Tox-1 Flashcards
(99 cards)
1
Q
Xenobiotic
A
Foreign substance
2
Q
Antidote
A
Any substance that prevents/relieves the effects of a toxicant (no antidote works on all toxicants)
3
Q
NOAEL
A
No Observed Adverse Effect Level; the highest experimental point that is without adverse effect
4
Q
LOAEL
A
Lowest Observed Adverse Effect Level; the lowest concentration or amount of a substance that causes an adverse effect experimentally
5
Q
Additive
A
The sum of the effects of the chemicals involved in the reaction
6
Q
Antagonistic
A
When the net effect of the chemical reaction is zero (antidotes for poisons)
7
Q
Synergism
A
When the sum of the effects is more than each chemical individually
8
Q
Cats are deficient in this type of metabolism
A
Glucuronidation
9
Q
Dogs are deficient in this type of metabolism
A
Acetylation
10
Q
Pigs are deficient in this type of metabolism
A
Sulfation
11
Q
Bioactivation
A
When metabolism increases the toxicity of a compound
12
Q
These three conditions make patients candidates for intubation
A
Unconscious, paralyzed, and severe respiratory distress
13
Q
Ventilation may be needed if there is…
A
Hypoventilation and hypercapnia, metabolic acidosis, or hypoxia
14
Q
At what concentration of oxygen do you treat hypoxia?
A
40%
15
Q
What are three cardiovascular signs of toxicity?
A
Tachycardia, arrhythmias, and hypertension
16
Q
What two drugs were mentioned that can be used to treat toxicity-associated tachycardia and arrhythmias?
A
Lidocaine and propranolol
17
Q
What two drugs were mentioned that can be used to treat toxicity-associated hypertension?
A
Nitroprusside and Hydralazine
18
Q
What are two CNS signs of toxicity?
A
Hyperactivity (seizures) and depression
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
20
Q
What drug was mentioned that can be used to treat toxicity-associated CNS depression (decreased respiratory rate)?
A
Doxapram
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
22
Q
What are the two most common methods of GI decontamination?
A
Emesis and activated charcoal
23
Q
What is the goal of inducing emesis after a suspected toxic exposure?
A
Prevent toxicant absorption
24
Q
Within how much time is inducing emesis successful in preventing toxicant absorption?
A
60 minutes
25
What are the contraindications of inducing emesis?
Too long, chronic exposure, caustic material, recent gastric sx, some species, oils/gasoline
26
What is the rule of thumb for when to induce emesis?
Toxic dose of the substance was ingested, no vomiting has yet occurred, and activated charcoal is not an option
27
What is the goal of using activated charcoal after a suspected toxic exposure?
Prevent toxicant absorption
28
What are the contraindications of activated charcoal?
Corrosive agents (acids, alkaloids), oil/gas, cyanide, obstructed airway/altered state, ruptured intestinal wall, chronic exposures
29
What is the rule of thumb for when to use activated charcoal?
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
30
What substances are not adsorbed by activated charcoal?
Acids, alkalis, alcohols/glycols, metals, oils, petroleum distillates, detergents
31
What is the goal of administering cathartics after a suspected toxic ingestion?
Facilitate toxicant removal
32
What are examples of cathartics?
Mineral oil, saline cathartics (milk of magnesia)
33
For corrosives, strong acids or bases, use ___ instead of emesis
Dilution with milk, water, or eggs
34
Lipid infusion is a relatively new treatment and is specifically used in _____ toxicosis
Ivermectin
35
What are the common names of organophosphate pesticides?
Parathion, malathion, chlorpyrifos
36
What is the mechanism of activity of organophosphate pesticides?
Irreversible inhibition of acetylcholine esterase (AChE) activity (anticholinesterase)
37
What are the clinical signs of organophosphate pesticide toxicity?
Muscarinic (SLUDGE-M), nicotinic (muscle fasciculations beginning with the face, generalized tremors, weakness, paralysis), CNS (depression, ataxia, nervousness, seizures)
38
How do you diagnose organophosphate pesticide toxicity?
