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Toxicology > Heavy metals (Bergfelt)--lead > Flashcards

Heavy metals (Bergfelt)--lead Flashcards

1
Q

What is a toxic heavy metal?

A

Dense metal or metalloid that is noted for its potential toxicity, especially in environmental contexts

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2
Q

What are 4 elements on the World Health Organization’s list of 10 chemicals of major public concern?

A

Cadmium (Cd)

Mercury (Hg)

Lead (Pb)

Arsenic (As)

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3
Q

What characteristics must a metal have to be considered a ‘heavy metal?’

A

Metal having an atomic weight greater than sodium (23) and specific gravity (density) > 5 g/cm3

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4
Q

On the health effects basis, which heavy metals are essential?

A

Cu, Zn, Co, Cr, Mn, Fe

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5
Q

On the health effects basis, which heavy metals are non-essential?

A

Ba, Li, Zr

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6
Q

On the health effects basis, which heavy metals are highly toxic and which are less toxic?

A

Highly toxic = Pb, Hg, Cd

Less toxic = Sn, Al

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7
Q

What are the 7 toxicological properties of heavy metals?

A
  • Persistence–long residual and half-life
  • Soil residence time–> 1000 years
  • Acute toxicity–plants, animals, microorganisms
  • Bioaccumulation and biomagnification–through food chain
  • Chronic and sub-lethal effects at low conc.
  • Synergistic effects
  • Teratogenic and carcinogenic properties
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8
Q

Is lead readily degraded in the environment?

A

No

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9
Q

T/F: Lead is easily absorbed and metabolized

A

FALSE

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10
Q

What occurs with oral exposure to lead?

A

Forms insoluble compounds in GIT–small amount absorbed (acidic environment)

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11
Q

How does the type of lead affect absorption?

A

Organic lead is more readily absorbed than metallic lead

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12
Q

What conditions favor dissolution and absorption?

A

Acid conditions

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13
Q

What was the Flint water crisis (in a nutshell)?

A
  • Allowable lead levels in water = 15ppb
  • What comes out of faucets = 2ppb
  • What came out of Flint’s faucets = 13,200ppb
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14
Q

What is an anthropogenic source of lead toxicity?

A

Aerial emission from combustion of leaded fuel, batteries waste, insecticides and herbicides

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15
Q

What is the most common source of lead toxicosis in animals?

A

Lead-based paints

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16
Q

T/F: A thumbnail sized chip of lead-based paint may contain 50-200 mg of lead

A

TRUE–the lowest lethal dose in dogs is 191 mg/kg!

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17
Q

Sources of exposure to lead toxicity?

A
  • Paint (old painted surfaces, fences)
  • Old batteries
  • Plumbing, solder, putty
  • Galvanized wire
  • Some linoleum, imported ceramics/pottery
  • Contamination from industry (lead oxide)
  • Lead shots, weights, fishing sinkers
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18
Q

T/F: An estimated 10-20 million birds and other animals die from lead poisoning each year in the US

A

TRUE

:(

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19
Q

Which birds are most vulnerable to lead toxicosis?

A

Waterfowl–can ingest spent pellets or lost fishing tackle

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20
Q

What can become a source of secondary lead poisoning for wild animals?

A

Birds shot with lead pellets and not retrieved

(bioaccumulation/biomagnification)

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21
Q

How common is lead toxicosis?

A

It is one of the most common toxicoses! Acute to chronic, Pb displaces Ca and Zn!

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22
Q

Why are young animals more sensitive to lead toxicosis than adults?

A

Greater GIT absorption and immature BBB

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23
Q

Which species are most susceptible?

A

Cattle, horses, pets, waterfowl, and pet/wild birds

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24
Q

T/F: Dogs are more frequently poisoned because of their indiscriminate eating habits

A

TRUE

(freakn labs)

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25
Q

Which species are more resistant to lead toxicosis?

A

Goats, swine, and chickens

(avian plumbism or avian saturnism)

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26
Q

What is the most common route of lead poisoning?

A

Ingestion

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27
Q

How can lead be absorbed?

A

Dermal (poor), inhalation (rare), ingestion (oral absorption is poor, but is increased by GI acidity)

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28
Q

What decreases led absorption?

A

Calcium, zinc, or protein

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29
Q

What is the mechanism of lead absorption?

