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Also known as: '''''Addison's disease
Also known as: '''''Addison's disease
==Introduction==
==Introduction==
[[Image:Adrenal necrosis.jpg|thumb|200px|Histological section of an adrenal gland undergoing necrosis<br><small>A. Jefferies 2008</small>]]
Addison's disease occurs due to a failure to produce adequate amounts of glucocorticoid and mineralocorticoid hormones from the adrenal cortex. The majority of cases are '''primary''' and occur due to an autoimmune response directed at the endocrine cells of the adrenal glands, resulting in adrenocortical atrophy. This is an example of a [[Type IV Hypersensitivity|type IV (delayed type) hypersensitivity response]]. Smaller numbers of primary cases are caused by haemorrhage, necrosis or neoplasia within the adrenal glands. '''Secondary''' hypoadrenocorticism occurs due to a reduction in the secretion of ACTH from the anterior pituitary gland.
Addison's disease occurs due to a failure to produce adequate amounts of glucocorticoid and mineralocorticoid hormones from the adrenal cortex. The majority of cases are '''primary''' and occur due to an autoimmune response directed at the endocrine cells of the adrenal glands, resulting in adrenocortical atrophy. This is an example of a [[Type IV Hypersensitivity|type IV (delayed type) hypersensitivity response]]. Smaller numbers of primary cases are caused by haemorrhage, necrosis or neoplasia within the adrenal glands. '''Secondary''' hypoadrenocorticism occurs due to a reduction in the secretion of ACTH from the anterior pituitary gland.
===Primary Hypoadrenocorticism===
===Primary Hypoadrenocorticism===
[[Image:Adrenal atrophy.jpg|thumb|150px|Image of an adrenal gland undergoing atrophy.<br><small>A. Jefferies 2008</small>]]
[[Image:Adrenal atrophy.jpg|thumb|200px|Image of an adrenal gland undergoing atrophy.<br><small>A. Jefferies 2008</small>]]
There are several possible causes of primary hypoadrenocorticism, including:
There are several possible causes of primary hypoadrenocorticism, including:
*'''Adrenal atrophy''' is thought to be an autoimmune disease caused by a type IV immune response. Affected animals have an increased risk of developing other immune-mediated diseases, including [[Immune Mediated Haemolytic Anaemia|immune-mediated haemolytic anaemia]]. Grossly, the adrenal glands are small, difficult to locate and they are dark brown on cut sections. Histological analysis reveals the presence of an infiltrate of lymphocytes, plasma cells and macrophages.
*'''Adrenal atrophy''' is thought to be an autoimmune disease caused by a type IV immune response. Affected animals have an increased risk of developing other immune-mediated diseases, including [[Immune Mediated Haemolytic Anaemia|immune-mediated haemolytic anaemia]]. Grossly, the adrenal glands are small, difficult to locate and they are dark brown on cut sections. Histological analysis reveals the presence of an infiltrate of lymphocytes, plasma cells and macrophages.
[[Image:Adrenal necrosis2.jpg|thumb|150px|Image of an adrenal gland undergoing necrosis. Note the areas of haemorrhage within the cortex of the gland.<br><small>A. Jefferies 2008</small>]]
[[Image:Adrenal necrosis2.jpg|thumb|200px|Image of an adrenal gland undergoing necrosis. Note the areas of haemorrhage within the cortex of the gland.<br><small>A. Jefferies 2008</small>]]
*'''Adrenal necrosis''' may be caused by certain infections or it may be a sequel to other metabolic diseases. In horses, [[Salmonella|'''salmonellosis''']] may cause adrenal necrosis but, in small animals, necrosis is more likely to occur due to myoarteritis in uraemic animals resulting in ischaemia of the adrenal gland. Idiopathic necrosis may occur with no apparent cause. Grossly, the glands contain areas of red haemorrhage with yellow necrotic foci.
*'''Adrenal necrosis''' may be caused by certain infections or it may be a sequel to other metabolic diseases. In horses, [[Salmonella|'''salmonellosis''']] may cause adrenal necrosis but, in small animals, necrosis is more likely to occur due to myoarteritis in uraemic animals resulting in ischaemia of the adrenal gland. Idiopathic necrosis may occur with no apparent cause. Grossly, the glands contain areas of red haemorrhage with yellow necrotic foci.
===Secondary Hypoadrenocortisism===
===Secondary Hypoadrenocortisism===
Deficient pituitary secretion of ACTH. Often '''iatrogenic''' due to withdrawal of glucocorticoid treatment. Prolonged high dose treatment induce adrenal atrophy due to the effect of negative feedback on the pituitary. The withdrawal of drug must be gradual to allow to adrenal gland to return to function over a period of time.
Deficient pituitary secretion of ACTH. Often '''iatrogenic''' due to withdrawal of glucocorticoid treatment. Prolonged high dose treatment induce adrenal atrophy due to the effect of negative feedback on the pituitary. The withdrawal of drug must be gradual to allow the adrenal gland to return to function over a period of time.
Usually little effect on mineralocorticoids as ACTH has little trophic effect on their production.
