Hair and Nails Dan Flashcards
What are the causes of Pityriasis amiantacea?
what is treatment?
Psoriasis
seb derm
eczema
use strong keratolytics e.g. leave in coal tar and sal acid prep then topical steroids; diagnosis may become clear later
What are Terry’s nails?
What are the associations?
White nails with a narrow distal pink/red/brown band May or may not see the lunulae Assoc; Liver failure Renal failure CCF Diabetes Hyperthyroidism Malnutrition POEMS
T/F
FFA has been triggered by starting TNFα blockers
T
How long is anagen phase for scalp hairs?
2-6 years
How many scalp hairs are in anagen or telogen in the scalp?
90% in anagen
10% in telogen
small number in catagen - less than 1%
How quickly does scalp hair grow?
1cm per month
T/F
catagen phase is always about 2 weeks in all human hairs
T
No matter follicle type or site
How long does telogen phase last on scalp?
3 months
what is exogen?
end stage of telogen when new hair starts growing and telogen hair is shed from follice
which keratins are found in hair?
mainly keratin 1 and 2 almost 50/50 ratio
how many hairs are normally in a scalp follicular unit?
3-5 follicles connected to a single erector pili muscle
how much scalp hair is lost before thinning become evident in most cases?
over 50%
T/F
miniaturization is the process of terminal scalp hairs turning into vellus hairs mainly in pattern hair loss
T
what is kenogen?
when a telogen follicle has lost its club fibre (telogen hair) but not yet transitioned to anagen
T/F
type 1 5alpha reductase is found in the scalp, beard and chest hair follicles
F
type 2 5alpha reductase
converts testosterone to DHT which drives male AGA
what are the major DDs for diffuse hairloss?
PHL/AGA acute TE chronic TE diffuse AA (rare) diffuse anagen effluvium - nearly always drug or disease
T/F
AGA in prepubertal children who do not have precocious puberty/hyperandrogenism is rare and usually male pattern type
F
rare but usually female pattern type
what is grading system for MPHL?
Hamilton or Norwood systems
what is grading system for FPHL?
Sinclair or Ludwig systems
what is trichodynia?
scalp paraesthesia
often occurs in PHL esp FPHL in 20-30% of women
what is the Sinclair grading system of FPHL?
1 - normal
2 - widened central part line
3 - widened part + tanslucent border of central part line
4 - bald area along anterior of part line
5 - advanced hair loss
what are key trichoscopic and histo features of AGA?
Trichoscopy;
variable hair shaft thickness due to miniturization
Peripilar sign - brown halos around hair ostia
yellow dots (yellow ostia)
Histo;
reduced ratio of terminal:vellus hairs from over 8:1 (nomal) to
less than 4:1
+ some increase in telogen follicle count and fibrous streamers
what investigations should be done in PHL?
None routinely
If young women w/ not FHx or any other indication then do hormone screen
Consider TFTs, ferritin and zinc in all cases
sometimes B12, folate, VitD, ANA
If diagnosis unclear consider biopsy
What is treatment ladder for PHL
reassure and do nothing - eg if normal temporal loss; does not indicate increased risk of further PHL in men or women
treat dandruff/scalp disease and any reversible causes of hairloss or nutritional deficiency
advise sun protection if scalp visible
assess psychosocial impact and manage as necessary
camouflage - hair styles, wig, toppik thickener, scalp dye
topical - minoxidil 5%
oral - minoxidil, finasteride, dutastride (men only)
women - cOCP, spironolactone, CPA
surgical - excision, flap, scalp expander, follicular unit transplants
what are the associations of alopecia areata?
Nail changes Atopy inc eczema Hypothyroid (hashimotos) LS IBD Vitiligo Autoimmune polyendocrinopathy syndrome 1
what nail changes are seen in alopecia areata?
brittle nails onycholysis Beau's lines Onychomadesis Koilonychia Trachyonychia Pitting - fine, organized (stippled), in grid pattern
what are poor prognostic factors in alopecia areata?
POLE V Yellow Paediatric onset Ophiasis Long standing Extensive trichoscopy - vellus hairs, yellow dots
how long do nails take to grow?
fingernails 3mm/month
toenails 1mm/month
T/F
treating associated hypothyroidism will improve alopecia areata
F
usually not but worth checking for and treating anyway
what is treatment ladder for AA?
