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80 Cards in this Set
- Front
- Back
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List some common hepatotoxins
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paracetamol, aflatoxins, trimethoprim‐sulpha drugs, zinc, iron |
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List some common nephrotoxins
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ethylene glycol, easter lily (cats), raisin ingestion (dogs + cats), aminoglycosides, paraquat, NSAIDS |
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what poisoning is oxygen supplementation contraindicated?
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paraquat poisoning |
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Give 3 examples of anticonvulsant drugs used to control seizures?
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Diazepam Barbiturates Propofol (care in cats with CRI) |
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When should emesis NOT be induced in a poison case?
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NOT if impaired consciousness or absent gag reflex NOT if the toxin is caustic/corrosive/liquid paraffin |
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List 4 emetic drugs
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Apomorphine (0.04mg/kg IV or into the conjunctival sac) Ipechacuana syrup (1‐2mls/kg PO) Xylazine in cats (0.5mg/kg IV) Dexmedetomidine in cats |
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Describe how to perform a gastric lavage |
- Light anaesthesia may be necessary -Endotracheal intubation (inflated cuff) to reduce the risk of aspiration of lavage -Stomach tube passed -Lavage repeatedly with warm saline/water (5‐10ml/kg) |
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What can be given to reduce further absorption of the toxin?
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Purgatives |
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When are repeated doses of activated charcoal required?
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for toxins with enterohepatic circulation e.g. ibuprofen |
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Give 2 examples of diaretics
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frusemide (1‐2mg/kg) mannitol (0.5‐1g/kg infusion) |
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When can intravenous fat emulsion be given?
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-CNS toxicities e.g. permethrins, ivomectin, mycotoxins, etc. -Life‐threatening arrhythmias caused by lipid‐soluble drugs |
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What are the risks of using intravenous fat emulsion?
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Risk of pancreatitis (dog), peri‐vascular inflammation |
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How is paracetamol eliminated? Why is this a problem for cats?
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-conjugation with glucuronide and sulphates in the liver -non‐toxic conjugates are excreted in the bile and urine cats have limited capacity of sulphates and cannot use the glucuronide pathway --> instead paracetamol metabolised by cytochrome p450 --> toxic metabolites |
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The toxic metabolites from paracetamol metabolism by cp450 result in? |
- depletion of production and stores of glutathione |
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Paracetamol toxicity is dose dependent, what are the doses for dogs and cats?
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200‐600mg/kg in dogs 50‐100mg/kg in cats |
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How does paracetamol toxicity result in chocolat coloured membranes?
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hb is also denatured --haemoglobinuria --haemolytic anaemi |
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How can paracetemol result in jaundice?
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Hepatocellular damage by toxic metabolites |
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List some CS of paracetamol poisoning? |
Facial, paw and pulmonary oedema Vomiting, ataxia and collapse (cats) Depression, weakness, anorexia (dogs) Facial, paw and pulmonary oedema Vomiting, ataxia and collapse (cats) Depression, weakness, anorexia (dogs) Facial and distal limb oedema Chocolate‐coloured mucous membranes |
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What reduces methaemoglobin back to haemoglobin?
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Methylene blue |
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What is Heinz body anaemia?
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inclusions within red blood cells composed of denatured haemoglobin often in association with haemolytic anaemia
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What 3 drugs can be given as a specific treatment for paracetamol treatment?
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N‐acetylcysteine S‐adenosyl‐methionine (SAM) Methylene blue |
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What does N-acetylcysteine do? When is it used?
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- replenishes glutathione stores - detoxifies TM to nontoxic metabolites - directly conjugates TM to reduce toxicity - acts as sulphur donor to increase capacity for non toxic metabolites |
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What is s-adenosyl-methionine? WHen is it used? |
- precursor for glutathione |
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What is methylene blue used for?
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(* care in cats can lead to haemolytic anaemia) used in paracetamol poisoning |
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What is the function of COX-1?
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- production of gastric PGE → mucus & bicarbonate secretion - renal PGE → maintenance of renal blood flow in hypotensive states |
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WHat are the CS of NSAID toxicity?
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Acute renal failure (oliguric) Neurological signs (ataxia and seizures) |
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What is the initial treatment 1-2 hours post ingestion of NSAIDs? |
-Assess patient’s renal function & electrolytes -Gastrointestinal decontamination --> induce emesis/gastic lavage -->activated charcoal (continue for 72 hours due to enterohepatic circulation of NSAIDs) -IVFT to maintain renal perfusion |
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What fluids should be given after NSAIDs toxicity and why? |
IVFT to maintain renal perfusion -Especially if the patient is vomiting or dehydrated -To maintain renal perfusion if anaesthesia is required -Crystalloids – lactated ringer’s solution |
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What can happen in aspirin toxicity that doesn't occur with other NSAIDs? |
-Irreversible COX inhibition -Hepatic metabolism to salicylic acid --> hyperventilation (direct effect on resp centre) -->metabolic acidosis |
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What can be done to limit the gastric injury during NSAIDs toxicity?
