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RUSVM Toxicology Summer 2019 > Lead, Zinc, and Selenium Toxicosis > Flashcards

Lead, Zinc, and Selenium Toxicosis Flashcards

1
Q

What is the most common sources of lead toxicosis?

A

Lead based paints
Batteries, plumbing solder, galvanized wire, lead shots, fishing sinkers.

Contaminated pastures from industry

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2
Q

T/F: lead is not degraded in the environment

A

True

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3
Q

How much lead is absorbed from he GI tract?

A

Only 1-2% because it forms insoluble compounds

Acid conditions favor dissolution

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4
Q

What species are most susceptible to lead toxicosis?

A

Cattle, horse, pet, water fowl

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5
Q

Why are puppies more sensitive than adults to lead toxicosis?

A

Greater absorption and immature blood-brain barrier

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6
Q

Oral absorption of lead is poor but is increased by ________

A

Acidity

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7
Q

How is lead transported in the body?

A

As lead proteinate on erythrocytes membrane

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8
Q

How long does lead stay in soft tissues?

A

4-6weeks

Slowly stored in bone and stays for several years

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9
Q

Where is lead excreted?

A

Urine
Small amount in bile

Can be in milk in toxic levels

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10
Q

What are the target tissues of lead toxicity?

A

CNS, GI tract, and hematopoietic system

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11
Q

What is the MOA of of lead?

A

Binds with the SH and other nucleophilic functional groups
Inhibits SH containing enzymes and other proteins

Chronic exposure causes anemia due to inhibition of enzymes in heme synthesis, delay in RBC maturation, and shortening the life span of erythrocytes

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12
Q

What clinical signs would you see due to lead toxicosis?

A

GI- anorexia, vomiting, colic, diarrhea, or constipation

CNS- anxiety, hyperexcitability, vocalization, head pressing, circling, running, manical behavior, seizures, tremors, and blindness.
Pharyngeal paralysis and roaring in the horse
CNS depression in horses and sheep

Anemia in chronic cases

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13
Q

What lesions can be causes by lead toxicosis?

A

Microscopic

  • cerebral cortical necrosis and poliomalacia in cattle
  • acid fast eosinophilic intranuclear inclusion bodies in renal tubular epithelium or hepatocytes
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14
Q

What laboratory diagnostics would you do if you suspect lead toxicosis?

A

Chemical analysis - antemortem specimen of choice, above 0.4ppm

Hematology

  • increased nucleated RBC
  • basophilic stippling of RBC in dogs
  • increased stippling protoporphyrin in dog
  • fluorescence of plasma porphyrins under UV light in cattle

Radiography
-object in GI

UA
-increased delta-ALA levels

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15
Q

What is the DDX for the following clinical signs..

Anxiety, hyperexcitability, vocalization, head pressing, circling, running, manical behaviour, seizures, tremors, and blindness

A

Chlorinated hydrocarbons
-neuromuscular signs and convulsive activity, but no blindness

Urea
-no abnormal posturing or head pressing

OP and carbamates
-PSNSmimetic signs/ neuromuscular, less behavioural

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16
Q

What is the treatment for lead toxicosis?

A

Calcium EDTA is cheating agent of choice for 5 days
-oral admin may increase absorption

Dimercaprol prior to EDTA May improve effect because it crosses the BBB and enhances renal and biliary excretion of lead

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17
Q

What is recommended as part of treatment for pet birds with lead toxicosis?

A

Dimercaptosuccinic acid (DMSA)

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18
Q

What is recommended for treatment following EDTA in treatment of chronic lead toxicosis?

A

D-penicillamine PO

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19
Q

What can be given for supportive treatment in lead toxicosis?

A 
Thiamine 
Glucocorticoids 
Zinc supplement 
Diazepam or barbiturates 
Fluid therapy

Decontaminate with magnesium sulfate and removal of the lead object

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20
Q

What are common sources of zinc toxicosis?

A

Ingestion of zinc containing pennies
Galvanized wire
Zinc oxide skin ointment
Zinc containing lotions, shampoo, wound healing agents

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21
Q

What is the normal function of zinc in the body?

A

Growth, cell proliferation, skeletal development, collagen formation, skin feathering, wound healing reproduction, immune system, direct stabilizing effect on cellular membranes.

Component of many important enzymes and proteins
-alcohol dehydrogenase (ALD), lactic dehydrogenase (LDH), alkaline phosphatase (AP), carbonic anhydrase, DNA polymerase, RNA polymerase, superoxide dismutase

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22
Q

What is the toxicity of zinc?

A

100mg/kg

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23
Q

A ________ environment enhances zinc release and absorption

A

Acid

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24
Q

What is the MOA of zinc toxicosis?

A

Irritant to GI mucosa
May interfere with enzymes
Direct damage to cell membranes and organelles
Excessive dietary zinc intake interferes with absorption and utilization of copper and iron
Antagonizes copper and iron in hemoglobin synthesis
Causes hemolytic anemia

25
Q

What are the clinical signs associated with zinc toxicosis?

A

GI- vomiting, anorexia, lethargy, abdominal pain, diarrhea, pica

Hematologic - hemolytic anemia, icterus, and hemoglobinuria

Renal - azotemia, hypercreatinemia, and hyperphosphatemia

26
Q

What are the lesions seen with zinc toxicosis?

A

Gastritis, gastric ulcers, liver damage, and tubular casts

27
Q

What changes would you see in lab values in zinc toxicosis?

