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Showing posts with label O. Show all posts
Thursday, January 6, 2011
Wednesday, January 5, 2011
Mycosis axillary and pubic
Tricomicoza axillary and pubicTricomicoza is a superficial bacterial colonization of axillary and pubic hair follicles. The condition is characterized by granular deposits, yellow, black or red, which binds to the hair.
While many patients are asymptomatic, they accuse the axillary or pubic rash, growths on the hair and odor. It tells the color pink and sweat-cromhidroza. Lesions are pruritic and can become infected by dermatophytes. Tricomicoza is caused by several species of fungi Corynebacterii and not, as the name implies.
Treatment of hyperhidrosis improvement involves the use of drying agents. Topical clindamycin is indicated for severe cases. Complications include septicemia occur in immunocompromised and secondary colonization of catheters and surgical wounds. Recurrence is common, but proper care and treatment are simple treatment. The prognosis is excellent.
Pathogenesis and causes
Tricomicoza is a characteristic disorder of hair and sweat glands in the pubic and axillary region. Causative organism is Corynebacterium tenuis who prefer a moist environment of the groin and underarms. 33% of healthy adults are colonized by this bacterium epidermal, but only some develop disease. Tricomicoza risk factors include strict hygiene and lack of hyperhidrosis, with immunosuppressed status.The exact origin of the substance of the cement grains that cause hair colored is still debated.
Signs and symptoms
Tricomicoza can affect any age group from puberty until senescence. Axillary Tricomicoza is typically asymptomatic, though patients may experience an unpleasant odor of sweat. The hairs are present in granules of 1-2 mm red, black and yellow that adheres firmly to the hair. The insoluble substance elaborated by the bacteria invade and destroy cuticulara and cortical keratin. The yellow color is seen more frequently and with yellow stain clothes.Black and red colors are observed especially in tropical climates.The hair can be sfarimicios and thus easier to break. Alopecia typically is not present. The adjacent normal skin, hyperhidrosis, although the affected region is common. The lesions are present and in the groin, scrotum and penis sheath. Injuries can be associated with redness and itching, superinfection with dermatophytes.
Treatment
The fastest way to shave hair therapy is affected. Shower gels with benzoyl peroxide helps to prevent recurrences. Antiperspirants help treat and prevent the condition by reducing axillary hyperhidrosis. Preparations for topical antibiotics such as clindamycin and erythromycin are also effective. Drying powders are helpful. Hydrochloric naftidina cream 1% is useful for combined antibacterial and antifungal actions. The prognosis is excellent condition.
While many patients are asymptomatic, they accuse the axillary or pubic rash, growths on the hair and odor. It tells the color pink and sweat-cromhidroza. Lesions are pruritic and can become infected by dermatophytes. Tricomicoza is caused by several species of fungi Corynebacterii and not, as the name implies.
Treatment of hyperhidrosis improvement involves the use of drying agents. Topical clindamycin is indicated for severe cases. Complications include septicemia occur in immunocompromised and secondary colonization of catheters and surgical wounds. Recurrence is common, but proper care and treatment are simple treatment. The prognosis is excellent.
Pathogenesis and causes
Tricomicoza is a characteristic disorder of hair and sweat glands in the pubic and axillary region. Causative organism is Corynebacterium tenuis who prefer a moist environment of the groin and underarms. 33% of healthy adults are colonized by this bacterium epidermal, but only some develop disease. Tricomicoza risk factors include strict hygiene and lack of hyperhidrosis, with immunosuppressed status.The exact origin of the substance of the cement grains that cause hair colored is still debated.
Signs and symptoms
Tricomicoza can affect any age group from puberty until senescence. Axillary Tricomicoza is typically asymptomatic, though patients may experience an unpleasant odor of sweat. The hairs are present in granules of 1-2 mm red, black and yellow that adheres firmly to the hair. The insoluble substance elaborated by the bacteria invade and destroy cuticulara and cortical keratin. The yellow color is seen more frequently and with yellow stain clothes.Black and red colors are observed especially in tropical climates.The hair can be sfarimicios and thus easier to break. Alopecia typically is not present. The adjacent normal skin, hyperhidrosis, although the affected region is common. The lesions are present and in the groin, scrotum and penis sheath. Injuries can be associated with redness and itching, superinfection with dermatophytes.
Treatment
The fastest way to shave hair therapy is affected. Shower gels with benzoyl peroxide helps to prevent recurrences. Antiperspirants help treat and prevent the condition by reducing axillary hyperhidrosis. Preparations for topical antibiotics such as clindamycin and erythromycin are also effective. Drying powders are helpful. Hydrochloric naftidina cream 1% is useful for combined antibacterial and antifungal actions. The prognosis is excellent condition.
Tinea nigra
Tinea nigraTinea nigra is a superficial ringworm usually caused unusual Hortaea wemeckii. It appears as a hyperpigmented macule on her hands. Plants and rarely other parts of the body may be affected. Although nigra can be alarming aspect is unusual because of high incidence and potential confusion with a more severe medical condition (malignant melanoma), tinea nigra is a benign and easily curable disease.
After tinea nigra is described and diagnosed based on patient history, physical examination and appropriate laboratory tests indicate a treatment to eradicate the fungal infection. Dermatological agents are used as salicylic acid, tretinoin, topical imidazoles, piridone topical alilamine.
Because the infection is considered to occur after secondary inoculation trauma, patients should avoid sources of contamination such as soil, compost and rotted wood. Tinea nigra is a benign superficial fungal infection that does not cause serious complications. It is curable and treatment is not appropriate.
Pathogenesis and causes
Tinea nigra is a superficial mycosis of the stratum corneum. Infection occurs as a result of inoculation out of a contaminated source such as soil, compost timber or a trauma to the affected area. Typical incubation is 2-7 weeks. Lipophilic fungus shows adhesion to human skin. It is found exclusively in the stratum corneum and stratum lucidum does not extend to.Fungus takes nutrients from the breakdown of fats. It is tolerant to salt and a low pH environment. Cause changes to skin pigmentation patches colored black by the accumulation of substance melaninlike in fungi. Ringworm tends to occur in areas with a higher concentration of eccrine glands. Hyperhidrosis seems to be a risk factor.
Signs and symptoms
Tinea nigra is most common in pediatric and adolescent populations, yet people of all ages can be infected. Generally patients are asymptomatic tinea nigra. Rarely pruritus can be reported. The absence of any discomfort the patient's decision to postpone doctor.
Physical examination.Tinea nigra is characterized by the presence of a brown-black macules painless. The macula appears as a black dot initially insidious. Macular hyperpigmentation varies from brown to black up similar to silver nitrate. Edges are typically discrete. Pigmentary changes appear smooth. Typical lesion is solitary, although multiple lesions may be present. Solitary lesions are located on the surfaces and planting palm, but can extend to the fingers. Areas like the neck or chest are rarely affected.Shape ovoid lesion varies and can be round or irregular. The lesion grows slowly in a few weeks or months. Size varies from a few millimeters to inches in diameter, depending on the duration of infection. Other natural elements such as redness or mercy are absent. Rarely is this peeling.
Diagnosis
Laboratory studies:Microscopic examination of scales peilii-treated with potassium hydroxide showed septated hyphae, branched cxare containing black pigment in the wallsIncreases intro-week culture.Histological examination of biopsy specimens showed mild hyperkeratosis and acanthosis. One can describe a lymphoma perivascular infiltrates in the papillary layer of dermis and subpapilar.The differential diagnosis is made with the following diseases: Addison's disease, dysplastic nevus, malignant melanoma, nevi melanocitici, syphilis, candida, pint, chemical contamination.
Treatment
Topical antifungal preparations are used to eradicate the infection. Dermatological agents are used to treat tinea nigra due to their action on the skin. They can help remove excess keratin in hyperkeratotic skin disorders or modify the cellular turnover. Or fungicides are used alongside medical fungistaticele.
Salicylic acid peeling of the stratum corneum determined by dissolving the intercellular cementum without affecting the structure of viable dermis. Tretinoin topical drops coalescence of follicular epithelial cells and stimulate their mitotic activity with a rapid turnover of epithelial cells.
Imidazolii topical antifungal spectrum are typically used for tinea pedis and tinea but are useful nigra. Examples: Clotrimazole, ketoconazole, miconazole. Piridonele are topical agents with broad spectrum activity anticandidozica, antidermatofitica and antibacterial. Examples: Ciclopirox. Topical Alilaminele epoxidaza inhibit a key enzyme in the biosynthesis of squalene sterol in fungi fungus causes death. Examples: terbinafine. Fungistatic agents not only kill fungi prevent their replication. Examples: undeclenic acid.
After tinea nigra is described and diagnosed based on patient history, physical examination and appropriate laboratory tests indicate a treatment to eradicate the fungal infection. Dermatological agents are used as salicylic acid, tretinoin, topical imidazoles, piridone topical alilamine.
Because the infection is considered to occur after secondary inoculation trauma, patients should avoid sources of contamination such as soil, compost and rotted wood. Tinea nigra is a benign superficial fungal infection that does not cause serious complications. It is curable and treatment is not appropriate.
Pathogenesis and causes
Tinea nigra is a superficial mycosis of the stratum corneum. Infection occurs as a result of inoculation out of a contaminated source such as soil, compost timber or a trauma to the affected area. Typical incubation is 2-7 weeks. Lipophilic fungus shows adhesion to human skin. It is found exclusively in the stratum corneum and stratum lucidum does not extend to.Fungus takes nutrients from the breakdown of fats. It is tolerant to salt and a low pH environment. Cause changes to skin pigmentation patches colored black by the accumulation of substance melaninlike in fungi. Ringworm tends to occur in areas with a higher concentration of eccrine glands. Hyperhidrosis seems to be a risk factor.
Signs and symptoms
Tinea nigra is most common in pediatric and adolescent populations, yet people of all ages can be infected. Generally patients are asymptomatic tinea nigra. Rarely pruritus can be reported. The absence of any discomfort the patient's decision to postpone doctor.
Physical examination.Tinea nigra is characterized by the presence of a brown-black macules painless. The macula appears as a black dot initially insidious. Macular hyperpigmentation varies from brown to black up similar to silver nitrate. Edges are typically discrete. Pigmentary changes appear smooth. Typical lesion is solitary, although multiple lesions may be present. Solitary lesions are located on the surfaces and planting palm, but can extend to the fingers. Areas like the neck or chest are rarely affected.Shape ovoid lesion varies and can be round or irregular. The lesion grows slowly in a few weeks or months. Size varies from a few millimeters to inches in diameter, depending on the duration of infection. Other natural elements such as redness or mercy are absent. Rarely is this peeling.
Diagnosis
Laboratory studies:Microscopic examination of scales peilii-treated with potassium hydroxide showed septated hyphae, branched cxare containing black pigment in the wallsIncreases intro-week culture.Histological examination of biopsy specimens showed mild hyperkeratosis and acanthosis. One can describe a lymphoma perivascular infiltrates in the papillary layer of dermis and subpapilar.The differential diagnosis is made with the following diseases: Addison's disease, dysplastic nevus, malignant melanoma, nevi melanocitici, syphilis, candida, pint, chemical contamination.
Treatment
Topical antifungal preparations are used to eradicate the infection. Dermatological agents are used to treat tinea nigra due to their action on the skin. They can help remove excess keratin in hyperkeratotic skin disorders or modify the cellular turnover. Or fungicides are used alongside medical fungistaticele.
Salicylic acid peeling of the stratum corneum determined by dissolving the intercellular cementum without affecting the structure of viable dermis. Tretinoin topical drops coalescence of follicular epithelial cells and stimulate their mitotic activity with a rapid turnover of epithelial cells.
Imidazolii topical antifungal spectrum are typically used for tinea pedis and tinea but are useful nigra. Examples: Clotrimazole, ketoconazole, miconazole. Piridonele are topical agents with broad spectrum activity anticandidozica, antidermatofitica and antibacterial. Examples: Ciclopirox. Topical Alilaminele epoxidaza inhibit a key enzyme in the biosynthesis of squalene sterol in fungi fungus causes death. Examples: terbinafine. Fungistatic agents not only kill fungi prevent their replication. Examples: undeclenic acid.
Schnitzler Syndrome
Schnitzler SyndromeSchnitzler syndrome is characterized by chronic urticaria, nonpruriginoasa in association with recurrent fever, bone pain, arthralgia and arthritis and gammopatie monoclonal immunoglobulin M with a concentration below 10 g / l. Most patients with Schnitzler's syndrome have a chronic benign evolution. Spontaneous remission has not been reported. About 10-15% of patients develop a lymphoproliferative disease, including limfoplasmocitic lymphoma, Waldenstrom macroglobulinemia or myeloma IgM.
All patients with chronic urticaria shows this syndrome, the appellant. Pruritus is absent, but may become slightly itchy lesions over time. There were no identified risk factors. Pathogenesis of the syndrome is not yet well defined.Nonsteroidal anti-inflammatory corticosteroids and immunosuppressants shows a degree of improvement in rash and arthralgia. Skin manifestations respond poorly to antihistamines. They used numerous medications to treat this syndrome but not effective.
Pathogenesis and causes
Exact pathogenesis of Schnitzler syndrome is unclear. It is believed that IgM paraproteinemic storage leads to the formation of immune complexes and complement activation cascade, responsible for skin manifestations. Another proposed theory is uncontrolled activation of interleukin 1.
Signs and symptoms
Schnitzler syndrome patients are aged between 13-71 years at diagnosis. All patients have chronic urticarial rash, appellant. Itching is not common but lesions are poorly pruritigene debut after 2-3 years at 45% of patients. Rash is usually the first symptom that appears affected mostly the trunk and extremities, and avoiding the palms and soles, neck and head.Approximately 90% of patients complain fever recurrence. Each febrile episode usually resolves in a few hours, however, fever may persist for up to 24-48 hours. The episodes can occur daily or infrequently, twice a year. 80% of patients experience pain, bone pain and myalgia 70%. Bone pain affects especially the hip bone and the tibia. Femur, spine, arms and collar bone are rarely involved. Fatigue and weight loss occur in some patients.
Physical examination.Urticarial rash consisting of papules and pink plates, slightly elevated, 0. 5-3 cm in diameter. Injuries occur every day in November. They persist for 12-24 hours and resolve without sequelae. Angioedema is possible but very rare. Lymphadenopathy can be found in 50% of patients, hepatomegaly and splenomegaly 30% to 10%.
There is a set of criteria to classify patients in Schnitzler syndrome:-Recurrent fever, arthralgia or arthritis, bone pain-Lymphadenopathy, hepatosplenomegaly, leukocytosisHigh-ESR, abnormal bone.
