Podcasts about neuroleptic

Send Me a Message! In this episode of The Dysregulated Podcast, I explore the vital role Seroquel plays in my ability to get a good night's sleep and how its absence leaves me battling through the day. Sleep deprivation exacerbates the negative ruminations that seem to take centre stage of my psyche, and today, they've been particularly focused on my inner workaholic—the sub-part of me constantly pushing to apply for new jobs and to (hopefully) improve my life! That is one part of me that doesn't slow down, even if the self has! Join me as I do my best to explain the challenges of sleeplessness, self-criticism, and the weight of unrelenting expectations, all before the Seroquel kicks in and I finally get some rest!-Follow my journey living with mental illness and the hard-fought lessons learned along the way. Lived experience is the driving force of this podcast, and through this lens, my stories are told. This is a raw, honest, and authentic account of how multiple psychological disorders have shaped my past and continue to influence my future.Support the showTo support the show, CLICK HEREYou can follow me on Instagram: @elliot.t.waters

Contributor: Taylor Lynch, MD Educational Pearls: What is NMS? Neuroleptic Malignant Syndrome Caused by anti-dopamine medication or rapid withdrawal of pro-dopamenergic medications Mechanism is poorly understood Life threatening What medications can cause it? Typical antipsychotics Haloperidol, chlorpromazine, prochlorperazine, fluphenazine, trifluoperazine Atypical antipsychotics Less risk Risperidone, clozapine, quetiapine, olanzapine, aripiprazole, ziprasidone Anti-emetic agents with anti dopamine activity Metoclopramide, promethazine, haloperidol Not ondansetron Abrupt withdrawal of levodopa How does it present? Slowly over 1-3 days (unlike serotonin syndrome which has a more acute onset) Altered mental status, 82% of patients, typically agitated delirium with confusion Peripheral muscle rigidity and decreased reflexes. AKA lead pipe rigidity. (As opposed to clonus and hyperreflexia in serotonin syndrome) Hyperthermia (>38C seen in 87% of patients) Can also have tachycardia, labile blood pressures, tachypnea, and tremor How is it diagnosed? Clinical diagnosis, focus on the timing of symptoms No confirmatory lab test but can see possible elevated CK levels and WBC of 10-40k with a left shift What else might be on the differential? Sepsis CNS infections Heat stroke Agitated delirium Status eptilepticus Drug induced extrapyramidal symptoms Serotonin syndrome Malignant hyperthermia What is the treatment? Start with ABC's Stop all anti-dopaminergic meds and restart pro-dopamine meds if recently stopped Maintain urine output with IV fluids if needed to avoid rhabdomyolysis Active or passive cooling if needed Benzodiazapines, such as lorazepam 1-2 mg IV q 4hrs What are active medical therapies? Controversial treatments Bromocriptine, dopamine agonist Dantrolene, classically used for malignant hyperthermia Amantadine, increases dopamine release Use as a last resort Dispo? Mortality is around 10% if not recognized and treated Most patients recover in 2-14 days Must wait 2 weeks before restarting any medications References Oruch, R., Pryme, I. F., Engelsen, B. A., & Lund, A. (2017). Neuroleptic malignant syndrome: an easily overlooked neurologic emergency. Neuropsychiatric disease and treatment, 13, 161–175. https://doi.org/10.2147/NDT.S118438 Tormoehlen, L. M., & Rusyniak, D. E. (2018). Neuroleptic malignant syndrome and serotonin syndrome. Handbook of clinical neurology, 157, 663–675. https://doi.org/10.1016/B978-0-444-64074-1.00039-2 Velamoor, V. R., Norman, R. M., Caroff, S. N., Mann, S. C., Sullivan, K. A., & Antelo, R. E. (1994). Progression of symptoms in neuroleptic malignant syndrome. The Journal of nervous and mental disease, 182(3), 168–173. https://doi.org/10.1097/00005053-199403000-00007 Ware, M. R., Feller, D. B., & Hall, K. L. (2018). Neuroleptic Malignant Syndrome: Diagnosis and Management. The primary care companion for CNS disorders, 20(1), 17r02185. https://doi.org/10.4088/PCC.17r02185 Summarized by Jeffrey Olson MS2 | Edited by Meg Joyce & Jorge Chalit, OMSIII  

