Dermatology

Dermatology
Introduction
In this lesson we'll review the assessment of the
skin, hair, nails, and mucous membranes, which
can provide clues to systemic disease,
cutaneous infection or injury, bites or stings,
parasite infestation, and skin cancer. We'll cover
the following topics:
History
Physical examination
Common screening and diagnostic tests
Health-promotion behaviors related to the
dermatologic system
Incidence
Problems of the skin account for 4% or 5% of
visits to primary-care providers
Nearly 20% of patients seen have signs and
symptoms related to dermatology
Skin cancer is now at epidemic proportions,
affecting about one in 88 people
Most skin cancer is nonmelanoma skin cancer
(NMSC)
The increase in the incidence of skin cancer rate
is associated with cumulative skin exposure to
ultraviolet light from the sun or tanning beds
History
Current complaint
Constitutional signs and symptoms
Signs and symptoms of problem with the skin,
hair, nails, or mucous membranes
Onset and progression of problem over time
Location
Pattern of spread
Change in individual lesions
Change in contact
Details of prodromal period, including
relationship of symptoms to provocative factors
Relieving factors, including previous treatment
Risk factors for skin cancer

History
Medical history
Allergic response produced by exposure to medications,
foods, or other substances
Contraceptive method
Serious illnesses or injuries
Hospitalizations
Radiation
Previous skin problems or skin cancer
Immunosuppression
Chronic illness, including diabetes mellitus and
hypertension
Tetanus prophylaxis status
Atopic history (e.g., asthma, hay fever, eczema)
History
Family history
Skin cancer
Psoriasis
Atopy
Tuberous sclerosis
Melanoma
Xanthomas
Genetic conditions
Medication history
Over-the-counter (OTC), prescription, or
complementary therapies related to the chief
complaint (including topical steroids) and
reasons for use
History
Psychosocial history
Occupation and leisure activities
Drug, alcohol, and tobacco use
Sunbathing and use of tanning beds
Use of sunscreen
Exposures
Travel
Sexual abuse, particularly that involving
exposure to pediculosis pubis
Risk factors for human immunodeficiency virus
(HIV) infection
Physical Examination
Conduct a comprehensive physical examination, paying special attention to particular areas
not usually exposed during an exam.
Examination
Prepare the appropriate tools and environment for the examination
Assess the patient's general appearance, including whether he or she seems well or
appears uncomfortable
Assess vital signs
Inspect the skin (with patient disrobed and draped appropriately) for color, texture, and
hydration status
Remember that skin characteristics vary with age
Pay particular attention to lesions that are consistent with skin cancer: NMSC, including
basal-cell carcinoma and squamous-cell carcinoma; premalignant lesions such as
dysplastic nevi and actinic keratoses; and malignant melanoma (use the mnemonic
ABCDE to help you remember the signs of malignant melanoma)
Note the configuration of any lesions and assess for epidermal, pigment, or dermal
involvement
Assess rashes for dermal or epidermal involvement
Note the pattern of distribution of lesions
Note the structure of the lesion, including whether it is primary or secondary; its
dimensions; whether it is elevated or depressed; its palpable or visible features, such as
atrophy or lichenification; and its color and other physical characteristics
Palpate skin surfaces, noting moisture, mobility, turgor, texture, and temperature
Palpate the lesion for consistency, temperature, mobility, and tenderness
Inspect the mucous membranes
Inspect the hair, scalp, eyelashes, eyebrows, and body hair
Inspect and palpate the nails and note the presence of lesions
Diagnostic procedures
Examine skin material (scrapings, scales, crusts,
exudates, tissue) under a microscope to detect yeast
and fungus, bacteria, virus, spirochetes, or parasites
Use a Wood light to help diagnose certain fungal and
bacterial diseases and disorders of pigmentation
Perform diascopy to differentiate erythema from purpura
or petechiae (erythema blanches with pressure, whereas
purpura and petechiae do not)
Perform laboratory tests (if indicated)
Use dermoscopy for noninvasive inspection of deeper
layers of the skin
Perform an incisional (punch or shave) or excisional
biopsy as indicated
Education
Provide the patient or caregiver with guidelines for safe
sun exposure and explain how to treat sunburn
Encourage the patient to avoid tanning beds
Stress caution in high altitudes or in the presence of
reflecting snow, sand, water, or concrete, all of which
increase penetration of harmful rays
Teach the patient how to perform self-examination of the
skin in accordance with American Academy of
Dermatology guidelines
Tell the patient to make an appointment for a clinical
examination if his or her self-examination reveals certain
findings
Caution patients against using public hot tubs because
of the potential for folliculitis
Provide guidelines for safe body piercing, tattoo art, and
application of artificial nails
Introduction
In this lesson we'll review the presentation,
diagnosis, and treatment of acne vulgaris and
acne rosacea, disorders of the sebaceous and
apocrine glands. Acne vulgaris is a multifactorial
disease of the pilosebaceous unit in men and
women in Westernized societies who are near
puberty; in most cases, the condition becomes
less active as adolescence ends. Acne rosacea,
a chronic skin eruption with flushing and dilation
of small blood vessels in the face, is most
common in midlife. Both disorders are often
seen by the family nurse practitioner.
Incidence
Acne vulgaris
An estimated 80% of people between the ages
of 11 and 30 years experience an acne outbreak
at some point
Acne vulgaris affects between 40 million and 50
million individuals a year in the United States
alone
Nearly 12% of women and 3% of men will
continue to have clinical acne until age 44
White boys and men have been shown to have
more severe nodulocystic acne than black boys
and men

Incidence
Acne rosacea
Acne rosacea is most common in those with
Celtic and Northern European ancestry (fair skin
makes it more apparent) and least common in
black patients (darker skin may hide the
condition)
More women than men are affected by acne
rosacea, but men have more severe forms
Rosacea mainly affects adults older than age 30
years
More than 14 million in the United States are
affected

Pathophysiology
Acne vulgaris
Increased size and activity of sebaceous
glands
Altered growth of follicles and abnormal
differentiation of follicular kerotinocytes,
leading to the formation of follicular plugs
Proliferation of Propionibacterium acnes in
follicles
Inflammatory and immune responses
Pathophysiology
Acne rosacea
Although the cause of acne rosacea is unknown,
theories exist
Pathologic findings include inflammation surrounding
hypertrophied sebaceous glands contributing to papules,
pustules, and cysts; vascular dilation and infiltrates of
lymphocytes; and no comedones or blocked ducts
The condition is associated with blepharitis, keratitis, and
conjunctivitis; the lesions are prominent on the convex
areas of the face: forehead, nose, cheeks, and chin
Rosacea is classified into four subtypes:
erythematotelangiectatic, papulopustular, phymatous,
and ocular

History
Current complaint
Duration of symptoms
Location
Seasonal variation
Premenstrual flare-up
Thinning of scalp hair or increase of androgen-
dependent hair such as facial hair (women)
Secondary features of acne rosacea

History
Medical history
Endocrine disorders
Drug allergies
Menstrual history and pregnancy status
Hormone tests
Family history
Other skin disorders
Atopy (irritation to topical acne treatment)
Hydradenitis suppurativa
History
Medication history
Current and past treatment (topical and
systemic) of acne
Current and past treatment of other diseases
Failure of previous therapies
Oral contraceptives or birth control method used
and effect on acne
Aggravation by stress
Disfigurement
Occupational disability
Cosmetics and moisturizer products used
Examination
Inspect and palpate the skin
Determine the number and location of the
lesions and whether the lesions are
noninflammatory or inflammatory
For each predominant type of lesion in each
location, note the severity
Look for complications such as rhinophyma
(acne rosacea) and scarring
Note the presence of associated conditions
In most cases, no screening or diagnostic tests are
needed in the assessment and diagnosis of acne
Hormone assessments are conducted in women with
suspected hyperandrogenemia
Serum and urine pregnancy tests are conducted to rule
out pregnancy before the initiation of treatment with a
potentially hazardous drug
Complete blood count with differential and renal, liver,
and lipid profile are performed initially and every 4 weeks
for patients treated with isotretinoin (Accutane)
The diagnosis of acne vulgaris is based on the presence
of comedones
The diagnosis of acne rosacea requires evidence of one
or more primary features in a central distribution on the
face
Differential diagnosis: acne vulgaris
Rosacea
Steroid acne
Molluscum contagiosum
Folliculitis
Differential diagnosis: acne rosacea
Acne vulgaris
Steroid abuse with rosacea
Fungal infection
Cutaneous features of lupus erythematosus
Drug eruptions (especially iodides and
bromides)
Treatment
Nonpharmacologic: acne vulgaris
Stress reduction
Gentle skin care with soap products for sensitive skin
Avoidance of oil-based cosmetics, moisturizers, and
sunscreens
Avoidance of greasy hair products near the face
Nonpharmacologic: acne rosacea
Avoidance of oily cosmetics
Use of camouflage makeup as appropriate
Reassurance
Stress reduction
Minimizing sun exposure
Avoiding known triggers
Avoiding certain medications, if possible, by informing
prescribers of an acne or rosacea diagnosis
Laser therapy for telangiectasia and ablative therapy for
rhinophyma
Treatment
Pharmacologic: acne vulgaris
Treatment is based on whether acne is
mild or moderate to severe
Pharmacologic: acne rosacea
Topical antibiotics
Oral antibiotics for cases involving
papulopustular (subtype 2)
Low-dose isotretinoin or topical retinoids
Education
Acne vulgaris
Explain the origins of the disease and reassure the patient
that the condition is not his or her fault
Stress that treatment success depends heavily on the
patient's compliance with prescribed therapies
Acknowledge the social and psychological impact of
having acne and offer appropriate support, counseling,
and referral, if needed
Encourage the patient to use adequate sun protection and
gentle skin care while taking topical and oral medications
Explain that acne treatment is a long-term process and tell
the patient that initial worsening is possible as the
medication brings out the acne waiting to emerge onto the
skin
Explain that it may take 12 to 16 weeks to reach maximum
reduction in the number of lesions
Education
Acne rosacea
Suggest the use of camouflage makeup, if
appropriate
Tell the patient to avoid unnecessary sun
exposure and to use sunscreen when sun
avoidance is not possible
Encourage the patient to avoid triggers that
worsen the condition
Tell the patient to notify prescribing health-care
providers of the disorder in an effort to avoid
vasodilator therapy if at all possible
Offer additional resources for information, such
as the National Rosacea Society
Follow-Up
Schedule three follow-up visits over 12 to 16
weeks to establish an effective plan of care
See patients at 4 to 6 weeks to assess
compliance and response to and tolerance of
prescribed regimen, then follow up at 1-month
intervals to further assess response and
compliance and make therapeutic changes as
indicated
See the patient taking long-term antibiotics
regularly with the plan of weaning him or her off
the drugs as other treatments (e.g., topical
retinoids, hormonal treatment) allow
Referral
Consult as needed with specialists (dermatologists,
gynecologists) to plan a safe, effective treatment for the
patient with acne
Refer the patient to a dermatologist if acne does not
respond to an adequate trial of initial treatments or if
isotretinoin (Accutane) is indicated
If endocrine disease is suspected, refer patient to an
endocrinologist
Refer the patient with acne rosacea who desires
electrodessication or sclerosis of permanently dilated
vessels in the face to a dermatologist
Refer the patient with rhinophyma to a surgeon for
surgical correction, if appropriate
Refer the patient with ocular effects of rosacea to an
ophthalmologist
Introduction
Atopic dermatitis (eczema) is a chronic, cyclic,
relapsing, inflammatory, intensely pruritic skin
disease with multiple clinical presentations.
Contact dermatitis is an eruption of the skin
related to contact with an irritating substance or
allergen. Seborrheic dermatitis is a chronic skin
condition affecting the scalp, face, central chest,
and intertriginous areas.
In this lesson we'll review the assessment,
diagnosis, and treatment of these common skin
conditions.
