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Pediatrics > Dermatology > Flashcards

Dermatology Flashcards

1
Q

How should a skin exam be performed?

A
  • Should be conducted in good light
  • Should be complete
    • Evaluation of scalp, hair, nails, eyes, mouth, palms, soles
  • Exam should be visual & tactile
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2
Q

What are the types of primary lesions?

A
  • Macule, patch
  • Papule, plaque
  • Nodule, tumor
  • Vesicle, bulla
  • Pustule
  • Cyst
  • Wheal
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3
Q

Macule

Patch

A
  • Macule
    • Flat & nonpalpable
    • Represent cutaneous color changes
  • Patch
    • Large macule
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4
Q

Papule

Plaque

A
  • Papule
    • Epidermal or superficial dermal lesions
    • Elevated above the skin surface
  • Plaque
    • Large or coalesced papules
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5
Q

Nodule

Tumor

A
  • Nodule
    • Dermal lesions below the skin surface
    • May have epidermal component
  • Tumor
    • Large nodule
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6
Q

Vesicle

Bulla

A
  • Vesicle
    • Fluid-filled papules
  • Bulla
    • Large vesicle
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7
Q

Pustule

A

purulent-filled papules

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8
Q

Cysts

A

nodules filled w/ expressible material

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9
Q

Wheals

A

cutaneous elevations caused by dermal edema

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10
Q

What are examples of secondary characteristics?

A
  • Scaling
  • Crusting
  • Pigmentation changes
  • Excoriations
  • Scars
  • Ulcers
  • Atrophy
  • Fissures
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11
Q

Scaling

A

desquamation of the stratum corneum

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12
Q

Crusting

A

dried exudate & debris

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13
Q

Excoriations

A

linear erosions into the epidermis

caused by fingernail scratches

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14
Q

Scars

A

thickened fibrotic dermis

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15
Q

Ulcers

A

absence of epidermis & some of dermis

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16
Q

Atrophy

A

thinning of epidermis or dermis

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17
Q

Fissures

A

linear cracks into the dermis

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18
Q

What are examples of configuration & distribution?

A
  • Configuration of lesions
    • Linear
    • Annular (circles)
    • Arcuate (half-circles)
    • Grouped
    • Discrete (distinct & separate)
  • Distributions
    • Generalized
    • Acral (hands, feet, buttocks)
    • Confined to dermatome
    • Other specific locations
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19
Q

What are some diagnostic procedures for dermatology?

A
  • Woods light
    • Identifies pigmentary changes & some dermatophytes
  • Scrapings
  • Cultures
    • Bacteria, virus, fungus
  • Invasive techniques
  • Immunofluorescent staining
    • Autoimmune vasculitic disorders
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20
Q

What scrapings are used for diagnosis in dermatology?

A
  • Fungus
    • 10% KOH added to scraping of scale or exudate to identify fungal hyphae
  • Scabies
    • Examine scraping of unscratched lesion or burrow for mites, eggs, feces
  • HSV
    • Base of vesicle scraped
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21
Q

What are some invasive techniques used for diagnosis in dermatology?

A
  • Incision & drainage
    • Diagnosis, cultures, therapy
  • Biopsy
    • Shave or tangenital
      • Epidermal or superficial dermal lesions
    • Punch
      • Epidermal, dermal, superficial subq
    • Excision
      • Complete lesion removal
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22
Q

Absorption of topical agents in children vs. adults

A
  • Skin of child = skin of adult
  • Exception
    • Premature infant
    • Absorption is greater
    • Thinner stratum corneum
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23
Q

Therapeutic efficacy of a topical agent is related to both the _________ and the ______.

A

active ingredient, vehicle

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24
Q

Hydration of the skin is critical. What are some examples of moisturizers?

A
  • Ointments
    • Little or no water
    • Maximal water-retaining properties
    • Useful for very dry skin
  • Creams
    • 20-50% water
    • Useful for skin of average dryness
  • Lotions
    • More water than creams
    • Useful for minimally dry skin, large SA
  • Solutions & alcohol-based gels
    • Useful for areas w/ hair (scalp)
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25
Q

What is thickened skin called?

What does it require?

