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MLSCI 466 > Trace Elements > Flashcards

Trace Elements Flashcards

1
Q

organic lead

A

tetraethyllead
exposure =rare since advent of unleaded gas

differ from signs of inorganic lead poisoning in that hematologic abnormalities are unusual and encephalopathy predominates

metabolized to inorganic lead so if chronic exposure will eventually present as same problems as inorganic lead exposure

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2
Q

mercury poisoning

A

used in dent, med (diuretics), ag, and industry (electrical components)

can be divided into three chemical classes:
> inorganic mercury salts (mercuric and mercurous salts)
> elemental mercury
> organic mercury salts (arylmercury and alkylmercury)

inorganic mercury released by industries into waterways can be converted to methylmercury by microflora

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3
Q

symptoms of mercury poisoning

A

chronic exposure to mercury produces significant effects on two organ systems: CNS & kidneys

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4
Q

elemental mercury poisoning

A

high lipid solubility and crosses cell membranes

chronic inhalation of merc vapour, mercury will preferentially attack CNS

crosses blood-brain barrier and accumulates in CNS

after rapidly accumulating in the brain, the mercury oxidizes to the mercuric form

cause degenerative changes through action on structural proteins and enzyme systems; synaptic and neuromuscular transmission is blocked

all mercury compounds will concentrate in the kidney to some extent

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5
Q

organic mercury poisoning

A
  • crosses BBB and placenta causing neurological and teratogenic disorders
  • 90% of a methylmerucry ingestion is absorbed compared to 10% with the soluble inorganic salts
  • organic mercury is less corrosive to intestinal mucosa than inorganic mercurials
  • the alkylmerucry compounds are almost completely absorbed from the GI tract - distributed to brain (target organ), liver and kidney and excreted primarily in the feces
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6
Q

chronic arsenic toxicity

A

malignant changes in almost all organs of the body

exact mechanism of carcinogenesis unknown

effective treatment of chronic exposure not yet established

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7
Q

arsine gas

A
  • rapid and fatal hemolysis is a unique characteristic (since cmombnies w Hb, reacting with oxygen to cause hemolysis)

classic arsine triad = hemolysis, abdominal pain, hematuria

jaundice after 24hrs

coppery skin pigmentation = due to metheme perhaps??

if patient survives hemolysis - death may result from renal failure (necrosis of proximal tubule)

at high levels produce direct multi-system cytotoxicity

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8
Q

cadmium poisoning

A

one of heavy metals of greatest toxicological concer

exposure due to electroplating, pigments, plastic stabilizers, batteries

found in nature with lead and zinc;during mining of these metals, cadmium may be released into air

poorly absorbed din GI tract = little as 5% entering blood

comes form contaminated food and water

inhalation of airborne cadmium from cigarette smoking

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9
Q

heavy metal most prone to accumulate in body

A

cadmium

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10
Q

bio half-life of cadmium

A

10-30 yrs

kevel increases throughout life

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11
Q

where does cadmium accumulate?

A

lung, liver, kidney

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12
Q

what enzymes does cadmium inhibit?

A

enzymes containing sulfhydryl groups
- binds to other ligands on proteins and purines

also inhibits alpha1-antitrypsin = responsible partly for pulmonary symptoms

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13
Q

cadmium competes with cellular uptake of various other metals in body such as _______ & _____

A

copper; zinc

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14
Q

oral symptoms of cadmium toxicity

A

severe nausea, diarrhea, vomiting
muscular cramps
salivation
dizziness
proteinuria
glycosuria
osteomalacia

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15
Q

inhalation symptoms of cadmium toxicity

A

rhinorrhea
difficulty breathing
chest pain
pulmonary edema
progressive emphysema
azotemia (presence of ura & other nitrogenous bodies in blood)
proteinuria
liver necrosis

