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📋 HAIR DISEASES - EASY STUDY NOTES

(Chapter 24 - Habif's Clinical Dermatology)

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🔬 ANATOMY & PHYSIOLOGY

Types of Hair

Hair Follicle Sections (Top to Bottom)

1. Infundibulum - surface to sebaceous gland duct
2. Isthmus - from sebaceous duct to erector pili muscle insertion
3. Inferior segment - exists only during anagen; from muscle to matrix

Hair Shaft Layers (outer → inner)

• Cuticle (outermost - protects cortex)
• Cortex (bulk of shaft - contains pigment melanosomes)
• Medulla (innermost - sometimes absent)

Key Facts

• Humans have ~5 million follicles at birth; NO new follicles form after birth
• Scalp has >100,000 hairs
• Scalp hair grows 0.3-0.4 mm/day (≈6 inches/year)
• The bulge (outer root sheath near arrector pili) = stem cell reservoir for follicle regeneration

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Hair Growth Cycle

ANAGEN (growing) → CATAGEN (transitional) → TELOGEN (resting) → ANAGEN
    2-6 years           2-3 weeks              2-3 months
    90-95%               <1%                    5-10%

Club hair = dead hair; solid white proximal end; shed during telogen

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🔍 EVALUATION OF HAIR LOSS

Systematic Approach (Box 24.1)

History Questions

• Sudden vs gradual
• Systemic disease or fever
• Recent stress (physical/psychological)
• Medications/chemicals

Examination

• Localized vs generalized
• Scarring vs non-scarring
• Inflammatory vs non-inflammatory
• Follicular plugging

Diagnostic Tools

Anagen vs Telogen Hair (Microscopy)

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📊 SIMPLIFIED DIAGNOSIS TABLE (97% of cases)

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🌊 GENERALIZED HAIR LOSS

1. Telogen Effluvium (TE)

• Normal scalp, diffuse loss, NO scarring
• Up to 50% hair affected
• Resting hairs shed ~100 days after trigger

• High fever
• Severe emotional/physical trauma
• Postpartum (1-4 months after delivery - delayed anagen release)
• Drugs (see below)
• Hypothyroidism, iron deficiency
• Crash diets

2. Anagen Effluvium

• Scalp hypothermia (DigniCap, Paxman) can minimize chemotherapy-induced loss

3. Loose Anagen Hair Syndrome (LAS)

• Children; female:male = 6:1
• Defective anchorage of hair shaft → easily, painlessly pluckable hair
• Young girl with short blond hair that won't grow long
• Pull test: >10 loose anagen hairs (normal = 1-2)
• Trichogram: ≥70% loose anagen, no telogen
• Most improve with age

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🎯 LOCALIZED HAIR LOSS

Androgenetic Alopecia (AGA) - Men (Male Pattern Baldness)

• Physiologic reaction; polygenic inheritance
• Begins age 12-40; ~50% express before age 50
• Androgen-sensitive follicles on top; androgen-independent on sides/back

Type I    = Normal (minimal frontotemporal recession)
Type II   = Slight frontotemporal recession
Type III  = Deep frontotemporal + midfrontal recession
III vertex= Hair loss on vertex
IV-VII    = Progressively increasing vertex + frontal baldness

• Testosterone (T) → DHT via 5α-reductase type II (in hair follicles + prostate)
• DHT binds follicle androgen receptor → miniaturizes follicles
• Terminal hairs → vellus hairs; anagen shortens progressively
• Inflammation around bulge area damages stem cells

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Female Pattern Hair Loss (AGA in Women)

• Ludwig pattern: Central scalp thinning; frontal hairline PRESERVED (key difference from men)
• Widening of central hair part
• "Pony tail is thinner"
• Pull test normal; miniaturized hairs of varying diameter
• More common with PCOS and other androgen excess states

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🧔 HIRSUTISM

Ferriman-Gallwey (mFG) Scoring

• 9 body sites (upper lip, chin, chest, upper/lower back, upper/lower abdomen, arm, thigh)
• Score 0-4 per site
• Score 6-8 = hirsutism in white/black women
• <5% of reproductive-age women score >7

