Lead, Zinc, and Selenium Toxicosis Flashcards
What is the most common sources of lead toxicosis?
Lead based paints
Batteries, plumbing solder, galvanized wire, lead shots, fishing sinkers.
Contaminated pastures from industry
T/F: lead is not degraded in the environment
True
How much lead is absorbed from he GI tract?
Only 1-2% because it forms insoluble compounds
Acid conditions favor dissolution
What species are most susceptible to lead toxicosis?
Cattle, horse, pet, water fowl
Why are puppies more sensitive than adults to lead toxicosis?
Greater absorption and immature blood-brain barrier
Oral absorption of lead is poor but is increased by ________
Acidity
How is lead transported in the body?
As lead proteinate on erythrocytes membrane
How long does lead stay in soft tissues?
4-6weeks
Slowly stored in bone and stays for several years
Where is lead excreted?
Urine
Small amount in bile
Can be in milk in toxic levels
What are the target tissues of lead toxicity?
CNS, GI tract, and hematopoietic system
What is the MOA of of lead?
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
What clinical signs would you see due to lead toxicosis?
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
What lesions can be causes by lead toxicosis?
Microscopic
- cerebral cortical necrosis and poliomalacia in cattle
- acid fast eosinophilic intranuclear inclusion bodies in renal tubular epithelium or hepatocytes
What laboratory diagnostics would you do if you suspect lead toxicosis?
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
What is the DDX for the following clinical signs..
Anxiety, hyperexcitability, vocalization, head pressing, circling, running, manical behaviour, seizures, tremors, and blindness
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
What is the treatment for lead toxicosis?
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
What is recommended as part of treatment for pet birds with lead toxicosis?
Dimercaptosuccinic acid (DMSA)
What is recommended for treatment following EDTA in treatment of chronic lead toxicosis?
D-penicillamine PO
What can be given for supportive treatment in lead toxicosis?
Thiamine Glucocorticoids Zinc supplement Diazepam or barbiturates Fluid therapy
Decontaminate with magnesium sulfate and removal of the lead object
What are common sources of zinc toxicosis?
Ingestion of zinc containing pennies
Galvanized wire
Zinc oxide skin ointment
Zinc containing lotions, shampoo, wound healing agents
What is the normal function of zinc in the body?
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
What is the toxicity of zinc?
100mg/kg
A ________ environment enhances zinc release and absorption
Acid
What is the MOA of zinc toxicosis?
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
What are the clinical signs associated with zinc toxicosis?
GI- vomiting, anorexia, lethargy, abdominal pain, diarrhea, pica
Hematologic - hemolytic anemia, icterus, and hemoglobinuria
Renal - azotemia, hypercreatinemia, and hyperphosphatemia
What are the lesions seen with zinc toxicosis?
Gastritis, gastric ulcers, liver damage, and tubular casts
What changes would you see in lab values in zinc toxicosis?
Sample - serum, liver,r kidney, pancreas, urine
Hemolytic anemia, icterus, hemoglobinuria
Azotemia, hypercreatinemia, and hyperphosphatemia
Decreased copper in chronic toxicosis
What is the DDX for zinc toxicosis?
Copper Naphthalene Onion Red maple Cotton seed Mustard Immune -mediated hemolytic anemia Hyperphosphatemia Phenolic DMSO Guaifenesin
What is the treatment of zinc toxicosis?
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
What disease is caused by selenium deficiency in lambs, calves, and foals?
White muscle disease
What disease is caused by selenium deficiency in young pigs?
Hepatosis dietetica
What disease is caused by selenium deficiency in chicks?
Exudative diathesis
What disease is caused by selenium deficiency in adult pigs
Porcine stress syndrome
What soils are deficient is selenium?
Northeast
Northwest
Southeast
Great Lakes
Where do you find selenium rich soils?
Midwest/western states
-> can have plants that accumulate high levels of Se
What is usually the source fo selenium toxicosis in cattle, sheep, and horses?
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)
What is usually a source of selenium toxicosis in small animals?
Improper use to selenium-medicated shampoos
What are the 3 states of selenium ?
Selenate (+6)
Selenite (+4)
Selenide (-2)
Selenium has similar properties to what compounds?
Arsenic —> can be used to enhance elimination
Sulfur —> often replace sulfur in enzymes
List the toxicity of the various forms of Se from most of least toxic.
Organic selenium in plants > selenate = selenide > synthetic organoselenium
Who has the lowest oral toxic dose of selenium, swine, cattle, or horse?
Horse < cattle < swine
What type of soils promote formation of selenate?
Arid alkaline soil (Great plains)
Toxicity of selenium can be reduced by??
High protein diet and ingestion of other elements that bind Se like copper
T/F: elemental Se is absorbed through the intestines
False
Elemental Se is not absorbed because it is insoluble in water
To what tissues is Selenium particularly distributed to?
Liver, kidney, and spleen
Chronic exposure of selenium results in high concentrations where?
Hair and food
What are the only meals that cross the BBB and cause CNS signs?
Lead and organic mercury
Where is selenium excreted?
Mainly in urine
Bile
Across placenta and milk (usually not in toxic levels)
What is the MOA of selenium toxicosis?
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
Clinical signs
Colic, bloat, watery diarrhea
Labored respiration, fluid sounds in lungs, bloody froth form nares, and cyanosis
DDX?
Acute Selenium toxicosis Pneumonia Infectious hepatitis Enterotoxemia Pasturellosis
The subacute toxicosis caused by selenium in cattle is AKA?
Blind staggers
What are the stages of blind staggers?
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
What condition do pigs get from subacute Se toxicosis ? What are the clinical signs?
Porcine focal symmetrical poliomyelomalacia
Neurological signs include incoordination, lameness, and paralysis
Other signs include alopecia, hoof abnormalities, and separation of the hoof
What are the specimens of choice for laboratory analysis (acute and chronic )?
Acute - blood, kidney, and liver
Chronic- hair and hoof (must be washed before analysis )
T/F: blood/plasma glutathione peroxidase activity correlates will with blood Se concentration in cattle, sheep, and swine
True
-does not correlate well in horses
What is the DDX for chronic Se toxicosis?
Molybdenum Fluoride Freezing Ergotism Laminitis
What is the treatment for acute Se toxicosis?
Saline cathartics
Symptomatic - oxygen and treatment of pulmonary edema and shock
Acetylcystine
How can you prevent Se toxicicity?
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
