STUDY - Technical - New Dacian's Medicine
Skin
Manifestations of Internal Diseases (5)
Translation Draft
I'm going to start this post with "discussions" about blisters/bubbles.
Depending on their size, skin lesions with liquid contents are called blisters (less than 0.5 cm) or bubbles (more than 0.5 cm). Primary bullous diseases include vulgar pemfigus, foliaceu pemfigus, erythematous pemfigus, bullos pemfigoid, gestationis herpes, scar pemigoid, acquired bullous epidermisis, linear IgA disease and herpetiform dermatitis.
Vesicles and bubbles are also found in contact dermatitis, both in the irritant and allergic forms. When there is a linear arrangement of vesicular lesions, an exogenous cause must be suspected. Bullous diseases secondary to drug ingestion can take one of the forms: phototoxic rash, isolated bubbles, toxic epidermal necrolysis and polymorphic erythema. Clinically, phototoxic eruptions resemble an exaggerated sunburn, diffuse erythema and bubbles in sun-exposed regions. The most commonly associated drugs are thiazides, tetracyclines, sulfonamides, phenothiazides, nonsteroidal anti-inflammatory drugs (NSAIDs) and psoralians. The occurrence of a phototoxic rash depends on the doses of the drug and UV-A irradiation.
Toxic epidermal necrolysis (NET) is characterized by bubbles that appear on the surface of large areas of erythema, which then take off. This leads to large areas of denuded skin. Associated morbidity, such as septicaemia, and mortality are relatively high and are depending on the extent of epidermal necrosis. In addition, these patients may also experience damage to the mucous membranes and intestinal tract. The drugs are the primary cause of NET and the most common etiological agents are phenytoin, barbiturates, sulfonamides, penicillins and NSAIDs. Severe acute graft-versus-host disease (grade 4) may also resemble NET.
In polymorphic erythema (EP), the primary lesions are pink-red macula and edematous papules, the center of which can become vesicular. What suggests the diagnosis of EP, rather than a drug-induced morbiliform examination, is the appearance of a dark purple color of the spots in the center of the lesions. "Target" or iris lesions are also characteristic for EP and they occur as a result of the appearance of the edges and the more intensely colored center, more active in combination with the centrifugal extension. However, lesions in the iris should not be present to confirm the diagnosis of EP.
The preferred regions of damage include hands, forearms (extensor faces), palms, plants and mucous membranes (oral, nasal, ocular and genital). Hemorrhagic lip crusts are characteristic for EP, as well as for two other bullous disorders (vulgar pemfigus and NET). Fever, malaise, myalgia, pharyngeal pain and cough may precede or accompany the rash. EP lesions usually heal within 3-6 weeks, but can be recurrent. Drugs can induce EP, especially subphoneamides, phenytoin, barbiturates, penicillins and carbamazepine, but they are not the triggers in most cases, especially in young adults. Herpes simplex infections are the most common cause of EP in this age group and lesions occur 7-12 days after viral eruption.
Other infectious agents associated with EP include Mycoplasma pneumoniae, Histoplasma capsulatum, Coccidiides immitis, Yersinia enterocolica and several viruses (echovirus, coxsackie, Epstein-Barr and influenza virus). EP may also follow after vaccinations with BCG, polio or vaccine virus and after radiation therapy (radiotherapy) and exposure to toxins from the environment. In addition to primary bullous diseases and hypersensitivity reactions, viral and bacterial infections can produce blisters and bubbles. The most common infectious agents are herpes simplex, herpes varicella-zoster and staphylococcus.
Staphylococcal epidermal necrolysis syndrome (SSSS) and bullos impetigo are two bullous conditions associated with staphylococcal infection (type I phages). In SSSS, the initial signs are erythema and pain in the region of the face, neck, torso and intertriginous areas. These are followed by short-lived flasce bubbles, take-off or exfoliation of the superficial epidermis. Crusty areas then appear, characteristically around the mouth. SSSS is distinguished from NET by the following traits: younger age group, the more superficial layer of bubble formation, no lesions in the oral cavity, shorter evolution, lower morbidity or mortality and an association with staphylococcal exfoliative toxin ("exfoliatin"), not associating with drugs.
