STUDY - Technical - New Dacian's Medicine
Common
Skin Conditions (1)
Translation Draft
In this short series of posts I will "talk" about eczema, psoriasis, skin infections, acne and other common skin conditions.
Eczema or dermatitis is a way of reaction manifested by variable clinical and histological signs. Eczema is the common expression for a number of conditions including atopic dermatitis, allergic and irritant contact dermatitis, dyshidrotic eczema, numulary eczema, chronic lichen simplex, astetitic eczema and seborrheic dermatitis.
Primary lesions may include papules, erythematous maculs and vesicles, which may join together to form plaques and spots. In severe eczema can predominate secondary lesions of infection or excoriation, which are marked by zemuir and crust formation. Long-term dermatitis is often dry and is characterized by thickened, descuamative skin (lichenization).
Atopic dermatitis is the skin expression of the atopic terrain, characterized in up to 70% of patients with a history of asthma, hay fever or dermatitis. It has been estimated that up to about 20% of children will experience some atopic eczema. Clinical criteria for the diagnosis of atopic dermatitis are represented by: 1. pruritus and grating, 2. evolution marked by exacerbations and remissions, 3. typical lesions of eczema dermatitis, 4. personal or family history of atopia (asthma, allergic rhinitis, food allergies or eczema) and 5. clinical evolution lasting more than 6 weeks.
The clinical aspect often varies with age. The infantile pattern is characterized by inflammatory spots and crusty plaques that appear on the face, neck, extension surfaces and groin. The large child's shape similar to that of the adolescent is marked by flexural skin dermatitis, especially in the antecubital and popliteal fossa. Atopic dermatitis can heal spontaneously in adults, but will persist in adult life in more than half of individuals affected in childhood.
The distribution of lesions may be similar to those occurring in children. However, adults affected by atopic dermatitis frequently have localized disease, manifested as eczema or as lichen simplex chronicus. Pruritus is an important feature of atopic dermatitis and many of the skin changes of affected patients are secondary to rubbing and scratching. Other stigmas of atopic dermatitis are perioral pallor, a cube lower eyelid (Denia line), increased palmar drawing and increased incidence of skin infection, especially with Staphylococcus aureus.
Atopic individuals often have dry, itchy skin, abnormalities of the skin vascular response and, in some cases, elevated levels of serum IgE. The therapy of atopic dermatitis should be based on the avoidance of skin irritants, adequate skin hydration, judicious use of topical glucocorticoids of low or medium potency and prompt treatment of secondary infected skin lesions. The most common irritants are soaps and hot water. Patients should be instructed to bathe using hot, not hot water, and limit the use of soaps.
Immediately after bathing, the skin should be lubricated with a topical glucocorticoid of low or medium potency, in the form of cream or ointment. Crusty and zemuind lesions should be treated with systemic antibiotics with activity against Staphylococcus aureus, as secondary infection often exacerbates eczema.
The role of food allergens in atopic dermatitis is controversial, but there is little evidence that it plays any role, except in early childhood. control of pruritus is essential for treatment, as atopic eczema is often "an itchy itch". Antihistamines are useful to control the itching that accompanies eczema, but sedation can limit their usefulness.
Unlike hives, non-sedative antihistamines are of limited use because the effectiveness of antihistamines in the treatment of pruritus associated with atopic dermatitis is primarily related to their sedative effects in opposition to any specific action on histamine-mediated pathways. Treatment with systemic glucocorticoids should be limited to severe exacerbations that do not respond to conservative topical treatment. In the patient with chronic atopic eczema, treatment with systemic glucocorticoids will generally heal the skin only briefly, but discontinuation of systemic therapy will invariably be accompanied by recurrence, if not worsening of dermatitis.
Patients who do not respond to conventional therapies should be assessed the appropriateness of an epicutan test to eliminate the possibility of allergic contact dermatitis. In rare cases, severe atopic dermatitis that does not recover may require systemic immunosuppressive therapy, but it should be used with extreme caution.
Contact dermatitis is an inflammatory process of the skin caused by one or more exogenous agents that directly or indirectly affect the skin. This impairment may be caused by an inherent characteristic of a compound; irritant contact dermatitis (ID). An example of DCI would be dermatitis induced by a base or a concentrated acid. Agents that cause allergic contact dermatitis (DCA) induce a specific antigen immune response. Clinical lesions of contact dermatitis can be acute (wet and erythematous) or chronic (dry, thickened and squamous) depending on the persistence of aggression.
