This work was written in 2005 having as documentation bibliography dating from 1959-1987. Research and studies conducted in dermatology after 2010 can be found in the works presented at international conferences.
1.Production and development of skin diseases
The action of the etiological factors on the epithelial tissue can sometimes occur directly, directly, but in the vast majority of cases it occurs indirectly, through the nervous system, by reflex, or through allergy phenomena or similar to allergies. Even in cases where the lesion seems to occur through the direct action, in reality it intervenes at the same time and to the more important extent the indirect reactivity.
Some external agents have a direct and direct mandatory action on the tegument, related to the fact that they are caustic, toxic or act physically. Thus, acids and concentrated bases, some mineral salts, high heat, intense and prolonged cold, mandatory cause chemical or physical burns, excoriation, acute dermis. The mechanism of production of these lesions is physico-chemical, by coagulating or modifying skin albumin, or mechanically, by removing cell layers.
At the same time with the direct action it intervenes as I specified the indirect, reflex action. The exteroceptors announce the powerful excitation produced by these agents, as well as the morpho-physical-chemical changes, cause reflexes that train the reactivity of the whole body. From here on the development and evolution of the lesions are determined by the reactivity of the body.
The action of microbes and parasites on the skin is inhibited in a first stage of the skin properties we talked about in the previous chapters. If the skin defense is outdated, the reactivity of the whole body intervenes. That is why the appearance, severity and evolution of the lesions are related to the state of the whole body, with its reactions, with the modification of the reactivity to the respective agent.
In most cases, causal factors act indirectly by reflex, by allergy.
Poisoning is characterized by the action of the precise cause, by the fact that accidents that appear at the same dose of toxic, are often almost identical to all individuals, are directly related to the respective toxic. Thus, after a precise toxic amount of mercury, all individuals make the same lesions: digestive, renal, skin. The reactivity of the body passes on the second plane.
Allergic or intolerance manifestations are primarily linked to the body’s reactivity. The cause is an elegant, a certain non -toxic reactogen, which in most individuals does not produce any morbid manifestation. Once these accidents occur, they are different in various patients, for the same cause. Thus, some do in the skin of the skin, prurigo, dermato-epidermis, nodular reactions, others have isolated or concomitant manifestations in the internal organs (gastritis, hepatitis, nephritis, asthma, etc.), or at the vessels (necrotizing capillary purple)
It is worth noting the importance of nerve disorders during dermatosis. It has been seen that eczema, hives, itching, psoriasis, etc., appear or worsen in case of upset, nervous fatigue, emotional states. Thus, the frequent symmetry of the lesions, as well as the changes in the skin in case of central or peripheral nerve lesions, was noted. Experimentally it was shown that during the neuroses caused in dogs eczema, ulcers, skin infections, hair loss, manifestations that are healed only with the healing of neurosis are observed.
Another observation is the different reactivity of the skin to various factors in the external environment. It has been shown that some external agents, food, medicines, substances found in the exercise of the profession, cosmetics or clothing, different individuals do not react the same. In some people there is no reaction from the tegument; Others, on the contrary they make analog type rashes, or different; Some individuals do not tolerate contact with the respective substance at first, others support it at first contact, but at the next or next touches make more or less intense, passing, or prolonged rash.
The allergy includes changes in the body’s reactions to foreign, living or chemical substances. This modified reaction can be more intense, weak or zero. In practice, they are understood by allergic manifestations, especially the most intense. The essential fact in the allergy is that the modification of the reaction occurs according to one or more prior contacts with the respective substance. Usually, the terms sensitivity, hypersensitivity, hyperalergie are usually used.
There are two major conditions for allergy:
In some infections, in some mycosis, allergy occurs in all individuals subjected to infection or parasitosis and can be called collective allergy.
Much more interesting for dermatology is individual allergy, which meets some people towards a certain allergen. This individual allergy, understood as an increased reaction, was also called intolerance.
Allergy can be highlighted most of the times through skin tests.
Para -para -rail is the appearance of a positive skin reaction to an infection, during another infection (for example vaccination)
MetaOalegia is the renewal or intensification of an old skin reaction, or a lesion, under the influence of the action of another substance. For example, a patient had an eruption caused by contact with a spore of a poison. On the occasion of the ingestion of a food or drug, the previous lesion reappears, at the same level.
The classic explanation of the allergy can be summarized as follows: the allergen, the antigen or the reactogen once entered the body, causes the formation of antibodies. At a new introduction of antigen (generally after repeated penetrations), the antibodies formed previously combine with the antigen and thus the conflict, the complex or the antigen-antibody reaction, which is the basis of the allergic manifestations.
Allergens or antigens are mostly protein with large molecule, which also have aromatic groups in their component. Some polysaccharide substances may also have antigenic properties. However, there are semantagenic substances, which do not have complete antigenic properties, in the sense that they cannot cause the production of antibodies. They are called Haptene.
In order to have this quality, it must be fixed by a protidal molecule indifferent and then they become complete antigens. The antibodies formed towards these antigens (haptena+protida molecule) react in the presence of the respective haptea in the same way as the antibodies formed towards the complete antigens react in the presence of the respective antigens.
The antibodies are formed in the reticulo-histocyst tissue, in lymphocytes. From a chemical point of view, antibodies are globulins. Some theories explain their formation in the presence of antigen, others admit the probable possibility of their subsequent formation even in the absence of antigen. It should be emphasized that the nervous system also intervenes in the phenomenon. Thus, the presence of modified globulins is reported to the bark by chemo receptors, and removed adapting to the need to form such globulins, modifies the metabolism through related influxs. It can be seen that the direct excitement of the receptors by the antigen, can lead to the formation of antibodies.
Once you form these antibodies sometimes remain in circulation, (humoral allergy), giving rise to antigen reintroduction to general allergic phenomena. Other times the antibodies are fixed on certain cells (cell allergy) or tissues where the reaction will occur when reintroduction. These cells, tissues, shock organs, are in dermatology the epidermis. Of what antibodies can be highlighted by different skin tests.
The conflict, the shock, the antigen-antibody reaction lead to the release at this level of some chemical mediators, histamine, acitylcoline and heparin. These substances produced in the epidermis act either directly or through the nervous system which leads to the appearance of allergic clinical phenomena.
Allergy tea through its composition has been designed precisely to intervene in the intimacy of phenomena and to counteract the conflict between antigen -antibody and thus avoid allergic manifestation.
The role of the nervous system in the skin pathological phenomena
Researchers have shown the role of the nervous system in the production of antibodies in infectious diseases in that antigens excite peripheral, vascular and even the central nervous system, and as a reflex, antibodies can be formed or without concomitant antigens on the formative tissues of the tissues. antibodies. Allergy and immunity are closely related to the nervous system, and the humoral phenomena are some of their manifestations.
Allergic phenomena are interpreted from the fact that weak excitators produce strong reactions, small doses produce sensitization with increased excitability. Once the pathological outbreak constituted on the bark and on the skin, it is reactivated by small doses, by weak excitations.
The role of conditioned reflexes
This role of the reflexes conditioned in the production and relapses of some skin lesions, of an allergic type or not, is obvious. The reproduction of the conditions in which a substance with mandatory action has acted causes the lesions, without the respective substance. In the usual conditions, many excitants from the external and internal environment produce weak excitations that do not seem to give birth to reflexes. These can be met and become active, they can coincide over time with excitants that produce skin lesions. If these coincidences are repeated, the conditions are fulfilled that the weak excitations will become conditioned excitants, to reproduce the lesions, without the ordinary, obligatory exciting. These cases are common in the working conditions where some professional dermitis appears through mandatory excitants.
In connection with the type of nervous system, these conditioned excitants act more or less intense and a shorter or longer time. Even in skin mycosis, the role of the nervous system and the reactivity of the whole body is very important. Microbes, parasites by their presence, by their secretions and toxins, excite exteroceptors, which transmit to the excitation. The cortical excitation outbreak sends the reflex of the related incit that causes the skin reaction and later through compensatory phenomena, the return to normal. If the cortical excitation outbreak is strong, the lesion does not heal even if we applied an energetic, anti -infectious or antiparasitic treatment. In this case, the central, cortical disorder should be treated.
2.Diagnosis of dermatological diseases
In this chapter I will present some things to take into account when we become patients with dermatological problems and eliminate from our thinking, the fact that we know what we have because we have seen someone else, or I read in a book about that problem.
Knowing the pathophysiological processes that occur in the sick skin and the elementary lesions, as well as the dynamics of their formation, will be easily analyzed these processes within the dermatoses and a dermatological diagnosis can be fixed.
The thorough analysis of the pathological skin processes requires a wonderful investigation of the patient, his manifestations, his general state, including his nervous system and the environment in which he lives.
The examination of the patient must be done in a suitable environment. The room in which the examination is done will have an optimum temperature of 18-20grades. The influence of the cold, the heat and the physiological reactions produced by the thermal factors, which must be taken into account, are well known.
The light on which the examination is made must be the right one. Natural light is the best. Direct sunlight is not suitable, it can change the appearance of lesions. When natural light is not conducive, artificial light will be used. When examining the hair, Wood light will be used, which through its phosphorescence, offers important details in establishing the alterations suffered by parasitic brushes.
By querying the patient, a series of data will be collected and useful in relation to the patient’s affection, his pathological past and the influences of the external environment in which the patient lives and exercises his profession.
The general orientation on the disease is done in order to know the reasons why the patient came to the doctor.
The history of the disease is necessary to know the date when the disease has been triggered, the circumstances in which it appeared, the connection with any cause that the patient can establish, as well as if the members of his family both on the ascending and descending branch have suffered from A similar disease or if the environment in which the patient lives or works, there are others suffering from the same disease.
It is also necessary to establish the evolution of the disease from the appearance of the first symptoms until the date of examination, as well as the possible treatments made and their effects.
Anamnesis will include the age and sex of the patient, his profession, working conditions, material condition, living conditions, housing hygiene, nutrition, sex life, previous diseases, possible laboratory analyzes, family history. All these elements contribute to the correct establishment of the diagnosis. Often it is necessary to study the personality of the patient, to determine the type of his nervous system, to discover all the harmful influences exerted on his nervous system. Possible physical and mental trauma suffered, the way the patient is asleep and wakes up; possible intense and long emotions and other diseases that can compromise the general condition through the excitations exerted on the brain bark.
It is necessary to determine the character of the fundamental processes of the central nervous system (excitation, inhibition, mobility)
Only after this information has been established, can the objective examination, an exam who interests the skin of the patient, have to specify all the particularities of the skin eruption.
The visual inspection allows to specify the shape, distribution of the color of the eruption, as well as other features. Palpia offers data on the consistency of the eruption and on its headquarters in the skin layers, as well as on the sensitive and thermal disorders.
The general skin examination should specify whether the skin is supple, or rough, wet, oily or dry, if the skin has suffered scars, pigmentation.
The distribution of eruptions may be interested, because there are generalized eruptions (throughout the body surface), eruptions located on certain regions (predilection localization), which can be symmetrical (psoriasis) or asymmetrical.
Anatomical-clinical analysis consists in specifying the lesions from which the eruption is composed.
After the wonderful analysis of the skin eruption, the examination of the internal organs must be followed. The skin should not be considered as an isolated organ, it is found in intimate interdependence with the whole body. Any disorder of the internal organs exerts through the brain bark an influence on all systems and appliances, implicitly on the skin. Many of the skin eruptions are morbid manifestations produced by the suffering of digestive, circulatory, respiratory, uro-genital, neurovegetative and endocrine organs.
The exam must be total, regarding the body as a unitary whole, as an inseparable unit.
Laboratory examination, cytological, histopathological examination, skin reactivity, also have a special importance in the diagnosis of dermatoses. Therefore, fixing the diagnosis will result from the analysis and synthesis of all the data regarding the respective condition and it is good to avoid fixing the diagnosis in a single look, the method that can lead to unintended errors.
3.Treatment of skin diseases
The dermatological treatment is one of the most important problems, which interest both the patient and the dermatologist, because both are interested in healing dermatosis during the shortest time and preventing any relapses.
The treatment of dermatoses produced by known etiological factors should not encounter difficulties, because many substances that allow causal treatment are known.
In the cases of unknown etiology dermatoses, numerous failures are encountered due to the misunderstanding of the pathological facts, the neglect of the discovery of the connections that exist between the body and the dermatosis and especially the non -knowledge of the influence that the nervous system has in all the morbid manifestations of the skin and the superficiality with which the superficiality is treat this important problem.
All the therapeutic measures will be futile if the role of the nervous system in the pathogenesis of the respective dermatosis and the role of any pathological disorders of the internal organs, viscero-visceral, viscero-cortical, which if they remain uninfected by treatment, will be played from the beginning of the respective dermatosis. , they will give room for relapses.
The establishment of a rational dermatological treatment can be done only after the establishment of the perticularities that can influence the progress of the morbid process. These considerations require the individualization of the dermatological treatment, which practically means establishing the treatment methods appropriate to the general condition of the body and the local state of skin manifestations. Even in full knowledge of these particularities, the dermatological treatment requires in most cases time and patience. During the treatment, a series of incidents can occur sometimes, due to the individual reactivity and intolerance, which can cause the healing to stop at a given time. That is why the treatment of skin diseases is as delicate as possible, requiring a rich experience, even for the specialist doctor, who can sometimes be hit by difficulty difficult to pass.
In general, dermatological treatment can be external and internally.
For the external treatment, physical and chemical means are available. The physical means are applied as such, while the use of pure chemicals is made very rarely. These substances, in most cases, are applied by special methods, they are incorporated into different vehicles, which applied to the sick skin exerts their action. External treatment can be drug, hydro-meal, physiotherapy, phytotherapy, balneotherapy.
The most important is of course the drug treatment, the drugs being made up of two components: the chemical and the vehicle or the excipient.
These components influence each other, that without taking into account the concentration of the drug, the same chemicals produces different effects, according to the application mode. This fact offers enormous possibilities, which the doctor can use in the therapeutic action, accommodating the way of using the patient’s reactionary particularities.
Different substances are called excipients in which the active drug is incorporated. There are several kinds of excipients:
- Liquid expansion are water, alcohol, ether, chloroform, acetone, glycerin, oil, etc.
When prescribing a medicine in liquid excipient, the solubility of the drug will be taken into account. It will generally be chosen as a liquid excipient a substance in which the active drug dissolves and at the same time, the effects we seek to obtain will be taken into account.
An aqueous solution does not act deeply, compared to an alcohol, ether, etc. solution, which dissolves the fat of the skin, will act deeper. It should also be kept in mind that the solutions are not too concentrated, because they can have a caustic action. Because the solutions macerate the skin and favor the penetration of microbes and pathogenic parasites, their use will be short -lived.
When the active substance is not soluble, the drug will be prescribed in the form of suspension or emulsion.
Powder excipients (powders), are powder substances of mineral or vegetable origin.
Mineral powders, more often used, include zinc oxide, talc, carbonate and bismuth subnitrate, magnesium carbonate, kaolina.
Vegetable powders are starch and coal.
In powders, solid, well sprayed active substances can be incorporated. The powders must be fine and non -irritating.
Fats are of three types: animals, vegetables, minerals.
Mineral fat excipients can be solid and liquid.
The pork lard should be fresh, because it raises quickly and becomes through its irritating acidity for the skin. To prevent this disadvantage, add 5% benzoe tincture.
Lanolina is extracted from sheep wool. It is viscous, it stretches hard, so it can only be prescribed with grease. It is hygroscopic, that it allows the incorporation of a large amount of water, becoming soft. It penetrates through the epidermis harder, but it has the advantage that it does not alter. Launoline can also incorporate liquid substances.
The most used liquid excipient is fish lard. This has the advantage that it is not irritating, it penetrates easily through the epidermis and the high content of vitamin A, accelerating the restoration of tissues. It is applied in rebel prurites and chronic ulcers, having an epithelizing effect.
Vegetable fat excipients are also liquid, solid.
Sweet almond oil is placed in the oils used for hair or in the protective oil against insulation. Its combination with water is contraindicated, because cyanhydric acid is formed, which is very toxic.
Olive oil is much used in cosmetics.
Castor oil is used in the oily drugs used for hair care.
The linen oil is used in burns.
Sunflower oil is very used and replaces previous oils.
Mineral fat excipients.
Vaseline is extracted from oil, being the most used excipient. It has the advantage that it does not alter, it stretches well on the skin, it is not irritating and it penetrates slightly in the skin. Do not mix with water. It can be prescribed alone, or in equal parts with lanolin, especially when an aqueous substance must be incorporated.
Paraffin oil is used in fatty creams, does not irritate the skin, does not alter.
Their medicines and action.
