Derm Flashcards
Macules
< 1 cm; circumscribed and flat
Patch
flat, >1 cm
Papules
raised, < 1cm
nodules
papules > 1 cm, in dermis or subcutatneous area
Plaques
well defined elevated confluence of papules > 1cm
Vesicles
circumscribed, fluid containing epidermal elevations < 1 cm
Bulla
vesicle > 1 cm
Pustules
circumscribed, small elevations with purulent exudate
Wheals
plateau-like edematous elevations, pink or red
Scale
dry or greasy flakes of stratum corneum
Crust
dried serum, blood or pus with debris on skin surface
Excoriation
shallow, hemorrhagic linear excavation
Erosions
loss of all or portions of epidermis from physical abrasions, vesicles, or bullae
Ulcer
rounded or irregular shaped excavations into dermis or deeper
Fissure
linear deep skin split through epidermis or into dermis
lichenification
thickened skin with accentuated skin markings
atrophy
decreased skin thickness
Congenital Melanocytic Nevi (CMN)
macules, papules or plaque AT BIRTH, +/- hair, lesions grow in proportion to individuals size
CMN Risk of malignancy
increased size of CMN = increased risk of malignant potential; risk of melanoma
Most common pigmented lesion in infants
Mongolian spot
Mongolian Spot other name
Congenital dermal melanocytosis (CDM)
Mongolian spot
bluish-grey patch with irregular border and normal texture
Mongolian spot dx
clinical; further work up if FTT or not meeting developmental milestones
Mongolian spot prognosis
fades by age 2 and disappears by age 10
may be mistaken for abuse
CDM (mongolian spot)
Nevus sebaceous
hyperplasia of epidermis, sebaceous glands, hair follicles, apocrine glands
Nevus sebaceous clinical presentation
usually on scalp or face; waxy solitary, smooth, yellow-orange hairless patch, often oval or linear; more pronounced in adolescence (bumpy, warty or scaly)
Goes away with age
Mongolian spot
Grows with age
CMN
More pronounced in adolescence
Nevus Sebaceous
nevus sebaceous dx
some may need histological evaluation; BCC or other malignancy may arise from lesions
Nevus sebaceous tx
f/u, refer to derm if concerning changes are observed
Malignant potential
CMN, Nevus Sebaceous
Aplasia Cutis Congenita (ACC)
absence of skin present at birth
ACC presentation
most commonly found midline posterior scalp (may have tuft of hair = neural tube defect), may be associated fluid-filled bulla, well demarcated
ACC tx
gentle cleaning and ointment, hypertrophic scar may develop, refer to neuro for surgical repair if large or multiple scalp lesions
ACC imaging
done if atypical/large or hair tuft
Cafe-au-lait Macultes (CALM)
uniformly pigmented macules/patches; most common in african americans; present at birth OR in early childhood
CALM lesions are associated with what conditions
McCune-Albright syndrome or NF1
Neurofibromatosis
autosomal dominant (50% new mutations)
Sx of NF1
cafe-au-lait, axillary or inguinal freckling, neurofibromas, lisch nodules, optil gliomas, skeletal abnormlaities
Kids with NFI need what
yearly ophthalmology exams starting at 1 year
Types of vascular anomalies
- Tumors: neoplasms proliferate and typically require tx to stop growth
- Malformations: abnormal blood vessels without rapid proliferation (static/slow growing)
Vascular Tumors
infantile hemangioma, congenital hemangioma, pyogenic granuloma
Vascular malformations
capillary malformations (CM), port-wine stain, nevus simplex
Port-Wine Stain (PWS)
cutaneous capillary malformation; present at birth and DOES NOT REGRESS; pink/dark red patch (may darken/thicken)
PWS associated with
soft tissue or bony overgrowth, Sturge Weber Syndrome in V1 distribution (congenital glaucoma concerns if patch affects eyelid)
Sturge Weber Syndrome
PWS in V1 distribution; concern for congenital glaucoma
PWS tx
No tx needed; Pulse dye laser, widespread/extremity overgrowth = refer to vascular specialist
Pulse dye laser
tx for PWS; causes intravascular coagulation in abnormal vasculature without damaging surrounding structures (do early before it progresses)
Most common benign vascular tumor
Infantile hemangiomas
Risk factors for infantile hemangiomas
LBW, female, twin gestation and fair-skin
Clinical presentation of infantile hemangiomas
NOT PRESENT AT BIRTH but appear shortly after, can be superficial (bright red and minimally elevated), deep (large with bluish color) or mixed; ulceration is common complication
Infantile hemangiomas stages
Proliferative:
1. Early- rapid growth during first 3 months of age (max: 5–7 weeks)
2. Late- less rapid but still ongoing; completed @ 9 mo
Involution: Color darkens and tumors softens, ultimate residual skin changes vary
Completed growth of infantile hemangioma
9 mo
Max growth period of infantile hemangioma
5-7 weeks of age (grows rapidly first 3 mo)
Nevus simplex is also known as…
Salmon Patch
Nevus Simplex presentation
faint, TRANSIENT capillary malformation; flat, pink/red patch typically midline of forehead, scalp, upper eyelids, posterior neck and back
Most common pediatric vascular lesion
Nevus simplex (salmon patch)
NS on nape of neck
stork bite
NS on eyelid
angel’s kiss
Time period for NS
fade within 1-2 years
Pyogenic Granuloma
acquired (not born with) lobular vascular tumor; occurs at any age and affects skin prone to traums (hands, fingers, face and mucous membrane); develop rapidly (days to months); FRIABLE, can recur despite treatment
