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Y4 EQ - Miscellaneous > Equine Urinary Medicine > Flashcards

Equine Urinary Medicine Flashcards

1
Q

What is acute renal failure?

A

An abrupt and sustained decrease in GFR resulting in azotaemia and disturbances in fluid, electrolyte and acid-base homeostasis

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2
Q

Why is it important to identify patients at risk of acute renal failure early?

A

Acute renal failure is reversible in the early stages

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3
Q

Are pre-renal, renal or post-renal acute renal failures most common in horses?

A

In adult horses usually pre-renal (haemodynamic) or renal
Post-renal less common - neonates with bladder rupture, rarely obstruction

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4
Q

What are the causes of pre-renal acute renal failure in horses?

A

Haemodynamic:
- Hypovolaemia e.g. colitis, sweat, blood loss
- Volume redistribution e.g. effusions
- Decreased cardiac output
- Altered vascular resistance e.g. sepsis and endotoxaemia

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5
Q

What are the common and less common causes of renal acute renal failure in horses?

A
  • Primarily acute tubular necrosis secondary to ischaemia or nephrotoxin exposure
  • Less commonly glomerulonephritis e.g. immune mediated (EIA) or post-infection e.g. Strep. Equi
  • or interstitial nephritis e.g. pyelonephritis
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6
Q

Describe ischaemia as a renal cause of acute renal failure

A
  • Prolonged haemodynamic changes, renal infarction, NSAID administration
  • Large blood flow (20% cardiac output)
  • Only 10 to 20% of blood flow to the kidneys reaches the medulla - more susceptible to ischaemic injury when there is damage to the blood supply
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7
Q

Describe nephrotoxins as a renal cause of acute renal failure

A
  • Antibiotics e.g. aminoglycosides, polymixin B, tetracyclines
  • Endogenous substances e.g. haemoglobin and myoglobin
  • Others e.g. NSAIDs, heavy metals
  • 90% of the blood flow is filtered by the cortex - susceptible to toxins
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8
Q

Most drug toxicities are exacerbated by …?

A

Concurrent dehydration

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9
Q

What should be monitored in horses on potentially nephrotoxic drug therapy? Why?

A

Serum creatinine
- Particularly if there is evidence of concurrent hypovolaemia, endotoxaemia, or renal insufficiency
- Treat aggressively if creatinine rises significantly

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10
Q

Describe the main features of aminoglycoside nephrotoxicity

A
  • Neomycin is the most nephrotoxic
  • Filtered by the glomerulus (no metabolism - all excreted by the kidneys)
  • Reabsorbed by proximal tubular epithelial cells
  • Accumulation in proximal tubular cells interferes
  • Reabsorption is time dependant - vs dose dependant, therefore single dose daily will reduce toxicity and accumulation
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11
Q

Describe the main features of NSAID nephrotoxicity

A
  • Toxicity due to renal medullary crest and papillary necrosis and sloughing of the tubular epithelial cells in the kidneys
  • Dose dependant effects
  • Secondary to ischaemia secondary to prostaglandin (PGE2 & PGI2 or COX 1) inhibition
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12
Q

What are the clinical signs of acute renal failure?

A
  • Usually referable to the primary problem e.g. acute colic or colitis
  • Anorexia and depression
  • Uraemia, fluid, electrolyte & acid-base disturbances
  • May be just a worsening of the primary problem, or an apparent lack of response to therapy
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13
Q

How is acute renal failure diagnosed?

A
  • History, clinical signs, results of urinalysis and serum biochemistry
  • Other tests: e.g. fractional excretion of electrolytes, GGT/creatinine ratio
  • Proteinuria, glucosuria
  • Sediment exam
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14
Q

Increases in … and … need to be differentiated from the effects of dehydration or pre-renal azotaemia

A

BUN
Creatinine

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15
Q

How can you determine if the azotaemia is pre-renal?

A

Pre-renal azotaemia should be quickly reversible with fluid therapy and present with maximally concentrated (>1.035) urine prior to fluid therapy

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16
Q

What causes GGT to increase?

A

Damage to tubules

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17
Q

Other tests: e.g. fractional excretion of electrolytes, GGT/creatinine ratio, can only be performed when?

A

Only on urine collected before fluid therpay

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18
Q

What makes the normal urine of horses cloudy?

