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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
this is widely used in galvanizing processes, paints, preserving wood, and alloy agent in brass
Zinc
26
this is used in medicinal preparations as topical astringents, antiseptics, antifungal agents and as lozenges for common col
zinc salts
27
metal fume fever
inhalation of freshly formed fumes of zinc oxide (eg. welding, metal cutting)
28
half life of zinc
5-16 months
29
zinc poisoning symptoms
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
30
zinc chloride fumes have caused death due to such complications as ________ ________ and ______________
pulmonary edema; bronchopneumonia
31
functions of copper
constituent of enzymes and proteins necessary for Hb synthesis component of superoxide dismutase = scavenges free radical superoxide (O2-)
32
symptoms of copper deficiencies
disorders in pigmentation retarded growth anemia in children arterial wall structure defect
33
Menkes' disease
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)
34
Wilson's disease
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
35
what happens when copper accumulates in liver?
cirrhosi
36
what happens when copper accumulates in brain?
destruction of nerve cells
37
what happens when copper accumulates in kidney and cornea?
Kayser-Fleischer rings
38
algicide
copper sulfate
39
copper poisoning
- 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
40
half-life of copper
26 days
41
acute exposure of copper: symptoms of poisoning
nausea, vomitting bloody diarrhea hypotnesion hemolytic anemia uremia CV collapse
42
chronic exposure of copper: symmptoms of poisoning
sporadic fever comiting epigastric pain diarrhea jaundice
43
inhalation of copper: symptoms of poisoning
metal fume fever ulceration and perforation of nasal septum necrotic hepatitis
44
functions of selenium
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)
45
thisi s reported to reduce the toxicity of many metals including mercury, cadmum, lead, silver, and to some extent, copper
selenium
46
symptoms of selenium deificencies
heart disease hypothyroidisim weakened immune system
47
this is associated with two endemic diseases found in China
selenium-poor regions Keshan Disease Kashin-Beck Disease
48
Keshan Disease
cardiomyopathy = cardiac enlargement, abnormal ECG, cardgiogenic shock, CHF, necrosis of myocardium
49
Acute Keshan Disease
nausea vomiting necrosis of myocardium
50
T or F. Keshan disease is reported to occur primarily in children and women of child-bearing age
T!
51
how do we treat Keshan disease?
selenium supplementation
52
Kashin=Beck disease
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
coal combustion
selenium
54
selenium poisoning
ubiquitous coal combustion potographic devices, plastics, paints, anti-dandruff shampoo, vitamin, mineral supplements, fungicides, types of glass, feed supplement for pultry and livestock
55
half life of sleenium
100 days
56
respuiraotry symptoms of selenium
dizziness, fatigue, irritaiton of mucus membranes extreme caes = pulmonary edema and severe bronchitis
57
acute oral exposure symptoms of selenium poisoning
nausea, voiting, diarrhea ocassionally = CV symptoms such as tachycardia
58
chronic oral exposure of selenium
selenosis dermal = loss of hair, deformation/loss of nails (white spots, streaks, breaks off easily), discoloration + excessive decay of teeth neurological = numbness, paralysis
59
marker of over-exposure to selenium compounds
garlic breath
60
sources of lead exposure
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
over 90% of asorbed lead is deposited here
bone
62
lead poisoning
- 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
half life of lead
0.4-3.6 yrs
64
symptoms of acute lead poisoning
uncommon lead dust non-specific; GI inflammation urinary output decreases due to renal damage massive ingestion may cause death due to CV collapse
65
plumbism
chornic lead poisoning
66
hematological symptoms of chronic lead poisoninh
baso stoppling anemia
67
GI symptoms of chronic lead poisoning
anorexia constipation metallic taste
68
neurological symptoms of chronic lead poisoning
lead encephalopathy ataxia, nausea, vomiting restlessness irritability convulsions coma
69
neuromuscular symptoms o chronic lead poisoning
