Hair Disorders Flashcards
1
Q
What is hair?
A
- complex structure composed of keratinized cells that grow from follicles embedded within skin
- basic anatomy = comprehending hair growth & various hair- related conditions
2
Q
Hair anatomy
A
- pilosebaceous unit
- dead, keratinized cells
- hair follicle within skin = hair shaft emerges
- hair shaft = part of hair not anchored to follicle, exposed at skin’s surface (eg: visible)
- rest of hair anchored in follicle, lies below surface of skin & referred to = hair root
- hair shaft = cuticle, cortex & medulla
- hair bulb surrounds hair papilla = connective tissue & contains blood capillaries & nerve endings from dermis
- hair root ends deep in dermis at hair bulb & layer of mitotically active basal cells = hair matrix
- hair bulge = specialised region of hair follicle located above hair bulb
— serves as reservoir of stem cells contribute to ongoing production of new hair cells during hair growth cycle & facilitate hair follicle regeneration
3
Q
Sebaceous glands
A
- associated with hair follicles & secrete sebum, oily substance that moisturizes & lubricates hair & surrounding skin
— sebum travels up hair shaft, helping to maintain its health & flexibility
4
Q
Arrector pili muscle
A
- small, involuntary muscle attached to hair follicle
- contracts, causes hair tot stand up = phenomenon known as “goosebumps”
5
Q
How does hair grow?
A
- grows on most parts of skin surface, except palms, soles, lips & eyelids
- hair thickness & length varies according to anatomic site
- vellus hair is fine, light in colour, short in length
- terminal hair is thicker, darker & longer
- hair shaft grows within follicle at rate 1cm/ month
— cell division within hair bulb at base of follicle
— cells produce = three layers of hair shaft (medulla, cortex, cuticle)
— hair shaft mainly composed of protein keratin (skin & nails)
6
Q
Hair growth cycle
A
- phases not synchronized & any hair may be at a particular phase at random
- anagen: active growth phase (1-6 yes, majority)
- catagen: transitional phase of 1-3 weeks when growth stops & follicle shrinks (1-3% of hairs)
- telogen: resting phase for 1-4 months (10% of hairs in normal scalp)
(- exogen a fourth phase, shedding)
7
Q
Scarring & non-scarring alopecia
A
- hair loss (alopecia) = isolated problem/ associated with another disease/ condition
- non-scarring (temporary/ reversible) or scarring (permanent), depending on cause
- pathophysiology crucial for accurate diagnosis & management of patients
8
Q
Non-scarring alopecia
A
- hair looks with non-scarring damage to hair follicles (hair loss usually reversible or treatable)
Common causes
= alopecia areata (hair loss, clumps/ patches, bald spots in various areas of body)
Telogen Effluvium (temporary hair loss = stressor/ change to your body)
Make & female pattern hair loss
9
Q
Scarring alopecia
A
- permanent damage to hair follicles
Common causes
= discoid lupus erythematous
Lichen planopilaris (inflammatory condition effecting skin & mucous membranes)
Chronic bacterial infections
Chronic fungal infections
10
Q
Alopecia areata
A
- autoimmune condition
- presents with discrete bald patches on scalp, cause hair loss from all hair-bearing areas in body
- immune system mistakenly targets hair follicles as foreign & launches an immune response against
- cause ?
- thought: loss of immune privilege in anagen hair follicles plays key role + genetic susceptibility
11
Q
Pathophysiology of alopecia areata
A
- immune system, CD8+ T-lymphocytes is thought = crucial role in development
- T-lymphocytes infiltrate hair follicles & recognize specific self-antigens expressed in hair follicle as foreign
- immune response is triggered = inflammation & subsequent damage to hair follicles
12
Q
Genetic & other factors of alopecia areata
A
- strong hereditary component
- 16 genetic risk loci detected
- numerous human leukocyte antigen (HLA) class I & II alleles & several alleles involved in immune pathways, hair pigmentation & response to oxidative stress
- mode of inheritance = complex & environmental influences
13
Q
Telogen effluvium
A
- healthy scalp, 85% of hair follicles = actively growing hair (anagen hair) & 15% resting hair (telogen hair)
- few hairs may also be in catagen
- new anagen hairs begins to grow under resting telogen hair & pushes out
- normal/ healthy scalp can lose up to about 100 hairs a day on one’s comb, basin or on pillow = normal hair cycle
- significant number of hair follicles prematurely enter telogen phase (resting phase) of hair growth cycle = increased hair shedding
- insult to system, 70% anagen hairs = telogen, reversing usual ratio
- triggered by variety of factors, physiological, psychological or environmental stressors
14
Q
Triggering factors of telogen effluvium
A
- physical/ emotional stress (childbirth, surgery, severe illness)
- hormonal changes (postpartum hormonal fluctuations, thyroid disorders, contraceptive pill)
- nutritional deficiencies (iron, zinc, biotin)
- certain medications (anticoagulants, retinoids)
- rapid weight loss
15
Q
Pathophysiology of telogen effluvium
A
- triggering factors disrupt normal balance of hair growth cycle
- large number hairs in anagen phase (growing phase) go abruptly enter telogen (resting)
