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Flashcards in Heavy Metals Deck (77):
1

What is a heavy metal

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

2

Toxic properties of heavy metals

- long residue and half life
- biomagnification
- teratogenic and carcinogenic

3

Lead tox properties

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

4

Which is more readily absorbed? Inorganic or organic lead

Organic

5

Where is inorganic lead found

- dyes, paints and pesticides

6

Inorganic lead is or ins't soluble in water

is not

7

Organic lead uses

anti knocking agents in gasoline products

8

Organic lead properties

- high soluble in organic solvents
- can be absorbed by skin
- accumulates in fat

9

Largest human source of exposure to lead

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

10

Most common source for animal lead toxicosis

- consumption of lead based paints

11

Birds and lead toxicity

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

12

Younger or older animals are most sensitive to lead toxicity?

- younger
- crosses BBB
- greater GI absorption

13

Which species is more frequently poisoned by lead?

dogs due to indiscriminate eating patterns

14

Which animals are more resistant to lead poisoning

goats, swine and chickens

15

Lead toxicokinetics

- dermal and GI absorption is poor (unless in acidic environment)
- Calcium, zinc and proteins decrease absorption

16

Calcium deficiency will have what effect on lead absorption

- greater effect as lead binds to the same carrier proteins
- will have more of a chance to jump on

17

How is lead distributed in the body

- system circulation
- binds to erythrocyte membrane transport

18

Is lead able to cross the placental barrier

YES!

19

How long does lead bind to proteins in soft tissue

- 4-6 weeks
- metallothionein= liver protein that stores metal ions

20

where can lead accumulate and be biologically inactive

- bone matrix
- reserve for several years

21

How is lead excreted

- urine mostly but also bile and milk

22

MOA of lead toxicity

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

23

lead toxicity clinical signs

- anorexia, salivation, vomiting, lead colic, rumen atony
- sometimes megaesophagus
- signs of anemia
- basophilic stippling of erythrocytes
- CNS signs
- pharyngeal paralysis

24

Lesions from lead poisoning

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

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