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Chronic inflammatory dermatoses



Psoriasis. A very common inflammatory chronic dermatosis - psoriasis - is found in people of any age. In some cases, it is associated with arthritis, myopathy, enteropathy, and AIDS. In particular, psoriatic arthritis (arthropatic psoriasis) can manifest itself in a mild form or, conversely, lead to severe joint deformations, resembling changes in rheumatoid arthritis. More often, psoriasis affects the skin of the elbows, knees, scalp, lumbosacral region, intergluteal fissure and glans penis. The most typical focal imaging is a clearly defined pink or orange-pink plaque covered with easily removable scales of a characteristic silver-white color (Fig. 25.19, A, B). There are other variants of psoriatic foci that have a ring-shaped, linear and sinuous configuration. Psoriasis sometimes causes erythema of the whole body and peeling - a condition known as erythroderma. In 30% of patients, the color of the nails changes to tan. Depressions and dimples appear on the nails, detachment of the nail plate from the main bed (onycholysis), as well as thickening and crumbling of the nail occur. In a rare variant, pustular psoriasis, small sterile pustules form on the surface of typical plaques and (or) in their circumference. This option is either benign and localized (usually on the extremities), or a generalized type of course with a threat to life. Generalized type of psoriasis is accompanied by fever, leukocytosis, arthralgia, pustules diffusely scattered in the skin and mucous membranes, as well as possible secondary infections and electrolyte disturbances.

A characteristic morphological picture is inherent in psoriatic lesions. Hyperplasia of the epidermis leads to a significant thickening (acanthosis) of the epidermis. Figures of mitosis are found significantly higher than the basal layer of the epidermis, where normally, as you know, the mitotic activity of cells is limited. The granular layer is thinned or absent, but on the surface of the epidermis there are abundant horny scales, reflecting the phenomena of parakeratosis. For psoriatic plaques, thinning of those sections of the epidermis that are located directly above the papillae of the dermis (the so-called suprapapillary plates), dilated, sinuous blood vessels in the dermal papilla are also typical. The described set of changes leads to an abnormal proximity of the vessels of the papillary dermis to the parakeratotic scales located above. This explains the appearance of multiple characteristic tiny bleeding spots after removing the scales (Auspitz symptom; H.Auspitz). Inside the spongy foci, as well as in the stratum corneum, where there are signs of parakeratosis, neutrophils form small clusters [spongy pustules and Munrow microabscesses (WJ Mungo)]. In pustular psoriasis, larger abscess-like accumulations of neutrophils are located directly under the stratum corneum.

In recent years, new information has been received on the pathogenesis of psoriasis. An increase in the incidence noted in connection with the presence of certain types of leukocyte antigens (HLA) in patients suggests that genetic factors play a role in predisposition to psoriasis. The emergence of new lesions in the area of ​​any trauma [the Koebner phenomenon (H. Koebner)] also gives a certain approach to understanding the pathogenesis of psoriasis. Recently, evidence has been obtained that psoriasis may reflect a type of complement-mediated reaction localized in the stratum corneum of the epidermis. According to this hypothesis, exogenous or endogenous damage to the stratum corneum in certain individuals leads to the unmasking of antigens of the stratum corneum. These antigens cause the formation of specific autoantibodies that bind to the stratum corneum, fix complement and activate the complement cascade. Then, the local release of the C3- and C5a components determines the activation and accumulation of neutrophils. Such a phenomenon is probably supported by metabolites of arachidonic acid, primarily leukotrienes. Later, neutrophils in the stratum corneum release serine proteases, which unmask even more antigens and support the process. Proliferative factors (for keratinocytes) that lead to epidermal hyperplasia and the formation of scales characteristic of psoriasis are also distinguished. Another possibility is that the initial defect in psoriasis is expressed in the increased ability of the microcirculatory bed of the surface layers of the dermis to collect neutrophils. Perhaps endothelial cells in psoriasis are unusually sensitive to cytokine stimuli that regulate the expression of leukocyte-endothelial adhesion molecules. Such regulation may result from genetically determined acceleration of cytokine receptor expression.

Lichen planus. Itchy purple-red polygonal papules are the main clinical symptoms of this disease of the skin and mucous membranes. Lichen planus is a self-stopping process. Usually, it spontaneously passes 1-2 years after the occurrence, often leaving areas of post-inflammatory hyperpigmentation (see below). However, lesions in the oral cavity can persist for years. Occasionally, with chronic lesions of the mucous membranes and submucosal tissues, malignancy occurs, but a direct pathogenetic relationship between the two types of skin lesions has not been proven. Skin changes are represented by papules, which can merge and form plaques. Papules often show white spots or lines forming a Wickham net (LFWickham). Multiple and symmetrical lesions are typical, especially on the limbs. They often occur around the wrists and elbows, as well as on the glans penis. Foci on the mucous membrane of the oral cavity in 70% of patients are presented in the form of white mesh or reticular zones. As with psoriasis, the Kebner phenomenon is sometimes noted.

