Flashcards
Basics of Veterinary Toxicology
Flashcards do conjunto (21)
- 1XenobioticChemical found in an organism that is not normally to be present e.g. toxins, drugs. They are not necessarily harmful.
- 2PoisonA xenobiotic that after having contact with, or being ingested/inhaled/injected in sufficient quantity will be detrimental to the organism.
- 3ToxinA poison of biological origin
- 4For a substance to be hazardous it must ...1. Be likely to be encountered in a form that can be assimilated
2. Be likely to be ingested, inhaled, or come into contact with the integument in sufficient quantities to cause harm.
3. Reach a site within the body where it can do harm which often requires uptake and transport
4. Interact with crucial metabolic pathways ans these may vary from species to species. - 5Toxicity rankingsVery toxic: if ingested, aspirated or injected at 25mg/kg
Toxic: kill at 25-200mg/kg
Harmful: toxic between 500-1500mg/kg - 6Cumulative poisonsToxin accumulates until it reaches threshold level at which clinical signs begin to appear. A mechanism of chronic intoxication.
- 7Why is determining the NOEL for carcinogens difficult?1. Carcinogenic doses vary widely with individuals and within a species
2. Multi-step nature of carcinogenesis
3. Long time between exposure and disease
4. Effects of other promotors (xenobiotics, environmental factors, physiological factors may be involved/required) - 8Chronic toxicityEntails long term exposure, but the onset of clinical signs may be acute or chronic.
Occurs due to persistent exposure resulting in small amounts of organ damage which are additive.
Or the toxin accumulates in tissues until levels are sufficient to cause harm. - 9Pyrrolizidine alkaloid toxicosisAn example of chronic toxicity with acute onset of clinical signs. The seasonal exposure to plants containing Pyrrolizidine alkaloid causes liver damage. Once the amount of liver damage exceeds its functional reserve (can be years) there is hepatongenous photosensitisation which chronic lesions in the liver.
- 10Copper toxicosis in sheepAn example of a chronic toxicity where the toxin accumulates. Copper accumulates in the liver until levels reach 600ppm and there is some kind of stressor triggering the sudden release of this copper into the blood which causes free radical damage to the RBCs and haemolysis.
- 11Secondary toxicosesIf carnivores eat the flesh or viscera of poisoned animals they may ingest sufficient toxin to cause acute toxicosis. E.g. cats and dogs eating rats poisoned with rodenticides
- 12To cause adverse effects the toxicant ...1. Must be able to reach the effector site in concentrations sufficient to cause damage. Completely insoluble compounds or non-volatile compounds usually have little to no toxicity.
2. The host/victim must have cell structures or metabolic pathways that will be adversely affected by the compound or it metabolites. - 13Main sites of biotransformationLiver, lungs and kidneys.
- 14Phases of biotransformation1. Degradative reaction involving oxidation, reduction or hydrolysis. Occurs in the SER and requires cytochrome p450. The metabolites may be more or less toxic.
2. Conjugation with a hydrophilic molecule so the compound is able to be excreted e.g. with bile or in urine. - 15InductionThe up-regulation of cytochrome P450 or mixed function oxidases in the liver in response to increased amount of substrates requiring biotransformation. There is SER hypertrophy and glassy hypertrophies cytoplasm of hepatocytes.
Induction usually decreases the potential toxicity of target compounds. It may increase toxicity if the metabolite produced by biotransformation is more toxic, or if there is increased metabolism or hormones or related molecules. - 16ResistanceInnate property developed by selection over generations and possessed by all members of the species. E.g. Koalas ability to obtain nutrients from eucalyptus leaves and minimal toxic effects.
- 17ToleranceAn acquired trait, developed by the individual
- 18Mechanisms of resistance1. Enhanced endogenous or exogenous biotransformation
2. Modification or circumvention of biochemical pathways that are vulnerable to the toxin
3. Development of metabolic pathways that produce less toxic metabolites
4. Alterations in uptake and transport. - 19Mechanisms for tolerance1. Ingestion of sublethal amounts altering absorption, storage or elimination rate.
2. Induction of metabolic pathways or alternative pathways
3. Altered uptake, storage of elimination through changes in transport mechanism
4. Partitioning of lipophilic substances into fat stores. - 20Toxin function at a cellular level can interfere with...1. Energy supply- respiration and energy production
2. Membrane integrity or function, esp of the mitochondria
3. Denaturation of structural or metabolic proteins
4. Inhibition of an enzyme, co-factor binding, competing for substrate or irreversibly binding to active sites etc.
5. DNA: mutations, epigenetic effects (stopping cell division, protein transcription etc.) - 21—
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- Veterinary Medicine FlashCards sobre Basics of Veterinary Toxicology , criado por Alice Kermond em 19-09-2016.
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- Alice Kermond
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