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Toxicology VAP845 > L3. Heavy Metals > Flashcards

L3. Heavy Metals Flashcards

1
Q

Arsenic (As)

A

Chemistry - metalloid

  1. Elemental, organic, inorganic
  2. Trivalent (+3) comes as organic and inorganic
  3. Pentavalent (+5) comes as organicn or inorganic
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2
Q

Arsenic (As)

Sources

A

Mining sites and smelters

Insecticides and Herbicides

Wood Preservative

Medicinal (Heartworm Therapy)

Feed Supplements

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3
Q

Inorganic Arsenic

Sources

A

Old pesticides - Iron arsenate, herbicides

Terro ant poison

Ashes of CCA lumber

Chromated copper arsenate

common source for cattle

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4
Q

Chromated Copper Arsenate

A

Discontinued as residentail areas in 2003

Still used in commercial, industrial and ag

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5
Q

Arsenic (As) Toxicokinetics

A
  1. Adsorption of different forms is variable
    1. This is a major factor in toxicity
  2. Distribution:
    1. Accumulation initially inliver then slowly distributed to other tissues later accumulates to keratinized tissue
    2. Crosses placenta and is embryotoxic
    3. Crosses blood-brain barrier
    4. Hair and keratinized tissue - eliminated int he feces and urine
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6
Q

Inorganic Arsenic (As)

Toxic Mechanisms

A

Binds with sulfydryl enzymes

Blocks cellular respiration

Acts on tissues with high respiration - gut epithelium, capillaries

Toxicity: Trivalent is 5-10X more toxic than pentavalent

Arsenite (3+) > arsenate (5+) > organic Arsenic

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7
Q

Heartworm Therapy with Arseinc:

Thiacetarsamide - Caparsolate

A

Vomiting

Liver and Kidney Damage

Ivermectin, melarsomine, and Diroban commobly used now to treat heartworm in dogs

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8
Q

Arsenic (As)

Toxic Mechanisms

A
  • Arsenite – As3+
    • inhibits ATP synthesis
    • Sulfhydryl inhibition
    • a-lipoic acid – TCA cycle
  • Phosphate Competition
    • uncouples oxidative-phosphorylation
  • Arsenate-As5+
    • resembles Pi in structures and reactivity, replaces phosphate
  • Arsenic is eliminated/detoxified rapidly compared to other heavy metals:
    • most intoxications are acute or subacute
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9
Q

Inorganic Arsenic (As)

Clinical Signs

A

Effects the GI tract

Vomiting, intense abdominal pain, diarrhea, fluid loss, maybe acute death, marked dehydration, weakness, staggering gait

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10
Q

Inorganic Arsenic (As)

Lesions

A

GI hemorrhage, edema, fluid filled, shoughing mucosa, renal tubular degeneration

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11
Q

Inorganic Arsenic (As)

Diagnosis

A

Arsenic analysis of kidney, liver >8ppm

Suspect material

Blood is not a good diagnostic source

Urine contains Arsenic if kidneys are functioning

Accumulates in hair for chronic exposure

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12
Q

Inorganic Arsenic (As)

Treatments

A

Most attempts are futile

Rehydration

BAL (dimercaprol) is classic antidote but best if used before signs occur

Thiotic acid (50mg/kg q8 hr)

Succimer (DMSA) same for lead tox (SA)

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13
Q

Iron (Fe)

A

Common in human dietary supplements and vitamin/mineral tablets

Ingestion fo concentrated iron sources can be toxic to children and pets

Takes a lot of flintstone vitamins to poison a 40 pound child with iron

Injections

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14
Q

Iron (Fe) Toxicity

A
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15
Q

Iron (Fe)

Pathogenesis

A
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16
Q

Iron (Fe)

Clinical effects:

4 stages

A
  1. 0-6hrs
    1. corrosive effect
    2. Nausea, vomiting, diarrhea, GI hemorrhage
  2. 6-12 hrs
    1. apparent remission
  3. 12-24 hrs
    1. severly poisoned dogs
    2. severe lethargy
    3. Reoccurence of GI sings
    4. metabolic acidosis
    5. Liver necrosis
    6. Coagulopathy
    7. Cardiovascular collapse, shock
  4. Several Weeks later
    1. scarring and stricture of GI tract
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17
Q

Iron (Fe)

Diagnosis

A

History, clinical signs

Abdominal radiographs (mass of pills in the stomach)

SerumL Fe

Normal 80-240 ug/dl

if 300-500 monitor closely

if > 500 - chelation therapy

Serum total iron binding capacity (if serum Fe >TIBC = poisoning likely)

