Tricyclic Antidepressant Toxicity Presentation

Tricyclic Antidepressant Toxicity Presentation Tricyclic Antidepressant Toxicity Presentation 1) Help with creation of a power point. 2) Integrate case study provided and annotated biography to create power points 3)please use the final version of our the annotated biography YOU WILL MAKE… HER’S WAS HORRIBLE. 4) https://images.app.goo.gl/ wZo6rZXL5WuMFFpg6 integrated the principal slides tittle of this PPT with those of the ppt attached to create a complete and comprehensive ppt on the study case only. ( USED TITLES OF THE SLIDES OF THIS POWER POINTS ASSOCIATED WITH THAT PF THE ATTACHED POWER POINT)THE TITLES OF THIS POWER FIRST THEN THE TITLES OF THE ATTACHED PPT) ALL RELATED TO THE ATTACHED CASE STUDY ONLY ( THE TITLE ARE USES TO KNOW WHAT SHOULD BE INCLUDED IN THE SLIDES OF THIS PPT). TOPIC: SEE CASE STUDY ONLY 5) PLEASE CHANGE MY DIAGNOSIS AND TITLE TO (Tricyclic Antidepressant Toxicity) THE CASE STUDY IS ABOUT Tricyclic Antidepressant Toxicity IN A GERIATRIC PATIENT. Tricyclic Antidepressant Toxicity Presentation LIKE LAST PPT WE DIS PLUS THE CASE STUDY PRESENTATION PART. NURS 6061 University Of Texas Tricyclic Antidepressant Toxicity Presentation empty_power_point.pptx case_study_mio.docx tricyclic_antidepressant_toxicity_article.docx ORDER NOW FOR CUSTOMIZED AND ORIGINAL ESSAY PAPERS Tricyclic Antidepressant Toxicity Presentation. Use of bbbbbbbbbbbb (Diagnosis). Dr. aaaaaaaaaaaaa School of Nursing at . PMHMP-NURS-6261 Dr. bbbbbbbbbbb. 06/30/2020 Topic Overview Topic: Should ketamine be approved officially as effective and durable treatment for suicide and suicidal ideation? Rationale: Existing treatments take a long time before alleviating the symptoms of depression and suicidal ideation. Problem Description • Suicide and suicide ideation are emergencies that need urgent interventions. • Depression is an emergency with social, cultural, and economic impacts on society. • There is no effective treatment approach to manage suicide and suicide ideation. Proposed Practice Change • Due to the urgency presented by suicide/suicide ideation, the healthcare department needs to approve the use of ketamine immediately to lighten the condition’s burden on the economy and society. • Practitioners can use ketamine to treat depression and its complications, including suicide and suicidal ideation. • Ketamine is an ideal treatment approach because it works immediately and has minimal side effects. Presentation of Evidence • Andrade (2017) claims that ketamine and derivatives are effective for treating MD, which can trigger suicidal behavior. • Zanos and Gould (2018) assert that ketamine inhibits NMDA and activates an acid receptor, which help in managing depression/suicide. • Duman (2018) affirms that ketamine is effective in treating depression/suicide ideation resistant to other medical approaches. • Grunebaum et al. (2018) posits that treatment of MD/suicide using ketamine has positive outcomes within 24 hours. Recommendations • The health care department should approve ketamine as a treatment approach for preventing suicide and managing suicide ideation because of its proven benefits and due to the ineffectiveness of existing approaches. • Ketamine can reduce the rate of suicide completed if practitioners conduct efficient patient screening, public education, and cultural support when implementing the approach. Implications for Practice Approving the use of ketamine for treating suicide and suicidal ideation will have numerous benefits including: • Decreased burden on health care. • Reduced health care costs. • Improved economic development. • Improved health care quality. References Andrade C. (2017). Ketamine for Depression, 2: Diagnostic and Contextual Indications. The Journal of Clinical Psychiatry, 78(5), Duman R. S. (2018). Ketamine and rapid-acting antidepressants: A new era in the battle against depression and suicide. F1000Research, 7 Grunebaum, M. F et al. (2018). Ketamine for Rapid Reduction of Suicidal Thoughts in Major Depression: A Midazolam-Controlled Randomized Clinical Trial. The American Journal of Psychiatry, 175(4), 327-335 References Meisner, R. C. (2019). Ketamine for major depression: New tool, new questions. Harvard Health Publishing. Retrieved from https://www.health.harvard.edu/blog/ketamine-formajor- depression-new-tool-new-questions-2019052216673 