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Toxicology > Exam 4: Metals > Flashcards

Exam 4: Metals Flashcards

1
Q

What form of chromium is considered to contribute most to observed toxicosis?

A

Hexavalent chromium (CrVI/Cr6+) is a recognized carcinogen

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2
Q

What role does copper disposition play in susceptibility to copper toxicity?

A

Accumulation of copper in the liver leads to chronic hepatitis in affected dogs that may progress to cirrhosis
Anorexia, lethargy, vomiting, weight loss

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3
Q

What role does genetics play in the copper disposition process?

A

Bedlington Terriers = inherited metabolic defect resulting in impaired biliary copper excretion - defect in COMMD1 gene

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4
Q

What is the primary mechanism by which copper exerts toxicosis?

A

When copper levels get too high and saturate copper reservoirs in the cell, “free” copper ions exist in the cell, undergo redox reactions, and lead to damage ot membranes, proteins, and nucleic acids primarily through reactive oxygen species

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5
Q

What is the primary mechanism by which Molybdenum exerts toxicosis?

A

Toxicity of Mo is intricately tied to its interactions with copper and sulfur - predominant manifestations of Mo poisoning are associated with secondary copper deficiency

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6
Q

What is the primary mechanism by which iron exerts toxicosis?

A

Hydroxyl radical reacts with the first thing it hits and can damage proteins, nucleic acids, and lipid
Damage it creates can also propagate as it reacts to generate another radical

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7
Q

What is the primary mechanism by which manganese exerts toxicosis?

A

Oxidative stress and generation of ROS
Mechanism is varied and may involve disruption of proteins involved in oxidative phosphorylation in the brain as well as mitochondrial calcium flux and sequestration

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8
Q

What is the primary mechanism by which zinc exerts toxicosis?

A

Unknown, but plays many roles in regulation of cell death and protection as well as interactions with other metals
Toxicity at high levels may have something to do with oxidative stress

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9
Q

What clinical signs predominate for copper toxicity?

A

Dogs (initial) = salivation, vomiting, nausea
Dogs (advanced) = pu/pd, icterus, diarrhea, ascites
Small ruminants = weakness, panting, pale mm, icterus, dark brown/red urine, abortion, death

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10
Q

What clinical signs predominate for molybdenum toxicity?

A

Sheep/cattle (acute)= feed withdrawal, lethargy, weakness, hind limb ataxia progressive to front limbs and recumbency
Chronic = teart scours (diarrhea), poor weight gain, anemia, achromatrichia, alopeciea, limb deformities

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11
Q

What clinical signs predominate for iron toxicity?

A

GI cell necrosis
Fluid loss
Cardiotoxicity

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12
Q

What clinical signs predominate for manganese toxicity?

A

Primary chronic effects are neurological
Reduced appetite and growth rate, anemia and abdominal discomfort, abortions and cystic ovaries

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13
Q

What clinical signs predominate for zinc toxicity?

A

Dogs/cats = vomiting, diarrhea, red urine, icterus, liver and kidney failure, anemia
Foals = non-painful joint involvement
Other livestock = lethargy and anorexia, decreased weight gain or milk production, anemia, icterus

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14
Q

What treatments are available for zinc poisonings?

A

Antacids, proton pump inhibitors, removal of FB
IV fluids, blood transfusion, sucrafate for GI bleeding, CBC + chem (liver/kidney function)
Chelation therapy is controversial as can facilitate zinc absorption from the stomach if FB are still present

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15
Q

What treatments are available for manganese poisonings?

A

GI decontamination
Chelation therapy (EDTA increases urinary excretion)
Antioxidant therapy (Vit E, N-acetylcysteine)
Symptomatic and supportive care

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16
Q

What treatments are available for iron poisonings?

A

GI decontamination
Chelating agents (enhance urinary elimination with deforoxamine)
Symptomatic and supportive care

17
Q

What treatments are available for copper poisonings?

A

Feed low copper diet (avoid high copper organ meats)
Chelating agents (D-penicillamine, trientine hydrochloride to enhance urinary elimination)

18
Q

What is the basis for the interaction of copper, molybdenum and sulfate in ruminants?

