9.2 - Introduction to Dermatology Part 2

Question 1

What are the functions of the hair?

Answer 1

• protection against external factors
• pilosebaceous unit produces sebum
• apocrine sweat
• thermoregulation
• social and sexual interaction
• reservoir epithelial and melanocyte stem cells

Question 2

What are the two types of hair we have and where?

Answer 2

• terminal hairs - scalp, eyebrows and eyelashes
• vellus hairs (thin and pale) - rest of body except palms, soles, mucosal regions of lips, and mucosal regions of external genitalia

Question 3

Describe the steps to the hair cycle

Answer 3

1. anagen (where new hair forms and grows) - lasts 2-6 years, 85% of hair is in this phase
2. catagen (regressing/shrinking phase) - lasts 3 weeks, 1% of hair
3. telogen (resting phase where blood supply to the hair is lost) - lasts 3 months, 10-15% of hair
4. then, hair is lost and cycle begins again

Question 4

What is the structure of the hair?

Answer 4

• human skin contains pilosebaceous follicles and sweat glands (next to each other)
• hair follicle (pilosebaceous unit) occupies a pocket of epithelium continuous with superficial epidermis, and envelopes a small papilla of dermis at the base
• holocrine sebaceous glands open up into the pilary canal –> in axillae = follicles associated with apocrine glands
• arrector pili (smooth muscle) extends at angle between surface of dermis and point in follicle wall

Question 5

What are the two portions of the hair follicle?

Answer 5

• infundibulum - uppermost portion of hair follicle extending from opening of sebaceous gland to surface of the skin
• isthmus - lower portion of upper part of hair follicle between opening of sebaceous gland and intrusion of arrector pili muscle - epithelial keratinisation begins with the lack of granular layer named ‘trichilemmal keratinisation’

Question 6

What does the bulge of the hair filament do?

Answer 6

• segment of the outer root sheath located at insertion of arrector pili
• hair follicle stem cells reside here
• they migrate down to generate new lower anagen hair follicle (enter bulb matrix, proliferate and undergo terminal differentiation to form hair shaft and inner root sheath)
• also migrate upwards (distally) to form sebaceous glands and to proliferate in response to wounding

Question 7

What does the bulb do?

Answer 7

Lowermost portion of the hair follicle, includes the follicular dermal papilla and the hair matrix

Question 8

What does the outer root sheath do?

Answer 8

Extends along from the hair bulb to the infundibulum, and epidermis serves as a reservoir of stem cells

Question 9

What does the inner sheath do?

Answer 9

• guides/shapes hair
• encloses follicular dermal papilla, mucopolysaccharide-rich strome, nerve fibre and capillary loop

Question 10

What are the functions of the nails?

Answer 10

• protection of underlying distal phalanx
• counterpressure effect to pulp - important for walking and tactile sensation
• increase dexterity/manipulation of small objects
• enhance sensory discrimination
• facilitate scratching or grooming (part of defence mechanisms to get rid of infestations/parasites)

Question 11

What is the structure of the nails?

Answer 11

• final product of proliferation and differentiation of nail matrix keratinocytes that have lost all organelles etc
• emerges from proximal nail fold
• grows at 1-3mm/month
• firmly attached to nail bed
• detaches at hyponychium
• lined laterally by lateral nail folds

Question 12

What is the nail matrix?

Answer 12

• produces nail plate
• lies under proximal nail fold, above bone of distal phalanx (to which it is connected by a tendon)
• lunula is the only visible portion
• nail matrix keratinocytes differentiate –> lose their nuclei and are strictly adherent - cytoplasm completely filled by hard keratins
• also contains melanocytes (but are inactive)

Question 13

What is psoriasis?

Answer 13

• chronic, immune-mediated disorder
• caused by polygenic predisposition combined with environmental triggers e.g. trauma, infections (like streptococcal throat infection), medications
• pathophysiology involves T cells and their interactions with dendritic cells, and cells involvement in innate immunity, including keratinocytes
• psoriatic arthritis is most common systemic manifestation

Question 14

Describe the pathophysiology of psoriasis?

Answer 14

• stressed keratinocytes release DNA/RNA which form complex with antimicrobial peptides (psoriasin) and induce cytokine production (TNF-a, IL-1 and IFN-a) which activate dermal dendritic cells (dDcs)
• dDcs migrate into lymph nodes –> promotes Th1, Th17, Th22 cell production –> chemokine release –> migration of inflammatory cells to dermis –> cytokine release –> keratinocyte proliferation –> psoriatic plaque

Question 15

What characterises the most common form of psoriasis?

Answer 15

Sharply demarcated, scaly, erythematous plaques

Question 16

What are the clinical features of psoriasis?

Answer 16

• keratin plaques on skin
• flexural psoriasis in genitalia where there’s no plaques as it is all rubbed away
• can get nail psoriasis as it affects nail matrix (signifies higher risk of psoriatic arthritis) - with nail psoriasis you can see pitting, onycholysis (lifting off nail bed) and salmon/oil stains due to this too, subungual hyperkeratosis
• psoriasis can lead to erythroderma
• guttate psoriasis = acne-like spots over body that look like teardrops

Question 17

What are common sites of psoriasis?

Answer 17

• scalp
• elbows
• knee
• nails
• hands
• feet
• trunk (including intergluteal fold)

Question 18

How do we manage psoriasis?

