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SAM module B Critical Care > Toxicology > Flashcards

Toxicology Flashcards

1
Q

What would generally be considered a minimum database?

A 
PCV/ TS
BG
BP
Lytes
Urea/ Crea
ECG
Lactate
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2
Q

How can you decontaminate the skin?

A

e.g. pyrethrins/ organophosphates
luke warm water, soapy detergent, wear gloves
If in petrol/ diesel - then use vegetable or mineral oil first

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3
Q

How long after ingestion of a substance can you induce emesis?

A

Normally up to 4 hours
EG - only an hour
Chocolate and neurotoxins can sit in the stomach - up to 8 hours

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4
Q

What are the contraindications for inducing v+?

A

Neuro signs
Already v+
Caustic
Bread dough

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5
Q

How can you do gastric lavage?

A 
GA - so can do on neuro patient
Ensure enflated ET tube
Lubricated stomach tube
Do in cycles of 30-40ml/kg
Keep doing it until the fluid runs clear
Remove the tube partially inflated
kink the stomach tube to prevent leakage when removing
Wash out the mouth
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6
Q

What is the use of charcoal?

A

Adsorbs to toxins to prevent absorption
Normally 1-2 doses, but do repeated dosages if there is enterohepatic circulation (e.g. NSAIDs/ ivermectins)
DO NOT GIVE WITH FOOD

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7
Q

What is theobromide?

A

A type of methylxanthine (like caffiene and theophylline)
Causes CNS stimulation
and cardiac and skeletal muscle stimulation by inhibiting Ca recycling
Both dogs and cats affected

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8
Q

What are the clinical signs of theobromide toxicity?

A 
Hyperactivity/ hyperreflexia
U+ incontinence from diuresis
V+/D+
Muscle twitching/ seizures
tachycardia/ tachy arrhythmia
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9
Q

How can you manage a theobromide toxicity?

A 
Decontaminate and activated charcoal if able 
Anti epileptic drugs
Anti arrhythmics (B blockers/ Ca channel blockers) - only give these if volume resuscitated first
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10
Q

How can grapes cause toxicity?

A

Mechanism unknown

Any grape product - juice/ raisins/ wine etc

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11
Q

What does lily toxicity cause?

A

Mechanism unknown but causes renal tubular death

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12
Q

How do you manage lily or grape toxicity?

A

If recent - decontaminate, activated charcoal, IV fluids for 24 hours, baseline urea creatinine and lytes
Monitor - weight, u+ output, bloods @ 24 hours

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13
Q

What would be the signs of a lily or grape toxicity developing?

A

Increase in weight/ decrease in urinary output
Increased urea/ crea
Granular casts in u+ microscopy

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14
Q

How should you treat a lily or grape toxicity that has clinical signs on presentation?

A

Fluids - balance lyte solution (CSL good to balance acid/ base)
Maintain BP and renal perfusion
Prevent further 2ndary injury
Correct pre existing lyte imbalance (e.g. low Cl from v+, low Ca from acidosis)
Encourage diuresis (fluids/ frusemide)

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15
Q

What is the use of frusemide for inducing diuresis?

A 
Na/K/Cl2 pump inhibitor
Acts on ascending loop of henle
4mg/kg IV bolus
Followed by 2mg/kg every 4-6 hours 
Little proven efficacy in anuric/ oliguric patients
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16
Q

What is the only real effective treatment for anuria/ oliguria?

A

Dialysis

not a specific treatment but buys the kidney time to recover

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17
Q

How often should you monitor bloods on AKI patients

A

Normally every 6-12 hours for lytes
24 hours urea and crea - expect these to get worse for at least the first 2 days, then plateau
numbers are not related to prognosis
Lower UO is what is related to prognosis

N.B takes 6 weeks to know prognosis, unlikely to get CKD

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18
Q

What is toxic with ethylene glycol?

A

Metabolites - the worst are glyco-aldehyde and glycolic acid

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19
Q

What are the stages of ethylene glycol toxicity?