Menard, C., Hodes, G. E., & Russo, S. J. (2016). Pathogenesis of depression: Insights from human and rodent studies. Neuroscience, 321, 138–162. https://doi.org/10.1016/j.neuroscience.2015.05.053 Zanos, P., & Gould, T. D. (2018). NURS 6061 University Of Texas Tricyclic Antidepressant Toxicity Presentation Tricyclic Antidepressant Toxicity Presentation. Mechanisms of ketamine action as an antidepressant. Molecular Psychiatry, 23(4), 801– 811. Wesley Brown, a 63-year-old businessman, was “found down” in the road by police and brought to the emergency room (ER) of a large university-affiliated hospital. The psychiatry service was consulted for management of “psychotic behavior” in the ER. The patient’s family reported that the patient had exhibited an approximately 2-week history of “strange behavior.” According to his sister, Mr. Brown had been running around the kitchen with knives, sending paranoid e-mails about the justice system to his friends, showing his guns to the neighbors, seeing people in the walls, having paranoid thoughts that his wife was having an affair, and not sleeping. The patient’s wife had reported him missing 3 days prior to admission. Notably, his car was found a few blocks away with a large box in its trunk containing numerous medications and the patient’s extensive gun collection. Mr. Brown’s vital signs were within normal limits. His medical records revealed a history of coronary artery disease and a coronary artery bypass graft 5 years prior to admission, as well as chronic back pain and several spinal surgeries, with an associated history of daily opiate use. He had no prior psychiatric history, including any history of depression or antidepressant medications. His outpatient medications included metoprolol, cyclobenzaprine, and morphine (in the form of MS-Contin). His physical examination was notable for heavy sedation, mydriasis, hypoactive bowel sounds, urinary retention, epistaxis, and depressed reflexes. A computed tomography (CT) scan of the head was negative, and CT of the cervical spine showed degeneration. His blood alcohol screen was negative, and complete blood count and comprehensive metabolic panel results were within normal limits, as were an electrocardiogram and cerebrospinal fluid from a lumbar puncture. His urine toxicology screen was positive for “benzodiazepines and tricyclics.” Mr. Brown’s mental status examination revealed waxing and waning alertness, an unkempt appearance, lack of cooperation with nursing and medical personnel, somewhat slurred speech, and signs of psychomotor retardation. His affect alternated between subdued/somnolent and restless/agitated. He denied suicidal or homicidal ideation but reported significant paranoid ideation that focused on his wife’s suspected affair. His thought process was notably tangential. He denied both auditory and visual hallucinations. His judgment and insight were impaired. During his initial evaluation, the patient was noted to have a Mini-Mental State Examination score of 16 of 30 possible points. He lost 7 of 10 points for orientation, 3 for attention and calculation, 2 for recall, and 1 each for sentence writing and copying design. Tricyclic Antidepressant Toxicity Muhammad M. Khalid; Muhammad Waseem. Author Information Last Update: July 5, 2020. Go to: Introduction Tricyclic antidepressants (TCAs) were introduced in the late 1950s for the treatment of depression. However, with the advent of selective serotonin reuptake inhibitors (SSRIs) and other new antidepressants, the use of TCAs has become limited, although it is still used to treat depression that has not responded to treatment with less toxic agents. In adults, TCAs are also used in migraine headache prophylaxis, treatment of neuralgic pain, including the pain associated with Ciguatera poisoning, and obsessive-compulsive disorder. In children, TCAs have been used to treat nocturnal enuresis. Despite the current limited use of TCAs, the curve for TCA-overdose associated hospitalization and fatality is on the rise.