STUDY - Technical - New Dacian's Medicine
Skin
Manifestations of Internal Diseases (2)
Translation Draft
We've reached alopecia.
We've reached alopecia.
The two major forms of
alopecia are: scarring and non-scar. In scar alopecia appear
associated with fibrosis, inflammation and loss of hair
follicles. On clinical examination, the scalp skins are smooth,
with a low number of follicular openings, but in some cases the
changes are visible only in biopsied samples collected from the
affected regions. In non-scarred alopecia, the aerial portions
of the hair have disappeared, but the hair follicles are
preserved, explaining the reversible nature of the non-scaricial
alopecia.
The causes of alopecia are represented by: A. non-scaral alopecia: 1. primary skin conditions (a. telogen efluvius, b. androgenetic alopecia, c. alopecia areata, d. tinea capitis and e. traumatic alopecia), 2. medicines and 3. systemic diseases (a. lupus erythematosus, b. secondary syphilis, c. hypothyroidism, d. hyperthyroidism, e. protein deficiencies, iron, biotin and zinc and f. HIV infection) and for B. scar alopecia: 1. primary skin diseases (a. skin lupus, b. lichen plan, c. calvant folliculitis and d. linear scleroderma/ morfea) and 2. systemic diseases (a. lupus erythematosus, 2. sarcoidosis and c. skin metastases).
Primary skin disorders are the most common causes of non-scaral alopecia and include telogen efluvius, androgenetic alopecia, alopecia areata, tinea capitis and traumatic alopecia. in women with androgenetic alopecia, an increase in the level of circulating androgens may occur as a result of ovarian or adrenal dysfunction. When there are signs of virilization, such as the thickened voice and enlarged clitoris, the possibility of a tumour of the ovary or adrenal gland should be considered.
Non-scaric alopecia (primary skin conditions) has as main causes the following: 1. telogen efluvius (clinically characterized by diffuse hair loss, which occurs either after major stress such as high fever, serious infection, etc., or after hormonal/ post partum changes being reversible without treatment; pathogenicity is that stress causes synchronization of the growth cycles of individual hairs, which are normally asynchronous, therefore a large number of growing/ anagenous hairs simultaneously enter the death/ telogen phase; treatment is surveillance, discontinuation of any drugs that have the side effect of alopecia and verification of the existence of an underlying metabolic cause such as hypo or hyperthyroidism) , 2. androgenetic alopecia (which has as clinical characteristics the miniaturization of hairs along the middle line of the scalp with the withdrawal of the anterior line in men and some women; pathogenic is noted an increased sensitivity of the affected hairs to the effects of testosterone and increased levels of circulating androgens, ovarian or adrenal origin in women; treatment, if there is no evidence of a state of hyperandrogenism, is represented by topical minoxidil with or without tretinoin and possibly hair transplantation), 3. alopecia areata (has as clinical characteristics circular, well-delimited areas, with diameter of 2-5 cm, hair loss, in extensive cases, the confusion of lesions and/ or damage to other hairy areas of the body and punctual nail depressions; pathogenic is noted that the germ areas of the hair follicles are surrounded by T lymphocytes and occasionally associated diseases such as hypo and hyperthyroidism, vitiligo and Down syndrome may be "retrieved"; treatment is the administration of topical anthralin, intralezional glucocorticoids and contact sensitizers), 4. (clinical characteristics represented by variations from descuamation with minimal hair loss, isolated spots with "black dots"/ broken threads and "swampy" plaque with pustules/ kerion; pathogenic is noted the invasion of hairs by dermatophytes, most commonly Trichophyton tonsurans; treatment is the administration of oral griseofulvin plus 2,5 % selenium sulfide shampoo or ketoconazole, also being done when examining family members) and 5. Traumatic alopecia (clinical characteristics represented by broken hairs and irregular contour; pathogenic is found to traction hair with curlers, rubber band or hair braiding, exposure to heat or chemicals as well as mechanical traction/ knittingmania; as a treatment it is necessary to change the style of the hairstyle or aggressive chemical treatments for hair, knittingmania may require hair cutting and examination of hairs or diagnostic biopsy, followed by psychotherapy).
Exposure to various drugs can also cause diffuse hair loss, usually by inducing a telogen eluvius. An exception is the anagen efluvius observed in antimycotic agents, such as dadoreubicin. Alopecia is a side effect of the following drugs: warfarin, heparin, propiltiouracil, carbimazole, vitamin A, isotretinoin, etretinate, lithium, beta-blockers, colchicine, amphetamines and thallium.