Diagnosis
Laboratory studies:-All cases are associated with serum gammopatie to imunoforezaESR and C-reactive protein-high, Leukocytosis, thrombocytosis, anemia-Abnormal lymphoid proliferation in the bone marrow.
Histological examination. Examination of skin samples showed perivascular infiltrates of neutrophils, neutrophilic, lymphocytic inflammation, lymph vessels are intact and slightly superficial dermis shows edema. Note deposit of IgM and complement in the upper dermis and at the junction dermoepidermica.The differential diagnosis is made with the following diseases: lupus erythematosus, acute urticarial vasculitis, chronic idiopathic urticaria, cryoglobulinemia, pressure urticaria.
Treatment
NSAIDs, corticosteroids and immunosuppressive shows an improvement of arthralgia and bone pain but not the eruption. Cutaneous and extracutaneous manifestations respond poorly to H1 and H2 antihistamines. Some patients responded to treatment with thalidomide, rituximab, cloroquina, chlorambucil, cyclophosphamide, azathioprine, plasmapheresis, intravenous immunoglobulin. Phototherapy with psoralen and ultraviolet A small eruption in some patients.It is also used pefloxacin mesylate and anakinra, a recombinant form of natural IL-1 receptor.
PrognosisSchnitzler syndrome require long-term assessment because of the potential of developing lymphoproliferative disease, particularly Waldenstrom macroglobulinemia. No recorded complete spontaneous remission. The prognosis is still good. 10-15% of patients will develop cancer limfoplasmocitar.
All patients with chronic urticaria shows this syndrome, the appellant. Pruritus is absent, but may become slightly itchy lesions over time. There were no identified risk factors. Pathogenesis of the syndrome is not yet well defined.Nonsteroidal anti-inflammatory corticosteroids and immunosuppressants shows a degree of improvement in rash and arthralgia. Skin manifestations respond poorly to antihistamines. They used numerous medications to treat this syndrome but not effective.
Pathogenesis and causes
Exact pathogenesis of Schnitzler syndrome is unclear. It is believed that IgM paraproteinemic storage leads to the formation of immune complexes and complement activation cascade, responsible for skin manifestations. Another proposed theory is uncontrolled activation of interleukin 1.
Signs and symptoms
Schnitzler syndrome patients are aged between 13-71 years at diagnosis. All patients have chronic urticarial rash, appellant. Itching is not common but lesions are poorly pruritigene debut after 2-3 years at 45% of patients. Rash is usually the first symptom that appears affected mostly the trunk and extremities, and avoiding the palms and soles, neck and head.Approximately 90% of patients complain fever recurrence. Each febrile episode usually resolves in a few hours, however, fever may persist for up to 24-48 hours. The episodes can occur daily or infrequently, twice a year. 80% of patients experience pain, bone pain and myalgia 70%. Bone pain affects especially the hip bone and the tibia. Femur, spine, arms and collar bone are rarely involved. Fatigue and weight loss occur in some patients.
Physical examination.Urticarial rash consisting of papules and pink plates, slightly elevated, 0. 5-3 cm in diameter. Injuries occur every day in November. They persist for 12-24 hours and resolve without sequelae. Angioedema is possible but very rare. Lymphadenopathy can be found in 50% of patients, hepatomegaly and splenomegaly 30% to 10%.
There is a set of criteria to classify patients in Schnitzler syndrome:-Recurrent fever, arthralgia or arthritis, bone pain-Lymphadenopathy, hepatosplenomegaly, leukocytosisHigh-ESR, abnormal bone.
Diagnosis
Laboratory studies:-All cases are associated with serum gammopatie to imunoforezaESR and C-reactive protein-high, Leukocytosis, thrombocytosis, anemia-Abnormal lymphoid proliferation in the bone marrow.
Histological examination. Examination of skin samples showed perivascular infiltrates of neutrophils, neutrophilic, lymphocytic inflammation, lymph vessels are intact and slightly superficial dermis shows edema. Note deposit of IgM and complement in the upper dermis and at the junction dermoepidermica.The differential diagnosis is made with the following diseases: lupus erythematosus, acute urticarial vasculitis, chronic idiopathic urticaria, cryoglobulinemia, pressure urticaria.
Treatment
NSAIDs, corticosteroids and immunosuppressive shows an improvement of arthralgia and bone pain but not the eruption. Cutaneous and extracutaneous manifestations respond poorly to H1 and H2 antihistamines. Some patients responded to treatment with thalidomide, rituximab, cloroquina, chlorambucil, cyclophosphamide, azathioprine, plasmapheresis, intravenous immunoglobulin. Phototherapy with psoralen and ultraviolet A small eruption in some patients.It is also used pefloxacin mesylate and anakinra, a recombinant form of natural IL-1 receptor.
PrognosisSchnitzler syndrome require long-term assessment because of the potential of developing lymphoproliferative disease, particularly Waldenstrom macroglobulinemia. No recorded complete spontaneous remission. The prognosis is still good. 10-15% of patients will develop cancer limfoplasmocitar.
Scabies
Scabies
* Introduction
* Who makes scabies
* How to transmit disease
* How to manifest disease
* What is the treatment of scabies
In practice scabies, and scabies popular name, is a disease that is seen quite often, affecting people of any age, sex, race, religion, social status and intellectual level.
In Romania, due to problems of large masses of population in the interwar period and especially during the first years after the Second World War, the period associated with material deprivation, low level of hygiene, but also by consulting the doctor, he stuck the idea that Scabies is a disease caused only misery and lack of personal hygiene. As a result, currently, many patients with this disease, especially among those with higher social status, refuse to accept that they might be suffering from scabies, following various treatments antiallergic addressing homeopathy, herbal or "healers", all kinds of therapies will more or less aggressive, getting to transform a relatively trivial illness, a disease "incurable. "
* Introduction
* Who makes scabies
* How to transmit disease
* How to manifest disease
* What is the treatment of scabies
In practice scabies, and scabies popular name, is a disease that is seen quite often, affecting people of any age, sex, race, religion, social status and intellectual level.
In Romania, due to problems of large masses of population in the interwar period and especially during the first years after the Second World War, the period associated with material deprivation, low level of hygiene, but also by consulting the doctor, he stuck the idea that Scabies is a disease caused only misery and lack of personal hygiene. As a result, currently, many patients with this disease, especially among those with higher social status, refuse to accept that they might be suffering from scabies, following various treatments antiallergic addressing homeopathy, herbal or "healers", all kinds of therapies will more or less aggressive, getting to transform a relatively trivial illness, a disease "incurable. "
Rinosclerom
RinoscleromRinoscleromul is a chronic granulomatous condition of the nose and other upper respiratory tract structures. Rinoscleromul is the result of infection with the bacterium Klebsiella rhinoscleromatis. Family incidence suggests genetic control of host response to bacteria. Nasal infection caused deformation, rhinorrhea, epistaxis, nasal obstruction. It affects the nasal cavities, pharynx, and bronchi trahea.
Treatment includes long-term antibiotics and surgery in patients with symptoms of obstruction. Given the high recurrence rate of disease requires a prolonged antibiotic therapy with follow-up bronchoscopy. Evolution is usually chronic recurrent.
Pathogenesis and causes
Rinoscleromul is contracted through inhalation of infectious droplets directly. The disease begins as epithelial transition zones nasal vestibule, the area of subglotica the larynx or nasopharynx and oropharynx. Cellular immunity is impaired in patients with rinosclerom, the humoral being maintained.Rinoscleromul usually affects the nasal cavity, but associated injuries can affect the larynx, nasofaringele, oral cavity, paranasal sinururile or soft tissues of the lips, nose, trachea and bronchi. Although it is mainly caused by Klebsiella rhinoscleromatis or isolated forms of K. ozaenae.
Signs and symptoms
Rinoscleromul is a rare chronic granulomatous infection that must be considered in perosanele with nasal polyps adhering to avoid sinus nasal septum. The most common presentation is not specific. Because of similar clinical picture of chronic rhinitis is often not recognized. The clinical picture includes the following allegations:-Nasal obstruction, rhinorrhea, epistaxis-Dysphagia, nasal deformity, anosmiaDifficulty breathing, which progresses to stridorAnesthesia-soft palate, hoarseness.
Physical Exam
The disease affects mainly the nasal cavities, but can also affect nasofaringele, oropharynx, larynx, trachea and bronchi. Oral cavity, paranasal sinuses, soft tissues of the nose, lips may also be affected. In rare cases rinoscleromul extend to the orbit. The presentation is often nonspecific.
Rinoscleromul is divided into three stages:Catarhal, or atrophic: the first stage begins with an intro that evolves nonspecific rhinitis fetid purulent rhinorrhea and crustificare. This stage can last for weeks or months.Granulomatous, or hypertrophic: nasal mucosa starts to become red and granular with the formation of polyps in the nose or muriforme formations. Appears once with the enlargement of nasal epistaxis, nasal cartilage deformation and destruction. Destruction can cause anosmia, anesthesia of the soft palate, uvula enlargement, hoarseness and varying degrees of airway obstruction. Lesions appear as atrophic changes and granulomatous, fibrotic stage of healing. Front-bottom of the antrum and medial wall are more often affected than other structures. Involvement of the maxillary antrum is suggested in sclerom and entrepre jaw can act as reservoir of infection.Soft palate is thickened at the junction with the hard palate. The sign may help early diagnosis of the condition. Physical examination showed granulomatous or nodular erythematous swelling covered with scabs. Similar appearance of tumors and are suggestive of local extension of cancer. Can be located intro pseudo Rinoscleromul variety of areas, including septum and rinofaringele.Sclerotic: characterized by sclerosis and fibrosis. In stage sclerotic nodules are replaced by fibrous tissue, leading to extensive scarring and stenosis.
Diagnosis
Studies:Klebsiella-culture is positive for only 50% of patients-Bacteria can be identified by Gram stain, Schiff, Giemsa and silverCT-assessment with and without contrast showed homogeneous lesions without involvement of adjacent fascial plans, forcing irregular concentric airway collapse, the trachea, similar lesions are characteristic of crypts, with calcifications, nodule, luminal narrowing and wall thickeningCytology analysis is performed by brushing the lesion are characteristic Mikulicz cellsShow signs of nasal endoscopy-three stadium-Bronchoscopy.
Histological examination. Features include rinoscleromului vacuolated Mikulicz cells and transformed plasma cells with Russell corpora. Mikulicz cell is a large macrophage with clear cytoplasm containing the bacilli. The disease is diagnosed mainly in proliferative phase clinical tablooul chic when it is easily recognized histologically.The differential diagnosis is made with the following conditions: actinomicoza, basal cell carcinoma, leishmaniasis, leprosy, nasopalatin duct cyst, sarcoidosis, sporotrichoza, syphilis, warts carcinoma, Wegener's granulomatosis.
Treatment
Medical therapy.Will receive long-term antibiotics. The infection responds to treatment with third generation cephalosporins and clindamycin. Sclerotic lesions respond well to therapy with ciprofloxacin.
Surgical therapy.Surgery combined with antibiotic therapy is beneficial in patients with granulomatous disease and nasal obstruction or throat or sinus disease through proliferation of lesions. Tracheotomy should be considered in patients with laryngeal obstruction in stage two and three of the disease. Plastic surgery is necessary in patients with scar stenosis or when the nasal cavity, pharynx, larynx or trachea remain imperforate. Extensive granulomatous lesions are treated by open excision.Surgery and laser therapy are required to treat airway compromise and tissue deformation. Advanced Scar Treatment with carbon dioxide laser shows excellent results. The advantages of this technique include: general operating field, complete relaxation of the patient, good gas exchange, eliminating the risk of aspiration and opportunity debriurilor blood and oxygen administration.
Treatment includes long-term antibiotics and surgery in patients with symptoms of obstruction. Given the high recurrence rate of disease requires a prolonged antibiotic therapy with follow-up bronchoscopy. Evolution is usually chronic recurrent.
Pathogenesis and causes
Rinoscleromul is contracted through inhalation of infectious droplets directly. The disease begins as epithelial transition zones nasal vestibule, the area of subglotica the larynx or nasopharynx and oropharynx. Cellular immunity is impaired in patients with rinosclerom, the humoral being maintained.Rinoscleromul usually affects the nasal cavity, but associated injuries can affect the larynx, nasofaringele, oral cavity, paranasal sinururile or soft tissues of the lips, nose, trachea and bronchi. Although it is mainly caused by Klebsiella rhinoscleromatis or isolated forms of K. ozaenae.
Signs and symptoms
Rinoscleromul is a rare chronic granulomatous infection that must be considered in perosanele with nasal polyps adhering to avoid sinus nasal septum. The most common presentation is not specific. Because of similar clinical picture of chronic rhinitis is often not recognized. The clinical picture includes the following allegations:-Nasal obstruction, rhinorrhea, epistaxis-Dysphagia, nasal deformity, anosmiaDifficulty breathing, which progresses to stridorAnesthesia-soft palate, hoarseness.
Physical Exam
The disease affects mainly the nasal cavities, but can also affect nasofaringele, oropharynx, larynx, trachea and bronchi. Oral cavity, paranasal sinuses, soft tissues of the nose, lips may also be affected. In rare cases rinoscleromul extend to the orbit. The presentation is often nonspecific.
Rinoscleromul is divided into three stages:Catarhal, or atrophic: the first stage begins with an intro that evolves nonspecific rhinitis fetid purulent rhinorrhea and crustificare. This stage can last for weeks or months.Granulomatous, or hypertrophic: nasal mucosa starts to become red and granular with the formation of polyps in the nose or muriforme formations. Appears once with the enlargement of nasal epistaxis, nasal cartilage deformation and destruction. Destruction can cause anosmia, anesthesia of the soft palate, uvula enlargement, hoarseness and varying degrees of airway obstruction. Lesions appear as atrophic changes and granulomatous, fibrotic stage of healing. Front-bottom of the antrum and medial wall are more often affected than other structures. Involvement of the maxillary antrum is suggested in sclerom and entrepre jaw can act as reservoir of infection.Soft palate is thickened at the junction with the hard palate. The sign may help early diagnosis of the condition. Physical examination showed granulomatous or nodular erythematous swelling covered with scabs. Similar appearance of tumors and are suggestive of local extension of cancer. Can be located intro pseudo Rinoscleromul variety of areas, including septum and rinofaringele.Sclerotic: characterized by sclerosis and fibrosis. In stage sclerotic nodules are replaced by fibrous tissue, leading to extensive scarring and stenosis.
Diagnosis
Studies:Klebsiella-culture is positive for only 50% of patients-Bacteria can be identified by Gram stain, Schiff, Giemsa and silverCT-assessment with and without contrast showed homogeneous lesions without involvement of adjacent fascial plans, forcing irregular concentric airway collapse, the trachea, similar lesions are characteristic of crypts, with calcifications, nodule, luminal narrowing and wall thickeningCytology analysis is performed by brushing the lesion are characteristic Mikulicz cellsShow signs of nasal endoscopy-three stadium-Bronchoscopy.
