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Toxicology > Quiz 1: Principles, Diagnosis, Treatment, Neurotoxicants > Flashcards

Quiz 1: Principles, Diagnosis, Treatment, Neurotoxicants Flashcards

1
Q

Paracelsus

A

“Father of Toxicology”

Swiss physician that said “all substances are poisons”

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2
Q

Toxicology is concerned with

A

Identification, treatment, and assessing risks of poisons

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3
Q

Definition of Toxicant

A

Compound that causes toxicity

May be natural or man-made

Xenobiotic = foreign substance

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4
Q

Definition of Antidote

A

Substance that prevents/relieves effects of a toxicant

No antidote works on all toxins (not even activated charcoal)

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5
Q

NOAEL

A

“No observed adverse effect level” on dose-response curve

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6
Q

LOAEL

A

“Lowest observable adverse effect level” on a dose-response curve

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7
Q

Classifications of chemical interactions in toxicity

A

Additive
Antagonistic
Synergism

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8
Q

Factors influencing toxicity

A

Factors related to exposure
Factors related to the subject
Factors related to the environment

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9
Q

Types of exposure classifications

A

Acute
Sub-acute/subchronic
Chronic

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10
Q

Acute exposure

A

A single exposure or multiple exposures in 24 hours

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11
Q

Sub-acute/subchronic exposure

A

Exposure over 7 to 90 days

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12
Q

Chronic exposure

A

Protracted exposure (6 months - lifetime)

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13
Q

Most important veterinary toxicants are absorbed by what routes?

A

Oral and dermal

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14
Q

What usually detoxifies a compound and increases its elimination?

A

Metabolism

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15
Q

When metabolism increases the toxicity of a compound

A

Bioactivation

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16
Q

Mechanism of Toxicity (4 steps)

A
  1. Delivery from site of exposure to target
  2. Reaction of the ultimate toxicant with the target molecule
  3. Cellular dysfunction and resultant toxicities
  4. Repair or disrepair
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17
Q

How do toxicants cause toxicity?

A

Cellular damage

Organ system dysfunction

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18
Q

Most common toxicants that cause death

A

Insecticides
Rodenticides
Ethylene Glycol

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19
Q

When treating a patient for a toxicosis, what do you do first?

A

Evaluate for immediate life-threatening problems

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20
Q

How to prevent aspiration of vomitus in an unconscious patient?

A

Keep head lower than body

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21
Q

A patients may need assisted ventilation if:

A

Hypoventilation, hypercapnia
Metabolic acidosis (venous pH 7.35)
Hypoxia, treat with 40% oxygen

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22
Q

How to treat CNS hyperactivity (seizures)

A

Diazepam
Phenobarbital
Methocarbamol

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23
Q

How to treat CNS depression

A

Analeptics

Doxapram

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24
Q

How to treat tachycardia and arrhythmias

A

Lidocaine

Propranolol

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25
Q

How to treat hypertension

A

Nitroprusside

Hydralazine

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26
Q

How to increase cardiac contractility

A

Dobutamine

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27
Q

Priority in animals with severe clinical signs

A
  1. Assess hypo/hyperthermia

2. Pull blood for laboratory profile and diagnostic testing (3cc EDTA tube and 2 serum tubes)

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28
Q

4 major themes of a History

A
  1. Health history
  2. Current clinical history
  3. Environment
  4. Diet
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29
Q

Two most common methods of decontamination

A

Emesis

Activated charcoal

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30
Q

Contraindications of emesis in decontamination

A
  1. > 30 minutes since exposure
  2. Chronic exposure
  3. Ingestion of caustic materials
  4. Recent GI surgery
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31
Q

Induce emesis if:

A
  1. Toxic dose of substance was ingested
  2. No vomiting has yet occurred
  3. Activated charcoal is not an option
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32
Q

Contraindications of using activated charcoal

A
  1. If it will not bind the toxin (inorganic compounds, oils, gasoline, ethylene glycol, cyanide, etc.)
  2. If airways are obstructed
  3. If patient has altered state of consciousness
  4. Chronic exposure
  5. If you suspect GI perforation
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33
Q

Activated charcoal is most useful for what type of toxins?

A

Toxic plants
Pesticides
Herbicides

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34
Q

Give charcoal if:

A
  1. Substance is known to be absorbed by it
  2. Ingestion was very recent/undergoes enterohepatic circulation/is sustained release
  3. The patient can tolerate it
  4. There is no immediate need to administer oral meds
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35
Q

Effect of cathartics

A

Decrease GI transit time
Increase movement of toxins/charcoal-toxin complex
Decrease absorption of the toxin

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36
Q

Example of a cathartic

A

Mineral Oil

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37
Q

What to do for corrosive toxins that have been ingested?

