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== Introduction<br>  ==
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ADH from the posterior pituitary stimulates water uptake from the distal convoluted tubule and collecting ducts of the kidney and so conserves water. Release is regulated by:
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Anti- Diuretic Hormone ADH, from the posterior pituitary stimulates water uptake from the distal convoluted tubule and collecting ducts of the kidney and so conserves water. Release is regulated by osmoreceptors in the hypothalamus and volume receptors in the hypothalamus.A deficiency of ADH is known as '''Diabetes insipidus'''.  
*Osmoreceptors in the hypothalamus.
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*Volume receptors in the hypothalamus.
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A deficiency of ADH is known as '''Diabetes insipidus'''.
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Causes of deficiany may by '''c''''''entral''': failure to synthesise or release ADH, or '''n''''''ephrogenic''': failure of the nephrons to respond to ADH present in the kidney.  
May be:
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*'''Central''': failure to synthesise or release ADH.
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*'''Nephrogenic''': Failure of the nephrons to respond to ADH present in the kidney.
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''Clinical Signs''
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<br>
*Marked polyuria; 5-20X normal output, often resulting in nocturia and incontinence.
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*Marked polydipsia; animal will search for water.
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*Dehydration.
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*Weight loss.
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*Anorexia.
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*Neurological signs if neoplastic in origin.
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''Differential diagnosis'':
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== Clinical Signs<br> ==
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Presents similarly to '''Psychogenic polydipsia'''.  Patients drink excessively leading to overhydration and a functional lack of ADH (none is released as water does not need to be conserved).  The kidney in this case will have decreased ability to concentrate urine due to '''medullary washout'''. The hypertonicity within the medulla is abolished by the excess water.  
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There will be a marked polyuria; '''5-20X normal outpu''''''t''', often resulting in nocturia and incontinence. There will also be a desperate polydipsia; animal will search for water.  
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''Diagnosis'':
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Other clinical signs include dehydration, weight loss, anorexia and neurological signs if neoplastic in origin.
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*Urine specific gravity is low ('''1.001-1.005''')<br>Solute is absorbed in excess of water thus demonstrating a good tubular function.
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<br>
*Dehydration so see mildly elevated PCV and TP.
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''Psychogenic polydipsia: plasma osmolality decreased due to excess water in contrast to increased plasma osmolality with DI due to dehydration.''
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== Diagnosis<br> ==
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*'''Water deprivation test''': Aims to measure urine osmolality after 12-24 hours water deprivation to determine whether ADH is indeed deficient.
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The differential diagnosis of '''psychogenic polydipsia '''must be excluded. In this disease, patients drink excessively leading to overhydration and a functional lack of ADH (none is released as water does not need to be conserved). The kidney in this case will have decreased ability to concentrate urine due to '''medullary washout'''. The hypertonicity within the medulla is abolished by the excess water.''<br>''
**Collect initil urine and plasma samples for osmolality.
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**Weigh patient.
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**Withhold food and fluid.
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**Collect urine and plasma after 6 hours and thence 2 hourly. 
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**'''STOP''' when:
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***Patient displays concentraing ability.
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***Patient loses >5% bodyweight.
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***24 hours have passed.
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A positive test for diabetes insipidus is a failure to concentrate urine >1.010 after 12-24 hours.
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A urine sample should be taken. In Diabetes insipidus, urine specific gravity is low ('''1.001-1.005''').<br>
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''If psychogenic polydipsia is suspected then gradually restrict water for 3 days prior to test to avoid medullary washout giving a false positive test.''
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Blood tests will show dehydration so will see mildly elevated PCV and TP.  
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*'''ADH response test''': Administer '''Desmopressin''' i/m.  Monitor specific gravity of urine 2 hourly. 
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<br>  
**'''Central''' diabetes insipidus will concentrate urine >1.020.
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**'''Nephrogenic''' diabetes insipidus will not be able to concentrate the urine at all in response to the synthetic ADH.  SG <1.010.<br> Nb. A positive ADH response test means nothing unless preceded by a water deprivation test to prove the presence of diabetes insipidus.
