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Ag Animal Test 3 > Urology in Ag Animal Medicine > Flashcards

Urology in Ag Animal Medicine Flashcards

1
Q

History and signalment info to gather for urologic problems

A
  • Age and sex
  • Duration
  • Dietary history
  • Breeding history
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2
Q

Physical exam things to get for urologic disease

A
  • Observe urination

- Get a urine sample

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3
Q

Appearance of dysuria, stranguria, incontinence

A
  • They may look like they have abdominal pain
  • They may be planking
  • Camelids start squatting whether or not they are trying to urinate or defecate
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4
Q

Common causes of stranguria or dysuria

A
  • Urethral obstruction or inflammation
  • Neurologic issues
  • This is more consistent with UMN
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5
Q

Causes of incontinence

A
  • Impaired neuromuscular control of urination, congenital abnormalities
  • This is more consistent with LMN
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6
Q

Differentials for a rectal prolapse?

A
  • Parasites

- Blocked animals and urethral obstruction

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7
Q

Hematuria

A
  • Blood in the urine
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8
Q

Hemoglobinuria

A
  • Hemoglobin in the urine
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9
Q

Myoglobinuria

A
  • Myoglobin in the urine
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10
Q

Bilirubinuria

A
  • Bilirubin in the urine
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11
Q

Pyuria

A
  • White blood cells in the urine
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12
Q

Differentials for hemoglobinuria?

A
  • Leptospirosis, bacillary hemoglobinuria, copper toxicity, post-parturient hemoglobinuria, water intoxication
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13
Q

Goat RBCs

A
  • Very thin cell walls and very sensitive to hypo-osmolarity
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14
Q

What is the pathogenesis of water intoxication?

A
  • Massive water intake –> hypotonicity of body fluid –> hemolysis of RBCs
  • Sudden decrease in osmolality
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15
Q

Clinical signs of water intoxication

A
  • Neurologic signs
  • Respiratory distress
  • Hemoglobinuria
  • Death
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16
Q

Treatment for water intoxication

A
  • Temporarily restricting water intake
  • Supportive care
  • Restore Na to 140-155 mmol/L without overcorrection
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17
Q

When do you see hemoglobinuria during urination?

A
  • Throughout
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18
Q

Color of hemoglobinuria

A
  • Deep red to black
  • Doesn’t spin out
  • hard to tell apart from myoglobinuria
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19
Q

What does hemoglobinuria suggest about plasma?

A
  • hemolytic state with icterus possibly developing
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20
Q

Hematuria

A
  • Blood in urine if you spine down the urine
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21
Q

Color of hematuria?

A
  • Red, pink, or brown
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22
Q

Urine cytology of hematuria

A
  • RBCs seen on microscopic examination
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23
Q

What does timing of hematuria during the stream tell you about where hematuria localizes?

  • Beginning? End? Throughout urination?
A
  • Beginning of urination - urethra, reproductive tract
  • End of urination from bladder
  • Throughout urination: kidney, ureters
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24
Q

Appearance of myoglobinuria?

A
  • Red/brown urine
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25
Q

Clues that red or brown urine might be myoglobinuria?

A
  • Blood CK, AST may be markedly elevated
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26
Q

Differentials for myoglobinuria?

A
  • Clostridial disease
  • Myopathies
  • Plant toxicosis
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27
Q

Bilirubinuria appearance of urine

A
  • Dark brown
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28
Q

Which type of bilirubin is excreted?

A
  • Conjugated bilirubin
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29
Q

Diagnosis of bilirubinuria

A
  • Strong positive on the dipstick
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30
Q

Approach to diagnosis of hematuria and pigmenturia

A
  • PE
  • CBC and/or examine serum or plasma
  • Full UA, centrifugation, and sediment exam
  • Look for any chance of toxins
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31
Q

What is important t odo when you see pigmenturia?

A
  • Maintain perfusion of the kidneys as pigments are nephrotoxic**
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32
Q

Pyuria definition

A
  • Gross or microscopic evidence of inflammatory cells and debris
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33
Q

What can cause pyuria?

A
  • Septic or nonseptic inflammatory disease
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34
Q

Approach to diagnosis of pyuria?

A
  • History and PE (including rectal palpation to check for pyelonephritis and transabdominal ultrasound)
  • Urinalysis
  • Culture
  • Determine source of pyuria
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35
Q

What finding on urinalysis suggests urinary tract inflammation?

A
  • > 10 WBC/HPF
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36
Q

Collection of urine for urinalysis

A
  • Midstream voided or catheterized, but CANNOT catheterize male ruminants
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37
Q

What are two reasons why it’s so challenging to catheterize male ruminants?

A
  • Sigmoid flexure

- urethral diverticulum

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38
Q

What finding on cultures suggests UTI?

A
  • Bacterial counts >1 x 10^4 bacteria/mL of urine
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39
Q

What suggests contamination on urine culture?

