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Marine Biotoxins: Symptoms and Monitoring Programs
Published in Hafiz Ansar Rasul Suleria, Megh R. Goyal, Health Benefits of Secondary Phytocompounds from Plant and Marine Sources, 2021
Huma Bader Ul Ain, Farhan Saeed, Hafiza Sidra Yaseen, Tabussam Tufail, Hafiz Ansar Rasul Suleria
There is no neutralizing agent accessible for ciguatera poison. Regurgitating must be initiated if the patient is wake and has eaten ciguatera poison containing fish in the last 3 to 4 hours. Ipecac drug is used because regurgitating, but numerous specialists think ipecac may cause electrolyte imbalance in the body, so that IV liquids are must in worst sickness. Initially, the administration of activated charcoal within 3 to 4 hours after the ingestion of toxicant may adsorb the poison. Amitriptyline and gabapentin may diminish neural side effects. Intravenous Mannitol is the main CFP treatment assessed by randomized single-or double-blind studies to counteract the symptoms during the initial 2–3 days of poisoning [13, 43, 54]. Diphenhydramine, hydroxyzine, and NSAID’s may help to treat irritation and eliminate painful sensation. Stay away from liquor, fish, nuts, and nut oils are strongly recommended after the use of ciguatera poison to reduce the chances of symptoms reoccurrence.
Restricted eating disorders
Published in Judy Bothamley, Maureen Boyle, Medical Conditions Affecting Pregnancy and Childbirth, 2020
It has been suggested that cardiac causes account for at least one-third of the deaths of those with restricted eating disorders7. Severe anorexia may result in reduced cardiac muscle mass, leading to impaired contractility with reduced cardiac output. In addition, the reduced mass can cause the cardiac valves to sag, with subsequent mitral valve prolapse. Electrolyte imbalance, particularly low potassium, can result in cardiac arrhythmias. Women who use syrup of ipecac (a medication that induces vomiting) can experience symptoms of chest pain, muscle weakness, shortness of breath and tachycardia and are at risk of cardiomyopathy, which can be fatal8. Prolonged use of laxatives with a purging type of eating disorder may cause malabsorption, further complicating electrolyte and nutrient balance.
Eating disorders
Published in Judy Bothamley, Maureen Boyle, Medical Conditions Affecting Pregnancy and Childbirth, 2020
Physical complications of anorexia nervosa and bulimia are summarised in Table 11.2 and Table 11.3, respectively. Impaired cardiac function has been reported to be as high as 10–21% for woman with eating disorders (James, 2001). Severe anorexia may result in reduced cardiac muscle mass, leading to impaired contractility with reduced cardiac output. In addition, the reduced mass can cause the cardiac valves to sag, with subsequent mitral valve prolapse (Perry, 2002). Electrolyte imbalance, particularly low potassium, can result in cardiac irregularities. Women who use syrup of ipecac (a medication that induces vomiting) can experience symptoms of chest pain, muscle weakness, shortness of breath and tachycardia and are at risk of cardiomyopathy, which can be fatal (James, 2001). Prolonged use of laxatives with a purging type of eating disorder may cause malabsorption, further complicating electrolyte and nutrient balance (Steffan, et al., 2007). Despite the many potential complications of eating disorders, physical findings may be normal, particularly in women with normal weight who have bulimia nervosa.
Treatment for beta-blocker poisoning: a systematic review
Published in Clinical Toxicology, 2020
Joe-Anthony Rotella, Shaun L. Greene, Zeff Koutsogiannis, Andis Graudins, Yit Hung Leang, Kelvin Kuan, Helen Baxter, Elyssia Bourke, Anselm Wong
Fifteen case reports [67–81] described the administration of activated charcoal. Seven studies reported the dose of activated charcoal (median dose 50 g, range 50–150 g) [68,69,72,74,79,82,83]. Of these cases, six involved atenolol, three involved bisoprolol, three involved propranolol, two involved metoprolol and two involved carvedilol. Death occurred in two cases as a result of progression of beta-blocker toxicity [75,80]. Five case reports [68–71,84] reported survival without complication following use of gastric lavage. One case report [85] described survival following copious vomiting of pill fragments induced by syrup of ipecac administration. Heise et al. [86] reported patient survival after removal of pill fragments by oesophageal gastroduodenoscopy 16 h post-ingestion of atenolol 4500 mg, coingested with chlorthalidone and lisinopril. Death resulted in one case following gastric lavage and administration of activated charcoal [69]. This was most likely the result of progression of beta-blocker toxicity following development of cardiogenic shock and pulmonary oedema.
