STUDY - Technical - New Dacian's Medicine
Skin
Manifestations of Internal Diseases (8)
Translation Draft
I have made an estimate of the volume of information I still have to present here and I have come to the conclusion that today will be dedicated to the signs attracted to internal diseases.
I have made an estimate of the volume of information I still have to present here and I have come to the conclusion that today will be dedicated to the signs attracted to internal diseases.
So let's get on with the
red lesions! Skin lesions that are red in color have a wide
variety of etiologies and, in an attempt to simplify their
identity, a subdivision into papules, papules/ subcutaneous
plaques and nodules will follow.
Ordinary red papules include arthroped bites/stings and cherry hemangiomas (the latter are small, red-lit, dome-shaped papules, which represent benign capillary proliferations). In AIDS patients, the occurrence of multiple red lesions resembling hemangiomas indicates bacillary angiomatosis, and biopsy shows piles of bacilli that are positive for Wartin-Starry staining (the pathogen has been identified as Rochalimaea henselae and Bartanella quintana). Visceral disseminated disease is primarily found in immunocompromised hosts, but can also occur in immunocompetent individuals.
Multiple angiokeratomas are found in Fabry disease, a recessive x-linked lysosome hoarding disease that is due to alpha-galactozidase A deficiency. Associated symptoms include: chronic renal failure, peripheral neuropathy and corneal opacity (verticellata cornea). Electronic photomicrographies of angiokeratomas and normal clinical skin show lamellar lipid deposits in fibroblas, pericytes and endothelial cells, which are diagnosed for this disease.
There are several infectious diseases that present themselves as sporotricoid-looking erythematous nodules or papules, i.e. in a linear arrangement along the lymphatic channels. The two most common etiologies are Sporothrix schenckii (sporotricosis) and Mycobacterium marinum (atypical mycobacteria). Microorganisms are introduced as a result of trauma and a primary site of inoculation is often found in addition to the lymph nodes. Additional causes include Nocardia, Leishmania and other dimorphic fungi (culture in lesional tissue orienting the diagnosis).
Other conditions with differential diagnosis in papules/red plaques include erysipelas, light polymorphic rash (EPML), skin lymphocytoma, skin lupus, skin lymphomas and skin leukaemia. The first three diseases are primary skin conditions. Polymorphic light rash (EPML) is characterized by papules and erythematous plaques, especially in areas of skin exposed to the sun (back of hands, extension faces of forearms and face).
Injuries are secondary to UV-B and UV-A exposure and, at northern latitudes, EPML is more severe in late spring and early summer. A process called "heating" occurs upon continuous exposure to UV, when the rash is erased, but in temperate climate it will recur in the spring season. EPML should be differentiated from skin lupus and this is done by histological examination and direct immunofluorescence of lesions. Cutaneous lymphocytoma (pseudolymphoma) is a benign proliferation of lymphocytes in the skin that present as papules and plaques infiltrated pink-red to purple red. It should be particularly lupus skin and skin lymphomas.
Several types of red plaques are found in patients with systemic lupus, including: 1. erythematous urticaria plaques affecting the cheeks and nose in a classic "butterfly" rash, 2. discoid erythematous lesions with fine squamous or with an appearance of "upholsterer nails", telangiectasis, central hypopigmentation, peripheral hyperpigmentation, follicular plugs and localized atrophy on the face, scalp, external ear , upper arms and torso and 3. psoriatic or ring lesions of subacute lupus, with hypopigmentation centers, localized on the face, extension regions of the arms and upper torso.
Other skin lesions are: 1. acute and temporary violet erythema of the face and V of the neck, 2. urticariavasculitis, 3. lupus paniculite, 4. diffuse alopecia, 5. secondary alopecia of discoid lesions, 6. telangiectasis and periangle erythema, 7. lesions resembling polymorphic erythema, which can become bullous and 8. distal ulcerations secondary to Raynaud's phenomenon, vasculitis or livedoid vasculitis. Patients with only lesions of discoid lupus usually have the form of lupus limited to the skin. However, 2-10% of these patients eventually develop systemic lupus. Direct immunofluorescence of the affected skin shows deposits of IgG or IgM and C3 in a granular distribution along the dermoepidermic junction.
