DISORDERS OF HAIR

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DISORDERS OF HAIR By Dr. Sahar Ismail
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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.
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• 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).

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Hair cycle The cycle has mosaic pattern. The hair
does not grow continuously but each follicle
unsynchronized with the other follicles.
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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
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Alopecias
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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.

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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.
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• 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).

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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).
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Alopecia areata It is a common asymptomatic
disease characterized by rapid (sudden) onset of
hair loss with an initial circumscribed, totally
bald, smooth patch.
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• 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.

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• 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.

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• 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.

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Clinical types Alopecia localisata. Described
before. Alopecia totalis. Means total loss of
scalp hair Alopecia universalis. Means loss of
all body hair.
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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.
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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).
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• 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.

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• 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.

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• Treatment
• Topical minoxidil.
• Systemic fenestride
• Hair transplantation.

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• 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).

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• 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.

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DISORDERS OF SKIN COLOR
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• 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 persons race or color.
• The number and size of the melanosomes or pigment
  granules, continuously synthesized by these
  melanocytes determine differences in skin color.

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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 worlds population.
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Etiology The etiology is still unknown and the
suggested theories are 1- Inheritance.
2-Autoimmune hypothesis. 3- Neurogenic
hypothesis. 4- Self-destruct theory.
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• 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.

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• 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.

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• 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.

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DISORDERS OF NAILS
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• Disorders of nails
• Nail Bed disorders
• Changes in nail colour
• Anemic pallor
• Cyanosis
• Salmon patch, oil drop
• Onycholysis
• Splinter hemorrhage
• Subungual hyperkeratosis
• Periungual fibromas

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• Nail plate disorders
• Koilonychia
• Anonychia
• Pitting
• Nail plate thickening
• Median nail dystrophy
• Beaus lines
• Brittle nail
• Pigmentary disorders
• Longitudinal melanonychia
• Nail fold disorders
• Paronychia
• Ingrown nail

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Pseudomonas infection
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Cyanosis
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Psoriasis oil drop
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Onycholysis
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Psoriasis onycholysis
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Subungual hyperkeratosis
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Koilonychia
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Psoriasis pitting
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Onychomycosis
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Traumatic changes
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Beaus line Zinc deficiency
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Brittle nail
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Paronychia
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Eczema