lead palsy wrist drop, foot drop fatigue muscular weakness
70
renal symptoms of chronic lead poisoning
impaired tublar reabsorption of glucose, phosphate, AAs, bicarbonate irreverisble chronic nephritis
71
lead levels of concern in children
5 ug/dL or 0.24 umol/L
72
why are children susceptible to neurotoxicity from lead
elevated GI absorption (they absorb 50% and retain 30%) they also have incompletely developed BBB that do not prevent CNS entry
73
T or F. 1/4 of lead encephalopathy victims will not survive
T > 40% of survivors experience intense neurological dysfunction
74
generalized CNS toxicity in children due to lead
- shorter attention span - impulsiveness - cant follow directions - inappropriate provlem solving - robust deficits in learned skills
75
T or F. Lead poisoning is a notifiable disease
T
76
lead levels of ____ are notifiable
greater than 0.5 umol/L
77
toxic effects of mercury dependent on:
chemical form route of admin duration of exposure or amount imdividual sensitivity
78
chronic exposure to mercury produces significant effects on two rogan systems
CNS kidney
79
T or F. Mercuric salt (HgCl2) is more toxic than mercurous salt (Hg2Cl2)
T ifi ngested, HgCl2 mo,re rapidly absorbed and greater toxicity
80
T or F. Monovalent inorgnic mercury salts are more soluble than divalent
F! divalent more soluble
81
This is the principle target organ for inorganic mercurials
kidney
82
symptoms of inorganic mercury exposure
- 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
"mad as a hatter"
mercuric nitrate = felt hat industry neurological changes due to exposure
84
sy,ptoms of elemntal mercury exposure
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
T or F. Organic mercurials cross BBB and placenta
T = neurological and teratogenic disorders
86
T or F. Organic mercury is more corrsive to intestinal mucoss than inorganic
F! LESS corrosive
87
target organ of alkulmercury compounds (prganic)
brain
88
symptoms of organomercurial exposure
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
chemotherapeutic agent for acute promyelocytic leukemia
arsenic
90
forms of arsenic
trivalent = arsenites pentavalent = arsenates
91
organic arsenic
either pentavalent or trivalent linked to a carbon
92
ASH3
gaseous hydride of As 3+
93
where is arsenic mainly stored
liver, kidney, <3, lung, etc.
94
where is the highest concentrations of arsenic found
hair and nails due to high sulfhydral content of kaeratin
95
arsenic is chemically similar to this
phosphorus so also deposited in bones and teeth
96
T or F. Arsenic readily causes placenta
T = fetal damage
97
arsenic half-life
10 hours
98
arsenobentaine
non-toxic organic seafood arsenic lobster
99
this uncouples ox phosphorylation by interfering in the formation of ATP
pentavalent arsenic
100
what does trivalent arsenic do?
- 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
symptoms of acute arsenic exposure
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
symptoms of chronic arsenic exposure
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
rapid and fatal hemolysiks is a unique characteris of this
arsine gas - arsine combines with Hb = react w O2 => hemolysis
104
classic arsine triad
hemolysis ab pain hematuria
105
arsine gas: jaundice appears after ___ hours
24
106
copper skin pigmentaiton
arsine gas due to methem???
107
high levels of arsine gas causes
direct multisystem cytotoxicity
108
one of heavy metals of greatest toxicological concern
cadmium
109
exposure of cadmium
electroplating pigments plastic stabilizers batteries also found in nature with lead and zinc (mining)
110
where does cadmium accumulate in the body
lung, liver, kidney
111
this is the heavy metal most prone to accumulate in the body
cadmium
112
what does cadmium do in the body
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
oral symptoms of cadmium toxicity
severe nausea, diarrhea, vomiting muscular cramps salivation dizziness proteinuria glycosuria osteomalacia
114
inhalation symptoms of cadmium
rhinorrhea difficulty breathing chest pain pulmonary edema progressive emphysema azotemia (urea/other nitrogenous bodies in blood) proteinuria liver necrosis
115
I'tai-I'tai Byo
ouch-ouch disease bone and muscle pain
116
what is ouch-ouch disease
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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