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Dermatology > Diseases of Hair Density > Flashcards

Diseases of Hair Density Flashcards

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Dermatology Board Prep flashcards
1
Q

Hair growth pattern

A

hair grows in a cyclic pattern that is defined in 3 stages (most scalp hairs are in anagen phase)

  1. growth stage = anagen phase
  2. transitional stage = catagen stage
  3. resting stage = telogen phase
  • total duration of the growth stage reflects the type and location of hair: eyebrow, eyelash, and axillary hairs have a short growth stage in relation to the resting stage
  • growth of the hair follicles is also based on the hormonal response to testosterone and DHT; this response is genetically controlled
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2
Q

Hair loss differential diagnosis

A

TOP HAT

Telogen effluvium, tinea capitis
Out of Fe, Zn
Physical: trichotillomania, “corn-row” braiding

Hormonal: hypothyroidism, androgenic
Autoimmune: SLE, alopecia areata
Toxins: heavy metals, anticoagulants, chemotherapy, vitamin A, SSRls

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3
Q

DDx of non-scarring (non-cicatricial) alopecia

A

Autoimmune
• Alopecia areata

Endocrine
• Hypothyroidism
• Androgens

Micronutrient deficiencies
• Iron
• Zinc

Toxins 
• Heavy metals 
• Anticoagulants 
• Chemotherapy 
• Vitamin A

Trauma to the hair follicle
• Trichotillomania
• ‘Corn-row’ braiding

Other
• Syphilis
• Severe illness
• Childbirth

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4
Q

Androgenetic alopecia clinical presentation

A
  • male- or female-pattern alopecia
  • males: fronto-temporal areas progressing to vertex, entire scalp may be bald
  • females: widening of central part, “Christmas tree” pattern
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5
Q

Androgenetic alopecia pathophysiology

A

action of testosterone on hair follicles

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6
Q

Androgenetic alopecia epidemiology

A

• males: early 20s-30s • females: 40s-50s

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7
Q

Androgenetic alopecia management

A
  • minoxidil (Rogaine®) solution or foam to reduce rate of loss/partial restoration
  • females: spironolactone (anti-androgenic effects), cyproterone acetate (Diane-35®)
  • males: finasteride (Propecia®) (5-α-reductase inhibitor) 1 mg/d
  • hair transplant
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8
Q

Physical hair loss etiologies

A
  • trichotillomania: impulse-control disorder characterized by compulsive hair pulling with irregular patches of hair loss, and with remaining hairs broken at varying lengths
  • traumatic (e.g. tight “corn-row” braiding of hair, wearing tight pony tails, tight tying of turbans)
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9
Q

Telogen effluvium clinical presentation

A

• uniform decrease in hair density secondary to hairs leaving the growth (anagen) stage and entering the resting (telogen) stage of the cycle

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10
Q

Telogen effluvium pathophysiology

A

variety of precipitating factors

  • hair loss typically occurs 2-4 mo after exposure to precipitant
  • regrowth occurs within a few months but may not be complete
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11
Q

Precipitants of Telogen Effluvium

A

“SEND” hair follicles out of anagen and into telogen

Stress and Scalp disease (surgery)
Endocrine (hypothyroidism, post-partum)
Nutritional (iron and protein deficiency)
Drugs (citretin, heparin, lithium, IFN, β-blockers, valproic acid, SSRIs)

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12
Q

Anagen effluvium clinical presentation

A

• hair loss due to insult to hair follicle impairing its mitotic activity (growth stage)

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13
Q

Anagen effluvium pathophysiology

A
  • precipitated by chemotherapeutic agents (most common), other meds (bismuth, levodopa, colchicine, cyclosporine), exposure to chemicals (thallium, boron arsenic)
  • dose-dependent effect
  • hair loss 7-14 d after single pulse of chemotherapy; most clinically apparent after 1-2 mo
  • reversible effect; follicles resume normal mitotic activity few weeks after agent stopped
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14
Q

Non vs scarring alopecia difference on physical exam

A

Non scarring alopecia: intact hair follicles on exam -> biopsy not required (but may be helpful)

Scarring alopecia: absent hair follicles on exam -> biopsy required

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15
Q

Alopecia areata subtypes

A

Alopecia totalis: loss of all scalp hair and eyebrows

Alopecia universais: loss of all body hair

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16
Q

Alopecia areata clinical presentation

A
  • autoimmune disorder characterized by patches of complete hair loss often localized to scalp but can affect eyebrows, beard, eyelashes, etc.
  • may be associated with dystrophic nail changes – fine stippling, pitting
  • “exclamation mark” pattern (hairs fractured and have tapered shafts, i.e looks like “!”)
  • may be associated with pernicious anemia, vitiligo, thyroid disease, Addison’s disease
  • spontaneous regrowth may occur within months of first attack (worse prognosis if young at age of onset and extensive loss)
  • frequent recurrence often precipitated by emotional distress
17
Q

Alopecia areata management

A
  • generally unsatisfactory
  • intralesional triamcinolone acetonide (corticosteroids) can be used for isolated patches
  • UV or PUVA therapy
  • immunomodulatory (diphencyprone)
18
Q

Scarring (Cicatricial) Alopecia clinical presentation

A

• irreversible loss of hair follicles with fibrosis

19
Q

Scarring (Cicatricial) Alopecia etiology

A
  • physical: radiation, burns
  • infections: fungal, bacterial, TB, leprosy, viral (HZV)

• inflammatory
■ lichen planus (lichen planopilaris)
■ DLE (note that SLE can cause an alopecia unrelated to DLE lesions which are non-scarring)
■ morphea: “coup de sabre” with involvement of centre of scalp
■ central centrifugal cicatricial alopecia (CCCA): seen in up to 40% of black women, starting at central scalp; one of most commonly diagnosed scarring alopecias, may be associated with hair care practices in this population

20
Q

Scarring (Cicatricial) Alopecia investigations

A

biopsy from active border

21
Q

Scarring (Cicatricial) Alopecia management

A
  • infections: treat underlying infection

* inflammatory: topical/intralesional steroids, anti-inflammatory antibiotics, antimalarials

22
Q

DDx of scarring (cicatricial) alopecia

A 
Developmental/Hereditary Disorders 
• Aplasia cutis congenita 
• Epidermal nevi 
• Romberg’s syndrome 
• Generalized follicular hamartoma 
Primary Causes 
• Group 1: Lymphocytic 
• DLE 
• Lichen planopilaris 
• Central centrifugal cicatricial alopecia 
• Classic pseudopelade
  • Group 2: Neutrophilic
  • Folliculitis decalvans
  • Dissecting scalp cellulitis
  • Group 3: Mixed
  • Acne keloidalis nuchae
Secondary Causes 
• Infectious agents 
- Bacterial (e.g. post-cellulitis) 
- Fungal (e.g. kerion tinea capitis) 
• Neoplasms (e.g. BCC, SCC,  lymphomas, and metastatic tumours) 
• Physical agents
- Mechanical trauma 
- Burns 
- Radiotherapy 
- Caustic chemicals

Dermatology (11 decks)

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