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Hair nail and colour - hind.cc

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					DISORDERS OF HAIR
         By
   Dr. Sahar Ismail
   Hair has no vital function in humans,
yet its psychological functions are
extremely important. Hair is present all
over the body except the palms, soles,
glans and prepuce.
Types of hair:
Lanugo hair: (prenatal) Fine hair, usually shed in
utero.
Vellus hair: (postnatal) Similar to lanugo hair,
seldom exceeds 2 cm in length.
Terminal hair: Long, coarse and pigmented.
Androgen dependent hair:
 Pubic and axillary hair in both sexes.
 Facial, trunk and extremities in males only.
The average scalp hair is about 100,000 hair and
the average number of hair shed is 25-100/day.
Scalp hair growth is about 0.35 mm/day (1 cm
/month).
  Hair cycle
The cycle has mosaic pattern. The hair does not
grow continuously but each follicle unsynchronized
with the other follicles.
  Stages of the hair cycle
1- Anagen (growth stage)
   duration 2-6 years (3 years)   ± 85-90% of hairs

2- Catagen (involution stage)
   duration 1-2 weeks             ±1% of hairs

3- Telogen (resting stage)
   duration about 3 months        ±10-15% of hairs
Alopecias
   Alopecia means loss of hair. It may be cicatricial
or non-cicatricial.

A- Cicatricial alopecia
It results from destruction of hair follicles by scar
tissue formed in the scalp.
Clinical picture
•Presence of scarring.
•Evidence of the disease or condition which caused
scarring may be present.
•Cicatricial alopecia is a permanent condition and
re-growth of hairs in the affected area is not
expected.
   Causes:
   A-Congenital: A scarred area in which hair follicles are
destroyed is present at birth due to a developmental defect.
   B- Acquired:
   1. Trauma - Mechanical,
              - Thermal (e.g. burns).
              - Physical (e.g. radiodermatitis).
   2. Infection:- Pyogenic (abscess).
                - Fungal (kerion, favus).
                - Bacillary (lupus vulgaris).
               - Spirochaetal (gumma).
   3. Collagen diseases
              - Discoid lupus erythematosus of the scalp.
              - Scleroderma (morphea).
   4. Diseases of unknown etiology
              - Pseudopelade.
              - Folliculitis decalvans.
B- Non-Cicatricial alopecia
A. Congenital
 Congenital atrichia. Due to failure of development
of hair follicles.
 Congenital hypotrichia. The hair follicles are poorly
developed.
B. Acquired
1- Circumscribed
 Alopecia areata.
 Infections e.g. tinea capitis, secondary syphilis
                    (moth eaten alopecia).
 Traumatic (trichotillomania).
2- Diffuse:
1-Telogen effluvium (stress induced).
2-Anagen effluvium. (affects only anagen hairs and seen
following treatment with cancer chemotherapeutics; the
process is entirely reversible).
3-Androgenetic alopecia.
4-Endocrinal (hypo-pituitarism, hypothyroidism and hyper-
thyroidism).
5-Drugs (thyroid antagonists, anticoagulants, arsenic,
thallium salts).
6-Nutritional and metabolic disorders (deficiency of iron, zinc
or protein).
7-Severe chronic illness (malignancy, liver disease, kidney
disease).
        Alopecia areata:
   It is a common asymptomatic disease
characterized by rapid (sudden) onset of
hair loss with an initial circumscribed,
totally bald, smooth patch.
  Etiology:
    The etiology is unknown, but many factors
appear to have a role:
• Genetic factors: Positive family history in
about 20%.
• Immunological factors: Autoimmune theory
is supported by the association with other
autoimmune diseases.
• Emotional stress: May be a precipitating
factor.
Clinical picture:

Occurs mostly in patients below 40 years age.
Both sexes are equally affected.
Usually on the scalp (60%), beard area,
eyebrows, eyelashes, and less commonly, on
other hairy areas of the body.
The course of the disease is unpredictable.
There is a tendency to complete re-growth (4-6
months up to 2 years) especially the localized
type, but some cases never recover.
It is characterized by rapid and complete loss of hair in
one or more circumscribed, round or oval patches.
The size of the patch may vary from 1 to 5 cm in
diameter.
Exclamation mark hairs “thin proximally and thick distally
and can be easily pulled-out” may be present around the
patch indicating progression of the disease.
Clinical types
Alopecia localisata. Described before.
Alopecia totalis. Means total loss of scalp hair
Alopecia universalis. Means loss of all body hair.
Treatment
Psychological assurance is needed.
1- Topical treatment
a- Topical steroids.
b- Local irritants e.g. dithranol, phenol.
c- Minoxidil 5% “Regaine”.
d- Topical immunotherapy e.g.
   dinitrochlorobenzene (DNCB).
e- Topical cyclosporine.
2- Intra-cutaneous injection of steroids
3- Systemic treatment
 a- Systemic steroids, can lead to hair growth
   but hair may be lost when the treatment is
   stopped.
b- Systemic cyclosporine.
c- Photochemotherapy (PUVA).
        Androgenetic alopecia
  (Male-pattern alopecia Common baldness)