Pyogenic granuloma tx
biopsy to confirm dx (surgical excision with primary closure, curettage or shave remove w/ electrodessication, pulsed dye laser); risk of recurrence is high; tx is traumatic (viscious cycle)
When to refer hemangiomas to emergent ENT
mandibular hemangioma with stridor or hoarseness; evaluate for airway compromise
Diaper dermatitis causes
irritant/contact; seborrheic dermatitis, atopic dermatitis or other underlying skin conditions
Diaper derm presentation
episodic with varying severity, persistnec = secondary infection with C. albicans, etc
Candidal superinfecton
beefy red plaques (involves skin folds); dx with KOH
impetigo
secondary infection of S. aureus or S. pyogenes; fragile pustules and honey crusted erosions
Honey crusted erosions
impetigo
Bacteria behind impetigo
S. aureus and s. pyogenes
Diaper dermatitis therapeutic options
EDUCATE; barrier cream (paste/ointment), low-potency topical steroid if severe or not resolving; breast-milk (anti-inflammatory and anitmicrobial); DON”T USE POWDERS
Tx for diaper derm candida infection
Topical antifungal
Tx for diaper derm bacterial superinfection (impetigo)
Mupirocin
Lice
Pediculus humanus capitis
Clinical presentation of lice
asymptomatic; itching if allergic to saliva, cervical LAD, febrile w/ secondary staph infection
Dx for Lice
visualize live lice (wet-combing); nits may persist for months and does not indicate active infection
Tx for lice
topical pediculicides (pyrethroids, malathion, benzyl alcohol, spinosad)- rinse in sink to avoid skin irritation; wet combing (mechanical removal) w/ conditioner, 15-60 minutes every 3-4 days for several weeks
Prophylactic tx for lice
only bedmates
Topical pedicullices
pyrethroid, malathion, benzyl alcohol, spinosad
Neonatal cephalic pustulosis (Neonatal acne)
not true acnes; inflammation due to Malassezia; self-limited; presents first 2-3 weeks and resolves by 6-12 months
Neonatal acne presentation
first 2-3 weeks
Neonatal acne resolution
by 6-12 months (usually by 4 months without scarring)
Not true acne
neonatal acne
Clinical presentation of neonatal acne
inflammed papules/pustules on forehead, nose and cheeks; no comedones
Tx for neonatal acne
self-limiting
Mild- cleanse w/ mild soap and water
persistent acne: ketoconazole or hydrocortisone to expedite clearance
Infantile Acne
hyperplasia of sebaceous glands; inflammatory papules, comedones, pustules
Presentation of infantile acne
3-4 months
Resolution of infantile acne
2-3 years
Tx for infantile acne
benzoyl peroxide, topical abx, topical retinoids; oral tx only in severe cases
“true acne”
infantile acne
“the itch that rashes”
atopic dermatitis
Atopic dermatitis presentation
infants: cheeks, trunk and extensor surfaces
Adults: neck, flexors, hands and feet
Tx for atopic derm
petroleum (vaseline) AAA 2x daily; topical steroids, topical calcineurin inhibitors (elidel, protopic), antihistamines
Cradle cap
seborrheic dermatitis
yellow, greasy adherent scales on vertex of scalp (may also effect diaper area and axilla)
cradle cap
herald patch
pityriasis rosea
Pityriasis rosea
benign, viral skin exanthem, mild pruritis, large salmon colored herald patch with colarrette scale followed by smaller lesions; christmas tree patern
Vitiligo
acquired skin depigmentation via autoimmune process against melocytes
Vitiligo presentation
milk-white macules with homogenous depigmentation and well-defined border, slowly progressive; tx with topical steroids
Measles (rubeola)
highly contagious; clinical stages: 1. incubation (2-3 weeks), asymptomatic
- Prodrome (anorexia, malaise, fever >105
- Enanthem (koplik spots- bluish white papules (48 hours prior to rahs)
- exanthem: blanching, maculopapular rash starting on face and spreading head to toe (spares palms and soles)
Erythema infectiosum also known as…
Fifth’s disease
Etiology of Erythema infectiosum
Parvovirus B-19
Erythema infectiosum presentation
Stages:
- Incubation 7-14 days
- Prodrome: flue like 2-3 days (mild fever, malaise, coryza)
- Facial rash: slapped cheek
- Body rash: 2-3 days after face rash/ lacy, pink macular rash of trunk and xtremitites
Lacy pink rash
Fifth’s disease
Slapp Cheek
Fifth’s disease
Hydrops fetalis
fifth’s disease
Blueberry muffin
Congenital rubella syndrome (lethal)
Roseola Infantum
caused by HHV-6; peak 7-13 months; high fever, resolves, rash appears (blanchable, pink macules), starts on neck /trunk then spreads to face
Measles symptoms (prodrome)
3 C’s: cough, coryza, conjunctivitis
Etiology of hand, foot, mouth
coxsackie A16 virus
Etiology of molluscum
Poxvirus
Clinical presentation of molluscum
flesh colored, pearly, papules with umbiliciation; not on palms or soles; resolve 6-12 months
Verruca Vulgaris etiology
HPV
Varicella presentation
Pruritic, lesions at different stages (papule, blister, ulcer) over 4 days and crust over in 6 days
Herpes Zoster (shingles)
neuritic pain (throbbing, stabbing, burning), grouped vesicles on erythematous base in dermatomal distribution (unilateral)
Etiology of tinea versicolor
Malassezia
Etiology of thrush
candida albicans
Thrush
mouth pain; creamy-white patches/plaques with underlying erythematous mucosa; thrush will brush