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Dermatology 2 > Diseases of the Hair > Flashcards

Diseases of the Hair Flashcards

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Dermatology Board Prep flashcards
1
Q

What are the 3 hair growth phases?

A
  1. anagen
  2. catagen
  3. telogen
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2
Q

Define anagen hairs

A

growing hairs (about 3 yrs) (85-90%)

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3
Q

Define catagen hairs

A

undergoing transition from growing to resting stage (1-2 weeks) (<1%)

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4
Q

Define telogen hairs

A

resting hairs, remain in the follicles for variable periods before they fall out (3-5 months) (10-15%)

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5
Q

When working up diseases of the hair, what should you ask about?

A
  • is the hair loss related to “thinning” or “shedding
  • hair care habits and products used
  • use of prescription/nonprescription meds
  • pain, itch, burning
  • body hair (too much or too little)
  • nail abnormalities
  • recent surgeries
  • signs of androgen excess
  • h/o autoimmune /endocrinediseases
  • recentorchronicillnesses
  • female pts: menstrual cycle and pregnancies
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6
Q

PE for chief complaint of “hair loss”

A
  • Closelyexaminethescalp and document any erythema, scale, folliculitis, evidenceofscarring
  • Lookfornewhairgrowth(fiberswithtaperedends)orhairbreakage
  • Pulltest – put pressure on the hair and see how many are shed
  • Notebodyhairdensityanddistribution
  • Documentanynailabnormalities
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7
Q

List the noncicatricial forms of alopecia (3)

A
  1. Alopecia Areata
  2. Androgenetic Alopecia
  3. Telogen Effluvium
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8
Q

List the cicatricial forms of alopecia

A
  1. DLE-Discoid Lupus Erythematous
  2. Lichen planopilaris
  3. Central Centrifulgal Cicatricial Alopecia
  4. Folliculitis decalvans
  5. Dissecting Cellulitis
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9
Q

Define alopecia areata

A
  • rapid, complete hair loss, 1 or > round patches 1-5 cm diameter
  • seen in young adults (< 25 years); children are affected more frequently
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10
Q

Etiology of alopecia areata

A
  • etiology unknown  25% with + FMH.

- associated with higher incidence AD, Downs synd, and autoimmune dz

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11
Q

How does alopecia areata present?

A
  • Asymptomatic sharply defined, patchy hair loss from any hair-bearing area.
  • Loss of all scalp hair (alopecia totalis), loss of all body hair (alopecia universalis)
  • No visible inflammation
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12
Q

Hair sign of alopecia areata

A

“Exclamation point” hairs : broken-off stubby hairs (distal ends are broader than proximal ends) seen at margins of hair loss

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13
Q

List the other physical features of alopecia areata

A
  • Nail pitting to severe dystrophy is possible

- Spontaneous remission common in patchy, less so in widespread

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14
Q

Tx of alopecia areata

A
  • topical high potency steroids
  • IL (intralesional) injections esp for localized.
  • topical minoxidil in combination with other tx
  • See Dr. Letassy’s handout
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15
Q

What is the MC type of human hair loss?

A

Androgenetic alopecia

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16
Q

Define androgenetic alopecia

A
  • combined effect of genetic predisposition and influence of androgen on hair follicles
  • androgen susceptibility of the follicles plays an important role
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17
Q

What is the principle agent of androgenetic alopecia in men?

A
  • 5α-dihydroxytestosterone (DHT) thought to be the principal agent.
  • DHT made by action of 5α-reductase on testosterone; binds 5x more potently to theandrogen receptors (ARs); localized around hair follicles.
  • Balding scalp has been shown to contain higher levels of 5α-reductase as well as DHT compared to nonbalding scalp.
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18
Q

What is the age of onset for androgenetic alopecia?

A
  • Men develop teens, 20s or early 30s.
  • Females later, usually 6th decade but as early as the mid teens
  • it has gender specific patterns
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19
Q

Characterization of androgenetic alopecia

A

progressive follicular miniaturization, shortening of the anagen phase with more telogen hairs and transition to “baby” vellus fibers on the scalp in a characteristic distribution

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20
Q

How does scalp appear in androgenetic alopecia?

A
  • scalp is normal - no inflammation

- in women, look for signs of virilization

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21
Q

Lab for androgenetic alopecia

A
  • No lab required but consider Free and Total Testosterone, DHEA-S, prolactin with signs of virilization.
  • Also consider TSH, T4, CBC, Iron profile to r/o other forms of hair loss
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22
Q

Should you biopsy for dx of androgenetic alopecia?

