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URI 2 > Diagnostic approach to polyuria and polydipsia (PUPD) > Flashcards

Diagnostic approach to polyuria and polydipsia (PUPD) Flashcards

1
Q

Define Polyuria and Polydipsia?

A
  • Polyuria = Increased urination
  • Polydipsia = Increased thirst
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2
Q

Most animals with PUPD have?

A

Primary polyuria causing a secondary compensatory polydipsia – they drink more because they have lost water and are thirsty, because they cannot concentrate their urine

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3
Q

Thirst and urination are determined by interplay of:

A

Plasma osmolality (tonicity of the blood), especially plasma sodium

•Determines blood pressure – baroreceptors (pressure) and osmoreceptors (water)

Hypothalamic - Pituitary gland – ADH axis

•Regulates water reabsorption in collecting duct

Renal function

•Needed to produce concentrated urine

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4
Q

Clinical signs of PUPD – what do owners see?

A
  • Seen to drink more often from bowl
  • Need to fill water bowl more often
  • Drinking from puddles, shower, glasses
  • Longer than normal stream of urine
  • Need to urinate more frequently (may see as incontinence)
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5
Q

Discuss Primary polydipsia?

A
  • RARE
  • Psychogenic polydipsia – horse>others
  • Hepatic insufficiency/ portosystemic shunt – can give changes in mentation causing PD
  • Central lesion effecting hypothalamus
  • Dietary change e.g. wet to dry

–No compensatory PU

•Compensation for increased loss eg heat

–No compensatory PU

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6
Q

List causes of Primary polyuria?

A
  • Hepatic disease
  • Hyperthyroidism (C)
  • Hyperadrenocorticism*
  • Hypoadrenocorticism
  • Hypokalemia
  • Hypercalcaemia*
  • Diabetes mellitus (DM)*
  • Diabetes insipidus (DI)
  • Pyometra*

–Cause 2ndary nephrogenic disabetes inspidus in the male seen with prostatitis.

  • Pyelonephritis
  • Post-obstructive
  • Renal disease*
  • Iatrogenic

* = most common in dogs

C= cats only

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7
Q

How else can causes of primary polyuria be categorised?

A

•Renal

•Hepatic

•Endocrine – diabetes mellitus, diabetes insipidus, hyperthyroidism, hyperadrenocorticism, hypoadrenocorticism

•Infectious – pyelonephritis, pyometra

•Electrolytes – hypokalemia, hypercalcaemia

  • Iatrogenic – diuretics, steroids etc
  • Hyperviscosity syndromes: interefere with ADH production
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8
Q

What is ADH’s role in PU/PD caused by Primary central diabetes insipidus?

A

Primary central diabetes insipidus

–Congenital, very rare (secondary central also v rare from tumours)

–No ADH produced so cannot concentrate urine

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9
Q

What is ADH’s role in PU/PD caused by Nephrogenic diabetes insipidus?

A

Nephrogenic diabetes insipidus

–Only common as an acquired disease (pyometra and protastitis)

–Congenital, exceptionally rare!

–No ADH receptors so no ADH action in DCT

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10
Q

what is young animal urine like?

A

Young animals, v dilute urine, almost like water.

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11
Q

Discuss what causes Reduced sensitivity to ADH that causes Failure of tubule to respond to ADH?

A

Reduced sensitivity to ADH

–E.coli toxins in pyelonephritis and pyometra

–Hyperadrenocorticism

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12
Q

Discuss what causes Interference with action of ADH at tubule that causes Failure of tubule to respond to ADH?

A

Interference with action of ADH at tubule

–Hypercalcaemia

–Hypokalemia

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13
Q

Discuss what causes ADH receptor downregulation that causes Failure of tubule to respond to ADH?

A

ADH receptor downregulation

–Obstuction of ureters/ bladder

–Hypokalemia

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14
Q

What is osmotic diuresis?

A

Increased excreted solute with high osmotic potential needs dilution

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15
Q

What can lead to osmotic diuresis?

A
  • Diabetes mellitus (glucose)
  • Chronic kidney disease (BUN) multifactoral animals with renal disease of variable degrees of PU/PD
  • Post-obstructive diuresis (BUN) e.g blocked cat build up lots of electrolytes behind obstruction and then when freed it floods out.
  • Liver failure inc portosystemic shunt (cortisol, other solutes not broken down)
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16
Q

What is Reduced medullary concentration gradient?

A

Unable to concentrate urine in Loop of Henle

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17
Q

What can lead to reduced medullary concentration gradient?

A

Long period of PU of any cause (reduced BUN present in medulla)

  • Including fluid therapy and corticosteroids

Liver failure (reduced BUN production)

Hypoadrenocorticism (hyponatremia) Addisons: pre-renal azotaemia as they cannot retain Na so they cant increase their USG.

Hyperthyroidism (increased renal blood flow)

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18
Q

Look at this if you feel like it?

