PATHOPHYSIOLOGY NR 507WK1 TD1

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PATHOPHYSIOLOGY NR 507 WK1TD1 Week 1: Altered Immune System and Altered Inflammatory Response - Discussion Part One Loading... Discussion This week's graded topics relate to the following Course Out... comes (COs). 1 2 3 6 5 6 7 Analyze pathophysiologic mechanisms associated with selected disease states. (PO 1) Differentiate the epidemiology, etiology, developmental considerations, pathogenesis, and clinical and laboratory manifestations of specific disease processes. (PO 1) Examine the way in which homeostatic, adaptive, and compensatory physiological mechanisms can be supported and/or altered through specific therapeutic interventions. (PO 1, 7) Distinguish risk factors associated with selected disease states. (PO 1) Describe outcomes of disruptive or alterations in specific physiologic processes. (PO 1) Distinguish risk factors associated with selected disease states. (PO 1) Explore age-specific and developmental alterations in physiologic and disease states. (PO 1, 4) Discussion Part One (graded)John is a 19-year-old college football player who presents with sneezing, itchy eyes, and nasal congestion that worsens at night. He states that he has a history of asthma, eczema and allergies to pollen. There is also one other person on the football team that has similar symptoms. His vitals are BP 110/70, P 84, R 18, T 100 F. Write a differential of at least five (5) possible items from the most likely to less likely. For each disease include information about the epidemiology, pathophysiology and briefly argue why this disease fits the presentation and why it might not fit the presentation. Responses Rechel DelAntar Introduction 4/26/2016 7:11:48 PM Hello Professor and Class, I would like to greet everyone a warm Hello and hope everyone is doing great. My name is Rechel Delantar and I have been a nurse for what seems like ages (graduated 1990). I have been in critical care and recovery room for most of my nursing career. The last 12 years I have specialized in Cardiovascular Recovery Room caring for post Heart Assist device, ECMOs, open hearts and organ transplant patients among others before moving to my current position as a Heart transplant coordinator. I have always wanted to pursue my masters degree but found it difficult with time and family and later on going back to school online became a little intimidating. When my parents died I then decided to pursue my dream of obtaining my APN. I have been blessed to have good instructors and classmates and I'm getting comfortable with school. It is a pleasure to meet everyone and good luck with class. Rochelle Elayda Discussion part 1 4/26/2016 9:49:02 PM Allergic rhinitis Epidemiology: Allergic rhinitis is a common chronic disease with a prevalence between five and twenty-two percent in the United States (Khan, 2014). Many patients who have asthma also have allergic rhinitis. Rhinitis is most common in patients ages 15-25, and it affects more boys than girls (Batt, 2014). Allergic rhinitis is usually diagnosed before asthma and sensitization occurs at a very young age when the immune system is still immature (Batt, 2014). Symptoms include sneezing, itching, nasal irritation, and rhinorrhea. The symptoms occur when the patient breathes in allergens such as pollen, dust, food, and pet dander. Pathophysiology: When the patient is exposed to an allergen, the allergen-specific T cells is activated and causes the production of allergen-specific IgE (Batt, 2014). The IgE binds to receptors on mast cells and basophils. The allergen causes cell degranulation and releases mediators such as histamine, leukotrienes, and prostaglandins which causes the symptoms associated with allergic rhinitis (Batt, 2014). Argument: I think that John could be suffering from allergic rhinitis. With his history of asthma and pollen allergy as well as his symptoms of sneezing and nasal congestion, allergic rhinitis would be a perfect fit. Rhinosinusitis Epidemiology: Rhinosinusitis is the inflammation of the paranasal sinuses and nasal mucosa. About 31 million people are affected by sinusitis in the United States and is the fifth most common diagnosis in which antibiotics are prescribed (Shoup, 2011). About $3-$5 billion dollars of healthcare costs are due to patients with sinusitis.Pathophysiology: Rhinosinusitis is either acute or chronic. Acute rhinosinusitis can be either bacterial or viral. Viral rhinosinusitis is caused by exposure to viruses such as the rhinovirus, influenza A and B, parainfluenza, respiratory syncytial virus, adenovirus, and enterovirus (Shoup, 2011). When viruses enter the nasal passage, they attach to cell walls and activate several inflammatory pathways which causes an excess of turbinate vasculature, intercellular leakage, and seromucinous discharge (Shoup, 2011). Acute bacterial rhinosinusitis is commonly caused by Streptococcus pneumonia, Haemophilus influenzaie, Moraxella catarrhalis, and Stapholocoous aureus (Shoup, 2011). Chronic rhinosinusitis is caused by infection, allergies, genetics, or systemic disorders. The inflammatory cells that are triggered are eosinophils (Shoup, 2011). Argument: Symptoms of rhinosinusitis are cough, sneezing, rhinorrhea, nasal congestion, facial pain or pressure headache, and sore throat (Shoup, 2011). John has some of these symptoms but does not have a headache or facial pain which is a significant feature of rhinosinusitis. There is really no connection between rhinosinusitis and asthma or allergies to pollen. Rochelle Reference: Batt, R. (2014). Treatment of seasonal allergic rhinitis and impact on the adolescent. Nurse Prescribing, 12(3), 120-126. Retrieved from http://www.nurseprescribing.com/cgi-bin/go.pl/library/article.html? uid=103680;article=NP_12_3_120_126 Kahn, D. (2014). Allergic rhinitis and asthma: epidemiology and common pathophysiology. Allergy and Asthma Proceedings, 35, 357- 361. doi: 10.2500/aap.2014.35.3794 Shoup, J. (2011). Management of adult rhinosinusitis. The Nurse Practitioner, 36(11), 23-26. Retrieved from http://www.tnpj.com Rochelle Elayda reply to Rochelle Elayda RE: Discussion part 1 Continuation of original post: The Common Cold (Rhinovirus Infection): The common cold was discovered in 1956 by Dr. Winston Price where he was able to isolate the rhinovirus (Kennedy, Turner, Braciale, Heymann, & Borish, 2012). Adults experience two to three colds per year and children experience an average of eight to twelve per year. The virus affects the upper and lower airways. There is no cure for the common cold, but palliative relief help with symptoms. The common cold is largely responsible to loss of productivity, high healthcare costs, and triggering other illnesses (Witek, Ramsey, Carr, & Riker, 2014). Pathophysiology: The rhinovirus, which is the main virus that causes symptoms of the common cold, is a single-stranded non-enveloped RNA virus that has over 100 serotypes (Kennedy et al., 2012). When the RV enters the cell, the viral genome is translated into a polyprotein, which goes through a process called proteolytic cleavage which produces the structural and non-structural gene products (Kennedy et al., 2012). Argument: Symptoms of the common cold are sneezing, headache, malaise, chilliness, nasal discharge, nasal obstruction, sore throat, and cough. Although this diagnosis could be a possibility, John does not have many of those symptoms and does not feel malaise. Seasonal allergy: Epidemiology: Allergies affect approximately 15-20 percent of the population and has 5/2/2016 4:32:42 PMincreased dramatically in the last 20-30 years. It is a huge hindrance for those affected by it. The most common cause of allergy symptoms is pollen, molds, and fungi(Middleton, 2016). Pathophysiology: When an allergen enters the body and invades the immune system, T helper cells and their mediators begin to respond by attacking this invader (Middleton, 2016). Antigen-presenting cells detect the allergen and then the allergen is absorbed, processed, and displayed on its surface. The invaded antigen-presenting cell migrates to the T-lymphocyte which stimulates