A

Yes, if help needed ruling out other types of alopecia

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23
Q

In men, what is the tx for androgenetic alopecia?

A
  • topical minoxidil (Rogaine)
  • finasteride (Propecia)
  • hair transplant
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24
Q

Topical minoxidil MOA for androgenetic alopecia

A

promotes survival of dermal papilla cells, prolongs anagen phase and enlargement of shaft diameter.
*apply BID

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25
Q

Dose of finasteride for androgenetic alopecia

A

*finasteride = type 2 5alpha-reductase inhibitor.
-1 mg daily helps to prevent further hair loss
~65% observe regrowth.
-if no effect after 12 mo d/c

26
Q

List the tx for androgenetic alopecia in women

A

-topical minoxidil

Oral antiandrogens:

  • spironolactone
  • cyproterone acetate
  • cimetidine
  • flutamide
27
Q

What is the only FDA approved tx for androgenetic alopecia in women?

A

topical minoxidil

28
Q

What are the tx for both men and women for androgenetic alopecia?

A
  • dutasteride (Avodart)
  • fluridil (Eucapil)
  • low-level light therapy
  • topical lantanoprost 0.1%
29
Q

Define telogen effluvium

A
  • Excessive shedding of normal telogen hairs
  • Shedding occurs 2-5 months after premature conversion of many anagen hairs to telogen hairs.
  • Reaction pattern to a variety of stressors
  • Widespread scalp involvement
  • F > M
30
Q

List stressors of telogen effluvium

A
  • endocrine (thyroid)
  • nutritional deficiency (consider in pts undergoing bariatric sx)
  • physical stress
  • psychological stress
  • intoxication
  • drugs (oral contraceptives)
31
Q

What are 2 “signs” for telogen effluvium?

A
  • “bag” sign: pts can literally bring in bags of hair that has fallen out
  • beau lines on the fingernails
32
Q

Other PE findings for telogen effluvium

A
  • No abnormalities to scalp
  • Diffuse thinning esp. to temporal regions
  • Pull test- grasping approx. 40 hairs with slow pull.
  • Pulling out 3-6 hairs is positive and indicates active shedding
33
Q

Dx of telogen effluvium

A
  • mostly clinical diagnosis
  • punch biopsy where increased ratio of telogen hairs can be confirmed
  • consider blood work
34
Q

Tx of telogen effluvium

A
  • Removal/treatment of the cause is primary goal, if possible
  • Topicalminoxidilmay help to induce anagen
  • Complete regrowth of hair is the rule
  • Reassurance as TE may continue for up to a year after the precipitating cause
  • Can reoccur
35
Q

Define cicatricial alopecia

A
  • Results from damage/destruction of hair follicles by inflammatory processes.
  • Usually not infectious
36
Q

Cicatricial alopecia is characterized by…

A

their inflammatory infiltrate, either lymphocytic, neutrophilic, or mixed

37
Q

End result of cicatricial alopecia

A

destruction of hair follicles and replacement of the follicular structure by fibrous tissue and permanent hair loss

38
Q

Which of the cicatricial alopecias are lymphoid-mediated disorders?

A
  1. DLE- discoid lupus erythematous
  2. Lichen planopilaris
  3. Central centrifulgal cicatricial alopecia
39
Q

Which of the cicatricial alopecies are neutrophil-mediated disorders?

A
  1. Folliculitis decalvans

2. Dissecting cellulitis

40
Q

Etiology of DLE

A
  • F»M, first onset typically at the age of 20–40 years

- Systemic lupus erythematosus (SLE) will develop in 5%–10% of adult patients with DLE

41
Q

How does DLE patient present?

A
  • Presents with one or more erythematous, atrophic patches of alopecia
  • Follicular hyperkeratosis, hyperpigmentation, hypopigmentation and telangiectasia can be present
  • Can be sensitive or pruritic, and the patient might report a worsening after UV exposure
  • May have other DLE lesions to other parts of body, always check external ear/concha**
42
Q

Dx of DLE

A
  • Always check for systemic lupus with ANA.

