HAIR SHAFT DISORDERS
Hair shaft
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Contains three layer:medula ,cortex,cuticle
Diseases contain in 4 category:
1)fractures:trichorexisnodusa,t.invaginata,
trichoshisis,trichoclasis
2)irregularities:longtundal ridging
,grooving,pili bifurcati,monilitrix
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3)Twisting: pili torti ,woolly hair, trichonododsis,circle
hair
4)Extraneus matter attached to hair follicle
For examination of hair shaft abnormalities the best
site is the proximal 1-2 inches of the shaft under
microscope (with immersion oil or polarized light )
Pili torti
Increased hair fragility
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1)bubble hair:
- in young women a localized area of uneven fragile hair
- hair is straighter and stiffer than normal
-under microscope hair contains large,irregularly spaced
bubbles and hair fractures at the site of bubbles
-etiology:traumatic hair care technique and malfunctioning
hair dryer
- treatment: trimming the affected hair
Monilitrix(beaded hair)
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-AD inheritance
-normal hairs at birth but fibers replaced by short
broken, fragile hair within few months
-always in the scalp but sometimes eyebrow and
eye lash and nails have abnormality
-perifolicular erythema and folicular hyperkeratosis
Uniform nodes on the hair with abnormal hair
constrictions
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Pili Torti ;twisting of hair around its long axis and
flattening of hair.the hair has spangled appearance
No treatment but it may improve d during puberty
The acquired form is after anorexia nevrosa and oral
retinoid therapy
Trichorrehexis nodosa
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Commonest form of hair shaft abnormality
The hair is brocken like two brushes merging to each
other
Three types:1)proximal:in patients after years of
uncomplicated straightening of hair
2)distal:acquired progressive cutical
damage
3)circumscribed in scalp ,mustache or
beard
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The type 1 is almost always in black patients
Type 2 is always in blond hair and asians associated
with trichoptilosis, or longitudinal split ends known as
split ends
In type 3 which pruritus is a prominent symptom;
scratching and rubbing may be the cause.
Among such diseases are circumscribed
neurodermatitis,contact dermatitis, and atopic
dermatitis.
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The curly hair that may result from isotretinoin
therapy has been attributed to extensive
trichorrhexis nodosa.
Treatment is directed toward the avoidance of
trauma to the hair.
Hair abnormalities not associated with
hair fragility
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Acquired progressive kinking of hair:
acquired curling of scalp hair
Young men developing curly, fizzy and lusterless
hair in fronto parietal area or vertex with
subsequent progression to androgenetic alopecia
Loose anagen hair syndrome
Young girl with short blond hair which
seldom needs cutting
 Diffuse or patchy alopecia without any
increase in hair fragility
 Hairs can be easily pulled from the scalp
 Fault in configuration of inner root sheat
 Improve with aging
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Pilli multi gemini: multiple hair shafts arising from
one papilla almost in the beard area
Uncombable hair:
Wooly hair:
Hair color
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Melanocytes producing hair pigment are associated
with the hair matrix, and melanogenesis occurs only
during anagen. This cyclic melanin synthesis
distinguishes follicular melanogenesis from the
continuous melanogenesis of the epidermis.
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With age, cyclic melanocytic activity in the follicular
unit declines.
By 40 years of age most individuals show evidence
of graying.
Graying mechanism:
tyrosinase activity within
hair bulb,defective migration of melanocyte from
defective hair melanocyte reservoir in ors,damage
of reactive oxygen specis to DNA of melanocytes
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In gray hair (canities), melanogenic activity is
decreased as a result of fewer melanocytes and
melanosomes, as well as a gradual loss of
tyrosinase activity.
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Typically, white people start going gray in their
mid-30s, Asians in their late 30s, and AfricanAmericans in their mid-40s.
Half of all people have a significant amount of
gray hair by the time they turn 50.
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Graying of the scalp hair is genetically determined
and may start at any age.
begins at the temples then beard and the body
hair is the last
Premature whitening of scalp hair is usually caused
by vitiligo, sometimes without recognized, or
actually without, lesions of glabrous skin.
Early graying (before age 20 in white or before
age 30 in black persons) is usually familial;
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Blond hair may become green in the swimming pool
or may stain brown near the tar or crysarobin
Alternating red and brown color or whitening of
hair is seen in iron deficiency anemia it responds
completely to iron suppliments
Whitening of hair is seen in B12 deficiency and IFN
therapy and with chloroquin therapy
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Selenium sulfide shampoo make the hairs yellow
discoloration
HIV elongated eyelashes and eyebrow and
strengtening of the curled hair
Hair casts (pseudonits)
remnants of the inner root sheath.often occur in great
numbers and may mimic nits in the scalp.
