Skin Appendages and Hair Disorders😊

Skin Appendages and Hair Disorders

• In humans, cuticle covers entire length

Skin appendages include:

Hair Structure

• Hair divided into two parts:
• Upper Part
• Infundibulum: Upper part above the isthmus.
• Isthmus: From sebaceous glands to erector pili muscle.
• Comprise the constant part of the hair follicle.
• Lower Part
• Bulb
• Suprabulbar Area
• Not constant; regresses and reforms.
• Differs in telogen and anagen hair.

Adamson's Fringe

• Mnemonic: Adams fridge → prevent fungal infections

• Area just above the bulb, over the suprabulbar area.
• Separates
• Lower part: Keratinized hair follicle.
• Upper part: Non-keratinized hair follicle.

• Important in fungal infections;

• restricts invasion above the fringe.

Types of Hair

Three types:

• Lanugo Hair



• Newborn babies, more common in premature babies.
• Soft, unpigmented, unmedullated.

• Vellus Hair (Adults)



• Very soft, unmedullated.
• < 2 cm long, less pigmented.
• Common on the face.

• Terminal Hair (Adults)



• Thick, coarse, medullated.
• Longer, pigmented.
• Androgen-dependent (pubic, axillary, beard).

Hair Cycle

Three phases:

• Anagen, Catagen, Telogen.

Phase	Duration	% of Hair	Characteristics
Anagen	2-3 years	90%	Growth phase; responsible for length.
Catagen	2-3 weeks	1%	Transition phase.
Telogen (Normal)	2-3 months (Falls 50-100/day)	9%	Fall phase. (Hair goes back to anagen eventually).

• Normal Anagen to Telogen Ratio: ~9:1

• Mnemonic:
• Ana → Elephant → big → 2 - 3 yrs → Grow big → Growth phase
• Cat → Smallest → 2 -3 weeks → Become small → Transformation phase

Hair Disorders

• Categorized into:
• Hair fall (Alopecia)
• Disorders of hair growth (Hirsutism/Hypertrichosis)

Disorders of Hair Loss (Alopecia)

• Two types:
• Non-scarring (Non-cicatricial) Alopecia
• Scarring (Cicatricial) Alopecia

Non-scarring (Non-cicatricial) Alopecia

• No damage to the hair bulb.

• High chances of regrowth (stem cells in hair bulb).

Three main types:

1. Patterned Alopecia:
• Androgenetic alopecia (AGA).
• Female and male pattern

2. Diffuse Alopecia:
• Effluviums (anagen, telogen)

3. Patchy Alopecia:
• Alopecia areata.

• Tinea capitis (KOH+, scales).
• Moth-eaten alopecia (secondary syphilis, VDRL+).
• Trichotillomania

Patterned Alopecia

• Types: Male AGA, Female AGA.

• Mechanism:
• Testosterone converted to Dihydrotestosterone (DHT) by 5-alpha reductase.
• DHT converts terminal hair to vellus hair (soft, hypopigmented, miniaturized).
• Mnemonic: Villous hair is the Villain
• Culprit: 5-alpha reductase.

Patient Presentation:

• Usually adults.

Males:

• Pattern: Frontotemporal recession and vertex balding.

• Asymptomatic.

• No significant hair fall, but reduced density/visible scalp.

• Norwood Hamilton classification (starts frontotemporal, widens, balding).

Females:

• Pattern: Widening of central parting, loss of density.

• Stage 3: Almost Christmas tree / Fur tree pattern.

• Ludwig's pattern (type 1, 2, 3).

• Mnemonic: Ludwig → Ladies Wig → Alopecia

Treatment:

• Counselling (long-standing process).

• Topical Minoxidil + Anti-androgens = Drug of choice.

• Topical Minoxidil:
• 2% for females, 5% for males.
• Potassium channel opener; increases blood flow.

• Anti-androgens:
• Males: 5-alpha reductase inhibitors:
• Finasteride (specific 5-alpha reductase type 1 inhibitor).
• Dutasteride (inhibits both type 1 and 2).
• Females: Oral anti-androgens (Spironolactone, Cyproterone acetate).

• Severe cases:
• Surgical (hair transplantation).

• Nowadays:
• Platelet-rich plasma therapy (PRP).

Diffuse Alopecia: Effluvium

• Characterized by diffuse hair shedding (no pattern or patch).

• Disorder of hair cycle.

Two major phases:

• Anagen Effluvium
• Cause: Chemotherapy (inhibits actively dividing cells).
• 90% of anagen hair fall (global alopecia).

• Telogen Effluvium (TE)
• Acute or Chronic.

Chronic TE:

• Hypothyroidism

• anemia.

Acute TE

• Onset: 2-3 months after an insult.

• Insult: Any physical, emotional, or physiological stress.
1. Physical:
• Prolonged infection
• TB, chikungunya, COVID, CAD, stroke, hospitalization, typhoid
2. Emotional:
• Exam, loss of family member.
3. Physiological:
• Pregnancy.

