Hematopoietic disorders - non-infectious causes of anemia

Question 1

Water intoxication pathogenesis

Answer 1

• Massive water intake –> hypotonicity of body fluid –> hemolysis of RBCs

Question 2

Who gets water intoxication?

Answer 2

• Milk reared calves when they are first given access to unlimited water
• Sudden decrease in osmolality

Question 3

Clinical signs of water intoxication

Answer 3

• Neurologic signs (swelling)
• Respiratory distress (fluid overload)
• Hemoglobinuria
• Death

Question 4

Clinical pathology of water intoxication

Answer 4

• Hemolytic anemia
• Hemoglobinuria
• Hyposthenuria (dilute urine)
• marked hyponatremia (110 or lower)

Question 5

Treatment for water intoxication

Answer 5

• Temporarily restricting water intake
• Supportive care
• Restore Na to 120-125 mmol/L without overcorrection (reintroduce electrolytes slowly)

Question 6

Treatment for calves with Na <110mmol/L that are exhibiting neuro signs

Answer 6

• Hypertonic saline
• Mannitol
• Corticosteroids

Question 7

Who gets post-parturient hemoglobinemia?

Answer 7

• Sporadic and low incidence
• High producing multiparous cows
• Signs develop in the first month after calving

Question 8

Pathophys of post-parturient hemoglobinemia

Answer 8

• Similar to Brassica and onion with oxidative stress
• Main thing is hypophosphatemia (ATP doesn’t work)
• Major risk factor in developing RBC lysis
• Impairs Na/K pump yielding increased fragility –> decreased ATP production in RBC
• Intravascular hemolysis
• Copper and Selenium deficiency

Question 9

Signs of post-parturient hemoglobinemia

Answer 9

• Depression, decreased feed consumption, decreased milk production
• Icterus
• Dark red to port wine colored hemoglobinuria
• Tachycardia
• Ketosis

Question 10

Clin path for post-parturient Hemoglobinemia

Answer 10

• hemoglobinuria
• Heinz bodies
• Erythropoietic response after 4-5 days
• Low serum phosphorus

Question 11

Treatment for post-parturient hemoglobinemia

Answer 11

• Blood transfusion and supportive fluids
• Correct hypophosphatemia
• Must give oral phosphate salts instead of CMPK which is phosphite (must also have rumen function)
• Correct dietary imbalances
• Slow recovery

Question 12

What causes Heinz body anemias?

Answer 12

• Brassica plants (Rape, Kale, Turnips)

- Also onions (any member of the allium familY)

Question 13

Toxin in Brassica plants

Answer 13

• S-methyl cysteine sulfoxide

- Converted to dimethyl disulfide in the rumen

Question 14

Toxic principle in Brassicas

Answer 14

• S-methyl cysteine sulfoxide which is converted to dimethyl disulfide in the rumen

Question 15

Who is more susceptible to Brassica toxicity?

Answer 15

Cattle

Question 16

Other signs associated with Brassica plants?

Answer 16

• Goitergenic effects, atypical interstitial pneumonia, choke

Question 17

Who is susceptible to onion toxicity?

Answer 17

• All ruminants

Question 18

Toxic principle in onions?

Answer 18

• N-propyl disulfide and s-methyl cysteine sulfoxide

- Difficult to predict toxicity

Question 19

Pathophysiology of Heinz body anemia

Answer 19

• Heinz body formation by precipitation of oxidatively denatured Hgb
• RBC are less deformable –> removed from the circulation by RES in spleen –> phagocytized and broken down
• Hemoglobinuria is rare

Question 20

Clinical signs of heinz body anemia?

Answer 20

• Weakness, lethargy, anorexia, exercise intolerance
• Death losses
• Pale mucous membranes +/- icterus
• Elevated HR and RR, normal temp
• Decreased production

Question 21

Clin Path and Dx of Heinz body anemia

Answer 21

• Early stages can see high % of RBC with Heinz body inclusions
• RBC destruction in 3-4 days
• TP WNL
• Negative Coombs test
• +/- hemoglobinemia and hemoglobinuria (most often extravascular)
• +/- UA changes due to hemoglobinuria if it exists

Question 22

Treatment for Heinz body anemia

Answer 22

• Remove source
• Supportive care (blood transfusion, IVF and diuresis if hemoglobinuria or azotemia)
• Pain
• Keep them quiet management - NSAIDs

Question 23

Prognosis for Heinz body anemia

Answer 23

• Good if inciting factor controlled or eliminated and anemia is modest
• Poor if rapidly progressive and profound anemia without blood transfusion

Question 24

Who tends to get copper toxicity?

Answer 24

• SHEEEEP

- Also camelids

Question 25

Toxic dose for sheep relative to cattle

Answer 25

-MUCH lower in sheep than in cattle

Question 26

What diets are most likely to result in Cu toxicity?

Answer 26

- Copper molybdenum ratios over 6:1

Question 27

Sources of copper toxicity

Answer 27

- mixing errors, injections

Question 28

Pathophysiology of copper toxicity

Answer 28

- Ionized copper internalized by hepatocytes - Hepatocytes become saturated and die and release large amounts of cuprous Cu into the blood - Free inorganic Cu is an oxidant --> cellular damage due to oxidative stress - Production of Heinz bodies and methemoglobinemia - RBC lyse intravascularly or are sequestered by spleen

Question 29

Signs of acute Copper toxicity if ingested

Answer 29

- Abdominal pain - Severe diarrhea - Vomiting (quidding or regurgitation; can run rumen chloride which would be high) - Green feces - Severe shock, dehydration, death in 24 hours

Question 30

Injected acute copper toxicity clinical signs

Answer 30

- Anorexia, depression, dehydration - Ascites, pleural transudate - Hemoglobinuria - Dyspnea - Head pressing, ataxia, aimless wandering

Question 31

When would you see hemoglobinuria from acute copper toxicity?

Answer 31

- Injection

Question 32

Clinical signs of chronic copper toxicity

Answer 32

- can take weeks to occur - Acute onset of depression, anorexia, thirst - Hemoglobinuria, anemia, icterus - Death in 24-48 hours

Question 33

Which samples to take for copper toxicity?

Answer 33

- Liver and kidney samples always | - Liver is best place to look

Question 34

Diagnosis of copper toxicity

Answer 34

- measure plasma or hepatic copper levels - Heinz body formation - Intravascular hemolysis - methemoglobinemia - Decreased PCV - Azotemia - Increased plasma ceruloplasmin (enzyme that takes copper to the liver to store it) - Increased liver enzymes - Urinalysis is dark brown to black in color, high protein, blood, and hemoglobin

Question 35

Where to do a liver biopsy?

Answer 35

- Clip the entire animal - Tuber coxae to the elbow and between 9th and 10th rib - Lidocaine - Ultrasound guide if you can

Question 36

Treatment for copper toxicity

Answer 36

- Transfusion - Oxygen support - Maybe methylene blue for methemoglobinemia - Chelators (amybe can't use; D-penicillamine; anhydrous sodium sulfate; ammonium molybdate)

Question 37

Prognosis of copper toxicity

Answer 37

- Poor

Question 38

Prevention of copper toxicity

Answer 38

- Restrict copper supplementation especially in sheep - Dress contaminated pastures with molybdenum phosphate to decrease Cu:Mo ratio down below 6:1 - Educate new sheep owners!