the B-cell to produce the antibody, IgE. The IgE attaches itself on the surfaces of mast cells causing an inflammatory mediator such as histamine (Middleton, 2016). Argument: John is allergic to pollen which could trigger the symptoms described in the scenario. Seasonal Influenza: Epidemiology: Seasonal outbreaks for influenza in the United States occurs in the winter months. Globally, this illness has caused about half a million deaths each year (Goodband, Oakley, Rayner, Toms, & Brostoff, 2014). Influenza causes approximately 7.6 million working days a year (Goodband et al., 2014). One of the most important steps in the prevention of influenza is vaccination. Despite the well-known benefits of vaccination, many people continue to refuse to get vaccinated. Pathophysiology: The influenza virus is an RNA virus which is surrounded by a viral envelope containing glycoproteins (Goodband et al., 2014). Because this is an RNA virus (and not a DNA virus), the influenza genome is susceptible to spontaneous genetic mutations. These mutations may effect the genes that encode the H and N antibody- binding sites which in turn reduce the binding of existing antibodies. New viral strains tend to spread more rapidly. Argument: Although the influenza virus causes the symptoms that John currently has, this would be the last diagnosis I feel he would have. The flu causes fever, malaise, and body aches. John is still playing football, and if he had the flu, he would not feel well enough to play. Reference: Goodband, A., Oakley, S., Rayner, J., Toms, J., & Brostoff, J. (2014). Influenza: disease, epidemiology, and the importance of vaccination uptake by healthcare workers. Primary Health Care, 24(7), 33-38. Retrieved from http://www.journals.rcni.com/doi/pdfplus/10.7748.phc.24.7.33.e860 Kennedy, J., Turner, R., Braciale, T., Heymann, P., & Borish, L. (2012). Pathogenesis of rhinovirus infection. Current Opinion in Virology, 2(3), 287-293. Retrieved from http://www.ncbi.nlm.gov/pmc/articles/PMC3378761/ Middleton, J. (2016). The pathophysiology of allergic responses. Nursing Times. Retrieved from http://www.nursingtimes.net Rechel DelAntar Differential Diagnoses Hello professor and Class, Differential Diagnoses A case of a 19 year old college Football player John, with sneezing, itchy eyes and nasal congestion with symptoms worsening at night with a history of asthma, allergies to pollen and eczema. Vital 5/1/2016 2:35:58 PMsigns appear normal except for a low grade fever of 100F. And although another teammate is experiencing the same signs and symptoms, it does not say when it has started, are the symptoms on and off or continuous and did both players experienced the symptoms at the same time or one after the other. In the case of our patient, 5 possible differential diagnoses are: 1. Rhinovirus = Commonly known as the common colds. Incubation period is usually 12-72 hours and may last 7-11 days or longer. Signs and symptoms would be nasal discharge, nasal congestion, sneezing itchy eyes, fever (typically low grade), headache and facial and ear pressure. In some cases, Rhinovirus may exacerbate an asthma attack. The RV will infect the epithelium inducing an innate immune response. Engagement of receptors causes cytokine response, which drives neutrophil recruitment manifested by neutrophil laden discharges. In response, the Humoral immune system activates B cells with sero- specific IgA and IgG antibodies (Kennedy, J., et al., 2012). Transmission is through droplet spray or direct contact and the organism can be identified through a nasal swab. The patient presents the same signs and symptoms of this disease and could easily be infected by this virus through contact with his friends and specially sharing sports equipment with his teammates. 2. RSV/Respiratory Syncytial Virus = is a respiratory virus that infects the lungs and breathing passages and in healthy people is manifested as a mild cold like symptoms and recovers in 1-2 weeks and although it occurs mostly in children, it can occur in different age groups (Centers for Disease Control and Prevention, 2014). Symptoms ranging from very mild to life threatening. Typical initial symptoms are nasal congestion, runny nose, mild cough and low grade fever. The RSV Virus is spread when an infected person coughs and sneezes. The virus enters the body through the nose, or mouth and very often the eyes when people wipe their eyes from droplet spray or direct contact. The pathogenesis of this disease is not fully known but the virus attacks the respiratory tree causing inflammation. The inflammatory response causes the symptoms wherein the host cell recognizes the virus and secretes inflammatory cytokines and in the process drawing immune cells from the periphery and since it is self-limiting, patients require supportive care (America Lung Association, 2016). Diagnosis is through nasal swab for Respiratory panel. This could be a likely diagnosis as he is exhibiting some of the signs of the disease except for cough and contacted the disease from one of his team mates. Although he is not experiencing cough, he may just be starting with the disease process at this time. 3. Acute Bacterial rhinosinusitis = This is characterized by the inflammation in the lining of the paranasal sinuses. Since sinusitis rarely occurs without rhinitis, rhinosinusitis is the preferred term. Symptoms include nasal congestion, fever, nasal drip, fatigue and cough later on as post nasal drip sets in. It is spread through aerosol and direct contact. The early stage of sinusitis is viral however a small number of patients develop secondary bacterial infections generally caused by aerobic bacteria. Patient immune system has been compromised from the first infection and is not strong enough to fight a second opportunisticorganism. The symptoms are similar to the one experienced by John except that it is unclear how long has the patient had these symptoms that may suggest that this is indeed a secondary infection (Kennedy, J., et al., 2012). 4. Influenza = Influenza is a respiratory infection caused by the Influenza virus. Although it is largely categorized as A, B and C, new subtypes of the virus have been identified such as the H1N1 and H3N2 that have caused mortality in the population (Centers for Disease Control, 2016). Signs and symptoms include sore throat, nasal discharge, myalgia, red and watery eyes, weakness, fever cough and other respiratory symptoms. Transmission is through aerosol or by contact with saliva or other respiratory secretions. The virus attached itself to the respiratory tract and the viral replication combined with immune response to infection leads to the destruction and loss of cells in the lining. Although these are viruses, they have a segmented genome, which causes them to rapidly evolve causing an epidemic (Zambon, M., 2016). The Flu could be a reason for the patient to be experiencing the sign and symptoms he is exhibiting however, he has not been complaining of any myalgia despite having low grade fever. 5. Allergic Rhinitis (Hay fever) = This an allergic reaction triggered by outdoor pollens and molds, smoke pollution and strong smells causing nasal congestion, itchy eyes and sneezing and no fever. It affects all ages and unlike viral infections, they are not contagious. They are cause by an overactive immune system who mistakes dust or pollen for germs and attacks them. Upon exposure to the allergen specific IgE antibodies bind to receptors in the mast cells of the respiratory mucosa. When the allergen is inhaled again, the IgE antibodies bind with the allergen resulting in activation of the cell and the symptoms of hay fever (DeShazo, R. and Kemp, S., 2014). The signs and symptoms of allergic rhinitis maybe similar but John is exhibiting low grade fever which is not a typical sign for an allergic reaction. References: American Lung Association. (2016). RSV Symptoms, Causes and Risk Factors. Retrieved from http://www.lung.org/lung-health-and-diseases/lung-disease- lookup/rsv/rsv-symptoms- causes-risk.html. Centers for Disease Control and Prevention. (2014). Respiratory Syncytial Virus Infection. Retrieved from http://www.cdc.gov/rsv/. Centers for Disease Control. (2016). Influenza (Flu). Retrieved from http://www.cdc.gov/flu/. DeShazo, R. and Kemp, S. (2014). Pathogenesis of Allergic rhinitis. Retrieved from http://www.uptodate.com/contents/pathogenesis-of-allergic- rhinitis-rhinosinusitis. Kennedy, J., Turner, R., Braciale, T., Heymann, P and Borish, L. (2012). Pathogenesis of Rhinovirus Infection. Current Opinion in Virology. 