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ALOPECIA

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					HAIR DISORDERS



         GROUP 5
Objectives

 Describe the normal hair growth cycle
 Discuss the etiology, clinical features
  and management of androgenetic
  alopecia and alopecia areata.
 Discuss drug induced alopecia

 Discuss vitamins which are beneficial
  for healthy hair.
HAIR STRUCTURE

 Hair is composed of strong structural
  protein called keratin.
 This is the same kind of protein that
  makes up the nails and the outer layer
  of skin.
 Each strand of hair consists of 3
  layers.
Cont’d

   An innermost layer or medulla which is
    only present in large thick hairs.
   The middle layer known as the cortex.
    The cortex provides strength and both
    the color and the texture of hair.
   The outermost layer is known as the
    cuticle. The cuticle is thin and colorless
    and serves as a protector of the cortex.
STRUCTURE OF HAIR ROOT

   Below the surface of the skin is the hair
    root, which is enclosed within a hair
    follicle.
   At the base of the hair follicle is the
    dermal papilla.
   The dermal papilla is feed by the
    bloodstream which carries nourishment
    to produce new hair.
Cont’d

   The dermal papilla is a structure very
    important to hair growth because it
    contains receptors for male hormones and
    androgens.
   Androgens regulate hair growth and in
    scalp hair Androgens may cause the hair
    follicle to get progressively smaller and
    the hairs to become finer in individuals
    who are genetically predisposed to this
    type of hair loss.
THE HAIR GROWTH CYCLE

   Hair follicles grow in repeated cycles.
    One cycle can be broken down into
    three phases.
   Anagen - Growth Phase
   Catagen - Transitional phase
   Telogen - Resting Phase
   Each hair passes through the phases
    independent of the neighboring hairs.
ANAGEN PHASE – GROWTH
PHASE
   Approximately 85% of all hairs are in the
    growing phase at any one time.
   The growing phase of the normal hair
    growth cycle is responsible for producing
    new hair and for allowing the continued
    lengthening of that new hair.
   The Anagen phase or growth phase can
    vary from two to six years.
ANAGEN PHASE

   In this cycle hair is produced at the root
    and growth is maintained through the
    blood vessels, which feed the hair strand
    its nourishment.
   Hair grows approximately 10cm per year
    and any individual hair is unlikely to grow
    more than one meter long.
CATAGEN PHASE – TRASITIONAL
PHASE

   At the end of the Anagen phase the hairs
    enters into a Catagen phase which lasts
    about one or two weeks.
   During the Catagen phase the hair
    follicle shrinks to about 1/6 of the normal
    length.
    The lower part is destroyed and the
    dermal papilla breaks away to rest
    below.
TELOGEN PHASE – RESTING
PHASE
   The resting phase follows the catagen
    phase and normally lasts about 5-6
    weeks.
   During this time the hair does not grow
    but stays attached to the follicle while the
    dermal papilla stays in a resting phase
    below.
   Approximately 10-15 percent of all hairs
    are in this phase at any one time.
TELOGEN PHASE cont’d

   At the end of the Telogen phase the hair
    follicle re-enters the Anagen phase.
   The dermal papilla and the base of the
    follicle join together again and a new hair
    begins to form.
   If the old hair has not already been shed
    the new hair pushes the old one out and
    the growth cycle starts all over again.
   Each day anywhere from 50 to 100 hair
    strands are shed during the normal process
    of this phase.
   This is also the phase that is most
    associated with baldness.
    If a person is suffering from alopecia or hair
    loss they will first notice an abnormally high
    rate of shedding.
   At first this excessive hair loss will result in
    hair thinning but the end result could be
    baldness.
   Abnormal hair loss or shedding is defined as
    the loss of more than 150 hair strands each
    day for an extended period of time.
HAIR HEALTH

