1 / 41

Hair and Nail Disorders

Hair and Nail Disorders. Hair. Structure and functions Alopecia Excessive growth of hair Hair pigmentation and hair cosmetics. Structure of hair. Types of hair: 1) Lanugo ( seen in utero ) 2) Vellus 3) Terminal Hair is a keratinized product of hair follicle.

marvin
Download Presentation

Hair and Nail Disorders

An Image/Link below is provided (as is) to download presentation Download Policy: Content on the Website is provided to you AS IS for your information and personal use and may not be sold / licensed / shared on other websites without getting consent from its author. Content is provided to you AS IS for your information and personal use only. Download presentation by click this link. While downloading, if for some reason you are not able to download a presentation, the publisher may have deleted the file from their server. During download, if you can't get a presentation, the file might be deleted by the publisher.

E N D

Presentation Transcript


  1. Hair and Nail Disorders

  2. Hair • Structure and functions • Alopecia • Excessive growth of hair • Hair pigmentation and hair cosmetics

  3. Structure of hair Types of hair: 1) Lanugo( seen in utero) 2) Vellus 3) Terminal • Hair is a keratinized product of hair follicle. It is present all over skin except on vermillion of lips, palms, soles and skin of nail folds.

  4. Functions of hair • Concerned with sexual and social communication • Protective role eg. nasal and eyelash hair • Sensory function: touch sensation

  5. Hair Cycle • Hair follicles undergo a repetitive sequence of growth and rest called the hair cycle. • Period of active hair growth is Anagen. Duration of this phase decides the length of hair. In humans, it is maximum on scalp. • Catagen is the regressive phase in which the follicular activity declines and ceases. • The hair stays in the Telogen (resting) phase till the beginning of next anagen phase.

  6. Disorders of hair Disorders of hair can either be due to : • loss of hair from hair bearing areas (alopecia) • Excessive hair Androgen dependent hair patterns of typically terminal hair (hirsutism) Patterns of increased hair growth other than in androgenic distribution (hypertrichosis)

  7. Alopecia Can be classified as : 1) Non-cicatricial: preservation of follicles on clinical and histologic examination. Common causes are alopecia areata, androgenetic alopecia, female patterned hair loss and telogen effluvium. 2) Cicatricial (scarring): destruction of follicles due to conditions eg: trauma, infections, cutaneous lupus erythematosus, lichen planus. It is irreversible There can be either diffuse or localised (patterned / non-patterned ) hair loss.

  8. Alopecia areata Can be classified as : • Chronic inflammatory disease probably due to a T-cell mediated response in genetically predisposed individuals. Environmental factors may trigger the condition. • Affects any hair bearing area; can be localized, extensive or diffuse. The involvement of all scalp hair is alopecia totalisand all body hair is alopecia universalis. • Associated with atopy, Down’s syndrome, vitiligo, pernicious anemia, myxoedema, diabetes or hypertension in the family.

  9. Alopecia areata • The affected area shows total hair loss without any inflammation; sometimes with short, easily extractable ‘exclamation-mark’ hair at margin. • Grey hair spared (going white overnight). • Regrowth either spontaneous or following treatment; at first fine and unpigmented but later resumes normal colour and calibre • Nail pitting, onycholysis may be associated

  10. Differential diagnosis • Tineacapitis • Trichotillomania • Secondary syphilis • Androgenetic alopecia

  11. Treatment • Majority of cases have spontaneous regrowth of hair without any treatment. • Steroids (usually topical or intra- lesional) • Topical minoxidil • Topical anthralin, phenol • Topical immunotherapy: Dinitrochlorobenzene (DNCB), squaric acid dibutyl ester (SADBE), diphencyprone (DPCP) • Immunomodulators : Cyclosporin • Photochemotherapy

  12. Prognosis Majority will get complete regrowth sometimes without treatment in 1 year. A small percentage end up with severe chronic form. • Poor prognostic indicators : Onset in childhood, atopy, positive family history, extensive involvement , nail dystrophy, other auto-immune conditions.

