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[Fitz 9ed - Part 16] Disorders of the Hair and Nails > Ch 88: Cicatricial Alopecia > Flashcards

Ch 88: Cicatricial Alopecia Flashcards

1
Q

All scarring alopecias are characterized by clinically by _______, and pathologically by _______.

A

Clinical: (+) loss of follicular ostia
Pathological: (+) replacement of hair follicles with fibrous tissue

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2
Q

Etiology and pathogenesis of Primary Cicatricial Alopecias

A

Not completely understood

Inflammatory infiltrate affecting infundibulum and isthmus –> damage to bulge and sebaceous glands –> incomplete hair cycle –> chronic follicular inflammation and foreign-body reaction

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3
Q

Cells responsible for renewal of the upper part of the hair follicle and sebaceous glands, as well as restoration of the lower cyclical component of the follicles at the onset of a new anagen period

A

Pluripotent hair follicle stem cells (found in the bulge region of the isthmus)

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4
Q

Sites affected first in Primary Cicatricial Alopecia

A

Central and parietal scalp

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5
Q

Clinical presentation of Primary Cicatricial Alopecia

A

(+) isolated alopecic patches with atrophy and lack of follicular ostia
(+) diffuse/perifollicular erythema
(+) follicular hyperkeratosis, pigment changes, tufting, pustules

*clinically visible inflammation may be absent, seen on HP in the deep dermis and SQ

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6
Q

Diagnostic Tools

A

Dermatoscope
Punch biopsy (4mm), with SQ
- 1 horizontal: H&E, elastin (acid alcohololic orcein), mucin, PAS
- 1 vertical: transverse cut, IHC

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7
Q

Findings on dermoscopy (10x)

A

(+) absence of follicular ostia
(+) perifollicular erythema
(+) follicular hyperkeratosis

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8
Q

Prognosis once hair follicle is destroyed and replaced by fibrous tissue:

A

No hope for hair regrowth. :(

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9
Q

Requirements for hair restoration surgery (eg. hair transplantation, scalp reduction)

A

No disease activity should occur on the scalp for at least 1 year after therapy

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10
Q

Classifications of Primary Cicatricial Alopecias

A

Lymphocytic
Neutrophilic
Mixed

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11
Q

Lymphocytic Primary Cicatricial Alopecias

A 
Chronic cutaneous LE (DLE)
Lichen planopilaris
Classic lichen planopilaris
Frontal fibrosing alopecia
Graham-Little syndrome
Classic pseudopelade of Brocq
Central centrifugal cicatricial alopecia
Alopecia mucinosa
Keratosis follicularis spinulosa decalvans
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12
Q

Neutrophilic Primary Cicatricial Alopecias (higher risk of limited graft survival and disease recurrence)

A

Folliculitis decalvans

Dissecting cellulites/folliculitis (perifolliculitis abscedens et suffodiens)

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13
Q

Mixed Cicatricial Alopecias

A

Folliculitis (acne) keloidalis
Folliculitis (acne) necrotica
Erosive pustular dermatitis

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14
Q

Most common cause of inflammatory Cicatricial Alopecia

A

DLE, Lichen Planopilaris

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15
Q

Percentage of patients with DLE that will progress to SLE

A

Children: 26 to 31%
Adults: 5 to 10%

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16
Q

Conditions associated with DLE

A

Verruciform xanthoma

Papulonodular dermal mucinosis

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17
Q

Histopathologic findings of DLE

A

(+) lymphocyte-mediated interface dermatitis with vacuolar degeneration of the basal cell layer and necrotic keratinocytes
(+) thickening of basement membrabce
(+) destruction of sebaceous glands and elastic fibers

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18
Q

DIF findings of DLE

A

(+) linear, granular deposition of IgG and C3 at the DEJ

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19
Q

Treatment for DLE

A

Baseline: ophthalmologic examination, CBC
Hydroxychloroquine (adults: 200 to 400mg OD, children: 4 to 6mg/kg)
Bridge tx: oral Prednisone (1 mg/kg) over the first 8 weeks of treatment

