Hair (also refer to Yip notes) Flashcards
History
Gradual thinning in a pattern over time (THINNING)
vs
Rapid increase in amount of hair shed I.e. in shower, on pillow, carpet, when brushed (SHEDDING)
Symptoms
Usually asymptomatic
Itch, burning, pain —> inflammation —> possible scarring hair loss
Itch —> pediculosis capitals, tinea capitis
Gradual thinning - Family history of premature hair loss in male/female pattern Menstrual irregularity Hirsutism/other signs of androgenisation Contraceptive history
Shedding I.e. telegenic effluvium -
Life events few months before onset I.e. psychological stress, physical illness
New meds started few months before onset
Dieting/weight loss
Relationship between iron stores and hair loss controversial
Acute telogen effluvium - may identify trigger
Chronic/episodic telogen effluvium - difficult to identify specific trigger
Clinical exam
Clinically evident hair loss
Pattern -
- Diffuse
- Patchy
- Distinctive distribution
Extent
Hair colour, shine, texture
If patchy - ? patent follicular ostia (non-scarring) or lost of follicular ostia (scarring)
Scalp inflammation - Perifollicular erythema Follicular hyperkeratosis Follicular plugging Pustules/swellings
Trichoscopy - Variation in hair fibre diameter Hair shaft abnormalities Exclamation mark hairs Cadaverised hairs (black dots visible under the scalp surface repressenting hair remnants) Abnormal scalp vessels
Hair pull test for diagnosis/assessment generalised hair shedding I.e telogen effluvium -
Avoid part lines
Gather approx 60 hairs with non-dominant thumb and forefinger
Grasp hairs between dominant thumb and forefinger near scalp, apply gentle traction in a smooth gradual manner away from the scalp
Assess number and type of hairs extracted
Repeat from a few sites on the scalp
Hair pull test for disease activity in focal area of hair loss -
Grasp a few hairs from edge of focal hair loss area
Telogen hairs from periphery of patch of AA
Anagen hairs from active areas of scarring alopecia
Modified hair pull test to assess hair breakage -
If hair breaks/snaps —> hair brittleness —> shaft abnormality
Trichogram (forced pluck of hair including hair roots) -
Needle holder/armed forceps grasping hairs near the scalp surface, then firmly and rapidly tug hair away from scalp
Hairs analysed under microscope - % hairs in telogen and anagen
Time consuming
Doubtful value
Trichoscopy
AA - Yellow dots (sebum within follicular ostia) Black dots Broken hairs Exclamation mark hairs
Female pattern hair loss -
Variation in hair fibre diameter
LPP -
Follicular hyperkeratosis
DLE -
Arborising vessels
Folliculitis decalvans -
Tufting
Erythema
Children with hair loss
Part of genetic syndrome
Ectodermal abnormality affecting hair, teeth, nail, heat intolerance/anhidrosis
Assoc hair shaft abnormality
History -
Pattern of hair at birth
Evolution during 1st year of life
Patches of Alopecia early in life —> aplastic cutis (absent hair follicle development), triangular Alopecia (vellus hairs fail to develop into terminal hairs)
Acquired patches of Alopecia —> infective cause I.e. tinea capitis —> hair samples for mycology
Teeth/nail development
Heat intolerance due to anhidrosis —> ? Ectodermal dysplasia
Family history
Failure of hair to grow beyond a certain length —>
- Hair shaft abnormality I.e. monilethrix
- Increase in hair loss I.e. loose anagen syndrome
- Decreased growth phase I.e. short anagen syndrome
Investigation
Light microscopy for possible hair shaft disorders
Hair shaft disorders may be focal, sufficient hairs should be submitted for analysis
Trim hairs near to the base (not plucked from the roots)
Polarisation of hair shafts - tiger tail pattern in trichothiodystrophy due to low sulphur content
Microscopy of plucked hair useful for detecting ruffled cuticle in the roots in loose anagen syndrome
Scalp biopsy
2 x 4mm punch biopsies
