Inflammatory Dermatoses Flashcards
Inflammatory dermatoses: summarise the biology and significant clinical manifestations of specific inflammatory dermatoses including acne, eczema, psoriasis, bullous pemphigoid and pemphigus vulgaris.
Skin Microanatomy
- The skin is divided up into the epidermis, the dermis and the hypodermis (subcutaneous tissue).
- Some important cells found in the stratum basale are – merkel cells, melanocytes, dividing keratinocytes
- Keratinocyte differentiation pathway – basal cell -> prickle cell -> granular cell -> keratin.
Stratum corneum:
- Very important barrier function of the skin.
- Defects lead to eczema.
- Composed of corneocytes (differentiated keratinocytes) with lipids in between each of them.
- Filagrin protein gene defect: predispotition to develop excema and other allergic condition
Eczema
Eczema/Dermatitis
Types of eczema:
Atopic
- “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.
- Rellapsing - remitting
- Cause – defective barrier of skin.
- Filagrin (an epidermal protein) gene mutation in ~10% of patients - allows influx of irritant proteins
- Defective barrier then allows entry of irritants, allergens and pathogens which then cause inflammation.
- The atopic march: sequence of allergy related health problems (eczema, food allergy, asthma, renitis)
- Palmar hyperlinearity is a sign of the mutation
- Chronic eczema: extentuated lichenification -> cut-off between normal and eczematic skin
- Herpes simplex: virus causing eczema herpeticum
- Treatment: moisturizers, topical steroids
Seborrhoeic:
- 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.
- Vulnerale to allergic contact dermititis - sensitised to particular allergens (cosmetics, eyedrops, hair dye)
Discoid – occurs in small discrete discs.
- Allergic contact
Psoriasis
Psoriasis
- common inflammatory dermatoses usually starting in teens or 40s/50s.
- Psoriatic arthritis affects approx. 30% of people with cutaneous disease.
- Types of psoriasis:
- Chronic plaque.
- Guttate.
- Palmoplantar pustulosis (exacerbated by smoking stress obesity).
- Generalised pustular psoriasis – same as above just everywhere- pustules with sterile neutrophils
Cause of psoriasis:
- Genetic susceptibility – many genes are implicated including PSOR1:
- Environmental causes.
- Drugs: antimalariar b blockers lithium
- Infections: streptococcus infections (better after tonsilar removal)
Pathophysiology:
- 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.
Triggers include infections, drugs and stress.
Hystology:
Hyperkeratosis
Parakeratosis: normally this layer shouldn’t have nuclei, in psoriasis they do
Acanthosis: thickenning of the epidermis
Occurs in skalp, extensin surfaces, ambilicus, genitals, nails (Subungual hyperkeratosis, Dystophic nail and loss of cuticle, onycholysis and pitting)
Guttate: mainly affect teenagers - individual red papules rather than patches - exacerbated by strptococcal infections
Acne
Acne
- very common condition affecting mainly teenagers and young adults.
- Pathophysiology – disease of the pilosebaceous unit of the skin.
- Pathogenesis – 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 à further inflammation of surrounding skin.
Clinical features
- open (blackhead)/closed (whitehead) comedones, papules, pustules, nodules and scars on face, chest and back.
Treatment:
- sterilise benzoproxine
- topical/oral AB - erithromycin (lipid philic)
- contraceptive pills reducing the free testosterone (yasmide)
Bullous Pemphigoid
- autoimmune bullous inflammatory condition most common in the elderly.
Basement membrane zone - epidermis embryologically frm ectoderm and dermis from misoderm -> this means that there is some specialised proteins in sticking them together -
BP antigen 1 or 2 - targets of autoantibody -> inflammaotry reaction: splitting of that level of the BM
Clinical features – intense pruritus followed by development of tense blisters on an erythematous background of skin or mucous membrane – E.G. Epidermolysis bullosa.
Pathogenesis:
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.
Treatment: steroids
Betweem tje leracynotyes - connections - autoantibody targeted against these proteins ??
Pempigus vulgaris
Split between the epidermis and not the BM
- uncommon AI bullous inflammatory disease most common in middle-aged people.
Clinical features – flaccid blisters which break easily leaving erosions and crusted lesions.
Pathogenesis:
- IgG auto-antibodies to epidermal cell surface proteins desmogleins 1 & 3 à loss of cell-cell adhesion (acantholysis) within the epidermis causing flaccid blisters in the skin or mucous membranes.
Rarer: most likely to occur in Asians, younger people, 30s, 40s
