5. PU/PD and concentration disorders Flashcards
1
Q
what is the normal urine production in dogs and cats
A
26-44 ml/kg/day
2
Q
what are maintenance fluids in dogs and cats
A
2ml/kg/hr
3
Q
what is polyuria
A
excreting an increased volume of urine
4
Q
what is pollakiuria
A
passing urine more frequently
5
Q
normal water intake is affected by what factors
A
- ambient temp
- respiratory evaporative loss
- exercise level
- water content of food
- faecal water content
- age
- physiological state (pregnancy/lactation)
6
Q
what are the most common causes of PUPD in dogs and cats
A
- renal insufficiency
- chronic renal disease
- diabetes mellitus
- hyperadrenocorticism
- hyperthyroidism
7
Q
the production of concentrated urine is dependent on which three mechanisms
A
- the ability to make and secrete ADH
- functional kidneys that are able to respond to ADH
- the presence of an osmotic gradient in the renal medulla
8
Q
list causes of primary polyuria
A
- central diabetes insipidus = rare, partial or complete deficiency of ADH due to issue with pituitary
- primary nephrogenic diabetes insipidus = very rare congenital disorder = kidneys cant respond to ADH due to aquaporin channel insertion defect
- secondary nephrogenic diabetes insipidus = acquired inability to respond to ADH, due to many conditions which interfere with the normal interaction of ADH and tubular receptors affecting tubular function or decreased hypertonicity of the medullary interstitium resultin in loss/reduction of concentration gradient
- in both cases of nephrogenic DI, ADH levels will be high but no response to synthetic vasopressin or water deprivation
9
Q
list causes for renal insufficiency
A
- osmotic diuresis in remnant nephrons (water followig solutes that are not resorbed)
- disruption of medulalry hypertonicity
- decreased functional nephrons
- decreased number of functional nephrons in CKD must excrete the normal daily solute load leading to solute diuresis with impaired urinary concentrating ability
10
Q
how does hyperadrenocoricism caus PUPD
A
- defective ADH release
- impaired tubule response to ADH action
11
Q
how does hypoadrenocorticism cause PUPD
A
- loss of the osmotic gradient in renal medulla due to chronic sodium wasting
- loss of renal medullary hypertonicity leading to inadequate urine concentration
- also loss of aldosterone
12
Q
how does diabetes mellitus cause PUPD
A
- glucose normally freely filtered by the glomerulus so large amounts enter the ultrafiltrate for active resorption (none or very little should be present in urine)
- in DM blood glucose is high and therefore glucose levels in ultrafiltrate will be high
- active transport of glucose in the tubule reaches maximum (TMAX) and is overloaded
- excess glucose remains in the filtrate and is excreted in the urine
- PUPD in DM is via osmotic diuriesis = high osmolality filtrate (lots of glucose in the filtrate) prevents water moving out of the tubule via osmosis. ADH is present and may be working fine but the large concentration gradient for water to move down is significantly lessened
13
Q
how does hyperthyroidism caus PUPD
A
- primary polyuria may occur as a result of thyrotoxicosis = increasing cardiac output and GFR as well as increased renal medullary blood flow wich has the potential to decrease renal medullary hypertonicity and urine concentrating ability
- some cats with hyperthyroidism may also have primary polydipsia secondary to the effect of high thyroid hormone concentrations on the thirst centre
14
Q
how does liver disease cause PUPD
A
- due to loss of medullary hypertonicity
- urea is made in the liver
- in chronic/severe liver disease decreased production of urea leads to decreased renal medullary hypertonicity
- increased levels of corticosteroids (mimics HAC) that inhibit the release of ADH thus causing a degree od central diabetes insipidus
15
Q
what is psychogenic polydipsia
A
- psychiatric disturbance leading to huge drive to drink
- result is hypo-osmolality when water intake exceeds the ability of kidneys to remove it
- very large amounts of very dilute urine are produced
- ADH not the problem - controlled water deprivation is the only definitive test (to see if the kidneys can concentrate urine when animal is given less water)