Inflammatory dermatoses Flashcards

1
Q

Describe the basic micro anatomy of the skin

A

3 layers:
Epidermis
Dermis
Subcutaneous tissue

Sweat glands, sebaceous glands, hair follicle and blood vessels found throughout

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2
Q

Describe the structure of the stratum corneum

A

Very important for barrier function of the skin
Defects lead to eczema
Filagrin gene mutation common in eczema patients

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3
Q

What is atopy and give examples of atopic diseases

A

Tendency to develop hypersensitivity

Eczema, asthma, hayfever

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4
Q

What are the types of eczema

A

Atopic
Seborrhoeic
Allergic contact dermatitis
Discoid

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5
Q

What are the intrinsic and extrinsic factors contributing to atopic eczema

A

intrinsic - leads to defects in epidermal skin barrier e.g. filagrin gene mutation

Extrinsic - Allergens (house-dust mite), irritants (detergents in soaps), pathogens (staphylococcus)

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6
Q

Describe the immunology of atopic eczema

A

Activation of CD4+ lymphocytes and the Th2 immune response
Mast cell degranulation, releasing histamine

Chronic - Activation of CD4 and CD8 lymphocytes and Th1 immune response

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7
Q

Describe the histology of psoriasis

A
Hyperkeratosis
Parakeratosis
Acanthosis
Inflammation
Dilated blood vessels
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8
Q

Give examples of areas where psoriasis might manifest

A
Soles
Subungual hyperkeratosis (under nails)
Nails
Palms
Back (guttate)
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9
Q

What is acne

A

Disease of the pilosebaceous unit of the skin

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10
Q

Describe acne pathogenesis

A
  1. Hyperkeratinisation of the epidermis in the infundibulum of the hair follicles
  2. Accumulation of dead keratinocytes in hair follicle lumen
  3. Increase sebum production stimulated by androgens
  4. Proliferation of propionibacterium acnes within the pilosebaceous unit
  5. Rupture of the inflamed pilosebaceous unit, with further inflammation of the surrounding skin
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11
Q

What are some factors that lead to acne

A

Comedone formation
Genetic predisposition
Propionibacteria acnes
Androgenic stimulation

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12
Q

What are the clinical features of acne

A
Whiteheads (closed comedones)
Blackheads (open comedones)
Papule
Nodules
Pustules
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13
Q

What is bullous pemphigoid

A

An autoimmune bullous inflammatory condition most common in the elderly.

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14
Q

Describe the pathology of bullous pemphigoid

A

IgG autoantibodies to basement membrane antigens BP180 (type XVII collagen) or BP230 result in cleavage of the skin at the dermo epidermal junction leading to sub epidermal blisters.

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15
Q

What is a clinical sign of the filagrin gene mutation

A

Palmar hyperlinearity

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16
Q

What is eczema

A

Very common itchy skin condition. Onset often within first 6 months of life. Many children will grow out of it, but a proportion does not.

17
Q

Describe the biology of eczema

A

Defective barrier function of the skin, leading to dry skin.
Filagrin gene mutations in 10% of cases.
Defective barrier function allows penetration of irritants, allergens (eg house dust mite particles) and pathogens eg staph aureus. Inflammation of the skin then occurs.

18
Q

What is filagrin

A

Filagrin is an epidermal protein important in maintaining barrier function of the skin.

19
Q

Describe seborrheic eczema

A

A very common type of eczema affecting babies and adults.
Often not itchy.
There is overgrowth of malassezia species of yeast on the skin with associated skin inflammation.
The rash has a distinctive distribution including nasolabial folds, eyebrows, scalp, central chest and sometimes axillae and groins.

20
Q

Describe the biology of psoriasis

A

Many genes are implicated including PSOR1
Immune process occurs where T lymphocytes move out of blood vessels into the dermis and initiate the release of cytokines, eg Tumour Necrosis Factor Alpha
The Epidermis becomes thickened and produces more keratinocytes than normal, neutrophils infiltrate the epidermis and lymphocytes infiltrate the dermis.

21
Q

Give examples of psoriasis triggers

A

Infections, drugs and stress.

22
Q

What are the clinical features of bullous pemphigoid

A

intense pruritus followed by the development of tense blisters on an erythematous background of skin or mucous membranes

23
Q

What is pemphigus vulgaris

A

An uncommon autoimmune bullous inflammatory disease, which usually affects middle aged individuals.

24
Q

What are the clinical features of pemphigus vulgaris

A

flaccid blisters which easily break leaving erosions and crusted lesions.

25
Q

Describe the biology of pemphigus vulgaris

A

IgG autoantibodies to epidermal cell surface proteins desmogleins 1 and 3 lead to loss of cell-cell adhesion (acantholysis) within the epidermis causing flaccid blisters in the skin or mucous membranes.