A
  • Large variety of bacterial species
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40
Q

Crystalluria significance

A
  • Can lead to formation of calculi

- May see crystals on the hair

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41
Q

Polyuria definition

A

Passage of abnormally large amounts of urine

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42
Q

Causes of polyuria

A
  • Renal failure: tubular function is impaired or loss of nephrons
  • Neurogenic or nephrogenic diabetes insipidus
  • Renal medullary washout
  • Excessive drinking
  • Liver failure
  • Other electrolyte abnormalities
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43
Q

Approach to diagnosis of polyuria

A
  • HISTORY (have you seen them urinate more often or less)?
  • Clin path
  • Water deprivation test (ONLY in stable patients**)
  • Fractional clearance
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44
Q

Clin path changes possible with PU

A
  • Hyposthenuria (USG <1.007)

- Isosthenuria

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45
Q

Fractional clearance vs creatinine clearance - for which do you need to know the flow rate?

A
  • For creatinine you need to know the flow rate, but not for fractional clearance of sodium
  • This makes fractional clearancce of sodium more practical
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46
Q

Normal fractional clearance of Na

A
  • Don’t need to know the flow rate
  • More practical
  • Normal is 0-4% (usually greater than 1% except in dairy cattle)
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47
Q

Equation for fractional clearance of sodium

A

[Na in urine]/[Na in serum] x [Creatinine in serum]/[creatinine in urine]

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48
Q

What is anuria?

A
  • Absence of urine production
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49
Q

pre-renal causes of anuria?

A
  • Dehydration, decreased perfusion
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50
Q

Renal causes of anuria

A
  • Acute tubular nephrosis

- End stage renal disease

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51
Q

Post renal causes of anuria

A
  • Urethral obstruction
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52
Q

Oliguria

A
  • Scant or subnormal urine production
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53
Q

Oliguria causes

A
  • Dehydration and acute and chronic renal disease
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54
Q

Glucosuria

A
  • glucose in urine
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55
Q

What is the renal threshold for glucose in most large animal species?

A

> 150 mg/dL

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56
Q

Other findings on urinalysis?

A
  • ketonuria

- Proteinuria

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57
Q

What can cause a false positive with proteinuria on a dipstick?

A
  • Alkaline urine
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58
Q

What can cause increases in urinary protein?

A
  • Glomerulonephritis or amyloidosis

- UTI

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59
Q

Normal urinalysis in an adult cattle/sheep/goat/camelid?

USG: 
Protein 
Glucose
Ketones
Blood 
pH 
WBC
RBC
Casts 
Crystals 
Urine culture results
A
  • USG >1.022
  • Protein neg to 1+
  • Glucose, ketones, blood: negative
  • pH 7.0 to 8.5
    WBC: 0-3/HPF
    RBC: 0-5/hpf
    Casts: none
    Crystals: rare
    Urine culture: sterile with catheter
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60
Q

What are casts?

A
  • Protein or cellular material from renal tubules
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61
Q

What do casts indicate?

A
  • renal damage or tubular disease
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62
Q

Occult blood on urinalysis significance?

A
  • Hard to interpret
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63
Q

Meaning of transitional cells on urinalysis?

A
  • Neoplasia
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64
Q

Hyposthenuria definition

A

USG below 1.010

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65
Q

isosthenuria

A

USG around 1.010

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66
Q

Hypersthenuria

A

> 1.030-1.035

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67
Q

What are the three possible categories for azotemia?

A
  • pre-renal
  • Renal
  • Post-renal
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68
Q

What is BUN?

A
  • Urea is non-toxic means of excreting ammonia
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69
Q

What determines urea excretion in ruminants?

A
  • Nitrogen intake
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70
Q

Where is urea nitrogen secreted and metabolized?

A
  • Urea nitrogen is secreted in saliva and metabolized by ruminal flora
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71
Q

High BUN but normal creatinine?

A
  • Less reliable for specific kidney function
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72
Q

Where does creatinine come from?

A
  • Generated by muscle metabolism as a constant
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73
Q

Creatinine excretion and reabsorption

A
  • Excreted by kidney and not reabsorbed
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74
Q

Sensitivity of creatinine

A
  • Very sensitive and early indicator of renal insufficiency
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75
Q

Creatinine as an indicator compared to BUN?

A
  • More reliable
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76
Q

Physiologic increase in creatinine?

A
  • Double muscled animals
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77
Q

What can lead to a more acidic urine in ruminants physiologically?

A
  • High concentrate forage
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78
Q

What can lead to hyperphosphatemia?

A
  • Decreased GFR
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79
Q

Significance of hyperphosphatemia in ruminants?

A
  • Less significant because kidney is not the major excretory route for phosphorus
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80
Q

What can lead to hypocalcemia in ruminants?

A
  • Renal disease
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81
Q

Fibrinogen levels in bovine renal failure?

A
  • Can be very high (exceeding 1800 mg/dL)
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82
Q

Collecting urine:

  • Cattle
  • Sheep
  • Camelids
A
  • Cattle you can tickle the vulva in females
  • In sheep you can hold off their nose
  • Camelids are tough
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83
Q

What should you think with a paradoxical aciduria?

A
  • Abomasal outflow tract obstruction
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84
Q

Signs of paradoxical aciduria?

