Toxicology Flashcards
Method of decontamination (5)
Dilution, emesis, gastric lavage, absorbents, cathartics
Indication dilution and what can be used?
Ingested an irritant or corosive
2-6ml/kg water or milk
When to induce emesis
Within 2-3 hours of ingestion
Can be effective >3 hours if coalesce to form a bezoar e.g. chewable medication, chocolate
Contraindication to emesis (5)
Corrosive agent, petroleum distillate (risk of aspiration), coma, seizures, recumbency
Indication gastric lavage
When emesis is controintdicated or unsucessful
Name an absorbent
Activated charcoal
Name three drugs than under go enterohepatic recirculation
Digoxin, NSAID and cannabis
What do absorbents not bind to? (6)
Heavy metals, alcohol, fertiliser, nitrates, iodies, clorate
Contra-indication to absorbents, why
Caustic material - unlikley to bind and impairs visulaisation of burns/ulcers
What electrolyte abnormality can be associated with activated charcoal
Hypernatraemia
Why use activated charcoal with a catthartic
Only finds with weak chemical fores, these will break down if the substance resides in the GIT for a prolonger periord»_space;> re-release of the toxins
Three type of cathartics
Bulk (psyllium, canned pumpkin)
Osmotic (sorbital frequently added to activated charcoal)
Lubricants (minerral oil - not with activated charcoal)
Antidote to amphetamine
Acepromazine
Antidote to amitraz
Atimpamazole
Atropine is an antidote for what (2)
Carbamates, organophosphates
Antidote for selective serotonin uptake inhibitors
5-hydroxtryptophan
Cyprohepadine is a antidote for what?
Balcofen
Antidote for ethylene glycol?
Ethanol, fomepizole
Flumazenil is an antidote for what?
Benzodipazepine
When can intralipid emulsion be useful? (6)
Bupivicaine, verampil, propranolol, clompipramine, lidocaine, moxidectin
When can methcarbamol be an antidote? (4)
Permethrin, metaldehyde, strychinine, tremorgenic mycotoxins
Antidote for cholecalciferol toxicity
Pamidronate
MOA methocarbamol
Inhibition of AchE (similar to carbamate)
Types of rodenticides (4)
Anticoagulant, neurotoxic, vitamin D3, corrosive to GIT
Action of bromethalin
Neurotoxic rodenticide - uncoupling oxidative phosphorylation in the brain and liver mitochronidria leading to decreased ATP (affecting Na/K ATPase pump)
Lipid peroxidation and sodium accumulation in cell –> CNS oedema.
Treatment of bromethalin intoxication
Early decontamination, mannitol, supportive care, activated charcoal
MOA phosphide rodenticides
Corrosive, direct GIT irritant
Zinc phosphide combines with gastric acid or mositure to form phosphide gas
Treatment of phosphite intoxication
emesis, absorbents, well ventilated room
Vitamin K depenent coagulation factors
II VII IX and X
Which coagulation factor has the shortest half-life
VII
Why are cats sensitive to pyrethrins?
Cat’s altered glucuronidation metabollism
Clincial signs of pyrethrin intoxication
GI - hypersalivation, v+, nausea
CNS - disorentation, hyperexcitability, seizures
Respiratory - dyspnoea, tachypnoea
Treatment of pyrethrin intoxication (3)
Dermal decontamination, mucscle relaxant (methocarbamol), anticonvulsants
MOA carbamates and organophosphates
Competetively inhibit AchE»_space; excess Ach accumulation
Clinical signs of organophosphate intoxication
Cholinergic crisis - Salivation, lacrimation, urinate, defecation, emesis, bradycardia, bronchoconstriction
MOA amitraz
Monoamine oxidase inhibitor and alpha-adrenergic agonist
What do paintballs contain? (4)
Contain polyethylene glycol, sorbitol, glycerine and gelatin
Toxicity associated with paintballs, what is therefore contra-indicated
Hypernatraemia
Activated charcoal contra-inidcated
What can mouldy food contain
Tremorgenic mycotoxins
Adverse effect of 3-6% sodium hypochlorite?
