Poisons and toxins 1 & 2 Flashcards

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1
Q

Hx important for toxicology

A
  • what?
  • signalment
  • how much and toxic dose
  • when (decontaminate, should they be showing CS?)
  • CS
  • vomiting?
  • other hx (meds, chronic illness)
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2
Q

Common presenting problems with toxicology

A
  • neuro (seizure, tremor)
  • renal azotaemia
  • haematologic (anaemia, coagulopathy)
  • CV (tachycardia, arrhythmia)
  • hepatic/ GIT
  • metabolic (hypoglycaemia, acidaemia)
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3
Q

Classic signs indicating toxin ingestion

A
  • known toxin ingestion
  • acute onset
  • scavenger (walk off lead, children, parties)
  • excluded other cause
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4
Q

Natural toxin groups

A

plants, animals, fungi, inorganic matter

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5
Q

Chemical toxin groups

A
  • drugs/ meds
  • pesticides (domestic, agricultural)
  • household chemicals
  • industrial chemicals
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6
Q

Aspects of toxicokinetics

A

= between administered dose and compound at site of action
- uptake, transport, metabolism and transformation, sequestration, excretion (i.e absorption, distribution, metabolism and excretion)

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7
Q

Aspects of toxicodynamics

A

= between compound at site of action and adverse or toxic effect

  • binding
  • interaction
  • induction of toxic effects
  • depends on protein binding and cellular changes and cytoprotection
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8
Q

What are important things to know relating to toxin toxicokinetics and toxicodynamics?

A
  • time to peak
  • T (1/2)
  • route of elimination / site of metabolism
  • GI recirculation
  • Target receptors
  • antidotes
  • whether lipophilic
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9
Q

How can the cardiovascular system be affected? Tx?

A
  • arrhythmia - ECG, anti-arrhythmics

- shock - IV bolus

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10
Q

How can the respiratory system be affected? Tx?

A
  • oxygen
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11
Q

How can the neurological system be affected?

A
  • SEIZURES - diazepam, propofol and phenobarbital (this order, diazepam better for idiopathic epilepsy so often need propofol, phenobarbital takes 20-30 minutes to work
  • TREMORS - methocarbamol and diazepam (methocarbamol is a mm relaxant)
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12
Q

If hyperthermic, what should you do?

A

Cool to 39.3 degrees (don’t cool below this or the temperature will rapidly drop), running water, fan, IVF

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13
Q

After addressing the MBS with acute toxicity, what are your considerations?

A
  • temperature
  • blood glucose
  • PCV/ TP and smear
  • coagulation (PT, APTT)
  • biochemistry (renal, hepatic)
  • haematology
  • UA
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14
Q

What needs to be considered when tx a toxicity?

A
  • what? caustic? (acid, alkali, bleach)
  • when?
  • amount? toxic dose/ LD50? volume?
  • CS
  • recumbent/ seizure/ gag reflex present?
  • pharmacokinetics (enterohepatic metabolism? renal excretion? binds charcoal? antidote?)
  • risk of tx?
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15
Q

List tx options for toxicity

A
  • emesis
  • milk
  • gastric lavage
  • enema
  • activated charcoal
  • sorbitol (cathartic)
  • IVF
  • dermal decontamination
  • antidotes
  • lipids (Intralipid)
  • dialysis
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16
Q

What is a cathartic drug?

A

one that accelerates defaecation, opposite of a laxative, example is sorbitol

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17
Q

Indications - emesis

A

Recent ingestion (

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18
Q

Contraindications - emesis

A
  • recumbent, unconscious, no gag, seizure
  • caustic (acid, alkali, bleach)
  • petroleum
  • detergents
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19
Q

Method to induce emesis - 4

A
  • Apopmorphine: give one dose, second if not working, don’t give a third time
  • Xylazine (cats)
  • Medetomidine (cats)
  • Hydrogen peroxide (USA)
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20
Q

Gastric/colonic lavage - indications

A
  • ingestion
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21
Q

CI - gastric/colonic lavage

A

caustic

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22
Q

Complications gastric lavage

A
  • aspiration pneumonia (cuff ETT)

