papulo-erytroskuamosa kuliah sm vii edit.ppt

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dr. Luh Made Mas Rusyati, Sp.KK

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Page 1: Papulo-Erytroskuamosa kuliah  sm vII edit.ppt

dr. Luh Made Mas Rusyati, Sp.KK

Page 2: Papulo-Erytroskuamosa kuliah  sm vII edit.ppt
Page 3: Papulo-Erytroskuamosa kuliah  sm vII edit.ppt
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Difinition: recurrent, kronik, skin inflammatory ds with variations in clinical presentations

Belongs to dermatosis erythroskuamous lesionsmarked by increase in vascularization (erythema) and scales production in the epidermis

Universal, variations in incidence 0,1-11,8%

Highest incidence in Europe (Denmark 2,9%), no case has been reported from India

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Psoriasis may began at any ages Uncommon under the age of 10 years It most to appear between ages of 15

and 30 Christophers Divided into Type I

and II Type I before 40 yr and HLA

associated, type II after 40 yr, lacking HLA associated

No evidence that type I and type II respond differently to different therapies.

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Psoriasis Classification and Psoriasis Classification and Clinical Patterns of Skin Clinical Patterns of Skin

PresentationPresentation Psoriasis Vulgaris Eruptive (guttate) psoriasis Psoriasis eritrodermi Generalized pustular psoriasis (von

Zumbusch) Annular pustular psoriasis Localized pustular psoriasis

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4 Characteristics findings in psoriatic lesions:

1.Well-demarcated lesions2.Silvery, layered, rough scales at the

surface of the lesions 3.The skin are erythema and coiled

beneath the scales 4.Positive Auspitz sign

Koebner phenomenon presents in 20% cases

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LESION ON THE NAILS LESION ON THE KNEES

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Physical trauma Infections Stress Drugs

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DIAGNOSIS Anamnesis Clinical findings Histopathological

examinations

DD Seborrheic

dermatitis Pityriasis rosea Syphilis PRP

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Laboratory FindingsLaboratory Findings

Laboratory examinationsunspecific Histopathologic findings epidermal

and upper dermal changes Initial changes: oedeme of str

papillare of the dermis with mononuclear cells infiltrates and spongiosis

Late changes: neutrofil migration to the str korneum Munro’s microabcess

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PASI PASI ((Psoriasis Area and Severity Psoriasis Area and Severity

IndexIndex)) Badan dibagi 4 kuadran dgn bobot : Kepala (K=0.1), Badan (B=0.3), Ekstrimitas Atas (EA=0.2), Ekstrimitas Bawah (EB=0.4)

Area (A) yang terlibat diberi bobot : tidak ada=0, < 10%=1, 10-30%=2, 30-50%=3, 50-70%=4, 70-90%=5, 90-100%=6

Keparahan (S) diberi gradasi 0-4 Gejala klinis : Eritema (E), Infiltrat (I),

Deskuamasi (D) PASI = 0.1(EK+IK+DK)AK +

0.3(EB+IB+DB)AB + 0.2(EEA+IEA+DEA)AEA + 0.4 (EEB+IEB+DEB)AEB

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TreatmentTreatment

Treatment based on the extent and location of lesions, health problem.- lesions < 5% of the body topical drugs- lesions 5-10% of the body topical drugs + phototherapy/systemic drugs- lesions > 10% of the body phototherapy or systemic drugs

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TreatmentTreatment

Topical drugs :- Antralin (dithranol)- Vit D3 and analogues- Tazarotene- Tar- Topical corticosteroids- Emolient

Ultraviolet light- PUVA (Psoralen Ultra Violet A)- UVB

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TreatmentTreatment Systemic therapysevere cases with

extensive lesions or pustular or active psoriasis- Metotrexate (MTX)- Cyclosphorine- Retinoid- Esther Fumarat Acid- Glucocorticoids systemic- Macrolactam (Calcineurin Inhibitor)- Excimer Laser

