Metal poisoning – copper, zinc, thallium, tin, selenium, arsenic Lecture No. 10

Август 13, 2022

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Metal poisoning – copper, zinc, thallium, tin, selenium, arsenic Lecture No. 10

Содержание

2. Copper - Cu Intoxications quite rare Mainly from copper fungicides, coins etc. CuSO4 – for seeds,
3. In blood transported bound to albumin, ceruloplasmin Stored in liver and bone marrow Excretion in bile
4. Mechanism of action: Haematotrophic poison – directly toxic to erythrocytes Hepatotoxic – directly toxic to hepatocytes
5. Pathological examination: Inflammatory changes on GIT mucosa, green-blue colour of mucosa, hypertrophy of kidneys and liver,
6. Zinc - Zn Poisonings quite rare Zinc from medicines – common in dogs; zinc from containers
7. Intestinal absorption of zinc influenced by iron and copper Transported bound to albumin and macroglobulin Excreted
8. Clinical signs: gastrointestinal upset from direct irritation, anorexia, lethargy, hyperventilation, liver damage, pancreatitis, arthritis, multiorgan (mainly
9. Pathological examination: Degeneration of liver, kidneys, pancreas, petechias, haemorrhage in lymphatic nodes, spleen and brain, gastroenteritis,
10. Thallium - Tl Used for making low-melting point special glass for highly reflective lenses In developing
11. Mechanism of action: Inhibition of respiration enzymes and oxidative phosphorylation Interference with porphyrin and collagen metabolism
12. Often consequences such as trembling, paralyses and behavioural changes remain Pathological examination: haemorrhagic gastritis, ulceration, damage
13. Tin - Sn Mainly applied as various organic substances – phenyl- and methyl- tin compounds used
14. Acute intoxication: - Local irritation on mucosas, eye and skin irritations, headaches, stomach ache, severe sweating,
15. Selenium - Se In soil, cumulation in plants – can transform it into more toxic compounds
16. Acute form: - depression, ataxia, dyspnoe, salivation, cyanosis, anaemia, decreased fibrinogen and prothrombin, death due to
17. Arsenic - As Metallic arsenic not toxic – insoluble in water and acids Its compounds toxic
18. Mechanism of action: Trivalent compounds most toxic (pentavalent less) Binds to –SH groups – block of
19. Acute poisoning: - violent stomach pains, tenderness and pressure, retching, vomiting, sense of dryness and tightness
20. Pathological examination: haemorrhage on mucosa of GIT, pseudomembranes, necrotisation, fatty degeneration of parenchymatic organs Treatment: dimercaprol,
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Copper - Cu
Intoxications quite rare
Mainly from copper fungicides, coins etc.
CuSO4 –

for seeds, plants, antiparasitic for fish, Cu(OH)2, CuCl2.3Cu(OH)2, Cu2O
Cu1+ salts are water insoluble, Cu2+ salts are water soluble
Nutritional essential element
A part of superoxiddismutase, cytochrome- c-oxidase, monoamine oxidases etc.

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In blood transported bound to albumin, ceruloplasmin
Stored in liver and bone

marrow
Excretion in bile
Most sensitive species are sheep (unable to increase elimination process into bile – Cu/adenosine ATPase), other ruminants less, monogasters are quite insenstitive
In dogs – Bedlington + West higland white + Skye terriers, Dalmatians, Labrador retrievers and Doberman pinschers can have genetic predisposition for Wilson disease

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Mechanism of action:
Haematotrophic poison – directly toxic to erythrocytes
Hepatotoxic – directly

toxic to hepatocytes
Probably due to oxidation potential - catalyzes the production of very reactive radical ions – oxidative stress
Clinical signs:
Corrosive effect on GIT mucosa (haemorrhagic gastritis and enteritis), vomiting (green colour), colic, black excrements
Hypoxia – acute hemolytic crisis, damage to liver and kidneys
In chronic intake: apathy, anorexia, icterus, hepatic encephalopathy – neurological signs

