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Disease and Ther. Final > Heavy metals Chelators > Flashcards

Heavy metals Chelators Flashcards

1
Q

Toxicology

A

study of adverse effects of a chemical, physical, or biological agent

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2
Q

Toxicity

A

the ability of a material to damage a biological system, cause injury, or impair function

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3
Q

What effects degree of toxicity

A

dose, route of exposure, and chemical species, as well as the age, gender, genetics, and nutritional status of exposed individuals

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4
Q

Hazard

A

ability of an agent to cause toxicity

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5
Q

Risk

A

the expected frequency of exposure to a hazardous agent

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6
Q

Route of exposure

A

Route of entry into body

inhalation, transdermal, oral mucosal

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7
Q

Duration of Exposure

A

may effect selection of treatment

acute vs. chronic

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8
Q

ADME

A

the Adsorption, Distribution, Metabolism, and Excretion of toxic substances and their metabolites

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9
Q

Clearance

A

measure of plasma cleared per unit time

sum of both renal and hepatic contributions

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10
Q

1st order clearance

A

normal conditions

eliminations of drugs/chemicals is proportional to their plasma concentration

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11
Q

Zero order kinetics

A

when plasma levels become very high, protein binding and normal metabolism can both become saturated, rate of elimination can become fixed
More drug will be delivered into circulation in unbound fraction

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12
Q

Volume of distribution

A

apparent volume into which a substance is distributed

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13
Q

Which volume of distribution is more difficult to remove (like with hemodialysis)

A

Large volume of distribution is more difficult to remove than small volume of distribution

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14
Q

Bioaccumulation

Biomagnification

A
  • accumulation of a toxic agent when the uptake exceeds the organism’s ability to metabolize/excrete
  • Biomagnification: increases in the relative amount of contaminant in a biological system as it passes up the food chain
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15
Q

Why, at very high blood concentrations, do normal kinetic properties of drugs or toxins change

A

Larger, unbound free fractions

prolonged half life and increase toxicity

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16
Q

What defines metals as heavy

A

high atomic weight and having a density at least five times greater than that of water (specific density of more than 5g/cm3)

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17
Q

Top 3 most toxic substances

A
  1. Lead
  2. Mercury
  3. Arsenic
  4. Cadmium
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18
Q

How do heavy metals interfere with normal biological processes

A

by competing with normal substrates

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19
Q

Chelators and half life

A

the shorter the half life, the more effective it is to use chelators to remove heavy metals

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20
Q

Primary exposure sources of lead

A 
Building materials/construction
Batteries
Lead pipes
paint
soil, dust, water 
industry
fold remedies
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21
Q

Why is lead exposure particularly detrimental to young children

A

Their bodies absorb b/c Pb competes with Ca and growing bodies require more Ca.
children absorb more than 50% consumed
adults - about 10-15%
Kids suck on stuff

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22
Q

Half life of lead

A

1-2 months

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23
Q

Symptoms of lead poisoning

A

Headaches
neurocognitive deficits
kidney damage

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24
Q

Main repository in body for lead burden

A

Substitutes for Ca in bone

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25
Q

What are Burtonian lines

A

Lead lines causing a darkening of the gingiva

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26
Q

Mechanism of leads toxicity

A

Interferes with Ca us
Causes anemia
Causes immunosuppression

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27
Q

treatment regimen for lead toxicity - recommended chelators

A

Remove exposure

Chelators - EDTA, removes Pb from bone slowly and requires multiple chelating treatments

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28
Q

Mercury primarily used in what form

A

methyl/Hg form

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29
Q

Primary exposure sources of mercury

A

Fish
Amalgam (CDC says it’s not a problem)
Thermometers

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30
Q

Mechanism of mercury toxicity

A

Reacts with selenium (necessary for reducing oxidized vitamin C and E)
Can cause gingivostomatitis

31
Q

Symptoms of mercury poisoning

A

Mad hatter disease
Neurological
Psychiatric problems
Gingivostomatitis

32
Q

CDC’s conclusions regarding mercury exposure in thimerosal in flu vaccines
and dental amalgam

A

other than redness and swelling at injection site

neither have evidence of causing harm

33
Q

Treatment regimen for mercury toxicity - including chelators

A

Chelators - Dimercaprol and Succimer

34
Q

Why is dimercaprol contraindicated in chronic mercury intoxication

A

Chronic use of dimercaprol can cause serious renal toxicity

35
Q

Exposure sources of Arsenic

A

Industry
Groundwater
Arsenite - used in chemotherapeutics for leukemia

36
Q

Toxicokinetics of Arsenic - route of intake

A

absorbed through respiratory mucosa and GI tract

poor skin absorption

37
Q

Symptoms/effects of arsenic

A

Fatigue, anemia, renal failure, hyperpigmentation
Carcinogenic in lungs, skin, and bladder
hemolytic on RBCs

