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Veterinary Textbook of Internal Medicine > Toxicology > Flashcards

Toxicology Flashcards

Neurotoxicoses, hepatotoxicoses, Renal, GI, Cardiorespiratory and Haemtologic toxicosis

1
Q

What are the two main goals of decontamination?

A
  • Prevention of systemic absorption
  • Enhancing elimination
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2
Q

What are the methods of decontamination?

A
  1. Oral decontamination
  2. Enemas
  3. Ocular decontamination
  4. Dermal decontamination
  5. Inhalant decontamination
  6. Advanced elimination
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3
Q

What are the methods of oral decontamination?

A
  1. Dilution
  2. Emesis
  3. Activated charcol
  4. Cholestramine
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4
Q

What are the methods of dermal decontamination?

A

Bathing and clipping

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5
Q

What are the methods of advanced elimination?

A
  1. Intravenous lipid emulsion
  2. Therapeutic plasma exchange
  3. Haemodialysis and charcoal haemoperfusion
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6
Q

How is oral decontamination used in the management of toxicosis?

A

It is used to:
1. Prevent systemic absorption of orally ingested toxicants
2. To make a toxin less irritating or corrosive
3. To enhance elimination of toxicants

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7
Q

When should oral decontamination be avoided in case of toxin exposure?

A

When a patient is unable to protects its airways.

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8
Q

What is the purpose of dilution in cases of toxin exposure?

A

Used to decrease oral and gastric irritation

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9
Q

What is the dose rate of dilution?

A

2ml/kg PO milk or water in a bowl or via syringe

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10
Q

When is dilution indicated in toxin exposure?

A

In cases of ingestion or petrol, corrosive or caustic agents and plants containing insoluble calcium oxaletes

The calcium in milk may also be of benefit in decreasing absorption of some toxicants including fluroquinalones, fluroide, tetracyclines and bisphosphonate.

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11
Q

What is the purpose of emesis in cases of toxin exposure?

A

To remove ingested toxins from the stomach

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12
Q

What percentage of stomach contents are expected to be recovered following emesis?

A

40-60%

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13
Q

What time frame is emesis recovery most likely to be successful?

A

30-90 minutes following ingestion

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14
Q

When is emesis contraindicated?

A

In cases of ingestion or caustic substances or petrol or if the patient is at high risk of aspiration.

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15
Q

What are the common medications used to induced emesis in dogs?

A
  1. Apomorphine at 0.03mg/kg IV , SC or in the conjunctival sac - centrally acting
  2. Ropinirole eye drops which act by stimulating the dopamine receptors in the CRTZ
  3. 3% hydrogen peroxide at 0.5ml/kg PO up to 50ml total dose, can be repeated after 10mins if no vomiting has occured
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16
Q

What are the common medications used to induced emesis in cats?

A
  1. Dexmedetomidine 7mcg/kg IV
  2. Xylazine 0.44 mg/kg IM
    Additional motion can also be used in combination
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17
Q

Why can’t hydrogen peroxide not be used in cats?

A

Can induce necroulcerative haemorrhage gastritis

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18
Q

What is the purpose of activated charcoal?

A

To prevent absorption of toxins in the gastrointestinal tract

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19
Q

When should activated charcoal be used in cases of intoxication?

A

Should be considered in pets with recent toxin exposure that are still in the gastrointestinal tract or toxins that undergo enterohepatic recirculation

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20
Q

What should the first dose of activated charcoal be given with?

A

A cathartic such as sorbitol

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21
Q

In which cases should multiple dose of activated charcoal be given?

A

In some cases (not all) of toxins that undergo enterohepatic recirculation, these follow up dose should be given at half the initial dose and without a cathartic.

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22
Q

Which toxins is activated charcoal ineffective?

A
  • heavy metal
  • corrosive materials
  • hydrocarbons
  • fluroide
  • xylitol
  • ethanol
  • petrol
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23
Q

What is the main risk of administering activated charcoal?

A

Life threating hypernatraemia

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24
Q

What are the risk factors of developement of hypernatraemia in causes of intoxication?

A
  1. Small animals
  2. Dehydration
  3. Ingestion of osmotically active substances e.g. chocolate, paintballs or soft chew medications/supplements
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25
Q

How should a patient be handled/monitored after activated charcoal administration?

A
  1. Monitoring or serum sodium
  2. IVFT
  3. FA to water
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26
Q

How does activated charcoal, paintballs, chocolate and soft chew medications cause hypernatraemia?

A

Because of the osmotic effects of activated charcoal, the cathartic present in activated charcoal, or both it draw free water out and into the GI tract resulting in hypernatraemic dehydration.

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27
Q

What are the signs of hypernatraemia?

A

Neurological signs e.g. tremors, seizures secondary to cerebral odema. GI signs. Lethargy.

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28
Q

How is activated charcoal induced hypernatraemia treated?

A

Since it is an acute onset this can be correctly quickly.
1. Resuscitating or hydration with LRS
2. Then IVFT 0.45% saline solution with 2.5% dextrose at a rate of 40 ml/hour (92 ml/kg/day).
3. Diazepam (0.5-1 mg/kg intravenously) and/or methocarbamol (75 mg/kg intravenously) to control the tremors.
4. Warm water enemas

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29
Q

Why is a 0.45% saline solution combined 2.5% dextrose used to treat acute hypernatraemia?

A

when we are administering 0.45% NaCL + 2.5% dextrose, that extra 2.5% dextrose is mixed in to the 500 ml bag to make the fluid isosmolar. Giving 0.45% NaCL ALONE is contraindicated, as it’s not an isotonic fluid (it’s osmolality is only 154 mEq/L) Our normal body’s osmolality is approximately 300 mosml/L, so we should always give a fluid that is approximately 300 mosm/L (any balanced, isotonic fluid is usually 300 mosm/L). That extra dextrose increases the osmolality of a bag of 0.45%NaCL to approximately 300 mosm/L, making it a safe fluid to give. That dextrose is also metabolized by cells and provides free water to the patient, helping to lower the sodium in the body.