Histologically, lichen planus is characterized by an extensive and dense lymphocytic infiltrate that appears along the dermatoepidermal junction. Lymphocytes are closely associated with keratinocytes of the basal layer, which undergo degeneration, necrosis and resemble more mature cells of the stratum corneum in size and contours. The consequences of such destructive lymphocytic infiltration are expressed in a change in the configuration of the dermatoepidermal junction, which becomes sawtooth. Nuclear-free necrotic cells of the basal layer can be drawn into the inflamed papillary layer of the dermis, where they turn into colloidal bodies.

The relationship between lymphocytes and epidermal cells resembles that of erythema multiforme (see above). Changes of the chronic type are characteristic of lichen planus: hyperplasia (less often atrophy) of the epidermis; thickening of the granular and horny layers (hypergranulosis and hyperkeratosis, respectively). Another variant of the disease is lichen planus, which affects the epithelium of the hair follicles, - lichen planus follicularis.
The exact pathogenesis of lichen planus is unknown. It is likely that the release of antigens at the level of the basal layer and the dermatoepidermal junction may explain the response of the cell-mediated immune response in this disease. There is evidence confirming just such a point of view, since the initial infiltrates from T-lymphocytes associated with Langerhans cell hyperplasia serve as triggering factors for the formation and evolution of focal lesions.

Lupus erythematosus. Manifestations of systemic lupus erythematosus are described in detail in Chapter 5. However, there is a skin form of lupus erythematosus without associated systemic manifestations, which is called discoid (chronic) lupus erythematosus. In individuals with a clinical picture of discoid lupus erythematosus, systemic lesion, as a rule, does not develop. However, more than 30% of patients with systemic lupus erythematosus may have changes that are neither clinically nor morphologically indistinguishable from those with the discoid type. In other words, if



Fig. 25.20.

Discoid form of lupus erythematosus

. Atrophy of the epidermis, hyperkeratosis, perivascular lymphocytic infiltration [from Grundmann E., Geller SA, 1989}.

based only on changes in the skin, it is often impossible to distinguish systemic lupus erythematosus from discoid lupus erythematosus.

Skin manifestations are usually represented either by mild erythema of the cheeks, or by large erythematous scaly plaques with clearly defined borders. Such discoid plaques are formed either with a purely cutaneous form of lupus erythematosus, or with systemic lupus erythematosus. Skin manifestations of lupus erythematosus may begin or worsen when exposed to sunlight. The epidermal surface of the lesions is shiny or flaky, and squeezing from the sides often leads to their wrinkling - a sign of atrophy of the epidermis. Through the thinned epidermis, dilated and sinuous blood vessels (telangiectasias), as well as small areas of hypo- and hyperpigmentation, can be seen. Under the usual magnifying glass, small horn plugs are visible in the openings of the hair bags.

Histologically, changes in discoid lupus erythematosus are characterized by lymphocytic infiltrate located along the dermatoepidermal or dermatofollicular junction, or along both. Massive infiltrates around blood vessels and appendages of the skin, for example around sweat glands, are also noted (Fig. 25.20). A more intense infiltration of subcutaneous fat develops with the so-called deep lupus. In the basal layer of the epidermis, diffuse vacuolization of epithelial cells is usually determined. The epidermis is strongly thinned or atrophied, the line of its junction with the dermis is smoothed. Hyperkeratosis is expressed on the surface of the epidermis. Atrophy of epithelial structures is detected in the hair follicles, the openings of the hair bags are often dilated and clogged with keratin. Using the PAS reaction, a significant thickening of the basement membrane of the epidermis is determined, and the direct immunofluorescence technique allows revealing a characteristic granular band of immunoglobulin and complement along the dermatoepidermal and dermatofollicular joints. The immunopathogenesis of lupus erythematosus is discussed in chapter 5. It is believed that both humoral and cell-mediated mechanisms act in parallel to destroy pigment-containing basal cells in the skin. Humoral mechanisms can include both the formation and deposition of immune complexes and the C5b – C9 complement components (membrane-attacking complex) at the dermatoepidermal joints.