2(3), 287- 293.Zambon, M. (2016). Epidemiology and Pathogenesis of Influenza. Journal of Antimicrobial Chemotherapy. 71(5), 3-9. Lorna Durfee Discussion Part 1 - Differentials 5/1/2016 3:45:14 PM John is a 19-year-old college football player who presents with sneezing, itchy eyes, and nasal congestion that worsens at night. He states that he has a history of asthma, eczema and allergies to pollen. There is also one other person on the football team that has similar symptoms. His vitals are BP 110/70, P 84, R 18, T 100 F. Write a differential of at least five (5) possible items from the most likely to less likely. For each disease include information about the epidemiology, pathophysiology and briefly argue why this disease fits the presentation and why it might not fit the presentation. Dr. Brown and Class: Subjectively, the patient presents with a history of sneezing, itchy eyes, and nasal congestion worsening at night. There is a history of asthma, allergies to pollen and eczema. Objectively, he shows an elevated temperature, but other vital signs appear to be normal. He mentioned that there is another contact on his football team that has similar symptoms and is having an exacerbation of allergy symptoms. The differentials are as follows: Differential #1: Allergic rhinitis – Because John has allergies, he could be exhibiting allergic symptoms. When researching information regarding allergic rhinitis and the pathophysiology, Sin and Togias (2011) inform the reader that allergic rhinitis is one of the most common IgE-mediated diseases. The reaction occurs from inhaling an allergen and sets the stage for a type 1 hypersensitivity reaction. The results are events that are both immunological and biochemical. Pollen can set off an allergic reaction because the particles of the allergen are ingested and are incorporated into the nasal mucus and then into the tissues of the nose (Togias & Sin, 2011, p. 108). Sensitization happens because the antigen-presenting cells (APCs), which are dendritic, swallow up the allergen and then break them down into peptides that move into lymph nodes. The presentation of these peptides is to the not yet specific epitope CD4 T lymphocytes or T cells. The dendritic cells set up a network inside the epithelium and the respiratory mucosa and nasal mucosa. Dendritic cells and T cells increase on the surface of the epithelium with rhinitis. Also, other signals that affect DCs and T cells include prostaglandin E and lymphopoietin from the epithelial cells and this, in turn, expresses ligand (Togias & Sin, 2011, p. 108). 2 The regulatory T cells (Treg cells) suppress the immune responses through cytokines. Tregs can also induce apoptosis. Most allergic patients can have allergen-specific IL-4 effector T cells, IL-10 Tr1 cells, and Tregs. The balance of these can decide if allergy will develop. There is some indication that regulatory T cells are not working and are defective in allergic rhinitis (Togias & Sin, 2011, p. 108). The B lymphocytes synthesize IgE from direction and regulation of the cytokines. IgE- expressing memory B-cell cytokines will then produce clonal expansion. Another sign between ligand CD40 on the T cell and CD40 on the B cell produces co-stimulation. This co-simulation urges B-cell activation and recombination for producing IgE. The (FcεRI) interactions on the basophils and the mast cells produce an allergic reaction, and this is atthe cellular level (Togias & Sin, 2011, p. 108). This patient may also have nonallergic rhinitis and vasomotor rhinitis instead. Consideration must include allergy and infection (Togias & Sin, 2011 p. 111). Allergic rhinitis fits the presentation of the symptoms he is currently exhibiting. Differential # 2: Seasonal allergy to pollen – The National Institute of Allergy and Infectious Diseases (2016) tell us that pollen is a major trigger for allergies. Usually known in layman’s terms as hay fever, the National Institute of Allergy and Infectious Diseases refers to it as “seasonal allergic rhinitis.” The statistics state that pollen allergy affects 7 percent of adults and 9 percent of children living in the United States. The body sets off an allergic reaction through the immune system to an allergen that may seem harmless to some but for others, it can cause major problems. It appears that this patient has some pollen allergy that arises in the fall. His symptoms could be from weeds that are present in the fall or some other allergen such as mold. Ragweed causes problems for many people. If he only has symptoms for a period, perhaps he is allergic to the pollens in the air at the time. These can cause allergy symptoms. (National Institute of Allergy and Infectious Diseases, 2016). To determine if he has an allergy to certain antigens he will need to be tested to confirm. If not, then he could have some other condition. Seasonal allergy appears to fit the presentation as well. Differential # 3: Sinus infection - Aring and Chan (2012) explain that acute sinusitis or rhinosinusitis is inflammation of the mucosa in the nasal passages. The American Academy of Otolaryngology defines rhinosinusitis based on duration and is considered either bacterial or viral (Aring & Chan, 2011, p. 1057). The authors inform us that sinusitis can result from viruses associated with the common cold. The lining of the mucosa of the nose and nasal passages leads to edema which in turn causes obstruction of the sinus and in the ostia. Also, the bacterial and viral infections can impede the action of the cilia (little hairs) inside the nose, which have the ability to transport mucus. Because there is an obstruction, it slows down the mucus transport; the secretions become stagnate, and reduction of oxygen tension in the sinus cavities results (Aring & Chan, 2011, p. 1057). This condition allows for the proliferation of virus and bacteria. Common organisms in acute sinusitis are those of Streptococcus pneumonia, Staphylococcus Aureus, and Haemophilus influenza as well as Moraxella catarrhal. Viruses commonly associated with viral sinusitis are; rhinovirus, parainfluenza and influenza and adenovirus (Aring & Chan, 2011, p. 1058). Because there is no way of knowing how long this has been going on, it is hard to tell whether this is a prolonged infection. To diagnose this, we must see that the symptoms become worse after seven to 10 days or last for longer than 10 days (Aring & Chan, 2011, p. 1058). Differential # 4: Common cold - Because there is another athlete with similar symptoms, John has been near that athlete and in an environment where transmission of viruses could occur. The locker room could be the actual physical environment that may subject him to infection. Colds or flu can be easily passed with contact sports or in a close, warm and humid environment. This disease might fit the presentation. Kennedy, Turner, Braciale, Heymann, & Borish (2012) inform us that rhinovirus is the virus most likely responsible for producing common cold infection. The rhinovirus is an RNA virus which contains no envelope surrounding it. With cell replication, RNA serves as the messenger that informs the capsid proteins responsible for viral replication and assembly. When the virus enters the cell, viral translation occurs. The RNA genome has four viral capsid proteins. The differences in amino acids in the capsid proteins have differences among the different strains of Rhinovirus infection as well as serotypes. When the virus attaches and binds to the cell the virus loses the protein capsid. The uncoating by intermediate particles and the loss of the viral capsid proteins in VP1 and VP4 leads to transmigration of viral RNA. Transmigration of viral RNA is also