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30
Q

What is the action of cholestyramine?

A

Binds to bile acids in the intestines forming an insoluble complex and is excreted in the faeces.

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31
Q

When is cholestyramine indicated?

A

It is used off-label is cases of cholecalciferol, sago palm, blue green algae and NSAIDs.

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32
Q

What is the dose of cholestyramine?

A

0.3-1g/kg PO q8

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33
Q

What is the amount used for warm water enema?

A

5-10ml/kg

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34
Q

How is ocular decontamination performed?

A

Large quantities of flush (eye wash or artificial tears) for 20-30mins.

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35
Q

What is intravenous lipid emulsion?

A

It is a sterile emulsion of soybean, oil, egg phospholipids and glycerins.

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36
Q

When is intravenous lipid emulsion therapy indicated?

A

It is used in the treatment of severe lipophilic intoxications e.g.
- bupivicaine and other local anaethetics
- moxidectin
- ivermectin
- calcium channel blockers
- baclofen
- permethrin
- THC
- ibuprofen

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37
Q

What is the dose regime for intravenous lipid emulsion therapy?

A

Use a 20% lipid solution with an initial bolus of 1.5ml/kg IV followed by 0.25ml/kg/min for 30-60 minutes. Doses can be repeated q4-6hrs if the patient is still showing clinical signs and the patient is no longer lipaemic (lipaemia occurs as a side effect of ILE therapy).

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38
Q

What are the side effects of intravenous lipid emulsion therapy?

A
  1. Hypertriglyceridaemia
  2. Volume overload
  3. Persistent and gross lipaemia
  4. Corneal lipidosis
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39
Q

What is therapeutic plasma exchange?

A

it has been used on veterminary medicine to remove toxicants with high protein binding and low volume of distribution. It removed a patients plasma and associated protein bound toxin and replaces it with new plasma.

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40
Q

In what cases can therapeutic plasma exchange be used?

A

Been suggested for NSAIDs

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41
Q

What are the potential sides effects of therapeutic plasma exchange?

A
  • hypotension
  • bleeding
  • clot formation
  • sepsis
  • allergic reaction
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42
Q

What are the indications for acepromazine in cases of toxicosis?

A

Agitation and hypertension

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43
Q

What is the dose of acepromazine?

A

0.05-0.1mg/kg IV

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44
Q

What is atipamezole used for in cases of toxicosis? What are the indications?

A

Toxicosis with amitraz, xylazine, dexmedetomidine, brimonidine, clonidine and tizanidine

Sedation, bradycardia, hypotension

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45
Q

What is the dose of atipamezole?

A

50 mcg/kg IM

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46
Q

What is atropine used for in cases of toxicosis? What are the indications?

A

Organophosphates and carbomates, solanum spp, clitocybe and inocyte mushrooms.

Indications: Bradycardia, AV block, SLUDGE - M signs.

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47
Q

What are SLUDGE-M signs?

A

Salivation
Lacrimation
Urination
Defecation / Diarrhea
Gastrointestinal upset
Emesis
Miosis and muscle spasms

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48
Q

What are the indications for cyproheptadine in causes of toxicosis?

A

Serotonin syndrome

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49
Q

What are the indications for levetiracetam in causes of toxicosis?

A

seizures

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50
Q

What are the indications of methocarbamol in cases of toxicosis?

A

Generalised muscle tremors

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51
Q

What is the dose of methocarbamol?

A

55-220 mg/kg slow IV titrated to effect

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52
Q

When is propanolol indicated?

A

It’s a beta blocker used in cases of albuterol intoxication resulting in sinus tachycardia

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53
Q

When is pyridoxine indicated?

A

Isoniazid and gyromitra mushroom intoxication when causing seizures. Also an adjustive therapy for etheylene glycol intoxication

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54
Q

When is vitamin K indicated?

A

Known or suspected exposure to an anticoagulant or prolonged coagulation values

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55
Q

What is the dose of vitmain K?

A

1.5 - 2.5 mg/kg PO q12 for 7-30 days

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56
Q

How do we known when to discontinue vit K therapy?

A

check pt 60-72 hours after last dose of vit K to ensure continued treatment is not required.

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57
Q

What are the side effects of vit K?

A

Can cause anaphylaxis

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58
Q

What are the indications for yohimbine?

A

Same as atipamezole.

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59
Q

What is the mechanism of action of aminopyridine (avitrol)?

A

Blocks potassium channels and increased acetylcholine release

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60
Q

What are the clinical signs of aminopyridine intoxication?

A

Weakness, hypersalivation, vomiting, dyspnoea, tachycardia, tremors and seizures.

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61
Q

How do you treat aminopyridine intoxication?

A

Supportive care.

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62
Q

What is the mechanism of action of 5-fluorouracil?

A

Chemo drug - neuro signs possibly due to disruption of the krebs cycle or inhibition of gaba production.

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63
Q

What are the signs of 5-fluorouracil intoxication?

A

vomiting, altered mentation, ataxia, tremors or seizures. BM suppression in 2-4 weeks.

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64
Q

How is 5-fluorouracil treated?

A

Supportive. Levetiracetam for seizures.

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65
Q

What is the mechanism of neurotoxicosis of 5-hydroxytryptophan?

A

Increased production of serotonin.

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66
Q

What are the clinical signs of 5-hydroxytryptophan?

A

Serotonin syndrome

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67
Q

What do products with 5-hydroxytryptophan commonly contain?

A

xylitol

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68
Q

What are the signs of serotonin syndrome?

