This is followed by spontaneous involution over several years and therefore active non-intervention is advised. However, treatment should be considered for lesions which are large with potential for disfigurement, ulcerating, threaten vital function, e. Until recently, steroids topical, intralesional and oral were the mainstay of treatment.
However, the serendipitous discovery of a non-selective oral beta blocker as an effective treatment has revolutionized its management. Oral propranolol has become the treatment of choice for complicated lesions. The exact mechanism for its action is not completely understood, but is postulated to inhibit angiogenesis and recruitment of endothelial progenitor cells as well as inducing apoptosis. More recently, topical beta blockade in the form of eye drops usually used for glaucoma applied directly to the lesions has been shown to be effective.
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A number of genes are involved in the formation and migration of neural crest cells. Genetic mutations causing defects in the neural crest can lead to the development of neurocutaneous syndromes i. Examples of neurocutaneous syndromes include tuberous sclerosis, neurofibromatosis and Sturge—Weber syndrome Table For years, management of infantile haemangiomas consisted of active monitoring, surgery, steroids, interferon or vincristine. Since then, the use of propranolol for infantile haemangiomas has been reported in over publications and it has become the first-line therapy for haemangiomas requiring treatment.
Hyperactive mTOR causes unchecked cell growth, proliferation, metabolism and angiogenesis, all of which can give rise to tumour growth, which may affect many organs. Neurological abnormalities e. The development of the skin appendages hair, nails, eccrine, apocrine and sebaceous glands begins during the first trimester and matures in the second trimester. The epidermis is thought to convey signals to the dermis to initiate appendage formation. Abnormalities in epidermal development and the associated signalling pathways can result in skin appendage abnormalities.
A 2-year-old boy presents with a firm rubbery nodule on his right eyebrow. This child is likely to have a dermoid cyst, which, despite its name, is an overgrowth of epidermis and adnexal structures such as sebaceous, eccrine and apocrine glands due to a defect in the skin development in fusion lines. It typically presents as a firm rubbery nodule at birth, or by 5 years of age. It can be associated with a pit or sinus tract to underlying structures. Imaging may be required before surgical excision plastic surgery. The epidermis is a stratified squamous epithelium.
It has four or five layers:. The skin epithelium changes and becomes super-specialized as the cells migrate to the skin surface, forming a squamous shape elongated flattened cells. This is achieved by filling of the cytoplasm with proteins, especially keratin, and cross-linking these polymer fibres into strong stable networks.
The squamous shape means the skin is resistant to mechanical trauma and allows shedding without disruption of the whole surface. The epidermal cells, known as keratinocytes, are held together by organelles called desmosomes. Desmosomes are cell adhesion structures that are especially prominent in the epidermis and mucous membranes.
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The basal cell layer is the source of new epidermal cells, and rete pegs ensure attachment of the dermis to the epidermis via the basement membrane the multi-layered structure forming the DEJ. Melanogenesis occurs in specific ovoid organelles, known as melanosomes, which are produced in dendritic melanocytes. Each melanocyte is associated with about 36 keratinocytes and one Langerhans cell epidermal melanin unit.
Melanin synthesized within melanosomes is transported via dendrites to adjacent keratinocytes, and accumulate within keratinocytes and melanocytes in the perinuclear areas.
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Melanin serves as a physical barrier that scatters UV radiation, and reduces its penetration through the epidermis. The epidermal turnover time migration of cells from stratum basale to stratum corneum is approximately 30 days. The epidermis is supported and nourished by a thick layer of dense tissue underneath, the dermis. Collectively, they provide structural stability and elasticity to the skin.
The dermis consists of two layers: papillary dermis and reticular dermis.
It also contains vascular plexus supplied from vessels within the subcutaneous fat, and an extensive lymphatic and nerve system. The efferent system controls the cutaneous vasculature and its appendages, whereas the afferent system provides appreciation of cutaneous sensation. The dermis is attached to the underlying tissues by a layer of loose tissue called the hypodermis or subcutaneous layer, which contains variable amounts of adipose tissues.
