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Clinical lectures: Yr2 > Scarring and Non-scarring hair loss & Excessive hair growth > Flashcards

Scarring and Non-scarring hair loss & Excessive hair growth Flashcards

1
Q

What is the anagen to telogen ratio in hair cycle physiology?

A

9:1

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2
Q

What is the duration of the anagen/growth phase?

A

~3 years

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3
Q

What is the duration of the catagen/regression phase?

A

1-2 weeks

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4
Q

What is the duration of the telogen/rest phase?

A

~3 months

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5
Q

What is the duration of the exogen/shedding phase?

A

~3 months

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6
Q

How is hair loss classified?

A

Diffuse or patchy, and scarring or non-scarring alopecia

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7
Q

What characterizes alopecia areata?

A

Chronic autoimmune disease with non-scarring round or oval bald patches

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8
Q

What is the pathophysiology of alopecia areata?

A

Own immune cells attack hairs in anagen phase, causing inflammation and hair loss

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9
Q

How does alopecia areata typically present?

A

Round/oval bald patches with smooth skin or short hair stubs

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10
Q

What is diffuse alopecia areata?

A

Overall hair thinning, uncommonly associated with alopecia areata

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11
Q

What is alopecia totalis?

A

Total loss of scalp hair

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12
Q

What is alopecia universalis?

A

Total loss of body hair

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13
Q

What is ophiasis in the context of alopecia areata?

A

Bandlike pattern of hair loss along occipital or temporal scalp margins

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14
Q

What are hallmark features of alopecia areata?

A
  • Exclamation mark hairs
  • White hair regrowth
  • Nail pitting
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15
Q

What is the management approach for a single patch of alopecia areata?

A

No treatment, as there is an 80% chance of regrowth

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16
Q

What is the management for patchy alopecia areata?

A
  • Intralesional injection/topical corticosteroids
  • Minoxidil with localized PUVA therapy
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17
Q

What is the management for diffuse alopecia areata?

A

Diphencyprone contact immunotherapy

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18
Q

What is the mechanism of action for diphencyprone contact immunotherapy?

A

Induces contact dermatitis to distract the immune system from attacking hair follicles

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19
Q

What is the management for over 50% scalp hair loss in alopecia areata?

A

Systemic immunosuppressants, e.g., methotrexate

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20
Q

What is Trichotillomania?

A

Non-scarring, self-induced hair pulling.

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21
Q

What is the presentation of Trichotillomania?

A

Irregularly-shaped spiky patches with angular borders, containing random distribution of short, broken hair shafts and different-length hairs.

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22
Q

Where is Trichotillomania commonly distributed?

A

In areas that are easy to reach with hands, e.g., scalp, eyelashes, eyebrows.

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23
Q

What is the management for Trichotillomania?

A

Initial treatment of underlying psychogenic disorder in adults, followed by behavioral therapy, e.g., habit reversal and conservative ways to stop hair pulling, e.g., wearing gloves or putting socks on child’s hand, cutting hair close to scalp.

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24
Q

What is Androgenic alopecia?

A

Non-scarring hair thinning due to excess androgen levels, especially dihydrotestosterone (DHT) and genetic factors.

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25
Q

What is the pathophysiology of Androgenic alopecia?

A

Excess DHT causes hair to become shorter, thinner, and stay in telogen phase for longer periods.

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26
Q

What is a common family history associated with Androgenic alopecia?

A

Patient usually has a family history of pattern hair loss.

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27
Q

What is the presentation of Androgenic alopecia in men?

A

Hair thinning at the top and front of the scalp (receding hairline) to form a characteristic M-pattern.

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28
Q

What is the presentation of Androgenic alopecia in women?

A

Hair thinning at the crown of the scalp and surrounding hair-parting in a characteristic ‘christmas tree’ pattern.

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29
Q

What management options are available for women with Androgenic alopecia?

A

Only women are entitled to NHS treatments including topical minoxidil and anti-androgenic drugs, e.g., finasteride, spironolactone.

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30
Q

What private treatment options are available for Androgenic alopecia?

A

Private treatments include hair transplant and wigs.

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31
Q

What is Telogen Effluvium?

A

Nonscarring, noninflammatory, diffuse hair loss often triggered by systemic stress events.

Examples include childbirth, severe medical illness, crash dieting/malnutrition, psychological stressors, surgery, medication, and thyroid disease.

