Urinary tract disorders pt 2 Flashcards
Chronic Renal Failure
- how common?
- causes?
- Uncommon in horses
- Causes:
– Congenital abnormalities
– Primary glomerular disease
> Proliferative glomerulonephritis (Ag:Ab)
– Primary tubulointerstitial disease
> Chronic interstitial necrosis and fibrosis
> Pyelonephritis
CRF – Diagnosis, signs
Vague signs:
* Chronic weight loss
* Lethargy, anorexia
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* PU/PD
* Peripheral edema
* Poor hair coat
* Oral ulceration or increased dental tartar
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* Combine urinalysis with serum biochemistry
– Azotemia without urine concentration (!proteinuria)
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* Complete Blood Count:
– Anemia, hypoproteinemia
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* Serum Biochemical Profile
– Azotemia
– Hypoproteinemia, hypoalbuminemia
– Mild hyponatremia, hypochloremia
– Hypercalcemia, hypophosphatemia
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* Trans-rectal palpation
* Renal ultrasonography
* Renal biopsy
* Urine culture
CRF – Treatment
- Not curative, but may prolong life
- Address causes of acute exacerbation
- Supportive care:
– Fresh water
– Salt block
– Reduce feeding of high Ca++ feeds (eg alfalfa hay)
– Limit protein in diet (while maintaining body weight)
Polydipsia / Polyuria main causes?
- Psychogenic Polydipsia
<><> - Diabetes Insipidus
– Neurogenic (lack of ADH production)
– Nephrogenic (lack of nephron response to ADH)
<><> - High sodium content in feed
water deprivation test - when to do it? what do the results mean?
- start by measuring USG: what do we do if greater or less than 1.025 USG?
- > 1.025: normal nephron function
<><><><> - < 1.025: pertial water deprivation 40ml/kg/day for 4 or more days
- Water Deprivation Test:
- result > 1.025? medullary washout from psychogenic polydipsia
- result <1.025? exogenous ADH administration
> result >1.025: Diabetes Insipidus (Neurogenic)
> result < 1.025: Diabetes Insipidus (Nephrogenic)
Psychogenic Polydipsia
- how common? what is it? treatment?
- Most common cause of PU/PD in horses
– A behavioral vice
– No abnormalities on clinical exam, biochemistry, or
urinalysis (except hyposthenuria/isosthenuria)
<><><><> - Treatment?
– Behavioral modification (environmental enrichment)
Ruptured Bladder / Uroperitoneum
- when do we see this? what can rupture?
Most commonly occurs in neonatal foals
* During parturition
* NICU Patients: secondary to improper handling,
sepsis
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Rupture of any site:
– Bladder (most commonly dorsal aspect)
– Urachus
– Urethra
– Ureters
Ruptured Bladder / Uroperitoneum
- Clinical Signs
Progressive onset of:
– Depression, reduced nursing
– Colic, straining or posturing to urinate frequently
– Tachycardia
– Abdominal distension
– Respiratory compromise
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*Passage of urine does not rule out rupture
Uroperitoneum – Diagnosis
- Azotemia, acidosis
- Electrolyte abnormalities are significant:
> decreased Na, Cl
> increased K - Simultaneous biochemistry and abdominocentesis
> Compare creatinine in abdominal fluid to blood:
> creatinine in abdomen / creatinine in serum > 2
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Trans-abdominal ultrasonography
– Large volume of free fluid, may see bladder wall defect
– Assess urachus
<><><><> - Contrast radiography
<><><><> - Catheterization and infuse new methylene blue
dye, followed by abdominocentesis
Uroperitoneum – Treatment
Correct electrolyte derangements, especially K!
– Physiologic saline
– Glucose, NaHCO3, calcium borogluconate
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Abdominal drainage (slowly)
– Foley catheter
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* Surgical correction (only once fully stabilized)
Urolithiasis
- how common?
- associated with what?
- Uncommon in horses
- Diagnosed most often associated with problems of
the bladder and urethra
> (May detect renal uroliths during ultrasonography)
Urolithiasis
* Risk Factors:
– Increased occurrence with age
– Male
– Preexisting renal disease (“nidus”)
common urolith in horses?
