Urinary tract disorders pt 2 Flashcards

1
Q

Chronic Renal Failure
- how common?
- causes?

A
  • Uncommon in horses
  • Causes:
    – Congenital abnormalities
    – Primary glomerular disease
    > Proliferative glomerulonephritis (Ag:Ab)
    – Primary tubulointerstitial disease
    > Chronic interstitial necrosis and fibrosis
    > Pyelonephritis
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2
Q

CRF – Diagnosis, signs

A

Vague signs:
* Chronic weight loss
* Lethargy, anorexia
<><>
* PU/PD
* Peripheral edema
* Poor hair coat
* Oral ulceration or increased dental tartar
<><><><>
* Combine urinalysis with serum biochemistry
Azotemia without urine concentration (!proteinuria)
<><>
* Complete Blood Count:
– Anemia, hypoproteinemia
<><>
* Serum Biochemical Profile
– Azotemia
– Hypoproteinemia, hypoalbuminemia
– Mild hyponatremia, hypochloremia
– Hypercalcemia, hypophosphatemia
<><>
* Trans-rectal palpation
* Renal ultrasonography
* Renal biopsy
* Urine culture

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3
Q

CRF – Treatment

A
  • 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)
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4
Q

Polydipsia / Polyuria main causes?

A
  • Psychogenic Polydipsia
    <><>
  • Diabetes Insipidus
    – Neurogenic (lack of ADH production)
    – Nephrogenic (lack of nephron response to ADH)
    <><>
  • High sodium content in feed
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5
Q

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?
A
  • > 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)
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6
Q

Psychogenic Polydipsia
- how common? what is it? treatment?

A
  • 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)
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7
Q

Ruptured Bladder / Uroperitoneum
- when do we see this? what can rupture?

A

Most commonly occurs in neonatal foals
* During parturition
* NICU Patients: secondary to improper handling,
sepsis
<><><><>
Rupture of any site:
– Bladder (most commonly dorsal aspect)
– Urachus
– Urethra
– Ureters

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8
Q

Ruptured Bladder / Uroperitoneum
- Clinical Signs

A

Progressive onset of:
– Depression, reduced nursing
– Colic, straining or posturing to urinate frequently
– Tachycardia
– Abdominal distension
– Respiratory compromise
<><><><>
*Passage of urine does not rule out rupture

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9
Q

Uroperitoneum – Diagnosis

A
  • 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
    <><><><>
    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
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10
Q

Uroperitoneum – Treatment

A

Correct electrolyte derangements, especially K!
– Physiologic saline
– Glucose, NaHCO3, calcium borogluconate
<><><><>
Abdominal drainage (slowly)
– Foley catheter
<><><><>
* Surgical correction (only once fully stabilized)

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11
Q

Urolithiasis
- how common?
- associated with what?

A
  • Uncommon in horses
  • Diagnosed most often associated with problems of
    the bladder and urethra
    > (May detect renal uroliths during ultrasonography)
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12
Q

Urolithiasis
* Risk Factors:

A

– Increased occurrence with age
– Male
– Preexisting renal disease (“nidus”)

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13
Q

common urolith in horses?

A
  • Calcium carbonate
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14
Q

Urolithiasis – clinical signs

A

– Colic
– Pollakiuria
– Dysuria
– Incontinence
– Hematuria

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15
Q

Urolithiasis – Diagnosis

A
  • Urinalysis and culture
  • Trans-rectal palpation (empty bladder)
  • Cystoscopy
  • Ultrasonography (trans-rectal, trans-abdominal)
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16
Q

Urolithiasis – Treatment

A
  • Surgical Removal +/- Lithotripsy
  • Urine acidification?
    > Ammonium chloride, ammonium sulfate (unpalatable)
    > Reduction in dietary calcium?
17
Q

Pyelonephritis
- origins?
- significance?

A
  • Usually ascending infection
    > Bladder paralysis
    > Urethral obstruction
  • May be hematogenous (from bacteremia)
  • Can be life threatening
18
Q

Pyelonephritis – Diagnosis

A
  • Systemic signs (fever, depression)
    <><><><>
  • Clinicopathology
    – CBC: inflammatory leukogram
    – Biochemical Profile:
  • Azotemia if bilateral
  • Elevated acute phase proteins
    <><><><>
    Urinalysis (catheterization)
    – Lower pH?
    – Leukocytes, blood
    – Protein
    – Bacteria
    <><><><>
    Cystoscopy with ureteral catheterization
    – Culture each kidney
    <><><><>
  • Ultrasonography (trans-abdominal)
  • Blood culture
  • Neurological examination
19
Q

Pyelonephritis – Treatment, prognosis

A

Antibiotics (based on culture and sensitivity)
– Consider drug concentration achieved in urine versus
potential for nephrotoxicity
– Prolonged administration
* Trimethoprim-sulfadiazine
* Penicillin
* Ceftiofur
<><><><>
* Diuresis
* Heminephrectomy > Ensure that function of the contralateral kidney is normal!
* Prognosis: poor unless diagnosed very early and
treated aggressively (rarely occurs)

20
Q

Bacterial Cystitis - origins? which sex?

A

Most commonly occurs secondary to another
disorder of the urinary system
– Urolithiasis
– Bladder paralysis
– Neoplasia
– Iatrogenic infection following bladder catheterization
<><><><>
- female > male

21
Q

Bacterial Cystitis – Diagnosis

A

Clinical Signs
– Rarely see systemic signs (eg. fever, depression)
– Pollakiuria, stranguria
<><>
* Trans-rectal palpation of bladder
<><>
* CBC, biochemical profile, plasma fibrinogen ?
<><>
Urinalysis
– Catheterized sample (culture!)
– Urinalysis:
* Lower pH?
* Leukocytes (>10/hpf), erythrocytes
* Bacteria (>20/hpf)
* Protein
<><>
* Ultrasonography of bladder (per rectum)
<><>
* Cystoscopy
– Check for a urolith
– Lavage the bladder
<><>
* Urine culture

22
Q

Bacterial Cystitis – Treatment

A
  • Antibiotics (based on culture and sensitivity)
    > As for pyelonephritis
  • Correct underlying cause (eg. remove urolith)
  • Diuresis by increased water intake (fluids, salt)
  • Lavage bladder
23
Q

how common are neoplasias in the kidneys?

A

rare

24
Q

types of neoplasia we might see in bladder

A

– Squamous cell carcinoma, transitional cell carcinoma,
fibromatous polyps

25
Q

types of neoplasia we might see in kidneys

A

– Renal cell carcinoma, lymphosarcoma

26
Q

Blister beetle ingestion - what toxin?

A

= Cantharidin toxicosis

27
Q

Blister Beetle (Cantharidin) - risk factors

A
  • Ingestion of blister beetles in hay
  • Increased risk with:
    – Alfalfa
    – Stage of harvesting (post-bloom)
    – Hay conditioners
28
Q

Blister Beetle (Cantharidin) - what does it do? signs?

A

Necrosis of mucous membranes:
– Gastrointestinal ulcers (mouth, stomach, intestines)
– Renal failure
– Cardiotoxic in high concentrations
<><><><>
Signs:
– Colic, vague
– Urinary signs

29
Q

Blister Beetle (Cantharidin) diagnosis

A

– Detection of toxin (cantharidin) in blood or urine
– Evidence of feeding alfalfa hay > See beetles in hay (not reliable)

30
Q

Blister Beetle (Cantharidin) treatment

A

– As with any oral intoxication
– Mineral oil, charcoal
– Supportive care, diuresis