STUDY - Technical - New Dacian's Medicine
Skin
Manifestations of Internal Diseases (9)
Translation Draft
We've reached the blue lesions, which are the result of vascular tumors and ectasis or the melanic pigment in the dermis. Venous lakes (ectasis) are dark blue compressible lesions, which are usually found in the head and neck region. Venous malformations are also blue lumps and compressible papules that can occur anywhere on the body, including the oral mucosa. When there are multiple congenital lesions, rather than single, the patient may have blue hematoma syndrome or Mafucci syndrome.
Patients with blue hematoma syndrome also have bleeding vascular abnormalities of the gastrointestinal tract, while patients with Mafucci syndrome have osteochondromas and associated discondroplasis. In the case of isolated hemangiomas of relatively large size there may be associated platelet destruction (Kasabach-Merritt syndrome) or musculoskeletal defects. Blue nevi are found when there are groups of pigment-producing non-vice cells in the dermis. These benign papular lesions are dome-shaped and most commonly occur on the back of the hands and arms.
With regard to violaceous lesions, plaques and violet papules are found in lupus pernio, skin lymphoma and skin lupus. Lupus pernio is a particular type of sarcoidosis, affecting the tip of the nose and earlobes, with lesions that are violet in color rather than red-brown. This form of sarcoidosis is associated with upper airway damage. The plaques of skin lymphoma and skin lupus may be red or violet and have been discussed above.
Papules and purple plaques are found in vascular tumors, such as Kaposi sarcoma and angiosarcoma, and when there is extravasation of erythrocytes in the skin associated with inflammation, as in palpable purpura. Patients with congenital or acquired arteriovenous fistulas and venous hypertension may have violet papules on the lower limbs, which may resemble Kaposi sarcoma clinically and histologically, and this condition is called pseudo-Kaposi sarcoma (acral angiodermatitis). Angiosarcoma is most common lyusand in the scalp and face in elderly patients or in regions with chronic lymphedema and presents as papules and violet wounds. In the region of the head and neck the tumor often extends beyond the defined edges and can be accompanied by facial edema.
Brown and black papules were "discussed" with presentations on hyperpigmentation.
At the end of these "color" presentations I will approach skin metastases, as they can have a wide range of colors. It is most commonly presented as firm subcutaneous nodules of skin color, either as red, red-brown papulo-nodules. Injuries to skin lymphoma range from pink-red to plum color, while metastatic melanoma can be pink, blue or black in color. Skin metastases occur by hematogenous or lymphatic dissemination and are most commonly due to the following primary carcinomas: in men in the lung, colon, melanoma and oral cavity, while in women, in the breast, colon and lung. These metastatic lesions may be the initial presentation of carcinoma, especially when the location is the lung, kidney or ovary.
And so, I came to purple... The causes of purpura are represented by: I. primary skin disorders (represented by A. non-palpable with 1. trauma, 2. solar purpura, 3. steroidal purpura, 4. capillary and 5. livedoid vasculitis), II. systemic diseases (A. non-palpable with 1. coagulation disorders represented by a. thrombocytopenia, including ITP, b. abnormal platelet function and c. defects in coagulation factors, 2. vascular fragility with a. amyloidosis, b. Ehlers-Danlos syndrome and c. scurvy, 3. thrombi with a. disseminated intravascular coagulation, b. monoclonal cryoglobulinemia, c. thrombocytopenic thrombotic purpura and d. warfarin reaction , 4. embolisms of a. cholesterol and b. fat, 5. possible immune complexes such as a. Gardner-Diamond self-erythrocytic sensitization syndrome, b. hypergamaglobulinemic purpura Waldenstrom and B. palpable as is the case of 1- vasculitis with a. leukocytoclastic vasculitis and b. node polyarteritis and 2. embolisms with acute meningococcalemia, b. disseminated gonococcal infection, c. spotted fever and d. ectima gangrenosum). Purpura occurs when there is an extravasation of erythrocytes in the dermis and, as a result, the lesions do not whiten at pressure. This is in contrast to those erythematous or purple lesions due to localized vasodilation (which whiten at pressure). Purpura (greater than or equal to 3 mm) and spots (more ici or 2 mm) are divided into two large groups: palpable and non-palpable. The most common causes of purpura and non-palpable spots are primary skin conditions such as trauma, solar purpura and capillary. Rarer causes are steroid purpura and livedoid vasculitis. Solar purpura is primarily found on the forearm extension face, while glucocorticoid purpura (secondary to potent topical steroids) or that of endogenous or exogenous Cushing syndrome may be more extensive. In both cases there is a change in the supporting connective tissue surrounding the dermal blood vessels. In contrast, the spots from the capillary are found mainly on the lower limbs. In capillary there is an extravasation of erythrocytes as a result of lymphocytic perivascular inflammation. The spots are bright red, 1-2 mm in size and disseminated inside a yellow-caffeine ring macul or coin form. The yellow-caffeine color is caused by hemosiderin deposits in the dermis.
