Download to read offline
Lectureำนำนกวสหสหสกสกสกสสกสกสกสกสกสสกสกสกสกสหสหสหส
- 1. Purit Pureesrisak, MD Divisionof Dermatology, Department of Medicine, Rajavithi Hospital, Ministry of Public Health often GannG
- 4. Outline • Terminology anddescribe lesion • Dermatitis and eczema • Urticaria • Dyshidrosis • Miliaria • Sexually transmitted diseases • Leprosy • Erythema multiforme /SJS/TEN • Erythema nodosum
- 5. Primary lesion blesimainan Intoe eiE banence bqee. m pn i ga hterfEii. l.int
- 6. Primary lesion 62s but ahemtr.net roseby I 2 mar iit.is 077m V1 4
- 7. Primary lesion f pub www.msaswomtt.c Gone 006.000 19thtobutafzuiydip.pe Come 90 Me 6ⁿ no 6 WE
- 8. Primary lesion c TE distant C pDS breenivend c Coins LACI W 960
- 9.
- 10. Secondary lesion he g analysing www.go.it fi Thefull the listof epiden I horns non beds
- 11.
- 12.
- 13.
- 14. PI i in i t.ph Primelesinaviarpa put them 2 a igli string ones 6 assist
- 15.
- 16.
- 17.
- 18. Eczema/ Dermatitis Inflammation ofthe skin characterised by itching, redness, scaling and clustered papulovesicles.
- 19.
- 20. Stages of eczema •Acute eczema: there is erythema, minute papules and vesicles which may rupture leading to oosing and crust formation. • Subacute eczema: edema and vesiculation are less apparent while papules, erythema and some scales are predominant • Chronic eczema: no oosing or crusting are present. The skin is dry, scaly and may be fissured. The repeated attacks of pruritic skin may lead to lichenification which means: thickening, hyperkeratosis, hyperpigmentation and increased skin markings. Into iii 6st sept 3sta if piiind089 ua cuetwb 17 c stinarians 84 21 152 p athperpigment ar Enn Cha F ftp.fifg 042m 052 84msec Whperpigmatan a crest
- 21. Acute eczema aug 7 again 0122verydokubniygddlutfaugrapefves.de loutails terpressler 9 Lalu detecting Else mold
- 22.
- 23.
- 24. Classification of eczema Endogenouseczema Exogenous eczema • Atopic eczema • Seborrheic eczema • Discoid eczema (Nummular) • Pityriasis alba • Stasis eczema • Asteatotic eczema (Xerotic) • Dyshidrosis (Pompholyx) • Prurigo nodularis • Lichen simplex chronicus • Irritant contact dermatitis • Allergic contact dermatitis • Photodermatitis mm mm i C an ii tii l figy g i fgfgg.MIL ii Ji
- 25. At.pl Atty a unionink gas 25dg 0 thenod sold Mum
- 26.
- 27. Treatment of eczema •Correction of underlying factors Avoidance of exposure to sensitizers and solvents, treatment of varicose veins, foci of infection, hot water etc. • Broad spectrum antibiotics if secondary infection • Oral antihistamines • Topical corticosteroids of appropriate strength for the patient's age and affected area twice daily for days. Creams are used for acute and subacute cases and ointments for dry chronic cases • Topical emollients as vaseline for dry skin and in chronic cases • Topical immunomodulators: tacrolimus ointment 0.03% or pemicrolimus 1% cream twice daily • Short course of systemic steroids in acute, severe and wide spread cases • Ultraviolet rays therapy with PUVA and narrowband UVB (NBUVB) a mmesiit.tn ii irkatf GE and in 322 steroid 26Jakewas 118mmol be aging if a band agg unto use but if adamantasion ellulity iffunnair
- 28.
