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Structure of the skin and its appendages

Leather - a multifunctional organ that covers the human body and serves as a boundary separating it
from the external environment, is closely interconnected with all other organs and systems. In this
regard, a variety of physiological and pathological processes in a certain extent, are reflected in the
skin or leaking from its participation.

Skin covers the entire body surface. In the natural openings (mouth, nose, urethra, vagina and
anus), skin moves in the mucosa. The total area of skin in an adult is from 1.5 to 1.8 m 2 , the child is
age dependent.

During the ontogeny of skin develops two germ layers - the outer layer (ectoderm) and
middle (mesoderm), and consists of two types of tissue - epidermal junction and which are closely
linked.

Layers of the skin

Allocate 3 of the skin (Figure 1-1):

epidermis (epidermis);

dermis (derma);

subcutaneous fat (subcutis), or hypodermis (hypodermis).

Epidermis

Epidermis and its appendages (hair, nails, sweat and sebaceous glands) develop from the
ectoderm. On the 2nd week of embryogenesis in the basal layer of the epidermis from the neural
crest melanocytes penetrate.
Fig. 1-1. Skin structure

Epidermis presented stratified squamous epithelium squamous whose thickness is on the most
delicate areas (eyelids) is 0.04 mm, in the rough (palms, soles) - up to 1.6 mm.

In the epidermis there is mandatory 3 kinds of cells:

keratinocytes (epidermotsitov) are presented in different evolutive forms and form the main mass
of cells of the epidermis.

pigment cells (melanocytes).

immune cells (macrophages intraepidermal).

Also in the epidermis show Merkel cells, but they are neyroretseptornogo structures and associated
with nerve endings that penetrate from the dermis.

In the epidermis distinguish five layers (Figure 1-2):

horn (stratum corneum);

brilliant (stratum lucidum);


granular (stratum granulosum);

prickly (stratum spinosum);

basal (stratum basale).

The basal layer

The basal layer is composed of a number of cylindrical cells 1 (basal keratinocytes) having mitotic
activity. Between keratinocytes of the basal layer are connected through desmosomes and are
attached to the basement membrane poludesmosomami.Poludesmosomy are microscopic
protuberances cytoplasmic cells penetrating the basement membrane, they determine a firm
connection to the basement membrane of the epidermis and dermis.

2 keratinocytes isolated subpopulations: one of them is constantly proliferates, 2nd is dormant


(backup). The primary function of the basal layer of keratinocytes - the constant proliferation and
regeneration of epidermal defects.

Fig. 1-2. structure of the epidermis

Melanocytes - Process-large pigment cells lie on the basement membrane and form the basal layer
of the epidermis. Melanocytes are even in the mucosa. An exception is the thick epidermis of the
palms and soles, where these cells do not. In the adult human melanocytes amount is about 10% of
all cells of the epidermis (in newborns - 3.7%, and the children - 7%). Number of melanocytic cells
does not depend on race, nor of gender. Melanocytes synthesize the pigment melanin, which
protects the skin from harmful ultraviolet (UV) rays. Melanocytes produce melanin from tyrosine with
the participation of the enzyme tyrosinase.
Prickle layer

Located above the basal layer prickle layer comprises 3-8 layers of cells, with "spikes". Prickly
keratinocytes contain large amounts of outgrowths (desmosomes), penetrating into the recesses of
the neighboring cells and joining them on the principle of fasteners "lightning" with the formation of
nodules Bitstsotsero. All this adds strength and elasticity to the epidermis.

Langerhans cells (intraepidermal macrophages) are also located in the prickle layer and represent
cells with long processes that extend up to the basement membrane and the granular layer. In
inflammatory processes can migrate to lymph nodes and dermis.Langerhans cells differs from other
macrophages in the presence of these special raketkoobraznyh Birbeka granules containing chalone
- a substance that inhibits the proliferation of keratinocytes. Langerhans cells are from 2 to 7% of the
epidermal cells, have mesodermal origins.

The main function of Langerhans cells:

regulation of the population of keratinocytes;

antigenpredstavlenie on T-helper lymphocytes, secretion of interleukins (IL) 1, IL-4, interferon


(IFN), tumor necrosis factor (TNF), etc., and are also involved in immunopathological processes of
the skin.

Greenstein cells resemble Langerhans cells, but without granules Birbeka. The number of cells is
1-3% of all cells of the epidermis.Function as antigen-presenting cells for T-suppressor lymphocytes.

Basal and prickle layer collectively called Malpighian or germ layer of the epidermis.

Granular layer

Granular layer consists of 1-2 layers of cells (2-4 rows on the palms and soles) in the form of an
elongated lozenge - granular keratinocytes. A characteristic feature of the cells of this series - the
presence of a plurality of granules in the cytoplasm and granules eleidin Orlanda lamellar bodies
with lipid vesicles (keratinosom). In the future, these substances form a layer between bilipidnye
horny scales. By highly specialized epidermal lipids include ceramides, cholesterol, fatty acids,
phospholipids and other lipid compound.

Shiny coat

Shiny (eleidinovy) layer looks like a shiny structureless narrow strip separating the granular layer of
the stratum (available on the palms and soles).

Stratum corneum

Stratum corneum - the end product of the evolution of keratinocytes. Horny layer consists of many
imbricate scales (corneocytes), representing the dead, filled with keratin residues
keratinocytes. Corneocytes are flush with each other, but on the surface in contact with the external
environment, lose strength and can be easily separated - physiological desquamation, imperceptible
to the eye. The thickness of the stratum corneum at different areas of the skin varies considerably
(maximum - on the soles and palms, in the calluses).

Corneocytes and lipid layers of the granular layer keratinosom form multilayer lipid structure of the
stratum corneum and form theepidermal lipid barrier, which protects the skin from the trans-
epidermal water loss and provides water resistance of the epidermis.Epidermal lipid barrier also
plays the role of a special intercellular cementing substance, providing the adhesive strength of the
horny layer structures and preserving the integrity of the skin. Epidermal ceramides not only retain
water in the skin, but also to regulate the rate of desquamation influencing the differentiation of
keratinocytes, and also have pronounced antimicrobial action.

The cycle of development of epithelial cells (cells from the basal layer to ottorgshihsya horny
plates) is normally 28 days.

Epidermis separated from the dermis of the basal membrane, which is a specialized extracellular
matrix. Electron microscopy in the basal membrane of isolated light and dense

plates, as well as plasmolemma. In plasmolemma reveal numerous pinocytic vesicles, indicating that
the active involvement of the basal membrane in the exchange processes between the epidermis
and dermis. Due to the lack of blood vessels in the epidermis of its supply is provided by the
diffusion of nutrients through the basement membrane of the dermis.

Features of the structure of the epidermis in children

In children, the epidermis is thin, it determined mainly basal, prickle and horny layers. Stratum
corneum in children thin and loose.Up to the upper rows cells contain a nucleus. Stratum corneum
exfoliation processes in young children occur 4-5 times faster than adults. Due to the lack of young
children in the epidermis of the granular layer of the skin practically synthesized ceramides and
inconsistency arises epidermal lipid barrier. Due to these structural features of the skin of the child,
especially the young, thin-skinned at the slightest adverse effects (violations of hygiene, frequent
bathing and use of soaps, tight swaddling) and prone to the development of maceration.

The skin of children more intensely than adults, are the processes of mitotic division. Mitosis are
not only in the cells of the basal layer, but also partly in the thorny layer, which contributes to more
rapid reparative processes (epithelialization) when damaged epidermis.

An important feature of the skin in children - a tenuous connection between the basal layer of
keratinocytes themselves, as well as the basement membrane, associated with a small number of
desmosomes and poludesmosom in these cells. Because of this, children are more likely than adults
are epidermolitichesky processes that lead to a breach of the dermal-epidermal junction and
clinically manifested bullous dermatoses (pemphigus neonatal Ritter exfoliative dermatitis, bullous
impetigo, etc.).
The skin of children reduced the number of melanocytes compared with the skin in adults and up
to 6 months of age melotsitarnye cells are functionally active and contain a small amount of melanin
granules that determines skin sensitization children to UV radiation (UVR).

neonatal skin differs from the skin of adults, and the reaction pH. In adults, slightly acidic pH of the
skin, newborns IME-

a neutral reaction, and seborrheic areas and folds (due to caseous grease) - alkaline. Only 2 to 4
weeks of age the child begins to shift skin reaction in an acidic environment. This feature leads to
more frequent development in young children pyoderma and Candida infections.

Dermis

The dermis consists of two layers: the papillary and reticular. The papillary layer is formed by loose
connective tissue and capillary network, and mesh - dense, fibrous connective tissue unformed. Both
layers are composed of three components: cells, fibers and ground substance. In the dermis, also
located blood, lymph vessels and nerve endings.

Cells dermis

Fibroblasts - the main cells of the dermis. They provide the synthesis of collagen, elastin and
retikulinovyh fibers and ground substance.

Mast cells (mast cells, tissue basophils) refer to the descendants of blood stem cells and tissue
analogs basophilic leukocytes. In the cytoplasm of mast cells contain specific granules with
biologically active substances: histamine, heparin, serotonin, and hyaluronic acid. These substances
have a regulating effect on vascular permeability of skin differentiation of various cells involved in the
development of inflammatory and immune reactions, etc. Have a great migration ability.

Histiocytes (tissue macrophages) is carried out phagocytosis. Their cytoplasm


has lysosomes containing hydrolytic lysosomal enzymes (collagenase, elastase, lysozyme , etc.),
which is carried out through the destruction of phagocytosed particles. Histiocytes secrete
mediators: IL-1, IFN- a , TNF , etc., which activate and inhibit cell division and functions of
connective tissue and immunocompetent cells.

T-cells - red blood cells, are located around the blood and lymph vessels. If necessary, can quickly
migrate into the lower parts of the epidermis to dermal tissue. 3 species isolated T lymphocytes: T-
helper cells, T suppressor cells, T-killer cells. Helper T cellsactivate production of antibodies by B
lymphocytes. suppressor T inhibit incorporation of B-lymphocytes

differentiation and delay the production of antibodies. T-killer cells - lymphocytes, asking yourself
lysis of foreign cells.

Plasma cells (plasma cells) in normal conditions are rarely in the dermis, is usually only around the
vessels. Function plasmacytoid - secretion of antibodies (immunoglobulins - IgA, IgM, IgG, etc.).
Fiber

Collagen fibers - staple fibers of the dermis, are built of protein type 1 - collagen, which provides
mechanical strength of the dermis.

Elastic fibers form a thin extensive network in the dermis contain the protein elastin, whose
distinctive properties - stretch and contractility.

Reticular fibers are placed directly under the epidermis, have a pronounced elongation. They are
especially numerous around the skin appendages (hair follicles, sweat glands), where they serve as
a framework.

Dermal connective tissue fibers are arranged in a certain direction, they are linear and
form Langer's line (Figure 1-3). The skin is stretched stronger in the direction perpendicular to the
course of the fibers and hence the least conspicuous scar skin obtained after cutting the substrate
along the wound fibers, which must be considered during surgical interventions, during massaging.

3. .
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: , , .
The main histopathological changes in the epidermis:

hyperkeratosis - thickening of the stratum corneum (excessive formation or delayed exfoliation


horny scales);

parakeratosis - incomplete keratinization characterized by the presence of nuclei in the stratum


corneum (accompanied by an underdevelopment or absence of the granular layer);

granulosa - thickening of the granular layer;

acanthosis - increasing the number of rows of cells thorny layer;

dyskeratosis - premature keratinization of individual keratinocytes;

intracellular edema (vacuolation) is characterized by the appearance of vacuoles in the


protoplasm epidermotsitov, deformation of the nucleus, pyknosis;

spongiosis (intercellular edema of the epidermis) is characterized by accumulation of fluid


between the cells, dilation and rupture of intercellular bridges can end intraepidermal vesicle
formation;

ballooning degeneration - necrobiotic process, leading to rupture of intercellular bridges; cells or


groups of cells that have lost touch with each other, swim freely in the extended

intercellular spaces in the form of swollen spherical structures (cylinders);


acantholysis - loss of communication between the epidermal cells due to damage to their
desmosomal contacts, leading to the formation of cavities intraepidermalnyh;

epidermolysis - loss of communication between the epidermis and dermis in the basement
membrane due to damage poludesmosom, leading to the formation of cavities subepidermal.

The main histopathological changes in the dermis and hypodermis:

papillomatosis - elongation, branching dermal papilla uneven lifting the epidermis;

granulomatosis - inflammation that leads to the formation of granulomas. Granuloma


characterized by the presence of focal chronic inflammatory response to tissue damage. By the
nature of the cellular composition of granulomas can judge the character of inflammation: acute
purulent - polymorphonuclear leukocytes; syphilis, tuberculosis - histiocytes, epithelioid cells; chronic
inflammation - plasma cells etc.;

granulation tissue - immature connective tissue consisting of fibroblasts, young collagen fibers,
capillaries;

subpapillyarit - edema of the papillary layer of the skin;

Multiple sclerosis - an increase and thickening of collagen fibers in the dermis, resulting in scar
formation;

mucoid swelling of connective tissue - connective tissue swelling occur and swelling of the
fibers, as well as the accumulation of glycosaminoglycans uncharacteristic;

fibrinoid swelling of the connective tissue - the destruction of collagen fibers and accumulation
of connective tissue fibrinoid.Histologically, the connective tissue looks homogeneously;

elastosis - disorganization, adhesives, thickening of elastic fibers;

elastolysis - destruction of elastic fibers;

hyalinosis - degeneration of connective tissue deposition in her hyaline;

amyloidosis - degeneration of connective tissue deposition of amyloid in her glycoprotein;

micro-abscesses - small focal accumulations of cells in the epidermis or dermis. Munro


microabscesses - Cluster neutron

fils in the horny layer of the epidermis in psoriasis, microabscesses Potro - accumulation in the
epidermis of immature lymphocytes in lymphomas;

metachromasia - coloring phenomenon of tissues and cells in a different color than the color of
the dye is detected in the presence of acid mucopolysaccharides and amyloid;
atrophy - a decrease in the number of layers of the skin or its volume. Can be treated as separate
layers of the skin and generally to the skin;

bionecrosis - the process of dying tissue, accompanied by cheesy and fibrinoid necrosis.

4 .. The concept of primary cells. Clinical examples


Primary elements

Spot (macula) is characterized by a change in color of the skin without changing its relief and consistency. Skin color mainly
depends on the blood flow and the amount of pigment. Therefore isolated vascular spots, pigmentation, as well as artificial resulting
from the exogenous or endogenous chemical skin penetration of dyes.

Vascular patches are classified into congestive, ischemic, hemorrhagic and telangiectasia.

1. congestive spots develop mainly as inflammatory, at least - by a reflex mechanism (erythema modesty). Roseola isolated by size
(up to 2 cm in diameter) and erythema (more than 2 cm in diameter).

2. Ischemic spots are rare and are associated usually with vascular spasm or congenital absence at selected sites (malformations).

3. Hemorrhagic spots developed by two mechanisms - per Rexin and per diapedesin. In the first case, the output form-

elements outside the bloodstream occurs due to rupture of blood vessels in the second - as a result of violations of the permeability
of the vascular wall. All varieties of hemorrhagic spots called purpura. However, isolated spots up to 1 cm in diameter - petechiae,
more than 1 cm - ecchymosis and extensive hemorrhage - suggilyatsio. When diascopy hemorrhagic spots disappear.

4. venules are paralytic vasodilatation small vessels (venules, capillaries, arterioles) or neovascularization. Arterioles showed little
bright red elements, not raised above the skin; venules somewhat broader bluish, often act on the skin surface. Distinguish linear in
shape, tree and spider telangiectasia. The reasons for their development are genetic factors (vascular nevi), hormonal (pregnancy,
estrogen therapy, corticosteroids) and physical (actinic, ionizing radiation).

Pigment spots are formed at an elevated amount of melanin (giperpigmentnye spots) under reduced (hy-popigmentnye) and in the
absence of melanin (depigmentny

e).

Giperpigmentnye spots may be present at birth (birthmarks) or acquired (chloasma, freckles). Congenital depigmentnye spots are
called partial albinism purchased - vitiligo. Gipopigmentnye primary spots (leucoderma) are rare and are associated usually with
neuroendocrine disorders, due to the regulation of melanogenesis sympathetic nervous system and pituitary hormones.

Artificial stains occur most often in contact with chemical substances into the skin coloring exogenously (tattoo, traces of
gunpowder), at least - endogenously (deposition of carotene, silver, bismuth).

Blister (urtica) represents bespolostnoy element, which developed as a result of acute edema limited sosoch-kovogo layer. Blisters
may be pink color of varying intensity or white. White color means of expression edema, leading to compression of blood vessels
and blood flow. Blisters there for several hours and allowed without leaving any change in the skin. Outlines blistering round, oval or
irregular, the most value-diversity

different. As a rule, they are accompanied by itching, excoriation but never meet.

Bubble (Bulla) - this cavity element, towering above the skin or mucous membranes, resulting in-traili subepidermal. Content his
serous, clear or cloudy, sometimes mixed with blood. In bladder distinguish tire cavity and bottom. It may be hemispherical, tense or
flat, flabby. The quantity of bubbles varies from small pea to a hen's egg and more. For the development of bladder requires prior
destruction of intercellular connections or dermoepidermalnyh. This can happen as a result of exogenous chemical or physical
factors leading to necrosis epidermotsitov and separation, as well as due to autoimmune processes, genetic defects (acantholysis,
epidermolysis).

Vesicle (bubble, vesicula) is a hemispherical, slightly raised above the skin cavitary education in size from a pinhead to a small
pea.Intraepidermalno formed by the following mechanisms: spongiosis (intercellular edema), intracellular edema, ballooning
degeneration.

Pustule (abscess, pustula) is a cavity formed pus. It can be primary (in this case the presence of leukocytes is not always due to
infection, and in these cases it is sterile) or secondary, forming vesicles from the bladder or when connecting a secondary infection
is intra-epidermal or subepidermal. In some cases, the microbes in the contents of pustules are not detected (amikrobnye
pustulosis).

Abscess formed in the dermis or subcutaneous tissue, is called an abscess.

2 . Primary proliferative elements

Papule (nodule, papula) is an element that is more or less raised above the skin, tight palpation and reflecting changes in the
epidermis or dermis. Papules, with a few exceptions (for example, lichen planus), allowed without consequences, but often remain
pigmentation disorders.

Hemispherical in shape isolated papules, flat and pointed.

Hemispherical shape papules reflect pathological processes in the dermis without the participation of the epidermis (at the
microscopic level changes are detected in the epidermis). Most often to the formation of hemispherical or dermal

papules causes chronic inflammation (limfogistiotsitar-ITATION infiltrates around the blood vessels lift the epidermis); proliferation of
various elements of the dermis - vessels (Angioma), connective tissue (fibroids), glands (adenoma); smooth muscle (LM), the
deposition of lipids (Xanthi-ma), calcium salts (calcification), amyloid (amyloidosis), mucin (mutsinoz).

Flat papules indicate that the formation of the epidermis necessarily involved. They are divided into epi-dermal and
epidermodermalnye. These papules are distinguished by color: as there are no vessels in the epidermis, the epidermal papules
painted in the color of the skin or have dingy grayish hue, while epidermodermalnye elements pinkish-red due to the vascular
component. Epidermal papules formed or due to expansion of one of the layers of the epidermis (corn) or all layers (wart).

Genital papules (follicular) are always associated with hair follicles.

Largest distinguish miliary papules (the size of a millet grain), lenticular - with lentils, nummulyarnye - coin.

Pumping at the confluence of papules or plaques formed. At the confluence of hemispherical papules smooth surface plaque, at the
confluence of flat papules - with severe skin pattern, follicular - a float.

Funds are also seropapulu - element characterized by papules, located on the blister and topped vesicle. Since blister quickly
allowed and bubble dries to form a crust, usually represented seropapula bundle with a crust in the center.

Tubercle (tuberculum) is a towering, or is at the level of the skin more or less dense, or soft consistency education. Element reflects
the changes in the dermis associated with infiltrates consisting mainly of mononuclear phagocytic system cells-Leary
(macrophages, epithelioid cells, giant cells) in chronic granulomatous inflammation. When diascopy tubercles they tend to be more
or less yellow.Tubercles resolved in two ways: leaving scar or atrophy, and open in the future to heal with scar formation. They are
arranged in the limited areas of the skin, grouping or merging with each other.

Knot (nodus) is characterized by pathological changes in the hypodermis, which may be a manifestation of the banal (acute or
chronic inflammation), specific granules lematoznogo process often - tumors. Clinical manifestations node in acute and chronic
inflammation are different. In the first case, patients complain of pain, especially during palpation elements nodes bright pink color,
with indistinct borders, pasty consistency, in the second - nodes cyanotic color, dense palpation, with clear boundaries. Nodes at a
specific granulomatous inflammation allowed to form scar atrophy, opened with the formation of ulcers or fibrosing. However, it
should be noted that the least informative sites for the diagnosis, so when dermatoses, manifested nodes often used histological
methods
5. Notion of secondary elements rash. Clinical examples

Secondary elements

Secondary spot relates to pigment spots and develops at the site of any primary cell, except blister. It may be hypo
giperpigmentnym.

Scale (squama) - a visible accumulation of rejects from the skin horny plates. Distinguish mu-kovidnoe peeling, scaly, lamellar and
eksfolia-tive. Isolated parakeratoticheskie and giperkeratoticheskie flakes. First formed in parakeratosis, ie, incomplete keratinization
of keratinocytes (remnants of the nuclei), characterized by weak bonds between themselves and easily rejected at poskablivanii or
friction. The second image on the background of hyperkeratosis, flush with each other and with difficulty
rejected.Parakeratoticheskie are primary flakes dandruff, giperkeratoticheskie - with ichthyosis.

Erosion (erosio) - limited defect of the epidermis, growing on the site revealed the intraepidermal cavity-elements or due to
maceration. Outlines erosion rounded, square dimensions match the primary element, the surface of pink-red, moist due to serous
fluid or pus. Microvesicles formed by opening the smallest erosion (mikroerozii), which are found only in droplets sometimes parting
of serous fluid (drip moknutie, "serous dew"). When maceration (softening the stratum corneum under the influence of long-term
impact-

the action of water, sweat in the folds of the skin, urine in infants) horny layer becomes white, swollen and torn away, exposing a
variety of sizes and shapes of erosion. Epitelizi-ruetsya erosion, leaving no trace, except for temporary pigmentation disorders.

Excoriation (excoriatio) is a linear defect of the epidermis or dermis that occurs when combing, at least - in other mechanical
influences. In case of damage to the dermis heals excoriation with scar formation. When traumatizing papules or seropapuly
excoriation may be oval or round.

Crack (fissura) is formed by stretching the skin against her increased dryness, infiltration or hyperkeratosis, with deep lesions heal
with scarring.

Ulcer (ulcus) is a defect within the dermis or hypodermis, resulting from the collapse of a number of primary cells or rejection
scab.Assessing the ulcer, you should pay attention to its size, depth contours (round, oval, polycyclic), character edges, bottom,
state of the skin. Greater role played by the edges of the ulcer. In particular, the steep edges indicate the presence of necrotic rod
saped - melting of the deep tissues with a break of pus through a narrow opening or circumferential growth of the inflammatory
process in depth. Blyudtseob differently ulcer develops as a result of malnutrition due to damage to blood vessels or skin tumor
infiltration powerful.

The above characteristics make often set the primary element from which a plague. For example, small-area sores develop after
opening epidermodermalnyh deep pustules or tubercles in the decay. In the first case the edges are slightly podrytymi ulcers, soft,
bottom is covered with purulent coating around - active hyperemia. In the second case the edges of steep, tight at the bottom -
necrotic mass on the periphery - congestive hyperemia. Larger lesions develop at the site subepidermal strength bubble node
abscess. When opening the bladder ulcer surface with soft edges, serous discharge, fringed collar stratum corneum. When opening
the abscess with deep ulcer podrytymi edges, purulent discharge and active hyperemia around. In the decay of a deep ulcer site
with sheer hard edges, necrotic bottom and congestive hyperemia

circumferentially. In some cases, ulcers can develop primary. This forms a trophic ulcer due to malnutrition and necrosis. All the
ulcers heal by scarring.

Ulcer should be distinguished from the wound, which is a defect in tissue injury due to the unaffected skin.
Cork (crusta) is an element formed during drying of blood or fluid in the cavity elements or effused on the surface of the skin. Yellow
crusts indicate serous inflammation, greenish - about purulent, brownish-black - the presence of blood. Laminated to each other
peel significantly protruding above the skin, called rupees.

It is advisable to allocate a scab - an element that is a manifestation of necrosis of the skin. It differs from cover in black and
demarcation zone of reactive inflammation.

Scar (cicatrix) develops at the site of the defect or the dermis and hypodermis is a newly formed tissue, consisting mainly of
collagen (the elastic fibers are absent). Fresh red scar through the active formation of new vessels, old - white due zapustevaniya
vessels.Skin appendages in no scar, skin pattern is not detected.

Distinguish normotroficheskie, hypertrophic and atrophic scars-cal. Hypertrophic scars are raised above the skin due to excessive
proliferation of connective tissue; atrophic - below the level of the surrounding skin due to lack of regeneration (thinned they gather
in folds). Also isolated keloid scars, which in some cases can not be distinguished from hypertrophic either clinically or
histologically.However, in their differential diagnosis should be considered that hypertrophic scars occur quickly enough to the site of
trauma, in its configuration reflect damage, do not go beyond the defect; keloid scars appear after an indefinite time, do not reflect
the shape of damage and go beyond it.

A distinction is also scar atrophy, developing without prior skin defect, usually at a resolution of chronic granulomatous processes or
in severe vacuolization of the basal keratinocytes.

Atrophy is characterized by thinning of all layers of the skin with preservation of their structure. Physiological characteristic of senile
atrophy of the skin. Pathological atrophy is extremely rare, accompanying inflammatory processes in some dermatoses. It may be
diffuse, strip (striae pregnant, etc.) and spotty.

Lihenifikatsiya (lichenification) is a pathological condition of the skin characterized by a pronounced skin pattern. Last acanthosis
and papillomatosis caused.

Vegetation formed when sprawl dermal papilla. Clinically, they resemble a cauliflower. There are dry - peplno gray or soft -
succulent eroziro-suite. Most often, they are developing at the bottom of erosions or ulcers due to irritation.

6. Features dermatological clinical examination of patients. Laboratory


methods of diagnosis of skin diseases.
On examination, you should pay attention not only on the affected skin imposed patients, but also on
the entire skin and visible mucous membranes. This is necessary for several reasons: first, to
diagnose critical assessment of unaffected skin - its humidity, greasiness, dryness; Second, patients
often for various reasons, do not show all the lesions, and among them may be the most
demonstrative; thirdly, some dermatoses inherent characteristic changes in the mucous membranes,
enabling the correct diagnosis.In addition to visual evaluation of skin lesions are presented and
palpation, which allows to determine consistency, slip-dependence of the skin and the depth
distribution of the process; vitropression - viewing surface lesions through the glass, which are
pressed against the affected skin, and many other research methods that will be presented in the
appropriate sections.

Skin diseases are manifested primarily by various eruptions, consisting of individual elements,
conventionally divided into primary and secondary.
In addition to defining the elements of skin rashes, dermatitis diagnosis include an assessment of
skin rashes as a whole in terms of:

1) monomorphic or polymorphic rash. Under monomorphic rash understood rash, consisting of the
same elements. Polymorphic rash includes a variety of elements, and if there are different primary
cells, then we speak of true polymorphism; if polymorphism caused secondary elements that have
developed from a single primary - a false (evolutionary);

2) the prevalence of rash - skin lesions may be limited (localized), more or less common and
universal;

3) symmetrically or asymmetrically rash;

4) localization of the rash. Essential for diagnosis has, for example, the exclusive defeat uncovered
body parts or large folds of skin, predominant involvement of flexor or extensor surfaces of the
extremities, involvement in the process of the mucous membranes, etc.;

5) relative positioning of elements of a skin rash. On this basis distinguish disseminated rash,
grouped, annular inclined to merge, curly, gray-piginoznuyu ("the sprawling" in either direction with a
resolution in the center);

6) the nature of the borders of the lesions (clear or vague);

7) the reasons for the expansion of the lesions - they sprawl on the periphery or the rash of new
elements around them;

8) is isomorphic to the reaction - the emergence of fresh primary cells specific to the disease, the
site of skin irritation in some exogenous factor (scratch, prick injection needle burn sunlight, etc.).

Often, the diagnosis of skin disease requires the use of a variety of additional research methods,
which are discussed in the relevant sections. It is the microscopic diagnosis of the fungal culture and
skin diseases, damaged skin histological examination, in some cases - the lymph nodes,
determining the blood cells of lupus erythematosus, bullous dermatoses cytodiagnosis, determining
dermographism, pain, heat and tactile sensitivity, the sensitivity of the skin to chemicals UV rays, etc.
In some cases it is necessary to resort to trial for the treatment of specific suspect dermatosis
means (EX juvantibus diagnosis - diagnosis through treatment).

It should be noted that in recent years to identify a clear trend in the development of new methods
for diagnosis of skin diseases, allowing in vivo visualization of the structure of the skin. Among these
methods, the most studied and applied in diagnostic practice the following:

1) optical coherence tomography;

2) confocal microscopy;
3) magnetic resonance imaging;

4) epilyuminestsentnaya microscopy;

5) ultrasound skin.

Optical coherence tomography (OCT) allows you to visualize in vivo epidermis and papillary dermis
and most successfully used in the diagnosis of bullous dermatoses and some tumors.

Confocal microscopy has a higher resolution than OCT, and allows us to study changes in the skin at
a greater depth.

Magnetic resonance imaging is used to visualize tumors of the skin and appendages.

Epilyuminestsentnaya microscopy allows in vivo study the changes in the skin surface at various
pigmented tumors, particularly in the complex diagnosis of melanoma nom.

Ultrasound examination is used for veracity of pathological changes of the surface layers of the skin,
characterized by different echogenicity (sclerosis, edema, deposition of calcium).

Finally, after diagnosis, many patients undergo a general clinical examination in order to identify the
causes of endogenous dermatosis, including predisposing factors.

7. Neoplasms skin.
Skin neoplasms
Definition. Neoplasms skin are a heterogeneous group of diseases consisting of skin tumors, nevi,
secondary metastatic tumors and specific gemodermy.

Tumor foci represent the abnormal proliferation of tissue, continuing after the termination of the
etiological factors caused it.According to the forecast tumors are classified as benign,
malignant and prekankrozy (precancerous). On the origin of the tumor may be primary, ie, arise
from their own skin tissue (skin tumors) and secondary, developing as a result of metastasis of
malignant cells in her oncology

cal internal diseases (secondary metastatic tumors) or proliferation of abnormal cells in the skin
malignancies of the hematopoietic system (specific gemodermii or leukemia of the skin).

Benign skin tumors should be distinguished from non-vusov (malformations of the skin). The latter
are benign growths (both innate and manifested in different periods of life), which consist of normal
cells and structures pathologically coordinated with each other ("tissue deformity"). In some cases
there are mixed tumors, with signs of both benign skin tumors, and nevi.
Skin tumors and malformations of its development are divided into epithelial (originating from the
epidermis and skin appendages), mesenchymal-mum (developing of connective tissue, adipose
tissue, blood vessels) and neuroectodermal (arising from the nerves).pigmented nevi called
malformations skin originating from nevus cells (melanocytes).

Etiology and pathogenesis of skin lesions have been insufficiently studied. It is believed that their
causes may be genetic predisposition, ultraviolet, X-rays or radiation, viral infection, chronic skin
trauma and their impact on carcinogenic substances, insect bites, cancer metastasis, nonhealing
skin ulcers. In most cases, the etiology is not established tumors. In the pathogenesis of skin cancer
also plays a role and a weakening of the immune function of the skin Supervisory tumor cells caused
by immunosuppressive therapy comorbidities, and other etiological factors.

Diagnosis of tumors based on clinical data, refining the results of mandatory histological studies.

28.1. Benign neoplasms

Seborrheic wart

Definition. Seborrheic wart (senile warts, basal cell papilloma) - benign neoplasm associated with
impaired differentiation of basal cells of the epidermis, which is a clearly-from

Bordering towering papule or plaque with a rough surface.

The clinical picture usually begins to develop in elderly and senile age. Often observed defeat the
closed areas of the body, face and scalp. Senile warts look like papules and plaques round or oval,
yellow-brown, sometimes almost black in color, clearly delineated, rises above the surface of the
skin and with a slightly flattened warty surface (resembling in shape a lump of chewing gum adhered
to a solid surface). Tumor diameter of 0.5-4 cm possible spontaneous resolution elements.

The differential diagnosis is carried out dermatofib-Roma, pigmented nevi and melanoma.

Treatment. underwent surgical excision, laser therapy, electrocautery, radiotherapy, cryotherapy.

Pigmented nevi

Definition. Pigmented nevi (see col. incl., Fig. 34) - a group of benign tumors (malformations),
developing from cells melanogennoy system - chalk monocytes, which are otherwise called nevus
cells.

The clinical picture of pigmented nevi diverse. They all share the characteristic color rashes (from
yellow-brown to black), due to different concentrations of melanin content. Most often they appear as
dark spots of varying size and smooth flat papules, but may take the form of giant plaque
papillomatous surface. Some pigmented nevi are densely covered with hair.
Some pigmented nevi melanomoopasny, ie, under appropriate conditions can be transformed into
less lanomu. The most pronounced capacity for malignancy have borderline pigmented
nevi, melanocytes are located in the area of the basement membrane of the epidermis. Clinically,
they are black or dark gray spots (papules) with a flat smooth surface, devoid of vellus hair.They can
be localized in any areas of the skin, but most are melanomoopasnymi located on the palms, soles,
and genitals. About starting ma-lignizatsii pigment nevus evidenced by the following

signs that a diagnosis of malignant lentigo:

1) increasing the diameter of the nevus, especially in uneven sprawl of its borders;

2) The gain or loss of pigmentation;

3) the formation of pigment spots around the nevus or the appearance on the surface of dense
papules - "satellites";

4) seal nevus or the appearance of infiltration and hyperemia around him;

5) the appearance of pain or itching;

6) increase in the regional lymph nodes.

The differential diagnosis of pigmented nevi conducted with senile warts, melanoma and
dermatofibro-my.

Treatment. If there melanomoopasnogo nevus or malignant lentigo performed surgical excision of


all tumors with the surrounding healthy skin and subcutaneous fat.

Dermatofibroma

Definition. Dermatofibroma (fibroma) - a benign mesenchymal tumor of connective tissue, which is


a hemispherical papule or node.

The clinical picture. tumor occurs more often in the lower limbs, and open areas of the body (in a
spot exposed trauma and insect bites). Fibroids are dense hemispherical heavily pigmented nodules
or knots, protruding above the surface of the skin, the size of 0.5-3 cm Eruptions occur at any age
and have no tendency to progression. The number of elements from single to multiple.

The differential diagnosis is carried out with seborrheic wart, pigmented nevi and melanoma.

Treatment. required surgical excision, laser therapy, cryotherapy.

Angioma
Definition. Angiomas are benign tumors composed of altered vascular walls of various types (blood
and lymph capillaries, venules, arteries, veins).

The clinical picture of capillary hemangioma is characterized by vascular spots of various sizes,
with irregular borders, pink-red or cherry color, blanching at diascopy. Surface stains flat, smooth,
sometimes slightly rising. Favourite localization - face.

Starry hemangioma is a miliary red papules, which radiate from the vascular branches. More
localized on the face - the nose and cheeks.

Cavernous hemangioma looks soft node, from 1 to 5 cm, with a rough surface, sometimes falling
on palpation. Color education varies and depends on its depth in the skin. Superficial hemangioma
bluish-red, deep - with a bluish tinge.

The differential diagnosis is carried out with Kaposi's sarcoma and other vascular tumors.

Treatment. required surgical excision, radiotherapy, laser therapy, cryotherapy, diathermy.

Lipoma

Definition. Lipoma - a benign tumor of adipose tissue derived from fat cells - adipocytes.

The clinical picture. tumor is a soft, often lobed node size from a few to tens of centimeters, often
protruding above the surface of the skin. Color of the skin over the lipoma is not changed. Tumours
can be either single or plural.

The differential diagnosis is carried out with atheroma der matofibromoy, secondary metastatic
tumors.

Treatment - surgical excision.

28.2. Skin cancers

Basalioma

Definition. bazaliomah (basal cell epithelioma, see col. incl., Fig. 35) - the most common malignant
epithelial tumor that develops from atypical basal cells of the epidermis and follicular epithelium. It is
characterized by extremely slow growth, accompanied by inflammatory infiltration and destruction of
the surrounding tissue, and no tendency to metastasis.

The clinical picture. occurs predominantly in elderly and senile age. The most frequent localization
- face, scalp. Characterized by extremely slow growth, slightly increasing in size over the
years. Basal cell epithelioma not metastasize. It is characterized by only a peripheral growth involves
destroying tissue. Because of these features, called tumor with BAZALIT mestnodestruiruyu-schim
growth.And because of the possibility under certain conditions (for example, due to inadequate
radiotherapy) metatipichesky its transformation into cancer, some authors refer to this tumor
prekankrozam.

Rodent begins with the appearance of a single plane or a dense hemispherical papules 2-5 mm in
diameter, slightly pinkish or normal skin color. Subjective feelings are absent. Papule and slowly
growing for several years reaches 1-2 cm at the same time the central part splits and covered with
bloody crust, which is found in the rejection of easy bleeding ulcer or surface erosion. Along its
periphery observed narrow roller, solid or consisting of individual miliary papules slightly
pinkish. Sometimes it can be pearlescent paint or dark brown. Ulcer formed, increasing in size, while
in the central part of the rumen.

Depending on the nature of basal cell growth can turn into a large (10 cm or more) flat plaque with
scaly surface; in significantly protruding above the surface of the skin mushroom node; a deep ulcer
that destroys the underlying tissues, including bone (ulcus rodens, ulcus terebrans).

The differential diagnosis is carried out with seborrheic wart, Bowen's disease, actinic keratosis,
chalk-noma, various nevi.

Treatment: surgical excision, radiotherapy, laser therapy, cryotherapy.

Squamous cell carcinoma

Definition. Squamous cell carcinoma (spinotsellyulyarnaya epithelioma, squamous cell carcinoma) -


malignant epithelial neoplasm of proliferating atypical keratinocytes in the epidermis and starts
turning into invasive metastatic tumor.

The clinical picture. Disease occurs 10 times rarer than basal cell carcinoma, men are 2 times
more often than women.Development of neoplastic process most susceptible to white-skinned
patients living in hot sunny countries (Central America, Australia, etc.). Squamous cell carcinoma-
tion can begin anywhere on the skin and mucous membranes, most often in places where they
transition into each other (lips, genitals). Initially, there is a small infiltration, with a slightly rising gi-
perkeratotichnoy surface gray or yellow-brown color. Subjective feelings are absent in the initial
period. Tumor size, starting from a few millimeters, is gradually increased up to 1 cm, after which it is
defined a tight knot, which rapidly reaches a walnut. Depending on the direction of growth or tumor
may protrude above the surface of the skin or tissue to grow into the depth, undergoing decay to
form ulcers. Ulcerative infiltrative growth spinotsellyulyarnoy epithelioma embodiment leads to the
destruction not only the skin but also the underlying tissues (muscles, bone) but also tends to rapid
first metastasis to regional lymph nodes and then to other organs. Emerging ulcer is extremely
dense, slightly raised edges and twisted; its bottom is covered with blood crusts and grayish
masses, bleeds easily, and sometimes shows white corns ("horn pearls"). Tendency to ulcer healing
missing, appear local excruciating pain, further develop cachexia and secondary infectious
complications.
The differential diagnosis is carried out with the disease Bow Cohen, basal cell carcinoma, actinic
keratosis and vulgar warts.

Treatment. resorted to surgical excision of the entire tumor, surrounding skin, subcutaneous fat, and
if necessary - regional lymph nodes and other tissues involved. Used as radiotherapy, laser therapy,
cryotherapy, medication tsitosta-narcotic drugs.

Melanoma

Definition. Melanoma (malignant melanoma) is the most malignant tumor of the skin of developing
melanoma cells (malignant melanocytes) and tending to rapid metastasis.

The clinical picture. Melanoma occurs much less frequently basal cell carcinoma and squamous
cell carcinoma, predominantly in Caucasians suffer excessive insolation, usually after puberty. The
tumor can occur anywhere on the skin, including the nail bed(melanotic felon, acrolentiginous
melanoma), or primary (on intact skin) or second (30% of cases) as a result of malignancy nevus
pigment, such as by a chronic injury. In the latter case exophytic nevus begins to grow and change
their pigmentation (see "Pigmented nevi"). Melanoma is an easy bleeding papule or flat, slightly
raised, domed or knobby knot with uniform dark brown or black with a bluish tinge. Sometimes some
parts of the tumor may be deprived of color, and in rare cases, melanoma does not contain
melanin (amelanotic melanoma). Due to early nodal metastasis at first about the primary node
appear dense pigmented hemispherical papules, and subsequently - multiple pigmented and
depigmented-ITATION papules and nodes scattered throughout the body. Metastases appear in the
internal organs and as a rule, before the collapse of the primary tumor begins.

Diagnostics. melanoma biopsy strictly contraindicated, so the diagnosis is based on characteristic


clinical picture, after which the patient with suspected less lanomu sent to specialized oncological
dispensary for diagnosis and treatment.

The differential diagnosis is carried out with pigmented nevi, seborrheic wart and dermatofibroma.

Treatment. necessary surgical excision of the tumor throughout the surrounding skin, subcutaneous
fat, and regional lymph nodes.For the prevention of relapse assigned chemotherapy.

Kaposi's sarcoma

Definition. Kaposi's sarcoma (Kaposi's disease) is a malignant immune diseases caused by


multifocal proliferation in the skin and internal organs and hemo-endothelial limfokapillyarov and
perivascular connective tissue cells.

Etiology and pathogenesis. multifactorial etiology of the disease-Thorne. Expected to participate


oncogenic virus (HHV8), local trauma, genetic predisposition. Pathological process is more frequent
in patients immunoskomprometiro-bathrooms (old age, which preceded immunosuppressive therapy,
HIV infection) and in patients with endocrine diseases.
The clinical picture. Allocate the following clinical forms of Kaposi's sarcoma:

1) classic (sporadic idiopathic); 2) immunosuppressive; 3) endemic; 4) Epidemic (associated with


HIV infection).

Clinical manifestations of classical Kaposi's sarcoma characterized by initial symmetric skin lesions,
usually of the lower limbs, and sometimes the hands and forearms. Men more likely to suffer elderly
(over 60 years). Eruptions are slightly swollen, reddish-brown or bluish-purple spots and papules,
which gradually transformed into flat infiltrated plaques and painful knots, against which often shine
telangiectasia. Fresh nodes develop at the edges of the primary foci, merge with them, forming
different degrees of density larger lumpy tumor infiltrates. Individual elements spontaneously
resolved, leaving pigmented, slightly atrophic spots.

The disease has a chronic course and flows over the years, long lesion limited to the same body
parts (foot, leg, hand). Outbreaks eventually become n-morragichnymi with ocher-yellow color
purpuroznoy, marked their bleeding after minor injury and ulceration.Eventually, around the nodes
develops pronounced swelling of the surrounding tissues, causing elephantiasis of the
limbs.Dissemination occurs rash, swollen lymph nodes affected skin torso, genitals, face, mucous
membranes of the nose and mouth, internal organs (gastrointestinal tract, kidneys, liver, lungs).

Immunosuppressive disease develops in patients, long-term use immunosuppressants (about


organ transplantation, autoimmune diseases, malignant lymphoma, etc.) and clinically resembles the
classical form. Cancel immunosuppressive therapy often leads to recovery.

Endemic Kaposi's sarcoma occurs in endemic HHV8 virus and HIV geographical areas Equatorial
Africa (especially in Uganda) in Alaska. Common in younger patients (25-40 years), mainly men and
children of both sexes. Clinically occurs in three variants.

In the first variant manifestations of the disease correspond to the clinical picture of the idiopathic
form of the disease.

In the second variant of the disease process develops in the form of localized aggressive Kaposi's
sarcoma, characterized by the appearance of rapidly increasing, with a tendency to invasive
penetration into subcutaneous fat, muscle and bone infiltrated vegetating tumors.

Third, the most severe variant of this form of Kaposi's sarcoma is characterized by diffuse disease of
the lymph nodes (sometimes without cutaneous manifestations), frequent ulceration of skin lesions,
wider involvement of the visceral organs and rapid (within 1 year) deaths.

Epidemic Kaposi's sarcoma is one of the clinical diagnostic signs of AIDS, as occurs in HIV-infected
patients (in any period of infection). Usually develops in men aged 25-30 years (most homosexuals
and drug addicts). Characterized by a marked character of a large number of metastatic lesions that
may appear anywhere on the body (face, ears, neck, chest, abdomen, palms, soles).Despite the
unusual location and a significant amount of eruptive elements, skin lesions clinically consistent
classical Kaposi's sarcoma.