Atopic Dermatitis: Incidence
May occur at any age
Prevalent in infants, children, and young adults; the most
common skin disease of childhood (7%17.2%)
Scientists estimate that symptoms develop in 65% of
patients in their first year of life and in 90% before the
age of 5 years
Prevalence in school-age children has increased greatly
since the early 1960s
Onset after age 30 is less common and often results
from exposure of the skin to harsh or wet conditions
Affects both male and female patients
Accounts for 10% to 20% of visits to dermatologists
More than 15 million people in the United States are
believed to have symptoms
U.S. insurance companies are believed to spend more
than $1 billion a year on the disease
Atopic Dermatitis: Pathophysiology
Develops as a result of a complex interrelationship of
environmental, immunological, genetic, and
pharmacological factors leading to compromised skin
barrier function
Appears to be associated with immune-system
malfunctions that result in increased serum IgE synthesis
and is associated with a personal or family history of
atopic disease
May be exacerbated by staphylococcal infection,
psychological stress, seasonal/climate changes, activity,
irritants, and allergens
Risk factors include emotional stress, exposure to
irritating clothing or chemicals, excessively hot or cold
climates, and exposure to smoke
Atopic Dermatitis: History
Current complaint
Incessant pruritus and uncontrollable itching are the cardinal
symptoms
Determine the age of onset (<2 years is characteristic)
Ask about itching, appearance, and distribution of rash or lesions
and whether dermatitis is chronic or chronically relapsing
Ask about associated symptoms (e.g., wheezing, runny nose,
tearing)
Question adults regarding hand dermatitis
Medical history
Seasonal or food allergies
Asthma
Other skin disorders
Family history
Allergic rhinitis and age of onset
Asthma and age of onset
Atopic dermatitis and age of onset
Atopic Dermatitis: History
Medication history
New medications, particularly topical agents
Routine skin care, including frequency of bathing
and products used
Presence of pets in the home
Use of chemical-free laundry products
Types of clothing worn (e.g., wool, cotton)
Heating and cooling in the home, usual
temperature inside the home, and humidity level
Stigma of having a visible skin disorder
Psychological stressors that may act as triggers
Atopic Dermatitis: Physical Examination
Examination
Have the patient undress completely and don a gown for privacy
Examine the skin systematically to determine the extent and
distribution of the lesions
Identify primary and secondary lesions
Examine areas of flexure for erythema (redness) and scaling but
also look for lichenification (thickening) in these areas
Examine the hands, looking for erythema, scaling, and hyperlinear
palm creases and dry, fissured fingertip pads
In infants (birth2 years), look for redness and blisters on the
cheeks, forehead, scalp and extensor aspects of arms and legs
In children (212 years), look for dry, scaly rash on antecubital and
popliteal areas and flexures of wrists, ankles, neck, and buttock-
thigh creases
In adolescents and adults, look for hand dermatitis and lesions on
the face, neck, and body characterized by scaling skin with xerosis
and lichenification
Look for other associated features
Diagnostic procedures are usually unnecessary
Blood eosinophilia may be noted
Serum IgE levels will be increased
Cultures of drainage may help rule out other
causes or confirm skin infection
Skin biopsy, interpreted by a
dermatopathologist, is helpful if doubts exist
For a diagnosis of atopic dermatitis, the patient
must have an itchy skin condition (or parental
report of scratching or rubbing of skin), plus
three or more additional characteristics
The presence of pruritus, characteristic history, and the structure and
distribution of lesions help distinguish atopic dermatitis.
Differential diagnosis
Contact dermatitis, allergic
Contact dermatitis, irritant
Lichen simplex chronicus
Nummular dermatitis
Psoriasis and plaque
Scabies
Ichthyosis
Seborrheic dermatitis
Tinea corporis
Primary immunodeficiency in infants (rare but life-threatening; e.g.,
Wiskott-Aldrich syndrome)
Cutaneous T-cell lymphoma in adolescents or adults (also rare but
life-threatening)
Atopic Dermatitis: Treatment
Nonpharmacologic
Short, cool showers or baths, depending on the climate,
followed by the application of a moisturizer
"Soaking and greasing" regimen
Soft clothing next to the skin
Cool temperatures, particularly at night, to avoid the
irritation and itching that sweating can cause
Humidifier (cool mist) to prevent excess drying
Laundering of clothes in a mild detergent, with no bleach
or fabric softener
Avoidance of cigarette smoke and other irritants (e.g.,
grass pollen, dust mites, irritant foods)
Avoidance of animals, including pets in the home
Atopic Dermatitis: Treatment
Pharmacologic
Topical steroids, topical antipruritics, and antihistamines are the mainstays of
treatment
When combined with moisturization, this regimen yields excellent results
Ointment bases are preferred for topical preparations, particularly in dry
environments
Antibiotics are used in the treatment of clinical infection caused by Staphylococcus
aureus or flares of disease
Oral or parenteral corticosteroids may be used in severe cases or cases of
extensive flaring
Hospitalization or "home hospitalization" may be required in severe or unresponsive
cases
Immunomodulators that act as calcineurin inhibitors, such as tacrolimus and
Pimecrolimus (Elidel) 1%, are effective but carry a black-box warning
UV-radiation therapy can be helpful
In patients with eczema herpeticum, acyclovir is effective
In patients with severe disease, particularly adults, phototherapy, methotrexate,
azathioprine, and cyclosporine have been used with success
Both hydroxyzine and diphenhydramine hydrochloride provide a certain degree of
relief from itching but are not effective without other treatments
Ketotifen (a calcium-channel blocker) may be effective
Other medications, such as oil of evening primrose, thymopentin, -interferon, and
Chinese herbs, have disappointing results, may be impractical, and can be
expensive
Atopic Dermatitis: Education
Reinforce treatment and maintenance regimens
Show videos that illustrate how to apply medication and
discuss the role of moisturizing
Teach the appropriate use of topical corticosteroids and
explain complications when they are used
inappropriately
Tell patients with verrucae vulgaris that episodes may be
more frequent, more widespread, and more difficult to
eliminate
Warn patients to avoid the current smallpox vaccine and
to exercise caution when coming into close contact with
a person who has been recently vaccinated
For excellent patient education resources, visit
eMedicine's patient-education resources on skin, hair,
and nails and eczema
Atopic Dermatitis: Follow-Up
The first follow-up visit should be scheduled
within 1 to 4 weeks, depending on the severity of
eczema, to determine the effectiveness of
therapy
Monthly visits are appropriate until the patient is
using lubricants only, then every 3 to 6 months
Because atopic dermatitis is a chronic, recurrent
disorder, offer practical counseling at each visit
regarding ways to deal with the disorder
If there is no concern about overuse or
inappropriate use of topical corticosteroids,
provide ample refills so that the patient can
control the condition on his or her own
Check up with the patient and reinforce
compliance with treatment regimens
Atopic Dermatitis: Referral
Consider consulting with an allergist if
asthma, hay fever, or an acute reaction to
a particular food develops
Refer any patient who does not respond to
conventional therapies after a 2- to 4-week
trial to a dermatologist for management
Contact Dermatitis: Incidence
Nonimmunologic or irritant contact dermatitis
(ICD) accounts for 80% of cases
Immunologic allergic contact dermatitis (ACD), a
delayed cell-mediated hypersensitivity reaction,
accounts for 20% of cases
Contact dermatitis is one of the most common
skin conditions seen by the nurse practitioner
Contact dermatitis accounts for approximately
5.7 million visits each year to health-care
providers
Contact dermatitis affects all age groups and
both genders
ACD is more common in families with allergies
than in unaffected families
Contact Dermatitis: Pathophysiology
ICD is caused by a direct injury to the skin
wherein exposure to the irritative agent
produces immediate discomfort
ACD affects only individuals who have been
previously exposed to an agent
Causes of contact dermatitis include plants,
household chemicals, dyes and industrial
chemicals, elastic, cleaning agents, and
anesthetics and topical medicines
Risk factors include occupational or leisure
exposure to allergens, the use of cosmetics, the
wearing of leather or fur garments, and hair
dyeing
Contact Dermatitis: History
Current complaint
Acute symptoms include papules, vesicles, and bullae
surrounded by redness, itching, and oozing with crusting
The chronic form involves lichenification, an
erythematous base, scaling, and fissures
Lesions are distributed in areas of thin skin and those in
contact with the allergen; the palms and soles are more
resistant, and deep skin folds are usually not affected
Lesions may take the shape of the irritant (zipper,
jewelry, latex) and display sharp borders
Ask the patient about itching, appearance, and
distribution of the rash or lesions
Determine whether dermatitis is chronic or chronically
relapsing
Ask about use of new cleansing routines, laundry
products, clothing, belts, jewelry, cosmetics, hair
products, or medications
Contact Dermatitis: History
Medical history
Previous exposure to offending agent (to identify
acute or allergic form of dermatitis)
Family history
Dermatitis
Medication history
New medication, particularly a topical agent (to
rule out contact dermatitis)
Stigma of having a visible skin disorder
Psychological stressors that may act as triggers
Living conditions and exposures that trigger
dermatitis
Contact Dermatitis: Physical Examination
Examination
Have the patient undress completely, then don a
gown to maintain privacy
Examine the skin systematically to determine the
extent and distribution of the lesions
Compare potential source of irritative contact
with the physical findings
Pay attention to distribution of spared and
affected areas
Contact Dermatitis: Physical Examination
The diagnosis is based on clinical
impression
A patch or prick test may be performed if
ACD is suspected
Herpes simplex
Bullous pemphigoid
Atopic dermatitis
Contact Dermatitis: Treatment
Removal of the agent causing the
symptoms
Lukewarm water or Aveeno oatmeal baths
to relieve itching
Topical soaks in cool water, 25.5% silver
nitrate solution, Burows solution, or
saltwater (1 tsp of salt per pint of water)
Contact Dermatitis: Education
Explain the need to avoid the irritant and discuss ways
for the patient to do so
Teach the patient to keep secondary sources such as
clothing and fingernails clean
Explain that fluid from vesicles does not cause the
spread of disease
Tell the patient that white petrolatum or Eucerin may be
used as an emollient for long-term use
Warn the patient about drowsiness caused by
antihistamines and untoward local skin effects
(specifically, atrophy, stria, telangiectasia, and
tachyphylaxis) resulting from prolonged use of potent
topical steroids
Explain that autoinoculation may progress to generalized
eruption and that secondary skin infections are not
uncommon
Contact Dermatitis: Follow-Up and Referral
Follow-up
Contact dermatitis is generally benign and self-
limited, so follow-up is typically not necessary
unless the problem recurs or the course is
complicated
Referral
Refer the patient for patch testing after
dermatitis resolves
Refer any patient whose dermatitis does not
respond to conventional therapies after a 2- to 4-
week trial to a dermatologist for management
Seborrheic Dermatitis: Incidence
Common disorder, mainly affecting infants,
adolescents, and adults
Affects both men and women
Family history of the disorder is common

Seborrheic Dermatitis: Pathophysiology
Flares are associated with stressors and illness
The common skin-surface yeast Pityrosporum
ovale may contribute
Associated with increased sebaceous-gland
activity in infants and teens
Acnegenic medications may cause this condition
Risk factors include Parkinson disease, acquired
immune deficiency syndrome (severity
correlates positively with progressive immune
deficiency), and emotional stress
Seborrheic Dermatitis: History
Current complaint: infants
Onset around 1 month of age; resolves by the child's first
birthday
Greasy, sometimes reddened scaling of the scalp,
commonly called cradle cap
Rash in axillary and diaper areas
Current complaint: adults
Patches and plaques with scales and distinct margins in
hairy areas with numerous sebaceous glands
Dandruff (visible desquamation of scalp) may be a
precursor
Red, smooth, glazed appearance in skin folds
Mild itching
Bilateral and symmetrical features
Intermittent symptoms
Seborrheic Dermatitis: History
Family history
Stigma of a visible skin disorder
Psychological stressors that may act as
triggers
Living conditions and exposures that
trigger dermatitis
Seborrheic Dermatitis: Physical Examination
Examination
Have the patient disrobe, then don a gown to
maintain privacy
Examine the skin systematically to determine the
extent of the lesions and the distribution of the
lesions
Look for symmetrical and bilateral appearance
and presence of greasy, scaly areas in areas of
hair and high sebaceous activity
Note localization and periodicity
Seborrheic Dermatitis: Physical Examination
Diagnosis is based on clinical findings; no
special procedures are necessary
Atopic dermatitis (infants)
Psoriasis
Tinea capitis or cruris
Rosacea
Lupus erythematosus
Dandruff
Candidiasis
Seborrheic Dermatitis: Treatment
Infants
Treatment consists of frequent
shampooing of the baby's hair with a mild
shampoo, with removal of thick scales
several hours before shampooing
If a nonmedicated shampoo is ineffective,
a ketoconazole shampoo (Nizoral) or coal-
tar shampoo may be required
Seborrheic Dermatitis: Treatment
Adults
Wash affected areas with antiseborrheic shampoos,
starting with over-the-counter brands such as Tegrin or
Selsun Blue and moving to more potent coal-tar, salicylic
acid, sulfur, or selium agents if needed
Use 10% liquor carbonic detergents in Nivea Oil at
bedtime, covering the scalp with a shower cap, and
continue the regimen nightly for 3 weeks
Use ketoconazole cream (Nizoral) to clear scales in
nonscalp areas, followed by topical steroids to relieve
inflammation; start with 1% hydrocortisone and progress
to a more potent fluorinated preparation if needed
When the problem is under control, facilitate remission
with the use of a zinc soap or selenium lotion and
periodic applications of steroid cream
Treat secondary infections of lesions with a short-term
regimen of erythromycin or dicloxacillin

Seborrheic Dermatitis: Education
Tell the parent or caregiver that cradle cap
usually resolves after 6 to 8 months; inform the
adult patient that the disorder is chronic but
controllable
Teach the appropriate use of topical
corticosteroids and explain the complications
that may result if they are used inappropriately
Warn the patient that use of fluorinated steroids
around the eyes may contribute to glaucoma
Tell the patient that tar products may contribute
to photosensitivity
Seborrheic Dermatitis: Follow-Up and
Referral
Follow-up
The scheduling of follow-up visits depends
on the disease course; most patients
should be seen at least every 3 months
Referral
Refer the patient whose dermatitis does
not respond to conventional therapies after
a 2- to 4-week trial to a dermatologist for
management
Introduction
Intertrigoinflammation caused by skin-to-skin contact,
generally found in the groin, axilla, or inframammary
foldshas the potential to result in secondary fungal or
bacterial infection when microorganisms invade the body
through broken skin. Left unmanaged, fungal infection
may provide a portal for lymphangitis or cellulitis,
especially in patients whose leg veins have been used
for open-heart surgery; chronic untreated kerions can
result in scarring alopecia, and untreated cutaneous
candidiasis can result in bacterial infection.