Biopsies orientated in the direction of hair growth to minimise transaction of follicles
Extend to subcut fat
Scarring Alopecia protocol -
Both biopsies from peripheral active border/edge
1 for Vertical section by doctor - half for immunofluorescence, half for lab vertical sectioning
1 for Horizontal section
Non-scarring alopecia protocol -
1 from involved area I.e. vertex in androgenetic alopecia, edge of AA patch
1 from control area I.e. occiput in androgenetic alopecia
Both horizontal sectioning
Biopsies useful in -
Possible scarring alopecia
Distinguish between AA and trichotillomania
Excessive hair shedding without clinical reduction in hair density (DDx telogen effluvium vs early pattern hair loss) for evidence of follicular miniaturisation (early pattern hair loss)
Diagnose diffuse hair loss of uncertain cause I.e. diffuse AA, SLE
Diagnose rare causes I.e. secondary syphilis, granulomatous disease, cutaneous lymphoma, malignancies
Non-scarring alopecia
Androgenetic alopecia (patterned hair loss)
Telogen effluvium
Alopecia areata
Androgenetic alopecia (male balding) and female pattern hair loss
Patterned hair loss over the crown
Male balding (AGA) - Hamilton-Norwood scale Bitemporal recession —> vertex balding Early onset —> more rapid progression Genetic predisposition + androgens
FPHL -
Ludwig scale - 3 stages
Sinclair scale - 5 stages (stage 1 is normal) - clinical severity and Rx response
Christmas tree pattern (widening of central part line in mid-frontal scalp, may extend ear to ear) —> Diffuse reduction of hair density over the crown
Complete/near complete preservation of frontal hairline I.e. minimal/no bitemporal recession - although not all maintain frontal/temporal hairline
Onset later than in men
Episodic or continuous
Increase in hair shedding w/o noticeable reduction in volume
Increase in hair shedding with loss of volume over crown
Diffuse thinning over crown w/o Hx hair shedding
? Change in thickness of ponytail —> degree of hair loss
Most have no other evidence of virilisation
DDx of early FPHL - chronic telogen effluvium (chronic diffuse hair shedding w/o noticeable widening of central parting, loss of ponytail volume of up to 1/3, mild bitemporal recession)
Assoc diseases AGA -
Trichodynia (scalp pain) - common in context of increased hair shedding
Positive assoc Vertex balding and prostate CA
Weak assoc vertex balding and coronary hear disease
Kennedy disease assoc with reduced risk of AGA
Assoc diseases FPHL - HTN Elevated cholesterol Late onset diabetes Hyperandrogenism PCOS Hyperaldosteronism
Ix (general) -
Hair pull test ? Hair cycle disturbance I.e. telogen effluvium, active pattern hair loss
Trichoscopy ? Different hair density between mid frontal and occipital scalp ? Miniaturisation (hair diameter diversity)
Photos
Ix (men) -
Unnecessary in AGA unless there is diagnostic uncertainty
Ix (all women with FPHL) - FBC Serum ferritin TFT Fasting lipids ? Hypercholesterolaemia Fasting glucose ? Diabetes Blood pressure ? HTN
Ix (FPHL If signs of virilisation/hirsutism)
- Sudden onset, rapidly progressive, advanced —> exclude virilizing/androgen secreting tumour
- Menstrual disturbance, infertility, hirsutism, acne —> PCOS
Serum testosterone
DHEAS morning sample days 1-5 menstrual cycle, ensure not on OCP
17-OH progesterone
Androstenedione
Scalp biopsy (non-scarring alopecia protocol, vertex + occiput as control area) in FPHL useful in women with excessive hair shedding and minimal reduction in hair density ? Early FPHL vs chronic TE -
Ratio terminal to vellus hairs in horizontal section 4mm PBx
FPHL <4:1
Chronic TE >8:1
Indeterminate if ratios are in between these values
Prognosis -
Progressive without Rx
General Mx -
Need for maintenance Rx for sustained effect
Avoid internet products
Camouflage - small fibres, dyeing the scalp
Wigs (synthetic vs natural) - full wig vs smaller hair piece interwoven with existing hair or worn over top, difficult to wear in summer due to heat