Common eels (acne, comedo). This is a chronic inflammatory dermatosis that affects the hair follicle. Acne is more common in adolescents of the middle and older age group and affects people of both sexes. In boys, the disease is more severe. Acne is observed in people of all races, but in people of Asian descent they occur in a milder form. In adolescents, acne is believed to occur as a result of hormonal changes and changes in the maturation of hair follicles. The occurrence of acne can be triggered, and their course is aggravated by iatrogenic factors, i.e. certain medications (corticosteroids, ACTH, testosterone, gonadotropins, contraceptives, trimethine, iodine and bromine compounds); contact with harmful industrial substances (oils, chlorinated hydrocarbon and coal tar); excess clothing; being in tropical latitudes. Perhaps hereditary factors also play a role, since in some families there is a special exposure to acne in blood relatives.

Acne appears in two ways: non-inflammatory and inflammatory. Both options can "coexist" in one person. The first option is open and closed type acne. Open acne is built from small follicular papules containing a black horn plug in the center. This color results from the oxidation of melanin. Closed acne is a follicular papule without a visible central plug. Since the stratum corneum is hidden beneath the surface of the epidermis, closed acne are potential sources of rupture of the affected follicle and inflammation. The inflammatory variant of acne is characterized by erythematous papules, nodules and pustules. Heavily leaking options, such as spherical acne, lead to the formation of deep scars and sinuses.

In the middle part of the affected hair follicle, abundant masses of lipids and horny matter (keratin) are determined. Over time, such a follicle expands, and its epithelium and adjacent sebaceous glands atrophy. In the case of the development of open acne, large gaping holes appear, while the openings of closed eels can be distinguished only under a microscope. Lymphohistiocytic infiltrates appear in or around the affected hair follicles. With a rupture of the follicles, acute and then chronic inflammation is noted. Due to rupture, skin abscesses may form. However, gradual healing then follows, often with scarring. The pathogenesis of acne remains unclear. It is believed that endocrine factors (especially androgens) are involved in this process, since in castrated people this disease never develops. Apparently, the dishormonal state is not the only or primary cause. It is believed that bacterial lipases of the pathogen Propionibacterium acnes break down sebaceous oils, while releasing fatty acids that have a strong irritating effect on the tissue and trigger the inflammatory phase of the development of acne. Delayed lipase synthesis is the basis for prescribing antibiotics to patients with an inflammatory form of acne.

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Chronic inflammatory dermatoses