A

Carbonate crystals

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19
Q

What can cause an increase in protein in horses urine (normal)

A

Mucus which lubricates the urinary tract

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20
Q

Describe the electrolyte changes seen in acute renal failure

A

Hyponatraemia and hypochloraemia – May also see hypocalcaemia & hyperphosphataemia

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21
Q

Why are IV fluids used as a part of acute renal failure treatement?

A
  • Improve renal perfusion, correct metabolic disturbances and induce diuresis
  • Aim to prevent pre-renal failure developing into intrinsic renal failure
  • Replace fluid deficits and maintain on twice maintenance provided polyuric
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22
Q

What needs to be monitored when treating acute renal failure?

A
  • Monitor body weight, PCV and serum protein
  • Estimate dehydration and continue to monitor - if increase above expected baseline, may be overhydrating or use CVP
  • Monitor serum biochemistry
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23
Q

Which 2 drugs can be used for diuretic therpay?

A

Furosemide
Dopamine

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24
Q

Compare furosemide and dopamine as diuretics

A

Furosemide:
- Must be filtered at the glomerulus to work
- Care with exacerbating volume depletion and potentiating drug effects
- May make things worse in a dehydrated pateint
Dopamine:
- Recommended
- Potent renal vasodilator that acts directly on specific receptors on arterioles. Give via infusion - care with arrhythmias

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25
Q

Is glomerular disease seen more as chronic or acute renal failure?

A

Chronic

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26
Q

List the clinical signs of chronic renal failure

A
  • Chronic weight loss
  • Lethargy, poor hair coat, PU/PD, poor performance (mild anaemia)
  • May see oral ulceration, gastroenteritis, excessive tartar and halitosis
  • Ventral oedema inconsistent
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27
Q

Describe the test results which indicate chronic renal failure

A
  • Persistent isosthenuria (1.008 - 1.014) with azotaemia and clinical signs
  • Mild anaemia, mild hypoalbuminaemia
  • Electrolyte abnormalities – hypercalcaemia, hypo PO4,hypoNa, HypoCl and low bicarbonate
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28
Q

Why is hypercalcemia seen in chronic renal failure?

A

In horses its normal to absorb large amount of Ca from the diet for the kidneys to eliminate (not like this in SAs)
So when the kidneys stop working you get large amount of Ca accumulation

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29
Q

How is ultrasound used in diagnosing chronic renal failure?

A
  • Left kidneys lies deep to the spleen
  • Right kidney lies next to the caecum and duodenum
  • Endoscopy collection of ureter samples to look at relative severity of effect in each kidney, culture, biopsy
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30
Q

How is chronic renal failure in horses treated?

A
  • Palliative only
  • Ensure water and salt always available
  • Improve nutrition with lower protein (< 10% if possible) to manage BUN
  • Decrease calcium if high calcium diet (alfalfa)
  • Care with excessive fat supplementation due to risk of hyperlipaemia
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31
Q

Describe the prognosis of chronic renal failure in horses

A
  • If mild to moderate elevations in creatinine (<200 U/L), some horses can survive a long time
  • Poor long term prognosis and shorter time if creatinine is higher.
  • > 800 U/L prognosis is grave
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32
Q

How is polyuria define in horses?

A

Urine output exceeding 50 mL/Kg/day ≈ 25 L of urine in 500 Kg horse

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33
Q

How is polydipsia define in horses?

A

Fluid intake of more than 100 mL/Kg/day ≈ 50 L of water in 500 Kg horse

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34
Q

Urine production and water consumption vary with which factors?

A

Age
Diet
Workload
Environmental temperature

35
Q

In which cases is active water excretion important in horses?

A

Foals ingest up to 20% of their body weight in milk a day (250 mL/Kg/day)
→ failure to produce a large volume of hyposthenuric urine would result in water retention

36
Q

How are polyuria and polydipsia confirmed?

A

Measure accurately water intake over 24 hours
How to collect all urine produced by a horse over 24 hours?
Polyuria Vs Dysuria

37
Q

What is dysuria?

A

Abnormal urination
Pollakiuria (frequent, small amounts)
Stranguria (difficulty urinating)
Haematuria, and/or pyuria

38
Q

What are the signs of dysuria?

