Introduction to Dermatology
in the
Young Adult
Jennifer Nevas, CRNP
Philadelphia VA Medical Center,
Department of Dermatology
Benign Skin Lesions
• Warts
• Molluscum Contagiosum
• Dermatofibroma
• Epidermal inclusion cysts
Warts
• Etiology: Human papilloma virus (HPV)
• Common in children, adolescents, and immunosuppressed
individuals
• Presentation: verrucous topped papules
• DDx: cutaneous horn, SK, SCC
• Lesions may spontaneously resolve
• Treatment (nongenital warts):
– Cryotherapy (LN2), topical salicylic acid, surgical removal
– Refer if no improvement with topicals
• Treatment (genital warts):
– Cryotherapy, imiquimod, Podofilox, surgical removal
– Refer to derm (GI if anal involvement) if no improvement
with topicals
Molluscum Contagiosum
• Etiology: benign viral infection with a DNA poxvirus
• Most common in children – infection through direct skin-to-
skin contact or indirect skin contact w/ fomites (bath towels)
• In adults, molluscum are sexually transmitted
• Presentation: ~2-5mm, discrete, nontender, flesh-colored,
umbilicated papules
- Generally asymptomatic
- Most common on the face, trunk, and extremities in
children and on the genitalia in adults
• DDx: Milia, keratosis pilaris, wart
• Treatment: spontaneously resolution can occur or can treat
with LN2, curettage, salicylic acid, topical tretinoin, or
imiquimod
- Refer if no improvement with topicals and LN2 needed
Umbilicated
papules
Umbilicated
papules
Dermatofibroma (DF)
• Etiology: unknown
• Can develop at any age, but usually young adulthood; more
common in women
• Presentation: Usually solitary (0.5 to 1 cm) lesions on extremities
– Overlying skin color can range in color
– May feel like a small pebble fixed to the skin surface
– Tethering of overlying epidermis to the underlying lesion with
lateral compression is called the “dimple sign”
– Generally asymptomatic, but can be tenderness or itch
– Historically attributed to a trauma to the skin (e.g., bug bite)
• DDx: Nevus, keloid, melanoma, SCC, prurigo nodule
• Treatment: None, can refer for ILK or excision if the lesion is very
symptomatic
Dimple sign
Epidermal Inclusion Cyst (EIC)
• Etiology: result from the proliferation of epidermal cells
within a circumscribed space of the dermis
• Can occur at any age but most common in 3rd and 4th
decades; twice as common in men
• Presentation: Appear as flesh–colored-to-yellowish, firm,
round, mobile nodules often with central punctum (pore)
– Discharge of a foul-smelling “cheese-like” material is
common
– Occur most frequently on the face, scalp, neck, and trunk
– Usually asymptomatic but may become inflamed or infected
• DDx: lipoma, milia
• Treatment: None required, can refer for tx with ILK or
excision (refer larger lesions to general surgery)
EIC with central punctum
Epidermal Inclusion Cyst, inflamed
• Cyst rupture due to trauma
 inflammation
• Can become infected
• Treatment:
– warm compresses
– intra-lesional steroids
– I & D
– +/- oral antibiotics
• Do NOT squeeze or
excise at this time!
Common Skin Disorders
• Tinea
• Tinea Versicolor
• Vitiligo
• Scabies
• Herpes
• Folliculitis
• MRSA
• Acne
• Atopic
dermatitis/eczema
• Contact dermatitis
• Keratosis Pilaris
• Pityriasis Rosea
• Seborrheic dermatitis
• Psoriasis
• Intertrigo
Atopic Dermatitis
• Etiology: pruritic disease of unknown origin; evidence indicates that
genetic factors are important
• Prevalence - 15-30% of children; 2-10% of adults
• Male-to-female ratio is 1:1.4; affects persons of all races
• 85% of cases occur in 1st
year of life; 95% occur before age 5
• Presentation: incessant pruritus
– ill-defined, erythematous, scaly, and crusted (eczematous) patches and
plaques
– Xerosis and lichenification is seen in children and adults
• DDx: contact derm, psoriasis, CTCL, scabies, TV, seb derm
• Treatment: moisturization, topical steroids, topical calcineurin
inhibitors, antihistimines, phototherapy, mild soaps & detergents,
cotton clothing; methotrexate, prednisone, or cyclosporine for
severe cases; antibiotics or antivirals for secondary infections
• Refer if symptoms persistent despite tx or if weird presentation
Atopic Dermatitis
Major Features
 Pruritus
 Typical morphology and
distribution
 Facial and extensor
eczema in infants and
children (though can have
flexural involvement in
children)
 Flexural eczema in adults
 Dermatitis—chronic or
chronically relapsing
 Personal or family history or
atopy—asthma, allergic
rhinitis, atopic dermatitis
Minor Features
 Xerosis
 Ichthyosis/keratosis pilaris/hyperlinear palms
 IgE reactivity (immediate skin test reactivity; + RAST)
 Elevated serum IgE
 Early age of onset
 Tendency for cutaneous infection (ie. Staph, HSV)
 Nonspecific hand/foot dermatitis
 Nipple eczema
 Cheilitis
 Conjunctivitis (recurrent)
 Dennie-Morgan infraorbital fold
 Keratoconus
 Cataracts
 Orbital darkening
 Facial pallor/facial erythema
 Pityriasis alba
 Itch when sweating
 Wool intolerance
 Perifollicular accentuation
 Food hypersensitivity
 Influenced by environmental & emotional factors
 White dermatographism or delayed blanch to
cholinergic agents
Need: 3 Major + 3 Minor
Secondarily infected: Impetiginized
Hygiene Changes/Lubrication
• Avoid barrier disruption
– Harsh soaps
– Washcloths
– Bathing too frequently
• Moisturize, moisturize, moisturize!
