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Bovine hematuria and hemoglobinuria Flashcards

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1
Q

How do you differentiate hematuria and hemoglobinuria/myoglobinuria?

A

spin down the urine

hematuria when centrifuged leaves clear supernatant

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2
Q

What will you find with myoglobinuria that does not occur with hemoglobinuria?

A

increased CK, AST

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3
Q

Where might blood in the urine arise from?

A
  1. urethra
  2. bladder
  3. kidney
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4
Q

What are differentials of hematuria?

A
  1. urethra: caluli, trauma, urethritis
  2. bladder: bracken fern, cystitis, papilloma, neoplasia, calculi, polyps
  3. kidney: pyelonephritis, infarction, trauma, malignant catarrhal fever, endotoxic shock
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5
Q

What are the major calculi in ruminants?

A
  1. struvite–seen in feed lot–phosphatic on grain based diets
  2. silica–rangeland
  3. calcium carbonate–most comon on lush clover pasture
  4. calcium oxalate: idiopathic
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6
Q

Who is most likely to get urinary calculi?

A

males

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7
Q

When do urinary calculi occur?

A

when high mineral concentratrions in urine overwhelm crystallization inhibitors

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8
Q

What forms a matrix for calculus formation?

A

mucoproteins

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9
Q

How are calculi diagnosed?

A
  1. hematuria
  2. colic and straining to urinate
  3. enlarged ureter or urethra (rectal exam, urethra pulsing without urination)
  4. post renal azotemia
  5. endoscopy?
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10
Q

How are calculi diagnosed?

A
  1. surgical
  2. salvage if not uremic
  3. medical (tranquilizer, NSAID, IV fluids)
  4. Walpole’s solution (acetic acid)
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11
Q

How are struvite crystals prevented?

A
  1. increase long stem forage in diet (hard to convince in feedlot)
  2. 3-5% salt in feedlot diets
  3. ammonium chloride (alkalinize the urine) but reduces palatability
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12
Q

How do you prevent silica calculi?

A

sodium or ammonium chloride

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13
Q

What is urethral trauma commonly associated with?

A

uroliths

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14
Q

What is bacterial urethritis sometime sassociated with?

A

pseudomonas

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15
Q

What does bacterial urethritis suually manifest as?

A

hemospermia. treated by rest from reprod acitvity and antibiotics that concentrate in urine like penicillin

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16
Q

What are the clinical signs of bracken fern poisoning?

A

bladder wall thickneing, tumors
blood and clots in urine
anemia may be present
usually sporadic

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17
Q

what is the cause of enzootic hematuria?

A

pteridium aquilinum (braken fern)

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18
Q

What are the toxic agents of pteridium aquilinum toxicity?

A

ptaquiloside, quercetin, A ecdysone

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19
Q

What is the treatmetn for braken fern?

A

supportive care, removal of braken fern from diet

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20
Q

Who most commonly gets cystitis?

A

females

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21
Q

What are the common etiological agents of cystitis?

A

C. renale, or e. colie

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22
Q

is grosshematuria common with cystitis?

A

no

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23
Q

What are common clinical signs of cystitsi?

A
  1. dysuria,
  2. pollalkuria,
  3. decreased urinary flow rate
  4. thickened bladder wall
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24
Q

What is a good treatment for cystitis?

A

penicillin, actually gets such high levels in urine that can get e. coli

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25
Q

Who does pyelonephritis usually affect?

A

females

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26
Q

Are animals systemically ill with cystitis? what about pyelonephritis?

A
  1. no

2. yes

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27
Q

What are the clinical signs of pyelonephritis?

A

systemic clinical signs

smooth enlarged painful kidney occasionally palpable on rectal

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28
Q

What is the treatment for pyelonephritis?

A

antibiotics (penicillin) and supporitve care

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29
Q

What is the prognosis for pyelonephritis?

A

guarded

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30
Q

What are the most common causes of renal infarction?