- Always bx if you suspect scarring changes

43
Q

Management of DLE

A
  • Class I or II topical steroid
  • IL Kenalog 10mg/cc Q 4-8 weeks
  • Systemic therapy often needed: Hydroxychloroquine at a dose of 200–400 mg daily in adults
  • Emphasize sun protection
44
Q

Etiology of lichen planopilaris

A
  • May or may not be associated with lichen planus of the skin or mucosa
  • MC in middle-age women
  • Occasionally can be result of lichenoid drug reaction (most common are gold, antimalarials and captopril)
45
Q

How does lichen planopilaris start?

A
  • Usually starts at the crown with patches of perifollicular erythema and follicular hyperkeratosis with scarring changes
  • Itching, burning sensations and sensitivity of the scalp
46
Q

What is frontal fibrosing alopecia?

A
  • a variant of lichen planopilaris
  • older women with band-like frontotemporal alopecia.
  • alopecia of eyebrows often seen
47
Q

Dx and management of lichen planopilaris

A

*Always bx if consider scarring process

  • Potent topical steroids
  • IL Kenalog 10 mg / cc Q 4-8 weeks
  • Oral steroids as bridge therapy
  • Systemic meds may likely be needed: doxycycline, hydroxychloroquine, cell-cept, cyclosporine, acitretin
48
Q

Etiology of central centrifugal cicatricial alopecia (CCCA)

A
  • unclear
  • thought that one or more may contribute to its formation: chemical processing, heat, traction or other traumas
  • MC seen in African American women
49
Q

Presentation of CCCA

A
  • skin colored patch of scarring alopecia on the crown, gradually progressing centrifugally to parietal areas
  • some have crops of crusts at periphery of patches
  • possible polytrichia: multiple hair follicles in the same opening
  • often c/o itching or tenderness
50
Q

Management of CCCA

A
  • Bx if you consider scarring process
  • Encourage d/c of chemical/heat processing and reduction of traction
  • Strong topical steroids
  • IL Kenalog 10 mg /cc at periphery Q 4-8 weeks
  • Doxycyline/minocycline
  • Topical minoxidil
  • Other systemic meds may be needed- cyclosporine, cell-cept
51
Q

Define folliculitis decalvans

A

Neutrophilic inflammation of scalp with crops of pustules that result in scarring alopecia

52
Q

Etiology of folliculitis decalvans

A
  • Predominantly occurs in young and middle-aged adults
  • Slight preference of the male gender
  • Etiology unclear but thought to be body’s abnormal suppurative immune response to staph or other organism
53
Q

Where does folliculitis decalvans start?

A
  • Usually starts vertex area with erythematous patches of alopecia, follicular pustules and follicular hyperkeratosis
  • C/o pain, itching and burning are common
54
Q

What is tufted folliculitis?

A
  • AKA doll’s hairs
  • often present in folliculitis decalvans
  • multiple hairs from one follicle and dilated orifice
55
Q

Management of folliculitis decalvans

A
  • Long term oral abx (doxy/MNC/clarithromycin) as will generally recur when d/c
  • Topical abx: clindamycin solution
  • Topical steroids
  • Selenium sulfide shampoo as adjunct
  • Oral isotretinoin (Accutane) can result in longer term remission but not cure
56
Q

What is dissecting cellulitis related to?

A

acne conglobata and hidradenitis suppurativa- follicular occlusion triad

57
Q

Who gets dissecting cellulitis

A
  • Young men between 18 and 40 years of age

- African-American MC

58
Q

Pathogenesis of dissecting cellulitis

A

may include follicular occlusion (hair follicle becomes blocked with keratin and ruptures, resulting in inflammatory response), seborrhea, androgens and secondary bacterial overpopulation as well as an abnormal host response to bacterial antigens

59
Q

What part of the scalp is typically involved with dissecting cellulitis?

A

Most often vertex and occipital scalp

60
Q

Clinical presentation of dissecting cellulitis

A
  • Erythematous pustules and deep, boggy, tender nodules, abscesses and sinuses
  • Suppurative with purulent drainage
  • Multifocal lesions can form an intercommunicating ridge
  • Pruritic and tender
  • Results in scarring which can be hypertrophic or keloidal
61
Q

Management of dissecting cellulitis

A
  • Oral/topical antibiotics
  • Topical steroids
  • IL Kenalog 10 mg/cc
  • Oral isotretinoin has shown prolonged remission but not cure
  • Possible I&D
  • Excision with skin grafting but only and exception for extreme cases

Dermatology 2 (10 decks)

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