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Module 4 Week 1 > Toxicology > Flashcards

Toxicology Flashcards

1
Q

Define poison

A

Any substance which destroys life or injures health when introduced into a living organism

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2
Q

Toxicity is due to…

A

High dose or high sensitivity

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3
Q

What does Lethal dose (LD) LD50 mean

A

Dose to kill 50% of test population

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4
Q

Effective dose (ED) ED50

A

Dose to benefit 50% population

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5
Q

What does Therapeutic index (TI) mean

A

Ratio between the two LD50/ED50

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6
Q

5 routes of intoxication

A

Ingestion (food, water)
Cutaneous (insecticides, ectoparasiticides)
Inhalation (aerosols)
Injection (blood) e.g thorn prick
Ocular

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7
Q

What is the VPIS

A

Veterinary poisons information service

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8
Q

Aim of VPIS

A

• Provide information & advice by telephone on the management of acute poisoning
• Provide risk assessment for cases (toxic doses/effects/breed specific)
• Lab services available to subscribers
• Referral to ‘expert’ contacts
• Identify tablets/capsules/foreign drugs
• Provide information about constituents of commercial/agricultural products
• Antidote/antivenom supply
• Perform toxicovigilance/ surveillance
• Access to TOXBOX

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9
Q

What is ToxBox

A

Drugs used to treat poison

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10
Q

Name the ToxBox drugs

A

• Activated Charcoal – binds toxins
• Apomorphine – aids vomiting
• European viper antiserum - for snakebites
• Fresh frozen plasma
• Methocarbamol – muscle relaxant
• Acetylcysteine – paracetamol antidote
• Vitamin K1 – rat poison antidote
• Intralipid 20% - binds lipophilic drugs

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11
Q

Top 10 poisons for animals. According to VPIS

A
  1. NSAIDs e.g iboprofen
  2. Anti coagulant rodenticides (e.g. warfarin)
  3. Chocolate
  4. Paracetamol
  5. Permethrin (insecticide)
  6. Metaldehyde
  7. Lilies
  8. Grapes etc
  9. Adder bite
  10. Benzalkonium chloride e.g in eye drops

Also of note are fungi, blue green algae, Xylitol (E967) artificial sweetener, e-cigarettes

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12
Q

How is poisoned animal treated?

A

• Breathing, heart rate, temperature stabilised
• Information from owner gathered
• Prevent continued absorption of the poison
• Elimination of the absorbed poison is attempted – eg make sick
• An antidote may be given if available
• Symptomatic and supportive care is given

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13
Q

How to prevent continued absorption of a poison?

A

• Wash (surface, eyes)
• Gastric evacuation
• Gastric lavage
• Adsorbent such as charcoal
• Elimination

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14
Q

What is gastric evacuation

A

Processing in which the contents of stomach are moved over duodenum- vomiting

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15
Q

Chemicals used to stimulate gastric evacuation

A

• 3% hydrogen peroxide (Irritant)
• Syrup of Ipecac (huana) (Irritant and CTZ stimulant) – quite toxic
•Xylazine (iv, cats) ( Alpha 2 agonist trigger of CTZ)
•Apomorphine (pills, dogs) (Dopamine agonist; CTZ)

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16
Q

Times when gastric evacuation should not be used

A

-Seizures – risk of fluid entering lungs
-depression / coma – unlikely to be sick
-loss of gag reflex – can check
-hypoxia
-species unable to vomit (e.g. sheep, rodents)
-ingestion of corrosives / volatile petroleum products
– damage on way up
-recent abdominal surgery, hernia

17
Q

What is gastric lavage

A

Process of cleaning out contents of the stomach- adding water into stomach and diluting out any toxin that’s there

18
Q

How do we stimulate gastric evacuation/vomiting

A

Centres in the brain induce vomiting. Drugs are provided that stimulate that nervous system in the brain that send signals to stomach to cause vomiting

19
Q

Describe process of gastric lavage

A

-give animal light anaesthesia
-put a tube down with tepid tap water/normal saline
-then bring back out
-repeat multiple times

20
Q

Absorbents
-What do they do
-Example

A

Stops toxins being absorbed into. Other tissues
-Activated Charcoal (slurry)
acts as sponge – commonly used Give orally – causes black faeces/urine

21
Q

Chelating agents
-what do they do & how do they work
-examples

A

-Bind metal ions non specifically eg arsenic, lead
-once bound the ions are chemically inert and therefore stops the poison from working
-examples; EDTA (Ethyl Diamine Tetra Acetic acid) & Desferrioxamine (for ferrous ions)

