pigment, hair, nail, and misc derm disorders

hyperpigmentation causes

systemic disorders, medications, cancer, addison disease, B12 deficiency, hemochromatosis, Wilson disease

hypopigmentation types

focal, diffuse

focal hypopigmentation

vitiligo, tinea versicolor

diffuse hypopigmentation

albinism

pigment disorder pathophysiology

amount of melanin produced changes, not number of melanocytes

melanin production

stimulated by UV radiation

vitiligo

acquired autoimmune pigmentary skin disorders

vitiligo potential causes

melanocyte destruction, hyperactive immune system

vitiligo associated diseases

thyroid disease, diabetes, pernicious anemia, addison’s disease

vitiligo clinical presentation

depigmentation of fingertips, knuckles, ventral wrist, axilla, toes, ankles, around eyes/mouth, hairline, genitals

sharply demarcated, usually symmetric hypopigmented/depigmented macules/patches on skin

vitiligo diagnostics

skin bopsy/electron microscopy to show absence of melanocytes

CBC, ACTH, B12, A1C, Thyroid function

vitiligo treatment <20% involvement

topical tacrolimus 0.1%

topical superpotent corticosteroid

topical JAK inhibitor (ruxolitinib)

vitiligo treatment >20% involvement

narrowband UVB

PUVA

melasma

facial hyperpigmentation common in women/pregnancy/OCP/HRT

more common in non-white

melasma clinical presentation

well demarcated light to dark brown hyperpigmented macules or patches usually on face and symmetrical

melasma treatment

gold standard - hydroquinone to decrease melanin formation

sun avoidance/protection

often resolves after pregnancy

acanthosis nigricans

hyperpigmentation, common predictor of metabolic syndrome/insulin resistance

metabolic syndrome

cluster of conditions that occur together increasing risk of heart disease, stroke, and T2D

obesity, hypertriglyceridemia, low HDL, HTN, hyperglycemia

acanthosis nigricans clinical presentation

brown to black ill defined velvety hyperpigmented plaques

often on lateral neck folds, axilla, groin, elbows, knuckles

acanthosis nigricans diagnostics

A1C, lipid panel, thyroid function

acanthosis nigricans treatment

topical: salicylic acid, tretinoin, vit D ointment

oral: metformin, fish oil

laser therapy

melanocytic nevi

benign mole, usually <6mm with well defined border

early on are flat, small “junctional nevi” that can later enlarge and become raised “compound nevi”

atypical/dysplastic nevi

larger moles (>6mm) with ill defined irregular border and irregular pigmentation

risks: sun exposure

atypical nevi melaooma risk

50+ total, one ≥8mm, many atypical moles

blue nevi

small, slightly elevated, blue-black moles common on dorsal hands

MC in Asian pts

malignancy is rare

hair composition

elastic keratin filaments

hair growth phases

anagen → catagen → telogen

scarring/cicatricial alopecia

absent follicular markings/scar

follows trauma/inflammation that prevents hair growth

irreversible and permanent

scarring alopecia

present follicular markings

often in association with systemic disease

types of nonscarring alopecia

androgenetic alopecia, telogen effluvium, alopecia areata, trichotillomania

common trauma preceeding scarring alopecia

chemical/physical trauma, burns, infection, skin conditions (lupus), radiation, trichotillomania

scarring/cicatricial alopecia diagnostics

scalp biopsy from active border

scarring/cicatricial alopecia treatment

derm referral

1st line - topical/intralesional steroids and tetracyclines

2nd line - hydroxychloroquine, immunosuppressant

androgenetic alopecia

MC type of alopecia usually following puberty and worsens with age

androgenetic alopecia PE

males: widow’s peak and vertex

females: vertex and widening part

light hair pull test

grab 50-60 hairs and pull lightly in 2+ areas

6+ removed = positive

androgenetic alopecia diagnostics

males: none

females: assess hyperandrogenism

androgenetic alopecia nonpharmacologic treatments

follicular hair transplant

laser comb

hair pieces

platelet rich plasma

androgenetic alopecia pharmacologic treatments

minoxidil 5% topical daily

males: finasteride 1mg PO

females: spironolactone 50-200mg

telogen effluvium

transitory increase in number of hairs in telogen/resting phase

telogen effluvium causes

postpartum, crash dieting, malnutrition, fever/illness, stress, hormonal contraceptives

telogen effluvium clinical presentation

hair loss with large number of hairs with white bulbs coming out with gentle tugging of hair

telogen effluvium diagnostics

examine hair - anagen:telogen ratio

scalp biopsy

ferritin labs if iron deficiency suspected

telogen effluvium treatment

observation, maybe topical minoxidil

if d/t iron deficiency, supplements

alopecia areata

complex genetic, immune mediated disease that targets anagen follicles

associated with hashimoto’s, pernicious anemia, addison’s, vitiligo, SLE, mental health, atopy

