love all your videos! I just ordered your book and cant wait for it to come in! thank you so much for taking the time to do this. It has really helped me so much and will allow me to give my patients the care they deserve. thanks again!
I think you made a huge generalization with drug interactions here. As pharmacokinetics process of absorption, metabolism, distribution and excretion can be places 2 drugs can interact. Same with pharmacodynamics it's not just synergistic response
can you do the most common psych drugs individually? including how to escalate the doses in your opinion and how to wean people off and possible interaction with other commonly prescribed drugs?
Hi Dileep, check out my entire lecture series for each psych drug individually. For overall practice guidelines, unfortunately I can't update videos once they're uploaded to CZcams, but I have included this in my book: a.co/3DbhDip Hope it helps!
At 1:05 this is an error shared among many MDs (and even prominent texts), one which is NOT conveyed by the latest research, about Serotonin Syndrome. There is a widespread belief that SS can be caused by practically any 2 drugs that increase serotonin. REALITY: the SSRIs/SNRIs combined with the more powerful MAOIs can cause SERIOUS Serotonin Syndrome. Other combos are hardly ever worthy of a hospital visit - why? - because they can't increase serotonin NEARLY enough. PERIOD. Combinations with other drugs that work for instance on opioid receptors or NET can together give the impression of Serotonin Toxicity to the untrained eye. I've seen the most ridiculous assertions in papers that were actually published, including that Mirtazapine (a good 5HT2A blocker which has been used as an antidote to Serotonin Toxicity) and Codeine have caused ST.
It is true that the majority of cases of life-threatening or serious serotonin syndrome involve MAOIs combined with another serotonergic medication. However, there are many reports of patients who are on different combinations developing clinically significant serotonin syndrome, including tramadol/SSRI, mirtazapine/fentanyl, buspirone/SSRI, etc. I am basing this off of a brief review article summarizing the evidence which you can find here: www.ncbi.nlm.nih.gov/pubmed/24358002
The Volpi-Abadie article you cited is almost as unmemorable as it is misleading. The following is information from much better and more highly cited studies, and if you'd like I'll send you the bibliography. I should divulge now that the international authorities on this syndrome (ST) will tell you they are fed up with bogus case reports of ST precipitated by any number of drugs incapable of doing so. Appears to be mostly because A) the writers are ER doctors and/or B) the doctor (even a psychiatrist or neurologist) is untrained either in pharmacology (more common than one would like to admit) or identifying what Serotonin Toxicity actually looks like. Responses: 1) Tramadol is a very weak SRI (in addition to being an opioid analgaesic) and and anyway its effect on serotonin is simply additive - like adding another 10mg or whatever the dose of the SSRI the patient is already taking, i.e., this is a bogus assertion. 2) Mirtazapine increases serotonin levels only about 30%, less than taking a brisk walk around the block. Its sideways method of coupling with serotonin-containing neurons to increase SER (see Stahl's Psychopharmacology) is the weakest of all mechanisms, and has been used successfully as an ST antidote. Fentanyl is incapable. 3) Buspirone + SSRI is again incapable. Vilazodone and vortioxetine are SSRIs with (among other miniature serotonin-modulating capabilities) 5HT-1A partial agonism (there's no full agonism in pharmacology, although Lundbeck likes to say so) and therefore, ought to be causing Serotonin Syndrome left, right and center!... Only they're NOT, again, because they pharmacologically CANNOT.
@@MemorablePsych As a recent grad, we were taught to monitor for serotonin syndrome in patients receiving meds that increase levels. In clinicals I encountered a patient who was taking 3 meds which increase serotonin levels. My instructor asked what I should be monitoring for and the answer he wanted was serotonin syndrome. I can't speak for others but we were taught this in my PMHNP program.