Thank you Miranda "Spitfire" Speth, OMS III, for developing this podcast. Thank you Bayli Zimmerman, OMS IV, for another guest star appearance! This podcast discusses these two syndromes based on Miranda's review of the literature. She did a great job and helped me learn more about the similarities between the two conditions. She also clarified the differences I didn't know. This is a great refresh on recognition and treatment of the psychiatric condition. We enjoyed our discussion and hope you do too! Thank you to the immortal Jordan Turner for creating the perfect bumper music!

Live Nursing Review with Regina MSN, RN! Every Monday & Wednesday we are live. LIKE, FOLLOW, & SUB @ReMarNurse for more.     7 Day of NCLEX: https://ReMarNurse.com/7days   Quick Facts for NCLEX Next Gen Study Guide here - https://bit.ly/QF-NGN Study with Professor Regina MSN, RN every Monday as you prepare for NCLEX Next Gen.   ► Create Free V2 Account - http://www.ReMarNurse.com ► Get Quick Facts Next Gen - https://bit.ly/QF-NGN ► Subscribe Now - http://bit.ly/ReMar-Subscription ► GET THE PODCAST: https://remarnurse.podbean.com/ ► WATCH LESSONS: http://bit.ly/ReMarNCLEXLectures/ ► FOLLOW ReMar on Instagram: https://www.instagram.com/ReMarNurse/ ► LIKE ReMar on Facebook: https://www.facebook.com/ReMarReview/   ReMar Review features weekly NCLEX review questions and lectures from Regina M. Callion MSN, RN. ReMar is the #1 content-based NCLEX review and has helped thousands of repeat testers pass NCLEX with a 99.2% student success rate! ReMar focuses on 100% core nursing content and as a result, has the best review to help nursing students to pass boards - fast!

In this weeks episode you'll learn about two often confused syndromes that cause elevated body temperature! Episode written by Dr. Thomas Kiebalo (Internal Medicine Resident) and reviewed by Dr. Peter Wu (Clinical Pharmacology and Toxicology and General Internal Medicine) and Dr. Gillian Spiegle (General Internal Medicine). Infographic by Dr. Shannon Gui (Internal Medicine Resident). Support the show

Show notes at pharmacyjoe.com/episode829. In this episode, I'll discuss three ways to tell the difference between serotonin syndrome and neuroleptic malignant syndrome. The post 829: Three ways to tell the difference between serotonin syndrome and neuroleptic malignant syndrome appeared first on Pharmacy Joe.

Show notes at pharmacyjoe.com/episode829. In this episode, I ll discuss three ways to tell the difference between serotonin syndrome and neuroleptic malignant syndrome. The post 829: Three ways to tell the difference between serotonin syndrome and neuroleptic malignant syndrome appeared first on Pharmacy Joe.

The First Principles of Antipsychotics that can more than get you through your psychiatry rotation: is it all about the dopamine? === Other Links === Check out our new website ⁠⁠⁠1pm.wiki⁠⁠⁠ for the ⁠⁠⁠Notion document⁠⁠⁠, free Anki flashcards, and podcast episodes. Check out our Instagram: ⁠⁠⁠https://www.instagram.com/firstprinciplesofmedicine/⁠⁠⁠ Recorded 7 March 2023 Co-hosts: Broska Zeynel & Jason D'Silva feat. Renae Long & Alexander Lawrie. Produced by Adian Izwan. If you have any ideas or feedback, comment on this Notion document, or shoot us an email at ⁠⁠⁠hello@1pm.wiki⁠⁠⁠ *** We're really excited to be collaborating with Becky from Becky's notes, a UK based resource, to produce infographics for our visual learners out there. Becky's notes brings together all the key topics medical students need to know in a readily available place, reviewed by specialists in the field. These visually striking notes are a refreshing change from all the boring textbooks. You can check her out on Instagram at @beckysnotes01 and get her books at ⁠⁠⁠https://linktr.ee/Beckysnotes⁠⁠⁠ === Timestamps === (01:33) The First Principles of pathways (02:59) Dopaminergic pathways (03:28) Mesolimbic - positive symptoms (04:13) Mesocortical - negative symptoms (07:17) Nigrostriatal - motor symptoms (08:15) Tuberoinfundibular - prolactin (09:06) Pathway summary (10:53) Other receptors (13:47) Antipsychotics (finally) (14:19) Typical antipsychotics (17:43) Negative symptoms mnemonic (19:36) Neuroleptic malignant syndrome (22:28) Atypical antipsychotics (24:23) Metabolic side effects (25:07) Summary

