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 club-shaped.
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
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
Localised
Non-scarring
Tinea capitis
Alopecia areata
Androgenetic alopecia
Traumatic (trichotillomania, traction, cosmetic)
Syphilis
Scarring
Idiopathic
Developmental defects
Discoid lupus erythematosus
Herpes zoster
Pseudopelade
Tinea capitis/kerion

15. Localized alopecia
Alopecia areata

16. Etiology
An immunological basis is suspected because of an association with
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 broken off about 4 mm from the scalp
Are 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 (ophiasiform type)

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 (male-pattern 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 baldness is androgen dependent
In 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 2- 3mths after the precipitating factor
Severe cases associated with anemia and beau’s lines of the nails.
Treatment: stops spontaneously after2- 3mths

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
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 excessive growth of hair in Signs of virilization
Beard area and side burn
Chest
Shoulder-tips
Around the nipples
Abdomen
Male pattern of pubic hair
Androgenetic alopecia
Signs 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
Clitoral enlargement

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 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 mg for 10 days each cycle
Spironolactone 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.