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TOX > Heavy Metals > Flashcards

Heavy Metals Flashcards

1
Q

What is a heavy metal

A

metal having a weight greater than sodium and a specific gravity density greater than 5 gm/cm3

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2
Q

Toxic properties of heavy metals

A
  • long residue and half life
  • biomagnification
  • teratogenic and carcinogenic
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3
Q

Lead tox properties

A
  • not degraded in environment
  • not absorbed or metabolized
  • In the GI tract, tends to form insoluble compounds, however acid conditions help absorption
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4
Q

Which is more readily absorbed? Inorganic or organic lead

A

Organic

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5
Q

Where is inorganic lead found

A
  • dyes, paints and pesticides
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6
Q

Inorganic lead is or ins’t soluble in water

A

is not

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7
Q

Organic lead uses

A

anti knocking agents in gasoline products

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8
Q

Organic lead properties

A
  • high soluble in organic solvents
  • can be absorbed by skin
  • accumulates in fat
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9
Q

Largest human source of exposure to lead

A

aerial emission from combustion of leaded fuel, battery waste, insecticides and herbicides

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10
Q

Most common source for animal lead toxicosis

A
  • consumption of lead based paints
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11
Q

Birds and lead toxicity

A
  • waterfowl are most vulnerable (spent lead pellets or lost fishing tackle)
  • Birds shot with lead pellets are a source of secondary infection
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12
Q

Younger or older animals are most sensitive to lead toxicity?

A
  • younger
  • crosses BBB
  • greater GI absorption
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13
Q

Which species is more frequently poisoned by lead?

A

dogs due to indiscriminate eating patterns

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14
Q

Which animals are more resistant to lead poisoning

A

goats, swine and chickens

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15
Q

Lead toxicokinetics

A
  • dermal and GI absorption is poor (unless in acidic environment)
  • Calcium, zinc and proteins decrease absorption
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16
Q

Calcium deficiency will have what effect on lead absorption

A
  • greater effect as lead binds to the same carrier proteins

- will have more of a chance to jump on

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17
Q

How is lead distributed in the body

A
  • system circulation

- binds to erythrocyte membrane transport

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18
Q

Is lead able to cross the placental barrier

A

YES!

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19
Q

How long does lead bind to proteins in soft tissue

A
  • 4-6 weeks

- metallothionein= liver protein that stores metal ions

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20
Q

where can lead accumulate and be biologically inactive

A
  • bone matrix

- reserve for several years

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21
Q

How is lead excreted

A
  • urine mostly but also bile and milk
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22
Q

MOA of lead toxicity

A
  • competes with calcium in bones and alters its movement across membranes
  • can interfere with GABA neurotransmission
  • chronic exposure inhibits heme synthesis = anemia
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23
Q

lead toxicity clinical signs

A
  • anorexia, salivation, vomiting, lead colic, rumen atony
  • sometimes megaesophagus
  • signs of anemia
  • basophilic stippling of erythrocytes
  • CNS signs
  • pharyngeal paralysis
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24
Q

Lesions from lead poisoning

A
  • non- specific grossly
  • can see cerebral cortical necrosis and poliomalacia in cattle
    eosinophilic intranuclear bodies in renal tubular epithelium
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25
Q

Hematology Lab results from lead toxicosis

A
  • non regenerative anemia
  • few reticulocytes
  • basophilic stippling in dogs and rabbits
  • abnormal hemoglobin conc.
  • fluorescence of porphyrins
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26
Q

Chemical analysis results with lead toxicosis

A
  • lead bound to erythrocytes

- blood is with lead greater than 0.4 ppm is diagnostic

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27
Q

Treatment for lead toxicosis

A
  • fluids and electrolytes

- eliminate by washing animal, gastric lavage, cathartics

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28
Q

What should you not use in treatment of lead toxicosis

A

ACTIVATED CHARCOAL

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29
Q

What is chelation therapy

A
  • an agent that forms multiple bonds with metal ions in order to make them inert and excretable
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30
Q

Calcium disodium EDTA

A
  • most common chelating agent
  • given IV
  • cannot give for more than 5 days due to renal injury
  • need to supplement with Zn because it will also bind to that
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31
Q

Dimercaptosuccinic acid (DMSA, Succimer)

A
  • BEST in birds
  • Orally administered
  • can be used alone or after treatment with EDTA
  • doesn’t bind to essential minerals
  • less nephrotoxic
32
Q

Dimercaprol (BAL)

A
  • Can be used alone or with EDTA
  • crossed the BBB and enhances excretion
  • avoid with liver and renal disease
  • Given IM- PAINFUL
33
Q

D- penicillamine

A
  • Given orally
  • used following EDTA
  • less effective
  • can be nephrotoxic
  • vomiting is common
34
Q

Lead toxicity prognosis

A
  • mild-moderate signs = good

- severe central nervous signs= guarded to poor

35
Q

lead toxicity on radiograph

A
  • accumulates in active bone matrix
  • inhibits normal remodeling of long bones
  • lead lines
36
Q

Zinc toxicity

A
  • Ingestion will cause zinc salts when combined with acid in the stomach
37
Q

Zinc properties

A
  • needed for growth, wound healing, reproduction
  • helps taste and smell receptors work
  • component of many enzymes and proteins
38
Q

