Please write 2 pages for a conclusion. Please read the paper that I will upload. Use citations if needed. Do not give your opinion. Facts and evidence. The Impact of Cystic Fibrosis on Children Heather Kirk November 20, 2021 English 102 For Assistant Professor Donald Scott Page Break Research Proposal Paragraph Thesis Question: What is Cystic Fibrosis and how does it affect children? Thesis Answer Cystic Fibrosis is: (1) an inherited genetic condition with severe respiratory symptoms that develops in children who get a defective gene from both parents; (2) it affects the secretory gland that produces mucus, tears, sweat, and saliva, (3) as well as it impacts the digestive system, hampering physical development. Cystic fibrosis (CF) is an inherited genetic condition with severe respiratory symptoms. Cystic fibrosis affects the lungs by causing formation of thick sticky mucus that blocks the airways. The blockages cause inflammation which leads to lung damage resulting in difficulty breathing. The prevalence of Cystic fibrosis is higher among populations from Northern Europe as compared to African Americans, Asian Americans, Native Americans, and Hispanics. Many children with Cystic fibrosis face problems with physical development, growth, and difficulty gaining weight. (Pool, 2019). Multiple treatments are prescribed daily, some examples are chest therapy to help loosen and clear lung secretions, exercise to help loosen mucus and to help physical conditions, and bronchodilators to decrease inflammation and to reduce mucus. Cystic fibrosis is an illness that requires children, with the help of family, to accept multiple health-related behavioral and developmental demands. The morbidity and mortality factors of cystic fibrosis cause cognitive, emotional, and behavioral challenges among many of its victims (Ernst, 2016). Over the last decade, many advances have been made in the diagnosis and treatment of Cystic fibrosis (Agrawal 2017). Cystic fibrosis is (1) an inherited genetic condition with severe respiratory symptoms that develops in children who get a defective gene from both parents; (2) it affects the secretory gland that produces mucus, tears, sweat, and saliva, (3) as well as it impacts the digestive system, hampering physical development. Page Break Sentence Outline Thesis Question: What is Cystic fibrosis and how does it affect children? Thesis Answer: Cystic fibrosis Is (1) an inherited genetic condition with severe respiratory symptoms that develops in children who get a defective gene from both parents; (2) it affects the secretory glands that produce mucus, tears, sweat, and saliva, (3) as well as it impacts the digestive system, hampering physical development. Cystic fibrosis is: (1) an inherited genetic condition with severe respiratory symptoms that develops in children who get a defective gene from both parents. A. Children must inherit two copies of the mutated CFTR gene from both parents. B. Inheriting one copy of the gene will make you a carrier of Cystic fibrosis. 2. Cystic fibrosis affects the secretory glands that produce mucus, tears, sweat, and saliva. A. Disrupts the normal function of epithelial cells. B. CFTR mutation interferes with normal CFTR protein. 3. Cystic fibrosis impacts the digestive system, hampering physical development. A. Slows down physical development, growth, and weight gain. B. Growth and development require energy and nutrients. C. Mucus blocks the pancreatic duct and interferes with digestion. CONCLUSION Page Break Heather Kirk English 102 November 20, 2021 Assistant Professor Donald Scott The Impact of Cystic Fibrosis on Children Cystic fibrosis (CF) is an inherited genetic condition with severe respiratory symptoms. Cystic fibrosis affects the lungs by causing the formation of thick sticky mucus that blocks the airways. The blockages cause inflammation which leads to lung damage resulting in difficulty breathing. The prevalence of cystic fibrosis is higher among populations from Northern Europe as compared to African Americans, Asian Americans, Native Americans, and Hispanics. Many children with cystic fibrosis face problems with physical development, growth, and difficulty gaining weight (August 2019). Cystic fibrosis is an illness that requires children, with the help of family, to accept multiple health-related behavioral and developmental demands. The morbidity and mortality factors of cystic fibrosis cause cognitive, emotional, and behavioral challenges among many of its victims (October 2016). Over the last decade, many advances have been made in the diagnosis and treatment of cystic fibrosis. (Agrawal 2017) Cystic fibrosis is (1) an inherited genetic condition with severe respiratory symptoms that develops in children who get a defective gene from both parents; (2) it affects the secretory gland that produces mucus, tears, sweat, and saliva, (3) as well as it impacts the digestive system, hampering physical development. Cystic fibrosis is an inherited disorder caused by cystic fibrosis transmembrane Conductance Regulator (CFTR) gene mutation (Saint-Criq & Gray 2017). CFTR gene controls salt and fluid movement across cells by instructing the CFTR protein found in all mucus-secreting organs in the body (Saint-Criq & Gray 2017). CFTR gene mutation prevents the CFTR protein from functioning normally which results in the build-up of thick sticky mucus in the mucus-secreting organs (Janeczko 2016). Cystic fibrosis (CF) is an autosomal recessive genetic condition that most frequently reduces life expectancy in Caucasians (Kelly 2015). Respiratory infections are the primary cause of morbidity and mortality in individuals with cystic fibrosis. Acute pulmonary clinical symptoms associated