38
Q

Mechanism of arsenic toxicity

A 
interferes with enzyme function
increases ROS and oxidative stress
interferes with signal transduction
hemolytic effects on RBCs
Carcinogenic
39
Q

Treatment for acute arsenic intoxication

A

Decontamination and supportive care
Chelators: Unithiol or Dimercaprol
Emperic chelation if exposure is suspected

40
Q

Treatment for chronic arsenic intoxication

A

Supportive care
Dietary supplementation with folate
No chelators since chronic arsenosis leads to irreversible damage to several vital organs, carcinogenic

41
Q

Treatment for acute arsine gas intoxication

A

Blood exchange hemodialysis and transfusions
aggressive hydration
No chelators - no benefit

42
Q

How do chelators work on heavy metals

A

They render heavy metal ions unavailable for covalent interactions

43
Q

How does the half-life of the heavy metal effect the ability of a chelator to remove it from a target organ

A

The longer the half life, the less effective the chelator action

44
Q

Is it better to treat with chelators quickly or to wait

A

Most effective if administered ASAP after exposure

45
Q

Dimercaprol: Approved for which heavy metal poisonings as a monotherapy

A

Arsenic (acute) and Mercury

Combo with Edetate calcium disodium for severe lead poisoning

46
Q

Dimercaprol monotherapy contraindicated for what

A

Chronic exposure to lead

b/c it redistributes larger doses of lead to CNS

47
Q

Dimercaprol Combo with what for chronic poisoning of what

A

Combo with CaNa2-EDTA (edetate calcium disodium) for severe lead exposure

48
Q

Is Dimercaprol water soluble

A

no (cannot give orally)

49
Q

Only route of administration for dimercaprol

A

Intramuscular (i.m.)

50
Q

Therapeutic index of dimercaprol compared to succimer or unithiol

A

It can be very toxic, especially on kidneys

Succimer has replaced dimercaprol for the most part

51
Q

Succimer

A

Water-soluble form of dimercaprol

For oral use only

52
Q

Succimer approved for which heavy metal poisonings

A

Lead
Arsenic
Mercury

53
Q

Succimer’s main mechanism for removing heavy metals

A

Binds to cysteine to form mixed disulfides which are excreted by the kidney

54
Q

Half life of Succimer

A

2-4 hours

55
Q

Adverse effects of Succimer

A

only diarrhea/GI upset, maybe mild rashes

much better than dimercaprol

56
Q

Edetate Calcium Disodium (CaNa2-EDTA) approved for which heavy metal poisonings

A

Lead

57
Q

Edetate Calcium disodium targets intra or extra-cellular lead

A

Extra cellular

58
Q

Edetate calcium only route of administration

A

Intravenous

59
Q

Half life of edetate calcium disodium

excretion

A

1 hour

excreted 100% by kidney

60
Q

Edetate calcium disodium contraindicated for what population

A

Anuric patients

excreted by kidneys

61
Q

Unithiol
another form of what
routes of administration

A

Another water-soluble form of dimercaprol

Orally or IV

62
Q

Half life of Unithiol

A

20 hours

63
Q

Unithiol effective against which heavy metals

FDA approved for which

A

Mercury
Arsenic
Lead
FDA approved for none

64
Q

Biocompatibility

A

ability of a material to elicit an appropriate biological response in a given application in the body

65
Q

4 biocompatibility criteria for the ideal dental material

A

Should not be harmful to pulp or soft tissues
Should not contain toxic diffusable substances that may be released and absorbed into the circulatory system to cause systemic toxicity
Should be free of potentially sensitizing agents that may cause allergic reactions
Should have NO carcinogenic potential

66
Q

Most common allergic reactions observed in dental practices

How to avoid them

A

Allergic contact dermatitis: distal fingers and tips after repeated exposure to monomers of bond - wear gloves wash hands
Latex Allergies - use non-latex
Allergies to denture base materials - soak in water 24 hours before first-time use

67
Q

What step releases mercury the most

A

Polishing amalgam

68
Q

How to avoid pulpitis from unpolymerized monomers in resin composite deep fillings

A

Use twice the recommended time of exposure
Cure in increments
Zinc phosphate cement
Glass ionomer

69
Q

How to avoid lesions caused by zinc phosphate cement

A

Use proper mix or alternatively use a resin-modified glass ionomer cement
Make sure it isn’t too thin

70
Q

How to reduce cytotoxicity of acrylate bonding agents

A

rinse with tap water between applications of subsequent reagents

71
Q

Importance of ventilation in lab with metals

A

Beryllium dust
Nickel dust
Beryllium vapors

72
Q

Mechanism of cyanide poisoning

A

not a heavy metal, but very common

prevents cells of body from getting oxygen and ATP, causing cell death

73
Q

Antidote for Cyanide

A

hydroxycobalamin - reacts with cyanide to form cyanocobalamin which is excreted by kidneys

Disease and Ther. Final (7 decks)

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