[1][2][3][4] Go to: Etiology Since TCAs are mostly used for treating patients with chronic pain and neuropsychiatric disorders, toxicity and overdoses are mostly seen in these patients, who are taking them for these debilitating diseases. NURS 6061 University Of Texas Tricyclic Antidepressant Toxicity Presentation Tricyclic Antidepressant Toxicity Presentation. These drugs are commonly prescribed for these diseases, and therefore are readily available to these patients. Go to: Epidemiology According to the database, TCA overdose accounted for 1.12 exposures per 10,000 population in 1992. Recently, the trend for antidepressant overdose has shifted more towards SSRIs. However, the rate of hospitalization is higher in cases of TCA overdose compared to SSRI, because of the narrower therapeutic index with TCAs. Go to: Pathophysiology Tricyclic antidepressants impose their therapeutic effects by inhibiting presynaptic reuptake of norepinephrine and serotonin in the central nervous system (CNS). This effect in the CNS can cause seizures. TCAs are weakly basic, and an acidic environment facilitates the formation of the ionized form and potentiates this effect. In cases of toxicity, TCAs block a number of receptors, including peripheral alpha-adrenergic, histaminic, muscarinic, and central serotonin receptors. Blockade of alpha-adrenergic receptors can cause hypotension. Blockade of muscarinic receptors can cause signs of anticholinergic toxicity, such as tachycardia, fever, dry mouth and skin, decreased bowel sounds, and altered mental status. Blockade of histamine receptors can also cause altered mental status. TCAs can cause cardiac toxicity. Blockade of fast sodium channels in myocardial cells slows the action potential and provides a membrane stabilizing effect. The characteristic QRS prolongation seen in TCA overdose occurs secondary to prolongation of phase “0” of the myocardial action potential. This effect can lead to heart block and bradycardia. QT prolongation seen in cases of TCA overdose occurs due to potassium channel blockade that may potentially cause torsades de pointes. TCAs can also exert a quinidine-like toxic effect on the myocardium that can cause decreased cardiac contractility and hypotension.[5][6][7] Go to: Toxicokinetics TCAs are rapidly absorbed in the gastrointestinal tract. However, following an overdose, owing to the inherent anticholinergic effects, TCAs may decrease the gastrointestinal motility and cause delayed absorption and toxicity. Coingestion of other anticholinergic medications may cause more erratic absorption. TCAs have a long elimination half-life as these drugs are largely bound to the plasma protein and highly lipid-soluble. Renal excretion occurs after significant first-pass hepatic metabolism. TCAs are primarily metabolized by CYP2D6, and the enzyme inducers and inhibitors of this pathway may alter their metabolism. Toxicity may occur because of the primary compound or its metabolite. Respiratory or metabolic acidosis may increase the unbound fraction of TCA and may potentiate the harmful effects. Signs of toxicity usually appear within 2 hours’ post-ingestion. If 6 hours post-ingestion, there are no signs of toxicity seen both clinically and on the electrocardiogram, and the patient has normal bowel sounds, then most likely, the patient has not taken a significant overdose and can be medically cleared for psychiatric evaluation if needed. Once significant toxicity occurs, it usually lasts for 24-48 hours. However, there are case reports of significant toxicity due to Amitriptyline that lasted up to 5 days postingestion. Go to: History and Physical All patients with suspected TCA overdose should be immediately evaluated, and a 12 lead EKG should be obtained. The therapeutic index of TCAs is narrow, and therefore, the ingestion of 10 to 20 mg/kg is potentially life-threatening. Symptoms usually start in 30 to 40 minutes, and signs of toxicity are usually clinically apparent within 2 hours, but delayed toxicity may occur. History of co-ingestion or access to other medications, including acetaminophen and aspirin, is essential. Close attention to the patient’s vital signs and repeated physical examination for evidence of an anticholinergic toxidrome, cardiac toxicity, and neurologic toxicity should be done and will help guide proper management. Go to: Evaluation Cardiovascular, anticholinergic, and neurologic manifestations are common. Vital signs may be abnormal. The patient may not be able to protect his or her airway. NURS 6061 University Of Texas Tricyclic Antidepressant Toxicity Presentation Tricyclic Antidepressant Toxicity Presentation. Respiratory depression may occur. Sinus tachycardia