Hematopoietic disorders - non-infectious causes of anemia Flashcards
Water intoxication pathogenesis
- Massive water intake –> hypotonicity of body fluid –> hemolysis of RBCs
Who gets water intoxication?
- Milk reared calves when they are first given access to unlimited water
- Sudden decrease in osmolality
Clinical signs of water intoxication
- Neurologic signs (swelling)
- Respiratory distress (fluid overload)
- Hemoglobinuria
- Death
Clinical pathology of water intoxication
- Hemolytic anemia
- Hemoglobinuria
- Hyposthenuria (dilute urine)
- marked hyponatremia (110 or lower)
Treatment for water intoxication
- Temporarily restricting water intake
- Supportive care
- Restore Na to 120-125 mmol/L without overcorrection (reintroduce electrolytes slowly)
Treatment for calves with Na <110mmol/L that are exhibiting neuro signs
- Hypertonic saline
- Mannitol
- Corticosteroids
Who gets post-parturient hemoglobinemia?
- Sporadic and low incidence
- High producing multiparous cows
- Signs develop in the first month after calving
Pathophys of post-parturient hemoglobinemia
- 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
Signs of post-parturient hemoglobinemia
- Depression, decreased feed consumption, decreased milk production
- Icterus
- Dark red to port wine colored hemoglobinuria
- Tachycardia
- Ketosis
Clin path for post-parturient Hemoglobinemia
- hemoglobinuria
- Heinz bodies
- Erythropoietic response after 4-5 days
- Low serum phosphorus
Treatment for post-parturient hemoglobinemia
- 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
What causes Heinz body anemias?
- Brassica plants (Rape, Kale, Turnips)
- Also onions (any member of the allium familY)
Toxin in Brassica plants
- S-methyl cysteine sulfoxide
- Converted to dimethyl disulfide in the rumen
Toxic principle in Brassicas
- S-methyl cysteine sulfoxide which is converted to dimethyl disulfide in the rumen
Who is more susceptible to Brassica toxicity?
Cattle
Other signs associated with Brassica plants?
- Goitergenic effects, atypical interstitial pneumonia, choke
Who is susceptible to onion toxicity?
- All ruminants
Toxic principle in onions?
- N-propyl disulfide and s-methyl cysteine sulfoxide
- Difficult to predict toxicity
Pathophysiology of Heinz body anemia
- 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
Clinical signs of heinz body anemia?
- Weakness, lethargy, anorexia, exercise intolerance
- Death losses
- Pale mucous membranes +/- icterus
- Elevated HR and RR, normal temp
- Decreased production
Clin Path and Dx of Heinz body anemia
- 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
Treatment for Heinz body anemia
- Remove source
- Supportive care (blood transfusion, IVF and diuresis if hemoglobinuria or azotemia)
- Pain
- Keep them quiet management - NSAIDs
Prognosis for Heinz body anemia
- Good if inciting factor controlled or eliminated and anemia is modest
- Poor if rapidly progressive and profound anemia without blood transfusion
Who tends to get copper toxicity?
- SHEEEEP
- Also camelids
Toxic dose for sheep relative to cattle
-MUCH lower in sheep than in cattle
What diets are most likely to result in Cu toxicity?
- Copper molybdenum ratios over 6:1
Sources of copper toxicity
- mixing errors, injections
Pathophysiology of copper toxicity
- 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
Signs of acute Copper toxicity if ingested
- 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
Injected acute copper toxicity clinical signs
- Anorexia, depression, dehydration
- Ascites, pleural transudate
- Hemoglobinuria
- Dyspnea
- Head pressing, ataxia, aimless wandering
When would you see hemoglobinuria from acute copper toxicity?
- Injection
Clinical signs of chronic copper toxicity
- can take weeks to occur
- Acute onset of depression, anorexia, thirst
- Hemoglobinuria, anemia, icterus
- Death in 24-48 hours
Which samples to take for copper toxicity?
- Liver and kidney samples always
- Liver is best place to look
Diagnosis of copper toxicity
- 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
Where to do a liver biopsy?
- Clip the entire animal
- Tuber coxae to the elbow and between 9th and 10th rib
- Lidocaine
- Ultrasound guide if you can
Treatment for copper toxicity
- Transfusion
- Oxygen support
- Maybe methylene blue for methemoglobinemia
- Chelators (amybe can’t use; D-penicillamine; anhydrous sodium sulfate; ammonium molybdate)
Prognosis of copper toxicity
- Poor
Prevention of copper toxicity
- 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!
