dermatología 1

7/28/2019 Dermatologa 1

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Recopilacin realizada por: Dr. Ren Njera Alvarado - Neurlogo

Dermatologa 1

1. El tratamiento de eleccin para la tia de la cabeza en los pacientes peditricos es:

a) La nistatinab) El ketoconazolc) El fluconazold) La griseofulvinae) El clotrimazol

D) LA GRISEOFULVINA.- Las dermatofitosis o tias son infecciones micticas que afectan a lapiel y estructuras queratinizadas como pelos y uas. La tia del cuero cabelludo (tambindenominada Tinea capitis o Tinea tonsurans) es un tipo de tipo de tia no inflamatoria sonpropias de la infancia cursando con placas alopcicas con pelos rotos y descamacin. Por logeneral, al llegar la pubertad suelen curar espontneamente sin dejar cicatriz. El tratamiento deeleccin de la tia del cuero cabelludo en nios es la griseofulvina. La griseofulvina es deprimera eleccin en el tratamiento de las tias por su bajo precio, pero nunca est indicada enel tratamiento de una candidiasis cutnea. Otros frmacos tiles en el tratamiento de lasdermatofitosis son los imidazoles y la terbinafina.

2. En tipo de lepra que predomina en Mxico es la:

a) Precoz indeterminadab) Tuberculoidec) Multibacilard) Limtrofee) Lepromatosa

B) TUBERCULOIDE.- La lepra o enfermedad de Hansen est producida por Mycobacterium

leprae. Afecta sobre todo a piel y al sistema nervioso perifrico. Se requiere un contacto ntimo

y duradero para su transmisin. La inmunidad celular en determinante en la evolucin de la

enfermedad. La forma ms frecuente es la lepra tuberculoide polar, que se da en individuos con

buena inmunidad celular: placas hipocrmicas de bordes bien definidos con prdida precoz de

la sensibilidad. La baciloscopia es negativa y el Mitsuda es positivo. La lepra lepromatosa polar

se da en gente con mala respuesta inmune celular, es una forma multibacilar. La opcin que

dice precoz indeterminada hace referencia a la forma de comienza de casi todos los pacientes,

puede evolucionar hacia la curacin o hacia las otras formas clnicas. La forma borderline o

limtrofe presenta caractersticas clnicas de ambas formas polares.

3. Los tablejeros que manipulan carne de bovino infectada con Mycobacterium tuberculosisvariedad bovis tienen el riesgo de contraer tuberculosis:

a) Colicuativab) Micronodularc) Ndulo necrticad) Verrugosae) Escrufulosa


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4. En los preescolares y escolares la dermatitis atpica se localiza ms frecuentemente en:

a) las mejillasb) la cara posterior del cuelloc) los pliegues flexuralesd) los glteos

e) las manos y los pies

C) LOS PLIEGUES FLEXURALES.- La dermatitis atpica es un trastorno de la piel de cursocrnico y recidivante, cuya manifestacin principal es un eccema pruriginoso y la piel seca quedan lugar a un rascado continuo y a la posterior liquenificacin de las lesiones. Suele debutaren la infancia pudindose distinguir tres fases segn la localizacin de las lesiones. En ellactante predominan las lesiones en el cuero cabelludo y cara respetando el tringulonasogeniano, en la infancia estas se localizan principalmente a nivel de las flexionesantecubital y popltea, mientras que en el adulto suelen aparecer en cuellos, flexuras, dorso delas manos y en la cara.

5.- El medicamento de eleccin para tratar el imptigo en un lactante de ocho meses es:

a) Amoxicilinab) Fosfomicinac) Dicloxacilinad) Amikacinae) Rifampicina

El imptigo es una infeccin vesiculopustular y/o encostrada de la piel debida a Streptococcuspyogenes y/o Staphylococcus aureus. El imptigo buloso ocurre frecuentemente en el recin nacido oen los lactantes y es debido a S aureus. Aunque este padecimiento suele resuelve de maneraespontnea, se recomienda la inclusin de antibiticos para acelerar la curacin y evitarcomplicaciones como celulitis o glomerulonefritis. El tratamiento incluye 10 das con dicloxacilina,

cefalosporina de 1 generacin (cefalexina), clindamicina o mucopirocin tpico.