 Slow hair growth, brittle and/or
  damaged hair may be due to
  nutritional deficiencies.
 Certain vitamins and supplements can
  boost hair growth and encourage
  healthy hair.
   Vitamin B-complex - 50 mg. of the major B-
    vitamins (including folate, biotin and inositol)
   Vitamin B-6 - 50 mg.
   Vitamin C with bioflavonoids – 1-2 grams
    daily.
    Vitamin E - 400 to 800 IU daily.
   Beta-Carotene - 10,000 to 15,000 IU daily.
   One recommended daily dose of
    magnesium, sulfur, zinc.
   Flaxseed oil - one tbsp daily or one tablet.
ANDROGENETIC ALOPECIA

   A genetically determined, patterned,
    progressive loss of hair from the scalp.
   Hair loss is caused by androgen-
    mediated follicular miniaturization that
    leads to fine, short, non-pigmented,
    vellus hair formation.
   It affects both men and women at a
    similar prevalence of approximately
    40%.
 Men present with gradual thinning in
  the temporal areas, producing a
  characteristic M shape with gradual
  extension to the crown (vertex) area.
 Women usually present with diffuse
  thinning on the crown area while
  maintaining a frontal hairline.
AETIOLOGY

 The condition is generally considered
  to be a dominantly inherited disorder.
 In women, autosomal-dominant
  inheritance and a link to polycystic
  ovary syndrome have been found.
PATHOPHYSIOLOGY

   Androgenic alopecia is characterized by
    progressive shortening of the Anagen
    growth phase with each hair cycle
    associated with increased Telogen and
    catagen hair transformation.
   This process leads to follicular
    miniaturization with conversion of long,
    terminal hairs to short and fine vellus
    hairs.
CLINICAL FEATURES

 Progressive thinning of hair in women,
  over the frontal area, over a period of
  years.
 Progressively receding hairline in
  males.
 Thinning of hair on top of head in
  males.
MANAGEMENT

 In men –Topical Minoxidil or Oral
  Finasteride.
 In women - Topical Minoxidil or Anti-
  androgenic therapy with
  spironolactone or cyproterone.
TOPICAL MINOXIDIL

 Minoxidil is the currently preferred
  treatment for androgenetic alopecia
  and is topically administered as 2
  percent Minoxidil.
 Its also available in 5% formulations.
Cont’d

 The exact mechanism by which
  Minoxidil works is not known, but the
  treatment appears to affect the hair
  follicle in three ways.
 It increases the span of time follicles
  spend in Anagen, it rouses follicles
  that are in catagen and it enlarges the
  actual follicles.
Cont’d

 In effect, vellus hairs enlarge and are
  converted to terminal hairs, and
  shedding is reduced.
 Earlier, exogenous estrogen was used
  to treat androgenetic alopecia, but this
  treatment is used less often now,
  because of the efficacy of Minoxidil.
 Hypertrichosis may occur with use of
  Minoxidil.
FINASTERIDE

 Finasteride has been shown to be
  effective in men with alopecia.
 The agent should not be used in
  women of childbearing age, because
  5a-reductase inhibitors may cause
  abnormalities of the external genitalia
  in the male fetus.
Cont’d

   Additionally, Finasteride has not been
    shown to be useful in postmenopausal
    women with androgenetic alopecia.
 When hair loss is extensive, wigs may
  be worn.
 Hair transplantation, an accepted (but
  expensive) treatment for male balding,
  is increasingly being used in female
  hair loss.
ALOPECIA AREATA

 Alopecia areata (AA) is an
  autoimmune disease that affects
  almost 2% of the population.
 Inflammatory cells target the hair
  follicle, thus preventing hair growth.
 Typically, a small round patch of hair
  is noticed. This patchy hair loss may
  regrow spontaneously. (Patchy
  alopecia areata)
 In other cases there can be extensive
  hair loss - Alopecia totalis, indicating
  total loss of scalp hair
 In rare cases there is loss of all scalp
  and body hair (alopecia areata
  universalis).
ALOPECIA AREATA
ALOPECIA UNIVERSALIS
ALOPECIA AREATA
TOTALIS
AETIOLOGY

 The aetiology of AA has not been
  determined.
 However, it is hypothesized to be an
  organ-specific autoimmune disease
  mediated by T lymphocytes directed
  at hair follicles.
PATHOPHYSIOLOGY

 As in many other autoimmune
  diseases, there is a strong association
  of AA with human leukocyte antigen
  (HLA) class II alleles.
 There also appears to be a link
  between AA and Down’s syndrome
  suggesting that chromosome 21 may
  also be involved.
CLINICAL FEATURES

 Hair loss.
 Balding.