A

Copper:molybdenum ration of 6:1 is optimal
Less than 2:1, molybdenum toxicosis will occur
Greater than 15:1 may cause copper toxicosis
Toxicity of Mo is intricately ties to its interactions with copper and sulfur, predominant manifestations of Mo poisoning are associated with secondary copper deficiency

19
Q

What role does the copper, molybdenum, sulfate interaction in ruminants play in potential toxicities?

A

Molybdenum and sulfur form thiomolybdate in the rumen and form an insoluble complex with copper - therefore, adding molybednum and sulfur to the diet of ruminants decreases copper availability

20
Q

How does iron “exist” in living systems?

A

Bound to transferrin in blood
Bound to lactoferrin in mild
80% bound to Hb, Mb, and other heme-containing enzymes
Remaining bound intracellularly to ferritin and hemosiderin

21
Q

What role does pH play in potential zinc poisoning?

A

Stomach acid provides for rapid release of zinc from ingested metallic objects

22
Q

How does zinc differ from other metals with regards to chelation therapy?

A

Chelation therapy is controversial as it can facilitate zinc absorption from the stomach if FB are still present and eluting zinc

23
Q

What role do metals play in biology?

A

Certain metals are needed for many biological reactions
Vital biochemical processes require energy inputs and catalysts

24
Q

Where are thiols found in biomolecules?

A

Present mainly in cysteine, tripeptide glutathione, and cysteine residues of proteins and enzymes
Located within the the active site of many enzymes

25
Q

Why are thiols important in the mechanism of action of many metals and metalloids?

A

Play fundamentally important structural and functional roles
Located within the active sites of many enzymes
Directly involved in catalysis

26
Q

What is metallothionein and what role does it play in the mammalian cell?

A

Low MW protein with cysteine residues - can bind 7 atoms of Cd and other metals
MT can sequester heavy metals and prevent oxidation of critical protein or non-protein thiols

27
Q

What is the primary source for exposure to mercury (Hg)?

A

Global contaminant - emissions (mining, coal combustion, volcanic eruptions)
Rare in domestic animals - usually due to accidental consumption of obsolete products containing Hg, high fish consumption in Yukon sled dogs

28
Q

What is the primary source for exposure to cadmium (Cd)?

A

Mineral supplements in feed
Application of phosphate fertilizers
Sewage sludge on pastures/fields
Clover, willow, tobacco plants
Cigarette burning

29
Q

What is the primary source for exposure to Arsenic (As)?

A

Insecticides
Immiticides
Herbicides
Treated wood
Water

30
Q

What is the primary source for exposure to Lead (Pb)?

A

Batteries
Pb weights (curtains, fishing)
Pb based paints
Pb shot
Pastures near Pb smelters
Leaded gas

31
Q

What “form” of mercury is considered the most significant with regards to toxicity and what specifically about the molecular makeup allows it to access the CNS?

A

MeHg (organic) - methylmercury
Highly bioavailability
Crosses the BBB - amino acid transporter helps cross the BBB through moleculary mimicry
Potent neurotoxicant especially for the developing fetus

32
Q

What effective treatments exist for cadmium toxicosis?

A

Minimize/reduce exposure
EDTA, BAL/dimercaprol, DMSA NOT effective
BAL can increase nephrotoxicity

33
Q

How do the different forms of arsenic differentially target metabolism and what is the selectivity of target tissues to arsenic toxicosis?

A

Arsenite more toxic than arsenate and inorganic forms are more toxic than organic forms
Arsenite = binds with lipoic acid (TCA cofactor) effecting energy metabolism
Arsenate = uncouples ox phos because it competes with phosphate during conversion of ADP to ATP

34
Q

What is the most likely source of lead poisoning in cattle in North America?

A

Lead-acid batteries found on agricultural pasture lands

35
Q

What treatment options are available for acute lead poisoning?

A

Remove Pb objects from GI tract
Ca-EDTA
DMSA (dimercaptosuccinic acid)

Toxicology (13 decks)

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