- hypothermia

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23
Q

Complications - emesis

A

aspiration pneumonia

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24
Q

Method - gastric lavage

A

GA –> ETT –> pass stomach tube (length muzzle to last rib, wide bore, lubricate) –> lavage stomach (instil 10-20ml/kg of water into stomach, slosh around abdomen, place end of stomach tube below animal to empty, repeat until no more contents retrieved) –> 3 sided lavage (R/L lateral and sternal recumbency) –> remove stomach tube (kink so no leakage into oesophagus)

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25
Q

Activated charcoal (AC) - indications

A
  • toxins which bind to AC

- enterohepatic metabolism

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26
Q

CI - activated charcoal

A
  • recumbent, unconscious, no gag, seziure

- toxins which DON’T bind AC (ethylene glycol, alcohol, alkali, petroleum, heavy metals, xylitol)

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27
Q

What is xylitol?

A

synthetic sweetener

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28
Q

Complications - activated charcoal

A
  • aspiration pneumonia

- if contains sorbitol –> dehydration (therefore only use this type of AC once/ first time, subsequently just AC)

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29
Q

Method of administration - AC

A
  • 1-2g/kg PO: food, syringe

- q4 hours or until faeces black (warn clients)

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30
Q

Diuresis - indications

A
  • renal excretion of toxins in toxic form (lilies, raisin, EG)
  • nephrotoxic
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31
Q

Diuresis - CI

A

risk of fluid overload (anuric/ oliguric, cardiac dz, pulmonary dz)

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32
Q

Distinguish anuria and oliguria

A
anuria = no passage of urine
oliguria = reduced urine production and excretion
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33
Q

Dermal decontamination - indications

A

Dermal toxins (permethrin - cats, engine oil, oil on birds)

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34
Q

Dermal decontamination - considerations

A
  • hypothermia

- sedation

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35
Q

Method - dermal decontamination

A

Clip contaminated area, wash with vegetable oil and washing up liquid (dog shampoo not good for this)

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36
Q

Indications - intralipid

A

Lipophilic toxins (i.e. Log P >1):

  • local anaesthetics
  • ivermectin
  • permethrin
  • baclofen
  • marijuana
  • mycotoxin
  • TCA, beta-blcoked, Ca channel blocker
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37
Q

Adverse effects - intralipid

A

RARE:

  • lipaemia
  • pancreatitis
  • hypersensitivity
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38
Q

CS - permethrin toxicity in cats

A

mm fasiculations (mild), although not a seizure, animal can be very hypothermic. Tx with IVF, usually 24 hr hospitalisation

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39
Q

Opioid antidote

A

naloxone

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40
Q

Alpha-2 agonist antidote

A

atipamezole

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41
Q

Benzodizepine antidote

A

flumazenil

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42
Q

Ethylene glycol (EG) antidote

A

ethanol (or just vodka!), 4- methylpyrazole is hard to get and expensive but also works

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43
Q

Paracetamol antidote

A

N- acetylcyssteine

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44
Q

NSAID antidote

A

misoprostol

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45
Q

Anticoagulant rodenticide antidote

A

vitamin K

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46
Q

Which toxins would you treat with dialysis? (not needed to memorise this)

A
  • ethylene glycol
  • baclofen
  • paracetamol
  • aminoglycosides
  • ethanol
  • mushroom
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47
Q

Ddx - toxins causing seizures and tremors

A
  • metaldehyde (snail/slug pellets)
  • mycotoxin (mouldy bread)
  • theobromine (chocolate, caffeine)
  • permethrin (topical flea tx, toxic to cats
  • recreational drugs
  • lead
  • OPs/ carbamates
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48
Q

Outline metaldehyde toxicosis

A
  • commonest cause of death in dogs (VPIS cases)
  • kills slugs/snails by dehydration and paralysis
  • method in mammals unclear
  • is a tetramer of acetaldehyde
  • is hydrolysed by gastric acid to acetaldehyde but clinical relevance of this is doubtful
  • metaldehyde itself or unknown metabolite may be responsible
  • disruption of GABAergic system may cause the convulsant activity
  • not lipophilic
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49
Q

LD50 - metaldehyde in dgs

A
  • 100-1000mg
  • variable individual resonse
  • other threshold indicated to be > 2mg/kg
50
Q

Tx - metaldehyde

A
  • gastric decontamination and observation (if
51
Q

Toxic dose - metaldehyde

A

LD50 = 500mg/kg

52
Q

Source - tremorgenic mycotocins

A

some mouldy foods, silage and compost

53
Q

Tx - mycotoxins

A
  • apomorphine
  • activated charcoal
  • diazepam
  • cool IV fluids
54
Q

What is roquefortine C?