A

Hyperkeratosis

  • Keratolytics
    • Salicylic acid
    • Urea
    • Alpha-hydroxy acids
    • Retinoic acid
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26
Q

What are some examples of destructive therapies?

A

Used for warts, molluscum contagiosum

  • High dose salicylic acid
  • Podophyllin
  • 5-FU
  • Cryotherapy
  • Electrotherapy
  • Laser therapy
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27
Q

What are some examples of anti-infective agents?

A
  • Topical antibiotics
  • Antifungals
  • Antivirals
  • Antiparasitic agents
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28
Q

What anti-inflammatory agents are used for treatment in dermatology?

A

Topical corticosteroids

  • Weakest steroid that will achieve the treatment goal should be used first
  • Low-potency on the face or groin
    • Epidermis is thinner, increased side effects
  • Systemic vs. local side effects
  • Other
    • Tacrolimus ointment (atopic dermatitis)
    • 1-5% sulfer (acne)
    • Tar (eczema & psoriasis)
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29
Q

What are the local side effects of topical corticosteroids?

A
  • Acne (acne rosacea)
  • Hirsutism
  • Folliculitis
  • Striae (axilla, groin)
  • Hyper/hypo-pigmentation
  • Atrophy
  • Ecchymoses & telangiectasias
  • Tachyphylaxis (insensitivity)
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30
Q

What is contact dermatitis?

What are the 2 categories?

A
  • Inflammation of the epidermis & superficial dermis secondary to direct contact w/ the skin by a sensitizing substance
  • Categories
    • Allergic contact dermatitis
    • Primary irritant contact dermatitis
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31
Q

What is the etiology of allergic contact dermatitis?

A
  • Direct T-cell mediated response to an exogenous applied allergen
  • Steps for rxn
    • Initial sensitization
    • Rechallenge (small, not dose-dependent)
  • Common causes
    • Poison ivy, oak, sumac
    • Nickel-containing jewelry & belt buckles
    • Topical lotions & creams
    • Perfumes & soaps
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32
Q

Allergic contact dermatitis

clinical features

management

A
  • Erythematous papules & vesicles in the area that came into contact w/ the allergen
  • Treatment
    • Topical corticosteroids
    • Avoidance of the offending allergen
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33
Q

What is the etiology of primary irritant contact dermatitis?

What is the most common type?

A
  • Caustic substances that irritate the skin
  • Not an allergic rxn, no sensitization needed
  • Dose-dependent
  • Most common type: diaper dermatitis
    • Multifactoral disorder
    • Prolonged contact w/ urine & fecal matter, friction, maceration, proteases in feces
    • Secondary infection: Candida albicans
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34
Q

What are the clinical features of primary irritant contact dermatitis?

A
  • Erythema w/ papules on upper thighs, buttocks, genitourinary area
  • NO involvement of inguinal creases
  • Candidal superinfection
    • Involvement of inguinal creases
    • More-intense confluent erythema
    • Satellite lesions
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35
Q

How is primary irritant contact dermatitis managed?

A
  • Keep skin free from urine & stool
  • Skin moisturizers
  • Barrier creams & ointments (zinc oxide)
  • Frequent diaper changes
  • Low-potency corticosteroids
    • Severe inflammation
  • Nystatin, Clotrimazole (anti-fungal)
    • Candidal infection
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36
Q

Seborrheic Dermatitis

epidemiology

etiology

A
  • Infants & adolescents
  • Cause unknown
  • Hypersensitivity rxn to saprophytic yeast
    • Pityrosporum ovale
    • Lives in areas that overproduce sebum
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37
Q

What are the clinical features of Seborrheic Dermatitis?

A
  • Eruption of red scales & crusts in areas w/ high numbers of sebaceous glands
    • Scalp, face (eyebrows, nose, beard), chest, groin
    • Skin lesions may be greasy
  • Infants
    • Dermatitis limited to scalp (“cradle cap”)
    • Face, upper chest, flexor creases of extrem
  • Adolescents
    • Dermatitis in nasolabial folds, pinna, scalp
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38
Q

How is Seborrheic Dermatitis managed?

