STUDY - Technical - New Dacian's Medicine
Skin
Manifestations of Internal Diseases (1)
Translation Draft
It is now a generally accepted fact in medicine that the skin may show signs of internal
diseases. Therefore, in the medical treaties there will always be a chapter describing in detail the major systemic conditions that can be identified by skin signs.
The assumption behind such a chapter is that a clinician has been able to identify the patient's medical condition and only needs to read about it in a treatise. In reality, rapid differential diagnosis and identification of these conditions are actually difficult for a nondermatologist, as it is not versed in the recognition of skin lesions or their presentation spectrum.
Therefore, general approaches seek to cover the particular theme of skin medicine not by discussing individual conditions, but by describing and discussing the various clinical signs and symptoms of presentation indicating the presence of these conditions. Concise differential diagnoses are thus presented, in which significant diseases are briefly discussed and separated from more common diseases that have no significance for internal diseases.
The latter are summarized in descriptions/ tables and should always be excluded when thinking of a dermatological condition. For a detailed description of individual diseases, the reader must study a dermatological text. The categories of skin lesions discussed include papuloscuamous lesions, erythroderma, alopecia, figurative lesions, acne, pustules, telangiectasis, hypopigmentation, hyperpigmentation, vesicles/ bubbles, exantems, urticaria, papulonodular lesions, purpura and ulcers.
In trying to determine the appropriate category for called lesion, it is important to examine its surface appearance, shape and color, as well as location and distribution.
We'll start with the papuloscuamous skin lesions. The important causes of papuloscumus skin lesions are represented by: 1. primary skin conditions (psoriasis, tinea, pinkish pitiriazis, lichen plan, parapsoriasis and Bowen's disease/ spinocellular carcinoma in situ), 2. medicines, 3. systemic diseases (lupus erythematosus, T-cell skin lymphoma, secondary syphilis and Reiter syndrome). When an eruption is characterized by elevated lesions, papules less than 1 cm or plaques larger than 1 cm in combination with scuba, it is called papuloscuamy. The most common papuloscuamous conditions (psoriasis, tinea, pinkish pitiriazis and plan lichen) are primary skin conditions. These primary skin conditions/ primary skin conditions are represented by: 1. psoriasis (with characteristic red-red lesion, silvery scuba and net demarcation, localized at the elbows, knees, scalp and pressed area, having as other signs nail dystrophy with puncitiform/ pitting depressions, onicolesis and yellow color change including arthritis, especially in small joints of the hands and feet, causing as useful investigations for the diagnosis of skin biopsy and culture for beta-hemolytic streptococcus and treatment represented by the interruption of possible provocative agents, topical glucocorticoids, keratolitics, tardons and vitamin D, UV-B, PUVA and methotrexate), 2. (with characteristic pink-red lesions, with frequent central healing, active edge with descuamations, localized on the inner face of the thigh/ tinea cruris, palms, plants or any surface of the body, having as other signs the invasion of the corneal layer by dermatophytes, causing as useful investigations KOH and/ or mycotic culture of scumes and treatment represented by topical or systemic antimycotics, e.g. imidazoles, triazoli, allylamines and griseofulvin), 3. pinkish pitiriazis (with characteristic pink-orange lesions, oval shape, long axis following the cleavage lines of the skin, peripheral and squamous coloured, localized on the trunk and proximal extremities, having as other signs heraldic spots as initial lesions and usually the largest in size with spontaneous healing in 2-3 months, determining as useful investigations skin biopsy and VDRL for the exclusion of secondary syphilis and treatment represented by discontinuation of possible provoking agents, antihistamines, topical glucocorticoids and exposure to UV-B if disseminated) and 4. plane lichen (with characteristic purple, polygonal, flat-roofed lesions, crossed by thin white lines/ Wickham streaks, with localization in flexion regions of the hand joints, ankles, the pressed area and the penis gland, having as other signs reticulated white plaques and/ or erosions on the oral mucosa, pruritus and nail dystrophy with pterigium and longitudinal grooves, determining as a useful investigation skin biopsy, with a treatment represented by the removal of possible provoking agents such as topical glucocorticoids, PUVA and per os glucocorticoids).
