HAIR SHAFT DISORDERSBy:Dr Neda Adibidermatologist

Hair shaft

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

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 )

Increased hair fragility

• 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)

• -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

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

• 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

• 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

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

Pilli multi gemini: multiple hair shafts arising from one papilla almost in the beard area

Uncombable hair: Wooly hair:

Hair color

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.

• 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

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.

Typically, white people start going gray in their mid-30s, Asians in their late 30s, and African-Americans in their mid-40s.

Half of all people have a significant amount of gray hair by the time they turn 50.

• 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;

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

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

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• shaving to alleviate the disorder..• White persons are uncommonly affected; however, it is more• common in renal transplant recipients. • Tenderness responds to mid-strength topical steroids. • The use of clippers or chemical depilatories, glycolic acid

lotion, and adjunctive antibiotic therapy may be helpful.• Benzoyl peroxide 5%/ clindamycin 1% gel has

been shown to be effective in double-blind evaluation.• 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

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 .

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!

 

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.

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

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 ofCushing's disease, hypothyroidism, or

acromegaly.

PCO:FBS and lipid profile Adrenal cause:DHEA-s Cushing:24h cortisol Hypo TYRoidism:TSH Acromegaly:GH Late onset CAH:17 OH prog

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

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