PNS II - ANS II Flashcards
Provide the locations of nicotinic receptors. What type of receptors are they? How do they function?
- 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
What is the effect of nicotine on the parasympathetic ganglia?
- stimulates then blocks them
Describe how to treat nicotine toxicosis in a dog.
- 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
What is used to acidify urine? Why is urine acidification useful in treating nicotine toxicosis?
- ammonium chloride - hastens excretion
Name three toxic compounds found in tobacco. What are their toxic effects?
- pyridine alkaloids (nicotine)
- teratogens (anabasine, anatabine)
- polycyclic aromatic hydrocarbons (PAHs) on combustion - carcinogenic, mutagenic, teratogenic
What is the most appropriate method for decontamination following ingestion of tobacco plants and why?
- emesis, enterogastric lavage, activated charcoal
- charcoal is most common as most cases are livestock
- in livestock decontamination is limited to charcoal
What is the purpose of administering atropine to treat tobacco plant toxicosis?
- to treat parasympathetic effects
Name three toxins found in poison hemlock. What is the general name of these toxins and how do they act?
- 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
Which of the toxins in poison hemlock is most toxic?
- y-coniceine
What is the characteristic smell of urine and breath of animals with poison hemlock toxicosis?
- musty and mousy, smells like rotting cardboard
Name the toxins found in lupine. What are the mechanisms of action of these toxins? What is lupinosis?
- quinolizidine alkaloids - nicotinic
- piperidine alkaloids - nicotinic
- anagyrine - teratogenic
- lupinosis - acute liver atrophy due to eating lupines
Which domestic animal species is most commonly affected by lupine poisoning and why?
- sheep - they will eat anything
Name two US states in which lupine toxicity is prevalent.
- montana
- idaho
- utah
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.
- 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
Describe how to treat poison hemlock or lupine toxicosis.
- nonspecific - charcoal, gastric lavage, assisted respiration
- avoid overexcitement and stress
Name a toxin present in lobelia and its mechanism of action.
- nicotinic alkaloids - lobeline, lobelidine
Name the toxin found in golden chain and its mechanism of action.
- nicotinic quinolizidine alkaloid - cytisine
Provide the mechanism(s) of toxicity of levamisole (imidazothiazole) .
- 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
Describe how to treat levamisole toxicosis.
- no antidote
- just supportive and symptomatic care
- atropine ca be used to help control some cholinergic signs
Why is decontamination not possible or advisable for poisoning by bronchodilators?
- rapid absorption and onset of clinical signs - don’t have time
- emesis only possible within 15-30 minutes of ingestion
Describe how to treat poisoning due to bronchodilators.
- supportive therapy for clinical signs
- IV fluids for hypotension
- diazepam for hyperactivity
- IV propranolol for tachycardia
Name a drug used to treat tachycardia.
- propranolol
What are the clinical signs of β-adrenergic syndrome (decongestant toxins)?
- weakness
- tachycardia
- vasodilation (hypotension)
- bronchodilation
- hypokalemia
- hyperactivity
- tachypnea
- depression
- muscle tremors
- death
Describe how to treat poisoning due to decongestants.
- 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
Identify two drugs that can be used and one that should not be used to control seizures following poisoning by decongestants.
- yes use - acepromazine, chlorpromazine
- no use - diazepam (can make dogs more agitated)
Provide the mechanism(s) of toxicity of amitraz (found in mange, mite, tick, and lice treatments and pesticides). Why is amitraz contraindicated in horses?
- 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
What is the antidote for amitraz toxicosis? What is its mechanism of action?
- a adrenergic antagonists - atipamezole, yohimbine
- reverse bradycardia, hyperglycemia, and CNS depression
Provide four clinical signs of adrenergic syndrome and two toxic agents that can cause them.
- 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
Provide four clinical signs of sympatholytic syndrome and two toxic agents that can cause them.
- 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
