Toxo clinical signs and treatment Flashcards
Lily
topical exposure
big issue = acute kidney injury 24-72hrs later
nephrotoxic to cats
topical exposure - needle-sharp crystals and clinically may cause stomatitis, glossitis and severe burning ocular pain
consumption - gastritis in first 3 hrs, may vomit
vomiting, salivation, neurological
Urinalyis = epithelial casts
proteinuria and glycosuria then inc urea and creatinine
Treat = emesis (xylazine/ dexmedetomidine), aggressive GI contamination- activated charcoal and cathartic and IVF diuresis
permethrin/ pyrethroids (spot on)
NOT for cats
CNS affected by reversibly prolonging sodium conductance => increased depolarising AP which results in repetative nerve firing
CS - Excessive salivation, tremors, ataxia, depression, hyperthermia/hypothermia
anorexia, vomiting
Treatment: decontaminate to prevent further absorption
topical = bath
oral - emetics (xylazine cat), activated charcoal and cathartics
muscle tremor - diazepam
paracetamol
Non immune mediated anaemia
cats v sensitive as deficient in substance that detoxified the more toxic intermediate once metabolised by liver = accumulates. but dogs can be toxic too
CS = CNS depression, vomiting, methaemoglobinaemia (haemolysis), tachycardia, hyperpnoea and weakness
Cats primarily develop methaemoglobinaemia (chocolate coloured MM, pale, cyanotic as cannot release oxygen normally) within a few hours, followed by Heinz body formation that can lead to haemolysis.
jaundice, vomiting, hypothermia, facial or paw oedema (more common in cats), cyanosis, dyspnoea, hepatic necrosis and death. Liver damage (centrilobular necrosis) occurs most commonly in dogs and is often delayed, with signs and clinicopathologic changes appearing 24 or more hours after ingestion.
Treatment - emesis if within 2 hrs activated charcoal cathartics (promote gut motility) aggressive IVFT - oxygen therapy, blood transfusion
ethylene glycol
Antifreeze!
toxicosis is caused by metabolites
Glycolic acid can cause severe metabolic acidosis and oxalic acid binds Ca ions in the renal tubules (and other tissues) to form calcium oxalate crystals, leading to hypocalcaemia, obstruction of tubules and renal epithelial damage.
CS:
- GI irritation
- CNS toxicity
- Nephrotoxicity
3 phaseS:
1 - 30 mins following = ataxic, tachycardia, tachypnoea, PU/PD dogs PU cats
vomiting
2 - 8 hrs following ingestion = metabolic acidosis = anorexic, emesis, depression, hypothermia. large dose may be fatal- coma
3- 1-3 days following, more often fatal
oliguric renal failure
large painful kidney, oral ulceration, salivation, vomiting, seizure
Fatal mostly once here
treatment = fomepizole and supportive: IVFT
rodenticides (anticoagulant)
inhibiting the recycling of vitamin K1 from vitamin K1 epoxide reductase. leads to a reduction in the active forms of clotting factors II, VII, IX and X in the circulation. The reduction in the active forms of these factors leads to prolonged clotting times.
Diagnosis = history and coagulation screen
Treat - emesis, activated charcoal
replace vit K1 and blood before clotting factors working
Thoracocentesis if dysnpoic related to bleeding in pleural space
metaldehyde
banned!
sly and snail pellets
CNS stimulation - loss of GABA inhibition
acute onset neurotoxicity then hepatotoxicity
CS = Hyperaesthesia, anxiety, restlessness, salivation, muscle tremors, incoordination, opisthotonus, tachycardia, seizures, coma, death
Emesis, gastric levage, cathartic
Fluid therapy
diazepam - tremor or seizure
nutrition and warms supportive
NSAIDS
most commonly seen. in practice: high dose or long exposure
Inhibit prostaglandin synthesis through COX inhibition
CS - vomiting, CNS depression, anorexia, diarrhoea and ataxia.
GI effect - Mild epigastric pain
Erosive gastritis, ulceration and haemorrhage
Nephrotoxicity
Acute kidney injury
Hepatoxicity, decreased platelet function, bone marrow suppression, seizures
Treatment: Emesis Gastric lavage, adsorbents, cathartics Repeat doses of activated charcoal NSAIDs often have long half-lives
Sucralfate
H2 antagonist cimetidine, ranitidine, famotidine
PPI omeprazole
Misoprostal (synthetic prostaglandin)
Treat AKI INTRAVENOUS FLUID THERAPY Monitor urine output Furosemide, mannitol (for oliguria or anuria) Monitor potassium
methylxanthines
caffeine and theobromine (choc, tea, coffee)
small = GI upset
large = cardiac supra ventricular or ventricular arrhythmia
anxious
Tremore ans seizure
Treat: emesis up to 12hrs post ingestion
activated charcoal
Grapes
AKI secondary to acute tubular necrosis
treat: emesis, activated charcoal, IVFT
Garlic onions leek
Non imune mediated anaemia
Disulfide and thiosulfates are metabolised to compounds that damage RBCs
Heinz bodies, haemolysis, methaemoglobinemia
Cats and dog breeds with hereditary RBC enzyme deficiencies more sensitive
The damage to the RBCs can be cumulative (days to weeks)
Supportive care, oxygen, blood transfusion
Canabis
rarely fatal
CS - Depression, disorientation, lethargy, incoordination. Come in looking comatosed but can respond to stimulation
Hypothermia, compulsive eating, symptomatic therapy and supportive care
repeated activated charcoal
xylitol
sweetener, chewing gum, Calpol, peanut butter
hige insulin release collapsed and hyperglycaemic hepatic necrosis emesis if chewing gum supportive treatment IVFT, glucose
activated charcoal not suede
