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Veterinary Toxicology > Hematotoxicology, Pt. 2 > Flashcards

Hematotoxicology, Pt. 2 Flashcards

1
Q

What is the toxic principle of Red Maple (Acer rubrum)? What species are affected?

A

gallic acid and tannins

equids - horses and Grevy’s zebra following ingestion of wilted/dried leaves or bark

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2
Q

What are the 3 steps to the proposed metabolism of the toxic principles of red maple?

A
  1. tannic acid is metabolized to gallic acid in the equine ileum by Klebsiella pneumonia or Enterobacter cloacae
  2. gallic acid is further metabolized to pyrogallol by the same bacteria
  3. pyrogallol is absorbed in the ileum and interacts with iron to form free radicals leading to its oxidation into Fe3+ to form methemoglobin
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3
Q

What is the mechanism of toxicity of red maple?

A

oxidative damage to hemoglobin causes precipitation as Heinz bodies on the RBC either causing direct damage to the RBC membrane, altering its permeability (intravascular hemolysis) or physical removal by the spleen

  • RESULTING in progressive anemia
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4
Q

Other than the spleen, what other organ can RBCs with Heinz bodies be filtered to?

A

kidney —> precipitation in renal tubules —> renal failure

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5
Q

When is red maple poisoning most common? What are the 2 characteristic clinical signs? What else can be seen?

A

fall/late summer (July-October) after a storm when fallen red maple leaves or branches are accessible to horses

acute hemolytic anemia and red-brown discoloration of urine

  • depression, anorexia, weakness
  • increased respiratory and heart rates
  • cyanosis, icterus, decreased PCV
  • Heinz bodies, proteinuria
  • abortion
  • paracute death from tissue anoxia
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6
Q

What supportive care should be given to horses with red maple toxicosis? What are 2 possible antidotes? Which one may be contraindicated in horses? What pain relief is recommended?

A

IV fluids, whole blood transfusion, oxyglobin, oxygen

  1. ascorbic acid
  2. methylene blue - may oxidize Hb into MetHb

NSAIDs, pentazocine, butorphanol

(aggressive therapy tends to be unrewarding - prognosis is guarded)

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7
Q

What members of the Allium family commonly cause toxicosis? What is the toxic principle?

A

onion, garlic, leek, chives

n-propyl disulfide

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8
Q

How does the type of onion affect toxicosis? What 3 animals are most susceptible? Which RBCs are most susceptible to this oxidative damage?

A

wild onions rarely cause toxicity, but may impart offensive odor in milk

  1. cats - high number of -SH groups
  2. dogs (minced onions)
  3. cattle
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9
Q

What 3 species of dogs are especially susceptible to onion toxicosis? Why?

A
  1. Akitas
  2. Shibas
  3. Tosas

high levels of reduced glutathione and potassium in RBCs

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10
Q

What are the 2 main mechanisms of toxicity of onion toxicosis?

A
  1. n-propyl disulfide blocks glucose-6-phosphate dehydrogenase, which impairs the hexose monophosphate pathway in the RBCs
  2. n-propyl disulfide oxidizes Hb resulting in insufficient NADPH or glutathione and precipitation into Heinz bodies —> spleen removal/hemolysis —> anemia
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11
Q

What is the major function of glucose-6-phosphate dehydrogenase?

A

generates cellular reducing power (NADPH) and ribose (RNA, DNA)

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12
Q

What are clinical signs of onion toxicosis?

A
  • anorexia, vomiting, salivation, lethargy
  • ataxia, recumbency
  • rapid breathing and heart rates
  • pale/icteric MM
  • onion odor in breath and flavor in milk
  • hemoglobinuria, hemoglobinuria
  • reduced PCV and hematocrit, elevated WBC
  • Heinz bodies
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13
Q

Onion toxicosis, hemoglobinuria and hemoglobinemia:

A
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14
Q

What supportive care is most important for onion toxicosis?

A

cardiovascular

  • IV fluids
  • oxygen
  • whole blood transfusion or oxyglobin
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15
Q

What part of the bracken fern is most toxic? What is the main toxic principle?

A

young plants and rhizomes

ptaquiloside (thiaminase, cyanogenic glycoside)

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16
Q

What are the 3 mechanisms of toxicity of bracken fern toxicosis?

A

PTAQUILOSIDE

  1. causes death of precursor cells in the BM
  2. causes urinary tract neoplasia by alkylating DNA and inducting protooncogenes
  3. secreted in milk
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17
Q

What are the 4 common syndromes of bracken fern toxicosis?

