Term
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Definition
| poisoning of the nervous system |
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Term
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Definition
| compounds which occur naturally in the environment (produced by living organisms) |
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Term
| what are xenobiotic agents? |
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Definition
| man made neurotoxic compounds |
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Term
| what are the gross manifestations of neurotoxicity? |
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Definition
| physical s/s and mental s/s |
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Term
| if there is suspicion of neurotoxic syndrome, what 3 areas need to be addressed? |
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Definition
| clinical, neurophysiological and psychological |
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Term
| what does the clinical exam consist of? |
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Definition
| fatigue, memory (may need to cross check w/fam member), depression, sleep, muscle strength, h/a, skin rashes, vision, nausea, taste, urination and breathing |
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Term
| what does the neurophysiological exam consist of? |
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Definition
| gait/posture, cranial nerves, motor function, tendon reflexes, and sensory evaluation |
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Term
| what does the psychological exam consist of? |
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Definition
| level of consciousness, attention, prevailing mood, learning/memory, language and cognitive functions |
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Term
| what does neurotoxicity need to be differentiated from? |
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Definition
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Term
| how can an uncertain etiology for a possible neurotoxicity be r/o? |
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Definition
| environmental sampling, evidence of exposure, biological indicators of absorption and demographic factors |
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Term
| what is the cellular response to injury? |
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Definition
| swelling of the cell and cytoplasmic organelles, dispersion of the RER, swelling of the nucleolus, decrease in cytoplasmic pH, decrease in oxidative enzymes, and decrease in protein synthesis (not able to repair itself) |
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Term
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Definition
| inadequate O2 supply w/adequate perfusion. |
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Term
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Definition
| inadequate O2 supply due to inadequate perfusion |
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Term
| what is cytotoxic anoxia? |
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Definition
| adequate O2 supply w/adequate perfusion - but a decrease in cell metabolism |
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Term
| where does neural damage occur? |
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Definition
| w/an insult at the cell body, the processes (axons/dendrites), or supporting structures (myelin/glia) |
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Term
| what is functional damage? what are the degrees of this? |
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Definition
| residual loss of function following a neural insult it occurs in the following degrees: *permanent damage (enough cell death = loss of function), *functional recovery (remaining cells maintain function/other cells develop function), and *reversible damage (new growth). |
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Term
| what neurotoxic agents can cause anoxia? |
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Definition
| barbiturates (OD: prolonged coma and degeneration of neurons [but not that bad b/c of reduced demand during coma]), carbon monoxide (acute: degeneration of CNS gray matter, secondary: degeneration of white matter), and cyanide (degeneration of gray matter). |
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Term
| what neurotoxic agents damage myelin (MS-like)? |
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Definition
| isoniazid (peripheral neuritis), lead (adults: segmental myelin degeneration, children: encephalopathy/central demyelinization/cerebral edema), NO (often used in dental offices, can cause combined system disease/pernicious anemia and knocks out posterior columns/corticospinal pathway) |
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Term
| what neurotoxic agents can cause peripheral axonopathies? |
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Definition
| alcohol (degeneration of distal segments of motor neurons), carbon disulfide (3 phases: 1st polyneuritis, 2nd tremor, 3rd psychosis), organophosphates (affect ACh: cause peripheral axon degeneration, weakness, ataxia), triethyltin (myelin degeneration and spasticity), and n-hexane (axon degeneration, polyneuropathy of motor functions, severe muscular atrophy) |
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Term
| what neurotoxic agents damage the cell? |
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Definition
| organomercurials (damages the DRG/CNS = vision/hearing/speech/balance/movement/cognitive problems) and vinca alkaloids (damage to cell cytoplasm and motor nerve atrophy) |
