Inflammatory Dermatoses

Question 1

What cells are found in the stratum basale?

Answer 1

• merkel cells
• melanocytes
• dividing keratinocytes

Question 2

What is the keratinocyte differentiation pathway?

Answer 2

basal cell -> pricle cell -> granular cell -> keratin

Question 3

What are the types of eczema?

Answer 3

1. Atopic
2. Seborrhoeic
3. Discoid – occurs in small discrete discs
4. Allergic contact

Question 4

What are the features of atopic eczema?

Answer 4

“the tendency to develop hypersensitivity” – includes eczema, hay fever & asthma:
- Very common, itchy skin condition with onset from first 6 months of life. Many grow out of it

Cause : defective barrier of skin
then allows entry of irritants, allergens and pathogens which then cause inflammation.

• Filagrin (an epidermal protein) gene mutation in ~10% of patients
  > Palmar hyperlinearity is a sign of the mutation.

Question 5

What are the features of seborrhoeic eczema?

Answer 5

• Common skin condition affecting babies and adults but is NOT itchy
• Associated with an overgrowth of malassezia (species of yeast on the skin that causes inflammation)
• The rash has a distinctive distribution involving – nasolabial folds, eyebrows, scalp, central chest, axilla and groin

Question 6

What are the types of psoriasis?

Answer 6

• Chronic plaque
• Guttate
• Palmoplantar pustulosis
• Generalised pustular psoriasis – same as above just everywhere

Question 7

What are the causes of psoriasis?

Answer 7

• Genetic susceptibility – many genes are implicated including PSOR1
• Environmental causes

*Triggers include infections, drugs and stress

Question 8

Describe the pathophysiology of psoriasis

Answer 8

T-lymphocytes move out of blood vessels into the dermis and initiate release of cytokines (e.g. TNFa). The epidermis thickens in response (produces more keratinocytes). Neutrophils infiltrate the epidermis and lymphocytes infiltrate the dermis

Question 9

Describe the pathogenesis of acne

Answer 9

disease of the pilosebaceous unit of the skin

multifactorial:

• Hyperkeratinisation of the epidermis in the infundibulum of hair follicles - Accumulation of dead keratinocytes in the lumen of the hair follicle
• Increase sebum production stimulated by androgens
• Proliferation of Propionibacterium acnes within pilosebaceous unit
• Rupture of inflamed pilosebaceous unit -> further inflammation of surrounding skin

Question 10

What are the clinical features of acne?

Answer 10

• open (blackhead)/closed (whitehead) comedones
• papules
• pustules
• nodules and scars on face, chest and back

Question 11

What is bullous pemphigoid?

Answer 11

autoimmune bullous inflammatory condition most common in the elderly

Question 12

What are the clinical features of bullous pemphigoid?

Answer 12

intense pruritus followed by development of tense blisters on an erythematous background of skin or mucous membrane – E.G. Epidermolysis bullosa

Question 13

Describe the pathogenesis of bullous pemphigoid

Answer 13

IgG auto-antibodies against basement membrane antigens BP180 (T17 collagen) or BP230 result in cleavage of skin at the dermo-epidermal junction leading to sub-epidermal blisters

Question 14

What is pemphigus vulgaris?

Answer 14

uncommon AI bullous inflammatory disease most common in middle-aged people

• Clinical features – flaccid blisters which break easily leaving erosions and crusted lesions

Question 15

What causes pemphigus vulgaris?

Answer 15

o IgG auto-antibodies to epidermal cell surface proteins desmogleins 1 & 3 -> loss of cell-cell adhesion (acantholysis) within the epidermis causing flaccid blisters in the skin or mucous membranes