– The more the better
– Soak and smear technique – soak in tub of luke
warm water for 20 minutes, pat dry, and
liberally apply topical medication or lubricant
Topical Treatment
• Topical steroids – may alternate high potency
with mid potency to reduce risk or use on
weekends only
– Risks of overuse of topical steroids include: atrophy,
striae, telangiectasias, hypopigmentation
(temporary), can have systemic absorption if using
long-term on a large body surface area
• Topical calcineurin inhibitors (steroid sparing
agents)
– Tacrolimus (Protopic) ointment
– Pimecrolimus (Elidel) cream
Steroid Classes
• 7 classes based on vasoconstrictive properties
• Note: ointment form is stronger than cream form
– Class 1 = superpotent
• Clobetasol propionate
• Betamethasone dipropionate
– Class 3 and 4 = mid-strength
• Fluocinonide
• Betamethasone valerate
• Triamcinolone
– Class 6 and 7= low potency
• Fluocinolone
• Desonide
• Hydrocortisone
Scalp, palms, soles
Trunk, extremities
Face, genitals,
intertriginous areas
Allergic Contact Dermatitis
• Etiology: delayed type of induced sensitivity resulting from cutaneous
contact with a specific allergen to which the patient has developed a
specific sensitivity
• ~25 chemicals are responsible for as many as one half of all cases
• Common culprits: Poison ivy, topical antibiotics (e.g., Neosporin,
neomycin, bacitracin), nickel, rubber gloves, hair dye, textiles,
preservatives, fragrances, benzocaine
• Presentation: pruritic papules and vesicles on an erythematous base
– Acute onset
– Geometric morphology (circles, lines, etc)
– Lichenified pruritic plaques may indicate chronic ACD
– Initial site of dermatitis often provides best clue regarding the potential cause
• DDx: drug rash, nummular dermatitis, seb derm, tinea, urticaria
• Treatment: avoid offending agent, topical steroids or calcineurin
inhibitors, antihistamines, cool soaks, emollients, oral prednisone in
severe cases, can refer for patch testing to help determine allergen
Keratosis Pilaris
• Etiology: benign, genetic disorder of keratinization of hair
follicles
• Affects nearly 50-80% of all adolescents and ~40% of adults;
often improves with age
• Presentation: small folliculocentric keratotic papules
(gooseflesh appearance)
• Most common on outer-upper arms and thighs
• Usually asymptomatic
• Worse in wintertime
• DDx: acne, folliculitis, atopic dermatitis, milia, lichen nitidus
• Treatment: none required but ammonium lactate lotion or
urea cream may help
Pityriasis Rosea
• Etiology: benign, self-limited disease; considered to be a viral exanthem
• More common in women, children, & young adults
• Presentation: typically begins with a solitary macule that heralds the
eruption (“herald patch”)
• This lesion is usually a salmon-colored macule that enlarges over a
few days to become a patch with a collarette of fine
• Within the next 1-2 weeks, a generalized exanthem usually
appears as bilateral and symmetric salmon-colored macules with
a collarette scale oriented with their long axes along cleavage lines
(creates classic Christmas tree pattern)
• Tends to resolve over a 6 week period, but variability is common
• DDx: syphilis (so important to check RPR if there are risk factors),
nummular dermatitis, psoriasis, lichen planus, tinea corporis
• Treatment: None required but can treat pruritus with topical steroids,
oral antihistamines, topical menthol-phenol lotions
• Refer if skin lesions not resolving in a few months
Seborrheic Dermatitis
• Etiology: related to a pathologic overproduction of
sebum; may involve an inflammatory reaction to the
yeast Malassezia
• Presentation:
– Erythema with greasy yellowish scale on the “T-
zone” of the face, scalp, behind the ears, central chest
– Dandruff
– Can affect intertriginous areas
• Usual onset occurs with puberty
• Worsens with changes in seasons, trauma, stress,
Parkinson disease, AIDS, certain medications
• DDx: Atopic or contact dermatitis, rosacea, perioral
dermatitis, tinea, impetigo
Treatment for Seborrheic Dermatitis
• Shampoo at least every other day (shampoos that contain
ketoconazole, salicylic acid, tar, selenium, sulfur, or zinc
are especially helpful) – leave on for 5 minutes before
washing off
• Clobetasol 0.05% solution or Derma-Smoothe/FS
(mineral/peanut oil + fluocinolone 0.1%) for severe flaking
on the scalp
• Ketoconazole 2% cream twice a day (for face, ears chest)
• Hydrocortisone 2.5% cream – short-term use during flares
• Tacrolimus ointment or pimecrolimus cream as steroid
sparing agents
Psoriasis
• Etiology: Multifactorial
disease that appears to be
influenced by genetic and
immune-mediated
components
• Presentation: Characterized
by red papules and plaques
with adherent silvery scale
• Triggers: Physical trauma,
stress, infection (Strep, HIV),
pregnancy, medications
Drugs that can Trigger Psoriasis
• NSAIDs
• Antibiotics
• Steroids
• Antimalarials
• Lithium
• ACE inhibitors
• Beta-blockers
• Calcium channel blockers
• Interferon
• Tetanus
• Antihistamines
For Each Clinic Visit
• Ask about joint pain
– 10% of patients have Psoriatic Arthritis (PsA)
(Refer to Derm or Rheum)
• Estimate body surface area (BSA)
– An average palm = 1%
– Disease Severity:
• Mild <5% BSA
• Moderate = 5-10% BSA (Refer to Derm)
• Severe >=10% BSA (Refer to Derm)
• Note – psoriasis is associated with cardiovascular
disease, smoking, alcohol, metabolic syndrome,
lymphoma, depression, suicide
Psoriasis Vulgaris
• Chronic and stationary - lesions can persist for years
• Distribution:
– Elbows
– Knees
– Scalp
– Lumbosacral
– Umbilicus
Koebner’s Phenomenon
• Occurs in 20% of patients
• Non-specific trauma can lead to formation of psoriasis in
the area of irritation
Inverse Psoriasis
• Involvement limited to skin fold regions
• Usually associated with minimal scaling
• Distribution: axilla, inframammary region, genitocrural
region, neck
• Often confused with intertrigo
Topical Treatments for Psoriasis
• Topical steroids
• Hydrocortisone 2.5% ointment (low strength) – good for short term
use on face, penis, and intertriginous areas
• Triamcinolone 0.1% ointment (medium strength)
• Clobetasol 0.05% ointment (high strength)
• Synthetic Vitamin D
• Dovonex (calcipotriene) cream – helps reduce scale
• Topical calcineurin inhibitors – steroid sparing
agents (good for face, penis, intertriginous areas)
• Protopic ointment
• Elidel cream
• Common treatment regimen
• calcipotriene bid Mon-Fri and clobetasol oint bid Sat-Sun for lesions
on trunk and extremities; hydrocortisone or calcineurin inhibitor for
face, penis, and intertriginous areas
Intertrigo
• Etiology: an inflammatory condition of skin folds resulting from heat,
moisture, and friction
• Often colonized by infection - usually candida but can also be
bacterial, fungal, or viral
• A common complication of obesity and diabetes
• Presentation: Erythema, cracking, and maceration with burning
and itching at sites in which skin surfaces are in close proximity
(axillae, perineum, inframammary creases, abdominal folds,
inguinal creases)
• DDx: contact dermatitis, seborrheic dermatitis, cellulitis, inverse
psoriasis, acanthuses nigricans
• Treatment: Barrier creams such as zinc oxide paste, compresses with
Burow solution 1:40 or dilute vinegar, absorbent powders and