Usually little effect on mineralocorticoids as ACTH has little trophic effect on their production.
==Treatment==
==Treatment==
===Stabilisation===
===Stabilisation===
It is important to get as much information during initial triage of a collapsed animal as possible. Some differentials include anaphylaxis, HGE, Parvo, arrythmias, pericardial effusion, any cause of hyperkalemia, hemoabdomen. A FAST ultrasound exam can be used to investigate anaphylaxis (gall bladder edema), pericardial effusion, and hemoabdomen. ECG can evaluate for heart block and bradycardias as well as typical hyperkalemia induced changes (prolonged S-T interval, enlarged T waves). Electrolytes, PCV, blood gas, lactate can all help with initial work up and diagnosis.
The classic Addisonian is ~ 3 years old and as such anaphylaxis and HGE are the most common differentials. Differentiating anaphylaxis from Addison's early on is critical to saving these patients.
Since collapsed, bradycardic animals are unlikely to survive for long, urgent intervention is required to stabilise these patients. '''Intra-venous 0.9% sodium chloride (saline) solution''' should be provided at shock rates to restore normovolaemia and begin to correct the electrolyte imbalances. Additional '''glucose''' can be added to fluids in hypoglycaemic animals but blood glucose levels should be monitored closely if this is undertaken.
Since collapsed, bradycardic animals are unlikely to survive for long, urgent intervention is required to stabilise these patients. '''Intra-venous 0.9% sodium chloride (saline) solution''' should be provided at shock rates to restore normovolaemia and begin to correct the electrolyte imbalances. Additional '''glucose''' can be added to fluids in hypoglycaemic animals but blood glucose levels should be monitored closely if this is undertaken.
When the diagnosis has been made with some certainty, '''intra-venous glucocorticoid replacement therapy''' can be initiated together with a '''mineralocorticoid'''. Dexamethasone is the corticosteroid of choice as it has greater mineralocorticoid activity than other products. Although there is an intra-muscular injectable mineralocorticoid (desoxycorticosterone acetate) available in the USA, this is not usually required for stabilisation.
Hypothermia must be corrected slowly so as not to cause cell shrinkage in the brain. Hyperkalemia will improve with [[Fluid therapy|IV fluid therapy]], but in the case of life threatening arrhythmias 10% CaGluconate can be given to protect the heart (1ml/kg @ 1ml/minute to effect). Insulin and Dextrose can be used to drive potassium into the cells and sodium bicarbonate can be used to correct acidosis.
When the diagnosis has been made with some certainty, '''intra-venous glucocorticoid replacement therapy''' can be initiated together with a '''mineralocorticoid'''. Hydrocortisone sodium succinate is the steroid of choice as it is short acting and provides equal glucocorticoid and mineralocorticoid activity. Although there is an intra-muscular injectable mineralocorticoid (desoxycorticosterone acetate) available in the USA, this is not usually required for stabilisation.
Avoid giving prednisone or prednisolone as it will alter the results of ACTH stim test. Dexamethasone or Dex-SP are accetable pre-test steroids.
[[Gastroprotective Drugs|'''Gastro-protectant drugs''']] (such as sucralfate, ranitidine or omeprazole) may be administered to vomiting animals and '''antibiotics''' should be provided to any animals that develop pyrexia.
[[Gastroprotective Drugs|'''Gastro-protectant drugs''']] (such as sucralfate, ranitidine or omeprazole) may be administered to vomiting animals and '''antibiotics''' should be provided to any animals that develop pyrexia.
The prognosis for long term survival is excellent for animals with hypoadrenocorticism provided that any crisis is controlled.
The prognosis for long term survival is excellent for animals with hypoadrenocorticism provided that any crisis is controlled.
==Literature Search==
{{Learning
|flashcards = [[Small Animal Abdominal and Metabolic Disorders Q&A 07]]
|literature search = [http://www.cabdirect.org/search.html?it=any&q2=Addison%27s+disease&q1=Hypoadrenocorticism&calendarInput=yyyy-mm-dd&q3=Addisons+disease&occuring1=title&show=all&rowId=1&rowId=2&rowId=3&options1=AND&options2=OR&options3=OR&occuring3=title&occuring2=title&publishedend=yyyy&la=any&publishedstart=yyyy&fq=sc%3A%22ve%22&y=12&x=43 Hypoadrenocorticism publications]
}}
==References==
Ettinger, S.J, Feldman, E.C. (2005) '''Textbook of Veterinary Internal Medicine''' (6th edition, volume 2) Elsevier Saunders Company
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[[Category:Cell Mediated Autoimmune Diseases]][[Category:Dog - Endocrine System]][[Category:Expert Review]]
[[Category:Cell Mediated Autoimmune Diseases]][[Category:Endocrine Diseases - Dog]][[Category:Expert Review]]
[[Category:Neurological Pathology - Dog]]
[[Category:Neurological Diseases - Dog]][[Category:Immunological Diseases - Dog]]
[[Category:Adrenal Glands - Pathology]]