STUDY - Technical - New Dacian's Medicine
Common
Skin Conditions (4)
Translation Draft
A slightly shorter post will follow (lack of time available). But let's "move on" with the "open" presentation in previous posts...
Warts are skin neoplasias caused by papiloviruses. For 50 different human papillomaviruses (HPV) have been described and their number will almost certainly continue to increase. The lesions of typical vulgar warts are sessiles, dome-shaped, usually about 1 cm in diameter and have an area made up of numerous small filamentous projections. HPV that causes vulgar warts also causes typical planting warts, flat warts (flat verruca) and filiform warts in intertriginous regions.
Planting warts are endophytic and are covered with thick keratin. the decapation of the wart will generally highlight a central core of keratinized residue and punctual bleeding places. Filiform warts are most common on the face, neck and skin folds and present as papillomatous lesions with a narrow base. Flat warts are only slightly elevated and have a velvety, untrighting surface. They have a tropism for their faces, arms and legs and often spread through shaving.
Many types of HPV have been associated with genital tract lesions. They generally start as small papillomas and can grow to form extensive lesions. In women they can affect the labia, perineum or perianal skin. In addition, the vaginal mucosa, urethra and anus may be involved, as may the cervical epithelium. In men, lesions often occur in the balanopreputial trench but can be found on the penis, scrotum, perianal skin or in the urethra.
In recent times, considerable evidence has accumulated suggesting that HPV would play a role in the development of cervical cervical cervical neoplasia and external genitalia. HPV types 16 and 18 have been most extensively studied, while recent evidence also involves other types. These lesions may initially appear as small, flat, velvety, hyperpigmented papules that appear on the genitals or perianal skin.
Histological examination of biopsies in affected regions may reveal changes associated with typical warts and/ or typical characters for intraepidermal carcinoma (Bowen's disease). Spinocellular carcinomas associated with papilovirus infections have also been observed in extragenital skin. This was most common in patients who were immunosuppressants after organ transplantation.
There are many ways to treat warts, but none is universally effective. Perhaps the most useful and convenient method for treating warts with any localization is liquid nitrogen cryotherapy. Equally effective, but requiring much more compliance on the part of the patient is the use of keratolytic agents such as patches with salicylic acid or combinations of lactic acid and salicylic acid. For genital warts, the application of podofiline solution is moderately effective, but may be associated with intense local reactions in certain patients. Other topical agents used are tricloracetic acid or cantaridine.
Electrocauterization and curettage or excision with carbon dioxide laser are also effective, but require local anesthesia. The recurrence of warts appears to be common to all these variants, as viral genomic material is present in normal-looking skin adjacent to clinical lesions. Treatment of warts should be tempered by the recognition that most warts in normal individuals heal spontaneously within 1-2 years. Also, only an extremely small proportion of warts is associated with neoplasia and they are almost exclusively localized on the genitals or perianal skin.
I will now approach acne with its two forms, vulgar and rosacea.
Vulgar acne is usually a self-limiting condition, predominantly in adolescents and young adults, although 10-20% of adults may have some form of the condition. The permissive factor for the expression of the disease in adolescence is the increase in the release of sebum by the sebaceous glands after puberty. Small cysts, called comedones, are formed in the hair follicles due to the blockage of the follicular orifice through retention of sebum and keratinous material. The action of lipophilic levs (Pytirosporum orbicular) and bacteria (Propionobacterium acnes) inside comedones releasefree fatty acids from sebum, cause inflammation in the cyst and lead to rupture of the cyst wall.
An inflammatory reaction of the foreign body occurs as a result of the externalization of oily and keratinous residues from the cyst. The hallmark of vulgar acne is comedon, which can be closed (white dot) or open (black dot). Closed comedones appear as 1-2 mm granular white papules that are accentuated when the skin is stretched. They are precursors of inflammatory lesions of vulgar acne.
The contents of the included comedones are not easily evacuated. Open comedones, which rarely turn into inflammatory lesions of acne, have a much dilated follicular orifice and are filled with oxidized, dark and easily discharged oily residues. Comedones are usually accompanied by inflammatory lesions: papules, pustules or nodules.