A

dehydration and/or NSAID treatment

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31
Q

What occurs with renal infarction?

A

acute tubular necrosis, primarily at loop of henle

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32
Q

What are the clinical signs of renal infarction?

A

polyuria, anuria, dysuria

renal azotemia on blood work

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33
Q

What is the treatment for renal infarction?

A

resotration of adequate renal perfusion–fluids

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34
Q

What is hemoglobinuria caused by?

A

severe haemolysis

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35
Q

What is the issue of hemoglobin and the kidney?

A

nephrotoxic and causes renal damage

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36
Q

What are the bacterial causes of hemoglobinuria?

A
  1. clostridia

2. leptospira

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37
Q

What are the parasitic causes of hemoglobinuria

A
  1. babesia
  2. eperythrozoon
  3. theileria
  4. trypanosoma
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38
Q

What are the immune causes of hemoglobinuria?

A
  1. neonatal isoerythrolysis

2. autoimmune

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39
Q

What are the causes of heinz body (cause of hemoglobinuria)

A
  1. drug
  2. plants
  3. molybdenum deficiency
  4. selenium deficiency
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40
Q

What are 3 micellaneous causes of hemoglobinuria?

A
  1. water
  2. copper
  3. post partum
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41
Q

What causes bacillary hemoglobinuria?

A

clostridium hemolyticum (C. novyi type D)

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42
Q

Where do spores of clostridium haemolyticum go?

A

to the kupffer cells of liver

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43
Q

What is clinical disease of bacillary hemoglobinuria exacerbated by?

A

liver fluke infestation

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44
Q

What are the clinical signs of bacillary hemoglobinuria?

A
  1. sudden death
  2. fever
  3. anorexia
  4. blood in feces
  5. red urine
  6. blood is usually thin, water and slow to coagulate
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45
Q

How is diagnosis made for bacillary hemoglobinuria?

A
  1. necropsy–gram stain of liver impression

2. FAT on liver

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46
Q

How is bacillary hemoglobinuria treated?

A

rarely attempte because acute/fatal. could try penicillin

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47
Q

What should you do with bacillary hemoglobinuria carcus?

A

deep burial/burned

48
Q

What provide protection against bacillary hemoglobinuria?

A

most 8 ways vaccines

49
Q

Is leptospirosis a zoonosis?

A

yes

50
Q

Is leptospirosis common in western canada?

A

no

51
Q

What are the three leptospira species that cause renal disease?

A
  1. L hardjo
  2. L pomona
  3. L gripptophyosa
52
Q

What are the clinical signs of leptospirosis?

A
  1. repro failure
  2. agalactia
  3. mastitis
  4. occasionally hemoglobinuria
53
Q

HOw is diagnosis of lepto mde?

A

PCR

others possible

54
Q

How is lepto traeted?

A

penicillin, oxytetracylcine but careful using oxy in animal with impaired renal function

55
Q

What is prevention of lepto?

A
  1. avoid stnading water
  2. screen animals before enter herd
  3. control rodents
  4. vaccine is good
56
Q

Who is more susceptible to copper intoxiciation?

A

small ruminants

57
Q

What is the pathogenesis of copper intoxication?

A

liver copper accumulates, once a certain level there is a massive release of copper.

58
Q

What is the most common history of copper intoxication?

A

small ruminant fed a cattle mineral

59
Q

What is treatment for copper intoxication?

A 
supportive care (blood transfusion)
chelation therapy with D-penicillamine or ammonium tetrathimoybdate if available
60
Q

What can exacerbate copper intoxication?

A

molybdenum

61
Q

When does heinz body anemia occur?

A

exposure to oxidizing agents such as phenothiazines, methylene blue, onions, brassicas or molybdenum or selenium deficiency

62
Q

What are clinical signs of heinz body anemia?

A
  1. weakness
  2. depression
  3. anemia
63
Q

How is heinz body anemia diagnosed?