accomplished through the cell membrane of the host (Kennedy et. al, 2012, pp. 1-2).In patients without asthma, the symptoms are limited to the upper respiratory tract. There is rhinorrhea, obstruction of the nasal passages with the permeability of the vascular structures as well as the stimulation of mucus. Coughing is a less common manifestation of rhinovirus upper respiratory infection. Coughing is caused by drainage from the back portion of the pharynx because of infection in the lung airways. There is some sinus involvement with cold symptoms (Kennedy et. al, 2012, p. 2). Given this patient has a history of eczema, allergies, and asthma, he would be showing infection of the respiratory tract (lower) and the symptoms more prominent with a cold. There can be coughing, tightness in the chest, shortness of breath and sometimes wheezing. There is debate about whether RV can actually infect cells in the lower respiratory tract or whether infection (bronchial) is the basis for the respiratory symptoms in opposition to influences that are are indirectly related to the immune response in the infection (Kennedy et. al. 2012, p. 2). This presentation would not appear to fit the presentation. Differential # 5: Nasal congestion - According to Fried (2016) nasal congestion and a runny nose commonly occur together but sometimes alone. They suggest that causes for nasal congestion and rhinorrhea can be related to viral infection or upper respiratory infections or allergic reactions. Also, dry air can be a factor for congestion in nasal passages as well as an acute sinusitis or perhaps a foreign body (Fried, 2016). John also may be having rebound congestion because of the use of a decongestant. References Aring, A. M., & Chan, M. M. (2011). Acute rhinosinusitis in adults. American Family Physician, 83(9), 1057-1063. Fried, M. P. (2016). Nasal congestion and rhinorrhea. Merck Manual Online. Retrieved from http://www.merckmanuals.com/professional/ear,-nose,-and-throat- disorders/approach-to-the-patient-with-nasal-and-pharyngeal-symptoms/nasal- congestion-and-rhinorrhea Kennedy, J. L., Turner, R. B., Braciale, T., Heymann, P. W., & Borish, L. (2012). Pathogenesis of rhinovirus infection. Current Opinion in Virology, 2(3), 287-293. Retrieved from doi.org/10.1016/j.coviro.2012.03.008 National Institute of Allergy and Infectious Diseases. (2016). Pollen allergy fact sheet. Retrieved from https://www.niaid.nih.gov/Pages/default.aspxTogias, A., & Sin, B. (2011). Pathophysiology of allergic and nonallergic rhinitis. Proceedings of the American Thoracic Society, 8(1), 106-114. Retrieved from http://www.atsjournals.org/action/doSearch? AllField=Pathophysiology+of+Allergic+and+Nonallergic+Rhinitis 5/3/2016 10:23:06 AM Lorna Durfee reply to Lorna Durfee RE: Discussion Part 1 - Differentials Addendum: Professor Brown and Class: In the prior thread, I outlined the differentials and the pathology from the case study. The following is the epidemiology that is required. Epidemiology Differential #1: Allergic rhinitis - The estimation, Bhattacharyya (2014) informs us, is that approximately 15% to 20% of the population in the United States suffers from chronic or recurrent congestion. Allergic rhinitis is the cause of most of the patient cases (Bhattacharyya, 2014, p. 1447). Differential # 2: Seasonal allergy to pollen - The first effects of seasonal allergic rhinitis from pollen (hay fever) in the United States happened around 1872. It was also first observed in England a year later. The identification of this disease in England and Germany was by the turn of the 20 century. The United States identified it around 1920. In the beginning, hay fever was considered a disease of the affluent but not for the working-class people. Ironically, in the early part of the 20 century, the affluent patients from New England that suffered from hay fever retreated to resorts in the mountains in an attempt to escape the pollen. The first published written paper on pollen was in 1911 (Platts-Mills & Cummins, 2016). th th Differential # 3: Sinus infection - The Centers for Disease Control and Prevention (2016) statistics show that the number of adults diagnosed with this condition is 29.4 million and the percentage diagnosed is 12.3%. Also, the number of office visits for patients with this diagnosis is 11.7 million (Centers for Disease Control and Prevention, 2016). Differential # 4: Common cold - The rhinovirus is responsible for most of the colds that are seen and is the primary cause of anywhere from 33% to 50% of adult cases seen annually. There are more than 100 micro-organisms and serotypes found in rhinovirus. An interesting fact is that adults have two to three colds a year whereas children have around eight to 12. Children are a good reservoir (carrier) for this virus (Pappas, 2016). Differential # 5: Nasal congestion - The American Academy of Otolaryngology – Head and Neck Surgery, state that nasal congestion or stuffy nose is one of the oldest and most common complaints. This condition may be a nuisance for some as it can cause a considerable amount of discomfort. There are various causes, including infection, allergy and anatomical defects such as septal deviation (American Academy of Otolaryngology-Head and Neck Surgery, 2016). ReferencesAmerican Academy of Otolaryngology-Head and Neck Surgery. (2016). Stuffy nose. Retrieved from http://www.entnet.org/content/stuffy-nose Bhattacharyya, N. (2014). Approach to the patient with chronic nasal congestion and discharge. In Goroll, A. H., & Mulley, A. G. (Eds.), Primary care medicine: Office evaluation and management of the adult patient (7th ed., p. 1447). Philadelphia, PA: Wolters Kluwer/Lippincott Williams & Wilkins Health. Centers for Disease Control and Prevention. (2016). Sinus conditions. Retrieved from http://www.cdc.gov/nchs/fastats/sinuses.htm Pappas, D. E. (2016). Epidemiology, clinical manifestations, and pathogenesis of rhinovirus infections. Retrieved May 3, 2016, from http://www.uptodate.com/contents/epidemiology-clinical-manifestations-and- pathogenesis-of-rhinovirus-infections Platts-Mills, T. A., & Cummins, S. P. (2016). Increasing prevalence of asthma and allergic rhinitis and the role of environmental factors. Retrieved from http://www.uptodate.com/contents/increasing-prevalence-of-asthma-and- allergic-rhinitis-and-the-role-of-environmental-factors#H2 Rochelle Elayda reply to Lorna Durfee RE: Discussion Part 1 - Differentials 5/3/2016 3:25:18 PM Lorna, I agree with your differentials. I also placed allergic rhinitis at the top of my list. John displays symptoms of rhinitis, which are sneezing, nasal congestion, and itchy eyes. As a football player, John is outside and on grass for many hours each day. According to Ryan (2016), up to 40% of patients with allergic rhinitis also have asthma. Although pollen is heaviest in spring and summer, it also appears in other seasons such as the falls (which is when football season starts). People with asthma have a greater risk to experience allergic rhinitis that those who do not have a history of asthma. Rochelle Reference: Ryan, D. (2016). How to identify and manage seasonal allergic rhinitis. Journal ofCommunity Nursing, 30(2), 54-59. Retrieved from http://search.ebscohost.com.proxy.chamberlain.edu:8080/login.aspx? direct=true&db=rzh&AN=114567503&site=nrc-live Rechel DelAntar reply to Rochelle Elayda RE: Discussion Part 1 - Differentials 5/3/2016 8:04:16 PM Hello Lorna, Rochelle and class, I had originally thought about putting allergic rhinitis as my first differential diagnosis but I was hesitant because the patient was exhibiting a low grade fever. Fever is a biochemical response to inflammatory process from the release of pyrogens (endotoxins) from bacteria, viruses and parasitic infections (McCance, K.L., et. al., 2013). Allergies to my understanding is a result of an overactive immune system and do not produce fever. Allergic Rhinitis and Viral infection both has similar symptoms except for presence of low grade fever of 100F. I was undecided which diagnosis best suited the scenario but decided with the common cold at the end. Reference: