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Toxicology > Dipyridyl herbicides > Flashcards

Dipyridyl herbicides Flashcards

1
Q

2 specific dipyridyl herbicides?

A

Paraquat and diquat

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2
Q

4 uses?

A
  • Broad spectrum dessicant contact herbicides
  • Paraquat is RUP, diquat GUP
  • Concentrated forms (5-20%) for agriculture use and dilute forms for lawns/gardens
  • Sprayed as 0.5 lb/acre for ag use
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3
Q

Sources of toxication?

A
  • Ingestion of concentrates
  • Malicious
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4
Q

Stability?

A

Unstable, rapidly inactivated by light and soil

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5
Q

Solubility?

A

Salts are soluble in water, poorly soluble in alcohol, and insoluble in hydrocarbon solvents

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6
Q

Stability of solutions?

A

Stable in neutral or acidic conditions but destroyed by alkali

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7
Q

What does paraquat bind strongly to?

A

Soil

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8
Q

what are dipyridyl herbicides caustic to?

A

Mucous membranes

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9
Q

Which animals are susceptible?

A

All animals, especially dogs

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10
Q

Oral LD50?

A

Ranges from 25-75 mg/kg in cats, dogs, pigs, sheep, and humans

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11
Q

What enhances paraquat’s toxicity?

A
  • Selenium
  • Vitamin E deficiency
  • Depletion of tissue glutathione
  • Oxygen therapy
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12
Q

What will cause chronic toxicity and death in dogs?

A

Daily oral exposure to 170ppm paraquat

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13
Q

Where is diquat absorbed from?

A

Poorly absorbed from GI tract

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14
Q

Where is paraquat absorbed from? Where is it distributed?

A
  • Absorbed from GI tract (<20%) and skin (<10%)
  • Distributed all over the body and achieves high conc. in lungs (10x)
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15
Q

How is paraquat excreted?

A

Excreted w/in 24hrs mainly unchanged in urine (minimal metabolism)

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16
Q

Mechanism of action?

A
  • Reduced by nicotinamide-adenine dinucleotide phosphate (NADPH) to produce singlet oxygen
  • Singlet oxygen reacts w/ lipids of cell membranes to form hydroperoxides
  • Production of free radical and membrane damage and cellular degeneration and necrosis (esp lung tissue)
17
Q

What are the early signs of acute toxicosis?

A
  • May be vomiting, anorexia, or depression
  • High doses may cause ataxia, dyspnea, and seizures
  • Signs may not be observed until 3 days after exposure to paraquat
18
Q

What are the delayed signs of acute toxicosis?

A
  • (2-7 days)
  • Respiratory signs: tachypnea, dyspnea, harsh resp sounds, cyanosis, and reduced pulmonary compliance
19
Q

What are the signs of subacute or chronic toxicosis and when do they occur?

A
  • 1-3 weeks
  • Resp signs due to progressive pulmonary fibrosis
20
Q

Where are the lesions mainly found?

A

Respiratory tract

21
Q

Specific lesions? Other findings?

A
  • Pulmonary congestion edema, congestion, hemorrhage, fibrosis, and failure of lungs to collapse
  • Lingual ulcers may be seen
  • Liver, kidney, and spleen may be congested and enlarged
  • Microscopic lesions are consistent with gross findings
22
Q

Chemical analysis?

A
  • Specimens are suspected plant, stomach contents and urine (acute cases) or lungs (chronic cases)
  • Urine samples may be negative after 48hrs from exposure
23
Q

Radiography?

A

Mild changes in lungs

24
Q

DDx?

A
  • Pneumonias
  • Inhalent toxicants such as toxic gases, vapors, and dusts
25
Q

What is the specific antidote?

A

There is none

:(

26
Q

Detoxification?

A
  • Emetics
  • Activated charcoal preferred
  • Bentonite or Fuller’s earth orally (several times daily for 2 days)
  • Saline cathartics following the adsorbent
27
Q

Supportive treatment?

A
  • Oxygen contraindicated b/c it may increase toxicity
  • Fluid therapy may be used to cause diuresis and support kidney fx
  • Hemodialysis or peritoneal dialysis
28
Q

Biochemical antagonists (antioxidants)?

A
  • Orgotein (superoxide dismutase)
  • Acetylcysteine
  • Ascorbic acid
  • Niacin or riboflavin
29
Q

Are the treatments helpful?

A

None of the treatments are likely to be of much help unless begun w/in 24hrs of exposure

30
Q

Prognosis?

A

Guarded or grave

Toxicology (22 decks)

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