Lecture Keywords: (★)

Nail Changes (3 most common conditions):

• Tinea unguium – distal, proximal, superficial types; brittle nails
• Candidal onychomycosis – paronychia, nail discoloration, nails not brittle
• Psoriatic nail – brittle nails, distal onycholysis, lesions (pits, oil spots, salmon patch)
Erythematous Non-Scaly Papules:
• Miliaria rubra – tiny papules, body folds, hot weather
• Scabies – Circle of Hebra, nocturnal itching, other contacts
• Insect bites – papules with puncta, arms and legs
• Pediculosis – papules near hairy areas, nits
• Acne vulgaris – not itchy, no vesicles, face chest and back, comedones (lesions with plugs)

Alopecia:
• Alopecia areata – round bald patches, exclamation point hairs
• Trichotillomania – irregularly shaped bald patches, varying lengths of hairs within a patch, girls, patient pulls
hairs
• Telogen effluvium – no bald patches, diffuse hair loss, 3-5 months after cause

Onychomycosis (Tinea Unguium)

Description:
• Infection of the nail plate by fungus, represents up to 30% of diagnosed superficial fungal infections
• 4 classic types:
o Distal subungual onychomycosis – most common (★)
▪ Distal nail bed and hyponychium + secondary involvement of the underside of the nail plate of
fingernails and toenails
▪ Usually caused by T. rubrum, T. tonsurans growing in prevalence in children
o White superficial onychomycosis (leukonychia trichophytica)
▪ Invasion of the toenail plate on the nail surface
▪ T. mentagrophytes, Cephalosporium, Aspergillus, and Fusarium oxysporum fungi
▪ HIV – T. rubrum
o Proximal subungual onychomycosis
▪ Nail plate mainly from the proximal nailfold, may indicate HIV
▪ T. rubrum, Trichophyton megninii
o Candida onychomycosis (C. albicans)
▪ Destruction of the nail + massive nail bed hyperkeratosis
▪ Seen in patients who are immunocompromised and have chronic mucocutaneous candidiasis,
also diabetic patients and those with an atopic background
• Chronic mucocutaneous candidiasis (CMCC):
o Heterogenous group of patients whose infection with Candida is chronic but limited to mucosal
surfaces, skin, and nails
o Onset is typically before age 6, onset in adulthood may herald thymoma
▪ Inherited (linked to endocrinopathy) or sporadic
o Oral lesions are diffuse, perlèche and lip fissures are common
o Nails become thickened and dystrophic, with associated paronychia
o Hyperkeratotic, hornlike, or granulomatous lesions are often seen
• Pathogen is influenced by heredity, geography, and footwear
o Many are asymptomatic and may not seek treatment
o Diabetes, peripheral neuropathy – higher risk for bacterial cellulitis related to onychomycosis
o Acute paronychia – typically staphylococcal in origin; chronic paronychia – multifactorial (irritant
dermatitis and candidiasis may play important roles)

VHCC 3A-MED | ANDREW’S 13TH ED + LECTURE NOTES (★)

 • KOH – can be performed rapidly in the office
o Dermatophyte – long septated hyphae; Candida – pseudohyphae
Differentials:
• Psoriasis
o May involve other nails with pitting, onycholysis, oil spots, and salmon patches or by heaped-up
subungual keratinization
o Lesions typically start at the center of the nail (★)
o Typical features of psoriasis may be present on other areas of skin
o 22% of cases, men > women, important to get family history (skin is usually the CC, not nails)
• Lichen planus
o May produce rough nails or pterygium formation
o May involve the oral mucosa or skin
• Eczema, contact dermatitis
o Affects adjacent nail fold
• Langerhans cell histiocytosis
o Subungual debris and hemorrhage, may be a marker for systemic disease
• Hyperkeratotic (“Norwegian”) scabies
o May also produce dystrophic nails but is associated with generalized hyperkeratosis
• Repetitive contact urticaria, allergic contact dermatitis to foods and spices
o May mimic candida paronychia

