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Ag Animal II > Hematopoietic disorders - non-infectious causes of anemia > Flashcards

Hematopoietic disorders - non-infectious causes of anemia Flashcards

1
Q

Water intoxication pathogenesis

A
  • Massive water intake –> hypotonicity of body fluid –> hemolysis of RBCs
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2
Q

Who gets water intoxication?

A
  • Milk reared calves when they are first given access to unlimited water
  • Sudden decrease in osmolality
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3
Q

Clinical signs of water intoxication

A
  • Neurologic signs (swelling)
  • Respiratory distress (fluid overload)
  • Hemoglobinuria
  • Death
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4
Q

Clinical pathology of water intoxication

A
  • Hemolytic anemia
  • Hemoglobinuria
  • Hyposthenuria (dilute urine)
  • marked hyponatremia (110 or lower)
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5
Q

Treatment for water intoxication

A
  • Temporarily restricting water intake
  • Supportive care
  • Restore Na to 120-125 mmol/L without overcorrection (reintroduce electrolytes slowly)
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6
Q

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

A
  • Hypertonic saline
  • Mannitol
  • Corticosteroids
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7
Q

Who gets post-parturient hemoglobinemia?

A
  • Sporadic and low incidence
  • High producing multiparous cows
  • Signs develop in the first month after calving
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8
Q

Pathophys of post-parturient hemoglobinemia

A
  • 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
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9
Q

Signs of post-parturient hemoglobinemia

A
  • Depression, decreased feed consumption, decreased milk production
  • Icterus
  • Dark red to port wine colored hemoglobinuria
  • Tachycardia
  • Ketosis
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10
Q

Clin path for post-parturient Hemoglobinemia

A
  • hemoglobinuria
  • Heinz bodies
  • Erythropoietic response after 4-5 days
  • Low serum phosphorus
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11
Q

Treatment for post-parturient hemoglobinemia

A
  • 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
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12
Q

What causes Heinz body anemias?

A
  • Brassica plants (Rape, Kale, Turnips)

- Also onions (any member of the allium familY)

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13
Q

Toxin in Brassica plants

A
  • S-methyl cysteine sulfoxide

- Converted to dimethyl disulfide in the rumen

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14
Q

Toxic principle in Brassicas

A
  • S-methyl cysteine sulfoxide which is converted to dimethyl disulfide in the rumen
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15
Q

Who is more susceptible to Brassica toxicity?

A

Cattle

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16
Q

Other signs associated with Brassica plants?

A
  • Goitergenic effects, atypical interstitial pneumonia, choke
17
Q

Who is susceptible to onion toxicity?

A
  • All ruminants
18
Q

Toxic principle in onions?

A
  • N-propyl disulfide and s-methyl cysteine sulfoxide

- Difficult to predict toxicity

19
Q

Pathophysiology of Heinz body anemia

A
  • 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
20
Q

Clinical signs of heinz body anemia?

A
  • Weakness, lethargy, anorexia, exercise intolerance
  • Death losses
  • Pale mucous membranes +/- icterus
  • Elevated HR and RR, normal temp
  • Decreased production
21
Q

Clin Path and Dx of Heinz body anemia

A
  • 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
22
Q

Treatment for Heinz body anemia

A
  • Remove source
  • Supportive care (blood transfusion, IVF and diuresis if hemoglobinuria or azotemia)
  • Pain
  • Keep them quiet management - NSAIDs
23
Q

Prognosis for Heinz body anemia

A
  • Good if inciting factor controlled or eliminated and anemia is modest
  • Poor if rapidly progressive and profound anemia without blood transfusion
24
Q

Who tends to get copper toxicity?

A
  • SHEEEEP

- Also camelids

25
Q

Toxic dose for sheep relative to cattle

A

-MUCH lower in sheep than in cattle

26
Q

What diets are most likely to result in Cu toxicity?

A
  • Copper molybdenum ratios over 6:1
27
Q

Sources of copper toxicity

A
  • mixing errors, injections
28
Q

Pathophysiology of copper toxicity

A
  • 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
29
Q

Signs of acute Copper toxicity if ingested

A
  • 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
30
Q

Injected acute copper toxicity clinical signs

A
  • Anorexia, depression, dehydration
  • Ascites, pleural transudate
  • Hemoglobinuria
  • Dyspnea
  • Head pressing, ataxia, aimless wandering
31
Q

When would you see hemoglobinuria from acute copper toxicity?

A
  • Injection
32
Q

Clinical signs of chronic copper toxicity

A
  • can take weeks to occur
  • Acute onset of depression, anorexia, thirst
  • Hemoglobinuria, anemia, icterus
  • Death in 24-48 hours
33
Q

Which samples to take for copper toxicity?

A
  • Liver and kidney samples always

- Liver is best place to look

34
Q

Diagnosis of copper toxicity

A
  • 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
35
Q

Where to do a liver biopsy?

A
  • Clip the entire animal
  • Tuber coxae to the elbow and between 9th and 10th rib
  • Lidocaine
  • Ultrasound guide if you can
36
Q

Treatment for copper toxicity

A
  • Transfusion
  • Oxygen support
  • Maybe methylene blue for methemoglobinemia
  • Chelators (amybe can’t use; D-penicillamine; anhydrous sodium sulfate; ammonium molybdate)
37
Q

Prognosis of copper toxicity

A
  • Poor
38
Q

Prevention of copper toxicity

A
  • 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!

Ag Animal II (13 decks)

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