Zinc sources of exposure

A
  • ingestion of pennies
  • used to galvanize metals to prevent rusting
  • batteries
  • zinc oxide ointments
  • overdose of dietary supplement
39
Q

Zinc toxicity

A

Acute LD50 is 100 mg.kg zince salts

40
Q

How many pennies does a dog have to eat for subacute zinc poisoning

A

around 5

41
Q

Why does chronic zinc typically occur

A

In the diet

42
Q

Zinc toxicokinetics

A
  • absorbed through small intestines
  • acid and chelating agents helps to increase absorption
  • interferes with copper and iron use by the body
43
Q

Where is most zinc metabolized/ extracted from

A
  • the liver
44
Q

MOA of zinc toxicosis

A
  • largely affects RBC, kidney liver and pancreas

- often causes intravascular hemolysis

45
Q

Accumulation of zinc

A
  • Rapid accumulation in pancreas, liver, kidney, spleen and reproductive organs
46
Q

Excretion of zinc

A
  • primarily in the feces (bile), pancreatic juice and mucosal cells
  • 10% in urine
47
Q

Zinc Toxicity clinical signs

A
  • GI irritation
  • RBC damage (hemolytic anemia)
  • Renal damage
  • livestock= decreased milk/ weight gain
  • lameness and stiffness in foals
48
Q

Lesions with zinc poisoning

A
  • gastritis/ gastric ulcers
  • renal tubular casts
  • liver damage
  • pancreatitis
49
Q

Chemical analysis results with zinc toxicosis

A
  • need to use trace elements tube for analysis

- royal blue top

50
Q

Lab work results for zinc tox.

A
  • hemolytic anemia
  • icterus
  • hemoglobinuria
  • azotemia
  • hyper phosphatemia
51
Q

Zinc toxicosis treatment

A
  • remove foreign bodies (emesis, endoscopy, surgery)
  • cathartics
  • supportive care
52
Q

Should you use chelating agents with zinc toxicosis

A
  • not initially as it may cause zinc redistribution

- can use after EDTA

53
Q

Zinc prognosis

A
  • guarded to poor with severe hemolytic crisis but good otherwise
54
Q

25% of Iron in the body is in what form

A
  • Ferric (Fe3+)
55
Q

Source of iron toxicity

A
  • oral supplements
  • mineral fortified fertilizers
  • slug/ snail bait
  • oxygen absorbing sachets
  • hand warming pads
56
Q

Least and most toxic sources of iron

A
  • IV is the most toxic
  • IM is middle toxic
  • oral is least toxic
57
Q

When would you give injectable iron to an animal

A
  • baby piglets

- born with low amounts of iron and need supplementation when in production

58
Q

What are the three forms of iron

A

elemental, divalent (ferrous) or trivalent (ferric)

59
Q

Is iron reactive or stable

A

very reactive and can switch from divalent to trivalent very quickly

60
Q

what increased iron toxicity in piglets after iron supplementation

A

selenium and vitamin E def in pregnant sows

61
Q

Is organic or inorganic iron more toxic?

A

inorganic

62
Q

Is ferrous or ferric iron more toxic

A

ferric (Fe3)

63
Q

Lethal dose of oral iron

A

greater than 200 mg/ kg or elemental iron

64
Q

How is iron regulated in the body

A
  • level of absorption and reabsorption rather than excretion in urine or feces
65
Q

Percentages of iron in different parts of the body

A
  • 70% in hemoglobin
  • 10% in myoglobin
  • 20% in enzymes or stored in the liver
66
Q

Iron toxicokinetics

A
  • overwhelms the selective absorption mechanism and saturates iron in the GI mucosal cells
  • circulating iron = free radicals
67
Q

MOA of iron toxicity

A
  • free radicals from iron ions cause lipid peroxidation and damage cell membranes
  • causes fatty necrosis of the myocardium and causes other cardio issues
  • corrosion of the GIT mucosa
  • ions damage liver and cause systemic acidosis
68
Q

Per acute iron toxicity clinical signs

A
  • anaphylactic reaction
  • shock
  • death in a few minutes/ sec.
69
Q

Acute iron toxicosis CS

A
  • severe depression
  • shock
  • acidosis
  • death in a few hours
70
Q

Stage 1 of acute iron toxicosis

A

nausea, vomiting, diarrhea, GI hemorrhage

71
Q

Stage 2 of acute iron toxicosis

A

FALSE apparent recovery

72
Q

stage 3 of acute iron toxicosis

A
  • most serious clinical signs

- GI, coagulation, hepatic and cardiovascular problems

73
Q

Stage 4 of acute toxicosis

A

GIT obstruction secondary to fibrosing of damaged GI

74
Q

Lesions with iron toxicity

A
  • yellow-brown discoloration at injection site
  • GI ulceration and hemorrhagic enteritis
  • liver issues
75
Q

Lab results with iron toxicity

A
  • elevated serum iron
  • increased saturation of the serum total iron binding capacity
  • increased PCV
  • acidosis
  • hemoglobinuria
76
Q

Iron toxicity treatment

A
  • GI decontamination within 4 hours of ingestion
  • emesis and gastric lavage before CS
  • Do NOT use activated charcoal
  • milk of magnesia
77
Q

Deferoxamine

A
  • given as a SLOW IV infusion
  • may cause hypotension, arrhythmias, and pulmonary toxicity
  • enhances excretion of iron
  • urine will be reddish brown

TOX (15 decks)

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