A
  1. aplastic anemia in cattle and sheep (most common in North America)
  2. enzootic bovine hematuria
  3. tumors of the upper GI tract following prolonged low-dose exposure
  4. progressive renal degeneration in sheep depending on age, consumption, and toxin content
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18
Q

When is aplastic anemia seen following bracken fern toxicosis? What are the 4 common clinical signs?

A

suppression of bone marrow activity after >3-4 weeks of exposure

  1. fever, lethargy, loss of appetite
  2. severe pancytopenia
  3. hemorrhaging from natural orifices - vulva, mouth, conjunctiva, anterior chamber of the eye
  4. bloody stool and urine
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19
Q

What is characteristic of enzootic hematuria caused by bracken fern toxicosis? What is necessary for this to develop? What does this result in?

A

intermittent blood loss in urine from hemorrhages and tumors in the urinary bladder of cows - “red water disease”

prolonged (>2 years) consumption of low levels

anemia, elevated heart rate, weakness —> death from anemia

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20
Q

What are the 6 most common clinical signs seen in animals with upper GI tumors caused by bracken fern toxicosis?

A
  1. choking
  2. coughing
  3. bloat
  4. emaciation
  5. regurgitation of greenish fluid
  6. extended neck posture
21
Q

What is recommended for treating bracken fern toxicosis?

A
  • blood or platelet transfusion in cattle with aplastic anemia
  • antibiotics to prevent secondary infection
22
Q

What members of the Brassica family cause toxicosis? What are 4 toxic principles?

A

cabbage, kale, broccoli, turnips, and mustards commonly used as winter feed for cattle and sheep

  1. S-methyl cysteine sulfoxide (SMCO)
  2. glucosinolates
  3. goitrin
  4. nitrile, nitrates
23
Q

What species are susceptible to Brassica toxicosis?

A

poultry, swine, cattle, sheep

24
Q

How is SMCO found in Brassica metabolized? What are the 5 mechanisms of toxicity based on the toxic principles?

A

reduced into toxic dimethyl disulfide by microbial fermentation in the GIT

  1. dimethyl disulfide oxidizes hemoglobin to form Heinz bodies, resulting in hemolytic anemia
  2. glucosinolates give rise to isothiocyanates, causing gastroenteritis
  3. goitrin is goitregenic
  4. nitrate is converted into nitrite in the rumen, which oxides hemoglobin and causes methemoglobinemia
  5. nitrile causes pulmonary emphysema, hepatic necrosis, and blindness
25
Q

What are the 2 most common signs of Brassica toxicity? What may also be observed?

A

anemia and GI upset

  • hemoglobinuria, hemoglobinemia
  • tachycardia, polypnea
  • cyanosis, jaundice
  • diarrhea, colic, rumen stasis
  • poor conception rate, reduced milk, growth retardation
  • goiter
26
Q

What supportive treatment is recommended for Brassica toxicity?

A
  • blood transfusion
  • diuresis with fluids to reduce hemoglobinuric nephrosis
27
Q

What 3 syndromes are associated with copper toxicity?

A
  1. acute copper toxicosis - sheep
  2. enzootic icteurus - sheep (South Africa)
  3. genetic canine copper toxicosis - Bedlington terriers, West Highland white terriers, Skye terriers, Dalmatians, Dobermans (Wilson’s disease in humans)
28
Q

What causes genetic copper toxicosis in Bedlington terriers?

A

autosomal recessive disorder of biliary copper excretion

29
Q

What is the main cause of copper toxicosis? What increases the risk of developing this?

A

ingestion or administration of copper-containing formulations/materials - anthelmintics, footbaths, pesticides, dietary additives, copper salts, poultry litter, feeding food for other species to sheep

feeding ionophores (Monensin) - increases copper absorption

30
Q

How does the species sensitivity to copper toxicosis compare?

A
  • sheep are very sensitive, especially British breeds (Suffolks, Shropshires, Oxfords) and Texel sheep (hepatocytes have high affinity for copper and low excretion)
  • swine, horses, cattle (except Jerseys!), poultry, and dogs are relatively resistant
31
Q

What is the mechanism of toxicity of copper toxicosis?

A
  • Cu regulation involves its sequestration in the liver by metallothionein and excretion through bile and urine
  • toxicity occurs when the capacity of the liver to regulate Cu is exceeded, leading to accumulation in hepatocytes
  • this allows redox recycling, which generates ROS that cause hepatocyte necrosis and allows Cu to be released into the blood and damage of RBCs

RESULTS in intravascular hemolysis, release of Hb and anoxia —> centrilobular hepatic necrosis, accumulatiom in the kidney

32
Q

How does copper toxicosis affect proteins?