A
  • Low potency topical corticosteroids
  • Sulfer, zinc, salicylic acid-based shampoos
    • Light scrubbing w/ brush to remove crusts
    • Loose scales removed w/ mineral oil
  • Topical anti-fungal medication
    • Eradicate Pityrosporum ovale
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39
Q

Pityriasis Rosea

epidemiology

etiology

A
  • Uncommon <5 YO
  • Extremely common during late childhood/adolescence
  • Cause unknown
  • Similar to hypersensitivity rxn to virus
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40
Q

What are the clinical features of Pityriasis Rosea?

A
  • Papulosquamous disorder
    • Solitary, large 2-5 cm scaly, erythematous lesion (herald patch)
    • Trunk or extremities
    • 1-30 days
  • Oval erythematous macules & papules
    • 1-2 wks after herald patch
    • 3-6 wks from chin to mid-thigh
    • Skin lines: “Christmas tree” distribution
    • Lesions are pruritic (50%)
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41
Q

How is Pityriasis Rosea managed?

A
  • Topical or systemic anti-histamines
  • Exposure to UV light may shorten course
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42
Q

Psoriasis

epidemiology

etiology

A
  • 3% of children in the US
    • More common in adults
    • 30% develop in childhood
  • Autosomal dominant inheritance
  • Immune dysregulation –> epidermal proliferation
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43
Q

What are the clinical features of Psoriasis?

A
  • Distribution of skin lesions & severity variable
  • Scaling papules & plaques
    • Scalp: non-greasy w/o hair loss
    • Ears, elbows, lumbosacral, groin
    • Classic: silvery scale
  • Koebner phenomenon
    • New lesions at sites of skin trauma
  • Nail involvement common
    • Pits, distal thickening, lifting of nail bed, nail destruction
  • Arthritis during childhood uncommon
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44
Q

How is Psoriasis managed?

A
  • Moderate/high-potency corticosteroids
  • UV light therapy
  • Analogs of Vitamin D
  • 3% salicylic acid in mineral oil for scalp
  • Retinoids
  • Anthralin (downgrades EGF)
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45
Q

What is Miliaria Rubra (Heat Rash)?

What is the etiology?

A
  • Distrupted sweat ducts near the upper dermis (occlusion/friction) that result in sweat being released onto the skin
  • Sweat on skin –> inflammatory response
  • More sweat, more occlusion, heat rash
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46
Q

What are the clinical features of Malaria Rubra?

How is it managed?

A
  • Small erythematous pruritic papules/vesicles
  • Areas of occlusion or rubbed areas
  • Inguinal region, axilla, chest, neck
  • Treatment
    • Avoidance of occlusive clothing
    • No medications
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47
Q

What are the 4 types of hypersensitivity disorders?

A
  • Urticaria
  • Serum sickness
  • Erythema Multiforme
  • Toxic Epidermal Necrolysis
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48
Q

What is serum sickness?

A
  • May initially appear as urticaria
  • Systemic signs & symptoms
    • Fever
    • Arthralgias
    • Adenopathy
    • Evidence of organ injury
  • Medications are common causes
    • Cephalosporins
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49
Q

What is Erythema Multiforme?

A
  • Hypersensitivity rxn to many stimuli
  • Drugs, viruses, bacteria, fungi, protozoa, systemic disease
50
Q

What are the 3 major categories of Erythema Multiforme?

What is the classic skin lesion?

A
  • Categories
    • Erythema multiforme minor
    • Erythema multiforme major
    • Stevens-Johnson syndrome
  • Classic lesion
    • Target lesion
    • Fixed, dull red, oval macule
    • Duskey center w/ papule or vesicle
51
Q

Erythema Multiforme Minor

  • major cause
  • skin findings
  • mucous membrane findings
  • systemic findings
  • management
  • prognosis
A
  • major cause
    • HSV
  • skin findings
    • Symmetric target lesions (acral)
  • mucous membrane findings
    • One surface (mouth, 25%)
  • systemic findings
    • Prodrome: low fever, arthralgias, myalgias
  • management
    • Supportive care, Acyclovir (preventative)
  • prognosis
    • Good, possible recurrence
52
Q