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16
Q

symptoms of cadmium toxicity

A
  • severe cadmium poisoning in residents of Toyoma, Japan due to contamination of rice fields by cadmium released from a metal poisoning plant upstream
  • renal damage leading to disturbances in calcium and phosphorus metabolism were believed to be responsible for skeletal abnormalities and severe leg and back pain
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17
Q

essential elements needed for normal physiological functionig

A

chromium
cobalt
copper
manganese
molybdenum
selenium
vanadium
zinc

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18
Q

sources of zinc

A

oytsers
red meat
pultry
cheese
shellfish
legumes
whole grains
mushrooms
brewer’s yeast

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19
Q

sources of copper

A

oysters
liver
whole grains
shellfish
legumes
nuts
choclate

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20
Q

sources of chromium

A

bbrewer’s yeast
lean meats
cheeses
whole grains
mmolasses
spices
bran cereals

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21
Q

sources of selenium

A

rbazil nut
brewer’s yeast
liver
butter
fish
shellfish
garlic
whole grains

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22
Q

functions of zinc

A

protein synthesis
carbohydrate metabolism
zinc dependent enzymes = alc dehydrogenase
acts as an antioxidant and free radical scavenger
gatekeeper of immune response

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23
Q

symptoms of zinc deficiencies

A

growth retardation
delayed sexual maturation
anorexia with altered taste and smell
acrodermatitis (inflam of skin - hands or feet)
impaored wound healing + immunity
alteration of vitamin A emtabolism

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24
Q

acrodermatitis enteropathicaa

A

inherited as an autosomal recessive trait attributed to a defect in zinc metabolism

after weaning from breastfeeding = babies get pustular dermatitis combined with severe GI disturbances

zinc supplementation = free of symptoms

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25
Q

this is widely used in galvanizing processes, paints, preserving wood, and alloy agent in brass

A

Zinc

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26
Q

this is used in medicinal preparations as topical astringents, antiseptics, antifungal agents and as lozenges for common col

A

zinc salts

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27
Q

metal fume fever

A

inhalation of freshly formed fumes of zinc oxide (eg. welding, metal cutting)

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28
Q

half life of zinc

A

5-16 months

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29
Q

zinc poisoning symptoms

A

oral = lassitude (tiredness, listlessness), enteritis, diarrhea (bloody or watery), intense ab pain, CNS depression, tremors

inhaltion = sudden onset of thirst, fever, chills, myalgias (musc headached and pains), headaches

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30
Q

zinc chloride fumes have caused death due to such complications as ________ ________ and ______________

A

pulmonary edema; bronchopneumonia

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31
Q

functions of copper

A

constituent of enzymes and proteins

necessary for Hb synthesis
component of superoxide dismutase = scavenges free radical superoxide (O2-)

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32
Q

symptoms of copper deficiencies

A

disorders in pigmentation

retarded growth

anemia in children

arterial wall structure defect

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33
Q

Menkes’ disease

A

steely or kinky hair syndrome = sex-linked recessive disorder of copper absorption

extremely low level of copper

name of disease = defective keratinization and pigmentation of hair

bone changes, severe cerebral degeneration (early infancy, failure to thrive, lethargy, hypothermia, seizures)

sopper supplementations allows clinical improvement (parenteral administration; other routes than digestive tract)

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34
Q

Wilson’s disease

A

hepatolenticular degeneration

severe autosomal recessive disorder of copper metabolism
onset = 4-5 yrs

diminished synthesis of copper-transporting protein ceruloplasmin and impaired excretion of copper into bile

copper low in serum but high in urine

zinc therapy used to prevent copper absorption

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35
Q

what happens when copper accumulates in liver?

A

cirrhosi

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36
Q

what happens when copper accumulates in brain?

A

destruction of nerve cells

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37
Q

what happens when copper accumulates in kidney and cornea?