Histological examination. Features include rinoscleromului vacuolated Mikulicz cells and transformed plasma cells with Russell corpora. Mikulicz cell is a large macrophage with clear cytoplasm containing the bacilli. The disease is diagnosed mainly in proliferative phase clinical tablooul chic when it is easily recognized histologically.The differential diagnosis is made with the following conditions: actinomicoza, basal cell carcinoma, leishmaniasis, leprosy, nasopalatin duct cyst, sarcoidosis, sporotrichoza, syphilis, warts carcinoma, Wegener's granulomatosis.
Treatment
Medical therapy.Will receive long-term antibiotics. The infection responds to treatment with third generation cephalosporins and clindamycin. Sclerotic lesions respond well to therapy with ciprofloxacin.
Surgical therapy.Surgery combined with antibiotic therapy is beneficial in patients with granulomatous disease and nasal obstruction or throat or sinus disease through proliferation of lesions. Tracheotomy should be considered in patients with laryngeal obstruction in stage two and three of the disease. Plastic surgery is necessary in patients with scar stenosis or when the nasal cavity, pharynx, larynx or trachea remain imperforate. Extensive granulomatous lesions are treated by open excision.Surgery and laser therapy are required to treat airway compromise and tissue deformation. Advanced Scar Treatment with carbon dioxide laser shows excellent results. The advantages of this technique include: general operating field, complete relaxation of the patient, good gas exchange, eliminating the risk of aspiration and opportunity debriurilor blood and oxygen administration.
Porphyrias
Porphyrias are metabolic disorders of heme synthesis. Partial enzyme deficiencies result in excessive accumulation and excretion of 5-aminolevulinic acid, porphyrins and porfobilinogenului. Porphyria cutanea tarda porphyria is most commonly found in Europe and North America. Bullous photosensitivity Pseudoporfiria describe a physically and clinically mimicking porphyria cutanea tarda.
Porphyria cutanea tarda is caused by deficiency of an enzyme of heme biosynthesis. Porphyrins accumulate in the liver, are transported in plasma and excreted in urine. Sun exposure of these patients to determine the fragility of skin, blisters, bubbles, hypertrichosis, hypopigmentation, scleroderma changes, dystrophic calcifications, milia and scarring. In porphyrins pseudoporfirie no abnormalities. The skin lesions can not be distinguished from those of porphyria cutanea tarda. Pseudoporfiria has been reported in hemodialysis patients with excessive exposure to ultraviolet A.
Pseudoporfiriei are numerous causes including exposure to ultraviolet A, hemodialysis, some drugs, vitiligo. The main treatment is discontinuation of medication pseudoporfiriei if this is possible. Clinical resolution may require several months, especially in drug-induced form. The prognosis is good once you removed pseudoporfirie triggering agent.
Pathogenesis
Pathologie pseudoporfiriei precise mechanism is unknown. It impugned the role of visible light or ultraviolet A drug-induced fit. It turns out that fotosensibilizatorii are deposited along the endothelium of blood vessels in affected skin. Triggered an immune response against antigens is believed to develop after exposure to light of the dermis. It is considered that damages the endothelium by elberarea fotosensibilizantii exogenous protease after exposure to the sun. Then immunoglobulin G binds to altered endothelium result in the formation of bubbles in the lamina lucid.Pseudoporfiriei pathogenesis caused by hemodialysis is considered to be due to aluminum hydroxide. This solution is found in hemodialysis and cause similar diseases porphyrias after long term administration.
Causes and Risk FactorsPseudoporfiriile can be produced by various drugs, excessive sun exposure and hemodialysis.
Medicines that may cause pseudoporfirie include:-Naproxen, ketoprofen, nabumetone, oxaprozin, mefenamic acid, rofecoxibNalidixic acid, tetracycline, ampicillin-sulbactam, cefepime, ciprofloxacin-Voriconazole, furosemic, butamida, triamterene, hydrochlorothiazide, torsemida, bumetamida-Amiodarone, 5-fluorouracil, imatinib, cyclosporine, dapsone, pyridoxine-Etretinat, isotretinoin, aspirin, flutamide, cola, ultraviolet A, oral contraceptivesUV-B phototherapy, hemodialysis, vitiligo.
Signs and symptoms
A careful history is important to detect cases of exogenous pseudoporfiriei. Pseudoporfiria clinically characterized by increased fragility of skin, redness and appearance of bubbles in the blood and erosions on sun-exposed skin, identical to those seen in patients with porphyria cutanea tarda. Hypertrichosis, hyperpigmentation and scleroderma changes found in porphyria cutanea tarda are not observed in pseudoporfirie.Pseudoporfiria which is clinically similar to erythropoietic protoporfiria is described only in children who have juvenile rheumatoid arthritis naproxen.
Diagnosis
Laboratory studies:-The most important test is to evaluate serum porphyrin, which is negative if the patient has no real porphyriaOther causes of photosensitivity, which must be excluded by obtaining connective tissue disease antinuclear antibody, antiRo, ribonucleoproteina Smith, antiADN.The differential diagnosis is made with the following disorders: bullous pemphigoid, epidermolysis bullosa, protoporfiria erythropoietic, lupus erythematosus, porphyria cutanea tarda.
Treatment
In drug-induced pseudoporfiriei it to the interruption of drug therapy trigger. Resolution of signs require a few months.
Porphyria cutanea tarda is caused by deficiency of an enzyme of heme biosynthesis. Porphyrins accumulate in the liver, are transported in plasma and excreted in urine. Sun exposure of these patients to determine the fragility of skin, blisters, bubbles, hypertrichosis, hypopigmentation, scleroderma changes, dystrophic calcifications, milia and scarring. In porphyrins pseudoporfirie no abnormalities. The skin lesions can not be distinguished from those of porphyria cutanea tarda. Pseudoporfiria has been reported in hemodialysis patients with excessive exposure to ultraviolet A.
Pseudoporfiriei are numerous causes including exposure to ultraviolet A, hemodialysis, some drugs, vitiligo. The main treatment is discontinuation of medication pseudoporfiriei if this is possible. Clinical resolution may require several months, especially in drug-induced form. The prognosis is good once you removed pseudoporfirie triggering agent.
Pathogenesis
Pathologie pseudoporfiriei precise mechanism is unknown. It impugned the role of visible light or ultraviolet A drug-induced fit. It turns out that fotosensibilizatorii are deposited along the endothelium of blood vessels in affected skin. Triggered an immune response against antigens is believed to develop after exposure to light of the dermis. It is considered that damages the endothelium by elberarea fotosensibilizantii exogenous protease after exposure to the sun. Then immunoglobulin G binds to altered endothelium result in the formation of bubbles in the lamina lucid.Pseudoporfiriei pathogenesis caused by hemodialysis is considered to be due to aluminum hydroxide. This solution is found in hemodialysis and cause similar diseases porphyrias after long term administration.
Causes and Risk FactorsPseudoporfiriile can be produced by various drugs, excessive sun exposure and hemodialysis.
Medicines that may cause pseudoporfirie include:-Naproxen, ketoprofen, nabumetone, oxaprozin, mefenamic acid, rofecoxibNalidixic acid, tetracycline, ampicillin-sulbactam, cefepime, ciprofloxacin-Voriconazole, furosemic, butamida, triamterene, hydrochlorothiazide, torsemida, bumetamida-Amiodarone, 5-fluorouracil, imatinib, cyclosporine, dapsone, pyridoxine-Etretinat, isotretinoin, aspirin, flutamide, cola, ultraviolet A, oral contraceptivesUV-B phototherapy, hemodialysis, vitiligo.
Signs and symptoms
A careful history is important to detect cases of exogenous pseudoporfiriei. Pseudoporfiria clinically characterized by increased fragility of skin, redness and appearance of bubbles in the blood and erosions on sun-exposed skin, identical to those seen in patients with porphyria cutanea tarda. Hypertrichosis, hyperpigmentation and scleroderma changes found in porphyria cutanea tarda are not observed in pseudoporfirie.Pseudoporfiria which is clinically similar to erythropoietic protoporfiria is described only in children who have juvenile rheumatoid arthritis naproxen.
Diagnosis
Laboratory studies:-The most important test is to evaluate serum porphyrin, which is negative if the patient has no real porphyriaOther causes of photosensitivity, which must be excluded by obtaining connective tissue disease antinuclear antibody, antiRo, ribonucleoproteina Smith, antiADN.The differential diagnosis is made with the following disorders: bullous pemphigoid, epidermolysis bullosa, protoporfiria erythropoietic, lupus erythematosus, porphyria cutanea tarda.
Treatment
In drug-induced pseudoporfiriei it to the interruption of drug therapy trigger. Resolution of signs require a few months.
Porom
PoromPoromul is a benign neoplasm composed of annexes that shows differentiation of tubular epithelial cells. Malignant variant is called porocarcinom poromului. Apocrine Poromul is more common than the eccrine. Poromul acrospiromului spectrum belongs, with nodular hidradenoamele, hidradenoamele clear cells, and dermal duct tumors Simplex hidroacantomul.Poromul manifests as a solitary nodule or papule. Most lesions are asymptomatic, but may be accompanied by minor pain. Rarely the patient develops multiple poroame simultaneously, a phenomenon known as poromatoza. Poroamele multiple negative can become a cosmetic issue.
Poromul not require medical treatment, they are treated by surgical excision. There are no complications associated with poromul. The prognosis is favorable because the lesions have clinical significance. Even poromatoza not associated with other anomalies. The risk of malignant transformation of a porom is minimal and is considered to be similar to that of normal skin.
Pathogenesis and causes
Poromul is a benign neoplasm that shows differentiation poroida. Malignant variant is porocarcinomul. Poroamele appear only on the skin and does not affect other tissues.
Signs and symptoms
Poromul can occur at any age but is typical of adult age. Are asymptomatic and manifest as stable or nodule with some slow growth. Some are associated with pain. Poroamele are some of the many types of benign neoplasms may occur secondary annexes printrun nevus sebaceous. They look like colored papules or nodules under the skin 2 cm. Occasionally may be pigmented. Lesions may protrusion erosion or ulceration.
Diagnosis
Blood examinations are not needed for this lesion. Poromului diagnosis can not be placed solely on history and clinical examination. Diagnosis is established by histopathology.Histological examination. Most poroame tend to be small, consisting of di cuboid epithelial cells. Neoplastic cells have eosinophilic cytoplasm. Areas of ductal differentiation occurs as a tube lined by a thick cuticle and sometimes eosinophilic cytoplasmic vacuoles. Rarely shows focal necrosis and a well-vascularized stroma-combination that thinks malignant.The differential diagnosis is made with urmataorele aefctiuni: seborrheic keratosis, squamous cell carcinoma, trichilemoma, hidradenom, acrospirom, hidradenom poroid.
Treatment
Poromul not require medical treatment, but surgical excision. Poromului prognosis is favorable because the lesions shows no known clinical significance. Multiple-poroamele Poromatoza not associated with other anomalies. The risk of malignant transformation is minimal.
Poromul not require medical treatment, they are treated by surgical excision. There are no complications associated with poromul. The prognosis is favorable because the lesions have clinical significance. Even poromatoza not associated with other anomalies. The risk of malignant transformation of a porom is minimal and is considered to be similar to that of normal skin.
Pathogenesis and causes
Poromul is a benign neoplasm that shows differentiation poroida. Malignant variant is porocarcinomul. Poroamele appear only on the skin and does not affect other tissues.
Signs and symptoms
Poromul can occur at any age but is typical of adult age. Are asymptomatic and manifest as stable or nodule with some slow growth. Some are associated with pain. Poroamele are some of the many types of benign neoplasms may occur secondary annexes printrun nevus sebaceous. They look like colored papules or nodules under the skin 2 cm. Occasionally may be pigmented. Lesions may protrusion erosion or ulceration.
Diagnosis
Blood examinations are not needed for this lesion. Poromului diagnosis can not be placed solely on history and clinical examination. Diagnosis is established by histopathology.Histological examination. Most poroame tend to be small, consisting of di cuboid epithelial cells. Neoplastic cells have eosinophilic cytoplasm. Areas of ductal differentiation occurs as a tube lined by a thick cuticle and sometimes eosinophilic cytoplasmic vacuoles. Rarely shows focal necrosis and a well-vascularized stroma-combination that thinks malignant.The differential diagnosis is made with urmataorele aefctiuni: seborrheic keratosis, squamous cell carcinoma, trichilemoma, hidradenom, acrospirom, hidradenom poroid.
Treatment
Poromul not require medical treatment, but surgical excision. Poromului prognosis is favorable because the lesions shows no known clinical significance. Multiple-poroamele Poromatoza not associated with other anomalies. The risk of malignant transformation is minimal.
Porphyria cutanea tarda
Porphyria cutanea tardaPorphyria cutanea tarda is a term that spans a group of diseases in which heme synthesis enzyme activity is uroporfinogena decarboxylase deficiency. Porphyria cutanea tarda include enzyme gene mutations in hereditary and earned may occur in genetically predisposed people after exposure to hepatotoxine or in the context of liver tumors.Clinical expression of hereditary porphyrias earned and usually follows exposure to agents or conditions that affect hepatocytes and lead to hepatosideroza. These agents include ethanol, estrogen, hepatitis and HIV, along with hemochromatosis genes.
Excess iron triggers the formation of toxic oxygen species and oxidative stress increases facilitating porfirinogeneza. Reduction of the heme synthesis enzyme activity to 25% of normal clinical signs cause. Exposure to hydrocarbon compounds, polyhalogenated aromatic compounds in the environment cause disease in many people-toxic porphyrin epidemic porphyria. Liver tumors that produce excess porphyrins are rare cases of porphyria cutanea tarda.
Clinical appears veziculizare and petechiae on the arms, hands and face. As observed hypertrichosis, urine discoloration, pigmentation type facial melasma, alopecia scleredemului scar and related lesions. Avoiding the sun is the primary prevention of photosensitivity. Alcohol should be avoided, estrogen. The practice of therapeutic phlebotomy to reduce iron stores.
Pathogenesis
When missing liver enzyme activity porphyrin synthesis this pathway of synthesis byproducts accumulate in the liver, plasma and other organs. Porphyrins with many carboxyl groups are water soluble and excreted by the kidneys. 8 groups of carboxyl porphyrins are called uroporfirine, those four groups isocoproporfirine coproporfirine and excreted mostly in feces. Photoactive porphyrins are molecules that abseorb energy from visible light spectrum violet. Leather so excited porphyrins mediate oxidative determine the sign of skin lesions.