A

the mould present in blue cheese, humans tolerate this well, dogs don’t

55
Q

At what levels does theobromine cause toxic effects, severe signs and seizures in dogs?

A
  • TOXIC EFFECTS: >20 mg/kg
  • SEVERE SIGNS: 40-50mg/kg
  • SEIZURES: 60 mg/kg
56
Q

What quantities of theobromine do dark, milk and white chocolate cause toxicity?

A
  • DARK: treat for > 3.5g/kg
  • MILK: treat for > 14g/kg
  • WHITE: by law, can only contain cocoa butter and thus minimal concentrations of theobromine
57
Q

CS - theobromine toxicity

A
  • vomitting
  • diarrhoea
  • PD
  • salivation
  • dehydration
  • CNS/ myocardial stimulation: tremor, convulsions, tachycardia, hypertension, arrhythmias
  • Renal failure
  • fatal cases - severe convulsions/ circulatory failure
58
Q

Tx - theobromine toxicity

A
  • emesis
  • activated charcoal
  • adequate hydration
  • benzodiazepines for CNS stimulation
  • lidocaine or beta-blocker for rapid tachycardia/ arrhythmia
59
Q

Mechanism - permethrin toxicity - cats

A

alteration of voltage- dependent sodium channels in nerve membranes causes repetitive discharges or membrane depolarisation. Some may also inhibit GABA-R. Loss of this inhibition can lead to hyperexcitability of nervous tissue.

60
Q

Timings of effect of permethrin toxicity in cats

A
  • onset at 1-3 hours (up to 36 hours)

- duration of effects 1-3 days, rarely up to 7 d

61
Q

3 main CS of permethrin toxicity in cats

A
  • hypersalivation
  • tremor
  • fasciculations
  • many others too
62
Q

Tx - feline permethrin toxicity

A
  • Intravenous lipid infusion *
  • diazepam,
  • pentobarbital
  • propofol
  • methocarbamol (a centrally acting skeletal mm relaxant, has been effective where benzodiazepines have failed)
63
Q

Toxins which can cause coagulopathy

A
  • anticoagulant rodenticide

- coagulopathy secondary to hepatopathy (xylitol)

64
Q

Toxins –> haemolysis - 2

A
  • paracetamol (cats)

- onion/ garlic

65
Q

What is the toxin in anticoagulant rodenticide?

A
  • most are second generation
  • commonest are bromodioloe and difenacoum
  • others: brodifacoum, flocoumafen
  • commonly at 0.005% strength baits, some professional compounds may be more concentrated (0.1%)
66
Q

How do anticoagulant rodenticides cause toxicity?

A

inhibit vitamin K expoxide reductase which converts vitamin K epoxide to vitamin K –> depletion of vitamin K which converts precursor coagulation proteins to their activated forms.

67
Q

Outline pharmacodynamics/kinetics of anticoagulant rodenticide

A
  • peak plasma levels vary (mins to hours)

- plasma elimination half life is 14 hr (warfarin) and 6 days (brodifacoum)

68
Q

CS - anticoagulant rodenticide

A
  • CS relatively uncommon as clotting facotrs have a long half life so there is a delay between exposure and CS>
  • onset of CS at 27 - 72 hours: increased clotting or PT time, main effect is haemorrhage with bruising, bleeding, gums, nose, GIT, wounds
  • other CS: dyspnoea, lethargy, weakness…
69
Q

Difenacoum - treatment threshold for acute exposure

A

100g bait/ kg at 0.005%

70
Q

Flucoumafen - treatment threshold for acute exposure

A
71
Q

Potentially toxic dose - bodifacoum

A

0.04 mg/kg

72
Q

Potentially toxic dose - bromadiolone

A

0.35 mg/kg

73
Q

Potentially toxic dose - difenacoum

A

5 mg/kg

74
Q

Potentially toxic dose - flocoumafen

A

0.0075 mg/kg

75
Q

Tx - anticoagulant rodenticide with CS or elevations in clotting/ PT

A

Vitamin K1 therapy (until PT normalises and then orally in divided doses for about 3 weeks, before finally discontinuing tx, check PT 1-3 days after). Whole blood/ plasma transfusions may be required. Monitor PCV and TS q 12 hours.