Fortunately, the hair usually grows spontaneously again after discontinuation of the provoking agent. Less often, non-ciccaral alopecia is associated with lupus erythematosus or secondary syphilis. In systemic lupus there are two forms of alopecia: one is scarring and the other is non-scar. This latter form can be diffuse dyed and affect the entire scalp or be located in the frontal scalp in the form of multiple short hairs ("wolf brushes").
Disseminated areas of alopecia, poorly circumscribed, with the appearance of "moth eaten" are a manifestation of the secondary stage of syphilis. Diffuse hair thinning is also associated with hypo and hyperthyroidism, hypopituitarism, HIV infection and protein, iron, biotin and zinc deficiencies. Scar alopecia is more commonly the result of a primary skin disease, such as plan lichen, decalitis, skin lupus or linear scleroderma (morphea), than the sign of a systemic disease. Although scar lesions of discoid lupus can be found in patients with systemic lupus, in most cases the pathological process is limited to the skin.
Uncommon causes of scar alopecia include sarcoidosis and skin metastases. In the early stages of discoid lupus, plan lichen and calcalvante folliculitis there are circumscribed regions of alopecia. Fibrosis and consecutive loss of follicles are observed especially in the center of individual lesions, while the inflammatory process is most intense in the periphery. The regions of active inflammation in discoid lupus are erythematous, with squamous, while the regions of anterior inflammation are often hypopigmented, with a hyperpigmentation edge. In the plane lichen, peripheral perifolicular maculas are purple in color and post-inflammatory hyperpigmentation is a characteristic sign.
Complete examination of the skin and oral mucosa, combined with a biopsy and direct immunofluorescence, will help in distinguishing these two entities. Peripheral active lesions in the decalating follicleare are perifolicular pustules that usually contain Staphylococcus aureus or normal flora. These patients often have other forms of acne and folliculitis and may have reactive arthritis.
Let's move on to the figurative skin lesions! In figurative rashes, lesions form rings and springs that are usually erythematous, but can be skin-colored, up to brown. Most commonly are due to primary skin diseases such as tinea, urticaria, centrifugal annular edema and annular granuloma. An underlying systemic disease is present in a second, less common group of migratory annulment erythema. It comprises erythema gyratum repens, erythema migrans, erytema marginatum and necrolitic migratory erythema. In the erythema gyratum repens you can see hundreds of movable concentric arches and wave fronts that resemble wood fibers.
The search for an underlying malignant disease is mandatory in a patient with this rash. Migratory erythema (erythema migrans) is the skin manifestation of Lyme disease, which is caused by the spirocheta Borrelia burgdorferi. At the initial stage (3-30 days after the tick bite), a small ring lesion usually occurs, which can extend to almost 10 cm in diameter. Within a few days, in about half of patients, multiple smaller erythematous lesions occur in remote areas of the bite. Associated symptoms include headache, fever, myalgia, photophobia, arthralgia and rash.
Margined erythema (erythema marginatum) is found in patients with acute articular rheumatism, especially on the trunk. The lesions are pinkish-red in color, flat or slightly elevated and transient. There are also skin diseases that present as ring rashes, but do not have an obvious migratory component. Examples include LCCT, annular skin lupus, also called subacute lupus, secondary syphilis and sarcoidosis.
I'll finish with the presentation of a few items about acne. Vulgar acne and rosacea are the two important forms of acne. The etiology of acneiform rashes is represented by: 1. primary skin conditions (vulgar acne and rosacea acne), 2. medicines, 3. systemic conditions (increased production of androgens with a. adrenal origin, e.g. Cushing's disease, 21-hydroxylase deficiency and b. of ovarian origin, e.g. polycystic ovary disease and, apart from all this, disseminated cryptococosis and Behcet disease). Estrogens decrease the activity of the sebaceous glands, while androgens increase the production of sebum.
Therefore, vulgar acne in an adult, especially if it is recent onset, may be reflected in increased levels of circulating androgens. Ovarian or adrenal dysfunction, for example, polycystic ovary disease, Cushing syndrome or partial deficiency of 21-hydroxylase can lead to hormonal imbalance. Examining the patient in search of signs such as hirsutism, adrogenetic alopecia, hypertension and subcutaneous fat redistribution will help to specify the diagnosis.
Exacerbations of vulgar acne follow the ingestion of certain drugs, such as iodines, bromides, glucocorticoids and lithium, as well as local applications of compounds containing oils. Acneiform lesions may occur in patients with Behcet's disease, and in immunocompromised patients, disseminated cryptococosis may occur as an acne-shaped rash. Patients with carcinoid syndrome have episodes of acute and transient congestion (flushing) in the head, neck and sometimes torso. The resulting facial skin changes, especially telangiectasis, mimic the clinical appearance of rosacea. Facial suctions, as found in polycytemia vera, can also be confused with rosacea.