Erythema Multiforme Major

  • major cause
  • skin findings
  • mucous membrane findings
  • systemic findings
  • management
  • prognosis
A
  • major cause
    • Mycoplasma pneumonaie, drugs
  • skin findings
    • Symmetric target lesions (acral, truncal)
  • mucous membrane findings
    • 2 mucosal surfaces (mouth, eyes)
  • systemic findings
    • Prodrome: low fever, arthralgias, myalgias
  • management
    • Supportive care, erythromycin/azithromycin (M. pneumoniae), stop offending drug
  • prognosis
    • Good
53
Q

Stevens-Johnson Syndrome

  • major cause
  • skin findings
  • mucous membrane findings
  • systemic findings
  • management
  • prognosis
A
  • major cause
    • Drugs
  • skin findings
    • Widespread atypical, asymmetric target lesions, blisters, necrosis
  • mucous membrane findings
    • 2 mucosal surfaces (mouth, eyes)
  • systemic findings
    • Prodrome: high fever, cough, malaise, headache, arthralgias
  • management
    • Supportive care, stop offending drug, optho consult, steroids, IVIG, burn unit
  • prognosis
    • High morbidity & mortality (5%)
54
Q

What is Toxic Epidermal Necrolysis?

What are the clinical features?

What is the prognosis?

A
  • Severe rxn to drugs
    • Anti-convulsants
    • Antibiotics
    • Anti-inflammatory drugs
  • Widespread epidermal necrosis
  • Sloughing of the epidermis (>30% skin loss)
  • Severe mucous membrane involvement
  • No target lesions
  • Nikolsky sign: skin peels away w/ lateral pressure
  • Mortality (10-30%)
    • Sepsis, dehydration, electrolyte abnormalities
55
Q

Fungal infections are common during childhood & are most associated with _________ & with _______ living conditions.

A

humidity

urban/crowded

56
Q

What are the 4 categories of fungal infections?

A
  • Tinea capitis (hair)
  • Skin infections
    • Tinea corporis (body)
    • Tinea pedis (foot)
    • Tinea cruris (groin)
  • Tinea unguium (onychomycosis)
  • Tinea versicolor
57
Q

What is the etiology of tinea capitis?

A
  • Trichophyton tonsurans (95%)
    • Human-to-human contact
  • Microsporum canis (5%)
    • Cats & dogs
58
Q

What are the clinical features of tinea capitis?

A
  • Patchy hair loss
    • Black dot ringworm: hairs break at scalp
    • M. canis: broken hairs thick & white
  • Scales & pustules
  • Kerion
    • Large red boggy nodule
    • Hypersensitivity rxn to dermatophyte
  • Occipital & posterior cervical lymphadenopathy
59
Q

How is tinea capitis diagnosed?

A
  • Microscopic evaluation of hairs w/ 10% KOH
    • Identify fungal hyphae, fungal culture
  • Hairs fluoresce under Woods light w/ M. canis
60
Q

How is tinea capitis treated?

A
  • Systemic oral antifungal therapy (griseofulvin)
    • 6-8 wks
  • Topical antifungal agents ineffective
  • Topical 2.5% or 5% selenium sulfate shampoo
    • Reduces infectivity
61
Q

Pathogens for fungal infections of the skin include….

A
  • M. canis
  • T. tonsurans
  • Other Trichophyton species
62
Q

Clinical features

  • tinea corporis
  • tinea pedis
  • tinea cruris
A
  • tinea corporis (“ringworm”)
    • Oval or circular scaly erythematous patches w/ partial central clearing
  • tinea pedis (athlete’s foot)
    • Post-pubertal adolescents w/ scaling & erythema btwn toes or on the plantar aspect of the foot
    • Vesicles may be seen
  • tinea cruris
    • Scales & erythema in groin/inguinal creases
63
Q

How are fungal infections of the skin diagnosed?

How are they managed?

A
  • Clinical features
  • KOH examination of skin scrapings
    • Fungal hyphae & culture
  • Treatment
    • Topical antifungal medications
    • Clotrimazole, terbinafine, ketoconazole
64
Q

What is tinea unguium?

How is it treated?

A
  • Fungal infection of the nails (onychomycosis)
  • Thickening & yellow discoloration of 1 or several nails (usually toenails)
  • Topical management challenging
  • Prolonged therapy required
  • Systemic medictations
    • Griseofulvin
    • Terbinafine
    • Ketoconazole
65
Q

What is tinea versicolor?