In this lesson, we'll cover data collection, diagnosis, and
management of the following fungal disorders that may
result from intertrigo:
Tinea (fungal infections caused by dermatophytes)
Cutaneous candidiasis (diaper rash)
About Tinea
Tinea is a fungal infection caused by a dermatophyte
Tinea capitis (ringworm of the scalp) is a fungal infection of the hair
follicles and the surrounding skin, presenting with hair loss
Tinea barbae (ringworm of the beard) is similar to tinea capitis but
affects the beard and mustache
Tinea corporis (ringworm of the glabrous skin) affects the trunk and
extremities but excludes the palms, soles, and groin
Tinea versicolor typically appears on the trunk, neck, and proximal
extremities
Tinea pedis ("athlete's foot"), a fungal infection of the feet, is the
most common infection
Tinea manuum is a fungal infection of the palmar and interdigital
areas of the hand
Tinea cruris ("jock itch") is a fungal infection of the groin areas,
including genitalia, pubic area, and perineal and perianal skin
Tinea unguium, or onychomycosis (ringworm of the nails) affects the
toenails more commonly than it does the fingernails
Tinea: Incidence
The estimated cost of treatment of fungal
infections in the United States in 1994 was $400
million
Tinea is manifested most commonly in children
as scalp infections
Tinea capitis is more common in African-
American children than in children of other races
The incidence of onychomycosis increases with
age
Tinea: Pathophysiology
Infection begins when a fungal spore adheres to the skin under
suitable conditions (e.g., trauma or a moist, occlusive
environment)
Within 4 to 6 hours, the spore germinates
The germinating spores develop hyphae and complete the life
cycle by producing more spores
As the dermatophyte grows on the skin, there may be no clinical
signs of infection; some persons may be symptomatic carriers
Inflammation associated with the fungal growth is usually an
allergic response to fungal antigens that have affected the
epidermal layer, composed of living cells
Common pathogens include Epidermophyton, Microsporum,
and trichophyton rubrum
A potassium hydroxide (KOH) slide shows the characteristic
"spaghetti-and-meatball" appearance of tinea versicolor under
the microscope
Tinea: History
Current complaint
Location and duration of occurrence
Associated symptoms, including itching, burning,
pain, or excessive sweating
Current treatments
Contact with infected animals or persons
History of shared combs, towels, or clothing
Recent travel
Use of communal showers or swimming areas
Environmental exposures, such as contact
sports and use of sports facilities or activities
such as swimming and gardening
Tinea: History
Medical history
General medical condition, especially status of hepatic,
renal, and endocrine systems and presence of
immunosuppressive disorders
History of previous occurrence and past treatments
History of other skin disorders or allergies
Medication history
Current medications
Family history
History of tinea infections
History of other skin disorders
Other family members with skin disorders
Living conditions

Tinea: Physical Examination
Conduct a comprehensive physical
examination of the skin, using a good light
source and paying special attention to
areas of particular concern.
Examination
Check all body surfaces with clothes
removed
Check for lymph node enlargement
Observe for characteristic lesions of
corporis, barbae or capitis, cruris,
onychomycosis, pedis, and versicolor
Microscopic observation with the use of a
KOH preparation
Inspection of infected areas under a Wood
lamp
Fungal culture consisting of several hairs
or scrapings from an infected area, placed
on appropriate test medium
Differential diagnosis: capitis
Atopic dermatitis (skin lesions in flexure folds)
Seborrheic dermatitis (no hair loss)
Psoriasis (nail changes and silvery lesions on knees and elbows)
Alopecia areata (complete hair loss, not patchy)
Impetigo
Bacterial folliculitis
Trichotillomania (hair of differing lengths and history of compulsive
hair-pulling)
Differential diagnosis: barbae
Bacterial folliculitis
Herpes
Contact dermatitis
Differential diagnosis: corporis
Nummular eczema
Psoriasis
Pityriasis rosea

Differential diagnosis: pedis
Contact dermatitis
Interdigital psoriasis
Eczema
Differential diagnosis: cruris
Candidiasis or intertrigo (uniformly red, no central clearing, satellite
lesions)
Contact dermatitis
Lyme disease
Erythrasma (uniformly brown scales, bright coral-red fluorescence)
Differential diagnosis: onychomycosis
Psoriasis
Candidiasis
Yellow-nail syndrome
Differential diagnosis: versicolor
Pityriasis alba (see image)
Vitiligo (development of totally white macules, complete absence of
melanocytes)
Tinea: Treatment
Pharmacologic
Topical creams are the preferred treatment for all forms of tinea
except tinea capitis, tinea barbae, and onychomycosis, which
require a combination of topical and oral medications
Common adverse effects of oral antifungal medications include
gastrointestinal complaints and headache
Pharmacologic: capitis and barbae
Prescribe 2.5% selenium sulfide shampoo to prevent the spread of
infection
Advise use of 1% Selsun Blue shampoo (can be purchased over the
counter [OTC])
Griseofulvin (Fulvicin) is the only agent approved for tinea capitis;
however, resistant organisms require an increased dosage and
longer duration of treatment
Griseofulvin, terbinafine (Lamisil), ketoconazole (Nizoral), and other
agents differ in their dosages for children and adults
Griseofulvin has the most adverse effects, followed by ketoconazole,
itraconazole, and terbinafine
Prescribe prednisone 1 to 2 mg/kg daily for 5 to 10 days for adults
with inflammatory tinea capitis
Check drug interactions before prescribing
Tinea: Treatment
Pharmacologic: corporis
A topical agent such as miconazole nitrate 1%
(Monistat), clotrimazole 2% (Lotrimin), and econazole
1% (Spectazole) is usually effective
Advise patients to continue applying topical agents twice
daily for 2 weeks after clinical signs and symptoms have
disappeared
Oral agents are for widespread, inflammatory, or
resistant infections
Pharmacologic: versicolor
Topical agents such as selenium sulfide lotion 2.5%
(Selsun), miconazole cream 2.5%, clotrimazole 1%, and
thiosulfate 25% are effective
Advise patients to apply beyond the borders of the
affected areas for 5 to 10 minutes every day for 2 weeks
Oral medications usually are not needed but may be
used in resistant cases or for prophylaxis
Tinea: Treatment
Pharmacologic: pedia and manuum
Clotrimazole, miconazole, tolnaftate, or terbinafine hydrochloride
cream, applied twice daily to the feet, should be continued for 2
weeks after the condition has cleared
Butenafine 1% may also be used daily after bathing for 4 weeks
Talcum powder or antifungal powders (OTC) can be used
In severe cases, Burows solution can help with oozing lesions
Pharmacologic: cruris
Clotrimazole or miconazole topical cream may be applied twice daily
for 3 to 4 weeks
In children, 1% terbinafine may be applied daily for 7 days
Butenafine 1% may be applied daily after bathing for 2 weeks
Oral treatment may be administered in resistant cases
Pharmacologic: onychomycosis
Oral medications are more effective than topical medications
Advise patients to avoid antacids within 2 hours of taking oral
medications
Tinea: Treatment
Nonpharmacologic
The affected child may return to school
after beginning oral therapy
A child in the daycare setting does not
need to be isolated once treatment has
begun

Tinea: Education
Explain that adverse effects and drug interactions are associated with oral
antifungal medications
Teach the patients to avoid sharing brushes, combs, hats, towels, and other
items that can transmit fungal scales and to keep his or her own items clean
Stress the importance of good hygiene and suggest the use of a benzoyl
peroxide wash
Encourage the patient to treat pets that may be infected
Tell the patient to avoid braiding their hair or using oils on the hair or scalp
Suggest the application of creams after bathing and reapplying after
swimming or exercising
Encourage the patient to keep the skin dry and to remove wet swimsuits as
soon as possible
Suggest cotton undergarments and loose-fitting clothes
Advise the patient with fungal disorders of the feet to wear leather or
nonocclusive shoes with cotton socks, to use drying powders on the feet,
and to wear sandals or rubber shoes in communal areas as appropriate
Explain that the recurrence rate is high and that treatment may be needed
each spring before sun exposure, especially to stop the redevelopment of
tinea versicolor
Explain that it may be necessary to order cultures and treat other family
members
Encourage all family members to use selenium sulfide shampoo to prevent
recurrences caused by asymptomatic carriers
Tinea: Follow-Up and Referral
Follow-up
Reevaluate all cases of tinea after 2 weeks for response
to therapy
Follow up with patients with resistant infections and tinea
capitis every 2 to 4 weeks until clear
Monitor patients taking oral antifungal medications
monthly
Monitor for superimposed bacterial infections at the
follow-up visit; cultures and Gram staining may be
needed to determine the appropriate antibiotic therapy
Check for resolution of lesions
Referral
Collaborate with a physician in regard to patients who
require oral antifungal medications
Collaborate with physician in regard to patients who do
not show improvement within 2 weeks
Cutaneous Candidiasis: Incidence
The exact incidence of cutaneous
candidiasis (also known as diaper rash) is
unknown
The condition may present anywhere
between 2 weeks of life and when a child
is toilet trained
It also affects patients with diabetes or in
those with decreased immunity
Young and old patients are more likely to
be colonized
Cutaneous Candidiasis: Pathophysiology
Cutaneous candidiasis occurs in moist, occluded
cutaneous sites
Dermatitis results from prolonged contact of urine and
feces with skin, leading to skin irritation or from skin
surfaces rubbing together causing irritation
In 80% of cases, if the dermatitis lasts more than 3 days,
the area is colonized with Candida even before the
characteristic lesions are seen
Some cases may be caused by Candida and passed to
the child from the mother by way of maternal vaginal
candidiasis at birth
The rash is usually caused by the yeast Candida
albicans and less often by other Candida species
Heat and other factors can increase susceptibility
Cutaneous Candidiasis: History
Current complaint
Rash in diaper area
Irritability
Crying while voiding
Complaints of a rash under the breasts, in the
groin, or on the intergluteal cheeks
Associated symptoms, including eczema or
other skin lesions or oral thrush
Medical history
Prior episodes of rash (suggesting neglect or
carelessness)
Cutaneous Candidiasis: History
Family history
Maternal vaginal candidiasis
Medication history
Use of neomycin ointment (can cause allergic
dermatitis in infants)
Recent antibiotic use (may suggest candidal
infection)
Abuse or neglect
Cultural differences in hygiene
Parents' low education level
Cutaneous Candidiasis: Physical
Examination
Conduct a comprehensive physical examination
of the skin, using a good light source.