In this episode, we review the high-yield topic of Neuroleptic Malignant Syndrome from the Psychiatry section. Follow Medbullets on social media: Facebook: www.facebook.com/medbullets Instagram: www.instagram.com/medbulletsofficial Twitter: www.twitter.com/medbullets

Good morning and welcome to your Wednesday dose of Your Daily Meds.Bonus Review: At what level in the body does control of iron stores occur? Answer: Control of iron in the body occurs at the level of the small bowel mucosal cells. These enterocytes are responsible for the control of iron absorption. When body iron stores are low - plasma transferrin is high, its iron saturation is low, more iron passes from ferritin in the eneterocytes to transferrin in bloodWhen body iron stores are adequate - transferin saturation is higher, the iron remains in the enterocyte and the unwanted iron is lost from the available absorption pool when the enterocyte is shedRemember that iron is readily absorbed by these enterocytes, but the absorption across the enterocyte basal membrane is regulated by levels of ferritin and transferrin and transferrin saturation.If we overload this mucosal block with excessive iron supplementation, we will absorb excess ironOr if the function of the control mechanism is defective, such as in haemochromatosis, we will be overloaded with iron, resulting in iron deposition in the tissuesCase:A 45-year-old male is brought to the Emergency Department by ambulance.On examination, he has a temperature of 38.2°C and is agitated.There is tremor, muscle rigidity and a marked deep tendon hyperreflexia of the lower limbs more so than the upper limbs.His pupils are dilated and mucus membranes dry.Relatives at his home informed the paramedics that he has a history of depression for which he is known to a Psychiatrist.Which of the following is the most likely diagnosis?Serotonin syndromeNeuroleptic malignant syndromeMalignant hyperthermiaSympathomimetic toxicitySeizureHave a think.Scroll for the chat.Procedure:Alright then.As if in an OSCE situation, tell me how you would approach, prepare for and conduct the ‘procedure’ of local anaesthetic infiltration.Have a think.Jot some things down.Scroll for the chat.The Syndrome:This man has signs suggestive of serotonin syndrome.Serotonin syndrome can be a life-threatening condition with increased serotonergic activity in the central nervous system. It can be caused by therapeutic medication use, interactions between medications and intentional overdose. Classically, serotonin syndrome is a clinical diagnosis of mental status changes, autonomic hyperactivity and neuromuscular abnormalities. In this case, serotonin syndrome is manifested by hyperthermia, agitation, muscular rigidity and hyperreflexia, along with the history of antidepressant use. Common antidepressants like Sertraline are Selective Serotonin Reuptake Inhibitors (SSRIs), which increase the extracellular levels of serotonin and serotonergic neurotransmission in the brain. Neuroleptic malignant syndrome is a life-threatening neurological emergency associated with the use of neuroleptic medication. It is characterised by mental status change, rigidity, fever and dysautonomia. In this case, the physical signs more prominent in the lower limbs and the associated SSRI usage are more suggestive of serotonin syndrome. Malignant hyperthermia is characterised by hypermetabolic crisis when a susceptible individual is exposed to a volatile anaesthetic agent, which is unlikely given the history in this case.Sympathomimetic toxicity is manifested by stimulation of alpha- and beta-adrenergic receptors and characterised by typical adrenergic signs and symptoms, including hyperthermia, tachycardia, diaphoresis, hypertension and cardiac arrhythmias. Sympathomimetic toxicity can be caused by prescribed and non-prescribed substances, such as ecstasy.Seizure is unlikely given the autonomic changes and neuromuscular abnormalities in this