The differential diagnosis is carried out with hemangiomas and lichen planus.

Treatment. Overall therapy includes course application of cytostatic therapy (prospidin 100-200 mg
per day, a course of 3-4 g intervals between courses of 3-4 months), interferon preparations, and in
severe cases - polychemotherapy.

Physiotherapy. Used radiotherapy large nodular elements.

Outdoor therapy. symptomatic therapy (disinfectant ointment) for ulcerated lesions.

Lymphoma of the skin

Definition. Lymphomas are a large group of malignant diseases caused by proliferation of


neoplastic cells in the immune system (lymphocytes, their precursors and derivatives).

Lymphoid tissue is widely distributed in the body and form lymphoid organs - central (bone marrow,
thymus) and peripheral (spleen, lymph nodes, lymphoid tissue of the gastrointestinal tract, broncho-
pulmonary lymphoid tissue and skin). Each of these bodies can be a source of lymphoma, which
begins with the proliferation of malignant lymphoid cells therein. Traditionally distinguished Hodgkin's
disease (Hodgkin's disease) and Nekhoda-zhkinskie lymphoma. The latter may be nodal (derived
from lymph nodes) and extranodal (arising from any other lymphoid organ, including the
skin). Lymphoma of the skin are the second most frequent lesion after lymphoma of the
gastrointestinal tract. Distinguish primary lymphoma of the skin, developing primarily in the skin, and
secondary skin lesions in lymphomas other localizations.

Skin primary lymphoma (see col. incl. Fig. 36) - is the immune system of the tumor characterized
by proliferation of T-or B-lymphocytes, which have a specific tropism for the skin. In 1975 he was
offered a single concept of T-cell lymphomas, and in 1988 the first international symposium on skin
lymphoma officially recognized the existence of primary B-cell lymphomas of the skin. Among all
primary cutaneous lymphomas accounts for 60-65% of T-cell lymphoma, 20-25% of B-cell and 10%
naredkost form (NK-cell lines or indeterminate).

Currently, cutaneous lymphomas using the new WHO-EORTC classification (2005), based on the
WHO classification of lymphoid neoplasms of the hematopoietic tissues and classification of
cutaneous lymphomas and the European Organization for Research and Treatment of Cancer
(EORTC-classification).

According to this classification, isolated T-and NK-cell lymphomas, and B-cell lymphoma. For T-and
NK-cell lymphomas ethyl include the following: mycosis fungoides and its variants (follikulotropny,
pedzhetoidny reticulosis, granulomatous loose skin syndrome);Sezary syndrome; T-cell
ing leukemia / lymphoma adults; Primary cutaneous CD30 + lymphoproliferative disease (primary
cutaneous anaplastic large cell lymphoma-Terrorism, lymphomatoid dad les); pannikulitopodobnuyu
subcutaneous T-cell lymphoma; extranodal NK / T-cell lymphoma; primary cutaneous peripheral T-
cell lymphoma, unspecified (primary cutaneous aggressive epidermotropnaya CD8 + T-cell-tion
lymphoma, cutaneous / T-cell lymphoma, primary cutaneous CD4 + pleomorphic T-cell
lymphoma cells of small and medium-sized).

For B-cell lymphomas include primary cutaneous B-cell lymphoma, marginal zone accurate; primary
cutaneous lymphoma Thomas of follicular center cell; primary cutaneous diffuse large B-cell
lymphoma, a type of lower extremities.

Also isolated hematologic neoplasia from precursor cells-CD4 + / CD56 + blood-cutaneous


neoplasia (blastic NK-cell lymphoma).

The clinical picture of cutaneous lymphomas is very diverse and depends on the type of
proliferating tumor cells (lymphocytes morphological analogues, lymphoblasts, plasma cell-ing,
plazmoblastov, centrocytes, centroblasts or immunoblotting region) and the stage of disease, as
pathological changes over time due to growing developing more expressed malignant neoplastic
cells gradually weighting the clinical course of the disease.

Cutaneous T-cell lymphoma

Mycosis fungoides. aliber first described this disease in 1806, calling it mycosis fungoides due to
the fact that elements of the tumor resembled large mushrooms. Ba-zen in 1876 allocated during
three stages of dermatosis: spotty (erythematous), plaque and tumor.Usually granulosarcoid ill
elderly. The disease begins with spots that gradually infiltrated, turning into plaque. In erythematous
stage disease manifests diverse and uncharacteristic erythema urtikaropodobny-E, psoriasis and
parapsoriazopodobnymi, ekzemopodobnye eruptions. In some cases there are clearly defined
elements eritematoskvamoznye sizes from 2-3 cm to 10-15 cm or more. Number of lesions varies
from a few to many. They are accompanied by intense itching,

sometimes unbearable. The first manifestations of the disease can spontaneously disappear after a
few months to re-emerge. After repeated alternation of partial remissions and relapses spotted stage
gradually moves into the second - plaque stage.

It is characterized by the formation of indurated plaques of various sizes, yellowish red or bluish
color, with lihenifitsirovannoy surface.In the plaques, and the scalp and outside, often hair fall. Nail
plate deformed, become brittle. The average duration of spotty and patchy stages is 3-5 years. In
some cases, patchy stage can last for decades.

The third stage of the disease manifests tumor-nodes, which may be formed both in existing plaque
or on unaffected skin previously.Localization and number of tumors can be very different. They have
a size from plum to orange, wide or, conversely, a narrower base, soft or testovatoy
consistency. Reaching a certain size, they eroziruyutsya or deep ulcerate.

Peripheral lymph nodes in the first stages of the disease is usually not raised in the second stage is
often increased, and the third - as a rule. In tumor stage possible dissemination process in the
internal organs, lymph nodes, bone marrow and blood.

At the moment there are the following options for mycosis fungoides: 1) follikulotropny with follicular
mucin-Zoom or without (clinically follicular papules, plaques, tumors caused perifolliku molar
infiltration of neoplastic lymphocytes); 2) pedzhetoidny reticulosis(psoriaziformnye rash, localized
mainly in the distal extremities);

3) granulomatous loose skin syndrome (determined in large folds infiltrated lacking elasticity, folded
education).

Subtype of mycosis fungoides include the following: bd's disease, ichthyosiform, gipopigmentny,
poykilodermiche-sky, etc. More than one hundred and twenty years isolated headless mycosis
fungoides, in which there is direct tumor stage, bypassing spotty and patchy. Currently

the emergence of new methods of investigation proved that this form of lymphoma is not a mycosis
fungoides.

Sezary syndrome is characterized by erythroderma, an increase of peripheral lymph nodes, the


presence of cells Se-dawn, representing more than 5% of all lymphocytes, and in absolute numbers
- more than 1000/mm 3 . In addition, marked itching of bottom-la-plantar hyperkeratosis, alopecia,
onychodystrophy.

Primary cutaneous CD30 + lymphoproliferative disease

Lymphomatoid papulosis. Makauley in 1968 coined the term lymphomatoid papulosis to refer to
the disease, which lasted for years, sometimes - for decades, and was characterized by
spontaneous permitted papular elements. Noteworthy is that in benign clinical course,
histopathological data showed malignant neoplastic process. Lymphomatoid papulosis usually
begins in 35-45 years with reddish spots, gradually turning into papules that have a smooth surface
may peel or crusted. By the above elements can join purpura, necrosis. Elements left on the
resolution or gipopigmentnye giperpigmentnye spots, in rare cases - atrophic scars. The preferential
localization of lesions - trunk, proximal extremities; less involved in the process of the palms, soles,
face, scalp.

Primary cutaneous anaplastic large cell lymphoma has the second highest frequency of T-cell
lymphomas of the skin. Can occur at any age, although it most often 60-70 years.

The disease is manifested by single or grouped nodes, often ulcerated, at least - papules localized
on the limbs or trunk. The possibility of spontaneous remission.
Pannikulitopodobnaya Subcutaneous T-cell lymphoma is characterized by infiltration of the
subcutaneous tissue neoplastic cells that histologically evident lobular panniculitis determining
lymphoma clinic. The disease is characterized by single or multiple subcutaneous nodules, which in
some cases is gradually ulcerate. They are located mainly in the lower extremities. Lesions can be
both single and generalized.

This lymphoma is a benign, extracutaneous dis-seminatsiya observed in 20% of cases.

Extranodal NK / T-cell lymphoma kletognaya, nasal type. suffer more adult males. For the
disease characterized by multiple plaques and tumors predominantly on the trunk and extremities, in
the case of nasal forms - destructive tumor in the midface.

Primary cutaneous peripheral T-cell lymphoma, unspecified. For various versions of this lymph
we characteristic papules, plaques, nodes often eroziruyuschiesya or ulcerate.

Cutaneous B-cell lymphoma

Cutaneous B-cell lymphoma, marginal zone.

Among the primary B-cell lymphoma occurs in about 50% of cases. Disease presented papules from
pink, red to violet, plaques, or nodes, are localized mainly on the trunk or limbs, especially the top.

Primary cutaneous lymphoma cell follicular center. Among the primary B-cell lymphomas of the
skin occurs in 30% of cases.Disease represented by single or grouped pinkish papules (from a few
millimeters in diameter and larger), and tumor-like plaques nodes are localized mainly on the scalp,
forehead and torso.

Primary cutaneous diffuse large B-cell lymphoma of the exact type of the lower limbs is
predominantly found in elderly people, mostly women. The eruptions are rapidly growing reddish or
bluish-reddish tumor on one or both lower extremities.

Diagnostics. For diagnosis of cutaneous lymphomas in addition to assessing the clinical picture
must be used in combination the following diagnostic methods: histological (description cytological
characteristics of tumor cells), immunohistochemistry (definition of the phenotype of tumor cells),
cytogenetic (detection of chromosomal abnormalities), molecular biology (tumor clonality
determination process ). To identify the possible involvement of other bodies shall mapping skin

General clinical and biochemical blood tests, chest radiography, computed tomography, ultrasound
of the abdomen and retroperitoneum, sternal puncture, biopsy lymph node biopsy.

The differential diagnosis of cutaneous lymphomas performed with many diseases. In


eritematoskvamoznoy and plaque stage mycosis fungoides differentiate with eczema, psoriasis
vulgaris, focal neurodermatitis, allergic dermatitis, drug reaction. Sezary syndrome differential
diagnosis spend with nonspecific erythroderma-E arising in therapy of inflammatory dermatoses
irrational (Pink zoster, psoriasis, eczema, atopic dermatitis), and toksikodermiya. Lymphomatoid
papulosis with vasculitis and differentiate gemodermiyami. Various lymph we manifested nodes
should be differentiated from the pan-nikulitami.

Treatment of lymphoma depends on the type of skin lymphoma stage.

General Therapy T-cell lymphomas. Initially used restorative and immunostimulating agents
(vitamins, ginseng, Eleutherococcus, interferon). In the second stage uses phototherapy (PUVA,
UVB), radiation therapy (radiotherapy, fast electrons), appointed cytostatic monotherapy (pro-spidin
100 mg daily, on a course of 3-5 g or cyclophosphamide 200 mg daily, on a course of up to 6
g ).When eritrodermicheskoy indolent lymphomas, treatment is initiated with corticosteroids
(prednisolone per os at 30-40 mg per day or diprospan 1 1 ml intramuscularly once a week) and
then connect prospidina (cyclophosphamide) in the same course dose. In tumor stage disease using
radiotherapy and chemotherapy.

Outdoor therapy - is symptomatic. On infiltration, papules and plaques designate glucocorticosteroid


ointments and creams, and disintegrating units - disinfectants (to prevent secondary infection).

Therapy of B-cell lymphomas. applied surgical removal of lesions and / or radiation therapy with
systemic process - chemotherapy.

28.3. PREKANKROZY

Actinic keratosis

Definition. Actinic keratosis (solar keratosis, senile keratome) - precancerous growths appearing on
the skin exposed to chronic sun exposure, and subsequently tending to transform into squamous cell
carcinoma.

Etiology and pathogenesis. disease occurs as a result of regular extended sunlight or UV


irradiation, especially with wavelength of 280-320 nm, after a latent period of 10-20 years old. It is
considered that insolation UV genetic material gives epidermal cells, whereby they are transformed
into anaplastic cells (carcinoma in situ). These abnormal cells gradually replace normal
keratinocytes and lead to a breach of keratinization of the epidermis. Transformation into squamous
cell carcinoma occurs at that moment when they break through the basement membrane and
penetrate into the dermis.

The clinical picture develops, usually over the age of 45 years on the open, exposed to insolation
areas of the body (forehead, scalp, back of the nose, ears, cheeks, neck, shoulders).

Tumor begins with the appearance of round, oval, sometimes irregularly shaped, reddish, slightly
inflamed plaques, against which shine telangiectasia, and palpation reveals a rough surface horn. In
other cases, more pronounced hyperkeratosis and constitutes horny masses yellow. Strongly
expressed hyperkeratosis can significantly protrude above the surface of the skin and lead to the
development of cutaneous horns, which is more common in the eyelids and forehead. Sometimes
senile keratoma giperpigmentiruetsya outwardly resembling seborrheic wart.

Actinic keratosis is subject to very slow development, malignancy in squamous cell carcinoma does
not occur in all cases and occurs after a few years or decades. Clinically this moment manifests
increased inflammation, thickening and plaque ulceration.

The differential diagnosis is carried out and disseminated discoid lupus erythematosus, Bowen's
disease, seborrheic wart, basal cell carcinoma.

Treatment. Applied cryotherapy, radiation therapy, laser therapy, surgical excision.

Bowen's disease

Definition. Bowen's disease - a chronic inflammatory disease caused by abnormal proliferation of


keratinocytes in the epidermis, characterized by slow growth and invasive ability to transform into
squamous cell carcinoma.

Etiology and pathogenesis. disease is an intraepidermal carcinoma (carcinoma in situ), arising


from the proliferation of atypical keratinocytes. Developing first only intraepidermal tumor, eventually
breaks a basal membrane and transformed into squamous cell carcinoma. Bowen's disease occurs
as a rule, in older patients, most often in people who have used cosmetic or topically medicaments
containing carcinogenic substances (e.g., arsenic). It is believed that foods which contain arsenic
compounds (wine, tonic), may also be provoking factors.

The clinical picture. Lesions of the skin may be single or multiple, hitting any skin and mucous
membranes. The most frequent localization - the skin of the trunk, forehead, temporal area and
fingers.

Affected skin look as rounded or irregular outlines pink spots or plaques ranging in size from 2-5 mm
to 10 cm They are slightly infiltrated and slightly raised above the surface of the skin, rough and
covered with a grayish-white or yellowish scales, scales, crusts or scabs . After removal of flakes,
platelets appear red with eroded or slightly keratinized papilloma toznoy surface. From the mucous
membranes are mainly affected oral mucosa, glans penis, vulva, changed parts which demonstrate
actinic.

The disease develops slowly, sometimes the process is allowed to spontaneously, transformation
into squamous cell carcinoma occurs only in a few years. Patients with the disease Bow Ena often
find related cancers of internal organs, especially the lungs, gastrointestinal tract and urogenital
system.
The differential diagnosis is carried out with psoriasis vulgaris, nummulyarnye eczema and
disseminated discoid lupus erythematosus, actinic keratosis, basal cell carcinoma.

Treatment. resort to surgical excision, radiotherapy, laser therapy, cryotherapy, the use of 5% or
ftoruratsilovoy 30% prospidinovoy ointment.

Paget's disease

Definition. Paget's disease is an intra-epidermal adenocarcinoma developing in the nipple and


areola of the breast (usually unilateral).

Etiology and pathogenesis. tumor develops from atypical epidermotropnyh breast ductal
cells (Paget cells) has infiltrative growth into surrounding tissue followed by metastasis.

The clinical picture. Paget's disease occurs almost exclusively in females and usually after the age
of 40 years. The disease begins with a unilateral lesion of the nipple or peripapillary fields in which
there is an itchy, painful, well-delineated, erythematous plaque, scaly-crusted. Plaque slowly
increases in size and goes beyond the areola, hitting the skin of the breast, at the same time
remaining sharply demarcated from healthy skin. At the same time, due to the invasive growth, the
tumor grows in depth, becoming a painful knot. The process ends with metastasis to nearby lymph
nodes and the development of breast cancer.

As a variant of the disease, also occurs ekstramammar-tion Paget's disease, which develops from
the cells of the ducts of apocrine sweat glands, and therefore affects the anogenital and axillary
region, occasionally - the navel. This pathological process also occurs more often in women and has
clinical manifestations similar classical Paget's disease.

The differential diagnosis is carried out with eczema nipples, psoriasis vulgaris, streptococcal
intertrigo, Bowen's disease, basal cell carcinoma.

Treatment. requires surgical excision of the affected area within the involved tissues.

28.4. SECONDARY metastatic tumors

Definition. secondary metastatic tumors are malignant tumor cell proliferation of cancer of the
internal organs, skin falling in hematogenous or lymphatic metastasis by due. Of malignant diseases
of the internal organs most commonly metastasize to the skin cancers, causing the development in
her secondary carcinomas of the skin.

The clinical picture. Skin lesions occur in 35% of patients with metastatic tumors of internal
organs. Sometimes they are the first symptoms suggestive of the presence of metastases. In depth,
location may be affected by different parts of the skin, secondary metastatic tumors can be
exophytic, intradermal-E, epidermal. They usually represent the nodes of different sizes, the skin
over which varies in color from normal skin color to bright red. In the subsequent nodes may break
forming sluggish granulating ulcer.

Localization of tumors is dependent on the location of the primary tumor. Skin of the abdomen often
affected in lung tumors, stomach, kidneys and ovaries. In the skin of the breast is usually detected
metastases in women with breast cancer. On the scalp metastases of malignant tumors predominate
lung, kidney and breast cancer.

Secondary hematogenous metastatic tumors can occur anywhere on the skin and are both single
and multiple. Their favorite localization - leather abdomen and thighs. By secondary lymphatic
metastatic tumors entered into the skin mainly in breast cancer.

The differential diagnosis is carried out with benign and malignant skin tumors, specific
gemodermiyami, erythema nodosum, erythema induratum, skrofuloderme.

Treatment is similar to that in Paget's disease.

28.5. GEMODERMII

Definition. gemodermiyam To include skin lesions caused by malignant diseases of hematopoietic


myeloma colloid and lymphatic systems (myeloma and lymphoma).

Leukemia can cause the development of the pathological process in the skin due to the proliferation
of abnormal cells in her blood system, morphologically identical ley plots. Such gemodermii are skin
growths are called specific gemodermiyami leukemia or skin. In addition, the skin may develop an
inflammatory response associated with the general toxic-allergic influence leukemia body as a whole
due to them caused by disturbances in the endocrine, immune, nervous and other systems.

These inflammatory reactions are called nonspecific or gemodermiyami leykemidami.

The clinical picture. When myeloid leukemias process can affect any area of skin. Eruptions
occur more often on the legs and are single or multiple, towering, with a clear boundary nodules and
plaques bluish-red, red-brown, or bluish-gray color. Sometimes there are sites on which skin color is
unchanged. Elements are characterized by a pronounced tendency to decay with the formation of
ulcers of varying depth.

Myeloid leykemidy more common and specific myeloid gemodermy represent primarily
hemorrhagic manifestations in the skin and mucous membranes (vibitses bubbles with hemorrhagic
content).

Specific gemodermii with lymphocytic leukemia (lymphoid leukemia) occur in 20-50% of


patients. Neoplasms are arranged symmetrically, often in the face and scalp, but can occur on any
other parts of the body. They are smooth, moderately dense nodes and tumor infiltration of various
sizes, which can sometimes coalesce reaching the size of an apple. The skin over them may be red-
brown or color normal color. Ulceration nodes is rare. Diffuse infiltration of the person accompanying
the periorbital edema, gives it a superficial resemblance to the muzzle of a lion (leonine
facies). characteristic is the presence of a bluish-red or red-brown tumor infiltrates in the
earlobes. Possible occurrence of infiltrates in the mucous membranes of the mouth. Another
manifestation of lymphoid leukemias are pruritic papular rash on various parts of the body,
resembling those at strofulyuse adults.

Lymphoid leykemidy manifested mainly generalized pruritus, which occurs in 10-20% of cases,
simple and nonspecific subacute prurigo rodermiey red blood, and sometimes - chronic urticaria and
purpuroz-governmental rash on skin and mucous membranes.

Differential diagnosis of specific gemodermy conducted with benign and malignant skin tumors
(primarily lymphoma), secondary metastatic tumors, Kaposi's sarcoma, leprosy.

Treatment of symptomatic gemodermy.

8. Principles external treatment of skin diseases


General principles of treatment. External treatment

Skin diseases are closely related with the state of the entire human body.
Treatment of diseases of the nervous system, internal organs, endocrine
glands, the expulsion of worms and treatment of foci of infection are of great
importance for the successful treatment of patients with skin diseases. With
knowledge of the etiology of the disease treatment is carried out primarily
for the purpose of removing the cause of the disease (eg, destruction of
scabies mite). Therapy of patients with skin diseases should be
comprehensive and include the correct mode, and general outdoor treatment
modalities.

External treatment of skin diseases are common in conjunction with


medication and rational diet. It aims to accelerate the elimination of lesions
and reduce the feeling of itching, burning, contraction pain. External
treatment is carried out, usually a nurse.

Outside treatment begins with cleaning the lesion from flakes crusts, pus,
scraps of wall bubbles and bubbles. This time with tweezers, curved scissors
and cotton swabs soaked in 3% hydrogen peroxide. You can not forcibly
remove scales, crusts, the remnants of ointments. Such sites are abundantly
moistened sunflower, peach, linseed oil, or any other, and re-treated in 10-15
minutes or leave the oil patch over a longer time. Contaminated soil erosion
and ulcers treated with 3% hydrogen peroxide solution, and wipe the skin
around the lesions camphor or 2% salicylic alcohol.

If a patient with a skin disease move difficult or even impossible (for


erythroderma, in severe cases of mycosis fungoides, pemphigus vulgaris,
systemic lupus erythematosus, psoriasis, etc.), change the sheets produces a
nurse with a nurse, as is discussed in the chapter on "Personal Care of the
patient. " Linen sheet and such patients should always be well straightened
to avoid the formation of bedsores. Change shirts in such patients produce
as: shirt pulled up to the edge of the underarms and removed from the head
first, then with it. In severe cases, common dermatoses (for example,
erythroderma) on the patient wear baby's undershirt.

When serious condition dermatological patients medical staff (paramedic,


nurse, nursing sister) performs a number of hygiene procedures. So, for
washing patients from a pitcher pour water over the basin. Tempted such
patients with a weak solution of potassium permanganate (1:1000) with a
cotton swab mounted on forceps. Cotton swab dipped 2% boric acid solution,
washed ever. Oral cavity is rinsed with a weak solution furatsilina (0.02%
-1:5000), potassium permanganate (0.01% -1:10000) etakridina lactate
(rivanol) (0.05% -1:2000). Tongue and mouth wipe 1% solution of borax to
the 10% glycerol solution, wrapped with gauze moistened with a spatula and
the solution.

For topical treatment of skin disease most often use powders, lotions, wet
dressings, lubrication, agitated water and oil mist (mash), pastes, ointments,
patches and other dosage forms.

Powders composed of a powdery substance which deposited a thin layer on


flat portion lesion. Indifferent powder containing zinc oxide, talc, starch, terra
alba zudouspokaivayuschee and exert anti-inflammatory activity, they dry
the skin (for diaper rash), it is cooled and absorb exudate. Sulfonamides
(white streptocid, etc.) in the form of powder, xeroform, dermatological
powders are part of the treatment of erosions and ulcers.

Lotions. Drug solutions, pre-cooling, moisten 2-4 gauze, lightly squeezed and
applied to the affected area of the skin. Change lotions made in 5-15 minutes
(as it dries) for half an hour, the procedure is repeated 3-5 times a day
(depending on the severity of the process). Moknutie lotions reduce puffiness
and weaken the itching and burning, ie, anti-inflammatory effect due to
vasoconstriction. Most use 1-2% solution of tannin, 0.25-0.5% solution of
silver nitrate (lapis), 2-3% solution of boric acid, 0.25-3% solution
amidopirina, lead water.

Disinfectant lotions used in cases where joins pyogenic infection. These


lotions are ethacridine lactate solution (rivanol) (0.1%) Frc (1:5000),
potassium permanganate (0.05%), resorcinol (1.2%).

Humidity drying up bandage doing on the same principle as a lotion, but


have 8-12 gauze layers. Dressings changed every half an hour - an hour or
less (as it dries). If prisyhaniya bandage forcibly removed and soaked with
the same solution.

Such dressings are used with limited skin lesions with marked infiltration and
moist. Pustular skin diseases and common acute inflammatory processes are
contraindications to the use of wet-drying bandages.

Warming packs used in chronic inflammatory processes with profound


disabilities infiltrates the skin and subcutaneous tissue (atopic dermatitis,
etc.). 10-12 folded layers of gauze moistened with a solution (lead water, 2%
boric acid, etc.), squeezing and superposed respectively on the lesion size.
Gauze is applied over the sheet of paper voschanoy somewhat larger size,
and then - a layer of cotton wool and tape up. Compress change 1-2 times a
day.

In contrast, warming is no dermatological wool compress.

Lubrication produce alcohol and aqueous solutions of aniline dyes (eg,


brilliant green). Pruritus, neurodermatitis - aqueous-alcoholic solution of
menthol (1.2%), carbolic acid (1-1.5%) and aqueous solutions of copper
sulphate (2-10%), silver nitrate (lapis) (2-10%) .

Water and oil agitated suspension (mash). Water, glycerol and powdery
substance (30% of total weight) of the aqueous mash up. Powdery
substances are often zinc oxide, talc, white clay, starch. Water talkers are
anti-inflammatory, soothing itching and burning. Hydroalcoholic mash
contain alcohol. Oil mash is prepared from the same powders and liquid fat
base (sunflower, peach oil or liquid). Frequently used "zinc" oil (30% zinc
oxide and 70% vegetable oil). Oil talkers soften the skin, help to remove
scales, crusts and reduce feelings of tension, contraction.

Before the use of aqueous and oily suspensions shaken and a piece of cotton
is applied to the affected area. These drugs can be added sulfur ihtiol, tar,
menthol and other agitated mixture dries quickly on the skin, do not impose
the armband. Should not be applied with abundant soak and hairy areas of
the head.

Pasta. They are made up of equal amounts of powders (zinc oxide, talc etc.)
and fatty base (lanolin, petrolatum, etc.). They are deeper than talkers, but
less active than the ointment, anti-inflammatory and drying effect. Pasta
dough stick to the skin without a bandage. On the scalp soak in the presence
of pasta is not applicable. Pastes are applied to the skin 1-2 times a day.
Once in 3 days pasta remove swab dipped in vegetable oil.

Frequently applied zinc paste, consisting of equal parts of zinc oxide, talc,
lanolin and petroleum jelly. During the testimony of the paste include ihtiol,
naphthalene, resorcinol, sulfur preparations, tar and other paste is applied to
lesions with a spatula and lightly smear on the hearth strips. The surface
area lubricated gauze and tape up applied (no more than 2-3 rounds).

Ointments are composed of one or more medicinal substances are uniformly


mixed with the fat ointment base (vaseline, lanolin, lard, naphthalene, etc.).
Assign ointment in subacute and chronic skin diseases, the presence of
inflammatory infiltrate in the skin, since they have a profound effect.
Consume 2-10% sulfuric ointment 2-3% coal tar, white mercury 1-3%, 2%
salicylic, ihtiolovye 2-5%, 2-3% naphthalane and other ointments and
antibiotic ointments (erythromycin, and biomitsin etc.). In the treatment of
the bubble and herpes zoster used interferon ointment.

Used as ointments containing corticosteroids (Prednisolone, hydrocortisone,


deperzolonovaya), corticosteroids and antibiotics - Oksikort, Geokorton,
lokakorten (with neomycin, vioformom, tar), ultralayte, dermozolon,
deperzolon, monomitsin-prednizolonovuyu, sinalar-H - with neomycin or
sinalar C - with hinoformom.
For a long time, especially on large areas of skin steroid creams and
ointments should be used with great caution, as due to suction (especially if
eroded surface of the skin) steroid hormones may have an adverse effect on
the patient's body and give local complications (formation of atrophic skin
areas appearance of telangiectasia, etc.).

Spatula ointment applied evenly on a piece of cloth and put it on the lesion,
strengthen bandage or ointment applied directly to the skin, leaving without
a bandage. Scabies, pityriasis versicolor ointment rubbed into the skin.
Affected areas smeared paste or ointment 1-2 times a day. Sometimes ihtiol,
tar used in pure form (without ointment base), then produce lubrication 1
every 2 days. During the procedure, ointments and pastes in glass beams
put on a separate table, the amount of medication nurse gives a patient on
voschanoy paper.

Nurse should make sure that on the banks that hold ointments, lotions,
solutions, neatly and clearly written name and the date of preparation.
Application of external funds at the end of their life-cycle is not permitted, as
they can cause irritation and inflammation of the skin (dermatitis).

Plaster. In emplastic basis than fat, wax or resin is included. Patch compared
with the ointment has a thick and sticky consistency. It is preheated, and is
applied to the affected area of a thick layer, it acts more deeply than an
ointment. Plaster containing no drugs used for fixation bandages for skin. If
an ordinary bad patch stick to the skin, it is slightly warmed.

Soap. By therapeutic soaps are brimstone, tar, ihtiolovye, resorcinol, sulfur-


salicylic acid, sulfur-tar, etc.

Bath. Therapeutic shared bath with the addition of pine extract, potassium
permanganate (1:10,000), oak bark (1 kg of bark boiled in 6 liters of water),
decoction of bran (1 kg of wheat bran boiled in 3 liters of water) and local
(37-40 C ) is used in skin diseases, hands, feet, genitalia, anus. So, hot
baths for arms prescribed for chills, vasomotor disorders.
Depending on the temperature of bath water divide to neutral (34-36 C),
warm (36-38 C), hot (39 C and above), cool (33-21 C) and cold (20 C
and below). Duration conventional baths - 15-25 min-10 min warm, hot - 5
min.

First bath wash with hot soapy water, sponge or brush, which are pre-boiled
and stored in a 1% solution of bleach and disinfect 1-2% solution of bleach or
1% bleach solution. Then wash off with disinfectant solution with hot water.
Once a week, clean bath of dilute hydrochloric acid, sodium bicarbonate,
kerosene or a special paste. Rusty spots purified oxalic acid.

Therapeutic baths should be taken 30-40 minutes after a light breakfast or 1-


2 hours after lunch.

Bath with the addition of starch and bran (wheat or almond) is taken as an
antipruritic and soothing agent. Starch or bran (500-1000 g) in a linen bag
immersed in a water bath or indifferent lukewarm (37 C) temperature, and
the contents received into the water from time to time squeeze bag. Of 1-2
kg can be prepared in advance bran broth, drain and add to the bath.
Almond bran can be added directly into the bath. Duration of therapeutic
baths for 30 minutes - 1 hour or more.

Shared bath, shower shown in psoriasis, neyrodermatozah. Water cleanses


the skin from the remnants of drugs, crusts, loosens thickened horny layer of
the epidermis, has a calming effect on the nervous system, improves blood
circulation.

9. Modern views on the etiology and pathogenesis of psoriasis.


Psoriasis (psoriasis) - a chronic skin disease of multifactorial nature with a dominant value of genetic factors in its
development, characterized by hyperproliferation of epidermal cells, keratinization disorder, an inflammatory reaction
in the dermis.

Psoriasis affects about 2% of the world population. The disease can occur in newborns and infants.

Etiology and pathogenesis

Distinguish two types of psoriasis.

Psoriasis type 1 in the 60-65% associated with heredity: for it is typical early manifestation of the disease, the
peak incidence - in 16-21 years. Characterized by a large area of damage, torpid course and frequent relapses. A
relationship with the disease antigens HLA-B13, HLA-B17, HLA-Bw57, HLA-Cw6.
Psoriasis 2nd type is not associated with a system of HLA, characterized late manifestations of the disease peaks
in 50 years.Communication with heredity was found in 1%.

Psoriasis is an autoimmune nature of the disease with involvement in the process of primary T lymphocytes and
secondary activation and keratinocyte proliferation (division of accelerated 10 times). Activation of CD4 lymphocytes
induces a variety of immunological reactions, including the increased activity of macrophages, synthesizing a wide
range of pro-inflammatory mediators, especially cytokines (TNF-), interleukin-1.

Trigger mechanisms of development of psoriasis are often chronic foci of infection (tonsillitis, sinusitis, etc.). The
disease can occur after mechanical injury to the skin, medication (especially tetracycline).

In preschool children psoriasis often appears after the psycho-emotional surge in the period expressed as a result of
reactions vegetonevroticheskih fright.

Distinguish winter, summer and off-season forms of psoriasis.

Etiology ... ... cause of psoriasis remains unclear. None of the existing hypotheses about the origin of psoriasis did
not become generally accepted. The most common viral, hereditary (genetic), neurogenic and exchange (metabolic)
theory of disease, but none of them is not universally accepted. Apparently has psoriasis multifaktornuyu nature. In
its pathogenesis assign a role immunological, enzymatic and other biochemical abnormalities in the body. Significant
role for genetic factors. The structure of genetic determination is not deciphered. Of the triggers of psoriasis are
important primarily emotional stress and psycho-emotional status of the patient. Infectious diseases, chronic foci of
infection (tonsillitis, sinusitis, urinary diseases, etc.) can also trigger the appearance of psoriasis. It is proved that the
infectious agent causing teardrop-shaped psoriasis is related to streptococcus. Quite often, psoriasis occurs in areas
of mechanical damage to the skin, namely in the field of cuts, scrapes, punctures, scratching, abrasions, burns,
acupuncture dermoabraziya, vaccinations, insect bites, punctures, operational scars, abrasions, tattoos, burns, and
solar X-ray irradiation or psoriasis frequently appears after administration of drugs (-blockers, nonsteroidal anti-
inflammatories, interferon). One can not ignore the influence of climatic factors (illness, usually acute in
winter). Pathogenesis ... ... in the pathogenesis of psoriasis play an important role immune disorders. Skin lesions
accompanied by an influx of activated T lymphocytes. Increased synthesis by activated macrophages and
keratinocytes interleukin-1 induces T cells to produce interleukin-2, which in turn is a potent stimulator of proliferation
of T-lymphocytes. Activation of T-helper pathogenesis associated with the proliferation of epidermal cells. Excessive
migration from peripheral blood lymphocytes in the affected skin can cause the epidermis of infiltration of these cells
due to changes in the cytoplasmic membranes, increasing adhesion to endothelial cells, chemotaxis of T
lymphocytes, and interleukin-1 stimulation of migration into the epidermis. Active inflammatory mediators are
histamine, released during mast cell degranulation and influence vascular permeability; hydrolase released from
neutrophils; prostaglandins, leukotrienes and other arachidonic acid derivatives. Increased local production of
arachidonic acid metabolites may be caused by cytokines produced by macrophages or keratinocytes.

Histopathology ... ... in the epidermis observed parakeratosis, acanthosis in mezhsosochkovyh sites Malpighian
layer and thinning it nadsosochkovyh sites spongiosis and intracellular edema, congestion in the intercellular gaps,
penetrating from the dermis neutrophils (Munro microabscesses). Papule on the horny layer is thickened, loosened,
consists mainly of parakeratoticheskih cells with elongated, rod-shaped nuclei. Numerous gap between the plates
filled with air, through which the scales have a silvery appearance. In the old elements hyperkeratosis more
pronounced than parakeratosis;nuclei in the stratum corneum occur regardless of how long ago papules. Granular
layer disappears or persists interrupted one row of its cells. In acute cases, and no shiny coat. Malpighian layer over
papillae thinned, elongated epidermal outgrowths. In styloid layer between the papillae pronounced
acanthosis. Capillaries of the papillary layer of expanded strongly crimped, overfilled with blood. In the papilla and
papillar layer around the vessels there is an inflammatory infiltrate composed of lymphocytes and histiocytes. Clinical
forms ... ... depending on the size and nature of eruptive elements are distinguished: (1) point psoriasis,
characterized by papules the size of a pinhead to a millet or grain, (2 ) guttate psoriasis - elements reach the size of a
grain of lentil; (3) Coin-type psoriasis with eruptions magnitude 3-5 cm; (4) Psoriasis manifested lichenoid
papules; (5) psoriasis, where the sprawling formed papillomatous lesions; (6) annular psoriasis - elements form a
ring; (7) with psoriasis rashes ranging in form of arcs and garlands; (8) shaped, or geographic, psoriasis - outlines
lesions resemble a map; (9) seborrheic psoriasis - localized rash characteristic of seborrhea on the ground in the
form of small pinkish scaly spots; (10) "chronic" psoriasis, etc

10. Clinical features of psoriasis. Severe psoriasis.


Clinical manifestations ... ... classic vulgar psoriasis is a clearly demarcated erythematous papules and plaques,
varying widely in size and covered with white scales. Removing scales leads to the appearance of tiny droplets of
blood (a sign auspices). Often appear on the nails pitted and develops their dystrophy. Mainly affects the elbows,
knees, scalp, genitals and lumbar region, although the process may involve any part of the body. A favorite place of
psoriasis are extensor surfaces of the extremities. However, the degree of damage varies. Young elements rash
usually small (1-3 mm), but can easily be combined with the formation of large plaques (type of concentric
circles). Psoriasis is one of those skin diseases (along with flat lichen, vitiligo, warts) which are characterized by
Koebner phenomenon. Last means new items on the site of traumatic injury to the skin (such as scratches and
scratches).

11. The principles of treatment of psoriasis.


Principles of treatment ... ... now modern medicine does not cure psoriasis. Treatment of psoriasis is directed to
inhibition of proliferation of epithelial cells and elimination of inflammation. Psoriasis Treatment needs to be
individualized for each patient and assigned based on anamnestic data, forms, stages, the distribution process,
comorbidities, age and sex of the patient, contraindications to a particular method of treatment or medication. Due to
the fact that psoriasis is a chronic course and does not represent a threat to the life of the patient, priority is given to
topical treatment, except for severe diseases that require an integrated system of treatment with detoxification,
desensitizing, anti-inflammatory drugs of different groups, physiotherapy therapies, outdoor drugs etc. It is necessary
to pay attention to the overall physical and psychological condition of the patient, the patient's tolerance to find the
disease.Recommended various methods of psychotherapy, such as cognitive-behavioral therapy, climate. Systemic
therapy ... ... during the progressive stage appointed detoxification therapy, used externally emollient cream or 1-2%
salicylic ointment. Within the framework of systemic therapy applied: (1) aromatic retinoids (acitretin (neotigazon))
mechanism of action is to inhibit proliferation of epidermal cells, the normalization process of
keratinization. Particularly effective formulation in combination with PUVA therapy; (2) cytotoxic agents
(methotrexate), which is used in cases of persistent course of psoriasis and contraindications to other treatments; (3),
immunosuppressants (e.g., cyclosporine A dose of 5 mg per 1 kg of body weight per day) are assigned in common
cases of severe, resistant to other treatments for psoriasis; (4) NSAIDs prescribed for artropaticheskom, as well as to
reduce acute inflammation in exudative psoriasis and erythrodermic; (5), systemic corticosteroids: use of these drugs
in the treatment of psoriasis is considered inexpedient since it leads to the development of the disease torpid forms
resistant to different kinds of therapy (in severe cases of psoriasis may arthropathic intraarticular injection of depot
corticosteroids); (6) physical therapy treatments (PUVA therapy, photochemotherapy (FHT), selective phototherapy
(SFT)); (7) spa treatment (advantageously carried out in a few years is the progression of psoriasis, patients
traditionally sent to Matsesta Sochi, Pyatigorsk and other resorts). External treatment ... ... widely used drugs
salicylic acid naftalan tar, corticosteroids. Outdoor therapy depends on the clinical stage and form of psoriasis, plaque
localization, the presence of secondary infection. At all stages of psoriasis on limited areas of the skin may be
administered corticosteroid creams and ointments (tselestoderm, flutsinar, ultralayte etc.). For treatment of areas of
delicate skin fluorinated corticosteroids are applied, for example, mometasone furoate 0.1% (Elokim Advantan). High
efficacy and good tolerability different combination of drugs, for example, Diprosalik (beta metazona dipropionate
0.05% and salicylic acid 3% (ointment), 2% (lotion)). Apply ointment affecting pathogenetic mechanisms of psoriasis -
Psorkutan (it is composed of calcipotriol - a synthetic analogue of the most active metabolite of vitamin D3, which
interacts with receptors of keratinocytes inhibits their excessive division normalizes the process of cell
differentiation). For the prevention and treatment of psoriasis of the scalp is recommended to use shampoos series
Friderm.Alternative Treatments ... ... to these methods are those that rely primarily on non-drug approaches. Among
them: the method of microwave resonance therapy ozoterapiya method effects ultralow temperatures, the method of
transcranial electrostimulation, hypnosis. These methods are used in conjunction with conventional
treatments. Prevention of psoriasis ... ... is the prevention and timely elimination of disorders of the various organs
and systems of the body, contributing to the emergence of psoriasis. At the same importance is the normalization of
mental status, adherence to labor, leisure, food. To prevent a recurrence general treatment of psoriasis patients
should continue for some time after the disappearance of the rash. Suitable clinical examination of patients with
psoriasis. For psoriasis patients and first-degree relatives who have an increased risk of psoriasis, it is desirable long-
term follow, during which address issues of laboratory examination, consultation doctors of different specialties,
employment,9 development of rehabilitation, vocational guidance.
12. Contact dermatitis. Etiology, pathogenesis, diagnosis of atopic dermatitis.
Principles of treatment.

Definition. Dermatitis (dermatitis) - a disease characterized by inflammation of the skin that have arisen as a result of a direct impact on her agents
ambient physical or chemical nature. In English literature, the term dermatitis is not a nosological form, and describes inflammation in the dermis of any
etiology. Therefore, usually accompanied by definition the term dermatitis (contact, seborrheic atopic etc.).

Etiology and pathogenesis. Among physical factors isolated mechanical stimuli (friction, pressure), ultraviolet rays, high and low temperatures,
exposure to ionizing radiation. Chemical agents are divided into obligate and facultative. First cause dermatitis in anyone, the second - only in
individuals with hypersensitivity to any allergen. Dermatitis caused by obligate stimuli factors - allergic.

Dermatitis on physical factors, as well as simple dermatitis is a reaction not related to immune mechanisms, developed as a result of the release of
cellular mediators (prostaglandins and interleukins) of ke-ratinotsitov in response to the damaging effects of environmental factors.

Some authors have nonimmunological (IRRI mutant) dermatitis, which are subdivided into acute toxic dermatitis and cumulative dermatitis (chronic
cumulative reaction). Last develops as a result of prolonged exposure (from several months to several years) weak stimuli (soap, shampoo) and is
manifested by erythema, desquamation, lihenifikatsii. Atopic dermatitis is a clinical manifestation of hypersensitivity (cell-mediated) type 4.

Atopic dermatitis (dermatitis allergica)

Etiology and pathogenesis. most frequent following allergens that cause allergic dermatitis: benzocaine, nickel sulfate, potassium dichromate,
neomycin sulfate, ethylene, formaldehyde, epoxy resin, etc. They are part of the skin, cement, local anesthetics, fungicide-tion funds antibiotics and
other drugs used topically, cosmetics, metal jewelry, rubber, hair dye, glue, plastic. On the mechanism of the development of allergic dermatitis refers
to a type IV allergic reactions - delayed-type hypersensitivity. Hapten (antigen with low molecular weight) falling on the skin forms a hapten-protein
complex which is captured by epidermal Langerhans cells and after processing as a complete antigen is presented to T-helper cells, which ends the
release of various mediators.Subsequently, T cells enter the regional lymph nodes and produce specific memory cells and effector T which circulate in
the blood.This process takes up to three weeks. Re-exposure to the antigen occurs proliferation of activated T-lymphocytes, migration and release of
mediators of cytotoxic T cells, which is accompanied by the development of vesicular skin reaction at the site of contact.This phase lasts for 48-72
hours.

The clinical picture. At the point of contact with the allergen develops erythema, against which the vesicles are formed, which are either dry up to
form crusts or opened, exposing the erosion.

Diagnostics. diagnosis of atopic dermatitis in plays an important role determining the allergen. The most widely used for this application
tests. Commonly used standard panel, composed of 20 allergens. Testing is carried out only with the known substances in conventional
concentrations. The most widely used camera Finn. A small amount of allergen is placed in the wells of aluminum reinforced with paper tape. Tape

attached to the upper part of the back for 48 hours, then removed and an assessment results. Classic positive test is characterized by erythema,
edema, vesicles.

Differential diagnosis is carried out with eczema.