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Term
| which are the neurotoxic agents which affect the neuromuscular junction? |
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Definition
| botulinum toxin (binds to presynaptic ACh terminal), tetrodotoxin (blocks all Na+ channels, can block all nerve transmission [puffer fish]), batrachotoxin (increases permeability, causes greater flow of Na+ and thus membranes stay depolarized), DDT (keeps Na+ channels open longer = tremors/convulsions), pyrethrins (Na+ channels held open longer - but this is rapidly biotransformed so not as poisonous for humans), nicotine (ganglionic stimulation, h/a, disturbed hearing/vision, weakness, chronic convulsions, breathing cessation), and lead (competitively inhibits Ca+ - keeps NT from release and muscle contractions from occurring). |
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Term
| what are neurotoxic agents which cause localized CNS lesions? |
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Definition
| carbon tetrachloride (increases the size of astrocytes in basal ganglia/cerebellum), glutamate (increases intracellular Ca++/Na+ = seizures/excitotoxicity), organic mercury (atrophy/cell depletion esp in the granular layer of the cerebellum), manganese (decreased DA synthesis), and MPTP (kills catecholaminergic neurons [esp DAnergic]) |
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Term
| what does management of a neurotoxin-exposed pt consist of? |
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Definition
| stabilize (ABCs, IV dextrose/thiamine/naloxone and O2), identify (hx and exam), minimize (remove pt from source and emesis/lavage/cathartics if necessary), antidote, excrete (activated charcoal, forced saline diuresis, alkaline diuresis, hemodialysis, and hemoperfusion), and support (manage cardiac arrhythmias, seizures, ionic imbalance, pH imbalance) |
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Term
| what are common neurotoxin-antidote combinations? |
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Definition
| deferoxamine-iron, ethanol-ethylene glycol/methanol, naloxone-opiates, D-penicillamine-arsenic/lead/mercury, pralidoxime-organophosphates, and antivenin-pit vipers |
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Term
| what can be used as an antidote for most metal poisonings? |
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Definition
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Term
| is there an antidote to methane/ethane/propane/butane toxicity (convulsions)? |
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Definition
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Term
| what does gasoline/kerosene toxicity present as? |
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Definition
| similar to drunken behavior. no known antidote. |
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Term
| what does toluene (glue) toxicity present as? |
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Definition
| euphoria, hallucinations, seizures, coma, optic neuropathy, ataxia and quadriparesis. no known antidote. |
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Term
| what is the antidote for methanol and ethylene glycol? |
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Definition
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Term
| what is the main difference between the insecticides: organochlorines (DDT/chlordecone) and organophosphates (parathion/paraoxon/malathion)? |
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Definition
| the organochlorines have no antidote but pyridine-1-aldoxime methyl chloride (2-PAM) and atropine can be used for the organophosphates. the symptoms are similar for both however. |
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Term
| what is the antidote for cyanide? |
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Definition
| amyl nitrate (which can produce priapism itself) |
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Term
| what are the most commonly used herbicides which have neurotoxic effects? |
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Definition
| chlorophenoxy compounds: 2,4,-D and 2,4,5-T - affects farmers. |
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Term
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Definition
| a non-neurotoxic herbicide which can cause dysphagia. not used in the US, but in mexican mj crops |
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Term
| what are the rodenticides? |
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Definition
| warfarin, red squill, sodium fluoroacetate, and strychnine (CNS excitation, antagonizes the glycine inhibitory receptor in the spinal cord = tetanus like rigidity, convulsions) |
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Term
| what are the phytotoxins? |
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Definition
| castor bean (little kids may eat these if on a necklace), water hemlock (rapid death, dilated pupils, delirium convulsions), mistletoe (seizures, death), mushrooms group 1 (acetaldehyde dehydrogenase inhibitor activity [etoh interaction], death angel), mushrooms group 2 (hallucinations/anticholinergic, antidote: physostigmine), mushrooms group 3 (seizures, delirium, hyperreflexia, antidote: pyridoxine), mushrooms group 4 (muscarine - parasympathetic stimulation, cholinergic poisoning, blurred vision, antidote: atropine), mushrooms group 5 (ANS symptoms), mushrooms group 6 (psilocybin - hallucinations), azalea, rhododendron, and apple/choke cherry/peach/apricot/plum seeds/pits (contain cyanide, antidote: amyl nitrite) |
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