1 figures title7week 8 business level and corporate-level stra

1. 1
Figures title: 7Week 8 Business-Level and Corporate-Level
Strategies Assignment
Student’s Full Name
BUS499 Business Administration Capstone
Professor’s Name
Date
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REMINDERS
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resources to support what you have written in your own words.
Week 8 Business-Level and Corporate-Level Strategies
Assignment
Write your introduction to this 6 page paper here. Include one
paragraph (not more than 6 lines of text) that explains what
your paper will discuss. Much of your introduction may be
taken from the assignment instructions (in your own words).
Read all assignment resources to understand what should be
included in your paper. Be sure to review the assignment
instructions in Blackboard, the grading rubric, and relevant

3. course announcements to understand the requirements. Do not
exceed 6 lines of text in this introduction. There should be no
direct quotes in this section. After reading these instructions,
replace this blue text with your introduction and change the font
color to black.Business-Level Strategies
Analyze the business-level strategies for the corporation you
chose to determine the business-level strategy you think is most
important to the long-term success of the firm. You will also
need to determine whether or not you judge this to be a good
choice (Note: in this step you need to choose and write about
only one business-level strategy from the text book (not
Google). Hint: See Figure 4.1 in the textbook. Include a
thorough justification for your choice that is backed by facts
and sound judgement. For background, be sure to research and
explain the industry in which your selected corporation
operates. You could also briefly (1 – 2 sentences) define the
business-level strategy (cite your sources) you are writing about
using the textbook/Learn, as an introduction to your analysis.
Read Chapter 4 in the course textbook. Review the Week 4
Learn Reading for supporting content. Your response here
should demonstrate that you understand the key concepts
regarding the selected business-level strategy and can apply
them to a real-world corporation. Keep in mind that this is a 6
page paper and as such your analysis should thoroughly address
the concepts discussed in the course. Avoid unsubstantiated
statements, extended introductory commentary, direct quotes,
and unrelated content. Strive for about 1 ½ to 2 pages of well -
constructed, in-depth analysis in this section.
In this section, you could research and identify the core
competencies your chosen firm uses to implement its business-
level strategies and discuss their effectiveness. You could also
demonstrate from your research how the firm uses its core
competencies to create and sell its products in the marketplace.
Consider the actions & choices your firm has made to compete
in individual product markets. Review Chapters 4-9 for
specifics on the business-level strategies. Your response should

4. clearly identify the one business-level strategy from the
textbook that you think is most important to the long-term
success of the corporation. Your response must also include a
clearly stated and justified judgement on whether that strategy
is a good choice. Include enough content and depth to
demonstrate a thorough analysis of your selected corporation’s
business-level strategy. Remember that this is a 6 page paper
and as such, you will need to dig deep. After reading these
instructions, replace this blue text with your analysis and
change the font color to black. Corporate-Level Strategies
Analyze the corporate-level strategies for the corporation you
chose to determine the corporate-level strategy you think is
most important to the long-term success of the firm. You will
also need to determine whether or not you judge this to be a
good choice. (Note: in this step you need to choose and wr ite
about only one corporate-level strategy from the text book (not
Google). Hint: See chapter 6 in the textbook. Include a thorough
justification for your choice that is backed by facts and sound
judgement. You could also briefly (1 – 2 sentences) define the
corporate-level strategy (cite your sources) you are writing
about using the textbook/Learn, as an introduction to your
analysis. Read Chapter 6 in the course textbook. Review the
Week 6 Learn Reading for supporting content. Your response
here should demonstrate that you understand the key concepts
regarding the selected corporate-level strategy and can apply
them to a real-world corporation. Keep in mind that this is a 6-
page paper and as such your analysis should thoroughly address
the concepts discussed in the course. Avoid unsubstantiated
statements, extended introductory commentary, direct quotes,
and unrelated content. Strive for about 1 ½ to 2 pages of well -
constructed, in-depth analysis in this section.
Your response should clearly identify the one corporate-level
strategy from the textbook that you think is most important to
the long-term success of the corporation. Your response must
also include a clearly stated and justified judgement on whether
that strategy is a good choice. Include enough content and depth

