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toxicology > Heavy Metals > Flashcards

Heavy Metals Flashcards

1
Q

Mode of action for Lead

A

Altered GABA transmission, Displaced Calcium from binding sites, altered nerve and muscle transmission, decreased smooth muscle contraction and interference with mineral absorption.

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2
Q

Lead Clinical sings in a dog

A

Primarily GI signs- V, D, anorexia, tender abdomen

Secondarily: Neurologic signs- lethargy, ataxia, convulsions

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3
Q

Lead Clinical signs in a cow

A

NEurologic signs predominate (blindness, increased vocalization, ataxia, circling, aimless wandering)
GI signs are secondary- Rumen stasis, Gaunt, anorexia

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4
Q

Lead Clinical signs in horse

A

Paralysis of recurrent laryngeal nerve -> Roaring

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5
Q

Birds clinical signs with lead

A

Neurologic, muscle wasting

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6
Q

What Diagnostic samples do you want with Lead. Both post-moretem and ante-moretem

A

Antemortem- Whole blood in a purple tp tube, Milk

Post mortem- Liver, Kidney, Bone, Brain

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7
Q

Treatment methods for Lead

A

NO LEGAL ANTEDOTE IN FOOD ANIMALS**

CaEDTA given IV or SQ- must remove any foreign body to prevent continued absorption
Succimer- oral but is extremely expensive

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8
Q

Arsenic Mode of action

A

3+ binds to Lipoic Acid & blocks cellular respiration -> decreased ATP, capillary dilation -> Edema

5+ substitutes for P, uncouples oxidative phosphorylation -> Decreased ATP

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9
Q

Clinical signs associated with Arsenic

A

Gastrointesstinal, bloody diarrhea

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10
Q

Swine Clinical signs associated with Arsenic

A

Goose stepping, lack of proptioception, blindness

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11
Q

Appropriate samples for Arsenic

A

Sciatic and optic nerve- demyelination of the nerve

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12
Q

Gross lesions seen with Arsenic

A

Necrohemorrhagic gastroenteritis, ulcerations

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13
Q

Microscopic lesions associated with arsenic

A

GI and renal necrosis, peripheral neuromuscular degeneration, submucosal edema

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14
Q

Treatment for Arsenic

A

Decontamination: cathartics, gastric lavage, emesis
Supportive care: correct dehydration and acidosis
Chelators:
Succimer- Extremely expensive
Dimercaprol: must be given before clinical signs are present- expensive
Thiotic ACid- not for food animals - increases antioxidants

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15
Q

Mercury Toxicity

A

Organic > Inorganic > Elemental

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16
Q

Mercury Mode of action

A

Organic- inhibition of protein synthesis decreasing proteins, and funciton, resulting in necrosis

Inorganic- binds to sulfhydryl groups -> inhibits sulfhydryl enzymes, decreasing energy and funciton, resulting in necrosis

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17
Q

Clinical signs associated with Mercury

A

ORganic- stomatitis, conjunctivitis, blindness, ataxia, paresis, abnormal posture, paralysis, coma, death

Inorganic- vomiting, diarrhea, stomatitis, oliguria, death

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18
Q

What samples are appropriate for Mercury

A

Liver, kidney, Brain for Hg testing

Whole blood and urine in acute cases

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19
Q

Lesions associated with Mercury

A

Ulcerative/necrotic gastroenteritis, renal tubular necrosis, demyelination of peripheral nerves in swine

Cerebellar hypoplasia in cats

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20
Q

Treatment of Mercury

A

Oral decontamination: Egg whites, D-penicillamine, Na Thiosulfate, Saline cathartic

Succimer- expensive and not practical in LA

Organic= damage is generally extensive and too late

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21
Q

environmental concerns associated with Mercury

A

Contaminated livestock should not be used for consumption

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22
Q

Mode of Action for Zinc

A

Unknown, but causes hemolysis, GI irritation and erosion

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23
Q

Clinical sign of dogs with Zinc

A

Hemolytic anemia, GI irritation , anorexia, V, D

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24
Q

Clinical signs of ruminants associated with Zinc

A

Decreased growth and efficiency

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25
Q

Clinical signs associated with equine and Zinc

A

Lameness, and Laryngeal paralysis

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26
Q

Swine clinical signs associated with Zinc

A

Lameness

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27
Q

Sheep clinical signs associated with Zinc

A

diarrhea

28
Q

Sample collection for suspect Zinc cases

A

Pancreas, Liver, GI tract

Royal blue top tube with Red stripe for TM evaluation

29
Q

Gross lesions associated with Zinc

A

Pancreatitis, icterus, GI erosions & ulcerations, hemorrhagic joints in swine, OCD in horses

30
Q

Treatment of zinc

A

Remove foreign body, Supportive care
CaEDTA
D-penicillamine- oral, but very expensive

31
Q

Iron toxicity: routes of administrations

A

IV >IM>oral

32
Q

Iron MoA

A

cutely it is very corrosive and causes necrosis, decreased cardiac output. Metabolic acidosis from hypovolemia and hypotension.

