Hair Loss

drug-induced alopecia

-A lot of drugs that can cause alopecia (drug induced) - ACE inhibitors/anticoagulants can cause hair loss, birth control, beta-blockers -Can change the medication

hirsutism etiology

-Where are the hormones coming from? Tumor, amenorrhea (no periods) -Can be drug induced, no known cause, ovarian problems/adrenal problems

pattern hair loss DDX

Diffuse nonscarring scalp alopecia Telogen defluvium Secondary syphilis SLE Fe deficiency Hypothyroidism Trichotillomania Seborrheic dermatitis

pattern hair loss male vs women

Hamilton classification for males Ludwig classification for women (thinning from the top and out) higher the value the worse the hair loss is

excessive hair growth

Hirsutism: occurs in women at sites where hair is under androgenic control (puberty hair growth sites) Hypertrichosis: hair density or length beyond accepted limits of normal age, race, and sex (can be normal in some cultures)

alopecia is classified into 2 types

Noncicatricial alopecia: non-scarring - no clinical signs of tissue destruction (hair can come back) cicatricial alopecia: scarring - evidence of tissue destruction (e.g., inflammation, atrophy, scarring; no hair growth again) ** allows distinguish between scarring and nonscarring alopecia

alopecia areata diagnostics

Serology •ANA to r/o SLE •RPR test to r/o 2/2 syphilis KOH prep to r/o tinea capitis Dermatopathology -Any hair loss - rule out lupus with ANA (anti-nuclear antibody test) -RPR: rapid plasma test -KOH prep - know how to do basic steps - know why they are doing it and the general steps of how to do it (hyperlink in lecture on blackboard)

Central centrifugal cicatricial alopecia (CCCA)

cicatricial alopecia •Aka "hot comb alopecia" •MC black women •Starts in crown/midvertex •Possible relation to chemical processing, heat, chronic tension on hair - educate pts on - Less chemicals/less heat to help with this

Pseudopelade of Brocq

cicatricial alopecia •End stage of all noninflammatory scarring alopecias •Discrete, smooth, skin/pink colored lesions •Irregularly shaped areas of alopecia •Early moth-eaten pattern (in early stage) •Eventual large patches of loss (footprints in the snow) -All scarring alopecia can progress to this or pt just has this -Irregularly shaped -Lead to a lot of scarring -Islands of hair surrounded by a sea of scalp (skin tufts) -Inflammation -Islands = hairs are tufted together

chronic cutaneous lupus erythematosus

cicatricial alopecia •Erythematous plaques •Discrete discoid lesions •Keratotic follicular plugs (carpet tacks) •Post-inflammatory hypopigmentation - hair loss area - red -Scarring and irritating with scaling on the ears

folliculitis decalvans

cicatricial alopecia •Hair loss 2/2 to pustular folliculitis •Surviving hairs cluster •Boggy or indurated scalp/beard w/ pustules, erosions, crusts, and scale •Staph aureus is common - Skin is boggy to touch = wet/spongy, soft give to it; erosions and crusts and scales of the folliculitis - different stages seen; folliculitis is most commonly caused by S. aureus

folliculitis keloidalis nuchae

cicatricial alopecia •MC black men •Occiput of scalp and nape of neck •Starts w/ chronic papular or pustular erosion •May lead to keloidal scarring -Nuchae - back of the neck -Won't see very often -Look like papular and pustulars - if doesn't heal well can lead to keloidal scarring - refer out

dissecting folliculitis

cicatricial alopecia •MC black men •Initial deep inflammatory nodules over occiput (occipital region - back of the head) •Progress to coalescing regions of boggy scalp •Staph aureus -nodular/keloidal -Boggy to touch, purulent material , sinus tracts; suspicious of S. aureus

Lichen planopilaris

cicatricial alopecia •MC middle-aged women •MC Parietal scalp •Perifollicular erythema (near follicles) +/- hyperkeratosis of the skin •Violaceous (purple) discoloration and scalp pain ••Scarring if prolonged

Alopecia Areata

noncicatricial alopecia - More unique and have distinguishing factors that makes it different than pattern hair loss •Localized loss of hair in round or oval areas •No apparent inflammation of the skin •Nonscarring w/ hair follicles intact •Hair can regrow (with remission) - May see exclamation mark hair - broken hair follicles look like exclamation marks (!)