5. to demonstrate a thorough analysis of your selected
corporation’s corporate-level strategy. Remember that this is a 6
page paper and as such, you will need to dig deep. After reading
these instructions, replace this blue text with your analysis and
change the font color to black. Competitive Environment
Analyze the competitive environment to determine the
corporation's most significant competitor (this will require
research outside of the course material). Compare their
strategies at each level and evaluate which company you think
is most likely to be successful in the long term. Justify your
choice. Hint: read chapters 1 through 10 in the course textbook
as they provide a solid background for this section. Review the
Week 1 through 8 Learn readings for supporting content.
Remember that this is a 6 page paper and requires a thorough
competitive analysis. Strive for about a 1 ½ to 2 pages of well -
constructed, in-depth analysis in this section. Cite your sources
and avoid the use of direct quotes. After reading these
instructions, replace this blue text with your analysis and
change the font color to black.Market Cycles
Determine whether your choice from Question 3 (Competitive
Environment section above) would differ in slow-cycle and fast-
cycle markets. It would be a good idea to briefly explain what
the slow-cycle and fast-cycle markets are from the textbook
(cite your sources) as a short introduction to your
determination. Hint: read Chapter 5 in the course textbook.
Remember that this is a 6-page paper and therefore each section
requires a thorough response that demonstrates your
understanding of key concepts covered in the course and your
ability to apply them to a real-world corporation. Cite your
sources and avoid the use of direct quotes. After reading these
instructions, replace this blue text with your response and
change the font color to black.
Sources
1. Hitt, Ireland, & Hoskisson. 2020. Strategic management:
Concepts and cases: Competitiveness and globalization (13th
ed.). Mason, OH: South-Western Cengage Learning

6. 2. Author. Publication Date. Title. Page # (written as p. #). How
to Find (e.g. web address)
3. Author. Publication Date. Title. Page # (written as p. #). How
to Find (e.g. web address)
Name Illness or Condition:
Epidemiology
(Definition, Demographics, Risk Factors, Exposures)
Time Course
(Duration & Pattern of Prodrome or Symptoms)
Clinical Presentation with Classic S&S
(Key & Differentiating Features - Must have features, rejecting
features)
Mechanism of Disease Process
(Pathophysiology - known derangements in anatomy,
physiology, immunology, biochemical, genetics, metabolomics
AND environmental contributors)
FORM: Illness Script NURS612
Diagnostic Test(s) & Findings
(Common diagnostic tests used to support diagnostic impression
and their specific findings)
Illness or Disorder: Herpes Zoster
Epidemiology
Time Course

7. Clinical Presentation with Classic S&S
Mechanism of Disease Process
Define: Herpes zoster (HZ) or shingles, is the reactivation of
the latent varicella zoster virus (VZV) or chicken pox, in the
dorsal root ganglia (Sandy, 2005).
Demographics: People over the age of 60 who had the chicken
pox or varicella vaccine.
Risk Factors: Those who had the natural infection of varicella-
zoster virus, varicella vaccination, malignancies such as
lymphoma or leukemia, bone marrow and solid organ transplant,
HIV with CD4 count <200 cells/microL, cancer chemotherapy,
corticosteroid therapy, immune-modulatory therapy, or over the
age of 60.
Incidence: 4 cases per 1,000 U.S. population annually (Center
for Disease Control and Prevention [CDC], 2016).
Exposures: Close contact with ill persons
Duration of Prodromal Symptoms: The pre-eruptive phase can
last 1-10 days with an average of 48 hours (Sandy, 2005).
Pattern of Prodrome or Symptoms: The eruptive phase is next
marked by the emergency of vesicular eruptions resolves in 10-
15 days. The chronic phase is characterized by persistent or
recurring pain lasting 30 or more days after the lesions have
crusted, which occurs in 9-45% of all cases (Sandy, 2005).
Symptoms: Muscle or toothache like pain, fever, loss of
appetite, rash that is painful, itchy or tingly, headache,
sensitivity to light, malaise (CDC, 2016).
Signs: Itching or burning pain and paresthesia or puritis lasting
from one day to three weeks, followed by a maculopapular
vesicular rash on an erythematous base. The rash is most
commonly confined to the thoracic region at the fifth and sixth
dermatome levels in a belt like fashion and distributed in
irregular groupings of vesicles that vary in size and do not cross
the midline of the body (Sandy, 2005).
Must-Have Features: Rash appearance and distribution are
unilateral and vesicular on an erythematous base and confined