The prevalence of contact dermatitis in industrialized areas can reach levels of 5-20%, with DCI much more common than DCA. the most common presentation of contact dermatitis is hand eczema and is frequently related to occupational exposures. DCI is generally demarcated and often located in regions with thin skin (eyelids, intertriginous regions) or regions where the irritant has had abusive contact. Injuries can range from minimal skin erythema to areas with marked edema, blisters and ulcers. Chronic irritant dermatitis of moderate intensity is the most common type of DCI, and the most commonly affected regions are hands.
Treatment should be directed towards avoiding irritants and the use of protective clothing or gloves. DCA is a manifestation of delayed type hypersensitivity mediated by T lymphocytes with memory in the skin. The most commonly recognized form of DCA occurs in response to plant-derived antigens.
Members of the Toxicodendron genus, including venomous ivy, oak and sumac, cause an allergic reaction marked by erythema, vesicle and intense pruritus. The rash is often linear, corresponding to areas where plants have touched the skin. However, other allergens can be much more difficult to identify, especially if the exposure is chronic and the skin becomes thickened and scupamy.
From a treatment point of view, if DCA is suspected and an aggressive agent is identified and removed, the rash heals. Usually, treatment with a topical high potency fluorinate is sufficient to relieve symptoms while DCA is taking its course. Patients with particularly extensive disease or of interest to the face or genitals may require oral treatment with glucocorticoids.
Since the natural evolution of DCA is 2-3 weeks, therapy should be continued for the entire period of time. Treatment of DCA by short, rapidly low cures of oral glucocorticoids is almost always accompanied by recurrence of skin lesions. In addition, when using systemic glucocorticoids, they are optimally administered in single morning doses to limit potential side effects. Identifying a contact allergen can be a difficult task and can take a long time.
Patients with conventionally refractory dermatitis or unusual distribution and pattern should be suspected of DCA. They should be carefully questioned about occupational exposures, topical and oral medications. More frequent sensitizing agents include preservatives in topical preparations, nickel sulphate, potassium dichromate, neomycin sulfate, flavourings, formaldehyde and rubber treatment agents. Epicutian testing is useful in identifying these agents, but should not be used in patients with disseminated active dermatitis or those treated with systemic glucocorticoids.
Eczema of the hands is a very common chronic skin condition. It accounts for the overwhelming majority of occupation-related skin diseases, which is responsible for a significant proportion of occupational impairments and loss of working time. It can be associated with other skin disorders like atopic dermatitis, or it can occur in isolation. Like other forms of dermatitis, both exogenous and endogenous factors play important roles in the expression of hand dermatitis. Chronic, excessive exposure to water and detergents may initiate or aggravate this condition. It can present with dryness and cracking of the skin of the hands, as well as with varying degrees of erythema and edema.
Often, dermatitis begins under the rings, where water and irritants are trapped. A variant of dermatitis of the hands, dyshidrotic eczema, presents with multiple papules and small, intensely itchy vesicles, on the tenar and hypotenar eminences and on the sides of the fingers. Injuries tend to occur in bunches, which slowly form crusts and heal. The assessment of a patient with hand eczema should include a determination of the potential associated occupational exposures.
Predominant damage to the dorsal surface of the hands with respect to the palmar face should suggest a possible contact dermatitis. Anamnesis should be directed to identify possible exposures to irritation or allergens. The use of rubber gloves to protect dermatitis skin is sometimes associated with the occurrence of delayed hypersensitivity reactions in agents used to cross-link the rubber. These delayed hypersensitivity reactions can be detected by epicutan testing.
Less commonly, patients may develop hand dermatitis as a consequence of immediate latex hypersensitivity reactions. These reactions are of particular interest because these patients are at risk of anaphylactic reactions. The most sensitive method of detection is the use of scarification testing with latex extract. However, this should only be taken with maximum caution in a place where an anaphylactic reaction can be treated. A radioallergosorbent test (RAST) is available for latex, but it has a sensitivity of only 60%.
Treatment of hand dermatitis is directed to avoid irritants, identify possible contact allergens, treat coexisting infection and apply topical glucocorticoids. Whenever possible, hands should be protected with gloves, preferably vinyl gloves. Most patients can be treated by applying moist, refreshing compresses (pansages) to dry and debride acute inflammatory lesions and relieve swelling, followed by the application of a topical glucocorticoid of medium potency in the form of cream or ointment. As with atopic dermatitis, the treatment of secondary staph infection is essential for good control. In addition, patients with hand dermatitis should be examined for dermatophyte infection by preparation with KOH and culture.
That's enough for today... We've got a long way to go...
