Cutaneous horn Cutaneous horn is a clinical diagnosis that refers to a conical projection on the skin that is similar to a miniature horn. The base of the horn may be flat, nodular or crateriforma. Cutaneous horn is composed of compacted keratin. More histological lesions have been documented based on quantity of keratin, and histologic confirmation is often necessary to exclude malignant changes. No clinical feature to distinguish between malignant and benign lesions. The sensitivity and large favors malignant lesions.
The lesion is benign in most cases. Malignancy is present in 20% of cases, the most common type was squamous cell carcinoma. The incidence of carcinoma increases to 33% when the cutaneous horn is present on the penis. Sensitivity to the lesion is usually a sign of the possible presence of a squamous cell carcinoma. Appropriate treatment varies depending on the type of lesion. To exclude a malignant biopsy is important horn base. Neoplasms are excised. Benign lesions do not require treatment other than diagnostic biopsy. In patients with squamous cell carcinoma or basal cell carcinoma are given further consideration to follow appellant in the first three years after treatment.
Pathogenesis and causes
Horn skin rash usually appears on sun-exposed areas but may also occur on the unexposed. Resulting in the formation of hyperkeratosis develops on the surface of a horn hiperproliferative injuries. It is most commonly a benign wart or seborrheic keratosis, or may be a premalignant actinic keratoses. Over half of the croissant skin are benign, and 37% develop from actinic keratoses. Malignancy is reported to the horn in 20% of cases. Benign lesions associated with cutaneous horns include angiokeratomul, angioma, benign lichenoid keratosis, cutaneous leishmaniasis, dermatofibromul, discoid lupus, infundibulare cysts, nevus anemicus, acantomul epidermolitic, fibroids, Balan, organoid nevus, prurigo nodularis, piogenic granuloma, sebaceous adenoma, seborrheic keratosis and warts. Premalignant or malignant lesions with the potential that can give rise to a cutaneous horn include adenoacantomul, actinic keratoses, arsenic keratoses, basal cell carcinoma, Bowen's disease, Kaposi's sarcoma, malignant melanoma, Paget's disease, renal cell carcinoma, sebaceous carcinoma and squamous cell carcinoma.
Signs and symptoms
The peak incidence for cutaneous horn is to persons of 60 years. Lesions in the neoplasia to occur more often in patients over 70 years. Cutaneous horn is usually asymptomatic. Due to excessive height they can be traumatized. Trauma pain cause inflammation at the base. Rapid proliferation may also occur. Distribution of cutaneous horn usually appears on sun-exposed areas, especially on the face, nose, arms, back of hands against siureche. It is a hyperkeratotic papule with a height more than half the width of the base. Is typically a few mm in length.
Diagnosis
Diagnosis is confirmed through a biopsy. Histological examination showed keratosis can be compact or parakeratotica ortokeratotica. Is frequently associated acanthosis. The differential diagnosis is made with warts and pilomatricoma nongenitale piercing.
Treatment
Recommended treatment varies depending on the type of lesion. To exclude malignancy is essential to perform a biopsy of the horn base. In the case of benign lesions and benign biopsy is therapeutic. Aporpiate neoplasms are excised with margins. Patients with squamous cell carcinoma shows croissants should be evaluated for metastasis. Lozala destruction by cryosurgery is first-line treatment for cutaneous horn. In patients with squamous cell carcinoma or basal cell carcinoma are given further consideration to follow appellant in the first three years after treatment.
Showing posts with label Diseases and disorders. Show all posts
Showing posts with label Diseases and disorders. Show all posts
Friday, January 7, 2011
Sebaceous cysts
Sebaceous cysts The skin may appear more benign skin tumors. These formations reproduce the structure of tissue of origin, are well defined, with the tendency of local development without metastasis.
After histological structure of these tumors can be: a.Epiteliale b.Conjunctive c.Ale melanogen system
Benign tumors grow by epithelial hyperplasia, retention or mixed. Cysts are tumors formed by retention, retention and content varies depending on the nature of each. Sebaceous retention cysts are formed by secretion of the sebaceous glands which were obstructed, for various reasons, the excretory ducts. They occur in people young or adult seborrheic syndrome tend to develop a location and have an addiction Range sebaceous glands: anterior and posterior chest, scalp, face, States. It should be noted that the occurrence of these cysts is random and not of a hereditary transmission of the disease. Their appearance varies from small skin tumors subepidermice coverage with normal appearance, soft consistency, large tumors to some aspect erythematosus and live, because superinfection. Sometimes, cyst contents can drain spontaneously or after expression, leaving to eliminate a white-yellow or purulent material, foul-smelling. In evolution, sebaceous cysts can remain stationary for relatively large periods of time (years), it can be disposed of periodically or suptainfecta.
Treatment is exclusively surgical excision and target the entire gland with all the content retention.
After histological structure of these tumors can be: a.Epiteliale b.Conjunctive c.Ale melanogen system
Benign tumors grow by epithelial hyperplasia, retention or mixed. Cysts are tumors formed by retention, retention and content varies depending on the nature of each. Sebaceous retention cysts are formed by secretion of the sebaceous glands which were obstructed, for various reasons, the excretory ducts. They occur in people young or adult seborrheic syndrome tend to develop a location and have an addiction Range sebaceous glands: anterior and posterior chest, scalp, face, States. It should be noted that the occurrence of these cysts is random and not of a hereditary transmission of the disease. Their appearance varies from small skin tumors subepidermice coverage with normal appearance, soft consistency, large tumors to some aspect erythematosus and live, because superinfection. Sometimes, cyst contents can drain spontaneously or after expression, leaving to eliminate a white-yellow or purulent material, foul-smelling. In evolution, sebaceous cysts can remain stationary for relatively large periods of time (years), it can be disposed of periodically or suptainfecta.
Treatment is exclusively surgical excision and target the entire gland with all the content retention.
Mucous cyst
Mucous cyst Mucous cyst is a benign cystic lesion, the mucosa of oral cavity minor salivary glands. Mucocel preferred name because these formations do not show their epithelial wall and cysts. The lesions may be located directly under the mucosa, superficial mucocele, the submucosa-classical or chorion mucocelele deep-deep mucocele. There are two types of mucocele according to histological characteristics of the cyst wall: a mucous extravasation, police formed a wall surrounded by mucous-92% granulation tissue and a mucous retention cyst wall epithelial-8%.
Multiple accused persons affected vesicles that spontaneously break leaving superficial ulcers. They fully recover within a few days. Deeper lesions present as papules in domcare become yellow in a few months. Patients with superficial cysts require no treatment. For multiple lesions is intralesional injection of triamcinolone and indicate electrodesicare. Treatment of choice is surgical excision for deep cysts classic. Cryosurgery is a therapeutic alternative, argon and carbon dioxide laser. Patients with this disorder have an excellent prognosis, recurrence is still frequent in the absence of associated salivary gland resection.
Pathogenesis and causes
Mucous cyst formation mechanism is not entirely clear, however, suggesting a traumatic than an obstructive etiology. Location frequent side formations on the surface of the lower lip supports the role of trauma as an etiological factor. Although obstruction may play a role in the etiology of mucous cysts was shown to bind to the mucous gland duct Cobia has not determined the formation of mucocele.
Signs and symptoms
Although patients of all ages can be affected, the most frequent cases of mucous cysts occurring in those younger than 30 years. Mucous retention cysts are more common in older people. Clinical presentation varies depending on the type and location of lesions. People with superficial cysts may experience the emergence of multiple vesicles that rupture and leave shallow ulcers. These lesions completely healed in a few days. Sometimes lesions recur in the same place. Classical cysts presents as dome-shaped papules, which become bright yellow as wax and disappear in a few months. A cyst located in deep tissue shows a slow growth phase, forcing masses firm root.
