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Disorders of hair

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  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.

  3. 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.

  4. 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.

  5. 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.

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

  7. Terminalhair • Fully developed • Long coarse medullated hair in the scalp or pubic regions. • Their growth is influenced by circulating androgen levels.

  8. 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.

  9. 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.

  10. 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.

  11. CLASSIFICATION OF ALOPECIA • Localised • Non-scarring • Tineacapitis • Alopecia areata • Androgenetic alopecia • Traumatic (trichotillomania, traction, cosmetic) • Syphilis • Scarring • Idiopathic • Developmental defects • Discoid lupus erythematosus • Herpes zoster • Pseudopelade • Tineacapitis/kerion • 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 • Folliculitisdecalvans • Lichen planuspilaris

  12. Localized alopecia Alopecia areata

  13. 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

  14. 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.

  15. Epidemiology • AA is the common type • Both gender affected • Can start at any age

  16. 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

  17. 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.

  18. The characteristic uninflamed patches of alopecia areata.

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

  20. 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.

  21. 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)

  22. Alopecia totalis Alopecia universalis

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

  24. 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

  25. 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.

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

  27. 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.

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

  29. 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.

  30. 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.

  31. Androgenetic alopecia beginning in the frontal area

  32. 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

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

  34. 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.

  35. 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

  36. 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

  37. Etiology: • Infections: typhoid, malaria, dengue • Childbirth:prolonged • Surgical trauma • Haemorrhage • Emotional stress

  38. 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

  39. Excessive hair Hypertrichosis Hirsutism

  40. 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

  41. 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.

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

  43. Acquired hypertrichosis