Skin lesions of general medical importance. Skin diseases How diet errors affect the skin

Thomas B. Fitzpatrick, Jeffrey R. Bernhard

The skin is one of the most sensitive indicators of a serious illness: even with an untrained eye, it can be distinguished by cyanosis, icterus or ash-gray pallor in shock. An experienced physician should be able to identify mild skin manifestations of life-threatening diseases and know the diagnostic criteria by which diseases of other organ systems are diagnosed. Skin manifestations are often critical to a definitive diagnosis. Thus, some skin "marker syndromes", such as erythema nodosum, may indicate a multisystem disease and require a correspondingly careful medical evaluation.

The skin (Fig. 48-1) consists of three layers: 1) the epidermis - the superficial part, which includes two main types of cells (keratinocytes and melanocytes); 2) the dermis, on which the epidermis rests; it is a complex of connective tissue elements, nerves, blood and lymphatic vessels, bodies, skin appendages and some cells (mast, fibroblasts, histiocytes); 3) subcutaneous adipose tissue (subcutaneous tissue), acting as a soft layer between the outer layers and the underlying bone. Keratinocytes produce and accumulate intermediate filaments of keratin in the cytoplasm. They are constantly changing; about 27 days are enough for their differentiation and maturation. In the process of maturation, the keratinocyte loses its nucleus, retaining only the cytoplasm, which turns into a highly organized two-phase system of keratin filaments immersed in an amorphous matrix, which is in many ways similar to the fiber-lignin system of wood fiber, which is recognized as a high degree of resistance to stretching and pressure. The nuclear-free outer part of the epidermis (stratum corneum) acts as a dense keratin membrane. This stratum corneum functions virtually as a waterproof barrier between the internal fluid environment and the external environment. This is the main skin barrier that prevents the loss of fluid in the body and the penetration of toxic agents into it. It also functions as a passive membrane: some substances pass through the skin by passive diffusion in the direction of the concentration gradient.

The skin has a relatively limited number of pathological reactions. If we represent specific skin lesions with letters of the alphabet, then their groups, figuratively speaking, will form words and phrases. This allows an experienced specialist to recognize clinically significant syndromes or establish a diagnosis. In most patients, the changes on the skin detected by the therapist are comparable to those in one of the groups of syndromes (see Table 47-3) or types of skin lesions (see Table 47-1). These skin changes or clinical manifestations may be one type of lesion, such as a vesicle or nodule, or an accumulation of different types of skin elements, such as papules or vesicles. Single or multiple elements can be found in any part of the body; in some pathological processes, their boundaries are not defined: this type of diffuse lesion occurs in systemic sclerosis and pigmentation disorders.

Rice. 48-1. Skin Anatomy (courtesy of Frank H. Netter).

Skin manifestations of systemic diseases such as generalized pruritus (see Chapter 50), sensitivity to light (see Chapter 52), and malignancy in internal organs are not discussed in this section. Skin reactions in diseases of other organs, such as hyperpigmentation in Addison's disease (see Chapter 51) or café-au-lait spots in neurofibromatosis, are also discussed in their respective sections.

When attempting to determine a specific type of skin lesion, it is important to identify the primary affected skin element, i.e. the epidermis, dermis, blood vessels, or subcutaneous fat. This method contributes to the improvement of the diagnostic capabilities of the doctor, since the number of diseases that cause pathological changes in each of these skin components is limited. For example, although erythema multiforme causes changes in the dermis and epidermis, blood vessels are primarily involved in the process, while erythematous spots are explained by the secondary involvement of other components in the process, the inflammatory process leads to the development of cellular infiltrates, clinically determined in the form of papules, to the destruction of the basal membranes and blister formation.

Damage classification by primary element

Epidermis

Scaly patches, papules or plaques. Generalized scaly macules, papules or plaques are common and significant diagnostic features that the patient usually pays attention to (see Fig. 47-2, 47-3, 47-11).

The sudden appearance of symmetrical, scaly, erythematous macules or papules is often indicative of drug hypersensitivity reactions. Scaly, erythematous papules on the scalp and extensor surfaces of the arms and legs suggest psoriasis. Psoriasis elements are often especially pronounced in places prone to repeated injuries (elbow and knee joints). Psoriatic papules or plaques often have silvery-white, mica-like scales that can be removed in layers relatively easily. The number of basal cells of the epidermis in psoriasis increases many times. This increase in the population of basal cells reduces the time of renewal of the epidermis from 27 days normally to 3-4 days. As the migration of epidermal cells from the basal layer to the skin surface accelerates, the process of cell maturation and keratinization is disrupted (see Fig. 47-12, A), which determines the localization of morphological and biochemical changes. Along with hyperplasia of basal cells, metabolism increases. the synthesis and breakdown of nucleoproteins are accelerated, which leads to increased excretion of nucleic acid metabolites, such as uric acid, in the urine. In addition, in connection with the need to ensure the acceleration of cell division, subepidermal vessels proliferate. These numerous cytological, histological, histochemical and biochemical changes are currently considered as a result rather than a cause of the development of the disease. The only significant point currently known regarding the underlying cause of psoriasis is the inheritance of a predisposition to it. Erosive joint disease, psoriatic arthritis are discussed in the relevant chapter.

Treatment for psoriasis is still the responsibility of a dermatologist. For localized psoriasis, topical corticosteroids, tar preparations, ultraviolet radiation, or exposure to sunlight are most effective in most patients. Corticosteroids can be injected directly into small elastic plates. Their systemic administration is not only ineffective, but can cause a generalization of the process. Some patients with generalized psoriasis need to be treated with complex chemotherapeutic drugs, especially methotrexate, which can suppress cell reproduction to a greater extent than their function, i.e., keratinization.

In 1974, a new form of photochemotherapy was proposed, in which powerful long-wave ultraviolet irradiation was performed while the patient was receiving methoxsalen. This method can replace many others. With the so-called PUFL treatment (psoralen in combination with ultraviolet rays), 2 hours before the general irradiation of the body using a special system that allows you to receive predominantly UFL with a wavelength of 320-400 nm (UFL-A), the patient must take psoralen (P ). For the appearance of erythema or the achievement of remission in psoriatic lesions, radiation itself is ineffective, however, in the presence of one of the psoralens (methoxsalen), UFL-A turns into an effective light-active factor, and after repeated use, the intensity of psoriatic changes decreases. The mechanism of this action may be partly explained by the binding of psoralen to DNA under the influence of UV-A. An analysis of more than 5,000 points performed in a number of clinics in the USA and Europe showed the high efficiency of photochemotherapy against the background of taking methoxalen in severe psoriasis: more than 80% of patients were completely cured after 3-4 weeks of treatment (2-4 times exposure per week). Subsequently, it is desirable to carry out maintenance radiation sessions weekly or less frequently. While effective, methoxsalen photochemotherapy requires specialized knowledge and equipment to accurately calculate UFL-A;

PUFL-therapy is recommended only for patients with a disabling form of psoriasis, since the long-term effects of treatment include premature skin aging, skin cancer in some susceptible patients (i.e., with a history of exposure to arsenic or ionizing radiation), cataracts. In exceptional cases of disabling and persistent psoriasis, it may be necessary to combine PUFL or UVB (medium wavelength ultraviolet rays) with other agents, such as systemic administration of methotrexate after or in combination with a course of radiation.

The therapist does not always take into account the possible role of psoriasis as the cause of disability or changes in the patient's appearance. In the US, psoriasis affects 2-8 million people, with about 100,000 in a serious form.

With glucagon syndrome, psoriasis-like changes appear on the skin of the face, lower abdomen, buttocks, inguinal region, perineum, and legs. Sometimes they are difficult to distinguish from changes in subacute psoriasis, but often they are distinguished by superficial necrosis in the center of the plates. Stomatitis and anemia also join, the patient's body weight is clearly reduced. Hyperglycemia may be absent. Ulceration quickly disappears after removal of the glucagon-secreting tumor of the pancreas. Psoriasis-like skin changes also occur in Reiter's syndrome (keratoderma blennorrhagicum), mycosis fungoides (cutaneous T-cell lymphoma), nummular eczematous dermatitis, parapsoriasis, some drug reactions, and dermatophytosis.

