Decoding Hair: Structure, Function, & Disorders

Hair disorders range from the most common Alopecia to rare conditions like Monilethrix. Hair disorders are a crucial part of Dermatology paper.

Read this blog post thoroughly to ace master a key topic of the Dermatology paper and ace your NEET PG preparation. 

Let’s begin. 

• Integumentary system is composed of 
  • Skin
  • Appendages 
• Appendages composed of
  • Hair
  • Nails
  • Different glands. 

Structure of Hair 

• Hair bulb
  • Present at the root of hair
• epidermis and sebaceous gland 
  • present at the level of hair follicle . Arrector Pili Muscle, present below the attachment of sebaceous follicles.  It attaches from the hair follicle from one end and the lower part of the epidermis at the other end. 
• Based on their attachment, hair follicle gets divided into two parts: 
  • Upper - Hair strand part
  • Lower - determines the type of hair. 
  • Lower part keeps changing. 
• Upper part: (two parts based on the attachment of sebaceous glands) 
  • Infundibulum: Above the attachment of sebaceous glands 
  • Isthmus: Below the attachment of sebaceous gland 
• Lower part
  • Bulb region
  • Supra bulbar region. 
• Stem cells are located at supra bulbar region. This region is also known as Bulge. 
• Cicatricial alopecia
  • Anything that causes damage to outer root sheath will cause alopecia and where the hair will not grow back is cicatricial alopecia 
• Non cicatricial alopecia 
  • Here, hair will grow back because stem cells are not damaged.

Hair, transverse section of hair root

• Cross section of hair: layers are as follow
  • Medulla - inner most layer
  • Cortex  
  • Cuticle (part of inner root sheath) and on the outside, there is outer root sheath. 
  • The inner root sheath has three parts: 
    • Henley's layer
    • Huxley's layer
    • Cuticle, cortex, and medulla. 
    • Mnemonic - hens hugs cute chicken mom's

Medullary index

• The thicker the hair, the thicker the medulla will be. Animal hairs will be thicker than human hairs.   Medullary index = Diameter of medulla / diameter of whole shaft. Humans: medullary index < 1/3. Animals: medullary index > 1/2. Adamson's fringe is just around the bulge, this area is known as keratogenous zone. It differentiates between the keratogenous and non keratogenous parts. Dermatophytes are keratinophilic, so dermatophytes will not enter this area because this will be limited by Adamson’s fringe that marks the end of the keratogenous zone of the hair follicle. 

Types of hair

• Three types of hair
  • Lanugo hair
  • Vellus hair
  • Terminal hair

Lanugo hair

• Seen in premature baby, Soft non, medullated - thin, 
• Unpigmented hair
• In utero
• Premature babies 

Vellus hair

• Hair on the face, forehead
• Soft 
• non medullated
• Less pigmented 
• < 2cm long 
• Till adolescent 

Terminal hair 

• Coarser
• Hair on bearded area, pubic area
• medullated
• Pigmented
• Longer
• Present in androgen-dependent areas because it has hormones. 

Hair Cycle 

• Growth phase is followed by the transition phase which is followed by the falling phase. This is the continuous cycle of growth. 
• Growth phase - Anagen hair
• Transition phase – Catagen hair
• Falling phase – Telogen hair
• When entering the Telogen phase, the club root shape is formed. When hair shades off, it will go again to anagen stage. 

• That is why we have 50-100 hairs falling per day.
• Anagen: Telogen = 9:1 
• Hair growth rate: 1cm/month

Hair Disorders

• Loss of hair - Alopecia
• Excessive hair growth

Tests for hair

• Hair pull test - 
  • Pull hair and see how many hairs are coming. If it is more than 6, it is insignificant
• Trichogram 
  • Pull and take out certain hair and mount it to count no of anagen and telogen based on the hair bulb
• Trichoscan 
  • Like dermoscope. Computer based program where one can see hair growth in magnified form
• Scalp biopsy
  • Helps us to know different disorders. 