What causes it?

A
  • Superficial fungal disorder
  • Adolescents & young adults
  • Pityrosporum orbiculare
    • Yeast of the stratum corneum
66
Q

What are the clinical features of tinea versicolor?

A
  • Fine, scaly oval macules
  • Trunk, proximal arms, face
  • Hypo/hyper-pigmented
  • More prominent w/ sun exposure
  • Infection may be asymptomatic
67
Q

How is tinea versicolor diagnosed?

How is it managed?

A
  • KOH examination of scraping of lesion
    • Fungal hyphae or circular spores
    • “spaghetti & meatballs”
  • Woods light
    • Yellow or orange fluorescence
  • Treatment
    • Overnight application of 2.5% selenium sulfide weekly for 3-4 wks
    • Ketoconazole shampoo or cream
    • Systemic anti-fungal medications
68
Q

What are the 10 viral skin infections of children?

A
  • Viral exanthem
  • Measles & rubella
  • Erythema infectiosum (5th disease)
  • Roseola infantum (exanthem subitum)
  • Gianotti-Crosti syndrome (papular acrodermatitis)
  • Varicella (chickenpox)
  • HSV-1, HSV-2
  • Hand-foot-mouth disease & herpangina
  • Warts
  • Molluscum contagiosum
69
Q

What is viral exanthem?

A
  • Skin rash associated w/ viral infection
  • Enanthem: involvement of oral mucosa
  • Morbilliform: measles-like
  • Scarlatiniform: scarlet fever-like; papular, vesicular, petechial
70
Q

What is the etiology of Erythema infectiosum?

A
  • Most common in school-age children
  • Parvovirus B19
  • 5th disease transmitted by respiratory secretions
  • Aplastic crisis (pts w/ hemoglobinopathies)
  • Prolonged anemia (immunosuppressed pts)
  • Fetal hydrops
  • Miscarriage in pregnant women
71
Q

What are the clinical features of 5th disease?

A
  • UR symptoms
    • Cough, fever, rhinorrhea
  • “Slapped-cheek” rash (1-2 wks after URI)
    • Red macular rash
    • Lasts several days
  • No longer contagious when facial rash appears
  • Lacy, reticular rash on trunk & extremities
    • Lasts 3-5 days
    • Exercise, heat, sunlight can induce rash
  • Arthralgias (adults > children)
72
Q

How is 5th disease treated?

A
  • Supportive
  • IVIG for chronic anemia (immunosuppressed pts)
73
Q

Roseola infantum (exanthem subitum)

  • age group
  • etiology
  • clinical features
  • treatment
A
  • Children <2 YO
  • Most common: HHV-6, HHV-7
    • Adenovirus, parvovirus B19, echovirus 16
  • Clinical
    • 3-5 days of high fever
    • Pink papular eruption on trunk
    • Fades in 24-48 hrs
  • Treatment is supportive
74
Q

What is Gianotti-Crosti syndrome?

(papular acrodermatitis)

What are the clinical features? Treatment?

A
  • Children <3 YO
  • HepB, EBV, CMV, Coxsackie virus
  • Clinical features
    • Red or flesh-colored flat-topped papules
    • Acral areas (extremities, buttocks, cheeks)
    • Skin lesions last wks, may recur
    • URI symptoms precede eruption
  • Treatment is supportive
75
Q

What is the incidence of varicella?

What is the age group?

A
  • Incidence has decrased since vaccinations
  • Any age in unimmunized children & adults
76
Q

What are the clinical features of varicella?

A
  • 7-21 day incubation period
  • Intensely pruritic erythematous macules
  • Central vesicles w/i 1-2 days
  • Classic lesion: “dew drop on rose petal”
  • Crops of lesions over 2-5 days
    • Crusting, hundreds of vesicles
  • Fever is common
77
Q

How is varicella managed?

A
  • Anti-pyretics
  • Cleansing w/ anti-bacterial soaps
    • Prevent bacterial superinfection
  • Antihistamines for itching
  • Monitoring
  • Treatment of complications
  • IV Acyclovir
    • Varicella pneumonia & encephalitis
    • Pts at high risk for complications
    • Pts w/ ophthalmic involvement
78
Q

What is the pathophysiology of HSV?