76
Q

Tx - anticoagulant rodenticide without CS and normal PT for 3 days

A

Tx not required

77
Q

Advice to client if pet has ingested anticoagulant rodenticide

A
  • no off-lead walks
  • care when playing with other animals
  • no bones
78
Q

In which species does paracetamol toxicity cause the most porblems?

A

dogs

79
Q

Other terms for paracetamol

A

acetaminophen or APAP

80
Q

Mechanism of paracetamol toxicity

A
  • saturation of metabolic pathways
  • toxic metabolite conjugated by glutathione
  • glutathione promptly depleted
  • cats lack metabolic capacity to detoxify paracetamol
81
Q

Paracetamol - early cs (

A
  • progressive cyanosis (fails to respond to O2 tx)
  • brown/blue MM
  • weak and lethargic
82
Q

Mid CS - paracetamol (2-24 hours)

A
  • facial/ paw oedema
  • vomiting
  • depression
  • dark brown blood (methaemoglobinaemia) and remains dark on aeration
83
Q

Longer CS - paracetamol (> 24 hours)

A
  • severe methaemoglobinaemia

- hepatic necrosis

84
Q

Toxic dose - paracetamol - dogs and cats

A

DOG: 150 mg/kg
CAT: 20 mg/kg

85
Q

Tx - paracetamol toxicity

A
  • emesis (within 2 hours)
  • activated charcol
  • ANTIDOTE: acetylcysteine (precursor of glutathione)
86
Q

What UA sign is typically seen with acute kidney injury?

A

Casts (a type of sediment)

87
Q

Toxins causing renal damage

A
  • ethylene glycol (EG) - occasionally
  • NSAIDs - one of commonest
  • aminoglycosides (gentamicin)
  • lilly (cats)
  • grapes/ raisins (dogs)
88
Q

Which NSAID is most commonly ingested by pets?

A

ibuprofen and meloxicam

n.b. in veterinary, COX-2 specific inhibitors are commonly used

89
Q

What is NSAID toxicity largely due to?

A

COX-1 inhibition

90
Q

NSAID toxicity - early CS - 3

A
  • GIT erosion, ulcer, perforation
  • V/D - both may be bloody
  • CNS (rarely, ataxia, lethargy, drowsiness), large doses
91
Q

NSAID toxicity - late CS - 2

A
  • renal failure

- hepatic damage

92
Q

Toxic dose - ibuprogen

A

10 mg/kg

93
Q

Toxic dose - carprofen (commonest veterinary NSAID)

A

40 mg/kg

94
Q

Toxic dose - meloxicam

A
  • Oral > 1mg/kg

- SC 0.2 mg/kg

95
Q

Tx - NSAID toxicity

A
DECONTAMINATION:
- emesis (optimal within 2 hrs ingestion)
- activated charcoal (repeat dose)
MAINTAIN RENAL FUNCTION
- oral fluid therapy
- IVF - maintenance for 24-48 hours
* be guided by renal function tests*
96
Q

How can gastric ulceration be prevention with NSAID toxicity?

A
  • H2 receptor antangonists - Cimetidine, Ranitidine, Famotidine
  • Proton pump inhibitors - Omeprazole
  • Ulcer healing / coating - sucralfate
  • Prostaglandin supplementation - Misoprostol
97
Q

Tx - renal toxicity

A
  • DIURESIS: IVF at 2-3x maintenance, furosemide if anurix despite IVF
  • GASTROPROTECTION: omeprazole (easier to give in dogs than cats)
  • ANTI-EMETIC: maropitant (1mg/kg)
98
Q

Monitoring - renal toxicity

A
  • urine output
  • BWt
  • urea:creatinine
  • K+
  • ECG
99
Q

Outline Ethylene glycol (EG) absorption

A
  • rapid - peak plasma concentrations
100
Q

Mechanism of EG toxicity

A
  • metabolism catalysed by alcohol dehydrogenase
  • various intermediate metabolites with toxic actions (glycoaldehyde; glycolic acid = rate limiting step, acidosis and high urine levels indicative; glyoxylic acid; oxalic acid)
101
Q

