PNS II - ANS II Flashcards

1
Q

Provide the locations of nicotinic receptors. What type of receptors are they? How do they function?

A
  • nicotinic N
    • ligand gated
    • autonomic ganglia, adrenal medulla
  • nicotinic M
    • ligand gated
    • neuromuscular junctions
  • function - channel protein, ACh binds and allows cations to rush in
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2
Q

What is the effect of nicotine on the parasympathetic ganglia?

A
  • stimulates then blocks them
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3
Q

Describe how to treat nicotine toxicosis in a dog.

A
  • decontamination
    • emesis if orally exposed in past hour
    • gastric lavage within 2-4 hours, give activated charcoal and cathartic, whole bowel irrigation
    • dermal exposure - wash with mild hand dishwashing detergent
  • control seizures - benzodiazepines (diazepam, lorazepam), barbiturates
  • treat hyperthermia - external cooling with tepid running water and fanning
  • positive pressure ventilation and supplemental oxygen
  • treat symptoms - isotonic crystalloid fluids for cardovascular effects
  • atropine for severe bradycardia
  • acidification of urine with ammonium chloride to hasten excretion
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4
Q

What is used to acidify urine? Why is urine acidification useful in treating nicotine toxicosis?

A
  • ammonium chloride - hastens excretion
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5
Q

Name three toxic compounds found in tobacco. What are their toxic effects?

A
  • pyridine alkaloids (nicotine)
  • teratogens (anabasine, anatabine)
  • polycyclic aromatic hydrocarbons (PAHs) on combustion - carcinogenic, mutagenic, teratogenic
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6
Q

What is the most appropriate method for decontamination following ingestion of tobacco plants and why?

A
  • emesis, enterogastric lavage, activated charcoal
  • charcoal is most common as most cases are livestock
    • in livestock decontamination is limited to charcoal
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7
Q

What is the purpose of administering atropine to treat tobacco plant toxicosis?

A
  • to treat parasympathetic effects
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8
Q

Name three toxins found in poison hemlock. What is the general name of these toxins and how do they act?

A
  • piperidine alkaloids
    • stimulates then blocks nicotinic receptors at autonomic ganglia, neuromuscular junction, adrenal medulla
  • effect depends on toxin
    • y-coniceine is stimulatory, teratogenesis, early stages of plant, most toxic
    • coniine has mixed effects, teratogenesis, late stages of plant (seeds)
    • N-methyl coniine is inhibitory
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9
Q

Which of the toxins in poison hemlock is most toxic?

A
  • y-coniceine
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10
Q

What is the characteristic smell of urine and breath of animals with poison hemlock toxicosis?

A
  • musty and mousy, smells like rotting cardboard
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11
Q

Name the toxins found in lupine. What are the mechanisms of action of these toxins? What is lupinosis?

A
  • quinolizidine alkaloids - nicotinic
  • piperidine alkaloids - nicotinic
  • anagyrine - teratogenic
  • lupinosis - acute liver atrophy due to eating lupines
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12
Q

Which domestic animal species is most commonly affected by lupine poisoning and why?

A
  • sheep - they will eat anything
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13
Q

Name two US states in which lupine toxicity is prevalent.

A
  • montana
  • idaho
  • utah
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14
Q

Name the lupine toxin associated with teratogenesis. What is the appearance of animals affected by the teratogenic syndrome induced by lupine toxins? Explain this teratogeny.

A
  • anagyrine
  • animals have crooked front limbs, neck, and spine
  • may have a cleft palate
  • happens in utero - dam eats toxic lupines and it affects embryo/fetus
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15
Q

Describe how to treat poison hemlock or lupine toxicosis.

A
  • nonspecific - charcoal, gastric lavage, assisted respiration
  • avoid overexcitement and stress
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16
Q

Name a toxin present in lobelia and its mechanism of action.

A
  • nicotinic alkaloids - lobeline, lobelidine
17
Q

Name the toxin found in golden chain and its mechanism of action.

A
  • nicotinic quinolizidine alkaloid - cytisine
18
Q

Provide the mechanism(s) of toxicity of levamisole (imidazothiazole) .