A
  • Neonatal infection
    • Passage through birth canal
    • Mother w/ primary HSV infection
    • 2/3 HSV-2, 1/3 HSV-1
  • Gingivostomatitis
    • Most common HSV infection during infancy & childhood (HSV-1)
79
Q

What are the complications of varicella infection?

A
  • Bacterial superinfection (Staph aureus)
  • Necrotizing fasciitis (group A strep)
  • Scarring
  • Reye syndrome (ingestion of salicylates)
  • Pneumonia
  • Encephalitis
  • Acute cerebellar ataxia
  • Hepatitis
  • Herpes zoster
  • Infection during pregnancy
80
Q

What are the complications of varicella infection during pregnancy?

A
  • Teratogenic effects
  • Congenital varicella syndrome
    • Zigzag scarring of the skin
    • Shortened or malformed extremities
    • CNS damage
    • Eye abnormalities
      • Cataracts, chorioretinitis
  • Severe varicella infection of neonate
    • Mother acquires varicella w/i 1 wk of delivery
81
Q

What are the clinical features of HSV?

A
  • HSV gingivostomatitis
  • Neonatal HSV
  • Herpetic whitlow
  • Recurrent HSV infection
82
Q

What is HSV gingivostomatitis?

A
  • Young infants
  • Grouped vesicles & ulcers
    • Lips, corners of mouth, tongue
  • Pain on swallowing
  • Drooling
  • Fever
  • Infection lasts 1-2 wks
83
Q

What is neonatal HSV?

What are the serious sequelae?

A
  • 1st wk of life w/ variable signs & symptoms
  • Few vesicles at the site (scalp) in contact w/ maternal lesions
  • Signs & symptoms of sepsis
    • Apnea, lethargy, irritability, seizures
  • Serious sequelae
    • Meningoencephalitis
    • Hepatitis
    • Sepsis
    • Shock
    • Death
84
Q

What is herpectic whitlow?

A
  • HSV-1 infection of the thumb or fingers
  • Secondary to thumb/finger sucking by child w/ oral HSV lesion
85
Q

How does recurrent HSV infection occur?

A
  • HSV resides in the dorsal root ganglion
  • Mild & less symptomatic
  • Generally occur on the lip
  • Reactivation by fever, sunlight, emotional stress, trauma
86
Q

How is HSV diagnosed?

A
  • Tzanck preparation
    • Epidermal giant cells on microscopy
  • Direct fluorescent ab testing
    • Detection of HSV antigen
  • Culture of base of lesion
  • PCR to identify HSV in CSF
87
Q

How is HSV managed?

A
  • Neonatal HSV
    • Medical emergency
    • Immediate hospitalization
    • IV acyclovir
  • Cutaneous & oral HSV
    • Oral acyclovir
    • Prevents recurrent infection also
88
Q

What is hand-foot-mouth disease & herpangina?

What are the clinical features?

How is it treated?

A
  • Coxsackie virus type A16 (most common)
    • A2, A5, A10
  • Clinical features
    • Vesicles, papules, pustules
    • Palms, soles, fingertips
    • Shallow ulcers/erosions on soft palate/tongue
    • Fever
  • Only oral lesions = herpangina
  • Treatment is supportive
89
Q

What are the clinical features of warts?

A

HSV

  • Any skin surface
  • Irregularly-shaped discrete flesh-colored papules
  • Smooth or rough
  • Increase in size, contagious, spreads adjacently
  • Condyloma acuminata
    • Multiple external warts in genital area
90
Q

How are warts managed?

A
  • Resolve spontaneously w/i 1-2 yrs
  • Treatment
    • Liquid nitrogen
    • Salicylic acid
    • Cantharidin
    • Podophyllin
    • Surgical excision
  • Recurrance after any treatment is high
91
Q

What are the clinical features of molluscum contagiosum?

A

Poxvirus

  • Small asymptomatic flesh-colored papules w/ central umbilication
  • Anywhere on skin w/ hair follicles
  • Face, proximal extremities, trunk
  • Lesions are contagious
  • HIV infection: extensive eruptions
92
Q

How is molluscum contagiosum treated?

