Pharmacology for Nursing Care

Question: Discuss about the Pharmacology for Nursing Care. Answer: Introduction: Fever is an abnormal increase in body temperature. A body temperature beyond the standard oral measurement of 37C or the standard rectal temperature of 37.2C is considered as raised temperature (Marieb Hoehn, 2016). Fever which is controlled by the hypothalamus do not rise above 41oC, demonstrating a built-in thermostatic safety mechanism. Fever is a non-specific response that is mediated by exogenous pyrogens (Bacteria or virus) and endogenous pyrogens secreted from host cells. Endogenous pyrogens are Interleukin -6, Interleukin -1, and tumor necrosis factors. These cytokines are synthesized by epithelial cells, endothelial cells, fibroblasts, lymphocytes, and monocytes types of cells (Marieb Hoehn, 2016). Macrophages, T and B cells are produced to promote defence against infection. In addition, generated prostaglandins bind to receptors in hypothalamus and persuade modifications in the set-point. Once the set-point is amplified, the blood flow through the hypothalamus is perceived as being beneath the appropriate temperature, thus, heat production and conservation starts till blood temperature extents to the new set-point (Craft et al., 2015). Fever serves as natural defense system of the body against pathogens that cannot survive at a higher temperature. The rise in body's core temperature reduces the load of microbes in the body. The increasing temperature also activates the immune system by activating CD8+ cytotoxic T cells and also increases immunity by transformation of lymphocytes into B and T cells, enhances phagocytosis, increases neutrophil motility and amplifies production of antiviral interferon (Marieb Hoehn, 2016). According to Craft et al. (2015), the main reason is that viral and bacterial infections may look similar in early stages and so it is prophylactic. In many cases it could be due to people demanding antibiotics from their doctor. But these antibiotics are inadequate in a viral infection such as influenza. Doctors occasionally prescribe antibiotics to reduce the risk of co-infection or secondary bacterial infection during influenza. Phenoxymethylpenicillin is narrow spectrum bactericidal antibiotic. It is effective against susceptible bacteria during their active multiplication stage. Phenoxymethylpenicillin is an orally active antibiotic which has highest bioavailabilitywhen taken orally (Craft et al., 2015). Phenoxymethylpenicillin is less effective against Gram-negative bacteria but possesses a range of an antimicrobial activity against Gram-positive bacteria. It acts by inhibiting the biosynthesis of bacterial cell wall peptidoglycan. Inhibition of the construction of peptidoglycan cross-links in the bacterial cell wall creates an imbalance between cell wall assembly and degradation, causing the bacterial cell to die rapidly (Bullock Manias, 2014). Antibiotics target either the multiplication mechanism of microorganisms or the mechanism of homeostasis protein (Snyder et al., 2013). Antibiotics either kill microbes or make them unable to multiply or divide. Bacteria and fungi must be continuously active metabolically and can be poisoned at any stage by antibiotics. Unlike bacteria and fungi, viruses proliferate and spread by injecting their genetic material into the host's cells and letting it infect cells into producing more viral particles. Viruses use many host cell genes for replication and antibiotics cannot not specifically distinguish and target only viral proteins from host proteins. Therefore, making antibiotics inadequate and ineffective against viruses (Lehne Rosenthal, 2014). Peter could have contracted the influenza virus from an infected person who coughed, sneezed or talked in front him. Peter also could be infected by shaking hand with an infected person or touching infected objects. When an infected person coughs sneezes or talks, tiny infected droplets get into the air. (Boland et al., 2011). The portal of entry of these virus containing droplets is the respiratory tract. The incubation period is about 18 to 72 hours. The portal of exit is through the mouth or nose of the infected person when they sneezes and coughs (Influenza, 2016). The virus can also be spread by hands, objects or surfaces contaminated with influenza viruses. When healthy people touch these contaminated objects and subsequently touch their nose, mouth or eyes becomes infected with this virus. Researchers have found that influenza virus can survive on objects for about two to eight hours (Boland et al., 2011). The portal of entry of the virus is the respiratory tract. The incubation period is about 18 to 72 hours. The portal of exit is through the mouth or nose of the