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Small Animal Final Year > Toxicities > Flashcards

Toxicities Flashcards

1
Q

What can neuroexcitatory toxins cause in:

A) CNS?

B) PNS?

A

A) CNS: hyperexcitability, seizures, ataxia

B) PNS: muscles tremors and fasciculation

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2
Q

What can neuroinhibitory toxins cause in:

A) CNS?

B) PNS?

A

A) CNS: obtundation, stupour, coma

B) PNS: weakness, flaccid paralysis

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3
Q

How can you decontaminate gastrointestinally absorbed toxins?

A

–Emesis (within 2 hrs from ingestion) in alert patients

–Gastric lavage (within 2 hrs from ingestion) in subdue/comatose animals. Has to be done under GA and extreme care taken to protect airways

–Activated charcoal 1-5g/kg every 6-8 hrs for up to 24 hrs. In alert patients!

–Colonic lavage and cathartics

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4
Q

How can you decontaminate a cutaneous toxin?

A

–Bath, in stable patients

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5
Q

How can you decontaminate an inhaled toxin?

A

–Ventilation (mechanical in severe cases)

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6
Q

How can you decontaminate if an animal was exposed to a lipophilic substance?

A

Lipid infusion (Intralipid®), if exposure to lipophilic substances, acts as lipid sink. Bolus of 2mg/kg, followed by CRI of 4mg/kg/hr for 4 hrs

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7
Q

Name 6 neuroexcitatory toxins (8)

A
  • Ivermectin and macrolide parasiticides
  • Metaldehyde
  • Methylxanthines
  • Organophosphate and carbamates
  • Permethrin
  • Mycotoxines
  • Strychnine
  • Lead
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8
Q

How can Ivermectin, moxidectin, selamectin, milbemycin cause toxicity after ingestion? (3)

A

–Large-animals deworming products or contaminated faeces

–Iatrogenic by overdosing or wrong route or administration (ie per os instead of topic)

–Care with collie breeds (MDR1 mutation)

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9
Q

How does Ivermectin and macrolide parasiticides cause toxicity?

A
  • Mechanism of action –> agonist at the GABAA-gated chloride channels in the CNS
  • Initial neuroexcitation, followed at high doses by flaccid paralysis and coma
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10
Q

What is the toxicity of Ivermectin and macrolide parasiticides in:

A) Susceptible breeds?

B) Other breeds?

C) Cats?

A

A) 0.1mg/kg

B) 2.5mg/kg

C) 0.3-1.3mg/kg sc

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11
Q

What is the half life of Ivermectin and macrolide parasiticides?

A

2-19 days

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12
Q

How is Ivermectin and macrolide parasiticides toxicity diagnosed?

A

History

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13
Q

What is the clinical presentation of Ivermectin and macrolide parasiticides toxicity?

A

–Ataxia

–Lethargy

–Tremors

–Mydriasis

–Blindness

–Hypersalivation

–Disorientation

–Seizures

–Weakness

–Stupor

–Coma

–Respiratory failure

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14
Q

How can we manage Ivermectin and macrolide parasiticides toxicity?

A

–Emesis

–Activated charcoal

–Lipid infusion

–Phenobarbital for seizure control or propofol CRI if not responding

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15
Q

What is the prognosis of Ivermectin and macrolide parasiticides toxicity?

A

Dose related - can be guarded. Long recovery.

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16
Q

What is found in slug and snail baits which causes toxicity?

A

Metaldehyde

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17
Q

What is the mechanism of toxicity for metaldehyde?

A

•Mechanism of action

–Reduces levels of GABA (reduced inhibition à means excitation)

–Reduces levels of noradrenaline and serotonin

=Pro-convulsive effect

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18
Q

What are the clinical signs of metaldehyde?

A

–Anxiety

–Muscle tremors

–Fasciculations

–Ataxia

–Seizures

–Tachypnoea

–Tachycardia

–Hyperthermia

= HEAT STROKE

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19
Q

How do you diagnose metaldehyde toxicity?

A

History

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20
Q

How do you manage metaldehye toxicity?

A

–Emesis or gastric lavage

–Activated charcoal

–Benzodiazepine/phenobarbital (muscle tremors and seizures)

–Propofol infusion (severe cases of refractory seizures)

–Monitor body temperature!!!

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21
Q

What is the prognosis of metaldehyde toxicity?

A

Good if prompt intervention

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22
Q

What are caffeine, thoebromine (chocolate), theophylline?

A

Methylxanthines

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23
Q

What is the mechanism of action of Methylxanthines toxicity?

A

–Causes elevation of intracellular cyclic AMP, this results in increase in intracellular CA++ = neuromuscular excitability and inoptropic effect

–Competitive inhibition of adenosine receptors = CNS stimulation

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24
Q

With caffeine and theobromine:

A) When do you have clinical signs?

