Dr Jennifer Martinick shares this informative slide show to spread awareness about Hair Disorders.

1. Disorders of hair
Less
hair
Excessive hair

2. The
hair can be divided into three parts
(1) The bulb
A swelling at the base which originates
from the dermis
(2) The root
The hair lying beneath the skin surface
(3) The shaft
Which lies above the skin surface.

4.  In
cross-section,
(1) The medulla
An area in the core which contains loose
cells
and airspaces
(2) The cortex
Which contains densely packed keratin and
(3) The cuticle
Which is a single layer of cells arranged like
roof shingles.

5. Classification
Hairs
are classified into three main types
◦ Lanugo hair
◦ Vellus hair
◦ Terminal hair
Terminal
hairs convert to vellus hairs in male
pattern alopecia
Vellus hairs convert to terminal hairs in hirsutism.

6. Lanugo hair
 Fine long hair
covering the foetus
 Shed about 1
month before birth
unless born
prematurely.
 May reappear
sometimes in
severe malnutrition
and anorexia
nervosa.

7. Vellus hair
 Fine, short
unmedullated hair
covering much of
the body surface.
 They replace the
lanugo hair just
before birth.

8. Terminal hair
 Fully developed
 Long coarse
medullated hair in the
scalp or pubic regions.
 Their growth is
influenced by
circulating androgen
levels.

9. The hair cycle
Each
follicle passes through regular cycles of
growth and shedding.
There are three phases of follicular activity
◦ Anagen
 The active phase of hair production.
◦ Catagen
 A short phase of conversion from active growth to the
resting phase.
 Growth stops, and the end of the hair becomes clubshaped.
◦ Telogen
 A resting phase at the end of which the club hair is
shed.

11. The
duration of each of these stages varies
from region to region.
On the scalp it is said to contain an average of
100,000 hairs
◦ Anagen lasts for upto 5 years
◦ Catagen for about 2 weeks
◦ Telogen for about 3 months
As
many as 100 hairs may be shed from the
normal scalp every day as a normal
consequence of cycling.

13. Alopecia
 The
term alopecia means loss
of hair
 Alopecia has many causes and
patterns.
 One convenient division is into
◦ Localized
◦ Diffused
 It
is also important to decide if
the hair follicles are replaced by
scar tissue; if they have,
regrowth cannot occur.

14. CLASSIFICATION OF ALOPECIA
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Localised
Non-scarring
Tinea capitis
Alopecia areata
Androgenetic alopecia
Traumatic (trichotillomania, traction,
cosmetic)
Syphilis
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Scarring
Idiopathic
Developmental defects
Discoid lupus erythematosus
Herpes zoster
Pseudopelade
Tinea capitis/kerion
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Diffuse
Androgenetic alopecia
Telogen effluvium
Metabolic
Hypothyroidism
Hyperthyroidism
Hypopituitarism
Diabetes mellitus
HIV disease
Nutritional deficiency
Liver disease
Post-partum
Alopecia areata
Syphilis
Discoid lupus erythematosus
Radiotherapy
Folliculitis decalvans
Lichen planus pilaris

15. Localized alopecia
Alopecia areata

16. Etiology
 An
immunological basis is suspected because of an
association with
◦
◦
◦
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Autoimmune thyroid disease
Pernicious anemia
Vitiligo
Atopy
 Histologically,
T lymphocytes cluster like a swarm of
bees around affected hair bulbs because cytokines
produced by the dermal papillae in lesions not only
attract lymphocytes to perifollicular region but also
stimulate them to multiply

17.  Alopecia
areata is probably inherited as a
complex genetic trait
 Sometimes
HLA-DQ3, -DR11 or -DR4 act as
susceptibility factors
◦ With an increased occurrence in the first-degree
relatives of affected subjects and twin concordance.
 It
affects some 10% of patients with Down’s
syndrome, suggesting the involvement of genes
on chromosome 21.
 Environmental
factors as well as emotional
factors may trigger alopecia areata in the
genetically predisposed.

18. Epidemiology
AA
is the common type
Both gender affected
Can start at any age

19. Presentation
A
typical patch of hair loss area is uninflamed,
with no scaling, but with empty hair follicles
 Pathognomonic
‘exclamation-mark’ hairs may be
seen around the edge of enlarging areas.
 They
 Are
are broken off about 4 mm from the scalp
narrowed and less pigmented proximally

20. Incidence
is most common in
the scalp and beard but
other areas, especially the
eyelashes and eyebrows, can
be affected too.
An
uncommon diffuse
pattern is recognized, with
exclamation-mark hairs
scattered widely over a
diffusely thinned scalp.
Up
to 50% of patients show
fine pitting or wrinkling of
the nails.

