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Stevens-Johnson syndrome is a severe form of erythema multiforme complicated by severe blistering of skin and mucosae including the mouth, eyes, and genitalia, and accompanied systemic features such as fever. The target lesions of erythema multiforme may be evident, but in its most severe form, toxic epidermal necrolysis (TEN, associated with a positive Nikolsky sign) causes widespread blistering of the skin. Other complications include diarrhoea, anterior uveitis, pneumonia, renal failure, and polyarthritis, A wide variety of triggers may be responsible, including drugs (e.g. sulphonamides; thiacetazone in HIV +ve patients), streptococcal infections, viral infections (e.g. HSV Orf), malignancy, and some systemic diseases (e.g. SLE). Management: Stop any potential drug trigger. Nurse patients as for extensive burns, with careful attention to fluids, nutrition, and prevention of 2° bacterial infection. In the absence of good nursing care and attention to fluids, the mortality from fluid loss is high. The role of steroids is controversial: they reduce progression but also significantly increase the risk of infection. IV immunoglobulins are sometimes used but large controlled trials are required to confirm their benefit. TEN is associated with a high mortality.

Buruli ulcers are a chronic necrotizing skin disease of tropical forest areas caused by infection with Mycobacterium ulcerans. Cases have been reported in east, central, and west Africa, Asia, central and south America, Papua New Guinea, and Australia. The mode of transmission is unknown but possibilities include inoculation by minor trauma, biting insect, or contaminated aerosols of water.
Lesions start as a painless nodule which may be itchy. Some resolve spontaneously, but many enlarge and break down to form a relatively painless ulcer with edges that may be undermined for 5-15 cm. Mycolactone, a bacterial exotoxin, contributes to necrosis and ulcers may spread rapidly to become very large and disfiguring. There are few systemic signs (although lymphadenopathy and lymphoedema may occur). Complications include 2° bacterial infection and tetanus. Without treatment, many lesions eventually slowly heal after a few years, often causing severe scarring, contractures, and deformities.

The suprabasal cell layer is composed of five to ten layers that appear connected to each other by prickle-like structures. Suprabasal (prickle) cells are polygonal in the lower layer and flattened in the upper layers. They are larger than basal cells and contain a small amount of chromatin in their circular nucleus.

The part that gives the appearance of a prickle corresponds to the desmosome (a form of intercellular bridge).

The granular cell layer is composed of two or three layers of cells containing basophilic keratohyalin granules. The cells and nuclei in the granular cell layers are even flatter than those in the suprabasal layer. Spherical lamellar granules, each with a diameter of approximately 300 nm (also known as Odland bodies or

ketatosomes), can be observed in the granular cell layers by electron microscopy. The main component of lamellar granules is released into the intercellular space of horny cells as stratum corneum lipid.