  13. Androgenetic alopecia (AGA) • Most common cause of hair loss • Male patterned baldness(MPB) : 50% men affected by the age of 50 years • Female patterned hair loss(FPHL): 20-50% women affected by age of 50 years • Most likely inherited as autosomal dominant/ polygenic trait from either parent

  14. Pathogenesis • Hormonal factors- Type 5 alfareductase changes testosterone to dihydrotestosterone (5-DHT). 5DHT facilitates miniaturization of hair. Aromatase in contrast inhibits process of miniaturization. • Androgen receptors may be increased or may be hyper-responsive in areas affected by AGA

  15. Clinical features • Pigmented terminal hairs are progressively replaced by finer, short and virtually non-pigmented hairs. • MPB: pattern of progression is uniform; starts as frontoparietal recession and involves the entire scalp sparing the occipital fringe; graded into 8 stages by Hamilton. • FPHL: widened central parting earliest sign; progresses through 3 stages of Ludwig.

  16. Treatment • Medical : Topical Minoxidil (2 to 10%) Oral Finasteride (1 to 2.5 mg) • Surgical : Follicular unit transplant Scalp reduction • Cosmetic cover : wigs, hair bonding, hair weaving

  17. Telogen effluvium (TE) • Sudden significant hair loss 2-3 months after an offending insult where hair follicles are pushed prematurely from anagen to telogen phase. • Offending insults: fever, post partum, crash dieting, hypoproteinemia, iron deficiency, major surgeries, prolonged anaesthesia, hypo and hyperthyroidism, major internal disease, acute psychologic stress and medication.

  18. Trichotillomania • Psychiatric disorder in which there is a compulsive habit of pulling out the hair. • Bizarre pattern of hair loss in which hair is twisted and broken at various distances from clinically normal scalp • Management: may vary from identification of stressful episode with accompanying support, parent education, support of psychologist and psychiatrist, drug therapy (antidepressants etc.)

  19. Alopecia due to tinea capitis • Seen essentially in prepubertal age group • It is patchy, incomplete and is due to breakage of hair shaft invaded by dermatophytes. • It is fully reversible except in cases of inflammatory involvement due to species of dermatophytes accidently derived from animals/soil.

  20. Cicatricial alopecia • Seen as an area of thin, shiny, dry and depressed skin with telangiectasia; absence of follicular openings. • Could be developmental/ hereditary, traumatic, secondary to tineacapitis, discoid lupus erythematosus, herpes zoster, bacterial infections, neoplastic disorders, cicatricialpemphigoid, pseudopelade of Brocq • Excision and primary closure for small patches, autografting and scalp expansion, cosmetic camouflage for large patches.

  21. Excessive hair • Growth of hair that in any given site is coarser, longer or profuse than is normal for the age, sex and race • Hirsutism: androgen dependent hair patterns of typically terminal hair • Hypertrichosis: patterns of increased hair growth involving non-androgen dependent follicles

  22. Hirsutism • Growth in female of coarse terminal hair in adult male pattern of distribution i.e. face, chest, upper back • Androgen dependent • Idiopathic or due to hyperplasia / tumors involving ovaries, adrenal cortex or pituitary • May be due to drugs, reduced plasma sex hormone binding globulin, increased androgen receptor or 5 alfareductase activity in skin • Other causes: HAIR-AN and SAHA syndromes

  23. Approach to a hirsute patient • Enquire about the pattern of hirsutism, alopecia, features of virilisation • Probe into the menstrual history, family history and intake of drugs such as glucocorticoids, anabolic steroids. • Systemic examination: Deepening of voice, muscle bulk, loss of body contours, hypertension, striaedistensae and clitoromegaly • Cutaneous examination: Associated acne, acanthosisnigricans, androgenetic alopecia • Investigate to rule out hormonal aberrations like polycystic ovarian or androgen secreting tumors

  24. Treatment • Cosmetic: depilatory creams, plucking, bleaching, electrolysis, eflornithine • Lasers: Nd:YAG, intense pulse light, diode, alexandrite • Hormonal correction: any tumors have to be removed • Drugs: cyproterone acetate, finasteride, flutamide, spironolactone, leuprolide, ketoconazole, medroxyprogesterone acetate

