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Tox Exam 1 > PNS III - Neuromuscular > Flashcards

PNS III - Neuromuscular Flashcards

1
Q

Briefly discuss the physiology of the neuromuscular junction.

A
  • the neuromuscular junction is a cholinergic synapse between a motor neuron and skeletal muscle
  • action potential arrives at terminal button of motor neuron causing the opening of Ca channels
  • this causes the release of ACh which binds to nicotinic receptors on the muscle fiber
  • binding to these causes the opening of Na channels and sodium rushes back into the fiber and stimulates the action potential
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2
Q

What is the origin of the phrase ‘black widow spider’?

A
  • the female eats the male after mating
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3
Q

Name the black widow spider toxin. What is the mechanism of action of this toxin?

A
  • a-latrotoxin
  • binds to 2 neuronal receptors (neurexins, calcium independent receptor for latrotoxin [CIRL]) causing release of neurotransmitters via 2 mechanisms
    • Ca-independent and Ca- dependent
  • this inhibits presynaptic neurotransmitter reuptake
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4
Q

Differentiate the Ca-dependent and Ca-independent mechanisms of action of a-latrotoxin.

A
  • Ca dependent
    • affects ACh, GABA, glutamate
    • direct action via CIRL
  • Ca independent
    • catecholamines (dopamine, EPI, NE)
    • neurexin receptor, pore formation - Ca entry
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5
Q

Name the drugs recommended for control of muscle cramping in black widow toxicosis.

A
  • benzodiazepines (diazepam)
  • methocarbamol
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6
Q

Is there an antivenin for black widow venom?

A
  • yes, Lyovac Antivenin
  • used for high risk patients (neonates, geriatric) or those not responding to symptomatic treatment
  • be prepared to respond to anaphylactic reaction
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7
Q

Name the sources of botulinum neurotoxin toxin.

A
  • Clostridium botulinum
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8
Q

Which botulinum toxin subtype(s) most commonly affect animals and birds?

A
  • A, B, C, D - most important in animals
  • cattle - B, C, D
  • horse - A, B, C
  • avian - A, B, C, E
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9
Q

Provide the mechanism of toxicity of botulinum toxin and the resulting clinical signs.

A
  • toxins enter presynaptic nerve endings by endocytosis, light chain bonds to synaptotagmin
  • blocks release of ACh at neuromuscular junction - flaccid paralysis
  • inhibits exocytosis of ACh by cleaving proteins essential for fusion of the vesicle membrane with the neuronal cell membrane
  • clinical signs
    • sudden death progressive neuromuscular dysfunction, progressive flaccid paralysis
    • ataxia, depression, weakness of tongue and tail
    • poor reflexes of eyes and throat - mydriasis, slow pupillary light response, decreased palpebral reflex, decreased gag reflex, weak vocalization
    • ANS signs - bradycardia, vomiting, inability to swallow, ileus, constipation, ruminal atony, frequent attempts to urinate (horses)
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10
Q

Name the proteins involved in the docking of ACh vesicles at the presynaptic cell membrane. Identify the botulinum toxin subtypes that affect these proteins.

A
  • SNARE and NSF proteins
    • SNARE includes synaptobrevin (VAMP), SNAP-25, syntaxin
  • A, B, C, D, E, F, G
    • B, D, F, G - cleave synaptobrevin (VAMP)
    • A, C, E - cleave SNAP
    • C - cleaves syntaxin
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11
Q

What are the characteristic signs of botulism in foals and waterfowl?

A
  • foals - tremors, shaker foal syndrome
  • waterfowl - progressive paralysis of neck (limberneck), wings, legs
    • death by drowning
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12
Q

What is the diagnosis of botulinum toxicosis based on?

A
  • analysis of serum, GI contents, vomit, ruminal fluids, and feed for the toxin
  • mouse bioassay
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13
Q

Describe the treatment procedures for botulinum toxicosis.