patient.Infiltration:Ok, so lets start with Indications:Local anaesthesia (LA) for painful procedures egSuturingDebridement of woundForeign body removalReduction of disclocated small jointArterial punctureThen some Contraindications:Local anaesthetic allergy - rareAvoid lignocaine with adrenaline in areas of end-arterial supply eg:FingersToesPenisPinnaNose(Even though amputated digits can be reattached (after a period of literally zero blood supply) and adrenaline is used in local anaesthetics for digital blocks of fingers and toes… best stick to the safe answer in the test…)Equipment:Alcohol swabSkin cleansing solution eg some chlorhexidineLocal Anaesthetic agent of choiceSyringe: 5mL or 10mLNeedle: 25G and 21GChoice:Small volumes of concentrated anaesthetic for small areas or jointsLarge volumes of less concentrated anaesthetic for large areas or jointsSelect adrenaline-containing anaesthetic for vascular sites - causes vasoconstrictionLikely help reduce bleedingReduce systemic absorption of lignocaineMaintain higher anaesthetic concentration near nerve fibresProlong local anaesthetic conduction blockadeLignocaine is most commonly usedBupivacaine and Ropivacaine are longer acting, usually used for nerve blocks or epiduralsCalculate:Maximum safe dose of your chosen agent:Lignocaine - Max dose 3mg/kg - Duration 0.5-1 hourLignocaine with adrenaline - Max dose 7mg/kg - Duration 2-5 hoursThis means you will need to do some maths to work out how many mL of a particular % concentration lignocaine +/- adrenaline you can safely inject.Just make sure you calculate your maximum mg for the particular patient FIRST, then work out the mL from the bottle SECOND.Procedure:Consent, explain procedure blah blah blahClean the siteRecheck dose, safe maximum, dilution, allergies etcDraw LA into syringe with 25G needleEnter dermis of skin at 45deg, aspirate to ensure needle not in blood vesselInfiltrate 1-2mL of LA to make a blebExchange 25G for 21G needleEnter skin through previously anaesthetised bleb siteAdvance subcutaneously, aspirate and injectRepeat: Advance, aspirate, injectIf you aspirate blood, withdraw a bit, aspirate then inject and continueRepeat such that the desired area is infiltrated with LAWait at least two minutes to take effectThen get on to cutting or suturing or realigning or whatever.Bonus: How is iron carried (or transferred) in the blood? Answer in tomorrow’s dose.Closing:Thank you for taking your Meds and we will see you tomorrow for your MANE dose. As always, please contact us with any questions, concerns, tips or suggestions. Have a great day!Luke.Remember, you are free to rip these questions and answers and use them for your own flashcards, study and question banks. Just credit us where credit is due. This is a public episode. If you would like to discuss this with other subscribers or get access to bonus episodes, visit yourdailymeds.substack.com

You are called to see a 31 yr old woman on the ward who is 8 hours postop after a diagnostic laparoscopy to investigate her longterm chronic pelvic pain. The nurse treating her is concerned because she is still complaining of pain despite many analgesics, however she is more concerned by the patient's increasingly erratic behaviour and agitation. Her heart rate is 108/min, NIBP 155/95, she appears sweaty, temp = 38.9C, appears restless and has some noticeable tremor. When you examine her she has very brisk reflexes and three beats of clonus in her ankles. Glancing at her med chart you see she is usually on desvenlafaxine 50mg/day, tramadol 100mg BD, and admits to using methamphetamine recreationally. Join Graeme and I as we discuss a rational approach to this sort of scenario, share some real life anecdotes and trade a few more dodgy dad jokes. Differential diagnoses (don't miss these)Deeper dive into SS syndrome, and NLMS References Tutorial of the Week 2010 Serotonergic Syndrome Serotonin Syndrome in the Perioperative Period BJA Education 2020