moisture-wicking undergarments, exposing the skin folds to air,
topical antifungal agents for secondary infections (e.g., clotrimazole,
econazole, ciclopirox, miconazole, ketoconazole, nystatin)
Tinea aka “Ringworm”
• Etiology: superficial fungal infection of skin
• More common in preadolescents and in hot,
humid climates
• Presentation: scaly, ring-shaped,
erythematous plaque that enlarges and
displays central clearing; often mildly itchy
• Confirm diagnosis with KOH prep
• DDx: nummular dermatitis, granuloma
annulare, lupus, psoriasis, pityriasis rosea
Tinea Corporis
Tinea Pedis
Positive KOH
Tinea Incognito (Majocchi’s Granuloma)
• A deep folliculitis due to a cutaneous dermatophyte infection
• Two types:
1) Follicular type - secondary to trauma or topical corticosteroids
2) Subcutaneous nodular type - occurs in immunocompromised pts
Treatment of Dermatophytosis
• Topicals (localized disease)
– Azoles (ketoconazole)
– Allylamines (terbinafine)
– Applied to the lesion and at least 2 cm beyond this
area once or twice/day for at least 2 weeks,
depending on which agent is used
• Systemic (extensive disease, nail or scalp
involvement, Majocchi’s granuloma)
– Griseofulvin, itraconazole, terbinafine
– May consider referral to dermatology
Tinea Versicolor
• Etiology: benign superficial cutaneous fungal infection
with Malassezia furfur (yeast); not contagious
• Most common in persons aged 15-24 years, when the
sebaceous glands are more active
• Presentation: Fine scaling, salmon-pink, hypo- or
hyperpigmented macules and patches
– Chronic, recurrent eruption occurring on upper trunk and
proximal extremities
– Exacerbated by warm, humid conditions
• KOH confirms diagnosis
• DDx: vitiligo, pityriasis alba, guttate psoriasis, CTCL
• Therapy: topical azole antifungals, selenium sulfide
Classic “spaghetti and meatballs”
on KOH of Tinea Versicolor
Vitiligo
• Etiology: An acquired progressive disorder resulting in the
destruction of melanocytes caused by genetic and nongenetic
factors
• Often associated with autoimmune disorders (usually
thyroid)
• Average age of onset is 20 years
• Presentation: Usually well demarcated white or
hypopigmented macules and patches that enlarge
centrifugally over time
• Common sites - face, neck, scalp, areas subjected to repeated
trauma (bony prominences, ventral wrists, dorsl hands), and
around body orifices (lips, genitals, gingiva, areolas, nipples)
• Body hair in affected areas may be depigmented
• DDx: tinea versicolor, post inflammatory hypopigmentation,
pityriasis alba, mycosis fungoides
• Treatment: Phototherapy, topical steroids, tacrolimus,
vitamin D analogs, cosmetics, depigmentation with
hydroquinone
• No single therapy produces predictably good results so
the response to therapy is highly variable
• Hands, feet, genitals can be most difficult areas to treat
Scabies
• Etiology: Sarcoptes scabiei
• In developed countries, scabies occur primarily in institutional settings
and long-term care facilities; also common among children
• Presentation: Extremely itchy, especially at night
– Often involves armpits, groin, umbilicus, wrists, fingerwebs, nipples
– Primary lesions typically include small papules, vesicles, & burrows
• DDx: atopic dermatitis, bug bites, folliculitis, psoriasis
• Treatment: topical antiscabietic agents (e.g., Permethrin 5%) are
applied from the neck down with repeat application in 7 days, oral
ivermectin is also effective
– Pruritus may continue for several weeks after successful treatment
– Antipruritic agents (e.g. sedating antihistamines) and/or
antimicrobial agents (for secondary infection) may be needed
– All family members and close contacts must be evaluated and
treated for scabies, even if they do not have symptoms
Itchy papules on the
penis are scabies until
proven otherwise
Scabies mite
Herpes Simplex
• Etiology: caused by the herpes simplex virus (two types exist)
– HSV-1 (associated with orofacial disease)
– HSV-2 (associated with genital disease)
• HSV is ubiquitous
• Presentation:
– Primary infections are often accompanied by systemic signs, longer duration
of symptoms, and higher rates of complications
– Recurrent episodes are milder and shorter
– Lesions are painful & progress to vesicles; new lesions can erupt over 1-2 wks
– Often on the mucosal surface of the oral/genital area & on surrounding skin
– Mucosal vesicles form shallow painful ulcers; cutaneous lesions evolve into
crusted ulcers that heal in 5-7 days
– Oral recurrences often triggered by pyrexia, stress or sunburn; genital
recurrences often linked to stress or menstrual cycle
• DDx: hand-foot-and-mouth disease, zoster, syphilis
• Treatment: antivirals
Folliculitis
• Etiology: primary inflammation of the hair follicle resulting from
infections, follicular trauma or occlusion
• Superficial folliculitis is common and often self-limited
• Affects all races, ages, and men and women equally
• Presentation: acute onset of erythematous, folliculocentric
papules and pustules associated with pruritus or mild discomfort
• DDx: Acne, contact dermatitis, milia, miliaria, insect bites
• Treatment:
• uncomplicated superficial folliculitis can be treated with
antibacterial soaps and good hand washing technique
• refractory or deep lesions with a suspected infectious etiology
may need empiric treatment with topical and/or oral antibiotics
that cover gram-positive organisms (choose a drug that covers
MRSA in areas of high prevalence or in predisposed patients)
• mupirocin ointment in the nasal vestibule twice a day for 5 days
may eliminate the S aureus carrier state in recurrent folliculitis
• Prevalence: Studies have shown ~ 25-30% of the population is
colonized with MSSA (usually on skin or in nasal passages)
• A study in a California ED found 51% of patients presenting for
evaluation of a skin infection had +MRSA cultures
• Presentation: infections usually manifest as folliculitis or a similar
skin infection (patients often present with a “spider bite” or
“infected pimple”)
• Transmission of CA-MRSA is though an open wound or from
contact with a CA-MRSA carrier
• Treatment: I & D of the abscess and tx with appropriate
antibiotics when indicated; wound exudates should be cultured
to determine the causative organism and appropriate antibiotics
• Oral antibiotics: Trimethoprim-sulfamethoxazole DS twice daily,
w/ or w/o rifampin 600 mg/d; doxycycline 100 mg twice daily;
clindamycin 450 mg 3 times a day (96% sensitive)
Community Acquired MRSA (CA-MRSA)
Acne
• Etiology: multifactorial but key factor is genetics (the
propensity for follicular epidermal hyperproliferation with
subsequent plugging of the follicle is inherited)
• Characterized by chronic inflammatory disease of the
pilosebaceous follicles (recurrence and relapse is common)
• Sebum production by sebaceous gland
• Propionibacterium acnes (P acnes) follicular colonization
• Alteration in keratinization process
• Release of inflammatory mediators
• Acne is a common skin disease affecting 60-70% of
Americans at some time during their lives
Key Elements in the History
• Men vs. women
– Menstrual history
– PCOS
• Previous Hx
– Acne as a teenager
• Habits
– Picking or rubbing
• Previous Tx
– How long did you use?
