Exam II: Equine and Large Animal Nephrology Flashcards

Lectures from Oliver and Applegate

1
Q

Urinary Assessment

Be able to determine given bloodwork and a urinalysis if a horse is most likely to have pre-renal, renal or post renal disease (azotemia)

What will be on bloodwork? electrolyte abnormalities?

When is is not the kidney? (creatinine)
What non-renal diseases cause increased creatinine?

A

BUN is unpredicatable and difficult to assess, “I don’t use it” - Dr. Oliver

Creatinine: Normal: 0.4-1.8 mg/dL
in foals, creatinine is 30-50% higher if there is asphyxia or prematurity (5-15 mg/dL is okay in the first few years of life)
Non-renal examples of high creatinine include, rhabdo, muscle wasting, and fasting.

pre-renal disease is azotemia with a USG >1.020
renal is with isosthenuria (1.008-1.012)
post-renal azotemia may occue with failure to urinate

Electrolyte abnormalities will include low sodium, low chloride, and hyperkalemia

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2
Q

Urinary assessment objectives

Be able to determine given a blood and urine sample, the likely source of pigmenturia.

A

Whole blood (blood spins down in urine and blood samples)
hemoglobin (pink urine and plasma)
myoglobin (pink urine, blood spins down in blood, ie clear plasma)

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3
Q

Urinary Assessment objectives

Be able to identify a normal equine urine sample (grossly) and identify abnormal urinalysis findings.

A

a normal equine sample will have mucous, calcium carbonate crystlas and concentration. urine samples can be “turbid and goopy”.

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4
Q

urinary assessment objectives

Discuss clinical signs of equine urinary disease.

A

clinical signs of equine urinary diesease includes:
weight loss
abnormal urination
differentials for polyuria is PPID, renal disease, polydipsia, and diabetes.
differentials for pollakiuria include things that would irritate the bladder or urethra like cystc calculi, cystitis, and mare in estrous

less common: fever, anorexia, ventral edema (in worst cases), oral ulcers/ dental tartar (from changes in calcium and phosophorous ratios), nephroliths/neoplasia (“kidney colic”)

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5
Q

urinary pathology

Be able to identify the major equine nephrotoxins

A

the most common acute kidney injury in the horse is acute tubular necrosis (ATN) caused by:

nephrotoxins: tetracyclines (oxytet), aminoglycosides (gentamicin), banamine, bute, and Equiox (NSAIDS), biphosphonates (osphos) and myoglobin and hemoglobin.

or ischaemia: dehydration, hypovolemia, and hypoxia

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6
Q

urinary pathogens objectives

Discuss appropriate treatment options for acute kidney injury in horses

A

JUDICIOUS EUVOLEMIA

prevent prevent prevent

restore plasma volume and maintain euvolemia

dialysis: with risks of peritonitis and knowing it does not make kidney heal faster.

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7
Q

urinary pathology objectives

Discuss the risk factors for the development of cystitis, nephrolithiasis and sabulous cystitis

What kind of cystitis could bladder atony lead to?

A

bacterial cystitis can happen for any good reason and some of those reasons include: damage from pre-existing stones, indwelling urinary catheters, bladder paresis/ paralysis, underlying neoplasia
be mindful that in the case of bacterial cystitis, they notoriously develop antibiotic sistance

ideopathic cystitis is a hemorrhagic cystits that is not typically associated with bacterial infection or increased WBC in urine, it may be associated with stress/ exercise. it does have a good chance for a resolution.

the sabulous cystitis is associated with a collection of inflammatory debris, usually the result of poor bladder emptying. with this cystitis, there is a high chance of reocurrence.

cystic calculi (stones) generally form in the bladder and almost always are calcium carbonate stones. they may originate from diets high in calcium or previous infection. surgucal removal is warranted.

sabulous

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8
Q

What protective mechanisms does the kidney have to increase vasodilation during time of low oxygen and blood flow?

A

prostaglandins
nitric oxide
dopamine

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9
Q

Ruminant Urinary Objectives

Describe the location of the urethral recess, sigmoid flexure, and the urethral process, as well as identify the species in which each of these structures is found and their relevance to clinical medicine

pathology?

A

In the male cattle, you have to think about the urethral recess and sigmoid flexure. During catheterization, knowing the urethral recess exists is helpful to avoid. For the sigmoid flexure know that is is the number 1 place for obstruction in the cattle and number two in small ruminants.
The urethral process is number one for obstruction in the small ruminant. It is also called the pizzle.

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10
Q

Ruminant Urinary Objectives

Identify the lesion of ulcerative posthitis and name the causative agent.