21. The characteristic uninflamed patches of
alopecia areata.

22. Exclamation-mark hairs: Pathognomonic of
alopecia areata.

24. Course
 The
outcome is unpredictable.
 In a first attack, regrowth is usual within a few
months.
 New hairs appear in the centre of patches as fine
pale down, and gradually regain their normal colour
 The new hair may remain white in older patients.
 Fifty percent of cases resolve spontaneously
without treatment within 1 year
 Only 10% have severe chronic disease
 Subsequent episodes tend to be more extensive
 Regrowth is slower.

25.  Hair
loss in some areas may coexist with regrowth
in others.
A
few of those who go on to have chronic disease
loose all the hair from their heads (alopecia
totalis) or from the whole skin surface (alopecia
universalis).
 other variant is ophiasis which is lose of hair in a
band like patternat the periphery of scalp
 Regrowth
is tiresomely erratic but the following
suggest a poor prognosis:
1. Onset before puberty
2. Association with Atopy or Down’s
syndrome
3. Unusually widespread alopecia and
4. Involvement of the scalp margin
type)
(ophiasiform

26. Alopecia totalis
Alopecia universalis

27. Differential diagnosis
Ringworm
infection
Lupus erythematosus
Lichen planus
Hair-pulling habit of children
Traction alopecia
Secondary
Pseudopelade

28. Investigations
None
are usually needed.
The
histology of bald skin shows
lymphocytes around and in the hair matrix.
Syphilis
can be excluded with serological
tests
Organ-specific
autoantibody screens

29. Treatment
A
patient with a first or minor attack can be
reassured about the prospects for regrowth.
Topical corticosteroid creams of high potency
can be prescribed
The use of systemic steroids should be avoided
in most cases
Intradermal injection of 0.2 ml intralesional
triamcinolone acetonide (5–10 mg/ml), raising a
small bleb within an affected patch, leads to
localized tufts of regrowth.
 Side effects dermal atrophy evident as
depressed areas at the sites of injections.

30. Regrowth within a patch of alopecia areata after
a triamcinolone injection.

31. Ultraviolet
radiation or even psoralen
with ultraviolet A (PUVA) therapy may
help in extensive cases, but hair fall often
returns when treatment is stopped.
Contact sensitizers (e.g. diphencyprone)
seemed promising but the long-term
effect of persistent antigen stimulation is
worrying; they are still being used only in
a few centres under trial conditions.
Wigs are necessary for extensive cases.

32. A trial of diphencyprone to one side of the scalp
caused some regrowth

33. Androgenetic alopecia (malepattern baldness)
Cause
It
is because of miniaturization of hair follicles
Although
clearly familial, the exact mode of
inheritance has not yet been clarified.
Male-pattern
In
baldness is androgen dependent
females, androgenetic alopecia (female-pattern
hair loss), with circulating levels of androgen within
normal limits, is seen only in those who are strongly
predisposed genetically.

34. Presentation
The
common pattern in men is the loss
of hair first from the temples, and then
from the crown
However,
in women the hair loss may be
much more diffuse, particularly over the
crown
In
bald areas, terminal hairs are replaced
by finer vellus ones.

35. Androgenetic alopecia beginning in the frontal
area

38. Complications
Anxiety
Bald
scalps burn easily in the sun
It has been suggested recently that bald
men are more likely to have a heart
attack and prostate cancer than those
with a full head of hair

39. Differential diagnosis
The
diagnosis is usually obvious in men, but
other causes of diffuse hair loss have to be
considered in women

41. Treatment
 Scalp
surgery
 Hair transplants
 Wigs
 Topical application of minoxidil lotion may slow early hair
loss and even stimulate new growth of hair but the results
are not dramatic
◦ Small and recently acquired patches respond best.
◦ When minoxidil treatment stops, the new hairs fall out
after about 3 months.
 Antiandrogens help some women with the diffuse type of
androgenetic alopecia.

42. Treatment
 Finasteride
(Propecia), an inhibitor of human type
II 5α-reductase, reduces serum and scalp skin
levels of dihydrotestosterone in balding men and
at the dosage of 1 mg/day, it may increase hair
counts
◦ Lead to a noticeable improvement in both frontal and
vertex hair thinning.
◦ However, the beneficial effects slowly reverse once
treatment has stopped.
◦ This treatment is not indicated in women or children.
 Side-effects
are rare, but include
◦ Decreased libido, erectile dysfunction and altered
prostate-specific antigen levels

43. Telogen effluvium
All
the hair follicle are not synchronous
in their cycle
If anagen phase of several adjoining hair
follicles is aborted and these follicles
enter telogen phase at the same time and
several hair are shed simultaneously this
is called telogen effluvium