Alopecia 

• Stem cells
  • When stem cells are affected, one gets Cicatricial/scarring area.  Here, the hair does not come back.  If stem cells are not damaged, one can get hair. 
• Non Cicatricial/ non scarring 

• Also known as Non Cicatricial alopecia 
• Patterned -
  • Androgenetic Alopecia
• Diffuse -
  • Effluvium
• Patchy -
  • Alopecia 
  • Areata
  • Trichotillomania
  • Tinea capitis 
  • moth eaten alopecia

Androgenetic Alopecia

• Dependent on androgen. In males - male patterned hair loss . In female - female patterned hair loss. These are non-genetic.  Genetic susceptibility: polygenic inheritance 

• Testosterone converts to dihydrotestosterone
  • The enzyme used is 5 alpha-reductase.
  • reduces the anagen phase
  • hair becomes short and causes miniaturisation of hair. 
• So, terminal hair is converting into vellus hair now.  In males, bitemporal recession happens - from temple and vertex balding happens.  If they progress, they will get little hair while keeping the vertex empty. 
• This is male Androgenetic Alopecia
  • The vertex has no hair. But little fringe of hair is present around the side because this area is occipital, which is not androgen dependent.  Graded into I to VII sections and is given by Norwood- Hamilton
• In female patterned hair loss:  Widening of central parting. 
• There are three divisions of female Alopecia. 
  • Type I
  • Type II 
  • Type III
• This pattern was given by Ludwig. Grade III looks like an air tree / Christmas tree pattern in females. 

Management of these patient: 

• Counselling - it requires long period treatment. 
• Topical management
  • Minoxidil
  • Potassium channel opener
  • It causes Vasodilation (increase in blood flow of scalpy)
• 2% Minoxidil - female pattern hair loss
• 5-10% Minoxidil - male pattern hair loss 
• Side effects of Minoxidil: 
  • Contact Dermatitis 
  • Headache
• This is FDA approved treatment. 
• Systemic management 
  • Finasteride - 5 alpha reductase inhibitor - type 1 & 2 given 1 mg/day
  • Dutasteride - type 1 & 2 inhibitor. Dose 0.5 mg/day
• For females 
  • Oral anti-androgens, which can be cyproterone acetate, spironolactone, and flutamide. 
• Surgical management: 
  • Hair transplantation. Transplant hair from occipital area because it is not androgen dependent
  • When transplantation from the donor area, it retains the quality of the donor area. So if it is androgen dependent, it will remain androgen dependent. 

Effluvium

• Diffused hair fall
• If Effluvium affects anagen - Anagen Effluvium 
• If Effluvium affects telogen - Telogen Effluvium
• When a patient is given Chemotherapy.  Chemotherapy acts against all the mitotically active cells.  So, in the hair, it will act against anagen and thus patient losses all the hair.  When all the hair is gone - anagen Effluvium
• Telogen Effluvium
  • Physical stress in the form of surgery, trauma, or prolonged illness.  Prolonged illness can be Dengue, malaria, Covid, TB, chikungunya, pregnancy. When it happens in pregnancy, we call it Telogen gravidarum.  So, when stressed, Anagen prematurely converts into Telogen.  Hair in the telogen phase stays for three months and then hair fall happens. 
• Chronic TE: 
  • Iron deficiency, thyroid, crash diet or malnutrition. If repeated insults, patients will face hair fall for many years.  Then, there will be subsequent thinning of the ponytail. 

Dermatology Related Articles:

Alopecia Areata

• It is a patchy kind of hair fall . It is a non-cicatricial alopecia. It is an autoimmune T-cell mediated disorder where the T-cell acts against hair follicles. 