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18
Q

Iron (Fe)

Treatment

A

Emetic in alert animals, gastric lavage or gastrostomy

Fluids, electrolytes, acid/base balance

GI Protectants (tagament)

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19
Q

Iron (Fe)

Chelation Therapy

A

Deferoxamine

Initial IV infusion …. 15mg/kg/hr

IM 40mg/kg every 4-8 hrs

Continue until serum Fe is below 350 ug/dl or less than the TIBC

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20
Q

Mercury (Hg)

A

Long history of toxicosis and pollution

Toxicosis is infrequent and sporadic

Cases in the last 30 yrs are associated with Hg fungicide treated seed

Fungicide treatment has been cancelled for most countries

Current issues are mostly from environmental pollution

21
Q

Mercury (Hg)

Traits

A

unusual metal becuase it is a liquid at normal temperatures

Hg vapor poses a substantial hazard

Inorganic and orgnaic forms exist

22
Q

Mercury (Hg)

Environmental Concern

A

3 different forms in the environment

  • Elemental Hg, Hg0 - metallic or vapor
  • Inorganic mercury, Hg salts, HgCl2
  • Organomercurial compounds, alkyl forms = elthyl, methyl, propyl, dimethal, and aryl forms of Hg such as phenylmercuric acetate

Hg accumulates as alkyl, methyl, and ethyl merucry

23
Q

Mercury (Hg)

Sources

A

Batteries - discontinued in USA in 1996

Some disc batteries contian mercury oxide = small risk

Some pharmaceuticals - calomel - used as an antiseptic save, in laboratory electrodes ans as a fungicide

Idustrial effluents, sewage sludge

Ocean waters - marine fish, shell fish, mackerel, shark, swordfish, tilefish, tuna

Elemental Hg - used in thermometers, barometers, fluorescent tubes

24
Q

Mercury (Hg)

Toxicosis

A

Elemental Hg is low in toxicity orally

Hg salts; 1mg/kg/day is toxic to cats in 15 days

Hg salts: large animals 8-12 mg/kg

Methyl (alkyl) mercury 0.2-0.5mg/kg

Phenyl (aryl) mercury: swine 1 mg/kg

Overall highly toxic on a chronic basis

25
Q

Mercury (Hg)

Clinical Effect

A
  • Inorganic:
    • GI and renal tubular necrosis
  • Organic:
    • neurologic fibrinoid degeneration of arterioles, neuronal necrosis → blindness, staggering, incoordination, recumbancy, death
26
Q

Mercury (Hg)

Absorption

A

elemental Hg poor GIT absorption, but vapors are absorbed and dangerous

Salts and organ mercurial are absorbed in the GIT

27
Q

Mercury (Hg)

Excretion

A

kidney → urine; fecal; lungs

28
Q

Mercury (Hg)

Mechanisms of Toxicity

A

Primary targets are the kidneys and CNS

Bind to sulfhydryl groups

Inhibits enzymes and protein synthesis

Inhibit mitochondrial function by binding to alpha lipoic acid and thioctic acid

Sulfer containing organic acid cofactor involved in aerobic mtabolism

Pyruvate dehydrogenase complex

29
Q

Mercury (Hg)

Diagnosis

A

Whole Blood >1ppm

LIver

kidney

hair

urine

feeds

30
Q

Mercury (Hg)

Treatment

A

Acute Exposure: egg white, activated charcoal; sodium thiosulfate

Saline cathartic or sorbitol

Oral penicillamine orally

DMSA

Chronic organic - Se, Vitamin E

31
Q

Mercury (Hg)

Public Health

A

Bioaccumulation and bio magnification int he food chain

Sediments → fish → mammals, including humans

Hg residues in kidney and muscle tissue, currently most concern in fish

Higher concentrations range form 0.7-1.5 ppm

32
Q

Thallium (Tl)

A

Discovered in 1861 by Sir Williams Crooks

1862 by French Chemistr Claude-Auguste Lamy

In Greek, Thallos “green twig”

Monovalent and trivalent salts are very toxic

Elementary Tl is non toxic

33
Q

Thallium (Tl)

States

A

Thallic +3 oxidation state

Thallous +1 oxidation state

34
Q

Thallium (Tl)

Source

A

World production is 12 tons/year

Emissions 1500 tons/year in granite and coal

Semiconductors, photocells, optic glass, thermometers

Tl201 radiocative tracer used in heart scintigraphy to detect myocardial ischemia