A
  • Observation, no therapy
  • Removal
    • Curettage
    • Podophyllin, trichloroacetic acid, liquid nitrogen, salicylic acid, cantharidin
93
Q

What are 2 examples of Ectoparasites?

A
  • Louse infestation
  • Scabies
94
Q

Louse infestation

  • types
  • etiology
  • epidemiology
A
  • Types
    • Head lice (scalp)
    • Body lice (body)
    • Pubic lice (groin)
  • Organisms
    • Pediculus humanus: head & body lice
    • Phthirus pubis: pubic lice
    • Small 6-legged insect that attaches to skin & ingests blood
  • Crowded living conditions, sharing of hats, clothes, combs, hairbrushes
95
Q

What are the clinical features of Louse infestation?

A
  • Head lice
    • Itching, bodies found on scalp
    • Nits (eggs): oval-white bodies attached to the hair shaft
  • Body lice
    • Papules & pustules on trunk w/ excoriations
  • Pubic lice
    • Lice or nits in groin
    • Black crusted papules or blue macules (macula cerulea)
96
Q

What are the clinical features of scabies?

A

Sarcoptes scabiei

  • Pruritic papules or vesicles
  • Abdomen, dorsum of hands, groin, axilla, flexor surfaces of wrists, interdigital spaces
  • Infants: facial & neck involvement
  • Itching is severe
  • S-shaped burrows
97
Q

How is scabies diagnosed & treated?

A
  • Microscopic examination of scraping of unscratched burrow (mite, eggs, feces)
  • Treatment
    • Overnight application of 5% permethrin lotion or 1% lindane (adolescents/adults)
  • Highly contagious (treat all contacts)
  • Itching up to 30 days after treatment
  • Bed sheets, pillowcases, clothes washed in hot water
98
Q

What are the 4 types of hypopigmentation?

A
  • Postinflammatory hypopigmentation
  • Pityriasis alba
  • Vitiligo
  • Oculocutaneous albinism
99
Q

What is postinflammatory hypopigmentation?

A
  • May follow any skin inflammation
    • ex: atopic dermatitis
  • Generally resolves over months to yrs
100
Q

What is Pityrasis alba?

A
  • Related to atopic dermatitis
  • Hypopigmented, dry, scaly patches
  • Commonly on cheeks
  • Treatment
    • Moisturizers
    • Mild corticosteroids
101
Q

What is vitiligo?

A
  • Complete loss of skin pigment in patchy areas
  • Melanocyte destruction
  • Partial repigmentation may occur
  • No effective treatement
  • Psoralen + UV light may be helpful
102
Q

What is oculocutaneous albinism?

A
  • Genetic defect in melanin synthesis
  • White skin & hair, blue eyes
  • Photophobia, nystagmus
  • No treatment
103
Q

Tuberous Sclerosis

inheritance

skin findings

A
  • Autosomal dominant
  • Ash-leaf spots
    • ​hypopigmented macules seen best under Woods light
  • Adenoma sebaceum
    • ​angiofibromas on nose/face
  • Shagreen patch
    • thickened orange peel appearance
  • Ungual fibromas
104
Q

Tuberous Sclerosis

CNS findings

A
  • Seizures (95%)
    • Infantile spasms
  • Intracranial calcifications
  • Cortical or subependymal tubers
105
Q

Tuberous Sclerosis

systemic findings

A
  • Renal cysts
  • Cardiac rhabdomyomas
    • # 1 cause of neonatal cardiac tumors
  • Retinal astrocytoma or hamartoma
  • Mental retardation
106
Q

Neurofibromatosis type 1

inheritance

skin findings

A
  • Autosomal dominant
  • Cafe-au-lait spots
  • Axillary or inguinal freckling
  • Plexiform neurofibroma or skin neurofibromas
107
Q

Neurofibromatosis type 1

CNS findings

A
  • Optic glioma (3 YO)
  • Intracranial calcifications
  • CNS neurofibromas
108
Q

Neurofibromatosis type 1

systemic findings

A
  • Osseous lesions (1 YO)
    • Sphenoid dysplasia
    • Thinning of long bone cortex
  • Scoliosis
  • HTN
  • Learning problems
109
Q

What are congenital nevi?