Symmetrically located on the palmar and subliminal surfaces, scaly spots or papules are often mistaken for a manifestation of secondary syphilis, while generalized lymphadenopathy and ulcerations in the oral cavity are very often noted.

Quite banal and often baffling the doctor, generalized scaly rashes appear with pink lichen. In this case, the scale is very thin on the periphery of the lesion and forms a kind of "collar", in the center there may be no peeling. Pityriasis rosea usually spreads like a coniferous tree, which is especially noticeable on the back. Not always, but quite often, a few days before the generalization of the process, a single isolated scaly precursor spot appears on the skin.

Peeling spots and papules are formed with dermatophytosis and candidiasis, therefore, in any case of peeling, it is necessary to examine some scales for the detection of mycelium (see "Laboratory tests" in chapter 47).

Susceptibility to superficial dermatophytosis is variable and appears to be at least in part dependent on the reactivity of the organism. The effect of taking griseofulvin inside is also variable: it depends on the localization of the infection. Griseofulvin is effective even in the treatment of short courses of fungal infections of the skin of the scalp, trunk, inguinal region, but even with long-term treatment, it is rarely possible to cope with damage to the skin of the hands, nails of the fingers and toes. When infecting the plantar surface, skin of the trunk, inguinal region, local treatment with any of the antifungal drugs of the imidazole series is highly effective, but it is ineffective when the nails of the fingers and toes are affected.

Another large group of fungal infections is represented by candidiasis. They are completely unresponsive to oral griseofulvin and are caused mainly by Candida albicans, sometimes by C. tropicalis, C. krusei, and C. stellatoidea. C. albicans can saprophyte in the gastrointestinal tract and vagina, especially in pregnant women or in women taking oral contraceptives or broad-spectrum antibiotics. However, these infections are so associated with diabetes that all patients with candidiasis, regardless of gender, should be examined for this disease.

Although C. albicans is a common saprophytic fungus found in the vagina and gastrointestinal tract, it is rarely isolated from healthy exposed skin. It can penetrate the epidermis at high skin moisture and maceration. Thus, candidiasis usually occurs in areas of diaper rash (under the mammary glands and in the navel, groin, axillary pits) and in the mucous membrane of the oral cavity and vagina. C. albicans usually causes chronic paronychia. In candidiasis infections, the lungs, urinary tract, and heart may be involved.

Treatment for candidiasis of the skin and mucous membranes depends on the location of the infection and the type of damage. Maceration of the skin should be combated by drying the affected area with an air stream. In places of diaper rash, it is very useful to apply lotions and powders with nystatin. Its oral administration with cutaneous candidiasis is ineffective. With untreated candidiasis, its sexual transmission is inevitable. The most successful treatment for fungal paronychia is the use of a 2% alcohol solution of gentian violet. In some cases, for example, in chronic mucocutaneous candidiasis, systemic administration of ketaconazole is indicated.

Without culture, it is difficult, if not impossible, to differentiate dermatophytosis caused by one of these types of fungi from candidiasis. A direct study of the scales of a scaly rash in the area of diaper rash has no diagnostic value, since the mycelium can be detected both in dermatophytosis and in candidiasis, but spores are found only in candidiasis. Therapists too often start using topical antifungals or griseofulvin without determining whether the rash is dermatophytosis or candidiasis. Since parenterally administered griseofulvin is ineffective in candidiasis, and dermatophytes are resistant to nystatin, the use of these drugs for unspecified rashes can lead to prolongation of the disease. Newer drugs, such as haloprogin and miconazole, are effective in both dermatophytosis and candidiasis.

Due to the increase in the number of patients treated with chemotherapy for leukemia and other neoplastic processes, fungal diseases have acquired a new meaning in medicine. Patients, including kidney transplant recipients, are exposed to almost all saprophytic fungi that invade their tissues.

Vesicles and blisters. A number of diseases (erythema multiforme and tardive porphyria cutaneous) can be accompanied by the formation of vesicles and blisters, which, however, are manifestations of certain bacterial and viral infections, allergic contact dermatitis (for example, in connection with poison ivy), trauma, thermal and chemical burns and , most importantly, bullous diseases of unknown etiology (pemphigus and pemphigoid).

With herpes zoster and herpes simplex, group vesicles form, with chickenpox - isolated, discrete vesicles. In determining their nature, the Zanka test plays an important role (see, about laboratory research methods in Chapter 47). Giant epithelial cells are found in herpes simplex, herpes zoster, and varicella, but absent in vaccinia and varicella. The nature of a vesicle or bladder can be identified by skin biopsy, regardless of their intra- (viral infections and pemphigus) or subepidermal (bullous pemphigoid) localization (see Fig. 47-7-47-9).

Vesicles lining up in linear stripes are typical of poison ivy dermatitis. The most reliable diagnostic sign of both allergic and primary contact dermatitis is the localization of vesicles in skin areas exposed to the corresponding factor. Isolated vesicles and blisters on the skin of the dorsal surface of the hands and face may be the only manifestation of late cutaneous and mixed porphyria. In the first case, the diagnosis can be quickly confirmed by examining the urine with a Wood's lamp. These patients do not suffer from photosensitivity, although the topography of the lesions suggests that sunlight plays a role in their localization.

Isolated disseminated blisters in adults represent a major challenge in terms of diagnosis and treatment. Bullous pemphigoid and pemphigus a are chronic and occur predominantly in adults. Pemphigus has serious consequences for the patient. These two diseases should be differentiated using skin biopsy and immunofluorescent techniques. Only by the clinical picture it is impossible to differentiate bullous pemphigoid, which proceeds chronically and benignly, from pemphigus vulgaris, a serious disease that inevitably ends in the death of the patient, if he. not receiving immunosuppressants. There are four distinct types of pemphigus, but the most important in terms of recognition for the therapist is pemphigus vulgaris. It can begin on the mucous membrane of the nasal cavity or mouth, so the patient often first turns to the dentist or otorhinolaryngologist about non-healing erosions in the larynx (hoarseness), mouth or nosebleeds. Damage tends to spread to other areas without any patterns, but with a predominant localization in the navel, scalp, torso. Pemphigus vulgaris occurs predominantly in middle-aged people (40-60 years old) and rarely in people under the age of 17 and older than 75. From the very beginning, it is clinically manifested by the formation of flabby blisters in the skin, easily bursting and rarely increasing to large sizes. Erosions formed at the site of a bursting bladder increase in area due to exfoliation of the epidermis, which poses a serious problem in combating secondary infection and maintaining fluid balance; approximately the same difficulties arise in the treatment of patients with extensive burns. The mucous membranes of the mouth and nose are affected in almost all patients; in more than half of the cases, the first manifestations of the disease are damage to the oral mucosa. More often at first they are not numerous and within a few weeks can retain their original size. The process then spreads to other areas of the skin.

The diagnosis of pemphigus is made on the basis of a light-optical study of early vesicle biopsy specimens and direct immunofluorescence. The earliest changes in pemphigus vulgaris include intercellular edema, followed by the disappearance of intercellular bridges in the deep layers of the epidermis (see Fig. 47-9, A). In this regard, the bonds between the epidermal cells (acantholysis) are weakened and gaps are formed, and then bubbles, most often in the suprabasal layer. In other words, the basal cells, being separated from one another, retain their connection with the dermis like tombstones.

Immunofluorescence makes it possible to detect in the serum of patients with pemphigus IgG antibodies specific for the intercellular substance of the skin and mucous membranes, and to differentiate pemphigus from pemphigoid by their localization. In pemphigus, fluorescence is detected exactly at the sites of acantholysis, since IgGs are associated with the intercellular glycocalyx of epidermal cells. In bullous pemphigoid, antibodies interact with the antigen in the area of the basement membrane and fluorescence is noted in this zone.