The earliest lesions that occur in adolescence are generally slightly inflamed or non-inflammatory comedones on the forehead. Subsequently, more characteristic inflammatory lesions appear on the cheeks, nose and chin. The most common localization of acne is the face, but damage to the chest and back is not unusual. Most forms remain light and do not produce scarring. Yet a small subgroup of patients develops large cysts and inflammatory nodules, which can drain and cause significant scarring.
Exogenous and endogenous factors can alter the expression of vulgar acne. Friction and trauma can break preexisting microcomedones and cause inflammatory acne lesions. It is commonly found in head bandages and chin straps of sports helmets. Application of cosmetic comedognic topical agents or in hair preparations and chronic topical exposure to certain industrial compounds that are comedogenecan can cause or aggravate acne. Glucocorticoids, topically applied or systemically administered as lithium, isoniazide, halogens, phenytoin and phenobarbital may cause acne-shaped rashes or aggravate pre-existing acne.
Treatment of vulgar acne is directed towards the elimination of comedones, the decrease of the population of bacteria and lipophilic levs and the reduction of inflammation. Although acne-affected regions should be kept clean, there is little evidence that surface fat removal would play an important role in therapy. Excessive vigorous cleansing can aggravate acne due to mechanical rupture of the comedones. Tetracycline or erythromycin per bone will decrease follicular colonization with some lipophilic microorganisms. They also appear to have an anti-inflammatory effect independent of the antibacterial effect.
Topical agents, such as retinoic acid, benzoyl-peroxide or salicylic acid, can change the way of epidermal descuamation, preventing the formation of comedones and helping to cure pre-existing cysts. Topical antibacterial agents like benzoyl-peroxide, erythromycin, clindamycin or tetracycline topical are also useful additions in therapy. Serious nodulocystic acne that does not respond to oral antibiotics and topical therapy can be treated with synthetic retinoid isotretinoin.
The use of this medicine is limited by its teratogenicity and women should be tested for pregnancy before initiation of therapy, a method of contraception is required during treatment and tested for pregnancy while therapy lasts. Patients receiving this medication develop extremely dry skin and cheilitis and should be followed for the development of hypertriglycerideemia.
Rosacea acne is an inflammatory disorder predominantly affecting the center of the face. It is found almost exclusively in adults affecting only rarely patients under 30 years of age. Rosacea is more common in women, but the most severely affected are men. It is characterized by the presence of erythema, telangiectasis and superficial pustules but is not associated with the presence of comedones.
Rosacea rarely affects the chest and back. There is a relationship between the tendency to pronounced facial erythema (flushing) and the subsequent development of rosacea. Often, individuals with rosacea initially experience a pronounced flushing reaction. It can be in response to heat, emotional stimuli, alcohol, hot drinks or spicy foods. As the disease progresses, the erythema persists more and more, eventually becoming permanent.
Papules, pustules and telangiectasis are then over-added to persistent erythema. Long-lasting rosacea can lead to the proliferation of connective tissue, especially the nose (rhinophima). It can also be complicated by various inflammatory disorders of the eye, including keratitis, blepharitis, irritate and recurrent chalazion. These eye problems potentially threaten vision and require ophthalmological evaluation.
Rosacea acne can generally be effectively treated with oral tetracycline. Topical metronidazole is also effective. In addition, the use of low potency non-fluoridated topical glucocorticoids, especially after refreshing baths, is useful in improving facial erythema. Topic fluorinated glucocorticoids should be avoided, since chronic use of these preparations can effectively cause rosacea. Topical therapy is not effective for eye disease.
And with that, I've completed this group of posts. From tomorrow I will address the drug-induced skin reactions and then proceed to address the skin manifestations of internal diseases (a fairly consistent group of posts) and finally photosensitivity and other light reactions. It is only after all this series of posts (I hope to complete them by 1 August) that I will be able to move on (to haematological alterations, etc.).