22
Q

Cathartics

A

-Sodium (Glauber salts) or magnesium sulphate (Epsom salts); ^ rate of something passing through GI tract by pulling water into gut and therefore flushing it out faster
-Sorbitol; pulls water into gut and helps movement through gut

23
Q

Chocolate
-sources
-toxicity
-clinical signs
-treatment

A

-theobromine (a methylxanthine) in chocolate products
-toxicity: dark chocolate-> ED50 1.25g/kg
Milk chocolate->ED50 9g/kg
White chocolate-> ED50 2.2 kg/kg
-vomiting, excitability, ataxia and tachycardia
-decontamination; induce vomiting by giving charcoal/lavage etc, no antidote for chocolate

24
Q

Poisons that have specific antidotes available

A

Anticoagulant rodenticides
Ethylene Glycol (anti-freeze)
Psychoactive drugs
Paracetamol (acetaminophen)

25
Q

Anticoagulant rodenticides (used as rat poison)
-sources
-occurrence
-toxicity

A

-Warfarin (less toxic) and Difenacoum & bromadiolone (highly toxic)
-high on VPIS toxic list
-mechanism: any rat poison acts as an antagonist of vitamin K (reversible). Interferes with production of clotting factors. Overtime start to see defects of bleeding

26
Q

Clinical signs of Anticoagulant rodenticides

A

Depression and anorexia (early signs even before bleeding)
Acute ingestion of very high doses
-vascular collapse
Repeated intake
haemorrhage - internal/external and symptoms of this eg weakness
Diagnosis
prolonged clotting time, urine analysis (blood in urine)
- post mortem: haemorrhage

27
Q

Treatment of anticoagulant rodenticides
(Which vitamin is not effective?)

A

Give vitamin K

Menadione – provit K, (vitamin K3 is not effective)

28
Q

Ethylene glycol (present in antifreeze)
-source
-occurrence
-toxicity

A

-Attractive taste
-High mortality rare, common in cats and dogs
-Toxicity: LD50: cats 1.5 ml / kg; dogs 6.6 ml / kg Mechanism: metabolites are toxic (glycoaldehyde, glycolic acid & oxalic acid) i.e doesn’t need much to cause toxicity

29
Q

Ethylene glycol poisoning clinical signs

A

Early clinical signs (1-2 hrs)
• weakness,vomiting,uncoordination
Delayed signs (24-96 hrs)
• thirst,inhibitionofurineproduction,bloodinurine, convulsions………death

30
Q

Ethylene Glycol poisoning treatment

A

Ethanol is an alternative substrate for ADH enzyme (this way animal metabolises the ethanol instead of the poison therefore a much less toxic compound is broken down)
• 20%ethanolIV5.5ml/kg
• with5%sodiumbicarbonate8.8ml/kg–counteracts/balances up acidosis caused by glycolic acid
• 4-methylpyrazole(4MP;Fomepizole,usedinUSA) – acts as an inhibitor for ADH enzyme (expensive)

31
Q

Psychoactive drugs
-sources
-occurrence
-toxicity
-clinical signs
-treatment

A

-Cocaine, amphetamine, narcotics
-little documentation as owners have difficulty owning up to leaving drugs out which animal has ingested
-toxicity: rapid CNS effects; hyperactivity, ^ heart rate, in-coordination of animal
-decontamination or give absorbents or give specific antagonist (antidote that reverses effects)

32
Q

Paracetamol poisoning
-sources
-occurrence
-toxicity

A

-Household supplies
-Cats especially susceptible
- cats are deficient in glucuronyl transferase enzyme
required for glucuronide conjugation (metabolism of paracetamol)
-toxicity: LD50 cats 50-100 mg/kg
N-acetyl-p-benzoquinone forms (intermediate), oxidises Hb to metHb (leads to cyanosis and RBC lysis-toxic to RBCs) (humans are usually able to metabolise N-acetyl-p-benzoquinone so wouldn’t lead to formation of intermediate)

33
Q

Clinical signs of paracetamol poisoning

A

Facial/pulmonary oedema, cyanosis (paler colour of membranes as not getting 02 delivered to tissue) (MetHb) Liver damage …haemolysis, jaundice

34
Q

Treatment for paracetamol poisoning

A

Decontamination
N-acetylcysteine –glutathione precursor (acts as antioxidant) (ToxBox)
Sodium sulphate - alternative substrate
Vitamin C (ascorbic acid – reducing agent)
Methylene blue (reduces metHb to Hb)

antioxidant=reducing agent

Module 4 Week 1 (5 decks)

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