Answer 18

• treatment - therapeutic ladder
• secondary prevention - reducing alcohol intake and smoking
• comorbidities - you are at higher risk of coronary heart disease, inflammatory bowel disease, inflammation of liver - some med used to treat psoriasis also treats bowel disease

Question 19

What is the first step of the therapeutic ladder to treat psoriasis?

Answer 19

• topical therapies e.g. vitamin D analogues, topical corticosteroids, retinoids, tropical tacrolimus/pimecrolimus
• other first step therapies if >20% of body covered with psoriasis is phototherapy (causes T cell apoptosis) with narrowband UVB (safe as no increased risk of skin cancer) or PUVA (psoralen + UVA) - this goes deeper into skin than UVB so does increase skin cancer risk

Question 20

What are the second and third steps of the therapeutic ladder to treat psoriasis?

Answer 20

• systemic treatments that you take into system
• acitretin - oral retinoid, vitamin A analogue - helps bring order to differentiation of keratinocytes from deep to superficial (which psoriasis messes up)
• systemic immunosuppression - methotrexate (diverse anti-inflammatory effect) and ciclosporin (inhibits T cells)
• advanced therapies - PDE4 inhibitors (apremilast) which reduces TNF, biologics (injected monoclonal antibodies e.g. anti-TNF-a, anti-IL17, anti-IL23), JAK inhibitors which inhibit many cytokines

Question 21

What is atopic eczema?

Answer 21

• intensely pruritic (itchy) chronic inflammatory condition
• complex genetic disease with environmental influences
• typically begins during infancy or early childhood
• often associated with other ‘atopic’ disorders e.g. asthma, rhinoconjunctivitis

Question 22

How does atopic eczema present in kids vs adults?

Answer 22

• acute inflammation of cheeks, scalp and extensors in infants (infantile phase of atopic dermatitis: erythematous, oedematous papules and plaques)
• flexural (inner surface of limbs) inflammation and lichenification/thickening of skin due to scratching, in children / adults

Question 23

What types of eczema are there?

Answer 23

• eczema and dermatitis are the same thing
• atopic eczema
• seborrhoiec dermatitis
• venous stasis eczema
• allergic contact dermatitis
• irritant contact dermatitis

Question 24

What is the barrier defect in the pathophysiology of atopic eczema?

Answer 24

• filaggrin is a protein that binds and aggregates keratin fibres and intermediate filaments to form cellular scaffold in stratum corneum cells (mutated in those with atopic eczema)
• reduced extracellular lipids and impaired ceramide production
• increased transepidermal water loss (TWL) –> fissuring (cracking of skin) which can be very painful and affects QOL
• there is impaired protection against microbes and environmental allergens

Question 25

What is immune dysregulation in the pathophysiology of atopic eczema?

Answer 25

• since skin is abnormal, Staphylococcus aureus finds it hospitable
• Staphylococcus superantigens stimulate Th2 lymphocyte responses and subvert T regs
• eosinophils also get excited and play a role

Question 26

How is atopic eczema managed?

Answer 26

• lifestyle changes - stop using soap, use of emollients
• clinical nurse specialist involvement - topical application technique (apply moisturiser 3 times a day in a specific way), day treatment, habit reversal (learn to stop scratching themselves as this can lead to itch-scratch cycle)
• comorbidities - some eczema treatments also used for asthma
• patch testing - they may have an allergy which is aggravating eczema which is why it is not getting better
• biopsy - not usually done but sometimes e.g. nipple eczema not improving –> Paget’s disease (underlying breast cancer)

Question 27

What are first line treatments in the therapeutic ladder for eczema?

Answer 27

• topical corticosteroids (correct potency for correct site) which are anti-inflammatory
• topical tacrolimus (T cell inhibitor) / pimecrolimus
• counselling to learn how to apply as underuse –> poor adherence and overuse –> tachyphylaxis/adverse effects - amount to use measured by fingertip units
• phototherapy - narrowband UVB, PUVA (for hand dermatitis)

Question 28

What are the adverse effects of topical corticosteroids?

Answer 28

• rare - skin atrophy, folliculitis, exacerbation of acne and rosacea, infection
• very rare - perioral dermatitis, rebound syndrome (tachyphylaxis - less of a response over time to taking a drug), allergy
• extremely rare - hormone imbalance (suppression of hypothalamic-pituitary-adrenal axis), hirsutism

Question 29

What are the adverse effects of topical calcineurin inhibitors?

Answer 29

Burning sensation

Question 30

What are second line treatments in the therapeutic ladder for eczema?

Answer 30

• systemic immunosuppression - methotrexate, ciclosporin, azathioprine, mycophenolate mofetil
• advanced therapies - biologics (anti-IL-4a, anti-IL13), JAK inhibitors

Question 31

What is allergic contact dermatitis?

Answer 31

• allergic eczema e.g. to poison ivy, nickel in cheap jewellery, cobalt in shoes
• you can get allergic dermatitis with or without atopic eczema

Question 32

What is impetiginisation?

Answer 32

• a complication of eczema where you have superficial infection of eczema usually caused by Staphylococcus aureus or Streptococcus
• gold crust seen

Question 33

What is venous stasis eczema?

Answer 33

• swollen legs, keratinocytes do not adhere to each other anymore so barrier function is lost
• eczematous cascade occurs

Question 34

What is eczema herpeticum?

Answer 34

• emergency situation where HSV can rapidly spread (internally too) as eczema has caused immune dysregulation
• causes erosions (breaches in epidermis that do not go all the way through - if they did they would be ulcers) and are monomorphic when they all look the same size/shape
• should not misinterpret as eczema getting worse and intensify treatment with oral steroids - could make it worse