In this short series of posts I will "talk" about eczema, psoriasis, skin infections, acne and other common skin conditions.
Eczema or dermatitis is a way of reaction manifested by variable clinical and histological signs. Eczema is the common expression for a number of conditions including atopic dermatitis, allergic and irritant contact dermatitis, dyshidrotic eczema, numulary eczema, chronic lichen simplex, astetitic eczema and seborrheic dermatitis.
Primary lesions may include papules, erythematous maculs and vesicles, which may join together to form plaques and spots. In severe eczema can predominate secondary lesions of infection or excoriation, which are marked by zemuir and crust formation. Long-term dermatitis is often dry and is characterized by thickened, descuamative skin (lichenization).
Atopic dermatitis is the skin expression of the atopic terrain, characterized in up to 70% of patients with a history of asthma, hay fever or dermatitis. It has been estimated that up to about 20% of children will experience some atopic eczema. Clinical criteria for the diagnosis of atopic dermatitis are represented by: 1. pruritus and grating, 2. evolution marked by exacerbations and remissions, 3. typical lesions of eczema dermatitis, 4. personal or family history of atopia (asthma, allergic rhinitis, food allergies or eczema) and 5. clinical evolution lasting more than 6 weeks.
The clinical aspect often varies with age. The infantile pattern is characterized by inflammatory spots and crusty plaques that appear on the face, neck, extension surfaces and groin. The large child's shape similar to that of the adolescent is marked by flexural skin dermatitis, especially in the antecubital and popliteal fossa. Atopic dermatitis can heal spontaneously in adults, but will persist in adult life in more than half of individuals affected in childhood.
The distribution of lesions may be similar to those occurring in children. However, adults affected by atopic dermatitis frequently have localized disease, manifested as eczema or as lichen simplex chronicus. Pruritus is an important feature of atopic dermatitis and many of the skin changes of affected patients are secondary to rubbing and scratching. Other stigmas of atopic dermatitis are perioral pallor, a cube lower eyelid (Denia line), increased palmar drawing and increased incidence of skin infection, especially with Staphylococcus aureus.
Atopic individuals often have dry, itchy skin, abnormalities of the skin vascular response and, in some cases, elevated levels of serum IgE. The therapy of atopic dermatitis should be based on the avoidance of skin irritants, adequate skin hydration, judicious use of topical glucocorticoids of low or medium potency and prompt treatment of secondary infected skin lesions. The most common irritants are soaps and hot water. Patients should be instructed to bathe using hot, not hot water, and limit the use of soaps.
Immediately after bathing, the skin should be lubricated with a topical glucocorticoid of low or medium potency, in the form of cream or ointment. Crusty and zemuind lesions should be treated with systemic antibiotics with activity against Staphylococcus aureus, as secondary infection often exacerbates eczema.
The role of food allergens in atopic dermatitis is controversial, but there is little evidence that it plays any role, except in early childhood. control of pruritus is essential for treatment, as atopic eczema is often "an itchy itch". Antihistamines are useful to control the itching that accompanies eczema, but sedation can limit their usefulness.
Unlike hives, non-sedative antihistamines are of limited use because the effectiveness of antihistamines in the treatment of pruritus associated with atopic dermatitis is primarily related to their sedative effects in opposition to any specific action on histamine-mediated pathways. Treatment with systemic glucocorticoids should be limited to severe exacerbations that do not respond to conservative topical treatment. In the patient with chronic atopic eczema, treatment with systemic glucocorticoids will generally heal the skin only briefly, but discontinuation of systemic therapy will invariably be accompanied by recurrence, if not worsening of dermatitis.
Patients who do not respond to conventional therapies should be assessed the appropriateness of an epicutan test to eliminate the possibility of allergic contact dermatitis. In rare cases, severe atopic dermatitis that does not recover may require systemic immunosuppressive therapy, but it should be used with extreme caution.
Contact dermatitis is an inflammatory process of the skin caused by one or more exogenous agents that directly or indirectly affect the skin. This impairment may be caused by an inherent characteristic of a compound; irritant contact dermatitis (ID). An example of DCI would be dermatitis induced by a base or a concentrated acid. Agents that cause allergic contact dermatitis (DCA) induce a specific antigen immune response. Clinical lesions of contact dermatitis can be acute (wet and erythematous) or chronic (dry, thickened and squamous) depending on the persistence of aggression.