8. to the thoracic region.
Rejecting Features: Dermatomal pain without rash, rash
eruption affecting bilateral dermatomes (Sandy, 2005).
Diagnostics: Tzanck viral culture smear to differentiate VZV
from herpes simplex virus, fluid culture for VZV DNA by
polymerase chain reaction to differentiate wild type from
vaccine virus, or VZV immunohistochemistry by
immunoglobulin M and immunoglobulin G antibody testing to
differentiate the presence of acute or previous infection (Sandy,
2005).
Pathophysiology: VZV viral particles remain dormant in the
dorsal root and cranial sensory ganglia after infection or
vaccination. Immunologic mechanisms suppress replication of
the virus, but VZV reactivate when the host fails to contain the
virus. Once VZV is activated at the spinal root or cranial nerve
neurons, an inflammatory response occurs. This inflammation in
the dorsal root ganglion causes hemorrhagic necrosis of nerve
cells, leading to neuronal loss and fibrosis. The virus then
travels from the sensory ganglion back down the nerve to the
skin, where it produces the characteristic dermatomal rash of
herpes zoster (Sandy, 2005).
Known Derangements: Declining virus-specific cell mediated
immune responses due to aging causes the body to lack the
ability to suppress replication of the virus. With weakening of
VZV-specific cellular immunity due to immunosuppression the
virus may reactivate and travel peripherally along sensory
nerves to reach the mucocutaneous surface that is innervated by
the ganglia in which the virus is reactivated (Sandy, 2005).
Illness or Disorder: Inherited Ichthyosis Vulgaris
Epidemiology
Time Course

9. Clinical Presentation with Classic S&S
Mechanism of Disease Process
Define: Ichthyosis is a family of disorders characterized by dry
or scaly and thickened skin (National Institute of Arthritis and
Musculoskeletal and Skin Disease [NIAMS], 2012). There are
more than 20 types of ichthyosis, but Ichthyosis Vulgaris is the
most common type affecting 95% of patients who have this skin
disease.
Demographics: Presents in early childhood-usually from 3
months to 5 years of age and more common in Europeans.
Risk Factors: Inherited genes for ichthyosis from one or both
parents or develop a gene mutation for ichthyosis while in the
womb (American Academy of Dermatology, 2016).
Incidence: A common disease in the U.S., with a prevalence of
1 case in 300 persons (American Academy of Dermatology,
2016).
Exposure: Hereditary
Pattern of Symptoms: Absent at birth, typically appears within
the first year of life to five years, intensifying up until puberty
then decreases with age (NIAMS, 2012).
Symptoms: Dry skin, itchy skin, flaky scalp, tile-like small
scales, and deep, painful cracks in skin
Signs: Scales that are white, gray, or brown appearing on the
fronts of legs, backs of arms, scalp, or abdomen typically,
thickened skin on the palms and soles, deep cracks on the palms
and soles, puritis, keratosis pilaris, and decreased ability to
sweat causing temperature dysregulation (American Academy of
Dermatology, 2016).
Must-Have Features: Hyperkeratosis and onset in infancy or
early childhood

10. Rejecting Features: Skin takes on a “dry river bed” appearance
with inflammation, or fine, silvery scale.
Diagnostics: Genetic testing
Pathophysiology: Ichthyosis vulgaris is caused by a loss-of-
function mutation in the gene encoding the protein filaggrin.
This mutation leads to defection production of filaggrin.
Filaggrin is a filament-associated protein require for the binding
of keratin fibres in epidermal cells to form an effective skin
barrier. It helps to maintain the skin pH, retain moisture, and
reduce trans-epidermal water loss. Dryness results from the
reduced skin hydration due to the defective filaggrin. Excessive
scales are caused by the inability of the skin cells to remain
hydrated as they move upward through the stratum coreum.
Hyperkeratosis results from compensatory repair mechanisms
increasing cell proliferation (NIAMS, 2012).
Known Derangements: Autosomal dominant genetic disorder
leading to defective production of filaggrin. Symptoms worsen
in the winter months due to decreased moisture from the cold,
dry air.
Illness or Disorder: Erythema Multiforme
Epidemiology
Time Course
Clinical Presentation with Classic S&S
Mechanism of Disease Process
Define: Erythema multiforme is a skin condition considered to
be a hypersensitivity reaction associated with certain infections
and medications (Lamoreux, Sternbach, & Hsu, 2006).
Demographics: Typically occurs in adults 20 to 40 years of age,
but it can occur at any age.
Risk Factors: Herpes simplex virus infection, mycoplasma
pneumonia, hepatitis B virus infection, fungal infections, HIV