A
  • decontaminate
    • emesis, gastric lavage, charcoal
  • supportive and symptomatic care
    • ventilation, physostigmine for muscle function with atropine for muscarinic signs, IV fluids, remove bad feed
  • nutritional support - hand feeding and watering
  • antitoxin if diagnosis made early
    • polyvalent (anti-B and anti-C) and monovalent (anti-B) antitoxins available for adult horses and foals and should be given ASAP
  • antibiotic - penicillin, metronidazole, amoxicillin
  • debride wounds for animals suffering from wound botulism
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14
Q

Name two tick species associated with tick paralysis in North America.

A
  • Dermacentor andersoni
  • Dermacentor variables
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15
Q

Provide the mechanism of action of tick toxins. What is the general name of these toxins?

A
  • holocyclotoxins block ACh release at neuromuscular junction and inhibit depolarization of lower motor neurons - leading to paralysis
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16
Q

How is tick paralysis treated?

A
  • remove tick, tick dip solution, support respiration in severe cases
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17
Q

What is anatoxin-a? Provide the mechanism of action of anatoxin-a including clinical signs associated with its action.

A
  • nicotinic agonist produced by blue-green algae
  • rapid onset of muscle rigidity and tremors, cyanosis, convulsion
  • paralysis and respiratory distress leading to death
18
Q

Differentiate between anatoxin-a and anatoxin-a(s) toxicoses.

A
  • anatoxin-a
    • agonist of nicotinic ACh receptors at both neuromuscular junction and neurons
    • stimulation at neuromuscular junction in weakness, respiratory paralysis, death
  • anatoxin-a(s)
    • irreversible acetylcholinesterase inhibitor in PNS
    • build up of ACh results in ataxia, seizures, respiratory arrest, death
    • ”s” - salivation
19
Q

Describe the diagnostic procedures for anatoxin-a toxicosis.

A
  • evidence of ingestion of blue-green algae and compatible clinical signs
  • decreased cholinesterase activity in blood and plasma
  • examine water for appropriate algae type
  • mouse bioassay with suspect water
  • identify toxin in water by HPLC or GC-MS
20
Q

Why is it difficult to treat anatoxin-a toxicosis?

A
  • there is no antidote
  • onset is so rapid that treatment may not be possible
21
Q

Give 3 examples of ionophores. Provide the mechanism of action of ionophores.

A
  • sources - coccidiostats (parasite treatment), growth promotants
    • monesin - rumesin, coban
    • lasalocid - bovatec, avatec
    • narasin - maxiban, monteban
    • salinomycin - biocox, saccox
    • laidlomycin propionate - cattlyst
  • binds and preferentially transports cations across cell membranes
  • net effect is ion imbalance (Na, K, Ca, H) and deficits in the function of excitable tissues (neurons and muscles)
  • mitochondrial ion imbalance leads to decreased ATP
22
Q

Name the body systems most affected during ionophore toxicosis.

A
  • neurologic
  • muscular
  • GI
  • cardiovascular
23
Q

Describe the treatment of ionophore toxicosis.

A
  • no specific antidote
  • decontamination
    • emesis in dogs and cats, charcoal, cathartic
  • supportive therapy
    • IV fluids, minimize stress
  • antioxidants
    • vitamin E, selenium
24
Q

In which geographic region of the US does larkspur poisoning commonly occur?

A
  • western US
25
Q

What are the toxic agents in larkspur?

A
  • diterpene alkaloids
    • methyllcaconitine (MLA)
    • 14-deacetylnudicauline (DAN)
  • DAN is more toxic, but MLA occurs in greater quantities
26
Q

Which domestic animal species is most susceptible to larkspur toxins? Why are sheep used for biological control of larkspur?

A
  • cattle are most susceptible
  • sheep used for biological control becase they can tolerate 4-5x the amount lethal to cattle
    • can eat it without getting sick and trample stalks
27
Q

Provide the mechanisms of toxicity of larkspur toxins?

A
  • block nicotinic receptors of ACh at neuromuscular junctions and in CNS (MLA)
28
Q

Describe the diagnostic procedures for larkspur toxicosis.

A
  • evidence that animals have grazed it
  • plant presence in ruminal contents
  • presence of bloat and ruminal contents in bronchi
29
Q

Describe the treatment of larkspur toxicosis.