Etiology (Box 24.4)

Virilization = Hirsutism PLUS:

• Clitoral hypertrophy
• Deepening voice
• Temporal balding
• Decreased breast size
• Amenorrhea
• Increased muscle mass
• Acne + increased sebum → Suggests ovarian or adrenal tumor

Polycystic Ovary Syndrome (PCOS)

1. Oligomenorrhea/anovulation
2. Clinical/biochemical hyperandrogenism (hirsutism, acne, elevated T)
3. Polycystic ovaries on ultrasound (>8 follicles/ovary, all <10mm) (After excluding: congenital adrenal hyperplasia, Cushing, androgen-secreting tumor, acromegaly)

• 6% of reproductive-age women
• Insulin resistance + hyperinsulinemia
• Elevated LH, T; reduced SHBG
• Obesity in 70%
• 3× increased risk of endometrial cancer
• Risk of type 2 DM (up to 40%)
• Impaired glucose tolerance in up to 40%

Alarm Values (Tumor Workup):

• Total T > 6.9 nmol/L (>200 ng/dL)
• DHEA-S > 18.9 nmol/L (>7000 ng/mL) → Suggests ovarian or adrenal androgen-producing tumor

Hirsutism Treatment Principles

• First-line: Oral contraceptives (suppress LH → ↓ ovarian androgens; ↑ SHBG → ↓ free androgen)
• Add antiandrogen after 6 months if poor response
• At least 6 months of treatment needed for response
• Cosmetic: shaving, waxing, eflornithine cream (Vaniqa), laser/IPL

• All equally effective
• Teratogenic → always use with contraception

• Irreversible inhibitor of ornithine decarboxylase
• Slows hair growth (not permanent)
• Results in 6-8 weeks; regrows when stopped

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🔵 ALOPECIA AREATA (AA)

• AA = Patchy scalp hair loss
• Alopecia totalis = 100% scalp hair loss
• Alopecia universalis = 100% loss of scalp + body hair
• Ophiasis pattern = Band-like loss in parietotemporo-occipital area (poor prognosis)

Clinical Features

• Smooth, white/normal scalp
• "Exclamation point" hairs - normal upper shaft, narrowed base - at periphery of patch
• Regrowth in 1-3 months; may be white/fine initially
• Eyelashes + beard are second most common sites

Nail Changes (10-66%):

• Pitting (irregular, organized rows, or longitudinal)
• "Sandpaper nails" appearance

Prognosis

• Majority regrow within 1 year without treatment
• 10% develop chronic disease and may never regrow
• Poor prognosis: family history AA, young age, nail dystrophy, atopy, extensive loss, immune diseases

Pathology

• "Swarm of bees" = peribulbar lymphocytic infiltrate
• NO scarring
• Inflammation terminates anagen → catagen
• Bulge SPARED → new hair can regrow after inflammation resolves

Etiology

• Unknown; autoimmune T-lymphocyte mediated
• Associations: thyroid disease (8-11.8%), vitiligo (4× increased), atopy (2×)

Differential Diagnosis

• Tinea capitis (KOH+, scale)
• Trichotillomania (irregular, broken hairs, not completely bald)
• Secondary syphilis (moth-eaten pattern)
• Telogen effluvium (diffuse, not patchy)

AA Treatment by Age & Severity

• Topical midpotent corticosteroid + 5% minoxidil solution
• Alternative: Anthralin (short contact)

• Intralesional corticosteroids (triamcinolone acetonide 5-10 mg/mL)
  • Regrowth in 4-8 weeks; 60-67% response rate; repeat every 4-6 weeks
• ± 5% topical minoxidil twice daily
• ± Topical corticosteroid

• 5% topical minoxidil + topical corticosteroid
• Topical immunotherapy (DPCP) - treatment of choice for >50% scalp in adults
• Anthralin (20-25% response)
• Oral corticosteroids (rarely; high relapse rate)

• Diphenylcyclopropenone - first choice for >50% scalp
• Squaric acid dibutyl ester (SADBE) - alternative
• ~60% success rate in experienced hands
• Goal: mild itching, erythema, scaling