The number of dermatological drugs is high and cannot be entirely in this paper.
According to the action that the incorporated chemicals performs, the external medication is divided as follows:
- Detective and soothing medication.
- antiseptic medication.
- Anti -infectious medication.
- Antiparasitic medication.
- Decapant and keratolytic medication.
- Reductive and Siciva medication.
- Antipuriginal medication.
- exciting and rustic medication.
- discolor medication.
- Caustic medication.
The detective and soothing medication aims to clean the rashes of different secondary bands. For this purpose, it is used: wet applications, powders, mixtures, glycerols.
Antiseptic medication is applied in the treatment of staphylo-successococcal pyodermatitis, in imitiginized dermatoses and in other piococcal dermatoses. It can use: lotions, badijonation, dyes, cheeks and pasta, antiseptic powder.
The anti -infectious medication is based on the biological methods, which try to create immunity from different infectious agents. Local applies with antibiotics, penicillin, sulfamide, etc.
Antiparasitic medication. Iodine tincture can be used in superficial tricophytes. Salicylic acid, benzoic acid can be applied in epidermomicosis.
The decapant and keratolytic medication follows the exfoliation of the horny layer and the removal of the deposits formed by them. For this purpose, the alkaline soap with which the affected region is used can be used. More pronounced decapant and keratolytic effects has salicylic acid, used to remove psoriatic scales.
The medication reducing, decongesting and suicidal is based on the preparations with oxygen greedy substances. This medication is at the same time keratoplastic, decongestant and antipruriginal as well as desensitizer.
Antipuriginal medication is used to combat itching. She is palliative. In itching diseases it is important to know the cause of itching. Here we meet lotions, bandijonari, cheeks, pasta and mixtures. All formulas with phenol, menthol, camphor are often irritating. They will only be used in chronic, rebellious, non -irritable dermatoses.
Exciting, ruby and revulsive medication. In some dermatoses it is necessary to irritate the skin to excite nerve endings, in order to cause a congestive inflammatory reaction. For this purpose, alcoholic tinctures, chloroforms based on camphor, iodine and various acids are used.
The discoloration medication is indicated in the treatment of hyperchromes consecutive to dermatoses and hyperpigmentation in the wishes, etc. Lotions and cheese are used, and for calming the irritation is prescribed a stirring mixture.
Caustic medication is used to destroy, cauterize certain tissues. Concentrated phenic acid, zinc chloride, salicylic acid, silver nitrate, arsenic are used.
In the external medication it is good to take into account the following practical considerations:
If the diagnosis is not accurately fixed, it is good that the external treatment does not change the clinical picture.
In inflammatory conditions, treatment should be started with non -active meduations that can sometimes lead to healing or allow to tolerance of the skin.
When the medication is changed, it is good to try its effect on a small territory. If the treatment is supported, it will be applied on the entire surface of the eruption.
When it cannot be decided for one method or another and when the eruption is symmetrical and stretched, different treatment methods can be tried.
The initial method will not change too often, it is continued for a well -determined time to convince us if it is effective.
When no method will give positive results, the situation will be examined again, to specify if the patient has performed exactly what the doctor has prescribed, or if there is no individual reactivity or microbial factors that keep the morbid state or if the diagnosis is not wrong.
It is recommended that in the prescription of the drugs it is taken into account that in small territories, 20-30 grams of cheeks, pasta, etc., and in the larger territories, the quantity can reach up to 100 grams.
Internal medication in dermatology
For a long time the internal medication in dermatology is limited to iodine, arsenic, mercury, sulfur and calcium. With the development of physiopathology, the connection between dermatoses and the disorders of the central nervous system and internal organs was insisted. Many internal medication are still empirical, based on hypothetical assumptions, but in the future there will be a special emphasis on the connection between dermatoses and diseases of the internal organs. The conceptions of the effects of different drug substances are viewed under the influence that the nervous system exerts in the healing mechanism. In fact, even local treatments can produce some reflex reactions that contribute to the healing of the morbid process.
Various drugs used in combating general metabolism disorders, gastrointestinal disorders, endocrine disorders, have given spectacular results in combating dermatological disorders.
Eating and diet have been shown that they are not just an adjuvant factor in dermatology. Spectacular results were obtained in skin tuberculosis and in all dermatoses where there is a chlorinated retention with a tendency to eczema formation. It has also been observed that in the dermatoses that have as a starting point a gastrointestinal disorder, the establishment of a diet is an indispensable condition for obtaining the most hasty healing.
In itching dermatoses, in food toxiderms it is good to avoid especially spirits, coffee, tea, chocolate, canned meat, sausages, spices, fermented cheeses.
Vaccinotherapy is indicated in pyoderma, furunculosis, erysipel.
Staphyl-Streptococcal anatoxin also gives good results in staphy-states. Antibiotics can be used in erysipelas, boils and secondary infections from eczema, burns, toxicoderma.
4.Elementary lesions of the skin and its appendages
Different harmful causes, represented by physical, chemical, microbial and unknown agents, cause a series of anatomical lesions on the skin.
These anatomical lesions actually constitute defense phenomena against external and internal harmful agents. They result from the defense processes of the skin, a vital organ, endowed with a high reaction capacity.
The morphological changes of the cells are conditioned by several factors, namely the action of the harmful factor exerted on the cell and the reaction that the cell opposes to the aggression of the harmful factor. This reaction occurs under the influence of the central nervous system, through reflexes starting from the cortex. The result of this reaction translates into anatomical lesions that are divided into two groups: passive and active.
Inflammation is the totality of biological reactions determined by the penetration of a flogogenic agent into the skin, either from the external environment or from the internal one.
Elementary lesions in the dermis
Dermal inflammation (dermatitis)
Elementary lesions of the dermis translate into circulatory lesions, hyperplastic lesions and degenerative and neoplastic lesions.
Congestion or hyperemia
In any inflammatory pathological condition, the amount of blood in the vessels of the affected tissues increases, a phenomenon called congestion. This can be active – through exaggerated arterial flow and passive – through venous stasis.
Active congestion is clinically manifested by a limited or diffuse redness, which disappears with digital pressure and is hyperthermic. If the redness is limited, we speak of erythema, if it is generalized, it is called erythroderma.
Passive congestion is clinically manifested by a purplish redness, which disappears with digital pressure. The local temperature is low and the injury is slightly painful.
The edema is formed by the serosity that accumulates in the lacunar system. In most cases, the edema is inflammatory, being accompanied by congestion, and in rare cases it can be non-inflammatory, of mechanical, toxic or nervous origin.
Hemorrhage is produced by the spreading of blood, with or without rupture of the vascular walls. Clinically, the hemorrhage occurs on healthy skin, in the form of red-purple spots, called petesia or ecchymoses according to their size and shape.
Inflammatory disorders of the dermis
When the harmful cause acts through the excitations received from the skin receptors, and the processes are not limited to the circulatory disorders that are in the initial phase of the inflammation, but they are amplified, then they give rise to cellular hyperplasia.
The infiltrate is an agglomeration of cells that modify or transform the structure of the dermis. The infiltrate has a different cellular composition, as the inflammation is acute, subacute or chronic.
In general terms, infiltrates of chronic inflammation are called granulomas. The best known types are: tuberculous granuloma, syphilitic granuloma, mycotic tubercle, leprous tubercle, leukemic and sarcoid tubercle.
Degenerative lesions of the dermis
Degenerative lesions of the skin tissue result in necrosis, necrobiosis, gangrene and infiltration of the skin with substances foreign to the structure of the skin tissue.
Necrosis occurs through circumscribed or total tissue mortification, resulting from a sudden and brutal process.
Necrobiosis is a process identical to necrosis, but the tissue mortification occurs slowly and progressively.
Gangrene is produced by the mortification of tissues that are later invaded by anaerobic microbes, causing gas bubbles and gangrenous emphysema. The color of the gangrenous parts is livid violet, then brown, having a fetid smell due to putrefaction.
Degeneration is due to metabolic disorders and the deposition of particular substances in the skin. Metabolic disorders initially produce a hyperfunction of the cells, and later they reach their vitality, realizing a slow death.
The degeneration of the elastic tissue occurs in the elderly as a manifestation of senility or under the influence of various metabolic disorders.
Inflammatory lesions of the epidermis
The epidermis being devoid of vessels, the inflammatory processes take place differently compared to those of the dermis. The changes are conditioned by the lesions of the dermis. They are varied and translate through exoserosis, exocytosis and through evolutionary changes of the epithelial cells in the different layers of the epidermis.
Sweat gland lesions are called hydrosis. Their inflammation, due to staphylococcal infection, gives rise to hydrosadenitis, characterized by an acute process followed by suppuration.
Inflammation of the appendages of the skin
The inflammation of the hair follicle results in a prominent perifollicular pustule, centered by a strand of hair. The content of the pustule is purulent or seropurulent. One can meet superficial folliculitis in which the hair does not fall out and deep folliculitis in which the hair falls out easily.
Inflammatory lesions of the nails (onychosis, onyxis)
The nail formed by the corneous blade can be the seat of inflammatory processes located either at the matrix or at the nail bed. The inflammatory process leads to the fall of the nail, and the newly formed nail is not compact at first, but consists of soft horny lamellae.
When the nail is invaded by cryptogamic parasites, it partially or totally dissociates, it becomes brittle.
Elementary injuries produced by color changes.
A spot or macula is an elementary lesion characterized by a special color, which forms on the skin in a circumscribed or diffuse territory. This difference in coloration is conditioned by the modification of the factors that as a whole affect the normal coloration of the skin, namely the melanic pigment, the blood vessels and the structure of the epidermis.
Dyschromic spots are characterized by the fact that they do not disappear with finger pressure, are permanent or transient and are not accompanied by inflammatory phenomena.
They can meet:
Hyperchromic or pigmented spots, conditioned by an excess of pigment, having a brown-black color:
-congenital (pigment nevi)
Achromic spots, conditioned by the lack of melanic pigment.
- congenital albinism
-acquired- primitive (vitiligo)
Artificial spots, conditioned by coloring substances artificially introduced into the skin or substances that are formed in the skin by hematogenous means.
-circumscribed: macules, ceruleus, tattoo
-diffuse: argyria (ingestion of silver-based preparations)
Vascular-blood spots are caused by the alteration of two elements, closely linked from a physiological point of view, that is, blood vessels and circulating blood. The common feature of these stains is their red-violet color, due to the presence of blood.
-Vascular spots: congenital-vascular nevi, angiomas
-Erythematous spots, caused by an inflammatory process. They have a pink or violet color, disappear with digital pressure and evolve quickly
-Purple spots, conditioned by the overflow of blood in the skin tissues. They do not disappear with digital pressure, they evolve quickly, they are not inflammatory. According to their size, we distinguish petesia, ecchymoses, suffusions. Their color varies with age: blue, brown, greenish, yellow.
Solid elemental damage
The elementary lesions included in this group are caused by acute, sub-acute and chronic inflammatory processes (edema, infiltration, hyperplasia, hypertrophy and degeneration).
Their common characteristic is the fact that they are solid, have a hard consistency, are prominent and do not contain liquid.
The urticaria plaque is a circumscribed, flattened or hemispherical, prominent, red or porcelain-white, surrounded by an erythematous halo. Its size varies from a grain of rice to large sizes. Its duration is ephemeral, it can appear without subjective symptoms, but it is usually accompanied by itching or stinging.
The papule is a circumscribed elevation of the skin, hard, resistant to palpation, resolving and containing no liquid. It does not leave a scar.
- The tubercle is a circumscribed, round elevation. It has a slow evolution, often with a tendency to necrobiosis and the formation of ulcers.
- The goma is a formation characterized by a nodule, usually larger, at first hard, round, which successively catches all the layers of the skin, having the starting point in the hypodermis. Due to its evolutionary phases, goma leads through necrosis to the destruction of the skin and the formation of deep ulcers.
- Keratosis is characterized by a circumscribed or diffuse hyperplasia of the stratum corneum, which leads to the thickening of this layer and to changes in the consistency of the skin. When keratosis is generalized, corneous production is more discrete (eg ichthyosis).
- Lichenification is characterized by an excessive thickening of a more or less limited skin territory, its surface presenting a grid with deep folds crossed in opposite directions. It can be primary or secondary, when it is produced by repeated rubbing, scratching, and can occur, therefore, in chronic itchy diseases.
- The vegetation is characterized by a soft, filiform or globular excrescence, with a branched surface like a cauliflower. The vegetations can be primitive (venereal vegetations) or secondary to chronic inflammations (pyoderma vegetatus).
- The tumor is a circumscribed formation of the skin, non-inflammatory, which tends to persist or grow. This definition includes a whole series of lesions that are very different from each other in terms of size and histological substrate.
Elementary lesions with liquid content
- The vesicle is a clear, circumscribed, hemispherical collection of serositis, like a point or a needle. The evolution is characterized by the rupture of the ceiling of the vesicle and the formation of an erosion that is covered with a crust. It does not leave a scar.
- Bula, or flictena, is a collection of circumscribed serosity larger than the vesicle.
- Pustule is a circumscribed collection of the skin with purulent liquid content. It can be primary, when the liquid content was purulent from the very beginning, or secondary, when the pustule resulted from the purulent transformation of a vesicle or bubble.
Cutaneous wastes are morbid formations that result from the accumulation on the surface of the skin of physiological or pathological secretions, or of necrotic tissues or epithelial cells that are more abundantly shed from the surface of the stratum corneum.
- Scales are small fragments, horny crumbs, which come off on the surface of the epidermis. According to their size, we find pityriaziform scales having the dimensions of callus elements (pityriasis)
- lamellar scales, up to several centimeters in diameter (psoriasis, exfoliative dermatitis.)
- scales in the form of large flaps (scarlatina, some erythrodermas)
- The crust is a concretion that forms on the surface of the epidermis following the drying of physiological or pathological secretions (serosity, pus, blood, sebum, parasites). The crust appears as a phase in the evolution of vesicles, bullae, pustules and ulcers. It can also result from the accumulation of parasites.
- An eschar or boil is the injury that results from the necrosis of a limited part of the skin. The lesion is black. It is removed from the skin leaving an ulceration that ends in a scar (gangrene).
The scar is the consecutive formation of the processes that destroy the layers of the skin, being made up of an unformed tissue, meant to replace the substance losses suffered. It can be, as the case may be, pearl-white or pigmented. We can talk about a normal scar, when it is smooth, with a surface free of hairs and pores; vicious when there is adherence to the underlying plans; keloid when it is hard, painful red, fibrous and often hypertrophic. The scar is the posthumous witness of ulceration.
Atrophy translates into an alteration of the skin, especially of the elastic and connective tissue. In this case, the skin thins, becomes smooth, dry.
Skin damage caused by cold
Frostbite is a local condition, sometimes accompanied by general phenomena, produced by the action of cold on the body.
The determining cause of frostbite is the cold. In most cases, a number of favorable factors are added to the action of the cold, both internal, in which nervous reactivity is decisive, and external (meteorological, clothing).
Frostbite was classified from an anatomical-clinical point of view into 4 degrees.
First degree frostbite is characterized by a red-violet erythema, with slight edema, accompanied by severe pain, burning sensation, itching, stinging or paresthesias. After healing, the patient is left with itching and an exaggerated sensitivity to cold.
Second degree frostbite is characterized by the appearance of blisters, filled with clear or bloody liquid and necrosis of the epidermis. After the opening of the blisters, you can see the dermis with a purplish, sometimes greyish, mortified appearance. Atonic gray ulcers are very difficult to repair. The intense pain at the beginning, especially when the secondary infection appears, disappears after some time.
Degree III frostbite. The skin and hypodermic tissue are mortified, cold, livid, being covered by large, bluish blisters with hemorrhagic content. Part of the tissue is removed in the form of eschar, leaving ulcerations that usually develop over a long time and heal very slowly.
Degree IV frostbite is characterized by dry or wet gangrene phenomena affecting the skin, soft tissues and even bones. after 9-17 days, a demarcation groove appears, which separates the necrotic tissues from the healthy ones. Necrotic tissues are removed in 2-3 months. The healing period is very long and followed by nervous disorders that explain the persistence of trophic disorders and osteoporosis at the level of the injured limb segment.
The complications of frostbite are of three types: infectious, general infectious, residual trophic disorders.
The emergency treatment of reversible phenomena in the pre-reactive period must follow:
- the reactivation of local thermal conditions: the frostbite is removed from the action of the cold and the heating is done gradually. Friction with snow is prohibited. Prolonged warm baths (balneological baths with plants) are preferred, which combat spasm. The water gradually heats up in 20-30 minutes from 18-37 degrees.
- the reactivity of the local circulation through vasodilators.
