Phenoxy derivatives of fatty acids (2,4-D) Flashcards

1
Q

3 sources of exposure

A
  • Accidental ingestion of concentrates or sprays (cattle)
  • Grazing freshly sprayed pastures (cattle)
  • Access to freshly sprayed lawns (pets)
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2
Q

T/F: Generally, srayed forages in the recommended concentrations do not cause poisoning

A

TRUE

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3
Q

What do phenoxy derivatives of FAs do to plant metaboisms?

A

Alter the metabolism of plants–> increases their toxicity by increasing accumulation of nitrate or cyanide

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4
Q

T/F: Phenoxy derivatives of FAs also decrease palatability of some poisonous plants, decreasing poisoning

A

FALSE–they increase palatability of some poisonous plants, increasing poisoning

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5
Q

Are phenoxy derivatives of FAs stable in the environment?

A

NO

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6
Q

Are phenoxy derivatives of FAs degraded by rumen flora, thus altering it?

A

Nope

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7
Q

T/F: Phenoxy derivatives of FAs are an irritant to GI mucosa

A

TRUE

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8
Q

Which species are the most susceptible to phenoxy derivatives of FAs?

A

Cattle and dogs

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9
Q

T/F: Cattle are more sensitive to phenoxy derivatives of FA’s than other species

A

FALSE–it’s dogs

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10
Q

What does toxicity depend on?

A

Species and duration of exposure

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11
Q

What’s the acute oral LD50 in dogs?

A

Approximately 100mg/kg

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12
Q

Where are phenoxy derivatives of FAs readily absorbed from? Where are they poorly absorbed from?

A
  • Readily absorbed from GI tract or by inhalation
  • Poorly absorbed from skin
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13
Q

Where are phenoxy derivatives of FAs distributed?

A

All over body, including liver, kidney, and brain

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14
Q

T/F: Meat residues in cattle and sheep are likely even with exposure to low concentrations of 2,4-D

A

FALSE–residues unlikely unless exposed to very high concentrations

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15
Q

What are the half lives of phenoxy derivatives of FAs?

A

Generally short (few hours), but longer in dogs (up to 3-4 days)

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16
Q

How is 2,4-D mainly metabolized? How is it excreted?

A
  • Metabolized mainly by hydrolysis
  • Excreted mainly unchanged in urine by tubular secretion
17
Q

T/F: Alkalinization of urine enhances renal excretion

A

TRUE

18
Q

Mechanism of action (3)?

A
  • Irritation of GI mucosa
  • Affect skeletal muscle membranes in dogs
  • Uncouple oxidative phosphorylation, and depress ribonuclease synthesis (unknown relationship to clinical signs)
19
Q

What are the general clinical signs of 2,4-D toxicity?

A

Generally non-specific; mainly GI and NM

20
Q

Clinical signs in ruminants?

A
  • Anorexia, rumen atony, may be bloat and diarrhea and ulcers in buccal mucosa
  • Depression, muscle weakness and emaciation with no convulsions
21
Q

Clinical signs in dogs?

A
  • Anorexia, vomiting, bloody diarrhea
  • Myotonia and weakness of the muscles especially posterior muscles and ataxia w/ rigidity of skeletal muscles
  • At high doses, onset is rapid (< 1 hr), opisthotonos may occur and posterior paralysis in addition to severe GI signs
22
Q

Clinical signs in swine?

A

Vomiting, diarrhea, muscle weakness and depression

23
Q

Various lesions of 2,4-D toxicosis?

A
  • Nonspecific
  • Mainly GI damage and degeneration of liver and kidney
  • Rumen stasis with ingested food is a characteristic finding
24
Q

Laboratory diagnosis?

A
  • Elevated ALP, LDH, CPK
  • Chemical analysis
    • Analytical methods are expensive and time consuming
    • Specimens are suspected forage, water, kidney, urine, liver, stomach, feces
25
Q

Diagnosis?

A
  • Difficult from clinical signs and lesions b/c they are nonspecific
  • History of ingestion is important
  • Chemical analysis might be helpful
  • Rule out other diseases
26
Q

Treatment?

A
  • No specific antidote
  • Detoxification
    • Wash skin w/ soap + water
    • Activated charcoal
  • Supportive/symptomatic treatment
    • IV fluids
    • Antidiarrheals and rumenatorics