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32
Q

What are the two types of Telogen Effluvium?

A

Acute and Chronic.

Acute occurs abruptly after a trigger and lasts less than 12 months; Chronic occurs after a trigger with acute or slow onset and lasts more than 12 months.

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33
Q

How long does hair regrowth take in Telogen Effluvium?

A

Hair regrowth takes months to years.

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34
Q

What is Tinea capitis?

A

A fungal skin infection causing patchy, inflamed, non-scarring hair loss on the scalp due to kerions.

Kerions are abscesses formed in response to severe fungal infection.

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35
Q

How is Tinea capitis diagnosed?

A

Wood’s lamp examination shows yellow-green fluorescence if microsporum canis is present, but mycology scrapings can confirm the diagnosis.

36
Q

What is the management for Tinea capitis?

A

Oral antifungals are required because the fungus grows deep into the hair follicle, making topicals insufficient.

37
Q

What is scarring/cicatricial alopecia?

A

A type of hair loss characterized by the replacement of hair follicles with scar tissue.

38
Q

What are the characteristics of lichen planopilaris?

A

Cicatricial alopecia with white, smooth bald patches on the scalp and a receding hairline with perifollicular erythema.

Also check for nail changes and wickham’s striae in oral mucosa.

39
Q

What is frontal fibrosing alopecia?

A

Cicatricial alopecia predominantly along the frontotemporal hairline, usually occurring in postmenopausal women.

Commonly affects other areas such as eyebrows and eyelashes.

40
Q

What characterizes discoid lupus erythematosus (DLE)?

A

UV-induced cicatricial alopecia with circular lesions of erythema, scale, and follicular plugging.

Most common in women of colour.

41
Q

What is central centrifugal cicatricial alopecia (CCCA)?

A

Slowly progressive scarring hair loss centered on the crown/vertex and midline, extending outwards.

Most common in black ethnic groups.

42
Q

What are the features of folliculitis decalvans?

A

Inflammatory scarring alopecia with perifollicular papules and pustules, scale, and tufting.

Characterized by pustules, erosions, scaling, ulceration, and tufts of hair growing from the same follicle.

43
Q

What are some causes of scarring alopecia?

A

Trauma, congenital and autoimmune skin disorders, post-radiotherapy or post-operative scarring, traction alopecia (due to hair styling products and devices).

44
Q

Why is early recognition of scarring alopecia important?

A

It must be recognised early and referred to dermatology as it can cause permanent hair loss.

45
Q

What are some management options for scarring alopecia?

A

Potent/very potent topical steroids (e.g., dermovate) and systemic antibiotics (e.g., doxycycline, hydroxychloroquine).

46
Q

What is the initial investigation for hair loss?

A

Can be a clinical diagnosis due to hallmark features.

47
Q

What tests should be conducted if a patient presents with thyroid symptoms?

A

Thyroid function tests.

48
Q

What serum level is indicative of hair loss?

A

Serum ferritin level below 70 micrograms.

49
Q

What tests are advised to rule out hyperandrogenism?

A

Free testosterone, androstenedione, and dehydroepiandrosterone (DHEA) if the patient presents with acne, irregular menses, or hirsutism.

50
Q

What test should be conducted for patients with suspected DLE and SLE?

A

ANA test.

51
Q

What screening should be done for hair loss presenting in a moth-eaten pattern?

A

Syphilis screen.

52
Q

What is hirsutism?

A

Androgen-dependent excessive hair growth.

53
Q

In which gender is hirsutism more prevalent?

A

Much more prevalent in females than males.

54
Q

What causes hirsutism?

A

Hirsutism occurs due to hyperandrogenism, which can be caused by underlying conditions.

55
Q

What is an established cause of hirsutism?

A

Obesity.

56
Q

What are idiopathic causes of hirsutism?

A

Hirsutism can have idiopathic causes where androgen levels are normal.

57
Q

What endocrine diseases can cause hirsutism?

A

Ovarian disease (e.g., PCOS, benign/malignant ovarian tumors), adrenal disease (e.g., congenital adrenal hyperplasia, benign/malignant adrenal tumors), and pituitary gland disease (e.g., Cushing’s disease, prolactinoma).

58
Q

What are iatrogenic causes of hirsutism?

A

Drugs such as anabolic steroids, oral contraceptives, phenytoin, and androgenic drugs.

59
Q

What is the typical presentation of hirsutism?