- infection prevention.
Injuries caused by X-rays and radioactive substances
X-rays and radioactive substances, if overdosed, produce a series of skin lesions called radiodermatitis. The clinical aspect and evolution of these poor inflammatory reactions vary in relation to the intensity and penetration power of the irradiations.
Radiodermatitis can be early or late.
Early radiodermatitis occurs in patients irradiated all at once or at a short interval with a dose of X-rays that exceeds the minimum dose (500r)
After a latent period of a maximum of 3 weeks, lesions appear that vary from erythema and pigmentation to radionecrosis. The softer the rays and the higher the dose, the shorter the latency period.
And here you can find radiodermatitis of the first, second and third degrees (radionecrosis).
Late radiodermatitis occurs several years after irradiation, as a result of the accumulation of small and repeated doses of radiation. They are mostly found in radiologists who do not take sufficient protective measures.
Radiodermatitis cancer is rare and appears 10-20 years after irradiation. Neoplasias occur at the level of hyperkeratotic lesions, or atonic fissures and ulcerations.
Skin diseases caused by light rays
The rays of the solar spectrum are capable of producing a series of skin conditions known as lucites or photodermatoses.
In relation to their pathogenic mechanism, photodermatoses are divided into:
Traumatic photodermatoses are the changes suffered by normal skin exposed to light rays that are too intense or for a long time.
-Solar erythema is the typical phototraumatic lesion and is compared with a first degree burn, and in the case of flash burns, with a second degree.
The lesions appear a few hours or even a day after exposure, and may be accompanied by headache and fever. The condition heals in a few days, being followed by scaling and diffuse pigmentation. Solar erythema is easy to prevent if exposure to the sun is done gradually. The application of creams or oily solutions on the skin, which contain chemical substances that absorb ultraviolet rays, makes the epidermis resistant even to prolonged exposure.
Sailor’s or farmer’s skin. Prolonged and repeated exposure to the sun’s rays, especially in particular weather conditions (wind), causes pigmentation, atrophy and degeneration of the skin known as farmer’s or sailor’s skin in the uncovered regions of the body. In individuals with such skin alterations, senile keratomas and skin cancers appear more frequently.
Photodynamic dermatoses occur under the influence of substances in the skin that strengthen the effect of light rays.
Burns are local injuries similar to wounds, very often infected with serious repercussions on the whole body. They are caused by the action of heat on the tissues. Somewhat similar injuries are produced by electricity, some chemical agents, caustics or irradiation.
In essence, the tissue changes produced under the influence of heat are due to the coagulation of tissue proteins, followed by inflammation and sometimes necrosis.
Burns are accompanied by general “burn disease” phenomena, the first being shock (similar to traumatic shock) on which the patient’s life sometimes depends.
The burns were classified from an anatomo-clinical point of view in relation to the intensity of the tissue alterations and the depth of the lesions, in three degrees, to which a fourth is added (tissue carbonization)
First-degree burns (erythematous burn dermatitis) is a reversible alteration of the epidermis and dermis, which translates into erythema, which exceeds the burned surface, has blurred edges and is accompanied by edema. For an adult, it does not present any seriousness if it is not extended, but it can cause death in infants and children.
Second degree burn (bullous dermatitis due to burn). Shortly after the accident, blisters filled with plasma form on the red and inflamed skin, located either between the epidermis and the dermis, or in the thickness of the epidermis.
Third degree burn (burn necrosis) is the result of necrosis by coagulation, which affects, apart from the epidermis, the dermis and the hypodermis and sometimes even the muscles. Because the nerve endings are destroyed, the lesions are less painful than those of the second degree.
IV degree burn (carbonization) occurs when the heat has destroyed a segment of a limb (finger, hand, etc.) by carbonization, leaving the patient mutilated.
Burns that exceed 10% of the body surface are accompanied by shock phenomena, which appear in the first hours after the accident. This shock goes through a period of excitation and a period of inhibition. During the period of excitement, the patient is agitated, delirious, screams of pain, and the pulse is fast.
During the inhibition period, the patient is adynamic, pale, has difficulty answering questions or is in a state of unconsciousness. The pulse is weak, the temperature and blood pressure low. This last period is often followed by coma and death, which occurs in 12-24 hours.
Even if the patient has passed the critical phase, created by the neurogenic shock in the first 24 hours, the situation continues to be serious, due to the hemodynamic and metabolic disorders, following the plasmorrhage. At the level of the burn, a large amount of plasma transudates, producing a hemoconcentration and an immortal loss of proteins. The patient is in a state of numbness, with slow and irregular breathing, oliguric, febrile.
The burn that has overcome these accidents remains exposed to the serious danger of secondary infection, which is a constant complication of burns. Infected burns are accompanied by a toxic-infectious syndrome that can sometimes lead to death through septicemia. Resistance to infection, as well as scarring, are hampered by the so-called chronic burn shock, characterized by hypotension, hypoproteinemia and anemia.
The treatment of burns must be local and general. General treatment is essential in all cases that exceed 10% of the body surface. This general treatment must first address the shock and the moderate heating of the patient to 22-24 degrees Celsius. The treatment of shock is an emergency treatment and must be done preventively, before its occurrence or during the period of excitement. The infection must be prevented starting from the first 24 hours.
The local treatment is generally done after the shock has passed, because applying the dressing would exaggerate the shock.
One of the revolutionary theories for treating serious skin diseases is to treat the patient in the open air with a bath of light and infrared rays simultaneously with the application of an extract of animal and vegetable origin to the skin, and internally using special teas. They can prevent shock, hemodynamic and metabolic disorders, prevent secondary infections and the skin heals quickly. For now, this product called epithelial bioregenerator is still in the experimental stage.
Pyodermas are inflammations of the skin due to pyococci, ie staphylococcus and streptococcus, the usual germs of suppuration. Both staphylococcus and streptococcus constantly colonize the skin, the number being directly related to the state of cleanliness and hygiene of the skin. Staphylococcus is 10 times more common than streptococcus and is located especially in pilo-sebaceous openings.
Staphylococcus infections are more common in adults, while streptococcus infections are more common in children.
In certain regions of the body, such as the envelopes, parts covered by hair, saprophytic pyogenic germs are much more frequent, due to the conditions of heat, humidity, pH and mechanical irritation, which favor the multiplication and development of microorganisms.
Pyococci can live indefinitely on normal skin, in a saprophilic state, producing pathogenic changes only when the epidermal barrier was removed by a microorganism and it became possible to inoculate the deeper layers. Rarely, pyococci from a skin or mucosal lesion are transported by hematological route and cause skin lesions of endogenous origin.
The extent of the lesions is determined by two factors: the virulence of the germ and the body’s susceptibility to infection, which is conditioned by age, fatigue, intercurrent diseases (diabetes, jaundice, nephritis, etc.)
Acute superficial folliculitis (impetigo) occurs, especially around various wounds, burns, microbial dermatoses, or after prolonged wet dressings.
The conditions of heat and humidity, the maceration of the envelopes through sweat or pathogenic secretions, as well as the lack of local hygiene, favor the appearance of folliculitis lesions. Among acute superficial folliculitis we mention: folliculitis after shaving, follicles following the application of pomades with tar, mercury or professional folliculitis (on contact with mineral oils, hypochlorite, cement, etc.).
The elementary lesion is a superficial pustule with a diameter of 5-6 mm that starts with redness, followed by a grayish-yellowish pustule the size of a needle. After an evolution of a few days, the pustule dries up and turns into a grayish-yellow crust that detaches without leaving a scar.
Deep acute folliculitis (jug) is eyelash folliculitis. The appearance is not sudden, but is preceded by redness, swelling and pain. After 1-2 days, a pustule appears centered on a strand of hair. After a few days, the contents of the pustule are removed or dry, giving rise to a crust. This condition is relapsing.
Folliculitis of the nostrils is caused by chronic rhinitis, epilation or a more or less delicate cleaning of the nasal passages. It starts with itching, a feeling of tension and redness of the affected nostril. When the lesion expands, a boil of the nose is born, which can lead to complications.
Subacute and deep chronic folliculitis is an infection of the pilo-sebaceous follicles, with chronic evolution, which can be located in the beard, armpit, pubic region, or in any part of the body covered with thick hair. In general, the lesions start at the mustache, in the middle, due to rhinitis and from here they spread symmetrically to the beard. Less often it is limited only to the mustache. A sensation of pain, stinging and itching appears. The pustules heal spontaneously in a few weeks, but are followed by new lesions that give the eruption a chronic evolution, with internal and external disturbances. Rarely, the follicular papillae are destroyed, leading to alopecia.
Chronic alopecic folliculitis are chronic follicular inflammations of the beard, which appear in the form of a plaque, usually unilateral, whose central part is alopecic, due to a scarring process. Alopecia is permanent.
Furuncle is an inflammation of the pilo-sebaceous follicle, which constantly affects the sebaceous gland and the tissues around the follicle. The inflammation is caused by infection of the follicle with staphylococcus. The condition can also be located outside the pilo-sebaceous follicle, at the level of the sweat or ceruminous glands. The nodular lesion is constantly accompanied by central necrosis, which leads to the elimination of a central plug. Small traumas caused by scratches, scratching and rubbing favor the penetration of the staphylococcus in the depth of the skin tissues. The general condition conditions the appearance of boils. The body’s defense reaction to staphylococcus is reduced during diabetes, chronic nephritis, hypovitaminosis, constipation and individuals who do excessive physical work.
The causes that cause dermatosis
The causes that can cause dermatosis are particularly numerous. They can come from the external or internal environment.
External causes can be: trauma, stings, dust. Scratching and rubbing can be important provoking and aggravating factors.
Thermal factors; heat, cold, especially associated with humidity, dryness and wind.
Radiation: sunlight, X-rays, radium.
Chemical factors: medicines, and organic substances of animal or vegetable origin, with which the skin comes into contact.
Animal parasites (mites, insects) and plant parasites (pathogenic fungi, various microbes, are also part of the external causes that produce dermatosis.
- Factors that, although coming from the external environment, act internally. These are: foods, drugs and toxins, microbes that cause general infections with skin symptoms or outbreak infections. Along with microbes, intestinal worms can also be reported.
- Morpho-functional disorders of the viscera and systems also play an important role.
- Dry, seborrheic or hyperhidrosis skin, as well as alkaline skin, predispose to some dermatoses.
-Gastrointestinal and liver disorders play a significant role.
- Endocrine disorders, especially ovarian and less thyroid, adrenal disorders, can sometimes be highlighted.
- Blood and vascular diseases can be accompanied by skin lesions.
-The morpho-functional disorders of the nervous system and the character of the fundamental processes of the central nervous system, excitation, inhibition, mobility, which together allow the identification of a mode of higher nervous activity, have a particularly important role on the appearance and evolution of many dermatoses.
-A series of nutritional and metabolic disorders cause or worsen some dermatoses. Diabetes favors the development of infections, gangrene, skin mycoses; metabolic disorders in the course of gastro-intestinal and liver diseases, hormonal disorders. Avitaminoses, nutritional deficiencies, which can cause skin disorders, should also be included here.
- Heredity and individual predisposition play an important role. It cannot be ignored that the same cause, acting equally on different people, can cause dermatosis in some of them, while others remain immune, and the skin lesions that appear, although caused by the same cause, often have different aspects. On the other hand, it is known that the same skin lesion can be caused by different causes. It is clear that these facts are due to the individual’s own reactivity. This own reactivity is due to: a) heredity, i.e. the transmission not only of innate qualities, but also of those acquired during life; these skills are transmitted through individual metabolism and through the type of nervous system; b) the influence of the external environment (living conditions, food, work) as well as the influence of the internal environment (different morpho-functional and metabolic disorders), which can change the reaction properties of the nervous system and therefore of the whole organism.
The existence of some diseases
There are families in which there are congenital, constitutional predispositions, unmodified by other influences, because the way of life, food and work are the same. The disease, once it appears, tends to reproduce in the family. It can be exemplified by the palmo-plantar keratoderma that appears on the island of Meleda, in families that have lived the same life for generations.
Another example would be the psoriasis disease that affects almost a quarter of the population of an area in southern Italy, where family traditions have been preserved for over hundreds of years.
Changing the external, internal, social environmental factors can make the disease with a hereditary predisposition no longer appear in the offspring
- The economic and social factors are very numerous and complex. Their role is in the foreground. The economic level, living and food conditions, the degree of health education culture, are a series of factors that have a great importance on the frequency of skin diseases.
If we analyze the internal and external causes, we see that they can be of two types: predisposing and determining.
Sometimes, especially when it comes to external factors (heat, cold, chemical substances), the connection between cause and effect is obvious. Other times, for example when it comes to internal metabolic factors, they are harder to highlight, and their role harder to appreciate. Often the etiological factors are multiple and it is difficult to specify which of them are provocative and which are predisposing. In these cases, it is necessary to determine the cause that constitutes the etiological dominance.
Parasitic dermatoses of animal origin
Dermatoses caused by insects.
Pediculosis is caused by lice, parasites that belong to the class of insects. There are three varieties of lice, according to their shape and size, according to the type of lesions they cause and according to their locations. Thus, pediculosis of the head, dediculosis of the body and that located in the hairy regions can be found.
Among other insects that cause rashes are mentioned fleas, bedbugs or wood lice, mosquitoes.
Bees and wasps cause severe pain at the site of the sting, followed by redness and swelling of the region. When the stings were numerous, the pain is more intense, the swelling more pronounced, everything being accompanied by serious general phenomena, fever, dyspnea, asthenia and sometimes even death.
Caterpillars also cause itchy, erythematous and vesicular rashes on human skin, which can become generalized. The lesions are more linear, due to the path traveled by the insect, which deposits, through its bristles, the irritating venom of its subcuticular glands. Lesions usually heal spontaneously.
Scabies or scabies is a dermatosis caused by the parasite called the scabies mite. In general, the infection starts from the female, which lays its eggs in the thickness of the stratum corneum. For this purpose, it pierces the epidermis with its beak and inserts itself into it, where it slowly digs a gallery, from which it cannot get out, it finally dies at the extremity of this trench, not before laying eggs, which in a few days turns into larvae. They come out through small holes and spread on the surface of the skin, where after a few more days they turn into nymphs. During all this time, the nymphs, males and females, spread over the whole body, bite the integuments to feed and give rise to a series of other injuries. The treatment of these injuries is done with antiparasitic pomades containing sulfur, calcium carbonate, petroleum jelly.
Ticks are larger mites up to 4mm long, which attack all animals and people who live more in forests. Through the stings of larvae or adults, these parasites cause a series of itchy lesions to humans, which can lead to complications. Because when the biting parasite remains embedded in the skin, it is advisable not to pull it out violently, because it can give rise to skin suppurations. A few drops of gasoline or oil applied to it are enough to remove it easily.
Spiders can also cause, through their stings, especially at night, after a 24-hour incubation, inflammatory and painful lesions, in the middle of which blisters appear with a reddish-purple exudate, which then leave behind ulcers that heal through scars. In the more serious forms, found more often in tropical countries, the skin lesions can become necrotic and expand, accompanied by high fever and other serious general forms that can sometimes even lead to death. The treatment consists in opening and disinfecting the blister, with subsequent applications of wet antiseptic dressings.
The scorpions, through their stings in the skin, also cause, with the help of a needle, along which the venom flows, a papular lesion, of a violet color, on the surface of which a flictena appears surrounded by an accentuated inflammatory area. Sometimes the skin lesion is accompanied by general nervous phenomena in the form of convulsive seizures. The treatment consists in extracting the needle with tweezers, opening and disinfecting the blister, followed by wet antiseptic dressings.
Dermatoses produced by bacilli
Leprosy is a chronic, generalized infectious disease produced by the Hansen bacillus. It is located especially on the skin, the peripheral nervous system, but also affects the lymphatic system and various viscera. The evolution is long, chronic, with outbreaks and remissions, often fatal, death occurring through visceral injuries or intercurrent infections. Leprosy is a contagious, transmissible disease.
The bacilli enter the body either through the skin (in warm countries) or through the mucous membranes and primarily through the nasal mucosa. The role of the nervous system is very important in mobilizing the body’s defense systems. Once the bacilli enter the body, they slowly multiply at the inoculation site, then spread regionally and throughout the body. The leprous process affects the reticulo-endothelial tissue, including the ganglia, and causes a true chronic, inflammatory infection. Leprosy incubation is variable, but in any case long, at least months, sometimes 10-20 years. In reality, the infection is slow, which explains the apparent long incubation period. In the beginning, uncharacteristic general symptoms appear: fatigue, anemia, apathy, drowsiness, rheumatic pain, muscle pain, digestive disorders, anorexia, diarrhea, tingling, localized or generalized itching, neuralgia, cold sensations, mild febrile attacks. Some particular signs are: rebellious, dry rhinitis. Characteristic lesions called leprosy may appear on the skin during this period.