- 29. Atopic dermatitis • 15–20%in early childhood • Major features - Pruritus - Eczematous dermatitis (acute, subacute, or chronic) with typical morphology and age specific patterns Facial and extensor involvement in infancy Flexural eczema/lichenification in children and adults - Chronic or chronically relapsing disorder - Personal or family history of atopy (allergic rhinitis, asthma, atopic dermatitis) 2fleea AP Ctropil iffanis to animator I80 maintain childhood a CC in infant 653 angina tidily
- 30.
- 31.
- 32.
- 33.
- 34.
- 35. • Frequently affectschildren and adolescents with AD • Multiple ill-defined hypopigmented macules and patches (usually 0.5 to 2 cm in diameter) with fine scaling, which are typically located on the face, shoulders and arms. • Following sun exposure • Treatment : topical steroid , sunscreens Pityriasis alba Emo AP 1500258 5N 96 ancestor if g Indus Asteroid Pitunyiu.vetoo
- 36.
- 37. Seborrheic dermatitis • 1-3% of adult population (23% in elderly) • Chronic, multifactorial (endogenous and exogenous factor) • Inflammatory response to Malassezia yeast Ñ 2iwv 1 1 gang 10T Solders prep essen iiii.IE
- 38. Seborrheic dermatitis :Clinical • Mild form of scaling limited to the scalp (dandruff) • Poorly demarcated erythematous patches with greasy scaling • Location : scalp, nasolabial folds, ears, eyebrows, anterior chest, or upper back malaise a dinner no and Invert is Unu Sebastien Clegg
- 39. Seborrheic dermatitis :Risk factor • Older age • Male sex • Obesity • Stress depression • Winter climate • Alcohol consumption, tobacco exposure • Hypertension • HIV • Neurologic disease (Cerebrovascular event and Parkinson disease) r H aaw th
- 40.
- 41. Seborrheic dermatitis :Treatment •Life style management • Topical drugs - Corticosteroids - Shampoos and topical antifungals - Calcineurin inhibitors in a tritt that on To sled ea 1 molasserio wey anionrota Crm but I
- 42.
- 43. Stasis dermatitis • Stasiseczema, hypostatic eczema, varicose eczema • Associated with the lower extremities in long-standing venous insufficiency • Can be complicated by allergic contact dermatitis - Topical antibiotics, lanolin, emulsifiers, paraben, iodine, balsam of Peru , fragrances, chemical of plant origin an retiring among
- 44. Stasis dermatitis :Clinical • Bilateral circumferential dermatitis of the ankle and calf areas • Triad : alopecia, waxy appearance, and yellow- brown pigment from hemosiderin deposition • Complications : ulcer, cellulitis or lymphangitis IGma a 8 yellenbrin a denftenaid.mn
- 45. Stasis dermatitis :Treatment • Compression therapy - Stocking, elastic bandage • Topical steroid • Emollient co staeon
- 47. Xerotic eczema • Asteatoticdermatitis, eczema craquele • Skin disease the most frequently diagnosed in the elderly • Common in the elderly but can be seen in any age group • Associated with cutaneous loss of lipids, transepidermal water loss • Common in winter in inside btrare 2 Wow 0771N bob
- 48. Xerotic eczema :Clinical • Desquamation, erythema, fissuring, and pruritus • Polygonal erythematous fissures separating plates of dry scaly skin, sometimes described as “cracked porcelain,” “crazy pavement,” or a “dry riverbed” • Location : most often on the anterolateral portion of the lower legs fation f1t .tk i i adult
- 49. Extensive xerotic eczema •Should be investigated for internal malignancy, such as malignant lymphoma • On a diuretic • General dryness of the skin >> atopic eczema, chronic renal or liver failure, AIDS, myxedema, and in malabsorption especially of vitamin A or zinc C pantsuit 11 295 0552
- 50.
- 51.
- 52. Dyshidrosis(Pompholyx) • Most commonamong adolescents and young adults • Deep-seated vesicles on the palms, the lateral aspects of the fingers and soles • “Tapioca” appearance • Itching • Secondary bacterial infection is common 0tG 91 no 85502
- 53.