A

One - 2-12 hours after
sweeth breath, drunk, V+

Two - 6-24 hours
Show neuro signs

Three - 24-48 hours after
AKI

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20
Q

What can help dx ethylene glycol toxicity

A

Clinical signs
Severe acute azotaemia
There are test kits available
Ca oxalate monohydrate crystals in large numbers
On U/S - kidney halo - bilateral hyperechoic corticomedullary junction
High Anion gap

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21
Q

How do you treat EG toxicity when no clinical signs are yet noted

A

Emesis within an hour - one of the few indicatons of at home emesis
Prevent EG metabolism - competitively inhibit alcohol dehydrogenase enzyme
Ethanol given IV then a CRI - give for 12 hours if a test is -ve
48 hours if no signs of azotaemia
Best treatment would still be dialysis as it removes it from the body

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22
Q

How does metaldehyde cause issues

A

Metabolised to acetylaldehyde
Decreases GABA, nor adrenaline and 5 HT activity
Therefore lack of CNS inhibition

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23
Q

What are the signs of metaldehyde toxicity?

A

Restlessness, anxiety, p+
Ataxia, ptyalism, muscle fasciculations
Seizures, hyperthermia, coma, death

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24
Q

How can you Dx metaldehyde toxicity?

A

Acute onset progressive seizures
Possible exposure
green v+/ f+
Rule out other causes (low Ca or BG)

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25
Q

How do you treat an acute metaldehyde with no clinical signs?

A

Emesis

Gastric and colonic lavage

26
Q

How do you treat a metaldehyde toxicity with clinical signs?

A

Control seizures with standard drugs
CV support - IV fluids to maintain BP and volume status
Kidney support - fluids to prevent myoglobin induced AKI
Do gastric and colonic lavage
If needed propofol, maintain for at least 12 hours before trying to turn off.
Monitor GA as you would for any other (ECG, capnograph, BP
Continue phenobarb 2mg/kg BID for 3-5 days
minimum database at 0, 24, 48 hours
Survival >80%, poorer prognosis if AKI or DIC

27
Q

How do rodenticides cause issues?

A

Interfere with the vitamin K cycle - this is needed for factors VII, IX, X
Takes at least 48 hours before you start seeing signs

28
Q

How do you treat an asymtomatic rodenticide poisoning?

A

Induce emesis and provide charcoal
Do not give vit K
check PT 48 hours after ingestion

29
Q

How do you treat a rodenticide poisoing with a coagulopathy?

A

FFP -20 ml/kg over 4 hours
Vit K s/c then move to oral
check PT again 48 hours after finished meds

30
Q

How do anticoagulants exert their effects?

A

The anticoagulants inhibit vitamin K1 epoxide reductase

Takes at least 2-3 days to start showing signs of haemorrhage

31
Q

What are the most common signs of rodenticide toxicity?

A

dyspnea, coughing, lethargy, and hemoptysis.
Bleeding into body cavities such as the chest, abdomen, and joints is also common. Many patients present with vague clinical signs of lethargy, weakness, and anemia without any overt external hemorrhage
Bleeding into the brain or spinal cord may result in severe central nervous system (CNS) disturbances, seizing, paresis, paralysis, or acute death.3 Tracheal constriction caused by thymic, peritracheal, or laryngeal bleeding may result in severe dyspnea

32
Q

Which clotting time goes up with rodenticide poisoning fastest and why/ how?

A

Because it has the shortest half-life, factor VII is the first to be affected. Depletion of factor VII leads to an increase of the PT.
Levels of PIVKA, the collective term for the precursors of the vitamin K–dependent clotting factors, also become increased.
The PT may be increased within 36 to 72 hours. Beyond 72 hours, as other factors become depleted, increases in activated partial thromboplastin time and activated clotting time develop

33
Q

Which blood abnormalities occur with rodenticide toxicity and why?

A

anemia, thrombocytopenia, hypoproteinemia, and decreases in CO2 and Po2

34
Q

How long should vitamin K therapy be given if the generation of anticoagulant is unknown?