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🧠 TRICHOTILLOMANIA (TTM)

DSM-5 Diagnostic Criteria (Box 24.11)

1. Hair loss from recurrent hair-pulling
2. Repeated attempts to stop
3. Significant distress/impairment
4. Not due to dermatologic condition
5. Not better explained by another mental disorder

Clinical Features

• Frontoparietal scalp most common (easily reached)
• Irregular, angulated border
• Area is NEVER completely bald (unlike AA)
• Short, broken hairs of varying lengths randomly distributed
• Eyebrows and eyelashes may be involved

Diagnosis

• Ask patient directly about hair manipulation
• No telogen hairs on pull test (nearly 100% anagen)
• Biopsy: normal hairs, absent hairs in follicles, NO leukocyte infiltration; catagen hairs in 74%
• Hair growth window test: cover shaved area for 1 week → normal growth proves hair is growing

Difference from AA:

Treatment

• Supportive counseling (physician/parent)
• Habit reversal therapy (superior to pharmacotherapy)
• Clomipramine (more effective than placebo; SSRIs = NOT proven superior to placebo)
• Consider psychiatric referral for extensive cases

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➡️ TRACTION ALOPECIA

• Caused by: braids, ponytails, rollers, hot straightening combs
• Hair loss corresponds exactly to the stressed area
• Usually temporary; rarely permanent
• Treatment: Avoid the causative hairstyle

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🔥 SCARRING ALOPECIAS

Key principle: Permanent hair loss because follicle is DESTROYED (unlike non-scarring)

Primary vs Secondary Scarring Alopecia

1. Central Centrifugal Cicatricial Alopecia (CCCA)

• Most common cicatricial alopecia in black women
• Starts at vertex, spreads forward/outward
• Early stage: erythema, scaling around follicles; pruritus, scalp tenderness
• Late stage: scarring, fibrosis
• Association with type 2 diabetes mellitus
• Treatment: topical/intralesional corticosteroids, topical minoxidil; doxycycline for inflammatory disease

2. Chronic Cutaneous Lupus Erythematosus (Discoid LE)

• Common cause of scarring alopecia
• More common in women
• Classic lesion: "carpet tack scale" (follicular plugging with scale attached to underside)
• Well-circumscribed, erythematous, scaly plaques → atrophic hypopigmented/hyperpigmented scars
• Immunofluorescence: IgG, IgM deposits at dermoepidermal junction
• Treatment: Topical/intralesional corticosteroids, hydroxychloroquine, oral agents (azathioprine, cyclosporine)

3. Lichen Planopilaris (LPP)

• More common in adult women
• Lesions: centrifugal pattern, vertex-centered
• Spinous, hyperkeratotic follicular papules with perifollicular erythema
• Smooth, atrophic, polygonal-shaped patches; scarring central, active at margins
• Patients: pain, stinging, burning
• Immunofluorescence: cytoid body staining (IgM, IgA) - positive in 50%
• Differential: DLE, pseudopelade, folliculitis decalvans
• Treatment: Superpotent topical steroids, intralesional steroids, short oral steroids; hydroxychloroquine; doxycycline, tetracycline, cyclosporine

4. Frontal Fibrosing Alopecia (FFA)

• Variant of LPP
• Mainly postmenopausal women
• Scarring from frontal hairline extending backward
• Perifollicular erythema + minute perifollicular papules at advancing edge
• Eyebrow loss common
• Biopsy = same as LPP
• Poor prognosis for recovery

5. Pseudopelade (of Brocq)

• Rare, slowly progressive, non-inflammatory scarring alopecia
• "Footprints in the snow" appearance - skin-colored, slightly depressed patches
• Starts on crown; moth-eaten-like patches coalesce
• May be end-stage of other scarring alopecias
• Treatment resistant to topicals; intradermal steroids

6. Folliculitis Decalvans

• Chronic pustular eruption → patchy permanent alopecia
• Crops of pustules surrounding multiple expanding oval areas of alopecia
• Staphylococcus aureus cultured from pustules
• Biopsy: follicular neutrophilic abscesses (early); dermal lymphocytes + scarring (late)
• Treatment: Culture pustules; antibiotics (rifampicin + clindamycin × 10 weeks; dapsone); topical mupirocin