telogen effluvium

noncicatricial alopecia shedding! •Transient increase in shedding of normal telogen hairs from resting scalp follicles •2/2 to accelerated shift of anagen into catagen and telogen phase •Results in increased daily hair loss (often > 150 hairs/day) •If severe, diffuse thinning of scalp - Telogen - end of hair cycle - can lose normally but more than normal - make noticeable hair loss and thinning of the scalp

pattern hair loss

noncicatricial alopecias - MC •Hair follicle is not permanently damaged (just loosing hair) •Spontaneous or treatment-induced regrowth is possible •Pattern hair loss is MC type of progressive balding •Aka: androgenetic alopecia (AGA), male-pattern baldness, common baldness (males). Hereditary thinning, female-pattern baldness (females). -More classic with males -(genetic predisposed) - spontaneous hair loss -Vertex of hair, crown of the head

effluvium or defluvium

shedding of hair

alopecia areata epidemiology

•**Onset: young adults < 25y/o; children more frequently - Young adults/children hair loss think AA!

pattern hair loss treatment

•**Oral finasteride (Propecia) 1mg qd for men •Topical minoxidil (Rogaine) 2% or 5% solution •Use of antiandrogens in women w/ AGA and elevated adrenal androgen levels (more to come in endocrine) •Hairpiece •Hair transplantation (answer isn't always medication!) -Propecia: not safe for women premetapause (child bearing women) - works! Can stop hair loss and bring back some hair - can help; inhibits 5alpha reductase inhibitor -Rogaine: better for females

pattern hair loss: epidemiology

•Age of onset: •Males: any time after puberty (male patterned baldness); often expressed in 40s •Females: later in life; approx. 40% occurs in 60s •Males > Females

Pseudofolliculitis Barbae** know

•Aka "razor bumps"* •MC black men that shave •Related to curved hair follicles •Any shaved area e.g. beard, scalp, pubic •Keloidal scarring -Any shaving areas you can get this -Has to do with the type of hair - get ingrown hairs that don't grow well (and under the skin) and papules form; forms keloidal scarring (bumps) where they shave - not a ton you can do with keloids if it progresses this far -C. Alopeica - does if beard area cannot grow over time - but in general no -Only in shaving area - long standing condition that can progress

alopecia areata clinical manifestation

•Alopecia is sharply defined •Normal-appearing skin •"Exclamation mark hairs" (see at the margins of the lesion) •Hair loss patches can be stable and often show spontaneous regrowth •Scattered, discrete areas of alopecia or confluent w/ total loss of scalp hair •AA effects the scalp MC •Any hair-bearing area is susceptible -picture: confluencing area on the top of head - Different types and could affect different hairs: scalp and eyebrows are gone

pattern hair loss: etiology

•Combination of androgenic effects and genetic predisposition -Autosomal dominant and/or polygenic -Inherited from either or both parents -Change in male hormones (androgenic effect) -If parents have it you could or couldn't loss hair

hirsutism treatment

•Cosmetic (if idiopathic) •Shaving, waxing, chemical •Laser epilation, electrolysis •Bleaching •Weight loss (if hormones) •Oral contraceptives (adding or removing them) •Endo consult (if hormone imbalance possible/adrenal gland tumor possible)

pattern hair loss pathogenesis

•Dihydrotestosterone → growth of prostate, terminal hair •In male pattern baldness, causes hair follicles to decrease in size •Testosterone → growth of axillary hair and pubic hair •5α-reductase (5α-R) converts testosterone to DHT •Type I 5α-R: sebaceous glands (face, scalp), chest/back •Type II 5α-R: scalp hair follicle, beard, chest, foreskin/scrotum -Why is it happening -Hormone involvement -DHT and testosterone; 5 alpha reductase coverts T to DHT - imbalance in these processes creates the male pattern baldness -DHT: grows body hair and enlarge the prostate; too much - acne, increase level more sensitive to the hormone DHT which decreases hair follicles - stop the process of 5alpha reductase to treat!! -Meds targets type 2 5alpah-R -Mostly in males from testosterone to DHT (but can happen in women too)

hypertrichosis

•Excessive hair growth (density, length) beyond accepted limits of normal for age, race, sex in areas that are not androgen sensitive •May be universal or localized •May consist of lanugo, vellus, or terminal hair -Could be one spot or all over -Thickened hair

hirsutism

•Excessive hair growth (women) in androgen-dependent hair patterns •2/2 to increased androgenic activity •Normally only postpubescent males have terminal hair in these sites -chest, increase hair in axillae regions -Sign of underlying potential issues

alopecia areata pathogenesis

•Follicular damage occurs in anagen followed by rapid transformation to catagen and telogen; then to dystrophic anagen status •Follicular stem cells are spared (so the hair can grow back) -Increase turnover in the hair stages and the hair stages start to fall out