• Mechanism:
• Body converts anagen hair prematurely to telogen phase
• reduces hair growth requirements

• Ratio Reversal:
• ~50% hair in telogen phase.

• Fall:
• Hair stays in telogen 2-3 months, then falls off.

• History:
• Insult followed by severe hair shedding 2-3 months later.

• Diagnosis: 
• Hair pull test positive.

• Treatment:
• Counselling (hair will go into anagen, regrow).
• Hair supplements (biotin).

Alopecia Areata

Patchy alopecia

• Called Pelade.

• Type: Autoimmune disorder.

• Associations: Hypothyroidism, pernicious anemia, Down syndrome.

• Patient Presentation:
• H/o Atopy
• Asymptomatic
• Smooth surface, no scaling, no itching.
• Single or multiple patches.
• Location: Scalp, eyebrows, beard area (any terminal hair).

• Grey hairs typically spared.
• Turning Grey Syndrome:
• All black hair falls off,
• only grey remains
  (immune process targets pigmented hair bulbs).

• Severe Forms:
• Alopecia totalis:
• Total scalp hair loss.
• Alopecia universalis:
• Total body hair loss.

• Specific Pattern:
• Ophiasis pattern:
• Band-like hair fall in the occipital area.

Diagnosis:

• Trichoscopy: 
• Exclamation mark hairs (periphery of patch).

• Histopathology:
• Intense lymphocytic infiltrate (swarm of bees appearance).

• Primarily a clinical diagnosis.

Associated Nail Changes:

• Pitting:
• Geometric pattern pitting of nails:
• Fine, superficial, regularly placed
• Contrast: Psoriatic pitting (deep, random, irregular).

• Trachyonychia:
• Longitudinal ridging and roughening of nail plate.

Treatment:

• Single, recent patch in child:
• May spontaneously resolve.

• Otherwise: 
• Intralesional steroids (treatment of choice).

• 6-8 patches: 
• Oral corticosteroids.

• Contact Immunotherapy:
• (Applied to patches to create irritant reaction, sparing hair).
• Agents:
• Dinitrochlorobenzene,
• Squaric acid dibutyl ester,
• DPCp (Diphencyprone).

• Recent drugs: 
• JAK kinase inhibitors 
• Tofacitinib,
• Baricitinib,
• Abrocitinib

• Other oral agents:
• Levamisole
• Cyclosporine
• Oral Minoxidil

Trichotillomania

• Trio = hair; Mania = maniac/psychiatric condition.

• Type:
• Psychiatric disorder;
• patient pulls out own hair.

• Falls under DSM-4 criteria.

• Patient denies/unaware; family observes.

• Pulls hair when thinking.

On Examination:

• Hairs of various lengths.

• History of psychiatric disturbance
• withdrawn, not socially active/intelligent

• Patchy alopecia
• not smooth, unlike alopecia areata

• Perifollicular hemorrhages (due to trauma).

• "Frier tux sign":



• Patchy alopecia with various hair lengths.

• Complications:
• Trichophagia,
• trichobezoar,
• GI obstruction.

• Skin Biopsy:
• Empty hair follicles,
• perifollicular hemosiderin deposition.

• Treatment:
• Cognitive Behavior Therapy (CBT).
• Psychiatric treatment:
• SSRIs (Paroxetine, N-acetylcysteine).

Scarring (Cicatricial) Alopecia

• Hair bulb is damaged.
• No hair regrowth (counsel patient).

• Mnemonic:
• Hair bulb broke (pseudopalede of broq) Like (Lichen planus) SLE (SLE)

Lichen Planus (follicular LP):

• Violaceous,

• itchy papules on periphery,

• leading to cicatricial alopecia.

Discoid Lupus Erythematosus (DLE):

• Scales,

• perifollicular erythema,

• leading to cicatricial alopecia.



• Remember:
• DLE → Cicatricial;
• Acute Cutaneous LE (ACLE) → Non-cicatricial.

Pseudopelade of Brocq:

• Idiopathic (cause unknown).

• Chronic, slowly progressive cicatricial alopecia.

• Biopsy: No inflammation, just patchy cicatricial alopecia.

• Sign: Patch resembles "footprints in snow".

Disorders of Hair Growth (Hirsutism)

Hirsutism:

• Hair growth in male pattern + Alopecia + Acne.

• Excessive hair growth in androgen-dependent areas in females.

• Conversion of vellus hair to terminal hair (opposite of AGA).

• Seen in: Increased Androgen.
• PCOS
• Congenital adrenal hyperplasias
• Virilizing tumors
• SAHA syndrome
• Idiopathic

• Androgens in Females
• Mild increase: Hirsutism.
• Excessive increase: Virilisation.

• Score: Ferriman-Gallwey scoring. ( ≥8 ).

• Rule out hyperandrogenism

• 1st line: 
• OCP: DOC.
• leading to ↓↓ Androgen,
• Use for 6 months
• If not relieved →
• Anti-androgens 
• Add Spironolactone + OCPs
• spironolactone is antiandrogenic → can affect external genitalia of a male fetus in case of conception → Hence OCPs are added in reproductive age group.