Physical Exam Clinical presentation depends on the depth of the lesion. Superficial cysts: mucus accumulates just under the lining of forcing small vesicles, translucent on the soft palate, buccal mucosa and retromolara region. While these vesicles are broken spontaneously or by trauma leaving pale ulcers or erosions. Cysts classic form it is presented as a collection of material in the submucosa mucosal swelling in producing high dome, well-defined, mobile and painless. These lesions have a smooth blue. Sizes range from several mm to cm, but 75% of lesions less than 1 cm. lesion surface can become white due to numerous irregularities and rupture and healing caused by trauma or puncture.
The most common location is on the lower lip, floor of mouth, cheeks, palate, dorsal surface of the tank retromolara and language. Lesions prevent the upper lip. Most large lesions affecting the mouth floor. They are called ranula due to similarity with an anatomical feature in the form of oral cavity frog bag. This collection of mucus may extend outside the oral cavity until the top or bottom medistinul head. When mucus accumulates in deep soft tissue masses appear large, painless Pink lining.
Diagnosis
Studies: Flat-ray showed soft tissue density Sonogram shows a round-table or hipoecogena lobe with well-defined edges -Computed tomography showed a well-defined formation water density Fine-needle aspiration is used to evaluate deep lesions, it demonstrates a few histiocite mucoid fluid and inflammatory cells.
Histological examination. It shows collections with eosinophilic mucus mixed with inflammatory cells present in the mucosa superficial or deep. Roigine epithelial mucin is only a fibroblast. Formations wall is composed of granulation tissue, while it is replaced by fibrocite and inflammatory cells. It is rare to see a wall derived from epithelial minor salivary glands. Lesions shows lymphocytic infiltrates, ductal distension, root degeneration and varying degrees of fibrosis. The differential diagnosis is made with the following conditions: aphthous stomatitis, lichen planus, lipomas, mucous pemphigoid, hemangiomas, fibromas, schwannoma.
Treatment
Patients with superficial cysts only require monitoring. For multiple cysts with Intralesional triamcinolone injections are recommended and electrodesicare.
Surgical therapy. Minor salivary glands should be excised only if persistent irritation. Treatment of choice for the classic deep cysts is surgical excision, which should include immediately adjacent glandular tissue. Cryosurgery with liquid nitrogen is a therapeutic alternative. After a week necrotic area is observed in the treated area. Later that separates from healthy tissue in 1-2 weeks, showing a surface reepitelizata. Benefits include the application process simple, minor discomfort during the procedure and the low incidence of complications such as infection, bleeding. There is the possibility of recurrence.
Another therapeutic strategy is argon laser therapy. The area is completely healed in two weeks. Advantages of cruichirurgiei consist in the absence of postoperative discomfort, swelling and irritation diminished and a reduced healing time. The disadvantage is the need for specialized equipment. Using carbon dioxide laser treatment has been tried mucocelelor. Shows the advantage of precise surgical techniques, and wound lack singerarii minimal. The prognosis of these patients is good. Recurrence is common if the salivary glands were not excised.
Multiple accused persons affected vesicles that spontaneously break leaving superficial ulcers. They fully recover within a few days. Deeper lesions present as papules in domcare become yellow in a few months. Patients with superficial cysts require no treatment. For multiple lesions is intralesional injection of triamcinolone and indicate electrodesicare. Treatment of choice is surgical excision for deep cysts classic. Cryosurgery is a therapeutic alternative, argon and carbon dioxide laser. Patients with this disorder have an excellent prognosis, recurrence is still frequent in the absence of associated salivary gland resection.
Pathogenesis and causes
Mucous cyst formation mechanism is not entirely clear, however, suggesting a traumatic than an obstructive etiology. Location frequent side formations on the surface of the lower lip supports the role of trauma as an etiological factor. Although obstruction may play a role in the etiology of mucous cysts was shown to bind to the mucous gland duct Cobia has not determined the formation of mucocele.
Signs and symptoms
Although patients of all ages can be affected, the most frequent cases of mucous cysts occurring in those younger than 30 years. Mucous retention cysts are more common in older people. Clinical presentation varies depending on the type and location of lesions. People with superficial cysts may experience the emergence of multiple vesicles that rupture and leave shallow ulcers. These lesions completely healed in a few days. Sometimes lesions recur in the same place. Classical cysts presents as dome-shaped papules, which become bright yellow as wax and disappear in a few months. A cyst located in deep tissue shows a slow growth phase, forcing masses firm root.
Physical Exam Clinical presentation depends on the depth of the lesion. Superficial cysts: mucus accumulates just under the lining of forcing small vesicles, translucent on the soft palate, buccal mucosa and retromolara region. While these vesicles are broken spontaneously or by trauma leaving pale ulcers or erosions. Cysts classic form it is presented as a collection of material in the submucosa mucosal swelling in producing high dome, well-defined, mobile and painless. These lesions have a smooth blue. Sizes range from several mm to cm, but 75% of lesions less than 1 cm. lesion surface can become white due to numerous irregularities and rupture and healing caused by trauma or puncture.
The most common location is on the lower lip, floor of mouth, cheeks, palate, dorsal surface of the tank retromolara and language. Lesions prevent the upper lip. Most large lesions affecting the mouth floor. They are called ranula due to similarity with an anatomical feature in the form of oral cavity frog bag. This collection of mucus may extend outside the oral cavity until the top or bottom medistinul head. When mucus accumulates in deep soft tissue masses appear large, painless Pink lining.
Diagnosis
Studies: Flat-ray showed soft tissue density Sonogram shows a round-table or hipoecogena lobe with well-defined edges -Computed tomography showed a well-defined formation water density Fine-needle aspiration is used to evaluate deep lesions, it demonstrates a few histiocite mucoid fluid and inflammatory cells.
Histological examination. It shows collections with eosinophilic mucus mixed with inflammatory cells present in the mucosa superficial or deep. Roigine epithelial mucin is only a fibroblast. Formations wall is composed of granulation tissue, while it is replaced by fibrocite and inflammatory cells. It is rare to see a wall derived from epithelial minor salivary glands. Lesions shows lymphocytic infiltrates, ductal distension, root degeneration and varying degrees of fibrosis. The differential diagnosis is made with the following conditions: aphthous stomatitis, lichen planus, lipomas, mucous pemphigoid, hemangiomas, fibromas, schwannoma.
Treatment
Patients with superficial cysts only require monitoring. For multiple cysts with Intralesional triamcinolone injections are recommended and electrodesicare.
Surgical therapy. Minor salivary glands should be excised only if persistent irritation. Treatment of choice for the classic deep cysts is surgical excision, which should include immediately adjacent glandular tissue. Cryosurgery with liquid nitrogen is a therapeutic alternative. After a week necrotic area is observed in the treated area. Later that separates from healthy tissue in 1-2 weeks, showing a surface reepitelizata. Benefits include the application process simple, minor discomfort during the procedure and the low incidence of complications such as infection, bleeding. There is the possibility of recurrence.
Another therapeutic strategy is argon laser therapy. The area is completely healed in two weeks. Advantages of cruichirurgiei consist in the absence of postoperative discomfort, swelling and irritation diminished and a reduced healing time. The disadvantage is the need for specialized equipment. Using carbon dioxide laser treatment has been tried mucocelelor. Shows the advantage of precise surgical techniques, and wound lack singerarii minimal. The prognosis of these patients is good. Recurrence is common if the salivary glands were not excised.
Cellulite
Cellulite
* Introduction
* Symptoms of Cellulite
* Cellulite Causes and Risk Factors
* Treatment and prevention
Denotes second term cellulite problems, which have no connection between them: the cell or common aesthetic, characterized by the deposition of subcutaneous fat, and medical or infectious cellulitis.