Parenteral administration of corticosteroids, sometimes in combination with azathioprine, is quite effective in pemphigus. In some patients, the desired result can be obtained only through the use of this drug.

Pustules. This skin reaction (see Fig. 47-10) may be the result of an infectious or aseptic inflammatory process. Pustules may arise from previous vesicles of any etiology. Infection with pyogenic bacteria, especially staphylococci and some types of fungi and mycobacteria, can lead to the development of pustules without a vesicular stage. Of the causes of non-infectious nature, acne, pustular psoriasis and hypersensitivity to drugs, especially to sulfonamides, iodides and bromides, should be noted. Purple pustules on the arms and legs are characteristic of disseminated gonococcemia but may occur in other forms of bacterial sepsis.

Exudative (impetiginous) rashes. Acute infection with gram-positive cocci may develop primarily or superimpose on eczematous dermatitis, and sometimes on any vesiculobullous disease, and is characterized by the appearance of scabs (see Fig. 47-13). This process in the skin leads to the same consequences as streptococcal pharyngitis, since acute glomerular nephritis develops in a significant proportion of patients with dermatitis with rashes. These patients should receive a full course of parenteral antibiotic treatment.

Eczematous dermatitis. This type of skin damage is a typical inflammatory response to both endogenous and exogenous factors, and not an independent nosological unit. It must therefore be defined by an etiologically justified term, namely "a topical eczematous dermatitis". This disease requires serious attention due to the very high incidence of skin lesions. About 1/3 of all patients observed by dermatologists in the United States suffered from eczema, which caused incalculable loss of working time and reduced productivity. Some forms of eczematous dermatitis are given in table. 48-1 and 48-2 (see also figs. 47-8 and 47-11). Of all the disorders of this kind, atopic eczematous dermatitis is the most important for the therapist. More than 30% of patients develop respiratory disorders of an allergic nature (asthma and hay fever). In addition, the disease continues for 15-20 years. 15% of young people develop cataracts. Finally, patients with atonic eczematous dermatitis are particularly susceptible to infections such as lichen simplex and cowpox. Most of them have elevated serum IgE levels. It is very difficult to reduce the intensity of persistent itching, the most effective topical application of corticosteroids, tar gels, oil baths, emollient ointments and the prevention of emotional stress.

Erythrodermal syndrome (exfoliative dermatitis). This serious disease may develop as a reaction to drugs, complicate generalized spread of dermatitis (eg, psoriasis) or atopic dermatitis, or be associated with lymphoma and leukemia. The syndrome manifests itself in the form of generalized erythematous scaly rashes on the entire surface of the skin and is of great importance due to systemic disorders resulting from massive and prolonged skin desquamation. The severity of metabolic changes in response to peeling depends on the duration and severity of the process itself. Significant metabolic disturbances in chronic exfoliative dermatitis occur at a desquamation rate of about 17 g/mm2 per day. In patients with this form of dermatitis, a negative nitrogen balance, edema, hypoalbuminemia, and a decrease in muscle mass can be detected. Another notable feature of these patients is the large extrarenal water loss due to a distinct increase in its transepidermal exit through the damaged skin barrier. The course of exfoliative dermatitis is determined by its etiology: at present, this disease is not a mystery in patients with psoriasis or atopic dermatitis, but in lymphoma and leukemia, the prognosis of the disease is unclear. About 60% of patients with exfoliative dermatitis recover within 8-10 months, 30% die, and treatment is ineffective in 10% of patients.

Diffuse or limited (focal) atrophy. Epidermal atrophy is manifested by almost complete transparency of the epidermis and is associated with a decrease in the number of endermocytes. Atrophied epidermis may retain signs of healthy cells, and atrophy is often accompanied by changes in the dermis. A limited form of atrophy accompanies discoid lupus erythematosus, diabetic lipoid necrobiosis, occurs with atrophic stretch marks of the skin, diffuse atrophy of the epidermis, with aging and scleroderma.

The most significant disorder in the atrophic type is diabetic lipoid necrobiosis- (NLD). Such lesions are usually asymptomatic, appear more often in women in places prone to trauma, for example, on the anterior and lateral surfaces of the lower leg, and may also appear on the skin of the hands and even the face. Initially, a small raised nodule with distinct reddish edges is formed,

Table 48-1. Types of eczematous dermatitis of unknown etiology

The term is used by many clinicians in connection with at least four types of eczematous dermatitis that can only occur on the hands (atopic eczematous, allergic contact eczematous, nummular eczematous, and dyshidrotic eczematous dermatitis). It is possible that contact irritants, which are often exposed to the skin of the hands, play the role of provoking or aggravating factors in the development of one of the listed types of eczematous dermatitis.

Such rashes are considered manifestations of eczematous dermatitis, but the necessary clinical descriptions and data on the results of skin biopsy are often lacking. For example, constitutional diathesis and contact dermatitis, which gradually (as skin atrophy develops) increases and flattens, becomes not so high. The skin becomes brownish-yellow to orange in color, and blood vessels can be clearly seen due to the evenness, thinning, and translucency of the atrophic epidermis. NLD is typically indolent, but may develop shallow ulcerations that are resistant to medication. In all likelihood, NLD may develop in individuals with undiagnosed diabetes mellitus, but sufficiently complete examinations of patients in this group using glucose tolerance tests, in particular cortisone-glucose tolerance, have not been carried out. With NLD, focal changes appear in the dermis, which are acellular and intensely infiltrated by eosinophils areas of necrosis, surrounded by areas of inflammation. The main feature is granulomatous inflammation with epithelioid cells, histiocytes, and multinucleated giant cells. The process always involves blood vessels, the endothelium of which proliferates, and sometimes occlusion of arterioles and deep arteries of the dermis occurs; capillary walls thicken, they accumulate PAS-positive material. Some patients are cured by careful injections of suspensions of triamcinolone acetonide into the lesions.

Table 48-2. Types of eczematous dermatitis, known etiology

Hypomelanotic spots, diffuse hypomelanosis, hypermelanotic spots and diffuse brown hypermelanosis syndrome, see Chap. 51.

Papules and nodules (with and without inflammation). With an unchanged epidermis (i.e., without peeling), papules and nodules may have the color of healthy skin, be erythematous, sometimes poorly pigmented (yellow or brownish). Since they may be manifestations of a more significant pathological process of a general nature, such as sarcoidosis, histocytosis X, tuberculosis, lymphoma, or cancer metastases, a biopsy of dermal papules and all nodules is necessary to establish a definitive diagnosis. Since dermal nodules also appear with deep fungal lesions, such as coccidioidomycosis, it is necessary to biopsy not only to exclude their malignancy, but also to sow part of the excised tissue to identify fungi. For sowing, the tissue of the nodules is crushed with a pestle in a mortar. If nodules resemble leprosy or tuberculous nodules, histological preparations should be carefully examined for acid-fast bacteria. Material obtained from skin areas in which the leishmanial process is usually localized (face and hands) must be carefully examined for the presence of leishmania.

Papules and nodules with or without signs of inflammation may occur with pathology of the sebaceous glands. The latter are widely distributed in the skin of the face and scalp, although they are also found in the skin of the labia minora and scrotum, trunk, breast nipple and eyelids. The sebaceous gland refers to the holocrine glands, characterized by desquamation of the entire cell into the excretory duct. The sebum it secretes is a complex lipid mixture of squalene (the main product of the steroid cycle), triglycerides and wax esters. The work of the sebaceous glands is regulated by androgens secreted by the gonads. In women, unlike men, adrenal androgens may be an important factor involved in maintaining the function of the sebaceous glands. The main disease of these glands are common acne (acne vulgaris), mainly on the face, to a lesser extent on the back, chest and shoulders. Papules and nodules appear on the skin with and without an inflammatory reaction. Non-inflamed papules, called acne, may be open (black dot) or closed (white dot). Closed blackheads are precursors of papules, pustules, and large inflammatory nodules. In addition, cysts and scars of various sizes may appear, a typical acne scar looks like a clear depression with a hole. Pustular and cystic changes, despite the abundance of purulent exudate, in which the incision is quite effective, are usually sterile, but may contain Propionibacterium acnes.