Examination
Check the head, ears, eyes, nose, throat
particularly the mouth and throatfor white
patches on the tongue and buccal mucosa
Examine the genitalia for erythema, papules or
vesicles, or ulcerations
Observe skin in the diaper and interdigital areas
for a rash or burned, scalded, or shiny
appearance
If bullae or yellow crusts are present, suspect a
secondary infection (Staphylococcus aureus)
Cutaneous Candidiasis: Physical
Examination
Culture to rule out Staphylococcus aureus
KOH wet prep to reveal Candida yeast
cells and pseudohyphae
Atopic dermatitis
Impetigo
Psoriasis
Irritant dermatitis
Cutaneous Candidiasis: Treatment
Nonpharmacologic
Increase fluids
Provide cranberry juice if child is 1 year or older
Withhold other juices
Pharmacologic
A glucocorticoid preparation will speed
resolution with judicious short-term use
Topical antifungal agentssuch as nystatin,
azole, or imidazole creamcan be applied to
the affected area twice daily or more often with
diaper dermatitis
Oral antifungal agents such as nystatin
Cutaneous Candidiasis: Education
Tell the patient or caregiver to avoid petroleum products
because they trap moisture
Advise the caregiver to change diapers frequently,
cleanse the diaper area with water at each diaper
change, and avoid commercial wipes, which contain
alcohol
Suggest that caregivers let the child go without diapers
as much as possible to keep the area dry
Suggest changing the brand of diapers
Teach caregivers to wash hands carefully
Suggest the daily application of a powder with
miconazole but tell caregivers to avoid talcum powder
because it may produce aspiration pneumonia
Suggest washing with benzoyl peroxide to help reduce
Candida colonization
Cutaneous Candidiasis: Follow-Up and
Referral
Follow-up
Follow up by telephone or schedule a
return visit in 48 hours
Referral
If candidiasis fails to respond in 1 week,
refer the case to a dermatologist
If the condition worsens, refer to the
collaborating physician; an
immunodeficiency may be present
Introduction
Skin problems caused by infestations of lice
(body, head, or pubic) and scabies are inevitable
diagnoses faced by the family nurse practitioner
in practice today. Left untreated, infestations can
result in continued infestation, "vagabond's skin"
(lichenified, scaling, hyperpigmented papules,
most commonly on the trunk), and multiple
pyodermas of the scalp, as well as secondary
infection, plus psychosocial discomfort because
of the stigma attached to these disorders.
This lesson focuses on recognizing, managing,
and preventing the spread of such infestations.
Lice: Incidence
Pedicular infestation of the skin or hair is caused by a species of
blood-sucking lice capable of living as external parasites on the
human host
Three types of lice that inhabit the human host are Pediculus
humanus corporis, Pediculus humanus capitis, and Phthirus pubis
Between 6 million and 12 million cases occur each year in the
United States and hundreds of millions of cases exist worldwide
Most cases of lice infestation (50% to 75%) occur in children
younger than 12 years old
Lice can be epidemic in daycare centers, kindergartens, and schools
Lice infestation occurs in all ages and socioeconomic groups and in
all geographic regions
Infestations are less common in blacks than in whites
Infestations may occur in any season but are most common August
through November
Lice are generally transmitted by way of contact with bedding or
other human beings, but each type of infestation has a specific
incidence
Lice: Pathophysiology
Lice are ectoparasites that, when spread by way of direct
or fomite contact, pierce the skin to feed (shown here)
When the louse bites, it first infuses saliva to prevent
clotting and then probes for a vessel
The female louse lays 100 to 300 eggs (nits) during its
lifetime
The louse cannot live away from a human host for more
than 50 to 55 hours
The saliva of the louse provokes symptoms through a
histamine response
Secondary skin lesions are common because of
scratching; lymphadenopathy and irritation at the
scratched sites may indicate infection
Certain factors increase susceptibility to pediculosis
capitis, pediculosis corporis, and pediculosis pubis
Lice: History
Current complaint
Known exposure to lice
Intense itching (the hallmark of louse
infestation), often worse at night, particularly on
the back and at the side of the scalp and, in
pediculosis capitis, at the occipital hairline and in
the postauricular area
Sleeplessness
Irritability
Difficulty concentrating in school because of
itching and fatigue resulting from interrupted
sleep
Lice: History
Family history
Infestation in any family member or close associate
Enrollment in daycare, kindergarten, school, or camp
Sharing of clothing or hairbrushes, combs, barrettes, wigs, hats, and
other hair-care items
Participation in sports in which equipment is shared
Homelessness, residence in a crowded environment, or other factor
preventing regular bathing, shampooing, and laundering of clothing
Sharing of clothing, pillows, or bedding
Whether the patient wears clothing from yard sales or thrift shops
and whether he or she launders these items before use
Number of sexual partners
Possibility of sexual abuse in a child
Perceptions of the problem (infestation carries a stigma, and many
misconceptions about lice infestation exist)
Lice: Physical Examination
Conduct a comprehensive physical examination of the skin, using a
good light source, wearing gloves, and paying special attention to
particular areas.
Examination
Visualize lice on hair shaft
Identify nits
Note red pinpoint bites or black specks (louse feces)
Look for erythema at the nape of the neck and in the postauricular
areas
Look for 3- to 15-mm blue, nonblanching, asymmetrical tracks on
the thighs and trunk
Check for red macules, papules, or crusting pustules with central
hemorrhagic punctures
Be alert to lesions of secondary infection caused by scratching
Look for symptoms of other sexually transmitted diseases (STDs)
that may coexist with pediculosis pubis
Lice: Physical Examination
Remove a louse and place it in mineral oil for
examination under a microscope for
confirmation if desired
Because lice fluoresce and appear pearly, use a
Wood lamp (normally not necessary for
diagnosis); dead nits do not fluoresce
Confirm the type of infestation
For pediculosis capitis, rule out hair artifacts
(e.g., hairspray or gel), dandruff, seborrhea,
psoriasis, impetigo, and tinea capitis
Lice: Treatment
Nonpharmacologic
Commercial preparations such as
GenDerm's Step 2 ease nit removal
A solution of one part white vinegar to one
part water may also be used to loosen nits
A nit comb (metal works best) helps
remove all nits from the hair
Petrolatum applied twice a day for 10 days
aids in the treatment of infested eyelashes
Lice: Treatment
Pharmacologic
A pediculicide such as a pyrethrin, permethrin,
lindane, ivermectin, or malathion is required to
kill lice and nits
During application of a pediculicide, the patient's
eyes must be covered and shut
Most pediculicides are contraindicated in
children younger than 2 years, in pregnant
women and in lactating women
Treat secondary infections with antibiotics such
as erythromycin, dicloxicillin, or cephalosporin
Treat eyelash infestations on the basis of the
age of the patient
Lice: Education
Reassure the patient and family that pediculosis is curable,
does not cause long-term effects, and is a common problem
in all socioeconomic groups
Because lice are transmitted from person to person, educate
children and parents about transmission and preventive
measures
Teach the patient or caregiver how to disinfect the personal
articles of the infested individual and how to clean the
environment
Recommend that all family members and close contacts be
examined for infestation and undergo treatment at the same
time as the patient (in the case of pediculosis pubis, this
includes sexual partners)
Advise parents to inform school authorities about any child
with lice infestation
Reinforce the importance of exposing all lice and nits to
pediculicide and destroying or removing all nits from infested
hair
Lice: Follow-Up
During louse season, have the parent
check the child's hair every 3 days
Several days after treatment, have a
family member reexamine the child
Ensure that pediculicide is reapplied 7 to
10 days after the initial treatment
For pediculosis pubis, ensure that all of
the patient's sexual contacts during the
previous month undergo treatment
Lice: Referral
Refer children younger than 2 years to a
physician
Refer a pregnant or lactating woman to a
physician
Referral is indicated if treatment fails
Any patient with a coexisting dermatologic
condition should be referred to a physician
Pediculosis pubis in a child should cause the
nurse practitioner to suspect sexual abuse; the
appropriate authorities should be notified in such
cases
Scabies: Incidence
Scabies (Sarcoptes scabiei) exists in two
variants: nodular and crusted (Norwegian)
Scabies is most common in children, young
adults, institutionalized persons of all ages, and
persons with acquired immune deficiency
syndrome
Incidence is persistently high in developing
countries and in overcrowded housing
elsewhere
Norwegian scabies is more common than the
nodular variant among the immunodeficient and
those with mental or physical disabilities such as
Down syndrome, neurologic disease, or
malnutrition
Scabies: Pathophysiology
The mite that causes scabies infestation is an obligate parasitethe human skin itch
mite, known as Sarcoptes scabieian oval, gray, or translucent parasite 0.3 to 0.5
mm long
Close contact is necessary for transmission
The impregnated female mite Burows into the skin, using chemical factors in the
saliva to dissolve keratin on the skin's surface
Once in the Burow, the female remains there her entire life (approximately 30 days),
laying two or three eggs per day
The eggs hatch in 3 or 4 days and the mites reach maturity in approximately 4 days,
after which they migrate to the surface, mate, and repeat the cycle
A person infested with classic (nodular) scabies who bathes frequently may have
more than 50 mites in the skin; with the Norwegian type, thousands of mites may be
involved
Symptoms, which occur 4 to 6 weeks after the first infestation, are the result of a
hypersensitivity reaction caused by mite saliva and feces (scybala) deposited in the
skin
People who are infested with scabies more than once experience symptoms in 24 to
48 hours after succeeding exposures
In rare cases transmission occurs by way of fomites such as towels and linens; the
mite can live for as long as 5 days away from the human host
Diagnosis is sometimes difficult because the scratching provoked by intense itching
obscures the classic signs
The distribution of lesions and multiple individuals affected in the same residential
setting should increase the index of suspicion for scabies infestation
Scabies: History
Current complaint
Generalized pruritic rash, particularly on the
hands, flexor portion of the wrists, elbows,
axillary folds, buttocks, breasts, abdomen, and
genitals
Intense intermittent itching, especially nocturnal,
intensifying with increased warmth of skin and
persisting for weeks after treatment; itching may
not be noted, however, by an
immunosuppressed patient
Sleeplessness resulting from intense pruritus
Scabies: History
Medical history
Previous infestation
Previous episodes of itching
Family history
Similar symptoms in family members or close
contacts, especially those living with the patient
Multiple sexual partners
Daycare, school, or camp attendance
Institutionalization
Residence in a nursing home
Scabies: Physical Examination
Conduct a comprehensive physical examination of the skin,
using a good light source and a magnifying lens. Wear
gloves, and pay special attention to areas of concern in
scabies infestation.