Systemic causes of non-palpable purpura fall into several categories. First, those secondary to some coagulation disorders and vascular fragility will be addressed. The first group comprises thrombocytopenia, abnormal platelet function, as in uremia, and defects of clotting factors. The initial localization of thrombocytopenia-induced spots is in the distal extremities of the lower limbs. Capillary fragility leads to non-palpable purpura in patients with systemic amyloidosis, disorders of collagen production, such as Ehlers-Danlos syndrome, and scurvy. In scurvy appear hairs in the corkscrew, with surrounding hemorrhage, arranged on the lower limbs, plus gingivitis. Vitamin C is a cofactor for lysyl-hydroxylase, an enzyme involved in posttranslational modification of procolagen, which is necessary for the formation of a cross-link.
In contrast to the previous group of conditions, in which either a clotting abnormality or capillary fragility is responsible for the non-palpable purpura, which occurs in the next group of conditions is associated with the formation of thrombus in vessels. It is important to note that these thrombi are noticeable in skin biopsies. This group of conditions includes disseminated intravascular coagulation (CID), monoclonal cryoglobulinemia, thrombotic thrombocytopenic purpura and warfarin reactions. Disseminated intravascular coagulation (CID) is triggered by several types of infection (gram-negative, gram-positive, viral and rickettsii), as well as neoplasms and tissue damage. Extended (disseminated) purpura and hemorrhagic infarctions of the distal extremities are encountered.
Similar lesions occur in purpura fulminants, which is a form of CID associated with fever and hypotension, which occurs more frequently in children after an infectious disease like chickenpox, scarlet fever or an upper respiratory tract infection. Hemorrhagic bubbles may appear on the affected skin in both conditions. Monoclonal cryoglobulinemia is associated with multiple myeloma, Waldenstrom macroglobulinemia, lymphocytic leukemia and lymphomas. Purpura, especially on the lower limbs, and hemorrhagic infarctions of the fingers of the hands and feet are found in these patients. Exacerbation of the activity of the disease may occur after exposure to cold or an increase in serum viscosity. Biopsies show precipitated cryoglobulin in dermal vessels. Similar deposits were found in the lung, brain and renal glomerules.
Patients with thrombocytopenic purpura, fever and microangiopathic hemolytic anaemia. The administration of warfarin can cause painful areas of erythema, which become purple and then necrotic, with a black adhering scale. This reaction is common in women and areas with abundant subcutaneous fat (breasts, abdomen, buttocks, thighs and calves). Erythema and purpura occur between the 3rd and 10th day of therapy, most likely as a result of a transient imbalance between levels of anticoagulants and procoagulants dependent on vitamin K. Continuous therapy does not exacerbate pre-existing lesions and patients with a hereditary or acquired deficiency of protein C are at increased risk for this particular reaction , as for purpura fulminans.
Purpura secondary to collecterolic embolisms is usually found on the lower limbs of patients with atherosclerotic vascular disease. She frequently follows anticoagulant therapy or an invasive vascular procedure like arteriography, but can also occur spontaneously, by disintegrating atheromarous plaques. Associated lesions are livedo reticularis, gangrene, cyanosis, subcutaneous nodules and systemic ulcerations. Multiple sections of the piece harvested by biopsy may be needed to highlight the cholesterol cracks in the vessels. Spots are also an important sign of fatty embolism and occur especially in the upper body 2-3 days after a major injury. By using special fixatives, embolisms can be highlighted in the biopsy samples in the spots. Tumor embolisms or thrombus are found in patients with atrial mixomas and marantic endocarditis.
In Gardner-Diamond syndrome (self-erythrocytic sensitivity), patients have extensive bruising within regions of warm, painful erythema. An episode of significant trauma frequently precedes the onset of this syndrome. Intradermal injections of autologous or phosphatidyl serine derived from the erythrocytic membrane may cause injury in some patients (however there are cases when a reaction occurs at the injection site on the forearm, but not in the middle region of the back). This has led some researchers to consider this syndrome as a skin manifestation of a severe emotional stressor. Waldenstrom hypergamaglobulinemic purpura is a chronic condition characterized by spots on the lower limbs. There are circulating complexes of IgG and anti IgG molecules and exacerbations are associated with orthostatism or long walking.
We continue tomorrow with purple, completing the "section" of the skin manifestations of internal diseases... Yeshhh, I did it!