The root cause of the formation of acne, both closed and open, is still not exactly known, but the initial histological phenomenon is excessive keratinization in the follicle canal. Currently, it is believed that in the process of triglyceride lipolysis, carried out by Propionibacterium acnes, fatty acids are released that can cause an inflammatory reaction in the follicle wall, followed by its rupture. The entry of the contents of the follicle into the tissue is accompanied by perifollicular inflammation. The inflammatory infiltrate has a lymphocytic character, but later (due to the presence of keratin material, gram-positive diphtheria-like bacteria and sebum) in it. giant cell reaction to a foreign body.

The action of antibiotics in acne is not well understood, but it is known that they reduce the amount of propionobacteria (Propionibacteria) and free fatty acids on the surface of the skin. Since these microorganisms have an in vitro lipolytic effect, it is assumed that the decrease in the level of free fatty acids is associated with the action of antibiotics. It is believed that lotions and gels with benzene peroxide, which are highly effective and widely used by dermatologists, have an antibacterial effect (decrease in the population of microorganisms).

Initially, it was assumed that the combined use of estrogens and progestins (oral contraceptives) should be effective in acne, but their value turned out to be not so high in the treatment of women, while they are contraindicated in men. There are no convincing data on any effect of food products on the dynamics and severity of acne vulgaris. The latter may appear in the 8th year of life or be absent until the age of 20 years, remain for several years, and then spontaneously disappear, usually at the beginning of the third 10th anniversary of life. For some individuals, however, acne vulgaris continues to bother later in life. New effective treatments for acne include topical solutions of antibiotics such as clindamycin and erythromycin. With a pronounced cystic form of acne, the most effective, but unsafe, 13-c15-retinoic acid, taken orally. It has a quick and pronounced effect, but at the same time it has teratogenic activity. It should not be given to women of childbearing age unless effective contraception is guaranteed. Some other side effects, such as dry skin, hypertriglyceridemia, bone growths, make this drug only used in severe cases when other treatments have failed.

Pretibial myxedema can also lead to the formation of nodules on the legs, the back of the feet. The process is usually bilateral, nodules and plaques are dense, raised, and difficult to move. They can be the color of healthy skin, pink, sometimes brown, and appear yellow, waxy in diascopy. The epidermis above the nodules in some cases is not changed, in others it has a distinct warty surface. The pathogenesis of pretibial myxedema is unclear. It can develop alone or in combination with hyperthyroidism (Graves' disease), both before treatment of the latter and after it, the dynamics of its manifestations does not correspond to the dynamics of changes in the eyes (if any). Nodules in this disease serve as sites of accumulation of mucopolysaccharides, which can be demonstrated by special methods of staining histological preparations. In the pathogenesis of pretibial myxedema, exophthalmos, and acropathy, the role of a long-acting thyroid stimulator bound in plasma to immunoglobulin G (7S β-globulin) has been discussed, but its significance in the development of pretibial myxedema has not been elucidated.

The most important etiological factors in the development of ulcers on the legs and feet are circulatory disorders. Chronic venous insufficiency leads to ulceration, especially in the region of the medial malleolus and the medial surface of the lower third of the leg, ulcers develop in areas of the skin with brownish hemosiderin pigmentation, sometimes edematous and sclerotic. In the area of the lateral malleolus, ulcers of a hypertensive and ischemic nature develop predominantly. Ulceration may be due to tissue infarction in the area receiving blood from large or small vessels (arteries, arterioles). Infarction may result from occlusion or narrowing of a vessel associated with embolism, thrombosis, exposure to cryoagglutinins, macroglobulin-, cryoglobulinemia, thrombotic thrombocytopenic purpura, polycythemia, systemic lupus erythematosus, Raynaud's disease, arteriosclerosis obliterans and thromboangiitis. Leg ulcers can also occur with hemolytic anemia, including sickle cell anemia, thalassemia, and congenital spherocytosis.

Some types of ulcers, such as pyoderma gangrenosum, are characterized by severe marginal necrosis. Usually they are localized on the legs, are characterized by a sluggish course, often combined with ulcerative colitis or regional ileitis. Ulcers in pyoderma gangrenosum are surrounded by uneven bluish-red edges and have a necrotic bottom. In the initial stage they are often represented by pustules or small red nodules at the site of injury, gradually increasing in size until the development of liquefying necrosis and the formation of an irregularly shaped ulcer. They are often multiple and can occupy a significant part of the surface of the lower leg. Histopathological findings are nonspecific. The healing process proceeds more frequently in accordance with the course of ulcerative colitis, and as the ulceration extends to the reticular dermis and subcutaneous tissue, a scarring process occurs. Pyoderma gangrenosum and its variants can also develop in other diseases, such as myeloproliferative disorders and rheumatoid arthritis. The term “tropical ulcer” now refers not only to ulcers in cutaneous leishmaniasis, but also to those developing in cutaneous diphtheria, syphilis, yaws and tropical syphilis, as well as to corrosive ulcer (chronic ulceration on the dorsum of the foot or lower leg, caused by a variety of bacteria starving homeless people).

Ulcers can also form with peripheral neuropathy ("neuropathic" ulcer, or malum perforans-perforating ulcer), complicating diabetes, dorsal tassels, polyneuritis, leprosy, congenital anesthesia, hereditary sensory radicular neuropathy.

In histiocytosis X and amebiasis, ulcers are localized in the anal and perianal regions. A hanging drop test is required to detect Entamoeba histolytica.

With an unusual form of ulcers, one should think about their possible artificial origin, for example, when exposed to acid or cauterized with a burning cigarette. Most doctors pay too much attention to these ulcers when examining a patient, but, unfortunately, they do not know how to recognize their nature. Nodular and ulcerative formations of stony density, especially around the joints (elbow, knee, finger), may indicate skin calcification or gout. Radiography contributes to the detection of calcification, but with gout, seals are not detected by this method.

Diffuse or focal sclerosis. Diffuse sclerosis of the skin is more common on the arms, chest, and face in systemic sclerosis, sometimes called progressive systemic sclerosis. At first, the skin appears yellowish and slightly edematous, pressure on it leaves no imprints; later it thickens, the affected area becomes delineated and may be distinctly hyperpigmented. Skin calcification and Raynaud's phenomenon are usually determined.

Focal sclerosis accompanies limited scleroderma. In this case, one or more rounded or oval dense reddish plaques with a diameter of up to several centimeters appear, the center of which subsequently turns white or yellow, and the edge often differs in a lilac tint - with telangiectasias. This process does not spread to other organs and is a localized cutaneous form of scleroderma. Another type of localized scleroderma is linear scleroderma, the morphological changes in which are the same as in limited sclerosis, but the process develops in areas of the skin in the form of strips parallel to the axis of the limb, or along the near-median line in the forehead and scalp. This form of scleroderma is not associated with progressive systemic sclerosis.

Edema. In addition to local and generalized, there is another form of leg edema, rarely recognized by a doctor. This is a bilateral swelling of the feet, a fairly common process in patients with subacute or chronic dermatitis of the feet, most often with chronic eczematous dermatitis and psoriasis. It has nothing to do with heart disease and occlusion of the lymphatic vessels, it may be associated with increased permeability due to local capillary damage, which is part of the inflammatory process in the skin. Increased permeability of capillaries leads to an increased transition of fluid from them into the extravascular space. This form of edema is characterized by the formation of pits in places of pressure on the skin; when dermatitis is relieved, the edema disappears completely.

Diffuse or focal atrophy. Atrophy of the dermis is caused by a decrease in the amount of connective tissue in the papillary and reticular layers and is manifested by a retraction of the skin surface. Focal atrophy of the dermis may remain after an injury, combined with atrophy of the epidermis, for example, during the formation of pregnancy bands or Cushing's disease.