A

4 weeks

If possible, avoid the use of other highly protein-bound drugs (corticosteroids, nonsteroidal antiinflammatory drugs, and so forth) during the treatment, and instruct the owner to restrict exercise during this time

35
Q

Which toxins cause CNS signs (excitation/ seizures)?

A

Metaldehyde (hyperthermia, tremors)
Amphetamines or cocaine (ingestion in dogs: sympathomimetic effects and hyperthermia)
Tremorgenic mycotoxins (Penitrem A, roquefortine) from eating moldy foods (GI signs, hyperthermia, and tremors)
Cold medications: pseudoephedrine, ephedrine, some antihistamines (sympathomimetic effects, hyperthermia)
Organophosphate or carbamate pesticides (cholinergic crisis; SLUD signs)
Pyrethrin/pyrethroid-type pesticides (especially permethrin in cats: tremors, shaking, ataxia, seizures, GI signs)
Organochlorine pesticides (tremors, shaking, ataxia, seizures)
Chocolate: caffeine, theobromine, methylxanthines (polydipsia, polyuria, GI and CV effects)
Zinc phosphide: mole or gopher baits (GI signs, shaking, dyspnea due to pulmonary edema)
Bromethalin toxicosis: rat or mouse bait (paresis, weakness, ataxia, tremor)
Lead (GI signs, hematologic abnormalities [nucleated RBCs, basophilic stippling, anemia])
Metronidazole toxicosis (in dogs with repeated use and/or high dosage: nystagmus, ataxia, weakness, paresis, seizures)
Nicotine: tobacco or cigarettes (ingestion in dogs: spontaneous vomiting, tremors, CV effects)
Tricyclic antidepressant toxicosis: amitriptyline, clomipramine, imipramine, nortriptyline (agitation, nervousness, ataxia, CV effects)

36
Q

Which toxins can cause CNS signs (depression/ seizures)

A

Ivermectin, moxidectin, and other avermectin toxicosis (ataxia, weakness, depression, tremors, seizures, blindness)
Marijuana ingestion (ataxia, hypothermia, urinary incontinence)
Benzodiazepines ingestion: alprazolam, clonazepam, diazepam, lorazepam (hyporeflexia, ataxia, CNS excitation: paradoxical reaction)
Barbiturate overdose: short acting or long acting (coma, hypothermia, weakness, ataxia)
Ethylene glycol (ataxia, disorientation, GI signs)
Methanol or ethanol ingestion (GI signs, ataxia, weakness, depression)
Propylene glycol: antifreeze (depression, ataxia, GI signs)
Baclofen or other centrally acting muscle relaxant ingestion in dogs (vocalization, ataxia, disorientation, coma, hypothermia)
Amitraz insecticide exposure (depression, ataxia, CV effects, paralytic ileus)

37
Q

Which toxins can cause muscle weakness, paresis, paralysis

A

herbicides (dogs: ataxia, weakness, GI signs)
Metronidazole (see Seizures, above)
Bromethalin rodenticide
Coral snake envenomation (cats: local swelling, pain, puncture wound)
Macadamia nuts ingestion in dogs (weakness, ataxia)
Concentrated tea tree oil exposure: Melaleuca oil (cats and dogs: weakness, ataxia, CNS depression)

38
Q

Which toxins can cause acute blindness?

A

Lead
Ivermectin, moxidectin, and other avermectin toxicosis;
Salt poisoning (in dogs: polydipsia, GI signs, tremors, ataxia, seizures, serum sodium >160 mEq/L is strongly supportive)

39
Q

Which toxins can cause AKI?

