PU/PD in Small Animals Flashcards

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1
Q

What is the main hormone that governs urine production?
Where is it made, and where it is stored?

Where does it take its effect?

A

Anti-Diuretic Hormone (aka Vasopressin)

Made: Supraoptic and paraventricular nuclei of the hypothalamus
Stored: In the posterior pituitary

Effects: the Kidneys (distal renal tubules and collecting ducts) and blood vessels

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2
Q

What causes ADH to be released from the posterior pituitary?

A
  • Changes in plasma osmolality
  • Blood volume depletion
  • Decreased blood pressure
  • RAAS activation
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3
Q

Where and what is the effect of ADH on the kidneys?

A
  • ADH affects the distal tubules and the collecting ducts, leading to resorption of water via binding to its receptors, leading to an increased expression of aquaporin-2 channels
  • This will decrease urine output, and increase urine concentration
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4
Q

Where and what is the effect of ADH on the blood vessels?

A
  • Binds to Endothelial receptors of blood vessels to release vWF
  • Increases vasoconstriction + BP
  • Increases platelet aggregation
  • Causes an increase in CRH (corticotropin-releasing hormone) and thus increases ACTH secretion
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5
Q

Does ADH have any effect on water loss from the feces, evaporation/ sweating, saliva etc.?

A

No!

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6
Q

What is needed in order to allow for ADH to have its effects?

A
  • Intact hypothalamus + posterior pituitary gland
  • 1/3 of functioning renal system
  • Normal binding and stimulation of the ADH-receptors in the kidneys
  • Medullary concentration gradient must be sufficient: which is dependent on urea and Na+ concentrations to allow for the resorption of water
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7
Q

What is a normal water intake in dogs and cats?

A

20 - 90 ml/kg/day

Note: this is highly dependent on many factors such as diet, environment, exercise, productivity status (lactating or not) etc.

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8
Q

What is a normal urine output in dogs and cats?

A

20 - 45 ml/kg/day

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9
Q

What is defined as Primary polydipsia?

A

Excess drinking causing excess urination

What goes in, must come out

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10
Q

What is defined as Primary polyuria?

A

Excess urination with compensatory polydipsia

What is lost must be replaced

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11
Q

What is more common, primary polydipsia or polyuria?

A

Primary Polyuria, leading to a compensatory polydipsia

Primary polydipsia is extremely RARE!

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12
Q

What are the DDx for Primary Polydipsia?

A
  • Behavioural: environmental or emotional cause
  • Dipsogenic Diabetes Insipidus: hypothalamic lesions: idiopathic or infections, or neoplastic leading to increased thirst response
  • Intestinal disease, particularly diarrhea
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13
Q

What are the DDx for Primary Polyuria?

A
  • ADH deficiency: due to central diabetes insipidus (DI)
  • Primary nephrogenic DI
  • Acquired nephrogenic DI
  • Osmotic diuresis
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14
Q

What are the causes of Central Diabetes Insipidus, leading to Primary Polyuria?

A
  • Idiopathic: most common cause as we never find an actual cause
  • Trauma: to the head leading to the pituitary stalk separation
  • Neoplasia
  • Surgery: Hypophysectomy
  • Developmental defects in structure
  • Infection
  • Inflammation
  • Cysts

These will all lead to an ADH deficiency

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15
Q

What is Diabetes Insipidus?

A

Diabetes insipidus (DI) is a condition characterized by large amounts of dilute urine and increased thirst.

More common in dogs than cats

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16
Q

What are the causes for Primary nephrogenic DI, leading to Primary Polyuria?

A
  • Genetic mutations of the ADH-receptor or aquaporin channel

- Usually inherited, and breeds such as Huskies are commonly affected

17
Q

What are the causes for Acquired nephrogenic DI, leading to Primary Polyuria?

A
  • Kidney disease
  • Liver disease
  • Pyelonephritis
  • Pyometra/ E.coli endotoxemia
  • Hypercalcemia
  • Hypokalemia
  • Hyperthyroidism
  • Hyperadrenocorticism
  • Hypoadrenocorticism
  • Drugs/ diet
  • Hyperviscosity Syndrome: overproduction of erythropoietin leading to erythrocytosis
18
Q

What are the causes for Osmotic diuresis, leading to Primary Polyuria?