is commonly present due to anticholinergic toxicity, but more dangerous tachydysrhythmias and even bradycardia with or without heart block can occur. Hypotension can occur due to dehydration, cardiac toxicity, and alpha-adrenergic blockade. The patient may often demonstrate anticholinergic toxicity, such as fever, dilated pupils, dry mouth, dry, warm skin, decreased bowel sounds, and altered mental status. The patient may be agitated or seizing, or the patient may have decreased mental status, and may even become comatose. An EKG should be obtained early in the management of these patients, and any evidence of sodium and/or potassium channel blockade should be promptly addressed. Prolongation of QRS, due to sodium channel blockade of more than 100 milliseconds, is predictive of seizures while QRS > 160 milliseconds is predictive of arrhythmia. An R/S ratio in AVR of 0.7 or more and an R wave in the AVR lead more than 3 mm is strongly predictive of seizures and arrhythmias. In addition to basic lab investigations, including levels of possible co-investments, such as acetaminophen and aspirin, a CT scan of the head to rule out other causes of altered mental status should be done if clinically indicated. It should be noted that TCA levels do not correlate with toxicity, but may be helpful in diagnosing an unknown overdose when the clinical symptoms and signs point to a possible TCA ingestion. Any sign of toxicity warrants admission in an intensive care setting for at least 24 hours. Asymptomatic patients should be continuously monitored for signs of toxicity, changes in vital signs, and EKG for at least 6 hours.[8][9][10][11] Go to: Treatment / Management Proper management of airway, breathing, and circulation is critical in cases of TCA poisoning. Gastrointestinal decontamination by activated charcoal should be done only if conditions are appropriate and the airway is protected. Charcoal decontamination may be effective up to 2 hours’ post-ingestion, especially if the bowel sounds are diminished. Every effort should be made to minimize the formation of acidosis, as acidosis may increase cardiac and neurologic toxicity. Seizures usually respond to benzodiazepines, but in cases of refractory seizures, prompt administration of anticonvulsants, such as phenobarbital or propofol, or even general anesthesia, should be considered. Sodium bicarbonate should be given to hemodynamically unstable patients, patients with seizures, and patients with QRS prolongation of more than 100 msec. Sodium bicarbonate is given as a bolus of 1 meq/kg, followed by an intravenous infusion containing sodium bicarbonate. The aim of this therapy is to narrow the QRS and to keep the serum pH between 7.5 and 7.55. Hypotensive patients should be treated with IV fluids and sodium bicarbonate, and if their hypotension does not respond to this, alpha-adrenergic agents, such as norepinephrine, should be used. Sodium bicarbonate should be used to treat dysrhythmias associated with QRS widening. Temporary pacemakers have been used to treat refractory symptomatic bradycardias not responsive to sodium bicarbonate. Physostigmine, Type 1A, Type 1C, and Type 3 Anti-dysrhythmic agents should be strictly avoided, as should Flumazenil. Intralipid emulsion treatment should be considered in hemodynamically unstable patients with overdoses of lipophilic TCAs. Since TCA are highly protein bound with an extensive volume of distribution, enhanced elimination with dialysis and hemoperfusion is not effective. NURS 6061 University Of Texas Tricyclic Antidepressant Toxicity Presentation Tricyclic Antidepressant Toxicity Presentation. Go to: Enhancing Healthcare Team Outcomes Tricyclic antidepressant toxicity can be life-threatening and is best managed by an interprofessional team that consists of an emergency department physician, nurse practitioner, poison control specialist, cardiologist, neurologist, and an emergency or critical care nurse. As with all cases of poisoning, proper management of airway, breathing, and circulation is critical in cases of TCA poisoning. Gastrointestinal decontamination by activated charcoal should be done only if conditions are appropriate and the airway is protected. Sodium bicarbonate should be given to hemodynamically unstable patients, patients with seizures, and patients with QRS prolongation of more than 100 msec. Some patients may even require temporary pacing for bradycardia. Hydration and close monitoring in an ICU setting are recommended. It is vital to make sure that the patient has no other coingestants in the systemic circulation. For patients managed promptly, the outcomes are good. However, if treatment is delayed or the patient has ingested multiple other agents, the prognosis is guarded. Before discharge, if attempted suicide is suspected, the patient should be referred to a mental health counselor. Parents should be urged to keep all medications in a locked cabinet away from the reach of children.