 Bald patches.

 Nails may have pitting or
  trachyonychia.
 Exclamation point hairs.
MANAGEMENT
Corticosteroids
   Corticosteroid therapies can include
    intralesional injections or topical
    application.
   Intralesional steroids are the first-line
    treatment in localized conditions.
   Hair growth may persist for 6-9 months
    after a single injection.
   Adverse effects mostly include pain
    during injection.
   Injections are administered every 4-6
    weeks.
TOPICAL STEROIDS

 Fluocinolone acetonide cream 0.2%
  (Synalar HP) twice per day.
 Betamethasone dipropionate cream
  0.05% (Diprosone).
   Treatment must be continued for a
    minimum of 3 months before regrowth
    can be expected, and maintenance
    therapy often is necessary.
TOPICAL
IMMUNOTHERAPY
 Topical immunotherapy is defined as
  the induction and periodic elicitation of
  an allergic contact dermatitis by
  topical application of potent contact
  allergens.
 Commonly used agents for
  immunotherapy include squaric acid
  dibutylester (SADBE) and
  diphencyprone (DPCP)
 Topical immunotherapy has been
  used for almost 20 years; no serious
  adverse effects have been reported.
 The most common side effect, which
  is desired, is a mild contact dermatitis
  (redness, scaling, itching).
 Both SADBE and DPCP appear to be
  equally effective.
 The mechanism of action of topical
  immunotherapy is unknown.
 Antigenic competition has been
  hypothesized. That is, the introduction
  of a second antigen can initiate a new
  infiltrate containing T-suppressor cells
  and suppressor macrophages that
  may modify the preexisting infiltrate
  and allow regrowth.
MINOXIDIL

 Minoxidil appears to be effective in the
  treatment of alopecia areata in
  patients with extensive disease (50-
  99% hair loss).
 The 5% solution appears to be more
  effective.
 No more than 25 drops are applied
  twice per day regardless of the extent
  of the affected area.
 Initial regrowth can be seen within 12
  weeks, but continued application is
  needed to achieve cosmetically
  acceptable regrowth.
 Minoxidil usually is well tolerated.
  Adverse effects include distant
  Hypertrichosis and irritation.
DRUG INDUCED ALOPECIA

 This may be partial or complete and
  can involve sites other than the scalp,
  although the scalp is commonly
  affected.
 Medications can lead to two types of
  hair loss: Telogen effluvium and
  Anagen effluvium.
TELOGEN EFFLUVIUM

 Telogen effluvium is the most
  common form of drug-induced hair
  loss.
 It usually appears within two to four
  months after taking the drug.
 This condition causes the hair follicles
  to go into their resting phase
  (Telogen) and fall out too early.
   People with Telogen effluvium usually
    shed between 100 and 150 hairs a
    day.
ANAGEN EFFLUVIUM

 Anagen effluvium is hair loss that
  occurs during the Anagen phase of
  the hair cycle, when the hairs are
  actively growing.
 It prevents the matrix cells, which
  produce new hairs, from dividing
  normally.
 This type of hair loss usually occurs
  within a few days to weeks after
  taking the medication.
 It's most common in people who are
  taking chemotherapy drugs and is
  often severe, causing people to lose
  most or all of the hair on their head,
  as well as their eyebrows, eyelashes,
  and other body hairs.
DRUGS CAUSING ALOPECIA

   Anticoagulants
   Anticonvulsants
   Antithyroid drugs
   Beta-blockers
   Withdrawal of oral contraceptives
   Cytotoxic drugs
   Gold salts
   Interferon's
   Lithium
   Retinoid
   Sodium valproate
PIGMENTATION
DISORDERS
  Hyperpigmentation