A

Grapes and raisins ingestion in dogs (initial GI signs, then azotemia in >24 h, possible pancreatitis)
NSAIDs: ibuprofen, naproxen, nabumetone, piroxicam, carprofen, diclofenac, ketoprofen, indomethacin, ketorolac, oxaprozin, etodolac, flurbiprofen, sulindac (initially GI signs, azotemia in 24–74 h after acute ingestions)
Zinc toxicosis
Ethylene glycol toxicosis (ataxia, altered mentation/depression, GI signs, urine may fluoresce with Wood’s lamp; azotemia, calcium oxalate monohydrate crystalluria appear after kidney injury has occurred)
Lillies (ingestion in cats: initially GI signs, azotemia in generally 24–72 h after ingestion)
Cholecalciferol rodenticide and other vitamin D3 analogs: calcipotriene, calcitriol (initial GI signs, then CV, CNS signs; azotemia; hypercalcemia with hyperphosphatemia differentiates from hypercalcemia of malignancy or hyperparathyroidism)

40
Q

Which toxins can cause acute hepatic damage?

A

Mushrooms: amanita type (delayed onset GI signs [12 hours after ingestion], acute liver injury in 1–3 days)
Blue-green algae: Microcystis sp (exposure to stagnant body of water; acute onset GI signs, hypovolemic shock, acute liver injury in 1–2 days)
Iron: multivitamin ingestion (GI signs, hypovolemic shock, acute liver injury in 1–2 days)
Acetaminophen toxicosis (methemoglobinemia within a few hours, GI signs, increased liver enzymes in 1–3 d)
Aflatoxicosis (dogs: mostly from contaminated dog food, several outbreaks reported in the United States)
Copper storage (breed: bedlington Terrier, others)
Xylitol (see Hypoglycemia)
Other drugs (carprofen: GI signs, increased ALT days after starting treatment; cortidosteroids: steroid hepatopathy after weeks/months of use; phenobarbital: chronic hepatopathy after months of use)

41
Q

Which toxins can cause the presence of oral burns/ ulcers

A

Acid ingestion (corrosive lesions on lips, gums, tongue, salivation, vomiting, fever)
Alkali ingestion (same as with acid, esophageal perforation more likely)
Cationic detergents: present in several disinfectants (oral burns, salivation, vomiting, fever)
Alkaline battery chewing/ingestion (oral burns, salivation, vomiting)
Potpourri ingestion (cats > dogs: oral burns, salivation, vomiting, tongue protrusion, fever)
Bleaches: sodium or calcium hypochlorite (bleach-like smell, salivation, vomiting, wheezing, gagging)
Ingestion of phenolic compounds (especially in cats: oral ulcers/lesion may be present; Heinz body anemia and hemolysis may be seen)

42
Q

What are the ddx for oral ulcers other than toxins?

A

Uremic stomatitis (uremic halitosis, azotemia, GI signs)
Periodontal disease (associated with dental calculus; gingival lesions)
Trauma (presence of foreign body, recent tooth fracture)
Electrical cord chewing (sharply demarcated ulcers, dyspnea due to noncardiogenic pulmonary edema)
Systemic lupus erythematosus and other autoimmune diseases (lesions are characteristically at the mucocutaneous junction; joint pain, other systemic signs can be present)
Infectious (feline calcivirus infection, FeLV, FIV, nocardiasis, ulcerative necrotizing stomatitis, Fusobacterium spp. infection; identify other characteristic features of individual diseases)

43
Q

Which toxins can cause acute blood loss/ anaemia/ or methaeglobinuria?

A

Acetaminophen (chocolate-brown colored mucous membrane within hours, dyspnea)
Naphthalene mothball ingestion (moth ball-like odor in the breath, hemolysis)
Onions and garlic toxicosis (hemolysis in 2–3 d, anemia, coffee-color urine)
Zinc toxicosis (metallic object in the GI tract, gastritis, pancreatitis, hemolysis, hemoglobinuria)
Iron (see Acute Hepatic Injury)
Anticoagulant rodenticides: brodifacoum, bromadiolone, chlorophacinone, difethialone, diphacinone, pindone, warfarin (lethargy, dyspnea due to pulmoney hemorrhage, persistent bleeding at venipuncture site; increased PT +/− aPTT)
Rattlesnake envenomation (swelling, pain, +/− fang puncture marks in skin; endemic region)
Other Drugs (local anesthetic toxicosis [lidocaine, benzocaine, tetracaine, dibucaine]: methemoglobinemia, CV and CNS effects; phenazopyridine and other azo dyes toxicosis [methemoglobinemia, hemoglobinuria])

44
Q

Which toxins can cause cardiac arrhythmias?

