PU/PD Flashcards
polyuria
production of large volumes of dilute or unconcentrated urine
what causes polyuria
inability of the kidneys to concentrate urine
- renal dysfunction
- nephrogenic DI
- calcium interfering with renal signaling
- osmotic diuresis
normal UOP
1-2 mL/kg/hr
50 mL/kg/day
UOP for polyuria
> 50 mL/kg/day
polydipsia
increased water intake
more often secondary to a primary polyuria than primary polydipsia
normal water intake
50-100 mL/kg/day
majority are 50-80 but increases with activity level
water intake for polydipsia
> “80”-100 mL/kg/day
80-100 is considered a “gray zone” - may be elevated for an individual animal
hyposthenuria
dilute urine with USG < 1.008
isosthenuria
urine that is neither concentrated or dilute
USG = 1.008-1.012
hypersthenuria
concentrated urine with USG > 1.012
vasopressin
antidiuretic hormone (ADH)
produced by the hypothalamus and released by the posterior pituitary
released in response to dehydration to stimulate water reabsorption in the kidneys
ADH levels in a hydrated state
hydration –> less ADH –> less water absorbed –> dilute urine
ADH levels in a dehydrated state
dehydration –> more ADH –> more water absorbed –> concentrated urine
desmopressin
synthetic vasopressin (DDAVP)
administered as a test OR treatment for central diabetes insipidus
what must you do before administering DDAVP
rule out ALL causes for secondary nephrogenic diabetes insipidus before administering DDAVP
if responsive to DDAVP - suggests central DI
if unresponsive to DDAVP - suggests nephrogenic DI
common causes of PU/PD
- cushing’s (dogs)
- hyperthyroid (cats)
- diabetes mellitus
- renal disease
- medications (prednisone, phenobarbital)
- hypercalcemia
- post obstructive diuresis
central diabetes inspidius
RARE
deficiency or malfunction of the pituitary gland resulting in low to no ADH production
causes: traumatic, neoplasia, cysts, malformation
nephrogenic diabetes insipidus
malfunction of the kidney’s ability to respond to ADH
most commonly SECONDARY to underlying disease - pyometra, hypercalcemia, Cushing’s, pyelonephritis, hyperthyroidism
primary is rare (congenital)
how to confirm PU/PD
- quantify the water intake
- ask owner how many cups per day the patient drinks - measure USG
- use first morning sample (most concentrated) - pertinent history questions
- differentiate polyuria from lower urinary tract signs
how many mL in a cup of water
240 mL
how many cups of water should a 10 kg dog drink in 1 day
50-100 mL/kg/day
10 kg –> 500 - 1000 mL/day
daily water intake = 2 to 4 cups per day
> 4 cups per day indicates polydipsia
what USG can be expected if a patient is truly PU/PD
< 1.025
what history questions should you always ask an owner in PU/PD cases
- how many times is the patient going out to urinate?
- is the urination large or small volume?
- is the patient getting up at night to drink or urinate?
- any other clinical signs? (straining, dribbling, etc)
ALWAYS ask about current medications - prednisone, phenobarbital can cause PU/PD
what specific testing can be done for Cushing’s
urine cortisol:creatinine ratio
what specific testing can be done for hyperthyroidism
total T4
what specific testing can be done for renal disease
chemistry panel (BUN, creatinine)
clinical consequences of PU/PD
- urinary incontinence
- QOL (for pet and owner)
- atonic bladder
at home management consideration
must NOT withhold water from a PU/PD patient - can lead to life threatening dehydration, hypovolemia, and electrolyte derangements
in hospital management considerations
IV fluid therapy can cause loss of the medullary concentration gradient - once the underlying condition is treated, may need time to re-establish the gradient to properly concentrate urine
must TAPER fluids - stopping suddenly will cause a transient PU/PD leading to dehydration