infected person when they sneezes and coughs (Influenza, 2016). The susceptible host for influenza virus infection are children below two years, aged people over sixty-five years, pregnant women and individuals with certain medical conditions (Influenza, 2016). To prevent the modes of transmission, people should cover their mouth and nose with a tissue when coughing. Washing hands with soap and water can help to avoid infection (Lee Bishop, 2016). When soap and water are not available, using an alcohol-based hand sanitizer can be effective (Influenza, 2016). Inflammatory responses begins with chemicals released into ECF by infected tissues, blood proteins and immune cells. The mast cell is perhaps the most significant activator of the inflammatory response (Porth Matfin, 2014). Inflammatory mediators like prostaglandins, kinins and complement activation have inflammatory roles and chemotaxis allows inflammatory cells to move to the infection site. They dilate the local arterioles (hyperemia) causing redness and heat of inflamed region (Craft et al., 2015). The swollen throat can be a result of swollen lymph glands. During infection, the lymph glands swell rapidly and become tender as the immune system deals with the infecting virus (Porth Matfin, 2014). Tissue swells during inflammationwhen the endothelial lining of capillaries becomes leakier permitting more blood plasma to exude into the spaces of connected tissue. Inflammation shifts the balance between fluid leaving vascular spaces and re-entering the system. This causes fluid build-up called edema and resulting tissue swelling (Craft et al., 2015). Patchy covering of yellow-white exudate over tonsils indicates tonsillitis due to infection. Tonsils produce antibodies which fight infection and prevent it from further spreading to other body parts. Sometimes inflamed tonsils become swollen with a yellowish coating. It happens because within the tonsils neutrophils, monocytes and lymphocytes destroy the viruses by producing inflammatory cytokines such as phospholipase A2 (Porth Matfin, 2014). Virus lack necessary components and use the ribosomes, enzymes and other cellular machinery of the host cell to replicate (Bauman et al., 2012). Bacteria contain their genetic material DNA and all the essential tools like ribosomes, proteins that they need to replicate themselves (Snyder et al., 2013). Replication of virus: In lytic cycle, the virus first get attached to the host cell by adsorption and secrets an enzyme that hydrolyses the host cell wall component to form a pore. The virus then injects nucleic acid into the host cell through the pore and induces infection. Viral nucleic acid destroys the synthesis of host proteins and initiates to the production of required viral particles (Snyder et al., 2013). The majority of the viral DNA performances as a template for its own synthesis and rest of the DNA is used to synthesize viral m-RNA. This newly moulded m-RNA constitutes viral coat proteins. Thus, new viral particles are produced by the assemblage freshly synthesized nucleic acid and proteins (Bauman et al., 2012). In lysogenic cycle, viral DNA becomes incorporated into the DNA of host genome. The viral DNA then replicates with the host DNA as a single unit and after a number of generations, the viral DNA gets separated and come into the lytic cycle (Bauman et al., 2012). Bacterial replication involves 3 gradual stages: initiation, elongation, and termination. The initiation of DNA replication in bacteria is facilitated by the protein DnaA. Binding of the DnaA to the initiation site breaks the hydrogen bonds. This event forms the replication fork which causes the DNA to loop in preparation for melting open by the helicase DnaB. Now, DNA polymerase III holoenzyme commences the replication and elongation progression. Termination of DNA replication in bacteria is accomplished by the aid of termination sequences and the Tus protein (Snyder et al., 2013). References Bauman, R. W., Machunis-Masuoka, E., Cosby, C. D. (2012).Microbiology: With diseases by body system. Benjamin Cummings. Boland, M., Wilson, J., Santall, J., Video Education Australasia. (2011).Infection control in healthcare. Bendigo, VIC: VEA. Bullock, S., Manias, E. (2014).Fundamentals of pharmacology. Pearson Higher Education AU. Craft, J., Gordon, C., Huether, S. E., McCance, K. L., Brashers, V. L. (2015).Understanding pathophysiology-ANZ adaptation. Elsevier Health Sciences. Influenza. (2016).World Health Organization. Lee, G., Bishop, P. (2016).Microbiology and infection control for health professionals. Pearson Higher Education AU. Lehne, R. A., Rosenthal, L. (2014).Pharmacology for nursing care. Elsevier Health Sciences. Marieb, E. 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