A

CNS stimulation, vomiting, tremoring, seizures, hyperthermia (secondary to tremoring and seizuring), diarrhea, abdominal pain, and mydriasis

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69
Q

What is the mechanism of neurotoxicosis of acetylcholinesterase insecticides e.g. organophosphates and carbamol?

A

Inhibits acetylcholinesterase

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70
Q

What are the signs of organophophate or carbamol intoxication?

A

SLUDGE signs

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71
Q

What is the mechanism of neurotoxicosis of alcohols?

A

Enhances inhibitor effects of gaba and inhibits glycine binding

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72
Q

What is the treatment of alcohol intoxication?

A

Naloxone, atipamezole or yohimbine may reverse CNS depression; haemodialysis.

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73
Q

What is the mechanism of neurotoxicosis of a2 agonist intoxication?

A

Potentiates a2 adrenergic receptors to inhibit the release of noradrenaline

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74
Q

What is the treatment of a2 agonist intoxication?

A

atipamezole or yohimbine

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75
Q

What is the mechanism of neurotoxicosis of amphetamines/MDMA intoxicosis?

A

Sympathomimetic result in adrenaline release and serotonin release resulting in hypertension, tachycardia, CNS excitation, seizure, hyperthermia etc.

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76
Q

What is the treatment of amphetamines/MDMA intoxicosis?

A
  • Acepromazine for agitation
  • Propanolol for inappropriate and persistent sinus tachycardia
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77
Q

Why should benzos be avoided in causes of amphetamine and MDMA intoxication?

A

As it can cause paradoxical excitation

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78
Q

What is the mechanism of neurotoxicosis of MAO inhibitors (selegiline)?

A

Inhibits serotonin breakdown by inhibiting MAO resulting in serotonin syndrome

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79
Q

What is the mechanism of neurotoxicosis of SSRI intoxication?

A

Inhibits serotonin reuptake and some also inhibit noradrenaline results in serotonin syndrome

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80
Q

What is the treatment for anti-depressant intoxication include MAO inhibitor and SSRIS?

A

cyproheptadoine and acepromazine for their anti-serotonin effects

Propanolol for persistent sinus tachycardia

ILE may be effective

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81
Q

What is the treatment of TCA intoxication?

A

Titrate pH to 7.55 with IV sodium bicarbonate

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82
Q

What is the mechanism of neurotoxicosis of baclofen iontoxication?

A

It is a centrally acting muscle relaxant, it is a gaba b agonist that binds to both the pre and post synaptic receptors results in CNS and respiratory depression, paralysis of muscles arrhythmias hyotension and seizures

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83
Q

How is baclofen intoxication treated?

A

ventilatory support and haeodialysis

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84
Q

What is the mechanism of neurotoxicosis of barbiturate intoxication?

A

Activated gaba a receptors, inhibits glutamate receptors and inhibits the release of noradrenaline and acetylocholine

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85
Q

What is the treatment of action of barbiturate intoxication?

A

supportive/ILE

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86
Q

What is the mechanism of neurotoxicosis of benzodiazepines?

A

activates gaba a receptors

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87
Q

What is the treatment of benzodiazepine intoxication?

A

Flumazenil

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88
Q

What is the mechanism of neurotoxicosis of bromethalin (type of rat poision)?

A

uncouple oxidative phosphorylation in neurol and glial cell mitochondria resulting in fluid accummulatgion within myelin results in neuro signs

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89
Q

What is the treatment of bromethalin (type of rat poison) intoxication?

A

Decontamination is most important

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90
Q

What is the mechanism of neurotoxicosis of bupropion (anti-depressant)?

A

Inhibits reuptake of dopamine and noradrenaline and antagonises nicotine acetylcholine receptors

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91
Q

What is the treatment of bupropion (anti-depressant) intoxication?

A

supportive, ILE

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92
Q

What is the treatment of cannibis intoxication?

A

supportive, ILE

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93
Q

What is the mechanim of neurotoxicosis of carbon monoxide intoxication?

A

Binds to haemohglobin reducing oxygen carrying capacity

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94
Q

What is the mechanism of neurotoxicosis of cocaine intoxication?

A

CNS stimulant, block reuptake of noradrenaline and serotonin

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95
Q

What the treatment for cocaine intoxication?

A

Supportive ILE

96
Q

What are the clinical signs of ethylene glycol in toxication?

A

Neuro - ataxia and seizures
Renal failure
Vomiting

97
Q

What is the mechanism of neurotoxicosis of ethylene glycol intoxication?

A

Alcohol effects of parent compound, metabolites causes a severe acidosis

98
Q

What is the mechanism of neurotoxicosis of grayanotoxins (Kalmia, Rhododendron, pieris spp.)?

A

Inhibits sodium channels

99
Q

What are the clinical signs of grayanotoxins intoxication?

A

Vomiting, cardiac arrhythmias, ataxia, seizures

100
Q

What is the mechanism of neurotoxicosis of Isoxazole mushrooms Amanita muscaria, A. pantherina) toxicosis?

A

Ibotenic acid, a glutamate and glycine receptor agonist, and muscimol, a GABAA agonist

101
Q

What are the clinical signs of Isoxazole mushrooms Amanita muscaria, A. pantherina) toxicosis?

A

GI upset, CNS depression, disorientation, paresis, opisthotonos, seizures, respiratory depression, or coma

102
Q

What should be avoided in Isoxazole mushrooms toxicosis?

A

Benzodiazepines

103
Q

What is the mechanism of neurotoxicosis of isoxazoline toxicosis?

A

Inhibits GABA and glutamate receptors in insects

104
Q

What are the clinical signs of isoxazoline insecticide toxicosis?

A

GI upset, lethargy, ataxia, rare tremors and seizures (often singular)

105
Q

What is the treatment for isoxazoline toxicosis?

A

Supportive, if topical, dermal decontamination

106
Q

What is the mechanism of action of lead toxicosis that leads to neurological signs?

