69-70

Question 1

Christmas tree pattern

Answer 1

Widened part line seen in female pattern hair loss

Question 2

occipital hair loss

Answer 2

ophiasis

Question 3

Genetic loci implicated in male pattern hair loss

Answer 3

Androgen receptor, estrogen receptor-beta, and aromatase

Question 4

Enzyme implicated in androgenic alopecia

Answer 4

5 alpha reductase, type 2

Question 5

Possible new therapeutic target for treatment of AGA

Answer 5

Prostaglandin H2

Question 6

Scales used to classify pattern of mail AGA versus female

Answer 6

For male: Hamilton and Norwood

For female: Ludwig; for part line: Sinclair scale

Question 7

AGA trichoscopy

Answer 7

Brown halos

Question 8

AA trichoscopy

Answer 8

Yellow dots, exclamation point hairs, and dystrophic hairs

Question 9

Trichotillomania trichoscopy

Answer 9

Hair shafts of different lengths, broken hairs, and black dots

Question 10

Tinea capitis trichoscopy

Answer 10

Comma and zigzag hairs

Question 11

DLE trichoscopy

Answer 11

Red dots

Question 12

LPP trichoscopy

Answer 12

White dots (due the loss of melanin over scarred fibrotic tracts and perifollicular fibrosis)

Question 13

Monolethrix trichoscopy

Answer 13

Broken hair shafts plus hairs with beads

Question 14

Trichorrhexis invaginata

Answer 14

Bamboo hairs, broken hair shafts and nodose swellings

Question 15

Pathophys of CCCA

Answer 15

–Premature dislocation of the inner cheek
–Eccentric epithelial atrophy
–Concentric lamellar fibroplasia (onion skin like fibrosis)
-Variable intensity specific particular location, primarily at the level of the upper isthmus and lower

Question 16

Pathophys of LPP

Answer 16

–Bandlike mononuclear cell infiltrate obscuring the interface follicular epithelium and dermis; vacuolar alteration at the interface hypergranulosis with infundibula typical
–Colloid and Civatte bodies are occasionally found as part of the interface alteration
–Inflammation affects the upper portion of the follicle (infundibulum and isthmus) most severely
–Additionally, epidermal changes of LP are found

Question 17

Pathophys of discoid lesions of lupus erythematosus

Answer 17

–Vacuolar interface alteration of the follicular epithelium; epidermis may be spared
–The interface change in follicles is usually vacuolar rather than lichenoid (less inflammation)
–Chronic inflammation (often including plasma cells) of the eccrine sweat glands and arrector pili is sometimes present
–Increased dermal mucin is often present
–Granular deposits of IgG and C3 at the dermal epidermal junction and/or the junction of the follicular epithelium and dermis are typical

Question 18

Drugs associated with telogen effluvium

Answer 18

Retinoids, anti-convulsant, anti-thyroid medication, anticoagulants (especially heparin), lithium, and interferons

Question 19

What reflects the total body iron storage?

Answer 19

Ferritin

Question 20

Which cell type drives the autoimmune process seen and alopecia areata?

Answer 20

CD8+ T cells

Question 21

Cytokines involved in alopecia areata

Answer 21

T cells produce IFN gamma and gamma chain cytokines (IL 2, 7, 15, 21) which indicates signaling via the JAK/STAT pathway

Question 22

Immune privilege seen in hair follicles during which phase?

Answer 22

Anagen phase

Question 23

Hair color and alopecia areata

Answer 23

During active disease, non-pigmented hairs are initially spared; with regrowth, the hairspray initially be gray or white, but re-pigmentation is usually observed within a few weeks or months

Question 24

Most common nail findings and alopecia areata

Answer 24

Nail pitting, trachyonychia (sandpaper like roughness due to excessive longitudinal raging), brittle nails, onycholysis, koilonychia and, rarely, onychomadesis

Question 25

Systemic steroids and alopecia areata

Answer 25

Approximately 80% of patients will respond to high-dose systemic corticosteroids; however about 50% will relapse with dose reduction or cessation of therapy