Infectious Cellulitis
Acute infectious cellulitis is an inflammation of the skin accompanied by pain, erythema (redness), swelling and local heat. Cellulitis can be caused by external pathogenic bacteria, but also the indigenous microbiota that colonize the skin and its annexes (S.aureus, S.pyogenes). Careful anamnesis may guide the etiological diagnosis because ltcari handle single external pathogens in nature. Business continuity is a gateway for bacteria in the skin (cuts, stings, bites, surgical incisions).
S.aureus infection spreads from a limited central focus (abscess, folliculitis), while infection caused by S.pyogenes is a diffuse inflammation that expands more rapidly, the fever and lymphadenopathy isotita satellite.
Surgery for removal of fragments of safena vein may be followed by streptococcal cellulitis. Streptococci can produce cellulitis in patients with chronic lymphedema (elephantiasis). In individuals with diabetes mellitus frequently cellulite is caused by group B streptococcus and the child, periorbital cellulitis is caused by Haemophilus influenzae; H.influenzae spread of infection through vaccination may be offset.
There are other situations in which certain bacteria can cause cellulite, these infections occur in typical situations, that a careful history can identify the precise cause. For example, the cell that occur as a cat or dog bite is most commonly caused by Pasteurella multocida, Staphylococcus intermedius and Capnocytophaga canimorsus, plus a variety of anaerobic microorganisms (including the bite man). Pasteurella species are resistant to nafcillin and dicloxacina but sensitive to quinolones, tetracycline and erythromycin. Infections associated with animal or human bites can be treated successfully by administration of ampicillin and cefotixina.
P.aeruginosa penetrate the nail from an injury (when someone is standing board = 'sweaty shoe syndrome''), three types of bacteria can cause infection: ectima gangrenosum, cellulitis folliculitis, and subsequent to penetrating wounds. Treatment requires mandatory, surgical drainage of purulent collections. Empire (until the results of DST) can be used an aminoglycoside, a third-generation cephalosporin to a penicillin (semisynthetic) or a fluoroquinolone.
Incapacitated patients hospitalized and immunocompromised people (HIV) often suffer from the cells with gram-negative bacilli (including P.aeruginosa). In such cases, we recommend to culture and sensitivity testing because it is a multidrug resistant hospital flora.
From the above, we notice that the etiology of cellulite can be determined by history, where there is a solution of continuity, samples for culture can, in some cases is difficult to identify the causative agent as the needle punctures the center of lesion will lead to a positive culture in only one fifth of cases. Lesion size does not correlate with an increased number of bacteria, inflamtia axtinzandu is through the action of microbial toxins or inflammatory mediators of the host.
Risk factors for cellulitis
People who have an increased risk of cellulitis are those who suffer from some diseases:
-Diabetes -Poor peripheral circulation Chronic hepatitis, liver cirrhosis, Skin-disease-eczema, psoriasis, diseases that cause skin lesions: chicken pox or acne Insect-sting -Use of corticosteroids or immunosuppressive drugs
* Introduction
* Symptoms of Cellulite
* Cellulite Causes and Risk Factors
* Treatment and prevention
Denotes second term cellulite problems, which have no connection between them: the cell or common aesthetic, characterized by the deposition of subcutaneous fat, and medical or infectious cellulitis.
Infectious Cellulitis
Acute infectious cellulitis is an inflammation of the skin accompanied by pain, erythema (redness), swelling and local heat. Cellulitis can be caused by external pathogenic bacteria, but also the indigenous microbiota that colonize the skin and its annexes (S.aureus, S.pyogenes). Careful anamnesis may guide the etiological diagnosis because ltcari handle single external pathogens in nature. Business continuity is a gateway for bacteria in the skin (cuts, stings, bites, surgical incisions).
S.aureus infection spreads from a limited central focus (abscess, folliculitis), while infection caused by S.pyogenes is a diffuse inflammation that expands more rapidly, the fever and lymphadenopathy isotita satellite.
Surgery for removal of fragments of safena vein may be followed by streptococcal cellulitis. Streptococci can produce cellulitis in patients with chronic lymphedema (elephantiasis). In individuals with diabetes mellitus frequently cellulite is caused by group B streptococcus and the child, periorbital cellulitis is caused by Haemophilus influenzae; H.influenzae spread of infection through vaccination may be offset.
There are other situations in which certain bacteria can cause cellulite, these infections occur in typical situations, that a careful history can identify the precise cause. For example, the cell that occur as a cat or dog bite is most commonly caused by Pasteurella multocida, Staphylococcus intermedius and Capnocytophaga canimorsus, plus a variety of anaerobic microorganisms (including the bite man). Pasteurella species are resistant to nafcillin and dicloxacina but sensitive to quinolones, tetracycline and erythromycin. Infections associated with animal or human bites can be treated successfully by administration of ampicillin and cefotixina.
P.aeruginosa penetrate the nail from an injury (when someone is standing board = 'sweaty shoe syndrome''), three types of bacteria can cause infection: ectima gangrenosum, cellulitis folliculitis, and subsequent to penetrating wounds. Treatment requires mandatory, surgical drainage of purulent collections. Empire (until the results of DST) can be used an aminoglycoside, a third-generation cephalosporin to a penicillin (semisynthetic) or a fluoroquinolone.
Incapacitated patients hospitalized and immunocompromised people (HIV) often suffer from the cells with gram-negative bacilli (including P.aeruginosa). In such cases, we recommend to culture and sensitivity testing because it is a multidrug resistant hospital flora.
From the above, we notice that the etiology of cellulite can be determined by history, where there is a solution of continuity, samples for culture can, in some cases is difficult to identify the causative agent as the needle punctures the center of lesion will lead to a positive culture in only one fifth of cases. Lesion size does not correlate with an increased number of bacteria, inflamtia axtinzandu is through the action of microbial toxins or inflammatory mediators of the host.
Risk factors for cellulitis
People who have an increased risk of cellulitis are those who suffer from some diseases:
-Diabetes -Poor peripheral circulation Chronic hepatitis, liver cirrhosis, Skin-disease-eczema, psoriasis, diseases that cause skin lesions: chicken pox or acne Insect-sting -Use of corticosteroids or immunosuppressive drugs
Squamous cell carcinoma
Squamous cell carcinoma
* Introduction
* Signs and symptoms
* Diagnosis
* Treatment
Squamous cell carcinoma is the second form of skin cancer and has over 20% of cutaneous neoplasms. It appears on sun-exposed skin in people of middle or advanced age. Most squamous cell carcinomas are immediately identified and removed through small surgical. Larger and more severe lesions require aggressive surgery, radiation therapy or both. High-risk squamous cell carcinoma carries a significant risk of metastasis and thus require careful evaluation and treatment.
One cause for the increased incidence of squamous cell carcinoma is due to sun exposure. It postulates that rarefied ozone layer can increase exposure to ultraviolet light. Other contributing factors include the increasing incidence of old age. In addition the number of patients with immunosuppressive therapy used in organ transplantation and various rheumatologic and dermatologic diseases is increasing. Most squamous cell carcinomas are treated and produce few sequelae. A subset of high risk lesions determine the increased morbidity and mortality associated with this type of cancer. These injuries can cause extensive tissue destruction and their removal may leave a significant cosmetic deformity. The risk of metastasis is 2-6%, though rates have been described and 47% when perineural invasion. Lymphatic metastases are associated with significant morbidity. Once installed metastasis to lung disease is incurable.
Non-surgical options for treatment of squamous cell carcinoma is chemotherapy, immunomodulatory topical photodynamic therapy, radiotherapy and systemic chemotherapy. Radiotherapy is the choice for patients who can not apply and is adjuvant surgery for those with metastases. Most squamous cell carcinomas can be treated by surgical or destructive methods, with high rates vinecare. The use cryotherapy, and curettage electrodesicarea, conventional excision with margins, Mohs surgery. Because squamous cell carcinoma is a lesion that may reverse the cause of death and metastasis as it carries a negative prognosis, tumor removal should be attempted at first presentation to the doctor.
