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Toxicology VAP845 > L2. Introduction to Heavy Metals > Flashcards

L2. Introduction to Heavy Metals Flashcards

1
Q

Metals in Biology

A

Easily donate and accept electrons

Form water soluble cations through electron loss

  • Perform essential biological functions
    • Electron transfer
    • Redox reactions
    • Electrochemistry and signaling
    • Structural
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2
Q

Toxicity Mechanisms

A

Oxidative Damage: zinc

Altered electrophysiology and osmotic states: Na

Competition with “normal” elements for absorption: Mo/Cu

Incorporation into protiens in place of normal constituents: Pb/Ca

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3
Q

Metals of Most Veterinary Concern

A

lead

copper

zinc

sodium

iron

arsenic

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4
Q

Meatals - What are they?

A

A metal is a chemical element whose atoms readily lose electrons to form cations, and form metallic bonds between other metal atoms and ionic bonds with nonmetal atoms

Exist as elements or compounds

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5
Q

What is a Heavy Metal?

A

Poorly defined subset of elements that exhibit metallic properties

Relatively toxic (Pb, Sn, Hg, Ti, Au, Pt, Ba)

Considered meaningless by IUPAC

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6
Q

Toxilogical Properties

A

Cumulative in biological systems

Can change valence

Complex with organic molecules

Persistent in the environment

Can be strong oxidant

Bind to essential molecules

Many metal to metal interactions

Clinical toxic effects vary widely

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7
Q

General Considerations

A

In order to understand the basis fo heavy metal toxicity be familiar with their chemical properties and reactivity

Oxidation states

Bonding

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8
Q

Oxidation States

A

Heavy metals have multiple oxidation states

Common oxidation states of Se: -2, 0, +4, +6

This leads to the formation of different compounds having different toxicological properties

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9
Q

Bonding

A

Many heavy metals have coordinate covalent bonds

Sulfur, Oxygen, and Nitrogen bind to heavy metals through this type of bond

Can be basis for toxicity

Example: Heavy metals can bind to S atom on proteins and inactivate the enzymes

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10
Q

Lead

A

Killing people and animals for 4000+ years

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11
Q

Lead:

The king of toxic metals

A

Long use in human history

Maleable and low melting point

Forms many compounds (oxides, halides, sulfides, proteinates)

No offensive odor or taste

Highly cumulative in biological systems

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12
Q

Pb in Veterinary Medicine

A

The most common cause of Heavy metal intoxication

Poisoning most frequent in:

Cattle

Dogs

Cats, pet birds, zoo animals

Sporadically horse, sheep

Pigs resistant

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13
Q

Pb In Veterinary Medicine:

Example

A

Budgies in the zoo were poisoned by and old door in the exhibit that contained lead based paint

Curators set up the exhibit to look like an old mining set up in australia

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14
Q

Lead:

Major Effects

A

nervous system in the primary target

Mildly irritant to the GI mucosa

Anemia due to interference iwht RBC maturation

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15
Q

Lead (Pb):

Major Public Health Concern

A

Persistent in the environment

Increase Pb = Decreased IQ

No safe exposure level in people

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16
Q

Lead (Pb):

Significant in Animals

A

very commonly diagnosed in KSVDL in cattle, also often seen in dogs and pet birds

High risk to birds of prey, water fowl

17
Q

Lead (Pb):

Source

A
  • Lead carbonate used to be a common component of paint
    • strictly controlled since the 1970s
    • Old buildings/stored paint remain important sourses
  • Lead-acid batteries:
    • dumb sites, scrap cars
  • Industrial/mining pollution
  • Lead shot, Fishing weights, toys, ect.
18
Q

Lead (Pb):

Important Kinetic Factors

A
  • More surface area = more absorption
    • lead/acid battery plates
    • GIT mucosal surface area
  • Acidic environments = more absorption
    • Low pH leads ot ionization
  • More time = more absorption
    • lead particles may be trapped in the reticulum
  • Relative tissue half lives
    • blood → a few days
    • liver/kidney → weeks
    • Brain → months
    • Bone → 1000 days
19
Q

Lead (pB):

Sources for small animals

A

Pb based paint, chips, solder

Lead weights, sinkers, toys

Pb batteries

Motor oil form leaded gas engines

Old grease

Old linoleum

Pollution

20
Q

Lead (Pb):

Signalment

A
  • Seasonal incidence, spring, early summer
  • Age:
    • often younger animals
  • Location:
    • Dogs:
      • older homes, lower income areas, work places
      • Cities grew west ward from a river, east part of town has Pb, newer part does not
    • Cattle:
      • casual management, old buildings, junk piles, old machinery, unattended batteries
  • Species:
    • dogs, cattle most frequently
21
Q

Lead (Pb):

Toxicokinetics

A

Poorly absorbed …. 2% form GI tract

Dust Inhalation … Fine particles <0.5um

Lead shot/bullets in tissue …. 90% binds to RBC, some to albumin

  • Ingested lead typically requires solubilizing
    • acid environment of stomach vs, lead in soft tissue
  • Tissue binding - first to erythrocytes
  • Crosses blood-brain barrier and plancenta
    • embryo toxicity
  • Incorporation into bone:
    • storage sites, detoxification mechanism
    • Lead line: in radiographs, in gums
  • Elimination:
    • fecal
    • urinary
22
Q