– How did you use?
– Why did you stop?
• Medications
– Dilantin, lithium, prednisone,
etc.
The Severity of Acne Varies
• Mild
– Primarily comedones,
pustules and papules
(<10)
• Moderate
– Primarily pustules and
papules (10-40),
comedones
• Moderately severe
– Numerous papules and
pustules (40-100),
comedones, deeper
nodular lesions
[Refer to derm]
• Severe
– Nodulocystic acne and
acne conglobata
[Refer to derm]
Mild Acne
Moderate Acne
Moderately Severe Acne
Severe Acne
Hormonal Acne
• Women
• Associated with PCOS,
hirsutism, and menstrual
irregularity
• Treatment:
- Multiple estrogen-
based OCPs
- Spironolactone
• Check labs - DHEAS and
testosterone
Treatment of Acne
Mechanism of Action
Topical retinoids
Anticomedogenic
Comedolytic
Anti-inflammatory
Benzoyl peroxide
Antimicrobial
Keratolytic
Antibiotics
Anti-inflammatory
Antimicrobial
Anti-hormonal
Inhibits sebum
production
Systemic retinoids
Inhibits sebum
production
Comedolytic
Antimicrobial (indirect)
Mild Acne
• Primary Treatment:
• Topical tretinoin (Retin-A) + topical antimicrobial
• Tretinoin at night (0.025%, 0.05%, or 0.1% cream) and
topical clindamycin gel or lotion in the morning
• Adjunctive Treatment:
• Salicylic acid 2% wash or benzoyl peroxide 2.5-5% (BPO)
wash to entire face once or twice daily
• BPO cream, gel, or lotion in the morning as spot
treatment (let patients know that BPO bleaches
clothing/bedding)
• Faux pas: Using topical antimicrobial as monotherapy
or for > 3 mos duration as this encourages antimicrobial
resistance
Moderate Acne
• Primary Treatment:
• Topical retinoid + ORAL antibiotic
• Tretinoin or tazarotene at night
• Oral doxycycline or minocycline once daily
• Amoxicillin and Bactrim (low dose) are also options
• Adjunctive Treatment:
• Salicylic acid 2% wash or benzoyl peroxide 2.5-5% (BPO)
wash to entire face once or twice daily
• BPO cream, gel, or lotion in the morning to entire face
• In women, consider oral contraceptive pills and/or
spironolactone
• Faux pas: Not aggressively using topical retinoid, not
having low threshold for oral antibiotics during acute
phase, not considering OCPs and/or spironolactone
Moderate-Severe Acne
• Primary Treatment:
• Refer to Dermatology is reasonable
• Topical retinoid + ORAL antibiotic (high dose)
• Tretinoin or tazarotene at night
• Oral doxycycline or minocycline twice daily
• Amoxicillin and Bactrim (low dose) are also options
• Adjunctive Treatment:
• Salicylic acid 2% wash or benzoyl peroxide 2.5-5% (BPO)
wash to entire face once or twice daily
• BPO cream, gel, or lotion in the morning to entire face
• In women, highly consider spironolactone (alternative
in addition to OCPs)
• Faux pas: Same as with moderate acne but also not
considering Accutane
Severe Acne
• Primary Treatment:
• Refer to Dermatology
• Oral isotretinoin (Accutane) as monotherapy OR potent
topical retinoid (tazarotene) + ORAL antibiotic (high
dose) + topical BPO
• Adjunctive Treatment:
• Women are automatically on OCPs and consider adding
spironolactone
• OK to add oral or topical antibiotics but be mindful or
drug interations
• Faux pas: not being on Accutane, not bridging to topical
retinoids when weaning from Accutane, not considering
bridging to oral antibiotics or spironolactone when
weaning from Accutane
Topical retinoids should be 1st
line in maintenance therapy
• Target microcomedo formation
• Topical retinoid monotherapy is effective
• No issue with antimicrobial resistance
• Add BPO and not antibiotics for
maintenance
Therapeutic Considerations
• All discussed therapies for acne are pregnancy class
C or worse
• Spironolactone - can raise K level so renal function
must be normal
• Oral antibiotics should be used to shutdown acute
inflammatory acne over a few months only
• If previously on oral antibiotic and patient flares,
then restart on the same oral antibiotic (no need to
switch)
• Start Accutane slowly, especially in those with
nodulocystic acne (can paradoxically induce flare)
Reducing Antibiotic Resistance
• Concurrent use of oral and topical
antibiotics should be avoided
• Avoid using antibiotics as monotherapy
• Antibiotics should be discontinued as soon
as inflammatory lesions disappear
• Topical antibiotics may be used in mild to
moderate acne but should be used in
combo with a retinoid or BPO
Acknowledgements:
•Brian Kim, MD
•Karolyn Wanat, MD
•Campbell Stewart, MD
References:
•Thiboutot et al. New insights into the management of acne: An update from the
Global Alliance to Improve Outcomes in Acne Group. JAAD 2009; 60:S1-50.
•Tan et al. Hormonal treatment of acne: review of current best evidence. J Cutan Med
Surg 2004; 8:S4:11-5.