When psoriatic lesions are accompanied by arthritis, the possibility of psoriatic arthritis or Reiter disease should be considered. A history of oral ulceration, conjunctivitis, uveitis and/ or urethritis indicates this last diagnosis. In gout psoriasis there is an acute onset with small, uniform lesions, disseminated over large areas, often in association with a streptococcal infection. Lithium, beta-blockers, HIV infection and rapidly decreasing the dose of systemic glucocorticoids are also known as factors exacerbating psoriasis.
Epidermal hyperproliferation and incomplete maturation are responsible for the formation of plaques and scubates characteristic for psoriasis. Always when making the diagnosis of pinkish pitiriazis or lichen plan it is good to check the patient's medication, since the rash can be treated by simple interruption of the provoking agent. Medicinally induced eruptions similar to pink pityriasis are most commonly found as reactions to beta-blockers, captopril, gold and metronidazole, while drugs that can cause a lichenoid rash include gold, antimalarials, thiazides, quinidine, phenothiazides, sulfonilation, beta-blockers and captopril. Lichen plan lesions are also found in chronic graft-versus-host disease.
Parapsoriasis is an intermediate disease, as it can remain only as a primary skin disease or progress to T-cell skin lymphoma (LCCT) after a latency period of up to 40 years. There are several forms of parapsoriasis, comprising the shape with smaller plates (0.5 - 5 cm), with large plates (larger than 6 cm) and the retiform one. The lesions of parapsoriasis with small plates and those of parapsoriasis with large plates are superficial, orange in color, with fine, white smes. In forms with small plates, lesions are usually on the trunk, but can be widely disseminated.
In large plate forms, the most common localization is the area of the "belt" and often a fine wrinkle secondary to epidermal atrophy is encountered. Retiform parapsoriasis causes a networked appearance and the individual papules are red-brown and flat. The last two forms of parapsoriasis, with large plates and retiform, can evolve to LCCT. An indication of the development of LCCT in lesions of parapsoriasis with large or retiform plaques is an amplification of the palpable component of the plaque (increased infiltration). In the early stages, LCCT may be mistaken for eczema or psoriasis, but often does not respond to appropriate therapy for these inflammatory diseases.
Diagnosis of LCCT is established by skin biopsy that highlights collections of atypical T lymphocytes found in the epidermis and dermis. As the disease progresses, skin tumors and lymph node damage may occur. In secondary syphilis appear disseminated red-brown papules with thin scuba. The rash often affects palms and plants and can resemble pinkish pitiriazis. The associated findings are useful in establishing the diagnosis and include annulment plaques on the face, non-scarcation alopecia, wide candyloma (wide and moist base) and mucous plaques, as well as adenopathy, malaise, fever, headache and myalgia. The interval between primary and secondary stage is usually 4-8 weeks and spontaneous resolution in the absence of adequate therapy is encountered.
Erythroderma is the term used when most of the skin surface is erythematous (red in color). It can be associated with scabs, erosions or pustules, as well as hair or nail loss. Potential systemic manifestations include fever, chills, hypothermia, reactive adenopathy, peripheral edema, hypoalbuminemia and high-flow heart failure. the main causes of erythroderma are: 1. skin diseases, such as psoriasis and dermatitis, 2. drugs, 3. systemic diseases, most commonly LCCT and 4. Idiopathic.
In the first three groups, the location and description of the initial lesions, before the occurrence of erythroderma, helps with the diagnosis. For example, a history of squamous red plaques on the elbows and knees would indicate psoriasis. It is also important to examine the skin carefully, following the possible migration of erythema and associated secondary changes, such as pustules or erosions. Migratory erythema spouts sprinkled with superficial pustules are found in pustulous psoriasis. A secondary erythroderma of an underlying skin disease is most commonly due to psoriasis or one of the various forms of dermatitis (eczema). Each type of dermatitis has its distinctive features, but these may be limited to initial lesions.