Causes:
• Not all nail changes are due to fungi, but soaking in water increases the risk of fungal infection (★)
• T. rubrum – most common cause
o Usually starts at the distal nail corner, involves the junction of the nail and its bed
o Yellowish discoloration that spreads proximally as a nail streak
o Later, subungual hyperkeratosis becomes prominent and spreads until the entire nail is affected
o Entire nail gradually becomes brittle and separated from its bed (result of piling up of subungual
keratin)
o Fingernails, toenails – similar appearance
o Skin of the soles – likely involved, characteristic branny scaling and erythema
• T. mentagrophytes
o Usually superficial, no paronychial inflammation
o Generally begins with scaling of the nail under the overhanging cuticle
o Remains localized to a portion of the nail, may involve entire nail plate over time
o White superficial onychomycosis – small, chalky white spots appear on or in the nail plate; can be easily
shaved off
• T. violaceum, T. schoenleinii, T. tonsurans, Trichosporon beigelii – occasionally invades the nails
• Scopulariopsis brevicaulis, other nondermatophyte molds – infrequently isolated
o Infection usually begins at the lateral edge of the nail, burrows beneath the plate, and produces large
quantities of cheesy debris
• Nattrassia mangiferae (Hendersonula toruloidea), Scytalidium hyalinum – can also cause moccasin-type tinea
pedis
• Common nondermatophyte molds: Aspergillus species, Fusarium, Acremonium
o More common features of onychomycosis (nail plate thickening, opacification, onycholysis) +lateral nail
invasion alone, paronychia, transverse fracture of the proximal nail plate
o Culture in medium without cycloheximide (found in Mycosel agar)
• C. albicans
o Inflammation of the nailfold → redness, edema, and tenderness of the proximal nailfolds + gradual
thickening and brownish discoloration of the nail plates
o Usually only the fingernails are affected
• Other various fungi – E. floccosum, Microsporum, Trichyphyton, yeasts, nondermatophytic molds

VHCC 3A-MED | ANDREW’S 13TH ED + LECTURE NOTES (★)

 Treatment:
• Nail changes are very difficult to treat since you need to wait for them to slough off then grow (★)
o 3-4 months for fingernails, 6-12 months for toenails (★)
o Always check the proximal, slowly proximal becomes normal first until entire nail sloughs off then
becomes normal again (★)
• No topical agent achieves the cure rates possible with oral therapy, but topical agents have lower risk of side
effects because they are not systemic
o Mild nail involvement – may give topicals but penetration is slow (★)
o Infection may be difficult to eradicate → treat with both systemic antifungals and topical nail lacquers
o Give oral agents to patients with diabetes, soaking cannot be avoided, immunocompromised (★)
▪ Generally effective on Aspergillus spp., Scopulariopsis brevicaulis and Fusarium spp
o Oral griseofulvin – not effective for common nondermatophyte molds (Aspergillus species, Fusarium,
Acremonium)
o Nail avulsion – another option but painful and recurrence is still possible
• #1 treatment of fungal infection – avoid water immersion (★)
• Terbinafine
o Fingernails:
▪ Adults – 250 mg/day for 6 weeks
▪ Children – 250 mg daily for patients over 40 kg, 125 mg (1/2 tablet) for those 20–40 kg, 62.5 mg
(1/4 tablet) for 4 tablet) for those under 20 kg
o Toenails:
▪ Generally 12 weeks
• Itraconazole
o Generally given as pulsed dosing, 200 mg twice daily for 1 week of each month
o 2 months when treating fingernails, 3–4 months when treating toenails
o Pulsed treatment – low incidence of liver function abnormalities
▪ Liver function tests for patients receiving continuous itraconazole for periods exceeding 1
month
• Fluconazole 150–300 mg once weekly for 6–12 months
• Ciclopirox, eficonazole, amorolfine nail lacquers – topical, modestly effective at moderate cost
o Eficonazole, ciclopirox – use for 48 weeks
• C. albicans – most topicals marketed for tinea will also be effective for candidiasis
o Anticandidal agents – can be combined with topical corticosteroids
▪ Fluconazole – remarkable safety record, even when used long term
o Itraconazole or fluconazole but relapses are the rule
▪ Combine topical and systemic treatment (synergistic effect) - topical amorolfine + oral
itraconazole
▪ Oral fluconazole once a week or itraconazole in pulsed dosing – if topical treatment fails
• CMCC – systemic fluconazole, itraconazole, or ketoconazole is necessary for control
o Courses are typically prolonged, repeated, and given at higher doses than usual recommended dose
o Patients with achlorhydria may have problems with absorption of itraconazole and ketoconazole
• Neodymium:yttrium-aluminum-garnet (Nd:YAG) laser therapy
• 20% will not respond to treatment
o Presence of dermatophytoma within the nail may be associated with a higher risk of failure
▪ Yellow streaks within the nail, may respond to unroofing and curettage
o Recurrence rates may be lower with itraconazole than with terbinafine monotherapy, but combined
therapy does not result in a lower rate
• Ozone gas, UV light, visible light – molds are sensitive
o T. rubrum – susceptible to UVC radiation, photodynamic therapy (PDT), psoralen with UVA (PUVA), and
various forms of laser light
o Phthalocyanines, Photofrin – PDT with broad-band white light is fungistatic, porphyrins caused
photodynamic killing
VHCC 3A-MED | ANDREW’S 13TH ED + LECTURE NOTES (★)
 o 5,10,15-Tris(4-methylpyridinium)-20-phenyl-(21H,23H)-porphine trichloride, deuteroporphyrin
monomethylester

