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Cell Biochemistry and Biophysics Jul 2015Myocardial infarction (MI) is a term used for an event of heart attack which is due to formation of plaques in the interior walls of the arteries resulting in reduced... (Review)
Review
Myocardial infarction (MI) is a term used for an event of heart attack which is due to formation of plaques in the interior walls of the arteries resulting in reduced blood flow to the heart and injuring heart muscles because of lack of oxygen supply. The symptoms of MI include chest pain, which travels from left arm to neck, shortness of breath, sweating, nausea, vomiting, abnormal heart beating, anxiety, fatigue, weakness, stress, depression, and other factors. The immediate treatment of MI include, taking aspirin, which prevents blood from clotting, and nitro-glycerin to treat chest pain and oxygen. The heart attack can be prevented by taking an earlier action to lower those risks by controlling diet, fat, cholesterol, salt, smoking, nicotine, alcohol, drugs, monitoring of blood pressure every week, doing exercise every day, and loosing body weight. The treatment of MI includes, aspirin tablets, and to dissolve arterial blockage injection of thrombolytic or clot dissolving drugs such as tissue plasminogen activator, streptokinase or urokinase in blood within 3 h of the onset of a heart attack. The painkillers such as morphine or meperidine can be administered to relieve pain. Nitroglycerin and antihypertensive drugs such as beta-blockers, ACE inhibitors or calcium channel blockers may also be used to lower blood pressure and to improve the oxygen demand of heart. The ECG, coronary angiography and X-ray of heart and blood vessels can be performed to observe the narrowing of coronary arteries. In this article the causes, symptoms and treatments of MI are described.
Topics: Humans; Myocardial Infarction
PubMed: 25638347
DOI: 10.1007/s12013-015-0553-4 -
European Journal of Drug Metabolism and... Oct 2019Pain management in the pediatric population is complex for many reasons. Mild pain is usually managed quite well with oral acetaminophen or ibuprofen. Situations... (Review)
Review
Pain management in the pediatric population is complex for many reasons. Mild pain is usually managed quite well with oral acetaminophen or ibuprofen. Situations involving more severe pain often require the use of an opioid, which may be administered by many different routes, depending on clinical necessity. Acute and chronic disease states, as well as the constantly changing maturational process, produce unique challenges at every level of pediatrics in dosing and management of all medications, especially with regard to high-risk opioids. Although there has been significant progress in the understanding of opioid pharmacokinetics and pharmacodynamics in neonates, infants, children, and adolescents, somewhat limited data exist from which necessary information, concerning the safe and effective use of these agents, may be drawn. The evidence here provided is intended to be helpful in directing the practitioner to patient-specific reasons for preferring one opioid over another. As our knowledge of opioids and their effects has grown, it has become clear that older medications like codeine and meperidine (pethidine) have very limited use in pediatrics. This review provides pharmacokinetic and pharmacodynamic evidence on the currently available opioids: morphine, fentanyl (and derivatives), codeine, meperidine, oxycodone, hydrocodone, hydromorphone, methadone, buprenorphine, butorphanol, nalbuphine, pentazocin, ketobemidone, tramadol, piritramide, naloxone and naltrexone. Morphine, being the most studied opioid analgesic, is the standard against which all others are compared. Pharmacokinetic parameters of morphine that have been found in neonates, i.e., higher volume of distribution, immature metabolic processes that develop at various rates, elimination that is variable based on age and weight, as well as treated and untreated disease processes, are an example of all opioids in the population discussed in this review. Outside the premature and neonatal population, the use of opioids in infants, children, and adolescents quickly begins to resemble the established values found in adults. As such, the concerns (risks) of these medications become comparable to those seen in adults.
