28 - Neurotoxins Flashcards
non specific vs. specific toxins: what are they important for
non specific: important for public health. specific: more important scientifically; tell us something about neuronal function. some have therapeutic use
lead poisoning: aka? interferes with? particularly toxic to?
plubism, saturnism, painter’s colic: interferes with development of NS. particularly toxic to children and fetuses
lead poisoning: what disorders? symptoms?
learning + behavioural disorders. abdominal pain, headache, irritability, muscle weakness, coma, seizures, death
lead mechanisms of action: 3?
interferes with NT release, probably by competing with Ca. blocks blutamate NMDA-Rs. causes demyelination.
lead: what level is toxic? therapy?
any detectable level is toxic. sometimes can be treated with disodium calcium edetate: chelation therapy.
disodium calcium edetate
chelation therapy for lead poisoning
mercury poisoning; aka? symptoms
acrodynia, pink disease, minimata disease. peripheral neuropathy, skin discoloration, edema, ataxia, blindness, deafness, convulsions, dementia, paralysis, muscle weakness
mercury blocks degradation pathway of? so causes?
catecholamines = hyperhidrosis aka increased sweating, tachycardia, hypertension
mercury inactivates?
inactivates s-adenosyl methionin, which is necessary for CA catabolism by COMT
mercury and myelin? what is esp toxic?
affects myelin: leads to neuronopathy where whole neuron dies. organic salts like methylmercury are esp toxic.
2 examples of organophosphates
malathion. soman. nerve gas, insecticides
what do organophosphates do
irreversible block of AChase = similar effects to direct acting cholinergic agonists
4 effects of organophosphates
eyes = miosis, decreased IOP, myopia. respiration = bronchiole constriction, increased secretion. increased gut mobility and bladder stimulation. heart: bardycardia, decreased CO
organophosphates: 3 effects on neuromusc transmission?
increased strenth of contraction. higher conc = muscle fasciculation. highest conc = depolarizing neuromusc blockade.
2 effects of nerve gas/insecticide poisoning
cardiac arrest. fluid in lungs + bronchioconstriction. blockade of respiratory skeletal muscle contraction
organosphosphate poisoning: treat with what, which will do what?
atropine: antagonizes muscarinic effects, but not effects at NMJ
organosphophates also produce? aka? delayed how long?
OPIDN: induced delayed neuropathy, aka dying back neuropathy. delayed 7 - 10 days after exposure.
OPIDN: what regenerates? what doesn’t? symptoms look like?
peripheral NS tracts regenerate. CNS/motor tracts don’t. symptoms look like MS.
MPTP: toxic? metabolism? which cells and enzyme?
itself not toxic, but crosses BBB and is metabolized into toxic cation MPP+ by glial cell MAO-B
MPP+ effects?
taken up by DA transporter; kills DA producing neurons in SN
MPP+ mechanism of action?
interferes with complex 1 of ETC, affects mitochondrial metabolism = buildup of free radicals
MPTP treatment
MPTP not directly harmful, so can mitigate poisoning via MAO-B inhibitors like selegiline
selegiline
MAO-B inhibitor, can treat acute MPTP poisoning
