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Flashcards in Inorganic arsenic Deck (37)
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1

Sources?

  • 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

2

What 3 states does arsenic exist in?

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

3

What group does arsenic react with?

-SH group

4

What is the lethal oral dose in most species?

 1-25mg/kg

Very toxic

5

Types of toxicity?

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

6

Which species are susceptible?

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

7

What forms of arsenic are more toxic?

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

8

Pentavalent arsenic is converted to what?

Trivalent in-vivo

9

Where is arsenic absorbed from?

GI tract, intact skin, and by inhalation

10

Where is arsenic distributed?

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

11

T/F: Arsenic poorly crosses the BBB

TRUE

12

Where is pentavalent reduced to trivalent? What occurs next?

Liver

Then is partly metabolized in the liver and kidney by methylation

13

How is arsenic excreted?

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

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

14

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

FALSE

15

What does the trivalent bind to?

2-SH groups of lipoic (thioctic acid)

16

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

Lipoic acid

17

What occurs following inhibition of lipoic acid?

Inhibition/slowing of glycolysis and citric acid cycle

--> inhibits oxidative enzymes and inactivates glutathione (GSH)

18

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

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

--> local corrosive effect

19

Which tissues/cells are most sensitive?

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

Capillary endothelial cells are most sensitive

20

Clinical signs of peracute toxicosis?

Sudden death or severe colic, collapse and death

21

Clinical signs of acute toxicosis?

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

22

Clinical signs of subacute toxicosis?

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

23

Lesions?

  • 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

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

TRUE

25

What are other specimens used for chemical analysis?

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

26

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

Normal tissue residues is 0.5ppm

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

27

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

PCV, BUN

28

Diagnosis?

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

29

DDx?

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

30

Emergency and supportive treatment?

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

31

Decontamination?

  • 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

What is the chelator of choice for inorganic arsenic?

Dimercaprol (BAL, British antilewisite)

Must confirm diagnosis before giving antidote--very toxic

33

Is Dimercaprol 100% effective?

No

34

How might Dimercaprol increase toxicity?

By mobilizing arsenic

35

What are the toxic side effects of Dimercaprol?

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

36

Dimercaptosuccinic acid

(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

Prognosis of inorganic arsenic poisoning?

Grave if not treated early