A
  • decontaminate - charcoal, cathartic
  • move animals to new pasture
  • give cholinesterase inhibitors (physostigmine)
  • avoid stress and excitement
  • relieve bloat by stomach tube or trocarisation
  • antibiotics for inhalation pneumonia
30
Q

In which geographic region of the US are locoweeds most commonly found?

A
  • pacific northwest
31
Q

Name the toxins present in locoweeds. Which of these toxins cause neuromuscular toxicity?

A
  • nitroptopanol glycosides (miserotoxins)
    • hydrolyzed to nitrotoxins by rumen microbes
  • nitrotoxins - 3-NPOH, 3-NPA
    • 3-NPOH is absorbed and metabolized in the liver to 3-NPA
    • 3-NPA is responsible for toxicity
    • if ingested as 3-NPA, most of it is biodegraded in the GI tract, so there is a lower toxicity
    • 3-NPA causes axonal degeneration in the spinal cord
  • indolizidine alkaloid (swainsonine) and selenium
    • CNS and skin toxicity
32
Q

What is nitrotoxicosis? Provide the clinical signs of this condition.

A
  • nitrotoxicosis - the clinical signs associated with nitrotoxin ingestion and toxicosis
  • acute
    • constipation, ataxia, staggering gait, recumbency, death from cardiac-respiratory failure
  • in most cases, signs are gradual
    • dyspnea, salivation, weakness, muscular spasms, docile appearance, goose-stepping, cracker heels, fetlock knuckling, posterior paresis/paralysis
    • loss of body condition as toxicosis progresses
33
Q

Identify a locoweed toxin and provide its mechanism of action.

A
  • 3-NPA inhibits the krebs cycle leading to decreased energy (ATP) production and loss of cellular homeostasis
  • axonal degradation in spinal cord, hypotension via vasodilation and cardiodepression
34
Q

Describe the diagnostic procedures for nitrotoxicosis.

A
  • clinical signs, evidence of plant consumption
  • gross and histo respiratory and neuro lesions
  • identification of NPA and NPH in plasma and serum by HPLC
35
Q

Describe the treatment of nitrotoxicosis.

A
  • withdraw animals from source of plant
  • cattle will avoid locoweed when other forage available
  • toxin concentration decreases rapidly as plants mature and undergo senescence
36
Q

Name two sources of tremorgenic mycotoxins.

A
  • tremorgenic forages - bermuda grass, ryegrass, dallis grass
  • moldy cheese, bread, walnuts, and pasta
  • garbage
37
Q

Identify the mycotoxins referred to as tremorgens and the fungi that produce them. Which of these mycotoxins affect dogs?

A
  • dogs
    • Penicillium crustosum produces penitrem A
    • Penicillium roquefort produces roquefortine C
  • livestock
    • Acemonium lolii produces lilitrem B
    • Claviceps paspali produces paspalitrem
38
Q

Provide the mechanisms of action of tremorgens and the main clinical signs of toxicosis.

A
  • tremorgens cause presynaptic release of ACh and prolong depolarization at the neuromuscular junction
    • facilitate transmission at motor end plate
  • reduce levels of GABA and glycine
    • CNS stimulation
  • cerebral vasoconstriction
    • leads to anoxia and CNS signs
  • opisthotonus
    • spasm of muscles causing backward arching of head, neck, and spine
39
Q

Describe the decontamination procedures for tremorgenic mycotoxicosis in dogs.

A
  • asymptomatic animals
    • emesis, activated charcoal, cathartic
  • symptomatic animals
    • sedate/anesthesia and perform gastric lavage, then give activated charcoal and cathartic
40
Q

Describe the treatment of tremorgenic mycotoxicosis in dogs.

A
  • decontaminate then symptomatic and supportive therapy
  • diazepam to control agitation, seizures, muscle tremors
    • in patients that do not repsond to diazepam use methocarbamol or barbiturate
  • IV fluids
41
Q

Describe the treatment of tremorgenic mycotoxicosis in livestock.

A
  • replace contaminated forage and keep animals in a quiet place until recovery

Tox Exam 1 (6 decks)

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