How should we approach the management of neuroleptic malignant syndrome? What is the role of bromocriptine, dantrolene, and ECT? Faculty: Jim Phelps, M.D. Hosts: Jessica Diaz, M.D.; Flavio Guzman, M.D. Learn more about Premium Membership here Earn 0.5 CMEs: Quick Take Vol. 23 The Neuroleptic Malignant Syndrome—A Systematic Case Series Analysis Focusing on Therapy Regimes and Outcome

Podcast summary of articles from the February 2021 edition of the Journal of Emergency Medicine from the American Academy of Emergency Medicine.  Topics include Echocardiographic findings in PE, cardiovascular emergencies in the COVID era, antibiotics for nasal packing, serotonin syndrome, diphenhydramine for neuroleptic drugs, and board review on monocular vision loss.  Guest speaker is Dr. Paul Koscumb.

This episode covers neuroleptic malignant syndrome!

Show notes at pharmacyjoe.com/episode534. In this episode, I ll discuss three ways to tell the difference between serotonin syndrome and neuroleptic malignant syndrome. The post 534: Three ways to tell the difference between serotonin syndrome and neuroleptic malignant syndrome appeared first on Pharmacy Joe.

This week on MIA Radio, we interview Dr. Sandy Steingard. Dr. Steingard is Medical Director at Howard Center, a community mental health center where she has worked for the past 21 years. She is also Clinical Associate Professor of Psychiatry at the College of Medicine of the University of Vermont. For more than 25 years, her clinical practice has primarily included patients who have experienced psychotic states. Dr. Steingard serves as Board Chair of the Foundation for Excellence in Mental Health Care. She was named to Best Doctors in America in 2003 and writes regularly for Mad in America. She is editor of the book Critical Psychiatry, Controversies and Clinical Implications due in 2019. In this episode we discuss: What led Sandy to her career in psychiatry and her particular interest in the critical aspects of psychiatry and psychology. That Sandy’s initial interest was in biomedical explanations of psychotic experiences. How, in the late 80s, the advent of new antipsychotic drugs caused an initial excitement because of the promises made about safety and efficacy, but that Sandy came to realise the problems with the drugs. How she witnessed the over-promotion of the drugs and that the promotion was markedly different to the results of studies and her observations of patients that were taking them. How a series of disappointments and recognition of some inherent flaws in psychiatry led Sandy to her interest in alternatives. That the book, The Truth About the Drug Companies by Marcia Angel MD, had a big impact on Sandy’s view of the drugs during the 2000s. Other influential books were The Daily Meds by Melody Petersen and Side Effects by Alison Bass. That reading Anatomy of an Epidemic and particularly the problematic aspects of the long-term use of antipsychotic drugs caused Sandy to question how she was practising. That she found colleagues were sometimes angry at the conclusion that antipsychotic drugs might not be safe or lead to better outcomes for patients. That this led to the investigation of alternatives such as Open Dialog, training with Mary Olsen at the Institute of Dialogic Practice and discovering the Critical Psychiatry Network and the work of Dr. Joanna Moncreiff. How Sandy approaches practising from a critical perspective, particularly when expectations are in line with the dominant biomedical narrative. Her book, Critical Psychiatry, due in 2019 which aims to help clinicians apply transformational strategies in their clinical practices. That psychiatrists would be well served by welcoming lived experience input to their daily practice. Why informed consent should be viewed as an ongoing process rather than a one-time agreement. The problems that arise in clinical studies where experience is translated into a numerical form. Relevant links: Critical Psychiatry, Controversies and Clinical Implications (due 2019) How Well Do Neuroleptics Work? What We Are Talking About When We Talk About Community Mental Health The Truth About The Drug Companies by Marcia Angel MD (video) The Daily Meds by Melody Petersen (review) Side Effects by Alison Bass Open Dialog The Institute for Dialogic Practice Critical Psychiatry Network