A

Competes with zinc ions which disrupts GABA production and activity; alters synaptic transmission at smooth muscle neuromuscular junctions

107
Q

What are the clinical signs of lead toxicosis?

A

Acute: GI upset, ataxia, tremors, agitation, seizures

Chronic: GI upset, lethargy, behavior changes, intermittent seizures, anemia, megaesophagus

108
Q

How do you treat lead toxicosis?

A

Blood lead level; chelation with succimer (DMSA), calcium EDTA, BAL, or penicillamine

109
Q

What is the mechanism of neurotoxicosis of local anaesthetic toxicosis?

A

Inhibits recovery of sodium channels

110
Q

What are the clinical signs of local anaesthetic toxicosis?

A

GI upset, methemoglobinemia, cardiac arrhythmias, seizures

111
Q

How do you treat local anaesthetic toxicosis?

A

Supportive care

112
Q

What is the mechanism of neurotoxicosis of LSD toxicosis?

A

Increases serotonin

113
Q

What are the clinical signs of LSD toxicosis?

A

Ataxia, mydriasis, depression or excitation, vocalization

114
Q

What is the treatment for LSD toxicosis?

A

Supportive care

115
Q

What is the mechanism of action of macadamia toxicosis?

116
Q

What are the clinical signs of macadamia toxicosis?

A

Weakness, CNS depression, GI upset, ataxia, tremors, nonfebrile hyperthermia

117
Q

What is the treatment for macadamia toxicosis?

A

Supportive; most resolve in 24 hours

118
Q

What is the mechanism of neurotoxicosis of macrocyclic lactone intoxication?

A

At low doses, inhibits GABA; at high doses, potentiates GABA

119
Q

What are the clinical signs of macrocyclic lactone intoxicosis?

A

CNS depression, ataxia, weakness, blindness, respiratory depression, bradycardia, hypothermia, coma

120
Q

What is the treatment of macrocyclic lactone toxicosis?

A

Supportive care; ILE

121
Q

What is the mechanism of neurotoxicosis of metaldehyde toxicosis?

A

Exact mechanism unknown; decreases serotonin, norepinephrine, monoamine oxidase and GABA

122
Q

What are the clinical signs of metaldehyde toxicosis?

A

Rapid onset of tremors, seizures, nonfebrile hyperthermia, tachycardia

123
Q

How is metaldehyde toxicosis treated?

A

Methocarbamol for tremors

124
Q

What is the mechanism of neurotoxicosis of methylxanthine (Caffeine, theobromine, theophylle) toxicosis?

A

Inhibit cyclic nucleotide phosphodiesterases and antagonize the effects of adenosine

125
Q

What are the clinical signs of methylxanthine toxicosis?

A
  • GI upset (dogs, cats: 20 mg/kg); agitation, tachycardia (>40 mg/kg)
  • tremors, seizures (>60 mg/kg).

Signs begin within minutes (caffeine-only products) to 6-12 hours (chocolate).

126
Q

How do you treat methylxanthine toxicosis?

A

Supportive, as appropriate: emesis if not showing any clinical signs; IV fluids; beta-blockers if cardiac tachyarrhythmias; seizures respond to barbiturates (e.g., phenobarbital); activated charcoal is rarely given due to risk of hypernatremia (fluid shifts)

127
Q

What is the mechanism of action of metronidazole toxicosis?

128
Q

What are the clinical signs of metronidazole toxicosis?

A

GI upset, ataxia, hypermetria, tremors, vertical nystagmus, seizures

129
Q

What is the treatment of metronidazole toxicosis?

A

Discontinue metronidazole; diazepam to hasten recovery

  • Oral diazepam (at approximately 0.43 mg/kg orally every 8 hours for three days)
130
Q

What is the mechanism of neurotoxicosis of nicotine toxicosis?

A

Low dose: stimulates nicotinic acetylcholine receptors

High dose: blocks nicotinic receptors due to persistent depolarization

131
Q

What are the clinical signs of nicotine toxicosis?

A

Vomiting. Low dose: agitation, tachycardia, tremors. High dose: bradycardia, respiratory depression, weakness, paresis

132
Q

What should be avoided in cases of nicotine toxicosis?

A

Antacids as they enhance absorption

133
Q

What are the clinical signs of opioid toxicosis?

A

Lethargy, ataxia, GI upset, bradycardia, hypothermia, hypotension, nonfebrile hyperthermia (cats), CNS depression, coma

134
Q

What is the treatment of opioid toxicosis?

A

Naloxone to reverse

135
Q

What is the mechanism of action of phenylpropanolamine toxicosis?

A

Vasoconstriction

136
Q

What are the clinical signs of phenylpropanolamine?

A

Agitation, tachycardia (followed by bradycardia), hypertension, tremors, piloerection

137
Q

What is the mechanism of action of pyrethrin toxicosis?

A

Prolongs sodium influx and reduces potassium efflux, which enhances the action potential and results in repetitive nerve discharge

138
Q

What are the clinical signs of pyrethrin toxicosis?

A

Tremors, dermal paresthesia, agitation, seizures, GI upset with oral exposure

139
Q

Which animal is more sensitive to pyrethrin toxicosis?

140
Q

What is the treatment of pyrethrin toxicosis?

A

Bathe if dermal, methocarbamol for tremors; ILE

141
Q

What is the mechanism of action of zinc toxicosis?

A

Direct irritant to GI tract; releases phosphine gas, which interrupts cellular aerobic respiration in mitochondria, leading to decreased energy production, free radical formation, and damaged cellular membranes, proteins, and nucleic acids

142
Q

What are the clinical signs of zinc toxicosis?

A

Vomiting, lethargy, CNS depression, tremors, agitation, seizures, coma, ataxia, rigidity, nystagmus, tachypnea, dyspnea, pulmonary edema, increased renal values and liver enzyme activities, acidosis

143
Q

What is the treatment for zinc toxicosis?