11. infection, lymphoma, hepatitis B vaccine, allergic response to
tattoos, syphilis, cytomegalovirus infection, Epstein-Barr virus,
and medications such as barbiturates, anticonv ulsants,
penicillin, phenothiazine, hydantoins, and NSAIDs (Lamoreux,
Sternbach, & Hsu, 2006).
Exposures: Close contacts with ill persons, tattoos, and
vaccinations.
Duration of Prodromal Symptoms: Typically, no prodromal
symptoms.
Pattern of Symptoms: Target lesions appear 7 days after the
onset of itching and/or burning at the site of eruption, and then
resolves spontaneously in three to five weeks.
Symptoms: Red spots, ridges, and sometimes blisters appear on
the tops of hands, forearms, face, neck, legs, or trunk, some
spots may evolve into concentric circles that resemble a target
with a grayish discoloration in the center, muscular stiffness,
fever, and malaise may occur.
Signs: The individual lesions begin acutely as numerous sharply
demarcated red or pink macules that then become papular. The
papules may enlarge gradually into plaques several centimeters
in diameter. The central portion of the papules gradually
becomes darker red, brown, dusky, or purpuric. Crusting or
blistering sometimes ensues in the center of the lesions. The
characteristic “target” or “iris” lesionhas a regular round shape
and three concentric zones: a central dusky or darker red area, a
paler pink or edematous zone, and a peripheral red ring. The
skin lesions of erythema multiforme usually appear
symmetrically on the distal extremities and progress proximally.
Lesions on the dorsal surfaces of the hands and extensor aspects
of the extremities are most characteristic. Palms and soles also
may be involved (Lamoreux, Sternbach, & Hsu, 2006).
Must Have Features: Individual lesions are present and in a
fixed location for at least one week and some evolve into target
lesions.

12. Rejecting Features: Lesions at the same site for less than 24
hours, center of the lesions appears normal, target lesions with
dusky or purpuric center, or bullous lesions.
Diagnostics: No specific laboratory tests or biopsies are
indicated to make the diagnosis of erythema multiforme.
Pathophysiology: The pathophysiology of erythema multiforme
is still not completely understood but it is thought to be
immunologically mediated and involves a hypersensitivity
reaction that can be triggered by stimuli such as bacterial, viral,
or chemical products (Lamoreux, Sternbach, & Hsu, 2006).
Known Derangements: Herpes associated erythema multiforme
is thought to be due to a delayed type hypersensitivity reaction.
The disease begins with the transport of viral DNA fragments to
distant skin sites by peripheral blood mononuclear cells. HSV
genes within DNA fragments are expressed on keratinocytes,
leading to the recruitment of HSV-specific CD4 helper T cells
involved in cell-mediated immunity. The CD4 cells react to
viral antigens with production of interferon-γ, starting an
inflammatory cascade (Lamoreux, Sternbach, & Hsu, 2006).
Patients taking medications such as barbiturates,
anticonvulsants, penicillin, phenothiazine, hydantoins, and
NSAIDs that develop erythema multiforme often have an altered
metabolism of the responsible drug and are considered to be
slow acetylators. This means that an increased proportion of
drug metabolism is directed toward the alternative pathway of
oxidation by the cytochrome P-450 system, causing in increased
production of reactive and possibly toxic metabolites. Affected
individuals have a defect in the ability to detoxify these reactive
metabolites, which may then behave as happens by binding
covalently to proteins on the surface of epithelial cells. This
may then induce the immune response, leading to the severe
skin reaction (Lamoreux, Sternbach, & Hsu, 2006).