A

Excess hair growth in a male pattern (e.g., upper lip, cheeks, chin, pubic hair extending to umbilicus, inner thighs, chest, upper back).

60
Q

What are associated virilisation symptoms of hirsutism?

A

Acne, irregular or absent periods, clitoromegaly, deepened voice, increased muscle bulk, frontotemporal hair loss.

61
Q

What causes rapid onset hirsutism with severe virilisation?

A

Adrenal tumors or ovarian tumors that secrete androgens.

62
Q

What is the purpose of a fasting blood glucose test in hirsutism investigation?

A

Screens for type 2 diabetes which can be associated with PCOS.

63
Q

What does a plasma testosterone level test screen for?

A

Testosterone-secreting tumors.

64
Q

What does an elevation in 17-hydroxyprogesterone and progesterone levels indicate?

A

Can indicate congenital adrenal hyperplasia.

65
Q

What do cortisol levels at 9am and midnight screen for?

A

Cushing’s disease.

66
Q

What do prolactin levels screen for?

A

Prolactinoma; moderately elevated values should prompt imaging of the pituitary-hypothalamic region.

67
Q

What is typically elevated in PCOS regarding LH and FSH levels?

A

LH is typically elevated, while FSH is low or normal.

68
Q

What does dehydroepiandrosterone sulfate (DHEA-S) screen for?

A

Adrenal androgen production; elevated levels can indicate adrenal androgen-secreting tumors.

69
Q

What is the initial management approach for hirsutism?

A

Initially treat the underlying cause, then address hirsutism.

70
Q

What are some private treatments for hirsutism?

A

Temporary removal methods such as bleaching and laser removal.

71
Q

What is eflornithine hydrochloride?

A

A topical cream that decreases facial hair growth, with effects seen in about 8 weeks.

72
Q

What is the initial treatment approach for hirsutism?

A

Initially treat the underlying cause, then address hirsutism.

73
Q

What are private treatments for hirsutism?

A

Private treatments provide temporary removal, e.g., bleaching and laser removal.

74
Q

What is Eflornithine hydrochloride?

A

A topical cream that decreases facial hair growth, with gradual improvement seen over 6-8 weeks.

75
Q

What are spironolactone and cyproterone acetate?

A

Anti-androgenic drugs used to treat hirsutism.

76
Q

What is the function of finasteride?

A

It is a 5-alpha reductase inhibitor used for hirsutism.

77
Q

How does the Combined Oral Contraceptive pill help with hirsutism?

A

It reduces androgen production and should be offered particularly to women desiring contraception.

78
Q

What conservative measures should be advised for women with PCOS or overweight?

A

Diet and exercise should be advised to all women with PCOS or who are overweight.

79
Q

What is hypertrichosis?

A

Non androgen-dependent excessive hair growth.

80
Q

What causes localized hypertrichosis?

A

Causes include porphyria cutanea tarda, naevoid hypertrichosis, spina bifida, and chronic rubbing or trauma.

81
Q

What is naevoid hypertrichosis?

A

A congenital condition characterized by a solitary circumscribed area of terminal hair growth.

82
Q

What is spina bifida?

A

Incomplete closing of the spine and membranes around the spinal cord during early development in pregnancy, which can cause a faun-tail tuft on a newborn’s lower back.

83
Q

What causes generalized hypertrichosis?

A

Causes include malnutrition (e.g., anorexia nervosa), foetal alcohol syndrome, paraneoplastic effect, drugs (e.g., minoxidil, phenytoin, androgenic drugs, ciclosporin, diazoxide), and porphyria cutanea tarda.

84
Q

What are the two classification systems for hypertrichosis?

A
  1. Congenital or acquired hypertrichosis
  2. Generalised or localised hypertrichosis
85
Q

What are the three types of hair in hypertrichosis?

A
  1. Lanugo: long fine hair that should be shed in utero and the first few weeks of life.
  2. Vellus: short fair hair that covers most of the body.
  3. Terminal: thick pigmented hair.
86
Q

What investigations are done for hypertrichosis?

A

Investigations depend on the cause and may include FBC, U&E, LFT, fasting glucose level, serum iron and ferritin, serology for hep A-C, and serum porphyrins.

87
Q

What imaging study may be used in the investigation of hypertrichosis?

A

Liver ultrasound.

Clinical lectures: Yr2 (46 decks)

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