Documente Academic
Documente Profesional
Documente Cultură
Carbon monoxide
• One of the most common fatal poisonings, occurs by inhalation.
• CO is a colorless, odorless gas that results from incomplete
combustion of hydrocarbons.
Common sources of CO in poisonings:
• House fires and improperly vented automobiles, gas heaters,
furnaces, hot water heaters, wood- or charcoal-burning stoves,
and kerosene heaters.
• Carbon monoxide is produced due to incomplete combustion of
organic matter.
• CO is produced when natural gas (methane or propane) burns.
• Inhaling tobacco smoke results in CO in the blood but not enough
to cause poisoning
CO
• Carbon monoxide has 200 times more affinity than oxygen for
haemoglobin.
• Carbon monoxide converts haemoglobin to carboxyhaemoglobin
and thus the oxygen carrying capacity is affected.
CO...contd
• Blood is bright red in colour and the mucous membrane is
healthy pink
• This poisoning commonly arises from exhaust fumes when
chicks are being transported by truck or from improper
ventilation in hatchers.
• Mortality may be high unless fresh air is provided immediately
• At necropsy, the beak is cyanotic, and a characteristic bright
pink color is noted throughout the viscera, particularly the
lungs.
• Diagnosis can be confirmed by a spectroscopic analysis of the
blood.
Treatment
• Patients should be removed from the source of CO and
stabilized as necessary.
• They are given 100% O2 (by nonrebreather mask) and
treated supportively.
• Hyperbaric O2 therapy (in a chamber at 2 to 3
atmospheres of 100% O2) typically should be
considered for patients who have any of the following:
Life-threatening cardiopulmonary complications, Loss
of consciousness (no matter how brief), A
carboxyhemoglobin level > 25%
• (the efficacy of hyperbaric O2 therapy is becoming more
controversial, with some studies suggesting harm)
Prevention
• Prevention involves checking sources of indoor combustion to
make sure they are correctly installed and vented to the
outdoors.
• Exhaust pipes should be inspected periodically for leaks.
• Cars should never be left running in an enclosed garage (near
pets).
• CO detectors should be installed because they provide early
warning that CO is free in a dwelling's atmosphere.
• If CO is suspected in a dwelling, windows should be opened, and
the dwelling should be evacuated and evaluated for the source
of CO
SELENIUM TOXICITY
(ALKALI DISEASE/BLIND STAGGERS)
SELENIUM
• As a micronutrient (0.1-0.3 ppm), it is added to the diet to
prevent several deficiency disease states of cellular
degeneration and cell mEmbrane damage such as white
muscle disease in cattle and sheep, hepatosis dietetica in
swine and exudative diathesis in chicken.
• Dietary allowance of selenium above the requirements during
pregnancy has been reported to improve selenium status of
the newborn calves
• Enhances calf vitality and immune response; -important
micronutrients in the feed/diet of animals.
Sources of Selenium
• Plants – important source in ruminants
(acute)
• Parenteral Se products (younger ones)
• Medicated Shampoos( SeS-in pets dermatitis,
dandruff)
• Insect repellants, lubrcicating oils, fungicides
( Se as antioxidant)
Seleniferous plants
• WOODY ASTERS (Xylorrhiza spp.);
• Astragalus (LOCOWEEDS, POISON-VETCHES);
• GOLDENWEEDS (Oonopsis spp.);
• Oxytropis spp.);
• Oonopsis spp. (GOLDENWEEDS);
• PRINCESS'S PLUME (Stanleya pinnata)
• Atriplex spp
• Selenium is present in inorganic and organic forms and all
animal species are susceptible to selenium toxicosis.
• Poisoning is, however, more common in forage eating
animals when dietary selenium level exceeds 5 ppm
• Severity of disease depends upon
– the oxidation state of selenium (selenide, selenite or selenate)
– quantity ingested
– Organo-selenium, after absorption in the form of selanomethionine
– May bc oxidize from selenide state to selenite or reduced from
inorganic selenate form to selenite.
– It is the selenite form which (selenium in selenite state may substitute
sulphur in the synthesis of aminoacids and proteins) is responsible for
toxicosis.
• Variable amounts (25-70 %) of dietary selenium may be
eliminated within 2 days of ingestion of a large dose
Toxicodynamics:
• Gastrointestinal signs and lesions in acute selenium toxicity
are, in part, due to the irritant nature of selenium in large
concentrations.
• The biochemical effects due to
• (i) Replacement of sulphur of aminoacids such as cysteine
and methionine resulting in the synthesis of abnormal
proteins and enzymes.(hoof and hair defects of chronic
selenosis.)
• (ii) Inhibition of SH - containing enzymes, such as succinic
and other dehydrogenases, may result in decreased ATP
synthesis.
• As a result of this, oxygen utilisation is decreased in liver,
kidneys and brain.
• Inhibition of cell oxidation-also due to interference with
haeme containing selenoprotein found in muscle tissue of
selenium - treated animals.
Toxicodynamics: ….contd