PATHOPHYSIOLOGY WEEK
6 TD2 Dermatologic and
Musculoskeletal Disorders
Discussion Part Two
,Week 6: Dermatologic and Musculoskeletal Disorders - Discussion Part Two
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Discussion
This week's graded topics relate to the following Course Outcomes (COs).
1 Analyze pathophysiologic mechanisms associated with selected disease states. (PO 1)
2 Differentiate the epidemiology, etiology, developmental considerations, pathogenesis, and
clinical and laboratory manifestations of specific disease processes. (PO 1)
3
Examine the way in which homeostatic, adaptive, and compensatory physiological
mechanisms can be supported and/or altered through specific therapeutic interventions.
4
(PO 1, 7)
Distinguish risk factors associated with selected disease states. (PO 1)
5 Describe outcomes of disruptive or alterations in specific physiologic processes. (PO 1)
6 Distinguish risk factors associated with selected disease states. (PO 1)
7 Explore age-specific and developmental alterations in physiologic and disease states. (PO
1, 4)
Discussion Part Two (graded)
Johnny is a 5-year-old Asian boy who is brought to a family practice office with a “runny” nose that started about 1
week ago but has not resolved. He has been blowing his nose quite frequently and “sores” have developed
around his nose. His mother states, “The sores started as ‘big blisters’ that rupture; sometimes, a scab forms with a
crust that looks like “dried maple syrup” but continues to seep and drain.” She is worried because the lesions are
now also on his forearm. Johnny’s past medical and family histories are normal. He has been febrile but is
otherwise asymptomatic. The physical examination was unremarkable except for moderate, purulent rhinorrhea
and 0.5- to 1-cm diameter weeping lesions around the nose and mouth and on the radial surface of the right
forearm. There is no regional lymphadenopathy.
• Write a differential of at least five (5) possible diagnosis’s and explain how each may be a possible answer to
the clinical presentation above. Remember, to list the differential in the order of most likely to less likely.
• Based upon what you have at the top of the differential how would you treat this patient?
differential diagnosis for this clinical presentation and justify it.
• When would you allow the student back to school? Elaborate on your reasoning?
,Responses
Lorna Durfee 6/5/2016 8:06:15 PM
Discussion Part Two
Johnny is a 5-year-old Asian boy who is brought to a family practice office with a “runny” nose that started about 1
week ago but has not resolved. He has been blowing his nose quite frequently and “sores” have developed around his
nose. His mother states, “The sores started as ‘big blisters’ that rupture; sometimes, a scab forms with a crust that
looks like “dried maple syrup” but continues to seep and drain.” She is worried because the lesions are now also on
his forearm. Johnny’s past medical and family histories are normal. He has been febrile but is otherwise
asymptomatic. The physical examination was unremarkable except for moderate, purulent rhinorrhea and 0.5- to
1-cm diameter weeping lesions around the nose and mouth and on the radial surface of the right forearm. There is
no regional lymphadenopathy.
Write a differential of at least five (5) possible diagnosis’s and explain how each may be a possible answer to the
clinical presentation above. Remember, to list the differential in the order of most likely to less likely.
Based upon what you have at the top of the differential how would you treat this patient?
Differential diagnosis for this clinical presentation and justify it.
When would you allow the student back to school? Elaborate on your reasoning.
Doctor Brown:
With my experience as a school nurse and physical trainer, I have seen many students come to the clinic with various
complaints. However, I distinctly remember a particular student who exhibited the signs above and symptoms similar
to these.
Differential Diagnoses:
#1 Impetigo
#2 Molluscum Contagiosum
#3 Rubella
#4 Chicken pox
#5 Hand, foot and mouth disease
Differential Diagnoses:
This patient exhibits the signs and symptoms of impetigo. He appears to have non-bullous impetigo. The blisters start
as small vesicles and burst then have honey-colored serum. Yellow to white-brown or tan crust develops, and it looks
like it is coated with honey or brown sugar. He has all the signs and symptoms that are part of the bacterial infection.