Fotocutanata most common manifestation of porphyria cutanea tarda is due to increased mechanical fragility of blood vessels in the dermis, the occurrence of erosions, ulcers and painful blisters after sun exposure. They heal with depigmentation and scarring. Other common features of late cutaneous porphyria include hypertrichosis, scleroderma similar boards that may develop dystrophic calcifications and similar colored urine excretion of wine or tea.
Causes and Risk Factors
Common cause of late cutaneous porphyria is to reduce the enzymatic activity of heme cycle. Many risk factors acting simultaneously or separately to inhibit this enzyme. Hepatic viral infections are often associated with porphyria cutanea tarda. Hepatitis C cause 50% risk of developing this disease. The association with HIV virus is also incriminated. There is also a close relationship between porphyria and hemochromatosis genes.
Excess iron triggers the formation of toxic oxygen species and oxidative stress increases facilitating porfirinogeneza. Reduction of the heme synthesis enzyme activity to 25% of normal clinical signs cause. Exposure to hydrocarbon compounds, polyhalogenated aromatic compounds in the environment cause disease in many people-toxic porphyrin epidemic porphyria. Liver tumors that produce excess porphyrins are rare cases of porphyria cutanea tarda.
Clinical appears veziculizare and petechiae on the arms, hands and face. As observed hypertrichosis, urine discoloration, pigmentation type facial melasma, alopecia scleredemului scar and related lesions. Avoiding the sun is the primary prevention of photosensitivity. Alcohol should be avoided, estrogen. The practice of therapeutic phlebotomy to reduce iron stores.
Pathogenesis
When missing liver enzyme activity porphyrin synthesis this pathway of synthesis byproducts accumulate in the liver, plasma and other organs. Porphyrins with many carboxyl groups are water soluble and excreted by the kidneys. 8 groups of carboxyl porphyrins are called uroporfirine, those four groups isocoproporfirine coproporfirine and excreted mostly in feces. Photoactive porphyrins are molecules that abseorb energy from visible light spectrum violet. Leather so excited porphyrins mediate oxidative determine the sign of skin lesions.
Fotocutanata most common manifestation of porphyria cutanea tarda is due to increased mechanical fragility of blood vessels in the dermis, the occurrence of erosions, ulcers and painful blisters after sun exposure. They heal with depigmentation and scarring. Other common features of late cutaneous porphyria include hypertrichosis, scleroderma similar boards that may develop dystrophic calcifications and similar colored urine excretion of wine or tea.
Causes and Risk Factors
Common cause of late cutaneous porphyria is to reduce the enzymatic activity of heme cycle. Many risk factors acting simultaneously or separately to inhibit this enzyme. Hepatic viral infections are often associated with porphyria cutanea tarda. Hepatitis C cause 50% risk of developing this disease. The association with HIV virus is also incriminated. There is also a close relationship between porphyria and hemochromatosis genes.
Pityriasis rosea
Pityriasis roseaMeans fine pink pink pityriasis scaling. It is a common skin disease seen in healthy individuals, most often in children and young adults. It manifests as an acute eruption papuloscuamoasa duration from 6-8 weeks. May show some variants and the diagnosis is important because it can signify or secondary syphilis. The disease is most common in spring and autumn in temperate zones. It is favored by warm, dry season.The disease typically begins through a solitary macule that trigger the eruption. Pink initial lesion increases in a few days to devein a spot with fine scales within well-demarcated edges. In a few weeks is a generalized exanthem. Itching is common.
The rash resolves spontaneously. Improvement of pruritus by topical steroids, oral anrihistaminice, lotions and bath oils local menthol menthol is indicated. In cases resistant to ultraviolet B phototherapy is beneficial dynamics. Low dose acyclovir reduces the duration of the eruption.Pityriasis generally resolves in 12 weeks pink. Most cases do not return, but some patients may relapse. Pink pityriasis persistent over three months is correctly classified as chronic pityriasis lichenoides. The prognosis is excellent. Patients are not considered contagious.
Pathogenesis and causes of pityriasis roseaPityriasis pink was considered to be a viral exanthem. Clinical presentation supports this concept. He was associated with upper respiratory tract infections, may run in families and close contact and have an increased incidence in immunocompromised individuals. The incidence increases in spring, and the disease seems to cause life-long immunity. Despite viral etiological considerations have not discovered any virus.
Signs and symptomsPityriasis pink is more common in women than in men. It develops mainly in children and young adults, although any age group can be affected. Most patients are between 10-35 years. The condition begins to trigger the eruption through a solitary macule. Initial lesion grows in a few days and becomes a pink stain with fine scales well demarcated in the periphery. Over the next two weeks is a generalized exanthem, although it can occur in a few hours or months. This secondary phase consists of bilateral and symmetrical appearance of patches with scales long axis oriented along the lines of cleavage. This phase tends to resolve within 6 weeks. Itching is common, easy-moderate.
Physical ExamTrigger spot is one of 2-10cm in diameter, located on the neck or trunk with fine scales. It is seen in over 50% of patients and can occur as multiple lesions with atypical localization. Secondary lesions appear on the abdomen, trunk, upper back and proximal limbs. They are described as having an appearance of cigarette paper, with the long axis oriented parallel along the lines of cleavage giving a classic Christmas tree look.
Atypical pityriasis occurs in 20% of patients. These variations can be separated into lesions or changes in their distribution. Photosensitivity may occur. Lesions may be localized to one area. One can see an inverse pityriasis. This form of damage appears on the face and distal extremities and is more common in children. Pata trigger may be the only manifestation of disease. He also described a variant in which unilateral lesions do not exceed the median line.Impaired oral hemorrhage may occur as spotty, ulcers, papulovezicule, erythematous bubbles or tiles. The incidence is less than 10%.
Diagnosis of pityriasis roseaHistological examination. Biopsy specimen is helpful in atypical cases. Show perivascular dermatitis, parakeratoza focal epidermal hyperplasia and focal sponginess. May epidermal cell exocytosis, sponginess variable acanthosis and a slight fine granular layer. There is an inflammatory infiltrate in the dermis.The differential diagnosis is made with the following conditions: stains erythema perstans, lichen planus, numulara dermatitis, pityriasis lichenoides, gutat psoriasis, seborrheic dermatitis, syphilis, tinea corporis, viral exanthema.
TreatmentTreatment is not necessary in most cases because it is self-limited pink pityriasis without sequelae. If severe itching can take measures for improvement. Patients should avoid harsh soaps, tight clothes and scratching. Mild Emolientele are helpful. Topical preparations with calamine, menthol, pramoxine, starch and colloidal oatmeal are good.Topical steroids can relieve itching. Sedative effect of antihistamines to help patients sleep better at night. Ultraviolet B therapy relieves itching within 24 hours, but increase postinflamatorie hyperpigmentation. Aciclovir shows resolution of the eruption if given early.
Prognosis
Pink is a self-limited disease pityriasis, benign that resolves without treatment in 6-12 weeks. Not cause lesions leave scars hyperpigmentation postinflamatorie though. The prognosis is excellent, the recurrence rate is 2%.
The rash resolves spontaneously. Improvement of pruritus by topical steroids, oral anrihistaminice, lotions and bath oils local menthol menthol is indicated. In cases resistant to ultraviolet B phototherapy is beneficial dynamics. Low dose acyclovir reduces the duration of the eruption.Pityriasis generally resolves in 12 weeks pink. Most cases do not return, but some patients may relapse. Pink pityriasis persistent over three months is correctly classified as chronic pityriasis lichenoides. The prognosis is excellent. Patients are not considered contagious.
Pathogenesis and causes of pityriasis roseaPityriasis pink was considered to be a viral exanthem. Clinical presentation supports this concept. He was associated with upper respiratory tract infections, may run in families and close contact and have an increased incidence in immunocompromised individuals. The incidence increases in spring, and the disease seems to cause life-long immunity. Despite viral etiological considerations have not discovered any virus.
Signs and symptomsPityriasis pink is more common in women than in men. It develops mainly in children and young adults, although any age group can be affected. Most patients are between 10-35 years. The condition begins to trigger the eruption through a solitary macule. Initial lesion grows in a few days and becomes a pink stain with fine scales well demarcated in the periphery. Over the next two weeks is a generalized exanthem, although it can occur in a few hours or months. This secondary phase consists of bilateral and symmetrical appearance of patches with scales long axis oriented along the lines of cleavage. This phase tends to resolve within 6 weeks. Itching is common, easy-moderate.
Physical ExamTrigger spot is one of 2-10cm in diameter, located on the neck or trunk with fine scales. It is seen in over 50% of patients and can occur as multiple lesions with atypical localization. Secondary lesions appear on the abdomen, trunk, upper back and proximal limbs. They are described as having an appearance of cigarette paper, with the long axis oriented parallel along the lines of cleavage giving a classic Christmas tree look.
Atypical pityriasis occurs in 20% of patients. These variations can be separated into lesions or changes in their distribution. Photosensitivity may occur. Lesions may be localized to one area. One can see an inverse pityriasis. This form of damage appears on the face and distal extremities and is more common in children. Pata trigger may be the only manifestation of disease. He also described a variant in which unilateral lesions do not exceed the median line.Impaired oral hemorrhage may occur as spotty, ulcers, papulovezicule, erythematous bubbles or tiles. The incidence is less than 10%.
Diagnosis of pityriasis roseaHistological examination. Biopsy specimen is helpful in atypical cases. Show perivascular dermatitis, parakeratoza focal epidermal hyperplasia and focal sponginess. May epidermal cell exocytosis, sponginess variable acanthosis and a slight fine granular layer. There is an inflammatory infiltrate in the dermis.The differential diagnosis is made with the following conditions: stains erythema perstans, lichen planus, numulara dermatitis, pityriasis lichenoides, gutat psoriasis, seborrheic dermatitis, syphilis, tinea corporis, viral exanthema.
TreatmentTreatment is not necessary in most cases because it is self-limited pink pityriasis without sequelae. If severe itching can take measures for improvement. Patients should avoid harsh soaps, tight clothes and scratching. Mild Emolientele are helpful. Topical preparations with calamine, menthol, pramoxine, starch and colloidal oatmeal are good.Topical steroids can relieve itching. Sedative effect of antihistamines to help patients sleep better at night. Ultraviolet B therapy relieves itching within 24 hours, but increase postinflamatorie hyperpigmentation. Aciclovir shows resolution of the eruption if given early.
Prognosis
Pink is a self-limited disease pityriasis, benign that resolves without treatment in 6-12 weeks. Not cause lesions leave scars hyperpigmentation postinflamatorie though. The prognosis is excellent, the recurrence rate is 2%.
Freckle
FreckleFreckles Synonyms: efelide, macula solaris
Or efelidele Freckles are small patches, thin skin surface. They are usually multiple in number. With exposure to sunlight and therefore become more apparent in winter months are almost imperceptible. Although efelidele are predominantly benign can be observed in association with systemic disease.
People who are genetically succeptibile somatic mutations in melanocytes may have to promote the growth of epidermal melanogenesis. Melanocytes are increased in number and even that number may be low. With exposure to ultraviolet A and B increases dopa reaction leading to production of large melanosomes and characteristic clinical appearance.Efelidele occur during childhood as areas of increased pigmentation confined to regions of the body above the waist. At more advanced ages their number decreases. Efelidele appear at age 2 years and increase in number during adolescence. Macules are asymptomatic, more numerous in areas exposed to sun and fade, little in the winter.
Physical ExemenEfelidele are many simple, small, thin patches 1-5 mm in diameter with uniform pigmentation. It is commonly found on sun-exposed areas such as nose, cheeks, shoulders and upper back. Macules may be discrete or confluent. Similar simple sunburn freckles freckles are darker, and irregular edges of a few centimeters.Efelidele are common in people blondes and redheads. Are distributed equally between sexes. Can this be some impact on cosmetic and are not associated with increased mortality. Mortality may be increased in diseases associated with efelide such as xeroderma pigmentosum.
Causes and risk factors for frecklesFreckles tend to be inherited autosomal dominant. Are more common in people with lighter skin and thin and blond or red hair. Individuals succeptibile ultraviolet sun exposure induces pistruiii A and B by stimulating melanocytes to produce melanin.
Xeroderma pigmentosum. Freckles and even prominent blacks in heterozygous carriers of the disease autosomal recessive. Excessive Their appearance suggests the possibility of people with black hair disease. Neurofibromatosis. Freckles can be found in regions with folds of skin in individuals with this autosomal dominant disease.
Treatment of frecklesTreatment is not necessary. If the patient wants to change the cosmetic appearance indicate avoiding exposure to sun and makeup. SPF creams can be used to prevent efelidelor pigmentation caused by sun exposure. If you want you can try chemical peels, cryotherapy and laser treatment to make less efelidele poeminente. Efelidele cosmetic problem but may be associated with any complications. However, recent studies show that people with different skin types to efelide succeptibile are at increased risk of developing skin cancers. This combination is simply because efelidele and skin cancer are more common in people exposed to the sun with skin type I and II towards other people.
Or efelidele Freckles are small patches, thin skin surface. They are usually multiple in number. With exposure to sunlight and therefore become more apparent in winter months are almost imperceptible. Although efelidele are predominantly benign can be observed in association with systemic disease.
People who are genetically succeptibile somatic mutations in melanocytes may have to promote the growth of epidermal melanogenesis. Melanocytes are increased in number and even that number may be low. With exposure to ultraviolet A and B increases dopa reaction leading to production of large melanosomes and characteristic clinical appearance.Efelidele occur during childhood as areas of increased pigmentation confined to regions of the body above the waist. At more advanced ages their number decreases. Efelidele appear at age 2 years and increase in number during adolescence. Macules are asymptomatic, more numerous in areas exposed to sun and fade, little in the winter.
Physical ExemenEfelidele are many simple, small, thin patches 1-5 mm in diameter with uniform pigmentation. It is commonly found on sun-exposed areas such as nose, cheeks, shoulders and upper back. Macules may be discrete or confluent. Similar simple sunburn freckles freckles are darker, and irregular edges of a few centimeters.Efelidele are common in people blondes and redheads. Are distributed equally between sexes. Can this be some impact on cosmetic and are not associated with increased mortality. Mortality may be increased in diseases associated with efelide such as xeroderma pigmentosum.
Causes and risk factors for frecklesFreckles tend to be inherited autosomal dominant. Are more common in people with lighter skin and thin and blond or red hair. Individuals succeptibile ultraviolet sun exposure induces pistruiii A and B by stimulating melanocytes to produce melanin.
Xeroderma pigmentosum. Freckles and even prominent blacks in heterozygous carriers of the disease autosomal recessive. Excessive Their appearance suggests the possibility of people with black hair disease. Neurofibromatosis. Freckles can be found in regions with folds of skin in individuals with this autosomal dominant disease.