Low-risk tumors are healed surgical therapy, however patients who develop squamous cell carcinoma u have 40% risk of developing other squamous tumors in the next two years. The risk is increased as the patient progresses in age. Therefore patients should be assessed every 6-12 months. Patients with high risk tumors require examination of skin and lymph nodes within 3-6 months for at least 2 years after diagnosis.
Pathogenesis and causes
Squamous cell carcinoma is a malignant tumor of epidermal keratinocytes. Some cases occur de novo in the absence of precursor lesions, however, most tumors arise from precancerous lesions known as actinic keratoses. Patients with multiple actinic keratoses are at increased risk of developing tumors. Squamous cell carcinoma is able to infiltrate local, to expand the regional lymph nodes and distant metastases to determine, especially in the lungs.
The main reason is the cumulative exposure to sunlight during their lifetime. Other causes include: Exposure to ultraviolet therapy with psoralen and UV Therapy -People with skin type I and II -Ionizing radiation, chemical carcinogens-arsenic (heavy water, Chinese herbs) -Failure of DNA repair-xeroderma pigmentosum -Iatrogenic immunosuppression: sunlight, organ transplantation HPV-infection, chronic inflammation: Marjolin ulcer, dystrophic epidermolysis bullosa.
Pathological conditions that predispose to the development of squamous cell carcinoma: -Burns, venous ulcers, lymphedema, lupus erythematosus, discoid -Erosive oral lichen planus, keratodermie mutilating, Necrobiosis lipoidica -Osteomyelitis, acne Conglobata, hidraadenita suppurativa Dissecans-cellulitis of the scalp, lupus vulgaris, limfogranulomul venerian, -Inguinal granuloma, chronic deep fungal infections Oculocutanat-albinism, xeroderma pigmentosum, dyskeratosis congenital -Porokeratoza, nevus sebaceous syndrome, KID.
General risk factors associated with squamous cell carcinoma development include: Over 50 years-old, male -White skin, blond hair, blue eyes, green or gray -Skin that burns easily in the sun-type I and II -Areas near the equator, history of previous skin cancer nonmelanozic Exposure to ultraviolet: recreational, medical or artificial Exposure to chemical carcinogens, exposure to ionizing Immunosuppression, chronic, healing of chronic conditions, human papillomavirus.
* Introduction
* Signs and symptoms
* Diagnosis
* Treatment
Squamous cell carcinoma is the second form of skin cancer and has over 20% of cutaneous neoplasms. It appears on sun-exposed skin in people of middle or advanced age. Most squamous cell carcinomas are immediately identified and removed through small surgical. Larger and more severe lesions require aggressive surgery, radiation therapy or both. High-risk squamous cell carcinoma carries a significant risk of metastasis and thus require careful evaluation and treatment.
One cause for the increased incidence of squamous cell carcinoma is due to sun exposure. It postulates that rarefied ozone layer can increase exposure to ultraviolet light. Other contributing factors include the increasing incidence of old age. In addition the number of patients with immunosuppressive therapy used in organ transplantation and various rheumatologic and dermatologic diseases is increasing. Most squamous cell carcinomas are treated and produce few sequelae. A subset of high risk lesions determine the increased morbidity and mortality associated with this type of cancer. These injuries can cause extensive tissue destruction and their removal may leave a significant cosmetic deformity. The risk of metastasis is 2-6%, though rates have been described and 47% when perineural invasion. Lymphatic metastases are associated with significant morbidity. Once installed metastasis to lung disease is incurable.
Non-surgical options for treatment of squamous cell carcinoma is chemotherapy, immunomodulatory topical photodynamic therapy, radiotherapy and systemic chemotherapy. Radiotherapy is the choice for patients who can not apply and is adjuvant surgery for those with metastases. Most squamous cell carcinomas can be treated by surgical or destructive methods, with high rates vinecare. The use cryotherapy, and curettage electrodesicarea, conventional excision with margins, Mohs surgery. Because squamous cell carcinoma is a lesion that may reverse the cause of death and metastasis as it carries a negative prognosis, tumor removal should be attempted at first presentation to the doctor.
Low-risk tumors are healed surgical therapy, however patients who develop squamous cell carcinoma u have 40% risk of developing other squamous tumors in the next two years. The risk is increased as the patient progresses in age. Therefore patients should be assessed every 6-12 months. Patients with high risk tumors require examination of skin and lymph nodes within 3-6 months for at least 2 years after diagnosis.
Pathogenesis and causes
Squamous cell carcinoma is a malignant tumor of epidermal keratinocytes. Some cases occur de novo in the absence of precursor lesions, however, most tumors arise from precancerous lesions known as actinic keratoses. Patients with multiple actinic keratoses are at increased risk of developing tumors. Squamous cell carcinoma is able to infiltrate local, to expand the regional lymph nodes and distant metastases to determine, especially in the lungs.
The main reason is the cumulative exposure to sunlight during their lifetime. Other causes include: Exposure to ultraviolet therapy with psoralen and UV Therapy -People with skin type I and II -Ionizing radiation, chemical carcinogens-arsenic (heavy water, Chinese herbs) -Failure of DNA repair-xeroderma pigmentosum -Iatrogenic immunosuppression: sunlight, organ transplantation HPV-infection, chronic inflammation: Marjolin ulcer, dystrophic epidermolysis bullosa.
Pathological conditions that predispose to the development of squamous cell carcinoma: -Burns, venous ulcers, lymphedema, lupus erythematosus, discoid -Erosive oral lichen planus, keratodermie mutilating, Necrobiosis lipoidica -Osteomyelitis, acne Conglobata, hidraadenita suppurativa Dissecans-cellulitis of the scalp, lupus vulgaris, limfogranulomul venerian, -Inguinal granuloma, chronic deep fungal infections Oculocutanat-albinism, xeroderma pigmentosum, dyskeratosis congenital -Porokeratoza, nevus sebaceous syndrome, KID.
General risk factors associated with squamous cell carcinoma development include: Over 50 years-old, male -White skin, blond hair, blue eyes, green or gray -Skin that burns easily in the sun-type I and II -Areas near the equator, history of previous skin cancer nonmelanozic Exposure to ultraviolet: recreational, medical or artificial Exposure to chemical carcinogens, exposure to ionizing Immunosuppression, chronic, healing of chronic conditions, human papillomavirus.
Oral Candidiasis
Candidiasis describes a group of fungal infections involving skin and mucous membranes. Infection is caused by species of Candida, especially Candida albicans. The most common classification of oral candidiasis infection divided into four types including acute pseudomembranous candidosis, acute atrophic candidiasis, chronic candidiasis hyperplasia and chronic atrophic candidiasis. Hyperplasia, chronic candidiasis was then divided in 4 groups depending on location and endocrine involvement: chronic oral candidiasis (leucoplakia candozica), endocrine candidiasis syndrome, chronic localized mucocutaneous candidiasis and diffuse chronic candidiasis. Erythematous candidiasis is the term used for red lesions of candidiasis.
Candidiasis is a disease predominantly of older people or those immunosuppressed by medication chemotherapy, HIV infection, long-term antibiotic therapy, chronic diseases: diabetes, immune deficiencies, neoplasms. If corticosteroids or antibiotics is the cause of candidiasis is advisable to reduce the dose or change in treatment. If the fund because of the condition is not known or can not be avoided it is recommended systemic or topical antifungal therapy. In patients with severe immunosuppression is important to prevent extension of infection and colonization of other areas. Oropharyngeal region is the main source of colonization and allow secondary spread of infection. Resistance to azole antifungals is a well known problem, especially in people with HIV infection and other immunosuppressive conditions. We recommend changing antifungal used. The prognosis is good for most immunocompetent hosts, but in immunocompromised patients is common antifungal resistance.