7. Dissecting Cellulitis

• Young black men
• Boggy, fluctuant scalp nodules on crown/vertex/occiput
• Interconnected abscesses with sinus tracts → extensive scarring
• Part of "follicular occlusion triad" (dissecting folliculitis + hidradenitis suppurativa + acne conglobata)
• Treatment: Antibiotics; isotretinoin; adalimumab (reported effective)

8. Acne Keloidalis Nuchae

• Young black men (much less common in white men)
• Occipital scalp and posterior neck
• Follicular papules/pustules → fibrosis → firm keloidal papules
• Initially neutrophilic inflammation
• Treatment: Antibiotics (topical and oral); topical/intralesional steroids; surgery in advanced cases

9. Tufted Folliculitis

• End stage of other scarring alopecias (folliculitis decalvans, acne keloidalis, etc.)
• Multiple hairs (2-10+) emerging from single dilated follicular orifice
• Follicular rupture + abscess + fibrosis around follicles
• Treatment: Same as folliculitis decalvans

10. Acne Necrotica

• Severe scalp folliculitis
• Papules/pustules → crusts → depressed scars
• Can also affect face
• Treatment: Minocycline, topical clobetasol

11. Erosive Pustular Dermatosis

• Elderly; actinically damaged scalp
• Often follows trauma or destructive treatment
• Red, pustular, crusted, eroded plaques
• Progressive scarring alopecia
• Biopsy: lymphocytes and plasma cells in dermis
• Treatment: Potent topical steroids, tacrolimus, calcipotriol, acitretin, isotretinoin, topical dapsone gel

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🦠 TRICHOMYCOSIS

• Asymptomatic infection of axillary or pubic hair by Corynebacterium
• Hair shaft coated with adherent yellow (occasionally red or black) firm concretions
• Associated with hyperhidrosis
• Treatment: Shave hair; control hyperhidrosis with antiperspirants; Naftifine 1% cream

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🏥 QUICK COMPARISON CHART: KEY DISEASES

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🧪 ANDROGEN METABOLISM SUMMARY

Testosterone (T)
        ↓  [5α-reductase Type I: sebaceous glands]
        ↓  [5α-reductase Type II: hair follicles, prostate]
       DHT (Dihydrotestosterone)
        ↓
Androgen receptor in dermal papilla
        ↓
- Scalp: miniaturizes follicles → AGA
- Beard/chest/pubic: enlarges follicles → terminal hair growth

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⚠️ HIGH-YIELD POINTS FOR EXAMS

1. Telogen effluvium occurs ~3 months after the trigger
2. Postpartum hair loss = delayed anagen release (1-4 months post-delivery)
3. Exclamation point hairs = pathognomonic of alopecia areata
4. "Swarm of bees" peribulbar infiltrate = alopecia areata (no scarring)
5. "Carpet tack scale" = Discoid lupus erythematosus
6. "Footprints in the snow" = Pseudopelade
7. Tufted folliculitis = multiple hairs from single orifice
8. Follicular occlusion triad = dissecting folliculitis + hidradenitis suppurativa + acne conglobata
9. CCCA is most common cicatricial alopecia in black women
10. Dissecting cellulitis + acne keloidalis = young black men
11. Anagen hairs = all affected in trichotillomania (no telogen on pull test)
12. Hamilton classification = male AGA; Ludwig classification = female AGA
13. Ophiasis pattern AA = poor prognosis
14. AA prognosis: >1 year disease, alopecia totalis, nail dystrophy, atopy = poor outcome
15. PCOS diagnosis requires 2 of 3: oligomenorrhea, hyperandrogenism, polycystic ovaries
16. Ferriman-Gallwey score ≥ 6-8 = hirsutism
17. 5α-reductase absent congenitally → AGA does NOT develop (confirms DHT role)
18. Finasteride NOT effective in postmenopausal women with AGA
19. Habit reversal therapy > pharmacotherapy for trichotillomania
20. Trichomycosis = Corynebacterium (NOT fungi, despite the name)

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