Equine Urinary Medicine Flashcards
(34 cards)
What are haemodynamic causes of acute renal failure?
– Hypovolaemia e.g. colitis, sweat, blood loss
– Volume redistribution e.g. effusions
– Decreased cardiac output
– Altered vascular resistance e.g. sepsis and endotoxaemia
What are renal causes of acute renal failure?
- 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
How can ischaemia cause ARF?
- 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
What are examples of nephrotoxins?
- antibiotics e.g. aminoglycosides (gentimicin), polymixin B,
tetracyclines - Endogenous substances e.g. haemoglobin and myoglobin
- Others e.g. NSAIDs, heavy metals
What should be monitored on potentially nephrotoxic drugs?
- Serum Creatinine
-treat aggressively if rises significantly
How does aminoglycoside nephrotoxicity occur?
- 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
How does NSAID toxicity occur?
- 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
What are CS of nephrotoxicity?
- 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
How is nephrotoxicity diagnosed?
- Hx, CS
- Urinalysis
- Serum Biochemistry - increased BUN + creatinine
How do you treat nephrotoxicity?
- 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
How do you treat nephrotoxic horse if oliguric?
- Furosemide (4x a day)
- Dopamine - renal vasodilator
(synergistic)
What are examples of chronic renal failure in horses?
- 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
What are CS of chronic renal failure?
- 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
How is Chronic renal failure diagnosed?
- Persistent isothenuria (1.008-1.014), with azotaemia + CS
- Mild anaemia + hypoalbuminaemia
- Electrolyte abnormalities =
-hyperalcaemia
-hypophosphataemia
-hyponatremia
-hypochloride
-low bicarbonate
What is treatment of chronic renal failure?
- Palliative
-improve nutrition + lower protein
-Decrease calcium (avoid alfalfa)
-ensure water + salts always available - if creatinine >800U/L = grave prognosis
What is classed as PU/PD?
- 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
What is Dysuria?
- Abnormal urination =
-pollakiuria - more frequent
-stranguria - difficulty urinating
-haematuira
-pyuria
What are causes of PUPD?
- 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
What would you do to approach PUPD?
- 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)
How can you distinguish between psychogenic polydipsia + Diabetes insipidus?
- 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
How can you distinguish neurogenic + nephrogenic diabetes insipidus?
- Neurogenic = USG increases to >1.020 following ADH / vasopressin administration
- Nephrogenic = no change in USG after administration of ADH , vasopressin
What is treatment of PUPD?
- 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
What are 3 main causes of pigmenturia?
- Blood (haematuria)
- Haemoglobin
- Myoglobin
How do you differentiate different causes of pigmenturia?
- 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