McCance, Huether, and Brasher (2014) tell us that the crust is the identifying factor with a moist base that weeps when
the scab is removed that identifies impetigo. The blisters can be on the face and the nose, but other areas such as the
hands can be involved and extremities. There is no lymphadenitis (McCance et al., 2014, p. 1656). If we compare it to
the differential diagnosis of the herpes simplex virus, we can see that HSV-1 is the type that induces oral infection
(such as cold sores and fever blisters). However, there must be contact with saliva. With this infection, the virus
affects cells of the epithelium and remains there in the dorsal root ganglion where it is latent. These lesions present
with clusters and painful vesicles (on mouth, tongue and around the nose). Burning and paresthesias occur before
onset. The vesicles rupture and form a crust. However, the lesions last for 2 to 6 weeks. Stress, light, fever and
fatigue can cause reactivation (McCance, Huether & Brashers, 2014, p. 1636). The presentation and signs and
symptoms of herpes do not coincide with the findings that we have with our current patient. Therefore, the differential
diagnosis of Impetigo fits the presentation and the symptoms.
#1 - Impetigo:
Baddour (2016) has stated that Impetigo is a contagious bacterial infection observed more often in children. It has two
distinct classifications, one of primary impetigo which is an invasion of the previously normal skin or direct bacterial
invasion. The other classification is secondary impetigo which comes from skin trauma. This can include abrasions,
minor trauma, and bites from insects. Eczema can also be an underlying condition. Impetigo is seen in children from
two to five years old. It is not to say that adults and older children do not get the infection because they can. This
infection is noted in warm and humid conditions and can spread easily through close contact. Carriage of group A
Streptococcus and Staphylococcus aureus has been noted in patients with impetigo (Baddour, 2016).
McCance, Huether, and Brashers (2014) explain that there are two types of impetigo; nonbullous and bullous. Both
types start with vesicles with a thin vesicular roof that is formed from stratum corneum. Nonbullous is contagious,
with superficial vesicles that are pustular and caused by Staphylococcus aureus or group A Streptococcus pyogenes.
These microorganisms spread by direct contact with others who are infected or through insect bites. The lesions are
smaller vesicles at first with honey-colored serum. There is a crust that forms as the vesicles rupture that is yellow to
white-brown. There is lymphadenitis with nonbullous impetigo. Bullous impetigo is caused by Staph aureus. This
organism is carried in the nose, perineal area and fingernails. It can be transmitted by an individual or with
contaminated equipment. The bacterial toxins or exfoliative toxins cause disruption in the desmosomal adhesion
, molecules and form blisters. The blisters then coalesces to form bullae. There are lesions scattered over the skin. As
these lesions rupture, they develop a honey-colored, flat crust that appears on the skin. The crust is the distinctive
feature of impetigo. When the crust is removed, the skin base will be moist, inflamed and weeping. Lesions are found
on the face, the nose, mouth and hands. It is possible that other areas of the body could develop lesions. There is
usually no lymphadenitis (McCance et al., 2014, p. 1656).
Treatment of Impetigo:
Shim, Lanier, and Qui (2014) explain that The Infectious Diseases Society of America recommends topical mupirocin
as first-line therapy, although known resistance to the drug exists. If the patient has numerous lesions and does not
respond to topical treatment, then they should get treatment with oral antibiotics for S. pyogenes and S. aureus. The
recommended antibiotics (oral) are dicloxacillin, amoxicillin/clavulanate, cephalexin. Also, the list includes
erythromycin and clindamycin (Shim, Lanier, & Qui, 2014, p. 335). McCance et al., (2014) tell us that antibiotic
therapy should be determined by bacterial culture and drug sensitivity because the prevalence of impetigo in the
community is increasing. Methicillin-resistant S. aureus and impetigo are increasing. For more extensive impetigo
systemic antibiotics may be needed. However, beta-lactam antibiotics should be avoided if MRSA is suspected
(McCance et al., 2014, p. 1656).
When will the child be allowed back in school?