Association 

• Other autoimmune disorder
  • Type 1 DM
  • Thyroid disorders 
  • Pernicious anemia 
• There are certain HLA association too 

• The Anagen are being targeted. T cell starts acting against the anagen hair root.  The hair compensates and converts the anagen hair into the telogen hair.  The telogen hair falls and goes back to the anagen hair.  This happens repeatedly, and eventually, the person is left with a bald patch.
• Single or multiple patches of hair loss are seen in this condition
  • These patches are smooth. No scaling, and no itching, no redness and are well defined. Also called Pelade 
• Inflammation affects the pigment in the hair and does not affect the grey area
  • The person will keep on losing hair. But the grey hair will stay there.  All the grey hairs are retained in a person suffering from Alopecia Areata.  It is called Turning grey syndrome  Alopecia Areata does not affect grey hair.  
•  It is asymptomatic. 

Exclamation mark hair

Recreate this image or confirm its presence 

• Broken hair present on the periphery of the lesion.
  • These hairs will appear tapering down and with a little bulbar area below.  These exclamation mark hairs are seen on the periphery of the patches of Alopecia Areata. 
• Variants: 
  • Complete hair loss from all over the body - Alopecia Universalis . Complete hair loss over scalp - Alopecia Totalis. Band of Alopecia Areata occurs called Ophiasis pattern and forms an O on the scalp.  In Sisaipho, only an occipital band is left, and all the hair is gone. 
• Sometimes the Alopecia Areata does not affect the scalp and may have associated involvement with 
  • Eyebrows 
  • Eyelashes 
  • Beard area  
• Nail findings in the patients of Alopecia Areata (AA)
  • Pits
    • In psoriasis pits were deep random, and irregular. Here the pits are superficial, geometric and they are not random (regular)
  • Longitudinal ridging or Trachyonychia - all 20 nails may be affected. 
• In 80 per cent of cases AA spontaneously resolves. 

Differential diagnosis 

• Tinea capitis 
  • Also present with non-cicatricial, patchy hair fall, non-scarring alopecia, broken off hair - This is common. Scaling, itching, KOH positive (absent in alopecia areata)
  • It does not have exclamation mark hair. 
• Moth eaten alopecia
  • Associated with syphilis in the secondary stage . It will not be a standalone finding, and the patient will have other symptoms including VDRL positive 
• Trichotillomania 

Treatment

• Spontaneous resolution is an option 

Topical treatment 

• Corticosteroids. But the better method is giving it intralesional - Intralesional steroids (ILS) is the treatment of choice. Triamcinolone or kenacort of the strength 10 mg/ml dilute it 1:4 or 1:2 and it is injected intradermally in the Alopecia Areata. 
• Contact immunotherapy 
  • Like simulating a contact irritant reaction
  • Three agents are used
    • Di nitro chlorobenzene 
    • Squaric acid dibutyl ester 
    • Diphencyprone 
  • A little concentration is applied on the patch, and these agents act as contact irritants which generate an irritant reaction and divert the T cells here, and they free the hair follicle, and they improve.

Oral agents 

• Systemic therapy - for extensive alopecia areata 
  • Levamisole 
  • Cyclosporine 
  • Oral mini pulse therapy - Betamethasone or methylprednisolone given twice a week to minimise the side effect. 
• JAK kinase inhibitor called tofacitinib is a new agent increasingly being used. 

Trichotillomania

• It is Differential Diagnosis of alopecia. It is a psychiatric disorder and OCD of pulling hair.  It is classified into DSM 4 criteria. History will not be given by patients, some others will give hints about psychiatric issues. . Often seen in adolescence or young adults. 
• Site: 
  • Happens on an accessible site which can be fronto parietal area. Patchy hair loss.  This patchy hair loss will be broken hairs of variable lengths. Happens on the dominant part of the scalp. 
• Sometimes, because of the trauma, one may see perifollicular haemorrhages. Patients may also eat hairs which leads to trichophagia or trichobezoar obstruction.  It is also called the sign-friar tuck sign. 
• On skin biopsy
  • Empty cast, p/f hemosiderin 
• Treatment: 
  • Cognitive behavioural therapy (CBT) 
  • Antipsychotic Medicines like SSRI, paroxetine, or NAC - N-acetyl cysteine. 

