Aetiology of skin conditions - other skin lecture is more important this one don't need to know in too much detail

How long is cell turnover?

28 days - longer cycles as you age

What are the layers of the Skin structure and what seperates these layers

• Epidermis: thin tough outer layer, prevents loss of water and body fluids and acts as protective layer, thickness depends on part of the body

• Dermis - elastic tissue, where collagen, elastin and fibrinogen are = flexibility and stretch of skin, decompromises as you get older. Also contains nerve ending s

• Subcutaneous tissue - Fatty layer that insulates body and acts as padding and energy storage

How long is cell turnover?

28 days - longer cycles as you age

What are the layers of the Skin structure and what seperates these layers

• Epidermis: thin tough outer layer, prevents loss of water and body fluids and acts as protective layer, thickness depends on part of the body

• Dermis - elastic tissue, where collagen, elastin and fibrinogen are = flexibility and stretch of skin, decompromises as you get older. Also contains nerve ending s

• Subcutaneous tissue - Fatty layer that insulates body and acts as padding and energy storage

What is Psoriasis?

• Chronic inflammatory skin disease

• Increased epidermal cell turnover = thickening and scaling

• Inflammatory cell infiltration

• Relapsing / remitting

Note : affects men and women the same

BIG HINT THIS PART WILL BE IN THE EXAM AS A CASE QUESTION: What is the cause of Psoriasis?

• T-cells (Th1 & Th17) become overactive due to faulty signaling of Immune mediated antigen

• These T-cells release inflammatory cytokines (IL-17, IL-23, TNF-α).

• These cytokines accelerate skin cell growth (keratinocyte hyperproliferation). Epidermal hyper proliferation

• Normally, skin cells replace every 28-30 days—in psoriasis, this happens in 3-4 days, leading to thick, scaly plaques.

—

Trigger (e.g., stress, infection, trauma) →

• Immune mediated antigen →

• T cell activation →

• Release of inflammatory cytokines (e.g. IL 23 or 17 etc.) - these are updriven in psoriasis →

• Epidermal hyper proliferation

• = Plaques

—

Genetic factor also

What else can trigger Psoriasis (what are the precipitating factors)?

• Injuries such as cuts, abrasions, sunburn

• Streptococcal infection

• Hormonal events – often improves during pregnancy and relapses in the postpartum period

• Sunlight – usually improves but 10% will get worse

• Drugs (beta-blockers, lithium, NSAIDS, antimalarials, withdrawal of systemic steroids) - KEY FOR THE EXAM!!!!!

• Alcohol

• Smoking

• Stress

• Obesity

What area the different types of Psoriasis ?

CHRONIC PLAQUE PSORIASIS: - MAIN ONE

• Plaque = thickened/raised patch > 2 cm across

• Red plaques – well defined edge covered with silvery scales

• Plaques can be any size

• Scale = flakes of stratum corneum, accumulate or shed

• Can affect any area (usually scalp, kness/shins, outside of elbows, lower back)

• Plaques can crack and bleed – scratching/removing scales → pinpoint bleeding

• Usually symmetrical in distribution across the body

GUTTATE PSORIASIS (drop like):

• Acute

• Children and young adults usually

• Often after a streptococcal throat infection

• Multiple, small, pink, scaly drop-like plaques over trunk + limbs

FLEXURAL PSORIASIS:

• Affects skin folds e.g. armpits, groin, under breasts

• Shiny and moist

• Prone to secondary infection

What is the difference between eczema and dermatitis ?

• Eczema is endogenously caused [Internal factors (genetics, immune dysfunction, skin barrier defects)]

• Dermatitis is cause by exogenous factors e.g. allergic or irritant contact dermatitis

What is eczema and what is it caused by ?

• Impaired barrier function of skin

• Dry, itchy, cracked skin (due to impaired barrier function).

• Redness, swelling, and recurrent flares (acute: oozing; chronic: thickened skin).

• Commonly affects flexures (e.g., elbows, knees) in children, but can occur anywhere.

1. Genetic Factor: Filaggrin (FLG) Mutation

• Filaggrin is a protein crucial for:

  • Binding keratinocytes (skin cells) together.

  • Producing natural moisturizing factor (NMF) to retain water.

• FLG mutations → weak skin barrier →:

  • Transepidermal water loss (dry, cracked skin).

  • Easier penetration of irritants/allergens (soap, pollen, microbes).

2. Immune System Overreaction

• Allergens/irritants trigger Th2 immune response → release of IL-4, IL-13, IL-31 (cause itching/inflammation).

• Chronic inflammation → skin thickening (lichenification).

Can be acute or chronic

What is atopic eczema ?

• A genetic tendency to develop allergic diseases

• Genetic factors involved – 70% have family history of eczema/ asthma/ hay-fever/ urticaria

• e.g. eczema - affects children mostly

• Suggested due to immature immune system and high IgE levels (also in asthma)

• Asymmetrical appearance

• Red skin, scratched bleeding

Precipitating factors:

- Dry skin

- Stress

- Extremes of temperature

- Infection

What is allergic contact dermatitis??

• Allergy to usually harmless substances that have been in contact with the skin

• E.g. nickel, components of creams/ointments, fragrances, rubber gloves, plants

• Cause: Activation of T-cells → release of cytokines

• Visible in 48 / 96 hours after contact with allergen

• Patch testing can be useful in patients

Questions to ask patient with suspected allergic contact dermatitis

area affected

timing

exposure?

What is irritant contact dermatitis?

• Caused by Chemical / Mechanical irritation of the skin

• E.g. detergents, abrasives, water

• Irritants remove oils and lipids from stratum corneum → deeper penetration of irritant → triggers inflammation

• No allergy involved

What do irritants do ?

Irritants remove oils and lipids from stratum corneum → deeper penetration of irritant → triggers inflammation

What is acne ?

• Inflammation of the sebaceous glands in the skin

• Usually affects face/back/chest where sebaceous glands most numerous and active

How do we assess severity of acne ?

• Mild = non-inflam, <20 comedones

• Severe = extensive nodular cysts, scarring, >125 lesions

What are the types of acne and their symptoms?

Symptoms of acne in general:

• Greasiness

• Comedone formation

Blackheads:

•Small open follicular papules containing a central black keratin plug

•Pigmenation from oxidised melanin (not dirt)

Whiteheads:

• Small closed follicular papules

• no visible central keratin plug

Pathogenesis of Acne

• Driven by sebaceous glands

• Bigger sebaceous glands can cause an increased activity by androgens (hormones) that effect the formation of comodones as more sebum is being produced

• Keratin plugs stop the outflow of the sebum produced by the sebaceous glands = build up of sebum comodone formation