Plant-Related Toxicants Flashcards

1
Q

Describe the accumulation of nitrate by plants

A
  • nitrate is absorbed from the soil by the plant and converted to nitrite by nitrate reductase
  • nitrite is converted to ammonia
  • ammonia is converted to amino acids, then to vegetable protein
  • accumulation occurs with the conversion of nitrate to nitrite is reduced, but nitrate is still being taken up
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2
Q

Which part of the plants/what age have the highest concentrations of nitrate?

A
  • stalks contain the highest

- young plants have higher concentrations

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3
Q

What are the properties of nitrate?

solubility, palatability

A
  • soluble in water

- salty and palatable

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4
Q

Which species are the most susceptible to nitrate poisoning?

Which are the least?

A
  • ruminants are most susceptible

- pigs are resistant

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5
Q

Describe the toxicokinetics of nitrate poisoining

A
  • rumen microflora convert nitrate to nitrite faster than nitrite is converted to ammonia
  • excess nitrite is absorbed and enters erythrocytes in exchange for Cl ions
  • crosses placenta
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6
Q

Describe the mechanism of action of nitrate poisoning

A
  • nitrite interacts with hemoglobin: ferrous oxidized to ferric and hemoglobin converts to methemoglobin
  • high mHb causes death from anoxemia
  • abortions occur
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7
Q

What are the clinical signs of nitrate poisoning?

A
  • sudden death without signs
  • rapid breathing, restlessness, weakness, ataxia, cyaosis, convulsions and death
  • abortion
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8
Q

What are the observed lesions in nitrate poisoning?

A
  • congestion of organs

- brown colored blood

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9
Q

How is nitrate poisoning treated?

A
  • methylene blue 1% IV

- activated charcoal, rumen lavage, or oral antibiotics

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10
Q

How are large animals usually poisoned with cyandide?

Small animals?

A

LA: ingestion of cyanogenic plants (wild cherry, sudan grass, johnson grass, and sorghums)
SA: ingestion of hydrogen cyanide and cyanide salts in many materials

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11
Q

Which animals are more susceptible to cyanide poisoning?

A
  • ruminants are most susceptible

- sheep less than cattle

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12
Q

Describe the toxicokinetics of cyanide poisoning

A
  • HCN absorbed through GI tract, inhalation, and intact skin
  • distributed throughout body
  • CN with thiosulfate is metabolized to thiocyanate which is less toxic and excreted in urine
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13
Q

Describe the mechanism of action of acute cyanide toxicity

A
  • excess cyanide in blood and tissue binds with ferric iron and copper
  • blocks electron transport and inhibit cells from using oxygen
  • metabolic acidosis
  • decreases cellular energy
  • vasoconstriction
  • neuronal damage from anoxia
  • irritation of mucus membranes
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14
Q

Describe the mechanism of action of chronic cyanide toxicity

A
  • neuronal degeneration and demyelination of spinal cord and brain
  • low levels of cyanide are goitrogenic
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15
Q

What are the clinical signs of acute cyanide toxicosis?

A
  • rapid onset
  • tachypnea, anxiety, severe panting, gasping, and behavioral alarm
  • death in 4-5 minutes
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16
Q

What are the clinical signs of chronic cyanide toxicosis?

A
  • posterior paralysis, urinary incontinence, and cystitis
  • constipation due to lower spinal cord degeneration
  • possible goitrogenic effect
17
Q

What lesions are found in cyanide toxicosis?

A
  • mucus membranes bright red
  • blood is cherry red and may not clot
  • congestion and petechiae in GI and lungs
  • cyanide smell
18
Q

How is cyanide toxicosis diagnosed?

A
  • elevated thiocyanate levels in urine
  • lactic acidosis and increased anion gap
  • sodium picrate paper test
19
Q

How is cyanide toxicosis treated?

A
  • sodium nitrate 20% IV (vasodilation and methemoglobin)
  • sodium thiosulfate 20% IV (converts cyanide to thiocyanate)
  • sodium thiosulfate orally
  • oxygen
  • mineral oil, vinegar
20
Q

Which species are the most susceptible to soluble oxalate poisoning?

A

sheep and cattle

21
Q

What will reduce the toxicity of soluble oxalate?

A
  • ruminants allowed to graze small quantities of oxalate containing plants
  • presence of food in rumen
  • calcium or calcium rich diets
22
Q

Describe the mechanism of action of soluble oxalate poisoning

A
  • after absorption, oxalates combine with calcium ion to form insoluble ca oxalate
  • leads to hypocalcemia and tetany, or affects bone and milk production
  • precipitation of ca oxalate crystals in kidney tubules
23
Q

What are the clinical signs of soluble oxalate poisoning?

A
  • colic, dullness, depression, muscle weakness and twitching, head and neck pulled to one side, prostration, coma, and death
  • rapid breathing and blood-tinged froth around mouth
  • fatal renal tubular toxicosis, oliguria, hyperkalemia, and cardiac failure
24
Q

What lesions are seen in soluble oxalate toxicosis?

A
  • excess fluid in abdomen and thoracic cavities
  • petechial hemorrhage in GI mucosa
  • emphysema of lungs
  • blood tinged froth in mouth and esophagus
  • kidneys have dark red cortex and medullar separated by a gray line
25
Q

How is soluble oxalate toxicosis diagnosed?

A
  • presence of Ca oxalate crystals in kidney tubules
  • hypocalcemia
  • high BUN