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Toxicology Question

Discussion in 'Medical Toxicology (MD, DO, PharmD)' started by Sparda29, Jan 30, 2011.

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  1. Sparda29

    Sparda29 En Taro Adun Gold Donor

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    So my toxicology professor told us that the best drugs to commit suicide with would be Tricyclic Antidepressants. I'm trying to figure out, why is it these over CNS depressants?
  2. All4MyDaughter

    All4MyDaughter SDN Mommystrator Staff Member Administrator SDN Senior Moderator Lifetime Donor Partner Organization

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    Cardiovascular and neurologic toxicity. Narrow therapeutic index.
  3. Aznfarmerboi

    Aznfarmerboi Senior Member

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    Also, there is really no treatment for Tricyclic antidepressants. However, I dont know if the pain and agnony is worth it...
  4. Ackj

    Ackj

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    I've always heard these are the easiest way since you first fall asleep and then you don't even notice the heart block. Plus there's no real antidote either.

    IV barbiturates probably wouldn't be a bad choice, if not for the difficulty administering them. You pass out before you can push the plunger all the way down :laugh:
  5. PharmDstudent

    PharmDstudent

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    Nick Drake died this way.
  6. nafcillin

    nafcillin

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    sick topic
  7. njac

    njac Senior Member

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    Relatively quick, very effective. Not so peaceful until you get through the anticholinergic psychosis though.

    But we do have an antidote. It covers two mechanisms for reversing toxicity. What is it and what are the mechanisms?
  8. UMN_MJS_2010

    UMN_MJS_2010 MJ

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    physostigmine....

    but why is everyone so scared of using it? i know why, but wondering if anyone else knows the story behind the (false) feeling that it is a bad drug for TCA/anticholinergic o/d ....
  9. njac

    njac Senior Member

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    Not my first choice. Or fourth.
  10. PharmDstudent

    PharmDstudent

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    Activated charcoal if it's early enough, NaBicarb for acidosis, lidocaine for arrythmia, and dopamine for heart block or hypotension.
  11. UMN_MJS_2010

    UMN_MJS_2010 MJ

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    why not? how much toxicology experience do you have?

    ok i'll bite, how about high dose insulin?
  12. njac

    njac Senior Member

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    Why is norepi preferable to bicarb in tca-associated hypotension, particularly if pt on tca chronically?
  13. UMN_MJS_2010

    UMN_MJS_2010 MJ

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    in my experience working within a tox service at a level 1 trauma hospital, activated charcoal is rarely used for several reasons but mostly due its risk for aspiration and lack of accurate information about actual timeline of ingestion to presentation (unless it is witnessed)...
  14. PharmDstudent

    PharmDstudent

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    Supposedly due to CNS depression, it can take longer to digest.
  15. njac

    njac Senior Member

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    I'll get back to your physo question when I'm not finishing up some stuff for a meeting... But I think this is a great discussion point.

    While younger toxicologists are quick to avoid AC for the above reasons - what is the actual incidence of charcoal aspiration or charcoal empyema? With an anticholinergic o/d and possible (probable?) coingestants, what would one dose of AC hurt?
  16. njac

    njac Senior Member

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    How does altered mental status affect absorption
  17. UMN_MJS_2010

    UMN_MJS_2010 MJ

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    Here is an interesting article to consider when discussing the treatment of TCA overdose... It was published by the group I worked with and seems to offer a promising treatment modality for the future. I know its a case report but there are many more where this came from but are simply unpublished as of yet.

    Clin Toxicol (Phila). 2009 Apr;47(4):303-7.
    High dose insulin in toxic cardiogenic shock.

    Holger JS, Engebretsen KM, Marini JJ.

    Department of Emergency Medicine, Regions Hospital, St. Paul, MN 55101, USA.
    Abstract

    OBJECTIVE: To report the successful use of high dose insulin (HDI) in previously unreported insulin dosing ranges in a patient with severe myocardial toxicity due to an amitriptyline and citalopram overdose.