13. Illness or Disorder: Melanoma
Epidemiology
Time Course
Clinical Presentation with Classic S&S
Mechanism of Disease Process
Define: Melanoma is the tumor of melanin-forming cells,
typically a malignant tumor associated with skin cancer
(American Cancer Society, 2016).
Demographics: White, male> females, and over the age of 60.
Incidence: About 87,110 new melanomas will be diagnosed
(about 52,170 in men and 34,940 in women). About 9,730
people are expected to die of melanoma (about 6,380 men and
3,350 women) (American Cancer Society, 2016).
Risk Factors: Sun exposure, moles, fairer skin, blue or green
eyes, freckles, blonde or red hair, immunocompromised, family
history of melanoma, genetic mutations to genes associated with
melanoma, history of basal or squamous cell skin cancers, and
older age
Exposures: Indoor tanning bed, not applying sunscreen when in
the sun, and living in an area with a warmer climate and more
UV light.
Pattern of Symptoms: Melanomas have two growth phases,
radial and vertical. During the radial growth phase, malignant
cells grow in a radial way in the epidermis. With time, most
melanomas progress to the vertical growth phase, in which the
malignant cells occupy the dermis and develop the ability to
metastasize (American Cancer Society, 2016).
Classifications for melanomas are called stages. The stage
refers to the thickness, depth of penetration, and the degree to
which the melanoma has spread. The staging is used to
determine treatment. Early melanomas (Stages 0 and I) are

14. localized; Stage 0 tumors are in situ, meaning that they are
noninvasive and have not penetrated below the surface of the
skin, while Stage I tumors have invaded the skin but are small,
non-ulcerated, and are growing at a slow mitotic rate. Stage II
tumors, though localized, are larger (generally over 1 mm.
thick) and/or may be ulcerated or have a mitotic rate of greater
than than 1/mm2; they are considered intermediate melanomas.
More advanced melanomas (Stages III and IV) have
metastasized to other parts of the body. There are also
subdivisions within stages (Skin Cancer Foundation, 2017).
Symptoms: New spot on the skin or a spot that is changing in
size, shape, or color, spot that looks different from all other
spots on your skin.
Signs: A is for Asymmetry: One half of a mole or birthmark
does not match the other. B is for Border:The edges are
irregular, ragged, notched, or blurred. C is for Color:The color
is not the same all over and may include different shades of
brown or black, or sometimes with patches of pink, red, white,
or blue. D is for Diameter:The spot is larger than 6 millimeters
across (about ¼ inch – the size of a pencil eraser), although
melanomas can sometimes be smaller than this. E is for
Evolving: The mole is changing in size, shape, or color
(American Cancer Society, 2016).
Must Have Features: Abnormal skin area with one or more signs
that is confirmed with a positive skin biopsy.
Rejecting Features: Negative skin biopsy
Diagnostics: Skin exam & skin biopsy
Pathophysiology: Melanomas begin from melanocytes, which
emerge from the neural crest and travel to the epidermis, uvea,
meninges, and ectodermal mucosa. The melanocytes, which live
in the skin and produce a protective melanin, are contained
within the basal layer of the epidermis, at the junction of the
dermis and epidermis. Melanomas may develop in or near a
previously existing precursor lesion or in healthy-appearing

15. skin. A malignant melanoma developing in healthy skin is said
to arise de novo, without evidence of a precursor lesion. Many
of these melanomas are stimulated by solar irradiation (Skin
Cancer Foundation, 2017).
Known Derangements: Many genes are implicated in the
development of melanoma, including CDKN2A (p16), CDK4,
RB1, CDKN2A (p19), PTEN/MMAC1, and ras. CDKN2A
(p16) appears to be especially important in both random and
hereditary melanomas (American Cancer Society, 2016).
Exposure to ultraviolet radiation (UVR) is a serious factor in
the development of most melanomas. Ultraviolet A (UVA),
wavelength 320-400 nm, and ultraviolet B (UVB), 290-320 nm,
possibly are carcinogenic and actually may work in concert to
induce a melanoma.
UVR appears to be an effective inducer of melanoma through
many mechanisms, including suppression of the immune system
of the skin, generation of melanocyte cell division, free radical
production, and damage of melanocyte DNA (Skin Cancer
Foundation, 2017).
Illness or Disorder: Vasculitis
Epidemiology
Time Course
Clinical Presentation with Classic S&S
Mechanism of Disease Process
Define: Vasculitis is a term for a group of rare diseases that
have in common inflammation of blood vessels. These vessels
include arteries and veins. When such inflammation occurs, it