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IntroductionIntroduction

Definition chronic dermatosis papulosquamous disease, associated with increase in sebum production (seborea)

Insidence 2 peaks, the first 3 month of life and 4th and 7th decade of adulthood with male preponderence

Clinical lesions on the scalp,, face, body parts with plenty of sebaceous follicle, varies in severity

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Seborrheic DermatitisSeborrheic Dermatitisin Infantsin Infants

Thick, oily crust on hairy scalp, crease area for examples on the retroauricular fold, ear peak, mid face, neck, chest

Sometimes accompanied by fissures (crusta lactea, milk crust, cradle cap)

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Desquamative Erythroderma Desquamative Erythroderma ((Leiner’s DiseasesLeiner’s Diseases))

Skin lesions quickly coalescence into wide lesions all over the body, erythematous, covered with scales erythroderma

Look severly ill, with anemia, diarrhea, and vomitting

Frequently followed by secondary infections

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Seborrheic Dermatitis Seborrheic Dermatitis in Adultin Adult

Seborrhoeic eczematid Pityriasis sicca Erythema paranasale Patchy dermatitis seborrhoeic Pityriasiform type seborrheic

dermatitis Folliculare type seborrheic dermatitis Chronic Otitis Media Blefaritis

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Triggering FactorTriggering Factor

Seborrhea Microbial impact Drugs Neurologic/neurotransmitter

dysfunction Physical factors Nutritional imbalance

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Diagnosis and Differential Diagnosis and Differential DiagnosisDiagnosis

Diagnosisanamnesis + clinical findings

DD/ in infant : atophic dermatitis, psoriasis, scabies, Langerhans Cells Histiocytosis

DD/ in adult depends on location : psoriasis, atophic dermatitis, impetigo, contact dermatitis, allergic reactions, pityriasis versikolor, pityriasis rosea, demodocosis/demodicidosis, candidiasis

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TreatmentTreatment

Aim: releasing the scales, inhibiting yeast colonization, preventing secondary infections, reducing pruritus and oedeme

Treatment depends on the location of the lesion

Some therapeutic modalitiesantifungal, topical

Steroid topikal

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PrognosisPrognosis

Infantgood prognosis, mostly mild and healed spontaneously

Adultchronic disease, treatments for reducing symptoms and not for healingpatients education

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IntroductionIntroduction

The term first used by Gilbert in 1860 Definition: common, acute, self-limited

skin eruption that typically begins as a single thin oval scaly plaque on the trunkherald patch

Followed by numerous similar-appearing smaller lessions along the lines of cleavage of the trunkchristmas tree pattern

Usually asymptomatic, sometimes associated with pruritus and mild flu-like symptoms

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EpidemiologyEpidemiology

Reported in all races, irrespective of the climates

Average annual incidence: 0,16% Occurs most commonly in teenagers

and young adultbetween 10-35 years old

Slight female preponderance 1.5:1 Recurrences are raresuggests

lasting immunity after initial episode

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Etiology and Pathogenesis Etiology and Pathogenesis

Historically pityriasis rosea has been considered to be caused by an infectious agent

Scientific evident theory that pityriasis rosea represents a viral exanthem associated with reactivation of human herpesvirus (HHV-7) and (HHV-6)

The mech of reactivation is unknown The characteristic distribution of the

lesions are unexplained

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Clinical FindingsClinical Findings

Historysingle truncal lesion followed by numerous smaller lession in several days to weeks later, asymptomatic-pruritic, flu like symptoms

Cutaneous lesions: - herald patch well demarcated, Ø 2-4 cm, oval/round, salmon coloured, with fine scales- secondary lesions small plaque resembling primary plaque with christmas tree pattern or small, red, non-scaly papules spread peripherally

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Differential DiagnosisDifferential Diagnosis

Secondary syphilis Tinea corporis Nummular dermatitis Guttate psoriasis Pityriasis lichenoides chronica Pityriasis rosea – like drug eruption