A

Supportive; antacids to raise stomach pH;

Chelation with succimer or CaEDTA or d-penicillamine

public health concern with humans inhaling phosphine gas from ingesta (move patient to well-ventilated area)

144
Q

How can you diagnose neurotoxicoses?

A
  1. Mostly history and clinical signs
  2. Radiographs for suspect metal toxicosis
  3. A serum ethylene glycol test for suspected toxicosis
  4. Over the counter urine drug screen test
  5. Electrolytes/blood gas
145
Q

What toxins can causes acute blindness?

A
  • Hypernatremia (activated charcoal, ice melts, play dough, salt)
  • Ivermectin
  • Lead
  • Metaldehyde
  • Paintballs
146
Q

What toxins can cause tremors?

A
  • Hypernatremia (activated charcoal, ice melts, play dough, salt)
  • Metaldehyde
  • Pyrethrin/pyrethroids (bifenthrin, permethrin)
  • Strychnine
  • Tremorgenic mycotoxins (penitrem A, roquefortine)
147
Q

What toxins can cause muscle weakness, paresis, paralysis?

A
  • Black widow spider (Lactrodectus spp.)
  • Bromethalin
  • Coral snake (Elapidae spp.)
  • Fertilizers (especially manure-based)
  • Ionophores (lasalocid, monensin)
  • Macadamia nut
  • Metronidazole
  • Tea tree oil (Melaleuca spp.)
  • 2,4-D and phenoxy herbicides
148
Q

Which toxins can causes nervous system depression?

A
  • Alcohols
  • Alpha-2 agonists
  • Antidepressants
  • Antihistamines—low doses
  • Baclofen
  • Barbiturates
  • Benzodiazepines (alprazolam, clonazepam, diazepam, lorazepam)
  • Diethylene glycol
  • Ethylene glycol
  • Hypernatremia
  • Imidazoline decongestants
  • Ivermectin (abamectin, moxidectin, etc.)
  • Lead
  • Marijuana
  • Muscle relaxants (cyclobenzaprine, methocarbamol)
  • Mushrooms
  • Nicotine
  • Non-steroidal anti-inflammatory drugs—high doses
  • Opioids
  • Phenothiazines
  • Piperazine
  • Propylene glycol
149
Q

What toxins can cause Nervous system excitation +/- seizures?

A

Amphetamines
Antidepressants (TCA, SSRI, atypical)—high doses
Antihistamines (diphenhydramine, loratadine)—high doses
Baclofen
Bromethalin
Brunfelsia spp.
Cicuta spp. (water hemlock)
Cocaine
Cold medications (pseudoephedrine, ephedrine, phenylephrine)
Cyanobacteria
5-Fluorouracil
5-Hydroxytryptophan
Hypernatremia (activated charcoal, ice melts, play dough, salt)
Isoniazid
Isoxazoline insecticides (afoxolaner, fluralaner, sarolaner)
Lead
LSD
Metaldehyde
Methylxanthines (caffeine, chocolate, theophylline)
Metronidazole
Mushrooms (isoxazole, Psilocybe spp.)
Nicotine
Organophosphate or carbamate insecticides (aldicarb, methomyl, disulfoton)
Phenylpropanolamine
Pyrethrin/pyrethroid insecticides
Toads (Rhinella marina, Incilius alvarius)
Tremorgenic mycotoxins (penitrem A, roquefortine)
Yohimbine
Zinc phosphide/aluminum phosphide

150
Q

What is the minimum diagnostic database for suspected neurotoxicosis?

A
  • Thorough history
  • CBC
  • Biochemistry with lytes
  • Blood pressure
  • Blood gas
151
Q

What are the medications used for chelation of lead? What are the doses?

A

Chelators effective for lead elimination include:
- succimer (10 mg/kg PO q8h for 10 days)
- edetate calcium disodium (CaEDTA, 25 mg/kg SQ q6h for 5 days or 75 mg/kg IV q6h for 2-5 days, diluted to 10 mg/mL for administration)
- d-penicillamine (30-110 mg/kg/day PO divided q6h for 7 days), or dimercaprol (British anti-Lewsite [BAL], 3-6 mg/kg IM q6-8h

152
Q

What medications can be used for stimulatory signs/seizures?

A
  • acepromazine
  • Diazepam in some case but can worsen certain toxins
  • Seizure can be controlled with diazepam, levetiracetam, midazolan or phenobarbital or inhalant anaesthesia
153
Q

How is serotonin syndrome treated?

A

A serotonin antagonist such as cyproheptadine. Propranolol may also antagonize serotonin activity

154
Q

How are tremors treated in toxicosis?

A

Methocarbamol

155
Q

What are the hepatotoxicants of veterinary importances?

A
  1. Drugs/supplements:
  2. Plants e.g. cycads
  3. Mushrooms/fungi: Amatoxins, aflatoxins, blue green algae (Cyanobacteria)
  4. Heavy metals: iron
156
Q

What are the hepatotoxic drugs of veterinary importance?

A

Acetaminophen
Anabolic steroids (e.g., stanozolol)
Aspirin
Azathioprine
Azole antifungals
CCNU (lomustine)
Corticosteroids
Diazepam
Diethylcarbamazine
Halothane
Ketoconazole
Mebendazole
Megestrol acetate
Methimazole
NSAID (e.g., carprofen)
Phenobarbital
Phenytoin
Primidone
Tetracycline
Trimethoprim-sulfa
Zonisamide

157
Q

What are some common supplements that can result in hepatotoxicity?

A
  • alpha-lipoic acid
  • joint supplements
158
Q

How long does it take paracetamol to reach peak plasma levels after oral dosing?

159
Q

What is the toxic dose of paracetamol in dogs?