A

Use dilution instead of emesis

Milk water or eggs

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38
Q

How to treat dermal toxicant exposure?

A

Bathe in liquid dish soap

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39
Q

Lipid infusion

A

Relatively new treatment for toxicant ingestion

Off label-use of IV fluids

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40
Q

Emetic agent for dog, pigs

A

Apomorphine

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41
Q

Emetic agent for cats

A

Xylazine

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42
Q

Good agent for at-home emesis induction

A

Salt water

Hydrogen peroxide

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43
Q

Treatment for sustained-release toxicants

A

Gastric lavage or whole bowel irrigation

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44
Q

Common antidotes to know

A

Vitamin K for rodenticide toxicities

Digoxin for plant toxicities

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45
Q

Analytic testing

A

Testing for toxicants
Not one test that will screen for all toxicants
Can be costly

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46
Q

Ancillary support includes

A

Managing any hepatic or renal injury

Maintain body temperature (hyperthermia- cold baths, ice; hypothermia- blankets, circulating warm water pads, NO HEAT LAMPS)

Ensure adequate urine output

Prevent irritation of skin/membranes with demulcents, milk, sucralfate

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47
Q

How to prevent future toxicant exposures

A

Change pasture, feed, water, etc.
Remove baits, pesticides, etc.
Bathe or flush cutaneous or ocular exposures
Educate clients

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48
Q

Types of Neurotoxicants

A 
Pesticides
Pharmaceuticals
Mycotoxins
Ammoniated feed toxicosis 
Strychnine 
Salt
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49
Q

Largest class of chemicals inducing toxicosis

A

Neurotoxicants

50
Q

Pesticide usage

A 
Billions of pounds made each year in US
300 types of pesticides in US
>50% use is non-commercial 
Improper use and storage 
Many benefits (higher crop yields, better health)
51
Q

Organophosphate Pesticides

A

Agricultural and residential use has increased
Used in flea collars, dips, fly, ant, roach bait
Parathion, malathion, chlorpyrifos
Highly water soluble and acute toxicity

52
Q

Mechanism of action of Organophosphates

A

Irreversible inhibition of Acetylcholinesterase activity (anti-cholinesterase)

Leads to cholinergic overstimulation within minutes to hours

53
Q

Clinical signs of anti-cholinesterase toxicity

A

Clinical signs may last 1-5 days

Muscarinic: SLUDGE-M

Nicotinic: Muscle fasciculations, tremors, weakness, paralysis

CNS: Respiratory depression, ataxia, nervousness, clinic-tonic seizures

54
Q

Atropine Challenge

A

Used to diagnose anti-cholinesterase toxicity

Administer pre-anesthetic dose of atropine and see if patient responds normally

If normal, toxicity is NOT due to anti-cholinesterase toxicant

55
Q

Treatment of anti-cholinesterase toxicity

A 
GI decontamination
Bathe if dermal exposure
Atropine sulfate for muscarinic signs 
Oxides (protopam, 2-PAM) to reactivate AChE
Diazepam or barbiturates for seizures 
Time
56
Q

Histopathology of patient following OP toxicity

A

Vacuolization of brain

Degeneration of neurons

57
Q

Organophosphate-induced Delayed Neurotoxicity

A

Axonal degeneration of long motor neurons
Hindlimb weakness, paralysis
No treatment
Poor prognosis

58
Q

What is Ivermectin?

A

Antihelminthic

59
Q

What breeds are susceptible to Ivermectin toxicosis?

A

Border Collies
Australian Shepherds
Shelties

60
Q

Mechanism of action of ivermectin toxicosis

A

GABA receptor agonist

Increased inhibitory input = DEPRESSIVE effect

Can see cumulative toxicity with repeat doses

61
Q

Clinical signs of ivermectin toxicosis

A

Ataxia, lethargy, mydriasis, coma, blindness, bradycardia, recumbency, disorientation, seizures, respiratory distress, anaphylactic reactions

62
Q

Diagnosis of ivermectin toxicosis

A

History of administration
Brain concentration >100 ppb
Can also measure in GI content, fat, liver, and feces
No visible lesions, no diagnostic bloodwork

63
Q

Treatment for ivermectin toxicosis

A 
Recent exposure: multiple doses of activated charcoal 
Supportive care
Electrolyte therapy
Epinephrine 
Barbiturates for seizures
64
Q

How to prevent ivermectin toxicosis

A

Test dogs prior to administering higher doses

65
Q

What are pyrethroid pesticides?

