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The Metabolic Medicine Postoperative Bariatric Surgery Consultation
Published in Michael M. Rothkopf, Jennifer C. Johnson, Optimizing Metabolic Status for the Hospitalized Patient, 2023
Michael M. Rothkopf, Jennifer C. Johnson
The disadvantage of transdermal clonidine is that its onset of action begins after about 8 hours and reaches the steady state at 2–3 days. Therefore, a fast-acting agent may be needed on day 1. In our practice, the drug of choice is amlodipine. This drug is taken either crushed or dissolved in a small amount of water. A second option we have employed is to give oral clonidine at the 0.1 mg dose. This tablet is small enough that it can be taken with a few sips of water. It can be given repeatedly for blood pressure control.
Nausea/Vomiting of Pregnancy and Hyperemesis Gravidarum
Published in Vincenzo Berghella, Maternal-Fetal Evidence Based Guidelines, 2022
Clonidine is a centrally acting alpha-2 adrenergic agonist commonly used as an anti-hypertensive agent. It has been studied in the prevention of post-operative nausea and vomiting. One small cross over design RCT (N = 12) evaluated transdermal clonidine in addition to other anti-emetic therapy for the treatment of refractory HG and found subjective and objective improvement in measures of nausea and vomiting. Of note on this small study, it was also reported one patient whose pregnancy course was complicated by central venous catheter associated sepsis [112]. Given this small limited study, there is insufficient data on safety or efficacy to recommend clonidine for the treatment of NVP or HG.
Complications of extracranial carotid aneurysm repair and resection of carotid body tumor
Published in Sachinder Singh Hans, Mark F. Conrad, Vascular and Endovascular Complications, 2021
Sachinder Singh Hans, Mary Lee
Barorecetor failure is a very rare but an important complication following bilateral carotid body tumor resection. It should be suspected in patients with tachycardia and labile hypertension 24–72 hours following tumor removal.4 Other symptoms include headache, emotional lability, and anxiety. Prompt diagnosis of this syndrome is imperative as patients can develop hypertensive encephalopathy with stroke.4 The baroreflex failure has not been described following unilateral carotid body tumor resection, suggesting that contralateral preservation of baroreceptor is adequate to maintain normal physiology.4 Interruption of the baroreceptors results in unopposed sympathetic signals from the brain stem leads to tachycardia and labile hypertension with BP increasing to very high values. An incidence of 20% of baroreflex failure following bilateral common carotid body tumor resection has been reported.4 Treatment is largely empiric. Antihypertensive complications with quick onset of action and short half-life such as labetalol, phentolamine, hydrolozine, and nitroprusside are recommended. For long-term management, clonidine is a preferred therapy. Clonidine treats both hypertension and tachycardia associated with this syndrome by stimulating alpha-2 receptors in the brain stem and stimulating parasympathetic outflow.4
Management of Pregabalin Use Disorder: A Case Series
Published in Journal of Psychoactive Drugs, 2022
Lisa Langlumé, Céline Eiden, Sophie Roy, Floriane Taruffi, Julien Gambier, Hélène Donnadieu-Rigole, Hélène Peyrière
In this series of patients, management of withdrawal was based, for some anxious patients, on the short-term use of diazepam with a programmed dose reduction. Importantly, the diazepam dose should be adapted in patients with a history of benzodiazepine abuse and/or current use. At the time of the study, the long-term effectiveness of this adjuvant treatment was unknown. However, two patients who took diazepam relapsed and restarted pregabalin consumption. One of the limitations is the risk of the shift of dependence from pregabalin to diazepam or another substance (Gahr et al. 2015). Clonidine (used in patient no. 8) might be another possible option to manage pregabalin-related withdrawal symptoms. Clonidine is an alpha-adrenergic agonist used off-label for the management of opioid withdrawal (Toce et al. 2018). Clonidine helps to reduce the signs and symptoms of excessive autonomic activity (e.g. anxiety, chills, piloerection, tachycardia, and hypertension). Clonidine has been previously used for pregabalin withdrawal management outside the context of pregabalin use disorder and was effective on agitation (Barrett, Kittler, and Singarajah 2015).
Immunomodulatory properties of antihypertensive drugs and digitalis glycosides
Published in Expert Review of Cardiovascular Therapy, 2022
Paweł Bryniarski, Katarzyna Nazimek, Janusz Marcinkiewicz
Clonidine, agonist of alfa-2 receptor, is used in medium and severe hypertension, Gilles de la Tourette syndrome, treatment of opioid and alcohol addiction, as well as in Attention Deficit Hyperactivity Disorder (ADHD). Clonidine lowers blood pressure, slows down the heart rate, reduces stroke volume, relieves pain, has a calming and anxiolytic effect, and increases appetite. This drug, by stimulating receptors in the solitary tract, reduces the activity of sympathetic neurons, which go to the heart and blood vessels, and stimulates the vagus nerve. This leads to dilation of arterial vessels, slowdown of the heart, and reduction of minute capacity. The immune effects of clonidine have not been thoroughly investigated. In placental tissue and peripheral blood mononuclear cells during normal pregnancy, we can observe increases anti-inflammatory IL-10 production and decreases pro-inflammatory TNF-alpha and IL-6 [16]. Because of anti-TNF activity, this drug increases eNOS mRNA expression in human uterine myometrial microvascular endothelial cells [18] (Table 1).
Impact of chronic medications in the perioperative period: mechanisms of action and adverse drug effects (Part I)
Published in Postgraduate Medicine, 2021
Ofelia Loani Elvir-Lazo, Paul F White, Hillenn Cruz Eng, Firuz Yumul, Raissa Chua, Roya Yumul
Alpha2 agonists act predominantly on central α2-receptors. Their activation leads to inhibition of norepinephrine release from presynaptic neurons, sedation via stimulation of receptors in the locus coeruleus, and modification of centrally mediated pain via dorsal horn stimulation [11]. Clonidine is a mixed alpha2 agonist-antagonist used orally to treat hypertension, anxiety, attention deficit hyperactivity disorder (ADHD), chronic pain, postoperative shivering, and opioid withdrawal symptoms. Clonidines are metabolized mainly through CYP2D6 and to a lesser extent by CYP3A4/5 and CYP1A1/2. Tizanidine, another mixed α2 agonist/antagonist, is used to treat muscle spasms and cramps associated with a wide variety of CNS disorders. The primary cytochrome P450 isoenzyme involved in tizanidine metabolism is CYP1A2. Dexmedetomidine, a pure α2 agonist, is used for sedation and analgesia in the operating room (OR) and postanesthesia care unit (PACU) and in the intensive care unit (ICU) [11]. Dexmedetomidine is metabolized by cytochrome P450 (CYP2A6) and uridine diphosphate glucuronosyltransferase (UGTs), UGT1A4, and UGT2B10, to inactive metabolites.