A
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19
Q

What is a Reduced medullary concentration gradient?

A

Unable to concentrate urine in Loop of Henle

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20
Q

What causes Reduced medullary concentration gradient?

A
  • Long period of PU of any cause (reduced BUN present in medulla)
  • Including fluid therapy and corticosteroids
  • Liver failure (reduced BUN production)
  • Hypoadrenocorticism (hyponatraemia)
  • Hyperthyroidism (increased renal blood flow)
21
Q

History check

If the owner has noticed a change in urinary behaviour, ask them to describe what has changed:

A

–Any change in food, treats, management?

–Is the animal on any medications which may cause PUPD?

–Straining to urinate?

–Small volume of urine frequently or big ones?

–Urine on the bed in the morning?

–Conscious/unconscious urination?

–Discoloured/smelly urine?

22
Q

Step 1. Is it really PUPD?

A

Is it drinking more than it should?

–Ask owners to measure intake over 24h

•Measure over 2-3 days which makes for easier calculation

–Normal = 40-60ml/kg/d (but compare relative to what is normal to the dog. Has the owner said it is drinking more this is enough to trigger investigation)

–PD is 100ml/kg a day roughly twice normal.

Is its urine concentrated?

–Get a free catch sample and check with your refractometer –NOT dipstick!

–typically >1.035 to be concentrated (relative to the patient)

23
Q

In step 1 if the USG is acceptable what do we do?

A

If the USG is acceptable (moderately concentrated):

–Thorough clinical examination - palpate relevant areas e.g. thyroid, kidneys, liver.

–go back to the clients for a better history of the nature of the problem (often pollakiuria/dysuria)

24
Q

If it is PUPD, or the USG is low or both, continue to step 2.

What is step 2?

A

Is there glucose in the urine on your dipstick?

–If so, this animal may have diabetes mellitus.

–ALWAYS check with a concurrent blood glucose (there are rare causes of primary renal glycosuria)

–Check not contamination from the container!

–Remember stressed cats…..

–If not, go to step 3.

–Renal threshold for cats of glucose: 12mmol/L

25
Q

What is step 3?

A

Step 3 – is there evidence of chronic kidney disease?

  • Is the animal in poor body condition?
  • Skin tent? Small kidneys if palpable?
  • Halitosis/oral ulceration
  • USG 1.008-1.012?

–Concentrated urine less than 1.008. A hyposthenuric urine suggest kidneys are still working and diluting urine.

–Or is the USG commensurate with the level of dehydration?

If suspicious, check:

Blood urea nitrogen AND serum creatinine with serum phosphate

(remember high BUN could just be from dehydration/ high protein meal)

26
Q

Step 4– review the clinical examination and signalment.

Which animals are likely to get which diseases?

DAMNITV?

A

Young animals?

  • Congenital abnormality: cPSS, congenital renal disease

Female entire dogs?

  • Pyometra

Old cats?

  • CKD, hyperthyroidism, Lymphoma, diabetes, primary hypertension (not common on its own)

Old dogs?

  • HyperAC, neoplasia (stuff causing hypercalcaemia), diabetes, kidney disease, liver disease
27
Q

Got a suspicion of pyometra? Next steps….

A

Pyometra – diagnostic imaging

28
Q

Got a suspicion of Hypercalcaemia? Next steps….

A

Hypercalcaemia – check serum and ionised Ca and phosphate then look at differentials

29
Q

Got a suspicion of Liver disease ? Next steps….

A

Liver disease – bile acid stimulation test

30
Q

Got a suspicion of Hyperadenocorticism? Next steps….

A

Hyperadenocorticism – ACTH stim

31
Q

Got a suspicion of Hypoadrenocorticism? Next steps….

A

Hypoadrenocorticism – ACTH stim (if wanted to rule it out measure basal cortisol)

32
Q

Got a suspicion of Hyperthyroidism? Next steps….

A

Hyperthyroidism – total T4

33
Q

Got a suspicion of Pyelonephritis? Next steps….

A

Pyelonephritis – sediment/urine culture (but may be negative……)

34
Q

Discuss the Water deprivation test?

A
  • There is a “water deprivation test” which has been used to diagnose diabetes insipidus in the past
  • It is now thought best to rule out all other differentials and then trial treat with DDAVP rather than use this test
  • Also consider ADH assay along with blood and urine osmolality measurements
35
Q

Summary?

A
  • There is a finite list of causes of PUPD – follow a systematic approach
  • Always check urine specific gravity on a refractometer, not the dipstick
  • Bear in mind that common things are much more likely than the weird ones
36
Q

“Sally”, 10yo F Staffordshire bull terrier

  • Drinking more for last 2 weeks
  • Off colour and vomiting, normal faeces
  • Possible weight loss?
  • Not sure whether spayed

Clinical examination

  • Mucus membranes slightly tacky
  • Thoracic auscultation normal
  • Abdomen tense, difficult to palpate
  • No visible vaginal discharge
  • Temperature 39.2C

What is the problem list?