A

≥75-100 mg/kg

160
Q

What is the toxic dose of paracetamol in cats?

161
Q

What is the toxic metabolite in paracetamol?

A

N-acetyl-para-benzoquinone imine (NAPQI)

162
Q

Describe the mechanism of action of liver injury of acetominophen toxicosis?

A

N-acetyl-para-benzoquinone imine (NAPQI) is generated by cytochrome P450 oxidation in the liver and kidney when the normal glucuronidation and sulfation pathways are saturated. Intrinsic antioxidants such as glutathione or cysteine bind NAPQI, preventing cellular injury, but when these antioxidant systems are depleted, NAPQI binds to cellular macromolecules, resulting in hepatocellular injury and death.

163
Q

What is the onset of action of acetominophen toxicosis?

A

2-4 hours for methemoglobinemia and 24-48 hours for liver injury

164
Q

What laboratory abnormalities do you see for liver injury?

A

AST, ALT and TBIL elevations

165
Q

How do you manage paracetamol toxicosis?

A
  1. Supportive care, management of clinical signs
  2. IVFT
  3. GI decontamination
  4. Administration of glutathione precursors such as n-acetylcysteine at 140mg/kg IV loading dose, followed by 70 mg/kg IV q6 for 6 doses and s-adenosylmethionine at 20mg/kg PO q24 or can divide into q8-12 doses
  5. Ascorbic acid (30 mg/kg PO, SQ, IV q6h) helps reduce methemoglobin to hemoglobin
166
Q

What is the mechanism of liver injury of Alpha lipoic acid toxicosis?

A

Oxidative injury, binding of cellular thiol groups

167
Q

What is the toxic dose of alpha lipoic acid in cats?

A

Cats are 10× more sensitive than dogs; dosages >13 mg/kg = hepatocellular damage

168
Q

What is the toxic dose of alpha lipoic acid in dogs?

A

> 126 mg/kg = hepatocellular injury

169
Q

What is the mechanism of liver injury of diazepam toxicosis?

A

immune-mediate response in suspected

170
Q

What is the onset of action of diazepam toxicosis?

A

Onset after 3-7 days of oral dosing

171
Q

What is the mechanism of liver injury or iron toxicosis?

A

Free radical production causing oxidative injury

172
Q

What chelation therapy is recommended for iron toxicosis?

A

chelate with deferoxamine (15 mg/kg/h or 40 mg/kg slow IV q4-8h) when serum iron >300 mcg/dL

173
Q

What is the dose of iron toxicosis in dogs?

A

20 mg/kg, gastrointestinal injury; ≥60 mg/kg, hepatic injury

174
Q

What is the mechanism of liver injury of joint supplement toxicosis?

A

Suspected manganese toxicosis. Reported only in dogs.

175
Q

What is the dose of joint supplement toxicosis in dogs?

A

Reported in dogs only; oral manganese dosage of 86 mg/kg from joint chews was lethal.

176
Q

What is the mechanism of liver injury of NSAID toxicosis?

A

Unknown, theories include mitochondrial injury, oxidative injury, neoantigen formation

177
Q

What does NSAID toxicosis do to the liver?

A

Causes an idiosyncratic hepatopathy in dogs generally occurs after 2-3 weeks or more of therapy; usually reversible; hepatopathy not reported in cats

178
Q

When is methimazole toxicity seen? How is it treated?

A

Usually in first month of therapy; usually reversible

179
Q

What is the mechanism of liver injury of sulfonamide toxicosis?

A

Neoantigen formation triggers immune response

180
Q

Which fungi is most commonly associated with aflatoxins?

A

Aspergillus

181
Q

What are the common sources of aflatoxins?

A

corn and other grains, peanuts, soybeans, tree nuts, and cottonseed

182
Q

Describe the mechanism of liver injury of aflatoxins.

A

The toxicity of AFB1 is due to its biotransformation into toxic epoxides that bind cellular proteins and nucleic acid, resulting in altered protein synthesis, energy production, cellular metabolism, enzyme activity, and nucleic acid transcription and translation. These processes lead to hepatocellular degeneration, necrosis and apoptosis. The low levels of toxic metabolites generated under normal circumstances are dealt with by endogenous antioxidant molecules such as glutathione, and it is only in the face of excessive exposure that significant cell injury occurs. Aflatoxin-induced DNA damage can result in genetic and epigenetic alterations that can persist and lead to chronic liver injury and carcinogenesis.

183
Q

Why are dogs and cats more sensitive to aflatoxins?

A

Compared to most other mammalian species, dogs and cats have inherently low hepatic glutathione concentrations and low glutathione-s-transferase activity, making them more sensitive to aflatoxin-induced liver injury.

184
Q

How soon do clinical signs develop in cases of alfaxatoin exposure?

A

Clinical signs of aflatoxicosis may develop within 1-2 days of ingestion of feeds contaminated with very high levels of aflatoxin but may be delayed for weeks to months in cases of chronic exposure to more moderately elevated aflatoxin concentrations.

185
Q

How is aflatoxin toxicosis treated?

A

Non-specific
- Anti-emetic
- GI protectants
- IVFT
- Vit K for coagulopathies
- N-acetycysteine or s-AME or silymarin for glutothionine precursors and hepatoprotection

186
Q

Describe the mechanism of liver injury of blue-green algae (Cyanobacteria) toxicosis?

A

Hepatocyanotoxins are absorbed from the ileum and are taken up by hepatocytes via a bile acid transporter. Within the hepatocyte, these peptides bind and disable cytoskeletal proteins, initiate lipid peroxidation, and bind to and fragment DNA. The overall cellular effect of HCs is loss of membrane integrity, decreased protein synthesis, necrosis, and apoptosis leading to rounding and detachment of hepatocytes from the basement membrane and intrahepatic “hemorrhage” into areas devoid of hepatocytes. In severe intoxications, massive loss of hepatocytes results in pooling of large volumes of blood within the liver, resulting in hepatomegaly and rapid death due to hypovolemia. Surviving patients experience acute hepatic insufficiency that can lead to hepatic failure

187
Q

What laboratory finding are often seen with cyanobacteria toxicosis?