- increased number of hairs in telogen phase at any given time
- leads to excess shedding of hair (gentle manipulation of scalp)
- increased shedding = pt as diffuse hair loss/ thinning
- NB = self-limiting condition in vast majority of people
- underlying triggering factor is resolved/ managed, affected hair follicles gradually return to normal growth cycle
- new hair begins to grow, shedding diminishes over time
16
Q
Male & female pattern hair loss
A
- androgenetic alopecia
- male pattern = most common of diffuse thinning of hair & balding that occurs in adult males
- combo of hormones (androgens) & genetic predisposition
- receding hairline & hair loss on top & front of head
- similar type of hair loss in women = thinning hair on mid-frontal area of scalp & less severe than occurs in males
17
Q
Genetic predisposition of male & female pattern hair loss
A
- androgenetic alopecia = genetically determined
- influenced material & paternal inherited susceptibility genes
- several genes = differing age of onset, progression, pattern & severity of hair loss in family members
18
Q
Androgen sensitivity in male & female pattern hair loss
A
- hallmark in increased sensitivity of hair follicles to androgens, dihydrotestosterone (DHT)
- DHT by product of testosterone conversion = enzyme 5-alpha reductase
- DHT shorten the growth anagen, phase of hair cycle from usual duration of 3-6 years to weeks/months
— together with miniaturization of follicles - hair follicles located in certain areas of scalp, frontal & vertex regions in men & central scalp in women = more susceptible to DHTs effects
19
Q
Miniaturization of hair follicles in male & female pattern hair loss
A
- presence of DHT leads gradual miniaturization of hair follicles
- miniaturization = progressive shrinking of hair follicles over time
- hair follicles produce thinner, shorter & less pigmented hairs during each hair growth cycle = appearance of thinning or balding areas
20
Q
Female pattern hair loss
A
- present with male pattern = excessive levels of androgens + genetic predisposition
- women = acne, irregular menses & excessive facial & body hair
- PCOS although majority don’t experience hair loss
- less often congenital adrenal hyperplasia may be responsible
- losing hair with age = more likely to present with female pattern loss in which hormone tests normal
21
Q
Discoid Lupus Erythematous (DLE)
A
- chronic scarring condition
- most common form of cutaneous lupus erythematous
- sub-type chronic cutaneous…
- Persistent scaly plaques on scalp, face & ears
— progress to scarring, atrophy, dyspigmentation & permanent hair loss affected hair-bearing areas
22
Q
Pathophysiology of DLE
A
- LE is polygenic autoimmune disease linked to various HLA subtypes, immune signaling & environmental factors which ultimately leads to autoantibody production & T-cell dysfunction
- exact etiology?
- likely genetically predisposed individuals by exact genetic connection has not been determined
- exogenous factors eg: smoking & UV
— smoking more common
— UV can provoke DLE as it is photosensitive disorder (non-sun exposed areas as well)
23
Q
Lichen planopilaris (LPP)
A
- uncommon inflammatory condition = permanent hair loss
- disease form of lichen planus = hair follicles, similar Pathogenesis
= patchy, progressive, permanent hair loss mainly on scalp, other hair-bearing skin may be affected
24
Q
Pathophysiology of LPP
A
- exact cause?
- thought cytotoxic autoimmune response to unknown antigen = hair follicles
- exact trigger ?
- gene-related, rarely drug-induced
25
Q
Chronic bacterial infection in hair loss
A
Depends on
- type of bacteria (eg: staph aureus)
- location & severity of infection (eg: scalp)
- individual patient factors (eg: underlying HIV)
Bacterial scalp infections presents as scalp Folliculitis do not usually = scarring hair loss
26
Q
Severe bacterial superinfection
A
Chronic scalp conditions
Eg: seborrhaoeic eczema, dermatitis
May = severe inflammation & damage & eventually permanent destruction of hair follicles
27
Q
Dissecting cellulitis of scalp
A
- rare cause of scarring alopecia
- primarily related to follicular hyperkeratosis, rather than infection
- bacterial superinfection may occur
28
Q
Folliculitis decalvans
A
Applied to forms of highly inflammatory scarring alopecia = inflammatory, follicular papules & pustules dominate clinical picture
- often, not always staph aureus can be grown from pustular or crusted lesions
- primary staph infection of scalp is cause
Tufted hair - multiple hair shafts from one orifice
29
Q
Fungal infections with hair loss
A
- tinea capitis is common of scalp, presents with pruritic scaling areas of non-scarring hair loss
- trichophytom & microsporum species of Dermatophyte fungi = major causes of tinea capitis
- contracted human to human/ animal through direct contact
- tinea capitis does not usually cause scarring alopecia, unless infection long-standing & untreated/ severe/ clinical variant = kerion develops
30
Q
Kerion
A
- severe manifestation of tinea capitis = dramatic immune response to infection
- development of inflammatory plaque with pustules, thick crusting, & drainage
- most commonly in children 5-10 = rare in infancy
- most often caused zoophilic dermatophyte, anthropophilic fungi can also cause
- persistent = scarring alopecia