•James et al. Clinical Practice. Acne. NEJM 2005; 352:1463-72.
•James et al. Andrews’ Diseases of the Skin: Clinical Dermatology 2006, 10th
edition.
•James, WD, NEJM, 2005, 352 (14); 1463-72.
•USPFTF website

Dermatology for the young adult 2016

  • 1.
    Introduction to Dermatology inthe Young Adult Jennifer Nevas, CRNP Philadelphia VA Medical Center, Department of Dermatology
  • 2.
    Benign Skin Lesions •Warts • Molluscum Contagiosum • Dermatofibroma • Epidermal inclusion cysts
  • 3.
    Warts • Etiology: Humanpapilloma virus (HPV) • Common in children, adolescents, and immunosuppressed individuals • Presentation: verrucous topped papules • DDx: cutaneous horn, SK, SCC • Lesions may spontaneously resolve • Treatment (nongenital warts): – Cryotherapy (LN2), topical salicylic acid, surgical removal – Refer if no improvement with topicals • Treatment (genital warts): – Cryotherapy, imiquimod, Podofilox, surgical removal – Refer to derm (GI if anal involvement) if no improvement with topicals
  • 6.
    Molluscum Contagiosum • Etiology:benign viral infection with a DNA poxvirus • Most common in children – infection through direct skin-to- skin contact or indirect skin contact w/ fomites (bath towels) • In adults, molluscum are sexually transmitted • Presentation: ~2-5mm, discrete, nontender, flesh-colored, umbilicated papules - Generally asymptomatic - Most common on the face, trunk, and extremities in children and on the genitalia in adults • DDx: Milia, keratosis pilaris, wart • Treatment: spontaneously resolution can occur or can treat with LN2, curettage, salicylic acid, topical tretinoin, or imiquimod - Refer if no improvement with topicals and LN2 needed
  • 7.
  • 8.
    Dermatofibroma (DF) • Etiology:unknown • Can develop at any age, but usually young adulthood; more common in women • Presentation: Usually solitary (0.5 to 1 cm) lesions on extremities – Overlying skin color can range in color – May feel like a small pebble fixed to the skin surface – Tethering of overlying epidermis to the underlying lesion with lateral compression is called the “dimple sign” – Generally asymptomatic, but can be tenderness or itch – Historically attributed to a trauma to the skin (e.g., bug bite) • DDx: Nevus, keloid, melanoma, SCC, prurigo nodule • Treatment: None, can refer for ILK or excision if the lesion is very symptomatic
  • 10.
  • 11.
    Epidermal Inclusion Cyst(EIC) • Etiology: result from the proliferation of epidermal cells within a circumscribed space of the dermis • Can occur at any age but most common in 3rd and 4th decades; twice as common in men • Presentation: Appear as flesh–colored-to-yellowish, firm, round, mobile nodules often with central punctum (pore) – Discharge of a foul-smelling “cheese-like” material is common – Occur most frequently on the face, scalp, neck, and trunk – Usually asymptomatic but may become inflamed or infected • DDx: lipoma, milia • Treatment: None required, can refer for tx with ILK or excision (refer larger lesions to general surgery)
  • 12.
  • 13.
    Epidermal Inclusion Cyst,inflamed • Cyst rupture due to trauma  inflammation • Can become infected • Treatment: – warm compresses – intra-lesional steroids – I & D – +/- oral antibiotics • Do NOT squeeze or excise at this time!
  • 14.
    Common Skin Disorders •Tinea • Tinea Versicolor • Vitiligo • Scabies • Herpes • Folliculitis • MRSA • Acne • Atopic dermatitis/eczema • Contact dermatitis • Keratosis Pilaris • Pityriasis Rosea • Seborrheic dermatitis • Psoriasis • Intertrigo
  • 15.
    Atopic Dermatitis • Etiology:pruritic disease of unknown origin; evidence indicates that genetic factors are important • Prevalence - 15-30% of children; 2-10% of adults • Male-to-female ratio is 1:1.4; affects persons of all races • 85% of cases occur in 1st year of life; 95% occur before age 5 • Presentation: incessant pruritus – ill-defined, erythematous, scaly, and crusted (eczematous) patches and plaques – Xerosis and lichenification is seen in children and adults • DDx: contact derm, psoriasis, CTCL, scabies, TV, seb derm • Treatment: moisturization, topical steroids, topical calcineurin inhibitors, antihistimines, phototherapy, mild soaps & detergents, cotton clothing; methotrexate, prednisone, or cyclosporine for severe cases; antibiotics or antivirals for secondary infections • Refer if symptoms persistent despite tx or if weird presentation
  • 16.
    Atopic Dermatitis Major Features Pruritus  Typical morphology and distribution  Facial and extensor eczema in infants and children (though can have flexural involvement in children)  Flexural eczema in adults  Dermatitis—chronic or chronically relapsing  Personal or family history or atopy—asthma, allergic rhinitis, atopic dermatitis Minor Features  Xerosis  Ichthyosis/keratosis pilaris/hyperlinear palms  IgE reactivity (immediate skin test reactivity; + RAST)  Elevated serum IgE  Early age of onset  Tendency for cutaneous infection (ie. Staph, HSV)  Nonspecific hand/foot dermatitis  Nipple eczema  Cheilitis  Conjunctivitis (recurrent)  Dennie-Morgan infraorbital fold  Keratoconus  Cataracts  Orbital darkening  Facial pallor/facial erythema  Pityriasis alba  Itch when sweating  Wool intolerance  Perifollicular accentuation  Food hypersensitivity  Influenced by environmental & emotional factors  White dermatographism or delayed blanch to cholinergic agents Need: 3 Major + 3 Minor
  • 20.
  • 21.
    Hygiene Changes/Lubrication • Avoidbarrier disruption – Harsh soaps – Washcloths – Bathing too frequently • Moisturize, moisturize, moisturize! – The more the better – Soak and smear technique – soak in tub of luke warm water for 20 minutes, pat dry, and liberally apply topical medication or lubricant
  • 23.
    Topical Treatment • Topicalsteroids – may alternate high potency with mid potency to reduce risk or use on weekends only – Risks of overuse of topical steroids include: atrophy, striae, telangiectasias, hypopigmentation (temporary), can have systemic absorption if using long-term on a large body surface area • Topical calcineurin inhibitors (steroid sparing agents) – Tacrolimus (Protopic) ointment – Pimecrolimus (Elidel) cream
  • 24.