Alopecia support group
Serial photos every 6-12 months
Medical Mx AGA -
5% Minoxidil lotion/foam continued indefinitely OD-BD —> useful in early AGA, benefit most pronounced in first 6/12, marginal thereafter; S/E local irritation, contact dermatitis, hypertrichosis of temples, if stopped clinical regression within 6/12 to state of baldness that would have existed if no Rx
Finasteride 1mg OD (5-alpha reductase 2 selective antagonist, reverse miniaturisation process, arrest but does not reverse bitemporal recession) —> early initiation will achieve better results as potential for regrowth diminishes as AGA progresses; S/Es reduced libido, erectile dysfunction (may or may not resolve on cessation of Rx), reduced PSA by 50% and underestimation of prostate CA risk (need to double the PSA value to correct for the finasteride effect), ? Impair genital development/feminisation in male fetus if pregnant women exposed to semen containing finasteride but there are currently no recommendations regarding use of condoms in product leaflet
Dutasteride 0.5mg OD (combined 5-alpha reductase 1 & 2 antagonist) —> more effective than finasteride, sexual side effects more common than finasteride and dose related, reversible retrograde ejaculation
Medical Mx FPHL -
5% Minoxidil lotion/foam continued indefinitely OD-BD
Spironolactone 50-300mg OD for premenopausal/post menopausal women —> best tolerated, easiest to use; S/Es menstrual irregularities, post menopausal bleeding, breast tenderness/enlargement, fatigue, feminisation of male fetus (contraindicated in pregnancy), hyperkalaemia, reduce BP (insignificant in absence of renal impairment); take OCP to to reduce hormonal side effects
Cyproterone acetate 50-100mg OD for 1st 10 days of menstrual cycle for premenopausal women, continuously +/- oral oestrogen for post menopausal women —> more effective in women with hyperandrogenism; S/Es lassitude, weight gain, breast tenderness, loss of libido, nausea, depression, feminisation of male fetus (contraindicated in pregnancy)
Flutamide - limited use d/t potentially fatal hepatotoxicity
Finasteride 1mg OD in post menopausal women —> relative contraindication in premenopausal women d/t teratogenicity
Telogen effluvium
Increase in shedding of telogen/club hairs d/t premature termination of anagen hairs of the hair cycle
In infancy, follicular cycling within anatomical regions is synchronous —> synchronous shedding
Hair length affects perception of hair loss
Hair pluck —> 13% telogen, 86% anagen, 1% catagen
5 functional types of TE -
Immediate anagen release I.e. physiological stress, drug-induced hair loss (follicles stimulated to leave anagen and enter telogen -rematurely)
Delayed anagen release I.e. post partum hair loss (anagen duration prolonged in pregnancy —> large number of follicles cycle into telogen —> shed together)
Short anagen syndrome I.e. androgenetic alopecia where TE precedes visible balding (shortening of anagen —> persistent telogen hair shedding)
Immediate telogen release I.e. temporary increase in hair shedding 4-6 weeks after starting minoxidil (premature exogenous —> shortening of telogen duration —> does not necessarily initiate anagen —> telogen follicles may remain empty for weeks)
Delayed telogen release
Acute TE vs chronic TE vs drug-induced TE
ACUTE TE
Mechanism: Immediate anagen release
Acute onset diffuse scalp hair loss 2-3 months after triggering event
- high fever
- surgical trauma
- sudden starvation
- haemorrhage
- pregnancy (telogen gravidarum) I.e. 2-3 months after childbirth —> resolves, small proportion persistent episodic diffuse/localised shedding
- OCP —> synchronous hair growth —> shedding when OCP ceased
- no trigger
No evidence that stresses of everyday life sufficient to induce diffuse hair loss
Lower rate of shedding + short period —> No obvious baldness
High rate of shedding —> noticeable balding