pattern hair loss diagnosis

•History (family hx) •Pattern of alopecia •Family incidence of AGA •Skin bx may be necessary in some cases - Can do clinically most of the time

hirsutism pathogenesis

•In hyperandrogenic women, there is an increased percentage of androgens secreted directly by the ovaries

hirsutism clinical presentation

•New growth of terminal hair, especially on the face •Chest •Abdomen •Upper back •Shoulders •Signs of virilization (female that has more of a male pattern balding - signs of male characteristics - increase muscles in males, deeper voice, etc - save for endocrine) - not due to puberty -Areas where it is present on males than females

alopecia areata treatment

•No curative tx is available; efforts aimed at inflammatory infiltrate •Psychological support is important •Hair piece •Makeup applied to eyebrows; brow tattoos •Intralesional injection w/ triamcinolone acetonide 3-7mg/mL •For few and small lesions ( in the lesion - sterioid - may stop the inflammation and stop changes in antagen and telogen phases) •Systemic glucocorticoids* •Systemic cyclosporine* (immunosuppressant - can't be on forever) - don't know what causes it so we don't know how to treat it -Systemic steroids may help with the hair growth but can't be on forever -Can't be on either systemic drugs forever

alopecia areata DDX

•Nonscarring alopecia •White-patch tinea capitis •Trichotillomania (psychiatric hair pulling) •Early scarring alopecia •Pattern hair loss •2/2 syphilis (alopecia areolaris)

pattern hair loss course

•Progression of alopecia is usually very gradual •Over years to decades

hirsutism epidemiology

•Race: white > black > Asian •Prevalence: Survey of college-aged women: 25% had easily noticeable facial hair and 17% had periareolar hair

cicatricial alopecia diagnostics

•Scalp biopsy: 4mm punch biopsy including SQ tissue - Scalp biopsy if etiology is not clear - see what is going on under the surface; pseduofolliculitis - if hx is clear and cause is know then no you don't need this

pattern hair loss clinical manifestation

•Scalp skin is normal (not scarring, not red) •Hair in areas of pattern hair loss becomes finer in texture, shorter in length, and reduced diameter •In time, hair becomes vellus (hair on the rest of your body) and will atrophy - Picture = class 4 Hamilton - distribution of loss is: frontal loss, temporal loss, thinning of the vertex •Men usually exhibit patterned hair loss in the frontotemporal and vertex areas •Paradoxical excessive growth of secondary sexual hair e.g. axillae, pubic, chest, beard is possible (not always the case) •Women also lose scalp hair in male-pattern distribution •Hair loss is less pronounced and more diffuse typically Male patterned baldness - increase in chest hair or facial hair - could be hormonal imbalance - endocrine issue in women

hirsutism diagnostics

•Serum testosterone •Serum free testosterone and DHEA -Don't need to know right now - workup hormone is necessary though

alopecia areata course

•Spontaneous remission is common in patchy AA (no SLE or syphilis) •Poor prognosis if: onset in childhood, loss of body hair, nail involvement, atopy, family hx AA - hair may not come back •Recurrences are frequent (cyclical fashion is possible)

cicatricial alopecia treatment

•Topical high-potency and **intralesional glucocorticoids •E.g. triamcinolone •Improves sx and hair growth •Antibiotics if S. aureus is documented - Not many available: injectable high potent steroids

pattern hair loss diagnostics

•Trichogram will show an increase in the number of telogen hairs •Dermatopathology will show an abundance of telogen-state follicles, follicles of decreasing size, and eventually nearly complete atrophy •Hormone studies •In women w/ hair loss and evidence of increased androgens (irregular menstruation, infertility, hirsutism , severe cystic acne, virilization) determine the following: - Trichogram - pluck out hairs and look under the microscope and look at what stages the hair are in (telogen - 10% of hair and more than anagen then something is off) -Do hormone studies especially if: listed above -Hirsutism: hairy than they should be - hormone imbalance for potential underlying disease -Virilization: male sex hormones effect - increase clitoris

alopecia areata etiology

•Unknown - can happen at any age •Association w/ other autoimmune diseases •10-20% have familial hx of AA

cicatricial alopecia

**Scarring alopecia •Results from damage or destruction of hair follicle stem cells by: •Inflammatory processes •Infection •Other pathology e.g. surgical scar, primary or metastatic neoplasm •Scarring is irreversible** •Therapies are not effective (take ability to grow hair as stem cells are compromised) - Damage to hair follicle stem cells - no hair growth back