Atropine challenge
39
If you observe dry mouth, mydriasis, and increased heart rate after an atropine challenge during a suspected organophosphate pesticide toxicity, what do you conclude?
Toxicity is NOT due to AChE (not OP toxicity)
40
What drugs can you use to treat organophosphate pesticide toxicity?
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
What syndrome is characterized by axonal degeneration of long motor neurons (hindlimb weakness, paralysis)?
OPIDN: Organophosphate-Induced Delayed Neurotoxicity
42
What breeds are the most susceptible to Ivermectin toxicosis?
Border collies, australian shepherds, and shelties
43
Why are certain breeds susceptible to Ivermectin toxicosis?
Blood Brain Barrier
44
What is the mechanism of action of Ivermectin?
GABA receptor agonist
45
Is the half-life of Ivermectin short or long?
Long (2-3 days); can see cumulative toxicity with repeat doses
46
What are the clinical signs associated with an Ivermectin toxicosis?
Increased inhibition! Ataxia, lethargy, mydriasis, coma, blindness, bradycardia; recumbency, disorientation, and seizures in collies; respiratory distress; anaphylactic reactions
47
How do you diagnosis Ivermectin toxicity>
History of administration
48
What organ systems can one use to diagnose Ivermectin toxicity?
Brain, GI content, liver, fat, and feces (no visible lesions, no diagnostic blood work)
49
What is the appropriate treatment plan for Ivermectin toxicosis?
GI decontamination for recent exposures (multiple doses of activated charcoal), supportive care (fluid and lyte therapy, epinephrine, short acting barbiturates)
50
What is the prognosis for non-susceptible breeds of dogs if exposed to <5 mg/kg of Ivermectin?
Good
51
What is the prognosis for any breed at dosages > 5 mg/kg of Ivermectin?
Guarded
52
What is the cardinal rule of pyrethroid pesticides?
DO NOT USE ON CATS
53
What is the mechanism of action of pyrethroid pesticides?
Binds voltage-gated sodium channel (causes hyperactivity)
54
What makes pyrethroid pesticides so toxic in cats?
Cats are not efficient at glucuronide conjugation
55
What are the clinical signs of pyrethroid pesticide toxicity?
In cats: drooling, paresthesia , muscle tremors and seizures, excessive muscle activity, and hyperthermia
56
How do you diagnose pyrethroid pesticide toxicity?
Difficult! Clinical values normal, nonspecific lesions, history of exposure, chemical analysis for pyrethrum/pyrethroid
57
What drug can be used to control the muscle tremors associated with pyrethroid pesticide toxicity?
Methocarbamol
58
What is the treatment plan for pyrethroid pesticide toxicity?
Stabilize tremors/seizures, bathe multiple times, IV fluids
59
What is the mechanism of action of bromethalin?
Damages mitochondrial function (uncouple oxidative phosphorylation in CNS -> loss of ion gradient -> fluid accumulation in myelin sheaths -> decreased nerve conduction and respiratory arrest)
60
What are the clinical signs of bromethalin toxicity?
Ataxia, hindlimb paralysis, hyper-excitability, severe muscle tremors, running fits, grand mal seizures
61
How do you diagnose bromethalin toxicity?
Cerebral edema and cerebellar degeneration; histological evidence of neuronal vacuolization and edema
62
How do you treat bromethalin toxicity?
Emesis (if recent exposure), repeated administration of activated charcoal, furosemide, treat seizures
63
What is the primary cause of pharmaceutical toxicosis?
Careless storage
64
What is the mechanism of action of Alprazolam (Xanax)?
GABAa receptor modulator that acts at the limbic, thalamic, and hypothalamic level of the CNS
65
What are the clinical signs of an Alprazolam toxicity?
Ataxia, depression, vomiting, tremors, tachycardia, diarrhea, and ptyalism (Depressive effect); some may initially show excitation at a high dose
66
What drug can be used as an antidote to Alprazolam toxicity?
Flumazenil (GABAa antagonist)
67
Can you use GI decontamination with Alprazolam toxicity?
Yes; emesis if recent, activated charcoal if toxic dose ingested
68
What is the mechanism of action of Zolpidem (Ambien)?