A

Pesticides made from pyrethrins of chrysanthemum flowers
Considered “safer” than organophosphates
Used in dog flea/tick topical prevention

66
Q

Mechanism of action of pyrethroid pesticides

A

Lipophilic, absorbed by all routes
Binds voltage-gated sodium channels
Causes repetitive nerve discharges -> hyperactivity and overstimulation

67
Q

Why are cats more susceptible to pyrethroid toxicity than dogs?

A

Inefficient glucuronide conjugation

68
Q

Clinical signs of pyrethroid toxicosis in cats

A

Drooling, paresthesia, muscle tremors, seizures, excessive muscle activity, hyperthermia

69
Q

Clinical signs of pyrethroid toxicosis in dogs

A

Paresthesia, shaking of legs, muscle fasciculation, rubbing of application site, agitation, nervousness

70
Q

Diagnosis of pyrethroid toxicosis

A

Difficult
Look at clinical signs, history of exposure
Chemical analysis for pyrethrin/pyrethroid

71
Q

Treatment of pyrethrin toxicity

A

Stabilize: treat seizures (methocarbamol)
WASH IT OFF
IV fluids, furosemide

72
Q

Bromethalin

A

Single-dose rodenticide

Kills in 3-5 days -> delayed toxicosis

73
Q

Mode of action of bromethalin toxicosis

A

Parent and metabolite uncouple oxidative phosphorylation in CNS

Loss of ion gradients in leads to fluid accumulation in myelin sheaths

Causes decreased nerve conduction, respiratory arrest, and edema

74
Q

Clinical signs of bromethalin toxicosis

A

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

75
Q

Diagnosis of bromethalin toxicosis

A
  1. Cerebral edema and cerebellar degeneration

2. Histological evidence of neuronal vacuolization and edema

76
Q

Treatment of bromethalin toxicosis

A 
Emesis if recent exposure
Give activated charcoal/sorbitol 
Maintain hydration and electrolytes 
Furosemide for edema 
Treat seizures
77
Q

Primary cause of pharmaceutical toxicosis

A

Careless storage

78
Q

Top prescribed pharmaceuticals that cause toxicoses in animals

A 
Vicodin 
Synthyroid
Zocor
Lipitor 
Lisinopril
79
Q

Mechanism of action for alprazolam toxicosis

A

Acts at limbic, thalamic, and hypothalamic levels of CNS

Depressive effects

80
Q

Clinical signs of alprazolam toxicosis

A

Ataxia, vomiting, depression, tremors, tachycardia, diarrhea, ptyalism, hypothermia

Usually occurs within 30 minutes of ingestion

Some animals may initially show CNS excitation

81
Q

Diagnosis of alprazolam toxicosis

A

Based on clinical signs and history of exposure

82
Q

Treatment of alprazolam toxicosis

A 
Emesis with apomorphine if recent ingestion
Activated charcoal 
Flumazenil for severe CNS depression
Close monitoring
Fluids
83
Q

Zolpidem

A

Ambien
Sleep aid
Non-benzodiazepine hypnotic drug

84
Q

Mechanism of action of zolpidem toxicosis

A

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

85
Q

Clinical signs of zolpidem toxicosis

A

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

86
Q

Diagnosis of zolapidem toxicosis

A

Based on clinical signs and history of exposure

87
Q

Treatment of zolpidem toxicosis

A

Supportive
Keep patient in a quiet place
Treat clinical signs if needed

88
Q

What are mycotoxins?

A

Fungal metabolites that cause pathological, physiological, and/or biochemical alterations usually on several organ systems

Can affect all species

Includes aflatoxins, slaframine, and fumonisin

89
Q

What is Slaframine?

A

Produced by “black patch” fungus on red clover
Rain, high humidity, cool weather triggers growth
Occurs in central, SE, SW USA

90
Q

Mechanism of action of Slaframine

A

ACh mimic, partially acts as a muscarinic cholinergic agonist, especially in exocrine glands

91
Q

Slaframine toxicity is most common in what species?

A

Horses and cattle

92
Q

Clinical signs of slaframine toxicosis

A

Copious salvation (the “slobbers”)
Bloat, diarrhea, frequent urination
Feed refusal

93
Q

Diagnosis of slaframine toxicosis

A

Consumption of clovers with “black patch”

94
Q

Treatment of slaframine toxicosis

A

Remove source
Maintain hydration and electrolytes
Atropine
Rarely fatal

95
Q

What is fumonisin?

A

Metabolite of Fusarium spp.
Found almost exclusively on corn
Usually occurs in years of drought followed by wet weather
Presence of Fusarium spp. Is not indicative of fumonisin

96
Q

Mechanism of action of fumonisin toxicosis

A

Inhibition of sphingosine-N-acetyltransferase causing increased levels of sphingosine, which is cytotoxic

Affects vascular epithelial cells, which can lead to stroke, hepatic injury, and pulmonary edema

97
Q

Which species are susceptible to fumonisin toxicosis?

