Tox-1 Flashcards

1
Q

Xenobiotic

A

Foreign substance

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2
Q

Antidote

A

Any substance that prevents/relieves the effects of a toxicant (no antidote works on all toxicants)

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3
Q

NOAEL

A

No Observed Adverse Effect Level; the highest experimental point that is without adverse effect

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4
Q

LOAEL

A

Lowest Observed Adverse Effect Level; the lowest concentration or amount of a substance that causes an adverse effect experimentally

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5
Q

Additive

A

The sum of the effects of the chemicals involved in the reaction

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6
Q

Antagonistic

A

When the net effect of the chemical reaction is zero (antidotes for poisons)

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7
Q

Synergism

A

When the sum of the effects is more than each chemical individually

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8
Q

Cats are deficient in this type of metabolism

A

Glucuronidation

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9
Q

Dogs are deficient in this type of metabolism

A

Acetylation

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10
Q

Pigs are deficient in this type of metabolism

A

Sulfation

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11
Q

Bioactivation

A

When metabolism increases the toxicity of a compound

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12
Q

These three conditions make patients candidates for intubation

A

Unconscious, paralyzed, and severe respiratory distress

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13
Q

Ventilation may be needed if there is…

A

Hypoventilation and hypercapnia, metabolic acidosis, or hypoxia

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14
Q

At what concentration of oxygen do you treat hypoxia?

A

40%

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15
Q

What are three cardiovascular signs of toxicity?

A

Tachycardia, arrhythmias, and hypertension

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16
Q

What two drugs were mentioned that can be used to treat toxicity-associated tachycardia and arrhythmias?

A

Lidocaine and propranolol

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17
Q

What two drugs were mentioned that can be used to treat toxicity-associated hypertension?

A

Nitroprusside and Hydralazine

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18
Q

What are two CNS signs of toxicity?

A

Hyperactivity (seizures) and depression

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19
Q

What three drugs were mentioned that can be used to treat toxicity-associated CNS hyperactivity (seizures)?

A

Diazepam (GABA modulator), Phenobarbital, and Methocarbamol

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20
Q

What drug was mentioned that can be used to treat toxicity-associated CNS depression (decreased respiratory rate)?

A

Doxapram

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21
Q

What are the four major themes of the complete history for a patient presenting with a potential toxicity?

A

Health history, current clinical, environment, diet

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22
Q

What are the two most common methods of GI decontamination?

A

Emesis and activated charcoal

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23
Q

What is the goal of inducing emesis after a suspected toxic exposure?

A

Prevent toxicant absorption

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24
Q

Within how much time is inducing emesis successful in preventing toxicant absorption?

A

60 minutes

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25
Q

What are the contraindications of inducing emesis?

A

Too long, chronic exposure, caustic material, recent gastric sx, some species, oils/gasoline

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26
Q

What is the rule of thumb for when to induce emesis?

A

Toxic dose of the substance was ingested, no vomiting has yet occurred, and activated charcoal is not an option

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27
Q

What is the goal of using activated charcoal after a suspected toxic exposure?

A

Prevent toxicant absorption

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28
Q

What are the contraindications of activated charcoal?

A

Corrosive agents (acids, alkaloids), oil/gas, cyanide, obstructed airway/altered state, ruptured intestinal wall, chronic exposures

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29
Q

What is the rule of thumb for when to use activated charcoal?

A

Substance is known/thought to be adsorbed by it, ingestion was very recent/undergoes enterohepatic circulation/is sustained released, can tolerate it, and there is no immediate need to administer oral meds

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30
Q

What substances are not adsorbed by activated charcoal?

A

Acids, alkalis, alcohols/glycols, metals, oils, petroleum distillates, detergents

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31
Q

What is the goal of administering cathartics after a suspected toxic ingestion?

A

Facilitate toxicant removal

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32
Q

What are examples of cathartics?

A

Mineral oil, saline cathartics (milk of magnesia)

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33
Q

For corrosives, strong acids or bases, use ___ instead of emesis

A

Dilution with milk, water, or eggs

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34
Q

Lipid infusion is a relatively new treatment and is specifically used in _____ toxicosis

A

Ivermectin

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35
Q

What are the common names of organophosphate pesticides?

A

Parathion, malathion, chlorpyrifos

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36
Q

What is the mechanism of activity of organophosphate pesticides?

A

Irreversible inhibition of acetylcholine esterase (AChE) activity (anticholinesterase)

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37
Q

What are the clinical signs of organophosphate pesticide toxicity?

A

Muscarinic (SLUDGE-M), nicotinic (muscle fasciculations beginning with the face, generalized tremors, weakness, paralysis), CNS (depression, ataxia, nervousness, seizures)

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38
Q

How do you diagnose organophosphate pesticide toxicity?