We've reached the blue lesions, which are the result of vascular tumors and ectasis or the melanic pigment in the dermis. Venous lakes (ectasis) are dark blue compressible lesions, which are usually found in the head and neck region. Venous malformations are also blue lumps and compressible papules that can occur anywhere on the body, including the oral mucosa. When there are multiple congenital lesions, rather than single, the patient may have blue hematoma syndrome or Mafucci syndrome.
Patients with blue hematoma syndrome also have bleeding vascular abnormalities of the gastrointestinal tract, while patients with Mafucci syndrome have osteochondromas and associated discondroplasis. In the case of isolated hemangiomas of relatively large size there may be associated platelet destruction (Kasabach-Merritt syndrome) or musculoskeletal defects. Blue nevi are found when there are groups of pigment-producing non-vice cells in the dermis. These benign papular lesions are dome-shaped and most commonly occur on the back of the hands and arms.
With regard to violaceous lesions, plaques and violet papules are found in lupus pernio, skin lymphoma and skin lupus. Lupus pernio is a particular type of sarcoidosis, affecting the tip of the nose and earlobes, with lesions that are violet in color rather than red-brown. This form of sarcoidosis is associated with upper airway damage. The plaques of skin lymphoma and skin lupus may be red or violet and have been discussed above.
Papules and purple plaques are found in vascular tumors, such as Kaposi sarcoma and angiosarcoma, and when there is extravasation of erythrocytes in the skin associated with inflammation, as in palpable purpura. Patients with congenital or acquired arteriovenous fistulas and venous hypertension may have violet papules on the lower limbs, which may resemble Kaposi sarcoma clinically and histologically, and this condition is called pseudo-Kaposi sarcoma (acral angiodermatitis). Angiosarcoma is most common lyusand in the scalp and face in elderly patients or in regions with chronic lymphedema and presents as papules and violet wounds. In the region of the head and neck the tumor often extends beyond the defined edges and can be accompanied by facial edema.
Brown and black papules were "discussed" with presentations on hyperpigmentation.
At the end of these "color" presentations I will approach skin metastases, as they can have a wide range of colors. It is most commonly presented as firm subcutaneous nodules of skin color, either as red, red-brown papulo-nodules. Injuries to skin lymphoma range from pink-red to plum color, while metastatic melanoma can be pink, blue or black in color. Skin metastases occur by hematogenous or lymphatic dissemination and are most commonly due to the following primary carcinomas: in men in the lung, colon, melanoma and oral cavity, while in women, in the breast, colon and lung. These metastatic lesions may be the initial presentation of carcinoma, especially when the location is the lung, kidney or ovary.
And so, I came to purple... The causes of purpura are represented by: I. primary skin disorders (represented by A. non-palpable with 1. trauma, 2. solar purpura, 3. steroidal purpura, 4. capillary and 5. livedoid vasculitis), II. systemic diseases (A. non-palpable with 1. coagulation disorders represented by a. thrombocytopenia, including ITP, b. abnormal platelet function and c. defects in coagulation factors, 2. vascular fragility with a. amyloidosis, b. Ehlers-Danlos syndrome and c. scurvy, 3. thrombi with a. disseminated intravascular coagulation, b. monoclonal cryoglobulinemia, c. thrombocytopenic thrombotic purpura and d. warfarin reaction , 4. embolisms of a. cholesterol and b. fat, 5. possible immune complexes such as a. Gardner-Diamond self-erythrocytic sensitization syndrome, b. hypergamaglobulinemic purpura Waldenstrom and B. palpable as is the case of 1- vasculitis with a. leukocytoclastic vasculitis and b. node polyarteritis and 2. embolisms with acute meningococcalemia, b. disseminated gonococcal infection, c. spotted fever and d. ectima gangrenosum). Purpura occurs when there is an extravasation of erythrocytes in the dermis and, as a result, the lesions do not whiten at pressure. This is in contrast to those erythematous or purple lesions due to localized vasodilation (which whiten at pressure). Purpura (greater than or equal to 3 mm) and spots (more ici or 2 mm) are divided into two large groups: palpable and non-palpable. The most common causes of purpura and non-palpable spots are primary skin conditions such as trauma, solar purpura and capillary. Rarer causes are steroid purpura and livedoid vasculitis. Solar purpura is primarily found on the forearm extension face, while glucocorticoid purpura (secondary to potent topical steroids) or that of endogenous or exogenous Cushing syndrome may be more extensive. In both cases there is a change in the supporting connective tissue surrounding the dermal blood vessels. In contrast, the spots from the capillary are found mainly on the lower limbs. In capillary there is an extravasation of erythrocytes as a result of lymphocytic perivascular inflammation. The spots are bright red, 1-2 mm in size and disseminated inside a yellow-caffeine ring macul or coin form. The yellow-caffeine color is caused by hemosiderin deposits in the dermis.
