5: Inflammatory Dermatoses

Question 1

Explain the differentiation of keratinocytes

Answer 1

Basal cell -> Prickle cell -> Granular cell -> Keratin (barrier)

Question 2

Atopic eczema

Answer 2

Atopy = tendency to develop hypersensitivity
Atopic eczema is common, relapsing and remitting
Filagrin gene commonly mutated, important for holding keratinocytes together in epidermal layer of skin

Defect in skin barrier allows penetration of exogenous agents (allergens, Staph Aureus, irritants)
Taken up by APCs, activates Th2 type immune response
Produces IgE antibodies that stimulate mast cell degranulation (release of histamine) -> inflammation

Usually occurs at flexual areas of skin

Question 3

What is the atopic march?

Answer 3

1. Within 3 months of age you tend to develop eczema FIRST
2. Food allergies (also peaks around 1yr)
3. Astham (peaks around 5yrs)
4. Rhinitis (peaks around 9-10yrs)

Question 4

Signs of filagrin gene mutation?

Answer 4

Palmar hyperlinearity

Lines are more visible

Question 5

Chronic changes in eczema?

Answer 5

Skin become less red
Lichenification - skin markings become more visible due to chronic rubbing/scratching
Results in thicker leathery skin

Question 6

What is severe eczema?

Answer 6

Erythrodermic eczema
Redness over whole skin surface
Systemically unwell
Should be admitted to hospital

Question 7

What is eczema herpeticum

Answer 7

Herpes virus can infiltrate skin as well

Spreads around skin forming ulcers

Question 8

Other types of eczema?

Answer 8

Seborrhoeic - overgrowth of yeast
Allergic contact dermititis - allergy to skin products (could be medications)
Discoid

Question 9

Pathophysiology of Psoriasis

Answer 9

Number of genes give susceptibility to psoriasis
Environmental trigger causes immune response
Resulting in psoriasis
T-cells in dermis release cytokines
Neutrophils go to epidermis -> overproduction of keratinocytes -> thickening of epidermis
Scaling of outermost layer of skin

Question 10

Histology of psoriasis

Answer 10

Hyperkeratosis
Parakeratosis - retention of nuclei in stratum corneum
Acanthosis
Inflammation
Dilated blood vessels

Question 11

Histology of psoriasis

Answer 11

Hyperkeratosis
Parakeratosis - retention of nuclei in stratum corneum
Acanthosis (thickening of skin)
Inflammation
Dilated blood vessels

Question 12

Presentation of psoriasis

Answer 12

Commonly in places of trauma: scalp, outside of elbows/knees (eczema is INSIDE), feet soles
Scaly plaques
SYMMETRICAL

Question 13

Types of psoriasis

Answer 13

Psoriasis soles (on the sole of feet)
Nail psoriasis - subungual hyperkeratosis, roughening of nail and loss of cuticle, pitting
Guttate psoriasis - ‘rain drops’
Palmar psoriasis -> pustules
Generalised pustular psoriasis (need to be admitted to hospital)

Question 14

3 things that cause pustules

Answer 14

Infection
Psoriasis
Drug reaction

Question 15

Pathophysiology of acne

Answer 15

1. Comedone formation - build up of keratin in hair follice causing a plug
2. Androgen production -> increased sebum production
3. Overgrowth of P.acnes -> inflammation
4. rupture of follicular canal
5. Inflammatory molecules/dead particles spill into dermis causing more inflammation

Genetic + hormonal factors

Question 16

Clinical features of acne

Answer 16

Whiteheads - Closed comedone
Blackheads - Open comedone, can see dead keratin
Papules (inflammatory)
Pustules (pus)
Nodules

Question 17

Treatment for acne?

Answer 17

Topical agents: Lipid soluble antibiotics targeting P.acnes
Oral antibiotics (anti-inflammatory effect)
Oral contraceptive pill for females

If none of that works, isotretinoin (anti-inflammatory/anti-proliferative)

Question 18

Bullous pemphigoid

Answer 18

Autoimmune skin disease common in elderly
Auto-antibodies agianst BP1 and BP2 proteins in basement membrane (between dermis and epidermis)
Skin splits away from dermis splits forming blisters

Treat with steroids/immunosuppressants

Question 19

Epidermolysis Bullosa

Answer 19

Genetic abnormality in BP1 or BP2
Sub-epidermal blisters (i.e. BELOW epidermis)\
Treated with immunosuppressants (suppresses auto-antibodies)
Red patches can form before blistering occurs

Question 20

Pemphigus vulgaris

Answer 20

Auto-antibodies against desmogleins (protein in desmosomes) that hold keratinocytes together in epidermis
Superficial blisters that erode easily, causing superficial erosions
Tends to occur in middle-aged, middle-eastern/oriental ethnicities