6.- Un marinero de 58 aos presenta desde hace 3 meses una neoformacin nodular de 1centmetro de dimetro localizada en la nariz. La lesin es brillante y tiene bordes perlados;adems, se observan telangiectasias. El diagnstico clnico ms probable es de:

a) Nevo atpico displsicob) Carcinoma espinocelularc) Melanoma nodulard) Nevo azule) Carcinoma basocelular

Los tumores malignos de la epidermis son: carcinoma basocelular y espinocelular. El carcinomabasocelular es el tumor maligno ms comn en el ser humano, mas frecuente en pieles claras conexposicin crnica a la luz solar. Con un frecuencia ligeramente > en hombres y en edad avanzada.La variedad nodular es la forma clnica ms comn, de aspecto papular, ligero eritema, contelangiectasias en la superficie, se puede observar depresin y ulceracin, tienen bordes perlados yelevados.


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7. - Which of the following diseases is caused by Bartonella species:

a) Strongilosisb) Miocardosisc) cat scratch diseased) Death

e) tularemia

Key signs and symptoms of Bartonella infections include dermal lesion (bacillary angiomatosis andchronic phase ofBartonella bacilliformis infection); papule at inoculation site followed by proximallymphadenopathy (cat scratch disease); fever, bacteremia, acute hemolytic anemia (acute phase ofB bacilliformis infection); persistent or relapsing fever (fever and bacteremia/endocarditis). Predisposingfactors include louse exposure, low income, and homelessness (Bartonella quintana-associatedbacillary angiomatosis, fever, and bacteremia/endocarditis); cat exposure (cat scratch disease andBartonella henselae-associated bacillary angiomatosis, fever and bacteremia/endocarditis);sandfly exposure in endemic areas of South American Andes (B bacilliformis infection). History of HIVor immunocompromise (bacillary angiomatosis). Key laboratory findings include small, curved,pleomorphic weakly gram-negative bacilli, best visualized with Warthin-Starry silver stain of tissue.

8.- Un hombre de 19 aos se presenta a consulta con lesiones pruriginosas en los pliegues delos codos el cuello y los huecos poplteos, constituidas por placas eccematosas yliquenificadas. El diagnstico ms probable es:

a) Dermatitis por contactob) Liquen planoc) Dermatitis atpicad) Psoriasise) Neurodermatitis

Criterios diagnsticos de la dermatitis atpica

CRITERIOS MAYORES1. Prurito2. Liquenificacin en flexuras en adultos3. Afectacin cara, flexuras y superficies de extensin en nios y jvenes4. Combinacin de estos patrones en nios y adultos5. Carcter crnica y recidivante6. Historia personal o familiar de atpia

CRITERIOS MENORES1. Xerosis2. Ictiosis/exageracin pliegues palmares/queratoris pilar3. Reactividad cutnea inmediata (tipo I) a los test cutneos

4. Elevacin valores sricos de IgE5. Edad precoz de comienzo6. Tendencia a infecciones cutneas y dficit de la inmunidad celular7. Tendencia a dermatitis inespecificas de pies y manos8. Eczema de pezn9. Queilitis10. Conjuntivitis recidivante11. Pliegue infraorbitario de Dennie-Morgan12. Queratocono


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13. Catarata subcapsular anterior14. Ojeras u oscurecimiento periocular15. Palidez facial o eritema en cara16. Pitiriasis alba17. Pliegues en parte anterior de cuello18. Prurito provocado por sudoracin

19. Intolerancia a la lana y los solventes de las grasas20. Acentuacin perifolicular21. Intolerancia a algunos alimentos22. Evolucin influenciada por factores ambientales y emocionales23. Dermografismo blanco

9.- En la piel la regulacin trmica se lleva a cabo por intervencin de:

a) Hipotlamob) Corteza cerebralc) Tlamod) Cerebeloe) Protuberancia

Las seales que activan los centros hipotlamicos reguladores de la temperatura provienen de dosfuentes: las clulas en la porcin anterior del hipotlamo, y los receptores cutneos para latemperatura, en especial los que perciben el frio.

10.- La dermatosis qu se transmite de persona a persona por contacto directo con la piel y quese manifiesta por la presencia de lneas de hebra es la:

a) Erisipelab) Escabiosisc) Pitiriasis albad) Paragonimiasis

e) Tia del cuerpo

La escabiosis o sarna es una enfermedad contagiosa producida porSarcoptes scabiei, el caro oarador de la sarna, caracterizada por prurito intenso de la piel y excoriaciones debidas al rascado. Elcaro, que se transmite porel contacto estrecho con seres humanos o animales domsticosinfestados, excava tneles en las capas externas de la piel, donde las hembras depositan sushuevos. De 2 a 4 meses despus de la primera infestacin comienza la sensibilizacin a los caros ysus productos, dando lugar a una erupcin papular pruriginosa. Pueden producirse infeccionesbacterianas secundarias.