Treatment of frecklesTreatment is not necessary. If the patient wants to change the cosmetic appearance indicate avoiding exposure to sun and makeup. SPF creams can be used to prevent efelidelor pigmentation caused by sun exposure. If you want you can try chemical peels, cryotherapy and laser treatment to make less efelidele poeminente. Efelidele cosmetic problem but may be associated with any complications. However, recent studies show that people with different skin types to efelide succeptibile are at increased risk of developing skin cancers. This combination is simply because efelidele and skin cancer are more common in people exposed to the sun with skin type I and II towards other people.
Gestational pemphigoid
Gestational pemphigoidGestational pemphigoid is an autoimmune dermatosis of pregnancy. It was originally named because of the characteristic features of gestational herpes herpetiform of vesicles, but the term is a misnomer because the condition is not associated with active viral herpetic infection or a history.
The disease does not cause fetal growth or maternal mortality. It is associated with an increased prevalence of premature babies and small gestational age. 5-10% of all babies may resolve transitional skin damage as maternal antibodies disappear. Patients with gestational pemphigoid have an increased prevalence of autoimmune diseases, including Hashimoto's thyroiditis, pernicious anemia and Graves' disease, also associated with HLA-DR3 haplotype-4.The disease manifests during the third quarter of pregnancy by urticarial rash, pruritic papular on the abdomen and torso. Including persistent disease has been reported for several years after birth.
Treatment aims relieve itching and blocked vesicle enlargement. It shows warm baths and compresses to relieve itching, antihistamines and corticosteroids. It will use first the lowest therapeutic dose because the mother's pregnancy status. If they do not opt for the efficient drugs are more powerful. Gestational pemphigoid regresses in a few weeks or months after delivrenta without scars. May return during other tasks, may be precipitated by menstruation or oral contraceptives.
Pathogenesis and causes
Gestational pemphigoid is an autoimmune disease associated with pregnancy. Most patients develop antibodies against two proteins hemidesmosomale. Known as herpes factor gestational gestational these antibodies belong to immunoglobulin class G1 heat. This triggers an autoimmune response leading to vesicle formation subepidermice. Trigger disease still remains unidentified. He proposed an activation reaction cross between placental tissue and skin. Gestational pemphigoid is closely linked to the haplotype HLA-DR3-4. Placenta is known to be the main source of antibodies and so parents can be a target immune during pregnancy.
Signs and symptoms
Gestational pemphigoid occurs in pregnant women. It typically manifests in advanced pregnancy with sudden onset of pruritic urticarial papules and vesicles on the abdomen and torso. Itching can be so severe, that you can interrupt daily activities. Injuries can occur anytime during pregnancy, but developed mainly during the second and third quarter. Symptoms may occur in pregnancy but also sfirsutul immediate delivery. Gestational pemphigoid usually resolves spontaneously within a few weeks or months after delivrenta even earlier if the nursing breast. The persistence of disease activity is described even after a few years after birth. The disease can be triggered by the use of contraceptives and menstrual periods, and the tasks ahead.
Physical examination.Initial clinical manifestations are typical erythematous patches and urticarial periombilicale boards. These lesions progress to vesicles energized. Some patients may experience only pleasure without veziculizare urticarial. The rash expands peripherally, avoiding the face, palms and soles. Mucosal lesions occur in 20% of cases. Patients may develop secondary infections at veziculizarii.
Diagnosis
Routine laboratory tests are not helpful in diagnosing the disease. Blood results are normal, although peripheral eosinophilia is observed. Tests also showed increased immunoglobulins, erythrocyte sedimentation rate, acute phase reactants and antithyroid antibodies. HLA-DR haplotype 3-4 is present in 45% of cases.Histological examination.Prelevatele affected skin biopsy showed infiltration with predominantly eosinophilic veziculizare subepidermica. The inflammatory infiltrate is located at the dermo-epidermal junction and perivascular. Keratinocyte necrosis and dermal edema are often present.The differential diagnosis is made with the following disorders: bullous pemphigoid, pemphigoid scar, linear IgA dermatosis, acute urticaria, contact dermatitis, dermatitis herpetiformis, erythema multiforme, bullous diseases induced by drugs, papular dermatitis of pregnancy, pruritic folliculitis of pregnancy.
Treatment
Treatment tries to relieve itching and peripheral extension of the eruption. To minimize the risk to the fetus and mother are used therapeutically to lower levels of disease suppression. Assessed the risks and benefits must always tried terapeiilor.
Medical therapy.It shows warm baths, and compresses to relieve itching emolientele. Patients with mild can be treated with antihistamines and topical or intralesional steroids like triamcinolone. However, these regimens are usually ineffective in severe cases, making the necessary systemic corticosteroids: prednisone. Once veziculizarea stopped and the lesions begin to heal until the dose of prednisone is decreased to the minimum that controls the disease. Other regimens include azathioprine, pyridoxine, plasmapheresis, dapsone, intravenous immunoglobulin, cyclosporine and minocycline / nicotinamide. It is promising and chemical oophorectomy with goserelin.
Prognosis
Women with gestational pemphigoid delivrentei have a higher incidence of premature and newborn babies in the optimal gestational age. It has been observed and a risk of immunological diseases. Children born out of a mother with the disease may be rarely veziculizare. They are however at risk of infection, and thermoregulatory disorders of fluid and electrolyte balance. Pemphigoid regresses in a few weeks or months after delivery. May return to other tasks and can be precipitated by menstruation or oral contraceptives. Impaired skin of newborn babies is rare and decreases with the disappearance of maternal antibodies.
The disease does not cause fetal growth or maternal mortality. It is associated with an increased prevalence of premature babies and small gestational age. 5-10% of all babies may resolve transitional skin damage as maternal antibodies disappear. Patients with gestational pemphigoid have an increased prevalence of autoimmune diseases, including Hashimoto's thyroiditis, pernicious anemia and Graves' disease, also associated with HLA-DR3 haplotype-4.The disease manifests during the third quarter of pregnancy by urticarial rash, pruritic papular on the abdomen and torso. Including persistent disease has been reported for several years after birth.
Treatment aims relieve itching and blocked vesicle enlargement. It shows warm baths and compresses to relieve itching, antihistamines and corticosteroids. It will use first the lowest therapeutic dose because the mother's pregnancy status. If they do not opt for the efficient drugs are more powerful. Gestational pemphigoid regresses in a few weeks or months after delivrenta without scars. May return during other tasks, may be precipitated by menstruation or oral contraceptives.
Pathogenesis and causes
Gestational pemphigoid is an autoimmune disease associated with pregnancy. Most patients develop antibodies against two proteins hemidesmosomale. Known as herpes factor gestational gestational these antibodies belong to immunoglobulin class G1 heat. This triggers an autoimmune response leading to vesicle formation subepidermice. Trigger disease still remains unidentified. He proposed an activation reaction cross between placental tissue and skin. Gestational pemphigoid is closely linked to the haplotype HLA-DR3-4. Placenta is known to be the main source of antibodies and so parents can be a target immune during pregnancy.
Signs and symptoms
Gestational pemphigoid occurs in pregnant women. It typically manifests in advanced pregnancy with sudden onset of pruritic urticarial papules and vesicles on the abdomen and torso. Itching can be so severe, that you can interrupt daily activities. Injuries can occur anytime during pregnancy, but developed mainly during the second and third quarter. Symptoms may occur in pregnancy but also sfirsutul immediate delivery. Gestational pemphigoid usually resolves spontaneously within a few weeks or months after delivrenta even earlier if the nursing breast. The persistence of disease activity is described even after a few years after birth. The disease can be triggered by the use of contraceptives and menstrual periods, and the tasks ahead.
Physical examination.Initial clinical manifestations are typical erythematous patches and urticarial periombilicale boards. These lesions progress to vesicles energized. Some patients may experience only pleasure without veziculizare urticarial. The rash expands peripherally, avoiding the face, palms and soles. Mucosal lesions occur in 20% of cases. Patients may develop secondary infections at veziculizarii.
Diagnosis
Routine laboratory tests are not helpful in diagnosing the disease. Blood results are normal, although peripheral eosinophilia is observed. Tests also showed increased immunoglobulins, erythrocyte sedimentation rate, acute phase reactants and antithyroid antibodies. HLA-DR haplotype 3-4 is present in 45% of cases.Histological examination.Prelevatele affected skin biopsy showed infiltration with predominantly eosinophilic veziculizare subepidermica. The inflammatory infiltrate is located at the dermo-epidermal junction and perivascular. Keratinocyte necrosis and dermal edema are often present.The differential diagnosis is made with the following disorders: bullous pemphigoid, pemphigoid scar, linear IgA dermatosis, acute urticaria, contact dermatitis, dermatitis herpetiformis, erythema multiforme, bullous diseases induced by drugs, papular dermatitis of pregnancy, pruritic folliculitis of pregnancy.
Treatment
Treatment tries to relieve itching and peripheral extension of the eruption. To minimize the risk to the fetus and mother are used therapeutically to lower levels of disease suppression. Assessed the risks and benefits must always tried terapeiilor.
Medical therapy.It shows warm baths, and compresses to relieve itching emolientele. Patients with mild can be treated with antihistamines and topical or intralesional steroids like triamcinolone. However, these regimens are usually ineffective in severe cases, making the necessary systemic corticosteroids: prednisone. Once veziculizarea stopped and the lesions begin to heal until the dose of prednisone is decreased to the minimum that controls the disease. Other regimens include azathioprine, pyridoxine, plasmapheresis, dapsone, intravenous immunoglobulin, cyclosporine and minocycline / nicotinamide. It is promising and chemical oophorectomy with goserelin.
Prognosis
Women with gestational pemphigoid delivrentei have a higher incidence of premature and newborn babies in the optimal gestational age. It has been observed and a risk of immunological diseases. Children born out of a mother with the disease may be rarely veziculizare. They are however at risk of infection, and thermoregulatory disorders of fluid and electrolyte balance. Pemphigoid regresses in a few weeks or months after delivery. May return to other tasks and can be precipitated by menstruation or oral contraceptives. Impaired skin of newborn babies is rare and decreases with the disappearance of maternal antibodies.
Pearly penile papules
Pearly penile papulesTilt penile papules are small dome-shaped papules or filiform skin-colored crown ditch located on the glans penis typical. Circumferential lesions are arranged in one or a few lumps. It is transmitted sexually. They are benign and not associated with an infectious etiology.The injuries do not require specific therapy. The patient may want treatment for cosmetic reasons. Cryotherapy and laser ablation are reported as effective.
Pathogenesis and causes
Tilt penile papules are considered a normal variant and does not have any malignant potential. Are not contracted or spread through sexual contact. Lesions are observed more frequently in uncircumcised men, their growth mechanism is still unknown. In the past considered a condition caused by the accumulation of smegma in uncircumcised men, actually proved to be false today.
Signs and symptoms
Because the anatomical distribution condition is described only in men. Those affected are aged between 20-30 years with a gradual decrease with age. Most patients with penile papules tilt to the doctor because they are worried about possible sexual nature of transmission condition. The disease is not transmitted sexually. Papules are often confused with condyloma acuminata, genital warts or molluscum contagiosum less.
Physical ExamOn physical examination, describing single or multiple small papules, white or colored, dome-shaped or filiform circumferential located around the crown of the glans. Lesions are asymptomatic and persist throughout life, however, become less visible over time.
Diagnosis
Histological examination. It demonstrates a number of vessels in the dermis with proliferation ectaziate fibroblasitca. Structures surrounded by concentric fibrosis is a feature annexes. These facts indicate angiofibromul and papules are characteristic tilt.The differential diagnosis is made with the following diseases: molluscum contagiosum, genital warts, ectopic sebaceous glands.
Treatment
Lesions are asymptomatic and require no treatment. Some patients may require treatment regimens to relieve anxiety and discomfort cosmetic. You can opt for laser ablation carbon electrodesicare and curettage and excisional surgery to remove lesions. Podofilina topical application does not work. The condition is associated with personal cleanliness and sexual activity. There are no topical or oral pharmacological therapies to cure the condition.
Pathogenesis and causes
Tilt penile papules are considered a normal variant and does not have any malignant potential. Are not contracted or spread through sexual contact. Lesions are observed more frequently in uncircumcised men, their growth mechanism is still unknown. In the past considered a condition caused by the accumulation of smegma in uncircumcised men, actually proved to be false today.
Signs and symptoms
Because the anatomical distribution condition is described only in men. Those affected are aged between 20-30 years with a gradual decrease with age. Most patients with penile papules tilt to the doctor because they are worried about possible sexual nature of transmission condition. The disease is not transmitted sexually. Papules are often confused with condyloma acuminata, genital warts or molluscum contagiosum less.
Physical ExamOn physical examination, describing single or multiple small papules, white or colored, dome-shaped or filiform circumferential located around the crown of the glans. Lesions are asymptomatic and persist throughout life, however, become less visible over time.
Diagnosis
Histological examination. It demonstrates a number of vessels in the dermis with proliferation ectaziate fibroblasitca. Structures surrounded by concentric fibrosis is a feature annexes. These facts indicate angiofibromul and papules are characteristic tilt.The differential diagnosis is made with the following diseases: molluscum contagiosum, genital warts, ectopic sebaceous glands.
Treatment
Lesions are asymptomatic and require no treatment. Some patients may require treatment regimens to relieve anxiety and discomfort cosmetic. You can opt for laser ablation carbon electrodesicare and curettage and excisional surgery to remove lesions. Podofilina topical application does not work. The condition is associated with personal cleanliness and sexual activity. There are no topical or oral pharmacological therapies to cure the condition.
Onychomycosis
Onychomycosis refers to a fungal infection that affects the toes and hands. It can affect any part of the nail unit, including the nail matrix, nail or nail bed itself. Onychomycosis is not life threatening but can cause pain, discomfort and local deformation, along with occupational and psychological limitations. Effects of psychological and psychosocial impact on quality of life.
Main subtypes of onychomycosis are distal lateral subunghiala onychomycosis, white superficial onychomycosis, onychomycosis subunghiala proximal endonix onychomycosis and candidal onychomycosis. Patients may experience a combination of these. Total distofica Onychomycosis is the most advanced of any subtype.
Onychomycosis is usually asymptomatic patients are so disturbed by the cosmetic discomfort. As the disease progresses it may interfere with walking, bipedal position and exercise. Onychomycosis is caused by dermatophytes, molds and fungi nondermatofite. Risk factors include family history, advanced age, poor health, previous trauma, hot and humid climate, immunosuppression, use of communal bathrooms and shoes rank.
The antifungal treatment of onychomycosis using topical, oral and surgical techniques. Treatment depends on the number of fingers affected, type and severity of onychomycosis. A combination of topical and systemic regimes increase the cure rate.