Others: TAC ILSI 10mg/mL q4-6wks, oral acitretin and isotretinoin, MMF, MTX, azathioprine

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20
Q

Classic LPP most commonly seen in

A

Women, fifth decade

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21
Q

Clinical manifestations of Graham-Little Syndrome

A

LPP of the scalp
Noncicatricial alopecia of the eyebrows, axilla, groin
Keratosis pilaris

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22
Q

Frontal Fibrosing Alopecia (FFA) most commonly seen in

A

postmenopausal women

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23
Q

Triggers for lichenoid drug eruptions

A

Gold, antimalarials, captopril, quinine, thiazide diuretics

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24
Q

Sites affected first in Classic LPP

A

Crown and vertex of scalp

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25
Q

Classic LPP vs DLE

A

Classic LPP: alopecic areas are smaller, irregularly shaped, and interconnected (may appear reticulated), (+) itching, burning sensation, sensitivity of scalp

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26
Q

Clinical presentation of FFA

A

(+) frontal, band-like or circumferential scarring alopecia, with (+) follicular hyperkeratosis and perifollicular/diffuse erythema
(+) sparing of few hairs on original frontal hairline
(+) alopecia of the eyebrows

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27
Q

Histopathologic findings of LPP/FFA

A

(+) lymphocytic infiltrate and interface dermatitis in and around upper permanent part of hair follicle

(-) vascular plexus not affected by inflammation, no mucin deposits –> both seen in DLE

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28
Q

DIF findings of LPP/FFA

A

(+) globular cytoid depositions of IgM

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29
Q

First-line treatment for Classic LPP/FFA

A

TAC ILSI 10mg/mL q4-6wks +/- Class I or II topical corticosteroids

Near the face: TAC 2.5mg/mL injected 1cm behind the hairline

Others: minoxidil, platelet-rich plasma, oral cyclosporine, retunoids, antimalarials, griseofulvin, oral corticosteroids

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30
Q

Pseudopelade of Brocq (PPB) most commonly seen in

A

Women, 30-50yo

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31
Q

Sites affected first in PPB

A

Vertex and occiput of scalp

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32
Q

Clinical presentation of PPB

A

(+) small flesh-toned alopecic patches with irregular margins (“footprints in the snow”

OR (+) non-inflammatory centrifugally spreading patch of alopecia

(-) follicular hyperkeratosis
(-) perifollicular/diffuse erythema

33
Q

Clinical presentation of DLE

A

(+) >=1 erythemtatous, atrophic, alopecic patches on scalp
(+) follicular hyperkeratosis, hyperpigmentation, hypopigmentation, telangiectasia

(+/-) sensitivity, pruritus, worsening with UV exposure

34
Q

Histopathologic findings of PPB

A

(+) sparse to moderate lymphocytic infiltrate around follicular infundibulum
(+) complete destruction of sebaceous glands
(+) replacement of hair follicles with fibrous tracts (late stage)

(-) interface dermatitis; elastic fibers preserved and thickened

35
Q

Treatment of PPB

A

1st Line: TAC ILSI 10mg/mL +/- corticosteroids

Hydroxychloroquine, oral prednisone, isotretinoin

36
Q

Central Centrifugal Cicatricial Alopecia (CCCA) most commonly seen in

A

Women of African descent

37
Q

Etiology of CCCA

A

Autosomal dominant inheritance
Chemical hair grooming
Traction-inducing hair styles

38
Q

Clinical presentation of CCCA

A

(+) skin-colored patch of scarring alopecia on the crown, progressing centrifugally
(+) perifollicular hyperpigmentation, polytrichia

(+/-) pain, itching, tenderness, “pins-and-needles” sensation

39
Q

Histopathologic Findings of CCCA

A

(+) dermal hyalinization, hair fiber granulomas, loss of follicular epithelium, follicular lymphocytic inflammation of the lower infundibulum to isthmus, premature desquamation of inner root sheath and fibrous connective tissue

40
Q

Treatment of CCCA

A

Early diagnosis is crucial
More natural, less traumatizing hair practices

ILSI/topical steroids, tetracycline, HCQ, immunosuppressants (MMF, cyclosporine), antiandrogens

