Diseases of Hair Density Flashcards
Hair growth pattern
hair grows in a cyclic pattern that is defined in 3 stages (most scalp hairs are in anagen phase)
- growth stage = anagen phase
- transitional stage = catagen stage
- 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
Hair loss differential diagnosis
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
DDx of non-scarring (non-cicatricial) alopecia
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
Androgenetic alopecia clinical presentation
- 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
Androgenetic alopecia pathophysiology
action of testosterone on hair follicles
Androgenetic alopecia epidemiology
• males: early 20s-30s • females: 40s-50s
Androgenetic alopecia management
- 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
Physical hair loss etiologies
- 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)
Telogen effluvium clinical presentation
• uniform decrease in hair density secondary to hairs leaving the growth (anagen) stage and entering the resting (telogen) stage of the cycle
Telogen effluvium pathophysiology
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
Precipitants of Telogen Effluvium
“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)
Anagen effluvium clinical presentation
• hair loss due to insult to hair follicle impairing its mitotic activity (growth stage)
Anagen effluvium pathophysiology
- 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
Non vs scarring alopecia difference on physical exam
Non scarring alopecia: intact hair follicles on exam -> biopsy not required (but may be helpful)
Scarring alopecia: absent hair follicles on exam -> biopsy required
Alopecia areata subtypes
Alopecia totalis: loss of all scalp hair and eyebrows
Alopecia universais: loss of all body hair
Alopecia areata clinical presentation
- 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
Alopecia areata management
- generally unsatisfactory
- intralesional triamcinolone acetonide (corticosteroids) can be used for isolated patches
- UV or PUVA therapy
- immunomodulatory (diphencyprone)
Scarring (Cicatricial) Alopecia clinical presentation
• irreversible loss of hair follicles with fibrosis
Scarring (Cicatricial) Alopecia etiology
- 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
Scarring (Cicatricial) Alopecia investigations
biopsy from active border
Scarring (Cicatricial) Alopecia management
- infections: treat underlying infection
* inflammatory: topical/intralesional steroids, anti-inflammatory antibiotics, antimalarials
DDx of scarring (cicatricial) alopecia
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