In skin lymphoma there is a proliferation of histocytes or malignant lymphocytes in the skin and the clinical appearance resembles that of the skin lymphocytoma (papules and plaques infiltrated pink-red to red-purple). Skin lymphoma can occur anywhere on the surface of the skin, while the predilection regions of lymphoma are the malal protrusions, the tip of the nose, earlobes, forearms and scrotum. Patients with non-Hodgkin lymphomahave specific skin lesions more often than those with Hodgkin's disease and sometimes skin nodules precede the development of extracutaneous nonhodgkin lymphoma.
Arcuate lesions are sometimes found in lymphoma and skin lymphocytoma, as in LCCT. Skin leukaemia has the same appearance as skin lymphoma and specific lesions are most common in monocytic leukaemias than in lymphocytic or granulocyte strips. Skin chloromas (granulocyte sarcomas) may precede the appearance of circulating blasts in acute non-lymphocytic leukaemia and, as such, are a form of aleucemic skin leukaemia. Common causes of erythematous skin nodules include inflamed inclusion epidermal cysts, acne cysts and boils.
Paniculitis, an inflammation of the fatty layer, also presents as subcutaneous nodules and is frequently a sign of systemic disease. There are several forms of paniculitis, including nodos erythema, endured erythema, deep lupus, Weber-Christian disease, a1-antitrypsin deficiency, fact-like form and necrosis of adipose tissue secondary to pancreatic disease. In all of these diseases, with the exception of nodos erythema, lesions can crack and ulcerate or heal with scarring.
The pretibial region is the most common localization for nodos erythema nodules, while the posterior face of the calf is the most common localization for pained erythema lesions. In nodos erythema, the nodules are initially red, but then they get a blue color as they heal. Patients with nodos erythema and without an underlying systemic disease may, however, experience fever, malaise, leukocytosis, arthralgia and/ or arthritis. However, the possibility of an underlying disease should be excluded and the most common associations are streptococcal infections, upper respiratory tract infections, sarcoidosis and inflammatory bowel disease.
Rarer associations are tuberculosis, histoplasmosis, coccidioidomycosis, psitacosis, drugs (oral contraceptives, sulfonamides, aspartame, bromides, iodines), cat claw disease and infections with Yersinia, Salmonella and Chlamydia. In most patients, endured erythema/ nodular vasculitis is an idiopathic disease, however, in approximately 25-50% of patients, the chain polymerization reaction (PCR) will demonstrate the presence of DNA belonging to Mycobacterium tuberculosis. Deep lupus lesions are found primarily on the face, arms, upper region and buttocks (areas with abundant adiposity) and are found in both skin and systemic forms of lupus.
The skin above may be normal, erythematous or may show changes in discoid lupus. Necrosis of subcutaneous adipose tissue that is associated with pancreatic disease is probably secondary to circulating lipases and is found in patients with pancreatic carcinoma, as well as in those with acute and chronic pancreatitis. Associated symptoms may occur in this condition and Weber-Christian disease: arthritis, fever and inflammation of visceral fat. Histological examination of biopsies collected by deep incision will help in the diagnosis of this particular type of paniculite.
Subcutaneous erythematous nodules are also found in the skin's node polyarteritis (PAN) and as a manifestation of systemic vasculitis, e.g. systemic PAN, allergic granulomatosis or Wegener granulomatosis. Cutaneous PAN presents with painful subcutaneous nodules and ulcers against the background of a red-violet network of livedo reticularis. The latter is due to low blood flow through the superficial horizontal venous plexuses. Most lesions are found on the lower limbs and while arthralgia and myalgia may accompany cutaneous PAN, there are no signs of systemic impairment. And in skin forms, and in systemic vasculitis, skin biopsy samples from the associated nodules will show changes characteristic of a vasculitis (the size of the affected vessel depends on each condition).
I will complete this post with the presentation of some elements about red-brown lesions. Skin lesions in sarcoidosis are, classically, red, red-brown and at diascopy (pressure with a glass blade) a residual yellow-brown color is observed, which is secondary to granulomatous infiltration. Papules and waxy plaques can be found anywhere on the skin, but the face is the most common localization. Usually, there are no surface changes, but sometimes the lesions will have smes. Biopsies in the papules show "nude" granulomas in the dermis, i.e. granulomas surrounded by a minimum number of lymphocytes. Other skin lesions in sarcoidosis are ring lesions with atrophic or squamous center, papules on scars, hypopigmented macula and papules, alopecia, acquired ihtiosis, erythema nodos and lupus pernio. Associated symptoms are peripheral adenopathy and enlargement of the parotid and tear glands. When there is skin damage to the hands, X-rays will show lithic lesions in the underlying bone.