Panniculitis of adipose tissue (subcutaneous)

Nodules (inflammatory, usually soft, red). The localization of nodules in the subcutaneous tissue is judged on the basis of a sign of displacement of the skin above them. However, in some cases, during inflammatory processes, the nodule can be related to both the subcutaneous base and the dermis, so it is not possible to displace the skin over it. Acute, soft, red nodules on the legs are typical of erythema nodosum syndrome and nodular subcutaneous fat necrosis associated with pancreatitis.

Erythema nodosum syndrome includes bilateral formation, mainly on the anterior surface of the lower leg or less often on the hands and skin of the face, multiple soft nodules. This syndrome is combined with a number of other disorders that are not related to one another, their common properties include only a distinct hypersensitivity reaction.

Nodules with erythema nodosum rise slightly above the surface of the surrounding skin, they are swollen, sometimes very tender. The disease is characterized by the formation of bruises as a result of hemorrhage. The lesions never ulcerate or thicken, and very rarely leave scars or signs of atrophy. Erythema nodosum is associated with primary tuberculosis, primary coccidioidomycosis, histoplasmosis, yersiniosis, infections caused by? contraceptive preparations containing ethinyl estradiol and norethinodrel.

Soft red subcutaneous nodules can appear on the legs and in acute pancreatitis, pancreatic tumors and are mistakenly regarded as manifestations of erythema nodosum. This pathology of the skin is called melting panniculitis nodosa (URP), the accompanying formations are distinct and morphologically different from those in classic erythema nodosum. In URP, they vary in size from a few millimeters to several centimeters, and they are mobile, in contrast to the nodules in erythema nodosum. Within 2-3 weeks they undergo reverse development, sometimes leaving behind hyperpigmented scars with a slightly depressed surface. The appearance of nodules may be accompanied by pain in the abdomen, fever, joint pain. Sometimes nodules can develop in other areas of the body. Some of the larger nodules develop similarly to abscesses: they begin to fluctuate, rupture, and exude whitish, creamy or oily, viscous masses. In erythema nodosum, the formation of draining abscesses is not typical. Of pancreatic tumors accompanied by URP, acinar adenocarcinoma is more often detected. With Weber-Christian panniculitis, at first, sedentary nodules are soldered to the surrounding skin, and then, as the edema decreases, a depression appears in the center of the compaction zone.

In addition to the mentioned nosological forms, various types of vasculitis can also be the cause of the formation of soft subcutaneous nodules. Thus, a biopsy through excision or incisions is often required to diagnose these lesions.

Nodules (non-inflamed, usually indurated, non-erythematous). Displaceable, painless, seemingly non-inflammatory nodules appear around the joints in articular rheumatism, rheumatoid arthritis, and a number of metabolic diseases such as xanthoma, gout, and calcification. Mobile rather firm, subcutaneous nodules may represent skin metastases of cancer and malignant melanoma. Subcutaneous nodules on the legs may manifest sarcoidosis. They can also form in onchocerciasis and filariasis. Quite often, they are caused by lipomas (benign tumors represented by adipose tissue, single or multiple, often lobulated). They are more often elastic and compressible, in most cases they are determined on the trunk, back of the neck and forearm. Subcutaneous lipoma can be painful and associated with severe obesity. This condition, known as Derkum's disease, is more common in middle-aged women,

Diffuse or focal atrophy. Atrophy of the subcutaneous tissue causes retraction of the skin surface and occurs with lipodystrophy, melting panniculitis, and localized fatty atrophy at the injection sites of insulin. Almost 25% of diabetic patients taking insulin (most often women under the age of 20 years) experience atrophy of this nature. In places of depressions with local fatty atrophy, the subcutaneous base is completely absent, there are no signs of inflammation. With lipodystrophy, diffuse atrophy of the skin can spread to large areas of the skin,

Blood vessels

Measles-like and scarlet fever-like eruption. These forms of skin eruptions are macules and papules and may occur in response to treatment with certain drugs, in measles, rubella, erythema infectiosum, other skin eruptions of viral origin, and in rickettsiosis, including endemic murine typhus and Rocky Mountain fever, scarlet fever, and secondary syphilis. Many diseases accompanied by the appearance of spots or papules in acutely ill and febrile patients are shown in Table. 48-3.

Hives. Urticaria is characterized by the formation of blisters, the distinguishing feature of which is that they exist for only a few hours (see Fig. 47-6). On this basis, they are differentiated from papules with erythema multiforme, which remain for 1-2 days or more. An acute onset usually indicates a connection between urticaria and medications or certain types of food (oysters, fresh berries).

Table 48-3. Rash and fever in acutely ill patients: diagnosis according to the nature of the manifestations

May be accompanied by arthralgia and musculoskeletal pain. "A typical sign is spider-like depressed papules or vesicles. 11 Often represented by infarcts.

But: Fitzpatrick T. B., Johnson R. A. Dermatology in General Medicine.- 3d ed.- New York: McGrow-Hill, 1987.

Erythema multiforme syndrome. This syndrome is a specific type of reaction of the skin and mucous membranes to the action of a number of factors, including infectious agents (human herpes virus, pulmonary mycoplasma) and drugs (especially penicillin, antipyretics, barbiturates, hydantoins and sulfonamides). In 50% of patients, the etiology of the syndrome remains unclear. The main pathological sign is an acute lymphohistiocytic inflammatory infiltration around the blood vessels and at the border between the dermis and epidermis. Degenerative changes also appear in capillary endotheliocytes, marked swelling of the papillary dermis and necrosis of keratinocytes. There is also some evidence linking the syndrome with the immune complex and hypocomplementary vasculitis.

Skin changes are characterized by symmetry, develop mainly on the extensor surfaces of the distal parts of the arms and legs, on the back surfaces of the hands and feet. The process often involves the palmar and plantar surfaces even in the absence of changes on the dorsal surfaces. Bubbles appear in the oral cavity, on its mucous membrane, gums and tongue, later eroding. The lips are often swollen, and scabs form on them. Acute toxemia, weakness, high fever, cough and "spotted" inflammatory process in the lungs can join. Skin elements are often bright red in color, the intensity of their color gradually decreases, these areas thicken, they form centers of pale color, which may contain blisters. Such target- or diaphragm-like changes, variable but typical of erythema multiforme, are identified by a bright red rim around a pale pink area with a cyanotic center, which may contain a bubble. Systemic treatment with corticosteroids is widely used, but its effectiveness has not yet been proven.

Purpura (with or without inflammation). When a purple rash appears, it is necessary to immediately determine its etiology. Almost always, purpura is associated with the vessels of the dermis. Depending on their size, purple spots gradually disappear over several days or weeks. Dotted and small spots are called petechiae, larger ones (more than 2 cm in size) are called bruises, and extensive purple spots are called ecchymosis (see Fig. 47-2, D).

Purpura with inflammation is usually palpable, that is, it looks like papules, and occurs with systemic vasculitis and bacteremia such as staphylococcus, gonococcus, and meningococcemia. In these conditions, a diagnosis can be made by skin biopsy within 8 hours (the time required for tissue processing). Careful scraping of the area of the purplish spot may provide sufficient material for a Gram stain; intracellular gram-positive diplococci are sometimes found in acute, meningococcal and gonococcemia. Recognition of elements of palpable purpura and infarcts that occur with systemic vasculitis (necrotizing vasculitis), on the one hand, and with chronic meningococcemia, on the other, is difficult. Skin lesions in systemic vasculitis are usually bilateral and nearly symmetrical, tending to be concentrated on the legs, especially in the lower sections, around the ankles, and on the dorsum of the foot. In chronic meningococcemia, they can appear on the trunk, arms and legs, and on the face. However, in this case, the rash can be bilateral, which complicates, if not impossible, the timely differential diagnosis of chronic meningococcemia and systemic vasculitis. The type of skin elements in both conditions can be identical: a complex of palpable elements of purpura and papules inherent in urticaria without purpura. It is also not possible to distinguish them histologically in biopsy specimens. Thus, it is preferable for patients with bilateral palpable purpura and fever to undergo antibiotic therapy until blood culture results are obtained.