GI irritant
Adverse effects of ultra bleach (5-10% sodium hypochlorite and 0.2-2% sodium hydroxide)
Corrosive
Toxic ingredient in windshield wiper fluid, metabolism and management
Methanol
Metabolised to formaldehyde (with alcohol dehydrogenase) which is rapidly oxidised to formic acid and then metbaolised to CO2 and H2o
Supportive care - decontamination ineffective and activated charcoal contraindicated
3 stages of ethylene glycol toxicity
Stage 1 - 30 min -12 hr : alcohol poisoning (ataxia, hypersalivation, v+, pu/pd, seizures)
Stage 2 - 12-24 hr: Clinical signs resolve but severe internal injury
Stage 3 12-24 hours (c), 36-72 hours (d): severe AKI secondary to Ca oxalate crystalluria
Diagnosis of ethyelene glycol intoxication
EG blood test within 24 hours
Venous blood gas - metabolic acidosis with high anion gap
Metabolism of propylene glycol
Metabolised to D- and L- lactate which can contribute to metabolic acidosis.
MOA calcium channel blocker
Inhibit transmembrane influx of extracellular calcium through slow or long-lasting L-type ion channels»_space;> decreased myocardial contractility and arterial smooth muscle relaxation»_space;> decrease peripheral resistace, BP and afterload
Treatment of CCB overdose (3)
Ca gluconate to increase transmembrane flow
Intralipid
High dose insulin therapy (with concurrent dextrose)
MOA high dose insulin for CCB intoxication
Supression of PDE III»_space;> increased intracellular calcium influx
Mild hypokalaemia causing enhanced myocardial inotropy
Characteristics of serotonin toxicity syndrome (6)
Muscle rigidity, increased reflexes, tremors, hyperthermia, hypertension and transient blindness.
MOA tricyclic antidepressants
Inhbit neuronal reuptake of norepinepherine, serotonin and dopamine in the CNS
Also affinity of muscarininc and H1 receptors and can cause Na/K channel blockade of varying degrees
MOA benzodiazepines
Enhance inhibitory neurotranmitter, GABA
Signs of benzodiazepine toxicity
CNS depression, ataxia, aggression
MOA phenylpropanolamine
Alpha adrenergic agonist - increases urethral outflow resistance
Adverse effects of phyenylpropanolamine (4) and mechanism
Associated with Alpha receptor and B1 receptor stimulation : agitation, mydriasis, hypertension, tachycardia (or bradycardia secondary to hypertension)
Management NSAID toxicity
Decontamination IVFT Gastroprotectants Multiple doses activated charcoal (undergoes enterohepatic recirculation) TPE
NSAID toxcity and TPE
11/11 dogs survived, 6 had bleeding complications
Why is haemodialysis not helpful with NSAID toxicity
Highly protein bound
Signs of paracetamol toxicity (4)
Methemoglobinemia, cyanosis, hepatitoxicosis, hepatic encephalopathy
Adverse effect of albuterol intoxication
Hypoklaemia
MOA albuterol
Beta adrenergic agonist
MOA balcofen
centrally acting skeletal muscle relaxant
Class of drug caffine
Methylxanthine
MOA methylxanthine
Non-selective PDE inhibitor
Adverse effects diphenhydramine (4)
Hyperactivity, tachycardia, vocalisation, hypethermia
Prevelence of diphenydramine toxicosis in one study
23.5%, 3 dogs died
Action amphetamines
CNS and CVS stimulants due to release of NE and catecholamines which acts on alpha and beta adrenergic receptors
Clinical signs ketamine intoxication - low, high and severe doses
Small doses - mild stimulation, halucinations (30-60 mins)
High doses - opsthotonus, mydriasis, ataxia, increased muscle tone
Severe - coma, respiratory depression, hyperthermia, seizures, death
MOA gamm hydroxybutanoic acid
Synthetic derivative of GABA
What is LSD
synthetic hallucinogen
What types of plants are Calla lilly, pholdendron, peace lilly
oxalate containing plants
Clinical signs of oxalate containing plant ingestion
Calcium oxalate and crystals result in mechanical and inflammatory injury to the skin and mucous membranes
Plant proteolytic enzymes may contribute to local inflammation by promoting release of kinins and histamine.
