Heavy Metals Flashcards
Mode of action for Lead
Altered GABA transmission, Displaced Calcium from binding sites, altered nerve and muscle transmission, decreased smooth muscle contraction and interference with mineral absorption.
Lead Clinical sings in a dog
Primarily GI signs- V, D, anorexia, tender abdomen
Secondarily: Neurologic signs- lethargy, ataxia, convulsions
Lead Clinical signs in a cow
NEurologic signs predominate (blindness, increased vocalization, ataxia, circling, aimless wandering)
GI signs are secondary- Rumen stasis, Gaunt, anorexia
Lead Clinical signs in horse
Paralysis of recurrent laryngeal nerve -> Roaring
Birds clinical signs with lead
Neurologic, muscle wasting
What Diagnostic samples do you want with Lead. Both post-moretem and ante-moretem
Antemortem- Whole blood in a purple tp tube, Milk
Post mortem- Liver, Kidney, Bone, Brain
Treatment methods for Lead
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
Arsenic Mode of action
3+ binds to Lipoic Acid & blocks cellular respiration -> decreased ATP, capillary dilation -> Edema
5+ substitutes for P, uncouples oxidative phosphorylation -> Decreased ATP
Clinical signs associated with Arsenic
Gastrointesstinal, bloody diarrhea
Swine Clinical signs associated with Arsenic
Goose stepping, lack of proptioception, blindness
Appropriate samples for Arsenic
Sciatic and optic nerve- demyelination of the nerve
Gross lesions seen with Arsenic
Necrohemorrhagic gastroenteritis, ulcerations
Microscopic lesions associated with arsenic
GI and renal necrosis, peripheral neuromuscular degeneration, submucosal edema
Treatment for Arsenic
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
Mercury Toxicity
Organic > Inorganic > Elemental
Mercury Mode of action
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
Clinical signs associated with Mercury
ORganic- stomatitis, conjunctivitis, blindness, ataxia, paresis, abnormal posture, paralysis, coma, death
Inorganic- vomiting, diarrhea, stomatitis, oliguria, death
What samples are appropriate for Mercury
Liver, kidney, Brain for Hg testing
Whole blood and urine in acute cases
Lesions associated with Mercury
Ulcerative/necrotic gastroenteritis, renal tubular necrosis, demyelination of peripheral nerves in swine
Cerebellar hypoplasia in cats
Treatment of Mercury
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
environmental concerns associated with Mercury
Contaminated livestock should not be used for consumption
Mode of Action for Zinc
Unknown, but causes hemolysis, GI irritation and erosion
Clinical sign of dogs with Zinc
Hemolytic anemia, GI irritation , anorexia, V, D
Clinical signs of ruminants associated with Zinc
Decreased growth and efficiency
Clinical signs associated with equine and Zinc
Lameness, and Laryngeal paralysis
Swine clinical signs associated with Zinc
Lameness
Sheep clinical signs associated with Zinc
diarrhea
Sample collection for suspect Zinc cases
Pancreas, Liver, GI tract
Royal blue top tube with Red stripe for TM evaluation
Gross lesions associated with Zinc
Pancreatitis, icterus, GI erosions & ulcerations, hemorrhagic joints in swine, OCD in horses
Treatment of zinc
Remove foreign body, Supportive care
CaEDTA
D-penicillamine- oral, but very expensive
Iron toxicity: routes of administrations
IV >IM>oral
Iron MoA
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
Samples for Iron cases
Serum , liver, feed, radiographs
Lesions for Iron cases
Brown staining at injection sites, GI errosion and ulceration
Treatment for Iron cases
Deferoxamine until effect.
Wine colored urine is associated with what heavy metal?
Iron
Fluoride MoA
REplaces hydroxy appetite in crystaline structure of bone. Mineralization is delayed/altered
Presentations for Fluoride cases
Osteofluorisis- lameness, exostosis
Dental fluoresis: dystrophic formation of the dentin and enamel in erupting teeth. Softening of toothe enamel- early wear
Appropriate sample for Fluoride cases
Bone, urine, Radiography looking for exostosis
Treatment for fluoride cases
reduce fluoride in the diet
Thallium source
Mycoplasma agar plate
Clinical signs associated with Thallium
Gastrointestinal (profuse vomiting)
Neurologic (tremors, decreased mentation, paralysis)
Dermal (sloughing of skin, alopecia)
Lesions associated with Thallium
Hemorrhagic gastritis, enteritis, colitis, pulmonary edema & hemorrhage.
Dermal necrosis
Treatment of Thallium
Prussian blue and Dithizone- ineffective if clinical signs are present
What heavy metal is associated with foot baths?
Copper
What Cu:Mo ratio has Cu tox potential in sheep
> 20:1
Copper MoA
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
Clinical signs associated with Copper
Diarrhea, liver damage, schock.
No clinical signs during the accumulation phase
Icteric, and hemoglobinuria
What samples are good choices for Copper
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
Gross lesions for Copper case
Icteric MM, visceral tissues, fat Gun metal- black kidney Liver is very friable Serum- hemolyzed -dark red - brown Urine- hemoglobinuria
What stain is specific for Copper
Rhodanine Stain-
Herd level treatment for Copper
Na molybdate
Zinc
Individual level treatment for copper
D-penicillamine (very expensive)
Ammonium Tetrathiomolybdate- must be compounded
Bedlington terrier having decreased liver function associated with what heavy metal
Copper
Molybdenum MoA
Copper antagonist
Promotes Cu excretion.
What species is most susceptible to Mo
Cattle- especially in beef herds
Clinical effects of Molybdenum
greenish.bubbly diarrhea
Copper deficiency (decreased immune system funciton, decreased melanin synthesis) “Red” Black angus
Anemia
What samples should you collect for Mo testing?
Liver, serum, feed, forage, water, soil
Treatment fo rMo
decrease exposure
Increase Cu
Copper glycinate
Multimin 90
What is the only regulated essential mineral in feed?
Selenium
MoA for Selenium
Produciton of free radicals, displacement of S from proteins, inhibition of RNA synthesis (embryotoic)
Decreased ATP synthesis
Clincal signs associated with swine and Selenium
Hind limb ataxia progressing to posterior paresis, lameness, decreased intake and growth
Clinical signs associated with chronic Selenium intoxication
Hair loss (most reported symptom) discoloration
Weakness/depression
Lameness
sample collection for Selenium
Serum, whole blood, liver, kidney, hair, hoof wall all are good options
Microscopic lesions associated with selenium
Bilateral poliomyelomalacia
Lungs: edema, congestion, hemorrhage
Kidneys: cortical necrosis
Treatment for Selenium
No effective treatment for acute cases
Subacute- wait for depletion
Chronic- no good treatment, focus on prevention.
Eliminate the exposure