A

Serum liver enzyme activities, bile acid concentrations, and bilirubin concentrations are abnormal; hypoglycemia, hypokalemia and hyperammonemia may occur. Depending on the degree of hepatic injury, coagulopathy or encephalopathy may develop

188
Q

How is cyanobacteria toxicosis treated?

A
  • supportive care
  • symptomatic therapy
  • Cholestyramine (300-1000 mg/kg PO q8h) should be considered if the patient’s condition is amenable to oral administration
  • Hepatoprotection with N-acetylcysteine, s-AME or silymarin should be considered
189
Q

Describe the mechanism of liver injury of cycad toxicosis?

A

Cycasin, the primary hepatotoxin, is biotransformed in the intestine to methylazoxymethanol (MAM), a metabolite that is hepatotoxic, neurotoxic, mutagenic, teratogenic, and carcinogenic. MAM alkylates nucleic acids, impairing cellular protein synthesis and resulting in cell death.

190
Q

What are the clinicopathological findings is cases of cycad toxicosis?

A

Clinicopathologic alterations consistent with liver failure (elevated bilirubin concentrations, liver enzyme activities, and bile acid concentrations; elevated coagulation times; hypoglycemia) may take up to 24-48 hours to develop. Azotemia, bilirubinuria, hematuria, and cylindruria may occur.

191
Q

How do you treat cycad intoxication?

A
  1. Decontamination with emesis and activated charcoal
  2. IVFT
  3. Anti-emetics
  4. GI protectants
  5. Vit K
  6. Hepatoprotectants
192
Q

Where is xylitol found?

A

Gum, lollies, toothpastes, cosmetics and oral medications

193
Q

Describe the mechanism of action of xylitol toxicosis.

A

Dogs have a unique physiologic response to xylitol that results in a rapid, sustained, and dose-dependent rise in insulin release, which in turn triggers a precipitous drop in blood glucose levels. Some dog also develop elevated liver enzymes and some progress to severe hepatic necrosis.

194
Q

How do you treat xylitol toxicosis?

A

Decontamination and supportive care. If concerned for hepatic necrosis/ coagulopathy vit K and hepatoprotectants.

195
Q

What are the common renal toxicants in dogs and cats?

A
  1. Allium spp
  2. Aminoglycosides
  3. Amphotericin B
  4. Cholecalciferol and Vit D analogues
  5. Cisplatin
  6. Ethylene glycol
  7. Lilium and hemerocallis spp.
  8. Pit vipers
  9. NSAIDS
  10. Sulfonamides
  11. Tetracyclines
  12. Vitis spp. e.g. grapes and raisins
  13. Zinc
196
Q

How does cholecalciferol/vit D analogues causes an AKI?

A

It has the potential to cause an AKI secondary to hypercalcaemia and renal mineralisation.

197
Q

What are the most common sources of cholecalciferol/vit D analogues?

A

Rodenticides and human medications

198
Q

How do you managecholecalcifierol/vit D toxicosis?

A
  1. Decontamination e.g. emesis and activated charcoal
  2. Cholestyramine resin
  3. Ca+, Phosp, BUN and creat should be monitored daily until 96 hours after exposure
  4. Once hypercalcaemia develops treatment is focused on returning calcium and phosp to normal

Once serum Ca++ levels normalize, the patient should be weaned off saline diuresis and discharged on oral medications. Following discharge Ca++ should be monitored at least 2-3 times per weeks for 2-3 weeks

Treatment may be required for weeks due to the long half-life of calcidio

199
Q

What is the prognosis of vit D toxicosis?

A

The prognosis is good if the exposure is treated promptly. The prognosis is guarded to poor once hypercalcemia develops and grave once soft-tissue mineralization develops.

200
Q

Where is ethylene glycol found?

A

automotive antifreeze, de-icers, home solar units, inks, brake fluids, and snow globe-type decorations.

201
Q

How do you diagnose ethylene glycol toxicosis?

A

While the gold standard is gas chromatography-mass spectroscopy quantitative analysis of serum EG levels, cage-side EG tests are available. They have good sensitivity but are lacking in specificity. False positives can be seen from the presence of alcohols, propylene glycol, glycerol, and sorbitol.7-9 Osmolal gap and acid-base testing can be used in conjunction with a cage-side EG test to best determine the need for treatment. An increased serum osmolal gap (>20 mOsm/kg) within 1-2 hours of the exposure is indicative of the presence of an exogenous solute like EG.

202
Q

How do you calculate osmolal gap?

A

measured serum osmolality minus the calculated serum osmolality.

Serum osmolality is calculated using the following formula: 1.86 × (Na+ + K+ + glucose/18 + BUN/2.8),

assuming Na+ and K+ are in mEq/L and glucose and BUN are in mg/dL; with metric units (all mmol/L), the formula is 1.86 × (Na+ + K+ + glucose + BUN).

203
Q

How do you treat ethylene glycol toxicity?

A

Fomepizole (4-methylpyrazole) is the preferred ADeH inhibitor.

Or Ethanol

204
Q

How does fomepizole work?

A

It directly inhibits the enzyme and causes less central nervous system (CNS) depression, diuresis, and acidosis than ethanol does.

205
Q

How long should fomepizole be used for in the treatment of ethylene glycol toxicity?

A

Fomepizole should be continued until at least 36 hours post-exposure or until an EG test is negative.

206
Q

How does ethanol work in treating ethylene glycol toxicity?

A

Ethanol does not directly inhibit Alcool dehydrogenase, but rather serves as a competitive substrate for the enzyme.