A rapid differential diagnosis between SS and NET can be made through a section of the bubble (with the cryoseeker) or by exfoliative cytology of the bubble content. In SSS, the location of staphylococcal infection is usually extracutaneous (conjunctivitis, rhinorrhea, otitis media, pharyngitis, tonsillitis) and lesions are sterile, while in the impetigo bulos lesions are in the region of infection. The impetigo is more localized than SSSS and is usually presented with melicitic crusts. Sometimes purulent superficial bubbles can also form. Cutaneous embolisms from gram-negative infections may present as isolated bubbles, but the basis of the lesion is purple or necrotic and may progress to ulcers.
Several metabolic disorders are associated with bubble formation, including diabetes mellitus, renal failure and porphyria. Local hypoxia secondary to low blood flow can also produce bubbles, which explains the presence of bubbles on pressure points in comatous patients (coma bubbles). In diabetes mellitus, bubbles strained with clear viscous fluid appear on normal skin. The lesions can be up to 6 cm in diameter and are localized on the distal extremities. There are several types of porphyria, but the most common form with skin signs is late skin porphyria (PCT). On solar exposed regions (especially face and hands), the skin is very fragile and trauma causes erosion and bubbles in tension.
These lesions are subsequently cured with scarring and formation of mirium (the latter are firm, white or yellow papules, of 2-3 mm, which represent inclusion epidermoid cysts). Associated lesions may be hypertrichosis of the lateral malarial regions (in men) or face (in women) and, in areas exposed to sunlight, hyperpigmentation and firm sclerous papules. An increased level of urinary uroporphyrin confirms the diagnosis and is due to a decrease in the activity of uroporphyrinogen-decarboxylase. Favourable agents include alcohol, iron, chlorinated hydrocarbons and hepatitis C virus infection.
Differential diagnosis of PCT includes: 1. porfiria variegata (pct skin signs plus systemic findings of acute intermittent porphyria, having a diagnostic fluorescent emission of plasma porphyrin at 626 nm), 2. photosensitivity reactions of a drug-induced bulos character (pseudoforfiria - clinical and histological findings are similar to PCT, but porphyrins are normal, etiological agents being furosemide, tetracycline, nalidixic acid, dapsona, naproxen and pyridoxine), 3. bullous dermatosis of hemodialysis (the same aspect as PCT, but porphyrins are usually normal or sometimes elevated to the limit of normal, patients having chronic renal failure and are hemodialysis), 4. PCT associated with hepatomas, liver carcinomas and hemodialysis and 5. acquired bullous epidermolysis.
I will complete this post with the presentation of some elements about exanthemas. The causes of exanthema are represented by: I. for those morbiliforms with A. drugs, B. viral (1. rubella, 2. measles/ measles, 3. infectious erythema, 4. Epstein-Barr, echovirus, Coxsackie virus and adenovirus, 5. EARLY HIV), Bacterial C. (1. typhoid fever, early secondary syphilis, 3. early in rickettsioze, early in meningococemia), D. acute graft-versus-host disease and II. for those scarlet fever with A. scarlet fever, B. toxic shock syndrome and C. Kawasaki disease.
Exantems are characterized by a generalized acute rash. The two modes of presentation with maximum frequency are: papules and erythematous macula (morbiliforms) and confluent erythema (scarlatiniform). Morbiliform rashes are usually due to either drugs or viral infections. For example, up to 5% of patients receiving penicillins, sulfonamides, captopril, phenytoin or gold will develop a maculopapular rash. Accompanying signs may include pruritus, fever, eosinophilia and transient adenopathy.
Similar maculopapular eruptions are found in the classic viral exanthemas of childhood, including: 1. measles/ measles (a prodrom with chorise, cough, conjunctivitis and Koplik spots on the oral mucosa, the rash starting retroauricular, at the hair implantation line and on the forehead and then spreads down the body, often becoming confluence), 2. rubella (starts on the forehead and face and then spreads down the body, healing in the same order and is associated with retrouricular and suboccipital adenopathy) and 3. infectious erythema (fifth disease, cheek erythema is followed by a reticulated drawing on the extremities, being secondary to an infection with parvovirus and in adults associated arthritis is found).