Doesn’t not produce total baldness
Spontaneous complete regrowth 3-6 months (unless trigger repeated)
Ix - hair pull positive with normal club hairs
CHRONIC TE
Telogen hair shedding persisting > 6 months
Primary vs secondary
Primary - idiopathic change in hair cycle dynamics
Secondary -
- thyroid disorders (both hyper/hypothyroidism) - reversible with euthyroid state restored
- severe iron deficiency anaemia - corrected by iron replacement
- acrodermatitis enteropathica, acquired zinc deficiency from long-standing TPN (diffuse hair loss w/o other symptoms/signs —> never due to diet zinc deficiency, low zinc levels on routine screen in these patients prob incidental finding)
- malnutrition i.e. crash dieting with protein-calorie restriction, marasmus (also have hair shaft abnormalities), pancreatic disease, essential fatty acid deficiencies
- Liver disorders
- chronic renal failure
- SLE
- dermatomyositis
- secondary syphilis (moth eaten border not always present)
Shedding in early FPHL (diffuse, episodic) can mimic TE —> if suspected, PBx mid frontal scalp
DRUG-INDUCED TE
Mechanism: immediate anagen release
6-12 weeks after starting —> progressive whilst drug continued
shedding can recur with biochemically unrelated drugs (true cross reactivity rare)
Testing - Stop drug for at least 3 months —> regrowth following discontinuation and recurrence on re-exposure supports drug as the cause
Full recovery may take 6 months
Persistent shedding after 3 months/incomplete recovering after 6 months —> possible coincidental androgenetic alopecia
Common drugs -
- Acitretin > isotretinoin
- Minoxidil (immediate telogen release —> temporary telogen shedding)
DDx - chronic TE, AGA
PRIMARY CHRONIC TE (DDx early AGA)
Idiopathic, most cases no trigger
Unknown mechanism
Sometimes self-limiting
Middle-aged women 30-50 yrs
Sudden onset increased hair shedding persisting at least 6 months
Fluctuating course over few years
May have trichodynia, scalp dysaesthesia
Reduction in ponytail volume by up to 50%
Hx of ability to grow hair very long in childhood —> suggestive of long anagen phase
Reports high hair density prior to onset of hair loss
Usually neg fam Hx of AGA
Clinical exam -
- Bitemporal recession w/o widening of central part line (if this is present then supports dx of AGA) —> but AGA can mimic this presentation
- Positive hair pull over vertex + occiput —> though if neg does not exclude dx
- Trichoscopy - no miniaturisation
Dx of exclusion -
- detailed drug Hx
- diet Hx
- scalp exam
- hair pull test
- FBC
- TFT
- ANA
- syphilis serology
- serum zinc
- other Ix of nutritional status if clinically warranted I.e. iron studies
- scalp biopsy 4mm PBx from vertex scalp for horizontal sectioning may be needed to differentiate from early AGA —> terminal to vellus ratio < 4:1 = AGA
Rx -
- nil necessary, hair is replaced and condition does not lead to baldness
- may respond to minoxidil
Alopecia areata
Non scarring
Autoimmune disease
T-cell mediated autoimmune mechanism in predisposed individuals
Collapse of normal immune privilege at hair follicle
? target hair bulb melanocytes
Genetic predisposition/family history
Associated diseases - Atopy esp eczema - early onset, more severe forms of AA Thyroiditis LE Vitiligo Psoriasis
Triggers -
Psychological stress
Clinical features -
Circumscribed hairless smooth patch
Skin normal/slightly red
Exclamation mark hairs at margins of bald patch
Occasionally diffuse without discrete bald patches
Ophiasis pattern
Scalp, beard, eyebrows, eyelashes +/- trunk/limbs
Nail involvement usually in severe disease - fine stippled organised pitting, trachyonychia
Sparing of white hair (less susceptible but not immune)
Unpredictable course - regrowth within few months vs further patches vs alopecia totalis vs alopecia universalis
Regrowth - fine and non-pigmented —> normal calibre and colour recovers completely
If regrowing hairs remain non-pigmented, consider concurrent vitiligo