Occurs with other minerals

Heavy Metals: Very toxic and highly comulative

Rodenticide: 1920’s-60’s: tasteless, oderless, easily masked in baits

Once used as a depilatory

Off the market since 1965

Occasional exposure form old products, cleanout of buildings

35
Q

Thallium (Tl)

MOA

A

Half life is 1-30 days

Similarities in charge between K+ (Tl will substitutes for K+)

1) Blocks energy utilization by Na-K ATPase channel; blocks active transport of K+ across the cell membrane

Tl ahs a 10 fold greater affinity than K+ in neuronal, cardiac and skeletal muscle cells

2) Blocks energy production from glucose: ADP to ATP by pyruvate kinase = K requiring enzyme

Inhibition by binding with 50 fold affinity compared to K+

3) Damages riboflavin, forming and insoluble complex and intracellular sequestration of Vitamin B6
4) Binds to SH groups and interferes with formation of disulphide bonds in heratin, structural damage to hair and nails → depilatory
5) causes activation or inhibition of other enzymes

36
Q

Thallium (Tl)

Clinical Effects

A

Multisystemic Disease:

  • Gi necorsis - similar to arsenic, severe hemorrhagic gastritis, congested oral mucosa
  • Neurologic - trembling, motor paralysis, mental retardation
  • Alopecia and skin sloughing form 7 days to 2-3 weeks after ingestion, renal and liver injury
  • Blindness
37
Q

Thallium (Tl)

DIagnosis

A

Urine thallium (any concentration is significant)

Kidney, liver, feces,

Feces

38
Q

Thallium (Tl)

Treatment

A

Radiofardase - prussian blue insoluble capsules

Treatment is ineffective once clinical signs are apparent

Dithizon: specific chelatory fot Tl

39
Q

Fluoride (Fl)

A

Reactive, water soluble non-metal common in nature, but variable in distribution

Sources include:

Minind deposits

Rock phosphate

Water form deep wells/geothermal water

Industrial pollution

40
Q

Fluoride (Fl)

Sources

A

Drinking water and plants

Mineral deposits – effluent, tailings

Pesticides

Product of industrial processing of aluminum ores or phosphate fertilizers

Fertilizers and calcium/phosphate minerals must be deflourinated

Past history: Aerial contamination form aluminum smelters and steel mills

41
Q

Fluoride (Fl)

MOA

A

Affects mineralized tissue — teeth,a nd bone

Deposited in hydroxyapatite crystal of bone and distorts normal haversian system remodeling

Dental fluorosis si dystrophic formation of dentin and enamel in erupting teeth only

42
Q

Fluoride (Fl)

Clinical Effects

A

Chonic Exposure:

Progressive debilitating disease

Cattle, horses, wild herbivores

Osteroflourosis:

Bone formation on outside of long bones produces lameness

Dental Fluorsis:

Softening of tooth enamel, early wear

Does not readily cross the placenta

43
Q

Fluoride (Fl)

Kinetics

A

Rapidly absorbed; excreted through urine

About 50% of asbsorbed dose requesters in bone

Mostly in developing/remodeling bone

Developing teeth

erupted teeth are unaffected

44
Q

Fluoride (fl)

Clinical Signs

A

Large, acute exposure cause GI irritation and kidney damage

Moderate, chornic exposures are more common, affects bones and developing teeth

45
Q

Fluoride (Fl)

Diagnosis

A

History: exposure to feeds, environment

Clinical Signs: Lameness, weight loss, elongated hooves, Lapping water

Lesions:

Dental Fluorosis in erupting teeth

Exostosis of limbs, ribs, mandible

Fl analysis: uring, bone

Feed, water

46
Q

Fluoride (Fl)

Treatment / Management

A

No Specific Treatment

Poor prognosis

Pain management and soft feed may allow salvage following extended recovery periods

Avoid exposure

Aluminum or Ca-carbonate at 1% of diet will reduce fluoride absorption

47
Q

Fluoride (Fl)

Prevention

A

Best to prevent

Environmental impact

Food Safety - not significant

48
Q

Fluoride in drinking water

A

Controversial

  1. Fluoridation is a violation of the individual’s right to informed consent to medication
  2. Fluoride is not an essential nutrient
  3. Hundreds of research articles published over the past several decades have demonstrated potential harm to humans form fluoride at various levels of exposure, including levels currently deemed as safe
  4. It also poses threats to animals as wellas the environment as large

Toxicology VAP845 (15 decks)

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