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Veterinary Toxicology > Nicotinic and Adrenergic Toxicants > Flashcards

Nicotinic and Adrenergic Toxicants Flashcards

1
Q

What are nicotinic receptors selectively blocked by?

A

hexamethonium

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2
Q

What are the most common early signs of nicotinic stimulation? What are some clinical signs?

A

CNS stimulation

  • salivation, lacrimation
  • emesis, diarrhea
  • tachycardia, tachypnea
  • shallow, slow respiration
  • collapse, coma
  • cyanosis
  • bradycardia, weak pulse
  • cardiac arrest
  • excitation/depression
  • muscle weakness, tremors, convulsions
  • paralysis, loss of reflexes
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3
Q

What are the main sources of nicotine? What potent effect does it tend to have?

A
  • plants
  • tobacco products
  • nicotine gum
  • snuff
  • nicotine sulfate (insecticides, immobilizing agent)

emetic effect —> limits absorption

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4
Q

What is the mechanism of toxicity of nicotine? How does it affect the adrenal medulla and CNS?

A

mimics ACh at sympathetic and parasympathetic ganglia, NMJ, and CNS causing immediate stimulation followed by a blockade

  • causes the release of catecholamines
  • stimulates chemoreceptor trigger zone to cause emesis
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5
Q

What is the major clinical sign of nicotine poisoning?

A

nicotinic stimulation followed by depression and paralysis

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6
Q

What is recommended for decontamination for nicotine poisoning? How can hyperthermia be resolved?

A
  • emesis if orally exposed within past 1 hr
  • gastric lavage, activated charcoal, catharsis, whole bowel irrigation
  • wash animal with warm water and mild hand dishwashing soap with dermal exposure

external cooling with tepid running water and/or fanning

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7
Q

What drugs are recommended to control seizures associated with nicotine poisoning? With severe bradycardia?

A
  • benzodiazepines: Diazepam, Lorazepam
  • barbiturates

Atropine

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8
Q

What is a good way to hasten nicotine excretion?

A

acidification of the urine with ammonium chloride

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9
Q

Where is Tobacco (Nicotiana spp.) most commonly found? Why is risk of toxicity low?

A

all US, mostly in SW states

plant in unpalatable and animals will stay away if good quality forage is available

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10
Q

What are the 3 toxic principles of Tobacco (Nicotiana spp.)? What species are affected?

A
  1. pyridine alkaloids - nicotine
  2. teratogens - anabistine, anatabine
  3. polycyclic aromatic hydrocarbons (PAHs) - produced upon combustion (carcinogenic, mutagenic, teratogenic)

cattle, swine, sheep, horses, birds

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11
Q

What are some clinical signs of Tobacco (Nicotiana spp.)?

A
  • dullness
  • vomiting, salivation, diarrhea
  • abdominal cramps
  • bloat, colic
  • frequent urination
  • muscular weakness
  • staggering, trembling, shivering, spasms, tremors
  • 3rd eyelid protrusion, blindness
  • prostration, opisthotonus
  • irregular and weak pulse, heart palpitation
  • elevated body temperature with colt extremities
  • diaphragmatic spasms, respiratory paralysis, dyspnea, death
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12
Q

What is the main clinical signs of Tobacco (Nicotiana spp.) associated with swine?

A

TERATOGENESIS - pregnant sows may give birth to piglets with arthrogryposis if exposed within 35 days of gestation, causing prolongation of parturition and death of the piglet from neonatal asphyxiation

(sows do not show signs of toxicosis before giving birth to malformed piglets)

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13
Q

How can Tobacco (Nicotiana spp.) be diagnosed?

A
  • history of exposure and clinical signs
  • confirm by identifying nicotine or other nicotine-like alkaloids in blood, urine, GI contents, liver, or kidney
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14
Q

What are the main 2 options for decontamination of Tobacco (Nicotiana spp.) Which is most common?

A
  1. emesis or enterogastric lavage
  2. administer activated charcoal*

most cases are in livestock

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15
Q

What is recommended for treating the parasympathetic effects of Tobacco (Nicotiana spp.)?

A

Atropine

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16
Q

What is Conium maculatum (poison hemlock) known to contaminate? Where does it grow?

A

hay and grain

most of USA and southern Canada

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17
Q

What is the toxic principles of Conium maculatum (poison hemlock)? What 2 chemicals are present in each stage of the plant’s growth?

A

piperidine alkaloids

  • LATE STAGES (seeds) = coniine
  • EARLY STAGES = γ-coniceine (most toxic)
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18
Q

What species are most sensitive to Conium maculatum (poison hemlock)? What is the mechanism of toxicity? How does the toxic principle cause different effects?

