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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Arrector pili muscle

A
  • small, involuntary muscle attached to hair follicle
  • contracts, causes hair tot stand up = phenomenon known as “goosebumps”
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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