Equine Urinary Medicine Flashcards

1
Q

What are haemodynamic causes of acute renal failure?

A

– 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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2
Q

What are renal causes of acute renal failure?

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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3
Q

How can ischaemia cause ARF?

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
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4
Q

What are examples of nephrotoxins?

A
  • antibiotics e.g. aminoglycosides (gentimicin), polymixin B,
    tetracyclines
  • Endogenous substances e.g. haemoglobin and myoglobin
  • Others e.g. NSAIDs, heavy metals
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5
Q

What should be monitored on potentially nephrotoxic drugs?

A
  • Serum Creatinine
    -treat aggressively if rises significantly
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6
Q

How does aminoglycoside nephrotoxicity occur?

A
  • Neomycin is the most nephrotoxic
    –gentamicin & amikacin similar
  • Filtered by the glomerulus (no metabolism - all excreted by the kidneys)
  • Reabsorbed by proximal tubular epithelial cells
  • Accumulation in proximal tubular cells interferes with cells function
  • Pre-treatment with calcium may reduce nephrotoxicity
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7
Q

How does NSAID toxicity occur?

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 2ary to prostaglandin (PGE2 & PGI2 or COX 1) inhibition
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8
Q

What are CS of nephrotoxicity?

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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9
Q

How is nephrotoxicity diagnosed?

A
  • Hx, CS
  • Urinalysis
  • Serum Biochemistry - increased BUN + creatinine
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10
Q

How do you treat nephrotoxicity?

A
  • IV fluids to improve renal perfusion, correct metabolic disturbances + induce diuresis
    -replace loss + 2x maintenace if polyuric
  • Discontinue nephrotoxic drugs
  • Monitor BW, PCV, serum protein + biochem
  • Poor prognosis if poor initial response to fluid therapy
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11
Q

How do you treat nephrotoxic horse if oliguric?

A
  • Furosemide (4x a day)
  • Dopamine - renal vasodilator
    (synergistic)
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12
Q

What are examples of chronic renal failure in horses?

A
  • Glomerular disease is seen more as chronic vs. acute renal failure
  • Acute tubular necrosis may progress to chronic interstitial nephritis
  • Other acquired include renal neoplasia (e.g. adenocarcinoma, lymphoma), amyloidosis
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13
Q

What are CS 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
    –hypoalbuminaemia relatively mild and offset by increase in globulins, except for glomerulonephritis
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14
Q

How is Chronic renal failure diagnosed?

A
  • Persistent isothenuria (1.008-1.014), with azotaemia + CS
  • Mild anaemia + hypoalbuminaemia
  • Electrolyte abnormalities =
    -hyperalcaemia
    -hypophosphataemia
    -hyponatremia
    -hypochloride
    -low bicarbonate
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15
Q

What is treatment of chronic renal failure?

A
  • Palliative
    -improve nutrition + lower protein
    -Decrease calcium (avoid alfalfa)
    -ensure water + salts always available
  • if creatinine >800U/L = grave prognosis
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16
Q

What is classed as PU/PD?

A
  • PU = urine output >50ml/Kg/day
  • PD = intake of more than 100ml/Kg/day
  • Urine production + water consumption vary with = age, diet, workload, environmental temp
17
Q

What is Dysuria?

A
  • Abnormal urination =
    -pollakiuria - more frequent
    -stranguria - difficulty urinating
    -haematuira
    -pyuria
18
Q

What are causes of PUPD?

A
  • Renal failure
  • PPID (Cushing’s disease)
  • Primary or psychogenic polydipsia - most common
  • Excessive salt consumption
  • Diabetes insipidus
  • Diabetes mellitus
  • Sepsis and endotoxaemia
  • Iatrogenic - fluid therapy
19
Q

What would you do to approach PUPD?

A
  • CONFIRM!! =
    -complete blood count
    -serum biochem
    -Urinalysis = SG, glucose, protein
  • Azotaemia + isosthenuria = chronic renal failure
  • Azotaemia + hyposthenuria = recovery from acute renal failure
  • Hyposthenuria without azotaemia = psychogenic polydipsia / Diabetes insipidus
  • PPID = specific endocrine testing (ACTH)
20
Q

How can you distinguish between psychogenic polydipsia + Diabetes insipidus?

A
  • Water deprivation test
    -do not perform in dehydrated horse
    -empty bladder + get baseline body weight
    -deprive from access to water
    -measure USG, BW + urea
  • If USG increases = psychogenic polydipsia
    -If USG = hyposthenuric = diabetes insipidus
21
Q

How can you distinguish neurogenic + nephrogenic diabetes insipidus?