41
Q

Clinical presentation of Alopecia Mucinosa

A

(+) well-demarcated, indurated, erythematous or skin-colored patches of scarring/nonscarring alopecia
(+) diffuse hair loss
(+) alopecia of the eyebrows
(+/-) grouped follicular papules, follicular cysts, follicular hyperkeratosis

42
Q

Histopathologic findings of Alopecia Mucinosa

A

(+) mucin deposition in the outer root sheath
(+) replacement of entire pilosebaceous unit by pools of mucin

*strictly speaking, not a primary cicatricial alopecia because hair follicle is not replaced by a true scar

43
Q

Conditions associated with Alopecia Mucinosa

A

Cutaneous T-cell lymphoma

Mycosis fungoides, Sezary syndrome

44
Q

Treatment for Alopecia Mucinosa

A

Oral corticosteroids, minocycline, isotretinoin, topical/intralesional CS, dapsone, indomethacin, light therapy

45
Q

Keratosis follicularis spinulosa decalvans (other names)

A

Keratosis atrophicans faciei
Ulerythema ophyrogenes
Keratosis pilaris rubra atrophicans faciei

46
Q

Etiology of KFSD

A

X-linked inheritance

47
Q

KFSD usually seen in

A

Adolescence

48
Q

Clinical presentation of KFSD

A

(+) scarring alopecic patches, follicular hyperkeratosis, +/- pustules
(+/-) involvement of eyebrows/lashes

49
Q

Histopathologic findings of KFSD

A

(+) mixed infiltrate of lymphocytes and neutrophils in the infundibular area (early)
(+) predominantly lymphocytic, follicle replaced by fibrous tissue (late)

50
Q

Treatment of KFSD

A

May improve with age

Topica/intralesional CS, oral retinoids

51
Q

Folliculitis Decalvans most commonly seen in ____, starts at ____

A

Young and middle-aged adults, male

Vertex of scalp

52
Q

Etiology of Folliculitis Decalvans

A

S. aureas infection in combination with hypersensitivity reaction to “superantigens’ and defects in host cell-mediated immunity

53
Q

Clinical presentation of Folliculitis Decalvans

A

(+) erythematous, alopecic patches, follicular pustules, follicular hyperkeratosis
(+) tufted folliculitis - 5 to 15 hairs emerging from single dilated orifice
(+) pain, itching, burning sensation

54
Q

Histopathologic findings of Folliculitis Decalvans

A

(+) keratin aggregation in infundibulum with numerous neutrophils
(+) intra/perifollicular neutrophilic infiltrate
(+) sebaceous glands destroyed early

(+) neuts, lymphocytes, plasma cells extend into dermis; hair-shaft granulomas with FB giant cells (advanced)

(+) follicular and interstitial dermal fibrosis, hypertrophic scarring (end-stage)

55
Q

Treatment of Folliculitis Decalvans

A

Low-dose antibiotics for many years

Eradication of S. aureus: minocycline, erythromycin, cephalosporins, TMP-SMX, rifampicin + clindamycin, oral fucidic acid, mupirocin,

TAC ILSI 10mg/mL to reduce inflamm

56
Q

Dissecting Folliculitis (other names)

A

Dissecting cellulites

Perifolliculitis capitis abscedens et suffodiens of Hoffman

57
Q

Follicular Occlusion Triad

A

Dissecting folliculitis
Acne Conglobata
Hidradenitis suppurativa

58
Q

Dissecting Folliculitis most commonly seen in

A

Young men, 18-40yo, African-American

59
Q

Pathophysiology of Dissecting Folliculitis

A

Follicular occlusion, seborrhea, androgens, secondary bacterial population, abnormal host response

60
Q

Clinical presentation of Dissecting Folliculitis

A

(+) fluctuating nodules, abscesses, sinuses with spontaneous discharge of pus
(+) erythematous, follicular papules and pustules
(+) multifocal lesions - form intercommunicating ridge and seropurulent exudates
(+) tenderness, pruritus
(+) keloids/HS (chronic/relapsing)