Treatment is primarily aimed at the identification and elimination of the allergen. Outwardly shown corticosteroid creams and ointments, if necessary -
total desensitizing therapy.
13. Toksikodermiya. Etiology, pathogenesis, diagnosis, treatment.

toksidermii (toksikodermii, toxicoder-Mia) - skin diseases, developing as a result of exposure to chemicals at her
admitted into the body and circulated hematogenically. This term is quite conventional, as the disease occurs more
frequently allergic and not toxic mechanisms.

Etiology and pathogenesis. toksidermii reasons - drugs, food, industrial and household chemicals that are toxic and
allergenic properties. These substances enter the body primarily through the digestive and respiratory tracts,
moreover, the drugs may cause drug reaction by intravenous, subcutaneous, intramuscular, vaginal, rectal, urethral
administration, for absorption through the skin when applied topically. Most frequent medicinal drug reaction, followed
by frequency - food. Medicinal drug reaction can be caused by any drugs, including antihistamines and corticosteroid-
E, but the most often - antibiotics, sulfonamides, analgesics, barbiturates.Food toksidermii account for about 15% of
all drug reaction. The reasons for their development are or food itself or the substances formed during its prolonged
storage, cooking, and various impurities - preservatives, dyes, etc.

In the pathogenesis toksidermii sometimes plays the role of idiosyncrasy - intolerance of a drug or food.

The clinical picture. toksidermii clinical picture usually nonspecific and may be submitted by any

primary element rash except protuberance and the particular node. However, are the following features characteristic
of most drug reaction: acute onset, symmetry, prevalence, monomorphic, stagnant shade rash, a tendency to merge
elements (especially in the folds), itching, peeling at the resolution elements.

Spotted toksidermii (see col. incl., Fig. 16) appear most often hyperemic spots, at least - and hemorrhagic pigment
(toxic melasma).

Papular drug reaction characterized is disseminated en-ostrovospalitelnyh hemispherical papules (occasionally


follicular or flat) from miliary to flax-tikulyarnyh, in rare cases - plaques. Emit a peculiar form of papular toksidermii -
lichenoid, which, in some cases, it is difficult to distinguish from lichen planus.

Knotty toksidermii ostrovospalitelnyh nodes appear, sometimes in the form of acute erythema nodosum.

Vesicular toksidermii presented large vesicles or microvesicles, bordered rim flushing. In the case of restrictions
defeat the palms and soles they manifest type dyshydrosis.

Pustular drug reaction most often occur in areas rich in sebaceous glands, because they tend to be associated with
the action of halogen released from the body with sebum. Clinically they appear pustules or eel elements.

Bullous drug reaction can be both common and limited (fixed drug reaction). LATEST localized most frequently in
the genital and oral mucosa and is characterized by the formation of bluish-reddish spots, sometimes - edematous
plaques, which develop on the background of bubbles. According to the resolution process is stored persistent
pigmentation. The disease recurs at the same location after each dosing. Bullez-tion drug reaction can occur in the
form ekssu-dative multiforme erythema, including heavy variety - syndrome of Stevens - Johnson.

There are also rare forms of drug reaction: allergic vasculitis, medical lyupoidny syndrome similar to systemic lupus
erythematosus, palmoplantar ceramics todermiya, tuberous bromoili yododerma.
Diagnostics. toksidermii In diagnostics plays an important role carefully collected history about the possible causes
of the disease, these diagnostic tests in vitro, ho- cha and false positives are not uncommon lozhnootritsa-tional
results.

Differential diagnosis. roseolous toksider-Mia should be differentiated from roseolous sifilid, pink lichen, plaque
psoriasis. Papular toksider Prize differentiate with lenticular psoriasis lentiku polar sifilid, lichen planus.

Vesicular drug reaction is diagnosed by exclusion pioallergidov, mikidov, eczema, atopic dermatitis.

Pustular drug reaction is differentiated from acne vulgaris on the basis of the patient's age, the acute onset of the
disease and there are no signs of seborrhea.

Toksikodermiya similar exudative erythema multiforme, differentiate from infectious erythema multiforme. Toksidermii
differentiate with a number of infectious diseases characterized, unlike toxin dermis, severe general condition:
measles, rubella, scarlet fever, chicken pox.

Treatment toksidermii conducted in the following areas:

1) the termination of access to the body of the etiological factor (cancel medicines exception with professional and
household chemicals);

2) elimination of the etiological factor of the body (excessive drinking, the appointment of diuretics enterosor Bento
laxatives);

3) desensitization and detoxification (parenteral administration of drugs, calcium, sodium thiosulfate, antihistamines,
ascorbic acid, at elevated temperatures - corticosteroids, gemodez, reopoligljukin, hemosorption). Topically applied
anti-inflammatory agents in the form of solutions, creams.

14. Eczema. Classification, etiology, pathogenesis, clinical features, principles


of treatment.
Eczema (eczema) - polietiologicheskoe relapsing chronic inflammatory skin disease, which manifests itself
evolutionary polymorphism rashes pathognomonic sign which - serous wells.

The term "eczema" is derived from the Greek word ekzeo - flush, boil. Prior to the beginning of the XIX century. he
used to refer to erythema, erysipelas, acute urticaria and other emerging diseases of the skin.

As an independent disease eczema has been allocated Uillanom (Villan) in 1808 and Batemanom (Bateman) in 1813
they relate it to vesicular dermatoses. In 1819 Bitt (Biett) during eczema identified acute and chronic variants. In 1854
Deverzhi described pathognomonic sign of eczema - serous (eczema) wells.

Eczema is the most common dermatoses, occurs predominantly in persons aged 20 to 50 years. Women are affected
more often than men.

Etiology and pathogenesis

The mechanism of disease is changing reactivity entailing increased skin sensitivity to exogenous and endogenous
stimuli in two ways: neurogenic and allergic.

Endogenous stimuli: a neuropsychiatric injury foci of chronic infection, immunodeficiency disorders, gastrointestinal
disease, intoxication, genetic factors, etc.
Exogenous stimuli: all kinds of physical, chemical, and other allergens.

Onset of the disease, its exacerbation and relapse are also associated with emotional stress and the positive effects
of hypnotherapy. By type vistserokutannogo reflex realized eczematous process induced organ failure (usually the
abdomen). Damage to the peripheral nervous system can also lead to the development of eczematous lesions. An
example is the post-traumatic eczema.

Allergic component plays a predominant role in the pathogenesis of microbial and especially contact eczema. In favor
of this view convincingly demonstrate positive results of skin tests.

In recent years investigating the role of the immune system in the pathogenesis of eczema. Spotted its relative
deficiency in patients with eczema due to inhibition of function of T lymphocytes and increasing the number of B-
lymphocytes, immunoglobulins synthesizing, which leads to a violation of the class of proteins in the blood.

However, not all individuals suffering from disorders of the central or peripheral nervous system, burdened
vistseropatiyami having foci of chronic infection or exposed to chemical irritants, there eczematous lesion.

For the development of eczema need more genetic predisposition. Formed eczema responsible exacerbations in the
active period and in remission relapsed multiple and diverse effects of exogenous and endogenous factors.

Classification

Standard classification of eczema does not exist. In Russia isolated following forms of eczema:

True (idiopathic) eczema.

Microbial eczema.

Baby Eczema.

Seborrheic eczema.

Occupational eczema.

However, children's eczema, different age evolution serous lack of wells, and intense itching, currently referred to as
atopic dermatitis.

Seborrheic eczema, seborrheic flowing on background, not having serous wells, caused by the fungus Pityrosporum
ovale, usually referred to seborrheic dermatitis.

Thus, these two terms (children and seborrheic dermatitis) is necessary to exclude from classification.

Occupational eczema occurs as a result of contact with irritants in terms of production, but contact with chemicals
and other irritants possible and at home (washing powder, a variety of paints, cosmetics, etc.). In this regard, the term
"professional eczema" expedient is replaced by "contact eczema."

Such a classification was developed in 1964 ST Pavlov.

True (idiopathic) eczema.

Contact eczema.

Microbial eczema.
According to NS Potekaeva, this classification should be added and posttraumatic eczema, which was considered
one of the varieties of microbial eczema.

However, unlike microbial eczema, where staphylococci and streptococci are not acting etiological factors and
sensitizing, posttraumatic eczema caused by trauma or injury is directly related to pyogenic agent. Develops a few
weeks after injury. Clinical manifestations and course corresponds to the true eczema.

Adrift distinguish acute, subacute and chronic eczema, respectively occurring within 2-6 months or indefinitely.

The clinical picture

True (idiopathic) eczema

True (idiopathic) eczema - the most common form. Its main feature is that it occurs without apparent clinically defined
pathogenetic component. The only known precipitating factors.

Acute eczema develops as follows.

Initially appear pink-red spots. Rapidly increasing in number and size, merging with each other, they form
erythematous rash, and then diffuse erythema. Due to a small swelling erythema will stand slightly above the environ-

tal skin. This stage of acute eczema was named erythematous.

Soon the background of erythema there are numerous small exudative papules they are swollen, juicy, have a pink-
red color and consistency testovatoy - papular stage.

With an increase in inflammation increases swelling, papules transformed into vesicles with serous contents sterile
- vesicularstage. Vesicles, revealing, exposing the bright red erosion, continuously separating transparent serous
exudates. Such erosion are called serous (eczematous) wells (Fig. 12-18).

Serous wells merge to form a solid red lesions, but serous wells on this background are distinct. Foci located on the
basis of edematous and deprived of the stratum corneum, intensely separated serous exudate that flows from their
surface, and impregnates bandage lingerie - weeping stage.

weeping stage - the culmination of acute eczema. After this stage, the inflammation begins to fade, and the disease
goes into the next, krustoznuyu stage, characterized by the cessation of new vesicles.

The contents of surviving in small bubbles shrinking cake. Under crusts gradually restored stratum corneum,
painting foci becomes bluish-pink, crusts fall off. Develops limited peeling scaly scales - squamous

step. Gradually, the skin gets discolored, peeling stops, indicating that the complete regression of acute eczema. In
subsequent relapses occur. It should be remembered that acute eczema runs jerky: it does not replace the stage in
series with each other, and laminated to each other. In this regard, the erythematous-edematous background
eczematous lesions at the same time there are papules, vesicles, serous wells, peel and flake. The combination of
these lesions creates a picture of the evolution of polymorphism.

Development of acute eczema can be abortifacient - not necessarily goes through all stages. Vesicular stage,
bypassing moknutie can move in step krustoznuyu or squamous, and erythematous or papular stage may end
peeling and complete resolution of the disease.

For acute eczema is characterized by fuzzy boundaries foci. Acute eczema can be transformed through 1.5-2 months
in subacute eczema, the main morphological element which is infiltration, formed as a result of decay of exudative
phenomena and accumulation of cellular infiltrate. In this case, the foci of subacute eczema take distinct paths,
swelling and moknutie become small or clinically not defined, the color loses its brightness, becoming pinkish-bluish.

Papules and vesicles few, saved crusts and scales can be detected conspicuous skin patterns. After about 6 months
subacute eczema becomes chronic.

For lesions of chronic eczema characterized by clear boundaries, B

nyushnaya paint a rosy tint, no puffiness and soak, small groups of papules and vesicles, excoriations (the result of
scratching), scales and crusts, including hemorrhagic, exaggerated picture of the skin and dense consistency on
palpation (Fig. 12-19).

However, chronic eczema may occur without prior acute and subacute stages. For non-chronic eczema

definitely long. As subacute eczema, and chronic, acute type are regular episodes of acute eczema. Along with the
aggravation of subacute and chronic eczema possible new eczematous lesions as near old homes, and at a distance
from them.

Possible involvement in the eczematous process all or nearly all of the skin, respectively, with the development of a
total or partial erythroderma. localization of foci of true eczema is extremely diverse, they can occur anywhere on the
skin. However, most often affects the face, hands, forearms and shins are usually symmetrical.

Typically true for eczema infection complication pyococcus to form impetiginoznyh crusts, sometimes quite massive.

Disgidroticheskaya eczema

Kind of true eczema - disgidroticheskaya eczema that affects only the palms and soles. Its clinical features are
caused by the epidermis (especially the stratum corneum) of the palms and soles, having over other large skin
portions, the greatest thickness (Fig. 12-20).

For dyshidrotic eczema is characterized by vesicles with a diameter of 4-5 mm with a tense, tight palpation tire and
transparent serous contents. They are grouped in small pockets located on slightly erythematous background, but
sometimes merge into a multi-chamber cavity.

Vesicles with an increase in inflammation opened with the formation of erosions and dry up when fading into flat
yellowish crust.These rashes are complemented scarce small scales. Outbreaks dyshidrotic eczema clearly
distinguished and often surrounded by a collar peeling of the epidermis.

Itching - a permanent feature of eczema. The exception is weeping eczema, in which due to the rejection of the
stratum, and sometimes granular layer, itching disappears, replaced by soreness. Small or moderate itching. It does
not reach great strength, as in atopic dermatitis. Often, it is joined by burning.

Microbial eczema

Microbial eczema develops as a result of sensitization to microorganisms, and have got long-existing, such as after
an injury and the occurrence of skin lesions pyococcus. Contribute additional sensitization and endogenous foci of
chronic infection (sinusitis, tonsillitis, etc.). Children often appears between the ages 5 and older.

Outbreaks of microbial eczema clearly distinguished, have rounded or krupnofestonchatye shape, fringed collar
peeling of the epidermis, often with a peripheral rim of pink. Outbreaks fully or partially covered by crusts yellowish,
greenish-yellow and brown.
Free areas crusts, as well as surface lesions after removing crusts begin to soak acquire bluish-pink color, covered
with eczematous wells separating drops of serous fluid. Near the hearths, and sometimes on the surface, be
individual and small phlyctenas folliculitis.

In the long exudative manifestations undergo regression: microbial eczema becomes dry type. Dry stagnant brilliant
bluish-surface pockets of easily removable cover large scales, there are single vesicles and eczematous wells (Fig.
12-21, 12-22).

The most frequent localization of microbial eczema - shin, foot, especially the interdigital folds, forearm, hand, the
area around the nipple of the breast and under the breasts in women, with the auricles. Asymmetry characteristic
rash.

A peculiar kind of microbial eczema - nummulyarnye (nummular) eczema, developing, apparently under the
influence of

chronic foci of infection: chronic tonsillitis, granulomas teeth, chronic appendicitis, etc. For its foci characterized by
sharp boundaries, right round the outline with a diameter of 1.5 to 3 cm drip moknutie (Fig. 12-23).

Fig. 12-23. nummulyarnye eczema

Outbreaks will stand slightly above the surrounding skin. During the chronic moknutie fades in color is dominated by
bluish tone, develops limited peeling scaly scales, the center may take the form of healthy skin. Localization diverse,
can be disseminated.Nummulyarnye eczema exceptionally resistant in relation to therapy and particularly prone to
relapse.

In domestic dermatology assumed options microbial eczema and varicose eczema posttraumatic.

The defeat at varicose eczema can capture not only the epidermis and dermis, but hypodermis. In this case, joining
local and general hyperthermia, lymphangitis and lymphadenitis. Serous wells do not show (Fig. 12-24).

Contact eczema

Contact eczema is a sequential stage of atopic dermatitis, which is formed by prolonged exposure to the sensitizing
agent. As atopic dermatitis, eczema is related to work or at home with a contact with the skin sensitizer and the basis
of its pathogenesis is monovalent sensitization.

Contact eczema affects mainly the back of hands, forearms, face, neck, external genitalia, usually in the form of
limited foci. The clinical picture is consistent with true eczema. However, there are differences: less pronounced
polymorphism, rapid regression in addressing the appropriate stimulus and the absence of independent
exacerbations and relapses (Fig. 12-25).

Diagnostics

Eczema diagnosis is relatively straightforward. Its form (true, microbial and posttraumatic) recognize on the basis of
the characteristics of their clinical picture. Identifying eczematous wells - a pathognomonic sign of eczema, a
convincing diagnostic evidence.

If necessary, a survey to identify laboratory abnormalities and comorbidities.

Accurate diagnosis of contact eczema are adjusted based on positive skin tests. They identify monovalent

character sensitization. In the long monovalent sensitization can be transformed into a polyvalent, that means turning
to the true contact eczema.
Differential diagnosis

Eczema differentiate from atopic dermatitis, allergic contact dermatitis, toksikodermii, neurodermatitis.

Treatment

In the treatment of patients with eczema crucial role played by the combination of pathogenetic and external therapy,
conducted with all its clinical forms.

Pathogenetic drugs eczema patients prescribed antihistamines (Chloropyramine, mebgidrolin, cetirizine,


levocetirizine, etc.) as a means of having antiallergic and antipruritic effect.

Use as intravenous sodium thiosulfate, calcium chloride, magnesium sulfate.

Precautions need to be treated to the appointment of vitamins, especially vitamin B 12 (cyanocobalamin), which
includes cobalt, having the properties of the sensitizer.

In acute eczema during shows only vitamin C (ascorbic acid), from the use of other vitamins is advisable to
abstain. During the chronic vitamin C in addition to the testimony can be received and other vitamins.

Also required correction of violations and related diseases, especially the central nervous system and gastrointestinal
tract.Correction is carried out in coordination with the appropriate professionals. Particular attention should be paid to
the regulation of the chair and cleanse the intestines.

Promote regression of the manifestations of eczema hydrolytic lignin, colloidal silicon dioxide and other endosorbenty
and enterosan *having not only absorbent, but also detoxification and complex effects on the gastrointestinal tract and
its microflora.

In embodiments, common and persistent systemic glucocorticoids resorted to, often prednisolone tablets in initial
dosages between 20 and 60 mg. To achieve the therapeutic effect of the daily dose is gradually reduced until the total
abolition. With the suc-

hamsters can be assigned betamethasone 1-2 ml per 1 injection 2-3 injections with an interval therebetween in one
week.

The mainstay of treatment is the removal of contact eczema sensitizing stimulus that leads to the gradual extinction
of its manifestations. Microbial eczema need therapy foci of chronic infection. When antibiotics are shown
posttraumatic eczema.

Strictly necessary balanced diet, especially when true eczema. From the diet is necessary to avoid those foods which
are associated with the beginning of eczematous process, its exacerbation and relapse. If necessary, designate a
hypoallergenic diet.

Plays an important role in view of external therapy stage of the inflammatory process.

Water is necessary to limit the procedure to prevent provocative effect of water on eczematous lesions, and for
common variants and total eczema should be eliminated completely.

With abundant soak that is usually found in true eczema (acute or exacerbation of subacute and chronic), prescribe
lotions or dressings vlazhnovysyhayuschie of antiseptic solutions, while the slim but stubborn soak - from astringent
solutions.
The former include boric acid solution (Sol. al. borici, 1-2-3%), resorcinol (1-2%), potassium permanganate
(1:5000). The latter solution also has deodorant properties. Group binding solution is leaden water * (Aq.
plumbi), liquid Burov * (Liq. Burowi).

In chronic eczema is exacerbations treatment begins with ointments. By the combination of high efficacy and good
tolerability should give preference to creams and ointments with betamethasone and especially cream and ointment
mometasone. Mometasone (0.1% lotion, cream, ointment) has a potent combination of advantages outdoor
glucocorticoid with the virtual absence of local and systemic side effects. Convenient dosing - 1 time per day provides
better adherence to treatment and the presence of three dosage forms (cream, ointment and lotion) allows the use of
the drug, taking into account the stage of the inflammatory process.

To avoid side effects include the duration of application of creams and ointments can not exceed 1,5-2 months.

After 2-3 weeks of use in the prevention of infection go to recommend creams and ointments, which in addition
includes glucocorticoid hormones and antimicrobials. Most effective cream and ointment betamethasone +
gentamicin + clotrimazole containing glucocorticoid, antibacterial and antimycotic agent.

Cream and ointment betamethasone + gentamicin + clotrimazole also shown microbial eczema. Pockets of chronic
eczema covered with dry crusts and abundant scales, pockets of dyshidrotic eczema prescribe creams and
ointments containing both glucocorticoid hormones, and salicylic acid.

Salicylic acid helps apostasy crusts and scales and deeper penetration into the tissue lesions of glucocorticoid
hormones. Highly effective drugs betamethasone + salicylic acid and salicylic acid + mometasone. With massive
infiltration ointment therapy complement warm baths, paraffin and mineral wax applications and other physiotherapy
treatments.

Complex pathogenetic individual therapy and clinical supervision of the patient help increase interrecurrent period.

Features of the eczema in children

The development of eczema is not typical for young children. In infancy only possible development of atopic
dermatitis and seborrheic dermatitis.

The most frequently develops microbial eczema (mycotic, postskabioznaya).

The younger the child, the more important in the exacerbation of the disease play exogenous irritants (food,
physical, etc.), and in adolescent and adult patients, on the contrary, - endogenous factors.

In children, eczema often occurs in acute and subacute forms, clinically vesicular-papular rash, weeping, serous
crusts, rarely lihenifikatsii centers.

Treatment is carried out on the basis of atopic dermatitis, but taking into account the clinical varieties of eczema
and their pathogenesis.

Counseling

Should pay attention to the patient's chronic relapsing nature of the flow of eczema. Necessary to identify the factors
contributing to the occurrence and recurrence of eczema.
15. Neyrodermatozy. The notion of atopy. Etiology, classification
neyrodermatozov
Neurodermatitis

Neurodermatitis (Neurodermitis) - chronic itching dermatosis, characterized by the appearance of papules and
development lihenifikatsii. Occurs more frequently in older children and adults.

Etiology and pathogenesis

The disease is associated with functional changes in the central nervous system and organic changes of nerve fibers
and the receptor apparatus of the skin.

Also play a role endocrine disorders and gastrointestinal pathology.

The clinical picture

Appears painful itching, and under the influence of constant scratching there are small, flat, diamond-shaped, shiny
papules. In the beginning they normal skin color in the future - rozovatokorichnevatye. Lihenifitsirovannye formed
plaques. Their boundaries are blurred, on the surface of visible flakes, excoriating, bloody crusts. There are three
forms of neurodermatitis: limited, disseminated and diffuse.

Limited neurodermatitis

Outbreaks size 10x5 cm or slightly more localized on the back or side of the neck, leg, ankle joint, hip folds in
mezhyagodichnoy crease in the perineum, scrotum or labia majora (Fig. 12-26, 12-27) . There are three zones in the
center - lihenifikatsiya around her - small lichenoid papules on the periphery - hyperpigmentation.

Disseminated neurodermatitis

Disseminated neurodermatitis characterized by multiple foci described neurodermatitis.

Fig. 12-27. Neurodermite limited legs and feet

Atopic dermatitis

For atopica characteristic diffuse lesions in the form of individual and lihenifikatsii papular flat elements. Skin - earthy.

Diagnostics

In the diagnosis of clinical matters. Necessary to exclude a history of atopic dermatitis and eczema.

Differential diagnosis

Differentiate disease from eczema, atopic dermatitis, pruritus adults.

Treatment

With limited form displays local therapy in the form of ointments glucocorticoid (betamethasone, betamethasone +
salicylic acid, clobetasol, fluticasone), ointment naphthalane oil, cream-gel Aysida * Cream * Foretal etc.
In the diffuse form prescribed hyposensitization therapy, short course of corticosteroids by mouth (prednisone 20 - 40
mg), antihistamines. Showing spa treatment, especially hydrogen sulfide baths, physiotherapy (electric, selective
phototherapy, etc.).External treatment is prescribed, as in other forms.

16. Hives: etiopathogenesis, diagnosis and treatment.


Urticaria and angioedema, urticaria , at least one case of hives in their lifetime mark of 10-20% of the
population. Urticaria is characterized by sudden rash, mainly on the closed parts of the body, blisters, causing
severe itching. They have a variety of shapes and sizes, often fused together, forming a bizarre, girlyandovidnye
figures. After a few tens of minutes or hours blisters disappear, but the rash of new elements continues. Attacks rash
may result in a few hours or days (acute urticaria), but can last for many weeks, months and even years (chronic
urticaria). Sometimes blisters barely raised above the skin (spotted urticaria), in other cases, and accompanied by
bleeding, allowing leave temporary pigmentation (gemorrargicheskaya urticaria). As an exception occurs bullous
urticaria: blisters formed in the center of the bubble, and the clinical picture is very similar to erythema multiforme
exudative. Urticaria may occur or in the form of acute episodes lasting a few hours or days, or have chronic when
attacks occur every day and sometimes several times a night for many weeks, months and even years.
Ehtiopatogenez. Urticaria is an allergic skin reaction of immediate type caused by a variety of exogenous and
endogenous factors. Blisters hives - not a manifestation of the inflammatory response, but a peculiar swelling of the
skin, due to the resulting increase sharply emerging vascular wall permeability when exposed to certain chemically
active substances. Of the latter, the most important are histamines and some products of protein metabolism,
providing histamine action. These substances can be made to the external skin (insect bites, sting), it formed a direct
action on the skin of external factors of mechanical, physical or chemical nature or be produced in the body due to its
various pathological states.urticaria Very often occurs as a result of outbreaks of acute hypersensitivity to different,
often food (eggs, cheeses sharp, strawberries, cancers, certain grades of fish, meat and the like) or drug ( quinine,
morphine, inkikun, therapeutic serum, penicillin, etc.) substances. urticaria often develops as a result of increased
sensitivity to cold, at least - to heat, sunlight. In some cases, you may experience the conditioned reflex
urticaria. represents a special form of the so-called angioedema (limited acute angioedema).The disease is
expressed by the sudden appearance of limited swelling of the skin and subcutaneous tissue, most often on the face
(lips, cheeks, eyelids) or in the genital area. Dramatically affected area above the level of the surrounding skin, has
plotnoelasticheskuyu consistency and porcelain-white, at least - slightly pink, color. The appearance of edema
accompanied by a burning sensation, at least - itching. held for several hours, sometimes 1-2 days, the swelling
disappears. In some patients, seizures recur at regular intervals. Sometimes limited angioedema combined with
conventional hives. As a special kind of urticaria usually considered artificial hives - blistering often linear forms in
response to mechanical stimulation of the skin, such as holding a blunt stick. Unlike artificial sublime dermographism
urticaria hives true accompanies itching. treatment. At an acute attack of urticaria caused by ingestion of food or
drugs, it is necessary, first of all, clean the intestines, take a laxative (magnesium sulfate). Thereafter prescribe
antihistamines are administered intravenously 10% solution of calcium chloride, in severe cases - hormones. At the
same time the larynx 0.5-1.0 ml epinephrine 1:1000. Children urticaria (strofulyus) prurigo baby is close to the hive
disease. observed in children aged from 5-6 months to 2-3 years. Characterized by a rash on the skin of the trunk
and limbs of small blisters in the center of which is formed papulovezikula size of a pin head. Rarely occurs in the
center of the blister bubble greater magnitude similar to bubble chickenpox. The rash is accompanied by severe
itching. As a result of scratching on the spot papulovezikul formed bloody crusts frequently observed complication of
pyogenic infection, usually in the form of vulgar impetigo. The disease is chronic, with minor remissions and upon
reaching the age of three are usually independently passes. most common cause of childhood urticaria is wrong,
sometimes excessive, child nutrition. Often detected hypersensitivity (allergy) to any certain foods (eggs, milk, meat,
sweets).treatment. necessary to establish a right to the child's diet, eliminating those foods which are suspected as
possible allergens. Along with this prescribed oral medications for the content of calcium. External treatment is the
appointment antipruritic agents in the form of mash, weak alcoholic solutions. Useful warm baths with potassium
permanganate. Chronic forms of urticaria are often associated with impaired liver, kidney, gastrointestinal,
metabolic changes, worm infestation, hidden pockets of infection (tonsillitis, etc.). Such forms may occur as a
manifestation of toxicity in pregnant women, as a consequence of malignant tumors of internal organs, blood
diseases. Chronic urticaria is necessary to carefully examine the patient to determine the cause of the disease and
appropriate treatment. In case of an allergen (pollen, food, etc.) shows specific desensitization. Necessary treatment
of detected foci of chronic infection, inflammation of the gastrointestinal tract; beneficial therapeutic effect is
subaqueous bath. When held degelminizatsiya helminthic infestation. For the normalization of the central nervous
system are shown sedatives may be recommended hypnotherapy autohaemotherapy. Whether chronic urticaria
mainly allergic disease? No. Studies have shown that patients with chronic urticaria allergy, even a family tendency to
it, marked with the same frequency as that of the general population. On the other hand, patients with atopic
diseases (eczema, hay fever, asthma) acute urticaria lasting 1-3 days is more common than among healthy
individuals. In this group, it has an allergic nature and in many cases is associated with food. What is the cause of
most chronic hives? Causes of chronic hives, despite extensive study, as a rule, remain outstanding. Except physical
and chronic autoimmune, 95% of cases are considered as idiopathic urticaria. Is there a relationship between chronic
urticaria and the presence of autoantibodies? In 13-14% of patients with idiopathic chronic urticaria identified
antithyroid microsomal antibodies (2 times more often than in the control group).Some people with chronic urticaria
respond to intradermal serum own blistering and redness persists for 8 hours Many of these patients were
determined by IgG antibodies in the serum reacting with a-subunit vysokoaffinitetnogo IgE-receptor kletkok mast and
basophils. Other patients IgG-antibody apparently reacts with itself IgG. Detection rate of IgG-antibodies in patients
with chronic urticaria yet to be finalized, but, according to some clinics, these antibodies are detected in one third of
patients. Forecast.Champion RH, observing 554 patients with urticaria, contact the clinical department of a hospital
in England , reported that at 6 months in 50% of patients still noted the active stage of the disease. Of these, there
were 40%, at least periodically, the symptoms of urticaria and 10 years later. The forecast was slightly worse in
patients with angioedema as the sole manifestation and even worse - when combined with urticaria
angioedema. characteristic histological finding in chronic (in the absence of vasculitis), urticaria is a perivascular
infiltrate. Revealed an increase in the number of lymphocytes. The number of mast cells increased about 10 times,
been an increase in histamine content. Although eosinophils usually small, intense deposition of alkali main protein of
eosinophils observed in the tissues of 50% of patients, thus indicating the involvement of eosinophils in the
inflammatory process. Patients with urticarial vasculitis usually detected necrotizing vasculitis of small venules with
the accumulation of immunoglobulin and complement. In patients with low serum complement (gipokomplementarny
urticarial vasculitis), polymorphonuclear leukocytes predominate, whereas in patients with normal levels of serum
complement in the presence of a typical lymphocytic infiltration. Is the prevalence of physical urticaria? Champion
AD reported that of 554 patients with urticaria observed at the University Hospital in England, physical urticaria was
observed in 17.5%; most other forms - idiopathic. Physical urticaria often represented dermographism (8.5%),
cholinergic (5.1%) and acquired cold urticaria (2.5%). Some hives caused by physical factors, may be passively
transferred with serum the blood of patients. There are reports of IgE-mediated transfer of acquired cold urticaria,
some types of solar urticaria and dermographism. The disappearance of this effect by inactivating the heat and allow
the application of adsorbents to determine experimentally the role of IgE as an intermediary in the transfer. patients
with acquired cold urticaria stay in cold water can cause a massive release of mediators. In this case the patient is
not excluded development of shock, in which he can drown. How soon after exposure to cold blisters occur in
acquired cold urticaria? Blisters do not develop in the moment of action cold and appear more as it warms. The delay
is likely due to a decrease in blood supply to the skin during cold exposure. Only when one form of urticaria are
blisters which presence is enough to make an accurate diagnosis - with cholinergic urticaria, they are completely
different from those in other forms of urticaria are usually small, spot ( often compared in size with a pencil eraser),
characterized by severe redness, but sometimes merge to form larger elements. Develops cholinergic urticaria
usually on the upper chest and neck. Defeat can capture and limbs.Which factors contribute to cholinergic
urticaria? By what mechanism they cause blisters? Exercise, warm baths, showers and emotional experiences are a
classic trigger cholinergic urticaria. Increased body temperature, which is perceived centrally, resulting in the release
of cholinergic efferent skin and mast cell degranulation. Solar urticaria are classified by the wavelength of light,
causing them (see Table. 41.) Table 41. Classification of solar urticaria. How often aspirin causes or enhances
hives? Aspirin rarely causes hives in a patient not having any other symptoms, but many patients with chronic
urticaria rash blisters increases with aspirin or non-steroidal anti-inflammatory agent in the active phase of the
disease. Typically, patients are those aspirin without risk if the disease is in an inactive phase. This suggests that
aspirin is not causal, and non-specific enhancer factor acting probably at a pharmacological level. According to the
retrospective and prospective studies of aspirin causes an exacerbation in 20-40% of patients with urticaria in the
acute stage. Angioedema Certain information from the medical history of the patient may indicate that recurrent
angioedema is hereditary. From 75 to 85% of patients with hereditary angioedema (NANO) indicate the presence of
seizures with relatives.Angioedema attacks characterized by the absence of blisters and itching associated idiopathic
angioedema. When NANO angioedema attacks often triggered by trauma or surgery. Severe upper airway stricture is
observed almost exclusively in nano and not typical for conventional idiopathic angioedema. Frequent in nano -
attacks of acute abdominal pain caused by swelling of the intestinal wall. In addition, the severity of the attack NANO
usually increases within a few days, and they are poorly cropped antihistamines or epinephrine. Why C1-esterase
deficiency is not considered in the differential diagnosis of chronic urticaria? At the heart of NANO is a hereditary
deficiency of C1 esterase inhibitor. Patients have recurrent attacks of angioedema without itching, but in the absence
of urticaria. Thus, NANO never a part of the differential diagnosis of urticaria. Having determined NANO screening
laboratory test for serum C4. C2 content between attacks within the norm. In 15-20% of patients with C1 esterase
inhibitor may be in the normal range, but not function, and the standard immunological research did not identify these
patients. Required functional study is not always available, and, moreover, it is more expensive than the definition of
the level of C4. Which treatment method to give preference in NANO? NANO is inherited in an autosomal dominant
manner. Androgens weak masculinizing effects such as danazol or stanozolol stimulates the synthesis of a normal
C1-esterase inhibitor in the liver such patients. Patients with a dysfunctional C1 esterase inhibitor also treatable,
because they have one normal gene. effective preventive measures to prevent the attack NANO, which can be
triggered by surgery, is the appointment of epsilon-aminocaproic acid (15 g per day for 2-3 day) prior to surgery or
administration [2-3 units 450 mL X 2 (3)] of fresh frozen plasma for recovery from C1-esterase inhibitor. patient 60
years there are new episodes angioneurotic edema and itching observed without lowering C4. What disease should
assume in the first place? Acquired C1 inhibitor deficiency esterase. This condition is usually observed in patients
with lymphomas, in which the blood circulating IgM with a low molecular weight as well as reduced levels of C1
esterase inhibitor and small levels of C1-C4. The mechanism of activation is carried out by reacting a C1 to immune
complex binding, or with C1-idiotype antibody attached to an immunoglobulin on the cell surface of the
tumor. Acquired deficiency of C1-esterase was also seen with connective tissue diseases (systemic lupus
erythematosus), and the presence of carcinoma of the IgG-antibodies against C1 esterase inhibitor. In the latter case,
levels of C1 - within limits. androgen treatment can be successful in patients with acquired deficiency of C1 esterase
inhibitor due to an increase of its production by the liver

17. Atopic dermatitis: etiology, pathogenesis, diagnosis, treatment principles. Age


dynamics, diagnostic criteria.

Atopic dermatitis (dermatitis allergica)

Etiology and pathogenesis. most frequent following allergens that cause allergic dermatitis: benzocaine, nickel sulfate, potassium dichromate,
neomycin sulfate, ethylene, formaldehyde, epoxy resin, etc. They are part of the skin, cement, local anesthetics, fungicide-tion funds antibiotics and
other drugs used topically, cosmetics, metal jewelry, rubber, hair dye, glue, plastic. On the mechanism of the development of allergic dermatitis refers
to a type IV allergic reactions - delayed-type hypersensitivity. Hapten (antigen with low molecular weight) falling on the skin forms a hapten-protein
complex which is captured by epidermal Langerhans cells and after processing as a complete antigen is presented to T-helper cells, which ends the
release of various mediators.Subsequently, T cells enter the regional lymph nodes and produce specific memory cells and effector T which circulate in
the blood.This process takes up to three weeks. Re-exposure to the antigen occurs proliferation of activated T-lymphocytes, migration and release of
mediators of cytotoxic T cells, which is accompanied by the development of vesicular skin reaction at the site of contact.This phase lasts for 48-72
hours.

The clinical picture. At the point of contact with the allergen develops erythema, against which the vesicles are formed, which are either dry up to
form crusts or opened, exposing the erosion.

Diagnostics. diagnosis of atopic dermatitis in plays an important role determining the allergen. The most widely used for this application
tests. Commonly used standard panel, composed of 20 allergens. Testing is carried out only with the known substances in conventional
concentrations. The most widely used camera Finn. A small amount of allergen is placed in the wells of aluminum reinforced with paper tape. Tape

attached to the upper part of the back for 48 hours, then removed and an assessment results. Classic positive test is characterized by erythema,
edema, vesicles.

Differential diagnosis is carried out with eczema.

Treatment is primarily aimed at the identification and elimination of the allergen. Outwardly shown corticosteroid creams and ointments, if necessary -
total desensitizing therapy.

18. Acantholytic pemphigus. Etiological, pathogenetic features. Criteria for


the diagnosis, treatment principles.
What is true Pemphigus (acantholytic)
True or acantholytic, pemphigus - bullous dermatosis characterized by the formation of
intraepithelial blisters on intact skin, or (and) the mucous membranes as a result of acantholysis.

The disease has a long chronic course with remissions of varying severity and varying duration.

Distinguish four clinical forms of pemphigus acantholytic:

vulgar,

vegetating,

leaf-,

seborrhea (erythematous).

What triggers Pemphigus true (acantholytic)


The etiology is unknown. There are viral and autoimmune theory of the disease. Currently proven
leading role in the pathogenesis of autoimmune processes true (acantholytic) pemphigus.

Pemphigus vulgaris (pemphigus vulgaris), or vulgar , is more common in other forms. Basically
ill men and women from 40 to 60 years, in childhood and adolescence - very rare.

Symptoms of true pemphigus (acantholytic)


Most often, oral mucosa affected in common (vulgar) pemphigus (75% of patients), so it is of the
greatest interest to dentists. Pemphigus vulgaris almost always starts with the mucosa of the mouth
or throat, and then spreads to the skin. Even if the disease begins with skin lesions, later almost
always reveal the defeat of the oral mucosa.

Mucosal lesion in the mouth and lips pemphigus characterized by the formation of single bubbles with
serous or hemorrhagic content with a very thin tire. Due to constant maceration bubbles in the mouth
very quickly opened, so to see them can be extremely rare. On the periphery of erosion often find
scraps of tire blistering. Bubbles are formed on the site of painful erosions round, oval or elongated in
the form of a crack forms, long-term healing.Erosion bright red color are arranged on a background of
unmodified or slightly inflamed mucosa. Their sizes vary with pemphigus - from small to large surface
abrasions zastoynokrasnogo color. Plaque on the surface erosions usually does not happen or it may
be a thin layer can be easily removed fibrinous plaque. Sometimes, instead of bubbles formed white
(color greasy) film, which is exposed after rejection erosive surface. A progressive course of the
disease due to the emergence of new bubbles and expressed acantholysis number of erosions and
their size increases. At the confluence of erosions formed extensive lesions covering almost the entire
oral mucosa. Available hypersalivation. Most often localized erosion of the mucous membrane of the
cheeks (especially in the retromolar area), the lower surface of the tongue, palate and floor of the
mouth area. Sometimes the lesions occur on the mucous membrane of the alveolar processes,
transitional fold, top and bottom lips. In these cases, erosion epiteliziruyutsya very slowly, even in
patients receiving high doses of corticosteroids.

If untreated, there are new erosion, which merge together to form extensive erosive surface without
tendency to healing. The pain is quite strong, the most intense when eating and speaking. Erosion
quickly become infected, especially in nesanirovannoy mouth. Joining coccal, fungal flora and
fuzospirohetoza aggravates the patient's condition, there is a specific fetid breath. Salivation
increases. Saliva macerated corners of the mouth, painful cracks appear. On the red border of lips in
the corners of the mouth are also possible blisters and erosions covered with hemorrhagic
crusts. Sometimes there is hoarseness, indicating the larynx.

Bubbles are formed on the skin mainly in the field of friction of clothing (abdomen, back, inguinal
folds, etc.). After opening the blistering of the skin are very painful erosions. Any contact with them
clothes, linen or bandages causes a sharp pain and forcing the patient to spend hours in a stationary
state.

Symptom Nikolsky with pemphigus usually positive. There are three variants:

if tweezers to grab the tire bladder or upper layer of the epithelium at the edge of erosion and
pull it, prois37 Zack. 5491. M. Maksimovskiy film epithelium detachment goes on apparently
healthy intact skin and mucosa.Thin film epithelium very fragile and easily dissected with
tweezers;

rubbing unmodified form on the skin or mucosal lesions between regions leads to the rapid
formation of blisters or erosions;

if you rub areas located away from the affected area, there are also exfoliate the upper layers
of the epithelium. The second and especially the third species symptom Nikolsky indicate the
intensification of intensity acantholysis.

In pemphigus than skin and mucous membranes of the mouth, and may be affected by other mucosa
(intestines, stomach, esophagus, pharynx), and the internal organs and the central nervous system.

Pemphigus is characterized by undulating course, periods of exacerbation followed by periods of


remission, which rarely occur spontaneously, usually after treatment. In the absence of timely and
proper treatment the disease progresses steadily. Can fast generalization skin rash and mucous
membrane of the mouth, worsening general condition of patients, there is a weakness, malaise, loss
of appetite, fever up to 38-39 C, diarrhea; edema of the lower extremities. Joining secondary
infection accompanied by cachexia intoxication. Without treatment, the process ends with fatal after a
few months of onset.

However, due to the widespread use of corticosteroids is now such cases are rare. Corticosteroid
therapy interrupts the progressive course of pemphigus, and a stage of remission.

Dermatitis herpetiformis Duhring location characterized by subepithelial blistering. Small bubbles,


intense, located on the edematous hyperemic background, tend to merge their formation is
accompanied by burning and itching.Unlike pemphigus lesions in dermatitis Dhring rarely localized in
the mucous membranes. Symptom negative Nikolsky, acantholytic cells are absent. In bubbles
significant content of eosinophils in the blood also eosinophilia. In patients with dermatitis
herpetiformis Duhring sensitivity to iodine is often increased.

In some cases, pemphigoid, lichen planus and other cystic diseases in the subepithelial location of
bubbles around them or erosions can quite easily peel off the top layer of the adjacent epithelium. At
the same tire bladder thick, hardly broken. This symptom is called a false symptom Nikolsky, or a
symptom of perifocal subepithelial detachment.

Benign Pemphigus neakantoliticheskaya oral mucosa differs from pemphigus vulgaris localized bubbles
only on the oral mucosa, subepithelial location, dense tire blistering, often with hemorrhagic content,
lack of acantholytic cells.

True diagnosis of pemphigus (acantholytic)


Diagnosis is based on clinical manifestations, positive symptom Nikolsky, cytology results and direct
immunofluorescence.

Cytological examination mazkovotpechatkov or scrapings from the bottom of erosions required


diagnosis of pemphigus. Presence in them of acantholytic cells confirms the diagnosis of pemphigus
acantholytic. Acantholytic cells, or cells Ttsanka representing altered cells thorny layer, have round
shape and a size smaller than normal cells thorny layer. Relatively large nucleus of the whole cell, its
diameter is y - y and a diameter of the cell is painted in dark blue color, often having from 1 to 6 and
a light nucleoli. The cytoplasm of cells heterogeneous coloring: light-blue and dark blue around the
nucleus at the periphery. Acantholytic cells characteristic polymorphism in the color, size of cells and
nuclei. There are giant multinucleated cells - "monsters". At the height of the disease and the number
of acantholytic multinucleated cells increases dramatically. They merge into a solid conglomerate
polymorphic cells. In remission and during treatment with corticosteroids decreases the number of
acantholytic cells.

Cytological picture with vegetating pemphigus does not differ from that in the vulgar. In seborrheic
pemphigus multinucleated cells typically do not detect, acantholytic cells were found in smaller
quantity, they are monomorphic.

Histopathological study. Found that the major morphological changes are in acantholytic pemphigus
acantholysis and swelling, resulting in formation of intraepithelial blisters. Between the cells are
broken due spinous layer - acantholysis phenomenon, thereby melting the intercellular bridges the
gap formed between the cells, and then bubbles. The bottom of such bubbles, as subsequently surface
erosions, mostly lined with acantholytic cells.

Differential diagnosis

Acantholytic (true) pemphigus must be differentiated from other bullous lesions of the oral mucosa:

exudative erythema multiforme;

pemphigoid;

drug allergy;

bullous lichen planus;

herpeto many forms of dermatitis Dhring;

neakantoliticheskoy benign pemphigus only oral mucosa.

Differential diagnosis of pemphigus acantholytic other diseases accompanied by the formation of


bubbles, mainly based on the localization of bubbles with respect to the epithelium.