    Steroid Classes • 7classes based on vasoconstrictive properties • Note: ointment form is stronger than cream form – Class 1 = superpotent • Clobetasol propionate • Betamethasone dipropionate – Class 3 and 4 = mid-strength • Fluocinonide • Betamethasone valerate • Triamcinolone – Class 6 and 7= low potency • Fluocinolone • Desonide • Hydrocortisone Scalp, palms, soles Trunk, extremities Face, genitals, intertriginous areas
  • 25.
    Allergic Contact Dermatitis •Etiology: delayed type of induced sensitivity resulting from cutaneous contact with a specific allergen to which the patient has developed a specific sensitivity • ~25 chemicals are responsible for as many as one half of all cases • Common culprits: Poison ivy, topical antibiotics (e.g., Neosporin, neomycin, bacitracin), nickel, rubber gloves, hair dye, textiles, preservatives, fragrances, benzocaine • Presentation: pruritic papules and vesicles on an erythematous base – Acute onset – Geometric morphology (circles, lines, etc) – Lichenified pruritic plaques may indicate chronic ACD – Initial site of dermatitis often provides best clue regarding the potential cause • DDx: drug rash, nummular dermatitis, seb derm, tinea, urticaria • Treatment: avoid offending agent, topical steroids or calcineurin inhibitors, antihistamines, cool soaks, emollients, oral prednisone in severe cases, can refer for patch testing to help determine allergen
  • 28.
    Keratosis Pilaris • Etiology:benign, genetic disorder of keratinization of hair follicles • Affects nearly 50-80% of all adolescents and ~40% of adults; often improves with age • Presentation: small folliculocentric keratotic papules (gooseflesh appearance) • Most common on outer-upper arms and thighs • Usually asymptomatic • Worse in wintertime • DDx: acne, folliculitis, atopic dermatitis, milia, lichen nitidus • Treatment: none required but ammonium lactate lotion or urea cream may help
  • 30.
    Pityriasis Rosea • Etiology:benign, self-limited disease; considered to be a viral exanthem • More common in women, children, & young adults • Presentation: typically begins with a solitary macule that heralds the eruption (“herald patch”) • This lesion is usually a salmon-colored macule that enlarges over a few days to become a patch with a collarette of fine • Within the next 1-2 weeks, a generalized exanthem usually appears as bilateral and symmetric salmon-colored macules with a collarette scale oriented with their long axes along cleavage lines (creates classic Christmas tree pattern) • Tends to resolve over a 6 week period, but variability is common • DDx: syphilis (so important to check RPR if there are risk factors), nummular dermatitis, psoriasis, lichen planus, tinea corporis • Treatment: None required but can treat pruritus with topical steroids, oral antihistamines, topical menthol-phenol lotions • Refer if skin lesions not resolving in a few months
  • 32.
    Seborrheic Dermatitis • Etiology:related to a pathologic overproduction of sebum; may involve an inflammatory reaction to the yeast Malassezia • Presentation: – Erythema with greasy yellowish scale on the “T- zone” of the face, scalp, behind the ears, central chest – Dandruff – Can affect intertriginous areas • Usual onset occurs with puberty • Worsens with changes in seasons, trauma, stress, Parkinson disease, AIDS, certain medications • DDx: Atopic or contact dermatitis, rosacea, perioral dermatitis, tinea, impetigo
  • 35.
    Treatment for SeborrheicDermatitis • Shampoo at least every other day (shampoos that contain ketoconazole, salicylic acid, tar, selenium, sulfur, or zinc are especially helpful) – leave on for 5 minutes before washing off • Clobetasol 0.05% solution or Derma-Smoothe/FS (mineral/peanut oil + fluocinolone 0.1%) for severe flaking on the scalp • Ketoconazole 2% cream twice a day (for face, ears chest) • Hydrocortisone 2.5% cream – short-term use during flares • Tacrolimus ointment or pimecrolimus cream as steroid sparing agents
  • 36.
    Psoriasis • Etiology: Multifactorial diseasethat appears to be influenced by genetic and immune-mediated components • Presentation: Characterized by red papules and plaques with adherent silvery scale • Triggers: Physical trauma, stress, infection (Strep, HIV), pregnancy, medications
  • 37.
    Drugs that canTrigger Psoriasis • NSAIDs • Antibiotics • Steroids • Antimalarials • Lithium • ACE inhibitors • Beta-blockers • Calcium channel blockers • Interferon • Tetanus • Antihistamines
  • 38.
    For Each ClinicVisit • Ask about joint pain – 10% of patients have Psoriatic Arthritis (PsA) (Refer to Derm or Rheum) • Estimate body surface area (BSA) – An average palm = 1% – Disease Severity: • Mild <5% BSA • Moderate = 5-10% BSA (Refer to Derm) • Severe >=10% BSA (Refer to Derm) • Note – psoriasis is associated with cardiovascular disease, smoking, alcohol, metabolic syndrome, lymphoma, depression, suicide
  • 39.
    Psoriasis Vulgaris • Chronicand stationary - lesions can persist for years • Distribution: – Elbows – Knees – Scalp – Lumbosacral – Umbilicus
  • 40.
    Koebner’s Phenomenon • Occursin 20% of patients • Non-specific trauma can lead to formation of psoriasis in the area of irritation
  • 41.
    Inverse Psoriasis • Involvementlimited to skin fold regions • Usually associated with minimal scaling • Distribution: axilla, inframammary region, genitocrural region, neck • Often confused with intertrigo
  • 42.
    Topical Treatments forPsoriasis • Topical steroids • Hydrocortisone 2.5% ointment (low strength) – good for short term use on face, penis, and intertriginous areas • Triamcinolone 0.1% ointment (medium strength) • Clobetasol 0.05% ointment (high strength) • Synthetic Vitamin D • Dovonex (calcipotriene) cream – helps reduce scale • Topical calcineurin inhibitors – steroid sparing agents (good for face, penis, intertriginous areas) • Protopic ointment • Elidel cream • Common treatment regimen • calcipotriene bid Mon-Fri and clobetasol oint bid Sat-Sun for lesions on trunk and extremities; hydrocortisone or calcineurin inhibitor for face, penis, and intertriginous areas
  • 43.