Systemic causes of non-palpable purpura fall into several categories. First, those secondary to some coagulation disorders and vascular fragility will be addressed. The first group comprises thrombocytopenia, abnormal platelet function, as in uremia, and defects of clotting factors. The initial localization of thrombocytopenia-induced spots is in the distal extremities of the lower limbs. Capillary fragility leads to non-palpable purpura in patients with systemic amyloidosis, disorders of collagen production, such as Ehlers-Danlos syndrome, and scurvy. In scurvy appear hairs in the corkscrew, with surrounding hemorrhage, arranged on the lower limbs, plus gingivitis. Vitamin C is a cofactor for lysyl-hydroxylase, an enzyme involved in posttranslational modification of procolagen, which is necessary for the formation of a cross-link.
In contrast to the previous group of conditions, in which either a clotting abnormality or capillary fragility is responsible for the non-palpable purpura, which occurs in the next group of conditions is associated with the formation of thrombus in vessels. It is important to note that these thrombi are noticeable in skin biopsies. This group of conditions includes disseminated intravascular coagulation (CID), monoclonal cryoglobulinemia, thrombotic thrombocytopenic purpura and warfarin reactions. Disseminated intravascular coagulation (CID) is triggered by several types of infection (gram-negative, gram-positive, viral and rickettsii), as well as neoplasms and tissue damage. Extended (disseminated) purpura and hemorrhagic infarctions of the distal extremities are encountered.
Similar lesions occur in purpura fulminants, which is a form of CID associated with fever and hypotension, which occurs more frequently in children after an infectious disease like chickenpox, scarlet fever or an upper respiratory tract infection. Hemorrhagic bubbles may appear on the affected skin in both conditions. Monoclonal cryoglobulinemia is associated with multiple myeloma, Waldenstrom macroglobulinemia, lymphocytic leukemia and lymphomas. Purpura, especially on the lower limbs, and hemorrhagic infarctions of the fingers of the hands and feet are found in these patients. Exacerbation of the activity of the disease may occur after exposure to cold or an increase in serum viscosity. Biopsies show precipitated cryoglobulin in dermal vessels. Similar deposits were found in the lung, brain and renal glomerules.
Patients with thrombocytopenic purpura, fever and microangiopathic hemolytic anaemia. The administration of warfarin can cause painful areas of erythema, which become purple and then necrotic, with a black adhering scale. This reaction is common in women and areas with abundant subcutaneous fat (breasts, abdomen, buttocks, thighs and calves). Erythema and purpura occur between the 3rd and 10th day of therapy, most likely as a result of a transient imbalance between levels of anticoagulants and procoagulants dependent on vitamin K. Continuous therapy does not exacerbate pre-existing lesions and patients with a hereditary or acquired deficiency of protein C are at increased risk for this particular reaction , as for purpura fulminans.
Purpura secondary to collecterolic embolisms is usually found on the lower limbs of patients with atherosclerotic vascular disease. She frequently follows anticoagulant therapy or an invasive vascular procedure like arteriography, but can also occur spontaneously, by disintegrating atheromarous plaques. Associated lesions are livedo reticularis, gangrene, cyanosis, subcutaneous nodules and systemic ulcerations. Multiple sections of the piece harvested by biopsy may be needed to highlight the cholesterol cracks in the vessels. Spots are also an important sign of fatty embolism and occur especially in the upper body 2-3 days after a major injury. By using special fixatives, embolisms can be highlighted in the biopsy samples in the spots. Tumor embolisms or thrombus are found in patients with atrial mixomas and marantic endocarditis.
In Gardner-Diamond syndrome (self-erythrocytic sensitivity), patients have extensive bruising within regions of warm, painful erythema. An episode of significant trauma frequently precedes the onset of this syndrome. Intradermal injections of autologous or phosphatidyl serine derived from the erythrocytic membrane may cause injury in some patients (however there are cases when a reaction occurs at the injection site on the forearm, but not in the middle region of the back). This has led some researchers to consider this syndrome as a skin manifestation of a severe emotional stressor. Waldenstrom hypergamaglobulinemic purpura is a chronic condition characterized by spots on the lower limbs. There are circulating complexes of IgG and anti IgG molecules and exacerbations are associated with orthostatism or long walking.
We continue tomorrow with purple, completing the "section" of the skin manifestations of internal diseases... Yeshhh, I did it!
Have a good day!
Dorin, Merticaru