androgenetic alopecia

progressive minaturization of terminal hairs or shortening of anlagen phase. presents as a pattern type hair loss classified using the Hamilton-norwood scale in males or the Ludwig scale (females). considered to be an androgen-dependent trait with polygenetic inheritance and variable penetrance.

testosterone --> dihydroteesotserone (associated with pattern baldness, chest, beard hair, leg and arm hair)

in most situations person is healthy but is possible to have abnormal hormone production that results in pattern thinning.

alopecia areata

complex, genetic immune mediated disease that targets anlagen hair follicles. affects 2% of population. disease may be limited and patchy, extensive or with complete body and scalp hair loss. in AA, the hair follicle is not destroyed and maintains the potential to regrow hair. it can affect anybody!

it can also affect the nails. the most common clinical feature is nail pitting. nails may also be thin and brittle and may shed.

telogen effluviuvm

premature conversion of anagens follicles to telgen. associated with many situations including postpartum period, medications, weight loss, acute/chronic illness. it may be acute or chronic and persist. when it persists it is associated with significant temporal thinning.

lichen planopilaris

more common in Females. caucasians. clinically presents with perifollicular scale and inflammation that eventually leads to scarring. 50% have associated lichen plans maybe use itching during of the scalp. histology: band like lymphocytic infiltrate affecting hair follicle mostly at the bulge region. perifollicual fibrosis noted early; later more extensive fibrosis with loss of sebaceous glands and hair follicles.

frontal fibrosis alopecia

central centrifugal cicatricial alopecia

Shiny ivory, atrophic appearance. loss of hair follicles can be seen on ndermoscopy. goal of treatment into t prevent scaring or further scaring.

lichen plalnopilaris is an example of this.

Hirsutism

presence of terminal hair growth following a similar pattern to that developing in androgen-dependent sites in men after puberty. it is frequently associated with androgenetic alopecia or other signs of androgen excess such as acne. may be end-organ specific (hair follicle only), inherited or associated with ovarian or adrenal gland disease.

infectious

dermatophyte is the most common. trichophyton rubum is the most common organism and often occurs with tines pedis. presents with white,yellow, orange or brown streaks or pathches under a thickens nail plate. it is usually chronic and progressive if not treated.

bacterial infections: pseudomonas= common colonizer of onycholytic nails. the nail us usally discolored green or black. patients often have a history of wetwork

papulosquamous

psoriasis: commonly presents with pitting, onycholysis, sublingual debris and discoloration. patients with nail involvement are more likely to have psorati arthritis. psoriatic nails can be secondarily infected with a dermatophyte.

lichen Plans: commonly occurs in isolation without any evidence of skin/mucosal lichen plants. presents abruptly with longitudinal ridging, thinning, and fissuring of the nail plate and possible pterygium.

traumatic

habit tic deformity: roughly parallel, horizontal depressions most often over the median nail plate caused by picking, rubbing or scratching the proximal nail fold or cuticle.

onycholysis: nail plate is detached from the nail bed. most often caused by exposure to irritants or physical trauma, but can also be caused by onychomycosis, psoriases and medications.

systemic

beau lines: horizontal depressed white nonbonding bands of the nail plate. can be caused by systemic insults, drugs, or trauma.

clubbing: over curvature of the nail can be idiopathic or related to cardiovascular pulmonary or gastrointestinal disorders.

koilonchychia (spoon nails): center of the nail is depressed relative to the edges. can be caused by iron deficieny,hyporthyroidism, trauma or congenital

spinter hemorrhage: small, longitudinal lines of dark discoloration, usually aged by trauma but can be related to systemic illnesses or drugs

terry's nails: nails are white proximally with a narrow pink or brown distal band. can be related to liver disease or aging.

tumors

newborn skin

thinner , less hair and more fragile. body surface area to weight is 5X higher--> increased risk for percutaneous absorption of topical medications and infections.

preterm infants <32 weeks GA have immature stratum corner--> inc. risk for dehydration and electrolyte imbalances

cutis marmorata

common. physiologic pattern of erythema on newborn spin. prominent mottling of the skin on exposure to cold, resultant dilatation of capillaries and venues. warming improves the appearance. it is usually transient and no treatment is required.