Purpura without inflammation always looks like papules, and the determination of platelets in a blood smear makes it possible to exclude thrombocytopenic purpura with confidence.

On the legs of elderly people suffering from purpura, a number of skin inflammatory processes can be detected, including various types of contact dermatitis. Under these conditions, purpura does not have the importance that is attached to it when it develops on the trunk and arms. However, perifollicular purpura on the skin of the legs (usually accompanied by follicular hyperkeratosis) is almost pathognomonic of scurvy. Purpura often develops in amyloidosis when squeezing skin lesions (waxy spots and papules). Such "incarcerated" purpura can form in healthy skin in patients with thrombocytopenic purpura and in the elderly.

Heart attacks. Unlike kidney infarcts, infarction foci in the skin are characterized not by pale, but by dark red color with a grayish tint and a motley pattern. They are represented by irregularly shaped spots, sometimes slightly deepened in relation to the skin surface and often surrounded by a pink, hyperemic rim. Zones of heart attacks are usually somewhat softer. Skin infarction is one of the important and often diagnostic symptoms of diseases affecting a number of systems (acute and chronic meningococcemia, streptococcal and staphylococcal septicemia, systemic vasculitis, fulminant purpura, systemic lupus erythematosus, gonococcemia, false septicemia and sometimes dermatomyositis). Dego's disease (malignant atrophic papulosis), in which white-porcelain spots are surrounded by a narrow telangiectatic and erythematous rim, is often accompanied by the development of similar infarctions in the gastrointestinal tract and central nervous system.

Telangiectasias. Redness of the skin is most often due to transient dilation of blood vessels (erythema). In contrast to the hue acquired due to the fixation of blood pigments, which is noted in purpura, erythema disappears when pressed with a glass or plastic plate. Telangiectasia, on the other hand, refers to a condition in which the red tint of the skin is determined by the constant expansion of small blood vessels (can be detected with a conventional hand-held magnifier) and their increase in number. Telangiectasia may present as single thin vascular branches, is distinctly red (i.e., not blue) in appearance, and is often localized to the face and nose. It may look like confluent patchy areas that have the character of permanent erythema. With discoid (in the form of a butterfly on the face) and systemic lupus erythematosus, dermatomyositis, psoriasis, erythema is more caused by telangiectasia.

Scattered isolated telangiectasias on the upper trunk or arms and legs are typical of progressive systemic sclerosis (systemic scleroderma). Teleangiectasias of the nail bed, that is, periungual telangiectasias, are important diagnostic features in lupus erythematosus (its discoid and systemic forms) and dermatomyositis. These changes are rare, if ever found, in systemic scleroderma and rheumatoid arthritis. Clearly defined red spots and papules with a diameter of 1-2 mm with areas of radiant telangiectasia are found in hereditary hemorrhagic telangiectasia. They are localized on rv6ax, tongue, nasal mucosa, face and hands.

Generalized telangiectasias in the form of red spots on most of the surface of the body may be a sign of mastocytosis and urticaria pigmentosa. Telangiectasias are a special feature of great diagnostic value in ataxia-telangiectasia or Louis Barr syndrome. They may appear as early as the 2nd year of life, but most often appear around the age of 5 years, first on the conjunctiva, and then spread to the auricles, eyelids, butterfly face, upper chest, arms and notes.

Telangiectasias can have a special form, known as an arterial spider, or spider nevus, spider angioma, nevus, araneus. The main vessel in this formation is usually a weakly pulsating arteriole, which can be detected by diascopy. Less common skin changes found along with vascular nevi in liver disease include telangiecgatic plexuses or networks, i.e., small red spots consisting of thin intertwined vessels that turn pale when pressed. Spider angiomas, often three or less, are not uncommon in healthy children and adults. Multiple angiomas of this type often develop during pregnancy, after ingestion of progestin drugs, in rheumatoid arthritis, and thyrotoxicosis. Most lipes with pronounced multiple vascular "spiders", however, reveal a form of diffuse liver damage, i.e. alcoholic cirrhosis Progression to subacute hepatitis is often accompanied by the appearance of rashes in the form of spiders, and with alcoholic and postnecrotic cirrhosis, almost half of the patients have multiple vascular "spiders". The mechanism of their development in hepatic pathology is unknown, and the relationship of these changes with impaired strogen metabolism in the liver has not been sufficiently established.

Bibliography

Brauerman/. Skin signs of systemic disease. -Philadelphia: Saunuers, 1981.

Farber E. M., Cox A. 1. (eds). Psoriasis: Proceedings of the third International Symposium. - New York: Yorke Medical, 1981.

Fitzpatrick T. W., Bernhard J. D. The structure of skin lesions and fundamentals ot diagnosis. - In: Dermatology in genera! medicine/T.ds. T. W. Fitzpatrick et al. - 3d ed. - New York: McGraw-Hill, 1987.

Henseler T. et al. Oral 8-rnethoxypsoralen photochemotherapy of psoriasis - Lancet, 1981, 1:853.

Honigsmann H. et al. Oral photochemotherapy with psoralens and UVA (PUVA):

principles and practice. - In: Dermatology in general medecine/Eds. T. W. Fitzpatrick et al. - 3d ed - New York: McOraw-HiH, 1987.

Leyden J. ]., Kligman A. M. The role of bacteria in acne vulgaris. -- In: Progress in diseases o! the skin/Ed. R. Fieischmajer. - Orlando: Grune and Stratton, 1984, p. 21, 29.

Parrish J. A. et a!. Photochemotherapy of psoriasis with oral methoxsalen and longwave ultraviolet light. - N. Engl. J. Med., 1974, 291:1207.

Peck G. L. et al. Prolonged remissions of cystic acne with 13-cis-retinoic acid. - N. Engl. J. Med, 1979, 300:329

What are the layers of the skin?

Describe the protective function of the skin.

There are two main layers of the skin: the outer - the epidermis, the inner - the dermis and subcutaneous fatty tissue - the hypodermis.

The skin protects the internal environment of the body from drying out, the introduction of microorganisms and various damage.

Numerous skin receptors protect us from contact with dangerous objects, help maintain a constant body temperature, and allow us to recognize objects by touching them.

1. How are errors in the diet reflected on the skin?

As a result of errors in the diet, rashes, inflammation, spots, swelling, peeling, black dots appear on the skin. With a diet for weight loss, the skin may lose elasticity and healthy color, sag with ugly folds, and wrinkles will become more noticeable.

2. Is it possible to determine, by the condition of a person's skin, which vitamin he lacks?

If there is not enough vitamin A, the skin becomes dry, cracked, darkened, and baldness often occurs. A lack of vitamin B2 can lead to cracks in the corners of the mouth, brittle nails, eczema, and a lack of vitamin C can lead to subcutaneous hemorrhages.

3. How to provide first aid to a person who has received a thermal burn?

Light thermal burns cause burning. The skin swells and turns red. The burned area is cooled under running water. Then wipe with cologne or a weak solution of potassium permanganate. If blisters form, apply a bandage after they burst. You can not pierce the blisters, microbes can get into the wound. In case of severe burns, the victim is covered with a sterile bandage and taken to the hospital.

4. What should be done if caustic acid gets on the skin; alkali?

Acid burnt skin (chemical burn) is first washed with running water, and then with a two percent soda solution. If alkali gets on the skin, then it is first washed off with water, and then treated with weak solutions of acetic or citric acid. After these procedures, the affected area is washed again with clean water and a sterile bandage is applied.

5. What are the first aid measures for frostbite.

The first sign of frostbite is the appearance of white spots on the skin and loss of sensation. In this case, the whitened nose, ears, cheeks are rubbed with a soft cloth. Rubbing should be done carefully so as not to damage the skin. Frostbite areas should not be rubbed with snow, as snow crystals can scratch it. If the sensitivity is not restored, and the spots darken, you should consult a doctor. In case of severe frostbite of the hands or feet of the victim, they are taken to a warm room. The limb is wrapped with cotton, wool, so that warming occurs slowly, due to the heat generated by the body. Useful warming drink.

