1. Hair and Nail Disorders
Digital Lecture Series : Chapter 24
Col. Manas Chatterjee
Senior Adviser, Professor and Head
Maj. Shekhar Neema
Graded Specialist and Asst Professor
Department of Dermatology, Command Hospital (EC), Kolkata

2. CONTENTS HAIR Structure Function Alopecia Excessive hair growth
Hair pigmentation
Hair cosmetics
NAIL
Structure
Function
Nail changes in systemic diseases
Nail changes due to drugs
Common diseases of nail
Basic procedures
MCQs
Photoquiz

3. Structure of hair Types of hair : Lanugo (seen in utero) Vellus
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.

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

6. Hair Cycle
Hair follicles undergo a repetitive sequence of growth and rest called the hair cycle.
Anagen is period of active hair growth. 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.
Telogen is the resting phase in which hair stays till the beginning of next anagen phase.

8. 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)

9. Alopecia Classification:
Non-cicatricial: preservation of follicles on clinical and histologic examination. Common causes are alopecia areata, androgenetic alopecia, female patterned hair loss and telogen effluvium.
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.

10. Alopecia areata
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 totalis and all body hair is alopecia universalis.
May be associated with atopy, Down’s syndrome, vitiligo, pernicious anemia, myxoedema, diabetes or hypertension in the family.

11. 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.

12. Localised Non Scarring Alopecia : Alopecia Areata

13. Differential diagnosis
Tinea capitis
Trichotillomania
Secondary syphilis
Androgenetic alopecia

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

15. Prognosis
Majority will get complete regrowth sometimes without treatment in 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.

16. 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; more from father.

17. Pathogenesis
Hormonal factors - 5 alfa reductase changes testosterone to dihydrotestosterone (5-DHT).
5 DHT 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.

18. Clinical features
Pigmented terminal hairs are progressively replaced by finer, short and virtually non-pigmented hairs.
MPHL: 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.

19. Male Pattern Alopecia

20. Female Pattern Alopecia

21. Androgenetic Alopecia
Patterned Non scarring alopecia : Androgenetic Alopecia

22. Female Pattern Hair Loss
Patterned Non scarring alopecia

23. Treatment Medical : Topical Minoxidil (2 to 10%)
Oral Finasteride (1 mg or less)
Surgical :
Follicular unit transplant/extraction
Scalp reduction
Cosmetic cover :
Wigs, hair bonding, hair weaving

24. 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.

25. 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.)

26. Trichotillomania

27. Alopecia due to tinea capitis
Seen essentially in pre-pubertal 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 derived from animals/soil or if inflammatory process destroys the hair follicles

28. 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 tinea capitis, discoid lupus erythematosus, herpes zoster, bacterial infections, neoplastic disorders, cicatricial pemphigoid, pseudopelade of Brocq
Treatment: Excision and primary closure for small patches, autografting and scalp expansion, cosmetic camouflage for large patches.

29. Scarring Alopecia

30. Excessive hair
Growth of hair that in any given site is coarser, longer or more 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.

31. Hirsutism
Growth in females 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 alfa reductase activity in skin.
Other causes : HAIR-AN and SAHA syndromes.

32. 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, striae distensae and clitoromegaly.
Cutaneous examination: Associated acne, acanthosis nigricans, androgenetic alopecia.
Investigate to rule out hormonal aberrations like polycystic ovarian disease or androgen secreting tumors.

33. Treatment
Cosmetic : depilatory creams, plucking, bleaching, electrolysis, eflornithine.
Lasers : Long pulse 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.

34. Hair pigmentation and cosmetics
Canities : greying of hair with age.
Premature canities : onset of greying before 20 years in Caucasians and 30 years in Africans.
Poliosis : localised patch of grey hair; congenital and acquired.
Hair cosmetics : shampoos, conditioners, hair dyes and bleaches.

35. Nails

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

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

38. 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 like Inflammatory bowel disease.

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

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

41. 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.

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

43. Nail psoriasis Seen in up to 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.

44. Nail psoriasis

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

46. Lichen planus

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

48. 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, immunosuppression, trauma, poor peripheral circulation.
Most common pathogens are Trichophyton rubrum, Trichophyton mentagrophytes and candida species.

49. Onychomycosis : see one hand involvement

50. Ingrown nail
Common condition due to piercing of nail plate into lateral nail fold
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

51. Colour changes in nails
Leuconychia
Nail hyperpigmentation

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

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

54. MCQ’s
Q.1) Which phase of hair cycle has maximum duration among the following?
Catagen
Telogen
Kenogen
Anagen
Q.2) Which of the following is not a poor prognostic marker in alopecia areata?
Nail involvement
Oophiasis pattern
Solitary patch
Associated Autoimmune diseases
Ans : Q. 1 – D, Q. 2 – C

55. MCQ’s
Q.3) Nail involvement is seen in what percentage of psoriasis patient?
10 %
50%
20%
None
Q.4) What is the most common pattern of nail involvement in onychomycosis?
Distal - lateral subungal onychomycosis (DLSO)
Proximal subungal onychomycosis (PSO)
Total dystrophic onychomycosis (TDO)
White superficial onychomycosis (WSO)
Ans : Q. 3 – B, Q. 4 – A

56. Classify the type of alopecia and enumerate few causes
Photo Quiz
Ans : Cicatricial alopecia. It can result due to trauma, infections, cutaneous lupus erythematosus, lichen planus
Classify the type of alopecia and enumerate few causes

57. Identify the nail disorder
Photo Quiz
Ans : Subungual hematoma
Identify the nail disorder

58. Thank You!