We still have plenty to talk about here. See you tomorrow!
The causes of alopecia are represented by: A. non-scaral alopecia: 1. primary skin conditions (a. telogen efluvius, b. androgenetic alopecia, c. alopecia areata, d. tinea capitis and e. traumatic alopecia), 2. medicines and 3. systemic diseases (a. lupus erythematosus, b. secondary syphilis, c. hypothyroidism, d. hyperthyroidism, e. protein deficiencies, iron, biotin and zinc and f. HIV infection) and for B. scar alopecia: 1. primary skin diseases (a. skin lupus, b. lichen plan, c. calvant folliculitis and d. linear scleroderma/ morfea) and 2. systemic diseases (a. lupus erythematosus, 2. sarcoidosis and c. skin metastases).
Primary skin disorders are the most common causes of non-scaral alopecia and include telogen efluvius, androgenetic alopecia, alopecia areata, tinea capitis and traumatic alopecia. in women with androgenetic alopecia, an increase in the level of circulating androgens may occur as a result of ovarian or adrenal dysfunction. When there are signs of virilization, such as the thickened voice and enlarged clitoris, the possibility of a tumour of the ovary or adrenal gland should be considered.
Non-scaric alopecia (primary skin conditions) has as main causes the following: 1. telogen efluvius (clinically characterized by diffuse hair loss, which occurs either after major stress such as high fever, serious infection, etc., or after hormonal/ post partum changes being reversible without treatment; pathogenicity is that stress causes synchronization of the growth cycles of individual hairs, which are normally asynchronous, therefore a large number of growing/ anagenous hairs simultaneously enter the death/ telogen phase; treatment is surveillance, discontinuation of any drugs that have the side effect of alopecia and verification of the existence of an underlying metabolic cause such as hypo or hyperthyroidism) , 2. androgenetic alopecia (which has as clinical characteristics the miniaturization of hairs along the middle line of the scalp with the withdrawal of the anterior line in men and some women; pathogenic is noted an increased sensitivity of the affected hairs to the effects of testosterone and increased levels of circulating androgens, ovarian or adrenal origin in women; treatment, if there is no evidence of a state of hyperandrogenism, is represented by topical minoxidil with or without tretinoin and possibly hair transplantation), 3. alopecia areata (has as clinical characteristics circular, well-delimited areas, with diameter of 2-5 cm, hair loss, in extensive cases, the confusion of lesions and/ or damage to other hairy areas of the body and punctual nail depressions; pathogenic is noted that the germ areas of the hair follicles are surrounded by T lymphocytes and occasionally associated diseases such as hypo and hyperthyroidism, vitiligo and Down syndrome may be "retrieved"; treatment is the administration of topical anthralin, intralezional glucocorticoids and contact sensitizers), 4. (clinical characteristics represented by variations from descuamation with minimal hair loss, isolated spots with "black dots"/ broken threads and "swampy" plaque with pustules/ kerion; pathogenic is noted the invasion of hairs by dermatophytes, most commonly Trichophyton tonsurans; treatment is the administration of oral griseofulvin plus 2,5 % selenium sulfide shampoo or ketoconazole, also being done when examining family members) and 5. Traumatic alopecia (clinical characteristics represented by broken hairs and irregular contour; pathogenic is found to traction hair with curlers, rubber band or hair braiding, exposure to heat or chemicals as well as mechanical traction/ knittingmania; as a treatment it is necessary to change the style of the hairstyle or aggressive chemical treatments for hair, knittingmania may require hair cutting and examination of hairs or diagnostic biopsy, followed by psychotherapy).
Exposure to various drugs can also cause diffuse hair loss, usually by inducing a telogen eluvius. An exception is the anagen efluvius observed in antimycotic agents, such as dadoreubicin. Alopecia is a side effect of the following drugs: warfarin, heparin, propiltiouracil, carbimazole, vitamin A, isotretinoin, etretinate, lithium, beta-blockers, colchicine, amphetamines and thallium.
Fortunately, the hair usually grows spontaneously again after discontinuation of the provoking agent. Less often, non-ciccaral alopecia is associated with lupus erythematosus or secondary syphilis. In systemic lupus there are two forms of alopecia: one is scarring and the other is non-scar. This latter form can be diffuse dyed and affect the entire scalp or be located in the frontal scalp in the form of multiple short hairs ("wolf brushes").