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11. - In the treatment of dermatitis in the diaper area is essential:

a) Application of zinc pasteb) Abolition of contact with dirty diapersc) Addition of a topical corticosteroidd) Application of a topical antifungal

e) Application of a topical antibiotic

Diaper dermatitis, the most common form of primary irritant contact dermatitis seen in pediatricpractice, is caused by prolonged contact of the skin with urine and feces, which contain irritatingchemical such as urea and intestinal enzymes. Treatment consists of changing diapers frequently.

12 .- A man of 35 years represent a disseminated dermatosis on the face, trunk and extremities,flaccid blisters formed by burning and sparing normal surrounding skin. Additionally there areulcers in the mucous membranes. In the skin biopsy is intradermal acantholytic blister. Themost likely diagnosis is:

a) Pemphigoid

b) Epidermolysis bullosac) Pemphigus Vulgarisd) Pemphigus foliaceuse) Dermatitis herpetiformis

Pemphigus vulgaris (PV) is a blistering skin disease seen predominantly in elderly patients. Patientswith PV have an increased incidence of the HLA-DR4 and -DRw6 serologically defined haplotypes.This disorder is characterized by the loss of cohesion between epidermal cells (a process termedacantholysis) with the resultant formation of intraepidermal blisters. Clinical lesions of PV typicallyconsist of flaccid blisters on either normal-appearing or erythematous skin. These blisters ruptureeasily, leaving denuded areas that may crust and enlarge peripherally. Substantial portions of the bodysurface may be denuded in severe cases. Manual pressure to the skin of these patients may elicit the

separation of the epidermis (Nikolsky's sign). This finding, while characteristic of PV, is not specific tothis disorder and is also seen in toxic epidermal necrolysis, Stevens-Johnson syndrome, and a fewother skin diseases. Lesions in PV typically present on the oral mucosa, scalp, face, neck, axilla, andtrunk. In most patients, lesions begin in the mouth; involvement of other mucosal surfaces (e.g.,pharyngeal, laryngeal, esophageal, conjunctival, vulval, or rectal) can occur in severe disease. Pruritusmay be a feature of early pemphigus lesions; extensive denudation may be associated with severepain. Lesions usually heal without scarring, except at sites complicated by secondary infection ormechanically induced dermal wounds. Nonetheless, postinflammatory hyperpigmentation is usuallypresent at sites of healed lesions for some time. Biopsies of early lesions demonstrate intraepidermalvesicle formation secondary to loss of cohesion between epidermal cells (i.e., acantholytic blisters).Blister cavities contain acantholytic epidermal cells, which appear as round homogeneous cellscontaining hyperchromatic nuclei. Basal keratinocytes remain attached to the epidermal basement

membrane, hence blister formation is within the suprabasal portion of the epidermis. Lesional skin maycontain focal collections of intraepidermal eosinophils within blister cavities; dermal alterations areslight, often limited to an eosinophil-predominant leukocytic infiltrate. Direct immunofluorescencemicroscopy of lesional or intact patient skin shows deposits of IgG on the surface of keratinocytes; incontrast, deposits of complement components are typically found in lesional but not uninvolved skin.Deposits of IgG on keratinocytes are derived from circulating autoantibodies directed against cell-surface antigens. Circulating autoantibodies can be demonstrated in 80 to 90% of PV1 patients byindirect immunofluorescence microscopy; monkey esophagus is the optimal substrate for these studies.Patients with PV have IgG autoantibodies directed against desmogleins (Dsgs), transmembrane


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desmosomal glycoproteins that belong to the cadherin supergene family of calcium-dependentadhesion molecules. Such autoantibodies can now be precisely quantitated by enzyme-linkedimmunosorbent assay (ELISA). Most patients with early PV (i.e., only mucosal involvement) have onlyanti-Dsg3 autoantibodies; most patients with advanced disease (i.e., involvement of skin and mucosa)have both anti-Dsg3 and anti-Dsg1 autoantibodies. Recent studies have shown that the anti-Dsgautoantibody profile in these patients' sera as well as the tissue distribution of Dsg3 and Dsg1