Thus, when erythema multiforme exudative bubbles surrounded by a zone of erythema peripherally
located subepithelial, Nikolsky negative symptom. In addition, for exudative erythema multiforme
characterized by acute onset, seasonality relapse marked inflammation of the mucous membrane of
the mouth, shortness of flow.

When bullous pemphigoid bubbles located under the epithelium, their fat tire, so the time of their
existence longer.Bullous pemphigoid sick more often people over 60 years old. Symptom negative
Nikolsky, acantholytic cells do not show.

Distinguish akantoligicheskuyu pemphigus from allergic stomatitis help drug history (information on
medication) and the results of allergy tests. After discontinuation - allergen stomatitis rapidly
disappearing. Bubbles in drug stomatitis located beneath the epithelium, Nikolsky sign is negative, no
acantholytic cells.

When bullosa form planus subepithelial bubbles, no acantholysis. Around bubbles or other areas of the
oral mucosa are multiple papules typical of lichen planus.

Treatment of pemphigus true (acantholytic)


Treatment of pemphigus currently include corticosteroids, which are the primary means of
treatment for this disease. All other drugs, including cytostatics used to eliminate complications
associated with glucocorticoid.Glucocorticoid treatment success depends on the timing of the
application and their dosages. More correctly matched doses of corticosteroids before their early
administration, the more opportunities to achieve stable and long-term remission of the
disease. Treatment of patients with pemphigus acantholytic should only be undertaken in a specialized
hospital.

For treatment of patients with pemphigus prednisolone, methylprednisolone (metipred, urbazon),


dexamethasone (deksazon), triamcinolone (polkortolon, kenakort) in shock doses that depend on the
patient's condition.Prednisolone appoint 60-80 (up to 100) mg / day, triamcinolone on 40-80 mg /
day, dexamethasone 8-10 mg / day.Such high, the so-called shock-dose patients take to cease the
formation of new bubbles and almost complete epithelialization of erosions, an average of 10-15
days. Then slowly reduce the daily dose of prednisone first 5 mg every 5 days, in the future, these
terms are extended to 7-10 days. Upon reaching a daily dose of 20-30 mg reduce it very carefully. In
the future, the daily dose is reduced until the minimum is not defined yet, so-called individual
maintenance daily dose, which is introduced permanently. For prednisolone is usually 2.5-5 mg for
dexamethasone - 0.5 - 1 mg every 4-5 days.

Prolonged use of corticosteroids causes side effects (increased blood pressure and glucose in the
urine, bone osteoporosis, increased thrombus formation, etc.). In this connection, in order to reduce
complications from corticosteroid therapy is recommended dietary restriction of salt and water. Meals
should be mostly protein with reduced fat and carbohydrates. Inside prescribe drugs potassium
(potash asparkam), ascorbic acid, B vitamins, calcium supplements, calcitonin.

Along with glucocorticoids in patients with pemphigus acantholytic used immunosuppressants.

Some authors have noted a good therapeutic effect of simultaneous administration of cytotoxic drugs
(cyclophosphamide, azathioprine, methotrexate) and glucocorticoids.

For treatment of patients with pemphigus acantholytic use plasmapheresis hemosorption that
reduce the side effects of glucocorticoids and cytotoxic drugs, as well as help to reduce their dose.

Local treatment is mainly aimed at the prevention of secondary infection of erosions and ulcers and
accelerate their epithelialization includes painkillers as trays for the oral cavity; non-irritating
antiseptic preparations in concentrations; application to the buccal mucosa or lubrication corticosteroid
ointments. After each meal and prior to application of ointments kortikosteroidsoderzhaschih
necessary rinse with warm weak solution of potassium permanganate, 0.25% chlorine bleach, 0.02%
chlorhexidine and others is important for rapid epithelialization of erosions in the mucosa has a
thorough oral hygiene. With the defeat of the vermilion border and lubrication applications spend
ointments containing corticosteroids and antibiotics, as well as oil solution of vitamin A. When
complications of pemphigus candidiasis prescribe antifungal medications. To accelerate epithelialization
of erosions and ulcers on the oral mucosa shows laser (geliyneonovy and infrared laser).

However, even with proper and timely treatment, the prognosis in true (acantholytic) pemphigus
remains serious.Patients who take a long time corticosteroids need sanatornokurortnom treatment
(gastrointestinal and cardiovascular profile). Cooking them is absolutely contraindicated.

19. Herpetiformis Duhring dermatosis. Etiological, pathogenetic features.


Diagnostic criteria. Principles of treatment.

Definition. Dermatitis herpetiformis Duhring (dermatitis herpetiformis) - benign chronic dermatosis characterized
polymorphism, grouping elements, and itching.

Etiology and pathogenesis. etiology is unknown. In the pathogenesis of matter of malabsorption syndrome, caused
by an unusual organism sensitivity towards cereal proteins (gluten) and autoimmune reactions. Found that the most
important role in the sensitization by ente neuropathy plays protein gliadin. Immune complexes (GLIA-din-IgA) are
recorded in the tops of dermal papilla, causing an inflammatory reaction. Due to increased chemotaxis subepidermal
zone formed clusters of neutrophils and eosinophils, their enzymes are released, causing detachment of the
epidermis from the dermis.

The clinical picture. disease can begin at any age, it takes years (20-30 years), punctuated by periods of complete
recovery lasting from several weeks to months to years. The disease is characterized by the following clinical signs:

1) true polymorphism (bubbles, blisters, spots, papules);

2) grouping rash;

3) itching.

Blisters filled with clear or cloudy, at least - hemorrhagic content, tensions arise on a background of erythema or
outwardly healthy skin. They can be arranged annularly, girlyandoobrazno. Bubbles or opened, forming erosion, or
dry out to form a honey-yellow

bloody or brown-black crusts, under which occurs gradually epithelialization. After healing bubbles remains
pigmentation. Symptoms Nikolsky, peripheral growth erosions, pears, Asbo - Hansen negative. Distinguish the
following forms of the disease:

1) bullous;

2) gerpesopodobnaya (small bubbles);

3) trihofitoidnaya (ring-shaped layout rash);

4) strofulopodobnaya;

5) vegetans;

6) localized (on the extensor surfaces of the joints, legs, arms as a result of constant scratching skin lihenifitsiruetsya:
from time to time on a background of lichen-fication bubbles form).

Relatively rare at the same time with skin lesions observed rash blisters on the oral mucosa.

Diagnosis is based on histological data, cytological methods, direct RIF. Histological study revealed subepidermal
cavity formed on the basis of neutrophilic and eosinophilic microabscesses-tion in the dermal papilla. When
cytodiagnosis have large numbers of eosinophils - 10-30%, RIF reveals deposition in the dermal papilla IgA and C3
complement fraction. In blood eosinophilia possible.

Differential diagnosis is performed with pemphigus vulgaris, pemphigoid, strofulyusom, common herpes, scabies.

Treatment. Gluten-free diet, diaminodiphenyl sulfone (DDS). DDS appoint 0.05-0.1 g, 2 times a day, in cycles of 5-7
days with one-, two-day intervals. More effective combination of SDS and corticosteroids (especially in bullous form) -
10-20 mg prednisolone. In the treatment of VAT should be administered ascorbic acid and iron supplements,
metilura-cylinder in order to strengthen its action and reduce the toxic effects.

In some cases very effective vitamins B, C, F with phosphorus and calcium preparations.
Localized dermatosis herpetiformis amenable radiotherapy.

Outdoor therapy is limited to puncture bubbles and lubrication lesions aniline dyes.

20. Toxic epidermal necrolysis (Lyell's syndrome).


Lyell syndrome;

Acute epidermal necrolysis (toxic epidermal necrolysis - TEN) - developing acute dermatosis characterized by
necrosis of the epidermis with its subsequent detachment throughout the skin.

Etiology and pathogenesis. A. Lyell identified 4 etiological factor TEN - medicinal, staphylococcal, mixed and
idiopathic. At present the cause of development of PETN mainly medicaments - sulfonamides, antibiotics,
barbiturates, pyrazolo-on. In the pathogenesis of the disease into play all types of immunopathological reactions, in
particular autoimmune.

The clinical picture. disease begins with a sharp increase in body temperature to 38-40 C, deterioration of the
general condition of the patient, the appearance of the skin roseola, erythema, rash type exudative erythema
multiforme, at least - urticarnaya elements and purple, often disease like Stevens - Johnson.

A few days later formed diffuse universal erythema, against which starts peeling of the epidermis with formation of
painful erosions and flaccid blisters. Affected skin becomes scalded with boiling water. Characterized by sharp pain
as diseased and healthy-looking skin. Symptom Nikolsky (finger skin friction leads to detachment of the epidermis) in
the areas of healthy-looking skin is very positive.

Patient's general condition is extremely difficult. In peripheral blood eosinophils are absent, increased the number of
pas lochkoyadernyh neutrophils (55%) indicated toxic granularity of neutrophils, laboratory parameters witness-

exist inappropriate water, electrolyte and protein balance.

Diagnosis is based on TEN following data: detachment of the epidermis, fever, sharp pain affected and healthy-
looking skin, the lack of blood eosinophils.

Differential diagnosis. Acute epidermal necrolysis-tion in the early stages (before clinical manifestations of
detachment of the epidermis) is differentiated with drug reaction.

Treatment of patients with TEN is preferably carried out in the intensive care units burn centers, with the success of
therapy depends on the timing of its start. Apply the following drugs: corticosteroids, starting with 150 mg of
prednisolone means normalizing the water-electrolyte and protein balance, broad-spectrum antibiotics, prolonged
and not providing nephrotoxicity. Outwardly symptomatic therapy. Very important is a thorough patient care with the
use of modern technology - water mattresses, etc.

21. Planus. Clinical features, treatment principles.

Definition. planus (lichen planus, lichen ruber planus) - non-communicable diseases with subacute
or chronic course, affecting the skin and mucous membranes, characterized clinically monomorphic
rash pruritic papular-tion elements.

Etiology and pathogenesis. etiology of lichen planus is not installed.


It is assumed that the pathogenesis of the role played by infectious agents that damage,
keratinocytes, causing the appearance of new membranes at their antigens by Langerhans cells
attacked the nearby. Last begin to strengthen the production of interleukin-1.This cytokine acting on
keratinocytes and lymphocytes stimulates production of interleukin-2, -interferon and epidermal
timotsitakti viruyuschego-factor, which in turn causes the epidermal cells on the HLA antigens. In
response, T helper cells and cytotoxic damage corneocytes reacting antigens as II (HLA-DR), and a
main class I MHC. Connect to this reaction Labro-cytes secrete tumor necrosis factor, which causes
the appearance on epidermotsitov intercellular adhesion molecule-1, which further attract immune
cells, causing ultimately, the emergence and development gipergranuleza lichenoid reaction.

Among infectious agents that provoke the development of inflammation, act as Gram-negative
bacteria (which fragments are detected by electron microscopy) and fungi (Candida) and various
viruses (viruses papillomatoznye 6, 11, 16, la virus varitsel zoster).Factors contributing to the
development of the disease are stress, endocrinopathy, gastro-intestinal tract, which preceded the
immunosuppressive therapy, insolation. Defeat the oral mucosa promote tobacco smoking, dental
amalgam. There is information about the genetic predisposition to the disease.

The clinical picture is diverse and characterized by many clinical forms of lichen planus. Classic
skin lesions may represent a rash-injectivity, flat, shiny, polygonal, miliary, pale pink papules, which
further increase somewhat in size and become purple-violet (Do-henoidny) shade. Some of the
nodules have a characteristic central pupkoobraznoe impression. Papules may fuse together,
forming small plaques, covered with small scales. At some sites you will notice a kind of grayish-
white mesh pattern ("grid Wickham"), clearly manifested in lubrication papules or plaques with oil
and is a clinical manifestation expressed gipergranuleza epidermis.

The disease is accompanied by itching, often intense. Eruptions are localized mainly on the inner
surface of the forearm, the area of the wrist, the sacrum, the front surface of the tibia, the genitals. In
some cases, they are distributed over the entire body except the face. Some patients with papules
arranged linearly (zosteriformno) during the individual nerves.

Mucous membranes of the mouth occurs in 20-35% of cases at the same time with rashes on the
skin, sometimes in isolation. On the mucous membranes of the cheeks appear mi-ary white nodules,
which merge to show "grid Wickham." On periglottis papules form small plaques. On the red border
of lips rashes appear as purple plaques on the surface revealed a grayish-white grid.

To nail lesions characterized by longitudinal grooves in the nail plate, tuberosity, splitting, thinning
and loss, subungual hyperkeratosis.

The disease is prolonged for many months. The onset of acute or subacute process progresses first,
then in a few months, it should be fixed period. In the subsequent defeat gradually resolved, leaving
hyperpigmented patches. In the acute phase may be a "isomorphic response" (Koebner
phenomenon) - fresh appearance of papules in place of mechanical or chemical injury to the skin
(cuts, abrasions, bites, chemical and thermal burns).
In some patients, peripherally sprawling papules and plaques exposed central resolution, forming a
ring with hyperpigmentation in the central part - is ringed form of lichen planus (lichen planus
annularis) . Outside some cases permit the central portion undergoes atrophic changes (annular
atrophic lichen planus).

Bullous, or pemfigoidnaya form of the disease (lichen planus bullous, pemphigoides) is


characterized by a rash in the acute period, along with the usual papules, blisters in size from a pea
to a cherry, filled with serous or sero-n-hemorrhagic content. Bubbles appear on both the apparently
intact skin, and on the surface of papules and plaques.

Gipertrofigeskaya form (hypertrophic lichen planus) often develops on the front surface of the tibia,
at least in other parts of the body. Lichenoid plaques formed hue significantly elevated above the
surface of the body and covered with thick horny layers. This form of the disease is difficult to cure,
in connection with which there are plaques for years, eventually undergoing sclerosis.

Lichen planopilaris - perifollicular form, in which the observed precipitation perifollicular conical
nodules in the central part covered with horny Shih peaks. Defeat the scalp ends scar atrophy.

Aktinigesky, or tropical, lichen planus (actinic lichen planus, lichen planus tropicus) occurs more
frequently in people of the Middle East, Central Asia and parts of Africa. The most common among
the inhabitants of Egypt, about 40% of them suffer from this dermatosis. Endemicity of the disease
associated with concomitant gastrointestinal infections (schistosomiasis), which defeated on a
background of intense UFO (spectrum B) leads to the development of dermatosis. Rashes appear
on the open areas of the body exposed to sun exposure: face, hands, arms, neck. Papules very
superficial peel slightly, painted in dark purple color, have clear boundaries and sloping
edge. Expressed slightly itchy, and no Koebner phenomenon. Addition to those described, in this
form in closed areas of the body can be observed eruptions, clinically identical to the classical form
of lichen planus. Most susceptible to the disease-wives

ness and persons performing work outdoors. Process proceeds cyclically, sharpening in the spring
and summer and winter undergoing spontaneous remission. Scalp and nails are not involved in the
process.

Diagnosis is based on characteristic clinical picture (flat, shiny, polygonal, pale pink, with
pupkoobraznym impression papules subsequently acquires characteristic lichenoid shade and mesh
Wickham and Koebner phenomenon). In severe cases, use the histological diagnosis method.

The differential diagnosis is carried out with psoriasis vulgaris, and lichenoid papules sifilid
toksider-Mia, in which rash may be clinically identical to idiopathic lichen planus. Lesions of the
mucous membranes of the mouth is differentiated with leukoplakia, lupus erythematosus, syphilitic
papules.
Treatment. Held treatment of opportunistic diseases (especially gastrointestinal) and elimination of
precipitating factors (normalization of mental status).

General Medicine. In the acute period prescribed broad-spectrum antibiotics (doxycycline,


methacycline) or sulfa drugs ("Biseptolum"), sedatives (bromine, valerian) chloride injection or
calcium gluconate, vitamin B 1 , niacin preparations (ksantinola nicotinate, "Teonikol").

Most successfully used in the treatment of derivatives chloroquinoline ("delagil", "Plaquenil"), which
are more effective in combination with small doses glyukokortikosteroi-rows (20 mg prednisolone per
day). In the treatment of lesions of the mucous membranes used "neotigazon."

Physiotherapy. Showing electrosleep inductothermy lumbar-sacral spine, PUVA therapy. In the


topical treatment of verrucous lesions used kriomas-blacks diathermocoagulation.

Outdoor therapy is usually not available. In the presence of severe itching appointed "fenistil gel" or
wiping alcohol solutions other antipruritic agents. Therapy warty lesions by means of
glucocorticosteroid ointments or retinoids (Retin-hand ointment), which is applied to the affected
areas of the skin under occlusive dressing.

22. Pyoderma. Etiology, classification. Principles of treatment of pyoderma.

Streptococcal, staphylococcal piodermity streptococci, Pioallergidy main morphological


element streptoderma - conflict - a cavity in the epidermis with a thin and flabby tire filled with
serous-purulent or purulent contents located on the smooth skin and is not associated with the
sebaceous hair follicles. Distinguish strep impetigo, bullous impetigo and ecthyma vulgar.

Strep impetigo - a contagious disease that affects children and young women. Characterized by a
rash of conflicts fringed rim flushing. Often conflict tire bursting with the formation of surface erosions
pink-red color separating copious exudate. Exudate, as well as the contents of conflict, quickly dries
to form honey-yellow crusts, which are found in backsliding pink spots, soon disappearing. With the
progression of multiple become phlyctenas may merge into large pockets, covered with thick
crusts. There have been mild itching or slight burning sensation. Overall condition is generally not
disturbed.

clinical varieties : 1) bullous impetigo - the most severe variant of streptococcal impetigo; usually
develops in adults on the feet, legs and hands. Characterized by large tense blisters have serous or
sanioserous exudate and thick tire. Inflamed skin around them, 2) Zayed - in the corners of the
mouth in the form of cracks, 3) okolonogtevoy impetigo - sometimes conflict horseshoe nail
covers; 4) annular impetigo. Formed by drying flat bubbles in the center and spread them on the
periphery, the formation of arcs and garlands; 5) strep diaper rash - in large skin folds arise eroded
areas with border exfoliated epidermis; 6) papules erosive streptoderma. Occurs in infancy. Red
nodules, dense consistency, value to the bean. Can join lymphangitis, lymphadenitis, general
disorders, changes in the hemogram. Outbreaks of impetigo smeared with aniline dyes, ointments
with antibiotics (with bullous impetigo pre reveal bubbles).

Simple versicolor - LPAI streptoderma causing indolent disease. Manifests the appearance of light
pink or pink-red spots with melkoplastinchatymi, grayish-white scales on the surface.Occur more
often in children and women. Localization: face, torso and shoulders.
Vulgar ecthyma - the only form of streptococcal deep. Location: often in adults in the legs, buttocks,
thighs and torso. May be caused by mixed infection. Clinic: there is a large, deep-seated conflict with
purulent or purulent hemorrhagic content, dries in thick crust, which is found under the ulcer. Healing
is superficial, less scar drawn with clear contours. Ecthyma amount varies from single to multiple. In
immunocompromised individuals, they acquire a prolonged duration. Forms: regular, gangrenous,
penetrating (deep).

Treatment "Sumamed" 500 mg per day for 3 days 1 hour before meals. Nasal ointment "Baktroban" -
inside the nostril 2-3 times a day for 7 days. Topical solution "Fukortsin" 2-4 times a day, after drying
- ointment. Ointment "gioksizon" 2 times a day with a thin layer. "Lorinden C" 3 times per day
(cream), 2 times a day after improvement (ointment). Ointment and spray "Oksikort" 2 times a
day. Aerosol "Oksitsiklozol" 2-3 times a day - 2-3 times a week. Aerosol "Polkortolon" 1-3 times a
day. streptococci stafilodermii deep Chronic ulcerative pyoderma vegetans - of sycosis, or folliculitis
occurs phlyctenas ulcer with infiltrative margins. Bottom is covered with growths papilliform and
vegetations.botryomycoma (pyogenic granuloma) - on-site implementation of the microorganism
formed tumor with a lobular structure ("raspberry"), which must excise. Shankriformnaya
pyoderma reminds chancre, is localized on the genitals, not clinically different from syphilitic. Often
in people with AIDS, but shankriformnoy pyoderma seal beyond ulcers, syphilis - comes out. Vulgar
impetigo - a contagious disease. Starting with typical streptococcal phlyctenas. After joining a staph
infection phlyctenas turbid liquid, shrinking into layered light yellow rind. All are prone to rashes
peripheral growth. Rejection crusts accompanied by the formation of erosion and granulation
growths. Antibiotics are prescribed for advanced character. Pioallergidy formed as a result of large
and deep pyoderma forms, resulting in sensitization of the organism. Morphologically - mottled
nodular or nodular urticaria, vesicular elements. During eruptions patients feel itching. Treatment:
externally - indifferent talkers and powder, total desensitizing therapy (calcium gluconate)
autohaemotherapy. 2. Therapy of chronic pyoderma treatment of pyoderma . When multiple foci total
wash prohibited at single foci problem is solved individually. Always avoid washing themselves
foci. Household items must be individual. Treatment of common phenomena preferably carried out in
the hospital. "Cephalexin" 250-500 mg four times daily for 7 days. "Sumamed" 500 mg per day for 3
days 1 hour before meals. In chronic pyoderma - "Prospidin" 100 mg / m / in every day, the course
was 3.0 Solution for external use "Fukortsin" 2-4 times a day, after drying - ointment. Nasal ointment
"Baktroban" - inside the nostril 2-3 times a day for 7 days.Ointment "gioksizon" 2 times a day with a
thin layer. Aerosol "Levovinizol" 2-3 times per week (on infected wounds limited, erosion,
ulceration). Aerosol "Oksitsiklozol" 2-3 times a day - 2-3 times a week. Aerosol "olazol" after removal
of necrotic and purulent masses from the surface - 2-4 times a day. Prevention, prognosis. Hygienic
common mode, full and regular meals, physical education and sports. Treatment of common
diseases. Prevention and immediate treatment of microtrauma. Personal hygiene. Isolation of
children with streptococcal impetigo and vulgar, of collectives. Prompt treatment of initial
manifestations. The prognosis for cure in acute forms, is generally favorable, chronic, especially
occurring against the backdrop of heavy locations in the face - for delayed. General principles for the
treatment of chronic pyoderma: 1) a thorough examination of the patient, the elimination of
comorbidities, readjustment of foci of infection; 2) general therapy a) etiotropic means: - antibiotics (if
necessary conduct antibiotikogrammy), sulfonamides, nitrofurans; - polyvalent staphylococcal
vaccine; glycopeptide; staphylococcal toxoid subcutaneously into the undercut region (0.2 ml, 0.5 ml,
1.0 ml, 1.5 ml, 2.0 ml, 10.6 injections every 4-5 days, one month repeat rate) - subcutaneous
antifagin staphylococcal specific (from 0.2 to 1 ml a day, each successive dose increases of 0.2 ml;
course - 8-10 injections, conduct three courses every three weeks); antistaphylococcal
immunoglobulin intramuscularly every other day, 3 ml 4-6 times; b) pathogenic agents: - pirogenal -
2.5 micrograms a day, the temperature should not be more than 38 on ; plasmol (2 ml subcutaneous
injections of 15); intravitreal (sc injection 15); splenin (sc injection 15); Aloe (subcutaneously, 15
injections) , immunostimulants (metiluratsil Pentax, autohaemotherapy staphylococcal hyperimmune
plasma transfusions 4-5 times), immunomodulators (levomizol - 150 mg 3 days, 4 days break;
nukleinat sodium 3 times a day 3 weeks) - vitamin (A, B1, B6, B12, C, folic acid) - antihistamine
treatment; - enzymes (chymotrypsin, himopsin); c) symptomatic treatment: - painkillers (Analginum,
Trigan, maksigan) - lowering the temperature (Panadol, paracetamol ) Local therapy: a) the stage of
infiltration: - obkalyvanie hearth antibiotics; - electrophoresis with antibiotics; - UFO, UHF,
ultrasound b) under suppuration: - with a clean bandage ihtiola, aloe liniment; - Treatment of skin
around the hearth boric, salicylic alcohol ; - surgical excision in) stage ulceration: - turundy with
hypertonic saline; - rinsing with hydrogen peroxide; - aniline dyes tushirovanie potassium
permanganate; - antibiotic ointments, emulsions with sulfonamides; - antibacterials animal and
vegetable origin (hlorofillipt, baliz-2 , ekteritsid).

23. Staphylococcal pyoderma. Classification, clinical features and treatment.

7.1. STAFILODERMII

Ostiofollikulit

Definition. ostiofollikulit (superficial folliculitis, ostiofolliculitis) - an acute purulent inflammation of the mouth of the hair follicle (Fig.
5).
Etiology and pathogenesis. causative agent of the disease is koagulazopozitivny Staphylococcus aureus. The main predisposing
cause of the disease appears excessive pollution of the skin, especially under conditions of increased sweating, damp clothes and
skin maceration.
The clinical picture. characterized by the formation in the mouth (ostium) of the hair follicle pustules the size of a pinhead, imbued
with hair and lined rim flushing. After 2-4 days in pustule shrinking crust, which disappears, leaving no trace. Some pustules can
grow peripherally, increasing in size to a value large pea (staphylococcal impetigo Bokhar da). Sycosis may be single or
multiple. Pustules rash can occur anywhere on the skin, covered with hair, but the most common is the localization of their facial
skin, neck and extremities. Sometimes the disease can take recurrent nature.

Diagnosis is based on sycosis characteristic clinical picture: small, short-lived existing follicular pustules with mild inflammation
around them are located in different areas of the skin.
Differential diagnosis. Differentiate ostiofollikulit be vulgar with sycosis, pustular form of acne vulgaris, acne methyl iodide, eel
sifilid.
Treatment. Overall therapy is not required. Carried out in exceptional cases, when the disease is resistant chronic recurrent
nature.Appointed stimulated

Fig. 5. ostiofollikulit. Arrow indicates the path of penetration of staphylococci

Glare means (autohaemotherapy, metiluratsil aloe).

Physiotherapy. With the spread of assigned UFO - total suberitemnymi doses.

Outdoor therapy limited to the treatment of pustules 1% solution of brilliant green, or 2% tincture of iodine. Also used other
disinfectants in the form of ointments or powders. The skin around the lesions treated with 2% ethyl alcohol solution of boric acid or
salicylic.

Sycosis

Definition. Sycosis (perifolliculitis beard, sycosis staphylogenes) - chronic recurrent suppurative folliculitis limited area of the skin,
mostly the beard and mustache (Fig. 6).Etiology and pathogenesis. Causes of disease are rooted mainly in skin sensitization to
staphylococci and suppressing sterilizing properties of sebum due to neuroendocrine disorders. Patients often suffer
hypogonadal.The clinical picture. disease occurs almost exclusively in males. Localized in the growth of beard, mustache,
eyebrows, sometimes pubic, scalp, armpits. Defeat begins with the appearance of follicular pustules like sycosis that continually
recur in a limited area of the skin. Gradually develops around the affected follicles to form a reactive inflammation diffuse dermal
infiltrate. On its surface formed purulent crusts. Plucked hairs are surrounded in the root of the vitreous clutch. The disease occurs
torus-lipid.

Diagnosis is based on sycosis characteristic clinical picture: a plurality of permanent recurrent follicular pustules on a limited area
of the skin (usually

Fig. 6. Sycosis. Arrow indicates the path of penetration of staphylococci

beard and mustache area), accompanied by the development of a chronic inflammatory reaction.

Differential diagnosis. Differentiate vulgar Sycosis follows with sycosis, pustular form of acne vulgaris, infiltrative-suppurative
trichophytosis (barber's itch), methyl iodide eels, eel sifilid.

Treatment. Overall therapy includes antibiotics (oxacillin, cephalexin, rifampicin, Augmentin), and stimulants (autohaemotherapy,
pirogenal, immuno-cash, taktivin), if necessary - correction of hormonal disorders.

Physiotherapy - UFO erythemal doses.

Outdoor therapy. pustules In the acute phase treated with an alcoholic solution of aniline dyes, to infiltrate impose pastes or creams
with anti-inflammatory, disinfectant and permitting means (boric Degtyar in kind, sulfur-tar), creams or ointments containing
glyukokor-tikosteroidnye and antibacterials ( "Oksikort" "In a tselestoderm-garamitsinom" "futsikort" etc.). To prevent a recurrence,
careful skin care (2 rubdown% alcoholic solution of salicylic or boric acid).

Folliculitis

Definition. follicles (folliculitis deep, folliculitis) - an acute purulent inflammation of the middle and lower segments of the hair follicle
(Fig. 7).

Etiology and pathogenesis. Pathogens folliculitis are various types of staphylococci, among which the most common is
Staphylococcus aureus koagulazopozitivny. Microorganisms infiltrating the hair follicle, consistently penetrate the middle and lower
part of the follicular epithelium, causing purulent fusion of the latter. Process is limited perifollicular tissue.

Fig. 7. folliculitis. Arrow indicates the path of penetration of staphylococci

The clinical picture. Folliculitis differs from ostio-folliculitis deeper location of the inflammatory process in the hair follicle. It is a pink
papule the size of a pea. In the center of it often develops a pustule, filled with hair. Papule in a few days or dissolves, or
nagnaivayas, opened with the formation of pitting ulcer healing and subsequently leave behind a scar. Predisposing causes of the
development of folliculitis most frequently are exogenous factors.

Diagnosis of folliculitis is based on characteristic clinical picture manifested rash lenticular inflammatory nodules, opened with the
release of creamy pus, or spontaneously resolves.

Differential diagnosis. Differentiate folliculitis followed with papular form of acne vulgaris, acne methyl iodide, eel sifilid.

Treatment is similar to treatment sycosis.


Boil

Definition. Boil (furunculus) - acute necrotic inflammation of the hair follicle and the surrounding tissues (Fig. 8) (see col. incl., Fig.
1).

Etiology and pathogenesis. pathogen of the disease - CoA gulazopozitivny Staphylococcus aureus. Due to the high pathogenicity
of the pathogen, providing release of considerable enzymes (esterases, proteases, collagenase, etc.), the initial infectious process
(folliculitis) goes into perifolliculitis, causing extensive necrosis of the surrounding tissue. Infection often occurs through airborne
droplets from nasopharyngeal carriers, as well as due mikrotravmatizma and wear contaminated clothing.

The clinical picture. Boil develops as a result of acute purulent necrotic

Fig. 8. Boil. Arrows indicate pathways staphylococci

matic inflammation of the hair follicle and the surrounding tissues. Initial manifestations boil look like ostio-folliculitis or folliculitis, but
differ in morbidity. After 1-2 days the inflammatory site is formed rapidly growing to the size of the forest or walnut, with pain
worse. A few days later assembly opened with pus. Thus there is a dead tissue greenish - "necrotic core." After his demarcation and
exclusion remains ulcer with pus, which quickly heals by scarring.

In some cases there is purulent fusion of almost all infiltration with necrotic core and formed an abscess (boil abscessed). In other
cases, on the contrary, festering expressed very little - so-called dry boil.

Sometimes there are various complications boil. Due to the penetration of staphylococci in lymphatic vessels develop lymphangitis
and regional lymphadenitis. The spread of infection to adjacent tissues leads to the development of cellulitis, osteomyelitis. The
close relationship of the skin of the chin with the periosteum (dense connective thanks tyazham) contributes to the development of
osteomyelitis of the mandible. Weakened patients boil on the shin can be transformed into a chronic ulcer pyoderma. Staphylococci
entering the blood causes the formation of metastatic abscesses in the bones, muscles, perirenal fat, kidneys and other organs. To
this may predispose the relevant body injury with hemorrhage (even small), which creates favorable conditions for settling of
microorganisms. Finally, during the boil may acquire malignant character: infiltration increases in size, swelling increases, allowing
tissues become tense and tight around the boil developed thrombophlebitis and lymphangitis and regional lymphadenitis, sharply
increased pain, increased body temperature (40 C) , the number of leukocytes in peripheral blood, increased erythrocyte
sedimentation rate, a headache, obscured consciousness. The result of this development can be boil pyosepticemia sepsis or with
the formation of multiple abscesses in the internal organs, leading to death. The most dangerous carbuncle, growing on the face
and in particular in nasolabial triangle, nose and lips

(Especially upper). In these cases, the presence of a very thick and a superficial venous network creates favorable conditions for
infection control in the vessels and the development of purulent meningitis. Dissemination contribute to the high mobility of the
mimic muscles, squeezing the initial elements boil, cutting them while shaving, irrational local treatment.

Abrasions. furunculosis Under understand multiple boils rash or persistent recurrence single boils. Furunculosis can be localized
(e.g., on the back of the neck, lumbar region) or general - boils at dissemination throughout the skin.

Localized abrasions, as well as single boils, due to the influence of exogenous predisposing causes abrasions common - mainly
influenced by endogenous causes. For short periods of predisposing factors develops acute abrasions, with prolonged exposure -
chronic. Recurrent boils that relate to chronic furunculosis, mainly related to skin sensitization to staphylococci. Abrasions,
especially sharp, often accompanied by general malaise, fever. Sometimes these phenomena are observed at single furuncle.
Diagnosis and boil boils is based on characteristic clinical picture: painful inflammatory sites in central necrotic forming rods that
are rejected with the formation of purulent crateriform ulcers.

Differential diagnosis. Boils should be differentiated from deep folliculitis, carbuncle, gidrade-nit, skrofuloderme.

Treatment. Overall therapy in the treatment of uncomplicated single-nennogo boil, rapolozhennogo is the face, is not
required.General treatment is used for localization boils on the face (with the obligatory bed rest), complicated boils any location, as
well as abrasions. In these cases, certainly with antibiotics. Effective drugs are semisynthetic penicillin, cephalosporin-sporiny,
rifamycins, Augmentin. In chronic abrasions should apply immunostimulatory therapy (preparative

Rata thymus interferon Immunal, pirogenal) and restorative (vitamins A, B 1 , B 2 , C, E, F) therapy.

Physiotherapy is used in the developing stage of infiltration, when appropriate to apply dry heat (UHF therapy SoLux).

Outdoor therapy. Before treatment, the hair should be cut out around the boil (but not shave!). In the initial stage, characterized by
the development of the inflammatory infiltrate, apply clean ihtiol that 1-2 times a day is applied to the lesion in the form of lozenges,
covered with wool. While dressing or labels are not required, as ihtiol well kept on the skin. During dressings cash ihtiol previously
removed with warm water. The surrounding healthy skin wipes with a 2% ethanolic solution of boric acid or salicylic in the direction
from the periphery to the center. Washing in the bath tub or shower prohibited. After opening the boil ihtiol contraindicated and may
only be imposed on the edge area of infiltration. In the central part of which revealed boil superimposed gauze tissue or introduced
turundami with hypertonic sodium chloride solution. Doily attached plaster or kleolom, circular bandages are not used because they
may cause autoinoku-lyatsiyu and spread of infection. Ligation performed at least 2 times per day. This local therapy is up to full
sloughing. After the rejection of necrotic rod apply ointments containing antibacterial agents (streptocid, tetracycline, erythromycin,
lin-komitsin "baneotsin," etc.). When localizing a boil on the face ihtiol not applicable, creates maximum peace of facial muscles, in
connection with which the patient no longer talk and translate it to food liquid food. Abscessed boils treated surgically: autopsy
performed abscess.

Carbuncle

Definition. Carbuncle (carbunculus) - extensive acute necrotic inflammation of the dermis and subcutaneous fat, in the
inflammatory process involving several nearby hair follicles (Fig. 9).

Etiology and pathogenesis. causative agent acts koagulazopozitivny Staphylococcus aureus, sometimes in conjunction with the
streptococci. Carbuncle development is due

Fig. 9. Carbuncle. Arrows indicate pathways staphylococci

but, on the one hand, high virulent and pathogenic properties of staphylococci, on the other - a pronounced effect of endogenous
predisposing causes. The combination of these two factors leads to a vast area necrotic inflammation with the development of deep
cellulitis, reaching the fascia and muscles. clinical picture. Development carbuncle begins as well as boils, but staphylococci in this
case quickly penetrate the hair follicle of the lymph vessels in the deep departments of the dermis and subcutaneous tissue, which
leads to the spread of necrotic suppurative inflammation and increase infiltration originally formed to large sizes. Infiltrate around the
expressed edema. Patients concerned about a sharp pain.

Carbuncles are usually solitary. However, they are usually accompanied by fever, chills, headache. Further characterized by the
formation during the carbuncle on the surface of multiple perforations of which is allocated thick pus mixed with blood. Soon melts
the entire skin covering the carbuncle, and then exposed deep ulcer (sometimes reaching to the fascia and even muscle), the
bottom of which is a solid mass of necrotic dirty green color. After demarcation and exclusion last filled with granulation and ulcer
healing with the formation of rough scar. In some cases, for carbuncle complicated as well as during the boil.

Diagnosis is based on carbuncle characteristic clinical picture manifested the development of large, fester and turn into an abscess
inflammatory node, located in the deeper parts of the skin, accompanied by a syndrome of intoxication and reveals a few holes with
the common cavity containing a thick creamy pus.

Differential diagnosis. Carbuncle differentiate with boils, gidradenity, skrofuloderme.

Treatment is carried out according to the same principles as in the treatment of complicated boil mandatory appointment of
antibiotics and stimulants. Feature is the external therapy prior surgical opening of the abscess.

Hydradenitis

Definition. hydradenitis (Hidradenitis) - an acute purulent inflammation of apocrine sweat glands (Fig. 10).

Etiology and pathogenesis. causative gidradenity is koagulazopozitivny aureus, sometimes in combination with other Gram-
negative bacteria such as Proteus, Klebsiela, E. coli. predisposing causes development of staphylococcal lesions of apocrine sweat
glands are mainly sweating, skin contamination, rubbing her clothes , damage shaving armpits, as well as dysfunction of the
gonads.

The clinical picture. armpits, at least - to a great sex lip or other areas of skin containing apocrine glands (in the anus, navel pubis,
teat field, in the groin area), there is a node, often reaching the size of a hen's egg. Skin over it purplish-red. Painful
knot. Sometimes the body temperature rises. Soon he softened and opened with the release of large amounts of pus. Healing
occurs with scar formation. In some cases hydradenitis permitted without purulent fusion infiltrate and leaves no scar. From different
boil hydradenitis hemispherical shape and lack of necrotic core. With the defeat of several glands develops a group of nodes that
are turning into abscesses, may merge with each other. Course of the disease sometimes becomes chronic, recurrent nature.

Diagnosis of the disease is made on clinical grounds - pus-

Fig. 10. hydradenitis. Arrows indicate pathways staphylococci

but inflammatory node, located in anatomic areas of skin containing apocrine sweat glands, and opened with the release of
significant amounts of pus formation without necrotic core.

Differential diagnosis. hydradenitis differentiate with skrofuloderme, folliculitis deep, furuncle, carbuncle.

Treatment gidradenity similarly treat boils. With recurrent gidradenity appoint more bracing and an immunomodulating agent (see
"Treatment of boils"). Often used surgical treatments (opening nodes).

7.2. STAFILODERMII NEWBORN,

INFANTS AND CHILDHOOD

Ostioporit
Definition. Ostioporit (periporit, vezikulopustulez) - an acute purulent inflammation of the mouths of the sweat glands in the
newborn.

Etiology and pathogenesis. Staphylococcal defeat the mouths of the sweat glands develops in the first days of life on the
background of predisposing factors, which include, first and foremost, maceration of the skin due to excessive sweating when
violations swaddling children. The common predisposing factors include premature birth, bottle-feeding a baby.

The clinical picture. at the inguinal and axillary folds, the skin of the trunk and scalp poured numerous pustules quantity of millet
grain to pea. Pustules surrounded by hyperemic rim, they quickly shrivel in the crust, which subsequently disappear, leaving no
trace of this illness. In asteroid-border, debilitated children process covers vast areas and tends to merge.

Diagnosis vezikulopustuleza conducted on the basis of history (violation of child care) and a characteristic clinical picture - multiple
pustules rash in areas of increased sweating.

The differential diagnosis is carried out ostiofolliku-cast and scabies.

Treatment is to lubricate the affected skin 1-2% alcohol or aqueous solutions of aniline dyes. Surrounding healthy skin
obrabatyvayut2% self-litsilovym or boric alcohol. The period of treatment is not recommended to bathe the baby.

Multiple skin abscesses

Definition. Multiple skin abscesses (psevdofurunkulez Finger) - an acute purulent inflammation of eccrine sweat glands in neonates
and infants and early childhood.

Etiology and pathogenesis. causative agent is Staphylococcus aureus, sometimes in combination with steptokokka-E and other
microorganisms. The main cause of the disease is a maceration of the skin, caused by excessive sweating of the child against its
raunchy content (foul swaddling and skin care). Concomitant predisposing factors are the children borne infection, rickets, gastro-
intestinal tract, reduced food, artificial feeding.

The clinical picture. disease begins with the appearance of the back, back of the neck, thighs and buttocks numerous dense knots
the size of a large pea, the skin over which becomes bluish-red hue. Nodes slowly increased, reaching a size of cherries and
gradually turning into abscesses, then a fluctuation and they burst, releasing bloody pus. Over some of the nodes can be observed
in the mouths of superficial pustules eccrine sweat gland ducts (ostioporit).

Diagnosis of the disease is on the basis of history (violation of baby changing) and the characteristic clinical picture - packed
inflammatory lesions of multiple nodes, forming an abscess and is often combined with manifestations vezikulopustuleza.

Differential diagnosis should be made with folliculitis and furunculosis.

Treatment. Overall therapy involves the administration of broad-spectrum antibiotics and stimulants (injections maternal blood
gamma globulin).

Outdoor therapy is to impose ihtiolovye patties for developing components and lancing abscesses which developed in conjunction
with the lubrication of alcohol solutions of aniline dyes. Healthy skin of the trunk and extremities rubbed colorless disinfectant
solution (2% alcoholic solution of salicylic or boric acid).

Epidemic pemphigoid
Definition. Epidemic pemphigoid (epidemic pemphigus neonatal pyococcus pemphigoid, pemphigus neonatorum) - highly
contagious acute staphylococcal disease of newborns, characterized by diffuse skin lesions with blistering in the epidermis.

Etiology and pathogenesis. causative agent is Staphylococcus aureus phage type 71, releasing eksfo liativny-exotoxin
(epidermolizin), which causes acantholysis epidermis under his horny layer with the formation of surface bubbles. The source of
infection is a medical staff of maternity hospitals and mothers of newborns, including bacillicarriers nasopharyngeal
staphylococci.The highly contagious pathogen causes outbreaks and epidemics in hospitals. The emergence of the disease
contribute to premature labor and toxemia of pregnancy.

The clinical picture. disease usually begins at 2-3 weeks of life. Characterized by eruptions in the trunk, neck, head, limbs intact or
slightly erythematous skin small (pea-sized) bubbles filled with serous contents. Bubbles gradually increase in size, their contents
become cloudy later they opened, forming moist bright inflammatory erosion. Infiltrate at the base erosion is missing and they
quickly epiteliziruyutsya. Relapsing disease occurs with repeated outbreaks of fresh eruptions, in preterm or debilitated children may
be accompanied by common occurrences - fever, increased erythrocyte sedimentation rate, leukocytosis, eosinophilia.

Diagnosis pyococcus pemphigoid is based on characteristic clinical picture (vspyshkoobraznoe development of smaller bubbles
with rapidly mutneyuschim content) and data

tion history (the first appearance of the rash within 1-2 weeks after birth).

Differential diagnosis. Epidemic pemphigoid should be differentiated from syphilitic pemphigus newborns (study of cystic fluid for
acyanotic and blood - by serological tests), varicella, epidermolysis bullosa.

Treatment. Overall therapy performed in severe cases, accompanied by a syndrome of intoxication, and includes the appointment
of broad-spectrum antibiotics, vitamins, parenteral administration of the mother's blood.

Outdoor therapy is to remove the tire blistering and appointment warm baths with a solution of potassium permanganate. After
termination soak - creams with anti-inflammatory and disinfectant.

Staphylococcal scalded skin syndrome

Definition. Staphylococcal scalded skin syndrome (exfoliative dermatitis newborn Ritter von Rieth-terskhayna, Staphylococcal
Lyell's syndrome) - acute severe staphylococcal disease characterized by diffuse skin lesions with formation of large bubbles flabby,
clinically resembling second-degree burns.

Etiology and pathogenesis. pathogen of the disease - II fagogruppy Staphylococcus aureus, phage type 71, stands out exotoxin
(eksfoliatin, epidermolizin), which causes extensive subkornealny acantholysis of the epidermis with formation of large surface
bubbles. Infectious process develops in children in the first 3 months of life, most often in hospitals where nurses are the sources of
infection or puerperal. Perhaps the development of the disease in older children or even adults immunosuppressed, most typical of
patients on long-term immunosuppressive therapy (eg, about the transplanted kidney).

The clinical picture. disease begins with a bright ostrovospalitelnyh periorifitsialnoy erythema, exanthema resembling scarlet
fever.Beginning around the mouth, navel, anus, genitals, erythema spreads rapidly, and on it for 1-2 days, large bubbles appear,
quickly opened up and baring extensive oozing erosion.