- 54. Nummular eczema • Achronic disorder of unknown etiology • Papules and papulovesicles coalesce to form nummular plaques with oozing, crust, and scale • Most common sites of involvement are upper extremities, including the dorsal hands in women, and the lower extremities in men. I crine
- 55.
- 56. Prurigo nodularis • Apruritic disorder that runs a chronic course • Hyperkeratotic firm nodules vary in size from 0.5 to 3 cm and may be excoriated • Associations include atopic dermatitis, or systemic causes of pruritus c ftp.G C Lan
- 57.
- 58. Lichen simplex chronicus •A chronic, severely pruritic disorder characterized by one or more lichenified plaques • Most common sites of involvement are scalp, nape of neck, extensor aspects of extremities, ankles, and anogenital area lictimist Shinchstemoning
- 59.
- 60. Allergic contact dermatitis •Cell-mediated (type IV), delayed type hypersensitivity reaction • Clinical manifestation of ACD is an eczematous dermatitis (acute, chronic) • The hands, feet, and face (including the eyelids) are some of the common sites for ACD M 11W inardaladalaithner y i ñ Fiurio
- 61. Allergic contact dermatitis avw.mh tpeJtnninsurin ir aic C.e.am iifi 2022604 s 3ndaug
- 62. Irritant contact dermatitis •Nonimmunologic inflammation of the skin caused by contact with a chemical, physical, or biologic agent • 80% percent of contact dermatitis is irritant and is commonly related to occupation • Atopic dermatitis is a major risk factor for irritant hand dermatitis N Yift 1 Who 470 ptysigatomialla.us 8211429 p GerminG looioni twifordtwfai.sn Cotcldematii I
- 63. Irritant contact dermatitis Acute Patchtesting should be performed in cases with suspected chronic irritant dermatitis to exclude an allergic contact dermatitis Chronic a feminine ms Vinny 002 6110 row i suddennial Elina oppitch
- 64.
- 65. Miliaria • From disruptionof sweat ductal integrity • Ultraviolet light exposure, resident organisms on skin, and repeated sweating episodes are facilitating factors • Common in infants and warmed environments • Subsides within a day moshi dearie Milian US Milio Tone sweatdish Cloud wnlooonnio m.ie Tourisick lifinson 101m 400 2 aug monsoon nN 2mi
- 66.
- 67.
- 68.
- 69. Urticaria and angioedema •Urticaria : itchy well demarcated reddish evanescent swellings of the skin (wheals) and flare • Angioedema : swellings of deep dermal and subcutaneous/submucosal tissues. Swellings are painful rather than itchy, poorly defined and pale or normal skin colored. flavono It'sb 200 Pro Inn Fem IEY.EE 881 11 n if angioedema butbvavityettaifh.gs
- 71. Urticaria : pathophysiology •Allergic : histamine is an important mediator in urticaria. Mast cells are the major histamine releasing cells in the skin. Allergens react with IgE molecules which are bound to the surface of mast cells leading to mast cell degranulation and release of histamine and other mediators. This results in local increase of permeability of capillaries and venules. • Non allergic : direct degranulation of mast cells occurs without antigen antibody reaction due to the effect of substances like - aspirin, neuropeptides, nonsteroidal anti-inflammatory drugs (NSAID), opiates, ciprofloxacin, polymixin, rifampicin and vancomycin we Unreamestrellor histamine 4128841022 Tomiskell Efs Gouldroscions has i.ie i i 10220 trainman mistreat 2 pathing