A

cattle

nicotinic stimulation, then blockade of autonomic ganglia, NMJs, and adrenal medulla

  • γ-coniceine = stimulatory
  • coniine = mixed
  • methyl coniine = inhibitory
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19
Q

What unique toxic effect do γ-coniceine and coniine in Conium maculatum (poison hemlock) have?

A

teratogenesis

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20
Q

What are the nicotinic clinical signs of Conium maculatum (poison hemlock) poisoning?

A
  • muscular weakness and trembling
  • ataxia
  • rapid pulse
  • mydriasis
  • salivation
  • abdominal pain
  • frequent urination and defecation
  • lacrimation
  • depression
  • paresis, respiratory paralysis
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21
Q

What 2 non-nicotinic clinical signs are associated with Conium maculatum (poison hemlock) poisoning?

A
  1. musty, mousy smell in breath and urine
  2. teratogenic syndrome - joint deformities, crooked legs, kinked tails, cleft palate depending on gestation stage of exposure
  • CATTLE: day 40-50 = cleft palate
  • CATTLE: day 40-100 = contractures and cleft palate
22
Q

Where is it most common to find Lupinus (Lupine/Bluebonnet)?

A

Rocky Mountains westward (cause the most deaths in Montana, Idaho, and Utah)

23
Q

What are the 2 toxic principles of Lupinus (Lupine/Bluebonnet)? Where are they most concentrated in the plant?

A
  1. quinolizidine and piperidine alkaloids
  2. anagyrine

pods and seeds

24
Q

What is the mechanism of toxicity of Lupinus (Lupine/Bluebonnet)? What species is most affected?

A
  • alkaloids = nicotinic
  • anagyrine = teratogenic

sheep

25
Q

What 2 species rarely develop Lupinus (Lupine/Bluebonnet) toxicity? Why?

A
  1. cattle
  2. horses

do not usually eat pods

26
Q

How do clinical signs of Lupinus (Lupine/Bluebonnet) compare in sheep and cattle?

A

SHEEP = labored breathing, depression, salivation, ataxia, clonic spasms, seizures, butting other animals and pressing against the fence, respiratory failure, coma, death (most susceptible)

CATTLE = excessive salivation, teeth-grinding, muscular weakness, ataxia, recumbency, respiratory paralysis, death (rare)

27
Q

What causes teratogenic syndrome in Lupinus (Lupine/Bluebonnet) toxicity? How are calves affected? In what 2 states has this been reported?

A

anagyrine

crooked calf disease affecting front limbs, neck, and spine due to impairment of fetal movement during gestation (+/- cleft palate)

SD, NE

28
Q

How can poison hemlock and Lupinus toxicity be diagnosed?

A
  • history of plant ingestion
  • clinical signs
  • chemical analysis of blood, stomach contents, liver, and kidney
29
Q

What makes Lobelia cardinalis (Cardinal flower) toxic?

A

contains nicotinic alkaloids - lobeline, lobelidine and others

30
Q

What makes Laburnum anagyroides (Golden chain) toxic?

A

nicotinic quinolizidine alkaloid - cytisine

31
Q

What is the main source of Imidazothiazoles, like Levamisole? What is the mechanism of toxicity?

A

antiparasitics (antinematode, microfilaricide) and immunostimulants

acts as a nicotine-like ganglionic stimulant with both nicotinic and muscarinic effects to cause stimulation, then a blockade of ganglionic and skeletal muscle transmission

32
Q

What are the main clinical signs of Imidazothiazole toxicity?

A
  • DUMBELS
  • anxiety, irritability
  • head shaking, lip licking
  • muscle tremors and seizures
  • ataxia
  • hyperesthesia
  • clonic convulsions with CNS depression
  • behavioral changes
  • tachypnea
  • collapse and death due to respiratory failure
33
Q

What species are susceptible to Imidazothiazole toxicity?

A
  • sheep
  • swine
  • cattle
  • dogs
  • horses
34
Q

No antidote is available for Imidazothiazole toxicity. What symptomatic therapy is used?

A

Atropine - controls cholinergic signs

35
Q

Adrenergic receptors locations and responses:

A
36
Q

What are some non-specific, α1 selective, and α2 selective adrenergic agonists? What are they used to treat?

A

Epinephrine, Norepinephrine - anaphylaxis, cardiac arrest

Phenylephrine, Methozamine - decongestants

Clonidine - hypertension, anxiety

37
Q

What are some non-specific, β1 selective, and β2 selective adrenergic agonists? What are they used to treat?