- Calcium carbonate
Urolithiasis – clinical signs
– Colic
– Pollakiuria
– Dysuria
– Incontinence
– Hematuria
Urolithiasis – Diagnosis
- Urinalysis and culture
- Trans-rectal palpation (empty bladder)
- Cystoscopy
- Ultrasonography (trans-rectal, trans-abdominal)
Urolithiasis – Treatment
- Surgical Removal +/- Lithotripsy
- Urine acidification?
> Ammonium chloride, ammonium sulfate (unpalatable)
> Reduction in dietary calcium?
Pyelonephritis
- origins?
- significance?
- Usually ascending infection
> Bladder paralysis
> Urethral obstruction - May be hematogenous (from bacteremia)
- Can be life threatening
Pyelonephritis – Diagnosis
- Systemic signs (fever, depression)
<><><><> - Clinicopathology
– CBC: inflammatory leukogram
– Biochemical Profile: - Azotemia if bilateral
- Elevated acute phase proteins
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Urinalysis (catheterization)
– Lower pH?
– Leukocytes, blood
– Protein
– Bacteria
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Cystoscopy with ureteral catheterization
– Culture each kidney
<><><><> - Ultrasonography (trans-abdominal)
- Blood culture
- Neurological examination
Pyelonephritis – Treatment, prognosis
Antibiotics (based on culture and sensitivity)
– Consider drug concentration achieved in urine versus
potential for nephrotoxicity
– Prolonged administration
* Trimethoprim-sulfadiazine
* Penicillin
* Ceftiofur
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* Diuresis
* Heminephrectomy > Ensure that function of the contralateral kidney is normal!
* Prognosis: poor unless diagnosed very early and
treated aggressively (rarely occurs)
Bacterial Cystitis - origins? which sex?
Most commonly occurs secondary to another
disorder of the urinary system
– Urolithiasis
– Bladder paralysis
– Neoplasia
– Iatrogenic infection following bladder catheterization
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- female > male
Bacterial Cystitis – Diagnosis
Clinical Signs
– Rarely see systemic signs (eg. fever, depression)
– Pollakiuria, stranguria
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* Trans-rectal palpation of bladder
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* CBC, biochemical profile, plasma fibrinogen ?
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Urinalysis
– Catheterized sample (culture!)
– Urinalysis:
* Lower pH?
* Leukocytes (>10/hpf), erythrocytes
* Bacteria (>20/hpf)
* Protein
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* Ultrasonography of bladder (per rectum)
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* Cystoscopy
– Check for a urolith
– Lavage the bladder
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* Urine culture
Bacterial Cystitis – Treatment
- Antibiotics (based on culture and sensitivity)
> As for pyelonephritis - Correct underlying cause (eg. remove urolith)
- Diuresis by increased water intake (fluids, salt)
- Lavage bladder
how common are neoplasias in the kidneys?
rare
types of neoplasia we might see in bladder
– Squamous cell carcinoma, transitional cell carcinoma,
fibromatous polyps
types of neoplasia we might see in kidneys
– Renal cell carcinoma, lymphosarcoma
Blister beetle ingestion - what toxin?
= Cantharidin toxicosis
Blister Beetle (Cantharidin) - risk factors
- Ingestion of blister beetles in hay
- Increased risk with:
– Alfalfa
– Stage of harvesting (post-bloom)
– Hay conditioners
Blister Beetle (Cantharidin) - what does it do? signs?
Necrosis of mucous membranes:
– Gastrointestinal ulcers (mouth, stomach, intestines)
– Renal failure
– Cardiotoxic in high concentrations
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Signs:
– Colic, vague
– Urinary signs
Blister Beetle (Cantharidin) diagnosis
– Detection of toxin (cantharidin) in blood or urine
– Evidence of feeding alfalfa hay > See beetles in hay (not reliable)
Blister Beetle (Cantharidin) treatment
– As with any oral intoxication
– Mineral oil, charcoal
– Supportive care, diuresis