   Hypopigmentation
HYPERPIGMENTATION
o   Also known as Hypermelanosis

o    Due to an increased number of pigment
    cells (melanocytes) or from increased
    production of melanin.

o    Hormones that stimulate melanin
    synthesis, such as melanocyte-
    stimulating hormone (MSH), are
    frequently elevated.
TYPES
   Darker skin patches
   Post- inflammatory (trauma, burns, skin
    disease)
   Purpura
   Urticaria
   Melanoma
   Pigmented purpura
   Mastocytosis
   Chloasma (melasma)
   Freckles
Chloasma

   Also known as melasma – a blotchy,
    brownish pigmentation on the face
    that develops slowly and fades with
    time. The pigmentation is due to
    overproduction of melanin by the
    pigment cells, melanocytes.


   Often found in pregnant women
Causes
   Genetic predisposition to melasma.
   Pregnancy – the pigment often fades a
    few months after delivery.
   Hormonal contraceptives, including oral
    contraceptive pills and injected
    progesterone
   Sun exposure
   Scented or deodorant soaps, toiletries
    and cosmetics – a phototoxic reaction
   Unknown factors, when it arises in
    apparently healthy, normal, non-
    pregnant women
Clinical features

   Melasma usually affects women; only one in
    twenty affected individuals are male.
   Starts between the age of 30 and 40.
   Common in people that tan well or have
    naturally dark skin compared with those
    who have fair skin.
   Affects the forehead, cheeks and upper lips
    resulting in macules (freckle-like spots) and
    larger patches.
Clinical features

Type      Clinical features
Epidermal Well-defined border
          Dark brown color

          Appears more obvious under black light

          Responds well to treatment

Dermal    Ill-defined border

          Light brown color

          Unchanged under black light

          Responds poorly to treatment

Mixed     Combination of light and brown patches

          Partial improvement with treatment
MANAGEMENT

 Response to treatment very slow.
 Start gently – Sensitive skin. Harsh
  treatments may result in an irritant
  contact dermatitis, and this can result
  in postinflammatory pigmentation.
 Discontinuing hormonal contraception.

 Year-round sun protection.
 Use a broad-spectrum very high
  protection factor sunscreen of
  reflectant type and apply it to the
  whole face.
 E.g Aquasun SPF4 Lotion(Octyl
  methosycinnamate 3, butyl
  methoxydibenzoylmethane 1.5%, Zinc
  oxide 5%
 Titanium dioxide 3%).
 Alternatively, use a make-up
  containing sunscreen.
 Use   of a mild cleanser, and if the
  skin is dry, a light moisturiser.
 Preventing new pigment formation.
  Bleaching creams inhibit the
  formation of melanin by the
  melanocytes. They include:
    Hydroquinone 2-4%, for 2 to 4
     months. This sometimes causes
     stinging and redness.
    Azelaic acid can be used
     longterm, and is safe even in
     pregnancy. It may sting.
    Kojic acid
   Topical corticosteroid such as
    hydrocortisone works quickly to fade the
    colour and has an additional benefit of
    reducing the likelihood of a contact
    dermatitis caused by other agents.
   Hydrocortisone 0.5-2.5% (DermAid
    Cream/Soft Cream and Lotion-HC 1%)
   Peeling off the pigment.
      Salicylic acid creams
      Topical alpha hydroxyacids including
       glycolic acid and lactic acid, as
       creams or as repeated superficial
       chemical peels.
 Topical retinoids, such as tretinoin,
  works in several ways to improve
  skin color, but can be hard to
  tolerate and might cause dermatiits.
 Not to be used during pregnancy.