Blood results - EG toxicity

A
  • azotaemia
  • hyperglycaemia
  • increased osmolaality
  • increased anion gap
  • increased urea: creatinine
  • decreased USG
  • URINALYSIS: proteinuria, glucosuria, haematuria, albuminuria, calcium oxaluria
102
Q

Diagnosis - EG toxicity

A

stains can lend fluorescence to urine and other contaminated tissue examined under Wood’s lamp within 6 hours BUT negative results don’t rule it out

103
Q

Tx - EG toxicity

A
  • early dx and aggressive intervention (
104
Q

T/F: true lily (Liliaceae) and day lily (Hemerocallis) cause renal toxicity in cats

A

True

105
Q

Outline lilly toxicity

A
  • all parts of plant are toxic
  • small amount of plant can have serious consequences
  • mechanism of toxicity unknown
  • rapid development of CS: GIT irritation, PU, dehydration, renal failure, seizures (severe cases)
106
Q

Tx - lilly toxicity

A
  • REDUCE ABSORPTION: emesis +/- AC

- PREVENT RENAL SHUTDOWN AND ENHANCE RENAL PERFUSION: IVF diuresis for at least 48 hours

107
Q

Prognosis - lilly toxicity

A
  • tx options limited once renal failure occurred so guarded.
  • good if tx before onset of renal impairment.
108
Q

What is xylitol?

A
  • natural 5-C sugar alcohol
  • in fruits/ vegetables
  • not denatured or modified in baking/ cooking
  • rapid and potent stimulator of insulin release (dogs, dose-dependent)
  • -> liver damage (unknown mechanism)
  • e.g. smint pastilles, wrigleys gum
109
Q

Tx - xylitol toxicity

A
  • aggressive
  • treat for > 0.05g/kg (50 mg/kg)
  • gastric decontamination
110
Q

Monitoring - xylitol toxicity

A
  • baseline glucose, K+, phosphorous, total bilirubin, LFTs and clotting tests
  • monitor glucose concentrations every 1- 2 hours for at least 12 hours.
  • re-check the other tests every 24 hours, for at least 72 hours.
111
Q

Xylitol effects and tx - 2

A
  • HYPOGLYCAEMIA (tx with frequent small meals, oral sugar for 8-12 hours), glucose/dextrose (severe cases), ECG (risk of hypokalaemia-induced arrhythmias)
  • HEPATOTOXICITY: consider immediate dextrose therapy, s-adenosyl-l-methionine or acetylcystein as hepatoprotectants
112
Q

Overall tx - xylitol

A
  • EMESIS - apomorphine
  • Glucose correction
  • Monitor: blood glucose (BG), biochem, PCV?TS, coagulation (since liver failure can cause problems with this)
113
Q

Hepatoxicity - ddx

A
  • xylitol
  • mushroom
  • paracetamol
114
Q

What is bendiocarb? CS? Tx?

A

a widely-used insecticide –> moderate ataxia, abnormal lung sounds, tachycardia, small pupil and increased bowel sounds.
- Tx: single dose of diazepam and atropine

115
Q

Toxins causing seizure/ tremor (LEARN!!!) - 7

A
  • metaldehyde
  • mycotoxin
  • theobromine
  • permethrin
  • lead
  • OP
  • recreational drugs
116
Q

Toxins causing anaemia (LEARN!!!) - 6

A
  • COAGULATION:
  • rodenticide
  • hepatotoxin
  • HAEMOLYSIS:
  • paracetamol (cats)
  • onion/ garlic
  • heavy metals
117
Q

Toxins causing renal problems (LEARN!!!) - 7

A
  • EG
  • NSAIDs
  • aminoglycosides
  • lillies (cats)
  • raisin/grapes (dogs)
118
Q

Toxins causing hepatic problems (LEARN!!!) - 4

A
  • xylitol (also hypoglycaemia)
  • cycad (plant that looks like pineapple growing out of ground)
  • mushroom
  • paracetamol
119
Q

General methods to treat toxin

A
  • emesis
  • milk
  • gastric lavage
  • enema
  • AC
  • sorbitol (cathartic)
  • IVF
  • dermal decontamination
  • antidotes
  • intralipid
  • dialysis
120
Q

What are the most important systems to treat?

A

MBS (also toxins often affect GIT)