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Pathological examination:
Inflammatory changes on GIT mucosa, green-blue colour of mucosa, hypertrophy

of kidneys and liver, icterus and dark kidneys in chronic poisoning
Treatment:
Activated charcoal, laxatives, GIT protection – sucralfat, treatment of anaemia, hypoxia, etc.
Addition of molybdenum and zinc in diet in sheep – decrease in copper absorption
Chelating agents – penicilamin (in Wilson disease)

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Zinc - Zn
Poisonings quite rare
Zinc from medicines – common in dogs;

zinc from containers made of galvanized metal plates – cattle
An essential element of the body
Present in about 200 metalloenzymes – e.g. carbonic anhydrase, alkaline phosphatase, lactate and alcohol dehydrogenases
Necessary for nervous system development, for immune system, required for vitamin A metabolism and calcification of bones, etc.
Chelates with cysteine and histidine, forms so called zinc fingers – bind to DNA, regulation of genetic activity

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Intestinal absorption of zinc influenced by iron and copper
Transported bound to

albumin and macroglobulin
Excreted in faeces, less in urine, milk, saliva
Detectable in every organ system, especially the prostate and liver, and is at its highest concentration in the tapetum lucidum
Mechanism of action:
Probably competes with copper and iron in the organism – decreased serum copper (in breathing enzymes, hematopoesis) – decreased utilisation of oxygen, oxidative stress
Decreased ceruloplasmin – antioxidant
Decreases glutathione levels

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Clinical signs:
gastrointestinal upset from direct irritation, anorexia, lethargy, hyperventilation, liver damage,

pancreatitis, arthritis, multiorgan (mainly kidney) failure
intravascular haemolytic anaemia, morphological changes of erythrocytes including nucleated erythrocytes, Heinz bodies and spherocytes

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Pathological examination:
Degeneration of liver, kidneys, pancreas, petechias, haemorrhage in lymphatic nodes,

spleen and brain, gastroenteritis, arthritis, in ZnO inhalation intoxication lung emphysema and oedemas in chest area
Treatment:
Eradication of metal particles from stomach, administration of Na2CO3 – formation of insoluble ZnCO3
Blood transfusion in severely anaemic patients
EDTA

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Thallium - Tl
Used for making low-melting point
special glass for highly

reflective lenses
In developing countries still permitted as a pesticide (rodenticide, insecticide)
Body absorbs thallium very effectively, especially through the skin, lungs, GIT
Two-phase elimination – most within 24 hours in urine, but the rest stays for weeks and is excreted via faeces
Undergoes enterohepatic circulation
Cummulated in brain, kidneys, bones

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Mechanism of action:
Inhibition of respiration enzymes and oxidative phosphorylation
Interference with porphyrin

and collagen metabolism
Exchange with K+ in muscles, neurons (Na/K ATPase), stabilisation of ribosomes etc.
Inhibition of mitosis, sweating and sebaceous glands
Clinical signs:
Acute - Stomach ache, colic, diarrhoea, bradycardia or tachycardia (exchange with K+, damage to nervus vagus), nervous system damaged – tremors, paralysis, reversible hair loss
Chronic – anorexia, stomach ache, nerve pains and joint pains, peripheral neuropathies, alopecia, red skin, kidney damage

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Often consequences such as trembling, paralyses and behavioural changes remain
Pathological examination:

haemorrhagic gastritis, ulceration, damage of spleen, kidneys, hyperaemia of brain
Treatment: Prussian blue - Fe7(CN)18(H2O)x – p.o., formation of non-soluble complexes that are excreted in bile – inhibition of enterohepatic circulation
+ fluid therapy to maintain kidney function

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Tin - Sn
Mainly applied as various organic
substances – phenyl-

and methyl-
tin compounds used as fungicides
The number of applications of organic tin substances is still increasing - the paint industry, the plastic industry, agriculture
Triethyltin is the most dangerous organic tin substance
Absorption through food, breathing and skin
Accumulation in an organism
Mechanism of action:
Increases permeability of mitochondria membranes for anions – mineral imbalance (Ca2+). Also inhibition of Ala-D, but weaker then in lead. Disturbance in steroid hormone synthesis.