Therapeutic options for COVID-19: a quick review
Published in Journal of Chemotherapy, 2020
Muhammad Sani Ismaila, Faruku Bande, Aminu Ishaka, Aminatu Abubakar Sani, Karla Georges
Among the literature analyzed in the present work are those focusing on the use of antiparasitic drugs like emetine and ivermectin to treat patients with COVID-19. Emetine, for example, is an isoquinoline, an alkaloid from ipecac. It has been extensively used as an antiparasitic drug reported to inhibit both ribosomal and mitochondrial protein synthesis as well as interfere with the integration and activities of DNA and RNA.80–82 Ivermectin is a broad-spectrum antiparasitic drug. The proposed anti-COVID-19 viral mechanism reported for ivermectin from the in-vitro study is by blocking importin heterodimer responsible for nuclear import. Ivermectin is originally an antiparasitic drug shown to bind with and destabilize the Impα/β1 heterodimer, thereby preventing it from binding to the viral protein and from entering the nucleus, this results in decreased inhibition of the antiviral responses, leading to more efficient antiviral response.29 In vitro experimentation in Vero/hSLAM cells infected with SARS-CoV-2 clinical isolate, Australia/VIC01/2020 (MOI = 0.1) resulted in a ∼5000-fold reduction in viral RNA at 48 h with no toxicity observed.29 But some controversy arose which made the FDA to issue a warning explaining that in vitro studies as reported in Antiviral Research (AVR) were commonly used in the early stages of drug development; thus, additional testing was needed to determine whether ivermectin might be safe or effective in preventing or treating coronavirus or COVID-19 (FDA:https://www.fda.gov/animal-veterinary/product-safety-information/fda-letter-stakeholders-do-not-use-ivermectin-intended-animals-treatment-covid-19-humans).
Attenuation of brain mitochondria oxidative damage by Albizia julibrissin Durazz: neuroprotective and antiemetic effects
Published in Drug and Chemical Toxicology, 2019
Mohammad Ali Ebrahimzadeh, Hamed Fathi, Ali Ziar, Hamidreza Mohammadi
In this study, the flower extract of A. julibrissin significantly reduced frequency of emesis generated by copper sulfate and ipecac in young chickens (Figures 1 and 2). Ipecac induces emesis by stimulation the chemoreceptor trigger zone (CTZ) in the area postrema (central action) and by directly stimulating the gastric mucosa (peripheral action) (Hosseinzadeh et al. 2008). Ipecac-induced emesis was effectively prevented by multiple doses of the extract, suggesting that the extract has antiemetic activity in both the central and peripheral nervous systems. Copper sulfate induces emesis through a peripheral action, by increasing the concentration of 5-HT released from enterochromaffin (EC) cells in the intestinal mucosa (Endo et al. 2000, Hosseinzadeh et al. 2008). A. julibrissin extract also efficiently prevented copper sulfate-induced emesis. These data suggest that the extract has appropriate peripheral antiemetic activity. Furthermore, the antiemetic effect of the extract also increased dose dependently, and the 200 mg/kg dose showed the most effective antiemetic effect (Figures 1 and 2). Flavonoids, glucosides, lignans, saponins, and terpenes are classes of compounds that have been identified to have antiemetic activity (Ahmed et al. 2013). The proposed mechanisms of action for these natural resources are inhibition of the stimulation of dopaminergic signaling in visceral afferent innervations, antioxidant action, antagonism of 5-HT3/5-HT4 receptors, δ (enkephalinergic)-receptor inhibition, tachykinin NK1 receptor antagonism, and cannabinoid CB1 receptor activation (Ahmed et al. 2013). Since these compounds are present in the A. julibrissin extract, it could be inferred that they may be involved in its antiemetic activity. Further studies are necessary to examine the mechanism of action of the various active compounds that could be responsible for the antiemetic activity of the A. julibrissin extract. Stimulation of the dopaminergic neurons at the CTZ can induce emesis. Additionally, release of 5-HT by enterochromaffin cells can occur after mucosal damage. The released 5-HT activates 5-HT3 receptors, stimulating the vagal afferent nerves. Moreover, stimulation of the tachykinin NK1 receptors after release of substance P from the gastric mucosa may act cooperatively with 5-HT3 receptors to induce vomiting in the upper gastrointestinal tract (Endo et al. 2000). Some plant extracts inhibit both the induced 5-HT and increased substance P in abdominal vagal nerve activity (Ahmed et al. 2013). It is possible that the extract containing flavonoids and terpenes, which have been determined to be antiemetic, could penetrate to the central nervous system and have antiemetic activity in the chicken emesis model.