A
  • Neurogenic = USG increases to >1.020 following ADH / vasopressin administration
  • Nephrogenic = no change in USG after administration of ADH , vasopressin
22
Q

What is treatment of PUPD?

A
  • Depends on primary cause =
  • Psychogenic salt ingestion =
    -Prevent access to mineral salt
  • Psychogenic polydipsia =
    -Environmental changes to relieve boredom
  • Renal failure =
    -Allow constant access to water
    -Good diet
    -Avoid feeds rich in Ca (alfalfa)
  • PPID =
    -Specific treatment: dopamine agonists (pergolide)
  • Diabetes insipidus =
  • Allow constant access to water
  • Neurogenic = Vasopressin (short half life → impractical), Chlorpropamide, clofibrate → potentiate vasopressin action
    -Nephrogenic = Restrict Na intake, Thiazide
23
Q

What are 3 main causes of pigmenturia?

A
  • Blood (haematuria)
  • Haemoglobin
  • Myoglobin
24
Q

How do you differentiate different causes of pigmenturia?

A
  • Spin it down - if still red = haemoglobin / myoglobin
    -if not red = haematuria
  • Blondheim Test (ammonium sulphate precipitation test)
  • haemoglobin = haemolysed serum, haemolytic anaemia
  • Myoglobin = serum biochem = increase CK + AST
25
Q

What are causes of myoglobinuira?

A
  • Muscle cells rupture =
  • Rhabdomyolysis =
    –Sporadic/recurrent exertional rhabdomyolysis
    –Polysaccharide storage myopathy
    –Atypical myopathy
    –Post-anaesthetic myositis
26
Q

What causes haemoglobinuria?

A
  • Haemolysis =
    –Immune mediated haemolytic anaemia
    –Neonatal isoerythrolysis
    –Infectious causes (Babesia, EIA…)
27
Q

How is haemoglobinuria diagnosed?

A

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

28
Q

What are common causes of haematuria?

A

– Urinary tract infection - pyelonephritis / cystitis
– Urolithiasis
– Neoplasia

29
Q

What does timing of haematuria tell us?

A
  • Throughout urination =
    -Kidneys
    -Ureters
    -Bladder
  • Start of urination =
    -Distal urethra
  • End of urination =
    -Proximal urethra and bladder neck
30
Q

What is seen with pyelonephritis? Dx? Tx?

A
  • Ascending infections or consequence of septicaemia
  • Signs = haematuria or pyuria without stranguria or pollakiuria
  • Fever, weight loss, depression
  • Diagnosis = urinalysis (uretheral catheterization) + bacterial culture
  • Treatment = Prolonged antimicrobial course
31
Q

What is seen with cystitis? Dx? Tx?

A
  • CS = haematuria or pyuria with stranguria or pollakiuria
  • Dx = urinalysis, cystoscopy, bacterial culture
  • Tx = Address primary cause + Antimicrobials
32
Q

What animals get urolithiasis? What are contributing factors? CS? Dx? Tx? Px?

A
  • Males predisposed
  • > 10years old
  • Lower urinary tract more common (60% bladder)
  • Contributing factors = Urine retention, UTI, genetic
  • CS = Haematuria, stanguria, pollakiuria, pyuira, incontinence, recurrent colic + loss of condition
  • Dx = Rectal palp bladder, US bladder, cystoscopy
  • Tx = Mares = manual removal
    -Stallions = laparocystotomy, lithotripsy
  • Px = decrease Ca in diet, urine acidifiers
33
Q

What is Sabulous cystitis? What causes it? Tx?

A
  • Accumulation of crystalloid sediment in ventral bladder
  • Secondary to bladder paralysis / problems with bladder emptying = EHV-1, polyneuritis equi, sacral fractures
  • Tx = regular emptying + bladder lavage + control of 2ary UTI
34
Q

What are other causes of haematuria?

A
  • Idiopathic renal haematuria =
    -Arab horse, Uni- or bilateral (unilateral more common)
    -Often severe enough to require blood transfusions
    -Tx = supportive; nephrectomy in severe cases
  • Exercise associated haematuria =
    -Typically microscopic, Due to bladder trauma against pelvis
  • Urethral defects =
    -Urethral rents or tears = Stallions and geldings
    -Haematuria at the end of urination
    -Dx = endoscopy → lesion on dorsal area of urethra at the level of the ischial arch
    -Tx = most resolve spontaneously; if persistent then perform temporary urethrostomy