Polydipsia and Polyuria
what needs to be included in the PE
be complete, include weight and hydration status, P.C.V, plasma proteins, S.G Measure animals water consumption
Dipsinogenic
chemical compounds that stimulate thirst by direct action on neurons in the thirst center
Pseudopsychogenic Pd
compulsive water drinking due to anxiety, boredom, or compulsive neurotic owners
renal disease
decrease renal concentrating mechanisms
Renin and Angiotensin
dipsinogenic compounds produced in systemic diseases that result in Pd
Hyperadrenocorticism
disorder caused by excessive adrenal cortex production of glucocorticoid, resulting in increased urination due to ADH inhibition at collecting ducts; also called Cushing's disease
Diagnostic plan
document that the problems exist data base; clues for diagnosis perform urine concentration tests perform special diagnostic tests
nephrogenic
enzyme deficiency causes an unresponsiveness to ADH
hyperthyroidism
excessive activity of the thyroid gland produces abnormally high levels of thyroid hormone. Results in high metabolic rate, skinny, eating a lot
polyuria
excessive production of urine, usually urine has a decreased S.G
what is ADH control center controlled by
extracellular fluid osmolality
Iososthenuric
glomerular filtrate has a SG equal to plasma which is 1.008-1.012
where is thirst center located
hypothalamus gets stimulated to drink
when not to do water deprivation tests
if animal is azotemic, dehydrated, or hypercalcemic
ADH osmoreceptor control system
increased extracellular fluid osmolality > increased ADH release > increased collecting tubule permeability > water reabsorbed
iatrogenic
induced by humans; "drug induced" in this case alcohol causes inhibition of ADH release
diabetes mellitus
insulin deficiency that results in hyperglycemia and consequent glycosuria (glucose in urine)
Furosemide
large macromolecule that does not cross the blood brain barrier so not good to give for fluid in the brain
concurrent system
loops of henle- water is reabsorbed along concentration gradients established in the renal medulla; decreases osmolality
Medullary washout
loss of countercurrent multiplier system (loops of henle)
Neurogenic
neural injury causes a def. in ADH
pathologic thirst causes
neuronal irritation (tumor, trauma, inflammation) psuedopsychogenic pd increased plasma renin hypercalcemia thoracic caval constriction
secondary polydipsia
not as well understood, but more common cause of Pd animal is anticipating water needs prior to actual deficiencies
pathologic thirst/polydipsia
not compensatory, primary Pd
ADH response test steps
obtain urine SG, without water and food, give S.G vasopressin. Take urine SG @ 30 mins
2nd basic principle
over-hydration (excessive amounts of water in the body) vs dehydration (low amounts of water in the body)
what is the main cause: Pu or Pd?
polyuria usually results in a Pd
pseudopsychogenic pd
primary pd, compensatory pu
failure to respond to ADH response test indicates
primary renal disease diabetes insipidus medullary washout
pyometra
pus in the uterus that results in unresponsiveness to ADH
where is ADH produced and released by
specialized neurons in the hypothalamus called pituicytes stored in nerve endings
how are Pu and Pd produced
through disorders that disturb distal and collecting tubular function
1st Basic Principle
water in = water out
primary polydipsia
well understood, but not a primary mechanism that determines water intake, d/t intracellular dehydration and when pressure receptors decrease in blood volume
when is ADH response test give?
when animals fail to concentrate their urine
when to terminate water deprivation test
when concentrated urine is produced weight loss of 7% or more occurs theres an increase in plasma protein theres an increase in plasma osmolality
Water deprivation test
12 hr fast; measure blood serum osmolality, obtain urine SG and evaluate every 3-4 hrs
normal SG for ADH response test
> 1.015 are normal
What S.G is not Pu?
> 1.035
Failure to concentrate urine can be contributed to
ADH deficiency ADH unresponsiveness primary renal disease medullary washout
Two renal concentrating mechanisms
ADH osmoreceptor control system concurrent system
disorders that produce Pu/Pd
Diabetes insipidus, diabetes mellitus, hyperadrenocorticism, liver failure, medullar washout, pyometra, pseudopsychogenic pd, renal disease, iatrogenic
Diuretics
Drugs that elevate the rate of bodily urine excretion Mannitol. dextrose and furosemide
polydipsia
Excessive thirst persisting for long periods of time
antidiuretic hormone (ADH)
Hormone produced by the neurosecretory cells in the hypothalamus that alters permeability of the membrane and stimulates water reabsorption from kidneys
diabetes insipidus
Neurogenic or nephrogenic
what does the water deprivation test rule out
Pd
thirst
a desire for water
Azotemic
a toxic condition caused by failure of the kidneys to remove urea from the blood
where is ADH control center located
adjacent to thirst center in hypothalamus
Hypercalcemia
an abnormally high level of calcium in the blood cancer*** inhibits ADH and leads to mineralization of the kidney and chronic renal failure
what is normally the primary problem
animal normally have Pu as their primary problem which results in a compensatory Pd