Symptoms Diagnosis and Treatment

When excessive dosage of aspirin is ingested by an individual it is known as aspirin toxicity or salicylate toxicity [1]. With salicylate toxicity or poisoning the common symptomatic manifestations that appears which aids the process of diagnosis are nausea, ringing within ears, pain in the stomach and tachycardia [1]. With excessive dosage poisoning inflammation of the cerebrum, diminished level of sugar within blood and arrest of heart might also occur [1]. To diagnose the exact level of aspirin within the blood plasma consecutive blood examinations are required along with the blood gas analysis. The treatment procedure for salicylate poisoning incorporates activated charcoal, administration of intravenous fluid with sodium bicarbonate, dextrose and potassium chloride [2]. It was found that dextrose application is beneficial though the sugar level of the blood is typical. Aspirin is considered to be a weak acid with PKa value of 3.5 [2]. The mechanism behind the toxicity is uncoupling oxidative phosphorylation. The phenomenon hinders the citric acid cycle and therefore to generate ATP the body opts for anaerobic metabolism which eventually results in the enhanced level of ketones and lactate within the blood [2]. As the child has ingested over dosage of aspirin three hours before, the toxicity should be considered within phase 1 level that may show the phenomenon of hyperventilation followed by respiratory alkalosis and alkaluria. This phase lasts for up to 12 hours and urine sample examination confirms the presence of potassium and sodium bicarbonate. Therefore, the child was treated with repeated dosage of activated charcoal for gastric decontamination process along with IV fluid administration with 5% dextrose that would generate the output of urine within the range of 3 ml/kg/h and resuscitation as the primary treatment [3].

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Most of the insecticide poisoning is due to organo phosphorous (OP) insecticide [4]. These compounds make an attachment and in turn phosphorylate several proteins and enzymes all within the system. Though the exact mechanism is still unclear, however several studies have shown that inhibition of synapse junction of acetylcholine esterase (AChE) plays the major or central role in the mechanism of toxicity [4]. The physiological phenomenon helps in the concentration of acetylcholine and hyper stimulation of the receptors of acetylcholine within the Central Nervous System (CNS), Autonomic Nervous System (ANS) and Neuromuscular Junction (NMJ) [4]. The toxicity results in acute failure of the respiratory system as a result of neuromuscular system, bronchorrhoea and diminished central respiration drive [4]. The poisoning results in rapid arrest of the respiratory system might be within 30 minutes. The farmer patient was showing the signs of insecticide poisoning with profuse salivation and problems during breathing. The rate of the pulse was 35 beats/ min (bradycardia) which was much lower showing the risk of cardiac arrest and his pupils were also constricted. Therefore his respiratory rate and nervous system is affected [5]. Therefore for the treatment of Organophosphate‐induced delayed neuropathy (OPIDN) conventional anti muscarinic drugs are administered. The drug atropine is an antagonist of muscarinic receptor showing the unfocused competitive action. The drug results in better penetration within the CNS [5]. The dosage mechanism is administered with bolus loaded dose of 0.6 to 3 mg via IV fluid. Then after repeated dosing (after 5 mins) is required until the patient becomes atropinized. Following that an infusion of 10 to 20% is necessary and the patient should be monitored carefully [5].

Schizophrenia is a complicated mental health disorder that is also chronic in nature. The symptomatic manifestations may range from illusions, unorganised way of expression and conduct with dysfunctional cognitive actions [6]. The most suitable drugs according to NICE are the second generation antipsychotics (SGAs) in comparison to the first generation due to the reduced side effects. The example of SGAs is Aripiprazole [6]. The mechanism of action of SGAs is the blockage of the post synapse of the dopamine D2 receptors within brain [7]. Drugs Aripiprazole is exceptional as it acts as partial agonist of the D2 receptors. The receptor specifically D2 plays a major role in the clinical mechanism of action of antipsychotics [7]. The SGAs especially has a different working principle when compared with older medication where the affinity for binding to receptor serotonin 5HT2 is more than binding to the D2 receptors [8]. However, the pharmacology of these drugs is complex and still not clearly elucidated by any established hypothesis. Another drug clozapine is used for the treatment management of schizophrenia and it is generally prescribed for those patients who did not show proper response to other antipsychotics [7]. However this drug has a side effect due to which its use is restricted namely agranulocytosis [7]. It is also an example of antipsychotic drug that makes bonding with both serotonin and dopamine receptors. The drug acts as an antagonist of receptor subunit 5-HT2A of the serotonin. The mechanism improves the symptomatic manifestations of adverse cognitive signs of schizophrenia and other disorders [7, 8].

Chemotherapy is often associated with adverse side effects of nausea and vomiting among 50% of the patients [9]. Evidence suggests that vomiting has been observed among 40 % of the patients who had been exposed to chemotherapy with anthracycline + cyclophosphamide and also among 50% of the populace who had been exposed to extreme dosage of cisplatin [9]. To encounter this problem of emesis pharmacological interventions with dexamethasone and octreotide can be considered beneficial but often shows the symptoms of obstruction in the process of bowel. Therapy with antagonist of neurokinin 1 receptor named aprepitant had also shown positive effects upon the management of emesis with more reduction of 15%–20% among the patient population [9].