A

ID heinz bodies in blood smears stained with methylene blue, wrights or crystal violet

64
Q

Why should you not ix blood smears with methanol?

A

will inhibit stain uptake

65
Q

What are hemoparasites in cattle?

A

babesia
eperythrozoon (e. weyoni, e. ovis)
thelia
trypanosomes

66
Q

What is neonatal isoerythrolysis associated with in ruminants?

A

vaccines of blood origin (babesia, anaplasma) (there ar eno blood based vaccines currently available in canada)

67
Q

What is post-parturient hemoglobinuria?

A

a sporadic syndrome characterized by intravascular hemolysis, hemoglobinuria, anemia which occurs in first month post partum
related to hypophoshpatemia
treatment consists of supportive care and phosphate supplementation
(phosphite does nothing to phosphate concentrations)

68
Q

What is water intoxication?

A

large amounts of water will cause RBCs to become osmotically fragile resulting in haemolysis
exacerbated by cold water
clinical signs: associated with large scale haemolysis–neuro signs, hemolysis

69
Q

How can you classify hemorrhage?

A
  1. acute: internal/external

2. chronic: bleeding GI lesion, renal

70
Q

What can cause acute externa hemorrhage?

A
  1. surgery: e.g. dehorning and castration

2. trauma: external laceration

71
Q

What is the treatment for acute external hemorrhagg?

A
  1. surgery to close vessel
  2. wund management
  3. supportive care (blood transfusion, fluid and electrolyte therapy)
72
Q

What are the clinical signs of anthrax?

A
  1. sudden death

2. clinical signs may include hematuria and/or bloody diarrhea

73
Q

What should you do with a suspected anthrax case?

A
  1. blood smear
  2. do not open carcass
  3. saskatchewan anthrax response plan
  4. call provincial chief vet officer
74
Q

What can cause internal hemorrhage?

A
  1. splenic rupture (trauma)
  2. middle uterine artery rupture (spontaneous, sporadic, usually following uterine prolapse)
  3. blood vessel erosion
75
Q

What can cause blood vessel erosions

A
  1. abscess, neoplasia, mycotic

2. caval syndrome following rumen acidosis

76
Q

How is internal hemorrhage diagnosed?

A
  1. anemia by hypoproteinemia
  2. ultrasound
  3. abdominocentesis–not very rewarding in cattle
77
Q

What is the treatment for internal hemorrhage?

A
  1. may have to attempt surgery
  2. anesthetic risk
  3. treat shock
  4. blood transfusion
78
Q

What are causes of bleeding GI lesions?

A
  1. abomasal lymphosarcoma
  2. ulceration
  3. parasitism (type II dz, post hemonchus treatment–not most common treatment of hemonchus)
79
Q

How are bleeding GI lesions diagnosed?

A
  1. melena may not always be present
  2. fecal occult blood
  3. perform fecal occult blood test BEFORE rectal exam
80
Q

What are features of abomasal lymphosarcoma?

A
  1. may cause bleeding into abomasum
  2. melena
  3. intenral iliac LN may be enlarged on rectal
  4. large tumor may be palpable on rectal
  5. abdominal exploratory surgery may help
  6. seropositive does not equal tumour
81
Q

Type 2 abomasal ulcers associated with what?

A

significant blood loss

82
Q

What are clinical signs of abomasal ucleration

A 
sudden death
bruxism
abdominal pain
melena
anaemia
83
Q

What is treatment for abomasal ulceration?

A
  1. supportive care

2. surgery? antacids?

84
Q

What is type II disease?

A

hypobiotic larvae excyst and may cause severe disease with hemorrhage into abomasum and melena

85
Q

What are renal causes of bleeding?

A
  1. bracken fern

2. rare causes include: neoplasia, renal vascular anomalies

86
Q

What are signs of renal cause of bleeding

A

blood observed in urine

87
Q

What are inherited hemostatic dysfunction disorders?