A

Absorbed by active transport using the same carrier protein as calcium

–> If patient is deficient in Ca, vitamin D, Zn, or Fe, then Pb is more readily absorbed

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30
Q

Which species is GIT absorption of lead greater in?

A

GIT absorption is greater in non-ruminants (~10%) than in ruminants (~3%)

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31
Q

What age is GIT absorption greater in?

A

Greater in immature animals (up to >50%) compared to adults (5-15%)

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32
Q

Where/how is lead distributed?

A

Throughout the body by systemic circulation–binds to erythrocyte membranes for transport (60-90%, depending on species)

33
Q

What is the main route of absorption?

A

GIT

34
Q

T/F: Lead crosses the BBB, placenta, and binds to proteins in soft tissues for 8-10 weeks

A

FALSE–it binds to proteins in soft tissues for 4-6 weeks

Everything else is true

35
Q

What is metallothionein?

A

Liver protein involved in cellular detoxification of inorganics–sequesters metal ions present in elevated concentrations

36
Q

Where does lead accumulate?

A

Active bone matrix–a reserve for several years

~83-95% in mature animals

~70-75% in immature animals

Activated by pregnancy, lactation, chelating agents

37
Q

How is lead excreted?

A

Primarily through urine, but also in milk and bile

38
Q

What does lead interfere with? What can it substitute for?

A

Interferes with biological structure and function

Can substitute for Ca2+, Mg2+, Fe2+

39
Q

What does lead form complexes with?

A
  • Forms complexes with nucleophilic functional groups (COOH, NH2, SH)
    • Most stable complex with sulfhydryl groups (-SH)
    • Increases stability (S-S to S-P to S-P-S)
    • Pb may displace Zn in some enzymes
40
Q

What does lead compete with?

A

Ca2+ in bone and alters Ca2+ movement across membranes (e.g., BBB)

41
Q

T/F: Alterations in cerebral endothelium due to lead competing with Fe2+ may lead to edema

A

FALSE–it’s due to lead competing with Ca2+

42
Q

What are the target tissues of toxicity?

A

GIT, blood, and CNS

43
Q

What might lead interfere with in the CNS?

A

GABA neurotransmission

44
Q

What does chronic exposure inhibit?

A

Heme synthesis that leads to anemia

45
Q

What else might lead to anemia?

A

Delayed erythrocyte maturation and fragility–short lifespan

46
Q

T/F: Lead can alter the release of neurotransmitters (dopamine, acetylcholine, GABA)

A

TRUE

47
Q

How can lead cause brain edema?

A

Breakdown of the BBB through toxic effect on the endothelial cells and alteration of microvascular systems

48
Q

How long can clinical signs take to appear?

A

A few hours, days, weeks, to months, depending on amount, duration, species, and other factors

49
Q

What are the main systems effected by lead poisoning?

A

GIT, hematologic, CNS

50
Q

What GIT signs are seen in lead toxicosis?

A
  • Anorexia, maybe salivation, vomiting, ‘lead colic,’ diarrhea, constipation, or rumen atony
  • Rarely megaesophagus has been reported in small animals
51
Q

What hematologic signs are seen in lead toxicosis?

A
  • Clinical signs related to anemia
  • Basophilic stippling of erythrocytes
  • Blood analysis
    • Antemortem: whole blood conc. in mammals <0.1 ppm for background and >0.35 for lead toxicosis
    • Postmortem: kidney and liver >10ppm for lead toxicosis
52
Q

What CNS signs are seen in lead toxicosis?

A
  • Anxiety, hyperexcitability, vocalization, head pressing, circling, running, maniacal behavior, seizures, tremors, blindness (more acute)
  • Pharyngeal paralysis and ‘roaring’ and seizure-like activity in the horse w/ more acute toxicity
  • CNS depression may be seen in horses and sheep and in chronic toxicosis
53
Q

What CNS signs are seen in avians with lead toxicosis?

A
  • Raptors and waterfowl show peripheral neuropathy and chronic wasting
  • Psittacines show neuro and GIT abnormalities
54
Q

What are the gross lesions associated w/ Pb toxicosis?

A

Non-specific; lead objects may be found in GIT

55
Q

What microscopic lesions are seen in Pb toxicosis?

A
  • May see cerebral cortical necrosis and poliomalacia in cattle
  • Acid-fast eosinophilic intranuclear inclusion bodies in renal tubular epithelium or hepatocytes
56
Q

What hematology changes are seen?