McCance, K. L., Huether, S. E., Brashers, V. L., & Rote, N. S. (2013). Pathophysiology: The biologic basis for disease in adults and children (7th ed.). St. Louis, MO: Mosby. Lorna Durfee reply to Rochelle Elayda RE: Discussion Part 1 - Differentials Rochelle: I agree with you. However, the patient may be in the initial phase of a viral infection or prodromal phase. His history shows that he has known allergies, eczema, and asthma. His symptoms range from sneezing and itchy eyes to nasal congestion that is worse at night. These symptoms also occur with allergic rhinitis, as I have stated in my first post. As we know from our readings this week, clinical infection is an ongoing process that includes stages. This patient could be in a prodromal stage. Nursing involves observing patients and it is then when we usually can recognize symptoms that are related to the initial onset of a viral infection. These symptoms can mimic the signs and symptoms outlined in our case study. The only thing that stands out as being different with this patient information is that his temperature is somewhat elevated. We do not have enough information to make a definitive diagnosis. Trunkel (2012) informs us that body temperature varies from lowest in the morning to highest in the afternoon. The temperature of the body has a balance between heat production by tissues and heat loss from the periphery of the body. Fever happens when the hypothalamic set point is raised. The set point rises and causes vasoconstriction and shunting to the periphery. When it decreases, it induces shivering, and this increases heat production. The hypothalamus sets a new point. There are also pyrogens that can cause fever. Disorders that can cause fever can be infectious, neoplastic, and inflammatory. When a patient has a fever that is less than or equal to four days in duration, it is considered infectious. We do not know how long our patient has had this elevation in his temperature. The causes of fevers can be upper and lower tract respiratory infections, infection in the GI tract, urinary tract infections, and skin. This fever could be self-limited ( Trunkel, 2012). 5/5/2016 11:48:36 AMIn conclusion, we need a further assessment to evaluate. Also, it is not known what medications he is taking for his allergies. Nor do we know his immunization history. Trunkel (2012) relates that the degree of elevation of the temperature does not seem to predict the cause of infection. Fever has many infectious and drug causes. So far, in this case, there are so many unknowns. We have to consider the underlying chronic disorders and those that impair the immune system (Trunkel, 2012). I still feel it is what I had stated in my differential, allergic rhinitis. References Trunkel, A. R. (2012). Fever. In Merck manual online. Retrieved from http://www.merckmanuals.com/professional/infectious-diseases/biology- of-infectious-disease/fever Matthew Dove reply to Lorna Durfee RE: Discussion Part 1 - Differentials 5/8/2016 5:53:11 AM Healthcare is in good hands with all the thoughtful responses and holistic attitudes presented in class this week. I agree with many of your summations, Lorna, Rechel, and Rochelle and you raise a salient point that more assessment is needed to fully understand what is going on with this patient. Specifically, there were a couple contentious characteristics of the case study to appreciate--like the implications of one elevated temp or more available information of lifestyle for assessment. While the literature suggests that allergic rhinitis is commonly present in the absence of fever (Porth, 2014), I would add that empiricism also has a moderate level of evidence that advocates for diet modification of a patient struggling with IgE mediated hypersensitivity responses. Further assessment would look at potential triggers in environment and food allergies such as with gluten. Gluten as an example is omnipresent ingredient in many foods and can trigger exacerbations of an altered immune system. Studies even show that it is present in many non-food items such as hydrolyzed wheat protein in soap (Fukutomi, Taniguchi, Nakamura, Akiyama, 2014). Inflammation is often a major reaction affecting many physiological responses systemically as a result of gluten in the compromised immune system. Elli, Roncoroni, Bardella research states that the pathogenesis and mechanism of the gluten triggering further allergic responses is, “largely unknown, but a mixture of factors such as the stimulation of the innate immune system, the direct cytotoxic effects of gluten, and probably the synergy with other wheat molecules...In addition, the diagnostic procedures still remain problematic due to the absence of efficient diagnostic markers; thus, diagnosis is based upon the symptomatic response to a gluten-free diet and the recurrence of symptoms after gluten reintroduction.” The study demonstrates that, “temporary withdrawal of gluten seems a reasonable therapy, but the timing of gluten reintroduction and the correct patient management approach are have not yet been determined” (Elli, Roncoroni, Bardella, 2015). Mameri , Brossard, Gaudin, Gohon, Paty, Beaudouin, Moneret-Vautrin, Drouet, Sole, Wien, Lupi, Larre, Snegaroff, and Denery-Papini relate that, “Allergenicity was evaluated from patients who had a wheat food allergy or baker's asthma and it was determined that Wheat products cause and exacerbate IgE-mediated allergies because of molecular α- and γ-gliadin proteins” (Mameri, et. al, 2015). Whilecausation is an audacious claim, the study represents how a patient with pre- disposing hypersensitivities can be further aggravated by other factors outside insulting stimuli. In terms of hypersensitivity to food allergens, Lombardo, Bolla, Chignola, Senna, Rossin, Caruso, Tomelleri, Cecconi, Brandolini, and Zoccatelli agree that the issue could harm those already sensitized and prone to anaphylaxis, allergies and propose solution through bio-engineered foods. The researchers suggest that “Wheat [Triticum aestivum (T.a.)] ingestion can cause a specific allergic reaction, which is called wheat-dependent exercise-induced anaphylaxis (WDEIA). The major allergen involved is ω-5 gliadin, a gluten protein coded by genes located on the B genome. Our aim was to study the immunoreactivity of proteins in Triticum monococcum (einkorn, T.m.), a diploid ancestral wheat lacking B chromosomes, for possible use in the production of hypoallergenic foods” (Lombardo et al., 2015). Although Genetically Modified Organisms (GMO) are generally met with consternation, eliminating certain proteins in food might represent a potential candidate in the production of hypoallergenic products like peanut butter or bakery items. I was cued into this research because of the considerable improvement in my son who experiences seasonal allergies and asthma when reducing his gluten intake. While Celiac disease was ruled out, he went from multiple asthma exacerbations per week to none after altering what he ate. Ultimately, there is something to be said for (at the very least) screening and developing a holistic care plan that potentially includes diet modification in improving a patient’s life and experiences with IgE allergies. Refferece Elli, L., Roncoroni, L., Bardella, M.T. (2015). Non-celiac gluten sensitivity: Time for sifting the grain. World Journal of Gastroenterology, 21(27), 8221-6. DOI: 10.3748/wjg.v21.i27.8221. Fukutomi, Y., Taniguchi, M., Nakamura, H., Akiyama, K. (2014). Epidemiological link between wheat allergy and exposure to hydrolyzed wheat protein in facial soap. Allergy, 69(10):1405-11. DOI: 10.1111/all.12481. Lombardo, C., Bolla, M., Chignola, R., Senna, G., Rossin, G., Caruso, B., Tomelleri, C., Cecconi, D., Brandolini, A., Zoccatelli, G. (2015). Study on the Immunoreactivity of Triticum monococcum (Einkorn) Wheat in Patients with Wheat-Dependent Exercise-Induced Anaphylaxis for the Production of Hypoallergenic Foods. Journal of Agricultural Food Chemistry, 23;63 (37):8299-306. DOI: 10.1021/acs.jafc.5b02648. Porth, C.M. (2014). Essentials of Pathophysiology: Concepts of Altered Health States (4th Ed.) Philadelphia, PA: Lippincott Williams & Wilkins. Mameri, H., Brossard, C., Gaudin, J.C., Gohon, Y., Paty, E., Beaudouin, E., Moneret- Vautrin, D.A>, Drouet, M., Sole, V., Wien, F., Lupi, R., Larre, C., Snegaroff, J., Denery-Papini, S. (2015). Structural Basis of IgE Binding to α- and γ-Gliadins: Contribution of Disulfide Bonds and Repetitive and Nonrepetitive Domains. Journal of Agricultural Food Chemistry, 63(29):6546-54. DOI: 10.1021/acs.jafc.5b01922. Liberty Neoh Discussion Part One 5/1/2016 5:56:46 PMDr. Brown and Class, Part One: Differential Diagnosis: 1. Allergic Rhinitis caused by exposure to certain allergens can cause swelling or inflammation of the mucous membranes which can lead to sneezing, nasal congestion, and itchy eyes. According to Hollier (2016), allergic rhinitis is “caused by any substance or condition which causes an IgE mediated response characterized by rupture of mast cells and release of histamines, leukotrienes, prostaglandins, and other substances”. Tran, Vickery, and Blaiss (2011) reported that there are approximately 10-30 % of adults in the United States are affected by this condition. Week 1 lecture explained that the antigen- antibody response is the basic protective mechanism of our immune system (Chamberlain, 2016). Based from this information, I believe that John has allergic rhinitis. 2. Asthma is a chronic condition caused by inflammation of the bronchial mucosa and spasms of the bronchial smooth muscle which can lead to narrowing of the small and occasionally large airways. Asthma affects more than 22 million Americans (Hollier, 2016). John did have a history of asthma but I need to obtain a comprehensive health history and physical assessment if he has any wheezing, cough (non-productive early symptom), shortness of breath, and tachypnea, just to name some of the symptoms associated with asthma. John’s symptoms did not include shortness of breath nor tachypnea. 3. Common Cold is an infection of the upper respiratory tract caused by a virus. The symptoms may last for 3-10 days (Hollier, 2016). The scenario has limited information regarding the duration of present symptoms, therefore, I did choose this as my primary diagnosis. 4. Influenza is a highly contagious, acute viral illness of the respiratory tract which involves the nasal mucosa, pharynx, and conjunctiva. Influenza is common during the months of October to April. Prevalence is highest in school-age population (Hollier, 2016). The casestudy did mention that there was another player with similar symptoms. Since influenza is highly contagious, I would expect more football players and other students to have the illness. 5. Respiratory Infections involve direct invasion of the mucosa lining the upper airway. Inoculation of bacteria or viruses occurs when a person’s hand comes in contact with pathogens and the person then touches the nose or mouth or when a person directly inhales respiratory droplets from an infected person who is coughing or sneezing. Upper Respiratory Infections (URIs) are the most common infectious illness in the general population and are the leading cause of missed days at work or school. They represent the most frequent acute diagnosis in the office setting (Meneghetti & Mosenifar, 2015). References Chamberlain College of Nursing. (2016). NR-507 Week 1: Altered immune system and altered inflammatory response [Online lesson]. Downers Grove, IL: DeVry Education Group. Hollier, A. (2016). Clinical Guidelines in Primary Care. Scott, LA: Advanced Practice Education Associates, Inc. Tran, N. P., Vickery, J., & Blaiss, M. S. (2011). Management of rhinitis: Allergic and non- allergic. Allergy, Asthma, & Immunology Research, 3(3). doi:10.4168/aair.2011.3.3.148 Meneghetti, A. & Mosenifar, Z. (2015). Upper respiratory tract infection. Medscape News & Perspective. Retrieved from http://emedicine.medscape.com/article/302460- overview#a7 Sarah Boulware Part One Dr. Brown and Class, 1. Hayfever (Seasonal Allergic Rhinitis) 5/2/2016 4:21:19 PMa. Epidemiology: Rhinitis is characterized as an upper respiratory tract disorder involving inflammation of all mucous membranes of the upper airway when exposed to pollen triggers. It is most likely to affect people who have become sensitized to a specific pollen. People with hayfever often have a history of other allergies such as eczema and asthma. Hayfever affects 1 out of 4 people, 4 out of 10 teenagers, and 9 out of 10 occurrences are due to grass allergens. b. Pathology: Pollen is inhaled through the nose, triggering a cascade of inflammatory reactions that lead to sneezing, increased mucous production and swelling, itchy eyes and an itchy nose. This reaction is continuously stimulated until there is no longer pollen in the air. The most common implicated allergen is grass. c. Fits Presentation: John has a history of eczema and asthma, which is associated with hayfever as well being previously sensitized to pollen. He exhibits the common signs and symptoms of hayfever, which include itchy eyes, sneezing, and nasal congestion. He is a teenager that plays football so he is likely going to be affected by grass allergens which is the most common allergen and he is in the most common age group for allergies. d. Does not fit presentation: There are many conditions that present with the same signs and symptoms of rhinitis. John has a low-grade fever, which may be associated with the common cold and not hayfever. There is also another player with similar symptoms, which means it could be a contagious virus and not an allergy issue. (Bartle & Emberlin, 2011) 2. The Common Cold (Viral) a. Epidemiology: The common cold dates back to the 16 century. There are many misconceptions on how the common cold is acquired. There are more than 200 viruses that can cause a cold and produce a large variability of symptoms. Primary symptoms are nasal congestion, sneezing, pharyngitis, and cough. th b. Pathology: Cold symptoms develop due to an inflammatory response to viral antigens. Chemical mediators are released affecting the vascular tissues in the nasal epithelium, causing engorgement and increased vascular permeability. This leads to sneezing, nasal congestion, and rhinitis. Symptoms can lead to fever, malaise, watery eyes, and a general discomfort. A common cold is self-limiting and symptoms typically last for 7 to 10 days but may persist for up to 3 weeks c. Fits presentation: John presents with congestion and a low-grade fever, which are symptoms of a cold. There is also another teammate with the same symptoms, which means that it could be a contagious virus. d. Does not fit presentation: John has a history of allergies and eczema, which favors his symptoms being related to hayfever and more of an allergy than a virus. He does not present with a cough, which is a common symptom of a cold but not always present. e. (KinyonMunch, 2011) 3. Sinus Infection (Sinusitis) a. Epidemiology: Sinusitis is one of the most common conditions treated by Primary care providers. It can be caused by viral or bacterial infections. It is the fifth most common diagnosis for which antibiotics are prescribed. The pattern and duration of the illness is key to determine if it is viral or bacterial and prescribe appropriate treatment. b. Pathology: Mucosal edema leads to obstruction of the sinus ostia. Viral and bacterial infections impair the cilia, which transport mucus. This causes stagnation of secretions and lowered oxygen tension within the sinuses, creating a perfect environment for infections. Streptococcus pneumonia, Haemophilus influenzae, Staphlyococcus aureus, and Moraxella catarrhalis are the most common organisms associated with sinusitis. Many people experience symptoms similar to an upper respiratory tract infection, facial pain or pressure, purulent rhinorrhea, maxillary toothache, and nasal obstruction. c. Fits presentation: John is suffering from nasal congestion that worsens at night, which could be related to sinusitis. There is also another person with similar symptoms.d. Does not fit presentation: John does not exhibit many symptoms of sinusitis. He does have nasal congestions but that could be caused by several other