Symptom Nikolsky positive. Bubbles and erosion exposed peripheral growth, merging, they can capture almost all the baby's
skin. At this stage of lesion may be accompanied by fever, increased erythrocyte sedimentation rate, leukocytosis, eosinophilia, and
anemia.When assigning adequate therapy due to lower intensity of hyperemia and edema of the skin re-epithelialization of erosions
occurs within one week.
Diagnosis exfoliative dermatitis newborns based on characteristic clinical picture - multiple bubbles increasing in size, showing
extensive acantholysis epidermis (positive Nikolsky sign) and is often accompanied by a syndrome of intoxication.

The differential diagnosis is carried out with thermal burns, syphilitic pemphigus newborn's disease epidermolysis bul. In adults,
staphylococcal scalded skin syndrome, toxic epidermal differentiate with ethyl necrolysis.

Treatment. Overall therapy involves assigning penalties-tsillinazoustoychivyh antibiotics (amoxiclav) or other antibiotics with a
broad spectrum of action.

Outdoor therapy begins with the appointment to the field weeping erosions warm baths with a solution of potassium
permanganate.On the cover is applied ointment with disinfectants.

24. Streptococcal pyoderma. Classification, clinical features and treatment.


Streptococcal Impetigo

Definition. Impetigo (impetigo streptogenes) - acute diffuse serous inflammation of the skin to form subkorne-cial or
intraepidermalnyh bubbles.

Etiology and pathogenesis. The causative agent of the disease is the -hemolytic streptococcus group A. In rare cases (bullous
impetigo) in the pathogenesis of intraepidermal blistering-tion participate koagulazopozitivnye phage type 71 staphylococci causing
intraepidermalny Akan-toliz. Leading predisposing cause of the development of impetigo are microtrauma (shaving, scratches,
insect bites).

The clinical picture. Strep impetigo is characterized by sudden onset, severe in Education

against the background of hyperemia subkornealnyh bubbles are transformed within a few hours or rough crust layered honey-
yellow color, which are exposed by removing erosion, fringed collar narrow stratum corneum. The primary element is the surface
(under the stratum corneum) flabby bubble up to 1 cm with a clear serous content - conflict. It is so fast shrinking in the crust that is
usually visible. With the addition of a staph infection crust acquire a greenish-yellow color (streptostafilokokkovoe or vulgar
impetigo).disease is accompanied by itching, so the crust can be hemorrhagic. Impetiginoznye elements have a tendency to
peripheral growth and mergers. Often develops regional lymphadenitis. Often children suffer. Favourite localization - the person of
men - the area of growth of beard and mustache, women - the scalp. Sometimes, especially in children, in the process involves the
mucous membranes of the mouth, nose, eyes: there phlyctenas quickly opened with the formation of painful erosions.

In some patients on long-term resolution of impetigo on the faces remain mukovidno or scaly scaly congestive spots. Similar items
can be primary, mainly in children before puberty, as well as adults, working outdoors. Summer, under the influence of sunlight,
stains may disappear, but the skin on their tans place to a lesser extent and becomes lighter than healthy. This skin lesion is
regarded as worn out, the dry form of impetigo is called simple or white, deprive a person.

In some cases, conflict grows in shrinking crust (plate) only in the central part, and remains on the periphery of the cystic
roller(annular impetigo.) In other cases, the conflict persists, located in the deeper layers of the epidermis. She is not opening and
not in ssyhayas crust expands and reaches the size of a large bubble (bullous impetigo). bullous impetigo often develops in the
field of nail ridges (usually in the presence of burrs), horseshoe surrounding the nail plate (surface felon).

In persons who have a habit of licking his lips, as well as in sleeping with his mouth open, which implies saliva, excessive moisture
occurs corners of the mouth, which contributes to time-

vitiyu slotted impetigo ("perleches"). The latter represents erosion surrounded by a collar of the horny layer of the remaining tires
phlyctenas; in the depth of a crack mouth and the skin around it - honey-yellow crust. During perleches very stubborn. A similar
pattern with slit impetigo have candidiasis of the oral (if it does not form a crust) and papular sifilid appropriate localization which is
characterized by infiltration at the base erosion.

Papules erosive sifilid resembles another impetigo, observed in infants. On the buttocks and back of the thighs appear phlyctenas
who quickly opened, leaving erosion. At the base erosion soon developed papular infiltration. This form of strep-called
todermiisifilopodobnym posterozivnym papular impetigo. predisposing cause of its development are maceration and irritation feces
with insufficient childcare (hence another name - nappy rash). This explains the uniqueness of the clinical picture: moisture prevents
the formation of crusts, "washes away" collar erosion around the stratum corneum (the remnants of conflict tires); causes irritation
reactance infiltrative inflammation in their basement.

Diagnosis is based on data impetigo history (mikrotravmatizm, skin contamination) and characteristic clinical picture
(vspyshkoobraznoe mutneyuschih appearance quickly and drying surface bubbles).

Differential diagnosis. Impetigo should be differentiated from artefitsialnym and atopic dermatitis. Slit with Zayed impetigo
differentiate lesions in yeast. Differential diagnosis of diaper dermatitis is carried out with papular infiltration of congenital
syphilis.Diagnosis sifilopodobnogo posterozivnogo papular impetigo must be confirmed by the negative results of the study on
discharge erosion pale ponemy friction and negative results of serological tests for syphilis.

Treatment. Overall therapy conducted at the widespread nature of the process and the presence of complications such as
lymphangitis and lymphadenitis. In these cases with antibiotics (semi-synthetic penicillins, rifamycins, cephalosporin-width).

Outdoor therapy may be used depending on the clinical form of impetigo. The skin around the lesions 3-4 times a day wiped
disinfectants (2% alcoholic solution of salicylic, boric, boric levomitse Ting-salicylic acid). Bubbles opened with the removal of
tires.Under moist erosions apply lotions or wet-drying bandage with a solution of 0.25% silver nitrate, 2.1% resorcinol, 2.1% boric
acid, liquid Alibura. After termination of the presence or soak dry crusts apply ointment with disinfectants. In marked inflammation at
the periphery of the lesions is possible for a short period (1-2 days) use of ointments and creams containing in its composition
glyukokortikoste-roidy and antibacterials ("belogent", "diprogent", "futsikort", "Lorinden- C ").

Intertriginoznaya streptoderma

Definition. intertriginoznaya streptoderma (strep diaper rash, strep intertrigo) - seropurulent diffuse inflammation of the skin to form
bubbles in the developing inguinal-femoral and mezhyagodichnoy folds, armpits, in the folds of the abdomen and neck in obese
subjects, at least - in the interdigital folds stop sometimes - brushes.

Etiology and pathogenesis. pathogen of the disease - -n-molitichesky streptococcus group A. The process is streptokokovoe skin
lesions predisposing causes of which are enhanced flow and salootdele-tion, beli, urinary incontinence, discharge from the fistula,
hemorrhoids, hot compress, insufficient drying the skin folds after bathing, etc. Sometimes the cause is saccharephidrosis diabetics.

The clinical picture. Clinically strep in-tertrigo is a wet erosive surface formed as a result of opening conflict bordered collar
stratum corneum. Its boundaries clear, krupnofestonchatye. Deep folds longitudinally arranged superficial, non-bleeding visible
cracks.Lesions have peripheral growth occurring by detachment of the stratum corneum. Outside the contiguous areas of the skin
clinical picture becomes impetigo. Subjective feelings are expressed in the form of itching (less marked pain, burning).

Diagnosis of the disease is based on characteristic clinical picture (large scalloped wet erosion, located in large folds of the skin). In
complex cases, a laboratory diagnosis (microscopic or culture methods).

Differential diagnosis. strep diaper rash should be differentiated from intertriginoznaya Candido Zom (yeast intertrigo).

Treatment. Overall therapy is conducted in the presence of complications (lymphangitis, lymphadenitis) or chronically recurrent
course of disease present and includes antibiotics and stimulants.

Physical therapy is administered after removal ostrovospalitelnyh phenomena and soak in the form of termination of UVR erythemal
doses to the affected skin.

Outdoor therapy. When soak - lotions and wet-drying bonnets of disinfectants and anti-inflammatory drugs (2% alcoholic solution of
boric acid, 2% solution of resorcinol, Alibura liquid, etc.). After termination and removal soak ostrovospalitelnyh phenomena use
pasta with disinfectant and anti-inflammatory drugs (a 2% gentsianvioletovaya, ethacridine-boron-naftalanovaja, a 2% methylene),
application of creams containing glucocorticosteroids and disinfectants ("polkortolon-TS" "Oksikort", "target stoderm with
garamitsinom-In", "futsikort", etc.). In resistant cases occurring, characterized by the development of chronic inflammation,
ointments permissive and disinfectants - 5-10% sulfuric-tar ointment wil Parkinson's, a 10% ihtiolovye. Since intertriginoznaya
streptoderma not always possible to differentiate from inter-triginoznogo candidiasis, medication should be used, acting as
streptococci, and the yeast-like fungi.

Chronic diffuse streptoderma

Definition. Chronic diffuse streptoderma is a vast hearth chronic serous or sero-purulent inflammation diffusely affects the skin of
the tibia, at least - of the scalp.

Etiology and pathogenesis. disease is strep streptococci or staphylococcal disease


skin, the peculiarity of the clinical picture and a chronic course which caused persistent local circulatory disorders that cause tissue
hypoxia skin. Most often they are associated with a constant supercooling shins or head varicose veins, daily prolonged stay on his
feet, etc.

The clinical picture is characterized by hyperemia, often stagnant, low infiltration, krupnofestonchatymi clear boundaries formed
collar stratum corneum. Surface covered with large hearth plate seropurulent and serous-hemorrhagic crusts between them -
erosion. By removing crusts exposed solid surface moist. The lesion was gradually "spreads" on the periphery. Around it can not
detect the primary elements - large phlyctenas. The disease is characterized by torpid, is prolonged, acute inflammatory process
that, then subsides. In the latter case moknutie terminated and replaced cover large scales. Long term course of the disease
contributes to its transformation into microbial eczema, resulting in an appearance on an erythematous background mikroerozy
separating drops of serous fluid.

Diagnosis of chronic diffuse streptoderma based on clinical features (large wet erosion, sometimes covered with purulent
hemorrhagic crusts and scales krupnoplastinchatoe which is most often in the legs and often in patients with impaired trophics lower
limbs).

The differential diagnosis is carried out with microbial eczema.

Treatment. Overall therapy. funds from the general treatment applied by intramuscular injection of 10% solution of calcium
gluconate 10 ml daily or every other day, antihistamines, vitamins (B 1 , B 6 , C, P, PP), immunostimulatory therapy
(autohaemotherapy, pirogenal, metiluratsil taktivin, reaferon), as well as broad-spectrum antibiotics (ampicillin, azlocillin, amoxiclav).

Physical therapy is the same as in-noznoy streptococcal intertrigo.

Outdoor therapy. When soak is recommended to use lotions and wet-drying bandages from solutions with disinfectant and
astringent (0.25% silver nitrate solution, 2% alcoholic solution of resorcinol, boric

acid liquid Alibura). On the cover - ointment with disinfectants. After removing ostrovospalitelnyh phenomena and termination soak
use pasta with disinfectant and anti-inflammatory drugs (Etacryl-din-boron-naftalanovaja, a 2% methylene 3-5% probability
ihtiolovaja), you can use creams containing glucocorticosteroids and disinfectants ("white -Gent "" diprogent "" Lorinden-C ","
futsikort "" derma-celestite-B with garamitsinom "). In the stage of chronic inflammation, torpid flow shown ointment permissive and
disinfectants - sulfur-Tar-naftalanovaja, tar and naphthalene in equal parts.

Ecthyma

Definition. Ecthyma - acute serous-purulent necrotic-parameter skin inflammation that develops as a result of microorganisms into
the depth of the skin (epidermis under) and causing necrosis of the dermis to produce ulceration (see col. incl., Fig. 2).

Etiology and pathogenesis. Ecthyma can be not only streptococcal but streptococci staph, staphylococcus, and in exceptional
cases - gonococcal. Penetration deep into the skin infection caused microtraumas and mainly scratching due to lice, scabies and
other pruritic dermatoses. The disease often develops due to lower immune reactivity due to hypovitaminosis, stress, chronic
intercurrent disease-E.

The clinical picture. Due to the nature etiopato-genesis disease starts with the formation not phlyctenas and deep, amid the
inflammatory infiltrate, bladder or epidermal-dermal blisters the size of a large pea and more. Bubble or pustule rapidly shrinking in
serous-hemorrhagic-ragicheskuyu or purulent hemorrhagic crust immersed in a thick skin and inconspicuous area bordered
hyperemia. By removing the cover reveals an ulcer with steep edges, filling in time granulation. Ecthyma usually multiple, often
linear (in the direction of scratching); favorite localization - the lower limbs and buttocks. We unscrupulous people in the presence of
stagnation in the legs, in frail patients, the disease without treatment may acquire chronic.

Diagnosis ecthyma is based on characteristic clinical picture (inlaid into the skin purulent hemorrhagic crusts, and rounded surface
ulcers located in the lower extremities).

Differential diagnosis. vulgarity ecthyma should be differentiated from chronic ulcer pyococcus, acute necrotizing type of
cutaneous leishmaniasis indurativ-tion and erythema syphiloma.

Treatment. Overall therapy. Out of the total treatment prescribed vitamins (A, B 1 , B 6 , C, P) and stimulating therapy (autogemote-
rapiya, metiluratsil pirogenal, timalin). With widespread process, complicated course used broad-spectrum antibiotics.

Physiotherapy treatment is carried out similarly streptococcal intertrigo and chronic diffuse streptoderma.

Outdoor therapy. skin around the affected areas wiped with disinfectant alcohol or processed aniline dyes. Tyres conflicts are
removed and stacked on the cover ointment with disinfectants. After removing the tire blistering or discharge of crusts apply lotions
or wet-drying bandage with disinfectant and anti-inflammatory drugs (1% silver nitrate solution, a 2% solution of boric acid, 1%
solution of resorcinol). A dried ulcer impose the same ointment with disinfectants. With a weak tendency to apply ointment to heal
Mikulicz iruksol, Levosin, a 10% ointment metiluratsila.

25. Fungal infections of the skin. Etiology, classification, pathogenesis.

Fungi are widely distributed in soil, air, fruit plants, rich in sugars. Leading role in the development of
fungal infections playsScopulariopsis brevicaulis.

Etiology and pathogenesis. Mushrooms can affect the stratum corneum, skin appendages, the
mucous membranes of the mouth and genitals, dermis, hypodermis, and other deep tissue (with
deep mycosis).

Development of fungal infections of the skin caused by the following factors: the pathogenicity and
virulence of the pathogen status of host, environmental conditions.

Diagnosis. Diagnosis of fungal infections of the skin in most cases should be confirmed

laboratory methods isledovanija: microscopic, allowing to establish the presence of the fungus by
culture, identifying the fungus, in rare cases, a histological study. In a number of fungal infections
used fluorescent diagnostics.

Microscopic method we study scales, tire vesicles, nail plates, hair. Pathogen fungal disease can be
detected after clearing the horny substance in a hot solution of caustic alkali. To this end, the
crushed pieces of the test material was placed on a glass slide and a drop applied to them 20%
potassium hydroxide solution. Following this, the glass is heated over a flame until the burner on the
periphery of the rim drops white crystals of alkali. Then the drug is applied coverslip and study it
under a microscope. Positive results of the study are findings fungus - strands of mycelium and
spores, which, however, does not allow to identify the fungus.

Cultures study identifies the genus and species of fungus, moreover, it is more informative than
microscopy. The most widely used Wednesday Saburo or wort agar containing antibiotics.

Fluorescent diagnostics is to ultraviolet light through a filter lesions Wood and is used mainly in the
defeat at mikrosporii hair and favuse.

Classification. In recent years, domestic dermatology applied ND Sheklakova classification,


according to which there are four groups of fungal infections and psevdomikozov group. To mycosis
include:

1) keratomikozy (pityriasis versicolor, etc.);

2) ringworm (tinea, athlete's foot, caused by red trihofitonom, trichophytia, microsporia crusted
ringworm);
3) candidiasis;

4) deep mycoses.

The group attributed psevdomikozov erythrasma, actinomycosis, etc.

Currently, in most countries, the most widely used classification of fungal diseases of the skin,
depending on the etiology. Isolated fungal infections caused by dermatophytes (further specification
is based on specifying the localization of mycosis), yeast-like fungi and molds. Mycoses caused by
dermatophytes:

1) of the scalp;

2) the beard and mustache;

3) smooth skin;

4) persons;

5) large folds of the body;

6) feet;

7) brushes;

8) nails.

26. Tinea pedis. Etiopathogenesis, epidemiology. Clinical forms.


Tinea pedis

Tinea pedis - an umbrella term that includes fungal infection of the skin and nails of feet. Defeat stop often causes Tr. rubrum (70-75%), less often
- Tr. mertagrophytes interdigitale (18-19%), Epidermophyton floccosum (2-3%), yeast-like fungi of the genusCandida, fungi (7-8%).

Place primary localization pathogenic fungi in tinea pedis - interdigital folds. With the progression of the process rashes go beyond them.

Defeat stop at various kinds of fungus clinically occurs almost the same way.

Etiology

Most often defeat feet and nails caused by fungi Tr. rubrum and Tr. mentagrophytes interdigitale. penetration of fungi in the epidermis contributes to the
violation of his integrity as a result of microtrauma, diaper rash, scrapes, excessive dryness or excessive sweating. Background for the development of
infection - endocrine disorders, immunodeficiency disorders, circulatory disorders, trophic tissue stop.

Spread of athlete's foot is basically promotes the visiting public baths, saunas, showers, especially in industries (mines, metallurgical plant, etc.),
swimming pools, etc.

The clinical picture

There are several clinical varieties of athlete's foot. Worn form - beginning mycotic process. Celebrating slight peeling interdigital folds, often -
between IV
and V toes, sometimes small surface cracks. Subjective disorders are absent.

Squamous form is manifested by small peeling of scales in the interdigital plate folds, as well as on the lateral surface of the sole (Fig. 5-
8). Sometimes there is congestion specified locations and tingling.

intertriginoznaya form - affected interdigital folds, often - between III and IV, IV and V of the toes. In addition to diaper rash, redness present, edema,
maceration, moknutie, frequent erosion and cracks, accompanied by itching, burning, pain (Figure 5-9).

Fig. 5-8. Mycosis stop squamous form

Fig. 5-9. Mycosis stop intertriginoznaya form

disgidroticheskaya form - on the arch of the foot there are numerous bubbles and bubbles with thick cap. Eruptions seize vast areas of the soles,
interdigital folds of skin and fingers. Fused multi-chamber formed bubbles in their showdown - wet erosion pink-red color.Arise hyperemia and edema
of the skin (Figure 5-10).

Fig. 5-10. Mycosis stop disgidroticheskaya form

Inflammatory process gradually fades away, formed three zones:

Central - smooth skin pinkish-red color with a bluish tint, and a few thin scales;

average - numerous erosion separating scant serous fluid, redness, swelling;

Peripheral - vesicles and multi-chamber bubbles, bubbles.

There are features of the clinical picture, depending on age. Aggravation and exudative clinical manifestations characteristic of the young and middle-
aged, monotonous for dry skin - for patients of elderly and senile age.

The acute form of athlete's foot. Aggravation expressed or intertriginoznaya disgidroticheskaya athlete's foot can lead to the development of the
acute form, considered as a manifestation of severe sensitization to fungi pathogens: grow exudative phenomena, leather feet and legs becomes
sharply giperemirovanoy and edematous. Against this background, you can see numerous vesicles and blisters with serous and sero-purulent
contents. Their opening leads to the merging of erosions. Maceration in the interdigital folds goes beyond them, there are erosion, cracks. On the
hands, body, face possible allergid as swollen spots, papules, vesicles. Increased body temperature, developing bilateral pahovobedrenny
lymphadenitis, lymphangitis. Subjectively, weakness, headache, difficulty in walking.

hyperkeratotic form - Dry flat papules, plaques nummulyarnye lihenifitsirovannye slightly reddish color on krasnovatozheltovatogo arch of the foot
(Fig. 5-11). Surface lesions, especially in the center, covered with various thicknesses layering grayish-white scales, their boundaries clear. On the
periphery - curb exfoliated epidermis, individual bubbles. Eruptions merge, forming serpiginiruyuschie diffuse, large-sized pockets, exciting the entire
sole, sides and rear feet. Along with scaly patches occur hypertangent

ratoticheskie education by type of limited or diffuse callus yellowish with cracks on the surface. Subjectively - dry skin, mild itching, and sometimes
painful. Giperkeratoticheskaya form is often associated with squamous - squamous giperkeratoticheskaya.
Onychomycosis (onychomycosis). Normally fungi penetrate the nail plate from the centers of fungal infection of the interdigital folds feet
soles. However, allow the possibility of the development of isolated onychomycosis when driver is embedded in the nail plate from her distal, lateral,
proximal edges or directly through the dorsal surface (Fig. 5-12). Russian mycologists distinguish 3 types of onychomycosis: normotrofichesky,
hypertrophic, oniholitichesky (atrophic).

- Normotrofichesky type: changes only painting nails - in the distal appear spots and stripes, varying in color from white to yellow ocher (Figure 5-
13). Then the entire nail changes color, shine and keeping unchanged thickness.

- Hypertrophic type: a color change joins growing subungual hyperkeratosis. Nail loses luster

becomes dull, thickened and deformed, partially destroyed laterally (Figure 5-14). - Oniholitichesky (atrophic) type: dull brownish-gray, dirty-gray color
of the affected part of the nail, it atrophy and exclusion from the bed (Fig. 5 - 15). Exposed portion is covered with layers of loose
giperkeratoticheskaya. Proximal portion of the long-term remains unchanged.

Features of current fungal infections in children


The disease is practically does not occur in young children.

Fungal infections diagnosed stop from about 3-5 to 10-13% of school-age children and increase progressively in

boys and girls aged 15-18. Variability in the frequency of infection tinea pedis children is primarily due, anatomical and physiological characteristics of
their skin, peculiar to each age.

Boys are sick more often than girls (this helps the swimming pools, showers, gyms, more frequent use of rubber boots).

Diagnostics

Diagnosis is based on clinical lesions of skin, nails, laboratory data and microscopic cultural studies to identify the type of fungus.

Differential diagnosis

Differential diagnosis is performed with traumatic nail psoriasis, eczema, lichen planus, a disease Reiter onihopatiyami.

With the localization of the feet, hands differentsruyut disease eczema, congenital hyperkeratosis.

Treatment

Worn form:

- Use of any acceptable dosage forms: solutions, sprays, creams, ointments containing naftifine, terbinafine, ketoconazole, ciclopirox,
sertaconazole. Preparations applied to the cleaned and the dried skin, 1 per day, duration of treatment is an average of 2 weeks. It is possible to
alternate the application of the solution, lotions and ointments;

- antimycotics isoconazole econazole, ciclopirox, miconazole applied 2 times a day until resolution of clinical symptoms, then treatment was continued
for another 1-2 weeks, but one time a day;

- obsolete treatments include lubrication interdigital folds 2% iodine solution or liquid Castellani (fukortsin) in the morning and 5.10% sulfur-salicylic
ointment - evening.

squamous giperkeratoticheskaya form:

- to remove the horny layers can be applied to the soles of 5-10-15% salicylic vaseline at night under the wax paper to completely remove the horny
masses;

- more effective detachment on Arievich: on the soles on the 2 days in the hospital and at home - at night for 4-5 days

for poultice is applied successively ointment containing salicylic acid (12.0), lactic acid (6.0) and petrolatum (to 100.0);

- easy to use milk-salicylic collodion (lactic and salicylic acid 10.0 to 100.0 collodion), which lubricate the soles of your feet in the morning and evening
for 7 days, then at night under a compress applied 5% salicylic vaseline, do morning foot soap-soda baths and peeling of the epidermis is removed
poskablivanii pumice. Later transferred to these antifungal creams, ointments.

intertriginoznaya form:

- apply sprays terbinafine cream diflucortolone + isoconazole zinc paste. After removing the diaper rash, maceration, epithelialization cracks apply
conventional antifungals external actions (naftifine, terbinafine, etc.).

disgidroticheskaya form. Acute form:

- acute inflammation of the skin of feet (disgidroticheskaya form, acute form) treatment is carried out as eczema. As hyposensitizing therapy
administered one of the solutions was: Calcium chloride (10%), sodium thiosulfate (30%) intravenously, calcium gluconate (10%) intramuscularly; one
of antihistamines (Chloropyramine, mebgidrolin, ketotifen, cetirizine, loratadine, desloratadine, levocetirizine - from the age of 2 years in the form of
droplets);

- exterior of drugs used lotion with a boric acid solution (2%), resorcinol (2%), silver nitrate (0.25%) 0.01 *% miramistina etc. When bacterial infections
occur designate trays with potassium permanganate solution (1:6000), soda baths (1 tablespoon per 200 ml of water). Crusts removed, bubbles reveal
sterile scissors and treated lesions water solution of 1% methylene blue or brilliant green.Then apply boric Naftalan paste kremgel Aysida *. You can
assign spray terbinafine;

- it is expedient to use formulations having, besides an antifungal, antiinflammatory, and (or) an antibacterial action: creams diflucortolone +
isoconazole, isoconazole, hydrocortisone + neomycin + natamycin, naftifine, terbinafine, bacitracin, neomycin + (in the form of a powder or an
ointment), etc.
Treatment of onychomycosis

Causal treatment - the only effective treatment for fungal nail infections. Distinguish local, systemic and combination therapy.

Advantages of local therapy - no side effects and toxic effects observed with systemic drugs as topical antifungals are not absorbed into the systemic
circulation.

Indications for local therapy:

distal-lateral form of onychomycosis;

white surface (initial stage);

defeat than 1 / 2 of the nail;

mild subungual hyperkeratosis;

defeat 1 or 2 nails.

The disadvantage of local therapy is that the drug when applied to the surface of the nail plate is not always reaches the fungus in the nail bed
positioned and (or) in the matrix. In the latter case, local media treatment is ineffective, and to take stock of the drug to the infected box is necessary to
resort to the destruction of the nail plate - use keratolytic patches, removal of the nail plate by mechanical means.

It is most convenient for this purpose use devices with different particle c mills that enables you to painlessly remove the nail for 10-15 min.

There is a set for the removal and treatment of nails - bifonazole. Active substance in it is bifonazole - imidazole derivative having a broad spectrum of
activity on dermatophytes, molds, yeast-like fungi. The kit includes a 1% ointment in a tube at 10.0 g with dispenser, waterproof plasters and
scraper. Ointment has keratolytic action (procedure takes 10-15 days). Subsequently, the cream is applied to 1% bifonazole for 4-6 weeks.

The most effective and convenient means of proper treatment of onychomycosis - lacquers ciclopirox, amorolfin. They can be used without having to
remove the nail or making it partially.

Effective in treating onychomycosis naftifine 1% solution. It is active against dermatophytes, fungi of the genus Candida and most fungi, and has a
pronounced anti-inflammatory effect, also provides local bactericidal effect on gram-positive and gram-negative bacteria, which provides warning
complications foot mycoses pyoderma, microbial eczema, erysipelas.

Topical therapy is continued until complete recovery shaped configuration, the transparency and surface smoothness of the nail. The course of
treatment - 4-6 months.

Systemic therapy. Through the introduction of modern antifungals in therapy became possible to achieve high efficiency in the treatment of
onychomycosis.

Indications for systemic therapy:

distal-lateral form of onychomycosis (late stage);

proximal and total form of onychomycosis;

defeat over 1 / 2 of the nail;

involvement in the matrix;

pronounced changes in the nail (hyperkeratosis, onycholysis);

2-3 defeat nails;

inefficiency of local therapy;

combination of onychomycosis with common skin lesions or hair.

The effectiveness of systemic therapy is determined by the flow characteristics of onychomycosis, clinical and etiological indications schemes,
adequate for a specific case of onychomycosis, treatment of comorbidities (diabetes, varicose veins, obliterating endarteritis, etc.).

Of systemic antimycotics in the treatment of onychomycosis is most often used terbinafine and itraconazole.
The duration of treatment depends on the rate of regrowth of different nails and their growth - from the patient's age.

27. Keratomikozy: clinical features, diagnosis, treatment principles.


5.1. Keratomikozy

Under keratomikozy understand fungal skin diseases in which pathogens infect only the horny layer
of the epidermis.

In our country, this group is represented by colored (pityriasis) versicolor.

Etiology

Pathogen - Pityrosporum orbiculare (Malassezia furfur), referring to the lipophilic yeast-


fungi. Basically ill persons young and middle age.

Pityrosporum orbiculare as a saprophyte is on human skin and under favorable conditions for it
causes symptoms. The disease most often occurs in individuals suffering from excessive sweating,
changes in the chemical composition of sweat, digestive diseases, endocrine disorders, vegetative-
vascular disorders and immune deficiency.

Overheating children irrational hygienic regimen contribute to the emergence of the disease and its
recurrence.

The clinical picture

Characterized by small spots on the skin of the chest, neck, back, stomach, at least - the upper and
lower extremities, axillary and pahobedrennyh areas, sometimes on the scalp.

First appear yellowish points located at the mouth of the hair follicles. Then comes their peripheral
growth and formed rounded contoured spot diameter of 1 cm pinkish, then svetloi dark brown color
(Fig. 5-1, 5-2). Uneven coloring eruptive elements in different patients and even in the same patient
led to the term "colorful lichen." The surface is covered with scaly rash scales by loosening fungus
stratum corneum (2nd term - "chromophytosis"). Sometimes peeling reveal only when poskablivanii
spots.

Spots may merge, forming pockets of up to 10-15 cm in diameter with scalloped edges or even
larger sizes. Increasingly common process observed in HIV infection, and the transformation is
possible in spots papules and plaques.

After peeling and insolation amplified spots become white in color (Figure 5-3). For the disease
characterized by a long course with frequent exacerbations.

Features of the flow in children. Colorful lichen rarely develops in young children (sometimes in
combination with common gneiss), and in adolescents the disease observed in the presence of
comorbidities (dystonia, endocrinopathies, obesity).
Fig. 5-1. Colorful lichen. Skin lesions of the chest
Fig. 5-2. Colorful lichen. Skin lesions of the chest and abdomen
Fig. 5-3. Colorful lichen. Skin lesions of the chest and abdomen after insolation

Diagnostics

Diagnosis is based on clinical manifestations, detection of the pathogen in skin flakes under
microscopic examination, the characteristic yellow or brownish glow under fluorescent Wood, iodine
positive sample (sample Balzer).

Balzer sample reveals invisible peeling. To this end, a cotton swab dipped in a 5% solution of iodine,
lubricate the lesion border and healthy skin. Due to peeling spots tinea versicolor become more
intense color than healthy skin (Figure 5-4). This test can be applied to establish the cure when the
skin stays whitish spots.
Fig. 5-4. Colorful lichen. Trial Balzer

Differential diagnosis

Colorful lichen differentiate from pink lichen Gibert (should be "mother plaque" spots bright pink-
red); syphilitic roseola (spot the same size, do not merge); syphilitic leukoderma (spots do not
merge, white, surrounded by a zone of hyperpigmentation, a negative test Balzer); dry streptococcal
(whitish spots, isolated, large, more children).

Treatment

In the treatment of multi-colored lichen effective spray terbinafine 1% used 2 times a day for 1
week; Terbinafine 1% cream - rub 2 times a day for 2 weeks; bifonazole as a 1% cream or a solution
of 1% - 1 times a day for 2-3 weeks; ciclopirox in a 1% cream or solution, 2 times a day for 10-12
days; Cream 2% sertaconazole; Clotrimazole 1% solution (for 1-3 weeks), etc.

Treated not only places lesions, and areas of the skin from the neck to the waist. Desirable solutions
in massaging the scalp. When common form with frequent relapses co-administered antimycotics for
systemic effects: itraconazole 200 mg daily for 7 days or 100 mg for 2 weeks; fluconazole 50 mg 1
time a day every day for 2-4 weeks; terbinafine 250 mg 1 time a day for 7 days.

Counseling

The patient may need to explain that in the period of treatment should be normal (car) wash
underwear and bed linen and stroking his iron. Wearing underwear previously subjected to similar
treatment. Contagiousness pitirosporalnoy flora questionable - in need of treatment of the underlying
disease.

28. Dermatophytes: clinical and epidemiological features, diagnosis, treatment


principles.
5.2. Dermatophytes

Dermatophytes - group filamentous fungi affecting horny keratinocytes (the horny layer of the
epidermis, nails, hair).

Pathogens dermatofty (tinea) belong to the genera Trichophyton,


Microsporum and Epidermophyton.

Ringworm can be divided into epidermomikozy, trihomikozy, onychomycosis - depending on the


defeat of a particular tissue, but often resorted to the classification based on the anatomic location of
the lesion (jock itch, athlete's foot, etc.).

Jock itch
Mainly affected large folds, mainly inguinal and adjacent areas of the skin, as well as the pubic area,
thighs (Fig. 5-5). In children is rare, can occur during puberty.

Etiology

Pathogen - fungus Epidermophyton floccosum. disease occurs more frequently in patients suffering
from sweating, obesity, when wearing tight clothes in a hot humid climate, long-term external
treatment of glucocorticoid.

The clinical picture

In the inguinal region there are small, slightly swollen spots pinkish-red color with clear boundaries,
rounded outlines. In the future, they increase in size, coalesce, forming a solid center (sometimes
plaque) with scalloped contours, desquamation. Edge spots (plaques) are raised. Eruptions beyond
groin. May be affected by axillary

Fig. 5-5. Inguinal athlete

ITATION cavities, folds under the breasts, popliteal fossa, etc. Sometimes the marginal zone is
covered with bubbles, crusts.Subjectively, patients feel itching. Over time, inflammation fading,
peeling enhanced prevails brownish coloration.

Diagnostics

Diagnosis is based on clinical presentation, results confirmed microscopy (mycelium).


Differential diagnosis

Differential diagnosis is performed erythrasma (lesions do not extend beyond the groin, under the
Wood's lamp - korallovokrasnoe light); intertrigo, candidiasis of skin folds (whitish coating, eroded
land); psoriasis skin folds (swollen, bright red patches).

Treatment

In acute inflammation using 1% 1% spray or creams terbinafine, naftifine, bifonazole, ketoconazole,


miconazole, sertaconazole and other antifungals.

When failure of external agents inside terbinafine administered at 250 mg daily for 14 days or 200
mg of itraconazole per day for 7 days.

Counseling

Patient is informed about the need to address the factors contributing to the emergence of the
disease. Should apply powder with antifungal agents in areas of former eruptions, disinfect
underwear and bed linen (machine wash and iron stroking

29. Fungal infections of the scalp. Epidemiology, differential diagnosis.


Microsporia

Microsporia - the most common mycotic infection after athlete's foot.

Etiology

In Russia mikrosporiya cause mainly 2 exciter: Microsporum Canis (dog), a synonym for - M. lanosum (cat) and Microsporum
ferrugineum (rusty). Other mikrosporumov rare and epidemiological irrelevant.

M. Canis - zoofilny fungus major carriers are cats (especially kittens) and dogs. Human infection occurs through direct contact with sick animals or
through objects contaminated hair or scales containing M. canis; 3-4% contamination with people from each other.

M. ferrugineum - anthropophilic fungus, its carriers are patients with mycosis these people. The infection is transmitted from an infected person
healthy by direct contact or through contaminated objects (combs, hats, clothing, towels, bedding, barber tools, etc.).

Pathogens microsporia on household items, clothing, toys retain pathogenicity than 1 year, in the environment (soil, sand) - more than 1 month.

The incubation period for microsporia caused M. canis, 5-7 days and caused M. ferrugineum, - 4-6 weeks. Fluorescence at the base of the hair in the
glow of fluorescent lamp appears on the 10-12th day, the hair break off after 3 weeks of onset.

Sick more often, young children and students. Overcrowding (kindergartens, schools, nursing homes) facilitates transmission of the disease to others.

The clinical picture

Fungi of the genus Microsporum can affect hair, smooth skin and very rarely - nails. Clinical manifestations of mycosis have features depending on the
causative agent.

When microsporia caused M. canis, on the hairy part of the head are usually formed by 1 or 2 (sometimes more) of large hearth diameter of 3-5 cm
and over, round or oval, with clear boundaries, pink in color, covered with grayish scales. In the hearth of all affected hair broken off at 5-7 mm (Figure
5-16). On the periphery of these large lesions detected many small, with a diameter of 0.1 to 0.3 cm may occur infiltrative and even suppurative forms
of the disease.
Fig. 5-16. Microsporia scalp

On smooth skin lesions are located more in the open, but often closed parts of the body, 0.5-1.5 cm in diameter, round or oval, from pink to bright red in
color, with clear boundaries. On the periphery of the surface is covered with scales, bubbles and thin crusts, in the center reveal defurfuration. Within
the lesions may occur perifollicular nodules red. Sometimes multiple lesions lesions coalesce to form irregular shapes lesion (Figure 5-17). In this form
microsporia often amazed eyebrows and eyelashes (Fig. 5-18). The majority of patients involved in the process of vellus hair.

Fig. 5-17. Microsporia smooth skin. Multiple foci

Fig. 5-18. Microsporia smooth skin and eyelashes

When microsporia called M. ferrugineum (fungus most contagious of all tinea) on the hairy part of the head deep pockets, usually small, multiple,
irregular shapes. When tendencies to merge and can form large foci (up to 5-7 cm in diameter), sometimes exciting to 1 / 3 of the scalp. Small foci are
located mostly in the marginal zones of the Taking of adjacent sections of smooth skin. On the head can be one large area with multiple small lesions
centers around. Inflammatory effects are not expressed. Affected skin pale pink or changed. In outbreaks has slight peeling. Affected hair break off and
not all at different levels (usually 6-8 mm). Sometimes imperceptible inflammation and destruction of land can be detected only when viewed from a
patient with a fluorescent lamp.

On smooth skin lesions frequently observed single round, in the center of the skin has a normal color, and on the periphery arises congested roller.

In some patients the lesions represent a ring consisting of bubbles, nodules and crusts, one inscribed in the other (Figure 5-19). May be affected by
vellus hair.

When microsporia sharp deterioration in cases of basic lesions sometimes have allergic rashes - microsporidia as erythematous or lichenoid spots
bubbles and general

Fig. 5-19. Microsporia smooth skin caused by M. ferrugineum

conditions: fever, weakness, loss of appetite, malaise, increase in regional lymph nodes, lymphadenitis, etc.

Diagnostics

Diagnosis is based on clinical presentation, microscopic scales, hair (mycelium), greenish glow hair under a Wood's lamp, the identification of the
fungus on Sabouraud medium.

Differential diagnosis

Differential diagnosis spend with seborrheic dermatitis, psoriasis, neurodermatitis limited form, alopecia areata, discoid lupus erythematosus; with
suppurative form - with furuncle, carbuncle; trichophytosis, favuse.

10 . Tinea pedis : pathogens , diagnosis , clinical forms , treatment and prevention .

Tinea pedis

Tinea pedis - an umbrella term that includes fungal infection of the skin and nails of feet. Defeat stop often causes Tr. rubrum (70-75%), less often
- Tr. mertagrophytes interdigitale (18-19%), Epidermophyton floccosum (2-3%), yeast-like fungi of the genusCandida, fungi (7-8%).

Place primary localization pathogenic fungi in tinea pedis - interdigital folds. With the progression of the process rashes go beyond them.

Defeat stop at various kinds of fungus clinically occurs almost the same way.

Etiology

Most often defeat feet and nails caused by fungi Tr. rubrum and Tr. mentagrophytes interdigitale. penetration of fungi in the epidermis contributes to the
violation of his integrity as a result of microtrauma, diaper rash, scrapes, excessive dryness or excessive sweating. Background for the development of
infection - endocrine disorders, immunodeficiency disorders, circulatory disorders, trophic tissue stop.
Spread of athlete's foot is basically promotes the visiting public baths, saunas, showers, especially in industries (mines, metallurgical plant, etc.),
swimming pools, etc.

The clinical picture

There are several clinical varieties of athlete's foot. Worn form - beginning mycotic process. Celebrating slight peeling interdigital folds, often -
between IV

and V toes, sometimes small surface cracks. Subjective disorders are absent.

Squamous form is manifested by small peeling of scales in the interdigital plate folds, as well as on the lateral surface of the sole (Fig. 5-
8). Sometimes there is congestion specified locations and tingling.

intertriginoznaya form - affected interdigital folds, often - between III and IV, IV and V of the toes. In addition to diaper rash, redness present, edema,
maceration, moknutie, frequent erosion and cracks, accompanied by itching, burning, pain (Figure 5-9).

Fig. 5-8. Mycosis stop squamous form

Fig. 5-9. Mycosis stop intertriginoznaya form

disgidroticheskaya form - on the arch of the foot there are numerous bubbles and bubbles with thick cap. Eruptions seize vast areas of the soles,
interdigital folds of skin and fingers. Fused multi-chamber formed bubbles in their showdown - wet erosion pink-red color.Arise hyperemia and edema
of the skin (Figure 5-10).

Fig. 5-10. Mycosis stop disgidroticheskaya form

Inflammatory process gradually fades away, formed three zones:

Central - smooth skin pinkish-red color with a bluish tint, and a few thin scales;

average - numerous erosion separating scant serous fluid, redness, swelling;

Peripheral - vesicles and multi-chamber bubbles, bubbles.

There are features of the clinical picture, depending on age. Aggravation and exudative clinical manifestations characteristic of the young and middle-
aged, monotonous for dry skin - for patients of elderly and senile age.

The acute form of athlete's foot. Aggravation expressed or intertriginoznaya disgidroticheskaya athlete's foot can lead to the development of the
acute form, considered as a manifestation of severe sensitization to fungi pathogens: grow exudative phenomena, leather feet and legs becomes
sharply giperemirovanoy and edematous. Against this background, you can see numerous vesicles and blisters with serous and sero-purulent
contents. Their opening leads to the merging of erosions. Maceration in the interdigital folds goes beyond them, there are erosion, cracks. On the
hands, body, face possible allergid as swollen spots, papules, vesicles. Increased body temperature, developing bilateral pahovobedrenny
lymphadenitis, lymphangitis. Subjectively, weakness, headache, difficulty in walking.

hyperkeratotic form - Dry flat papules, plaques nummulyarnye lihenifitsirovannye slightly reddish color on krasnovatozheltovatogo arch of the foot
(Fig. 5-11). Surface lesions, especially in the center, covered with various thicknesses layering grayish-white scales, their boundaries clear. On the
periphery - curb exfoliated epidermis, individual bubbles. Eruptions merge, forming serpiginiruyuschie diffuse, large-sized pockets, exciting the entire
sole, sides and rear feet. Along with scaly patches occur hypertangent

ratoticheskie education by type of limited or diffuse callus yellowish with cracks on the surface. Subjectively - dry skin, mild itching, and sometimes
painful. Giperkeratoticheskaya form is often associated with squamous - squamous giperkeratoticheskaya.
Onychomycosis (onychomycosis). Normally fungi penetrate the nail plate from the centers of fungal infection of the interdigital folds feet
soles. However, allow the possibility of the development of isolated onychomycosis when driver is embedded in the nail plate from her distal, lateral,
proximal edges or directly through the dorsal surface (Fig. 5-12). Russian mycologists distinguish 3 types of onychomycosis: normotrofichesky,
hypertrophic, oniholitichesky (atrophic).

- Normotrofichesky type: changes only painting nails - in the distal appear spots and stripes, varying in color from white to yellow ocher (Figure 5-
13). Then the entire nail changes color, shine and keeping unchanged thickness.

- Hypertrophic type: a color change joins growing subungual hyperkeratosis. Nail loses luster
becomes dull, thickened and deformed, partially destroyed laterally (Figure 5-14). - Oniholitichesky (atrophic) type: dull brownish-gray, dirty-gray color
of the affected part of the nail, it atrophy and exclusion from the bed (Fig. 5 - 15). Exposed portion is covered with layers of loose
giperkeratoticheskaya. Proximal portion of the long-term remains unchanged.

Features of current fungal infections in children

The disease is practically does not occur in young children.

Fungal infections diagnosed stop from about 3-5 to 10-13% of school-age children and increase progressively in

boys and girls aged 15-18. Variability in the frequency of infection tinea pedis children is primarily due, anatomical and physiological characteristics of
their skin, peculiar to each age.

Boys are sick more often than girls (this helps the swimming pools, showers, gyms, more frequent use of rubber boots).

Diagnostics

Diagnosis is based on clinical lesions of skin, nails, laboratory data and microscopic cultural studies to identify the type of fungus.

Differential diagnosis

Differential diagnosis is performed with traumatic nail psoriasis, eczema, lichen planus, a disease Reiter onihopatiyami.

With the localization of the feet, hands differentsruyut disease eczema, congenital hyperkeratosis.