Management of oxalate plant ingestion
Decontamination - rinse mouth with water or milk
Signs of liliaceae (Eater lilly/tiger lilly) intoxication (3)
First phase: GIT within minutes to hours
Second phase - oliguric/anuric renal failure CNS depression
36% develop neureo signs - ataxia, depression, tremors
Toxic dose of lilly ingestion
<1 leaf
Management of lilly ingestion
decontamination, intensive IVFT
Active component of canabis
delta-tetrahydrocannabinol which interact with cannabinoid type 1 receptors
Clinical signs of canabis intoxication
CNS depression, mydriasis, hyperesthesia, ptyalism, tremors
Will emetics work with canabis ingestion
No, strong anti-emetic properties
Toxin associated with rhododendrums and MOA
Grananotoxin - binds Na channels and maintains excitable membranes in a state of depolarisation
Clinical signs of rhododendrum intoxication
Abdominal pain, tenesmus, CNS depression, skeletal muscle weakness, pulmonary oedema, arrythmia, hypotension
Toxin associated with castor bean
Ricin - inactivates RNA, inhibiting protein synthesis
Clinical signs associated wiht iris or tulip intoxication
Gastrointestinal irritant - potent emetic (interaction NK-1)
Toxicity associated with macadamia nuts
Acute toxic syndrome with in 1-2 hours characterised by weakness, CNS depression, vomiting, ataxia, tremors
Toxicity associated wiht onion, garlic, chives
Sulphoxides broken down to N-propyl disulphide»_space; oxidate damage to haemoglobin and erythrocyte membranes»_space;> methemoglobin, heinz bodies and eccentrocytes (intravascular haemolysis)
What treatment can be given for heinz body anaemia and methemoglobinemia associated with onion/garlic intoxication
ascorbic acid
Toxicity associated with raisins and grapes
AKI +/- vestibilar/forebrain signs (not associated with azotaemia)
Prognosis raisin/grape toxocity
53% survived
MOA of nicotine
Cholinergic (nicotine) receptor agonist - stimulant at low doses and depressent at high doses
What toxic componentsdo E-cigarettes contain
Nicotine along with glycerol, propylene glycol and ethylene glycol
Management nicotine intoxication
Gastric decontamination, symptomatic care, atropine if bradycardia, activated charcoal q6-8 hr post ingestion transdermal patches (delayed nictotine relase may occur)
Types of pit vipers (2)
Rattlesnakes, copperheads
Purpose of toxin from pit vipers
Neurotoxin to immobilise prey
Clinical signs of pit viper bite
Local - bleeding, swelling, ecchymosis, erythema, sloughing
60% develop hypocoagulablity - correlates with plt not TEG
Systemically pain, weakness, nausea, muscle fasiculations
MOA coral snake venom
Neurotoxic - non-depolarising post synpatic neuromuscular blockade with little tissue reaction
Clinical sign of coral snake envenomation
Ascending flacid paralysis
Management coral snake envenomation (4)
Assisted ventilation
Elastic compression bandage around bitten limb
Antivenom
Supportive care
MOA brown spider venom
Single bite can be fatal
Sphingomyelinase D binds to cell membranes and induces leukocyte infiltration
Induces rapid coagulation and occlusion of small capillaries causing tissue necrosis
Clinical signs of brown spider bite
Local - pruritus, oedema (bulls-eye lesion) and sorness (vasoconstriction and ischemia)
systemic (less common) - Coombs negative IMHA, DIC
Management brown spide bite
Supportive care local and systemically
MOA black widow spider venom
Promotes calcium-independent release of Ach and NA and inhibits reuptake
Clinical signs of black widow spider bite
Pain, abdominal rigitidy, systemic hypertension
Signs of european adder bite
57% ventricular arrythmia (increased cTnI)