    Intertrigo • Etiology: aninflammatory condition of skin folds resulting from heat, moisture, and friction • Often colonized by infection - usually candida but can also be bacterial, fungal, or viral • A common complication of obesity and diabetes • Presentation: Erythema, cracking, and maceration with burning and itching at sites in which skin surfaces are in close proximity (axillae, perineum, inframammary creases, abdominal folds, inguinal creases) • DDx: contact dermatitis, seborrheic dermatitis, cellulitis, inverse psoriasis, acanthuses nigricans • Treatment: Barrier creams such as zinc oxide paste, compresses with Burow solution 1:40 or dilute vinegar, absorbent powders and moisture-wicking undergarments, exposing the skin folds to air, topical antifungal agents for secondary infections (e.g., clotrimazole, econazole, ciclopirox, miconazole, ketoconazole, nystatin)
  • 45.
    Tinea aka “Ringworm” •Etiology: superficial fungal infection of skin • More common in preadolescents and in hot, humid climates • Presentation: scaly, ring-shaped, erythematous plaque that enlarges and displays central clearing; often mildly itchy • Confirm diagnosis with KOH prep • DDx: nummular dermatitis, granuloma annulare, lupus, psoriasis, pityriasis rosea
  • 46.
  • 48.
  • 49.
  • 50.
    Tinea Incognito (Majocchi’sGranuloma) • A deep folliculitis due to a cutaneous dermatophyte infection • Two types: 1) Follicular type - secondary to trauma or topical corticosteroids 2) Subcutaneous nodular type - occurs in immunocompromised pts
  • 51.
    Treatment of Dermatophytosis •Topicals (localized disease) – Azoles (ketoconazole) – Allylamines (terbinafine) – Applied to the lesion and at least 2 cm beyond this area once or twice/day for at least 2 weeks, depending on which agent is used • Systemic (extensive disease, nail or scalp involvement, Majocchi’s granuloma) – Griseofulvin, itraconazole, terbinafine – May consider referral to dermatology
  • 52.
    Tinea Versicolor • Etiology:benign superficial cutaneous fungal infection with Malassezia furfur (yeast); not contagious • Most common in persons aged 15-24 years, when the sebaceous glands are more active • Presentation: Fine scaling, salmon-pink, hypo- or hyperpigmented macules and patches – Chronic, recurrent eruption occurring on upper trunk and proximal extremities – Exacerbated by warm, humid conditions • KOH confirms diagnosis • DDx: vitiligo, pityriasis alba, guttate psoriasis, CTCL • Therapy: topical azole antifungals, selenium sulfide
  • 55.
    Classic “spaghetti andmeatballs” on KOH of Tinea Versicolor
  • 56.
    Vitiligo • Etiology: Anacquired progressive disorder resulting in the destruction of melanocytes caused by genetic and nongenetic factors • Often associated with autoimmune disorders (usually thyroid) • Average age of onset is 20 years • Presentation: Usually well demarcated white or hypopigmented macules and patches that enlarge centrifugally over time • Common sites - face, neck, scalp, areas subjected to repeated trauma (bony prominences, ventral wrists, dorsl hands), and around body orifices (lips, genitals, gingiva, areolas, nipples) • Body hair in affected areas may be depigmented • DDx: tinea versicolor, post inflammatory hypopigmentation, pityriasis alba, mycosis fungoides
  • 57.
    • Treatment: Phototherapy,topical steroids, tacrolimus, vitamin D analogs, cosmetics, depigmentation with hydroquinone • No single therapy produces predictably good results so the response to therapy is highly variable • Hands, feet, genitals can be most difficult areas to treat
  • 58.
    Scabies • Etiology: Sarcoptesscabiei • In developed countries, scabies occur primarily in institutional settings and long-term care facilities; also common among children • Presentation: Extremely itchy, especially at night – Often involves armpits, groin, umbilicus, wrists, fingerwebs, nipples – Primary lesions typically include small papules, vesicles, & burrows • DDx: atopic dermatitis, bug bites, folliculitis, psoriasis • Treatment: topical antiscabietic agents (e.g., Permethrin 5%) are applied from the neck down with repeat application in 7 days, oral ivermectin is also effective – Pruritus may continue for several weeks after successful treatment – Antipruritic agents (e.g. sedating antihistamines) and/or antimicrobial agents (for secondary infection) may be needed – All family members and close contacts must be evaluated and treated for scabies, even if they do not have symptoms
  • 60.
    Itchy papules onthe penis are scabies until proven otherwise
  • 61.
  • 62.
    Herpes Simplex • Etiology:caused by the herpes simplex virus (two types exist) – HSV-1 (associated with orofacial disease) – HSV-2 (associated with genital disease) • HSV is ubiquitous • Presentation: – Primary infections are often accompanied by systemic signs, longer duration of symptoms, and higher rates of complications – Recurrent episodes are milder and shorter – Lesions are painful & progress to vesicles; new lesions can erupt over 1-2 wks – Often on the mucosal surface of the oral/genital area & on surrounding skin – Mucosal vesicles form shallow painful ulcers; cutaneous lesions evolve into crusted ulcers that heal in 5-7 days – Oral recurrences often triggered by pyrexia, stress or sunburn; genital recurrences often linked to stress or menstrual cycle • DDx: hand-foot-and-mouth disease, zoster, syphilis • Treatment: antivirals
  • 64.
    Folliculitis • Etiology: primaryinflammation of the hair follicle resulting from infections, follicular trauma or occlusion • Superficial folliculitis is common and often self-limited • Affects all races, ages, and men and women equally • Presentation: acute onset of erythematous, folliculocentric papules and pustules associated with pruritus or mild discomfort • DDx: Acne, contact dermatitis, milia, miliaria, insect bites • Treatment: • uncomplicated superficial folliculitis can be treated with antibacterial soaps and good hand washing technique • refractory or deep lesions with a suspected infectious etiology may need empiric treatment with topical and/or oral antibiotics that cover gram-positive organisms (choose a drug that covers MRSA in areas of high prevalence or in predisposed patients) • mupirocin ointment in the nasal vestibule twice a day for 5 days may eliminate the S aureus carrier state in recurrent folliculitis
  • 66.