The patient should remain out of school initially for 24 hours after starting antibiotics. If the lesions are still weepy,
oozing and wet, they should be covered. Washing hands with soap can reduce the incidence of impetigo. Schools may
have policies that vary when it comes to the amount of time to remain out of school after the 24 hour period
(Dynamed, 2015). Additional care includes covering the lesions with a watertight dressing. Also, make sure to wash
all clothes, towels, and bedding with hot water and keep separate.
#2 - Molluscum contagiosum:
Molluscum contagiosum is a poxvirus that causes a localized infection with small papules on the skin. It is not as fatal
as smallpox. However, it is similar to that virus. The only know host for Molluscum contagiosum is humans. Like the
vaccinia and variola viruses molluscum replicates in the cytoplasm of the cells. The human genome study revealed
that more than one-half of the genes are similar to those in variola and vaccinia viruses. Because the diseases are
different, there are also many genes found in variola and vaccinia that are not found in the genome for molluscum
contagiosum. Molluscum has unique genes that encode proteins for host defense mechanisms. These inhibit the host
inflammatory response and response to the infection (Isaacs, 2016). There are four genotypes, but genotype 1
represents 90 percent of cases in the United States. There is also an indication that mild cases that are subclinical may
be more prevalent in the community (Isaacs, 2016).
McCance, Huether, and Brashers (2014) explain that the aformentioned virus will induce cell proliferation that blocks
responses that would control the virus. The epidermis grows into the dermis and forms saccules that contain virus
clusters. The cell is composed of mature, immature and incomplete viruses and debris. The lesions are dome-shaped
and can appear on the face, trunk, and extremities. They are usually quite quiet unless they are traumatized, or there is
a secondary infection (McCance et al., 2014, p. 1658). This condition does not fit our patient’s symptomatology and
presentation.
#3 - Rubella (German Measles):
Rubella is a communicable disease of children caused by a ribonucleic acid (RNA) virus that enters into the system
through the respiratory route. It is a mild disease, and incubation is from 14 to 21 days. There are enlarged lymph
nodes, fever (low-grade), sore throat and runny nose with a cough. There is a faint pink to red rash that is
maculopapular. This rash can develop on the face and then trunk and extremities. The rash is not seen on the palms or
soles of the feet. The virus causes dissemination of the skin. Children are not contagious after the development of the
rash. There is lifelong immunity to rubella, along with measles, chickenpox, and roseola if you contact the disease
(McCance et al., 2014, p. 1658). The rash presentation is not the same as the patient’s presentation.
#4 - Varicella (chickenpox):
Varicella is a disease that is seen in childhood and approximately 90 percent of children develop the disease during
their first decade in life. This virus is very contagious and spreads from person-to-person via airborne droplets. With
infection in the household, there is a 90 percent chance that people who are susceptible will get the disease within 14
days. Children remain contagious for one day before the rash develops. Transmission can happen up to 5 to 6 days
after onset of lesions in healthy children. There are no prodromal signs (McCance et al., 2014, p. 1660). The illness
may appear with vesicles on the trunk, scalp, and face. Later on, it spreads to the extremities. The lesions have various
stages. They can present as macules, papules, and vesicles. They rupture easily. They develop a crust. Sometimes
they can be found in the mouth, conjunctiva, and pharynx. There is a fever for 2 to 3 days (McCance et al., 2014,
p. 1660). This disease fits some of the signs and symptoms but not all. The presentation is different.
#5 - Hand, foot, and mouth disease:
The Centers for Disease and Control and Prevention (2015) explain that hand, foot and mouth disease is a common
viral illness that affects children younger than 5. It does, however, occur in adults. It usually starts with a fever, lack
of appetite and sore throat and just not feeling well. Once the fever starts, about two days later, painful sores develop
in the mouth. A skin rash with red spots develops that blister. The blisters can appear on the palms, hand, feet (soles)
or the elbow, knees or buttocks. Some people do not show signs, but they still pass the virus to others. The viruses that
belong to the Enterovirus genus (polioviruses, coxsackieviruses, and echoviruses and enteroviruses. Coxsackievirus