A

Sample - serum, liver,r kidney, pancreas, urine

Hemolytic anemia, icterus, hemoglobinuria
Azotemia, hypercreatinemia, and hyperphosphatemia

Decreased copper in chronic toxicosis

28
Q

What is the DDX for zinc toxicosis?

A 
Copper 
Naphthalene 
Onion 
Red maple 
Cotton seed 
Mustard 
Immune -mediated hemolytic anemia 
Hyperphosphatemia 
Phenolic 
DMSO
Guaifenesin
29
Q

What is the treatment of zinc toxicosis?

A

Decontamination -cathartics, surgical removal

Supportive care - blood transfusion, oxygen therapy, fluid therapy, furosemide, mannitol, or dopamine for acute renal failure

Chelation- calcium disodium EDTA, and D-penicillamine

30
Q

What disease is caused by selenium deficiency in lambs, calves, and foals?

A

White muscle disease

31
Q

What disease is caused by selenium deficiency in young pigs?

A

Hepatosis dietetica

32
Q

What disease is caused by selenium deficiency in chicks?

A

Exudative diathesis

33
Q

What disease is caused by selenium deficiency in adult pigs

A

Porcine stress syndrome

34
Q

What soils are deficient is selenium?

A

Northeast
Northwest
Southeast
Great Lakes

35
Q

Where do you find selenium rich soils?

A

Midwest/western states

-> can have plants that accumulate high levels of Se

36
Q

What is usually the source fo selenium toxicosis in cattle, sheep, and horses?

A

Graze seleniferous plants

  • obligate accumulators -> locoweed, milk vetch, princes plume (contain high Se levels 15000ppm and are generally not palatable)
  • facultative accumulators —> aster, saltbrush, and paintbrush (accumulate 25-100ppm)
  • passive accumulators —> corn, wheat, oat, barely grass, and hay (accumulate 1-25ppm, MOST common source)
37
Q

What is usually a source of selenium toxicosis in small animals?

A

Improper use to selenium-medicated shampoos

38
Q

What are the 3 states of selenium ?

A

Selenate (+6)
Selenite (+4)
Selenide (-2)

39
Q

Selenium has similar properties to what compounds?

A

Arsenic —> can be used to enhance elimination

Sulfur —> often replace sulfur in enzymes

40
Q

List the toxicity of the various forms of Se from most of least toxic.

A

Organic selenium in plants > selenate = selenide > synthetic organoselenium

41
Q

Who has the lowest oral toxic dose of selenium, swine, cattle, or horse?

A

Horse < cattle < swine

42
Q

What type of soils promote formation of selenate?

A

Arid alkaline soil (Great plains)

43
Q

Toxicity of selenium can be reduced by??

A

High protein diet and ingestion of other elements that bind Se like copper

44
Q

T/F: elemental Se is absorbed through the intestines

A

False

Elemental Se is not absorbed because it is insoluble in water

45
Q

To what tissues is Selenium particularly distributed to?

A

Liver, kidney, and spleen

46
Q

Chronic exposure of selenium results in high concentrations where?

A

Hair and food

47
Q

What are the only meals that cross the BBB and cause CNS signs?

A

Lead and organic mercury

48
Q

Where is selenium excreted?

A

Mainly in urine
Bile
Across placenta and milk (usually not in toxic levels)

49
Q

What is the MOA of selenium toxicosis?

A

Irritation of GI mucosa

Deplete tissue glutathione (GSH)
Selenium requires sulfur in amino acids causing abnormal proteins
Decrease ATP in chronic toxicosis

Death due to respiratory insufficiency —> pulmonary edema and hemorrhage

50
Q

Clinical signs
Colic, bloat, watery diarrhea
Labored respiration, fluid sounds in lungs, bloody froth form nares, and cyanosis

DDX?

A 
Acute Selenium toxicosis 
Pneumonia 
Infectious hepatitis
Enterotoxemia 
Pasturellosis
51
Q

The subacute toxicosis caused by selenium in cattle is AKA?

A

Blind staggers

52
Q

What are the stages of blind staggers?

A

1- poor appetite, aimless wandering, circling, walking through objects, with normal respiration and temp

2- depression, incoordination, foreleg weakness and walking on knees, anorexia

3- colic, hypothermia, emaciation, clouded cornea, paresis, coma and death

53
Q

What condition do pigs get from subacute Se toxicosis ? What are the clinical signs?

A

Porcine focal symmetrical poliomyelomalacia

Neurological signs include incoordination, lameness, and paralysis
Other signs include alopecia, hoof abnormalities, and separation of the hoof

54
Q

What are the specimens of choice for laboratory analysis (acute and chronic )?

A

Acute - blood, kidney, and liver

Chronic- hair and hoof (must be washed before analysis )

55
Q

T/F: blood/plasma glutathione peroxidase activity correlates will with blood Se concentration in cattle, sheep, and swine

A

True

-does not correlate well in horses

56
Q

What is the DDX for chronic Se toxicosis?

A 
Molybdenum 
Fluoride
Freezing 
Ergotism 
Laminitis
57
Q

What is the treatment for acute Se toxicosis?

A

Saline cathartics
Symptomatic - oxygen and treatment of pulmonary edema and shock
Acetylcystine

58
Q

How can you prevent Se toxicicity?

A

Soil and forage testing
Remove from seleniferous areas
Addition of copper to the diet, high protein diet, increasing sulfur-containing proteins may reduce toxicosis
Addition of organic arsenicals to diet increase biliary excretion of selenium

RUSVM Toxicology Summer 2019 (10 decks)

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