Flashcards
Neurological Toxicants
Cards in this deck (26)
- 1Histological changes of the nervous system-Neurons: necrosis, red and dead chromatolysis, swelling, accumulations of neurofilaments, axonal swelling, fragmentation, wallerian degeneration.
-Astrocytes: swelling, hypertrophy, accumulation of glycogen granules, increased GFAP, Alzheimer type II cells.
-Microglia: microgliosis, enlargement
-Oligodendrocytes: swelling, demyelination - 2Why is the nervous system so susceptible?-contains lots of myelin and lipoproteins with low levels of antioxidant enzymes and so is very sensitive to lipid peroxidation
-has high metabolic rates and is exclusively dependent on aerobic glucose-dependent metabolic pathways. Brain is highly sensitive to toxicants disrupting mitochondrial function and energy metabolism. - 3CNS protection from toxicosis1. Blood brain barrier
-physical barrier reducing permeability of endothelial cells.
-metabolic barrier containing P glycoproteins with are efflux pumps on the the endothelial cells which actively pump out xenobiotics. - 4When does the BBB fail?1. Certain brain regions dont have a BBB (circumventricular organs, autonomic ganglia)
2. Infants, neonates can have an open BBB.
3. Lipophilic agents readily cross the BBB, hydrophilic agents are excluded.
4. Trauma ischemia, and toxicosis may damage the BBB. - 5Major nervous toxicants that cause sudden death1. Urea/Ammonia
2. Neurotoxic cyanobacteria
3. Cyanogenic glycosides
4. Theraphosid spider venom (dogs) - 6Toxicants that cause clonic seizuresThose that cause polioencephalomalacia syndromes (Thiaminase, sulphur associated).
Corynetoxins
Lead
Organophosphorous compounds.
Carbamates
Metaldehyde
Sodium ion
Brunfelsia spp. in fruits (dog) - 7Toxins that cause tetanic seizuresStrychnine
Phosphide rodenticides
Duranta erecta - 8Toxins that cause tremorsIndole alkaloids of Phalaris spp.
Lolitrems
Paspalitrems
Synthetic pyrethroids
Macrocycline lactone anthelmintics. - 9Toxins that cause ataxiaCycads (cattle)
Xanthorrhoea spp (cattle)
Aliphatic nitrocompounds
Thiaminase (horse)
Cyanogenic glycosides - 10Toxins that cause deranged behaviour/deep depression-Swainsonine
-Fumonisins (horse)
-Tetrahydrocannabinol
-Barbituates
-Calystegines
-Lead
-Hepatoencephalopathies - 11Toxins that cause paralysis/paresisBotulism
Ciguatoxin
Tetrodotoxin
Polyether inonophore antibiotics.
Selenium (pig)
Macadamias (dogs). - 12Toxins causing blindness-Stypandrol, halogenated salycylanides, Ptaquilosie --> Retinal degeneration.
-Minosine ,xanthrrhoea --> cataracts
Furanocoumarins, organic aresenicals.
Hepatic encephalopathies, polioencephalomalacia, fumonisn. - 13Ammonia toxicityRuminants: oral lethal dose is 0.4-1.5g urea/kg.
Horses: lethal at 3.5g urea/kg - 14Conditions of ammonia poisoning1. Excessive or rapid intake of urea containing feedstuff. This can occur in feed mixing errors, supplements to hungry cattle, failing to dissolve urea completely in molasses, mixing rainwater with M8U so cattle drink conc urea, or if there is a malfunction of urea dispensing mechanism to water supply.
2. Contamination of drinking water with urea
3. Unrestricted intake of high protein feed e.g. soya bean meal. - 15Clinical signs of urea toxicity1. onset is 10-30mins after dose, high case fatality rate
2. Rapid death
3. Clonic convulsions
4. Abdominal pain, ruminal tympany
5. Dyspnoea,
6. Muscle tremor - 16Pathological signs of urea toxicityIncreased serum urea
Non-specific necropsy (agonal petechiation, rapid bloat, pulmonary oedema). - 17Treatment of Urea toxicityEmpty rumen via stomach tube or rumenotomy
Drench with cold water to decrease concentration and temperature to reduce speed of ammonia production from urea
Drench with acetic acid to alter rumen pH
Monitor for relapses - 18Pathogenesis of cyanobacterial alkaloid neurotoxinsParalytic shellfish toxins block sodium channels = saxitoxin.
Anatoxin-a and homoanatoxin-a mimic Ach act the nicotinic and muscarinic receptors causing constant depolarization resulting in paralysis of skeletal muscle and respiratory muscles.
Anatoxin-a also has a sudden death factor which irreversibly inhibits cholinesterase - 19Clinical signs of cyanobacterial alkaloid neurotoxins-Sudden death, dyspnoea, respiratory arrest, +/- blue or blue-green stains around mouth and on legs. +/- signs of cholinesterase inhibition
- 20Conditions of cyanobacterial poisoningIncreased water nutrient concentrations from human/animal waste or fertiliser runoff. + wind which concentrates the algae blooms at livestock access points. Or using irrigated water contaminated with cyanobacteria to water crops fed to animals.
- 21Treatment of cyanobacterial poisoningPrognosis is grave. Can try atropine and oximes. Oximes can reactivate cholinesterases by removing phosphorous.
- 22Cyanogenic glycosides -source, species affected, conditions of poisoningSource: Sorghum spp, Eucalyptus cladocalyx
Species: all, but ruminants much more susceptible
Conditions: young leaf material, stressed plants, sorghum hay can retain toxicity. - 23Pathogenesis of cyanogenic glycosides poisoningCyanide blocks cytochrome C oxidase inhibiting mitochondrial cellular respiration.
- 24CSx and pathological findings of cyanogenic glycosidesSudden death, may see rapid deep breathing, weak irregular pulse, muscle weakness, coma, bright red venous blood (as cyanide binds to Hb instead of O2, so lots of free O2 in the blood).
Chronic toxicity: ataxia, urinary incontinence, cystitis, white matter degeneration in spinal cord and brain, foetal arthrogryposis. Goitre in sheep. - 25Cyanid poisoning treatmentDeliberate induction of methaemoglobinaemia (MetHb) which competes with cytochrome oxidase of cyanide ions. Can induce with nitrites.
- 26Theraphosid spider venomOnly dogs affected, neurotoxic. Flaccid paralysis, death within hours of being bitten.
Information
- Description
- Veterinary Medicine Flashcards on Neurological Toxicants , created by Alice Kermond on 25/09/2016.
- Created by
- Alice Kermond · Sep 2016
- Updated
- Apr 6, 2018
- Views
- 0
- Tags
- Rating