with the stomach indicate pancreatic, gastrointestinal, and hepatobiliary breakdown (Kelly 2015). Therefore, many children who are affected admit to gastrointestinal, pancreatic, and hepatic symptoms during their lives. This poorly influences the development of the illness, standards of living, and survival chances (Gelfond 2013). With cystic fibrosis, genetic mutation alters the generation of the cystic fibrosis transmembrane conductance regulator (CFTR) that controls the production of mucus in the exocrine and bronchial glands, colon, pancreas, biliary, and reproductive structures. Different mutations contribute to faulty and unbalanced CFTR proteins. Consequently, children suffering from cystic fibrosis will produce thick mucus, which blocks the opening of the cavity structures, leading to swelling and alteration of the regular operation of the involved organs (Sathe 2016). The molecular and operational variances, linked with ecological and specific aspects, lead to fluctuating phenotypes of the illness, deterring the prognosis with undesirable implications (Kelly 2015). Cystic fibrosis is an inherited genetic condition with severe respiratory symptoms. Cystic fibrosis can lower the lifespan of an individual, because of a genetic mutation of a gene on chromosome 7 that codes for CFTR protein. This protein operates as a transmembrane Campinitiated chloride conduit. Two copies of the gene are altered in clinical illness. CFTR protein mutation can either be categorized as malfunctioning protein, disordered regulation, unreliable chloride conductance, or accelerated conduit turnover (Awatade 2018). Delta F508 is the most frequently occurring alteration; therefore, it is present in 70% of American individuals living with Cystic fibrosis and over 60% of global cases. It is a class 2 gene alteration of irregular collapsed CFTR protein. Therefore, it contributes to untimely obliteration in the Golgi bodies. In children, the delta F508 alteration usually adds to exocrine pancreatic inadequacy and a higher possibility for an infant’s first stool to be thicker and stickier than normal (Pallin 2019). Defective protein synthesis forms from a splice-site alteration. This is responsible for the untimely end of the mRNA sequence. As a result, genetic information will not become decoded into a protein product. This contributes to minimal chances of children developing cystic fibrosis. Even then, irregular post-decoding processing of the CFTR protein can occur. This is significant as it facilitates the appropriate intracellular transfer of the protein. However, due to this irregularity, the CFTR cannot be transited to a suitable cellular site. Furthermore, cystic fibrosis dysfunction in children is described by reduced protein function based on intracellular motioning. This contributes to the development of a wholly formed protein conduit in the cellular structure that is not operational. Nonetheless, the frequency of chloride ion flow and the time taken to initiate the conduit is diminished considerably. Regardless, a dysfunction involving a net reduction of CFTR saturation conduits in the cell surfaces due to quick destruction by the cellular process is likely to occur. The mutations, in this case, change the equilibrium of mRNA as well as that of advanced CFTR protein. Many of these irregular mutations lead to reduced emission of chloride and an apparent increase in the reabsorption of sodium into the cells. This increases the reabsorption of water. Therefore, leading to signs of thicker mucus emission on epithelial coatings as well as highly viscous emissions from exocrine tissues. This leads to mucous plugging with barrier pathologies in organs such as the sinuses, lungs, pancreas, biliary and hepatic systems, intestines, and sweat glands (Sathe 2016). The risk factors associated with cystic fibrosis are family history, ethnicity, and race. Children must inherit two copies of the mutated CFTR genes from both parents for them to show symptoms (Saint-Criq & Gray 2017). Inheritance of a single copy makes one a cystic fibrosis carrier with a chance of passing the gene to offsprings. Children are at higher risks of developing cystic fibrosis if one or both parents have a mutated CFTR gene or if they have a close relative with cystic fibrosis. Cystic fibrosis has various adverse effects on children. cystic fibrosis slows down physical development, growth, and weight gain (Oliwko et al 2020). Cystic fibrosis causes clogging of the pancreatic duct preventing the release of digestive enzymes into the digestive tract (Patel 2020). This interferes with the digestion and absorption of nutrients. Growth and development require energy and nutrients, children with cystic fibrosis face difficulties digesting and absorbing nutrients (Patel 2020). They also need extra energy to fight cystic fibrosis-related infections and respiratory related infections. At birth, infants with cystic fibrosis tend to have symptoms such as delayed growth which makes them smaller compared to others their age. They may also have difficulty breathing and performing exercises, and repeated sinusitis (Janeczko 2016). Children with cystic fibrosis may also experience chronic coughing with thick sputum and wheezing due to the accumulation of thick sticky mucus in the bronchial tubes and airway, this may be associated with repeated pneumonia (Janeczko 2016). A sinus infection occurs when emission thickness increases which blocks the sinus Ostia. This can further lead to ciliary dysfunction, augmented provocative mediators as well as an amplified bacterial settlement with pathogens (Sathe 2016). The prolonged effect of this syndrome is likely to lead to structural damage. Lung disease results