A

The bacterial infection of the skin of the sheath, the prepuce, and
the glans penis is caused by Corynebacterium renale. If the penis is also involved, the
more appropriate description would be balanoposthitis.

can also be called pizzle rot if extended to there.

The organism typically proliferates in male small ruminants fed forages, hay, or total
mixed rations that are high in protein (generally, over 14-15% crude protein on a dry
matter basis).
Painful urination and reluctance to breed

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11
Q

Ruminant Urinary Objectives

Describe the role of dietary crude protein, urea, and ammonia in the pathogenesis of ulcerative posthitis.

A

The organism (c. renale) typically proliferates in male small ruminants fed forages, hay, or total
mixed rations that are high in protein (generally, over 14-15% crude protein on a dry
matter basis).

the high protein leads to a higher metaolbism to urea where c. renale can proliferate. the break down of urea causes a higher ammmonia which can produce a chemical dermatitis

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12
Q

Ruminant Urinary Objectives

Describe the common risk factors for, and historical and physical examination features of urolithiasis

A

common risk factors include:
lower water intake (is it accessible, is it frozen)
dietary mineral imbalances
castration (urethral diameter)
and sex (predilection for MALES»females)

struvite is finely granular white to brown, calcium carbonate is pear pretty, calcium oxolate is pearlish pink, silica and calcium phospahte are seen the most. middle 3 cannot be dissolved. struvite better chance of dissolving in acid solution like

for history, it would be helpful to know diet (for struvite, common signalment is feedlot calves and lambs, show animal on high grain diet, and pet goats on inappropriate diets. for silica, the native rangeland grasses in the western US and Canada have a high silica content. calcium carbonate in high calcium diets (clover, alfalfa). calcium oxolate in high oxolate diets (rhubarb, peanuts, pig’s weeed, lamb’q quarter))

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13
Q

Ruminant Urinary Objectives

Contrast the clinical signs, blood work, and urinalysis/urine sediment
findings of an animal with cystitis with those of an animal with
pyelonephritis

A

■ Ascending UTI:
– Urethra to bladder = cystitis.
– Bladder to one or both ureters =
ureteritis
– Ureters to kidney(s) = pyelonephritis
■ Corynebacterium renale
– Confined cattle UTIs: Vulva – vulva
contact
– Aka contagious bovine pyelonephritis
■ E. coli (and rarely, other coliforms)
– Damage to lower urinary tract defenses
e.g. dystocia, metritis
■ Ascending UTI w/ patent urachus in neonate

■ 1. Cystitis
* Pollakiuria
* Dysuria: May vocalize during voiding, cow
retains urination posture long after urine flow
has ceased
* Blood and purulent debris on vulva, perineum,
hindlegs
* Blood and protein on dipstick urinalysis
* WBCs too if stick has a WBC
panel…unreliable though
* Inflammatory sediment
* Usually, no fever or CBC changes
* Unless accompanied by umbilical infection
in neonates, metritis in adults

■ 2. Pyelonephritis
– One or both kidneys
■ Same signs as Cystitis, plus:
– Colic
– Fever more consistently found
– CBC – inflammatory leukogram
– Casts of WBCs/Debris on urine
sediment
– If renal azotemia exists and
concurrent isosthenuria, then likely
both kidneys are involved

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14
Q

Ruminant Urinary Objectives

Describe the differences between disease caused by host-adapted and nonhost-
adapted serovars of Leptospira in cattle

A

■ Host-adapted serovar for cattle = Leptospira borgpetersenii serovar
hardjo type hardjo-bovis
– Just call it “hardjo”
■ Acute infection and leptospiremia often go unnoticed – no acute
signs!
■ Infection of adult cattle may produce chronic interstitial nephritis of
variable severity, but overt renal dysfunction rarely results
■ Chronic infection of the urogenital tract is established with
protracted (often lifelong!) shedding of the organism in the urine

NON Host-Adapted Serovars in Cattle
■ Serovars pomona &
grippotyphosa
■ These are NOT host-adapted to
cattle
■ Tend to cause more severe and
acute disease in cattle
■ These HURT the kidneys

■ Cows are SICK!
■ Acute, sever nephritis
– Azotemia, hematuria, oligouria or
anuria
■ Sever hemolytic disease
– Icterus, fever
■ Can also see agalactia and mastitis
– Known as Flabby udder or Milk-drop
syndrome
■ Abortion
– Soon after infection

  1. Vaccinate
  2. Drain or fence off wetlands
  3. Limit (if possible) rodent &
    wildlife exposure
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