Examination
Look for primary lesions, including papules and vesicles
Assess the interdigital areas of the fingers and the flexor
aspects of the wrists for Burows
In infants and young children, look for generalized skin
eruptions on the scalp, face, palms, and soles
In Norwegian scabies, thick, crusted plaques are present
on the hands and feet, including the palms and soles
Look for associated lesions, including excoriation caused
by scratching, impetigo, and firm reddish-brown nodules
(nodular scabies)
Practice handwashing and universal precautions to
protect against scabies infestation
Scabies: Physical Examination
Confirm the presence of mites, eggs, or feces under the
microscope or, if these items cannot be found, confirm
the presence of Burows
Use mineral oil or a marker to help identify Burows
Scrapings do not always yield mites, so the diagnosis is
often made on the basis of clinical presentation alone
Atopic dermatitis
Allergic dermatitis
Contact dermatitis
Insect bites
Secondary syphilis
Scabies: Treatment
Nonpharmacologic
All bed linens and clothing that have been used
or worn in the preceding 3 days should be
washed in hot water with detergent and dried in
a hot dryer or dry cleaned
Bed linens should be washed in hot water daily
until the course of treatment is finished
Because the mite cannot survive off the host for
more than 3 days, items that are not washable
can be sealed in a plastic bag for 7 days to kill
the mites
Scabies: Treatment
Pharmacologic
Oral antihistamines and mild topical corticosteroid agents may be
needed after treatment to help control pruritus
Permethrin 5% (Elimite) is the preferred treatment because of its low
toxicity and high efficacy
Lindane 1% (Kwell) lotion is considered an alternative treatment
because of organism resistance and its neurotoxic effects in infants
Crotamiton 10% (Eurax) cream or lotion is less effective than
permethrin but is considered safe for infants and pregnant and
nursing women
A sulfur preparation (precipitated sulfur 5% to 10%) is the preferred
treatment for infants younger than 2 months, pregnant or nursing
women, and people who cannot afford other treatments
Ivermectin can also be used as an alternative treatment, but its
safety and efficacy have not been established in children weighing
less than 15 kg
Secondary bacterial infections should be treated as well
Scabies: Education
Reassure the patient or caregiver that scabies is curable and is a
common problem in all socioeconomic groups
Explain that symptoms generally occur 4 to 6 weeks after infestation,
coinciding with the development of the immune response
Also explain that because of the lag time between infestation and
symptoms, transmission may have occurred unrecognized
Encourage all infested family members to be treated simultaneously to
avoid reinfestation, and explain that asymptomatic family members and
close contacts should also be treated because of delay in symptoms
Teach adults to apply the scabicide from the neck down to the toes, with
special attention to interdigital areas of the fingers and toes, umbilicus,
and skin folds
Tell the parent or caregiver that treatment of an infant or young child
should include the scalp and face if lesions are present
Explain that relief from itching may not occur until 3 to 6 weeks after
treatment because of the skin's hypersensitivity to the debris left in the
Burow, and itching will continue until the natural turnover of skin occurs
Tell patients that retreatment is not indicated for continued itching
Teach patients to wash linens in hot water and to dry-clean other
bedding and cloths or place in sealed plastic bags for 7 days
Scabies: Follow-Up and Referral
Follow-up
Reexamine the patient 2 weeks after the start of therapy
to look for irritant dermatitis and to treat residual pruritus
Schedule a second follow-up examination in 4 weeks to
check for new lesions; an absence of new lesions 4
weeks after treatment indicates that the therapy has
been successful
Referral
Refer a pregnant or lactating woman to a physician
Refer any child younger than 2 years to a physician
Refer any patient with Norwegian scabies to a physician
Refer the patient with coexisting dermatologic conditions
to a physician
Introduction
In this lesson we'll review several skin
conditions seen in primary-care practice:
Paronychia
Pityriasis rosea
Erythema multiforme
Stevens-Johnson syndrome
Paronychia: Incidence and Pathophysiology
Paronychia is an acute or chronic inflammation of the folds
surrounding the nail plate of the fingernails and toenails.
Incidence
Affects people in all age groups
Three times as many women as men are affected
Pathophysiology
Acute infection is precipitated by trauma or chemical
damage
The chronic form is associated with frequent immersion
of the hands, finger-sucking, or diabetes mellitus
Causes of acute infection include Staphylococcus
aureus (most common), streptococci, and Pseudomonas
The most common cause of the chronic form is Candida
Paronychia: History
Current complaint
Pain or throbbing in the affected finger or
toe
Swelling and redness around the nail
Changes in the nail plate
Onset and progression of symptoms
Relieving and aggravating factors
Treatment strategies attempted
Associated symptoms
Trauma of the affected area
Paronychia: History
Medical history
Chronic illness, particularly diabetes
mellitus
Allergies
Medication history
Any prescription or nonprescription drugs
taken
Employment or leisure activities that
require immersion of hands for long
periods
Paronychia: Physical Examination
Examination
Separation of the nail fold from the nail plate
Erythema and swelling around the nail plate
Purulent drainage (some cases)
Changes in the nail plate
Green coloration of the nail in cases caused by Pseudomonas
Gram stain
Culture and sensitivity test
Potassium hydroxide (KOH) prep and study
Fungal culture
Herpetic whitlow
Reiter disease
Psoriasis
Paronychia: Treatment
Nonpharmacologic
Elevation of the affected digit to relieve throbbing pain
Warm compresses or vinegar soaks in the acute form
Keep the digits dry in the chronic form
Incision and drainage if an abscess forms
Partial or complete removal of an ingrown toenail to
promote healing
Pharmacologic
Antibiotics for acute condition in patients with diabetes,
in cases involving suppuration, and in severe cases
Topical or systemic treatment for chronic paronychia of
bacterial or fungal origin
Paronychia: Education
Teach bartenders, nurses, dishwashers, and other
patients whose work involves prolonged immersion of
the hands to keep the hands dry and encourage the use
of lined rubber gloves when possible
Educate the parents or caregiver of a thumb- or finger-
sucking child about the condition and encourage the
child to quit
Teach the proper procedure for cutting the nails to help
prevent ingrown nails
Discuss ways to minimize the risk of trauma to the
fingers or toes
Encourage patients with diabetes to maintain good
control of the disease
Explain that complications include abscess and chronic
changes to the nail and, possibly, nail loss
Paronychia: Follow-Up and
Referral
Follow-up
Healing is expected with adequate treatment
Follow up routinely as appropriate until the
condition is cured
Referral
Referral is generally not required unless
treatment is ineffective or the patient is
immunosuppressed
Consider consultation in diabetic patients with
uncontrolled glycemia
Pityriasis Rosea: Incidence and
Pathophysiology
Pityriasis rosea is a common, self-limited eruption involving
the skin and mucous membranes, possibly of viral origin.
Incidence
The condition is often categorized as a papulosquamous
condition
It affects people of both sexes and all races, most
commonly children and young adults
In the United States, the condition is most common in
the spring
Nearly 0.14% of the U.S. population is affected at some
point
Pathophysiology
The cause is unknown, but the condition may be either a
viral or an autoimmune disorder
Pityriasis Rosea: History
Current complaint
Mild pruritus
Malaise and fever in rare instances
Skin lesions
Pityriasis Rosea: Physical Examination
Conduct a comprehensive skin examination.
Examination
A herald patch may appear days to weeks
before generalized rash materializes
This generalized rash, containing smaller
plaques similar in features to the herald
patch, may be seen predominantly on the
trunk
Lesions frequently occur along skin-
cleavage lines in a "Christmas tree"
pattern
Pityriasis Rosea: Physical Examination
No specific laboratory tests are available
The white blood cell count will be normal
Serologic study may be needed to rule out syphilis
A KOH preparation will help differentiate pityriasis rosea
from tinea corporis
Secondary syphilis
Viral exanthem
Drug eruption
Psoriasis
Eczema
Tinea corporis
Pityriasis Rosea: Treatment
Nonpharmacologic
Warm oatmeal baths to relieve itching (hot water
exacerbates itching)
Good skin hygiene to prevent secondary
infection
Ultraviolet light to help hasten resolution
Pharmacologic
Topical antipruritics as needed
Topical steroids to reduce itching as needed
(triamcinolone 0.1% cream)
Oral antihistamine (e.g., Benadryl 25 mg three
times daily) if needed for relief of itching
Pityriasis Rosea: Education, Follow-Up,
and Referral
Education
Reassure the patient that the disease is self-limiting
Teach the patient how to avoid secondary infections
such as impetigo
Follow-up
The condition will likely resolve 2 to 6 weeks after
symptoms appear
If lesions persist for more than 10 weeks, have the
patient return for reevaluation
Referral
Because pityriasis rosea is a self-limiting disease, it does
not usually require consultation or referral
Erythema Multiforme: Incidence and
Pathophysiology
Incidence
Erythema multiforme is characterized as a hypersensitivity skin
disorder; it varies in severity and its clinical manifestations
Most common in people ages 20 to 30 years; rarely occurs in
subjects younger than 3 years or older than 50 years
Affects people of all races
More common in male subjects than in female ones
A history of the disorder increases the risk of future appearances
Immunodeficient patients are particularly susceptible
Incidence is increased in the spring and fall, consistent with the
increase in infectious organisms
Erythema multiforme accounts for up to 1% of dermatologic
outpatient visits
Pathophysiology
The most common cause is a preceding viral or bacterial infection
Other causes include protozoans, fungi, collagen vascular disease,
malignancy, pregnancy, premenstrual hormone changes,
consumption of beer, Reiter syndrome, sarcoidosis, drugs and
vaccines, and radiotherapy
Erythema Multiforme: History
Mild burning sensation of the skin (no pruritus)
Mixture of macules and papules of various sizes
and target lesions
Each eruption comprises central inflammation
and a superficially necrotic area surrounded by a
halo of less inflamed skin and an erythematous
outer rim
Occurs on the palms, soles, dorsal surfaces of
the hands, extensor surfaces of the extremities,
and the face
May involve the mucous membranes (the oral
mucosa are involved in two thirds of cases)
Vesicles may be present if the antecedent agent
is HSV
Erythema Multiforme: Physical
Examination
Examination
Petechiae, vesicles, bullae (disseminated
and symmetric on the extremities and
face), and fixed target lesions
Assess for absent or mild prodrome
Look for vesicles and ulcers on the oral
mucosa
Try to elicit the Nikolsky sign, in which the
superficial layers of skin slide free of the
lower ones under slight pressure; it is not
present in erythema multiforme
Erythema Multiforme: Physical
Examination
Laboratory tests are not useful in
diagnosis
Skin biopsy is diagnostic
Urticaria
Drug eruption
Paroneoplastic pemphigus
Pemphigoid
Erythema Multiforme: Treatment
Nonpharmacologic
Elimination of the causative agent, if known
Symptomatic treatment for mild cases
Meticulous wound care and wet dressings with Burows
or Domeboro solution in severe cases
Increased fluid intake
Warm saline mouthwashes for oral lesions
Pharmacologic
Acyclovir (if HSV is the causative agent)
Tamoxifen (may prevent premenstrual attack)
Steroids (controversial, but tapered systemic therapy
with prednisone is common)
Oral rinses with warm saline solution or a solution of
diphenhydramine, Xylocaine, and Kaopectate for relief of
symptoms and to facilitate oral fluid intake
Erythema Multiforme: Education
Reassure the patient that the disease is self-
limiting and generally disappears within 3 weeks
without scarring or other complications
Remember that many people see erythema
multiforme as an early form of Stevens-Johnson
Syndrome; explain the proper categorization
Explain that erythema multiforme recurs in 30%
of cases
Encourage the patient to avoid the known
causative agent and others of the same class
that can cross-react
Encourage the patient to wear a MedicAlert
bracelet
Teach wound and lesion care
Erythema Multiforme: Follow-Up and
Referral
Follow-up
Follow-up is usually not necessary
Referral
Because erythema multiforme is not
associated with complications and is
associated with drug exposure, referral is
generally unnecessary
Referral to a dermatologist may be
appropriate if erythema multiforme minor
recurs
Stevens-Johnson Syndrome: Incidence
Stevens-Johnson syndrome (SJS) was once known as
erythema multiforme major but is now considered a
separate entity. A generalized hypersensitivity reaction,
usually to a drug, causes early lesions of the skin and
mucous membranes. SJS may progress to a more
severe form known as toxic epidermal necrolysis (TEN),
which has a mortality rate of 40%. SJS, considered a
dermatologic emergency, has a rapid onset, evolves
over 1 to 2 weeks, and persists for 4 to 6 weeks.