44. Etiology:
Infections:
typhoid, malaria, dengue
Childbirth:prolonged
Surgical trauma
Haemorrhage
Emotional stress

45. Clinical
features: hair loss occurs after 23mths after the precipitating factor
Severe cases associated with anemia and
beau’s lines of the nails.
Treatment: stops spontaneously after23mths

46. Excessive hair
Hypertrichosis
Hirsutism

47. Hirsutism and hypertrichosis
Hirsutism
is the growth of terminal hair in a
woman which is distributed in a pattern
normally seen in a man (for example,
mustache, beard, central chest, shoulders,
lower abdomen, back, and inner thighs).
Hypertrichosis
is an excessive growth of
terminal hair in either sex that does not
follow an androgen-induced pattern

48. Types of hypertrichosis
Congenital
Hypertrichosis is very rare.
◦ A fetus is covered with lanugo and it does not fall
off but continues to grow.
Acquired
Hypertrichosis
◦ Occurs after birth.
◦ Unpigmented vellus hair or pigmented terminal
hair.
◦ The excessive hair may cover the entire body
(Generalized), or it could be localized to one
area.

49. Congenital
Localized forms:
Hypertrichosis cubiti (Congenital hairs
on elbows)
Hairy pinna (Congenital hairs on the
external ears)

50. Acquired hypertrichosis

51. Causes of hypertrichosis
Localized
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Melanocytic naevi
Becker’s naevi
Satyr’s tuft in sacral area- in patients with spina bifida
Chronically inflamed joints
Under plaster casts
Carrying weights over shoulder

52. Causes of hypertrichosis
Generalized

Anorexia nervosa, starving, malnutrition

Drug induced- minoxidil, diazoxide, ciclosporin
anabolic steroids.

porphyrias

Fetal alcohol syndrome

Fetal phenytoin syndrome

Hypertrichosis lanuginosa(congenital or acpuired)

General systemic illness (such as advanced HIV infection)

Hypothyroidism or other endocrine disorders

53. Hirsutism
Cause
Increased level of androgens or an oversensitivity of hair follicles to androgens

Racial or familial trait (Mediterranean, Caucasians and Asians)

Idiopathic hirsutism

Hormonal:

Polycystic Ovarian Syndrome

Cushing's disease

Tumors in the ovaries or adrenal gland

Congenital adrenal hyperplasia

postmenopausal women

Itragenic:

Drugs- androgens or progesterones, anabolic steroids.

55. Presentation
An
in
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excessive growth of hair
Beard area and side burn
Chest
Shoulder-tips
Around the nipples
Abdomen
Male pattern of pubic hair
Androgenetic alopecia
Signs
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of virilization
Temporal hair recession
Acne
Deep voice, increased size of Adam's apple
Oily perspiration
Breast atrophy
Muscle hypertrophy
Loss of female body contour

58. Investigations
 Significant
hormonal abnormalities are not usually found in
patients with a normal menstrual cycle.
 Investigations
◦
◦
◦
◦
are needed if:
Hirsutism occurs in childhood
There are features of virilization
Hirsutism is of sudden or recent onset
There is menstrual irregularity or cessation

59. The tests sent are
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Total and free testosterone
Sex hormone binding globulin
Free androgen index
Dihydroxyepiandrosterone sulfate
Androstenedione (drawn after 10 a.m.)
If there is also menstrual disorder, additional tests may be requested.
◦ Luteinizing hormone (LH) and follicle stimulating hormone (FSH)
◦ Oestradiol, 17-hydroxy progesterone
◦ Prolactin
Tests may be requested to evaluate other related aspects of health, for
example:
◦ Thyroid function
◦ Cortisol or overnight dexamethasone test
◦ Glucose
◦ Lipids (cholesterol and triglyceride)
Pelvic ultrasounds

60. Treatment
 Treat
underlying disorder
 Home remedies for minor hirsutism include
commercial, waxing or shaving, or making its
appearance less obvious by bleaching
 Plucking should be avoided as it can stimulate hair
roots into Anagen.
 The abnormally active follicles can be destroyed by
electrolysis.
 If numerous, by laser
 Topical therapy with eflornithine, an inhibitor of
ornithine decarboxylase, can slow regrowth.

61. Oral
antiandrogens
◦ Oral contraceptive pills with oestrogen and
cyproterone- antiandrogenic activity
◦ Cyproterone acetate 50-200 mg for 10 days
each cycle
◦ Spironolactone 50-200 mg daily can slowly
reduce excessive hair growth-long term.
Pregnancy
must be avoided during such
treatment as it carries the risk of feminizing
a male fetus.