determine the site of blister formation in patients with pemphigus. Experimental studies have alsoshown that these autoantibodies are pathogenic (i.e., responsible for blister formation) and that theirtiter correlates with disease activity. PV can be life-threatening. Prior to the availability ofglucocorticoids, the mortality ranged from 60 to 90%; the current mortality is approximately 5%.Common causes of morbidity and mortality are infection and complications of treatment withglucocorticoids. Bad prognostic factors include advanced age, widespread involvement, and therequirement for high doses of glucocorticoids (with or without other immunosuppressive agents) forcontrol of disease. The course of PV in individual patients is variable and difficult to predict. Somepatients achieve remission (40% of patients in some series), but others may require long-termtreatment or succumb to complications of their disease or its treatment. The mainstay of treatment issystemic glucocorticoids. Patients with moderate to severe disease are usually started on prednisone,60 to 80 mg/d. If new lesions continue to appear after 1 to 2 weeks of treatment, the dose may need to

be increased. Many regimens combine an immunosuppressive agent with systemic glucocorticoids forcontrol of PV. The most frequently used are either azathioprine (1 to 2 mg/kg per day), ormycophenolate mofetil (20 to 35 mg/kg per day), cyclophosphamide (1 to 2 mg/kg per day). It isimportant to bring severe or progressive disease under control quickly to lessen the severity and/orduration of this disorder.

13. - For the treatment of tinea capitis is indicated for use:

a) Shampoo with ketoconazoleb) Miconazole topical applicationsc) Oral Ketoconazoled) Oral mycostatin

e) Oral Griseofulvin

Dermatophytes are fungi that infect skin, hair, and nails and include members of the generaTrichophyton, Microsporum, and Epidermophyton. Tinea corporis, or infection of the relatively hairlessskin of the body (glabrous skin), may have a variable appearance depending on the extent of theassociated inflammatory reaction. It may have the typical annular appearance of "ringworm" or appearas deep inflammatory nodules or granulomas. Involvement of the groin (tinea cruris) is more common inmales than females. It presents as a scaling, erythematous eruption that spares the scrotum. Infectionof the foot (tinea pedis) is the most common dermatophyte infection and is often chronic; it ischaracterized by variable erythema, edema, scaling, pruritus, and occasionally vesiculation.Involvement may be widespread or localized, but almost invariably involves the web space between thefourth and fifth toes. Infection of the nails (tinea unguium or onychomycosis) occurs in many patients

with tinea pedis and is characterized by opacified, thickened nails and subungual debris. Dermatophyteinfection of the scalp (tinea capitis) has returned in epidemic proportions, particularly affecting inner-citychildren, but it also affects adults. The predominant organism is T. tonsurans, which can produce arelatively noninflammatory infection with mild scale and hair loss that is diffuse or localized. Localizeddisease may be well defined or irregular. T. tonsurans can also cause a markedly inflammatorydermatosis with edema and nodules. This latter presentation is a kerion. The diagnosis of tinea can bemade from skin scrapings, nail scrapings, or hair by culture or direct microscopic examination withpotassium hydroxide (KOH). Hair, nail scrapings, and scrapings from markedly inflamed skin may fail toshow hyphae on direct examination.


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Both topical and systemic therapies may be used to treat dermatophyte infections. Treatment dependson the site involved and the type of infection. Topical therapy is generally effective for uncomplicatedtinea corporis, tinea cruris, and limited tinea pedis. It is not effective as a monotherapy for tinea capitisor onychomycosis. Topical imidazoles, triazoles, and allylamines may all be effective topical therapiesfor dermatophyte infections. Haloprogin, undecylenic acid, ciclopirox olamine, and tolnaftate are alsoeffective, but nystatin is not active against dermatophytes. Topicals are generally applied twice daily,

and treatment should continue 1 week beyond clinical resolution of the infection. Tinea pedis oftenrequires longer treatment courses and frequently relapses. Oral antifungal agents may be required forrecalcitrant tinea pedis or tinea corporis with a nodular (granulomatous) component. Oral antifungalagents are required for dermatophyte infections involving the hair and nails and for other infectionsunresponsive to topical therapy. A fungal etiology should be confirmed by direct microscopicexamination or by culture prior to prescribing oral antifungal agents. All of the oral agents may causehepatotoxicity and should not be used in women who are pregnant or breast-feeding. Griseofulvin is theonly oral agent approved in the United States for dermatophyte infections involving the skin, hair, ornails. Itraconazole and terbinafine are approved for onychomycosis; however, the literature citesmultiple examples of their effective use in other dermatophyte infections. When griseofulvin is used, adaily dose of 500 mg of microsized or 350 mg of ultramicrosized griseofulvin administered with a fattymeal is an adequate dose for most dermatophyte infections. Higher doses are required for tinea pedis