A

inactivates then by displacing other essential metals from them, oxidizing -SH groups, and depleting antioxidants —> causing oxidative stress

33
Q

When do clinical signs of copper toxicosis appear in sheep/cattle? What is observed when this happens?

A

stress - decreased food, transportation, handling, shearing, weather, exercise

  • massive liver necrosis causes Cu to be released and RBC damage (hemolysis)
  • hemoglobinuria, icterus, anoxia
  • hemolytic crisis: port wine urine, swollen blue kidneys, swollen spleen with dark brown parenchyma
34
Q

What swine are most susceptible to copper toxicosis? What clinical signs are seen?

A

generally resistant - young are more susceptible than adults

  • anorexia, depression, poor weight gain
  • icterus
  • hemoglobinuria
  • bloody feces
35
Q

What is copper toxicosis in companion animals commonly associated with? What are the typical signs?

A

acute toxicity is rare in cats and dogs —> ingestion of Canadian and US pennies

  • depression, dehydration, anorexia
  • intermittent vomiting
  • mild abdominal pain
  • diarrhea
36
Q

What causes copper storage disease in dogs? What does this cause? What do affected dogs show? What never develops?

A

autosomal recessive defect of Cu excretion —> chronic active hepatitis with slow hepatocellular death

  • anorexia, weight loss
  • ascites
  • CNS signs due to toxemia
  • icterus is uncommon though liver function marker enzymes are elevated

hemolytic crisis or hemoglobinuria

37
Q

When does subacute Cu poisoning commonly occur? What do signs include? What does not occur?

A

when lambs in Cu-deficient areas, like FL, southeastern coastal areas, and west of the Rockies, are given Cu compounds (even at normal dosage)

  • GIT hemorrhage
  • pulmonary edema
  • ascites

liver damage occurs, but there is no icterus or hemolytic crisis

38
Q

What are common ways to diagnose copper toxicosis?

A
  • evidence of blue-green ingesta
  • elevated serum and liver/kidney Cu concentrations
  • CBC, serum panel: hemolysis, elevated liver enzymes
  • abnormal radiographs showing foreign objects
  • liver histopathology
  • breed of dog
39
Q

What 3 treatments are recommended for animals with copper toxicosis?

A
  1. surgery to remove foreign body
  2. supportive care (IV fluids)
  3. D-penicillamine to chelate Cu and promote urinay excretion
40
Q

What 2 treatments are recommended in ruminants with copper toxicosis?

A
  1. ammonium molybdate, sodium thiosulfate, or ammonium tetrathiomolybdate to reduce liver Cu concentrations
  2. dietary supplementation with zinc acetate to reduce Cu absorption

(treatment of acute toxicosis is often not successful)

41
Q

What is the main source of zinc? What species are most susceptible to toxicosis?

A

zinc-containing foreign bodies - PENNIES, galvanized metals, rash ointment, sunscreen, feed mixing errors, contaminated forage

  • dogs, especially younger small breeds
  • caged birds
42
Q

Where is zinc absorbed? What 3 factors tend to affect its rate of absorption? How is it excreted?

A

small intestine

  1. dietary components - Cu, Ca, Mg, phytate, protein
  2. age
  3. growth rate

bile, feces, intestinal secretions, pancreatic fluid (some chelated zinc is lost in urine)

43
Q

What are the 3 mechanisms of toxicity of zinc?

A
  1. direct irritation to GIT
  2. hemolytic anemia by causing direct damage to RBC membrane, inhibiting RBC enzymes, and increasing RBC susceptibility to oxidative damage
  3. competitive interactions with Cu and Fe (anemia) and Ca
44
Q

What clinical signs are commonly seen with zinc toxicosis?

A
  • depression, vomiting, diarrhea
  • anorexia, abdominal pain
  • icterus, hemolytic anemia
  • decreased PCV, hemoglobinemia, hematuria
45
Q

How are blood smears commonly affected by zinc toxicosis? What may occur in sheep?

A

increased nucleated RBCs and basophilic stippling caused by aggregation of rRNA

Cu deficiency

46
Q

How is zinc toxicosis diagnosed?

A
  • zinc analysis in serum, kidney, liver, and urine by collection in royal blue-top tubes (no rubber due to zinc contamination)
  • radiography
47
Q

What GI protectants and chelation therapy is recommended for zinc toxicosis?

A

PPI, H2-blockers, sucralfate

Ca-EDTA, BAL, or D-penicillamine

48
Q

How does lead cause anemia?

A
  • increases RBC fragility and basophilic stippling (nucleotidase inhibition)
  • interferes with heme synthesis by inhibiting ALAD, ferrochelatase, and heme synthase

Veterinary Toxicology (29 decks)

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