nevus simplex

most common vascular birthmark present in 80% of all newborns. midline facial nape of neck (tend to persist in neck) locations. immature innervation of dermal capillaries. facial lesions face over first 1-2 years, no treatment necessary. in extensive cases or on other areas of the body further work up could be indicated.

erythema toxic neonatorum

may present at birth but typically appears within 24-48 hours.

morphology: erythematous macules and papules that rapidly progress to flaccid pustules (non infectious) on an erythematous base.

distribution: face, trunk, buttocks and proximal extremities. palms and soles re almost never affected. aside from the rash, the infant is otherwise healthy.

transient pustular melanosis

benign, asymptomatic, self-limited. mainly seen I healthy newborn with skin of color. etiology unknown.

morphology: vesicles superficial pustules and pigmented macules. vesicles and pustules are fragile and May present with a rim of surrounding scale.

distribution: usually located on the chin, neck forehead, chest, buttocks and less often on palms and soles. improves 1-2 weeks, no treatment necessary

congenital nevi

benign proliferation of melanocytes present at birth. grow in proportion to patients. classified based on size. 1% of newborns have a small CMN. risk of melanoma is very low. periodic surveillance of CMN recommended.

cafe au lait macules

very common. light tan to brown, oval maculs that can occur anywhere on body. many children have 1 or a few. in a setting of > 5 CALM can be seen in the setting of several conditions including nueurofibromatosis type 1. they arise due to mutations in the NF1 gene (further evaluation and or referral to a specialist) expressed in melanocytes. children may acquire more over time.

neurofibromatosis type 1: autosomal dominant. fairly common. due to mutations in nuerofibromin gene leading to age related abnormalities tissue proliferation. NF gene is involved in the ras/map kinase signaling pathway. children with a diagnosis of NF require age related anticipatory counseling and management.

criteria: 2 or more of the following: 6 cafe aux lai, 2 or more neurofibromas, optic glioma, 2+ litchi nodules, first degree relative with NF1

selected syndrome

infantile hemangioma ( see more under vascular birthmarks)

most common benign vascular tumors (4%). risk factors: low birth weight, female gender, twin gestation and fair skin. after birth, a premonitory mark may be present such as a bruise-like patch, area of vasoconstriction/pallor or telangiectasia.

infantile hemangioma

most common benign vascular tumors (4%). risk factors: low birth weight, female gender, twin gestation and fair skin. after birth, a premonitory mark may be present such as a bruise-like patch, area of vasoconstriction/pallor or telangiectasia.

proliferate during first 2-3 months of life with rapid growth of superficial IH between 5-7 weeks. growth usually stabilizes around 4-6 mo. followed by involution over years. larger deeper IH grow for longer and involute more slowly. based on these growth characteristics. IH requiring intervention should be referred for treatment before 3 months of age.most require no intervention

possible complications: ulceration ,visual impairment, multifocal presentation, aesthetic complications, complex associations ( PHACE, LUMBAR/SACRAL). oral propranolol = new treatment.

capillary malformations (prot wine stain)

capillary malformation that is fully present at birth though may not be noted. it occurs in 0.3% of newborns. V1 distribution is associated with Sturge Weber Syndrome.

note: storage-weber syndrome: facial PWS in V1 distribution. have a mutation in GNAQ. ocular and leptomeningeal anomalies. neurological involvement (seizures, contralateral hemiparesis, developmental delay, migraine headaches, tram track calcifications ) and ocular findings( congenital glaucoma, increased choroidal vascularity)

progressive and thicken over time, and dilate further with age. they can be treated with laser, usally pulsed dye. Redarkening may occur but not extent of baseline. recommended ophthalmology follow up in V1 and v2 PWS.

Hypopigmented birthmarks

segmental pigmentation disorder: block like areas of hypertension or hyper pigmentation that follow lines of blaschko, benign and persist throughout life. not associated with other syndromes.

, nevus depigmentosus,

ash leaf macules/confetti macules (often seen with tuberous sclerosis and may be the presenting sign) oval ill defined hypo pigmented macules or patches >3 further workup is needed.

tuberous sclerosis: neurocutaneous disorder due to mutations in TSC1/2 genes. presents during infancy with cutaneous findings, or seizures. 80% of patients present with the confetti or ash leaf maces. infants develop multiple benign tumors in skin, CNS, kidney, lungs and heart.