A
  • acts as a nicotine like ganglionic stimulant
  • has both nicotinic and muscarinic effects
  • first there is stimulation than blockade of ganglionic and skeletal muscle transmission
19
Q

Describe how to treat levamisole toxicosis.

A
  • no antidote
  • just supportive and symptomatic care
  • atropine ca be used to help control some cholinergic signs
20
Q

Why is decontamination not possible or advisable for poisoning by bronchodilators?

A
  • rapid absorption and onset of clinical signs - don’t have time
  • emesis only possible within 15-30 minutes of ingestion
21
Q

Describe how to treat poisoning due to bronchodilators.

A
  • supportive therapy for clinical signs
    • IV fluids for hypotension
    • diazepam for hyperactivity
    • IV propranolol for tachycardia
22
Q

Name a drug used to treat tachycardia.

A
  • propranolol
23
Q

What are the clinical signs of β-adrenergic syndrome (decongestant toxins)?

A
  • weakness
  • tachycardia
  • vasodilation (hypotension)
  • bronchodilation
  • hypokalemia
  • hyperactivity
  • tachypnea
  • depression
  • muscle tremors
  • death
24
Q

Describe how to treat poisoning due to decongestants.

A
  • decontamination
    • emesis in early toxicosis
    • activated charcoal, cathartic
    • gastric lavage
  • control seizures, hyperactivity, tremors
    • phenothiazine (acepromazine, chlorpromazine) or barbiturate
  • give IV fluids, treat hyperthermia
  • treat tachycardia with IV propranolol
  • acidify urine with ammonium chloride to enhance drug elimination
25
Q

Identify two drugs that can be used and one that should not be used to control seizures following poisoning by decongestants.

A
  • yes use - acepromazine, chlorpromazine
  • no use - diazepam (can make dogs more agitated)
26
Q

Provide the mechanism(s) of toxicity of amitraz (found in mange, mite, tick, and lice treatments and pesticides). Why is amitraz contraindicated in horses?

A
  • binds to a2 adrenergic receptors in CNS causing sedation (agonism)
    • a2 receptor is presynaptic
    • stimulation - decreased neurotransmitter (NE) release
  • binds to a1 and a2 receptors in PNS causing agonism
  • inhibits monoamine oxidase (MOA) causing behavioral and neurotoxic effects
    • MAO catabolizes catecholamine neurotransmitters intraneuronal
  • amitraz is contraindicated in horses because it causes ileus
27
Q

What is the antidote for amitraz toxicosis? What is its mechanism of action?

A
  • a adrenergic antagonists - atipamezole, yohimbine
  • reverse bradycardia, hyperglycemia, and CNS depression
28
Q

Provide four clinical signs of adrenergic syndrome and two toxic agents that can cause them.

A
  • a adrenergic syndrome
    • hypertension, tachycardia, pale mucous membranes, mydriasis, decreased GI motility, hyperactivity
  • B adrenergic syndrome
    • weakness (hypotension), bronchodilation, hypokalemia, hyperactivity, tachypnea, depression, muscle tremors, death
  • mixed a and B adrenergic syndrome
    • hypertension, tachycardia, mydriasis, dry mucous membranes
  • toxins causing adrenergic syndromes - decongestants
    • pseudoephedrine
    • phenylephrine
    • phenylpropanolamine
    • ephedrine
29
Q

Provide four clinical signs of sympatholytic syndrome and two toxic agents that can cause them.

A
  • sympatholytic - adrenergic drugs that inhibit the SNS by affecting the release of NE or EPI
    • anti adrenergic syndrome
  • vomiting, hyperventilation, convulsion, hypotension, bradycardia or tachycardia, heart block, arrhythmias, lethargy, decreased or absent bowel sounds
  • a adrenergic antagonists
    • non specific - phentolamine, phenoxybenzamine
    • a1 specific - prazosin, doxazosin, tamsulosin
    • a2 specific - yohimbine, idazoxan
  • B adrenergic antagonists
    • non specific - propranolol, timolol, nadolol, pindolol
    • B1 specific - metoprolol, acebutolol, atenolol, esmolol
    • B2 specific - butoxamine