6. How to protect yourself from ringworm and scabies? What causes these diseases and how do they spread? Why is it necessary to urgently consult a doctor in both cases?

Skin disorders and skin lesions

Causes of skin disorders

Usually distinguish internal and external causes of violations normal condition of the skin.

Among internal reasons may be errors in the diet, contact with substances that cause allergies, hormonal imbalance, lack of vitamins.

So, too much food leads to the fact that the skin turns red, becomes greasy. The consumption of alcoholic beverages changes the complexion, leads to puffiness and other cosmetic defects due to impaired functioning of the skin vessels.

The effect on the condition of the skin of a lack of vitamins is especially great. If there is not enough vitamin BUT, the skin becomes dry, cracks, darkens, baldness often occurs. vitamin deficiency AT 2 can cause cracks in the corners of the mouth, breakage of nails, eczema and vitamin deficiency With- to subcutaneous hemorrhages.

First aid for burns

Careless handling of fire, flammable and caustic liquids, prolonged exposure to the sun can lead to thermal (from the Greek. therme- heat, heat) and chemical burns skin.

Sunburn and First Aid

After prolonged exposure to the sun without clothes, burns of the first degree often appear, burns of individual areas are of the second degree.

Signs of sunburn:

Sharp redness, pain, swelling, and blisters disturb the victim from 3 to 5 days.
Signs of a skin burn are sometimes supplemented by signs of general overheating of the body.

First aid for sunburn:

The victim should be doused with cold water, drink cool water, tea, milk.
Lubricate the skin with boron vaseline.
With extensive lesions, hospitalization is necessary after the administration of painkillers.

Thermal burns and first aid

Most often, burns appear as a result of hot liquids, flames, skin contact with hot objects on the body. Depending on the temperature and duration of exposure to the skin, burns of varying degrees are formed.

Signs of burns and their degree

Burns of the 1st degree.Damage to the cells of the stratum corneum of the skin, which is manifested by redness of the burned areas of the skin, their swelling and burning pain.

Burns II degree.The stratum corneum of the skin is completely damaged, a sharp reddening of the burnt skin, the appearance of blisters on it, and a sharp pain.

Burns III degree. The deep layers of the skin are damaged, crusts, scabs appear.

III A degree- the skin does not die to its full thickness, and its lower layers are preserved.
III B degree- All layers of the skin are destroyed.

Burns IV degree.There is charring of the skin, subcutaneous tissue and underlying tissues.

Burns I, II, III A degree are called superficial, such burns are capable of self-healing. Healing of deep burns III B and IV degree is impossible without skin grafting.

The course and severity of burns, as well as the time of recovery, depend on several circumstances:

the origin of the burn and its degree;
burnt surface area;
features of first aid to the victim.

First aid for thermal burns

It is necessary to quickly remove the victim from the fire zone.
If a person’s clothing catches fire, you must immediately remove it or throw a blanket, coat, bag over the victim, that is, stop the access of air to clothing.
Flames on clothes can be extinguished with water, sand, extinguished by rolling on the ground on their own. In no case should you run in burning clothes.
You can also use fire extinguishers. But we must remember that the foam from fire extinguishers is dangerous to the eyes. In addition, the foam from some fire extinguishers is electrically conductive. Therefore, before proceeding to extinguish the flame with them, it is necessary to turn off electrical appliances located nearby.
After the flame is knocked down from the victim or he is removed from under a jet of hot steam or liquid, sterile gauze or simply clean dressings from improvised material should be applied to burn wounds. At the same time, adhering clothing should not be torn off the burnt surface, it is better to cut it off with scissors.
It is better to wrap a victim with extensive burns in a freshly ironed sheet and put him to bed.
Under no circumstances should bubbles be pierced.
If the burned person has a chill, it is necessary to warm him up: cover, give plenty of warm drink.
It is very important to create peace for the victim, not to disturb him with repeated shifting, turning over, dressings.
If the victim has lost consciousness as a result of carbon monoxide poisoning, it is necessary to bring cotton wool, a napkin or a handkerchief soaked in ammonia to the nose. If he has lost his breath, give artificial respiration in the fresh air.
Burns of I and II degrees over 10% of the body surface are always accompanied by burn shock. At first, the victims are excited, restless. Then comes a state of sharp weakness and general oppression of all body functions: the victims become indifferent to everything around them. Since shock is associated with pain, measures are taken to reduce it, give painkillers and urgently call a doctor.

Chemical burns and first aid

Chemical burns occur after exposure to the skin and mucous membranes of acids, alkalis and phosphorus.

Acid burns.Acid burns are usually deep, with a dry eschar forming at the site of the burn.

First aid for acid burns:

Remove acid-soaked clothing.
Wash affected areas with a 2% baking soda solution or soapy water to neutralize the acid.
Apply a dry bandage.

Alkali burns.Alkali-dead tissues are moist, so alkali burns are more severe than acid burns.

First aid for burns with alkalis:

Alkaline-soaked clothing should be removed.
Rinse the affected areas thoroughly under running water.
Wash the affected areas with a 2% solution of boric acid, a solution of citric acid or table vinegar.
Apply dry bandages.

Phosphorus burns.Phosphorus burns cause deep damage due to the fact that phosphorus dissolves in fats, therefore it penetrates deeply into tissues, causing, in addition to signs of a burn (redness, swelling, necrosis of tissues), signs of general poisoning.

First aid for burns with phosphorus:

Immediate neutralization of phosphorus in the affected areas with a 5% solution of copper sulfate (copper sulfate).
Then apply napkins soaked in the same solution.
Ointment dressings should not be applied to wounds.

So, the general rules for first aid for chemical burns can be formulated as follows. burnt acid the skin is first washed with running water, and then with a two percent soda solution. If it gets on the skin alkali, then it is first washed off with water, and then treated with weak solutions of acetic or citric acid. After these procedures, the affected area is washed again with clean water and a sterile bandage is applied.

For burns of the esophagus and stomach acids and alkalis due to the rapid spread of the burn through the digestive canal, first aid should be as early as possible. After interaction with a chemical substance, the surface layer of the mucous membrane dies, severe pain appears, vomiting with an admixture of bloody mucus, the temperature rises, and excruciating thirst begins. With severe burns, the initial symptoms in the form of a burning sensation and pain do not disappear for a long time, the victims often die. Burns of the stomach are relatively rare, especially isolated burns of the stomach, without simultaneous burns of the esophagus. The victim needs to drink plenty of milk, water, the introduction of antidotes. He should be sent to the hospital as soon as possible.

Skin diseases

Fungal diseases of the skin. One of the most common fungal diseases of the skin - ringworm . This disease got its name because the hair on the infected areas of the skin becomes fragile. They break off, and it seems that they were cut in these places. There are two forms of ringworm. One of them can be infected only from a sick person. In open areas of the skin, bright red spots appear, scaly in the middle. This lichen usually affects the upper layers of the skin. The second form of the disease is common among both humans and animals. It is very difficult, because in addition to the skin, the fungus also affects deeper tissues. The disease is very contagious, but it can be prevented if you follow simple rules: do not wash with a common washcloth, do not use other people's slippers and other people's clothes. You need to be especially careful when in contact with animals: cats, dogs, goats, etc. After communicating with animals, you should wash your hands thoroughly, do not touch their hair with your face.

If there is a suspicion that a person or animal is ill with ringworm, you should contact the clinic, and show the animal to a veterinarian. The room in which there was a sick animal, things used by a sick person, are thoroughly disinfected.

Lesson 2

Lesson topic: Skin disorders and skin lesions.

The purpose of the lesson: to identify the causes of violations of the skin and skin lesions.

Developing: to develop the intellectual abilities of students, using for this problematic and other tasks that encourage them to think independently, compare, generalize, specify;

Educational: the formation of the need to care for one's skin, compliance with the rules of skin hygiene, as well as respect for one's health.

Lesson type: combined.

New concepts: thermal burn, chemical burn, frostbite, ringworm, scabies itch, scabies.