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Induce emesis/gastric lavage (1-2 hrs PI) Gut protectants to prevent ulceration |
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List some gut protectants that are given for NSAID toxicity
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- H2 blockers - proton pump inhibitors ie. omeprazole - prostaglandin PGE1 analogues |
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Why can bicarbonate be administered during aspirin toxicity? |
Bicarbonate also enhances renal elimination |
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What is the recommended treatment for NSAIDs toxicity? |
Reduce further absorption; induce emesis or perform gastric lavage if within 1-2 hours of ingestion. Administer activated charcoal – this should be continued every 6 hours for 72 hours due to the entero-hepatic circulation of ibuprofen. Supportive therapy; IVFT to maintain renal perfusion. Specific Therapy; Misoprostol (synthetic PGE1 analogue), H2-antagonists (cimetidine, ranitidine or famotidine), proton-pump inhibitors (omeprazole) and sucralfate. |
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What are the clinical signs of NSAID toxicity?
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vomiting, depression, anorexia, diarrhoea, melaena and anuria/oliguria or PUPD |
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What drugs are contraindicated to be used with NSAIDs?
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glucocorticoids |
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How can elimination of salicylate be enhanced?
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forced diuresis (combination of IVFT and diuretics e.g. frusemide) with careful attention to fluid balance to avoid overload. |
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How does ethylene glycol result in mortality?
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Mortality due to acute oliguric renal failure 60-70% in dogs, and is higher in cats. |
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List some DDx for acute renal failure to be aware of as well as ethylene glycol poisoning
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Lily toxicity in cats Grape/raisin toxicity in dogs & cats Leptospirosis in dogs |
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What does ethylene glycol cause before it is metabolised? How long till symptons occur?
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Vomiting and CNS depression (lethargy, ataxia, seizures, stupor, coma)
within 30 mins of ingestion |
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What is Ethylene glycol metabolised to ? |
EG----> glycoaldehyde ---> glycolic acid ----> glycoxylic adic ---> oxalte, glycine and a-hydroxyl-b-ketodipate |
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What metabolised ethylene glycol to glycoaldehyde?
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alcohol dehydrogenase to glycoaldehyde, glycolic acid and oxalate |
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What are the CS of EG toxicity within 30 mins PI?
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vomiting and CNS depression (caused by EG)
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What are the CS of EG toxicity within 12-24 hours?
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- Acute renal failure (manifests as anorexia, depression, vomiting, oral ulceration and renal pain) develops within 12-24 hours in cats and 36-72 hours in the dog. |
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Why does metabolic acidosis occur with EG toxicity?
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Severe metabolic acidosis occurs as a result of glycolic acid accumulation |
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How does kidney damage occur during EG toxicity?
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Most of the metabolites are directly toxic to the renal tubular epithelium and in addition the formation of calcium oxalate crystals within the renal tubules contributes to anuric/oliguric renal failure.
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What is the serum biochemistry results in EG toxicity? |
azotaemia hyperphosphataemia hyperkalaemia hypocalcaemia hyperglycaemia (shows up after renal damage) |
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How would urine analysis present with EG toxicity?
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- isosthenuria is seen in dogs (USG 1.008-1.012) - reduced USG in cats (<1.035) due to osmotic diuresis - calcium oxalate (monohydrate) crystalluria (3 hours after ingestion in the cat and 6 hours in the dog) |
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What is osmotic diuresis?
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increase of urination rate caused by the presence of certain substances in the small tubes of the kidneys eg. glucose. The excretion occurs when substances such as glucose enter the kidney tubules and cannot be reabsorbed (due to a pathological state or the normal nature of the substance) --> increase in osmotic pressure within the tubule--> retention of water within the lumen, and thus reduces the reabsorption of water, increasing urine output (i.e. diuresis). The same effect can be seen in therapeutics such as mannitol, which is used to increase urine output and decrease extracellular fluid volume. |
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To diagnose EG toxicity the kidneys can be ultrasounded --> how would they appear?
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increased cortical echogenicity and medullary rim sign |
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How can EG toxicity be diagnosed BEFORE the onset of acute renal failure?
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High anion gap (AG) metabolic acidosis; low HCO3-, high AG. This may be observed as early as 1-3 hours after ingestion, before the onset of ARF |
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What is the recommended therapy for EG toxicity?
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- Decontamination as previously described - Emesis, activated charcoal - Aggressive IVFT/dialysis - Bicarbonate therapy for acidosis |
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What 3 drugs can be given as specific therapy for EG toxicity?
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- 4‐methyl‐pyrazole ( inhibit alcohol dehydrogenase) - Vit B1 and Vit B6 (enhance metabolism of glycoxylic acid to non-toxic metabolites) |
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What enhances metabolism of glycoxylic acid to non-toxic metabolites?