B) When do you have seizures?

A

A) 20mg/kg

B) 60mg/kg

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25
Q

What are the clinical signs within 1-2 hours of ingestion of Methylxanthines?

A

–Restlessness

–Hyperactivity

–V+ve and D+ve

–Tachycardia/tachypnoea

–Polyuria

–Muscles twitching

–Seizures (tonic or tetanic)

–Hyperthermia

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26
Q

How do you diagnose Methylxanthines ingestion?

A

History

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27
Q

How do you manage Methylxanthines toxicity?

A

–Emesis/activated charcoal

–Control ventricular arrhythmias (lidocaine, procainamide, Ca channel blockers, B blockers)

–Control muscle tremors and seizures with benzodiazepines (diazepam)

–Control temperature

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28
Q

What is the prognosis if Methylxanthines are ingested?

A

Good if early treatment

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29
Q

What is the mechanism of toxicity with Organophosphate and carbamates?

A

•Inhibit the action of the AChE (acetylcholinesterase)

=Ach accumulates in the synaptic space

30
Q

What are the 3 syndromes of ingesting Organophosphate and carbamates?

A
  • Acute toxicity
  • Intermediate
  • Delayed (neuropathy)
31
Q

With organophosphate and carbamate acute toxicity:

A) Muscarnic clinical signs?

B) Nicotinic signs?

C) CNS signs?

A

A) Hypersalivation, lacrimation, urination, defecation vomiting, miosis, bradycardia, bronchospasm

B)–Muscle fasciculation, twitches and tremors

–(delay NM signs) weakness and paralysis

C)

–Anxiety, ataxia, seizure, obtundation, coma

32
Q

What are the clinical signs of intermediate syndrome (7-96 hours) with Organophosphate and carbamates?

A

•Severe NM signs, weakness, neck ventroflexion, forelimbs weakness and hypoventilation

33
Q

When is delayed neuropathy and what is seen with Organophosphate and carbamates?

A

•1-4 weeks after exposure

–Anorexia, lethargy, pelvic limbs paresis, hyperaesthesia, neck venroflexion (cat)

34
Q

How do you diagnose organophosphate and carbamate ingestion?

A
  • Known exposure
  • Whole blood (heparin) cholinesterase activity <25-50%
  • Gastric content
35
Q

How do you manage Organophosphate and carbamates ingestion?

A
  • Skin decontamination, emesis, activated charcoal (depending on exposure)
  • Atropine 0.02mg/kg iv (muscarinic signs)
  • Pralidoxime (2-PAM) 10—20mg/kg sc, im or iv (care, may worsen clinical signs!)
  • Supportive care
36
Q

What is the prognosis of ingesting organophosphate and carbamates?

A

Good if they survive initial toxicity

37
Q

Why are cats susceptible to permethrin toxicity?

A

Deficiency in hepatic glucuronidatin

38
Q

What is the mechanism of toxcitiy of permethrin?

A
  • Slows both opening and closing of voltage sensitive Na+ channels
  • Resulting prolonged depolarisation
39
Q

What is the clinical presentation of permethrin toxicity?

A
  • Muscle fasciculation
  • Ears twitching
  • Tremors
  • Ataxia
  • Seizures
  • Hyperthermia
  • Hyperaesthesia
40
Q

When do animals present with permethrin toxicity?

A

3 hours - 3 days

41
Q

How do you diagnose permethrin toxicity?

A

History of exposure

42
Q

How do you manage permethrin exposure?

A
  • Decontamination of skin if dermal exposure (use washing up liquid!)
  • Control temperature hyperthermia but also hypothermia (after bath)
  • Drug therapy aimed at controlling tremors and seizures

–Benzodiazepine

–Phenobarbital

•Intravenous lipid administration

43
Q

What is the prognosis of permethrin expsosure?

A
  • Usually good if treatment/decontamination is promptly started
  • Recovery takes between 2 to 7 days
44
Q

What are penitrem A and roquefortine?

A

Mycotoxines (tremogenic)

45
Q

What is the mechanism of action of mycotoxines (tremogenic)

A

Unknown- –Likely inhibition of glycine function or release (in the CNS)

46
Q

What are the clinical signs of Mycotoxines (tremogenic)?

A
  • Hyperaesthesia, restlessness, vomiting, salivation, muscle tremors, seizures and status epilepticus (dose dependent)
  • Heat stroke!!!
47
Q

When do clinical sigs present with mycotoxines?

A

30 minutes to several hours

48
Q

How do you diagnose Mycotoxines (tremogenic) toxicity?

A
  • History
  • Mass spectroscopy
  • Chromatography
  • Culture of vomitus
49
Q

How do you manage Mycotoxines (tremogenic) exposure?