Both measles and rubella are found in young unvaccinated adults and an atypical form of measles is found in adults immunized with either measles (inactivated) or vaccine (inactivated) followed by live virus vaccine. Unlike classical measles, the rash in atypical measles begins on the palms, plants, fist joint and wrists of the fingers and the lesions can become purple. The patient with atypical measles may have lung damage and an altered general condition. Rubella and rozeoliform rashes are also associated with Epstein-Barr virus infections (5-15% of patients), echovirus, coxsackie virus and adenovirus. Detection of specific IgM antibodies or a four-fold increase in serum IgG levels allows correct diagnosis.
Sometimes a maculopapular rash is the result of a virus-drug interaction. For example, about 95% of patients with infectious mononucleosis receiving ampicillin will develop a rash. Note, early in the evolution of infections with Rickettsia and meningococcal, before the appearance of purple, lesions can be macula and erythematous papules. The same happens in chickenpox before blisters appear. Maculopapulous rashes are associated with early HIV infection, early secondary syphilis, typhoid fever and acute graft-versus-host disease. At the latter, lesions frequently begin on palms and plants and pink macular spots of typhoid fever mainly include the anterior trunk.
Typical scarlet fever rash is found in scarlet fever and is due to an erythrotoxin produced by group A beta-hemolytic streptococcus infections, most commonly pharyngitis. There is a diffuse erythema that begins on the neck and upper torso and perifolicular red dots. The associated lesions are the white-raspberry tongue (white surface with red papillae), followed by red-raspberry tongue (red tongue with red papillae), palate spots, a facial flush with pallor around the mouth, linear spots in the antecubital fossa and peeling of the affected skin, palms and plants 5-20 days after the onset of the rash. A similar descuation of the palms and plants is found in toxic shock syndrome, Kawasaki disease and after severe febrile diseases. Certain strains of staphylococcus also produce an erythrotoxin that causes the same clinical signs as in streptococcal scarlet fever except for the antistreptolysis O titre (ASLO) which is not increased.
In septic shock syndrome (TSS), staphylococcal infections (group I phages) produce an exotoxin (TSST-1) that causes fever and rash, as well as enterotoxins. Initially the majority of cases were reported in women who used tampons during the menstrual period. However, other sites of infection, including wounds and vaginitis, can produce TSS. The diagnosis is based on clinical criteria and three of these include monocutaneous localizations. Clinical criteria are: 1. fever, 2. diffuse skin erythema, 3. palm-plantar descuamation 1-2 weeks after the onset of the disease, 4. hypotension and 5. damage to three or more organ systems, including the gastrointestinal tract, musculature, kidneys, liver, CNS, blood (thrombocytopenia) and mucous membranes. The latter lesions are represented by hyperemia of the vagina, oropharynx or conjunctiva. Similar systemic lesions have also been described in streptococcal septic shock-like syndrome, stroptococcal toxic skin-like syndrome, and although an examination is observed less frequently than in TSS caused by a staphylococcal infection, the underlying infection is often found in soft tissues.
The rash of Kawasaki disease (mucocutaneous and lymph node syndrome) is polymorphic, but the most common clinical forms are morbiliform and scarlet fever. Most cases occur in children under 5 years of age, but cases have also been reported in adults. Diagnosis is based on fever, exceeding 5 days, plus four or five of the following criteria: 1. bilateral conjunctival erythema, 2. exanthema, 3. cervical adenopathy, usually unilateral, 4. erythema and edema of the hands and feet, followed by descuamation and 5. diffuse erythema of the oropharynx, raspberry tongue and erosions of the lips with crust formation. This clinical picture may resemble septic shock and scarlet fever, but the clues for the diagnosis of Kawasaki disease are cervical adenopathy, labial erosions and thrombocytosis. The most serious systemic manifestation associated with this disease is coronary aneurysm secondary to arteritis. Aneurysms can lead to sudden death, especially during the first 30 days of illness. Scarlet rash is also found in the early stages of SSS, and as drug reactions.