Topics: Analgesics, Opioid; Animals; Child; Humans; Infant; Infant, Newborn; Pain; Pain Management
PubMed: 31006834
DOI: 10.1007/s13318-019-00552-0 -
American Journal of Obstetrics and... May 2023Labor pain is among the most severe types of physical pain that women may experience during their lifetime. Thus, pain relief is an essential part of medical care during... (Review)
Review
Labor pain is among the most severe types of physical pain that women may experience during their lifetime. Thus, pain relief is an essential part of medical care during childbirth. Epidural analgesia is considered to be the most efficient method of pain relief during labor. Nevertheless, patient preferences, contraindications, limited availability, and technical failure may require the use of alternative pain reliving methods during labor including systemic pharmacologic agents, and nonpharmacologic methods. Nonpharmacologic methods for pain alleviation during vaginal birth have become popular over the years, either as a complement to pharmacologic agents or at times as the principal therapy. Methods such as relaxation techniques (ie, yoga, hypnosis, and music), manual techniques (ie, massage, reflexology, and shiatsu), acupuncture, birthing ball, and transcutaneous electrical nerve stimulation are considered safe, although the evidence supporting their effectiveness for pain relief is not as robust as it is for pharmacologic agents. Systemic pharmacologic agents are mostly administered by inhalation (nitrous oxide) or through the parenteral route. These agents include opioids such as meperidine, nalbuphine, tramadol, butorphanol, morphine, and remifentanil, and non-opioid agents such as parenteral acetaminophen and nonsteroidal anti-inflammatory drugs. Systemic pharmacologic agents suggest a diverse armamentarium of medication for pain management during labor. Their efficacy in treating pain associated with labor varies, and some continue to be used even though they have not been proven effective for pain relief. In addition, the maternal and perinatal side effects differ markedly among these agents. There is a relative abundance of data regarding the effectiveness of analgesic drugs compared with epidural, but the data regarding comparisons among the different types of alternative analgesic agents are scarce, and there is no consistency regarding the drug of choice for women who do not receive epidural pain management. This review aims to present the available data regarding the effectiveness of the different methods of relieving pain during labor other than epidural. The data presented are mainly based on recent level I evidence regarding pharmacologic and nonpharmacologic methods for pain relief during labor.
Topics: Pregnancy; Female; Humans; Pain Management; Labor, Obstetric; Analgesics; Analgesics, Opioid; Labor Pain
PubMed: 37005099
DOI: 10.1016/j.ajog.2023.03.003 -
Archives of Toxicology Aug 2021Opioid-induced respiratory depression is potentially life-threatening and often regarded as the main hazard of opioid use. Main cause of death is cardiorespiratory... (Review)
Review
Opioid-induced respiratory depression is potentially life-threatening and often regarded as the main hazard of opioid use. Main cause of death is cardiorespiratory arrest with hypoxia and hypercapnia. Respiratory depression is mediated by opioid μ receptors expressed on respiratory neurons in the CNS. Studies on the major sites in the brainstem mediating respiratory rate suppression, the pre-Bӧtzinger complex and parabrachial complex (including the Kӧlliker Fuse nucleus), have yielded conflicting findings and interpretations but recent investigations involving deletion of μ receptors from neurons have led to greater consensus. Some opioid analgesic drugs are histamine releasers. The range of clinical effects of released histamine include increased cardiac output due to an increase in heart rate, increased force of myocardial contraction, and a dilatatory effect on small blood vessels leading to flushing, decreased vascular resistance and hypotension. Resultant hemodynamic changes do not necessarily relate directly to the concentration of histamine in plasma due to a range of variables including functional differences between mast cells and histamine-induced anaphylactoid reactions may occur less often than commonly believed. Opioid-induced histamine release rarely if ever provokes bronchospasm and histamine released by opioids in normal doses does not lead to anaphylactoid reactions or result in IgE-mediated reactions in normal patients. Hypersensitivities to opioids, mainly some skin reactions and occasional type I hypersensitivities, chiefly anaphylaxis and urticaria, are uncommon. Hypersensitivities to morphine, codeine, heroin, methadone, meperidine, fentanyl, remifentanil, buprenorphine, tramadol, and dextromethorphan are summarized. In 2016, the FDA issued a Drug Safety Communication concerning the association of opioids with serotonin syndrome, a toxicity associated with raised intra-synaptic concentrations of serotonin in the CNS, inhibition of serotonin reuptake, and activation of 5-HT receptors. Opioids may provoke serotonin toxicity especially if administered in conjunction with other serotonergic medications. The increasing use of opioid analgesics and widespread prescribing of antidepressants and psychiatric medicines, indicates the likelihood of an increased incidence of serotonin toxicity in opioid-treated patients.
