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NR 507 Week 1 TD (Part 1, Part 2, Part 3)

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NR 507 Week 1 TD (Part 1, Part 2, Part 3) NR 507 Week 1 Quiz (Questions & Answers) PART 1: John is a 19-year-old college football player who presents with sneezing, itchy eyes, & nasal congestion that worsens at night. He states that he has a history of asthma, eczema & 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 three (3) possible items from the most likely to less likely. For each disease include information about the epidemiology, pathophysiology & briefly argue why this disease fits the presentation & why it might not fit the presentation. Nasal congestion viral rhinitis, allergic rhinitis, sinusitis, rhinitis medicamentosa (rebound from nasal decongestants) Sneezing allergic rhinitis, URI DX: 1. Allergic response to stimulant from being outside – i.e. allergic rhinitis/ sinusitis?

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NR 507 Week 1 TD (Part 1, Part 2, Part 3)

NR 507 Week 1 Quiz (Questions & Answers)

PART 1:
John is a 19-year-old college football player who presents with sneezing, itchy
eyes, & nasal congestion that worsens at night. He states that he has a history of
asthma, eczema & 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 three (3) possible items from the most likely to
less likely. For each disease include information about the epidemiology,
pathophysiology & briefly argue why this disease fits the presentation & why
it might not fit the presentation.


Nasal congestion viral rhinitis, allergic rhinitis, sinusitis, rhinitis medicamentosa
(rebound from nasal decongestants)

Sneezing allergic rhinitis, URI

DX:
1. Allergic response to stimulant from being outside – i.e. allergic
rhinitis/ sinusitis?

,2. Viral rhinitis /URI?

3. Bacterial rhinitis/ sinusitis?

“Type 1 allergic responses mediators (such as epinephrine, acetylcholine, &
inflammatory mediators) bind to receptors on mast cells & the target cells of
inflammation (i.e. smooth muscle), thereby controlling the release of
inflammatory mediators from mast cells & the degree to which target cells
respond to inflammatory mediators (p. 272).




Differential Diagnoses:

• Allergic Rhinitis. Since John reports a history of allergies, specifically to pollen,
he could be experiencing an exacerbation of his allergies.
Epidemiology: The increasing prevalence of allergic rhinitis has epidemiologists
questioning what changed. The rise was too quick to be attributed to genetics, therefore
epidemiologist deduce that it is environment related (Platts-Mills & Commins, 2017).
Indoor & outdoor allergen exposure has increased since the 1800’s, which likely
influenced the development of allergic rhinitis as well as asthma (Platts-Mills &
Commins, 2017). Allergic rhinitis is one of the most IgE-mediated diseases (Sin &
Togias, 2010). When an allergen is inhaled, a type 1 hypersensitivity reaction begins,
which ultimately results in a reaction that is both immunological & biochemical (Sin &
Togias, 2010). Pollen is an allergen that can set this reaction into motion.
Pathophysiology: “Type 1 reactions are mediated by antigen-specific IgE & the
products of tissue mast cells” (McCance, Huether, Brashers, & Rote, 2013, p. 263).
When a person experiences repeated exposure to such an antigen (i.e. pollen), IgE
production is enhanced & the person becomes sensitized (McCance, Huether, Brashers,
& Rote, 2013,
p. 263). When more exposure with the antigen occurs, a molecule from the antigen binds
“simultaneously to two molecules of IgE-Fc receptor complexes on the mast cell’s
surface (cross-link) resulting in activation of intracellular signaling pathways & mast cell
degranulation” (McCance, Huether, Brashers, & Rote, 2013, p. 265). Mast cell
degranulation products stimulate an acute inflammatory response (McCance, Huether,
Brashers, & Rote, 2013).
IgE is synthesized by B –lymphocytes by way of cytokines (Sin & Togias, 2010). When
basophils & mast cells react, they produce an allergic reaction at the cellular level (Sin
& Togias, 2010).
Presentation of Disease: Allergic rhinitis is characterized by signs & symptoms
that include sneezing, nasal obstruction, rhinorrhea, postnasal drip, fatigue, & itchy
eyes,

, nose, & throat (DeShazo & Kemp, 2017). When considering rhinitis, allergy & infection
should be considered (Sin & Togias, 2010). However, allergic rhinitis does best fit the
symptoms the patient is exhibiting.

2. Viral Rhinitis. Since there is another person on John’s team experiencing similar
symptoms, John’s symptoms could be viral. John & his teammate share some of the same
physical environment, making them susceptive to this kind of infection.
Epidemiology: Also known as the common cold, more than 200 subtypes of viruses can
cause the common cold (Sexton & McClain, 2017). Viruses can have seasonal patterns.
Rhinoviruses are typically seen in the fall & late spring (Sexton & McClain, 2017). The
common cold can be spread 3 ways: droplets via small particles, droplets via large
particles, & via direct contact (Sexton & McClain, 2017). Viruses can remain viable on
skin for approximately 2 hours post contact (Sexton & McClain, 2017). The rhinovirus,
which is one of the most common viruses that cause the common cold, can live on
surfaces for many hours, therefore increasing the chance of transmission (Sexton &
McClain, 2017).
Pathophysiology: Viruses are simple organisms when compared to human cells &
bacteria (McCance, Huether, Brashers, & Rote, 2013). The classification of a virus
depends on the format of their nucleic acid in the virion; this format is either RNA or
DNA & if it is single-str&ed or double-str&ed (McCance, Huether, Brashers, & Rote,
2013). The classification also depends on if the virus uses the reverse transcriptase (RT)
enzyme to replicate (McCance, Huether, Brashers, & Rote, 2013). Seven classifications
of viruses are present; ssRNA + sense (+ sense works as mRNA) represents the
rhinovirus (McCance, Huether, Brashers, & Rote, 2013). Therefore, the rhinovirus is an
RNA virus that does not have an envelope around it (McCance, Huether, Brashers, &
Rote, 2013).
Presentation of Disease: Being as John & his teammate exhibit some of the same
symptoms & they share a physical environment where a virus could easily be passed to
one another, this disease may fit the presentation. There are a few conditions that mimic
the common cold, such as allergic rhinitis & bacterial rhinosinusitis (Sexton & McClain,
2017). One can distinguish between the common cold & simple rhinitis by their
symptoms; the common cold typically presents with sore throat & cough (Sexton &
McClain, 2017). At this time, John does not have any complaints of a sore throat or a
cough, therefore this diagnosis does not fully fit the presentation.

• Bacterial Rhinitis or Acute Bacterial rhinosinusitis (ARS).
Epidemiology: ABRS is a common problem that can be uncomplicated or complicated.
For this purpose, uncomplicated will be the focus. Uncomplicated ABRS stems from a
bacterial etiology that does not extend outside the paranasal sinuses & nasal cavity
(Hwang & Patel, 2017). The most common bacterial associated with ABRS are
Streptococcus pneumoniae, Haemophilus influenzae, & Moraxella catarrhalis (Hwang &
Patel, 2017). Streptococcus pneumonia & Haemophilus influenza account for 75 percent
of ABRS infections (Hwang & Patel, 2017).
Pathophysiology: Bacterial & viral infections can hinder the action of the cilia within the
nostril, which transport mucus. When the cilia cannot do their job, secretions become

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