Erythroderma (primary skin disorders) may be secondary to the following conditions: 1. psoriasis (with initial pink-red lesions, with silver squamous, with net delimitation, in which the initial lesions are localized in the elbows, knees, scalp and presacrate area, including nail dystrophy, arthritis and pustules, determining as useful investigations for skin biopsy diagnosis and treatment with/ without PUVA and methotrexate), 2. atopic dermatitis (in acute form having initial lesions in the form of erythema, fine squamous, crust, diffuse edges and in the chronic form in the form of lichenification/ accentuated skin drawing, localized in the antecubital and popliteal fossa, neck and hands, finding and pruritus, family history of atopia including asthma, allergic rhinitis, allergic conjunctivitis and atopic dermatitis, as well as the elimination of S. aureus infection or the elimination of over-additional irritant contact dermatitis, causing as useful investigations skin biopsy and treatment with topical glucocorticoids, tar and antipruriginous, antihistamines per bone, non-occlusive wet wraps, UV-B plus UV-A, PUVA, glucocorticoids per bone/ im, topical antibiotics or per bone), 3. stasis (with initial lesions represented by erythema, crusts, excoriations, with localization in the lower extremities, having as additional signs pruritus, edema of the lower limbs, history of venous ulcers, thrombophlebitis and/ or cellulitis, exclusion of the existence of cellulite, exclusion of over-added contact dermatitis, e.g. that given by topically applied neomycin, causing as useful investigations skin biopsy and treatment with topical glucocorticoids, non-occlusive wet compresses, lifting the foot above the horizontal plane and the use of compressive medical stockings), 4. local contact (with initial lesions represented by erythema, crusts, blisters and bubbles, localized depending on the provoking agent, additional irritant signs with onset within a few hours or allergic with delayed type hypersensitivity with a latency time of 48 hours, causing as a diagnostic reaction epicutan testing and as a treatment the removal of irritant or allergen, administration of topical glucocorticoids, or per bone/ im and oral antihistamines), 5. systemic contact (with initial lesions represented by erythema, fine scuba, crust with generalized localization, with additional signs represented by the fact that the patient has a history of allergic contact dermatitis to a topical agent and then receives systemic medication that is structurally related to it, e.g. topical ethylendiamide and aminophilin iv), 6. seborrheic (with initial pink-red lesions, with fatty squamous, localized to the scalp, nasolabial folds, eyebrows and intertriginous areas, or additional signs of stress exacerbation, HIV infection and association with Parkinson's disease, causing as a diagnostic reaction skin biopsy and as treatment topical glucocorticoids and imidazoles) and 7. pitiriazis rubra pilaris (with initial red-orange, perifolicular and papule lesions, with generalised localization, but with characteristic regions of normal skin/ "omissed", with additional signs represented by kerous keratodermy and exclusion of the existence of T-cell skin lymphoma, causing as a diagnostic reaction the skin biopsy and as a treatment the administration of isotretinoin or etretinate and methotrexate).
Medicinally induced erythroderma (exfoliative dermatitis) may begin with a morbiliform rash or may begin as a diffuse erythema. Peripheral fever and eosinophilia often accompany the rash, and sometimes allergic interstitial nephritis is associated. A number of drugs can cause erythroderma, including penicillins, sulfonamides, carbamazepine, phenytoin, gold, allopurinol, captopril and the stimulating factor of granulocytes-macrophage colonies. While reactions to anticonvulsants may cause pseudolymphomatos syndrome, allopurinol reactions may be accompanied by hepatitis, gastrointestinal bleeding and nephropathy.
The most common malignant disease associated with erythroderma is LCCT (in some series, up to 25% of cases of erythroderma were due to LCCT). Patient lesions may be papules and isolated tumors, but most commonly erythroderma is present throughout the course of the disease (Sesary syndrome). In Sesary syndrome there are circulating atypical T lymphocytes, pruritus and adenopathy. In cases of erythrodermy, including Hodgkin's and nonhodgkinian lymphomas, the first being the most common. Isolated cases of secondary erythrodermy have also been reported for solid tumours of the lung, liver, prostate, thyroid and colon (but usually at a late stage of the disease).