A
  • Ruminants with a hypochloremic, hypokalemic, metabolic alkalosis
  • urine pH 5-6
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85
Q

Paradoxical aciduria pathophysiology

A
  • Abomasum/rumen fluid retention –> decreased circulating fluid volume –> hypovolemia –> aldosterone –> Na resorption and cation secretion –> K+ depletion (due to decreased K intake and sequestration) therefore H+ secreted leading to lower H+ in blood and paradoxic aciduria
  • Abomasal HCl reflux and sequestration also leads to H+ and Cl- depletion and metabolic alkalosis, which drives K+ into cells and H+ out of cells futher contributing to the K+ depletion
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86
Q

Protein in urine

  • Normal?
  • Significance?
A
  • Not normal

- GN or amyloidosis or UTI

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87
Q

Other diagnostics for urologic problems

A
  • Rectal examination to feel bladder and kidneys
  • neuro exam
  • Radiology, US, scintigraphy, biopsy, and endoscopic exam (special)
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88
Q

Ulcerative posthitis and vulvitis - what is it?

A
  • ulcerative bacterial infection of the mucous membrane
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89
Q

Etiology of ulcerative posthitis and vulvitis

A
  • Corynebacterium renale
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90
Q

Risk factors ofr ulcerative posthitis and vulvitis

A
  • males are more predisposed because the prepuce can pool the urine
  • Increase or excessive dietary protein concentration
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91
Q

How long can corynebacterium renale persist?

A
  • Can persist in wool, hair, and scabs for as long as 6 months
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92
Q

What are main losses with ulcerative posthitis and vulvitis?

A
  • Production losses
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93
Q

Pathophysiology of ulcerative posthisis and vulvitis?

A
  • Corynebacterium renale
  • High protein diets –> increased ammonia production in the rumen –> converted to urea in the liver –> urea is eliminated through the renal system –> C. renale proliferates
  • urease in organism converts urea back to ammonia –> chemical irritation and ulceration of the prepuce and surrounding skin
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94
Q

Clinical signs of ulcerative posthitis and vulvitis?

A
  • Dysuria, vocalization while voiding
  • Inflammation progresses, ulceration may result in fibrous adhesion between the penis and prepuce
  • Severe inflammation can lead to obstruction of the urethra
  • Impairment of breeding soundness
  • Weight loss in chronic cases
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95
Q

Dfdx for ulcerative posthitis and vulvitis

A
  • Ulcerative dermatosis
  • Contagious ecthyma
  • Urolithiasis
  • Caprine herpesvirus
  • Mycoplasma mycoides subspecies Mycoides large Colonya
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96
Q

Treatment for ulcerative posthitis and vulvitis

A
  • Reduce protein and NPN intake (* THE BIGGEST THING)
  • Limit contact
  • Clip wool or hair from skin surrounding the prepuce or vulva (goes quite a ways)
  • Topical abx (Petercillin, mastitis treatment tubes, triple abx)
  • Systemic antibiotics (Penicillin, ampicillin, oxytetracycline but careful with cephalosporins)
  • NSAIDs
  • Surgery
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97
Q

What three things should you be using ceftiofur for?

A
  • Respiratory, metritis, and foot rot
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98
Q

Prognosis for ulcerative posthitis and vulvitis

A
  • Poor if diet not changed

- Recovery for breeding? (GUARDED)

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99
Q

Prevention of ulcerative posthitis and vulvitis

A
  • Limit protein and NPN
  • Slow weight gains
  • Separate affected males to decrease spread
  • Shear at the time of highest protein intake
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100
Q

Etiology of urolithiasis

A
  • Metabolic disease in all livestock species
  • Disease due to trauma of the urinary tract and obstruction of urinary outflow
  • Diagnosis in a single animal = all males in a group at risk
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101
Q

What does it mean if one male gets urolithiasis in a group? Are the others at risk?

A
  • All males in a group are then at risk
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102
Q

Environmental risks for urolithiasis

A
  • Cold weather

- Drink a lot less

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103
Q

Why are males more predisposed to urolithiasis?

A
  • Longer, narrow, and contains the sigmoid
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104
Q

Special anatomical features of male cattle?

A
  • Distal sigmoid flexure, near the insertion of hte retractor penis muscle
105
Q

Special anatomical features of male small ruminants?

A
  • Urethral process and distal sigmoid flexure
106
Q

Age of castration with urolithiasis?

A
  • Castrating younger raises the risk, but castrating older is harder to do
107
Q

Which breed is classic for urolithiasis?

A
  • Nigerian Dwarf Goats
108
Q

Pathophysiology of urolithiasis?

A
  • Supersaturation of urine with calculus-forming crystalloid (this is why hydration is huge in prevention)
  • Capabilities of crystallization inhibitors in urine are overwhelmed
  • Dehydration
  • Urinary pH
  • UTIs
  • Anatomy of the ruminant urethra contributes to obstruction
109
Q

Phosphatic stones - risk factors in diet for formation?

A
  • Rations high in phosphorus (grain-based rations)

- Calcium/Phosphorus ratio less than 2:1

110
Q

Struvite calculi fancy name

A
  • Magnesium ammonium phosphate hexahydrate
111
Q

Apatite calculi fancy name

A
  • Calcium phosphate
112
Q

What can phosphatic stones look like?

A

Single stone or sand-like debris

113
Q

What type of cattle tends to get phosphatic stones?

A
  • Feed lot steers due to high phosphorus grain-based diets
114
Q

Three primary type of calculi

A
  • Phosphate, calcium, and silica
115
Q

Silica calculi feed risks

A
  • Primarily grazing native rangeland grasses or western North America
116
Q

How does water deprivation factor into silica calculi formation?

A
  • Periods of water deprivation and urine becomes concentrated
117
Q

Appearance of silica calculi?