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TreatmentTreatment

Self-limited Education dan reassurance Pruritic lesion topikal

corticosteroids medium potency Flu-like symptoms and extensive

lesions acyclovir oral 5 x 800 mg for a week

Special considerationphototherapy

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Prognosis andPrognosis andClinical CourseClinical Course

All patients have spontaneous resolutions

Disease durations 4-10 weeks No residual effects secondary to

occurance of pityriasis rosea Reccurency is possible, but rare

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IntroductionIntroduction

Exfoliativa dermatitis, exfoliativa erythroderma, Red Man syndrome

Definitioninflammatory skin ds with erythematous and scales formation all over the body either idiopathic or caused by extention of other skin ds (psoriasis, atophic dermatitis, drug eruption, cutaneus T-cell lymphoma)

almost 50% associated with underlying ds

25% idiophatic

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EpidemiologyEpidemiology

Rare case male : female = 2:1 to 4:1 Average age of onset are 40-60 years

old, but can also affecting neonates and infants

In the adulthood mostly related to psoriasis, atophic dermatitis, drug eruption, idiophatic

In neonates and infants mostly caused by atophic dermatitis, seborrheic dermatitis, drug eruption, psoriasis, infections (for example Staphylococcal Scalded Skin Syndrome)

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EtiopathogenesisEtiopathogenesis

Pathogenesisunclear Increase in germinativum cells mitosis

and shortening of functional epidermal keratinization

Increase in scales degradation rate Increase in vascular endothelial growth

factor/vascular permeability factorincrease in permeability and vascularization

Increase in adhession molecules expressionaffecting production and proliferation of inflammatory mediators

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EtiopathogenesisEtiopathogenesis Drug eruption eritroderma: alopurinol,

ampisillin/amoxcysilin, dapson, carbamazepine, fenbarbital, sulfonamide, Ca-channel blockers, simetidine, gold, obat tradisional

Eritroderma ec systemic disease : malignancy (solid tumor and haematologic), infection (syphillis, HIV)

Psoriatic erythroderma : effect of the disease, corticosteroid, methotrexate, phototherapy, lithium, pregnancy, infection

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Clinical ManifestationClinical Manifestation Eritema generalisata, 90% with scales

formation, without affecting the mucousa Acute: erithemawhite/yellowish fine

scales starting in flexures areaforming platelike leson on the palmsgrey, dry scales, with light red skin lesions

Secondary infections: wet lesions, tightly adherent scales, bad odour caused by colonization of bacteria

Chronic: thick skin and nails, induration, oedeme and lichenifications, hair fall, subungual hyperkeratosis, onykilosis, beau lines of the nails

Drug eruption: shoreline feature in the nails

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Clinical ManifestationClinical Manifestation Primary type(idiopathic)erythem starts

in the trunk, spreading with scales production mostly in old man, chronic, relaps, severe pruritus, limfadenopati, dermatopati, extensive keratoderma palmoplantarRed Man Syndrome

Secondary typewith associated underlying ds- topical drug eruption: initial lesion as dermatitis- systemic drug eruption: initial lesion morbiliformis/skarlatiniformis-2/3 histopathologic findings are consistent with underlying ds- exacerbation occurs in lesion with sunlight exposure

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Systemic Findings in Systemic Findings in ErythrodermaErythroderma

62% cases present with axillaris and inguinalis limfadenopati, >37% hepatomegaly, 23% splenomegaly

Poikilothermia Decrease in systemic blood flowheart

failure 80% cases presents with fever and

tachycardia Dehidration Increase in blood ureum level Protein loss dan nitrogen, potassium,

folate imbalancehipoalbuminemia, oedeme, reduce in muscle mass

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Commonly find erythroderma

Psoriasis Athopic

dermatitis Drug eruption Idiophatic

Rare form of erythroderma

Cutaneus T-Cell Lymphoma (CTCL)

Pitiriasis Rubra Pilaris (PRP)

Dermatosis Bulosa- Pemfigus foliaseus- Pemfigoid bulosa- Pemfigus paraneoplastik

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Laboratory FindingsLaboratory Findings

