· Numbers table
· Purpose
· Localised toxicity
· CNS toxicity
· CVS toxicity
· Final answer
|
Concentration presented |
Toxic plasma concentration |
Toxic subcutaneous dose |
Cocaine |
5% = 50mg/mL |
0.5mcg/mL |
2mg/kg = 140mg = ~3mL |
Lignocaine |
2% = 20mg/mL |
5mcg/mL |
7mg/kg w adr = 490mg = ~25mL |
Adrenaline |
1:100k = 10mcg/mL |
? |
? |
|
Mechanism of action |
Function |
Cocaine |
Inhibit VdNaC Monoamine reuptake Norad : dopamine : serotonin 5:3:2 |
Local anaesthetic Vasoconstriction |
Lignocaine |
Inhibit VDNaC |
Local anaesthetic |
Adrenaline |
α1 agonist |
Vasoconstriction |
Cocaine |
· Septal necrosis possible even with single use |
Lignocaine |
· Rare |
Adrenaline |
· Necrosis if large amount of drug |
LAST |
· Cause: inhibition of neuronal VDNaC · Initial excitation (block inhibitory interneurons): paraesthesia, peri-oral tingling, vertigo, tinnitus, inattention, slurred speech, muscle twitching, seizure · Then inhibition: coma, apnoea |
Cocaine (non-LAST) |
· Cause: dopamine and serotonin reuptake inhibition · Euphoria, delirium, seizure |
LAST |
· Inhibit VDNaC;, also VDKC and VDCC at higher concentration · ECG “pulled apart” (long Q, wide QRS), tachyarrhythmia, VF arrest · First phase: ↑HR, ↑mAP · Second phase: myocardial depression, ↓mAP · Terminal phase: vasodilatation, arrhythmia, arrest |
Cocaine (non-LAST) |
· NRI, ↑ICF Ca2+ · Tachyarrhythmia, ↑mAP, coronary vasospasm, ischaemia, arrest |
Adrenaline |
· ↑ICF Ca2+ -> tachyarrhythmia, ischaemia, stroke, arrest |
Considerations |
· Nasal mucosa is highly vascular -> ↑absorption rate · Vasoconstriction by cocaine/adrenaline -> ↓ absorption rate -> ↓peak plasma concentration · Interaction unclear: ? synergistic for inducing seizures |
How much |
· ? Cocaine 1mL · ? Lignocaine with adrenaline 5mL (I have no idea. Suggestions for a definitive answer are welcome) |
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