- 72. Causes of urticaria 1-Food: food additives or preservatives, fishes, banana, nuts, eggs, chocolate and cheese. 2- Drugs: aspirin, NSAIDs, antibiotics eg; penicillin..etc 3- Inhalants: pollens, dust or animal fur 4- Intestinal parasites 5- Stress 6- Septic foci eg; in teeth, tonsils or urinary tract 7- Physical causes: heat, cold, water, vibration, sunlight or pressure 8- Cholinergic urticaria: is a specific type in which small weals occur in association with sweating due to heat or emotional stress 9- Insect bites or stings 10- Contact urticaria eg; occupational exposure 11- Medical causes: like hepattitis, obstructive jaundice and Helicobacter pylori infection 12- Serum sickness I analata PUawidaiauiwonvessoo.tl02TUiwodr worse a É in fdt panwodamide provaana ita arrannigtiitiFet 27109 onnankiaci.us
- 73. Acute VS Chronicurticaria • Acute : present continuously or intermittenly for less than 6 weeks • Chronic : present for at least 6 weeks or more. When no underlying cause is identified it is termed chronic idiopathic urticaria. cai wt
- 74. Urticaria: treatment 1-Treatment ofthe cause if possible 2- AntiH1 antihistamines are the first line of treatment: - traditional classic antiH1 eg; chlorpheneramine maleate, diphenhydramine, and hydroxizine - non sedating antiH1: cetrizine hydrochloride, loratadine, fexofenadine, desloratadine and acrivastine 3- AntiH2 antihistamines may be needed in addition to antiH1 eg; cimetidine and ranitidine 4- Systemic drug 5- Locally: calamine lotion is used for soothing the sensation of pruritus. 6- In angioedema: distressing the respiratory passages from oropharyngeal-laryngeal edema; epinephrine (adrenaline) in 1/1000 solution is the first line of management. It is given subcutaneously in a dose ml. -
- 75.
- 76.
- 77.
- 80.
- 81. Syphillis A disease causedby the spirochete Trepomena pallidum subspecies pallidum 1. Primary stage, characterized by a chancre 2. Secondary stage, characterized typically by skin eruption(s) with or without lymphadenopathy and organ disease 3. A latent period of varied duration, characterized by the absence of signs or symptoms of disease, with only reactive serologic tests as evidence of infection 4. Tertiary stage, with cutaneous, neurologic, or cardiovascular manifestations prime syphil Iis
- 82.
- 83.
- 84. Secondary Syphillis Prodomal symptoms Generalizedlymphadenopathy (50-85%) Skin manifestatons - Early (10%): generalized eruption; non-pruritic, roseola-like, discrete macules - Late (70%): generalized maculopapular and papulosquamous eruptions – Palms and soles: symmetric papules and plaques with a collarette of scale (Biett collaretes) – Anogenital area: condyloma lata – Seborrheic area: “corona veneris” along the hairline Mucous membrane (30%) - Mucous patches Patchy alopecia (7%) “moth-eaten” localized areas of hair loss c Try so mean a batwar 6 note it 202 c Ic t.tn iwyTtge Sous 14200 Morph in mi c iiiii an iffaint pole s le
- 85.
- 86.
- 87.
- 88.
- 89.
- 90.
- 91. Syphillis milliontoo If 2211ft noakmiaiei.FI g for ifeng.rem.net y ne.to ii.ftaE i honour birdtoot if wea 54 I metin today I atan total Listing
- 92.
- 93.
- 94.
- 95.
- 96.
- 97. Gonorrhea : DGI 2naNIINONT.in 8ai i 1242224526C Gilliminedgentle than 9 Trial in mintg.to rtnritti Gi tarkbdinnot
- 98. Gonorrhea S4 Gore itwmadavauavinty.be septi at hits a it was une anzhecritic1211420654 feeling it is Effi c
- 99.
- 100.
- 101.
- 102.
- 103.
- 104. Leprosy Winalidmay 9 TE 1821isno Iwa TWioe atcans eye aizshrmllenee.IE
- 105. Leprosy 61 or tthe differentiation must2
- 106.
- 107.
- 108.
- 109.
- 110. Leprosy Éuaap man as has a aeFE Drow Ein C 2ⁿᵈ if toolepry Jiff qq.gg ff
- 111.
- 112.
- 113.
