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Dermatology Board Prep > DERM (10) Hair, Nails, and Mucous Membranes > Alopecias > Flashcards

Alopecias Flashcards

1
Q

Two major types of alopecia?

A

Scarring and non-scarring

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2
Q

What do you look for to see if an alopecia is inflammatory vs not?

A

Look to see if the ostia is present or not

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3
Q

Difference between male and female androgenic alopecia?

A

Male pattern: Starts at the temporal area and reshapes anterior hairline

Women: Diffuse thinning on crown, less temporal recession and the frontal hairline is maintained. Has a more Christmas tree shape to loss.

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4
Q

Histology of androgen-dependent alopecia?

A

Increased vellus hairs (diameter of the hair shaft < inner root sheath width), mildly increased telogen to anagen ratio (follicles will be higher in the dermis, anagen should be near subcutis).

  • In final stage connective tissue can replace follicular structure (scarring)
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5
Q

Treatment for androgen-dependent alopecia?

A
  • minoxidil 2 or 5%
  • finasteride
  • dutasteride (both 5-ɑ reductase isoforms) [some stuff suggesting this may be more effective]
  • hair transplant
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6
Q

At what stage in the hair cycle is the bulb lowest in the dermis?

A

Mature anagen, most shallow during telogen

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7
Q

Two major types of alopecia?

A

Scarring and non-scarring

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8
Q

Major types of scarring alopecia?

A

DLE, Morphea, Infections/Tinea capitis, Radiation, Burn, Lichen planopilaris

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9
Q

Major types of non-scarring alopecia?

A

Alopecia areata, androgenitic alopecia, telogen effluvium, trichotillomania, traction alopecia

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10
Q

What are the two main divisions of alopecias within the non-inflammatory category?

A

Normal follicle number and decreased follicle number

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11
Q

What are the types of alopecia associated with non-inflammatory processes that have normal follicle numbers?

A

Androgenetic alopecia, telogen effluvium, trichotillomania

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12
Q

What are the types of alopecia associated with non-inflammatory processes that have decreased follicle numbers?

A

Traction alopecia

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13
Q

How are the inflammatory alopecias divided?

A

They can be divided by cell type: lymphocytic, neutrophilic, histiocytic/plasma cells, and little or no inflammation

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14
Q

What are the major lymphocyte driven inflammatory alopecias?

A

Discoid lupus erythematosus, alopecia areata, lichen planopilaris

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15
Q

What are the major neutrophil driven inflammatory alopecias?

A

Folliculitis decalvans, tinea capitis, zoster, dissecting cellulitis, burns, radiation

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16
Q

What are the major Histiocytes and Plasma Cells driven inflammatory alopecias?

A

Secondary Syphilis

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17
Q

What inflammatory alopecias have little or no inflammation?

A

alopecia areata, late lichen planopilaris, late discoid lupus, late scleroderma, late burn, radiation associated

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18
Q

Epidemiology of androgenetic alopecia?

A

M>>F (80% caucasian men affected by age 70). The incidence in women increases after menopause.

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19
Q

Groups with the lowest rates of androgenetic alopecia?

A

Native Americans and Eskimos

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20
Q

Genetics of androgenetic alopecia?

A

Both polygenic and autosomal dominant

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21
Q

What is the hormone that drives androgenetic alopecia?

A

DHT… it is an androgen-dependent process. If men are castrated before puberty no androgenetic alopecia occurs.

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22
Q

What is the pattern seen with male androgenetic alopecia?

A

Starts at the temporal area, reshapes the anterior hairline

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23
Q

What is the pattern seen with female androgenetic alopecia?

A

Diffuse thinning on the crown, less temporal recession and the frontal hairline is maintained

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24
Q

What is the workup for androgenetic alopecia in women?

A

Evidence of hirsutism/PCOS/virilization: check DHEA-S, total and free testosterone, prolactin

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25
Q

What is the workup for androgenetic alopecia in both men and women?

A

TSH, debatably ferritin, consider telogen effluvium which can lead to an accelerated rate of pattern alopecia

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26
Q

Histopathology of androgenetic alopecia?