and onychomycosis. The duration of therapy may be 2 weeks for uncomplicated tinea corporis or aslong as 6 to 18 months for nail infections. Due to high relapse rates, griseofulvin is seldom used for nailinfections. The usual adult dose of griseofulvin for tinea capitis is 1 g of microsized or 0.5 g ofultramicrosized given daily for 6 to 8 weeks or until cultures are negative. The adjunctive use of topicalantifungal agents may be useful, but topical therapy alone is not adequate for tinea capitis. Markedlyinflammatory tinea capitis may result in scarring and hair loss, and systemic or topical glucocorticoidsmay be helpful in preventing these sequelae. Common side effects of griseofulvin includegastrointestinal distress, headache, and urticaria. Oral itraconazole and terbinafine are approved foronychomycosis. Itraconazole is given as either continuous daily therapy (200 mg/d) or pulses (200 mgtwice daily for 1 week per month) administered with food. Fingernails require 2 months of continuoustherapy or two pulses. Toenails require 3 months of continuous therapy or three pulses. Itraconazolehas the potential for serious interactions with other drugs requiring the P450 enzyme system for

metabolism. Terbinafine (250 mg/d) is also effective for onychomycosis. Therapy with terbinafine iscontinued for 6 weeks for fingernail infections and 12 weeks for toenail infections. Terbinafine has fewerdrug-drug interactions, but caution should be used when patients are on multiple medications.

14.- Una mujer de 20 aos, en tratamiento con ibuprofeno porque padece tensin premenstrual,presenta un cuadro de dos das de evolucin manifestado por ppulas en zonas de pieleritematosa localizadas en la cara, la V del escote, los antebrazos y el dorso de las manos. Lapaciente refiere prurito y ardor en las zonas afectadas. El diagnstico ms probable es:

a) Fotodermatosisb) Eritrodermiac) Dermatitis de atpica

d) Neurodermatitise) Urticaria

Se trata de una dermatitis fotoalrgica que es una reaccin cutnea papulovesicular, eccematosa oexudativa que se produce de 24 a 48 horas despus de la exposicin a la luz en una personapreviamente sensibilizada. La sustancia sensibilizante se concentra en la piel y necesita experimentaruna alteracin qumica provocada por la luz para convertirse en un antgeno activo, al parecer elibuprofeno no tiene relacin con el padecimiento.


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15. - The blisters patients presenting with dermatitis herpetiformis is located at:

a) Subepidermalb) Dermisc) Stratum lucidumd) Stratum granulosum

e) Stratum basale

Dermatitis herpetiformis is a rare and fascinating entity characterized by urticaria and vesicles. Malestend to be affected more frequently than are females, and the age at onset is often in the third andfourth decades, although disease has been known to develop at any age after weaning. A majorassociation is with celiac disease; both the vesicular dermatosis and the enteropathy respond to a dietfree of gluten. The urticarial plaques and vesicles of dermatitis herpetiformis are extremely pruritic.They characteristically occur bilaterally and symmetrically, involving preferentially the extensorsurfaces, elbows, knees, upper back, and buttocks. Vesicles are frequently grouped, as are those oftrue herpesvirus, and hence the name herpetiform. The early lesions of dermatitis herpetiformis arehistologically characteristic. Fibrin and neutrophils accumulate selectively at the tips of dermal papillae,forming small "microabscesses". The basal cells overlying these microabscesses show vacuolization,

and minute zones of dermoepidermal separation (microscopic blisters) may occur at the tips of involvedpapillae. In time, these zones coalesce to form a true subepidermal blister. Eosinophils may occur inthe infiltrates of older lesions, creating confusion with the histologic picture of bullous pemphigoid.

Attention to the early alterations at the blister edge, however, usually allows separation of these twodisorders. By direct immunofluorescence, dermatitis herpetiformis shows granular deposits of IgAselectively localized in the tips of dermal papillae, where they are deposited on anchoring fibrils. Glutenis the protein moiety that persists subsequent to the removal of water and starch from defatted flour.Gliadin is a class of protein found in the gluten fraction of flour. Patients with dermatitis herpetiformismay develop antibodies of the IgA and IgG classes to gliadin and reticulin, a component of theanchoring fibrils that tether the epidermal basement membrane to the superficial dermis. In addition,individuals with certain histocompatibility types (HLA-B8 and HLA-DRw3) are particularly prone to thisdisease. It is thus thought that genetically predisposed persons may develop IgA antibodies in the gut

to components of dietary gluten and that these antibodies (or immune complexes) then cross-react orare deposited in the dermal papillae of the skin, resulting in clinical disease. Some individuals withdermatitis herpetiformis and enteropathy respond to a gluten-free diet (as with celiac disease).