16. causes changes in the walls of blood vessels, such as weakening
and narrowing that can advance to the point of blood vessel
blockage. A result of vasculitis is that the tissues and organs
supplied by affected blood vessels do not get enough blood.
This can cause organ and tissue damage that can even lead to
death (Hasan, 2017). Giant cell arteritis (GCA) is the most
common form of vasculitis. In GCA, the vessels most often
involved are the arteries of the scalp and head, especially the
arteries over the temples, which is why another term for GCA is
“temporal arteritis.”
Demographics: Whites> non-whites, women> men, and over the
age of 50.
Incidence: Data from population-based studies estimate that 1 in
5,000 people over the age of 50 years are affected by GCA each
year. The prevalence of GCA is estimated at 278 per 100,000
people over the age of 50 years (Hajj-Ali, 2012).
Risk Factors: Over the age of 50, women, Northern European
descent, polymyalgia rheumatic, and family history.
Exposures: Age
Prodromal Symptoms: May occur for a few days to weeks
Pattern of Symptoms: Chronic and worsening if not treated
Symptoms: Headache around the temples, pain in jaw muscle
while chewing, decreased appetite, tenderness of the scalp,
vision changes, and shoulder or hip joint aching and stiffness
Signs: Low grade temperature, weight loss, polymyalgia
rheumatic, swelling or decreased pulses in the temporal artery,
tenderness to pressure on the carotid artery, generalized
tenderness, jaw claudication, and blurred vision
Must Have Features: One or more symptom and a superficial
temporal artery biopsy that shows inflammation
Rejecting Features: No inflammation present in the temporal
arteries
Diagnostics: Elevated erythrocyte sedimentation rate and C-
reactive protein levels, elevated platelet counts, positive
temporal artery biopsy (Hajj-Ali, 2012).

17. Pathophysiology: GCA is an autoimmune disorder causing
immune cells to be involved in an inflammatory reaction. The
primary inflammatory response involves the activation of
dendritic cells in the adventitia of arteries by an unknown
antigen, with production of chemokines that recruit CD4+T
helper cells. Activated CD4+ T helper cells differentiate into
Th1 cells (producing interferon gamma) and Th17 cells
(producing interleukin 17).
Interferon gamma causes endothelial cells and vascular smooth
muscle to recruit more Th1 cells, CD8+ T cells, and monocytes.
The monocytes differentiate into macrophages and the
characteristic giant cells that produce growth factors, other
interleukins and proteolytic enzymes that increasingly narrow
and obstruct the vessel wall. Narrowing of the blood vessel
lumen causing decreased blood supply to the neighboring
tissues. The blood vessel may also become thrombosed causing
severe ischemia or necrosis of tissues ordinarily supplied by the
blood vessel (Hajj-Ali, 2012).
Known Derangements: A cellular immune reaction to elastin has
been associated in the pathogenesis of GCA. In support of the
hypothesis that elastin is the inciting antigen, disease severity
has been shown to correlate with the amount of elastic tissue
within the vessels (Hajj-Ali, 2012).
Illness or Disorder: Erythema Nodosum
Epidemiology
Time Course
Clinical Presentation with Classic S&S
Mechanism of Disease Process

18. Define: acute, nodular, erythematous eruption that usually is
limited to the extensor aspects of the lower legs (Schwartz &
Nervi, 2007).
Demographics: Women> men, more common in young adults
18-34 years
Incidence: erythema nodosum occurs in approximately one to
five per 100,000 persons (Schwartz & Nervi, 2007).
Risk Factors: Streptococcal infections, inflammatory bowel
disease, sarcoidosis, Hodgkin disease and lymphoma,
pregnancy, sulfonamides and halides.
Exposures: Working in close contact with the ill, and recent
streptococcal
infection
Pattern of Symptoms: A prodrome commonly occurs as early as
one to three weeks before the onset of erythema nodosum.
Individual nodules may last for two weeks; new outcroppings
may continue to develop for up to six weeks. These nodules
often take approximately one to two months to heal completely
and may assume a bruise-like appearance as they fade. The
active disease may last up to 18 weeks (Schwartz & Nervi,
2007).
Symptoms: Fever, malaise, painful, symmetric, red nodules on
the anterior leg
Signs: Lesion borders are poorly defined, and lesions var y from
2-6 cm. During the first week, lesions become tense, hard, and
painful; during the second week, they may become fluctuant, as
in an abscess, but do not weep or ulcerate. Individual lesions
last approximately 2 weeks, but occasionally, new lesions
continue to appear for 3-6 weeks. Lesions change color in the
second week from bright red to bluish or livid. As absorption
progresses, the color gradually fades to a yellowish hue,
resembling a bruise. Aching legs and swelling ankles may

