9.2 - Introduction to Dermatology Part 2 Flashcards
1
Q
What are the functions of the hair?
A
- protection against external factors
- pilosebaceous unit produces sebum
- apocrine sweat
- thermoregulation
- social and sexual interaction
- reservoir epithelial and melanocyte stem cells
2
Q
What are the two types of hair we have and where?
A
- 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
3
Q
Describe the steps to the hair cycle
A
- anagen (where new hair forms and grows) - lasts 2-6 years, 85% of hair is in this phase
- catagen (regressing/shrinking phase) - lasts 3 weeks, 1% of hair
- telogen (resting phase where blood supply to the hair is lost) - lasts 3 months, 10-15% of hair
- then, hair is lost and cycle begins again
4
Q
What is the structure of the hair?
A
- 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
5
Q
What are the two portions of the hair follicle?
A
- 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’
6
Q
What does the bulge of the hair filament do?
A
- 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
7
Q
What does the bulb do?
A
Lowermost portion of the hair follicle, includes the follicular dermal papilla and the hair matrix
8
Q
What does the outer root sheath do?
A
Extends along from the hair bulb to the infundibulum, and epidermis serves as a reservoir of stem cells
9
Q
What does the inner sheath do?
A
- guides/shapes hair
- encloses follicular dermal papilla, mucopolysaccharide-rich strome, nerve fibre and capillary loop
10
Q
What are the functions of the nails?
A
- 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)
11
Q
What is the structure of the nails?
A
- 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
12
Q
What is the nail matrix?
A
- 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)
13
Q
What is psoriasis?
A
- 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
14
Q
Describe the pathophysiology of psoriasis?
A
- 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
15
Q
What characterises the most common form of psoriasis?
A
Sharply demarcated, scaly, erythematous plaques
16
Q
What are the clinical features of psoriasis?
A
- 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
17
Q
What are common sites of psoriasis?
A
- scalp
- elbows
- knee
- nails
- hands
- feet
- trunk (including intergluteal fold)
18
Q
How do we manage psoriasis?
A
- 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
19
Q
What is the first step of the therapeutic ladder to treat psoriasis?
A
- 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
20
Q
What are the second and third steps of the therapeutic ladder to treat psoriasis?
A
- 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
21
Q
What is atopic eczema?
A
- 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
22
Q
How does atopic eczema present in kids vs adults?
A
- 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
23
Q
What types of eczema are there?
A
- eczema and dermatitis are the same thing
- atopic eczema
- seborrhoiec dermatitis
- venous stasis eczema
- allergic contact dermatitis
- irritant contact dermatitis
24
Q
What is the barrier defect in the pathophysiology of atopic eczema?
A
- 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
25
Q
What is immune dysregulation in the pathophysiology of atopic eczema?
A
- 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
26
Q
How is atopic eczema managed?
A
- 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)
27
Q
What are first line treatments in the therapeutic ladder for eczema?
A
- 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)
28
Q
What are the adverse effects of topical corticosteroids?
A
- 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
29
Q
What are the adverse effects of topical calcineurin inhibitors?
A
Burning sensation
30
Q
What are second line treatments in the therapeutic ladder for eczema?
A
- systemic immunosuppression - methotrexate, ciclosporin, azathioprine, mycophenolate mofetil
- advanced therapies - biologics (anti-IL-4a, anti-IL13), JAK inhibitors
31
Q
What is allergic contact dermatitis?
A
- allergic eczema e.g. to poison ivy, nickel in cheap jewellery, cobalt in shoes
- you can get allergic dermatitis with or without atopic eczema
32
Q
What is impetiginisation?
A
- a complication of eczema where you have superficial infection of eczema usually caused by Staphylococcus aureus or Streptococcus
- gold crust seen
33
Q
What is venous stasis eczema?
A
- swollen legs, keratinocytes do not adhere to each other anymore so barrier function is lost
- eczematous cascade occurs
34
Q
What is eczema herpeticum?
A
- 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
