Hair shaft disorders

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Hair shaft disorders
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Hair shaft

• Contains three layermedula ,cortex,cuticle
• Diseases contain in 4 category
• 1)fracturestrichorexisnodusa,t.invagin
  ata,
• trichoshisis,trichoclasis
• 2)irregularitieslongtundal 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 )

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Pili torti
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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
• -etiologytraumatic hair care technique and
  malfunctioning hair dryer
• - treatment trimming the affected hair

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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

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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

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Trichorrehexis nodosa

• Commonest form of hair shaft abnormality
• The hair is brocken like two brushes merging to
  each other
• Three types1)proximalin patients after years
  of uncomplicated straightening of hair
• 2)distalacquired
  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.

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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

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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

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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.

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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
  African-Americans 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

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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 groups1) 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

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Psudo nit
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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 NdY AG
  laser and diod or alexandrite

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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

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• - 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

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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 .

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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.

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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

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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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• PCOFBS and lipid profile
• Adrenal causeDHEA-s
• Cushing24h cortisol
• Hypo TYRoidismTSH
• AcromegalyGH
• Late onset CAH17 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.

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Treatment

• Finasteride2.5-5 mg/day
• Spirinolacton50-200 mg/day
• CPA12.5 mg/day (10 days in the cycle)
• Metformin
• Flutamide500 mg/day