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Small Animal Medicine > Polyuria & Polydipsia > Flashcards

Polyuria & Polydipsia Flashcards

1
Q

What are the 4 steps to urine formation?

A
  1. filtration of plasma through glomerulus
  2. reabsorption
  3. secretion
  4. excretion
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2
Q

What is the greatest contributor to the urine concentration gradient?

A

urea

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3
Q

How does the pituitary gland control water absorption and urine concentration?

A
  • releases ADH in response to an increased plasma osmolarity (sodium, glucose) or low ECF volume
  • ADH enhances water permeability, causing it to be passively absorbed along the osmotic gradient
  • this results in more concentrated urine
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4
Q

At what USG is urine considered normally concentrated by the renal tubules?

A
  • DOGS = > 1.030
  • CATS = > 1.035

(always analyze with Hx of the patient!)

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5
Q

What amount of water intake is necessary for maintenance? What is considered polydipsia?

A

50-60 mL/kg/day, based on insensible loss caused by breathing or urine excretion

drinking 2x the maintenance —> 100 mL/kg/day

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6
Q

What is the normal amount urine expected to be produced in a day? What is polyuria?

A

~ 40 mL/kg/day

excessive increase in urination with increased volumes

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7
Q

What is the difference between polyuria and pollakiuria?

A

POLYURIA - excessive and increased volume

POLLAKIURIA - excessive urination in small amounts (sign of LUT disease)

ASK CLIENTS about size of puddles, frequency, duration, urine stream, or litter box clumps

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8
Q

What are 3 causes of primary polyuria with compensatory polydipsia?

A
  1. lack of ADH
  2. lack of response to ADH
  3. lack of medullary concentration gradient
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9
Q

What are 3 causes of primary polydipsia with compensatory polyuria?

A
  1. physiologic
  2. behavioral
  3. pathologic

(psychogenic due to brain tumors or head trauma)

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10
Q

What is central diabetes insipidus?

A

lack of ADH release due to pituitary disease

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11
Q

What is nephrogenic diabetes insipidus?

A

lack of response to ADH most commonly caused by substances that interfere with ADH binding to receptors in kidneys

  • bacterial endotoxins: E. coli from pyelonephritis, pyometra, or prostatitis
  • calcium
  • cortisol
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12
Q

What are 3 causes of of loss of medullary concentration gradient?

A
  1. hyponatremia, hypokalemia, or decreased BUN, which decreases the osmolality of plasma
  2. osmotic diuresis - diabetes mellitus or renal glucosuria, where glucose in filtrated urine pulls water
  3. reduced nephron function - chronic renal failure
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13
Q

What are some disease pathways that lead to primary polyuria?

A
  • central and nephrogenic diabetes insipidus
  • endotoxins from pyometra, pyelonephritis, and prostatitis
  • hyperadrenocorticism, hypercalcemia: cortisol and calcium block renal receptors for ADH
  • DM, renal glucosuria: osmotic
  • hypoadrenocorticism: decreased aldosterone causes hyponatremia
  • hyperthyroidism: increased renal blood flow
  • chronic renal disease: damage to kidneys
  • leptospirosis: tubular damage
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14
Q

What are the most common causes of PU/PD in dogs and cats?

A

DOGS: CKD, hyperadrenocorticism (Cushings), DM

CATS: CKD, hyperthyroidism, DM

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15
Q

How can we ask clients to quantify water intake?

A
  • fill water bowl as normal, measuring total water volume
  • refill bowl as needed through the next 24 hours while measuring each refill
  • quantify the amonut of water left and subtract it from the total volume
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16
Q

What are the components of the minimum database for diagnosing the cause behind PU/PD?

A
  • UA
  • urine culture
  • CBC
  • chemistry
17
Q

How is USG helpful for diagnosing the cause of PU/DP?

A

indicates whether the patient is able to concentrate urine

  • hypersthenuria and hyposthenuria = kidneys able to concentrate/dilute urine, unlikely kidney disease
18
Q

Why is sedimentation on UA helpful for diagnosing the cause of PU/PD?

A

active sedimentation, like bacteriuria, pyuria, and hematuria, can indicate pyelonephritis

19
Q

Why is the presence of proteinuria helpful for diagnosing the cause of PU/PD?

A

indicates renal, tubular, or glomerular disease

20
Q

Why is the presence of glucosuria helpful for diagnosing the cause of PU/PD?

A

indicates diabetes mellitus or tubular disease

21
Q

What are the 3 major values evaluated on normal serum chemistry when trying to diagnose the cause of PU/PD?

A
  1. liver enzymes - decreased markers of synthetic function, like glucose, albumin, and BUN —> liver failure causes decreased urea, which also alters medullary concentration
  2. kidney values - azotemia indicative of kidney disease
  3. electrolytes - calcium, sodium, potassium
22
Q

What additional values of serum biochemistry are helpful for diagnosing the cause of PU/PD in cats and dogs?

A

CATS = total T4 for hyperthyroidism

DOGS = LDDST for hyperadrenocorticism (Cushing’s)

23
Q

What 3 diagnostics other than routine blood work can be used to diagnose the cause of PU/PD?

A
  1. abdominal ultrasounds - observe urinary tract and adrenals (Cushing’s!)
  2. SDMA - indicates GFR
  3. desmopressin (DDVAP) trial
24
Q

How is psychogenic polydipsia diagnosed after ruling out every other option? Why must this be done carefully?

A
  • modified water deprivation test - not given water, still results in concentrated urine
  • first morning urine - not given water all night, concentrated urine
25
Q

How does central and nephrogenic diabetes insipidus compare on the desmopressin (DDAVP) when diagnosing for the cause of PU/PD?

A

CENTRAL - no ADH produced from pituitary, so oral/conjunctival DDAVP should cause the urine to become concentrated, since the receptors in the kidney still work (+ decrease in water intake)

NEPHROGENIC - ADH not acting on kidney, so even if oral/conjunctival DDAVP is given, the urine will not become concentrated

26
Q

Why should modified water deprivation tests and desmopressin (DDAVP) trials be done carefully?

A

withholding water can be dangerous in certain circumstances

rarely, patients with psychogenic polydipsia treated with DDAVP can undergo water toxicity

Small Animal Medicine (52 decks)

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