Equipment: tables "Structure of the skin", "Scabies itch", magnifiers, paper napkins.

During the classes;

Frontal practical work: determination of skin oiliness in different parts of the face (using a napkin). A conversation about oily, dry and normal skin. Different areas of the skin may have different oil content, and therefore require different care.

Individual survey.

The structure and functions of the skin (using the Wall Chart "The Structure of the Skin")

Student messages on topics:

a) skin care

b) hair and nail care.

Preparing students for active and conscious assimilation of new material

(3 min)

Summarizing the students' answers, the teacher points out the important protective functions of the skin, so it is very important not to allow any violations and damage to it, which we will talk about today.

Write the topic of the lesson on the board.

Setting the objectives of the lesson.

Causes of skin disorders

First aid for burns and frostbite

Identify the causes of skin diseases (lichen, scabies)

Learning new material

(25 min)

1 Causes of skin disorders.

Explanation with elements of conversation, drawing up a diagram, working with the text of the textbook,

And why do guys call the skin a mirror of our body? (children express their assumptions)

Summarizing the statements of students, the teacher concludes that the state of the skin can determine the internal state of the body.

Using text from the textbook. 165. Determine the causes of violation of the skin.

Causes of skin disorders

External Causes: Internal Causes

trauma;

viral and fungal diseases;

non-compliance with the rules of skin hygiene.

Internal reasons:

yellowing of the skin, mucous membranes

eyelid and scleraliver and gallbladder disease;

teenage acnea consequence of the restructuring of the endocrine glands;

violation of the skin -result of vitamin deficiency.

Vitamin deficiency:

A - the skin is dry, cracking.

AT 2 - cracks in the corners of the mouth, breaking of nails.

C - subcutaneous hemorrhages.

2. First aid for burns and frostbite.

Explanation with elements of conversation, work with the text of the textbook,

What are burns?

Conversationbased on knowledge of safety rules in chemistry lessons

chemical

burns

thermal

CHEMICAL BURNS- caused by contact with the skin of various caustic substances.

Acid burn:

b) rinse with 2% soda solution.

2. Alkali burn:

a) wash off the reagent with plenty of water;

b) rinse with 1% solution of acetic or citric acid.

THERMAL BURNS

Idegree - reddens /epidermis/;

IIdegree - blisters filled with tissue fluid (epidermis, dermis);

IIIdegree - more serious violations (epidermis, dermis, subcutaneous fatty tissue);

IVdegree - charring (epidermis, dermis, subcutaneous fatty tissue, muscles and bones).

First aid for burns work with the text of the textbook p. 165-166, 2nd paragraph.

Idegree - rinse with cold water, treat with alcohol, cologne.

II, III, IV- go to the hospital with a sterile dressing.

Frostbite

Mild frostbite - rub the skin with a soft cloth until it reddens and restores sensitivity.

With severe frostbite - make a heat-insulating bandage on the brush and give a hot drink. It is important that the warming of the tissue comes from the inside due to the restoration of blood circulation.

3. Causes of skin diseases.

Explanation with elements of conversation, work with the text of the textbook.

Fungal diseases.

Ringworm.

Prevention:

a) do not wash with a common washcloth;

b) do not use other people's slippers and other people's clothes;

c) be careful when dealing with animals: cats,

dogs, goats, etc.;

d) Wash your hands thoroughly.

Skin disease scabies.

Let's remember from the zoology course who is the scabies itch? Why is he dangerous? How to deal with it?

The text of the textbook "Scabies" will help you rememberindependent work with the text of the textbook from 167.

Answer the questions:

who is the causative agent of this disease?

How does a tick get into the skin?

what size is it?

what causes severe itching?

where do ticks most often live?

what is the danger of severe itching, except for the inconvenience that it delivers?

how can infection occur?

What should be done if scabies is suspected?

is this disease curable?

Consolidation and application of new knowledge

(5 minutes).

Conversation on:

1. How to provide first aid to a person who has received a thermal burn?

2. How to protect yourself from ringworm and scabies?

3. Why is it necessary to urgently consult a doctor in both cases?

Homework. (1 min)

Homework Information .

§42, answer questions p.167.

Carry out the experiment described in the appendix on p. 266 textbook "On heat and cold"

The skin has two important functions:
- coverage of all internal organs and systems;
- protection.

The outer surface of the skin is regularly exposed to aggressive environmental influences. The skin is involved in the process of evaporation of moisture, prevents overheating and retains heat. The skin is the organ of touch. It is able to contract, stretch, withstand mechanical shocks. Through the skin, the body removes harmful and toxic substances.

Skin structure

The skin is made up of several layers. The epidermis of a person (the upper outer layer of the skin) of average build and height weighs half a kilogram and has an average area of 1.5-2 m2. On the border with the atmosphere is the first outer layer of the epidermis - the barrier (horny). The horny layer of the skin is the first to be exposed to external influences. It consists of cells filled to such an extent with keratohyalin (a substance of a protein nature) that they become similar to a lamellar horny scale. The horny cells adjoin very tightly to each other and have special outgrowths on the outer part of the shell, with the help of which they are connected. Most microorganisms, contaminants, viruses cannot penetrate beyond the stratum corneum. Damage or removal of the stratum corneum greatly increases the permeability to pathogenic microorganisms, liquids, irritants. The cells of the stratum corneum are in an ongoing process of wear and tear and renewal.

Beneath the epidermis is a layer of skin called the dermis. It contains lymphatic and blood vessels. With their help, there is a constant nourishment of the entire skin.

Skin damage

The skin is regularly stressed. External physical and chemical influences can break its integrity. Physically, the skin is affected by: mechanical stimuli, electric current, low and high temperatures. Among chemical influences, acids and alkalis are the most destructive. The degree of skin damage depends on the properties of the aggressive factor, the time of its exposure, the depth of physical damage.

The most common causes of skin damage are household injuries, as a result of which a person can receive stab or cut wounds, bruises, irritations, and burns. Different types of wounds require different approaches to treatment. If the wound is deep, surgery may be needed. In this case, the edges of the wound are sutured. A scar may remain in its place after healing.

Abrasions are superficial skin lesions. They are extensive and painful, but almost never leave scars after healing. Cuts are deeper damage to the skin. They affect, in addition to the epidermis, also the dermis, in which there are many small blood vessels that cause profuse bleeding.

Wounds due to bites are not very deep, but almost always lacerated and fraught with the risk of bacterial and viral infection. Such wounds require special treatment and medical advice.

Stab and deep incised wounds are distinguished by the fact that the hole on the surface of the skin is almost always less than the depth of the lesion. Stab wounds can lead to severe tissue damage and underlying internal organs.

Medications for the treatment of skin lesions

To prevent infection of superficial abrasions and scratches, shallow wounds, burns, it is useful to have emergency supplies in the first-aid kit. This is a group of antiseptic and disinfectant substances. Bactericidal agents actively affect bacilli, protozoa, bacteria, fungi. Iodine-containing solutions (iodine, iodinol, Lugol's solution, iodoform, iododicerin) are halogen-containing antiseptic agents (preventing the vital activity of microorganisms) action. Such compositions treat superficial damage to the skin. Contact with sensitive mucous membranes and eyes can cause serious irritation.

The well-known potassium permanganate (potassium permanganate) and hydrogen peroxide at a concentration of 3% belong to the subgroup of oxidizing agents in the line of antiseptics.

A large group of antiseptics intended for local external use is represented by medicinal formulations based on a number of metals (zinc, lead, bismuth). Metal compounds in various concentrations destroy microorganisms, have an astringent effect, reduce the severity of inflammatory processes, create a film of albuminates on the wound surface due to protein denaturation.

Local disinfectants include:
- anionic disinfectant detergents (soap);
- ethyl alcohol (medical);
- acids (salicylic, azelaic, boric);
- phenols (resorcinol);
- alkalis (tetraborate);
- aldehydes (cidipol);
- dyes (brilliant green, methylene blue);
- herbal medicines (chamomile, calendula, sage).