The pathogenesis of oral candidiasis Candida albicans is the organism most predominant cause thrush. Other species, including Candida krusei occur in severely immunocompromised persons. Candida glabrata is an issue in the growth of oropharyngeal candidiasis in patients receiving radiation therapy for head and neck cancer. In patients with HIV have been known and new species such as Candida dubliniensis and Candida inconspicua. Candida albicans is a harmless commensal of the human body and especially your mouth at over 50% of the population is still very favorable terms opportunistic pathogen. One such alteration is favoring the normal bacterial flora of oral cavity or reducing immune defense.
Acute pseudomembranous candidiasis. It is seen in healthy infants or those in which treatment with antibiotics, corticosteroids, or xerostomia altering oral microbial flora. Complications occasionally use corticosteroid inhalers. Immunodeficiencies, HIV infection, immunosuppressive therapy, leukemia, lymphoma, cancer and diabetes are more prone to candida infection.
Erythematous candidiasis. It can cause ulcers and fissures on the tongue and especially in patients with broad-spectrum antibiotic therapy. It can also be a feature of HIV infection. Median rhomboid glossitis is a red patch on the middle of the face back in two thirds of the tongue before and is mostly seen in smokers and those with HIV.
Chronic mucocutaneous candidiasis. Describes a group of rare syndromes that include an immune defect, in which persistent mucocutaneous candidiasis responds poorly to topical treatment. In general how to be more severe candidiasis is more likely to both identify an immunological defect.
Causes and risk factors for oral candidiasis Family members in Candidiasis Candida are causative organisms. Secretion of antimicrobial proteins and peptides is low in the saliva of patients with oral candidiasis.
Factors which favor candidiasis include: Carrier-state is more common in women than in men and in summer months High-rate carrier status is seen in immunocompromised, blood group antigens A and lack of salivary secretion Carrier-state is higher for saliva acid Xerostomia increases the carrier-state -Use of psychotropic drugs that cause dry mouth Micelles, the amount is increased during sleep and decreases in food and brushing teeth Smoking increases the state-run carrier, increases the risk of infection in people with HIV, especially cause multifocal candidosis and median rhomboid glossitis Therapy with tetracycline Oral microbial flora-imbalance by bacterial suppression, impaired salivary flow, immune defects -Topical corticosteroid therapy, systemic or adhering -Diabetes mellitus.
Candidiasis is a disease predominantly of older people or those immunosuppressed by medication chemotherapy, HIV infection, long-term antibiotic therapy, chronic diseases: diabetes, immune deficiencies, neoplasms. If corticosteroids or antibiotics is the cause of candidiasis is advisable to reduce the dose or change in treatment. If the fund because of the condition is not known or can not be avoided it is recommended systemic or topical antifungal therapy. In patients with severe immunosuppression is important to prevent extension of infection and colonization of other areas. Oropharyngeal region is the main source of colonization and allow secondary spread of infection. Resistance to azole antifungals is a well known problem, especially in people with HIV infection and other immunosuppressive conditions. We recommend changing antifungal used. The prognosis is good for most immunocompetent hosts, but in immunocompromised patients is common antifungal resistance.
The pathogenesis of oral candidiasis Candida albicans is the organism most predominant cause thrush. Other species, including Candida krusei occur in severely immunocompromised persons. Candida glabrata is an issue in the growth of oropharyngeal candidiasis in patients receiving radiation therapy for head and neck cancer. In patients with HIV have been known and new species such as Candida dubliniensis and Candida inconspicua. Candida albicans is a harmless commensal of the human body and especially your mouth at over 50% of the population is still very favorable terms opportunistic pathogen. One such alteration is favoring the normal bacterial flora of oral cavity or reducing immune defense.
Acute pseudomembranous candidiasis. It is seen in healthy infants or those in which treatment with antibiotics, corticosteroids, or xerostomia altering oral microbial flora. Complications occasionally use corticosteroid inhalers. Immunodeficiencies, HIV infection, immunosuppressive therapy, leukemia, lymphoma, cancer and diabetes are more prone to candida infection.
Erythematous candidiasis. It can cause ulcers and fissures on the tongue and especially in patients with broad-spectrum antibiotic therapy. It can also be a feature of HIV infection. Median rhomboid glossitis is a red patch on the middle of the face back in two thirds of the tongue before and is mostly seen in smokers and those with HIV.
Chronic mucocutaneous candidiasis. Describes a group of rare syndromes that include an immune defect, in which persistent mucocutaneous candidiasis responds poorly to topical treatment. In general how to be more severe candidiasis is more likely to both identify an immunological defect.
Causes and risk factors for oral candidiasis Family members in Candidiasis Candida are causative organisms. Secretion of antimicrobial proteins and peptides is low in the saliva of patients with oral candidiasis.
Factors which favor candidiasis include: Carrier-state is more common in women than in men and in summer months High-rate carrier status is seen in immunocompromised, blood group antigens A and lack of salivary secretion Carrier-state is higher for saliva acid Xerostomia increases the carrier-state -Use of psychotropic drugs that cause dry mouth Micelles, the amount is increased during sleep and decreases in food and brushing teeth Smoking increases the state-run carrier, increases the risk of infection in people with HIV, especially cause multifocal candidosis and median rhomboid glossitis Therapy with tetracycline Oral microbial flora-imbalance by bacterial suppression, impaired salivary flow, immune defects -Topical corticosteroid therapy, systemic or adhering -Diabetes mellitus.
Skin Cancer
What is the skin cancer?
Skin Cancer (excessive proliferation of skin cells) usually occur on sun-exposed skin portions.
There are three main types of skin cancer: basal cell carcinoma, squamous cell carcinoma and melanoma. The first two forms have a slow and are treatable in most patients, especially if detected early. In contrast, melanoma is the most serious form, because it affects the deeper layers of skin and shows the greatest potential for further extension to other body tissues. Incidence of skin cancer is increasing.
To reduce the risk of skin cancer, avoid or limit excessive exposure to ultraviolet rays. Detected in its early stages, most cancers can be treated successfully.
Skin Cancer (excessive proliferation of skin cells) usually occur on sun-exposed skin portions.
There are three main types of skin cancer: basal cell carcinoma, squamous cell carcinoma and melanoma. The first two forms have a slow and are treatable in most patients, especially if detected early. In contrast, melanoma is the most serious form, because it affects the deeper layers of skin and shows the greatest potential for further extension to other body tissues. Incidence of skin cancer is increasing.
To reduce the risk of skin cancer, avoid or limit excessive exposure to ultraviolet rays. Detected in its early stages, most cancers can be treated successfully.
Pilonidal disease
What is Pilonidal disease?
Pilonidal disease is a chronic skin infection sacrococcigeana region. It develops as a cyst, pilonidal cyst on the sacrum at the base line interfesiere. It appears initially that one or more small sinuses that can come out hairs. Pilonidal cyst is painful, making walking painful sitting position and adoption. Frequently infected, eliminating pus and blood.
Pilonidal cyst is often encountered in young people between the ages of 15 and 35 years after puberty when sex hormones affect the glands pilosebacee and modify the normal development of body hair. Development of pilonidal disease is rare after 40 years. It is common in obese people.
Pilonidal disease incidence rate is 0. 7%. Men are affected four times more often than women. Onset occurs at younger ages in women due to puberty earlier installation. Incidence is also affected by hair characteristics such as their growth rate, thickness, roughness. White persons are affected more often than those belonging to African or Asian race. Associated risk factors are prolonged in seated, excessive sweating, poor hygiene, friction at this level, obesity and trauma.