SALT (severity alopecia tool) grading
Up to 50% recover within 1 year
Almost all experience more than 1 episode
Up to 25% experience alopecia totalis/universalis —> full recovery unusual
Less favourable prognosis - family Hx, onset childhood, ophiasis pattern, ? atopy, duration > 1 year
DDx -
Children - tinea capitis, trichotillomania
Early scarring alopecia
SLE
Secondary syphilis (diffuse/patchy hair loss)
Ix -
Straightforward clinical dx on most cases —> Ix usually not needed
Biopsy may be necessary/helpful if diagnostic uncertainty —> diffuse alopecia, early scarring alopecia
Selected cases -
- fungal MCS ? tinea capitis
- ANA, ENA ? SLE
- syphilis serology / secondary syphilis
Risk for other autoimmune disease small and lifelong —> debatable if routine one off screening for these is appropriate or not
Path -
Affects anagen follicles
Perifollicular and intrafollicular infiltrate mainly of T cell lymphocytes in and around hair bulb “swarm of bees”
In contrast to inflammatory scarring alopecias, little/no inflammation around isthmus of hair follicle (where stem cells are) —> follicles not destroyed in AA
Both anagen and telogen follicles found in affected sites (higher proportion in telogen as anagen follicles are precipitated into telogen/return to telogen prematurely, follicles smaller than normal)
Mx -
General -
Treatments induce hair growth but NONE alter course of the disease
Response rate for extensive hair loss low
Counselling of patient + family important -
- nature of disease
- natural history
- regrowth cannot be expected within 3 months of any individual patch
- available treatments
- chances of success
Patient support
Camouflage/wig
Semipermanent tattooing of eyebrows
First line Limited patchy alopecia -
Potent TCS I.e. clobetasol lotion/foam/shampoo for at least 3 months to hasten recovery (may be complicated by folliculitis) - not effective for alopecia totalis/universalis
ILCS is best I.e. triamcinolone acetonide 5-10mg/mL fine needle injection to upper subcutis (local atrophy common S/E —> recovers within few months) - not suited for rapidly progressive alopecia/alopecia totalis/alopecia universalis
Uncertain benefits for topical minoxidil and dithranol
Second line extensive/rapidly progressive alopecia -
6 week daily tapering course of oral pred starting at 40mg/d
Third line -
Contact immunotherapy most effective I.e. DPCP, squaric acid dibutyl ester (SADBE), dinitrochlorobenzene (DNCB) for at least 6 months -
- sensitise using 2% DPCP in acetone under Finn chamber for 2 days on upper arm
- assoc temporary occipital/cervical LN during and throughout Rx
- possible severe dermatitis, minimise risk by careful titration
- other S/E —> urticaria, vitiligo, hyperpigmentation
PUVA (topical, oral) - continued Rx usually needed to maintain hair growth —> risk of cumulative UVA dose
Scarring (cicatricial) alopecia
ACQUIRED CICATRICIAL ALOPECIA
Primary vs secondary
PRIMARY Inflammatory Lymphocytic - - Follicular lichen planus —> Lichen planopilaris —> Frontal fibrosing alopecia —> Graham-Little syndrome - Chronic cutaneous LE (DLE) - Pseudopelade of Brocq - Central centrifugal alopecia - Alopecia mucinosis - Keratosis pilaris spinulosa decalvans Neutrophilic - - Folliculitis decalvans —> tufted folliculitis - Dissecting cellulitis Mixed - Acne keloidalis - Acne necrotica - Erosive pustular dermatosis
Non-specific
- End stage cicatricial alopecia
SECONDARY Traumatic - - Radiodermatitis - Post-op - Burns - Artefactual alopecia —> Trichotillomania —> Dermatitis artefacta —> Cosmetic alopecia —> Traction alopecia —> Hot comb alopecia —> Medical trauma hair loss Sclerosing disorder - - Morphoea - Scleroderma - Lichen sclerosus - Sclerodermoid PCT - Chronic GVHD Granulomatous - - Sarcoidosis - Necrobiosis lipoidica - Infectious granulomas Infectious - - Bacterial —> Folliculitis —> Carbuncle/furuncle - Fungal —> Kerion —> Favus —> Tinea capitis - Viral —> Shingles —> Varicella —> HIV Protozoal —> leishmaniasis Treponemal —> Syphilis Mycobacterial —> TB Neoplastic - - Benign —> Cylindroma —> Other adnexal tumours - Primary malignant —> BCC —> SCC —> CTCL - Secondary malignant —> Lymphoma/leukaemia —> Breast —> Lung —> GI —> Renal