A slightly shorter post will follow (lack of time available). But let's "move on" with the "open" presentation in previous posts...
Warts are skin neoplasias caused by papiloviruses. For 50 different human papillomaviruses (HPV) have been described and their number will almost certainly continue to increase. The lesions of typical vulgar warts are sessiles, dome-shaped, usually about 1 cm in diameter and have an area made up of numerous small filamentous projections. HPV that causes vulgar warts also causes typical planting warts, flat warts (flat verruca) and filiform warts in intertriginous regions.
Planting warts are endophytic and are covered with thick keratin. the decapation of the wart will generally highlight a central core of keratinized residue and punctual bleeding places. Filiform warts are most common on the face, neck and skin folds and present as papillomatous lesions with a narrow base. Flat warts are only slightly elevated and have a velvety, untrighting surface. They have a tropism for their faces, arms and legs and often spread through shaving.
Many types of HPV have been associated with genital tract lesions. They generally start as small papillomas and can grow to form extensive lesions. In women they can affect the labia, perineum or perianal skin. In addition, the vaginal mucosa, urethra and anus may be involved, as may the cervical epithelium. In men, lesions often occur in the balanopreputial trench but can be found on the penis, scrotum, perianal skin or in the urethra.
In recent times, considerable evidence has accumulated suggesting that HPV would play a role in the development of cervical cervical cervical neoplasia and external genitalia. HPV types 16 and 18 have been most extensively studied, while recent evidence also involves other types. These lesions may initially appear as small, flat, velvety, hyperpigmented papules that appear on the genitals or perianal skin.
Histological examination of biopsies in affected regions may reveal changes associated with typical warts and/ or typical characters for intraepidermal carcinoma (Bowen's disease). Spinocellular carcinomas associated with papilovirus infections have also been observed in extragenital skin. This was most common in patients who were immunosuppressants after organ transplantation.
There are many ways to treat warts, but none is universally effective. Perhaps the most useful and convenient method for treating warts with any localization is liquid nitrogen cryotherapy. Equally effective, but requiring much more compliance on the part of the patient is the use of keratolytic agents such as patches with salicylic acid or combinations of lactic acid and salicylic acid. For genital warts, the application of podofiline solution is moderately effective, but may be associated with intense local reactions in certain patients. Other topical agents used are tricloracetic acid or cantaridine.
Electrocauterization and curettage or excision with carbon dioxide laser are also effective, but require local anesthesia. The recurrence of warts appears to be common to all these variants, as viral genomic material is present in normal-looking skin adjacent to clinical lesions. Treatment of warts should be tempered by the recognition that most warts in normal individuals heal spontaneously within 1-2 years. Also, only an extremely small proportion of warts is associated with neoplasia and they are almost exclusively localized on the genitals or perianal skin.
I will now approach acne with its two forms, vulgar and rosacea.
Vulgar acne is usually a self-limiting condition, predominantly in adolescents and young adults, although 10-20% of adults may have some form of the condition. The permissive factor for the expression of the disease in adolescence is the increase in the release of sebum by the sebaceous glands after puberty. Small cysts, called comedones, are formed in the hair follicles due to the blockage of the follicular orifice through retention of sebum and keratinous material. The action of lipophilic levs (Pytirosporum orbicular) and bacteria (Propionobacterium acnes) inside comedones releasefree fatty acids from sebum, cause inflammation in the cyst and lead to rupture of the cyst wall.
An inflammatory reaction of the foreign body occurs as a result of the externalization of oily and keratinous residues from the cyst. The hallmark of vulgar acne is comedon, which can be closed (white dot) or open (black dot). Closed comedones appear as 1-2 mm granular white papules that are accentuated when the skin is stretched. They are precursors of inflammatory lesions of vulgar acne.
The contents of the included comedones are not easily evacuated. Open comedones, which rarely turn into inflammatory lesions of acne, have a much dilated follicular orifice and are filled with oxidized, dark and easily discharged oily residues. Comedones are usually accompanied by inflammatory lesions: papules, pustules or nodules.