Symptoms and signs vary from simple holes in the skin up to a large mass, painful. Common area will drain fluid that may be clear layout, bleeding or pus. The infection affected area becomes red, sensitive, and foul-smelling pus removed. The infection can cause fever and installation, grata and general malaise.
Treatment depends on the clinical disease. An acute abscess treated by incision and drainage to release the pus and reduce swelling and pain. A pilonidal sinus excision will require chronic or open surgery. Recurrent disease should be treated surgically. Procedures vary from opening until sinus excision and possible closure by flaps. Operations require extended periods of recovery. If the wound is left open will require compresses and bandages to keep it clean. Although you several weeks during healing, the success rate is higher for open wounds.
Pathogenesis
After the onset of puberty, sex hormones affect pilosebacee glands and hair follicles become secondary distensionati with keratin. As a result of folliculitis develops that causes swelling and follicular occlusion. Infected follicles extend into the subcutaneous tissue and break forcing pilonidal abscess. The result is a sinus paths leading deep into the subcutaneous space.
In 90% of cases of sinus tract is centripetal direction corresponding with the direction of hair growth. Follicle is usually involved at 5-8 cm from the anus. In rare cases the sinus is located caudal and is found at 4-5 cm from the anus. Lateral sinus is created when communicating pilonidal abscess spontaneously drains to the skin surface. Santa primitive sinus tract is a tube epithelizant buttocks. A sinus tract becomes grainy side that opens. Hairs pilonidal sinus involved are attracted by movement and friction buttocks every time or go sit down.
Medical physical examination shows a bunch of hair that rises from the buttocks region. The hair that is sequestered type determines the installation of a foreign body reaction and infection. Rare foreign bodies other than human hair can cause this disease. Were reported kidnapped in the hair not from the host and bird feathers were feather out of a blanket.
Pilonidal sinus can occur in many parts of the body but most commonly is found in the region sacrococcigeana at the top of the line interfesiere at 5 cm from the anus.
Predisposing factors for the onset of pilonidal disease: Pubertal-age-sex hormone involvement -Male sex, poor hygiene Excessive-sweating, acne -Obese people, the trauma region Adoption-friction and prolonged sitting position.
Pilonidal disease is a chronic skin infection sacrococcigeana region. It develops as a cyst, pilonidal cyst on the sacrum at the base line interfesiere. It appears initially that one or more small sinuses that can come out hairs. Pilonidal cyst is painful, making walking painful sitting position and adoption. Frequently infected, eliminating pus and blood.
Pilonidal cyst is often encountered in young people between the ages of 15 and 35 years after puberty when sex hormones affect the glands pilosebacee and modify the normal development of body hair. Development of pilonidal disease is rare after 40 years. It is common in obese people.
Pilonidal disease incidence rate is 0. 7%. Men are affected four times more often than women. Onset occurs at younger ages in women due to puberty earlier installation. Incidence is also affected by hair characteristics such as their growth rate, thickness, roughness. White persons are affected more often than those belonging to African or Asian race. Associated risk factors are prolonged in seated, excessive sweating, poor hygiene, friction at this level, obesity and trauma.
Symptoms and signs vary from simple holes in the skin up to a large mass, painful. Common area will drain fluid that may be clear layout, bleeding or pus. The infection affected area becomes red, sensitive, and foul-smelling pus removed. The infection can cause fever and installation, grata and general malaise.
Treatment depends on the clinical disease. An acute abscess treated by incision and drainage to release the pus and reduce swelling and pain. A pilonidal sinus excision will require chronic or open surgery. Recurrent disease should be treated surgically. Procedures vary from opening until sinus excision and possible closure by flaps. Operations require extended periods of recovery. If the wound is left open will require compresses and bandages to keep it clean. Although you several weeks during healing, the success rate is higher for open wounds.
Pathogenesis
After the onset of puberty, sex hormones affect pilosebacee glands and hair follicles become secondary distensionati with keratin. As a result of folliculitis develops that causes swelling and follicular occlusion. Infected follicles extend into the subcutaneous tissue and break forcing pilonidal abscess. The result is a sinus paths leading deep into the subcutaneous space.
In 90% of cases of sinus tract is centripetal direction corresponding with the direction of hair growth. Follicle is usually involved at 5-8 cm from the anus. In rare cases the sinus is located caudal and is found at 4-5 cm from the anus. Lateral sinus is created when communicating pilonidal abscess spontaneously drains to the skin surface. Santa primitive sinus tract is a tube epithelizant buttocks. A sinus tract becomes grainy side that opens. Hairs pilonidal sinus involved are attracted by movement and friction buttocks every time or go sit down.
Medical physical examination shows a bunch of hair that rises from the buttocks region. The hair that is sequestered type determines the installation of a foreign body reaction and infection. Rare foreign bodies other than human hair can cause this disease. Were reported kidnapped in the hair not from the host and bird feathers were feather out of a blanket.
Pilonidal sinus can occur in many parts of the body but most commonly is found in the region sacrococcigeana at the top of the line interfesiere at 5 cm from the anus.
Predisposing factors for the onset of pilonidal disease: Pubertal-age-sex hormone involvement -Male sex, poor hygiene Excessive-sweating, acne -Obese people, the trauma region Adoption-friction and prolonged sitting position.
Bullous disease of dialysis
Bullous disease of dialysis Bullous disease of dialysis is a skin fragility syndrome and veziculizare. The skin lesions are clinically and histologically similar to porphyria cutanea tarda. Lesions typically occur on sun-exposed skin on the dorsal hands in individuals who are treated with continuous dialysis for chronic renal failure. Mecanobuloasa disease was observed in patients with end stage renal disease treated by chronic ambulatory peritoneal dialysis and hemodialysis.
The level of porphyrins in urine and stool is normal. The level is slightly elevated plasma porphyrins excluding true that porphyria patients anefrici coarse determine abnormal values.
These skin lesions cause cosmetic discomfort and interfere with the use of hands. May become painful and can scar secondarily infected but are not life threatening.
Causes and Risk Factors Bullous dermatosis of dialysis etiology remains unclear, although the propensity worsening lesions and fragility of sun exposure suggests a phototoxic mechanism.
Since the level of plasma porphyrins in people with chronic renal failure is a little high, photosensitisation the porphyrins may play an important role in some cases. However photosensitisation porphyrins seems to be the main cause because most dialysis patients with similar levels of porphyrins and serum fotocutanate not develop lesions. Speculation that fotosensibilizantii during dialysis (produced emanate from pipes) are responsible remains unproven. Concomitant use of phototoxic potential therapeutic agents (furosemide) can not be identified in most cases. Effects of high concentrations of aluminum in therapeutic sources or external sources of heme biosynthesis enzymes, leading to overproduction of porphyrins has been suggested as possible etiology, but still unproven.
Signs and symptoms People with chronic renal dialysis bullous dermatosis presenting these lesions develop after months or years of maintenance dialysis regimes. The lesions are more florid after exposure to sunlight, patients still do not realize the role of sunlight in causing damage than when they start to become painful.
Physical Exam: Vesicles and hemorrhagic fluid-filled blisters or erosions exuding clear and mostly occur on the dorsal of the hands, scalp, face and neck. Healing of crusted erosions leave atrophic scars. Milia, pigmentation and hypertrichosis occurred more frequently.
Diagnosis Laboratory studies: To exclude porphyria true will evaluate plasma porphyrins. The test may be abnormal coarse a person with compromised renal function.
Histological examination: Microscopic examination of biopsy samples from a vesicle showed subepidermice bubbles can not be distinguished from those of true porphyria, with oedematous dermal papillae and perivascular lymphocytic infiltrate. Ultrastructural studies show thickening of the walls of dermal venules and basal lamina junction due dermoepidermice replicated to degranulate mast cells and hyaline masses granulofilamentos secreted by fibroblasts. Examination by direct immunofluorescence shows the presence of immunoglobulin G and immunoglobulin A versatile, M, complement and fibrin around dermal venules.