A

Foxglove: Digitalis sp (plant ingestion: GI signs, ventricular and/or supraventricular arrhythmias)
Lily of the valley: Convallaria majalis (plant ingestion, GI signs, ventricular and/or supraventricular arrhythmias)
Oleander: Nerium oleander (GI signs, ventricular and/or supraventricular arrhythmias)
Bufo toads: Bufo sp (endemic region; GI signs, collapse, seizures, sinus tachycardia, ventricular arrhythmias)
Azalea and other Rhododendron plants (GI signs and possible cardiac arrhythmias)
Antidepressant toxicosis: (CNS signs, anticholinergic effects)

45
Q

What are the ddx for cardiac arrhythmias aside from toxins?

A

Automobile trauma (evidence of other injuries)
Gastric dilation and volvulus (abdominal distention, dyspnea, shock; radiographs confirmatory)
Severe anemia (due to any cause)
Severe hypokalemia (due to any cause)
Acidosis (due to any cause)
Hypoxia (due to any cause)
Primary heart disease (cardiomyopathy, valvular heart disease, congenital heart problems, heartworm infestation: heart murmur, cardiomegaly, or evidence of congestive heart failure)

46
Q

Which toxins can cause dyspnoea?

A

Petroleum distillates: kerosene, gasoline, and other hydrocarbons (hydrocarbon smell in the breath, salivation, vomiting, CNS depression, diarrhea, aspiration)
Zinc phosphide (exposure to gopher bait or similar; GI and CNS signs, dyspnea due to noncardiogenic pulmonary edema)
Smoke inhalation (dyspnea, collapse, panting, shock; smell of smoke on fur in virtually every case)
Organophosphate or carbamate pesticides (cholinergic crisis, SLUD signs)
Paraquat herbicide (rare; progressive dyspnea, panting, delayed onset after exposure)
Cardiogenic (multiple causes of left-sided congestive heart failure)
Noncardiogenic (seizures, head trauma, electrical shock, drowning and near-drowning)
Some organic arsenicals (mainly injectable, melarsamine)
Calcium channel blockers toxicosis, see cardiac abnormalities (noncardiogenic pulmonary edema along with cardiac signs

47
Q

Which toxins can cause GI signs?

A

Garbage poisoning (vomiting, diarrhea, dehydration, abdominal pain)
Chocolate toxicosis (initial stages: polydipsia, polyuria, vomiting, hyperactivity, tachycardia)
Fertilizer ingestion (NPK: vomiting, diarrhea, polydipsia)
NSAID toxicosis (initial stages: GI signs with or without blood in vomitus, diarrhea)
Endotoxins and enterotoxins: staphylococcal, clostridial, Escherichia coli, salmonella (severe GI signs, progressive lethargy, dehydration, hypothermia)
Zinc oxide (diaper rash ointment ingestion in dogs; mild to severe gastritis)
Iron Toxicosis
Aresnical herbicides (initial stages: vomiting, abdominal pain, watery diarrhea)
Caster beans: (initial GI signs within several hours)
Insoluble calcium oxalate containing plants: elephants ear (Caladium sp.), dumb cane (Dieffenbachia sp.), philodendron (Philodendron sp.), peace lily (Spathiphyllum sp.) (vomiting, diarrhea, oral swelling, salivation)
Zinc phosphide (GI and CNS signs, pulmonary edema; liver and kidney damage possible)

48
Q

Which toxins can cause salt poisoning?

A 
Paint ball ingestion (dogs: history of paintball ingestion, polydipsia, vomiting, diarrhea, ataxia)
Salt toxicosis (history of inducing emesis with sodium chloride, ingestion of excessive amounts of salt-containing objects [play dough/plasticine] and foods)
Activated charcoal administration (can occur sporadically in some dogs, possibly due to fluid shift)
Seawater ingestion (history of visit to a beach, lack of access to fresh water, swimming)
49
Q

Which toxins can cause hypoglycaemia?