The earliest lesions that occur in adolescence are generally slightly inflamed or non-inflammatory comedones on the forehead. Subsequently, more characteristic inflammatory lesions appear on the cheeks, nose and chin. The most common localization of acne is the face, but damage to the chest and back is not unusual. Most forms remain light and do not produce scarring. Yet a small subgroup of patients develops large cysts and inflammatory nodules, which can drain and cause significant scarring.
Exogenous and endogenous factors can alter the expression of vulgar acne. Friction and trauma can break preexisting microcomedones and cause inflammatory acne lesions. It is commonly found in head bandages and chin straps of sports helmets. Application of cosmetic comedognic topical agents or in hair preparations and chronic topical exposure to certain industrial compounds that are comedogenecan can cause or aggravate acne. Glucocorticoids, topically applied or systemically administered as lithium, isoniazide, halogens, phenytoin and phenobarbital may cause acne-shaped rashes or aggravate pre-existing acne.
Treatment of vulgar acne is directed towards the elimination of comedones, the decrease of the population of bacteria and lipophilic levs and the reduction of inflammation. Although acne-affected regions should be kept clean, there is little evidence that surface fat removal would play an important role in therapy. Excessive vigorous cleansing can aggravate acne due to mechanical rupture of the comedones. Tetracycline or erythromycin per bone will decrease follicular colonization with some lipophilic microorganisms. They also appear to have an anti-inflammatory effect independent of the antibacterial effect.
Topical agents, such as retinoic acid, benzoyl-peroxide or salicylic acid, can change the way of epidermal descuamation, preventing the formation of comedones and helping to cure pre-existing cysts. Topical antibacterial agents like benzoyl-peroxide, erythromycin, clindamycin or tetracycline topical are also useful additions in therapy. Serious nodulocystic acne that does not respond to oral antibiotics and topical therapy can be treated with synthetic retinoid isotretinoin.
The use of this medicine is limited by its teratogenicity and women should be tested for pregnancy before initiation of therapy, a method of contraception is required during treatment and tested for pregnancy while therapy lasts. Patients receiving this medication develop extremely dry skin and cheilitis and should be followed for the development of hypertriglycerideemia.
Rosacea acne is an inflammatory disorder predominantly affecting the center of the face. It is found almost exclusively in adults affecting only rarely patients under 30 years of age. Rosacea is more common in women, but the most severely affected are men. It is characterized by the presence of erythema, telangiectasis and superficial pustules but is not associated with the presence of comedones.
Rosacea rarely affects the chest and back. There is a relationship between the tendency to pronounced facial erythema (flushing) and the subsequent development of rosacea. Often, individuals with rosacea initially experience a pronounced flushing reaction. It can be in response to heat, emotional stimuli, alcohol, hot drinks or spicy foods. As the disease progresses, the erythema persists more and more, eventually becoming permanent.
Papules, pustules and telangiectasis are then over-added to persistent erythema. Long-lasting rosacea can lead to the proliferation of connective tissue, especially the nose (rhinophima). It can also be complicated by various inflammatory disorders of the eye, including keratitis, blepharitis, irritate and recurrent chalazion. These eye problems potentially threaten vision and require ophthalmological evaluation.
Rosacea acne can generally be effectively treated with oral tetracycline. Topical metronidazole is also effective. In addition, the use of low potency non-fluoridated topical glucocorticoids, especially after refreshing baths, is useful in improving facial erythema. Topic fluorinated glucocorticoids should be avoided, since chronic use of these preparations can effectively cause rosacea. Topical therapy is not effective for eye disease.
And with that, I've completed this group of posts. From tomorrow I will address the drug-induced skin reactions and then proceed to address the skin manifestations of internal diseases (a fairly consistent group of posts) and finally photosensitivity and other light reactions. It is only after all this series of posts (I hope to complete them by 1 August) that I will be able to move on (to haematological alterations, etc.).
Have a good day, full of
peace, understanding, love and gratitude!
Dorin, Merticaru