Toxicology Flashcards
(34 cards)
Toxicological terms
poison: any substance which when introduced into a living organism destroys life or injures health
toxicity: may be due to high dose or high sensitivity
Lethal dose and effective dose
Therapeutic index (TI) is the ratio between Ld50 and Ed50
v. high value=relatively safe
low value=narrow therapeutic range
LD50: dose at which 50% of animals are killed
ED50: dose at which 50% of animals get alleviation from whatever you’re trying to fix.
Five basic routes of intoxication
ingestion: food, water source; vomitus, urine, feces
cutaneous: insecticides, topical applications like ectoparasiticides; blood
inhalation: aerosols
injection: blood
ocular
often seen non-specific signs with intoxication
How is a poisoned animal treated?
1st: breathing, HR, temp stabilized
information is gathered from owner
continued absorption of poison is prevented
elimination of absorbed poison is attempted
an antidote may be given
symptomatic and supportive care
Prevention of continued absorption of poison
wash- cutaneous i.e. bird covered in oil
gastric evacuation
gastric lavage
adsorbent and chelating agents
elimination
Stimulation of gastric evacuation
fourth ventricle: chemotrigger zone
vestibular apparatus
medulla: vomiting centre
stomach: vagal and sympathetic afferents from GI tract stimulate trigger zone
small intestine: serotonin is released from enterochromaffin cells in GI tract
3% hydrogen peroxide
syrup of ipecac- toxic alkaloid that causes GI irriation- only give once
Xylazine: alpha 2 agonist- works on MCTZ
Apomorphine (Dopamine agonist: MCTZ)- opioid, but actions via dopamine receptor (agonist). very useful in dogs, can give in eye, gingival mucosa.
Vomiting gets rid of 40-60% of gastric content- not much use after 6 hours. can put salt or mustard at back of tongue.
Contraindications of gastric evacuation
seizures
depression/coma
loss of gag reflex
hypoxia
species unable to vomit
ingestion of corrosives/volatile petroleum products
recent abdominal surgery/hernia
Gastric lavage
light anaesthesia/cuffed ET tube
tepid tap water/normal saline (5-10ml/kg)
Gravity flow to aspirate
repeat until clear. Useful to keep 1st lavage for analysis
Adsorbents
all adsorbents taken orally (cf. chelating agents)
activated charcoal most commonly used- exposed to O2, makes lots of pores and fissures
fuller’s earth
Fecal elimination
no chemical reaction between toxin and adsorbent
good for large non-polar molecules, bad for hydrocarbons, heavy metals or ethanol
Cathartics
ways of getting things out of system fast
sodium (glauber’s salts) or magnesium sulphate (epsom salts)- speed transit through gut
sorbitol (often used in activated charcoal which tends to constipate)- or lactulose–helps move things through gut.
Enhancing elimination via urinary tract
Acidify: ammonium chloride
Alkalinization: sodium bicarbonate
Close patient monitoring- acid/base balance
Symptomatic, supportive care and monitoring is often sufficient
Chelating agents
useful for diagnosis of heavy metal poisoning- usualy eliminated through urine–> can take urine sample to check for heavy metal
Chemical reaction: agent binds metal ions
bound ions are chemically inert and thus prevent poisoning
examples: EDTA, desferrioxamine (particularly good for iron).
Chocolate
theobromine (a methylxanthine) in chocolate products
toxicity: white choc 2.2kg/kg
milk: 9g/kg
dark 1.25g/kg
Clinical signs: vomiting, excitability, ataxia, tachycardia
Treatment: decontamination (adsorbent) and symptomatic
Ethylene glycol
source: main component of antifreeze
attractive taste; commonly seen in cats and dogs; high mortality
has specific antidote
Toxicity: cats 1.5ml/kg, dogs 6.6ml/kg
Mechanism: metabolites are toxic (glycoaldehyde, glycolic acid and oxalic acid). Calcium+oxalic acid–>crystals in kidney–>renale failure.
Alcohol dehydrogenase=enzyme that metabolises. Can lead to metabolic acidosis– need to counteract metabolic acidosis.