A
  • Typically hard, smooth white to brown, radiopaque, and layered
118
Q

Incidence of silica calculi in urinary tracts of range cattle

A
  • 50-80%

- Obstruction is variable however

119
Q

What are the two calcium based calculi?

A
  • calcium carbonate and calcium oxalate
120
Q

Risk factor for calcium carbonate?

A
  • Ruminants grazing lush, rapidly growing clover pastures or being fed alfalfa hay
  • Rich in calcium, low in phosphorus and magnesium
  • Increased urinary calcium excretion and alkaline urine –> calcium carbonate calculogenesis
121
Q

Urine pH that can contribute to calcium carbonate?

A
  • Alkaline urine
122
Q

Calcium carbonate urolith appearance?

A
  • Typically round, smooth shape and golden and are often present as multiple uroliths scattered throughout the lower urinary tract
123
Q

Appearance of calcium oxalate

A
  • Typically dense, hard, white to yellow, and either smooth or jagged
124
Q

Signs of acute urinary obstruction

A
  • Bladder distention
  • Stranguria and abdominal pain, anuria, or dribbling urine
  • restless, tread, swish tails, grind their teeth (bruxism), may vocalize
  • Tachycardia, tachypnea, and mild bloat secondary to ruminal stasis
  • may see secondary rectal prolapse due to straining
  • Crystals or blodo on the hairs of preputial tuft, dry
  • Rectal exam shows pulsation of the pelvic urethral
  • Abdominal palpation possible in small ruminants and camelids
125
Q

What are common sequele to urolithiasis?

A
  • urethral rupture

- Bladder rupture

126
Q

Urethral rupture signs

A
  • Ventral edema***
  • Depression
  • Inappetence
  • bilateral pitting edema in the ventral perineum, inguinal region, prepuce, ventral abdomen
127
Q

Bladder rupture clinical signs

A
  • Relief of bladder distention causes cessation of stranguria
  • Distention of abdomen develops within 1-2 days after rupture, ballottement of abdomen may elicit a flluid wave
  • Depression anorexia, weakness, dehydration, and shock
  • Animal’s breath may smell like ammonia
128
Q

Diagnostics for urolithiasis?

A
  • Abdominal ultrasound to reveal distended bladder
  • Radiographs
  • Examination of the urethral process in small ruminants
129
Q

What size bladder on ultrasound is considered significant in small ruminants?

A
  • > 8 cm
130
Q

How to do examination of the urethral process?

A
  • Tip them and take the penis out
  • Light sedation and lidocaine in the prepuce
  • Anesthetize goats
  • Allis tissue forceps and pull out the stone
  • Hard to do
131
Q

Clin Path with Acute Urolithiasis

A
  • May be unremarkable
  • Hyperglycemia and stress leukogram
  • Hemoconcentration and azotemia
  • Hematuria and proteinuria
132
Q

Clin Path with chronic urolithiasis

A
  • Hyponatremia, hypochloremia , hypocalcemia, hyperphosphatemia, and severe azotemia with isosthenuria (extensive nephron damage)
133
Q

Potassium with bladder rupture

A
  • Don’t worry so much about it as hyperkalemia isn’t always a thing
134
Q

Treatment of urolithiasis

A
  • Salvage (reasonable if feedlot steer)
  • Medical management
  • Surgical management
135
Q

Medical management for urolithiasis?

A
  • Antispasmotic tranquilizer (Acepromazine)
  • Bladder drinage (percutaneous infusion with Walpole solution)
  • Fluid therapy
136
Q

Walpole solution

A
  • Acetic acid

- May help dissolve struvites

137
Q

Should you also give pain management if you’re giving acepromazine?

A
  • YES
138
Q

Fluid therapy for urolithiasis?

A
  • be VERY judicious
  • Patients with uroperitoneum to stabilize hypovolemia and correct electrolyte abnormalities
  • Avoid supplementation of potassium as hyperkalemia is still a risk
  • Watch for fluid overload
139
Q

Fluid overload signs in small ruminants

A
  • Pulmonary edema
140
Q

Surgical management of urolithiasis

A
  • Urethral catheterization and retrograde flushing
  • Amputation of urethral process
  • Perineal urethrostomy (PU)
  • Urethrotomy and stone removal
  • Tube cystotomy
  • Bladder marsupialization
141
Q

Catheterization and retrograde flushing difficulties

A
  • Very hard to catheterize male ruminants
142
Q

Perineal urethrostomy

A
  • Used in feedlot steers a bit

- Not meant to be long-term but more salvage

143
Q

Tube cystotomy

A
  • Often preferred

- Gives time for inflammation to go down

144
Q

Pain medications post-op

A
  • Meloxicam (if well-hydrated)

- gabapentin

145
Q

How do you close the urethra for a urethrotomy?

A
  • Let it heal by second intention
146
Q

Perineal urethrostomy surgery

A
  • Last ditch effort

- Going into the perineum and cutting the urethra as it comes down

147
Q

Cons of perineal urethrostomy vs tube cystostomy?

A
  • You don’t get to look at the bladder to know if it’s compromised or not
148
Q

What determines prevention and management for urolithiasis?

