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Y3 MOD Nutrition > SA Toxicology > Flashcards

SA Toxicology Flashcards

1
Q

What are some routes of intoxication?

A

Oral
Cutaneous/topical
Inhalation
Injection
Ocular

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2
Q

What are the first steps to take when an owner calls suggesting there has been an intoxication?

A
  • Take relevant history (What? When? Are there clinical signs?)
  • Prevent further intoxication
  • Ask them to bring a sample of the substance if available
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3
Q

What can you recommend owners to do if their pet has had a topical contamination?

A

Recommend washing:
- Water only, watch temperature
- Gloves for owner
- Do not want the toxin to become systemic through grooming

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4
Q

On admission, what are the first steps to take in stabilising a pateint?

A
  • Respiration (airway patency/normal ventilation)
  • Cardiovascular (arrhythmia, shock, severe haemorrhage)
  • CNS signs (seizures, convulsions)
  • Thermoregulation (hyper- or hypothermia)
  • Severe electrolyte or acid-base derangement
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5
Q

How should ocular contamination me managed/treated?

A
  1. Irrigate the eye(s) with saline for 20-30mins - Use tepid water if saline unavailable
  2. Treat for ulceration - Fluorescein staining should be performed after flushing and again at 12–24 hours post-exposure to assess for corneal ulceration.
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6
Q

What is the aim of treatment when a toxin has been ingested?

A

Aim: to decrease absorbed dose
- Prevent further absorption
- Increase elimination
- Bind toxin in inert form

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7
Q

Which drug is used to induce emesis in dogs?

A

Apomorphine

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8
Q

How is apomorphine administered?

A

Parenteral administration can result in protracted vomiting
- 0.04mg/kg IV (rapid onset) or IM
- 0.08mg/kg SC (slow onset)
- Reverse with naloxone as necessary (this does not stop the vomiting!)

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9
Q

Which emesis inducing drug can be used in dogs and cats?

A

Xylazine

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10
Q

How is xylazine reversed?

A

Atipamezole

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11
Q

Why drug can be used to induce emesis in just cats?

A

Dexmedetomidine

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12
Q

What must you remember to do when you have induced emesis in a toxic ingestion pateint?

A

Retain a sample of vomit

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13
Q

When is emesis induction indicated?

A

Within 3h of ingestion
- As soon as possible
- Up to 6h for aspirin and 12h for chocolate

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14
Q

When is emesis induction contraindicated?

A
  • Animal has been vomiting
  • Absent gag reflex
  • Sedation or loss of consciousness
  • Seizuring
  • Ingestion of corrosive substance or volatile petroleum based product
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15
Q

Which procedure can be performed when it is not possible to induce emesis?

A

Gastric lavage

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16
Q

Describe how gastric lavage is performed

A
  • Must have a cuffed ET tube in place
  • Lower head and neck relative to thorax
  • Use an orogastric tube
  • 5-10ml/kg of warmed water
  • Repeat 10-15 times or until lavage is clear
  • Can add activated charcoal to lavage and leave in for 10-15 minutes
  • Retain a sample of the initial lavage
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17
Q

Name an adsorbent used in toxin ingestion cases

A

Activated charcoal

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18
Q

What are the role of cathartics in toxin ingestion?

A

Enhance toxin clearance i.e. Reduce the time a toxin is exposed to the gastrointestinal tract

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19
Q

When are cathartics contraindicted?

A

If the animal has diarrhoea, is dehydrated, if ileus is present, or if intestinal obstruction or perforation are possible.

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20
Q

Name some cathartic drugs

A
  • Psyllium hydrophilic mucilloid
  • Sorbitol
  • Sodium or magnesium sulphate
  • Liquid paraffin
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21
Q

Name another method that will enhance toxin clearance

A

Diuresis

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22
Q

Describe the process of diuresis

A
  • IVFT (monitor urine output – normal 0.5-1mL/kg/hr)
  • Diuretic therapy (furosemide 1mg/kg or mannitol 0.5g/kg for oliguric or anuric AKI non-responsive to fluid replacement (ensure the animal is hydrated first!)
  • Furosemide can be used to treat hypercalcaemia secondary to cholecalciforal toxicity
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23
Q

What is one of the most important components of toxin treatment?

A

Supportive care
- Thermoregulation
- Respiratory support
- Cardiovascular support
- Analgesia
- CNS disturbances
- Nutritional support

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24
Q

At what temperature is an animal described as being hyperthermic?