Dermatoses caused by physical agents
Normal skin, by its structure, is able to withstand, without being damaged, external physical and chemical excitations up to a certain intensity. After these excitations are too intense, the body reacts differently, in relation to the nature of the stimulus. Reactions to external physical and chemical agents are generally limited to the place of action of the respective agent.
-Mechanical agents that act with a low intensity produce injuries that only affect the epidermis and heal without a scar. Such injuries are erosions, exulcerations, excoriations following scratching caused by pruritic diseases. When the respective traumatic agent acts more intensely, the lesions affect the dermis and hypodermis, giving the appearance of a wound, contusion, hematoma.
- Intermittent pressure, repeated for a long time, produces inflammation, pigmentation of the skin and as a process of physiological adaptation hyperkeratosis occurs, which can be of two types:
a) The callus is a yellowish or brown hyperkeratotic lesion, wider on the surface, discretely prominent, whose edges are imperceptibly continuous with the normal epidermis. Only some plantar injuries are painful, especially when they are accompanied by cracks. The most frequent location is at the level of the legs and is due to the pressure exerted while walking.
b) The corn is a round, well-defined hyperkeratotic lesion, with a diameter varying between 5-10mm, painful. The callus is prominent, but it sinks into the underlying dermis, irritating the skin nerves and causing spontaneous pain, especially when pressure is applied. The hyperkeratotic epidermis is often translucent and very hard, having the consistency of a nail.
Permanent pressure can produce necrosis through ischemia (eschar that occurs in immobilized patients).
Dermatoses caused by chemical agents
The skin is equipped with a fairly marked resistance to chemical agents. However, there are substances that, in certain concentrations, constantly produce skin inflammation or necrosis. Along with these toxic substances, there are others to which the body only reacts after a prior sensitizing contact. Chemical agents that are toxic only to the skin of sensitized individuals through repeated contact are called allergens. The skin reaction to various allergens does not depend so much on their nature, as on the state of hypersensitivity in which the respective individual is. The skin of these individuals reacts to contact with small doses of the allergen, through inflammation of the eczema type. This is the mechanism of production of many occupational eczemas. Initially, at the point of contact of the chemical substance with the sensitized skin, an irritation dermatitis characterized by erythema, edema, and bubbles occurs, so that later, as the sensitivity increases, an erythematous-vesicular eczematiform eruption occurs, which exceeds the surface of contact.
Chemical eczematiform dermatitis, like any eczema of external cause, is capable of producing secondary reactions at a distance, of the eczematide type.
The skin of the young and old is less resistant to irritating chemical agents. Dry skin is more susceptible than oily skin.
Skin with normal reactivity usually responds to chemical irritations with an inflammatory reaction, called chemical irritation dermatitis, the type of which is dermatitis produced by vesicating substances. There are individuals who develop contact dermatitis in the presence of substances generally well tolerated by others. In these cases, individual susceptibility probably related to a state of special sensitization intervenes.
Chemical irritation dermatitis is the simplest skin reaction to a chemical agent. At the point of contact, an acute erythemato-edematous reaction occurs, which is covered with vesicles or bubbles, through the rupture of which, exuding exulcerations and crusts are born. The injuries are strictly limited to the region where the contact with the irritating substance occurred.
Dermatoses following the absorption of a chemical or medicinal substance
Ingestion of some chemical substances (in the vast majority of cases it is about medicines or substances handled in various professions), can give rise to skin eruptions of different types.
The chemical substance can also enter the body through the respiratory, cutaneous, intravenous or intramuscular route. The skin manifestations that arise in this way are called toxidermia or toxicodermia, wrong terms, because they are not toxic processes, but intolerance. Their clinical type is generally unrelated to the chemical substance in question. However, some drugs produce quite characteristic rashes.
Antipyrine causes various eruptions, the most common of which is erythema bullous, characterized by erythematous spots located on the skin, oral and genital mucosa.
Iodine and especially iodines produce a wide variety of skin eruptions, covering almost all aspects of skin reactions.
Bromines frequently cause acne-like lesions, which appear in the form of small papules-pustules and often turn into boils surrounded by redness.
Gold salts produce, in addition to the characteristic erythroderma, lichenoid eruptions and pigmentation.
Arsenic gives rise to a series of skin accidents.
Sulfamides produce, among other skin accidents, erythema nodosum.
Penicillin produces urticaria, eczematiform dermatitis and an erythroderma that appears a few days after starting the treatment.
Allergic dermatoses are a series of skin conditions produced by the body’s “sensitization” to certain exogenous or endogenous substances. The sensitized skin acquires the property of reacting to these substances in a very special way (allergy = modified reaction). This group of dermatoses includes eczema, urticaria, prurigo, neurodermatitis, some professional eruptions and some erythroderma.
Food allergic rashes
In addition to chemical intolerances, food intolerances must also be described. These have particularly varied clinical manifestations (most often in the form of hives), so the food in question cannot be identified only by the appearance of the lesions. Food intolerances are often preceded or accompanied, but not necessarily, by general and digestive disorders (nausea, vomiting, diarrhea, temperature, dizziness. Among the foods most often incriminated are: preserved, salted, smoked meat and fish; game; fermented cheeses; mushrooms; strawberries; coffee; alcohol.
As treatment, it is recommended to suppress the food in question, a hypotoxic and non-allergenic diet (flour-vegetarian), the non-specific medication mentioned for medicinal eruptions, antihistamines, oxygen therapy. Sometimes, after the disappearance of the eruption, the body is tried to get used to the respective food, by taking it in minimal and progressive doses.
Special results were obtained in these cases following the use of Imuniplant tea.
In the evolution of an eczema plaque, we distinguish five phases:
- The erythematous phase, characterized by a more or less intense redness, accompanied, especially in regions rich in loose connective tissue, by an edema of variable intensity.
- Vesiculation. On the described reddish background, numerous vesicles the size of a needle tip, with clear, transparent contents, do not take long to appear.
- The sloughing phase is characterized by the rupture of the vesicles and the spilling of their contents on the surface of the skin. During this period, the plaque appears scattered with small holes that are nothing more than blister craters. In cases of intense depression, the entire surface of the plaque is flooded with a citrine liquid. By drying this exudate, greyish-yellowish or brown crusts result.
- Thinned and shiny epidermis phase. After a variable time, the sloughing stops, the crusts fall off and do not recover, and the thinned epidermis continues to remain red, taking on a smooth, glossy appearance as if it were coated with varnish.
- The peeling phase. The epidermized plaque is covered with lamellar or furfuraceous scales, which reproduce for some time, until the skin regains its normal color and appearance.
The succession of the various phases described do not occur synchronously, during the entire eruption. These phases can coexist on the surface of the same plaque, a fact due to which the eczematous eruption, as a whole, acquires a polymorphic character. In practice, the picture of eczema sometimes shows deviations from the type described, either by the shortening or prolongation beyond measure of one or more of the phases described above, or by the changes imprinted on the eruption by the region where it develops.
Among the subjective symptoms, we point out the burning sensation in the initial period and the itching that is almost constant in all the evolutionary stages of eczema, sometimes becoming unbearable.
Eczema can be acute, when it appears suddenly, being accompanied by an accentuated itching, intense erythema, edema and vesiculation and chronic in which vesiculation and exudation is less, predominating dry eczema and sometimes lichenification. Chronic eczema usually develops in the form of successive outbreaks.
The most well-known forms of eczema are: vulgar eczema, papulo-vesicular eczema and nummular eczema.
Papulo-vesicular eczema is characterized by a disseminated eruption, consisting of grouped or isolated papulo-vesicular lesions, with a slightly raised erythematous base. The central vesicle is small, it can dry out without breaking or it can be opened by scratching, allowing a drop of serositis to flow out, which turns into a punctate crust.
Nummular eczema consists of well-defined round or oval plaques. The plaque has the characteristics of a vesicular or papulo-vesicular eczema. Sometimes, the center flattens, dries and is covered with crusts or scales, while active vesicles persist on the periphery. The places of predilection are: the dorsal side of the hands, feet, fist and tibio-tarsal joints.
Eczema occurs at any age, but is more common in infants, early childhood and adults. The factors involved in the etiology of this syndrome are divided into predisposing and provocative ones.
- The predisposing causes, although very numerous, have an etiological significance that is difficult to specify.
Heredity and family predisposition play an important role in infant eczema and in some adult eczema and, on the contrary, do not intervene in any way in contact dermatitis
The condition of the skin plays an important role in the pathogenesis of eczema, because skin reactivity depends, among other things, on local conditions. Thin skin, poor in pigment, seborrheic, or hyperhidrotic, is more susceptible to the toxic and even sensitizing action of chemical agents. Xeroderma (dry skin) is also a predisposing factor for eczema. Venous stasis, the special trophic conditions, following varicose veins, favor the appearance of eczema.
Visceral diseases have been considered by many specialists as one of the important causes of eczema. The digestive tract has often been assigned an important role, considering that it would favor the penetration of allergens into the body. There are known cases of eczema (which coexists with gastric disorders or with a latent or manifest colitis) that evolves favorably after treating the digestive condition.
Alteration of liver functions, especially the antitoxic one, is often blamed in the etiology of eczema, arguing that in eczema patients the liver cell would not be able to assimilate heteroproteins resorbed in the intestine, leaving them to sensitize the skin via hematogenous route. The insufficient liver cell allows a large amount of histamine substances to pass into the circulation. Even if most of the time the liver function tests in eczema patients are negative, the role of the liver in protecting the body against toxic substances resorbed through the intestinal mucosa cannot be minimized.
The endocrine glands also play an important role in creating that morbid predisposition that we talked about. It is known that puberty sometimes makes eczema disappear before this period. There are known cases of eczema whose evolution is paced by menstruation, most times getting worse during it
Menopause also intervenes in the etiology of eczema, favoring the appearance of sensitization. There are frequent cases of eczema and prurigo that appear with the onset of menopause.
Dysfunctions of the thyroid gland also have some role in the occurrence of eczema. It has been experimentally demonstrated that thyroidectomized animals can only be sensitized after ingestion or injection of thyroid extract.
An important role can also be attributed to the adrenal cortical and pituitary glands in the occurrence of eczema. The anti-allergic action of cortisone and ACTH is well known.
Food factors and nutritional disorders. Clinical and experimental facts are known that show the role played by these factors in the production of eczema. It should be remembered that nutritional imbalances favor eczema, both when the food ration is insufficient and when it is increased.
A hypoalimentary regime, low in proteins, causes them to be absorbed, insufficiently digested and therefore susceptible to play the role of allergen. The hypoproteinemia found in some eczematous patients is often not the cause of the condition, but the effect of the plasma loss that occurs in the waning phase of eczema. The excess of carbohydrates, as well as the reduction of the ratio of unsaturated fatty acids, favors the appearance of eczema, especially in infants and small children. Based on these considerations, some authors saw eczema as a deficiency disease and recommend treatment with vit.F, which gives some results, especially in children.
The deficiency of vitamins C, K and P complicates the cellular oxidation-reduction processes and increases the capillary permeability, and the insufficient ration of vitamins from group B does not ensure the trophicity and normal protection of the skin. All these tissue biochemical disorders favor the appearance of eczema. It has been experimentally shown that animals deficient in pantothenic acid develop a skin syndrome similar to seborrhea, and those lacking vitamin B6 develop eczematiform dermatitis.
Food deficits, disorders of intermediate metabolism, and of endocrine functions influence the metabolism of electrolytes and water in the body and at the same time act on the acid-base balance, factors also incriminated in the etio-pathogenesis of eczema.
It is known that calcium levels are low in some eczema sufferers. The sodium and magnesium content of humors is also important. The change in the acid-base balance usually consists of a tendency to alkalosis. The possibility of acidosis is also not excluded.
It has been proven that the metabolism of water in the body is related to the cause of the exudate, especially in infant eczema.
The correction of these metabolic imbalances is often followed by the healing of eczema, which is also explained by the proven fact that only by drinking a certain tea (Imuniplant or Deniplant), certain skin conditions were resolved favorably.
Chronic infections and focal infection (dental, sinus, tonsillar, cholecystic, appendicular) favor the body’s sensitivity, maintaining the state of excitation of the cortical foci responsible for skin disorders. Sometimes the foci of infection are the source of the reactogen that sensitized the skin, eczema behaving as a secondary eruption compared to the primary extracutaneous infectious foci.
The role of the central nervous system and neurovegetative disorders must be highlighted in particular. Eczema patients are often overworked, irritable, with irregular sleep, with exaggerated reactions, with a lack of inhibition or pathological inertia, in a word, they are individuals with a more excitable, unbalanced nervous system or in a period of abnormal reactions.
- The provocative causes are also very numerous. They can be divided into external causes and internal causes.
a) External causes. Any external stimulus, acting strongly or repeatedly on the skin, can trigger an eczema. This is how mechanical and physical agents act, such as small traumas, cold, heat, solar radiation, wind.
Chemical and medicinal agents are very common. In addition to the chemical agents mentioned in the previous chapters, we also mention soap, cosmetics, hair dyes, fabric dyes, etc. We also mention here the pollen and juices of plants such as primrose, lily.
Some insects, through contact or their stings, can be eczematogenic factors.
Microbes that are found on the surface of the skin as well as various cryptogamic parasites can also cause eczema in some circumstances.
The predilection site of microbial eczema is generally in the retroauricular groove, inguinal-crural fold, perianal region, armpit and calves, and for those determined by cryptogamic parasites, inguinal-crural, submammary, plantar, palmar and interdigital regions.
b) Internal causes or those that act internally can be: food, medicinal, metabolic.
-The most varied foods, especially the protein ones, can be the cause. We quote as follows: meat, especially preserved meat, fish, crustaceans, eggs, cheeses, milk, and sometimes vegetables and fruits.
-Ingested or injected drugs rarely cause eczema-type eruptions.
- Abnormal metabolic products, which appear in the course of various gastro-intestinal, liver, diabetes, uricemia diseases are sometimes provocative causes.
To identify the provocative substance, it is recommended to practice the tests, which sometimes give conclusive results.
Pathology of eczema
Eczema being considered an allergic reaction, results from sensitization of the skin to an allergen with which it came into contact externally or internally. In the immunological conception of eczema, it was admitted that the tissues subjected to contact with the allergen produce antibodies capable, upon new contact, of conflicting with it. The antigen-antibody conflict triggers chemical mediators such as histamine and related substances that produce eczematous lesions. It has been shown that acetylcholine also intervenes in the triggering of allergic accidents.
However, we can say that allergy is a side of increasing the body’s general reactivity.
Often, the antigen cannot be identified, and the eczematous reaction is triggered by other factors.
a) Sometimes the irritants that cause eczema are associated with other irritants in work, life, and food conditions. The latter can thus become conditional excitants and can cause the appearance of eczema, without the first excitant acting anymore. This explains the so-called polysensitivities.
b) In other cases, the excitants that act either on the exteroceptors or on the interoceptors of the internal organs, cause foci of excitation at the level of the central end of the cortical analyzer. If the action of these excitants is strong, the foci of pathological excitation do not disappear, but persist on the bark, becoming vestigial, residual, stagnant foci of excitation. From these foci emanate radiations, related excitations that reach the skin and cause eczematous morphological changes, by disturbing the trophic, vasomotor function, which the bark excites on the skin.
The foci of stagnant excitation, which persist at the level of the cerebral cortex after an eczema, also explains the fact that the action of indifferent excitants during the period of stagnant, dominant excitation, results in the reactivation of this foci and as a consequence the recurrence of eczema.
In all these cases, the type of nervous system and the disorders in the dynamics of the cerebral cortex that occur during neuroses, various toxic infections, and psychological traumas play an important role. Some authors would explain the allergy as a consequence of some phasic phenomena in the corresponding areas of the cerebral cortex, with the paradoxical phase, in which a weak stimulus causes an intense effect.
Finally, the pathogenesis of distant, disseminated or generalized lesions that appear in patients with initially localized eczema must be explained. These lesions, labeled secondary, are considered to be due to sensitization. We can often see how the lesions spread during the period of exacerbation of the initial outbreak and spontaneously regress when the initial lesion improves.
In relation to the etio-pathogenesis of an eczema, often the clinical appearance is also different.
Thus, when the predominant cause is external, we generally speak of a contact eczematiform or microbial, parasitic dermatitis. They are localized, without a tendency to spread, sometimes regressing after the removal of the cause and a local treatment.
