5: Inflammatory Dermatoses Flashcards
Explain the differentiation of keratinocytes
Basal cell -> Prickle cell -> Granular cell -> Keratin (barrier)
Atopic eczema
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
What is the atopic march?
- Within 3 months of age you tend to develop eczema FIRST
- Food allergies (also peaks around 1yr)
- Astham (peaks around 5yrs)
- Rhinitis (peaks around 9-10yrs)
Signs of filagrin gene mutation?
Palmar hyperlinearity
Lines are more visible
Chronic changes in eczema?
Skin become less red
Lichenification - skin markings become more visible due to chronic rubbing/scratching
Results in thicker leathery skin
What is severe eczema?
Erythrodermic eczema
Redness over whole skin surface
Systemically unwell
Should be admitted to hospital
What is eczema herpeticum
Herpes virus can infiltrate skin as well
Spreads around skin forming ulcers
Other types of eczema?
Seborrhoeic - overgrowth of yeast
Allergic contact dermititis - allergy to skin products (could be medications)
Discoid
Pathophysiology of Psoriasis
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
Histology of psoriasis
Hyperkeratosis Parakeratosis - retention of nuclei in stratum corneum Acanthosis Inflammation Dilated blood vessels
Histology of psoriasis
Hyperkeratosis Parakeratosis - retention of nuclei in stratum corneum Acanthosis (thickening of skin) Inflammation Dilated blood vessels
Presentation of psoriasis
Commonly in places of trauma: scalp, outside of elbows/knees (eczema is INSIDE), feet soles
Scaly plaques
SYMMETRICAL
Types of psoriasis
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)
3 things that cause pustules
Infection
Psoriasis
Drug reaction
Pathophysiology of acne
- Comedone formation - build up of keratin in hair follice causing a plug
- Androgen production -> increased sebum production
- Overgrowth of P.acnes -> inflammation
- rupture of follicular canal
- Inflammatory molecules/dead particles spill into dermis causing more inflammation
Genetic + hormonal factors
Clinical features of acne
Whiteheads - Closed comedone Blackheads - Open comedone, can see dead keratin Papules (inflammatory) Pustules (pus) Nodules
Treatment for acne?
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)
Bullous pemphigoid
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
Epidermolysis Bullosa
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
Pemphigus vulgaris
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