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Acute intoxication: - Local irritation on mucosas, eye and skin irritations, headaches,

stomach ache, severe sweating, urination problems, severe tremor and convulsions
Chronic intoxication: - Depressions, liver damage, shortage of red blood cells, brain damage (anger, sleeping disorders, forgetfulness, headaches)
- Malfunction of immune system – inhibition of NK cells function – thus increased risk of carcinogenesis
Pathological examination: necrosis on liver and kidneys, brain oedema, corrosive lesions on mucosa
Treatment: Carbo adsorbens, symptomatic

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Selenium - Se
In soil, cumulation in plants –
can transform

it into more toxic compounds
In middle Europe lack of selenium in soil and food !
Poisonings in north America and south Africa, here due to overdose during treatment (in pigs and cattle)
Very good absorption through guts, deposition in liver, spleen, kidneys, hair and horn of hoof
Substitutes sulphur in amino-acids, inhibition of oxidation-reduction enzymes

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Acute form:
- depression, ataxia, dyspnoe, salivation, cyanosis, anaemia, decreased fibrinogen

and prothrombin, death due to respiration collapse
Chronic form:
- weight decrease, anorexia, loss of hair, disturbances in hoof formation, leg paresis, damage of joints and long bones
Pathological examination: generalised haemorrhages, ascites, lung oedema, degenerative changes on liver, kidneys – acute form; atrophy of myocardium and liver cirrhosis in chronic form
Treatment: symptomatic

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Arsenic - As
Metallic arsenic not toxic –
insoluble in water

and acids
Its compounds toxic
Nowadays poisonings quite rare, but its effect known since ancient times
Used as a pesticide, in industry
Absorption via guts or skin – systemic toxicity
Excretion via urine
Deposition in skin, in nails and hair for many years
If administered in low doses – addiction - mithridatism

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Mechanism of action:
Trivalent compounds most toxic (pentavalent less)
Binds to –SH groups

– block of many enzymes (oxidative phosphorylation, glycolysis)
Damage of mucosa, endothelium,
Increased permeability of vessels, decrease in blood pressure
Clinical signs:
Peracute poisoning (within a few seconds to a few minutes):
- collapse of blood circulation, dilatation of vessels, sometimes vomiting and diarrhoea

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Acute poisoning:
- violent stomach pains, tenderness and pressure, retching, vomiting,

sense of dryness and tightness in the throat, thirst, hoarseness and difficulty of speech
- the matter vomited, greenish or yellowish, sometimes streaked with blood
- convulsions, delirium, death due to circulatory collapse
Chronic poisoning:
- strong profuse diarrhoea, inappetence, dehydration
- changes in skin colour, formation of hard patches on the skin
- skin cancer, lung cancer, cancer of the kidney and bladder

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Pathological examination:
haemorrhage on mucosa of GIT, pseudomembranes, necrotisation, fatty degeneration

of parenchymatic organs
Treatment:
dimercaprol, sodium thiosulphate, symptomatic

Metal poisoning – copper, zinc, thallium, tin, selenium, arsenic Lecture No. 10

Содержание

Copper - CuIntoxications quite rareMainly from copper fungicides, coins etc.CuSO4 –

In blood transported bound to albumin, ceruloplasminStored in liver and bone

Mechanism of action:Haematotrophic poison – directly toxic to erythrocytesHepatotoxic – directly

Pathological examination:Inflammatory changes on GIT mucosa, green-blue colour of mucosa, hypertrophy

Zinc - ZnPoisonings quite rareZinc from medicines – common in dogs;

Intestinal absorption of zinc influenced by iron and copperTransported bound to

Clinical signs:gastrointestinal upset from direct irritation, anorexia, lethargy, hyperventilation, liver damage,

Pathological examination:Degeneration of liver, kidneys, pancreas, petechias, haemorrhage in lymphatic nodes,

Thallium - TlUsed for making low-melting point special glass for highly

Mechanism of action:Inhibition of respiration enzymes and oxidative phosphorylationInterference with porphyrin

Often consequences such as trembling, paralyses and behavioural changes remainPathological examination:

Tin - SnMainly applied as various organic substances – phenyl-