The differential diagnosis is made with the following disorders: bullous pemphigoid, epidermolysis bullosa, bullous lupus erythematosus, porphyria cutanea tarda.
Treatment Any photosensitiser drug that the patient could use it to be identified and stopped. Oral N-acetylcysteine used as a healing vesicle determine radiation protection studies in patient groups. Avoiding sunlight, using sunscreens and avoiding mechanical trauma may help reduce the severity of injuries. For bubbles secondarily infected may need treatment with antibiotics.
The level of porphyrins in urine and stool is normal. The level is slightly elevated plasma porphyrins excluding true that porphyria patients anefrici coarse determine abnormal values.
These skin lesions cause cosmetic discomfort and interfere with the use of hands. May become painful and can scar secondarily infected but are not life threatening.
Causes and Risk Factors Bullous dermatosis of dialysis etiology remains unclear, although the propensity worsening lesions and fragility of sun exposure suggests a phototoxic mechanism.
Since the level of plasma porphyrins in people with chronic renal failure is a little high, photosensitisation the porphyrins may play an important role in some cases. However photosensitisation porphyrins seems to be the main cause because most dialysis patients with similar levels of porphyrins and serum fotocutanate not develop lesions. Speculation that fotosensibilizantii during dialysis (produced emanate from pipes) are responsible remains unproven. Concomitant use of phototoxic potential therapeutic agents (furosemide) can not be identified in most cases. Effects of high concentrations of aluminum in therapeutic sources or external sources of heme biosynthesis enzymes, leading to overproduction of porphyrins has been suggested as possible etiology, but still unproven.
Signs and symptoms People with chronic renal dialysis bullous dermatosis presenting these lesions develop after months or years of maintenance dialysis regimes. The lesions are more florid after exposure to sunlight, patients still do not realize the role of sunlight in causing damage than when they start to become painful.
Physical Exam: Vesicles and hemorrhagic fluid-filled blisters or erosions exuding clear and mostly occur on the dorsal of the hands, scalp, face and neck. Healing of crusted erosions leave atrophic scars. Milia, pigmentation and hypertrichosis occurred more frequently.
Diagnosis Laboratory studies: To exclude porphyria true will evaluate plasma porphyrins. The test may be abnormal coarse a person with compromised renal function.
Histological examination: Microscopic examination of biopsy samples from a vesicle showed subepidermice bubbles can not be distinguished from those of true porphyria, with oedematous dermal papillae and perivascular lymphocytic infiltrate. Ultrastructural studies show thickening of the walls of dermal venules and basal lamina junction due dermoepidermice replicated to degranulate mast cells and hyaline masses granulofilamentos secreted by fibroblasts. Examination by direct immunofluorescence shows the presence of immunoglobulin G and immunoglobulin A versatile, M, complement and fibrin around dermal venules.
The differential diagnosis is made with the following disorders: bullous pemphigoid, epidermolysis bullosa, bullous lupus erythematosus, porphyria cutanea tarda.
Treatment Any photosensitiser drug that the patient could use it to be identified and stopped. Oral N-acetylcysteine used as a healing vesicle determine radiation protection studies in patient groups. Avoiding sunlight, using sunscreens and avoiding mechanical trauma may help reduce the severity of injuries. For bubbles secondarily infected may need treatment with antibiotics.
Peripheral xerotica Balance
Peripheral xerotica Balance Lichen sclera is a chronic inflammatory dermatosis, sclerosing, progressive, etiology unclear. Most cases of lichen scleral involve the genitals. In men, genital damage is known as the balance xerotica Peripheral or penile lichen sclera.
Penis changes are insignificant debut. While these include changes in color and texture. These include itching, dysuria, painful erections, with or without urethritis debacluri. The penis shows phimosis and paraphimosis. The etiology of the disease is unknown but believed to be multifactorial. The following factors are incriminated: circumcision after 13 years, hormonal factors, autoimmune diseases, genetic factors and human papilloma virus present.
Effective treatment has not been discovered yet. Some therapies with varying degrees of success have been tested: topical or intralesional steroids, tacrolimus, testosterone topical etretinat, carbon dioxide laser. And surgical methods are used for signs and symptoms of urethral stenosis or malignant change. As the disease progresses retrograde retention of urine occurs with impaired renal parenchyma. Erectile painful intercourse life limiting. Neoplasms have been reported and lesions that develop in the penis. Lichen sclera of the penis is chronic and progressive regression or improvement of the affected areas is unusual.
Pathogenesis and causes
The etiology of penile lichen sclera is unknown but is believed to be multifactorial. The occurrence of several factors contributing balanitei xerotice obstructive disease:
Circumcision after 13 years / uncircumcised status. The involvement of this factor may be due to the effect known as the Koebner or isomorphic phenomenon. What ami large majority of male genitalia inflammatory dermatoses, including lichen sclera occur in uncircumcised men, or belated circumscribed. The foreskin may promote chronic irritation or serves to maintain a favorable environment for infectious agents. Such chronic infection may initiate changes seen in lichen sclera.
Hormonal factors. Hormonal influences in the development of lichen have been incriminated much sclera, especially in the form of vulvar female. Most studies have focused on the role of testosterone in the pathogenesis of penile lesions. Vulvar lichen sclera in children resolves pubertal onset of menarche and increasing testosterone in genital skin. In addition, adults were evaluated for low levels of testosterone, androstenedione and dihidrostestosteron comparable to control subjects. Defect can be the altered function of 5-alpha reductase.
Autoimmune diseases. Many autoantibodies, including antinuclear, antimicrosomali thyroid, gastric parietal anticelule, anticortex adrenal, smooth and antimitochondrial antimuschi were detected in patients with lichen sclera. Vitiligo, thyroid disease, diabetes and alopecia areata have been reported frequently with lichen sclera.
Genetics. Lichen sclera has been reported in families, including twins, siblings, mothers and daughters and brother and sister. However it has not been identified yet heredity.
The human papilloma virus. This virus has been reported it in some cases of penile lichen sclera. If lichen is secondary infection, or it promotes the appearance is still a fact not disputed.
Signs and symptoms
Peripheral xerotica Balance is more common in middle-aged men. Early in the disease, penile lichen sclera is relatively asymptomatic with only a few noticeable changes. Later symptoms are more obvious with the passage of years, equipment and changes color and texture. Early symptoms are more prevalent in uncircumcised patients.
The clinical picture includes: -Itching, burning, dysuria Glans penis, hypoesthesia Painful erections, impaired sexual function Strength-reducing urinary bladder and jet size Debacluri-with or without urethritis.
Symptoms of late stage Peripheral xerotica balanitei include: Phimosis-unable-to decalota glans Paraphimosis-unable-to recalota glans. Development of squamous cell carcinoma in individuals with multifocal scleral and atrophic lichen of the penis and infection with hepatitis C were reported.
Physical examination. Lichen sclera shows only subtle physical changes in the initial phase, nonspecific erythema, mild hypopigmentation. As the condition progresses, multiple erythematous papules appear discreet or patches that merge intro or splash plate or purple-white ivories. The lesions affect mainly the glans and foreskin. Frenulum, urethral meatus, fossa naviculara, sheath of penis and perianal area may be involved. A sclerotic white ring in place at this stage the foreskin is diagnostic. Erosion, cracks, spots, bubbles and sero-haemorrhagic teleangiectaziile gland are reported, although unusual.
With progression of the disease may become adherent to the glans foreskin. Coronary groove and sclerotic frenulum may be destroyed. Urinary meatus may be al until urinary retention. Urinary retention can be severe to cause retrograde ureterohidronefroza. Significant collapse of the urinary meatus may lead to retrograde urethral blockage. Phimosis and paraphimosis in uncircumcised patients may occur in the late stage.