Pathogenesis of onychomycosisPathogenesis of onychomycosis depends on the clinical subtype. In onychomycosis subunghiala distal side, the most common form of onychomycosis, fungi extend from the plantar skin and invades the nail bed by hiponichium. Inflammation of the musculoskeletal physical signs typical nail onychomycosis determine subunghiale distal side. In contrast, white superficial onychomycosis is a rare presentation caused by direct invasion of the nail surface. In subunghiala proximal onychomycosis, the rarest subtype, the fungi penetrate the nail matrix and proximal nail fold colonize the deep portion of the proximal nail. Endonix Onychomycosis Onychomycosis is a variant of subunghiale distal side, the nail fungus infects the skin and directly invade the nail. Total dystrophic onychomycosis involves the whole nail unit.Invasion by candida fungus is not common because it requires an altered immune response as a factor predisposing to penetrate the nail.
Causes and risk factors for onychomycosisOnychomycosis is caused by three main classes of fungi: dermatophytic fungi and fungi nondermatofitici. Dermatophytic are the most common causes of onychomycosis. Two major pathogens are responsible for 90% of cases of onychomycosis. Trichophyton rubrum and T. mentagrophytes. Nondermatofite onychomycosis caused by fungi, species of Fusarium, Scopulariopsis, Aspergillus is becoming increasingly common. Onychomycosis by candida is rare.
Associations between subtypes of onychomycosis and the causative factors:-T. rubrum is the most common pathogen in distal lateral onychomycosis subunghialaSubunghiala-proximal onychomycosis due to T. tubrum is typical for immunosuppressed patientsSubunghiala-proximal onychomycosis with inflammation is caused by fungi nondermatofitice periunghialaSuperficial white onychomycosis, is caused by T. mentagrophytes-Candidate is observed in premature children, immunocompromised and those with chronic mucocutaneous candida.
Risk factors for onychomycosis are these:-History of contact with people affected-Health and poor hygiene-Previous trauma, hot and humid climateClose-shoes, communal bathrooms
Main subtypes of onychomycosis are distal lateral subunghiala onychomycosis, white superficial onychomycosis, onychomycosis subunghiala proximal endonix onychomycosis and candidal onychomycosis. Patients may experience a combination of these. Total distofica Onychomycosis is the most advanced of any subtype.
Onychomycosis is usually asymptomatic patients are so disturbed by the cosmetic discomfort. As the disease progresses it may interfere with walking, bipedal position and exercise. Onychomycosis is caused by dermatophytes, molds and fungi nondermatofite. Risk factors include family history, advanced age, poor health, previous trauma, hot and humid climate, immunosuppression, use of communal bathrooms and shoes rank.
The antifungal treatment of onychomycosis using topical, oral and surgical techniques. Treatment depends on the number of fingers affected, type and severity of onychomycosis. A combination of topical and systemic regimes increase the cure rate.
Pathogenesis of onychomycosisPathogenesis of onychomycosis depends on the clinical subtype. In onychomycosis subunghiala distal side, the most common form of onychomycosis, fungi extend from the plantar skin and invades the nail bed by hiponichium. Inflammation of the musculoskeletal physical signs typical nail onychomycosis determine subunghiale distal side. In contrast, white superficial onychomycosis is a rare presentation caused by direct invasion of the nail surface. In subunghiala proximal onychomycosis, the rarest subtype, the fungi penetrate the nail matrix and proximal nail fold colonize the deep portion of the proximal nail. Endonix Onychomycosis Onychomycosis is a variant of subunghiale distal side, the nail fungus infects the skin and directly invade the nail. Total dystrophic onychomycosis involves the whole nail unit.Invasion by candida fungus is not common because it requires an altered immune response as a factor predisposing to penetrate the nail.
Causes and risk factors for onychomycosisOnychomycosis is caused by three main classes of fungi: dermatophytic fungi and fungi nondermatofitici. Dermatophytic are the most common causes of onychomycosis. Two major pathogens are responsible for 90% of cases of onychomycosis. Trichophyton rubrum and T. mentagrophytes. Nondermatofite onychomycosis caused by fungi, species of Fusarium, Scopulariopsis, Aspergillus is becoming increasingly common. Onychomycosis by candida is rare.
Associations between subtypes of onychomycosis and the causative factors:-T. rubrum is the most common pathogen in distal lateral onychomycosis subunghialaSubunghiala-proximal onychomycosis due to T. tubrum is typical for immunosuppressed patientsSubunghiala-proximal onychomycosis with inflammation is caused by fungi nondermatofitice periunghialaSuperficial white onychomycosis, is caused by T. mentagrophytes-Candidate is observed in premature children, immunocompromised and those with chronic mucocutaneous candida.
Risk factors for onychomycosis are these:-History of contact with people affected-Health and poor hygiene-Previous trauma, hot and humid climateClose-shoes, communal bathrooms
Onycholysis
OnycholysisOnycholysis is a nail disorder frequently encountered. It is characterized by a spontaneous separation of the nail starting at the edge of progressive proximal and distal free. Nail is separated from the underlying structures and lateral support. Less separation starts at the proximal and expands, the distal free edge, as seen especially in nail psoriasis onicomadesis.
Treatment varies and depends on the cause onycholysis. It is important to remove the causative factor. Onycholysis of psoriasis can be treated with topical corticosteroids. Patients should avoid trauma, irritants and moisture. To prevent infection with bacteria and fungi indicate antibacterine and oral antifungal regimens. Severe cases left untreated can lead to permanent loss of nails and scars.
Pathogenesis
Nails with onycholysis usually are smooth, firm and without inflammatory reaction. Onycholysis is a matrix ugnhiei disease, but the underlying nail discoloration may occur as a result of secondary infection. Treatment of primary and secondary factors that exacerbate the condition is important. Left untreated, severe cases can cause scarring of the nail bed.
Causes and Risk Factors
Etiological factors may be exogenous, endogenous, hereditary or idiopathic. Contact irritants, trauma and moisture are the most common causes for onycholysis.
Systemic causes:-Multiple myeloma, amyloidosis, diabetes, bronsiectazie, erythropoietic porphyriaHistiocytosis X-, hyper-, hypothyroidism, ischemia, leprosy, lupus, Neural, pellagra-Pemphigus vulgaris, porphyria cutanea tarda, pregnancy, Reiter syndrome, psoriatic arthritis,, Sarcoidosis, scleroderma, shell nail syndrome, syphilis, yellow nail syndrome.
Causes skin:-Psoroazis, lichen planus, dermatitis, hyperhidrosis, congenital paconichiaVegetant-pemphigus, lichen streaked, atopic dermatitis, congenital abnormalities of the nails.
Causes cancer:Squamous-cell carcinoma of nail bedLung-carcinoma.
Nonmicrobieni exogenous factors:-Repetitive mechanical trauma, contact dermatitis, paints, OJE, ugnhii adhesives, gas, solvents, bleach-Irritant contact dermatitis by prolonged immersion of nails in water, sweet solutions, exposure to acids and bases.
Microbial factors:-Dermatophytosis: T. rubrum, Trichophyton mentagrophytes-Fungus-Candida-Pseudomonas bacteria, viruses-herpes simplex.
Causes photosensitivity madicamentoase by agents (sun):-Tetracycline, psoralen, fluoroquinolones, chloramphenicol, chlorpromazine, doxycycline-Minocycline, oral contraceptives, aminolevulinic acid.
Pharmacological Causes:-Doxorubicin, mitoxantrone, captopril, bleomycin, 5-fluorouracil-Retinoids, tetracycline, etoposide, paclitaxel.
Other causes:-Onycholysis congenital hereditary partial onycholysis-Onycholysis gained idiopathic congenital distal onycholysis.
Signs and symptoms
People of any age may onycholysis, although it is a disease of adults. Pacentilor careful anamnesis usually show exposure to different agents nail injury. Affected nails are smooth, firm and without inflammation. Nail bed discoloration is due to secondary infection. Spontaneous separation of the nail starts at free distal edge and progresses proximally. Less separation begins at the proximal nail and extends to the free edge. Nail is separated from the underlying structures and side.
Diagnosis
It will undertake studies to exclude onychomycosis, treatment with potassium hydroxide to reveal the nail fungus. Biopsy staining with hematoxylin and eosin nails for fungi.
Treatment
Depending on the cause onycholysis treatment must deal with underlying conditions. Patients should avoid trauma to the affected nail and keep the area dry. Must avoid exposure to irritants and wet, wear cotton socks at home and in the synthetic work if it shows a wet environment.Intralesional corticosteroid injections are associated with nail dystrophy in psoriasis.The practice of diluted triamcinolone injections in the proximal nail fold every 4 weeks in 4-6 sessions. Apply topical antifungal azoles alilamine or twice a day to avoid superinfection nail. To use concurrent onychomycosis fluconazole, itraconazole, terbinafine. The 1% 5-fluorouracil in massage twice a day for 4 months is effective for patients with psoriasis. Other regimens tested relative onycholysis results include PUVA in psoriasis, etretinat oral hydroxyurea and isotretinoin.
Treatment varies and depends on the cause onycholysis. It is important to remove the causative factor. Onycholysis of psoriasis can be treated with topical corticosteroids. Patients should avoid trauma, irritants and moisture. To prevent infection with bacteria and fungi indicate antibacterine and oral antifungal regimens. Severe cases left untreated can lead to permanent loss of nails and scars.
Pathogenesis
Nails with onycholysis usually are smooth, firm and without inflammatory reaction. Onycholysis is a matrix ugnhiei disease, but the underlying nail discoloration may occur as a result of secondary infection. Treatment of primary and secondary factors that exacerbate the condition is important. Left untreated, severe cases can cause scarring of the nail bed.
Causes and Risk Factors
Etiological factors may be exogenous, endogenous, hereditary or idiopathic. Contact irritants, trauma and moisture are the most common causes for onycholysis.
Systemic causes:-Multiple myeloma, amyloidosis, diabetes, bronsiectazie, erythropoietic porphyriaHistiocytosis X-, hyper-, hypothyroidism, ischemia, leprosy, lupus, Neural, pellagra-Pemphigus vulgaris, porphyria cutanea tarda, pregnancy, Reiter syndrome, psoriatic arthritis,, Sarcoidosis, scleroderma, shell nail syndrome, syphilis, yellow nail syndrome.
Causes skin:-Psoroazis, lichen planus, dermatitis, hyperhidrosis, congenital paconichiaVegetant-pemphigus, lichen streaked, atopic dermatitis, congenital abnormalities of the nails.
Causes cancer:Squamous-cell carcinoma of nail bedLung-carcinoma.
Nonmicrobieni exogenous factors:-Repetitive mechanical trauma, contact dermatitis, paints, OJE, ugnhii adhesives, gas, solvents, bleach-Irritant contact dermatitis by prolonged immersion of nails in water, sweet solutions, exposure to acids and bases.
Microbial factors:-Dermatophytosis: T. rubrum, Trichophyton mentagrophytes-Fungus-Candida-Pseudomonas bacteria, viruses-herpes simplex.
Causes photosensitivity madicamentoase by agents (sun):-Tetracycline, psoralen, fluoroquinolones, chloramphenicol, chlorpromazine, doxycycline-Minocycline, oral contraceptives, aminolevulinic acid.
Pharmacological Causes:-Doxorubicin, mitoxantrone, captopril, bleomycin, 5-fluorouracil-Retinoids, tetracycline, etoposide, paclitaxel.
Other causes:-Onycholysis congenital hereditary partial onycholysis-Onycholysis gained idiopathic congenital distal onycholysis.
Signs and symptoms
People of any age may onycholysis, although it is a disease of adults. Pacentilor careful anamnesis usually show exposure to different agents nail injury. Affected nails are smooth, firm and without inflammation. Nail bed discoloration is due to secondary infection. Spontaneous separation of the nail starts at free distal edge and progresses proximally. Less separation begins at the proximal nail and extends to the free edge. Nail is separated from the underlying structures and side.
Diagnosis
It will undertake studies to exclude onychomycosis, treatment with potassium hydroxide to reveal the nail fungus. Biopsy staining with hematoxylin and eosin nails for fungi.
Treatment
Depending on the cause onycholysis treatment must deal with underlying conditions. Patients should avoid trauma to the affected nail and keep the area dry. Must avoid exposure to irritants and wet, wear cotton socks at home and in the synthetic work if it shows a wet environment.Intralesional corticosteroid injections are associated with nail dystrophy in psoriasis.The practice of diluted triamcinolone injections in the proximal nail fold every 4 weeks in 4-6 sessions. Apply topical antifungal azoles alilamine or twice a day to avoid superinfection nail. To use concurrent onychomycosis fluconazole, itraconazole, terbinafine. The 1% 5-fluorouracil in massage twice a day for 4 months is effective for patients with psoriasis. Other regimens tested relative onycholysis results include PUVA in psoriasis, etretinat oral hydroxyurea and isotretinoin.
Nevomelanocitic congenital nevu
Nevomelanocitic congenital nevus known as congenital hairy nevus is a pigmented surface lesion present at birth. Nevomelanocitele melanoblastelor and forms are derivatives of the cancer cell group. Multiple definitions have been used to classify non-living in small, medium and giant. These include the diameter, total body surface area and the possibility of intervention in a single excised nevus.
Giant congenital nevi potential to become malignant is significant and an important consideration in treatment and control of this clinical entity. Multiple studies have attempted to elucidate the cumulative risk of developing cutaneous melanoma in patients with congenital nevi. Have recent study showed that cumulative risk of melanoma is 5 to 5 years, 7% for people with large or giant congenital nevi. For small nevi risk was assessed at 0. 8% and 5%. Malignancy should be suspected in increasing length of a nevus, pain, bleeding, or itching significant pigmentation.
Treatment of patients with congenital nevi depends on lesion size, location and propensity for malignant transformation. Aesthetic considerations are important. Surgery for giant congenital nevi is shown at the age of 6 months. The procedures used in the surgical treatment include serial excision and reconstruction with skin grafts, tissue expansion, local flaps and free tissue transfer. Adjuvant treatments include chemical peeling, dermoabraziunea, laser. Surgical excision remains the treatment of adjuvant therapy mainly because the cells do not completely remove nevice. Control of small lesions include photographic documentation and monitoring by surgical excision.
Pathogenesis
Nevomelanocite congenital nevi were arranged in clusters in the epidermis and dermis or well ordered in the form of nests or cords. This nevomelanocitelor in the lower third of the dermis is typical of congenital nevi. Nevomelanocitele may extend into subcutaneous tissue. They tend to be associated with the nerves and blood vessels.