A
  • Post-obstructive diuresis: urine blockage that we have unblocked, and for a short time after urea is excreted acting as an osmotic substance, pulling water out with it and causing diuresis
  • Glucosuria: due to Primary renal glycosuria, Diabetes mellitus or Fanconi syndrome (Basenji’s predisposed)
  • Drugs: Mannitol
19
Q

What are the unusual causes of PU/PD in a patient where the more normal causes have been ruled out?

A
  • Polyuric phase of Acute Kidney Injury from Raisin ingestion
  • Syndrome of inappropriate antidiuretic hormone secretion (SIADH)
  • Phaeochromocytoma
  • Leptospirosis
  • Splenic hemangiosarcoma
  • Intestinal leiomyosarcoma
20
Q

What are the most common causes of PU/PD in dogs? (8)

A
  • Hyperadrenocorticism
  • Diabetes mellitus
  • Chronic kidney disease
  • Pyelonephritis
  • Pyometra
  • Hypercalcemia
  • Liver disease
  • Diabetes insipidus
21
Q

What are the most common causes of PU/PD in cats? (3)

A
  • Chronic renal failure
  • Diabetes mellitus
  • Hyperthyroidism
22
Q

How can you confirm the presence of PU/PD in a patient?

A

Urine analysis

  • Presence of glucose
  • Specific Gravity: would expect it to be low. Urine that is appropriately concentrated or higher means the animal is NOT polyuric
23
Q

You are presented with a patient that the owners claim is PU/PD, you take a urine sample and note Hyposthenuria
What DDx list can now be made?

A
  • Dipsogenic/ Psycogenic
  • Central DI
  • Hyperadrenocorticism
  • Hypercalcemia
  • Liver disease
  • Hypoadrenocorticism
  • Infections such as pyelonephritis/ pyometra
24
Q

You suspect primary polydipsia in a dog even though it is rare, plasma osmolality may be helpful is ruling it in or out
How do you calculate plasma osmolality?

A

2[Na] + [glucose] + [urea]

Reference range = 290 -310/330 mOsm

A dog with primary polydipsia will have a plasma osmolality that is at the lower end of this range or below

e.g.
Na+ = 142.1 mmol/L
Glucose = 6.0 mmol/L
Urea = 4.6 IU/L

2(142.1) + 6 + 4.6 = 294.8
294.8 is at the low end of the Reference Range

25
Q

You suspect Primary Polydipsia in a dog, even though it is rare, what diagnostic tests can be done to rule it in/out?

A
  • Hematology + Biochemistry
  • Calculate Plasma osmolality from the biochem results
  • Request urine analysis on different samples from different times and days
26
Q

You are presented with a patient who is PU/PD, and proves to be PU/PD based on low SG.
After additional tests and repeat urine tests, you have narrowed down to Central Diabetes Insipidus, what test can be performed to rule in Central DI?

Describe this test

A

Test: Modified Water Deprivation Test

Stage 1: Gradual Water restriction to repair Medullary concentration gradient

  • Day 1: limit water to 120 - 150 ml/kg/day
  • Day 2: limit water to 80 - 100 ml/kg/day
  • Day 3: limit water to 60 - 80 ml/kg/day

Stage 2:
- Day 4: Assess response to complete water deprivation
Confine the animal
Catheterize the bladder (+ antibiotics given after due to the high risk associated with UTI’s)
Empty bladder
Record urinalysis, weight, hydration status, urine and electrolytes every 30-60 mins

The test is discontinued when:

  • Urine SG is > 1.025: this means a diagnosis is achieved as Primary Polydipsia
  • 5% weight loss
  • 5% dehydration
  • Marked increase in [Na+] ( > 160 mmol/L)
  • Dullness

However, if the test is stopped for any other reason besides Urine concentration, we proceed with the following:

1) Assess response to Desmopressin administration (2-10 ug IV)
2) Urine is monitored every 30mins
3) Maintenance fluids at 2.5-3 ml/kg/hr
4) Test is carried on for 4 - 24 hours (usually peak action is at 4 hours)
5) Assess SG, expect it to concentrate above 1.010 - 1.015: confirmation of Central DI
6) Must now investigate the underlying cause
7) Re-hydrate the patient now CAREFULLY

27
Q

What is the treatment of Central Diabetes Insipidus?

A
  • DDAVP = Desmopressin acetate
    This is a synthetic analogue of ADH, and has a potent anti-diuretic effect with a prolonged duration of action

note: has smaller effect on blood vessels compared to ADH
caution: increased blood clotting effect