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TYPES OF HAİR

TYPES OF HAİR. Lanugo hair: Soft fine hair that covers much of fetus; usually shed before birth Vellus hair: Fine, nonpigmented hair that covers the body of children and adults; growth not affected by hormones.

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TYPES OF HAİR

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  1. TYPES OF HAİR • Lanugo hair: Soft fine hair that covers much of fetus; usually shed before birth • Vellus hair: Fine, nonpigmented hair that covers the body of children and adults; growth not affected by hormones. • Terminal hair: Thick pigmented hair found on scalp, beard, axillae, pubic area; growth is influenced by hormones. Eyebrow/eyelash hair are terminal hairs.

  2. BIOLOGY OF HAIR GROWTH • Hair growth on the scalp occurs in cycles of intermittent activity; phases of growth are followed by periods of quiescence. • Anagen: Phase of normal active growth. Catagen: Brief transition phase(between anagen and telogen) during which hair growth stops. Telogen: Resting phase. • Duration and rate of growth of anagen phase ( varying at different body sites, in different individuals, and at various ages) determine the ultimate length of hair in that area.

  3. HAIR LOSS: ALOPECIA: EFFLUVIUM or DEFLUVIUM

  4. ETİOLOGY OF HAİR LOSS • Diffuse (global) hair loss (nonscarring) • Failure of follicle production • Hair shaft abnormality • Abnormality of cycling (shedding) • Telogen effluvium • Anagen effluvium • Loose anagen syndrome • Alopecia areata • Focal (patchy,localized) hair loss • Nonscarring • Production decline • Triangular alopecia • Pattern hair loss ( androgenetic alopecia) • Hair breakage • Trichotillomania • Traction alopecia • Tinea capitis • Primary or acquired hair shaft abnormality • Unruly hair • Abnormality of cycling • Alopecia areata • Syphilis • Cicatricial (scarring) alopecia

  5. ALOPECIA AREATA (AA) AA is a localized loss of hair in round or oval areas without any visible inflammation of the skin in hair bearing areas; the most common presenting site is the scalp. AA totalis: total absence of terminal scalp hair. AA universalis: total loss of terminal body and scalp hair. Ophiasis: Bandlike pattern of hair loss over periphery of scalp.

  6. Epidemiology and Etiology • Age of onset: Young adults(< 25 years; children are affected more frequently. • Sex: female=male • Prevalence: Relatively common. • Etiology: Unknown. Association with other autoimmune diseases suggests an anti-hair bulb autoimmune process.

  7. Pathogenesis • An autoimmune disease; not a sign of any multisystem disease. Associated autoimmune disorders: vitiligo, thyroid disease (Hashimoto’s disease), familial autoimmune polyendocrinopathy syndrome, myasthenia gravis. Folicular damage occurs in anagen followed by rapid transformation to telogen. With fulminant AA, persons may experience” going gray overnight”

  8. History • Duration of hair loss: Gradual over weeks to moths. Patces of AA can be stable and often show spontaneous regrowth over a period of several months; new patches may appear while others resolve. • Skin symptoms: Not symptomatic

  9. Physical Examination • Skin findings: Usually none. Possibly minimal erythema in area of hair loss. • Hair: Alpocia, normal- appearing skin. No scarring, no atrophy; Alopecia often sharply defined. Sometimes hair loss in AAT may follow a diffuse (noncircumscribed) pattern. • Sites of Predilection: Scalp, eyebrows, eyelashes, pubic hair, beard. • Nails: Fine pitting, mottled lunula, trachyonychia (rough nails), onychomadesis

  10. Differential diagnosis • Nonscarring alopecia: Secondary syphilis, white-patch tinea capitis, trichotillomania, traction alopecia, early DLE, androgenetic alopecia.

  11. Laboratory examinations • Serology: ANA, RPR • KOH preparation • Dermatopathology

  12. Course Spontaneous remission is common in patchy AA but is less so with AAT or AAU. Poor prognosis associated with ophiasis, age of onset, association of atopy, duration of hair loss in given area. If occurring after puberty, 80% regrow hair. After first episode of AA, 33% completely regrow the hair within 1 year. Recurrences of AA, however, are frequent. Systemic glucocorticoids or cyclosporine can induce remission of AA but do not alter the course.

  13. Management • No curative treatment is currently available. • Glucocorticoids: Topical, intralesional, systemic • Systemic cyclosporine • Induction of allergic contact dermatitis • Oral PUVA ( Photochemotherapy)

  14. TELOGEN EFFLUVIUM TE is the transient increased shedding of normal club telogen hairs from resting scalp follicles secondary to accelerated shift of anagen (growth phase) into catagen and telogen (resting phase), resulting in increased daily hair loss and, if severe, diffuse thinning of scalp hair.