The first class of drugs that will be discussed belongs to 5-HT3 receptor antagonists for example Ondansetron which is approved by the Food and Drug Administration in the year, 1991 [10]. The agent is effective against CINV (broad types of nausea and vomiting among the cancer patients) by showing antagonistic reactions to the receptor 5-HT3. This mechanism of antagonism is observed either in the vagal and peripheral terminals of nerve along with or in the central position of the triggering zone of chemoreceptor. The most usual adverse contraindications with this class of drugs are generally constipation and headache [10].

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NK1 receptor antagonists is the second class of drug. It shows inhibition against substance P within the central and peripheral pathways. Within this class aprepitant is the first drug which got approved with the dosage range of 125 mg on the first day (day 1) and 80 mg on the second and third days (day 2 and 3) via oral administration to control nausea and vomiting. The drug is essentially metabolized within the cytochrome (CY)P-450 3A4 followed by mild metabolism CYP-2C9 and CYP-1A2. Aprepitant is considered to be an inhibitor of CYP-3A4 and a stimulator of CYP-2A9. It is generally co administered with drug dexamethasone, which is a substrate of CYP-3A4 for the inhibition of CINV [9,10].

Corticosteroids is the third drug of choice. It is considered as the mainstream drugs for the late and acute emesis. It shows better effect when administered alone. To augment the efficacy the drug is co administered with antagonist of 5-HT3 receptor. Dexamethasone is the preferred corticosteroid and its mechanism of working is related to the actions within the central nervous system (CNS) and peripheral nervous system (PNS). It also acts by antagonism of receptors of serotonin. The usual adverse effects include insomnia, gain in weight, hyperglycemia etc [10].

Dopamine receptor antagonists is the fourth class. Antagonist of dopamine receptors can also be used for prevention of CINV. The antagonism phenomenon is observed within the trigger zone of chemoreceptor. Most frequent adverse reactions include dystonia and feeling sleepy [9].

With the discovery of insulin the clinical developmental prospects of patients with diabetics have improved but soon the challenges were also understood as due to the short half life of insulin the drug required multiple injections subcutaneously on an every day basis [11]. To encounter with this problem an approach to alter the chemical properties of the drug was taken into consideration so that the time span of its glucose diminishing activity within the blood can be extended. The first prominent attempt was the formulation of "intermediate-acting" named Neutral Protamine Hagedorn (NPH) insulin around 1940, however it has few limitations [11]. In 1980, the attention was shifted to prepare a "long-acting" known as insulin glargine that required only one or two injections on a daily basis [12]. Two long acting analogs namely insulin detemir and insulin glargine are considered to be playing the major roles in the clinical practice now. Another “ultra long acting” insulin namely insulin degludec also known as Tresiba which is characterized by the extended release of the drug into the blood stream and therefore results in extended period of action. The half life of this particular ultra long acting analog is 25 hours and its action period was found to be above 42 hours [12]. The level of flat insulin was noticed after 72 hours of the initial injection with comparatively lower variability during the day time with the analog glargine insulin and it demonstrated no variation with respect to localised reactions and weight gain [12].

References:

Pearlman BL, Gambhir R. Salicylate intoxication: a clinical review. Postgraduate medicine. 2009 Jul 1;121(4):162-8.

Temple AR. Acute and chronic effects of aspirin toxicity and their treatment. Archives of Internal Medicine. 1981 Feb 23;141(3):364-9.

O'Malley GF. Emergency department management of the salicylate-poisoned patient. Emergency medicine clinics of North America. 2007 May 1;25(2):333-46.

Eddleston M, Chowdhury FR. Pharmacological treatment of organophosphorus insecticide poisoning: the old and the (possible) new. British journal of clinical pharmacology. 2016 Mar;81(3):462-70.

Eddleston M, Buckley NA, Eyer P, Dawson AH. Management of acute organophosphorus pesticide poisoning. The Lancet. 2008 Feb 16;371(9612):597-607.

Kuipers E, Kendall T, Antoniou J. The NICE Guidelines on core interventions in the treatment and management of schizophrenia in adults in primary and secondary care. The British Psychological Society & The Royal College of Psychiatrists. 2010.

Patel KR, Cherian J, Gohil K, Atkinson D. Schizophrenia: overview and treatment options. Pharmacy and Therapeutics. 2014 Sep;39(9):638.

Jibson MD. Second-generation antipsychotic medications: Pharmacology, administration, and side effects. UpToDate. Waltham, MA (accessed 12 January 2017). 2016.

Warr DG. Chemotherapy-and cancer-related nausea and vomiting. Current oncology. 2008 Jan;15(Suppl 1):S4.

Rao KV, Faso A. Chemotherapy-induced nausea and vomiting: optimizing prevention and management. American health & drug benefits. 2012 Jul;5(4):232.

Owens DR. Insulin preparations with prolonged effect. Diabetes technology & therapeutics. 2011 Jun 1;13(S1):S-5.

Donner T, Sarkar S. Insulin–pharmacology, therapeutic regimens, and principles of intensive insulin therapy. InEndotext [Internet] 2019 Feb 23. MDText. com, Inc..

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