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A comprehensive set of flashcards covering sources, forms, mechanisms, symptoms, diseases, diagnosis, and treatment of mercury, cadmium, chromium, and copper toxicities.
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What three chemical forms can mercury exist in?
Elemental (metallic), inorganic (mercuric/mercurous salts), and organic (methyl-, dimethyl-, etc.).
Which form of mercury is non-toxic when swallowed as a liquid but highly toxic when inhaled as a vapor?
Elemental (metallic) mercury.
Which general form of mercury is considered the most toxic to humans?
Organic mercury, especially methyl- and dimethyl-mercury.
Among WHO’s priorities, how is mercury classified for public health?
One of the top ten chemicals of major public-health concern.
Name the major target organs for mercury toxicity.
Brain (CNS), kidneys, digestive tract, immune system, and lungs.
List at least four common sources of mercury exposure.
Fluorescent bulbs, thermometers/medical devices, contaminated seafood, dental amalgam, fungicides, seed preservatives, cosmetics, drinking water.
Through which routes can mercury be absorbed?
Inhalation (vapor), dermal absorption (moderate), ingestion (poor for elemental, effective for organic/inorganic salts).
Which form of mercury readily crosses the blood-brain barrier?
Elemental mercury vapor (metallic Hg).
Which form of mercury shows the greatest affinity for, and highest concentration in, the kidney?
Inorganic mercuric salts.
Describe the principal biochemical mechanism of mercury toxicity.
Strong binding to sulfhydryl (-SH) groups— inhibits key enzymes, increases membrane permeability, disrupts active transport, and causes mutagenesis.
By which routes is mercury primarily excreted?
Urine, feces, and breast milk; organic mercury is eliminated mainly in feces.
State four key acute symptoms after inhalation of mercury vapor.
Metallic taste, pneumonitis/pulmonary edema, headache/nausea/salivation, neurological signs such as ataxia or delirium.
What oral and renal signs follow ingestion of inorganic HgCl₂?
Grey-white erosions in mouth/tongue, abdominal pain, hemorrhagic GI tract, bloody diarrhea, acute tubular necrosis leading to scanty urine and kidney failure.
Which major neuro-sensory problems appear after ingestion of organic mercury compounds?
Visual and hearing loss, ataxia, tremors, and paralysis.
What is the term for chronic mercury poisoning?
Hydrargyrism.
What classic gum lesion is seen in chronic mercury poisoning?
A blue-gray line along the gingival margins.
Define Acrodynia (“pink disease”).
A hypersensitivity reaction in young children (<2 yrs) producing pink, peeling skin on hands, feet, cheeks, and ears, plus irritability and photophobia.
Which age group is most commonly affected by acrodynia?
Children under two years of age.
What caused Minamata disease?
Severe methyl-mercury toxicity from eating fish contaminated by industrial mercury discharged into water and converted by bacteria.
How does methyl-mercury reach humans in Minamata-type episodes?
Inorganic Hg → bacterial methylation → bioaccumulation in fish → human consumption → CNS injury.
List four hallmark neurological signs of methyl-mercury poisoning.
Disturbed gait, speech impairment, numbness/tremor, anxiety/depression (may progress to paralysis or coma).
How is mercury exposure confirmed in the laboratory?
Measurement of Hg in urine, blood, or hair; mercury is not a normal body constituent.
Name a chelating agent used to treat mercury poisoning.
Penicillamine (others include dimercaprol/DMPS/DMSA).
Identify four major environmental or consumer sources of cadmium.
Contaminated soils/fertilizers, batteries, plastics, tobacco smoke.
What lifestyle habit is one of the highest sources of cadmium exposure?
Cigarette smoking.
Which two organs accumulate the greatest cadmium burden?
Kidney and liver.
Cadmium in the liver binds to which low-molecular-weight protein?
Metallothionein.
Give two molecular mechanisms of cadmium toxicity.
Binds to sulfhydryl groups; competes with Ca, Zn, and Se in enzymes and bone, disrupting mineral metabolism and stimulating carcinogenesis.
Distinguish primary and secondary organ effects of cadmium.
Primary: lung, liver, kidney; Secondary: skeletal system (bone demineralization).
List two acute respiratory signs of cadmium inhalation.
Bronchospasm/irritation, pulmonary edema or chemical pneumonia.
What is the hallmark chronic renal lesion from cadmium?
Proximal tubular dysfunction leading to kidney failure.
Name two bone disorders linked to chronic cadmium exposure.
Osteomalacia and osteoporosis with fragile bones (pseudo-fractures).
Describe Itai-Itai disease.
Severe bone pain, fractures, and renal dysfunction due to chronic cadmium exposure from polluted irrigation water in Japan.
Mention two systemic effects of cadmium on reproduction or immunity.
Reproductive failure/infertility and immune system damage; also CNS injury.
Which dietary or supplemental elements have protective effects against cadmium toxicity?
Calcium, selenium, and zinc (plus antioxidants vitamins C & E, methionine).
Differentiate Cr³⁺ and Cr⁶⁺ with respect to toxicity.
Cr³⁺ is insoluble, non-corrosive, and essential; Cr⁶⁺ is corrosive, oxidizing, crosses cell membranes, and is carcinogenic.
How does hexavalent chromium (Cr⁶⁺) enter cells?
Via sulfate and phosphate anion transport pathways, then is reduced to Cr³⁺ intracellularly.
What is the major target organ of Cr⁶⁺ after inhalation?
Respiratory tract (nasal passages, bronchi, lungs).
State two acute respiratory effects of Cr⁶⁺ exposure.
Upper airway irritation and pulmonary edema.
Name two chronic respiratory consequences of Cr⁶⁺ exposure.
Bronchial asthma/sensitization and increased risk of lung cancer.
What two life-threatening effects follow acute ingestion of Cr⁶⁺?
Hemorrhagic gastroenteritis and acute renal failure (via tubular necrosis).
What are “chrome ulcers”?
Deep penetrating skin ulcers caused by direct or chronic Cr⁶⁺ contact.
Through which biological samples is chromium eliminated?
Urine primarily, also milk, hair, and nails.
By which main route does copper enter the body?
Oral ingestion (food, water, or veterinary/agricultural chemicals).
Name the principal plasma transport protein for copper.
Ceruloplasmin.
Explain how copper acts as a hematotrophic poison.
Weakens RBC membranes, creating Heinz bodies, causing hemolysis and methemoglobinemia.
What distinctive color may appear in vomitus during acute copper poisoning?
Blue-green vomitus.
What chronic oral sign suggests prolonged copper exposure?
Green or purple lines along the gum margins.
What genetic disorder causes pathological copper accumulation?
Wilson’s disease.
Which three organs are chiefly affected in Wilson’s disease?
Liver, brain (basal ganglia), and eyes (Kayser-Fleischer rings).
What is the major excretory pathway for excess copper?
Biliary excretion into the intestine, with some urinary and fecal loss.