Treatment

Worn form:

- Use of any acceptable dosage forms: solutions, sprays, creams, ointments containing naftifine, terbinafine, ketoconazole, ciclopirox,
sertaconazole. Preparations applied to the cleaned and the dried skin, 1 per day, duration of treatment is an average of 2 weeks. It is possible to
alternate the application of the solution, lotions and ointments;

- antimycotics isoconazole econazole, ciclopirox, miconazole applied 2 times a day until resolution of clinical symptoms, then treatment was continued
for another 1-2 weeks, but one time a day;

- obsolete treatments include lubrication interdigital folds 2% iodine solution or liquid Castellani (fukortsin) in the morning and 5.10% sulfur-salicylic
ointment - evening.

squamous giperkeratoticheskaya form:

- to remove the horny layers can be applied to the soles of 5-10-15% salicylic vaseline at night under the wax paper to completely remove the horny
masses;

- more effective detachment on Arievich: on the soles on the 2 days in the hospital and at home - at night for 4-5 days

for poultice is applied successively ointment containing salicylic acid (12.0), lactic acid (6.0) and petrolatum (to 100.0);

- easy to use milk-salicylic collodion (lactic and salicylic acid 10.0 to 100.0 collodion), which lubricate the soles of your feet in the morning and evening
for 7 days, then at night under a compress applied 5% salicylic vaseline, do morning foot soap-soda baths and peeling of the epidermis is removed
poskablivanii pumice. Later transferred to these antifungal creams, ointments.

intertriginoznaya form:

- apply sprays terbinafine cream diflucortolone + isoconazole zinc paste. After removing the diaper rash, maceration, epithelialization cracks apply
conventional antifungals external actions (naftifine, terbinafine, etc.).

disgidroticheskaya form. Acute form:

- acute inflammation of the skin of feet (disgidroticheskaya form, acute form) treatment is carried out as eczema. As hyposensitizing therapy
administered one of the solutions was: Calcium chloride (10%), sodium thiosulfate (30%) intravenously, calcium gluconate (10%) intramuscularly; one
of antihistamines (Chloropyramine, mebgidrolin, ketotifen, cetirizine, loratadine, desloratadine, levocetirizine - from the age of 2 years in the form of
droplets);
- exterior of drugs used lotion with a boric acid solution (2%), resorcinol (2%), silver nitrate (0.25%) 0.01 *% miramistina etc. When bacterial infections
occur designate trays with potassium permanganate solution (1:6000), soda baths (1 tablespoon per 200 ml of water). Crusts removed, bubbles reveal
sterile scissors and treated lesions water solution of 1% methylene blue or brilliant green.Then apply boric Naftalan paste kremgel Aysida *. You can
assign spray terbinafine;

- it is expedient to use formulations having, besides an antifungal, antiinflammatory, and (or) an antibacterial action: creams diflucortolone +
isoconazole, isoconazole, hydrocortisone + neomycin + natamycin, naftifine, terbinafine, bacitracin, neomycin + (in the form of a powder or an
ointment), etc.

Treatment of onychomycosis

Causal treatment - the only effective treatment for fungal nail infections. Distinguish local, systemic and combination therapy.

Advantages of local therapy - no side effects and toxic effects observed with systemic drugs as topical antifungals are not absorbed into the systemic
circulation.

Indications for local therapy:

distal-lateral form of onychomycosis;

white surface (initial stage);

defeat than 1 / 2 of the nail;

mild subungual hyperkeratosis;

defeat 1 or 2 nails.

The disadvantage of local therapy is that the drug when applied to the surface of the nail plate is not always reaches the fungus in the nail bed
positioned and (or) in the matrix. In the latter case, local media treatment is ineffective, and to take stock of the drug to the infected box is necessary to
resort to the destruction of the nail plate - use keratolytic patches, removal of the nail plate by mechanical means.

It is most convenient for this purpose use devices with different particle c mills that enables you to painlessly remove the nail for 10-15 min.

There is a set for the removal and treatment of nails - bifonazole. Active substance in it is bifonazole - imidazole derivative having a broad spectrum of
activity on dermatophytes, molds, yeast-like fungi. The kit includes a 1% ointment in a tube at 10.0 g with dispenser, waterproof plasters and
scraper. Ointment has keratolytic action (procedure takes 10-15 days). Subsequently, the cream is applied to 1% bifonazole for 4-6 weeks.

The most effective and convenient means of proper treatment of onychomycosis - lacquers ciclopirox, amorolfin. They can be used without having to
remove the nail or making it partially.

Effective in treating onychomycosis naftifine 1% solution. It is active against dermatophytes, fungi of the genus Candida and most fungi, and has a
pronounced anti-inflammatory effect, also provides local bactericidal effect on gram-positive and gram-negative bacteria, which provides warning
complications foot mycoses pyoderma, microbial eczema, erysipelas.

Topical therapy is continued until complete recovery shaped configuration, the transparency and surface smoothness of the nail. The course of
treatment - 4-6 months.

Systemic therapy. Through the introduction of modern antifungals in therapy became possible to achieve high efficiency in the treatment of
onychomycosis.

Indications for systemic therapy:

distal-lateral form of onychomycosis (late stage);

proximal and total form of onychomycosis;

defeat over 1 / 2 of the nail;

involvement in the matrix;

pronounced changes in the nail (hyperkeratosis, onycholysis);

2-3 defeat nails;

inefficiency of local therapy;


combination of onychomycosis with common skin lesions or hair.

The effectiveness of systemic therapy is determined by the flow characteristics of onychomycosis, clinical and etiological indications schemes,
adequate for a specific case of onychomycosis, treatment of comorbidities (diabetes, varicose veins, obliterating endarteritis, etc.).

Of systemic antimycotics in the treatment of onychomycosis is most often used terbinafine and itraconazole.

The duration of treatment depends on the rate of regrowth of different nails and their growth - from the patient's age.

30. Viral dermatoses. Etiology, classification, diagnosis, treatment principles.

Dermatoses * viral etiology constitute a fairly large group of skin diseases and common. These include
herpes, warts, molluscum contagiosum, genital warts. Among adults viral skin diseases constitute 3-4% of
children (usually aged 5-8 years) - to

* Chapter "Viral dermatoses" written by Dr. A.A.Kubanovym Medical Sciences.

9.5% of dermatoses. Despite the fact that the virus infection can occur in utero, at birth or in the first days of life, the
disease does not develop, since the mother's blood come antiviral antibodies that the body creates in the fetus and
child passive immunity. By the beginning of the 2nd year of life, immunity wanes, so maybe the development of viral
dermatoses. Numerous pathways virus: through the skin, infected objects, mucous membranes (sexual contact with
patients or virus carriers, kissing), airborne. When lowered immunity incubation period varies from a few days to 2-3
weeks.

17.1. Herpes Simplex

Herpes simplex (herpes simplex), or herpes, the most common.

Infections caused by herpes simplex virus (HSV), are known to mankind since ancient times. The name "herpes" is of
Greek origin and means "crawl", "creep up." According to the Center for Disease Control in the U.S. registered 500
000 new cases of herpes infections per year, and reported the news media, such infections amazed 2-20 million
Americans. In the UK, genital herpes infections are significantly higher than other infections, sexually transmitted
diseases. This infection is common in Scandinavia, where it was detected in 8% of women attending sexually
transmitted infection clinics. Unfortunately, cases of herpes are not registered in the country, although this disease is
spread widely, and can lead to serious complications, including death.

Etiology and pathogenesis. By herpes viruses include four morphologically similar virus: HSV
virus, varicella zoster - the causative agent of varicella zoster virus, Epstein-Barr virus and cytomegalovirus.

There are two serotypes of HSV. Contact with HSV-1, according to the serological tests happens to the 18th month of
life in almost all people. After initial contact with an organism virus falls into it, usually via the respiratory tract, enters
the trigeminal ganglion cells where it may be stored in latent form indefinitely, sometimes for life without causing
clinical symptoms. In France, 60% of patients older than 50 years Serop transitively to HSV-1 and 15% - to HSV-2.

The first contact with HSV-2 usually occurs after puberty in early sexual activity. After primary infection, the virus
displays, as well as HSV-1, enters into an inactive form and is localized in the sacral ganglion cells, and is able to
persist in a latent form there indefinitely.

In both cases, some, often directly opposite conditions (hypothermia, overheating, colds, stress, HIV carrier, etc.)
both viruses can be reactivated, causing recurrent infections.
HSV-1 usually causes a rash around the mouth, lips, kerato-conjunctivitis, and HSV-2 - rashes in the genital
area. sexual behavior can also lead to the opposite phenomenon, when HSV-1 is found in the outbreaks on the
genitals, and HSV-2 - in the outbreaks on the face.

Very important is the fact that HSV has oncogenic properties, especially HSV-2.

The disease is seen in both sexes and all age groups. Several distinct clinical forms of herpes simplex, different
localization, severity, propensity to relapse.

The clinical picture. Elements herpes simplex localized around the orifices: the wings of the nose, in the corners of
the mouth, on genitals and red border of lips (herpes labialis) (Fig. 52). First, at one place, at least two or more limited
amid hyperemia appear small diameter of 1 to 3 mm vials. Each locus from 2 to 10 and more bubbles (Figure
67). Bubbles within the group, contain a clear fluid, which becomes cloudy after 2-3 days. Sometimes as a result of
the merger of small bubbles formed one or two multi-bubble diameter 1-1.5 cm with scalloped contours. If bubbles
are not subjected to friction or maceration, further shrinking their contents yellowish-gray crust that disappears after
5-6 days, leaving a slightly hyperon remirovannoe or pigmented spot. On the skin

Fig. 52. Herpes simplex (localization on the lips - herpes labialis)

subject to friction, maceration, and on the mucous membranes and vesicles opened erosion formed a bright red color
with polycyclic contours. Rash accompanied by a feeling of bubbles tingling, burning, pain, in some cases, severe
swelling of the surrounding tissue.Overall condition is usually not affected, although some patients report malaise,
muscle aches, chills. Body temperature may rise to 38-39 C. On average, the entire process completed within 1-1.5
weeks, but the duration of the disease increases with few complications secondary infection.

Herpetic stomatitis is one of the species herpes simplex. Common rashes bubbles appear on the mucous
membranes of the lips, cheeks, on the gums, palate. On the background of edematous and hyper-renormalized
mucosa there are small groups of bubbles, which opened in the wee hours of the occurrence. In their place are
wrong erosion melkofestonchatymi outlines. 2-4-day erosion of delicate fibrinous film. 6-14 days, and sometimes
later, epithelialization occurs erosions. Patients complain of pain, increased salivation.

Acute herpetic (acute aphthous) stomatitis diagnosed in children under 6 years. The disease begins suddenly, often
with prodromal phenomena as malaise, weakness, fever. Edematous and congested on the oral mucosa lesions
arise aftopodobnye diameter of 0.5 to 1 cm Unlike conventional herpes sores have views of the AFL with necrosis in
the center and a pronounced inflammatory rim around the periphery. Eruptions first isolated, which gives them an
even greater resemblance to aphthae, but a large number of merge, forming extensive erosive and ulcerative
areas. Process is accompanied by profuse salivation and severe morbidity.

Herpes simplex is a kind of recurrent herpes. Relapses can occur at different frequencies and in different seasons. In
some patients, relapses are 3-4 times a month and the disease becomes permanent. Recurrent herpes in clinical
manifestations are not different from herpes simplex.

In the pathogenesis of recurrent herpes important role belongs to the predisposing factors that reduce cellular
immunity - overheating and overcooling, infectious diseases, especially colds, severe general diseases in the first

vuyu all leukemia, cancer, etc. The women of recurrent herpes is often linked to the menstrual cycle.
Diagnosis is not difficult for a typical clinical picture and localization.

Herpes simplex genital sometimes may have some clinical similarities with chancre, but unlike herpes chancre
erosion has polycyclic outlines eruptions consist of individual fused small erosions, located on the grounds without
inflamed infiltrate characteristic chancre.Unlike syphilis for herpes acute, often recurrent. In doubtful cases resort to
the study of erosion on discharge acyanotic.

Herpes on the oral mucosa type herpetic stomatitis should be differentiated from exudative erythema multiforme and
pemphigus vulgaris. When erythema multiforme exudative unlike herpes recurrences a marked seasonality (spring
and fall); against the background of sharply hyperemic and edematous mucosa of the mouth appear large bubbles
that quickly opened. On-site erosion revealed the bubbles are irregular shapes, covered with dense fibrinous film. On
the red border of lips Filter bubbles rapidly shrinking in massive bloody crusts. Profuse salivation noted, eating
difficult. When pemphigus vulgaris erosion located on apparently did not change in the membrane, they are not prone
to epithelialization, positive Nikolsky sign in smears from the surface erosions detected acantholytic cells.

To confirm the diagnosis of herpes simplex can be used cytological. Study scraping spend the first 2-3 days after the
appearance of bubbles. When staining with Romanovsky-mu-Giemsa revealed giant cells with basophilic cytoplasm,
nucleus and having 3-4 more.Nuclei are arranged densely, stratifying on each other, giving the impression of a
conglomerate. Sometimes, the kernel does not have clear contours due to poor staining.

PCR is the most sensitive for the detection of HSV DNA. There is a set of PCR primers HSV-1 and HSV-2, but this
method requires expensive special equipment.

Treatment. Externally applied alcoholic solutions of aniline dyes, including fukortsin, an ointment containing the
antiviral agent: 3% oxolinic 3-5% tebrofenovuyu (Zovirax, acyclic

sup). Good therapeutic effect was observed in cases of early (in the first 4-5 h) the use of drugs. Leukocyte interferon
solution is applied to the lesion 6-7 times a day.

Much more difficult to treat recurrent herpes. To prevent recurrence necessary to increase cell-mediated
immunity. Herpetic polyvalent vaccine administered intradermally by 0.1-0.2 ml in the outer surface of the shoulder
with an interval of 2-3 days; the course of 10 injections. Several smaller therapeutic effect is dezok-siribonukleaza
(DNase), which is administered by intramuscular injection of 10-25 mg, powder dissolved in distilled water or isotonic
sodium chloride solution. Injections made in a day; the course of 6-10 injections. Pronounced therapeutic effect in
relapsing forms of herpes has acyclovir (Zovirax, viroleks), which is prescribed from the first day of relapse into 200
mg 5 times a day for 5 days, along with the 5% ointment Zovirax, which lubricate the lesion 6 times a day.

Prevention. prevention of recurrences of herpes in a certain role to play media, enhances immunity.

17.2. Shingles

The disease causes neurotrophic filterable virus that antigenic structure and ability to develop human
embryonic tissues similar to varicella or identical to it. Cases children varicella after contact with patients with
herpes zoster and herpes zoster disease adults after contact with children, those suffering from chickenpox confirm
the closeness of these strains. Finally, there is the observation that the disease begins as a typical shingles,
chickenpox is transformed into, spreading over the skin of the trunk and extremities.

Distinguish the following clinical types:


- Generalized shingles (herpes zoster generalisatus, disseminatus) at bilateral and generalized rash;

- Hemorrhagic lichen when first transparent content bubbles becomes purulent, and a deeper propagation process in
the dermis - hemorrhagic (herpes zoster haemor-rhagicus), then remain scar changes;

- Gangrenous form, the most severe in which develop necrotic changes bottom bubbles and deeper layers of the
skin;

- Lightweight (abortive) form;

- Bullous with the advent of large bubbles.

After an incubation period (7-8 days) dermatosis group manifested rash bubbles, which are located on the hyper-ated
a background on the skin to one or more neural segments (Fig. 53). Eruptions are preceded by paroxysmal pain
radiating along the nerve trunks, burning, redness of the affected sites, weakness, fever, headache.

Bubbles appeared tense, with clear serous content, up to 1 cm in diameter after vesicle fusion formed lesions with
melkofestonchatymi edges. Layout unilateral, patients complain of intense pain in the neuralgic type rash and far
beyond. Elderly pain can last for months or even years after the disappearance of skin rashes.

With the defeat of motor and sensory fibers of the VII cranial nerve sometimes develops so-called Hunt syndrome,
including herpes zoster, facial paralysis and pain in the ear with the hearing loss. It should be borne in mind that the
pain of herpes zoster usually increases sharply with little friction lesion dress and even with a light touch to the
affected area. Intensity of subjective feelings do not always correspond to the severity and distribution of skin
cells. Soreness is stronger, for example, herpes zoster, in the first branch of the trigeminal nerve (Fig. 54). Since
painful

sensation often 3-5 days ahead of the clinical manifestations in the skin, there are cases of herpes zoster mimicking
acute appendicitis, cholecystitis, myocardial infarction, etc.

Shingles can be located anywhere on the skin, ie can affect any nerve. Favourite localization - the scalp, forehead,
eye area and other parts of the face, neck and occipital region, chest, abdomen, shoulders, thighs and buttocks.

Isolated lesions of the oral mucosa is rare, it is one-sided, what distinguishes the simple herpes zoster. Rash
accompanied by neuralgic pains that often precede eruptions. Bubbles can be placed on the mucosa of the sky,
cheeks, lips, tongue.

The big danger is the localization process in the eye (herpes zoster ophtalmicus), conducting sometimes to ulceration
of the cornea and Panophthalmitis. Other serious complications are paresis of the trigeminal or facial nerve, hearing
impairment. The disease may be complicated by meningitis (herpes zoster meningitidem), encephalitis.

Manifestations of viral infections contribute to infectious diseases, immunodeficiency, intoxication, metabolic


disorders, diseases of the blood, cooling injury. Process occurs more often and is exacerbated in cold seasons
(spring and autumn). Meeting in persons of any age, shingles rarely in young children.

In frail or persons suffering from a serious illness may be gangrenous form, in these cases, on-site rash ulcers are
formed, leaving scars.
Shingles usually leaves behind immunity; relapses were not observed. However, patients with severe diseases of the
sharp decline in immunity (cancer, leukemia, AIDS), there may be recurrent and generalized form of the disease.

Diagnosis is based on the pain along the nerve branches in conjunction with grouped herpetic vesicles on an
erythematous edematous background, arranged linearly in accordance with the location of neural structures.

From a simple bubble stripping and erysipelas shingles different radiating pain sensations that precede and are often
associated with rashes, as well as the linear arrangement of grouped vesicles on neural segments.

In the diagnosis of herpes zoster, often accompanying immunodeficiency, you must make sure that the patient is HIV
positive.

Treatment. When administered mild course of acyclovir into 800 mg five times a day for 7-10 days or famciclovir 250
mg three times a day for 5-6 days. In severe acyclovir introduced in / at 5-7.5 mg / kg every 8 hours for 4-7
days. When starting the secondary infection or to prevent it displays broad-spectrum antibiotics. When pain
Recommend paracetamol 500 mg 3-4 times a day, indomethacin at 50-150 mg / day or 800 mg ibuprofen two times a
day. Locally shows the same means that the treatment of herpes simplex 3% vidarabinovaya ointment, aniline dyes,
antibiotic ointment, and lotion klokvinolom.

Rp: Cloquinoli 2,0 Zinci oxydi 20,0 Talci aa 20,0 Glycerini 85% 30,0 Aq. destillatae ad 100,0 MDS Outside

17.3. Warts

There are simple (verrucae vulgaris); flat or youth (verrucae planae s. juveniles); genital (genital
warts); plantar warts.Pathogen - certain types of human papillomavirus (HPV). Affects people of any age, but
most often the first two varieties of children and young people. Contagious disease.

Simple warts caused by HPV-2 and HPV-3, localized mainly on the hands, but can appear on the face, the red
border of the lips, especially near the corner of the mouth, they are rarely on the oral mucosa. Simple wart is a bundle
diameter of 1 cm, significantly above the surface of the skin, grayish, gray-brown and flesh-colored, dense
consistency. On major long-existing wart usually have papillary growths with keratinization on the surface (Fig. 55).

Flat, or youth, warts, caused by HPV-3, occur more frequently in children and young adults. These nodules are up
to 3 mm in diameter with a flat, slightly protruding above the skin surface

completely, often polygonal shape. The color is not always different from normal skin, but sometimes have a pink or
brownish tint, often localized on the back of hands and face. With abundant rash on the face and they are often on
the red border of lips.Sometimes patients complain of a little itchy.

Palmar-plantar warts are localized only on the palms and (mostly) on the soles. Keratotiches distinguish deep-Kuyu
variety of HPV-1, and the surface (HPV-2 and HPV-4). Deep pockets of species appears painful hyperkeratosis
rounded, 1 cm in diameter or more.These warts occur almost exclusively in the field of pressure, mostly shoes. The
number of elements thus can be varied, there are several more warts. The central part is relatively easy to manage
warts removed mechanically, and then found a few papillary wet surface with a soft consistency, she remains tight
circle horn ring.

Surface species painless years there as diffuse lesions hyperkeratosis, reminding callus.
The diagnosis is easy to install. Sometimes you have to differentiate with lichen planus, in which the papules are
waxy luster pupkoobraznoe indentation in the center, purple-red color and cause itching. When warty lupus marked
inflammatory infiltrate and reddish-purple corolla around the periphery of the lesions.

In recent years, for the diagnosis of HPV infection using a signal amplification method, which is based on system

double gene trap - Digene Hybrid Capture System II (HCS-II). With this method, a highly specific carcinogenic HPV
types detected (16, 18, 31, 33, 39, 45, 51, 52, 56, 58, 59, 68) and low-risk types (6, 11, 42, 43, 44). 16th type of virus
detected in 50-70% of cases of cervical cancer.

Treatment. prescribe antiviral ointment 3% oksolinovuyu 5% tebrofenovuyu 0.5% bonafton-finance, information and
5% ftoruratsilovuyu,

Fig. 55. papillomavirus infection

20% podophyllin solution, 10-15% solutions of lactic and salicylic acids. In refractory cases shown intralesional
administration of interferon 1.5 million IU a day (only 6-8 injections). Good therapeutic effect give cryotherapy and
electrocautery, cauterization ferezolom, drug solkoderm.

The expediency of using common in patients with relapsing forms of infection and recombinant interferon (Intron A).

Genital warts (condylomata acuminata) caused by HPV-6 and HPV-11. This education testovatoy consistency with
lobed structure, shaped like a cauliflower or cockscomb, located on a narrow base (leg), first diameter of 2-3
mm. Warts are skin-colored or pink, with maceration of the surface becomes bright red and bleeds easily
traumatizing. Growing, they can form extensive conglomerates. Genital warts are often located in the genital area - in
the coronary sulcus on the inner layer of the foreskin in men at the entrance of the vagina, near the anus - in
women. In children, they occur in nososchechnoy or nasolabial fold.

Treatment with single elements usually surgery (electrocautery, cryosurgery, excision). With the spread of prescribed
Zovirax (acyclovir) inside ointment 20-25% beneath-Fellini, 5% fluorouracil solkoderm.

17.4. Molluscum contagiosum

Called the largest virus filter - Molitor hominis, infectivity has been proven experimentally. Transmission occurs
through direct contact with infected or virus-co-support, as well as through contaminated objects of care, bath,
swimming pool, household items.Most sick children. In groups of children observed outbreaks. The incubation period
ranges from 2 weeks to several months.

Clinical manifestations. nodules ranging in size from 1 to 8 mm, normal skin color or pearl-gray ("pearl"),
hemispherical shape with a crater-like impression in the center and cheesy contents. It microscopically determined
degenerative epithelial shiny oval cells with large inclusions protoplazmatiches-Kimi (shellfish calf). Subjective
feelings

absent. Nodules can be either single or multiple (disseminated clams).

In children, nodules are localized mainly on the face (in a circle eyes), neck, chest, back of hands, adults - often on
the external genitals, pubic area, and skin of the abdomen, indicating that the sexual route of infection.
There are several clinical variants of molluscum contagiosum: Molluscum contagiosum miliare as multiple small
lesions, Molluscum contagiosum pediculatum - Clam nodules sitting on legs. At the confluence of individual nodules
formed giant clams.

Diagnostics. Pressing on the knot at the sides of the central part of the tweezers out pappy white curdled mass,
consisting of dead cells and special shellfish (ovoid) cells. Warts do not have central depressions and pearlescent
paint surface.

Treatment - squeezing with tweezers or sharp spoon scraping followed lubrication 5-10% alcoholic solution of iodine,
diathermy, cryotherapy.

31. Pediculosis. Classification, diagnosis, treatment.

Lice or lice - a contagious disease caused by a parasite on the body of three types of
lice.Danger lice that insects can be carriers of some serious diseases - typhus or relapsing
fever.

Causes of head lice

Pediculosis cause three types of lice:

Head lice live on the scalp, mustache, beard, eyebrows and eyelashes,

lice, live on television and in skin folds concerning garments

ploschitsy or pubic lice, live in pubic hair.

Lice can reproduce only in conditions of heat, cooling below 15-10 degrees, they die.Pubic
and head lice lay nits on the basis of hair lice lay eggs in the folds of clothing.After a week of
them hatch into larvae, which mature and feed on blood.Adults live up to 40 days.

Methods of infection

The source of infection - the only person transmission of lice carried by close contact in
organized groups, public transport, using common things and bed for pubic lice - infection
through sexual intercourse.

Widespread incidence of head lice, especially the chances are high in countries with low
health culture.The incubation period is about a week in lousy, the intensity of symptoms
depends on the degree.Manifestations biting lice arise because the skin of the head or body,
whereby the symptoms of lice arise.
Photo: head lice and pubic lice

Symptoms of head lice

Head lice

- Manifested by intense itching in the head, causing the patient is constantly scratching his
head.

On examination of the scalp identify areas of skin damage at the site of bites with bright
yellow "honey" crusts, as well as signs offolliculitis- inflammation of hair follicles,
ekzemopodobnye skin lesions on his head, at the temples and behind the ears.

Can be detectedlymphadenitisof the ears and neck.With long-term neglect and lice formed
mats of hair, matted and glued purulent wounds.

Patients with head lice when viewed head on the hair can be found nits - eggs laid by
insects.They can be full, whitish or yellowish, crush between the nails they click.Empty nits
appear gray.

http://diagnos.ru/diseases/parasit/pediculosis
Hanging pediculosis
- Affects the fate of the skin under the clothes on their shoulders, back, underarms, neck and
abdomen, lower back and groin.

On-site there are small bites rash type of mosquito bites with a dark dot in the middle.With
the development of elements arises their cyanosis, pigmentation, and often because of
scratching join pustular lesions.

Long duration wardrobe lice leads to thickening of the skin and melasma (brown color), on
the ground peeling bites.On-site septic and scratching lesions formed scars.

Pubic lice

If pubic lice worried little itchy skin, bites occur on the ground round or oval patches of gray-
blue color size to 1 centimeter.When pressed on these spots, they fade
dramatically.Ploschitsy have low mobility, they may be found in the hair root.

Diagnostics

Diagnosis and treatment carries a dermatologist.Basis of diagnosis - the typical complaints


of itching and scratching on the head, body or pubic skin.First, examination is conducted of
the head, body and groin.Find nits on the head and scratching the bite.In other cases, the
typical clinical data.

Head lice can be combed over a sheet of white paper for other diagnosis - Clinical.

Differential diagnosis

Lice must be distinguished frommange, which is also manifested by itching skin and
vulgarimpetigo, strep skin lesions.

Lice Treatment

Lice treatment is carried out at home, and certainly all the contact persons.Tools are used to
kill lice and nits in different forms - shampoos, sprays, lotions and emulsions.

If head lice are applicable:

trim the hair nalyso

combing lice and nits special comb antiv,

shampoo or lotion malathion 0.5-1%

drugs permethrin (nittifor, para-plus chloride, sumitrin, phenothrin)

20% water-soap emulsion benzyl,

boric ointment

Pedilin.

When pubic lice are applicable:


shaving pubic hair

treatment of skin and hair medifoks emulsion 20%

treatment of benzyl benzoate 20% emulsion,

lontsida solution followed by a dip and a change of clothes.

spray solution-pair-plus spray-pax.

When the wardrobe base lice treatment - treatment of all things and a thorough body wash
in the shower with soap and a washcloth.Clothes and accessories patient boiled or steamed,
failing treatment temperature - is placed in a tight package using aerosols
protivopedikuleznyh means - (malathion, sulfidos).

Remedies for lice

Permethrin: Carefully wipe the scalp undiluted drug, wait until dry hair (do not wipe or
wash).After 2-3 weeks the hair washed, dried and if necessary, re-treated

Shampoo Reed applied to the affected area for 10 minutes, then washed with a conventional
shampoo or soap.A hair treatment was carried out for 10 days

Shampoo Anti-Bit: hair is wetted with water, the drug is applied and rubbed into the roots of
the hair for 3 minutes, then washed and the procedure repeated.A second course - only for 2
days

Phenothrin (Ithaca) lotion is applied to wet hair, rub, then thoroughly rinsed, applied again,
waiting 5 minutes, then carefully washed and hair combed fine-toothed comb.The next day the
procedure was repeated.Aerosol spray on the scalp 20-30 times, waiting 30 minutes, then
carefully washed and combed fine-tooth comb;the next day the procedure was repeated

Note:drugs destroy lice, never used to treat lesions eyelashes!

Lice of the eyelashes and eyebrows are usually removed with tweezers.Lice on the eyelashes
can kill or weaken the simple Vaseline.

Lice Prevention

Should regularly monitor the condition of the hair and body hygiene, avoid casual sex to
prevent pubic lice.In transport, women are advised to remove hair in a ponytail or under
clothing.

Prohibited use other people's hats, hairbrushes and combs, hair clips and rubber bands,
wearing someone else's clothes.

http://diagnos.ru/diseases/parasit/pediculosis
33. Scabies. Epidemiology, diagnosis, treatment.
Mange (scabies)

Scabies - a contagious parasitic skin disease caused by scabies. Scabies - the most common parasitic disease found
in the practice of any profession and patients of any age.

Etiology
Pathogen - Sarcoptes scabiei hominis, itch mite - belongs to the class of arachnids, acariform squad. It is an obligate
ectoparasite of humans, that host Sarcoptes scabiei hominis is only a man and a parasite mite on the skin only, not
gouged.

The life cycle of the mite begins with skin contact person fertilized females, which immediately penetrates the skin (to
the granular layer of the epidermis). Moving forward on the go scabies, female eats the cells of the granular layer. We
mite digestion occurs outside of the intestine using evolved in the course of secret itch, containing a large amount of
proteolytic enzymes. Daily fecundity of females is 2-3 eggs. 3-4 days after oviposition of them hatch into larvae,
which leave through the course "vents" and again in the skin. After 4-6 days of larvae formed adult mature
individuals. And the cycle begins again. Female life expectancy is 1-2 months.

For scabies mites strong emphasis on the diurnal rhythm of activity. Happy female is in a dormant state. Evening and
in the 1st half of the night it gnaws 1 or 2 egg knee at an angle to the main direction of the course and in each of
them lays an egg, pre-deepening bottom stroke and performing in the "roof" "vent" for the larvae. Second half of the
night nibbles move in a straight line, intensive feeding, day stops and freezes. The daily program is executed
synchronously by all females, which explains the appearance of itching in the evening, the prevalence of infection in
the direct path of bed at night, the effectiveness of the application of acaricides in the evening and at night.

Epidemiology

Seasonality - a disease often recorded in the autumn-winter season, which is associated with the highest fecundity of
females at this time of year. Transduction pathways:

direct way (directly from person to person) is the most common. Scabies - a disease of close bodily contact. The
main circumstance in which there is an infection - sexual contact (more than 60% of cases), which was the basis
include scabies in the STI group. Infection also occurs during sleep in the same bed, with child care, etc. The family
in the presence of 1 patient with common scabies infected almost all members of the family;

indirect, or mediated pathway (through the objects used by the patient) is much rarer. The causative agent is
transmitted from sharing bedding, linens, clothing, gloves, sponges, toys, etc. In children's groups indirect
transmission occurs much more frequently than adults, due to the exchange of clothes, toys, stationery, etc.

Invasive stage mite - young female scabies mite and the larva. It is in these stages of the mite is able to pass from
the owner to another person and for some time to exist in the external environment.

In the external environment adults and larvae living no more than 4 days at 22 C and 35% humidity. At 60 C mite
death occurs within 1 hour and at boiling temperature and below 0 C mites die immediately. Eggs are more resistant
to mites acaricidal antiparasitic agents.

The most favorable conditions for the life of the tick is the "master" - fabrics made of natural materials (cotton, wool,
leather), as well as house-dust, wood surface.

Contribute to the spread of scabies if proper sanitation and hygiene measures, migration, population density, as well
as diagnostic errors, late diagnosis, atypical unrecognized form of the disease.

The clinical picture

The incubation period varies from 1-2 days to 1.5 months, depending on the number of ticks that fall on the skin,
stage, where the data mites tendency to allergic reactions, as well as the cleanliness of the person.

The main clinical symptoms of scabies itching at night, the presence of burrows, polymorphism characteristic rash
and localization.
Itch

The main complaint of patients with scabies - itching, worse at night time.

In the pathogenesis of itching in scabies point to several factors. The main cause of itching - mechanical stimulation
of nerve endings in promoting females, which explains the nature of the night itching. Reflex may cause itching.

Also in the formation of pruritus are important allergic reactions that occur during sensitization to mite itself and the
products of its life (saliva, feces, shell eggs, etc.). Of allergic reactions during infection with scabies has the greatest
value delayed hypersensitivity reaction type 4. Immune response, manifested increased itching develops 2-3 weeks
after infection. When repeated infection itching appears in a few hours.

Itching can be regarded as a protective reaction of the organism, since scratching itch moves destroyed and killed a
large number of eggs.

Itch move

Itch move - the main diagnostic symptom of scabies, which distinguishes it from other pruritic dermatoses. Progress
looks slightly rising line dirty gray, curved or straight, 5-7 mm in length. Identify symptom Sezary - palpation detection
burrows as a light elevation.Itch turn ends towering blind end with a female. Itch moves can detect with the naked
eye, if necessary, use a magnifying glass or a dermatoscope.

Upon detection of burrows can be used with a sample of ink. Ink or any solution of the aniline dye process suspicious
area of skin, and a few seconds later erase paint residue with an alcohol swab. Occurs uneven staining of the skin
over the course of itch by getting paint in the "vents".

Polymorphism rash

Polymorphism rash characterized by diverse morphological elements that appear on the skin for scabies.

Most frequent papules, vesicles size of 1-3 mm, pustules, erosions, scratches, purulent and hemorrhagic crust, post-
inflammatory pigmentation spots (Fig. 4-31, 4-32). Seropapuly, or papules, vesicles are formed on the place of
introduction into the skin of the larva. Pustular elements appear when connecting a secondary infection, itchy papules
hemispherical - when limfoplazii.

The greatest number of burrows detected on the hands, wrists, and the young men - and on the genitals (Figure 4-
33).

Polymorphism in scabies rash is often determined by symptom-Ardi Gorchakov - the presence of pustules, purulent
and hemorrhagic
Localization

Characteristic localized rash scabies - interdigital folds of the fingers, the area of the wrist, flexor surface of the
forearm, women - the nipple breast and belly, and men - genitals.

Brush most significant defeat for scabies, as it is here localized principal amount of burrows and formed the bulk of
the larvae, which hands passively spread throughout the body.

In adults with scabies are not affected face, scalp, upper third of the chest and back.

Localized rash scabies in children depends on the child's age and differs significantly from the skin lesions in adults.

Complications

Complications often alter the clinical picture and greatly complicate diagnosis.

Pyoderma - the most common complication, and with the spread of scabies always accompanies the disease (Fig.
4-36, 4-37). Most often develop folliculitis, impetiginoznye elements, boils, ecthyma may develop abscesses,
phlebitis, sepsis.

Dermatitis is characterized by mild, clinically centers erythema with indistinct borders. Often localized in the folds
on the stomach.

Eczema develops in long-existing common scabies and is characterized by torpid course. Most often develops
microbial eczema.Outbreaks have clear boundaries, there are numerous vesicles moknutie, serous-purulent
crusts. Localized rash on the hands (may cause

and bullous elements), feet, women - in a circle nipples, and men - on the inner thigh.

Hives.

Defeat nails reveal only in infants; characterized by thickening and clouding of the nail plate.

Features of the flow of scabies in children

Clinical manifestations of scabies in children depends on the child's age. Features scabies in infants

The process has a generalized, localized rashes all over the skin surface (Figure 4-38). Eruptions pre-

presented small papular elements bright pink color and erythematous-squamous foci (Figure 4-39).

pathognomonic symptom of scabies in infants - a symmetrical vesicular-pustular elements on the palms and soles
(Fig. 4-40, 4-41).

Lack of excoriations and hemorrhagic crusts.

Connection of secondary infection, manifested by patchy erythematous-squamous foci covered purulent crusts.

The majority of infants allergic dermatitis complicated by scabies, torpid to antiallergic therapy.
In a study of mothers of sick children or persons performing basic child care, identify typical symptoms of scabies.

Features of scabies in infants

rash similar to rashes in adults. Characterized by excoriation, hemorrhagic crusts.

Favourite localization lesions - "panty area": abdomen, buttocks, boys - genitals. In some cases remain vesicular-
pustular elements on palms and soles, which are complicated by eczematous eruptions. Face and scalp are not
affected.

Frequent common complication of scabies pyoderma: folliculitis, furunculosis, ecthyma, etc.

Strong night itching can cause sleep disorders in children, irritability, decrease in school performance.

In adolescents, the clinical picture of scabies psoroid adults. Celebrating frequent connection with the development of
secondary infections common forms of pyoderma.

Clinical varieties of scabies typical form

Described the typical form includes fresh and scabies spread of scabies.

Fresh scabies - the initial stage of the disease with incomplete clinical disease. Characterized by the absence of
the skin burrows and rashes presented follicular papules seropapulami. Diagnosis when examining patients exposed
to scabies persons.

The diagnosis of common scabies put in the long course and complete clinical picture of the disease (itching, itch
moves, polymorphism rash with typical localization).

Malosimptomno scabies

Scabies malosimptomno or "worn out", is characterized by mild skin rashes and minor itching. Reasons for the
development of this form of scabies may be the following:

Careful patient compliance with the rules of hygiene, frequent washing with a washcloth, promoting "washout" ticks,
especially in the evening;

skin care, comprising regular use of moisturizing creams for the body, closing vents and livelihoods infringing mite;

occupational hazards, consisting in contact with the patient's skin substances with acaricidal activity (motor oil,
gasoline, kerosene, diesel oil, household chemicals, etc.), which leads to a change in the clinical picture (no

rashes on the hands and exposed areas of the skin, but significant lesions on the skin of the body).

Norwegian scabies

Norwegian (cortical, krustoznaya) scabies - a rare and highly contagious form of scabies. Characterized by a
predominance of massive cortical layers in the typical places, which are exposed at the rejection erosive
surface. Typical itch moves even appear on the face and neck. This form of scabies is accompanied by violation of
the general condition of the patient: fever, lymphadenopathy, leukocytosis in the blood. Develops in people with
impaired skin sensitivity, mental disorders, immunodeficiency (Down's disease, senile dementia, siringimieliya, HIV
infection, etc.).

Scabies "incognito"
Scabies "incognito" or unrecognized scabies develops in the medical treatment with drugs that suppress the
inflammatory and allergic reactions, has antipruritic and sedative effect. Glucocorticoids, antihistamines, drugs and
other neurotropic agents suppress itching and scratching in patients, which creates favorable conditions for the
spread of mites on the skin. The clinical picture is dominated itch moves, no excoriation. Such patients are highly
contagious to others.

Postskabioznaya limfoplaziya

Postskabioznaya limfoplaziya - state after scabies, characterized by the appearance on the skin of the patient
hemispherical nodules pea-sized bluish-pink or brownish in color, smooth, thick consistency and accompanied by
severe itching. The disease is often observed in infants and young children (Figure 4-42).

Postskabioznaya limfoplaziya represents a reactive hyperplasia of lymphoid tissue at the point of greatest
congestion. Favourite localization - the crotch area, scrotum, inner thighs, armpits. Number of items - from 1 to 10-
15. Course of the disease - long, from several weeks to several months. Antiscabietic therapy is ineffective. Possible
spontaneous regression elements.

Diagnostics

Diagnosis of scabies is determined based on a combination of clinical manifestations of epidemic data, lab results
and test treatments.

Most important to confirm the diagnosis results of laboratory diagnosis with detection of female larvae, eggs, the
empty egg membranes under a microscope.

There are several methods of detecting tick. The easiest - method of layering scraping, which is carried out on a
suspicious area of skin with a scalpel, or lancet until the point of bleeding (for this method-

dike scraping treated with alkali) or acute stomach after prior application of 40% lactic acid solution. The resulting
scraping mikroskopiruyut.

Differential diagnosis

Scabies differentiate from atopic dermatitis, pruritus, pyoderma, etc.

Treatment

Treatment is aimed at the destruction of the pathogen acaricides. Mainly used drugs outdoor activities.

General principles of treatment of scabies patients, the choice of drugs, the terms defined dispensary "Treatment
Protocol. Scabies "(order of the MoH number 162 of 24.04.2003).

General rules for the appointment Antiscabietic drugs:

use of the drug in the evening, before going to sleep better;

the patient should take a shower and make a change of underwear and bed linen before treatment and at the end;

apply the drug must be on all areas of the skin, except for the face and scalp;

drug should only be applied by hand (do not swab or cloth), due to the high number of burrows on the hands;
Do not spray the drug on the mucosa of the eyes, nasal passages, mouth, and genitals; in case of contact with
mucous membranes should be flushed with running water;

exposure applied to the skin of the drug should not be less than 12 hours;

rub the medication should be in the direction of hair growth vellus (which reduces the possibility of contact
dermatitis, folliculitis);

hands after washing processing is over 3 hours, subsequently rubbed into the skin preparation of each of the
brushes after cleaning;

Do not use excessive amounts of drugs Antiscabietic time (exceeding the recommended scheme) since the toxic
effects of drugs will grow and Antiscabietic activity will remain unchanged;

treatment of patients identified in one outbreak (eg family) are carried out simultaneously in order to avoid
reinfection.

The most effective drugs Antiscabietic: benzyl benzoate, 5% solution of permethrin, piperonyl butoxide + esbiol
sulfuric ointment.

Water and soap emulsion of benzyl benzoate (20% - for adults, 10% - for children or as a 10% ointment) is used as
follows: drug treatment administered twice - in 1 and 4 days of treatment. Before use, the suspension was shaken
thoroughly, then double carefully applied to the skin with a 10-minute break. Side effects of the drug include the
possible development of contact dermatitis, dry skin.

5% solution of permethrin is approved for use in infants and pregnant women. Side effects with its use are
rare. Drug treatment produce three times: on the 1st, 2nd and 3rd days. Before each treatment should be prepared
fresh aqueous emulsion formulation, for which 1 / 3 of the vial (8 ml of a 5% solution) is mixed with 100 ml of water at
room temperature.

Piperonyl butoxide + esbiol aerosol - low emission drug approved for the treatment of infants, pregnant. Spray
applied to the skin from a distance of 20-30 cm from the surface in a downward direction. In infants treated as the
scalp and face. Mouth, nose and eyes pre-cover with a cotton swab. Upon the recommendation of treatment is
carried out once, but from experience we know that the spread of scabies requires 2 to 3-fold use of the drug (1, 5
and 10 th days) and only with fresh mange a single application of the drug leads to a complete cure of patients.

Sulfuric ointment (33% ointment is used in adults, 10% - in children). Among the side effects often occur contact
dermatitis. Apply for 5-7 consecutive days.

Particular attention is paid to the management of complications, which is carried out in parallel with antiscabietic
treatment. When pyoderma appoint (if necessary) antibiotics, topically used aniline dyes, antibacterial
ointment. Dermatitis prescribe antihistamines, hyposensitization therapy, externally - glucocorticoids combined with
antibiotics (oxytetracycline + hydrocortisone, hydrocortisone + natamycin + neomycin, oxytetracycline +
hydrocortisone, etc.). When insomnia prescribed sedatives (valerian tincture, motherwort, Percy *, etc.).

Postskabioznaya itching after a full treatment is not an indication for additional course specific treatment. Itching
regarded as the body's reaction to the mite killed. To eliminate prescribe antihistamines, and glucocorticoid ointment
aminofillinovuyu 5-10% ointment.

The patient is invited to readmission 3 days after the end of treatment for scabies, and then - every 10 days for 1.5
months.
Postskabioznaya limfoplaziya Antiscabietic does not require therapy. Use of antihistamines, indomethacin,
glucocorticoid ointment under an occlusive dressing, laser.

Features of scabies in children

Rubbing Antiscabietic drugs into the skin of the child holds the mother or other caregiver him face.

The drug is necessarily applied to all areas of the skin, even in the case of limited lesions, including the skin of the
face and scalp.

In order to avoid contact with the eyes when touching them with your hands young children wear baby's undershirt
(shirt) with protective sleeves or mittens (mittens); can cause the drug to the child during sleep.

Features scabies in pregnant and lactating women

Drugs of choice - benzyl benzoate, permethrin and piperonyl butoxide + esbiol for which proven safe use in
pregnancy and lactation.