On the contrary, when eczema is of internal cause, the clinical aspect is different. Eczema is very quickly disseminated from the beginning, has a chronic, relapsing evolution, with multiple outbreaks and is rebellious to local treatment.
It should also be pointed out here that even when the provocative, occasional cause was local and therefore the lesions start in a limited territory, if there is an organic, nervous predisposition, the clinical appearance changes quickly and takes the type of eczema of internal cause.
It is recommended that the following principles be taken into account in the treatment of eczema:
- Research and elimination of the causes that favored or determined skin sensitization.
- Eczema being a central nervous reaction with a complex pathogenic mechanism, the treatment should follow the interruption of the physio-pathological chain, especially at the level of the nervous system.
- Eczema patients are easily sensitized to medicinal substances applied to the skin for therapeutic purposes, which is why it is recommended to be very cautious in the indication of local treatments.
Eczema in infants and children
Eczema of early childhood, especially of infants, must be studied separately, because it has particular clinical, etio-pathogenic characteristics and requires special treatment, especially from a dietary point of view. Eczema in children appears early and generally heals up to two years, rarely later. After four years, eczema has the same characteristics as that of an adult.
According to the moment of appearance, according to topography, clinical aspect and evolution, two clinical types of infant eczema can be described: 1. seborrheic eczema and 2 eczema proper.
- Seborrheic eczema (or dermatitis) always starts in the first 2-3 months after birth. – Cephalic eczema starts at the level of the scalp and is manifested by grey-yellow scales-crusts, greasy, juicy, adherent to the hair, which is agglutinated. When the crust is removed by peeling off or by sectioning the hair, a bright red, smooth, scaly surface can be seen underneath. It must be specified that there are no blisters as in eczema proper, nor exulcerations as in impetigo. Very quickly the lesions spread to the ears, eyebrows, then partially to the cheek, in the folds of the neck. Isolated round elements of 1-2 cm diameter squamo-crusted or scaly, vaguely psoriasiform, can appear on the rest of the thoraco-abdomen, especially in the subumbilical region.
The treatment of seborrheic eczema must be primarily local. Since wet compresses are often difficult to bear, it is recommended that the removal of the crusts be done sooner with Vaseline or 2% salicylic acid oil. Then specific ointments are applied. During the healing period and to prevent relapses, a rigorous hygiene, broad powdering with mineral powders or application of boiled oil is recommended.
From a dietary point of view, some general rules that will be developed for eczema proper also find their application here. It is often good to add 200 g of cow’s milk to the diet. Biotin also gives good results.
The infant’s eczema always appears later, namely after the third month, often at 5-6 months. The usual location is at the level of the face, namely in the middle of the cheeks, where it forms two symmetrical round plates of 5-8cm diameter. The middle of the chin, as well as the center of the forehead can also be affected. The scalp, ears, neck are rarely affected. The itching is very intense and rebellious. Because of the violent scratching, excoriations and blood crusts form.
If the mistake is made of vaccinating children affected by eczema, sometimes a generalized vaccination occurs, with lesions especially on the eczematous areas, with a serious general condition.
Dietetics is the essential point of the treatment. This must be adapted taking into account two essential elements: correcting mistakes in nutrition and adopting the regime in relation to the type of eczema. Thus, weak, dystrophic children will be fed abundantly and not undernourished. Mother’s milk will only be suppressed in exceptional cases, and then it will be switched to diluted cow’s milk, acidified, creamed, added with flour. Pasty children will be given a little liquid and food without salt to dehydrate them. Fat children will be given a limited diet, so that they do not gain excessive weight. In all cases, if the eczema is rebellious, the amount of milk will tend to decrease, especially after 4 months. The diet will be supplemented by a regimen rich in vitamins, with vegetables, fruits (soups, vegetable purees boiled in water without salt, compote, tomato juice if it is tolerated, lemon juice). In older children, the cure of vegetables and raw fruits can give good results. From 4-5 months, DENIPLANT BABY tea can be introduced into the diet.
An essential rule is that the child should not be malnourished, should not lose weight (except fat children). It is preferable for the child to gain weight normally even while maintaining his eczema, than to get better from eczema but lose weight.
The internal treatment must be adapted to the case and established only by the attending physician. Thyroid or pancreatic extracts can be tried with caution. Synthetic antihistamines have given some results, but inconstant, partial or transient. They are not without their drawbacks. Corticotherapy should only be applied rarely, in acute attacks and for a limited time.
The change of air (plain or moderate altitude) often favorably influences the development of eczema.
Local treatment is very important. First of all, scratching will be avoided by applying bandages. In acute periods, compresses with weak solutions of chamomile tea, boric acid, borax will be applied. Very quickly, especially in the subacute phases, you will switch to creams, pastes, then progressively light or medium reducers will be added. Children will not be washed with soap, but wiped with chamomile tea, boric acid, vegetable oil. A little less frequent and then warm baths, with starch or bran, are expected.
Eczematides represent a group of erythemato-scaly, pruritic dermatoses, with a histological appearance and pathogenic mechanism similar to eczema.
Figured seborrheic eczematides begin with punctate lesions. with a clear outline, red or pink in color, covered with thick-looking scales. As the lesions spread on the surface, their center acquires a reddish-yellow color, and the slightly raised periphery keeps its red color. The element that has reached its full development is round, numerical, covered with scales, having the same appearance as in the initial lesions. The diagnosis of eczema must be differentiated from pityriasis versicolor, whose color is light brown, sometimes pale pink, is non-itchy, or from nummular psoriasis, which has thicker and drier scales.
Pityriasis-like eczematids are erythematous-scaly eruptions whose elements can be located or disseminated throughout the trunk, limbs and scalp.
Psoriasiform eczematides differ from the previous ones in that the eruptive elements are covered by thicker, stratified scales, and the eruption tends to extend and persist. These eczematids differ from psoriasis by the greasy appearance of the scales and by the absence of the candle spot sign. In addition, in psoriasiform eczematids, the edges of the plaques are less smooth than in psoriasis.
The treatment of these eczematids is almost identical to that of eczema, because they represent an accentuated form of eczema.
Neurodermatitis or chronic lichen simplex
Neurodermatitis consists of one or more lichenified plaques, conditioned by itching and its consequence, scratching. Sometimes the neurodermatitis is primitive, or proper, other times it is secondary to eczema. The skin in the affected regions undergoes special changes, thanks to which it thickens, becomes dry, rough, with greatly accentuated interpapillary furrows.
Two forms of neurodermatitis are distinguished: chronic and diffuse.
- Chronic circumscribed neurodermatitis begins with intermittent itching, which is exacerbated in the evening and under the influence of food abuse or emotions. Scratching following the itching produces changes in the skin in the affected area, which becomes reddish and has flattened, slightly shiny bumps. These changes are progressively accentuated and achieve the appearance characteristic of the disease state period.
The itching that precedes the appearance of the lesions persists throughout their evolution. This symptom appears intermittently in crises and induces the need to scratch.
Dermatosis has a chronic, prolonged evolution, being able to persist for years, or disappearing spontaneously, only to reappear later in another region.
- Diffuse neurodermatitis differs from the previous form, in that the itching and lichenification are diffuse.
The appearance of the lesions is preceded by generalized and intermittent itching. Under the influence of scratching, wide and shiny point papules first appear, which eventually coalesce to produce lichenified, diffuse plaques with irregular edges.
Neurodermatitis must be differentiated from chronic lichenified eczema, which is always preceded by vesiculation and sloughing, as well as from lichen planus, in which flat, glossy oval papules have the characteristic striations in the center and are usually isolated.
The treatment primarily aims at reducing itching. For this, helio-marine belts, mud baths and belts with arsenical or sulphurous mineral waters are indicated as the case may be.
Urticaria is an acute, itchy skin rash, characterized by raised white or reddish papules or plaques, similar to the lesions produced by contact with nettle leaves.
Its appearance means an allergic reaction, predominantly vascular, of individuals sensitized to macromolecular allergens.
Urticaria appears suddenly, sometimes accompanied by fever, gastrointestinal disorders (nausea, vomiting, diarrhea), the initial symptom that attracts the patient’s attention is itching, after which the characteristic urticarial lesions appear in a few minutes.
Itching is a constant subjective symptom. Scratching causes the appearance of new urticaria lesions.
The urticarial eruption is characterized by the fact that the elements disappear after a few hours, only to reappear after variable intervals, in the same place or in other regions.
In some urticarial patients, the simple rubbing of the skin with the uncle is followed by the appearance of a red stripe, which in 40-90 seconds takes on an urticarial appearance. This phenomenon is called figura dermographism. Dermographism lasts for months or even years.
Itching is a particular sensation that causes scratching; it is as undefined as the tactile, thermal sensation, etc.
The causes of itching are multiple: eczema, internal, toxic, autotoxic, etc. In general, these causes are associated, forming the so-called itchy summation, dominated by a cortical neurogenic factor.
The only objective symptom of pruritus is the scratch lesion. In the beginning, the patient tries to dominate the imperious need to scratch, so that eventually he gives in, scratching violently and producing excoriations.
Itchy attacks last 5-15 minutes, sometimes an hour or even more. The frequency and rhythm of crises do not follow any rule.
Itching can be diffuse, generalized, or localized in a more or less extensive skin region. It is usually not permanent and equal in intensity, but presents evening and nighttime exacerbations, with characteristic intermittents.
The itching crisis can be acute or subacute, accompanied by the imperious need to scratch, which gives a sensation of pleasure and once triggered cannot be stopped.
The immediate consequences of scratching are varied and strictly related to its intensity. They can range from simple transient erythema to the characteristic linear excoriations.
The late consequences of itching are mainly due to the secondary infection with pyococci, which scratching gives them the opportunity to penetrate the skin and produce various aspects of pyoderma.
It is called itching-symptom when it accompanies some dermatosis and itching-disease when it is accompanied by characteristic skin lesions.
From a clinical point of view, two forms of pruritus-disease are distinguished: generalized and localized.
Dyshidrosis is a vesicular dermatosis located on the extremities, most often on the palms and soles, in the interdigital spaces and on the sides of the fingers.
The rash appears suddenly, especially in warm seasons, being preceded by itching and sometimes swelling of the extremities. The elementary lesion is a blister, at the level of which the skin keeps its normal color or is more easily congested. The vesicles are initially the size of a needle tip, they quickly reach the size of a lentil grain. The dyshidrosis vesicle is hard to the touch and has a thick, resistant and transparent epidermal cover. It contains a clear, flowing liquid.
Dyshidrosis itself evolves in 10-15 days, healing spontaneously, but frequently recurs.
The treatment of dyshidrosis must be related to the cause that produced the dermatosis. First of all, fungal outbreaks must be sought and treated. Other times, foci of infection with pyococci must be detected and treated (tonsillar, dental, etc.) Local treatment is recommended: iodized alcohol and salicylate 1-2% or other antimycotic preparations. For dyshidrosis of undetermined cause, the treatment is identical to that of eczema
Occupational dermatoses are skin conditions that occur exclusively or predominantly in connection with the exercise of certain professions and whose total or partial cause results from the conditions in which the work is carried out.
In general, about 65% of occupational diseases are occupational dermatoses. Approximately 1-2% of chemical and oil workers are affected by such dermatoses.
In practice, the cause of most professional dermatoses, namely toxidermas, dermatitis and professional eczemas, as well as associated lesions of the skin, nails, hair, sweat and sebaceous glands, are chemical agents. These chemical products are very frequently encountered in the production process, either as raw materials or often as intermediate or finished substances. They are also sometimes used as solvents, catalysts.
We list below the chemical substances that most frequently cause occupational dermatoses:
Substances with mandatory action; sulfuric, nitric, hydrochloric, oxalic, formic, chromic, cresolic acids. Potassium, sodium, calcium hydrate. Sodium carbonate, sodium bicarbonate, potassium bichromate. Zinc chloride, arsenic, arsenic salts, chlorine and chlorinated products. Sulfur dioxide, acetic anhydride, turpentine, acetone, carbon tetrachloride, benzene, carbon sulfide.
Substances with sensitizing action: bismuth, nitrate and other salts, mercury, metal and various salts, Lead, acetate and other salts, Sodium cyanide, Nickel and potassium cyanide, Zinc and potassium double cyanide, Copper and potassium double cyanide , Nickel sulfate, Zinc sulfate, Beryllium, Sodium sulfide, Potassium alum, Chromium sulfate, Cobalt salts, Ammonium chloride, Hydrogen sulfide, Hydrazine, Ethyl oxalate, Phenylacetates, Creolin, Naphthenic soaps, Phenylcresols, Paramidophenols , Benzidine, Various dyes, Aniline, Folliculin, Chloroform, Lacquers, Synthetic and natural resins, Bakelite, Synthetic plastics, acrylics, nylon, various explosive substances, Insecticides, Cosmetics, Perfumes, Various soaps, Various medicines.
The group of hydrocarbons contains various petroleum derivatives: Kerosene, petrol, With spirit, Diesel, Mineral oils, Tars, Residues, Tar, bitumen.
Substances that are absorbed through the skin (causing general damage without skin damage): Trinitroglycerine, TNT, Phenetol, Phenetidine.
In relation to the importance, location and etiology of the lesions:
1.Professional stigmata, 2.Toxidermia. 3. Dermatitis, eczema. 4. Melanodermas. 5. Keratodermas. 6. Injuries by physical agents and chemical caustics. 7. Professional infections. 8. Lesions of the skin appendages.
The diagnosis of an occupational dermatosis involves two stages. In the first stage, the morphological diagnosis is made as in any dermatosis. In the second stage, the most important, it is established whether or not the injuries are related to the profession and what exactly are their causes and pathogenesis.
Local treatment is the usual treatment of lesions. Thus, dermatitis, eczema, pyoderma, burns will be treated according to the stage and clinical form. Chemical burns require special treatments
9.Autoimmune skin manifestations
Autoimmune diseases are due to the loss of immunological tolerance (recognition and tolerance defect of autoantigens), which can be primitive or secondary.
Collagenoses are “collagen diseases” which include lupus erythematosus, rheumatoid arthritis, scleroderma, dermatomyositis and periarteritis nodosa.
Anticorpogenesis in the conditions of primitive genetic abnormalities is especially valid for systemic and scleroderma lupus erythematosus. In the other autoimmune manifestations, it is a secondary autoimmunity, in which the different tissue components, in order to play the role of antigens, must be previously damaged by various toxins.
Lupus erythematosus is an erythemato-squamo-atrophic dermatosis, sometimes scarring, chronic, of indefinite duration and often symmetrically located on the face. Although lupus erythematosus has a well-defined symptomatology, this condition cannot be considered as a well-defined morbid entity, but is considered as a skin syndrome allergic to various factors.
From the multiple clinical and biological aspects regarding chronic lupus erythematosus, it can be said that this is a benign, but potentially evolutionary form of lupus erythematosus. It is assumed that the rarity of chronic lupus transformations into an acute form is due to genetic differences in predisposing factors.
The genetic factor plays a primary role in the pathology of lupus erythematosus, the transmission being most likely through multiple genes.
There are 3 clinical forms of lupus erythematosus:
- Chronic localized lupus erythematosus, with the two aspects:
- fixed or discoid lupus erythematosus.
- centrifugal lupus erythematosus.
- Chronic and subacute disseminated lupus erythematosus.
- Acute systemic lupus erythematosus (acute disseminated lupus erythematosus)
It should be mentioned from the beginning that a localized lupus erythematosus can sometimes start suddenly, with general symptoms (fever, headache, facial edema, etc.) On the other hand, a fixed chronic lupus erythematosus can be exacerbated, presenting multiple plaques variable sizes also on the hands, mid-thoracic region, less often in the rest of the body.
Centrifugal lupus erythematosus is characterized by erythematous plaques, with rapid evolution, centrifugal and with very little developed scales, so superficial forms. It sometimes starts with general symptoms such as fever, headache, acute inflammatory edema, especially of the eyelids. It can be confused at first with erysipelas. In the centrifugal form, the atrophy or scar is also very reduced or completely absent. It is the most benign variety and susceptible to healing, even spontaneously. It is often found on the face, occupying the nose and cheekbones, where it takes on the appearance of a butterfly or bat with outstretched wings, hence the name vespertilio.
Fixed or discoid lupus erythematosus also has an eccentric but very slow evolution. In months, it advances by a few millimeters. They are forms with a deep infiltration, with thick adherent scales and disfiguring scars. Erythema is a main element, which is maintained throughout the evolution. Even when the scale appears, the erythema persists on the periphery, where it constitutes the area of disease progression. There are types in which all forms are reduced to a purple-red spot, which disappears under pressure.