Differential diagnosis of sarcoidosis is made with foreign body granulomas produced by chemicals such as beryllium and zirconium, with late secondary syphilis and vulgar lupus. Vulgar lupus is a form of skin tuberculosis found in previously infected or sensitized individuals. There is often an underlying active tuberculosis elsewhere, usually pulmonary or lymph nodes. At least 90% of lesions occur in the head and neck region and are red-brown or yellow-brown plaques at diascopy. Secondary scarring and spinal carcinomas may occur in plaques. Crops should be made from lesions or PCR analysis, as rarely the colors for acid-alcohol-resistant germs highlight bacilli in dermal granulomas.
Sweet syndrome is characterized by red-brown plaques and nodules that are frequently painful and appear primarily on the head, neck and upper extremities. Patients experience fever, neutrophilia and a dense dermal neutrophil infiltration into the lesions. In about 10% of patients there is associated a malignant disease, most commonly acute nonlymphocytic leukemia. It has also been reported concurrently with lymphomas, chronic leukemia, myeloma, myelodysplastic syndromes and solid tumors (especially urogenital tract). Regions, extracutaneous damage comprise the joints, muscles, eye, kidney (proteinuria, sometimes glomerulonephritis) and lung (neutrophil infiltration). The idiopathic form of Sweet syndrome is more common in women after an infection of the airways.
A generalized distribution of red-brown maculas and papules is found in the form of mastocytosis known as urticaria pigmentosa. Each lesion represents a collection of mast cells in the dermis, with hyperpigmentation of the supraiacent epidermis. Stimuli such as friction or heat cause the degranulation of mastocytes and this causes the formation of localized urticaria (the Darier sign). Additional symptoms may result from mastocyte degranulation and include headache, flushing, diarrhoea and itching. Mastocytes also infiltrate various organs such as the liver, spleen and gastrointestinal tract in about 30-50% of patients with urticaria pigmentosa, and accumulations of mastocytes in the bones can produce osteosclerotic or osteolytic shadows on X-rays. In most of these patients, internal damage remains obviously static. A subtype of chronic leukocytocplastic vasculitis, erythema elevatum diuitinum (EED), is also presented with red-brown papules. These papules fuse into plaques on the extensor surfaces of the knees, elbows and small joints of the hand. EED products have been associated with streptococcal infections.
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Ordinary red papules include arthroped bites/stings and cherry hemangiomas (the latter are small, red-lit, dome-shaped papules, which represent benign capillary proliferations). In AIDS patients, the occurrence of multiple red lesions resembling hemangiomas indicates bacillary angiomatosis, and biopsy shows piles of bacilli that are positive for Wartin-Starry staining (the pathogen has been identified as Rochalimaea henselae and Bartanella quintana). Visceral disseminated disease is primarily found in immunocompromised hosts, but can also occur in immunocompetent individuals.
Multiple angiokeratomas are found in Fabry disease, a recessive x-linked lysosome hoarding disease that is due to alpha-galactozidase A deficiency. Associated symptoms include: chronic renal failure, peripheral neuropathy and corneal opacity (verticellata cornea). Electronic photomicrographies of angiokeratomas and normal clinical skin show lamellar lipid deposits in fibroblas, pericytes and endothelial cells, which are diagnosed for this disease.
There are several infectious diseases that present themselves as sporotricoid-looking erythematous nodules or papules, i.e. in a linear arrangement along the lymphatic channels. The two most common etiologies are Sporothrix schenckii (sporotricosis) and Mycobacterium marinum (atypical mycobacteria). Microorganisms are introduced as a result of trauma and a primary site of inoculation is often found in addition to the lymph nodes. Additional causes include Nocardia, Leishmania and other dimorphic fungi (culture in lesional tissue orienting the diagnosis).
Other conditions with differential diagnosis in papules/red plaques include erysipelas, light polymorphic rash (EPML), skin lymphocytoma, skin lupus, skin lymphomas and skin leukaemia. The first three diseases are primary skin conditions. Polymorphic light rash (EPML) is characterized by papules and erythematous plaques, especially in areas of skin exposed to the sun (back of hands, extension faces of forearms and face).