A

Ingestion of xylitol-containing products (dogs; sugar-free gum, sugar-free bakery products, etc.; hypoglycemia within 12 hours; seizures, acute hepatic damage and coagulopathy in 1–3 days)
Ingestion of oral diabetic/hypoglycemic agents (sulfonylureas)

50
Q

What the the ddx for hypoglycaemia, not including toxins

A

Insulinoma
Acute hepatic disease, portosystemic shunt
Functional hypoglycemia (idiopathic in neonates, insufficient caloric intake in young puppies and kittens, severe exercise)
Intestinal parasitism
Hypoadrenocorticism
Leiomyosarcoma/smooth muscle tumor
Endotoxemia

51
Q

What are the main indications for IV lipid emulsion treatment?

A

amlodipine, amphetamines, baclofen, diltiazem, lamotrigine, local anesthetics, loperamide, macrocyclic lactones (eg, ivermectin, moxidectin), marijuana, minoxidil, permethrin, phenobarbital, Pieris japonica, synthetic cannabinoids, and tremorgenic mycotoxins

High recommended for cats with lidocaine toxicosis, comatosed weed patients, permethrin if standard treatment fails

52
Q

What are the reported adverse events of lipid emulsions?

A

Pancreatitis, pain if extravated, hyperlipidaemia, hypersensitivity reactions
Can affect blood results so take blood first

53
Q

What are the main results of NSAID toxicity?

A

result from gastric irritation and ulceration, and include vomiting (sometimes bloody), anorexia, diarrhoea, melaena, abdominal pain or colic; gastric perforation may occur
Also renal dysfunction

54
Q

What are the signs of paracetamol toxicity in the dog?

A

nausea, vomiting, anorexia, abdominal pain, tachypnoea, tachycardia, jaundice and death (Sellon, 2006). Methaemoglobinaemia is also observed in dogs following high doses of paracetamol (>200 mg/kg) and is more likely to cause death than liver failure

55
Q

What are the signs of paracetamol toxicity in the cat?

A

depression, vomiting, hypothermia, respiratory distress, cyanosis and oedema of the face and paws. Haemolysis, anaemia, icterus and pigmenturia
Methaemoglobinuria.
More RBC injury than hepatic but can get that too, more in males

56
Q

How do you treat paracetemol toxicity?

A

supportive care and specific antidotal therapy including N-acetylcysteine, ascorbic acid and cimetidine

57
Q

What are the signs of antihistamine toxicity?

A

usually evident within 30 min
Signs of CNS depression are common, sometimes leading to coma and fatal respiratory depression. Higher doses of antihistamine can have CNS stimulatory effects, particularly in young animals. Anticholinergic signs, such as dry mucous membranes, dilated pupils and tachycardia, along with vomiting and diarrhoea, are possible

58
Q

How does amanita mushroom poisoning develop?

A

The initial phase is a latency period of approximately 6 to 12 hours, during which no clinical signs of illness occur after the ingestion.11 During the second phase, poisoned animals develop GI signs (vomiting, diarrhea, evidence of abdominal pain, lethargy, anorexia) between 6 and 24 hours after ingestion. After a period of false recovery of 12 to 24 hours, which signifies the third phase of poisoning, fulminant liver failure develops. During this third phase, close monitoring of liver and kidney function is essential to prevent misdiagnosis. After the GI phase, severe hypoglycemia as a result of the breakdown of liver glycogen can occur
The fourth and final phase begins 36 to 48 hours after exposure and is characterized by fulminant hepatic failure with subsequent coagulation disorders, encephalopathy, and renal failure

59
Q

How can you diagnose amanita mushroom toxicity?

A

Test for amanitim in urine or serum

60
Q

How do you treat amanita mushroom toxicity?

A

Charcoal if has eaten it within the last 24 hours
Mostly supportive
Dextrose, vitamin K1, blood products, and intravenous (IV) fluids must be considered as beneficial therapeutic agents for case management.
Silybin IV
SAM-e
Control nausea/ any pain

SAM module B Critical Care (9 decks)

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