That's really enough for today...
It is now a generally accepted fact in medicine that the skin may show signs of internal
diseases. Therefore, in the medical treaties there will always be a chapter describing in detail the major systemic conditions that can be identified by skin signs.
The assumption behind such a chapter is that a clinician has been able to identify the patient's medical condition and only needs to read about it in a treatise. In reality, rapid differential diagnosis and identification of these conditions are actually difficult for a nondermatologist, as it is not versed in the recognition of skin lesions or their presentation spectrum.
Therefore, general approaches seek to cover the particular theme of skin medicine not by discussing individual conditions, but by describing and discussing the various clinical signs and symptoms of presentation indicating the presence of these conditions. Concise differential diagnoses are thus presented, in which significant diseases are briefly discussed and separated from more common diseases that have no significance for internal diseases.
The latter are summarized in descriptions/ tables and should always be excluded when thinking of a dermatological condition. For a detailed description of individual diseases, the reader must study a dermatological text. The categories of skin lesions discussed include papuloscuamous lesions, erythroderma, alopecia, figurative lesions, acne, pustules, telangiectasis, hypopigmentation, hyperpigmentation, vesicles/ bubbles, exantems, urticaria, papulonodular lesions, purpura and ulcers.
In trying to determine the appropriate category for called lesion, it is important to examine its surface appearance, shape and color, as well as location and distribution.
We'll start with the papuloscuamous skin lesions. The important causes of papuloscumus skin lesions are represented by: 1. primary skin conditions (psoriasis, tinea, pinkish pitiriazis, lichen plan, parapsoriasis and Bowen's disease/ spinocellular carcinoma in situ), 2. medicines, 3. systemic diseases (lupus erythematosus, T-cell skin lymphoma, secondary syphilis and Reiter syndrome). When an eruption is characterized by elevated lesions, papules less than 1 cm or plaques larger than 1 cm in combination with scuba, it is called papuloscuamy. The most common papuloscuamous conditions (psoriasis, tinea, pinkish pitiriazis and plan lichen) are primary skin conditions. These primary skin conditions/ primary skin conditions are represented by: 1. psoriasis (with characteristic red-red lesion, silvery scuba and net demarcation, localized at the elbows, knees, scalp and pressed area, having as other signs nail dystrophy with puncitiform/ pitting depressions, onicolesis and yellow color change including arthritis, especially in small joints of the hands and feet, causing as useful investigations for the diagnosis of skin biopsy and culture for beta-hemolytic streptococcus and treatment represented by the interruption of possible provocative agents, topical glucocorticoids, keratolitics, tardons and vitamin D, UV-B, PUVA and methotrexate), 2. (with characteristic pink-red lesions, with frequent central healing, active edge with descuamations, localized on the inner face of the thigh/ tinea cruris, palms, plants or any surface of the body, having as other signs the invasion of the corneal layer by dermatophytes, causing as useful investigations KOH and/ or mycotic culture of scumes and treatment represented by topical or systemic antimycotics, e.g. imidazoles, triazoli, allylamines and griseofulvin), 3. pinkish pitiriazis (with characteristic pink-orange lesions, oval shape, long axis following the cleavage lines of the skin, peripheral and squamous coloured, localized on the trunk and proximal extremities, having as other signs heraldic spots as initial lesions and usually the largest in size with spontaneous healing in 2-3 months, determining as useful investigations skin biopsy and VDRL for the exclusion of secondary syphilis and treatment represented by discontinuation of possible provoking agents, antihistamines, topical glucocorticoids and exposure to UV-B if disseminated) and 4. plane lichen (with characteristic purple, polygonal, flat-roofed lesions, crossed by thin white lines/ Wickham streaks, with localization in flexion regions of the hand joints, ankles, the pressed area and the penis gland, having as other signs reticulated white plaques and/ or erosions on the oral mucosa, pruritus and nail dystrophy with pterigium and longitudinal grooves, determining as a useful investigation skin biopsy, with a treatment represented by the removal of possible provoking agents such as topical glucocorticoids, PUVA and per os glucocorticoids).