Injuries are secondary to UV-B and UV-A exposure and, at northern latitudes, EPML is more severe in late spring and early summer. A process called "heating" occurs upon continuous exposure to UV, when the rash is erased, but in temperate climate it will recur in the spring season. EPML should be differentiated from skin lupus and this is done by histological examination and direct immunofluorescence of lesions. Cutaneous lymphocytoma (pseudolymphoma) is a benign proliferation of lymphocytes in the skin that present as papules and plaques infiltrated pink-red to purple red. It should be particularly lupus skin and skin lymphomas.
Several types of red plaques are found in patients with systemic lupus, including: 1. erythematous urticaria plaques affecting the cheeks and nose in a classic "butterfly" rash, 2. discoid erythematous lesions with fine squamous or with an appearance of "upholsterer nails", telangiectasis, central hypopigmentation, peripheral hyperpigmentation, follicular plugs and localized atrophy on the face, scalp, external ear , upper arms and torso and 3. psoriatic or ring lesions of subacute lupus, with hypopigmentation centers, localized on the face, extension regions of the arms and upper torso.
Other skin lesions are: 1. acute and temporary violet erythema of the face and V of the neck, 2. urticariavasculitis, 3. lupus paniculite, 4. diffuse alopecia, 5. secondary alopecia of discoid lesions, 6. telangiectasis and periangle erythema, 7. lesions resembling polymorphic erythema, which can become bullous and 8. distal ulcerations secondary to Raynaud's phenomenon, vasculitis or livedoid vasculitis. Patients with only lesions of discoid lupus usually have the form of lupus limited to the skin. However, 2-10% of these patients eventually develop systemic lupus. Direct immunofluorescence of the affected skin shows deposits of IgG or IgM and C3 in a granular distribution along the dermoepidermic junction.
In skin lymphoma there is a proliferation of histocytes or malignant lymphocytes in the skin and the clinical appearance resembles that of the skin lymphocytoma (papules and plaques infiltrated pink-red to red-purple). Skin lymphoma can occur anywhere on the surface of the skin, while the predilection regions of lymphoma are the malal protrusions, the tip of the nose, earlobes, forearms and scrotum. Patients with non-Hodgkin lymphomahave specific skin lesions more often than those with Hodgkin's disease and sometimes skin nodules precede the development of extracutaneous nonhodgkin lymphoma.
Arcuate lesions are sometimes found in lymphoma and skin lymphocytoma, as in LCCT. Skin leukaemia has the same appearance as skin lymphoma and specific lesions are most common in monocytic leukaemias than in lymphocytic or granulocyte strips. Skin chloromas (granulocyte sarcomas) may precede the appearance of circulating blasts in acute non-lymphocytic leukaemia and, as such, are a form of aleucemic skin leukaemia. Common causes of erythematous skin nodules include inflamed inclusion epidermal cysts, acne cysts and boils.
Paniculitis, an inflammation of the fatty layer, also presents as subcutaneous nodules and is frequently a sign of systemic disease. There are several forms of paniculitis, including nodos erythema, endured erythema, deep lupus, Weber-Christian disease, a1-antitrypsin deficiency, fact-like form and necrosis of adipose tissue secondary to pancreatic disease. In all of these diseases, with the exception of nodos erythema, lesions can crack and ulcerate or heal with scarring.
The pretibial region is the most common localization for nodos erythema nodules, while the posterior face of the calf is the most common localization for pained erythema lesions. In nodos erythema, the nodules are initially red, but then they get a blue color as they heal. Patients with nodos erythema and without an underlying systemic disease may, however, experience fever, malaise, leukocytosis, arthralgia and/ or arthritis. However, the possibility of an underlying disease should be excluded and the most common associations are streptococcal infections, upper respiratory tract infections, sarcoidosis and inflammatory bowel disease.
Rarer associations are tuberculosis, histoplasmosis, coccidioidomycosis, psitacosis, drugs (oral contraceptives, sulfonamides, aspartame, bromides, iodines), cat claw disease and infections with Yersinia, Salmonella and Chlamydia. In most patients, endured erythema/ nodular vasculitis is an idiopathic disease, however, in approximately 25-50% of patients, the chain polymerization reaction (PCR) will demonstrate the presence of DNA belonging to Mycobacterium tuberculosis. Deep lupus lesions are found primarily on the face, arms, upper region and buttocks (areas with abundant adiposity) and are found in both skin and systemic forms of lupus.