A
  • increased vellus hairs
  • mildly increased telogen to anagen ratio
  • in final stage, connective tissue can replace follicular structure (scarring)
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27
Q

Treatment for androgenetic alopecia?

A
  • minoxidil 2 or 5%
  • finasteride
  • dutasteride (both 5-ɑ reductase isoforms)
  • hair transplant
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28
Q

On histology, how can a vellous hair be distinguished?

A

In vellous hair, the hair shaft is smaller than the inner root sheath.

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29
Q

What is the usual timing of telogen effluvium?

A

Precipitating event usually 3 months prior to diffuse shedding

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30
Q

How does telogen effluvium present?

A

Reduced density of hair, hair growth usually returns after months to years

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31
Q

Most common causes of telogen effluvium?

A
  • postfebrile
  • severe infection
  • severe chronic illness
  • severe, prolonged psychological stress
  • hypothyroidism / hyperparathyroidism
  • malnutrition
  • drugs (retinoids, stopping OCPs, heparin, antidepressants, lithium, amphetamines, antithyroid meds, anticonvulsants, β-blockers)

*some cases can be idiopathic

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32
Q

Most common drugs associated with telogen effluvium?

A

retinoids, stopping OCPs, heparin, antidepressants, lithium, amphetamines, antithyroid meds, anticonvulsants, β-blockers

33
Q

What is alopecia areata?

A

Autoimmune disease with increased CD8+ T-cells in the hair matrix → surround the hair bulb in deep dermis

34
Q

What type of T-cells drive alopecia areata?

A

CD8+ t-cells

35
Q

What other conditions is alopecia areata associated with?

A

Atopy, Hashimoto’s thyroiditis, vitiligo, IBD

36
Q

What signaling molecules are key in alopecia areata?

A

IL-15 and IFN-gamma

37
Q

How do JAK-inhibitors work in alopecia areata?

A

They break the IFN-gamma signalling

38
Q

What are the clinical varients of alopecia areata?

A

Alopecia totalis (loss of total scalp hair), or universalis (loss of all hair), or ophiasis pattern (band-like pattern of loss along temporal/occipital scalp).

39
Q

What pattern of alopecia areata is resistant to treatment?

A

Ophiasis pattern

40
Q

What types of hair can be seen at the borders of alopecia areata lesions?

A

Exclamation point hairs. These are wider at the top than at the bottom

41
Q

What physical exam findings can be found in alopecia areata?

A

exclamation point hairs at borders of lesions, regular nail pitting, trachyonychia

42
Q

Treatment options for alopecia areata?

A

intralesional kenalog (5mg/mL), topical irritants (anthralin, tazarotene), JAK inhibitors in the future For rapidly progressive disease –> oral CS pulsed over 2-3 months

43
Q

What is trichotillomania?

A

Self-induced hair loss from twirling, pulling and or breaking the hair

*Often underlying psychological stressor or disorder

44
Q

Exam findings suggestive of trichotillomania?

A

Hair tends to be of different length, occiput often spared, can do the clipped hair test where the hair is clipped short and the regrowth can be observed before it is long enough to pull

45
Q

Treatment for trichotillomania?

A

Behavioral modification is the primary modality. SSRI second line and clomipramine in children and adolescents.

46
Q

What is pressure-induced alopecia

A

Most commonly after very long surgical procedures. Most common resulting location is the occiput (solitary, oval patch)

47
Q

Histopathology in trichotillomania?

A

Look for tracheomalacia which is deformed hair shafts

48
Q

What chemo drugs are associated with anagen effluvium?

A

cyclophosphamide, doxorubicin, paclitaxel, etoposide

49
Q

What is anagen effluvium?

A

You get loss of growth phase hairs… so the hairs remain short before being shed.

50
Q

What pattern is seen in alopecia secondary to secondary syphilis?

A

Moth-eaten alopecia and telogen effluvium

51
Q

Where is central centrifugal cicatricial alopecia seen most commonly?

A

Black women 2/2 use of chemical hair relaxers or flat iron

52
Q

Presentation of central centrifugal cicatricial alopecia?

A

progressive scarring alopecia centered on the crown and midline. Usually asymptomatic but sometimes a secondary change of crusting or pustules can occur

53
Q

Treatment of central centrifugal cicatricial alopecia?