Must assess psychosocial impact - if very concerned may treat more aggressively
General;
- Reassurance - 50% resolve in 1 year so if seen early can reassure only
camouflage - hairstyle, wig, toppik, scalp dye
artificial eye lashes, eyeliner pencil, wear glasses to disguise loss
Topical
- potent TCS
- tacrolimus - alone or as topical steroid sparer
- minoxidil (esp less extensive cases)
- dithranol 1% + 2% sal acid in YSP; apply 30mins initially inc to 2 hrs
- DPCP immunotherapy (3rd line)
systemic
- oral minoxidil
- steroid; esp if widespread inv. pred 25-40mg daily until regrown and reduce over 6-8 wks
can use IV methyl pred or IM triamcinolone
- Cyclosporin
- simvastatin-ezetimibe (40/10mg); small JAAD study
physicial;
- ILCS - 2nd lne after topicals for small areas of AA; 2.5-5mg/ml; must wait at least 4 weeks before repeating, usually 6
- PUVA has been reported
Surgery - usually not indicated
how is DPCP performed?
explain process to pt; 50% response rate; slow to see effects
- pts should not touch scalp for 6 hrs after application
- must avoid sunlight as degrades DPCP
- CIs - pregnancy, blood dyscrazia, malignancy
- AEs - severe erutpion, dyspigmentation, caregiver sensitization
sensitize on scalp or upper inner arm w/ 2% DPCP in acetone on filter paper in Finn chamber for 48 hrs
wait 1 week before starting immunotherapy
some advocate treating half the scalp initially and add in other half when response confirmed
start w/ 0.001% in acetone
Titrate up conc weekly as tolerated to reach point of; erythema +scale and itch lasting 2-3 days after application
0.01, 0.025, 0.05, 0.1, 0.25, 0.5, 1.0, 2.0
start to see response by 12 weeks
stop if no response at 24 wks
when hair fully regrown taper off by reducing frequency of application
how many hairs are normally lost from the scalp each day?
50-100
T/F
75% of cases of telogen effluvium are idiopathic
F
30%
what are the causes of telogen effluvium?
Physiological shed - women post partum, newborns
physical illness - shed some time after trigger
high fever - eg dengue, malaria
severe infection
major surgery or GA
chronic illness - HIV, SLE, SCLE, dermatomyositis
endo - thyroid disease, chronic hyperparathyroidism
nutritional deficiency eg iron, zinc, or massive weight loss, anorexia nervosa, bulimia, crash dieting
Drugs - ABCD ROME
chronic (idiopathic) TE
what are drug causes of telogen effluvium?
ABCD ROME ACEi Beta blockers anti-coags anti-depressants Retinoids OCP or stopping long term OCP Minoxidil (initial shed), anti-Micorbials (isoniazid, indanivir) Epileptics - valproate, phenytoin, carbamazepine
what are features of chronic TE?
usually women
age 30-60
TE lasting over 6 months
up to 30% get trichodynia
Can be caused by any of the causes of TE esp drugs and chronic disease as trigger is ongoing
Idiopathic if no cause found after investigation - diagnosis of exclusion
In what condition do you typically see short hairs regrowing at frontal hairline and parting?
resolving telogen effluvium
T/F
hair pull test is negative in TE
False
usually highly positive
5-6 telogen hairs from each part of scalp as TE affects whole scalp
how many scalp hairs are in telogen in TE?
Over 20% is diagnostic
usually less than 50%
(normal is up to 10%)
what are trichoscopy features of TE?
Similar to PHL but affect whole scalp not just frontal and vertex
some miniaturization
peripilar sign
increased proportion of follicular units producing only 1-2 hairs
what is management of TE?
decide if acute or chronic (>6 months)
look for trigger in Hx +/- tests
assess for other cause of hair loss e.g. unmasked PHL
If isolated and acute w/ trigger reassure - resolves completely in 3-6 months
If chronic must investigate for triggers
can use topical or oral minoxidil
treat any scalp disease or other types of hairloss
camouflage usually not necessary as mainly an issue of shedding not thinning
T/F
hairs lost in alopecia areata are catagen hairs
F
dystrophic tapered anagen hairs
T/F
anagen effluvium usually causes more widespread hair loss than telogen effluvium
T
thinning and often body affected not just scalp
cf - TE usually noticed by shedding and not much thinning
what are causes of anagen effluvium?