A
  1. factor VIII (hemphilia, sex linnked, recessive)–holstein, hereford
  2. factor XI (autosomal, recessive)
    simmental hereditary thrombopathy: autosomal recessive primary platelet disorder
88
Q

Why are inherited hemostatic dysfunctions not common in dairy cattle?

A

lots of genetic testing esp of bulls

89
Q

What measures intrinsic pathway?

A

PTT

90
Q

What are causes of aquired hemostatic dysfunction

A
  1. vasculitis
  2. thromobocytopeina
  3. DIC
  4. warfarin toxicosis
  5. moudly sweet clover
91
Q

What are causes of vasculitis?

A

secondary to some septicemias–malignant catarrhal fever, blue tongue

92
Q

What are clinical signs of vasculitis

A

petechiae, ecchymoses, hmoerrhages may occur anywehere

other signs: edema, skin infarction, lameness, colic, dyspnea, ataxia

93
Q

How is vasculitis definitively diagnosed

A

biopsy

94
Q

How is vasculitis treated?

A

treat primary cause

supportive care

95
Q

What are the mechanisms of thrombocytopenia?

A
  1. decreased production
  2. sequestration
  3. consumption/destruction
    (IMPORTANT TO KNOW)
96
Q

What are clinical signs of thrombocytopenia

A 
petichiae and ecchymoses
prolonged buccal mucosal bleeding time
spontaneous GI or renal bleeding
tendancy to bleed with minor trauma, venipuncture
ischemic organ damage
97
Q

What are the two most common causes of thrombocytopenia?

A
  1. bovine viral diarrhea

2. bovine leucosis virus

98
Q

What does DIC usually follow?

A

usually following sepsis

99
Q

What does DIC require?

A

a thrombotic stimulus:
increased pro-coagulant activity
abnormal surface
–>increased and unregulated procoagulant acitvity

100
Q

What occurs due to DIC?

A 
Dysregulated thrombotic stimulus
Formation of multiple thrombi
Ischaemic damage and consption of prothrombotic factors
Production of FDPs
ischaemic organ damage
101
Q

HOw do you diagnose DIC?

A

numerous hemostatic tests will be abnormal

102
Q

What is treatment of DIC?

A

rarely practical–euthanasia

maybe flunixin meglumine, treat sock, plasma/heparin therapy? avoid glucocorticoids?

103
Q

How does warfarin toxicosis occur?

A
  1. usually ingested rodenticide
  2. competitive inhibitor of vit K
  3. vit K dependent clotting factors II, VII, IX, X affected
  4. half life VII is shortest so PT increased
104
Q

HOw does warfarin toxicosis manifest?

A

increased or spontaneous bleeding

105
Q

What is the treatment of warfarin toxicosis?

A

vit K supplementation

106
Q

Where is mouldy sweet clover usualyl found?

A

hay or silage

107
Q

What is the toxic agent of mouldy sweet clover?

A

dicoumarol

108
Q

What does dicoumarol do?

A

interfere with synthesis of vit K synthesis

109
Q

What are signs of mouldy sweet clover poisoning?

A

increased bleeding, may develop hematomas

110
Q

What are the indications for blood transfuions in ruminants?

A

acute PCV

111
Q

Is cross-matching for blood transfusion practical?

A

not in field

first transufions usually otlerated well

112
Q

HOw do you collect blood from donor for blood transfusion?

A
  1. ACD (acid citrate dextrose) or sodium citrate
113
Q

How much blood should you replace with blood trasnfusion?

A

20-40% of blood loss

114
Q

HOw do you administer blood transfusion?

A 
through in line filter
evaluate vitals before transfusion
give 0.1mL/kg over 5-10min
re-evaluate vitals
give 20ml/kg/hr
115
Q

What are transfusion reactions?

A
  1. changes in respiration, behavior, muscle fasciculations
116
Q

What is the treatment for transfusion reactions?

A
  1. shut off transfusion
  2. epinephrine
  3. corticosteroids

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