Disseminated areas of alopecia, poorly circumscribed, with the appearance of "moth eaten" are a manifestation of the secondary stage of syphilis. Diffuse hair thinning is also associated with hypo and hyperthyroidism, hypopituitarism, HIV infection and protein, iron, biotin and zinc deficiencies. Scar alopecia is more commonly the result of a primary skin disease, such as plan lichen, decalitis, skin lupus or linear scleroderma (morphea), than the sign of a systemic disease. Although scar lesions of discoid lupus can be found in patients with systemic lupus, in most cases the pathological process is limited to the skin.
Uncommon causes of scar alopecia include sarcoidosis and skin metastases. In the early stages of discoid lupus, plan lichen and calcalvante folliculitis there are circumscribed regions of alopecia. Fibrosis and consecutive loss of follicles are observed especially in the center of individual lesions, while the inflammatory process is most intense in the periphery. The regions of active inflammation in discoid lupus are erythematous, with squamous, while the regions of anterior inflammation are often hypopigmented, with a hyperpigmentation edge. In the plane lichen, peripheral perifolicular maculas are purple in color and post-inflammatory hyperpigmentation is a characteristic sign.
Complete examination of the skin and oral mucosa, combined with a biopsy and direct immunofluorescence, will help in distinguishing these two entities. Peripheral active lesions in the decalating follicleare are perifolicular pustules that usually contain Staphylococcus aureus or normal flora. These patients often have other forms of acne and folliculitis and may have reactive arthritis.
Let's move on to the figurative skin lesions! In figurative rashes, lesions form rings and springs that are usually erythematous, but can be skin-colored, up to brown. Most commonly are due to primary skin diseases such as tinea, urticaria, centrifugal annular edema and annular granuloma. An underlying systemic disease is present in a second, less common group of migratory annulment erythema. It comprises erythema gyratum repens, erythema migrans, erytema marginatum and necrolitic migratory erythema. In the erythema gyratum repens you can see hundreds of movable concentric arches and wave fronts that resemble wood fibers.
The search for an underlying malignant disease is mandatory in a patient with this rash. Migratory erythema (erythema migrans) is the skin manifestation of Lyme disease, which is caused by the spirocheta Borrelia burgdorferi. At the initial stage (3-30 days after the tick bite), a small ring lesion usually occurs, which can extend to almost 10 cm in diameter. Within a few days, in about half of patients, multiple smaller erythematous lesions occur in remote areas of the bite. Associated symptoms include headache, fever, myalgia, photophobia, arthralgia and rash.
Margined erythema (erythema marginatum) is found in patients with acute articular rheumatism, especially on the trunk. The lesions are pinkish-red in color, flat or slightly elevated and transient. There are also skin diseases that present as ring rashes, but do not have an obvious migratory component. Examples include LCCT, annular skin lupus, also called subacute lupus, secondary syphilis and sarcoidosis.
I'll finish with the presentation of a few items about acne. Vulgar acne and rosacea are the two important forms of acne. The etiology of acneiform rashes is represented by: 1. primary skin conditions (vulgar acne and rosacea acne), 2. medicines, 3. systemic conditions (increased production of androgens with a. adrenal origin, e.g. Cushing's disease, 21-hydroxylase deficiency and b. of ovarian origin, e.g. polycystic ovary disease and, apart from all this, disseminated cryptococosis and Behcet disease). Estrogens decrease the activity of the sebaceous glands, while androgens increase the production of sebum.
Therefore, vulgar acne in an adult, especially if it is recent onset, may be reflected in increased levels of circulating androgens. Ovarian or adrenal dysfunction, for example, polycystic ovary disease, Cushing syndrome or partial deficiency of 21-hydroxylase can lead to hormonal imbalance. Examining the patient in search of signs such as hirsutism, adrogenetic alopecia, hypertension and subcutaneous fat redistribution will help to specify the diagnosis.
Exacerbations of vulgar acne follow the ingestion of certain drugs, such as iodines, bromides, glucocorticoids and lithium, as well as local applications of compounds containing oils. Acneiform lesions may occur in patients with Behcet's disease, and in immunocompromised patients, disseminated cryptococosis may occur as an acne-shaped rash. Patients with carcinoid syndrome have episodes of acute and transient congestion (flushing) in the head, neck and sometimes torso. The resulting facial skin changes, especially telangiectasis, mimic the clinical appearance of rosacea. Facial suctions, as found in polycytemia vera, can also be confused with rosacea.
We still have plenty to talk about here. See you tomorrow!
Have a good day!
Dorin, Merticaru