Weeks later can cause scarring and strictures of the GI tract

33
Q

Samples for Iron cases

A

Serum , liver, feed, radiographs

34
Q

Lesions for Iron cases

A

Brown staining at injection sites, GI errosion and ulceration

35
Q

Treatment for Iron cases

A

Deferoxamine until effect.

36
Q

Wine colored urine is associated with what heavy metal?

A

Iron

37
Q

Fluoride MoA

A

REplaces hydroxy appetite in crystaline structure of bone. Mineralization is delayed/altered

38
Q

Presentations for Fluoride cases

A

Osteofluorisis- lameness, exostosis
Dental fluoresis: dystrophic formation of the dentin and enamel in erupting teeth. Softening of toothe enamel- early wear

39
Q

Appropriate sample for Fluoride cases

A

Bone, urine, Radiography looking for exostosis

40
Q

Treatment for fluoride cases

A

reduce fluoride in the diet

41
Q

Thallium source

A

Mycoplasma agar plate

42
Q

Clinical signs associated with Thallium

A

Gastrointestinal (profuse vomiting)
Neurologic (tremors, decreased mentation, paralysis)
Dermal (sloughing of skin, alopecia)

43
Q

Lesions associated with Thallium

A

Hemorrhagic gastritis, enteritis, colitis, pulmonary edema & hemorrhage.
Dermal necrosis

44
Q

Treatment of Thallium

A

Prussian blue and Dithizone- ineffective if clinical signs are present

45
Q

What heavy metal is associated with foot baths?

A

Copper

46
Q

What Cu:Mo ratio has Cu tox potential in sheep

A

> 20:1

47
Q

Copper MoA

A

Predominantlly stored in the liver, a stress event causes Cu to enter the blood stream, and a hemolytic crisis and lysis of RBCs occurs. Hemoglobinemia

“Gun-metal kidney”

Hemoglobinuria and death

48
Q

Clinical signs associated with Copper

A

Diarrhea, liver damage, schock.
No clinical signs during the accumulation phase

Icteric, and hemoglobinuria

49
Q

What samples are good choices for Copper

A

Liver- optimal and can be performed on live animals
Kidney-indicates massive release of copper
Feed, and feed labels

Serum is of little diagnostic value- liver maintains levels

50
Q

Gross lesions for Copper case

A 
Icteric MM, visceral tissues, fat
Gun metal- black kidney
Liver is very friable
Serum- hemolyzed -dark red - brown
Urine- hemoglobinuria
51
Q

What stain is specific for Copper

A

Rhodanine Stain-

52
Q

Herd level treatment for Copper

A

Na molybdate

Zinc

53
Q

Individual level treatment for copper

A

D-penicillamine (very expensive)

Ammonium Tetrathiomolybdate- must be compounded

54
Q

Bedlington terrier having decreased liver function associated with what heavy metal

A

Copper

55
Q

Molybdenum MoA

A

Copper antagonist

Promotes Cu excretion.

56
Q

What species is most susceptible to Mo

A

Cattle- especially in beef herds

57
Q

Clinical effects of Molybdenum

A

greenish.bubbly diarrhea
Copper deficiency (decreased immune system funciton, decreased melanin synthesis) “Red” Black angus
Anemia

58
Q

What samples should you collect for Mo testing?

A

Liver, serum, feed, forage, water, soil

59
Q

Treatment fo rMo

A

decrease exposure
Increase Cu
Copper glycinate
Multimin 90

60
Q

What is the only regulated essential mineral in feed?

A

Selenium

61
Q

MoA for Selenium

A

Produciton of free radicals, displacement of S from proteins, inhibition of RNA synthesis (embryotoic)
Decreased ATP synthesis

62
Q

Clincal signs associated with swine and Selenium

A

Hind limb ataxia progressing to posterior paresis, lameness, decreased intake and growth

63
Q

Clinical signs associated with chronic Selenium intoxication

A

Hair loss (most reported symptom) discoloration

Weakness/depression
Lameness

64
Q

sample collection for Selenium

A

Serum, whole blood, liver, kidney, hair, hoof wall all are good options

65
Q

Microscopic lesions associated with selenium

A

Bilateral poliomyelomalacia
Lungs: edema, congestion, hemorrhage
Kidneys: cortical necrosis

66
Q

Treatment for Selenium

A

No effective treatment for acute cases
Subacute- wait for depletion
Chronic- no good treatment, focus on prevention.
Eliminate the exposure

toxicology (7 decks)

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