Clinical signs and treatment for ethylene glycol
Signs: early (1-2 hours): weakness, vomiting, incoordination
Delayed signs (24-96 hours): thirst, anuria, hematuria, convulsions, death d/t renal failure
Treatment: ethanol is an alternative substrate for enzyme alcohol dehydrogenase. Ethanol has 100x more affinity for enzyme than ethylene glycol
20% ethanol with 5% sodium bicarb (to counteract metabolic acidosis)
can also use 4-methylpyrazole but it’s not super available and it’s expensive.
Organophosphates
source: ectoparasitic dips, collars, powders; insecticides
Toxicity: inhibit acetylcholinesterase–> stop ACh from being broken down. acts at muscarinic and nicotinic
Clinical signs: parasympathetic and neuromuscular activity
Treatment: atropine- blocks muscarinic receptors
oximes: regenerates acetylcholinesterase.
Arsenic/mercury
sources: inorganic arsenic: weed killers, insecticide, seed dressing, wood preservatives, mineral ores
organic: growth promoter
both arsenic and mercury are heavy metals
Occurence: ant baits attractive to cats; over usage of feed additives (arsenic growth promoters banned in EU)
Toxicity: 1-25mg/kg
Mechanism: general tissue poison
- inactivation of sulphydryl groups on enzymes
- uncouple oxidative phosphorylation
cause problems in intestinal epithelium and in kidneys, liver and skin
antidote= chelating agents
Arsenic/mecury poisoning signs
Acute toxicity: GIT most susceptible- severe gastroenteritis, vomiting, diarrhea, shock; massive ulceration and shedding of mucosa
Chronic toxicity: nervous signs; degeneration of peripheral nerves; ataxia, incoordination, blindness
Treatment of arsenic/mercury poisoning
GI decontamination
Chelating agents: sodium thiosulphate 15-30g in 100-200ml water IV or 30-60g orally every 6 hours
Dimercaprol: 3mg/kg IM every 3-4 hours.
Illicit drugs
sources: cocaine, amphetamines, narcotics
Toxicity: generally rapid CNS effects
clincial signs depend on agent
tx: decontamination, largely symptomatic, specific antagonists (i.e. naloxone for opiates).
Paracetamol
cats especially susceptible, deficient in glucuronyl transferase which is required for glucuronide conjugation
Toxicity: 50-100mg/kg in cats
N-acetyl p-benzoquinone (intermediary) oxidises Hb to metHB (affects O2 carriage).
cP450- metabolises paracetamol to NAPB–> lethal to animal
Can be metabolized to mercapteric acid–> glutathione helps excrete this but there’s only a certain amount in the body.
Clinical signs and treatment for paracetamol toxicity
Clinical signs: facial/pulmonary oedemia, cyanosis; liver damage (hemolysis, jaundice)
Treatment:
decontamination; supportive
N-acetylcysteine (glutathione precursor)
Sodium sulphate: helps alleviate symptoms
Vitamin C and methylene blue: help hemoglobin issues
Anticoagulant rodenticides
1st gen: warfarin; 2nd gen: difenacoum, bromadiolone (highly toxic, single feeding causes problems)
toxicity depends on agent
mechanism: vitamin K antagonist (reversible)
intereferes with production of clotting factors I, II, VII, IX, and X
Clinical signs and treatment for anticoagulant rodenticides
Clinical signs: depression and anorexia even before bleeding
Acute ingestion of very high doses: vascular collapse
Repeated intake: hemorrhage- internal/external (and symptoms of this e.g. weakness)
Diagnosis: prolonged clotting time, urine analysis; hemorrhage at PM
Treatment: vitamin K1 0.25-2.5 mg/kg subcut for warfarin, or 2.5-5mg/kg in case of long acting formulations
Menadione (vitamin K2) not effective.
Poisonous plants
occur in fields, hedgerows, hillsides, woods, gardens and in house
herbivores graze, browse, touch or are fed with them in hay or straw or other fodder
Carnivores will eat plants in house or in garden or on walks or get fed poisonous plants.