A

Atropine challenge

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39
Q

If you observe dry mouth, mydriasis, and increased heart rate after an atropine challenge during a suspected organophosphate pesticide toxicity, what do you conclude?

A

Toxicity is NOT due to AChE (not OP toxicity)

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40
Q

What drugs can you use to treat organophosphate pesticide toxicity?

A

Oximes (protopam, 2-PAM) - reactivates AChE unless it has been too long since the ingestion; diazepam or barbiturates for seizures, GI decontamination, Atropine sulfate for muscarinic signs

41
Q

What syndrome is characterized by axonal degeneration of long motor neurons (hindlimb weakness, paralysis)?

A

OPIDN: Organophosphate-Induced Delayed Neurotoxicity

42
Q

What breeds are the most susceptible to Ivermectin toxicosis?

A

Border collies, australian shepherds, and shelties

43
Q

Why are certain breeds susceptible to Ivermectin toxicosis?

A

Blood Brain Barrier

44
Q

What is the mechanism of action of Ivermectin?

A

GABA receptor agonist

45
Q

Is the half-life of Ivermectin short or long?

A

Long (2-3 days); can see cumulative toxicity with repeat doses

46
Q

What are the clinical signs associated with an Ivermectin toxicosis?

A

Increased inhibition! Ataxia, lethargy, mydriasis, coma, blindness, bradycardia; recumbency, disorientation, and seizures in collies; respiratory distress; anaphylactic reactions

47
Q

How do you diagnosis Ivermectin toxicity>

A

History of administration

48
Q

What organ systems can one use to diagnose Ivermectin toxicity?

A

Brain, GI content, liver, fat, and feces (no visible lesions, no diagnostic blood work)

49
Q

What is the appropriate treatment plan for Ivermectin toxicosis?

A

GI decontamination for recent exposures (multiple doses of activated charcoal), supportive care (fluid and lyte therapy, epinephrine, short acting barbiturates)

50
Q

What is the prognosis for non-susceptible breeds of dogs if exposed to <5 mg/kg of Ivermectin?

A

Good

51
Q

What is the prognosis for any breed at dosages > 5 mg/kg of Ivermectin?

A

Guarded

52
Q

What is the cardinal rule of pyrethroid pesticides?

A

DO NOT USE ON CATS

53
Q

What is the mechanism of action of pyrethroid pesticides?

A

Binds voltage-gated sodium channel (causes hyperactivity)

54
Q

What makes pyrethroid pesticides so toxic in cats?

A

Cats are not efficient at glucuronide conjugation

55
Q

What are the clinical signs of pyrethroid pesticide toxicity?

A

In cats: drooling, paresthesia , muscle tremors and seizures, excessive muscle activity, and hyperthermia

56
Q

How do you diagnose pyrethroid pesticide toxicity?

A

Difficult! Clinical values normal, nonspecific lesions, history of exposure, chemical analysis for pyrethrum/pyrethroid

57
Q

What drug can be used to control the muscle tremors associated with pyrethroid pesticide toxicity?

A

Methocarbamol

58
Q

What is the treatment plan for pyrethroid pesticide toxicity?

A

Stabilize tremors/seizures, bathe multiple times, IV fluids

59
Q

What is the mechanism of action of bromethalin?

A

Damages mitochondrial function (uncouple oxidative phosphorylation in CNS -> loss of ion gradient -> fluid accumulation in myelin sheaths -> decreased nerve conduction and respiratory arrest)

60
Q

What are the clinical signs of bromethalin toxicity?

A

Ataxia, hindlimb paralysis, hyper-excitability, severe muscle tremors, running fits, grand mal seizures

61
Q

How do you diagnose bromethalin toxicity?

A

Cerebral edema and cerebellar degeneration; histological evidence of neuronal vacuolization and edema

62
Q

How do you treat bromethalin toxicity?

A

Emesis (if recent exposure), repeated administration of activated charcoal, furosemide, treat seizures

63
Q

What is the primary cause of pharmaceutical toxicosis?

A

Careless storage

64
Q

What is the mechanism of action of Alprazolam (Xanax)?

A

GABAa receptor modulator that acts at the limbic, thalamic, and hypothalamic level of the CNS

65
Q

What are the clinical signs of an Alprazolam toxicity?

A

Ataxia, depression, vomiting, tremors, tachycardia, diarrhea, and ptyalism (Depressive effect); some may initially show excitation at a high dose

66
Q

What drug can be used as an antidote to Alprazolam toxicity?

A

Flumazenil (GABAa antagonist)

67
Q

Can you use GI decontamination with Alprazolam toxicity?

A

Yes; emesis if recent, activated charcoal if toxic dose ingested

68
Q

What is the mechanism of action of Zolpidem (Ambien)?