No more of this post.
I'm going to start this post with "discussions" about blisters/bubbles.
Depending on their size, skin lesions with liquid contents are called blisters (less than 0.5 cm) or bubbles (more than 0.5 cm). Primary bullous diseases include vulgar pemfigus, foliaceu pemfigus, erythematous pemfigus, bullos pemfigoid, gestationis herpes, scar pemigoid, acquired bullous epidermisis, linear IgA disease and herpetiform dermatitis.
Vesicles and bubbles are also found in contact dermatitis, both in the irritant and allergic forms. When there is a linear arrangement of vesicular lesions, an exogenous cause must be suspected. Bullous diseases secondary to drug ingestion can take one of the forms: phototoxic rash, isolated bubbles, toxic epidermal necrolysis and polymorphic erythema. Clinically, phototoxic eruptions resemble an exaggerated sunburn, diffuse erythema and bubbles in sun-exposed regions. The most commonly associated drugs are thiazides, tetracyclines, sulfonamides, phenothiazides, nonsteroidal anti-inflammatory drugs (NSAIDs) and psoralians. The occurrence of a phototoxic rash depends on the doses of the drug and UV-A irradiation.
Toxic epidermal necrolysis (NET) is characterized by bubbles that appear on the surface of large areas of erythema, which then take off. This leads to large areas of denuded skin. Associated morbidity, such as septicaemia, and mortality are relatively high and are depending on the extent of epidermal necrosis. In addition, these patients may also experience damage to the mucous membranes and intestinal tract. The drugs are the primary cause of NET and the most common etiological agents are phenytoin, barbiturates, sulfonamides, penicillins and NSAIDs. Severe acute graft-versus-host disease (grade 4) may also resemble NET.
In polymorphic erythema (EP), the primary lesions are pink-red macula and edematous papules, the center of which can become vesicular. What suggests the diagnosis of EP, rather than a drug-induced morbiliform examination, is the appearance of a dark purple color of the spots in the center of the lesions. "Target" or iris lesions are also characteristic for EP and they occur as a result of the appearance of the edges and the more intensely colored center, more active in combination with the centrifugal extension. However, lesions in the iris should not be present to confirm the diagnosis of EP.
The preferred regions of damage include hands, forearms (extensor faces), palms, plants and mucous membranes (oral, nasal, ocular and genital). Hemorrhagic lip crusts are characteristic for EP, as well as for two other bullous disorders (vulgar pemfigus and NET). Fever, malaise, myalgia, pharyngeal pain and cough may precede or accompany the rash. EP lesions usually heal within 3-6 weeks, but can be recurrent. Drugs can induce EP, especially subphoneamides, phenytoin, barbiturates, penicillins and carbamazepine, but they are not the triggers in most cases, especially in young adults. Herpes simplex infections are the most common cause of EP in this age group and lesions occur 7-12 days after viral eruption.
Other infectious agents associated with EP include Mycoplasma pneumoniae, Histoplasma capsulatum, Coccidiides immitis, Yersinia enterocolica and several viruses (echovirus, coxsackie, Epstein-Barr and influenza virus). EP may also follow after vaccinations with BCG, polio or vaccine virus and after radiation therapy (radiotherapy) and exposure to toxins from the environment. In addition to primary bullous diseases and hypersensitivity reactions, viral and bacterial infections can produce blisters and bubbles. The most common infectious agents are herpes simplex, herpes varicella-zoster and staphylococcus.
Staphylococcal epidermal necrolysis syndrome (SSSS) and bullos impetigo are two bullous conditions associated with staphylococcal infection (type I phages). In SSSS, the initial signs are erythema and pain in the region of the face, neck, torso and intertriginous areas. These are followed by short-lived flasce bubbles, take-off or exfoliation of the superficial epidermis. Crusty areas then appear, characteristically around the mouth. SSSS is distinguished from NET by the following traits: younger age group, the more superficial layer of bubble formation, no lesions in the oral cavity, shorter evolution, lower morbidity or mortality and an association with staphylococcal exfoliative toxin ("exfoliatin"), not associating with drugs.