Androgenetic alopecia is a physiological process in
a genetically predisposed individuals.
Etiology:
It is unknown. The factors suggested are:
•Genetic predisposition.
•Androgen stimulation of susceptible hair follicles.
Clinical picture:
The essential clinical feature of androgenetic
alopecia in both sexes is the replacement of
terminal hairs by the finer vellus hairs.
This process may begin at any age after
puberty.
In males, loss of hair, occurs chiefly from the
fronto-temporal and vertex regions.
In females, diffuse alopecia is the main
presentation with no recession to the anterior
hairline as in males.
  Treatment:

- Topical minoxidil.
- Systemic fenestride
- Hair transplantation.
Telogen effluvium

Following stress conditions many anagen hair
follicles enter prematurely into telogen with
excessive loss of normal hairs.

    Causes
-   Labour
-   Acute blood loss and surgical operations
-   High fever
-   Emotional stress
-   Crash diet (inadequate protein diet).
  Clinical picture

Diffuse shedding of hair occurs 1.5 to 4 months
after exposure to stressful event.
All the shed hairs are in the telogen phase.
 Usually no more than 50% of the hairs are
affected.
The prognosis is good as complete re-growth
of hairs occur in about 6 months.
DISORDERS OF SKIN COLOR
 The  melanocyte is the pigment-producing cell
of the epidermis.
It is derived from the neural crest.
The melanocyte is a dendritic cell and resides
in the basal cell layer.
The number of melanocytes in the epidermis
is the same, regardless of the person’s race or
color.
The number and size of the melanosomes or
pigment granules, continuously synthesized by
these melanocytes determine differences in
skin color.
Vitiligo
 It is an acquired loss of pigment of the skin.
Vitiligo usually begins in childhood and affects
both sexes. It occurs in about 1 % of the
world’s population.
Etiology
The etiology is still unknown and the suggested
theories are:
1- Inheritance.
2-Autoimmune hypothesis.
3- Neurogenic hypothesis.
4- Self-destruct theory.
Clinical picture
The disease is manifested by de-pigmented
white patches surrounded by a normal or a hyper-
pigmented border.
The hairs in the vitiliginous areas usually
become white also.
The lesions are found particularly in areas that
are normally hyperpigmented e.g. the face,
axillae, groins, areolae and genetalia in addition to
areas subjected to repeated friction and trauma
e.g. the dorsa of hands, feet, elbows and knees.
Vitiligo may involve the entire body surface.
Differential Diagnosis:
Partial albinism. The lesions are present at
birth and remain unchanged throughout life,
and usually confined to the head and trunk.

Hypopigmentation:
  Pityriasis alba,
  Pityriasis versicolor
  Leprosy.
Treatment
 The treatment of vitiligo is generally
unsatisfactory.
The use of cosmetic camouflage for the lesions
on the exposed skin.
Potent topical corticosteroids.
PUVA therapy or narrow-band UVB.
The use of grafting techniques e.g. minigrafts.
Laser for limited cases.
DISORDERS OF NAILS
Disorders of nails:
Nail Bed disorders:
  Changes in nail colour
    •Anemic pallor
    •Cyanosis
    •Salmon patch, oil drop
  Onycholysis
  Splinter hemorrhage
  Subungual hyperkeratosis
  Periungual fibromas
Nail plate disorders:
  Koilonychia
  Anonychia
  Pitting
  Nail plate thickening
  Median nail dystrophy
  Beau’s lines
  Brittle nail
Pigmentary disorders:
  Longitudinal melanonychia
Nail fold disorders:
  Paronychia
  Ingrown nail
Pseudomonas
infection
Cyanosis
Psoriasis;
oil drop
Onycholysis
Psoriasis;
onycholysis
Subungual
hyperkeratosis
Koilonychia
Psoriasis;
pitting
Onychomycosis
Traumatic changes
Beau’s line;
Zinc deficiency
Brittle nail
Paronychia
Eczema

				
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posted:7/26/2011
language:English
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