alopecia areata PE

1-4cm well demarcated patches of hair loss

exclamation hairs 2-3mm

can affect nails and cause pitting/onychodystrophy

alopecia areata diagnostics

autoimmune labs

scalp biopsy

alopecia areata treatment

usually self limiting

topical/intralesional corticosteroids (triamcinolone acetonide) or minoxidil

trichotillomania

pulling out one’s own hair

trichotillomania PE

irregular patches of hair loss, almost always short growing hairs present and unilateral to dominant hand side

trichotillomania treatment

CBT, n-acetylcysteine

onychophagia

nail biting

fingernail growth rate

3mm/month

toenail growth rate

1mm/month

decreased nail growth causes

age >50, fever, onychomycosis, malnutrition

increased nail growth causes

pregnancy, hyperthyroid

onycholysis

distal separation of nail plate from nail bed

paronychia

inflammation of lateral or proximal nail folds

onychoschizia

splitting of nails

systemic/generalized skin diseases that cause nail disorders

beau lines, vascular/neurologic disease, hypoxemia (clubbing), anemia (spoon nails), psoriasis/alopecia areata (pitting), hyperpigmentation (chemo)

onychomycosis

tinea unguium, fungal infection of nail

onychomycosis risk factors

diabetes, tobacco, immunocompromised, recurrent trauma, vascular disorders

local nail disorders

onycholycosis, dermatophyte, paronychia, distortion

onychomycosis MCC

dermatophytes (require keratin to grow, trichophyton/epidermophyton) then yeasts (candida albicans)

onychomycosis PE

nails are lusterless, brittle, hypertrophic, friable

onychomycosis diagnostics

KOH prep, fungal culture, periodic acid-Schiff stain

onychomycosis treatment

difficult!

topical antifungal therapy with limited value (efinaconazole 10%, tavaborole 5% not as effective)

systemic preferred - terbinafine 250mg daily x6-12 weeks, itraconazole 200-400mg daily 7 days per month x 2-12 months

watch LFTs/CBC with antifungals

paronychia

inflammation and pus accumulation along lateral nail fold usually due to mixed flora

paronychia treatment

if no abscess - warm soak, maybe augmentin

if abscess - I&D, augmentin

urticaria pathophysiology

IgE attach to mast cells and release histamine in superficial dermis, vascular permeability increases and fluid accumulation causes cutaneous lesions

herpetic whitlow

HSV infection usually on hands of dentists, HC workers

5 Is of urticaria

infection, injection (drug/venom), inhaled (pollen), ingestion (food), internal disease

urticaria clinical presentation

pruritis and wheals

check for anaphylaxis!!! (airway, GI, hypotension)

chronic inducible urticaria triggers

cholinergic, solar, cold, dermatographism

urticaria diagnostics

patch testing, autoimmune labs

urticaria treatment

stop offending agent, cool baths, loose clothing, antihistamines, leukotriene inhibitors, oral corticosteroids if severe

photosensitivity reactions

photodermatitis reaction to UV radiation

4 photosensitivity reactions

primary idiopathic, drug/chemical induced, UV exposure, genetic diseases

phototoxic photosensitivity

nonallergic, MC, associated with medications

photoallergy

delayed type hypersensitivity reaction to UV exposure

photosensitivity reaction clinical presentation

acute inflammatory phase, pain, fever, GI upset, malaise, erythema, edema, vesicles/oozing

key - rash only on photoexposed areas

photosensitivity management

identify offending agent, symptomatic treatment (cool compress, topical/oral glucocorticoids)

if persistent - systemic corticosteroid, immunosuppressant

lipoma

common soft tissue mobile subcutaneous nodules of fat cells MC in males

lipoma clinical presentation

slow growing, soft, mobile painless <5cm subcutaneous nodule often on trunk, shoulder, upper arm, neck

lipoma treatment

not necessary

can remove if >5cm/fast growing/concerning

epidermal inclusion cyst

benign growth of upper part of hair follicle common in Gardner syndrome

epidermal inclusion cyst clinical presentation

firm, dermal papule maybe with overlying black comedone/punctum on face/trunk

expresses foul smelling cheesy material

epidermal inclusion cyst diagnostics

culture, biopsy

epidermal inclusion cyst treatment

none if asymptomatic

surgical removal and be sure to get entire cyst wall to prevent recurrence

intralesional corticosteroids

pressure ulcer

maceration/friction/shearing causes injury, common over bony prominences

pressure ulcer clinical presentation

localized damage to skin and underlying soft tissue often over bony prominence

intact skin or open ulcer

stage 1 pressure ulcer

nonblanchable erythema of intact skin

stage 2 pressure ulcer

extends through epidermis/dermis, superficial and appears like abrasion/lac/blister

stage 3 pressure ulcer

full thickness skin loss involving damage or necrosis of sub-q tissue, can extend down to but NOT through fascia, appears as deep crater

stage 4 pressure ulcer

full thickness wounds with extensive destruction, tissue necrosis, damage to muscle/bone

pressure ulcer labs

CBC for infection

ESR/CRP for osteomyelitis

CMP for BF, albumin, LFT/KF

wound culture

maybe blood culture/bone biopsy

pressure ulcer imaging

XR

MRI for osteomyelitis

pressure ulcer treatment

prevention, moist wound environment, maybe surgical debridement