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 Outcomes (COs).
1 2 3
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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 Outcomes (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
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