A

Kayser-Fleischer rings

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38
Q

algicide

A

copper sulfate

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39
Q

copper poisoning

A
  • electrical wiring
  • algicide
  • acute oral ingestion of copper salt or food contam by copper utensils
  • industrial exposure due to inhalation of copper fumes or dust
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40
Q

half-life of copper

A

26 days

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41
Q

acute exposure of copper: symptoms of poisoning

A

nausea, vomitting
bloody diarrhea
hypotnesion
hemolytic anemia
uremia
CV collapse

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42
Q

chronic exposure of copper: symmptoms of poisoning

A

sporadic fever
comiting
epigastric pain
diarrhea
jaundice

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43
Q

inhalation of copper: symptoms of poisoning

A

metal fume fever
ulceration and perforation of nasal septum
necrotic hepatitis

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44
Q

functions of selenium

A

biologically active part of proteins, esp enzymes involved in antioxidant defense mechanisms (glutathione peroxidases), thyroid hormone metabolism (deiodinase enzymes), redox control of intracelular rxns (thoredoxin reductase)

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45
Q

thisi s reported to reduce the toxicity of many metals including mercury, cadmum, lead, silver, and to some extent, copper

A

selenium

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46
Q

symptoms of selenium deificencies

A

heart disease
hypothyroidisim
weakened immune system

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47
Q

this is associated with two endemic diseases found in China

A

selenium-poor regions
Keshan Disease
Kashin-Beck Disease

48
Q

Keshan Disease

A

cardiomyopathy = cardiac enlargement, abnormal ECG, cardgiogenic shock, CHF, necrosis of myocardium

49
Q

Acute Keshan Disease

A

nausea
vomiting
necrosis of myocardium

50
Q

T or F. Keshan disease is reported to occur primarily in children and women of child-bearing age

A

T!

51
Q

how do we treat Keshan disease?

A

selenium supplementation

52
Q

Kashin=Beck disease

A

atrophy, degeneration, and necrosis of cartilage tissue

occurs in children 5-13 years of age

treat with selenium supplements

factors other than selenium could be at work

53
Q

coal combustion

A

selenium

54
Q

selenium poisoning

A

ubiquitous
coal combustion
potographic devices, plastics, paints, anti-dandruff shampoo, vitamin, mineral supplements, fungicides, types of glass, feed supplement for pultry and livestock

55
Q

half life of sleenium

A

100 days

56
Q

respuiraotry symptoms of selenium

A

dizziness, fatigue, irritaiton of mucus membranes
extreme caes = pulmonary edema and severe bronchitis

57
Q

acute oral exposure symptoms of selenium poisoning

A

nausea, voiting, diarrhea
ocassionally = CV symptoms such as tachycardia

58
Q

chronic oral exposure of selenium

A

selenosis

dermal = loss of hair, deformation/loss of nails (white spots, streaks, breaks off easily), discoloration + excessive decay of teeth

neurological = numbness, paralysis

59
Q

marker of over-exposure to selenium compounds

A

garlic breath

60
Q

sources of lead exposure

A

water, air, soil, food (ENVIRONMENTAL)

crayons, toys, paper, clothes, dirt, sand, paint flakes, plastics, etc. (HOUSEHOLD)

miners, smelters, automobile finishers, storage battery workers, sheet metal workers, spray painters (HIGH INDUSTRIAL RISK)

61
Q

over 90% of asorbed lead is deposited here

A

bone

62
Q

lead poisoning

A
  • cumulative = both acyte and chronic intoxication
  • acute poisoning rare; chronic more common and serious
  • manifestation of toxicity = binding sulfhydryl groups of protein molecules = inactivates enzyme systems such as production of heme
63
Q

half life of lead

A

0.4-3.6 yrs

64
Q

symptoms of acute lead poisoning

A

uncommon
lead dust
non-specific; GI inflammation
urinary output decreases due to renal damage
massive ingestion may cause death due to CV collapse