 Dermabrasion(is a cosmetic
  medical procedure in which the
  surface of the epidermis of the
  skin(the stratum corneum) is
  removed by abrasion (sanding).
 Microdermabrasion      (a cosmetic
  procedue in which the stratum corneum
  (dead outermost surface of the skin) is
  partially or completely removed by
  light abrasion, to remove sun-damaged
  skin and to remove or lessen scars and
  dark spots on the skin.
 damage to the melanocytes may
  increase pigment production and
  darken the melasma.
   Laser resurfacing – results may be
    unpredictable. Newer fractional lasers
    may prove safer.
   Destroying the pigment with pigment laser
    or intense pulsed light device – this is
    possibly the best treatment for a quick result
    but several treatments may be necessary.
   Applying cosmetic camouflage (make-up).
 Results take time and the above
  measures are rarely completely
  successful.
 About 30% of patients can achieve
  complete clearance with a prescription
  agent that contains a combination of
  hydroquinone, tretinoin and a topical
  corticosteroid.
   Unfortunately, even in those that get a
    good result from treatment,
    pigmentation may reappear on
    exposure to summer sun and/or
    because of hormonal factors.
HYPOPIGMENTATION

 Generalized reduction in pigmentation
  of the skin.
 It is caused by melanocyte depletion
  i.e. a decrease in the amino acid
  tyrosine, which is used by
  melanocytes to make melanin
 Localized hypopigmentation may be
  due to partial or complete loss of
  melanin
Types of hypopigmentation

   Albinism
   Bleaching creams
   Chemical leukoderma
   Leprosy
   Vitiligo
VITILIGO

   Vitiligo is an autoimmune disease in which
    pigment cells (melanocytes) are destroyed
    resulting in irregularly shaped white patches
    on the skin.
   Any part of the body may be affected but
    common sites are face, neck, eyes, nostrils,
    nipples, navel, genitalia), body folds
    (armpits, groin), sites of injury (cuts,
    scrapes, burns) and around pigmented
    moles
TYPES OF VITILIGO

 TypeA-include all cases of vitiligo not
  in type B. Can occur at any age.
 New depigmented patches continue to
  appear through out patients lives.
 Type B -depigment patches are
  confined to a defined dermatome in
  the same manner as herpes zoster
  virus.
 generally affect youngsters.
 activity ceased after one year
  following rapid spread over the
  dermatomal areas.
CAUSES

 Melanin is the pigment that
  determines the color of skin, hair, and
  eyes.
 It is produced in cells called
  melanocytes.
 If melanocytes cannot form melanin or
  if their number decreases, skin color
  will become progressively lighter.
 The cause of vitiligo is not known.
 It sometimes follows physical injury
  such as sunburn, or emotional stress.
 There are three theories on the cause
  of vitiligo:
 The pigment cells are injured by
  abnormally functioning nerve cells.
MANAGEMENT

 Topical steroid e.g. cortisol cream.
 Calciniurin inhibitors like topical
  pimecrolimus and tacrolimus.(safe
  and effective to use on face and neck
  where strong steroid cream can cause
  skin thinning).
 There may be an autoimmune
  reaction against the pigment cells (the
  body may destroy its own tissue,
  which it perceives as foreign).
 Autotoxic theory - the pigment cells
  are self-destructive.
 Narrowband UVB
  phototherapy(helpful particularly in
  combination with calcineurin
  inhibitors, and perhaps with
  calcipotriol cream
 PUVA- form of light treatment requires
  the patient to take a psoralen
  medicine and then be exposed to
  ultraviolet .
 Gradual but partial repigmentation
  may results light (UVA).
 When the treatment is stopped, some
  of the pigment disappears again.
 PUVA takes less than five minutes
  twice weekly, and is continued for up
  to two years.
 PUVA is unsuitable for children or
  very fair skinned people.
 Surgical treatment- Experimentally
  some centres are removing the top
  layer of skin by various techniques
  (including dermabrasion or
  sandpapering) and replacing it with
  skin with normal pigmentation from
  another site.
 Sun protection.
 Protection from injury.
DEPIGMENTATION
THERAPY
 If a dark skinned person has vitiligo
  affecting a large part of the exposed
  areas, he or she may wish to undergo
  depigmentation.
 A cream containing monobenzyl ether
  of hydroquinone is applied to the skin.
 This causes all the skin to lose its
  pigment. Its effect is usually
  permanent.
ALBINISM

