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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
Q

How can a patient be actively cooled?

A
  • 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
Q

For which toxin is 100% oxygen supplementation contraindicted?

A

Paraquat exposure

27
Q

Name some toxins that can cause arrythmias

A

Foxglove, Lily of the valley, Oleander, Rhododendron, Antidepressents

28
Q

When is analgesia indicated for toxic pateints?

A
  • Ingestion of a caustic substance
  • Use an opioid unless contraindicated
  • Pethidine has short duration of action
  • Buprenorphine – partial agonist
29
Q

How should seizures due to a toxin be managed?

A
  • 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
Q

Which samples can be used to identify toxins?

A
  • Heparinised blood
  • Urine
  • Stomach contents
  • Sample of product ingested if available
  • PM tissues: liver, kidney, brain, stomach
31
Q

All members of which plant spp are nephrotoxic to cats?

A

Lilium and Hemerocallis
- All parts of the plant are considered toxic (leaves, flowers, seeds, pollen, stem).

32
Q

Describe the signs of lily toxicity

A

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
Q

When does permethrin toxicity most commonly occur?

A

Toxicities occurs when products “for dog use only” are used on cats

34
Q

Describe the signs of permethrin toxicity

A

Excessive salivation, tremors, ataxia, depression, hyperthermia/hypothermia

35
Q

Describe the pathophysiology of paracetamol toxicity in cats

A

Oxidative injury to RBCs - Methaemoglobin formation (cats)
Hepatotoxic (>24 hrs after ingestion)

36
Q

What are the clinical signs of paracetamol toxicity?

A
  • Vomiting, abdominal pain, tachycardia, pallor, cyanosis, chocolate- coloured mucous membranes
  • Occasionally facial oedema in cats
  • Depression (within hours)
  • Progression to hepatic failure
37
Q

What is the mainstay treatment for paracetamol toxicity?

A

N-acetylcysteine detoxifies the toxic metabolites

38
Q

What are some other methods of treating paracetamol toxicity?

A
  • Emesis if within 2h of ingestion
  • Activated charcoal (multi-dose regime)
  • Cathartics
  • Aggressive IVFT
  • Oxygen therapy, whole blood transfusion (cats)
39
Q

Name the toxin usually found in antifreeze, also found in de-icer, brake and transmission fluid, motor oils, paint, ink and industrial solvents

A

Ethylene glycol

40
Q

Describe the pathophysiology of ethylene glycol toxicity

A
  • 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
Q

Describe the signs seen in phase 1 of ethylene glycol toxicity

A

30 minutes following ingestion- lasts 2-12h
- Ataxia (look drunk)
- Tachycardia, tachypnoea
- PU/PD in dogs
- PU in cats
- Vomiting

42
Q

Describe the signs seen in phase 2 of ethylene glycol toxicity

A

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
Q

Describe the signs seen in phase 3 of ethylene glycol toxicity

A

1-3 days following exposure
- Oliguric renal failure
- Large painful kidneys, oral ulceration, salivation, vomiting, seizures

44
Q

How is ethylene glycol toxicity treated?

A
  • 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
Q

Which drug prevents metabolism of EG to glycolic acid by inhibiting alcohol dehydrogenase

A

Ethanol

46
Q

Which drug is the treatment of choice for ethylene glycol toxicity?

A

Fomepizole

47
Q

How do Anticoagulant rodenticide toxicities present?

A

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
Q

How are anticoagulant rodenticide toxicities treated?

A

Vitamin K1 orally

49
Q

What is the main effect on the body of cholecalciferol toxicity?

A

Hypercalcaemia

50
Q

Which toxin is found in slug and snail pellets?

A

Metaldehyde

51
Q

What are the effects of Metaldehyde toxicity?

A

Acute neurotoxicity, then hepatotoxicity
Hyperaesthesia, anxiety, restlessness, salivation, muscle tremors, incoordination, opisthotonus, tachycardia, seizures, coma, death

52
Q

How do NSAIDs cause toxicity?

A

Inhibit prostaglandin synthesis through COX inhibition
- GI effects
- Nephrotoxicity

53
Q

How is NSAID toxicity treated?

A
  • Emesis
  • Gastric lavage, adsorbents, cathartics
  • Repeat doses of activated charcoal
54
Q

How is GI ulceration treated?

A

Sucralfate

55
Q

Name the toxin found in chocolate, tea and coffee

A

Methylxanthines

56
Q

How are Methylxanthines linked to the bladder?

A

Methylxanthines are absorbed across the bladder wall - keep the bladder small when treating

57
Q

How do grapes and raisins cause toxicity?

A

Acute kidney injury secondary to acute proximal tubular necrosis

58
Q

What are the toxic effects of Xylitol (sweetener)?

A

Massive insulin release => profound hypoglycaemia
Clinical signs can appear within 30min

59
Q

What are the toxic effects of onions, garlic and leeks?

A

Disulfide and thiosulfates are metabolised to compounds that damage RBCs
Heinz bodies, haemolysis, methaemoglobinemia

Y3 MOD Nutrition (3 decks)

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