The reason why chronic alcoholism acts as an inducer is complex and not immediately intuitive. This post explains it well (thanks SBR249!): "When the normal alcohol metabolic pathway (alcohol dehydrogenase/aldehyde dehydrogenase) is saturated (remember alcohol, aspirin, and phenytoin metabolism follow zero order kinetics which means they are saturable), the cytochrome P450 pathway starts metabolizing alcohol. For a person not used to drinking alcohol (acute alcohol intake), the low capacity cytochrome P450 is easy to saturate which means it is no longer available for metabolizing other toxins and drugs (aka it's metabolic and detoxification actions are inhibited). Because CYp450 is an inducible system, for someone who is a chronic drinker, CYP450 is induced so that the capacity of the system increases due to increased enzyme production in order to both handle the chronic alcohol intake and to perform the other essential metabolic/detox functions of the CYP450 system." Source: forums.studentdoctor.net/threads/cyp450-interaction-with-alcohol.1092799/
Ah understood. I used the phrase "liver damage" somewhat carelessly in the video. The text explanation above is more accurate. Thanks for catching that!
im looking for literature on the effects of mixing a SSRI and barbituate with a herb called Kanna (sceletium tortuesum). i have a doctor trying to harm me i had 5 days of total psycosis and a brain anurisum from this drug to herb interaction, if anyone can help me i would be appreciative
16:40 grapefruit juice is a cyp3a4 inhibitor opposite of carb and barb
You're absolutely correct, my mistake!
dxm user?
@@noahlee8200 😳
I watch these videos for fun in my spare time, nothing is more interesting than pharmacology to me.
You are unique 😮
love all your videos! I just ordered your book and cant wait for it to come in! thank you so much for taking the time to do this. It has really helped me so much and will allow me to give my patients the care they deserve. thanks again!
your videos RULE! Thank you for making them.
I think you made a huge generalization with drug interactions here. As pharmacokinetics process of absorption, metabolism, distribution and excretion can be places 2 drugs can interact. Same with pharmacodynamics it's not just synergistic response
Thank you for these gems of videos
Sertaline is one of SSRI And they are metabolised by 2D6
Absolutely fantastic.
Excellent presentation !!! Absolutely simplified. Thank you so much!
can you do the most common psych drugs individually? including how to escalate the doses in your opinion and how to wean people off and possible interaction with other commonly prescribed drugs?
Hi Dileep, check out my entire lecture series for each psych drug individually. For overall practice guidelines, unfortunately I can't update videos once they're uploaded to CZcams, but I have included this in my book: a.co/3DbhDip
Hope it helps!
Strong work. Thank you for putting this together
Excellent presentation, extremely helpful methods to facilitate absorption of knowledge. I am rushing to buy your book.
Wish I had it when I did medical school
Thank You 🩺🙏
This was awesome. Thank you.
Linagliptin is not a secretagogue. It decrease GI emptying and glucagon secretion. It is a DPP4 inhibitor... (14:40)
You are correct - sorry for any confusion there!
Amazing! Thank you for this.
Thank you for this video 🙏
Thank you very much!
Plz explain the pharmacokinetic drug interactions of Amla
Fluoxetine inhibitor substrate same time?
At 1:05 this is an error shared among many MDs (and even prominent texts), one which is NOT conveyed by the latest research, about Serotonin Syndrome. There is a widespread belief that SS can be caused by practically any 2 drugs that increase serotonin. REALITY: the SSRIs/SNRIs combined with the more powerful MAOIs can cause SERIOUS Serotonin Syndrome. Other combos are hardly ever worthy of a hospital visit - why? - because they can't increase serotonin NEARLY enough. PERIOD.
Combinations with other drugs that work for instance on opioid receptors or NET can together give the impression of Serotonin Toxicity to the untrained eye. I've seen the most ridiculous assertions in papers that were actually published, including that Mirtazapine (a good 5HT2A blocker which has been used as an antidote to Serotonin Toxicity) and Codeine have caused ST.
