Week 4 - skin, atopy Flashcards
(31 cards)
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
Psoriasis - therapy
Local topical therapy (corticosteroids, dithranol, Vit D analogues, tar/salacylic acid/sulphur preparations), UV light therapy, Systemic (methotrexate, cyclosporine, acitretin)
Atopic dermatitis
Eczema
Inflammatory skin condition, all ages usual onset 2yrs, intense pruritis induces rubbing and scratching of skin, skin often dry with poorly defined papules or plaques, with/without scale, high risk 2ndary infection
- flexures
Atopic dermatitis - complications
Bacterial: Staph aureus (impetiginisation)
Viral: HSV (eczema herpeticum), molluscum contagiosum
Erythroderma - systemically unwell
Atopic dermatitis - triggers
Drying of skin, worsening barrier function (soaps, detergents)
Allergen inhalation (dust mite, animal hair, pollen)
Irritants (cleaning agents, wool, damp
Climate
Social/emotional stress
Atopic dermatitis - treatment
General: educate parents, avoid irritants, emollients
For exacerbation: topical corticosteroids, antihistamines
Acne vulgaris
Disease of the folliculosebaceous unit.
Keratin plugging of follicular opening, hormones
Bacteria: propionibacterium acnes
Primary vs secondary acne vulgaris
Primary: closed and open comedo (black head and white head)
Secondary: Papules, pustules, papulopustules, cysts, nodules
Acne vulgaris - treatment
- Hormonal manipulation - in women ocp with anti-androgenic progesterone (i.e. Diane, Yasmin)
- Reduce keratin build up blocking follicle openings - topical: differin gel (Vit A); oral: roaccutane (vit A) –> teratogenic, mental health side effects)
- Antibiotics (wash - benzylperoxide; topical - erythromycin etc; oral)
An adverse food reaction due to nonimmunologic mechanism is called….
Food intolerance
