Applied Pharmacology

Applied Pharmacology

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The main organ that deals in metabolism of paracetamol is the liver. In this organ, most of the paracetamol contents are absorbed, leaving the dose being excreted in about 90 % of the intake drug. During its metabolism, the drug combines with glucuronidea and sulphate and this simplifies the intake of the drug (Pharmweb 2011). During the metabolism of paracetamol, the peak blood level lowers to around 20mg/l, indicating that it is a complex drug that requires many body functions. Upon ingestion, paracetamol is oxidized with glutathione to produce benzoquinoneimine (Stoelting 1999).
Hepatotoxity is influenced by the depletion of glutathione in the liver. This is because of excessive intake of paracetamol that causes the drug to be oxidized. When there is increased intake of the drug, there are many adverse reactions that inhibit the production of glutathione. This leads to the production of hepapotoxity, one of the adverse effects associated with taking paracetamol (Pharmweb 2011). Hepapotoxity is mainly caused by the buildup of benzoquinoniemine, after complete depletion of glutathione from the liver. The effects are too severe that liver failure may occur.
In the event of an overdose, N-acetylcysteine is administered. This drug causes the liver to restructure itself and take on important tasks and functions. The liver is restored to its original state and this makes it more functional and ready to work on any foreign particles. The liver is restored and this helps in the generation of glutathione that is meant to combine with benzoquinoneimine. Timely use of N-acetylcysteine makes the liver to be safe and positively impacts on its fundamental roles. For this reason, early treatment of paracetamol overdose is recommended (Stoelting & Miller 2000).
Opioids are absorbed at the opioid receptors of the central nervous system. One of the key issues that happen at the receptors is the absorption of the drug at the cellular membranes (Department of Health 2011). The drug alters interchange of stimuli at the cellular membranes and this causes the transmissions at the central nervous system to be altered. This inhibits pain and other feelings, making the patient to appear numb and docile. Morphine mostly reacts with pain reactors and causes the patients to develop adverse effects that prevent pain and other physical feelings (National Center for Biotechnology Information 2011).
Opioid overdose is influenced by the intake of other drugs like alcohol. In the event that a person consumes excessive opioids like morphine or such related drugs, there is a chance of complete numbness that may even lead to death.

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Applied Pharmacology Essay

- The main organ that deals in metabolism of paracetamol is the liver. In this organ, most of the paracetamol contents are absorbed, leaving the dose being excreted in about 90 % of the intake drug. During its metabolism, the drug combines with glucuronidea and sulphate and this simplifies the intake of the drug (Pharmweb 2011). During the metabolism of paracetamol, the peak blood level lowers to around 20mg/l, indicating that it is a complex drug that requires many body functions. Upon ingestion, paracetamol is oxidized with glutathione to produce benzoquinoneimine (Stoelting 1999)....   [tags: Effects, Liver]

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Most of the patients who take an overdose of morphine cause the central nervous system to switch off completely due to excessive and mandatory command from the drugs.
Warfarin and amiodarone react to produce an effect that may trigger cardiac arrhythmiasis, especially in patients already suffering from arterial fibrillation. The drugs can cause anticoagulation if used for a prolonged duration of time (Pharm, Pharm, Nelson, Qi, & Rausch 2008). Both of these drugs affect the blood flow and hemorrhage is likely to occur. For this reason, these elements should not be used at the same time especially for sick people.

Works Cited

Pharm, YL, Pharm, KA, Nelson, BJ, Qi, D & Rausch, DJ 2008, ‘Characteristics of the Amiodarone-Warfarin Interaction During Long-term Follow-Up’, American Journal of Health-System Pharmacy, vol. 65, no. 10, pp. 947-952.
Department of Health 2011, Opioid Overdose Prevention, viewed 31 August 2011,
National Center for Biotechnology Information 2011, Morphine dependence, National Center for Biotechnology Information, Bethesda, MD.
Stoelting, RK & Miller, RD 2000, Intravenous anesthetics, in basics of anesthesia, Churchill-Livingstone, Oxford, UK.
Stoelting, RK 1999, ‘Pharmacokinetics and Pharmacodynamics of Injected and Inhaled Drugs’, Pharmacology and Physiology in Anesthetic Practice, vol. 3, pp. 1-17.
Pharmweb 2011, Metabolism, Biochemistry of overdose and its treatment, viewed 31 August 2011,

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