A

-oral tetracyclines plus potent topical steroids -severe disease - oral rifampin plus clindamycin -if perifollicular erythema present - ILK -change or decrease the use of chemical hair products

54
Q

Epidemiology of lichen planopilaris?

A

Affects W>>M, 50% have associated LP of the skin, mucous membranes, or nails

55
Q

Clinical presentation of lichen planopilaris?

A
  • clinically, p/w several foci of alopecia with loss of follicles and scarring centrally. Look for perifollicular erythema or scale
  • m/c locations: crown/vertex or midline vs frontal hairline and eyebrows (frontal fibrosing alopecia)
  • perifollicular erythema to violaceous color signify inflammation
56
Q

Most common areas for lichen planopilaris?

A

crown/vertex or midline vs frontal hairline and eyebrows (frontal fibrosing alopecia)

57
Q

What is Graham-Little syndrome?

A

Scarring scalp alopecia, alopecia of axillary/pubic areas that is not scarring and grouped spinous follicular papules on trunk/extremities

58
Q

Treatment for lichen planopilaris?

A
  • oral antimalarials
  • topical or ILK
  • oral doxycycline
  • MMF for severe or recalcitrant cases
59
Q

Clinical presentation of discoid lupus erythematosus?

A
  • clinically p/w circular lesions of erythema, atrophy, dilated/plugged follicles with scale and alopecia
  • later stage shows central hypopigmentation and peripheral hyperpigmentation + scarring
60
Q

Treatment for discoid lupus erythematosus?

A

anti-malarials

61
Q

Key distinguisher of discoid lupus erythematosus vs lichen planopilaris on histology?

A

Discoid lupus affects the acrosyringium whereas lichen planopilaris does not.

62
Q

What is the occlusion tetrad?

A

Dissecting cellulitis, acne conglobata, HS, pilonidal cysts/sinus

63
Q

How does dissecting cellulitis present?

A

Multiple, firm, scalp nodules over crown and occiput → boggy and fluctuant with purulent discharge with interconnections

+/- pain

64
Q

Treatment for dissecting cellulitis?

A
  • ILK
  • abx based on cx
  • incision and drainage
  • excision
65
Q

What is folliculitis decalvans?

A

Inflammatory scarring alopecia with perifollicular papules and pustules

66
Q

Presentation for folliculitis decalvans?

A

Recurrent crops of epilating follicular pustules

67
Q

Treatment for folliculitis decalvans?

A

Dapsone (neutrophil driven process), tetracyclines

68
Q

What is pseudopelade?

A

This is the end-stage or burned out stage of different types of scarring alopecias.

69
Q

Most common etiology of pseudopelade?

A

End-stage lichen planopilaris

70
Q

What is the histology of pseudopelade?

A

Shrunken, deep red dermis - fibrous tract remnants - thickened elastic fibers in dermis

71
Q

What is traction alopecia?

A

It is seen after years of hairstyling that causes excessive traction.

Essentially a scarring alopecia that can resemble trichotillomania early on but progresses usually from anterior hairline and moves towards the vertex

72
Q

What are poor prognostic indicators for alopecia areata?

A

the severity of onset, ophiasis pattern, younger age of onset; diffuse-type has good prognosis; m/c a/w vitiligo

73
Q

Most commonly associated diseases with alopecia areata?

A

Vitiligo

74
Q

What must patients be warned of prior to starting minoxidil?

A

Immediate release of telogen hair… more hair will fall out initially

75
Q

Important side effects of finasteride?

A

Change in the prostate (ejaculate volume), depression, decreased libido, erection problems, increased risk of HIGH-grade prostate cancer

76
Q

What are the two primary types of 5-a reductase and where are they located?

A

type I mainly on the scalp, sebaceous glands, and liver type II mainly in prostate and liver

77
Q

What things are related to DHT levels?

A

Growth of beard, prostate, acne at puberty, and temporal hair recession

78
Q

What 5-a reductase subtypes does finasteride block?

A

Finasteride blocks just the type II 5a reductase

79
Q

What 5a reductase subtypes does the dutasteride block?

A

Dutasteride blocks both the type I and the type II

DERM (10) Hair, Nails, and Mucous Membranes (6 decks)

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