things. It could be early in the disease process and his symptoms could be mild but there is not enough information to determine if he has sinusitis. (Aring & Chan, 2011) 4.Influenza (Viral) a. Epidemiology: Influenza is a highly contagious viral disease that can affect any age group. It is regarded as a serious public health problem. It has the potential to worsen existing medical problems such as asthma. b. Pathology: Influenza is caused by one of three influenza viruses (A, B, and C). Influenza type B is generally a more mild form than type A and type C is associated with minor symptoms. It is spread form one person to another via respiratory secretions that invade the airway of a susceptible individual. If antibodies do not effectively attack the virus it is able to replicate and causes cellular function to be disrupted. Usual signs and symptoms in younger patients are fever, muscle aches and pains, headaches, and chills. Fever is the most common symptom of influenza. c. Fits Presentation: John and his teammate could have a mild version of the Type C influenza virus. John presents with a low-grade fever so there is a possible influenza infection occurring. d. Does not fit presentation: Generally the symptoms of sneezing, itchy eyes, and nasal congestion are not associated with the influenza virus. (Perry, 2012) 5. Wiskott-Aldrich Syndrome (WAS) a. Epidemiology: WAS is a primary immunodeficiency. Hallmark symptoms include thrombocytopenia, immunodeficiency, and eczema. Patients with WAS are more prone to recurrent respiratory and skin infections and susceptible to lymphomas. b. Pathology: WAS is an X-linked primary immunodeficiency caused by a mutation in the gene encoding the WAS protein, which is an important regulator of branched actin chain polymerization. c. Fits presentation: John has a history of eczema which is a sign of WAS. Additional healthy history is needed to determine if recurrent infections and thrombocytopenia occur. d. Does not fit presentation: John would most likely be diagnosed at a young age with WAS because it usually manifest itself after the first month of life. He does not appear to have symptoms of thrombocytopenia. (Jesenak, Plamenoa, Plank, & Banovcin, 2013) References Aring, A. & Chang, M. (2011). Acute rhinosinusitis in adults. American Family Physician, 83(9), 1057-1063 . Retrieved from www.aafp.org/afp Bartle, J. & Emberlin, J. (2011). Understanding the main causes of hayfever. Practice Nursing, 22(5), 231-235. KinyonMunch, K. (2011). What do you tell parents when their child is sick with the common cold? Journal for Specialists in Pediatric Nursing, 16(1), 8-15. doi: 10.1111/j.1744-6155.2010.00262.x Jesenak, M., Plamenoa, I., Plank, L., & Banovcin, P. (2013). Wiskott-Aldrich syndrome caused by a new mutation associated with multfocal dermal juvenile xanthogranulomas. Pediatric Dermatology, 30(5), 91-93. doi: 10.1111/pde.12040 Perry, M. (2012). How the signs and symptoms of common infections vary with age. Practice Nursing, 23(4), 176-181.Liberty Neoh reply to Sarah Boulware RE: Part One 5/7/2016 2:13:07 PM Sarah, Thank you for your post. I was not familiar with Wiskott-Aldrich Syndrome (WAS). An article by Kerfoot and her colleagues (2012) concerning WAS suggested that early screening for Primary Immunodeficiency Disorders (PID D), such as WAS will help maximize patients’ survival and clinical outcomes. WAS is one of the immunodeficiency disorder that fall under PIDDs. According to the authors, “High- throughput sequencing techniques are now being utilized to simultaneously screen for genetic defects in a large number of genes or even throughout the genome. These may identify genetic alterations in a number of genes in a single individual. The evaluation of protein expression or function will then be required to determine which of these are relevant and pathogenic” (Kerfoot et al, 2012). As of now, WAS is not one of the diseases that is include in metabolic screening of newborns. The goal is to also include PIDDs in the newborn screening in the future. Reference Kerfoot, S. A., Jung, S., Golob, K., Torgeson, T. R., & Hahn, S. (2012). Tryptic Peptide screening for primary immunodeficiency disease. Proteomics Clinical Application, 6(7). doi: 10.1002/prca.201100096 Lanre Abawonse Discussion Part One 5/3/2016 12:01:46 AM Allergic rhinitis is a collection of symptoms, involving mucous membranes of the nose, eyes, ears, and throat after an exposure to allergens like pollen, dust, or dander. In their study, Holmes and Scullion (2012) stated that allergic Rhinitis is inflammation of the mucosa of the nasal airways, clinically identified by symptoms of nasal discharge, nasal blockage or congestion, and at times itching/sneezing. It can be seasonal or perennial. When this happens, IgE-mediated inflammation of the nasal mucosa follows exposure to an extrinsic protein; an immediate symptomatic response is characterized by sneezing, congestion, and rhinorrhea followed by a persistent late phase dominated by congestion and mucosal hyper-reactivity (Domino, 2014).Pathophysiology: Aeroallergen-driven mucosal inflammation is due to resident and infiltrating inflammatory cells, as well as vasoactive and pro-inflammatory mediators (e.g., cytokines). The cytokines are the most important pro-inflammatory mediators, especially the helper T cell activation that gives rise to macrophages, which stimulates interleukins 3, 4, 5, and 13. There are other contributing factors to the full understanding of the mechanism of Allergic Rhinitis. One is the allergic inflammatory cascade. Nathan (2008) contends that it comprises of a series of linked local and systemic immune events that are triggered by mast-cell activation after the immuno-globulin E-receptor is activated. This activation causes degranulation and release of pre-formed mediators, such as histamine and tryptase, from the mast cell. Activated mast cells also mobilize arachi-donic acid from membrane stores, which are then fed into eicosanoid synthetic pathways to produce leuko- trienes and other related mediators. Epidemiology: Onset is usually in first 2 decades, rarely before 6 months of age, with tendency to decline with advancing age. The mean age of onset is 8–11 years, and about 80% of cases have established allergic rhinitis by age 20. 10–25% of the US adult population and 9–42% of the US pediatric population are affected. 44–87% of patients with allergic rhinitis have mixed allergic and non-allergic rhinitis, which is more common than either pure form (Domino, 2014). Conclusion: Considering the physical signs presented by John, allergic rhinitis would fit his situation as the clinical signs of sneezing, itchy eyes, and nasal congestion that worsens at night. In addition, John’s known history of asthma and eczema are considered risk factors for allergic rhinitis (Rafiq, 2016) Upper respiratory infections (URIs) are the 2nd most common medical diagnosis, contributing to 20 million/year office visits. Inflammation of nasal passages resulting from infection occurs with various respiratory viruses. Eccles and Wilkinson (2015) noted that URIs are commonly associated with cold exposure and this may be the origin of the term ‘common cold’ which implies exposure to cold or a feeling of chilliness and cold. Domino (2014) contends that URI in most cases are self-treated, usually mild–moderate in severity. Self-limited systems that affected are ENT and Pulmonary (Domino, 2014). Pathophysiology: Rhinoviruses infect the ciliated epithelium lining the nose, resulting in edema and hyperemia of nasal mucous membranes. Klemens et al., 2007 contends that URI is characterized by neutrophil tissue infiltration and monocytes that become tissue macrophages soon after the inoculation of the virus. Domino (2014) stated that many strains present within the same geographic region or patient family: Rhinovirus, with> 100 serotypes: 30–50% Influenzavirus types A, B, C: 15% Coronaviruses: 15% Parainfluenza, respiratory syncytial virus (RSV): 10%; more common in children Enteroviruses, adenoviruses: <10%In 30% of cases, no pathogen is identified. Epidemiology: Each virus has different