Inflammatory dermatoses Flashcards

1
Q

What are the 3 layers of the skin?

A

Epidermis
Dermis
Hypodermis

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2
Q

What is dermatitis also known as?

A

Eczema

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3
Q

What are the different types of eczema?

A

Atopic
Seborrhoeic
Discoid
Allergic contact

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4
Q

What is the definition of atopy?

A

Tendency to develop hypersensitivity

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5
Q

What is atopic eczema?

A

Very common itchy skin condition

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6
Q

What is the onset of atopic eczema like?

A

It is often within first 6 months of life. Many children grow out of it but a proportion doesn’t

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7
Q

What is the biology of eczema?

A

Defective barrier function of the skin leading to dry skin

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8
Q

What is mutated in 10% of eczema cases?

A

Filagrin gene

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9
Q

What is filagrin?

A

Epidermal protein important in maintaining barrier function of the skin

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10
Q

What does defective barrier function in eczema allow?

A

Penetration of irritants, allergens (e.g. house dust mite particles) and pathogens e.g. staph aureus. Inflammation of the skin then occurs

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11
Q

What is seborrhoeic eczema?

A

Very common type of eczema affecting babies and adults, often not itchy

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12
Q

What is the pathology of seborrhoeic eczema?

A

There is overgrowth of malassezia species of yeast on the skin with associated skin inflammation.

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13
Q

What is distinctive in seborrhoeic eczema?

A

The rash has a distinctive distribution including nasolabial folds, eyebrows, scalp, central chest and sometimes axillae and groins

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14
Q

What is psoriasis?

A

Another common inflammatory dermatosis

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15
Q

When does psoriasis usually start?

A

Teens or 40s/50s

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16
Q

What are the different types of psoriasis?

A

Chronic plaque
Guttate
Palmoplantar pustulosis
Generalised pustular psoriasis

17
Q

What percentage of patients with cutaneous disease are affected by psoriatic arthritis?

A

Approximately 30%

18
Q

What are the underlying cause of psoriasis?

A

Genetic susceptibility and environmental triggers- many genes are implicated including PSOR1

19
Q

What is the pathophysiology of psoriasis?

A

Immune process occurs where T lymphocytes move out of blood vessels into the dermis and initiate the release of cytokines e.g. tumour necrosis factor alpha. The epidermis becomes thickened and produces more keratinocytes than normal, neutrophils infiltrate the epidermis and lymphocytes infiltrate the dermis

20
Q

What triggers for psoriasis are there?

A

Infections
Drugs
Stress

21
Q

Who is mainly infected by acne?

A

A very common condition which mainly affects teenagers and young adults

22
Q

What is the biology of acne?

A

It is disease of the pilosebaceous unit of the skin

23
Q

What is the pathogenesis of acne?

A

It is multifactorial and includes:
Hyperkeratinisation of the epidermis in the infundibulum of the hair follicles
Accumulation of dead keratinocytes in lumen of the hair follicle
Increased sebum production stimulated by androgens
Proliferation of propionibacterium acnes within the pilosebaceous unit
Rupture of the inflamed pilosebaceous unit with further inflammation of the surrounding skin

24
Q

What are the key clinical features of acne?

A
Open and closed comedones
Papules
Pustules
Nodules
Scars
on face, chest and back
25
Q

What is bullous pemphigoid?

A

An autoimmune bullous inflammatory condition most common in the elderly

26
Q

What are the clinical features of bullous pemphigoid?

A

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

27
Q

What is the biology of bullous pemphigoid?

A

IgG antibodies to basement membrane antigens BP180 or BP230 result in cleavage of skin at the demo-epidermal junction leading to sub-epidermal blisters

28
Q

What is pemphigus vulgaris?

A

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

29
Q

What do the clinical features of pemphigus vulgaris include?

A

Flaccid blisters which easily break leaving erosions and crusted lesions

30
Q

What is the biology of pemphigus vulgaris?

A

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