A
  • Depends on forage and stone analysis
149
Q

Silica stone management

A
  • Restricting silica intake is not feasible in ruminants grazing native grasses
  • Dietary management limited to salt supplementation to increase water consumption (diuresis)
150
Q

Prevention of phosphatic calculi

A
  • Dietary calcium/phosphorus ratio to a level of 2:1 or greater
  • Decrease the amount of grain or other high-phosphorus dietary components
  • Increase the quantity of long-stem forage in the ration to increase salivary flow and fecal phosphate excretion (salivary gland helps with phosphorus recycling)
  • Or, increase calcium in the diet with forages like alfalfa (BE CAREFUL)
151
Q

Why do you have to be careful with increasing calcium in the diet to prevent phosphatic calculi?

A
  • Could lead to a calcium stone
152
Q

Prevention of calcium carbonate calculi

A
  • feeding or supplementing with grass hay instead of feeding alfalfa
  • Salting grass hay to increase water consumption to help dilute urine
  • Acidifyng urine
153
Q

Ammonium chloride uspplementation - what’s hte idea behind it?

A
  • 0.5% to 1.5% of ration dry matter decrease urine pH to 6-6.5

In theory should increase the solubility of struvite and apatite crystals

154
Q

Cons of ammonium chloride supplementation

A
  • Long term complications can lead to chronic metabolic acidosis with decrease in bone density
  • Renal adaptation and will go back to normal
  • Not palatable and animals may stop eating the ration
155
Q

What is the MOST important aspect of prevention of urolithiasis?

A
  • Maximizing water intake!!!!
156
Q

Reoccurrence with urolithisis - how common?

A
  • VERY COMMON
157
Q

Definition of urachal disorders

A
  • Abnormalities of the umbilicus and umbilical remnants are frequently seen in neonatal calves - urachus included
158
Q

What is associated with urachal disorders?

A
  • Omphalitis
159
Q

Pathophysiology of urachal disorders

A
  • Bacterial infection of the urachus –> inflammatory response in the abdomen –> fibrinous adhesions form between the urachus and surrounding viscera –> abscess formation
  • Urachal fibrosis and adhesions may interfere with bladder emptying –> urine retention and secondary cystitis
160
Q

What is the most common bacteria associated with urachal disorders?***

A
  • Trueperella pyogenes or E. coli
161
Q

Clinical signs with urachal disorders

A
  • > 4 weeks old
  • Omphalitis
  • Fever, lethargy, poor body condition, rough hair coat, and poor growth
  • Dysuria, pollakiuria, stranguria, and colic, hematuria, or pyuria
  • May palpate an enlarged and painful umbilical remnant
  • may see urine dribble from umbilicus
  • Signs of UTI
162
Q

Differentials for urachal disorders

A
  • Urolithiasis, urethritis, or neurologic disease
163
Q

How acute are urachal disorders usually?

A
  • Often the owners will see them suddenly, but they aren’t considered that acute
164
Q

Diagnosis of urachal disorders

A
  • Transabdominal ultrasound of the umbilicus and ventral abdomen***
  • Clin path variable
165
Q

Clinical pathology findings with a urachal disorder

A
  • Variable
  • Inflammatory leukogram
  • Hyperfibrinogenemia
  • Hyperglobulinemia
166
Q

Treatment of urachal disorders

A
  • SURGERY
  • Ventral midline celiotomy, paramedian celiotomy, laparoscopy under general anesthesia is recommended
  • Perioperative and postoperative antibiotics are essential
167
Q

Prognosis for urachal disorders

A
  • Guarded to poor if adhesions are extensive and severe peritonitis
168
Q

What causes enzootic hematuria?

A
  • Bracken fern (Pteridium aquilinum)
169
Q

How acute or chronic is Bracken fern toxicity (i.e. enzootic hematuria)?

A
  • Poisoning requires prolonged exposure

- Characterized by intermittent hematuria and anemia

170
Q

Carcinogenic properties of Bracken Fern

A
  • Continued ingestion and infection with bovine papillomavirus type 2
171
Q

What is acute Bracken Fern poisoning?

A
  • An acute coagulopathy or fulminant septicemic crisis associated with severe bone marrow suppression
172
Q

Distribution of enzootic hematuria

A
  • Wide distribution
  • PNW and upper Midwest
  • Grows in well-drained fertile soils
173
Q

Who gets enzootic hematuria?

A
  • Primarily seen in adult sheep and cattle

- Not goats

174
Q

Which parts of the Bracken fern are toxic to sheep and cattle?**

A
  • All parts!**
175
Q

What properties of Bracken Fern lead to the clinical signs?

A
  • irritant, mutagenic, immunosuppressive, or carcinogenic activities
176
Q

What is the active agent in Bracken Fern?**

A
  • Ptaquiloside (aquilide A)
177
Q

Can bracken fern compounds be excreted or secreted by affected cattle?

A
  • Yes, carcinogenic principles are present in the milk of cows grazing bracken fern
  • Can cause GI inflammatory disease
  • Gastric ulcers in people
178
Q

Relationship between enzootic hematuria and Bovine papillomavirus-2?

A
  • Compounds may cause recrudescence of latent BPV-2 through immunosuppression
  • Mutagenic compounds interact with BPV-2 in bladder –> neoplasia
179
Q

Clinical signs of enzootic hematuria?

