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Boards: Neurology + Ophthalmology > Neuro Emerg 28: Neurological toxicities > Flashcards

Neuro Emerg 28: Neurological toxicities Flashcards

1
Q

Are cutaneously absorbed toxins usually hydrophilic or lipophilic?

A

lipophilic

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2
Q

At what time frame post toxin ingestion is colonic lavage indicated?

A

4-6 hours after ingestion

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3
Q

Name two toxins tracking more rapidly through the GI tract, indicating earlier colonic lavage

A
  • organophosphates
  • carbamates
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4
Q

Name the types of toxins that are not absorbed by activated charcoal

A
  • Alcohols
  • strong acids or alkalis
  • dissociable salts and metals (e.g., iron, lithium)
  • petroleum products
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5
Q

Explain the MOA of sorbitol

A

cathartic –> decreases transit time of toxins through GI tract –> reduces toxin absorption

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6
Q

What are the two broad categories of neurotoxins?

A
  • neuroexcitatory
  • neuroinhibitory
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7
Q

What is the mechanism of action of bromethalin toxicity

A
  • uncoupling of oxidative phosphorylation –> less ATP available
  • –> decreased function of Na-K-ATPase pumps –> increased intracellular Na
  • water accumulating in cellls –> cerebram edema –> increased ICP
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8
Q

What are the two different clinical pictures of bromethalin toxicity?

A

High dosages –> acute hyperexcitability (2-24 hours after exposure) –> seizures, hyperaesthesia, tremors

More common –> delayed ataxia, paresis, decreased conscious proprioception (1-3 days after exposure)

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9
Q

What class of medication is ivermectin?

A

avermectins or macrocyclic lactones

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10
Q

What breeds are more sensitive to ivermectin toxicity and why?

A

Collies and related breeds (Australian Shepherds, Border Collies, Shetland Sheepdogs, other herding dogs)

MDR1 mutation –> inefficient blood-brain barrier efflux pumps –> increased accumulation of the drug in the CNS

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11
Q

What is the mechanism of action of macrocytic lactones?

A

agonist for GABA(A)-gated chloride channels in the CNS

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12
Q

Are benzodiazepines contraindicated in ivermectin toxicity?

A

Historically thought to be contraindicated - due to drugs proximity to same GABA binding site

now postulated that this is actually not the case - can use benzos

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13
Q

What is the mechanism of action of lead toxicity

A
  • leads binds to sulfhydryl groups and interferes with sulfhydryl-containing enzymes –> interference in haem synthesis, RBC fragility, basophilic stippling
  • neurotoxic mechanisms unclear, proposed: GABA-interferences, capillary damage leading to cerebral hemorrhage + cerebral necrosis, Ca-inhibition, dopamine-interference
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14
Q

What would you see on a blood smear cytology in case of lead toxicity

A

nucleated red blood cells and basophilic stippling

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15
Q

Name chelation options for lead toxicity

A

Succimer PO
Ca-EDTA SQ or IV
D-Penicillamine

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16
Q

Why is MgSO4 indicated in lead toxicity

A

PO –> cathartic and binds to lead forming insoluble lead sulphate, that cannot be absorbed

17
Q

What is the MOA of methaldehyde toxicity

A
  • decreases levels of GABA - inhibitory neurotransmitter
  • increased monoamine oxidase activity
  • decreased noradrenaline and serotonin levels (5-HT)
18
Q

What is the MOA of chocolate toxicity?

A

methylxanthine (contains theobromine)
phosphodiesterase inhibitor –> increases levels of cyclic AMP/cAMP
–> increased IC Ca levels –> neuromuscular excitability + positive inotropic effects

19
Q

What are the most common tremorgenic mycotoxins?

A
  • Penitrem A
  • Roquefortine
20
Q

What is the MOA of tremorgenic mycotoxins?

A
  • unknown, but glycine inhibition is suspected
21
Q

What is the MOA of nicotine toxicity?

A
  • low doses –> acts on nicotinic acetylcholine receptors –> neuroexcitatory
  • higher doses –> neuromuscular blockage, persistent depolarization
  • stimulates the emetic chemoreceptor trigger zone
22
Q

What medications should be avoided in nicotine toxicity?

A

H2-blockers or PPIs – alkalination of the stomach increases absorption

23
Q

What is the MOA of organochloride toxicity?

A
  • unknown
  • suspected: opening on Na channels in neurons –> repetetive firing of action potential
  • suspected: GABA inhibition
24
Q

What is the mechanism of action of organophosphate and carbamate toxicity and what are the three different groups of clinical signs?

A

inhibits ACh-esterase –> ACh accumulates at cholinergic synapses

CS:
* Cholinergic signs (SLUDGE + bronchospasms and respiratory signs)
* CNS toxicity
* nicotinic toxicity (muscle tremors and weakness)

25
Q

What are the three different types of organophosphate toxicity clinical presentation?

A

1) Acute toxicity
2) Intermediate syndrome
3) organophosphate-induced delayed neuropathy

26
Q

How do organophosphates and carbamate differ in their mechanism of toxicity?

A

Organophosphates bind permanently to AChE
Carbamates bind reversible to AChE - shorter duration of CS

27
Q

Explain specific treatments for organophosphate and carbamate toxicity

A
  • Atropine for cholinergic signs
  • 2-PAM (Pralidoxime) –> reactivates phosphorylated cholinesterase (for severe nicotinic signs)
28
Q

What is the MOA fo permethrin toxicity?

A
  • slow the opening and closing of voltage-gated Na-channels –> leads to repetetive impulse firing
29
Q

What is the MOA of strychnine?

A

glycine inhibition –> glycine is an inhibitory neurotransmitter
prevents the release of glycine from Renshaw cells

30
Q

What is the MOA of metronidazole neurotoxicity?

A

mechanism of action unknown
suspected: inhibition of neuronal protein synthesis by binding to RNA + thiamine antagonism

31
Q

List 5 types of toxins found in snake venom

A
  1. Neurotoxins
  2. Procoagulants
  3. Anticoagulants
  4. Hemolysins
  5. Myotoxins
32
Q

Why should you avoid hypothermia in permethrin toxicity?

A

hypothermia may enhances intracellular Na movement –> worsens clinical signs

Boards: Neurology + Ophthalmology (14 decks)

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