Topics: Analgesics, Opioid; Animals; Drug Hypersensitivity; Hemodynamics; Histamine Release; Humans; Respiratory Insufficiency; Serotonin Syndrome
PubMed: 33974096
DOI: 10.1007/s00204-021-03068-2 -
Clinical Reviews in Allergy & Immunology Jun 2022Hypersensitivity reactions (HSRs) to chemotherapy may prevent patients from receiving the most effective therapy. This review was undertaken to identify evidence-based... (Review)
Review
Hypersensitivity reactions (HSRs) to chemotherapy may prevent patients from receiving the most effective therapy. This review was undertaken to identify evidence-based preventive premedication strategies that reduce the likelihood of HSR in the first instance and improve the safety of subsequent infusions in patients who have demonstrated HSR to a certain class of chemotherapy. PubMed was searched until October 2021 using the key words: "hypersensitivity to chemotherapeutic drugs," "hypersensitivity to antineoplastic agents," "taxanes hypersensitivity," "platinum compound hypersensitivity," "premedication," "dexamethasone," "prednisone," "hydrocortisone," "antihistamine," "diphenhydramine," "cetirizine," "famotidine," "meperidine," "aspirin," "ibuprofen," and "montelukast." The search was restricted to articles published in English. A total of 73 abstracts were selected for inclusion in the review. Most premedication regimens have been derived empirically rather than determined through randomized trials. Based on the available evidence, we provide an update on likely HSR mechanisms and a practical guide for classifying systemic HSR. The evidence indicates that a combination of prevention strategies using newer antihistamines, H2 antagonists, leukotriene receptor antagonists, and corticosteroids and other interventions used judiciously reduces the occurrence and severity of HSR and improves safety.
Topics: Drug Hypersensitivity; Histamine Antagonists; Humans; Paclitaxel; Premedication; Taxoids
PubMed: 35258842
DOI: 10.1007/s12016-022-08932-2 -
Headache Jan 2015The study aims to provide an updated assessment of the evidence for individual pharmacological therapies for acute migraine treatment. Pharmacological therapy is... (Review)
Review
The study aims to provide an updated assessment of the evidence for individual pharmacological therapies for acute migraine treatment. Pharmacological therapy is frequently required for acutely treating migraine attacks. The American Academy of Neurology Guidelines published in 2000 summarized the available evidence relating to the efficacy of acute migraine medications. This review, conducted by the members of the Guidelines Section of the American Headache Society, is an updated assessment of evidence for the migraine acute medications. A standardized literature search was performed to identify articles related to acute migraine treatment that were published between 1998 and 2013. The American Academy of Neurology Guidelines Development procedures were followed. Two authors reviewed each abstract resulting from the search and determined whether the full manuscript qualified for review. Two reviewers studied each qualifying full manuscript for its level of evidence. Level A evidence requires at least 2 Class I studies, and Level B evidence requires 1 Class I or 2 Class II studies. The specific medications - triptans (almotriptan, eletriptan, frovatriptan, naratriptan, rizatriptan, sumatriptan [oral, nasal spray, injectable, transcutaneous patch], zolmitriptan [oral and nasal spray]) and dihydroergotamine (nasal spray, inhaler) are effective (Level A). Ergotamine and other forms of dihydroergotamine are probably effective (Level B). Effective nonspecific medications include acetaminophen, nonsteroidal anti-inflammatory drugs (aspirin, diclofenac, ibuprofen, and naproxen), opioids (butorphanol nasal spray), sumatriptan/naproxen, and the combination of acetaminophen/aspirin/caffeine (Level A). Ketoprofen, intravenous and intramuscular ketorolac, flurbiprofen, intravenous magnesium (in migraine with aura), and the combination of isometheptene compounds, codeine/acetaminophen and tramadol/acetaminophen are probably effective (Level B). The antiemetics prochlorperazine, droperidol, chlorpromazine, and metoclopramide are probably effective (Level B). There is inadequate evidence for butalbital and butalbital combinations, phenazone, intravenous tramadol, methadone, butorphanol or meperidine injections, intranasal lidocaine, and corticosteroids, including dexamethasone (Level C). Octreotide is probably not effective (Level B). There is inadequate evidence to refute the efficacy of ketorolac nasal spray, intravenous acetaminophen, chlorpromazine injection, and intravenous granisetron (Level C). There are many acute migraine treatments for which evidence supports efficacy. Clinicians must consider medication efficacy, potential side effects, and potential medication-related adverse events when prescribing acute medications for migraine. Although opioids, such as butorphanol, codeine/acetaminophen, and tramadol/acetaminophen, are probably effective, they are not recommended for regular use.
