5. Inflammatory dermatoses Flashcards
What are eccrine and apocrine glands?
- Eccrine - make watery sweat (all over the body)
* Apocrine - make viscous sweat - on axillae and groin
What are the adnexal structures of the dermis?
Pilosebaceous unit
• hair follicle
• sebaceous glands
• erector pili muscle
What is the dermal matrix made up of?
- Collagen
- Elastin
- GAGs
- Blood vessels
- Nerves
Is the papillary or reticular dermis more deep?
Reticular dermis
How are keratinocytes formed?
Basal cell => prickle cell => granular cell => keratinocyte
Which gene mutation is common in eczema patients?
Filagrin gene
What is atopic eczema?
• Dry skin
• Barrier may become defective e.g. filagrin mutation
• Allergens or pathogens can penetrate - sensitisation
• Immune response activated via Langerhans cells
=> acute atopic dermatitis with activation of CD4+ (Th2 response)
=> chronic atopic eczema if left (Th1 response)
• Inflammatory response
• Common, relapsing and remitting
• The first atopic disease to come about in an individual’s life
What is a common sign of the filagrin mutation?
Palmar hyperlinearity
What are the most affected areas in infantile atopic eczema?
Face, arms, elbows, knees
What are the common sites of eczema outbreaks as a child gets older?
Remains on face, but particularly effects the antecubital fossa, popliteal fossa, hands, face and neck
What does acute and chronic eczema look like?
Acute
• Red and slightly blistery
• Often colonised with bacteria
Chronic
• Less red
• Excoriated and lichenified (thickened and accentuation of skin lines)
What bacteria particularly activates eczema?
S. aureus on the skin
How is eczema treated?
- Antibiotics
- Emollients
- Topical and oral steroids
What is eczema herpeticum?
Herpes simplex virus has proliferated on the surface of the skin
What dangerous disease can eczema herpeticum progress to?
Encephalitis => brain damage + death
What is seborrhoeic eczema?
- Just the scalp => dandruff
- Face => redness and greasy, scaly skin
- Mainly affects the nasolabial folds, eyebrows, forehead, chest and back
- Not itchy, but can be sore
- Cause by natural yeast on the skin
How can seborrhoeic eczema be treated?
Anti-dandruff/fungal shampoo, anti-fungal cream, topical steroid
When does seborrhoeic eczema get worse?
- Stress
- Staying up late
- Drinking too much alcohol
- Immunodeficiency
When does seborrhoeic eczema get better?
- No stress
- Sleeping well
- Exposed to sun
What is allergic contact dermatits and what can cause it?
- Very allergic to certain allergens when they come into contact with skin
- Eyelids affected may be due to makeup, preservatives in contact lens fluid and eyedrops
- PPD (pigment in henna) can cause sensitisation
- More likely in patients with atopic eczema
What is discoid eczema?
- Often on legs but can be anywhere
- Discs looking like eczema
- Intervening skin may look normal
- Often just dry skin with secondary dermatitis
What is the treatment for discoid eczema?
- Emollient use
- Topical steroid
- Avoiding soap/shower gel
What is psioriasis?
- Inflammatory dermatoses
- Psoriatic plaques (Raised areas) - salmon pink coloured, well defined, and silvery scaled
- Too many keratinocytes
What causes psoriasis?
- Polygenetic
- More likely to occur in monozygotic twins than dizygotic (shows genetic affect)
- Environmental triggers e.g. infection, stress, drugs
- Pressure and trauma to areas of the skin
- Immune response triggered => overproduction of keratinocytes
Describe the histology of psoriasis
- Thicker epidermis - acanthosis
- Thicker stratum corneum - hyperkeratosis
- Individual cells don’t lose their nuclei - parakeratosis
- Influx of neutrophils within epidermis, can form pustules and lead to inflammation
- Lymphocytes in dermis
- Dilatation of blood vessels - redness
What drives the immune reaction in psoriasis?
Lymphocytes and excess cytokines/TNF-alpha
What are the common sites of psoriasis?
- Scalp
- Elbows
- Knees
- Gentical areas
- Around umbilicals
- Natal cleft of buttocks
- Most nails (thickening, loss of cuticle, pitting)
Very symmetrical
What is Guttate psoriasis?
- Lots of little, raindrop like lesions on the skin
- Affects teenagers, and can occur after a streptococcal sore throat
- Weeks, months
- Genetic susceptibility
- Treat with antibiotics and topical steroids
What is palmoplantar pustulosis and who is often susceptible?
Pustules forming on the palms of the hands and soles of the feet, instead of plaques
• different genetic susceptibility
• often smokers (but cessation doesn’t help)
What is generalised pustular psoriasis and the treatment?
- Pustules all over the body
- Patient becomes very unwell - febrile and toxic, cannot function
- High HR and low BP
- Treated with immunosuppressants (and emollients + topical steroids)
- Rare condition, and high mortality without treatment
What is acne and when does it occur?
- Disease of the pilosebaceous unit
- Can occur at any age (common at onset of puberty)
- Driven by hormones - androgenic stimulation causes hypertrophy of sebaceous glands
- Build up of dead cells, hyperkeratinisation (thickening of infundibulum of hair follicle) => comedone
What are propionibacteria acnes?
- Secondary overgrowth of a bacteria within the follicle
- Secondary inflammation => rupture
- Products of inflammation in dermis
What are blackheads and whiteheads?
- Blackheads - open comedones, build up of keratin in hair follicle pore
- Whiteheads - closed comedone (blackhead, but covered with skin)
Both clinical features of acne
What are inflammatory lesions and what can happen when they heal?
- Papules (small)
- Pustules (puss-filled)
- Nodules (thickened)
- Can heal with scarring, which is difficult to treat
Clinical features of acne
What parts of the body does acne affect?
- Areas where sebaceous glands are predominant
* Face, neck, upper chest
What is the treatment for acne?
- Topical and oral antibiotics
* Isotretinoin (roaccutane) - anti-proliferative effects on keratinocytes
What is the epidermis and dermis derived from embryologically?
- Epidermis from ectoderm
* Dermis from mesoderm
Where is the basement membrane zone?
Between the epidermis and dermis
What causes bullous pemphigoid and pemphigus?
- Both autoimmune conditions
* Antibody acts against particular protein in BM
Describe bullous pemphigoid, complications and the proteins involved
- Deep (at BM)
- Tense blisters
- Usually elderly patient in their 70-90s
- Rash (like eczema) => blisters
- Can become infected without treatment
- Patients can then die from sepsis
- BPAg 1 and BPAg 2 involved (B cells produce antibodies against these proteins)
- These proteins are located on the BM
- Disease causes inflammation here, and splitting of the epidermis from the dermis
What is the treatment for bullous pemphigoid?
- High dose oral steroids
- Other immunosuppressant drugs (methotrexate)
- Treatment for a number of years
What happens if there is a mutation in one of the genes for the BPAg proteins?
Genetic blistering condition - epidermolysis bullosa (presents in babies)
Describe pemphigus vulgaris and its cause
- Superficial
- Auto-antibody directed at desmoglein of the hemidesmosomes within the epidermis (holding the cells together)
- Target is different in paraneoplastic pemphigus
- Splitting within the epidermis - acatholysis
- Causes blisters
- As they are superficial, they break down and flake off
What is the most common pemphigus?
Pemphigus vulgaris
What can be used to detect where the antibodies are present in pemphigus vulgaris?
Immunofluorescence
Wha happens if pemphigus vulgaris isn’t treated?
- Gets worse
* Can result in sepsis
What is the treatment for pemphigus vulgaris?
Oral steroids and immunosuppressants
