Flashcards
Neuro toxicity 2
Cards in this deck (44)
- 1Clonic seizureRecumbent, unconscious, with paddling, running, nystagmus
- 2Toxic causes of polioencephalomalaciaThamine deficiency due to thiaminase
Sulphur excess (inhibition of cytochrome C oxidase --> cell energy starvation) - 3Pathology in horsesDecreased blood thiamine
Increased blood pyruvate.
Maybe some myocardial oedema, cerebral congestion. Gross lesions usually not very specific - 4Pathology in sheepLarge amount of fern in rumen. Polioencephalomalacia. All cerebral lobes affected. Lesions in cerebral lobes fluoresce under UV light.
- 5Treatment horses and sheepHorses: good prognosis if able to stand. Give thiamine parenterally 100mg bid for 1 day then sid for 7 days.
Sheep: if no response after 6-8hrs prognosis poor. Give thiamine parenterally. - 6Sources of excess sulphur1. Molasses
2. some plants
3. manure gas
4. H2S from petroleum, goethermal wells - 7CSx signs-intermittent excitement
convulsions
sudden death may occur from inhalation of large amounts of H2S
An odour of sulphur
anorexia
hepatic necrosis, cyanosis, dyspnoea - 8Pathology of sulphur poisoningTransient odour of H2S in rumen.
Polioencephalomalacia, lesions fluoresce under UV if well developed.
+/- mucosa blackened by metal sulphides of animals receiving mineral supplements. +/- hepatic necrosis and haemorrhage. - 9Treatment and prevention of Sulphur poisoningCases not always responsive to thiamine admin. Increased dietary thiamine may be protective. Use ammonia chloride as a urinary acidifier, instead of ammonium sulphate.
- 10CorynetoxinsBacterial pre-formed toxins.
Associated with annual ryegrass. - 11Sources of corynetoxinsPasture grasses carrying bacteriophage-infected Rathayibacter toxicus bacteria infecting seedhead galls initiated by Anguina agrostis nematodes.
Host grasses include annual ryegrass, yellow slime on seedheads. - 12Pathogenesis of corynetoxinsInhibit N-glycosylation of proteins and thus cell membrane synthesis. Impairs cardiovascular function and vascular integrity, interfering with peripheral circulation and oxygen distribution.
- 13Conditions of corynetoxinsClinical signs are delayed, as its a cummulative poisoning usually.
Infected by eating mature seedheads on standing pasture (most cases in Nov-Jan).
Can be a long term contaminant of hay containing galls.
Cobalt deficient sheep more susceptible.
CSx after 2-6 days grazing. - 14CSx of corynetoxin poisoningAcute: intermittent convulsions --> death
Subacute: high stepping gait, muscle tremor, collapse, neck ventroflexion, limb paddling.
Affected animals left undisturbed often regain their feet and return to apparent normality. Death occurs within a few hours or up to 8 days after onset. - 15Pathology of corynetoxin poisoningIncreased liver enzymes
Pale liver (fatty change)
Haemorrhages
Perivascular oedema in the brain
Hepatocyte vacuolation - 16Treatment of corynetoxinsRemove from pasture in low stress manner. Cyclodextrin toxin binding agent. Monitor pastures for presence of galls (eliminate nematode from pasture).
- 17Lead poisoningSources: lead based paint, batteries, old lead pipes, young are more susceptible than adults. Lead shot contaminating pasture a problem for birds.
- 18Minor sources of lead and species affectedDomestic sources: solder, linoleum, golf balls, fishing sinkers, putty --> dogs
Lead mines and smelters --> pasture contamination
Lead based parasiticides used on crops.
Industrial and vehicular emissions contaminating urban air and vegetation. - 19Mode of action of lead poisoningStored in liver, excreted in bile and urine and milk. May form insoluble complexes in kidneys and in liver (bright pink intranuclear inclusion bodies).
Deposited in bone and forms a reservoir.So any osteolytic process e.g. releasing Ca from bones, also release lead. - 20Pathogenesis of leadInhibits enzymes systems with free sulphydryl groups which affects many target organs. Mimics enzyme co-factors like Ca, Fe, Zn, but non-functional.
Lead in the blood blocks haeme synthesis by blocking delta-aminoevulinic acid --> anaemia and build up of porphyrinuria.
Binds to brain capillary endothelial cells increasing capillary permeability resulting in oedema in the brain.
Generates free radicals.
Neuronal necrosis --> induce seizures.
In PNS have demyelination --> wallerian degeneration - 21CSx lead poisoningAtaxia
Sudden death or may take days.
Insidious onset makes Dx difficult.
Can have convulsions.
Dogs can vomit +nervous signs.
Cats rarely have seizures, but do vomit.
Horses: violent convulsions, peripheral neuropathy (induced roarers syndrome). - 22Lead poisoning GM findingsUsually non-specific
-enlarged kidneys, mild enteritis, possible dehydration, emaciation, bone (growth retardation lattice at physis).
Lead fragments in reticulum, sump oil.
Lead pellets in upper GIT of birds. - 23Lead histopathCerebral odema, polioencephalomalacia (sometimes).
Acid fast intranuclear inclusion bodies in renal cortex, hepatocytes and osteoclasts of canine metaphyseal bone.