65
Q

plumbism

A

chornic lead poisoning

66
Q

hematological symptoms of chronic lead poisoninh

A

baso stoppling
anemia

67
Q

GI symptoms of chronic lead poisoning

A

anorexia
constipation
metallic taste

68
Q

neurological symptoms of chronic lead poisoning

A

lead encephalopathy
ataxia, nausea, vomiting
restlessness
irritability
convulsions
coma

69
Q

neuromuscular symptoms o chronic lead poisoning

A

lead palsy
wrist drop, foot drop
fatigue
muscular weakness

70
Q

renal symptoms of chronic lead poisoning

A

impaired tublar reabsorption of glucose, phosphate, AAs, bicarbonate

irreverisble chronic nephritis

71
Q

lead levels of concern in children

A

5 ug/dL or 0.24 umol/L

72
Q

why are children susceptible to neurotoxicity from lead

A

elevated GI absorption (they absorb 50% and retain 30%)

they also have incompletely developed BBB that do not prevent CNS entry

73
Q

T or F. 1/4 of lead encephalopathy victims will not survive

A

T
> 40% of survivors experience intense neurological dysfunction

74
Q

generalized CNS toxicity in children due to lead

A
  • shorter attention span
  • impulsiveness
  • cant follow directions
  • inappropriate provlem solving
  • robust deficits in learned skills
75
Q

T or F. Lead poisoning is a notifiable disease

A

T

76
Q

lead levels of ____ are notifiable

A

greater than 0.5 umol/L

77
Q

toxic effects of mercury dependent on:

A

chemical form
route of admin
duration of exposure or amount
imdividual sensitivity

78
Q

chronic exposure to mercury produces significant effects on two rogan systems

A

CNS
kidney

79
Q

T or F. Mercuric salt (HgCl2) is more toxic than mercurous salt (Hg2Cl2)

A

T
ifi ngested, HgCl2 mo,re rapidly absorbed and greater toxicity

80
Q

T or F. Monovalent inorgnic mercury salts are more soluble than divalent

A

F! divalent more soluble

81
Q

This is the principle target organ for inorganic mercurials

A

kidney

82
Q

symptoms of inorganic mercury exposure

A
  • immediate corrosive injury to mouth mucosa, throat, esophagus and stomach (INGESTION)
  • mouth, pharynx and gastric mucosa appear ashen and painful
  • profuse vomiting of mucoid mateiral, bloody diarrhea, circulatory collapse, shock and sudden death
  • tubular necrosis
83
Q

“mad as a hatter”

A

mercuric nitrate = felt hat industry
neurological changes due to exposure

84
Q

sy,ptoms of elemntal mercury exposure

A

nonspecific = anorexia, weight loss, fatigue, muscular weakness
(inhalation or absorption through skin)
neurological/behavuioural problems frmo accumulation in cerebral/cerebellar cortex
= tremors in fingers, eyes or tongue => entire limp, slurred speech, illegible handwriting, anger attacks, high irritability, memory loss, drowsiness, loss of interest in life +{ withdrawal from society(erethism)

limited tubular necrosis

85
Q

T or F. Organic mercurials cross BBB and placenta

A

T = neurological and teratogenic disorders

86
Q

T or F. Organic mercury is more corrsive to intestinal mucoss than inorganic

A

F! LESS corrosive

87
Q

target organ of alkulmercury compounds (prganic)

A

brain

88
Q

symptoms of organomercurial exposure

A

oral infestion (food chain)

NOTE: symptoms may not occur until weeks/months after acute exposure

neurological manifestations = ataxia, tremors, unsteady gait, illegible handwriting, slurred speech

sensory involvement = parethesias of lips, hands, feet and visual + hearing impairment

  • emotional disturbances and erethism
  • severe poisoning = may be irreversible
89
Q

chemotherapeutic agent for acute promyelocytic leukemia

A

arsenic

90
Q

forms of arsenic

A

trivalent = arsenites
pentavalent = arsenates

91
Q

organic arsenic

A

either pentavalent or trivalent linked to a carbon

92
Q

ASH3

A

gaseous hydride of As 3+

93
Q

where is arsenic mainly stored

A

liver, kidney, <3, lung, etc.

