Week 4 - skin, atopy Flashcards
Type I Hypersensitivity
“immediate”, atopy, allergens often environmental
MoA: IgE and degranulation of mast cells
e.g. allergic rhinitis, asthma, anaphylaxis
Atopy
Increased tendency of certain individuals to type I hypersensitivity
Type II Hypersensitivity
Antibody-dependent cytotoxic hypersensitivity
Antibody binds self or foreign antigens; phagocytosis, NK cells or complement mediated lysis
MoA: IgG, IgM, complement
e.g. Rh incompatibility, transfusion rxn, haemolytic anaemia, Graves’
Type III Hypersensitivity
Immune-complex disease (deposition of immune complexes in blood vessels and tissues)
MoA: IgG, antigen, complement
e.g. vasculitis, nephritis, arthritis, pneumonitis, tetanus injection
Type IV Hypersensitivity
Delayed-type, mediated by T cells and macrophages
Rxns develop hour to days after contact (typically 12-48hrs)
e.g. contact dermatitis, TB test,
Infective causes of rash
Bacterial: staph, strep
Viral: molluscum contagiosum, HPV, HSV, EBV
Fungal: tinea corporis/capitis
Parasitic: scabies
Autoimmune/inflammatory causes of rash
Atopic dermatitis, psoriasis, neonatal lupus, acne
Papule
Elevated, solid lesion <0.5cm (e.g. bite reaction, rosacea)
Macule
Area of change in skin colour without elevation/depression, <0.5cm (e.g. drug or viral exanthem, scarlet fever)
Plaque
Plateau-like elevation above skin surface, usually >1cm (e.g. psoriasis)
Pustule
Papule containing purulent exudate, often centred on hair follicle (e.g. rosacea)
Vesicle
Elevated, superficial cavity containing fluid, )
Wheal/urticaria
Flat topped papule or plaque which migrates over 24hrs, due to dermal oedema (“hives” due to food intolerance, allergic rxn etc)
Psoriasis - clinical features
Erythema ‘salmon pink’, scale, thickened plaques, predilection for extensor surfaces, scalp, joint
Psoriasis - triggers
Physical trauma (Koebner phenomenon), stress, drugs (e.g. anti-hypertensives), infections (strep throat), nutrition and alcohol, UV light