Psoriasis
(book chapter too long – just read the trans on this and focus on appearance of lesions, associated s/s, causes (if
meron), differentials, and treatment)

Alopecia Areata
Alopecia areata can have nail pitting
Description:
• Characterized by rapid and complete loss of hair in one or more round or oval patches, typically 1–5 cm in
diameter, usually on the scalp, bearded area, eyebrows, eyelashes, and, less frequently, other hairy areas of the
body
o Sharply circumscribed patch of alopecia with exclamation point hairs at the periphery + absence of
scarring – indicative of alopecia areata
▪ Round, perfect shape; hair bulb becomes payat (★)
o A few resting hairs may be found within the patches
o Early in the course – may have sparing of gray hair, white hairs are rarely affected
o Sudden whitening of hair may represent widespread alopecia areata in a patient with salt-and-pepper
hair
• Associated with atopic dermatitis, Down syndrome, lichen planus, autoimmune diseases (ex. SLE), thyroiditis,
diabetes mellitus, myasthenia gravis, vitiligo
o Most cases can also occur without associated disease
o 25% have family history of alopecia areata
• 10% of patients (especially long-standing cases with extensive involvement) – nails develop uniform pits that
may form transverse or longitudinal lines
o Trachyonychia, onychomadesis, red or spotted lunulae – occur less often
o Dermoscopic exam – diffuse, round, or polycyclic perifollicular yellow dots
• Types of alopecia:
o Alopecia totalis – complete loss of scalp hair
o Alopecia universalis – complete loss of all hair
o Ophiasis – loss occurs confluently along the temporal and occipital scalp
o Sisaipho – inverse of ophiasis (almost the reverse spelling too haha), loss occurs on all areas except the
temporal and occipital scalp
o Acute diffuse and total alopecia – newly defined subtype occurring in young adults, good prognosis
• Migratory poliosis of the scalp – may represent a forme fruste of alopecia areata
o Migrating circular patches of white hair, but never lose hair
Differential:
• Pattern alopecia
o Rarely, alopecia areata may present in a diffuse pattern that may mimic pattern alopecia
▪ Look for history of periodic regrowth, nail pitting, presence of tapered fractures or “exclamation
point” hairs
▪ Alopecia areata – generally presents as an anagen effluvium, with an inflammatory insult to the
hair matrix resulting in tapering of the hair shaft and fracture of anagen hairs
▪ As the hair miniaturizes or converts from anagen to telogen, the remaining lower portion of the
hair rises above the level of the scalp, producing the exclamation point hair
• Tinea capitis, androgenetic alopecia, early lupus erythematosus (LE), syphilis, congenital triangular alopecia,
alopecia neoplastica, trichotillomania
• Pheidole ants – endemic areas of Southwest Asia
o Ants shear hair shafts during the night → overnight loss of clumps of hair
Cause:
• Follicular melanocytes in hair are the targets of activated T cells in alopecia areata
VHCC 3A-MED | ANDREW’S 13TH ED + LECTURE NOTES (★)
 Treatment:
• Natural course of hair loss is highly variable, some patches regrow without treatment
o Tendency for spontaneous recovery if postpubertal onset
▪ Regrowing hairs are downy and light in color → replaced with stronger and darker hair with full
growth
▪ Poor prognosis – atopic dermatitis, childhood onset, widespread involvement, ophiasis,
duration of longer than 5 years, onychodystrophy
o Long-term treatment frequently needed to maintain growth
o Patient education, wigs, innovative therapies – to alleviate psychological stress
• Intralesional injections of corticosteroid suspensions – treatment of choice for localized, cosmetically
conspicuous patches (those in the frontal hairline or in the eyebrows)
o Injections of triamcinolone 2–10 mg/mL – given intradermally or in the superficial subcutaneous tissue
▪ Large volumes and higher concentrations of triamcinolone – greater risk of atrophy
o Injection under significant pressure/with a small-bore syringe – increased likelihood of retinal artery
embolization
• High-strength topical corticosteroids – may be safer first-line therapy, less reliable than injections
• Other treatment options:
o Monthly methylprednisolone 500 mg/day for 3 days, 5 mg/kg twice daily over 3 days in children
o Oral and topical Janus kinase (JAK) inhibitors (tofacitinib, ruxolitinib)
o Phosphodiesterase 4 inhibitors, platelet-rich plasma – unclear
o Short-contact topical anthralin 1% cream – applied for 15-20 minutes then shampooed off
o Topical minoxidil – can be combined with other treatments or used alone
o Psoriatic doses of methotrexate and sulfasalazine up to 1.5 g three times daily
o Cyclosporine – alone or with other modalities
o 308-nm xenon chloride excimer laser (300–2300 mJ/cm2/session)
o Travopost, bimatoprost, latanoprost – for eyelash disease, associated with periocular pigmentation and
iris darkening
o Botanicals (including peony glucosides and glycyrrhizin)
• Refractory cases
o Induction of contact sensitivity to squaric acid dibutyl ester, dinitrochlorobenzene (DNCB), and
diphencyprone
o Topical/oral methoxsalen (psoralen), ultraviolet A (PUVA) therapy – also for widespread lesions
• Biologic agents are not recommended and may even cause alopecia areata