A
  • Increased nucleated RBCs: high demand for bone marrow to produce RBCs–> immature nRBCs released into circulation
    • Non-regenerative anemia w/ inappropriate release of nRBCs
    • 5-140 nRBCs/100WBCs
    • Basophilic stippling of erythrocytes in dogs, rabbits–differentiate from regenerative anemias
  • Fluorescence of plasma or urine porphyrins
57
Q

What is seen on radiographs following lead toxicosis?

A
  • Objects in the GIT
  • Metaphyseal sclerosis in young animals w/ chronic toxicosis
  • Rarely megaesophagus
58
Q

Urinalysis?

A
  • Inc. delta aminolevulinic acid dehydrase levels (porphyroobilinogen synthase–involved in heme synthesis)
  • Inc. urinary lead (4x or more) following EDTA administration–can result in kidney damage
59
Q

What is the specimen of choice for an antemortem chemical analysis?

A

Whole blood

>90% of circulating lead is bound to erythrocytes

60
Q

What are the blood Pb levels?

A
  • Blood Pb >0.4 ppm along w/ clinical signs is considered diagnostic
  • Blood Pb >0.6 ppm is considered diagnostic
  • Blood levels may not correlate w/ clinical signs
61
Q

T/F: Liver, kidney, and GI contents can be tested as well for chemical analysis

A

TRUE

62
Q

DDx?

A
  • Other toxicants that cause neuro signs
  • Other causes of anemia–assoc. w/ nRBCs
  • Lupinosis (acute liver atrophy) may be a differential
63
Q

Treatment: what should be done to stabilize the patient?

A

Fluid/electrolyte therapy (and ensure point of exposure is removed)

64
Q

Treatment: how can you eliminate Pb if present?

A
  • Wash it if in haircoat
  • Remove any lead from the gut before chelation
    • Chelation may enhance absorption further
  • Cathartics–magnesium sulfate may bind with Pb to form Pb-sulfate (harder to absorb and accelerates defecation)
65
Q

T/F: Activated charcoal is recommended to remove lead

A

FALSE–it is NOT recommended–does not bind well to heavy metals!

66
Q

Treatment: what is chelation therapy?

A

Use of chelating agents to detoxify an exposure to heavy metals (e.g., Pb, Hg, As) by converting them to a chemically inert form that can be excreted w/o further interaction w/ the body

67
Q

Treatment: should you be cautious w/ chelating agents?

A

YES–chelating agents can also be dangerous

Use of disodium-EDTA instead of Ca-disodium-EDTA has resulted in fatalities due to hypocalcemia and kidney damage

68
Q

What is the most common chelating agent used?

A

Calcium-disodium-EDTA

69
Q

How is Ca-disodium-EDTA administered?

A

IV–diluted and given in multiple doses (painful when used IM or SC in large animals)

70
Q

What is the primary concern with Ca-disodium-EDTA?

A

Renal injury

Treat max 5 days–if longer treatment is needed, ‘rest’ for 5 days, then resume

71
Q

Does Ca-disodium-EDTA bind to other minerals?

A

YES–Zn, Cu, Fe, and Ca; concurrent Zn supplementation is recommended

72
Q

What is ‘rebound?’

A

Pulling the lead out of the bone –> increases blood levels

Must be distinguished from re-exposure

73
Q

What is DMSA?

A
  • Dimercaptosuccinic acid (Succimer)
  • Structurally analogous to BAL (Dimercaprol)
74
Q

How is DMSA administered? What is it used for?

A
  • Orally administered, can be used alone or after treatment with EDTA or BAL
  • Used in children to treat lead toxicity
75
Q

Dimercaprol (BAL)

A
  • Can be used alone or w/ CaEDTA
    • May improve effect–crosses BBB and enhances excretion
    • Avoid if liver or renal disease
    • Given by IM injection–painful
76
Q

D-penicillamine

A
  • Given orally (can bind oral minerals)
  • Used following EDTA for chronic toxicosis
  • May be less effective
  • Potentially nephrotoxic, vomiting common
77
Q

What can be used to treat neuro signs?

A

Mannitol, diazepam or barbiturates, glucocorticoids (?)

78
Q

Adjunct therapies?

A

Taurine (inc. depleted glutathione), thiamine, Zn supplementation (if treating w/ EDTA)

79
Q

Prognosis?

A

Guarded–better if caught early

Animals may act as sentinels for human exposure–house pets

Toxicology (22 decks)

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