Question 26

Topical immunotherapy for alopecia areata

Answer 26

diphencyprone or aquatic acid dibutyl ester; applied once weekly to affected areas; titrated according to the severity of the reaction of the previous week – tolerable degree of erythema, scaling, and pruritus

Question 27

First line pharmacologic therapy for trichotillomania

Answer 27

Clomipramine

Question 28

A patch of alopecia present at birth or acquired during the first decade of life, in the temporal area, which persists for life

Answer 28

Temporal triangular alopecia

Question 29

Disease of black women with thick scalp and alopecia

Answer 29

Lipedematous alopecia

Question 30

psoriasiform alopecia

Answer 30

Seen in association with the TNF alpha inhibitor (infliximab and adalimumab)

Question 31

Baby that fails to regrow nearly all their hair after shedding their initial growth of hair shortly after birth

Answer 31

Congenital atrichia with papules

Question 32

What does scarring alopecia mean?

Answer 32

It means that the follicular epithelium has been replaced by connective tissue leading to permanent hair loss

Question 33

Difference between primary scarring alopecia versus secondary

Answer 33

In primary, the target of information appears to be the follicle, whereas with secondary, the follicle is an “innocent bystander” in the disease process for example 2/2 deep burns, radiation dermatitis, cutaneous malignancies, cutaneous sarcoidosis, morphea, necrobiosis lipoidica, and certain chronic infections such as cutaneous TB

Question 34

List of lymphocytic scarring alopecia’s

Answer 34

Discoid lesions of lupus erythematosus, LPP (including frontal fibrosing alopecia), classic pseudopelade (Brocq’s alopecia), CCCA

Question 35

List of neutrophilic scarring alopecia’s

Answer 35

Folliculitis decalvans, dissecting cellulitis

Question 36

List of mixed scarring alopecia’s

Answer 36

Acne keloidalis, acne necrotica, erosive pustular dermatosis

Question 37

For treatment of non-inflammatory CCCA

Answer 37

Combination of long acting oral tetracycline plus a potent topical corticosteroid

Question 38

For highly inflamed CCCA

Answer 38

May do an initial 10 week regimen of oral rifampin and clindamycin

Question 39

Another name for end stage scarring alopecia

Answer 39

Brocq’s alopecia

Question 40

Most common location of discoid lupus erythematosus lesions

Answer 40

Face, ears, and scalp

Question 41

What is the follicular occlusion triad

Answer 41

Dissecting cellulitis, hidradenitis suppurativa, and acne conglobata

Question 42

Pathophysiology of dissecting cellulitis

Answer 42

Follicular hyperkeratosis rather than infection start to play a primary role in pathogenesis, however bacterial superinfection can occur

Question 43

Clinical description of dissecting cellulitis

Answer 43

Lesions begin as multiple, firms scalp nodules, most commonly on the med and posterior vertex an upper occiput. The nodules rapidly develop into interconnecting, foggy, fluctuant, overall and linear ridges that eventually discharge purulent material

Question 44

Treatment of dissecting cellulitis

Answer 44

Isotretinoin (0.5 to 1.5 mg per kilogram daily until four months after achieving a clinical remission)

Question 45

Define folliculitis decalvans

Answer 45

A highly inflammatory form of scarring alopecia or inflammatory, follicular papules and pustules dominate the clinical picture; often but not always staphylococcus aureus can be grown from pustular or crusted lesions

Question 46

Monilethrix

Answer 46

Beaded hair, inherited in an autosomal dominant fashion, affected keratin and desmoglien genes (in the AR form), usually only involves the scalp Dash hair shops have uniform elliptical nodes of normal thickness and intermittent abnormal constrictions

Question 47

What test must children with pili torti have?

Answer 47

Early testing for hearing loss

Question 48

X linked recessive disorder of copper metabolism (ATP7A gene), with the affected males having pili torti, severe psychomotor retardation, growth failure, seizures, and other neurologic abnormalities

Answer 48

Menkes disease

Question 49

Syndrome associated with trichorrhexis invaginata

Answer 49

Netherton syndrome (SPIK5 mutation)

Question 50

Most common structural hair abnormality characterized by shaft fracture in which the individual cortical cells and their fragments splayed out

Answer 50

Trichorrhexis nodosa