19. continue for weeks. Hilar adenopathy may develop as part of the
hypersensitivity reaction of erythema nodosum. Arthralgia
occurs in more than 50% of patients and begins during the
eruptive phase or precedes the eruption by 2-4 weeks.
Erythema, swelling, and tenderness occur over the joint,
sometimes with effusions. Joint tenderness and morning
stiffness may occur (Schwartz & Nervi, 2007).
Must Have Features: Symmetrical nodular red lesions with
poorly defined borders
Rejecting Features: Lesions that weep, lesions that appear for
less than 2 weeks, lesions that do not change color over time to
appear like a bruise, and vasculitis
Diagnostics: CBC with differential, evaluation for streptococcal
infection, excisional biopsy showing septal panniculitis
(Schwartz & Nervi, 2007).
Pathophysiology: Erythema nodosum is a nonspecific cutaneous
reaction pattern to a variety of antigens, with many immune-
mediated mechanisms involved. Most direct and indirect
evidence supports the involvement of a type IV delayed
hypersensitivity response to numerous antigens (Schwartz &
Nervi, 2007). The exact pathophysiology is not known today.
Known Derangements: Ulcerative colitis and Crohn disease may
cause erythema nodosum. Erythema nodosum associated with
enteropathies correlates with flares of the disease. Erythema
nodosum occurs in up to 4.6 percent of women who are
pregnant, possibly as a result of estrogen production or relative
levels of estrogen and progesterone. Estrogen also has been
suggested as the linking factor behind the adult male-to-female
incidence ratio of 1:6. Combination estrogen and progesterone
oral contraceptive medications have been associated with
erythema nodosum for decades (Schwartz & Nervi, 2007).

20. Illness or Disorder: Vitiligo
Epidemiology
Time Course
Clinical Presentation with Classic S&S
Mechanism of Disease Process
Define: Vitiligo causes the skin to lose its natural color. Patches
of lighter skin appear. Some people develop a few patches,
while others lose much more skin color.
Demographics: Occurs at any age and affects all races and both
sexes equally
Risk Factors: Family history of vitiligo or an autoimmune
disease especially Hashimoto’s or alopecia
Exposures: None
Pattern of Symptoms: There is no way to tell if vitiligo will
spread. For some people, the white patches do not spread. But
often the white patches will spread to other areas of the body.
For some people, vitiligo spreads slowly, over many years. For
other people, spreading happens quickly. Some people have
reported more white patches after physical or emotional stress
(National Institute of Arthritis and Musculoskeletal and Skin
Disease [NIAMS], 2014).
Symptoms: White patches on the skin that may itch or feel
painful
Signs: Depigmentation of the skin commonly in areas where the
skin is exposed to the sun, but can appear anywhere on the
body. Hair may turn gray earlier and those with dark skin may
notice a loss of color in their mouths.
Must Have Features: Biopsy of the skin showing complete
absence of melanocytes
Rejecting Features: Visual changes, white patches that go away
over time

21. Diagnostics: Microscopic examination of the skin with biopsy
shows total loss of epidermal pigmentation (NIAMS, 2014).
Pathophysiology: Vitiligo is a multifactorial polygenic disorder
with a complex pathogenesis. It is related to both genetic and
non-genetic factors. Although several theories have been
propositioned about the pathogenesis of vitiligo, the exact cause
remains unknown. Generally agreed upon principles are an
absence of functional melanocytes in vitiligo skin and a loss of
melanocytes, due to their destruction. However, the destruction
is most likely a slow process resulting in a progressive decrease
of melanocytes. Theories regarding destruction of melanocytes
include autoimmune mechanisms, cytotoxic mechanisms,
intrinsic melanocyte defects, oxidant-antioxidant mechanisms,
and neural mechanisms (NIAMS, 2014).
Known Derangements: Family and twin studies have shown that
inheritance is complex and likely involves both genetic and
environmental factors. It is thought that genetic factors may
impact the age of onset of vitiligo. The inheritance of vitiligo
may include genes associated with the biosynthesis of melanin,
a response to oxidative stress, and regulation of autoimmunity
(NIAMS, 2014).
Illness or Disorder: Rosacea
Epidemiology
Time Course
Clinical Presentation with Classic S&S
Mechanism of Disease Process
Define: Rosacea is a common skin condition that causes redness
and visible blood vessels in your face. It may also produce

