2. 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.

8. Hair follicles
Infundibular segment (from its surface opening to the entrance of the sebaceous duct)
Isthmus (between the sebaceous duct and the insertion of the arrector pili muscle)
Hair bulb

11. 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.

12. On the scalp, anagen, active growth phase, lasts about 3-5 years
85-90 % of all scalp hairs are in the anagen phase (0.37 mm / day)
Catagen (involution phase): 2 weeks
Telogen (resting phase): 3-5 months
Each follicle functions as an independent unit

15. DIFFERENTIAL DIAGNOSIS OF DIFFUSE NONSCARRING HAIR LOSS

16. HAIR LOSS: ALOPECIA: EFFLUVIUM or DEFLUVIUM

17. 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
Syphilis
Cicatricial (scarring) alopecia

18. 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.

19. 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.

20. 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”

21. 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

22. Physical Examination
Skin findings: Usually none. Possibly minimal erythema in area of hair loss.
Hair: 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

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

24. Laboratory examinations
Serology: ANA, RPR
KOH preparation
Dermatopathology

25. 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.

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

27. 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.

28. 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.

29. Etiology Endocrine Nutritional Drugs
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.

30. Pathogenesis
Premature shift of anagen follicles into the telogen phase.

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

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

34. 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.

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

36. 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.

37. 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.

39. 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.

40. In genetically predisposed individuals, and under the influence of androgens, predisposed follicles are gradually miniaturized, and large, pigmented hairs (terminal hairs) are replaced by thin, depigmented hairs (vellus hairs).

41. Skin Androgen Metabolism
Testosterone is converted to the more potent dihydrotestosterone by 5 alpha reductase.
Skin cells contain 5 alpha reductase (types I and II).
The type I enzyme is found in sebaceous glands, and the type II enzyme is found in hair follicles and the prostate gland.

42. 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.

43. COMPARISON OF MALE PATTERN AND FEMALE PATTERN ANDROGENETIC ALOPESIA
Male pattern baldness results in a gradual regression of the hair on the central scalp and gradual frontotemporal recession, as well as a gradual decrease in hair shaft diameter in the areas of hair loss.
In contrast, most women with diffuse alopecia experience a gradual loss of hair on the central scalp, with retention of the normal hairline without frontotemporal recession.
There are a variety of anagen hair diameters.
With advancing age, the central thinning becomes more pronounced; in contrast to male pattern baldness, a fringe of hair along the frontal hairline persists.
In exceptional cases, a course similar to that in men is seen, with deep frontotemporal recession.
Male pattern
Female pattern

44. Hamilton Patterns
The progression and various patterns of hair loss are classified by the Hamilton male baldness classification system.
Triangular frontotemporal recession occurs normally in most young men (type I) and women after puberty.
The first signs of balding are increased frontotemporal recession accompanied by midfrontal recession (type II).
Hair loss in a round area on the vertex follows, and the density of hair decreases, sometimes rapidly, over the top of the scalp (types III through VII).

46. Physical examination
Skin findings: Scalp skin is normal. With advanced AGA, scalp is smooth and shiny.
Distribution: Hamilton classified male-pattern hair loss into V stages; Ludwig classified hair loss in females.

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

48. 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.

49. 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.

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