Trichotillomania (Trichotillosis)
Description:
• Compulsive practice of plucking hair from the scalp, brows, or eyelashes
o Seen mostly in girls younger than 10, although boys and all adults may engage in the practice
▪ Since pulling, it’s not a perfect round shape (★)
o Some relate exquisite pain localized to a follicle that can only be relieved by plucking the hair
▪ Usually a manifestation of obsessive-compulsive disorder
▪ May be associated with depression, anxiety, trichophagia (compulsive swallowing of the
plucked hairs)
▪ May result in formation of a gastric bezoar (Rapunzel syndrome)
o Better to ask “how” removal of the hair is done than “if” they remove hair
▪ If this fails – shaving a 3 cm2 area in the involved part of the scalp will result in hairs too short
for plucking and normal regrowth in the “skin window” within 3 weeks
• Typical areas are irregular patches of alopecia that contain hairs of varying length
o Scalp has a rough texture because of the short remnants of broken-off hairs

Differential:
• Alopecia areata – shares many histologic features, look for peribulbar lymphocytes or inflammatory cells

VHCC 3A-MED | ANDREW’S 13TH ED + LECTURE NOTES (★)

 Treatment:
• Behavior modification, psychotherapy
o Refer to psychologist (★)
• Appropriate psychopharmacologic medication (ex. clomipramine, olanzapine)
• Other treatment options:
o N-acetylcysteine – found to be effective in adults but not in children
o Valproic acid, quetiapine, naltrexone
o Bimatoprost – for eyelashes

Telogen Effluvium
Description:
• Presents with excessive shedding of normal telogen club hairs
o Estimates of loss – 150 to >400
o Most often occurs 3–5 months after the premature conversion of many anagen hairs to telogen hairs
o Induced by surgery, parturition, fever, drugs, dieting, or traction – no matter the cause, hair is lost “at
the root”
▪ Local patches of early telogen conversion may be induced by papulosquamous diseases
affecting the scalp
▪ Pattern (androgenetic) alopecia, chronic telegon effluvium
▪ Topical minoxidil
▪ May be related to protein or other nutrient deprivation – assess dietary habits, iron saturation,
ferritin, diseases involving blood loss (menstruation, GI blood loss)
▪ Associated diseases: hypothyroidism, allergic contact dermatitis to hair dyes, renal dialysis with
secondary hypervitaminosis A
o Affected by other factors – age, gender, race, genetics
▪ Postnatal telogen effluvium of infants – may occur between birth and first 4 months, regrowth
usually occurs by 6 months
• Each hair will have a visible depigmented club-shaped bulb + no sheath
• Trichodynia – common symptom, may also coexist with depression, OCD, anxiety
• Estimate telogen shed:
o Normal hair loss – 100 hairs
o Pull test – grasp 40 hairs firmly between thumb and forefinger, followed by a slow pull that causes
minimal discomfort
▪ >4-6 club hairs – abnormal
▪ Take note of influencing factors: recent shampooing (2–3 hairs being abnormal in a freshly
shampooed scalp), combing, phase of telogen effluvium (whether resolving or entering a
chronic phase)
o Clip test – 25-30 hairs are cut just above the scalp surface and mounted
o Trichogram evaluation – 50 hairs plucked with Kelly clamp with rubber drains over teeth
o 1 minute combing session
• Idiopathic chronic telogen effluvium – diffuse generalized thinning of scalp hair
o Mostly 30-60 years old, with abrupt hair loss and increased shedding and thinning
o Fluctuating course, accompanied by bitemporal recession

Treatment:
• Look for the cause, usually stressful events 3-5 months before or nutritional causes, then reassure (★)
o General rule – >1 year is pattern baldness (★)
• No specific therapy is required for most patients, most cases will stop spontaneously
o Give supplements and eat a balanced varied diet if nutrient deficient
o Discontinue offending agent if drug-induced
o Address papulosquamous scalp disorders since these may precipitate hair loss
o Determine iron and thyroid status if course is prolonged or if history and PE suggest abnormalities

VHCC 3A-MED | ANDREW’S 13TH ED + LECTURE NOTES (★)