    • Prevalence: Studieshave shown ~ 25-30% of the population is colonized with MSSA (usually on skin or in nasal passages) • A study in a California ED found 51% of patients presenting for evaluation of a skin infection had +MRSA cultures • Presentation: infections usually manifest as folliculitis or a similar skin infection (patients often present with a “spider bite” or “infected pimple”) • Transmission of CA-MRSA is though an open wound or from contact with a CA-MRSA carrier • Treatment: I & D of the abscess and tx with appropriate antibiotics when indicated; wound exudates should be cultured to determine the causative organism and appropriate antibiotics • Oral antibiotics: Trimethoprim-sulfamethoxazole DS twice daily, w/ or w/o rifampin 600 mg/d; doxycycline 100 mg twice daily; clindamycin 450 mg 3 times a day (96% sensitive) Community Acquired MRSA (CA-MRSA)
  • 68.
    Acne • Etiology: multifactorialbut key factor is genetics (the propensity for follicular epidermal hyperproliferation with subsequent plugging of the follicle is inherited) • Characterized by chronic inflammatory disease of the pilosebaceous follicles (recurrence and relapse is common) • Sebum production by sebaceous gland • Propionibacterium acnes (P acnes) follicular colonization • Alteration in keratinization process • Release of inflammatory mediators • Acne is a common skin disease affecting 60-70% of Americans at some time during their lives
  • 69.
    Key Elements inthe History • Men vs. women – Menstrual history – PCOS • Previous Hx – Acne as a teenager • Habits – Picking or rubbing • Previous Tx – How long did you use? – How did you use? – Why did you stop? • Medications – Dilantin, lithium, prednisone, etc.
  • 70.
    The Severity ofAcne Varies • Mild – Primarily comedones, pustules and papules (<10) • Moderate – Primarily pustules and papules (10-40), comedones • Moderately severe – Numerous papules and pustules (40-100), comedones, deeper nodular lesions [Refer to derm] • Severe – Nodulocystic acne and acne conglobata [Refer to derm]
  • 71.
  • 72.
  • 73.
  • 74.
  • 75.
    Hormonal Acne • Women •Associated with PCOS, hirsutism, and menstrual irregularity • Treatment: - Multiple estrogen- based OCPs - Spironolactone • Check labs - DHEAS and testosterone
  • 76.
  • 77.
    Mechanism of Action Topicalretinoids Anticomedogenic Comedolytic Anti-inflammatory Benzoyl peroxide Antimicrobial Keratolytic Antibiotics Anti-inflammatory Antimicrobial Anti-hormonal Inhibits sebum production Systemic retinoids Inhibits sebum production Comedolytic Antimicrobial (indirect)
  • 78.
    Mild Acne • PrimaryTreatment: • Topical tretinoin (Retin-A) + topical antimicrobial • Tretinoin at night (0.025%, 0.05%, or 0.1% cream) and topical clindamycin gel or lotion in the morning • Adjunctive Treatment: • Salicylic acid 2% wash or benzoyl peroxide 2.5-5% (BPO) wash to entire face once or twice daily • BPO cream, gel, or lotion in the morning as spot treatment (let patients know that BPO bleaches clothing/bedding) • Faux pas: Using topical antimicrobial as monotherapy or for > 3 mos duration as this encourages antimicrobial resistance
  • 79.
    Moderate Acne • PrimaryTreatment: • Topical retinoid + ORAL antibiotic • Tretinoin or tazarotene at night • Oral doxycycline or minocycline once daily • Amoxicillin and Bactrim (low dose) are also options • Adjunctive Treatment: • Salicylic acid 2% wash or benzoyl peroxide 2.5-5% (BPO) wash to entire face once or twice daily • BPO cream, gel, or lotion in the morning to entire face • In women, consider oral contraceptive pills and/or spironolactone • Faux pas: Not aggressively using topical retinoid, not having low threshold for oral antibiotics during acute phase, not considering OCPs and/or spironolactone
  • 80.
    Moderate-Severe Acne • PrimaryTreatment: • Refer to Dermatology is reasonable • Topical retinoid + ORAL antibiotic (high dose) • Tretinoin or tazarotene at night • Oral doxycycline or minocycline twice daily • Amoxicillin and Bactrim (low dose) are also options • Adjunctive Treatment: • Salicylic acid 2% wash or benzoyl peroxide 2.5-5% (BPO) wash to entire face once or twice daily • BPO cream, gel, or lotion in the morning to entire face • In women, highly consider spironolactone (alternative in addition to OCPs) • Faux pas: Same as with moderate acne but also not considering Accutane
  • 81.
    Severe Acne • PrimaryTreatment: • Refer to Dermatology • Oral isotretinoin (Accutane) as monotherapy OR potent topical retinoid (tazarotene) + ORAL antibiotic (high dose) + topical BPO • Adjunctive Treatment: • Women are automatically on OCPs and consider adding spironolactone • OK to add oral or topical antibiotics but be mindful or drug interations • Faux pas: not being on Accutane, not bridging to topical retinoids when weaning from Accutane, not considering bridging to oral antibiotics or spironolactone when weaning from Accutane
  • 82.
    Topical retinoids shouldbe 1st line in maintenance therapy • Target microcomedo formation • Topical retinoid monotherapy is effective • No issue with antimicrobial resistance • Add BPO and not antibiotics for maintenance
  • 83.
    Therapeutic Considerations • Alldiscussed therapies for acne are pregnancy class C or worse • Spironolactone - can raise K level so renal function must be normal • Oral antibiotics should be used to shutdown acute inflammatory acne over a few months only • If previously on oral antibiotic and patient flares, then restart on the same oral antibiotic (no need to switch) • Start Accutane slowly, especially in those with nodulocystic acne (can paradoxically induce flare)
  • 84.
    Reducing Antibiotic Resistance •Concurrent use of oral and topical antibiotics should be avoided • Avoid using antibiotics as monotherapy • Antibiotics should be discontinued as soon as inflammatory lesions disappear • Topical antibiotics may be used in mild to moderate acne but should be used in combo with a retinoid or BPO
  • 85.
    Acknowledgements: •Brian Kim, MD •KarolynWanat, MD •Campbell Stewart, MD References: •Thiboutot et al. New insights into the management of acne: An update from the Global Alliance to Improve Outcomes in Acne Group. JAAD 2009; 60:S1-50. •Tan et al. Hormonal treatment of acne: review of current best evidence. J Cutan Med Surg 2004; 8:S4:11-5. •James et al. Clinical Practice. Acne. NEJM 2005; 352:1463-72. •James et al. Andrews’ Diseases of the Skin: Clinical Dermatology 2006, 10th edition. •James, WD, NEJM, 2005, 352 (14); 1463-72. •USPFTF website