• Alternative:
• Flutamide.
• Finasteride.
• Ketoconazole.
• Cyproterone acetate.

• Topical: Eflornithine.

• Last resort: Continuous GnRH (decreased LH & FSH).

• Most important: 
• Laser hair reduction.
• Lasers:
• Diode
• long pulsed Nd:YAG laser.

• Mnemonic: Ocinu Ferriyil (Ferriman gellaway score) keetti → Spiral (Spironolactone) shape il odich → Flooril (Eflornithine) kidathi → Fine (Finasteride) Flute (Flutamide) keetti → Last continuous (Continuous GnRH) cheythu

Note

• Drug not used for hirsutism: Danazol (Causes hirsutism).

Female with Hirsutism:

• Check testosterone levels (Next step)



1. Normal: Idiopathic.
2. 70 - 200:
• PCOS.
• Late onset CAH.
3. ≥ 200:
• CAH.
• Androgen secreting tumour in ovaries.

• M/C cause of hirsutism in young:
• PCOS.

• M/C cause of rapid onset hirsutism in young females:
• Androgen secreting tumour of ovaries.

Other Miscell

Cutis Marmorata

• Infants.
• Marbled skin appearance.
• Physiological response to cold.
• Reverses on warming.
• Trunk.
• Extremities.

Lichen Nitidus

• Chronic inflammatory disease.

• Etiology:
• Unknown.

• Affected Children

• Key Feature:
• "Claw clutching the ball" appearance.
• Mnemonic: Clutching the ball at night (Nitidus)

• Components:



• Ball:
• Chronic inflammatory cell infiltrate.
• Claw:
• Rete ridges.

Trichothiodystrophy

 

• Genetics:
• Autosomal recessive

• Pathology:
• Abnormal sulfur-containing Keratins
• Leads to defective disulfide linkage
• Results in sparse & brittle hair

• PIBIDS
• (photosensitivity,
  ichthyosis, brittle hair,
  intellectual impairment,
  decreased fertility and
  short stature)

• Microscopy:
• Polarizing microscopy: Tiger tail appearance
• Alternating light/dark bands along hair shaft

• Mnemonic:
• Thio → Sulphate
• Thio → Tiger
• Dont confuse with trichorrhexis nodosa

Argininosuccinic Aciduria

Trichorrhexis nodosa (brittle hair)

• Enzyme deficient:
• Arginosuccinate lyase

• Also caused by
• Menke’s kinky hair
• Hypothyroidism
• Iron deficiency

• Mnemonic: Manka () was Iron () and thyroid deficent ()
• Urge (Arginosuccinate lyase) to pull hair

General Clinical Features

• Encephalopathy

• Respiratory alkalosis

• Tachypnoea

• Hyperammonemia + ↑ plasma glutamine

Neonates:

• feeding difficulties,

• failure to thrive,

• lethargy,

• convulsions, coma

NOTE: NETHERTON SYNDROME

• Netherland → Bamboo (Bamboo hair), Fish (Icthyosis), Spin (SPINK)

Dermatitis Artefacta

• Nature:
• Psychocutaneous disorder
• Self-induced

• Location:
• Accessible sites of the body

Meningococcemia

• Neisseria meningitidis

• Black central arch rashes

• Mnemonic: Nice black arch

Nail Disorders

Nail Structure

Nail Structure	Feature
Cuticle	Whitish area from proximal nail fold to nail plate.
Lunula	Semi-circular pinkish area at proximal nail.
Nail Bed	Beneath the nail plate.
Nail Matrix	• In proximal nail fold • forms the nail.

• Nail Plate

• Nail Folds

Important Disorders Associated with Nails

 

Trachyonychia

• Definition:
• Longitudinal ridging and roughening of the nail plate.

• Also Known As:
• “20-nail dystrophy” – all 20 nails can be affected.
• “Sand-blasted nails” – grey, roughened surface.

Causes of Trachyonychia

• Idiopathic

• Alopecia areata
• most common cause

• Lichen planus

• Typically occurs in children.

Treatment of Trachyonychia

• Children: Often self-resolving

• Topical options:
• Topical steroids
• Topical vitamin D analogues

• Adults:
• Oral or intramuscular corticosteroids (if needed)

Paronychia

• Definition: Inflammation of the nail folds.

Acute Paronychia

• Features:
• Pus accumulation
• Redness
• Swelling
• Tenderness and pain over the nail fold

• Cause: Bacterial infection of the nail fold.

Chronic Paronychia

• Common in:
• People involved in frequent wet work
• e.g., housewives, maids

• Pathogenesis:
• Repeated cuticle damage
• Recurrent inflammation
• Loss of cuticle

• Clinical Features:
• Swollen, red, itchy nail folds

Ingrown Toenail

• Cause: Improper nail cutting

• Pathogenesis: Nail grows inward into the lateral nail folds

• Features:
• Irritation
• Swelling
• Pain
• Crusting of lateral nail folds