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31 Cards in this Set
- Front
- Back
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Polydipsia
-define |
-increased thirst (>80-100 ml/kg/day)
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Polyuria
-define |
-increased urine production (>50 mL/kg/day)
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Normal maintenance fluid requirements
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60 mL/kg/day
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Thirst
-stimulated by |
-primarily by increased plasma osmolality
-non-osmotic factors: hypotension, hyperthermia, pain, drugs |
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cups = oz = mL
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1 cup = 8 oz = 240 mL
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Why is thirst stimulated primarily by increased plasma osmolality?
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-stimulate production and release of ADH
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Urine concentration requires
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-adequate ADH concentration
-kidney responsiveness to ADH |
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Kidney responsiveness to ADH relies on:
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- > 1/3 total nephron number
- hypertonic renal medullary interstitium |
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How is urine concentration usually measured?
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-refractometry
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Hyposthenuria
-urine concentration |
< 1.008
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Isosthenuria
-urine concentration |
1.008 - 1.012
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Range of minimal urine concentration
-dogs -cats |
-dogs = 1.013-1.029
-cats = 1.013 - 1.034 |
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Hypersthenuria urine concentration
-dogs -cats |
-dogs: > 1.030
-cats: > 1.035 |
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Hypersthenuria
-is an appropriate response when |
-dehydration
-azotemia |
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What is the more common cause of diagnosis of PU/PD?
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-Primary polyuria
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Primary Polydipsia
-define |
-hypersthenuric response to dehydration
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Primary polydipsia
-examples |
-psychogenic polydipsia (puppies)
-portosystemic shunt |
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Primary polydipsia
-effect on urine |
-should see normal response
-neurohypophysis and kidneys should all be normal, so ADH release should occur when deprived of water, and the kidneys should respond |
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Primary polyuria
-define |
-Diabetes insipidus
-no hypersthenuric response to dehydration |
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Primary polyuria
-rule outs |
-pituitary (central) DI
-nephrogenic DI |
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Differentiating Central DI from Nephrogenic DI
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Central DI = hypersthenuria with exogenous ADH administration
Nephrogenic DI = no hypersthenuria with exogenous ADH administration |
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Nephrogenic Diabetes insipidus
-examples |
-AKI/CKD (renal insufficiency/failure)
-hyperadrenocorticism -hypoadrenocorticism -pyometra -hypercalcemia -hypokalemia -drugs (diuretics, corticosteroids) -liver disease -renal medullary sinus washout -diabetes mellitus |
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Renal insufficiency/Failure
-cause for Nephrogenic DI |
-total nephron loss
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Hyperadrenocorticism
-cause for nephrogenic DI |
-cortisol interferes with ADH at the tubular epithelium
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Hypoadrenocorticism
-cause for nephrogenic DI |
-Aldosterone deficiency
--Na+ loss ---lose cortical hypertonicity |
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Pyometra
-cause for nephrogenic DI |
-E. coli endotoxin acts similar to cortisol and blocks ADH
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Hypercalcemia
-cause for nephrogenic DI |
-calcium interferes with ADH binding
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Hypokalemia
-cause for nephrogenic DI |
-decreased responsiveness of aquaporin
-decreased function of membrane proteins to make concentration gradient |
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Liver disease
-cause for nephrogenic DI |
-decreased renal medullary hypertonicity
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Renal medullary solute washout
-cause for nephrogenic DI |
-if lots of fluid is flushed through the system, eventually hypertonicity of the kidney is lost because high fluid rate makes it more difficult to absorb solutes
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Diabetes mellitus
-cause of nephrogenic DI |
-high solute concentration in urine causes in decreased concentration gradient
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