Clinical examination

Reception (inspection, consultation) dermatologist patient in the treatment of scabies is held five times: 1st time -
the day of treatment, diagnosis, and treatment assignment; 2 nd - 3 days after the end of treatment; 3, 4, 5 minutes -
once every 10 days. The total period of clinical supervision - 1.5 months.

When the diagnosis of scabies is necessary to identify the source of infection, contact persons, subject to
preventive treatment (family members and persons living with the patient in the same room).

- Members of organized groups (kindergartens, schools, classrooms) paramedics inspect the field. In identifying
scabies and school children excluded from visiting the child care institution for treatment. The question of the
treatment of contact persons decide individually (the identification of new cases of scabies are treated with all contact
persons).

- In organized communities where preventive treatment of contacts has been conducted, inspection is carried out
three times at intervals of 10 days.

Holding current disinfection in the outbreaks of scabies necessarily.

Prophylaxis

Basic preventive measures include early detection of scabies patients, contact persons and their
treatment. Disinfection of bedding and clothing can be accomplished by boiling, washing machine or in the
disinfection chamber. Things that can not be heat treated, disinfected ventilation for 5 days or 1 day in the cold, or
placed in a tightly tied plastic bag for 5-7 days.

For soft furniture, carpets, toys and clothing are also used aerosol A COUPLE *.

Counseling

Must warn patients about the contagiousness of the disease, strict adherence to sanitary measures in the family, the
community, the strict implementation of the methods of treatment, the need to re-visit a doctor to determine the
effectiveness of therapy.
34. Lupus erythematosus. Etiology, pathogenesis, classification, diagnosis,
treatment.
RED ERYTHEMATOSUS

Systemic lupus erythematosus (lupus erythematodes) - an autoimmune connective tissue disease


with unclear etiology, manifested on the skin erythema, hyperkeratosis and atrophy. In the general
structure of the skin disease are recorded in this dermatosis 1-1.5% of cases. Girls suffer from lupus
erythematosus were significantly more likely than boys.

Etiology and pathogenesis

In the pathogenesis of lupus principal role to the development of autoimmune reactions occurring at
the cellular components of the connective tissue (DNA - deoxyribonucleic acid, RNA - ribonucleic
acid, nucleoproteins), deposition of immune complexes on the border of the epidermis and dermis,
with the formation of complement fixing membranopovrezhdayuschego complex. Procatarxis - UFO.

The clinical picture

Clinical forms

There are four varieties of clinical chronic lupus: discoid, disseminated, centrifugal erythema Biett
and deeper form of sarcoma-Irganga.

Discoid shape

For discoid shape characteristic triad of symptoms: erythema, hyperkeratosis, atrophy. Outbreaks
often localized on the face in the form of a butterfly, wings exciting nose and cheeks (Figure 7-
1). May be affected by the exposed areas of the skin: the ears, the upper part of the skin of the
chest, scalp (Fig. 7-2).
Fig. 7-1. lupus erythematosus. Symptom butterfly
Fig. 7-2. lupus erythematosus. The defeat of the scalp

Initially, there is hyperemic spot, increasing in size and infiltrating into the plaque with raised-kai

Coy on the periphery and in the center of scaling. On the background of erythema
occur telangiectasia, formed follicular hyperkeratosis. When removing scales (pain) on its inner
surface visible spines - a symptom of "ladies' heel." In the future, there ishyperkeratosis across the
surface of the center (Figure 7-3). Resolution lesions occurs first in the central portion, and then
along the periphery. Formed scar atrophy.

Disseminated form
There are multiple erythematous lesions with a diameter of 2 cm, on their surface - TV

Fig. 7-3. Lupus

angiectasis, melkoplastinchatye flakes. Outbreaks have clear boundaries, their shape is oval,
ringed. Localization - often on the upper surface of the trunk, scalp, face skin on the hands (Figure 7-
4, a). In this form there is no follicular keratosis and scarring.

Centrifugal erythema Biett

Centrifugal erythema Biett appears limited erythematous spot cyanotic, rounded shape with clear
boundaries, which spreads centrifugally. No subjective disorders, hyperkeratosis and
atrophy. Localization - asymmetrical, often affects the forehead and malar part of cheeks.

Profound form
Profound form of lupus is formed under former discoid lesions or independently. In the subcutaneous
tissue arise deep nodes nespayannye surrounding tissues, painful. Leather knots cherry
color. Nodes may ulcerate, leaving scars inverted (Figure 7-4 b). In addition to this location, there are
sites on the thighs, buttocks.

Fig. 7-4. Systemic lupus erythematosus: a - disseminated form; b - profound form

Features of current lupus erythematosus in children

The most characteristic of subacute cutaneous lupus erythematosus. Limited cutaneous not
typical childhood.

More often than adults, there vezikulobulleznye elements.

Characterized by severe photosensitivity.

When systemic form in children occur fever, fatigue, muscle weakness, weight loss, night sweats,
arthralgia, lymphadenopathy, Raynaud's syndrome, as well as have the pleurisy, heart damage,
kidney.

A special form - lupus syndrome baby - typical for newborns and children first months of
life. Development of the disease associated with the penetration of antibodies through the placenta
to the antigens Ro / SS-A and La / SS-B from mothers with autoimmune disease (more than 50% of
cases detected subacute lupus erythematosus, systemic lupus erythematosus, or Sjogren's
syndrome). Characterized by isolated or combined skin rashes and heart disease. Skin rashes are
ring-shaped, scaly, located on the face, around the eyes (a symptom of "points"), scalp (Fig. 7-5). At
6-12 months of life rashes are alone,
Fig. 7-5. Lupus syndrome infants

leaving no scars. Lupus syndrome - the most common cause of congenital AV block. Possible liver
damage.

Diagnostics

Diagnostic key: a typical clinical picture, pain when removing scales (symptom-Besnier
Meshcherskij; symptom of "ladies' heel"); in disseminated form - finding cell LE (lupus cells).

Differential diagnosis

Differential diagnosis is carried out with psoriasis, s

.olar keratosis, red acne, lichen planus.

Treatment

Prescribe chloroquine 250 mg 2-3 times a day, for 10 days with a 5-day break or hydroxychloroquine
200 mg under the same scheme. Spend 2-3 cycles. When disseminated form of the disease after a
10-day course with breaks in 5 days for 1-1.5 months 1 tablet per day.

Hydroxychloroquine for the initial dose is 400-800 mg / day maintenance dose - 200-400 mg /
day. Sometimes a combined preparation glucocorticoid (prednisolone 15-20 mg / day).
Parallel appoint ksantinola nicotinate, an immunomodulating drugs.

External appointed glucocorticoid creams, ointments (methylprednisolone atseponat, alclometasone,


hydrocortisone, mometasone) and photoprotective creams.

Counseling

The patient should be apprised of precipitating factors contributing to the aggravation of the
pathological process (foci of chronic infection, drugs - vaccines, antibiotics, sulfonamides, stress,
hormonal changes, and Cooking

etc.).

35. Scleroderma. Etiology, pathogenesis, classification, diagnosis, treatment.

Scleroderma

Scleroderma (sclerodermia) - a group of diffuse connective tissue diseases with severe fibrosis and
sclerosis of the skin, visceral, vascular pathology. The disease occurs at any age. Women suffer 5-
10 times more often than men.

Etiology and pathogenesis

Scleroderma - a multifactorial disease, which is based on violation of the synthesis of connective


tissue fibroblasts. In this disease fibroblasts synthesize a large number of immature collagen that
leads to defeat the small vessels and tissue hypoxia develop fibrotic changes.

In the pathogenesis of the disease are important immune factors: defect in T cell and humoral
immunity (hyperglobulinemia appearance of antinuclear antibodies, antibodies to RNA, DNA,
collagen).

Precipitating factors in the development of scleroderma - injuries, hypothermia, hormonal disorders,


Lyme disease, cancer, chronic intoxication.

The clinical picture

Distinguish and limited systemic sclerosis.

Limited scleroderma

With limited form only manifestation of the disease - skin sclerosis. Clinically for limited scleroderma
distinguish 3 stages: edema, induration, atrophy.
Stage I (inflammatory edema). Spot appears pale pink or pink-purple, growing in size to 5-10 cm in
diameter. Color fades gradually, remaining only on the periphery in the form of purple rim and land
destruction becomes edematous.

Stage II (seal). Compacted swelling, sometimes woody density. seal skin over it becomes
whitish-yellowish color, reminiscent of ivory, shiny, not going to fold, no hair on, in the hearth of
disturbed sensitivity.

Corolla purple disappears. On the surface of the plaque may develop petechiae, telangiectasia,
bubbles. III stage (atrophy). Seal gradually dissolve, skin becomes thinner, formed
scar atrophy, more pronounced in the central part of the plaque. Hypo hyperpigmentation occurs.

There are several types of localized scleroderma: patchy, linear, deep. Separately isolated lichen
sclerosus and idiopathic atrophoderma Pasini-Pierini.

Patchy sclerosis (Morpheus)

Patchy sclerosis (Morpheus) - the most common form. Characterized by a long relapsing. Favourite
localization of foci - torso. The eruptions are rounded or oval plaques. Clearly be seen staging
inflammatory process in the skin (Figure 7-6). Mostly occurs in women 40-60 years old.

Fig. 7-6. patchy scleroderma

The linear form of scleroderma


The linear form of scleroderma differs from patchy form deep lesions and configuration hearth. For
this form of characteristic rash linearly arranged along the length of the limb (in the course of the
neurovascular bundle), or recalling a scar from a saber blow, on the face (from the scalp down to the
nose and chin) (Fig. 7-7). When the linear form atrophic process applies not only to the skin, but also
on the fascia, muscles, bones, limbs breaking growth and causing the development of contractures
(Fig. 7-8), and for localization in the face - blurred vision, articulation, warp face.

Linear form often manifests in childhood (3-10 years). Without treatment, the disease progresses for
a long time.

Profound form

Profound form - a rare species, characterized by the appearance in the deeper skin layers of dense,
often towering over her hosts round or oblong. The skin over the entities is not changed. Resolution
nodes accompanied by the formation of scar atrophy in the subcutaneous fat and skin retraction.
Fig. 7-7. Scleroderma. The linear form

Fig. 7-8. linear form of scleroderma

Lichen sclerosus

Lichen sclerosus (illness "white spots") - a special form of the surface small focal scleroderma. Most
sick women (10:1). There are two peak age incidence: in childhood (3-5 years) and adulthood (45-55
years). For each age group is characterized by its favorite localized rash. In childhood, mainly
affected anogenital region, and mature - chest and back.

Clinically, the disease is characterized by the appearance on the skin of small lichenoid papules
brilliant, which subsequently flattened and the surface becomes atrophic, resembling cigarette paper
(Fig. 7-9). Outcome - multiple small (diameter from 2 to 10 mm) atrophic white patches with a
porcelain shade (disease "white spots").
For most typical childhood anogenital lesions location, where there are clearly limited areas of
whitish color (atrophy) with erythema around the periphery of the hearth (Figure 7-10). In
complicated cases, the surface of the center bubbles appear, erosion, may join a secondary
infection. Girls-eruption

Fig. 7-9. Lichen sclerosus

Fig. 7-10. Lichen sclerosus in a child


tion often localized around the vagina and the anus, creating outlines hourglass or figure 8. Boys
rash Lichen sclerosus localized on the foreskin and can be complicated by cicatricial phimosis.

Atrophoderma idiopathic Pasini-Pierini

Atrophoderma idiopathic Pasini-Pierini - a rare form of scleroderma, characterized primarily arises


on the skin atrophy (no staging inflammatory process). A distinctive feature of this form: the
emergence of atrophic spots purple-brown, mostly on the skin of the back along the spine, the slow
progression of the process and resistance to treatment (Figure 7-11). In childhood, does not occur.

Systemic scleroderma

Systemic scleroderma - a serious, progressive disease of connective tissue characterized by


sclerotic lesions of the skin and internal organs, as well as vasospastic disorders common type of
Raynaud's syndrome.

Most commonly in systemic sclerosis affects the lungs, cardiovascular system, gastrointestinal tract,
kidneys, joints, muscles.

In a laboratory study, identify antinuclear body, rheumatoid factor, eosinophilia.

Fig. 7-11. atrophoderma idiopathic Pasini-Pierini

Diffuse (generalized) form

Diffuse (generalized) form is acute or podost to defeat all of the skin. Develops first tight edema
(when pressed dimple is formed), the skin is soldered with under zhaschimi bodies atrophy of the
subcutaneous adipose cellular and muscle movement difficult (Figure 7-12). A person becomes
amimi nym nose is pointed, thinner lips, limited mobility of the tongue, brush resembles a bird's leg.

Akroskleroticheskaya form

Akroskleroticheskaya form occurs more often chronically and starting! smiling usually with
Raynaud's syndrome. The most significant sclerotic n reflection skin develop on the face and distal
extremities to form acroscleroderma. Option akroskleroticheskoy we pho -CREST-syndrome (C -
skin calcification, R - Raynaud's syndrome, E esophagitis, S - acroscleroderma, T - telangiectasia).

Features of the course of scleroderma in children

Children provoking factors are SARS and injury.

Fig. 7-12. diffuse scleroderma

When the linear form faster than adults, develop deep tissue damage with the formation of
contractures, shortening limb deformities of the face. The localization process on the face develops
neurological symptoms (hearing, vision).

Lichen sclerosus forecast for girls is very good - the disease resolves on its own, leaving a light
atrophy. The boys may develop scar phimosis.

Diagnostics

Diagnosis is based on a typical clinical picture.


Differential diagnosis

Depending on the clinical forms of the disease differentiated from atrophic form of lichen planus,
lupus erythematosus, vitiligo, etc.

Treatment

Basic principles of treatment:

early start (especially in children with a linear form);

long-term treatment;

phasing-course treatment: therapy 1.5-3 months with a break for 3-6 months.

General treatment

General treatment traditionally begins with penicillin: benzylpenicillin intramuscularly to 500 thousand
units, 4 times a day for 10 days (total dose per treatment course is 20 million units). Penicillin has a
pronounced anti-inflammatory action and kollagenstabiliziruyuschim. Perhaps the appointment of
penicillamine, methotrexate, cyclosporine.

A course of hyaluronidase by: 32-64 IU intramuscularly every other day until 15 injections.

In the treatment of scleroderma used vasoactive drugs (pentoxifylline, dipyridamole, nicotinic acid,
etc.), vitamins A and E, aloe vera leaves, trifosadenin.

Treatment of systemic sclerosis is carried out in a therapeutic hospital rheumatologist.

Physical therapy is not indicated in severe inflammatory response in the outbreaks. In stationary and
regressive steps were performed electromechanical fonoferez hyaluronidase, chymotrypsin,
glucocorticoids, paraffin baths, mud baths. Massage and physical therapy is recommended for motor
disorders.

External treatment

In the swelling step (I) administered topically fluorinated glucocorticoid creams (methylprednisolone
aceponate, mometasone, hydrocortisone, etc.), nonsteroidal antiinflammatory drugs (ointments
phenylbutazone, diclofenac). In stage II pockets of hyaluronidase administered in dimethyl sulfoxide
or 33% dimethyl sulfoxide solution in the form of daily applications, means of sodium heparin,
complex protivofibroticheskie means (kontraktubeks * mederma * madekassol *). In stage III shows
emollients, impeding the development of trophic disturbances.

Lichen sclerosus externally to the anogenital region administered glucocorticoid funds for 2-4 weeks,
it is recommended
mandatory use of mitigation nourishing creams as daily care (soft zinc paste, cream with zinc oxide,
mineral oil, etc.). The boys in the development of phimosis shown circular cut or cut the foreskin.

Counseling

Attention should be paid to the role of patient factors trigger (hypothermia, insolation, drugs, etc.) in
the development and exacerbation of the skin process. Lichen sclerosus in the anogenital region to
avoid trauma (for example, when doing cycling, etc.).

36. Leprosy. Etiology, classification, diagnostic methods if

Leprosy (leprosy, Hansen's disease, lepra) - a chronic systemic infectious disease caused by a special type of
mycobacteria characterized by weak contagious and progressive course with a primary lesion of the skin, mucous
membranes and peripheral nervous system.

Etiology and pathogenesis. The pathogen Myco-bacterium leprae is a small curved gram-positive Lactobacillus
acidophilus length 0.5-1.5 microns. In the laboratory, swabs or pieces of tissue microorganism looks tightly packed in
bundles resembling a pack of cigars, and detected when stained by Ziehl - Neelsen or Fite.

The disease is spread mainly in tropical and subtropical regions of the world (South and Southeast Asia, Africa, Latin
America), but the highest incidence occurs in some colder regions such as Nepal and Korea. In Europe, leprosy
patients are registered in Greece, Spain, Portugal, Italy and France. In Russia, there are small pockets in the mouths
of the Volga and the Don. In total there are about 15 million patients. The largest number found in India, Central
Africa and Oceania.

A method of transmission unknown patient from the patient, as well as unknown way of introduction into the organism
infection.Infection with the development of the disease occurs after the regular, long time contact with leprosy
patients, and therefore the duration of the incubation

period is not certain. It is assumed that it may vary from 3 to 20 years. M. leprae tend affect the skin, mucous
membranes, upper respiratory tract and peripheral nerves in the last pathogen found in Schwann cells. In healthy
people, there is a sufficiently high resistance to leprosy infection. Development of the disease contribute to factors
that weaken the immune system: alcoholism, drug addiction, poor and malnutrition, physical overload, chronic
intercurrent disease. Leprosy patients usually highly anergichny to antigen M. leprae in vnutrikozh leprominovom-tion
test, which indicates that they have perverted the immunological reactivity and a poor prognosis in terms of curing the
disease. The emergence of low positive and positive reactions to lepric antigen improves the chances of
recovery. With early treatment the disease is curable.

The clinical picture. There are four clinical types of leprosy: lepromatous, tuberculoid, borderline and
undifferentiated.Lepromatous and tuberculoid leprosy are two diametrically opposite clinical and immuno-logical
variants of the disease. Lepromatous leprosy is characterized by a large number of pathogen in the body at the same
time, almost always complete absence of reactivity to it. Tuberculoid leprosy is a clinical form, in which the patient
has a small amount of background on mikoboktery severe allergy to them. Undifferentiated and Border leprosy
occupy an intermediate position between the two specified types. Leprominovy intradermal test is not diagnostic, and
is used to clarify the type of leprosy.

Lepromatous leprosy is a malignant form of leprosy observed in frail malnourished patients, characterized by the
prevalence of pathological process (skin, eyes, mucous membranes, peripheral nerves, lymph nodes and internal
organs), no tendency of affected areas to spontaneous resolution and a poor prognosis. In infected tissues revealed
a large number of M. lep-rae, who also detected in clinically unaffected
skin. Leprominovy test shows negative reaction.

Dermatological manifestations characterized symmetrically arranged erythematous-pigment spots, nodules, plaques


and infiltrated nodes (leproma-mi) with fuzzy boundaries. The skin on some of the elements has a reddish-brown
rusty color. Characterized spots round or oval in shape and are arranged in closed areas of the body. Papules and
develop nodes of the spots, but they can also occur in intact skin. They vary in size - from a few millimeters to several
centimeters, and density - from hard elastic to soft. The nodes may be located subcutaneously. Their most frequent
localization - forearm, back of hands, shins, thighs, buttocks, face, ears.Characterized by a significant increase in the
affected ears. In addition to the ears, rash on the face are located in the nose, the zygomatic arches and
eyebrows. Defeat person causes alopecia beards, eyebrows and mustache. In the process often involved eyes with
lesions age, sclera and cornea. Leprosy-matous infiltration face combined with a twisted forms keratokonyunkti-
appearance of the patient, which resembles the face of a lion (leonine facies).

Leprosy surface smooth, shiny from excess sebum, sometimes - a little flaky. In addition to increased greasiness of
the skin, they are characterized by hair loss and consequential loss of temperature, pain and tactile
sensitivity. Leproma can be resolved with the formation of scar atrophy, or may ulcerate due to injury or
spontaneously. Complications izyaz-hovering Leprosy secondary infection.Ulcer healing is slow to produce disfiguring
scars. Individual nodes do not ulcerate and become denser, reduced in size and fibrosing.

A number of patients found diffuse lepromatous type of lesion (Lucio leprosis), which is characterized by generalized
skin waxy infiltration. Thus the skin of the upper and lower limb swelling, reddish cyanotic color, slightly
hyperpigmented, contains numerous telangiectasia.

Leproma unaffected skin is dry, atrophic, sometimes swollen and infiltrated. There is a lack of sweating, pain
sensitivity, as well as hair loss.

In addition to skin and eyes also affects the mucous membranes of the mouth (lips, hard and soft palate, tongue) and
upper respiratory tract (nose, larynx, trachea), and the peripheral nervous system, which is often involved in the
process at the time of resolution of skin rash and demonstrates paralysis infiltrated nerves.

Most often in the process involves the nasal mucosa, first in the form of rhinitis with frequent nosebleeds, then
disintegrating leproma lead to perforation of the nasal septum and cause deformation of the nose. The defeat of the
larynx and trachea (laryngitis, tracheitis) leads to hoarseness, aphonia and even stenosis.

The defeat of the peripheral nervous system often characterized by involvement in the process of radial and ulnar
nerves, causing skin atrophy in the thenar and hypothenar and gradually leading to a change mutiliruyuschim brush.

The lymphatic system responds poliadenita which is observed even in the initial period of the disease. Lymph nodes
are soft, painless, mobile and not soldered to the surrounding tissues.

Quite often affects the genitals (orhoepidedi-mit, prostatitis, urethritis), the process ends sclerosis and atrophy. Some
patients revealed an enlarged liver and spleen.

Sluggish for lepromatous leprosy can sometimes be replaced by lepromatous reaction - acute period in which there is
both an increase resorption and ulceration of leprosy old and new ones. This period is often marked by fever, fatigue,
swollen lymph nodes, which become painful. Blood found in M. leprae.

Tuberculoid leprosy refers to a benign form of non-communicable disease with a favorable prognosis and is
characterized by slow progression of the process, the lack of systemic change and a tendency to spontaneous
resolution of skin lesions. In the skin, found a very small number of sticks Hansen and leprosy-Minowa test reveals
pronounced allergic reaction to lepric antigen. However, this form of leprosy can cause serious mutiliruyuschie
changes caused severe involvement of the peripheral nerves.

Cutaneous manifestations of tuberculoid leprosy often begin with one or more reddish purple

shade spots, sharply demarcated from healthy skin, as well as small papules undergoing peripheral growth with
central resolution, leaving depigmented-ITATION atrophic lesions. As a result, formed annular shape oval or
polycyclic outlines. Recent rash characterized by hyperesthesia, but in the future there is a gradual loss of first
temperature, and then the pain and tactile sensitivity, and stops sweating.

Pathological changes in the peripheral nerves characterized by swelling and uneven beaded thickening of the nerve
trunks, which is accompanied by violation of their duties. Degree of their expression is more pronounced than with
leprosy lepromatoz-tion and localization is symmetrical. Nerve damage causes paresis and atrophy secondary
corresponding muscles. Upper limbs show atrophy-cal changes of forearm muscles bulge thenar and hypothenar to
the development of contractures, leading to the formation of chelated brushes. Lower limb muscle atrophy
characterized by causing an uncertain gait, and trophic ulcers of the skin.

Internal organs are usually not affected.

Undifferentiated leprosy is characterized by asymmetric dermatologically hypo-and hyperpigmented spots


slabovospalitelnymi, anesthesia and agidrozom. Changes nerves polyneuritis appear, accompanied by thickening of
the nerves and lead to their paralysis, education chelated brushes and trophic ulcerations of the lower extremities. In
leprominovom test says weakly positive or negative reaction in the tissues revealed a small amount of the
pathogen. Undifferentiated form of leprosy can be months or years later, it is transformed into a lepromatous form,
occasionally - in tuberculoid.

Pogranignaya Leprosy is a rare form of the disease and is clinically characterized by skin and nerves, pathogen
detection in tissues histologically as lepromatous and tuberculoid leprosy and lepromatous negative reaction to the
antigen.

Cutaneous lesions are presented rare asymmetrically arranged pigment spots and separate large rounded,
protruding domed nodes or

plaques with fuzzy edges, over which the skin has a reddish tinge to the wine. Rashes are more common in the lower
extremities. In the eyebrows is often found alopecia.

Neurological manifestations are characterized by asymmetric neurites, which are already evident in the initial period
of the disease.

Borderline leprosy in the absence of treatment is usually transformed in lepromatous, and the appointment of
adequate treatment - in the form of tuberculoid leprosy.

Diagnosis of leprosy is based on anamnesis (prolonged contact with patients living in endemic area) and the
characteristic clinical picture (as a simultaneous destruction of the skin in the form of patchy and nodular elements
with characteristic color and greasy surface and peripheral nerves with loss of pain, temperature and tactile
sensitivity). In complex cases use hysteresis Minowa test wherein 0.1 ml intradermal injection of a solution of
histamine (at a dilution of 1: 1000) in a patient leprosy, unlike healthy patient, causes blister without concomitant
erythematous reaction. In addition, use direct microscopic detection of the pathogen in smears and tissue specimens,
as well as a test to detect violations of sweating: 0.1 ml of a solution of pilocarpine hydrochloride (dilution 1: 100)
injected intradermally into the affected area of skin that is processed starch iodine-mal solution. Positive reaction to
the lack of sweating is unaltered color of the solution that people with normal sweating becomes blue.

The differential diagnosis is carried out with sarcoidosis tertiary sifilid, leishmaniasis, and erythema induratum
skrofuloderme.

Treatment. Overall therapy carried out in complex, foreign exchange method. Assign 4 Diaminodiphenylsulfone rate
(VAT) (administered orally every day from day break every 6 days), starting with a dose of 50 mg twice daily for 2
weeks. In the next two weeks, a dose of 100 mg two times a day. This gradual increase in the dose can prevent the
possibility of leprosy reactions. Use of antibiotics rifampicin, which is assigned at a dosage of 300-450 mg 2 times a
day. Of stimulating and on-

scheukreplyayuschih immunokorrigirujushchaja funds used drugs (timalin, taktivin, metiluratsil nukleinat sodium
pentoksil), vitamins, adaptogens gepatoprotekto Organization ("essentiale-forte", "geptral", "Syrepar"), iron
supplements ("Ferrum Lek" "ferropleks").

Outdoor therapy is conducted in the presence of complications (ulceration, secondary infection) according to the
rules of treatment of pyoderma.

37. Syphilis: etiology, epidemiology, D - and superinfection. Immunegenesis


syphilis.
38. Syphilis: pathogenetic features, for classification. Laboratory diagnostic
techniques. Serological diagnosis of syphilis
39. Primary syphilis. Clinical features, lab. diagnosis of primary syphilis. Atypical
chancres: diff. diagnostics.
40. Sifilis.Klinicheskie Secondary features and diagnostic criteria of secondary
syphilis. Secondary syphilides.
41. Congenital syphilis, especially the pathogenesis and classification. Pregnancy
outcomes in syphilis.
42. Visceral pathology in the Tertiary syphilis (neurosyphilis, the pathology of the
cardiovascular system, bone). Principles of treatment of syphilis.

39. Primary Syphilis : clinical , laboratory diagnosis , treatment.

Ways syphilis - Sexual, domestic, transfusion-- transplacental

Primary syphilis (I):

Seronegative; -Duration 3-4 weeks, begins with the appearance of


the chancre
A week-increasing regional lymph nodes (with one or two sides)

-seropositive starts since pozitivatsii RW,-Lasts up signs of


secondary syphilis-Duration 3-4 weeks

Hidden

Clinical varieties of chancre; Erosive, ulcerative, herpetiformis,


petechial, chancre-print, Cortical, Ozhogovidny

Atypical forms chancre; Indurativny edema, chancre-felon,


chancre-amygdala

. CLINICAL PICTURE primary period of syphilis

For chancre characteristic: painless, smooth flat bottom ulcers color of raw meat or
spoiled fat, lack of inflammation, the presence of the seal at the base in the form of
plates or cartilage nodule density. Chancre typically has a diameter of 10-20 mm, but
there are so-called dwarf chancre - 2-5 mm and giant - 40-50 mm Giant localized
chancre usually pubic abdomen, scrotum, inner thighs, chin. There have been some
features chancre depending on the location: on the bridle of the penis, they acquire an
elongated shape and bleed easily when erect, flanked by the bridle, they are difficult to
see and have little or no compaction; chancre urethral opening is always hard and
bleeds easily, with localization chancre in the urethra there is a slight soreness,
especially on palpation. In women, chancres in urethral opening is always dense, while
in vulvo-vaginal chancre fold seal is not expressed

In rare cases of chancroid-amygdala, characterized by an increase in the seal and


without the formation of tonsil erosion or ulceration and accompanied by pain and
difficulty in swallowing. Chancre gums, hard and soft palate, pharynx, are extremely
rare. Vnepolo of O-chancre chancre deserve attention brushes, occurred more
frequently in men, mainly on the right hand. Isolated chancre-felon. while finger appears
bluish-red, swollen, clavate-inflated, patients experience sharp, "shooting" pain on the
dorsum of the phalanx with the bottom of the ulcer is covered necrotic-purulent
discharge. Chancre around the anus look like cracks.Chancre of the rectum causes pain
in the rectum just before defecation and some time afterwards, and the glassy nature of
feces

The particular species chancre also include:

1) "Burn" (kombustiformny) representing the erosion-prone expressed in peripheral


growth

weak seal at the base; grows erosion borders lose its right shape, the bottom is red,
granular;

2) Folmanna balanitis - a rare variety of primary syphiloma characterized by many small,


partially confluent, sharply demarcated erosions without noticeable seal at the base on
the penis or on the outer labia;

3) herpetiformis chancre reminiscent Geni-tal herpes.


SIGNIFICANT treating patients with syphilis

Specific treatment of patients with syphilis is assigned only after the confirmation of the
clinical diagnosis by laboratory methods.Diagnosis is based on relevant clinical
manifestations, detection of the causative agent and the results of serological
examination of the patient. Antisyphyllitic funds without confirmation of the presence of
syphilitic infection is prescribed for preventive treatment, prophylactic treatment, as well
as in the treatment trial.

Preventive treatment is carried out with the aim of preventing syphilis persons who
had sexual and close household contact with patients early stages of syphilis.

Prophylactic treatment is carried out by indications pregnant, ill and bolevshim


syphilis, and children born to these women.

Presumptive treatment may be imposed in cases of suspected specific lesions of the internal
organs, the nervous system, sensory organs, musculoskeletal system in cases where the
diagnosis could not be confirmed conclusive laboratory data and clinical picture does not allow
to exclude the presence of syphilitic infection.

As the primary means of treatment for syphilis using different preparations of penicillin.

In outpatient settings apply foreign du rantnye drugs penicillin - and ekstentsillin


retarpen and their domestic counterpart - bicillin 1.This one-component preparations
presenting dibenzyl-vuyu penicillin. Their single injection at a dose of 2.4 million units
maintains the serum Treponema-

tsidnoy concentration of penicillin for 2-3 weeks, and injection ekstentsillina retarpena
held 1 time per week, bitsillina-1 - 1 in every 5 days. In-patient treatment may also be
used bicillin bicillin 3 and 5. Three-component domestic bicillin 3 consists of dibenzileti-
lendiaminovoy, procaine penicillin and sodium salts in a ratio of 1:1:1. Injection of the
drug at a dose of 1.8 million ED do 2 times a week. Two-bicillin 5 comprises procaine
and dibenzylethylenediamine salts of penicillin in the ratio 4: 1. Injection of the drug at a
dose of 1.5 million units produced 1 time in 4 days.

40. Secondary Syphilis : clinical differential diagnosis , laboratory


diagnosis , treatment.
(II):

;
,, ,,
Clinical manifestations secondary period of syphilis lesion characterized mainly skin and
visible mucous membranes, and to a lesser extent changes in the internal organs,
musculoskeletal system and the nervous system. To manifestations of secondary
syphilis are spotted on the skin, papular and pustular syphilides and syphilitic alopecia
and pigment sifilid. All secondary sifilid characterized by the following common features.

1. Peculiar color. Only at the very beginning they have a bright pink color. In the future,
the color of their stagnant or acquires a brownish tint, begins to fade ("boring" in the
figurative expression sifilidologii French).

2. Focus. Elements syphilitic rashes usually do not merge with each other, but remain
demarcated from each other.

3. Polymorphism. Often there is a simultaneous precipitation of various secondary


syphilides such as spotted and papular or pustular and papular (true polymorphism), or
rash occurs due to the diversity of elements

at different stages of development (evolutionary or false polymorphism).

4. Benign course. Typically, secondary syphilides, except in the rare cases of malignant
syphilis resolves, leaving no scars or some other persistent traces, is not accompanied
by a rash of impaired general condition and subjective disorders, in particular itch, a
common symptom of a variety of skin diseases.

5. Lack ostrovospalitelnyh phenomena.

6. The rapid disappearance of most syphilides influenced specific therapy.

7. Extremely high infectiousness erosive and ulcerated secondary syphilides.

The first eruption of the secondary period (secondary fresh syphilis) is characterized by
an abundance of rash, symmetrical, small value items. In secondary recurrent syphilis
rash often limited individual sections of the skin, have a tendency to grouping, formation
of arcs, rings, garlands, the number of elements decreases with each subsequent
relapse.

Spotted sifilid (syphilitic roseola, see col. incl., Fig. 42) is a hyperemic spot color
which varies from subtle pink (color peach color) to deep red, morbilliform, but
often it is a pale pink, "faded . " Due to the evolution of polymorphism of roseola
may have uneven saturation color pink hue in the same patient. When pressed
roseola completely disappears, but after the cessation of pressure
reappears. Vitropression roseola, there are about 1.5 weeks, reveals brownish
coloration due erythrocytolysis and education gemosideri-on. Outlines roseola
round or oval, fuzzy, like finely torn. Spots are isolated from each other, Focus,
do not tend to merge and peeling. Roseola is no different from the surrounding
skin or relief, or consistency, peeling absent even during the permit

Syphilitic papules on the mucous membranes gradually moistened, so the surface of


macerated, swells and becomes opalescent color, and later eroziruetsya. Erosive
(weeping) papule consists of three zones: in the center - erosion around it - opal ring,
and on the periphery - congestive-hyperemic.

Prolonged irritation papules saliva and food can cause their peripheral growth and
merging with each other in the plaque.

Rash papules in the vocal cords leading to hoarseness or even aphonia.

Erosive papules should be differentiated from the AFL, the initial element of which is a
small vial, quickly opened to form a sharply painful sores surrounded by a narrow rim
bright flare. Infiltrate at the base no. Bottom is covered with diphtheritic coating.

Extremely rare pustular sifilid mucous membranes manifests as painful swelling


testovatoy bright red, decaying to form ulcers.

Syphilitic lesions of the internal organs of

secondary period can be observed in any internal organ, but is most common syphilitic
hepatitis, gastritis, nephrosonephritis and myocarditis. In the majority of cases clinically
vistseropatii not expressed, moreover, they are not pathognomonic signs, which often
leads to diagnostic errors.

Syphilitic lesions of bones and joints in the secondary period, usually limited to
pain. Characteristic nocturnal bon

e pain, often in the long bones of the lower extremities, and arthralgia in the knee,
shoulder and other joints. Rarer periostitis, wasps, and teoperiostity hydrarthrosis.

Syphilitic lesions of the nervous system in early syphilis manifested mainly in the form of
hidden asymmetrical meningitis, vascular lesions (early meningovascular neurosyphilis)
and autonomic dysfunction.

41. Tertiary Syphilis : clinical , laboratory diagnosis , treatment.


(III):

CLINICAL PICTURE OF TERTIARY period of syphilis

Tertiary syphilides skin. morphological substrate is tertiary syphilides product specific


inflammation - infectious granuloma. Their clinical manifestations in the skin - and
gummy Cuspal sifilid - differ depth development of the inflammatory process: in the
subcutaneous tissue formed Gunma, in your own skin - bumps. Infectiousness of their
minor.
Gunma (see col. incl., Fig. 48) is a thick consistency knot the size of a walnut, towering

above the skin, painless at palpation, not soldered to the surrounding tissues. Skin over
it initially is not changed, then it becomes bluish-red. Subsequent development gummas
can occur in different ways.

Most often gummy node softened in the center and opened with the release of a few
drops of glue-like fluid. The resulting defect rapidly increases in size and becomes a
typical gummy ulcer. It is painless, sharply demarcated from the surrounding normal skin
roller nondecomposed gummy dense infiltrate its steep edges, bottom is covered with
necrotic masses. Gummy ulcer months there, and when the secondary infection and
irritation in malnourished patients - even years. For healing ulcers gummy remains very
distinctive scar. In the center, on the former site of the defect, it is dense, rough, on the
periphery, on the site of infiltration allowed - a gentle, atrophic. Often, the peripheral part
of the central contracted, and the scar becomes stellate appearance.

In other cases, the gummy node not allowed izyazv-lyayas, and the scar is formed in
depth. The material is only slightly sinks. The third possible outcome of the development
of gummy site - its replacement by fibrous tissue impregnation with calcium salts and
encapsulation. Node becomes almost woody density becomes smooth, spherical,
reduced in size, and as such there indefinitely.

Gummas usually sporadic. Most often, they develop on the front of the leg. Gummy
ulcers sometimes merge with each other.

Cuspal sifilid characterized by lesions in limited areas of the skin grouped dense, bluish-
red, painless bumps in size from small to large pea, occurring at different depths in the
dermis and do not merge with each other. Exodus development of tubercles may be
twofold: they are either absorbed, leaving a scar atrophy, or ulcerate. Painless ulcers,
sharply demarcated from the surrounding healthy skin tight roller nondecomposed
infiltrate their steep edge, the bottom of necrotic. Subsequently, they can crusted. Ulcer
healing ends scarring. There are four varieties Bugorkova sifilid: grouped, sulfuric
piginozny, diffuse and dwarf.

For grouped Bugorkova sifilid typical isolated from one another arrangement of tubercles
and education concerning focal round ridges, each of which is surrounded by pigment
border.

Serpiginous Cuspal sifilid different peripheral uneven growth of the lesion due to a rash
of new tubercles. As they appear between the old and tubercles is their partial merger,
allowing for healing hearth scar formation penetrated by normal skin strips (mosaic
scar). In the case of ulceration tubercles can identify three areas in the outbreak serpigi-
noznogo sifilid. The central zone is a mosaic scar, followed by ulcer area, and on the
periphery - the zone of fresh tubercles. Hearth Bugorkova serpiginous syphilis Lida has
krupnofestonchatye shape.

Diffuse Cuspal sifilid (Cuspal sifilid platform) is rare. It is formed by the close fit of
tubercles to each other and looks solid plaque. By healing his scar remains mosaic.
For dwarf Bugorkova sifilid characteristic rash grouped, small, size of a millet grain to
pinhead bumps, differing from the elements E biliary papular sifilid only on the hem.

Tertiary syphilides mucous membranes. on the mucosa (palate, nose, throat, tongue), or
tertiary syphilis is manifested in the form of individual nodes gummy, or as diffuse
gummy infiltration. The process usually begins in the underlying bone and cartilage,
much less - in the most mucosa.

Gummas localized mucosal characterized by the same traits as skin gummas. Their
decay often leads to perforation of the nasal septum or the sky. Perforations differ
painless.

Perforation of the hard palate, which is observed only in syphilis, causes that violated
phonation (voice becomes nasal) and swallowing - the food through the perforations
gets into the nasal cavity. In the case of diffuse ulceration gummy infiltration palate
produces several perforations. Thanks for this healing is "grid scar."

Gummy diffuse infiltration of the soft palate is a violation of phonation and difficulty
swallowing, with scarring

fusion can happen palate with the posterior pharyngeal wall, which leads to a narrowing
throat.

Perforated septum at the border of bone and cartilage pieces (lupus only destroys
cartilage). Extensive destruction of the nasal septum, especially the destruction of it,
together with the opener, causes saddle nose.

Internal organ in the Tertiary syphilis characterized by the development gummas or


gummy infiltration, degenerative processes and metabolic disorders.

Tertiary syphilis of bones and joints. Defeat bones with tertiary syphilis manifested as
osteoperiosti-one or osteomyelitis. A leading role in their diagnosis plays
radiography. Most often suffers tibia, at least - the bones of the forearm, clavicle, skull.

42. Criteria for the diagnosis of various periods of syphilis.

Diagnosis of congenital syphilis is carried out on the basis of clinical, serological data
and studies of CSF, the maternal history.

study research material produced mainly from the surface of the chancre and erosive
papules. Data should always be cleaned with saline washes of various types of pollution
and previously used external medicines. The best way to detect acyanotic method of
research is in the dark field microscope that allows it possible to watch live treponema
condition with all the features of its structure and movement.

Laboratory diagnosis of syphilis Treponema pallidum includes identifying and carrying


out serological tests
Serology is used for the following purposes: confirmation of the clinical diagnosis of
syphilis, diagnosis of latent syphilis, monitor the effectiveness of treatment, the definition
of cure of patients with syphilis.

In the immune response involved both cell (macrophages, T-lymphocytes) and humoral
mechanisms (synthesis of specific Ig).Protivosifili-cal appearance of antibodies occurs
in accordance with the general laws of the immune response: first produced IgM, as the
disease begins to dominate the synthesis of IgG; IgA produced in relatively small
quantities. Question of IgE synthesis and IgD currently insufficiently studied. Specific
IgM appear 2-4 weeks after infection and disappear in untreated patients after about 6
months in the treatment of early syphilis - after 1-2 months late - after 3-6 months. IgG
usually appear at the 4th week after infection and reach, as a rule, higher levels of titles
than IgM. Antibodies of this class can be stored for a long time even after clinical cure of
the patient.

Modern syphilis serology based on a combination of non-treponemal and treponemal


tests.

Nontreponemal tests detect antibodies to early lipoid nature, such as cardiolipin,


cholesterol, lecithin. Nontreponemal tests are used for primary screening and
quantitative determination of the variant with a titer to monitor the effectiveness of
treatment on the dynamics of reduction in serum antibody titer. For the diagnosis of
syphilis positive result in nontreponemal test must be confirmed in treponemal tests.

To nontreponemal tests are microprecipitation reaction (RMP) with cardiolipin antigen,


which is carried out with inactivated plasma or serum, or its analogue RPR / RPR (rapid
reaction with plasma) in qualitative and quantitative ways.

Treponemal tests detect specific antibodies to species-specific antigens of Treponema


pallidum. These include immunofluorescence (IFA), the reaction of immobilization
acyanotic (RHS), the reaction of passive-gemag glyutinatsii (PHA), enzyme-linked
immunosorbent assay (ELISA). They are used to confirm the diagnosis of
syphilis. ELISA, TPHA and FTA are more sensitive than RHS, however, ELISA, TPHA,
FTA after suffering and cured of syphilis remain positive for many years, sometimes - for
life. Due to the fact that the ELISA and TPHA a highly sensitive, specific and
reproducible methods can be used as qualifiers and confirmatory tests.

1. immunofluorescence assay (IFA).

Reaction Principle is that of serum processed antigen, which is a pale treponema


Nichols strain derived from rabbit orchitis, dried on a glass slide and fixed with
acetone. After washing the drug is processed luminescence nistsiruyuschey serum
against human immunoglobulins. Fluorescent complex (+ anti-human immunoglobulin
fluorescein isothiocyanate) binds to human

immunoglobulin on the surface of Treponema pallidum and can be identified by


fluorescent microscopy. For serodiagnosis of syphilis used several modifications RIF:

a) reaction of immunofluorescence absorption (RIF-abs.). antibodies are removed from


the Group of serum using ultrasonically disrupted treponem culture, which dramatically
increases the specificity of the reaction. Since only of serum diluted 1: 5, then a
modification retains high sensitivity. FTA-ABS. becomes positive at the beginning of the
third week after infection (before the appearance of the chancre, or simultaneously with
it) and is a method of early syphilis serodiagnosis. Often remains positive serum and a
few years later after a full treatment of early syphilis, and in patients with late syphilis -
for decades.

Indications for making FTA-ABS.:

elimination of false positives treponem-tion tests;

survey of persons with clinical manifestations characteristic of syphilis, but with a


negative nontreponemal tests;

b) the reaction of IgM-FTA-ABS. mentioned above that in patients with early syphilis in
the first weeks of the disease appear IgM, which in this period are the bearers of
specific properties of the serum. In later stages of the disease begin to dominate the
IgG. The same immunoglobulin class and responsible for false-positive results, as
group antibodies are the result of long time immunization saprophytic treponemes
(mouth, genitals, etc.). Separate study Ig classes of particular interest in serodiagnosis
of congenital syphilis, in which protivotreponemnye antibody synthesized in the body of
the child, represented almost exclusively IgM, IgG and predominantly maternal
origin. Reaction IgM-FTA-ABS. based on the use of the second phase conjugate
instead of the anti-IgM anti-human globulin fluorescer containing a mixture of
immunoglobulins.