A
  • Hematuria is the first clinical sign in most animals
  • Chronic blood loss –> tachycardia, tachypnea, exercise intolerance, pale mucous membranes, and decline in productivity
  • Bladder wall thickening, and bladder may be palpated rectally
  • Dysuria, pollakiuria
  • Obstruction of the bladder trigone by blood clots
180
Q

Are patients with enzootic hematuria ever icteric?

A
  • NO
181
Q

Key diagnostics for enzootic hematuria?

A
  • History of Bracken Fern ingestion
  • Clin Path changes
  • Necropsy findings
182
Q

Clin Path findings with enzootic hematuria?

A
  • Severe anemia +/- regeneration
  • May see decrease in segmented neutrophils and lymphocytes
  • Urinalysis shows hematuria, protienuria, and variably pyuria
183
Q

Necropsy findings with enzootic hematuria?

A
  • Bladder wall is thickened, mucosa hemorrhagic and ulcerated
  • Bladder tumors and mixed origin neoplasms
184
Q

Treatment of enzootic hematuria?

A
  • Limited to reduction or elimination of bracken fern in the diet
185
Q

Prognosis of enzootic hematuria

A
  • May stop if ingestion is discontinued before neoplasia occurs
  • Once you get neoplasia, it’s a pretty poor prognosis
186
Q

What are different localizations for UTI?

A
  • Cystitis, uteritis, and pyelonephritis
187
Q

Which bacteria are most commonly implicated with UTI?

A
  • Ascending infections from C. renale or E. coli
188
Q

Epidemiology of UTI

  • Sex predisposition?
A
  • Uncommon

- Females more than males due to a shorter urethra

189
Q

C. renale infection pathophysiology

A
  • Pathogen adheres to urinary tract epithelium which is enhanced by alkaline conditions –> organism produces ammonium to maintain a high pH
190
Q

E. coli infection pathophysiology

A
  • Serotypes involved in UTI are unknown at this time

- Infection likely arises from fecal contamination or a loss of natural defenses in the urogenital tract

191
Q

Clinical signs of UTI

A
  • Dysuria or pollakiuria
  • +/- hematuria and pyuria - may not be visible
  • May be able to feel a thickened and painful bladder on rectal palpation
192
Q

Clinical signs of acute cases of pyelonephritis

A
  • Sudden reduction of feed intake or milk production
  • Fever, tachycardia, tachypnea, decreased skin turgor, enophthalmos, ruminal stasis, scleral injection, and occasional episodes of mild colic
  • Left kidney felt on rectal palpation - may be enlarged and painful
  • Right kidney evaluation with ultrasound
193
Q

Clinical signs with chronic pyelonephritis

A
  • Signs more vague

- Weight loss, muscle wasting, poor growth, anorexia, diarrhea, and reduced milk production

194
Q

Differentials for mild colic

A
  • UTI, GI, other intrabdominal disorders

- Bloodwork to rule it out

195
Q

Dfdx for dysuria

A
  • UTI, vaginitis, prevaginal abscess, pelvic entrapment of the bladder, vulvar trauma, postparturient swelling of the vagina or vulva
  • Urolithiasis in males
  • Neurologic deficits: neuro exam to rule out
196
Q

Hematuria dfdx

A
  • Parturition
  • UTI
  • Papillomas in the urinary tract
  • Postparturient hemoglobinuria
  • Enzootic hematuria
197
Q

Diagnosis of UTI

A
  • Clin Path and UA
198
Q

Clin Path findings with UTI

A
  • Neutrophilic leukocytosis with significant hyperfibrinogenemia in pyelonephritis
  • With chronicity , hyperglobulinemia
  • Anemia due to decreased erythropoietin in the affected renal tissue and from blood loss through urination
  • Azotemia (need to differentiate pre-renal, renal, and post-renal)
199
Q

What is needed for definitive diagnosis of UTI?

A
  • Urinalysis
200
Q

Treatment with UTI

A
  • Aggressive and long-term antibiotics
  • Beta lactams (Procaine Penicillin G or Ampicillin trihydrate at very high doses)
  • Ceftiofur is not labeled for this
  • Diuresis with oral or parenteral fluid therapy to dilute urine
201
Q

Prognosis with UTI

A
  • Better the earlier patient is treated
  • Cystitis alone yields higher success rates
  • Recrudescence can occur
202
Q

Poor prognostic indicators with UTI

A
  • BUN >110mg/dL and/or creatinine above 1.5 mg/dL
203
Q

What is renal amyloidosis?

A
  • Deposition of insoluble fibrillar protein in various organs, including the kidney as well as spleen and liver
  • Protein losing nephropathy
204
Q

Pathophysiology of renal amyloidosis

A
  • Reactive type (AA protein) - frequently associated with chronic inflammatory disease
  • AA resistant to proteolysis
  • Accumulation in glomerulus alters filtration leading to sustained albuminuria and loss of plasma oncotic pressure
205
Q

What is the precursor to AA?

A
  • Serum amyloid A (SAA) protein
206
Q

Where is AA made?

A
  • In the liver
207
Q

What type of protein is AA?

A
  • Acute phase protein
208
Q

How can amyloidosis cause diarrhea?