16.- El tratamiento de eleccin para la tia de la cabeza en los pacientes peditricos es:

a) La nistatinab) El ketoconazolc) El fluconazold) La griseofulvinae) El clotrimazol

Las dermatofitosis o tias son infecciones micticas que afectan a la piel y estructuras queratinizadascomo pelos y uas. La tia del cuero cabelludo (tambin denominada Tinea capitis o Tinea tonsurans)es un tipo de tipo de tia no inflamatoria son propias de la infancia cursando con placas alopcicas conpelos rotos y descamacin. Por lo general, al llegar la pubertad suelen curar espontneamente sindejar cicatriz. El tratamiento de eleccin de la tia del cuero cabelludo en nios es la griseofulvina. Lagriseofulvina es de primera eleccin en el tratamiento de las tias por su bajo precio, pero nunca estindicada en el tratamiento de una candidiasis cutnea. Otros frmacos tiles en el tratamiento de lasdermatofitosis son los imidazoles y la terbinafina.


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17.- En los preescolares y escolares, la dermatitis atpica se localiza ms frecuentemente en:

a) Mejillasb) Cara posterior de cuelloc) Pliegues flexuralesd) Gluteos

e) Manos y pies

La dermatitis atpica es un trastorno inflamatorio de la piel de curso crnico y recidivante, cuyamanifestacin principal es un eccema pruriginoso y la piel seca que dan lugar a un rascado continuo ya la posterior liquenificacin de las lesiones. Suele debutar en la infancia pudindose distinguir tresfases segn la localizacin de las lesiones. En el lactante predominan las lesiones en cuero cabelludoy cara respetando el tringulo nasogeniano, en la infancia stas se localizan principalmente a nivel delas flexuras antecubital y popltea, mientras que en el adulto suelen aparecer en cuello, flexuras, dorsode las manos y en la cara.

18. - Age most commonly occurring in erythema nodosum:

a) 5 to 15 yearsb) 20 to 40 yearsc) 40 to 50 yearsd) Over 50 yearse) Infants under the age

Erythema nodosum is an uncommon reaction pattern seen mainly on the anterior tibial areas of thelegs. It appears as erythematous nodules in successive crops and is preceded by fever, malaise, andarthralgia. Bilateral red, tender, rather well-circumscribed nodules are seen mainly on the pretibialsurface of the legs but also on the arms and the body. Later, the flat lesions may become raised,confluent, and purpuric. Only a few lesions develop at one time. Careful clinical and laboratoryexamination is necessary to determine the cause of this toxic reaction pattern. The following tests

should be performed: complete blood cell count, erythrocyte sedimentation rate, urinalysis, serologictest for syphilis, chest roentgenogram, and specific skin tests, as indicated. The causes of erythemanodosum are streptococcal infection (rheumatic fever, pharyngitis, scarlet fever, arthritis), fungalinfection (coccidioidomycosis, trichophyton infection), pregnancy, sarcoidosis, lymphogranulomavenereum, syphilis, chancroid, drugs (contraceptive pills, sulfonamides, iodides, bromides), and, rarely,tuberculosis. The disorder occurs predominantly in adolescent girls and young women.

19. - What is the metabolic conversion of vitamin D in the skin:

a) Transformation of 7-dehydrocholesterol into vitamin D3b) Processing of vitamin D to 25-hydroxyvitamin Dc) Conversion of 25-hydroxyvitamin D to 1,25 dihydroxyvitamin D

d) Conversion of ergocalciferol cholecalciferole) Processing of vitamin D2 and 25-hydroxyvitamin D

The active transport of Ca2+ and PO43- from the intestine is increased by a metabolite of vitamin D.The term "vitamin D" is used to refer to a group of closely related sterols produced by the action ofultraviolet light on certain provitamins. Vitamin D3, which is also called cholecalciferol, is producedin the skin of mammals from 7-dehydrocholesterol by the action of sunlight. The reactioninvolves the rapid formation of previtamin D3, which is then converted more slowly to vitamin D3(cholecalciferol). In the liver, vitamin D3 is converted to 25-hydroxycholecalciferol (calcidiol, 25-OHD3).


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dermatología 1

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