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