    CASE REPORT: A 65-year-old female presented in respiratory arrest, which was followed by bradycardic pulseless electrical activity after ingesting multiple medications. After a prolonged resuscitation, the patient was maintained only on infusions of norepinephrine (40 mcg/min), vasopressin (4 units/h), insulin (80 units/h), and sodium bicarbonate. Due to a deteriorating clinical condition and limited prognosis, the insulin infusion was titrated incrementally upwards to 600 units/h (6 units/kg/h) over a 5 h time period while simultaneously completely weaning off both vasopressors. She developed brisk pulses and warm extremities, and her cardiac output nearly tripled. After 2 days of stabilization the insulin was slowly tapered, and the patient recovered.

    DISCUSSION: HDI as a single cardiovascular agent significantly improved clinical and cardiovascular parameters after the failure of vasopressor therapy in severe cardiovascular toxicity. Higher doses of insulin than previously recommended may be needed in toxic poisonings when severe myocardial depression is present.
  18. UMN_MJS_2010

    UMN_MJS_2010 MJ

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    kinda what i was thinking.... :confused:
  19. njac

    njac Senior Member

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    Nice case! Did they consider intralipids?
  20. UMN_MJS_2010

    UMN_MJS_2010 MJ

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    not in this case but they have attempted lipid as a last resort in other cases where most if not all other options have been exhausted... i think it too is a promising treatment alternative to consider but should be chosen based on the particular overall clinical picture. this group is focusing on HDI have a pretty decent size NIH grant to investigate its use. would be curious to see the cost comparison between the two modalities, insulin and dextrose are pretty cheap... i thought lipid emulsion was a little on the pricey side. could be wrong thought...
  21. eeyore spice

    eeyore spice

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    I disagree too. They wouldn't be the most painless, the fastest, or guaranteed to kill you, though if someone already has a script, they'd be readily accessible.
  22. PharmDstudent

    PharmDstudent

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    I don't know anything about that. Maybe drunk people? Tricyclics are highly lipophilic, so please, enlighten me. The source specifically talked about delayed gastric emptying.
  23. UMN_MJS_2010

    UMN_MJS_2010 MJ

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    i think njac was attempting to point out that AMS does not directly affect absorption and was responding to your comment: "Supposedly due to CNS depression, it can take longer to digest."

    what is supposedly due to CNS depression? how does CNS depression increase "digestion time"? does the term "digestion" refer to absorption or metabolism?

    not sure what you were going for there ...
  24. PharmDstudent

    PharmDstudent

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    Anticholenergic properties leading to delayed gastric emptying and CNS depression are similar descriptors... in my mind. Lol
  25. UMN_MJS_2010

    UMN_MJS_2010 MJ

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    ahhh, i am beginning to follow you now... typical woman, expecting you to read her mind ;) haha jk
  26. PharmDstudent

    PharmDstudent

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    It just shows that I suck at being a woman. I can't get anything across. My manipulation skills are too weak. Lol!
  27. WVUPharm2007

    WVUPharm2007 "I hear the WMD is the bomb."

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    Cyanide is still the best.
  28. UMN_MJS_2010

    UMN_MJS_2010 MJ

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    oh come on now, don't be so hard on yourself :D
  29. PharmDstudent

    PharmDstudent

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    Well. If being a woman meant saving money and being thrifty, then I'd be top notch. But no. Today, it's about spending, not saving, and preferably, it's about spending someone else's money. Oh well... Maybe next lifetime ;)
  30. Sparda29

    Sparda29 En Taro Adun Gold Donor

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    Chew a bunch of apple seeds.
  31. Pharmavixen

    Pharmavixen foxy pharmacist

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    On 2nd thought, maybe this thread should be deleted...
    Last edited: Jan 31, 2011
  32. Sparda29

    Sparda29 En Taro Adun Gold Donor

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    Why? It's a legit discussion about pharmacy.
  33. Pharmavixen