The other element is the scale, epidermal lesion with very large varieties in thickness and appearance. In more recent forms it is fine, barely visible, like a fine film of collodion. The scale, if it is thin, is transparent and does not mask the redness of the skin. In other older cases, the scales are layered, dry, adherent, chalky. If we lift the scale, which is always difficult, we notice on its inner face a series of filiform, follicular extensions, which fix the scale to the lesion. In other forms, the scales are much thicker, irregular and grainy, like a plaster. The scales are very adherent, and sometimes bleeding may occur when lifting them. Sometimes the plaque is slightly sensitive to pressure.
A third characteristic element is the atrophic scar. It is never the result of an ulceration, because this dermatosis does not ulcerate spontaneously, but is the result of an interstitial sclerosis, through the resorption of the pathogenic infiltrate. The scar is also variable in relation to the intensity and depth of the infiltrate. In superficial forms, it may be completely absent. in other cases it is more pronounced, gray or depigmented and depresses the tissues.
The disease has a very long duration, sometimes it persists throughout life. It is mainly located on the face; it can also develop in the scalp, where it produces a generally permanent alopecia. It is also located in the front part of the chest, especially in the presternal region, on the dorsal surface of the fingers, so with predilection in regions exposed to sunlight.
Disseminated lupus erythematosus is a generalized form, intermediate between the usual localized form and acute exanthematic lupus.
Sometimes a stationary lupus for years can turn into a disseminated form, without pronounced general symptoms, other times the eruption occurs with general phenomena. This variety of subacute disseminated lupus has a relatively benign prognosis, unlike the acute one. The healing does not occur completely, but the erythematous-scaly, atrophic, more or less extended and numerous plaques persist.
Acute lupus erythematosus presents, in most of the otherwise rare cases, clinical symptoms distinct from ordinary lupus erythematosus.
Disseminated lupus erythematosus was included in the groups of collagen diseases. Under this name, a series of conditions with unknown etiology were designated and in which the hypersensitivity process probably plays an important role, with identical anatomopathological changes, externalized by a diffuse fibrinoid degeneration of the vasco-conjunctival tissue.
In addition to disseminated lupus erythematosus, acute rheumatic polyarthritis and nodular periarthritis and the dermatoses: scleroderma and dermatomyositis would be included in this group. It is therefore a matter of system diseases, that is, of the vasculo-conjunctival system.
The conditions classified as collagen diseases are not just a few morbid entities, but rather different ways of reacting to various toxic or microbial causes. There would therefore be a closeness between collagen diseases and allergic diseases.
Acute lupus erythematosus also begins with general symptoms of high fever, septic condition, arthralgias, myalgias, followed quickly by pleurisy, pericarditis, nephritis and polyarthritis. The rash presents different clinical aspects: erythematous plaques more or less extended, bullous and purplish eruptions. Sometimes they may be missing.
In the treatment of these diseases, although progress has been made recently, the results are still awaited. Treatment with gold salts is the preferred method and gives some results, especially in the more recent, superficial forms. However, the accidents that may occur during this treatment must also be taken into account, such as: erythroderma, jaundice, stomatitis, nephritis. In these cases, the treatment must be stopped immediately. The introduction of cortisone, hydrocortisone and its other derivatives did not lead to spectacular effects, but in any case the improvements are considerable. Of course, the results also depend on the degree of damage to the vital organs (kidneys, heart). The action of these preparations is not etiotropic but morbistatic, that is, it stops the further evolution of the disease.
Under the name of parapsoriasis, we mention three rare eruptive types, of unknown nature, with chronic evolution and completely independent of psoriasis, with which they have only vague clinical similarities.
The most interesting to know from a practical point of view is the so-called parapsoriasis in drops. The eruption consists of non-pruritic papular elements the size of a lentil grain, disseminated in a variable number on the trunk and limbs.
Lichenoid parapsoriasis differs from the previous one, on the one hand, in that its constituent elements are more infiltrated, globular or flattened, scaly only in their central part, and on the other, in that the eruptive elements often join together, constituting reddish plaques, often reticulate, disseminated on the trunk and limbs, with an atrophic appearance in places.
Parapsoriasis in plaques is characterized by plaques of variable sizes, usually round or oval, sometimes arranged in the form of branched, zoniform, disseminated on the trunk, limbs, reddish-yellowish in color, very little infiltrated, covered with fine scales.
Pityriasis Rubra Hebra
Pityriasis rubra, is a generalized dermatosis, rare, with chronic evolution and often fatal outcome.
From an evolutionary point of view, the eruption usually begins with red and slightly scaly plaques, located in various regions, which then gradually expand to cover the entire skin. Having reached the stage of complete development, the dermatosis is characterized by an intense and generalized redness of the skin, of a dark shade, sometimes slightly purple, accompanied by a moderate pityriaziform desquamation. The skin is generally slightly infiltrated, and on the surface neither papules nor depressions should be observed. Over time, the skin tries a kind of atrophy, it thins, becomes stretched, shiny, in some places it retracts, presenting embarrassment when moving. The patient complains of cold, skin tension and sometimes severe itching. After a few months, sometimes later, the general condition begins to be felt, the patient loses weight, becomes cachectic and usually dies of pulmonary tuberculosis or some other intercurrent disease. However, cases of healing are also known.
In addition to pityriasis rubra hebra, pityriasis rubra pilar and pityriasis rosacea gibert can also be found.
Lichen planus is a chronic dermatosis, of an unspecified nature, characterized from a clinical point of view by a more or less extended pruritic rash, consisting of papules of a particular appearance.
The elementary lesion of lichen planus is a papule the size of a needle, reddish or reddish-yellow and sometimes reddish-lilac, round or polygonal in shape, with a smooth and shiny surface like a crystal facet, often presenting at its center a small puctiform plug. This papule is dry, of a firm consistency and without visible scales.
Lichen planus develops with a special predilection on the front face of the fist, forearm, in the subumbilical region, genitals, on the sides of the trunk and in the lower lumbar region. In discrete forms of the disease, the eruption can remain for a long time or even definitively circumscribed to the places of election. Most of the time, however, it ends up spreading over almost the entire length of the skin, which is sprinkled with eruptive elements belonging to one or another of the aspects described.
As the eruption ages, its elements begin to pigment diffusely or only at their periphery.
Lichen planus is an itchy dermatosis by definition, the itching being sometimes, especially in nervous, overworked, very intense and annoying, preventing the patient from sleeping. In the usual forms of the disease, the general condition is not influenced.
Clinical observations show that lichen planus is a disease of adulthood, being very rare in children and the elderly. It seems somewhat more frequent in men than in women, and intellectuals are more often affected. The intervention of the central nervous system, which plays such an important role in the development of many dermatoses, can often be invoked here as well. An important number of cases are known in which lichen planus appeared after a violent emotion.
Lichen planus is a disease with a chronic evolution, which can last for months and years. Sometimes the generalization of the eruption is done quickly, sometimes gradually, in the form of successive outbreaks, at variable intervals. New elements appear as some of the old ones begin to regress, leaving pigmented spots in their place and over time imprinting a tiger-like appearance on the skin. After healing, relapses are possible, either in the form of isolated plaques, or reproducing the type of internal eruption.
Under this name, a rare dermatosis was described, very similar, from a clinical point of view, to the elementary lesions of lichen planus, but differing from them by their tuberculoid structure. It usually presents itself as a localized eruption, preferably on the sheath of the penis, but which can be generalized with predominance in the envelope. The disease occurs more often in adult men.
Clinically, the eruption consists of small flat, shiny, whitish or brown, non-pruritic papules.
Lichen nitidus, considered by some as a lichenoid tuberculide, would be, for others, only a particular variety of lichen planus. In support of this latter opinion, its association in some cases with cutaneous or oral lichen planus was invoked.
Ichthyosis is a scaly dermatosis, consisting of scales of variable thickness, more or less juxtaposed, reminiscent of fish scales, which is where the name given to the disease comes from.
This condition, generally familial, appears in early childhood and persists throughout life.
Clinically, ichthyosis is characterized by two particular symptoms: a pronounced dryness of the skin and the existence of scales of a special appearance on its surface.
The dryness of the skin, more pronounced in cases with abundant scales, does not seem to be strictly conditioned by them, because it persists even if the scales are removed by therapeutic procedures. It is generally less pronounced at the level of the large envelopes than in the rest of the skin. This can be seen especially in certain forms that we often find in some of the members belonging to the ichthyotic families. Sometimes xeroderma is, for a longer or shorter time, the precursor symptom of a late-developing ichthyosis.
In constituted ichthyosis, the patient’s skin is permanently covered with dry scales, more or less large, generally thin and, importantly, adherent to the skin in most of their extent. For this reason, unlike what happens in scaly dermatoses with an inflammatory substrate, peeling and removing the scales is done here with some difficulty. Scratched with the fingernail, the scales crumble easily due to their dryness, drawing along the scratch a whitish powdery streak, as in psoriasis.
According to the appearance of the scales, several types of ichthyosis can be described:
- Pityriasis-like ichthyosis, with small furfuraceous scales,
- Scutular ichthyosis characterized by larger, lamellar, polygonal or oval scales, with detached edges and an adherent center.
- Smooth or pearly ichthyosis, as the scales present a smooth and shiny surface, or as they have a pearly or silvery hue.
- Black ichthyosis, when the scales, either due to the accumulation of impurities, under their detached edges, or due to chemical transformations of their constituent substance, acquire, in part or in whole, a blackish hue.
In its usual forms, ichthyosis is a generalized dermatosis with a symmetrical disposition. With the exception of the envelopes, ichthyosis is spread over the entire surface of the skin, predominating especially on the limbs and in the lower half of the trunk. In the palmo-plantar regions the scales are missing, but the skin is dry and rough. Nails can be normal or sometimes dry and showing cracks.
The secretion of sweat and sebaceous glands is low in ichthyosis.
The connection between the dryness of the skin and the actual ichthyosis process is obvious if we take into account the fact that in the milder forms of the disease the scales can disappear completely during the summer, only to reappear in the winter.
Ichthyosis is a not too rare condition, especially if we refer to its milder forms. The etiological factor that is imposed, by its frequency, is that of heredity, which we meet in 25% of cases. Transmission of the disease is usually done in a direct line, from parents to children, in the course of several successive generations, or sometimes it skips a generation. Heredity can also be collateral. In 50% of cases, ichthyosis takes on the character of a family disease, affecting, without any preference, both sexes. Ichthyosis is never present from birth, but it does not begin to manifest itself until the first 3 years of life, sometimes lasting a lifetime.
From a physiopathological point of view, ichthyosis appears as a malformation of the skin, characterized by a decrease in the glandular secretions of this organ (sweating and sebaceous) and as a consequence of this condition, by a dryness of the skin and a disturbance of the process flaky. In these conditions, the corneum cells of the disjunctum layer, instead of being eliminated as they are produced invisibly, as in a normal state, remain longer adherent to the skin, on the surface of which they accumulate in the form of scales of variable thickness. The intimate cause presiding over the genesis of this malformation is still unknown.
Some specialists, based on the frequent coexistence of ichthyosis with disorders in the function of the glands with internal secretion and especially of the thyroid and sexual glands, tend to admit its endocrine nature. Thyroid insufficiency must be looked for very carefully in ichthyotics, because in dances it usually takes the form of small hypothyroidism, the basal metabolism being rarely altered.
As in psoriasis or other scaly dermatoses, the external treatment only aims at removing the scales formed by physical methods and alleviating the dryness of the skin with the help of ointments, pomades, etc., therefore, to solve the problem itself, internal intervention is required.
Under this name, purely symptomatic, are generally included all skin processes that are accompanied by a more or less pronounced thickening of the stratum corneum. The usual seat of keratodermas is represented by the palmar and plantar regions, the stratum corneum of these regions presenting, due to its structure, a special tendency to respond by an abnormal thickening to the most diverse pathological causes.
These explain why all dermatoses, including reactions of the stratum corneum, such as psoriasis, pityriasis rubra pilar, lichen planus, eczema, etc. wears, when located in the mentioned regions, a more pronounced keratosic aspect than the one they have in the rest of the skin.
- Familial symmetric palmo-plantar keratoderma.
This disease is characterized in the first weeks after birth, or somewhat later, during the first years of existence. It usually begins with a diffuse redness of the palms and soles, which is soon accompanied by a progressive thickening of the stratum corneum of these regions. In the full development phase of the disease, the palms of the hands and the soles of the feet, as well as the corresponding faces of the respective fingers, are completely covered with a horny shell, the thickness of which can vary from a few millimeters to 1 cm, and on the soles even more a lot.
Usually the hyperkeratosis stops suddenly at the edge of the palms and fingers, its peripheral limits being surrounded by a reddish or lilac-red circle, 2-3 mm wide. Sometimes, however, the horny carapace can exceed the upper limit of the palm, overflowing symmetrically towards the fist and the lower extremities of the forearms; at the feet, it can also exceed the sole, dressing the Achilles tendon.
Normally, keratosis wears the appearance of a compact horny blade, without visible scales, of a gray or yellow color like old wax, with a smooth surface, covered only by the natural folds of the region.
Palmo-plantar keratosis is usually accompanied by an exaggerated sweat secretion, especially on the feet, where it can become, through the stagnation and maceration inherent in the region, a repulsive fetidity. The local sensitivity is diminished as the stratum corneum thickens. However, it is not a matter of actual sensitivity disorders, because if we pierce the corneous shell with the tip of a needle, the patient immediately feels the pain.
Injuries to the hands and fingers prevent the patient from doing anything that requires some dexterity or delicacy of the tactile sense. Injuries to the legs, in turn, can embarrass walking, due to the deep cracks that are often accompanied by them.
The essential factor of these dermatoses is the familial character, without precisely knowing the primary cause underlying the disease itself. The transmission of this morbid predisposition is usually done directly to the offspring, sometimes continuously for several generations.
Like all congenital dystrophies, palmo-plantar keratoderma, once developed, does not show any tendency to regression as long as the treatment is limited to thinning and removing the crusts, for this reason it can be one of the most embarrassing and difficult to hide infirmities.
Symmetric palmo-plantar keratoderma of adults, also called essential.
Apart from the previously described form, it is worth mentioning another type of keratoderma, symmetrical palmo-plantar, which differs from the first one in that it is not hereditary, but appears in adulthood and is curable.
From the eruptive point of view, the disease is also characterized here by a palmo-plantar and digital hyperkeratosis, symmetrical, always taking a greater development on the feet. The cracks are usually more pronounced in the poop area, and can become painful and embarrassing to walk. Sometimes plantar hyperkeratosis, instead of being diffuse, has a more partial character, being limited to the level of the heel and the head of the metatarsals, respecting the hollow of the soles and the inner edge of the foot.
In the hands, hyperkeratosis is usually less developed and can be diffuse or limited only to the inner edge of the palms or near the metacarpophalangeal joints.
Treated, the disease is generally cured in a few months.
Among the symmetric palmo-plantar keratodermas, with a well-defined etiology, we mention arsenic symmetric palmo-plantar keratoderma, due to arsenic, either ingested for a long time as a medicine, or introduced into the body as a result of chronic occupational poisoning, and blenorrhagic keratoderma, of microbial origin that develops usually during a complicated blenorrhagia with extragenital manifestations
Some inframicrobes (ultraviruses) are located on the skin and produce well-characterized diseases. Some ultraviruses have a high affinity for both the epidermis and the nervous system. For this reason, epidermovirosis (warts) and epidermo-neurovirosis are distinguished, which include herpes and zoster.
Apart from these viruses, local diseases, there are also some general viral infections, febrile and contagious diseases with skin manifestations.
This category also includes a series of dermatoses of viral origin that are less studied, such as pemphigus vulgaris and psoriasis.
Warts (warts, moles) are papillary and hyperkeratotic growths of variable sizes. They are due to an ultravirus or inframicrobe.
Veruca vulgara generally appears in children and adults, young people on the dorsal side of the fingers and hands, less often on the palms, soles of the feet, elbows, etc. Their number is different, sometimes only 2-3, sometimes they are very numerous. They are isolated or grouped. They appear as round bumps of varying sizes, from the size of a needle to an even larger pea. Their surface is convex or almost flat, often irregular in the center, showing warty bumps. The color of the warts is grey-yellowish, brown or blackish. Their consistency is hard, rough.
Once they appear, warts grow and persist indefinitely, they rarely heal spontaneously.
The plantar wart is a somewhat different clinical type, due to the nature of the skin on which it develops. The corneous, hypertrophied layer does not allow the wart to develop in relief, so it grows deeper, where it irritates the papillary dermis. Clinically, the plantar wart appears as a callus, but in the center you often see a papillomatosis or gray-brown irregularities, and in the periphery a hyperkeratotic border. Sharp pain when pressure is exerted on the middle of the wart is characteristic.