   Hypopigmentary congenital disorder
    characterized by a partial (in
    hypomelanism, also known as
    hypomelanosis) or total (amelanism
    or amelanosis) lack of melanin
    pigment in the eyes, skin and hair (or
    more rarely the eyes alone).
   Albinism results from inheritance of
    recessive alleles.
CLINICAL FEATURES

 Nystagmus.
 Photophobia.

 reduced visual acuity.

 a lack of stereopsis.
MANAGEMENT

 No specific medical treatment is
  available.
 For occular ablinism, Refractive errors
  should be corrected, and some
  patients benefit from bifocal lenses.
 If visual acuity is severely impaired,
  these patients can be helped with
  telescopic and other low-vision
  devices.
   The most promising treatment for
    nystagmus is the eye muscle surgery
    that reduces the movement of the
    eyes but vision may not improve in all
    cases due to other associated eye
    abnormalities.
 For photophobia the eye doctors
  prescribe dark glasses that shield the
  eyes from bright light.
 ophthalmologists prefer to treat the
  infants at the age of six months before
  the function of their eyes has
  developed fully.
 They may recommend that parents
  patch one eye to promote the use of
  the non-preferred eye.
 It is vital that people with albinism use
  sunscreen when exposed to sunlight
  to prevent premature skin aging or
  skin cancer.
 Special UV-proof clothing and
  swimsuits are available and are a
  good alternative to excessive use of
  sunscreen.
REFERENCES

   http:\Alopecia Areata Treatment &
    Medication - eMedicine Dermatology.mht
   Http:\American Hair Loss Association - Drug
    Induced Hair Loss.htm
   Http:\[Drug-induced alopecia review of the
    literature] [Therapie_ 1995 Mar-Apr] -
    PubMed result.mht
   http://www.hairlossexpert.co.uk/WhatIsNor
    malCycleHairLossReGrowth.html
 http://bestpractice.bmj.com/best-
  practice/monograph/222/basics/classif
  ication.html
 http://www.dermnet.org.nz/hair-nails-
  sweat/female-pattern-hairloss.html
 Walker,R., CLINICAL PHARMACY
  AND THERAPEUTICS 4th Edition.
 AMH 2008
 http://www.medindia.net/patients/patie
  ntinfo/Albinism-Treatment.htm
 http://health.nytimes.com/health/guide
  s/disease/albinism/overview.html
 http://www.antivitiligo.com/

 http://www.medicinenet.com/vitiligo/art
  icle.htm
 http://health.hpathy.com/chloasma-
  melasma-symptoms-treatment-
  cure.asp
APPENDIX
DRUG                  PIGMENTATION
Amiodarone            Blue - grey
Anticonvulsants       Brown
Antimalarials         Blue - grey
Beta - blockers       Brown
Imatinib              Hypo/hyperpigmentation
Imipramine            Blue - grey
Methyldopa            Brown
Oral contraceptives   Brown spots/patches
Phenothiazines        Brown / blue - grey
Tetracyclines         Blue - black
Methoxsalen           Brown
HYPERTRICHOSIS
   Hypertrichosis is excessive hair growth over
    and above the normal for the age, sex and
    race of an individual (in contrast to
    hirsutism, which is excess hair growth in
    women).
   Hypertrichosis can develop all over the
    body or can be isolated to small patches.
   Hypertrichosis may be congenital (present
    at birth) or acquired (arises later in life).
   The causes mat be genetic, metabolic, or
    due to drugs.
QUESTIONS

   Describe the different phases of the hair
    growth cycle.
   Differentiate between alopecia areata and
    androgenetic alopecia.
   Which vitamins are good for hair?
   Give 3 examples of hyperpigmentation
    and hypopigmentation.
   Discuss the causes of Vitiligo and
    Chloasma.

				
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