Cicatricial or scarring alopecia

• Damaged Stem cells
  • Leads to permanent hair loss. 
  • The area will look scarred.
• Counselling for patient
  • The purpose of counselling would be to avoid new patches of hair loss. 
• Role of scalp biopsy 
  • To know what kind of infiltrate it is and how deep it is to provide treatment to the patient. 

Follicular LP

• It is called Lichen Plano pilaris. It is affecting the hair or follicular lichen planer. There will be violaceous lesions and plaques, present in the perifollicular distribution. Itching, scaling present. A patch of cicatricial alopecia will be left behind.

Lupus erythematosus 

• Another cause of cicatricial alopecia. SLE or ACLE causes non scarring alopecia. DLE/ chronic cutaneous LE causes scarring alopecia
  • Scarred patches of alopecia which are associated with scaling and follicular plugging and can be seen on scalp.

Pseudopelade of BROCQ

• Smooth patches due to scarring alopecia.  It is an idiopathic condition, no inflammation, no scaling, no erythema present in the biopsy report. The only thing visible is patches of cicatricial alopecia which is spreading.
  • Footprint in snow appearance
• It is chronic and slowly progressive.

Folliculitis Decalvans / Tufted Folliculitis 

• Neutrophil disorders that can lead to Cicatricial alopecia. Kind of deep folliculitis caused by bacteria. Pustules are found which go deep and damage the stem cells and cause scarring alopecia.  Hair tufts are formed. It heals with boggy scars.
• Treatment - antibiotics 

Dissecting cellulitis

• Deep folliculitis. Causes cicatricial alopecia.
• This is a part of a triad - follicular occlusion has three features.
  • Dissecting cellulitis of the scalp
  • Acne conglobata 
  • Hidradenitis suppurativa

Traction Alopecia 

• Because of traction there is excess force applied on the hair follicle, leading them to causing Traction Alopecia . It is a hairstyle disorder. Hair is damaged due to constant pressure of force applied to them.

Excessive Hair Growth

• Hypertrichosis - if it happens on the body.
  • Seen commonly congenitally over the knee. Can be seen with use of topical steroid.
• Hirsutism - when hair growth happens on androgen dependent areas. 

Hirsutism

• Growth of unwanted hair on androgen dependent sites . Female - growth of terminal hair in beard area. Feature of female. Vellus hair is converted to terminal hair

Causes 

• Androgens are being produced by two sources.
  • Ovaries 
  • Adrenals 
• If there is PCOS or ovarian tumour or any cause which is stimulating the ovaries one can have Hyperandrogenism. 
• Adrenal glands produce more androgen if there is 

• Congenital adrenal hyperplasia (CAH) 
• Virilizing tumours 

• Sometimes there is idiopathic and no symptoms are found and perfect androgen levels. 
• SAHA syndrome has four components 

• Seborrhoea
• Acne 
• Hirsutism 
• AGA 

• There is a scoring which has been given by Ferriman and Galway 

Investigation 

• PCOS - LH, FSH, DHEAS
• Adrenals - Level of 5 DHT is seen, look for thyroid, look for prolactin . All these hormonal tests are done in a patient of Hirsutism to rule out the cause of Hyperandrogenism. 

Treatment 

• Topical agent - Eflornithine
• Not very effective 
• Antiandrogen 

• Spironolactone 
• OCP’s - if patient has PCOS
• Dutasteride
• Flutamide 
• Cyproterone acetate
• Physical 
• Hair removal lasers
  • Diode and long pulse ND Yag. 

And that is everything you need to know about Hair disorders for Dermatology preparation. For more interesting and informative blog posts like this, download the PrepLadder App and keep following our blog!