A

Inhibits neuronal excitation by binding to the benzodiazepine site of GABA receptors

69
Q

What are the clinical signs of Zolpidem toxicity?

A

Ataxia, vomiting, lethargy, disorientation, hyper-salivation, hyperactivity, and panting

70
Q

What is the recommended treatment for a pet showing mild signs of Zolpidem toxicity?

A

Keep quiet in a safe place; CS typically resolve in 12 hours

71
Q

What mycotoxin is regularly screened for in peanut butter and is linked to liver cancer?

A

Aflatoxin

72
Q

What mycotoxin is produced by “black patch” fungus on red clover?

A

Slaframine

73
Q

What is the mechanism of action of slaframine?

A

Muscarinic cholinergic agonist (ACh mimic), especially in exocrine glands

74
Q

What is the hallmark clinical sign in horses with slaframine toxicity?

A

the “slobbers”

75
Q

What other toxicities do you have to differentiate between when there is a suspected slaframine toxicity?

A

OPs, botulism

76
Q

How do you treat a slaframine toxicity?

A

Remove source, maintain hydration and lytes, Atropine if severe CSs

77
Q

What mycotoxin is a metabolite of Fusarium spp?

A

Fumonisin

78
Q

What mycotoxin is found almost exclusively on corn?

A

Fumonisin

79
Q

What is the mechanism of action of fumonisin?

A

Inhibits sphingosine-N-acetyltransferase causing increased levels of sphinganine which is cytotoxic

80
Q

What are two diseases linked to fumonisin toxicity?

A

Porcine pulmonary edema and equine leukoencephalomalacia (ELEM)

81
Q

What are the clinical signs of porcine pulmonary edema caused by fumonisin toxicity?

A

Inactivity, increased respiratory rate, decreased heart rate -> respiratory distress

82
Q

What are the two main target organs affected in equine leukoencephalomalacia (ELEM) caused by fumonisin toxicity?

A

Brain and liver

83
Q

During necrosis of a horse that died of ELEM caused by fumonisin toxicity, what would you find?

A

CNS necrosis and liquefaction

84
Q

What is the treatment of choice for fumonisin toxicity?

A

None available (isolate, change feed, ultrasorb S?)

85
Q

What syndrome is associated with ammoniated feed toxicosis in cows?

A

“Bovine bonkers”

86
Q

What is the hallmark sign of ammoniated feed toxicosis in cows caused by imidazoles?

A

Alternating between hyperexcitability and “normal” behavior

87
Q

Ammonia is at what level in blood when death occurs in cows?

A

> 2 mg/dL

88
Q

What are the specific clinical signs of ammoniated feed toxicosis?

A

Hyperexcitability: nervousness, rapid blinking, dilated pupils, trembling, ataxia, rapid respiration, SLUD, tonic convulsions induced by stimuli

89
Q

What other differentials must you consider in a suspected ammoniated feed toxicosis?

A

OPs, cyanide, grain overload, meningitis, and encephalitis

90
Q

What is the treatment for imidazole toxicosis?

A

No treatment, just feed removal (sedation PRN, milking out); prognosis good

91
Q

What is the treatment for NPN overdose toxicosis?

A

No specific treatment; cold water + vinegar by stomach tube? Time; prognosis poor for recumbent animals

92
Q

What is the mechanism of action of strychnine?

A

Competitive antagonist at postsynaptic spinal cord and medulla glycine receptors; glycine is an inhibitor transmitter, therefore evokes an overstimulation

93
Q

What are the clinical signs of strychnine toxicity?

A

Anxiety, restlessness, stiff neck and gait, “grinning” as facial muscles stiffen, ears twitch, proceeds to violent seizures and respiratory distress, sawhorse stance; death from respiratory failure (asphyxiation during seizures), exhaustion

94
Q

What PE and lab findings are typical in strychnine toxicosis?

A

Hyperthermia, elevated CPK and LDH, lactic acidosis, hyperkalemia, and leukocytosis

95
Q

How do you treat strychnine toxicity?

A

Aggressive decontamination, control seizures (phenobarb or methocarbamol), ion trapping with ammonium chloride if not acidotic

96
Q

What is the most common cause of salt toxicity?

A

Water deprivation

97
Q

What is the mechanism of salt toxicity?

A

Diffusion of sodium into CSF when plasma Na levels are high leading to inhibition of glycolysis and ATP and attraction of water

98
Q

What are the clinical signs of salt toxicity?

A

Salivation, increased thirst, abdominal pain; circling, wobbling, aimless wandering, head pressing, blindness, seizures, and partial paralysis

99
Q

How do you diagnose salt toxicity?

A

Na levels > 160 mEq/L