  15. Epidemiology and etiology • Age of onset: Any age • Sex: More common in women due to parturition, cessation of an oral contaceptive, and “crash” dieting. • Incidence: Second most common cause of alopecia after androgenetic alopecia. • Etiology: A reaction pattern to a variety of physical or mental stressors.

  16. Etiology • Endocrine • Hypo- or hyperthroidism • Postpartum • Peri- or postmenopausal state • Nutritional • Deficiency: biotin, zinc, iron, essential fatty acids • Deprivation: caloric, protein • Drugs • Antimitotic agents (dose dependent): cancer chemotherapy, benzimidazoles • Antihypertensives: ACE inhibitors, beta blockers • Anticoagulants • Interferon • CMS drugs: lithium, valproic acid • Hormonal: oral contraceptives • Retinoid effect: vitamin A excess, retinoids, indinavir • Physical stress: anemia, surgery, systemic illness • Psychological stress • Idiopathic: no obvious cause is apparent in a significant number of cases.

  17. Pathogenesis • Premature shift of anagen follicles into the telogen phase.

  18. History • Hair thinning. • The precipitating event precedes the TE by 6 to 16 weeks.

  19. Physical examination • Skin lesions: No abnormalities of the scalp are detected. • Hair: Diffuse shedding • Sites of predilection: Scalp. • Nails: Beau’s lines

  20. Differential diagnosis • Increased shedding of scalp hair ±Nonscarring alopecia: Androgenetic alopecia, diffuse pattern alopecia areata, loose anagen syndrome, hyperthyroidism, hypothyroidism, SLE, seconday syphilis, drug-induced alopecia.

  21. Laboratory examinations: • Hair pull test • Chemistry: CBC, serum iron, ferritin SIBC ( rule out iron deficiency anemia) • TSH • Serology: ANA, RPR • Histopathology

  22. Course and prognosis • Complete regrowth of hair is the rule. Hair density may take 6 to 12 months to return to baseline. In postpartum TE, if hair loss is severe recurs after successive pregnancies, regrowth may never be complete.

  23. ANAGEN EFFLUVIUM (AE) • AE results from a rapid growth arrest of cell division in hair matrix .Only actively growing anagen folicles are subject. Onset is usually is rapid and extensive. • After any insult to hair follicle that impairs its mitotic/metabolic activity: cancer chemotherapy, radiation therapy, intoxications ( mercury, boric acid, thallium, colchicines), severe protein deficiency. • AE is usually extensive with generalized loss of scalp, eyebrow/lashes, beard, etc.

  24. ANDROGENETIC ALOPECIA (AGA) AGA is the common progressive balding that occurs through the combined effect of (1) genetic predisposition (AD and/or polygenic), and (2) action of androgen on scalp hair follicles.

  25. Pathogenesis • Testosterone is converted to DHT by 5alfa-reductase (5alfa-R). Type I 5-alfa-R is localized to sebaceous glands(face, scalp),chest/ back, liver, adrenal gland, kidney. Type II 5alfa-R is localized to scalp hair follicle, beard, chest skin, liver, seminal vesicle, prostate, epididymis, foreskin/scrotum. • Role of testosterone: (1) prenatal: internal sex organ development of male fetus; (2): post-natal: spermatogenesis, libido, muscle/bone mass. • In males, testosterone produced by the testes is the major androgen. In females, androstenedione and DHEAS are the major peripheral androgens. • In genetically predisposed individuals, DHT causes terminal follicles to transform into vellus-like follicles, which in turn undergo atrophy. During successive follicular cycles, hairs produced are of shorter length and of decreasing diameter. Conversely, androgens induce vellus-to-terminal follicle production of secondary sexual hair. • Most women with AGA are endocrinologically normal.

  26. Physical examination • Skin findings: Scalp skin is normal. With advanced AGA, scalp is smooth and shiny. • Distribution:Hamiltonclassified male-pattern hair loss into V stages; Ludwigclassified hair loss in females.

  27. Differential diagnosis • Diffuse nonscarring scalpalopecia:Diffuse pattern of hair loss with alopecia areata, telogen effluvium, secondary syphilis, SLE, iron deficiency, hypo/hyper thyroidism, trichotillomania, seborrheic dermatitis.

  28. Laboratory examinations • Trichogram • Dermatopathology • Hormone studies: Total and free testosterone, FSH, LH, 17-OH-progesterone, DHEAS, prolactin • Other studies: TSH, T4, serum Fe, TIBC, ferritin, CBC, ANA.

  29. Diagnosis and course • Clinical diagnosis is made on the history, pattern of alopecia, and family incidence of AGA. • Skin biopsy may be necessary in some cases. • The progression of alopecia is usually very gradual, over years to decades.

  30. Management • Oral finasteride • Topical minoxidil • Antiandrogens: Spironolactone,cyproterone asetate, flutamide, cimetidine. • Hairpiece • Surgical treatment: Hair transplantation, scalp reduction/rotation flaps.

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