The exact incidence is unknown because of confusion
with erythema multiforme (major), but SJS likely affects
only 0.1 persons out of 100,000 or fewer
SJS affects twice as many males as females and is more
common in children and young adults, especially in
those infected with human immunodeficiency virus
Immunosuppression and history of previous episodes
are also risk factors
Stevens-Johnson Syndrome:
Pathophysiology
The causative agent is sometimes
unknown, but drug intolerance accounts
for 80% of cases
Infections, especially Mycoplasma, are a
less common cause
Some drugs are associated with SJS, and
some vaccines are considered
precipitators
The syndrome often begins with a flulike
prodrome
Stevens-Johnson Syndrome: History
Current complaint
Skin tenderness
Stinging eyes
"Burning" mucosa
Pain on swallowing
Erythema
Desquamation of the skin, possibly progressing to epidermal
necrosis and sloughing
Skin lesions
Constitutional symptoms
Other symptoms
Medical history
Ill feeling, with fever, sore throat, or cough
Prodrome
Medication history
Use of drugs for treatment of another problem
Recent vaccination
Stevens-Johnson Syndrome: Physical
Examination
Examination
Assess the skin for tenderness
Look for disseminated symmetrical lesions,
confluent on the face, neck, and trunk
Look for atypical target lesions with necrotic
centers
Try to elicit the Nikolsky sign, which is present in
SJS
Look for severe mucosal involvement at two or
three sites
Look for massive necrosis and sloughing of
epidermis
Stevens-Johnson Syndrome: Physical
Examination
No specific diagnostic tests are available
Serologic tests or cultures for suspected sources of
infection may be helpful
Skin biopsy will demonstrate necrotic changes compared
with the predominantly inflammatory changes in
erythema multiforme
Exfoliative dermatitis
Scalded-skin syndrome (Staphylococcus aureus
induced)
Paraneoplastic pemphigus
Drug eruption
Erythema multiforme major
Burns
Pressure blisters
Stevens-Johnson Syndrome: Treatment
Nonpharmacologic
Elimination of the causative agent, if it is known
Admission to a hospital intensive-care or burn unit under the care of
a multidisciplinary team including an ophthalmologist, a
dermatologist, and possibly a plastic surgeon
Intravenous (IV) fluids with electrolyte replacement similar to that
employed in victims of third-degree burns
Meticulous care of damaged skin
Oral hygiene
Reverse isolation in cases of extensive epidermal loss
Adequate caloric intake, including parenteral nutrition, if needed
Ophthalmologic consultation and monitoring for corneal damage
Bed rest until the patient's condition is stable
Surgical dbridement of areas of extensive epidermal loss with
application of biosynthetic dressings
Surgical repair, if necessary, of long-term damage to vulvovaginal
tissues or corneas
Stevens-Johnson Syndrome: Treatment
Pharmacologic
Antibiotics, if the patient exhibits evidence of
infection
Antihistamines and topical steroids for pruritus
Pain medications
Immunoglobulins administered IV early in the
course of illness; becoming the standard of care
to halt progression to TEN
Continuous IV pentoxyphylline drip
Conjunctival erythromycin ointment
Oral rinses with warm saline solution or a
solution of diphenhydramine, Xylocaine, and
Kaopectate for relief of symptoms and to
facilitate oral fluid intake
Stevens-Johnson Syndrome: Education
Keep the patient and significant others informed
of progress and treatment options
Explain that treatment needs are similar to those
of burn victims because skin sloughing is like a
third-degree burn
Warn the patient to avoid causative agents
indefinitely and suggest that he or she wear a
MedicAlert bracelet or pendant
Explain the dangers of cross-reaction between
drugs in the same class and to avoid them
Tell patients that a third of all patients with SJS
experience a recurrence of symptoms
Explain complications
Stevens-Johnson Syndrome: Follow-Up and
Referral
Follow-up
Because this dermatologic emergency will be referred to
a physician provider for diagnosis and management,
follow-up likely will not be conducted solely by the nurse
practitioner
Patients will be monitored for secondary or concurrent
infections, electrolyte and fluid status, malnutrition, and
end organ damage throughout the 4 to 6 weeks it takes
for the disease to resolve
Surgical repair of damaged corneas or of scarred
vulvovaginal tissue may be required
Referral
This condition demands immediate referral to a
dermatologist
A support group such as the Stevens-Johnson
Syndrome Foundation may be helpful
Introduction
Psoriasis is a chronic disorder that results
from a polygenic predisposition combined
with such triggering factors as trauma,
infections, and medications. In this lesson,
we'll review the presentation, diagnosis,
and management of this disorder.
Incidence
Two types of psoriasis exist: eruptive and chronic stable (plaque)
Approximately 1% to 2% of people in the United States, or about
5.5 million people, have plaque psoriasis
Psoriasis affects children and adults
Men and women are affected equally
Women develop plaque psoriasis earlier than men
The first peak of plaque psoriasis occurs at age 16 to 22 years;
the second peak occurs at age 57 to 60
Psoriasis can affect all races, although studies have shown that
more people in western European and Scandinavian populations
have psoriasis than those in other population groups
Genetics is a strong factor in the development of psoriasis
Up to 30% of people with plaque psoriasis also have psoriatic
arthritis
Plaque psoriasis can sometimes evolve into more severe
disease, such as pustular psoriasis or erythrodermic psoriasis
Pathophysiology
Both systemic and local factors are involved in the
pathogenesis of psoriasis
The abnormality in psoriasis is an alteration of the cell
kinetics of kerotinocytes
The cell cycle shortens from 311 to 36 hours, resulting in
28 times the normal production of epidermal cells
The epidermis and dermis react as an integrated system:
Cell production changes in the germinative layer of the
epidermis, and inflammatory changes in the dermis
trigger the epidermal changes
Psoriasis is a T-celldriven disease; many T-cells are
present in psoriatic lesions surrounding the upper dermal
blood vessels, and the cytokine spectrum is that of a Th1
response
Maintenance of psoriatic lesions is considered an
ongoing autoreactive immune response
History
Current complaint
Pruritus (particularly of the scalp and anogenital areas)
Pustules, papules, and red plaques
Lesions
Arthritis (resembles rheumatoid arthritis)
Fever
Symptoms of strep throat
Acute illness
Stripping, pitting, fraying or separation of the distal margin of
the nail and thickening discoloration and debris under the nail
plate
Associated symptoms such as joint pain (psoriatic arthritis);
weakness, chills, and fever (von Zumbusch syndrome);
hypothermia in older patients; and hemodynamic changes
such as shunting of blood to the skin
Duration and location of symptoms and whether onset was
sudden
History
Family history
Skin disorders
Medication history
Corticosteroids
Lithium
Chloroquine
-Blockers or interferon-
Patient's view of disorder (stigma of having a visible skin
disorder)
Stressors
Alcohol consumption
Dietary history (for calorie count, especially in older
patients, who have an increased metabolic rate)
Examination
Have the patient completely undress and put on a gown
for privacy
Note the patient's general appearance, ranging from well
to uncomfortable to toxic, based on the extent of
involvement of the psoriasis
Record vital signs: height and weight, blood pressure,
temperature, pulse, and respirations
Examine the skin and scalp systematically to determine
the extent, distribution, type, and shape of the lesions
Check the fingernails for pitting or other changes
Examine the mucous membranes and tongue
Examine all areas of flexure, including the groin and
buttocks
Check the lesions for the Auspitz sign (bleeding when a
scale is removed)
Estimate the body surface area (BSA) involved
Throat culture for group A -hemolytic
Streptococcus infection
Determination of human immunodeficiency virus
serostatus in at-risk individuals with sudden
onset of psoriasis
Rheumatoid factor determination, erythrocyte-
sedimentation rate, and uric acid level testing if
joint inflammation is present
Skin biopsy, read by a dermatopathologist if any
doubt exists about the diagnosis of psoriasis
Potassium hydroxide prep to rule out tinea of the
skin or nails
Guttate psoriasis: drug eruption, pityriasis rosea, or
secondary syphilis
Small scaling plaques: seborrheic dermatitis, lichen
simplex chronicus, psoriaform drug eruption, tinea
corporis, or mycosis fungoides
Large geographic plaques: tinea corporis, or mycosis
fungoides
Scalp psoriasis: seborrheic dermatitis or tinea capitis
Inverse psoriasis: tinea, candidiasis (see image),
intertrigo, extramammary Paget disease, glucagonoma
syndrome, Langerhans-cell histiocytosis, or Hailey-
Hailey disease
Nail involvement: onychomycosis
Treatment
The aim of treatment is to bring the psoriasis into remission
or an inactive state. Pharmacologic therapy may be
topical, photo, or systemic, depending on the type and
extent of disease. Treatment may be stopped when
lesions can no longer be felt as raised, even if residual
erythema, brown hyperpigmentation, or
hypopigmentation persists.
Nonpharmacologic
Stress-reduction techniques
Limited sun exposure
Weight-loss counseling
Smoking cessation
Emotional and psychological support
Good skin care, with an emphasis on keeping the skin
well hydrated and lubricated
Treatment
Pharmacologic: topical therapy
Most patients with localized plaques on the trunk and extremities can
be treated with the use of topical therapy alone
Therapy consists of topical fluorinated glucocorticoids in an ointment
base, applied once scales have been removed after soaking in water
Treatment for small lesions consists of intradermal injections with
triamcinolone suspension
Vitamin D analogues and Tazaroten (topical retinoid) are other
alternatives
Pharmacologic: phototherapy
Narrow-band UVB and psoralen and long-wave UV radiation (PUVA,
also called photochemotherapy) are used
Treatment consists of two or three sessions per week
Most patients respond to treatment after 19 to 25 sessions
Pharmacologic: systemic therapy
Oral retinoids are most effective when combined with
photochemotherapy
Methotrexate is not used in young patients because of its liver toxicity
Cyclosporine, which is nephrotoxic, is only used in patients without risk
factors
Monoclonal antibodies and fusion proteins, under development, are
used only by dermatologists at this time
Education
Explain that psoriasis is a chronic condition that can be
controlled but not cured
Reassure the patient that the disease is not contagious
Because most patients feel that psoriasis adversely
affects their quality of life, give them the opportunity to
discuss these feelings
Offer encouragement and assistance in smoking
cessation, weight loss, and development of an exercise
regimen
Teach stress-reduction techniques and help the patient
identify stressors
Advise the patient to avoid trauma to the skin that may
cause psoriasis to "Koebnerize" to areas injured during
invasive activities such as shaving
Explain the complications of misuse of topical
corticosteroids
Follow-Up
Follow up 2 to 3 weeks after therapy is initiated,
then see the patient to check for side effects
every 2 to 3 months
Reinforce the need for compliance with
prescribed treatment regimens
Because this is a chronic, recurrent disorder,
offer patients practical counseling at each visit
on ways to deal with the disorder
If you are not concerned that a patient will
overuse or misuse topical medications, provide
ample refills so the patient can control the
condition on his or her own
Referral
Refer patients whose psoriasis is difficult to
manage or unresponsive to treatment after 2 to
4 weeks to a dermatologist for management
Refer all pediatric patients and adult patients
with psoriatic involvement of more than 15% of
the BSA or with moderate to severe disease to a
dermatologist for management; many are
candidates for phototherapy or systemic therapy
Consider referring the patient to such sources of
patient information as the National Psoriasis
Foundation and eMedicine's Skin, Hair, and
Nails Center
Introduction
Alopecia is the loss of hair from any part of
the body where hair normally grows. The
condition can be extremely distressing to
the affected person, so careful, sensitive
assessment and management are
important.
In this lesson, we'll cover the presentation,
diagnosis, and management of the
nonscarring forms of this condition.
Incidence
Hair occurs everywhere on the body except for the lips, palms, and
soles. There are approximately 120,000 hairs on the scalp and 5
million fine vellus hairs all over the body.