Juvenile flat warts appear in children and adolescents, less often in adults, often suddenly, explosively. It is generally located on the face, sometimes on the back of the hands. They appear as flat, round or slightly polygonal papules, 1-2 mm in diameter, skin-colored or slightly darker. It often heals spontaneously.
Papillomatous warts or papillomas are some millimeters-long, pedicled, filiform growths that form on the face or neck.
Papillomas of the oral mucosa are rarer and fewer in number. It is associated either with filoform papillomas or with vulgar warts. Their surface is always flat, and their gray color contrasts with the red of the mucosa.
The treatment of warts is local. After local anesthesia, the wart is excised, cauterizing the base with silver nitrate. Since relapses are frequent with this method, it is preferable to cauterize the warts by diathermocoagulation, galvanocautery. The use of thermocautery is often followed by unsightly scars.
Flat warts are often cured with resorbed pomades and salicylic acid 5-10%.
Herpes is an acute eruption of vesicles located on an erythematous base with usual peribuco-nasal or genital area. The condition is due to a virus. In humans, it can be seen in skin lesions, in the spinal ganglia, often in the cerebrospinal fluid, sometimes even in the saliva and blood. One fact is obvious: the persistence of the virus in the body, especially in the spinal ganglia, from where periodically, under certain circumstances, it can return to the skin and cause lesions. The way the virus spreads is nervous, it spreads along the nerves, both from the skin to the center and from the center to the integuments. Some specialists consider that the virus persists at the level of healed lesions, which explains the relapses in the same place. This approach does not match the clinical observations, which show that the appearance of the eruption is often accompanied and even preceded by nervous manifestations. Sometimes herpes appears isolated, without apparent causes. Most of the time, however, it appears in the following circumstances:
a). infections of another nature, sometimes well characterized, such as cerebrospinal meningitis, pneumonia, influenza.
b). during some mood disorders, shocks or physiological states, such as menstruation, sexual relations.
c). after taking some medicines or vaccines
d). in case of local infections or traumas such as blenorrhagia for genital herpes, dental, sinus or tonsillar infections or traumas for perioral herpes.
The herpes eruption is preceded by a few hours or even a day, by subjective sensations of itching, local heat, often discrete local or even regional neuralgia. The eruption appears in the form of a small erythematous plaque, slightly edematous, raised, on the surface of which a bouquet of vesicles, with clear contents, of a pearly appearance, quickly develops. Vesicles can be numerous 3-4, sometimes there are more plates and bunches. In some cases, the vesicles are more isolated from each other. Herpes can become locally painful to palpation. Very quickly, the contents of the vesicles become disturbed, turning into grey-brown crusts, sometimes hemorrhagic, which fall off, leaving a small transient erythematous spot. The whole evolution takes 10-12 days. Herpes does not leave a scar except exceptionally. Rarely, herpes can become infected.
Genital herpes deserves to be known because of its frequency, both in men and in women, and because of its location on the mucous membranes, which gives it special characteristics. It is characterized by the fact that it is more painful, often preceded and accompanied by severe neuralgia. The vesicles break quickly and leave behind small erosions, often confluent, with polycyclic and microcyclic edges. The surface of the erosions is red, sunken, sometimes covered by a grayish-yellow exudate. On palpation, the lesion is not tender, unless the herpes has been treated impetuously with overactive drugs, in which case it can become tender, ulcerate and persist for a longer time. Vulvar herpes is sometimes extended, with multiple lesions, febrile. Genital herpes is often recurrent, potentially opening the door to venereal infections.
Oral herpes is often located on the tonsils, pharynx, is painful and can be accompanied by fever (herpetic angina)
The treatment of herpes is not special, it heals itself. Active, untimely treatments can irritate, eczematize, ulcerate the herpes and therefore prolong its evolution.
Simple, decongestant, slightly disinfecting treatments can still favorably influence the evolution, preventing additional infections. Thus, skin herpes benefits from touches with alcohol, talcum powder, genital herpes from compresses with chamomile tea, possibly a simple cream. In case of pain, anti-neuralgic drugs, vitamin B1 are administered. To avoid venereal infections, sexual intercourse is prohibited before healing.
Recurrent herpes is more difficult to treat. The eruption can sometimes be stopped if the incipient lesion is touched with 2-3% iodized or resorbed alcohol.
Treatment with antibiotics gives dubious or null results.
Zoster is a virosis characterized by an eruption consisting of several erythematous-vesicular plaques distributed unilaterally on a well-defined nerve territory and accompanied by clinical nervous disorders and alterations in the spinal ganglia of the respective territory. Shingles almost never recurs, but if not treated carefully, it can lead to unwanted side effects.
Shingles can appear in two different circumstances:
a) either in small epidemics or in the form of more frequent cases in spring and autumn.
b) either in special pathological circumstances.
Additional causes that can trigger the appearance of the eruption are:
- different acute or chronic infections; meningitis, pneumonia, tuberculosis, secondary or nervous syphilis.
-some drug intoxications; arsenic, carbon dioxide, lead, morphine,
-injuries and traumas of the nervous system, cranial, dental traumas, lumbar puncture.
The zoster zone is characterized by rash, swelling of the satellite ganglions and nervous symptoms.
Often the eruption is preceded by general symptoms, sometimes very discrete, sometimes more pronounced, such as fever, chills, asthenia, which quickly recede after the appearance of the eruption. The rash can also be preceded by local subjective symptoms that manifest in the form of itching, burning, paresthesias.
The eruption is manifested in the same way as herpes, through the same erythematous-edematous plaques, somewhat more infiltrated, on which after 6-24 hours bunches of pearly vesicles appear. The eruption generally consists of several bursts for 3 days. They are always unilateral, do not exceed the midline and cover a nervous territory, well delimited, in connection with a medullary segment or a spinal ganglion. Plaques can remain isolated but often they coalesce. The vesicles have a clear content for 2-3 days, then the liquid becomes cloudy, becoming clearly purulent. On the fifth day, a brown crust appears in the center of the blister. Very quickly, the liquid turns into a crust. It dries completely in a few days and comes off in 10-15 days, rarely later, leaving erythematous spots at first, then depigmentation or hyperpigmentation.
Shingles sometimes heals on its own, but I would not recommend waiting for this. Local treatment can prevent further infections. Alcohol or diluted Dalibour water can be applied to the lesions and powdered with talc. In case of extensive eruptions, with infiltrations and ulcerations, slightly disinfecting wet compresses will be applied, possibly coloring solutions or disinfectant pomades, and anti-neuralgic drugs will be administered against pain.
The varicose ulcer is part of a syndrome characterized by a series of skin manifestations located on the calves, conditioned by the presence of varicose veins, dermal capillarities and trophic phenomena that lead to tissue sclerosis and their ulceration.
Varicose veins are irregular dilations of the veins, which change their path and caliber, becoming linear, sinuous and ampullary.
Varicose veins must be distinguished from venectasias, which are linear dilations with a uniform increase in the caliber of the vein.
Varicose veins can be found everywhere where venous circulation is impeded, especially in the lower limbs, a fact primarily due to orthostatism, which causes a physiological difficulty in venous circulation at this level.
Varicose veins of the lower limbs belong to external pathology, therefore also to dermatology, while varicose dilatations of other territories, described under the name of collateral venous circulation, belong to the domain of internal pathology.
The causes that trigger varicose veins are those that act, either by increasing the hydrostatic pressure of the blood column, or by reducing the resistance of the venous walls. The causes that act by increasing the hydrostatic pressure are:
- professions that require a special effort from the lower limbs (shop assistants, waiters, barbers, postmen, dentists, etc.). In them, the permanently increased muscle activity requires an increased blood flow, which has the consequence of making the blood reflux even more difficult.
- mechanical: obstacles can favor and therefore increase the pressure of the blood column. Among these causes, pregnancy should be mentioned in the first place, which causes a compression of the iliac veins and the cava. Other causes of this order are female genital tumors.
To the above causes are added others that cause the weakening of the venous wall:
-constitutional causes: tall individuals, as well as those with abundant subcutaneous cellular tissue, have varicose veins more frequently.
-sex: in women they are more frequent than in men.
-endocrine causes: it is observed that varicose veins appear both in men and in women, especially at the “age of hormonal crises”, i.e. adolescence or menopause. Pregnancy, presenting a very pronounced hormonal imbalance, can be considered as part of the endocrine causes of varicose veins.
The consequence of varicose dilatation of the veins is the appearance of venous valvular insufficiency. The valves, due to dilation of the vein walls, no longer overlap and thus can no longer fulfill their important role of leveling the blood column and dividing its pressure into segments of several centimeters. Due to this insufficient valve, the blood from the large veins presses directly on the blood from the varicose veins, so the circulation is even more hindered. This fact leads through a vicious circle to the exaggeration of the dilatation of the veins.
In the pathology of varicose veins, the vegetative nervous system plays an important role, both directly and indirectly, as an intermediary between endocrine glands and veins.
At the level of the lower limbs, on the inner face of the calves, less of the thighs, dilated, bluish, flexible, ampullate, irregular venous cords can be seen. Smaller, irregular, anastomosed dilations can be seen around the main cord. These venous dilations, very apparent when the patient is standing, are significantly reduced when the patient is lying down.
Accompanying symptoms of varicose veins are caused by blood stasis, with all its consequences regarding tissue nutrition.
These symptoms are subjective and objective.
The objectives are: excessive fatigue with relatively moderate efforts, pain in the lower limbs, which does not subside after a normal rest. Patients wake up in the morning with a feeling of painful fatigue or even severe pain.
The objective ones are primarily interested in blood circulation. There is a peripheral stasis with cyanosis, with small venectasias and malleolar edema, which disappear at first, after a night’s rest.
It occurs on the malnourished ground of the calf’s integuments, where the decrease in sebaceous and sweat secretion has reduced the ability of the acid and fatty coat to defend against pyococci, which are also present on normal integuments.
This flora is inoculated on the skin with reduced resistance, which it slowly sensitizes. The sensitization is initially local, resulting in the appearance of an erythematous-vesicular or erythematous-scaly epidermis in the respective place, clearly delimited or with irregular contours, with scattered lesions in the vicinity, which end up merging with the main plaque.
Later, after 4-8 weeks, the sensitization expands and appear at short intervals, at a distance, eruptions in the plaques, so-called secondary eruptions, of a special type, usually erythematous-scaly, symmetrical and which often remain sterile when inseminated, a whose pathogenesis is purely allergic and which do not require any special treatment, extinguishing the main focus bringing about their disappearance.
The second way of producing varicose eczema is around a crural ulcer. In this case, it is also a pyococcal eczema, produced by the oozing of pus from the surface of the ulcer, to which is usually added the effect of an irrational therapy.
At this stage, the patient presents with the entire complex of symptoms: varicose veins, dermatosclerosis, ulcers and eczematization. The treatment of varicose veins consists in combating circulatory disorders, in eliminating the main factor that leads to these disorders, i.e. varicose veins, in the general and local treatment of established lesions, i.e. eczema and varicose ulcers.
Dyschromia is a change in skin color due to an excess or lack of pigment. When the pigmentation is exaggerated, a hyperchromia is produced, while the lack or diminution of pigment production produces achromia or hypochromia.
In hyperchromia, the skin color varies from lighter yellow to yellow-brown to black. The surfaces affected by hyperchromia can be circumscribed, constituting pigment spots, or diffuse when they are called melanodermia.
in achromia or hypochromia, the modified areas appear lighter or even completely discolored. Manifestations of this order, called leukodermia, can be acquired or congenital. Those in the first category arise as a result of a local pathological process. Congenital acromia is presented in two forms: one generalized, constituting albinism, and another partial, limited to a certain surface of the skin, in the appearance of small white spots like achromic nevi, corresponding to a nerve treytorium.
Dyschromias are due to disorders in the formation of the normal pigment-melanin. The causes underlying these disorders are numerous and varied. They intervene either directly, locally, as in the case of various external irritants (physical, chemical, mechanical agents), or indirectly, as a consequence of general conditions such as various infections, intoxications, metabolic, endocrine, nervous disorders, etc.
Vitiligo is an acquired dyschromia, always appearing primitively, that is, without having been preceded by any local pathological process. The manifestations are translated by white spots of irregular shape and surrounded by an area of hyperpigmentation.
Dyschromia occurs more frequently between 10 and 30 years of age. It seems that the female sex is more affected. The spots develop unnoticed, usually they are not accompanied by any subjective symptoms, but sometimes their appearance is preceded by a slightly congestive and itchy rash. They can develop on any region of the body surface; however, the exposed parts, the face, the neck, the backs of the hands, the forearms and the integuments of the genital organs are the places where they appear more frequently.
The affected integuments have a characteristic appearance: islands of white color, circular or polycyclic in shape, surrounded on their periphery by an intensely pigmented area. The brown color degrades as it moves away from the white center, until it is confused with healthy skin. Hyperpigmented islands of different sizes sometimes remain in the area of the achromic surfaces.
Once the elements appear, they expand gradually, with a faster or slower pace, while new lesions appear in other places. The evolution of a vitiligo happens without any rules, the spots remain stationary for years, sometimes the pace is fast, the spots expand, ending up discoloring most of the body.
According to the appearance, location and extent of the spots, several clinical forms of vitiligo can be found:
- Punctate vitiligo: small achromic spots are spread on the hyperchromic surface; in variegated vitiligo, small pigment islands are seen in the discolored areas.
- Universal vitiligo: the acromia has spread over the entire surface of the body.
-Perinevic vitiligo: pigmented nevi are surrounded by an achromatic area.
-Vitilogo on the scalp is represented by strands of white hair.
All general treatments only give exceptional results. Also, local treatments do not give homogeneous and lasting repigmentation.
13.Functional disorders of the sebaceous glands
The exaggerated hypersecretion of sebum is called seborrhea. It can appear pure, when the skin is covered only with a thick, oily layer, oily seborrhea, or it can be associated with a fine, tarry peeling of the skin, dry seborrhea. In both cases, when the disease is located in the scalp, it is followed by hair loss. A hypersecretion of the sebaceous glands is observed in workers who work in overheated and humid places (fireplaces). As a syndrome we find seborrhea in parkinsonism, where the face is covered with a thick, oily layer. The decrease in sebaceous secretions is not of great importance; we find it in all dermatoses characterized by keratosis processes (ichthyosis, congenital hyperkeratosis, etc.)
In seborrhea, a treatment with degreasing lotions will be applied; salicylic alcohol 1-2%, camphorated alcohol 1%, sulfur-based lotions, and necessarily an internal treatment.
Diseases of the pilo-sebaceous follicle
This disease is characterized by furfuraceous plaques, clearly defined, located on the face, around the lips, on a slight inflammatory background. It is infectious and sometimes occurs in epidemics. The eruption appears in children, starting from the age of 5-10 years. It is characterized by a chronic furfuraceous desquamation, which is located on the cheekbones, forming round plates, with an imprecise delimitation. The skin does not show inflammatory lesions. It can also appear on the hairy skin of the head, which is covered with fine, whitish, abundant scales, especially towards the periphery of the hairy region, accompanied by itching, variable in intensity. It is characteristic that these scales disappear easily when washed with soap or after applying a simple cream, only to reappear after some time. If it is associated with seborrhea, it turns into greasy, steatoid pityriasis, characterized by greasy, yellowish scales, slightly adherent to the skin in normal appearance.
Persistent local and internal treatment can give good results.
This name is given to a seborrheic condition associated with a number of lesions that derive from each other, namely: comedones, papules, superficial and deep pustules and deep abscesses. The varieties are the following:
- juvenile or polymorphic acne.
- necrotic acne.
- hypertrophic acne.
- keloid acne.
Comedones appear as small black dots, consisting of a plug of sebum that gets stuck in the pilo-sebaceous follicle. The black extremity of the comedone is due to sebum oxidation. This formation can be easily extracted in the form of a filiform plug, a small worm, by lateral pressure between two fingers or with the blackhead extractor. In its component, the presence of a microbacillus and a parasite can be highlighted. Comedones can exist as the only manifestation of the disease: punctate acne.
In general, however, a congestive reaction occurs around the comedone, and later a slightly prominent pustule appears in its place, in the center of which is the comedone plug: pustular acne. The removal of pus is done together with the consistent, comedonic plug. After removing the suppurating plug, a yellowish, brown crust forms, which falls off, leaving a round, slightly clogged scar.
