Difference between revisions of "Diabetes Insipidus"

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== Introduction  ==
 
  
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[[Pituitary Gland - Anatomy & Physiology#Antidiuretic Hormone|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.  
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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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*Osmoreceptors in the hypothalamus.
 +
*Volume receptors in the hypothalamus.
  
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Causes of deficiency may be:
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A deficiency of ADH is known as '''Diabetes insipidus'''.
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:'''Central''': Central DI is characterized by decreased secretion of antidiuretic hormone (ADH)—also known as arginine vasopressin (AVP)—which gives rise to polyuria and polydipsia by diminishing the patient’s ability to concentrate urine.
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May be:
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Diminished or absent ADH can be the result of a defect in 1 or more sites involving the hypothalamic osmoreceptors, the supraoptic or paraventricular nuclei, or the supraopticohypophyseal tract.
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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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:'''Nephrogenic''': failure of the [[:Category:Nephron|nephrons]] to respond to ADH present in the kidney.Is characterized by a decrease in the ability to concentrate urine due to a resistance to ADH action in the kidney. Nephrogenic DI can be observed in chronic renal insufficiency, lithium toxicity, hypercalcemia, hypokalemia, and tubulointerstitial disease, rarely, diabetes insipidus may be hereditary.
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''Clinical Signs''
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*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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'''Psychogenic diabetes insipidus (psychogenic polydipsia)''' : It results from a neurological disorder of thirst control or as a result of some behavioral problem that triggers excessive water intake. In either case, the abnormally large volume of excreted urine in animals with psychogenic polydipsia is caused by excessive water intake (polydipsia), rather than by some primary problem with kidney, pituitary or hypothalamic function.
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''Differential diagnosis'':
  
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== Clinical Signs ==
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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 output''', 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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*Dehydration so see mildly elevated PCV and TP.
  
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== Diagnosis  ==
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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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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.  
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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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**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 urine sample should be taken. In Diabetes insipidus, urine specific gravity is low ('''1.001-1.005''').
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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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Blood tests will show dehydration so will see mildly elevated PCV and TP.  
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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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When other differentials have been excluded, it may be necessary 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.  
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*'''ADH response test''': Administer '''Desmopressin''' i/m.  Monitor specific gravity of urine 2 hourly. 
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**'''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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Steps: Collect initial urine and plasma samples for osmolality and weigh patient. Withhold food and fluid. Collect urine and plasma after 6 hours and thence 2 hourly. This test can be damaging to the animals health and must not be performed unless diagnosis is strongly presumed as it can become an animal welfare issue if not. '''STOP''' when: patient displays concentrating ability or patient loses >5% bodyweight or 24 hours have passed.  
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''Treatment'':
 +
*'''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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A positive test for diabetes insipidus is a failure to concentrate urine >1.010 after 12-24 hours.
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''Prognosis'':
  
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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 (>1.020) whereas '''nephrogenic''' diabetes insipidus will not be able to concentrate the urine at all in response to the synthetic ADH (SG <1.010.)
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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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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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Any expanding tumour, particularly if neurological signs are present, carries a poor prognosis.
  
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== Treatment  ==
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Central diabtetes insipidus secondary to head trauma varies in prognosis and spontaneous recovery may occur.
  
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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.
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[[Category:To Do - Clinical]][[Category:Endocrine Pathology - Dog]]
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'''Thiazide diuretics''' work by ''paradoxical effect'' by inhibiting the reabsorption of sodium in the proximal convoluted tubule. The volume of fluid within the extracellular fluid (ECF) will fall and hence the [[GFR]] will also decrease, reducing water loss. '''Chlorpropamide '''works by potentiating the 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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== Prognosis  ==
 
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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 diabetes insipidus secondary to head trauma varies in prognosis and spontaneous recovery may occur.
 
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{{Learning
 
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|flashcards = [[Feline Medicine Q&A 04]]
 
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}}
 
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== References  ==
 
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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''
 
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Ettinger, S.J, Feldman, E.C. (2005) '''Textbook of Veterinary Internal Medicine '''(6th edition, volume 2) ''W.B. Saunders Company ''
 
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Nelson, R.W. and Couto, C.G. (2009) '''Small Animal Internal Medicine '''(Fourth Edition)'' Mosby Elsevier. ''
 
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{{review}}
 
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{{OpenPages}}
 
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[[Category:Expert_Review - Small Animal]] [[Category:Endocrine_Diseases_-_Dog]] [[Category:Endocrine_Diseases_-_Cat]] [[Category:Endocrine_System_-_Pathology]]
 

Revision as of 18:24, 15 December 2010


 This article is still under construction.


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.
  • Volume receptors in the hypothalamus.

A deficiency of ADH is known as Diabetes insipidus. May be:

  • Central: failure to synthesise or release ADH.
  • Nephrogenic: Failure of the nephrons to respond to ADH present in the kidney.

Clinical Signs

  • Marked polyuria; 5-20X normal output, often resulting in nocturia and incontinence.
  • Marked polydipsia; animal will search for water.
  • Dehydration.
  • Weight loss.
  • Anorexia.
  • Neurological signs if neoplastic in origin.

Differential diagnosis:

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.

Diagnosis:

  • Urine specific gravity is low (1.001-1.005)
    Solute is absorbed in excess of water thus demonstrating a good tubular function.
  • Dehydration so see mildly elevated PCV and TP.

Psychogenic polydipsia: plasma osmolality decreased due to excess water in contrast to increased plasma osmolality with DI due to dehydration.

  • Water deprivation test: Aims to measure urine osmolality after 12-24 hours water deprivation to determine whether ADH is indeed deficient.
    • Collect initil urine and plasma samples for osmolality.
    • Weigh patient.
    • Withhold food and fluid.
    • Collect urine and plasma after 6 hours and thence 2 hourly.
    • STOP when:
      • Patient displays concentraing ability.
      • Patient loses >5% bodyweight.
      • 24 hours have passed.

A positive test for diabetes insipidus is a failure to concentrate urine >1.010 after 12-24 hours.

If psychogenic polydipsia is suspected then gradually restrict water for 3 days prior to test to avoid medullary washout giving a false positive test.

  • ADH response test: Administer Desmopressin i/m. Monitor specific gravity of urine 2 hourly.
    • Central diabetes insipidus will concentrate urine >1.020.
    • Nephrogenic diabetes insipidus will not be able to concentrate the urine at all in response to the synthetic ADH. SG <1.010.
      Nb. A positive ADH response test means nothing unless preceded by a water deprivation test to prove the presence of diabetes insipidus.

Treatment:

  • Desmopressin: Central disease only. Expensive.
  • 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.
  • Chlorpropamide: Potentiates effect of ADH on the tubules.
  • Carbemazepine: Acts similarly to chlorpropamide.
  • No therapy: Animals kept outdoors with free access to water at all times.

Prognosis:

Congenital central diabetes insipidus has a favourable prognosis and can be treated with desmopressin. Nephrogenic diabetes insipidus has a more guarded prognosis.

Any expanding tumour, particularly if neurological signs are present, carries a poor prognosis.

Central diabtetes insipidus secondary to head trauma varies in prognosis and spontaneous recovery may occur.

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