The skin above may be normal, erythematous or may show changes in discoid lupus. Necrosis of subcutaneous adipose tissue that is associated with pancreatic disease is probably secondary to circulating lipases and is found in patients with pancreatic carcinoma, as well as in those with acute and chronic pancreatitis. Associated symptoms may occur in this condition and Weber-Christian disease: arthritis, fever and inflammation of visceral fat. Histological examination of biopsies collected by deep incision will help in the diagnosis of this particular type of paniculite.
Subcutaneous erythematous nodules are also found in the skin's node polyarteritis (PAN) and as a manifestation of systemic vasculitis, e.g. systemic PAN, allergic granulomatosis or Wegener granulomatosis. Cutaneous PAN presents with painful subcutaneous nodules and ulcers against the background of a red-violet network of livedo reticularis. The latter is due to low blood flow through the superficial horizontal venous plexuses. Most lesions are found on the lower limbs and while arthralgia and myalgia may accompany cutaneous PAN, there are no signs of systemic impairment. And in skin forms, and in systemic vasculitis, skin biopsy samples from the associated nodules will show changes characteristic of a vasculitis (the size of the affected vessel depends on each condition).
I will complete this post with the presentation of some elements about red-brown lesions. Skin lesions in sarcoidosis are, classically, red, red-brown and at diascopy (pressure with a glass blade) a residual yellow-brown color is observed, which is secondary to granulomatous infiltration. Papules and waxy plaques can be found anywhere on the skin, but the face is the most common localization. Usually, there are no surface changes, but sometimes the lesions will have smes. Biopsies in the papules show "nude" granulomas in the dermis, i.e. granulomas surrounded by a minimum number of lymphocytes. Other skin lesions in sarcoidosis are ring lesions with atrophic or squamous center, papules on scars, hypopigmented macula and papules, alopecia, acquired ihtiosis, erythema nodos and lupus pernio. Associated symptoms are peripheral adenopathy and enlargement of the parotid and tear glands. When there is skin damage to the hands, X-rays will show lithic lesions in the underlying bone.
Differential diagnosis of sarcoidosis is made with foreign body granulomas produced by chemicals such as beryllium and zirconium, with late secondary syphilis and vulgar lupus. Vulgar lupus is a form of skin tuberculosis found in previously infected or sensitized individuals. There is often an underlying active tuberculosis elsewhere, usually pulmonary or lymph nodes. At least 90% of lesions occur in the head and neck region and are red-brown or yellow-brown plaques at diascopy. Secondary scarring and spinal carcinomas may occur in plaques. Crops should be made from lesions or PCR analysis, as rarely the colors for acid-alcohol-resistant germs highlight bacilli in dermal granulomas.
Sweet syndrome is characterized by red-brown plaques and nodules that are frequently painful and appear primarily on the head, neck and upper extremities. Patients experience fever, neutrophilia and a dense dermal neutrophil infiltration into the lesions. In about 10% of patients there is associated a malignant disease, most commonly acute nonlymphocytic leukemia. It has also been reported concurrently with lymphomas, chronic leukemia, myeloma, myelodysplastic syndromes and solid tumors (especially urogenital tract). Regions, extracutaneous damage comprise the joints, muscles, eye, kidney (proteinuria, sometimes glomerulonephritis) and lung (neutrophil infiltration). The idiopathic form of Sweet syndrome is more common in women after an infection of the airways.
A generalized distribution of red-brown maculas and papules is found in the form of mastocytosis known as urticaria pigmentosa. Each lesion represents a collection of mast cells in the dermis, with hyperpigmentation of the supraiacent epidermis. Stimuli such as friction or heat cause the degranulation of mastocytes and this causes the formation of localized urticaria (the Darier sign). Additional symptoms may result from mastocyte degranulation and include headache, flushing, diarrhoea and itching. Mastocytes also infiltrate various organs such as the liver, spleen and gastrointestinal tract in about 30-50% of patients with urticaria pigmentosa, and accumulations of mastocytes in the bones can produce osteosclerotic or osteolytic shadows on X-rays. In most of these patients, internal damage remains obviously static. A subtype of chronic leukocytocplastic vasculitis, erythema elevatum diuitinum (EED), is also presented with red-brown papules. These papules fuse into plaques on the extensor surfaces of the knees, elbows and small joints of the hand. EED products have been associated with streptococcal infections.
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Have a good day!
Dorin, Merticaru