from cystic fibrosis as a range impediment from congealed mucous emission, leading to inflammatory processes. This then causes a blockage of airways that can lead to death in children with cystic fibrosis. Similarly, pancreatic symptoms of cystic fibrosis result from high blockages of the pancreatic ductile by viscous emissions. As a result, gastric contents cannot be transited to the duodenum and the pancreatic exocrine glands can no longer excrete pancreatic enzymes (Sathe 2016). This adversely affects the process of digestion and therefore, the energy needed for development and growth becomes insufficient. Moreover, autodigestion of the pancreas can occur since the enzymes excreted will be acting on the pancreatic tissues. This contributes to the development of pancreatitis, which might further lead to failure (Sathe 2016). Children over the age of four with cystic fibrosis often experience introversions where part of the intestines are displaced into another (Pejkovska 2020). Also, due to chronic coughing and sticky stool, children with Cystic fibrosis experience rectal prolapse, where the rectum protrudes out when passing stool (Pejkovska 2020) The development and impact of Cystic fibrosis on children is a result of gene mutation. As such, children can acquire two copies of the mutated Cystic fibrosis transmembrane conductance regulator gene from both parents, which hastens the development of cystic fibrosis. The condition adversely affects the respiratory systems through the deposition of thick mucus onto the surfaces of respiratory structures hindering breathing. In addition, the condition can negatively affect growth and development as it inhibits the generation of energy and absorption of nutrients in the stomach. Cystic fibrosis causes delays in physical growth, development, and weight gain due to cystic fibrosis-related gastrointestinal (GI) and respiratory complications. Growth is an energy-dependent process, and the clogging of the pancreatic interferes with digestion. The pancreatic duct obstruction means insufficient digestive enzymes are released into the GI tract (Patel 2020). As a result, digestion and absorption of nutrients become impaired. In addition, due to clogged airways and pulmonary complications, children with cystic fibrosis expend more energy to breathe and fight cystic fibrosis-related respiratory infections. They need twice the recommended daily caloric intake compared to a healthy pediatric population (Dennett 2017). Thus, children with cystic fibrosis are prone to malnutrition and have difficulty gaining weight due to problematic GI and respiratory symptoms. Other GI conditions that affect a childs ability to obtain sufficient calories and nutrients also contribute to delayed attaining of appropriate weight for age. Pancreatitis may develop when enzymes released by the pancreas begin to digest pancreatic tissues. The pancreatic exocrine glands may also stop producing enzymes required to digest proteins, fats, and carbohydrates into usable forms (Shei et al. 2019). Inadequate amino 3 acids lead to stunting, and this becomes needed for growth and tissue repair. The impaired ability to break down food causes malabsorption and malnutrition. Poor growth can also be attributed to cystic fibrosis-related impaired pancreatic exocrine functioning, resulting in insufficient insulin-like growth factor 1 involved in early development (Shei et al. 2019). Optimal levels of this hormone promote the growth of bones and tissue: thus, its deficiency will result in a lower height and weight (BMI) for a particular age. Cystic fibrosis also interferes with digestion, reducing nutrient bioavailability and metabolism to fuel growth and development. GI clogging by mucus prevents gastric contents from reaching the duodenum, causing bloating, stomachache, and acid reflux (Dennett 2017). The GI obstruction will slow down stomach emptying, resulting in a persistent feeling of being full. As a result, food intake will be inadequate to support the high calories and nutrients required for normal growth and development. For this reason, vitamin supplements and Naso enteric feeding are available to increase the nutritional status of the children (Le et al. 2019). Pancreatic enzyme replacement can also boost digestion and absorption of essential nutrients. Another GI complication prevalent in children with cystic fibrosis is introversion. This condition is characterized by a part intestine that turns inwards (Pejkovska, 2020). Intestinal epithelia play a critical role in nutrient absorption into the bloodstream. They contain specialized structures called villi that develop from enterocytes (Dennett 2017). In introverted intestines, the organization of these protrusions is disturbed, affecting nutrient uptake. In addition, due to chronic coughing and sticky stool in children with cystic fibrosis, rectal prolapse, whereby the rectum protrudes when passing stool (Pejkovska 2020). All these conditions reduce the nutrient absorption and nutritional status of the child with cystic fibrosis. High cystic fibrosis- respiratory morbidity and impaired lung function also slow down growth and development. Children with cystic fibrosis have a lower birth weight than healthy newborns. Early growth is affected by the clogging of airways and lungs that limits oxygen uptake efficiency (Le et al. 2019). Bacteria and viruses thrive in the thick mucus environment. Impaired lung structure and function during this critical period of development will slow down growth and development. Cystic fibrosis is a genetic disease in which the expression of a mutant CFTR allele affects ion transport across epithelia. 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