- 114. Erythema multiforme Ematecatizuucuriioidgain.ca what ify t necting Emg 51 bvtorurticaicerecet.int ysunoodTfecation Yvan wrong www in n tiiifi ME tupian 12tbiatiieyginnn.am C man at Bataanbutumanadaina talmwnwobutoroslitsns.sk
- 115.
- 116.
- 117. Erythema multiforme em tagetlesion my32m A n mnE
- 118.
- 119. Stevens-Johnson syndrome/toxic epidermal necrolysis(SJS/TEN) - Mortality rate for SJS 1- 5 %, TEN 25–35 % - Variants of epidermal necrolysis - They occur 4–28 days after drug exposure - Mycoplasma pneumoniae, Herpes simplex virus was recognized in several cases of SJS, especially in children - Factors that seem to impact on the incidence of SJS and TEN: the genetic background of patients (HLA, metabolizing enzymes), the coexistence of cancer, concomitant radiotherapy, and certain infectious diseases (e.g., HIV) Lancet,Vol 390 October 28, 2017 4T off death mag egg ale amazing bairnsamidst fEugnm.gg epidermenecrolies qt da.lu epidemtnEt ifeaemeepidermislaio
- 120. Stevens-Johnson syndrome/toxic epidermal necrolysis(SJS/TEN) : Clinical presentation - Early : fever, influenza- like illness, ocular symptoms, ear, nose, and throat - Initial lesions : erythematous, irregularly shaped, dusky-red macules. Atypical target lesions Harr and French Orphanet Journal of Rare Diseases 2010, 5:39 Iii right money.name mppI Tonicepiderminy Cb mail it t.ie
- 121. Stevens-Johnson syndrome/toxic epidermal necrolysis(SJS/TEN) : Clinical presentation Atypical target lesions in SJS Typical target lesions in erythema multiforme Trxicepidermalnav.lyg TriaieGEEIa. h a ne Elow
- 122. Stevens-Johnson syndrome/toxic epidermal necrolysis(SJS/TEN) : Clinical presentation dya fifteen
- 123. Stevens-Johnson syndrome/toxic epidermal necrolysis(SJS/TEN) : Clinical presentation - Necrotic lesion confluence leads to extensive erythema, flaccid blisters, and large epidermal sheets - Nikolsky sign m brinating into
- 124. Stevens-Johnson syndrome/toxic epidermal necrolysis(SJS/TEN) : Clinical presentation - 80% of cases : erythema, blisters, or erosions involve the nasopharynx, oropharynx, eyes, genitalia, or anus mucous membranes Harr and French Orphanet Journal of Rare Diseases 2010, 5:39 1 Gate and a shin mussa rindouf In genitalia 1101non
- 125.
- 126.
- 127.
- 128.
- 129.
- 130.
- 131.
- 132.
- 133.
- 134. Erythema nodosum Clinical • Symmetric,tender, erythematous, nodules, and plaques on the anterior aspects of the lower extremities • Acute onset; no ulceration or scarring • Fever, fatigue, arthralgias, arthritis, headache are common • More common in women • Lasts from 3 to 6 weeks, with new lesions appearing for up to 6 weeks tanniality gs't.to Easontw hy g Byan yyppy.name I EI µ W una iii win rain Union EA 8111214844 phanngiti.TMUE.nl
- 135. Erythema nodosum Etiology • Infections,medications, malignancies, autoimmune disease, and inflammatory disorders have all been documented to provoke the clinical findings of EN • Infectious causes include bacterial, viral, fungal, and protozoa, with streptococcal respiratory tract infections being the most common etiology in pediatric cases of EN • Idiopathic cases of EN (37% to 60%) 1 7 91 EN Eutheranoulestly g 2kg Te draw Eis T.name ii.t
- 136.
- 137.
- 138.
- 139. Erythema nodosum Treatment • Treatmentof any associated disorder • Bed rest, aspirin, nonsteroidal antiinflammatory drugs mniÉ iii DI Mannv15