Congenital nevi increase the child grows. The risk of melanoma is proportional to the size nevus. For 50% of malignant giant nevi were developed at three years old, 60% and 70% in infancy to puberty. Approximately 40% of malignant melanomas seen in children occur in large congenital nevi. When a large congenital nevus involving the head or neck or middle line of the trunk can be seen associated meningeal melanocitoze occasionally complicated by seizures, focal neurologic defects, hidrocefalus obstruction or malignant changes.
Giant congenital nevi potential to become malignant is significant and an important consideration in treatment and control of this clinical entity. Multiple studies have attempted to elucidate the cumulative risk of developing cutaneous melanoma in patients with congenital nevi. Have recent study showed that cumulative risk of melanoma is 5 to 5 years, 7% for people with large or giant congenital nevi. For small nevi risk was assessed at 0. 8% and 5%. Malignancy should be suspected in increasing length of a nevus, pain, bleeding, or itching significant pigmentation.
Treatment of patients with congenital nevi depends on lesion size, location and propensity for malignant transformation. Aesthetic considerations are important. Surgery for giant congenital nevi is shown at the age of 6 months. The procedures used in the surgical treatment include serial excision and reconstruction with skin grafts, tissue expansion, local flaps and free tissue transfer. Adjuvant treatments include chemical peeling, dermoabraziunea, laser. Surgical excision remains the treatment of adjuvant therapy mainly because the cells do not completely remove nevice. Control of small lesions include photographic documentation and monitoring by surgical excision.
Pathogenesis
Nevomelanocite congenital nevi were arranged in clusters in the epidermis and dermis or well ordered in the form of nests or cords. This nevomelanocitelor in the lower third of the dermis is typical of congenital nevi. Nevomelanocitele may extend into subcutaneous tissue. They tend to be associated with the nerves and blood vessels.
Congenital nevi increase the child grows. The risk of melanoma is proportional to the size nevus. For 50% of malignant giant nevi were developed at three years old, 60% and 70% in infancy to puberty. Approximately 40% of malignant melanomas seen in children occur in large congenital nevi. When a large congenital nevus involving the head or neck or middle line of the trunk can be seen associated meningeal melanocitoze occasionally complicated by seizures, focal neurologic defects, hidrocefalus obstruction or malignant changes.
Necrobiosis
Necrobiosis Necrobiosis known as asymptomatic diabeticorum shows bright spots which enlarge over time, until red-brown to yellow, atrophic by degeneration of collagen and granulomatous response, storing fat and thickening of blood vessel walls. The exact cause is not known but the widely accepted theory include diabetic microangiopathy. Other theories suggest trauma or inflammation.
Necrobiosis lipoidica is described in 0. 3% of diabetics. The presence and progression of this condition is not related to diabetes management. Treatment is not satisfactory. Chronic disease progression is variable and scars. Skin cancer has been reported in people with Necrobiosis lipoidica with ulceration and previous trauma. Intralesional corticosteroids are used, but with minor effects. Antiagregare therapy with aspirin and dipyridamole have been tried as Necrobiosis lipoidica is caused by vascular occlusion or platelet-mediated immune mechanisms. And immunomodulators are used with variable success. Therapy includes surgical excision and grafting, but recurrent vascular damage is secondary. The surgical wound is healing slowly. You can try laser therapy.
Necrobiosis lipoidica is the main accused in ulceration that occurs after trauma. Infection can occur but are unusual. Were squamous cell carcinoma reported develop and diversify into chronic lesions of Necrobiosis lipoidica. The prognosis for this disease is unfavorable cosmetic. Treatment is helpful in stopping the expansion of lesions tend to present a chronic evolution. Ulcers can be painful, infected and heal with scarring.
Pathogenesis and causes
Necrobiosis lipoidica is a condition in collagen degeneration with granulomatous response, thickening of the walls of blood vessels and fat storage. Pathogenesis has not been shown to be related to genetic factors. Because of the close links between diabetes Necrobiosis lipoidica diabeticorum many studies have targeted this etiology. Microangiopathy in the disease could trigger the disease.Another theory is based on the deposit of immunoglobulins, complement and fibrinogen in the blood vessel walls. It is considered to be an antibody-mediated vasculitis disease. An additional theory of Necrobiosis lipoidica observed abnormal collagen, other theories include trauma, inflammatory and metabolic changes as a possible etiology.
Signs and symptoms
Necrobiosis lipoidica is 3 times more common in women than in men. Mean age of onset is 30 years old but can develop at any age. In patients with diabetes tends to occur early. Asymptomatic patients shows bright spots which enlarge slowly in a few months or years. Red-brown spots are initially yellow and then become depressed, atrophic. Ulcers can occur after trauma and are typically associated with pain. The main accusation is patient cosmetic appearance of the lesions. The clinical aspect of necrobiosis lipoidice is distinctive.
Physical ExamThe skin lesions begin by 1-3 mm papules, nodules are well defined or extending an active edge and become atrophic, frosty, spotted the central round. Initially these boards are red, yellow and brown but progressively become atrophic. Most cases occur in the pretibial area, but are reported in the face, scalp, trunk and upper extremities. You may notice multiple teleangiectazii thin epidermis surface. Ulcers at the site of trauma and secondary infection are occasional complications of necrobiosis lipoidice.Koebner phenomenon is present in these patients, particularly those with vasculitis at the site of trauma. In most patients Necrobiosis lipoidica lesions are typically multiple and bilateral. This can become painful due to nerve damage in 75% of cutaneous cases and 25% are in extreme distress.
Diagnosis
Histological examination. The condition shows interstitial granuloma involving dermis and subcutaneous tissue. Granulomas are composed of histiocite, plasma cells and eosinophils. Reduce the number of cutaneous nerve is another feature. The main element is thickening and swelling of vascular endothelial walls found in the deep dermis, similar to diabetic microangiopathy.The differential diagnosis is made with the following conditions: anular granuloma, sarcoidosis, xantoamele.
Treatment
Treatment for Necrobiosis lipoidica is not very effective because the exact etiology is unclear. Because trauma cause localized ulceration and protection legs stockings legs rest are helpful. Topical steroids can reduce inflammation but intralesional early active lesions but with minimal effects on atrophic lesions. To these steroids can cause additional atrophy. We have tried topical tacrolimus, cyclosporine, antiplatelet therapy, etanercept, infliximab. One study used topical bovine collagen to improve granulation tissue and wound healing promoting fibroblast activity and ulceration. Other therapies used with variable success include ultraviolet phototherapy, ticlopidine, nicotinamide, clofazimina, Intralesional injections of heparin, tretinoin, hidroxicloroquina.
Surgical therapy.Excision and grafting are effective, but recurrence is secondary vascular alterations. This shows an impaired wound healing. Have been described and laser regimens.
Prognosis
In terms of cosmetic outcome is negative lipoidice necrobiosis. Treatments can improve chronic ongoing expansion of individual lesions. Ulcers can cause significant morbidity, requiring prolonged wound care. These ulcers can be painful, become infected and heal with scarring.
Necrobiosis lipoidica is described in 0. 3% of diabetics. The presence and progression of this condition is not related to diabetes management. Treatment is not satisfactory. Chronic disease progression is variable and scars. Skin cancer has been reported in people with Necrobiosis lipoidica with ulceration and previous trauma. Intralesional corticosteroids are used, but with minor effects. Antiagregare therapy with aspirin and dipyridamole have been tried as Necrobiosis lipoidica is caused by vascular occlusion or platelet-mediated immune mechanisms. And immunomodulators are used with variable success. Therapy includes surgical excision and grafting, but recurrent vascular damage is secondary. The surgical wound is healing slowly. You can try laser therapy.
Necrobiosis lipoidica is the main accused in ulceration that occurs after trauma. Infection can occur but are unusual. Were squamous cell carcinoma reported develop and diversify into chronic lesions of Necrobiosis lipoidica. The prognosis for this disease is unfavorable cosmetic. Treatment is helpful in stopping the expansion of lesions tend to present a chronic evolution. Ulcers can be painful, infected and heal with scarring.
Pathogenesis and causes
Necrobiosis lipoidica is a condition in collagen degeneration with granulomatous response, thickening of the walls of blood vessels and fat storage. Pathogenesis has not been shown to be related to genetic factors. Because of the close links between diabetes Necrobiosis lipoidica diabeticorum many studies have targeted this etiology. Microangiopathy in the disease could trigger the disease.Another theory is based on the deposit of immunoglobulins, complement and fibrinogen in the blood vessel walls. It is considered to be an antibody-mediated vasculitis disease. An additional theory of Necrobiosis lipoidica observed abnormal collagen, other theories include trauma, inflammatory and metabolic changes as a possible etiology.
Signs and symptoms
Necrobiosis lipoidica is 3 times more common in women than in men. Mean age of onset is 30 years old but can develop at any age. In patients with diabetes tends to occur early. Asymptomatic patients shows bright spots which enlarge slowly in a few months or years. Red-brown spots are initially yellow and then become depressed, atrophic. Ulcers can occur after trauma and are typically associated with pain. The main accusation is patient cosmetic appearance of the lesions. The clinical aspect of necrobiosis lipoidice is distinctive.
Physical ExamThe skin lesions begin by 1-3 mm papules, nodules are well defined or extending an active edge and become atrophic, frosty, spotted the central round. Initially these boards are red, yellow and brown but progressively become atrophic. Most cases occur in the pretibial area, but are reported in the face, scalp, trunk and upper extremities. You may notice multiple teleangiectazii thin epidermis surface. Ulcers at the site of trauma and secondary infection are occasional complications of necrobiosis lipoidice.Koebner phenomenon is present in these patients, particularly those with vasculitis at the site of trauma. In most patients Necrobiosis lipoidica lesions are typically multiple and bilateral. This can become painful due to nerve damage in 75% of cutaneous cases and 25% are in extreme distress.
Diagnosis
Histological examination. The condition shows interstitial granuloma involving dermis and subcutaneous tissue. Granulomas are composed of histiocite, plasma cells and eosinophils. Reduce the number of cutaneous nerve is another feature. The main element is thickening and swelling of vascular endothelial walls found in the deep dermis, similar to diabetic microangiopathy.The differential diagnosis is made with the following conditions: anular granuloma, sarcoidosis, xantoamele.
Treatment
Treatment for Necrobiosis lipoidica is not very effective because the exact etiology is unclear. Because trauma cause localized ulceration and protection legs stockings legs rest are helpful. Topical steroids can reduce inflammation but intralesional early active lesions but with minimal effects on atrophic lesions. To these steroids can cause additional atrophy. We have tried topical tacrolimus, cyclosporine, antiplatelet therapy, etanercept, infliximab. One study used topical bovine collagen to improve granulation tissue and wound healing promoting fibroblast activity and ulceration. Other therapies used with variable success include ultraviolet phototherapy, ticlopidine, nicotinamide, clofazimina, Intralesional injections of heparin, tretinoin, hidroxicloroquina.
Surgical therapy.Excision and grafting are effective, but recurrence is secondary vascular alterations. This shows an impaired wound healing. Have been described and laser regimens.
Prognosis
In terms of cosmetic outcome is negative lipoidice necrobiosis. Treatments can improve chronic ongoing expansion of individual lesions. Ulcers can cause significant morbidity, requiring prolonged wound care. These ulcers can be painful, become infected and heal with scarring.
Melasma
Melasma is a hipermelanoza gained in areas exposed to sunlight. It presents as symmetric hyperpigmented macules, which can be confluent or dashed. The most common localizations are the cheeks, forehead, upper lip, chin, but occasionally can occur in sun-exposed areas. Chloasma is a synonymous term used to describe the occurrence of melasma during pregnancy. Chloasma derives from the Greek word "chloazein" means "being green". "MELAS" in Greek also means "black." Since the green color of the skin is melasma preferred term.
The most important factor in the appearance of melasma is exposure to sunlight. Melasma tends to occur in pregnancy and in women who oral contraceptives, although it can occur in anyone. The disease is more common in sunny climates and among people with darker skin.Dark spots, irregular skin, usually on both sides of the face. Pigmentation occurs frequently in the center of the face and cheeks, forehead, upper lip and nose. Sometimes the spots are found only on one side of the face. The spots are not itchy or painful and have only cosmetic importance.
If the skin is protected from the sun, melasma fades after pregnancy or after stopping oral contraceptives. People with melasma can use creams with SPF on stains and avoid sun exposure to prevent worsening of the condition. Skin whitening creams and retinoic acid can hidroquinona closed white spots.
Pathogenesis and causes
Pathophysiology of melasma is uncertain. In many cases this seems to be a direct relationship between female hormonal activity because the condition occurs in pregnancy and oral contraceptive use. Other factors are involved in the etiopathogenesis malesmei photosensitising drugs, mild ovarian or thyroid dysfunction, and certain cosmetics. The most important factor in the development of melasma is exposure to sunlight. Without the strict avoidance of sunlight potential success of treatments for melasma are doomed to failure.
Genetic predisposition.It is a major factor in the development of melasma. It is more common in women than in men. People with brown skin types from regions of the world with intense sun exposure are more likely to develop melasma. Over 30% of patients have a family history.
Exposure to the sun.Another major factor is exposure to sunlight. Ultraviolet radiation can cause lipid peroxidation of cell membranes, leading to excessive generation of free radicals that stimulate melanocytes to produce melanin in excess. SPF creams that block UV-B are especially poor because UV-A and visible light also stimulates melanocytes to produce melanin.
Hormonal influences.Pregnancy mask is well known in obstetrical patients. The exact mechanism by which pregnancy affects melasma is unknown. Estrogen, progesterone and melanocitic stimulating hormone (MSH) are normally kept in the third semester of pregnancy. However, nulliparous patients with melasma have no increased levels of estrogen and MSH. In addition, the incidence of melasma with estrogen and progestin contraceptives and diethylstilbestrol treatment for prostate cancer has been reported. The observation that postmenopausal women receiving progesterone develop melasma, while those receiving only estrogen progesterone does not involve playing a critical role in the development of melasma.
The most important factor in the appearance of melasma is exposure to sunlight. Melasma tends to occur in pregnancy and in women who oral contraceptives, although it can occur in anyone. The disease is more common in sunny climates and among people with darker skin.Dark spots, irregular skin, usually on both sides of the face. Pigmentation occurs frequently in the center of the face and cheeks, forehead, upper lip and nose. Sometimes the spots are found only on one side of the face. The spots are not itchy or painful and have only cosmetic importance.
If the skin is protected from the sun, melasma fades after pregnancy or after stopping oral contraceptives. People with melasma can use creams with SPF on stains and avoid sun exposure to prevent worsening of the condition. Skin whitening creams and retinoic acid can hidroquinona closed white spots.