A
  • Owners may notice clinical signs specifically
  • May see urine dribbling or scalding
  • Must differentiate from normal oestrus behaviour in mares
  • Less commonly may see colic or tenesmus
39
Q

List the causes of PUPD

A
  • Renal failure
  • PPID (Cushing’s disease)
  • Primary or psychogenic polydipsia
  • Excessive salt consumption
  • Diabetes insipidus
  • Diabetes mellitus
  • Sepsis and endotoxaemia
  • Iatrogenic
40
Q

Describe PPID as a cause of PUPD, including the pathophysiology

A

Endocrine disorders of older horses
PU/PD not very severe
Pathophysiology
- Hyperadrenocorticism → Hyperglycaemia
- Cortisol antagonism of vasopressin on the collecting ducts
- Decreased vasopressin production and release

41
Q

What is the most common cause of PUPD in horses?

A

Primary or psychogenic polydipsia

42
Q

Describe the pathophysiology of primary or psychogenic polydipsia

A

PU/PD more severe than with renal failure or PPID
Boredom?
Change in environment, stabling, diet…

43
Q

Describe the pathophysiology of Diabetes insipidus

A

Neurogenic: vasopressin deficiency
Nephrogenic: insensitivity of renal collecting ducts to vasopressin (buts its being produced normally)

44
Q

Describe the pathophysiology of Diabetes Mellitus

A

Hyperglycaemia → glucosuria → osmotic PU → PD

45
Q

Name 3 iatrogenic causes of PUPD

A

Fluid therapy, corticosteroids, α2-agonists

46
Q

Describe the diagnostic approach to PUPD

A

PD may be a compensatory mechanism for pathologic PU or other diseases associated with body water loss → rule out physiologic causes of PD or pathologic causes of PU before doing some tests that can be potentially dangerous to the horse (e.g. water deprivation test)

47
Q

Which diagnostic tests can be used in cases of PUPD

A

Complete blood count
Serum biochemistry
Urinalysis

48
Q

What do the following test results indicate:
- Azotaemia + Isosthenuria (1.008-1.014)
- Azotaemia + Hyposthenuria (<1.007)
- Hyposthenuria without azotaemia

A
  • Chronic renal failure
  • Recovery from acute renal failure
  • Psychogenic polydipsia or diabetes insipidus
49
Q

What is the role of the water deprivation test?

A

To distinguish between diabetes insipidus and psychogenic polydipsia

50
Q

The water deprivation test should NOT be performed in which horses?

A

Should not be performed in horses that are azotaemic or dehydrated, and other pathologic causes of PU/PD should be ruled out in advance

51
Q

Describe how to carry out the water deprivation test

A
  • Empty bladder and get baseline body weight
  • Deprive horse from access to water
  • Measure urine specific gravity, body weight and urea periodically
52
Q

How do the results of the water deprivation test diagnose diabetes insipidus or psychogenic polydipsia?

A

If urine specific gravity increases to >1.025 within 24 hours → psychogenic polydipsia (Able to concentrate urine)

If still hyposthenuric → diabetes insipidus

53
Q

Describe the medullary washout test

A

Modified water deprivation test
Restrict water intake to 40 mL/Kg for 3-4 days
Test body weight, hydration and urine specific gravity periodically

54
Q

How do the results of the medullary washout test diagnose diabetes insipidus or psychogenic polydipsia?

A

If specific gravity >1.025 at the end of the testing period → psychogenic polydipsia
If urine cant be concentrated → diabetes insipidus

55
Q

How can neurogenic and nephrogenic diabetes insipidus be differentiated?

A

Neurogenic: USG increase to >1.020 following administration of ADH or vasopressin
Nephrogenic: No change in USG (hyposthenuric) following administration of ADH or vasopressin

56
Q

Treatment of PUPD depends on?

A

The primary cause

57
Q

How is psychogenic polydipsia treated?

A

Environmental changes to relieve boredom

58
Q

How is renal failure treated?

A

Allow constant access to water
Good diet
Avoid feeds rich in Ca (alfalfa)

59
Q

How is PPID treated?

A

Specific treatment: dopamine agonists (pergolide)

60
Q

What are the 3 main causes of pigmenturia?

A

Discoloured, normally red to brown, urine
Blood (haematuria)
Haemoglobin
Myoglobin

61
Q

How should you approach a case of pigmenturia?