A rapid differential diagnosis between SS and NET can be made through a section of the bubble (with the cryoseeker) or by exfoliative cytology of the bubble content. In SSS, the location of staphylococcal infection is usually extracutaneous (conjunctivitis, rhinorrhea, otitis media, pharyngitis, tonsillitis) and lesions are sterile, while in the impetigo bulos lesions are in the region of infection. The impetigo is more localized than SSSS and is usually presented with melicitic crusts. Sometimes purulent superficial bubbles can also form. Cutaneous embolisms from gram-negative infections may present as isolated bubbles, but the basis of the lesion is purple or necrotic and may progress to ulcers.
Several metabolic disorders are associated with bubble formation, including diabetes mellitus, renal failure and porphyria. Local hypoxia secondary to low blood flow can also produce bubbles, which explains the presence of bubbles on pressure points in comatous patients (coma bubbles). In diabetes mellitus, bubbles strained with clear viscous fluid appear on normal skin. The lesions can be up to 6 cm in diameter and are localized on the distal extremities. There are several types of porphyria, but the most common form with skin signs is late skin porphyria (PCT). On solar exposed regions (especially face and hands), the skin is very fragile and trauma causes erosion and bubbles in tension.
These lesions are subsequently cured with scarring and formation of mirium (the latter are firm, white or yellow papules, of 2-3 mm, which represent inclusion epidermoid cysts). Associated lesions may be hypertrichosis of the lateral malarial regions (in men) or face (in women) and, in areas exposed to sunlight, hyperpigmentation and firm sclerous papules. An increased level of urinary uroporphyrin confirms the diagnosis and is due to a decrease in the activity of uroporphyrinogen-decarboxylase. Favourable agents include alcohol, iron, chlorinated hydrocarbons and hepatitis C virus infection.
Differential diagnosis of PCT includes: 1. porfiria variegata (pct skin signs plus systemic findings of acute intermittent porphyria, having a diagnostic fluorescent emission of plasma porphyrin at 626 nm), 2. photosensitivity reactions of a drug-induced bulos character (pseudoforfiria - clinical and histological findings are similar to PCT, but porphyrins are normal, etiological agents being furosemide, tetracycline, nalidixic acid, dapsona, naproxen and pyridoxine), 3. bullous dermatosis of hemodialysis (the same aspect as PCT, but porphyrins are usually normal or sometimes elevated to the limit of normal, patients having chronic renal failure and are hemodialysis), 4. PCT associated with hepatomas, liver carcinomas and hemodialysis and 5. acquired bullous epidermolysis.
I will complete this post with the presentation of some elements about exanthemas. The causes of exanthema are represented by: I. for those morbiliforms with A. drugs, B. viral (1. rubella, 2. measles/ measles, 3. infectious erythema, 4. Epstein-Barr, echovirus, Coxsackie virus and adenovirus, 5. EARLY HIV), Bacterial C. (1. typhoid fever, early secondary syphilis, 3. early in rickettsioze, early in meningococemia), D. acute graft-versus-host disease and II. for those scarlet fever with A. scarlet fever, B. toxic shock syndrome and C. Kawasaki disease.
Exantems are characterized by a generalized acute rash. The two modes of presentation with maximum frequency are: papules and erythematous macula (morbiliforms) and confluent erythema (scarlatiniform). Morbiliform rashes are usually due to either drugs or viral infections. For example, up to 5% of patients receiving penicillins, sulfonamides, captopril, phenytoin or gold will develop a maculopapular rash. Accompanying signs may include pruritus, fever, eosinophilia and transient adenopathy.
Similar maculopapular eruptions are found in the classic viral exanthemas of childhood, including: 1. measles/ measles (a prodrom with chorise, cough, conjunctivitis and Koplik spots on the oral mucosa, the rash starting retroauricular, at the hair implantation line and on the forehead and then spreads down the body, often becoming confluence), 2. rubella (starts on the forehead and face and then spreads down the body, healing in the same order and is associated with retrouricular and suboccipital adenopathy) and 3. infectious erythema (fifth disease, cheek erythema is followed by a reticulated drawing on the extremities, being secondary to an infection with parvovirus and in adults associated arthritis is found).