A
  • Deposition of amyloid in the IGT
209
Q

Clinical signs of renal amyloidosis

A
  • Weight loss
  • Diarrhea
  • Ventral edema
  • Hypoproteinemia and proteinuria***
210
Q

Dfdx for hypoalbuminemia, edema, or chronic diarrhea

A
  • Johne’s
  • Right heart failure
  • Chronic parasitism
  • Liver failure
  • Chronic Salmonella
  • Post caval syndrome
  • Copper deficiency
  • Also Haemonchus in goats
211
Q

Clin Path with Renal Amyloidosis

A
  • Marked proteinuria and hypoalbuminemia
  • Hyperfibrinogenemia and/or hyperglobulinemia
  • Azotemia if it’s in the kidneys
  • Persistent heavy proteinuria without RBCs, WBCs, or bacteria in the urine sediment
  • +/- hyperphosphatemia
  • Be careful interpreting urine dipsticks when urine is alkaline (confirmation via more specific tests)
212
Q

Necropsy results for renal amyloidosis

A
  • Stain kidneys with Congo Red
213
Q

Example history of a cow with possible PLN or PLE

A
  • Weight loss, diarrhea, bottle jaw
  • BAR
  • Non-foul smelling diarrhea
  • T: 101.5F, P 60/min, R 20/min
  • Rectal shows loose stool and thickened bowel loops
214
Q

Treatment and prognosis of renal amyloidosis

A
  • Prognosis is poor
  • AA persistent in tissues and remains if inflammation is treated
  • No specific treatment
215
Q

How common is glomerulonephritis?

A
  • rare
216
Q

Underlying cause of glomerulonephritis

A
  • Immune system targeting of glomerular tissues leads to glomerular injury
217
Q

Pathophysiology of glomerulonephritis

A
  • Antibodies may be directed against host or addition, circulating immune complexes may deposit in the glomerulus –> activation of complement and chemotaxis of leukocytes –> damage of the glomerulus and increased glomerular permeability
218
Q

CLinical signs with glomerulonephritis

A
  • Hx of weight loss, poor productivity, and chronic diarrhea
  • Rectal may reveal an enlarged but non-painful left kidney
  • Been associated with persistently infected BVDV, cattle with fascioliasis (flukes), and associated with preg tox in ewes
219
Q

Dfdx for glomerulonephritis

A
  • SImilar to amyloidosis
220
Q

Clin Path findings with glomerulonephritis

A
  • Heavy proteinuria, mild anemia, and hypoalbuminemia
  • Granular casts, RBSs, and leukocytes may be found in urine sediment
  • Azotemia, proteinuria, and ketonuria in a ewe with pregnancy toxemia
221
Q

Treatment and prognosis of glomerulonephritis

A
  • Most GN advanced once diagnosed

- Prognosis very poor

222
Q

What is tubular necrosis?

A
  • Acute renal failure
223
Q

Causes of tubular necrosis

A
  • Can be primary (2° to endometritis or any disease in the animal) or secondary (2° to a toxin) in origin
  • Toxin exposure and vulnerable to ischemia and reperfusion injury
  • Sudden decrease in GFR, nitrogenous waste accumulation, and loss of the ability to manage electrolytes, protein, acid-base, and water balance
224
Q

Pathophysiology of tubular necrosis

A
  • Ischemic and toxic damage to tubular cells due to primary issue
  • Prolonged ischemia –> destroys basement membrane –> preventing tubular epithelial cell regeneration
  • Pigment nephrosis –> endogenous toxicity due to hemoglobin or myoglobin to the kidneys as a result of hemolytic disease or myopathies –> result in renal vasoconstriction and tubular obstruction from protein coagulation
  • Any injury is compounded by dehydration
225
Q

Clinical signs of tubular necrosis

A
  • No specific clinical signs
  • Anuria/ oliguria, or polyuria
  • Poor appetite, diarrhea, or epistaxis
  • Saliva may have an ammonia smell
  • Muscular weakness and recumbency from acid-base imbalances
  • Renal encephalopathy
226
Q

Renal encephalopathy

A
  • Intracranial disease
  • Altered behavior, weakness, motor dysfunction, convulsions
  • Rare
227
Q

Dfdx for renal encephalopathy

A
  • Generic systemic illness similar to those of renal origin

- Pneumonia, pleuritis, mastitis, metritis, peritonitis, endocarditis, and metabolic derangements

228
Q

Diagnosis of tubular necrosis

A
  • Inflammatory diseases common
  • Electrolytes
  • UA
229
Q

Inflammatory changes seen with tubular necrosis sometimes

A
  • Leukogram may reflect primary causes

- Hyperfibrinogenemia

230
Q

Electrolytes changes seen with tubular necrosis and underlying cause

A
  • Hypokalemia (anorexia)
  • Hypocalcemia (anorexia)
  • Hyperphosphatemia (
231
Q

Purpose of urinalysis with tubular necrosis

A
  • Differentiate prerenal, post-renal, and renal causes

- Proteinuria, hematuria, and granular casts

232
Q

Phosphate with tubular necrosis

A
  • Primarily excreted through glomerular filtration in the kidneys in most mammals, so decreased GFR leads to increased serum phosphate
  • However, cattle and horses with decreased GFR may not always have hyperphosphatemia due to other sources of phosphate elimination such as saliva and GIT
233
Q

Treatment with tubular necrosis

A
  • Remove and bind toxin or source (promote diuresis through IV fluids and diuretics)
  • Activated charcoal
  • Prophylactic diuresis
  • Restoration of adequate renal perfusion and urine production (isotonic fluids with Ca and K if needed; patient is producing sufficient urine; IVF ideal)
  • Supportive care (Broad spectrum antibiotics; parenteral nutrition or rumen transfaunation; use NSAIDs carefully)
234
Q

What can be given to anuric or oliguric animals with tubular necrosis

A
  • Furosemide
235
Q

Prognosis of tubular necrosis

A
  • If over 75% nephrons compromised, that’s a poor prognosis
  • Best prognosis with intensive care
  • Conditions that occlude tubular blood flow warrant a poor prognosis (DIC, renal vein thrombosis)
236
Q

Maintenance hosts clinical signs with leptospirosis

A
  • Causes little disease
237
Q

How do incidental hosts get leptospirosis?