, hair cast move freely along the shaft.
they are two groups:1) girls between 2 and 8 years of
age with diffuse involvement and no scalp disease,
2)and children and adults with psoriasis, lichen planus,
seborrheic dermatitis,or trichotillomania. .
• 0.025% tretinoin lotion effective. False hair casts may
occur as a result of hair spray or deodorant concretion
Psudo nit
Pseudofolliculitis barbae
, curve back hairs pierce the skin as ingrowing hairs.
results in inflammatory papules and pustules, which may scar .
is seen in more than 50% of black men, who must sometimes give up
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shaving to alleviate the disorder..
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White persons are uncommonly affected; however, it is more
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common in renal transplant recipients.
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Tenderness responds to mid-strength topical steroids.
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The use of clippers or chemical depilatories, glycolic acid lotion, and
adjunctive antibiotic therapy may be helpful.
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Benzoyl peroxide 5%/ clindamycin 1% gel has been shown
to be effective in double-blind evaluation.
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Laser hair removal with the long-pulse Nd:Y AG laser and diod or
alexandrite
Trichoptilosis
- split ends in the hair ( Trichoptilosis) common for dry
hair.
-occur when the protective layer of the hair, or cuticle,
becomes damaged.
- It is usually caused by frequent washing, excessive
dying, vigorous brushing, overuse of chemicals.
KETOCONAZOL SHAMPOO
- these weaken the hair, strip away the cuticle, and
make the middle layer, or cortex, unprotected, and,
consequently, lead to split ends and hair breakage.
 Unfortunately, it is impossible to mend broken hair.
The only way to get rid of split ends is to cut them
off
How to Prevent Split Ends
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not wash the hair with shampoo more than 2-3
times a week, as shampoo dries your hair out.
Do not brush wet hair. Hair is more vulnerable to
splitting when it is wet.
Instead of a round brush, use a flat paddle brush
with wide tooth for everyday styling.
, apply a leave-in conditioner for dry hair .
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Try to avoid hair dryers, straightening irons, hot curlers,
etc.
Make hair trimmed every 4-6 weeks to remove
damaged ends.
Never trim your with dull scissors. It may cause more
splits and damage healthy hair.
Wear a hat to protect your hair from the sun damage.
And finally, remember that dry hair is fragile hair!
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Drugs associated with hypertrichosis include
minoxidil, cyclosporine, phenitoin,
diazoxide,streptomycin, penicillamine,
corticosteroids, danazol,psoralens,
hexachlorobenzene, PUVA, topical
bimatoprost,topical steroids, and topical androgens.
hirsutism
Most medically significant hirsutism is related to the
PCO
-. In a study of 873 patients with medically
 significant hirsutism, pcos was present in 82%.
Idiopathic hirsutism was present in 4.7%, and
6.75% of the patients had elevated androgen
levels and hirsutism with normal ovulation.
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Ovarian causes include PCOS , and a variety of
ovarian tumors, both benign and malignant.
PCOS is defined by anovulation (fewer than nine
periods a year or periods longer than 40 days
apart) with clinical evidence of hyperandrogenism.
Ovarian cysts are not required for the diagnosis,
and laboratory and imaging
studies are not required to establish the diagnosis. l
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The pathogenesis of PCOS may relate to insulin
resistance with resultant elevated insulin levels
leading to ovaria overproduction ofandrogens.
Prevalence rates of PCOS for black and white
women in the US are 8.0% and 4.8%,
respectively
Evaluation
Most hirsutism is related to ethnic heritage or PCOS.
 HX: onset and progression,virilization, menstrual
and pregnancy history, and family /
 racial background.
 Physical examination may reveal signs of
Cushing's disease, hypothyroidism, or acromegaly.
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PCO:FBS and lipid profile
Adrenal cause:DHEA-s
Cushing:24h cortisol
Hypo TYRoidism:TSH
Acromegaly:GH
Late onset CAH:17 OH prog
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A prolactin level should be obtained in any patient
with galactorrhea, but is of limited value as a
routine screening test for patients with hirsutism
alone.
Treatment
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Finasteride:2.5-5 mg/day
Spirinolacton:50-200 mg/day
CPA:12.5 mg/day (10 days in the cycle)
Metformin
Flutamide:500 mg/day