When psoriatic lesions are accompanied by arthritis, the possibility of psoriatic arthritis or Reiter disease should be considered. A history of oral ulceration, conjunctivitis, uveitis and/ or urethritis indicates this last diagnosis. In gout psoriasis there is an acute onset with small, uniform lesions, disseminated over large areas, often in association with a streptococcal infection. Lithium, beta-blockers, HIV infection and rapidly decreasing the dose of systemic glucocorticoids are also known as factors exacerbating psoriasis.
Epidermal hyperproliferation and incomplete maturation are responsible for the formation of plaques and scubates characteristic for psoriasis. Always when making the diagnosis of pinkish pitiriazis or lichen plan it is good to check the patient's medication, since the rash can be treated by simple interruption of the provoking agent. Medicinally induced eruptions similar to pink pityriasis are most commonly found as reactions to beta-blockers, captopril, gold and metronidazole, while drugs that can cause a lichenoid rash include gold, antimalarials, thiazides, quinidine, phenothiazides, sulfonilation, beta-blockers and captopril. Lichen plan lesions are also found in chronic graft-versus-host disease.
Parapsoriasis is an intermediate disease, as it can remain only as a primary skin disease or progress to T-cell skin lymphoma (LCCT) after a latency period of up to 40 years. There are several forms of parapsoriasis, comprising the shape with smaller plates (0.5 - 5 cm), with large plates (larger than 6 cm) and the retiform one. The lesions of parapsoriasis with small plates and those of parapsoriasis with large plates are superficial, orange in color, with fine, white smes. In forms with small plates, lesions are usually on the trunk, but can be widely disseminated.
In large plate forms, the most common localization is the area of the "belt" and often a fine wrinkle secondary to epidermal atrophy is encountered. Retiform parapsoriasis causes a networked appearance and the individual papules are red-brown and flat. The last two forms of parapsoriasis, with large plates and retiform, can evolve to LCCT. An indication of the development of LCCT in lesions of parapsoriasis with large or retiform plaques is an amplification of the palpable component of the plaque (increased infiltration). In the early stages, LCCT may be mistaken for eczema or psoriasis, but often does not respond to appropriate therapy for these inflammatory diseases.
Diagnosis of LCCT is established by skin biopsy that highlights collections of atypical T lymphocytes found in the epidermis and dermis. As the disease progresses, skin tumors and lymph node damage may occur. In secondary syphilis appear disseminated red-brown papules with thin scuba. The rash often affects palms and plants and can resemble pinkish pitiriazis. The associated findings are useful in establishing the diagnosis and include annulment plaques on the face, non-scarcation alopecia, wide candyloma (wide and moist base) and mucous plaques, as well as adenopathy, malaise, fever, headache and myalgia. The interval between primary and secondary stage is usually 4-8 weeks and spontaneous resolution in the absence of adequate therapy is encountered.
Erythroderma is the term used when most of the skin surface is erythematous (red in color). It can be associated with scabs, erosions or pustules, as well as hair or nail loss. Potential systemic manifestations include fever, chills, hypothermia, reactive adenopathy, peripheral edema, hypoalbuminemia and high-flow heart failure. the main causes of erythroderma are: 1. skin diseases, such as psoriasis and dermatitis, 2. drugs, 3. systemic diseases, most commonly LCCT and 4. Idiopathic.
In the first three groups, the location and description of the initial lesions, before the occurrence of erythroderma, helps with the diagnosis. For example, a history of squamous red plaques on the elbows and knees would indicate psoriasis. It is also important to examine the skin carefully, following the possible migration of erythema and associated secondary changes, such as pustules or erosions. Migratory erythema spouts sprinkled with superficial pustules are found in pustulous psoriasis. A secondary erythroderma of an underlying skin disease is most commonly due to psoriasis or one of the various forms of dermatitis (eczema). Each type of dermatitis has its distinctive features, but these may be limited to initial lesions.