A
  • Incidental hosts via direct contact from urine from infected maintenance host or through contaminated environment
  • Contact with feed, environment, or water contaminated with urine from an infected maintenance host
  • Contact with infected fetus or uterine discharge
238
Q

Appearance of lepto

A
  • Motile, gram-negative, obligate aerobic, tightly coiled
239
Q

Preferred environments of leptospirosis

A
  • Prefer moist, warm environments pH 7.2-8
240
Q

Leptospirosis serovars where cattle are incidental hosts

A
  • Leptospira interrogans canicola
  • L. interrogans pomona
  • L. interrogans icterohaemorrhagiae
  • L. interrogans bratislava
  • L. kirschneri grippotyphosa
241
Q

Which leptospirosis serovars are cattle more of a maintenance host?

A
  • L. interrogans hardjo type hardjoprajitno

- L. borgpetersenii hardjo type hardjobovis

242
Q

Seasonal incidence of lepto

A
  • Higher in summer or fall in temperate regions
243
Q

Which serovars of leptospirosis are most often implicated in renal infection of cattle?

A
  • Hardjo, pomona, and gryppotyphos
244
Q

Is leptospirosis zoonotic?

A
  • YES
245
Q

Pathophys of lepto

A
  • Mucosal surfaces and macerated skin –> organism enters blood stream –> Leptospiremia
  • Bacteremia lasts 4-7 days during with time fever and other systemic signs are often present
  • Humoral antibodies detectable at this time –> convalescent phase
246
Q

When are humoral antibodies detectable with leptospirosis?

A
  • During bacteremia that lasts 4-7 days

- This is when they have a fever

247
Q

Where does lepto localize during convalescent phase?

A
  • Mammary gland, kidney, or genital tract
248
Q

Virulence factors of Leptospirosis***

A
  • LPS**
  • Adhesion to cells and extracellular matrix
  • Bacterial motility - contributes to invasion and dissemination of bacteria
  • Hemolysins
  • Iron sequestration
249
Q

Clinical signs with non-host adapted serovars

A
  • Severe systemic disease, hemolytic anemia, hepatitis, interstitial tubular nephritis, and tubular nephrosis in calves
  • Agalactia and mastitis in lactating cows
  • Abortion
  • Renal lesions from direct damage to vascular endothelium (hypoxia, hemolysis, tubular epithelial damage from hemoglobin, and interstitial nephritis)
  • Fever, anorexia, lethargy, decreased milk production, petechiation, hemolytic anemia, and hemoglobinuria
  • Oliguria may be seen with interstitial nephritis or hemoglobinuric nephrosis
250
Q

Do you get hemoglobinuria with leptospirosis?

A
  • yes
251
Q

Diagnosis of lepto with serology

A
  • Serology
  • Microscopic agglutination test (MAT) showing a fourfold increase in MAT titer between acute and convalescent serum samples
  • Conversion from a negative titer to a titer of 100x or greater
252
Q

Serologic response in vaccinated animals

A
  • May be diminished
253
Q

When is serology unsuitable for dx of lepto?

A
  • Screening individual animals for carrier status

- Many animals that are chronically infected and shedding ma have negative serologic status

254
Q

Other ways to diagnose leptospirosis

A
  • Leptospira shedding in urine and semen can be detected by other means (Darkfield microscopy, Fluorescent antibody, PCR)
  • Urine culture often unrewarding
  • Second-voiding urine samples collection after administration of IV furosemide - discard first voided sample
255
Q

Treatment of acute leptospirosis caused by non-host-adapted serovars

A
  • Antibiotics (Ampicillin, amoxicillin, procaine penicillin G, tetracycline, tylosin, and tilmicosin)
  • IV and oral fluids for diuresis
  • Blood transfusion with severe hemolysis
256
Q

What determines prognosis for acute leptospirosis caused by non-host-adapted serovars?

A
  • Depends on virulence of the serovar, host immunity, and extent of renal lesions
  • Poor if >75% of nephrons are affected
257
Q

Treatment for renal colonization and shedding of lepto in cattle?

A
  • Long acting oxytetracycline
258
Q

Prevention of lepto

A
  • Draining or fencing off standing water
  • Maintain dry, clean environment
  • Limit rodent and wildlife contact with cattle
  • Cull renal carriers to limit transmission
  • Vaccine works well!
259
Q

Lepto vaccine info

A
  • Works well
  • Pentavalent (L. canicola, grippotyphosa, hardjo, icterohaemorrhagiae, and Pomona)
  • Whole-cell, inactivated vaccines
  • DO NOT resolve current renal infection

Ag Animal Test 3 (7 decks)

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