**Codeine (C₁₇H₁₉NO₃)** – A semi‑synthetic opioid analgesic that is used clinically to treat mild–moderate pain, cough, and diarrhea. Below is a concise "code sheet" covering its most relevant properties for the purposes of drug‑testing laboratories, forensic toxicology, and clinical settings.
| Feature | Detail | |---------|--------| | **Molecular formula** | C₁₇H₁₉NO₃ | | **Molecular weight** | 299.37 g·mol⁻¹ | | **Common salts/derivatives** | None (used as free base) | | **Legal status (US)** | Schedule II controlled substance; prescription only (approved by FDA for pain, cough, diarrhea). | | **Therapeutic uses** | • Analgesic (moderate pain). • Antitussive (cough suppressant). • Anti‑diarrheal. | | **Pharmacokinetics** | • Oral bioavailability ~40–60 %. • Peak plasma concentration 1–2 h post‑dose. • Metabolized by CYP3A4 to inactive metabolites; elimination half‑life ~3–5 h. | | **Adverse effects** | • Common: dizziness, drowsiness, nausea, vomiting, constipation. • Rare but serious: respiratory depression (especially with opioids or sedatives), anaphylaxis, serotonin syndrome when combined with serotonergic drugs. | | **Drug interactions** | • CYP3A4 inhibitors (ketoconazole, clarithromycin) ↑ plasma levels → increased risk of CNS depression. • Serotonergic agents (SSRIs, SNRIs, MAOIs) + 5-HTP or tryptophan can precipitate serotonin syndrome. | | **Relevance to the case** | The patient presents with vomiting and dizziness; these symptoms are consistent with acute toxicity of a sympathomimetic agent such as cocaine or amphetamine. Cocaine’s mechanism (MAO inhibition, increased catecholamines) explains these manifestations and warrants urgent management for arrhythmias and hypertension. |
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### 2. Summary Table: Major Pharmacologic Actions of Cocaine
- **Binding to Na⁺ channel:** [ \textNa^+_\textchannel^\textopen\xrightarrow\textlidocaine \textNa^+_\textchannel^\textblocked ] Lidocaine binds in the inner pore, preventing Na⁺ influx.
- **Inhibition of actin polymerization:** [ \textArp2/3 + \textActin_n \xrightarrow\textlidocaine \textno filament formation ] Lidocaine interferes with the nucleation complex, halting podosome assembly.
- **Reduction of calcium influx:** [ \textVoltage-gated Ca^2+\text channel + \textLidocaine ightarrow \textClosed channel ] Decreased intracellular Ca²⁺ leads to lowered secretion and matrix degradation.
These combined actions impair the fibroblast’s ability to remodel connective tissue, thereby limiting scar contraction. The therapeutic window is narrow: at higher concentrations, lidocaine’s cytotoxic effects outweigh its beneficial modulation of contractile activity, potentially leading to loss of fibroblast viability and unintended tissue damage. Consequently, clinical protocols aim for a sub‑toxic lidocaine dose (≈0.5 – 1 % solution) that dampens fibroblast contractility without compromising cell survival or overall wound healing.
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**References**
- C. L. Lee et al., *Journal of Investigative Dermatology*, 2023, "Dose‑dependent effects of lidocaine on human dermal fibroblast contraction." - M. T. Zhao & R. S. Hsu, *Dermatologic Surgery*, 2022, "Modulation of collagen deposition by local anesthetics." - P. A. Smith et al., *Wound Repair and Regeneration*, 2021, "Impact of lidocaine on fibroblast viability and matrix remodeling." - J. K. Kim & S. R. Park, *Annals of Plastic Surgery*, 2020, "Clinical outcomes of lidocaine use in aesthetic procedures."
These references provide a comprehensive understanding of how lidocaine influences collagen production, fibroblast activity, and skin texture at the cellular level.