22. small, red, pus-filled bumps (American Academy of
Dermatology, 2017).
Demographics: Between the age of 30 and 50, Celtic or
Scandinavian ancestry, women> men
Risk Factors: Fair skinned, blonde hair and blue eyes, family
history of rosacea, lots of acne, between the age of 30 and 50,
and smoking
Exposures: Hereditary and smoke cigarettes
Pattern of Symptoms: Chronic and worsening
Symptoms: Facial redness, swollen red bumps, skin may feel
hot and tender, dry skin, eye dryness or irritation, and enlarged
nose.
Signs: Rosacea usually causes a persistent redness in the central
part of your face. Small blood vessels on your nose and cheeks
often swell and become visible. Many people who have rosacea
also develop pimples on their face that resemble acne. These
bumps sometimes contain pus (American Academy of
Dermatology, 2017).
Must Have Features: Rosacea is defined by persistent erythema
of the central portion of the face lasting for at least 3 months.
Supporting criteria include flushing, papules, and pustules
(American Academy of Dermatology, 2017).
Rejecting Features: Photosensitivity, acne alone, facial flushing
that goes away.
Diagnostics: Examination of the skin and eyes
Pathophysiology: The exact pathophysiology of rosacea is
unknown. There is not a single physiopathological model.
The pathophysiology of rosacea appears to be complex, as
virtually all cutaneous cells, including immune cells, seem to
have roles (American Academy of Dermatology, 2017).
Known Derangements: The higher incidence of rosacea in those
of Celtic or Northern European descent also suggests a possible
genetic component. Still, several genomic studies have failed to
pinpoint a causative gene.
The innate immune system seems to be disrupted in patients
who have rosacea. As discussed earlier, serine protease levels

23. are elevated in those with rosacea, and this may result in
epidermal barrier dysfunction. A stinging or burning sensation
results when a sensory irritant, such as lactic acid for example,
easily penetrates the skin through a disruption or abnormalit y in
the epidermal barrier (American Academy of Dermatology,
2017).
References:
American Academy of Dermatology. (2016). Ichthyosis
vulgaris. Retrieved from
https://www.aad.org/public/diseases/scaly-skin/ichthyosis-
vulgaris#treatment
American Academy of Dermatology. (2017). Rosacea. Retrieved
from https://www.aad.org/public/diseases/acne-and-
rosacea/rosacea#symptoms
American Cancer Society. (2016). Melanoma skin cancer.
Retrieved from
https://www.cancer.org/cancer/melanoma-skin-
cancer/about.html
Center for Disease Control and Prevention. (2016). Shingles
(herpes zoster). Retrieved from
https://www.cdc.gov/shingles/hcp/clinical-overview.html
Hajj-Ali, R. (2012). Giant cell arteritis (temporal arteritis).
Retrieved from

24. http://www.vasculitisfoundation.org/education/forms/giant-cell-
arteritis/
Lamoreux, M.R., Sternbach, M.R., & Hsu, W.T. (2006).
Erythema multiforme. American Family Physician, 74(11) pp.
1883-1888.
http://www.aafp.org/afp/2006/1201/p1883.html
National Institute of Arthritis and Musculoskeletal and Skin
Diseases. (2012). Ichthyosis overview. Retrieved from
https://www.niams.nih.gov/Health_Info/Ichthyosis/
National Institute of Arthritis and Musculoskeletal and Skin
Diseases. (2014). Vitiligo. Retrieved from
https://www.niams.nih.gov/health_info/vitiligo/vitiligo_ff.pdf
Sandy, M. (2005). Herpes zoster: medical and nursing
management. Clinical Journal of Oncology Nursing, 9(4), 443-
467 7p.
doi:10.1188/05.CJON.443-446
Schwartz, R.A., & Nervi, S.J. (2007). Erythema nodosum: A
sign of systemic disease. American Family Physician,
75(5):695-700.
http://www.aafp.org/afp/2007/0301/p695.html
Skin Cancer Foundation. (2017). Melanoma. Retrieved from
http://www.skincancer.org/skin-cancer-information/melanoma