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''Treatment'':
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When other differentials have been excluded, it may be neccessary to perform a'''water''''''deprivation test''': This aims to measure urine osmolality after 12-24 hours water deprivation to determine whether ADH is indeed deficient.  
*'''Desmopressin''': Central disease only.  Expensive.
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*'''Thiazide diuretics''': ''Paradoxical effect''.  By inhibiting the reabsorption of sodium in the proximal convoluted tubule the volume of fluid within the ECF will fall and hence the GFR will also decrease, reducing water loss. 
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*'''Chlorpropamide''': Potentiates effect of ADH on the tubules.
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*'''Carbemazepine''': Acts similarly to chlorpropamide.
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*'''No therapy''': Animals kept outdoors with free access to water at all times.
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''Prognosis'':
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Steps: Collect initial urine and plasma samples for osmolality and weigh patient. Withhold food and fluid.&nbsp;Collect urine and plasma after 6 hours and thence 2 hourly.This test can be damagine to the animals health and must not be performed unless diagnosis is stongly presumed as it can become an animal welfare issue if not. '''STOP''' when: patient displays concentraing ability or patient loses &gt;5% bodyweight or&nbsp;24 hours have passed.
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Congenital central diabetes insipidus has a favourable prognosis and can be treated with desmopressin. Nephrogenic diabetes insipidus has a more guarded prognosis.
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A positive test for diabetes insipidus is a failure to concentrate urine &gt;1.010 after 12-24 hours.  
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Any expanding tumour, particularly if neurological signs are present, carries a poor prognosis.
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''<br>''
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An'''ADH response test''' can also be performed. Administer '''Desmopressin''' i/m and monitor specific gravity of urine 2 hourly. '''Central''' diabetes insipidus will concentrate urine &gt;1.020 whereas n'''ephrogenic''' diabetes insipidus will not be able to concentrate the urine at all in response to the synthetic ADH. SG &lt;1.010.<br> Nb. A positive ADH response test means nothing unless preceded by a water deprivation test to prove the presence of diabetes insipidus.  
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Central diabtetes insipidus secondary to head trauma varies in prognosis and spontaneous recovery may occur.
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<br>
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[[Category:To Do - Clinical]][[Category:Endocrine Diseases - Dog]][[Category:Endocrine Diseases - Cat]]
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== Treatment<br> ==
[[Category:Endocrine System - Pathology]]
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A few different treatment options have been described for this disease such as '''Desmopressin''': used for central disease only as is expensive.&nbsp;'''Thiazide diuretics''' work by p''aradoxical effect'' by inhibiting the reabsorption of sodium in the proximal convoluted tubule the volume of fluid within the ECF will fall and hence the GFR will also decrease, reducing water loss. '''Chlorpropamide '''works by potentiates effect of ADH on the tubules. '''Carbemazepine''': Acts similarly to chlorpropamide.
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Many owners choose not to medicate and will manage the disease by keeping animal outdoors with free access to water at all times.
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<br>
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== Prognosis''<br>'' ==
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Congenital central diabetes insipidus has a favourable prognosis and can be treated with desmopressin. Nephrogenic diabetes insipidus has a more guarded prognosis.
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Any expanding tumour, particularly if neurological signs are present, carries a poor prognosis.
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Central diabtetes insipidus secondary to head trauma varies in prognosis and spontaneous recovery may occur.
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<br>
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== References<br> ==
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Ettinger, S.J. and Feldman, E. C. (2000) Textbook of Veterinary Internal Medicine Diseases of the Dog and Cat Volume 2 (Fifth Edition) W.B. Saunders Company<br>Ettinger, S.J, Feldman, E.C. (2005) Textbook of Veterinary Internal Medicine (6th edition, volume 2)W.B. Saunders Company <br>Nelson, R.W. and Couto, C.G. (2009) Small Animal Internal Medicine (Fourth Edition) Mosby Elsevier. <br><br>
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<br>
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[[Category:To_Do_-_Review]] [[Category:Endocrine_Diseases_-_Dog]] [[Category:Endocrine_Diseases_-_Cat]] [[Category:Endocrine_System_-_Pathology]]
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