Anemia, limfositosis, eosinofilia, increase in ESR (erythrocyte sedimentation rate)

Decrease in serum protein Decrease in electrolytes and renal

function Increase in IgE serum Sezary Syndrome>20% sel Sezary Erythroderma idiophatic bone

marrow biopsy: eosinofilia (32%)

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Pathologic ExaminationsPathologic Examinations

Multiple consecutive biopsy needed

Erythroderma psoriatic histopathologic findings have >90% accuracy, but in erythroderma associated with CTCL histopathologic examinations are difficult

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TreatmentTreatment Adequate nutrition, fluid and electrolytes

balance, high protein diet, folic acid supplementation

Warm and moist environmet Hospitalizationsevere cases, observation

in fluid intake and renal function, possibility of cardiac failure

Supportive skin careemolient, weak to mid potency topical corticosteroids

Antibiotics for bacteria superinfections, antihistamin and behavioural therapy to decrease itch and scratch

Consider corticosteroids and immunosuppresant therapy in severe/refracter cases

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IntroductionIntroduction

Definition unique, common inflammatory disorders efecting skins, mucous membranes, nails, hairs

Lessions symmetric, grouped, erythematous-violaceous, flat-topped, polygonals papules

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EpidemiologyEpidemiology

Overall prevalence less than 1% worlwide

2/3 of the cases occur between 30-60 years old

No sexual predilection is evident Predilection in flexural aspects of

arms and legs Familial lichen planus have been

reported

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Etiology & PathogenesisEtiology & Pathogenesis

Lichen planus almost certainly immunological mediated

The most characteristic change in lichenoid reactionsapoptosis

Cell-mediated immunity plays major role

Humoral immunity as a secondary response

Both CD4+ and CD8+ T cells are found in the skin lesions

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Clinical FindingsClinical Findings

Cutaneous lessions:faintly erythematous –violaceous, flat-topped, polygonal papules

Thin, transparent, adherent scales at the top

Wickham striae Lessions are symmetrically and

bilaterally distributed over the extrimities

Asymptomatic-quite pruritic

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Histopathologic DiagnosisHistopathologic Diagnosis

Major pathologic findings basal epidermal keratinocyte damage

Epidermal changeshyperkeratosis, hypergranulosis, elongation of rete ridges

Multiple apoptotic bodies or colloid-hyaline (Civatte) bodies at dermal-epidermal junction

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Differential DiagnosisDifferential Diagnosis Classic: psoriasis, drug eruption, lichen

simplex chronicus Annulare: granuloma annulare, tinea Linear: nevus unius lateris, lichen

striatus, linear epidermal nevus Hypertrophic: lichen simplex

chronicus, prurigo nodularis, lichenoid cutaneous, amylidosis, kaposi sarcoma

Atrophic: lichen sclerosus Follicular: lichen nitidus, lichen

spinulosus Childhood: lichen nitidus, lichen

striatus, pityriasis lichenoides, papular acrodermatitis of childhood

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TreatmentTreatment Cutaneous Lichen planus

- first line: topical topical steroids, intralesional

steroids, tacrolimus, pimecrolimus

physical psoralen and UVAsystemic systemic steroids, etretinate,

acitretin, isotretinoin

- second line (systemic): cyclosporine, dapsone, hydroxychloroquine, azathioprine

- special forms (systemic): doxycycline, tetracycline, nicotinamide, interferon α-2b, metronidazole, cyclophosphamide, methotrexate

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TreatmentTreatment Oral Lichen Planus

- first line: topical topical steroids, intralesional steroids,

tacrolimus, pimecrolimus, lidocaine, tretinoin gel, isotretinoin gel

systemic anti candidal-systemic steroids, etretinate, acitretin, isotretinoin - second line :

topical cyclosporine mouthwashphysical extracorporeal photochemotherapy,

photodynamic therapy systemic cyclosporine, griseovulfin,

hydroxychloroquine, azathioprine, mycophenolate mofetil, thalidomide, cyclophosphamide