[12][13][Level 5] Go to: Questions To access free multiple choice questions on this topic, click here. Go to: References 1. Avau B, Borra V, Vanhove AC, Vandekerckhove P, De Paepe P, De Buck E. First aid interventions by laypeople for acute oral poisoning. Cochrane Database Syst Rev. 2018 Dec 19;12:CD013230. [PMC free article] [PubMed] 2. Kassim T, Mahfood Haddad T, Rakhra A, Kabach A, Qurie A, Selim M, Nayfeh AS, Aly A, Holmberg MJ. A Case of Amitriptyline-induced Myocarditis. Cureus. 2018 Jun 19;10(6):e2840. [PMC free article] [PubMed] 3. Methling M, Krumbiegel F, Hartwig S, Parr MK, Tsokos M. Toxicological findings in suicides – frequency of antidepressant and antipsychotic substances. Forensic Sci Med Pathol. 2019 Mar;15(1):23-30. [PubMed] 4. Guan Y, Li X, Umetani M, Boini KM, Li PL, Zhang Y. Tricyclic antidepressant amitriptyline inhibits autophagic flux and prevents tube formation in vascular endothelial cells. Basic Clin. Pharmacol. Toxicol. 2019 Apr;124(4):370384. [PMC free article] [PubMed] 5. Giwa A, Oey E. The return of an old nemesis: Survival after severe tricyclic antidepressant toxicity, a case report. Toxicol Rep. 2018;5:357-362. [PMC free article] [PubMed] 6. Lubna NJ, Wada T, Nakamura Y, Chiba K, Cao X, Izumi-Nakaseko H, Ando K, Naito AT, Satoh Y, Sugiyama A. Amitriptyline May Have Possibility to Induce Brugada Syndrome Rather than Long QT Syndrome. Cardiovasc. Toxicol. 2018 Feb;18(1):91-98. [PubMed] 7. Dempsey SK, Poklis JL, Sweat K, Cumpston K, Wolf CE. Acute Toxicity From Intravenous Use of the Tricyclic Antidepressant Tianeptine. J Anal Toxicol. 2017 Jul 01;41(6):547-550. [PMC free article] [PubMed] 8. Carr MJ, Ashcroft DM, Kontopantelis E, While D, Awenat Y, Cooper J, ChewGraham C, Kapur N, Webb RT. Clinical management following self-harm in a UK-wide primary care cohort. J Affect Disord. 2016 Jun;197:182-8. [PMC free article] [PubMed] 9. Bergen H, Murphy E, Cooper J, Kapur N, Stalker C, Waters K, Hawton K. A comparative study of non-fatal self-poisoning with antidepressants relative to prescribing in three centres in England. J Affect Disord. 2010 Jun;123(1-3):95101. [PubMed] 10. Bek K, Ozkaya O, Mutlu B, Da?demir A, Sungur M, Açikgöz Y, I?lek I, Baysal K. Charcoal haemoperfusion in amitriptyline poisoning: experience in 20 children. Nephrology (Carlton). 2008 Jun;13(3):193-7. [PubMed] 11. Gillman PK. Tricyclic antidepressant pharmacology and therapeutic drug interactions updated. Br. J. Pharmacol. 2007 Jul;151(6):737-48. [PMC free article] [PubMed] 12. Cao D, Heard K, Foran M, Koyfman A. Intravenous lipid emulsion in the emergency department: a systematic review of recent literature. J Emerg Med. 2015 Mar;48(3):387-97. [PubMed] 13. Güloglu C, Orak M, Ustündag M, Altunci YA. Analysis of amitriptyline overdose in emergency medicine. Emerg Med J. 2011 Apr;28(4):296-9. [PubMed] Copyright © 2020, StatPearls Publishing LLC. This book is distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits use, duplication, adaptation, distribution, and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, a link is provided to the Creative Commons license, and any changes made are indicated. Bookshelf ID: NBK430931PMID: 28613681 • • • Share on Facebook Share on Twitter Share on Google+ Views • PubReader • Print View • Cite this Page In this Page • Introduction • Etiology • Epidemiology • Pathophysiology • Toxicokinetics • History and Physical • Evalu …NURS 6061 University Of Texas Tricyclic Antidepressant Toxicity Presentation Purchase answer to see full attachment Student has agreed that all tutoring, explanations, and answers provided by the tutor will be used to help in the learning process and in accordance with Studypool’s honor code & terms of service . 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