  1. Acute inflammatory dermatoses
    Inflammatory dermatoses mainly manifest as processes mediated by local or systemic immunological factors, although in most cases their causes remain unknown. There are thousands of forms of specific inflammatory dermatoses. Typically, acute processes last from several days to several weeks and are characterized by inflammation with mononuclear infiltration
  2. Chronic inflammatory diseases
    Chronic pharyngitis. Inflammation of the mucous membrane of the pharynx is sluggish, manifested by an unstable sensation of pain, dryness and discomfort in the pharynx, and rapid fatigue of the voice. Often this happens when exposed to domestic and professional factors, including alcohol, smoking, air pollution by dust (especially cement), caustic chemicals. In recent years, the impact of
  3. Chronic diffuse inflammatory lung disease
    in accordance with the functional and morphological features, the lesions of their air-conducting or respiratory departments are divided into three groups: obstructive, restrictive, mixed - obstructive with restrictive disorders or restrictive with obstructive disorders. The combination of restriction with obstruction is observed in the late stages of almost all chronic diffuse
  4. ROLE OF CHRONIC INFLAMMATORY PROCESSES OF THE ORAL CAVITY IN THE FORMATION OF PATHOLOGICAL IMMUNE REACTIVITY
    Currently, great importance in the autoallergenization of the body is given not only to tonsilogenic foci, but also to chronic odontogenic foci of inflammation, where the accumulation of toxins occurs. Endotoxins formed by the microflora of the oral cavity, which have antigenic activity, sensitize the body, alter the body's reactivity, distorting its reaction to many factors of influence.
  5. Chronic diffuse inflammatory diseases of the lungs. Bronchial asthma. Lungs' cancer. Pneumoconiosis
    1. The main types of diffuse lung lesions 1. interstitial 4. small focal 2. obstructive 5. panacinar 3. restrictive 2. Causes of death with obstructive emphysema 1. gas acidosis and coma 2. renal failure 3. left ventricular heart failure 4. right ventricular heart failure 5. collapse of the lungs with spontaneous pneumothorax 3. The most important
  6. BUBBLE (BULLY) DERMATOSIS
    Bubble (bullous) dermatoses is a group of diseases, the main morphological element of which is a bubble with localization both on the skin and on the mucous membranes. Classification of cystic dermatoses 1) Pemphigus true (acantholotic). 2) Herpetiform dermatitis of Dühring. 3) Pemphigoid (non-acantholytic pemphigus): - Lever's bullous pemphigoid;
  7. LUNG DISEASES. CHRONIC DIFFUSIVE ASTHMA. INTERSTITIAL LUNG DISEASES. CANCER INFLAMMATORY LUNG DISEASES. Bronchial lung
    LUNG DISEASES. CHRONIC DIFFUSIVE ASTHMA. INTERSTITIAL LUNG DISEASES. CANCER INFLAMMATORY LUNG DISEASES. BRONCHIAL
  8. PROFESSIONAL DERMATOSIS
    Профессиональным дерматозом считается такое заболевание, которое возникает под влиянием систематического и длительного действия на организм определенных вредных факторов химической, физической, инфекционной и паразитарной природы, свойственных данной профессии, либо условий труда, характерных для того или иного производства. Профессиональные заболевания кожи вследствие воздействия
  9. ПРИНЦИПЫ ДИАГНОСТИКИ ДЕРМАТОЗОВ
    Дерматология (греч. «derma» – кожа, «logos» – учение) – область клинической медицины, которая изучает структуру и функции кожи в норме и при патологии; разрабатывает вопросы этиологии, патогенеза, диагностики, терапии и профилактики дерматозов, а также взаимосвязь болезней кожи с другими патологическими состояниями организма. Dermatology is divided into general and private. Общая дерматология
  10. ВИРУСНЫЕ ДЕРМАТОЗЫ
    Вирусные дерматозы – инфекционные болезни кожи, вызываемые внутриклеточными паразитами – вирусами. Источник инфекции – больной человек или вирусоноситель. Пути передачи вируса: контактно-бытовой и воздушно-капельный. К вирусным дерматозам относятся: герпес простой, герпес опоясывающий, бородавки, в том числе остроконечные кондиломы, контагиозный моллюск. Герпес простой (пузырьковый
  11. Вирусные дерматозы
    Среди вирусных заболеваний человека одно из ведущих мест занимают герпесы. Возбудитель инфекции характеризуется дерматонейротропностью, выраженным сродством к коже, слизистым оболочкам и к нервной ткани. Инфицирование герпесом может происходить воздушно - капельным, контактным (прямой или опосредованный) путем, при поцелуях, со слюной. Эпидемиологическое значение в распространении инфекции имеет
  12. Тема № 9. Вирусные дерматозы
    Цель занятия – закрепить теоретические знания по вопросам этиологии, патогенеза, клиники и лечения вирусных дерматозов. Информационный материал Бородавки. Этиология – вирус папилломы человека, относящийся к семейству паповавирусов, содержащий двухцепочечную ДНК. Заражение происходит контактным путем. Заражению способствуют микротравмы и повышенная потливость кожи. Факторы риска –
  13. Пузырные дерматозы
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  14. Пузырные дерматозы
    Пузырчатка. Этиология и патогенез болезни полностью не изучены. Существует множество теорий возникновения патологического процесса: теория задержки хлоридов, токсического, неврогенного, энзимного, бактериального, вирусного, аутоиммунного происхождения. Различают следующие клинические формы: вульгарная, листовидная, вегетирующая, себорейная (эритематозная). Чаще встречается вульгарная форма
  15. Зудящие дерматозы
    Нейродермит (Атопический дерматит). В развитии нейродермита большую роль играют нейроэндокринные, обменные нарушения, состояние различных отделов нервной системы, наследственная предрасположенность. В детском возрасте болезнь часто развивается на фоне экссудативного диатеза, аллергической реактивности. Неблагоприятные факторы внешней среды могут отягощать течение болезни. Ухудшение кожного
  16. ВИРУСНЫЕ ДЕРМАТОЗЫ. КОЛЛАГЕНОЗЫ
    ВИРУСНЫЕ ДЕРМАТОЗЫ.
  17. Тема № 6. Диффузные болезни соединительной ткани. Пузырные дерматозы
    Красная волчанка- тяжелое заболевание, поражающее соединительную ткань и сосуды. Среди факторов, провоцирующих появление или обострение красной волчанки, прежде всего отмечают повышенную чувствительность к инсоляции и метеорологическим воздействиям. В некоторых случаях у женщин заболевание возникает после беременности и родов. Различают хроническую (ограниченную и диссеминированную) и системную
  18. АЛЛЕРГИЧЕСКИЕ ДЕРМАТОЗЫ: ПИЩЕВАЯ НЕПЕРЕНОСИМОСТЬ И АЛЛЕРГИЯ
    Проблема аллергических заболеваний актуальна не только для людей, но и для братьев наших меньших. Наиболее часто аллергические реакции развиваются в ответ на укусы и ужаливания насекомых (например, у кошек они нередко связаны с укусами блох), а также после введения лекарственных препаратов; в довольно редких случаях аллергическая реакция может быть вызвана пищевыми продуктами. Неблагоприятные
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