Hair loss is a common and distressing symptom that affects men
and women of all ages
Androgenetic alopecia (common balding) is the most common cause
of hair loss, typically beginning anytime after puberty, when
androgens are synthesized
In the United States, about half of all men and women show some
expression of androgenetic alopecia by age 40
Alopecia areata (patchy balding; see image) is found in 1.7% of the
population
The first patch appears in 60% of patients with alopecia areata
before age 20
Familial incidence of alopecia areata is 37% in patients who had
their first patch by age 30 and 7.1% in those whose first patch
appeared after age 30
Women commonly experience postpartum hair loss (telogen
effluvium)
One third to one half of all cases of alopecia areata start by age 20
Pathophysiology
Hair is composed of keratin, the same material that makes up the fingernails and
toenails
With baldness, hairs are not actually lost; instead, they become vellus
Each hair follicle perpetually goes through three stages in the growth cycle:
catagen (transitional phase), telogen (resting phase) and anagen (growing
phase)
Alopecia is classified on the basis of distribution (generalized versus localized)
and scarring potential (scarring, or cicatricial, versus nonscarring, or
noncicatricial)
Nonscarring hair loss appears to be caused by injury resulting from a physical or
physiologic agent or immunologically mediated inflammation. In the section of the
hair follicle known as the bulge, where stem celllike activity controls follicle
regeneration and cycling; if this area is permanently injured, hair will not regrow
Most localized, nonscarring hair loss is hereditary and is caused by androgens
present in both men and women (see image)
The immune system can also cause hair loss
Hair loss resulting from certain causes can be reversible when those causes are
eliminated
Localized, nonscarring alopecia usually results from changes in follicle cycling
Types of generalized, nonscarring alopecia include telogen effluvium and anagen
effluvium
Scarring alopecias have other causes (e.g., discoid lupus, lichen planopilaris,
folliculitis decalvans)
Hair loss that occurs rapidly can be a sign of serious disease
History
Current complaint
Onset, duration, and severity of symptoms
Rate and timing of hair loss
Local or generalized hair loss
Other scalp symptoms (e.g., itching, tingling, burning)
Medical history
Ask about crash diets, post-pregnancy status, trauma,
infection, tinea capitis, collagen vascular disease,
neoplasms, and thyroid disease
Assess drug allergies
Menstrual and reproductive history
Current birth-control method
Recent physical trauma
Recent weight loss or gain
Recent febrile illness
History
Family history
Male- or female-pattern baldness
Arthritis
Medication history
Prescription or over-the-counter (OTC) medications,
vitamins, or herbal supplements, some of which can
cause alopecia
Dieting
Increased stress
Use of curlers, hair dyes, straightening agents, or hot
combs
Impact of disease on patient and family with respect to
issues of disfigurement, occupational disability, and
psychosocial impact
Examination
Note the presence of scars, erythema, scaling, inflammation,
follicular plugging, folliculitis, bogginess, or induration
Observe the density and distribution of hair-focal, diffuse, and male-
pattern and female-pattern loss
Examine the hair shaft for caliber, length, shape, and fragility (in the
image shown here, a normal hair fiber under polarizing microscopy,
the medulla is blue, the cortex is pink-red, and the cuticle is yellow)
Look for a well-circumscribed oval or circular nonscaly patch of
nonscarring hair loss with proximally tapering exclamation-point
peripheral hairs (alopecia areata)
Palpate the thyroid to assess size, nodularity, and vascularity
Use the "pull test" technique for hair loss
Determine whether eyebrow, eyelash, axillary, or body hair is
affected and examine hair density in other areas (e.g., face,
extremities)
Examine the fingernails
Conduct a complete physical examination, if one is indicated on the
basis of the history and findings of the scalp examination
After ruling out other causes of hair loss,
consider laboratory tests for secondary
conditions
For female alopecia with symptoms of
hyperandrogenism, check total testosterone,
free testosterone, dehydroepiandrosterone
sulfate (DHEA-S), or prolactin levels
For male and female alopecia without symptoms
of hyperandrogenism, consider other tests to
rule out thyroid disease, syphilis, anemia,
autoimmune disease, fungal or other infection,
tinea capitis (see image), and neoplasm or
inflammatory process
Nonscarring local alopecia: androgenetic
or alopecia areata
Generalized nonscarring alopecia: telogen
and anagen effluvium caused by
medications, illness, or pregnancy
Trichotillomania or traction alopecia (see
image; caused by tight braiding)
Scarring alopecia (discoid lupus or
folliculitis decalvans)
Treatment
Nonpharmacologic
Cosmetic measures (e.g., changes in hairstyle, wigs, extensions,
hairpieces, and scarves)
Ceasing to wear tight braids, buns, or hairpins
In chemical/allergic causes, avoidance of the identified sources
Laser therapy is showing some promise
Pharmacologic
In secondary causes of alopecia, treat the underlying medical
condition
For trichotillomania, consider behavioral therapy, antianxiety or
antidepressant medication, or a combination, preferably under the
supervision of a mental-health professional
Treat alopecia areata with steroid intralesional scalp injections,
topical steroids, or anthralin or systemic corticosteroids
Consider a hair-growth stimulant such as minoxidil (Rogaine) or
finasteride (Propecia)
Also consider monotherapy or synergistic use, such as adding
estrogen to any therapy (women) or adding tretinoin (Retin-A)
topical as an adjunct toor synergistically withminoxidil (men and
women)
Education
Educate the patient about cause and treatment of hair loss, if known
Discuss the use of medication for regrowth in nonscarring alopecia
Explain the costs and side effects of drug therapies
Make patient aware of transplants (more effective in men) under the
appropriate conditions
Give advice on wigs and hairpieces
Tell the patient to avoid caustic agents in the hair and to avoid
alkaline shampoos
Instruct the patients to comb his or her hair and avoid excessive
brushing
Warn the patient against excessive dieting
For the patient with positive findings of the hair-pull test, provide
anticipatory guidance during the period of extensive hair loss as the
cycle reestablishes itself and regrowth begins; explain that changes
take time and encourage the patient to stick with the regimen for 3 to
6 months
Help the patient and family come to terms with hair loss
Help the patients evaluate his or her therapy, including willingness
to adhere to the treatment regimen and awareness of quality of life
and satisfaction with results
Follow-Up and Referral
Follow-up
Follow up monthly with patients receiving intralesional
steroid injections for alopecia areata until the condition
has resolved or treatment is no longer indicated
Follow up with other patients every 3 to 6 months
Adjust therapy and identify causes (e.g., compliance or
finances) if response is inadequate
Referral
Refer the patient with scarring alopecia or the patient in
whom diagnosis is unclear to a dermatologist for
evaluation and management
Refer the patient to an endocrinologist if endocrine
disease is suspected
Introduction
In this lesson we'll review three common
skin cancers: basal-cell carcinoma,
squamous-cell carcinoma, andthe most
seriousmalignant melanoma. The family
nurse practitioner plays a key role in
minimizing the risks of skin cancer through
patient education, early recognition of
cancer, and timely referral to a
dermatologist for management.
Incidence
Benign or premalignant lesions are seborrheic keratosis, actinic keratosis,
and nevi. Malignant lesions include basal-cell carcinoma (BSC), squamous-
cell carcinoma (SCC), and melanoma.
Seborrheic keratosis mainly affects men age 30 and older
Actinic keratosis is common in fair-skinned people in middle to old age
Nevi are more common in whites with a family history of nevi
Half of all new cancers are skin cancers
Both BSC and SCC, often referred to as nonmelanoma skin cancer
(NMSC), have cure rates of more than 95% if detected and treated early
SCC accounts for about 20% of NMSC cases
Melanoma is more common than any nonskin cancer among people
between ages 25 and 29
The incidence of all types of skin cancer have been increasing in the United
States over the last few years, likely because of more leisure activity in the
sun, the popularity of tanning salons, and a decrease in the protective
ozone layer
One in six Americans is affected by skin cancer at some point
The lifetime risk of malignant melanoma is 1:70; the risk in 1960 was 1:1500
One's lifetime risk of dying of malignant melanoma is 0.35% for men and
0.21% for women
Malignant melanoma is the eighth most common cancer in the United
States, accounting for 1% to 2% of cancer deaths
Whites are at 10 times greater risk than blacks and seven times greater risk
than Hispanics
Pathophysiology
It is not known exactly what triggers the conversion of a
precancerous lesion to a cancerous one, but a variety of
factors increase the likelihood of skin cancer:
History of sunburn or intense, intermittent sun exposure
Living or spending extended periods at high altitude (the
atmosphere provides less protection) or near the
equator, where the sun is more intense
Smoking
Immunosuppression
Exposure to industrial carcinogens
Light hair (red or blond) and blue eyes
White race
Inability to tan (more likely to sunburn or freckle)
Age
Radiation treatment and radiograph exposure
History
Current complaint
Duration of lesions
Changes in lesions over time, especially those that are
quick or aggressive
Systemic symptoms (e.g., fatigue, weight loss)
Signs or symptoms of suspected noncancerous and
cancerous lesions
Patient's coloration
Medical history
Chronic illness
Immunosuppression
Previous skin cancers or precancerous lesions (and their
treatment)
History
Medication history
Corticosteroids
Medicines containing arsenic
Family history
Melanoma
Familial atypical mole and melanoma syndrome
(FAMMS), which puts the patient at a lifetime risk
nearing 100% for the development of melanoma
Occupation involving exposure to the sun, radiation, or
industrial chemicals
Outdoor leisure activities and hobbies
Sunbathing or use of a tanning parlor
Use of sunscreens
Examination
Have the patient undress; provide draping for maximum privacy
Ask the patient to remove concealing cosmetics for good
observation of a lesion, if necessary
Inspect the entire body for lesions
Look for characteristics of BSC, SCC, lentigo maligna melanoma,
superficial spreading melanoma, acral lentiginous melanoma,
amelanotic melanoma, seborrheic keratosis, actinic keratosis, and
nevi
Use the ABCDE approach to skin inspection; positive findings
should inspire a high index of suspicion for malignant melanoma
If lesions were photographed during previous evaluations, compare
and contrast those images with the current findings
Note atypical nevi and the existence of more than 50 moles larger
than 2 mm in diameter
Check the scalp, mucous membranes, and the lymph nodes
draining the area of any lesions found
Use an epiluminescence microscope to magnify and illuminate
lesions
Skin biopsy (usually performed by a
dermatologist), particularly when certain signs
are present
Seborrheic keratosis
Traumatized nevus
Lentigo
BSC
SCC
Malignant melanoma
Hemangioma
Pigmented actinic keratosis
Treatment
Nonpharmacologic
Remove noncancerous lesions with the use of
electrocautery or liquid nitrogen
Before referring a patient with a cancerous lesion or one
suspected of being malignant for removal, photograph all
lesions and record the location, name, and size of each
lesion, along with the date, in the patient's record
Excisional biopsy and staging may be based on tumor
thickness in millimeters to the deepest penetration of the
tumor (Breslow measurement) or histologic microstaging
(Clark's level); the depth and margins of the surgical
excision are based on these two assessments
Removal of sentinel lymph nodes is also common
Treatment
Pharmacologic
Imiquimod 5% cream (Aldara) has been
shown in early trials to be an effective and
relatively safe nonsurgical alternative in
the treatment of superficial BSC
The use of interferon is controversial
Chemotherapy may be prescribed for
melanoma
Education
Explain that after lesions have been removed,
the patient may note hypopigmentation in the
area where they were
Tell the patient to perform a skin self-
examination every month and report changes to
the health-care provider; encourage family
members to assist in the inspection
Stress the importance of contacting the health-
care provider if certain signs are noticed
Provide guidelines for protection from sun
exposure
Warn women with melanoma lesions larger than
1 mm in diameter to avoid becoming pregnant
for 2 years; the risk of recurrence is greater
during that period
Follow-Up and Referral
Follow-up
Because new lesions of actinic keratosis often
occur, follow up every 6 months
Closely monitor any patient with melanoma
lesions, ordering chest radiographs, liver-
function test, complete blood count, and
computed tomography as clinically indicated
Referral
Refer the patient with a cancerous or suspected
malignant lesions to a dermatologist for removal
of lesions and for biopsy and pharmacologic
treatment
Introduction
In this lesson, we'll cover the following viral
skin disorders commonly seen in the
primary-care setting:
Warts
Herpes simplex
Herpes zoster
Molluscum Contagiosum: Incidence
Consists of benign viral skin lesions with a
predilection for the face, trunk, arms, and legs in
children and the genitalia and groin in adults
Autoinoculable lesions are spread by wet skin-
to-skin contact; in adults this typically involves
sexual transmission, explaining why lesions are
usually limited to the genitalia and inner thighs
More common in male subjects than in women
and girls
Common in subjects with acquired immune
deficiency syndrome (AIDS) and cancer; in
these individuals, lesions are larger and more
widespread
Molluscum Contagiosum: Pathophysiology
DNA virus of a poxvirus of the Molluscipox virus genus
(see image) penetrates skin that has incurred minor
trauma or excoriation
Periungal lesions can spread through autoinoculation as
a result of cuticle biting or shaving
Children and regular swimmers may be exposed in the
pool (concrete abrades skin, which is then irritated by
chlorinated water)
The incubation period ranges from 2 weeks to 2 months
In individuals with normal immune function, lesions may
persist for as long as 6 months and then regress
spontaneously
In immunocompromised patients, spontaneous
regression does not occur, and aggressive treatment is
required
Molluscum Contagiosum: History
Current complaint
Onset and location of lesions
Prodromal symptoms
Pain associated with secondary infection of
lesions
Symptoms associated with the onset of lesions
Relieving and exacerbating factors
Exposure to an infected person
Primary or recurrent case
Signs and symptoms of gingivostomatitis
Molluscum Contagiosum: History
Medical history
Previous skin problems (and their treatment)
Immunocompromise
Chronic illness
Allergies
Varicella
Family history
Epidermodysplasia verruciformis (EDV)
Varicella
Concern about appearance
Time spent in a swimming pool

Molluscum Contagiosum: Physical
Examination
Examination
Examine the lesions for characteristic
location, distribution, and appearance
Use illumination and magnification to
identify surface characteristics
Check for lymphadenopathy at lesion sites
that may be draining
Molluscum Contagiosum: Physical
Examination
Paring or dbridement and study of keratotic
plug extruded from center of lesion; Giemsa
staining reveals inclusion bodies
Testing for sexually transmitted diseases in
adults with genital lesions
Basal-cell carcinoma
Milia (see image)
Infected skin lesions
Warts
Molluscum Contagiosum: Treatment
Nonpharmacologic
Freezing of lesions with the use of liquid
nitrogen
Incision of papules and expression of contents
Curettage
Pharmacologic
Topical cantharidin
Imiquimod cream
Tretinoin cream
Cimetidine for children with widespread lesions
Molluscum Contagiosum: Education
Explain that the condition is self-limiting and
often disappears completely without treatment in
6 to 24 months
Teach the patient or caregiver that the condition
can spread through sexual or other skin-to-skin
contact and explain that autoinoculation is
common
Explain to the immunosuppressed patient or his
or her caregiver that the lesions may be
recalcitrant
Stress that the condition may recur but that this
is uncommon
Molluscum Contagiosum: Follow-
Up and Referral
Follow-up
Reevaluate the patient 4 to 6 weeks after
treatment to evaluate lesions
The condition can persist for as long as 24
months; continue to monitor the patient
Referral
Immediately refer any patient with lesions
affecting more than two dermatomes or
with ophthalmic involvement
Warts: Incidence
Warts are benign tumors of the skin
caused by the DNA human papillomavirus
(HPV). They are painless and appear on
hands or feet as a well-circumscribed
thickened lesion.