Topics: Adult; Anti-Inflammatory Agents; Humans; Migraine Disorders; Serotonin Receptor Agonists; Societies, Medical
PubMed: 25600718
DOI: 10.1111/head.12499 -
The anaesthetist, opioid analgesic drugs, and serotonin toxicity: a mechanistic and clinical review.British Journal of Anaesthesia Jan 2020Most cases of serotonin toxicity are provoked by therapeutic doses of a combination of two or more serotonergic drugs, defined as drugs affecting the serotonin... (Review)
Review
Most cases of serotonin toxicity are provoked by therapeutic doses of a combination of two or more serotonergic drugs, defined as drugs affecting the serotonin neurotransmitter system. Common serotonergic drugs include many antidepressants, antipsychotics, and opioid analgesics, particularly fentanyl, tramadol, meperidine (pethidine), and methadone, but rarely morphine and other related phenanthrenes. Symptoms of serotonin toxicity are attributable to an effect on monoaminergic transmission caused by an increased synaptic concentration of serotonin. The serotonin transporter (SERT) maintains low serotonin concentrations and is important for the reuptake of the neurotransmitter into the presynaptic nerve terminals. Some opioids inhibit the reuptake of serotonin by inhibiting SERT, thus increasing the plasma and synaptic cleft serotonin concentrations that activate the serotonin receptors. Opioids that are good inhibitors of SERT (tramadol, dextromethorphan, methadone, and meperidine) are most frequently associated with serotonin toxicity. Tramadol also has a direct serotonin-releasing action. Fentanyl produces an efflux of serotonin, and binds to 5-hydroxytryptamine (5-HT) and 5-HT receptors, whilst methadone, meperidine, and more weakly tapentadol, bind to 5-HT but not 5-HT receptors. The perioperative period is a time where opioids and other serotonergic drugs are frequently administered in rapid succession, sometimes to patients with other serotonergic drugs in their system. This makes the perioperative period a relatively risky time for serotonin toxicity to occur. The intraoperative recognition of serotonin toxicity is challenging as it can mimic other serious syndromes, such as malignant hyperthermia, sepsis, thyroid storm, and neuroleptic malignant syndrome. Anaesthetists must maintain a heightened awareness of its possible occurrence and a readiness to engage in early treatment to avoid poor outcomes.
Topics: Analgesics, Opioid; Anesthesiologists; Fever; Humans; Intraoperative Complications; Serotonin Agents; Serotonin Syndrome
PubMed: 31653394
DOI: 10.1016/j.bja.2019.08.010 -
Archives of Toxicology Aug 2018Drugs may cause serotonin toxicity by a number of different mechanisms including inhibition of serotonin uptake and metabolism, increased serotonin synthesis and... (Review)
Review
Drugs may cause serotonin toxicity by a number of different mechanisms including inhibition of serotonin uptake and metabolism, increased serotonin synthesis and release, activation of serotonin receptors, and inhibition of cytochrome P450 oxidases. Some drug interactions involving opioids can increase intrasynaptic levels of serotonin, and opioid analgesic drugs are now recognized as being involved in some cases of serotonin toxicity especially if administered in conjunction with other serotonergic medications including monoamine oxidase inhibitors, selective serotonin reuptake inhibitors, serotonin-norepinephrine reuptake inhibitors, and tricyclic antidepressants. In March 2016, the FDA issued a Drug Safety Communication concerning the association of the entire class of opioid pain medicines with serotonin toxicity. Reports of the involvement of individual opioids particularly tramadol, tapentadol, meperidine, methadone, oxycodone, fentanyl, and dextromethorphan are reviewed. While relevance to human serotonin toxicity of animal models, including many studies on rat brain synaptosomes, is questionable, important insights have recently been forthcoming from research utilizing 5-HT receptors, serotonin transporter (SERT), and knockout mice. In studies with human SERT-transfected human HEK293 cells, the synthetic opioids tramadol, meperidine, methadone, tapentadol, and dextromethorphan inhibited SERT, but fentanyl and a number of phenanthrenes including morphine and hydromorphone did not. Receptor ligand-binding assays revealed interaction of fentanyl with 5-HT receptors and interaction of meperidine, methadone, and fentanyl with 5-HT receptors. Although the opioids most often associated with serotonin toxicity in humans inhibit human SERT in vitro, fentanyl and oxycodone are not inhibitory even though their clinical involvement has been reported. This suggests some SERT-independent effects on the serotonin system in vivo. Heightened clinician awareness of the possibility of serotonin toxicity among patients taking opioids and serotonergic antidepressants is called for.
Topics: Analgesics, Opioid; Animals; Brain; Drug Interactions; Humans; Models, Animal; Serotonin; Serotonin Syndrome
PubMed: 29916050
DOI: 10.1007/s00204-018-2244-6