Both measles and rubella are found in young unvaccinated adults and an atypical form of measles is found in adults immunized with either measles (inactivated) or vaccine (inactivated) followed by live virus vaccine. Unlike classical measles, the rash in atypical measles begins on the palms, plants, fist joint and wrists of the fingers and the lesions can become purple. The patient with atypical measles may have lung damage and an altered general condition. Rubella and rozeoliform rashes are also associated with Epstein-Barr virus infections (5-15% of patients), echovirus, coxsackie virus and adenovirus. Detection of specific IgM antibodies or a four-fold increase in serum IgG levels allows correct diagnosis.
Sometimes a maculopapular rash is the result of a virus-drug interaction. For example, about 95% of patients with infectious mononucleosis receiving ampicillin will develop a rash. Note, early in the evolution of infections with Rickettsia and meningococcal, before the appearance of purple, lesions can be macula and erythematous papules. The same happens in chickenpox before blisters appear. Maculopapulous rashes are associated with early HIV infection, early secondary syphilis, typhoid fever and acute graft-versus-host disease. At the latter, lesions frequently begin on palms and plants and pink macular spots of typhoid fever mainly include the anterior trunk.
Typical scarlet fever rash is found in scarlet fever and is due to an erythrotoxin produced by group A beta-hemolytic streptococcus infections, most commonly pharyngitis. There is a diffuse erythema that begins on the neck and upper torso and perifolicular red dots. The associated lesions are the white-raspberry tongue (white surface with red papillae), followed by red-raspberry tongue (red tongue with red papillae), palate spots, a facial flush with pallor around the mouth, linear spots in the antecubital fossa and peeling of the affected skin, palms and plants 5-20 days after the onset of the rash. A similar descuation of the palms and plants is found in toxic shock syndrome, Kawasaki disease and after severe febrile diseases. Certain strains of staphylococcus also produce an erythrotoxin that causes the same clinical signs as in streptococcal scarlet fever except for the antistreptolysis O titre (ASLO) which is not increased.
In septic shock syndrome (TSS), staphylococcal infections (group I phages) produce an exotoxin (TSST-1) that causes fever and rash, as well as enterotoxins. Initially the majority of cases were reported in women who used tampons during the menstrual period. However, other sites of infection, including wounds and vaginitis, can produce TSS. The diagnosis is based on clinical criteria and three of these include monocutaneous localizations. Clinical criteria are: 1. fever, 2. diffuse skin erythema, 3. palm-plantar descuamation 1-2 weeks after the onset of the disease, 4. hypotension and 5. damage to three or more organ systems, including the gastrointestinal tract, musculature, kidneys, liver, CNS, blood (thrombocytopenia) and mucous membranes. The latter lesions are represented by hyperemia of the vagina, oropharynx or conjunctiva. Similar systemic lesions have also been described in streptococcal septic shock-like syndrome, stroptococcal toxic skin-like syndrome, and although an examination is observed less frequently than in TSS caused by a staphylococcal infection, the underlying infection is often found in soft tissues.
The rash of Kawasaki disease (mucocutaneous and lymph node syndrome) is polymorphic, but the most common clinical forms are morbiliform and scarlet fever. Most cases occur in children under 5 years of age, but cases have also been reported in adults. Diagnosis is based on fever, exceeding 5 days, plus four or five of the following criteria: 1. bilateral conjunctival erythema, 2. exanthema, 3. cervical adenopathy, usually unilateral, 4. erythema and edema of the hands and feet, followed by descuamation and 5. diffuse erythema of the oropharynx, raspberry tongue and erosions of the lips with crust formation. This clinical picture may resemble septic shock and scarlet fever, but the clues for the diagnosis of Kawasaki disease are cervical adenopathy, labial erosions and thrombocytosis. The most serious systemic manifestation associated with this disease is coronary aneurysm secondary to arteritis. Aneurysms can lead to sudden death, especially during the first 30 days of illness. Scarlet rash is also found in the early stages of SSS, and as drug reactions.
No more of this post.
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