Pathogenesis and causes
Pathophysiology of melasma is uncertain. In many cases this seems to be a direct relationship between female hormonal activity because the condition occurs in pregnancy and oral contraceptive use. Other factors are involved in the etiopathogenesis malesmei photosensitising drugs, mild ovarian or thyroid dysfunction, and certain cosmetics. The most important factor in the development of melasma is exposure to sunlight. Without the strict avoidance of sunlight potential success of treatments for melasma are doomed to failure.
Genetic predisposition.It is a major factor in the development of melasma. It is more common in women than in men. People with brown skin types from regions of the world with intense sun exposure are more likely to develop melasma. Over 30% of patients have a family history.
Exposure to the sun.Another major factor is exposure to sunlight. Ultraviolet radiation can cause lipid peroxidation of cell membranes, leading to excessive generation of free radicals that stimulate melanocytes to produce melanin in excess. SPF creams that block UV-B are especially poor because UV-A and visible light also stimulates melanocytes to produce melanin.
Hormonal influences.Pregnancy mask is well known in obstetrical patients. The exact mechanism by which pregnancy affects melasma is unknown. Estrogen, progesterone and melanocitic stimulating hormone (MSH) are normally kept in the third semester of pregnancy. However, nulliparous patients with melasma have no increased levels of estrogen and MSH. In addition, the incidence of melasma with estrogen and progestin contraceptives and diethylstilbestrol treatment for prostate cancer has been reported. The observation that postmenopausal women receiving progesterone develop melasma, while those receiving only estrogen progesterone does not involve playing a critical role in the development of melasma.
Melanoma
Melanoma is a malignant tumor that develops in the melanocytes - cells that produce melanin and are found in skin, hair and eye membranes. Melanin is a substance that determines skin color pigmentosa.
Melanoma is a rare but serious skin cancer, because metastasize rapidly, invading other organs. Though melanoma is only 5% of skin cancers, it causes 75% of deaths from skin cancer.
The most common forms of skin cancer are basal cell carcinoma and squamous cell carcinoma. Basal cell carcinoma affects mainly people over 50 years and represents 90% of skin cancers. Evolution is very slow and low metastasis ability.Discovered and treated early stage, 90% of melanoma cases can be treated successfully.
Early detection of skin cancer this is the best method of reducing mortality. The success rate in treating skin cancer is hypothetically 100% if all cases were treated before the appearance of metastases. Hence the importance of a medical examination at the first signs of suspicion, even more as the first manifestation of cancer is not painful. Although parts of the body exposed to the sun shows a high risk of skin cancer can develop in any region of the body.
Exposure to ultraviolet radiation from the sun is the main cause of skin cancers, artificial sources of radiation are also criminalized. Risks to develop this type of cancer depend on geographical area: South Africa and Australia recorded the highest number of cases (people with white skin).For carcinomas, the adverse outcome is cumulative exposure to ultraviolet radiation: effects on skin may begin in childhood and increase throughout life. In contrast, when melanomas, it seems that intense exposure, especially that caused by sunburn, can be extremely dangerous.Incidence of skin cancer increases every year by 5% worldwide.The average age of diagnosis of melanoma is 53 years. However, melanoma is the most common cancer in women 25-29 years old and in second place after breast cancer in women 30 -34 years.
Melanoma is a rare but serious skin cancer, because metastasize rapidly, invading other organs. Though melanoma is only 5% of skin cancers, it causes 75% of deaths from skin cancer.
The most common forms of skin cancer are basal cell carcinoma and squamous cell carcinoma. Basal cell carcinoma affects mainly people over 50 years and represents 90% of skin cancers. Evolution is very slow and low metastasis ability.Discovered and treated early stage, 90% of melanoma cases can be treated successfully.
Early detection of skin cancer this is the best method of reducing mortality. The success rate in treating skin cancer is hypothetically 100% if all cases were treated before the appearance of metastases. Hence the importance of a medical examination at the first signs of suspicion, even more as the first manifestation of cancer is not painful. Although parts of the body exposed to the sun shows a high risk of skin cancer can develop in any region of the body.
Exposure to ultraviolet radiation from the sun is the main cause of skin cancers, artificial sources of radiation are also criminalized. Risks to develop this type of cancer depend on geographical area: South Africa and Australia recorded the highest number of cases (people with white skin).For carcinomas, the adverse outcome is cumulative exposure to ultraviolet radiation: effects on skin may begin in childhood and increase throughout life. In contrast, when melanomas, it seems that intense exposure, especially that caused by sunburn, can be extremely dangerous.Incidence of skin cancer increases every year by 5% worldwide.The average age of diagnosis of melanoma is 53 years. However, melanoma is the most common cancer in women 25-29 years old and in second place after breast cancer in women 30 -34 years.
Skin Manifestations of smoking
Skin Manifestations of smokingCigarette smoking is number one cause of preventable death. Represents an addict usually associated closely with severe internal diseases like cancer, pulmonary disease and cardiovascular disease. Smoking has manifesatri and external skin.
Poor wound healing.Smoking is criminalized for wound healing TROUBLE, in particular the surgical and grafting. Determining mechanism is multifactorial. Sin nicotine cigarettes cause vasoconstriction in cutaneous vessels decreased tissue oxygenation. Smoking increases carboxihemoglobina, platelet aggregation, blood viscosity, reduced storage and decreases collagen formation of prostacyclin, with negative effects on wound healing. In addition to vasoconstriction associated with smoking is not a transient phenomenon. Smoking a single cigarette can cause cutaneous vasoconstriction for 90 minutes while a full day package cause hypoxia.
Wrinkles.The danger many smokers face wrinkle is a stronger reason than that of pulmonary cancer or other life-threatening disease to quit smoking. Studies indicate that women who smoke have a much more wrinkled skin, wrinkles is early, skin color is dark yellow or gray tint.The precise mechanism by which smoking cause wrinkles is poorly understood. Elastin in the skin of non-smokers exposed to sunlight is more fragmented and thick compared to the non-smokers. Chronic ischemia of the dermis is a predisposing factor. Decreased collagen synthesis in chronic ischemia may be a factor. Prooxidant effects of smoking may contribute to premature wrinkling of the face.
Hidrosadenita suppurativa.Although the mechanism is unknown, studies show that smoking contributes to hidrosadenita suppurativa by altering neutrophil function, impaired function of sweat glands, sweat excretion of compounds in tobacco and poor wound healing promotion.
Palmoplantara pustular.Some studies show close "Association of this disease and smoking. Smokers have a risk of July. 2 times more likely to develop the disease compared to nonsmokers. Unfortunately, smoking cessation is not always translate to the clinical improvement palmoplantare pustulosis.
Psoriasis.Numerous studies show the connection between smoking and psoriasis. They show a high incidence of psoriasis among smokers but the connection between smoking and psoriasis is not known.
Scuamo cell skin cancer.Some studies show that smokers are at increased risk of squamous cell cancer compared with nonsmokers. The risk increases with the number of packs smoked per day and duration of habit. Mechanisms are immunosuppressed due to the effects of cigarette smoke.
Melanoma.Although there is evidence that smoking was associated with an increased risk of melanoma, several studies show that when are compared with nonsmokers, smokers are more likely to have metastases at first presentation have a low survival rate after diagnosis, shows and visceral metastases are prone to dying from melanoma. Smokers have a negative prognosis for melanoma due to adverse effects of smoking on the immune system, including a diminished capacity to mount an immune response to melanoma tumors transplanted.
Anogenital cancer.Several studies associate smoking with anogenital cancers (vulvar, anal, penile, vaginal, cervical). Of these five areas, three are most common: vulva, anus, penis.
Oral lesions.Many oral lesions, including lip cancer are significantly more common in smokers. Smoking is a risk factor for lip cancer, combined with excessive sun exposure, the two are synergistic. Oral cancer is linked to smoking, and associated with alcohol consumption, the risk is even higher.
Leucoplakia occurs more often in smokers, while a small percentage of patients suffering malignant transformation leucoplakie. Palace leucokeratoza nicotine smoker or exclusive palaces is seen in smokers, especially in the pipe. Represents a uniform keratosis hard palate with multiple red papules which translate nipples swollen salivary glands. Language smoker nicotine leucoplakia gloss or a similar phenomenon is observed on the back of the tongue.Gingivitis is characterized by acute necrotizing ulcerative lesions of interdental papillae associated with pain, bleeding and a fetid odor of the mouth. Exclusive smokers and appears to correlate with the amount of cigarettes smoked per day.
Nutrition.Apart from nutritional deficiencies may occur in these patients smoking has some effect on nutritional status. It was demonstrated that low levels of vitamin C in smokers. Hypovitaminosis severe risk is increased in smokers, especially those who did not supplement. Skin manifestations of vitamin C deficiency include skin hyperkeratosis, and hemorrhages perifoliculare of closed spaces, gingival hypertrophy, poor wound healing.
Acne and oral thrush.It seems that smoking has a protective effect on the appearance of acne sia afetelor mouth. It is thought that nicotine has an anti-inflammatory effect against acne.
Other skin lesions.Burger's disease (Peripheral tromboangeita) featuring skin lesions: erythema, ulceration, necrosis is closely associated with smoking. Yellow and brown stains on fingers and nails are a sign of smoking. Mustache smoker smoker is analogous to fingernails. There is a brown or yellow discoloration on the distal hair mustache mustache gray or white until the hardcore smokers.Smoking is a risk factor in the development of discoid lupus erythematosus.
Nicotinic therapyNicotine is a pharmacologically active substance, and in some patients this activity has a beneficial effect as treatment. The reported benefits of nicotine therapy for pyoderma gangrenosum, pemphigus vulgaris.Recognizing dermatologic effects of tobacco consumption may be a key element in the diagnosis of internal diseases associated with smoking. For many smokers the most visible and rapid effect of this drug as yellow teeth, wrinkles and bad breath odor are more persuasive incentives for smoking cessation than the knowledge that smoking kills.
Poor wound healing.Smoking is criminalized for wound healing TROUBLE, in particular the surgical and grafting. Determining mechanism is multifactorial. Sin nicotine cigarettes cause vasoconstriction in cutaneous vessels decreased tissue oxygenation. Smoking increases carboxihemoglobina, platelet aggregation, blood viscosity, reduced storage and decreases collagen formation of prostacyclin, with negative effects on wound healing. In addition to vasoconstriction associated with smoking is not a transient phenomenon. Smoking a single cigarette can cause cutaneous vasoconstriction for 90 minutes while a full day package cause hypoxia.
Wrinkles.The danger many smokers face wrinkle is a stronger reason than that of pulmonary cancer or other life-threatening disease to quit smoking. Studies indicate that women who smoke have a much more wrinkled skin, wrinkles is early, skin color is dark yellow or gray tint.The precise mechanism by which smoking cause wrinkles is poorly understood. Elastin in the skin of non-smokers exposed to sunlight is more fragmented and thick compared to the non-smokers. Chronic ischemia of the dermis is a predisposing factor. Decreased collagen synthesis in chronic ischemia may be a factor. Prooxidant effects of smoking may contribute to premature wrinkling of the face.
Hidrosadenita suppurativa.Although the mechanism is unknown, studies show that smoking contributes to hidrosadenita suppurativa by altering neutrophil function, impaired function of sweat glands, sweat excretion of compounds in tobacco and poor wound healing promotion.
Palmoplantara pustular.Some studies show close "Association of this disease and smoking. Smokers have a risk of July. 2 times more likely to develop the disease compared to nonsmokers. Unfortunately, smoking cessation is not always translate to the clinical improvement palmoplantare pustulosis.
Psoriasis.Numerous studies show the connection between smoking and psoriasis. They show a high incidence of psoriasis among smokers but the connection between smoking and psoriasis is not known.
Scuamo cell skin cancer.Some studies show that smokers are at increased risk of squamous cell cancer compared with nonsmokers. The risk increases with the number of packs smoked per day and duration of habit. Mechanisms are immunosuppressed due to the effects of cigarette smoke.
Melanoma.Although there is evidence that smoking was associated with an increased risk of melanoma, several studies show that when are compared with nonsmokers, smokers are more likely to have metastases at first presentation have a low survival rate after diagnosis, shows and visceral metastases are prone to dying from melanoma. Smokers have a negative prognosis for melanoma due to adverse effects of smoking on the immune system, including a diminished capacity to mount an immune response to melanoma tumors transplanted.
Anogenital cancer.Several studies associate smoking with anogenital cancers (vulvar, anal, penile, vaginal, cervical). Of these five areas, three are most common: vulva, anus, penis.
Oral lesions.Many oral lesions, including lip cancer are significantly more common in smokers. Smoking is a risk factor for lip cancer, combined with excessive sun exposure, the two are synergistic. Oral cancer is linked to smoking, and associated with alcohol consumption, the risk is even higher.
Leucoplakia occurs more often in smokers, while a small percentage of patients suffering malignant transformation leucoplakie. Palace leucokeratoza nicotine smoker or exclusive palaces is seen in smokers, especially in the pipe. Represents a uniform keratosis hard palate with multiple red papules which translate nipples swollen salivary glands. Language smoker nicotine leucoplakia gloss or a similar phenomenon is observed on the back of the tongue.Gingivitis is characterized by acute necrotizing ulcerative lesions of interdental papillae associated with pain, bleeding and a fetid odor of the mouth. Exclusive smokers and appears to correlate with the amount of cigarettes smoked per day.
Nutrition.Apart from nutritional deficiencies may occur in these patients smoking has some effect on nutritional status. It was demonstrated that low levels of vitamin C in smokers. Hypovitaminosis severe risk is increased in smokers, especially those who did not supplement. Skin manifestations of vitamin C deficiency include skin hyperkeratosis, and hemorrhages perifoliculare of closed spaces, gingival hypertrophy, poor wound healing.
Acne and oral thrush.It seems that smoking has a protective effect on the appearance of acne sia afetelor mouth. It is thought that nicotine has an anti-inflammatory effect against acne.
Other skin lesions.Burger's disease (Peripheral tromboangeita) featuring skin lesions: erythema, ulceration, necrosis is closely associated with smoking. Yellow and brown stains on fingers and nails are a sign of smoking. Mustache smoker smoker is analogous to fingernails. There is a brown or yellow discoloration on the distal hair mustache mustache gray or white until the hardcore smokers.Smoking is a risk factor in the development of discoid lupus erythematosus.
Nicotinic therapyNicotine is a pharmacologically active substance, and in some patients this activity has a beneficial effect as treatment. The reported benefits of nicotine therapy for pyoderma gangrenosum, pemphigus vulgaris.Recognizing dermatologic effects of tobacco consumption may be a key element in the diagnosis of internal diseases associated with smoking. For many smokers the most visible and rapid effect of this drug as yellow teeth, wrinkles and bad breath odor are more persuasive incentives for smoking cessation than the knowledge that smoking kills.
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