seasonal peaks (e.g., rhinovirus: Late spring, fall). Domino (2014) suggested that cold climates do not increase susceptibility and that transmission is from hand contact with contaminated skin/surface followed by contact with mucous membranes aerosolized particles from sneezing and coughing. Most of the viral shedding peaks after 48–72 hours of illness and can last up to 2 weeks and virus may last up to 2 hours on skin or longer on environmental surfaces. Conclusion: The close relationships of URI to symptoms exhibited by John in terms of nasal passages make the diagnoses relevant but inconclusive to John’s presenting problems. Acute Sinusitis is a symptomatic inflammation of ≥1 paranasal sinuses of <4 weeks' duration resulting from impaired drainage and retained secretions. Because rhinitis and sinusitis usually coexist, “rhinosinusitis” is the preferred term. Sng and Wang (2015) described acute rhinosinusitis (ARS) as a sudden onset of two or more symptoms, including one of either two key symptoms of nasal blockage/obstruction/congestion or nasal discharge, and facial pain/pressure and reduction or loss of smell for less than 12 weeks. The disease is subacute when symptomatic for 4–12 weeks and chronic when symptomatic for >12 weeks. Systems affected: Head/Eyes/Ears/Nose/Throat (HEENT); Pulmonary Pathophysiology: Impaired mucociliary clearance. Secretions that are not cleared become hospitable to bacterial growth. The trapped mucus creates an environment for bacterial growth. (Gupta, 2016). Inflammatory response (neutrophil influx and release of cytokines) damages mucosal surfaces. Viral: Vast majority of cases (rhinovirus, influenza A and B; parainfluenza virus; respiratory syncytial; adeno-, corona-, and enteroviruses) Epidemiology: It is believed that as many as 31 million individuals in the US each year are affected. Domino (2014) noted that the diagnosis of acute bacterial rhinosinusitis remains the 5th leading reason for prescribing antibiotics and 2% of viral rhinosinusitis episodes have a bacterial superinfection. Thus the incidence is highest in early fall through early spring (related to incidence of viral upper respiratory infection [URI]). Conclusion: John’s presenting signs are well aligned to the problem faced by patients with acute sinusitis. The nasal congestion experienced by John at night time could be the result of impaired clearance causing major disturbance at night time and the possibility of full blown infection as an aftermath. At this time, John’s presenting symptoms suggest allergic rhinitis and acute sinusitis. In spite of this close relation between the two diagnoses, it can be said that there is no information in John’s history to indicate how long his symptoms have persisted to make the call for acute sinusitis.Vasomotor Rhinitis (VR) can describe symptoms in patients that are triggered by external stimuli, this external stimuli has been mostly associated with cold. Halderman and Sindwani (2015) stated that vasomotor Rhinitis is the most prevalent cause of nonallergic rhinitis (NAR). Pathophysiology: It is one of the poorly understood pathophysiologic disease processes. Goroll and Mulley (2014) noted that it involves abnormal autonomic responsiveness and vascular dilation of the submucosal vessels. The study further explains that the IgE levels are always normal, and the number of eosinophils in nasal secretions is usually, but not always, normal. It is believed that sexual and emotional upset contributes to the nasal stuffiness or rhinorrhea, which makes it mimic perennial allergic rhinitis. Epidemiology: Overall, the epidemiology of rhinitis conditions are difficult to assess due to challenges in classifying rhinitis. Domino (2014) noted that 57% of patients with rhinitis have non-allergic or mixed rhinitis and can occur in those with or without nasal disease. Conclusion: John’s presenting problem suggests allergic rhinitis. Uzzaman and story (2012) noted that itchy eyes and sneezing are a hallmark of allergic rhinitis. In the case of VR, Settipane and Kaliner, (2013) noted that symptoms such as sneezing and itchy eyes are rare. Influenza: It infects a wide variety of species, including humans, different strains of bird and swine (McCance & Huether , 2013). Duncan (2013) also stated that influenza is a respiratory infection caused by the influenza virus and causes symptoms such as fever, coryza (inflamed nasal mucosal membranes), headache, malaise, myalgia, and at times gastrointestinal upset. It is a highly contagious viral respiratory infection that is caused by one of the three types of myxovirus. Influenza illness can include any or all of these symptoms: fever, muscle ache, headache, lack of energy, dry cough, sore throat, and possibly runny nose (n.d., 2015) Pathophysiology: It is a single stranded negative sense RNA virus which attaches to epithelial cells of the host and utilizes its own reverse transcriptase to replicate the negative strand RNA to positive strand RNA, which is utilized like messenger RNA to replicate proteins. Viral RNA is more prone to mutations and antigenic evolution causes many variations of the virus (McCance, Huether, Brashers, & Rote, 2013). Epidemiology: Domino, (2014) noted that males and females are affected equally. It mostly affects young people and older people are protected because they have pre- existing antibodies.Conclusion: John’s presenting history is not entirely associated with the influenza cases that are usually presented in sick patients. Individuals with influenza often present with a temperature of 102 to 103 f, redness of the soft plate, tonsils and pharynx. Rhinitis or rhinorrhea are often common with influenza but this is not enough to diagnose John with influenza. Reference Duncan, D. (2013). Treatment and prevention of influenza. Nurse Prescribing, 11(12), 590- 596.http://www.markallengroup.com/ma-healthcare/ Domino, F. J. (2014). The 5 minute clinical consult standard, 2015. [electronic resource]. Philadelphia. Pa. : Wolters Kluwer Health, 2014. Eccles, R., & Wilkinson, J. E. (2015). Exposure to cold and acute upper respiratory tract infection. Rhinology, 53(2), 99-106. doi:10.4193/Rhin14.239 Goroll, A. H., & Mulley, A. G. (2014). Primary care medicine: Office evaluation and management of the adult patient (7th ed.). China: Wolters Kluwer Gupta, A. K. (2016). Sinusitis. In F. J. Domino (Ed.), The 5-minute clinical consult (pp. 1028-1029). Philadelphia, PA: Wolters Kluwer Health. Halderman, A., & Sindwani, R. (2015). Surgical management of vasomotor rhinitis: a systematic review. American Journal Of Rhinology & Allergy, 29(2), 128-134. doi:10.2500/ajra.2015.29.4141 Holmes, S., & Scullion, J. (2012). Allergic rhinitis: assessment and treatment. Nurse Prescribing, 10(5), 222-228 5p. Influenza symptoms and the role of laboratory diagnostics. (2015). MLO: Medical Laboratory Observer, 47(11), 12. Klemens, C., Rasp, G., Jund, F., Hilgert, E., Devens, C., Pfrogner, E., & Kramer, M. F. (2007). Mediators and cytokines in allergic and viral-triggered rhinitis. Allergy And Asthma Proceedings: The Official Journal Of Regional And State Allergy Societies, 28(4), 434-441. McCance, K. L., Huether, S. E., Brashers, V. L., & Rote, N. S. (2013). Study guide for pathophysiology: The biologic basis for disease in adults and children (7th ed.). St. Louis, MO: Mosby. Nathan, R. (2008). The pathophysiology, clinical impact, and management of nasal congestion in allergic rhinitis. Clinical Therapeutics, 30(4), 573-586 14p. Settipane, R. A., & Kaliner, M. A. (2013). Chapter 14: Nonallergic rhinitis. American Journal of Rhinology& Allergy, 27 Suppl 1S48-S51. doi:10.2500/ajra.2013.27.3927 Sng, W. J., & Wang, D. (2015). Efficacy and side effects of antibiotics in the treatment of acute rhinosinusitis: a systematic review. Rhinology, 53(1), 3-9. doi:10.4193/Rhin13.225Uzzaman, A., & Story, R. (2012). Chapter 5: Allergic rhinitis. Allergy And Asthma Proceedings: The Official Journal Of Regional And State Allergy Societies, 33 Suppl 1S15-S18. doi:10.2500/aap.2012.33.3535 Jonathan Bidey Discussion [Show More]

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