A

Epinephrine, Isoproterenol

Xamoterol, Dobutamine, Prenalterol - cardiogenic shock

Albuterol, Formoterol, Terbutaline, Clenbuterol - bronchodilators

38
Q

What is the mechanism of toxicity of bronchodilators? What are the main clinical signs of toxicity?

A

stimulation of β-adrenergic receptors

peripheral vasodilation causing…
- hypotension
- bronchodilation and pulmonary edema
- muscle tremors and weakness
- increased HR and arrhythmias
- tachypnea
- vomiting, hypokalemia

39
Q

Why is decontamination not possible or advisable in the case of bronchodilator toxicity?

A

rapid absorption and onset of clinical signs

  • can induce emesis if within 15-30 min of ingestion
  • activated charcoal can be used with large ingestions of syrup
40
Q

What are the main 3 clinical signs of bronchodilator toxicity that can be treated?

A
  1. hypotension - IV fluids
  2. hyperactivity - Diazepam
  3. tachycardia - IV propanolol
41
Q

What are 4 examples of decongestants? What is the mechanism of toxicity?

A
  1. Pseudoephedrine
  2. Phenylephrine
  3. Phenylpropanolamine
  4. Ephedrine

sympathomimetic stimulation of α and β adrenergic receptors

42
Q

What are the 3 syndromes associated with decongestant toxicity?

A
  1. α-adrenergic syndrome - hypertension, tachycardia, pale MM, mydriasis, reduced GI motility, hyperactivity (α1/α2)
  2. β-adrenergic syndrome - weakness, tachycardia, vasodilation (hypotension), bronchodilation, hypokalemia, hyperactivity, tachypnea, depression, muscle tremors, death (β1/β2)
  3. mixed syndrome - hypertension, tachycardia, mydriasis, dry MM
43
Q

What 2 drugs are recommended to control seizures with decongestant toxicity? What is usually avoided? Why?

A
  1. Phenothiazines - Acepromazine, Chlorpromaine
  2. Barbiturates

Benzodiazepeines (Diazepam) - dogs become more agitated

44
Q

What are the main sources of Amitraz? In what 2 animals should they be used carefully? In what species is it contraindicated?

A
  • products for demodectic mange, mite, tick, and lice control (dips, collars, shampoos, pour-ons)
  • agricultural pesticides (esp. on fruit trees)

cats and puppies

horses - causes ileus

45
Q

How does absorption compare with ingestion and dermal exposure?

A

INGESTION = rapid absorption

DERMAL = relatively slow absorption after dipping

46
Q

What are the 3 mechanisms of toxicity of Amitraz?

A
  1. α2-adrenergic receptor agonist in the CNS to decrease NE release —> sedation
  2. α1 and α2 adrenergic agonism in PNS
  3. inhibits monoamine oxidase (MAO) to cause behavioral and neurotoxic effects (MAO catabolizes catecholamine neurotransmitters)
47
Q

What are the 2 most common central α2 clinical signs upon Amitraz toxicity? What does chronic exposure cause?

A
  1. CNS depression/sedation —> coma
  2. bradycardia

endocrine disruption and developmental/reproductive toxicity

48
Q

How does Amitraz cause ileus in horses?

A

α-adrenergic agonism causes GI hypomotility —> ileus —> severe colic

49
Q

What are the 2 antidotes for Amitraz toxicity?

A

α-adrenergic antagonists to reverse bradycardia, hyperglycemia, and CNS depression)

  1. Atipamezole
  2. Yohimbine
50
Q

What are some non-specific, α1 selective, and α2 selective adrenergic antagonists? What are they used to treat?

A

Phentolanine, Phenoxybenzamine - hypertension

Prazosin, Doxazocin, Tamsulosin - hypertension, urinary flow

Yohimbine, Idazoxan

51
Q

What are some non-specific, β1 selective, and β2 selective adrenergic antagonists? What are they used to treat?

A

Propanolol, Timolol, Nadolol, Pindolol

Metoprolol, Acebutolol, Atenolol, Esmolol - angina, hypertension, dysrhythmias

Butoxamine

52
Q

What clinical signs are suggestive of sympatholytic syndrome?

A

(anti-adrenergic —> α and β antagonists)
- vomiting
- hyperventilation
- convulsions
- hypotension, bradycardia/tachycardia
- heart block, arrhythmias
- miosis
- depression
- bronchoconstriction
- lethargy
- decreased/absent bowel sounds

Veterinary Toxicology (29 decks)

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