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Vit B1 and B6 |
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What are the CS of excitatory neurotoxins? List 4 excitatory neurotoxins? |
muscle twitching, tremors, tonic contractions and seizures eg. metaldehyde, OP, theobromine, strychnine |
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What are the CS of inhibitory neurotoxins? List 3 inhibitory neurotoxins? |
CNS depression and coma in conjunction with respiratory depression, and bradycardia eg. alphachloralose, ivermectins |
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What is metaldehyde and how does it act? |
Inhibits GABA |
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What are the CS of metaldehyde ingestion by 1-3 hrs PI?
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- abdominal pain - salivation and vomiting and D -tachypnoea and tachycardia - muscle tremors and tonic contraction - seizures (hyperthermia) - +- opisthotonus and convulsions --> Convulsions may give way to CNS depression/narcosis --> Liver failure may develop within 2-3 days. |
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What is the treatment for metaldehyde toxicity?
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Control spasms and convulsions (diazepam +- barbituates) Decontaminate (gastric lavage, AC) Supportive care (IVFT, cooling, bicarb for acidosis, glutathione precursors) |
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For metaldehyde toxicity why is gastric lavage preferred to inducing emesis?
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induction of emesis may induce violent muscle activity and acetaldehyde in gastric contents is caustic |
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How do permethrins cause neurotoxicity?
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Permethrins affect sodium channels--> repetitive nerve stimulation--> excitatory neurological signs (tremors, seizures) ( ataxia and depression may also be seen) |
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What is the treatment for permethrin toxicity?
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decontaminate (wash where spot on applied) supportive care (IVFT, IV lipid, avoid external stimuli, control temperature) |
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What are the CS of chocolate toxicity? |
restlessness/anxiety, panting (centrally mediated tachypnoea), diuresis, vomiting and diarrhoea can progress to CNS excitation (tremors and seizures) and cardiac arrhythmias (tachycardia, VPCs, ventricular tachycardia) |
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What is the treatment for chocolate toxicity in dogs?
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control spasms (anticonvulsant drugs) control cardiac arrhythmias (beta-blockers for supraventricular tachycardias, lignocaine for ventricular tachycardia) supportive care (IVFT, cooling) |
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How do OP and carbamates act?
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inhibition of acetylcholinesterase (AChE) --> prolonged activity of acetylcholine at the neuromuscular junction. |
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How is OP poisoning diagnosed? |
Response to atropine |
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How is OP toxicity treated?
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decontaminate (gastric lavage, bathe, AC) anticonvulsants atropine sulphate for muscarinic signs pralidoxime chloride (reactivates cholinesterase) |
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What are the clinical signs of OP poisoning?
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nicotinic - muscle tremors, generalised muscle tetany followed by weakness due to the inability of the membranes to repolarise adequately muscarinic - SLUD (salivation, lacrimation, urination, defaecation) --> onset prior to N CNS - anxiety, hyperactivity, tonic-clonic seizures to severe CNS depression |
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What can be given for OP toxicity to reactivate cholinesterase?
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pralidoxime chloride |
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How do avermectins act? WHat breeds are sensitive?
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COLLIE BREEDS |
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CS of avermectin toxicity?
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bradycardia, respiratory depression, CNS depression and coma |
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What is the treatment for toxicosis associated with CNS depression? ie. avermectin poisoning
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supportive care (IVFT, maintain body temp, nutritional support, respiratory support--> resp acidosis may develop with severe resp depression) |
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How do anticoagulant rodenticides work? |
inhibit vitamin K epoxide reductase--> prevent recycling of vitamin K in the liver. --> synthesis of vitamin-K dependent coagulation factors (II, VII, IX and X) is impaired --> factors become depleted--> clinical coagulopathy. |
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What are the CS from
anticoagulant rodenticide intoxication? |
indicative of a secondary haemostatic disorder and reflect the site of bleeding; common presentations include epistaxis, haemoptysis, dyspnoea due to haemorrhage into the lungs, haematoma formation. Pallor of mucous membranes may be associated with extensive internal bleeding. |
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How is anticoagulant rodenticide intoxication diagnosed?
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PT - prothrombin time APTT - activated partial thromboplastin time * factor VII has shortest half life so monitor PT as changes first |
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What is the treatment for anticoagulant rodenticide intoxication?
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reduce further absorption (induce emesis/gastric lavage, AC) supportive therapy (+- blootransfusion, O2 if sever intra pulmonary haemorrhage) vitamin K1 therapy (subcut then oral, for as long as 4 weeks) |
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How do vitamin D rodenticides work?
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-anorexia & vomiting -lethargy -tremors/ seizures -constipation -polyuria/polydipsia -acute renal failure -cardiac arrhythmias |
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Treatment for vitamin D toxicosis? |
- Treating hypercalcaemia --> intravenous fluid therapy (0.9%Na+Cl‐) frusemide glucocorticoids bisphophonates |
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What are the CS of an adder bite?
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RANGE FROM - severe distributive shock, with haemolysis and DIC |
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Treatment and prognosis of adder bites
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prognosis depends on location - head and neck better than extremities supportive care (IVFT and analgesia) antiserum can be imported |
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