A
  • Black, brown, tan, flesh-colored papules/plaques
  • Birth-6 mo
  • 1-2% of neonates
  • Increased risk of malignancy
    • Giant nevi (>20 cm) have 6-7% lifetime risk of malignant melanoma
  • Management
    • Excision
    • Careful observation
110
Q

What are acquired nevi?

A
  • Moles
  • 2-3 yrs, 11-18 yrs
  • Well-demarcated brown/black papules
  • Increase in size & number during puberty or pregnancy & after sunburn
  • Most are junctional nevi
  • Risk of malignant transformation lower than congenital
  • Management: careful observation
111
Q

What are 4 common disorders of the hair?

A
  • Alopecia areata
  • Tinea capitis
  • Traumatic alopecia
    • Trichotillomania
    • Traction alopecia
  • Telogen effluvium
112
Q

Alopecia areata is caused by ________ & affects ______ persons.

A
  • Autoimmune lymphocyte-mediated injury to the hair follicle
  • 1 in 1,000 persons
113
Q

What are the clinical features of alopecia areata?

A
  • Complete hair loss
    • 1-3 sharply demarcated scalp areas
    • No scalp inflammation
    • Sudden, underlying skin smooth & soft
  • Pitting of nails (40%)
  • Subtypes
    • Alopecia totalis (loss of all scalp hair)
    • Alopecia universalis (body + scalp)
114
Q

How is alopecia areata managed?

A
  • Regrowth of hair w/i 1 yr without treatment
  • Accelerated hair growth
    • topical or injected corticosteroids
    • topical minoxidil
  • Wigs & counseling
115
Q

What is Trichotillomania?

A
  • Conscious or unconscious pulling/twisting of hair
  • Clinical features
    • Irregularly bordered areas of hair loss
    • Hairs broken off at different lengths
    • Scalp: perifollicular petechiae & excoriations
    • Eyelashes & eyebrows also
  • Cause unknown, associated w/ anxiety
  • Management
    • Stress relief
    • Search for precipitating events
    • Application of oils (harder to pull out)
116
Q

What is traction alopecia?

A
  • Hair loss caused by constant traction or friction
  • Tight hair braids or curlers, vigorous scalop massage, constant rubbing
  • Patchy areas of alopecia w/ thinned, small hairs
  • Few broken hairs
  • Management: stop inciting trauma
117
Q

What is Telogen effluvium?

A
  • 2nd most common type of alopecia
    • After male-pattern baldness
  • Acutely stressful event that converts hairs from growing phase (anagen) to resting phase (telogen)
    • Pregnancy, surgery, acute illness, trauma
  • Clinical features
    • Generalized excessive hair loss
      • >100 hairs/day 2-3 mo after event
      • Normal: 50-100 hairs/day
  • Hair loss continues for 3-4 mo, then spontaneously resolves (regrowth)
118
Q

What are some other conditions that cause hair loss?

A
  • Hypothyroidism
  • DM
  • Hypopituitarism
  • Nutrition disorders
    • Hypervitaminosis A
    • Zinc deficiency
    • Marasmus
  • Medications
    • Warfarin, heparin, chemotherapy, cyclophosphamide
  • Ectodermal dysplasia
  • Hair shaft structural defects
119
Q

_____ is the most common skin disease.

120
Q

What is the pathophysiology of acne?

A
  • Excessive shedding & cohesion of cells that line the sebaceous follicles located on the chest, back & face
  • Production of sebum by sebaceous glands under the influence of androgens
    • Obstruction of sebum outflow
    • Comedone formation
  • Inflammation from proliferation of P. acnes
121
Q

What are the clinical features of acne?

A
  • 1-2 yrs before puberty
  • Noninflammatory acne
    • Open comedones (blackheads)
    • Closed comedones (whiteheads)
  • Inflammatory acne
    • Erythematous papules, pustules, nodules, cysts
  • Most pts have both
122
Q

How is acne treated?

A
  • Both types
    • Topcial benzoyl peroxide
    • Tretinoin (Retin-A)
    • Salicylic acid
  • Inflammatory acne
    • Antibiotics (oral, topical)
    • Benzoyl peroxide
  • Systemic isotretinoin (Accutane)
    • All types (nodular & cystic also)
    • Pregnancy test & birth control due to teratogenic effects

Pediatrics (24 decks)

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