61
Q

Dissecting Folliculitis usually begins on

A

Vertex and occipital scalp

62
Q

Histopathologic findings of Dissecting Folliculitis

A

(+) intra/perifollicular neutrophilic infiltrate with follicular occlusion (early)
(+) interconnecting sinus tracts lined by squamous epithelium, follicular perforation, perifollicular and deep dermal abscesses

63
Q

Treatment of Dissecting Folliculitis

A

Multimodal tx: oral abx (anti-inflamm; minocycline, tetracycline, erythromycin, cephalosporin, clindamycin +/- rifampin) + intralesional CS + oral prednisolone

Isotretinoin 0.5-1mg/kg/day - prolongs remission

Surgical methods (extreme cases): I&D, marsupialization with curettage of cyst wall, complete scalp extirpation with skin grafting

64
Q

Acne Keloidalis Nuchae most commonly seen in

A

African-American men, 14-25yo

65
Q

Etiology of Acne Keloidalis Nuchae

A

Trauma (shirt collars)

Infection (Demodex, bacteria)

66
Q

Clinical presentation of Acne Keloidalis Nuchae

A

(+) skin-colored follicular papule,s pustules, plaques

(+) keloid-like scarred lesions in occipital scalp

67
Q

Histopathologic findings of Acne Keloidalis Nuchae

A

(+) acute inflamm with neutrophilic/lymphocytic infiltration

(+) chronic granulomatous inflamm around isthmus and lower infundibulum

68
Q

Treatment of Acne Keloidalis Nuchae

A

1st Line: TAC ILSI (10-40mg/mL) +/- topical clindamycin 2% or oral tetracyclines

Others: topical retinoids, cryotherapy, laser, surgical excision

69
Q

Clinical presentation of Acne Necrotica (Varioliformis)

A

Frontal and parietal scalp, seborrheic areas of face; adults
(+) umbilicated, pruritic/painful papules with central necrosis
(+) varioliform/smallpox-like scars

70
Q

Histopathologic findings of Acne Necrotica (Varioliformis)

A

(+) suppurative, necrotic, infundibular folliculitis with lymphocytic/mixed inflammatory infiltrate

71
Q

Clinical presentation of Erosive Pustular Dermatosis

A

Elderly women

(+) suppurative, necrotic, erosive papule or plaque

72
Q

Histopathologic findings of Acne Necrotica (Varioliformis)

A

(+) extensive, chronic, mixed inflamm infiltrate in the dermis, later with dermal fibrosis

73
Q

Treatment of Acne Necrotica (Varioliformis)

A

Class I or II topical CS +/- topical/systemic antibiotics + oral isotretinoin

74
Q

Possible causes of Secondary Cicatricial Alopecia

A

Congenital defects, trauma, inflammatory conditions, infections, neoplasms, drugs, chronic traction and surgical scars

75
Q

Etiologic agents of Tinea Capitis

A

Endothrix: Trichophyton tonsurans subspecies sulfureum (90% overall)

  • (+) black dots
  • hair loss, inflamm, scaling is minimal

Ectothrix: Microsporum canis, Epidermophyton spp.

  • (+) alopecic patches with signs of inflamm and scaling with brittle grayish hair stumps
  • Wood’s: (+) yellow-green fluoresence
76
Q

Patelliform scales (scutula) - sulfuric-yellow concretions of hyphae and skin debris in the follicular orifices; malodorous

A

Favus

77
Q

Deep, highly inflammatory fungal infection; (+) highly suppurative, boggy, nodular, deep folliculitis with fistulas and pus secretion

A

Kerion

78
Q

Treatment for tinea capitis

A

Systemic: terbinafine, itraconazole, ketoconazole, griseofulvin, fluconazole
Topical sporicidal agents (to limit spread of spores): selenium, ketoconazole

79
Q

Etiologies of traumatic hair loss (4)

A

Traumatic injuries
Traction alopecias (braided/weaved African-American hair, Sikh topknot, tight ponytails, rollers)
Trichotillomania
Pressure alopecia (d/t ischemia)

[Fitz 9ed - Part 16] Disorders of the Hair and Nails (7 decks)

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