94
Q

where is the highest concentrations of arsenic found

A

hair and nails due to high sulfhydral content of kaeratin

95
Q

arsenic is chemically similar to this

A

phosphorus so also deposited in bones and teeth

96
Q

T or F. Arsenic readily causes placenta

A

T = fetal damage

97
Q

arsenic half-life

A

10 hours

98
Q

arsenobentaine

A

non-toxic
organic seafood arsenic
lobster

99
Q

this uncouples ox phosphorylation by interfering in the formation of ATP

A

pentavalent arsenic

100
Q

what does trivalent arsenic do?

A
  • inhibit enzymes containing -SH groups
  • inhibit pyruvate dehydrogenase resulting in inhibition of pyruvate ox and tricarboxylic acid cycle
  • impaired gluconeogenesis and reduced ox phosphorylation
101
Q

symptoms of acute arsenic exposure

A

diffuse skin rash

GI:
- extreme gastroenteritis bc of corrosion; burning esophageal pain, difficulty swallowing, unbearable stomach pain
- nausea, projectile vomiting, explosive diarrhea
- rice-water stools, bloody diarrhea and vomitus

excessive bleeding compromises circulatory system, BP drops = vascular shock and death

renal:
- tubular necrosis and renal failure
- urine outflow decreases and uremia may develop

delayed actions:
- ECG abnormalities (delayed cardiomyopathy)
- peripheral neuropathy = paresthesias, foot drop, wrist drop, slow reflexes
- liver cirrhosis

102
Q

symptoms of chronic arsenic exposure

A

insidious non-specifc symptoms
- weakness, tiredness, lack of appetite, weight loss, irritability, garlic odor on breath

specific
- dark brown pigmentation and thickening of keratin layer
- nails thicken and Mee’s Lines develop = white bands across width of nail

peripheral neuropathies (LEGS > arms affected); paralysis of both motor and sensory pathways

ulcerations of GI

hepatic injury = hepatitis and cirrhosis

103
Q

rapid and fatal hemolysiks is a unique characteris of this

A

arsine gas
- arsine combines with Hb = react w O2 => hemolysis

104
Q

classic arsine triad

A

hemolysis
ab pain
hematuria

105
Q

arsine gas: jaundice appears after ___ hours

A

24

106
Q

copper skin pigmentaiton

A

arsine gas
due to methem???

107
Q

high levels of arsine gas causes

A

direct multisystem cytotoxicity

108
Q

one of heavy metals of greatest toxicological concern

A

cadmium

109
Q

exposure of cadmium

A

electroplating
pigments
plastic stabilizers
batteries
also found in nature with lead and zinc (mining)

110
Q

where does cadmium accumulate in the body

A

lung, liver, kidney

111
Q

this is the heavy metal most prone to accumulate in the body

A

cadmium

112
Q

what does cadmium do in the body

A

inhibits enymes containing sulfhydrul groups
- binds to other ligands on proteins and purines

inhibits alpha1-antitrypsin = pulmonary symptoms

competes w cellular uptake of various other metals in body such as copper and zinc

113
Q

oral symptoms of cadmium toxicity

A

severe nausea, diarrhea, vomiting
muscular cramps
salivation
dizziness
proteinuria
glycosuria
osteomalacia

114
Q

inhalation symptoms of cadmium

A

rhinorrhea
difficulty breathing
chest pain
pulmonary edema
progressive emphysema
azotemia (urea/other nitrogenous bodies in blood)
proteinuria
liver necrosis

115
Q

I’tai-I’tai Byo

A

ouch-ouch disease
bone and muscle pain

116
Q

what is ouch-ouch disease

A

severe cadmium poisoning
Toyama, Japan
rice fields
renal damage => disturbances in calcium and phosphorus metabolism = skeletal abnormalities, severe leg + back pain

MLSCI 466 (19 decks)

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