Show notes at www.medicalcasespodcast.libsyn.com.    Remember in medical school when you were taught to treat the patient and not the numbers? It sounded so good, right? So why are we so aggressive with treating fever in patients with sepsis? This episode reviews the article "Acetaminophen for Fever in Critically Ill Patients with Suspected Infection".   Bottom line: for septic patients with fever, you can use acetaminophen to treat symptoms but there is no mortality benefit. Furthermore, if patients are persistently tachycardic despite adequate resuscitation and all other causes of tachycardia have been ruled out there is no harm in giving acetaminophen to control fever/ tachycardia.  Background: acetaminophen is often used to control fever in patients with suspected infection in the ICU - there is little data to suggest that this is beneficial.  Population: 700 ICU patients with fever (temp ≥38°C) and suspected source of infection Design: Multi-center, prospective, parallel-group, blinded, randomized, controlled trial. Intervention: 1 gm IV acetaminophen Q6H until  1) ICU discharge, 2) Resolution of fever, 3) Cessation of antimicrobial therapy OR 4) Death Control: Placebo Q6H Results: Primary Outcome - No difference in ICU free days to day 28.  Secondary Outcome - No significant differences between the acetaminophen group and the placebo group with respect to mortality at day 28 or at day 90   It should be noted that acetaminophen WAS associated with a shorter ICU stay among survivors but a LONGER stay among non-survivors.      Acetaminophen has a low chance of harming your patient but it is clear that there is no pressing medical indication (other than discomfort) to treat mild fever in sepsis.   Keep in mind that we are talking about fever in suspected infection. There are many other cases where temperature management of some sort IS indicated. This is often acheived through medications or external cooling. Examples include: Neuroleptic malignant syndrome  Serotonin syndrome Environmental exposure like heat exhaustion and heat stroke Post cardiac arrest - 33℃ vs 36℃ Malignant hyperthermia Anticholinergic toxidrome Brain trauma. Premies with Hypoxic-Ischemic Encephalopathy    From the article - Young, Paul, Manoj Saxena, and Rinaldo Bellomo. "Acetaminophen for Fever in Critically Ill Patients with Suspected Infection." New England Journal of Medicine N Engl J Med 373.23 (2015): 2215-224.   

We review thisa post from Dr. Charles Bruen of Resus Review on Malignant Hyperthermia and dantrolene. Then, we delve into core content pearls on polypharmacy -  serotonin syndrome, neuroleptic malignant syndrome, and extrapyramidal side effects.  We do this using Tintinalli and Rosen's as guides.  As always, visit foamcast.org for show notes and the generously donated Rosh Review questions. Thanks y'all! -Jeremy Faust and Lauren Westafer

Interview with Robert W. McCarley, MD, author of Globally and Locally Reduced MRI Gray Matter Volumes in Neuroleptic-Naive Men With Schizotypal Personality Disorder: Association with Negative Symptoms

Visit Eleanor Slade's website via http://www.helsinki.fi/foodwebs/Eleanor.htm. Music credit: -the song Neuroleptic trio instrumental 6, and link http://freemusicarchive.org/music/Neuroleptic_Trio/Summer_Variations/Neuroleptic_trio_instrumental_6 -the artist: Neuroleptic Trio: http://www.myspace.com/neuroleptictrio

Try to work out what your differential would be and how you would investigate and manage this case.

The aim of this investigation was to compare the degree of striatal dopamine-(D2) receptor blockade by two atypical antipsychotic drugs, risperidone and olanzapine. The percentage of D2 receptor occupancy during treatment was calculated by comparing the results of 123I-iodobenzamide SPECT with those from healthy control subjects. Twenty inpatients suffering from schizophrenia or schizoaffective psychosis according to DSM IV/ICD-10 criteria were treated with clinically recommended doses of risperidone and compared with 13 inpatients treated with up to 20 mg olanzapine. Neuroleptic dose and D2 receptor blockade correlated strongly for both risperidone (Pearson r = –0.86, p = 0.0001) and olanzapine (Pearson r = –0.77, p = 0.002). There was no significant difference between the D2 receptor occupancy of the two substances when given in the clinically recommended dose range (unpaired t-test, t= –0.112, p=0.911).