Lead (Pb):

Mechanism of Action

A
  • Binding to sulfydryl groups
    • heme synthesis
    • Altered GABA transmission
  • Competition with divalent cations (Ca++) ions
    • displace Ca++ from binding proteins
    • Altered nerve and muscle transmission
  • Inhibition of membrane associated enzymes:
    • Calmodulin, Na/K pumps
  • Altered Vit D Metabolism
    • impaired Ca++ absorption and Zn related enzymes
23
Q

Lead (Pb):

Clinical Presentation

A

Clinical onset usually delayed several days.

Time for absorption, binding to active sites

Depends on form of Pb

Organic: rapidly absorbed and distributed

Metallic: Slower absorption and onset

Carbonate, nitrate, oxide salts > acetate and Chloride salts

24
Q

Lead (Pb):

Clinical Signs

Most Species

A

Onset = several days after exposure

Signs quite variable: slow vs, explosive

Gastrointestinal and Neurologic combo

Complete anorexia

CNS depression or convulsion

Species differences are important

25
Q

Lead (Pb):

Clinical Signs

Dogs

A

GI: vomiting, anorexia, tender abdomen, Diarrhea/constipation

CNS: lethargy, hysteria, convulsions, ataxia, blindness, mydraisis

Clin Path → Increased nucleated RBCs and basophilic stippling without severe anemia

26
Q

Lead (Pb):

Dogs

DDx:

A

Canine distemper, parasites

Methylxanthines, thremorgenic mycotoxins

NSAIDs

Salt Toxicolsis

27
Q

Lead (Pb):

Cats

Clinical Signs

A

Less common due to eating habits

Lethargy, anorexia, vomiting, weight loss, excessive salivation

Neurological signs can be minimal

Inconsistent nucleated RBCs and basophilic stippling

Elevated AST, ALP

28
Q

Lead (Pb):

Cats

DDx

A

OP’s, bromethalin, methylxanthines

Hepatic Encephalopathy

29
Q

Lead (Pb):

Cattle

Clinical Signs

A

More common in calves

  • GI:
    • anorexia, rummen stasis, gaunt, salivation
  • CNS:
    • blindness, muscle twitching, head bobbing, depression, bruxism, circling, convulsions
    • Acute convulsive death in calves
30
Q

Lead (Pb):

Cattle:

DDx

A

Water deprivation, polio, OPs, nervous coccidiosis, Rabies

31
Q

Lead (Pb):

Birds - pets, waterfowl

Clinical signs

A

Depressed, weak, anorectic, weight loss, esophageal paralysis, regurgitation, diarrhea,

wing droop

32
Q

Lead (Pb):

Horses

Clinical Signs

A

Recurrent laryngeal nerve paralysis results in “roaring”

Ataxia, incoordination

Foals: metaphyseal sclerosis

33
Q

Lead (Pb):

Pathology in cattle

A

Few Significant gross lesions

Pb objects in rumen or stomach

Rumen protozoa dead or inactive

Laminar Cortical necrosiss (DDx from PPM)

Inconsistent acidophilic intra-nuclear inclusions in renals tubules

Porphyrinuria

34
Q

Lead (Pb):

Diagnosis

A

History Clinical Signs

Pb in WHOLE BLOOD

>0.35ppm (0.25ppm avian)

Normal = <0.05ppm

Pb in kidney or liver

Radiography - Pb objects in gut

Peripheral blood smear in dogs

Ca-EDTA mobilization test

Urinalysis: increased delta aminolevulinic acid, Pb concentration

Submit whole blood in a Purple Top Tube

35
Q

Lead (Pb):

Therapy

A

*Remove animal from source*

  • Stop further absorption
    • decontaminate GI tract
      • cathartics, enema according to species
    • Endoscopy or gastrotomy to remove objects
    • Oral MgSA4 in cattle-laxative anf formation of insoluble PbSO4
    • Charcoal not effecitve for metals
36
Q

Lead (Pb):

Chelation

A

Treatment - increase excretion - chelators

CaEDTA-IV, SQ

D Penicillamine - Oral in SA

Succimer - approved in dogs 10mg/kg TID for 5 days then BID for 2 wks

Effective in cattle, but dosage and expensie preclude

37
Q

Lead (Pb):

Treatment

A

Supportive

  • Fluids, thiamine
  • Control Seizures:
    • valium
    • Pnetobarbital +/-
  • Mannitol, dexamethasone for cerebral edema
  • Antioxidants
    • Vit-C
    • Vit-E
    • N-acetylcysteine
  • Good Nursing care
38
Q

Lead (Pb):

Public Health

A

Children in household exposed to the same Pb source as pets - pets can be sentinals

  • Food Safety:
    • long residue time in bone
    • Transfer to milk in early lactation
    • Residues can vary from weeks to months
    • Contact state veterinarian recommended

Prevention: owner/producer education

Toxicology VAP845 (15 decks)

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