Indications for the formulation of this reaction are:

diagnosis of congenital syphilis (IgG response eliminates maternal origin, which pass
through the placenta and can cause lozhnopolo-

Positive results FTA-ABS. in the absence of the child's active syphilis); evaluation of
treatment of early syphilis, with full treatment of IgM-FTA-ABS. negativiruetsya
c) reaction 19SIgM-FTA-ABS. Underlying this modification RIF is preliminary separation
of larger molecules from smaller 19SIgM 7SIgG molecules of serum. This separation
may be performed by gel-filtration. Research in the FTA-ABS reaction. serum containing
only a fraction 19SIgM, eliminates possible sources of error. However, the technique
setting reaction (especially the fractionation of serum) complex and difficult, which
severely limits the possibility of its practical use.

2. Immobilization reaction acyanotic (RIBT,

RHS).

Reaction principle is that, when mixed with a suspension of patient serum pathogenic
acyanotic living in the presence of complement lost mobility acyanotic. Detected in this
reaction antibody-immobiliziny relate to antibodies and later reach the maximum level
by the 10th month of the disease. Therefore, early diagnosis is unsuitable
reaction. However, in secondary syphilis reaction is positive in 95% of cases. With
tertiary syphilis RHS gives positive results from 95 to 100% of cases. With syphilis
internal organs, the central nervous system, congenital syphilis rate of positive results
RHS is close to 100. RHS to negative as a result of effective treatment comes not
always; reaction may remain positive for many years. Indications for staged reactions
are the same as for the FTA-ABS. Of all the schmooze-bit tests RHS is the most difficult
and time-consuming.

3. Immunosorbent assay (ELISA).

The principle of the method is that the antigens of Treponema pallidum load surface
solid-phase carrier (wells of the polystyrene panels or acrylic). Then, in such wells were
studied serum. In the presence of serum antibodies against acyanotic formed antigen +
antibody bound to the surface of the carrier. The next step is poured into the wells of
antispecies (against human immunoglobulins) serum labeled with an enzyme
(peroxidase or alkaline phosphatase). Labeled antibody (conjugate)

interact with the antigen + antibody, forming a new complex. For detecting it is poured
into the wells of the substrate and indicator solution (tetramethylbenzidine). Under the
action of the enzyme substrate changes color, indicating a positive reaction. Sensitivity
and specificity of the method is similar to the FTA-ABS. Indications IFA formulation are
the same as for the FTA-ABS. The reaction may be automated.

4. the passive hemagglutination (PHA).

The principle of the reaction is that the antigen used as formalinized erythrocytes, which
absorbed antigens of Treponema pallidum.When you add to that antigen serum
agglutination of red blood cells of the patient occurs - hemagglutination. Specificity and
sensitivity of the reaction is higher than with other methods of detection of antibodies to
Treponema pallidum, provided high-quality antigen. Reaction becomes positive on the
third week after infection and remains so many years after recovery. Micromethod
developed this reaction, as well as automated response mikrogemagglyutinatsii.

For different types of syphilis screening recommend the following methods of


serological diagnosis:

1) examination of donors (ELISA or PHA always in combination with MCI, RPR);

2) The initial examination for suspected syphilis (RPR or RMP in qualitative and
quantitative variations in the case of positive confirmation of any treponemal test);

3) monitor the effectiveness of treatment (nontreponemal tests in quantitative


formulation).
43. Etiology , course, classification of syphilis.

Causative agent of syphilis - pale treponema (Treponema pal-lidum belongs to the


order Spirochaetales) - slabookrashiva-yuschiysya spiral organism with 8-14 correct
swirls, similar in shape and size, which is retained during any movement of Treponema
pallidum and even hit her between what- or dense particles (red cells, dust particles,
etc.). There are four types of motion of Treponema pallidum:

1) forward (forward and backward);

2) rotation;

3) flexion, including swinging, pendulum bicheobraznoe and (under the influence of the
first injection of penicillin);

4) contractile (undulating, convulsive). Sometimes observed corkscrew (helical)

movement due to a combination of the first three.

Propagated pale treponema by transverse division into two or more parts. Under
adverse conditions (impact antibodies, antibiotics, etc.) formed an L-shape and cysts,
and from the latter may again be formed spiral form under appropriate conditions.

Treponema pallidum are unstable to various external influences. The optimum


temperature for them is 37 C. At 40-42 C, they die within 3-6 hours and at 55 C - 15
minutes. Outside the human body in the biological substrates treponemy can survive a
short time (to dry). Antiseptics quickly cause the death of her.

Infection occurs through contact with syphilis - more direct, less indirect. Direct contact
is usually manifested sexual intercourse, sometimes kiss. Physicians should be aware
of the possibility of occupational infection by direct contact with the patient during his
inspection and treatment procedures.

Indirect contact through various parts contaminated with infectious materials (spoons,
cups, cigarette butts, medical instruments, used mainly in gynecological and dental
practice).

All manifestations of syphilis on the skin and mucous membranes called


sifilid. Infectious to human health is such syphilides that are wholly or partially deprived
of the epithelium. In these cases pale treponema appear on the surface of the skin or
mucosa. Under certain conditions, can be contagious breast milk, semen, cervical
secretions of the uterus, blood, including menstrual. Sometimes pale treponema found
in patients with syphilis in the elements of a skin rash some dermatoses, such as
contents of bubbles and blisters herpes dermatitis.
Horny layer impermeable to Treponema pallidum, so syphilis infection through the skin
occurs only when a violation of his integrity, which may not be visible to the eye,
microscopic.

( 2 )

( 2 )

( .. )

( 2 )

( 2 )

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( 5 )

( 5 )

CLINICAL PICTURE congenital syphilis

Congenital syphilis is caused by infection of the fetus from the sick mother. Possibility of
intrauterine infection occurs after the formation of the placenta, and therefore placental
circulation, ie by the end of the third and beginning of the fourth month of
pregnancy. The pathogenesis of congenital syphilis depends largely on the immune
response of the fetus and to a lesser extent - from tsitodestruktivnogo action Treponema
pallidum.

Pregnant women with syphilis ends differently: abortion (medical), neonatal death (on
average about 25%), preterm birth, birth of a child with active manifestations of syphilis
and the birth of the patient latent syphilis (average 12%) and, finally, birth of a healthy
child (10-15% of cases). One or the other outcome of pregnancy due degree of activity
of syphilitic infection. The highest probability of fetal infection exists among women
infected with syphilis during pregnancy or the year before its occurrence.

The undoubted signs distinguish Hutchinson triad:


1) Getginsona teeth: upper central incisors, differing in size, smaller than normal, form
a barrel or a screwdriver, tapering to the cutting edge of the semilunar notch at the
cutting edge;

2) parenchymatous keratitis manifested lacrimation, photophobia, blepharospasm,


clouding of the cornea, resulting in a decrease or loss of vision;

3) labyrinthine deafness, caused by inflammation and n-morragiyami in maze


combined with degenerative changes in the auditory nerve.

By probable grounds include the following:

1) saber tibia bending forward as a consequence of tibia (the diagnosis must be


confirmed by X-ray);

2) radiant scars Robinson - Fournier around the mouth opening;

3) yagoditseobrazny skull, developing as a result of oc-teoperiostita frontal and parietal


bones and limited hydrocephalus;

4) syphilitic chorioretinitis;

42 .. Gonorrhea: etiology, epidemiology, classification, pathogenesis, diagnosis.


Gonorrhea in men. Principles of treatment of gonorrhea (fresh and chronic).
GONORRHOEA
Gonorrhea - infectious disease caused by Neisseria gonococci kind and sexually transmitted.

Acute inflammation of the urethra in men, urethra and cervix in women, usually accompanied by the
release of pus out. That's what gave grounds Galen in the II century BC suggest the term
"gonorrhea". While this name gives a misconception about the nature of the disease (the exact
translation - "semyatechenie"), it has been preserved, completely displacing previously tried the
terms "ophthalmia", "clap". However, infectious diseases with the expiration of pus from the urethra
were known long before Galen. Only discovery in 1879 by German scientist Neisser pus patient
urethritis special microorganism naturally causes inflammation of urogenital organs in humans,
finding suggests gonorrhea independent venereal disease.

Etiology. Gonorrhoea - gonokokk - bean-shaped diplococcus gram length from 1,25-1,6 microns
and a width of 0.7-0.9 microns.Gonococci are well painted all aniline dyes. In acute processes in
stained smears reveal a large number of gonococci in leukocytes (Fig. 123, 124). In later (chronic)
stages of the disease, when the discharge becomes scarce, gonorrhea are less common, and their
detection is sometimes necessary to resort to provocation and culture diagnosis.

In the scanning electron microscope have gonorrhea or globular form diplokokkovyh education with
slightly bumpy surface.
In the study of ultrathin sections in gonococci can not identify the cell wall, the cytoplasmic
membrane, cytoplasm with numerous ribosomes mezosomy, with nucleoid DNA strands. On the
surface of Neisseria gonorrhoeae revealed thin tubular threads - drinking, which bind their ability to
genetically transfer some properties, in particular resistance to antibiotics. Revealed by electron
microscopy capsule-like substance used to match the pathogen to adverse conditions and its
persistence in the body of the patient. Cytoplasmic membrane is related to the metabolism of cells.

Under adverse conditions possible L-transformation of Neisseria gonorrhoeae to the loss of the outer
cell membrane. Gonococci grow on

artificial nutrient media in the presence of human protein (ascitic agar) at 37 C.

Some strains of gonococci produce penicillinase, which contributes to their resistance to penicillin
and its derivatives. In many countries in recent years for failing to treat increasingly highlighted
gonococci, penicillinase-producing -lactamase or.

Epidemiology. Gonokokki outside the human body die quickly. Detrimental effect on them various
antiseptic preparations, heat above 56 C, drying, direct sunlight. Temperature below the optimum
gonokokki tolerate poorly and die quickly at 18 C. In pus gonococci retain viability and
pathogenicity until dry pathological substrate (from 30 minutes to 4-5 hours). Infection usually occurs
through sexual contact

by direct contact with a healthy person sick (or outwardly healthy carriers). Occasionally it is not
infected during intercourse, but through an infected toilet articles, linen, most little girls are becoming
infected from their mothers. Anal or oral intercourse may gonococcal infection of the rectum,
nasopharynx, oral mucosa, tonsils. Eye infection in adults is possible when making gonokokkov dirty
hands. The newborn eye infection occurs during passage through the birth canal sick mothers.

Increased susceptibility of the mucous membranes of the urinary organs, rectum, nose, throat,
mouth, tonsils, conjunctiva explained by biochemical, hormonal, immune and anatomical and
physiological
Fig. 123. Gonococcus (methylene blue stain)
Fig. 124. Gonococcus (Gram stain)

characteristics of the organism. Gonokokki preferably affect mucous membranes covered by columnar epithelium.

Immunity. When gonococcal infection has both humoral and cellular response, but does not develop immunity to prevent reinfection.Detectable serum antibodies
protivogono-cocci belong to different classes of immunoglobulins (IgG, IgM, IgA).

A considerable part of it is infected with gonorrhea had been ill again and even repeatedly, despite the high titers of specific antibodies in serum and expressed
sensitization of lymphocytes to gonococci. Also reinfection and superinfection possible while maintaining gonorrhea in the body. Known relative immunity to the
homologous strain of gonorrhea in the "family gonorrhea" when gonococci do not cause their permanent carriers any significant inflammatory response, but cause
acute disease when infected by third parties. Superinfection foreign pathogens regular sexual partners followed by a clinical picture of acute gonorrhea.

Currently, the country put into practice the International Statistical Classification of X with the next revision of the classification of gonorrhea.

A54 Gonococcal infection

A54.0 Gonococcal infection of lower genitourinary tract without periurethral abscess and accessory glands gonorrhea:

- NOS cervicitis

- Cystitis NOS

- Urethritis NOS

- NOS vulvovaginitis

A54.1 Gonococcal infection of lower genitourinary tract with periurethral abscess formation and accessory glands

A54.2 Gonococcal pelvioperitonit gonococcal infection and other urinary organs

Gonococcal (th);

- Epididymitis

- Pelvic inflammatory disease in women

- Orchitis

- Prostatitis

A54.3 Gonococcal eye infection

Gonococcal

- Conjunctivitis

- Iridocyclitis

Gonococcal ophthalmia neonatorum

A54.4 Gonococcal infection of musculoskeletal system

Gonorrhea:

- Arthritis

- Bursitis

- Osteomyelitis
- Synovitis

- Tenosynovitis

A54.5 Gonococcal pharyngitis

A54.6 Gonococcal infection A54.8 Other anorectal gonococcal infections gonorrhea (st) (st):

- Brain abscess

- Endocarditis

- Meningitis

- Myocarditis

- Pericarditis

- Peritonitis

- Pneumonia

- Sepsis

- Dermal.

Gonococcus infection men, as a rule, leads to the appearance of subjective symptoms that force to seek medical help. In women, gonococcal infection often
causes no symptoms, and little is revealed in surveys of sexual partners or developing complications.Apparently, this can be explained by lower health-seeking
women.

This necessitates screening for gonorrhea women with high risk of infection.

28.1. Gonorrhea in men

A gateway for gonococci in men is the urethra. In the first 2 h gonokokki delayed in implementing and using personal prevention methods may be destroyed. On
the mucosa of the front part of the urethra (to the external sphincter) gonococci multiply rapidly as spreading over its surface

particular, and penetrating between epithelial cells in the connective tissue layer, in the urethral glands and lacunae. Gradually gonococci penetrate the posterior
urethra. In this case there is a danger of the seminal vesicles, prostate, epididymis. The incubation period of gonorrhea is often 3-5 days, but sometimes it can be
1-15 days or more.

The clinical picture. Males distinguish fresh sub-divided into acute, subacute and sluggish (torpid); chronic; latent gonorrhea. All forms of gonorrhea may be
accompanied by a variety of local and distant (metastatic) complications.

Gonorrheal urethritis manifested Urethral inflammatory exudate and pain. In acute inflammation, marked redness and swelling of large sponges meatus. From the
urethra, a large amount of yellowish green or pale yellow pus. Sometimes a slight burning or itching precedes mucopurulent secretions. Signs of inflammation are
rapidly increasing, and after 1-2 days formed Front acute gonococcal urethritis. Patients feel pain and stinging when urinating. In subacute anterior fresh
gonococcal urethritis mucopurulent discharge, not abundant, sore jaws meatus is weak, and the subjective feeling insignificant. When torpid fresh gonococcal
urethritis subjective feelings are absent, or allocating scarce almost imperceptible. Sponges meatus not changed. Patients in this case often do not seek medical
help and most dangerous in epidemiological terms.

Later in gonorrhea even without treatment inflammatory response gradually decreases subjective disorders weakened. Urethritis goes into subacute and then
chronic.

If gonococci of anterior urethral fall into the posterior urethra, there is an acute total urethritis (urethrocystitis). Patient has urgent need to urinate, the end of which
there is a sharp pain (terminal). The urine is very low. Sometimes at the end of a drop of blood appears urination (terminal hematuria). In some cases, the severity
of inflammation observed fever, malaise.

Diagnosis of both front and acute gonococcal urethritis total is not difficult. It is based on the data history, the typical picture of the disease, dvuhstakannoy urine
sample
and confirmed by laboratory detection of Neisseria gonorrhoeae (microscopically and culturally). If the inflammation is limited to the mucosa anterior urethra, the
sequential discharge of urine in two cups of urine in the first glass, washing away the pus from the urethra, is muddy, and the second - transparent.

Urethritis in total in two cups of urine is turbid because of pus due to posterior urethral sphincter insolvency internal flows into the bladder (total Piura).

Chronic gonococcal urethritis is caused by the transformation of fresh gonorrhea urethritis. Focal defeat - an inflammation of the mucous membrane of
individual sections, gaps and glands. In cases of lesions only the front part of the urethra subjective feelings expressed slightly, and sometimes
absent. Inflammatory process detected only when the discharge or bonding sponges urethra after a night's sleep. Allocating scarce, mucopurulent, as a single
drop. In chronic lesions of the posterior urethra marked painful ejaculation, frequent urination and pain at the end of urination. Observed disorders of the genitals:
decreased libido, weakened erection, premature ejaculation occurs, sometimes there is an admixture of blood and pus in the ejaculate. Latent chronic gonorrhea
may not be accompanied by subjective sensations. Objective symptom is urethral sponge bonding in the mornings can sometimes increase the selection (after
walking, physical exertion, alcohol intake, sexual intercourse). In some cases, discharge is so small that it is washed away in the urine as the individual strands
and flakes visible in the 1st urine sample at dvuhstakannoy sample.

Laboratory diagnosis of gonorrhea. diagnosing gonorrhea in laboratory studies are crucial. Etiologic diagnosis is performed using bacterioscopic (research
discharge mandatory staining with methylene blue and Gram) and bacteriological methods (crop discharge on special nutrient medium). Diagnosis of gonorrhea is
based on the determination of the pathogen Neisseria gonorrhoeae in the discharge from the urethra, cervical, rectal, oropharynx, conjunctiva, and others with
Detachable put a thin layer on a glass slide, dried, fixed with ethanol, and then produce color 1% methylene blue and Gram. Stained preparations viewed in the
light-optical microscope at magnification 10 100 with immersion.

In preparations stained with 1% methylene blue, the nuclei of epithelial cells and polymorphonuclear neutrophils are colored blue, the cytoplasm - in blue color of
varying intensity. Gonokokk dark blue, bean-shaped, located in pairs. Cocci convex outer surface, with the concave side facing each other. Location gonokokkov
resembles the shape of the coffee bean.

Gonokokki located intracellularly towards leukocytes and surfactants with respect to the cells of the squamous epithelium. Leukocytes within each pair diplokokkov
located at an angle to its neighbors.

Determining the differential diagnostic feature is obtained on Gram stain: gram-negative diplococci is gonococcus.

At short-term storage in the bleach solution (a mixture of ethyl alcohol and acetone) stained with crystal violet dye gonokokki give dokrashivayutsya and red dye
(safranin).

If microscopy revealed typical gonococci, the cultural research is not carried out. To accurately determine the localization of inflammation in the urethra dvuhstakan
apply-ing the trial. More accurate topical diagnosis is possible with ureteroscopy, but can only be performed in chronic gonorrhea. In acute disease, ureteroscopy
may facilitate the spread of infection in the sections lying above the genitourinary system.

Differential diagnosis of gonococcal urethritis urethritis other etiologies (viruses, yeast and other fungi, different cocci, trichomonas, chlamydia, mycoplasma,
etc.) due to the great similarity of the clinical picture can be almost exclusively on the results of microscopy and bacteriological research.

Complications. gonoreyny Acute urethritis may be complicated by the ball-nit, balanoposthitis and inflammatory phimosis, which are similar to the processes of
non-gonococcal etiology. Tyson is a rare complication (abscess glands foreskin - tizonovyh glands) with moderately painful erythematous swelling around frenulum
foreskin. Inflammation lacunar channels (parauretrit) has the form of a point, slightly infiltrated and hyperemic holes on the lips of the urethra. Located in the
urethra alveolar-tubular mucous glands (glands Littre) and lacunae (gaps Morgagni) are always amazed by gonococci (littreity and morganite). When littreite in the
first urine sample appear peculiar purulent filaments by a comma,

it casts ducts of urethral glands. Gonococcus infection of the excretory ducts of bulbourethral glands (Cowper's glands) - cooperite usually goes unnoticed. Only
when there abstsedirovanii pulsating perineal pain, pain during bowel movements and frequent urination. Body temperature rises to 38 C and above.

Stricture becomes resistant gonococcal urethritis chronic outcome. Stricture may be solitary or multiple, length 0.5-1.5 cm One of the first symptoms of stricture is
delayed emptying of the bladder.

Gonococcal epididymitis is caused by penetration of gonococci in the epididymis of the prostate through the urethra semyavy-bearing duct or bypassing it
through the lymph vessels. Contribute to this reduction anastaltic vas deferens arising from irritation verumontanitis, sexual arousal, physical exertion. Gonorrheal
epididymitis usually develops acutely. There is pain in the epididymis and in the groin. Testicle itself remains unchanged. Patients with increased body temperature
(40 C), there are chills, headache, and weakness. Scrotal skin tense, flushed. Epididymis increased egg covers the top, back and bottom, tight and painful. In
subacute and chronic epididymitis pain expressed mild, swelling and redness of the skin may be missing, the body temperature is normal or low-grade, the health
of patients is not impaired.
Gonococcal defeat eggs may occur during the transition from inflammation of the epididymis on the egg, but this is rare. Often inflammatory process involves the
shell eggs, causing accumulation of fluid (acute periorhit). In such cases, the affected half of the scrotum is palpated fluctuating education, which can not
determine the epididymis.

Gonococcal lesion of the prostate can be acute or chronic. Distinguish catarrhal, follicular and parenchymal prostatitis. Prostatitis is often associated with
inflammation of the seminal vesicles - vesiculitis. If the inflammation is limited to the excretory duct, then formed catarrhal prostatitis, no subjective disorder, the
disease remains asymptomatic. Dissemination of lesions on the development of the lobules they tend psevdoabstsessov follicular prostatitis. In this case, the
symptoms of the disease are expressed distinctly. As in the crotch

a sensation of heat at the end of urination there is pain. Possible chills and severe malaise. On palpation the prostate gland of normal size, but may be
increased. Of normal thyroid tissue palpable painful seal.

Acute prostatitis is accompanied by severe parenchymal common disorders with fever, pain in the perineum and suprapubic and dysuric disorders. At rectal
examination revealed diffusely enlarged, painful, plotnovata prostate. Purulent infiltration melting occurs prostate abscess. In these cases, pathological
phenomena are dramatically amplified up to the AUR. Chronic prostatitis has a prolonged duration with discharge from the urethra, itching and burning. The secret
of the prostate often stands after urinating (voiding prostatoreya) or defecation (Defeo-cations prostatoreya). There are various functional disorders of the
genitourinary system, weakening of erection, decreased libido, premature ejaculation. In secret inflamed prostate revealed elevated white blood cell count,
reducing the number of grains of lipoid and sometimes complete absence violated crystallization phenomenon secret.Gonococci are found rarely in bacterioscopic
study and more frequently when bacteriological. Under any form of gonorrhea observed changes in blood: anemia, leukopenia or leukocytosis, eosinophilia,
neutrophils and climbed monocytosis. ESR is often elevated in acute gonorrhea.

43 Gonorrhea: etiology, epidemiology, classification, pathogenesis, diagnosis


Features gonorrhea in women. Principles of treatment of gonorrhea (fresh and
chronic).

Gonorrhea women. most women, unlike men, gonorrhea occurs without subjective symptoms, but
with the defeat of almost all departments of the genitourinary system and the
rectum. Distinguish gonorrhea bottom of the genitourinary system (urethritis, parauretrit, vulvar
vestibulitis, Bartolo nits, vaginitis, cervicitis and endocervicitis) and rising gonorrhea - endometritis,
salpingitis, oophoritis, pelvioperitonit.

Acute urethritis is characterized by a purulent discharge from the urethra; Some patients complain of
pain (cramps) during urination.In chronic urethritis not detect scarce serous-purulent discharge only
after massage of the urethra, which is felt as a thick strand. As often as urethritis, gonorrhea patients
found inflammation of the cervix (cervicitis and endocervicitis).

Diagnosis of gonorrhea is based on the data history, characteristic clinical picture, confirmed by
laboratory tests required, which is used as a discharge of the urethra, parauretral-tion ducts,
endocervical, vaginal walls, a large gland vestibule, and the secret of the seminal vesicles, prostate,
lacunae and prostatic urethra. These laboratory tests are:

1) microscopic detection of gonorrhea with typical morphological and tinctorial properties (Gram-
negative diplococci arranged in pairs and intracellular);

2) selection of a pure culture of the gonococcus (culture method);


3) immunofluorescence and immunohistochemical methods for detection of gonococcal antigen or
nucleic acid.

The differential diagnosis is carried out with other inflammatory diseases of the genitourinary
system, accompanied by her defeat of the mucous membranes.

Treatment is carried out according to the order of gonorrhea? 415 Ministry of Health of the Russian
Federation "On approval of a new protocol, patients' Gonococcal infection" (Wiley, 2003) and
includes the use of antibiotics, immunostimulatory and symptomatic drugs, physical therapy and
surgical treatments. Mandatory means general treatment is antibiotics. Currently, the most effective
agents are cephalosporins, fluoroquinolone-Lona, aminotsiklion (spectinomycin). This is because the
individual gonococcal strains produce penicillin Naz or -lactamases that confer resistance to
penicillin and past its derivatives.

In the treatment of acute localized gonococcal infection used one of the offered products:

Ceftriaxone - 250 mg intramuscularly, ciprofloxacin - 500 mg once inside;

ofloxacin - 400 mg once inside;

spectinomycin - 2.0 g intramuscularly;

benzylpenicillin sodium and potassium salts - an initial dose of 600,000 IU intramuscularly,


subsequent to 400 000 units every 3 hours per course of treatment 3.4 million units.

In the treatment of gonococcal infections with systemic manifestations, the following scheme
antibiotics:

Ceftriaxone - 1.0 intramuscularly or intravenously every 24 hours;

Cefotaxime - 1,0 intravenously every eight hours; spectinomycin - 2.0 g intramuscularly every 12
hours; ciprofloxacin - 500 mg intravenously every 12 hours

Intravenous, intramuscular or therapy with one of these drugs should last at least 7 days.

Possible to use a different algorithm treating: started therapy with one of the above preparations was
continued for 24-48 hours, at a resolution of clinical symptoms of oral therapy for moving one of the
following antibiotics:

Ciprofloxacin - 500 mg orally every 12 hours; ofloxacin - 400 mg orally every 12 hours

Treatment is carried out within 14 days, the lengthening duration of therapy should be strictly
justified.
The choice of drugs is carried out in view of anamnestic data (allergic reactions, hypersensitivity to
study drugs and gonococcus sensitivity to antibiotics and the patient's age, etc.).

If after 10-12 days after antibiotic cotherapy exceptions gonococci inflammation (discharge from the
urethra, the threads in the urine, etc.) are saved, these phenomena should be considered as
postgonoreynye. The patient should be evaluated in accordance with the etiologic diagnosis and
topical begin treatment.

In case of failure of the post-antibiotic treatment, clinical improvement is short and usually occur
early relapse. 35 days (and sometimes later, within one month) after the introduction of antibiotic
usilivayutsyaivnih discharge from the urethra can be found again gonococci. For late recurrence

Islands, which are less common characteristic sluggish, Malaucene-ptomnoe clinical course. Most
relapses occur frequently due to unrecognized concomitant trichomoniasis, as captured by
Trichomonas, gonorrhea due endotsitobioza can maintain vital functions within them, succumbing to
the effects of weak antibiotics. In cases where there is a concomitant of trichomoniasis or suspected
him to be in parallel with antibiotics to prescribe drugs 5-nitro-imidazole (metronidazole, tinidazole,
ornidazole ("tiberal")). "Tiberal" used 0.5 g, 2 times a day for 5 days.

At worse the uncomplicated gonorrhea relapse to apply an antibiotic from another, previously used
by the Group (tetracyclines, macrolides, aminoglycosides, rifamycins, cephalosporins, etc.). Patients
with sluggish ma-losimptomnym relapse over antibiotics should be carried out only after local
treatment.

As immunotherapy vaccine used gonococcal and non-specific immunotherapy involves the use
pyrogenal, prodigiozan, levamisole, metiluratsila, potassium orotate, thymic preparations. Also used
biogenic stimulators (aloe extract, FIBS, vitreous body).

Of physiotherapy techniques used his own blood reinfusion irradiated with laser light, and the means
used for the symptomatic treatment of complications (orchiepididymitis, prostatitis, adneksita etc.) -
diathermy, inductothermy, phonophoresis, paraffin and ozokeritotherapy, mud.

Local facilities for the treatment of gonorrhea are: daily washing urethra solutions of potassium
permanganate (1: 10,000), furatsillina (1: 5000) or that way-pyridinyl lactate (1: 1000); vaginal
douching solution of potassium permanganate (1: 8000) or infusion of chamomile (1 tablespoon per
2 cups of water); urethral instillation of 0.25% silver nitrate solution or a 1-2% solution
protargola;bougienage urethra metal and elastic buzhami.

When proceeding sluggishly (torpid) and chronic form of gonorrhea treatment should be
comprehensive. When treating such patients should be preceded by prescribing antibiotics and
topical immunotherapy treatment. Suspected source of infection and who had sex with patients
gonorrhea-
Rhea individuals who have gonorrhea are found, treatment should be carried out according to the
schemes of chronic gonorrhea.

44. Trichomoniasis. Etiopathogenesis. The clinic, diagnosis, treatment.

Trichomoniasis. Prevention, symptoms and treatments for


trichomoniasis
Contagious nature of the disease that is passed between people through sexual contact, fairly
common in the modern world. To one of these diseases include trichomoniasis.

Venereal disease that affects the vagina in women, and urethral system for both women and
men. The causative agent is considered one-celled parasite - Trichomonas vaginalis.

If trichomoniasis in women following symptoms:

Itching in the vagina, as well as in the external genitalia;

Profuse vaginal discharge (yellow, frothy, foul-smelling);

Pain during urination and during sexual intercourse;

Redness of the genitals.

Symptoms of trichomoniasis in men:

Itching when urinating and during sexual intercourse;

Burning in the urethra and the glans penis;

Frequent urination;

White or gray discharge.

Also in medical practice, there are cases when a person is only a carrier of trichomoniasis in this
case, the symptoms do not occur.

The incubation period of trichomoniasis is one to four weeks. Besides that trichomoniasis are
sexually transmitted, they can still be infected with the personal belongings of students contact
person with trichomoniasis. This can be towels, soap, washcloth, bed linen.Another way to transfer it
from the mother to the fetus during pregnancy.
When detected at trichomoniasis symptoms, should immediately consult a doctor - dermatologist for
an examination. Diagnosis of trichomoniasis is done by examining the patient, and also conducted
laboratory studies. Taken vaginal swabs and urethra. As with any sexually transmitted disease
trichomoniasis is dangerous for its complications. In women, it can be vulvitis, bartholinitis,
cystitis;and prostatitis in men.

Treatment of trichomoniasis must pass all regardless of the form of the disease, whether chronic or
acute. Treatment of trichomoniasis requires an individual, integrated approach. Local treatment and
antibiotic treatment is not always effective. Therefore, treatment of trichomoniasis is carried out by
introducing protivotrihomonadnyh drugs and bracing products. These include bio-stimulants,
vitamins and immune protection. Because of the danger and widespread trichomoniasis, promote
the following methods of prevention. Having one regular sexual partner. Mandatory use of condoms,
douching after sex.

45. Chlamydia. Epidemiology, clinical features, diagnosis, treatment.


Chlamydia - infectious disease, sexually transmitted infections caused by chlamydia ( Chlamydia
trachomatis ). Is one of the most common STDs.
According to statistics, every year in the world ill chlamydia 100 million, while the number of people
infected with chlamydia around the
globe by the most conservative estimates reaches one billion. According to the WHO and numerous
domestic and foreign researchers, urogenital chlamydia is one of the most common diseases, sexually
transmitted, so a serious problem for modern Venereology search is the most effective means of
treatment of so-called non-gonococcal inflammatory diseases of the genitourinary system.
According to various estimates, from 5 up to 15% of sexually active young people amazed Chlamydia
trachomatis. Widespread chlamydial infection is primarily associated with asymptomatic disease.

Chlamydia can cause a range of human organ damage, many times overlapping such, for example,
pyogenic cocci Gram. Indeed, rare microorganism can damage both external and internal genital organs,
respiratory tract, blood vessels and the heart of the intima, the synovial lining of the joints, teeth, organs
of sight and hearing.
subtle long time in the light microscope Chlamydia trachomatis did not attract attention
medicine. Because they had no history of aggravated nor noisy history of the discovery.Chlamydia can
not be classed neither virus nor bacteria. Because they are arranged and operate much more difficult first,
but the second is much easier.
This microorganism is a very unusual story titles. Chlamydia, even long before enrolling them in a
separate family, and the family were awarded lush and unusual
names. "miyagavanelly "," galprovii "," bedsonii "- what is not only poetic names called this
microorganism. Etiology Main article : Chlamydia trachomatis Chlamydia trachomatis - are fixed,
cocci, gram-negative obligate intracellular bacteria. Chlamydial infection mainly affects the genitourinary
system. Currently urogenital chlamydia is the most common (60%) cause of NGU. Existing for a long time
hidden under unfavorable conditions (effects of antibiotics, overheating, hypothermia, cold) Chlamydia
can be transformed into the so-calledL-shape - like "hibernate". This phenomenon contributes to the long
intracellular parasitism without conflict with the host immune system. When dividing cells of the body
dormant chlamydia transmitted to daughter cells. Only in the period of immunosuppression (suppression
of protective forces) may active reproduction and so-called reversion (awakening) of chlamydia L-
forms. At Chlamydia trachomatis share the following antigenic serotypes:
A, B, Ba, C - cause trachoma;

D, E, F, G, H, IJ, K - cause conjunctivitis and urogenital infections;

L1, L2, L3 - cause venereal

Ways of infection
Chlamydia Infection usually occurs through sexual contact, however, the transfer does not occur in all
cases of gonorrhea if the patient will be infected partner during sexual intercourse 3 of 4 people,
chlamydia - 1 of 4. Women are more susceptible to chlamydia.
incubation period - from 2 weeks to 1 month. The main route of infection - vaginal, or anal sexual
contact. Children can become infected during the passage of the fetus through the mother's birth canal,
the patient chlamydia. It is also possible contact-household transmission (set to preserve the infectivity of
Chlamydia household items, including cotton fabrics, up to 2 days at a temperature of 18-19
degrees). Pathogenesis A - uptake by cells of elementary bodies; B, C - the transformation of elementary
body in reticular; D - the growth and development of the reticular cells; E - the transformation of reticular
cells in elementary bodies of the new generation; F - cell destruction and release of elementary
bodies Microbiological features Chlamydia trachomatis :

Intracellular parasitism - combines chlamydia virus, with chlamydia are not able to synthesize
ATP and totally dependent on energy cells - that is in the process of parasitism destroy it
completely.

The presence of the cell membrane - combines with the bacteria Chlamydia - it allows the use of
antibiotics to treat chlamydia.

Tropism for the epithelium of certain organs (urogenital organs, conjunctiva).

Presence of a unique life cycle.

From all other microorganisms Chlamydia differ very special life cycle that begins with infection of
susceptible cells by host-specific chlamydia process of phagocytosis.
Chlamydia exist in the body in 2 forms:

Elementary bodies (EB) - or extracellular infectious cells.

Reticular cells (PT) - the intracellular form of the parasite.

ET penetrating into the epithelial cell, a colony of RT (inclusion) that using the energy resources of the
host cells multiply, going first in the so-called intermediate calf, and then in the new ET that come out of
the destroyed cells into the extracellular space and infect new cells. The entire development cycle lasts
48-72 hours and one phase of development of new forms 200-1000 ET.
first stage of infection - the attachment of metabolically inactive but infectious elementary body to the host
cell. Usually it is not ciliated cylindrical or cubic epithelium (conjunctiva, urethra, endocervix,
endometrium, fallopian tubes).
After attachment should phagocytosis elementary body, and they also induced. Inside the cell, there are
elementary bodies in the cytoplasmic vacuoles - phagosome where chlamydia remain whole growth
cycle, and surface antigens inhibit microbe decay and lysis of the phagosome. Perhaps this is one of the
reasons for chronic infection. Further elementary body is converted into reticular cells already
metabolically active and able to divide. Noncommunicable reticular cells and can not survive outside the
cell. Reticular cells are divided into 8-24 hours, condensed and converted into new elementary
bodies. After 48-72 hours the cells are disrupted and the elementary bodies are allocated in the external
environment. This begins a new cycle of reproduction chlamydia, which lasts about 48 hours.
Chlamydia reminds virus that is completely intracellular bacterium: depends on the nutrients and energy
cells - host does not synthesize ATP, the energy being a parasite. But, like all bacteria, contains DNA and
RNA, multiplies by division, has a hard shell like a gram-negative bacteria, which contains similar
lipopolysaccharide. Clinical manifestations of Chlamydia is often asymptomatic or with minimal
symptoms. Absolutely no symptoms chlamydia occurs in 46% of men and 67% of women. If symptoms
are present, they are not clearly expressed. Symptoms of chlamydia in women: Chlamydia in women
manifests itself by symptoms such as vaginal mucous or mucopurulent. From normal secretions may
differ malodorous or yellowish tint. May appear not strong pain in the external and internal genital itching
and burning (including when urinating), desire to scratch, abdominal pain - in the pelvic area, increased
pain before menstruation, intermenstrual bleeding. Also, a woman may experience general weakness and
mild temperatures - symptoms of intoxication. Chlamydia in men Symptoms of chlamydia in men: Men
have symptoms of the presence of chlamydial infection occur at the beginning, in most cases, as a mild
inflammation of the urethra prolonged (chronic) flow - urethritis, which continues at least several
months. Males may appear meager glassy discharge from the urethra. When urinating may occur itching
and burning. May have different pain, mainly slack: can hurt in the urethra, scrotum, in the back, in the
testes. Temperature may rise - up to 37 degrees, a man may feel general weakness - a consequence of
intoxication. There may be clouding of the urine, the presence of yarns pyogenic therein. Some men may
even spotting after urination or ejaculation. In some cases, long-term preservation of chlamydia occur in
the body in the form of isolated microcolonies on mucous - the so-called carrier. In the clinical,
instrumental and laboratory examination no signs of organ damage is not detected - that is clinically
healthy people, and only when using high-precision methods for laboratory diagnostics (PCR, cultural
studies) revealed chlamydia. This condition is associated with the suppression of reproduction chlamydia
immune system.Complications

Reiter's syndrome (urethritis, oculo-synovial syndrome) - characterized by a triad of symptoms:


urethritis, conjunctivitis and arthritis. Also found in the syndrome of various kinds of skin damage
and tsirtsinarny balanoposthitis.

Urethral stricture

Orchiepididymitis, leading to a narrowing of efferent pathways spermovyvodyaschih and Leydig


cell death that leads to the cessation spermageneza (sperm production) and male infertility.

Chronic prostatitis.

Inflammatory diseases of the pelvic organs (PID) in women - chlamydial infection can get into the
uterus, uterine appendages, woman's fallopian tubes causing inflammation there - endometritis,
salpingoophoritis, salpingitis. Chlamydia is the hallmark of scarring and adhesions in the fallopian
tubes, causing an ectopic pregnancy and tubal infertility.

The main manifestations of chlamydial infections in newborns (congenital chlamydia)

Oftalmohlamidioz (20%) - inclusion conjunctivitis.

Chlamydial pneumonia of newborns (20-25%).

Generalized chlamydia with pulmonary, heart, liver, gastrointestinal tract.

Encephalopathy with seizures, apnea.

Chlamydial pneumonia of newborns - chlamydia infection of the newborn during delivery from the
sick mother often leads to their pneumonia (pneumonia) with extremely severe with a high
mortality rate.

Fitz-Hugh syndrome - Curtis (English) - it is considered early complications of chlamydia


infection. Manifests as acute peritonitis and peregepatit accompanied by ascites and can proceed
[1] [ unauthoritative citation ]
without causing pelvic inflammatory disease .

Diagnosis
Diagnosis of chlamydia complicated because Chlamydia trachomatis - intracellular parasite. In this
regard, for chlamydia take no smear (mucus and discharge), and scraping (cells of the diseased organ),
but the use of non-invasive tests are sometimes more acceptable to patients. Material for analysis for
chlamydia may also be blood, urine and semen in men.
To detect chlamydia, the following laboratory techniques:

Mini test.

You can buy it over the counter and make a analysis on chlamydia. It's quick, cheap, but the accuracy of
these tests will never exceed 20% . Therefore, you can not rely on the test.

Microscopic analysis (general smear).

With this type of survey in men smear taken from the urethra, women - both smears of the vagina, cervix
and external opening of the urethra.

Immunofluorescence (IFA).

Taken from the urethra material stained with a special substance, and then examined under a special
microscope (called fluorescence). If chlamydia are present, they glow like fireflies in the lens of the
microscope. The accuracy of this method - up to 60-70%. Time for analysis - no more than one
hour. immunoassay (ELISA). Determination of antibody (IgG, IgA, IgM) in the blood to chlamydia. These
antibodies are produced by the body in response to infection. However, accuracy and analysis of
Chlamydia not exceed 60% .However, this method is indispensable when conducted a comprehensive
diagnosis of the organism for chlamydia. Polymerase chain reaction (PCR). This method today has the
largest sensitivity and accuracy - up to 100% . To analyze the need quite a bit of material, and the results
are ready in a day or two. But this method sometimes gives false-positive results. To confirm the accuracy
of PCR analysis usually needs to be tested for chlamydia by another method, which will recommend a
doctor or hold a new study in a month, three months and six months.

Seeding for chlamydia (culture method) with the definition of sensitivity to antibiotics.

Prophylaxis in infants.
Neonatal prevention
most effective prevention of chlamydial infection in neonates should be recognized identification and
treatment of infected mothers. Prevention of silver nitrate (1%), erythromycin (0.5%), tetracycline (1%),
conducted after birth, is not an effective method of preventing transmission C.trachomatis from an
infected mother as provided locally and does not affect nasopharyngeal colonization. Such prevention is
only effective in preventing the transmission of gonococci. Children of mothers who are not treated for
chlamydial infection are at high risk of infection, however, antibiotic prophylaxis is not shown, and the
effectiveness of this approach is unknown. According to the authors of the publication, in women with
poor or absent prenatal control should sputum culture at admission to the hospital, and newborns should
be monitored until the results. Infants born to infected mothers treated and observed for symptoms of
infection. Treatment. Chlamydial infection - the most common cause of neonatal conjunctivitis that
develops between 5 and 12-day life. If gonococcal conjunctivitis has purulent, chlamydial usually
accompanied by watery discharge. Difficulties in the differential diagnosis in infants may be associated
with chemical stimulation of prophylactic agents used in the establishment of the nasal lacrimal duct
obstruction, viruses and bacteria. For accurate etiologic diagnosis requires culture-conjunctival exudate
cells. Pending the results of prophylactic treatment is justified newborn erythromycin eye ointment. If
culture is allocated C.trachomatis , shows the drug inside. Erythromycin ethylsuccinate 50 mg / kg / day,
orally for 4 doses 14 days is recommended CDC. Since chlamydia are distributed in the tear ducts and
nasal passages, of at least 33% of infants developing chlamydial pneumonia. In cases where there are no
signs of conjunctivitis, in 11-20% of infants of HIV-infected and treated mothers develop
pneumonia. Symptoms include paroxysmal hacking cough, tachypnea, and emphysema, and bilateral
diffuse infiltrates in the lungs during radiography. Chlamydial pneumonia should be treated with
macrolides inside, but repeated cultural and radiographic research would be appropriate for children with
more persistent symptoms. Without treatment, the disease extends over weeks and months and
promotes further significant increase in the frequency of reactive airways disease. Be aware of adverse
effects of erythromycin, such as hypertrophic pyloric stenosis in infants, which occurs 8 times more
common in children receiving erythromycin inside (but not topically) between 3 and 13 days of
age. Widely known gastrokinetic properties of erythromycin, presumably underlie this phenomenon. Risk
to other macrolides (azithromycin or clarithromycin) in respect of this phenomenon is not known. Although
erythromycin crosses the placenta was not confirmed pyloric stenosis increased risk neonates whose
mothers received erythromycin during pregnancy. Azithromycin 20 mg / kg as a single dose, and within
three days is an effective alternative to erythromycin, but AARP continues to recommend this drug for the
treatment of chlamydial infection. PracticesScreening is a cornerstone of control of chlamydial infection,
but the incidence of these events is low . Noninvasive screening - test on the urine of sexually active men
and women can improve patient compliance screening. Testing of urine specimens reveals 85% of cases
of chlamydial infection as compared to 91% using the vaginal swabs. Increased efficiency is possible by
combining the test for urine and vaginal swabs, which increases the frequency of the identification of
Chlamydia by 9% compared with those using only a vaginal smears. CDC recommended routine
screening includes examination of the pelvic organs in sexually active women under age 25 and older, if
the woman belongs to a group of risk on behavior. Authors publishing believe that any subject who is
sexually active, do not use barrier contraception and / or new or has more than one partner in the last 3
months, or a history of STDs, should be evaluated for C.trachomatis . Number of sexual partners a
woman, her sexual practices and recent changes partner may indicate that it relates to risk of chlamydial
infection or other STDs. Thus, screening for chlamydia is shown, if the patient requires the appointment of
contraceptives and interested in sexual activity with suspected pregnancy, pregnancy, or any history of
STDs, as well as rapes. The most effective method for controlling chlamydial infection in newborns, after
screening and treatment of pregnant women is the use of antibiotics inside. Even if the woman was
treated for chlamydial infection during pregnancy, the diagnosis of chlamydial conjunctivitis can not be
completely excluded. The high degree of vigilance must be in respect of those newborns who noted
cough, tachypnea, wheezing, bilateral infiltration and emphysema.