More common in children (7%-10% of the
population) between the ages of 12 and 16
years
More common in female patients than in
males
Warts: Pathophysiology
Various types of warts exist, including the common wart,
the flat wart, and the plantar wart
Susceptibility is increased in people taking
immunosuppressant agents, those who spend time in
locker rooms, and in those with atopic dermatitis
Butchers, meatpackers, and fish handlers are
susceptible to warts on their hands and forearms that
seem to be related to prolonged immersion in water and
microtrauma associated with the processing of meats
and fish
Health-care professionals may be exposed to HPV in a
plume of smoke during laser or electrosurgical
procedures
Heredity by way of autosomal recessive inheritance
pattern is a factor in epidermodysplasia verrucifomis
(EDV)
Warts: History
Current complaint
Location of warts
Onset of symptoms
Primary or recurrent
Prodromal symptoms
Pain associated with secondary infection of
lesions
Symptoms associated with the onset of lesions
Exposure to people infected with HPV
Signs and symptoms of gingivostomatitis
Warts: History
Medical history
Skin problems (and treatments)
Immunocompromise
Chronic illness
Allergies
Varicella
Family history
EDV
Varicella
Warts: Physical Examination
Examination
Examine warts for characteristic location,
distribution, and appearance
Use illumination and magnification to
identify surface characteristics
Check for lymphadenopathy at sites of
potentially draining lesions
Diagnosis is usually based on clinical
findings
Warts: Physical Examination
Differential diagnosis: warts
Seborrheic keratosis (see image)
Actinic keratosis
Squamous-cell carcinoma
Differential diagnosis: plantar warts
Callus
Corn
Keratosis
Exostosis
Warts: Treatment
Nonpharmacologic
Watchful waiting, unless warts cause pain
Cryotherapy
Removal with the use of electrocautery, laser ablation, or
curettage
Occlusion with duct or waterproof tape
Foot soaks to help soften and ease removal of plantar
warts
Pharmacologic
Salicylic acid, daily transdermal delivery for 6 weeks
Trichloroacetic acid
Topical retinoids (for flat warts)
Imiquimod cream
Warts: Education
Explain that warts in epidermodysplasia may become
malignant
Reassure the patient that complete resolution is
expected with or without treatment
Teach the patient to cover a wart being subjected to
cryotherapy to prevent the escape of fluid from the
wound
Tell the patient that he or she can help prevent warts by
using personal shower shoes in locker rooms
Explain that autoinoculation and scarring are possible,
that injury to a nail with warts may result in nail
deformity, and that plantar warts that scar may cause
chronic discomfort when weight is being borne by the
foot
Warts: Follow-Up and Referral
Follow-up
Follow-up is not usually required for warts
Referral
Immediately refer any patient with lesions
affecting more than two dermatomes or
with ophthalmic involvement
Herpes Simplex: Incidence
Herpes simplex is a viral disease associated with the herpes
simplex virus (HSV). The condition usually manifests as a group of
vesicular lesions arising on an erythematous base on keratinized
skin or a mucous membrane.
Most common in children and young adults
Four of five individuals harbor HSV-1, which affects sites above the
waist
One in six individuals harbors HSV-2, which mainly affects sites
below the waist
Risk is increased with irritation of the skin or mucosa (e.g., by UV
radiation)
Altered hormonal milieu (e.g., menstruation) increases the likelihood
of a herpes outbreak
Fever and the common cold both increase risk of an outbreak
Newborns are especially susceptible
Occupational exposure puts many people at risk
Previous HSV infection is a predisposing factor
Immunocompromising factors increase risk
Herpes Simplex: Pathophysiology
HSV is transmitted by way of skin-to-skin,
skin-to-mucosa, or mucosa-to-skin contact
After exposure, the virus replicates in
epithelial cells, contributing to lysis
HSV then ascends the peripheral sensory
nerves and enters the sensory nerve root,
where latency is established
Incubation ranges from 2 to 20 days, with
an average of 6 days
Herpes Simplex: History
Current complaint
Location of lesions
Onset of symptoms
Primary or recurrent episode
Pain associated with secondary infection
of lesions
Exposure to an infected persons
Common triggers for recurrent outbreaks
(e.g., stress, fever, UV light exposure,
trauma, menstruation)
Herpes Simplex: History
Medical history
Skin problems (and their treatment)
Immunocompromise
Chronic illness
Allergy
Varicella
Family history
EDV
Varicella
Number of sexual partners
Use of barrier contraception
Herpes Simplex: Physical Examination
Conduct a comprehensive skin examination. Remember to wear
gloves.
Examination
Examine lesions for characteristic appearance
Use illumination and magnification to identify surface characteristics
carefully
Look for lesions affecting the oral mucosa, the vermilion border of
the lip, the face, and the pharynx (herpes labialis)
Note increased salivation, irritability, fetid breath, and tender cervical
nodes
Check for lymphadenopathy at potentially draining lesion sites
Check temperature
Check the fingertips for vesicles (herpetic whitlow)
If vesicles consistent with herpes are observed on the tip or side of
the nose, check the patient's visual acuity
Assess the patient's eyes for infection and note photophobia,
lacrimation, discharge, and preauricular adenopathy
Herpes Simplex: Physical Examination
Tzanck smear to detect multinucleate
giant epithelial cells
Viral culture to help distinguish HSV-1
from HSV-2; results take 3 to 7 days
Polymerase chain reaction
Contact dermatitis
Impetigo (see image)
Conjunctivitis (with ocular involvement)
Herpes Simplex: Treatment
Nonpharmacologic
Apply cool dressings moistened with Domeboro or Burows
solution, 30 minutes per dressing, three times daily
Intravenous hydration may be required for gingivostomatitis
Pharmacologic
Several preparations are available with which to treat oral
lesions
For lip lesions, apply ice or lidocaine 2% and protect with a
lip sunscreen such as Blistex
Prescribe acetaminophen (Tylenol) for pain
Acyclovir antiviral ointment (Zovirax, by prescription) can be
applied with the use of a finger cot or glove every 3 hours
for 7 days
Nonprescription docosanol (Abreva) can be applied as
soon as the patient notes symptoms, five times a day, until
lesion is healed
Zovirax and the oral antiviral famciclovir (Famvir) are
approved to treat herpes in immunosuppressed persons
Herpes Simplex: Education
Warn the patient about the risk of transmitting
the disease through direct contact (e.g., kissing,
oral sex)
Explain the natural history of the disease and
emphasize the potential for recurrence and
asymptomatic viral shedding
Encourage good handwashing
Encourage the patient to start treatment when
prodromal symptoms appear before a recurrent
episode
Explain that prevention and treatment can
prevent complications such as herpes
encephalitis, meningitis, and pneumonia
Herpes Simplex: Follow-Up and Referral
Follow-up
No follow-up is indicated for uncomplicated herpes
simplex infection unless secondary infection occurs
If secondary infection occurs, follow up weekly with
patients with normal immune systems and 2 to 3 days in
patients who are immunosuppressed, elderly, or
debilitated
Monitor renal function in patients taking acyclovir
Referral
Consult with an infectious-disease or HIV specialist in
the case of an immunocompromised patient with herpes
Immediately refer the patient with lesions affecting more
than two dermatomes or with ophthalmic involvement
Herpes Zoster: Incidence and Pathophysiology
Herpes zoster is an acute dermatologic infection caused by
reactivation of a dormant varicella zoster (chickenpox) virus. The
infection presents in three stages: prodrome, active, and chronic.
The dermatologic lesions are painful, grouped, unilateral
dermatomal eruptions.
Incidence
Increases with aging
Herpes zoster affects both male and female individuals
Between 10% and 20% of the population is infected at some point
Immunosuppression increases risk, as do cancers such as
leukemia and lymphoma, spinal surgery or radiation, and a
history of chickenpox (varicella)
Pathophysiology
Herpes zoster is caused by reactivation of dormant varicella virus
in the dorsal root ganglia
Reactivation may be idiopathic or associated with stress
Herpes Zoster: History
Current complaint
Painful vesicular lesions, distributed in a
dermatomal manner
Prodromal symptoms
Pain associated with secondary infection
of lesions
Exposure to an infected person
Primary or recurrent case
Herpes Zoster: History
Medical history
Previous skin problems
Details about past treatments
Immunocompromise
Chronic illness
Allergy
Varicella
Family history
EDV
Varicella
Herpes Zoster: Physical Examination
Examination
Examine lesions for characteristic appearance
Use illumination and magnification to identify
surface characteristics carefully
Check for lymphadenopathy at potentially
draining lesion sites
Assess the patient for regional adenopathy
If vesicles consistent with herpes are observed
on the tip or side of the nose, check the patient's
visual acuity
Check for ocular infections and note
photophobia, lacrimation, discharge, or
preauricular adenopathy
Check the patient's temperature
Herpes Zoster: Physical Examination
Tzanck smear to reveal multinucleate giant
epithelial cells
Viral culture; results in 3 to 7 days
Polymerase chain reaction (PCR) test
Erythema multiforme
Pemphigus (see image)
Aphthous ulcers
Herpangina
Hand-foot-mouth disease
Herpes Zoster: Treatment
Nonpharmacologic
Compresses wet with Burows solution or
cool tap water may be applied for as long
as 30 minutes, several times a day
Topical alternatives include calamine and
starch shake lotions
Although such infection is rare, patients
with active and potentially infectious
lesions should be kept away from
neonates, pregnant women, people who
have not had chickenpox, and
immunosuppressed persons
Herpes Zoster: Treatment
Pharmacologic
Use nonsteroidal antiinflammatory drugs to relieve pain
and fever
Antiviral therapy is indicated for herpes zoster in any
immunosuppressed person, adults at greatest risk for
postherpetic neuralgia (>55 years), and younger ones
with acute pain
Corticosteroids reduce acute pain and can be used for
immunocompetent patients at an initial dose of 60
mg/dL, tapered over 3 weeks
For postherpetic neuralgia, topical capsaicin cream can
be used four times a day for 21 days after all vesicles
have resolved
Regional nerve blocks and amitriptyline (2575 mg
nightly) are other alternatives for postherpetic neuralgia
Herpes Zoster: Education
Prepare the patient for the expected course of the
disease and explain that acute rash resolves within 14 to
21 days
Warn the patient that he or she can transmit the virus as
varicella (chickenpox) to susceptible people, including
newborns, pregnant women, and those who have not
been previously infected
Note that the varicella vaccine in a noninfected person
can help prevent herpes zoster
Explain that complications of herpes zoster include
postherpetic neuralgia (mostly in people older than 50
years), ocular involvement (commonly occurs in people
older than 40 years), meningitis, encephalitis,
pneumonia, Guillain-Barr syndrome, large-vessel
arteritis, and systemic dissemination
Encourage good hand-washing
Encourage the patient to start treatment when prodromal
symptoms appear before a recurrent episode
Herpes Zoster: Follow-Up and Referral
Follow-up
Follow up weekly with patients with normal
immune systems and every 2 to 3 days in
patients who are immunosuppressed, elderly, or
debilitated
Monitor renal function in patients taking acyclovir
Referral
Consult with an infectious-disease or HIV
specialist in the case of any
immunocompromised patient with herpes
Immediately refer the patient with lesions
affecting more than two dermatomes or with
ophthalmic involvement

Dermatology

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