Inhibits neuronal excitation by binding to the benzodiazepine site of GABA receptors
69
What are the clinical signs of Zolpidem toxicity?
Ataxia, vomiting, lethargy, disorientation, hyper-salivation, hyperactivity, and panting
70
What is the recommended treatment for a pet showing mild signs of Zolpidem toxicity?
Keep quiet in a safe place; CS typically resolve in 12 hours
71
What mycotoxin is regularly screened for in peanut butter and is linked to liver cancer?
Aflatoxin
72
What mycotoxin is produced by "black patch" fungus on red clover?
Slaframine
73
What is the mechanism of action of slaframine?
Muscarinic cholinergic agonist (ACh mimic), especially in exocrine glands
74
What is the hallmark clinical sign in horses with slaframine toxicity?
the "slobbers"
75
What other toxicities do you have to differentiate between when there is a suspected slaframine toxicity?
OPs, botulism
76
How do you treat a slaframine toxicity?
Remove source, maintain hydration and lytes, Atropine if severe CSs
77
What mycotoxin is a metabolite of Fusarium spp?
Fumonisin
78
What mycotoxin is found almost exclusively on corn?
Fumonisin
79
What is the mechanism of action of fumonisin?
Inhibits sphingosine-N-acetyltransferase causing increased levels of sphinganine which is cytotoxic
80
What are two diseases linked to fumonisin toxicity?
Porcine pulmonary edema and equine leukoencephalomalacia (ELEM)
81
What are the clinical signs of porcine pulmonary edema caused by fumonisin toxicity?
Inactivity, increased respiratory rate, decreased heart rate -> respiratory distress
82
What are the two main target organs affected in equine leukoencephalomalacia (ELEM) caused by fumonisin toxicity?
Brain and liver
83
During necrosis of a horse that died of ELEM caused by fumonisin toxicity, what would you find?
CNS necrosis and liquefaction
84
What is the treatment of choice for fumonisin toxicity?
None available (isolate, change feed, ultrasorb S?)
85
What syndrome is associated with ammoniated feed toxicosis in cows?
"Bovine bonkers"
86
What is the hallmark sign of ammoniated feed toxicosis in cows caused by imidazoles?
Alternating between hyperexcitability and "normal" behavior
87
Ammonia is at what level in blood when death occurs in cows?
> 2 mg/dL
88
What are the specific clinical signs of ammoniated feed toxicosis?
Hyperexcitability: nervousness, rapid blinking, dilated pupils, trembling, ataxia, rapid respiration, SLUD, tonic convulsions induced by stimuli
89
What other differentials must you consider in a suspected ammoniated feed toxicosis?
OPs, cyanide, grain overload, meningitis, and encephalitis
90
What is the treatment for imidazole toxicosis?
No treatment, just feed removal (sedation PRN, milking out); prognosis good
91
What is the treatment for NPN overdose toxicosis?
No specific treatment; cold water + vinegar by stomach tube? Time; prognosis poor for recumbent animals
92
What is the mechanism of action of strychnine?
Competitive antagonist at postsynaptic spinal cord and medulla glycine receptors; glycine is an inhibitor transmitter, therefore evokes an overstimulation
93
What are the clinical signs of strychnine toxicity?
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
What PE and lab findings are typical in strychnine toxicosis?
Hyperthermia, elevated CPK and LDH, lactic acidosis, hyperkalemia, and leukocytosis
95
How do you treat strychnine toxicity?
Aggressive decontamination, control seizures (phenobarb or methocarbamol), ion trapping with ammonium chloride if not acidotic
96
What is the most common cause of salt toxicity?
Water deprivation
97
What is the mechanism of salt toxicity?
Diffusion of sodium into CSF when plasma Na levels are high leading to inhibition of glycolysis and ATP and attraction of water
98
What are the clinical signs of salt toxicity?
Salivation, increased thirst, abdominal pain; circling, wobbling, aimless wandering, head pressing, blindness, seizures, and partial paralysis
99
How do you diagnose salt toxicity?
Na levels > 160 mEq/L