Sebaceous glands produce sebum via hair follicles collectively called a pilosebaceous unit. They are most concentrated on the face and scalp. They are stimulated by androgens and become active at puberty. In general, sweat glands are divided into eccrine and apocrine glands. Eccrine glands are mostly concentrated on palms, soles, axillae and forehead. They regulate the body temperature. Apocrine glands are mainly found in axillae and perineal regions.
They open into pilosebaceous follicles and produce body odour. The hair is made up of modified keratin. The hair cortex is produced from medulla within the hair bulb.
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The cortex contains densely packed keratin and is surrounded by a single layer of cells called cuticle. The hair colour depends on the amount of melanin in the cortex. There are three phases in a hair cycle — growth phase anagen which lasts several years; short involutional phase catagen ; and resting phase telogen , which lasts several months. Most infants at term have a full scalp of terminal hair.
However, shortly after birth, infants undergo a brisk period of shedding, where the pattern of synchronous hair growth shifts to the dyssynchronous hair growth of a normal adult. Congenital and hereditary hair disorders tend to present with abnormal pattern of hair growth or shaft morphology. Localized patches of hair loss alopecia may be a result of vascular compromise secondary to perinatal trauma, hamartomatous malformation, the development of naevi such as epidermal naevus and sebaceous naevus, or aplasia cutis.
Generalized sparse hair may suggest an inherited structural hair defect or genodermatosis. In general, hair disorders can be broadly categorized into focal or diffuse, congenital or acquired and scarring or non-scarring Table Most are inherited in an autosomal dominant pattern and there is usually no internal abnormality. Ectodermal dysplasias are genodermatoses that are characterized by absent or inadequate development of one or more of the epidermal appendages i. Netherton syndrome — an autosomal recessive condition of ichthyosis associated with bamboo hair a ball-and-socket hair shaft , erythroderma, and atopy.
Menkes kinky hair syndrome — an X-linked recessive disorder of copper metabolism, causing microcephaly, brittle silvery hair, pale skin and neurological abnormalities. An excessive loss of telogen hair, which can be physiological in the newborn, or triggered by illnesses, stress, surgery, iron and protein deficiency.
An abrupt loss of anagen hairs, triggered by radiotherapy can cause scarring , systemic chemotherapy and any toxic agents. An eroded area on the scalp, which presents at birth and heals over time as a patch of scarring hair loss. It can be associated with or without developmental anomalies. As described above — a type of epidermal naevus, which presents early in life as a waxy hairless rough plaque on the head and neck area.
An example of this is morphoea localized scleroderma on the frontal scalp, which may present as a shiny plaque of firm skin with scarring hair alopecia. It may be associated with other autoimmune conditions such as thyroid disease. The majority of children achieve full regrowth of hair within 1 year.
A common cause of patchy hair loss in children, especially in developing countries. It represents fungal infection of the scalp by dermatophytes most commonly Trichophyton tonsurans in the UK. Positive culture requires systemic antifungals.
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A compulsive habit to pull out the hair. Results in a bizarre pattern of hair loss with twisted and broken-off hairs found on an otherwise normal scalp. The nail is made up of a nail plate hard keratin which arises from the matrix beneath the proximal nail fold. The nail plate rests on the nail bed, which contains blood capillaries that gives the pink colour of the nails. A white, crescent-shaped lunula extends from under the proximal nail fold. The lateral borders of the nail plate are enveloped by the lateral nail folds. The skin underlying the free end of the nail represents the hyponychium.
Congenital and hereditary disorders often present with absence, hypoplasia incomplete development , or dysplasia abnormal development of the nails. Congenital malalignment of the big toenail represents a lateral deviation of the nail plate from the longitudinal axis of the distal phalanx. As a result of repeated trauma, this congenital abnormality causes thickened nail plate, onycholysis separation of the nail plate from the nail bed and discoloration of the nail. With time, this can lead to an ingrowing painful toenail.
Spontaneous improvement occurs in some patients. In ectodermal dysplasia, nails may be brittle, abnormally shaped, thickened, discoloured or absent. In pachyonychia congenita an autosomal dominant disorder of keratinization , the nails usually appear packed and thickened hyperkeratotic and frequently discoloured.
Chapter By the end of this chapter the reader should:.
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