Birds may have a peripheral neuropathy, degenerative arteritis, cardiomyopathy. - 24Tx of leadControl seizures with anticonvulsants, anaesthetics.
Adsorption and removal from GIT.
Chelating agents to bind any circulating lead.
Thiamine hydrochloride reduced Pb deposition in nervous system. - 25Organophosphorous compounds SourcesInsecticides/acaricide in dips, sprays, pour-ons.
Deliberate poisoning of feral animals. - 26Pathogenesis of OPsOPs phosphorylate AChE molecules. So there is accumulation of ACh in gap junction resulting in the overstimulation of ACh receptors. Return to optimal AChE function in tissue depends on slow replacement (20-30 days) of phosphorylated AChE molecules by new molecules.
- 27How can OP toxicity occur at normally safe doses?If the animal has low tissue glutathione (as detoxification is mediated by glutathione dependent). Aliesterases (isomers of OPs) form from OPs out of date are more potent than normal OP.
- 28CSx of OP poisoning-Muscarinic effects: constricted pupils, excessive salivation, increased GI tone --> diarrhoea, abdominal pain. Bronchoconstriction --> dyspnoae. Bradycardia.
-Nicotinic effects: involuntary twitching, convulsions, generalised tetany, tachycardia, hypertension
CNS effects: restlessness, tremor, convulsions, - 29Pathology of OP poisoningNo lesions at necropsy in acute cases. May be a strong chemical odour in rumen/stomach.
- 30OP treatment1. Atropine: blocks excess Ach effects for immediate relief of acute muscarinic signs
2. Oxime 2-PAM: hydrolyses phosphorylated AChe if not aged and bound irreversibly yet. 2-PAM without atropine has minimal effect.
3. Reduce exposure: wash OP off skin, induce vomiting, dose with activated charcoal. - 31Carbamates: sources and speciesInsecticides and acaricides, affecting livestock, dogs and cats. It is molluscicide. So poisoning often due to accidental or careless treatment at abnormally high dose rates, or dogs/cats have access to molluscicide used in garden.
- 32Carbamates pathogenesisAnti-cholinesterase action. Directly toxic without hepatic activation. Carbamylated AChE is readily hydrolysed so can be reversed. Rapidly metabolised in liver. Clearance in 2-3 days.
Most break down in sunlight. - 33Carbamate CSx, path, Dx and xSame as for OPs, May see blue dye in stomach contents if they have eaten molluscicide pellets.
- 34MetaldehydeA molluscicide used in gardens so dogs and cats most at risk.
Greenish colour. - 35Pathogenesis of metaldehydeRapid hydrolysis in stomach into acetaldehyde which is rapidly absorbed to reach the liver which it is oxidised. If the rate of absorption exceeds the rate of oxidation toxicity occurs.
Acetaldehyde easily crosses the BBB to reduce GABA neurotransmitter and increase monoamine oxidase activity possibly causing the tremors and convulsions. - 36CSx of metaldehyde toxicityOnset is a few mins to several hours post ingestion.
Anxiety, depression, salivation, vomiting, incoordination, hyperaesthesia, muscle tremors, prostration with limbs extended in continuous spasms, convulsions and opisthotonus. Spasms not provoked by ext stimuli unlike strychnine. - 37Pathology of metaldehydeNon-specific, green dye from pellets in stomach contetns, may see hepatocellular degeneration.
- 38Conditions of sodium poisoningDepends on fresh water supply at time of salt ingestion, if there is an unlimited water supply then salt poisoning is highly unlikely.
Pigs and poultry most susceptible. - 39Mechanism of sodium toxicityDehydraton --> haemoconcetration --> brain astrocytes gradually adapt to high osmolality of blood --> cytoplasmic osmotic pressure increases.
When water become available animal drinks copious amounts so large amounts of water move from vasculature into brain cells --> cerebral oedema --> compression of blood vessels in skill --> ischaemia of cortex --> death or csx of brain injury - 40CSx of sodium poisoning in pigsSeries of seizures, repeated at specific time intervals in each affected animal.
Twitching of face and ears,
Dog sitting position, head drawn slowly back and upwards, muscle tremors,
Lateral recumbency + violent paddling and dyspnoea - 41Csx of sodium poisoning in cattleAcute effects from very rapid intake: hyperexcitable, seizures with paddling, opisthotonus, apparent blindness, knuckling of fetlocks, head pressing, circling, muscle tremors, urinary incontinence, death in 24hrs.
- 42CSx of sodium toxicity in chickensSudden death, depression, excessive thirst, increased water consumption, dyspnoea, ataxia, paralysis,
- 43Pathology of sodium poisoningCerebral oedema, +/- polioencephalomalacia.
In pigs only there is eosinophilic meningoencephalitis in first 48hrs. Cerebral laminar necrosis.
In poultry: subcutaenous oedema, ascites, hydropericardium, pulmonary oedema, liver congestion, cardiac dilation. - 44Brundelsia sppToxic plant in australia. Dogs may eat ripe fruit in large amounts.
CSx: convulsions, extensor rigidity, opisthotonus.
Gastroenteritis. Treat with emetics, activated charcoal and anti-convulsants.
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- Veterinary Medicine Flashcards on Neuro toxicity 2 , created by Alice Kermond on 25/09/2016.
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