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Toxicology > Inorganic arsenic > Flashcards

Inorganic arsenic Flashcards

1
Q

Sources?

A
  • Use of arsenic has declined
  • Ant and roach baits
  • Wood preservative (arsenic pentaoxide)
  • Insecticides, herbicides, fungicides and rodenticides
  • Milk from poisoned cows may be toxic to calves
  • Pastures near smelters may be contaminated
  • Found in paint, pigments, detergents, and building materials
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2
Q

What 3 states does arsenic exist in?

A

3 oxidative states: elemental, trivalent (arsenite), and pentavalent (arsenate)

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3
Q

What group does arsenic react with?

A

-SH group

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4
Q

What is the lethal oral dose in most species?

A

1-25mg/kg

Very toxic

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5
Q

Types of toxicity?

A

Peracute, acute, or subacute (chronic toxicosis has not been documented in animals)

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6
Q

Which species are susceptible?

A
  • Herbivores most susceptible
  • Dogs can get poisoned by ant and roach baits
  • Swine, chickens are rarely poisoned
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7
Q

What forms of arsenic are more toxic?

A

Inorganic trivalent is more toxic than pentavalent which is more toxic than organic

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8
Q

Pentavalent arsenic is converted to what?

A

Trivalent in-vivo

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9
Q

Where is arsenic absorbed from?

A

GI tract, intact skin, and by inhalation

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10
Q

Where is arsenic distributed?

A

Distributed all over the body and achieves higher concentrations in liver and kidney and also in hair, hoof, nail, and skin

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11
Q

T/F: Arsenic poorly crosses the BBB

A

TRUE

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12
Q

Where is pentavalent reduced to trivalent? What occurs next?

A

Liver

Then is partly metabolized in the liver and kidney by methylation

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13
Q

How is arsenic excreted?

A

Rapidly excreted mainly in urine (w/in 48 hrs)

Small amounts are excreted in feces, milk, saliva, sweat, hair, and by exhalation

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14
Q

T/F: Milk from poisoned cows does not contain toxic levels of arsenic

A

FALSE

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15
Q

What does the trivalent bind to?

A

2-SH groups of lipoic (thioctic acid)

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16
Q

What is the essential cofactor for the enzymatic decarboxylation of keto acids?

A

Lipoic acid

17
Q

What occurs following inhibition of lipoic acid?

A

Inhibition/slowing of glycolysis and citric acid cycle

–> inhibits oxidative enzymes and inactivates glutathione (GSH)

18
Q

What does the pentavalent uncouple? What does it lead to?

A

Pentavalent uncouples oxidative phosphorylation (no fever) and may interfere with vitamins B1 and B6 metabolism

–> local corrosive effect

19
Q

Which tissues/cells are most sensitive?

A

Tissues rich in oxidative enzymes such as intestines, kidney, liver are more sensitive

Capillary endothelial cells are most sensitive

20
Q

Clinical signs of peracute toxicosis?

A

Sudden death or severe colic, collapse and death

21
Q

Clinical signs of acute toxicosis?

A
  • Rapid onset
  • Severe colic
  • Staggoring
  • Salivation
  • Vomiting
  • Thirst
  • Watery diarrhea which may be hemorrhagic
  • Possible hematuria
  • Death in 1-3 days
22
Q

Clinical signs of subacute toxicosis?

A
  • Colic
  • Anorexia
  • Depression
  • Diarrhea w/ blood or mucosal shreds
  • Dehydration
  • Partial paralysis of hind limbs
  • Death in several days
23
Q

Lesions?

A
  • GI mucosal edema and hemorrhage with sloughing and perforation, liver and kidney damage
  • Microscopically: capillary degeneration
  • Skin exposure causes skin lesions and blistering in addition to systemic lesions
24
Q

T/F: Urine is the best antemortem specimen for chemical analysis; liver and kidney are the best postmortem specimens

A

TRUE

25
Q

What are other specimens used for chemical analysis?

A

GI contents, vomitus, feces, milk, and suspected source (feed, plant, soil)

26
Q

What is the normal arsenic level in tissues? What level (and where) is a strong indication of poisoning?

A

Normal tissue residues is 0.5ppm

> 7-10ppm in liver or kidney is a strong indication of toxicosis

27
Q

What 2 things on the lab diagnosis are increased following arsenic toxicosis?

A

PCV, BUN

28
Q

Diagnosis?

A
  • History
  • Signs of sudden onset bloody diarrhea
  • Watery diarrhea w/ mucosal shreds
  • Lesions
  • Lab diagnosis
29
Q

DDx?

A
  • Caustics
  • Irritant plants
  • Urea
  • Pesticides
  • Severe acute heavy metal toxicosis
  • Monensin
  • Blister beetles in horses
  • OP
  • Hypomagnesemia
  • Enteric bacterial and viral diseases
30
Q

Emergency and supportive treatment?

A
  • Fluids and electrolytes, poss. blood transfusion
  • Treatment of acidosis
  • Vitamins, antibiotics, analgesics, dopamine, acetylcysteine, and other treatments
31
Q

Decontamination?

A
  • Gastric lavage (only early)
  • Mineral oil
  • Activated charcoal
  • Emetics and strong cathartics are contraindicated
  • Demulcents to coat the GI mucosa such as kaolin-pectin
32
Q

What is the chelator of choice for inorganic arsenic?

A

Dimercaprol (BAL, British antilewisite)

Must confirm diagnosis before giving antidote–very toxic

33
Q

Is Dimercaprol 100% effective?

A

No

34
Q

How might Dimercaprol increase toxicity?

A

By mobilizing arsenic

35
Q

What are the toxic side effects of Dimercaprol?

A

Vomiting, tremors, convulsions, hypotension, shock, coma and death

36
Q

Dimercaptosuccinic acid

A

(DMSA, Succimer, Chemet)

  • Given orally or IM
  • Water soluble analog of BAL
  • Safer but may be less effective than BAL in severe toxicosis
    • Hydrophilicity and poor tissue distribution
37
Q

Prognosis of inorganic arsenic poisoning?

A

Grave if not treated early

Toxicology (22 decks)

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