A

Spin the urine in a centrifuge:
- If you have whole blood the RBCs will settle at the bottom once spun = haematuria
- If it remains the same colour once spun, haemoglobin or myoglobin is present

62
Q

How can you differentiate haemoglobin vs myoglobin in urine?

A

Blondheim test = ammonium sulphate precipitation test
Myoglobin excreted at plasma concentration of 0.2g/L → normal plasma
Haemoglobin excreted at plasma concentration of 1g/L → pink or red plasma

63
Q

Where is myoglobin from in the body?

A

Muscle cells

64
Q

What is the cause of myoglobinuria?

A

Muscle cells rupture → myoglobin
Rhabdomyolysis:
- Sporadic/recurrent exertional rhabdomyolysis
- Polysaccharide storage myopathy
- Atypical myopathy
- Post-anaesthetic myositis

65
Q

How is myoglobinuria diagnosed?

A

Clinical signs and ↑CK and AST

66
Q

What are 3 causes of haemolysis?

A

Immune mediated haemolytic anaemia
Neonatal isoerythrolysis
Infectious causes (Babesia, EIA…)

67
Q

How is haemoglobinuria diagnosed?

A

Haemolysed serum
Anaemia (regenerative)
↑ bilirubin
Assessment of blood film
Agglutination tests: Coombs test

68
Q

What is haematuria?

A

Red cells in urine
Normal: up to 5 RBCs per high power field on sediment examination

69
Q

List the 3 common causes of haematuria

A

Urinary tract infection
Urolithiasis
Neoplasia

70
Q

How is the timing of haematuria linked to the anatomical cause?

A

Throughout urination = Kidneys, Ureters or Bladder
Start of urination = Distal urethra
End of urination = Proximal urethra and bladder neck

71
Q

Describe pyelonephritis in horses

A
  • Rare in horses. Frequently unnoticed for months/years
  • Ascending infections or consequence of septicaemia
  • Signs: haematuria or pyuria without stranguria or pollakiuria
  • Fever, weight loss, depression…
72
Q

Describe diagnosis and treatment of pyelonephritis in horses

A

Diagnosis: urinalysis (uretheral catheterization) + bacterial culture
Treatment: Prolonged antimicrobial course

73
Q

Describe cystitis in horses

A

Uncommon in horses
Ascending infections: investigate alterations in urine flow (urolithiasis, bladder paralysis, neoplasia…)
Signs: haematuria or pyuria with stranguria or pollakiuria

74
Q

Describe diagnosis and treatment of cystitis in horses

A

Diagnosis: urinalysis, cystoscopy, bacterial culture
Treatment: Address primary cause + Antimicrobials

75
Q

Describe the predispositions of urolithiasis in horses

A

Lower urinary tract more common - 60% bladder
Male predisposed - Shorter, narrower urethra
Normally >10 years old

76
Q

Describe the pathophysiology of urolithiasis in horses

A

High amounts of CaCO3
Alkaline urine favours crystallization of Ca crystals
Normally inhibitors of crystal growth
Contributing factors:
- Urine retention
- UTI
- Genetic

77
Q

What are the clinical signs of urolithiasis in horses?

A

Haematuria, maybe more apparent after exercise
Stranguria, pollakiuria, pyuria, incontinence
Recurrent colic, loss of condition…

78
Q

How is urolithiasis in horses diagnosed?

A

Rectal palpation bladder
Ultrasound examination bladder
Cystoscopy
Consider UTI: investigate

79
Q

How is urolithiasis in horses treated?

A

Mares: Manual removal
Males:
- Laparocystotomy
- Lithotripsy

80
Q

How is urolithiasis in horses prevented?

A

Decrease Ca in diet
Urine acidifiers

81
Q

What is sabulous cystitis?

A
  • Accumulation of crystalloid sediment in the ventral aspect of the bladder
  • Secondary to bladder paralysis or problems with bladder emptying – EHV-1, Polyneuritis equi, sacral fractures…
  • Irritation of the bladder wall
82
Q

How is sabulous cystitis treated?

A

Regular emptying and bladder lavage + control of secondary UTI

83
Q

Idiopathic renal haematuria occurs in which horses?

A

Arabs

84
Q

What is the cause of exercise associated haematuria?

A

Due to bladder trauma against pelvis

Y4 EQ - Miscellaneous (6 decks)

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