of insulin by hormones from the adrenal and thyroid glands, anterior pituitary causing high levels of blood glucose (e.g. progesterone may initiate postoestrus DM in the bitch, hyperadrenocorticism)
- Complication of pancreatic fibrosis
- Immune-mediated disease
- Insulin binding antibodies, insulinase and plasma antagonists imbalance
- Chronic insulin resistance (due to excessive food intake and down regulation of receptors) results in hyperinsulinism leading to islet exhaustion
- Glycogenosis and hydropic degeneration, amyloidosis (esp. cats)
- Other factors, eg. stress, viral infection, genetic factors
Clinical signs
- Hyperglycaemia
- Polyuria
- Polydypsia
- Polyphagia
- Weight loss
- Muscle wasting (but some animals may present obese)
- Hepatomegaly
- Cataracts (dogs)
- Later stages when becoming ketoacidotic
- Dehydration
- Depression
- Inappetance
- Vomiting
- Diarrhoea
- Ketotic breath
- Reduced cardiac output (due to loss of water and sodium), reduced blood pressure and renal flow causing circulatory collapse, coma and death
Pathology
- Pancreas appers normal or reduced in size due to fibrosis
- In cats, amyloidosis is sometimes present in the islets
- Fatty change is consistently present in the liver and kidneys
- The lens in the eye of the dog is often opaque due to deposition of sorbitol and fructose causing it to swell as the are not freely permeable (glucose is converted into sorbitol and fructose once the glycolytic pathway is saturated)
- In immune-mediated isletitis - progressive lymphoplasmacytic infiltration and selective destruction of islet cells
- Possible vacuolation of islet cells and epithelium of small ducts