A

Probable primary problems

  • Polydipsia, likely due to polyuria
  • Vomiting
  • [Mild pyrexia]

Probable secondary problems (indirect manifestations of disease)

  • Weight loss (likely reduced intake/cachexia)
  • Inappetance (likely due to nausea)
  • 5% dehydration (likely due to PUPD)
37
Q

What are the Differential diagnoses - (PUPD) for this case?

A

Renal

Hepatic

Endocrine – diabetes mellitus, diabetes insipidus, hyperthyroidism, hyperadrenocorticism, hypoadrenocorticism

Infectious – pyelonephritis, pyometra

Electrolytes – hypokalemia, hypercalcaemia

Iatrogenic – diuretics, steroids etc

38
Q

What are the Differential diagnoses for vomiting in this case?

A

Primary GI tract problem

–Inflammatory, infectious, obstructive, motility disorder, toxic

Intra-abdominal, extra GI problem

–Pancreatitis, diabetes mellitus, hepatitis, renal disease, pyometra, splenitis, hypoadrenocorticism, obstruction from large mass

Extra-abdominal

–Fear, pain, vestibular disease, toxic

39
Q

The next steps in this case was?

A
  • Urinalysis? USG 1.020 inappropriately concentrated for a dog with PU/PD
  • Biochemistry to rule out renal disease and diabetes mellitus?
  • Mild pre-renal azotemia – dehydration
  • No evidence of diabetes mellitus
40
Q

Case outcome for case 1?

A

Pyometra

41
Q

Case 2

  • Harry, 5yo MN labarador
  • PUPD for 4 weeks
  • Marked weight loss
  • Clinical examination otherwise unremarkable

Problem list

  • PUPD
  • Weight loss

–Inadequate intake

–Unable to digest/metabolise food

–Metabolism in excess of intake

•Nothing remarkable on clinical examination!

Look at the biochem?

A

Glucose not above renal threshold

Moderate azotaemia

Both calciums are high (3 types of calcium: complex calcium, protein bound and ionised calcium) ionised is the physiologically relevant. Hypercalcaemia which is physiologically relevant and azotaemia

Most animals with kidney disease will not have a marked hypercalcaemia (Rare)

Hypercalcaemia is nephrotoxic which is directly damaging the tubules, reducing renal perfusion and mineralisation= secondary damage to kidneys from hypercalcaemia

42
Q

What are case 2s new problems?

A
  • Azotaemia
  • Hypercalcaemia (ionized and total)
  • Hyperphosphotemia
43
Q

What are the Differential diagnoses for hypercalcemia?

A

Hogs In Yard

Hyperparathyroidism

Osteolysis

Granulomatous disease

Spurious sample

Idiopathic (cats)

Neoplasia

Young animals

Addisons (Hypoadrenocorticism)

Renal disease

D Hypervitaminosis D

44
Q

Can we narrow down the list?

A
  • Harry is hypercalcemic and hyperphosphatemic
  • In most diseases, the normal Ca-Ph balance is maintained
  • This balance is lost in:

–Renal failure

–Hypervitaminosis D

45
Q

Could Harry have primary renal failure?

A
46
Q

What did case 2 have?

A

Hypervitaminosis D

Major differential diagnoses: fish oil toxicity causing Hypervitaminosis D

Owner had been giving these and had been causing the problem

47
Q

How was case 2 managed for hypercalcemia?

A
  • Aggressive IV fluids (0.9% NaCl)
  • Frusemide?
  • Prednisolone?
  • Bisphosphonates?
  • Hope that there hasn’t been too much renal calcification…….

Harry survived, but with chronic renal damage

48
Q

Discuss Hypervitaminosis D?

A

Vitamin D toxicity refers to the effects of excessive intake of bioactive metabolites of vitamin D. Toxicity caused by ergocalciferol(vitamin D2) or cholecalciferol (vitamin D3) can occur from excessive dietary supplementation (most common in young growing dogs) for treatment of primary hypoparathyroidism. Both of these forms of vitamin D have a slow onset of action and prolonged duration, making correct dosing difficult. Treatment is directed at discontinuing the supplement or decreasing the dose of vitamin D. Toxicity caused by calcitriol (1,25-dihydroxyvitamin D), the most active form of vitamin D, most commonly occurs after treatment of primary hypoparathyroidism. Calcitriol is also the active ingredient in some rodenticides, but these products are no longer widely available in the USA.

In dogs, a newly emerging cause of vitamin D toxicity is ingestion of the calcitriol analogue, calcipotriene (also called tacalcitol), which is a topical preparation used to treat psoriasis in people. Calcipotriene toxicity in dogs can result in severe metastatic calcification in the GI tract, kidney, and other tissues; the condition is commonly fatal.

URI 2 (44 decks)

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