Diagnosis
Histological examination. Sclera genital lichen histological elements are similar to those of nongenitale form. These include ortokeratoza, hyperkeratosis with follicular plugs, stoppers without hyperkeratosis, atrophy of the malpighian layer, hydropic degeneration of basal and splicing dermoepidermica dressed. Follicular plugs are not apparent in affected mucosa. Note the significant edema and homogenization of dermal collagen in the upper dermis with dilated blood and lymph vessels and loss of elastic fibers. The inflammatory infiltrate includes lymphocytes, plasma cells, histiocite in the middle dermis, it is less pronounced in advanced lesions. The differential diagnosis is made with the following conditions: Balan circumscribed plasmacytoma, mucosal candidiasis,'s eritroplazia Queyrat, lichen planus, psoriasis boards, phimosis, Balan.
Treatment
There is no specific treatment to deliver on all patients. Mode with intramuscular penicillin has proven benefits meet studio, improved sensitivity, itching and inflammatory changes in three weeks. Therapy for patients is more aggressive circumscribed. The following regimens have shown benefit in varying degrees: intrelezionali and topical steroids, tacrolimus, testosterone topical etretinat and carbon dioxide laser.
Surgical therapy. Therapeutic benefits of circumcision uncircumcised patients. The surgical intervention for urinary obstruction. The practice of oral mucous membrane uretroplastia.
Prognosis As the disease progresses, urinary retention occurs with retrograde kidney disease. Erectile are painful and can affect sex. Neoplasms may arise from penile lesions, rarely. Signs and symptoms include the appearance of a nodule malignant transformation, proliferation, ulceration, veziculizare, hematuria, erythema, pain, debacluri purulent lymphadenopathy. Peripheral xerotica Balance is a chronic and progressive. Regression or improvement of atrophic areas is unusual.
Penis changes are insignificant debut. While these include changes in color and texture. These include itching, dysuria, painful erections, with or without urethritis debacluri. The penis shows phimosis and paraphimosis. The etiology of the disease is unknown but believed to be multifactorial. The following factors are incriminated: circumcision after 13 years, hormonal factors, autoimmune diseases, genetic factors and human papilloma virus present.
Effective treatment has not been discovered yet. Some therapies with varying degrees of success have been tested: topical or intralesional steroids, tacrolimus, testosterone topical etretinat, carbon dioxide laser. And surgical methods are used for signs and symptoms of urethral stenosis or malignant change. As the disease progresses retrograde retention of urine occurs with impaired renal parenchyma. Erectile painful intercourse life limiting. Neoplasms have been reported and lesions that develop in the penis. Lichen sclera of the penis is chronic and progressive regression or improvement of the affected areas is unusual.
Pathogenesis and causes
The etiology of penile lichen sclera is unknown but is believed to be multifactorial. The occurrence of several factors contributing balanitei xerotice obstructive disease:
Circumcision after 13 years / uncircumcised status. The involvement of this factor may be due to the effect known as the Koebner or isomorphic phenomenon. What ami large majority of male genitalia inflammatory dermatoses, including lichen sclera occur in uncircumcised men, or belated circumscribed. The foreskin may promote chronic irritation or serves to maintain a favorable environment for infectious agents. Such chronic infection may initiate changes seen in lichen sclera.
Hormonal factors. Hormonal influences in the development of lichen have been incriminated much sclera, especially in the form of vulvar female. Most studies have focused on the role of testosterone in the pathogenesis of penile lesions. Vulvar lichen sclera in children resolves pubertal onset of menarche and increasing testosterone in genital skin. In addition, adults were evaluated for low levels of testosterone, androstenedione and dihidrostestosteron comparable to control subjects. Defect can be the altered function of 5-alpha reductase.
Autoimmune diseases. Many autoantibodies, including antinuclear, antimicrosomali thyroid, gastric parietal anticelule, anticortex adrenal, smooth and antimitochondrial antimuschi were detected in patients with lichen sclera. Vitiligo, thyroid disease, diabetes and alopecia areata have been reported frequently with lichen sclera.
Genetics. Lichen sclera has been reported in families, including twins, siblings, mothers and daughters and brother and sister. However it has not been identified yet heredity.
The human papilloma virus. This virus has been reported it in some cases of penile lichen sclera. If lichen is secondary infection, or it promotes the appearance is still a fact not disputed.
Signs and symptoms
Peripheral xerotica Balance is more common in middle-aged men. Early in the disease, penile lichen sclera is relatively asymptomatic with only a few noticeable changes. Later symptoms are more obvious with the passage of years, equipment and changes color and texture. Early symptoms are more prevalent in uncircumcised patients.
The clinical picture includes: -Itching, burning, dysuria Glans penis, hypoesthesia Painful erections, impaired sexual function Strength-reducing urinary bladder and jet size Debacluri-with or without urethritis.
Symptoms of late stage Peripheral xerotica balanitei include: Phimosis-unable-to decalota glans Paraphimosis-unable-to recalota glans. Development of squamous cell carcinoma in individuals with multifocal scleral and atrophic lichen of the penis and infection with hepatitis C were reported.
Physical examination. Lichen sclera shows only subtle physical changes in the initial phase, nonspecific erythema, mild hypopigmentation. As the condition progresses, multiple erythematous papules appear discreet or patches that merge intro or splash plate or purple-white ivories. The lesions affect mainly the glans and foreskin. Frenulum, urethral meatus, fossa naviculara, sheath of penis and perianal area may be involved. A sclerotic white ring in place at this stage the foreskin is diagnostic. Erosion, cracks, spots, bubbles and sero-haemorrhagic teleangiectaziile gland are reported, although unusual.
With progression of the disease may become adherent to the glans foreskin. Coronary groove and sclerotic frenulum may be destroyed. Urinary meatus may be al until urinary retention. Urinary retention can be severe to cause retrograde ureterohidronefroza. Significant collapse of the urinary meatus may lead to retrograde urethral blockage. Phimosis and paraphimosis in uncircumcised patients may occur in the late stage.
Diagnosis
Histological examination. Sclera genital lichen histological elements are similar to those of nongenitale form. These include ortokeratoza, hyperkeratosis with follicular plugs, stoppers without hyperkeratosis, atrophy of the malpighian layer, hydropic degeneration of basal and splicing dermoepidermica dressed. Follicular plugs are not apparent in affected mucosa. Note the significant edema and homogenization of dermal collagen in the upper dermis with dilated blood and lymph vessels and loss of elastic fibers. The inflammatory infiltrate includes lymphocytes, plasma cells, histiocite in the middle dermis, it is less pronounced in advanced lesions. The differential diagnosis is made with the following conditions: Balan circumscribed plasmacytoma, mucosal candidiasis,'s eritroplazia Queyrat, lichen planus, psoriasis boards, phimosis, Balan.
Treatment
There is no specific treatment to deliver on all patients. Mode with intramuscular penicillin has proven benefits meet studio, improved sensitivity, itching and inflammatory changes in three weeks. Therapy for patients is more aggressive circumscribed. The following regimens have shown benefit in varying degrees: intrelezionali and topical steroids, tacrolimus, testosterone topical etretinat and carbon dioxide laser.
Surgical therapy. Therapeutic benefits of circumcision uncircumcised patients. The surgical intervention for urinary obstruction. The practice of oral mucous membrane uretroplastia.
Prognosis As the disease progresses, urinary retention occurs with retrograde kidney disease. Erectile are painful and can affect sex. Neoplasms may arise from penile lesions, rarely. Signs and symptoms include the appearance of a nodule malignant transformation, proliferation, ulceration, veziculizare, hematuria, erythema, pain, debacluri purulent lymphadenopathy. Peripheral xerotica Balance is a chronic and progressive. Regression or improvement of atrophic areas is unusual.
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