    Pharmavixen foxy pharmacist

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    Certainly, a discussion of toxicology is interesting and potentially educational for SDN members, and I initially contributed to this thread in that spirit. But we have an uncommon knowledge of poisons, and I don't think it's appropriate for us to be using our professional knowledge to discuss the most effective way to kill yourself on the internet.
  34. Sparda29

    Sparda29 En Taro Adun Gold Donor

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    LOL! Reminds me of that time on another forum where I posted a formula of how to create really cool purple crystals. Anyone who had common sense would have known not to do it (ammonia and bleach were some of the reagents), but apparently some turd actually did it and came back to the forum bitching.
  35. PharmDstudent

    PharmDstudent

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    I keep thinking about this. Does norepi displace TCAs?
  36. njac

    njac Senior Member

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    Nope! But something else does.
  37. PharmDstudent

    PharmDstudent

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    Ok. I'll pull the package insert when I get to work on a few things... if they're still attached to the bottles! :laugh:
  38. Pharmavixen

    Pharmavixen foxy pharmacist

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    Well, if this discussion is successful in imparting the right toxicological information, I guess nobody would be coming back to complain. ROFLMAO
  39. njac

    njac Senior Member

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    These aren't answers youll find in package inserts...

    Only took 2 hours to drive the 11 miles home from my offsite rotation!
  40. rxlea

    rxlea Unicorn wannabe Moderator Emeritus Gold Donor

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    OK EDIT x3: "Norepinephrine is the drug of choice. Other vasopressors may also be used, but norepinephrine has been reported to reverse hypotension that was refractory to other agents. This is thought to be because severe TCA toxicity causes depletion of synaptic norepinephrine that can then only be reversed with exogenous norepinephrine administration. Norepinephrine's vasopressive effect is from its alpha alpha-adrenergic agonist properties. Vasopressors are indicated for persistent hypotension not responsive to judicious fluid loading and sodium bicarbonate.

    "Norepinephrine has been reported to reverse refractory hypotension."
    Last edited: Feb 1, 2011
  41. PharmDstudent

    PharmDstudent

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    I had planned on looking in the pharmacology and toxicology sections...

    I must need to find another Rosetta Stone to figure this mystery out ;)

    I think Rxlea found it!! Cool.
  42. njac

    njac Senior Member

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    that's part of it. But it's particularly in patients with chronic TCA use.

    What about TCA's mechanism as an antidepressant would make it more amenable to exogenous Norepinephrine than Dopamine?

    Ok my point about NE depletion was answered, but again, why NE over DA? Physiologically/Mechanistically?
  43. rxlea

    rxlea Unicorn wannabe Moderator Emeritus Gold Donor

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    I found the answer in the same article I quoted from above but I want to see what other students come up with.
  44. Rockinacoustic

    Rockinacoustic

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    Here's a crapshoot: TCA's have a high affinity for NA+ channels-> Lower rate of depolarization-> lower rate of pre-synaptic firing. So the DA that is up-taken into the neuronal body and converted to NE isn't going anywhere fast.

    Exogenous NE bypasses that mechanism though.

    (?)
  45. 2411t

    2411t

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    tell me you ppl are looking this information up and not spitting it off the top of the dome. buncha nerds...
  46. njac

    njac Senior Member

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    Well I'm going off the top of my head, but I'm giving a lecture on TCA-toxicity next week at a top-10 pharmacy school. I don't mind if the youngins are looking things up.
  47. rxlea

    rxlea Unicorn wannabe Moderator Emeritus Gold Donor

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    Will your lecture be streamed? :D
  48. xiphoid2010

    xiphoid2010

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    let a resident take a crack at this case:

    Patients die of TCA OD due to arrhythmia and seizures.

    my guess is phenytoin, takes care of the arrhythmia and seizure problem.
  49. njac

    njac Senior Member

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    NO.

    But why?
  50. rxlea

    rxlea Unicorn wannabe Moderator Emeritus Gold Donor

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    Phenytoin has a narrow therapeutic window and there is a possibility it can interact with TCAs?

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