  25. Hair pigmentation and cosmetics • Canities : greying of hair with age • Preamturecanities: onset of greying before 20 years in whites and 30 years in blacks • Poliosis : localised patch of grey hair; congenital and acquired • Hair cosmetics : shampoos, conditioners, hair dyes and bleaches

  26. Nails • Structure and functions • Nail changes in systemic diseases • Nail changes due to systemic drugs • Common skin diseases involving nails • Basic procedures and surgeries

  27. Functions of nails • Help to grasp and manipulate objects • Help in ‘pincer grip’ • Protect terminal phalanx and fingertip • Serve an aesthetic and cosmetic purpose

  28. Nail changes in systemic diseases • Clubbing • Koilonychia • Beau’s lines • Subungual hematoma / Splinter hemorrhages • Color changes of nails • Periungual / subungual tumors

  29. Clubbing 3 major categories: • Idiopathic • Hereditary - congenital • Acquired: • 80% cases associated with respiratory ailments, 10-15% with cardiovascular and the rest with various extrathoracic diseases.

  30. Koilonychia (spoon nails) 3 types: • Idiopathic • Hereditary • Acquired : • Trauma, dermatologic diseases, • Raynaud’s phenomenon, iron deficiency (not the most common cause)

  31. Beau’s lines • Transverse depression across nail plate • Caused by serious systemic illness, drug reaction, bullousdermatoses, severe psychologic stress, local trauma, eczemas, idiopathic

  32. Nail changes due to systemic drugs • Asymptomatic growth rate change and pigmentation abnormalities are the most common changes. • Other changes: Transient shedding, photo- onycholysis, brittle nails, Beau’s lines, permanent nail deformities. • Common drugs: Antibiotics like tetracycline, cephalosporins; fluoroquinolones, antimalarials, retinoids, psoralens, chemotherapeutic drugs.

  33. Common skin conditions with nail changes • Psoriasis • Lichen planus • Fungal infections • Bacterial infections • Viral infections • Ingrown nails (trauma induced)

  34. Nail psoriasis • Seen in upto 50% of patients with psoriasis • May be the first manifestation of psoriasis • Seen in several nails; both finger and toe nails may be affected • Diagnostic signs include extensive irregular pitting, oil drop sign and onycholysis with erythematous borders. • Other abnormalities often seen are nail thickening, subungual hyperkeratosis, nail crumbling etc.

  35. Nail Lichen planus • Nail abnormalities evident in 10% cases with skin / mucosal lichen planus • Commonly occurs in absence of skin / mucosal involvement • Thinning and longitudinal ridging / fisssuring of nail plate, pterygium formation, subungual hyperkeratosis • Permanent destruction may occur

  36. Onychomycosis • Involvement of one / few nails • Examination of skin may give a clue • Four patterns of onychomycosis • Distal and lateral subungualonychomycosis (DLSO) • Proximal subungualonychomycosis (PSO) • White superficial onychomycosis (WSO) • Total dystrophic onychomycosis (TDO)

  37. Onychomycosis: causes • Caused by dermatophytes , candida and moulds • Is known to affect >10% of population in western world • Predisposing factors: occlusive footwear, diabetes mellitus, hyperhidrosis, immunosuppresion, trauma, poor peripheral circulation • Most common pathogens are Trichophytonrubrum, Trichophytonmentagrophytesand candida

  38. Ingrown nail • Common condition due to piercing of nail plate into lateral nail fold • Most common causes are improper trimming of nails and tight, ill-fitting footwear • Great toe nail most commonly involved • Causes inflammation, pain and sometimes formation of extra granulation tissue

  39. Useful investigations • KOH mount • Mycologic culture • Nail clipping • Biopsy-nail plate/nail bed • Radiologic studies

  40. Some therapeutic procedures • Chemical nail avulsion using 40% urea • Nail avulsion: partial and total • Nail splinting • Nail matrix injections • Nail unit biopsy • Chemical/surgical matricectomy • Electrosurgery / radiosurgery / cryotherapy, laser ablation of growths like verrucae, myxoid cyst • Surgical removal of growths like glomus tumor

  41. Thank you

More Related