The prevalence of contact dermatitis in industrialized areas can reach levels of 5-20%, with DCI much more common than DCA. the most common presentation of contact dermatitis is hand eczema and is frequently related to occupational exposures. DCI is generally demarcated and often located in regions with thin skin (eyelids, intertriginous regions) or regions where the irritant has had abusive contact. Injuries can range from minimal skin erythema to areas with marked edema, blisters and ulcers. Chronic irritant dermatitis of moderate intensity is the most common type of DCI, and the most commonly affected regions are hands.
Treatment should be directed towards avoiding irritants and the use of protective clothing or gloves. DCA is a manifestation of delayed type hypersensitivity mediated by T lymphocytes with memory in the skin. The most commonly recognized form of DCA occurs in response to plant-derived antigens.
Members of the Toxicodendron genus, including venomous ivy, oak and sumac, cause an allergic reaction marked by erythema, vesicle and intense pruritus. The rash is often linear, corresponding to areas where plants have touched the skin. However, other allergens can be much more difficult to identify, especially if the exposure is chronic and the skin becomes thickened and scupamy.
From a treatment point of view, if DCA is suspected and an aggressive agent is identified and removed, the rash heals. Usually, treatment with a topical high potency fluorinate is sufficient to relieve symptoms while DCA is taking its course. Patients with particularly extensive disease or of interest to the face or genitals may require oral treatment with glucocorticoids.
Since the natural evolution of DCA is 2-3 weeks, therapy should be continued for the entire period of time. Treatment of DCA by short, rapidly low cures of oral glucocorticoids is almost always accompanied by recurrence of skin lesions. In addition, when using systemic glucocorticoids, they are optimally administered in single morning doses to limit potential side effects. Identifying a contact allergen can be a difficult task and can take a long time.
Patients with conventionally refractory dermatitis or unusual distribution and pattern should be suspected of DCA. They should be carefully questioned about occupational exposures, topical and oral medications. More frequent sensitizing agents include preservatives in topical preparations, nickel sulphate, potassium dichromate, neomycin sulfate, flavourings, formaldehyde and rubber treatment agents. Epicutian testing is useful in identifying these agents, but should not be used in patients with disseminated active dermatitis or those treated with systemic glucocorticoids.
Eczema of the hands is a very common chronic skin condition. It accounts for the overwhelming majority of occupation-related skin diseases, which is responsible for a significant proportion of occupational impairments and loss of working time. It can be associated with other skin disorders like atopic dermatitis, or it can occur in isolation. Like other forms of dermatitis, both exogenous and endogenous factors play important roles in the expression of hand dermatitis. Chronic, excessive exposure to water and detergents may initiate or aggravate this condition. It can present with dryness and cracking of the skin of the hands, as well as with varying degrees of erythema and edema.
Often, dermatitis begins under the rings, where water and irritants are trapped. A variant of dermatitis of the hands, dyshidrotic eczema, presents with multiple papules and small, intensely itchy vesicles, on the tenar and hypotenar eminences and on the sides of the fingers. Injuries tend to occur in bunches, which slowly form crusts and heal. The assessment of a patient with hand eczema should include a determination of the potential associated occupational exposures.
Predominant damage to the dorsal surface of the hands with respect to the palmar face should suggest a possible contact dermatitis. Anamnesis should be directed to identify possible exposures to irritation or allergens. The use of rubber gloves to protect dermatitis skin is sometimes associated with the occurrence of delayed hypersensitivity reactions in agents used to cross-link the rubber. These delayed hypersensitivity reactions can be detected by epicutan testing.
Less commonly, patients may develop hand dermatitis as a consequence of immediate latex hypersensitivity reactions. These reactions are of particular interest because these patients are at risk of anaphylactic reactions. The most sensitive method of detection is the use of scarification testing with latex extract. However, this should only be taken with maximum caution in a place where an anaphylactic reaction can be treated. A radioallergosorbent test (RAST) is available for latex, but it has a sensitivity of only 60%.
Treatment of hand dermatitis is directed to avoid irritants, identify possible contact allergens, treat coexisting infection and apply topical glucocorticoids. Whenever possible, hands should be protected with gloves, preferably vinyl gloves. Most patients can be treated by applying moist, refreshing compresses (pansages) to dry and debride acute inflammatory lesions and relieve swelling, followed by the application of a topical glucocorticoid of medium potency in the form of cream or ointment. As with atopic dermatitis, the treatment of secondary staph infection is essential for good control. In addition, patients with hand dermatitis should be examined for dermatophyte infection by preparation with KOH and culture.
That's enough for today... We've got a long way to go...
A restful or super-fun
Saturday, full of understanding, love and gratitude!
Dorin, Merticaru