Acne is the classic stigma of adolescence and has been viewed as a normal physiologic reaction in the skin. The increase in size of the sebaceous glands and the concomitant increased amount of sebum secretion during adolescence are physiologic, but the inflammatory changes of true acne represent a disease which may be extraordinarily chronic and sometimes produce severe residual physical and psychological scarring which may be lifelong.
The basic cause of acne is still unknown but four major pathogenetic factors are : (a) increased sebum production, (b) abnormality of the microbial flora, (c) hyperkeratinization of the pilosebaceous duct and (d) inflammation. Genetic and racial factors also play a role in the development of acne.
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Eczema is defined as a series of inflammatory changes in the skin induced by external or internal (constitutive) factors.
A simple classification divides eczemas into 'exogenous', where some external causative factor is identifiable and 'endogenous', where some internal or constitutional factors are thought to be causative.
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Irritant contact dermatitis:
Irritant contact dermatitis occurs as a result of the skin coming in contact with irritants which cause an altered state of sensation (burning, stinging) and some morphologic changes. This type of dermatitis is due to direct damage caused by non-immune mechanisms as opposed to allergic contact dermatitis. Strong irritants like acids and alkalies cause immediate damage to the skin but weak irritants, on repeated contact with the skin, will produce eczematous changes clinically and histologically similar to allergic contact dermatitis.
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Allergic contact dermatitis:
Allergic contact dermatitis is a disorder of the skin resulting from a delayed hypersensitivity reaction mediated by T-lymphocytes against certain chemicals (contact allergens) causing sensitisation on coming in contact with the skin. Most contact allergens are haptens (incomplete allergens) which become complete allergens after combining with epidermal carrier proteins.
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For photoallergy and phototoxicity reactions an interaction between the chemical (topically applied or systemically given) and solar radiation (ultraviolet or visible light) is required. Photoallergic contact dermatitis will occur when the skin is exposed to light following application of the chemicals to the skin of a sensitised person. Phototoxic reaction will occur in a majority of persons as opposed to photoallergic dermatitis which occurs only in sensitised persons. Substances producing photoallergy are sulphonamides, thiazides and sulphonylureas while those causing phototoxicity are psoralens, tar, etc.
This is due to an allergic reaction to organisms or their products. The eczema responds to treatment with antibiotics which eradicate the organisms. It is distinct from infected eczema and occurs commonly on the legs due to chronic folliculitis.
The word 'atopy', which literally means 'out of place', represents an inherited tendency which predisposes to atopic dermatitis, bronchial asthma and allergic rhinitis.
Atopic dermatitis is a chronic relapsing pruritic skin disorder of unknown aetiology, associated with personal and/or family history of atopy and a typical distribution and morphology. It is characterised by distressing symptoms due to a low threshold for itching, tendency of the skin to lichenification and frequently, raised level of serum IgE.
It is estimated that about 3% of all infants and 10% of school children suffer from atopic dermatitis. These figures are for Europe but in India, the prevalence and severity are less, though on the rise.
(i) Raised IgE levels in 80%, (ii) Defects in cell-mediated immunity, (iii) Defects in neutrophil and monocyte chemotaxis.
The symptom of itch is so central in the pathogenesis that atopic dermatitis is described as "the itch that rashes and not the rash that itches". The disorder is characterised by infantile, childhood and adult phases. The infantile phase starts between 2-6 months of age, and pruritic papulovesicular, oozing lesions are distributed on the face, scalp and front of the knees and legs (see colour atlas). By the age of 18 months, the childhood phase starts and is characterised by itchy lichenified lesions in the cubital and popliteal fossae, sides of the neck, wrists and ankles. The distribution in the adult phase is similar and there is a marked tendency to lichenification and generalisation. The disorder may begin and remit in any of these phases.
Complications are :
Secondary bacterial infection with pyogenic cocci,
Eczema herpeticum, a disseminated infection with herpes simplex virus
Eczema vaccinatum, a disseminated infection with vaccinia virus.
The tendency to itch is reduced by avoiding direct contact with irritants, wool, extremes of temperature and soaps. Topical therapy is with emollients and mild-potency topical corticosteroids. Potent topical steroids are required for lichenified lesion. Centrally acting systemic antihistaminics are useful for alleviating pruritus and systemic antibiotics are needed for sepsis.
Seborrhoeic dermatitis is a chronic dermatitis with a typical distribution in the areas with a rich supply of sebaceous glands and erythematous papulosquamous lesions with greasy scales. Pityriasis capitis (dandruff) is probably the mildest form.
Pityrosporum ovale, a yeast normally present on the skin, is increased in the scales of seborrhoeic dermatitis. The disorder is more common in AIDS where the patients have increased susceptibility to yeast infections.
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Stasis dermatitis (Gravitational eczema) or Varicose eczema:
Stasis dermatitis occurs in middle-aged or elderly patients around the ankles as a result of venous hypertension. History of deep vein thrombosis and presence of superficial varicose veins are usual features. Venous hypertension, when transmitted to the capillaries, results in widened endothelial pores through which fibrinogen escapes and forms deposition of fibrin around the capillaries. Reduced oxygenation of the tissues and skin around the medial malleolus is thought to be responsible for the eczema. There is pruritus, oozing, pigmentation, purpura and atrophy. Ulceration may occur. Contact dermatitis due to allergic sensitisation to various topically used medications is frequent.
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Psoriasis is a genetically determined disorder characterised by development of chronic, well-defined, scaly, erythematous plaques on the extensor aspect of the extremities, especially on the elbows and knees, trunk, back and scalp. Nail involvement is very frequent and often gives the clue to the diagnosis. Psoriasis can be localised or generalised. High variability and unpredictability is the hallmark of this chronic affliction. The estimated prevalence is 1.5% to 3% in the general population. There is wide ethnic and racial variation. It has a bimodal peak of incidence, at 16-22 years and 57-60 years. Female predominance is noted in the younger age group.
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This common, autoimmune skin disease results in the destruction of melanocytes(Pigment producing cells) and the total depigmentation of affected skin. However, an association with other autoimmune diseases and a family history of such is found in one-third of cases. The cause is unknown, but the melanocyte seems to be damaged by some, as yet, unidentified antibody or toxin. In many parts of the world where skins are deeply pigmented, vitiligo is a principal cause of attendances at a dermatology department.Vitiligo affects up to 1 per cent of the United Kingdom population but 8.8 per cent in India. It presents during the first decade of life in 25 per cent of those affected. Except in those people unable to protect themselves from bright sunlight the disability is purely cosmetic, but it causes more concern and social handicap than almost any other common disease.
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