207
Q

How long should ethanol be used for in the treatment of ethylene glycol toxicity?

A

Ethanol should be continued for at least 24 hours beyond the point where renal and acid-base values are normal

208
Q

What is the mechanism of renal toxicity of allium spp?

A

Secondary to hemolysis

209
Q

What is the mechanism of renal toxicity of aminoglycosides?

A

Interfere with phospholipid metabolism in the lysosome of proximal renal tubular cells

210
Q

What is the mechanism of renal toxicity of amphotericin B?

A

Renal vasoconstriction

211
Q

What is the mechanism of renal toxicity of cholecalciferol?

A

Hypercalcemia from enhanced GI Ca++ absorption, mobilization of osteoclasts, enhanced renal Ca++ resorption

212
Q

What is the mechanism of renal toxicity of cisplatin?

A

Activates signaling pathways causing tubular cell injury and death

213
Q

What is the mechanism of renal toxicity of ethylene glycol?

A

EG metabolites are cytotoxic to renal tubular cells. Accumulation of CaOx crystals in renal tubules, renal tubular acidosis.

214
Q

What is the mechanism of renal toxicity of lilium and hemerocallis spp.?

A

Cats only. Unknown. Renal injury occurs due to necrosis of the proximal renal tubular epithelium. The toxin has also caused degeneration of pancreatic acinar cell.

215
Q

What is the mechanism of renal toxicity of Pit vipers?

A

Venom causes hemolysis and thrombotic microangiopathy

216
Q

What is the mechanism of renal toxicity of NSAIDs?

A

Inhibition of prostaglandin synthesis via COX enzyme inhibition, leading to renal vasoconstriction, decreased GFR, anoxia.

217
Q

What is the mechanism of renal toxicity of sulfonamides?

A

Crystalluria

218
Q

What is the mechanism of renal toxicity of tetracyclines?

A

Decreased utilization of amino acids

219
Q

What is the mechanism of renal toxicity of vitis spp?

A

Unknown (tartaric acid suspected)

220
Q

What is the mechanism of renal toxicity of zinc?

A

Secondary to hemolysis

221
Q

What are the clinical signs of renal toxicants?

A
  1. Vomiting
  2. AKI
  3. Haemolysis in some cases
  4. PU/PD, anuria
222
Q

How do you manage actue hypercalcaemia secondary to Vit D toxicosis?

A
  1. IVFT 0.9% NaCL 100-180ml/kg/day initially then adjusted to maintain hydration
  2. Low calcium diet
  3. Bisphosphonates: Pamidronate or zoledronate
  4. Predniosolone
  5. Furosemide
  6. Phosphate binders
223
Q

What is the function of 0.9% NaCL in managing acute hypercalcaemia?

A

Na+ competes with Ca++ for resorption in renal tubules

224
Q

Why should LRS be avoided in hypercalcaemi patients?

A

It contains calcium

225
Q

What is the function of a low calcium diet in managing acute hypercalcaemia?

A

Reduce exogenous Ca++, upregulation of metabolizing enzymes, lowering calcidiol levels

226
Q

What are the options for a low calcium diet?

A

Macaroni and lean ground beef, many prescription renal and urinary tract diets

227
Q

What is the function of bisphosphonates in managing acute hypercalcaemia?

A

Inhibits osteoclastic bone resorption

228
Q

What is the function of prednisolone in managing acute hypercalcaemia?

A

Reduce bone resorption, decrease intestinal absorption and increase renal elimination of Ca++

229
Q

What is the function of furosemide in managing acute hypercalcaemia?

A

Promote calciuresis

230
Q

What is the function of phospahte binders in managing acute hypercalcaemia?

A

Reduces intestinal absorption of phosphorus

231
Q

How is lily toxicosis managed?

A
  1. Decontamination e.g. bathing, emesis and activated charcoal
  2. Intravenous diuresis: continuing diuresis for at least 48 hours is recommended to prevent anuric renal failure
232
Q

How is NSAID intoxication managed?

A
  1. Decontamination e.g. emesis and activated charcoal if alert and within 1 hour of ingestion. If the NSAID undergoes enterohepatic recirculation, a second dose of AC can be given 6-8 hours after the first dose
  2. Cholestyramine has been shown to bind many NSAIDs and can be used in the first 24-48 h after an exposure
  3. Base line UA, and biochem performed and rechecked daily
  4. IVT at 2 x maintenance
  5. PPI e.g. omeprazole or pantropazole
  6. Sulcralfate or misoprostal
  7. TPE - more evidence if need however before it can be recommended
233
Q

What is the toxic component of grapes and raisins?

A

Tartaric acid

234
Q

What are the clinicopathologic finding in grape and raisin intoxication?

A

Clinicopathologic findings can include azotemia, hypercalcemia, hyperphosphatemia, increased alanine aminotransferase (ALT) activity, hyperglycemia, hyperkalemia, hypokalemia, isosthenuria, hyposthenuria, proteinuria, glucosuria, pyuria, crystalluria, and cylindruria

235
Q

How is grape intoxication managed?

A
  1. Decontamination: induction of emesis, activated charcoal should only be given in patients with large exposure and poor emesis results.
  2. If emesis is successful risk of AKI is considered low and patients can be monitored at home

Monitoring at home - these patients should not be given an antiemetic prior to discharge so as not to mask the development of any vomiting. Patients should have a renal chemistry profile and urinalysis rechecked at 24-48 hours post exposure or sooner if any clinical signs develop at home.

If decontamination is unsuccessful should be admitted to the hospital for isotonic crystalloid fluid diuresis for 48 hours. Renal profiles and urinalyses should still be monitored. Most patients that are promptly treated with fluid diuresis do not develop AKI

236
Q

Up to Gastrointestinal toxicosis

Veterinary Textbook of Internal Medicine (16 decks)

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