6400815
Descrição
FlashCards por Alice Kermond, atualizado more than 1 year ago
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Criado por Alice Kermond
aproximadamente 8 anos atrás
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| Questão | Responda |
| Nutmeg liver? | Chronic passive congestion of the liver resulting in dilated sinusoids, atrophy or loss of hepatocytes around central veins. |
| General pathophysiology of toxins of the heart | 1. Altered cardiac function may occur from abnormalities in; ion movement, loss of membrane function, contractile function, or energy metabolism. 2. Effects of toxin exposure on the heart include; developmental anomalies, acquired alterations in function of the conduction system, myocardium or heart valves, and inflammation/necrosis and hypersensitivity. |
| Morphologic responses to toxicants | 1. Hypertrophy 2. Ventricle dilation 3. Scarring/ myocardial fibrosis 4. Myocardial degeneration, necrosis and apoptosis (cardiac glycosides) |
| Major CV toxins associated with sudden death | 1. Fluoroacetate 2. Cardiac glycosides 3. Cardioactive steroids of Bufo spp 4. Polyether ionophore antibiotics |
| Major CV toxins associated with chronic heart failure | 1. Irritant diterpenoids of Pimelea spp 2. Gossypol (in cotton seed) 3. Persin (in avocado) |
| Major CV toxins associated with peripheral vascular dysfunction | Ergot alkaloids |
| Sources of fluoroacetate | 1. Plant sources (shrubs or trees): in Africa, South America and Australia 2. 1080 baits (sodium monofluoroacetate) 3. Animal carcasses contaminated with 1080 bait and live marsupials and birds exposed to toxic plants --> secondary poisoning of carnivores. |
| Mode of action of fluoroacetate | 1. Disrupts the citric acid cycle by binding and inactivating coenzyme A 2. Fluorocitrate forms which ireversible blocks enzyme cis-aconitase 3. Markedly reduced cell ATP production |
| Example of plant containing fluoroacetate | Gastrolobium spp. |
| Clinical signs of fluoroacetate poisoning in dogs | GIT and CNS signs predominate. -initial hyperirritability -hyperactivity, vomiting, repeated urinating, defecation -dyspnoea + frothing at mouth - Hysteria, barking -tonic/clonic convulsions, opisthotonus, paddling -hyperthermia from seizures and running Time from onset of CSx to death is 2-12hrs. |
| Clinical signs of fluoroacetate poisoning in herbivores | CV signs predominate. -sudden death -may see tachycardia, arrhythmia, hyperventilation. -groaning and teeth grinding (sign of pain) -collapse, terminal convulsions, death |
| Fluroacetate treatment for dogs | -Provide acetate ions to compete with fluoroacetate for binding sites to reduce conversion of fluoroacetate to fluorocitrate. -Glyceryl monoacetin, acetate ions in electrolytes solution + sodium bicarbonate. Prognosis is grave. |
| Mechanism/conditions of cardiac glycoside poisoning | Cardiac glycoside containing plants are usually not palatable, so are only ingested if the animal is starving. They retain their toxicity when dried, and they are likely more palatable with dried so have a greater chance of being ingested along with other dry feed in this time. Toxic quantities can be accidentally mixed in with feed e.g. garden waste, weed contaminants in hay, or seed in the feed grains. |
| Action of cardiac glycosides | - cardiovascular: inhibit cardiac sodium pump (Na+ K+ ATPase), thus disrupt membrane potential resulting in influx of Ca2+ into cardiac myocytes and increased contractility. |
| Clinical signs of cardiac glycoside toxicity | - sudden death -diarrhoea +/- blood -cardiac arrhythmias -vomiting -dyspnoea -ruminal atony -abdominal pain |
| Treatment of cardiac glycoside toxicity | Ruminants: lots of activated charcoal, electrolyte replacement solution, antiarrhythmic drugs Horses: activated charcoal, treat abdominal pain, antiarrhythmic drugs. |
| Toad toxin | Steroid toxin secreted from parotid glands and skin glands over the body. Often then licked by young/curious dogs. Toxin is analogous to cardiac glycocides in plants. Death can follow one exposure. Fatal dose 1mg/kg or the contents of both parotid glands. Small young dogs most at risk. |
| Clinical signs of toad toxicosis | -Rapid onset after contact -buccal irritation manifesting as profuse salivation, head shaking, pawing at mouth and hyperaemia of the buccal mucosa. -systemic signs: vomiting, ataxia, cardiac arrhymthmia, diarrhoea, convulsive seizures in severe cases (precede death). |
| Treatment of toad toxicosis | Prognosis is good in mild cases, poor if severe (CNS signs). -remove venom from mouth (flushing with water for 10mins) -control salivation and bronchoconstriction e.g. with atropine -sedate -support and monitor heart function -oral activated charcoal. |
| Polyether ionophore antibiotics | -monensin -lasalocid -salinomycin (A few main ones) |
| Pathogenesis of toxicity with ionophore antibiotics | They interfere with ion flux across biological membranes --> hydropic swelling of striated muscle cells --> mitochondrial swelling and degeneration --> striated muscle necrosis --> heart failure, paresis. Horses have the highest sensitivity for damage to the heart. Peripheral polyneuropathy and myocardial degeneration occurs in cats that ingest salinomycin |
| Scenarios where ionophore antiobiotc poisoning may occur | -failure to dilute a concentrate -mixing errors -horses getting into cattle feed, or feed for animals mixed up -cattle/sheep fed poultry litter -dogs/cats fed contaminated commercial diets -dogs chewing intra-ruminal slow release devices containing monensin -interactions |
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