It is true that the majority of cases of life-threatening or serious serotonin syndrome involve MAOIs combined with another serotonergic medication. However, there are many reports of patients who are on different combinations developing clinically significant serotonin syndrome, including tramadol/SSRI, mirtazapine/fentanyl, buspirone/SSRI, etc. I am basing this off of a brief review article summarizing the evidence which you can find here: www.ncbi.nlm.nih.gov/pubmed/24358002
The Volpi-Abadie article you cited is almost as unmemorable as it is misleading. The following is information from much better and more highly cited studies, and if you'd like I'll send you the bibliography. I should divulge now that the international authorities on this syndrome (ST) will tell you they are fed up with bogus case reports of ST precipitated by any number of drugs incapable of doing so. Appears to be mostly because A) the writers are ER doctors and/or B) the doctor (even a psychiatrist or neurologist) is untrained either in pharmacology (more common than one would like to admit) or identifying what Serotonin Toxicity actually looks like.
Responses: 1) Tramadol is a very weak SRI (in addition to being an opioid analgaesic) and and anyway its effect on serotonin is simply additive - like adding another 10mg or whatever the dose of the SSRI the patient is already taking, i.e., this is a bogus assertion. 2) Mirtazapine increases serotonin levels only about 30%, less than taking a brisk walk around the block. Its sideways method of coupling with serotonin-containing neurons to increase SER (see Stahl's Psychopharmacology) is the weakest of all mechanisms, and has been used successfully as an ST antidote. Fentanyl is incapable. 3) Buspirone + SSRI is again incapable. Vilazodone and vortioxetine are SSRIs with (among other miniature serotonin-modulating capabilities) 5HT-1A partial agonism (there's no full agonism in pharmacology, although Lundbeck likes to say so) and therefore, ought to be causing Serotonin Syndrome left, right and center!... Only they're NOT, again, because they pharmacologically CANNOT.
Thanks for this. I am not an expert in serotonin syndrome in particular, and you've given me something to look into more! I appreciate it.
youre awesome dude
@@MemorablePsych As a recent grad, we were taught to monitor for serotonin syndrome in patients receiving meds that increase levels. In clinicals I encountered a patient who was taking 3 meds which increase serotonin levels. My instructor asked what I should be monitoring for and the answer he wanted was serotonin syndrome. I can't speak for others but we were taught this in my PMHNP program.
I hyperfocused on pharmacology in university, too bad I was in criminal justice
Wouldnt liver damage work as an inhibitor since it wouldnt be able to metabolize drugs? (16:32)
The reason why chronic alcoholism acts as an inducer is complex and not immediately intuitive. This post explains it well (thanks SBR249!): "When the normal alcohol metabolic pathway (alcohol dehydrogenase/aldehyde dehydrogenase) is saturated (remember alcohol, aspirin, and phenytoin metabolism follow zero order kinetics which means they are saturable), the cytochrome P450 pathway starts metabolizing alcohol. For a person not used to drinking alcohol (acute alcohol intake), the low capacity cytochrome P450 is easy to saturate which means it is no longer available for metabolizing other toxins and drugs (aka it's metabolic and detoxification actions are inhibited). Because CYp450 is an inducible system, for someone who is a chronic drinker, CYP450 is induced so that the capacity of the system increases due to increased enzyme production in order to both handle the chronic alcohol intake and to perform the other essential metabolic/detox functions of the CYP450 system." Source: forums.studentdoctor.net/threads/cyp450-interaction-with-alcohol.1092799/
Right, when I meant live damage, I meant cirrhosis not chronic alcohol intake.
Ah understood. I used the phrase "liver damage" somewhat carelessly in the video. The text explanation above is more accurate. Thanks for catching that!
🤔
im looking for literature on the effects of mixing a SSRI and barbituate with a herb called Kanna (sceletium tortuesum). i have a doctor trying to harm me i had 5 days of total psycosis and a brain anurisum from this drug to herb interaction, if anyone can help me i would be appreciative