In other cases, a nodule the size of a pea or even larger forms at the base of the pustule, sometimes associating several deep, hard, painful nodules that fester through fistulas. When trying to evacuate with the extractor, a bloody pus is removed at first, and with a higher pressure, a more compact mass consisting of sebum gushes out; the acne is hardened. Sometimes communication paths are formed between the conglomeration and suppurating nodules. After scarring, new nodules may form in the scar that suppurate in the same way as the initial ones, their depth reaching the hypodermis. They form torpid abscesses, evolving slowly, with skin destruction, leaving irregular keloid scars.
The usual locations of acne are: cheekbones, chin, forehead, nose, dorsal and pectoral region, i.e. the election regions of seborrhea.
Etiology. Acne is considered a seborrheic manifestation associated with an exogenous staphylococci. Digestive disorders, endocrine disorders are blamed as etiogenic factors. Exacerbation during the premenstrual period is characteristic for girls. Hypothyroidism, adrenal insufficiency with hypotension are adjuvant factors.
The treatment is local, internal and general.
Strict hygiene is applied locally, in addition to the reducing and antiseptic drugs that are prescribed for seborrhea. Facial hygiene is achieved by degreasing with hot water and alkaline soaps, at least twice a day. Degreasing and anti-seborrheic preparations, spirit lotions based on sulfur are used. The epithelial bioregenerator gave good results in this condition as well.
The general treatment involves a dechlorinated diet, predominantly vegetarian, with the avoidance of preserved meat preparations, fats, spices and alcoholic beverages.
Internal treatment involves solving gastrointestinal and endocrine disorders, foci of infection and regulation of cellular metabolism.
Rosacea acne is a condition localized on the cheekbones, nose, forehead and chin, consisting of two morbid elements: one congestive, transitory or long-lasting and another of acneiform papular lesions. The disease is more frequent in women aged 40-50 and especially in menopause. It was found that rosacea acne occurs in individuals who suffered from facial seborrhea during puberty. In its evolution, the disease presents two clinical forms that usually constitute two successive phases of the condition: the first is facial erythrosis, based on which a vascular process is found, the second is rosacea acne (properly so-called), which also presents pustulation.
The evolution of the disease is variable, it usually occurs in bouts; it can disappear spontaneously or remain stationary for a long time. Sometimes the phenomena are accentuated, the pustulation becomes deep, the skin thickens, resulting in hypertrophic acne.
Necrotic acne. The disease appears in men at the age of 40-50. The eruption is localized with predilection on the forehead and the temporal region, in the marginal area of the hairy skin, often passing on the neighboring skin of the head, then in the retroauricular, chin and occipital region. the eruption consists of small, papulo-pustular lesions, slightly prominent, surrounded by a discrete, erythematous halo. The pustule has a reduced content, seropurulent, with a slightly umbilical center. The central umbilical part quickly materializes into a brown, adherent crust, which falls off in 7-8 days, leaving a round scar. In the evolution of eruptions, it is characteristic that the lesions appear gradually, so that they are found in different evolutionary phases. Rarely these lesions can merge. Subjectively they are painful.
Keloid acne of the neck It is more likely a deep folliculitis, chronic rebel, recidivist, than actual acne. It is mostly found in men aged 40-50, often obese. This folliculitis is accompanied by a hard, hypertrophic keloidal fibrous reaction. It presents as a raised, linear, horizontal sclerotic lesion, with follicular pustules on the periphery. In depth, there are subcutaneous or chronic abscesses that cause the hypertrophic reaction. A characteristic syndrome is the existence in a hair follicle of several hairs gathered in the shape of a brush.
14.Functional disorders of the sweat glands
Functional alterations of the sweat gland are called hydrosis. According to the character of the functional disorders, we distinguish: hyperhidrosis, when sweat secretion is exaggerated, and anhidrosis, when it is low or absent.
Hyperhidrosis can be generalized or localized.
In generalized hyperhidrosis, the hypersecretion of sweat varies individually and regionally. The secretion is more pronounced on the forehead, on the scalp, on the chest and back, on the seborrheic regions. Sweating hypersecretion is generalized, when it fulfills the role of thermoregulation in heavy physical efforts, at a high temperature of the external environment and febrile diseases. A generalized hyperhidrosis is observed in hyperthyroidism and chronic erythroderma.
Hyperhidrosis of the legs is translated by an abundant secretion of the plant and interdigital spaces. The stagnation of the secretion macerates the stratum corneum, so the sole has a white color. On this background, the openings of the glands appear as crater-like depressions. During efforts, when walking, the skin of the macerated layers loosens, giving way to superficial erosions.
The sweat gave off an unpleasant smell.
Hyperhidrosis of the hands is often observed in emotional individuals. The surface of the palms and fingers is constantly wet, producing shortcomings in the execution of some professions. Among workers in chemical dyeing shops, hyperhidrosis of the hands is common, being caused by washing hands with calcium chlorate, used to remove colors.
Axial hyperhidrosis translates into an abundant odorous secretion. This sweat can stain your underwear. It is often associated with trichomycosis palmella; sometimes predisposes to staphylococcal infections.
Hyperhidrosis located in the inguinal, perianal region and sometimes in connection with nerve diseases is also found.
Hyperhidrosis occurs as a result of reflexes started from the central nervous system, which produce, through vasodilatation, the exaggeration of the secretory function.
As a general treatment, inhibitory drugs of the neurovegetative system are administered. Strict local hygiene, frequent washing with soap and water. Substances that inhibit sweat secretion can be used.
Other sweat alterations
Chromhidrosis is characterized by the blue color of the sweat, due to the indican it contains, which oxidizes in contact with air, giving the shade shown.
Osmhidrosis is smelly sweat due to various volatile substances that can also be eliminated through sweat: garlic, onion, turpentine, etc.
Urhidrosis is characterized by a mixture of urates in the sweat. After the sweat evaporates, whitish crystals remain on the skin.
Hemathidrosis is constituted by sweat mixed with blood.
As I mentioned before, the lack of sweat is called anhidrosis. The disease is rare, it can be a congenital dystrophy or it can occur in asthenic patients, in miners and laundry workers, where the air is warm and humid, in generalized erythroderma, in ichthyosis, prurigo and more rarely after typhoid fever. The skin of these patients is dry and prone to microbial infections.
15.Diseases of skin appendages
- THE HAIR
Hair diseases are one of the most common problems in dermatological practice. The causes that produce hair disorders are varied, as are the diversity of its alterations.
In general, the hair can undergo the following pathological changes: 1. color changes, 2. structural changes, 3. changes regarding its exaggerated development in unusual regions, 4. thinning, especially in the scalp, possibly leading to baldness.
- Color changes.
The darkening is represented by the changes in hair color towards the light shade that is observed in some people with advancing age. In the conditions shown, the browning is therefore a physiological process. The factors that determine the browning are not completely elucidated; it is claimed by some that the bulb no longer produces the pigment that colors the hair; others claim that during hair formation, air bubbles enter its parenchyma. Some research on rats has shown that a diet devoid of B complex vitamins, namely pantothenic acid, would produce white hair.
Chronic diseases, neuritis and trauma of the peripheral nerves as well as strong nervous shocks play an important role, causing sometimes very rapid browning.
- Structural changes of the hair.
Trichochisis or trichoptilosis is characterized by the splitting of the hair at its free end, in its longitudinal axis.
Tricorexa nodosa is characterized by the appearance of small nodules along the hairline. At the level of these nodules, the hair splits into filaments and breaks. These alterations are caused in most cases, by washing the hair too often, by using hard brushes and concentrated oxygenated water in order to change the color of the hair.
In addition to the above condition, we remind you that in pruritic dermatoses: eczema, prurigo, neurodermatitis, located on hairy areas, through repeated scratching, the hair becomes blunt, shortens, leaving only a few stumps on the surface. The elimination of the mechanical factor, and the healing of dermatosis, lead to hair restoration.
Trichomycosis palmella. The bristles are surrounded by numerous granular formations consisting of an accumulation of micrococci, stuck to each other and to the hair by a sticky mass. The bristles appear devoid of their natural luster, hard and thickened and, depending on the type of microbes, colored in yellow, red, blue and black. Their typical location is the armpit and rarely, the pubic region.
Idiopathic trichoclasia. The bristles break in circumscribed territories without any discernible cause. The usual location is the scalp.
Trichonodosis laqueata is characterized by the formation of one or two looped or wide knots on the hair, without any alteration of the hair.
Trichomalacia. Inside the hair follicle, the hair softens and twists into a spiral, forming a slightly prominent formation. A thinning of the bristles can be observed on the surface.
In certain territories, the brushes increase in volume, are thicker and more numerous. The factors that determine hypertrichosis are very varied; frequent plucking of hairs, hormonal disorders in elderly women, virilism, exaggerated treatments with male gonadotrope preparations.
Hypertrichosis is sometimes present from birth, localized on extended areas, covered with thick, rich hair, based on pigmented nevi.
- Hair loss and alopecia
Hair loss is not the same as alopecia, because not every hair loss leads to alopecia. Alopecia (baldness) means a circumscribed or total, definitive lack of hair.
For any hair loss, we must specify from the beginning the following two clinical features:
- if this hair loss is circumscribed, i.e. if it appears in isolated, well-defined patches of varying size, or if it is diffuse and extends over large territories.
- if it is conditioned by a transient functional suppression of the papilla, without its destruction, it being therefore able to resume its functions after the disappearance of the harmful cause that intervened, the hair being restored, or if it is due to an atrophy of the papilla, in which case the hair no longer regenerates.
They can be produced by physical and chemical causes that act exogenously.
Traumatic marginal alopecia is produced in women by excessive traction when arranging the hairstyle, when using curlers. Its location varies according to the regions that are damaged by trauma.
Trichotillomania occurs in patients with mental disorders or in some school children who have the habit of continuously pulling out their hair.
Symptomatic alopecia appears after a surgical shock, obstetric shock, anesthesia, after infectious-contagious diseases (scarlet fever, typhus, flu, pneumonia, etc.) approximately after 6-8 weeks. It is characterized by diffuse hair loss. Sometimes the skin shows a furfuraceous peeling. The pathogenic factor is related to the etiogenic factor of the respective disease.
Here we can frame the hair loss that is observed in girls during puberty. It corresponds to seborrheic alopecia in men. This fall is caused by greasy seborrhea, which makes the hair greasy, and a layer of thick scales forms on the scalp. Patients must wash more often to remove this layer of fat. This seborrhea is often accompanied by vulgar acne. The etiopathogenic factor is probably endocrine. A similar alopecia based on endocrine factors is observed in women aged 30-40 and after menopause. In general, in these alopecias, the bristles become rare; they recover, but they are not as strong as before.
Exogenous irreversible alopecias are caused by various traumas, chemical substances or some local infections, which destroy the skin together with the hair papillae, leaving a scar.
Irreversible alopecias due to endogenous causes begin at puberty, both in girls and boys. The hair becomes greasy, greasy, and a layer of scales forms on the scalp, consisting either of greasy scales (seborrhea) or of dry pityriaziform scales (pityriasis). According to the type of initial lesions, we distinguish between seborrheic alopecia and pityriasis alopecia. Sometimes hair loss is not accompanied by skin lesions; premature alopecia. These three variants have identical symptoms; the difference consists only in the fact that in girls hair loss is less, it lasts only a few months, then stops, while in young men the loss is progressive, lasting without interruption for years in a row. so that at the age of 25-40 years the hair will completely fall out, leaving only in the postero-lateral peripheral area of the hairy skin, in a territory with a varied diameter, hairs forming a crown around the head. In this way, the disease reaches the terminal phase characterized by baldness. The scalp, in the center, is devoid of hair, forming a territory similar to the full moon; the skin is thinned, it can wrinkle in coarse folds, it is slightly movable on the deep layers, slightly atrophied, it shines and is smooth.
In the initial phase, a discreet itching is signaled, which is accentuated in the evening when going to bed.
The etiology is not known. The same causes can be blamed, as in all alopecias, nervous disorders probably of central origin and endocrine disorders. Sometimes this baldness runs in the family. It is interesting that in women hair loss stops, but in men it is progressive.
Therapeutic results are modest. They can be used in dry or oily form, pomades or exciting lotions. Internally, good results are obtained by taking pantothenic acid, vitamin A, vitamin H, antiseborrheic.
- Color change
The normal color of the nails is pink because the capillaries of the nail bed can be seen through the transparency of the nail plate. This normal coloring can be changed in various shades. The white coloring is called leukonychia. It can be total, i.e. involve the entire nail, as in vitiligo, albinism, neuritis or after serious diseases, or it can be partial. Partial leukonychia is the usual form of the condition and is currently called leukonychia, without any other qualification. It is characterized by white spots that appear on the nail plate, spots that can be distributed regularly (linearly, etc.) or irregularly. These spots usually arise at the level of the nail root, from where they reach its free edge, along with its growth. The occurrence of leukonychia is linked to general diseases, especially of an endocrine nature.
In jaundice, the nails are yellow. In cyanosis, cachectic states, peripheral collapse, they are violaceous. In gangrene they become almost black. The post-traumatic subungual hematoma also appears black, usually followed by the removal of the nail.
- Changing the shape of the nails.
The most frequently encountered modification of the shape is achieved by the so-called Hippocratic nails. They consist in exaggerating the normal convexity of the nails, which become convex like a watch glass. The probable cause is an edema of the bed and especially of the matrix which, rising, reduces the angle of growth compared to the phalanx, so that the nail is molded on the bone plane. Hippocratic nails can be found in the following general conditions: congenital heart diseases, slow endocarditis, suppurations and pulmonary tuberculosis, intestinal papillomatosis and Pierre Marie hypertrophic osteoarthropathy.
- Changing the structure of the nails.
Beau’s arciform furrow is a transverse furrow, which appears in the vicinity of the matrix and advances with the growth of the nail towards the free edge. It can be present on one or more nails. Its appearance is related to nutritional disorders, general pyretic conditions, intoxications.
In women, it can be the consequence of infections or manicure traumas.
Depressions or punctate erosions can appear on one or more nails, in the form of round excavations that give the nail the appearance of a thimble. They can be arranged irregularly or arranged parallel, transversely or longitudinally. They can appear after acute rheumatism and in various dermatoses: eczema, syphilis, but especially in psoriasis.
Nail furrows are longitudinal stripes, frequently found in the elderly. Sometimes they can be accentuated to such an extent that they can cause the nail to detach, especially when it is associated with an accentuated fragility.
Median canaliform dystrophy is a condition characterized by the presence of a longitudinal groove in one or more nails. This groove is accompanied by the thinning, at its level, of the nail blade, which becomes friable. It is a rare condition, probably of nervous origin.
Hepalonychia is a condition characterized by the softening of the nails, which deteriorates under the macerated action of the sweat secretion, in hyperhidrosis or in spasmodic paralysis. Sometimes, the nails can also lend the blue-white appearance; they have the fragility of the internal membrane of the eggshell.
Nail sideratio is the syndrome characterized by the stoppage of the growth of the nails.
Platonychia is characterized by the disappearance of the normal convexity of the nail surface, becoming flat.
Koilonychia is the inversion of the nail curves, the surface presenting a depression in the center, at which level the nail is softer. The nails take the appearance of shovels. It is observed in anemia, eczema.
Onychoschiiasis is characterized by the peeling of the nails from the bed. If the new nail grows normally on the bed, the two nails nest together like the tiles on the house. This condition is found in onychomycosis, in serious toxicodermas, in psoriasis, in pemphigus.
Helconichia means the partial destruction of the nail, in the form of a loss of substance, which thus reveals the portion corresponding to the bed, sometimes semilunar.
Onychophagia is the destruction of the free edge, through the habit that some people, especially children, have of biting their nails. The condition denotes nervous tics and requires an examination by a psychiatrist.
The wear of the free edge is observed in certain professions and in pruritic dermatoses. The edge becomes glossy, smooth and concave.
Atrophy of nails is characterized by their thinning, they become papery. Their surface becomes wavy, and the consistency soft. They should not be confused with the epidermal nail, which takes the place of the normal one, after the extirpation of the matrix, and which is formed through processes of additional keratinization of the bed.
Anonychia is the absence of nails. It can be total or partial and is usually congenital. It can be found in ichthyosiform hyperkeratosis, congenital diffuse keratosis and palmo-plantar keratoderma.
Thickening of the nail is characterized by the fact that the nail becomes hard, rigid, longitudinally or transversely striated and turns brown or gray. It can be congenital, traumatic or accompany other skin manifestations, such as palmo-plantar lesions, oral leukoplakia, etc.
Subungual parakeratosis differs from pachyonychia, with which it can be confused, by the fact that the corneous blade is of unchanged thickness; however, the free edge of the nail is thickened by numerous scales that lift the nail off the bed. It can usually be accompanied by changes in the nail; thickening, striations, etc.
It is found in psoriasis, eczema, mycosis, Norwegian scabies
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