Erythroderma (primary skin disorders) may be secondary to the following conditions: 1. psoriasis (with initial pink-red lesions, with silver squamous, with net delimitation, in which the initial lesions are localized in the elbows, knees, scalp and presacrate area, including nail dystrophy, arthritis and pustules, determining as useful investigations for skin biopsy diagnosis and treatment with/ without PUVA and methotrexate), 2. atopic dermatitis (in acute form having initial lesions in the form of erythema, fine squamous, crust, diffuse edges and in the chronic form in the form of lichenification/ accentuated skin drawing, localized in the antecubital and popliteal fossa, neck and hands, finding and pruritus, family history of atopia including asthma, allergic rhinitis, allergic conjunctivitis and atopic dermatitis, as well as the elimination of S. aureus infection or the elimination of over-additional irritant contact dermatitis, causing as useful investigations skin biopsy and treatment with topical glucocorticoids, tar and antipruriginous, antihistamines per bone, non-occlusive wet wraps, UV-B plus UV-A, PUVA, glucocorticoids per bone/ im, topical antibiotics or per bone), 3. stasis (with initial lesions represented by erythema, crusts, excoriations, with localization in the lower extremities, having as additional signs pruritus, edema of the lower limbs, history of venous ulcers, thrombophlebitis and/ or cellulitis, exclusion of the existence of cellulite, exclusion of over-added contact dermatitis, e.g. that given by topically applied neomycin, causing as useful investigations skin biopsy and treatment with topical glucocorticoids, non-occlusive wet compresses, lifting the foot above the horizontal plane and the use of compressive medical stockings), 4. local contact (with initial lesions represented by erythema, crusts, blisters and bubbles, localized depending on the provoking agent, additional irritant signs with onset within a few hours or allergic with delayed type hypersensitivity with a latency time of 48 hours, causing as a diagnostic reaction epicutan testing and as a treatment the removal of irritant or allergen, administration of topical glucocorticoids, or per bone/ im and oral antihistamines), 5. systemic contact (with initial lesions represented by erythema, fine scuba, crust with generalized localization, with additional signs represented by the fact that the patient has a history of allergic contact dermatitis to a topical agent and then receives systemic medication that is structurally related to it, e.g. topical ethylendiamide and aminophilin iv), 6. seborrheic (with initial pink-red lesions, with fatty squamous, localized to the scalp, nasolabial folds, eyebrows and intertriginous areas, or additional signs of stress exacerbation, HIV infection and association with Parkinson's disease, causing as a diagnostic reaction skin biopsy and as treatment topical glucocorticoids and imidazoles) and 7. pitiriazis rubra pilaris (with initial red-orange, perifolicular and papule lesions, with generalised localization, but with characteristic regions of normal skin/ "omissed", with additional signs represented by kerous keratodermy and exclusion of the existence of T-cell skin lymphoma, causing as a diagnostic reaction the skin biopsy and as a treatment the administration of isotretinoin or etretinate and methotrexate).
Medicinally induced erythroderma (exfoliative dermatitis) may begin with a morbiliform rash or may begin as a diffuse erythema. Peripheral fever and eosinophilia often accompany the rash, and sometimes allergic interstitial nephritis is associated. A number of drugs can cause erythroderma, including penicillins, sulfonamides, carbamazepine, phenytoin, gold, allopurinol, captopril and the stimulating factor of granulocytes-macrophage colonies. While reactions to anticonvulsants may cause pseudolymphomatos syndrome, allopurinol reactions may be accompanied by hepatitis, gastrointestinal bleeding and nephropathy.
The most common malignant disease associated with erythroderma is LCCT (in some series, up to 25% of cases of erythroderma were due to LCCT). Patient lesions may be papules and isolated tumors, but most commonly erythroderma is present throughout the course of the disease (Sesary syndrome). In Sesary syndrome there are circulating atypical T lymphocytes, pruritus and adenopathy. In cases of erythrodermy, including Hodgkin's and nonhodgkinian lymphomas, the first being the most common. Isolated cases of secondary erythrodermy have also been reported for solid tumours of the lung, liver, prostate, thyroid and colon (but usually at a late stage of the disease).
That's really enough for today...
A good, fruitful week,
full of achievements, understanding, love and gratitude!
Dorin, Merticaru