Acquired cicatricial alopecia
Primary - chronic, progressive —> disfigurement
Generally symptomatic I.e. itching, burning, soreness, scaling, discharge
Look for related skin disease elsewhere
- skin
- nails
- oral mucosa
Examine scalp - Loss of follicular ostia ? Folliculitis ? Follicular plugging ? Broken hairs Pustules - folliculitis decalvans, LPP, DLE
Ix -
Extract hair from edge of bald patch for MCS
Swab pustule for MCS
Bx early lesions, several 4mm PBx
—> At least 1 from peripheral border/edge of clinically active area for horizontal section, H&E
—> 1 from peripheral border/edge of clinically active area for vertical section
—> +/- 1 from peripheral border/edge of clinically active area for DIF
—> +/- 1 from centre of bald patch ? loss of follicle/regrowth
—> +/- 1 for special stains
Mx - Reduce symptoms, slow/stop progression Camouflage - powders, sprays, wig Surgical correction (ideally for non-inflammatory or burnt out disorders in secondary cicatricial alopecia - - Scalp reduction - Hair transplant
Primary non-specific cicatricial alopecia
Idiopathic
Non-inflammatory
Irregular
Permanent
Slowly progressive
No distinguishing clinical/histo features
May be result from primary inflammatory cicatricial alopecia that have burnt out esp ? LPP —> look out for LP to other sites
Initial patch over crown, but may be anywhere on scalp
Tend to be oval lesions, several foci may coalesce
No erythema
Smooth shiny patches, slightly depressed
Small number irregularly twisted terminal hairs may persist within patch —> easily extracted
Variable, unpredictable course and prognosis
No effective Rx
Follicular lichen planus - lichen planopilaris
Commonest form of follicular LP
Progressive scarring alopecia of the scalp
Loss of function of hair follicle PPAR-gamma
Recent lesions = violaceous papules, erythema, scaling —> follicular plugs, scarring —> Follicular plugs shed —> white, smooth, atrophic surface, absent of follicular orifices
Active edge have horny plugs —> hair pull positive —> twisted anagen hairs
Punctate keratoses/follicular erythematous papules to following sites -
- Axilla
- Inguinal folds
- Limb flexures
- Sacrum
Dx = LP elsewhere + LP histology scalp lesions
Histo - Hypergranulosis Saw toothed rete ridges Perifollicular fibrosis, clefts DIF neg (pos in DLE)
Prognosis -
Slow vs rapidly extensive
Resolution of symptoms or absence of visible inflammation does not imply hair loss is arrested —> alopecia can still progress over many years
Mx/Rx —> no proven effective Rx to arrest disease progression -
Short course PO pred initially to stabilise disease
If active inflammatory changes present —> ILCS
Itch/pain relief + slightly inhibit process —> TCS I.e. clobetasol propionate shampoo/ointment daily
Systemic -
- HCQ (variable success)
- Acitretin (variable success)
- CSA (effective for skin LP, Graham-Little syndrome)
- Thalidomide
Follicular lichen planus - frontal fibrosing alopecia
Post menopausal women
Can be familial
? Assoc with DLE
? Environmental cause
Often symptomatic, but can have pain/itch
Cardinal feature = Recession of frontal hairline in a straight line
Sideburns commonly lost
(In contrast to AGA when frontal recession occurs bitemporally)
Early loss of eyebrows +/- body hair loss
Loss of follicular orifices
Perifollicular erythema
Hyperkeratosis
Small papules on cheeks, temples d/t involvement of vellus hair follicles
Natural Hx -
Slow progression over many years
Frontal hairline recession unpredictable
Mx/Rx —> no convincing evidence any Rx is effective - TCS ILCS Systemic - - Doxycycline - HCQ - Finasteride