A

Horses, ponies, swine, rabbits

98
Q

Two diseases cause by fumonisin toxicosis

A 
Equine leukoencephalomalacia (ELEM)
Porcine pulmonary edema (PPE)
99
Q

Porcine pulmonary edema

A

Lethal pulmonary edema that occurs 4-7 days after consuming fumonisin contaminated feed
Manifests as respiratory distress
Necropsy shoes pulmonary pathology and edema, hepatic lesions, tissue necrosis

100
Q

Most specific biochemical changes for PPE

A

Increase in tissue and serum sphingoid bases

Increased liver enzymes

101
Q

Equine Leukoencephalomalacia (ELEM)

A

Fumonisin toxicosis of horses
Most common in late fall/early winter
Target organs: brain and liver
CNS toxicity: hysteria that gets progressively worse
Liver toxicity: jaundice, hepatic encephalopathy
Necropsy: CNS liquefaction

102
Q

Treating fumonisin toxicosis

A

No treatment.

“Ultrasorb S”: newly created mycotoxin deactivator

Isolate infected animals, change feed

Pigs usually recover in 48 hours after removing contaminated feed

103
Q

Ammoniated feed toxicosis is caused by

A

Over consumption of

Non-protein nitrogen sources (ammonium, salts) that are added to cattle feed

Mineral licks

104
Q

“Bovine bonkers”

A

Hyperexcitability state caused by ammoniated feed toxicosis

105
Q

Onset of clinical signs or death in ammoniated feed toxicosis

A

15 minutes - several hours

Death within 24 hours when blood ammonia >2mg/dL

106
Q

Normal blood ammonia concentration

A

<0.5mg/dL

107
Q

Diagnosis of ammoniated feed toxicosis

A

Check blood ammonia levels (>0.5 mg/dL)
Increased glucose, BUN
Decreased blood pH

108
Q

Treatment of ammoniated feed toxicosis

A

No specific treatment
Remove feed
Sedation may help prevent self-mutilation
Milking out affected cows
Give 5 gallons cold water and 1 gal vinegar

109
Q

What is Strychnine?

A

Compound from seeds of Indian tree

Used as poison for pocket gophers

Often used as malicious poison

110
Q

Mechanism of action of strychnine toxicosis

A

Strychnine is a competitive agonist at post-synaptic spinal cord and medulla glycine receptors

Glycine is an inhibitory transmitter

Causes overstimulation of muscles

111
Q

Clinical signs of strychnine toxicosis

A

Anxiety, restlessness, stiff neck and gait, “grinning” as facial muscles stiffen, ears twitch

Proceeds to violent titanic seizures and respiratory distress

“Sawhorse stance”: rigid extension of all 4 limbs

Death from respiratory failure, exhaustion

112
Q

Diagnosis of strychnine toxicosis

A

Hyperthermia
Elevated CPK and LDH in serum
Lactic acidosis, hyperkalemia, leukocytosis

113
Q

Treatment of strychnine toxicosis

A

Aggressive decontamination (e.g. Gastric lavage)
Control seizures with phenobarbital/methocarbamol to prevent asphyxiation
Ion trapping with ammonium chloride

114
Q

What is salt toxicosis?

A

Too much salt in blood caused by dehydration or consumption of large amounts of salt

Most common in pigs

115
Q

Mechanism of action in salt toxicosis

A

Na moves passively into CNS which causes:

  1. Inhibition of glycolysis and ATP
  2. Attraction of water to maintain osmotic balance-> increased volume and pressure
116
Q

Clinical signs of salt toxicosis

A 
Salivation 
Increased thirst
Abdominal pain 
Circling, wandering
Head pressing
Blindness
Seizures
Partial paralysis
117
Q

Threshold of blood salt levels in salt toxicosis

A

2.2 g/kg

118
Q

Diagnosis of salt toxicosis

A

Na levels >160 meq/L

Brain Na >2000ppm

119
Q

Treatment of salt toxicosis

A

SLOW rehydration over 2-3 days

Lower serum sodium levels at 0.5-1 mEq/L/hr by IV

Give loop diuretic (furosemide) to prevent pulmonary edema

120
Q

What pharmaceutical would be most useful for treating salt toxicosis in a pig?

A

Furosemide

121
Q

True or False:

Ivermectin is a GABA receptor blocker, causing clinical signs such as depression and respiratory distress in animals

A

False

It’s a GABA receptor agonist

122
Q

True or False:

Hyperthermia following Strychnine toxicosis often happens in dogs

A

True

Toxicology (7 decks)

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