Infection - tinea capitis, kerion - boil or abscess AI disease - pemphigus vulgaris Drugs; 3Cs and T-BAG; - Chemo - MTX, 5FU, Doxorubicin, Bleomycin - Colchicine - Cyclosporin - Thallium - Bismuth - Arsenic - Gold Radiation therapy Loose anagen syndrome
what is trichoscopy of chemo-induced hairloss/ anagen effluvium?
Black dots
Exclamation mark hairs
Monilethrx-like hairs
how is anagen effluvium managed?
Treat cause
camouflage
minoxidil
For chemo - sometimes scalp cooling during chemo Rx can reduce haiross; hair grows back 3-6 months after end of chemo in most cases. Sometimes straight hair grows back curly
What is age and sex distribution for trichotillomania?
more common in kids;
peak in young kids, 5-12, rarely in preschool age
2nd peak in adolesence and young adults - more likely to persist
F:M 4:1 in older kids and adults, but in preschool boys more common than girls
what are the associations of trichotillomania in children, adolescents and adults?
Children - habits eg. nail biting, thumb sucking, nose picking, learning difficulty, anxiety, iron deficiency
Adolescents - bullying, abuse, body image issues, anxiety or depression
Adults - anxiety disorder, depression, OCD, eating disorder, substance abuse
what are DSM IV diagnostic criteria for trichotilomania?
- recurrent pulling causing hairloss
- tension when resisting and increase immediately before hair pulling
- relief or please immediately after pulling hairs out
- not part of another mental health disorder
- interferes with normal social life or work etc
what is a hair growth window?
diagnostic technique used in trichotillomania
shave small patch of hair in site and rw in one week to see normal uniform regrowth
T/F
axillary hair is often involved in tricotillomania
F
Uncommon site
eyebrows and lashes common in children
body hair common in adults
what are clinical findings in trichotillomania?
ask about tension before pulling and gratification afterwards
ask about symptoms of associations dependent on age group - screen for anxiety, depression and suicidality in adolescents and adults and for bullying and sexual abuse in adolescents
may be vertex, temporal, frontal or occipital or non-scalp sites
often on side of dominant hand
can extend in centrifugal or linear pattern
may be secondary folliculitis
always ask about GI symptoms and hallitosis as some have trichophagia and can get bezoar (ball of hair in stomach)
Must assess impact on life
Trichoscopy -
broken hairs, hair powder, coiled hairs, split ends, flame hairs, V-sign, no major scalp/perifollicular changes
T/F
biopsy plays minimal role in investigation of trichotillomania
F
Most useful investigation
Features -
normal size and number of follicles
empty follicles with no inflammation
pigment casts - boken off hairs leave small dark bodies
some increase in telogen and end-catagen hairs
may be follicular plugging or trichomalacia (deep distortion and curling of hair bulb)
How is trichotillomania managed?
Dont lay blame
consider need for barium swallow etc if bezoar suspected
Consider need for psych rw if suicidal, major anxiety, depression etc and for paeds admission/ child protection if abuse suspected
need good Hx for causes to address
esp in kids worth checking diet and testing for iron studies
some kids just need to address causes of stress or discourage behaviour
may need to refer to psych; TCAs can work
SSRI may help but best if combined with behavioural therapy
relaxation techniques
hypnosis
T/F
pressure induced alopecia always resolves w/ time
F
not always
can be permanent or scarring loss
T/F
temporal triangular alopecia affects young adult men
F
May be present at birth or onset in childhood, in 1st decade
temporal hair lost and replaced by vellus hair
follicle numbers the same
persists lifelong
what is lipoedematous alopecia?
mainly affects women w/ dark skin
thick boggy area of hairloss at vertex
oedema and thickening of fat layer on path but no inflammation
follicles replaced by fibrous tracts
can be boggy scalp and path changes without hair loss
T/F
thyroid disease causes hair loss known as ‘glades in the wood’
F
this is secondary syphylis - describes patchy hairloss
which systemic disease cause hairloss?
all typically telogen effluvium type except pempigus vulgaris which causes anagen effluvium; SLE - also causes 'lupus hair' SCLE Dermatomyositis thyroid disease esp hypo secondary syphylis iron deficiency zinc deficiency malnutrition or crash dieting
what is lupus hair?
dry coarse hair w/ non-scarring alopecia in SLE
what scalp skin diseases can cause hairloss?