A

Temperature >40.5 ACTIVE COOLING REQUIRED

25
How can a patient be actively cooled?
- Cold packs in axillae; luke warm to cool water (not cold or ice water) spray; IVFT - Cool to 39.4oC within 30-60 minutes. Cooling further/faster => shivering => heat gain => increased core temp
26
For which toxin is 100% oxygen supplementation contraindicted?
Paraquat exposure
27
Name some toxins that can cause arrythmias
Foxglove, Lily of the valley, Oleander, Rhododendron, Antidepressents
28
When is analgesia indicated for toxic pateints?
- Ingestion of a caustic substance - Use an opioid unless contraindicated - Pethidine has short duration of action - Buprenorphine – partial agonist
29
How should seizures due to a toxin be managed?
- Diazepam - 0.5-1.0mg/kg - Phenobarbital - 2-5mg/kg SLOW IV: may take 20-30min to have effect - Propofol Care if hepatic encephalopathy is suspected - diazepam/barbiturates may have profound affect and are not recommended
30
Which samples can be used to identify toxins?
- Heparinised blood - Urine - Stomach contents - Sample of product ingested if available - PM tissues: liver, kidney, brain, stomach
31
All members of which plant spp are nephrotoxic to cats?
Lilium and Hemerocallis - All parts of the plant are considered toxic (leaves, flowers, seeds, pollen, stem).
32
Describe the signs of lily toxicity
Signs of AKI occur after 24-72h: - Often present with vomiting, salivation, or neurological signs (tremors, seizures, ataxia). - Epithelial casts can be found in the urine as early as 12-18hr after ingestion. - Proteinuria and glucosuria are common.
33
When does permethrin toxicity most commonly occur?
Toxicities occurs when products “for dog use only” are used on cats
34
Describe the signs of permethrin toxicity
Excessive salivation, tremors, ataxia, depression, hyperthermia/hypothermia
35
Describe the pathophysiology of paracetamol toxicity in cats
Oxidative injury to RBCs - Methaemoglobin formation (cats) Hepatotoxic (>24 hrs after ingestion)
36
What are the clinical signs of paracetamol toxicity?
- Vomiting, abdominal pain, tachycardia, pallor, cyanosis, chocolate- coloured mucous membranes - Occasionally facial oedema in cats - Depression (within hours) - Progression to hepatic failure
37
What is the mainstay treatment for paracetamol toxicity?
N-acetylcysteine detoxifies the toxic metabolites
38
What are some other methods of treating paracetamol toxicity?
- Emesis if within 2h of ingestion - Activated charcoal (multi-dose regime) - Cathartics - Aggressive IVFT - Oxygen therapy, whole blood transfusion (cats)
39
Name the toxin usually found in antifreeze, also found in de-icer, brake and transmission fluid, motor oils, paint, ink and industrial solvents
Ethylene glycol
40
Describe the pathophysiology of ethylene glycol toxicity
- Ethylene glycol is metabolised in the liver by alcohol dehydrogenase to glycolic acid (-> Severe metabolic acidosis) and oxalic acid (most important final metabolite) - Combines with calcium in blood vessels and renal tubules => hypocalcaemia, obstructed tubules, renal epithelial damage
41
Describe the signs seen in phase 1 of ethylene glycol toxicity
30 minutes following ingestion- lasts 2-12h - Ataxia (look drunk) - Tachycardia, tachypnoea - PU/PD in dogs - PU in cats - Vomiting
42
Describe the signs seen in phase 2 of ethylene glycol toxicity
8-24h following ingestion - Metabolic acidosis - Anorexia, emesis - Depression, miosis, hypothermia - If large doses may be fatal in this phase (severe depression, tachypnoea, coma, death)
43
Describe the signs seen in phase 3 of ethylene glycol toxicity
1-3 days following exposure - Oliguric renal failure - Large painful kidneys, oral ulceration, salivation, vomiting, seizures
44
How is ethylene glycol toxicity treated?
- Management depends on the time of presentation - Animals treated in phase 1 = excellent prognosis - EG is very rapidly absorbed so gastrointestinal decontamination is unlikely to be beneficial - Supportive care
45
Which drug prevents metabolism of EG to glycolic acid by inhibiting alcohol dehydrogenase
Ethanol
46
Which drug is the treatment of choice for ethylene glycol toxicity?
Fomepizole
47
How do Anticoagulant rodenticide toxicities present?
Present as coagulopathies - very variable Onset of clinical signs 1-3 days following ingestion - usually ~48h Diagnosis based on history and coagulation screen (WBCT, ACT, PT, aPTT)
48
How are anticoagulant rodenticide toxicities treated?
Vitamin K1 orally
49
What is the main effect on the body of cholecalciferol toxicity?
Hypercalcaemia
50
Which toxin is found in slug and snail pellets?
Metaldehyde
51
What are the effects of Metaldehyde toxicity?
Acute neurotoxicity, then hepatotoxicity Hyperaesthesia, anxiety, restlessness, salivation, muscle tremors, incoordination, opisthotonus, tachycardia, seizures, coma, death
52
How do NSAIDs cause toxicity?
Inhibit prostaglandin synthesis through COX inhibition - GI effects - Nephrotoxicity
53
How is NSAID toxicity treated?
- Emesis - Gastric lavage, adsorbents, cathartics - Repeat doses of activated charcoal
54
How is GI ulceration treated?
Sucralfate
55
Name the toxin found in chocolate, tea and coffee
Methylxanthines
56
How are Methylxanthines linked to the bladder?
Methylxanthines are absorbed across the bladder wall - keep the bladder small when treating
57
How do grapes and raisins cause toxicity?
Acute kidney injury secondary to acute proximal tubular necrosis
58
What are the toxic effects of Xylitol (sweetener)?
Massive insulin release => profound hypoglycaemia Clinical signs can appear within 30min
59
What are the toxic effects of onions, garlic and leeks?
Disulfide and thiosulfates are metabolised to compounds that damage RBCs Heinz bodies, haemolysis, methaemoglobinemia

Y3 MOD Nutrition (3 decks)

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