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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
Hematology Lab results from lead toxicosis
- non regenerative anemia - few reticulocytes - basophilic stippling in dogs and rabbits - abnormal hemoglobin conc. - fluorescence of porphyrins
26
Chemical analysis results with lead toxicosis
- lead bound to erythrocytes | - blood is with lead greater than 0.4 ppm is diagnostic
27
Treatment for lead toxicosis
- fluids and electrolytes | - eliminate by washing animal, gastric lavage, cathartics
28
What should you not use in treatment of lead toxicosis
ACTIVATED CHARCOAL
29
What is chelation therapy
- an agent that forms multiple bonds with metal ions in order to make them inert and excretable
30
Calcium disodium EDTA
- 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
31
Dimercaptosuccinic acid (DMSA, Succimer)
- BEST in birds - Orally administered - can be used alone or after treatment with EDTA - doesn't bind to essential minerals - less nephrotoxic
32
Dimercaprol (BAL)
- Can be used alone or with EDTA - crossed the BBB and enhances excretion - avoid with liver and renal disease - Given IM- PAINFUL
33
D- penicillamine
- Given orally - used following EDTA - less effective - can be nephrotoxic - vomiting is common
34
Lead toxicity prognosis
- mild-moderate signs = good | - severe central nervous signs= guarded to poor
35
lead toxicity on radiograph
- accumulates in active bone matrix - inhibits normal remodeling of long bones - lead lines
36
Zinc toxicity
- Ingestion will cause zinc salts when combined with acid in the stomach
37
Zinc properties
- needed for growth, wound healing, reproduction - helps taste and smell receptors work - component of many enzymes and proteins
38
Zinc sources of exposure
- ingestion of pennies - used to galvanize metals to prevent rusting - batteries - zinc oxide ointments - overdose of dietary supplement
39
Zinc toxicity
Acute LD50 is 100 mg.kg zince salts
40
How many pennies does a dog have to eat for subacute zinc poisoning
around 5
41
Why does chronic zinc typically occur
In the diet
42
Zinc toxicokinetics
- absorbed through small intestines - acid and chelating agents helps to increase absorption - interferes with copper and iron use by the body
43
Where is most zinc metabolized/ extracted from
- the liver
44
MOA of zinc toxicosis
- largely affects RBC, kidney liver and pancreas | - often causes intravascular hemolysis
45
Accumulation of zinc
- Rapid accumulation in pancreas, liver, kidney, spleen and reproductive organs
46
Excretion of zinc
- primarily in the feces (bile), pancreatic juice and mucosal cells - 10% in urine
47
Zinc Toxicity clinical signs
- GI irritation - RBC damage (hemolytic anemia) - Renal damage - livestock= decreased milk/ weight gain - lameness and stiffness in foals
48
Lesions with zinc poisoning
- gastritis/ gastric ulcers - renal tubular casts - liver damage - pancreatitis
49
Chemical analysis results with zinc toxicosis
- need to use trace elements tube for analysis | - royal blue top
50
Lab work results for zinc tox.
- hemolytic anemia - icterus - hemoglobinuria - azotemia - hyper phosphatemia
51
Zinc toxicosis treatment
- remove foreign bodies (emesis, endoscopy, surgery) - cathartics - supportive care
52
Should you use chelating agents with zinc toxicosis
- not initially as it may cause zinc redistribution | - can use after EDTA
53
Zinc prognosis
- guarded to poor with severe hemolytic crisis but good otherwise
54
25% of Iron in the body is in what form
- Ferric (Fe3+)
55
Source of iron toxicity
- oral supplements - mineral fortified fertilizers - slug/ snail bait - oxygen absorbing sachets - hand warming pads
56
Least and most toxic sources of iron
- IV is the most toxic - IM is middle toxic - oral is least toxic
57
When would you give injectable iron to an animal
- baby piglets | - born with low amounts of iron and need supplementation when in production
58
What are the three forms of iron
elemental, divalent (ferrous) or trivalent (ferric)
59
Is iron reactive or stable
very reactive and can switch from divalent to trivalent very quickly
60
what increased iron toxicity in piglets after iron supplementation
selenium and vitamin E def in pregnant sows
61
Is organic or inorganic iron more toxic?
inorganic
62
Is ferrous or ferric iron more toxic
ferric (Fe3)
63
Lethal dose of oral iron
greater than 200 mg/ kg or elemental iron
64
How is iron regulated in the body
- level of absorption and reabsorption rather than excretion in urine or feces
65
Percentages of iron in different parts of the body
- 70% in hemoglobin - 10% in myoglobin - 20% in enzymes or stored in the liver
66
Iron toxicokinetics
- overwhelms the selective absorption mechanism and saturates iron in the GI mucosal cells - circulating iron = free radicals
67
MOA of iron toxicity
- 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
Per acute iron toxicity clinical signs
- anaphylactic reaction - shock - death in a few minutes/ sec.
69
Acute iron toxicosis CS
- severe depression - shock - acidosis - death in a few hours
70
Stage 1 of acute iron toxicosis
nausea, vomiting, diarrhea, GI hemorrhage
71
Stage 2 of acute iron toxicosis
FALSE apparent recovery
72
stage 3 of acute iron toxicosis
- most serious clinical signs | - GI, coagulation, hepatic and cardiovascular problems
73
Stage 4 of acute toxicosis
GIT obstruction secondary to fibrosing of damaged GI
74
Lesions with iron toxicity
- yellow-brown discoloration at injection site - GI ulceration and hemorrhagic enteritis - liver issues
75
Lab results with iron toxicity
- elevated serum iron - increased saturation of the serum total iron binding capacity - increased PCV - acidosis - hemoglobinuria
76
Iron toxicity treatment
- GI decontamination within 4 hours of ingestion - emesis and gastric lavage before CS - Do NOT use activated charcoal - milk of magnesia
77
Deferoxamine
- 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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