Tinea capitis esp kerion - can be scarring
psoriasis - can be scarring
thick seb derm
what are trichoscopy findings to tinea capitis?
comma hairs
corkscrew hairs - more tightly coiled comma hairs
black dots - esp endothrix
rare - morse code hairs
can combine w/ Woods lamp for UV-enhanced trichosocpy
what are biphasic types of alopecia?
Non-scarring types that can become scarring if continue for long time
E.g. AGA, AA, traction alopecia, pityriasis amiantacea
also alopecia due to psoriasis or tinea capitis
what are secondary causes of scarring alopecia?
Not primarily a scarring alopecia disease but causes follicle detruction
causes are trauma, sclerosing diseases, infection and malignancy;
E.g. skin cancer, deep burn, XRT, sarcoidoisis, radiation dermatitis, scleroderma, linear morphoea (eg en coupe de sabre), cicatricial pemphigoid (scalp affected in 10%), NLD, infections e.g. TB, tinea capitis
which scarring alopecias are lymphocytic and which are neutrophilic?
Lymphocytic: DLE LPP pseudopelade of Brocq CCCA (neuts too if infected pustular type) alopecia mucinosa
Neutrophilic:
FDC
Dissecting cellulitis
Mixed: acne keloidalis nuchae erosive pustular dermatosis inflammatory tinea capitis acne necrotica
what genetic or congenital disorders can cause scarring alopecias?
aplasia cutis epidermal naevus hair follicle hamartoma incontinentia pigmenti Goltz syndrome porokeratosis of Mibeli Icthyosis EB Conradi-Hunerman bullous porphyrias
what are major categories of causes of scarring alopecia?
Primary scarring alopecias
Biphasic alopecias
secondary causes of scarring alopecias; Trauma, sclerosing, infections, neoplasms
Genetic and congenital causes of scarring alopecia
what triggers erosive pustular dermatosis?
Surgery, cryotherapy, XRT, skin grafts on scalp most often in pts w/ existing advanced AGA
what are histo features of erosive pustular dermatosis
epidermal erosion
chronic lymphocytic infiltrate; often plasma cells
destruction of follicles often w/ surrounding fb granulomatous reaction
T/F
erosive pustular dermatosis is treated with potent steroids
T swab to exclude infection \+/- biopsy to exclude IEC sun protection potent TCS w/ slow taper over months then mod TCS for control
T/F
central centrifugal cicatricial alopecia is triggered by hair relaxers or hot combs
T
can be
but continues even after pt has stopped using these
what are clinical and histo features of CCCA?
chronic progressive scarring alopecia esp in black women
starts at crown or vertex and expands centrifugally and symmetrically - active inflammation at edge
can be some polytrichia tufts in central scarred area
can be infection and pustules at active edge
mild pruritus or tenderness
Histo
lymphocytic infiltrate
atrophy of follicle epithelium
concentric lamellar fibrosis of follicles (onion peel)
can be hair fragments and fb granulomatous reaction
How is CCCA treated?
stop using hot combs, relaxers etc
Potent TCS + Doxy 1st line
if pustules present start w/ 10 week course of rifampicin + clindamycin then Doxy and TCS
Can need long term Rx
what are the types of LPP?
Classic
FFA
Graham-little syndrome
T/F
LPP is the most common scarring alopecia
T
How many LPP pts have LP elsewhere?
50%
can be skin, nails, genital/mucosal
T/F
FFA has been triggered by starting ustekinumab
F
has been triggered by starting TNFalpha blockers
what are the associations of LPP?
autoimmune disease esp hypothyroidism
also reported; lupus, sjogrens, hep C
do FBC, ELFT, TFTs and ANA
