Intro To Dermatology 2

Question 1

What is psoriasis

Answer 1

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

Question 2

Describe the pathophysiology, and which Th bias does it have?

Answer 2

• Stressed keratinocytes release DNA/RNA which form complex with antimicrobial peptides (e.g. psoriasin) and induce cytokine production (TNF-alpha, IL-1 and IFN-alpha) which activate dermal dendritic cells (dDCs)
• dDCs migrate to lymph nodes → promotes Th1, 17 and 22 cell production → chemokine release → migration of inflammatory cells to dermis → cytokine release → keratinocyte proliferation → psoriatic plaque
• Th1 bias

Question 3

What features characterise the most common form of psoriasis?

Answer 3

Sharply demarcated, scaly, erythematous plaques

Question 4

Clinical features of psoriasis

Answer 4

Scaly Keratin plaques on skin
Form as The keratin differentiation process occurs so quickly due to increased kearatin proliferation that they do not differentiate correctly

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Not seen in flexural psoriasis as friction rubs it away where genetalia is

Question 5

What is the most common systemic manifestation of Psoriasis?

Answer 5

Psoriatic arthritis

Question 6

Treatment- what is the therapeutic ladder?

Answer 6

• First step- what does this include (2 things)?
  
  • topical therapies like vit D analogues, topical corticosteroids, retinoids, topical tacrolimus/pimecrolimus
  • Phototherapy, what is it and what does it do (in a 4 word VSAQ response)?Induces T-Cell apoptosiswith 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
• Second and third step- what does this include? (3 things)
• Acitretin- oral retinoid- a vitamin A analogue- helps brings order to differentiation of keratinocytes from deep to superficial (which psoriasis messes up)
• Systemic immunosuppression- methotrexate (has diverse anti-inflammatory effect) and ciclosporin (inhibits T cells)
• Advanced therapies- PDE4 inhibitors (apremilast) which reduces TNF, Biologics (injected monoclonal antibodies: anti-TNF-alpha, anti-IL17, anti-IL23), JAK inhibitors which inhibit many cytokines

Question 7

What is atopic eczema?

Answer 7

• Intensely pruritic (itchy) chronic inflammatory condition
• Complex genetic disease with environmental triggers
• Typically begins during infancy or early childhood

Question 8

• What are some of the other atopic disorders associated with atopic eczema (3)?

Answer 8

Rhinoconjunctivitis

Hay Fever

Asthma

Question 9

Give one word used to describe the thickening of skin due to scratching

Answer 9

lichenification

Question 10

How and where does it present in kids vs adults? (clinical features

Answer 10

Acute inflammation of cheeks, scalp and extensors in infants (infantile phase atopic dermatitis: erythematous, oedematous papules and plaques)

Flexural (inner surface of limbs) inflammation and lichenification (thickening of skin due to scratching) in children and adults

Question 11

What types of eczema are there?

Answer 11

• Eczema and dermatitis are the same thing
• atopic eczema is one type of eczema and others are seborrhoiec dermatitis, venous stasis eczema, allergic contact dermatitis, irritant contact dermatitis

Question 12

• Describe the pathophysiology of atopic eczema
  -

Answer 12

• filaggrin is protein that binds and aggregates keratin bundles and intermediate filaments to form cellular scaffold in stratum corneum cells (this is mutated in atopic eczema people): mutation in filaggrin
• This means reduced extracellular lipids and impaired ceramide productionCeramide locks moisture into your skin and without this, there is a net effect of Transepidermal Water Loss (TEWL)
• There’s more transepidermal water loss (TEWL)- what clinical feature does this lead to?Fissuring- cracking of skin- can be very painful and affects quality of life

Question 13

There’s immune dysregulation-

Answer 13

• Since skin is abnormal, Staphylococcus aureus finds it hospitable
• Staphylococcus superantigens stimulate Th2 lymphocyte responses and subvert Tregs
• Eosinophils also get excited and play a role
• Th2 bias

Question 14

Describe the management of atopic eczema

Answer 14

• Lifestyle choices
  
  • Stop using soap
  • Use of emollients
  • Habit reversal- learn to stop scratching themselves as this can lead to itch-scratch cycle
  • Apply moisturiser 3 times a day and in a specific way (not rubbing vigorously on skin) which clinical nurse specialist can help with
• Comorbidities- some eczema treatments are also used for asthma

Question 15

Why might patch testing be used to manage atopic eczema?

Answer 15

Patch testing is used to detect allergies

These allergies could be what is aggrevating the eczema if treatment is not working on the eczema

Question 16

If someone who has nipple eczema is not responding to treatment, why would you take a biopsy

Answer 16

Paget’s disease of the nipple is associated with underlying breast cancer which looks exactly the same as nipple eczema

Question 17

What is the therapeutic ladder for eczema?

Answer 17

• First line treatments
  
  • Topical corticosteroids (correct potency for correct site) which are anti-inflammatory, topical tacrolimus (t cell inhibitor)/pimecrolimus- counselling to learn how to apply it as underuse leads to poor adherence and overuse leads to tachyphylaxis/adverse effects- amount to use measured by fingertip units
    
    • What are the adverse effects of topical corticosteroids?
      
      • Rare- skin atrophy, folliculitis, exacerbation of acne and rosacea, infection
      • Very rare- perioral dermatitis (dermatitis around mouth), rebound syndrome (tachyphylaxis- less of a response over time of taking a drug), allergy (to steroid itself or vehicle)
      • Extremely rare- hormonal imbalance (suppression of hypothalamic-pituitary-adrenal axis), hirsuitism
    • What are the adverse effects of topical calcineurin inhibitors?Burning sensation
    • What is the amount of topical corticosteroids to use measured by? (3 word VSAQ)Fingertip units (FTU)
    • TABLE OF LEAST TO MOST POTENT STEROID LADDERLeast to most potent:
      • Hydrocortisone
      • Clobetasone (Eumovate)
      • Betamethasone (Betnovate)
      • Mometasone (Elocon)
      • Clobetasol (Dermovate)
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    • Which steroid is the least potent? (1 word VSAQ)Hydrocortisone
    • Which steroid is the most potent? (1 word VSAQ)Clobetasol
  • Phototherapy- narrowband UVB, PUVA (for hand dermatitis)
• Second line treatments

Question 18

What is allergic contact dermatitis?

Answer 18

Allergic eczema e.g. to poison ivy, nickel in cheap jewellery, cobalt in shoes

Question 19

What is impetiginisation (which bacteria is it usually caused by)?

Answer 19

A complication of eczema where you have superficial infection of eczema usually caused by Staphylococcus aureus or Streptococcus

Gold crust

Question 20

• What is venous stasis eczema?
  -

Answer 20

• When you get swollen legs, keratinocytes don’t adhere to each other anymore so barrier function is lost
• Eczematous cascade happens

Question 21

What is eczema herpeticum?

Answer 21

• Emergency situation where (life-threatening) HSV (herpes simplex virus) can rapidly spread (can spread internally too) as eczema has caused immune dysregulation
• Causes erosions (breaches in epidermis that don’t go all the way through (if they did they would be ulcers) and are monomorphic when they all look the same size, shape
• Shouldn’t misinterpret it as eczema getting worse and intensify treatment with oral steroids because this could make it worse
• Bottom kid could potentially go blind without treatment