A
  • Emesis, gastric lavage, activated charcoal (for 24 hrs to reduce enteroepatice recirculation of the toxin)
  • Benzodiazepine/phenobarbital
  • General anaesthesia
  • Supportive care
50
Q

What is the prognosis of Mycotoxines (tremogenic) exposure?

A

•Generally good, improvements in 1 to 5 days

51
Q

What is Strychnine?

A

A pesticide

52
Q

What is the mechanism of action of Strychnine?

A
  • Blocks the action of glycine (inhibitory neurotransmitter)
  • Prevents the release of glycine from Renshaw cells in the spinal cord
53
Q

What is the clinical presentation of Strychnine exposure?

A
  • Quick onset 10-120 minutes from exposure (inhalation, ingestion)
  • Progressive and severe muscle spasm and extensor rigidity (saw horse and risus sardonicus), convulsions, heat stroke
  • Paralysis of diaphragm, (hypoventilation = death)
54
Q

How do you diagnose Strychnine exposure?

A
  • History
  • Analysis of gastric content
55
Q

How do you manage exposure to Strychnine?

A
  • Emesis (not recommended if the clinical signs are already present)
  • Gastric lavage under GA
  • Activated charcoal
  • Muscle spasm and convulsions must be controlled by

–Benzodiazepines

–Phenobarbital

–CRI propofol (24-72hrs)

•Mechanical ventilation may be necessary

56
Q

What is the prognosis of Strychnine exposure?

A
  • Fair to guarded
  • One of the most painful toxicities
57
Q

What is the mechanism of action of lead toxicity?

A
  • Binds to sulfhydryl groups (interferes with haem synthesis, RBC fragility, basophilic stippling)
  • Neurotoxicicty likely linked to interference with action of GABA, capillary damage, neuronal necrosis, inhibition of Ca2+, interference with dopamine uptake.
58
Q

What are the clinical signs of lead ingestion?

A

•Systemic signs

–Vomiting, anorexia, abd pain, lethargy, PU/PD

•Neuro signs

–Behavioural changes, ataxia, head pressing, blindness, tremors, polyneuropathy, seizures. (signs can be intermittent and depend on duration of exposure and amount ingested)

59
Q

How do you diagnose exposure to lead?

A
  • History
  • Presence of nucleated RBC and basophilic stippling
  • Blood and urine lead levels (>0.35ppm in blood and >0.75ppm in urine à acute toxicity)

Radiographs?

60
Q

How do you decontaminate lead exposure?

A

–Emesis

–Surgical removal of lead foreign body

–Magnesium sulphate 200-500mg/kg PO, cathartic and reduces absorption

•Chelation therapy

–Succimer 10mg/kg q8 hrs for 10 days

–Calcium EDTA 27mg/kg q6hrs SC injection has to be diluted!!!(can cause renal tubular necrosis)

–D-penicillamine 10-15mg/kg per day for 1 week

  • Seizures should be controlled with benzodiazepine
  • Mannitol can be used to reduce ICP
61
Q

What is the prognosis of lead exposure?

A

•Variable, generally good if undergoing chelating therapy

62
Q

Name 2 neuroinhibtitory toxins (2)

A
  • Macadamia nuts
  • Metronidazole
63
Q

What is the mechanism of action of Macadamia nuts toxicity?

A

Unknown

64
Q

What is the clinical presentaton when Macadamia nuts have been consumed?

A
  • 12-24hrs after ingestion
  • Pelvic limb weakness, stifness, paresis and muscle tremors
  • Vomiting and hyperthermia
65
Q

How do you diagnose Macadamia nuts consumption?

A

History

66
Q

How do you manage a dog which has consumed macadamia nuts?

A
  • Emesis (within 2-4 hrs)
  • Supportive care (fluidotherapy, antiemetics, control temperature)
  • Methocarbamol (muscle tremors)
67
Q

Where will you find Metronidazole?

A

Commonly used antibacterial and antiprotozoal antibiotic

68
Q

What is the mechanism of action of metronidazole?

A

•Mechanism of action as neurotoxin not fully understood.

–Purkinje cell loss

–Axonal degeneration in vestibular tracts

69
Q

What is the toxic dose of metronidazole?

A

60mg/kg a day

70
Q

What is the clinical presentation of a dog exposed to metronidazole?

A
  • Ataxia
  • Vestibular signs
  • Tremors
  • Seizures
  • Peripheral neuropathies
71
Q

How do you diagnose metronidzole toxicity?

A

History

72
Q

How do you manage a dog exposed to metronidazole?

A
  • Discontinuing metronidazole
  • Supportive care
  • Diazepam 0.2-0.5mg/kg PO for 3 days

Small Animal Final Year (317 decks)

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